COLUMBIA LIBRARIES OFFSITE .HEALTH SCIENCES STANDARD r-Ao o HX64121429 C46.St811901 A text-book of medic THE LIBRARIES COLUMBIA UNIVERSITY |Eil iijiJ[rm3frm]rnAlfruiifRn]fr^ i 1 1 I 1 1 i I 1 1 i HEALTH SCIENCES LIBRARY )Ei riAJfiifnfrinlf|irgnuflfrOT3rfOi^ Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons http://www.archive.org/details/textbookofmediciOOstr A TEXT-BOOK OF MEDICINE FOR STUDENTS AND PRACTITIONERS BY Dr. ADOLF STRUMPELL PROFESSOR AND DIRECTOR OF/'flfHE MEDICAL CLINIQUE AT THE UNIVERSITY OF ERLANGEN Ublrb Hmerican BDition « TRANSLATED BY PERMISSION FROM THE THIRTEENTH GERMAN EDITION, BY HERMAN F. VICKERY, A. B., M. D. Instructor in Clinical ^Medicine, Harvard University ; Visiting Physician to the Massachusetts General Hospital ; Member of the Association of American Physicians ; Fellow of the Massachusetts Jledical Society, etc. AND PHILIP COOMBS KNAPP, A.M., M. D. Ex-President of the American Neurological Association ; Chnical Instructor in Diseases of the Nen'ous System, Han/ard University ; Physician for Diseases of the Nervous System, Boston City Hospital ; Fellow of the Massachusetts Medical Society, etc. WITH EDITORIAL NOTES BY FREDERICK C. SHATTUCK, A. M., M. D. Jackson Professor of Clinical Medicine, Harvard University ; Visiting Physician to the Massachusetts General Hospital ; Member of the Association of American Physicians ; Fellow of the Massachusetts Medical Society, etc. WITH ONE HUNDRED AND EIGHTY-FIVE ILLUSTRATIONS IN THE TEXT, AND ONE PLATE NEW YORK D. APPLETON AND COMPANY 1 90 1: >c Stf/ Copyright, 1886, 1893, 1901, By D. APPLETON AND COMPANY. All rights reserved. Electrotyped and Printed AT THE ApPLETON PreSS, U. S. A. AUTHOR'S PREFACE TO THE THIRTEENTH EDITION The extent to which my text-book has been used, both in Germany and in other countries,* justifies me in the assumption that it has exercised some little influence upon the professional thought and practice of numerous medical read- ers, and imposes iipon me the obligation of employing everj'- opportunity for the improvement and perfection of my work. Yet I must confess that this task seems more difficult to me with every new edition of the book, for scientific workers are making deep and extensive investigations into the many subdivisions of internal medicine, with such zeal and skill that it becomes difficult for any one man to keep step with the unceasing progress of investigation in this wide domain, and to maintain that complete and universal command of facts and theories which is essential for a presentation of the subject, which shall be at once brief and true to the present standpoint of science. The author has often been painfully sensible of these limitations of his personal knowledge and ability, but he hopes that this will be regarded not merely as subject for criticism, but also as an excuse and an incentive to clemency, in case a reader who is expert in any specialty finds here and there an omission or an error. Above all, I beg the reader to consider that no text -book such as the present one ought to replace, or could replace, the vast material of the larger reference books. My purpose was not to collect all the facts of pathology which have been discovered up to date, nor all the methods of treatment which may have been recommended, wisely or unwisely, nor all the theories or views which have been propounded. My wish was to give a complete presentation of the essentials of our present knowledge and views with regard to the various diseases, from a scientific and individual stand- point ; and I desired particularly to impart to the reader an insight into the origin and relation of the various morbid phenomena. To this end I have brought the facts of clinical experience into the closest possible relation with the data of path- ological anatomy and of general pathology, and have endeavored, also, in discuss- ing therapeutics, to deduce from the nature of the symptoms a basis for rational medical opinion and treatment, although I have not undervalued the importance * So far as I have been informed, translations of my text- book have appeared in the following lan- guages : French, English, Italian, Spanish, Russian, modern Greek, Turkish, and Japanese ; and some of these translations have had several editions. iii iy AUTHOE'S PEEFACE of simple experience. A text-book intended for students and a larger circle of graduate readers ought not to incline too decidedly toward any one of tlie pre- vailing currents of scientific opinion. It should, however, acquaint the reader to such an extent with the questions at present under discussion relating to internal medicine, as to give him at least a fair start in his further studies. The author has made an honest effort to bring the present thirteenth edition of this book up to the level of contemporary medical thought and knowledge. Large portions of the book have been almost completely rewritten — in particular, the whole doctrine of gastric diseases and several chapters in other sections, in- cluding gall-stones, intestinal parasites, etc. Almost all portions of the book have received numerous additions and improvements, so that this edition may be said with justice to be completely revised. That even now my work is imperfect I am well aware. I shall, therefore, be thankful to any one who will inform me of the mistakes or omissions he discovers. A. Strumpell. TEANSLATORS' PREFACE The work of Professor Striimpell has been so long familiar that it is hardly necessary for the translators to introduce it again to the English-speaking por- tion of the medical profession or to express again their admiration of the work. Since the second edition of this translation was published in 1893 seven new editions have appeared in Germany, so that the book has been almost wholly re- written, although it still retains all the merits of the earlier production, with the advantage of being ixdly in line with the most recent medical investigations. The translators have kept as close to the original as seemed consistent with clear- ness. The doses in the metric system have been changed to the approximate equivalents in apothecaries' weight, the original doses being retained in paren- theses. As in the former editions, the translators have substituted specimens of handwriting in English in the chapter on general paralysis for the original in German script. These specimens were kindly furnished them by the late Dr. E. P. Elliot, of the Danvers Insane Hospital. The translators have also added a chapter upon the plague and various notes which they hope may prove of assist- ance to the American practitioner. These additions are inclosed in brackets and signed by the initials of the translators, to distinguish them from the (unsigned) additions, also in brackets, of Dr. Shattuck. Boston, Jmie, 1901. 00l!TTE]:^TS by Separate Organs Acute General Infectious Diseases CHAPTER I. Typhoid Fever Phenomena and Complications relating to the Separate Organs Peculiarities in the Course of the Disease Kelapses of Typhoid Fever II. Typhus Fever . III. Relapsing Fever IV. Scarlet Fever V. Measles . VI. Rotheln . VII. Small-pox Variola Vera Varioloid Course of the Fever, Symptoms presented Complications VIII. Varicella IX. Erysipelas X. Diphtheria . . . XI. Influenza (Grippe) XII. Dysentery XIII. Cholera .... XIV. Malarial Diseases Intermittent Fever Pernicious Intermittent Fever Remittent and Continuous Forms of Chronic Malarial Cachexia Masked Intermittent Fever Typho-malarial Fever XV. Dengue .... XVI. Yellow Fever . XVn. Plague .... XVIII. Epidemic Cerebro-spinal Meningi XIX. Septic and Pysemic Diseases XX. Hydrophobia (Rabies canina) XXI. Glanders (Farcy) XXII. Malignant Pustule (Anthrax. Mycosis intestinalis) XXIII. Trichinosis itis Malarial Fever and FA&E 1 9 20 21 30 33 38 48 53 54 55 56 57 62 63 67 77 81 85 93 96 99 99 100 102 104 107 111 116 122 125 127 131 Diseases of the Respiratory Organs SECTION I DISEASES OF THE NOSE I. Coryza II. Chronic Rhinitis III. Nose-bleed 135 137 139 VIU CONTEisTTS I. II. III. IV. V. VI. VII. VIII. SECTION n DISEASES OF THE LARYNX Acute Laryngeal Catarrh (Acute Laryngitis) Chronic Laryngitis (Chronic Lai-yngeal Catarrh) Laryngeal Perichondritis ..... CEdema of the Glottis ...... Tuberculosis of the Larynx (Consumption of the Larynx) Paralyses of the Laryngeal Muscles .... Paralyses in the Distribution of the Superior Laryngeal Nerve . Paralyses in the Distribution of the Inferior Laryngeal or Recurrent Nerve Spasm of the Glottis ......... New Growths in the Larynx ........ Benignant Growths in the Larynx ....... Malignant Growths. Carcinoma of the Larynx .... PAGE . 140 . 143 . 145 . 146 .147 . 150 . 150 . 150 . 153 . 155 . 155 . 155 SECTION III DISEASES OF THE TRACHEA AND THE BRONCHI I. Acute Catarrh of the Trachea and the Bronchi . The Milder Forms of Acute Bronchitis The Severer Pebrile Forms of Acute Bronchitis . Catarrh of the Finer Bronchi. Capillary Bronchitis II. Chronic Bronchitis m. Fcetid Bronchitis (Putrid Bronchitis) rV. Croupous Bronchitis (Fibrinous Bronchitis) ■ V. Whooping Cough (Pertussis) VT. Bronchiectasis .... VII. Stenosis of the Trachea and Bronchi Tracheal Stenosis Bronchial Stenosis VIII. Bronchial Asthma 156 159 159 160 162 167 170 172 176 180 180 181 181 II. ni. IV. V. VI. SECTION IV DISEASES OF THE LUXGS I. Pulmonary Emphysema .......... 187 Symptoms and Course of the Disease ....... 190 Other Symptoms in the Lungs and in Other Organs . .' . . . 193 Pulmonary Atelectasis (Compression of the Lungs. Aplasia of the Lungs) . 195 Pulmonary QDdema .......... 197 Catarrhal Pneumonia (Broncho-pneumonia. Lobular Pneumonia) . . 199 Croupous Pneumonia .......... 204 Description of Single Symptoms and Complications ..... 209 Special Peculiarities and Anomalies in the Course of Pneumonia . . 218 Tuberculosis of the Lungs (Pulmonary Phthisis. Pulmonary Consumption) 226 General Pathology and etiology of Tuberculosis ..... 226 etiology of Tiierbculosis in Man ........ 228 Pathological Anatomy of Tuberculosis, especially of Pulmonary Tuberculosis 231 Clinical History of Tuberculosis in General and of Pulmonary Tuberculosis in Particular ........... 234 VII. Special Symptoms and Complications Symptoms on the Part of the Lungs . Symptoms on Physical Examination General Symptoms in Pulmonary Tuberculosis Symptoms and Complications on the Part of other Organs Acute General Miliary Tuberculosis . . . . . 237 237 241 246 248 261 CONTENTS IX CHAPTER VIII. IX. X. XI. XII. Gangrene of the Lungs .......... 266 Diseases from the Inhalation of Dust (Pneumonoconiosis) . . . 270 Embolic Processes in the Lungs (Hsemorrhagic Infarction of the Lungs) . 273 Brown Induration of the Lungs (Lungs of Heart Disease) .... 275 Tumors of the Lungs. Cancer of the Lungs. Echinococcus of the Lungs. Pulmonaiy Syphilis .......... 276 SECTION V DISEASES OF THE PLEUEA I. Pleurisy ..... Physical Signs . ■ . Various Forms of Pleurisy II. Peripleuritis .... III. Pneumothorax rV. Hydrothorax. Hsematothorax V. New Growths of the Pleura VI. Mediastinal Tumors . VII. Actinomycosis of the Thoracic Cavity 279 285 288 295 295 299 300 301 302 Diseases of the Circulatory Organs SECTION I DISEASES OF THE HEART I. Acute Endocarditis (Endocarditis verrucosa, Endocarditis ulcerosa) . . 304 II. Valvular Disease of the Heart ........ 308 , General Pathology of Valvular Disease of the Heart ..... 310 Insiifiiciency of the Mitral Valve ........ 311 Stenosis of the Mitral Orifice (Mitral Stenosis) ...... 314 Insufficiency of the Semilunar Valves of the Aorta ..... 316 Stenosis of the Aortic Orifice ......... 320 Insufficiency of the Tricuspid Valve ........ 321 Stenosis of the Tricuspid Orifice ........ 322 Insufficiency of the Pulmonary Valve ....... 323 Stenosis of the Pulmonary Orifice (Pulmonary Stenosis) and the other Con- genital Lesions of the Heart ........ 323 Combined Valvular Diseases of the Heart ....... 325 General Sequelae and Complications of Valvular Disease of the Heart . 326 General Course and Prognosis of Valvular Disease of the Heart . . 333 Treatment of Valvular Heart Disease ....... 334 III. Diseases of the Myocardium ......... 340 Interstitial Myocarditis (Fibrinous Degeneration of the Myocardium. Scle- rosis of the Coronary Arteries) ........ 340 So-called Idiopathic Hypertrophy of the Heart (Mechanical Strain of the Heart) 345 Hypertrophy of the Heart, Associated with Congenital Smallness of the Systemic Arteries .......... 350 Primary Weakness of the Myocardium (Congenital Weakness of the Heart; Weakened Heart; Acute Muscular Strain of the Heart; Toxic Weak- ness of the Heart) .......... 351 The So-called Fatty Heart 353 IV. Cardiac Neuroses ........... 355 Angina Pectoris (Stenocardia) ......... 355 Nervous Palpitation .......... 356 Tachycardia 357 CONTEIs'TS II. I. II. III. IV. V. SECTION II DISEASES OF THE PERICARDIUM Pericarditis . . . . . . . . . Special Forms of Pericarditis ....... Hydro-pericardium, Hsemo-pericardium, and Pneumo-pericardium SECTION III DISEASES OF THE VESSELS PAGE 359 363 369 Arterio- sclerosis (Endarteritis chronica deformans. Aneurism of the Thoracic Aorta Aneurisms of the Other Vessels .... Rupture of the Aorta ..... Narrowing of the Aorta ..... Atheroma of the Vessels) 370 .374 379 . 380 . . .380 Diseases of the Digestive Organs SECTION I DISEASES OF THE MOUTH, TONGUE, AND SALIVARY GLANDS I. Catarrhal Stomatitis II. Ulcerative Stomatitis III. Aphthous Stomatitis IV. Thrush .... V. Glossitis .... Acute Parenchymatous Glossitis Glossitis Dissecans . Lingual Psoriasis. Leucoplacia VI. Noma .... VII. Parotitis (Mumps) . Idiopathic, Primary Parotitis Secondary Suppurative Parotitis VIII. Angina Ludovici IX. Anomalies of Dentition 382 383 385 386 388 388 388 388 389 390 390 391 392 392 SECTION II DISEASES OF THE SOFT PALATE, TONSILS, PHARYNX, AND NASO-PHARYNX [. Sore Throat (Inflammation of the Soft Palate and of the Tonsils) . . 394 Catarrhal Sore Throat 395 Follicular Tonsillitis 396 Tonsillar and Peritonsillar Abscess (Parenchymatous Sore Throat) . . 396 Necrotic Tonsillitis (Necrotic Sore Throat) ...... 397 Chronic Hypertrophy of the Tonsils ........ 399 Chronic Pharyngitis .......... 400 Chronic Catarrh of the Naso-pharynx, Chronic Posterior Nasal Catarrh . 400 Pharyngitis Sicca ........... 401 Hypertrophic Catarrh in the Pharynx and Naso-pharynx .... 401 Retropharyngeal Abscess .......... 403 SECTION III DISEASES OF THE (ESOPHAGUS I. Inflammation and Ulcer of the CEsophagus ....... 404 TI. Dilatation of the Oilsophagus ......... 406 II. III. IV. CONTENTS XI Diffuse Dilatation Diverticula III. Stenosis of the Oesophagus IV. Cancer of the CEsophagus V. Rupture of the CEsophagus VI. Neuroses of the CEsophagus Spasm of the CEsophagus . Paralysis of the CEsophagus PAGE 406 406 409 412 414 414 414 415 II. III. IV. V. VI. VII. VIII. SECTION IV DISEASES OF THE STOMACH IX. Brief Preliminary Remarks on the Examination of the Gastric Contents . 415 Constituents of the Gastric Juice, particularly Free Hydrochloric Acid, Pepsine, and Lactic Acid ......... 417 Determination of the Motor Activity of the Stomach .... 419 Estimation of the Size and Position of the Stomach ..... 420 Testing the Absorptive Powers of the Stomach ...... 421 Demonstration of Blood in the Gastric Contents ..... 422 Acute Gastric Catarrh (Acute Gastritis) . . . . . . . 422 Chronic Gastritis. Chronic Catarrh of the Stomach ..... 425 Phlegmonous Gastritis .......... 432 Gastric Ulcer 432 Cancer of the Stomach .......... 444 Anomalies of the Secretion of Gastric Juice ...... 452 Anacidity of the Stomach (Achlorhydria). Achylia Gastrica . . . 452 Hyjjer secretion and Hyperacidity of the Gastric Juice (Acid Dyspepsia) . 455 Dyspepsia with Hypersecretion of the Gastric Juice ..... 457 Periodical (Intermittent) Hypersecretion (Gastroxynsis) .... 459 Abnormalities in the Size and Position of the Stomach. Motor Disturb- ances of the Stomach ......... 460 Abnormalities in the Size of the Stomach. Atony of the Stomach . . 460 Abnormal Position of the Stomach. Gastroptosis ..... 462 Nervous Dysjjepsia ........... 463 SECTION V DISEASES OF THE INTESTINES II. III. IV. V. VI. VII. VIII. IX. X. XL XII. Intestinal Catarrh ....'... Appendix. Membranous Enteritis and Mucous Colic Cholera Morbus (Cholera Infantum) . Intestinal Catarrh of Children . Typhlitis and Perityphlitis (Appendicitis) Perforating Ulcer of the Duodenum . Tuberculosis of the Intestines Syphilis of the Rectum .... Cancer of the Intestines .... Heemorrhoids ...... Habitual Constipation .... Stricture and Obstructions of the Intestines Intestinal Constriction .... Intestinal Obstruction .... Intestinal Parasites .... Tape-worms ...... Round-worms . . . Oxyuris vennicularis .... Anchylostoma duodenale .... Trichocephalus dispar . . 474 475 477 482 488 488 490 491 493 495 499 502 503 508 508 515 516 518 519 xu CONTE^s^TS SECTION VI DISEASES OF THE PEKITOXEUil CHAPTER I. Acute Peritonitis II. Chronic and. Tubercular Peritonitis III. Ascites ..... lY. Cancer of the Peritoneum . PAGE 520 529 533 535 SECTION VII DISEASES OF THE LIVER, BILE-DUCTS, A^"D POETAL VEEST I. Catarrhal Jaundice ........ II. Acute Febrile Jaundice (Infectious Jaundice. Weil's Disease) ni. Biliary Calculi IV. Suppurative Hepatitis V. Cirrhosis of the Liver VI. Biliary Cirrhosis and Hypertrophic Cirrhosis of the Liver VII. Acute Yellow Atrophy of the Liver Appendix. Pernicious Jaundice. Cholsemia and Acholia VIII. Icterus Neonatorum IX. Syphilis of the Liver .... X. Cancer of the Liver and Bile-ducts XI. Echinococcus of the Liver XII. Circulatory Disturbances in the Liver Xm. Atrophy, Hypertrophy, and Degenerations of the Liver XrV. Anomalies in the Shape and Position of the Liver XV. Suppurative Pylephlebitis XYI. Thrombosis of the Portal Vein Appendix. Diseases of the Pancreas Haemorrhages into the Pancreas Atrophy of the Pancreas Pancreatitis Cysts of the Pancreas Cancer of the Pancreas Pancreatic Calculi 536 542 543 553 555 562 565 569 570 571 572 575 578 579 581 582 583 585 585 585 585 586 586 587 Diseases of the Kidneys, the Pelvis of the Kidney, and the Bladder SECTION I DISEASES OF THE KIDNEYS I. General Preliminary Remarks upon the Pathology of Renal Disease Albuminuria .......... Casts and other Abnormal Morphological Constituents of the Urine in Disease . . . . . . . ... The Dropsy of Renal Disease ....... Uraemia ........... The Changes in the Cireulatoiy Apparatus in Renal Disease II. Acute Nephritis ......... III. The Subchronic and Chronic Forms of Nephritis, with the Exception Genuine Contracted Kidney ...... IV. Contracted Kidney ......... V. Amyloid Kidney ......... VI. Purulent Nephritis and Perinephritis . . Purulent Nephritis ......... Perinephritic (Paranephritic) Abscess ..... VII. Disturbances of Circulation in the Kidneys .... Renal of the 588 589 592 594 596 601 603 618 625 635 640 640 641 643 CONTEXTS Xlll VIII. IX. X. PAGE The Congested Kidney '.......... 643 Embolic Infarction in the Kidneys ........ 643 New Growths in the Kidneys ......... 644 Parasites of the Kidneys and of tlie Urinary Passages. Chyluria . . 646 Echinococcus of the Kidney ......... 646 Distoma Hsematobium (Bilharzia Heematobia) ...... 646 Strongylus or Eustrongylus Gigas ........ 647 Filaria Sanguinis. Chyluria ......... 647 Movable Kidney (Floating Kidney. Ren Mobilis) ..... 648 Appendix. The Diseases of the Suprarenal Capsules and Addison's Disease (Bronzed Skin) ......... 650 SECTION II DISEASES OF THE PELVIS OF THE KIDNEY AND OF THE BLADDER I. Inflammation of the Pelvis of the Kidney. Pyelitis II. Nephrolithiasis ...... III. Tuberculosis of the Genito-urinary Apparatus IV. Hydronephrosis ...... V. Cystitis ........ VI. New Growths in the Bladder .... VII. Enuresis Nocturna ...... 654 657 662 665 667 672 673 Diseases of the Organs of Locomotion I. Acute Articular Rheumatism ......... 675 II. Chronic Articular Rheumatism (Chronic Polyarthritis) and Arthritis Defonnans ........... 688 III. Acute and Chronic ]\Iuscular Rheumatism ....... 694 rV. Acute Polymyositis ........... 698 V. Rachitis 699 VI. Osteomalacia ............ 704 Diseases affecting the Blood and Tissue-metamorphosis (CONSTITUTIONAL DISEASES) I. Ansemia and Chlorosis .......... 708 General Preliminary Remarks as to the Classification and etiology of the Various Forms of Anaemia ........ 708 Symptomatology of Anaemia ......... 711 II. Progressive Pernicious Anasmia . . . . . . . .719 III. Leukaemia ............ 726 IV. Pseudo-leukaemia 733 V. Haemoglobinaemia and Haemoglobinuria ....... 736 Yl. Scurvy 738 Appendix. Barlow's Disease ........ 743 VII. Purpura. Morbus Maculosus Werlhofli. Peliosis ..... 744 VIII. Haemophilia 746 IX. Diabetes Mellitus 748 X. Diabetes Insipidus ........... 767 XI. Gout 770 XII. Obesity 779 XIII. Scrofula . . ' 787 XIV CONTENTS CHAPTER I. 11. III. IV. V. VI. VII. Diseases of the Nervous System /. The Diseases op the Peripheral Nerves SECTION I DISEASES OF THE SENSORY NERVES General Remarks upon the Disturbances of Sensibility Sensibility to Contact .... Sense of Locality (Localization of Sensation) Sense of Pressure ..... Sense of Temperature .... Sensation of Pain ..... Electro-cutaneous Sensibility Delay of Sensation, Summation of Irritation and After-sensations The Sensibility of the Muscles and Joints ..... The Special Sensibility to Touch (Stereognostic Sense, Active Touch) The Sensory Conduction Tracts and Anesthesia of the Skin Course of the Sensory Conduction Tracts . The General Causes of Cutaneous Anaesthesia The Symptoms of Cutaneous Anaesthesia . Anaesthesia of the Trigeminus . Treatment of Cutaneous Anaesthesia . Neuralgia in General .... The Individual Forms of Neuralgia . Neuralgia of the Trigeminus Occipital Neuralgia . . Neuralgia in the Region of the Brachial Plexus Intercostal Neuralgia .... Neuralgia in the Region of the Lumbar Plexus Sciatica ....... Neuralgia of the Genitals and the Rectal Region Aehillodynia. Talalgia. Tarsalgia. Metatarsalgia The So-called Articular Neuralgias (Articular Neuroses) Acroparaesthesia ..... Habitual Headache ..... Anomalies of the Sense of Smell Anomalies of the Sense of Taste PAGE 789 790 790 791 792 792 793 793 794 795 796 796 799 800 802 803 804 810 810 813 814 815 816 817 820 821 821 822 824 826 827 SECTION II DISEASES OF THE MOTOR NERVES II. General Remarks upon the Disturbances of Motility ..... 82& Paralysis 829- Symptoms of Motor Irritation ......... 835 Ataxia ............. 837 General Remarks upon testing the Reflexes and upon the Condition of them 838 General Remarks upon the Changes of Electrical Excitability in the Motor Nerves and Muscles .......... 842 Table of the Different Forms of Voluntary Motion and the Muscles and Nerves Concerned therein ......... 851 The Different Forms of Peripheral Paralysis ...... 854 Paralysis of the Ocular Muscles . . . . . . . . 854 Paralysis of the Motor Branch of the Trigeminus ..... 858 Facial Paralysis ........... 858 Paralyses in the Region of the Muscles of the Shoulder . . . . 863 Paralyses of the Muscles of the Back and Abdomen ..... 865 Paralyses in the Region of the Upper Extremity ...... 866 CONTENTS XV III. IV. V. Paralysis of the Diaphragm .... Paralyses in the Region of the Lower Extremity Toxic Paralyses ...... Lead Paralysis . . . ' . Arsenical Paralysis ...... The Different Forms of Localized Spasm . Spasm in the Motor Distribution of the Trigeminus Clonic Facial Spasm ..... Spasm in the Region of the Hypoglossal Nerve. Lingual Spasm Spasms in the Muscles of the Neck . Spasms in the Muscles of the Shoulder and Arm Spasms in the Muscles of the Lower Extremity . Saltatory Reflex Spasm ..... Arthrogryposis ...... Spasms in the Respiratory Muscles . Writer's Cramp and Allied Professional Neuroses Simple and Multiple Degenerative Neuritis Simple Neuritis .... Primary Simple Neuritis . Secondaiy Simple Neuritis Multiple Degenerative Neuritis Primary Acute and Chronic Multiple Neuritis The Ataxic Form of Multiple Neuritis ("Acute Curable Ataxia VI. The Acute and Chronic Neuritis of Alcoholic Subjects. (Pseudo-tabes [Ataxia] of Alcoholic Subjects) Beri-beri. Endemic Multiple Neuritis New Growths in the Peripheral Nerves . Alcoholic Paraly PAGE 871 871 873 873 875 875 875 876 877 878 880 , 880 , 881 881 , 881 , 882 , 885 . 885 . 885 , 885 , 886 . 890 . 892 /■sis . 893 . 895 II. in. IV. Raynaud's Disease //. Vasomotor and Trophic Neuroses General Preliminary Remarks Erythromelalgia Symmetrical Spontaneous Gangrene. Acute Angioneurotic CEdema Myxoedema Cretinism .... Myxoedematous Infantilism Adiposis Dolorosa Scleroderma .... Acromegaly .... Gigantism .... Hyperostosis Cranii . Hydrops Articulorum Intermittens Injuries and Diseases of the Cervical Migraine ..... Progressive Facial Hemiatrophy Exophthalmic Goitre Sympathetic 900 900 900 901 901 901 902 902 902 903 904 904 905 905 908 909 II. III. ///. The Diseases of the Spinal Cord Diseases of the Spinal Meninges ........ 915 Acute Inflammations of the Spinal Meninges ...... 915 Chronic Spinal Leptomeningitis ........ 917 Pachymeningitis cervicalis hypertrophica ....... 918 Haemorrhage into the Spinal Meninges ....... 919 Preliminary Remarks on the Localization and Topical Diagnosis (Segmental Diagnosis) of Diseases of the Spinal Cord ...... 920 Disturbances of Circulation, Haemorrhages, Traumatic Lesions, and Func- tional Disturbances of the Spinal Cord ...... 928 Disturbances of Circulation ......... 928 XVI CONTENTS Substance of the Spinal Cord. Spinal Apoplexy. 929 930 932 933 934 937 941 943 946 946 947 947 948 948 949 949 950 954 95 Hsemonhage into the Hsematomyelia . Traumatic Lesions of the Spinal Cord Diseases of the Spinal Cord after a Sudden Eeduction of the Atmospheric Pressure (Caisson Disease) . Functional Disturbances (Spinal Irritation. Spinal Neurasthenia) IV. The Pressure Paralyses of the Spinal Cord The Pressure Paralyses in Vertebral Caries The Pressure Paralyses in Cancer of the Vertebrae V. Acute and Chronic Myelitis Symptoms of Motor Paralysis Symptoms of Motor Irritation Ataxia .... Disturbances of Sensibility Cutaneous Reflexes . Tendon Reflexes Disturbances in the Bladder and Rectum Trophic Disturbances Disturbances in the Region of the Cerebral Nerves VI. Multiple Sclerosis of the Brain and Spinal Cord Appendix. The So-called Pseudo-sclerosis . VII. Tabes Dorsalis . Disturbances of Motility in the Extremities ...... 966 Disturbances of the Cutaneous and Muscular Sensibility .... 969 Disturbances of the Reflexes . . . . . . . . .971 Disturbances in the Eye and the other Organs of Special Sense . . . 972 Disturbances in the Bladder, the Rectum, and the Sexual Organs . . 973 Symptoms in the Internal Organs ........ 973 Trophic Disturbances . . . . . . . . . . 974 Cerebral Symptoms ........... 976 VIII. Hereditary (Juvenile) Ataxia (Friedreich's Disease) . . . . . 981 Appendix. Hereditary Cerebellar Ataxia 984 IX. The Primary Degenerations of the Motor Tract, including the Muscles . . 985 Preliminary Remarks .......... 985 Amyotrophic Lateral Sclerosis ......... 986 Spinal Progressive Muscular Atrophy ....... 990 Neurotic Muscular Atrophy ......... 996 Progressive Muscular Dystrophy ... ^ ... . 998 Primary Degeneration of the Pyramidal Tracts ..... 1007 Appendix. Congenital Spastic Paraplegia in Children (Spastic Cerebral Paralysis. Infantile Spastic Diplegia. Little's Disease) . . . 1012 X. Acute and Chronic Poliomyelitis ........ 1014 Spinal Paralysis of Children ......... 1014 Acute Poliomyelitis of Adults ........ 1019 Subacute and Chronic Poliomyelitis ....... 1020 XL The So-called Acute Ascending Spinal Paralysis (Landry's Paralysis) . . 1021 XII. New Growths of the Spinal Cord and of its Membranes .... 1024 XIII. The Syphilitic Afi'ections of the Spinal Cord 1026 Chronic Gummatous Spinal Meningitis and Meningo-myelitis . . . 1027 Syphilitic Myelitis and Syphilitic Spastic Spinal Paralysis . . . 1028 XIV. Syringomyelia and Hydromyelus ........ 1029 J.V. Spina Bifida . . . ' 1032 XVI. Secondary Degenerations in the Spinal Cord ...... 1033 XVII. Unilateral Lesion of the Spinal Cord 1036 IV. The Diseases of the Medulla Oblongata I. Progressive Bulbar Paralysis ......... 1039 II. The Rarer Forms of Chronic Bulbar Paralysis, Progressive Ophthalmo- plegia, and Asthenic Bulbar Paralysis ...... 1045 CONTENTS xvu III. IV. Progressive Ophthalmoplegia ...... Asthenic Bulbar Paralysis. Pseudo-paralytic Myasthenia Family Periodic Paralysis . ' . Acute and Apoplectiform Bulbar Paralysis Haemorrhage into the Medulla Oblongata and the Pons Embolism and Thrombosis of the Basilar Artery Acute Inflammatory Bulbar Paralysis Compression of the Medulla . . . PAGE 1045 1046 1047 1048 1048 1050 1051 1052 V. Tee Diseases of the Brain SECTION I DISEASES OE THE CEEEBKAL MENINGES I. Hsematoma of the Dura Mater II. Purulent Meningitis III. Tubercular Meningitis IV. Thrombosis of the Cerebral Sinuses 1053 1055 1059 1064 SECTION II DISEASES OF THE BRAIN-SUBSTANCE I. Disturbances of Circulation in the Brain ....... 1066 II. General Preliminary Remarks upon the Localization of Cerebral Diseases . 1068 The Motor Region of the Cortex Cerebri 1069 The other Parts of the Cortex Cerebri, except the Center for Speech . . 1074 The Centers of Speech and the Disturbances of Speech (Aphasia and Allied Conditions) 1077 The Centrum Ovale, Internal Capsule, Central Ganglia, and Region of the Corpora Quadrigemina ......... 1083 The Cerebellum 1086 III. Cerebral Haemorrhage .......... 1089 IV. Cerebral Embolism and Tlirombosis (Encephalo-malacia) . . . 1103 V. Inflammation of the Brain ......... 1106 Abscess of the Brain (Suppurative Encephalitis) ..... 1106 Acute and Chronic Non-suppurative Encephalitis ..... 1110 Idiopathic (Inflammatory) Softening of the Brain ..... 1110 Curable Forai of Encephalitis ........ 1110 Diffuse Cerebral Sclerosis ......... 1110 The Acute Encephalitis of Children . . . . . . .1111 VI. Insolation. Sunstroke. Heat Prostration. Thermic Fever . . . 1113 VII. Tumors of the Brain .1115 Glioma ............. 1116 Sarcoma ............. 1116 Gumma and Solitary Tubercle ......... 1116 Carcinoma . . . . . . . . . . . .1116 Psammoma ............ 1116 Cysts of the Brain . . . . . . . . . . .1117 The General Symptoms of Cerebral Tumors .... . 1117 Tumors in the Different Parts of the Brain and their Focal Symi)toms . 1119 Appendix. Hydatids of the Brain 1124 VIJI. Cerebral Syphilis 1125 IX. Progressive General Paralysis of the Insane (Paralytic Dementia) . . 1129 X. Chronic Hydrocephalus . . . . . . . . . .1137 XI. Meniere's Disease 1139 XVlll CONTENTS VI. Neuroses without Known Anatomwal Basis II. III. IV. V. VI. VII. VIII. IX. XI. Epilepsy ............ Appendix. Infantile Convulsions (Eclampsia Infantum) Chorea ............ Appendix. Chronic Hereditary Chorea. Electrical Chorea. Para myoclonus (Myoclonia) ........ Paralysis Agitans .......... Athetosis ........... Tetany . . . . . . Tetanus ............ Congenital Myotonia (Thomsen's Disease) ..... Catalepsy ........... Hysteria ........... The Symptoms and Manifestations of Hysteria .... The Hysterical Stigmata, especially Sensory Anaesthesia and Hyperaesthesia Hysterical Paralysis ......... Hysterical Contractures ........ Vaso-motor Disturbances. Secretory Disturbances. Symptoms in the Internal Organs ......... General Mental and Bodily Constitution of the Hysterical Hysterical Attacks, Conditions of Spasm, etc. ..... Neurasthenia .......... Symptoms of Neurasthenia. The Mental Symptoms The Physical Symptoms .......... The So-called Traumatic Neuroses (Accident Neuroses) Appendix I. Summary of the Symptoms and Treatment in Cases of Poisoning .......... Appendix II. Table of Weights and Measures .... Index ............ 1141 1151 1152 1156 1157 1161 1162 1165 1169 1170 1172 1175 1175 1178 1179 1179 1181 1182 1193 1194 1195 1201 1206 1214 1217 LIST OF ILLUSTEATIOl^S FIG. PAGE Table I. Distribution of the areas of the sensory roots upon the surface of the body .......... facing page 924 1. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21, 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. Typhoid bacilli ....... Temperatures in typhoid fever . . . Example of the temperature curve in relapsing fever Spirilli of relapsing fever in the blood ... Example of a normal scarlet-fever curve Example of the temperature curve in measles . Example of the temperature curve in true small-pox The cocci of erysipelas ...... Comma bacilli ....... Different forms of the malarial plasmodium Quotidian intermittent fever ..... Tertian intermittent fever ..... Anthrax bacilli ....... Anthrax bacilli; spore formation and spore germination Trichinae ........ Paralysis of left vocal cord ..... Bilateral paralysis of the posticus .... Paralysis of both internal thyro-arytsenoid muscles Paralysis of the arytsenoideus .... Paralysis of the thyro-arytsenoids and arytaenoideus 22. Pediculated fibromata ..... Turpentine pipe ....... Crystals of fat acids ...... Asthma crystals and Curschmann's spirals Pneumonia diplococci ...... Example of the temperature curv'e in croupous pneumonia Example of the temperature curve in " intermitting '" pneumon Cholesterine crystals ....... Influence of a pulmonary haemon-hage upon the temperature Elastic fibers ....... Tubercle bacilli in the sputum .... Sub-febrile state in chronic pulmonary tuberculosis Hectic fever in chronic pulmonary tuberculosis Expectoration of a worker in graphite Sputum containing " cells of heart disease "' Temperature curve in pleurisy before and after tapi)in{ Masses of actinomycosis ..... Pulse cui-\'e in marked mitral stenosis Pulse curve in aortic insufficiency .... Pulse curve in stenosis of the aortic orifice Pulsus bigeminus ....... Pseudo-hepatic cirrhosis due to pericarditis Plan of the dentition ...... Method of wa.shing out the stomach Hsemine crystals ....... 1 7 35 36 40 50 57 63 86 94 97 97 127 128 131 151 152 152 153 153 155 166 168 185 206 216 217 222 239 240 240 246 246 271 276 293 302 314 319 321 328 366 393 416 422 XX LIST or ILLUSTRATIOl^S FIG. 47. Head of taenia solium 48. Head of cysticercus of the brain 49. Tsenia solium 50. Eggs of intestinal parasites 51. Head of teenia mediocanellata 52. Tsenia mediocanellata 53. Head of bothriocephalus latus 54. Bothrioceplialus latus 55. Embryo of botbriocephalus latus 56. Ascaris lumbricoides 57. 58. Oxyuris vermicularis 59, 60. Ancbylostoma duodenale . 61. Egg of anchylostoma duodenale 62. Tricboceplialus dispar 63. Leucine and tyrosine crystals 64. Tsenia echinococcus 65. 66. Ecbinococcus scolices 67. Ecliinococcus booklets 68. Different forms of casts 69. Waxy casts . 70. Epithelial cast 71. Distoma hsematobium 72. Embryos of filaria 73. Pelvic renal epithelium 74. Crystals of triple phosphate and amnionic urate 75. Temperature chart in acute articular rheumatism . 76. Appearance of the hand in protracted arthritis deforman 77. Chronic arthritis deformans with contracture 78. Puerpei'al osteomalacia ...... 79. Changes in the red blood-corpuscles in pernicious anaemia 80. Leuksemic blood .... 81. Mixed leukaemia (myelaemia) 82. Acute attack of gout in the fingers . 83. Changes in the fingers in chronic gout 84. Course of the posterior root-fibers in the cord and medulla 85. Transverse section of the cord, showing the course of the posterior root-fibers 86. Course of the sensory conduction tracts . 87. 88. Distribution of the sensory cutaneous nerves in the trunk and upper extremities 89. Detailed distribution of the nerves to the dorsal surface of the fingers 90, 91. Distribution of the sensory cutaneous nerves to the lower extremities 92, 93. Distribution of the sensory cutaneous nerves in the head . 94. Sciatic scoliosis in severe sciatica ....... 95. Horizontal section through the right cerebral hemisphere 96. Transverse section through the crura cerebri in secondary degeneration 97. Transverse section through the cer^"ical enlargement 98. Transverse section through the lumbar enlargement 99. Motor points of face 100, 101. Motor points of arm 844, 102. Motor points of thigh 103, 104. Motor points of leg . 841 105. Right facial paralysis 106. Trunk of the facial 107. Paralysis of the right serratus 108. Position of the hand in paralysis of the radial nerv 109. Paralysis of the ulnar nerve . 110. Spasm of the accessory ner\-e . 111. Spasm of the right splenius capitis 112. Radial nerve in alcoholic polyneuritis LIST OF ILLUSTEATIONS XXI pon PIG. 113. Acromegaly in a patient thirty years old .... 114. Left facial hemiatrophy ....... 115. Patient with Basedow's disease (exopjithalmus, goitre) . 116. Position of the hand in pachymeningitis cervicalis hypertrophica 117. Distribution of the sensory root-areas from the lumbo-sacral plexus 118. Lesion at the level of the second lumbar segment 119. Lesion at the level of the third lumbar segment 120. Lesion at the level of the fifth lumbar segment 121. Lesion of the first sacral segment . 122. Lesion of the second sacral segment 123. Lesion of the third sacral segment . 124. Lesion of the fourth sacral segment 125. Relations of the vertebrae to the spinal roots 126. Vertebral displacement in spondylitis 127. Angular kyphosis in vertebral caries 128. Distribution of the sclerosed nodules on the surface. of the 129. Example of disease of the cord in multiple sclerosis 130. Degeneration of the jjosterior columns in advanced tabes 131. 132. Transverse section of the cord in beginning tabes dor.'^al 133. Paralysis of the left oculo-motor nerve in tabes 134. Tabetic arthropathy of the right knee and left ankle 135. Genu recurvatum in tabes dorsalis .... 136. Attitude of a patient with hereditary ataxia . 137. Diagram of the motor tract ..... 138. Section of the cervical cord in amyotrophic lateral sclerosis 139-141. Atrophy of the hand in spinal progressive muscular atrophy 142. Atrophy of the hand and forearm in spinal progressive muscular atrophy 143, 144. Spinal progressive muscular atrophy 145. Neurotic muscular atrophy 146. Peroneal muscular atrophy 147. Positions of a child with pseudo-hypertrophic paralysis on rising 148. Pseudo-hypertrophy of the muscles .... 149. Juvenile myopathic muscular atrophy .... 150. Two brothers with juvenile muscular atrophy . 151. Juvenile muscular dystrojjhy ..... 152. Muscular dystrophy ....... 153. Juvenile muscular dystrophy. Myopathic facies 154. Progressive myopathic muscular atrophy 155. Spastic spinal paralysis ....... 156. Spastic spinal paralysis. Impulsive laughing 157. Family spastic spinal paralysis ..... 158. Position of the legs in congenital spastic cerebral paralysis 159. Section of the cord in anterior poliomyelitis . 160. Old spinal infantile paralysis ..... 161. Deformity of the hand in syringomyelia .... 162. Secondary descending degeneration of the pyramidal tracts 163. Secondary ascending and descending degeneration . 164. Course of the main tracts in the cord .... 165. Representation of the chief symptoms in unilateral lesion 166. Position of the nuclei of the cranial nerves 167. Progressive ophthalmoplegia ...... 168. Diagram of focal diseases in the pons .... 169. 170. Lateral aspect of the brain ..... 171. Aspect of the median surface of the eerebnim . 172. Topographical relations between the surface of the brain and the skull 173. Localization in the cerebral cortex .... 174. Diagram of the course of the optic fibers in the chiasma 175. Patient with right hemiplegia .... 176. Cerebral infantile paralysis ..... 1009, PAGE 903 909 911 918 924 925 925 925 925 926 926 926 928 935 938 954 955 962 963 972 974 975 983 986 987 992 993 994 997 998 1000 1001 1002 1003 1004 1005 1005 1006 1009 1010 1011 1013 1014 1016 1031 1034 1035 1037 1038 1042 1046 1049 1070 1071 1072 1073 1075 1095 1111 xxn LIST OF illusteatio:j^s FIG. 177. Examples of hand"\vriting in general paralysis 178. Characteristic position of the body in paralysis agitans 179. Example of the position of the fingers in the movements 180. Hysterical contracture .... 181. Contracture of the foot in traumatic hysteria 182. Hysterical arc de cercle .... 183. Hysterical attack with catalepsy . 184. Hysterical abasia ..... 185. Accident case with hysterical paresis of athetosi PAGE 1132 1158 1161 1179 1180 1183 1184 1189 1202 ACUTE GENERAL INFECTIOUS DISEASES CHAPTER I TYPHOID FEVER ( Typhus ahclominalis. Enteric Fever. Ileotyphus) Etiology. — The sole cause of eveiy attack of typhoid fever is an infection -of the body by a deiinite pathogenic bacillus, the " typhoid bacillus " discovered by Eberth and Koch, and later made better known by the researches of Gaffky and others. Their length (see JFig. 1) is about one third the diameter of a red blood-glob- ule, and their breadth equals one third their length, but ■sometimes they may grow out in long fibers. It is not yet certain whether spore forma- tion takes place in their inte- Tior or not. The typhoid bacilli show a very active sponta- neous movement in water, caused probably by very fine filiform threads which Loffler has discovered on the ends of the rods and which he regards as the motor organs of the ' bacilli. That these typhoid bacilli •are specific, is shown, how- ever, as in the case of many micro-organisms, less by their external form than by their peculiarities, as observed in pure cultures of them, and by their other biological peculiarities (virulence, chemical reaction, etc.). By the latter the pure typhoid bacillus is distinguished from a form of bacillus morphologically similar and^perhaps allied to it, which often is found in the intestine, and is called hacterium coli commune (Escherich). The attempt has even been made to regard the typhoid Taacillus merely as a virulent form of the bacterium coli, but the weight of evidence is at present in favor of regarding the typhoid bacillus as an independ- ent form. In cultures on gelatine the typhoid bacilli develop along the line of puncture in little whitish or yellowish clusters, while a thin gray pellicle extends slowly over the surface, but the nutrient gelatine never liquefies. The manner of their growth on the cut surface of boiled potatoes is still more characteristic, and espe- cially valuable for their recognition. The whole cut surface is covered with a 1 1 Fig. 1.— Typhoid bacilli. Section from the spleen. 800 : 1. (From FlCgge.) 2 ACUTE GENERAL INFECTIOUS DISEASES dense pellicle, scarceh^ discernible ^n-ith the naked eye, and forming an absolutely- pure culture of typhoid bacilli. It is an important fact that typhoid bacilli may also thrive if deprived of oxygen, because we can thus understand their increase within the intestine. The typhoid bacilli have thus far been found chiefly in the typhoidal infiltra- tions in the intestine, where they lie between the cells, and also in single foci in the mesenteric glands, the spleen, the liver, the kidneys, the pleura, the me- ninges, in typhoidal foci in the bones, etc. By suitable methods of investigation they are often found in the stools of typhoid patients and also in the fluid ob- tained by puncture of the fresh splenic tumor, in the gall bladder, sometimes in the urine, and also in the blood taken from a spot of roseola. As a rule, they are not found in the rest of the blood. Numerous attempts have been made to produce typhoid fever artificially by introducing pure cultures of the typhoid bacilli into the bodies of animals, but the results of these efforts have not yet proved perfectly harmonious. The main cause of the discrepancy is probably that animals are in general very slightly susceptible to the disease. At any rate, the attempts at artificial infection up to this date have proved successful only in cases when the animals subjected to the experiment (rabbits, guinea-pigs) have received large amounts of the typhoid bacilli directly into a vein or into the abdominal cavity (E. Frankel and Simmonds), or when the bacilli have been introduced into the duodenum (A. Frankel). Probably, how- ever, we have here to do rather Avith the intoxication of the animals caused by the poisonous matters generated in the cultures of bacilli than with an actual in- fection, for the pathological changes of typhoid fever are but little developed in the animals, and the injected bacilli themselves appear to be for the most part destroyed within the body of the animal experimented upon (Fliigge and Sirotinin, and others). Attempts to produce the disease by mixing the dejecta of typhoid patients with the animal's food have thus far proved invariably un- successful. Probably the bacilli are immediately destroyed by the hydrochloric acid in the stomach. Investigation of the a-tiology of typhoid fever must consequently be directed to ascertaining in what manner and through what channels the specific typhoid bacilli penetrate into the human body, and what circumstances are then essen- tial to their further development and to the display of their pathogenic properties. It must be confessed that the ability to answer these questions accurately is a goal from which we are quite distant. It is almost universally believed that, as a rule, typhoid bacilli do not have any permanent, independent existence outside the human body, but sometimes under favorable conditions they seem to be able to remain for years in a " latent condi- tion " in the external world (in moist earth or stagnant water). Often, however, the conditions essential to an abundant development of the bacilli arise in certain places, and thus make it possible for a greater or less number of persons to absorb the pathogenic poison, and, as a result, to be attacked by typhoid fever. In this way occur the numerous greater or smaller epidemics of typhoid fever in contrast to the sporadic cases, which are likewise possible, and are not infrequent. If an epidemic of typhoid appears in a place till then entirely free from the disease, we must always refer it to an importation of the disease-germs, and seek their source in some previous case of typhoid. We must, therefore, take for granted that the poison of tj-phoid can in some way escape from the body of the patient into the outer world. If we believe this, we shall be sure to think, first of all, of the intestinal discharges as the source of infection. These discharges, as already stated, are known to contain the typhoid bacilli or perhaps their spores. As to the exact manner of infection, views are still widely different. Up to the present time there are chiefly two contrasted theories, called, respectively, the TYPHOID FEVER 3 " ground-soil " and the " drinking-water " * theories. According to the former, which is maintained principally by Pettenkofer and his pupils, the ground-soil is to be regarded as the chief place of development for the schizomycetic fungus of typhoid fever. Whether this will flourish depends chiefly on the condition of the soil (varying at different times and in different places), and this alone should ex- plain all the peculiarities observable in the spread of the disease — e. g., that single houses, streets, or wards of a city should suffer. According to Pettenkofer, a soil that air and water easily penetrate — e. g., one made up of alluvial or detrital de- posits — is most favorable for the spread of the disease, while a firm, rocky bottom makes its further development impossible ; and, where this " tendency of the ground-soil " is wanting, the disease can neither be introduced nor, if brought in by the sick, spread any further; for, according to Pettenkofer, the typhoid poison is seldom if ever transferred directly from one person to another. The poison in the stools must first be changed by the soil before it becomes infectious. The " ground-air," which is continually rising, carries the poison not only into the open atmosphere, but into the air of dwelling-rooms, and, being then inhaled, produces infection. We can thus understand why Pettenkofer regards typhoid fever as not directly contagious. The chief support of the ground-soil theory, beyond the results of comparing the character of the soil with the extent of the epidemics, consists in the proof which Buhl and Pettenkofer have given (taking Munich as an example, and later Berlin and other places) that a relation exists between the variations of the standing water in the soil and the frequency of typhoid cases. It appears that, when the water stands high (near the surface), fewer cases occur, and when it falls below the mean height cases are more numer- ous. Pettenkofer explains this relation by the fact that the level of the ground- water is certainly an index of the moisture and other conditions of the soil upon which the development of the tjrphoid bacilli depends. To be contrasted, or rather compared, with the " ground-air " theory is the view held by most physicians, despite the vigorous protest of Pettenkofer, that drinking- water plays an increasingly important role in the origin of many epidemics of typhoid. In fact, in the case of numerous epidemics, whose extent bears an un- mistakable relation to the water-supply, we are forced to believe that the typhoid germs are brought into the body by means of waterused in drinking or othenvise. Even then we are by no means wholly to disregard the character of the soil, for the disease-producing poison — not to speak of direct pollution — is probably often communicated to the well-water from the soil. The possibility of this will be especially great if the wells are near drains or cess-pools containing typhoid dis- charges. In epidemics spread by drinking-water, the typhoid bacilli have lately been repeatedly found in the suspected water. We believe the idea is continually gaining ground that no single " theory " can fully explain all the facts, and that the possibility of infection occurring in several different ways must be considered. The final source of infection is always to be sought for in a previous case of tj^phoid fever. From this patient the typhoid bacilli reach the external world through the dejections, and may some- times directly reach another human body and infect it. Hence the experience that nurses, laundresses who wash the soiled linen, etc., often have typhoid fever; but tj'phoid fever is not contagious by conduction through the air. In most hos- pitals typhoid patients are not isolated from the rest of the sick, and yet out- breaks of t5T)hoid hardly ever occur among them, provided they are not in close intercourse with the typhoid cases or do not carelessly use the same dishes, rec- tal thermometer, etc. In the further extension of the disease — that is, when * Compare with what follows the statements concerning the aetiology of cholera, where the same disputed points are considered. 4 ACUTE GENERAL INFECTIOUS DISEASES there is an epidemic — water contaminated with typhoid bacilli certainly plays a frequent and most important part. All persons who indulge directly or indirectly (rinsing cooking utensils, etc.) in water from an infected spring or infected aque- duct are in danger of becoming ill. For example, it has been remarked in Eng- land, and lately in Cologne, that the fever in certain epidemics was limited to individuals who had their milk from one common source. In such cases, however, the probable cause is not a disease in the cows, but a pollution of the milk or the milk-cans by water. It is as yet doubtful if animals can have typhoid fever. This fact makes it uncertain whether the illnesses which have been observed to follow the ingestion of the flesh of diseased calves (e. g., the epidemic of Kloten) are actually to be considered typhoid fever, although the pathological changes are said by Huguenin to be very similar to those found in typhoid. [It is not probable that sewer-gas in itself is an exciting cause of typhoid fever. Especially in large cities typhoid dejections are constantly finding their way into the sewers, which afford all the conditions favorable to the further growth and development of the poison. If, then, the drainage of any house is defective, the seeds of the disease can readily gain access to the interior of the house and infect susceptible individuals. One of the most instructive epidemics on record is that in Plymouth, Pennsyl- vania, a town of eight thousand inhabitants. In the spring of 1885 a disease, at first supposed to be of a strange character, broke out in the place, and, before it ceased, affected twelve hundred persons, causing one hundred and thirty deaths. It was soon found that the malady was typhoid fever, which arose from one case, briefly in this wise : In January, February, and March there was a case of typhoid in a house on a hill sloping toward a water-supply of the town. The dejec- tions were thrown out on the snow, under which the ground was deeply frozen. On March 25th a sudden and great thaw occurred, the water did not sink into the ground, but ran immediately into the natural surface channels, and on April 10th the epidemic began. There were reasons, which it is not necessary here to detail, why the above source of water-supply was drawn upon to an unusual de- gree just at that time, but it has been shown that those who derived their water from other sources were spared by the disease. The original case came from Phil- adelphia.] In almost all cases the intestine seems to be the actual gate of entrance for the typhoid poison into the human system. This is shown by the fact that in all cases which come to autopsy in early stages of the disease, the typhoid bacilli are mainly confined to the lymphatic tissues of the intestine. The typhoid poison (bacilli or spores) is probably SAvallowed, either directly with water or polluted food, or after being inhaled or in some other way introduced into the mouth. [Raw oysters grown in impure waters may convey the infection. — V.] If not destroyed in the stomach, it passes on in viable condition into the alkaline contents of the intestine, and here finds the conditions essential to its further development. It penetrates at first into the lymphatic follicles and Peyer's patches, and thence goes on into the mesenteric glands, the blood-current, the spleen, and other organs. As in the case of most other infectious diseases, the occurrence of infection in typhoid is dependent not only on outward conditions, but also on an individual predisposition. Details of the circumstances attending this latter are as yet not at all accurately understood. Even in the worst typhoid centers, where the pos- sibility of infection must be universal, many escape the disease. Age has an indubitable influence upon the liability to the disease. Tj^hoid is especially a disease of youthful, vigorous individuals, of fifteen to thirty j^ears. Above that age it is noticeably less frequent, although cases do occur at sixty and even seventy years. Formerly it was often said that young children were never TYPHOID FEVER 5 attacked ; but this was because the disease was not recognized, for in reality it is only children under one year old who seem to be seldom infected. At a later age, cases are by no means rare. Sex can not be shown with certainty to have an especial predisposing influence upon the frequency of typhoid fever. Mental excitement and gross errors in diet seem to predispose to the disease. On the other hand, a certain immunity has been alleged to be given by many cir- cumstances, especially pregnancy, the puerperal state, and other diseases already existing (tuberculosis, heart disease). Most of these statements are shown, how- ever, by more extended experience, to be very doubtful. It is certain, however, that the occurrence of typhoid fever gives very probable though not absolute immunity against any later new attack. Recent bacteriological investigations have suggested a reason for this immunity. Certain chemical albuminoid sub- stances (protective substance or " alexine " of Buchner) probably remain in the blood-serum and fluids of the tissues and prevent a new infection. Finally, it must be mentioned that the necessary conditions for an abundant development and conveyance of the typhoid germs are beyond doubt dependent on the season. According to statistics, most of the typhoid epidemics come in the months from August to November, while generally the number of cases greatly diminishes from December to spring. General Course of the Disease. — Extended experience shows that, after infec- tion with the typhoid poison has taken place, a certain time must elapse before the symptoms of the disease appear. The length of this time, the " stage of incuba- tion," is, unlike that of many other infectious diseases, not perfectly definite. On the average, it lasts two to three weeks, sometimes less time, sometimes longer. During this period the patient either feels perfectly well, or has certain slight symptoms, to which he pays more or less attention, according to his individual susceptibility. These prodromata consist of langiior, disinclination to exertion, anorexia, slight headache, pain in the limbs, etc. Often they last only a few days. Not infrequently the patients state afterward that they had felt the dis- ease coming on for weeks. The transition of the prodromata into the regular disease takes place some- times so gradually that it is utterly impossible to take any one day as the first of the illness, in order to reckon from it its duration. It is usually, however, the first symptoms of a high temperature, chilliness, feverishness, and the accompanying increase in general discomfort, which allow one to fix, with at least some accuracy, the beginning of the disease. A decided initial rigor is certainly exceptional.* After the fever begins, most patients soon take to their beds, although it happens often enough that the sick feel either unable or unwilling to give up, and keep on at work for days ! There have been manifold attempts to divide the whole course of the disease into separate periods. The most natural division seems to be into the three stages of development, height or fastigium, and decline (stadium incrementi, s. acmes, s. decrementi). Usually, however, physicians reckon according to the week of the disease. The first week corresponds to the developmental stage, the second, and in all severer cases the third as well, to the fastigium, the fourth (in light cases the third) to the decline. The course of the disease is very variable, however, and naturally there is the greatest diversity in the departures from this general plan. In the first week, the initial period, the general symptoms augment rapidly. The patients become, in severe cases, very languid and feeble, have generally an * According to the representations of many authors, a marked initial riiror seems to occur rather often in some places. In Leipsic, and also in Erlangen, a pronounced rigor at the beginning of typhoid is scarcely ever seen. 6 ACUTE GENERAL INFECTIOUS DISEASES intense headache, and complete anorexia, with great thirst. The fever, which is all the time gradually rising, is recognizable subjectively by alternating sensa- tions of heat and cold, and objectively by the hot, dry skin, the parched lips, and the dry and coated tongue. The sleep is disturbed. For the most part there are no prominent thoracic or abdominal symptoms, except that at times there is a sense of oppression in the chest, or sorae cough. The pulse is quickened, some- times even now dicrotic. There is often a temporary epistaxis. The belly is not much swollen as a rule, and but little if at all tender. There is generally consti- pation. Usually the spleen, even at this time, exhibits a swelling that can be easily demonstrated. Generally the fastigium has begun before the end of the first week. The severe general symptoms persist or even increase. The fever maintains constant- ly a considerable elevation. The patients become more stupid. Often delirium appears, especially at night. In the lungs there is developed a more or less in- tense and extensive bronchitis. The abdomen becomes more swollen. On the skin of the trunk appear, generally at the beginning of the second week, a number of small, pale-red spots, roseolae. Instead of constipation, there is a moderate diarrhoea. There are daily about two to four soft, thin, bright-yellow dejec- tions. The third week, during which in the severe eases the symptoms already men- tioned persist, is the chief time of the numerous complications and of especial clinical events, about which we shall speak below at length. If the disease takes a favorable course, there comes at the end of the third week a decline of the fever; and then the general symptoms also improve as a rule. The mind becomes clearer, the patient sleeps better, and gains some appetite. The pulmonary and digestive symptoms abate, and convalescence gradually begins. This short sketch of the course of the disease corresponds to most of the cases of medium severity. There are, however, besides these, so many forms and so many variations from the usual picture, that it seems almost impossible to enu- merate completely all the events of typhoid fever. And besides, the separate epi- demics vary in their general character according to the time and place of their occurrence. In many epidemics the cases run a peculiar course and have certain special complications not seen in others. We will begin the presentation of the chief peculiarities by speaking of the course of the fever. Course of the Fever. — Observation of the temperature in typhoid is so abso- lutely essential for the estimation of each individual case that no scientiiic physi- cian ought to treat a case without regular measurement of the temperature. The measurements should be taken, if possible, in the rectum. Their frequency must of course be modified by circumstances, but it will probably be possible to have three or four measurements daily. At night, especially if the patients are asleep, it is generally not requisite to take the temperature. A general idea of the course of the fever can be gained only by representing the separate measurements graphically in a continuous " temperature curve." The typical curve of typhoid fever (see Fig. 2) falls naturally into three or four divisions. The first division is the initial period, or the pyrogenetic stage, and is seldom observed, since at this time the patients are generally not yet under the doctor's care. The initial period of the fever lasts, as a rule, some three or four days, seldom longer; and during this time the temperature rises, generally by gradual steps, so that the morning as Avell as the evening temperature is each day 2° or 3° (1°-1.5° C.) higher than on the day before. A sudden and considerable rise of temperature, such as occurs in many other diseases, is very rarely seen in the beginning of typhoid fever. The second division of the curve represents the so-called fastigium, and cor- TYPHOID FEVER responds to the height of the disease. During this time the fever presents, in most of the severer cases, the general character of " febris contmua'^ — i.e., the spon- taneous remissions of the fever seldom exceed 2° (1° C). Almost always the lower temperatures come in the morn- ing hours and the higher in the even- ing. In cases of average severity the morning remissions touch 102° -103° (39°-39.5° C), and the evening ex- acerbations 104°-105° (40°^0.5° C). Temperatures which reach or ex- ceed 106° (41° C.) are seen only in very severe cases. Considerable morn- ing remissions are always a favorable symptom, while morning temperatures of 104° (40° C.) or higher generally show the case to be severe. The dura- tion of the fastigium varies with the severity and obstinacy of the case. It may last only a few days or one and a half to two weeks; in violent cases still longer. In many cases of slight or average severity the period of decline follows directly on the fastigium; but in severe cases there frequently inter- venes another stage, which Wunder- lich has graphically named the " am- biguous " period. The temperature- curve becomes irregular and more variable. The morning remissions may be great, even reaching the nor- mal, while the evening temperatures are often still very high. This stage has accordingly been termed the " period of the steep curves." It may be said that in general the longer a case of typhoid lasts the more irregular will be the course of the fever. The last stage — i. e., in cases of slight or average severity the third stage, and in severe cases commonly the fourth — is the period of defer- vescence or recovery. The peculiar- ity of this period in typhoid fever is that the fall of the fever is never by crisis, but always gradually, by lysis. Commonly the temperature descends by degrees, so that on each new day the morning remissions as well as o^ g^ o^ °, '^ ^ the evening exacerbations are l°to ^ g? ^ c5 '-'fa 2° (0.5°-l° C.) lower. The zigzag form of curve, in which there are of course very frequently slight irregularities, must be taken as the rule. The duration of the defervescence generally exceeds g BUBBIBinilHffllS s inniiniHgsa S5 BiiaiHM^n S sHuaiHgnH ^ mnBgasagHiiBBS S uaHHEiaunn n HaffignmniH u SBSSgasiSHaii at HBggSIBHiiniB o a^aBBEBBIIIIII 05 ■HiilSiSIIHaSB 00 SHS^ISilSHHIl t- mA^smmsmm tD iB^mmmm SHElBaSgBiliiBSBM ■* sampiaBaii CO Sill^^SBBSIH (N HSSBBBBHHB ^ IHiaBBSSSHlin O IHilBBBiSiSEyBSB 05 iSiSSSIIinEBBBBB 00 Hii^niHIBSn t- assjiiiBiESEninin CO liBssniusiBas in vmsmssssssR ■>!• BliiS'nniliniHllBI CO HiiiisBSBaBias O! inHHiissana " nnraniiiiSiH s ^ 8 ACUTE GENERAL INFECTIOUS DISEASES that of the initial period. It lasts five to eight days, often longer. It is not very" seldom that in defervescence the morning remissions become from the first very marked, even reaching the normal temperature, while the evening exacerbations become daily less and less, until they too are not above the normal. A third form of decline is much less frequent, in which the morning remissions become every day greater, while the evening temperature persists for some days at about the same height. Several times we have seen the fever take on a tertian type during; recovery. To this outline must be added a number of observations of practical importance. The initial period does not exhibit especial variations from the course we have stated. Its entire duration is bounded by certain relatively narrow limits. The fastigium presents, as already mentioned, the greatest varieties in its dura- tion. In light cases it is wholly wanting, so that these consist only of a period of gradually rising fever, and of a gradual defervescence almost immediately con- secutive to the rise. The entire duration of such light cases is only one and a half to two weeks. In other and tolerably frequent cases, which are often tedious, but still for the most part are light, the fever is not continuous, but remittent. Th& difference between the morning and evening temperatures amounts to 3° or 4 F. (1.5°-2.0° C), but the absolute height of the temperature is often not very con- siderable, so that the temperature curve at first leads to error and excites suspi- cion, for example, of tuberculosis. We have seen in Leipsic a number of cases in which the fever was perfectly intermittent during almost the entire illness^ and for two to three weeks afternoon elevations reaching 104° (40° C.) or more daily succeeded normal morning temperatures. These cases had the general course of light attacks. Various influences, not to speak of therapeutic interference, may produce a. considerable temporary remission of temperature in the course of the fastigium. Such a remission sometimes occurs spontaneously from the seventh to tenth day of the disease. If a marked intestinal haemorrhage happens (vide infra), the tem- perature generally falls several degrees centigrade, and the less frequent instances, of severe epistaxis have the same effect. If, in female patients, abortion or prema- ture delivery occurs, we often observe a similar considerable fall of temperature,, even without severe attendant haemorrhage. Perforation of the intestine often causes the temperature to fall rapidly. At times the occurrence of mental dis- turbances effects a moderate though noticeable lowering of temperature. Those great and sudden depressions of temperature remain to be mentioned which are accompanied by a very small but exceedingly rapid pulse and general prostration. Every such collapse, if severe, is a most dangerous event, and demands prompt and energetic medical treatment (vide infra). The development of local complications, such as pneumonia or inflammation of the parotid gland, is generally accompanied by a considerable rise of tempera- ture. The fever in such cases often becomes more irregular. This indicates the great practical value of thermometry. Almost every new rise of temperature or any considerable change in the ordinary course of the temperature has its special cause, and is therefore a warning to the attending physician to be vigilant. The cause of the change in the temperature is often not apparent until two or three days later. The period of defervescence departs most frequently from its typical behavior by being lengthened out into a " stage of retardation." The morning tempera- ture is then generally normal, while in the evening slight or moderate elevations continue. The reason for this long continuance of the fever may freqviently be found in some not yet completely healed local complication, but often no such lesion can be demonstrated. Then we are commonly inclined to surmise sluggish, intestinal ulcers which will not heal, or trouble in the mesenteric glands, etc. TYPHOID FEVER & This slow fever may continue for weeks. It is prone to follow severe cases^ but lighter attacks, especially in elderly or feeble patients, may also take on this sluggish character at a relatively early period. To these last-mentioned cases must finally be added a few others in which during the whole course of typhoid fever no febrile temperature at all or only a very slight rise can be detected. Entrance into complete convalescence is shown with far greater certainty by the absence of elevations of temperature than by any other single symptom. There sometimes come, however, temporary elevations of temperature during con- valescence, following some error in diet, long-continued constipation, or mental excitement. In other cases the new fever depends on some local sequela, e. g., a boil or a glandular abscess. Often, however, the most accurate investigation fails to demonstrate a cause. Especially in the beginning of convalescence there some- times comes a high fever, or even a rigor, which may recur several times, but which soon gives place to a normal temperature. Generally no definite cause for these brief but decided elevations of temperature can be pointed out. Perhaps we might consider the possibility of some affection of the mesenteric lymph-glands. These sudden and great elevations have seldom any grave significance. This new fever which we have just described is best termed febrile recrudes- cence, or febrile sequela, in contrast with the proper typhoid relapse. That is, after typhoid fever has ended, the whole process may be repeated; and this occurrence is called a relapse. Particulars as to the behavior of the fever in such cases will be considered below, in connection with all the other peculiarities of typhoid relapses. Phenomena and Complications relating to the Separate Organs * Before we undertake a detailed discussion of the individual symptoms of typhoid fever, we must first make a brief general statement which is of very great significance for the correct understanding of almost every infectious disease. We include among the direct typhoidal symptoms all those morbid phenomena which are produced immediately by the typhoid bacillus itself or by its toxic chemical action; but, on the other hand, every patient sick with typhoid fever is exposed to many secondary infections (from the intestinal ulcers, from the mouth, in the lungs, etc.) whose invasion is rendered possible, or at least rendered easier, by the pre-existing typhoid infection. All the morbid symptoms arising in this way, which unite with the pure typhoidal symptoms in making up the whole picture of the disease, must, strictly speaking, be termed complications of typhoid. In the individual case it is often hard to decide whether a particular symptom is of a typhoidal nature or a complication. We must, however, hold fast to the essential difference between these two kinds of morbid phenomena, if we would obtain a deep insight into the nature and origin of the whole course of the disease. 1. Digestive Organs. — We think it best to begin our consideration of the more special symptoms with the phenomena referable to the intestinal canal, for the reason that the anatomical changes in the intestine are pathognomonic. Indeed, these alterations may sometimes become of surpassing import in a clinical point of view, although in the majority of cases the intestinal symptoms are clinically not nearly so prominent as the general symptoms that result from the infection of the system as a whole. The characteristic typhoid lesion of the intestine consists of an affection of Peyer's patches, most marked in the lower part of the ileum. In the first week the patches swell gradually (stage of medullary infiltration). The rest of the * To avoid repetition, Ave have in what follows united a description of the anatomical changes with, the presentation of the clinical symptoms. 10 ACUTE GENERAL INFECTIOUS DISEASES mucous membrane exhibits at the same tim.e miore or less marked symptomis of simple catarrhal inflammation. In the second week, necrotic crusts form on the surface of the patches, which are cast off in the third week, leaving behind the typhoid ulcers. Toward the end of the third week the ulcers clean up, and then in the fourth week, if the case takes a favorable course, the ulcers heal. Smooth scars are formed, often diffusely pigmented. Experience shows that these scarcely ever lead to stricture of the intestine. The same process also goes on in a greater or less number of the solitary follicles as well as in the Peyer's patches themselves. We may add that probably in lighter cases of typhoid (vide infra) there is often no actual ulceration. The swelling of the lymphatic tissue subsides in this case before sloughing occurs. We have already mentioned the occurrence of typhoid bacilli in Peyer's patches and the intestinal follicles. The number and size of the ulcers formed have no direct relation whatever to the severity of the case. Although very extensive lesions in the intestine are often found in cases that end fatally, yet, on the other hand, we observe fatal cases in which only a few ulcers are found in the intestine. In cases with exten- sive intestinal lesions we often see follicular ulcers in the colon as well as in the small intestine (colo-typhoid). The clinical symptoms referable to the intestinal canal are, as we have said, prominent only in exceptional cases. In the beginning of typhoid fever there is usually constipation. This may last throughout the illness, so that the patients have but one dejection in every two or three days, or often none at all unless an enema be given. As a rule, a moderate diarrhoea begins during the second week. There are two to four stools, or sometimes more, each day. These usually have a characteristic bright-yellow color. On standing, they divide into an upper, cloudy, and quite liquid layer, and a lower layer composed of yellow, crumbly masses. They have generally an alkaline reaction, and upon microscopic exami- nation they are found to contain, besides remnants of the ingesta and granular detritus, a few epithelial cells, round cells, many crystals of triple phosphate, and numberless bacteria. Pfeiffer and other investigators have been able frequently, although not invariably, to demonstrate the true tjT)hoid bacilli in the dejecta by means of special methods of cultivation. Severe diarrhoea (ten or more stools daily) is relatively infrequent. In some bad cases we have seen the stools take on a dysenteric character. The autopsy showed in these cases unusually severe lesions of the colon and a diphtheritic inflammation of its mucous membrane. They were probably secondary compli- cations. Gaseous distention affecting the intestine, and especially the colon, is very frequent ; a slight but evident gaseous distention, with a fluctuating, " air-cush- ion " feeling, is a very valuable symptom in the diagnosis of typhoid fever, but, as a rule, the meteorism is moderate. Indeed, severe cases of typhoid are ob- served in which the abdomen always remains concave. Marked tympanites is always an unpleasant complication. We saw one case, which ended fatally, with very great tympanites, in which the lesions were almost exclusively in the colon, and it was the enormous distention of its entire length which had so swollen the abdomen. The noise that«an often be produced by pressure in the ileo-cfecal region (gurgling) used to be regarded, but probably erroneously, as especially characteristic of typhoid fever. Abdominal pain is often entirely absent. Some patients, however, complain of abdominal pain during almost the entire illness. On pressure, the belly is generally somewhat sensitive, but the tenderness is sel- dom extreme. It is more apt to be marked when there is constipation. Often such tenderness is due to a participation of the peritoneum in the disease, even when there is no perforation (vide infra). There still remain two symptoms of the greatest practical importance, both of TYPHOID FEVER 11 which have a direct connection with the intestinal lesions: they are intestinal haemorrhage and perforation. Intestinal hsemorrhages in the course of typhoid are almost always due to the erosion of the walls of blood-vessels in connection with the formation and throw- ing off of the crusts of the ulcers. The hsemorrhages occur, therefore, most fre- quently toward the end of the second and during the third week. The blood pours out into the intestine, and is passed with the stools. Its amount may be small, or it may reach to one or two pints, or even more. Its color is generally rather dark. The later discharges are generally tarry. Liebermeister states that he has ob- served intestinal hsemorrhages in 7.3 per cent, of typhoid patients, and Griesinger in 5.3 per cent. We have ourselves seen, in the medical wards in Leipsic, 45 intestinal haemorrhages in 472 cases, i. e., in 9.5 per cent. In individual epidemics the frequency varies greatly. It rose in 1880 to eighteen per cent. Intestinal hsemorrhage is always a grave symptom. Even slight hsemorrhages deserve consideration, for they may be the precursors of severer ones. Yet intestinal hsemorrhage, even if profuse, is not necessarily fatal. Of the above forty-five cases of typhoid with haemorrhage, twenty-six ended in complete recov- ery. In eight cases, death occurred as the immediate result of the loss of blood. Eleven ended fatally after a time. After every considerable intestinal hsemorrhage, the symptoms of general ansemia, often even of collapse, appear. The fall of the bodily temperature has been already mentioned. The hsemorrhage has sometimes a favorable influence on severe cerebral symptoms, for consciousness succeeds to the previous stupor or delirium. Often the haemorrhage is directly followed by recovery from the disease. Much more ominous than the intestinal haemorrhage is the occurrence of per- foration, as a result of the breaking through of a typhoid ulcer into the abdominal cavity, because, almost without exception, this is followed by a purulent or even ichorous peritonitis. Peritonitis is never caused by the typhoid bacillus itself, but by pyogenic organisms (cocci, perhaps bacterium coli?) which enter the ab- dominal cavity with the contents of the intestine. The amount of fluid peri- tonitic exudation is, as a rule, not very great. The serous membrane is often found covered merely with a fibrino-purulent or purulent-hsemorrhagic deposit. The occurrence of perforation is sometimes marked by a violent pain suddenly felt by the patient ; but it may also, even in severe cases, take place insidiously. The abdomen is generally (not always) greatly distended and very tender on pressure, so that even in stupor patients groan while being examined. If gas has entered through the opening into the peritoneal cavity, we often observe absence of the ordinary dullness over the liver ; but this symptom is to be employed cau- tiously as a factor in diagnosis, for absence of hepatic dullness may also result from distended intestines lying in front of the liver. When perforation has oc- curred, the patient soon looks collapsed, with cheeks fallen in and sharp, cool nose. Frequent eructations and vomiting often follow. The pulse becomes small and very frequent. The temperature generally falls as the peritonitis begins, and later it usually undergoes great variations. Perforation of the intestine occurs most frequently in the third or fourth week of the disease, and much oftener in men than in women. In sluggish cases, how- ever, we can not be without apprehensions of it till a late period. The perforation generally takes place in a coil of the lower part of the small intestine, and with marked relative frequency in the right side of the pelvis, though seldom in the ver- miform appendix or in the colon. With few exceptions, death comes quicklj^ after a few days at latest. Only when the perforation is small and the intestines have become agglutinated at the onset is the course of the peritonitis slower, so that the symptoms are less violent and cause death in a week or ten days. Out 12 ACUTE GENEEAL INFECTIOUS DISEASES of fifty-six fatal typhoid cases in the Leipsic medical clinique we lost five, or nine per cent., from peritonitis following perforation. Here and there a case of re- covery has been reported, probably resulting from a limitation of the peritonitis- through sppedy adhesion of the intestines. It should be mentioned here that sometimes in typhoid fever a local or general peritonitis may occur through direct extension of the process to the serous mem- brane without actual perforation. We have seen in one case, as the result of the peritonitic bands and false membranes, complete occlusion of the intestine (ileus), and death. Swelling of the mesenteric lymph-glands (less often of the retro-peritoneal glands as well) is found in typhoid almost as constantly as the anatomical changes. in the intestine. Sometimes they break down, i. e., suppurate. In cases that have passed through the disease we often find considerable deposits of lime in the glands. These changes have a certain clinical importance; for, as already men- . tioned, we may often venture to refer a more or less tedious recurrent febrile state which has no other demonstrable cause to this lesion of the mesenteric glands.. In some rare cases a general peritonitis has been observed as a result of the burst- ing of a suppurating gland. The swelling of the spleen (acute splenic tumor) is, in typhoid fever as well as in many other acute infectious diseases, one of the most constant symptoms. The enlargement of the spleen can often be demonstrated as early as the end of the first week, and is therefore of considerable diagnostic importance ; but percussion of the spleen is sometimes decidedly difiicult and deceptive in this disease because of the existence of tympanites. The surest demonstration of splenic enlargement is therefore always by means of palpation, which, after a little practice, gives a positive result in the majority of cases. Absence of splenic tumor is most fre- quently observed in elderly typhoid patients. The spleen may also diminish con- siderably in size after severe intestinal haemorrhage. Pain in the splenic region, resulting from tearing of the distended capsule, is comparatively rare. The splenic infarctions which sometimes occur may, in exceptional cases, prove the starting-point of a peritonitis. Hepatic symptoms are seldom seen in typhoid fever, except that there may be a moderate swelling of the organ. The anatomical changes of " parenchymatous, degeneration," and the frequent formation in the liver of the small lymphomata. which Wagner discovered, have no clinical significance. The bile secreted is gen- erally pale and scanty. This is a partial explanation of the light color of the stools. A very rare complication, which we ourselves observed in one case, is acute yellow atrophy of the liver. The stomach presents no especial anatomical changes in typhoid. Anorexia is an almost invariable symptom in the beginning and during the course of all severer cases. There is seldom any desire for food till recovery begins; but then, if convalescence is undisturbed, the appetite soon attains an enviable keen- ness. Vomiting in the beginning or course of the disease is an exception, unless after some error in diet. We have already mentioned it as a symptom of perito- nitis. The changes in the mouth and throat of typhoid patients deserve the careful attention of the physician. The lips and tongue are in severe cases dry and fis- sured. The lips are often covered with dry, black crusts, sometimes described as a " fuliginous coating." The tongue is apt to be thickly coated at first, but later cleans off from the edges and tip. In severe cases, especially if the mouth is not .properly cleansed, a rather severe stomatitis may occur and produce superficial ulceration of the buccal mucous membrane and of the edges of the tongue. The gums sometimes become spongy, and are apt to bleed, as if scorbutic. Actual sore throat, at least according to our experience in Leipsic, occurs but TYPHOID FEVER 13 seldom at the beginning of typhoid fever. The difficulty in swallowing, often complained of by patients, is generally due to dryness of the pharynx. In certain epidemics, however, the occurrence of sore throat at the beginning of the illness lias been frequently observed. It may even happen that this early sore throat is accompanied by an erythema diffused over the body, so that at first suspicions of scarlet fever arise. The cases are very interesting and quite rare (although we have repeatedly seen them) in which disturbances of swallowing exist with the general typhoid symptoms from the beginning. On examining the fauces we see on the tonsils peculiar white, slightly elevated spots, which later form superficial ulcers. After a time these places heal, and in other respects the disease pursues a normal course. The suspicion is justified that in these cases there is a specific typhoidal disease of the tonsils (due to the typhoid bacillus itself), and such cases are called tonsillar or pharyngeal typhoid (analogous to the laryngeal typhoid, pneumo- typhoid, and nephro-typhoid, to be mentioned later). In such cases the typhoid bacilli have probably attacked the tonsils at their first invasion. It should also he mentioned that in severe cases there is often an extensive growth of thrush in the mouth and throat, and this may spread quite a distance down the oesophagus. The changes in the mouth and throat are of especial interest, for the reason that they may be directly propagated to important neighboring organs. Starting from the pharyngeal cavity, the pathogenic agent, probably in most cases the staphylococcus, may penetrate through the Eustachian tube into the middle ear. Thus arise those inflammations of the middle ear which are not very rare in severe cases of typhoid, and which lead to perforation of the membrana tympani and to purulent discharges from the ear. The not infrequent inflammation of the parotid gland is also, as we believe, occasioned in a similar way, the inflammatory agent reaching the parotid gland from the mouth by way of Steno's duct. We do not regard the otitis and parotitis as especial localizations of the typhoid poison, but as secondary diseases, for the occurrence of which typhoid fever merely fur- nishes the occasion, as when the mouth is imperfectly cleansed. Purulent otitis in typhoid fever can easily be overlooked at first, since stuporous patients only Tarely complain, of themselves, of pain in the ear or deafness. The parotitis appears m^ost frequently in the third week, and generally on one side, though sometimes on both. It almost always becomes purulent, and discharges either externally or into the external auditory meatus, unless there is a timely incision. 2. Organs of Respiration. — Affections of the lungs are among the most fre- quent and important complications of typhoid fever, but are for the most part not a direct result of the typhoid infection, but pure complications. The bronchitis very often found in severe cases, and especially in patients who do not come till late under proper care, certainly is dependent on the imperfect expectoration of the bronchial secretions and on the inhalation of inflammatory agents coming from the mouth and throat. ISTumerous cases of typhoid of slight or average severity, under proper care, run their course without any considerable bronchitis. In many other cases, and even severe ones, the bronchitis remains within moderate bounds, especially if the patient is brought promptly under proper care and treatment ; but in severe ■cases, when marked disturbances of the nervous system arise, and the patient in his stupor expectorates little, swallows things the wrong way, and lies all the time on his back, passive and collapsed, the occurrence of a severe, diffuse bron- chitis, especially in the lower lobes of the lungs, can hardly be avoided. Wor in such cases is there generally a mere bronchitis, but a more or less extensive catarrhal, lobular pneumonia, to be classed therefore under the so-called inhala- tion pneumonias (cf. chapter on lobular pneumonia). What was formerly termed " hypostatic pneumonia " is also almost invariably to be put in this group. Erom the way in which these pulmonary disorders arise, we can understand 14 ACUTE GENERAL INFECTIOUS DISEASES why the bronchitis sometimes takes on a putrid character, and why the lobular infiltrations are, in severe cases, transformed into genuine gangrene. If such spots touch the pleura, they occasion the development of a pleurisy which is almost always purulent. In rare cases, pneumothorax may arise as a sequel to the perfo- ration of a gangrenous infiltration into the pleural cavity. Various circumstances promote the occurrence of pulmonary symptoms. Thus we find it especially easy for a severe bronchitis and its sequelae to be developed, in the case of elderly per- sons, or the kyphoskoliotic, or the corpulent, or patients who have previously suf- fered from emphysema or cardiac disease. The subjective thoracic symptoms, in typhoid patients who have pulmonary complications, are generally not very prominent. It is only occasionally that patients complain in the early stages of typhoid fever of pain, and of a sense of oppression in the chest, or of cough, or of a stitch in the side; and even when such symptoms exist, the physical examination may give comparatively insignifi- cant results. The severer pulmonary complications are seen mainly in those whose intelligence is more or less blunted, and who, therefore, make little com- plaint, are not much disturbed by the dyspnoea, and cough and expectorate little. A careful physical examination alone can enlighten us as to their condition. On auscultation, sibilant rhonchi are the chief signs observed in the milder cases. In the severer ones there are moist, fine, and coarse rales, especially numerous toward the base of the chest. If there are abundant moist rales, we may infer that there is a lobular pneumonia, although this can not be demonstrated with certainty till the separate islets of infiltration unite into a more extensive solidification, so as to afford dullness on percussion. In addition to the pulmonary lesions already mentioned, genuine croupous or lobar pneumonia does occur in typhoid fever. This is often an actual complica- tion, dependent upon a secondary infection with the genuine pneumonia diplo- coccus. Such a pneumonia may come on early or sometimes during convalescence, and affect both the upper and lower lobes. There is probably also a true typhoid pneumonia caused by the entrance of typhoid bacilli into the lungs. Such a pneumonia can not at present be recognized anatomically, but only by bacterio- logical investigation. Especial interest attaches to those cases of typhoid fever which begin with a lobar pneumonia. Often there is at first not the slightest suspicion of a typhoid fever, for the disease is regarded as an ordinary croupous- pneumonia; but it is usually to be noticed that the illness does not begin sud- denly with a rigor, but more gradually, and that from its incipiency the constitu- tional symptoms, the headache and splenic tumor, are more prominent than is usually the case in pneumonia. At the end of the first week's illness there is no crisis, but persistent fever. Now the pulmonary symptoms often retreat more and more to the background, while, on the contrary, diarrhoea and rose-spots appear. The spleen is enlarged. In short, the clinical picture of typhoid is developed. It is not unnatural to suppose, although there is yet no absolute proof of the fact, that in these cases, which are fittingly termed " pneumo- typhoid," the infection with the typhoid bacilli has taken place exceptionally in the pulmonary tissue, and that, therefore, the first pathological changes are devel- oped in the lungs. Laryngeal Lesions. — The same causes which produce the bronchitis result alao in a simple catarrhal laryngitis, with hoarseness. This is in severe cases accom- ■ panied by superficial ulcers on the vocal cords or the posterior wall of the larynx. Sometimes, again, the lesion is due to mechanical causes, constituting the so-called " decubitus laryngis." The disorders which attack the less superficial structures of the larynx are fortunately rare. Chief among them is a laryngeal perichon- dritis of the arytenoid cartilages. This complication is justly regarded as of bad omen, and may lead to the rapid development of cedema of the glottis, with great TYPHOID FEVER 15 laryngeal obstruction and threatening suffocation. These severe laryngeal affec- tions in typhoid are regarded by some authorities, especially by Klebs, as always the direct effect of the infecting poison; but in most cases they are probably due to an invasion of staphylococci or some similar microbes. We have several times seen croup in typhoid fever, and it is a very dangerous symptom. In regard to their origin most of these mild and severe laryngeal affections in the course of typhoid fever are to be regarded as secondary inflammations; but specific typhoid disease of the larynx also seems to exist. The cases are of interest where the whole morbid process begins with a severe laryngitis (" laryngeal typhoid ") and is followed later by the ordinary symptoms of typhoid (vide supra, pharyngeal typhoid). Among symptoms referable to the mucous membrane of the nose, epistaxis is important. It occurs in the beginning of typhoid with tolerable frequency, and is in one way not unfavorable, for it often mitigates the patient's headache. At a later period nose-bleed may become a most unpleasant complication, as it is some- times very difficult to check. We have even seen one fatal case due to persistent nose-bleed. Other nasal symptoms are exceptional. There is an old saying that typhoid never begins with a coryza. 3. Nervous System. — The old term " nervous fever," which is still used by the laity, shows how frequent and severe are the nervous derangements which occur in typhoid. In cases of any severity there is almost always a certain dullness of intellect, often amounting to apathy and somnolence. The patients give mono- syllabic and incomplete answers to all questions, and their statements about their previous history are often disordered and contradictory. There may even be sopor or a deep coma in the worst cases. All cases of this sort in which there was a condition of intellectual enfeeblement were termed by the old physicians " fehris nervosa stupida," in contrast to the " febris nervosa ver- satilis," that form in which abnormal mental activity or delirium predominates. In severe cases delirium is very frequent. It is generally worse at night, and at times when the patient happens to be left alone. Very often he tries to leave his bed, because of his delusions, and talks of persons and things with which he was fomierly familiar; or he is very noisy and restless, sometimes shrieking from groundless fears. We may add that these diverse nervous symptoms frequently succeed one another, or appear in combination. Sometimes a soporose patient may be heard softly whispering to himself in " muttering delirium." Certain motor disturbances are often combined with considerable impairment of consciousness. There is a slight twitching of the muscles of the face and ex- tremities. The old authorities gave the name suhsultus tendinum to the sudden leaping into prominence of the sinews thus caused. It is best seen on the back of the hands. In severe cases the patient is sometimes observed to grind the teeth together; this is due to a cramp-like condition of the muscles of mastication, and is justly regarded as ominous. We often see persistent tremor of the extremities and lower jaw; and it is especially in these cases, as we have demonstrated iipon numerous patients, that the tendon reflexes and the mechanical excitability of the muscles are much increased. If deep coma comes on, the muscles become lax, the motions of the eye are not co-ordinated, and reflex excitability diminishes, or is wholly extinguished. Headache is one of the most constant symptoms in the beginning of the dis- ease. It is usually referred to the forehead or temples. The pain may be very violent, and sometimes takes on almost a neuralgic character. It almost always subsides in the second week. If we seek the cause of these nervous symptoms, which are often so severe, we find that the anatomical changes in the nervous system, including the brain, bear no relation whatever to the severity of the symptoms observed during life. We 16 ACUTE GENERAL INFECTIOUS DISEASES sometimes meet with minute haemorrhages in the cerebral meninges, or meningeal opacity or oedema, or a moist condition of the cerebral parenchyma ; but the con- nection of these and similar changes with the symptoms of the disease is often more than doubtful. Nor can the microscopic alterations in the brain, which have been reported, be regarded as important and authoritative. It is only in very rare cases that large cerebral haemorrhages or purulent meningitis have been found. As to this last, we should always be very cautious in making a diag- nosis, as symptoms which would seem to be most conclusively meningeal — such as stiffness of the neck, rigidity of the whole spinal column, and occipital head- ache — may appear in typhoid patients, and yet the autopsy may show no trace of meningitis. One theory, which has Liebermeister for its chief supporter, and which has won a tolerably widespread acceptance among physicians, is that the nervous symptoms are chiefly a direct result of the febrile temperature. It is impossible, however, for us to regard this view as universally true. The unprejudiced con- sideration of a large number of personal observations prevents it. Although it is undeniable that elevated temperature has a harmful influence on the nervous sys- tem, yet in numerous cases there is no relation between the height of the fever and the severity of the nervous derangements. There are cases in which the fever remains continuously high for days, while the patient feels perfectly comfortable and presents no symptoms of any important cerebral disturbance. The opposite class of cases is still more numerous, in which from the very start there is always a low temperature, and, notwithstanding, the most severe nervous symptoms arise. Frantzel and others have published very striking cases of this sort. Hence we must seek for some other special cause of the severe nervous symp- toms, and according to our present views this cause must be the intoxication re- sulting from the specific infection. We know that all bacteria produce, by their own tissue-metamorphosis and the chemical processes which they excite in their neighborhood, certain chemical matters which, especially in the case of the so-called " pathogenic bacteria," seem to be similar to the alkaloids (" ptomaines " and "toxines"), and exercise a decidedly poisonous influence upon the body, and especially upon the nervous system. These products are formed by the typhoid bacilli, enter the blood, and are the chief cause of the nervous phenomena. The difference in the violence of the latter in different cases probably depends mainly on a difference in the amount, and perhaps also in the quality, of the toxines produced by the typhoid bacilli, and probably also in the different susceptibility of individuals to the poison. The reason that the influence of these poisons is not much greater than it is, is that they are in part destroyed within the body and in part excreted with great rapidity, the channel of exit being mainly the kidneys. Thus is explained the interesting fact observed by Lepine, Bouchard, and others, that the urine of typhoid patients possesses poisonous properties not present in normal urine. That the appearance of the nervous symptoms is dependent not only on the material causes, but also on the susceptibility of the individual, is shown by the fact that certain patients are especially prone to exhibit marked nervous phe- nomena ; for example, hard drinkers, " nervous " individuals, and also those who have suffered violent emotional disturbances shortly before the onset of the disease. Actual insanity is not very infrequent during the course of typhoid, or in con- valescence. It generally takes the form of melancholia. We have repeatedly seen patients in such a state that they would lie almost motionless in bed, with eyes open, and perhaps assert that they Avere dead ! In other cases there is mental excitement, sometimes combined with hallucinations, or there is confu- sion of ideas. In one case, in a girl who was evidently predisposed to nervous dis- TYPHOID FEVER 17 ■orders, we saw typical hystei'ical insanity break out during the fever. Sometimes the mental excitement at the beginning of a relapse terminates in actual insanity. Tew of the psychoses which arise during or at the end of typhoid outlast con- valescence. We have still to mention a number of nervous diseases that develop in the course of typhoid or after its decline. Neuralgia is sometimes seen, as well at the beginning as at the end of the disease. It is most frequent in the regions supplied by the trigeminus and the occipital nerves. Great hyper^esthesia of the skin and muscles is not rare during convalescence. It attacks the lower extremities by preference. Paralysis of single muscles (e.g., of the serratus magnus), or paralysis of a single extremity, has been repeatedly observed as a sequela. The paralysis is generally of the atrophic variety, and is probably, as a rule, due to neuritis. Ataxia and spastic paralysis of the lower extremities are rare se- quelae. Finally, there are sometimes developed, either in the course or at the conclusion of typhoid fever, the symptoms of a localized cerebral disorder (e. g., liemiplegia and aphasia), the anatomical cause of which varies. There may be a haemorrhage or an embolism, and probably in still other cases a localized en- cephalitis. 4. Circulatory System. — Disturbances of the heart such as to produce striking -anatomical changes are rare. The pericardium macroscopically almost always appears normal; the slight mitral or aortic endocarditis sometimes found has no clinical significance. The disturbances in the cardiac muscle seem more im- portant. It is often more flabby than normal. The cavities, especially on the right side, are often dilated. With the naked eye we frequently see in the muscle itself cloudiness or fatty changes. Microscopic lesions are usually present and are much more pronounced. They consists usually of a granular (" albumi- noid ") or more rarely of a fatty or hyaline degeneration of the fibers, and of ..genuine inflammatory foci of interstitial myocarditis (Hayem, Romberg). No marked disease of the cardiac ganglia has as yet been found. The clinical significance of these changes should not, we believe, be overesti- mated. In all probability they are often without serious consequences and dis- appear completely with recovery from the disease. Sudden death (heart-fail- ure?) occurs in typhoid, but it is very rare (see the chapter on diphtheria). Per- manent disturbances of the heart after typhoid are also rare. When they occur they are perhaps due to the passage from an acute myocarditis to a chronic inter- stitial degeneration. [This slowness of the pulse as compared with the fever is common enough to have some diagnostic value, provided brain trouble is ex- ■cluded. The pulse is almost always rapid, although often not so much so as the Tieight of the temperature might lead one to expect. — V.] It averages from 90 to 110, and often more. When it keeps at 140 or Tiigher, in adults, it is always an unfavorable symptom. The abnormal frequency is often due in part to the high temperature; but there are other factors. Tem- perature and pulse do not correspond in all cases. Sometimes the pulse will have a normal or even subnormal frequency throughout the entire attack, de- spite the fever. Temporary accelerations are easily produced by mental excite- ment or bodily exertion, as by sitting up in bed. In convalescence the rate is fre- quently subnormal. Slight irregularities of the pulse are not rare, either in the acme or the decline of typhoid. Marked irregularity is always a grave symptom, although in many •cases it passes off and the patient recovers. Dicrotism, due to loss of tension in the wall of the artery, is so common that it is still regarded by elderly physicians as characteristic of typhoid, although it often occurs in the same way in other acute diseases. In many severe cases the height and strength of the pulse may cause no alarm, but often the pulse is 3 18 ACUTE GENERAL INFECTIOUS DISEAS1,S notably weak and small. This is due not only to the influence of the disease, but also to the previous condition of the individual. The diminished cardiac activity may result in venous thrombosis, especially in the lower extremities and in a crural vein. This sometimes causes swelling of one of the lower extremities during the later stages or convalescence. The swollen member generally regains its normal size after some weeks. In other cases the thrombosis occurs earlier, and in patients who are still too vigorous to suffer from cardiac weakness, so that we are forced to the conclusion that there is some local specific cause, a local thrombo-phlebitis due to the typhoid bacillus itself, or, more probably, to the invasion of the walls of the vein by some secondary infection. A possible, but fortunately infrequent, result of these thrombi in the lower limbs is pulmonary embolism and sudden death. In severe cases, which end in death, cardiac thrombi are sometimes found, with emboli in the lungs, spleen, kidneys, or other organs. CEdema of the ankles and legs is very often seen in convalescents, especially when they first get out of bed. It is due to the weakness of the heart and changes in the vascular walls. Once we saw a general dropsy develop at the end of a severe attack in a girl of fourteen. The autopsy disclosed no other possible cause for it than the extreme atrophy and flabbiness of the heart. 5. Blood. — As in most febrile diseases associated with great emaciation, so in typhoid in severe cases the number of red blood-corpuscles (and correspond- ingly the amount of hjemoglobin in the blood) is much diminished. We found, for example, 2,800,000 to 3,200,000 in a cubic millimetre. In milder cases the figures do not differ materially from normal. It is a fact of greater interest and also of distinct diagnostic importance that many observers have found that leu- cocytosis is absent in typhoid fever, contrary to what is found in many other acute febrile diseases, pneumonia, erysipelas, sepsis, etc. We have often confirmed this fact in our clinique. We sometimes find with the general emaciation a de- crease in leucocytes ; for example, only 3,000 or 5,000 in a cubic millimetre instead of the normal number of about 8,000. 6. Skin. — The eruption seen in typhoid fever is characteristic and extremely important in diagnosis. The roseolse or rose-spots (light red, slightly elevated spots) appear at the beginning of the second week, usually on the trunk, and chiefly on the abdomen and back. The number varies greatly. Rarely they are entirely absent, most often in elderly persons. Sometimes they are very abun- dant, and extend to the thighs, the arms, and even to the neck and face. Often they vanish after a few days, but they may persist much longer. In the latter case they may become to a very slight degree petechial, so that they will not entirely disappear on pressure. They often occur in successive crops. We have even seen several cases where new rose-spots kept coming for some days after the fever had disappeared. As to other cutaneous eruptions, we may mention first of all that heiioes la- bialis is so rare in typhoid that in cases of doubtful diagnosis it is a factor in excluding that disease. Miliaria, urticaria, and superficial pustules are some- times observed. Occasionally little bluish spots appear, especially on the trunk. These used to be called " laches hleudtres " (pelioma typhosum) ; but later obser- vations show that they are not connected with typhoid fever particularly. They are due to pediculi. We might use the term pelioma tj'phosum to designate the kind of vesicles which we have repeatedly seen on the abdomen in severe cases. They are about the size of peas, and have sero-hfemorrhagic contents. Boils and superficial abscesses are frequent, especially as disagreeable sequelae in convales- cence from severe attacks. There are often abscesses of the sweat-glands in the skin of the axilla during convalescence. All these and similar cases of suppura- tion in typhoid fever do not depend, as a rule, upon the original cause of the dis- TYPHOID FEVER 19 ease, but upon secondary pathogenic germs, especially the staphylococcus, for whose entrance the typhoid process has merely prepared the way. Extensive ecchymoses are very rare, and are symptomatic of a general hsemorrhagic diath- esis. Petechias are frequent during recovery. They are generally seen in the follicles of the skin below the knee. There have been a few cases of gangrene in the lower extremities, especially in the toes. We saw in one patient an ex- tensive gangrene of the skin of the abdomen. Its cause could not be determined (ice-bag?). Finally, we must mention that bed-sores are prone to develop in severe or neglected cases. The localities most often attacked are the nates, the furrow be- tween them, and the heels. A bed-sore may be so extensive, and accompanied by such undermining of the skin, as to be a dangerous or even fatal complication. The epidermis often scales oif to a considerable extent during convalescence after a severe attack of typhoid. Everybody knows how the hair falls out after the fever, but it is sure to grow again. The nails also are not infrequently affected, becoming rough and brittle, or even falling off. 7. Muscles, Bones, Joints. — Zenker has discovered a degeneration of the vol- untary muscles which occurs in typhoid as well as in other severe diseases. It is called the " granular " or " waxy " degeneration. Whether it has clinical symp- toms can not be determined. Perhaps it may explain the great muscular hyper- sesthesia which is often observed, and the muscular pains, which may be very trying. Severe cases sometimes have haemorrhages into the muscles, particularly the rectus abdominis. Lesions of the bones and joints occur but seldom, although other observers and we ourselves have repeatedly seen periostitis and ostitis in the ribs, tibia, etc., fol- lowing typhoid. It is an interesting fact that lately typhoid bacilli have often been found in such foci of disease, so that it is a true typhoid localization. Swell- ing of the joints is rare. When of a purulent nature it is usually due to secondary " septic " infection. 8. Genito -urinary Apparatus. — Genuine, acute, hsemorrhagic nephritis is a very rare complication. It does occur, however, and has even given rise to the establishment of a special " renal form of typhoid fever " (nephro-typhoid). This name applies especially to those cases in which a severe acute nephritis is the pre- dominant symptom at the start, while at a later period the course of the fever, the intestinal symptoms, the rose-spots, etc., show the disease to be typhoid fever. Nephro-typhoid is analogous to pneumo-typhoid and tonsillo-typhoid. A simple so-called febrile albuminuria occurs very frequently at the acme of typhoid, and is not to be interpreted unfavorably. It is probably the result of that slight par- enchymatous degeneration of the kidneys which occurs in typhoid with the same frequency as in most of the other severe infectious diseases. There does not seem to be a direct relation between the albuminuria and the fever, although some authors assume it to exist. It is more likely that the renal epithelium is injured by the noxious products which have been formed in the body and excreted by the kidneys. In other respects the urine in typhoid presents the same peculiarities as in most other severe febrile diseases : its amount is diminished ; its color dark ; its specific gravity increased; the excretion of urea greater than normal. It should be added that the urine at the height of the disease presents Ehrlich's " diazo-reaction " in almost all cases.* Cystitis is not a rare development toward the end of the illness. It is probably always secondary. * Ehrlich's test is carried out as follows : Solution 1 consists of strong hydrochloric acid, one part mixed with twenty parts of a one-half-per-cent. solution of sulphanilic acid. Solution 2 is a one-liiilf- per-cent. solution of sodic nitrite in water. To 250 c. c. of solution 1 is added 6 c. c. of solution 2 ; an equal volume ot urine is then added, and, lastly, about 60 c. c. of ammonia. On shaking, the urine becomes crimson. 20 ACUTE GENERAL INFECTIOUS DISEASES In men, orchitis is sometimes observed. Women often have their catamenia at the beginning of typhoid. Later in the course of the disease, and in convales- cence from severe attacks, the menses are often absent for several periods. In pregnant women there is considerable danger of abortion or miscarriage. Peculiarities in the Course op the Disease The above statements show an almost inexhaustible variety in the possible symptoms and complications of typhoid. The course of the disease as a whole may likewise present many diverse forms and peculiarities. We shall attempt merely to cite the most essential. The numerous light and rudimentary attacks {typhus levissimus) are first to be mentioned. It was not recognized till lately that they belonged to typhoid fever at all (Griesinger). They used to have all sorts of names applied to them, the favorite term being " gastric fever." This light form lasts eight to fourteen days. The fever is moderate and often decidedly remittent. There is almost no proper fastigium. The typhoid symptoms are but slightly developed. There is no severe pulmonary or cerebral disturbance. There is generally a moderate diarrhoea, the spleen is plainly enlarged, and often rose-spots can be found. The diagnosis of these cases is of course difiicult in proportion to the scanty develop- ment of typhoid symptoms. It is best established by demonstrating an aetiolog- ical relation between these cases and others which are plainly typhoid fever. Abortive typhoid is justly distinguished by Liebermeister from typhus levis. The name belongs to cases which begin with severe symptoms and high fever, as if they were going to be grave, but in which these violent symptoms disappear after a few days and give place to a rapid convalescence. On the other hand, there are cases which for a long time cause so little subjec- tive discomfort that the patient does not even go to bed (walking typhoid). It is not till quite late that there occurs a sudden change for the worse, or some severe complication. Thus it has happened that persons who were apparently healthy have suddenly had all the symptoms of a severe peritonitis due to perforation and have died, the autopsy disclosing the lesions of the third week of typhoid fever; or a mild typhoid assumes the walking type and is not detected, but later a severe or dangerous relapse may occur. The individual circumstances are very important in weighing each case, for they may modify the disease in many ways. In children it is a remarkable fact that typhoid ulcers are much less frequent than in adults. This explains why intestinal haemorrhages and peritonitis are much rarer in children. Marked cerebral symptoms are, on the other hand, very frequent. In severe cases children sometimes exhibit the peculiar symptom of a continuous penetrating screaming. In other, mild, cases the children are sop- orose. In the aged the diagnosis of typhoid is often very difficult, since the course of the disease is frequently irregular. Generally the fever is not very high, and it very seldom exhibits distinctly the type described above. The pulmonary or cere- bral symptoms predominate as a rule. In the corpulent, typhoid fever is often very severe, so that our prognosis must always be rather grave, especially if pulmonary symptoms arise. Hard drinkers are also in especial peril in this as in all other acute diseases. Dangerous cardiac weakness is prone to appear. Severe cerebral symptoms are frequent. It is, however, surprising that true delirium tremens is relatively in- frequent, although so common in pneumonia. The influence of previous strong mental excitement and of certain already ex- isting diseases (cardiac disease, emphysema, kyphoskoliosis, etc.) has been already mentioned. Finally, we repeat that often the different epidemics present certain TYPHOID FEVER 21 peculiarities. For instance, in one the type of the disease will be severe, in another mild. In one epidemic relapses are comparatively frequent, in another exceptional. The same is true with regard to the frequency of the appearance of certain symptoms, such as intestinal haemorrhage, perforation, pneumonia, or nephritis. Indeed, it has even been observed that those cases which occur during a given epidemic in the same family or house or block sometimes present striking resemblances to one another (" group typhoid " of E. Wagner and others). Relapses op Typhoid Fever Typhoid fever exhibits in many cases the peculiarity of repeating itself com- pletely after having run its entire course and disappeared. This process is called a relapse. It is in all probability the result, not of a fresh infection of the system from without, but of a renewed development of the germs already present, or pos- sibly of a fresh auto-infection. A typical relapse is like a first attack in all clinical and anatomical particulars, with this difference that everything is more condensed, and lasts a shorter time than in the first attack. The interval between the two, during which there is no fever, lasts seven to ten days. It may be longer, and is often shorter. Sometimes the relapse follows immediately upon recovery. Indeed, it may even happen that, before the patient has completely recovered, his temperature begins to rise again in the characteristic step-like way. To such cases as this last the term recrudescence is applied. Except in the time of its beginning, it may be just the same as a genuine relapse. In the interval be- tween the two attacks many persons are perfectly comfortable, and appear to be fully convalescent. There is often, however, a slight evening rise of temperature. It is noticeable that the splenic tumor does not completely disappear after the first attack in many cases which are followed by a relapse. The relapse is generally briefer, as we have said, than the first attack, seldom lasting more than fifteen to eighteen days. The temperature rises more rapidly, perhaps in two or three days. The f astigium is shorter, the decline more abrupt. The absolute height of the temperature may be very considerable, even exceed- ing that in the first attack. Rose-spots appear as soon as the third or fourth day. The stools become liquid, the spleen enlarges again, and all sorts of complications may arise. The danger occasioned by a relapse may, however, be overestimated. On the whole, a relapse is not so very dangerous, and it is especially noticeable that the subjective symptoms, such as headache, are often slight. A severe re- lapse may follow a mild case. In other instances the relapse may prove merely rudimentary. The frequency of relapses varies considerably in different epidemics. In Leipsic, we had relapses in about nine per cent, of all cases, but in separate years the percentage varied between four and sixteen. Out of about five hundred cases we have seen three in which there were two successive and typical relapses. Diagnosis. — The diagnosis of typhoid fever may be perfectly easy, but, if the case be anomalous, or come under observation at a late period, it may be ex- tremely obscure. Inasmuch as a search for the specific bacilli is too difiicult and troublesome for the practicing ijhysician, the diagnosis of the disease must be made from its course and symptoms. Important factors are the gradual onset, then the height and course of the fever, with no demonstrable localized disease, and the rose-spots. Less characteristic, but still of value, are the stools, the tym- panites, and the swelling of the spleen. Etiological factors, such as the occur- rence of undoubted cases of typhoid in the neighborhood, are of great diagnostic value in obscure cases. Sometimes the diagnosis can not be established till the appearance of certain symptoms, like intestinal haemorrhage, a characteristic mode of convalescence — viz., by lysis — or a relapse. It is an important rule not to make a diagnosis of typhoid after a single examination. It is generally neces- 22 ACUTE GENERAL INFECTIOUS DISEASES sary to observe the case accurately for several days before the diagnosis can be established. The differential diagnosis from other acute diseases, such as miliary tuberculosis, acute endocarditis, meningitis, etc., will be considered in discussing these diseases. The diagnosis is usually most difficult in the cases with an imperfect history which are first seen in a severe " typhoidal " state, with high fever, disturbances of consciousness, etc. These are the cases in which we must also consider, beside typhoid fever, miliary tuberculosis, acute septic or pysemic infection (including acute malignant endocarditis), meningitis, severe " typhoid pneumonia," etc. The accurate differential diagnosis between typhoid and these conditions will be spoken of later. We may state here that in such cases a careful examination of the blood, especially the absence of leucocytosis in typhoid, may afford very valu- able diagnostic criteria. The ordinary diagnostic features are also to be consid- ered, such as the way the disease began, so far as can be learned, the geti- ological conditions (i. e., the connection with other cases of typhoid), rose-spots, thin pea-colored stools, meteorism, intestinal hemorrhage, etc. Widal has lately reported a method for diagnosticating typhoid (Widal's serum reaction), which is very interesting theoretically, but which, of course, can be used only in cliniques and hospitals. It is based on previous researches by Gruber and others. If we mix ten or fifteen drops of a fresh culture of typhoid bacilli with a drop of blood-serum from a typhoid patient, the bacilli lose their mobility in a few minutes, or at most in a quarter to half an hour, and come together in little clumps ("agglutinating" action of the serum). If we add blood-serum from a typhoid patient to a uniformly cloudy mixture of typhoid bacilli in bouillon, the bacilli again clump together and sink to the bottom, while the fluid becomes perfectly clear. Since the blood-serum of healthy persons, or those not suffering from typhoid, does not give this reaction at all, or only in a slight degree, a very positive result from this test is quite a sure diagnostic sign. The reaction often occurs in typhoid even in the first weeks of the disease, but it may be delayed. It persists long after the disease has subsided. Widal's reaction can also be obtained with serum from a blister or from serous inflamma- tory exudation in a typhoid patient. In otherwise doubtful cases a positive result is of definite diagnostic significance. Prognosis.— A perfectly favorable prognosis should never be made. Cases which seem the mildest may become dangerous (from intestinal perforation, etc.). Yet, if there are good nursing and good treatment, typhoid fever is not a particu- larly dangerous disease, and we may hope for recovery even in very severe attacks. The danger lies, first, in the severity of the infection, as shown chiefly (though not wholly) by the height of the fever and the intensity of the general symptoms. A further danger is the appearance of the complications already enumerated and discussed. Thirdly, the constitution and condition of the individual are impor- tant. The circumstances coming under this head have likewise been repeatedly mentioned above. All these factors must be carefully estimated before we decide as to the danger in each case and make our prognosis. The mortality in typhoid varies greatly in the separate epidemics. The severe cases are undoubtedly more frequent at some times than at others. This renders it difficult to give statistics which are universally applicable. We may in general reckon on an average mortality of about ten per cent., and measure the severity of separate epidemics by this standard. Numerous observers agree that the treat- ment now in vogue has decidedly diminished the mortality. It was formerly not rare for it to reach twenty or twenty-five per cent. Treatment. — A specific cure for typhoid — i. e., some remedy to destroy the specific cause of the disease within the system, or to render it harmless — is as yet unknown. The different remedies recommended for this purpose (carbolic acid, TYPHOID FEVER 23 iodine, thalline, ergotine, naphthaline, etc.) have none of them proved their value, and we can not advise further trial of them. The interesting experiments lately reported of injecting sterilized pure cultures of typhoid bacilli or the bacillus pyocyaneus into the patient (Rumpf and Frankel) has as yet led to no definite practical result. At present there is only one remedy, whose efficiency, of course, should in no way be overrated, which we would be unwilling wholly to give up in treating typhoid fever, and that is calomel. Wunderlich noticed that if a few rather large doses of calomel be given at the beginning of the disease, it will on the average run a lighter and more favorable course than otherwise would have been the case. Wunderlich believed that typhoid fever may sometimes be aborted by this method. Although we can hardly expect this, it is really an efficient means of procedure, which we have almost always employed, to give two or three powders of calomel, of five grains (0.30 gramme) each, as the first prescription, to patients who come under treatment in the first week or the be- ginning of the second. As there is generally constipation, the laxative effect is also beneficial. Moreover, it often lowers the temperature somewhat. A moder- ate diarrhosa is not a contra-indication, but, if the bowels be very loose, the calo- mel should be omitted. In other respects the treatment of typhoid must still be chiefly dietetic and symptomatic, and in one sense prophylactic. We must fight the symptoms al- ready present, and further seek, as far as possible, to defend the patient from the attack of certain dangerous secondary disorders. Starting out with this view, the proper treatment of typhoid fever is a task of the highest importance, and by no means a thankless one. We will begin by considering the general treatment. The sick-room must not be too warm, and must be frequently and thoroughly aired. The sick-bed must be well cared for. If effort be made to prevent bed-sores, we shall obviate one source of pain and danger {vide supra), and save ourselves and the nurse much trouble. Those who are very ill should therefore be laid on an air-cushion, or, if possible, a water-bed. The patient should be told not to lie always upon his back, but to change now and then upon his side. The back, the region of the sa- crum, and the heels are to be often bathed with spirits of camphor or brandy. The minutest bed-sore is to be treated carefully. It should be cleansed twice a day (rinsed off with a weak solution of salicylic or carbolic acid), and dressed with an ointment containing Peruvian balsam, 1-30.* If the bed-sore be extensive, dust- ing with iodoform is very efficient treatment. We should be particularly careful not to let the skin be undermined. If this has already occurred, we must be prompt in the use of the knife or drainage-tube. We can not recommend too strongly that the mouth should be kept clean. In a light case the patient can see to this himself, but otherwise the mouth and tongue must be frequently cleansed with a linen cloth wet in cold water or a solu- tion of borax (1 to 30). Perhaps we need hardly repeat the reason for this excess- ive cleanliness. It lies in the causative relation between stomatitis and inflam- mation of the parotid gland, and of the middle ear. If the tongue and lips be dry, they may be touched with glycerine. The diet must be at once liquid and nourishing. Milk is excellent, and it should always be ordered, but it can, unfortunately, be taken by very few patients continu- ously. It is often better borne if coffee or a little brandy be added to it. Cocoa made with milk may also be given for a change. In severe cases ISTestle's food (Kindermehl) has been often employed by us with benefit. Broths and soups, thick- ened with sago or rice, are also good. They may be made more nourishing by * The unguentum balsami peruviani is made by mixing one part of balsam very thoroughly with thirty parts of the glycerite of starch (B. P.). It is not officinal in Germany. — Trans. 24 ACUTE GENERAL INFECTIOUS DISEASES adding an egg to them. If the patient is very anxious to have more solid food^ as often happens, we need not hesitate to give him a roll or rusk (Zwieback) that has been softened by soaking. If a patient becomes exceedingly enfeebled we should give him fine shavings of raw beef, regardless of the fever. A little dilute hydrochloric acid might be given with the meat. Beef -tea would be still better than the raw meat, and is to be strongly recommended. The various prep- arations of meat which are now made (meat-juice, meat-peptones, etc.) may be useful. When the fever takes a sluggish course, we must often begin to give stronger nourishment before the fever has ended. The best drink is cold Avater, which must be offered to the patient even when he does not ask for it. Lem- onade and similar preparations generally become distasteful in time. Drinks containing carbonic dioxide are to be avoided, because they increase the me- teorism. Cold tea with milk is good. In severer cases we should give some good strong wine, such as port, Malaga, or Hungarian wine, but it is not necessary to force the patient to take wine if he does not care for it. If the patient desires beer, we need not hesitate to give it in moderate amount. During convalescence we should be very careful about diet, since errors often have disagreeable conse- quences. We must wait till there has been no fever at all for seven to ten days before we allow a solid, animal diet, and return by degrees to common sorts of food. The general and dietetic treatment which we have thus far discussed is very important. Outside of this, it is our opinion that there is only one method of treatment to be chiefly considered — at least under the present limitations of our therapeutic ability. This method consists in the persistent use of cool baths, as first practiced by Brand in Stettin. We do not indeed believe that the indica- tions for this method of treatment are exactly what its original promoter held them to be, and we think some of the minutiae of the treatment should be changed. Yet there is at present no other single method of treating typhoid fever which has so numerous and evident advantages for the patient when properly and moder- ately used. To carry it out in private practice may often be more difficult than in a well-appointed hospital. However, even in private houses it will generally be possible to manage it, and we regard it as the duty of every physician who under- takes to treat a severe case of typhoid to try his best to have the baths employed, y^ The great advantages of the treatment by baths are : 1. Thejjaths dimin ish ^ (I the JBY er. if Ih&ir te mperature bfi_j[inly sufficient! v low, by djrect jLbsorption _of • I heat. The baths thus obviate, as far as possible, all'"tKi~Bad effects which might result from a rise of temperature. 2. The direct influence of the baths upon the nervous system is still more important. The intellect becomes clearer, the apathy and dullness diminish. In fact, if baths be used, we do not see nearly so often as formerly the grave " typhoid condition." It is thus evident that bathing not only causes an improvement in the subjective sensations of the patient, but brings in its train many other beneficial effects. The patient takes his nourishment better, does not so often swallow the wrong way, coughs more effectively, is easier to move, and his body and his mouth can be better cleansed. 3. The influence of the baths upon the respiratory organs is of the greatest importance. We refer especially to the stimulation to deeper inspiration, and the promotion of expec- toration. The best proof of the benefit of this influence is the circumstance that if patients are subjected to baths from the start, it is comparatively a rare thing for severe bronchitis, atelectasis, and catarrhal pneumonia to develop. 4. The good care of the skin, which the bathing makes possible, is not to be despised. Since this treatment has been introduced, bed-sores are much rarer in typhoid than before. 5. Lastly, the baths are sometimes observed to have a diuretic effect. What has been said shows that the height of the fever is by no means the sole TYPHOID FEVER 25- indication for the employment of baths, at least in our opinion. The condition of the nervous system and of the respiratory organs is also to be considered. It is true that numerous mild cases run a favorable course without a single bath; but we should always remember that this treatment is not only directed against the symptoms already existing, but has also a prophylactic importance, since it tends- to prevent any severe cerebral or pulmonary manifestations. We will pass on to the special method of carrying out balneo-therapeutics in typhoid. Full baths are generally employed, immersing the patient to his neck. The tub must stand, if possible, by the bedside. In hospitals, where there are beds- on rollers, it is a better way to wheel the patients into the bathroom. All who are severely ill should be lifted into the bath and there held and supported, to avoid any bodily fatigue. During the bath the skin should be gently rubbed. This averts unpleasant sensations of chilliness. The temperature of the water should not be set too low, especially for the first baths. We begin at 85° to 90° (24° to 26° R.), or, if the individual be elderly or sensitive and timid, at even warmer temperatures. When the patient has become accustomed to the tempera- ture of the water, we can cool off the bath still further. Baths below 73° (18° to 20° R.) have scarcely ever been used by us, and we believe that they are seldom needed. A very satisfactory average temperature is 80° to 85° (20° to 24° R.). A bath lasts on the average ten minutes. If the patient feels very cold or very uneasy in the bath, it must be cut short. After the bath the patient is at once lifted into bed, wrapped up in a sheet previously made ready, and wiped dry, with rather vigorous rubbing of the extremities and back. The moist sheet is then removed. The patient is covered up rather warmly, and is given some hot brotK or a sip of good strong wine. The effect of the bath upon the temperature is measured about half an hour later by the rect-um. If the temperature be 2° to 3° (1° to 2° C.) lower than before, the result is deemed satisfactory. Often the dif- ference is greater, but in severe cases the fever may be so obstinate that the tem- perature remits only a small fraction of a degree. In such cases it is sometimes permissible to lower the temperature of the bath still more, or continue it a little longer. If cool baths are ill-borne, protracted baths of lukewarm water are some- times very efficient (Riess, and others). In so far as the height of the fever furnishes an indication for baths, we m.ay accept 103.6° (39.8° C.) in the rectum, as the temperature calling for a bath, but spontaneous variations of the temperature of the body are always to be re- garded. In cases which show a low morning temperature without special inter- ference, the height of the evening temperature is seldom an indication for a cold bath. We regard it as ver-f important that the baths be not given too frequent- ly, since their advantages may thus be overbalanced by their incontestable evil consequences. At present we rarely prescribe more than two to four baths a day. At night we have given baths only very seldom, when forced to by extremely high temperatures or other bad symptoms. It must be a mistake to wake a pa- tient who is quietly sleeping, and put him into cold water, even if his tempera- ture is above 104° (40° C). On the other hand, even if the temperature be not excessive, or even if it be normal, there is, as we have said, no better remedy than the baths for severe pulmonary or cerebral symptoms. In such cases we often raise the temperature of the baths a little, and during them we have colder water poured upon the head and back. If we do this, the ears must be stopped with cotton-wool, lest the cold water find its way into them. Advantageous as the bath treatment of typhoid generally is, it must, how- ever, like every other therapeutic method, be used with wise moderation and with constant regard to individual conditions. If the patients are very weak, show a strong aversion to the baths, or feel dull and exhaiasted instead of refreshed after them, it is well to consider whether we really do good by continuing their employ- 26 ACUTE GENERAL INFECTIOUS DISEASES ment. In such cases we liave of late years often advised cold wet packs of the whole body in bed, instead of the baths, and we consider such a use of cold as very advisable in these cases. The antithermic action of the pack is, of course, much less than that of the bath, but it can easily be aided by the exhibi- tion of antipyretics internally. The respiration and the nervous system, how- ever, are almost always most favorably affected. Most patients readily consent to the packs and lie quiet for an hour or two in the wet envelope. We would urgently recommend the more frequent use of jjacks, especially in private prac- tice, where the bath treatment often meets with greater difficulties than in hospitals. We should here always begin with higher temperatures, and only gradually go on to cold packs. There are a number of contra-indications to the use of baths which can not be disregarded. First, the occurrence of intes- tinal haemorrhage, however slight, and likewise the suspicion that peritonitis is developing, prohibit bathing. In these cases quiet is the very first re- quirement of the patient, and the baths must be at once discontinued. The onset of otitis, severe laryngeal affections, and acute nephritis are also complica- tions in which we should properly omit the baths entirely or employ them very cautiously, giving them warmer and less frequently. Sometimes rheumatic pains in the limbs or an attack of boils render the continued use of baths difficult. In short, we see that nothing could be more foolish than to try to establish a general rule for the bath treatment of typhoid. Passing to the consideration of the further symptomatic treatment of typhoid, the first important question is about giving drugs to reduce the fever. The one- sided point of view which considered that the chief task of the physician in the treatment of acute febrile disease was to lower the temperature has been grad- ually abandoned. In describing the bath treatment of typhoid we have em- phasized the fact that the action of the bath in reducing the temperature was only one factor, and perhaps neither the most efficient nor the most impor- tant factor, in the curative action aimed at. In giving antipyretics inter- nally their antifebrile action is of chief importance, but some of them also have a certain sedative action on the nervous system. The important influence of the bath on the respiration and skin they do not possess. If we had to decide whether to treat typhoid exclusively by baths or exclusively by antipyrine and similar drugs we should decidedly prefer the former. We would not wholly exclude the use of antipyretics internally in the treatment of typhoid, but we would limit their use more than is often the case. In our opinion they are indi- cated only when with existing high fever baths are for any reason impossible or contra-indicated (vide supra), or when, in spite of the baths, the fever remains constantly high. In such cases the baths can often be judiciously combined with the use of antipyretics internally if the patient bears the drug well and feels better subjectively after the reduction of temperature than before. We often treat typhoid patients by baths in the day. and, if the fever be high, by a dose of antipyrine (fifteen to thirty grains, grammes 1-2) at night. With severe head- ache, nervous restlessness, etc., this remedy is especially indicated; but we regard it as at least useless and often improper to give a patient with moderate fever large doses of an antipyretic without any sufficient reason, as unfortu- nately is often the case in practice; the only permanent result is to make the patient feel worse and upset his stomach. In regard to the different antipyretics so frequently brought forward and recommended of late, we are of the opinion that antipyrine is most to be rec- ommended. It was introduced by L. Knorr and first recommended by Filehne. In doses of fifteen to thirty grains (grammes 1-2). best given in wafers, it usiially reduces the temperature considerably, although we may find that the height and the obstinacy of the fever are not identical terms. We do not TYPHOID FEVER 27 often see unpleasant effects from antipyrine (such as vomiting, profuse sweat- ing with defervescence, a chill when the temperature rises again, and some- times a measles-like eruption). The patient often feels better than before while under the influence of antipyrine, since the drug, as we have said, also acts favor- ably on the nervous symptoms (headache, restlessness). The dose of fifteen to thirty grains (grammes 1-2) can in severe cases be repeated several times a day, but, as a rule, we should not exceed eighty or ninety grains (grammes 5-6) in the twenty-four hours. One or two doses a day are usually all-sufficient. Lactophe- nine is also much recommended and even held as a specific in typhoid. In doses of seven to fifteen grains (gramme 0.5-1) it reduces the temperature considerably and usually causes a marked improvement in the general condition. A total of eighty or ninety grains (grammes 5-6) can be used in a day. Of the many other antipyretics which, of course, have often been tried in typhoid, we may first men- tion antifebrine (acetanilide), which in doses of four to seven grains (gramme 0.25-0.5) has a similar action to antipyrine (Cahn and Hepp), and it should be used in practice among the poor because it is much cheaper. If we avoid too large doses we seldom see unpleasant results. The appearance of a pale-cyanotic hue of the skin is the only disturbing feature; this, as in aniline poisoning, is probably due to a change in the coloring matter of the blood, and therefore warns us to be cautious. Other new antipyretics are phenacetine (fifteen grains, gramme 1, at a dose), salipyrine, etc., which have no special advantages. Qui- nine in doses of fifteen to thirty grains (grammes 1-2) and salicylate of soda in doses of seventy-five grains (grammes 5) are now little used as antipyretics, and properly, since their unpleasant action (vomiting, tinnitus, sweating, etc.) is much greater than that of the other drugs mentioned above. [Water or an acid drink should be given frequently by the nurse without wait- ing for the patient to ask for it, unless the mind is unusually clear. Phenacetine seems to have proved itseK less depressing to the heart than its predecessors. The antipyretic dose usual in this country is five grains. A strong protest should be entered against the routine or frequent use of any of these internal antipyretics. If the temperature seems, in itself, to cause restlessness and discomfort, an occa- sional dose may be given. When used early in the course of the disease, anti- pyretics may seriously embarrass the diagnosis in doubtful cases. The method of Brand has been slowly working its way in America of late years, and perhaps would have spread more widely and rapidly were it not that we have long been in the habit of frequently sponging our typhoid patients with alcohol and water.] Another important symptom which needs special treatment is intestinal haemorrhage. It has been already mentioned that if this occurs, the baths should cease at once. Further than this, the chief remedies are ice and opium. Flat ice-bags are laid upon the abdomen. They should not be too heavy, and should, if possible, be suspended from a hoop. Internally, the patient is given every two hours fifteen or twenty drops of laudanum or a powder of one-half grain or one grain (gramme 0.03 to 0.05) of opium, either pure or combined with acetate of lead (opii, gr. ss., grm. 0.03; plumbi acetatis, gr. j, grm. 0.05; sacchari albi, gr. j, grm. 0.05). The object of the opium is to check peristalsis, and thus promote the formation of a clot in the bleeding vessel. In severe cases we may tiy injec- tions of ergotine or fluid extract of hydrastis, twenty drops three or four times. Liquor ferri chloridi (five to ten drops in water eveiy hour) is often employed, but is of extremely doubtful value. The baths can not be resumed till there has been no bleeding for at least three or four days — and then only cautiously. If peritonitis occurs, the treatment is much the same. Above all, opium must be used in still larger doses, but, unfortunately, as a rule, in vain. The surgical treatment of peritonitis has rather more of a future and more success, but experi- ence of this is still scanty. 28 ACUTE GENERAL INFECTIOUS DISEASES If there is considerable diarrhoea, we can give mistura gummosa [P. G., gunt arabic and sugar, each 15 parts; water, 170 parts], or small doses of opiiun, th& latter sometimes combined with tannin, tannigen, etc. In general it is certainly proper not to check the ordinary moderate diarrhoea of typhoid. Persistent con- stipation is always to be avoided. Constipation at the beginning of the disease is overcome by calomel {vide supra). In later stages we always try enemata first, to produce an operation. If this does not succeed, then we must employ rhubarb or castor-oil. Great tympanites may be diminished by laying cold wet cloths or ice-bags upon the belly. Considerable amounts of gas may often be removed by introducing a long rectal tube. As to puncturing the greatly inflated intestines, a method practiced by some physicians, we have no personal experience. If there are severe pulmonary symptoms, baths or wet packs are, as we have said, the best remedies. Internally we may try liquor anamonii anisatus [P. G., olei anisi, 1 part ; aquae destillatee, 24 parts ; aquse ammoniae, 5 parts] and benzoic acid (grains ij to iij, gramme 0.1 to 0.2, in powder). If the pulse be very rapid,^ we may put an ice-bag over the heart. If at the same time the pulse is small and weak, we give stimulants. Of late we have most frequently given tincture of strophanthus (ten to fifteen drops several times) with the best results. We only rarely use digitalis in typhoid. If symptoms of severe cardiac weakness — so-called collapse — suddenly occur a rapid and energetic interference is urgently demanded. Subcutaneous stimulation, injections of ether or camphorated oil,* should be given, with wine, stropanthus, etc., internally. If the respiration stops it can sometimes be started up again by douches of cold water on the back of the neck, or we may often restore it by artificial respiration. Digitalis (one-half grain of the leaves, gramme 0.03, two or three times daily) may also be employed if the pulse be rapid; but it should be used with great caution. For nervous symptoms the baths and douching are the most effective rerae- dies. The head is meanwhile covered by an ice-bag. Antipyrine sometimes acts favorably on the nervous symptoms. If there be great excitement, as shown by excessive restlessness or delirium, small doses of morphine internally, or, better, subcutaneously, are often very useful. The numerous other complications and sequelse which may occur, but which can not all be mentioned here, should be treated on general principles. The prophylactic measures to avoid the spreading of the disease can be only briefly referred to. Of chief importance is careful disinfection of the excreta. The best means for this purpose is a two-per-cent. solution of corrosive sublimate or a five-per-cent. solution of carbolic acid. We may also pour on milk of lime until the reaction becomes alkaline, or use concentrated mineral acids. We should take care that bed-pans, bed-clothes, linen, the rectal thermometer, etc., should be handled by other persons as little as possible, and should be care- fully disinfected. If there seems reason to suspect that the disease was due to bad water, of course the source of siich suspected water must be cut oif. [Eecent experiments tend to show that the above solution of carbolic acid does not kill spores except after prolonged contact. The following are the measures of disinfection recommended by the American Public Health Association. It will be observed that they apply to all infectious diseases, and it seems well to give them here nearly in extenso, as the directions for disinfection in most text -books are far too vague. Disinfection of Excreta, etc. — The infectious character of the dejections of patients suflering from cholera and from typhoid fever is well established; and this is true of mild cases and of the earlier stages of these diseases as well as of * One part of camphor to four of olive-oil in doses of seven to fifteen minims (gramme 0.5 to 1) every hour or two. TYPHOID FEVER 29 severe and fatal eases. It is probable that epidemic dysentery, tuberculosis, and perhaps diphtheria, yellow fever, scarlet fever, and typhus fever, may be trans- mitted by means of the alvine discharges of the sick. In cholera, diphtheria, yellow fever, and scarlet fever, all vomited material should be looked upon as infectious; and in tuberculosis, diphtheria, scarlet fever, and infectious pneu- monia, the sputa of the sick should be disinfected or destroyed by fire. It seems advisable also to treat the urine of patients sick with an infectious disease with one of the disinfecting solutions below recommended. Chloride of lime, or bleaching powder, is, perhaps, entitled to the first place for disinfecting excreta, on account of the rapidity of its action. The following standard solution is recommended: Standard Solution ISTo. 1 Dissolve chloride of lime, of the best quality,* in pure water, in the proportion of four ounces to the gallon. Use one quart of this solution for the disinfection of each discharge in cholera, typhoid fever, etc. Mix well and leave in vessel for at least one hour before throwing into privy-vault or water-closet. The same directions apply for the disinfection of vomited matters. Standard Solution ITo, 2 Dissolve corrosive sublimate and permanganate of potash in pure water, in the proportion of two drachms of each salt to the gallon. This is to be used for the same purposes and in the same manner as Standard Solution No. 1. It is equally effective, but it must be left a longer time in contact with the material to be dis- infected — at least four hours. The only advantage this solution has over ISTo. 1 consists in the fact that it is odorless. It costs about two cents a gallon. It is very poisonous, and will injure lead pipes if passed through them in considerable quantities. Solutions of corrosive sublimate should not be placed in metal re- ceptacles. Disinfection of the Person. — The surface of the body of a sick person, or of his attendants, when soiled with infectious discharges, should be at once cleansed •with a suitable disinfecting agent. For this purpose solution of chlorinated soda, diluted with three parts of water, or Standard Solution ISTo. 1, diluted with three parts of water, may be used. A two-per-cent. solution of carbolic acid is also suitable for this purpose, and, under proper supervision, the use of a solution of corrosive sublimate (1-1,000) is to be recommended. In diseases like small-pox and scarlet fever, in which the infectious agent is given oif from the entire surface of the body, occasional ablutions with solution of chlorinated soda, diluted with twenty parts of water, will be more suitable than the stronger solution above recommended. In all infectious diseases the body of the dead should be enveloped in a sheet saturated with Standard Solution N'o. 1, or with a five-per-cent. solution of car- bolic acid, or a 1-500 solution of corrosive sublimate. Disinfection of Clothing. — Boiling for half an hour will destroy the vitality of all known disease-germs, and there is no better way of disinfecting clothing or bedding which can be washed than to put it through the ordinary operations of the laundry. ISTo delay should occur, however, between the time of removing soiled clothing from the person or bed of the sick and its immersion in boiling water, or in one of the following solutions; and no article should be permitted to leave the infected room until so treated. * Good chloride of lime should contain at least twenty-five per cent, of available chlorine. The cost of the solution is less than one cent a gallon. The sediment does no harm. 30 ACUTE GENERAL INFECTIOUS DISEASES Standard Solution No. 3 Dissolve four ounces of corrosive sublimate and one pound of sulphate of copper in a gallon of water. Two fluid ounces of this standard solution to the gallon of water will make a suitable solution for the disinfection of clothing. The articles to be disinfected must be thoroughly soaked with the disinfecting solution, and left in it for at least two hours, after which they may be wrung out and sent to the wash. Clothing may also be disinfected by immersing it for four hours in a two-per- cent, solution of carbolic acid. Soiled mattresses, pillows, feather beds, and articles of this nature can not be eifectually disinfected by sulphur fumigation, owing to the fact that the gas does not penetrate to their interior in sufficient amount. For articles of this kind, and in general for articles of little value, which have been soiled by the discharges of the sick, destruction by fire will be advisable. Disinfection of the Sick-Boom. — No disinfectant can take the place of free ventilation and cleanliness, and it is impracticable to disinfect an occupied apart- ment. Neutralizing bad odors is not disinfection. All surfaces should be thoroughly washed with Standard Solution No. 1, diluted with three parts of water, or with a 1-1,000 solution of corrosive sublimate. Standard Solution No. 3, diluted in the proportion of four ounces to the gallon of water, may be used. The walls and ceiling, if plastered, should be brushed over with one of these solutions, and subsequently washed over with a lime-wash. Especial care must be taken to wash away all dust from window ledges and other places where it may have settled, and thoroughly to cleanse crevices and out-of-the-way places. After this application of the disinfecting solution, and an interval of twenty-four hours or longer for free ventilation, the floors and wood- work should be well scrubbed with soap and hot water, and this should be followed by a second more prolonged exposure to fresh air, admitted through open doors and windows. As an additional precaution, fumigation with sulphur-dioxide gas is to be recommended, especially for rooms which have been occupied by patients with small-pox, scarlet fever, diphtheria, typhus fever, and yellow fever. All apertures into the room should be carefully closed, and not less than three pounds of sul- phur for each thousand feet of air-space should be burned. To secure complete combustion, the sulphur, in powder or small fragments, and moistened with alcohol, should be placed in a shallow iron pan, and this should be placed on bricks in a tub partly filled with water to guard against fire. — Editor.] [Formaldehyde gas is superior to sulphur dioxide, because of its greater efficiency and rapidity of action, and because it does less harm to household goods. Both gases have merely a superficial action. — V.] CHAPTER IT TYPHUS FEVER (Spotted Fever. Ship Fever) Typhus fever is an acute infectious disease, perfectly distinct from typhoid fever, but formerly often confounded with it. The similarity of the two diseases, which led to their similar names, consists only in the grave general condition with TYPHUS FEVER 31 fever, and in a number of complications which may appear in both. There is, however, an essential difference in the whole course of the two diseases, and espe- cially in the circumstance that the intestinal lesion which is characteristic of typhoid is never seen in typhus. The chief distinction between the two affections, which must undoubtedly lie in the difference in their causes, can not yet be dem- onstrated. We do not yet know the organized pathogenic agents of typhus fever, although it must be presupposed that they exist. .Sltiology. — As to the way in which infection occurs, we have much less infor- mation even than in relation to typhoid. We know nothing as yet as to the supposed specific agents which produce typhus, although micro-organisms have been repeatedly found in the blood. It is an incontestable fact that the appear- ance of typhus in a place previously free from the disease is always to be referred to an importation of the pathogenic poison from without. It is likewise deter- mined, through numerous observations, that typhus is one of the contagious dis- eases — that is, that the specific poison can be directly transferred from the patient to others around him. How it is transferred we have no certain knowledge. Per- haps the poison is contained in the expired air; or, as is still more probable, in the scales of epidermis ; or, perhaps, in the other excretions and secretions of the patient. We are equally ignorant through what channel the infectious agent enters the system — whether it is inspired or swallowed. It is certain that the poison may be transferred in the clothes, etc., of the patient (fomites). Favorable hygienic surroundings decidedly diminish the contagiousness of typhus fever. For example, in the well-ventilated pavilions of the Leipsic hos- pital there have rarely been cases of transfer of the disease to physicians, nurses, or other patients. On the other hand, if the hygienic influences be unfavorable, typhus fever may appear in very widespread epidemics. Those terrible epidemics which have been described under the names of " famine fever," " camp fever " (Hungertyphus, Kriegstyphus), etc., were for the most part typhus fever. In the smaller epidemics it is often possible to trace the disease to some wretched, over- filled tenement-house. At present typhus fever appears constantly in Great Britain. Ireland has been notorious for many years as a breeding-place of the disease. It is also frequent in the eastern part of Germany (Posen, East Prussia and West Prussia, Silesia), in Poland, Galicia, Russia, and in parts of southern Europe. The isolated cases which occur every year here and there in central Germany, though more or less numerous, are, almost without exception, to be referred to an importation of the disease. Typhus fever attacks by preference young adults of twenty to forty years ; but it occurs in children, and is comparatively frequent in elderly persons. There is no marked dependence of the epidemics upon any particular season of the year. As in the case of typhoid fever, a person who has once had the disease seems to enjoy immunity from any fresh attack. [The practical acquaintance of American physicians with typhus fever is, for- tunately, limited. Many of the outbreaks which have occurred were traceable to immigrants, especially from Ireland. During our civil war the disease broke out neither among the armies in the field nor among the prisoners of war. A number of cases were reported at the time, but great doubt has since been thrown upon the correctness of the diagnosis.] Course and Symptoms of the Disease.— If we try to sketch the characteristic behavior of typhus fever, especially as contrasted with typhoid, we may say that the disease begins much more abruptly and rapidly, and that the fever quickly becomes very high and the general disturbance very severe, but the illness lasts a shorter time, seldom more than two weeks, and generally passes by crisis into recovery. 32 ACUTE GENERAL INFECTIOUS DISEASES The length of incubation seems to vary. Murchison thinks it is usually xaore than nine days. Sometimes, though not invariably, slight prodromata precede by some days the actual outbreak of the disease. These are languor, anorexia, headache, and pain in the limbs. Then the regular illness begins, as a Tule, rather suddenly, and often with a pronounced rigor. With this the tem- perature rises quickly, and may on the very first evening reach 104° or 105° (40°-40.5° C). Vomiting is not rare, and may be repeated. A grave general ■condition, with fever, is developed in a few days. The patient feels exhausted. There is often violent pain in the loins and extremities. Nervous symptoms soon appear: persistent and intense headache, vertigo, spots before the eyes, ringing in the ears, and in many cases quickly increasing stupor and delirium. In severe cases the fever often reaches 106° (41° C), and may be even higher, and it is almost constant, with but slight morning remissions. The skin is hot and ■dry, the tongue dry and thickly coated, the respiration moderate, the pulse very •rapid. We very frequently find in the chest the signs of an extensive bronchitis. ISTasal catarrh and conjunctivitis also occur. Serious intestinal symptoms are generally absent, although there may be slight tympanites or diarrhoea. The spleen is almost always greatly enlarged. Only in a few epidemics is the splenic tumor said to have been wanting ( ?). The urine is concentrated and scanty, and sometimes has a trace of albumen. On the third to the seventh day of the disease the characteristic eruption ap- pears. To this the disease owes its name of " spotted fever." The eruption con- sists of rose-spots, generally very numerous and widespread, upon the trunk and extremities, often also on the face. Sometimes the spots are larger, and may then I)ear great resemblance to a fresh eruption of measles. The skin between the sep- -arate rose-spots is not infrequently diffusely reddened. After two or three days "the roseolse become hsemorrhagic, and change into lighter or darker petechise. It is commonly only in the lighter cases that the rose-spots fade away without :first becoming petechial. In rare though well-substantiated cases the eruption has been scanty, or even wholly wanting. Herpes does occur, but only seldom. The fever begins to abate in light cases as early as the second week, coin- ■cidently with an improvement in the general symptoms. Often this change is indicated about the seventh day by a considerable remission in the temperature. On the other hand, in severe cases, all the symptoms grow worse. The weakness increases. The nervous derangement reaches the extreme of a severe " typhoidal •state," expressed either by marked stupor, which sometimes passes into complete <3oma, or by violent delirium. Lobular pneumonia attacks the lungs, and the fever continues with unabated violence. These symptoms may end with death, I)ut in favorable cases they decline rapidly. Sometimes this decline is preceded I)y a great rise in temperature (perturhatio critica), especially about the seven- teenth day, rarely a few days earlier or later. In such cases the temperature is apt to fall by crisis, sinking in a day or two, with but slight interruption, down to the normal level. Even in those cases in which the descent is by gradations it is always decidedly more abrupt than in typhoid. The eruption quickly fades, the patients gradually improve, and, as a rule, become completely and permanently convalescent. It is true that some observers have seen relapses, but they are, at least in our present epidemics, extreriiely rare. Complications and Varieties in the Course of the Disease. — From what we Tiave said of its course, it is evident that the symptoms are essentially those of an intense general infection of the system. The sole demonstrable local lesion which is almost invariably present is the characteristic eruption, and this has evidently no causal relation to the severe symptoms of the disease. It is likewise extremely probable that most of the complications, which not infrequently arise in severe •cases, are secondary, and occur in the way already described with considerable RELAPSING FEVER 33 detail in the preceding chapter. They are just such complications as are possible in every severe general disease, and embrace otitis, parotitis, extensive lobular pneumonia, more rarely gangrene of the lungs, and pleurisy; also furunculosis, jDurulent cellulitis, bed-sores, dysentery, icterus, etc. Whether some of the local lesions which are observed may not be direct results of the pathogenic poison, we can not at present decide. Among these would come, first of all, the rare cases of lobar pneumonia and nephritis. Sequelae are, on the whole, rare, though sometimes there is a tedious ansemic condition, or neuralgia, paralysis, etc. The separate epidemics of typhus present considerable variety, not only as regards the occurrence of individual complications, but more especially in the general course and character of the cases. For instance, some epidemics are dis- tinguished by the greater frequency of light attacks {typhus exanthematicus levissimus, unsuitably termed by some " febricula "). Here the entire attack runs its course in five to eight days. The fever is generally comparatively moderate; there are no severe general symptoras, and complications are exceptional. Diagnosis. — It may be very difficult for a time to distinguish typhus from typhoid. The following factors are of chief importance : 1. The onset is much more abrupt in typhus than in typhoid, and is often accompanied by a pronounced rigor. 2. In typhus, the nervous disturbances usually appear earlier and are more severe than in typhoid. 3. The rash is seldom so extensive in typhoid as in ty- phus, and in typhoid it hardly ever becomes petechial. 4. In typhus the pains in the loins and limbs are generally much more pronounced. 5. If we still find it hard to decide, the manner of recovery will almost always settle the question. Recovery in severe cases of typhoid is, on the average, much more tardy and gradual, by lysis. In typhus it occurs generally by the seventeenth day, and by crisis. The prognosis is chiefly determined by the severity of the fever and of the nervous symptoms. Extensive lobular pneumonia is the most frequent dangerous complication. The mortality varies greatly in the separate epidemics. It is some- times only six or seven per cent., but may rise to twenty per cent. Treatment is based on the same principles as in typhoid fever. There is no specific remedy. Besides good nursing, a judicious employment of baths is cer- tainly our chief reliance for lessening the severity of many of the symptoms, such as febrile, nervous, and pulmonary disturbances, as well as for averting many dangerous complications. For all details of treatment we may refer to the pre- ceding chapter. CHAPTER III RELAPSING FEVEB {Relapsing Typhus — Febris Tecwrens) .aitiolog-y. — This disease was first named by English pathologists relapsing fever, and by Griesinger feliris recurrens. It has a peculiar course, made up of separate attacks, and is further of great interest because it is one of the first infec- tious diseases in which the specific pathogenic organisms became known, and, being easily demonstrable in each separate case, were utilized for the speedy and certain diagnosis of the disease. Obermeier discovered in Berlin, in the year 1873, that in relapsing fever the blood, at certain times, invariably contains peculiar thread-like micro-organisms. This discoveiy has since been universally confirmed; and it may be maintained that if once the presence of these " spirilli " 34 ACUTE GENERAL INFECTIOUS DISEASES be demonstrated in the blood, we are justified in making an absolute diagnosis of relapsing fever. In Germany the disease did not become epidemic till the year 1868. In 1S72 and 1873 there were considerable epidemics in Breslau and Berlin. Its last exten- sive appearance was in 1879 and 1880, when it spread over most of northern and central Germany, and was accurately studied by numerous observers. People of the poorer classes were almost exclusively attacked, and especially the " tramps." The uncleanly dens where these people lodge were found everywhere to be the chief centers of infection. The precise manner of infection is as yet almost wholly unknown. All ob- servers agree that the disease is directly contagious ; but it can not be very con- tagious if the hygienic influences be good. At least the results of our late epi- demics would imply this. In the Leipsic hospital, where at that time over two hundred and fifty cases were treated, and isolation could not be at all perfectly carried out, not one case of infection occurred. It is certain that the disease can be transmitted by direct inoculation with the blood of patients. This has been established by a Russian physician, by the experimental inoculation of healthy persons. Doctors have been repeatedly inoculated at the autopsy of those who have died of relapsing fever. The disease may likewise be transferred by inocula- tion to monkeys, while other mammals seem to enjoy an immunity from it. [The first cases of relapsing fever observed in this country were in Irish immi- grants coming over in the same vessel in the year 1844. At several periods since then more or less limited outbreaks traceable to immigration have occurred, but the disease has never acquired any foothold with us, and comparatively few physi- cians have ever seen it. So far as I can learn, only one case has ever been seen in Boston, and that was in the person of a physician from another city, who brought, the disease with him and passed through it in the Massachusetts General Hos- pital.] Clinical History. — The stage of incubation lasts about five to eight days. It is. only exceptionally that some slight prodromal symptoms present themselves just before the outbreak of the disease proper. As a rule, it begins suddenly, with a more or less pronounced chill and intense constitutional symptoms. There are violent headache, great languor, anorexia, and especially marked pains in the loins and extremities. The temperature rises rapidly, reaching generally 106° (41° C.) or higher as early as the first or second day. The skin is hot and dry, and usually quickly assumes a very characteristic dirty-yellowish color. In Leip- sic, we often saw herpes labialis, which seems, however, to have been rarer in epidemics elsewhere. The tongue becomes dry and thickly coated. Sometimes there is vomiting. The bowels are constipated, or there is a slight diarrhoea. The spleen becomes rapidly enlarged, being, as a rule, even larger than in typhoid or typhus. The liver is slightly enlarged. The chest presents the signs of a bron- chitis, generally moderate, but in exceptional instances severe. The pulse is much quickened. It is seldom that there are severe cerebral symptoms beyond a certain apathy and stupor. We have seen delirium tremens sometimes, in drunk- ards. A very characteristic symptom, already mentioned, is the marked hyperses- thesia of the muscles, especially in the calves. After these symptoms, accompanied by persistent and generally very high fever, have lasted five days to a week, there is a critical decline of temperature, with profuse sweating. The patient now improves so rapidly and decidedly that he thinks himself completely cured, and generally gives little credence to the physician's prophecy of a relapse. In rare but well-attested cases there has been really but one attack. The rule is that, after about a week, a second attack occurs, often a third after that, and, infrequently, even a fourth and fifth. In each of these, the above-mentioned symptoms are repeated more or less completely and vio- RELAPSIls^G FEVER 35 lently. As the only certain and constant sign of the recurring attacks (the so-called relapses) is a fresh rise of temperature, it will be well to consider their peculiarities at the same time that we describe the course of the fever.^ During the intervals of normal temperature the other objective symptoms of disease are usually absent, except an evident splenic tumor, and, not infrequently, the peculiar pale-yellow hue. Course op the Fever (see Fig. 3). — The beginning of the fever in the first attack is, as we have said, almost always sudden, so that it may even in a few hours reach a considerable height. The fever lasts, as a rule, five to seven days, but not infrequently as short a time as three or four days, or as long as ten or 2 3 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Fig. 3. — Example of the temperature curve in relapsing fever. twelve days. During this time it may keep a tolerably uniform height, but oftener there are considerable remissions, which may even come to deserve the name of pseudo-crises. In such cases the temperature sinks in the morning to normal or even lower, so that we might believe the fever ended ; but in the even- ing the temperature rises again to its former level. These pseudo-crises are most frequent toward the end of the attack, but do occur sometimes in the very first days. The absolute height of the fever is, as a rule, very considerable. Tempera- tures between 105.5° and 106.5° (41° and 41.5° C.) are very often observed, and in themselves are not especially ominous in relapsing fever. The highest tempera- ture we have observed was 107.9° (42.2° C). Sometimes the temperature is more moderate (between 102° and 104°, 39° and 40° C). The fever almost always ends at the close of the attack by crisis, only rarely by a rapid, gradual decline. The crisis is often preceded by an especially great rise the evening before {per- turhatio critica) ; so that the subsequent fall of temperature is very considerable. It generally occurs at night, and is accompanied by profuse perspiration. The fall may amount to 9° or 10° (5° to 6° C). The temperature sinks almost always below normal, often as low as 95° (35° C.) or thereabouts. Once we saw it fall to 92.1° (33.4° C). To the first attack succeeds an interval during which there is no fever (a py- rexia), which lasts on the average about a week, sometimes a less time, and often a greater. The longest interval we have ever observed lasted seventeen days. During this interval the temperature, which, as a rule, is at first subnormal, rises to normal, and then generally remains there. Exceptionally there are slight evening exacerbations to above 100.5° (38° C). These may have no demon- strable cause, or may result from some complication, such as otitis, or a furun- cle. Then comes another change, and generally a sudden one, ushered in with a 36 ACUTE GEIsTEEAL INFECTIOUS DISEASES chill, and a new rise of temperature, the beginning of the second attack or first relapse. During this attack the fever has the same general peculiarities as in the first attack. Generally the first relapse is briefer by a day or two than the first attack ; but the reverse is sometimes true. We will add that we have observed not infrequently a rather high evening temperature (101.5°, 38.5° C.) for one or two days before the second attack began, as also before the third. Relapsing fever seems in many epidemics to have been made up of two attacks, so that not more than one tenth of the cases had a third attack. On the other hand, the majority of the cases in the last epidemic had two relapses. In these cases the rule was for the interval between the second and third attacks to be one or two days longer than the first apyrexia; but earlier epidemics seem to have had the second apyrexia, if there was one at all, briefer than the first. The third attack is set down in all reported cases as decidedly shorter than either of its predecessors. It lasts generally two or three days. Exceptionally we have seen it persist for four or even six days. A fourth and even a fifth attack may occur, but only exceptionally. If they do happen, they are usually imperfectly developed, and often are limited to a fever of one day's duration. The more ac- curately and persistently we take the tem- perature during convalescence, the oftener do we find slight rises of temperature oc- curring at intervals late in the history of the case. These are probably to be inter- preted as final, rudimentary attacks. The Spirilli. — The number of cases of relapsing fever in which no spirilli can be demonstrated in the blood, if the exami- nation be accurate, has become so small that it can be disregarded, when we com- pare it with the much greater number of cases where such demonstration is made with ease and certainty. The best way is to get a drop of blood by pricking the skin, and examine it as it is, without mix- ing anything with it. Staining (with the basic aniline colors) is easy but unneces- sary. With any good dry lens of 400 to 500 diameters the spirilli are seen with perfect distinctness. It requires a little practice to make them out ; but this is easily obtained. Often the attention is first caught by little jogglings and mo- tions of the red blood-corpuscles, and then we see the delicate, narrow threads. Their length equals about three to six times the diameter of the red globules (Fig. 4). They exhibit an active and almost continuous motion, like snakes. Often the whole thread bends upon itself, and then stretches out again. They are partly separate and partly tied up in knots composed of four to twenty individ- uals. The whole number visible in one field varies greatly in individual cases, and has no direct relation to the severity of the case. Often it requires long searching to find a few, while in other eases there may be twenty or more in the field at once. A very interesting fact is that their appearance in the blood de- pends upon the attacks of fever. On the first day of the attack we rarely find spirilli, and then only one or two. Upon succeeding days their number increases. Shortly before the end of the attack — that is, before the crisis — they generally disappear entirely ; but even after the crisis they have been found, exceptionally and in very small numbers. They have very often been found by the author as well as other observers during the pseudo-crisis described above, so that, after the Fig. 4.— Spirilli of relapsing fever in the blood. KELAPSING FEVER 37 temperature has become normal, the presence of spirilli makes it very probable that another rise of temperature is impending. The spirilli have thus far been found in the blood only, in the catamenia, in bloody urine, or in blood coughed up from the lungs, and never in the organs or secretions (urine, milk, sweat, contents of herpetic vesicles). There can hardly be any doubt that the spirilli which appear in the separate attacks are to be regarded as separate gener- ations. As to their manner and place of development we have as yet no knowl- edge. In the final, rudimentary attacks, we find few if any. If the patient dies during an attack, they are to be found in the blood after death. Artificial cultivations have not been very successful; nor have pure cultures of them, to our knowledge, ever succeeded. Albrecht states that they will subsequent- ly develop in blood taken from a patient during the ioiterval when he has no fever. The blood is otherwise modified during relapsing fever. "We very often find a slight increase in the white corpuscles. There is often a noticeable abundance of very small bodies, so-called granular elements (Kornchenbildungen). The signifi- cance of these (the remains of white corpuscles?) is still doubtful. There are, finally, peculiar cells, rather large, with fat-granules. They were demonstrated by Ponfick in the venous blood, and are said to come from the spleen. We also find fatty-degenerated endothelium in the blood. Complications are on the whole rare, and mostly secondary. Important among these are troublesome ophthalmic disturbances, especially iritis and irido- choroiditis. Sometimes parotitis, laryngitis, or pneumonia occur. Epistaxis is a not infrequent complication. It is usually profuse and persistent, and it may even be dangerous. Sometimes there has been rather severe dysenteric trouble. In one case which ended fatally we observed a very peculiar intestinal lesion, consisting of hsemorrhagic-necrotic foci in the colon and lower ileum. In severe cases acute hsemorrhagic nephritis occurs with comparative frequency. At the autopsy an important and characteristic phenomenon is the wedge-shaped white spots which occur in the spleen, like infarctions. They have a clinical interest, as they may become the starting-point of pygemic conditions or of peritonitis. Splenic abscesses have been observed in a few cases. Variations in the course of the disease occur in this, as in all other acute infectious diseases. First there are mild, abortive cases, in which the attacks are few and brief. Then cases have been described resembling intermittent fever. Of chief importance is that severe variety of relapsing fever first observed in Egypt by Griesinger, and described as " bilious typhoid." There is no longer any doubt about the proper classification of this disease, for spirilli have been proved to appear in it, and it has even been shown that its inoculation upon another person ( !) produces an ordinary case of relapsing fever. Bilious typhoid fever oc- casions successive attacks, like those of relapsing fever. The type is much more severe. As a rule, there appear marked icterus, grave nervous symptoms, hfemor- rhages into the skin and mucous membranes; and the termination is frequently fatal. The autopsy shows a greatly enlarged spleen, often containing infarctions and abscesses, and in some cases hepatic abscesses, septic nephritis, and similar lesions. The prognosis of ordinary relapsing fever is on the whole very favorable. In the last epidemics the usual mortality was only two to four per cent. The fatal cases could some of them be laid to wretched nursing. In the remaining portion death resulted from complications, such as pneumonia and nephritis. The treatment must as yet be purely symptomatic. Antipyretic treatment is generally needless, since the fever is relatively brief and often quite intermittent. Moreover, most patients can not well endure cold baths, because the muscles are so painful. As a rule, good nursing and proper food amply suflSce. If the mus- 38 ACUTE GENERAL INFECTIOUS DISEASES cular pains are very violent, we may order chloroform liniment as an embroca- tion. Complications are to be treated on general principles. We are not acquainted with any remedy that can influence the disease itself or avert the relapses. Large doses of quinine, salicylic acid, etc., have been fre- quently employed for this purpose, but never with success. Lately there has been ascribed to calomel a favorable influence upon the general course of the dis- ease, and its use is said to diminish the number of attacks. We must await fur- ther evidence in support of this statement. CHAPTEE IV SCABLET TEVEE {Scarlatina) We now begin the consideration of those acute infectious diseases which are usually embraced under the name of the " acute exanthemata." In this group are reckoned, besides scarlet fever, measles, rotheln, small-pox, and varicella. The point which these diseases have in common i^ that in all of them is developed a characteristic eruption, of slight clinical signiflcance in itself, in most cases, but of thoroughly characteristic appearance in each disease, and hence of essen- tial importance in diagnosis. A number of the acute exanthemata have this further point of mutual resemblance that they appear chiefly in children. These diseases are scarlet fever, measles, rotheln, and varicella. .Etiology. — Infection with the specific scarlatinal poison occurs almost always by contagion, which takes place very readily. A single approach to a patient ill with scarlet fever may suffice to communicate the disease. There is no doubt that the disease may be transferred by objects which the patient has touched, such as linen, clothing, furniture, or toys. Persons who have been with the sick may be the means of transmitting the disease, although themselves unaffected. In Eng- land it has been thought that the contagium may be carried by milk. Numerous observations show that the scarlatinal poison is with great difficulty destroyed, and that it may keep its contagious powers for months ("tenacity"). We can thus see how difficult, how impossible, it may be in an individual case to point out the source of contagion. Scarlet-fever patients can communicate the disease certainly as late as the end of the desquamative period, or perhaps some- what longer. Details as to the manner of contagion, or as to the specific poison itself, are as yet unknown. All statements made in regard to finding alleged specific micro- organisms of scarlet fever are extremely doubtful. The exciting agent of scarlet fever must, however, be contained in the blood and in the contents of the miliary vesicles of scarlet-fever patients, for the disease has repeatedly been artificially produced in healthy persons by inoculation with these fluids. Predisposition to scarlet fever is far less universal than is pi'edisposition to measles or small-pox. In families with several children often only one or two fall sick, while the rest escape, although equally exposed. As age increases, liability to the disease greatly diminishes, although there are cases of scarlet fever among adults. The majority of patients are between two and ten years of age. Scarlet fever is rare during the first year of life. It is an interesting fact that children with fresh wounds, either accidental or surgical, are especially liable to scarlet fever. An analogous and familiar fact is that women after delivery have a strong SCARLET FEVER 39 tendency to the disease.* As a rule, a person is attacked but once, so that, after the disease is over, an immunity from contagion is enjoyed; but there are excep- tions to this rule. Scarlet fever is now spread over the entire globe. In Germany there are almost always some sporadic cases in the larger towns, while from time to time, especially in autumn, there are more or less extensive epidemics in one place or another. There is considerable variation in the different epidemics of scarlet fever, as in many other infectious diseases, in the general character of the disease, and above all in the prevailing mildness or severity of the cases and the frequency of certain complications (nephritis, diphtheria), etc. Clinical History. — The period of incubation is not definitely known. Many observations seem certainly to indicate a short period of two to four days, but the incubation stage is perhaps often somewhat longer — four to seven days. There are hardly ever any decided prodromata. The disease begins rather suddenly, with fever, often introduced by chilliness, and sometimes by a well-marked rigor. There is almost invariably a painful, scarlatinal sore throat. A further symp- tom, in all cases of any severity, is cerebral disturbance, generally rather intense. There may be headache, dullness, uneasy sleep, delirium, and, in smaller chil- dren, sometimes even convulsions. A very frequent and characteristic early sjTQptom is vomiting, which raay be repeated. The characteristic rash usually appears as soon as the close of the first day, or on the second, and begins on the neck and on the chest and face, quickly becoming almost universal. The eruption consists at first of numberless small red points, crowded thickly together and soon united into a diffuse, intense, scarlet-colored erythema. The small and somewhat elevated points almost always correspond to the swollen hair-follicles. The diffuse redness is the result of an excessive hyper- emia of the skin, and vanishes completely on pressure. The skin as a whole seems slightly swollen and thickened. The back usually presents the most vivid tint. In the face there is generally pallor of the lips and chin, presenting a very striking and characteristic contrast to the bright-red cheeks. If some object like the end of a pen-holder be drawn over the red skin, there soon arise corre- sponding white lines, due to contraction of the blood-vessels. It is possible thus to make letters or pictures upon the back of the patient. We should add, how- ever, that this is not a peculiarity of the scarlatinal eruption, being seen in other erythematous eruptions. The rash persists for some three or four days, at first even increasing somewhat in vividness. It often appears more intense by artificial light than in the day- time. Meanwhile the severe general symptoms continue — the fever, the usually excessively rapid pulse, the cerebral sjonptoms, and the throat trouble. The spleen is often somewhat swollen, though seldom very large. Then the eruption begins to fade, the fever gradually ceases by lysis, the general condition and the difficulty in swallowing improve. With the end of the first week or the beginning of the second, the cases which run the tjTDical course become fully convalescent. When the rash disappears, the epideraiis usually begins to peel off, in a very character- istic way, in pieces of considerable size. The exfoliation upon the hands and feet is especially pronounced, and the little convalescents often amuse them- selves by peeling off the epidermis in strips. Cases which are apparently the mildest and most benign may have their convalescence interrupted by the oc- currence of a secondary scarlatinal nephritis. There is no sure prophylaxis against this. We will now pass on from this general summary to a more complete considera- * In puerperal cases genuine scarlet fever and septic diseases were formerly often confounded. (See Chapter XVIII.) 40 ACUTE GENERAL INFECTIOUS DISEASES 41.0° 40.0' 39.0° 38.0 37.0° Mwmmmmm ■■■■■■■■BnnBIHB ■iBBssaaffii Fig. 5. Eruption. -Example of a normal scarlet-fever curve. tion in detail of general and local symptoms; and we shall see how manifold are the clinical phenomena presented by scarlet fever. 1. Fever (see Fig. 5). — Although in a few undeveloped cases there is no fever, or scarcely any, almost all cases of any severity have high fever. It is only ex- ceptionally that severe cases are observed in which the bodily temperature is little if at all elevated. As a rule, the fever rises rapidly upon the very first day, cor- responding to the sudden onset of all the symptoms, to about 104° or 105° (40°-40.5° C). The next day it often becomes a little higher still, and then persists with but slight variations, as a rule, so long as the eruption is at its height. During this period a tempera- ture of 105° or more (40.5°^1° C.) is not infrequently observed. When the eruption fades, and the other symp- toms decline, defervescence occurs. This happens but rarely by crisis, and that in the slight attacks. It is almost always by prolonged lysis, as in ty- phoid, only more irregularly and more rapidly. If the fever lasts into the sec- ond week of the disease, it is almost always (though not without excep- tions) caused by demonstrable complications. The most frequent causes are the persistence of a severe sore throat, the occurrence of inflammatory changes in the cervical glands, or a purulent otitis media. In closing what we have to say about the fever in this disease, we would emphasize the fact that the pulse is often very rapid (140 to 160 a minute), even in comparison with the height of the tem- perature. 2. The Throat. — The throat presents the most constant local lesion of scarlet fever. Sore throat is only in the rarest cases wholly absent ; * but its form and intensity may vary extremely. The mildest variety is a simple, erythematous catarrh, without much swelling, but exhibiting usually a vivid and often punctate reddening of the soft palate and tonsils, the pharynx, and also the mucous mem- brane of the hard palate, frequently associated with enlargement of the little mucous follicles. Sometimes minute haemorrhages take place into the mucous membrane. In other cases the scarlatinal affection of the throat is from the start associated with considerable swelling of the parts, and especially of the tonsils, justifying the term " parenchymatous sore throat." Not infrequently small abscesses form in the lacunae of the tonsils ; or superficial spots of necrosis develop which leave behind them larger or smaller ulcers, and sometimes occasion con- siderable haemorrhage. There may even be a circumscribed gangrene of the tonsils. The most important, because it is also the most dangerous, of the affections of the throat resulting from scarlet fever is the so-called scarlatinal diphtheria — that is, a diphtheritic inflammation of the tonsils and soft palate. This usually develops on the third, fourth, or fifth day of the disease, replacing a simple in- * Absence of sore throat has been noted by others and by myself, especially in the scarlet fever of women in childbed. I suspect that the reason for this is that the infection does not enter in the usual ■way through the mouth, but from some wound due to parturition. On the other hand, it is to be noted that in the scarlet fever from wounds, when the infection follows an injury to the finger, etc., a sore throat occurs. SCAELET FEVER 41 flammatory condition of the parts. Whitish, dirty-colored spots develop on the tonsils, the arches of the palate, and the uvula. These rapidly increase in size, and cause a dry necrosis of the mucous membrane and subsequent ulceration. The process is a truly diphtheritic one — that is, there is an inflammation com- bined with an extension into the diseased tissues of a fibrinous exudation. It is especially characteristic of scarlatinal diphtheria that there is almost invariably a considerable swelling of the cervical lymph-glands, except in those cases which die very quickly. It is true that the glands are usually somewhat enlarged in the milder forms of pharyngitis accompanying scarlet fever, but they seldom attain the size observed in the true diphtheritic process. In this there is an inflammatory and oedematous infiltration affecting often not only the glands themselves, but also the surrounding connective tissue, so that in severe cases the whole cervical region and the floor of the buccal cavity presents a firm and usually a very painful enlargement. It should be added that the severity of the throat symptoms and the extent of the glandular swelling are not always com- mensurate. Almost always the scarlatinal diphtheria is associated with a marked stomatitis, and very often also with a severe purulent or even diphtheritic rhinitis, although an invasion of the larynx (vide infra) is only exceptionally seen. At the alse of the nose and the corners of the mouth there are often superficial ulcers from this cause. Otitis is also a frequent complication of scarlatina (vide infra) . The infiuence of the scarlatinal diphtheria upon the general condition of the patient is always considerable. Apart from the marked local discomfort, there is often a severe general septic condition. Grajre signs of cardiac weakness (a very rapid, small pulse) are very apt to appear early. Moreover, cases of scarlet fever associated with pharyngeal diphtheria often show at the same time other severe septic complications (inflammation of several joints, simple or purulent inflammation of the serous membranes, nephritis, etc.). Many cases end fatally in a few days, while others pursue a more tedious course, lasting perhaps several weeks before death comes. These are often associated with pysemic processes in other parts of the body. With regard to the pathogenesis of the throat troubles seen in scarlet fever, the more simple forms are in all probability directly associated with the scarlatinal process — that is, they are direct sequences of the affection. In regard, however, to the severer forms, and especially to the diphtheritic variety, it is almost cer- tain that these are not a direct result of the scarlatinal poison, but are due to some secondary infection which occurs on the soil furnished by the primary scar- latinal angina. The severe necrotic disease of the mucous membranes and the secondary changes in the lymph-glands and other septic complications are due chiefly to streptococci (Loffler) ; but we are almost compelled to suppose that there is some intimate connection between the two varieties of infection, else why should this peculiar secondary disease, the scarlatinal diphtheria, be so often con- joined with scarlet fever ? It seems to us certain that " scarlatinal diphtheria " should not without further evidence be identified with true diphtheria, in spite of the similarity of the anatomical (" diphtheritic ") changes. From a purely clin- ical standpoint the two present several important points of difference. In partic- ular the scarlatinal diphtheria, in contrast with the primary form of the disease, seldom spreads to the larynx. Laryngeal croup is therefore but rarely seen in scarlet fever. The severe dyspntea which sometimes develops in the course of scar- let fever is probably caused by an inflammatory cedema of the glottis. Another important clinical distinction between genuine and scarlatinal diphtheria is that paralysis of the soft palate, the ocular muscles, and other parts is scai'cely ever a sequel of scarlatinal diphtheria. On the other hand, however, it is easily con- ceivable that many similarities between the two diseases should exist, since 42 ACUTE GENERAL INFECTIOUS DISEASES severe secondary septic streptococcus infection may occur both in scarlatinal angina and in true diphtheria. It is also possible that in some cases an actual true diphtheria should appear as a secondary infection in scarlatinal angina. The reported cases of laryngeal croup after scarlet fever may thus be explained. All these conditions, which have been ranch discussed, will be made wholly plain when the accurate bacteriological investigations of individual cases become more numerous. 3. We proceed by a natural sequence 'to the consideration of the affections of certain parts adjacent to the throat, troubles which must be regarded as chiefly the result of direct extension, or of a conveyance of the inflammatory process from the throat. The stomatitis we have already mentioned, as well as the disturbance in the neighboring lymph-glands and the surrounding tissue. Parotitis is not rare in severe cases. Of especial importance is the scarlatinal inflammation of the middle ear, which often results in permanent deafness. This inflammation usually arises at the time of desquamation, but it may occur earlier. It is either a simple catarrh, a purulent otitis media, or, in severe cases, an actual diphtheritic process. The deafness and earache are easily overlooked, as the other symptoms of the patient occupy the attention, so that the ear trou- ble is first recognized by the occurrence of perforation of the tympanum and sub- sequent purulent otorrhoea. After this declines there very often remains behind, as we have said, permanent deafness. Statistics have shown that four or five per cent, of all cases of deafness are referable to an attack of scarlet fever in child- hood. The otitis is seldom immediately dangerous, but yet cases of purulent meningitis have been observed to follow it. We have already spoken of the purulent or even diphtheritic rhinitis which almost always accompanies the scarlatinal sore throat. In rare cases there may also occur a purulent conjunctivitis, which is most probably the result of a direct conveyance of inflammatory secretions. The tongue in scarlet fever deserves special mention. The first coating cleans off, and then the tongue usually presents a very characteristic appearance. It is diffusely reddened and covered with little elevations corresponding to swollen papillae (strawberry tongue, scarlatinal tongue). 4. The characteristic eruption, as developed in the great majority of cases, has been described above. It remains to describe certain variations from the usual appearances. First, the eruption may be rudimentary. It is then not pronounced, and visi- ble only on a limited portion of the body (face, trunk, or extremities). Variations from the type are not rare ; sometimes the papules are more strongly develoi)ed (scarlatina papulosa) ; very frequently there are little vesicles {scarla- tina miliaris). This latter form of the eruption appears by preference upon the trunk, but it may come also upon the extremities, and is often brought out by ex- cessive perspiration, or by wrapping up the patient too warmly. Many epidemics are noticeable from the frequent appearance of this miliary form. More rarely the rash has a spotted look, resembling the eruption of measles {scarlatina varie- gata). There may be minute ecchymoses, which are not very rare and not omi- nous. Well-developed cases of hemorrhagic scarlatina are, however, very danger- ous, because here the general infection of the system is almost always exceedingly severe, and probably due to secondary sepsis; and there is besides, as a rule, a general ha^morrhagic diathesis. Other cutaneous lesions, especially herpes and urticaria, are not so very unusual in connection with the scarlatinal eruption. Furunculosis has been repeatedly observed after the rash fades. Desquamation generally begins as soon as the rash has completely disappeared, but it may not occur till a few days or even one or two weeks later. Its extent SCAELET FEVER 43 corresponds in general to the severity of the eruption, although extensive desqua- mation may follow a rudimentary eruption. It is seldom bran-like or furfura- ceous, as in measles. The rule is for it to be in lamellae, so that, as we have stated, quite large strips of epidermis may be detached entire. In rare cases an cedema of the skin appears after scarlet fever, which can not be shown to depend upon nephritis {vide infra), but which may perhaps be due to an abnormal permeability of the walls of the cutaneous blood-vessels following the eruption (hydrops scarlatinosus sine nephritide) . 6. Kidneys. — Next to the severer forms of throat trouble, the most important and dangerous complications are located in the kidneys. They may appear as early as the acme of the disease, as in many other infectious diseases. The urine has a trace of albumen. In rare cases the amount of albumen may be consider- able. The appearance of the urine is generally not much changed, and the micro- scope reveals but few abnormal constituents. There are some white and red blood- globules, a few hyaline casts, sometimes one or two renal epithelial cells. This initial albuminuria very rarely gives cause for alarm. The genuine scarlatinal nephritis scarcely ever develops much before the end of the second or the beginning of the third week. Sometimes it comes even later. In one case under our own observation it did not begin till the thirty-third day of the disease. It may therefore be regarded to a certain degree as a localized re- lapse. It may be so mild as to cause no subjective symptoms whatever, so that it would be unnoticed if the urine were not carefully examined. On the other hand, it may be accompanied by the gravest symptoms, and may soon terminate fatally. It may follow either severe cases or the mildest, so that the rule should be to examine the urine in every case of convalescence from scarlet fever as often and as carefully as possible. No exact statement can be made as to the fre- quency of this complication, for it is much more common in some epidemics than in others. The development of nephritis is often marked by a fresh rise of temperature. The elevation may be slight or it may reach 104° (40° C). According to our own experience, the fever often comes a day or two earlier than the changes in the urine. As the nephritis goes on, it is very often accompanied by a moderate fever with remissions. This fever may be almost wholly absent, especially in mild cases. The pulse generally becomes harder, and is sometimes quickened; but in many cases it will be slow, and it is sometimes irregular. Among other objective symptoms, the first to excite notice is generally a slight pufiiness of the face, which is usually pale. The eyelids, particularly, present an evident oedema. In the milder cases this oedema remains limited, while in others it gradually increases in extent and degree, involving first, as a rule, the dependent parts of the trunk, and later the extremities. Severe cases develop a pronounced ana- sarca. There are then, usually, effusions into the serous cavities, especially ascites and hydrothorax. The latter is dangerous chiefly through disturbance of the respiration, particularly if it be associated with severe bronchitis or pneumonia (vide infra). Although in general the development of a universal dropsy is characteristic of scarlatinal nephritis, oedema may at times be wholly absent. On the other hand, it is noteworthy that the oedema may occasionally show a peculiar localization, especially in the mucous membranes (oedema of the con- junctiva;, oedema of the ary-epiglottic folds with symptoms of laryngeal stenosis, oedema of the uvula and soft palate, etc.). The urine exhibits the most important changes (vide the section on renal diseases). These may be insignificant in the milder cases, but they are very pro- nounced in the severe ones. The amount is much diminished. Sometimes there will be for several days almost complete anuria. In cases of any severity the urine is turbid, dark, often evidently bloody, with increased specific gravity (about 1015 44 ACUTE GENERAL INFECTIOUS DISEASES to 1025), and containing a large amount of albumen. The sediment is generally abundant, and exhibits numerous hyaline easts of various lengths and diameters. To these may be attached red or white blood-corpuscles, detritus, granules of hsematoidin, or bacteria. In cases of some duration the casts are often moderately fatty. Very frequently there are found noticeably long and broad waxy [fibrin- ous] casts, which are opaque and yellow. In many cases of scarlatinal nephritis the urine is peculiar in having very many white blood-corpuscles, either isolated or adhering to the casts. These undoubtedly originate for the most part in the kidneys. Red globules, some of them in the form of colorless rings, are found. They are usually present in small numbers, but may become more abundant, especially for a day at a time. We have seen a very h^emorrhagic urine after the special albuminuria had disappeared. Renal epithelium is frequently seen, but not invariably nor in very large amount. Ur^emic symptoms often develop in scarlatinal nephritis. They may be of all degrees of severity. They will be described in detail under diseases of the kidney (vide infra). The uraemia may be so severe as to cause convulsions, coma, and death; but it is remarkable how often children recover from what seems to be the most pronounced uraemia. The duration of scarlatinal nephritis varies greatly according to its severity. ' In cases which run a favorable course, the urine is generally abnormal for two to four weeks, or even longer. There is sometimes a very slight albuminuria present for months without causing any symptoms. Death may be due to uraemia or more frequently it may come on with severe dyspncea. The latter is due partly to dropsical conditions (hydrothorax, ascites), or often to a severe diffuse bronchitis or pneumonia accompanying the nephritis. Cardiac insufficiency also may be the cause of death. The transition of acute scarlatinal nephritis into chronic nephri- tis, especially into chronic contracted kidney, is rare, but it has certainly been seen both by ourselves and others. It is worthy of note that, after the nephritis has lasted some four to six weeks, beginning hypertrophy of the left ventricle can be detected by the displacement and strengthening of the apex-beat. Friedlander has demonstrated this early h^i^ertrophy at autopsy. The anatomical changes of scarlatinal nephritis can be mentioned only briefly here. The forms vary. We often find the " large white kidney " — that is, a dif- fuse acute nephritis with fatty degeneration of the epithelium — and usually also more or less numerous hsemorrhages. In other cases the kidneys macroscopically are apparently little altered, but we see in the cortex the gray, prominent, blood- less glomeruli, in which the microscope shows very marked changes (" glomerulo- nephritis " of Klebs and others). 6. Joints. — When desquamation begins, or even earlier, pain and swelling may attack a certain number of the joints. This trouble was formerly called scarlatinal rheumatism, but now it is usually known as scarlatinal synovitis. It is generally mild and quite temporary, but, exceptionally, it may be severe and even purulent. Then it is usually a part of a secondary sepsis or a general pyEemia, as evinced by such other lesions as empyema, subcutaneous abscesses, jaundice, splenic tumor, nephritis, etc.; and they all seem to be caused by a sec- ondary infection with streptococci, etc. We have seen a few instances of excessive pain in the muscles of the thighs, accompanied by a moderate, diffuse swelling. 7. Another important complication of scarlet fever is pneumonia. In severe cases lobular pneumonia sometimes appears as early as the first stage of the dis- ease; but it occurs more frequently in connection with the nephritis, when it may have the significance of so-called nephritic pneumonia (vide infra). The respiration may be very seriously embarrassed by it. Inflammations of serous membranes in the chest — viz., endocarditis, pericarditis, and pleurisy — are more SCAELET FEVER 45 rare. They may or may not be accompanied by disturbances in the joints {vide supra). Pericarditis, endocarditis, and myocarditis sometimes develop during scarlet fever, but it is usually hard to decide whether they are due to the direct action of the scarlatinal poison itself or to secondary septic com- plications. We refer the tendency to tachycardia or bradycardia, irregularity of the heart-beat, etc. (which sometimes last long after the scarlet fever), to myocarditic changes. Endocarditis may result in permanent valvular disease. Quite severe intestinal symptoms, such as diarrhoea, may appear. These are generally the result of a catarrhal inflammation of the intestinal follicles. Dysentery is less frequent. The enlargement of the spleen has been already mentioned. The liver is sometimes found to be considerably enlarged. A general moderate swelling of the lymph-glands (neck, axillae, groins) is usually present in scarlet fever at the time of the eruption. We usually find in the blood a pronounced leucocytosis which sometimes lasts long after the other morbid symptoms. Variations in the Course of the Disease. — The diversities of the clinical pic- ture in different cases of scarlatina will be understood when we consider the variety and number of the disturbances thus far cited. It is to be added that the general course of the disease may exhibit numerous peculiarities, of which it is hardly possible to give an exhaustive presentation. We will content ourselves with a cursory statement of the most important deviations from the typical course. 1. Rudimentary Forms. — To this class, in which the disease does not reach a perfect development, belong first the cases of simple sore throat with no erup- tion, or at most an extremely faint and partial one {scarlatina sine exanthe- mate). Soraetimes even the sore throat is hardly to be seen, and there is noth- ing but a brief and slight fever with mild symptoms of general disturbance. The recognition of these cases as scarlatinal is possible only when we consider their setiological relation to other undoubted cases of scarlet fever. We had an excel- lent opportunity to observe them when the disease broke out in the children's wards of the hospital at Leipsic. The diagnosis is sometimes confirmed by a slight though evident desquamation, affecting the hands, feet, legs, and back, or by an acute nephritis, which may follow the mildest attacks of this sort. Many cases of acute nephritis, though apparently wholly spontaneous and primary, must be regarded as setiologically scarlatinal. 2. Rudimentary hut Pernicious Forms. — Under this head belong those attacks of scarlet fever in which the eruption is scanty or absent, while from the very start the most violent general symptoms appear. There is a very high fever, enor- mously rapid pulse, and delirium. Such cases must be the result of an uncom- monly severe general infection. They usually end in speedy death. Other cases, ending fatally in a few days, have a well-developed rash without other localized disturbances. 3. Severe Forms with a more Protracted Course. — In these cases the long- duration is not the exclusive result of especial complications, but is likewise due to the severity of the intoxication. One variety is the so-called typhoidal form of scarlatina, with persistent high fever and severe constitutional symptoms. An- other variety is the hsemorrhagic form briefly mentioned above, in which there are extensive haemorrhages into the skin and into the mucous and serous mem- branes. This form may run an extremely acute course. Further, in all per- nicious forms, there may be severe local complications, particularly diphtheritic or gangrenous sore throat, inflammations of serous membranes, etc. Attacks of this sort are often not produced by the poison of scarlet fever alone, but by secondary complicating processes. While speaking of scarlatinal diphtheria it has already been pointed out that secondary infection of the system may result, 46 ACUTE GENERAL INFECTIOUS DISEASES principally orig-inating from the diseased, throat, and occasioning sometimes grave septic conditions of the whole body, sometimes local disease of different parts. 4. In extremely rare cases Relapses do occur. After the first illness a fresh eruption breaks out with all the other symptoms. of scarlet fever. In anomalous cases, running a severe course, there is sometimes, at an advanced stage, a fresh, imperfect eruption (generally in spots), which Thomas has termed a pseudo- relapse. Probably this is usually a septic eruption. Diag^nosis. — The diagnosis of scarlet fever is made in most cases from the characteristic eruption taken in connection with the other symptoms. We should, however, bear in mind that exceptionally other eruptions appear which exhibit the closest resemblance to that of scarlet fever. 1. After the use of certain drugs, especially atropine (belladonna), quinine, antipyrine, morphine, chloral; and likewise after the ingestion of crabs, fish, etc. 2. As a symptom of other infectious diseases, such as typhoid fever, small-pox; and, above all, in septic diseases {vide infra). In an uncertain or anomalous case, factors of importance for diagnosis are the aetiology (connection with other well-defined cases), the initial sore throat, and the eventual occurrence of desquamation or of a secondary nephritis. The prognosis must in every case be guarded. From what has been said of the course of the disease, it is evident that, even in cases which are at first appar- ently the most favorable, dangerous complications may appear. The commonest dangerous complication during the height of the disease is scarlatinal diph- theria, the commonest dangerous sequel is nephritis. Treatment. — The majority of those cases of scarlet fever which take a typical. course will recover completely without our aid. In these the task of the physi- cian, so far as treatment is concerned, consists in arranging the details of hygiene and the general care of the patient. The sick-room should be cool and well ven- tilated and the diet rather strict, consisting mainly of milk. Broths and eggs may also be allowed. We should see that the skin and the mouth are kept clean. To change the linen frequently, if done with proper precaution, is not only permissible, but very desirable. Rubbing the skin with olive-oil, vaseline, etc., has some merit, and is especially to be recommended if the skin be harsh and dry after the eruption has faded. [From the moment that the disease is declared the patient should be thor- oughly anointed daily with carbolized vaseline, lard, or the like; and this should be kept up until desquamation has ceased. Not only is the comfort of the patient promoted, but the danger of the spread of the infection is thereby greatly lessened.] The scarlatinal disease of the throat must be treated with the greatest atten- tion, the main duty of the physician in this regard being to prevent, if possible, the ingress of the above-mentioned secondary infection. It is therefore our opinion that in every case of scarlet fever the greatest pains should be taken' from the very commencement of the disease to maintain complete disinfection of the mouth and throat. Larger children may use a gargle (two-per-cent. solu- tion of chlorate of potash, one- or two-per-cent. solution of carbolic acid). In- halations of carbolic-acid spray, dilute lime-water, etc., are also to be recom- mended where practicable. If there is prostration, or if the child be young or willful, we must cleanse the mouth and throat at short intervals, by means of a spray-apparatus, with disinfectants, such as boracic acid or permanganate of potash in solution. Sometimes it is a good plan to let the patient swallow slowly a half- teaspoonful of a solution of potassic chlorate (about 1 to 40), every half-hour or oftener, with the object of contributing to the local disinfection of the throat. If scarlatinal diphtheria nevertheless develops and the cervical lymph-glands begin- SCARLET FEVER 47 to increase further in size, there is reason to hope, according to the experience of Taube and Heubner, that parenchymatous injections into the tissue of the tonsils or the palatine arches may yet check the spread of the secondary infection. About 6 miniuis (a Pravaz syringe half full) of a three-per-cent. solution of carbolic acid may be injected twice daily upon each side by means of a long hollow needle and a subcutaneous syringe. Catti recommends painting the affected parts with a l-to-1,000 solution of corrosive sublimate. Of the many other remedies ad- vised, we may add that the insufflation or dusting of the tonsils with powdered sugar is of advantage. In ordinary scarlatinal diphtheria we can expect no benefit from Behring's serum-therapy, but if there is a complication with true diphtheria a serum-injection is most advisable. If the nose be likewise affected, the chief thing to do is frequent cleansing and syringing while the head is bent forward. We should be on the watch for the possible occurrence of otitis. In this particular the physician is often guilty of sins of omission. Much harm may be averted by a prompt syringing of the ears, or, if need be, by insufflation of air into the middle ear, or paracentesis of the membrana tympani. Inflammation of the glands in the neck, if severe, is prone to pass on to sup- puration, and it must then be treated surgically. When the swelling has just begun, or is still moderate, we may try to cure it by rubbing in iodoform ointment (1 to 15) two or three times a day. Ice is generally not so well borne as warm applica- tions (poultices or warm bran-cushions). If there be continuous high fever, accompanied by rather severe constitutional symptoms, a moderate employment of the cold-water treatment in scarlet fever is strongly to be recoramended. The baths seldom need to be cooler than 81° to 88° (22°-25° R.), and are to be employed two or three times daily, or oftener in severe cases. If the nervous disturbance be serious, or if the respiration be impaired, the patient should be douched with cold water during the bath. Instead of baths, wet packs may be used to advantage. Internal antipyretics, such as antipyrine, may usually be dispensed with, although in private practice we may be obliged to employ them. We must watch the condition of the heart carefully. When the pulse is very rapid we may use an ice-bag on the heart. When the heart begins to grow weak we may prescribe tincture of strophanthus, wine, etc., and the most efficient remedy for threatening collapse is injections of camphor. With mild scarla- tinal arthritis salicylate of sodium and antipyrine act well as palliatives, but in severe cases they, of course, do little good. We know of no means to avert the nephritis. In justice to himself, the physi- cian must always at the start point out the possibility of its occurrence, and must avoid as far as possible errors in diet or exposure to cold on the part of his pa- tient. He may thus escape blame. The treatment of the nephritis and its results is fully described in the section on renal diseases. The most important remedies are a mild diet and the use of warm or hot baths and packs. The other complications of scarlet fever must be treated symptomatically in the ordi- nary way. The patient must, as a rule, keep his bed three or four weeks, even if convales- cence be uninterrupted. [This injunction is rather extreme. Xephritis is as likely to follow a mild as a severe case, and occurs sometimes in spite of every precaution. The physician should use his discretion as to the length of time the patient is kept in bed. care- fully guarding against exposure to cold and imprudence in diet.] After desquamation is completed the skin should be thoroughly cleaned by warm baths. The disease is so dangerous that, whenever a case occurs in a fam- ily, isolation is absolutely demanded, and, if possible, all the other children should 48 ACUTE GENERAL INFECTIOUS DISEASES be sent away. If this advice be disregarded, we can reject all responsibility for any further cases and their results. [Scarlet fever is a disease at once so highly contagious and so common that it may be taken as the type of its class. Its hygienic treatment and the measures needful to prevent its spread consequently deserve more minute detail. The sick-room should be at the top of the house, if possible, and exposed to the south; every unnecessary article of furniture and all ornaments should be re- moved beforehand, carpets, curtains, and stuffed or upholstered furniture being included. A window should be kept open constantly, top and bottom; in cool weather a fire should be burning; in warm weather ventilation is furthered by placing a gas-burner or large kerosene lamp near the throat of the chimney. Outside the door of the sick-room a sheet moistened with a disinfectant solution should be carefully hung. Only those whose presence is absolutely necessary are to be allowed in the sick-room, and the physician, when his visit is completed, should pass directly out of the house. A convalescent should be kept away from all who are liable to contract or con- vey the disease until desquamation has entirely ceased. Several warm soap-baths should be given before the child emerges into every-day life, and it should finally be dressed in uncontaminated clothing. For further directions as to the disinfection of the room, the clothing, and the excreta, see pages 28-30.] CHAPTER V MEASLES (Morbilli) iEtiology. — In contrast with the malignancy of scarlet fever is the compara- tively benign nature of measles, a disease of childhood which is but little feared even by mothers. It is so widespread, and the susceptibility to it is so universal, that measles passes for an almost unavoidable but comparatively insignificant an- noyance. Indeed, few escape it; and probably the reason why adults have mea- sles so much less frequently than children is simply that most adults have already suffered from it in childhood. A second attack of measles in the same individual may occur, but it is certainly extremely rare. [In highly civilized countries measles has prevailed so long that it would seem that a relative resistance against the poison has been acquired. The frightful ravages of the disease when it was planted in virgin soil, as among the Fiji Is- landers not many years ago, apparently bear out this view. The susceptibility to measles is greater and more widespread than is that to scarlet fever — that is to say, fewer individuals reach adult life without having experienced an attack of the former than of the latter.] Measles generally comes in epidemics. Sporadic cases are exceptional. In this respect measles differs decidedly from scarlet fever. The rapid spread of the disease when it has once broken out is a result of its great contagiousness. If one child in a family is attacked, the others almost always take the disease. The in- fection may be transmitted even by well persons and by means of articles with which the sick have come in contact, although this is not often the case. We are not yet acquainted with the specific poison of measles — although its existence is to be taken for gTanted — nor with the details of its transmission. Still it seems most probable that the poison is inhaled through the mouth and nose, iand that this is the reason why its effects are usually first developed in the MEASLES 49 respiratory passages (vide infra). The disease can be artificially produced by in- oculation of healthy children with the blood or liquid secretions of those suffer- ing from it. Clinical History. — The length of the stage of incubation is tolerably uniform. It is ten days to the beginning of the first symptoms, and thirteen or fourteen days to the breaking out of the eruption. These figures have been established by the observations of Panum, the opportunity having been afforded upon the first introduction of the disease into the Faroe Islands. As a rule, there are no espe- cial prodromata during the period of incubation except some slight elevations of temperature. At the end of ten days the initial stage * begins, generally sudden- ly, and with an abrupt rise of temperature to 102° or 104° (39°-40° C). At the same time the characteristic catarrhal symptoms appear: nasal catarrh (coryza), to be recognized by the abundant nasal secretion, the frequent sneezing, and sometimes also by nose-bleed; more or less severe conjunctivitis, characterized by photophobia, reddening of the eyes, and increased flow of tears; and, lastly, symptoms of a catarrh of the upper part of the respiratory tract, usually mod- erate, but nevertheless causing hoarseness and a slight cough. With all this the general condition is disturbed, the children are restless, have headache, and eat little. Symptoms of a mild sore throat are not infrequent, but are very far from being so prominent as in scarlet fever. These initial symptoms last, as we have said, three or four days. Then the eruption begins (stage of eruption). This is very often preceded for a day or two by a peculiar, usually spotted, reddening of the hard and soft palates, termed " eruption upon the mucous membrane." [Koplik, in 1898, called attention to an eruption of bluish-white specks, surrounded by a reddish area, upon the mu- cous membrane of the cheek and lips, occurring twenty-four to seventy-two hours before the cutaneous exanthem. Others confirm his observations and regard " Koplik's spots " as a great aid in early diagnosis. — V.] The true eruption of measles begins almost always in the face, on the cheeks, forehead, and around the mouth (contrasting with the characteristic pallor of the chin in scarlet fever), and spreads from there rapidly downward over all the rest of the body. The erup- tion consists at first of little papillae, corresponding to the follicles. These are soon surrounded by a pale-red, slightly elevated border, and in many cases become confluent. Perfectly flat elevations, of various sizes and of extremely irregular, dentated, roundish, or angular shape, develop. They are often so thickly crowded together as to touch one another, but usually limited portions of normal skin intervene between them. Within each raised spot the little follicular papillae remain visible. With the beginning of the eruption the fever rises, having been, as a rule, slight during the last days of the initial stage. It attains about 104° or 105° (40°-40.5° C). In thirty-six to forty-eight hours the eruption reaches its full development and its greatest extent. The fever and the catarrhal symptoms also persist for the same length of time. Sometimes we find a slight swelling of all the lymph-glands. Then follows a decline in the fever, usually rapid, and indeed almost by crisis, while the eruption after a short period of full development begins gradually to fade during the two or three days following. At the same time the catarrhal symptoms diminish. A more or less extensive desquamation of the epidermis begins, scarcely ever in large pieces as in scarlet fever, but in little scales, like bran. In eight or ten days, if the disease runs a normal course, the patient is fully convalescent. * We consider the term "initial stage" more correct than "prodromal stage." The "larodromal symptoms" are the first slight symptoms which occur during the time of incubation of an infectious disease, while the symptoms presented by measles before the breaking out of the eruption are a part of the already developed disease. 4 50 ACUTE GENERAL INFECTIOUS DISEASES After this brief description of the usual course, we must consider more closely some of the symptoms and possible complications. The fever (see Fig. 6) of measles exhibits, as has been already implied, a toler- ably typical course. It begins with a rather marked and rapid rise upon the com- mencement of the disease. On the morning of the second day there is usually a marked remission, often to normal. In the last two days of the initial stage the fever is moderate, very rarely being so high as at the beginning. With the eruption there is a new, rapid rise, usu- ally higher than the initial one, so that we may well divide the fever into two periods^ — the prodromal fever and the eruptive fever. This latter is but brief and does not persist, as in scarlet fever, during the entire duration of the erup- tion. It falls by crisis when the rash has attained full development. There may, to be sure, be slight elevations of tem- perature during the next day or two; but, if the fever is considerable and per- sistent, it is always a sign that complica- tions have arisen, probably in the respir- atory apparatus. 39.0' 38.0= 37.0° 36.0° Initial Fever. Eruptive Fever. Eruption. Fig. 6.— Example of the temperature curve in measles. The eruption usually assumes the form described above, but may present manifold varieties. Sometimes its de- velopment is rudimentary. Sometimes it does not begin on the face, but on some other part of the body. This is generally regarded as a sign that the case will be anomalous in other ways as well. The individual spots may be smaller than usual, and may remain entirely separate from each other {morhilli papulosi). In other cases the eruption is so confluent (morhilli confluent es) that it resembles the eruption of scarlatina. The forma- tion of vesicles {morhilli vesiculosi) also occurs, but much more rarely than in scarlet fever. Hsemorrhagic measles is also observed, but usually only in the form of small, capillary bleeding, and in cases that otherwise run a perfectly favorable course. Very rare cases have indeed been described, with a general haemorrhagic diathesis and severe symptoms, resembling hsemorrhagic scarlatina. It is doubtful whether the " black measles " of the old writers was actually mea- sles at all. In addition to the proper eruption of measles, other eruptions some- times develop — such as vesicles, wheals, and pustules. The pulse is generally not so rapid in measles as in scarlet fever. Enlarge- ment of the spleen can be made out only to a slight degree, if at all. As a rule, we find no pronounced leucocytosis in the blood. The complications of measles are for the most part exaggerations or abnormal varieties and extensions of those troubles which are observed during the usual mild course of the fever. As in scarlet fever (vide supra), we often have to deal with the effects not of the original, but of secondary infection. Compared with the great majority of mild attacks taking the typical course, cases presenting com- plications of any severity are rare, and much less frequent than in scarlet fever. Epidemics are only now and then distinguished by unusual severity. Often quite serious eye-diseases are developed, particularly blennorrhagic con- junctivitis, keratitis, and iritis. Marked inflammation of the mucous membrane of the nose, throat, and lar- ynx may prolong the course of the disease. This is often merely an exaggera- MEASLES 51 tion of the usual catarrh. Otitis media likewise sometimes occurs. A laryngitis of marked intensity, with considerable swelling of the parts involved, may pro- duce much discomfort, or even symptoms of stenosis ("false croup")- Actual croupous and diphtheritic lesions of the throat and larynx also occur (diphtheria of measles). This last is indeed much rarer than scarlatinal diphtheria, but it may have the same unhappy termination. It is worth mentioning that sometimes genuine laryngeal croup is observed in measles, unaccompanied by lesions of the pharynx. In all these affections secondary infection plays the chief part, as it does in scarlet fever (vide supra, page 41). It is, however, in the lungs that the most frequent and important of all compli- cations in measles occur. The usual mild bronchitis becomes very intense, ex- tends into the bronchioles (capillary bronchitis), and then results, for the most part, in a more or less extensive, lobular, catarrhal pneumonia (q. v.). Accord- ing- to Koster, measles pneumonia rises from an inflammatory proliferation of nuclei about the small bronchi, and it usually invades the neighboring- alveoli by continuity along the small branches of the pulmonary artery. It is then a " small nodular," but not strictly a lobular pneumonia. Measles pneumonia is to be diagnosticated when moist rales are heard in abundance over a large part of the chest, and when there is at the same time persistent fever and pronounced diffi- culty in respiration, with cough or dyspnoea. We get decided dullness on per- cussion only when the separate centers of infiltration are more than usually con- fluent. Genuine lobar, croupous pneumonia appears much less often than the lobular variety. It attacks one lobe, or several, is attended by high fever, and may end with a well-marked crisis. The foregoing pulmonary symptoms usually appear at the height of the dis- ease, and persist after the eruption fades. They may delay convalescence for weeks. In other cases measles will be seen at the start to run a normal course, the temperature will have already fallen, and then come new fever and the appear- ance of decided pulmonary disturbance. This is always to be regarded as a grave complication; and especially in feeble children it may lead to death, with the symptoms of impaired respiration or of constitutional exhaustion. At present we can not definitely state how far in measles pneumonia we have to do with the direct action of the measles poison itself or with secondary infection (strepto- cocci, diplococci, etc.). Marked intestinal symptoms sometimes appear, particularly an excessive diar- rhoea, due to intestinal catarrh. It is characteristic of measles that in severe cases such a diarrhoea may assume a pronounced dysenteric character, indicated by blood and slime in the dejections, symptoms which usually depend upon the devel- opment of follicular colitis with ulcerations. IvTow and then still other complications may present themselves, of which a full enumeration is impossible. Nephritis does occur, but far less often than in scar- let fever. A simple albuminuria during the acme of the disease is not infrequent, but as a rule it has no especial clinical significance. We should mention gangrene of the cheek, the so-called noma, as a complication, which is very rare but appar- ently characteristic. Peculiarities in the course of the disease are much rarer in measles than in scarlet fever. Yet we see, on the one hand, unusually mild or rudimentary cases, in which either the rash or the other local symptoms are remarkably slight, and on the other hand, abnormally severe cases. These latter are distinguished by the unusual height or persistence of the fever, by the severe constitutional and nervous sjanptoms, and further by the early appearance of complications. Such cases have been termed " typhoid measles." We have already mentioned the severe form of hsemorrhagic measles. We should notice the clinical relation which measles bears to two other in- 62 ACUTE GENERAL INFECTIOUS DISEASES fectious diseases — to whooping-cough and tuberculosis. Measles and pertussis (q. V.) may follow each other in the same individual at a short interval, some- times one and sometimes the other taking the initiative ; epidemics of the two dis- eases prevail with comparative frequency at the same time. Tuberculosis is like- wise to be mentioned as an important sequela of measles. In these cases it is probable that the children have a tubercular focus smoldering somewhere in the body (lymph-glands, lungs) before the attack of measles which kindles it and aids its further extension. The measles may also, of course, excite a predisposi- tion to infection with tubercle bacilli. The diagnosis of measles, as of the other acute exanthematous diseases, is based chiefly upon the eruption, but we must also regard, of course, other symp- toms which may be present (fever, catarrhal symptoms). Personal experience does more to sharpen the perception than can the fullest descriptions. We can merely suspect the disease during the initial stage unless an epidemic prevails. If, beside the characteristic catarrhal symptoms, the above-mentioned eruption on the mucous membrane of the palate exists, the diagnosis becomes tolerably cer- tain. We should consider that eruptions similar to that of measles appear in other diseases, more especially in rotheln, scarlet fever, typhus fever, in the begin- ning of small-pox, and sometimes in secondary syphilis. Furthermore, we need to exclude eruptions due to drugs, especially antipyrine, and also turpentine, balsam of copaiba, etc. In doubtful cases we shall be enabled to form a decided opinion by the other symptoms, and, above all, by the further course of the disease. Prognosis. — We have already remarked how favorable in general the prog- nosis is, but we must here repeat that all epidemics do not exhibit the same benign character, and that in every case the physician must bear in mind the pos- sibility of complications, and particularly the danger of severe pulmonary dis- turbances. Treatment. — The patient should in general be kept somewhat warmer than in scarlet fever. Even in what seem to be the mildest cases the child should be kept in bed till desquamation is over. The sick-chamber is to be somewhat dark- ened, on account of the photophobia which usually exists at first. In this way, normal cases run on favorably without any especial therapeutic interposition. The catarrhal symptoms, however, should always be heeded, since to disregard them may lead to their becoming aggravated. The chief requisite is cleanliness. At regular intervals the eyes, the nasal cavity, and the mouth should be washed out with lukewarm water. If, despite all this, certain disturbances appear in a worse form than usual, or if complications develop, these must receive especial attention. Severe eye trou- bles should be treated according to the usual ophthalmological practice. The treatment of croupous trouble in the throat or larynx will be fully described in a later chapter. For the pulmonary complications, lukewarm baths, combined if need be with rather cool douches, constitute the most effectual remedy. Cold packs are also very efiicient. These we shall speak of later in more detail in the chapter on catarrhal pneumonia. The chief task of the physician in the treat- ment of measles is, however, to hinder as far as possible the appearance of compli- cations. We are not acquainted with any internal remedies for the hmg troubles which are at all trustworthy. In rare instances the excessive accumulation of mucus in the bronchi requires the administration of an emetic. As expectorants we may try ipecac, liquor ammonii anisatus, etc. If considerable intestinal dis- turbance arises, we must employ small doses of opium, calomel, tannalbin, or sub- nitrate of bismuth. We hardly need to say that, whatever else is done, the strength of the patient should be kept up as much as possible by giving wine, broths, milk, eggs, etc. For at least two or three weeks after the disease has ended, the child must be very carefully watched. ROTHELN 53 As the disease is usually so raild, prophylaxis is not very strenuously at- tempted. If one child in a family is attacked, it is probably already too late to isolate the others, and it is even an advantage to the family to have all the chil- dren finish at once what they will hardly be able eventually to avoid. We would make an exception in favor of isolation if the disease prevailed in a severe form. [It is not customary with us to insist so strongly upon isolation and thorough disinfection as in scarlet fever, but the tendency of the present day is toward a wide application of the principles of preventive medicine. It is certainly of no advantage to a child to contract measles. Delicate children, especially those with tubercular predisposition, should be carefully guarded against it ; and, even if it is decided that it is not worth while to attempt to confine the disease to one member of a family, every precaution should be taken against infecting other families. Under suspicious circumstances, consequently, children are to be kept away from school and from contact with others. If there is any reason to fear the development of tuberculosis, every possible hygienic means should be employed in order that full vigor may be regained.] CHAPTER VI ROTHELIT {German Measles) EoTHELN is a disease similar to measles, but distinct from it, although formerly often confounded with it, and perhaps with scarlet fever as well. The observa- tions of Steiner, Thomas, and others leave now no room to doubt that these dis- eases are distinct, for epidemics occur in which all cases present the characteristic peculiarities ascribed to rotheln. But the best proof is that children who have had rotheln are not infrequently attacked by genuine measles later. It may in- deed be very difficult in an individual case to decide which disease is present ; but that rotheln does exist, as an independent form of disease, can be denied by those alone who have never seen it. After an incubation of about two or three weeks the disease begins with the appearance of the eruption, which is usually noticed first in the face. Initial symptoms (cough, sneezing, etc.), preceding the eruption, either are wholly absent or at most last for half a day. The eruption is decidedly like that of measles, but its individual spots are smaller. They are seldom larger than small peas and circular, being only exceptionally as dentated and irregular in outline as are the maculae of measles. They appear on the whole face, the head, the trunk, and the extremities, are pale red (sometimes deep red), only slightly elevated, and are not apt to become confluent. In rare instances, small vesicles develop upon the macules. The soft palate sometimes exhibits, as in measles, a faint macular eruption at the beginning of the disease. After two to four days the eruption fades. There is usually no decided desquama- tion. Other symptoms of disease than this eruption are slight. Fever in many cases appears to be entirely absent. As a rule, there is for a day or two a little elevation of temperature, reaching 102° (39° C.) at most. Tokens of a moderate catarrh of the conjunctiva, the nasal mucous membrane, the throat, and the larynx are also observed — viz., photophobia, nasal discharge, and cough. Often, the cervical lymph-glands are more or less swollen. The constitutional disturb- 54: ACUTE GENEEAL INFECTIOUS DISEASES ance is generally so slight that the child can hardly be kept in bed. Important complications hardly ever occur. The prognosis of rotheln is therefore perfectly favorable, and the employment of any special treatment is needless. CHAPTER VII SMALL-POX ( Variola. Varioloid) .ffitiology. — Small-pox has been known for centuries, although formerly often confounded with other diseases.* It is one of the most dreaded acute infectious diseases, and in earlier times it has destroyed thousands in its pestilential prog- ress. It was the discovery of the possibility of prophylactic inoculation, and the ever-increasing spread of this precautionary measure, which first robbed the dis- ease of some portion of its terrors. Numerous statements have been made about the occurrence of micro-organ- isms in the variolous eruptions on the skin and mucous membranes, but we are compelled to say that we are not yet acquainted with the specific, organized poison of small-pox, however strongly justified we may be in assuming its existence. Bacteria can in fact easily be demonstrated in the eruption of variola, but most of them come from the surrounding atmosphere, and have no relation to the spe- cific variolous processes. The foci of bacteria found in the internal organs (liver, spleen, kidneys) are also due, as their discoverer, Weigert, himself supposed, to the secondary ingress of other varieties of micro-organisms, and are not directly asso- ciated with the variolous process, the diseased condition of the skin furnishing a ready entrance for infectious matter. Predisposition to variola, except as diminished by vaccination (vide infra), is universal. The disease may appear at any age, even in utero. Women are believed to be especially liable to it during pregnancy and child-bed. It is said that persons ill with another acute infectious disease, such as scarlet fever, measles, or typhoid fever, are, for the time being, tolerably secure from infection with small-pox; but this rule certainly has exceptions. The same individual rarely takes the disease a second time. A case of variola is always the result of transmission of the poison to a healthy person from one who is already ill with it. The specific poison is most abundant in the diseased portions of the body and in the pus of the suppurating pocks, as well as the crusts and scales which are left when these have dried up; but the disease is also contagious in its earlier stages, before the pustules develop, and even, according to a few observations, during the stage of incubation. Cer- tainly the variolous poison is very volatile — that is, it is prone to disseminate itself through the air in the neighborhood of the patient. In order to catch the disease it is not necessary to touch the patient, but merely to remain in his vicin- ity. In many cases we can not, however, determine with exactness the mode of transmission, since the contagion may either be direct or by means of objects and* utensils with which a patient has come in contact — for example, the soiled linen. The dead body also is capable of transmitting the disease. In general, numerous instances point to a considerable " tenacity " in the poison. The precise manner * The very name small-pox (petite verole) is significant of its confusion with syphilis, which was termed the " great pox." SMALL-POX 55 of infection is not yet known. It is most probable that the poison is drawn into the lungs with the inspired air. It has been demonstrated that the disease can be transmitted to healthy per- sons by direct inoculation of the contents of the variolous pustules. It is stated that monkeys and other animals may be successfuly inoculated in the same way. Whether inoculations with the blood of the sick will reproduce the disease is not yet settled. The secretions (saliva, sweat, urine, and milk) do not apparently contain the infectious matter. Course of the Disease. Variola and Varioloid.— The stage of incubation lasts as a rule thirteen to fourteen days, sometimes a somewhat shorter time. During this period prodromal symptoms are absent or insignificant. The disease itself begins suddenly with what are usually very characteristic initial symptoms — rigor, fever, headache, and intense pain in the loins. It is only in comparatively few cases that one or another of these symptoms is slight or wanting. The constitutional symptoms may be very severe — a dry tongue, stupor, wakefulness, delirium. The fever continues intense for some days. The pulse is much quickened. There is almost total anorexia, and often there is vomiting. There is constipation, or, more rarely, diarrhoea. Frequently there is a slight sore throat, and sometimes a slight bronchitis. The spleen is enlarged in most of the severe cases, and the urine often has a trace of albumen. In women, menstrua- tion occurs in a remarkably large number of cases. The proper variolous eruption does not at once appear, but from the second day other characteristic efflores- cences are not rare. These are termed the initial rash of small-pox. We may &id either a diffuse or macular erythema, extending in varying degree over the trunk and extremities (especially on the extensor surface), or a h^emorrhagic eruption with small spots, appearing by preference upon the hypogastrium and the inner surface of the thighs (in the so-called femoral triangle of Simon) or on the lateral surface of the trunk and on the upper arm. The erythema soon dis- appears, but the hsemorrhagic spots can be seen longer. Both forms of the initial eruption may be combined. The initial stage, just pictured, lasts usually three days. Severe symptoms occurring at this time do not exclude the possibility that the further course of the disease may prove favorable, while mild symptoms are of good omen. At the end of the third or on the fourth day the temperature makes a decided fall, and the regular variolous eruption begins to be developed upon the skin — the stadium eruptionis. During this period an evident difference among the separate cases becomes manifest. This distinction can not indeed be always drawn with a narrow line, but it is noticeable enough to justify the establishment of two types of variolous disease. We refer to the division into a severe form (variola vera), and another, mild form (varioloid). The variola proper has a well-developed eruption with many pustules, and, as a result of this, a second stage of fever (stadium suppurationis). Varioloid has a much more scanty eruption, and little or no suppurative fever. We must now discuss these two forms separately. Variola Vera The eruption almost always begins in the face and upon the hairy scalp, ap- pearing somewhat later on the trunk and arms, and last of" all upon the legs. It begins in the form of little red dots and spots, which develop in about two days to small papules (stadium floritionis) . If the hand be passed over thickly set and well-developed papules of variola, a peculiar soft, satin-like feeling is perceived. On the points of these papilla a little vesicle forms. This keeps growing larger and larger, its contents becoming turbid and purulent, till at last, on the sixth day of the eruption and the ninth of the disease, the development of the genuine pus- -tule of variola is complete (stadium suppurationis) . The pustule usually presents 56 ACUTE GENERAL INFECTIOUS DISEASES upon its summit a little dimple (umbilication), and is surrounded by a red border or " halo." Where the pocks are especially close together, as in the face, the skin between them is diffusely swollen, and the consequent burning and pain are excessive. The countenance becomes much disfigured. Often the eyes can not be opened because of the oedema. The hands also are apt to be intensely affected, especially the back of the hands, and also all parts which have previously been injured in any way (pressure or friction of clothing, etc.). On the trunk the pustules are very rarely as close together as on the face and hands. It is worthy of note that often new eruptions of pustules keep appearing for two or three days. At the same time with the eruption upon the skin, or even somewhat earlier, a perfectly analogous efflorescence develops upon the mucous membranes. The chief places for its appearance are the mouth and throat, the tongue, the soft pal- ate, the nasal cavity, also the larynx, the trachea, and the upper part of the oesopha- gus. In the vagina and rectum it is rare and scanty. In this mucous efflores- cence, however, there are no proper pustules, but small, superficial ulcers. These result from the maceration of the uppermost layers of the mucous membrane. They sometimes become confluent. The annoyance produced by this eruption in the mouth and throat is, of course, very great. The pocks in the larynx manifest themselves by hoarseness, and occasionally by symptoms of stenosis. As we have said, the beginning of the eruption is the signal for a noticeable fall in the temperature; but in true variola the fall does not reach the normal, or only temporarily. The other symptoms likewise remit, especially the head- ache and lumbar pain. When, however, the suppuration begins, the fever rises once more, and there are fresh symptoms of constitutional disturbance. This is the time for the dreaded attacks of delirium, during which the patient must be vigilantly watched, lest some untoward event happen. Now, too, complications may arise (vide infra). On the twelfth or thirteenth day of the disease the pustules begin to dry up (stadium exsiccationis) . The purulent contents of the pustules, part of which have burst, form yellow crusts, the swelling of the skin subsides, and, a few days later, the crusts and scabs begin to fall off. With the beginning of desic- cation, the fever declines; the local as well as the constitutional symptoms become daily slighter, and convalescence follows. The healing of the pustules is frequently accompanied by an extremely troublesome itching. After the scabs have been cast off, the skin presents pigmented spots, which persist for months. Wherever the cutis vera has itself been destroyed by the suppuration, a scar is inevitable. Thus arise the familiar scars (pitting) of small-pox, which continue visible through life. Yery often, after the end of the disease, there is almost complete alopecia. The hair often grows again, but not always. Varioloid The distinction between varioloid and variola vera is not in kind, but in de- gree. Varioloid is only a milder form of variola. There is, as we have already said, no sharp boundary-line between the two. Varioloid is most often observed in those whose susceptibility to the variolous poison has been diminished by vaccination (vide infra). As above mentioned, the behavior of the disease during its initial stage will not permit us to decide positively whether variola or varioloid will be developed. It is true that if the symptoms be especially mild, we may guess that it will be varioloid ; and, likewise, the appearance of the initial erythema already spoken of is regarded as a favorable omen. Shortly after the pocks begin to appear, the decision can almost always be made with certainty. In varioloid the eruption is rather scanty. It is often SMALL-POX 57 irregular, and does not by any means always begin, like that of variola, in the face, but often on the trunk. The individual pocks are in no way different from those of variola ; but it often happens that they do not pass through all the regu- lar stages to full suppuration, but ^mdergo resolution before this occurs. Such cases, in which there is nothing beyond papillae or vesicles, are sometimes spoken of as variolois verrucosa seu miliaris. The scantiness of the eruption and the limited amount of suppuration have for their corollary an absence, or at least a very slight development, of the suppurative fever. When the eruption appears the temperature usually falls by crisis to the normal level and remains there. The desiccation may begin as early as the eighth or tenth day of the disease, so that the whole duration of varioloid is con- siderably shorter than that of variola. Grave complications are very exceptional. The pocks may develop upon the mucous membranes, but here, too, they are scanty and not very vigorous. Course of the Fever, Symptoms presented by Separate Organs, and Complications 1. Fever {vide Fig. 7). — In the initial stage, as we have said, the temperature rises rapidly as a rule, with a pronounced rigor ; and during the first days it very often reaches 104° to 106° (40°-41° C). It sinks on the third to the sixth day, when the first papillae develop, and then, in the case of varioloid, falls rapidly to normal, and remains there. In variola the decline is slower and less complete; and with the beginning of suppuration the temperature begins to rise again. The violence of this suppur-ative fever is usually in direct proportion to the severity of the eruption. It has manifold fluctuations, but seldom lasts, in severe cases, less 3 3 4 5 fi « 9 10 11 12 13 14 15 16 \7 18 40.0° 39.0° 38.0° 37.0° — iBi my mi iBHIIinillllSISSBHB Initial Fever Suppurative Fever. Eruption. Fig. 7. — Example of the temperature curve in true small-pox. than a week. Temperatures of 104° (40° C.) and higher are common. The fever declines by lysis. In case of approaching death, the temperature may be ex- tremely high, even reaching 108° or 109° (42°-43° C). 2. Shin. — We have already described the macroscopic appearance of the erup- tion. It remains to mention briefly the histological phenomena. The first de- monstrable changes are in the cells of the deeper layers of the rete Malpighii. As a result of the variolous infection, the cells perish, are swollen by the lymph which escapes from the papillary blood-vessels, and transformed into flaky, homogeneous masses without nuclei ("coagulation necrosis" of Weigert). The lymph becomes more and more abundant, and crowds the cells farther and far- ther apart. These are thereby finally changed into threads and membranes. 58 ACUTE GENERAL INFECTIOUS DISEASES forming a distinct net-work in the vesicle. This explains why, if such a vesicle be pricked, its entire contents are never discharged at once. Great numbers of white corpuscles escape, along with the lymph, from the blood-vessels, and finally render the contents of the original vesicle purulent. Proliferative processes occur in the surrounding epithelial cells, which are still intact, and thus the margin of the vesicle becomes elevated, while the dead portion in the center sinks in. Thus the pock becomes umbilicated. If a portion of the papilla itself suppurates, a scar must be left on healing. If the process remains limited to the epithelium, com- plete regeneration takes place, and the skin reassumes its normal appearance. Certain secondary complications, which sometimes attack the skin, remain to be mentioned : abscess, phlegmon, erysipelas, gangrene, and bed-sores. None of these are due directly to the specific variolous intoxication. 3. Respiratory Organs. — The disturbances here are in part symptoms of the specific process of the disease, and in part secondary. The frequent occurrence of secondary symptoms in small-pox is easy to understand (compare the chapter on lobular pneumonia). Of the primary symptoms, we should mention genuine pocks in the larynx, the trachea, and the larger bronchi. As sequels to these, naore or less severe secondary disorders are very frequent : laryngeal ulcerations, which may even lead to laryngeal perichondritis and oedema of the glottis ; diffuse bronchitis; lobular pneumonia, often of great extent, due to the inhalation of solid matter into the lungs, and frequently accompanied by pleurisy. It should be especially noticed that lobar, croupous pneumonia is not rare. Whether this be likewise secondary, or a direct result of the variolous poison, is not yet known. 4. Digestive System. — The genuine pocks often develop, as stated, in the mouth and pharynx, and likewise in the upper part of the oesophagus. They are not observed in the mucous membrane of the stomach or intestines. The active diarrhoea sometimes seen depends upon catarrh of the intestine. Dysentery is rare. The eruption in the mouth and throat may result in severe secondary trou- bles, purulent otitis, parotitis, pharyngeal diphtheria, etc. The spleen is almost always considerably enlarged, and often the liver also, but in a less degree. 5. Circulatory System. — Pathological changes in the heart are rare, if we except the slight parenchymatous degeneration of its muscular fibers, common to almost all severe infectious diseases. Sometimes there is a slight endocarditis (^q.v.), which is probably secondary. Pericarditis is rather more frequent. 6. Organs of Special Sense. — Genuine variolous pustules occur upon the eye- lids and the conjunctiva. Later in the disease there may be keratitis, iritis, or choroiditis. We have already mentioned the relative frequency of aural disturbances, par- ticularly purulent otitis media. 7. Articular swelling may appear in the suppurative stage. The shoulders and knees are most apt to be attacked. Periostitis also occurs. 8. Nervous System. — We find no pathological changes corresponding to the severe nervous derangements manifested during the disease. After the small-pox is over, spinal diseases sometimes occur, with either paralysis or ataxia. Westphal has shown that they are caused, in some cases, by numerous disseminated centers of inflammation in the spinal cord. . Encephalitic processes have also been ob- served in small-pox, and in some cases neuritic paralysis. 9. Albuminuria is quite common in severe attacks, but genuine nephritis is a very rare complication. In pregnant women attacked by small-pox abortion or premature labor is very apt to occur. If a living child be born, it usually dies soon after birth. Anomalies in the course of the disease are manifold. We will not speak of the two typical forms already considered. There are abnormally mild cases, with scarcely any initial symptoms, or with an obscure eruption, or with no eruption at SMALL-POX 59 all (fehris variolosa sine exanthemate). In such cases a correct diagnosis is pos- sible only at the time an epidemic prevails, and by the aid of the attendant setio- logical circumstances. There are also abortive cases in which the first symptoms are severe, but which recover with remarkable rapidity. The abnormally severe cases are more important. First, there is the confluent variety. This is merely the typical process in its completest development. The initial symptoms are themselves generally very severe, and are followed, without any considerable remission of the fever, by the eruption of hundreds of pustules. The skin of the face and hands is one continuous area of suppuration. The local discomfort is extreme, as is also the intensity of the fever and of the constitu- tional symptoms. The nervous system suffers most. There is at the same time an unusually abundant eruption upon the mucous membranes. The occurrence of the above-mentioned complications affecting the various organs of the body is frequent. Death is a common result; or, if recovery takes place, it may be delayed by tedious sequelae. Hsemorrhagic small-iDox is the worst anomalous form. The name is applied to several different varieties. In the first place, any variolous eruption may be- come more or less hsemorrhagic, and yet the general course of the disease not be essentially altered. Such cases are more common among elderly people, cachec- tic persons, and drunkards. Secondly, there is a very severe form of small-pox, which is generally quickly fatal. The initial stage is marked by the unusual severity of the symptoms. The abundant eruption soon becomes hsemorrhagic, and there are also ecchymoses in the mucous membranes and the internal organs. This has been called black small-pox, and by Curschmann variola hcemorrhagica pustulosa. There is another form of hsemorrhagic variola, different from these but linked to them by transitional varieties. In it the acute hsemorrhagic diathesis develops during the initial stage. Death almost always occurs before the regular variolous eruption. This most frightful form is usually termed purpura variolosa. That it is small-pox is proved by its setiological relations alone. Otherwise it would be impossible to distinguish it from certain other acute septic disorders. It is prone to attack the youthful and vigorous. Chills, headache, and pain in the loins are the first symptoms, just as in ordinary cases. Cutaneous ecchymoses appear as early as the second or third day. They increase in area so rapidly that one can almost see them grow. They are most extensive in the hypogastric region. There are also ecchymoses in the eyelids, the conjunctiva, the mouth and pharynx, and, as the autopsy discloses, many in the internal viscera. The constitutional symp- toms are most severe, and the patient seldom survives the fifth or sixth day of the disease. Diagnosis. — The certainty with which we can make the diagnosis of small-pox in any well-developed case is equaled by the difficulty of deciding about it during the beginning of the disease, or even during the beginning of the eruption. At this period diagnosis may be impossible. When the variolous eruption is in pro- cess of development, it may be qonfounded with typhus fever, with that form of measles in which the papillae are prominent, with syphilitic eruptions, and with certain forms of erythema exsudativum, just breaking out. We can not here fully discuss all the factors which should be considered in making this diagnosis. It is important not to regard the cutaneous appearances alone, but to note all the other symptoms besides. But it is often necessary to watch a doubtful case for some time before a diagnosis can be established. Prog-nosis. — The facts which are of greatest weight in prognosis have already been emphasized. We may repeat tliat during the initial stage the prognosis of any individual case can seldom be determined. If the first symptoms are mild, or if the initial erythema appears, the case is regarded hopefully. The abundance 60 ACtTTE GENERAL INFECTIOUS DISEASES of the eruption has an influence upon the severity of the disease. Circumstances peculiar to the individual are also important — e. g., age, constitution, or alcoholic habits. We have already called attention to the danger of confluent small-pox, and to the almost absolutely fatal prognosis in the genuine hsemorrhagic variety. The mortality varies greatly in different epidemics; on the average it may be taken at about fifteen to thirty per cent. Beyond doubt, the introduction of vaccination has decidedly lessened the fatality of the disease by diminishing- the frequency of the severe forms. Treatment. — 1. Prophylaxis — Vaccination. — As in all contagious diseases, isolation is of little avail unless complete. This fact has led to the erection in late years of small-pox hospitals. All utensils used by the patient, and his cloth- ing, bedding, and the like, should be most carefully disinfected. The best method is to employ a high degree of heat— viz., 240° to 250° (115°-120° C). These precautionary measures are employed in many other diseases as well, but for small-pox we are acquainted with a special method of prophylaxis. It is. founded upon a fact which is the most remarkable within the domain of the infec- tious diseases. We refer to prophylactic vaccination. It must long ago have been remarked that a person who has had the disease once, enjoys, to a large degree, immunity from any fresh infection. This suggested the idea of exposing- children purposely to contagion, so as to insure them from small-pox for the rest of their lives. The actual inoculation of small-pox is said to have been long practiced in India and China. In the year 1717 it was employed by Lady Mary Wortley Montagu, of England, upon her own son, and with success. Unfortu- nately, however, the inoculated small-pox proves fatal in many instances; and, being itself contagious, it serves to spread the disease still further. Then ap- peared an article written by the English surgeon, Edward Jenner, in 1798. This informed the medical profession of a fact already known to the rural population of his native place, but which Jenner first established scientifically, and recognized in all its importance. There sometimes occurs a disease similar to small-pox upon the teats and udder of the cow, called variola vaccina. It is apparently a local trouble, and it can easily be inoculated upon the skin of human beings. Vaccine pustules will be developed upon the spot inoculated. These almost invariably heal without any great constitutional disturbance ; but the person vaccinated pos- sesses the same immunity from small-pox as if he had had small-pox itself. This statement of Jenner's was soon confirmed upon every side. The result is the con- tinually spreading custom of prophylactic vaccination. In some countries it is enforced by law, and it can be opposed only by ignorance or by lamentable prejudice. To explain exactly how vaccination can protect against small-pox in this way is still beyond our powers ; but vaccination has at present lost much of its former enigmatical character, since we know that a similar immunity can be produced in almost all infections by inoculation with attenuated or altered virus (see the chapters on malignant pustule, diphtheria, tetanus, pneumonia, etc.). This anal- ogy has become the more certain since there is no longer any doubt, according to recent observations (Fischer and others), that vaccinia is, in fact, only a form of small-pox rendered milder and modified by transmission to animals. If we in- oculate a calf with the contents of a fresh small-pox vesicle from man, typical vac- cinia is produced. With the contents of this vaccine vesicle children can be inoculated without any danger, and they are no longer susceptible either to vac- cinia or small-pox. We can mention only the most important of the details relating to vaccination and the method of its performance. Only exceptionally do we vaccinate with the contents of a human vaccine vesicle ("humanized lymph"), but we almost invariably use animal lymph from vaccine vesicles of calves. This is now ob- SMALL-POX 61 -tained in large quantities and put on the market. The process of vaccination is to make three shallow incisions, 3 or 4 centimetres apart, in the skin of the upper arm, and to introduce the vaccine-lymph into them. The surrounding tissue hecomes swollen in three or four days. In seven or eight days the vaccine vesicles are well developed, if the disease takes its normal course. Next they become purulent, and then dry up, and finally, on healing, leave the familiar scar behind. The whole process occupies about three weeks. If the vaccination fails, or is but partially successful, it must be repeated after a few months. The protective power of vaccination does not last indefinitely, and therefore re-vaccination is necessary every five or six years. The first vaccination of children usually takes place when they are three or four months old. If they are feeble we wait longer, unless small-pox is prevalent. It must be confessed that vaccination is not without its dangers. The little cutaneous wound made by it may lead, like any other, to sepsis or to erysipelas. The latter has been called vaccination-erysipelas. But such misfortunes are ex- tremely rare. The not uncommon " vaccine roseola " deserves especial mention. It appears first upon the arm vaccinated, and spreads over the rest of the body; but it is not a serious matter. It is of course possible, by especially bad luck in the use of human lymph, that other diseases, among which syphilis is of chief importance, may be inoculated along with vaccinia ; but this is a very rare occur- rence — much more so than the enemies of vaccination pretend. If the physician exercise proper care in the selection of the person from whom to take humanized virus, it can be entirely avoided. [The incubation stage of vaccinia being shorter than that of small-pox, the prompt vaccination of an unprotected individual who has been exposed to infec- tion should always be practiced, if possible; oftentimes the severe disease may thus be prevented.] 2. The treatment of small-pox is purely symptomatic. When the disease has once begun it is too late for vaccination to have any influence upon its further course. During the initial period we may advantageously employ cool baths to diminish the fever and alleviate the constitutional symptoms. An ice-bag will relieve the headache. We must not let the lumbar pains lead us to any but a cautious use of local irritants, for the pocks come out in greater abundance upon such portions of the skin as have been in any way irritated. If the disease proves, during the stage of eruption, to be varioloid, there will be no further need of special treatment. Good nursing and proper food will suffice. The true small-pox, on the other hand, demands the interposition of the physi- cian. He must strive to guard the regular course of the disease in the skin and in those portions of the mucous membrane which are accessible from being disturbed by secondary inflammations; for we have no doubt that the ruptured pustules furnish a most easy ingress to septic impurities from the surrounding atmosphere, so that later, when there is extensive suppuration of the skin, or analogous and severe disturbance in the mucous membrane, it is impossible to discriminate between the effects of the small-pox itself and those due to the secondary suppura- tion. If we were able to have the whole process go on " antiseptically " we should certainly have made an important advance in therapeutics. Indeed, the methods of treatment which have been up to this time recommended fulfill this indication up to a certain point, e. g., painting the skin with tincture of iodine, or with a strong solution of nitrate of silver — methods formerly much in vogue. Schwimmer's suggestion seems still better. He recommends, from the beginning of the eruption, the use of a paste made as follows : Acid, carbol., parts 4 to 10 ; ol. olivse, 40; crette prseparat., 60. M. et ft. pasta mollis. This is spread on pieces of old linen and laid upon those parts where the eruption is apt to be worst — ^viz., the forearm, hand, and leg. The face is covered with a mask, having holes corre- 62 ACUTE GENERAL INFECTIOUS DISEASES sponding to the mouth, nose, and eyes. The applications are changed every twelve hours. Under this treatment the local distress is said to be diminished, suppuration slight, and healing comparatively rapid. The pain and sense of ten- sion in the skin are often relieved by cold applications, or by simple ointment or oil. Under Hebra, in Vienna, continuous warm baths were employed in severe cases with great success. The treatment of the affected mucous membrane in small-pox must also meet the indication above mentioned. The most thorough disinfection of the mouth and pharynx must be aimed at. The means to be used are careful washing and gargling with solutions of chlorate of potash (1 to 30), carbolic acid, borax, per- manganate of potash, or liquor ferri chloridi. The eyes, if they need it, must also be appropriately treated. As to all other complications, cool baths are relatively the most useful remedy. They can be given without difficulty. The chief indica- tions for them are severe pulmonary or nervous symptoms, or continuous high fever. Internal antipyretics, such as quinine or antipyrine, are also employed. Violent nervous disturbances, such as delirium, sometimes require the cautious use of narcotics. There is nothing to add as to the treatment of malignant hsem- orrhagic small-pox, for, as we have said, such cases are unfortunately almost hopeless. CHAPTER VIII VARICELLA ( Chicken-pox) Varicella is truly one of the diseases of childhood. Adults very rarely have it. It is contagious, and often conies in epidemics. The stage of incubation does not last over thirteen to seventeen days. The disease begins with the appearance of vesicles, the size of a pea or a little larger, usually having a small red areola, and varying in number from ten to one hun- dred or more. The trunk usually bears the greater part of the vesicles, while the extremities have few. The face is frequently the seat of a considerable number, and sometimes there are a few upon the hairy scalp. There may be a vesicle here and there upon the mucous membrane of the mouth or palate. There are seldom any prodromata. Slight symptoms of fever may attend the eruption itself. The eruption is usually over in a few days, although there may be repeated crops, so that we often see fresh vesicles by the side of others which are drying up. Each individual vesicle heals quickly, and the pustulation seen in small-pox is here ex- ceptional. The course of the disease is completed in a week or ten days. Most children feel perfectly well the whole time, although there may be in rare cases pain in the limbs, anorexia, and a slight coryza. A severe complication is hardly ever seen. An unusual event is a mild nephritis. Exceptionally, the disease may be rudimentary, with a varicelloid roseola and no formation of vesicles. On the other hand, some cases present quite severe con- stitutional symptoms and a high fever, even reaching 105° (41° C.) temporarily. In most cases, however, as we have said, the child is so slightly disturbed that a physician is hardly thought necessary. The diagnosis is almost always easy. Formerly varicella was often con- founded with small-pox, and to this day the followers of Hebra, in Vienna, for some inconceivable reason, maintain the identity of the two. That they are essen- tially distinct is shown (1) by the epidemics of the two appearing entirely separate from each other, (2) by the fact that having one does not give immunity from the ERYSIPELAS 63 other, and (3) by the uniform failure of attempts to produce variola by inoculat- ing varicella, or vice versa. Still, we must bear in mind, in order to avoid mis- takes, that many dermatologists class the mildest cases of small-pox as varicella. Those who devote themselves to general diseases are probably all now convinced that varicella is a separate disease. The prognosis is perfectly good. There is usually no special treatment neces- sary, but young children should be kept in bed till the eruption has dried up. CHAPTER IX ERYSIPELAS (.b'i. Anthony'^s Fire) .Sitiology. — Erysipelas is a peculiar inflammation of the skin, recognized by redness, swelling, and pain. It has the peculiarity of spreading gradually, by direct extension, from its point of origin over a larger or smaller portion of the body. The cause of this inflammation, as was first shown by Fehleisen, is a local infection by the streptococcus pyogenes and its further extension in the skin. The exciting agent of erysipelas is then bacteriologically identical with the strep- tococcus which is the cause of phlegmonous suppuration, severe septic infection, etc. The reason why in the individual case erysipelas develops, and not some other strep- ----iV^^^tAifSiSpij^^ tococcus disease, is the special variety of in- : ;;;'/' ;' - fection and the further spread of the strepto- ^^^^'^/(^ y/ /^ cocci in the deeper lymphatics of the skin, jff^Mi "^^^^m and in part perhaps the special " virulence " #3^RSf3||jr-- '^^-^S of the infecting germs. ^^Mf>^^^^0^^ '''^^^ifflWXS The former distinction between " trau- " "? /I?^^^:" '•:'■^■p^^^^^5^ matic " and " idiopathic " or " exanthe- matic " erysipelas can no longer be rigidly ^^^^m----:- '• ■•'.■^-^Ip- - maintained. Every erysipelas is in a certain Wrf^M, ' -'l^^M^i^f"'^' sense traumatic, since infection with strepto- cocci can not occur through the unbroken skin. The so-called " idiopathic " erysipelas is dis- 'W^i^'fiMi- tinguished from " wound erysipelas " (in W0''^^^--^^ which, of course, we include puerperal erysipe- ?^^Va" las, erysipelas of the newborn starting from -v/^i-:^"-' the umbilical wound, etc.) only by the fact fig. 8.-The cocci of erysipelas. x700. that in the former the infection takes place in Section through a lymph-vessel in the skin, small, insignificant wounds of the skin which are easily overlooked. Such an erysipelas occurs chiefly in the face and head, and the following description of the symptoms refers chiefly to this facial erysipelas. Most of these cases of erysipelas arise from little excoriations, cracks, and scratches about the nose or ears, or more rarely about other parts of the face or scalp. A previous coryza, by the accompanying slight erosions about the nose, sometimes gives the opportunity for an attack of erysipelas, but sometimes the infection oc- curs in the mucous membrane of the nose or pharynx; then we have a primary erysipelas of the mucous membrane, which extends through the nasal passages and finally appears on the external surface of the nose. . Facial erysipelas is most apt to attack the young, and seems to be somewhat more frequent in women than in men. The laity erroneously regard catching cold 64 ACUTE GEKEEAL INFECTIOUS DISEASES and getting frightened as frequent causes of the disease. If we except the pre- disposing causes above mentioned — viz., coryza, slight scratches, cuts, etc. — we usually find no cause of which we can feel certain. Often endemic influences are important. It has been long known that traumatic erysipelas can get so secure a footing in particular hospitals or wards that every wounded person treated in them is in danger of this disease; but the apparently idiopathic variety is some- times remarkably frequent in particular places (barracks, etc.). Several mem- bers of one family may likewise have facial erysipelas simultaneously. In nearly all such cases the sufferers are infected from some common source, for direct contagion is certainly exceptional; but patients with open wounds should never be put near erysipelas cases, because here the risk of infection can not be wholly excluded. Direct inoculation can, however, as has been proved, convey the dis- ease from a patient to other persons or to animals. In contrast with the behavior of many other infectious diseases (typhoid fever, measles, scarlet fever, small-pox, etc.), erysipelas is peculiarly apt to attack the same individual over and over again. There are persons who have facial erysipelas about every one or two years, and ten to fifteen times. Often the explanation of this apparently lies in some chronic disease — e. g., chronic oza;na, chronic eczema of the nostrils or ears — which makes infection easy, but in other cases no cause can be discovered. Of course when erysipelas afilicts the same person a number of times the individual attacks gradually be- come milder. Marasmus seems to predispose to erysipelas. At least we have observed that erysipelas occurred with relative frequency, in the Leipsic hos- pital, in patients suffering from the last stages of phthisis or cancer, or similar diseases. Clinical History, — In many cases the first subjective symptoms ai'e simultane- ous with the cutaneous swelling, and these are chiefly local. There is pain and a sense of tension in the skin. Soon subjective symptoms of fever also appear, such as general malaise, anorexia, headache, and sometimes vomiting. In other cases the disease starts with more violent constitutional symptoms : there is an initial rigor, with violent headache and great languor. The local erysipelatous swelling appears almost at the same time with these general symptoms or sometimes a few days later, either because the local inflammation is at first slight or because it is not noticed, as in the scalp when the hair is very thick. In rare instances the disease begins with sore throat. We saw three almost simultaneous cases of facial erysipelas in one family, in which a severe sore throat lasted for four or five days preceding the appearance of the cutaneous disorder. We have seen a number of similar cases since and believe that they are due to a true erysipelatous angina — that is, to an erysipelas of the soft palate which extends through the nostrils to the external skin. In cases of erysipelas which follow a coryza we may assume, as stated above, that there is an erysipelas of the nasal mucous membrane pre- ceding the erysipelas of the skin. The erysipelatous process in the skin is almost always circumscribed at first. It usually starts on the nose, less often upon the cheek, the ears, or the hairy scalp. The skin becomes considerably swollen, grows red, smooth, and shiny, and feels hot. The redness and swelling keep spreading. There is usually a sharp, elevated ridge, perceptible to sight and touch, separating the diseased from the still healthy portion of the skin. As long as the erysipelas is spreading, we see stretching out from its border, or somewhat removed from it, small red streaks and spots which gradually increase in area and intensity, and finally coalesce. Any decided fold in the skin may hinder for a time the extension of the disease. The naso-labial folds are particularly apt to limit it. The border of the hairy scalp frequently forms a terminal line; but the whole scalp may be attacked, the inflammation stopping only when it reaches the nape of the neck. The boundary of the erysipelas in the ERYSIPELAS 65 hairy scalp can usually be quite accurately deteiinined by palpation (swelling and local tenderness). It is only in a relatively small number of cases that it spreads farther yet, attacking the back, the arms, and -the anterior surface of the trunk, or even extending to the feet. This is known as erysipelas migrans. The facial erysipelas may be healed long before the disease ceases to extend over the other parts of the body. When the spreading process is about to cease, the inflammation usually becomes decidedly milder, appears only in isolated spots, and finally stops completely. In most cases, only the face, the ears, and a part of the scalp are attacked. It is not a rare thing for vesicles or bullse to form in the portions of skin attacked. Such cases are called erysipelas vesiculosum or erysipelas hullosum. The serum may change to pus in these blisters, and then we have erysipelas pustulosum. Exceptionally the infiltration of the skin becomes so intense as to result in a localized necrosis or gangrene — erysipelas gangrcenosum. The parts most apt to be attacked by this are the eyelids, where abscesses sometimes form. Microscopic examination of the skin shows a marked hypersemia of all the blood-vessels and a very considerable infiltration of both the skin and the subcu- taneous connective tissue with serum and cells. In those parts where vesicles are formed there are many dead and disintegrated epithelial cells in the rete Mal- pighi. In the parts where most streptococci develop there may also be necrosis of the deeper layers of the skin. We have already said that there may be many streptococci in the lymphatics of the skin, but they are found only in the first fresh stages of the inflammation. When the inflammatory exudation has reached its full height, the streptococci have usually wholly disappeared. As a rule we find only a few or no streptococci in the contents of erysipelas vesicles. The inflammation in any one spot usually ends four or five days after it has made its appearance there. There is apt to be much attendant desquamation. The face is often left with a finer complexion than it had before. The other symptoms, of which the constitutional disturbance and the fever are chief, correspond pretty closely to the severity and extent of the cutaneous lesion. It is comparatively seldom that this correspondence does not exist. The fever in facial erysipelas usually rises rapidly at first, and to a considerable height. We have seen but few cases where the high fever was delayed till a day or two after the skin was attacked. The temperatures observed in erysipelas are often extreme: 106° (41° C.) is not at all rare. The highest we ever saw was 107.2° (41.8° C). While the erysipelas continues or is spreading, the fever is sel- dom continuous, nor are the remissions insignificant. Pronounced intermissions, even down to normal, are very frequent, but are followed again by a rapid and great rise of temperature. The fever may terminate with a genuine crisis. In intense cases of considerable extent, or in erysipelas migrans, the termination is more apt to be by a more or less gradual lysis. We have seen the cutaneous inflammation in erysipelas migrans still extend itself a little, in a rudimentary form, after the fever had completely ceased. The headache is often intense, and seems to result not merely from the inflam- mation of the scalp but from disturbances of the circulation in the underlying parts, or more probably from the action of a toxine. Other severe cerebral symptoms are also relatively frequent. The patient may be very restless, excited, and wakeful. At night there may be mild or even violent delirium; or there may be decided stupor. All these sjanptoms are in chief part due to the general intoxication caused by the infection ; but they also justify a surmise, as we have said, that there is a circulatoiy derangeraent in the meninges and the brain itself, resulting from the inflammation of the scalp. In drunkards, delirium tremens is' not infrequent. 5 m ACUTE GENERAL IXEECTIOUS DISEASES One of the most constant symptoms in facial erysipelas is gastric and intestinal disturbance. There is usually complete anorexia. The tongue is thickly coated. Vomiting is frequent, not only at the beginning but during the course of the dis- ease. There is constipation ; or there may be quite severe diarrhoea. There is no pathological lesion known corresponding to these clinical symptoms. The spleen is usually moderately swollen. In all severe cases we find in the blood a pro- nounced leucocytosis (16,000 to 18,000 leucocytes in a cubic millimetre). Strep- tococci are not found in the blood. The entire duration of the disease varies greatly in different cases. A very light case may get well in a few days. Most cases of average severity last a week or ten days. Erysipelas migrans may continue for many weeks. We have sev- eral times seen a relapse come on after a number of days of complete apyrexia. Either the face would be once more attacked, or some portion of the skin which had previously escaped. Local complications are comparatively rare and insignificant in erysipelas. The lymphatic glands of the throat and back of the neck are very frequently somewhat swollen, but seldom attain great size. Bronchitis and lobular pneu- monia may develop in severe cases, but are not at all characteristic. Some ob- servers call attention to the occurrence of pleurisy, endocarditis, and pericarditis ; but these complications also are very rare. The spleen is usually slightly swollen. Sometimes there is an icteroid hue. The urine frequently contains a small amount of albumen, and in severe cases of erysipelas acute hsemorrhagic nephritis is not so very rare, but it almost always disappears entirely. The albuminuria usually disappears a few days after the fever. Swelling of the joints has been repeatedly observed. It is more frequent in the severe surgical forms of erysipelas, which are combined with universal septic and pysemic conditions of the system. Purulent meningitis may complicate an erysipelas located in the head, but it is very rare. We should be exceedingly cautious about asserting its existence even when the cerebral symptoms are very pronounced. Cutaneous complications are relatively frequent. We have seen herpes labialis quite often, and a number of cases of urticaria. Of much greater importance are the cutaneous abscesses which occur in severe cases. These are due to a phleg- monous or even gangrenous inflammation of the connective tissue. Their most frequent seat in the face is the eyelids, as already stated; and in that case the eye may itself be endangered. At the close of severe cases of erysipelas migrans, numerous abscesses may develop in the skin of the trunk and extremities, delay- ing convalescence. Since, as we have said, the streptococcus of erysipelas is abso- lutely identical with the streptococcus pyogenes, all purulent inflammatory com- plications of erysipelas are to be referred to the local or metastatic action of the original infectious germs, but erysipelatous nephritis is probably of purely toxic origin. The diagnosis of erysipelas is almost always easy when once the cutaneous lesion has developed. Phlegmonous inflammation of the skin and lymphangitis are to be eliminated ; but this is always possible, with proper care. After a single examination, we may confound it with acute facial eczema of great severity, or even with a marked urticaria. Chief attention should be paid to the characteristic border of erysipelas and to its manner of extension. In erysipelas beginning in the hairy scalp the local inflammation may easily be overlooked, being completely masked by the severe general symptoms. The prognosis of facial erysipelas, when it attacks a healthy person, is very favorable. In drunkards a severe case may be complicated by delirium tremens, and the issue be unfavorable. We saw one case end fatally because of gangrene of the eyelids, followed by purulent inflammation of the orbital connective tissue. Erysipelas migrans may so exhaust the powers of feeble patients as to become DIPHTHEEIA 67 dangerous. The prognosis of surgical erysipelas is relatively more unfavorable, but it can not be considered here. Treatment. — The treatment of ordinary erysipelas of the head and face, which is the main question here, is purely symptomatic. The large number of remedies recommended (tincture of iodine, nitrate of silver, iodoform, ichthyol, carbolic acid, collodion, etc.) shows that they can not any of them materially influence the morbid process. It is easy to be deceived about their efiicacy, as most cases are relatively benign. We therefore usually content ourselves with powder- ing the affected skin or covering it with oil or vaseline to relieve the tension, and also with putting on an ice-bag if the patient likes it. We have found no proof that we can limit the advance of the disease mechanically by applying firm ad- hesive plaster to the boundary of the erysipelas, etc. We can expect no specific action from internal remedies (Pirogoff's camphor cure, liquor ferri sesquichlo- rati, etc.). Apart from alleviating the local discomfort, some other symptoms occasionally demand special consideration. Severe headache and other severe nervous symp- toms may be relieved by the local use of cold or by antipyrine and similar remedies. With high temperature cool baths or antipyretics internally may be used with benefit, but in general the fever does not often demand energetic treatment, since in erysipelas, as we have said, considerable spontaneous remissions of temperature often occur. When there are marked gastro-intestinal symptoms we may pre- scribe hydrochloric acid, opium, etc. Only when there is a true migrating erysipelas and the disease spreads over the body should we try more energetic methods. Heuter recommended subcutaneous injections of a two-per-cent. solution of carbolic acid a little way from the edge of the erysipelas. Although this method is certainly rational, we have usually seen no striking results from it. It seems more effective to scarify the erysipela- tous skin and then wash it with a corrosive-sublimate solution, as lately recom- mended. In the severe cases the main point, after all, is to maintain the patient's strength by nursing and food. If cutaneous abscesses form, they should be opened promptly, when they usually soon heal. CHAPTEE X DIPHTHEEIA {Diplitheritis. Croup. C'ynanche contagiosa) .ffitiology and General Pathology. — Clinically, "diphtheria" means a certain well-characterized, specific, acute, infectious disease, the chief visible lesion of which is a croupous-diphtheritic inflammation of the pharynx and upper air-pas- sages. In a purely pathological sense, however, the terms " croupous " and " diph- theritic " have a broader meaning. They denote a certain form of inflammation which may occur in the mucous membrane of almost any part of the body. It is frequent in the intestine and bladder. There is great diversity in the causes which may produce it. The pathological characteristic of every croupous-diphtheritic inflammation consists in the formation of a fibrinous exudation. This may either be a croupous membrane, which is grayish white, rather firm and elastic, and which can be lifted off with comparative ease from the mucous membrane upon which it rests, or it may be a diphtheritic infiltration with necrosis of the tissues. Here the exudation is more or less deeply imbedded within the proper structure of the mucous mem- 68 ACUTE GENERAL IISTFECTIOUS DISEASES brane itself. There is no essential difference between croup and diphtheria ; diph- theritic inflammation is the severer form of the disease, croupous inflammation the milder. In diphtheria the fibrinous exudation is preceded by a necrosis of the epithelium and of the underlying tissues of the mucous membrane as ^vell, while in the case of croupous exudation the necrosis is limited to the epithelium. The croupous membrane never rests upon an intact mucous surface, but replaces the epithelium, which has already been totally or in very large part destroyed. Flaky remnants of the epithelium, no longer nucleated, are sometimes found in the meshes of the fibrine. The preceding destruction of the epithelium is essential to the occurrence of fibrinous, croupous inflammation. The fibrinous exudation can be formed in those places only where the cause which excites the inflammation kills the epithelium at the same time. It is still undecided whether or in what degree the epithelium takes part in the formation of the croupous membrane. Most pathologists hold that the material for the fibrine comes from the fibrinogen of the infiammatory matter which transudes through the walls of the vessels, and also from the disintegrated migratory white blood-globules. These last are abundant throughout the deposit itseK, and still more numerous in the entire tissue of the mucous membrane beneath the croupous or diphtheritic exudation. If recovery takes place in croup, all that is needed after the exudation has been cast off is the renewal of the epithelium, which can be accomplished through the exclusive agency of the remnants of epithelium left along the borders of the dis- eased spot. In diphtheria, however, the entire necrotic portion of mucous mem- brane must slough off, a line of demarkation being formed, and cicatricial tissue replaces the necrosed portion. The above is a bare outline of the present views about croupous and diph- theritic inflammations. They have been reached gradually through the labors of E, Wagner, Weigert, and others. We have not yet touched upon the setiological factors; but what precedes renders it evident how manifold they may be, for many causes which destroy the epithelial layer of the mucous membrane, and at the same time promote inflammation, may excite croup. We have mechanical causes, such as impacted f eeces, gall-stones, renal calculi ; chemical irritants, caustics, like ammonia and the acids; and, fijially, a number of specific, infec- tious, disease-producing poisons. Among these is the specific poison of diphtheria proper. There has been no doubt for a considerable period that true pharjTigeal diph- theria could be produced only by a specific organized cause. To demonstrate this, however, has been thus far extremely difficult, for there are in the diseased parts a great number of diverse micro-organisms, originating in the mouth and throat, and really secondary to the diphtheritic process; and, although they of course are entirely different from the specific " diphtheritic bacteria," it is very hard to separate them. Nevertheless Loffler has of late succeeded in solving the ques- tion of the origin of diphtheria in an apparently decisive way. From numerous investigations by Roux and Yersin, Heubner, and others, there can scarcely be a doubt at present that the specific diphtheria bacillus is a form of bacillus char- acterized by a definite and particular granular formation, a club-like swelling at the ends, and special methods of growth on blood-serum. The diphtheria bacilli are found only on the diseased portion of the mucous membrane or the point of inoculation, and never in the blood or the internal organs. This fact is of the greatest pathological significance, and it has been established not only for diph- theria in man, but also for experimental diphtheria in animals. In pharyn- geal diphtheria they are found chiefly on the under surface of fresh false mem- brane. The severe general symptoms of diphtheria, however, except when due to secondary infection (vide infra), depend upon the poisonous chemical action of certain substances produced by processes of metabolism in the bacilli. Little DIPHTHEEIA 69 that is definite is known, however, as to the precise chemical nature of these " toxines." We may accept it as a fact that the diphtheria bacilli or their spores reach the pharyngeal cavity directly through the inspired air or in some other way, and there, in case they attach themselves to the mucous membrane and increase,, produce diphtheria. In a few rare cases they seem to be inhaled into the larynx at once, and to excite there a " primary laryngeal croup " (vide infra) . The source of the infection is always to be referred ultimately to another case of diphtheria, but the way in which the disease spreads can not always be traced in detail. In many cases, of course, a direct (" contagious ") transmission of the poison is evident, as from coughing, or the many cases of the disease in physi- cians and nurses from sucking the croupous membrane out of the tracheotomy tube in children, etc. If several children in one house fall sick, as often hap- pens, we may here suspect a direct transmission of the disease, although it is also possible that in such an event several cases may arise from the same source of infection. We do not yet know positively how far the diphtheria bacilli can lead an independent existence outside of the human body (the earth, the floors of dwellings, etc.). It seems certain that the infection can be carried from one person to another by some intermediary, by clothing, linen, toys, and other objects to which the diphtheria poison clings. The resistance of the latter to external in- fluences — temperature, drying, etc. — is very considerable. After complete recov- ery from diphtheria, virulent diphtheria bacilli may be found in the oral cavity for a considerable time. This is particularly to be noted on account of its prac- tical importance. We must mention, in conclusion, that attention has lately been called to the possibility of the transmission of diphtheria from sick animals (hens, doves, calves, [cats] ) to man, since diseases resembling diphtheria undoubt- edly occur in the domestic animals mentioned. Diphtheria, as is well known, is a disease chiefly of childhood, but some cases, and even very severe ones, may occur in adults. In advanced life the dis- ease is very rarely seen. In large cities sporadic cases occur from time to time, but the disease often takes on an epidemic character. At such times some places appear to be much more subject to the disease than others. [While it seems in the highest degree probable that the poison is usually purely local at the start, cases occur which suggest that constitutional infection through the pulmonary blood-vessels may precede the local manifestations. Infection through the alimentary canal is not probable, though its occurrence can not be positively denied. There are still points in the etiology and pathology of this affection which are involved in obscurity. Much has been said and written in this country and in England about the relations of filth and diphtheria. That filthy surroundings contribute a soil favorable to the development of the poison, and at the same time diminish the resisting power of the human organism, can not be doubted ; but, as long as the parasitic theory of infectious diseases prevails, sewer-gas and the like must be classed among the predisposing or accessory causes. Some of the frightfully virulent epidemics of diphtheria in sparsely settled country districts and on the Western plains are difiicult to explain under the theory that each case is mediately or immediately the result of a previous case; these difficulties will, however, doubtless be cleared away in time.] Clinical History. — The incubation is rather brief, seldom exceeding two to five days. The disease itself almost always begins with general malaise, headache, fever, and pain on swallowing. Little children, however, often do not complain of this last symptom, and in older children the sore throat may not be very troublesome at first. It is therefore a very important rule for the physician to examine the throat carefully in every child who presents ill-defined general symp- 70 ACUTE GENEEAL INFECTIOUS DISEASES toms. If diphtheria is beginning, we find redness of the soft palate, and more or less swelling of the tonsils. Upon the inner surface of the latter, and perhaps upon the arch of the palate and the uvula also, are spots covered with a grayish- white coating, which is quite firmly adherent to the mucous membrane. They are less frequent at first upon the posterior wall of the pharynx and the hard palate. Their extent varies greatly in different cases. In the mildest they are chiefly confined to the tonsils, attacking the soft palate or the tonsillar surface of the uvula but little if at all. In severer attacks the spread of the false membrane during the first days of illness is rapid. Almost invariably there is a very early and considerable swelling of the lymph-glands at the angle of the jaw. The con- stitutional symptoms persist. The children are restless. There is complete an- orexia, and frequently vomiting. The temperature-curve is not typical. It is irregular, but is often rather elevated. In true diphtheria such high tempera- ture, 104°-105° (40°-41° C), as is common in follicular tonsillitis, is certainly exceptional. On the other hand, fever may be slight or almost absent, even in the worst cases. The pulse is very rapid. The urine may have a trace of albumen. In mild eases the local and constitutional symptoms remain moderate ; and at the end of a week or ten days there is decided improvement, with rapid convales- cence. In severe cases, however, dangerous symptoms appear, perhaps early ; the croupous inflammation involves neighboring organs, or a severe constitutional condition is developed. The diphtheria very frequently extends into the nose. This "diphtheritic eoryza," though not in itself dangerous, is usually a sign that the case is a severe one. The inflammation of the nasal mucous membrane may be simply muco- purulent (from secondary infection with streptococci?), but it may also be croupous. It is betrayed by the abundant purulent discharge. Excoriations and superficial ulcers are usually soon produced at the edge of the nostrils. There may be nose-bleed. A much more dangerous complication is the extension of the croupous infiam- mation into the larynx. This creates a mechanical hindrance to respiration, which proves fatal in a great many cases, as the child's larynx is so small. For- merly " croup " — i. e., croupous inflammation of the larynx — was regarded as a different disease from diphtheria. Many specialists in children's diseases still maintain this view ; but it is in direct opposition to all anatomical, clinical, and aatiological facts. We grant that there are cases where the pharynx is slightly affected, while the croupous inflammation of the larynx is extreme ; and once in a great while the diphtheritic infection results in croupous laryngitis and trache- itis alone, the pharynx escaping disease'. Still the proposition that there are two distinct diseases, "croup" and "diphtheria," is absolutely untenable. In the overwhelming majority of cases the throat is first affected and then the larynx. We should also consider how easily slight lesions in the phai-ynx may be over- looked, especially if located upon the posterior surface of the soft palate or upon the epiglottis. Cases of what is called " ascending croup," in which the laryngeal affection precedes the appearance of the disease in the pharynx, are, to say the least, very exceptional. Hoarseness is usually the first indication that the diphtheria has attacked the larynx. Then follows the peculiar, harsh, ringing, " croupy cough," so dreaded by the parents, and, finally, there are signs of beginning laryngeal stenosis. Kespira- tion is not much accelerated, but is labored, and the accessory muscles of respira- tion are called more and more into action. The child becomes more restless and anxious. Its face grows pale and livid. Even in children who can make no definite statement as to their subjective sensations these symptoms which we have mentioned are very noticeable. The chief cause of the dyspna?a is undoubt- DIPHTHEEIA Tl edly the mechanical stenosis due to the croupous deposit. Paralysis of the laryn- geal muscles may perhaps be a factor. If portions of the false membrane become partially detached, they may act like valves, being sucked in at each inspira- tion, and pushed aside by the current of expired air. If greater stenosis occurs, respiration becomes noisy, resembling snoring. Inspiration, particularly, is pro- longed and " sawing," and is attended by marked depression of the larynx toward the sternum. An important diagnostic point is the drawing in during inspiration of the supra-sternal region, the epigastrium, and the lower part of the sides of the thorax. This is the direct result of the obstructed flow of air into the lungs. As the lungs do not expand enough to correspond to the inspiratory dilatation of the thorax, the parts mentioned are forced in by atmospheric pressure. The degree of dyspnoea may vary at different times. The false membrane may be loosened and coughed up, rendering respiration easier for a time, till fresh exudations or dis- placements of membrane cause renewed distress. Recovery is still possible. The membrane may be expectorated and no more be formed. Unfortunately, this happy termination rarely occurs. In most cases the symptoms of suffocation in- crease more and more, respiration grows quicker and more superficial, and the child becopies more and more stupefied by the excess of carbonic dioxide in the blood. The pulse gets very small, rapid, and irregular. There are mild convul- sions and then death. The autopsy in these cases usually discloses that the croupous infiammation has extended into the larger bronchi or even into the smaller. The lumen of the bronchioles may be almost completely occluded by false membrane. This croup- ous bronchitis gives rise to no especial auscultatory phenomena during life, so that often we suspect it rather than diagnosticate it. Its clinical signifi- cance, however, is very great, since, even in adults, it may cause death by suffoca- tion without any especial stenosis of the larynx. If it is present, respiration may not be materially relieved in spite of tracheotomy. Beside the dangers attendant upon the local extension of the diphtheritic inflammation, the general intoxication of the body must be regarded as the second most important circumstance in our general estimate of the disease. As men- tioned above, the diphtheria bacilli produce an extremely poisonous toxine, which enters the circulation and which may give rise to the severest symptoms. Our knowledge of human diphtheria is not yet so far advanced that we can state posi- tively what particular symptoms are due to this intoxication, but special attention must be called to the fact that the general symptoms are often very slight, in spite of extensive local croupous inflammation. On the other hand, where the local dis- ease is relatively slight, severe general symptoms sometimes occur which may justly be referred to this diphtheritic intoxication. Among these severe general symptoms are somnolence, which may increase to complete sopor, an increase in the pulse to 120 or 140, progressive cardiac weakness, and collapse. The con- ditions are different in those cases which are termed septic diphtheria. Here the local disease in the pharynx usually has a special appearance : instead of the croupous deposits we see a deeper-seated necrotic destruction of mucous mem- brane covered with a foul-smelling, greasy, purulent deposit (" gangrenous diph- theria"). In such cases the lymph-glands in the neck are almost always much swollen. The tongue is dry and fissured, and a stinking secretion runs from the nose. The temperature is usually not very high, but the pulse is very rapid and small. In these cases there is certainly a secondary septic infection, probably in most cases from streptococci, as in scarlatinal diphtheria (vide supra). Gen- eral septic intoxication and secondary septic inflammation are now mixed with the original disease, and, as we have said, it is often hardly possible to trace in an individual case the precise origin of the morbid condition. These considerations must also be borne in mind in our study of the symptoms 72 ACUTE GEl^EEAL INEECTIOUS DISEASES manifested in other organs in diphtheria. We must iirst mention the direct local extension of the original specific diphtheritic process to the neighboring parts. "We have already said that the nose, larynx, trachea, and bronchi are often involved, but the dense squamous epithelium of the oesophagus and the mucous membrane of the stomach, which is protected by its secretion, are very rarely affected. We must add, however, that diphtheria often extends to the Eustachian tube and mid- dle ear, and also to the anterior part of the oral cavity (gums, lips), and through the nose to the lachrymal canal and the conjunctiva. The latter may also be affected by the direct conveyance of the infectious matter by the finger, etc. In a similar way diphtheria may sometimes involve the external genitals (in girls) or any accidental wounds or injuries of the skin, such as blistered sur- faces, etc. Of the internal organs, the lungs, heart, and kidneys demand chief attention. In the lungs, beside croupous bronchitis, pneumonia often develops in severe cases. This is usually a lobular catarrhal pneumonia, more rarely lobar croupous pneu- monia. Although we can not absolutely deny that the pneumonia may some- times be of a true diphtheritic nature, the majority of cases of pneumonia de- veloping in diphtheria must certainly be classed as secondary affections, due to the inhalation and development of secondary agents (probably streptococci), which may readily take place. After the original diphtheria has disappeared the secondary lobular pneumonia may long prevent recovery or even cause a fatal termination of the illness. The condition of the heart in diphtheria is of especial importance, because severe functional impairment, probably of toxic origin, is common. Even when the fever is slight the pulse may sometimes be very rapid, small, and often irregular. An abnormal slowness of beat is much rarer. It is especially to be borne in mind that even in apparently mild cases there may be ^ery dangerous cardiac weakness. Even during convalescence we repeatedly see sudden death which must be regarded solely as " heart-failure." The autopsy shows that gross disease of the heart is very exceptional in diphtheria, but degen- eration of the muscular fibers and little interstitial myocarditic foci of secondary origin are often found in severe cases. It is at present quite impossible to esti- mate the actual clinical significance of these anatomical changes, since it is at least probable that disturbances of the innervation of the heart cause the car- diac weakness as much as these lesions of the cardiac muscle. Since nephritis is especially common in septic diphtheria, it is hard to decide whether it is due to the primary disease or is to be considered a secondary compli- cation. Its clinical significance is not very great, since it neither materially modifies the general picture nor has any definite bearing on the result of the disease. (Edema, ursemia, etc., are only rarely seen in diphtheritic nephritis. The macroscopic changes in the kidney are usually very slight. Microscopically we find the various degenerative conditions of acute nephritis (vide infra). The Nervous Sequelae of Diphtheria. — The convalescent from diphtheria is liable to be attacked by certain nervous sequelae. Of these, diphtheritic paralysis is the most important. It appears about one or two weeks after the throat trouble ceases, or perhaps earlier, and it is quite as likely to follow mild cases as severe ones. It attacks the soft palate by preference. The voice becomes nasal and deglutition difficult. The naso-pharynx is imperfectly cut off during the act of swallowing, and with each attempt liquid regurgitates through the nose. Usually the pharyngeal mucous membrane is hyposesthetic at the same time, and de- prived of its reflex excitability. There may also be paralysis of the vocal cords upon one or both sides, and this again is frequently combined with angesthesia of the mucous membrane of the throat. There may be paralysis of the ocular mus- cles, of which those controlling accommodation are most apt to be affected, render- ing the vision for near objects imperfect. Paralysis of the muscles of the trunk DIPHTHEEIA 73 and extremities is least frequent, but it may be very extensive. Sometimes sev- eral of these parts are paralyzed simultaneously. Thus we see quite often paral- ysis of the soft palate and of the rauscles of accommodation combined. In some cases there is well-marked ataxia of the lower limbs with or without paresis. This renders the gait very uncertain and tottering, the tendon reflex is almost always abolished, while sensation is affected slightly if at all. Very rarely diph- theria is followed by contracture of the hands or other parts, by difficulty in artic- ulation and paresis of the bladder. A paralysis of the pharynx is sometimes left behind, so that the children have to be fed for weeks through an o3Sophageal tube. It is a remarkable fact that not only in almost every case of the nervous dis- orders which we have mentioned, but often also in individuals who have entirely escaped them, there may be no patellar reflex after diphtheria for weeks or even months. With regard to the pathological state, it is probably a degenerative con- dition of the corresponding peripheral nerves, not only in the post-diphtheritic paralysis, bvit also in the cases of post-diphtheritic ataxia (see the chapter on mul- tiple neuritis). These degenerations are probably due to the poisonous chemical action of certain toxines which are produced directly by the vital processes of the diphtheria bacilli. It is therefore of great interest to note that paralysis has been produced experimentally in animals by the action of diphtheritic toxine by Roux and Yersin and others. The prognosis of all the nervous sequelae of diph- theria is very favorable, and even in severe cases complete recovery usually takes place in the course of a few weeks or months. This is in harmony with the periph- eral nature of the disease. But there is one paralysis which is highly dangerous — that of the heart, as already mentioned. It may occur suddenly during convales- cence. Probably it is analogous to the other nervous derangements, and the result of degeneration in the [nuclei or] fibers of the pneumogastric. Diag'nosis. — The physician will seldom fail to recognize a case of actual diph- theria if he pays proper attention. The characteristic patches and the severe gen- eral and local symptoms make the diagnosis certain. It is much more common to mistake other forms of sore throat, particularly in adults, for diphtheria. The most deceptive are follicular and necrotic tonsillitis {vide infra). We must not suppose that every white spot upon the tonsils is diphtheritic, and we must speak of " diphtheria " only when there is an actual croupous inflammation in the phar- ynx with a true membranous deposit. The practiced eye can usually distinguish at the first glance the plugs of pus limited to the follicles of the tonsils, which are usually multiple, and also the slight and superficial necrosis of mucous membrane limited to the tonsils in necrotic angina. Of late, it has often been proved by bacteriological examination that in these tonsillar affections there are no diph- theria bacilli, and that they therefore are not true diphtheria. We must add, however, that there are light forms of true diphtheria in which the pathological changes assume a milder form, resembling the tonsillar affections just mentioned. In such cases we are therefore certainly justified, especially in dealing with children, in bearing in mind the necessary precautions, but in our opinion the physician should never alarm the family by the justly dreaded word " diphtheria " without sufficient reason. An absolutely definite diagnosis between diphtheria and the other tonsillar diseases can be made only by bacteriological examination. This is at present still too difficult a matter in diphtheria to be within the scope of every physician, but the constantly increasing number of good bacteriological laboratories renders it possible for almost every physician to obtain bacteriological examination of the suspected deposit in doubtful or important cases. An experienced clinician can usually make a correct diagnosis and prognosis even without a " culture." [When the membranes are confined to the nose, the diagnosis may be more or less difficult; but it is especially in cases in which the nasal mucous membrane is Y4 ACUTE GENERAL INFECTIOUS DISEASES involved that we encounter great swelling of the glands at the angles of the jaw. There is also apt to be a thin, acrid, bloody, or sero-purulent discharge. Jacobi states that while diffuse pharyngeal injection may or may not point to imminent diphtheria, marked local congestion is either traumatic or diphtheritic. An examination of the urine should never be neglected in doubtful cases : in diph- theria a trace of albumen is very common; in simple or follicular sore throat albumen is very rare, if indeed it occurs at all.] Prognosis. — The dubious prognosis of true diphtheria is universally known, even by the laity. The very fact that the best-developed and healthiest children so often fall victims to it associates the name diphtheria with the saddest mem- ories. There are indeed many mild cases which recover in a week or two, and severer ones which end happily in three or four weeks; but in most cases, where the process extends into the larynx, or the symptoms of a severe constitutional in- fection occur, the prognosis must be regarded as very serious. Only recently, however, since the introduction of the serum treatment, has the prognosis even of severe diphtheria become considerably more favorable. Formerly, before the serum treatment, it was regarded as a relatively favorable result if one half of the children with diphtheria in the hospitals, on whom tracheotomy was done, re- covered ! Sixty or seventy per cent, of the children operated on often died. At present, however, the mortality of the tracheotomy cases, treated at the same time with serum, has fallen to about twenty-five per cent., and these are only the severe cases in which the serum treatment was begun late. The improved prog- nosis under the serum treatment appears much more favorable if we compare the whole number of cases and the death-rate of diphtheria before and after the in- troduction of this treatment (Heubner, Widerhofer, Baginsky, etc.). In general, diphtheria is to be regarded as the more serious the younger the child is. In later childhood, after the eighth or tenth year, the number of dan- gerous cases is much less. The description of the symptoms shows sufficiently what the dangers of the disease are, and how they are to be recognized. We would state once more that, even in apparently mild cases, the danger of sudden paralysis of the heart, though fortunately rare, always demands the greatest caution. Treatment. — Up to a short time ago it was impossible to say anything in re- gard to any generally recognized treatment of diphtheria which was really effect- ive, but very recently a method of treatment has been discovered, chiefly by the important and interesting investigations of Behring and Roux, which de- serves to be called an actual specific. If further observations confirm the pres- ent results, this treatment is one of the most brilliant and triumphant medical acquisitions. Behring found, in continuing the important discoveries of Pasteur, Buchner, and others, that certain protective matter (" antitoxine ") was formed in the blood-serum of those animals (sheep, goats, horses, etc.) which had been infected with artificially weakened cultures of diphtheria bacilli. If the animal survive the milder infection, it is less sensitive to a severer infection, and, finally, by continued inoculation, it may even become completely immune to the severest in- fection. The blood-serum of such immune animals can now be used in the treat- ment of diphtheria in man. The treatment is simple, and consists in injecting the serum under the skin of the child who has diphtheria by means of a carefully disinfected syringe. The best places for injection are the anterior chest wall or the thigh. Since the amount of serum to be injected is usually about five cubic centimetres, we should use a special syringe which is not too small. The best are made like a Pravaz syringe with an asbestos packing. It is to be understood that the injections must be made with the strictest aseptic precautions. There are three different preparations of serum in the market, varying according to the DIPHTHEEIA 75 strength of their immunizing action. In fresh and milder cases we inject Serum I (" 600 units of antitoxine "), in severer and more advanced cases, especially if there be any signs of disease in the larynx, we use at once Serum II (" 1,000 units ■of antitoxine")? or even Serum III. According to the severity of the case, or according to its course, we repeat the same injection or a weaker dose of the same once in the next twelve to twenty-four hours. In many cases of moderate severity a single injection of Serum II suffices. The favorable action of the serum is shown chiefly by the fact that the affection does not extend after the injection. The existing croupous deposit is thrown off in the course of the next four or five days. The serum injections have no injurious action. Urticaria sometimes occurs after an injection, but it has no serious significance. There is no proof that albuminuria and post-diphtheritic paralysis are seen oftener in cases treated with serum than in other cases. We need not explain further that the serum must be ineffectual in severe septic diphtheria. Taking everything into consideration, it is therefore the duty of the physician, in accordance with our present knowl- edge, to use the serum in every case of true diphtheria in children. At present it is, of course, impossible to pronounce a final judgment on the whole question; but it seems beyond a doubt that we physicians are standing on the threshold of an entirely new era in the treatment of infectious diseases. It is of the greatest practical importance that the serum treatment be begun as early as possible. The most favorable results are seen in children treated on the very first days of the disease. [In merely suspicious cases, therefore, it would seem wise to administer the antitoxine at once, and thus give the patient the benefit of the doubt.- — V.] Local treatment of the affected places in the phar- ynx at the same time is unnecessary. We would, however, emphasize the impor- tance of a general cleansing and disinfection of the whole oral cavity by gargling and rinsing with dilute solutions of potassic chlorate, salicylic acid, corrosive sub- limate (1 to 3,000), etc. Inhalations naay also be used, with caution, for the same purpose. It is also very important to watch the child's nutrition carefully in order to keep up the strength. Milk, eggs, meat juice, small quantities of wine, etc., are most advisable. Since the introduction of serum-therapy all the former methods of treatment have been quite superseded. This is especially true of the many previous attempts to limit the morbid process and cause it to disappear by local disinfection. The practical difficulties in carrying out any really effective local treatment have always prevented the general recognition of the value of caustics, i^ainting, etc. Nevertheless some remedies, even up to the present time, are still recommended as efficient, especially liquor ferri sesquichlorati (pure or diluted), dabbing with a l-to-1,000 sublimate solution, etc. Of the many internal remedies which were formerly tried we can mention only chlorate of potassium and iodide of potassium. The former remedy may still be recommended and may be given in teaspoonful doses of a solution containing 1 part to 30 or 40 of water. [The tincture of the chloride of iron is much used in this country in the treat- ment of diphtheria, and appears to be of real service ; but it must be given in large doses. The following prescription is recommended by Jacobi, whose experience has been very large, for a child of two years : ]^ Tinct. ferri chloridi oij ; Potas. chlorat gr. xx ; Glycerin, pur ,^j ; Aquae ^r. M. S. : Teaspoonful every fifteen, twenty, or thirty minutes. 76 ACUTE GENEEAL IJ^FECTIOUS DISEASES Turpentine is better as an inhalation than by the stomach; a teaspoonful or two of the oil can be poured in water kept at the boiling point by an alcohol-lamp. The whole air of the room is thus charged with the remedy. ITo drug should be used with disorders the stomach. Tablet triturates containing one one-thou- sandth of a grain of corrosive sublimate can be allowed to melt in the mouth with the greatest freedom, and seem sometimes to exert a distinctly beneficial local action. The dose is, however, too small to secure the systemic effects of the drug unless the case is a mild one and free from notable dysphagia.] If the larynx is attacked, and if, in spite of the serum treatment, the conse- quent laryngeal stenosis threatens to cause suffocation, tracheotomy is our only resort. It is never indicated by the disease itself nor by the severity of the case^ but only by persistent obstruction of the larynx. It is therefore not invariably easy to decide whether tracheotomy is called for in any particular case. If the- general condition be bad and respiration already impaired, it is often very diffi- cult to determine whether laryngeal stenosis exists. Tracheotomy will be of no avail if the croup has already extended to the bronchi, or if the dangerous condi- tion of the patient is due to the severity of the constitutional infection or to incipient paralysis of the heart. We have already said that, since the introduc- tion of the serum treatment, the prognosis of diphtheria has become better even in the tracheotomy cases. How tracheotomy is performed, and in what the after- treatment consists, must be learned in the text-books on surgery, where we will also find the necessary description of the so-called intubation of the larynx. Intubation, as devised by Dr. O'Dwyer, is a procedure which makes a distinct advance in the treatment of laryngeal stenosis. In permitting the free access of air to the trachea, intubation may save life without resort to the serious operation of tracheotomy ; or it may tide over a time until tracheotomy becomes absolutely necessary or until the consent of the parents can be obtained to the use of the knife. In hopeless cases it may promote euthanasia. " If severe pulmonary symptoms occur in diphtheria, we should use first of all wet packs of the whole body or tepid baths with cool affusions. Such cutaneous stimulation refreshes and enlivens the whole nervous system, and we should there- fore try it also in the severe cases with secondary septic infection. In septic diphtheria we must also pay especial attention to the condition of the heart. So far as is possible we should try to avert the threatening cardiac paralysis by stimu- lants, such as wine, camphor, and strophanthus. The nervous sequelae of diphtheria are best treated with the constant current. As an internal remedy, iron is good, and also nux vomica or strychnine. The last may be given subcutaneously, if desired, in doses of gv.-io-^o (grm. 0.001-0.002). The prophylaxis of diphtheria demands that every child with diphtheria be absolutely isolated from healthy children. Behring [and many othe*-s] believe that a healthy child may be positively protected from infection by diphtheria for two or three weeks by the injection of a small dose of serum — the whole or one half of Dose I — that is, about three hundred units of antitoxine. It is, of course, very hard to judge of this, and for the present, therefore, it must be left to the individual judgment of the physician in what cases he will try prophylactic injec- tions of serum. [Diphtheria is a disease which involves commonly much exhaustion, and too much stress can hardly be laid on the importance of administering the maximum amount of nourislnnent in the most assimilable and easily swallowed forms from the start. It is also important to give stimulants early in most cases, not waiting for signs of exhaustion. Enormous quantities of brandy can often be given to small children without the slightest toxic effect. ISTo general rule can be laid down; the requirements of each case miist be studied and met. INFLUENZA 7Y When painful deglutition interferes with nutrition, peptonized milk, eggs, brandy, and the like, must be given by the rectum. Rectal alimentation and stimulation and feeding with the oesophageal tube are also to be resorted to in cases of post-diphtheritic paralysis o_f the oesophagus.] CHAPTER XI INFLUENZA {La Gri])pe) Influenza is a specific, acute, infectious disease which is especially distin- guished by the occasional enormous extent of its epidemics. While often years and decades pass without any especial attention being called to the disease, sud- denly cases of it will appear with such frequency that the largest part of the population is attacked, and the disease may better be described as pandemic than ■epidemic. Pandemics of influenza can be traced back with certainty into the six- teenth century. In the present century the influenza during the years 1830-33 traversed almost all of Asia and of Europe, then later there appeared numerous smaller epidemics, but these aroused general attention so little that the disease, upon its last pandemic appearance in the winter of 1889-90, was almost unknown to many physicians. Since that time the disease seems never to have wholly ■disappeared, as a few cases, and occasionally small groups of cases, are constantly seen. .Etiology. — The organized agents of influenza are still not positively known, but R. Pfeiffer has invariably found in the bronchial secretion of patients with the " catarrhal form " of influenza {^vide infra) a definite form of very small bacilli with rounded ends which stain darker than the central portion. These bacilli, which are either free in the mucus or in the pus-cells, are very probably of significance as a cause of the disease. The influenza bacilli very soon die if •dried, and also if put in water. In all probability the infection is usually due to inhaling the germs. The bacilli seem to appear at certain times over an immense territory, so that they or their spores are scattered everywhere through a large extent of country. Many observations upon the appearance of the disease in isolated institutions (convents and the like) render it very probable that the poison may also be carried by a person suffering from the influenza to another in regions pre- viously unaffected. Nevertheless, this contagious manner of spreading plays no great role in comparison with the direct infection from the outer world, this latter mode being everywhere possible during an epidemic of influenza. There is scarcely any reason for speaking of especial predisposing causes of influenza, inasmuch as at the time of a well-marked epidemic the overwhelm- ing majority of the population are attacked, both the healthy and the diseased, the vigorous and the feeble. Sex certainly makes no difference, and age only to this extent, that the disease is seen more rarely in little children under one year of age than in older children and adults. That catching cold has no special astiological significance is evident from the fact that influenza often appears in patients who are already sick in bed. It should finally be mentioned that animals also, and in particular horses, may be attacked by the influenza ; but, nevertheless, it is as yet a doubtful question whether all the diseases in animals which are described under this name are actu- ally identical with genuine influenza. Symptoms and Clinical History. — The best general idea of the extremely manifold symptoms of the disease will be obtained if we bear in mind that the 78 ACUTE GENERAL Il^EECTIOUS DISEASES influenza causes both, a marked infectious (or toxic) general constitutional dis- turbance of the body, and also certain local lesions with local symptoms. The clinical picture therefore varies greatly according to the predominance of one or the other group of symptoms, and also according to the special form of the local disease. ^ The onset of influenza is generally rather sudden. As a rule the marked cases begin with rather high fever, ushered in with a chill, violent headache, marked constitutional depression, and usually considerable pain in the back and loins. The weakness of the patient may be so great that, even if a vigorous individual, he will at once take to his bed. Severe nervous symptoms, such as stupor and de- lirium, are exceptional. Sometimes, but not very often, there is initial vomiting. The backache is often associated with pains in the muscles and joints. Oppressive pain in the eyes is quite characteristic also. This is particularly felt upon moving the eyeballs, and therefore is probably located in the external muscles. The spleen is occasionally somewhat swollen, but any great increase in its size is excep- tional. If the clinical symjDtoms as the case progresses are mainly limited to the above- named constitutional symptoms — fever, languor, headache, pain in the muscles — we may speak of a " typhoidal form " of the disease. Usually, however, certain local symptoms put in an early appearance, and it is especially the respiratory apparatus which, is attacked. The precise symptoms vary considerably in different cases. Sometimes the upper portion of the respiratory tract, the nose, larynx, and trachea are involved ; sometimes, from the start, the smaller bronchi. In the first instance there is marked coryza or hoarseness, in the other case there is cough, due to a dry bronchitis, which can be easily detected upon auscultation, and which involves especially the lower portion of the lungs. If these local symptoms out- weigh the constitutional, the case is described as belonging to the " catarrhal f onn " of influenza. Sometimes the influenza is localized in the digestive apparatus. This " gas- tro-intestinal form " is much rarer than the catarrhal. In this case, in addition to the more or less strongly characterized constitutional symptoms, there is marked disturbance of the stomach and intestines, as shown particularly by nausea with persistent vomiting, diarrhoea, abdominal pain, etc. In one case we observed jaundice. We may also mention in this connection the appearance of an initial pharyngitis. The pains in the back, loins, and extremities already mentioned may persist with unusual violence, and this peculiar form of the disease is known as the " rheumatoid." The muscles and the muscular attachments are probably the chief seat of these pains, which may be so violent that the patient is unable to lie com- fortably, and sometimes keeps up a continual moaning. The loins, in particular, may be the seat of most acute pain, also the upper arms, the knees, the thighs, and the eyes. Objective changes in the jjainful parts, such as swelling of the joints, are scarcely ever seen, nor are the nerve-trunks as a rule especially sensitive to pressure. The painful muscles are usually weaker than normal. The grouping of the clinical varieties of influenza under the four forms al- ready named affords a general idea of the manifold symptoms of the disease, but this division into separate forms must not be carried out too strenuously, for in reality many cases of the disease occur which present transition fonns and com- binations of the various groups of symptoms. Moreover, in all the forms a dis- tinction must be made between mild and severe attacks, for in influenza, just as in most other infectious diseases, there are many rudimentary and mild cases as- well as the fully developed ones, and some could not be properly interpreted but for the presence of the epidemic. The duration of the disease is best determined by the duration of the fever. INFLUENZA T9 In the very mildest cases there may be no fever whatever, or simply a slight evening rise of temperature. As a rule, there is a moderate fever, between 101.5° and 103° F. (38.5° and 39.5° C), although higher temperatures even to 104° F. (40° C.) and more are not infrequent. In the beginning of every severe attack the fever rises abruptly. After a duration of several days (four to seven) it may fall again in a manner approaching a crisis. More frequently, espe- cially when there exists diffuse, catarrhal trouble in the lungs, the fever ends by lysis. With comparative frequency there are found to be noticeable deviations in the temperature curve ; thus, for example, the high fever of the onset sinks on the second or third day, to be followed by an almost afebrile period of one or two days, whereupon a marked rise of temperature ensues. With this change in the temperature there are usually also corresponding variations in other symptoms. We see, then, that the duration of simple, uncomplicated influenza is in the mild eases about three or four days, in the severer cases about seven to ten days. To be sure, we should also consider in this connection that convalescence is often surprisingly slow, so that the after-pains (as it were) of the disease are felt for weeks. These consist, for instance, in a certain degree of debility, and in pain- fulness of the muscles. Sometimes also there are complete relapses, so that di- rectly or a short time after the disease has ended the symptoms begin anew. The special form of the disease may change in this case, so that, for example, the re- lapse of an influenza with predominant constitutional symptoms assumes the pro- nounced catarrhal form. Again, during the same epidemic it is not very rare for a patient to suffer from two attacks of influenza separated by a considerable inter- val of time. Complications and Sequelae. — While all the symptoms of influenza which we have thus far described are the direct effects of the original pathogenic cause, the majority of the frequent complications are undoubtedly dependent upon the in- gress of secondary infection. The system when attacked by influenza is greatly exposed to these secondary influences, and almost all the dangerous and tedious, cases of influenza become such only because of a mixed infection of this sort. This is particularly true of the lungs, in which secondary disease occurs most fre- quently — sometimes even in the flrst days of illness, but also in other cases later. The conditions here are similar to those seen in measles and whooping-cough. The simple, mild catarrh belongs to the original disease; the severe pulmonary affections are, however, invariably secondary complications occasioned by new pathogenic influences. These influences are not always the same. According to the investigations of Ribbert, Finkler, and others it is chiefly the pneumonia dip- lococcus and the streptococcus which are the true excitants of the secondary pneu- monia seen in influenza. These cases of pneumonia are either extensive catarrhal pneumonia especially affecting the lower lobes, or more rarely croupous pneu- monia with its characteristic sputum. We must also add that the influenza bacilli themselves may excite a lobular pneumonia, which shows a marked puru- lent character. If pneumonia be added to influenza, the former overshadows the whole picture. The patient is oppressed for breath, has a severe cough with pro- fuse expectoration, looks pale or cyanotic, and suffers from high fever. These symptoms persist for two or three weeks, and then gradually abate. It is in this way that influenza becomes dangerous for elderly and feeble or sickly persons. With noticeable frequency, pleurisy with effusion is conjoined with the influ- enza pneumonia. The exudation is generally serous, but exceptionally it is puru- lent. Complications in other organs are less frequent. We would make especial mention of purulent otitis media and keratitis and other severe diseases of the eye. We haVe several times observed acute nephritis, but this has always pursued a mild course. Among cutaneous eruptions herpes labialis is a frequent phenome- 80 ACUTE GE^^ERAL INFECTIOFS DISEASES non in all forms of influenza, even the milder. Other exanthems, such as urticaria and roseola, are much less frequent. Many of the complications named may con- tinue even after the fever and all other symptoms have ceased, so that they must be regarded as sequelse. This is particularly true of the diseases of the ear and eye and of persistent bronchitis, but only rarely of a pneumonia assuming the chronic form. An important and for the patient a troublesome and painful sequel is furunculosis, especially if some of the boils are located in the axilla or near the anus. Very often neuralgic pains in the distribution of the trigeminus or in the course of the sciatic or other nerves will persist for a considerable time after the influenza has ceased; but these pains may sometimes be located in the muscles; thus, for example, the frequent, persistent, and troublesome pain in the eyes. In a few cases more severe nervous sequelse, such as spinal symptoms and psychoses, have been seen after infltienza. A special form of acute hsemorrhagic encephalitis (vide infra) has been thought to have a relation to influenza. Diagnosis. — The diagnosis of influenza is in general not difiicult if one has to deal with a w^ell-marked case at the time of an influenza epidemic. The charac- teristic initial symptoms of fever, headache, and pain in the loins are to be con- sidered flrst of all. Their onset is much more rapid than, for example, in typhoid fever. Later on the pain in the various muscles as well as the catarrhal symp- toms are the most characteristic phenomena. Uncertainties and errors in diagnosis may arise from the fact that, on the one hand, we are disposed at the time of an epidemic to call almost all the catarrhal and indefinite mild affections we see " influenza," while, on the other hand, when there is no epidemic, we can not positively distinguish the sporadic " cases like influenza " from the ordinary acute febrile bronchitis, etc. It is indeed very possible, a priori, that different morbid agents may produce similar mild acute diseases of the accessible mucous membranes. In such cases, with pronounced general symptoms, high fever, etc., we must often be content with the diagnosis of "infectious" laryngitis, bronchitis, etc., without being able to decide defi- nitely whether the case is to be classed setiologically with influenza or not. At any rate in practice we should not abuse the diagnosis of influenza. Prognosis. — For an individual who is healthy and vigorous, influenza is not a dangerous disease, even in its severer forms; for elderly persons or invalids it may, however, be a serious affection. Patients with heart disease or pulmonary disease, or those suffering from chronic nervous troubles, sometimes succumb to it ; so that the general mortality at the time of a great epidemic of influenza is always considerably increased. The above-enumerated pulmonary complications are by far the most dangerous ; less often is a fatal termination caused by general or cardiac weakness. The above-mentioned nervous sequelse are also to be con- sidered in prognosis. Treatment. — IsFo specific remedy for the disease is known. Many physicians maintain that the exhibition of calomel at the beginning of the attack decidedly shortens its course, but confirmatory experience is wanting. In general we must, therefore, pursue a purely symptomatic method of treatment. For the initiatory fever, the headache, and the pain in the loins, antipyrine is sometimes a good remedy, and the same may be said also of phenacetine, antefebrine, and especially salipyrine. These drugs are also prescribed for the persistent pains in the mus- cles which come on later. Soothing liniments and ointments may be employed, with friction, for the same purpose. The treatment of the pulmonary complica- tions is according to the established methods. Morphine is mainly used for the troublesome cough. Apomorphine, senega, and other expectorants may be em- ployed, and, if indicated, external remedies such as an ice-bag or dry cupping. If the patient becomes very feeble, stimulants such as [strychnine], champagne, and strophanthus are demanded. DYSENTEEY 81 CHAPTEE XII DYSENTERY jSltiology. — By " dysentery " is meant a disease of the colon, which appears sporadically, but more often in epidemics; it is excited by infection with an organized pathogenic poison, about which we have as yet no definite knowledge ; and the infection is probably at first a local one. From the investigations of various men, especially Kartulis, it seems very probable that a certain form of amoeba must be regarded as the cause of " endemic tropical dysentery." At least in endemic dysentery we almost invariably find, both in the stools and in the walls of the dysenteric intestinal ulcers and in the dysenteric abscesses of the liver, many amoebae (amoeba coli), which are never found in any other intes- tinal affection. Dysentery may also be artificially produced in cats by means of f seces containing amoebse. In dysentery as it occurs in Germany, however, we do not apparently find amcebse in the stools as a rule, although even in Germany Quincke and others have described certain cases of " acute enteritis " (" amoebic enteritis ") in which there were a large number of amoebse. The question of the excitants of dysentery therefore needs further investigation, and it is not impossible that several intestinal affections with different aetiology have thus far been included under the name of dysentery, especially in the tropics. The true home of dysentery is in warmer and tropical countries, where the disease is much more violent and widespread than here. For example, the mortality among the soldiers of the Anglo-Indian army due to dysentery is said to be at times thirty per cent, of the entire number of deaths. In our climate most of the epidemics occur at the end of summer and in autumn. Endemic influences are certainly important. The special conditions in some places are evidently very favorable for the development and dissemination of dysenteric germs, and there are other places equally unfavorable. There can be no other explanation of the immunity of some localities contrasting with the great prevalence of the disease in others. How infection occurs we do not yet know. Many observations, especially in southern countries, support the idea that the germs may be taken into the system by drinking water. Dysentery does not seem to be directly contagious; but that it can be spread through the medium of the fsecal dejections of the sick — e. g., from privies, chamber-vessels, and bed-linen — is very probable. Many cases were formerly referred to catching cold or to some error in diet ; but we must, of course, regard these merely as predisposing influences. The objective pathological lesion of the colon, in all severe cases, consists in a pronounced croupous-diphtheritic inflammation. The remarks as to the general pathology of such inflammations made in the preceding chapter are equally ap- plicable to the analogous dysenteric inflammation. In this case, too, there is first a destruction of the epithelium and then the formation of a fibrinous exudation occupying its place, and penetrating down into the tissue of the mucous mem- brane itself. At the same time there is an intense purulent infiltration of the mucous and submucous tissue, accompanied by extensive ecchymoses. In the most virulent cases the macroscopic appearances are marked thickening of the whole wall of the intestine, congestion of the serous layer, and the conversion of the inner surface into a mottled, dark-red, irregularly roughened area of ulcera- tion. The disease may be confined to the rectum and the sigmoid flexure, but in severer cases it involves the entire colon as far as the ileo-cascal valve, or even extends to the lower portion of the ileum. Besides this severe form of diph- theritic or even gangrenous dysentery, there is a milder variety, termed catarrhal dysentery. In this the mucous membrane is found in a state of intense purulent 6 82 ACUTE GENERAL INFECTIOUS DISEASES inflammation, with ecchymoses. Even here little masses of croupous exudation, which can be torn off, have replaced the epithelium; but they never form con- tinuous layers of great extent. There is no sharp boundary-line between the two forms, the milder catarrhal-croupous and the severer diphtheritic dysentery. ISTumerous transitional and combined varieties exist. We must remark, in conclusion, that precisely the same anatomical changes as are presented in true dysentery may result from other causes. Important among these is persistent faecal impaction in the rectum, which, by a purely mechanical effect upon the epithelium, may excite a diphtheritic inflammation in the mucous membrane. And any severe constitutional disease whatsoever, such as typhoid fever, measles, small-pox, septicaemia, or phthisis, may be attended by a so-called " secondary dysentery." This is most frequent in hospitals. Whether it has the same aetiology as genuine dysenteiy is uncertain. Clinical History. — Throughout the entire illness the most prominent symp- toms are intestinal. There may be first of all some slight irregularity of the bowels for a few days, and then appears a moderate diarrhoea. The stools are at first feculent, although thin, and number two to six daily. After a few days the discharges increase in frequency, and become extremely characteristic. The stools are very frequent, occurring ten to twenty, and even sixty or more, times, in twenty-four hours. In severe cases there may be a distressing and almost constant desire to evacuate the bowels. After every operation, and to some extent during it, there is tenesmus attended by intense burning pain in the anus. The stools soon lose their usual feculent character in great part if not entirely. They become scanty, so that not more than about half an ounce is evacuated each time. For the most part they usually consist of a sero-mucous fluid, in which are suspended numerous shreds and particles of varying size. These are blood- stained bits of mucus, little coagula of blood, and necrosed pieces of mucous mem- brane. One or another of these constituent parts may predominate, so that there may be slimy, purulent, or bloody stools, or all sorts of combinations of these varieties. We often find, besides, a few small masses of faeces, usually covered with mucus. We sometimes see numerous clumps of mucus, resembling sago or frog's spawn ; they are probably mucous casts of the follicles. Under the micro- scope the greater part of the dysenteric discharge is seen to consist of pus-corpus- cles and blood. There are also cylinder epithelium and an enormous amount of detritus, and the bacteria of putrefaction. A purely dysenteric stool has no bad odor, except that in the worst cases of gangrenous dysentery the discharges become blackish and extremely offensive. The rectal tenesmus may be accompanied by a cramp-like pain during micturi- tion. There are often violent attacks of colic. The abdomen is usually rather tense, aud tender on pressure along the line of the colon, but without tympanites. The anus may be red, inflamed, and excoriated. Gastric symptoms are on the whole infrequent, if we except the complete anorexia which exists in all severe cases. Sometimes there is repeated vomiting. Occasionally hiccoughs prove dis- tressing. The tongue usually has a dry, greasy coating. The symptoms just depicted last about a Aveek or ten days. If the case is of much intensity, the general condition is also greatly affected. The patient seems much collapsed, and is very languid and feeble, with a small and rapid pulse. The skin becomes cool and rough, the voice weak and hoarse. There is pain in the muscles. The patient wastes away. The temperature has little that is char- acteristic or typical. In many cases there is no fever at all, and the temperature may even be subnormal. In most cases, however, there is an irregular fever seldom exceeding 104° (40° C), and having remissions. In the worst cases the general weakness may increase more and more, and death occur; but with us a favorable termination is much more frequent. The DYSEi^TERT 83 distress gradually diminishes, the stools assume more and more of a feculent char- acter, the patient becomes stronger, and after one and a half to three weeks con- valescence is established. It may be a long while, however, before a patient com- pletely recovers from a severe attack. A third possibility is the transition of the acute into a chronic dysentery. In this the symptoms of a chronic colitis, usually attended with cachexia, may persist for months and years. Mild, rudimentary forms of dysentery also occur, presenting no severe intes- tinal symptoms, and recovering at the end of a few days. In these cases, too, great sensitiveness of the intestine to disturbing influences frequently persists for quite a long time after the illness. There may be exacerbations of the disease, and relapses. Complications of dysentery, localized in other organs, are rare, at least in epidemics here. In tropical dysentery abscess of the liver is comparatively com- mon. It is dependent upon metastatic processes from the portal radicals. In some cases abscesses of the lungs and of the brain may follow abscess of the liver. Inflammation of the serous membranes or of one or more joints may also occur. If paraplegia follows it may be referred either to secondary myelitis or to poly- neuritis. Dysentery is also said to occur in connection with a " general scorbutic diathesis," but to all appearances this is usually a " septic " complication. The dysenteric ulcers rarely lead to perforation and consequent peritonitis. The diagnosis is seldom very difiicult. It is based exclusively upon the intes- tinal symptoms and the character of the stools. It is only the cases of secondary dysentery which occur in the course of other severe diseases that are likely to escape observation. The prognosis is mainly influenced by the character of the epidemic, which, as we have said, is in our climate usually benign. There may be danger, particu- larly to elderly people, from bodily weakness and collapse. Treatment. — Prophylaxis demands that the isolation of the patient and the disinfection of the stools be as complete as possible. The healthy must be very careful during an epidemic not to catch cold, and to avoid errors in diet, for experience shows that an opposite course predisposes to the disease. The patient must be kept warm, and must not leave his bed, even if the attack be mild. The diet must be rigorous. If the strength is fair, thin porridge, milk, and broths sufiice for some days. To a feebler person we should give somewhat stronger nourishment from the start, e. g., eggs, peptonized meat, and wine. Most patients bear liquids that are lukewarm better than those which are cold. As to drugs, the habit of almost all experienced physicians is to give at first a mild laxative. Although opiura does not usually control the diarrhoea and tenes- mus at all, it is the rule for decided improvement to follow the exhibition of the laxative. During the first days, or, if need be, later, we give two to four table- spoonfuls of castor-oil daily. If this medicine is very disagreeable to the patient, we can replace it by a strong infusion of rhubarb (10-100). In southern countries large doses of calomel (gr. x to xv, grm. 0.5-1) are customary, and are highly praised by the physicians there. Further on in the disease we may content oi;r- selves with giving mistura amygdalae ; or we may administer bismuth in the fol- lowing mixture: Bismuthi subnit. vel salicylat., grm. 5; mucilaginis acaciae, syrupi simpl., aa 15; aquse destil., 120 — to be shaken before taking. If the dis- ease should get worse again, however, we should always try a laxative. Emetics at the beginning of the disease are often employed in the tropics, but seldom with us. Ipecacuanha (radix antidysenterica) , given in large doses of fif- teen to thirty grains (grm. 1-2), is even regarded by many as a specific. Among antiparasitic remedies, naphthalin (gr. viij, grm. 0.5, thrice daily) and salol (one to two drachms, grm. 4.0-8.0, a day) have been especially recommended. ISTumer- ous attempts have been made at local treatment by enemata. No brilliant results. 84 ACUTE GEls^EEAL INFECTIOUS DISEASES however, can be claimed for any of these methods or medicines. A decided pallia- tive effect can be obtained from the injection of thin starch to which twenty or thirty drops of laudanum have been added. Suppositories of cocoa butter con- taining extract of opium often mitigate the tenesmus. Other injections are recom- mended, each to measure §ij to iijss. (grm. 60-100), and to contain either argenti nitrat., gr. j to vj (grm. 0.05-0.30), or plumbi acetat., gr. ij to viij (grm. 0.1-0.5), or potassii chlorat., gr. xv to xx (grm. 1-1.5), and especially tannin (three in- jections a day of a warm 0.5-per-cent. solution). In severe cases we may also try high injections of solutions of tannin as in cholera (vide infra). Many other solutions are used. The success of this treatment is, however, dubious. In all cases the margins of the anus must be protected from inflammation by frequently washing and anointing the skin. The treatment of weakness and collapse is by the usual stimulants — ^wine, ether, camphor, and the like. In chronic dysentery the main point is to persevere in a strict control of the diet. We may exhibit astringents, such as tannin and columbo. Subnitrate of bismuth is also given, and nitrate of silver and acetate of lead. And in these chronic cases a long-continued and thorough use of rectal irrigation with fluids containing some mild astringent or disinfectant may have a good effect. [Sporadic dysentery is a self -limited disease, and, as has been shown by Flint, runs its course within ten days without medication. Treatment, however, adds to the comfort of the patient and shortens the course. It is not customary with us to use daily laxatives. If there is any doubt as to whether the intestines have been emptied, a saline should be given, the action of which should be followed by opium in sufficient doses to allay pain and tenesmus. Subsequent action of the bowels is best obtained by simple large enemata. In weak persons castor-oil is to be preferred to salines. In epidemic dysentery active treatment is much more important. Laxatives are contra-indicated by sero-sanguinolent dejections or by asthenia, but enemata can be freely used. Stimulation is often required; nutrition must be carefully looked after, such articles being chosen as are digested and absorbed by the upper portions of the intestinal tract, leaving as little residue as possible to pass on to the inflamed colon. Opium is often demanded and tolerated in large doses, and astringents, such as the acetate of lead, gallic acid, and the pernitrate of iron, are of service. In acute dysentery the patient should be instructed not to yield to the desire to go to stool if he can help it, and tenesmus can often be much diminished by simple irrigation of the lower bowel with water, which may be warm or cold, whichever the patient finds more agreeable. Chronic dysentery is one of the most difficult maladies with which we have to deal. In its treatment a sea voyage, or removal for at least some months to a climate other than that in which the disease originated, is of far more value than drugs. Am(ebic Dysentery The amoeba coli, first found by Losch in the stools of a dysenteric patient, has received very careful study at the Johns Hopkins Hospital, and forms the subject of a most exhaustive and valuable monograph by Councilman and Lafleur. The living organism is readily seen, and recognized especially by its active amoeboid movements on the warm stage of the microscope. If the imees contain small gelatinous masses, these will be found to provide the most fruitful field for search. The numbers of the organisms vary widely in different cases, and even in the same case, from day to day. They are said to be present in this form of dysentei-y alone, and have been found in secondary abscesses of the liver and the CHOLERA 85 lung, alike after death and during life. They should be sought for in all obstinate cases with dysenteric symptoms. The prognosis is uncertain, and the cases are apt to drag along with exacerba- tions and remissions of the symptoms; but recovery does take place. There is notable danger of the formation of secondary abscesses, in which event re- covery is hardly to be hoped for. The only treatment which seems to have been of much service — beyond a general hygienic and supportive regimen — consists in the use of copious injections into the intestinal canal of solutions of quinine, in the strength of one to one thousand or even five thousand. Losch found that contact with a solution of the latter strength for one minute sufiices to kill the amoebae.] CHAPTER XIII CHOLERA (Asiatic Cholera) Historical Remarks. — The home of genuine Asiatic cholera is India. The first epidemic in that country with which we are accurately acquainted occurred in 1817. This was very widespread. The disease was probably endemic there at an earlier period. In the next few years the cholera extended in all directions, and reached Astrakhan by way of Persia. Between 1830 and 1832 the disease made its first great epidemic progress over Europe. Invading all European Russia, it reached Germany in 1831, and France and England in 1832. Then came many smaller epidemics up to 1838, when there was a complete cessation till 1846, in which year the disease, again starting from Asia, overspread Europe. There have in later years been epidemics in many places, but we can not here enter into the particulars of them. During the war of 1866 there were many cases of cholera in Germany, and from 1883 to 1886 Italy, France, and Spain were visited by the dis- ease. In August, 1892, cholera broke out suddenly and very unexpectedly in Hamburg, where within three months about 18,000 persons were attacked by the disease, and over 7,600 died of it. .ffitiology. — Some time ago it had become evident that the real cause of cholera consists in the infection of the system by a specific micro-organism. Koch was, however, the first to succeed in the search for the poisonous agent. He was in charge of the scientific expedition sent out by the German Government in 1883 to Egypt and India for the purpose of investigating the disease. Koch found in the intestines of all the victims of cholera whose bodies he examined a certain kind of micro-organism which he named the comma bacillus. It is shorter than the bacillus of tuberculosis, but somewhat thicker, and it is usually bent in the shape of a comma, or even like a semicircle (see Fig. 9). In pure cultures the comma bacilli grow into long spiral threads, resembling the spirilli of recurrent fever. Examined in a liquid, the individual bacilli are seen to make vigorous move- ments. This mobility is probably dependent upon the thin, filiform fibers at the ends of the comma bacilli discovered by LofSer. The comma bacilli flourish best at a temperature between 86° and 104° (30° and 40° C). Below 61° (16° C.) they cease to grow, but they are not killed even by a greater degree of cold. The free access of oxygen is desirable but not abso- lutely indispensable to their growth. They multiply veiy rapidly in liquids — e. g., broth or milk — and they may, under favorable circumstances, retain their vitality for many weeks, while they can be readily destroyed by desiccation. In this again they resemble the genuine spirilli, which can maintain their existence only in 86 ACUTE GENERAL USTFECTIOTJS DISEASES fluids. It is necessary that the nutrient material have an alkaline reaction. On neutral or acid material the growth of the comma bacilli ceases entirely. The characteristic features of pure cultures can not be described in detail here, but we may observe that the nutrient gelatin is slowly liquefied by the bacilli. JSToth- ing definite is yet known as to the occurrence and the formation of permanent spores. There can now be no doubt that the sole cause of cholera is infection by the comma bacilli. It has been shown that in every case of genuine Asiatic cholera the comma bacilli are present in the intestine, and that they are never found under any other circumstances. Even the last postulate which was needed to show their pathogenic significance has been fulfilled. Rietsch and ISTicati, followed by Koch himself and others, have succeeded in producing cholera in a guinea-pig by introducing into its duodenum or into the contents of the stomach previously made alkaline, pure comma bacilli. Investigation as to the origin of cholera must, therefore, now meet this culmi- nating question: Under what circumstances and through what channel do the comma bacilli penetrate into the human system, and in what raanner do they there excite the characteristic processes of the f'l^i''^'' ,^,\{ /''^// disease? There can be no doubt that among /"J- ji'' •z;;^' |'^^'_^' '/ Europeans, and probably everywhere except *''' '' ' jr'>J f- — " — "^ i^^ India,, the cholera is invariably imported. ' It is equally certain that the dejections of '' /-V,! '-> '^/' , }k)i'' , II cholera patients, which are rich in comma I ,',v/j>^''/ ^ 1/ jPj'Jf //I I bacilli, are the chief if not the only agent \''A - ~ /i /,.- r.i 1^ \ j^y which the disease is spread. The bacilli n -/■:>' Avhich escape into the outer world with the stools find abundant means to prolong their 'W-'.'ff!'''',' ,'0^/' '' 1 existence. They continue their growth " 'I ' \ ^i' 'f" J ) \\ upon moistened bed-clothes, or in water '' ',1 lu* 't j'f^i which contains a sufficient amount of or- ■ - / ///'/' // / ' ganic substances, or in food, such as fruit or /I '' ! '' milk, or in moist earth; and the ways by Fig. 9.— (From Koch.) Comma bacilli from which they Can in turn enter the system of a cholera deiection which had lain for two i i.i "^i i • • e. • j. • days on a wet cloth. The s-shaped bacilli a healthy human being are infinite m num- are at a. 600 diameters. hox. It is easy to understand why certain persons — e. g., laundresses and nurses — are more liable to infection than others; and it is equally intelligible that the spread of the disease should often bear a relation to certain outward circumstances. The fact has long been a familiar one, that the cholera almost always progresses along the world's most frequented highways, and that it never travels faster than the means of human intercommunication render possible. This is important, because it shows plainly that the germs of the disease are not disseminated by currents of air. It is easy to understand that the distribution of the disease should sometimes correspond with that of water destined for personal use. The experience of the last few years has again proved most clearly that the drinking- water is the chief, although of course not the only, source for the dissemination of cholera. If an extensive water-supply is contaminated by comma bacilli, as was the case in Hamburg, the disease may suddenly break out in a place with great severity. Sporadic cases usually arise from the use of a contaminated stream which is used for drinking only by a small number of men (sailors, etc.). A man falls sick with cholera, of course, not simply from swallowing the cholera bacilli, but because the bacilli remain in the intestine and multiply. It is safe to assume that many men swallow comma bacilli at the time of a cholera CHOLEEA 87 epidemic without falling sick at all, or without any but the slightest disturb- ance, because the comma bacilli are at once destroyed by the acid gastric juice or they develop in the intestine only in small numbers or perhaps in an attenuated form. In the last epidemic at Hamburg comma bacilli were sometimes found in the solid stools of healthy men, who were in close contact with cases of cholera, and also in the stools of men who had a very mild " cholera diarrhoea." These facts are extremely important. They lead to a correct estimate of the infection experiments repeatedly practiced of late on human beings, and, on the other hand, they have a great practical significance in regard to the danger of trans- mitting cholera. These theories may be brought into harmony with the observations collected by Pettenkofer, which go to show a connection between the dissemination of cholera and the character of the soil. The character of the soil can evidently influence the dissemination of the cholera bacilli in various ways. The conditions of the water in springs, etc., may depend very materially upon the character of the surrounding soil. The epidemiological facts especially emphasized by Petten- kofer are : 1. Certain places are immune, especially those lying in a rocky terrain. 2. The frequency of cholera (as of typhoid fever, vide supra) corresponds with variations in the ground-v/ater. Most cholera epidemics happen in the summer months. Liability to the dis- ease is very widespread, although some remarkable exceptions are seen. Sex is unimportant. Age has more influence. The disease occurs in sucklings, but, as a rule, is more rare among children than among adults. Elderly people are very apt to take the disease, while of typhoid fever the opposite is true. Most authors lay great stress upon predisposing causes. Among these, taking cold is not so important as are errors in diet and mild attacks of gastro-intestinal catarrh, which are shown by numerous observations to predispose strongly to the disease, because the acidity of the gastric contents is thus diminished, and the retention of comma bacilli in the intestine is thus facilitated. The stage of incu- bation seldom lasts over one to three days at most. Clinical History. — In cholera, as in most acute infectious diseases, the inten- sity of the illness varies between the extremes of mildness and severity, so that usually a correct interpretation of the mildest cases is rendered possible only by the fact that an epidemic exists and by the discovery of comma bacilli. These insignificant cases are called simple choleraic diarrhoea. The symptoms are those of a violent acute intestinal catarrh; the dejections are watery, rather large, painless, and number about three to eight in twenty-four hours. There is considerable malaise, complete anorexia, and thirst, and there may already be indications of severer choleraic symptoms — vomiting, slight pains in the calves of the legs, and diminished secretion of urine. Many cases recover after a few days or a week, but in others the first mild diarrhoea is succeeded, at the end of about one to three days, or rarely later still, by a severe attack of cholera. In such cases we speak of a " premonitory diarrhoea of cholera." The mild form is succeeded in a gradual transition by the cases designated as " cholerine." Cholerine exhibits the symptoms of a violent, rather sudden cholera morbus. It often begins at night. To the diarrhoea, which now and then displays even at this time the characteristics of pronounced cholera, vomiting is soon added. The accompanying constitutional symptoms are rather severe. There is great languor and depression. The voice grows weak, the extremities are cool, the pulse is small and accelerated, painful cramps occur in the calves of the legs, the urine grows scanty and perhaps albuminous. The whole attack lasts about a week or two, before recovery is complete. The course of the disease is not infrequently varied by repeated improvements and relapses. From these cases of medium severity there is again a continuous line of tran- 88 ACUTE GENEEAL INFECTIOUS DISEASES sition to the pronounced severe form of cholera. Statistics as to the frequency of the separate forms can not be given, since many of the milder cases escape observation. The true attack of cholera may begin suddenly with the severest symptoms. As a rule, however, it is preceded, as already stated, by a first stage of brief pre- monitory diarrhoea. This, after one to three days, is replaced with equal sudden- ness by the severe symptoms of the second or " algid stage," or " cholera asphyxia."^ Its first symptoms are the abrupt appearance of great bodily weakness, chilliness,, and vertigo. The characteristic gastro-intestinal symptoms soon declare them- selves. The diarrhcea grows very violent. At short intervals there are copious painless dejections, which at first retain somewhat of a feculent character, but very soon present a characteristic resemblance to rice-water, gruel, or whey. A single stool will measure a little less than half a pint (grammes 200). The stools have no color and almost no odor. They are watery, and usually deposit a finely granular, grayish-white sediment upon standing. Their reaction is neutral or alkaline. Only one or two per cent, is solid matter, with a little albumen and a relatively large amount of sodic chloride. In many severe cases the dejections, contain more or less blood. The microscope reveals epithelium, triple phosphate, and numerous micro-organisms. Of these last a part are the comma bacilli,, and a part are bacteria of putrefaction, etc. These excessive evacuations are but very rarely absent. They are more apt to fail if death occurs at the end of a few hours — cholera sicca. [In cholera sicca the intestines after death contain the characteristic rice- water material which, perhaps owing to paralysis of the muscular coat, was not expelled during life.] The appearance of the diarrhoea is soon followed by frequent though rarely distressing vomiting. The vomitus consists in part of ingested liquids and in part of an actual transudation through the mucous membrane of the stomach and intestine. Hiccoughs may accompany and follow the emesis. In addition to these prominent digestive symptoms of vomiting and profuse diarrhoea there are complete anorexia and excessive thirst. The tongue has a thick, dry coat. The abdomen is usually flat and soft, or it may be concave and hard. Sometimes we may feel fluctuation in the intestines, due to their being- filled with fluid. There is not much real abdominal pain; what there is, is de- scribed as a " feeling of heat and pressure " around the umbilicus. At the same time very severe symptoms develop in other organs. The circu- latory system is chiefly affected. The action of the heart may be stimulated at the beginning of the attack. The patient complains of palpitation and great precordial anxiety. After a brief time, however, cardiac weakness appears, and continually increases. The action of the heart becomes very weak, and the heart-sounds feebler and feebler. The pulse at the wrist grows very small, and is usually somewhat accelerated. In a severe case the pulse vanishes completely after a few hours. This collapse of circulation makes itself quickly evident in the appearance of the patient. The face and extremities grow cool, and then ice-cold ; the complex- ion becomes partly livid and partly a bluish gray; the lips are almost black. The surface temperature may fall below 95° (35° C), while in the rectum febrile tem- peratures may often be observed, reaching 102° (39° C.) and higher. The eye and cheek grow very hollow, the skin becomes wrinkled, and loses all its elasticity. The voice grows hoarse and feeble (voice of cholera). Respiration is laborious and superficial. The mind may remain unclouded to the end, but usually there is great apathy, and all acuteness of perception is destroyed. Only a few patients are restless and excited. Reflex action is much impaired. CHOLEEA 89 One characteristic symptom is the cramps in the muscles. These are usually very painful, and consist in tonic contractions of the muscles, particularly those of the calf of the leg, but also those of the toes, thighs, arms, and hands. The cramps occur spontaneously or upon the least provocation, last a few minutes, and recur at short intervals. The precise reason of their occurrence is not yet known. It may be the effect of poison (vide infra). They can be observed in other severe acute diseases, although most marked in cholera. They sometimes occur in chol- era morbus. In a well-developed attack of cholera there is almost invariably oliguria or anuria. The urine, if any be secreted, is concentrated, with abundant sediment, and it very often contains albumen. In many cases not one drop of urine reaches the bladder for days, and this condition persists till death or recovery. The symptoms thus far depicted, if taken as a whole, represent the algid stage, which seldom lasts more than one or two days. In many cases death occurs during this period. It is ushered in by the tokens of extreme general prostration, and may take place after a few hours, or more frequently in the second half of the first day. But in other cases the " stage of reaction " succeeds. This may be a true compensatory period, leading directly to convalescence. The evacuations become less frequent and more feculent, and the vomiting ceases. The pulse becomes stronger, the cyanosis and coolness of the extremities diminish, and an abundant perspiration is not infrequent. After a few days urine is again ex- creted. This is almost invariably quite albuminous, and usually contains casts and red blood-globules. If convalescence be uninterrupted, however, the urine very soon becomes perfectly normal, and after a week or two recovery is to be regarded as complete. Departures from this favorable course of the stage of reaction are frequent. Eecovery may be interrupted by repeated relapses into the previous condition, sometimes with a fatal result; instead of convalescence, there is developed a severe third stage, usually with fever. This stage ordinarily bears the generic name of cholera typhoid, although it is subject to manifold variations in its clin- ical symptoms as well as its exciting causes. Cholera typhoid may present an actually typhoidal general condition with severe fever. There is a considerable elevation of temperature, headache, and dullness. The pulse is full and rapid, the face flushed. The skin, particularly that of the extremities, sometimes presents the so-called choleraic eruption, in the form of an erythema, roseola, urticaria, or the like. This variety of cholera typhoid ends after a few days in recovery, or else passes into one of the following conditions. A second form of cholera typhoid is distinguished by the development of the most diverse local inflammations. Thus, there may be a severe dysenteric or diph- theritic inflammation of the small and large intestine, attended by offensive puru- lent and bloody stools. Pneumonia is also possible, as well as purulent bronchitis, diphtheritic inflammation of the larynx, pharynx, bladder, and female genitals, parotitis, and sometimes erysipelas and pyaemia. And when we consider that, besides all these conditions, the usual intestinal symptoms, or those of choleraic nephritis, may exist also, it is evident how varied the clinical picture may be. The development of these local affections frequently lays the foundation for numerous sequelae. Choleraic nephritis gives rise to the third or ura-mic variety of cholera typhoid. The secretion of urine is almost suspended. The region of the kidneys is some- times sensitive on pressure. The little urine that is still passed contains numer- ous casts, albumen, and frequently renal epithelium and white and red blood-glob- ules. Somewhere toward the end of the first week, or possibly earlier, there are grave nervous symptoms, to be regarded as uraemic : first there is headache and 90 ACUTE GENERAL IAtEECTIOUS DISEASES vomiting, then sopor and coma, or delirium and convulsions. Most of these cases are fatal. Patholog-y and Pathogenesis. — We are now acquainted with the manifold symptoms and varieties of the disease. If we seek for the pathological changes which control the process, and endeavor to find some correspondence between them and the symptoms, we shall be disappointed. At least, in its early stages, cholera is merely a severe local disease of the intestine. We find the serous layer of the coils of the small intestine rose-red from congestion. The mucous mem- brane is in a state of catarrhal inflaramation : it is swollen, reddened, and at first covered with a layer of tough, transparent mucus; but very soon an abundant transudation flows into the canal, so that the intestinal coils are filled with a large amount of clear fluid, looking like rice-water or gruel, and so devoid of bile as to indicate the suspension of its secretion. The signs of inflammation of the mucous membrane now grow more pronounced. The solitary follicles and Peyer's patches become swollen, with edges of a vivid red, and frequently there are many small ecchymoses in the mucous membrane. The extensive desquama- tion of the epithelial lining of the intestine has also been regarded as important, because it was regarded as in part the cause of the copious transudation. Still it may be questioned whether the desquamation is not, at least to some extent, a post-mortem change. In yet later stages of the disease the intestinal trouble very frequently assumes a croupous-diphtheritic character. The surface is ne- crosed and ulcerated in many places, and the contents of the intestine are no longer colorless, but sanious and bloody, with a foul odor. Otherwise most of the post-mortem lesions correspond to what was obvious at the bedside. The muscles exhibit an early and persistent rigor mortis, and fre- quently contract in such a way as to throw the corpse into some unusual posture. All the internal organs are remarkably dry, pale, and anemic. The left ventricle is contracted. The blood lies mostly in the large veins, the right side of the heart, and the cerebral sinuses. It is thickened, is but little clotted, and is said to resemble the juice of bilberries or huckleberries. The spleen is not enlarged — an exception to the rule in infectious diseases. The kidneys present marked passive congestion, most pronounced in the cortex. The microscope reveals a greater or less degree of parenchymatous nephritis, with great destruction of the epithelium. If death takes place at a rather advanced stage of the disease, the tissues have lost their characteristic dryness, and the most diverse local lesions, including nephri- tis, may be found to have occasioned death. If we search for the connection between the pathological changes just de- scribed and the cause of the disease, or again between these lesions and the clin- ical symptoms, the first point to guide us is that the comma bacilli are found only in the lumen of the intestine, and never in the blood or in other parts of the body. The intestinal symptoms are satisfactorily explained by this abnor- mal state of the intestine, but for all the other grave symptoms we have to seek some special cause. The desiccation which the body undergoes as a result of the excessive liquid dejections can not fail to affect the tissues, but can not fully explain the symptoms, for the circulatory disturbances and the cardiac failure at least may develop before large evacuations have occurred. It has also been settled beyond question by means of the newer investigations that precisely the worst symptoms of cholera — namely, the muscular cramps, the subnormal tem- perature, and the changes in the blood^are occasioned by the chemical results of tissue metamorphosis in the comma bacilli, that is, by the so-called toxines. Some of these have been already isolated chemically by Brieger and others. It is an interesting circumstance that the amount and virulence of the toxines formed by the comma bacilli seem to depend on the physical characteristics of the nutrient material on which the culture grows. CHOLEKA 91 As to the complications which occur in the later stages of the disease and which are embraced under the generic name of cholera typhoid, we regard them as mainly secondary. The choleraic process itself does not cause them, but is merely the occasion for their appearance. The examination of the intestine in such cases shows that numerous other varieties of bacteria follow closely upon the comma bacillus, gaining entrance to the system by treading in its footsteps. Cholera nephritis is probably due to various causes. Some forms of nephritis seem to be caused by specific cholera toxines (in analogy with scarlatinal nephritis), while others are probably of a secondary septic nature. Diagnosis. — A positive diagnosis of cholera can be made only by finding the comma bacilli in the stools. When an epidemic prevails it is often neither neces- sary nor possible to make the search in each individual case. Sporadic cases or the first cases of a beginning epidemic can and must be diagnosticated only in this way, which gives absolute certainty. We can not give here a detailed account of the bacteriological diagnosis, but we may state briefly that, when cholera exists, the simple microscopical examination of a smear preparation sometimes makes the diagnosis extremely probable. For this purpose a small clump of mucus is taken from a stool as fresh as possible, spread on a cover-glass as thinly as possi- ble, fixed by passing it carefully through the flame several times, and stained with an aqueous solution of methylene blue or carbol-fuchsine. In actual cholera we then find the comma bacilli sometimes in large amount (almost a pure culture) or especially arranged in characteristic small groups. To render our diagnosis un- assailable we must employ gelatine or agar plate cultures, etc., the details of which are to be found in the text-books of bacteriology. All those affections whose symptoms are like those of cholera may be con- founded with true cholera, especially cholera morbus (vide mfra) ; and also cer- tain cases of poisoning, especially acute arsenical poisoning, may give rise to symptoms wonderfully like cholera. The prognosis should always be guarded at the beginning, even if the symp- toms be mild, for, as already mentioned, a simple diarrhoea may prove to be '■^ premonitory " of a severe attack of cholera. During the real attack the prog- nosis grows graver in proportion as the case presents the characteristics of as- phyxia and cyanosis. The mortality in many epidemics is frightful. All the inhabitants of a house or street may in a brief period be swept away. Accurate statistics are difficult to give. If we count the typical cases alone, the mortality is not infrequently fifty to seventy per cent. In about two thirds of the fatal cases death occurs during the first days of the stage of asphyxia, and in about one third during the second period, known as " cholera tyiAoid." The influence of the diet and the hygienic surroundings of the patient before his illness is impor- tant. A greater proportion of children and old people perish than of the mid- dle-aged. Prophylaxis and Treatment.— The measures to be taken to prevent the spread of the disease, when it has once started in a place, can be only briefly discussed here. The chief things are the quickest isolation possible of the first cases that occur, the disinfection of the stools and all linen, objects, etc., soiled by the stools', and finally the determination of the source of infection (drinking-water, etc.), in order to prevent further infection. The evacuations (stools and vomitus) can be best disinfected with a five-per-cent. solution of carbolic acid or with milk of lime, chloride of lime, etc. ; the linen and other objects should be disinfected in a special disinfecting apparatus. It is veiy important to keep a strict oversight of the drinking-water, milk, and all articles of food eaten in an uncooked con- dition. In regard to individual prophylaxis, we must remember especially that any slight gastric or intestinal catarrh increases the liability to the disease. Hence, 92 ACUTE GEIsTEEAL nsTFECTIOUS DISEASES at the time of a cholera epidemic, careful dietetic restrictions are imperatively necessary and every disturbance of the stomach or the intestines, even the slight- est, needs the promptest and most careful treatment. It is best wholly to avoid the use of water that has not been boiled, raw vegetables, etc. [Various efforts have been made to render human beings immune to choleraic infection. The best results seem to have been attained by inoculating Haffkine's attenuated virus. — V.] In the treatment of the cholera attack itself many physicians even now use opium (laudanum or pure opium in powder, gr. ss.-j, grm. 0.03-0.05), while others,, especially at the beginning of the disease, prefer large doses of calomel (gr. v-x^ grm. 0.3-0.5, several times), and during the subsequent course they give con- tinued small doses of calomel (gr. ss.-j, grm. 0.03-0.05, every two hours). In the algid stage warmth is especially advisable. Hot baths, hot packs, sweat- boxes with dry or moist hot air, embrocations of hot oil, an abundant supply of hot drinks (coffee, tea, mulled wine, broths) are praised by all physicians, and they must certainly be used. The remaining treatment is symptomatic; morphine or ice for the vomiting and embrocations of chloroform oil or sub- cutaneous injections of morphine for the painful cramps in the calves. The weaker the heart becomes, the more energetically must we give stimulants (injec- tions of camphor or ether, champagne). Among the newer methods of treatment tried during the last epidemic we may mention subcutaneous infusions of warm "normal" (0.6 per cent.) salt solution in the infraclavicular region or under the skin of the abdomen. By uninter- rupted infusion by means of an irrigator or a funnel two or three quarts (litres) of salt solution can be infused in twenty-four hoi;irs. Intravenous injections have given still better results, and injections into the abdominal cavity have also been tried. Cantani strongly recommends intestinal injections (" enteroclysis ") with warm tannin solutions at a temperature of 100° to 10i° F. (38°-40° C). The fluid contains 5 to 10 parts of tannic acid, 50 parts of gum arable, and 2 or 3 parts of laudan-um to 2,000 parts of water. All these methods are believed to have shown some favorable results, but none of them has been able to attain gen- eral recognition and iise. After many experiments most physicians have finally gone back to the old forms of treatment. [The vital importance of the serious treatment of a beginning diarrhoea dur- ing a cholera epidemic can not be too strongly insisted on. Rest, simple diet, and a little medication will, in the vast majority of instances, entirely prevent grave consequences. The apparently trifling character of the symptoms is apt to lead people into a false security. Those who can leave an infected district should do- so without delay. With reference to the prevention of an epidemic, a pure water supply and strict cleanliness in its broad sense possess far more vii*tue than cordons of troops or measures of quarantine. It is more practicable to destroy the soil than to keep out the seed in these days of constant and rapid international communication^ The systematic disinfection of all cholera discharges or articles soiled by them should be a matter of course.] Great caution must be exercised about the diet, not merely during the attack itself, but for a considerable time afterward. At first we can allow only thin por- ridge, milk, broths, and toast or rusks. It is advisable to administer dilute hydrochloric acid with the food. The treatment of cholera typhoid varies greatly, of course, according to the kind of attack. The separate complications should receive their customary treatment. [In the first stage, absolute rest, opium, and lumps of ice by the mouth ad libi- tum are the chief measures on which reliance is to be placed. It should be remem- MALAEIAL DISEASES 93 Lered that the entire function of the intestinal tract is reversed; thus, instead of an absorbing-, it has become an excreting surface. In the stage of coHapse the nervous system is more or less paralyzed, the blood is damaged by the loss of its watery constitutents, and the circulation of that fluid is greatly impeded. The subcutaneous or gastric absorption of drugs is conse- a, tlirce parts of licorice, one part of orris-root, four parts of colt's-foot, and two parts each of mullein and anise- seed. — Traxs. 11 162 DISEASES OF THE EESPIRATOEY OEGANS racic symptoms. In severe cases a few dry cups may be very useful in adults, but local abstractions of blood are never necessary in simple bronchitis. If there is troublesome irritation on coughing, so as to disturb the rest at night, we may pre- scribe small doses of morphine, five to ten grains of Dover's powder (gramme 0.3-0.5), fifteen to twenty drops of cherry-laurel water, codeine, etc. When ex- pectoration is difiicult, we may use the so-called expectorants — ipecac, chloride of ammonium, apomorphine, senega, etc. We have already repeatedly mentioned the use of tepid baths and shower- baths, indicated in severe diffuse bronchitis developing secondarily in the course of other acute diseases. Tepid baths with shower-baths, two or three times a day, are also to be used as a most powerful remedy in severe cases of capillary bronchitis in children. The baths assist expectoration and guard against the possibility of the development of lobular pneumonia. Wet packs applied to the thorax or over the whole body are serviceable. The child should be wrapped to the neck in a sheet which has been pre- viously dipped in water at a temperature varying with the degree of the fever from 68° to 77° (16° to 20° E.) and well wrung out. It is best to leave the arms free. A dry woolen blanket may be wrapped around the moist sheet. This pro- cedure must be repeated three or four times a day. As to other remedies, we use the same as in adults. With weak children our care must be to keep up the strength by giving the most nourishing food possible and small amounts of wine. An emetic is sometimes indicated in cases with an abundant accumulation of mucus in the bronchi, and is of good service. As experience has shown, we should use opiates for small children only with the greatest caution. Senega and ben- zoin may be employed as expectorants. In the bronchitis of old people our chief aim should be to keep up and improve the patient's strength. We prescribe liquor ammonii anisatus, infusion of senega, etc., to aid expectoration, which is usually difficult, since the cough is feeble. We must keep close watch on the condition of the heart (digitalis). Tepid baths may be of advantage, but they must be used with care. CHAPTEE II CHRONIC BRONCHITIS {Chronic Bronchial Catarrh) .ffitiology. — Chronic bronchial catarrh may develop gradually from external causes, or in rare cases it may follow acute bronchitis. The same noxious influ- ences which excite acute bronchitis may, by the frequent repetition of their action, result in chronic bronchitis. The constant inhalation of dust is one of the commonest causes of primary chronic bronchitis (see the chapter on diseasec from the inhalation of dust). In maay cases it is therefore a definite occupation disease, and is seen in millers, bakers, wool-workers, stone-cutters, colliers, etc. In a large number of cases severe chronic bronchial catarrh is not an inde- pendent disease, but occurs as a complication or a result of other diseased condi- tions. The combination of chronic bronchitis with emphysema of the lungs {v'lde infra) is the most common. A large number of cases also are the result of some form of heart disease, such as valvular disease or myocarditis, or of disease of the vessels, leading to stasis in the pulmonary circulation, and finally to a chronic catarrh of the bronchi. Chronic bronchial catarrh in renal diseases also depends in part upon circulatory disturbances, and in part on the toxic action of urinary CHKONIC BEONCHITIS 163 constituents wHich have not been normally excreted. Finally, we find a more or less extensive chronic catarrh of the bronchi in other chronic affections of the lungs and pleura, as in tuberculosis or pleurisy. Chronic bronchitis is seen especially in adults and old people, and more fre- quently in men, on account of their exposure in the various trades, than in women,, but children may also have pronounced cases of chronic diffuse bronchitis. Such cases may often be referred to a previous acute disease of the respiratory organs, especially whooping-cough, less often measles, etc. Such cases in childhood often continue into later life, and on careful inquiry we may trace many of the severe^ cases of chronic bronchitis in adults back to childhood. Pathological Anatomy. — Chronic bronchitis is characterized anatomically by a persistent and chiefly venous hyper^emia and swelling of the bronchial mucous, membrane with increased secretion of mucus and morbid exudation of serum and pus-corpuscles. There is often a hyperplasia of the mucous membrane with puffi- ness of the surface. In old cases, however, we finally meet with an atrophy of all the layers of the mucous membrane. One of the most frequent results of chronic bronchitis is a cylindrical dilatation of the middle and lesser bronchi — bronchiectasis — especially in the lower lobes. This arises gradually from the loss of elasticity of the diseased bronchial walls, and their diminished resistant pow- ers, as well as from the pressure of the stagnating secretions. Symptoms and Course of the Disease. — The symptoms which are due to chronic bronchitis are dyspnoea, cough, and expectoration. To these should be added the results of a physical examination, in making a diagnosis. The cough is of very different severity in different cases. Usually it is worse early in the morning, in the evening, and at night, than in the daytime. The amount of expectoration is also subject to great variations. In many cases there is a dry cough (catarrhe sec, vide infra), in which only small amounts of tough, viscid sputum are expectorated. In other cases the expectoration is more abun- dant and muco-purulent, sometimes rather sero-purulent, and occasionally thin and separating into layers on standing. In catarrh of the finer bronchi the muco- purulent sputum at times indicates its origin by partly formed casts. We may also note the formation of so-called spirals (vide infra, bronchial asthma). Mi- croscopically, the expectoration has no special characteristic appearances, but contains only the usual elements of sputum — pus-corpuscles mixed with pavement epithelium, ciliated epithelium, often many bacteria, sometimes needles of fat acids, and rarely a few pointed octahedral crystals, the so-called asthma crystals (vide infra). Small amounts of blood may be seen in severe chronic bronchitis, especially in the catarrh of passive congestion, bronchitis with very severe at- tacks of coughing, etc., but they do not have any bad significance. Dyspnoea of moderate or even severe degree may be due solely to an extensive catarrh of the finer bronchi with narrowing of their lumen. In many cases in which there is bronchitis the dyspnoea is due chiefly to some co-existing abnormal condition of the heart or lungs. Physical Examination. — The percussion in bronchitis shows no special change. At most the resonance may be somewhat tympanitic from the relaxa- tion of the lung-tissue, especially in the lower and posterior portions of the lungs, or, with an abundant retention of secretion in the bronchi, it may be a little diminished. The inspiratory descent of the lower edge of the lung is lessened when the entrance of air is much impeded by the contracted or plugged bronchi. Auscultation may give either rhonchi, whistling, hissing, humming, etc., or moist rales, according to the extent of the catarrh and the amount and consistency of the secretion. The sounds are usually to be heard over the whole lung, or espe- cially over the lower lobes, because here the catarrh is usually most marked, and retention of secretion is most apt to occur. The respiratory murmur in some 164 DISEASES OF THE EESPIEATOEY OEGANS places may be quite obscured by the rales. Otherwise it is vesicular, sometimes exaggerated, sometimes rough and indefinite. Expiration is usually prolonged, because the exit of air from the alveoli is much hindered by the narrowed bron- chioles. The respiratory murmur may be much diminished, or even entirely sup- pressed in places where the bronchi are stopped by secretion, which happens most frequently in the lower lobes. Except in mild eases, we usually distinguish several different forms of chronic bronchial catarrh, which may run into one another. 1. The dry chronic catarrh (catarrhe sec of Laennec) is the form in which the mucous membrane has only a slight secretion. The cough is usually very trou- blesome and labored, but the patient raises merely a little tough sputum, or none at all. On auscultation we hear sibilant rhonchi, but no moist rales. This form of catarrh is usually associated with pulmonary emphysema, and asthmatic at- tacks are also frequent. The disease is stubborn, and usually lasts for years. 2. The so-called bronchial blennorrhcea is that form of chronic bronchitis in which we find a very copious sero-purulent exudation on the surface of the mucous membrane. The cough is therefore associated with a very abundant and quite thin expectoration, the amount of which in the twenty-four hours may exceed a pint (half a litre). The expectoration runs together in the sputa-cup and usually separates on standing, the more purulent portion sinking to the bottom, and the sero-mucous portion, which is usually frothy on the surface, remaining at the top. ISTumerous moist rales are heard in the lungs, especially in the lower portions. These diminish if large amounts of sputum are coughed up. Anatomically, the bronchi are almost always found dilated in this form of chronic bronchitis. 3. The so-called serous bronchorrhcea (" catarrhe pituiteux " of Laennec) is quite rare but very interesting. It is characterized by the expectoration of a very large amount of frothy, almost purely serous, or sero-mucous, thin sputum con- taining only a slight admixture of pus. The cough usually comes on in very vio- lent paroxysms which last from half an hour to an hour or more. The respiratory symptoms are quite severe, especially during these attacks, and have given rise to the old and useful term " asthma humidum." The expectoration collected in twenty-foiir hours may amount to one or two quarts (litres). Examination of the lungs usually reveals very abundant and extensive moist rales. The reso- nance on percussion is normal or a little diminished, from the accumulation of secretion. The special cause of this peculiar disease is quite obscure. There are mild afebrile and also very severe forms of this type of chronic bronchitis. We have seen several chronic cases, which were attended with persistent fever, and which led to great emaciation and weakness. In one case which came to autopsy there was found a marked tuberculosis of the retro-bronchial lymph-glands, while the lungs themselves showed hardly any striking changes. One vagus nerve was wholly imbedded in the tubercular mass of the glands, and it is not impossible that the peculiar attacks of serous expectoration were due to irritation of this nerve. At any rate, we should consider the possibility of such conditions in the future. It is worthy of note that attacks of " humid asthma," with expectoration of large amounts of serous sputum, have also been observed in chronic nephritis, espe- cially in contracted kidney (q. v.). Course of the Disease. — The course of most chronic bronchial catarrhs is very protracted. The disease usually has frequent remissions and fresh exacerbations. The patient is tolerably well in the pleasanter time of the year if he takes good care of himself, but in autumn and winter, or after exposure to various noxious influences, the catarrh grows worse and the patient's symptoms increase. If the disease has lasted for years, we usually find symptoms in the lungs, such as emphy- sema or chronic tuberculosis, or in the heart, such as secondaiy dilatation and CHKONIC BEONCHITIS 105 hypertrophy of the right ventricle, which symptoms gradually become more se- vere. The details of these conditions are to be found in the appropriate sections. Diagnosis. — The diagnosis of chronic bronchitis is not difficult in itself, and may easily be made by considering the patient's symptoms and by judging of the result of the physical examination. We must always consider, however, whether the bronchitis is actually a primary disease or a result or a complication of some other chronic disease. Therefore, in every case of chronic bronchitis, the heart and the kidneys (urine) must be carefully examined, as well as the lungs. Prognosis. — Chronic bronchitis is in most cases a very stubborn affection, which frequently, as we have said, shows improvement, but from which complete recovery is rare. The prognosis also depends greatly upon the patient's circum- stances, and upon the possibility of his taking care of himself and avoiding all harmful exposure. In secondary bronchitis the question whether the bronchitis is capable of material improvement or not of course depends mainly upon the prognosis of the primary disease. The danger in primary chronic bronchitis comes from the final development of its sequelse, especially from the gradual appearance of pulmonary emphysema, dilatation of the heart, secondary tuberculosis, etc. Treatment. — The only hope of success in severe cases in any method of treat- ing chronic bronchitis lies in removing the patient completely, at least for a time, from the action of injurious influences. The favorable result of the baths and health resorts that are employed depends largely upon this, that patients enjoy in them complete bodily rest, and are far better protected from dust and the changes in the weather than at home. We must make the patient comprehend the neces- sity of this condition as the basis of any treatment. If he can not go to a suit- able climate during the cold season, he must keep his room in all unpleasant weather, but at other times he may be permitted to stay in the open air. Further- more, the patient must be warned to avoid as completely as possible those harm- ful influences which his calling and manner of life entail, and among which especially to be mentioned is the bad air in our inns and restaurants. Food should be easily digestible, and, in persons inclined to corpulence, sparingly taken. Alco- hol is to be permitted only in a moderate degree. We combat the tendency to con- stipation, which is often present, by dietetic remedies, by taking fruit, especially grapes, prunes, etc., honey, Graham bread, or by mild laxatives, such as the bitter waters, Friedrichshall, Ofner, etc., since any persistent constipation aggravates the patient's symptoms. If the circumstances of the patient permit and his condition requires it, we should send him south in the autumn in order to avoid the evils of a northern winter, but we must always consider whether the patient has the strength to bear the burden and unavoidable discomfort of such a journey without permanent harm. The rule is to send patients with a bronchial catarrh when there is much secretion to health-resorts with a dry climate — for example, to the western Ri- viera, San Remo, Bordighera, Mentone, etc. The somewhat dry yet cooler cli- mate of Meran, Gries, or Arco is suitable for patients with a stronger constitu- tion. Patients with dry bronchitis usually find themselves at their best in a warm but not too dry climate. If we wish to be sure of avoiding the winter's cold, we must choose Sicily, Egypt, or Madeira for a residence. Of the more northern winter resorts we may mention places on the eastern Riviera, especially Nervi. We must recommend, in bronchitis, a suitable summer residence, particularly for those who dwell in large and dusty cities. Any private country house in a well-wooded and protected place is suitable. If we wish to send patients to a bath, Marienbad, Kissingen, or Homburg are proper places for corpulent people Avho also suffer from digestive disturbances, while we may send weaker patients to 166 DISEASES OF THE EESPIRATOET OEGANS Ems, Soden, Badenweiler, Ischl, Eeiclienhall, etc. A summer residence on the sea, best on the Baltic, is very serviceable for many patients. The inhalation treatment is much employed in chronic bronchitis, but we should not cherish too high hopes about its use. The best inhalations in dry catarrhs are simple steam, a one- or two-per-cent. solution of common salt or bicarbonate of sodium. Ems water, etc. In cases with marked secretion, inhala- tions of oil of turpentine are most to be praised. The simplest way is to pour a teaspoonful of oil of turpentine into hot water and inhale the vapor as it arises. The so-called turpentine-pipe, however, is more convenient and more efficacious (Fig. 23). This consists of a flask, which is filled to the height of several inches with water and then with a layer of oil of tur- pentine or of oleum pini pumilionis (P. G.), some two centimetres thick. Two glass tubes, open at both ends, are passed through the cork. One, straight, tube extends down into the layer of water : the lower end of the other is free in the upper part of the flask. The outer portion of this last tube is bent at an angle and is con- nected with the mouthpiece through which the patient inhales. The formation of turpentine vapor is aided by putting the flask in hot water. We have treated many patients in this way, who, for a number of hours a day, " smoked " their turpentine-pipes. In treating chronic bronchitis the pneu- matic method was considerably employed for a time; that is, the patient was made to breathe artificially compressed air, or to expire into air of less than the atmospheric pressure, by means of a movable pneumatic apparatus, as pro- posed by Waldenburg and others. Of late, however, this method of treatment has re- ceived less favor, inasmuch as actual results have fallen decidedly short of the benefit promised. In Eras, Eeichenhall, and other places special pneumatic cabinets have been arranged, filled with compressed air, in which patients remain for varying lengths of time. One of the most serviceable remedies in dry chronic bronchitis is a large amount of warm drink (pectoral tea. Ems water, Seltzer, etc.). Iodide of potas- sium in small doses (gr. iij-v, grm. 0.2-0.3, thrice daily) often acts favorably in making a tough secretion fluid. Of expectorants, ipecac and apomorphine are most recommended in this form of bronchitis. For distressing cough we may give Dover's powder, morphine, or codeine. In bronchial blennorrhoea we know empirically that the internal use of balsams causes a distinct diminution of the secretion. Oil of turpentine is the most active, and may be given internally in gelatine capsules, or mixed with milk, in doses of ten or fifteen drops three or four times a day. After each dose of turpentine we should give a glass of milk. Lepine, G. Seej and other French physicians recommend terpine as still more effectual. This is a derivative of turpentine, and is best employed in pills containing a grain and a half (gramme 0.1), of which two or even more are to be taken three times a day. It may also be given in solution as follows : Terpine, 2^ drachms (grm. 10) ; alcohol, q. s. ad sol. f aciendam ; aq. dest., 6 ounces, 6 drachms (200 grm). Misce. Sig: Two or three tablespoonfuls daily. Myrtol, balsam of copaiba, and balsam of Peru are also used internally. The chief ex- pectorants are infusion of senega root, liquor ammonii anisatus, etc. We should Turpentine-pipe. FCETID BEO:NrCHITIS 167 be very sparing of narcotics at first, but in severe cases "we can not wholly dis- pense "with them. [The iodide of potassium in doses of five to ten grains thrice daily is sometimes distinctly curative. An out-door life, free diet, moderate alcoholic stimulus, tonics, and woolen clothing do much to promote recovery.] Local applications to the chest in the form of embrocations, mustard plasters, dry cups, or cool or warm wet compresses are to be used, especially with severe dj^spnoea, or with pain and a feeling of oppression in the chest. Warm baths are very well borne by many patients with chronic bronchitis. Sometimes, too, vapor baths, if taken with caution, may be of service, especially in strong and corpu- lent patients. In dry chronic bronchitis we often give the patient a sweat in bed. In all secondary chronic catarrhs our chief attention, beyond the symptomatic treatment of the bronchitis, must be directed to the treatment of the underlying disease. If we succeed in once more regulating the heart's action by digitalis when there is uncompensated heart disease, or in establishing diuresis when there is renal disease, or in improving the general physical condition by proper dietetic measures in the corpulent, gouty, alcoholic, etc., we may also in that way cause improvement in the existing bronchial catarrh. CHAPTER ni rCETID BRONCHITIS [Putrid BroncJcitis) .31tiology. — By putrid or foetid bronchitis we mean that form of bronchitis in which the secretion of the mucous membrane undergoes a putrid decomposition, and in which, consequently, the expectoration takes on a peculiar and extremely foul odor. The special agents which cause foetid bronchitis are still unknown. The opportunity for the agents of putrefaction to enter the bronchi with the inspired air is of course often given, but a foetid bronchitis naturally is excited only when they can remain there and increase. Foetid bronchitis therefore de- velops quite rarely in a previously healthy lung (primary foetid bronchitis). The retention and the further development of the bacteria of putrefaction are chiefly favored, as we know, by diseased conditions which already exist in the bronchi. A great number of cases of foetid bronchial catarrh therefore develop secondarily upon other pulmonary affections of longer standing. Thus the expectoration may quite suddenly change and take on a foetid character in the course of a chronic or rarely of an acute bronchitis or of phthisis. Bronchiectasis {vide infra) great- ly favors the development of this putrid change, for in it the retention and stag- nation of large amounts of secretion promote and occasion the putrid decom- position. If a putrid decomposition of the secretion begins in one part of the bronchial system, the further extension of the process follows from direct infection. In rare cases putrid bronchitis also develops as a result of an embolic pulmo- nary gangrene. Symptoms and Course ; Anatomical Changes. — If a foetid bronchitis arises in the course of some other chronic pulmonary disease, its appearance may be marked by a sudden impairment of the general condition, by high fever, often associated with numerous chills, and by an increase of the thoracic symptoms, such as pain and cough. The change in the expectoration, the peculiarity of which was first accurately described by Traube, is characteristic. The expectoration shows the same character in cases of apparently primary foetid bronchitis. 168 DISEASES OF THE EESPIEATOEY OEGANS The sputum has a very repulsive, sweetish, putrid smell. The expectoration is usually quite abundant; the consistency is rather thin. On standing, the sputum shows a very marked division into three layers. This division is due to the abun- dant serous exudation in the bronchial mucous membrane and to the thin fluid character of the expectoration, Avhich permits an unequal division and a settling of the solid constituents. The upper layer consists of a very frothy, muco-puru- lent stratum, consisting in part of individual masses, from which a number of coarser or finer fibers float down into the middle layer. This middle layer con- sists of a dirty-green muco-serous fluid. At the bottom of the vessel is found the third layer, which is often the thickest, and is composed entirely of pus. It con- sists of pus-corpuscles which have sunk to the bottom, and is of a rather thin, greasy consistency. With the naked eye we generally recognize a number of little whitish-gray plugs and particles in it. These so-called " Dittrich's plugs," which are easily crushed under a cover-glass, are quite characteristic. Microscop- ically, they consist of decomposed pus-corpuscles, detritus, and bacteria, and usually contain very many needles of fat acids arranged in bundles (see Fig. 24). We often find also in the sputum large masses of fungi, especially great bunches of twisted lepto- thrix fibers, which, by an unpracticed eye, may readily be mistaken for elastic fibers. The latter are, of course, never found in the expectoration of a simple foetid bronchitis, but only in the deep-seated, destructive processes in the lung, like gangrene. On chemical examination of the sputum, the ordinary products of putrefaction may be found — volatile fat acids, especially butyric and valerianic acids, also sulphuretted hydrogen, leucine, tyrosine, etc. Fig. 24.— Crystals of fat acids. j^ jg ^.^^.j characteristic of many cases of foetid bronchitis that the sputum does not have a putrid character at all times. Sometimes for days the patient coughs up a simple catarrhal secretion, and then all at once comes an outburst of intolerable stinking expectoration. This is probably because a circumscribed putrid focus is fre- quently shut off, the expectoration coming solely from the other bronchi, where there is merely a simple catarrh, until finally the accumulation of putrid secretion is all at once coughed up again in large amount by mouthfuls. When foetid sputum is coughed up, the patient's breath also becomes very foul- smelling, so that he often becomes a burden to his associates. The signs which foetid bronchitis gives on physical examination are those of an ordinary bronchitis ; but it is characteristic of many cases, in distinction from ordinary chronic bronchitis, that the physical signs (rales, dry rhonchi) are limited chiefly to a definite portion of the lung, usually one lower lobe. In a great number of cases we also find signs of consolidation and contraction of the lung, of pleurisy, etc., which do not belong to foetid bronchitis as such, but are due to complications or sequelse. The most frequent of these sequelse is the development of a " reactive " lobular inflammation, a geniiine pneumonia, which follows a catarrh of the finer bronchi. These pneumonias frequently run into gangrene, so that Ave very often find a number of larger or smaller nodules of gangrene besides the extensive foetid bron- chitis in the lungs. In many of these cases the foetid bronchitis is certainly the primary process, and the development of the nodules of gangrene is sec- ondary; yet we shall see later that the reverse may also be true. Foetid bron- chitis and gangrene of the lungs run into each other so often, both clinically and anatomically, that there is no sharp line to be drawn between them. If the FCETID BR0:N^CHITIS 169 nodules are superficial, and reach the pleura, the infection attacks this, and we have a purulent or even an ichorous pleurisy. The smaller and medium-sized bronchi are almost always found in a condition of cylindrical dilatation in old foetid bronchitis. Their mucous membrane is in- tensely inflamed, and often ulcerated superficially. On its surface we see in the cadaver the greasy purulent masses and the plugs which we find in the expectora- tion during life. Whatever may be the case with the general course of foetid bronchitis, its beginning is often quite sudden and acute, both in the primary and in the second- ary forms, as we have said. The patient is attacked with fever, which may often be quite high, and with a stitch in the side, cough, and expectoration. Later, the characteristic peculiarities described above appear. The further course of the disease is almost always chronic, lasting for years, but subject to many variations. Very often manifest improvement, and even apparent recoveiy, takes place, when suddenly there is a new attack of fever and thoracic symptoms. The general condition and nutrition of the patient may be quite good for a long time, except during the periods of marked exacerbation of the disease. Patients with chronic foetid bronchitis often appear somewhat bloated, but also pale and slightly cyanotic. Peculiar clubbed thickenings of the terminal phalanges of the fingers, or more rarely of the toes, gradually develop, as in many cases of bronchiectasis. Slight oedema of the lower extremities is also sometimes present. Symptoms referable to other organs may be wholly absent. We see most fre- quently disturbances of the stomach, loss of appetite, and nausea, which proba- bly comes from swallowing the foetid sputum. Patients also complain of occa- sional rheumatic pains in the muscles and joints, which are probably due to an absorption of septic matter. In conclusion it must be mentioned that, in fortu- nately rare cases of foetid pulmonary disease, pyogenic germs reach the brain by metastasis, and give rise to purulent meningitis or cerebral abscess. The danger of the disease, apart from the exceptional occurrence just men- tioned, lies in the possible extension of the process to the lungs and the develop- ment of pulmonary gangrene and its sequelae. We hardly ever find a simple fcetid bronchitis in the cadaver, but we almost always see other processes besides, which have been mentioned above — reactive pneumonia, pulmonary gangrene, pleurisy, etc. All these processes develop very readily, and make rapid progress in old, decrepit persons, who live under bad hygienic conditions, in whom putrid processes in the lungs are frequent. The diagnosis of foetid bronchitis is not difficult in itself, for the diagnosis of a putrid process in the lung may be made from the stinking sputum alone. It may be difficult to decide whether we have to do merely with a foetid bronchitis, or with a pulmonary gangrene also. Decisive indications of pulmonary gangrene are derived from physical examination — dullness, bronchial respii'ation, and coarse, moist rales, signs of a cavity — and also the discovery of elastic fibers and frag- ments of parenchyma in the expectoration. The prognosis must be made with care in every case of foetid bronchitis. If the external circumstances of the patient are favorable, he may remain in toler- able health for years. We must always be prepared for the appearance of new exacerbations of the disease and of affections of the lung itself, and must also bear in mind the rarer scqueke (empyema, abscess of the brain). Treatment. — The chief aini of treatment must be to bring the putrid pro- cesses in the bronchi to a stand-still by the death of the agents of putrefaction. The difficulty of fulfilling this task lies in the impossibility of getting the disin- fecting material to act on the bronchial mucous membrane in the necessary amount and concentration. Xevertheless, we can, without doubt, at least relieve a foetid bronchitis and keep it in check by the judicious use of inhalations. Inhala- 170 DISEASES OF THE EESPIEATOET OKGAIs^S tions of a two-per-cent. solution of carbolic acid are most useful, given for five or ten minutes several times a day. These, however, are sometimes not well borne if long continued, and they may excite mild symptoms of carbolic poisoning — such as headache, malaise, and dark carbolic urine. We have often used with good re- sults the " carbolic mask " recommended by Curschmann, a kind of respirator fastened in front of the nose and mouth, containing cotton in a special receptacle impregnated with carbolic acid, equal parts of carbolic acid and alcohol, or other remedies such as turpentine or creasote. Many patients can wear these masks, with occasional interruptions, for many hours a day. Besides carbolic acid we may use inhalations of turpentine (turpentine-pipe or vapor), oleum pini pumil- ionis, creasote, etc. The internal use of these and similar remedies also seems fre- quently to be of service in putrid bronchitis. We recommend especially the in- ternal use of turpentine (in gelatine capsules), myrtol (also in gelatine capsules), also terpine hydrate (six to ten two-grain [gramme 0.1] pills a day), creasote, etc. In other respects all the general hygienic and symptomatic methods of treat- ment recommended for common chronic bronchitis (expectorants, narcotics., climatic health resorts, etc.) are also useful in foetid bronchitis. The sputum should be disinfected by putting strong carbolic acid, etc., into the sputum-cup to lessen the bad odor. It is a very good plan to keep the carbolic spray at work in the patient's room as often and as long as possible ; or the air may be impregnated with oleum pini pumilionis. CHAPTEE IV CBOUPOTJS BRONCHITIS {Fibrinous or Fseudo-membranous Bronchiti&) Croupous bronchitis is a peculiar form of disease of the bronchial mucous membrane, of very rare occurrence, in which there is a formation of extensive fibrinous patches in the bronchi. Only that form of croupous bronchitis which occurs primarily in the bronchi is to be considered here, and not the secondary form, which on the one side is associated with diphtheria in the pharynx and larynx, and on the other with croupous pneumonia. The aetiology of the disease is as yet wholly unknown. From analogy with other well-known croupous inflammations of mucous membranes, we must look here for some noxious influence which destroys the epithelium, but up to this time we are entirely ignorant of its character. Individuals in youth and middle age, somewhere between ten and thirty years old, are the chief victims. Men are attacked somewhat more frequently than women. The disease comes on either in persons who were previously healthy — the essential fibrinous or croupous bron- chitis — or in those who have already suffered from some other disease, especially some chronic pulmonary affection — the symptomatic, secondary croupous bron- chitis. It is not certain whether the last-named cases have the same astiological relations as the cases of genuine primary fibrinous bronchitis. Fibrinous bron- chitis has been observed in the course of typhoid fever and other acute infectious diseases. Symptoms and Course. — Primary fibrinous bronchitis occurs in two forms, acute and chronic. The acute form begins quite suddenly, with fever, cough, pain in the chest, and as a rule severe dyspnoea. The fibrinous coagula, which alone render the diagnosis possible, appear in the expectoration either at once, or after the existence for some days of what is apparently simple catarrhal bronchitis. These coagula form complete casts of the bronchi, and are more or less branch- CEOUPOUS BEOXCHITIS 171 ing. They are of a whitish color and of quite a dense, elastic consistency. The main stem may be a centimetre thick, and from it the further ramifications extend, dividing dichotomously. The largest casts are ten or fifteen centimetres long. On section, we usually find a free lumen within, and generally recognize a definite laminated structure in the membrane. In many places they are enlarged and swollen. Microscopically, we find white blood-corpuscles in and upon the hyaline ground-substance of the casts, and also red blood-corpuscles, sometimes epithelial cells, and quite often the peculiar pointed octahedral crystals which are also found in the expectoration in bronchial asthma {vide infra). The so-called "spirals" (vide infra) have also been found in the expectoration of fibrinous bronchitis. Chemically the casts apparently consist of coagulated albumen. It is doubtful whether they actually consist of fibrine. Weigert's fibrine stain does not affect them. Their solubility in alkalies, especially in lime-water, is of therapeutic importance. On coughing, the patient usually raises a simple mucous or muco-purulent ex- pectoration besides the casts, and in this sputum the casts are imbedded. They are often first discovered by pouring the whole amount of sputum into water, when they unfold and spread out. The expectoration also contains not infre- quently a slight admixture of blood. The subjective symptoms of the patient may be very violent. The dyspnijea sometimes attains a high and alarming degree. It ceases when a large cast is ex- pectorated after a severe paroxysm of coughing. Such attacks may recur every day or two. In other cases, however, the subjective symptoms are comparatively slight. Physical examination of the lungs reveals little that is characteristic. In un- complicated cases percussion shows nothing abnormal, or at most the signs of an acute emphysema. Auscultation gives the ordinary signs of bronchitis, not char- acteristic in themselves, such as rhonchi, or moist rales. If a large bronchus is plugged, the respiratory excursions and the respiratory murmur are almost en- tirely absent in the corresponding portion of the lung, but after the expectoration of a cast the murmur becomes once more audible. The duration of acute cases is sometimes only a few days, at most a few weeks. In favorable cases the fever, which at times is quite high, soon disappears, the respiratory symptoms grow milder, the expectoration of the casts ceases, and there is a complete and permanent recovery. In severe cases, however, death often ensues with all the symptoms of suffocation. The acute form sometimes becomes chronic, but this is rare. The chronic form of fibrinous bronchitis may last for years. Usually the con- dition grows worse periodically, at varying intervals of time, and at each exacer- bation casts are expectorated, while in the interval there is apparently merely a simple bronchial catarrh. Some observations are also recorded in medical litera- ture of persons who have expectorated these casts at intervals for years without any special disturbance of their health or their nutrition. In some cases other chronic pulmonary affections, such as tuberculosis, finally develop. The pathological anatomy of fibrinous bronchitis is not yet satisfactorily known on account of the rarity of the affection. The changes in the lungs found at the autopsy of fatal cases have usually been complications, such as pneu- monia, pleurisy, or tuberculosis, which stood in no direct relation to the fibrinous bronchitis. A loss of epithelium has been discovered in some cases in the parts of the bronchial mucous membrane that were attacked. Prognosis. — In all acute cases the prognosis should be guarded, for we know that about one fourth of the cases terminate fatally. The chronic cases, as has been said, are usually very protracted and are subject to frequent exacerbations, but they differ from the acute cases in being much less dangerous. 172 DISEASES OF THE EESPIRATOEY OEGANS Treatment. — We make special use for inhalations of those remedies which, as wo have said, have power to dissolve the casts. We usually employ a two- to five- per-cent. solution of carbonate or bicarbonate of sodium, and above all lime- water, either pure or diluted with an equal volume of water. The internal administration of iodide of potassium, in doses of twenty to forty-five grains (gramme 1.5-3.0) a day, proves of advantage in many cases. Energetic inimction with merctirial ointment is sometimes of service. Expectoration of the casts may be aided in many cases by such expectorants as senega and benzoic acid, or by the timely use of emetics. We do not know any remedies which can prevent a return of the attacks in the chronic form. The treatment, except at the time of the attacks, is the same as in ordinary chronic bronchial catarrh. - CHAPTEE V WHOOPING-COUGH {Pertussis. Tussis convulsiva) .Sltiology. — By the name "whooping-cough" we mean a specific disease of the mucous membrane of the air-passages, which is seen chiefly in children, and is characterized by a peculiar violent and paroxysmal cough. Sporadic cases are of almost constant occurrence in large cities, but the disease often appears in epi- demic outbreaks. Epidemics of whooping-cough follow epidemics of measles with remarkable frequency. Whooping-cough is without doubt contagious, and therefore often attacks one child after another in the same family. Kindergartens, orphan asylums, and day- nurseries aid very much in extending the disease. The contagious element seems to be connected with the air expired by the patient, particularly with the secretion from the mucous membrane expectorated after coughing. Children are most sub- ject to an attack up to the age of six years; from that age the liability to the disease decreases rapidly with increasing years. Whooping-cough is seen, indeed, in adults, but it is quite rare, and almost always without the pronounced features of tussis convulsiva. The epidemic onset, the contagiousness, and the whole course of the disease favor the theory of its infectious nature. The presence of the organisms which are supposed to be the poison of the disease has not yet been certainly demon- strated, although many have claimed to discover characteristic bacteria in the sputa of patients. These assertions, however, do not harmonize with one another, and lack well-attested and methodical proof. If a patient has once had the disease, he is almost invariably safe from a second attack. Symptoms and Course of the Disease. — Whooping-cough begins with the symptoms of a catarrh of the trachea and bronchi, which develops more or less rapidly, and which at first often shows nothing characteristic. We can at this period make a tolerably probable diagnosis only at a time when an epidemic is prevailing, or in case the child's associates have already been attacked with the disease. The cough is often very persistent, obstinate, and severe at the begin- ning, but it does not yet come on in distinct paroxysms. Examination of the chest shows nothing peculiar except a few rhonchi. There is often a coryza, with frequent sneezing, and there is sometimes a mild conjunctivitis. The child is restless and feverish, especially toward night. Tlie temperature may repeatedly reach 103° or 104° (39°-40° C.) in this initial fever. The duration of this first so-called catarrhal stage varies, but it usually lasts a week or ten days. WHOOPIXG-COUGH 173 The catarrhal stage gradually passes into the second, convulsive stage, without any sharp boundary. The cough becomes more violent, and comes on in the separate paroxysms of whooping-cough which are characteristic of the disease. We do not know the particular reason why the cough has this paroxysmal char- acter, but a nei-vous factor probably plays the chief part in it. The peculiarity of the attack consists in the violent, paroxysmal fits of cough- ing, which are from time to time interrupted by deep, long-drawn, loud, and shrill inspirations, due to the occurrence of a spasmodic contraction of the glottis. Exceptionally there are cases without this loud whistling inspiration. The child becomes markedly cyanotic during the attack, the veins in the neck swell, and tears come into the eyes. HaBmorrhage into the conjunctiva, nose-bleed, and in some cases haemorrhages into other organs, as the ear and the skin, often come on as a result of this stasis. Vomiting very often occurs either during a paroxysm or at its close. Involuntary evacuations of urine and fseces may also follow from the violent contraction of the abdominal muscles. Exceptionally we observe still more severe symptoms with a paroxysm : a complete spasmodic cessa- tion of respiration with imminent danger of suffocation, or sometimes general convulsions. In two cases we have seen hemiplegia in children which, accord- ing to the positive statements of their parents, came on suddenly during a severe attack of whooping-cough. It is still undetermined whether these "whooping- cough hemiplegias " are due to an actual cerebral hasmorrhage or whether they come from the enormous venous stasis in the brain. The paroxysms vary with the severity of the disease, frequently appearing ten or fifteen times in twenty-four hours; sometimes with greater frequency — fifty times or more. They also occur at night as often or even oftener than in the daytime. They come on either spontaneously or from some special predis- posing cause. The attacks which come on during eating cause the most dis- turbance, because the food taken is almost always vomited again. In chil- dren with whooping-cough we can often excite a spasm at any time, and this is important in diagnosis — by putting a spatula in the mouth, by pressing on the larynx, or by making the child cry. If there are several children with whooping-cough in the same room and a paroxysm attacks one of them, the others, as a rule, soon begin to cough too. Some prodromal symptoms often pre- cede the peculiar paroxysm, such as general uneasiness, rapid respiration, or vomiting. At the end of a paroxysm many children are very feeble and exhausted, but others recover rapidly, and are playing again quite briskly a few minutes after. In general the child feels quite well in the interval between the paroxysms, but the effects of the violent attacks of coughing may of course often be seen. Besides the occasional hemorrhages into the conjunctiva, we find the eyelids somewhat swollen, their veins dilated and blue, and showing through the skin. Many children grow very thin from the repeated vomiting. A small ulcer is quite frequently formed on the fraenum of the tongue, the origin of which is to be referred to mechanical causes. The tongue is violently protruded in the severe paroxysms of coughing, and the froenum is thus torn, or injured by the sharp lower incisors. Physical examination of the lungs shows nothing abnormal in uncomplicated cases except a few moist rales or rhonchi. Sometimes the rhonchi are wanting, or are present in small numbers only a short time before a paroxysm, but in other cases an intense diffuse bronchitis is developed, which often leads to the develop- ment of a lobular pneumonia (vide infra). Sometimes, but not always, there is an acute catarrhal inflammation of the bronchi, and especially of the posterior wall of the larynx. The fever, which is usually present in the first or catarrhal stage, is absent in the convulsive stage. The child is free from fever for the most part. " We often 174 DISEASES OE THE EESPIRATOEY ORGANS find a slight rise of temperature up to 100° or 101° (38°-38.5° C), but only toward night. Higher and more persistent fever points to the development of complications, especially on the part of the lungs. The convulsive stage seldom lasts less than three or four weeks, and often much longer, up to three or four months. The paroxysms gradually become less frequent and less violent (stadium decrementi), until they finally disappear entirely; but relapses and fresh exacerbations also occur in this stage. A cer- tain " irritability " of the bronchial mucous membrane remains for a long time after whooping-cough. Einally, however, the disease, in uncomplicated cases, goes on to a permanent and complete recovery. Complications and Sequelae. — The severe results which sometimes follow whooping-cough are probably due in part to the direct action of the specific causes of the disease, and in part to complications of a secondary nature whose develop- ment is merely favoi'ed by the whooping-cough. The most important are complica- tions in the lungs. A lobular catarrhal pneumonia often develops after a severe bronchitis which involves the finer bronchi. In such cases the respiration be- comes hurried and superficial, the fever higher, and the general condition bad even in the times between the paroxysms. On examination of the lungs, we hear numerous moist rales, especially over the lower lobes; and we can sometimes make out dullness on one or both sides, if there is extensive pneumonic infiltra- tion. Such cases are always very larotracted, and many children succumb, partly from the disturbance of respiration and partly from general weakness and in- anition. Complications in other organs are much rarer. Among the most frequent are attacks of diarrhoea which impair the child's nutrition. Many observers have also mentioned the quite frequent occurrence of a croupous or diphtheritic in- flammation in the pharynx and larynx in the course of whooping-cough. Finally, a case under our own observation may here be mentioned, in which death oc- curred with severe nervous symptoms, convulsions, and coma. At the autopsy very numerous capillary haemorrhages were found in the brain. Pulmonary emphysema is the first thing to be mentioned among the sequelae of whooping-cough. Erom the marked pressure which the severe and frequent outbursts of coughing exert from within upon the alveoli of the lungs, they gradu- ally become dilated. An acute lobular emphysema (" acute pulmonary infla- tion ") is set up, which sometimes passes into a typical chronic pulmonary emphy- sema (vide infra). Chronic bronchial catarrh may also remain for a long time after an attack of whooping-cough. We have already stated (see page 163) that many incurable cases of chronic bronchitis in adults are to be referred to an attack of whooping-cough in childhood. A third important sequel of whooping-cough is pulmonary tuberculosis. The bronchitis and lobular pneumonia which occur during whooping-cough some- times do not improve, especially in weak children with a tubercular tendency. The fever continues high, the child grows thin, and constantly becomes more and more miserable. At the autopsy we find cheesy nodules in the lungs, cheesy bron- chial glands, and at times tuberculosis of other organs. These cases signify that when a tubercular infection is present, but is still latent, the whooping-cough acts as an exciting cause for the outbreak of the disease, or that a greater receptivity to infection with tubercular poison is created by the whooping-cough. Mobius has lately reported the occurrence, in a few cases, of paralysis as a sequel of whooping-cough. This usually begins in the lower and extends to the upper extremities, and is due apparently to neuritis. The diagnosis of whooping-cough can not be made with certainty, as we have said, until the second or convulsive stage. It is easy then, however, since the characteristic attacks occur in no other affection of the lungs in like manner WHOOPING-COrGH 175 and with like frequency and duration. If we have no opportunity to observe the attack itself, and have to depend upon the description of the friends, the diagno- sis is sometimes more uncertain; but the accounts of the occurrence of cough, in individvxal paroxysms associated with vomiting, are usually so characteristic that errors are, on the whole, rare. Furthermore, the child between the parox- ysms usually presents certain signs: he has a bloated aspect, or we may find slight haemorrhages into the conjunctiva, or ulcers on the frsenum of the tongue, which make the diagnosis highly probable. Under some circumstances we may also make the attempt to bring on the paroxysm artificially (vide supra). In adults, as we have said, the attacks are rarely as characteristic as in children. There are usually the symptoms of a more or less severe bronchitis with obsti- nate paroxysmal covigh, but without the characteristic attacks and usually with- out vomiting. The diagnosis of whooping-cough therefore rests mainly upon the existence of special setiological conditions (the co-existence of the disease in children, etc.). The prognosis is favorable with the majority of children if they are previously strong and healthy. Very young children are in more danger than older ones. [Under two years there is great danger, and over five scarcely any. It has been said that whooping-cough causes one fourth the total mortality of children in London. — V.] There is danger if secondary pneumonia develops, and if the gen- eral nutrition and strength of the child suffer. As soon as the diagnosis is certain we must call thte attention of the parents to the probable long duration of the dis- ease. Regard must also be paid to the possibility of the development of sequelae, especially in weak children suspected of tuberculosis. Treatment. — Since the disease is protracted and is not devoid of danger, it is our duty, when an epidemic of whooping-cough prevails, to guard children from it as far as possible. If one child in a family is taken ill, the other children must be rigorously kept away from him. If circumstances permit, we should prefer to send them away to another place free from whooping-cough. With regard to the treatment of the disease, we must first endeavor to fulfill general dietetic and hygienic indications. The child should breathe good, pure air, and for this reason it is often advisable to transfer the patient to a larger room, with as much air and sunlight as possible. The atmosphere should not be too dry, and it is advisable to employ a spray of water (carbolic solution) fre- quently, or to hang up moist sheets in the room. In good weather the child should be out of doors a large part of the time, provided fever has ceased. City children are to be sent, if possible, into the country. The food should be good and nourishing, but dry and crumbly articles should be avoided, being apt to excite cough. W.arm or lukewarm baths frequently prove very beneficial, particularly when there is considerable bronchitis, as they lessen the danger of a lobular pneumonia. The medicinal treatment of whooping-cough has not yet shown brilliant results despite the large number of remedies recommended. During the ca- tarrhal stage it is usually sufficient to give a simple expectorant (ipecac, etc.) and plenty of warm drink. In the convulsive stage the best remedies to try are quinine, antipyrine, belladonna, bromide of potassium, and bromoform. The latter has been much recommended of late. Quinine is given in powders of one and a half to eight grains (grm. 0.1 to 0.5)several times a day, either in capsules or, in the case of smaller children, with chocolate. The earlier this remedy is em- ployed the more prompt is said to be its beneficial influence. Antipyrine is at present used more frequently than quinine, and in doses of four to eight grains (grm. 0.25-0.6) several times a day it often produces distinct improvement. Bella- donna is prescribed in powders containing one twelfth to one sixth grain (grm. 0.005 to 0.01) of the extract of belladonna, giving three to five such powders a 176 DISEASES OE THE EESPIRATOEY ORGAISTS day. This remedy has often seemed to the author to diminish the number and violence of the paroxysms. Bromide of potassium is employed in an aqueous solu- tion in the dose of fifteen to forty-five grains per diem (grm. 1 to 3). Its efficacy is probably due to its power to diminish reflex excitability. The same drug' employed in an atomizer often has a palliative effect. Bromoform is the remedy most used of late; two to five drops or more are given several times a day in sweetened water or fruit juice. It is readily taken, and it seems to act favorably both on the severity of the individual attacks and on the whole course of the disease. If the paroxysms are very violent we may cautiously administer small doses of morphine or codeia. Inhalations of chloroform and ether have also been recommended. The following mixture is a suitable one : ]^ Chloroformi §3 (grm. 30) ; iEtheris §ij (grm. 60) ; 01. terebinthinse ........................ Sijss. (grm. 10). M. Sig. One or two teaspoonfuls to be poured upon a pocket-handkerchief for in- halation. Finally, efforts have been repeatedly made to lessen the frequency and the severity of the attacks by anaBsthetizing the pharynx and larynx by painting with a ten- to fifteen-per-cent. solution of cocaine. Michael advocates the daily in- sufflation into the nostrils of powdered benzoin. Neither method of treatment has succeeded in establishing itself in practice. Sprays of various antiseptic remedies have been frequently employed be- cause of the infectious nature of the disease. The practitioner must not expect too much from them, however, although they sometimes act well. A one-per- cent, or two-per-cent. solution of carbolic acid is most frequently employed for inhalation. It may be given several times a day for periods of two or three minutes at a time, Next to this, turpentine and benzine are most to be recom- mended; of these, twenty or thirty drops are poured upon a sponge previously moistened with hot water. Turpentine and especially terpine hydrate (grains vij, gramme 0.5, thrice daily) are also given internally. [Earlow and others report marked success from spraying the upper air-passages with a two-per-cent. solution of resorcine.] In very many cases we finally content ourselves with taking good general care of the child, and, if the weather permit, with keeping him as much as possible in the open air. For the treatment of the complications and sequelse of whooping-cough the reader is referred to the appropriate chapters of this book. CHAPTER VI BRONCHIECTASIS {BroncJiial Dilatation) Dilatation of the bronchi is not a separate disease, but it is a result of various affections of the lungs and bronchi. Nevertheless, we will speak of it briefly in this connection since many cases actually present the appearance of a very char- acteristic disease. We distinguish anatomically the cylindrical and saccular bronchiectases. Cylindrical bronchiectasis consists of a uniform dilatation of a bronchial tube, and occurs most frequently in the medium-sized, or rarely in the finer BKONCHIECTASIS 177 bronchi of one or more lobes of tbe lung. We usually find at tlie autopsy tliat, on slitting up the bronchi, the point of the scissors can easily be pushed through the dilated bronchial tube close up to the pleura. Cylindrical bronchiectasis is usu- ally due to a long-continued bronchitis, and develops most frequently in cases of emphysema, and also in whooping-cough, measles, and sometimes in phthisis, etc. The primary process is probably always the atrophy which follows the catarrh, and the diminished resistance of the bronchial walls thus occasioned. The dila- tation of the lumen of the bronchus is produced gradually, partly by the trac- tion of the thorax during inspiration, and still more by the increased pressure in the bronchi due to the frequent and violent fits of coughing, and finally, perhaps, by the constant pressure of the stagnating secretion. The diagnosis of cylindrical dilatation of the bronchi is only a probable one. We suspect that a bronchiectasis has formed if the conditions are fulfilled which we know lead to it. In the chronic bronchial catarrh of emphysema we judge that there is cylindrical dilatation of the bronchi if the secretion is very abundant and comparatively thin, and separates into layers on standing in a sputum-cup. The dilatation is usually emptied by a severe paroxysm of coughing, such as is apt to occur in the morning if the secretion collects in great quantity during the night. Physical examination usually gives numerous, low, fine, and medium moist rales, especially in the lower lobes. The respiratory murmur some- times loses its vesicular character in marked cylindrical bronchiectasis, and has a more indefinite and tubular quality. Sometimes it is quite obscured in the lower part of the lung by the abundant rales. Saccular bronchiectases are spherical or oval dilatations which are confined to a definite portion of the bronchial tube. They may attain a diameter of several centimetres. The bronchus passes suddenly or gradually into the dilatation, and it is often obliterated so that the bronchiectasis forms a completely closed cavity. The wall of a saccular bronchiectasis loses in great measure the character of a normal bronchial wall. As a rule it is atrophied to a high degree, the atrophy involving not only the mucous glands, but also the muscular fibers, the elastic elements, and even the cartilages, so that the bronchiectatic cavities seem lined with nothing but a thin membrane. The occurrence of many dilated vessels in the walls of a bronchiectasis is due perhaps to an atrophy of the vessel walls and is a symptom of great clinical importance (vide infra). In other cases, however, we find hypertrophic processes, which involve the connective tissue of the mucous membrane, and lead to band-like projections and swellings. Finally, ulcerative processes may develop on the inner surface of a bronchiectasis and attack the surrounding lung-tissue, and change the bronchiectatic cavity into a typical ulcer- ating cavity. Only rarely, for example in emphysema, do we find a single saccular bron- chiectasis surrounded by tolerably normal lung-tissue. Its origin, then, is to be referred tp causes like those which have been given above for the much com- moner cylindrical bronchiectases. In the great majority of cases we find saccular bronchiectases, singly or in large numbers, surrounded by indurated and con- tracted lung-tissue. They form one of the complications of " pulmonary con- traction " [fibroid phthisis], which is almost always associated with contraction of the pleura. Since Corrigan's day we have with good reason looked upon this contraction as the chief cause for their origin. By the gradual shrinking and retraction of the lung, which as a rule has become adherent to the costal pleura, a traction is exerted upon the bronchial walls from without to which they grad- ually yield. Stagnation and pressure of the secretion work at the same time in like manner to dilate the bronchial tube. Thus arises the frequent combination of pulmonary contraction with the formation of bronchiectases. This combina- tion is usually unilateral, and involves the whole lung or only one of the upper 12 178 DISEASES OF THE EESPIEATOEY OEGAXS or lower lobes. Our knowledge is still very defective as to the cause of this " chronic interstitial pneumonia " leading to contraction. It often seems to be a quite insidious and gradual circumscribed chronic inflammatory process; in other cases by careful inquiry we can discover a previous acute process (pneu- monia, severe acute bronchitis, etc.) as a starting-point for the disease. Inha- lation of dust often plays a part in the causation. We sometimes see the form of pulmonary contraction in question developing as a result of pleurisy. Laennec first advanced the opinion that in such cases the pleurisy was the primary trouble, and that from it an interstitial inflammatory process attacked the connective tissue of the underlying lung and led to contrac- tion and then to the formation of bronchiectases. Unfortunately we lack further confirmatory evidence in this regard. Most saccular bronchiectases are situated in the lower lobes, but genuine bronchiectasis is not very rare in the upper lobes. As a rule, the trouble is uni- lateral, or at least afl'ects one side the most. Sometimes large portions of a lung may be completely transformed into a cicatricial tissue studded with many bronchiectatic cavities. " Pure cases " of bronchiectasis have nothing to do with tuberculosis. Before the discovery of the tubercle bacillus there was, of course, confusion between bronchiectatic and chronic tubercular contraction of the lungs; but we must remember that, under some circumstances, chronic tuberculosis may lead to the formation of bronchiectasis, and that, on the other hand, in bronchiectatic pro- cesses there is not infrequently a secondary development of tuberculosis. There are cases in which it is hard to decide, even at the autopsy, whether an exist- ing chronic contraction in a portion of the lung, with induration of tissue and the formation of bronchiectasis, was originally tubercular or of some other nature. The symptoms caused by saccular bronchiectasis are derived in part from phys- ical examination and in part from observation of the sputum and of the gen- eral course of the disease. If great bronchiectatic cavities lie near the chest- wall, they may give the same physical signs that we shall learn to recognize later in the description of tubercular cavities. Bronchiectases lying within the lung, however, are often devoid of definite physical signs, so that at most we may suspect them from other symptoms, such as the peculiarities of the sputum. The more abundant the formation of bronchiectases the more does the respiration lose its vesicular character and become harsh and finally bron- chial. Inasmuch as there is usually a very considerable secretion of mucus, we generally find, upon auscultation, abundant medium and even coarse moist rales. The percussion note over the bronchiectatic portion of the lung is usually dull or dull-tympanitic, a result of the chronic interstitial pneumonia about the bronchiectasis. The whole thorax near an extensive bronchiectasis is often much retracted and distorted. The expectoration is, as a rule, very abundant, and it is often raised by large mouthfuls. On standing, as a result of its thin fluid character, it exhibits a dis- tinct division into an upper frothy, muco-purulent layer, a middle muco-serous layer, and a lower purulent layer. It usually has ■ a peculiar stale, sweet- ish odor, but it may be foetid. The latter is almost always associated with stagnation of the secretion. So long as the expectoration is loose and easily evacuated, it is not foetid and the patient feels well. Then a cessation of the expectoration may ensue. The patient feels poorly, there may be a slight rise of temperature, and the expectoration becomes scanty and has a stinking foetid character. Periods of improvement may thus alternate with exacerbations. It is a favorable sign when the amount of the expectoration decreases, provided that it does not become foetid and that the patient does not feel worse. Since bronchi- BEONCHIECTASIS 179 ectasis may give rise to a permanent foetid bronchitis, and since, on the other hand, as we have said, foetid bronchitis itself often leads to the formation of bron- chiectasis, we can understand the manifold inter-relations and transitions which the two forms of disease present. The not infrequent pulmonary hsemorrhages in bronchiectasis are of great clinical importance. They are due to rupture of the dilated vessels (vide supra) in the walls of the bronchiectasis. They may also be due to ulcerative processes. Slight precursors may precede a severe haemoptysis. The haemorrhage may be" very abundant, and it may be repeated during a long period — several weeks — so that the patient becomes extremely anaemic. Finally the haemorrhages cease and the patient improves quite rapidly. Such attacks of haemoptysis may be repeated very often in the course of the year. When we hear comparatively well-nourished patients with lung disease say that they have suffered for years from frequent and severe haemoptyses, we can usually infer, from such statements, that there is a saccular bronchiectasis. The whole course of the disease is very variable, but it usually lasts for many years. It is doubtful whether a saccular bronchiectasis can actually be cured; but if no more serious sequelae occur, many patients may live for years in a tolerable condition, and may even reach an advanced age. The general nutrition often remains very good, although a certain very characteristic, anaemic, cyanotic tinge of the skin gives even to corpulent patients an unmistakable morbid ap- pearance. A very characteristic sign is that the terminal phalanges of the fingers gradually become clubbed and thickened, and the nails are much bent. This peculiar trophic change, the cause of which is still unexplained, is much rarer in chronic tubercular processes (vide infra). The diagnosis of extensive formation of bronchiectasis in the lungs is in many cases easy, but in other cases it may present great difficulties. In order to avoid confounding it with chronic tuberculosis the following should be espe- cially considered : In bronchiectasis the patient does not present a true cachexia ; he is usually somewhat cyanotic and pale at the same time. The layer of subcutaneous fat often remains well marked for a long time. The terminal phalanges of the fingers are often clubbed, as in foetid bronchitis. Fever is usually absent, unless there are some special complications. The expectoration is more abundant and more distinctly stratified than is often seen in tuberculosis; and, most important of all, it contains, of course, no tubercle bacilli. Finally, bron- chiectatic conditions ordinarily (though, of course, not always) develop in a lower lobe, while tuberculosis is apt to affect an upper lobe first. We will refer to the appropriate chapters for the relations of bronchiectasis to foetid bronchitis, pulmonary gangrene, etc. The treatment is never directed against the bronchial dilatation as such, but toward its causes or sequelae. The treatment of bronchiectasis, therefore, coin- cides with the treatment of chronic bronchitis, foetid bronchitis, etc. Besides general hygienic measures (climatic resorts), balsamic remedies (turpentine, etc.) are chiefly used. Any pulmonary ha3morrhage is to be treated symptomatically in the same way as haemoptysis in pulmonary tuberculosis (q.v.). 180 DISEASES OF THE EESPIEATOET OEGAXS CHAPTEE YII STENOSIS OF THE TRACHEA AND BRONCHI 1. Tracheal Stenosis Etiology. — Stenosis of the trachea may be caused either by diseases in the vicinity of the trachea, or by diseases of the trachea itself. The first-named mode of origin is the m^ore frequent. To this are due all the stenoses of the trachea from compression. Enlargements of the thyroid gland from simple struma and new growths, aneurisms of the arch of the aorta and of the in- nominate artery, tumors and abscesses in the anterior mediastinum, swelling of the lymph-glands at the bifurcation of the trachea, abscess on the anterior sur- face of the cervical vertebrte, etc., may exert so great a pressure on the trachea from without that its lumen is made narrower. Besides the direct action of pres- sure, iu most cases, a gradual atrophy and a softening of the rings of cartilage, due to pressure, sometimes play an important part, according to Eose, in the occurrence of stenosis. A collapse of the trachea may arise from this " flaccid softening," which may come on quite suddenly, and may cause many of the cases of sudden " death due to goitre." Changes in the trachea itself leading to stenosis are quite rare. Cicatricial stenosis as a result of syphilitic ulcerations is relatively the most frequent. New growths in the trachea are also to be mentioned, such as polypi and cancer, the latter almost always having invaded the trachea from the adjacent parts. Very rarely acute and chronic inflammatory processes such as perichondritis lead to a swelling of the mucous membrane sufficient to cause stenosis. In conclusion, we may mention that stenosis of the trachea may be due to the presence of foreign bodies. Symptcms. — If the stenosis is so extreme that there is a real hindrance to respiration, a very striking modification of the breathing occurs. It is difficult and labored, and is performed only by the help of the accessory muscles. Both expiration and inspiration are protracted, long drawn, and accompanied by a loud stridor. In many cases inspiration is more difficult than expiration, so that there is accordingly a preponderating inspiratory dyspno3a, and the number of respira- tions a minute is diminished. If the entrance of air into the lungs is incomplete in spite of the lengthening of the respirations, we see an inspiratory retraction of the lower part of the thorax, and sometimes of the throat and the supra-clavicular fossse. In tracheal stenosis the larynx, however, shows little or no to-and-fro movement on respiration. This fact is of value in diagnosis in distinguishing tracheal from laryngeal stenosis, for in the latter the respiratory movements of the larynx are quite well marked. We sometimes notice in the pulse during inspiration a marked fall in tension and in the height of the pulse-wave, the pulsus paradoxus. With the sphygmo- graph we can show still more plainly the changes in blood-pressure, which vary quite markedly with the respiration. The frequency of the pulse is usually a little increased, but sometimes it is diminished. The symptoms of the disease just described may form so characteristic a picture that we can recognize it at the first glance. More precise information as to the seat of the stenosis, or the accurate differentiation of tracheal stenosis from the very similar picture presented by larjmgeal stenosis, demands a direct laryngoscopic examination of the larynx and trachea, which, of course, is hardly practicable in a patient with a high degree of dyspna3a. BEONCHIAL ASTHMA 181 2. Bronchial Stenosis ISTarrowing of a primary bronchus, which is the only form to be mentioned here, arises most frequently as a result of the presence of foreign bodies — e. g., bits of bone, plum-stones, buttons, etc. These may enter the air-passages by means of a deep inspiration, especially while eating, or during sleep. We know that foreign bodies get into the right bronchus, which is wider, somewhat more frequently than they do into the left. Stenosis of the main bronchi from pres- sure also arises from aneurisms of the aorta, mediastinal tumors, enlarged bron- chial lymph-glands, etc. Stenosis of the left bronchus from the pressure of the greatly dilated left auricle has been observed in mitral stenosis. The symptoms are not equally distinct in all cases, and they depend upon the shutting off of the corresponding part of the lung. The dyspnoea is usually very evident, especially in acute cases. The respiratory excursions are much less on the affected side than on the sound side. The percussion-note remains clear; sometimes it is very deep, because the lung beyond the narrowed bronchus is con- stantly inflated. Auscultation shows complete absence of the vesicular respiratory murmur. We either hear nothing or we sometimes hear over the whole side a loud whistling or humming sound, the vibration of which can in some cases be felt by the hand applied to the chest-wall. The vocal fremitus is diminished on the affected side. A vicarious emphysema soon develops in the other lung. Lobular pneumonia frequently develops as a result of the entrance of foreign bodies into a bronchus, because the agents of inflammation have entered at the same time with these bodies, and, as the expectoration can be evacuated only with difficulty, and hence is more or less stagnant, these irritants can readily establish themselves in it. In stenosis from pressure the condition may of course be modi- fied in many ways by the primary disease. The prognosis and treatment of tracheal and bronchial stenosis depend en- tirely upon the nature of the primary disease. General statements as to treat- ment, therefore, need not be given here. A direct mechanical treatment of tracheal stenosis in appropriate cases, such as cicatricial stenosis, may be undertaken ac- cording to the different modes of dilatation above enumerated. The methods for removing foreign bodies from the larger air-passages belong to the domain of surgery. The employment of an emetic has met with distinct success in such cases, but it is not without danger, for the foreign body may wedge itself into the glottis during the act of vomiting and occasion danger of instant suffocation. CHAPTER VIII BRONCHIAL ASTHMA (Exudative Bvoncliiolitis. Asthmatic Bronchiolitis) Definition and Causes of the Disease. — Bronchial asthma is the name we give to a morbid condition whose chief symptom is a special form of severe dyspnoea. The characteristic features of the dyspnoea of bronchial asthma are, first, that it occurs in paroxysms, or at least that it grows worse paroxysmally, and, second, its peculiar manner of onset. The special character of the dyspnoea of bronchial asthma is explained by the fact that every true bronchial astlnna is due to an extensive and quite rapid contraction of the smaller and smallest bron- chial branches. This always gives rise to a form of distress for breath which differs materially from every other form of dyspnoea. 182 DISEASES OE THE EESPIRATORY OEGA:NtS The question as to the origin of bronchial asthma coincides, then, with the question as to the origin of that extensive contraction of the bronchioles which is the root of the disturbance. There seems to us no doubt that the latter should not always be referred to the same cause. We must therefore distinguish several forms of bronchial asthma, which, as a result of the similar conditions of dyspnoea, have many points of clinical similarity. Eormerly the so-called nervous bronchial astlnna was considered to be the commonest form. Asthma in many cases was regarded as a pure " neurosis," due to paroxysms of tonic spasm of the circular muscles in the small bronchi (Trous- seau, Biermer). The sudden contraction of the bronchi and the consequent dyspncea could, in fact, be very well explained in this way. The only thing left unexplained is the conditions causing the sudden onset of such a spasm. Many recent observations (Voltolini, B. Eriinkel, Hack, etc.) have rendered it extremely probable that, in at least a part of the cases, reflex processes play a great part, and especially reflex processes from the nasal mucous membrane. Many patients with asthma have been found to have marked changes in the nose, most frequently enlargement of the so-called erectile bodies on one or more tur- binated bones, also nasal polypi, chronic catarrh of the mucous membrane, etc. The evidence of the close connection between the attacks of bronchial asthma and those morbid processes rest, in the first place, upon the clinical fact that the asthmatic attack usually begins with a marked increase of the nasal symptoms (a stuffed nose, greater secretion, etc.) ; and, in the second place, especially upon the important therapeutic observation that in such cases the asthma may be made permanently to disappear by removing the nasal trouble. Accordingly there can hardly remain a doubt that in such instances it is proper to speak of a reflex bronchial asthma. Certain observations which have long been familiar are probably connected with these facts we have mentioned — namely, the cases in which persons are said to have genuine asthmatic attacks from particular odors (ipecac, burnt coffee, violets, etc.). This is probably a reflex process coming from the nose. Similar relations doubtless exist in the so-called hay asthma (see page 135). Although we may not question the occurrence of a reflex bronchial asthma, yet we can not regard the theory that it is caused by a tonic spasm of the bron- chial muscles as absolutely proved. So far as our own experience goes, even in " reflex asthma " there are usually during the attack plain signs of an abnormal secretion or exudation in the smaller bronchi (expectoration, bronchitic rales, etc.) ; but this condition requires further explanation than by the assumption of a muscular spasm. We are therefore of the opinion that we should not wholly reject the hypothesis advanced by many authors (Weber, Stork, Erantzel). Ac- cording to this hypothesis, acute stenosis of the bronchioles is caused much less by a muscular spasm than by an acute dilatation of the blood-vessels and acute swelling of the mucous membrane. Such a " vaso-motor " change may very well be excited by reflex causes, and it would much better explain the conditions in an asthmatic attack than would the assumption of a purely muscular spasm. It is doubtful whether genuine bronchial asthma may be due to a reflex from any other organ than the nose. The most credible statements are those in regard to the connection between bronchial asthma and disease of the pharynx (hyper- trophy of the tonsils), but the statements in regard to the occurrence of asthmatic attacks in diseases of the ear, stomach ("dyspeptic asthma"), intestines, female sexual organs, etc., are to be regarded with the greatest skepticism. In these cases there is usually confusion between true asthma and other conditions of dyspnoea (hysterical asthma, conditions of cardiac weakness, etc.). Although, from what has been said, it follows that the occurrence of a nervous reflex asthma can not be questioned, our knowledge as to the onset of nervous BKOXCHIAL ASTHMA 183 asthma as a primary affection is still very vague. At any rate the cases which, after careful investigation, allow no other explanation are very rare. It is also doubtful whether we have to do with a primary bronchial spasm or with vaso- motor conditions. The theory formerly maintained by many writers, that a tonic spasm of the diaphragm could be the cause of a true asthmatic attack, is at present almost universally abandoned. This theory is contradicted by the occurrence of manifest respiratory movements of the diaphragm during the asthmatic attack. These movements have also been demonstrated of late by the Rontgen rays. Apart from the reflex asthmatic conditions, most cases of so-called " bronchial asthma " are undoubtedly due to a primary catarrhal inflammation of the smallest bronchi and bronchioles; but since not even catarrh of the finer bronchi causes typical asthmatic attacks, we must assume that in asthma we have to do with a special form of bronchiolitis or at least with special attendant conditions which cause the asthma. Curschmann, to whom we owe the first accurate clinical investi- gation of this most common form of bronchial asthma, termed the bronchial affection, which forms the basis of it, " exudative bronchiolitis," but we have ourselves for a good while usually employed the name of " asthmatic bronchio- litis." We would indicate by this term a peculiar disease of the smaller bronchi and bronchioles whose characteristic features are a peculiar sort of expectoration (vide infra) and characteristic " asthmatic " {vide infra) attacks of dyspnoea which grow worse paroxysmally. It is indeed possible, but not certain, that in the latter regard nervous reflex processes in the bronchioles also play a part, somewhat like the spasm of the glottis in whooping-cough. The causes of this asthmatic exudative bronchiolitis are not always evident. Sometimes, however, circumstances apparently play a part similar to those producing ordinary bron- chitis, especially the continuous inhalation of vegetable dust (wool, meal, etc.). Many cases of bronchial asthma may also with great probability be referred to some severe bronchial disease in childhood (whooping-cough, severe bronchitis of measles, etc.). Symptoms and Course of the Disease. — We will begin the account of the symptomatology by a description of the asthmatic " attack." In its purest form " nervous " bronchial asthma consists, in fact, of single attacks of dyspnoea, dif- fering in frequency and duration, which occur at least without special cause or without any discoverable reason in persons otherwise apparently healthy. In the intervals between the attacks the patient is perfectly well, and, in partictilar, shows no signs of disease of the respiratory organs. In most cases of " bronchial asthma," however, the attacks, as we have said, are only more or less sudden ex- acerbations of a condition which in the intervals is not perfectly normal. While ordinarily only the signs of a chronic bronchitis are present, often associated with pulmonary emphysema, from time to time exacetbations occur, usually in the form of long-continued asthmatic dyspnoea, lasting for days or weeks. It is this latter form especially which can be explained only by the assumption of a true bronchiolitis. The asthmatic attack either begins quite suddenly, or, is preceded for a shorter or longer period by prodromata. These consist in a general feeling of dis- comfort, in abnormal sensations in the larynx or epigastrium, sometimes in re- markably frequent gaping, and often in a marked coryza associated with a good deal of secretion and frequent sneezing (compare the relation between many at- tacks of asthma and diseases of the nose, given above). The attack begins in most cases at night (before midnight). The patient wakes up with an intense feeling of pressure and anxiety. Sometimes he complains of a feeling of pain in the chest. He has to sit up straight, and in severe cases even to get out of bed. He often hurries to an open window in order to " get air." His ex- pression is anxious; his skin becomes pale and cyanotic, and sometimes is cov- 184 DISEASES OF THE EESPIEATORY OEGANS ered with a cold sweat. On objective examination we are at once struck by the characteristic change in the respiration. Both inspiration and, especially, expira- tion are almost always accompanied by a high-pitched whistling sound, audible at a distance. Both respiratory acts are labored, requiring the aid of the acces- sory muscles. On inspiration, only the upper part of the thorax is elevated to any extent. We see in the neck the inspiratory contraction of the sterno-cleido- mastoids, the scaleni, etc. Still more striking, however, is the labored, panting, long-protracted expiration, during which the abdominal muscles are contracted to a board-like hardness. We therefore recognize the disturbance of respiration in asthma as essentially an expiratory dyspnoea. The frequency of respiration is in many cases normal, oj even somewhat diminished, yet we have repeatedly counted thirty or forty respirations a minute. On physical examination of the lur^s during the paroxysm, we find the per- cussion-note over them normal or even strikingly loud and deep — the " box-tone." The lower boundary of the lung is usually found one or two intercostal spaces lower than normal, l^ot only is this condition shown in the cases with a perma- nent pulmonary emphysema, but during the asthmatic attack itself there occurs an acute inflation of the lung. The latter is probably explained by the fact that the lung is much stretched by the strenuous inspirations which are made by aid of the accessory muscles, while the weaker expiratory force is not enough wholly to drive out the air again through the contracted bronchioles. Therefore it hap- pens in bronchial asthma, as in every other bronchial disease, that the expiration is usually more labored and protracted than the inspiration. On auscultation, high-pitched whistling and creaking sounds, which quite obscure the vesicular murmur, are heard over most of the lung, especially during the long expiration^. In many places, indeed, where the bronchioles are almost completely closed, the respiratory murmur is entirely absent, or we hear only a low whistle on expira- tion. Toward the end of the paroxysm the noises become deeper and more boom- ing, and sometimes we hear a few moist rales. In brief paroxysms there may be scarcely any cough or expectoration. In most, particularly in the tedious cases of true asthmatic bronchiolitis, there is, however, a scanty tough mucous expectoration. In this are found, beside the ordinary constituents of simple bronchitic sputum, larger or smaller numbers of very characteristic clumps. These may be yellow or greenish-yellow, or, on the other hand, gray. The yellowish masses, which are usually very tough, and often consist of a bunch of thready matter, represent swollen and fatty-degenerated pus corpuscles, between which are very frequently interspersed a considerable number of pointed octahedral crystals. These crystals were first described by Leyden in the sputum of asthmatic patients, and are usually termed asthma crystals (see Fig. 25). Chemically they are identical with "Charcot's crystals," which are found in the leukemic spleen, the bone marrow, etc., and they probably represent the phosphoric-acid salt of an organic base (Schreiner's base, C^H^jST), although this has lately been questioned. As soon as the paroxysms cease the number of crystals in the sputum usually begins to diminish rapidly, and it is often possible to observe in them evident signs of disintegration. Nothing^is known, as to the origin of these crystals. Often, also, numerous ciliated epithelial cells are found, in addition to the crystals, in the yellow masses. The gray plugs in the sputum of asthmatic patients consist mainly of clumps of thready mucus, and contain the peculiar "spirals" which were first described by Ungar and by Cursch- mann. Many of these spiral threads are visible to the naked eye, but others demand the microscope for their recognition, through which they are seen as brilliant forms composed entirely of various sized bands and threads collected in spirals (see Fig. 25). Sometimes a brilliant central thread of small diameter is seen in the midst of the spiral. Around the spirals are found round cells, drops BEONCHIAL ASTHMA 185 of fat and myeline, and sometimes ciliated epithelium, and epithelial cells from the pulmonary alveoli. As to the precise way in which the spirals and their central thread develop, the question is not yet settled, but it is certain that the spirals represent casts of the minutest spirally twisted branches of the bronchi, R^^%>^ Fig. 25.— Asthma crystals and Curschmann's spirals (a, central fiber). and therefore clearly indicate the existence of a peculiar disease of the finest terminal bronchial twigs. Of the other peculiarities of the sputum in bronchial asthma we may mention, first of all, the almost invariable occurrence of very many eosinophilous cells in the sputum, and also, apparently, in the blood. The significance of this fact is still unknown. We occasionally find in the sputum of astlimatics crystals of calcic oxalate and calcic phosphate. The pulse is usually accelerated during the asthmatic paroxysm, the arteries contracted; the bodily temperature is normal, or sometimes even subnormal. In protracted attacks we have repeatedly seen a slight febrile movement up to about 102° (39° C). The duration of the asthmatic paroxysm is very different in individual cases, as has already been said. Sometimes it lasts only a few hours, but sometimes it lasts several days, and even weeks. Marked exacerbations and remissions of the disease usually alternate. The frequency of the paroxysms in ordinary astlmia also varies exceedingly. Sometimes they come on almost every night, and then there are long pauses of months and years, so that we can not make any general statements as to the course of the disease. Many asthmatic patients make very remarkable statements as to the individual exciting causes of their attacks. Many patients claim, for example, that the attacks occur only in certain places, while in other places they are wholly free from the trouble, that they can live only in the upper storeys of the house, etc. Such statements should not remain unheeded, although it is certain that they are often due to imagination. Definite recoveries are quite rare, since long-continued asthma almost always leads to chronic pulmonary emphysema with all its consequences. Diagnosis. — The diagnosis of the bronchial asthmatic condition as such is not difficult if we limit ourselves strictly to the characteristic type of the disease : the strenuous respiration with wheezing that can be heard at a distance, the labored, prolonged expiration, the characteristic physical signs in the lungs, and the peculiar sputum. Usually we can easily distinguish bronchial asthmatic dyspnoea from cardiac asthma (q.v.), spasm of the glottis (q.v.), and also from hysterical dyspnoea with its superficial and very rapid respiration and normal conditions in the lungs. This latter distinction of true bronchial asthma f i-om " hysterical asthma " is very important both in prognosis and treatment, since the two are frequently confounded. If we are sure that we are dealing 186 DISEASES OF THE EESPIEATOKT OEGAlv^S with true asthmatic attacks, the next question is whether it is a " pxirely nervous " reflex asthma qr an asthmatic exudative bronchiolitis. Here, of course, we can decide only after a careful and thorough examination of the patient (especially of the nasal cavities) and after observing the course of the disease. Finally, we must also consider the possibility of a purely symptomatic asthma in chronic pulmonary emphysema, in the chronic bronchitis of renal disease or arthritis, etc. We must, however, confine our iise of the term " symptomatic bronchial asthma " to those cases in which we actually have a dyspnoea with all the characteristic peculiari- ties of true bronchial asthma. Treatment. — In every case of asthma the first thing to be thought of is whether there is not a definite cause whose removal may cure the disease. In this connection we should examine the nose carefully, since numerous recent ob- servations have shown that a previously existing asthma may wholly disappear or at least be materially relieved after the treatment of some nasal disease which may be present, such as the removal of polypi, the destruction of the erectile bodies by the galvano-cautery, etc. Of course these results should not be over-estimated. It has repeatedly been claimed by nasal specialists that in many asthmatic patients we can find a definite spot in the nose and excite an asthmatic attack by touching it with a probe. This spot must then be treated first of all. "We will not wholly reject these statements, but we are somewhat skeptical in regard to them. At any rate, the nose should be treated, in our opinion, only when it presents actual morbid changes. If we can not satisfy the causal indication in this way, we should always try next a remedy which must pass for a direct specific against certain forms of asthma — iodide of potassium. In doses of twenty to forty-five grains a day (grm. 1.5-3.0), or even more if necessary, this usually causes a rapid improvement, which of course is not always, although it is frequently, permanent. In asthmatic bronchiolitis, especially, iodide of potassium in large doses often acts excellently. It seems to make the tough secretion more fluid, to ease the expectoration, and in this way to lessen the stenosis of the bronchioles. Of course a permanent and ^-complete cure is only rarely obtained from iodide of potassium. If iodide of potas- sium has been used in vain, we must turn to the other remedies which have been employed against asthma, although their action is often quite uncertain. We may mention here the nitrite of sodium (two parts in one hundred and twenty of water, two to three teaspoonfuls a day), and nitro-glycerine, which has an analogous action (twenty drops of a one-per-cent. alcoholic solution in six and a half ounces [grm. 200] of water, a tablespoonful two or three times a day) ; also bromide of potassium, belladonna, atropine, etc. In some cases pneumatic treatment, such as the inhalation of compressed air, has been successful, and sometimes, too, elec- tricity (galvanization and faradization of the neck), or hydrotherapy, has been claimed to give relief. Change of climate may sometimes be of distinct service. Many patients bear the sea-air well, while with others a mountain residence exerts a favorable influence. Special resorts (Marienbad, Kissingen, ferruginous baths, etc.) may often be recommended with advantage if appropriate to the patient's general constitution. In severe cases a special symptomatic treatment of the attack itself is often necessary. Narcotics are without doubt the most effective, especially chloral and morphine. In severe attacks we can not avoid injections of morphine, but we must always be cautious in order that the patient may not form the habit of using this to excess. Chloral hydrate (gr. xv-xxx, grm. 1.0-2.0) often relieves the individual attack. Among other symptomatic remedies we may mention mus- tard-plasters to the chest and calves, putting the hands and feet into hot water, inhalations of nitrite of amyl, turpentine, chloroform, pyridine, etc. Fumigation with saltpeter paper — unsized paper dipped in a concentrated solu- PULMOK"ARY EMPHYSEMA 187 tion of nitrate of potassium and dried — and the stramonium cigarettes to be had in most drug-stores, are much praised. The patient may also smoke with benefit stramonium or belladonna leaves which have previously been dipped in a solution of saltpeter and then dried. Many patients praise highly the different asthma cigarettes and smoke-producing powders or pastilles, which are sold as secret remedies, especially in America. Such apparent success is certainly due in great measure to the psychical suggestion wrought by these remedies. [Potassic iodide is more likely to prevent recurrence if it is given continu- ously, for several months at least, and it should not be thrown aside as useless until it has been pushed to the limit of toleration without avail. A convenient form of administration is in saturated aqueous solution, a minim of which repre- sents about a grain of the drug. The syrup of hydriodic acid may be substituted for potassic iodide in cases of intolerance of the latter. Grindelia robusta, a drachm of the fluid extract three or four times a day, serves sometimes to prevent recurrence of attacks. Marked alleviation of the paroxysms is often obtained from the inhalation of fifteen to thirty drops of the iodide of ethyl.] SECTIOISr IV Diseases of the Lungs CHAPTER I PULMONARY EMPHYSEMA {Alveolar Ectasia. Pneumatosis pidmonum) Nature and .^Etiology of the Disease. — Pulmonary emphysema, the abnormal inflation and dilatation of the lungs, is one of the commonest pulmonary affec- tions. It either develops in separate parts of the lung, in which case it is subordi- nate to other pathological changes which co-exist in the lungs, or it involves almost the whole extent of both lungs, and then presents the symptoms of a char- acteristic affection, which it is usually easy to recognize. The essence of pulmonary emphysema, the condition from which most symp- toms are immediately derived, is the loss of elasticity in the lungs. If we com- pare the sound lung, with its normal elastic force, to a new and very tense rub- ber band, the emphysematous lung must be compared to an old and lax band that is stretched and pulled out. We therefore see why the emphysematous lung takes up a greater space than the sound one, for, on account of its lack of elasticity, it can no longer contract to its former volume. We may therefore call emphysema a permanent inspiratory distention of the lung from which it can no longer return to its expiratory condition. If we open the thorax of a subject with nonnal lungs, they contract, as is well known, but the emphysematous lungs remain in their inflated condition after the thorax has been opened. If we inquire into the factors which cause this loss of elasticity in the lung. we find that they are the same kind of influences which tend to diminish the elas- ticity of any other elastic body. As a rubber band, by much pulling and stretch- ing, gradually gets longer and less elastic, so the lungs, as a result of their abnor- mally frequent and severe distention, gradually become inelastic and emphy- sematous. Emphysema in many cases is a true wearing out of the lung. The normal traction of inspiration, which is continually making new demands on 188 DISEASES OF THE EESPIEATOEY OEGA^tS the elastic powers of the lungs, finally leads to a loss of elasticity in them. In advanced age most lungs become more or less inelastic. The lungs of an old man are like an elastic band which has done its work for years but which has finally given out. We therefore class emphysema of the lungs in old age rather among the states of involution, such as develop in almost all organs in advanced life, than among special pathological changes. We distinguish, more- over, most lungs with senile emphysema from other emphysematous lungs by the fact that their volume as a whole is not increased, but is rather diminished below that of the healthy lung, since we find in them the extensive atrophic processes of old age. The condition becomes pathological, however, if the elasticity of the lung is deficient in earlier years and independently of the action of the special in- jurious influences which will soon be mentioned. In such cases of emphysema, developing in middle life or even in youth, the idea of a congenital weakness of the elastic elements in the lungs can not be set aside. It probably consists in a quantitative or a qualitative defect of the elastic tissue. Some observations seena to corroborate the statement that a disposition to emphysema may be present in several members of the same family. If a lung whose elasticity is previously subnormal can not persistently satisfy the ordinary demands upon it, a normal lung, on the other hand, also loses its elasticity if the demands made upon it are greater than it can perform. This is the reason why pulmonary emphysema is in some instances to be regarded as a dis- ease arising from the occupation. We mean here not only those influences which lead to chronic bronchitis and thus later to emphysema (vide infra), but more espe- cially the abnormal demands upon the lungs in all those callings which necessitate severe physical labor. We must not only regard the deeper and more rapid res- pirations, but also the increased pressure during expiration to wliich the lungs are often exposed in the raising of heavy weights, etc. This explains the common oc- currence of emphysema in the laboring classes, and also its greater frequency in men than in women. Besides this, we must add that in certain callings, such as glass-blowing and horn-blowing, the over-straining of the lungs is much more direct. In all such cases emphysema may be termed simply a premature exhaustion of the lungs. In very many cases emphysema develops as a result of other diseases of the lung, and especially as a result of chronic bronchitis. Dry catarrh of the medium- sized and finer bronchi when of long duration leads, as a rule, to pulmonary emphy- sema. The abnormal mechanical influences to which the lungs are thus exposed act both in inspiration and in expiration. Since the entrance of air to the alveoli is rendered more diflicult by the swelling of the mucous membrane in the smaller bronchi, abnormally deep and strong inspirations are necessary, with a marked expansion of the alveoli, in order to draw a sufficient quantity of air into the alveoli. The alveolar walls are therefore exposed to an abnormal traction at each inspiration. On expiration, a pressure from within, which is perhaps even more injurious, acts on the alveoli. The ordinary expiration, which usually needs only the elastic power of the lungs, is not sufficient in chronic bronchitis to drive the air out of the alveoli through the narrowed bronchi. Thus arise the difficulty and delay in expiration which are present in chronic bronchitis, and which lead to the active participation of the muscles of expiration, the abdominal group of muscles. On forced expiration, however, the pressure does not act simply upon the contents of the alveoli, but much more upon the smaller bronchi themselves. The channel of exit for the air from the alveoli, therefore, becomes still narrower. Since the air can not at once escape, the pressure within the alveoli is raised by the efforts at expiration, and the alveolar wall is thus again abnormally expanded. The cough, which is often present in chronic bronchitis, is a further factor, which PULMONAKY EMPHYSEMA 189 acts in a precisely similar injurious fashion. The attacks of coughing begin with a forced contraction of the muscles of expiration, which follows the closure of the glottis. Until the glottis opens, therefore, the lower parts of the lung especially are put under strong pressure. The air in them, which can not escape outward, is driven into the upper parts of the lung, and there leads to expansion of the alveoli, and finally to emphysema. We accordingly see that a number of injurious influences co-operate in the gradual development of emphysema from chronic bronchitis, and that, sooner or later, these influences have as their result the gradual dilatation of the lungs. Here, too, we must bear in mind the individual differences in the resisting power of the lungs. Conditions precisely similar to those in chronic bronchitis occur in other dis- eases, and lead in like manner to pulmonary emphysema. We very often see the development of emphysema in severe and persistent whooping-cough. The worst factor here, besides the existing bronchitis, is the f reqvient paroxysms of coughing. Many cases of pulmonary emphysema and chronic bronchitis may be ultimately referred to such a severe bronchial disease occurring in childhood. We have already mentioned, in the description of bronchial asthma, both the acute emphy- sema, which occurs during the attacks, and the final development of a permanent emphysema. In conclusion, we must here consider a theory advanced by Freund, which would make the development of an emphysema dependent upon a " primary rigid dilatation of the thorax." It is indeed conceivable that from certain pathological changes in the costal cartilages, as Freund claims, a thorax, which had become fixed in the position of inspiration, might exert a constant abnormal traction on the lungs and so give rise to an emphysema. The occurrence of this hypothetical • primary disease of the cartilages, however, has up to the present time not been established. It is rather considered by the majority of authors as a secondary change, developing as a result of emphysema or else simultaneously with it. On the other hand, it is certainly remarkable that we sometimes observe in children the " emphysematous habit " of the thorax and neck, which will be more fully de- scribed further on, and that in fact we can often discover in such children a beginning emphysema early in life. We might perhaps imagine a congenital, failure of harmony between the size of the thorax and the size of the lungs, whereby the latter are from the start in constant overtension. Besides the already described essential or substantial emphysema, which is a special disease attacking both lungs uniformly, we distinguish a so-called vicarious or complementary emphysema. If, by any disease, certain portions of the lungs are incapacitated in their functions, the parts which remain healthy must then assume the whole business of respiration. They become excessively expanded on inspiration, and as a result they become emphysematous. Thus we see emphysema of the upper lobes in affections of the lower lobes. Emphysema of one lung is most frequently observed clinically when the other lung is extensively diseased, especially in unilateral chronic contractions of the lungs and pleurae, usually seen in tuberculosis. Vicarious emphysema may also be confined to quite small por- tions of the lung, but then it is merely of pathological and not of clinical interest. Pathological Anatomy. — As we have seen, the actual abnormality of the lung in emphysema is not due to a pathological change, but to a change in its physical conditions. The loss of elasticity of the lung is shown in its greater volume, in its lack of contractility, and in its persistence in a position of inspiration. The single alveoli are of course just as much expanded as the whole lung, but their walls sljow at first no histological changes. We have here, then, a condi- tion which Traube has called " increased volume of the lungs," and has distin- guished from the " pulmonary emphysema " proper. This distinction is without 190 DISEASES OF THE EESPIRATORY OEGANS doubt justified anatomically, but clinically it can not well be maintained. As the distention is constant, the alveolar walls can not withstand the constant traction and pressure. This leads to progressive atrophy of their tissue from pressure — that is, it leads to a real disappearance of the elastic elements of the lung. The atrophy begins quite gradually. The partition-walls of the alveoli are first per- forated, and then they partly or wholly break down. The neighboring alveoli run more and more into one another, and thus finally arise alveolar ectasis and in- fundibular ectasis, which can be made out with the naked eye, and which may attain a diameter of five or ten millimetres or more. If single air-bubbles enter the interlobular, interstitial, or subpleural connective tissue, which may happen perhaps in severe fits of coughing, we speak of an interstitial or interlobular em- physema, in distinction from the ordinary vesicular or alveolar emphysema. The tissue atrophy in the septa of the alveoli affects not only the elastic tissue, however, but also the branches of the pulmonary capillaries in the alveo- lar walls. The affection of the elastic tissue adds no new conditions to the dis- turbed functions of the emphysematous lung, which we have just described. The destruction and final atrophy of the pulmonary capillaries, however, is the second important factor in the pathology of pulmonary emphysema, for, with the destruc- tion of so great a part of the vascular area in the lungs, the outflow from the right side of the heart is considerably impeded. There must therefore necessarily be a stasis in the pulmonary arteries and the right side of the heart, and the right side of the heart can overcome the increased resistance only by increased work, and thus in every chronic pulmonary emphysema there finally arise a dilatation and consecutive hypertrophy of the right ventricle with their further conse- quences, n, ^ ^ Symptoms and Course of the Disease General Course of the Disease. — Although a pulmonary emphysema may . sometimes, as in whooping-cough, develop in a comparatively short time, still its course is always very chronic. In most cases the origin of the disease is quite gradual, as in all those instances in which emphysema develops from chronic bronchitis or asthma, or as a result of some injurious occupation. The symp- toms gradually and insidiously associate themselves with those of the chronic bronchitis. The symptoms of emphysema usually begin in middle or advanced life, but marked emphysema may occur in youth and childhood. The disease always lasts for years, unless some fatal intercurrent disease arises. The objective and subjective symptoms are due either to the chronic bron- chitis, which very often co-exists, or to the emphysema itself. Not only is the bronchitis, as we have seen above, very often the cause of emphysema, but, on the other hand, the development of chronic bronchitis is greatly favored by the circulatory disturbances in the lung associated with emphysema. Thus the two diseases, emphysema and chronic bronchitis, are closely connected clinically. Bronchitis causes its well-known symptoms — cough, expectoration, moderate dyspnoea, and a feeling of pressure in the chest. The bronchiectases, which are often gradually formed, especially in the lower lobes, may lend a peculiar stamp to the cough and expectoration (see page 178). Emphysema increases the pa- tient's dyspnoea to a degree which can never be caused by chronic bronchitis alone. The emphysematous lungs soon become incapable of satisfying any extraordinary demands of respiration. Many patients are only slightly conscious of the diifi- eulty in breathing so long as they keep quiet, but whenever they make a trifling physical exertion, go up-stairs, or take a little longer walk than usual, the dyspnoea comes on. The variations in the intensity and extent of the bronchitis correspond to the frequent and quite marked variations in the patient's feelings. These variations PULMO]STAEY EMPHYSEMA 191 depend -upon the condition of the patient, his circumstances, and the possibility of his taking- care of himself ; the change of seasons, too, has an influence on him. In pleasant weather many patients live in tolerable comfort, but autumn and winter bring an aggravation of all their symptoms with the increase in their bronchitis. The last stage of the disease is characterized by the appearance of disturb- ance of compensation in the heart. We have seen above that the cause of the impairment of the pulmonary circulation, and of the resulting hypertrophy of the right ventricle, is the closure of numerous pulmonary capillaries. A further reason for the impairment of the circulation comes from the disturbance of res- piration itself, since the influence of the respiratoiy movements on the circulation is well known. The appearance of a marked disturbance of the circulation may be deferred for some time by the increased efforts of the right ventricle. The cyanosis of most patients, however, is due not only to incomplete oxidation but to the blood-stasis which extends backward from the right side of the heart into the veins of the body. Finally, the right ventricle becomes more and more feeble, the stasis in the veins increases, oedema of the extremities and transudation into the various cavities of the body ensue, and after long suffering the patient succumbs to dropsy. Emphysema is frequently combined in its later stages with other chronic dis- eases. Pulmonary emphysema with its sequela3 is seldom found at the autopsy as a single lesion, but we discover in the cadaver co-existing disease of the heart, the blood-vessels, or the kidneys, all a genuine wearing out of the aging body. Pulmonary, tuberculosis is often a final development in emphysema, but it is usually of the chronic indurated form, and is not very extensive. Physical Examination. 1. Inspection. — ^In many patients we can detect the disease with considerable confidence at the first glance ; we are therefore justified in speaking of an emphysematous habit. The patients are usually quite well nourished, at least in the early stages of the disease, and are often rather cor- pulent. They appear plump or even somewhat bloated, and their faces are more or less markedly cyanotic. The configuration of the neck and thorax is especially characteristic. The neck is usually short and thick; the sterno-eleido-mas- toid muscles, which have to act as auxiliaries in inspiration, are tense and hypertrophied. The inspiratory contraction of the scaleni may also be seen and felt. The veins in the neck are visibly dilated, and in severe cases are swollen to thick blue cords, and we sometimes see in them evident undulating or pulsating movements. The thorax is rather short, but broad and strikingly deep — the " bar- rel-shaped thorax." The intercostal spaces are narrow, and the lower ribs incline only a little downward. The epigastric angle is therefore obtuse, and sometimes becomes almost a straight line. The respiratory movements are almost always accelerated in severe cases. Inspiration becomes short and labored. The excur- sions of single ribs are therefore slight, and the thorax is raised rigidly and more as a whole. Expiration is visibly prolonged. There may be a noticeable retrac- tion of the intercostal spaces on inspiration, in the lower and lateral portions of the thorax. This characteristic form of the thorax in emphysema is regarded as a constant inspiratory position of the ribs, and corresponds to the permanent inspiratory dilatation of the lungs. The peculiar rigidity of the thorax is probably due to the changes in the costal cartilages already described, which, according to Ereund, are primary. In many cases the emphysematous form of the thorax gradually develops in the course of the disease, but in other cases it seems to depend on some original predisposition to the disease (vide supra). In conclusion, we must state that the above description corresponds to the typi- cal form of emphysema, from which we may have many deviations. In the para- 192 DISEASES OE THE EESPIEATOEY OEGANS lyzed thorax, for instance, we may meet with, a high degree of essential emphyseriia of the lungs, which has often given rise to errors in diagnosis. 2. Percussion. — Percussion gives very decided results in the diagnosis of pul- monary emphysema. We find the inferior border of the lungs one or two inter- costal spaces lower than under normal conditions, corresponding to their perma- nent inspiratory inflation. Clear pulmonary resonance on the right front in the line of the nipple extends to the lower border of the seventh, and sometimes of the eighth rib. On the left front it extends to the fifth or sixth rib, so that the cardiac dullness is lessened. The area of cardiac dullness can often not be made out at all; or at most, on strong percussion, it is made out in a limited extent as rela- tive dullness. The pulmonary resonance extends on both sides in the back to the first or second lumbar vertebra. These results of percussion in emphysema, how- ever, are frequently altered, because other conditions, such as passive congestion of the liver, meteorism, and ascites, may be present at the same time, and push up the diaphragm. Thus the detection of emphysema by percussion is made decid- edly difiicult. Qualitative changes in the percussion-note may be entirely wanting in emphy- sema. The pitch is sometimes remarkably loud and deep — the " box-tone " [tym- panitic resonance] ; but in other cases, especially in the back, we find it somewhat raised. This may depend in part upon the poor vibratory conditions in the rigid chest-walls, but in other cases it is caused by the retention of an abundant secre- tion in the lower lobes. On inspiration, the lower edge of the lung moves downward very little or not at all. This is an important sign in diagnosis. Since the lung is always in a state of abnormal inspiratory distention, and since the entrance of air is impeded by the accompanying catarrh of the bronchi, the difference between the inspiratory and expiratory expansion of the lung is much diminished. The difference caused by respiration in the lower limit of the lung affords a good measure of the respiratory disturbance in the lower lobes. The detection of dilatation and hypertrophy of the right ventricle by percus- sion is in many cases difficult, because the lungs cover the heart. A positive result can be obtained only by carefully defining the relative cardiac dullness [by very light percussion]. The epigastric pulsations frequently seen in emphysema, and also the marked undulating and pulsating movements in the jugular veins, are to be regarded as quite certain signs of dilatation of the right side of the heart. 3. Auscultation. — The characteristic auscultatory sign of emphysema is the prolonged expiration. As a flabby rubber band, when it is stretched and then let loose, no longer snaps back quickly and strongly, so the emphysematous lung, when it has been stretched in inspiration, comes back again only slowly. We hear with it a somewhat aspirated, sonorous sound, which plainly exceeds the vesicular inspiratory sound in duration. The vesicular murmur itself often undergoes a modification in pulmonary emphysema. It sounds exaggerated, and shuffling, or in other cases it is rougher and more indefinite. In a high degree of em- physema the vesicular respiration is sometimes very faint and obscure, because the inspiratory current of air is reduced to a small amount in the lungs, which are already excessively dilated. In many cases we hear rhonchi beside the respir- atory murmur, dry whistling, buzzing, and creaking sounds on inspiration and expiration. If cylindrical bronchiectases have already formed, we hear, especially over the lower lobes, numerous fine and medium moist rales, but no sonorous rhonchi. The adventitious sounds may wholly conceal the respiratory murmur. With a marked retention of secretion we sometimes hear nothing but a low, sup- pressed rattling. In the heart the sounds are usually rather feeble, because it is covered by the lung. The " functional systolic murmur of emphysema " at the apex, described by PULMOl^AKY EMPHYSEMA 193 some writers, we have heard much less frequently than we should expect after the statements relating to it. If present, it is probably due to co-existing valvular changes. The pulmonic second sound in emphysema is, as a rule, markedly accen- tuated, as a result of the stasis in the pulmonary circulation. The diminution of the expiratory pressure in emphysema may be measured with the manometer, or with Waldenburg's " pneumatometer." The normal ex- piratory pressure of 110 to 130 raillimetres sinks in emphysema to 100 or 80 milli- metres. As we should expect, the spirometer shows a diminution of the vital lung capacity, which can be readily explained. The normal lung capacity of about 3,500 cubic centimetres falls to 2,000 or 1,000 cubic centimetres. Other Symptoms in the Lungs and in Other Organs In regard to the other symptoms in the lungs we have only a little to add to what has already been said. The intensity of the cough naturally varies in individual cases according to the degree of the existing bronchial catarrh. Many patients are troubled by a dry cough, while others have abundant expectoration. There is nothing characteristic of emphysema in the composition of the latter. All the kinds of sputa which are found in the different forms of chronic bronchitis are also found in pulmonary emphysema. The dyspnoea, whose predominant ex- piratory character we have already mentioned, increases in advanced cases to a most marked degree. Sometimes the increase shows itself by the appearance of distinctly paroxysmal dyspnoea. This is often really to be regarded as a symptom- atic bronchial asthma, but, on the other hand, we must not overlook the fact that a temporaiy increase of the bronchitis, retention of secretion, and cardiac failure, may also excite attacks of dyspnoea, which can not properly be termed asthma. The important changes in the heart resulting from emphysema have already been described. The exhausted right ventricle can no longer overcome the in- creased resistance in the pulmonary circulation. The difficulty of respiration is still greater, from the passive congestion of the pulmonary vessels. The skin be- comes still more cyanotic, and finally oedema and general dropsy develop. The failure of compensation is indicated by the smallness of the pulse, its increased fre- •quency, and sometimes by its irregularity. The difficulty of an objective exam- ination of the heart in emphysema has been spoken of above. The appearances of blood-stasis in the internal organs are shown especially in the liver and kidneys. The liver is swollen, and its increase in size (the liver of passive congestion) can frequently be made out by percussion or palpation. The pains in the hepatic region, of which many patients complain, are per- haps due sometimes to the stretching of the capsule of the liver, but they are prob- ably more often muscular pains excited by the frequent coughing. In the kidneys the effect of stasis is first shown by a diminished excretion of urine. The urine is more scanty in amount, more concentrated, of a higher spe- cific gravity, and of a darker color. It generally gives an abundant sediment of urates, and it may contain a small amount of albumen. Microscopically we may '&nd a few hyaline casts, and a few red and white blood-corpuscles. It is evident that this diminished activity of the kidneys favors the development of dropsy. The spleen is not infrequently found congested at the autopsy. The evidence of this, however, is often uncertain during, life, for percussion of the spleen is •difficult on account of the emphysema, and palpation is difficult from the anasarca. Gastro-intestinal symptoms may be present in emphysema. The appetite seldom remains good throughout the disease. Many patients suffer from chronic constipation; and more rarely there is a tendency to diarrhoea. Fever is not present in simple pulmonary emphysema. Whenever fever exists for a long time it depends on other complications, such as severe bronchitis, pneu- monia, or tTiberculosis. 13 194 DISEASES OF THE EESPIEATORY OEGANS Complications of emphysema with other chronic diseases are frequent. The old opinion that emphysema and tuberculosis, and emphysema and chronic heart disease, were antagonistic to each other is entirely false. These complications are not very rare. We may also mention the complication with general arterio- sclerosis and with chronic nephritis, especially the contracted kidney. Among acute diseases we must mention particularly the acute accidental pulmonary complications, to which emphysematous patients, particularly of the lower classes, are much exposed as a result of over-exertion, exposure to cold, etc. Acute febrile bronchitis and lobular pneumonia cause marked exacerbations, and attacks of true influenza and croupous pneumonia in aged patients are not infrequently dangerous to life. The diagnosis of emphysema can be made directly from the results of the physical examination, and usually presents no difficulties. We think it important merely to say that too much stress should not be laid upon a low position of the lower edge of the lung alone. Many men apparently have dilated lungs but no symptoms at all. The chief thing, therefore (besides the dilatation of the lungs), is the presence of delayed and difficult expiration and lessened power of inspira- tion. The diagnosis is difficult when a patient with emphysema is not examined until the final, dropsical stage. In such cases it is often very difficult to avoid confusion with heart disease (primary hypertrophy, myocarditis, mitral stenosis), contracted kidney, etc. It is often difficult, also, to come to a decision in those cases in which there are evident signs of co-existing cardiac or renal disease besides the emphysema. In such cases it is often hardly possible to decide upon which of the different organic changes the chief stress is to be laid. In all such cases we must place especial confidence in an accurate history as well as a careful physical examination. The special nature and the sequence in development of the individual symptoms often afford valuable data for a correct appreciation of the whole clinicial picture. Prognosis. — Pulmonary emphysema of acute origin — that is, acute infla- tion of the lung — like that resulting from whooping-cough and analogous affec- tions, may be recovered from in many cases. Otherwise, as regards the final curability of the disease, the prognosis is wholly bad. The duration of the dis- ease and the intensity of the symptoms are of course very different in individ- ual cases. Here almost everything depends upon the circumstances in which the patient is placed. With sufficient care the disease may be tolerably well borne for many years, but without it the first symptoms of respiratory and cardiac insufficiency appear much earlier. The final termination is usually due to com- plications (vide supra). Treatment. — Since emphysema itself is only slightly amenable to treatment,, most of our therapeutic remedies are directed to that accompanying condition upon which the greater part of the symptoms depend — the chronic bronchitis.. If we succeed in improving this, or even in wholly removing it, we always obtain a decided improvement in all the patient's symptoms. The therapeutic agents mentioned in the description of chronic bronchitis are therefore of frequent use in emphysema. In the first place, we must seek the best hygienic conditions for the patient, and remove him from all injurious influences, such as dust, bad air, and great physical exertion. In drj- catarrh we should use the alkaline mineral waters, and when there is abundant mucous secretion the balsams, such as turpentine internally and by inhalation. The most valuable expectorants are iodide of potassium, apomorphine, and ipecac when the expectoration is tough, and liquor ammonii anisatus and senega when it is abundant. Their action, of course, too often fails of the desired result, so that we frequently have to change our remedies. When there is a troublesome cough, disturbing the sleep, we PULMOlSrAKY ATELECTASIS 195 can not dispense with narcotics, such as morphine, codeine, or Dover's powder. If severe dyspnoea comes on, we may try to obtain relief by mustard plasters to the chest, or by immersing the hands and feet in hot water. With asthmatic attacks we may try iodide of potassium, besides the other remedies mentioned for asthma. Here, too, we must finally resort to narcotics. We must carefully watch the condition of the heart, and use digitalis when there are signs of beginning disturbance of compensation and the pulse grows small and irregular, and this drug may prove very useful. If symptoms of dropsy set in, we may sometimes prescribe diuretic remedies, such juniper-tea, acetate of potassium, diuretine, calomel, etc., besides digitalis. When there is persistent weakness of the heart we should also use digitalis and other stimulants (stro- phanthus, camphor, wine, etc.). Besides the purely symptomatic treatment thus described, the attempt has been made to meet the causal indications in emphysema, and especially to aid the patient in expiration, and thus to improve the power of the lung to contract, where it is possible. To this end Gerhardt has recommended assisting expiration mechanically by compression of the thorax. This compression must be done methodically by another person,* about five or ten minutes every day, by the aid of both hands laid flat on the lower lateral portions of the thorax. The effect of this manipulation in diminishing the dyspnoea and making expectoration easier is in many cases very satisfactory. The " breathing chair " made by Eossbach has a similar mechanical action. The employment of the pneumatic treatment has also become quite general, especially since the introduction of Waldenburg's portable apparatus. The expi- ration into rarefied air, which meets the causal indication, may procure great relief for the patient in many cases, and sometimes, too, may result in an improve- ment of the emphysema which can be demonstrated on physical examination. In- halations of compressed air are also employed when there is severe bronchial catarrh. Still, too much must not be anticipated from pneumatic treatment. CHAPTEE II PULMONARY ATELECTASIS {Compression of the Lungs. Aplasia of the Lungs in Cases of IZyphoscoliosis) ^tiolog'y. — Atelectasis of the lungs is a condition the direct opposite of em- physema. While in the latter the lungs are abnormally inflated, in the former they are abnormally collapsed. The air has disappeared from the alveoli and lesser bronchi, and in the most advanced cases even from the larger bronchi. The atelectatic portions of the lung are not altered histologically, but are changed to a firm tissue, deprived of air — so-called splenization or carnification. The atelectasis of the new-born is due simply to deficient respiration and to the consequent imperfect entrance of air into the lungs. In weak children, who die soon after birth, we often find the lower lobes wholly or in part in a foetal, uninflated condition — that is, atelectatic. By artificial inflation we can readily * One of the author's patients at the policlinique in Leipsic made himself a very simple but very effective apparatus for producing this compression of the thorax on Jiimself by the aid of two nar- row boards, which are fastened together at one end by a cord of suitable length. These boards which are furnished with a pad at this end fitted to the wall of the chest, are laid fiat on the two sides of the thorax so that their free ends project forward some six inches or a foot, and serve as a one- armed lever. By pressing them together the patient himself can thus, without any strain, exert a con- siderable pressure on his thorax with each expiration. 196 DISEASES OF THE EESPIRATORY ORGANS expand the lungs to their normal extent. In many cases of weak, newly-born infants there is at first an atelectasis of parts of the lung, which gradually dis- appears entirely and is replaced by normal conditions. Acquired atelectasis occurs in two ways. We may mention, as the first and most frequent setiological factor, the plugging of the smaller bronchi. If a com- plete closure of a bronchus arises from the accumulation of secretion, as may easily happen in the narrow bronchi of children, the air can no longer enter, on inspiration, into that portion of lung supplied by the plugged bronchus. The air which is shut up in it is gradually absorbed by the blood. The adjacent parts of the lung expand, and the portion that is excluded from respiration collapses, leaving a circumscribed pulmonary atelectasis, usually rich in blood but devoid of air. Such atelectases, in greater or less number and extent, are very often found in the bodies of children who have suffered from severe bronchitis, espe- cially after measles, whooping-cough, or diphtheria. Besides the direct action of the plugging of the bronchus, the weakness of the respiratory movements and the cough, conditional upon the general state of the disease, play a significant part. The second very frequent and important cause of pulmonary atelectasis is compression of the lung. In all the diseases which diminish the space for the expansion of the lungs, the lungs are compressed to a greater or less extent, whereby the air is squeezed out of them. Thus arise the atelectases from pressure in pleuritic effusion, hydrothorax, pneumothorax, in marked cardiac hypertrophy, pericardial effusion, and aneurism of the aorta. Atelectasis of the lower lobes also arises in the same way from great upward pressure on the diaphragm by ascites, meteorism, abdominal tumors, etc. That form of pulmonary atelectasis which arises from deformities of the thorax is of great practical importance. In severe kyphoscoliosis, the half of the thorax corresponding to the convexity of the vertebral column is much narrowed. The lungs are materially hindered in their expansion, and even in their growth, if the deformity occurs in youth. This is called " aplasia of the lungs," a condition which may give rise to grave results (vide infra). Symptoms. — In the majority of eases the symptoms of atelectasis are subordi- nate to the disturbance caused by the primary disease. This is especially the case in most of the atelectases from pressure, although the most dangerous factor lies in the compression of the lung. The atelectasis of the lungs developing as a result of diffuse capillary bron- chitis, especially in children, can of course not be detected by physical examina- tion until it is of great extent. The respiration, in extensive formation of atel- ectasis, often shows a very striking and characterstic deviation from the ordinary type, especially when the atelectasis develops in the lower lobes. It is accelerated and labored, and is performed chiefly by the upper and anterior portions of the thorax. In the lower portions we see marked inspiratory retractions, which are caused in part by the external pressure of the air, and in part by the exaggerated contraction of the diaphragm. Physical examination can, of course, reveal abnormal conditions, especially dullness on percussion, only when the atelectasis is extensive. Dullness, however, is usually hard to make out in children. Auscultation gives signs of existing bronchitis ; and sometimes, too, with more extensive consolidation, there is bron- chial respiration. In other cases, as may be easily seen, the respiratory murmur is much diminished or wholly absent. Thus, the physical signs of atelectases are not easily distinguishable from those of pneumonia, especially of lobular pneu- monia. In fact, a sharp distinction between atelectatic nodules and nodules of lobular pneumonia in the lung can not be drawn clinically. Aplasia of the lungs in kyphoscoliosis demands a special description, because it is of great practical significance. Many patients with kyphoscoliosis may live for PULMONARY (EDEMA 197 years without special respiratory disturbance. Careful observation, of course, usually shows a somewhat labored and hurried respiration, but the patients have not paid much attention to it. In other cases the difficulty in breathing is more noticeable. The person affected is incapable of any severe physical ex- ertion; he always feels short of breath, and often suffers from cough and expec- toration. In the cases first mentioned, however, which for years have had little or no trouble, disturbances in respiration sometimes come on quite suddenly. They may also frequently arise without any special cause, and may attain a very threatening degree. The condition may improve, or it may lead to comparatively or even absolutely sudden death. Examination of the lungs during life usually shows nothing but the signs of an extensive bronchitis. By careful percussion we may quite frequently detect an increase of cardiac dullness to the right. Some- times a moderate oedema develops. In such cases the autopsy shows nothing as the cause of death but the changes in the chest. The lungs are deficient in air, small, and compressed, but in circumscribed portions, on the contrary, emphy- sematous and expanded. The right side of the heart in the great majority of cases is dilated and hypertrophied. There can scarcely be a doubt, therefore, that the cause of the onset of severe symptoms and the final cause of death is to be sought in the cardiac failure. Finally, it is worthy of mention that there is a frequent form of mild atelec- tasis in the lower lobes, which occurs in very sick and bed-ridden patients who usually keep in one position — on the back — as in typhoid fever. On making such patients sit up we hear during the first inspirations exquisite crepitant rales over the lower lobes, which sometimes disappear after a few deep inspirations. Here we have to do with a mild atelectatic condition, with a temporary collapse of the alveoli and smallest bronchi. The treatment of atelectasis coincides in great measure with the treatment of the primary disease, and is therefore to be looked for in the corresponding chap- ters. The prophylaxis of atelectasis, by constant attention to the respiration, is of great practical importance. We should try to keep the patient from lying con- tinually on his back, and we should make him take deep inspirations. The timely use of tepid baths, with shower-baths, is a special preventive of the development of atelectasis, and it may bring about a recovery when atelectasis is already present. Tepid baths may also be used with care in the treatment of dyspnoea caused by kyphoscoliosis. The condition of the heart, however, deserves especial attention (stimulants and digitalis). The reader is referred to the consideration of the general treatment of circulatory disturbances in the chapters on diseases of the heart. In other respects the symptomatic treatment by expectorants, etc., is the same as in other chronic pulmonary affections. CHAPTER III PULMONARY (EDEMA Etiology and General Pathology. — We have in pulmonary oedema the exuda- tion of a highly albuminous fluid, usually somewhat hfemorrhngic, not only into the interstitial tissue, but also into the alveoli themselves. The danger of the condition is easily understood from the high degree of dyspnoea. which immedi- ately ensues from it. In fact, pulmonary oedema is in many cases a terminal symptom, which comes on in all forms of acute and chronic disease. Many pa- 198 DISEASES OF THE EESPIRATOET ORGA^tS tients are said to die with the signs of pulmonary oedema, especially patients with heart disease, pulmonary and renal disease, and also with other affections of the most different kinds. In rare cases pulmonary oedema is a transitory symptom. Repeated attacks of it may occur, especially in heart disease and chronic renal disease, and, for a time at least, the patient recover from them. In spite of much clinical and experimental work, the special causes of pulmo- nary cedema are still quite obscure. For one class of cases the work of Cohn- heim and Welch shows that pulmonary oedema is to be considered as purely the result of stasis. Pulmonary oedema takes place when the outflow of venous blood in the lung meets an obstacle which can no longer be overcome by the mechanical force of the right ventricle. The obstacle which plays the most significant part here, and which may occur in all possible forms of disease — of course more read- ily in those mentioned above than in others — is paralysis of the left ventricle. If the further progress of the blood is much hindered by this, the overfilling of the pulmonary circulation and a consequent pulmonary oedema will necessarily follow, in spite of the most vigorous action of the right ventricle. Many cases of terminal pulmonary cedema seem to depend upon this fact, that the left ven- tricle is paralyzed in its action sooner than the right. The paralysis of the left ventricle, however, is certainly not the only factor to be considered in the origin of pulmonary oedema. We must also consider the condition of the walls of the blood-vessels in the lungs. In many cases, especially in renal disease, pulmonary oedema seems to depend upon local changes in the vessel walls (Sahli). This form of pulmonary oedema is somewhat akin to true inflammatoiy oedema. The latter is found chiefly in the vicinity of por- tions of lung infiltrated with pneumonia; it is usually of limited extent, and therefore it is of subordinate importance as a cause of disturbances in respiration compared with the diffuse oedema of stasis. In very rare cases, as we have ourselves seen, an apparently primary acute pul- monaiy oedema, with a speedily fatal termination, develops in men who are apparently perfectly healthy, and the autopsy gives no explanation of its origin. We perhaps have to do in these cases with the sudden failure of the left ven- tricle, but probably with acute vascular changes as well. Symptoms. — Marked dyspnoea is the most striking symptom in pulmonary oedema. It is subordinate only when the patient is found in the death agony and is no longer fully conscious. In pulmonary oedema the respiration is hurried, labored, and rattling. All the accessory muscles of respiration are called into play. The patient usually sits upright in bed. We see on his lips and cheeks a gradually and constantly in- creasing cyanosis, and we often hear at a distance the moist rales originating in the larger bronchi. On examination of the lungs, the percussion is essentially normal, if there is no other disease of the lungs. Sometimes the percussion-note is a little higher in pitch, and often it is slightly tympanitic. On' auscultation, we hear everywhere many fine and medium moist rales. If the patient can still expectorate, he raises a large amount of frothy, sero-sanguineous sputum. The whole picture of the disease is so characteristic that the condition can scarcely be mistaken. Treatment. — Since in most cases pulmonary oedema is not so much the cause as a symptom of approaching death, our remedies against it are apt to prove pow- erless, but it must always be our duty, at least in all cases that are not absolutely hopeless, to try to relieve the pulmonary circulation. From the pathogenesis of pulmonary oedema it follows that we must pay particular attention to the condition of the heart, especially of the left ventricle. Hence we should use energetic stimulants, especially subcutaneous injections of camphor or ether. CATAREHAL PNEUMONIA 199 ■every half hour or hour. Internally we give first strophanthus (ten drops of the tincture every hour) and also camphor, wine, and very strong cafe noir. Besides that, we apply strong irritants to the chest, such as large mustard plasters or hot sponges. Sometimes an actual improvement of the respiration, when it has nearly stopped, may be obtained by a bath with cold douching. When there is marked general cyanosis, if the patient is on the whole strong and well nour- ished, venesection is sometimes of manifest benefit. Emetics, however, accom- plish little, and are even dangerous on account of the collapse which is apt to come on after them. Expectorants (benzoin, liquor ammonii anisatus) are more frequently prescribed, and an energetic " derivation to the intestines," by senna, calomel, or enemata of vinegar, seems sometimes to be really of service. Acetate of lead in large doses, one or two grains (gramme 0.05-0.10), in powder, every hour, employed empirically by Traube, is deserving of trial. In this way, especially in acute diseases like typhoid and pneumonia, we in fact sometimes succeed in averting the danger of pulmonary oadema by rapid and energetic action. In the cases of oedema occurring in incurable chronic diseases of the heart and kidneys, the remedies employed are of course unfortunately incapable of preventing death. CHAPTER IV CATARRHAL PNEUMONIA (Bro7icho-p>ieumonia. Lobular Pneumonia) .ffitiology. — Catarrhal pneumonia is neither setiologically nor anatomically one single, absolutely independent disease, but from a clinical standpoint we are perfectly justified in grouping together the catarrhal, lobular pneumonias, which are usually secondary to other diseases, and especially to a previous bronchitis, and in contrasting them with croupous, lobar, " genuine " pneumonia. In the great majority of catarrhal pneumonias the belief is certainly correct, that the agents of inflammation do not enter the pulmonary alveoli directly from without, but that the inflammatory process is situated originally in the bronchi, and from this point extends downward to the special respiratory parenchyma of the lung. This extension of the inflammation may take place entirely by conti- nuity, or it may skip some part, as the germs are often inhaled from the bronchi directly into the infundibula and alveoli. The last-mentioned parts must, how- ever, possess considerable power of resisting germs, since the danger of an exten- sion of bronchitis to the alveoli generally exists only in the severer and more extensive cases of bronchitis or under other peculiar conditions. This exten- sion of the process is not uniform in all parts, but it occurs first in the distribu- tion of some small branches of the bronchi, and this is the reason why the pneu- monic infiltration affects first only a few bronchial areas — that is, individual lobules. In opposition to this generally accepted theory of the method of origin of the true " lobular " or " broncho-pneumonic " foci, the attempt has recently been made to show that the inflammatory process can pass through the walls of a small bronchus directly into the neighboring parenchyma of the lung, and that it may then extend further along the lymph-channels. Clinically, however, we can not yet distinguish this form of focal pneumonia from the ordinary catarrhal pneumonia. If we ask what are the conditions under which we are most apt to observe the development of lobular pneumonia, we must first mention a number of acute 200 DISEASES OE THE RESPIEATOEY OEGAl^S infectious diseases, in wMch. the air-passages are primarily affected, or in wMcli they may very readily be involved sympathetically. Chief among these are measles and whooping-cough, and next diphtheria, influenza, small-pox, etc. In all these diseases there is either a bronchitis at the beginning, or else it can de- velop very easily in them. It is in these same diseases, also, that simple bron- chitis comparatively often develops into lobular pneumonia. Eurthermore, in almost all severe acute and in many chronic diseases the conditions favor the development of secondary bronchitis and subsequently, at times, of lobular pneiunonia. Everywhere in the air-passages, as well as in the cavities of the mouth and pharynx, saliva, mucus, etc., readily collect if the patient is very ill. Expectoration is imperfect, and the constant dorsal decubitus favors the accumulation of secretion, especially in the lower lobes. The mouth and pharynx are harder to keep clean than under normal conditions. Fungi and bacteria collect in the secretion itself, as well as in the epithelium and particles of food which are left in the mouth, and these excite and keep up processes of decomposition. The inflammatory agents, which are carried into the air-pas- sages with the inspired air, find everywhere favorable conditions for settling and further development. From the upper portions they are drawn farther downward. From the larger bronchi the process invades the alveoli, and leads to catarrhal pneumonia. It is probably of significance, too, that in such very sick persons the vital resistance of the tissues has suffered, and that the development of such sec- ondary inflammation is consequently facilitated. We must also bear in mind that many patients who are very ill have difiiculty in swallowing. They get choked, and particles of food, with the germs of inflammation clinging to them, are carried into the air-passages. These particles, which a healthy person could easily cough up again, remain there, are decomposed, and give rise to bronchitis and lobular pneumonia. This is the explanation of the frequent development of lobular iDneumonia in the course of diseases which are entirely dissimilar. We observe it especially in severe bed-ridden cases, in all patients with stupor, in severe infectious diseases, in meningitis, and also in cases of nervous disease, in which coughing and deglutition are impaired as a result of bulbar affections. In all such cases lobular pneu- monia is to be considered a complication, and with reference to its origin de- serves the name of inhalation pneumonia or deglutition pneumonia. We shall soon see that this form, under some circumstances, may pass into circumscribed gangrene. Although in the preceding we have alwaj's spoken of " agents of inflamma- tion " in general, the precise variety is not necessarily the same in all cases. In the lobular pneumonias occurring in the course of measles, whooping-cough, influ- enza, etc., it is possible that the original specific germs may penetrate as far as the alveoli, and there cause an inflammatory exudation ; but this is certainly not always the case, and there are many reasons why in these affections, as well as in all the others mentioned above, catarrhal pneumonia should be regarded as a secondary complication, dependent upon the secondary invasion of other vari- eties of agents which cause inflammation. Different micro-organisms may prob- ably act as such agents. So far as our present investigations go, streptococci seem most frequently to be the special cause of broncho-pneumonia, and some- times in other cases staphylococci, diplococei, etc. Clinically, we can not at present make a complete separation on a strictly ^etiological basis. The development of lobular pnev;monia from bronchitis is most frequent, as we know, in children and old people. The frequency of catarrhal pneumonia in childhood is due in part to the limited dimensions of the bronchi. Besides that, however, the diseases in which it is especially frequent — namely, measles and whooping-cough — are children's diseases. In old people its comparatively CATAEEHAL PKEUMONIA 201 easy development is due to imperfect expectoration, and perhaps to the dimin- ished resistance of the tissues. The mild cases of primary bronchitis scarcely ever lead to lobular pneumonia, but sometimes in children, and less often in adults, a severe febrile bronchitis may occasion the formation of pneumonic foci. In Erlangen, the author has seen a good many cases which can not be regarded otherwise than as primary catarrhal pneumonia. We may also state that the inhalation of irritating chem- icals may occasion lobular pneumonia as well as bronchitis. Pathological Anatomy. — It is characteristic of catarrhal pneumonia that the inflammation is usually plainly circumscribed (vide supra), being limited to the territory of a small bronchus. Hence the name of " lobular " pneumonia or broncho-pneumonia, in distinction from croupous lobar pneumonia. An atelec- tasis (_vide supra) of the affected lobule, arising from the plugging of the bronchus leading to it, often, but not always, precedes the inflammation. The atelectasis of course becomes pneumonia only when germs enter the atelectatic spot. The inflammatory process itself consists of the exudation of a scanty fluid, which usually does not coagulate, and of numerous pus-corpuscles (white blood- corpuscles) into the lumen of the alveoli. With this is usually associated more or less marked desquamation of the alveolar epithelium, in which we often fljid necrosis or fatty degeneration. The alveolar cavities are completely filled with leucocytes and epithelium; few if any red blood-corpuscles are to be seen, al- though in some cases they may be more abundant. The vessels of the alveolar walls are hypersemic, and the connective tissue also contains a few wandering- leucocytes. The inflamed lobules are readily apparent to the eye and the touch by their firm consistence, being devoid of air. Their color at first, from the blood con- tained in the inflamed part, is a dark red (" splenization ")» but later it becomes m.ore grayish. A bit of such an inflamed spot, cut out with the scissors, does not float in water but sinks, because it contains no air. The lobular boundary of the individual nodules is usually easily distinguished from the neighboring healthy tissue, but, by confluence of adjacent nodules, large portions of the lung, and even whole lobes, may become infiltrated throughout — generalized lobular pneumonia. Symptoms. — 1. Primary Catarrhal Pneumonia of Adults. — The primary ca- tarrhal pneumonia which infrequently occurs in adults usually begins with the same phenomena as a severe attack of acute bronchitis. The patient feels pros- trated, and has cough, dyspnoea, and pain upon the side which is chiefly affected. There is almost never a pronounced initial chill, as in croupous pneumonia. The fever is usually not very high, from 101° to 103° (38.5° to 39.5° C), but higher temperatures sometimes occur, especially at the beginning of the disease. The expectoration is simply catarrhal or muco-purulent, never muco-sanguineous, as in croupous pneumonia. The physical examination gives almost invariably in one lower lobe many moist rales and a slight tympanitic or dull tympanitic per- cussion-note. Marked dullness and definite bronchial breathing are rare. In the lower lobe on the other, unaffected side, we often find signs of a slight bron- chitis; but in general the unilateral character of the symptoms is characteristic of primary catarrhal pneumonia, in distinction from ordinary bronchitis and secondary broncho-pneumonia. In mild cases the fever lasts from four to eight days, but the disease may last two or three weeks or more. There is never a crisis; the fever ends gradually by lysis. The getiology of primary catarrhal pneumonia has been little studied. Many cases may be streptococcus pneumonia ; we must also consider the influenza bacilli, since catarrhal pneumonia is especially common at the time of an influ- enza epidemic. 202 DISEASES OE THE EESPIEATORY OEGA^^S 2. Secondary Catarrhal Pneumonia. — Most of tlie cases of catarrhal pneu- monia develop, as we have already said, secondarily in the course of other affec- tions, hence the symptoms are frequently overshadowed by those of the other diseases. There are often found at autopsy a few foci of lobular pneumonia in the lower lobes which gave rise to no clinical symptoms whatever. In other cases, however, the development of extensive lobular pneumonia is of the greatest clinical significance. In many cases of chronic bronchitis, pul- monary emphysema, pulmonary tuberculosis, etc., in which the patient suddenly grows worse with a rise of temperature, the cause is certainly the development of foci of lobular pneumonia. Such complications may after a time completely disappear, or may cause a permanent aggravation of the original condition (e. g., tuberculosis). The onset of lobular pneumonia in other acute diseases is very important. The disturbance of respiration, during the patient's life, forms the most striking symptom of the disease, and lobular pneumonia is shown at the autopsy to be the immediate cause of death. The largest part of the fatal cases of measles and whooping-cough, and no very small part of those of diphtheria, scarlet fever, typhoid, small-pox, influenza, etc., are due, in the last instance, to the disturbance of respiration dependent upon lobular pneumonia. Since a diffuse bronchitis, extending into the finer bronchi, almost always pre- cedes the development of lobular pneumonia, and since it may also give rise in itself to marked disturbance in respiration, there is no sharp boundary to be drawn clinically between diffuse capillary bronchitis and lobular pneumonia. Only the experience, a hundred times repeated, that extensive capillary bronchitis is apt to lead to lobular pneumonia, permits us to suspect the latter, with con- siderable certainty, even if there is no direct clinical evidence of it. The most important objective physical sign of broncho-pneumonia is the not very loud, medium moist rales, almost always to be heard in the lower lobes. These rales are often high-pitched. Dullness of the percussion-note develops only when many lobular nodules coalesce and form a more extensive infiltration of the lung. Then we also find bronchial respiration. Catarrhal pneumonia is almost always associated with fever, which is mod- erately high and generally has a remitting character. We must, of course, judge of the fever in connection with the primary disease and any other complications. 1^0 general statements can be made as to the duration of secondary catarrhal pneumonia. Sometimes the acute symptoms last only a few days, in other cases they continue for weeks. Catarrhal pneumonia is not infrequently followed by pleuritic effusion, when the lobular infiltration reaches the pleura. Foci of lobu- lar pneumonia may develop into abscess or gangrene, but this is rare. 3. Catarrhal Pneumonia in Childhood. — The catarrhal pneumonia of child- hood is very characteristic and clinically important. It is observed most fre- quently in measles and whooping-cough, and also in weak, atrophic, and rachitic children. The increased frequency of respiration is most striking. The breath- ing is superficial, but labored, as is shown by the contraction of the auxiliary muscles of inspiration and the play of the nostrils. We also notice inspiratory retraction of the lower lateral portions of the thorax as a result of the incom- plete entrance of air. The number of respirations in a minute increases in chil- dren to sixty or eighty, or even more. In most cases the child has a frequent and apparently painful cough. Expectoration is entirely absent in small chil- dren. When it is present it shows no characteristic peculiarities different from ordinary catarrhal sputiam. The general condition is always bad. The child is restless, apathetic, and more or less stvipid. Its face is usually pale, but often quite cyanotic. The pulse is very rapid, and in small children may attain a frequency of 140 to 180 a minute. Fever is almost always present. It shows no typical course, it is now remitting and now intermitting, and toward evening CATARRHAL PI^EUMONIA 203 it perhaps rises to 104° or 105° (39.5°-40.5° C). The occurrence of such a rise in temperature is not without value in the diagnosis of catarrhal pneu- monia. If in diffuse capillary bronchitis a high fever is present for some time, we may assume with considerable certainty that the lobular infiltration has already begun. Physical examination furnishes direct evidence of the affection of the lungs, but its results are for the most part to be referred to the diffuse bronchitis and not to the lobular infiltration. Auscultation gives the most valuable signs. We hear over the lungs, in a greater or less extent, numerous fine and medium moist rales, often quite high-pitched. From these signs, strictly interpreted, we can diagnosticate merely bronchitis, but we may suspect pneumonia with the greatest probability. With very confluent broncho-pneumonia, auscultation sometimes gives bronchial breathing and bronchophony, besides the rales. It goes without saying that little lobular foci, surrounded by normal lung- tissue containing air, give no special signs on percussion. With numerous nodules running into one another, the percussion-note is duller, and there is sometimes tympanitic resonance. The dullness is often first to be made out over a stripe extending along the vertebral column — so-called " stripe-pneumonia." An attack of extensive lobular pneumonia is usually quite protracted. Even in favorable cases the disease rarely lasts less than two or three weeks, and it may persist much longer. The course of the disease is apt to be irregular, re- lapses succeeding improvement. The chief danger of the disease lies in this tendency to a protracted course, extending over weeks and months. Many chil- dren finally die, not of the lobular pneumonia itself, but from the general weak- ness and emaciation following the tedious febrile disease. We must remember, however, that complete recovery may sometimes take place quite late in the disease. The " transition of catarrhal pneumonia to caseation and tuberculosis " is a clinical fact with which physicians have long been conversant. In fact, we often find true tubercular changes in the lungs of children who have died after a tedious illness, as a result of measles, whooping-cough, etc. There can, of course, be no real question, however, of an actual transition from one disease to the other. In such cases either we have to do with an acquired tubercular infection, which has found a favorable soil in an already diseased lung, or (what is probably more frequently the case) the disease of the lung has promoted the development of a previously existing tuberculosis. It is usually weak children, with a hereditary predisposition to tubercle, who succumb to tuberculosis as a result of the above- named diseases. The diagnosis of a developing tuberculosis is not always easy, since it is only rarely that marked phthisical changes — like dullness at the apex, cavities, etc., which can be made out by a physical examination — are found in the lungs. We can usually suspect tuberculosis only from the general conditions (emaciation, persistent hectic fever, hereditary predisposition, or some secondary tubercular disease such as meningitis, etc.), especially as absolute proof, from the detection of tubercle bacilli in the sputum, is only rarely possible in children. Treatment. — Since we have already mentioned the proper treatment, in our description of the various diseases in which secondary pneumonia is especially prone to develop, we can now be brief. We have also laid repeated stress upon the possibility and the great practical importance of prophylaxis, which is self- evident from a just comprehension of the origin of lobular pneumonia. Besides keeping the nose, the mouth, and the pharynx as clean as possible, tepid baths, perhaps with cool douching, are the best means of preventing the de- velopment of lobular pneumonia, or of checking its further extension. Wet cold packs are often used with advantage (vide infra). It is an advantage, which is indeed to be considered in the second rank in comparison with the improvement 204 DISEASES OF THE RESPIEATOEY ORGANS in respiration, that by both the bath and the pack the febrile temperature is at the same time reduced. In the treatment of the lobular pneumonia of children a wet pack including the whole body is the best remedy. A sheet is dipped in water, wrung out, and wrapped around the whole of the patient except his head and arms. Outside of this is to be placed a dry woolen blanket or a layer of oiled muslin. The temper- ature of the water employed should be 68° to 77° (16° to 20° R.). The higher the fever the colder should the water be, and the oftener, say every hour or two, must the pack be renewed. In milder cases and at night it may be allowed to remain for three or four hours. The beneficial influence of the pack is shown not only by the temperature, but still more by the respiration. It is often strik- ing to see how much quieter the child becomes in the pack. • If the breathing, despite this remedy, remains unsatisfactory, and the patient becomes more and more stuporous, the treatment must be changed to lukewarm baths of a tem- perature of 77° to 86° (20° to 24° R.), with douchings of colder water. It is sometimes advisable in severe cases to add to the water employed for bathing or for the wet pack a few handfuls of mustard. The stimulation thus exerted upon the skin is quite marked. Among external applications to the chest, besides mustard plasters and poul- tices, dry cups are to be mentioned, which often do very good service in strong, older children, and especially in adults. We never need to use local blood-let- tings, however, in catarrhal pneumonia. Of internal remedies, expectorants are most used. Chief among these are ipecac, apomorphine, senega, and benzoic acid. This last is particularly useful in the lobular pneumonia of children. In strong children the abundant collec- tion of mucus in the bronchi may sometimes be relieved by the administration of an emetic, but we seldom need to resort to this. We should also be cautious in the use of narcotics. Stimulants (camphor, wine) must be used in severe cases. Antipyretics may be given to reduce the temperature, but if cool packs be used antipyretics can be wholly dispensed with. Inhalations or sprays are quite valueless in lobular pneumonia, yet it is recommended to keep the air in the sick- chamber constantly moist by hanging up wet towels, or by sprinkling with water. The room should also be as large and as well ventilated as possible. The general hygienic treatment is of the greatest importance. One of the most important duties, of which the physician must always be mindful, is to keep up the patient's strength by sufficient and proper food. When convalescence sets in, complete restoration to health may be materially furthered by going to a suitable place in the country. CHAPTER V CROUPOTJS PNEUMONIA {Lung Fever. Lobar Pneumonia. Fibrinous Pneumonia. Pleuro-pnevmonia) Croupous pneumonia is a sharply defined febrile disease of the lungs, which, in the great majority of cases, displays a distinct individuality in its clinical, anatomical, and usually, also, its setiological relations. Among the severe acute diseases it is decidedly one of the most important and frequent, and it is univer- sally familiar even to the laity under the names of pneumonia or inflammation of the lungs. In most cases this disease appears quite suddenly, and often, appar- ently without any special cause, in persons up to that time in perfect health. Such cases are described as primary, genuine, or frank pneumonia. On the other CEOUPOUS PNEUMONIA 205 hand, a case of croupous pneumonia will soinetimes occur as a complication of all sorts of other diseased conditions (secondary pneumonia). The clinical picture of pneumonia in these latter cases, however, is usually obscure and not well characterized, and consequently the following description is especially applicable to the primary form of the disease : .Sitiology. — The thought that croupous pneumonia might be an acute in- fectious disease had impressed the majority of physicians for a considerable length of time, but this suspicion did not receive satisfactory substantiation until the more recent investigations in bacteriology had been made. For instance, Friedlander demonstrated a special form of bacillus in lungs affected with pneumonia. Then, later, A. Frankel, and, soon after him, Weichselbaum, proved that while this " pneumonia bacillus of Friedlander " is perhaps to be regarded as the cause of croupous inflammation of the lungs in a few cases, yet in the overwhelming majority of instances the particular setiological factor is the so- called diplococcus pneumoniae (diplococcus lanceolatus capsulatus). The pneumonia diplococcus is characterized by its lancet-shaped outline (" like the flame of a candle "), and its frequent arrangement in pairs, the individuals of each pair having usually their broad ends apposed. Very often there are short chain-forms. The pairs of diplococci are usually surrounded by a delicate capsule. This is particularly common in preparations of the sputum. We have not space to describe particulars as to the pure cultures of the pneumococci upon agar and similar media. Pneumonia diplococci are among the most widely distributed of pathogenic organisms. They produce severe disease not only in the lungs, but in many other organs. With regard to the development of the pneumonic infection, it is a par- ticularly interesting fact that these diplococci have been not infrequently found in the mouths of healthy persons. This suggests the thought that the germs are drawn into the lungs with the inspired air, and there settle and proliferate when the conditions are especially favorable — for instance, if the resisting powers of the organism have been impaired, or perhaps if the diplococci are especially virulent. In animals the injection of diplococci into the lungs almost always excites pneumonia, but yet it is doubtful whether the incidence of the disease in man always bears out the surmise above mentioned. The severity of the con- stitutional disturbance at the very onset of many cases certainly justifies the supposition that at least often the infection takes place through the blood, and that the pathogenic organisms are carried to the lungs by way of the blood- vessels. Diplococci have been repeatedly found in the blood of pneumonia pa- tients, and the injection of diplococci into the subcutaneous cellular tissue of animals, particularly rabbits and mice, invariably excites a violent and fatal con- stitutional infection (so-called sputum-septicsemia). Certain clinical facts suggest that perhaps in individual cases there may be other modes of infection; for instance, by way of the intestine in cases with well-marked intestinal symp- toms. Starting from the lungs, the diplococci may invade the pleura, less often the pericardium, the meninges, and other organs, so that they are invariably deraonstrable in the pus of cases of meta-pneumonic empyema, pericarditis, and meningitis. From a clinical point of view their almost invariable presence in pneumonic expectoration (Fig. 26) is of the greatest importance. They can be easily demonstrated by the staining of a dried preparation with gentian-violet, although for absolute certainty of diagnosis further investigation is required. Supposing the infectious nature of pneumonia to be certain, all the other .alleged causes may of course be regarded as at most " predisposing causes." The old opinion, which is yet current, that pneumonia is due to catching cold, is to be received with great limitations, for croupous pneumonia is very frequently seen independently of any such influence. In many cases it will be found that 206 DISEASES OF THE EESPIEATOEY OEGANS an exposure to cold immediately preceded the commencement of the disease; but in these instances the cold is probably to be regarded merely as that circum- stance which promoted the occurrence of the infection, possibly because of the resultant injury to the bronchial and pul- monary epithelium. This explains the fact that pneumonia is especially frequent in certain classes, for instance, among day- laborers and soldiers. With regard to the so-called " traumatic pneumonia," the state of the case is similar to that of pneumonia due to cold. Patients from the laboring classes sometimes assert that they were taken ill as a result of heavy lifting or of a blow on the chest, but in such cases the subsequent FIG. se.-Pneumonia dipiococci. (After ^titch in the side was probably not the re- vierordt.) sult of the injury, but a symptom of the disease which had previously begun to de- velop. But still, in some few cases it may be that a preceding trauma injures the pulmonary tissue in such a way as to promote the occurrence of the infection. It is a strong argument in favor of our conception of pneumonia as an acute infectious disease that it may rarely be endemic. Extensive endemics of pneu- monia, usually of quite a malignant character, have been repeatedly observed in single buildings, especially in barracks or prisons, as well as in tenement houses and other localities. It is possible that precisely these severe cases of endemic pneu- monia are setiologically different from the ordinary croupous form and occasioned by some other pathogenic organism; but it is also true that the diplococcus of pneumonia itself appears to vary greatly in its virulence. Pneumonia does not, as a rule, show a decided epidemic character. In a large population sporadic cases occur at any season. It has been observed, how- ever, that the disease may become very frequent or almost completely disappear, and then again for a time be decidedly prevalent. In a limited way, therefore, it is quite proper to say that there are actual epidemics of pneumonia, and these, again, differ from one another in special peculiarities, particularly in their com- paratively benign or malignant character. Here again, no doubt, an important part is played by the varying virulence of the dipiococci which we have already referred to, which is also very evident under the influence of different modes of artificial cultivation of the organism. Most attacks occur in the winter or spring months, without any necessary relation, however,~between the frequency of pneumonia and the occurrence of especially bad, wet, or cold weather. Individual predisposition plays an unmistakable part in the disease, as we must suppose that it does in all infectious diseases. Like facial erysipelas and acute articular rheumatism, pneumonia is one of those diseases which is prone to attack the same individual several times. There are persons who have had acute pneumonia four or five or even more times in their lives. We can not affirm with certainty that the liability to pneumonia is due to a special bodily constitution. The strongest and most robust often fall ill with it, and, on the other hand, weak and delicate people, with a tendency to phthisis, are frequently attacked. Drunkards seem to have a special predisposition to the dis- ease, but of course it is exceedingly hard to give any definite statistics upon this point. . Pneumonia occurs at any time of life, most frequently in youth or middle age ; but it is by no means rare in early childhood, and also in more advanced years up to sixty or seventy. In general it is observed rather more often in men than in women. CEOUPOUS PNEUMONIA 207 [Defective house drainage seems to be a predisposing cause of pneumonia in some cases. A careful inspection of the local sanitary conditions is desirable, especially where more than one case occurs in a house.] Pathological Anatomy. — The anatomical process in croupous pneumonia con- sists in the formation of a hsemorrhagic, coagulable " fibrinous " or " croupous " exudation into the pulmonary alveoli and the smallest bronchi. The develop- ment of the exudation usually extends over one or more lobes to their whole extent, and, as the alveoli and finer bronchi are completely filled by the tough exudation, the spongy lung, filled with air, is changed to a firm tissue, devoid of air, except as it is penetrated by the large bronchi. Since Laennec's day we distinguish three stages in the development of the pro- cess. In the first stage (stage of inflammatory engorgement, engouement) the lung is very hypersemic, dark red, and the air contained in it is even now much diminished, but not entirely absent. The alveoli are filled with an abundant exudation, already hemorrhagic, but still fluid and not coagulated. In the second stage (stage of red hepatization) the coagulation of the exuda- tion is complete, and the lung has become throughout of the consistence of liver. The hepatized lung shows a somewhat increased volume, and is strikingly hard. The surface of the section has a red and manifestly granular appearance, which is due to the projection of the numerous little fibrinous plugs situated in the alveoli. With the knife we can scrape ofl^ a tenacious, creamy, grayish-red fluid from the surface of the section. In the small bronchi, divided by the knife, we find characteristic tubular bronchial casts. In the third stage (stage of yellow or gray hepatization), which gradually develops from the second, the red surface of the section changes to a yellowish- gray color, often mottled, while the lung grows anaamic and the exudation poor in red but rich in white blood-corpuscles. The consistency of the lung is still dense but more friable. The fluid scraped from the surface of the section is more abundant, milky, and puriform. The recovery from the process begins as the exudation becomes fluid. The fluid is in part absorbed and in part coughed up. It is not necessary for every pneumonia to go through all three stages com- pletely. In mild cases the process may stop sooner and recovery begin. Concerning the finer histological processes in croupous pneumonia, the pri- mary change is probably to be found in the injury and partial destruction of the epithelium in the alveoli and smallest bronchi, produced by inflammation due to the specific causes of the disease. As in every croupous inflanunation of a mucous membrane (see the chapter on diphtheria), a coagulable exudation is formed on the surface of the alveoli and smaller bronchi after the destruction of the epithe- lium. With the microscope we see the fibrinous net-work of the exudation filling the alveoli. Between its meshes lie numerous red blood-corpuscles — red hepatiza- tion. Where there is any of the alveolar epithelium left, we often notice active proliferation — increase and growth of cells. Later on the white blood-corpuscles increase, migrating from the vessels into the exudation — yellow hepatization. The red blood-corpuscles are dissolved unless they are removed by expectoration. The fibrinous exudation is also gradually dissolved as the result of chemical changes not yet clearly understood (peptonization of the albuminous sub- stances?), and is absorbed like the cells. The regeneration of the missing epi- thelium comes from the epithelium that has remained intact, and with that follows a gradual and complete restitutio ad integrum. The whole process is comparatively brief, usually running its course in a week or ten days. The most frequent termination is in complete recovery. The other methods of termination, as well as the complications in other organs, will be spoken of in connection with the clinical symptoms. We may here mention 208 DISEASES OF THE EESPIEATOEY OEGANS simply that the pleura over the affected portion of the lung takes part in the inflammation, without exception, as soon as the disease reaches the periphery, and a fibrinous pleurisy, which is not very intense, may then be recognized; hence the former use of the terms " pleuro-pneumonia " and " peripneumonia." Croupous pneumonia usually spreads rapidly over a great part of the lung. It is very often quite sharply limited to a single lobe — " lobar pneumonia " — so that the septum of connective tissue between two lobes also forms a strict boundary between pneumonic infiltration and healthy lung tissue ; but this boundary is by no means insurmountable, and quite frequently several lobes are wholly or in part attacked by pneumonia. According to all statistics, the lower lobes are more frequently affected than the upper. Isolated disease of the right middle lobe may occur, but it is much rarer than pneumonia of the upper lobes. Of the two lungs, the right is attacked with decidedly greater frequency than the left. We have ourselves seen, in 244 cases, 137 on the right, 86 on the left, and 21 in which both lungs were attacked to a great extent. Simultaneous affection of the lower lobe on one side and the upper lobe on the other — quite a rare occurrence — is termed " crossed pneumonia." General Course of the Disease. — In spite of the numerous modifications which the course of pneumonia may undergo in individual instances, we can still call pneumonia a typical disease, considering the great majority of cases. The sub- jective and objective symptoms dependent upon the local affection of the lung usually, but not always, take the chief place among the clinical phenomena. In this, pneumonia differs from many other infectious diseases, such as typhoid, in which the local organic disease is subordinated to the general infection. Pneumonia usually begins quite suddenly. In the majority of cases it starts with a pronounced chill of half an hour to an hour's duration, or at least with a marked and prolonged chilliness. The initial chill may attack the patient while in the best of health. Many patients are able to tell almost the very hour when, having been previously in perfect health, they were attacked by disease. The chill comes on in the daytime, in the evening, or even in the middle of the night, after a previously quiet sleep. At the same time the patient almost always feels as if a severe illness were beginning. Almost at once he is obliged to give up work, has violent headache, and loss of appetite. ISTot infrequently there is a single initial act of vomiting. Sometimes there are at once pulmonary symptoms, such as a stitch in the side and cough. Usually, however, these phenomena do not develop until later (vide infra). In other and somewhat rarer cases the beginning of pneumonia is more grad- ual. A prodromal stage of a few days, or even longer, precedes the severe illness. The symptoms are either of quite a general and indefinite nature, consisting of malaise, dullness, loss of appetite, and headache, or the prodromal symptoms point more strongly to a pulmonary affection. The patient complains several days, or even weeks, before the onset of the severe disease, of cough, thoracic discom- fort, slight dyspnoea, and similar symptoms. At the same time it is not possible to determine certainly whether these prodromata are caused by an already existing pneumonia or not. It is undoubtedly true that in most cases we have merely a simple bronchitis which furnishes a favorable soil for the develop- ment of pneumonia ; but perhaps the initiatory bronchitis may, in some cases, itself be an effect of the diplococcus infection, already begun, but not yet com- pletely developed. The subjective symptoms in the chest begin shortly after the onset of the disease, often on the very first day, but in other cases later. The patient has a stabbing pain in his side whenever he draws a deep breath; the respiration, therefore, becomes superficial and accelerated, and often somewhat irregular; his speech is interrupted by frequent pauses. In the further progress of a severe case CEOUPOUS PNEUMONIA 209 the dyspnoea becomes extreme and the respirations very frequent. With the stitch in the side is associated a desire to cough. The cough is painful, and hence short, half suppressed, and quite frequent and troublesome. From the second day the expectoration may assume its characteristic viscid, rusty, hsemor- rhagic appearance. Physical examination gives on percussion and auscultation the signs to be described more fully below. These are rarely to be found on the first day, but more frequently on the second, and sometimes not till later. In well-marked cases the severe constitutional symptoms persist or grow worse. We observe general weakness, headache, and complete loss of appetite. Some- times there are marked nervous symptoms, such as restlessness, wakefulness, stupor, and delirium; herpes appears on the lips or nose; the bowels are slug- gish, or, again, they may be loose; the urine is concentrated, and very often it contains a small amount of albumen. Almost always the pneumonia is associated with high fever. The typical •character of the disease and the peculiarities of the individual case are always well shown by the temperature chart. As the bodily temperature rises there is a corresponding increase in the frequency of the pulse. The course varies greatly according to the previous individual circumstances, the severity of the disease, and the existence of complications. In the majority of cases, after a comparatively short duration, the disease takes a favorable turn. The beginning of improvement is often sudden, like the onset of the disease. After the symptoms have lasted for some five to seven days, or in rarer cases a shorter or a longer time, at a constant height or with increasing intensity, there occurs in the regular course of the disease a critical decline of the fever — fre- Cjuently associated with quite a copious perspiration — and with that a very rapid improvement of all the other symptoms. In a short time complete recovery follows. In other cases, however, the course is not so favorable. The disease may have a fatal termination. In a third small class of cases the disease finally takes a protracted course, which is usually due to the occurrence of sequelae in the lungs or pleura. To this brief sketch of the disease we must append a description of the special symptoms. Description of Single Symptoms and Complications 1. Symptoms on the Part of the Lungs. — First among the subjective symp- toms comes the characteristic painful feeling or " stitch " in the side. This probably always has its origin in the dry pleurisy which accompanies the pneu- monia. It is therefore absent in the cases of central pneumonia (vide infra). In pneumonia of the lower and right middle lobes the pain is usually more severe than in pneumonia of the upper lobes. One result of the stitch in the side is the difiiculty, or even the impossibility, of deep inspiration. Hence the patient's dyspnoea is considerably increased, and this explains the incongruity between the shortness of breath and the relatively slight extent of the pneumonia in many oases. If the pneumonic infiltration of the lung is extensive, of course the dyspnoea of the patient is also referable in part to the diminution of the respira- tory surface. The subjective feeling of difficulty of breathing is prominent in the majority of cases, and it may become most distressing. Cough is one of the most constant symptoms in pneumonia, and is usually very painful ; hence the patient often tries to suppress it. Expectoration is apt to be very difficult at the onset of the disease, from the viscidity and scanty amount of the sputum; hence severe and distressing paroxysms of coughing are some- times observed. The cause of the cough is probably not to be found in the affec- tion of the alveoli, but in the co-existing bronchitis. The irritation of the pleura 14 210 DISEASES OF THE EESPIEATOEY ORGANS may also set up a reflex cough. In rare cases cough is entirely absent in pneu- monia. Except in the cases of limited or late localization (vide infra), we ob- serve this absence of cough chiefly in the pneumonia of old or very v^eak people^ and also, what is of practical importance, in the drunkard's pneumonia associated with delirium tremens. The pneumonic expectoration is so characteristic that we can often make the diagnosis of croupous pneumonia from this alone. It consists of a very tough viscid mucus, which sticks fast to the bottom of the cup even when inverted, and contains an intimate admixture of blood, which gives it a more or less pronounced red or yellow hsemorrhagic color. In individual cases there are numerous grada- tions. We usually call the pneumonic sputum " rusty," or " brick-red," or of a " prune-juice color," etc. Sometimes it has only a slight reddish or yellowish tint, and sometimes it consists almost entirely of blood. Often the sputum is very frothy. In some cases it assumes a peculiar grass-green [" green-gage "] color, which is due to a change in the blood coloring-matter, or to a mixture with bile pigment in " bilious pneumonia." The red color of the sputum, as microscopic examination shows, is due to numerous red blood-corpuscles, many of them still well preserved, mixed with it. They are, however, in part dissolved, and hence cause the uniform red color of the sputum. Separate spots containing much blood are often seen in it. Besides the red blood-corpuscles, the microscope shows numerous partly swollen or fatty-degen- erated pus-corpuscles. We also see long threads of mucus; sometimes large, round, pigmented cells (alveolar epithelium?) ; and finally, in rare cases, ciliated epithelium and crystals of h^matoidin. Frankel's diplococci are, as we have said, almost always easily demonstrable in the expectoration, and of course numerous other bacteria besides. We have still to mention the bronchial casts as important constituents of pneu- monic sputum. Since they are usually rolled up together, we may not find them except by spreading out the sputum in water. They consist of the most beautiful casts of the small bronchi, with many dichotomous divisions, and are a product of the croupous inflammation extending into the bronchi. The casts of the smallest bronchi are sometimes found in the form of " spirals," like those in asthmatic bronchitis (see page 184). The amount of the pneumonic sputum is, as a rule, not very considerable, but it differs a good deal in different cases. The chemical examination of the sputum has so far given no remarkable results. The amount of common salt contained in it is quite considerable. In many cases the pneumonic expectoration is absent, either because there is no cough or because the exudation is firmly coagulated and is absorbed with- out ever liquefying. Sometimes it is very tough and slimy, but without any admixture of blood; in other cases the sputum is simply catarrhal, when present at all, and then, of course, it comes not from the parts infiltrated with pneu- monia, but from the catarrh of the larger bronchi. In many severe cases the hsemorrhagic expectoration soon assumes more of a purulent character. We often find simple catarrhal sputum, too, besides the characteristic pneumonic sputum. The pneumonic sputum is sometimes seen in the first or second day of pneu- monia, but it may not appear until later. With the beginning of resolution it gradually loses its characteristic appearance. The expectoration then becomes less tenacious and simply muco-purulent, and finally disappears entirely. Physical Examination. — Inspection shows no especial anomaly in the general contour of the thorax. A marked bulging of the affected side occurs only when there is also abundant effusion into the pleural cavity. The action of the thorax in respiration is very important. With a. limited pneumonia we often notice CEOUPOUS PNEUMONIA 211 a very marked delay and limitation of motion of the affected side on inspiration. This is due in part to the pain in the side, which comes on with every deep inspi- ration, and also, in extensive pneumonia, of course, to the physical conditions resulting- from the anatomical changes. The unaffected portions of the lung act all the more forcibly. The acceleration of respiration is very striking, its frequency increasing to thirty or forty, or even more, a minute. We have repeatedly counted sixty res- pirations in adults, even in cases that finally resulted favorably. The breathing is shallow, but yet, in all severe cases, labored, and often also irregular, as a result of pleuritic pain or cough. We see the inspiratory contraction of the sterno-cleido-mastoids and scaleni in the neck, and often in the face a marked dilatation of the nostrils on inspiration. If there is marked dyspnoea the patient sometimes reclines in bed with the upper half of the body raised. The cheeks and lips are cyanotic. There is often a sharp contrast between the pale portions of the face near the corners of the mouth and the striking feverish and slightly cyanotic flush of the cheeks. The results of percussion are directly dependent upon the changed physical condition in the lung, due to the anatomical processes. In the beginning of pneu- monia, so long as the total amount of air in the lung remains but little altered, the percussion-note is clear, but when the elasticity and tension of the tissue in the diseased portion of the lung diminish, the resonance often becomes quite tympanitic. With increased exudation into the alveoli and smallest bronchi the amount of air in the lung constantly grows less, and therefore the percussion resonance becomes very dull, but it usually retains its tympanitic timbre. Since the pneumonic lung is rarely absolutely deprived of air — for a certain amount is always left in the larger bronchi — the percussion resonance seldom becomes so completely dull or flat, as it does, for example, with a large pleuritic effusion. The sensation of resistance upon the percussion of a pneumonic lung is likewise much less marked than over a pleuritic exudation. A marked sense of resistance implies, therefore, an unusual degree of involvement of the pleura in the inflam- mation. As soon as the absorption of the exudation begins, the volume of air in the lung increases, and the percussion-note becomes clearer, but remains for some time still markedly tympanitic, until the lung has regained its normal tension and elasticity. We have also to note that the intensity of the dullness m croupous pneumonia is sometimes subject to quite marked variations, since the secretion retained in the bronchi is at one time abundant and at another, after expectoration, scanty. The extent of the dullness or of the tympanitic resonance is naturally depend- ent upon the extent of the anatomical process. Small and central infiltrations may entirely escape detection by percussion. Auscultation is of almost greater importance than percussion in the detection of a beginning or limited pneumonic infiltration. The auscultatory signs depend upon the presence of the pneumonic exvidation, and upon the consequent trans- formation of the lung into a firm tissue devoid of air except in the larger bronchi. In the beginning of the disease we hear over the affected portions coarse or fine rales, and very often, too, the characteristic crepitant rale on inspiration discov- ered by Laennec. This arises because the walls of the alveoli and smallest bron- chi, which are glued together by the viscid exudation, are torn apart at each inspiration. The crepitation, however, is neither pathognomonic of pneumonia, nor heard in every case of pneumonia. With increasing infiltration, bronchial breathing replaces the vesicular. The bronchial breathing in pneumonia is usu- ally very loud, sharp, and close to the ear. When the infiltration is very com- plete there is often to be heard a pure and loud bronchial respiration, without any adventitious sounds; but of course there are often heard, besides the bronchial 212 DISEASES OF THE EESPIRATOHY ORGAJ^S breathing, high-pitched, moist rales in greater or less abundance. It is especially- true that with the eomniencement of " resolution " — that is, as soon as the exuda- tion becomes more fluid, abundant moist rales reappear, enough to obscure more or less the bronchial respiration. These rales are, for the most part, rather coarse, moist, and have a musical character. Often we hear at this time the character- istic crepitant rale again (crepitus redux). The rales gradually disappear, the respiratory murmur loses its bronchial character, becomes harsh and indefinite, and finally is normally vesicular once more. We often hear a few rhonchi over the unaffected portions of the lungs. On the diseased side, the respiratory murmur is often more or less diminished because of the diminished respiratory movenaent. Otherwise respiration in the unaffected portions of the lungs is usually completely normal. The auscultatory signs just described undergo an important change if the larger bronchi leading to the affected portion of the lung are completely plugged by the secretion, as they are quite liable to be. The respiratory murmur may then almost entirely disappear, and we hear, perhaps, only here and there a few obscure rales. Since such a plugging may be very transitory, we understand why in one day, over the same portion of the lung, we hear first loud bronchial breath- ing and rales, and then quite obscure and diminished breathing. Wherever there is bronchial breathing, we hear marked bronchophony. Some- times one can discover a beginning pneumonic infiltration by bronchophony sooner than by any other physical sign. The vocal fremitus persists or is some- what increased over a pneumonic lung so long as the large bronchi are open; but when they become plugged, as they are quite liable to be, the vocal fremitus is weakened or wholly abolished; and again, the voice sounds are weakened whenever there is a considerable amount of pleurisy accompanying the pneu- monia. We have yet to ad5, a few remarks about the parts of the lung in which we may expect first to perceive the physical signs of pneumonia, especially the aus- cultatory signs. In the first place, we should never neglect to examine carefully the lateral por- tions of the thorax and the axillary region when we suspect a developing pneu- monia. We often find the first rales here in pneumonia of the lower lobes. The first signs of infiltration may be found in the posterior middle portion of the thorax — that is, in the upper part of the lower pulmonary lobes — and thence they extend downward. Pneumonia of the upper lobes begins just as frequently behind in the apices as in front in the infra-clavicular fossae. Isolated jDneumonia of the right middle lobe also occurs, to be made out in front, on the right, between the fourth and sixth ribs. This may remain confined to the middle lobe, or extend to the neighboring lobes. Few general statements can be made about the nature or the rapidity of the extension of pneumonia, since in these respects the greatest differences are observed. The infiltration may remain confined to a small portion of the lung, or again it may spread over a whole lobe or more in a short time, even in one or two days. We call the pneumonia, whose constant extension by contiguity we can follow from day to day, wandering pneumonia (pneumonia migrans), or, from a purely superficial resemblance, which has given rise to many wrong ideas, " erysipelatous pneumonia." In these cases all the signs of resolution are present in the pai-ts first attacked, while the parts aifected later are found still at the height of the disease, or in the beginning of infiltration ; but we may also find in the autopsies of wandering pneumonia the parts of the lung affected later in a more advanced stage (gray hepatization) than the parts first attacked, which are still in the stage of red hepatization — that is, the inflammatory process in such cases seems to go through a more rapid evolution in the portions of lung CEOUPOUS PNEUMONIA 213 later affected. Wandering pneumonia is almost always severe and quite pro- tracted. Pneumonia in rare cases progresses by leaps. Such cases have been termed erratic pneumonia. In severe cases it is not unusual for both lungs to be affected. We then find the pneumonia either in both lower lobes, or in the lower lobe on one side and the upper lobe on the other side. 2. Symptoms on the Part of the Pleura. — As we have already mentioned, every case of pneumonia which reaches to the surface of the lung is associated with a fibrinous pleurisy, and, furthermore, it is not impossible that there should be an infection of the pleura without any direct extension from the neighboring pulmonary tissue. In many instances, the mild pleurisy which attends a pneu- monia causes no physical signs. On the other hand, the pain in the side in pneu- monia is probably always referable to the involvement of the pleura. In other cases the dry pleurisy attracts attention by the clearly audible friction, which may often be very loud, and is sometimes appreciable to the touch, if the hand is laid upon the side. We rarely hear the pleuritic friction sound in the begin- ning of pneumonia, but more frequently in the later stages, and perhaps not till many days after the crisis has taken place. The cases in which pleurisy with effusion complicates pneumonia are more im- portant. This may occur quite early. The abnormality of the clinical course is shown in these cases, as a rule, by the irregular behavior of the fever. There will be no typical crisis, but instead a slow lysis; or after the crisis occurs, the temperature will rise again. In most instances the exudation is serous, but it may be purulent (metapneumonic empyema). Long-continued fever should arouse suspicion of an empyema. In the pus of such cases of empyema the pneumonic diplococcus above mentioned (see page 205) has been repeatedly found. In two fatal cases the author has seen a hsemorrhagic pleurisy with a large amount of coagulated blood in the pleural cavity. The diagnosis of pleurisy with effusion complicating pneumonia is seldom difficult. The percussion resonance is duller, and the sense of resistance is more marked than in pure pneumonia (vide supra). The respiratory murmur and the vocal fremitus are constantly diminished and finally entirely absent. The symp- toms of pressure on the neighboring organs and cavities, the heart, the liver, and the semilunar space (see page 287), are especially important because they are most unequivocal. An exploratory puncture with a Pravaz's [hypodermic] syringe, that has been carefully cleansed and disinfected, gives a certain and safe method of recognizing pleurisy in doubtful cases. When there is suspicion that an empyema has begun, an exploratory puncture is imperative. A moderate degree of pleurisy may somewhat delay the course of the disease, but it has no special significance. Large effusions, however, may decidedly in- crease the difficulty in respiration and the duration of the illness. Again, the pneumonia may recover, leaving the pleuritic effusion quite undisturbed. In pneumonia of an upper lobe, too, the pleurisy may develop below and lead to an effusion there, while the lower lobe itself remains quite free from pneumonia. Metapneumonic empyema invariably requires surgical intervention, but after operation it almost always pursues a rapid course to recovery. 3. Circulatory Apparatus. Blood. — The pulse is accelerated from the begin- ning of the disease. In cases of moderate severity its frequency reaches 100 or 120; and, in very severe cases, a still higher rate up to 140 or 160 is seen, and is always a dangerous symptom. This high rate of the pulse does not have as bad a significance in children as it does in adults. The consideration of the quality of the pulse is important. Smallness, weakness, and irregularity of the pulse are of bad omen as symptoms of the onset of cardiac weakness. The attacks of col- lapse, which sometimes come on quite suddenly in severe cases of pneumonia as 214 DISEASES OF THE EESPIRATOEY OEGANS in other acute diseases, are especially dangerous. They occasion sudden weak- ness of the heart with a very- small and frequent pulse. The temperature sinks to subnormal, 95° to 93° (35°-34° C). The peripheral parts, the nose and ex- tremities, become cool, pale, and somewhat cyanotic. The general weakness and prostration become extreme. The collapse may be recovered from, especially with timely assistance, but patients may die in it. Pericarditis with fibrinous or sero-fibrinous exudation is one of the most serious cardiac complications. This can always be explained by a direct conduc- tion of the inflammatory process from the neighboring pleura, and is therefore somewhat more frequent in left-sided pneumonia than in right. It is a serious matter. Its diagnosis is seldom difficult if we make a careful physical examina- tion of the heart, but with very severe and extensive symptoms in the lungs a complicating pericarditis may be overlooked. A slight fresh endocarditis is sometimes found at the autopsy, but it has no clinical significance. Diseases of the cardiac muscle, especially fatty and paren- chymatous degeneration, may be discovered post mortem, but they are by no means frequent. In very weak persons, drunkards, etc., who die of pneumonia, we sometimes, indeed, find the heart remarkably flabby, with the right ventricle dilated, but in many cases of pneumonia we find the muscle of the heart at the autopsy perfectly normal. Here we almost always have to do with conditions of the heart which existed previously to the pneumonia, and merely became promi- nent during its course. When persons of vigorous and healthy constitution die of pneumonia, as, indeed, seldom occurs, the myocardium is found at the autopsy essentially healthy. It must be emphatically stated that our present knowledge does not enable us to establish before death any positive relation between the his- tological condition of the cardiac muscle and its functional ability. Frequent experience has made us certain of this fact. With regard to the blood, there is usually a well-marked leucocytosis in pneumonia. The exact count shows, not infrequently, twenty to twenty-five thousand or more of leucocytes in a cubic millimetre. With the crisis of the fever the number of leucocytes also falls abruptly, while in case of a pseudo-crisis theii number remains high. In some instances the leucocytosis is not marked. This is particularly frequent in severe and fatal cases, so that the absence of leucocy- tosis is regarded with some justice as an unfavorable element in prognosis. 4. Digestive Apparatus. — In severe cases of pneumonia the tongue is dry, coated, and quite like the tongue in typhoid. The appetite is also almost wholly lost from the beginning. Vomiting is not infrequent, especially in the begin- ning of pneumonia, and it also occurs later. It is observed with especial fre- quency in the pneumonia of children. Severe symptoms on the part of the intes- tinal canal are rare. As a rule the bowels are constipated, but there are also cases in which diarrhoea is so troublesome that we must believe that the mucous mem- brane of the intestine is considerably involved in the morbid process (vide infra). The complication of pneumonia with jaundice has a certain significance, but its causes are not always very clear. It is apparently sometimes due to an accom- panying catarrh of the duodenum. In other cases the veins of the liver, dilated from stasis, may exert a pressure on the bile-ducts. Slight jaundice has no special significance, and is frequent, even in mild cases; a marked jaundice, however, is seen only in severe cases, especially in drunkard's pneumonia. We call such cases, associated with jaundice, "bilious pneumonia." They have often other severe gastro-intestinal symptoms, such as vomiting, diarrhoea, and meteorism, and severe nervous symptoms, such as stupor and delirium. The liver may be somewhat enlarged, usually because of passive congestion. The spleen is often moderately swollen, particularly in severe cases, just as in other infectious diseases (acute splenic tumor). CROUPOUS P]SrEUMO:N"IA 215 5. Kidneys and Urine. — The infectious character of pneumonia is also shown hy frequent involvement of the kidneys. Careful examination of the urine almost always shows a trace, or even a considerable amount, of albumen. However, this . is very seldom of serious import, and vanishes promptly after the crisis. In many instances the changes in the urine are so considerable as to show an acute nephritis. There is a large amount of albumen, with casts, epithelium, and blood, in the urine. But even these cases of genuine pneumonic nephritis, which usually develop about the third to the sixth day of the illness, seldom prove to be serious, and scarcely ever result in oedema, uraemia, or other complications. Usually they get well rapidly. In one single case the author has observed a transition into chronic nephritis. The way in which pneumonia causes albuminuria and ne- phritis — between which no sharp dividing line can be drawn — is probably by the production and excretion of toxines. Great weight was formerly laid upon the diminution of the chlorides in the urine in pneumonia. In fact, the precipitate of chloride of silver, when we put a drop of solution of nitrate of silver into the urine, may be very slight or entirely absent. The chief cause of this diminution of the chlorides is the small amount of nourishment taken by the patient, but we must also bear in mind the large amount of chloride of sodium contained in the pneumonic exudation, and the retention of the chlorides in the body. Great significance was also formerly ascribed to the abundant sediment of sodium urate (exceptionally, uric acid) which is often noticed on the day of the crisis. This is known as brick-dust sediment (sedimentum lateritiurn), and is perhaps due in part to a material increase in uric acid (query : through de- struction of the large number of leucocytes in the blood?), but certainly in greater part to the fact that the conditions for the deposition of sediment are especially favorable on the day of the crisis. The urine is scanty in amount because per- spiration is so excessive, and hence it is concentrated and relatively very acid. It is, therefore, natural for the urates contained in it to be deposited in the form of a sediment. Pneumonia, in common with most of the other acute febrile diseases, is at- tended with an increased secretion of urea during the disease. The fact is of theoretic interest that during the resolution of pneumonia the urine often con- tains a demonstrable quantity of peptone, which is, in all probability, due to the destruction of the cells in the pneumonic exudation and their absorption into the blood. 6. Nervous System. — As in every severe febrile disease, nervous symptoms of a mild type are very rarely absent in any case of pneumonia. Among the nervous symptoms are general weakness and dullness, and especially headache, which is often very intense, and is usually increased by coughing. The onset of more severe cerebral symptoms, particularly delirium, is of great importance. Delirium may appear in any case of severe pneumonia, but it is most marked and has peculiar characteristics in alcoholic subjects. This delirium gives the pneumonia of drunkards {vide infra) its characteristic stamp. The usual cerebral symptoms in pneumonia do not correspond with macro- scopic changes in the brain, but result from the poisoning of the body with the toxines of the pneumonia diplococcus; and yet there is also a true cerebral dis- ease which has beyond a doubt a special relation to pneumonia, although it is an infrequent complication. We refer to purulent cerebro-spinal meningitis. This complication is particularly apt to appear at times when an epidemic of cerebro- spinal meningitis prevails, but it has been repeatedly observed at other times. The diagnosis of pneumonic meningitis may be obscured by the severe constitutional disturbances. Factors of importance are : the stiffness of the back and the neck ; the pain in the head and in the nape of the neck ; the stupor, changing to 216 DISEASES OF THE EESPIEATOEY OEGANS 10 deep coma; and, in many cases, optic neuritis, demonstrable by the opbthal- moscope. The termination of a well-marked case of meningitis is probably in- variably fatal, but we may have milder meningeal symptoms in pneumonia, such as pain and stiffness in the neck, followed by complete recovery. — With regard to the development of this meningitis, it is probably to be regarded as a true metastatic inflammation, inasmuch as the pneumonia diplococci have been re- peatedly found in the pus of the meningitis. As to the path which the pathogenic germs take to reach the meninges, we are not yet certain, but suppose that they travel along the lymph-channels of the intercostal nerves into the meninges sur- rounding the spinal cord, and thence further to the membranes of the brain. 7. Skin. — The frequent appearance of herpes in the course of pneumonia is characteristic, and is of diagnostic importance. It appears from the second to the fourth day of the disease, or sometimes later. Its ordinary seat is on the lips, especially at the corners of the mouth, also on the alse of the nose, and more rarely on the cheeks or the ear (herpes lahialis, nasalis, etc.). It has been seen only very rarely on other portions of the body besides the face, for example, on the forearm and the buttock, and in some cases on the cornea and on the mucous membrane of the tongue or gums. The herpes does not always come out all at once, but in fresh crops on successive days. We have several times seen two eruptions of herpes separated by an interval of several days. In repeated instances, under our own observation, herpes labialis, with a fresh rise of tem- perature, appeared some days after the crisis had taken place. Herpes may be ex- tensive in the mildest cases, while it is particularly apt to be scanty or absent in severe cases. We are, there- fore, on the whole, inclined to regard a well-marked eruption of herpes as of favorable prog- nosis. The true cause of the herpetic eruption is unknown. One might think of referring it to the action of toxines, just as in the herpes of other infec- tious diseases, such as inter- mittent and relapsing fevers, and epidemic meningitis. Other affections of the skin are of rare occurrence. We have seen urticaria in some cases. The jaundice occurring in pneumonia has already been described. 8. Course of the Fever (see Figs. 27 and 28). — Pneumonia is, almost without exception, accompanied by a more or less high fever with a very typical course. In the beginning of the fever the tem- perature rises very rapidly to a high point. Even during the initial chill the bodily heat increases from normal to about 104° (40° C.) and over. There are at present no observations to show whether, in the cases of pneumonia that begin gradually, there is also a gradual increase of the fever. During the course of the disease the fever shows on the whole a continuous or remitting character, but there is with this a decided tendency to single deep falls of temperature. Since these at first may easily be taken for the actual occurrence of crises, although later they are proved by the renewed rise in temperature to be a mere 40.0= 39.0° 38.0° 87.0<^ 36.0= SJ^SBJ^^SSSSBS sBiidsJiniHi ■■■■■■ WflHHIIH ■■■-=■■■■■ ■■■■■ ■BBBBBBB "" " Pseudo-crisis. Fig. 27.— Example of the temperature-curve in croupous pneumonia. (Personal observation.) CEOUPOUS PNEUMONIA 21Y 41.0° 40.0' 39.0° 38.0° ■■■■■HI rjil Fig. 28.- -Example of the temperature curve iu " intermitting" pneumonia. ^J:'ersonal observation.) temporary decline in the bodily heat, they are termed pseudo-crises. Pseudo- crises are usually seen in the first days of the disease, but in some cases they appear later and, what is remarkable, they are more apt to appear on those days, such as the fifth or seventh, on which the true crisis is apt to occur. They may be repeated one or more times, giving the fever a decidedly intermitting char- acter. These intermitting pneumonias, so called from ^ ^ the course of the fever, have nothing at all to do with malaria, which fact must be especially noted because of the frequency of erroneous statements. The fever may be decid- edly high in pneumonia, often reaching 104° or 106° (40°^1° C). The highest temperature ob- served by us was 107.8° (42.1° C). This was tem- porary. There is a cer- tain parallelism between the height of the fever and its severity to this ex- tent, that severe cases are often associated with per- sistent and especially high fever. But sometimes the most severe and even fatal cases have a comparatively low temperature — between 101° and 103° (38.5- 39.5 C). The highest temperatures are especially common in the first days of the illness, and yet, in spite of very high fever at the onset, the general course of the disease may turn out to be favorable, for the crisis may occur on the second or third day (inde infra, rudimentary and abortive pneumonia). In severe cases the progress of the disease often stamps itself plainly on the temperature. The pseudo-crises correspond to temporary improvements, and the fresh exacerbations of temperature to the invasion of a fresh lobe of the lung. We have certainly not seen a special rise immediately before the crisis — the so-called perturhatio critica — so often as many statements would lead us to expect. We have seen a gradual decline in temperature quite frequently in the closing days in fatal cases, but the opposite condition also obtains. A marked rise before death is not peculiar to pneumonia, but it does occur when there is a complicating meningitis. The decline of the fever is the most characteristic portion of the pneumonia curve. The fall in temperature usually comes on in the form of a decided crisis. Generally in the night there is a sinking of the temperature with a more or less abundant perspiration, in which as a rule the temperature may reach a sub- normal point — 96° to 95° (36°-35° C). The critical decline is often broken by new and slight elevations of temperature, so that on the morning of the next day there may be a definite increase of fever, the so-called protracted crisis. Only in a comparatively small number of cases does the fever end by lysis, in which the temperature goes down like steps. The duration of lysis is seldom more than three or four days at most. A decline of temperature by lysis is most frequent in severe and protracted cases, in so-called typhoid pneumonia (vide infra), and also particularly in pneumonia migrans. After the final crisis has occurred, the active pneumonic process ceases. The 218 DISEASES OF THE EESPIRaTORY ORGANS day of the crisis is therefore reckoned as the last day of actual illness. The pneumonia makes no advance after that, but resolution and absorption of the exudation and the restoration of the patient's strength still take time. Hippoc- rates knew when the time of the crisis occurs, and that the odd days, especially the fifth and the seventh, have a special significance in regard to it. In an infectious disease that has a typical course there can be nothing strange in the fact that the cessation of fever, to a certain degree, is associated with a definite period of time; but Hippocrates's rule has frequent exceptions. The crisis some- times occurs on the ninth, the twelfth, or the thirteenth day, and even later, and, on the other hand, there are quite short pneumonias of but one or two days' dura- tion {vide infra). In the days following the crisis the temperature, which, as we have said, falls to subnormal, regains its normal height. The pulse, which usually sinks to fifty or sixty during the crisis, when it often shows a slight irregularity, reaches its normal frequency again in a few days. We are quite apt to see, in the days inxmediately following the crisis, a slight temporary increase of temperature again, 100° to 102° at most (38°-39° C), but this has no special significance. In cases which run their course regularly, the signs in the lungs upon ausculta- tion and percussion become normal again in about six or eight days after the crisis. Often the time is even shorter than this, or it may be longer. Abnor- mally delayed resolution will be mentioned below. Special Peculiarities and Anomalies in the Course of Pneumonia 1. Pneumonia in Children. — Besides the common lobular pneumonia there is also a genuine, lobar, croupous pneumonia in children, which is by no means so rare as some authors formerly supposed. An initial chill is seen only in older chil- dren; initial vomiting, however, is very common in children. In many cases severe cerebral symptoms, like convulsions, drowsiness, or delirium, obscure the pulmonary symptoms at first. The further course, the development of physical signs, the fever, and the complications, are quite analogous to the appearances in adults. The pneumonic sputum is only exceptionally obtained for observation in children under eight years of age. In previously healthy children the prog- nosis of croupous pneumonia is almost invariably favorable. 2. Pneumonia in old people is, on the other hand, always dangerous. It may begin suddenly, as in people of middle age, but often it begins more slowly and insidiously. Its course is marked by the speedy onset of great weakness and debility. Nervous symptoms, like delirium, are not infrequent. Often there is fatal weakness of the heart. 3. Drunkard's Pneumonia. — We see croupous pneumonia in drunkards with remarkable frequency. The usually severe and dangerous course of the disease is due to the feeble resisting powers of their impaired organs. It is characterized by delirium tremens, which usually develops in the first days of the disease. The patient's mind is disturbed, he is very restless, constantly tries to get out of bed, and he fumbles night and day with his bed-clothes or night-gown. The alcoholic character of the delirium is shown by the patient's whole manner, the tremor of the hands and tongue, and the cast of his thoughts, which are usually happy but exceptionally anxious and terrified. His mind wanders to his former occupation or his usual boon companions, and the like. He becomes tearful or raving only when forcibly restrained. He may think himself involved in the tavern brawls. The alcoholic delirium is almost always associated with hallu- cinations. The hallucinations of little moving black figures are especially char- acteristic. They are either animals, rats or beetles, or little black men and similar weird shapes, and they give him much trouble. The subjective symptoms ■of pneumonia are wholly in the background. No delirious patient with pneu- CEOUPOUS PNEUMONIA 219 monia complains of cough, pain in the chest, or dyspnoea. Careful objective examination is the only thing that confirms the diagnosis. Very often patients with a happy delirium serve to entertain those about them, until suddenly very severe symptoms arise, and they become somnolent and succumb, with the symp- toms of pulmonary oedema. The prognosis of every case of drunkard's pneu- monia, therefore, is to be regarded as very unfavorable. 4. Pneumonia in Pre-existing Chronic Diseases. — Croupous pneumonia is oc- casionally seen in all forms of chronic disease. It is especially dangerous in persons who are already enfeebled, or afflicted with chronic cardiac or pulmonary disease, such as phthisis or emphysema. The pneumonia which often attacks pa- tients with emphysema is clinically important, since emphysema may render the objective evidence of pneumonia very obscure. The croupous exudation does not completely fill the dilated alveoli ; hence decided dullness and bronchial breathing are absent. 5. Pneumonia with Late Localization — Central Pneumonia. — Cases are quite often seen whose beginning, course, and subjective symptoms correspond through- out to a croupous pneumonia, but in which the objective evidence of pneumonic infiltration evades the most careful examination. The disease begins with a chill, the fever is high, the patient complains of pain in the chest, which is usu- ally slight, there is perhaps herpes, but not till the fourth, fifth, or sixth day can we make out anywhere any bronchial breathing or crepitant rales. In other cases even the crisis may set in before we are able to localize the pneumonia with cer- tainty. In most of these cases we probably have to do less with an actual late localization than with a central infiltration which nowhere approaches the periph- ery, and hence is made out objectively only late or not at all. A careful exami- nation of the sputum is of the greatest diagnostic importance, since it sometimes has a perfectly characteristic appearance in spite of the absence or the indefinite character of the physical signs. If there is no sputum, the diagnosis may of course remain very uncertain. The appearance of herpes and a critical fall in the temperature make the diagnosis of a pneumonic infection probable even in these cases. In one such case the author observed the development of a pleuritic friction rub upon the first day after the crisis, confirming the diagnosis of pneu- monia after the disease had run its course. 6. Rudiinentary and Ahortive Forms of Pneumonia — Unusual Localizations of the Pneumonic Infection. — Particularly at times of a pneumonia epidemic, but also at other times, the author has observed illnesses of short duration but often with high temperature which did not seem like clear cases of pneumonia, although they still were, in all probability, to be regarded as pneumonic — i. e., due to infec- tion with the specific diplococci. Cases of this sort usually begin suddenly with a chill, headache, and high temperature. Generally there is a cough and pain in the chest. Sometimes, however, there are no thoracic symptoms at all. The physician expects pneumonia to develop, but instead, on the first, second, or third day, the fever ceases abruptly, no changes in the lung having been discov- ered. Very often there will be a herpes facialis in such cases, and we doubt not that many instances of so-called herpes fehrilis, or fehris herpetica, are really cases of pneumonic infection, without any other localization than the herpes. In other instances, ujDon careful examination there will be found, at some place in the lungs, a slight crepitation, or limited bronchial breathing ; but the process does not extend; and in a very brief time, after a day or two, the fever ceases (rudimentary pneumonia; abortive pneumonia). In this connection we may remark that the diplococcus infection may be localized in still other places. Thus, for example, we regard it as very probable that many cases of sore throat or acute enteritis, associated with the svidden onset of high fever and with herpes, and especially when seen at the time of an 220 DISEASES OF THE EESPIEATOEY OEGAITS epidemic of pneumonia, are due to diplococcus infection. Associated with these attacks there may also be a late development of pulmonary symptoms. 7. Typhoid Pneumonia — Asthenic Pneumonia.— 'Qj typhoid pneumonia we mean those cases in which, beside the local pulmonary symptoms, which may be either slight or well marked, there are remarkably severe general symptoms. The cases do not often begin as suddenly as ordinary pneumonia, but more gradually, like typhoid. Even at first the general symptoms, such as great dull- ness, loss of appetite, or headache, predominate over the thoracic symptoms. At the height of the disease there is a decided typhoidal state, stupor, delirium, a very dry tongue, great general weakness, and also enlargement of the spleen, and fre- quently mild jaundice, albuminuria, etc. Such cases are to be regarded as pneu- monia with an unusually severe general infection (or intoxication). They some- times occur in epidemics. It is said that pneumonia of the upper lobes shows a somewhat more frequent tendency to severe nervous symptoms than pneumonia of the lower lobes. Eecovery from this typhoid or asthenic pneumonia, which may last two weeks or more, often follows by lysis. Typhoid pneumonia is by no means a sharply defined disease. The term serves merely as a short name for the grave constitutional disturbance. Clinically it is impossible to distinguish it sharply from pneumonia migrans, bilious pneumonia, and other forms. We must await further bacteriological investigations to determine whether there may not be some other special pathogenic organism in many cases of severe character. For instance, Finkler is inclined to regard certain cases of especially severe pneu- monia that seem to be endemic or contagious, as referable to streptococcus infec- tion. In this connection may be briefly mentioned, also, the peculiar and severe pneumonia which is contracted from diseased parrots. On the other hand, it is not improbable that another important factor may be a variation in the virulence of the ordinary pneumococcus. Piieumo -typhoid is to be carefully distinguished from typhoid pneumonia, although from a clinical point of view the diagnosis between them is often no easy matter. By pneumo-typhoid is meant typhoid fever with a localization of the typhoid bacilli in the lungs (see page 14), but it is also true that ordinary croupous pneumonia may occasionally appear as a complication of typhoid fever. 8. Pneumonia with Delayed Besolution. — While the resolution of pneumonia is complete, as a rule, in three days to a week after the occurrence of the crisis, there are cases in which this process demands a much longer time. Not infre- quently, and particularly in severe cases of pneumonia, one sees after the crisis a surprisingly rapid disappearance of all the physical signs, while, on the other hand, recovery is sometimes remarkably slow in apparently mild cases; but this rule is of course not without exceptions. The course of the disease is often enough precisely the opposite. Just what are the conditions upon which the rapidity or the slowness of resolution depends we do not know. Sometimes unfa- vorable constitutional conditions, such as anaemia, debility, phthisical tendencies, and kyphoscoliosis, appear to delay resolution. Sometimes, on the other hand, no such explanation can be found. It seems to us that at certain times all the cases of pneumonia exhibit more of a tendency to delayed resolution than at others, so that it is not impossible that there are variations in the pathological process itself. In many cases of delayed resolution it is our opinion that we have to do with genuine secondary diseases, or a mixed infection in the lungs for the development of which the precedent croupous pneumonia had prepared a favor- able soil. With regard to the symptoms of delayed resolution, there are various forms. In the first place, we see cases where the crisis takes place in the usual way, and the temperature thereafter remains permanently normal. The patients perhaps feel quite well, and are troubled little by thoracic symptoms; nevertheless, the CROUPOUS PNEUMONIA 221 dullness upon percussion remains unchanged, or diminishes at best very gradually, and the bronchial breathing and moist rales can still be heard. All the signs diminish very slowly, sometimes occupying several weeks in their disappearance, and then complete recovery ensues. In a few cases it is striking that, after the crisis, bronchial respiration and dullness persist, while there are scarcely any rales and no expectoration. In these cases it seems as if the pneumonic exuda- tion does not really liquefy at all, and is very slowly absorbed. In other cases there is no distinct crisis, but the fever continues, although lower than at first, and the physical signs remain to a greater or less extent. At the end of two or three weeks, or even still later, the fever slowly ceases, and thereupon normal resonance and vesicular breathing gradually return. In still other cases the patients remain free from fever for the first few days after the crisis has taken place, although the pneumonia is not completely re- solved. Then there appears again a rise of temperature which is mostly mod- erate, 100.5°-103.5° (38°-39.5° C), while the dullness continues and there are an abundance of moist rales and catarrhal expectoration. After two or three weeks the fever gradually ceases and the abnormal pulmonary signs also slowly disappear. In such cases we may indeed suppose that some secondary infection, a sort of secondary catarrhal pneumonia, has developed upon the seat of the croupous pneumonia. The disease may take still another course somewhat dif- ferent from those thus far described, and of this we have seen repeated instances much resembling one another. After the occurrence of the crisis the patient remains for about a week without fever. During this time the dullness and the not very loud bronchial breathing remain unchanged. Then appears a moderate intermitting fever, with elevations to about 103° or 103° (39.5° C). This fever may last two to four weeks, or even longer. Over the affected portion of the lungs are heard either no moist rales or only a very few. Gradually there appears a moderate but distinct contraction of the side involved, then the resonance gradually grows clear, the respiratory sounds louder and vesicular, the fever ceases, and finally health is completely restored. In many other cases of delayed resolution, as we have already said, we see this same striking absence of moist rales and the development of a moderate degree of contraction. Under such circumstances it is often very difiicult to exclude a secondary pleurisy, and we can not make sure except by repeated exploratory puncture. Moreover, it is not exceptional to find delayed resolution and secondary pleurisy both present in the same patient. 9. T ermination of Pneumonia in Phthisis, Contraction of the Lungs, Pulmo- nary Gangrene, or Pulmonary Abscess. — Four terminations of pneumonia are ordinarily mentioned as unusual and anomalous — the termination in " chronic pneumonia," in tuberculosis, in gangrene, and in abscess. Concerning the' termination in chronic pneumonia, we have already men- tioned a process belonging here, the termination in contraction with ultimate recovery. In rare cases the contraction is permanent. The anatomical process consists in the development of pulmonary cirrhosis, with the formation of a large amount of connective tissue. This proliferation, it should be said, takes place not only in the interstitial tissue, but also in the interior of the alveoli by extension from the alveolar walls. Few clinical observations of the fur.ther course of these cases, provided death does not shortly ensue, have as yet been published. When croupous pneumonia is said to terminate in pulmonary tuberculosis, of course the statement can be understood to mean only that the symptoms of tuber- culosis follow immediately upon an attack of pneumonia. When this is the case — it does not occur often — it is probable that the pneumonia attacked a per- son already suffering from tuberculosis, in whom, however, the symptoms did not become evident until after the pneumonia had rvm its course. It may also be 222 DISEASES OF THE EESPIRATORY ORGANS Fig. 29. — Cholesterine crystals. that exceptionally tlie pneumonia furnishes a soil for a secondary infection with tubercle bacilli. Pneumonia results in pulmonary gangrene in rare instances, when the patient is elderly, delicate, or diabetic. Here, too, in our opinion, a new infection, with a foul and putrid substance, must always take place, and this excites the gan- grene. The previous pneumonia furnishes only the occasion for the development of gangrene, and perhaps prepares the soil for the agents of decomposition. The development of gangrene is appreciated clinically (see the appropriate chapter) by the change in the sputum and the persistent fever. The transition from pneumonia to pulmonary abscess is very rare. We can not decide whether a further specific cause is also needed for this, or whether the pneumonic process may exceptionally go on into the formation of abscess. We know that the pneumococci sometimes excite purulent inflammation in the pleura and in the me- ninges, and so it would not seem impossible that, under peculiar circumstances, they should also cause the development of an ab- scess in the lungs. The transition to an abscess may be recognized by the character of the sputum, which contains fragments of pul- monary tissue, such as elastic fibers, besides abundant pus. Moreover, we sometimes find, on microscopic examination of the sputum in abscess, scales of cholesterine (Fig. 29) and hsematoidine crystals; the latter may be so abundant as to give the expectoration a brownish color. Sometimes we have seen a peculiar greenish color of the sputum. The signs of a pulmonary cavity are found if the abscess bursts. Diagnosis. — ISTo special remarks on diagnosis need to be added to the descrip- tion we have given of all the important symptoms which may occur in croupous pneumonia. In the first place, we must consider the sudden onset with a chill and high fever, shortly followed by subjective thoracic symptoms, such as cough and pain in the side; also the characteristic sputum and the objective physical signs, the appearance in many cases of herpes on the face, and finally the general course of the disease, particularly the temperature-curve with its final sudden drop. We will discuss the difi^erential diagnosis between pneumonia and pleurisy with effusion more fully in the description of the latter affection. Prognosis. — Croupous pneumonia belongs in general to the benignant infec- tious diseases. The great majority of cases, in previously strong and healthy individuals, run a favorable course, and end in complete recovery. On the other hand, pneumonia brings a number of perils with it, the knowledge of which should always make us cautious in giving a prognosis. One grave danger lies in the extension of the process. If the advance of the pneumonia can not be stopped, if the whole of one lung is involved, and, besides that, a great portion of the other lung, the diminution of the respiratory surfaces may of itself occasion a fatal termination. A further danger lies in the onset of certain complications. An intense pleu- risy, with effusion, especially if purulent, causes greater difficulty in respiration, and thus increases the danger. Still worse is a sero-fibrinous or purulent peri- carditis, which, in not very rare cases, is revealed at the autopsy as the special cause of death. We must note, however, that recovery sometimes finally takes place in spite of an empyema or of a purulent pericarditis. The complication with a purulent meningitis, which is fortunately very rare, is probably invariably fatal. CKOUPOUS PNEUMONIA 223 The dangers of constitutional infection and constitutional intoxication are, on the whole, much smaller in pneumonia than in other infectious diseases ; e. g., typhoid fever; but yet, this possibility deserves some consideration, particularly in certain forms of pneumonia already referred to and termed " typhoid " or " asthenic." Such particularly severe and malignant forms of pneumonia, with a high rate of mortality, sometimes appear as endemics and epidemics; but it should be added that these cases are also often marked by the extent of the local process and the development of the dangerous complications above enumerated. The individuality of the patient plays the most important part in the prognosis of pneumonia. While a constitution that was previously healthy and uninjured usually survives the disease, one that was previously weak and dis- eased readily succumbs. In this fact lies the danger of pneumonia in old, weak, badly nourished persons, and in persons with a pre-existing emphysema, kypho- scoliosis, heart disease, etc. In this, too, lies the great danger of every pneu- monia in drunkards. Since the nervous system is much affected by chronic alco- holism, we vei-y often see outbreaks of delirium tremens in pneumonia. In like manner the other nerve-centers are weakened and incapable of resistance, especially the regulatory centers for the heart and respiration. Hence we can understand why even moderate drinkers, though previously strong and well to all appear- ances, succumb to pneTimonia from failure of the heart and impairment of res- piration. If we ask upon what symptoms our prognosis in any given case should depend, we must reply that no single factor can be given especial prominence. Chief stress must always be laid upon the state of the lungs and the respiration, but attention must also be given to the general condition, the heart's action, the height of the fever, etc. The worst dangers of pneumonia have just been men- tioned. Of the abnormal terminations of pneumonia, contraction gives the best prog- nosis; but recovery, or at least a marked subsidence of all the symptoms, may sometimes take place after gangrene and abscess. Treatment. — Many of the milder cases of typical pneumonia need no special active treatment when the disease takes a favorable course. Most cases get well under, or, we can almost say, in spite of any treatment. From the now obsolete method of treatment by large bleedings, and from the use of certain drugs (vera- trine, tartar emetic), which are even now sometimes employed, we should expect harra rather than any benefit, yet under such treatment many patients have recovered. We do not know of any certain means favorably to influence the pneumonic process. Whether we are destined to learn of some specific mode of treatment, perhaps by means of some serum, after the analogy of other infectious diseases, as diphtheria, we can not say. A few beginnings have already been made in this direction, but without any practical results as yet. We are at present obliged, therefore, to fall back upon a purely symptomatic and constitutional treatment of pneumonia. The symptoms which are usually prominent in pneumonia, even in the milder cases, and of which the patient is especially desirous to be relieved, are the pain in the side, the troublesome cough, and the difiiculty and distress in breathing. Since the respiratory symptoms, as we have seen, are partly due to the pain, as this improves the patient's breathing often undergoes a decided improvement. For the pain, we may first mention a number of external applications to the skin on the affected side. An ice-bag sometimes gives marked relief. Many patients can not bear this, but prefer warm poultices or cold wet compresses. The application of mustard plasters or dry cups to the skin may be of advantage. Subcutaneous injections of morphine, however, are the most effective remedy, and 224 DISEASES OF THE EESPIRATOKY OEGANS are often indispensable. There is no reason why we should not use this remedy, with care and in moderate doses, for the relief of pain; and, as the disease is of short duration, we need not particularly fear the morphine habit. Small doses of morphine, subcutaneously or by the mouth, may also be required to alleviate the cough. Local blood-letting is a remedy the action of which can not be explained physiologically, and yet experience has shown that it is of undoubted advantage. The relief which many patients feel after the application of eight or twelve leeches to the affected side is very striking; but we should prescribe them only when there are severe symptoms at the beginning of the disease, and in persons who were strong and healthj^ before the attack. -Wet cups accomplish the same thing, but their effect is somewhat more powerful, and hence they should be re- served for strong and robust persons, such as laborers. The tepid or cold bath serves as the most effective means of improving the respiration, of aiding expectoration, and of stimulating and refreshing the whole system. We hold it useless, if not injurious, to give a patient baths if the dis- ease is progressing favorably, for almost every bath has some disagreeable feature. These disadvantages, however, are always less, in severe cases, than the bene- fit and improvement which baths give the patient, and which most patients recognize with gratitude. The main point is that the patient should make no physical exertion while in the bath, that he should be lifted into it, held and sup- ported while in it, and lifted into bed again after it. Since the baths are given primarily not on account of the fever, but to improve the respiration, and be- cause of their favorable influence on the nervous system, their temperature need not be especially low. We give them from 82° to 86° (22°-24° E..) ; somewhat warraer with sensitive and weak people, and cooler, down to 77° or even 72.5° (20°-18° R.), with strong persons, or with very high fever or severe nervous symp- toms. We need not employ more than two or three baths a day, and at night we employ them only when there are threatening symptoms. The favorable action of the baths is seen especially in the great relief and refreshment that the patient feels. The respiration is quieter and slower, but deeper. The patient often falls into a quiet sleep after the bath. Of late years we have often re- placed the baths by a wet pack, even in adults. This has been almost always very well received, and indeed seemed to make the patients quieter, with easier respira- tion and less discomfort. We would particularly and strongly recommend the pack for private patients, in whose case the employment of baths is associated with many difficulties. Among internal remedies for pneumonia, antipyretics are frequently em- ployed. We do not believe they are capable of exerting any decided infliience upon the general course of the disease, although we admit that antipyrine and, under some circumstances, also phenacetine and antifebrine have a good effect, since they not only modify the fever, but improve the nervous symptoms and the general condition. Antipyrine is prescribed in doses of fifteen to thirty grains (grammes 1-2), particularly toward night. To make the cough somewhat more effective, expectorants are prescribed. We ourselves most frequently employ infusion of ipecac, apomorphine, infusion of senega, liquor ammonii anisatus, and benzoin. The last two remedies are espe- cially favorable if the heart is feeble. It also seems to us of some importance, with regard to expectoration, to prescribe an abundance of liquid in the form of water, tea, lemonade, and similar drinks. The behavior of the heart should always be watched with vigilance, especially in elderly and delicate persons, and in the obese and alcoholic. If the pulse becomes very frequent, an ice-bag is placed upon the heart. If the pulse-rate is remarkably rapid from the start, we may order digitalis at once, either in infu- CROUPOUS PXEUMOXIA 225 sion, or, still better, in powders containing li to 3 grains (gramme 0.1-0.2), re- peated several times a day; and as digitalis acts slowly, requiring twelve to twenty-four hours to make its influence felt, if the weakness of the heart is dan- gerous, stimulants which act more promptly must be employed. As such, tinc- ture of strophanthus, repeated several times a day, deserves to be recommended, and, above all, subcutaneous injections of oleum camphoratum (1 to 4), of which three or four syringefuls (tii, xv), and more, may be employed (oss. to 5j). Again, ether injected subcutaneously is a powerful cardiac stimulant, but it should be employed cautiously because of its marked local effect (paralysis of the nerves), and the place of injection should be the skin of the abdomen or the thigh. We have yet to make some remarks upon the very extensive use of large amounts of alcohol in pneumonia. Without doubt a free use of alcohol is neces- sary in drunkards, especially when delirium tremens is beginning or is already pronounced. Since the withdrawal of any poison that is taken habitually, like nicotine or morphine, may excite the severest symptoms, the sudden withdrawal •of alcohol from drunkards may have the worst results, while, if we give an abun- ■dant supply of the stimulant to which the nervous system is accustomed, we some- times succeed in avoiding the onset of severe nervous symptoms, such as collapse and failure of the heart and respiration. Likewise wine should certainly be given to persons who are accustomed to it and themselves desire it. It is quite a •different matter with patients who before their illness have not been accustomed to take alcohol at all, or who took it only in small amounts. It may be true that in these cases moderate amounts of wine may have a stimulating and exciting action, although we never could satisfy ourselves of the often praised influence of alcohol upon the action of the heart. We hold it, however, unjustifiable to :force large amounts of alcohol indiscriminately upon every patient with pneu- monia, perhaps in spite of great resistance on his part. Why should we expect sick persons to bear doses of alcohol which have only bad results on healthy men unaccustomed to them? The assertion that fever patients " bear " alcohol better than healthy persons lacks proof. It should be admitted that perhaps alcohol is more rapidly consumed in fever than in health, but it should also be considered that the toxic effects of alcohol are less easily noticeable in comatose patients than in persons possessing normal consciousness. [Few American physicians of any experience will accept the reasoning of the author on the employment of alcoholic stimulants in those not accustomed to their use. The toxic effects of alcohol are as undesirable in pneumonia as in any other •disease, but there are few affections in which so great tolerance is shown for this agent. The chief indications for its exhibition are derived from the pulse and the first cardiac sound at the apex. A fiagging heart calls for alcohol, the effect •of which on the symptoms and on the circulation is to be carefully watched; the quantity is to be diminished, increased, maintained, or the agent is to be omitted 'entirely, according to the conditions present in the individual case. I am no ad- vocate of indiscriminate alcoholic stimulation ; but I believe that lives have been frequently saved in the past, and will be saved in the future, by the judicious and sometimes extremely free use of this class of remedies in acute pneumonia. In- halation of oxygen has won a prominent place in the treatment of severe pneu- monia of late years, and cases are reported in which life seems unquestionably to have been saved by it. In a considerable number of cases the editor has seen only •one which could come under this class. He has seen, however, marked tempo- Tary improvement in pulse and respiration, with diminution of cyanosis and in- duction of relatively quiet sleep. But the oxygen must be given in large quan- tities, sometimes continuously'. If its inhalation fatigues the patient, the gas may be allowed to escape before the mouth or under the nose of the patient. The 15 226 DISEASES OF THE KESPIEATOEY ORGANS objection to the efficient use of oxygen in some cases is the expense of perhaps some hundreds of gallons a day at five cents a gallon.] We scarcely need to lay special emphasis on the fact that the physican should endeavor, so far as possible, to maintain the bodily strength by means of appro- priate and sufficient nourishment. Soups, bouillon with toast or rusk, milk, and eggs are the most suitable articles of diet, and it is sometimes proper to give small amounts of finely minced meat. Care should be taken that the patient has an abundance of refreshing beverages. Wine and also moderate amounts of good beer may be allowed without hesitation. The treatment of complications follows the ordinary rules which have been given under the individual affections. We must also mention that, in delirium tremens, tepid baths with cold douches sometimes have a very good efl;ect. Be- sides this, we may try subcutaneous injections of strychnine, seven to fifteen minims of a one-per-cent. solution, once or twice a day. We can not wholly dis- pense with narcotics, such as morphine and chloral, but we must warn against the imprudent use of large doses of chloral, above thirty-five grains (grammes 2.5)^ CHAPTER VI TUBERCULOSIS OF THE LUNGS (^Pulmonary Phthuif. Pulmonary Consmnption) General Pathology and Etiology of Tuberculosis Ever since Bayle, in 1810, demonstrated the extensive distribution of peculiar- nodules in the various organs, and their relation to pulmonary consumption, few questions have so taxed clinical observers and pathologists as those relating to the cause and nature of tuberculosis. Harmony could not be reached, however, so long as the criterion for the decision of the questions was sought in the presence of definite anatomical changes, which were regarded as specific of tuberculosis. Laennec considered the peculiar change in the tubercular products, which later was named caseation by Virchow, to be characteristic, and called everything- tubercular in which it was found. He distinguished the isolated tubercle from diffuse, tubercular, cheesy infiltration. Thus Laennec recognized that many pro- cesses were allied whose affinity was often disputed afterward, and which has only recently been established, such as the affinity between " scrofulous " enlargement of the glands and tuberculosis. Another opinion became quite prevalent, after' Virchow discovered that precisely the same anatomical process as tubercular case- ation was also found in inflammatory products, which were certainly not tubercu- lar, and in cancerous ulcerations. Hence Virchow made a sharp distinction be- tween tubercle and those new growths and inflammatory processes which had become cheesy. The anatomical criterion of tuberculosis was, in his view, the presence of the miliary tubercle, a gray nodule, the size of a millet-seed at the- largest, made up of cells like lymph-corpuscles. The study of the finer structure- of the miliary tubercle was now pushed most eagerly by Wagner, Schiippel, Lang- hans, and others, but they were unable to reach perfect harmony regarding its origin and significance. As long ago as 1865, however, a discovery was made which pointed unequivo- cally to the only way which could lead to a correct knowledge of tubercvilosis. It was the fact, discovered by Villemin, that tuberculosis can be produced artificially by inoculating healthy animals with small amounts of tubercular and cheesy sub- stances. Although doubted and misinterpreted at first in various quarters, the- TUBERCULOSIS OF THE LUNGS 22Y fact that tuberculosis can be transmitted, and consequently the fact of its infec- tious character, must now be regarded as proved beyond a doubt. In the general change which our opinions upon the nature of infectious diseases have undergone, especially in the last few years, the existence of a specific, organized cause of tuberculosis, too, had to be assumed. Klebs, and later Cohnheim, had already without reserve defined tuberculosis as a specific, infectious disease and, sooner than we dared to hope, R. Koch discovered the special carriers of the disease in the shape of the tubercle bacilli, in the year 1881. The definition of tuberculosis no longer rests upon any external anatomical character. Every disease is tuber- cular which is excited by the pathogenic action of a specific kind of bacteria, the tubercle bacilli discovered by Koch. The pathogenic bacteria of tuberculosis belong to the group of bacilli. The tubercle bacilli are rod-like, of small diameter, slightly rounded at their extremi- ties, and either straight or somewhat bent. Their length is perhaps a fourth or a half that of the diameter of a red blood-corpuscle. In the interior of these rods it is not infrequently possible to distinguish very minute colorless spots which are probably to be regarded as endogenous spores. The tubercle bacilli have no inde- pendent motion whatever. Their reaction to certain coloring matters is very char- acteristic, and of the highest importance with regard to their recognition (vide infra). We know with absolute certainty that the tubercle bacilli are always present in all the different forms of pulmonary tuberculosis, both in the lung itself and in the expectoration (vide infra), and also in tubercular diseases of other organs, the brain, the intestines, the spleen, the liver, and the kidneys, and also in " scrofulous lymph-glands," in " fungous " diseases of the bones and joints, and in the so-called lupus, which is nothing but a local tuberculosis of the skin. Precisely the same bacilli are also found in the " spontaneous " tuberculosis of animals, such as monkeys, puppies, and guinea-pigs, and in every tuberciilosis that is artificially produced in animals by inoculation. Finally, by the discov- ery of tubercle bacilli in the " pearly distemper " of cattle, the identity of this disease with tuberculosis — an identity which had already been established by ex- periments in inoculation — was confirmed anew. Koch, by his successful " pure ctiltures " and inoculations with the cultivated bacilli, has established the fact that these bodies, known as tubercle bacilli, are to be regarded as organized, and as the special cause of tuberculosis. Bacilli coming from any fresh product of tubercular disease may be cultivated at a constant tem- perature of 98° to 100° (37°-38° C.) upon blood-serum which has been stiffened by heating, and upon several other artificially prepared soils. In this cultivation they show certain characteristic properties in their growth, which can not be fully described here, and they multiply to an unlimited extent. In this way we can keep up perfectly pure cultures of tubercle bacilli. Inoculation experi- ments tried with them on all sorts of creatures always give a positive result. The animals fall ill, lose flesh, and finally die, and at the autopsy we find undoubted tubercular disease of the internal organs, which may be more or less extensive. The most instructive inoculations are those into the anterior chamber of the eye in puppies or guinea-pigs, which were first tried by Cohnheim and Salomonsen. After an incubation of two or three weeks we see here very plainly an eruption of the first nodules of tubercle in the iris, and the tuberculosis spreads to the other organs of the body later. By these experiments it was first demonstrated that tuberculosis is always, at the start, a purely local disease, and that its further extension depends upon the spread of its germs. 228 DISEASES OF THE KESPIEATORY ORGANS ^Etiology of Tuberculosis in Man The distribution of tubercle bacilli must be remarkably extensive, for tuber- cular diseases occur in almost every country on earth. The predisposition of mankind to the disease is also very great, and thus we understand the frightful fact, which statistics show, that nearly one seventh of all deaths are from tuber- culosis ! It has neither been proved, nor is it probable, that tubercle bacilli multi- ply outside of the human body, like the bacilli of splenic fever, since they can develop only in a constant and uniformly warm temperature between 85° and 104° (30°-4:0° C). We must therefore regard them as true parasites, which can live — that is, which can propagate and multiply — only in the bodies of animals, but they (or their spores) seem to preserve their virulence and their ability to multiply outside of the body for a long time. Phthisical sputum may be used for inoculation with success, even if it has been dried for several weeks. The tuber- cle bacilli also resist most chemical reagents, such as nitric acid, very decidedly. If the body becomes infected, then, with tubercle bacilli, it is always probable that they have come from some other individual — ^man or beast — with tubercular disease. We need not mention how numerous the opportunities for infection may be, considering the present general distribution of tuberculosis. The chief stress in this respect is to be laid upon the expectoration of phthisical patients, which contains the bacilli. This dries on the floor, on the linen, and on other objects, and then the small particles which contain the germs of infection are carried off by the air. The extensive investigations of Cornet have well shown how fre- quently it is possible to obtain tuberculous material, which is capable of causing infection, from the dust in the neighborhood of phthisical patients who carelessly deposit their expectoration upon the floor and in handkerchiefs and elsewhere. On the other hand, Fliigge has lately emphasized the fact that, as shown by experiments, the inhalation of dry sputiun in the form of dust is far less dan- gerous than the breathing-in of fine particles of liquid expectoration. He points out that the consumptive with a cough can be shown to defile the surrounding air with numerous minute drops of sputum containing tubercle bacilli. These hover for a time in the air, and may be inhaled by other persons. This mode of infec- tion may actually be important as causing the direct transmission of tubercu- losis, and that such direct transmission is possible is shown by the cases of tuber- culosis in married couples, in nurses, and in patients who for a long time occupy a ward in which are many consumptives. Still, the experience of physicians proves that such direct infection with tuberculosis is of very infrequent occur- rence (vide infra). There are very many who fall sick with tuberculosis who have never been in close contact with other consumptives. In such cases it must be that the tubercle bacilli enter the body indirectly. The material which contains the bacilli or spores is taken into the body, in the majority of cases, along with the inspired air. This is probable, because, in most cases, tuberculosis has its starting-point in the air-passages, the lungs, or the lar- ynx. Inoculation experiments show that the first extension of the process depends upon the point of inoculation. If it be in the anterior chamber of the eye, the first nodules appear in the iris, as we have said ; if it be in the abdominal cavity, we have first a tuberculosis of the peritonexun; if the infectious matter be inhaled, we have first a tuberculosis of the lungs. Hence it seems very probable that, in tuberculosis in man, the infectious matter is taken directly into the air-passages by the breath. In this way it sometimes, though rarely, attacks the upper air- passages, as in primary tuberculosis of the nose, the pharynx, and the larynx, but more frequently it affects the deeper portions of the respiratory apparatus, as in primary tuberculosis of the lungs and bronchi. TUBEECULOSIS OF THE LUNGS 229 We must also consider other modes of infection, first among' wliich is tlie possibility of infection of the intestinal canal, from swallowing the infectious material. The transmission of tuberculosis from domestic animals to man plays a part in this connection which perhaps is not unimportant. Since the pearly distemper of cattle is identical with tuberculosis in man, the use of the flesh of such animals as food furnishes a possible means of infection. It is a still more important circumstance that, when pearly nodules are present on the udder, the milk of the diseased animal may be polluted by tubercle bacilli, and that the use of such milk as food, when it is uncooked, certainly involves the danger of the transmission of tuberculosis. Primary tuberculosis of the intestines, however, is not very frequent, probably because the tubercle bacilli which have been swallowed are usually destroyed in the stomach. Still, it is to be noticed that primary tuber- culosis of the intestine and of the abdominal lymph-glands (vide infra) is far more frequent in children than in adults, and that it is children who drink the most milk. In some eases the tubercular infection may probably arise from little fissures and excoriations of the skin. In this way either we get a local tuberculosis of the skin, such as lupus, or the bacilli are carried by the Ijonphatics to the neighboring glands of the neck or axilla, establish themselves there, and set up a tubercular disease in them. It should be stated that even when the tubercle bacilli are taken into the body through the lungs or the intestine, the infectious material often passes the primary seat of infection without fastening itself there, and does not take root until it reaches the nearest lymph-glands; or perhaps, often, still more distant regions, such as the kidneys or the bones (?). Thus arises the so- called primary tuberculosis of the bronchial or mesenteric glands, leading some- times, as we shall see later, to various severe tubercular diseases in other parts, such as the pleura or peritoneum. It remains to mention the possibility of a primary genito-urinary tubercu- losis. Primary infection of the uterus and ovaries might be referable to direct infection from without; but it is questionable whether genito-urinary tubercu- losis of the male, affecting the kidneys, testicles, and prostate, arises in this man- ner. In such cases we may be dealing with infection due to the excretion by the kidneys of tubercle bacilli which have got into the body in some other way. Considering the wide distribution of the tubercle bacilli, and the many chances for infection, it seems wonderful that in spite of it so many men escape the disease. One factor, which has been already mentioned by Koch, must be borne in mind, however, and that is the extremely slow growth of the tubercle bacilli. This is the reason why the bacilli do not always remain in the body, but in many cases are eliminated again before they have gained a definite foothold. Individual predisposition, however, is another factor which is probably still more important — a factor which we can not well explain, but which we can not get on without, at the present time, in the pathology of many infectious diseases. In our conception of most of the other infectious diseases, as well as of tubercu- losis, we must assume provisionally an unequal predisposition to disease in differ- ent individuals. Only a part fall ill of all who are exposed to the action of the poison. These are persons in whom it is particularly easy for the poison to estab- lish and propagate itself. It is very striking that the existence of the tendency to tuberculosis is often expressed in the general constitutional debility of the individual, and — still more remarkable — in certain peculiarities of his bodily frame, e. g., the shape of his thorax. This phthisical habitus (vide infra) is especially common in persons who come from f-amilies with a tendency to tuberculosis, and it is a peculiar and quite inexplicable expression of the predisposition to tuberculosis, due to family and hereditary influence (vide infra). It should be said that the hereditary tend- 230 DISEASES OF THE EESPIRATOEY ORGAl^S ency to tuberculosis is not invariably associated with any striking and self-evident weakness of the constitution. Persons who spring from tuberculous families may have a vigorous frame and yet fall victims to the disease; and likewise also, when there is no hereditary tendency, the most powerful build does not by any means render one invulnerable to the disease. We now believe that many evil influences which were once thought to be causes of tuberculosis act only in increasing the predisposition to the disease. In- sufficient food, bad air, severe illness, childbirth, want, and care — these alone, of course, can never produce tuberculosis; but we can easily imagine that the body which has become weakened affords less resistance to the injurious influence of the tubercular poison than does the strong and healthy body. Thus it seems to us, from our own observations, to be in the highest degree probable that chronic alcoholism increases the liability of the individual to tuberculosis. It is surpris- ing how often drunkards, possessed of a naturally most vigorous constitution, fall victims to tuberculosis; although in this connection we ought also to con- sider that drunkards are so often and so long in filthy and ill-ventilated saloons that they are particularly exposed to the danger of infection. People used often to speak of the transition of other affections of the lungs into pulmonary consumption — that is, into tuberculosis. It was imagined that an old bronchial catarrh, croupous inflammation of the lungs, or the catarrhal pneumonia accompanying measles, or whooping-cough, could readily become " tubercular." Of course the proper interpretation of such a connection is that the precedent disease prepares a favorable soil for infection with the tuberculous virus, and that consequently the tubercle bacilli fasten more readily upon the mucous membrane, which has been previuosly affected, than under normal con- ditions. Moreover, many of the infections which we formerly supposed to be apt to change into tuberculosis are themselves tuberculous. This is true in most of the so-called scrofulous diseases of the lymph-glands, bones, etc., and also, as we shall see later, in the overwhelming majority of cases of apparently primary pleurisy. No one will now admit the truth of the theory, which Nie- meyer once vigorously defended, that a primary pulmonary haemorrhage could cause the development of pulmonary phthisis. Certainly, in the cases which apparently support such an opinion, the pulmonary haemorrhage is not the cause, but a symptom, of pulmonary tuberculosis. IsTo single factor, however, of those which favor the predisposition to tuber- culosis, plays so manifest and so visible a part as does the hereditary tendency above mentioned — that is, the inborn predisposition of the individual. The fact of the heredity of phthisis meets us with such uncommon frequency that it must have forced itself upon the notice of the older physicians. In the great majority of all cases of phthisis we can make out, by close questioning, that in the family, either among the older members or among the brothers and sisters, one or more cases of tubercular disease have already occurred. The closer we investigate, and the more we search for some one of the different forms in which tuberculosis can show itself, like pleurisy, or affections of the bones and joints, the more frequently we can make out this hereditary predisposition. Some persons are indeed of the opinion that the hereditary transmission of the disease is often merely apparent, and not real, from the fact that the close relations between the children and their diseased parents, or brothers and sisters, greatly increases the danger of infection of the ordinary kind. Certainly this consideration should not be forgotten with regard to the occasional appearance of tuberculosis in families, but yet it would be impossible to explain in this way alone the extremely fre- quent development of tuberculosis in special families. There can be, therefore, scarcely any doubt as to the inheritance of tubercu- losis, but the explanation of this fact is far from clear. The hereditary charac- TUBERCULOSIS OF THE LUNGS 231 ter of tuberculosis may very well harmonize with its infectious character.* We might assume in this case a perfect analogy with syphilis — namely, a transition of the infectious material itself from the parent to the child before birth. There is only one striking difference between syphilis and tuberculosis — that the children of syphilitic parents very often come into the world with definite signs of infec- tion, while congenital tuberculosis in this sense is an extremely rare occurrence. We must accordingly compare tuberculosis to that form of hereditary syphilis (lues hereditaria tarda) in which the first symptoms of the affection come on at a late period. Since certain considerations, however, constantly oppose such a theory, we are of late disposed to assume that, as a rule, tuberculosis in itself is not inherited, but only the predisposition to tubercular disease. This opinion agrees with the facts that members of a family in which tuberculosis prevails very often show the so- called tubercular habit even without any real tubercular disease; and that they often have " weak lungs " — that is, that they easily get out of breath, and mani- fest a distinct tendency to catarrh of the respiratory organs. Another fact, which to a certain extent may be regarded as an argument against the assump- tion of a direct hereditary transmission of the disease, is that, in cases of appar- ently hereditary tuberculosis, as a rule those organs first show evidences of disease which are most exposed to an infection from the outer world— namely, the lungs and larynx. The age of the patient has an important influence upon the predisposition to tubercular disease. Pulmonary tuberculosis occurs with special frequency in youth, between fifteen and thirty. It is not rare in children. After forty it is much rarer in its pronounced and rapid forms, but it is seen even in the most advanced age. Slight tuberculous changes are very frequently found at autopsy in the lungs of old persons. These changes have, as a rule, no clinical sig- nificance. They are simply due to the inhalation of tuberculous germs with scarcely any tendency to further extension because of the lack of individual pre- disposition to the disease. It has not yet been shown that sex has a special influ- ence upon liability to the disease. Pathological Anatomy of Tuberculosis, especially op Pulmonary Tuberculosis If now we inquire wherein consists the injury which the tubercle bacilli in- flict upon the body, the first point to emphasize is that the action of the tubercle bacilli is at first invariably purely local. Tuberculosis does not belong to the ■*' general infectious diseases," in which the infection of the whole organism, the general infection of the body, predominates over the local disturbances. The essence of tuberculosis, at least in the great majority of cases, is the local disease. The tubercle bacilli give rise to definite anatomical changes in the organs where they settle, and the consequent disturbance of function in the organ has an effect on the rest of the body. In many cases the whole body may be so little affected that we may be justified in saying that there is a purely " local tuberculosis." The danger of tubercular diseases, however, consists in the fact that the local affection often attacks the most important organs, as the lungs and the brain, and sets up such extensive anatomical changes in them that because of these changes alone it becomes impossible for life to continue longer. Besides this, the infection in many cases does not always confine itself to one organ, but the infec- * Jani has made the interesting observation, that a few tubercle bacilli may be found in phthisis in the vas deferens and the prostate, or in the folds of the lining membrane of the tubes, without appar- ent disease of these parts. Whether this, however, explains the hereditary transmission of tuberculo sis, is as yet doubtful. 232 DISEASES OE THE KESPIEATOEY ORGANS tious material extends over the body by ways and means which we shall learn in part later on, and attacks one organ after another, or even many at once. Finally, it is to be said that the peculiar character of the changes caused by tuber- culosis explains why these are often the cause of manifold secondary processes, such as toxic effects and, particularly, secondary infections. Thus arise fever,, suppuration, secondary inflammation, and other important phenomena, which will be minutely considered later. The entire local action of the tubercle bacilli — that is, the pathological anat- omy of tuberculosis — is almost wholly independent of the organ attacked. Tu- berculosis belongs to the group of so-called " infectious tumors " — that is, the local action of the tubercle bacilli consists chiefly in the production of a prolifer- ation and accumulation of cells at their place of settlement, which is termed a tubercular new growth. Without going into histological details we may say, briefly, that the whole process consists in a primary injury of the tissue, due tO' the invasion of the tubercle bacilli, followed by a hyperplasia of the cells peculiar to the tissue itself, and involving not only the connective-tissue cells but also those of the epithelium. In this way are developed the so-called epithelioid cells and the giant cells. The next step in the process is the migration of numerous- leucocytes from the surrounding blood-vessels. The leucocytes, or round cells, collect about the above-mentioned new-formed cells, and may finally completely cover them. A network, or reticulum, is found between the individual new- formed cells and the wandering cells. This probably represents the remains of the original interstitial tissue, crowded apart by the increased number of cells. There is no new formation of vessels. The tubercle contains no blood-vessels. The tubercle bacilli lie especially inside the giant cells, but also in their vicinity. If these changes have progressed far enough, they become visible to the naked eye as a small, circumscribed grayish point, which is called a miliary tubercle. From these minute nodules the disease itself obtained its name of tuberculosis. By approximation and coalescence of neighboring tubercles — for these keep devel- oping because of the spread of the local infection — the tuberculous formation continually extends itself, and thus are gradually formed the large tubercular nodules, and finally the diffuse tuberculous new growth or the diffuse tubercu- lous infiltration. The tuberculous new growth, as such, can scarcely ever be distinguished histo- logically from other infectious tumors, such as those seen in syphilis and leprosy. Tuberculosis, however, has a characteristic difference in its final stages of cheesy degeneration and eventual disintegration of the new-formed tissue, processes which are apparently connected with the absence of blood-vessels and the conse- quent deficiency of nutrition of the new formation. Both the tuberculous infil- tration and also the portions of the original tissues inclosed by it perish, lose their nuclei, and finally become disintegrated. The manner in which they are de- stroyed — namely, " fatty degeneration " — belongs in the group of the so-called coagulation necroses. This process is recognizable to the naked eye, because the tuberculous infiltration when it becomes thus degenerated takes on a pronounced yellowish color. Wherever the necrotic portions of tissue are superficially situ- ated they are cast off, giving rise to tuberculous ulcers. Alongside the tuberculous new formation there are found in the organs affected with tuberculosis various inflammatory processes, either simple or sup- purative or hemorrhagic. We may therefore surmise that the tubercle bacilli (or the chemical toxines formed by them), besides their characteristic effects, act simultaneously in another role as excitants of inflammation; but it is very probable, and especially so in pulmonary tuberculosis, that many of the inflam- matory changes which arise are not peculiar to the tuberculosis as such, but are to be regarded as secondary processes (vide infra), for the development of which TUBEECULOSIS OF THE LUNGS 233 the preceding tuberculous new growth, as it disintegrates, furnishes a suit- able soil. As regards the special anatomical processes and appearances in pulmonary tuberculosis, the tubercular change usually begins in the walls of the smallest bronchi, or not rarely in the alveoli themselves. The disease does not begin, however, in many different parts of the lung at once, but probably in one or two circimiscribed spots only, and in a great majority of cases in one apex. We do not know why the apices are so often the starting-point of phthisis, but perhaps it is because of their relatively slight expiratory power, which renders them a favorable lodging-place for the tubercle bacilli. The tuberculous infiltration begins in the walls of the bronchi, and thence gradually extends toward the periphery. The original tuberculous bronchitis becomes a tuberculous peribronchitis. The infectious material extends from its original focus by means of the lymph- and blood-channels out into the sur- rounding tissue; and also as soon as superficial ulceration takes place, the in- fectious matter is liable to be carried by the inspired air into other bronchi. Thus the diseased spot, small at first, keeps gradually extending. Tubercular peribron- chitis is usually easily recognized with the naked eye. We notice the little lumen of the bronchus in the middle of the " cheesy " nodule, which at first is gray and later yellowish. Many of the adjacent nodules run together in part, and even entirely. The lumen of the bronchus is either wholly plugged by the infiltra- tion, or the destruction of the necrotic cells begins in the midst of the peri- bronchitis. In the latter case the lumen is enlarged to a little irregular hole — the first beginning of the formation of a cavity. The alveolar tissue of the lung can not long remain unaffected, with such a disease of the smaller bronchi. Lobular atelectasis, the necessary result of every permanent bronchial obstruction, miist arise, but this soon passes (by pene- tration or aspiration of the germs) into a lobular pneumonia, which from its specific nature later becomes caseous. We can not go into the histological de- tails here. The alveoli are filled with pus-corpuscles and large epithelioid cells, which are considered by many authors to be the offspring of the alveolar epithe- lium. The alveolar walls are also infiltrated. This finally results in the destruc- tion of the cheesy and necrotic tissue, and consequently in the formation of cavities. At other times the neighboring nodules run together, and the tuber- cular infiltration thus extends, giving rise to a diffuse caseous pneumonia. These processes may all be readily recognized by the naked eye. The earlier stages of atelectasis and infiltration correspond to the jelly-like, gray coloring seen in the so-called gelatinous infiltration of Laennec, and the transition to caseation is recognized by the eye from the yellowish color. Although all the processes thus far described are destructive in their nature, changes are also found in the lungs in tuberculosis which seem to have a tendency toward circumscribing the disease and toward healing. Prominent among these are the chronic interstitial processes. We meet with the formation of new con- nective tissue, partly about the tubercular infiltration, but especially where there is already destruction of tissue, and this leads to contraction and the formation of a firm cicatrix. The encapsulated cheesy masses may then be in part reab- sorbed; in part they undergo calcification. The possibility of such a halt in the tuberculous process depends, however, upon certain conditions. The tuberculous new growth and its destruction must not advance too rapidly, and the new-formed tissue must not itself be destroyed before it becomes cicatrized. We see the cicatricial formation, therefore, more especially in chronic cases; we find it in places which have been affected the longest, and where the tubercular process, perhaps, has finally come to a standstill of its own accord. Macroscopically, this cicatricial connective tissue is composed of a thick, firm substance, usually pig- 234 DISEASES OF THE KESPIKATORY ORGANS mented— the so-called pigment induration. If the cicatricial formation follows a previous extensive destruction of the pulmonary tissue, the affected portion of the lung may thus be diminished to less than half its original bulk. Cavities and firm cicatricial tissue form the anatomical basis of such an extensive " pulmonary contraction." Either the cavities are formed in the usual way from the destruc- tion of lung tissue, or they may be simple bronchial dilatations due to the trac- tion of the contracted tissue — bronchiectatic cavities. The contractile changes in pulmonary tuberculosis teach us that the tuber- cular process is in itself capable of healing. The incurability of most cases of phthisis is due to the fact that the infectious material from every existing tuber- cular nodule is carried into other bronchi, and there sets up a new tuberculosis. Thus the disease is constantly extended. The original tuberculosis, which was localized in one apex only, gradually spreads to the lower portion of the lung. The infectious material is carried by coughing into the trachea, and from this point may be carried by inspiration into the other lung. This becomes diseased, and finally there is such an extensive destruction of the lungs as to make the further continuance of life impossible. Besides the specific tuberculous lesions in phthisical lungs, there are very often found simple inflammatory processes, such as bronchitis and lobular catarrhal pneumonia; sometimes, also, although seldom of great extent, croupous pneu- monia; and finally, in exceptional instances, limited foci of gangrene. These secondary diseases not specifically tuberculous, and yet almost always associated with tuberculosis, are of the greatest clinical importance. They probably are due in most instances to the influence of secondary pathogenic germs (particularly streptococci, less often diplococci, etc.), for which the tuberculosis has merely prepared a favorable soil. Many clinical phenomena (particularly most of the febrile exacerbations of the disease) depend upon these secondary inflammatory processes which, in their turn, promote the further extension of the tuberculosis. Thus, frequently, inflammatory lesions which are due to secondary infection finally are transformed by the invasion of tubercle bacilli into foci of tuberculosis. If we consider the list of anatomical processes which are found in tuberculosis of the lungs, and which may be combined in the most manifold ways, we can understand the great diversity in the anatomical picture in different cases. Pri- mary tuberculosis of the bronchial wall and tubercular peribronchitis, diffuse cheesy pneumonia, and destruction of the tubercular new growths, with the for- mation of cavities, on the one hand; contracting interstitial pneumonia, cicatri- cial formation, and pigment induration on the other — these are the compara- tively simple anatomical lesions from which the whole process of pulmonary tuberculosis in its most varied forms is composed. Besides this, we often find here and there one or more miliary tubercles scattered through the lungs, which are probably due very largely to an extension of the infectious material by means of the blood or lymph current; and finally the already mentioned processes of sec- ondary infiammation, such as bronchitis and pneumonia. The secondary tubercular diseases of the pleura, the bronchial glands, and other organs, will receive a special description. Clinical History of Tuberculosis in General and of Pulmonary Tuberculosis IN Particular In judging of the various appearances in the clinical picture of tuberculosis we must especially consider the following points : The place of the first infec- tion is of the chief importance — that is, the place where a local affection, set up by the tubercular poison, first arises. One can readily understand why all those organs which are directly exposed to infection from without are most frequently TUBEECULOSIS OF THE LUNGS 235 affected with primary tuberculosis. Very often, as we have said, the lungs are the organs first attacked. Less often the upper respiratory passages — viz., the larynx and nose. In other cases the tubercle bacilli fasten first upon the digestive tract (the intestines, less often the pharynx and the tongue). In many other cases, how- ever, it can not be that the tubercle bacilli directly reach the organ which seems to be first affected. This is true of the so-called tuberculosis of serous membranes, of the tuberculosis of lymph-glands, of bones and joints, of the brain and of the genito-urinary tract. Investigators have yet to determine the paths by which the tubercle bacilli reach the respective organs in these cases. The glance which we have just taken at the organs most frequently attacked by tuberculosis shows the great clinical variety of tuberculous diseases viewed from this aspect. Another reason for the great variation in the course of tuberculosis is found in the fact that the extension of the local tubercular process may vary very greatly as regards time. Tuberculosis in one case may produce the most exten- sive destruction in both lungs in a few months or even weeks, and in another case it may remain almost quiescent for years, or advance only very slowly. We do not know fully on what these differences depend, but much is certainly due to the hygienic influences under which the patient lives. In the last analysis, however, we are often led to think of individual differences of constitution, which now check and now favor the rapid extension of the disease. This predisposition is, in most cases, congenital but sometimes acquired. This is particularly true of alcoholic subjects, who often evince a feeble power of re- sistance to tuberculosis, although originally of vigorous constitution, so that the rapidly spreading or " galloping " forms of tuberculosis are particularly common in drunkards. A third and final reason for the differences in the course of tubercular infec- tion is the manner of the further extension of the tubercular poison in the body. As we shall see in the description of tuberculosis in single organs, there are differ- ent ways in which tuberculosis may pass from one organ to another. Many con- tingencies are involved here, and we can easily comprehend how greatly the whole clinical course of the disease must be modified by the rapidity and the degree in which individual organs are affected. After these preliminary remarks we will pass on to the description of the clinical course of pulmonary tuberculosis. The onset of pulmonary tuberculosis is quite slow and gradual in the majority of cases. The patient can give only an approximate idea of the time when he began to be ill. The symptoms are referred directly to the respiratory organs The cough and its attendant expectoration are the chief things which affect him. Moreover, there is often pain in the chest, either the pleuritic stitch, or pain in the sternal region, or pain between the shoulder-blades. The patient is also apt to complain of shortness of breath, especially on severe physical exertion. Besides these symptoms, which point pretty directly to disease of the respira- tory organs, there are often quite striking general symptoms. The patient's ema- ciation is especially noticeable. This may be partly, though not wholly, explained by his loss of appetite. Besides the emaciation there is a steadily increasing pallor of the skin. The patient also shows a general dullness, weakness, and disinclina- tion to work. There is not infrequently a slight rise of temperature in the first stages of the disease, which causes subjective feelings of chilliness and fever. Severe night-sweats may also be noticed early. Any such constitutional disturbance should lead the physician not to regard the mild thoracic symptoms, which are also present, as insignificant, but to think of the possibility of incipient tuberculosis. It is very important to remember that the pulmonary symptoms may be entirely subordinate to the general symptoms mentioned, and that the patient himself is apt to pay little or no attention to 236 DISEASES OF THE EESPIRATORY OEGANS them. Incipient phthisis is therefore frequently diagnosticated as simple " chlo- rosis " or " gastric catarrh " for a long time, and is treated as such. An early and careful physical examination of the lungs and of the expectoration is the only protection against such an error. Both the pulmonary and the general symptoms assume significance, if we have to do with a patient in whom we suspect a " tubercular predisposition." We very often meet persons in whose family, either in the parents or the brothers and sisters, several cases of phthisis have occurred. They are persons who are always pale and weak, and who have previously shown a special liability to catarrh and other diseases of the respiratory organs — e. g., pneumonia. They have perhaps had diseases which our present theories bring into direct relation with tuber- cular infection. We refer to those quite frequent cases of pulmonary tuberculosis in individuals who have previously siiffered from " scrofulous diseases," such as chronic swelling of the lymph-glands, chronic affections of the eye or ear, or fungous diseases of the bones and joints, pleurisy, etc. (vide supra, page 230). Although the first symptoms of pulmonary tuberculosis often develop in those who were not quite well before, this is true in only a part of the cases. We often see precisely the same symptoms, both the pulmonary and the general, occurring in persons who previously seemed quite well and strong. ISTo consti- tution is perfectly protected against the disease. We have even seen the her- culean athlete of a circus die of phthisis. In distinction from the slow and gradual method of the development of tuber- culosis which has just been described, the first symptoms in other cases may be more sudden. A definite exposure is often given as a cause, after which the first symptoms of the disease have speedily developed. It goes without saying that we must consider these harmful influences — a chilling of the body, a cold draught, over-exertion, or marked mental excitement — at most, as exciting causes. When pulmonary tuberculosis begins somewhat abruptly, either the initial symptoms are from the start directly referable to the respiratory organs (cough, thoracic pain, dyspnoea), or the chest symptoms may be obscured by the severity of the constitutional disturbance. Thus we recall a number of cases in which young persons fell sick rather suddenly with somewhat severe, febrile con- stitutional disturbance. At first no cause of the fever could be found, so that the diagnosis was doubtful, or was supposed to be typhoid or some other disease. Then after a time, thoracic symptoms developed and pulmonary tuberculosis could be recognized. In most cases the illness would take a rather rapid course. That form of pulmonary tuberculosis which is termed " pneumonic " (vide infra) also exhibits a decidedly acute onset. Those cases of pulmonary tuberculosis which begin with hsemoptysis are of special practical importance. Of course, it must be understood that the tuber- cular process in the lung has existed for some time before the blood appears (vide supra, page 230). But in the midst of apparent health, or after some slight constitutional disturbance, comes a cough with bloody expectoration. Very often the further symptoms of pulmonary tuberculosis follow directly upon this initial hsemoptysis (vide infra). In conclusion, those cases are to be mentioned in which the first signs of tuberculosis appear not in the lungs but in the larynx. The full description of these cases has already been given in the chapter on laryngeal tuberculosis. The further course of pulmonary tuberculosis may vary so much that it is im- possible to give a complete enumeration of all the possibilities. In some cases it advances rapidly. We can make out the extension of the dis- ease objectively, almost from week to week. At first the apex of one lung alone is attacked, soon after the lower lobe of the same lung, then the other lung, either at the apex first or in the lower part. Besides the pulmonary symptoms, there is TUBERCULOSIS OF THE LUNGS 237 quite a high fever, rapidly increasing emaciation, and general loss of strength. Death ensues in a few months. We term such cases florid phthisis, or " gallop- ing consumption." In other cases, however, the disease has a remarkably chronic course. Its onset is very gradual, or else, after rather an acute onset, there is a comparative cessation of all symptoms. The thoracic symptoms do not disappear, but they are only trifling, and do not disturb the patient. Physical examination of the lungs does not show any extension of the process for months. The fever which accom- panies it is slight, if there be any. The patient remains quite well nourished, but in some cases there is a good deal of weakness. He feels better and worse by turns, his condition being greatly influenced by the care and nursing he receives. Unilateral contracting phthisis especially has this comparatively favorable course (vide supra). The affection remains confined to one lung for a long time. The occurrence of contraction shows the slight tendency of the tubercular process to advance, ^nd with satisfactory care the patient may remain quite well for years. In cases, too, which have had severe symptoms for a long time, a temporary standstill of the affection may take place, or an actual improvement in all the symptoms. At other times, in eases which have made no advance for a long time, the symptoms suddenly grow worse. There are all possible varieties between the extremes of florid phthisis and the very chronic cases which last for years and decades. If we recall the further modifications which the course of the disease may assume if complications arise, we can appreciate the manifold character of the clinical picture of phthisis. Most cases with definite signs of somewhat extensive disease terminate fatally. Death ensues, either with the signs of general exhaustion, or as a result of the final failure of respiration ; or it is due to the occurrence of complicatiorLS, such as tubercular meningitis, miliary tuberculosis, pulmonary haemorrhage, or pneu- mothorax. Yet, on the other hand, if the tuberculosis is not extensive, the disease may terminate in complete recovery. To say how frequent recovery is, is diffi- cult, for it is probable that many insignificant cases escape diagnosis. Further- more, a distinction should be drawn between recovery from a standpoint of patho- logical anatomy, meaning complete cicatrization, with disappearance of all tuber- cular new growth, and recovery from a clinical standpoint [arrest], meaning dis- appearance of all symptoms. Often apparent recovery proves deceptive. Special Symptoms and Complications 1. Symptoms on the Part of the Lungs. — Pain in the Chest. — Extensive de- struction of the lungs may occur without any feeling of pain. Many cases of phthisis are painless throughout their course. In other cases, however, the pa- tient's chief complaint is of severe pains in the side or in the front of the chest. These are probably always due to co-existing affections of the pleura, such as pleurisy, or pleuritic adhesions. In patients who suffer from severe cough, pains sometimes arise in the abdominal muscles and at the insertion of the dia- phragm, due to the excessive muscular contraction. Cough. — In the majority of instances cough is one of the most distressing symptoms of phthisis, but its severity varies very much in different individuals, and at different times in the same patient. We sometimes see cases, particularly in senile, insensitive individuals, in which, in spite of advancing phthisis, cough is remarkably slight, or entirely absent. In cases with severe cough, it is often worst at night, but paroxysms of coughing of long duration are also apt to come on in the morning or evening hours, which are painful and very distressing, and exhausting for the patient. The cough is usually associated with a more or less abundant expectoration, but sometimes there is chiefly a dry cough. The 238 DISEASES OF THE EESPIRATORY ORGAITS cough becomes very severe if the tubercular affection attacks the larynx and trachea (see laryngeal tuberculosis). Expectoration. — The amount of expectoration differs very much in different cases. It is most abundant when there is extensive formation of cavities in the lungs. In such cases it is often evacuated in the morning by persistent coughing. The consistency of the great part of the sputum is muco-purulent, and it differs little from that of simple bronchitis ; in fact, a large part of the phthisical expec- toration comes from the catarrhal inflammation of the bronchial mucous mem- brane. Usually, however, the amount of mucus as compared with the amount of pus is less in phthisical sputum than in that of simple bronchitis. The sputum is therefore less viscid and more fluid. The amount of mucus in the ex- pectoration is also apt to be greater in chronic bronchitis than in tuberculosis, although mucus is seen in the latter. The expectoration which comes from cav- ities is almost pure pus, with only a slight amount of serum and mucus inter- mixed. Such sputum consists often of large separate masses described as num- mular, or coin-shaped. If received in water, the uneven, rough surface of these masses is often evident, and suggests their formation in the irregular pulmonary cavities. The admixture of blood with the sputum is of great diagnostic and practical importance. Since no other disease so often gives rise to the presence of blood in the expectoration, coughing of blood (hsemoptysis) is almost synonymous with consumption among the laity. Little streaks of blood in the expectoration are quite frequent. They have no great significance, but, of course, they may some- times be the precursors of severe haemorrhages. Profuse haemoptysis takes place when the wall of a little pulmonary vessel— almost always a branch of the pul- monary artery — is infiltrated, destroyed, and finally eroded, by the tubercular new growth. The reason why haemoptysis is not more frequent is because the con- tents of the vessels usually undergo thrombosis. Severe haemorrhages very often have their origin in little aneurisms of the branches of the pulmonary artery, which penetrate into the interior of the cavities. In the cases of fatal haemoptysis we frequently succeed in finding the little aneurism and its point of rupture. Pulmonary haemorrhage occurs in all stages of phthisis. The initial haemopty- sis has already been mentioned (page 236). This may be followed by other symp- toms of pulmonary tuberculosis, or the haemoptysis may cease without any imme- diate sequels. Pulmonary haemorrhage may also occur at any time in the further progress of the disease. The amount of blood raised is variable. There may be one or more tablespoonfuls, or one or more pints. The blood is bright red, usually quite frothy, but little clotted, and in part mixed with other constituents of the sputum. After the first well-marked haemoptysis, the expectoration usually is mixed with blood for several days. Again, there may be repeated haemorrhages in a short time. Sometimes the haemoptysis begins abruptly, not infrequently at night, without any occasion. In other cases, the haemorrhage is referable to some distinct cause, such as bodily exertion, a violent paroxysm of coughing, strain- ing at stool, mental excitement, and the like. Many cases of phthisis are char- acterized by a special tendency to haemorrhage, while in many others haemoptysis never occurs. Severe haemoptyses are, of course, always an undesirable and dan- gerous complication, since they weaken the patient very much, and also depress his spirits. Many patients maintain their peculiar careless indifference, which is almost characteristic of the disease, despite the spitting of blood. The haemop- tysis may sometimes be the direct cause of death, but, as a rule, the patients sur- vive it. We have no better means of determining with certainty the influence which haemoptysis has upon the progress of tuberculosis than by the bodily tem- perature. If there was no fever before, and the haemoptysis also has an afebrile TUBEKCULOSIS OF THE LUNGS 239 course, or only a very brief rise of temperature, then we may hope in general that the patient may fully recover from the haemorrhage and be as well as before. If, however, the haemoptysis is followed by persistent fever, or if the fever which may have previously existed becomes higher and more persistent, we have every reason to suppose that the tuberculous process is making more rapid advances subsequently to the haemoptysis. We here append a temperature chart (Fig. 30) * Haemoptysis. Fig. 30.— Influence of a pulmonary haemorrhage upon the bodily temperature. (Erlangen medical clinique.) illustrating the temporary influence of a haemoptysis upon the temperature in a stationary afebrile case of pulmonary tuberculosis. The fact that the fever preceded the haemorrhage by a few days is probably due to the tuberculous arte- ritis, because of which material capable of exciting fever entered the circulation before the process had caused complete destruction and bursting of the arterial wall, and consequent pulmonary haemorrhage. A purulent sputum intimately mixed with blood is quite frequent and charac- teristic in many cases of phthisis with extensive formation of cavities. This is formed in the cavities from the mixture of the purulent secretion with little capillary haemorrhages. In this way the sputum, which is often nummular, assumes a greasy character and a reddish-brown or chocolate color. If foetid or gangrenous processes develop in the lungs, the sputum becomes foetid. In some cases we see temporarily in phthisis the characteristic sputum of croupous pneumonia, which comes from portions of the lung attacked with secondary pneumonia. Microscopic examination of the sputum may show — besides the ordinary mor- phological elements, such as pus-corpuscles, red blood-corpuscles, and epithelium — two constitutents which are of decided diagnostic importance: elastic fibers and tubercle bacilli. The demonstration of elastic fibers in the expectoration permits us to decide with certainty that there is a destructive process in the lungs, and thus it usually is direct proof of tuberculosis. Elastic fibers are also found in pulmonary gan- grene, and in the very rare cases of pulmonary abscess, as well as in tuberculosis, but gangrene is easily recognized by the other peculiarities of the sputum. The search for elastic fibers in the expectoration of tubercular patients demands a cer- tain amount of practice. We are most sure to find them if we look in the sputum, when it is sprend out, for little lentiform particles, which can easily be discerned with the naked eye. These consist of necrotic shreds of tissue torn off from th« walls of cavities. If we press one of these " kernels " under a cover-glass we find, in the midst of the granular detritus, beautifully twisted elastic fibers, which often have quite a definite alveolar arrangement (see Fig. 31). The elastic tissue is the only one spared in the general destruction. There is a special method of looking for elastic fibers. The sputum is boiled in sodic hydrate, diluted with 240 DISEASES OE THE KESPIEATOEY OEGAXS water, and we look for elastic fibers in the precipitate which then forms. We are never justified, however, in deciding that pulmonary tuberculosis is absent because we do not find elastic fibers in the sputum. Their presence is the only thing that has real diagnostic significance. The discovery of tubercle bacilli in the expectoration of phthisical patients is of much greater importance, and often this alone is decisive (see Fig. 32). They were first demonstrated by Koch, but Ehrlich devised the first simple method for their discovery, which can be easily employed by any physician. The simplest method and the one which we now employ almost exclusively for staining the bacilli, is as follows: Some of the sputum is rubbed between two cover-glasses, which are then slowly separated, leaving upon each cover-glass a Fig. 31. — Elastic fibers. Fig. 32.— Tubercle bacilli in the sputum. very thin layer of sputum. In order to fasten this sputum upon the cover-glass, the latter is passed three times slowly through a gas flame. The cover-glass is now held with a pair of forceps and covered with the following staining-fluid (carbol-fuchsine solution), which was first proposed by Ziehl and jSTeelsen: Dis- tilled water, 100 parts; crystals of carbolic acid, 5 parts; fuchsine, 1 part; mix, filter, and add alcohol, 10 parts. This staining solution upon the cover-glass is heated to boiling for a short time, and then the staining is completed. The cover- glass is now washed, first in absolute alcohol, then in distilled water, then placed for about two minutes in a solution of 2 parts of methyl-blue in 100 parts of a twenty-five-per-cent. solution of sulphuric acid. The acid bleaches out the dif- fused fuchsine stain, leaving the tubercle bacilli still colored, while the pus-cor- puscles are colored blue. The preparation is now rinsed in water, dried between two pieces of filter paper, and examined in Canada balsam. The whole process, when one has had a certain degree of experience, requires four or five minutes. The number of bacilli in different cases, and at different times in the same case, varies considerably. The more abundant the bacilli, the more reason have we to suppose there is a rapidly advancing process of ulceration, but of course we can never draw a broad conclusion as to the extent of the tuberculous disease from the number of bacilli in the sputum. Our only information on this point must come from the physical examination, and other clinical observations. On the other hand, the diagnostic significance of the demonstration of bacilli with regard to the recognition of a pulmonary tuberculosis can not be overrated. TUBERCULOSIS OF THE LUNGS 241 Every positive result is absolutely decisive, and the diagnosis of tuberculosis of the lungs ought certainly never to be made unless the bacilli have been demon- strated. Very frequently bacilli may be found in the sputum in early cases, at a time when no other certain sign of tuberculosis can be detected. On the other hand, we scarcely need to point out that the physician should be cautious in the interpretation of negative results. In all suspicious cases we must repeat the ex- amination of the sputum over and over again. Dyspnoea. — Many patients hardly ever complain of their breathing in spite of extensive destruction in the lungs. A patient who is much emaciated manifestly needs little oxygen, and the increased frequency of respiration, which is almost constant, can satisfy his needs. If there is a greater demand upon the respiration, a subjective feeling of dyspnoea may of course very readily occur, especially on a slight bodily exertion. In many cases, however, the patient complains of a dif- ficulty in breathing even when quiet, especially if pleuritic pains or adhesions between the surfaces of the pleura prevent him from taking a deep breath; and in the final stages the dyspnoea may be extreme. 2. Symptoms on Physical Examination. — In many eases inspection gives us that general impression of the patient which we term the " phthisical habit." The special signs of this are as follows : A slender but often quite a tall frame, weak muscular development, a thin layer of fat, a pale and perhaps very delicate skin with a bluish translucence, sometimes a circumscribed " hectic " flush in the cheeks, a long and slender neck, a long and flat thorax, small, thin hands, etc. Of course this characteristic constitutional habit is not equally well marked in all cases. The inspection of the thorax is of special value. The phthisical or " para- lytic " thorax is generally noticeable from its length, but it is narrow and flat. Unustial width of single intercostal spaces, and acuteness of the epigastric angle, are associated with a long thorax. The sternum is also long and narrow, and the sternal angle — Louis's angle — is sometimes particularly prominent. The supra- clavicular and infra-clavicular fossse are sunken, the neck is Avasted, and the shoulder-blades stand out from the thorax. On comparing the two halves of the thorax we very often observe a distinct drawing-in and flattening (con- traction) on the side most affected. This change is most frequent in the upper and anterior portions of the chest, bvit it is not rare even in the posterior and lower. The paralytic form of thorax is very often seen in phthisis, but it may be en- tirely absent. The respiration is usually somewhat accelerated, and sometimes quite mark- edly so in women with disease of the apices.. The feminine type of high thoracic breathing is largely changed to low thoracic or diaphragmatic breathing. A unilateral impairment of respiration is of greater importance; in such a case the apex in front or even the whole side, if there be phthisis of the lower lobe, lags in inspiration. The respiration is sometimes irregular, especially if there be pleuritic pains. The results of percussion are, of course, entirely dependent upon the sort of anatomical changes in the lungs, and hence differ very greatly in different cases. Since the phthisical process begins in the apices in the majority of cases, our chief attention is turned to the condition of the upper portions of the lungs on percussion. Slight changes in percussion may wholly escape discovery. Only when the air contained in the lung-tissue in the part affected is replaced to a cer- tain degree by the tubercular infiltration does the percussion-note become dull. Unilateral dullness at the apex is therefore one of the most frequent physical signs of phthisis. We can iisually make it out most plainly in the upper anterior intercostal spaces first, and in incipient cases often in the supra-clavicular f oss£)e only, but it is also observed sometimes in the back in the supra-scapular fossae. 16 242 DISEASES OF THE EESPIEATORY ORGAIsTS As the infiltration advances the dulhiess hecomes more extensive. For the accu- rate determination of the limits of dullness in the upper portions of the lungs, we recommend that percussion should be practiced in such a way as to proceed from the normal resonance of the lower portions upward toward the affected area. This method is particularly useful for the back of the chest. Often the dullness takes a tympanitic quality as a result of diminished tension in the lung, or more or less pulmonary retraction. Changes in tension may render the resonance, in begin- ning tuberculosis, deeply tympanitic without any accompanying dullness. The formation of cavities in tuberculosis has a great influence on the percus- sion-note. The dullness on percussion may thus become decidedly less, the degree of resonance depending, of course, upon the fullness of the cavity and the char- acter of the surrounding tissue. We often find a decided tympanitic resonance or a combination of dullness and tympany over a cavity. The different modifica- tions of the percussion-note in cavities are given feelow. The " cracked-pot reso- nance," or buckram sound, is met with in percussing over cavities, but we also find it in many other pathological conditions, and in children not infrequently when the lung is normal. Auscultation also gives no special pathognomonic signs of phthisis. Varying with the character and extent of the tubercular changes, abnonnal respiratory sounds and adventitious sounds are heard in place of the normal vesicular mur- mur. With slighter changes the vesicular breathing is merely modified; it seems remarkably diminished or interrupted, or sometimes exaggerated, with prolonged expiration. When the infiltration of the lungs increases, we find bronchial res- piration in place of the vesicular breathing; but, on the other hand, the forma- tion of a cavity is a frequent cause of bronchial respiration. Various sorts of moist rales are among the most frequent and diagnostically important of the auscultatory signs of phthisis. They are caused by the collection of secretion in the bronchi, or in pulmonary cavities. The more abundant and liquid the secretion is which is set in motion by the air current which traverses it, the more abundant and moister the rales. The larger the space is in which they develop, the coarser they are. Besides the true moist rales, there are also dry bronchitic rales (sibilant or sonorous) occasionally to bfe heard in portions of the tuberculous lung. In general, we may say that the extent of the tuberculous disease in the lungs can be determined by no symptom so surely as by the auscul- tatory signs relating to the respiration, and the adventitious sounds which may be present. Physical Diagnosis of Incipient Phthisis. — The importance of the diagnosis of early phthisis is so great that we will briefly sketch its most important physical signs. Now that the examination of the sputum for tubercle bacilli plays by far the most prominent part in the recognition of incipient tuberculosis, and is the only decisive evidence, the physical signs of this condition have lost much of their former importance. Still, even now, the determination of the seat and extent of the early process is extremely desirable. The auscultatory signs in the begin- ning of the disease are in general more certain and easier to recognize than those from percussion. He who lays too much weight on the so-called " slight dullness at the apex " will often make a false diagnosis. We will mention the following sjonptoms: 1. Constant and evident diminution of the respiratory murmur at one apex, especially if it is associated with marked deficiency of the respiratory movement on the affected side. In some cases the respiratory murmur on the diseased side is not weaker, but it has a more indefinite and harsher character; or again it may be rude, sharp, and " puerile." 2. Markedly interrupted respira- tion at one apex. 3. A prolonged expiratory murmur, which has a harsh charac- ter. 4. The discovery of dry rhonchi or moist rales at one apex is most important, since we know by experience thfvt " apex catarrhs " are, as a rule, tubercular. 5. TUBERCULOSIS OF THE LUNGS 243 Definite dullness, apparent on repeated examinations, or tympanitic dullness or tympany at one apex. 6. Evident contraction at one apex, as revealed by inspec- tion or perciission above the clavicles, 7. Some authors lay stress upon a systolic murmur in the subclavian artery, especially loud on expiration. This may occur in the beginning of phthisis, if the caliber of the vessel is narrowed by processes of contraction in the neighboring apex, but this symptom is neither frequent nor of great practical importance. The chief rule in the diagnosis of incipient phthisis must be held to be this — not to give a definite opinion until repeated examinations have been made. The other portions of the lungs are to be carefully examined as well as the apices, since in not very rare cases tuberculosis may begin in the lower lobes. We must always consider the patient's general symptoms as well as the physical signs (vide infra, diagnosis). Diagnosis of Cavities. — The positive diagnosis of pulmonary cavities by means of physical examination is often very difficult. Any one who will compare the discoveries at autopsies with the results of previous physical examination of consumptives will be in a position to confirm the truth of this statement. We may mention as the chief symptoms of a cavity: 1. Loud bronchial respiration, perhaps of an amphoric character, in places where the percussion-note is only slightly or not at all dull, but perhaps tympanitic. Such a condition means that the bronchial respiration is not due to an infiltration of lung-tissue. Bronchial respiration, however, may of course be heard over cavities which are surrounded by thickened lung-tissue, and hence give dullness on percussion. Pure amphoric respiration is very characteristic of a cavity, particularly if there is a clear, metallic quality to the sound; but this sort of respiratory murmur is heard only when the cavity is comparatively large, of regular shape, and with smooth walls. Under these circumstances the moist rales, if there are any, also have a clearly metallic sound (tinkle), and the percussion resonance may also be distinctly metallic. This last should be demonstrated by rod percussion with simultaneous auscultation. In many cases of this sort the differential diagnosis, between a large cavity and a sacculated pneumothorax (see page 298), is very difficult. 2. The so-called metamorphosing respiration, which begins as vesicular and sud- denly becomes bronchial, is heard especially over cavities, and hence has a diag- nostic value. 3. The different kinds of " changes in the percussion-note " over cavities are important signs. The most frequent and of greatest practical im- portance is Wintrich's change of note. This is when the tympanitic resonance, which is obtained over the cavity, becomes, on opening the mouth, more decided- ly tympanitic, louder, and especially, much higher. The respiratory change of pitch of Friedreich usually consists of a higher pitch on inspiration, but here there are numerous variations. Gerhardt's change of pitch (Weil) consists in a change of the tympanitic resonance when the patient changes his position, the pitch usually being higher when the patient sits up than when he is lying down. 4. Loud, bubbling rales are one of the most frequent signs of a cavity. They are definite indications of the occurrence of rales in a larger space than is nor- mally present in the apices of the lungs. If we have coarse and metallic rales in the apices of the lung, there is considerable probability of the existence of a cav- ity, inasmuch as the normal apices can not produce such sounds. Contraction of the Lungs [Fibroid Phthisis]. — Unilateral contraction of the lungs, much more frequent on the left than on the right, is a form of tuberculosis which is made apparent both by special physical signs and also by certain clinical peculiarities. It is usually recognized at once by inspection of the thorax, one side of the thorax being remarkably retracted. The upper anterior portions of the thorax, and, in all cases of a high degree of disease, the lower lateral and posterior portions, are much less tense than the corresponding parts on the other 2i:i DISEASES OE THE EESPIEATORY 0RGA:NTS healthy side. The fossae and intercostal spaces on the affected side are deeper, the shoulder-blade is drawn nearer the vertebral column, and the latter is even sometimes drawn over to the contracted side (scoliosis). The resonance is dimin- ished to a greater or less degree, over the affected side, which either lags behind or remains almost wholly at rest on respiration. The respiratory murmur is quite loud, and bronchial; and we also hear many rales, which are usually bubbling. Exceptionally the rales are few and the respiratory murmur feeble and indis- tinct. Anatomically, we have to do with a marked process of contraction of the interstitial connective tissue in the lungs, which is almost always associated with extensive formation of cavities, partly of an ulcerative, partly of a bronchiectatic character. The pleura is involved in the process almost without exception, but almost always secondarily; it is also thickened and contracted. If the pleuritic thickening is marked, the respiratory murmur and the vocal fremitus are de- cidedly weakened. The influence of the contraction on the neighboring organs is very decided, and usually it is easy to discover. The heart especially, whose external peri- cardium is in most cases very adherent to the pleura, is drawn well over to the side of the contraction. The apex-beat and the cardiac dullness are correspondingly displaced. With left-sided contraction the heart may be drawn over to the line of the left axilla, and with right-sided contraction it may be drawn to the median line, or even to the right of the sternum. With contraction of the left upper lobe the anterior surface of the heart comes into immediate contact with the an- terior chest-wall over a larger area than normal. We therefore see the motions of the heart over an abnormal extent, and we can often feel very plainly in the second left intercostal space the pulsation and the closure of the valves in dias- tole of the pulmonary artery. The upward traction of the diaphragm may be recognized by the position of the liver, or, in left-sided contraction, by the in- crease of the " semilunar " tympanitic space on the left. We usually find the sound lung on the other side quite emphysematous, as shown by the' downward displacement of the lower boundary of the lung, and also by the drawing over of the anterior median edge of the lung to the contracted side. In a part of the cases we can make out by percussion the development of consecutive dilatation and hypertrophy of the right ventricle. These are the chief physical signs of the so-called unilateral form of chronic pulmonary contraction. We would add here a few clinical remarks. These cases often, but of course not always, run a very chronic course, lasting for years. The general condition and the nutrition of the patient may thus remain com- paratively undisturbed for a long time. The patient looks somewhat pale and cyanotic, yet he is so well nourished as to present a very marked contrast to the appearance of the ordinary cases of phthisis. The appetite remains good, the fever is entirely absent, or else a slight degree of fever may be at times discov- ered by careful examination. The cough and expectoration, too, though often quite troublesome, are at other times very slight, especially when the patient has good care and nourishment. We need not wonder, then, that formerly many physicians did not consider that these cases had anything to do with phthi- sis — " consumption " ; and yet we are convinced by many clinical and anatomical observations that, setiologically, they are in by far the greatest part tubercular. They represent a very slow form of tuberculosis, which has time to develop inter- stitial processes which lead to contraction — that is, to local healing. If such cases come to autopsy, their tubercular character is usually definitely confirmed. We find undoubted tubercular lesions in the other lung and also in the remaining organs — e. g., the intestines. Sudden changes for the worse may occur in every " pulmonary contraction," even those cases which seem favorable ; the other lung may become highly tubercular, a miliary tuberculosis or a tubercular meningitis TUBERCULOSIS OF THE LUNGS 245 may develop, etc. On the whole, however, the slow course of this form of chronic tuberculosis is characteristic and of great practical significance, and its prognosis is therefore comparatively favorable^ We can not deny that a non-tubercular unilateral contraction of the lung may occur. As a result of bronchitis (particularly in cases due to the inhalation of dust), and also after pleurisy, processes of contraction develop, which are associated with the formation of bronchiectasis, and certainly have nothing to do with tuberculosis. In rare cases also croupous pneumonia is followed by unilat- eral contraction of the lung; and finally there is a rare and by no means satis- factorily investigated form of unilateral chronic interstitial pneumonia, with contraction, often associated with the formation of bronchiectasis. The differ- ential diagnosis of these conditions from tuberculous contraction rests in part upon the clinical history, which should be carefully taken, but mainly upon the absence of tubercle bacilli in the expectoration. In conclusion, we must mention that there are very many transitional forms between pulmonary contraction and the other varieties of pulmonary tuberculosis. We find more or less extensive processes of contraction in one apex in most cases of phthisis. Disseminated Pulmonary Tuberculosis. — There is a form of pulmonary tuber- culosis which it is very hard to make out on physical examination. In this we have to do with numerous peribronchial nodules disseminated over the whole lung. As there is still a good deal of normal tissue, containing air, between these nodules, percussion affords no dullness, and auscultation gives at most diffuse rhonchi ; hence this form is often confused with chronic bronchitis or pulmonary emphysema. The diagnosis can seldom be made from the physical signs, but only from the other symptoms, such as fever, emaciation, striking pallor of the skin, and the sputum. This form of phthisis sometimes runs a chronic course, but usually it is quite rapid. It occurs in elderly people, and also in children. Many forms of " dis- seminated, coarse granular " tuberculosis are transitional forms between this and genuine acute miliary tuberculosis. Pneumonic Form of Pulmonary Tuherciilosis. — A special clinical interest attaches to that form of pulmonary tuberculosis termed pneumonic, which we have already briefly mentioned. The disease begins in a decidedly acute manner with dyspnoea, frequent cough, and pain in the side. Sometimes we observe even a distinct initial chill. The expectoration is scanty, viscid, mucous, and often reddish or hsemorrhagic. It sometimes also has a peculiar greenish color. Even after a few days of illness we find, on examination, the well-marked signs of lobar infiltration. There is first pneumonic resonance, then a dull tympany, with fine moist rales and bronchial breathing. In most cases, but not all, a lower lobe is involved. The disease is almost invariably regarded at first as a croupous pneumonia, but the expected crisis does not appear. The fever remains high, the infiltration does not undergo resolution, the rales become coarser, the patient looks pale and wretched. Now, suspicion of tuberculosis being aroused, the sputum is carefully examined, and soon, although perhaps not at the first examination, tubercle bacilli are found. All cases of this sort take a rapid and unfavorable course. They may be called galloping consumption. L"''pon autopsy we find diffuse tubercular infiltration, and usually incipient cavity formation in numerous places. Other portions of the h;ngs than that first and most violently attacked ordinarily present considerable tuberculous change. In these instances it is evident that we have to do with an acute infection of a large portion of the lung with tubercle bacilli, Avhich of themselves exert a pow- erful inflammatory action, with unusual virulence. In rare cases there may also be a mixed infection, due. to the pneumococcus. 246 DISEASES OF THE EESPIEATOEY OEGANS ■■■flIHH ■BBBHHHBHBBI ■■■■n HBBBHHBHBBH ■EHBH nBBBBHBBBBH 39° BS8BB BhBBSSSBSbB SIHB IBBHBaBH ■■■HBB BBBBBmilBBBn iilBMBB MBIlBBBWBBBIfl 38° WBW.VSaB»WlilBHBf«aBH« MBBCIBViBBrSBnBBL^UIBH wisastssmiifs^ms or o UBMBBBBBlfiBIBBBBBBniB 0( BBBBBBBBD'IBBBBBBBUB ■BBBBBBBBBHBBBHBBB BSaBBBBBBSm Of o BBBBBBBBBBBBBBBBBB ot ■■■DiiPBBHHnHBHBHBIBB Fig. 33.— Sub-febrile state iu chronic pulmonary- tuberculosis. 3. General Symptoms in Pulmonary Tuberculosis. — In the description of the general course of pulmonary tuberculosis we have already mentioned the value of the constitutional symptoms in diagnosis and prognosis. Fever. — Only a few cases of phthisis run their course entirely without fever, but it may be absent for a time, even for weeks and months; and indeed, in cases with a very slow and favorable course (e. g., where there is unilateral con- traction), there may be no fever at all for years. The more carefully we measure the temperature the more often shall we find a slight evening rise up to 100° or 101° (38° to 38.5° C), or at least between 99° and 100° (37.5° to 38° C), even at times when the patient is doing well. Many cases that pursue a com- paratively favorable course have for a long while a . so-called sub-febrile condition. That is, the bodily tem- perature is normal in the morning, but in the evening invariably rises to about 100° or 100.7° (37.8° to 38.2° C), or even higher. (See Fig. 33). Very often, particularly in the more rapid cases, there is consider- able elevation of temperature, and the varieties and course of the fever are more or less characteristic. We should first mention the " hectic fe- ver " (see Fig. 34) which is often observed. For months the tempera- ture chart may present a uniform ap- pearance with a morning temperature approaching or reaching the normal, while there is a regular elevation every evening to 102° or 104° (39° to 40° C). In general, the higher the evening exacerbations the more unfavorable the case. In other cases the temperature chart is quite irregular; longer or shorter per- sistent periods of elevation alternate with periods when there is no fever. Particu- larly toward the end of the disease, as the bodily weakness increases, the previously regular, intermitting temperature grows irregular. At this time the intermis- sions often become more marked, and not infrequently general collapse tem- peratures— 95° to 93° (36° to 34° C.)— are observed. Again, the fever may for limited periods take on a more continu- ous character, probably in connection with exacerbations of the tuberculous process. In some few cases with acute onset (vide supra) we have also seen, in the beginning of the disease, a toler- ably high and approximately continuous fever, passing gradually into the ordi- nary fehris hectica. The cause of the fever in pulmonary tuberculosis is not yet settled. The special question is whether the tubercular process causes the fever of itself (by production of toxines), or whether the fever is due to the secondary inflammatory processes, such as the absorption of septic and toxic material from the decomposing contents of the bronchi and the pulmonary cav- 4U° BBBBBBBBBHBBBBBB BBBBBBBBBBBBBBBB ■■■■■BBBBBHBBHBB ■IBBBBIBBBBBBBIBBBB 39° BIIBBIBBBBilBBBIllBBBB BlBBinBBBIllBBIBIllBIIBB BHBIIBBBIIIB lIBHIBIIIBBJ ■■■■IIBHBIIIB tlBIIIBIIIBH BlHBMBIIBIIIB IIBIIIBHIBH 38° ■IHBA1BI11BWH BIBHIBIHBM ■IWBJBBMWBB I'BBB'BBn ■niWBB»BBB BBiBBBB'fl ■IBIHBIBBBBBBBJBBBBB ■IBHBIViBBIBlBBIVlBBIBiBB O'-O IIBIIBIMBIfniBBlTMIBmnBI o* m iBBiiBiiiBifiBiiB ngiijs IIBlWBMBIIIBIflBBBilBIIIB BSISBBB!SB!SBBB13BSS ■BBBBBBBBBBBMH 36° BBBBBBBBBBbbbbbb Fig. 34. -Hectic fever in chronic pulmonary tuberculosis. TUBEECULOSIS OF THE LUNGS 247 ities. The practical importance of the fever in puhnonary tuberculosis is very great. The emaciation and weakness of the patient are caused mainly by fever (vide infra), as are many subjective symptoms, including headache, chilliness, and persj)iration. It is important to remember that in observations of the fever we possess one of the most positive means of forming an opinion as to the course of pulmonary tuberculosis. In cases which are either completely stationary or very chronic there is no fever at all. The sub-febrile condition shows a slow, but still continuous, advance of the disease. Continuous hectic fever is an unfavor- able sign, and indicates a comparatively rapid march of the disease — the more rapid, the higher the evening temperature. In the florid or galloping forms we find tolerably high fever, at times continuous and at times remittent. Subnor- mal temperatures are almost always of bad omen. All changes in the general course of the disease for better or worse stamp them- selves clearly on the temperature chart. The onset of complications and secondary disease is often first indicated by the thermometer. Whether an attack of hgem- optysis passes over witho.ut permanent damage, or whether it is followed by an aggravation of the disease, can usually be told by the temperature sooner than in any other way (vide supra, page 238). Thus we see that the persistent and careful observation of the temperature in consumption deserves to rank as one of the most important means of estimating the status and course of the illness. Emaciation. — The great emaciation of the patient is very striking in most cases of phthisis. The muscular system and the fatty tissue are affected in equal degree. The soft parts of the thorax are often especially involved. The emacia- tion is due in part to the patient's loss of appetite, and to the small amount of food which he takes in consequence thereof, but the chief cause lies in the per- sistent fever and the increased metamorphosis of tissue. Quite a high degree of emaciation, however, may appear in the beginning of the disease with no fever. This we are wont to ascribe to the " general illness," but the special cause of it is unknown. Under favorable external conditions phthisical patients may make quite a decided gain in weight, especially at the times when they are free from fever. In very chronic cases, which run their course from the first without fever, the nutrition of the patient may remain good for a long time. Toward the end of the disease emaciation sometimes reaches its highest degree, and many phthis- ical patients die " wasted to a skeleton " in the true sense of the word. Ancemia — Color of the Skin. — In most cases anaemia appears in the course of the disease, to be recognized by the pale and sallow color of the skin and of the visible mucous membranes. The anaemia only rarely reaches that degree of peculiar waxy pallor that is found in idiopathic pernicious antemia. If the pallor is extreme, however, there is usually some special reason, such as profuse haemop- tysis or the complication of amyloid degeneration. The existence of the anaemia is also the reason why the phthisical patient does not look cyanotic in spite of the respiratory disturbance. In the more chronic. forms, where the general nutri- tion suffers less, we often see a cyanotic coloring of the lips and cheeks. Some- times the skin of phthisical patients assumes a dirty, dusky hue. We have already spoken of the circumscribed " hectic flush of the cheeks " seen with the fever. General WeaJcness — Night-Sweats — Nervous Disturbances. — We need not say that the general emaciation and anemia are accompanied by a marked decline in the patient's power of endurance. Tie finally becomes so helpless that he can scarcely move alone in the bed. The tendency which very many patients have to severe night-sweats is uni- versally acknowledged but not wholly explained. It may have some connection with the fall from the evening febrile temperature to the morning remission, and perhaps it is due to the greater accumulation of carbonic acid in the blood from the disturbance of respiration. i 218 DISEASES OF THE EESPIEATOEY OEGANS The disease has remarkably little influence upon the higher nervous functions, especially those of the mind. Most patients have a perfectly clear intellect to their latest breath. We all know the contented, hopeful, sanguine disposition of many patients, who do not recognize their own danger until the last stages of the disease. Occasionally the anaemia and the general disturbance of the nutrition of the brain lead to mental alterations, such as confusion, distraction, or melan- cholic conditions. We find, more frequently, disturbances in the peripheral nerves and muscles. Among these are neuralgic pains, and pains of an indefinite character, which have their seat in the legs, or sometimes in the arms, especially in the ulnar region and the sciatic nerve. These may be very distressing. Marked hypersesthesia of the skin and deeper parts is also not uncommon. The cause of such disturbances is probably often to be looked for in the degenerative changes in the peripheral nerves (Vierordt and others). Well-marked multiple neuritis has been repeat- edly observed in tuberculous patients (see section on nervous diseases). We very often see an increased reaction upon direct mechanical irritation in the emaciated muscles, and great liveliness of the so-called idiomuscular contrac- tions, which is shown, for example, on percussing the pectoral muscles on the an- terior wall of the chest. The phenomena grouped under the name of tendon re- flexes are also much increased in phthisis. 4. Symptoms and Complications on the Part of Other Organs. — 1. Pleura.— In pulmonary tuberculosis the pleura is also iuA^olved as a rule. The affection is almost always the result of a direct extension of the process from the lung to the pleura. At the avitopsy, we find in the pleura a few or many miliary tubercles, besides the simple inflammatory process — tubercular pleurisy. In many cases, in which we have to do only with an adhesive pleurisy and with pleuritic contraction, we can merely suspect the disease of the pleura, but it can not be directly made out and differentiated clinically from the pulmonary affection. In other cases we can diagnosticate a dry pleurisy in phthisis from the occurrence of the pleuritic friction-rub. The symptoms of pleurisy become more marked if there is a pleuritic effusion, which is usually readily discovered by a physical examination. The patient's pain and dyspnoea are usually much in- creased by such a complication. Besides a simple sero-fibrinous effusion we quite frequently find purulent and even heemorrhagic effusions in tuberculosis of the pleura. The formation of pneumothorax is an important complication in the pleura in phthisis. This is due to the rupture of a superficial pulmonary cavity into the pleural cavity, and the entrance of air into the latter. The different forms of pneumothorax and its symptoms will be described under diseases of the pleura. 2. Larynx, Pharynx, and Trachea. — The symptoms of laryngeal tuberculosis and their relation to pulmonary tuberculosis have already been given under dis- eases of the larynx (see page 148). We saw there that, although there is a primary laryngeal tuberculosis, most cases are secondary in their development to a pulmo- nary tuberculosis. The same holds true in regard to the much rarer tuberculosis of the pharynx. In some cases this may be of primary origin, but it is usually a result of re-inocu- lation with tuberculosis by means of the sputum, or of a direct extension of the tubercular process from the lai-ynx to the pharynx. Tubercular ulcers of the phar- ynx are found most frequently on the soft palate, on the tonsils, on the root of the tongue, and on the boundary between the pharynx and the larynx; they are rare in other parts of the pharynx. In exceptional cases tubercular affections are seen in the mouth — on the tongue. The local discomforts which all these ulcers cause is usually very considerable. Disseminated miliary tubercles, too, have been repeatedly seen in the mucous membrane of the pharynx. TUBEECULOSIS OF THE LUNGS 249 3. Stomach and Intestinal Canal — Peritoneum. — Tubercular ulcers in the mucous membrane of the stomach are exceedingly rare, but we very often notice some symptoms on the part of the stomach. Loss of appetite is a particularly common symptom in phthisis. Vomiting occurs often in phthisical patients, especially when the larynx is involved. It is usually brought on by paroxysms of coughing. Less frequently the cause of the vomiting is gastric catarrh, occa- sioned by the irritation of the sputa which have been swallowed; but in some cases the gastric symptoms depend upon the general condition — e. g., the anaemia. Although the tubercle bacilli swallowed with the sputum hardly ever infect the stomach, probably from the acid reaction of its contents, they very often at- tack the intestinal canal. In the majority of the cases of phthisis we find tuber- cular ulcers, either singly or in considerable numbers, in the vicinity of Bauhin's valves [the ileo-ca3cal valve], in the lower part of the ileum, and the upper part of the large intestine. Intestinal tuberculosis does not always cause very marked clinical symptoms, but as a rule we find diarrhoea in patients with tubercular ulcers of the intestine. They may have three or four stools in the twenty-four hours, and even more, but the stools have nothing characteristic. We rarely see a slight admixture of pus or blood in them. Tubercle bacilli have been repeatedly discovered in the de- jections, but the search for them is rather difficult. We must call attention, how- ever, to the fact that many patients have diarrhoea during life in whom we find at the autopsy no intestinal tuberculosis, but only a simple intestinal catarrh. Severe diarrhoea of a persistent and refractory character may also occur in asso- ciation with amyloid degeneration of the intestine, which is not infrequently seen in connection with other amyloid changes. Sometimes tuberculous ulcera- tions of the intestine are found at autopsy which, during life, had caused no diarrhoea. In cases of severe intestinal tuberculosis we sometimes meet with meteorism. With deep ulcers, extending to the peritoneum, we often see marked tenderness of the abdomen. The peritoneum may be affected by the tubercular ulcers of the intestine in a twofold manner. Genuine peritonitis from perforation, with a purulent or even a sanious exudation, is quite rare, and is excited by the rupture of an ulcer and the entrance of the contents of the intestine into the abdominal cavity. An in- fection of the peritoneum with the tubercular poison is more frequent. This may arise from deep-seated ulcers, which do not reach actual perforation, so that we have a peritoneal tuberculosis, or a tubercular peritonitis. During life peri- tonitis from perforation and that from tuberculosis are not always to be distin- guished. We must also mention that simple ascitic fluid is sometimes found in the abdominal cavity in phthisis, which may lead to a false diagnosis of peritoneal tuberculosis. Another way in which we may have a peritoneal tuberculosis in the course of phthisis is from the extension of the process in a tubercular pleurisy, through the diaphragm to the peritoneum. 4. Liver and Spleen. — We very often find a few or even many tubercles in the liver in phthisis, but they have no clinical significance. The liver is almost always infected with the tubercular poison from tubercular ulcers in the intestines, from which the poison passes to the branches of the portal vein and then to the liver. Fatty liver and amyloid or lardaceous liver are more important clinical changes. We can sometimes recognize the former by making out on physical examination the increase in the size of the organ, and by feeling its characteristic blunt lower edge. Moreover, we must emphasize the fact that, in our experience, fatty infil- tration of the liver is found much more rarely at the autopsy of consumptive subjects than the statements of many earlier authors wovild lead one to expect. 250 DISEASES OF THE EESPIEATOEY OEGAISTS Amyloid degeneration of the liver appears almost always in association with amyloid change in other organs (kidneys, spleen, intestine). If the amyloid degeneration is advanced, the liver is considerably enlarged, and it is usually pos- sible to feel distinctly its sharp and resistant edge; and, not infrequently also, its firm upper surface. Miliary tubercles or single large tubercular nodules in the spleen have a patho- logical interest only. Great splenic enlargement is found in amyloid degen- eration. 5. Kidneys, Urinary Passages, and Sexual Organs. — The presence of miliary tubercles in the kidneys is the first change in them to be mentioned, but it has no clinical significance. Extensive tuberculosis of the genito-urinary apparatus, however, may produce marked symptoms, such as pyuria. Genito-urinary tuber- culosis will be discussed in a later part of this work. In regard to the symptoms of amyloid kidney, which may develop in the course of phthisis in connection with amyloid disease in other organs, we will refer to the section on renal diseases. Genuine cases of nephritis, both acute and chronic, are also found quite fre- quently in phthisis, often combined with amyloid disease. These can not escape notice if the urine is carefully examined. Their development is probably always referable to the excretion of toxic material, arising from the disease in the lung. , 6. Circulatory Organs. — The rate of the pulse is often increased in consump- tion. This increase in frequency may be merely proportional to the fever, if any exists. It is also usually seen and it may be considerable when there is no fever. A persistently rapid pulse, when the temperature is little, if at all, ele- vated, may therefore be an important diagnostic sign of pulmonary (and all other) tuberculous diseases. The increase of the pulse, which readily comes on from comparatively trifling external causes, is especially noteworthy. It may be seen after slight physical exertion, or upon mental excitement, as during the physician's visit. Anatomical changes in the heart are rare, except that it is often remarkably small and flaccid. Moderate fatty degeneration of the heart, slight endocarditis of the valves, or occasional tubercles in the heart, causes no symptoms. The oc- currence of tubercular pericarditis, however, is important. This almost always arises from the extension of the tubercular process from the adjacent pleura, but in exceptional eases pericarditis has been seen as a result of rupture of a tuber- culous lymph-gland or a pulmonary cavity into the pericardium. 7. Lymph-glands. — The lymph-glands are a favorite seat for tubercular changes. We have stated above that the so-called scrofulous, cheesy lymph- glands, which are seen chiefly in the neck and the axillse, are afl'ected with tuber- cle in the majority of cases. The tubercular infection probably develops here from slight injuries and excoriations of the skin, by which the bacilli enter the body and reach the neighboring glands by means of the lymph-current. In other cases the infection comes perhaps from the mucous membrane of the phar- ynx. In tuberculosis of internal organs, too, we very often find the corresponding lymph-glands enlarged and more or less cheesy. The bronchial lymph-glands are swollen as a result of pulmonary tuberculosis, the mesenteric and retroperito- neal glands as a result of intestinal tuberculosis. The tuberculosis of the bron- chial lymph-glands is of especial importance in children. laideed, the tubercular virus which has gained access to the lungs may apparently reach the bronchial glands by means of the lymph-channels even without affecting the lungs them- selves, and occasion a tuberculous disease of the glands. Glands thus diseased break down and discharge into the lungs, and in this way generate a secondary pulmonary tuberculosis. This is one reason why the pulmonary tuberculosis of TIJBEKCULOSIS OF THE LUNGS 251 children so often begins not in the apex but in the middle or lower portion of the lung. Pressure from the enlarged glands may affect the air-passages, the branches of the pulmonary artery, the veins, the recurrent nerve (paralysis of the vocal cords), and even the aorta. Perforation of the cheesy bronchial glands into the cesoph- agus, the blood-vessels, etc., has also been observed. Tuberculosis of the bron- chial glands does not present any definite type of disease, however, and, although we may sometimes suspect it when there is pulmonary tuberculosis, we can only rarely diagnosticate it with certainty. The author himself observed a note- worthy case of tuberculosis of the bronchial glands, with compression of one vagus nerve in a patient who, during life, for weeks coughed up large amounts of a purely sero-mucous expectoration containing no bacilli. 8. Nervous System. — We have already mentioned various nervous symptoms in the description of the general symptoms. We must also add that tubercular meningitis is seen in the course of phthisis (see page 1059), and that large soli- tary tubercles may occasionally develop in the central nervous system. 9. Skin. — We have spoken of the great tendency which many patients have to severe sweats, especially at night. The frequent appearance of pityriasis versi- color, especially on the skin over the thorax, is also worthy of note. We often see moderate oedema of the legs and ankles, which is due to weakness of the heart. More marked oedema of one leg sometimes arises from thrombosis of the femoral vein. We must also mention here, in conclusion, the specific tubercular disease of the skin — lupus. This occurs alone, as a rule, without a co-existing pulmonary tuberculosis ; but, on the other hand, the old term " scrofulous lupus " had reference to the fact that we often find other tubercular affections in lupus besides the disease of the skin. Thus it does not seem strange that lupus and phthisis have been repeatedly observed to co-exist. Cutaneous tuberculosis may develop not only in the ordinary form of lupus, but also in nodules of consider- able size, or in rather extensive ulcers. Certainly some of the cases of so-called corpse-tubercle belong to true tuberculosis. We have seen a similar tuberculous cutaneous disease in a woman who for a long time had washed the soiled handker- chiefs of a consumptive patient. We have also seen a tuberculous affection of the skin upon the chin of a patient very ill with consumption. In this case, no doubt, the skin became infected by the sputum. Diagnosis. — The diagnosis of pulmonary tuberculosis has become absolutely certain, since the discovery of the tubercle bacilli, by the demonstration of their presence in the sputum (vide supra). In all incipient cases, in which the other symptoms of the disease have not yet made themselves manifest, but the sus- picion of incipient phthisis has been aroused by a persistent cough, by marked pallor and emaciation, by slight hoarseness, by an evening rise of temperature, by the appearance of night-sweats, by the presence of a hereditary predisposition, and similar symptoms, the finding of tubercle bacilli in the sputum is often the sole deciding factor. Still, it must not be forgotten that the examination for bacilli is decisive only when its result is positive, and that the greatest attention should be given also to all the other symptoms. To form an opinion as to the severity of a particular case, and as to its exact distribution and the variety of the tubercular process, is at present possible only by means of a consideration of the other symptoms, and in particular of the results of physical examination. The latter, therefore, has lost none of its importance by the discovery of the tubercle bacilli. Confusion between phthisis and other diseases is twofold. Where the consti- tutional symptoms are predominant, and there are no marked pulmonary symp- toms, an existing tuberculosis may be overlooked. In the beginning, especially, many cases of phthisis are considered to be merely anasmia, chronic gastric 252 DISEASES OF THE EESPIRATORY ORGANS catarrh, or simple bronchitis. If a continuous or intermitting fever appears in an early stage of phthisis, before any marked pulmonary symptoms have devel- oped, the disease may be mistaken for malaria or the like. On the other hand, it is by no means rare to consider patients phthisical who are suffering from some entirely different affection. He who lays too great stress .on the uncertain results of percussion will often make a false diagnosis. Severe latent diseases of the stomach, or certain general diseases, such as anaemia, diabetes, or chronic nephritis, may be mistaken for phthisis. Other pulmonary affections, too, may be confounded with tuberculosis, especially chronic bronchitis, emphysema, bronchiectasis, foetid and gangrenous, processes, and carcinoma of the lungs. A careful, unprejudiced, and complete examination of the patient is the only pos- sible protection against such errors. It is very important for the physician to know that there is such a thing as hypochondriacal phthiseophobia. Some nerv- ous individuals are tormented by a constant dread of becoming consumptive. Such persons complain of thoracic pain, dry cough, weakness, and other imagi- nary symptoms, which might readily mislead the physician into supposing that they actually have incipient pulmonary tuberculosis. Of course, the correct interpretation of such conditions is usually no difficult matter to the experienced physician, who is guided by the general impression of " nervousness," and by the comj)lete absence of any objective physical signs. In this connection we ought, furthermore, to express our opinion of the diag- nostic value of Koch's tuberculine (vide infra). Koch made the important dis- covery that tuberculous patients, particularly those suffering with pulmonary tuberculosis, exhibit a particular " reaction" after the injection of small amounts of tuberculine (gramme 0.001 to 0.002 of Koch's preparation). When this reac- tion occurs there develops, some four or five hours after the injection, a fever of 102° to 104° (39° to 40° C), associated with chilliness, headache, pain in the limbs, nausea, and languor. This constitutional reaction passes off after some twelve or fifteen hours. If the tuberculous process is located in the skin, trachea, or some other part where it is accessible to direct observation, a very decided local reaction may usually be observed besides the constitutional disturbance. The tuberculous tissue becomes swollen, red, and finally in part necrotic. In patients with tuberculosis of the internal organs, also, this local reaction probably takes place, but of course it can not be actu.ally seen, although it may perhaps be inferred because of the secondary phenomena. Thus, in pulmonary tuberculosis there may be an increase in the cough and expectoration. On the other hand, if an injection of tuberculine is made in a person who is healthy, or who is suffering from some disease other than tuberculosis, then, according to Koch, there will be no reaction at all to small doses. To obtain any reaction in persons who are healthy, or, at any rate, not tuberculous, it is said that the dose of Koch's prepa- ration must be increased to the amount of gramme 0.01. If these statements were true, the appearance or the absence of a reaction after the injection of a small amount of tuberculine would be an important and, indeed, a decisive factor in determining whether tuberculosis did or did not exist in any given case. These statements of Koch have been shown, hoAvever, by extensive investiga- tions, to be true only in general, and not in every case. Other observers as well as the present author have occasionally found that healthy persons, or persons free from tuberculosis, have reacted to doses of one or two milligrammes of tuber- culine ; while, on the other hand, patients with indubitable pulmonary tuberculo- sis have shown no distinct reaction even to considerable doses of tuberculine. Consequently the result of an injection of tuberculine can never be completely decisive from a diagnostic point of view, and in practice, therefore, the employ- ment of tuberculine for diagnosis has been adopted by only a few; but still, it would be a mistake to discard this means of diagnosis completely. In doubtful TUBEECULOSIS OF THE LUNGS 253 cases when we can not be sure of the diagnosis, the injection of about two milligrammes of tuberculine is of real importance, and the result of the test is certainly a valuable factor in summing up such a case; yet the verdict is never so unimpeachable as in cases in which the tubercle bacilli have been dis- covered. Prognosis. — It is very difficult to make a general statement as to the prog- nosis of pulmonary tuberculosis. There is no doubt that tuberculous foci in the lungs, if of limited extent, may become completely healed, at least from a clinical point of view. Indeed, such recovery probably takes place oftener than many suppose; at least, it is not very exceptional to find at the autopsy of elderly persons cicatricial contractions in the apices of the lungs which may, without doubt, be regarded as healed tuberculosis. In many of these cases the previous tuberculosis had never come to the knowledge of any physician. At the pres- ent day the discovery of tubercle bacilli in the sputum has rendered the diag- nosis of even very limited tuberculous processes an easy matter, and, consequent- ly, cases of recovery from pulmonary tuberculosis are now recognized much more often than formerly. Nevertheless, the prognosis of pulmonary tuberculosis must always be re- garded even now as very serious, and when the disease has made any great prog- ress the prognosis is decidedly unfavorable. Many cases of apparent recovery exhibit merely a temporary improvement, to grow worse again, and the assertion that treatment is absolutely hopeless in almost all cases in which the disease has reached an advanced stage is, unfortunately, too well established to require elab- orate argument. There is, however, one fact of extreme importance which should never be dis- regarded in the prognosis of pulmonary tuberculosis. There is a great difference in the duration of the disease. It is possible for the process to go on for years, while the patient feels tolerably well, and yet the disease smoulders. From this point of view cases may be distinguished as " benign," compared with those of rapid progress, and this prognostic distinction has the greatest importance in practice, although it is often very difficult to recognize. Many a consumptive, when first examined, gives one the impression that he can not live a fortnight longer, and yet the disease lasts many months, with improvement in most of the symptoms and general alleviation of the patient's condition. Again, one believes the disease to be incipient, encourages the family, and the patient dies in a few weeks of galloping consumption. Certain complications may occur which it is impossible to foresee, such as pulmonary haemorrhage, pneumothorax, tubercular meningitis, and miliary tu- berculosis. Apart from these, however, there are certain conditions which lead us to expect a comparatively favorable course for the disease : such are a vigorous constitution unimpaired by bad habits, of which drinking is particularly un- favorable ; a good weight ; freedom from hereditary taint ; limited extent of the local process ; later life ; the absence of complications ; and, finally, the persistent absence of fever. This last factor is so important that we must lay special stress upon it. If there is no fever whatever in a case of pulmonary tuberculosis, the patient is at that time in a condition in which the disease is quiescent ; and a decided improvement, perhaps even cure, may Be expected if appropriate means are employed. On the other hand, whenever fever appears we know that the dis- ease is not quiescent, but is actively advancing with more or less rapidity. The important points about the temperature in this regard have been already empha- sized (see page 246). It is self-evident, also, that the worldly circumstances of the patient, as well as the factors which we have just alluded to, are of great prognostic importance. On these, for instance, depends the possibility of i)roper care, of abundant nourishment, and, it may be, of a change of climate. 254 DISEASES OF THE EESPIEATOEY OEGANS Treatment. — 1. Prophylaxis. — The question of what prophylactic measures may effectually prevent the extension of the disease has entered upon a new stage since our definite knowledge as to the infectious nature of tuberculosis. We can no longer doubt the contagious character of phthisis, in support of which isolated examples were previously brought forward. Even if, according to all experience, the danger of contagion is not very great, still it is foolish to ignore it entirely. We must therefore call the attention of the relatives of phthisical patients to the possibility of this danger, and we should not permit the children of such patients to be uselessly exposed to it. We should take satisfactory pre- cautions for isolation, and also for disinfection of the sputum. Suitable sputum cups should be employed, and care should also be taken to prevent the dissemina- tion of the expectoration, either in its fresh state or after it has become dry. The future will teach us whether much evil may not be averted by such measures. The " prophjdaxis " till now employed was almost exclusively confined to hardening and strengthening the threatened individual as much as possible. We should ti-y to strengthen the bodies of children of a weak habit, with " scrofulous " symptoms, and children from families in which cases of tuberculosis have already occurred, and thus to arm them against the enemy that threatens them. Good food, fresh air, and a diminxition of the sensitiveness of the body by cold spon- ging and cold baths — these are the factors whose favorable influence is generally recognized. The removal of certain foci of tubercular disease, already existing, from the body may prove of great prophylactic importance. We refer to the timely treat- ment or extirpation of scrofulous — that is, tubercular — swellings of the lymph- glands, healing or resection of tubercular bones and joints, etc. Although in individual cases we can of course never know whether the part removed is the sole focus of disease in the body, still we are undoubtedly justified in trying to remove at least one possible source of some later general infection. A fuller discussion of this important point must be left to the works on surgery. 2. Therapeiisis. — Physicians have often thought that they had discovered a specific remedy for tuberculosis, but apparently they have thus far been mistaken. Formerly, the inhalation of antiseptic substances, such as carbolic acid, benzoate of sodium, and iodoform, was recommended, but this practice is now almost en- tirely given up. Arsenic was for a time much used, best given in pills containing ^'^- To (g'rm- 0.003) repeated several times a day; but this practice, again, has not held its own. Arsenic may be tried in incipient cases, particularly those associated with marked antemia, but great curative influence is not to be expected from it. Creasote has won far more advocates.' Continued for a considerable time in large doses (fifteen to thirty grains, grammes 1 to 2, or more, in the course of twenty-four hours), it is regarded by many physicians as an excellent remedy in incipient and even in advanced pulmonary consumption. It is best prescribed in gelatine capsules, or in a mixture of one part of creasote to two parts of the tincture of gentian, of which twenty to eighty drops may be given three times a day in a considerable amount of milk, or in wine. This remedy is usually fairly well borne, and the patients are pleased with the improvement it causes in their appetite and general condition. Of late, physicians have employed guaiacol, the active ingredient of creasote, instead of the drug itself, especially since carbonate of guaiacol has been brought forward, a preparation which has very little of the disagreeable odor and taste of creasote itself. Carbonate of guaiacol is admin- istered in powders containing about eight grains (gramme 0.5), in daily doses at first of twenty-five grains (gramme 1.5), gradually increasing to thirty or forty- five grains (grammes 2 to 3). Dyspeptic disturbance sometimes follows the use even of guaiacol, but still this remedy is, in general, better borne and more read- TUBEECULOSIS OF THE LU^tgs 255 ily taken than creasote. As to the specific and therapeutic use of guaiacol in pul- monary tuberculosis, it is not easy to foitn a decided opinion. It is certain that many jDatients praise these remedies, and improve considerably "while using- them ; but, on the other hand, the indiscriminate laudation of many authors is decidedly uiajustifiable. When the disease is slowly progressing- with persistent sub-febrile temperatures, the author has scarcely ever felt sure of any distinct influence ex- erted by guaiacol or creasote upon the temperature and the disease. ISTeverthe- less, it is often advisable in practice to make trial of these remedies, particularly of the carbonate of guaiacol. The remedy must be employed for months and, if possible, in increasing doses. Among the remedies which are recommended as having a specific influence, we will also mention cinnamic acid, which is con- tained in Peruvian balsam. This has been employed extensively by Landerer in the treatment of various tuberculous diseases, and particularly in pulmonary tuberculosis. He gives it in the form of small subcutaneous injections of a five- per-cent. emulsion, made up of the sweet oil of almonds and the yolk of e^g. The results obtained by Landerer, in the institute of Krahenbad, in the Black Forest, appear very favorable, but as yet they lack confirmation. The method has not yet been generally adopted. At the end of 1890 great interest was excited, as is well known, by the state- ment of R. Koch that he had extracted from pure cultures of tubercle bacilli, by means of glycerine, a substance called tuberculine, by Avhich he was able to heal tuberculous processes both in animals and men. This assertion aroused the thoughtless enthusiasm which is unfortunately so common with regard to ■ therapeutic questions, and which indeed in this case was rendered excusable by the high authority of the discoverer. In fact, within a few weeks after the remedy was made known, numerous reports were published of cures due to tuber- culine. But the longer the experiments were pursued the more evident it became that these extravagant opinions were not substantiated, and there set in a revul- sion of sentiment which has led to many adverse criticisms, perhaps equally un- justifiable with the CTrly praise. It is absolutely impossible to speak of tubercu- line as an established remedy for tuberculosis. In many patients there does in- deed appear a decided improvement under treatment, but these cases are such as were favorable any way, and therefore they may. owe their improvement to the general sjnuptomatic treatment and regimen which they have also enjoyed. At any rate, tuberculine has done no harm in such cases. Then, again, we have seen numerous cases of rather severe disease, in which it was not possible to notice any distinct influence of the tuberculine upon the general course of the illness. Per- haps the condition of the patient improved, or remained unchanged; or, again, it grew worse. Yet, whatever the change, it was such as might have occurred inde- pendently. Finally, there are, in the third place, cases which have been seen by the author as well as other observers, in which there was such a decided change for the worse shortly after the commencement of treatment, that one might really suppose that the remedy had exerted an actually harmful influence. We refer especially to cases in which the patient, previously without fever, exhibited after the injection a persistent elevation of temperature, Avith a more rapid ad- vance of the local process in the lungs. Consequently, we may say that, in all advanced cases, we can expect nothing from tuberculine. In incipient cases Ave may make trial of it, but we should be ex- tremely careful in our dosage, so as to avoid any chance of doing injuiy. Koch's rule at first was that the physician should begin with injections of gramme 0.001, and gradually increase. In this way was discoA'ered the interesting fact that the necessary dose for the production of the " reaction " (vide supra, page 252) became greater and greater. Many patients would finally bear the injection of one hundred milligrammes of tuberculine without any reaction at all. At first 256 DISEASES OF THE EESPIEATOEY OEGAXS it was regarded as the object of treatment to reach this point of tolerance, but the practice is now abandoned. One should begin with very small doses, about one fourth to one half a milligramme, and increase so slowly and by such minute gra- dations as to avoid any marked reaction. By such a method we can almost en- tirely exclude any harmful effect, and it may not be impossible that some of the patients who have had a favorable result actually owe their Improvement to the tubereuline, but it is extremely difficult to make sure of this. It would require the continuous observation of many patients for years, to enable one to form a reliable opinion with regard to this question. It may be seen that at present we can only speak with great reserve as to the possible therapeutic value of tubereuline, but nevertheless, its discovery was an event of the greatest value and interest, regarded from a therapeutical stand- point. There is no doubt of the specific influence of this substance upon tuber- culous processes. There is scarcely any sight more astonishing to the physician than the reaction of a patch of lupus upon the skin to a tiny dose of tubereuline introduced into the circulation! Taken into consideration with other bacterio- logical facts, this affords us a clear glance into a future when we shall succeed in making the wonderful influence of the material produced by the growth of bacteria available for the cure of infectious disease, and, in particular, of tuber- culosis. Perhaps there are the same possibilities for tuberculosis as in the case of diphtheria, the treatment of which, by means of the antitoxic serum pre- pared by Behring, is apparently so very successful; but with regard to tuber- culosis our methods are as yet incomplete, and a final opinion as to their value would be premature. Meanwhile, therefore, we physicians must continue to lay the greatest stress in the treatment of tuberculosis upon those methods which are termed in the widest sense hygienic and constitutional. It is undeniable that, by the correct and faithful emplo;vTi:ient of such methods, many very satisfactory successes may be obtained. Eor the present, we must be discreet, and seek to in- fluence the disease in the old accustomed manner by those therapeutic measures which have come down to us from ordinary medical observation and expe- rience. The hygienic and constitutional method of treating consumption has for its object the greatest possible promotion of the natural powers of healing. "We aim at this, in the first place, by avoiding as much as possible all influences which might cause a further extension of the disease, and by re-enforcing, so far as we can, all influences which increase the resisting powers of the individual, and the processes of spontaneous cure. The factors which are of most importance in this connection are, first, diet; second, rest; and third, the uninterrupted enjojTuent of good air. To obtain these three therapeutic factors all at once requires the renunciation by the patient of his calling, and his usual mode of life. The treatment of tuberculosis, therefore, should begin with the demand that the patient, for as long a time as possible, should devote himself exclusively to the care of his health. The next point is the choice of the place in which the " cure " shall be carried on. In many cases the proper management of the patient i^iay be pursued under the ordinary surroundings of home. Often, however, this is not the case because the last two, or even all three, of the essentials named can not be provided at home. It, therefore, is the duty of the physician in every indi- vidual case to determine how the desiderata are best to be obtained. According to the patient's means we consider respectively a residence in the country (if pos- sible, in a picturesque and wooded region); a special health-resort; or, finally, a suitable sanitarium. Erom a therapeutic standpoint, there is no doubt that treatment in a specially adapted sanitarium is chiefly to be recommended. In this all the requirements for recovery can be best carried out, and the patient constantly remain under medical obseiwation. In most cases it is only exter- TUBEECULOSIS OF THE LUNGS 257 nal considerations, for instance, pecuniary, -vvhicli keep the patient from a sani- tarium. It is a true philanthropy, therefore, which has of late led everywhere to efforts to render the benefits of institutional treatment accessible to the less wealthy classes. The requirements for proper treatment are also partially ful- filled in the so-called public health-resorts for pulmonary consumptives. These resorts, however, have the disadvantage that the patient is left far more to his own resources, and is consequently apt to be incautious, and hence jeopardize his recovery. A public health-resort would, therefore, be especially chosen for patients who have already been in an institution, and have learned what mode of life is proper for them; or for those who have already so far recovered that they may be allowed a certain degree of freedom. With regard to the minutiae in carrying out the above-enumerated essen- tials of treatment, we would add as follows : 1. Diet. This should be as nourish- ing and abundant as possible. Meat, milk, eggs, farinaceous foods, and butter are chiefly to be recommended, care being taken that the body should receive a sufficient amount of carbohydrates and fats, as well as an abundance of albumen. Many special " cures " for pulmonary consumption have a value, in so far as they lead to the ingestion of an abundant amount of easily assimilated nourishment. Such are cures with milk, koumyss, or kefir. It has even been proposed to in- troduce large amounts of such nourishment as milk and pulverized meat into the stomach by means of a stomach-tube, and thus accomplish " overfeeding." This method has not become very popular, although it may be indicated in some cases. It is very important to see that the patient has a diet that is not only abundant, but also palatable and varied. If pure milk is not readily taken, we may try the addition of coffee, tea, common salt, or brandy. With regard to the prescription of alcohol we recommend, unhesitatingly, moderate amounts of beer, and particularly such beer as is rich in extractive matter; and perhaps also extract of malt, and porter. Small amounts of good wine may contribute to the improvement of the appetite and the general condition. On the other hand, we think it useless and, in some circumstances, harmful, to order large amounts of the stronger alcoholic beverages, such as port wine and brandy, as prescribed in many sanitariums. Artificial foods, such as various preparations of meat, soma- tose, neutrose, and the like, should be used merely as makeshifts. The employ- ment of cod-liver oil to the amount of two to four tablespoonfuls a day is some- times not inappropriate, if it is well borne. 2. The two other factors of cure — rest, and the continuous enjoyment of good air — are best fulfilled by the fresh-air treatment, which is of late gaining in importance and popularity. The patients spend the greatest part of the day lying in the open air on comfortable reclining chairs. At the same time they avoid any unnecessary bodily exertion, any great demands upon respiration, and any irritation of the respiratory passages. Gain in bodily weight is promoted. The limitation of the diseased processes in the lungs is favored. Of course, in such matters also the individual should be considered, for moderate exercise in the open air is certainly for many patients not harmful, but rather beneficial. Often the methodical carrying out of the open-air treatment under suitable conditions demands the resources of a sanitarium, but we may find in a garden or on a veranda a sunny spot, screened from the wind, where the patient may lie com- fortably and pass the entire day till near sunset in the open air. In case of necessity the patient must content himself with a place by an open window. The advantages of the climatic health-resorts {vide infra) consist principally in the fact that they render possible a continuous enjoyment of the open air, even during the colder part of the year. It has been maintained that climatic factors, par- ticularly elevation, exercise a specific influence upon the healing of pulmonary tuberculosis; but this has not yet been proved. The best-known sanitariums for 17 258 DISEASES OF THE EESPIEATORT OEGANS pulmonary disease are found in Falkenstein in the T annus, Gorbersdorf, St. Bla- sien, Eeiboldsgriin, Hohenhonnef, and Andreasberg in the Hartz Mountains, and Davos and Arosa in Switzerland. Of the public health-resorts which are particu- larly suitable for consumptives, we would name for summer use the acidulated, alkaline, and chloride-of-sodium waters of Ems, Obersalzbrun, and Eeinerz; the chloride-of -sodium waters in Eeichenhall, Salzungen, and Soden; the mud springs in Lippspringe, Inselbad, and Weissenburg in Switzerland. Eor summer climate, the following are to be recommended: Beatenberg, Heiden, Engelberg in Switzer- land; Badenweiler, St. Blasien, Eippoldsau in the Black Forest, and many others. For the colder portion of the year we have, in their lofty situation, Davos, Arosa, and others. The more vigorous the constitution of the patient, the more proper it is to recommend him to go to a great elevation in the winter; while delicate subjects are usually better suited in the soitthern resorts. Of course only the very distant health-resorts in Algiers, Egypt, Malta, and the much-praised Madeira, can furnish a certain guarantee of constant mild weather. The Sicilian health-resorts (Catania and Palermo), and also Ajaccio, afford fa- vorable climatic conditions; while the health-resorts of the Eiviera, Meran, Gries, Arco, Gardone, Lugano, Pallanza, and Montreux, are much more uncertain in this respect, and therefore are to be used merely as stopping-places by the way during the spring and autumn months. We must also state that, in incipient cases, a residence by the sea, or a long sea-voyage, may sometimes be of great help. We have ourselves known severaj young physicians who have become ship surgeons on account of incipient phthisis, and who have returned from the voyage much stronger, and some of them appar- ently entirely well. We can not go into a full description here of all the health-resorts mentioned. We can not omit, however, calling special attention to the fact that we should always ask ourselves, in choosing a health-resort, whether the expense and incon- venience thus imposed upon the patient can be balanced by the possible benefit. The earlier the stage of the disease and the better the general condition of the patient, the more will his physician be justified in urging him to make every sacrifice in order to regain his health. We must particularly insist with the patient that no cure of tuberculosis can be accomplished by a single visit to any health-resort, but that recovery must be achieved by living continuously for years in accordance with all the demands of hygiene. On the other hand, it is wrong, both from a medical and from a humane standpoint, to send away consumptives in the last stages of their disease, to perish far from home and friends. Consumptives with fever should never be sent from home, unless they find refuge in a real sanitarium where they may enjoy the con- stant observation and treatment of a physician. [Our own health-resorts for consumptives are too well known to demand ex- tensive consideration here. The prime object is to secure for the patient a pure air, with such climatic conditions that he can pass the largest amount of time out of doors, at the same time that within doors his comfort is provided for, and a sufficiency of suitable and well-cooked foods is attainable. In Colorado, ISTew Mexico, and California, large numbers of fonner consumptives are leading active lives. Florida, Aiken, Thomasville, Asheville, and some other southern resorts, are good winter asylums for many cases, but patients should not return to jiSTew England before June 1st. An out-door life in the Maine or Adirondack woods during the warmer months is highly to be recommended for early and otherwise suitable cases. Saranac, IST. Y., affords every comfort during the colder months, combined with the very best medical attendance, and many people do well there. A relative disadvantage under which nearly all American health-resorts labor, as compared with those of Europe, consists in the greater difiiculty in providing oc- TUBEECULOSIS OF THE LUNGS 259 cupation and thus securing a mental attitude most favorable to recovery. In gen- eral, the northern sea-board is much less favorable than the interior, and early- cases often do well during the wint.er removed from the dampness of the coast, with its alternations of freezing and thawing. A change of climate is a very im- Ijortant step, and should receive the most careful consideration of the physician — • the circumstances of the patient, the stage and character of his disease, his tastes, etc., being carefully weighed before a decision is reached.] Finally, the employment of hydrotherapy should be mentioned in the hygienic treatment of tuberculosis. Although this can not exert any specific influ- ence on the disease, and therefore must not be prized too highly, yet it is often beneficial in the form of cold sponging, or brief cool douching and the like; and the stimulation of the skin has a favorable influence upon the general health. In severe febrile cases we may order sponging and rubbing in bed with cold water, brandy, vinegar, and the like. Also for the relief of symptoms (vide infra), such as pain, fever, and perspiration, we may often employ sponging, cold or warm compresses, and the wet pack. The symptomatic treatment of phthisis is directed in the first place against the pulmonary symptoms. We use much the same remedies to help the cough as in chronic bronchitis. We try inhalations with a solution of common salt, or of the alkaline carbonates, or, if there is much secretion, with solutions of tannin and the balsams, such as turpentine, or balsam of Peru. When there is severe, spas- modic cough, inhalations with narcotic solutions sometimes give some relief, such as cherry-laurel water, opium, or bromide of potassium. Morphine stands first among the drugs employed to check the cough. We should be cautious and sparing in its use at first, but it is an indispensable remedy in severe and hopeless cases. It relieves the irritation of coughing, the pain and the oppression in the chest, and at least gives the patient for a time the desired sleep. In chronic cases, with moderately severe symptoms, we may use for a long time the milder narcotics with advantage, particularly codeine (powders of gr. 0.5-1.0, gramme 0.03-0.05) or phosphate of codeine; also the extracts of hyos- cyamus and of belladonna (extracti hyoscyami 1, aquae lauro-cerasi 20, fifteen to twenty, drops every two hours). [Heroine is sometimes useful in doses of ^g- grain. — ^V.] It is important that the patient should learn to suppress his incli- nation to cough, at least up to a certain point. Sips of cold water often quiet the cough, as may also a " cough drop " held in the mouth, or a pastille contain- ing the salts found in Ems mineral water. If the patient complains of difiiculty in loosening the expectoration, we pre- scribe expectorants, the action of which often fails to meet our desires, but which can not be dispensed with in practice. The expectorants most frequently used are carbonate of ammonia, ipecacuanha, apomorphine, and senega. We very often combine expectorants with narcotics, as in Dover's powder. If severe pain in the chest comes on, we often use local applications : mustard plasters, warm poultices and cold compresses, painting with iodine, or embro- cations of chloroform. ISTarcotics, such as morphine, are indispensable in severe dyspnoea, which usually occurs only in the last stages of the disease or as a result of pneumothorax. The treatment of ha3moptysis is important. As a slight admixture of blood in the expectoration often precedes a severe haemoptysis, such an appearance always suggests caution. When there is any haemoptysis, absolute rest in bed is necessary. We should avoid any careful examination of the lungs, especially any severe percussion. We should lay a flat and not too heavy ice-bag over the lung on the side from which we suspect the haemorrhage; the cold is usually well borne, but sometimes it aggravates the cough, and must then be omitted. We would also recommend SAvallowing bits of cracked ice. Narcotics, such as 260 DISEASES OF THE KESPIEATORT ORGAlSrS morphine, are tlie most suitable internal remedies, since they aid the cessation of the hsemorrhag-e by suppressing the attacks of coughing-. The more troublesome the cough the more necessary is it, therefore, to administer morphine in solu- tion, by the mouth or even subcutaneously. Of remedies to check the blood we should name, first, extract of ergot or ergotine, which may be given by the mouth, or, still better, subcutaneously, in doses of 2 to 8 grains (grammes 0.1-0.5) several times a day. As to sphacelotoxine, and other special preparations of ergo- tine, there has been as yet no extended experience. We may also try the fluid extract of hydrastis, with equal parts of an elixir, giving thirty to forty drops of the mixture several times a day; also, acetate of lead and atropine. The in- fluence of these remedies, particularly those last named, is, however, quite uncer- tain. The inhalation of a one- to two-per-cent. solution of perchloride of iron usually excites cough, and is therefore more harmful than beneficial. A very popular remedy among the laity, and one almost always at hand, is common salt, of which several teaspoonfuls may be given in water. When the haemorrhage recurs frequently, it is also advisable to " tie off " the limbs — that is, to apply bandages rather firmly around the middle of the upper arms and the thighs. This causes venous congestion, and hinders the return of blood to the lungs. When pulmonary hsemorrhage has occurred, the diet should consist at first of nothing but cold milk, eggs, and similar food. Hot food, alcohol, and large amounts of meat are to be forbidden. It is a good thing to give acids, such as lemonade, or aromatic sulphuric acid, well diluted. Even when the bleeding has ceased we must keep the patient several days in bed, and for a loiiger time be extremely cautious, since the hsemorrhage is apt to be repeated. The hectic fever of consumption is remarkably little influenced by antipyretic drugs. It often is entirely useless, or even, on account of its evil effect upon the stomach, actually harmful to give to feverish consumptives, for long periods of time, large doses of such drugs as quinine, antipyrine, and antifebrine, particu- larly as the fever often of itself has deep morning remissions. The prescription of antipyretics is only justified when they make the patient feel better. On the other hand, it is very appropriate to give a cold sponging and rubbing to the whole body or chest, with water or alcohol, especially in the evening when the fever is high. The sponging is almost always well borne, and makes the patient feel brighter and easier. The cold pack may also be tried occasionally. Cold sponging often diminishes the troublesome sweats in phthisis, but if this does not check them, we may often prescribe atropine to advantage, grain tJt to •gV (gramme 0.0005-0.001) at night, but its action does not usually last very long. Lately agaricine in ^f" to -g-grain pills (gramme 0.005-0.01) has been recom- mended for the night-sweats in phthisis; also picrotoxine, of which grain i to J (gramme 0.008-0.01) is given in pill or solution at bed-time, and lately camphoric acid, grains 20-30 (grammes 1.5-2.0) in wafers. Dusting the body with a powder of five parts of salicylic acid to ninety-five of French chalk is also good. Sage tea is a favorite remedy for night-sweats — two or three cups of it cold at night — and so are milk and cognac. If there is loss of appetite, small doses of quinine, compound tincture of cin- chona, wine of cinchona, and other bitter remedies, such as tinctura amara (P. G.), are sometimes of service. It is also frequently a good thing to prescribe a little muriatic acid, five to ten drops of the dilute acid, with the meals. It is often very hard to check diarrhoea in phthisis. Opium, combined with tannin or acetate of lead, is most effective. This subject will be discussed more fully in the chapter on intestinal tuberculosis. We often prescribe preparations of iron, combined sometimes with quinine or arsenic (vide supra), in the beginning of the disease to improve the general con- ACUTE GENEKAL MILIAEY TUBERCULOSIS 261 dition and the anaemia, but, as experience shows, iron is contra-indicated in patients who are feverish or who have a tendency to haemoptysis. The treatment of the diseases complicating phthisis is to be found in the appro- priate chapters. CHAPTEE YII ACUTE GENERAL MILIARY TUBERCULOSIS .Sltiolog^. — Acute miliary tuberculosis is a form of tuberculosis which we are justified in describing particularly because of its anatomical relations and its peculiar clinical history. The disease is characterized anatomically by the ex- tremely abundant development of miliary tubercles in a comparatively short time in many organs of the body. We can not liken this process to anything but an overwhelming of the body with tubercle bacilli, which in some way reach the different organs simultaneously, and in them give rise to the eruption of tubercles. Buhl advanced the hypothesis a long time ago, that a cheesy focus could be found somewhere in the body in every case of acute miliary tuberculosis, and that the general infection of the body resulted from the absorption of these cheesy masses by the blood. Later investigations, however, have given us a much more definite explanation of the nature and manner of this general infection. Ponfick found, in some cases of acute miliary tuberculosis, an extensive tubercu- losis of the thoracic duct with breaking down of the tubercular new growth. It is easy to see how, in this way, a large amount of tubercular material could be brought directly into the circulation, from the free communication of the lymph- duct with the subclavian vein, and thus be " disseminated " through the different organs in a short time. Still more frequently, however, the tuberculosis of the large venous trunks, discovered by Weigert, especially the pulmonary veins, seems to be the starting-point for an acute general miliary tuberculosis. Usually there are tubercular lymph-glands, or sometimes other foci of tubercular disease, which involve the wall of a neighboring vein, gradually break through it, and project into its lumen. If caseation and ulceration result in this spot, the infec- tious material is of course constantly washed off by the blood-current and carried away, and thus it reaches the other organs. Since such a tubercular focus — e. g., a tubercular bronchial gland— may remain for a long time entirely without symptoms, we can understand how miliary tuber- culosis may break out in an acute form in persons who previously seemed per- fectly well. In other cases the patient has already suffered from some tubercular affection, and suddenly the conditions occur somewhere in the body which lead to the development of miliary tuberculosis. Thus we sometimes see it break out in a patient who has ordinary phthisis, but acute miliary tuberculosis is one of the rarities in advanced phthisis. If we find, at the autopsy of a case of acute general miliary tuberculosis, old phthisical changes in the lungs, which is by no means very common, they consist of old, partly cicatrized foci, pigment indura- tions, etc. We see miliary tuberculosis rather frequently as a sequel to pleuritic effusion. We have already previously called attention to the fact that in such cases the pleurisy itself is a tubercular disease. Miliary tuberculosis is also seen in persons with old tubercular affections of the bones and joints, such as coxitis and vertebral caries, with tubercular swellings of the lymph-glands, as in the neck and the axillae, or with tuberculosis of the genito-urinary organs. In such cases, of course, the tubercular affection which is discovered during life, is not always the source of the general miliary tuberculosis, but the discovery of the 262 DISEASES OF THE EESPIEATOET OEGAXS existence of such an afPection is of the greatest significance in diagnosis, as in this way our attention is strongly directed to the possibility of a general tubercular affection. In some cases an outbreak of miliary tuberculosis has been seen to follow other acute diseases, such as typhoid, or measles. Pathological Anatomy. — Except for the presence of an old tubercular affec- tion in some organ, and except for the tuberculosis of a vein or of the thoracic duct, which are as a rule apparent, and which have been described above, the anatomical lesion in acute miliary tuberculosis consists in the dissemination of miliary tubercles through a large number of the organs of the body. The lungs, the liver, and the spleen are constantly affected; almost as constantly the kid- neys, the thyroid gland, the marrow of the bones, the heart, and the choroid; less constantly, but still quite frequently, the serous membranes and the meninges. The miliary nodules may be found in large numbers in all the organs mentioned. They may in part be easily recognized by the naked eye, and in the kings they may be very plainly perceived by the touch. In many organs, however, especially in the liver and often in the spleen, they are hard to recognize with the naked eye, but they are easily discovered by the microscope. In regard to the histological structure of miliary tubercles, and the discovery of tubercle bacilli in them, we must refer to what has been said in the chapter on pulmonary tuberculosis, but we must also mention that, in some of the more chronic cases, some of the nodules may grow to be large tubercular foci, from the size of a lentil to that of a pea. Less developed cases of miliary tuberculosis are also found, in which only a lim- ited number of organs are attacked, and these with less severity. Clinical History. — The clinical symptoms of miliary tuberculosis depend upon two factors, the first being the general infection of the body, and the second the local tubercular affection of certain organs. Although in many organs miliary tuberculosis is entirely without symptoms, as in the liver, the kidneys, the heart, and the marrow of the bones, in two organs — the lungs, and more especially the brain — it leads to the most marked local symptoms. The miliary tuberculosis of the choroid, discovered by Cohnheim and Manz, is also without symptoms, but it can be made out with the ophthalmoscope, and it is therefore of great diagnostic value. Miliary tuberculosis affords quite different pictures, according to the predom- inance of one or the other of the groups of symptoms mentioned. We distinguish the four following forms : 1. Miliary Tuberculosis, with Predominant Symptoms of General Infection: the so-called Typhoidal Form. — This form may in part greatly resemble typhoid fever. The patient, who previously seemed quite well, or in whom some local manifestation of tuberculosis was suspected, falls ill with gradually increasing general symptoms, dullness, loss of appetite, headache, and fever. Since there is no local affection to be discovered to explain the symptoms, the disease at first may well be taken for typhoid. The general condition grows worse constantly, the fever is high and continually rises, and cerebral symptoms appear. In some cases an exanthematous eruption, like roseola, may increase the resemblance to typhoid. With careful observation, however, symptoms are almost always de- tected later in the disease which are, to a certain degree, characteristic of miliary tuberculosis, and are due to the existence of that disease either in the lungs or in the brain. The patient's complexion assumes a peculiar pallor, and with it a defi- nite cyanotic hue. The respiration becomes remarkably deep, and there is dysp- noea; or signs of a tubercular meningitis arise, such as rigidity of the neck, loss of consciousness, disturbances in the innervation of the ocular muscles, etc., and death follows with these symptoms. These cases last from ten days to three weeks, reckoning from the beginning of the severe symptoms. ACUTE GEXEEAL :MILIAEY TUBEECULOSIS 263 2. Miliary Tuberculosis, ivith Predominant Pulmonary Symptoms. — These cases, too, may begin quite suddenly, almost like an acute croupous pneumonia, or they may develop gradually with quite a long prodromal stage. From the onset the symptoms point especially to disease of the lungs or the pleura. The patient complains of a stitch in the side, cough, and dyspnoea. The expectora- tion may bear a decided resemblance to that of pneumonia. Such cases, espe- cially if they begin abruptly, are at first often erroneously regarded as croupous pneumonia, particularly if we find fine rales almost like crepitant rales over cer- tain portions of the lungs. But the expected crisis does not occur: the fever continues; the dyspnoea, general weakness, and anaemia of the patient increase; the physical signs of pulmonary disease (diffuse bronchitic rales) become more and more extensive. The patient's face is pale, cyanotic, and anxious. Death ensues with all the signs of impaired respiration. The course is usually some- what more protracted than in the tjTphoidal form, lasting for three or four weeks and more. 3. Miliary Tulerculosis, until Predominant Cerebral Symptoms, due to Tuber- cular Meningitis. — Tuberculosis of the meninges does not belong among the reg- ular lesions of general miliary tuberculosis. It develops in about haK the cases, according to our estimation; but where it occurs it almost always gives the whole case the characteristic imprint of tubercular meningitis, by which the other symp- toms are entirely concealed. The predominant symptoms are headache, fever, stupor increasing to deep coma, rigidity of the back and neck, and disturbances in the innervation of the ocular muscles. In such cases the tuberculous menin- gitis may alone be diagnosticated, and not the universal miliary tuberculosis. In fact, all the other signs of general miliary tuberculosis are not infrequently obscured by meningeal symptoms, and yet we have repeatedly observed, even in the deepest coma of the patient, a peculiarly deep and hurried respiration, which was the only noticeable sign referable to the miliary tuberculosis in the lungs. The sjonptoms of tubercular meningitis in many cases predominate in this type of the disease from the onset, but in other cases they come on during the attack and form its final period. The duration of the disease varies accord- ingly. 4. Miliary Tuberculosis witli a Protracted Course and Indefinite Symptoms for a Long Time — Intermitting Form. — ^Besides the forms already mentioned, cases occur which usually take quite a protracted course, lasting for eight or ten weeks, and having such indefinite symptoms that an absolute diagnosis is for a long time, or even throughout the disease, quite impossible. The patient com- plains of a number of general symptoms, such as headache and dullness, and also of thoracic symptoms, for which, however, we can find on examination no sufli- cient basis. There is almost always fever, usually not very high, and with a very irregular course ; hut we have seen a regular daily rise of temperature for a time in some cases, and attacks of fever with quite a severe chill, so that at first we thought of an irregular malarial intermittent fever — the intermitting form. Later on the symptoms gradually increase. The apparently inexplicable loss of strength, and the patient's ansemia and emaciation, are marked, and they are important in diagnosis. Einally, either severe pulmonary symptoms or the signs of tubercular meningitis set in, and to these the patient succumbs. We must mention particularly that the four forms of miliary tuberculosis just described are only the types of the disease. In individual cases we often meet with variations and transitional forms between these types. Single Symptoms. — 1. General Symptoms. — In all c^ses of acute miliary tu- berculosis the general condition of the patient is very serious. Most patients have a subjective feeling of severe illness, although they make little special com- plaint of it from the painless character of the disease. As the disease increases, 264 DISEASES OF THE EESPIRATOET OEGANS there is often a marked feeling' of anxiety and oppression besides the dyspnoea. There is, especially in the face, quite a peculiar pallor, characteristic of the disease, and associated with a marked cyanosis of the lips and cheeks. 2. Fever. — Acute miliary tuberculosis almost always runs its course with a more or less high fever, a course without fever having been observed in only a few instances. It often happens, in more protracted cases, that the temperature may be nearly normal for a time, or only slightly elevated. There is nothing characteristic or typical in the course of the fever. In the cases with typhoidal symptoms the fever is usually quite high, between 103° and 105° (39.5°-40.§° C), so that the temperature-curve may be exactly like that of typhoid. In other cases the fever is irregular and is broken by many remissions, remitting or intermit- ting quite regularly for some time. Death ensues with a moderately high tem- perature or in collapse. In cases with tubercular meningitis there is also a marked rise of temperature at the close, up to 108° (42° C.) and over. 3. Respiratory Apparatus. — It goes without saying that physical examination of the lungs may give no definite results. Almost all positive evidence is often wanting', and the contrast between the labored breathing and dyspnoea and the insignificance of the physical signs in the lungs is an important feature in diagnosis. Auscultation, as a rule, gives the signs of an intense bronchial ca- tarrh; we hear rhonchi or numerous fine and medium moist rales all over both lungs. The respiratory murmur itself is usually higher in pitch than normal, and in many cases it is obscure, rough, or harsh. In one of our cases there was heard, over a circumscribed area of the lung, a wholly peculiar, sharp, " lapping " sound on inspiration, which we have never heard under any other circumstances. Jiirgensen describes a soft friction sound, due to miliary tuberculosis of the pleura. Percussion usually gives no objective changes. At times the resonance is rather tympanitic, or slightly dull in some places. In some cases circumscribed pneumonic infiltration has been observed in the lungs in acute miliary tuberculosis, which, as we have said, may give rise to a confusion between miliary tuberculosis and croupous pneumonia, from the pres- ence of marked dullness, crepitant rales, and bronchial respiration. We must mention, finally, that in some of the eases physical examination of the lungs shows old changes in them, a phthisical affection of the apex, a former pleurisy, and the like. Positive evidence of such old tubercular affections may be of great diagnostic value in doubtful cases. Dyspnoea has been repeatedly mentioned among the pulmonary symptoms. The respiration is usually very much accelerated, especially during the more advanced stage of the disease, so that we see in adults forty, sixty, and even seventy respirations a minute. The respiration is also very deep, and is some- times noisy. As a rule there is cough, but it is usually troublesome only in the cases with severe bronchitis. It is often very slight. The expectoration is usu- ally scanty, and it is not characteristic. Special mention must be made of the fact that tubercle bacilli are absent in it, unless old ulcerated tubercular foci are present at the same time in the lungs. 4. Circulatory Apparatus. — The pulse is frequent, about 100 to 120 a minute, often weak and small, and sometimes irregular, especially if tubercular menin- gitis co-exists. The miliary tubercles, which post mortem are almost always to be found in the heart, especially in the endocardium, cause no symptoms. In uncomplicated, acute, miliary tuberculosis there is little if any increase in the number of white corpuscles in the blood. The presence of tubercle bacilli in the blood will be mentioned below. 5. Digestive Apparatus. — Vomiting is frequent at the onset of the disease. The bowels are usually constipated, but in many cases there is a moderate diar- rhoea. The loss of appetite, the thirst, and the dry tongue are due to the general ACUTE GENERAL MILIARY TUBERCIJLOSIS 265 disease and the fever. The spleen is usually somewhat, but not very much, enlarged. '6. Nervous System. — In many cases in which the pulmonary symptoms pre- dominate the intellect remains quite clear until the last, but in other cases cere- bral symptoms, such as headache, dizziness, stupor, and delirium, come on quite early, and are a part of the general infection. As has already been said, the nervous symptoms in the cases combined with tubercular meningitis become quite prominent, but in individual instances it may be hard to decide whether they are due to such a complication, or are merely severe general symptoms. 7. Eyes. — The ophthalmoscopic examination of the retina is of special diag- nostic importance, since the diagnosis may be made absolutely certain by finding miliary tubercles in the choroid. A negative result, however, is never decisive against the diagnosis, since the tubercles are sometimes absent, or at least are very few in number. Their discovery is almost always difficult, and demands much practice in the method of examination. In cases with tubercular menin- gitis we sometimes find an optic neuritis. Diagnosis. — The diagnosis of acute general miliary tuberculosis is ordinarily and justly considered very difficult. It quite often happens that at the autopsy a miliary tuberculosis is found which was not even suspected during life. It must be confessed that frequently, in such cases, we might very well have thought of acute tuberculosis. If, therefore, the possibility of acute miliary tuberculosis is brought to our attention during the patient's life, we can occasionally make an absolute diagnosis. The severe general condition, usually associated with fever, is most important, and for this no local cause can be found. Then come the pulmonary symptoms, especially the peculiar dyspnoea, for which there is also no adequate corresponding physical change to be discovered. It gives decided support to our suspicion if we can make out a distinct predisposition to tuberculosis, either hereditary or consti- tutional, or the history of a previous tubercular affection, especially pleurisy, and also chronic affections of the bones. The peculiar cyanotic pallor of the patient is very characteristic. On these factors rests the differential diagnosis between the " typhoidal " form of miliary tuberculosis and typhoid fever. Marked roseola and considerable enlargement of the spleen are distinct arguments for typhoid, although they sometimes occur in miliary tuberculosis, and so are the intestinal symptoms of typhoid, such as meteorism, the characteristic, loose yellow stools, and possi- bly intestinal hsemorrhage ; but we must not forget that both the roseola and the intestinal symptoms may be absent in typhoid. The course of the fever must always be considered in the differential diagnosis. It is much more frequently irregular and atypical in tuberculosis than in typhoid. Of course, the tempera- ture-curve is not an absolutely decisive factor. The blood does not afford any indubitable signs of distinction between the two, since in neither disease is there a decided leucocytosis. If the number of leucocytes is conspicuously small, 5,000 or less, typhoid is strongly suggested. The Widal serum-reaction with typhoid bacilli (see page 22) is very important, and, when it turns out positively, decisive. On the other hand, of course, the absolute demonstration of miliary tuberculosis in the choroid is unequivocal evidence in favor of miliary tuber- culosis. In many cases the onset of meningeal symptoms may aid the diagnosis. Of course, if the patient is not seen until the last stages of meningitis, especially when there is an incomplete history, the diagnosis is next to impossible. In this case, if the fluid obtained by lumbar puncture is found to contain tubercle bacilli, the diagnosis may be settled (compare the chapter on tubercular meningitis). Acute tuberculosis is often confounded with severe bronchitis, especially in old 266 DISEASES OF THE RESPIRATOEY ORGAINTS persons wlio are considered emphysematous. The very severe general condition, the pallor, the rapid loss of strength, and the fever, are the only things here which call our attention to acute tuberculosis, and render the diagnosis possible. We have already indicated the possibility of confusion at the onset between miliary tuberculosis and croupous pneumonia. Of decisive diagnostic value in all cases is the demonstration of tubercle bacilli in the blood, which is indeed a difficult matter, but it has already been ac- complished more than once (Weichselbaum and others). Prognosis. — The cases described in literature as " cured miliary tuberculosis " are so uncertain in their diagnosis that they can not be regarded as convincing. We must therefore consider the prognosis as absolutely fatal. The differences in the course of the disease have been already mentioned. Treatment. — Although drugs are absolutely powerless, still the case in hand must always receive treatment, especially if the diagnosis can not be made with absolute certainty. Our prescriptions are purely symptomatic. The cases with a typhoidal course are to be treated just like typhoid, with baths, stimulants, etc. Tepid baths, and also local applications to the chest, expectorants, and nar- cotics, are indicated when the thoracic symptoms predominate. If meningeal symptoms set in, we may try ice, perhaps local blood-letting, iodoform salve, or mercurial ointment externally, and iodide of potassium internally. CHAPTER VIII GANGRENE OF THE LUNGS .31tiology. — The sole cause of pulmonary gangrene — that is, the death and putrid decomposition of the lung-tissue — is the entrance of the bacteria of putre- faction into the lungs. The opportunity for inhaling them is certainly very great, but the normal organism apparently possesses the property of nullifying them and making them powerless. Under certain conditions, however, they take root in the lung and cause the death of the pulmonary parenchyma, which then, as a result of the presence of these specific bacteria of putrefaction, succumbs to that peculiar form of putrid decomposition known as " moist gangrene." The factor which most frequently gives rise to the development of pulmonary gangrene is the entrance of organic foreign substances, especially bits of food, into the lungs. The bacteria of putrefaction either enter the lungs with the foreign substance, or they settle there later and set up a putrid decomposition, first in that portion of the lungs, and then in the neighboring lung-tissue. The entrance of organic foreign substances into the lungs occurs in different ways. It often hap- pens from swallowing the wrong way, or from an accidental inhalation. In this way pulmonary gangrene may arise in previously healthy people, but it occurs especially in patients who are very low, very stupid, and soporose, and also in the insane, in patients who can not swallow or cough well, and in patients with paral- ysis of deglutition, as in bulbar paralysis. Bits of food may also reach the lungs from eructations and vomiting. Thus are explained the cases of pulmonary gan- grene which occur in patients with cancer of the stomach, and, still more fre- quently, with cancer of the oesophagus. Putrid organic material may also reach the lungs from ulcerative and ichorous processes in the mouth, the pharynx, and the larynx. In cancer of the tongue, the pharynx, and the larynx, in other ulcer- ative processes, and in injuries or wounds from operations in the mouth and phar- ynx that have become septic, pulmonary gangrene may develop quite readily. GAKGEE^^E OF THE LUNGS 267 Finally, septic foci in the vicinity may extend to the kings or perforate into a bronchus. In this way pulmonary gangrene may arise from the perforation through the pleura into the lungs of an ulcerated cancer of the stomach or a gastric ulcer, or in rare cases from vertebral caries, or from sanious lymph-glands. In some cases the cause of the pulmonary gangrene can not be made out, since the entrance of a foreign substance has perhaps been -wholly unnoticed, as may happen in children, or during sleep. We had a grown-up young woman under observation for a long time with pulmonary gangrene, and one day she coughed up several fragments of chicken-bones, but she could give no account of how they entered the lungs. Experience teaches us that pulmonary gangrene is more apt to develop in persons with impaired nutrition, in old, marantic individuals and drunkards, than in those who are healthy. The tendency of patients with diabetes mellitus to pulmonary gangrene is remarkable. Pulmonary gangrene often develops secondarily to some other pulmonary affection. We have already spoken of the relations between it and foetid bron- chitis. Foetid bronchitis, on the one hand, often leads to pulmonary gangrene through an extension of the process to the alveoli ; and, on the other hand, when there is a gangrenous focus in the lungs, the bronchi are often infected to a wide extent by the putrid secretion coming from it, and then there arises foetid bron- chitis. Both diseases often run into each other without any sharp boundary; but gangrene may develop secondarily in other affections of the lungs. A new infec- tion with putrid material, however, is always requisite, and the affection of the lungs that already exists furnishes merely a favorable soil. This is the only explanation of the process when croupous pneumonia " runs into gangrene," or when gangrene develops in catarrhal pneumonia, in bronchiectasis, or in phthisis. Although the agents of putrefaction enter the lungs through the bronchi in most of the modes of origin of pulmonary gangrene that have been mentioned, they may also be transported into the lungs by the blood-current. We call these forms embolic gangrene. We find such gangrenous nodules in the lungs in connection with extensive gangrenous bed-sores, puerperal processes, suppurative caries of the bones, etc. In these cases the putrid material enters a vein from the seat of the primary process and is brought to the lungs, and here we find, as a result of the putrid character of the embolus, not a simple infarction, but an embolic gangrene. Pathological Anatomy. — We more frequently find pulmonary gangrene in the lower lobes than in the upper, corresponding to its mode of origin. Either both lungs are affected or only one, and the right somewhat more freqiiently than the left. We distinguish a diffuse and a circumscribed form, according to the extent of the gangrene. Embolic gangrene belongs to the latter form, and its nodules, by preference, lie near the pleural surface. We can easily recognize the anatomical changes in gangrene. The lung-tissue is changed to a discolored, dirty, greenish-gray mass, Avhich gradually and pro- gressively becomes dissolved, forming a most foul-smelliug ichor. We find, left in it, necrotic fragments of tissue and vessels. Gangrene cavities, with irregular, ragged walls, are formed from the partial expectoration of the softened gangre- nous nodule. The lung-tissue in the vicinity of the gangrenous spot is to a greater or less extent inflamed, partly in the form of catarrhal pneumonia, partly in the form of circumscribed croupous pneumonia. The inflamed parts in the vicinity are gradually involved in the gangrene, so long as the process extends, but finally a suppurating line of demarkation may be formed about the gangrene, the whole gangrenous fragment is in a measure sequesti-ated, encapsuled, and gradually expelled, and so healing becomes possible. We have already stated that fcctid bronchitis may arise from a gangrenous nodule. 268 DISEASES OF THE RESPIEATOET OEGANS Whenever a gangrenous nodule reaches the pleura, a purulent and usually a sanious pleurisy follows from direct infection. Pneumothorax may arise from perforation of a gangrenous cavity. Clinical History. — The symptoms of gangrene depend for the most part upon the local affection in the lung. The condition of the expectoration is characteris- tic, and it alone may decide the diagnosis. In many ways the expectoration greatly resembles that of foetid bronchitis, and indeed a great part of it does not come directly from the gangrenous nodule, but is the secretion of the diseased bronchi. The penetrating stench of the sputum, a most repulsive, putrid odor, is very striking. The patient's breath and cough also have this stench, which infects the whole vicinity. The amount of the sputum is usually large; it may reach ten or twenty ounces (200-500 cubic centimetres) in twenty-four hours. If the sputum is collected in a glass it forms three layers, like the sputum of foetid bronchitis — an upper layer, muco-purulent, greasy, consisting in part of nummular sputa, and covered with much froth; a middle serous layer, in which some firm masses from the upper layer float; and a lower layer, almost wholly of pus, but greasy and greenish-yellow, which usually contains many large and small plugs and shreds of tissue. We find in these plugs, on microscopic examination, beautifully twisted needles of the fat acids (see Fig. 24, page 168) imbedded in countless bacteria, fat-drops, and detritus, and often collected in large bundles ; but besides these we find in the sputum the constituents of the parenchyma of the lungs, and this alone is the decisive factor in distinguishing between pulmonary gangrene and simple foetid bronchitis. Traube's statement that in pulmonary gangrene the expectoration contains few, if any, elastic fibers, because the elastic tissue itself is destroyed by gan- grene, is not correct ; or, at any rate, it is too sweeping. We have almost invariably found in the expectoration an abundance of elastic tissue, as well as other frag- ments of the parenchyma, pigment granules, and the like. Yet there is a prob- ability, no doubt, that in pulmonary gangrene the elastic tissue is for the most part destroyed. Filehne succeeded in extracting from the sputum of pulmonary gangrene, by means of glycerine, a ferment which in alkaline solution completely dissolved elastic tissue in a few days. The sputum always contains in enormous numbers bacteria of various kinds, both cocci and bacilli. Which of these are the special cause of the gangrene has not yet been definitely settled. The chem- ical examination of the sputum shows the presence of those substances which may always be found in the putrefaction of organic matter — tyrosine, leucine, am- monia, sulphuretted hydrogen, butyric acid, valerianic acid, caprylic acid, etc. The fresh sputum usually has an alkaline reaction, but on standing it becomes acid. Many cases of gangrene lead to erosion of the vessels and severe haemoptysis. Slight admixtures of blood in the sputum are not infrequent. The other symptoms on the part of the lungs are not especially characteristic of gangrene. Most patients complain of cough, pain in the side, and more or less severe dyspnoea. Physical examination, as a rule, permits us to make out the seat of the nodule, but not always, since the physical signs, of course, depend upon the situation and extent of the gangrene. Small nodules, situated centrally, often give no objective evidence of their presence. Every extensive infiltration, how- ever, must cause dullness on percussion. Over the area of dullness we hear bron- chial respiration, and usually quite numerous moist rales. If a gangrenous cavity is formed, the physical examination may show plain symptoms of a cavity — tym- panitic resonance on percussion, amphoric respiration, coarse moist rales, etc. The physical signs are sometimes due to the accompanying pleurisy ; the dull- ness is more complete, the respiratory murmur and the vocal fremitus are dimin- ished, and the adjacent organs are displaced by the abundant effusion; but an GAK"GKENE OF THE LUNGS 269 absolute diagnosis of an accompanying pleurisy is often to be made only by an exploratory puncture. We have already spoken of the occasional development of pneumothorax. In many cases there is fever, of quite an irregular character and of very vary- ing intensity. In the cases in which the gangrenous nodule is sequestrated, and the secretion can be freely emptied through the bronchi, so that there is no ab- sorption of septic material into the blood, fever may be entirely absent. We often see gastric and intestinal symptoms injpulmonary gangrene, the dis- turbance being without doubt due to swallowing some of the foetid sputum. Many patients complain of loss of appetite, and sometimes of vomiting or diarrhoea. In severe acute cases there is sometimes a well-marked typhoidal state, with such symptoms as stupor, delirium, and great cardiac weakness. This condition is probably caused by the absorption of septic material into the blood. Rheumatic pains in the muscles and joints are seen in this disease, just as in foetid bronchitis. Finally, it should be remarked that the appearance of secondary abscesses in the brain (see page 1107) has been repeatedly observed in pulmonary gangrene. This fact must be borne in mind when, in the course of pulmonary gangrene, marked brain symptoms are developed, especially if we have not only such general symp- toms as coma, but also such local symptoms as hemplegia and other forms of paralysis, and convulsions. The general course of the disease shows very great variations. In all cases in which the pulmonary gangrene is secondary to some other affection, the course and the general type of the disease depend very largely upon the primary attack, but the cases of idiopathic gangrene also present great variations. The onset is either quite gradual and slow, or quite acute, and associated with fever and tho- racic symptoms. The stinking expectoration and the bad odor from the patient's mouth first direct the attention to the existence of putrid processes in the lungs. The disease is usually very chronic, lasting for months or even years. Many remissions and intermissions occur. With proper care and treatment we may see a decided improvement, and often apparently a complete cessation of the disease. The bad odor ceases, the expectoration diminishes or disappears entirely, and the patient's strength and nutrition become almost normal; but relapses may occur after long intervals. When the affection is of slight extent we may even see a complete recovery. Pulmonary gangrene always takes a worse course in previously weak and marantic persons, and an unfavorable termination may follow in a comparatively short time. Death ensues either from a general loss of strength, as a result of the disease, or from complications, such as pulmonary haemorrhage, ichorous pleurisy, pneumothorax, or abscess of the brain. Rupture of an ichorous empyema out- wardly, or into the peritoneum, or into other cavities, is i*are. Special mention must be made of the fact that the symptoms of pulmonary gangrene are not always so very pronounced. In persons who are weak and run down we often see pulmonary gangrene at the autopsy, although during life there have been no marked symptoms, not even offensive sputum or foetor from the mouth. Diagnosis. — The diagnosis can not be made with certainty unless the charac- teristic sputum is present. We can decide whether the sputum comes from a foetid bronchitis or from the foetid contents of a bronchiectasis, or from actual gangrene, only by finding under the microscope the remains of lung-tissue in the expectoration. Physical examination in gangrene, at least in part of the cases, also gives the signs of infiltration or of cavity-formation in the lungs. Prognosis. — The prognosis depends first upon the nature of the underlying disease, and then upon the extent of the affection, the strength of the patient, and the possibility of sufficient care and proper treatment. If the process in the lung 270 DISEASES OF THE EESPIEATOKY OEGAI^S becomes sequestrated, marked improvement may follow, even in tlie severest con- ditions; but we must always remember that a relapse is possible. Complete re- covery from pulmonary gangrene is certainly extremely rare, if it ever occurs. We have already mentioned the dangers which may cause a fatal termination in pulmonary gangrene. Treatment.- — Prophylaxis plays an important part in those cases in which there is danger of the entrance of bits of food into the air-passages from de- fective deglutition. We must think of the possibility of this with all patients who show great stupor, and also with patients who have pharyngeal paralysis, in order to watch them while taking food, and eventually to try artificial feeding with the oesophageal tube. The treatment of already existing pulmonary gangrene has, as its chief aim, to check the putrid processes of decomposition in the lungs. Unfortunately, the remedies at our colnmand are not in all cases sufficient for this. The different disinfecting inhalations are the most effective. They are used in the same way as in foetid bronchitis (vide supra). Turpentine deserves the most confidence, and it may also be given internally with good results. According to Lepine, however, terpine acts even better than turpentine. We may also call attention to inhala- tions with carbolic acid, Curschmann's carbolic mask, inhalations with salicylic and boraeic acids (4 parts of salicylic and 20 of boracic acid to 1,200 of distilled water), bromine (bromine and bromide of potassium, 2 parts of each to 1,000 of water), and similar substances. Besides oil of turpentine, other internal remedies are recommended: half a grain to a grain (gramme 0.03-0.06) of acetate of lead every two hours, creasote, carbolic acid, etc. Their action is uncertain. Of late, myrtol has been greatly extolled. It is given in capsules containing gr. ijss. (grm, 0.15), of which two or three are to be taken every two hours. The general treatment of the patient is very important — he should have good food, and live in as good air as possible. We must treat the pain in the chest and the cough symptomatic ally, local applications and morphine being most useful. The fever seldom gives occasion for direct interference. We may try to relieve the g'astric and intestinal symptoms by giving antiseptics internally, especially by small doses of muriatic acid, salicylic acid, or creasote, as well as by the ordi- nary remedies, such as bitters and opium. If a secondary ichorous pleurisy develops, with or without pneumothorax, removal of the fluid by operation is necessary, if the patient has sufficient strength to bear it. In some few cases trial has been made of opening up the foci of gangrene by surgical means. As yet, it must be confessed, the results have not been very encouraging. CHAPTEE IX DISEASES FROM THE INHALATION OF DUST (P/ie^mwnoconiosis) Although there are a number of important contrivances in the respiratory apparatus to prevent the entrance of foreign substances into the lungs, still, if a person remains in a dusty atmosphere, so many particles of dust may be inhaled that they are not without effect on the lung-tissue. The diseases arising from the inhalation of dust are usually purely professional diseases, which occur espe- cially in workmen whose occupation involves the continual inhalation of some DISEASES FROM THE I^TIALATIOIT OF DUST 271 kind of dust. In earlier chapters of this book, particularly while considering chronic bronchitis, we have already emphasized the harmful influence of the inhalation of dust. We have seen how the habitual respiration of organic dust in particular (from grain, wool, wood, and tobacco) is very apt to lead to severe forms of bronchitis and bronchiolitis. We must now draw attention to certain specific diseases similarly caused. We must first mention, however, a condition of the lungs which can scarcely be regarded as pathological, although it has its origin in the constant inhalation of dust, especially of coal-dust — the ordinary black pigmentation of the lungs. There can now no longer be any doubt, although there was once a long dispute about it, that the black pigment in the lung comes, in large part at least, from the inhalation of carbon. The particles of carbon pass into the lungs themselves, and thence into the bronchial glands by means of the lymphatics. A certain part of the coal-dust inhaled is removed with the expectoration, and it may easily be found in it microscopically, and often by the naked eye, as we see it in the well- known black expectoration which we often have in the morning, if we have spent the previous evening in a room filled with smoke. In Germany, Traube was the first to discover the particles of carbon in the expectoration of a charcoal-burner. In the man's lungs, aftei death, the vegetable origin of •'^'^'?^^ "'.";.-7i^9% these particles could be rec- ^.,/ ^-,3^ ognized, and Traube gave the ,■-■■'•:;-'" ., • . ■■■'''■. jf correct exi^lanation of them. -if^^^^f *^ ■^•r ' In workmen who inhale large *^^^v, f^ ' ~ m' ' amounts of charcoal-dust, an- ^ ' ''■'•'' ;/*-;;, .r' thracite coal-dust, soot, or v^-. /^"~ '^ '#/ "^ graphite, the "normal" pig- v,!" *«»:: ■ '_^ . mentation of the lung passes '*?'! ^ 4-""-' into a pathological condi- -l::*;:.-- .■^^£_,. tion, anihracosis pulmonum. Fig. 35.— Expectoration of a man who worked on graphite. With this is usually associated meS clinfqlfe.f '"'^ '"'^ ^^''"''^'' ''' ""■^°°' ^^'■^^°^^° an extensive chronic bron- chitis. In the expectoration of such patients are found many cells, filled with black particles of coal, even long after they have left the dusty atmosphere. The pigmented cells are leucocytes, or perhaps some of them epithelial cells (see Fig. 35). Zenker first discussed comprehensively the fact of the entrance of the different sorts of dust into the lungs and the consequent results. Besides the anthracosis already mentioned, the pulmonary disease from inhaling the dust of flint and other stones is of especial importance, the so-called stone-cutter's lung — chaUcosis pulmonum — and also that from inhaling metallic dust, especially oxide of iron — siderosis pulmonum. The " stone-lungs " have been observed in workmen in the stamping-rooms of glass-factories, in mill-stone cutters, stone-polishers, stone- hammerers, plasterers, workers in porcelain, masons, slate-quarrymen, potters, etc. " Metal-dust lungs " occur in file-cutters, iron-workers, mirror-polishers, and especially in grinders, who inhale a mixture of stone- and iron-dust. The first case of a " red iron lung " was observed by Zenker, in a girl who had inhaled a thick dust of iron for ten or twelve hours a day. Her work was to color blotting- paper with a powder of red oxide of iron. During the inhalation of all these and similar kinds of dust, a portion of the inspired particles of dust are taken up by the leucocytes, and perhaps also by the epithelial cells, finally reaching the lymph-channels of the lungs. Some of the particles of dust remain in the inter- stitial connective tissue of the lungs. Others find their way to the bronchial and retro-bronchial lymph- glands. 2Y2 DISEASES OF THE EESPIEATOEY OEGANS If the inlialation of dust is long continued, it causes not only this abnormal pigmentation of the lungs, but also macroscopic auatomieal lesions. These con- sist, partly, in a more or less severe and extensive chronic bronchitis, and partly in an interstitial inflammation which is due to the chronic irritation of the for- eign matter (e.g., flinty particles), and leads to the formation of connective tissue. The lungs are studded with nodules, which feel hard to the touch, and grate on section with a knife. All of these nodules consist of firm connective tissue, in which the particles of stone or iron are encapsuled. By the union of single nodules we may get more extensive induration and cicatricial forma- tion. Chemical examination of such lungs gives, as might be supposed, a large amount of silicic acid, iron, etc. In most of the cases which come to autopsy we find further changes in the lungs, which are not the immediate result of the inhalation of dust, but consist of sequelae and complications. Chronic diffuse bronchitis in the worker in dust, like any other chronic bronchitis, may give rise to pulmonary emphysema, and later to cardiac hypertrophy, etc. We very often find in the lungs co-existing and pronounced tubercular changes. It need hardly be emphasized that these changes are not the direct result of the inhalation of dust, but that the changes in the lungs set up by such an inhalation furnish merely a favorable soil for infec- tion with tuberculosis. In most cases, the " dust-lungs " acquire a marked clinical significance chiefly from the sequelae mentioned — namely, emphysema and tuber- culosis. The circumscribed nodules of interstitial pneumonia have no very marked symptoms following them. In all cases in which there is a fatal termina- tion, with pulmonary symptoms, we should regard the immediate action of the dust as much less the cause of death than are the secondary diseases. The actual points to be considered in judging of the clinical symptoms of the diseases from inhaling dust are contained in what has been said. The symptoms are those of chronic bronchitis, pulmonary emphysema, or chronic phthisis, and attention to the injurious influences associated with the patient's calling is the only possible way of making a diagnosis, but in individual cases it may always be a matter of doubt how far other accidental causes of disease may come into play. The prognosis depends, in the first place, upon whether the patient can be removed from the action of these injurious influences or not, but we must also mention the fact, which has been often observed, that many individuals get some- what used to the dust. After they have once recovered from the initial bi'on- chitis, such persons can live in an atmosphere of dust for a long time without any noticeable injury. The prophylaxis of diseases from inhaling dust forms an extended chapter in the hygiene of occupations, which we can not dwell upon here. The workman must be taught the danger to which he is exposed, and the danger itself must be diminished as much as possible by sufficient ventilation of the work-rooms, by cleanliness, and, under some circumstances, by a change in the teclniicalities of the business. We need not give any special directions regarding the treatment of diseases from inhaling dust. It is founded on the same principles as the treatment of chronic bronchitis, emphysema, and chronic pulmonary tuberculosis. EMBOLIC PEOCESSES IN THE LUNGS CHAPTER X EMBOLIC PROCESSES IN THE LUNGS (IltemorrJiai/ic I/tfarctio7t of the Lvngn) Etiology. — The sources from which the material for an embolic plugging of branches of the pulmonary artery comes lie either in the right side of the heart or in the veins of the body. Pathological anatomj^ teaches us how often thrombi are formed in the veins, especially in the veins of the lower extremities and in the pelvic veins, and in the right side of the heart, in the recesses between the tra- beculse, in the auricles, on the valves and the chordse tendinge, and at the apex of the ventricle. The particles, torn loose from thrombi so situated, are carried on by the blood-current, reach the lungs, plug a larger or a smaller branch of the pulmonary artery, according to the size of the particles, and thus cause further changes in the lung-tissue. Since the branches of the pulmonary artery are " ter- minal arteries," and since thus the vascular territory belonging to each branch can not be supplied, or can be supplied only to a small amount, with blood by collateral circulation from other vessels, the closure of a branch of the artery shuts the territory supplied by it out of the circulation. The pressure, in the part of the vessel lying peripherally to the point of plugging, becomes almost nil, and, as a result, there is a collateral or backward current into the region shut off, flow- ing from the capillaries in the vicinity, and probably even from the veins belong- ing to it. Yet the blood which flows in is under so slight a pressure that it does not flow throiigh, but stagnates in the affected area. The walls of the capillaries and veins, in which the normal blood-current has ceased, lose their natural con- sistency as a result of this. The vascular walls become abnormally pervious. The fluid of the blood, the white blood-corpuscles, and also very many red blood- corpuscles, penetrate through the walls of the vessel into the surrounding tissue, and change it into the so-called hsemorrhagic infarction. Every embolic closure of a branch of the pulmonary artery does not necessarily result in the formation of an infarction. Upon the sudden plugging of a main trunk, or of several large branches of the pulmonary artery, death may ensue at once, so that naturally all further changes in the lung-tissue cease. We also find quite frequently, especially in central portions of the lung, embolism of single branches of the pulmonary artery without the formation of an infarction. In such cases there must necessarily be a little circulation in the vascular territory which has been shut off, either by anastomoses between the territory of the pul- monary artery and that of the bronchial or mediastinal artery, or by the neigh- boring capillaries, whose arteries of supply remain open. The changes thus far described are the result of a purely mechanical closure of a pulmonary artery. We have noticed this especially when simple fibrinous plugs have given the occasion for the embolic process. Pulmonary infarctions are most frequent in chronic heart disease, in all forms of primary and secondary dilatation of the heart, but especially in disease of the mitral orifice, most oftel^ mitral stenosis. Thrombus formation is frequent in the dilated right side of the heart, and furnishes material for pulmonary emboli ; but these emboli are seen in all other possible conditions of disease, in which thrombosis in the right side of the heart or in the veins may occur. The changes in the lungs assume quite a different appearance if the embolic material is not simple fibrine, but if it contains at the same time some specific infectious matter. If emboli reach the lungs from an acute malignant endocar- ditis in the right side of the heart, or, as is most frequently the case, from a puru- lent (septic) phlebitis anywhere in the body, giving rise to a puriform, liquefying 18 274 DISEASES OF THE EESPIEATOET OEGAE"S thrombus, the specific factors in inflartmiation — that is, bacteria — get into the lungs. Thus arise embolic abscesses and embolic gangrenous nodules in the lungs. We have already spoken of the latter, and the former are among the most constant lesions in every typical case of pyaemia. The fundamental facts as to the occurrence and significance of embolic pro- cesses in general, and those located in the lungs in particular, were discovered by Virchow. Eor a fuller understanding of the results of embolic closure of the vessels ve must thank chiefly Cohnheim. Pathological Anatomy. — ^Hgemorrhagic infarctions may involve one or more lobules, or almost a vhole lobe of the lung, according to the situation of the embolus. Most infarctions are situated at the periphery of the lung, and have approximately a conical shape, corresponding to the extent of the region of the vessel. The base of the cone lies against the surface of the pleura. It generally projects a little above that surface, and its dark color can usually be plainly rec- ognized through it. The pleura itself is the seat of a fibrinous inflammation at the point to which the infarction reaches, and sometimes for a large space around it. The conical shape of the infarction is plainly recognized on section. The lung-tissue is changed to a firm, fragile, uniformly black-red tissue, devoid of air. The embolus can usually be readily found in the branch of the pulmonary artery leading to the infarction. Under the microscope we see a diffuse infiltration of tissue, with red blood-corpuscles in the infarcted portion. The alveoli and finer bronchi are also filled with coagulated blood. Under favorable circumstances, in cases of longer standing, the blood may be reabsorbed in part ; so that the lung again contains air, but it remains much pigmented in that place, and more or less indurated from the development of interstitial connective tissue. In excep- tional cases there is complete destruction of the pulmonary tissue where the in- farction is situated. This brcken-do^wn material is either discharged or absorbed ; then cicatrization with contraction takes place. Hsemorrhagic infarctions are usually situated in the lower lobes, and more frequently on the right side than on the left. The smaller embolic abscesses are sometimes very numerous, and are dissemi- nated over the whole lung. In larger abscesses the conical shape may often be plainly recognized. When an abscess extends to the pleura, a purulent pleurisy arises from direct infection. Combinations and transitional forms between the ordinary heemorrhagic infarction and embolic abscesses are occasionally found in the lungs. Symptoms. — We often find at the autopsy embolism of single branches of the pulmonary artery, with or without infarction, which has caused no symptoms at all during life. Embolism of the main trunk, or of a large branch of the pulmonary artery, may cause sudden death, as has been repeatedly observed in patients with heart disease, or with venous thrombosis. If death be not immediate, sudden severe dyspnoea and oppression arise. The diagnosis may at least be suspected in such a case if we know of a possible source for an embolus. In some instances, when an embolus is situated in a large branch of the pulmonary artery, but has not com- pletely filled it, we can hear a systolic vascular murmur over the affected spot, as has been observed by Litten. The diagnosis, however, becomes certain if the further signs of infarction appear later. The most characteristic symptom of infarction in the lungs is the bloody expectoration. If we see quite suddenly bloody sputum in a patient with mitral stenosis, we are usually right in assuming a hsemorrhagic infarction of the lung. Either the sputum consists almost entirely of dark blood, or the blood is mixed with more or less mucus; but there is never much air in it. The bloody expecto- ration often lasts for several days. BROWN INDUEATION OE THE LUKGS 275 We try to learn more of the size and situation of the lesion by a physical ex- amination of the lungs. Of course this often gives a negative, or at least a doubt- ful, result. It goes without saying that small infarctions, and also those which are central, can not be made out by physical examination. Large peripheral infarctions may give rise in many cases to dullness on percussion, crepitant rales, and harsh or bronchial respiration, but it is often hard to decide in an individual case whether the physical signs which we meet with are not due to other patho- logical changes in the lungs, such as bronchitis or hydrothorax. We sometimes hear a pleuritic friction-sound in some part of the chest a few days after we sus- pect that an infarction has occurred, by which the diagnosis gains additional cer- tainty. We have already mentioned the subjective symptoms in embolism of a large pulmonary vessel — sudden dyspnoea and oppression. Small nodules often cause no special symptoms, but in other cases the patient feels a severe pleuritic pain, due to irritation of the pleura. Eever may be wholly absent, though we sometimes see a moderate rise of tem- perature at the onset. The embolic abscesses in the lungs hardly ever give rise directly to clinical symptoms. They form a part of the general picture of pyaemia and similar gen- eral infectious processes. Marked symptoms on the part of the respiratory appa- ratus are seen only when the abscesses are present in very large number. If an empyema develops from a focus which extends to the pleura, it sometimes occa- sions definite physical signs. It follows from all that has been said, that in the diagnosis of embolic pro- cesses the chief stress must always be laid on the presence of an ^etiological factor. We must regard the bloody sputum as the main direct symptom in hsemorhagic infarction. Embolic abscesses in the lungs may often be suspected in pysemic diseases, but they can hardly ever be diagnosticated with certainty. The prognosis is entirely dependent upon the underlying disease. In heart disease the occurrence of a hsemorrhagic infarction is usually on the whole an unfavorable sign, since it points to weakness of the right ventricle, and hence to the formation of a thrombus in it ; yet it often happens that the symptoms of a pulmonary infarction may pass away entirely. We need not give special directions for treatment. It is in part purely symp- tomatic, and in part coincident with treatment of the underlying affection. As regards prophylaxis, we must bear in mind the absolute necessity of as perfect rest as possible for those patients in whom the presence of venous thrombi — e. g., in the femoral veins, suggests the possibility of pulmonary embolism. CHAPTER XI BROWN INDURATION OF THE LUNGS {Lungs of Heart Disease) In heart disease, especially in mitral stenosis, we often find a peculiar change in the lungs, whose origin must be sought in the long-persisting engorgement of the pulmonary circulation. The lungs are hard and dense, and show on a fresh section an abnormal brownish-yellow color. In the larger pulmonary vessels, both arteries and veins, there is a thickening and cloudiness of the intima as a result of the stasis. We see here and there on the surface of the section, and beneath the pleura, little dark spots of pigment and fresh htemorrhages. We term this condi- tion brown induration of the lungs. 276 DISEASES OF THE EESPIRATOEY OEGANS Microscopic examination shows that the capillaries are evidently dilated and twisted as a result of the persistent stasis. They even extend a good way into the alveoli, whose lumen is thus actually diminished. The interstitial connective tis- sue seerris somewhat thickened, and we find in it many brown pigment-granules, the remains of the extravasated and decomposed red blood-corpuscles. The pig- ment-granules are some of them free, and some contained in cells (escaped leuco- cytes). In the intima of the larger vessels we often find fatty degeneration of the endothelium. With regard to the clinical importance of the pulmonary changes due to heart disease, we should say that it is very probable that the dyspnoBa of such patients is aggravated by the diminution of the alveolar spaces throughout the lungs, as a result of their being crowded with desquamated pulmonary epithelium. Clin- ically, however, we can not well distinguish this factor from the other causes of dyspnoea. We have no positive factors by which to diagnosticate brown induration of the lungs during life. The anatomical lesions, too, show a certain variation, not always to be explained, in that, under apparently the same conditions, the brown induration is often very marked, and often extremely slight. In cases . in which we find this in- duration in the cadaver we have re- peatedly heard, during the patient's life, a very sharp, puerile respiratory murmur, which seems to be character- istic of many cases of the " heart-dis- ease lung." We might lay still more stress upon the presence of large, characteristic cells in the expectora- tion, which are thickly filled with large and small yellow or bro-mi pigment - granules (see Fig. 36). These large pigmented cells (" cells of heart disease") are especially abundant in the expectoration of patients with extreme mitral stenosis. They are identical with the above- mentioned pigment-cells which are found in the lymph of the alveoli after death. Many investigators regard them as alveolar epithelium, while we are more in- clined to regard them as mainly leucocytes which have taken up the pigment of the disintegrated red blood-corpuscles. Besides these pigment-cells we also^ fre- quently see the still intact red blood-corpuscles in the expectoration of patients with heart disease. The prognosis and treatment coincide with those of the underlying cardiac disease. Fig. 36.— Sputum of a patient with mitral stenosis, containing the so-called "cells of heart disease." (.Personal observation.) CHAPTER XII TUMORS OF THE LUNGS. CANCER OF THE LUNGS. ECHINOCOCCUS OF THE LUNGS. PULMONARY SYPHILIS 1. ISTew Growths in the Lungs. Cancer of the Lungs. — Most of the new growths which are met with in the lungs are of a secondary nature. Secondary cancers are sometimes found in the lungs, with carcinoma of other organs, whose TUMOES OF THE LUNGS— PULMONAEY SYPHILIS 277 origin may always be explained by supposing a growth of the primary tumor into a vein, and the consequent carriage of the germs of the growth to the lungs. These secondary nodules in the lungs usually cause no special clinical symptoms, unless they are very numerous and extensive, when they give rise to dyspna3a, and physical signs. There once came to the clinique in Leipsic a case of sec- ondary, and very extensive, miliary carcinosis of the lungs, which ran a brief and fatal course, simulating acute miliary tuberculosis with predominant pulmonary symptoms. Other secondary new growths deserving mention are enchondroma and sar- coma. We have seen an extensive development of secondary pulmonary sarcoma, following primary sarcoma of the bronchial lymph-glands, and also following lympho-sarcoma of the lymph-glands of the neck, which grew into the jugular vein. We have also seen secondary deposits of sarcoma repeatedly in connection with primary congenital sarcoma of the kidney (see page 644). Enchondroma, sarcoma, and endothelioma appear, also, as primary new growths in the lung. Pulmonary cancer is, however, the only primary tumor which has any great clinical importance. In its clinical relations we can also rank with it certain malignant, metastatic forms of alveolar sarcoma. The typical cancer of the lungs is always a cylindrical-celled carcinoma, which un- doubtedly arises from the bronchial epithelium. It is especially common in elderly persons, over forty, and seems to be found somewhat more frequently in the right lung than in the left, and in the upper lobes than in the lower. By its diffusion the lung-tissue in the parts affected by cancer is changed to a yellow- ish-gray and quite soft and crumbling mass, devoid of air. We can usually scrape away from the section the characteristic cancer-juice, in which the micro- scope shows the typical cancerous elements. The pleura is very often involved. The new growth has either extended directly into it, or single, and more circum- scribed, secondary nodules have formed in it. The lymph-glands are almost invariably affected, especially the bronchial glands, and also the axillary and cei'vical glands. Secondary carcinoma of other organs is rare, but it is found in some cases in the other lung, the liver, the brain, and elsewhere. It is almost always difficult to interpret correctly the clinical symptoms of cancer of the lungs at the beginning of the disease. They are referred to some other, more common chronic pulmonary disease, such as chronic bronchitis, phthi- sis, or pleurisy, but in the further course of the disease we succeed, at least in a number of cases, in making a correct diagnosis. In other cases, especially in old people, the growth may remain latent. The general pulmonary symptoms have little that is characteristic. The patient complains of gradually increasing difficulty in respiration, and of pressure and distress in the chest, which may finally increase to the most intense dyspnoea. Most patients suffer very much from the labored, frequent, and spasmodic cough. The expectoration in some cases has no peculiarity, but it often assumes, at least for a time, a characteristic consistency which is extremely important for diagno- sis. It contains blood, and also has a peculiar " currant-jelly-like " appearance. Under the microscope we can sometimes make out the characteristic elements of the tvimor in it. Severe haemoptysis is also seen in cancer of the lungs. Physical examination of the lungs gives positive results in many cases, such as dullness, bronchial respiration, diminished respiration, rales, and sometimes pleuritic friction-sounds, none of which has anything characteristic in itself, although these signs may be of distinct significance in making out the seat and the extent of the new growth. Yet sometimes the area and peculiar limitations of the dullness — for example, if confined to the sternum — are so different from usual that from these factors alone suspicion of a new growth is excited. Thfe sense of resistance upon percussion is quite considerable; the respiratory murmur over the 2T8 DISEASES OF THE KESPIEATOKT OEGANS tumor is often inaudible or concealed by tlie stridor due to encroachment on tlie lumen of the larger bronchi. Finally should be noted the not infrequent appear- ance of a diffuse swelling, and sometimes of a slight oedema of the skin over the affected spot. The occurrence of certain sequelse is of great diagnostic significance. The chief one is swelling of the lymph-glands in the neck or axilla, and also certain symptoms of compression, which either are produced directly by the new growth, or are due to the secondary enlargement of the lymph-glands. Pressure on the superior vena cava, or a large branch of it, causes oedema in the face, neck, over the wall of the chest, or in one arm. The subcutaneous veins in the regions named appear dilated and tortuous. Pressure on the oesophagus causes diffi- culty in deglutition; pressure on the brachial plexus, intense neuralgic pains and paresis of one arm; pressure on the recurrent nerve, paralysis of the vocal cords and hoarseness; pressure on the trachea or a primary bronchus, the symptoms of tracheal or bronchial stenosis. The pleura is often involved so that the signs of a pleuritic effusion associate themselves with the other symp- toms. It is of diagnostic importance that in such cases the exudation is not infrequently hasmorrhagic (vide infra, new growths of the pleura). Besides the symptoms already mentioned we must consider the general symptoms. As in carcinoma in general, so in pulmonary carcinoma, the well-known cancerous cachexia gradually develops. The patient grows dull, loses his appetite more and more, disturbances of digestion and sometimes moderate elevations of tempera- ture develop, until he finally succumbs to general marasmus. The whole duration of the disease is from six months to two years. The prog- nosis is fatal. The treatment can be only symptomatic, and we employ the same remedies as in other pulmonary affections. We must still briefiy consider a new growth in the lungs which is extremely interesting from a theoretical point of view. In workmen in the cobalt mines of Schneeberg, in the Saxon Voigtland, the development of malignant lympho- sarcomata in the lungs, with the occasional formation of metastases in the glands, the liver, the spleen, etc., is of frequent occurrence. The disease runs its course under the type of a chronic pulmonary affection, and almost always ends fatally. The endemic occurrence seems to point to an infectious origin for the tumor. 2. EcHiNOCOCCUS OF THE LuNGS. — Primary echinococcus of the lungs is very rare. In most cases the echinococci are brought to the lungs secondarily from other organs, either by way of the blood-current, or, as is far oftener the case, by perforation of an echinococcus of the liver through the diaphragm. The symptoms of echinococcus of the lungs are manifold. The parasite some- times remains entirely concealed. In other cases a more or less severe, and often febrile, affection of the lungs, is developed, with pain in the chest, cough, and sometimes bloody expectoration, and dyspnoea. Physical examination of the lungs gives in some cases dullness, absence of respiratory murmur, and diminished vocal fremitus, while after the expectoration of the echinococcus (vide infra) symptoms of a cavity may ensue. A correct interpretation of all these symptoms is possible only when, as has often been observed, the echinococcus cysts are coughed up, or at least when parts of them, like the membranes or the booklets, are found in the expectoration. The termination of the disease may be favorable if the echinococci are expec- torated, or if we succeed in removing them by operative means. We can hardly hope to be able to kill the parasite by inhalations of turpentine or benzine. Some- times the echinococcus cyst becomes gangrenous, or suppurates. Rupture into the pleura, into the peritoneum, into the pericardium, and externally, has also been observed. This last termination is the most favorable, since otherwise, if the affection progresses, a fatal result may be caused by the sequelae, or rarely by the PLEUEISY 279 occurrence of suffocation. The details of the natural history of the echinococcus are given in the chapter on echinococcus of the liver. 3. Pulmonary Syphilis. — This would also be the place to speak of syphilitic new growths in the lungs, but, in our opinion, in spite of the quite abundant lit- erature of this subject in recent times, no definite clinical description of pulmo- nary syphilis can be made. Those physicians who are disposed to consider every pulmonary disease in a previously syphilitic subject to be of a syphilitic nature, certainly regard many things as pulmonary syphilis which have nothing at all to do with syphilis. At least, we have found that all those cases which at first sug- gested a diagnosis of pulmonary syphilis, finally, upon more accurate examina- tion and after longer observation, have turned out to be something else, usually tuberculosis. There are a few indubitable cases of chronic indurative contrac- tion of the lungs following primary syphilitic infiltration. The clinical picture here does not differ in any characteristic manner from that of ordinary chronic interstitial pneumonia. A probable diagnosis may be made from the knowledge of the syphilitic taint, the simultaneous existence of other syphilitic lesions — e. g., of the liver — the physical signs of chronic pulmonary disease, and the fail- ure to find tubercle bacilli in the sputum on repeated examinations. It is also well established that there may be syphilis of the larger and medium-sized bronchi, which is recognized at the autopsy by extensive radiating cicatrices in the bronchial mucous membrane, which sometimes lead to stenosis. Single gum- matous nodules in the lungs are of the greatest rarity. We sometimes find in the pleura peculiar radiating cicatrices, which probably are of syphilitic origin. The pulmonary syphilis of the new-born, which occurs in the form of single nod- ules or as a diffuse syphilitic infiltration, the so-called pneumonia alba, has only a pathological interest. If the existence of a syphilitic disease of the lungs is suspected, of course specific treatment should be employed. Iodide of potassium must be adminis- tered and perhaps also a course of mercurial inunctions. The results are not apt to be brilliant, however, because it is of course impossible to restore the portions which have been cicatrized. SECTION T Diseases of the Pleura CHAPTER I PLEURISY {Pleuintis) .31tiology. — Pleurisy is divided into primary and secondary. In a strict sense, the only cases of pleurisy which can be termed primary are those in which the pathogenic organisms penetrate into a healthy body, and become localized in the pleura without any previous organic lesion elsewhere, l^o doubt many a case of pleurisy seems primary from a clinical standpoint, which is really not so. The disease antecedent to the pleurisy may be so slight as to present no symptoms and attract no attention. The pleurisy appears as an apparently independent dis- ease, and is the first thing which attracts attention to the previously existing affection. Exclusive of traumatic pleurisy, resulting from such injuries as a penetrating 280 DISEASES OF THE EESPIRATOEY OEGAKS thoracic wound, xve know positively of only one form of pleurisy — viz., the rheu- matic — ^whicli is primary. This is, from an astiological point of view, most closely allied with acute articular rheumatism (Fiedler). In polyarthritis (see page 680) it is not very exceptional to have pleurisy develop secondarily. In many cases the rheumatic affection attacks the pleura at first, without any great involvement of the joints. Then often follow articular trouble, endocarditis, and the like, confirming, or for the first time disclosing, the setiology of the attack. Whether still other pathogenic influences may produce primary pleurisy is not settled. Some cases of acute pleurisy, setting in with high fever, we have felt justified in referring to diplococcus infection, as suggested by the association of herpes and other symptoms. In such instances it is scarcely possible to ex- clude with certainty the presence of a small focus of pneumonia. In genuine primary pleurisy the pathogenic germs must first enter the circulation, and by that means reach the pleura. It is frequently impossible to find out any special exciting cause for the attack. Often it is ascribed to catching cold. Among those varieties of pleurisy which appear from a clinical standpoint as primary, while their existence is really referable to a previous lesion of the body, by far the most frequent and important is the tubercular. On this point it was only gradually and by means of long experience that physicians obtained a cor- rect conception of the truth. We believe it right to say that the great major- ity of all cases of apparently primary pleurisy are tubercular. The infection of the pleura is due to the invasion of it by germs from some tuberculous focus, situated near by. Either there are small tuberculous patches in the lungs which extend to the pleura, or, probably yet more frequently, bronchial or retro-bron- chial lymph-glands, being tubercular, break into the pleural cavity and promptly excite pleurisy. In many of these cases the further course of this disease clearly shows that the pleurisy was tuberculous at the start, and not infrequently the physican is justified, even at the very beginning of the illness, in expressing his suspicion of tuberculosis (vide infra, diagnosis). In many other cases of pleu- risy its secondary character is clear from the start. Most of these occur from the direct extension of the inflammatory process, from some neighboring organ, to the pleura. When considering pulmonary diseases, we had occasion to point out that the various pathological changes in the lungs, when they extend to the pleura, involve it in the disease. Thus we see pleurisy associated with croupous pneumonia, lobular catarrhal pneumonia, pulmonary gangrene, haamorrhagic in- farction, embolic abscesses, and, most important of all, pulmonary tuberculosis. Many of the diseases just enumerated are frequent complications of the most diverse diseases. Hence, it is easy to understand that pleurisy is a not infre- quent phenomenon in all sorts of severe illnesses. ^ Inflammation from other neighboring organs beside the lungs may extend to the pleura. Inflammation of the contiguous serous membranes may spread to the pleura by continuity; thus pleurisy complicates pericarditis and peritonitis. In- asmuch as the pleura and the outer surface of the pericardium lie in direct appo- sition and, furthermore, the pleural cavity and the peritoneal cavity are directly connected by the lymph-channels of the diaphragm, we can easily understand that not only serous and purulent, but also diplococcus, inflammation of the peri- cardium and peritoneum may have pleurisy for a sequel. Another variety of secondary pleurisy is due to the conveyance of the inflam- matory organisms not from the immediate neighborhood, but from other parts, by way of the circulation. Here should be mentioned pleurisy due to general sepsis, to polyarthritis, to nephritis (see page 632), and to genuine gout (which see). The factors which give rise to the inflammation are either organic or. in the case of gout and nephritis, chemical in their nature. The inflammation they excite in the pleura is most varied in its kind and degree. • PLEUEISY 2S1 Of late years bacteriological investigations have been made by E. Levy, Prince Ludwig Ferdinand, and others, to obtain a more accurate knowledge as to the special variety of germs in the various forms of pleurisy, due to infection with org-anized material. It must not be forgotten, however, that these bacteriological investigations have been, for the most part, directed not to the diseased tissue, but to the inflammatoiy pleuritic exudation. This, however, in many cases con- tains no bacteria whatever. In particular, the exudation in most cases of tuber- culous pleurisy, whether serous or purulent, is absolutely sterile, and in the sec- ondary pleuritic exudations, in acute polyarthritis and nephritis, the search for bacteria has failed again and again. In other cases of pleiirisy, however, staphy- lococci have been found in the exudate, and in empyema streptococci also. Meta- pneumonic pleurisy, whether serous or purulent, is often, though not always, characterized by the presence of genuine pneumococci. In general, the question with regard to the special cause of the disease will have to be whether the pleu- risy, in each case, is a part of the original primary disease — that is, whether we find tubercle bacilli in tuberculosis and diploeocci in pneumonia, or whether thej pleurisy is a secondary complication, so that, for example, we find streptococci in typhoid fever. Further investigations are needed for complete enlightenment with regard to all these matters. Pathological Anatomy. — The inflamed pleura is markedly injected, it has lost its normal luster, and instead has a dull surface. This dullness is due to the coagulated fibrinous exudation upon the pleura, the exudation, in mild cases, forming only a thin layer. In more advanced cases, however, the surface of the pleura is covered with thick, rough, and shaggy masses of fibrine. As long as the fluid in the pleura is little or not at all increased, we speak of a simple fibrinous or dry pleurisy (pleuritis fihrinosa vel sicca). In other cases, however, besides the layer of fibrine there is an abundant exu- dation of fluid from the capillaries of the pleura, forming a pleuritic effusion. This is ordinarily of a simple serous character — serous and sero-fibrinous effu- sions. The fluid collects between the surfaces of the pleura, or, if there is at the same time an abundant coating of fibrine, between the gaps and in the meshes of the fibrinous exudation. In such cases there are often many flakes of fibrine floating in the fluid. Upon microscopic examination there are invariably found a few leucocytes even in serous exudations, and also sometimes a very few blood-corpuscles and endothelial cells (often swollen or fatty-degenerated), and plates of choles- terin. If the number of pus-corpuscles in the exudation becomes much increased, we have a sero-purulent, or a purulent exudation. This is always due to the presence of a specific organized poison which excites the suppuration. The pleurisies which come from embolic abscesses, from gangrenous foci in the lungs, and from carious ribs, and those which arise from the rupture of tubercular cavities into the pleura, are almost always of a suppurative character. We call the purulent pleuritic effusion empyema. If putrefactive agencies enter the pleural cavity at the same time with the pus poison, as in the pleurisies which develop in pulmonary gangrene, the purulent exudation assumes an ichorous, putrid character — ichorous effusion. Under certain circi^mstances the effusion assumes a hsemorrhagic character — • haemorrhagic effusion — especially if hsemorrhages occur from the old or newly formed capillaries dilated by the inflammation. They arise partly by diapedesis and partly from rupture of the walls of the vessels. The exact cause of the hsem- orrhages is usually unknown. We know by experience that haemorrhagic effu- sions are most frequent in tubercular pleurisy, a fact which is of diagnostic im- portance. The exudation may also be hasraorrhagic in connection with new 282 DISEASES OE THE KESPIEATOEY OKGANS growths of the pleura, after severe croupous pneumonia, in septic disease (e. g., puerperal fever), and finally when there is a general hsemorrhagic diathesis, as seen in scurvy, purpura hsemorrhagica, and leukaBmia. In all these last-men- tioned cases it should, of course, be considered that we are not always dealing with a true inflammatory exudation, but merely with a haemorrhage into the pleural cavity. The amount of fluid collected in one pleural cavity is, in the majority of cases, somewhere between a pint and a quart (500-1,000 cubic centimetres), but it may reach three or four quarts. Every large effusion must influence the position of the yielding walls of the pleural cavity, the chest-wall, the lungs, the medias- tinum, and the diaphragm, through the consequent increase of pressure in the affected pleural cavity ; and the resultant symptoms of pressure on the neighbor- ing organs are of the greatest clinical significance. Attention is first called to the lungs themselves. Since the normal lung is expanded in the thorax beyond its elastic equilibrium, it will retract as soon as a part of the pleural cavity is occupied with fluid. Until it has reached its position of elastic equilibrium there can be no question of a positive pressure on the lung. The lung floats on the effu- sion, in a certain way, if there be no adhesions, but, as the amount of the fluid further increases, compression of the lung follows. With a very large effusion the lung is pushed wholly up and back against the vertebral column, and is changed to an almost bloodless, airless, flat mass. It is, however, possible that the atelec- tasis of the lung is not caused exclusively by compression from without, but that, after the normal respiratory movements have ceased, a part of the air in the lung may be absorbed by the vessels, or even by the effusion. We also see the results of the pressure exerted by the pleuritic effusion on the mediastinum and diaphragm, as well as on the lungs. Displacements of the heart arise from the lateral pressure on the mediastinum, which must take place if the pressure in the diseased pleural cavity is equal to that of the atmosphere, for a greater and positive pressure is unnecessary, since a negative pressure prevails on the healthy side. The downward pressure of the diaphragm, which usually affects both halves of it, although in unequal degree, makes itself manifest on the right by the low posi- tion of the liver, and on the left by the downward displacement of the stomach and large intestine. It must be particularly noticed, however, that adhesions may prevent all the pressure-displacements which we have mentioned, both of the lungs and of the neighboring organs. As regards the further changes and terminations of the pleuritic processes, they depend upon the amount and character of the effusion. Favorable cases may result in complete recovery and absorption of the effusion. The fluid contents are taken up directly by the lymphatics of the pleura, and the solid constituents, the fibrine and the white blood-corpuscles, are decomposed, dissolved, and ab- sorbed. Old fibrinous patches sometimes become impregnated with lime salts, so-called "pleuritic ossification." Whenever a case of extensive pleurisy, with an abundant fibrinous or fluid exudation, gets well, there is a marked cicatricial contraction of the pleura, in which the whole thoracic wall is involved. It requires months for the lungs and the thorax to regain their normal expansion, if they can ever do so. That recovery from large pleuritic exudation is so often incomplete, is ex- plained for the most part by the nature of the original disease. We often find that temporary improvement is followed by a fresh relapse of pleurisy, or by the; appearance of extensive and usually tuberculous disease of the lungs or other organs. In the case of purulent exudations, also, final absorption of the fluid is possi- ble. This is especially likely when the empyema is meta-pneuraonic and benign. PLEUEIST 283 but this demands much time, and thick, cheesy masses of pus are often left in the pleural sac. In most cases of empyema, if there is not timely operative interfer- ence, the pus seeks an outlet for itself. It may break through the visceral pleura into a bronchus, and be emptied externally, thus giving rise to a pyo-pneumo- thorax ; but in many cases the pleura seems to be destroyed only superficially, and the pus is pressed into the alveoli as into a sponge, especially by the movements of coughing, and thence reaches the bronchi, without letting the air enter the pleural cavity (Traube). In other cases the empyema breaks externally through the chest-wall — empyema necessitatis. The point of rupture is usually found in the vicinity of the sternum, where the chest-wall is thinnest. In very rare cases the empyema breaks into the deeper parts of the trunk, or into the abdominal cavity. Course of the Disease. — We will speak in what follows especially of the course and symptoms of ordinary, apparently primary {vide supra), fibrinous or sero- fibrinous pleurisy, the so-called simple pleuritic effusion. What is said of it obtains in large measure in the other form of pleurisy also. The physical signs, of course, are almost wholly independent of the character of the effusion. As far as the different forms of pleurisy differ clinically, we will mention their peculiari- ties below. Only rarely is the onset of pleurisy quite acute and sudden, beginning with a rigor. In such cases we must guard against confusing it with croupous pneu- monia. Pleurisy usually begins slowly and gradually. The symptoms, which the patient himself feels, are in many cases to be referred directly to the disease of the pleura. One of the most constant is the pleuritic pain, the stitch in the side. A more or less severe pain comes on in the side at every deep breath, and hence upon any physical exertion; also upon movements of the body, in stooping, coughing, or gaping. Shortness of breath soon appears, and constantly increases. There is often a frequent, dry cough. Sometimes there ar'e scarcely any cough and expectoration. Such expectoration as there may be is usually simply mu- cous. Besides that, severe general symptoms almost always develop; the patient feels dull, looks pale, and has no appetite. Patients who can endure a good deal often keep at work for a long time, until, after feeling miserable for three or four weeks, they are forced to stay at home and summon a physician. It is very impor- tant to know that in not a few cases the general symptoms are much more promi- nent, at the beginning of pleurisy, than the local ones. The patient comes to the physician complaining only of weakness, loss of appetite, or headache, and the physical examination is the first thing that shows the presence of perhaps a large pleuritic effusion. In most of the severe cases the further course is slow like the beginning, but sometimes the severest symptoms, most intense dyspnoea, marked cyanosis, etc., may come on in a short time, owing to a sudden increase of the effusion. On the other hand, in mild cases the symptoms may disappear again in a few weeks, but the objective signs in such cases are generally to be made out for a longer time. The disease ordinarily lasts for at least five or six weeks, and often much longer. Gradual recovery follows, or the onset of some new disease, usually tubercular {vide infra). Single Symptoms. — The pleuritic pain, the stitch in the side, is one of the most frequent subjective symptoms. We have previously mentioned that in pri- mary diseases of the lungs, too, as in croupous pneumonia, the stitch in the side is due to the accompanying pleurisy. It is remarkable that the intensity, of the pain in no way corresponds to the apparent intensity of the disease. There is often the severest pain in the side when the physical examination shows almost nothing. On the other hand, we often hear a decided pleuritic rub without the patient's complaining of any special pain. Pressure on the chest-wall on the 284 DISEASES OF THE EESPIRATORT ORGAK^S affected side is often very painful. With severe pain we may consider the possi- bility of an invasion of the intercostal nerves by the inflammation. We have never observed cases, like those described by some authors, of " crossed pleuritic pain " — that is, cases in which the pain is localized on the side not affected. Cough and Expectoration. — The cough is probably excited directly by the dis- ease of the pleura. We often find that the pain in the side and also the cough are brought on by a deep inspiration. Expectoration is entirely absent in uncom- plicated pleurisy, or it is scanty, and consists simply of mucus. Much expectora- tion always means a pulmonary complication. A large amount of purulent sputum is evacuated if a purulent effusion breaks into the lungs {vide supra). Dyspnoea. — The respiration is usually shallow, and consequently frequent, be- cause of the pleuritic pain. In every large effusion which prevents respiration in one lung the dyspnoea becomes more severe, and may, with a very extensive effusion, reach the highest degree of orthopncea. The stronger the patient was before the disease, and the more rapidly the effusion develops, the more severe, as a rule, is the dyspnosa. Fever. — Most severe pleurisies are associated with fever, but its height is not very great, so that it quite rarely reaches 104° (40° C). The fever has no typical course. In cases with an acute beginning it is sometimes quite continuous, or slightly remitting at first. If improvement takes place, the fever goes down in about two or three weeks by lysis, so that this part of the temperature-curve may be precisely like the period of defervescence in typhoid. In the more protracted cases the fever gradually becomes more remitting, vary- ing between 100° and 101° (38°-38.5° C), and it assumes more and more the form of hectic fever. The longer the evening rise of temperature lasts, the more we are justified in suspecting tuberculosis. In empyema we see a higher, irregu- lar fever, sometimes associated with severe chills. The pulse is constantly rapid, up to 100 and over. In all severe cases the strength and tension of the pulse are much diminished. Irregularity of the pulse is not infrequent. All these changes are probably due in great part to the pres- sure of the effusion on the heart and large vessels. Lichtheim has discovered experimentally that it is not the compression of the vessels in the compressed lung which lowers the arterial tension. General Symptoms. — Pleurisy is almost always associated with a pronounced general malaise, muscular weakness, and dullness. The patient is pale, and often markedly cyanotic in cases with much disturbance of respiration. There is' great emaciation if the disease is of long duration. The appetite declines from the outset. There is often occasional vomiting, especially in the first period of the disease. The bowels are usually constipated. Many patients complain of headache. The condition of the urinary secretion is very important. In every pleuritic effusion the amoimt of urine is decidedly diminished so long as the effusion increases or remains at the same height. The daily amount is sometimes only eight or ten ounces (200-400 cubic centimetres). The urine is also concentrated, its specific gravity being about 1020-1028, Sediments of urates often form. This diminution of the excretion of water by the kidneys is largely the result of the diminished arterial pressure. An increase of the amount of urine is always a favorable symptom, often the first sign of beginning absorption of the effusion. If a large effusion is rapidly absorbed, the amount of urine may increase to eighty or a hundred ounces (2,500-3,000 cubic centimetres) daily. The urine, then, of course, is abnormally clear and of low specific gravity. PLEUEIST 285 Physical Signs 1. Fibrinous Pleurisy — Pleuritis- Sicca. — Simple fibrinous pleurisy sometimes gives rise to no physical signs at all. If it develops as a result of some pulmonary affection, the physical signs present are often dependent upon the latter alone. In many cases, however, dry pleurisy may cause marked objective signs. On inspection, we are struck by the impaired mobility of the affected side on respira- tion, which is due to the pain caused by breathing. Because of this same tender- ness the patient at first often lies on the sound side. Percussion gives no qualita- tive change of resonance as yet. With the beginning of exudation slight dullness appears, at first almost always in the posterior portion of the lungs. Sometimes the resonance becomes tympanitic as a result of retraction of the lung. We can almost constantly make out, especially in the back, that the lower edge of the lung moves less than usual on respiration. Auscultation gives a respiratory mur- mur that is either qualitatively unchanged or indefinite, but it is always dimin- ished. The peculiar pathognomonic sign of dry pleurisy, however, is the pleuritic friction-rub, that characteristic rubbing, grating, creaking sound, which arises from the sliding of the rough pleural surfaces over each other, and is detected especially in the lateral portions of the thorax. We can hear it both on inspira- tion and on expiration. It is often jerky, one rub following another after a con- siderable interval. If we are sure we hear a pleuritic rub, it is direct evidence of the existence of a dry pleurisy, but its absence will not let us exclude pleurisy. The friction-sound must be absent if there are pleuritic adhesions. We can often feel a marked rub by laying the hand on the chest. Sometimes the patient feels it himself, but in other cases he has no sensation of it. We may confound a slight rub with fine crepitant rales. Eepeated examinations before and after the patient has coughed usually confirm the diagnosis, since the rales are often changed by coughing. To be distinguished from the mild form of dry pleurisy just described is that variety in which there is an extensive and abundant fibrinous exudation, with scarcely any liquid. We have repeatedly seen severe cases following pneumonia, or even apparently primary cases, which displayed marked dullness and sense of resistance on percussion over the whole of one side of the chest, with diminished or absent respiration, and yet upon exploratory puncture only a few drops of serous exudation could be obtained. Evidently we had to do with the forma- tion of large amounts of coagulated fibrine. Attacks of this sort usually run a severe and tedious course, but they may, nevertheless, get well at last. 2. Pleuritic Effusion. — Small amounts of fluid in a pleural cavity escape discovery. Physical signs first appear when the amount of effusion reaches eight or ten ounces (200-300 cubic centimetres). Inspection shows first the more or less marked impairment of motion on the affected side on respiration. If the amount of the effusion is large, there is an evident distention of the affected side in the lower posterior and lateral portions of the thorax. The intercostal spaces are flattened or even a little convex. The nipples and shoulder-blades are farther removed from the median line on the affected side than on the healthy side. The hj-pochondrium on the affected side is more prominent. In an extraordinarily large effusion on the left side we have seen and felt, in the left hypochondrium, the lower surface of the diaphragm, which was actually arched downward. By direct measurement in severe cases we can make out that the affected side is expanded several centimetres. With every large effusion there is marked dyspncca and accelerated respira- tion. The slight excursions of the affected side on respiration are usually very striking, while the sound side moves so much the more. In this stage of pleurisy the patient often lies upon the affected side, in order to breathe with the healthy 286 DISEASES OE THE EESPIEATORY OEGAITS lung with as little restraint as possible. With large effusions complete orthopnoea may develop. The signs due to displacement of the neighboring organs, which are noticeable on inspection, will be mentioned below in the appropriate connection. Everywhere that a layer of fluid comes between the lung and the chest-wall there is a loss of clearness in the percussion-note. If the thickness of the layer of effusion is five or six centimetres, the resonance seems completely dull or flat. The pleuritic dullness is almost always made out first in the lower posterior por- tions of the thorax, more rarely in the lower lateral portions. With a slight effusion the height of the dullness is only a few centimetres, but, with much effusion, it rises higher in the back and the lateral portions of the thorax ; and on the right, resonance gradually grows dull anteriorly and inferiorly, above the liver. With very large effusions the dullness may begin in front at the second or third rib, or in rare cases even the whole half of the chest, front and back, may give a totally flat percussion-note. Pleuritic dullness is always attended with a marked feeling of resistance on percussion. With medium-sized effusions, when the dullness does not extend over the whole back, the upper boundary of the dullness usually forms an oblique line, highest at the vertebral column and thence running obliquely downward to the side of the thorax. Exceptionally the line runs the other way. On the right it is not possible to distinguish by percussion the lower limit of the exudation from the liver. On the left we can often distinguish its lower limit from the tympa- nitic resonance of the stomach, and are thus aided in diagnosis {vide infra, dis- placement of organs). [In moderate effusion without adhesions or pneumonic complications, the line of flatness in the back, the patient being in the vertical position, is lowest near the spinal column, and rises in a curve like the letter S as it passes outward toward the axillary region. The experiments by Dr. Garland, of Boston, with reference to this point are well known. Before attempting to mark out this line the patient should be told to take several deep inspirations, in order to inflate the triangular portion of lung which dips down near the vertebrae.] The percussion-note above a pleuritic effusion deserves attention. The begin- ning of pleuritic dullness is almost always relative, gradually passing to an abso- lute flatness. The pulmonary resonance above the beginning of dullness is usu- ally tympanitic, from retraction of the lung-tissue. We find the tympanitic resonance beautifully distinct in large effusions in the first and second intercostal spaces in front. It is loud and deep, and remains imchanged with the mouth open — Skoda's resonance. With very large effusions, which cause an actual com- pression of the lung, we sometimes find, in the second intercostal space, a dull tympanitic resonance, which becomes higher on opening the mouth. This reso- nance arises from the vibrations of air in a large bronchus surrounded by com- pressed lung — "Williams's tracheal tone." With large effusions we sometimes hear over the retracted lung, in the upper anterior intercostal spaces, a distinct buckram sound — the " cracked-pot sound." Displacement of the neighboring organs, which is made out chiefly by percus- sion, forms one of the most important physical signs in pleurisy with effusion. In right-sided effusions the liver, especially the right lobe, is displaced down- ward. We find the lower border of the liver dullness extending several centi- metres below the ribs. In very large effusions the liver may be pushed down to the level of the umbilicus. The pushing of the mediastinum to the left in large effusions may be recognized upon percussing from the right toward the left, by dullness over the upper part of the sternum, reaching to or beyond the left border of the sternum. The displacement of the heart to the left in the majority of well- marked cases is associated with a displacement of the apex of the heart upward. PLEUEISY 287 This is easily explained by considering the position of the heart and the direction of the pressure, which first acts from below. We recognize the displacement of the heart chiefly by the position of the apex-beat, which is seen and felt at or outside the left mammillary line in the fifth space, or often higher, as we have said — in the fourth. Percussion gives a corresponding displacement of the left boundary of the cardiac dullness to the left. In left-sided effusions the displacement of the heart to the right, which can usually be made out even in moderate effusions, is especially noticeable. Reso- nance over the lower part of the sternum is diminished, the heart's dullness extends to the right border of the sternum or several centimetres beyond it. In the most marked cases the heart is pushed to the right mammillary line. The displacement of the mediastinum is also to be made out over the upper part of the sternum, the dullness reaching to the right border of the sternum or beyond. The low position of the diaphragm is made out by a depression of the left, and in marked cases of the right, lobe of the liver. It is an especially important sign, however, that dullness occurs in the zone, about a hand-breadth wide, of normal tympanitic resonance above the left border of the ribs — the " semilunar space " of Traube. The normal tympanitic resonance here comes from the stomach or large intestine. As the diaphragm is pressed downward the pleuritic effusion presses on these organs. The semilunar space is therefore diminished, and finally, with large effusions, there is absolute dullness down to the edge of the ribs. Changes in dullness in pleuritic effusions may occur with a change of the patient's position, but they may often be absent on account of adhesions. As a rule the normal change in the position of the lower border of the lung corre- sponding with respiration is abolished. Auscultation always gives a diminished respiratory murmur over the pleuritic effusion. With a beginning effusion it may sound approximately vesicular, but later it becomes indefinite, harsh, and finally bronchial, if the larger bronchi re- main open for the respiratory current of air. The bronchial respiration sounds distant and low, and has the character of the sharp German ch, but in rare cases it also assumes a distinct amphoric tone, so that it sounds almost like a cavernous respiration. The respiratory murmur may finally disappear entirely over very large effusions. Above the upper boundary of the effusion the respiration almost always sounds harsh. Among the adventitious sounds we must mention the pleuritic friction sound, which of course can be heard only at the upper boundary of the effusion, where the two pleural surfaces meet. Moist rales and rhonchi signify a co-existing disease in the lungs. With slight effusions we often hear, on deep breathing, pure crepitant rales on inspiration, as the walls of the alve- oli and bronchioles in the atelectatic lung, which were stuck together, are torn apart. On auscultation of the voice we sometimes hear bronchophony, and sometimes that bleating, nasal sound known as segophojiy. Baccelli advanced the theory that auscultation of the whispered voice might be of service in diagnosticating the character of the effusion. With a serous effusion we can understand a whisper distinctly through the thorax, but not with a purulent effusion, since theoret- ically the cell-elements destroy the waves of resonance. This theory holds true in many cases, but by no means in all. On auscultation of the heart we notice, as a result of its displacement, an ab- normal extension of the region over which the heart-sounds are audible. If the inflammation spreads from the pleura to the outer surface of the pericardium, we can sometimes hear an extra-pericardial friction-rub, accompanying both the respiration and the action of the heart. The vocal fremitus is always diminished over the pleuritic effusion, and in marked cases is entirely absent. 288 ^ DISEASES OF THE EESPIEATOEY 0EGA:N'S 3. Absorption of the Effusion — Pleuritic Contraction. — The beginning ab- sorption of the effusion is usually first made evident by the percussion-note in the upper part of the dullness becoming clearer and sometimes tympanitic. The respiratory murmur is also plainer. Where it was bronchial it becomes in- definite and gradually vesicular again. The vocal fremitus is again to be felt. All these improvements take place gradually but'slowly. It is usually a very long time before the percussion-note resumes its normal clearness. The changes in the form of the thorax are especially striking. Only in pleu- risies with slight effusion does the somewhat expanded thorax resume its old form without further change. After every severe pleurisy with large effusion there is, during its absorption, a marked contraction of the affected half of the chest. In cases of moderate intensity the contraction affects only the lower lateral portions of the thorax, in severe cases the upper and anterior portions as well. "We find the most marked contractions in children and young persons with a yielding thorax. The circumference of the affected side is much less than that of the sound side. The ribs are pressed together and the intercostal spaces become very narrow. The fossae are deepened and the nipples and shoulder-blades are drawn nearer the vertebral column, which takes on an abnormal lateral curva- ture, in which its convexity is directed usually toward the affected side, but some- times to the sound side. Dullness and diminution of the respiratory murmur and vocal fremitus continue with the contraction of the pleura, but they no longer depend upon the presence of a fluid effusion, but are due to the pleuritic thick- ening. The process of marked contraction always lasts for months, or even longer. In favorable cases the contraction of the thorax may be readjusted very much later, often after years. The thickening is absorbed, and the lungs and thorax gradually expand, but in other cases there are extensive adhesions between the pleural surfaces, especially over the lower lobe, which result in a permanent dis- turbance of respiration. In almost all cases of pleurisy with contractions there arises a vicarious emphysema in the lung on the sound side. Complications. — Peculiar complications of pleurisy are rare. Where such occur they are due either to the primary disease v\-hich has led to the pleurisy, or to the simultaneous action of the same cause of disease, such as tuberculosis. Hence it happens that we speak of the frequent " complication " of pleurisy with chronic bronchitis or with tuberculosis of the lungs or other organs. It is impor- tant to bear in mind that, by a direct advance of the inflammation, the pleurisy may also invade the pericardium, and rarely the peritoneum, through the dia- phragm; but we see this extension of the process almost solely in tubercular and purulent pleurisies. We must mention, finally, that we have seen several cases with a large serous effusion, in which an acute hsemorrhagic nephritis occurred. For the paralysis of the arm on the corresponding side observed in some cases of empyema, compare what is said in regard to reflex paralyses on page 833. Various Forms of Pleurisy 1. Primary Rheumatic Pleurisy. — As we have already pointed out, when con- sidering the aetiology of pleurisy, clinical observations have lately led to the belief that some of the cases of acute primary pleurisy are due to the same cause as acute articular rheumatism (which see). Although there are as yet no suffi- cient number of decisive bacteriological investigations, we are, nevertheless, strongly inclined, from our present experience, to acknowledge the correctness of this view, even if we do not estimate the frequency of rheumatic pleurisy nearly so high, as, e. g., does Fiedler, on the ground of his observations in Dresden. Rheumatic pleurisy usually develops rather suddenly in persons previously healthy. Sometimes it is preceded by mild rheumatic pains in the muscles or PLEUKISY 289 some of the joints. The local discomforts, such as pain in the side, are often very severe, the fever is moderately high, though rarely over 104° (40° C.) ; and as the case progresses such rheum^itic symptoms as swelling of the joints and endocarditis may associate themselves with the pleurisy, and confirm the diag- nosis. In general, however, the course of the disease is favorable. The fever lasts, as a rule, only a week or two, and even when there is a large exudation it finally undergoes complete absorption with recovery. 2. Tubercular Pleurisy. — In an setiologieal sense we must declare the larger part of the ordinary " pleuritic effusions," which clinically seem primary, to be tubercular. The further course of the cases, if we can watch them long enough, almost always permits us finally to recognize the tubercular nature of the dis- ease; yet we can not say that some other tubercular disease, particularly phthisis, is always the immediate sequel of the pleurisy. In a comparatively small number of cases do the symptoms of acute tubercu- losis, or more frequently of chronic phthisis, appear as an immediate result of the pleurisy, which at that time is usually still present or in the contracting stage. The objective changes of phthisis are evident either in the apex or in the lower lobe of the affected side. The fever continues, the pulmonary affection advances, the other lung is also attacked, and the disease takes a fatal course under the type of an ordinary phthisis, now more acute and now more chronic. In other cases acute tubercular aifections arise sooner or later as a result of the pleurisy — tubercular meningitis, or general miliary tuberculosis. In other cases still the disease develops under the form of tuberculosis of the serous mem- branes, to which we will return again in the description of tubercular pericar- ditis and tubercular peritonitis. We often have to do with a double pleurisy with no evident complication in the lungs. In varying succession are added the symptoms of chronic tubercular peritonitis, with pain, swelling, and effusion of fluid into the abdomen, or the symptoms of tubercular pericarditis. Death finally ensues with persistent hectic fever and increasing general emaciation and weak- ness. The whole affection usually runs a chronic course, lasts for months, and often shows marked remissions and temporary improvements. In very many instances, on the other hand, the pleuritic effusion has through- out an apparently favorable course. After some weeks the fever ceases, the effu- sion is absorbed, the patient gets up, and is finally discharged as nearly well. Of course, some dullness and retarded motion often remain in the affected side, but even these may gradually disappear. These cases, too, very often turn out in the end to be tubercular. After a longer or shorter. period of apparent health, sometimes after the lapse of years, a " new " disease appears — that is, either a return of the pleurisy, a pleurisy on the other side, or some other acute or chronic tubercular affection. In such cases, too, we must look upon the former pleurisy, in an setiological sense, as tubercular. It is not impossible, however, for even a tuber- cular pleurisy to recover, and for the recovery to be permanent, if no other organ is at the same time affected by tuberculosis, especially if the lungs remain intact. Finally we must mention the cases in which a pleuritic effusion develops sec- ondarily to an already pronounced phthisis. Here too we almost always have to do with a tubercular pleurisy. The anatomical changes in tubercular pleurisy consist in the ordinary signs of inflammation, and also the presence of the specific nodules of tubercle. The number of tubercles differs very much in different cases. The pleura is in some cases completely studded with miliary nodules, and in others we find the tuber- cles, at least with the naked eye, only in single spots. The effusion is usually of a sero-fibrinous character. Sometimes it is ha9morrhagic, as the majority of cases of apparently primary " haemorrhagic pleurisy '' are generally of a tubercular nature. Empyema also (vide infra) occurs not infrequently in association with 19 290 DISEASES OF THE EESPIEATOEY OEGANS tuberculosis; and finally, in a few cases the exudation has been of a peculiar milky character, and has contained numerous oil-globules, probably originating from fatty-degenerated and disintegrated leucocytes and endothelium, 3. Purulent Pleurisy— Empyema.— A purulent exudation is developed in the pleura when the inflammation of that organ is due to a specific cause which excites suppuration. So far as is yet known, the streptococcus pyogenes seems to be the most frequent factor in producing empyema. It is found in the pus of empyema, due to such causes as external injury, caries of the ribs, pulmonary tuberculosis, pneumonia, and pyaemia. Less often empyema is excited by staphy- lococci. This is almost always a rather favorable form of the disease. Likewise comparatively benign is meta-pneumonic empyema, which in most instances is caused by the pneumococcus. The empyema of tuberculosis is, as has been already pointed out, in most cases devoid of bacteria (A. Frankel and others), and here we may have to do with the formation of chemical poisons capable of exciting suppuration. Empyema usually causes severe symptoms. The fever is higher than in the other forms of pleurisy, but it is irregularly intermittent, and is often associated with chills. There are severe general symptoms besides the fever, such as great languor, headache, a dry tongue, and a rapid pulse. We sometimes notice a slight oedema of the chest-wall on the affected side. Otherwise the local symptoms and disturbances are, of course, the same as in the other forms of pleurisy. If the pus is not evacuated artificially, the empyema may finally break externally or into the lungs (vide supra). In the latter case a very large expectoration of pus sud- denly occurs, and is usually followed by pneumothorax. Diagnosis. — Our chief attention in regard to diagnosis is directed to the dis- tinction between pleurisy and acute or chronic pneumonia, which is not very easy in all cases. We will briefly contrast the distinctive features as made out on physical examination. Inspection. — A marked distention of the affected side points to effusion; it does not occur in pneumonia. Percussion. — The dullness in pleurisy is complete, and the feeling of resistance on percussion is very marked; in pneumonia, however, the dullness is rarely so marked, and there is often a tympanitic sound. The discovery by percussion of signs of displacement of the neighboring organs is of especial weight, as these signs are always absent in uncomplicated pneumonia, while with few exceptions they can be easily demonstrated in every case of pleurisy when the exudation is at all considerable. Auscultation. — Diminished or suppressed respiratory murmur points to pleu- risy, loud bronchial breathing and rales to pneumonia; but we must not forget that in pneumonia auscultation may give the same signs as in pleurisy, if a bronchus is plugged. Vocal Fremitus. — Marked vocal fremitus over dullness is direct evidence of pneumonia, diminished or absent vocal fremitus of pleurisy ; but the vocal fremi- tus may also be diminished in pneumonia if a bronchus is plugged. Besides the physical signs, other phenomena to be observed are the mode of commencement, the course of the disease, the fever, the expectoration, and the appearance of herpes. The most reliable means of deciding in all doubtful cases is exploratory puncture, although even then we may of course be left in doubt whether an infiltration of the corresponding portion of the lung may not exist, in addition to pleurisy. If the exudation is largely fibrinous, or if there is an abundant new growth of inflammatory connective tissue, the results of aspira- tion may be negative. Hence, in doubtful cases we should always make re- peated trials. If we have diagnosticated a pleuritic effusion, the next question is always as PLETJKISY 291 to the character of the effusion, because the prognosis and treatment are to a large degree dependent upon this. Although certain well-known astiological circum- stances, and the severity of the fever and the general symptoms, often permit us to suspect the nature of the effusion, whether serous or purulent, the only certain information comes from an exploratory puncture with a hypodermic syringe. If the syringe is carefully disinfected, and the operation is cautiously conducted, this procedure is entirely devoid of danger, and we must urgently advise its employment in all doubtful cases in order to settle the diagnosis. It is indeed of practical importance to know that there is a likelihood in empyema of obtaining no fluid by means of exploratory puncture (vide supra), even when, upon incision, pus is found. We have had this experience repeatedly. In doubtful and severe cases in which there is suspicion of empyema, it is therefore decidedly advisable, when life is threatened, to make an incision of the pleura. Besides a macro- scopic inspection, a careful microscopic examination of the fluid withdrawn is sometimes of importance. Besides the ordinary constituents — red and white blood-corpuscles, endothelial cells, and cholesterine crystals — ^we may sometimes find something of special diagnostic significance, such as bacteria in septic pleu- risy, carcinoma-cells in cancerous pleurisy, etc. We can not always judge from the beginning whether a pleurisy is tuber- cular or not; but we should never forget, as has already been affirmed, that in every case of pleurisy, even if it is apparently primary, there is a strong sus- picion of tuberculosis. We must observe in particular the general habit and the nutrition of the patient, and inquire into the hereditary predisposition and any previous illnesses. In the further course of the disease persistent hectic fever, slowly increasing emaciation and pallor, fresh relapses, and the onset of pulmonary symptoms, point to the tubercular character of the pleurisy. Every double pleurisy, and every pleurisy associated with pericardial symptoms, leads us most decidedly to suspect tuberculosis. A hsemorrhagic effusion, as we have said, points strongly to tuberculosis. Tubercle bacilli are usually not present in the exudation of tuberculous pleurisy, because the tubercular nodules of the serous membrane scarcely ever ulcerate. On the other hand, we have often been able to demonstrate tubercle bacilli in the scanty expectoration of such patients, even when there were scarcely any pulmonary symptoms. The peculiarities of rheumatic pleurisy have been already detailed. Prognosis. — The prognosis, as regards the immediate danger of the disease, depends entirely upon the severity of the symptoms, and especially upon the dyspnoea. The prognosis, as regards the further course of the disease, depends chiefly upon the nature of the pleurisy. Many secondary and also many appar- ently primary pleurisies, although extensive, recover completely and permanently after weeks or months. Unfortunately, we only too frequently have to give a doubtful or an unfavorable prognosis, especially if the tubercular nature of the pleurisy be probable or certain. The prognosis of empyema depends partly upon the underlying disease, but especially upon judicious and timely operative inter- ference. In benign cases of empyema recovery is usually complete in a few weeks after operation, but sometimes months are required. The possibilities of a spon- taneous rupture of empyema, internally or externally, have been mentioned above. With incomplete healing, which leaves a pleural fistula, we must fear the appear- ance of general amyloid disease in various organs. In rare instances with large effusions sudden death occurs, an event which can not always be satisfactorily explained. Probably there are different factors in different cases, such as pulmonary embolism, cerebral embolism, sudden cerebral anaemia, weakness of the heart, or the onset of pulmonary cedema. Treatment. — In the beginning of the disease the treatment is purely symp- tomatic. We try to alleviate the patient's symptoms, the pain and dyspnoea, by 292 DISEASES OF THE EESPIEATORY ORGANS local applications, especially by mustard plasters, warm poultices, which are usually more grateful than cold applications, sometimes, too, by dry cups, also by embrocations with chloroform liniment, and, with severe symptoms, by mor- phine internally or subcutaneously. Unfortunately, we have but few remedies to check the inflammatory process in the pleura. If an ice-bag is well borne, it may be of service. The efficacy of the much-used painting with iodine is doubtful, but it may always be tried if there is a severe pleuritic pain. Perhaps more efficient is the application of iodized vasogen, or of iodoform ointment (1 to 15). If a large serous effusion has formed, it is the universal custom to prescribe diuretics. The idea is to cause, or at any rate promote, the absori)tion of the exudation by increasing the excretion of urine. It is, however, very difficult to obtain any real proof of the usefulness of diuretics in pleurisy with effusion. They often are of no use whatever, but again, the absorption of the fluid may follow the administration of a diuretic, so tha't it does not seem impossible that the latter has a therapeutic influence. With regard to a choice of the diuretics to be employed we would name, first, salicylate of sodium, 75 to 120 grains (grammes 5 to 8) a day, because a specific influence has been ascribed to this drug in pleu- risy. This applies particularly to cases of supposed rheumatic origin (vide supra). Many good observers assert that primary pleuritic exudations often run a remarkably rapid and favorable course, when treated with salicylate of sodium. Moreover, the drug has a direct diuretic effect. Besides this, the acetates of potas- sium and of sodium are frequently prescribed, as well as squills, and, of late, diu- retine (sodio-salicylate of theobromine), given in doses of thirty grains (grammes 2) two or three times a day. We have sometimes found this remedy apparently very efficient. If there are signs of cardiac weakness and diminished arterial tension, digitalis must be prescribed, alone or with a diuretic. Other internal remedies are at present seldom employed in pleurisy with effusion. The influence of iodide of potassium as an "absorbent " is extremely doubtful. Drastic purga- tives and such diaphoretic remedies as hot packs and pilocarpine usually affect the general condition unfavorably, and are of little use. Probably there are to- day few advocates of the so-called Schroth method of treatment, according to which the amount of fluid ingested is reduced to a minimum, so as to promote the absorption of the exudation. In many cases the operative treatment of pleu- risy (introduced by Trousseau) — the evacuation of the effusion by puncture — is of the greatest importance. Many cases of pleurisy with effusion run a favor- able course without it, and we consider it at least superfluous to puncture every effusion without sufficient grounds, but puncture is often one of the most service- able therapeutic influences at our command. The first and most important indi- cation for puncture is present when the effusion becomes so large as to be directly dangerous to life. As soon as the patient's dyspnoaa reaches a dangerous degree, and the cyanosis becomes marked and the pulse weaker, a puncture must be made as a direct vital indication. When the exudation is of considerable size there may be a very sudden aggravation of the symptoms, so that in such cases one should not wait too long. It is much better to puncture too early than too late! Trousseau urged that tapping should invariably be performed when the dullness caused by the exudation involves not only the back, but also the whole or nearly all of the anterior wall of the thorax, a rule which the author almost always follows. The benefit of such a puncture is often pronounced. The sec- ond indication is a too protracted absorption of the effusion. Puncture is indi- cated if the effusion does not disappear after an apparent remission of the in- flammatory symptoms, especially after the fever has gone. We often see the further absorption stimulated by such a puncture. It has been said that, if pos- sible, tapping should be delayed until the fever has ceased, but to us this does not seem at all necessary. When the exudation was large, or the absorption was PLEURISY 293 delayed, Ave have repeatedly aspirated even when the patient was still feverish, and have not infrequently found that the fever diminished remarkably upon the removal of the exudation (see the temperature chart, Fig. 37). * Puncture (1200 Ccm.) 40.' 39.° ifiiiaiiiiiiniiiiiiiii HinHaiiRiBeiiiiii "Bailiriaii Fig. 37. — Temperature-curve in pleurisy witli effusion before and after tappiufr. (Erlangen medical clinique.) [There is considerable danger in delaying interference with a large effusion, especially if it has come on pretty rapidly, however comfortable the patient may be. The liability to sudden and fatal dyspnoea under these circumstances is now well recognized.] As regards the performance of the puncture, we can not here go into all the numerous methods and forms of apparatus proposed. The distinctions are imma- terial. The simpler the method, the easier it is to perform, and hence the better it is. Every puncture must be preceded by an exploratory puncture in order to settle the diagnosis as to the presence and character of the exudation. A medium-sized trocar with a lateral openiug, to which a rubber catheter can be fastened, senses to evacuate the fluid. Billroth's and Frantzel's trocars are useful. Aspiration can be performed still more conveniently with a hollow needle, and best of all, according to our experience, with that proposed by Fiedler, which is now exclu- sively employed in the author's wards, because the point of this needle is guarded so that it can not scratch the tissues, and also, if it becomes plugged with clots of fibrine, these can be pushed out.* The instruments and the chest-wall at the point of puncture must be carefully disinfected. We usually choose a point for puncture, somewhere about the sixth intercostal space, in the middle or poste- rior axillary line. The patient sits up in bed, but is held and supported by another person, when it is possible. Before and during the puncture he takes a little strong wine, strophanthus, or similar stimulant. The pain of the opera- tion may be mitigated by previously injecting morphine [or still better, by caus- ing local anaesthesia with a half- to one-per-cent. solution of cocaine]. In the overwhelming majority of cases, and especially if the exudation is abundant, we can remove a large part of the fluid by simple puncture with siphonage. With few exceptions, the pleuritic exudation is under a positive pressure of 10 to 25 millimetres of mercury. The evacuating tube of the trocar must be previously filled with carbolized water and conducted under a layer of the same into the vessel prepared to receive the effusion. The evacuation of the effusion should always be slow and gradual. Many physicians advise stopping when 1,500 cubic centimetres have been removed, but if the fluid is allowed to escai^e slowly and everything is going well, this quantity may often be exceeded with im- * [Fiedler's instrument consists essentially of a sharp lioUovv needle, with anoutor jacket, which can be moved so as to cover the sharp point after the chest-wall has been penetrated. If the lumen is stopped up, a pointed steel wire thrust directly tlirough the attached rubber tubing displaces tlie obstruction. — Tkans.] 294 DISEASES OF THE EESPIRATOEY ORGANS punity in the case of large exudations. While, as we have said, in most in- stances the exudation may be satisfactorily removed by simple puncture and siphonage, it will sometimes prove necessary to employ aspiration. Hence some physicians invariably do so, and to this there is no objection, even if it is unne- cessary. The forms of apparatus most used for this are those invented by Dieulafoy and Potain. In puncture with aspiration we proceed more slowly and cautiously. [The necessity for two punctures — one exploratory, the other distinctly opera- tive — does not seem clear. The two can be perfectly combined, a fair-sized trocar or needle being as easy of introduction and producing really no more pain than a very fine one, and being more sure to give results on which reliance can be placed. An ordinary Davidson's syringe makes a very satisfactory pump and can always be obtained.] Unpleasant incidents which may cause a cessation of the process are rare. If the patient complains of dizziness or faintness we must cease, or at any rate, pause. Usually everything goes well until the needle begins to rub against the pleura: then there is pain and generally a violent cough. It is well, then, to remove the needle at once. The cough can usually be promptly quieted by rest and a little morphine, but sometimes after aspiration there will develop a sort of pulmonary oedema, with the expectoration of a large amount of frothy serous sputum (expectoration albumineuse). This is perhaps due to the increased per- meability of the vascular wall, or to feebleness of the left ventricle. When the process is over, we close the little opening with a bit of sticking- plaster or with iodoform collodion. A regular surgical dressing is scarcely ever necessary. If the exploratory puncture has shown a purulent effusion, we can first evacu- ate the pus by puncture, if the vital indication exists; but a permanent cure from tapping is exceptional. The pus almost always reappears. Empyema is like an abscess, which can not be cured until a permanent, free exit for the pus has been provided. We must, therefore, not only remove the pus, but institute drainage of the pleural cavity. The best method, and the one which is almost exclusively practiced in the surgical wards in Erlangen, is by incision of the pleural cavity, preceded by resection of a portion of a rib for the purpose of com- pletely emptying out the pus, and obtaining a better final result. This compara- tively simple method gives results so good and so entirely satisfactory that, to be frank, we can not understand why there has been so much discussion over the treatment of empyema. We are perfectly willing to allow that good results are likewise obtained with other methods, and in particular with the drainage by siphon action, advocated by Biilau. Yet there is not, in our opinion, any satis- factory ground for abandoning the ordinary surgical principles, relating to the treatment of internal suppuration, in the case of empyema. With regard to the minutiae of the operation, we must refer to text-books on surgery. In treating the chronic, contracted pleurisies with thickening, but without fluid effusion, methodical respiratory efforts, " lung-gymnastics," are of use. Be- sides these we should strengthen the general condition as much as possible. We should advise the patient to breathe deeply, and prescribe cold sponging of the chest daily. Inspiration of compressed air by means of a pneumatic apparatus is often accompanied by good results. Well-to-do patients, who have had a severe pleurisy, should be sent to a suitable climatic health-resort. PEEIPLEUKITIS 295 CHAPTER II PERIPLETJRITIS Under the name of " peripleuritis " Wvinderlich was the first to describe a rare form of disease, which consists of an inflammation of the connective tissue between the costal pleura and the ribs, and which terminates in the formation of an abscess. Similar cases have since been repeatedly observed, and all were char- acterized by the lack of any discoverable aetiology. There is neither a previous injury, nor a primary disease of the ribs or the pleura. Nevertheless the cause must be sought in an invasion of micrococci, which excite the suppuration. A knowledge of the particulars, however, can only be gained from future investiga- tions. They will determine whether peripleuritis can be regarded as an inde- pendent disease or not. The disease occurs chiefly in men. It usually begins suddenly with a chill, and runs its course with quite a high fever. In pronounced cases the local symp- toms have the greatest similarity to those of an empyema, but the greater protru- sion of the chest-wall is striking. The ribs are crowded apart by the abscess, and there is often spontaneous rupture externally, scarcely ever into the pleura. Per- cussion gives no symptoms of displacement of the neighboring organs, a distin- guishing point from empyema. It is of diagnostic significance that we can often discover normal lung-tissue containing air below the abscess. The mobility of the lower border of the lung is also usually retained, contrary to what is the case in empyema. Another important sign was first brought to notice by Bartels: the wall of the abscess relaxes on inspiration and becomes tense on expiration. We may also mention that acute nephritis has often been observed among the com- plications. From these points we may be able to make the diagnosis during life, at least in many cases. The prognosis is quite unfavorable, but recovery does occur. The treatment can be only operative, and it is quite analogous to that for empyema. CHAPTER III PNEUMOTHORAX {Pyv-pneumothoraz. Hydro-pneumotliora'x.) .31tiology. — Pneumothorax^ — that is, a collection of air or gas in the pleural cavity — arises, in an overwhelming majority of cases, from the penetration of air into the pleural cavity through an opening in the pleura. The opening may be in the external chest-wall from a penetrating wound of the chest or an empyema operation, or it may be in the pulmonary pleura. Pneumothorax is by far most frequently associated with phthisis, when a cavity lying beneath the pulmonary pleura perforates into the pleural cavity. This is more apt to happen in compara- tively acute phthisis than in very chronic forms, because the extensive adhesions and contractions in the latter hinder its development. It usually apj^ars in quite far advanced cases, but it may sometimes arise with but slight changes^ in the lung. Pulmonary gangrene or abscess, as well as phthisis, may cause pneumothorax by perforation into the pleural cavity. It may also arise from the rupture of an empyema into the lung. In some cases a perforation of the oesophagus or stom- 296 DISEASES OF THE EESPIRATOEY ORGAl^S acli into the pleura, as in gastric nicer, has been observed, with the formation of pneumothorax. The development of this condition from severe injuries, as from laceration of the previously healthy lung, without injury to the chest-wall, is rare. Forced respiratory movements, associated with physical exertion, seem especially capable of exciting svTch a process. We have ourselves seen pneumothorax develop sud- denly in a previously healthy woman while hanging out her washing, and another time in a young man during very labored rowing. Both cases recovered rapidly and completely. All the last-named causes, however, are far less important than pulmonary tuberculosis. We should mention that in phthisis, too, there is sometimes a defi- nite exciting cause — severe coughing, vomiting, or muscular exertion — which may favor the development of the pneumothorax. • Many authors maintain that, by decomposition of a putrid pleuritic effusion, gas may be produced, and thus we may have pneumothorax ; but such an event is extremely rare, if it ever happens. Pathological Anatomy. — On opening the pleural cavity a part of the air usu- ally rushes out, sometimes with an audible noise. We then look into a large cavity filled with air, and find, in total pneumothorax, the lung completely re- tracted and lying compressed against the vertebral column. If, however, the air fills only a part of the pleural cavity, as a result of extensive adhesions of the pleurse, we speak of a circumscribed or sacculated pneimiothorax. The amount of air contained in the pleural cavity may reach 2,000 cubic centimetres. The pressure which it is under is almost always positive — on an average five or ten centimetres of water. In the cases of pneumothorax arising from perforation of the pulmonary pleura we can usually make out the point of perforation in the lungs. This is more frequently situated in the upper lobe than in the lower. Sometimes it is already grown over or is covered by a layer of fibrine, and can no longer be found. The opening is usually quite small, but it may reach the size of a ten-cent piece. Left-sided pneumothorax seems to be somewhat more frequent than right-sided. The pleura itself is only rarely normal. Usually agents of inflammation have entered it with the air, and hence it is found in a state of inflammation. A part of the cavity is. then filled with effusion. This is usually wholly purulent — pyo- pneumothorax — or sero-purulent, but it may even be serous or sero-fibrinous — sero-pneumothorax, or hydro-pneumothorax. The neighboring organs, especially the heart and liver, are found pushed out of their normal position, as in large pleuritic effusions. Symptoms and Course. — The onset of pneumothorax (we speak in what fol- lows especially of pneumothorax in connection with pulmonary tuberculosis) is quite often made known by a sudden pain, usually associated with an increase of the dyspnoea and of the general symptoms. There is sometimes collapse. The temperature sinks below normal, the pulse rises to 140 and over. The patient looks pale and cyanotic. He usually sits upright or is in a half -sitting position in bed, either more on the aft'ected side, in order to use the normal lung as much as possible for breathing, or more on the sound side on account of the tenderness. If the pneumothorax has come on as a result of the rupture of an empyema into the lungs, there is at the same time a veiy abundant expectoration of pus. Although in many cases the symptoms mentioned lead to a suspicion of pneu- mothorax, yet a positive diagnosis can be made only after a physical exami- nation. Inspection gives a very marked distention of the affected side. The inter- costal spaces are stretched out, or even protruded. In some cases, as we have our- selves noticed, there is a marked elastic " air-cushion feeling " on palpating the PNEUMOTHOEAX 297 intercostal spaces. On respiration, the afFeeted side is almost entirely motionless, while the excursions of the other side are the more marked. The displacement of the heart is often evident from the. visible displacement of the apex-beat. Percussion gives over the pneumothorax a remarkably loud, full note, abnor- mally deep, but usiTally not tympanitic, on account of the tension of the walls. It is especially important to note that this resonance extends beyond the normal limits of the lung on the right down to the seventh or eighth rib, and on the left to the fifth or sixth rib, and sometimes even to the edge of the thorax. The lower limit of this abnormally loud percussion resonance shows no change of position with respiration. The displacement of the neighboring organs can also be made oi;t by percus- sion. With right-sided pneumothorax we find the lower border of the liver dull- ness abnormally low, and the left border of the cardiac dullness pushed over to the anterior axillary line. In left-sided pneumothorax the cardiac dullness is usually entirely absent from its normal place, and is found instead to the right of the sternum. The left lobe of the liver is pressed downward, and in the " semilu- nar space " we find, instead of the normal tympanitic resonance, the same deep, loud, and usually non-tympanitic note as in the upper parts of the thorax. Upon auscultation we are struck by the entire absence of respiratory murmur. This is in special contrast to the clear resonance on percussion. In other cases, however, we hear a number of metallic sounds, at least in many places and at many times, which are very characteristic of pneumothorax. First among these is amphoric, metallic respiration. This arises in open pneumothorax (vide infra) from the direct passage of the air in and out, but in all other cases it is the ordinary respiratory murmur, which has acquired a metallic timbre from reso- nance in the pneumothorax. In an analogous way arise the metallic-sounding rales ["metallic tinkling''], and the metallic resonr.nce of the cough and voice. Heubner has devised a particularly beautiful and practically important method for demonstrating the metallic sound in pneumothorax. If we strike lightly on a pleximeter with a little rod, usually the handle of a percussion hammer, while we auscult near it — " rod percussion " — we very often hear quite a distinct high metallic sound. The vocal fremitus over a pneumothorax is usually diminished, but it may be felt in spite of quite a large collection of air. A number of special physical signs are found if a purulent or serous effusion be added to the pneumothorax. In the first place, the resonance is thereby ren- dered dull, to a greater or less extent, in the lower parts of the chest. The bound- aries of the fluid by percussion show a very evident change with the patient's change of position, because the fluid in pneumothorax can move easily in all directions. Inasmuch as the shape of the remaining air space must change cor- respondingly, there is not infrequently a change in the pitch of any metallic sounds which may be produced, whether by percussion or respiration, varying with the posture of the patient (Biermer's change of note). In many cases, if the ear is applied to the chest-wall there is heard, on every motion of the fluid, produced, e. g., by gently shaking the patient, a metallic gurgling sound, so- called Hippocratic succussion. Forms of Pneumothorax. — According to the condition of the perforation dur- ing life, we distinguish three kinds of pneumothorax (Weil). We speak of an " open pneumothorax," if the point of perforation remains open, so that the air on respiration constantly passes in and out of the pleural cavity. If the perfora- tion is completely closed, we have a " closed pneumothorax." The third and most frequent form is the " valvular pneumothorax," in which air enters the pleural cavity at each inspiration, but on expiration there is a valve-like closure of the perforation, and thus the air can not escape again; but as soon as the pressure 298 DISEASES OF THE RESPIRATOEY ORGAITS in the pleural cavity increases so that no more air can enter it on inspiration, the valvular pneumothorax becomes closed. In open pneumothorax the pressure in the pleural cavity must be the same as the atmospheric pressure. A positive pressure in the pleural cavity can exist only in a closed or a valvular pneumo- thorax. A clinical diagnosis of the form of pneumothorax is not always possible, and has usually no great practical importance. The very loud, metallic, amphoric respiratory murmur, which may be heard in open pneumothorax, must be men- tioned, and Wintrich's change of pitch (see page 243) can sometimes be heard in this form. It is worthy of mention that symptoms of displacement of the neighboring organs must also arise in open pneumothorax. The predominant atmospheric pressure here is positive in contrast to the negative pressure in the other pleural cavity, and to the normal negative pressure which previously acted on the upper surface of the diaphragm. A very marked protrusion of the affected side, and great displacement of the heart and liver, however, speak most strongly against an open pneumothorax. Some authors have tried to find a point of distinction for the different forms of pneumothorax in the composition of the gas in the pleural cavity, but the results of chemical analysis are still contradic- tory. According to Ewald, we find in open pneumothorax not over five per cent. of carbonic acid and about twelve to eighteen per cent, of oxygen ; in closed pneu- mothorax, however, fifteen to twenty per cent, of carbonic acid and ten per cent, at most of oxygen. If in an open pyo-pneumothorax or hydro-pneumothorax the point of perforation lies below the level of the fluid, there sometimes arise on every inspiration metallic sounds, since the bubbles of air drawn in rise and come up through the fluid — " the water-pipe sound," " metallic tinkling." A peculiar sipping and short snapping sound on inspiration, heard by us in one case, seems to point directly to the existence of a valvular pneumothorax. Course of the Disease. — In many cases the occurrence of pneumothorax causes such a high degree of respiratory disturbance that death ensues in a few hours or days. In other cases the patient improves, and may feel quite well for a long time in spite of the condition. We have ourselves frequently observed patients who passed the entire day out of bed with scarcely any inconvenience. Usually, how- ever, the disease which gives rise to the pneumothorax, most often pulmonary tuberculosis, leads in a shorter or longer time to death. Sometimes, again, the patient recovers. This almost always occurs in those rare cases above mentioned, when a healthy lung has been torn, but sometimes, also, in cases of pulmonary tuberculosis. The healing takes place in this way, that the air is first replaced by a fluid effusion, and then the latter is gradually absorbed, but the air may also be directly absorbed in whole or in part. It depends upon the origin of the lesion, then, and upon the intensity of the underlying disease, whether the recovery is permanent or not. Diagnosis. — The diagnosis of pneumothorax is usually easy with careful ex- amination, but the symptoms may sometimes be of so little prominence as to excuse overlooking it. It is very difficult and often quite impossible to make a differential diagnosis between very large cavities and a saccular pneumothorax, since both conditions must have in part precisely the same symptoms. We may mention as the chief points in distinction : A cavity is apt to be situated in the apex, pneumothorax in the lower part of the thorax ; over a cavity the chest-wall is often sunken in, over pneumothorax it is prominent ; the vocal fremitus is usu- ally marked over a cavity, weak over pneumothorax. Signs of the displacement of organs point to pneumothorax, as does distinct succussion, while a metallic respiratory sound and metallic resonance on rod percussion may also be heard over large cavities with smooth walls. Besides the above signs, we should also carefully regard the general course of the disease. On careful questioning we HYDKOTHOEAX. H^MATOTHOEAX 299 shall almost always find that the severe symptoms depending upon the develop- ment of a pneumothorax, set in with more or less suddenness. Treatment. — Whenever pneumothorax has developed we must seek to obtain perfect quiet for the patient, as well as diminution of his sufferings, by means of morphine given subcutaneously or internally. The results of the administration of this drug, in a sufficient though careful dosage, is often very satisfactory. We must also stimulate cardiac activity, if it is impaired, by means of stro- phanthus or camphor. It is exceptional to find operative interference necessary because of the danger to life in the first days of the attack; and even later on we should usually wait to see how much spontaneous improvement of the condition may take place. If the symptoms remain severe and the displacement of organs is great, we should try to remove by aspiration as much air as possible from the pleural cavity. Likewise if there is an abundant exudation it is always useful to puncture and remove the fluid, repeating the operation if necessary. If the exudation is purulent, the treatment is precisely the same as for empyema, ex- cept that in hopeless cases of far-advanced tuberculosis we may limit our efforts to purely symptomatic treatment, or to the simple evacuation of the pus by puncture. CHAPTEE IV HYDROTHORAX. H^MATOTHORAX 1. Hydrothorax. — We term the occurrence of a serous transudation into the pleural cavity, independent of an inflammation of the pleura, hydrothorax, or thoracic dropsy. The cause of hydrothorax is in rare cases a local hindrance to the outflow of venous blood or lymph from the thorax, as in compression of the veins or of the thoracic duct by tumors; but in the great majority of cases the hydrothorax is part of a general dropsy, occurring especially in cardiac or renal disease. Hydrothorax is often first developed after marked oedema of the sub- cutaneous cellular tissue and ascites, but it may sometimes be one of the first symptoms of dropsy, particularly in renal cases. It is usually bilateral, but it is often unilateral, or at least much greater on one side than on the other. The pleura itself is normal or else oedematous. We often find it traversed v/ith a net- work of dilated lymphatics. The serous fluid in hydrothorax is distinguished from an inflammatory serous effusion by the smaller amount of albumen in it, and a correspondingly low specific gravity (usually below 1018), by the scanty number of cell-elements, and by the absence of or the slight tendency to spon- taneous coagulation. The clinical importance of hydrothorax lies in the hindrance to respiration which it causes. As a result of this the hydrothorax may be regarded in many cases, especially in renal disease, as the chief cause of death. The objective evi- dence of it comes from the physical examination, which must, in general, give dullness, diminished vocal resonance, and dislocation of neighboring organs, the same as in pleuritic effusion. We desire to emphasize also the bronchial res- piration from compression in hydrothorax, which is often very loud, although at the same time usually high and sharp, and which may even given rise to a confusion with pneumonic infiltration in the lungs. This very loud respira- tory murmur, contrasting with that of pleuritic effusion, is explained by the nor- mal condition of the lungs and the absence of all adhesions. For the same rea- son, too, the change in the boundary of the dullness, as a result of the patient's change of position, is usually more marked in hydrothorax than in pleuritic 300 DISEASES OF THE EESPIEATOEY ORGANS effusion. We often hear a few fine crepitant rales over the hydrothorax, which arise in the retracted and partly atelectatic lung. The main factor, however, in distinguishing hydrothorax from a pleuritic exudation is, in every case, the con- sideration of the primary disease. It should also be noticed that hydrothorax is usually bilateral, while pleuritic exudation is usually unilateral. Treatment is directed, first of all, to the primary disease. If we succeed in strengthening and regulating the action of the heart, or in restoring the secre- tion of urine, the hydrothorax often disappears with the other dropsical symptoms. If the dyspnoea caused by it reaches a dangerous degree, we often see great relief from aspirating the fluid. The nature of the underlying condition, of course, renders the benefit in many cases only transitory. 2. Hsematotliorax. — Effusions of blood into the pleural cavity (hsemato- thorax.) arise most frequently from traumatic lacerations of blood-vessels, rarely from the bursting of an aneurism of the aorta into the pleural cavity, from ero- sion of an intercostal artery in caries of the ribs, from the rupture of a cavity into the pleura in phthisis, if it simultaneously opens a blood-vessel, etc. In many such cases a typical exudative pleurisy follows the effusion of blood. The physical signs are the same as in other pleural effusions. Severe dyspnoea may demand the removal of the blood by puncture, or even by an incision. CHAPTER V NEW GROWTHS OF THE PLEURA The majority of new growths occurring in the pleura are of a secondary na- ture. We sometimes find single metastatic nodules of cancer in the pleura after primary carcinoma of other organs, especially of the mammary gland and the lungs, but most carcinomata of the pleura arise from primary carcinomata of the lungs and are due to a direct invasion of the pleura by the new growth. Of the primary new growths in the pleura, only one is of great importance — ■ the endothelial carcinoma, first described by E. Wagner. This develops de novo, in a diffuse manner, from a proliferation of the endothelial cells of the lymphatics and the connective tissue. Metastases occur in the lungs, in the lymph-glands, in the liver, in the muscles, etc. Single secondary nodules of cancer in the pleura cause no special clinical symptoms, but the cases of diffuse cancer of the pleura as a result of primary can- cer of the lungs are important, inasmuch as the sjmiptoms of disease of the pleura often quite predominate over the pulmonary disease. The dullness is intense, the respiratory murmur and the vocal fremitus diminished. In one such case we saw a proliferation of the cancer upon the ribs in front so that there was externally a very marked circumscribed swelling. The character of the sputum is the only thing that can give ns definite information as to the origin of the new growth in the lungs (see the chapter on cancer of the lungs). Primary endothelial carcinoma of the pleura runs a course similar to chronic pleurisy. As we sometimes find a co-existing fluid effusion in the pleural cavity, displacement of the neighboring organs may occur. The affection goes on for a long time without fever, or with slight and irregular elevations of temperature. Most cancers of the pleura are associated with severe pain. The diagnosis of new growths in the pleura can usually be made, if at all, only in the more advanced stages of the disease. At first almost all the cases are regarded as simple or tubercular chronic pleurisy. The diagnosis is founded less MEDIASTINAL TUMOES 301 upon the physical signs than upon the general course of the disease, the habit of the patient, and the evidence of metastases in the glands and other organs. In some cases characteristic elements of the new growth can be found by the micro- scope in the cloudy fluid obtained by an exploratory puncture. The prognosis is absolutely unfavorable, the treatment purely symptomatic. In endothelial carcinoma we might perhaps try the long-continued use of arsenic. CHAPTER YI MEDIASTIlSrAL TUMORS Ix the anterior mediastinum, in quite rare cases, extensive new growths occur, which are of importance on account of their severe clinical symptoms. The point of origin for the tumor is either the mediastinal lymph-glands, or the connective tissue, or sometimes the remains of the thymus gland. In their anatomical character the tumors are almost always sarcomata, usually lympho- sarcoma, rarely alveolar sarcoma. They usually occur in youth or middle age, and are somewhat more frequent in men than in women. The special setiological factors are unknown. In some cases an injury is stated to be the cause of their development. The first clinical symptoms are usually of a very indefinite nature. The patient complains of general languor, headache, pain in the chest, and slight diffi- culty in breathing, and only gradually do severe subjective and objective symp- toms develop in the chest. The symptoms are in part due directly to the tumor, but in larger part they are symptoms of compression from the gradually increasing pressure of the tumor on a number of neighboring organs. The pain in the chest, which is located chiefly in the sternal region, and is associated with a marked feeling of oppression, may be very severe. It sometimes shoots into the lateral portions of the chest and into the arms, showing pressure on the brachial plexus. The dyspnoea may finally increase to an extreme degree. A patient with lympho-sarcoma under our observation could, in the last days of her life, breathe only while standing. The dyspncea is due to a compression of the heart and lungs, and sometimes to actual stenosis of the trachea or a primary bronchus. Paralysis of the dilators of the glottis may also occur from a pressure paralysis of the recurrent nerves. Paralysis of one vocal cord has been repeatedly observed. In the case mentioned above a marked goitre developed, as a result of vascular stasis, which further increased the dyspnoea by pressure on the trachea. A hydro- thorax from local venous stasis may also aid in increasing the dyspnoea. Pressure on the oesophagus, and disturbances of deglutition due to it, are rare. Pressure on the vagus nerve and the sympathetic sometimes causes anomalies in the rate of the pulse — either marked acceleration or slowing of the pulse. If the sympathetic is involved there is inequality of the pupils. In some cases, by pressing on the tumor, an artificial dilatation of the pupil can be excited at will. By pressure on the vessels, especially on the superior vena cava, the subcla- vian vein, etc., oedema and cyanosis may arise in the coiTCsponding parts of the body. Objective examination of the chest gives a marked diffuse prominence of the sternal region in a part of the advanced cases; in other cases this swelling is absent. The discovery of an abnormal dullness in the anterior part of the chest 502 DISEASES OF THE EESPIEATORY ORGANS is of diagnostic importance; this usually joins the cardiac dullness on the left, and on the right it extends a varying distance beyond the right border of the sternum. The heart is often pushed somewhat to the left. We heard over the pulmonary artery in our case a marked systolic murmur, caused by compression of the vessel. A dissimilarity of the pulse on the two sides is not infrequent. The diagnosis of a mediastinal tumor is usually possible in cases with well- marked symptoms, but in other cases it is difficult and uncertain. The differential diagnosis between mediastinal tumors and aneurism of the aorta (g. v.) causes especially great difficulty. Tumors may also be confounded with abscesses in the anterior mediastinum. The prognosis is in all cases absolutely unfavorable. The disease terminates fatally, sometimes after a duration of six months or a year. The treatment can be merely symptomatic. Internally we may try iodide of potassium or arsenic. In the last stages of the disease we must try to alleviate the patient's great distress by narcotics. CHAPTER YII ACTINOMYCOSIS OF THE THORACIC CAVITY Bollinger and others have described a peculiar tumor affecting the jaw-bones of cattle, and occasioned by the presence of a special form of fungus, known as the actinomyces or ray-fimgus. More recently a class of diseases has been studied in human beings, occasioned by the same fungus (Ponfick, Israel, and others). These diseases may, as in cattle, affect the jaws, the floor of the mouth, and the neck; but in these cases they are mainly of surgical interest. The actinomycotic diseases of the internal organs, however, possess a great clinical importance; and, inasmuch as the lungs and pleura are the most frequently affected organs, it will be well to present briefly here the most important facts which have as yet been learned with regard to actinomycosis. The botanical position of actinomyces has not yet been definitely settled. Cohn and O. Israel regard it as a mould fungus. Bostrom, on the other hand, classes it with the algse, and namely with the variety eladothrix. In its growth, the fungus forms small or moderate-sized gray or sul- phur-yellow nodules which may be dis- tinguished with the naked eye in the pus of the diseased tissue (see below), and which upon microscopic examination re- solve themselves into a tangle of mycelium. It is an especial characteristic that many of these mycelia bear on their ends a club-shaped swelling. These are placed for the most part like radii on the periphery of a nodule, and so surround the entire mass like a circlet of rays (see Fig. 38). In nature actinomyces seems Fig. 38.— Classes of actinomycosis. (From Johne.j ACTDTOMYCOSIS OF THE THOEACIC CAVITY 303 to appear especially upon plants, for example upon the beard of spikes of wheat. Thus is explained the frequency of infection in the plant-eating cattle, and a similar direct infection seems occasionally to be possible in man. It is worthy of note that the fungus seems to locate itself often in carious teeth. Thus appar- ently arises the above-mentioned disease in the buccal cavity; while on the other hand, the fungus may be carried from its nidus in the mouth by inspiration into the respiratory tract, or by swallowing into the primce vice. Of course it may also be directly swallowed or inhaled. Wherever the fungus fastens itself in the body it occasions first a new growth of granulation-tissue, which hp^ a tendency to break down into a whitish or brownish pasty mass. The brown color is occasioned by the haemorrhage which frequently occurs. Very often actinomycosis goes on to suppuration; still, this probably depends upon the influence of pathogenic germs which have secondarily infected the part. Of especial importance is the tendency of the disease to extend from the lungs to the pleura and from the pleura to the peripleuritic connective tissue, and still further to the wall of the thorax. Thus arise not only extensive abscesses and wide-branching fistulous tracts, but also a very characteristic, extremely tough cicatricial infiltration of the affected part. Not infrequently there is at last a perforation reaching the outer surface of the body. The entire process, as a rule, is slow and insidious, but constantly progressive. The symptoms consist at first in slight thoracic discomfort, pain, cough, and ex- pectoration. Physical examination will often detect changes in the lungs, but the correct interpretation of the signs found is of course at first difficult, if not impos- sible. The more the disease spreads the greater is the distress. Usually there is hectic fever, which may assume a pysemic character if there is extensive suppura- tion. The patient gradually loses flesh, and in repeated instances amyloid degen- eration of the liver, spleen, and kidneys has been observed. If a focus breaks into a pulmonary vein, the disease may be developed by metastasis in other internal viscera. Moreover, there may be a direct extension of the disease to the pericar- dium, or through the diaphragm into the peritoneal cavity. The diagnosis of actinomycosis is at first difficult. It is established when the characteristic fungus is found in the sputum, but this has occurred in only a few cases as yet. If very extensive peripleuritic and pericostal suppuration has taken place, and the process has spontaneously broken outward or been laid open by surgical means, the demonstration above described in reference to the fungus is easy. The treatment can be only symptomatic, unless the diseased spot can be reached by operation, and then the treatment becomes surgical. Permanent cure has so far been attained in but rare instances. [Iodide of potassium has proved curative in a considerable number of cases, and it should certainly be tried, in doses of forty to sixty grains a day. — V.] DISEASES OF THE CIRCULATORY ORGANS SECTION" I Diseases of the Heart CHAPTER I ACUTE ENDOCARDITIS {Endocarditis verrucosa. Endocarditis ulcerosa) etiology. — Organized excitants of inflammation of different sorts, whicli cir- culate in the blood, may settle on the endocardium, especially on the valves of the heart, and there give rise to an acute endocarditis. Endocarditis, therefore, in its fetiological relations, is not to be regarded as a single disease. Pathogenic micro-organisms have been injected into the blood (the streptococcus pyogenes, staphylococcus aureus, and others), and in this way an artificial endocarditis has been set up in animals. The experiments are more apt to succeed if the valves or the inner coat of the vessels have been subjected to some slight injury before the injection, thus promoting the settling of the germs upon them (Orth and Wyssokowitsch, Ribbert). Most cases of endocarditis in man, both the vegeta- tive and ulcerative forms, appear to be caused by the staphylococcus pyogenes aureus. Streptococci are much less frequent than staphylococci, and it is only in rare cases that endocarditis is occasioned by the pneumococcus, gonococcus, and perhaps the diphtheria bacillus. In accord with these statements is the fact that in human beings acute articu- lar rheumatism, which is probably to be regarded as a staphylococcus infection, is that one of the infectious diseases which is especially apt to have acute endocar- ditis as a frequent and important complication. The staphylococcus infection need not appear, however, in the first place, as a typical acute polyarthritis. An acute endocarditis may appear as a sequel of many cases of apparently pri- mary pleurisy, tonsillitis, or other disease. Indeed, it is sometimes impossible to determine the gate of entry of the infection, and the whole disease takes the shape of an apparently primary endocarditis. In such cases the nature of the disease is made evident by the later appearance of multiple articular swellings. We also regard as allied to polyarthritis certain forms of infection called the "acute hsemorrhagic diseases" (e.g., purpura rheumatica), and also chorea (which see). It is therefore not surprising that acute endocarditis is not infre- quently observed in association with these affections. There are other acute infectious diseases with which acute endocarditis may be associated. Probably in these it is usually the result of a secondary mixed infection, generally with the staphylococcus. This explains the appearance of acute endocarditis in scarlet fever, small-pox, diphtheria, measles, and typhoid. Not infrequently mild cases of acute endocarditis, without clinical significance, are found in association with primary tuberculosis and ulcerating carcinoma. Again, acute and chronic nephritis may sometimes occasion a development of 304 ACUTE ENDOCAEDITIS 305 endocarditis. An especially important role in producing endocarditis is dis- played by grave septic and pyaemic conditions (vide supra). In these cases the acute endocarditis appears as one symptom, but it is often so prominent that the whole attack is called endocarditis (;vide infra). In such severe diseases we have often to do with a streptococcus disease, although it may be a staphylococcus in- fection of especial virulence. The ajtiology of gonorrhoeal endocarditis is not yet fully determined. Endocarditis as a sequel of gonorrhoea is fortunately very rare. It often seems to be an actual gonococcus infection, but in other instances is occasioned by some secondary germ. Finally, we have still to mention the important fact that acute endocarditis quite frequently develops on the soil of an already existing chronic endocarditis — the so-called acute recurrent endocarditis. In women, pregnancy and the puer- peral state sometimes seem to give the occasion for a recrudescence of the endo- carditis. Pathological Anatomy. — We usually distinguish an endocarditis verrucosa, with the formation of large or small papillary nodules on the endocardium, and an endocarditis ulcerosa (endocarditis diphtheritica) , with ulcerations as a result of the destruction and wasting away of the superficially necrosed tissue. The malignant, invariably fatal form of severe septic endocarditis is chiefly ulcerative endocarditis. Endocarditis verrucosa is the milder form, which is seen especially in acute polyarthritis and allied diseases, but we can not draw either a sharp ana- tomical or a sharp clinical distinction between the two, since malignant cases of endocarditis verrucosa are also observed. The endocardial growths are usually situated on the valves, especially on their edges of closure. More rarely we find them on the chordas tendinese and on the endocardium of the ventricle and auricle. In the mildest cases they are scarcely as large as the head of a pin, but in severe cases they may increase to quite large warty and glandular masses. Microscopically, the base of the nodule consists of a newly formed vascular tissue, infiltrated with small cells, which on its surface changes to a granular, coagulated mass. This last is formed partly of coagulated albumen, dead cells, and fibrine deposited from the blood, and partly of micrococci (vide supra). The micrococci are found without exception in all cases of ulcera- tive endocarditis — having been first discovered by Eberth. The endocardial ulcers arise from the destruction of the superficially necrosed nodules. If the thin valve in any place yields to the blood-pressure, we have the so-called acute val- vular aneurism. Complete perforation of a valve, and tearing off of fragments of a valve and of the chordae tendinese, are also seen. The great majority of cases of acute endocarditis are confined to the valves of the left side of the heart — the mitral and aortic valves. Endocarditis on the tri- cuspid valve is seldom seen except as a secondary affection in old cases of heart disease. In a case of acute ulcerative endocarditis in a grown man seen by us, the process was confined exclusively to the tricuspid valve, and there were very many embolic abscesses in the lungs. This may be considered a great rarity. In con- trast to the ordinary localization of endocarditis we find foetal endocarditis most frequently in the right side of the heart. Many other organs may be affected by the endocarditis, through embolism. In the benign endocarditis verrucosa, the masses of fibrine deposited on the irregu- larities of the valve furnish the embolic material. They cavise large or small in- farctions in the kidneys and spleen, embolic softening of the brain, etc. In the malignant, ulcerative forms, however, large numbers of bacteria get into the cir- culation at the same time with the necrotic masses of tissue which have been torn off. Here, then, we have to do not merely with simple mechanical obstruction but with infectious emboli. The emboli in ulcerative endocarditis, therefore, either give rise to embolic abscesses in the cardiac muscles, the kidneys, the spleen, the 20 306 DISEASES OF THE CIRCULATOKY ORGAIsTS lungs, the retina, etc., or they result in haemorrhages, especially into the skin, but also into the kidneys, the brain, the retina, and the serous membranes. It is not yet known why in some cases abscesses are more frequent and in others haemor- rhages. The two, however, may be combined. In general, we may suppose that the development of abscesses is everywhere connected with the presence of bac- teria, while haemorrhages may also arise from toxic influences ; but again changes in the vascular walls caused by bacteria might give rise to haemorrhages. Em- bolic abscesses belong almost exclusively to the severe form of septic endocarditis. Haemorrhages are seen in this form, and also — without co-existing abscesses — in certain severe forms of endocarditis occurring in the course of acute rheumatism and allied diseases. Clinical History. — Since acute endocarditis is not aatiologically a distinct dis- ease, and since its clinical course is very different in different cases, it seems ad- visable to us to describe, in what follows, the most important varieties separately ; but it must be expressly noted that the separate classes can by no means be sharply defined, and that there are many intermediate forms. 1. Slight endocarditis verrucosa is quite frequently found in the cadaver, without the slightest signs of any affection of the heart during life. The little papillary excrescences on the valves of the heart in phthisis, and carcinoma, whose aetiology has been explained above, are to be classed under this head. 2. The typical form of henign acute endocarditis is most frequent, clinically, in the course of acute articular rheumatism. It is much rarer in other infectious diseases (vide supra). In a few cases it is also seen as an apparently primary disease. Here there is a constitutional rheumatic infection which has taken place in some way, and which settles directly on the valves of the heart instead of in the joints (so-called primary rheumatic endocarditis). Careful questioning will sometimes reveal, or at least render probable, the place of infection (a mild case of tonsillitis or some slight external injury). Very often there will be later the symptoms of articular rheumatism. It is seldom that endocarditis as such is associated with special local disturbances, such as pain in the region of the heart, palpitation, and dyspnoea. Ordinarily the heart disease is discovered only by physical examination. The impulse of the heart in many cases is abnormally strong and diffuse; the pulse is accelerated, but strong, often somewhat jerky (pidsus celer), and usually regular, but sometimes a little irregular. Percussion at first shows no deviations from the limits of normal dullness. On auscultation, we hear at the apex, more rarely at the base, a loud blowing, systolic souffle. Diastolic murmurs are rare in acute endocarditis. The pulmonic second sound is often accentuated. The physical signs referable to the heart are only slightly marked in many cases of acute endocarditis. This is understood if we remember that the occurrence of a heart-murmur depends wholly on the localization of the endocarditis, on the development of some valvular insufficiency, etc. Besides the direct symptoms pointing to the cardiac affection, the onset of an acute endocarditis is often, but not always, associated with fever, or, if fever be already present, with an increase of it, and with a slight aggravation of the gen- eral disturbance. Embolic processes may occur in the brain, the spleen, the kid- neys, and the extremities, but they are comparatively rare. Sometimes a peri- carditis develops as a result of the endocarditis (vide infra). It is hard to make any accurate statements as to the duration of this form of endocarditis. The physical signs may last for days, or for several weeks. Com- plete recovery is possible, but in the majority of cases this variety passes into chronic valvular disease of the heart. 3. Malignant, non-septic form of acute endocarditis (" rheumatoid endocar- ditis" of Litten). In many cases this form is perhaps only a quantitative in- crease of the preceding form, but in other cases it is probably distinct from it ACUTE ENDOCAEDITIS 307 setiologically. The severe general infection is usually quite prominent here, and the disease resembles in many particulars grave septic endocarditis. The ob- jective signs in the heart are the same as in the preceding form, but more intense and extensive. The subjective cardiac symptoms, such as palpitation and distress, may be quite pronounced, but they may also be almost wholly absent in this form. The general condition, however, is usually bad. There is sometimes high fever with an irregular or intermitting course, but in many cases the fever is remark- ably low in spite of quite severe constitutional symptoms. The constitutional infection is very often manifested in these cases by the appearance of small or large haemorrhages in the skin, sometimes in the mucous membranes, as in the conjunctiva and the soft palate, and rarely in the retina. Secondary articular swellings often develop; they are always of a serous charac- ter, and never purulent. Renal haemorrhages and acute haemorrhagic nephritis are quite frequent. Large emboli may also occur in the different organs in this as in every other form of endocarditis. The duration of the disease extends over many weeks. In severe cases death ensues with a gradual aggravation of the general condition, and often with severe cerebral symptoms, such as stupor and delirium. In milder cases, however, the patient may finally get well. Regarding the occurrence of this form, we see it most frequently in acute articular rehumatism; also, in rare cases, in gonorrhoea, when it comes on some three or four weeks after the beginning of the urethral affection; also in ne- phritis, chorea, peliosis rheumatica, etc. The apparently primary cases of this sort usually belong to the recurrent form of acute endocarditis. 4. The recurrent form of acute endocarditis consists of an acute increase of the endocardial process, brought on by some exciting cause, in a patient already suffering from chronic endocarditis. The acute disease may show all the grada- tions from the mildest to the severest. The mild cases often run their course without any special symptoms. To this form we may frequently refer the more or less temporary elevations of temperature which we often see in patients with chronic valvular disease of the heart. In rarer cases the recurrent endo- carditis comes on quite suddenly in the form of a severe acute attack. This sometimes seems to be clinically a primary, independent disease, especially if the previous chronic heart disease has up to that time caused no special symptoms. The patient has general malaise, headache, chills, and fever. The last may be quite high — 104° (40° C.) and over — or moderate, varying between 100° and 102° (38°-39° C), or it may be entirely absent. In many cases it is intermittent, when the return of fever is often associated with a chill. The cardiac symp- toms may be quite pronounced, but in this form, too, they may be obscure and indefinite. In the further course of the disease we meet with cutaneous htBmor- rhages, retinal haemorrhages, articular swellings, large renal haemorrhages, or typical haemorrhagic nephritis — in short, just the same general type of disease as in the other malignant forms of acute endocarditis. The course is rarely rapid, and often lasts for weeks. Severe cases almost always end fatally. 5. The severe septic ulcerative endocarditis has already been described as a complication of a general septic state. We therefore refer to the appropriate chapter (see page 116) for all particulars. Septic endocarditis is probably en- tirely distinct aetiologically from the forms thus far described, and is manifested by quite a rapid fatal course, with severe typhoidal or pyaemic symptoms. It is characterized anatomically, apart from the cardiac affection, by the appearance of metastatic abscesses in the various organs, but in many cases, as we have said, abscesses and haemorrhages are combined. Diagnosis. — The diagnosis of an endocarditis, coming on secondarily in the course of articular rheumatism and other diseases, can be made only by a physical 308 DISEASES OE THE CIECULATORY ORGAITS examination of tlie heart. We must therefore give constant attention to the con- dition of the heart in diseases which we know may give rise to endocarditis. The diagnosis of the malignant form of endocarditis often causes great diffi- culty, especially if the patient is not seen until the later stages. It is confused with typhoid, meningitis, or acute miliary tuberculosis. Examination of the heart may furnish positive evidence, but sometimes, as we have said, there are no physical signs of cardiac disturbance, or the signs present are indefinite. Of other factors in diagnosis a special importance attaches to the secondary swelling of the joints, and also to the haemorrhages into the skin and retina, for these are much more infrequent in the diseases with which this form of endocarditis may be confounded. The acute hsemorrhagic nephritis, too, in connection with the other symptoms, is, at least to a certain degree, characteristic of malignant endocarditis. The course of the fever is of diagnostic value only when it is decidedly intermittent. A careful search for some setiological factor is very important for diagnosis in all cases. Eor other points the reader is referred to the consideration of septic diseases (page 116). Prognosis. — In the description of the course of the disease we have already mentioned the prognosis of the different forms. The severe cases of acute endo- carditis usually, and the cases of severe septic endocarditis always end fatally. Here, however, the cause of death is to be sought rather in the accompanying systemic infection than in the endocarditis itself. In mild cases recoverj^ is pos- sible, but the process of repair is often so incomplete that chronic valvular disease of the heart develops from the acute endocarditis. Treatment. — The chief requisite in the treatment of every endocarditis is as complete rest as possible for the patient. If ice is well borne, the continuous application of an ice-bag to the cardiac region is of service. If there are signs of cardiac weakness, such as a small, rapid, and irregular pulse, we must employ cardiac stimulants, strophanthus, camphor, and, above all, digitalis. It must be eonfessed that the effect of these is not very great. If there are marked sub- jective symptoms (such as dyspncea) narcotics, particularly morphine, are indis- pen-sable. Effort is made to combat the systemic infection by salicylic acid, salicylate of sodium, and similar remedies, including phenacetine and salipyrine. Quinine is usually entirely without effect, even when the fever is of an inter- mittent character. Arsenic, however, seems to be useful, particularly in the more protracted cases. [Eor remarks upon the alkaline treatment of rheumatism, see page 686.] CHAPTEE II VALVULAR DISEASE OF THE HEART (Clironie Endocarditis) .31tiology. — A large number of cases of chronic valvular disease of the heart proceed from acute endocarditis. Hence the frequent statement in the history of chronic valvular disease that the patient has had articular rheumatism, once or many times. In a collection of 163 cases of undoubted valvular heart disease, we were able to ascribe 86 to a previous attack of acute articular rheumatism. Fol- lowing the acute valvular endocarditis, which is often associated with this dis- ease, marked thickening of the valves occurs, due to the growth of connective tis- sue. There are also changes in the way of contraction, adhesion, and finally often of considerable calcification. The unavoidable result of all these processes is that VALVULAE DISEASE OF THE HEAET 309 the altered valves are rendered incapable of fulfilling their physiological function of regulating the circulation. Inasmuch as the mitral valve is most often attacked by endocarditis when associated with acute articular rheumatism, we find mitral disease predominating among rheumatic valvular troubles ; but lesions of the aortic valves, rheumatic in their origin, are by no means rare. If we find a valvular lesion in a patient who has never sufi'ered from articular rheumatism we may, in some cases, be able to refer the origin of the valvular trouble to a previous attack of acute endocarditis, excited by one of the other causes above mentioned. Thus it is well known that acute endocarditis may occur in the course of scarlet fever, diphtheria, and typhoid fever, and eventuate in chronic disease, but this is, according to our experience, very rare. In quite a large number of cases of heart disease, however, we can not obtain a history of acute endocarditis. We have to do here with an endocarditis which is chronic from the start, which also leads gradually to thickening, contraction, adhesion, and calcification of the valves. The causes of this chronic fibrous endocarditis are probably the same as of acute articular rheumatism, but in such cases they act from the start in a chronic manner. Perhaps often there may have been an incipient acute endo- carditis, whose course was unperceived. We not infrequently learn from patients with chronic heart disease, who have never had an attack of acute articular rheu- matism, that in former years they did suffer repeatedly from mild rheumatic pains, to which they paid little attention. Furthermore, it is by no means excep- tional to observe that such patients with a well-developed cardiac valvular lesion later on undergo one or more attacks of acute polyarthritis. Heart disease is also rarely associated with genuine chronic arthritis deformans. In other cases of valvular disease we must consider the possibility of other lesions, some infec- tious, some perhaps of a chemical and mechanical nature. Here belong, in the first place, those cases of cardiac disease which are associated with general arterio- sclerosis (atheroma of the blood-vessels). Indeed, atheromatous degeneration of the aorta seems sometimes to extend directly to the aortic valves, and thus cause a valvular lesion. Every setiological factor favorable to general arterio-sclerosis is, therefore, important in the aetiology of valvular disease. This includes ad- vanced life, excessive physical labor, alcoholism, and genuine gout. Another important cause is syphilis. Of late years, since we have paid more attention to this last factor than formerly, we have observed many cases of valvular disease which were almost certainly of syphilitic origin. In particular, lesions of the aortic valves, when there is no evidence of other causation, must awaken our suspicion of syphilis. There remains to be mentioned the influence of chronic nephritis upon the development of cardiac valvular disease, although in the not infrequent cases in which chronic nephritis, particularly of the interstitial vari- ety, is associated with chronic endocarditis, it is not always easy to determine whether both conditions are related in the way of cause and effect, or whether they are both secondary, and both alike the result of some third unfavorable influence. A hereditary predisposition to heart disease is not very frequent, but yet it can be made out with certainty in many cases. We have ourselves seen five members of the same family who have suffered from chronic heart disease, some from pure valvular disease and some from severe so-called idiopathic hyper- trophy. Perhaps the very frequent occurrence of heart disease in many families is also connected with a special family predisposition to rheumatic affections, the occurrence of which predisposition can not, in our opinion, be denied. Finally, a small number of cases of heart disease, especially in the right side of the heart, depend upon anomalies of development of the heart — congenital heart disease. Valvular disease of the heart occurs at every age of life. The time of origin of most cases, corresponding in part to the occurrence of acute articular rheuma- 310 DISEASES OF THE CIRCULATORY ORGAITS tism, falls in youth and middle age, somewhere between eighteen and forty; but severe valvular disease is not infrequent even in children; while late in life the clinical picture of valvular disease is often confused by the simultaneous presence of general arterio-sclerosis, pulmonary emphysema, or kidney trouble. Heart disease is said to be rather more frequent in the female sex than in the male. Women with heart disease not infrequently date their symptoms from pregnancy and the puerperium. General Pathology of Valvular Disease of the Heart. — Every valve of the heart, in order to fulfill its physiological task, must, on the one hand, open per- fectly at the right time in order to furnish a free passage to the blood-current through the appropriate orifice, and must, on the other hand, close firmly and perfectly at the right time in order to make any abnormal backward flow of blood impossible. In both relations the function of the valves may be disturbed by chronic endocarditis, the disturbance being the result of their anatomical changes. If the tips of the valves are shortened on their free edges by contrac- tion, or if the complete unfolding of the auriculo-ventricular valves is hindered by a shortening of their chordse tendinese, the closure of the valve can not be complete. At the moment when the closure of the valve is necessary a fissure remains open between its apices. We call this condition an insufficiency of the valve. On the other hand, the valves may lose their capability of free and suffi- cient separation from one another, as a result of thickening and calcification of the connective tissue, and also as a result of adhesions of the points of the valves with one another. At the moment when the blood-current should pass freely through the open orifice, the valve remains a stiff, narrow ring, through which the blood must force its way — stenosis of the orifice. The changes in the valves are often of such a sort that they cause at the same time both an insufficiency of the valve and a stenosis of the orifice. The thickening and calcification of the valves in stenosis cause, as a rule, a valvular insufficiency at the same time; but an insufficiency, set up by a contraction of the edges of the valves, may occur without a coincident stenosis of the orifice. The abnormal and injurious effect of a valvular lesion upon the circulation in the heart is felt in two directions. Either the obstacles to the circulation are increased in certain places, or there is a greater diastolic distention of certain portions of the heart. Both circumstances of course demand greater cardiac effort. If the heart were to labor with only the same degree of energy as under normal conditions, in spite of the increased resistance, or in spite of the greater distention, there would speedily be an impairment of circulation, incompatible with the continuance of life ; for, if the increased resistance were not overcome, or if the abnormally distended cavity were not properly emptied, there would at once be a rapidly increasing congestion behind the diseased valve, and beyond it a constantly diminishing pressure. We can speak of a circulation of the blood only when, in a given interval of time, exactly as much blood is driven out of the heart as flows into it. The slightest difference in this regard would, in a very brief period, produce such a congestion of blood in the veins and such a diminu- tion of blood in the arteries that the demand of the tissues for oxygen could no longer be satisfied, and death would be the necessary result. A normal circulation is maintained so long as the amount of arterial blood, which flows into the organs in a given interval of time, is sufficiently great and also capable of immediate increase, proportional to any temporary increase in the demands of the organs, as, for example, when there is bodily exertion. The amount of blood flowing through the organs in a given time depends upon the degree of distention, the frequency of contraction, and the complete emptying of the left side of the heart. This amount (" the size of the circulation ") may be diminished, and yet the circulation continue as such; but that the circulation can, in spite of the dis- VALVULAR DISEASE OF THE HEART 311 turbance occasioned by a valvular lesion, still be maintained in a satisfactory manner is due to the capability of the heart of overcoming the obstacles to the circulation by means of increased work. It is one of the wisest contrivances in our organism, that the heart has control of a reserve fund of strength, which comes into action, if need be, in a way to compensate as far as possible for any disturbance of the circulation. This explains why a man with valvular disease of the heart may be almost perfectly well for a long time, while the increased work of certain portions of his heart suffices to keep up an approximately normal circulation in spite of the existing valvular disease. We call a heart disease, in which there is at least no marked disturbance of circulation, a compensated heart disease. The abnormal increase in functional activity of certain portions of the heart, associated with every cardiac lesion, and referable in every case, as we have said, either to increased resistance or to increased distention, results in a hypertrophy of those particular portions of the heart, just as in the case of any other muscle. This hypertrophy does not consist of an increase in thickness of the individual muscular fibers, but chiefly of an increase in number. The total bulk of the cardiac muscle increases, and thus its capacity for work naturally becomes greater. It goes without saying that increased nutritive processes and a large supply of nourishment for the heart are necessary to bring about such a hypertrophy, by which alone a compensation of the heart disease is possible for any length of time. Hence we find the secondary hypertrophy of the heart absent, or at least only imperfectly developed, in feeble individuals, especially in those who have suffered from some other chronic wasting disease besides the heart disease, such as phthi- sis or carcinoma. Although the compensatory processes in the heart may prevent for a long time any marked disturbance of the circulation, the already overburdened heart can no longer completely satisfy any excessive demands upon it, even in a compensated heart disease. Hence patients with a compensated heart disease are free from sub- jective disturbance only when they remain at rest, while the signs of a disturbed circulation usually become quite apparent on slight physical exertion. The hypertrophied cardiac muscle can seldom supply permanently the ab- normally great drafts made upon it. There finally comes a condition of " fa- tigue," of " cardiac insufficiency." The cause lies either in the increase of the valvular disease, so that the hindrance to the blood-current caused by it can no longer be completely overcome, or in the fact that the nervous and muscular ele- ments in the heart have their powers gradually impaired by a disturbance of circulation in the heart itself. In short, in every heart disease the moment may finally come when the capacity of the heart has reached its limit,'%nd hence the compensation of the heart disease ceases. The results of stasis now appear with increasing severity in the different organs, as we shall learn to recognize later on, and the patient finally succumbs to them, unless some intercurrent event puts an end to life. After these general remarks, which will be understood better on reading what follows, we will pass on to the special description of the different forms of heart disease and their physical signs. 1. Insufficiency of the Mitral Valve Mitral insufficiency is one of the most frequent forms of heart disease. It develops in acute or chronic endocarditis of the mitral valve, from contraction of the free edges of the valve or from shortening of the chordte tendineas. In rare cases it comes on from partial adhesion of the valves to the walls of the ventricle. The closure of the mitral valve occurs normally at each systole of the left ven- 312 DISEASES OF THE CIKCULATOEY ORGANS tricle. It prevents the return of blood from the left ventricle to the left auricle. If the mitral valve is insufficient and its closure is incomplete, at every systole of the left ventricle a part of the blood is thrown back from it into the left auricle through the open space of the ostium venosum. This abnormal backward wave encounters the blood-current coming in an opposite direction into the left auri- cle from the pulmonary veins. The meeting of these two opposing currents, as well as the stream of regurgitant blood pressing through the open chink in the mitral valves, sets the blood in a whirl, and this impinging upon the tense edges of the valves produces a loud, blowing, systolic murmur. We hear this murmur loudest at the apex of the heart, corresponding to the laws of conduction in the thorax ; yet it usually is propagated so far that it may often be heard at the other cardiac orifices, although not so distinctly. A loud systolic mitral murmur cau also be heard sometimes in the back, on the left, and occasionally on the right. Tn some few cases the systolic murmur of mitral insufficiency is heard best in the second left intercostal space. This is probably because the murmur occasioned by the commotion in the left ventricle is conducted by the left auricular appendix to the anterior chest- wall (Naunyn). Curschmann has pointed out that this is par- ticularly apt to happen in cases of incipient mitral insufficiency; but, as a rule, even in these cases, the murmur is found at the apex of the heart. In most instances the systolic muscle-sound of the left ventricle, the so-called first sound of the heart, can also be heard besides the systolic murmur. It can be heard rather better if the ear is slightly removed from the ear-piece of the stethoscope [meaning the mon-aural instrument]. Exceptionally the sound may be com- pletely obscured by the murmur. The second sound is often not to be heard at the apex, probably because it is obscured by the relatively protracted murmur. Since the left auricle, at each systole of the ventricle, receives blood from two sides — its normal quantity from the pulmonary veins, and, besides that, the abnor- mal blood-wave from the left ventricle — it becomes much dilated. At the next diastole of the left ventricle the whole amount of blood collected in the auricle under increased pressure pours into the left ventricle through the mitral valve, which is now wide open (supposing a pure insufficiency of the valve without any stenosis). We see, then, that in pure mitral insufficiency the left ventricle must be filled beyond the normal amount during the diastole. The left ventricle must also expel in the following systole an abnormally large amount of blood. Al- though by this contraction only a part of the blood reaches the aorta in the direction of the normal blood-current while a part pours back into the auricle, the work of the left ventricle is of course excessive. Thus, in pure mitral insuffi- ciency, the left ventricle is dilated as a result of its increased filling in diastole, and is hypertrophied as a result of its increased labor. The general arterial tension remains approximately normal. It is not increased, since a part of the abnormal amount of blood, which pours out of the left ventricle at every systole, flows backward into the auricle. So long as the left ventricle is completely emp- tied by vigorous contractions, the aorta receives about the normal amount of blood, and the radial pulse remains, therefore, in cases of pure mitral insuffi- ciency, of about the normal strength and tension. The anomalies in the movements of the blood in mitral insufficiency produce still other effects. We have already seen that the left auricle is dilated from its overfilling. It also becomes hypertrophied, so far as its weak muscular structure permits, but it is not in itself capable of compensating for the disturbance which the pulmonary circulation suffers from the mitral insufficiency, for the back cur- rent from the left ventricle, and the consequent high pressure in the left auricle, must plainly offer an abnormal hindrance to the flow of blood from the pulmo- nary veins. This stasis sets back through the pulmonary capillaries and arteries into the right ventricle. This may be recognized, on physical examination, by VALVULAE DISEASE OF THE HEART 313 the change in the pulmonic second sound, which is louder, more valvular, and " accentuated," since the closure of the semilunar valves in the pulmonary artery now takes place under the abnormally high pressure which prevails in the arteries of the lungs. The right ventricle has the task of overcoming this abnormal stasis in the pulmonary circulation. It can overcome the abnormal resistance in the pulmonary circulation by increased work, and as a result it becomes hyper- trophied. So long as the hypertrophy of the right ventricle suffices to maintain the normal pulmonary circulation, the stasis extends no farther backward, but in the later stages of heart disease we see the right ventricle becoming paralyzed, and more and more dilated as a result of stasis. The flow of venous blood from the body into the right auricle and ventricle is now rendered more difficult. The signs of venous stasis become manifest; the patient has a cyanotic hue, con- gestive oedema appears in the face and the extremities, symptoms of passive congestion of the liver, spleen, and kidneys appear, and, in short, there is devel- oped the picture of an uncompensated heart disease. If we now sum up the physical signs of mitral insufficiency, the different methods of investigation give the following results: Inspection. — The cardiac region often seems rather prominent, as a result of the hypertrophy of the heart. This protrusion is most marked in young persons with a yielding thorax. The apex-beat is, as a result of the dilatation and hyper- trophy of the left ventricle, displaced toward the left and sometimes downward into the sixth intercostal space. It is more extensive and stronger than normal ("heaving"). The apex-beat is somewhat displaced toward the left as a result of the hypertrophy and dilatation of the left ventricle, and it is quite marked. Besides that, we often see a diffuse pulsation in the whole cardiac region. In the epigastrium we sometimes see an epigastric pulsation proceeding from the hypertrophied right ventricle. In cases which are no longer perfectly compen- sated the stasis in the veins of the body is rendered apparent by the general cyanotic appearance of the patient and the marked filling of the jugular veins in the neck, Undulatory or pulsating movements often occur in the latter (see tri- cuspid insufficiency, below). Palpation. — By palpation likewise we perceive the abnormal vigor and extent of the apex-beat, and the displacement of the same toward the left; and often, also, an extensive diffuse pulsation over the cardiac region, and in particvilar a distinct epigastric pulsation, due to the right ventricle. We often feel a systolic thrill at the apex of the heart — a " cat's purr " — by laying the hand flat on the chest. The same whirl of blood, which is audible as a murmur, may be per- ceived as a fine tremor of the chest-wall. The radial pulse is quite strong and usually regular. The sphygmographic tracing of it shows nothing characteristic in mitral insufficiency. Percussion. — This usually gives at first only a moderate increase of the heart's dullness to the left, and a little upward dilatation of the left auricle and left ventricle, but in the later stages there is at the same time an increase of the heart's dullness to the right, caused by hypertrophy and dilatation of the right ventricle. The whole area of cardiac dullness may finally extend two fingers' breadth beyond the right edge of the sternum, and to the left it may reach the mammillary line, or even pass far beyond it. Auscultation. — At the apex of the heart we hear a loud, quite long, pure sys- tolic blowing murmur, limited to the systole, either replacing the first sound or accompanying it. The second sound is often obscure or inaudible at the apex, but the pulmonic second sound is increased and accentuated. Auscultation of the vessels gives nothing characteristic. 314 DISEASES OF THE CIRCULATOEY ORGANS 2. Stenosis of the Mitral Orifice (Mitral Stenosis) Mitral stenosis often develops in chronic endocarditis of the mitral valve, as a sequel to a previous insufficiency. The valve constantly grows stiffer and more rigid, and the signs of stenosis gradually predominate over those of insufficiency. Hence we very often find stenosis and insufficiency of the mitral valve combined, but often the signs of stenosis are so much more prominent that we can properly speak of a pure mitral stenosis. Fig. 39. — Pulse curve in marked mitral stenosis. The disturbance which the circulation suffers in mitral stenosis is much greater than in mitral insufficiency. In mitral stenosis the orifice may finally become so narrow that it scarcely admits an ordinary lead-pencil. The influx of blood into the left ventricle is accordingly much impeded. During the diastole of the left ventricle the blood must force its way through the stiff and narrow ring of the mitral valve. In this way, again, are caused irregular whirling move- ments in the blood, and abnormal vibrations of the mitral valve, giving rise in most cases to an audible diastolic murmur. In mitral stenosis the left ventricle receives less than its normal amount of blood, and therefore it has no direct occa- sion for hypertrophy, and in fact it is sometimes found at the autopsy to be com- paratively small and to be crowded backward by the enormously dilated and hypertrophied right heart. ISTevertheless, we do often find hypertrophy of the left ventricle in cases of mitral stenosis, and for this reason, that mitral stenosis usually develops gradually from a previous insufficiency of the valves. That is, the chronic endocarditis occasions, probably in every case, first, an insufficiency of the valve, which is later followed by stenosis as the change progresses. We have already seen that insufficiency of the mitral valve always leads to hypertrophy of the left ventricle, and so we find it to persist even at a time when stenosis has become the prominent lesion. In other cases of stenosis, hypertrophy of the left ventricle is due to certain associated conditions, such as arterio-sclerosis or chronic nephritis. And finally we should also consider Friedreich's theory, that severe venous congestion may extend into the capillaries, and thence finally occasion abnormal resistance to the arterial circulation. The radial pulse in mitral stenosis is approximately normal, as long as the ventricle is sufficiently filled with blood during diastole. In spite of the stenosis of the mitral valve, the left ventricle may be satisfactorily filled, and this is more likely if the action of the heart is slow, allowing a longer diastole; and if, also, the left auricle is still capable of vigorous contraction. If, however, the action of the heart is hurried, and the left ventricle is no longer sufficiently dis- tended with blood during the diastole, the radial pulse becomes small and of low tension. Marked arhythmia is very often present in mitral stenosis, probably because of the insufficient amount of arterial blood supplied to the myocardium and its ganglia. The hindrance to the flow into the left ventricle in mitral stenosis soon lends to a marked stasis, which extends to the right side of the heart through the left auricle, and the pulmonary veins, capillaries, and arteries. The left auricle is dilated first (often to an enormous extent), and its walls are hypertrophied, but it can overcome only a very small part of the resistance at the mitral orifice. The right ventricle can, by more work, so increase the pressure in the pulmonary ves- VALVULAE DISEASE OF THE HEART 315 sels that, in spite of the narrowed orifice, an approximately sufficient quantity of blood may pour into the left ventricle. Hence we find in mitral stenosis a very marked hypertrophy and dilatation of the right ventricle. The stasis in the pulmonary circulation, manifested objectively by the accentuation of the pulmonic second sound, has as a result a gradually developing ectasis of the pulmonary capillaries. Thickening of the intima of the pulmonary arteries and veins also usually develops. (See the chapter on brown induration of the lungs.) The results of physical examination are as follows : Inspection. — The whole cardiac region may seem slightly prominent, as a re- sult of the hypertrophy of the heart. This protuberance is most marked in chil- dren with their yielding thoracic walls. The heart's action is usually extended over a larger area, but in pure mitral stenosis the apex-beat is no stronger than usual, though often displaced to the left. We have frequently noticed a marked pulsation in the epigastrium, produced by the right side of the heart. The jugu- lar veins are apt to be prominent, and show the different forms of undulatory and pulsating movement. Palpation. — This also gives signs corresponding to the more extended action of the heart. We sometimes feel the pulsation of the dilated right ventricle even to the right of the sternum. In some cases we feel a diastolic thrill at the apex of the heart, which alone may almost establish the diagnosis of mitral stenosis. This thrill arises from the same vertiginous currents in the blood which form the basis of the diastolic murmur (vide infra). The radial pulse is small in every case of severe mitral stenosis, and is very often irregular. Percussion. — Percussion shows, in the first place, an extension of cardiac dull- ness toward the right, reaching to the right edge of the sternum, or far beyond. Dullness also extends as a rule further to the left than normal. This is in part due to the hypertrophy of the left ventricle (vide supra), in part to a dilatation of the right side of the heart, so great as to push the left ventricle backward and to the left. The great distention of the left auricle causes an enlargement of the cardiac dullness upward. We observed one case in which the left auricle was so enormously dilated that it extended behind and beyond the right auricle toward the right, and was one factor in the increase of cardiac dullness toward the right, as observed during life. Auscultation. — The characteristic auscultatory sign of mitral stenosis is the diastolic [pre-systolic] murmur at the apex. This is never so loud and blowing as the systolic murmur of insufficiency, but it usually sounds more rolling or rippling. It is loudest at the apex, and it is transmitted only slightly toward the base. Since, as has been said, the left ventricle in mitral stenosis is sometimes pushed to the left and backward by the very much enlarged right ventricle, in looking for the murmur we must often go far to the left, in order not to auscult the right ventricle only. The origin of the murmur is easily explained. In the diastole of the left ventricle the blood-current must force its way through the narrow mitral orifice, whence vertiginous movements arise in the blood, and produce the murmur. Since the blood flowing through the narrow orifice has a current of relatively slight intensity, the murmur produced by it can not be very loud. Indeed, in the most extreme cases of mitral stenosis, the murmur is particularly apt to be very faint, and when the heart's action is hurried and irregular, entirely inaudible. Not infrequently the murmur is not heard until the second half of diastole. That is, when the contraction of the left auricle gives a fresh impulse to the current of blood streaming through the stenosed orifice. A murmur of this sort, which is audible only at the end of diastole, and passes with a distinct crescendo directly into the loud systolic sound and terminates with this, is called a pre-systolic 316 DISEASES OF THE CIECULATOEY OEGANS murmur. This murmur can often be plainly felt if the hand is laid upon the apex of the heart, as a pre-systolic thrill. It is not very exceptional to find no murmur audible in cases of extreme mitral stenosis. If such cases do not come under observation till the last stage of the disease, the mitral stenosis may readily be overlooked. We have ourselves re- peatedly found, in cases of mitral stenosis, that as the lesion grew worse the dis- tinct diastolic or pre-systolic murmur gradually and completely disappeared. This is explained by the fact that as the chink in the valve grows narrower and the weakness of the heart greater, the blood is not forced through the narrow orifice with siifiicient vigor to cause audible vibrations of the thickened valves. If the left ventricle is wholly displaced backward by the enormous increase in size of the right ventricle, we have also less favorable conditions for the propa- gation of the waves of sound from the mitral valve to the ear. The first sound at the apex is maintained in pure mitral stenosis. Indeed, it is often noticeably loud and valvular. All the later observations confirm the view that the systolic sound is a muscle sound, and consequently it is probable that this vigorous first sound is due to the contraction of the left ventricle, which, as we have seen above (page 314), is often hypertrophied, and also, as a result of the stenosis, only imperfectly filled. The strength of the first ventricular sound in mitral stenosis affords, at any rate, a marked contrast to its weakness in aortic insufficiency (vide infra). We have a strong sound when the ventricle is ill- filled, diminution and dullness of sound when the ventricle is over-filled. If in- sufficiency of the valve co-exists, we may hear a systolic murmur with the first sound or instead of it. The very marked accentuation of the pulmonic second sound, the result of the abnormally high tension in the pulmonary artery, is almost constant. It fails only in very anasmic, weak people, or in co-existing insufficiency of the tricuspid valve (vide infra). The second sound at the base is very often "di- vided " or reduplicated. The closure of the semilunar valves in diastole does not happen at the same time in the pulmonary artery and in the aorta, on account of the unequal tension in the two vessels, so that consequently the two sounds are heard, one shortly after the other. Although this division of the second sound is particularly frequent in mitral stenosis, it is by no nieans a pathognomonic sign of it. Mitral stenosis is one of the severest forms of heart disease. It almost always causes greater subjective disturbance than mitral insufficiency. Hypertrophy of the right ventricle may, indeed, maintain for a time an approximately complete cornpensation, but the signs of marked stasis in the pulmonary circulation, and further in the veins of the body, are apt to appear quite early. It must be admitted that the disturbances of compensation which occur in mitral stenosis are particularly susceptible of treatment, so that for many years there may be times of improvement, alternating with times of aggravation of the symptoms; but finally the time comes when it is impossible to regulate the circulation. The dyspnosa grows worse, and finally death occurs, usually preceded by dropsy. 3. Insufficiency of the Semilunar Valves of the Aorta Insufficiency of the aortic valves is due most frequently to contraction of the free edges of the valves. Tears, perforations, or adhesions of the valve to the wall of the vessel more rarely lead to insufficiency. The cause of all these changes is either a valvular endocarditis, which is usually a sequel of articular rheumatism, or a general arterial atheroma, which extends gradually from the intima of the aorta to the valves. We have already referred to syphilis as a not very infrequent cause of aortic lesions. A question of practical importance is VALVULAR DISEASE OF THE HEAET 317 whether violent bodily exertion may suddenly occasion the partial laceration of an aortic valve. Many clinical observations, including a recent case of the author's, seem to show the possibility of this extremely rare occurrence. The function of the aortic valves is to close tightly at the time of diastole of the left ventricle, in order to prevent any return of blood from the aorta into the ventricle. If these valves are insufficient — that is, if they do not close perfectly at each diastole — there is a return current of blood from the aorta into the left ventricle. This regurgitant diastolic wave sets the tense edges of the valve in vibration as it passes over them. Furthermore, the two currents of blood impinging upon each other in the left ventricle, the one an abnormal regurgitation from the aorta, the other the normal stream from the left auricle, produce irregular whirl- ing motions in the blood. All these vibrations are propagated to the surround- ing structures, and produce the long-continued, blowing, diastolic, and remark- ably characteristic murmur of aortic insufficiency. Aortic insufficiency causes an immediate and great increase in the demands upon the left ventricle, because of its abnormal distention, for it receives, as we have already said, not merely its normal quantum of blood from the left ven- tricle, but also the blood which regurgitates through the leaking valves of the aorta. It is consequently overfilled at every diastole, and finally becomes per- manently distended. Dilatation of the left ventricle forms a constant anatom- ical lesion in every case of aortic insufficiency, and is shown not only in the dila- tation of the whole ventricular cavity, but also in the very characteristic flatten- ing of the trabeculte and of the papillary muscles. There is iisually some fibrous thickening of the endocardium at the spot upon which the regurgitant blood-cur- rent is continally impinging. The left ventricle possesses sufficient reserve strength to discharge its contents completely for a long period by means of in- creased effort. This is indeed a task like that of Sisyphus, since the portion of the blood which is thrown into the aorta is constantly rolling back into the ven- tricle. The increased demands, however, lead necessarily at last to a hypertrophy of the left ventricle, often greater than is seen under any other conditions. From the facts enumerated we can easily understand the physical signs of insufficiency of the aortic valves. Inspection. — Great hypertrophy of the left ventricle often causes a marked protrusion of the whole cardiac region. The diffuse and very strong apex-beat, displaced downward and to the left, is especially striking. It may usually be seen in the sixth intercostal space, outside the left mammillary line, and some- times even at the anterior axillary line. Besides, we often see a marked diffuse tremor of the whole cardiac region. There is marked pulsation of the carotid arteries in the neck. The jugular veins show undulation and pulsation, when at last compensation begins to fail. Palpation. — ^We can appreciate the heart's action to a still greater extent by palpation than by inspection. The apex-beat is very resistant, massive, and plainly heaving — that is, the finger or stethoscope applied to the apex is lifted by the beat at every systole. In rare cases a diastolic thrill, corresponding to the diastolic murmur, can be felt over the base of the heart. In two such cases observed by us the murmur had a marked musical character (vide infra). The appearances in the arteries are given below. Percussion. — Percussion gives an extension of the cardiac dullness to the left, beyond the left mammillary line and even to the anterior axillary line, caused by the hypertrophy and dilatation of the left ventricle. The upper boundary of the cardiac dullness is normal, or it may extend up to the third rib. The right boundary is in its normal place at the left border of the sterniun, but it may also be pushed farther to the right, either, because the large left ventricle of itself 318 DISEASES OF THE CIECULATOEY OEGANS causes an extension of the "whole heart to the right, or because the right ventricle is also hypertrophied. The latter change occurs in pure aortic insufficiency "when the compensation is no longer complete, and the stasis extends back"ward from the left ventricle, through the pulmonary circulation, into the right side of the heart. It may also be remarked here that, in insufficiency of the aortic valves, the ascending aorta is often considerably dilated by the marked impulse frora the amount of blood pouring into it. A moderate degree of dullness is found over the dilated aorta, "n-hich may sometimes be made out at the sternal end of the second right intercostal space. Auscultation.— rlnsufficiency of the aortic valves is characterized by a long- dra"wn, loud, blowing diastolic murmur, the origin of "^'hich has been explained above. The place in "which the murmur is heard loudest is not the sternal end of the second right intercostal space, the ordinary point for auscultation of the aorta, but it almost al"ways lies farther to the left. Corresponding to the back- "ward current of blood to"ward the left ventricle, which begets the murmur, "we hear the latter loudest over the upper part of the sternum or even at its left bor- der. In some eases the murmur assumes a marked " musical character " — that is, there is a definite high musical tone, "which is due to a tendinous fiber arising from a "wearing a"way of the valve, and set in vibration by the diastole, or to some similar cause. The diastolic murmur is often audible at the apex, but it is faint there. It is only in a few exceptional cases that there is no diastolic murmur in aortic insufficiency. Sometimes we hear not only the murmur, but also the diastolic sound of the closing valve. During systole we scarcely ever hear over the aorta a pure, loud, first soimd, but almost always a short systolic murmur. This may, of course, be due to accompanying stenosis of the aortic valves, but yet is very common when there is insufficiency alone. It is explained by O. Eosenbach as being due to the fact that at the beginning of the systole of the left ventricle, the diastolic flow of blood has not yet completely ceased, so that the emerging blood-stream encounters this opposing current. This meeting of the two blood-currents in the root of the aorta during systole causes the vibrations which give rise to the short systolic murmur. It is to be noted that this circum- stance also may perhaps have some influence upon the development of the hyper- trophy of the left ventricle. It is very interesting and important that, as Traube pointed out, we find the first sound at the apex scarcely ever loud and pure, but often very indistinct and muffled; or else we hear a short systolic murmur instead of it. This veiling of the first sound at the apex of the heart has theoretic interest, because it has been employed as an argument against the view that the first mitral sound is a mus- cular sound; for it is not, in fact, at once apparent why the hypertrophied left ventricle should so often fail to produce a distinctly audible tone by its contrac- tion. But, as "we have already pointed out (see page 316), the probable explana- tion lies in the previous over-distention of the left ventricle during diastole. This renders the systolic contraction difficult and somewhat slow, and may be the cause of the indistinctness of the muscle-sound. In later stages of the disease we may also adduce parenchymatous degeneration of the myocardium, as an ex- planation of its feebleness. The systolic murmur, often heard at the apex in aortic insufficiency, may depend upon a co-existing true mitral insufficiency, but it is probably often due to a relative insufficiency of the mitral, since the valves, which are normal in themselves, can no longer cause a perfect closure of the left mitral orifice now that the left ventricle is dilated. Sympto5IS in the Peripheral Arteries. — Such remarkable symptoms are found in the peripheral arteries in aortic insufficiency that they demand a brief special description. The first striking symptom is the strong pulsation not only of the larger but also of the smaller arteries, even those the pulsation of which is VALVULAE DISEASE OF THE HEART 319 not generally visible. We see and feel not only a strong pulsation in the carotids, but also in the tortuous brachial artery, in the radial, ulnar, temporal, dorsalis pedis, etc. We sometimes feel an arterial pulse in the liver through the ab- dominal walls. The rapid decline of the pulse — the pulsus celer [Corrigan's pulse] — is most characteristic of aortic insuiEciency, and is to be felt especially in the radial artery, but also in the femoral, dorsalis pedis, and other vessels. An abnormally large quantity of blood is thrown into the arteries from the hypertrophied and dilated left ventricle; hence the high ascent of the pulse; but since the distended artery quickly contracts again, and particularly as at the next diastole of the ventricle the blood escapes in two directions, into the capillaries and back into the ventricle, an abnormally rapid and deep decline of the pulse follows the high ascent of its wave — a condition which explains the " jumping," " springing " pulse (pulsus celer) of aortic insufficiency. The quality of the pulse may be plainly recognized also in the sphygmographic tracing (see Fig. 40). The abnor- mal backward wave may even be detected in the capillaries. We often see a marked pallor of the finger- nails at every diastole of the heart in pa- tients with aortic insuf- ficiency — Quincke's ca- pillary pulse. The auscultatory phenomena over the ar- teries are connected partly with the chang- ing conditions of tension of the arterial walls. We very often hear a short, rough, systolic murmur in the carotid. The second sound, which is well known to be the transmitted aortic second sound, is absent. Instead of it we sometimes hear faintly transmitted the aortic diastolic murmur. The sound of the medium- sized and smaller arteries is very characteristic. By applying the stethoscope lightly we hear over the femoral, the brachial, and often over the radial, the ulnar, the palmar arch, and the dorsalis pedis, a marked valvular sound, which is changed by pressure on the artery, especially in the larger arteries, to a loud stenotic murmur. The quicker the pulse, the more certain are we to hear these sounds in the arteries. In the most marked cases of Corrigan's pulse these vas- cular sounds are so loud that we may hear almost any^vhere below the knee, by means of a stethoscope, a valvular sound. The double sound in the femoral (Traube's double sound) is quite a frequent phenomenon, about the origin and significance of which there has been much discussion. The double sounds either follow each other shortly, so that the first seems something like a preparatory blow for the second, or they are separated from each other by a longer interval, like the two sounds of the heart. Traube explained the origin of the first sound by the sudden tension of the vessel-wall, as in the simple femoral sound, and the second sound by the sudden relaxation of it. Friedreich has pointed out in regard to this that, in co-existing tricuspid insufficiency, a sound may also be produced in the femoral vein by tension of the venous valves. The double sound in the femoral may probably have different causes of origin. It is, of course, by far the most frequent in aortic insufficiency, but it has also been repeatedly observed in other forms of heart disease, as in mitral stenosis. The so-called Duroziez's double murmur in the femoral is more rare, and it is noticed almost exclusively in aortic Fig. 40.— Pulse curve in aortic insufficiency. 320 DISEASES OF THE CIECULATOEY OEGAKS insufficiency. This is when we hear, by pressing the stethoscope on the femoral, two murmurs plainly distinct from each other, of which the first comes from the passage of the systolic blood-wave, and the second from the passage of the abnor- mal backward wave coming from the periphery of the vascular system through the artificially contracted vessel. While the well-marked Corrigan's pulse and the arterial sounds associated with it are so characteristic, they do not appear with great distinctness in every case of aortic insufficiency, but only in many; while in other and apparently similar cases they are indistinct or quite absent. Probably this difference depends at least in part upon a diiference in the elasticity of the arterial walls. At any rate, we have seen well-marked Corrigan's pulse and sounding arteries in youthful patients; while in elderly persons with accompany- ing arterio-sclerosis or similar changes, these phenomena are not apt to be striking. Aortic insufficiency is a comparatively favorable form of heart disease, since it may be almost perfectly compensated for years by hypertrophy of the left ventricle. Many patients with moderate aortic insufficiency feel perfectly well, and are even capable of quite hard work. They have not the slightly cyanotic hue which almost all patients with mitral disease exhibit, but they have a nor- mal or even a pale complexion. If, however, the signs of disturbed compensa- tion once appear in aortic insufficiency the severest sequelae may develop quite rapidly. In aortic insufficiency it is exceptional to see such repeated changes from bad to good, and good to bad, as are often observed, for instance, in mitral stenosis. If the left ventricle becomes enfeebled, it can no longer satisfy the excessive demands made upon it. Passive congestion ensues, extending back- ward through the pulmonary circuit into the systemic veins, even while the pulse may still seem to be powerful. The average arterial tension becomes subnormal, dyspnoea increases, and there are attacks of cardiac asthma. CEdema appears, and the patient dies with the sjonptoms of anasarca. We will speak more fully below of certain intercurrent events in aortic insufficiency, such as cerebral haem- orrhage and pericarditis. 4. Stenosis of the Aortic Orifice Except for the mild forms of aortic stenosis, which often come on with aortic insufficiency, aortic stenosis is a rare disease. It arises from marked thick- enings and calcifications, and especially from adhesions of the aortic valves to one another. The stenosis may become so considerable that the orifice is finally reduced to a mere fissure, through which the left ventricle must force the blood at its systole. The fluttering of the valves and the vertiginous movements in the blood thus arising produce a loud systolic murmur. The left ventricle is com- pelled to do greater work in consequence of the increased resistance of the aortic orifice, and hence becomes hypertrophied. In spite of the increased effort, how- ever, comparatively little blood reaches the arterial system, and consequently the radial pulse is small and the arteries contracted. Inspection and Palpation. — Upon physical examination of the heart we find, in the first place, the apex-beat displaced outward as a result of the hypertrophy of the left ventricle, and also often more powerful than normal. It may, how- ever, be noticeably feeble, perhaps because of the slowness of the systole. A former explanation of this feebleness was the diminution of the recoil of the apex (the Gutbrod-Skoda theory of the apex-beat). Percussion. — Percussion gives an extension of the heart's dullness to the left. The right ventricle is also dilated and hypertrophied to a moderate degree in the later stages, if the stasis extends backward through the pulmonary circulation. Auscultation. — On auscultation, we hear over the aorta a very loud " sawing," long-drawn, systolic murmur, which is usually transmitted to the right, corre- VALVULAE DISEASE OF THE HEART 321 sponding to the course of the aorta, in distinction from the diastolic murmur of aortic insufficiency. It is usually to be heard loudest at the sternal end of the second right intercostal space, but it is audible to a lesser extent over almost the whole heart. It is usually quite loud over the carotids. The systolic sound at the apex is apt to be feeble. The second aortic sound is likewise faint or even inaudible. If there is co-existing insufficiency of the valve, the second aortic sound is replaced by a diastolic murmur. The pulse has been already described. It is small, and often surprises one by its contrast with the strength of the apex-beat. In well-compensated cases it is regular, and often moderately or even extremely slow. This slow pulse of aortic stenosis is often explained as a compensatory change in the heart's action, appro- priate to the existing lesion — the systole being lengthened, an increased amount of blood can be driven through the narrow aortic orifice. But the slowing of the cardiac action is really, in main part, a prolongation of the diastole, and there- fore the slow pulse is probably due chiefly to the fact that the wall of the left ven- tricle is ill-supplied with blood, just as in the case of sclerosis of the coronary Fig. 41. — Pulse curve in stenosis of the aortic orifice. arteries. The sphygmographic tracing of the radial pulse (see Eig. 41) shows a low wave and a comparatively slow rise and fall. Aortic stenosis of slight or moderate degree may be tolerably well borne by the patient. We have even seen a man with well-marked aortic stenosis who for years did not have the slightest subjective symptoms of heart-disease, until he finally died with an acute recurrent endocarditis. When the stenosis is more complete we sometimes have a most peculiar clinical picture. The pulse is very infrequent, as low as thirty to twenty-four beats in a minute. From time to time there are attacks of vertigo or syncope, the patient often falls, and has epi- leptiform attacks. These seizures, which may be repeated for months or even for some years, are probably connected with a sudden ansemia of the heart and brain. We have observed this remarkable group of symptoms particularly in elderly per- sons with aortic stenosis, due to arterio-sclerosis. In other respects the course of aortic stenosis is similar to that of the acute valvular diseases, and in the same way terminates in general circulatory derangement with its results. 5. Insufficiency of the Tricuspid Valve Insufficiency of the tricuspid valve is extremely rare as an independent dis- ease of the heart, but a secondary insufficiency of the tricuspid is quite fre- quent, and is therefore of practical interest, as it complicates other already-exist- ing valvular diseases in the left side of the heart. It arises either from a sec- ondary endocarditis, affecting the tricuspid, in quite an analogous manner with mitral insufficiency, or it is a so-called relative insufficiency. This name we give to that form of insufficiency which develops when the edges of the tricuspid valve, normal in themselves, at last fail to meet one another, from the increasing dilata- tion of the right ventricle, or at any rate from the inability of the enfeebled right ventricle properly to close the valve. The necessary result of tricuspid insufficiency is, that in every systole of the right ventricle a backward current passes through the open tricuspid orifice into the right auricle, and thence into the veins of the body. The tricuspid insuffi- ciency ensuing in other forms of heart disease must therefore increase the stasis 21 322 DISEASES OF THE CIECULATORY ORGAIsTS in the reins of the body, and it is thus far an unfavorable complication. It has a compensatory significance only as it affords relief to the pulmonary circulation. Since a part of the blood passes back from the right ventricle into the veins, less blood than usual must reach the pulmonary arteries. The decrease in ten- sion thus produced in these arteries makes itself apparent on auscultation, since the accentuation of the pulmonic second sound in valvular disease of the mitral orifice diminishes "R-hen tricuspid insufliciency takes place. That tricuspid insufliciency must result in a hypertrophy of the right ven- tricle is explained in just the same "way as the hypertrophy of the left ventricle in mitral insufliciency, from the increased influx of blood at increased tension into the right ventricle during diastole; but this effect of tricuspid insufficien- cy can rarely be made out in any individual case, since the right ventricle is usu- ally already hypertrophied as a result of the disease in the left side of the heart. The most important symptom from vhich we can diagnosticate tricuspid in- sufliciency is the venous pulse. The cause of this is the backward wave of blood produced at each systole of the right ventricle. So long as the venous valve above the bulbus jugularis is closed, we usually see only a " bulbar pulse," but very soon this valve also yields to the continued impulse of the blood, and then a strong, purely venous pulse is visible along the whole course of the jugular vein up to the vicinity of the mastoid process. The contraction of the right auricle very often causes a decidedly weaker elevation of the vein, which just precedes the marked pulsation caused by the ventricular systole (anadicrotic venous pulse) . On account of the straighter course of the right innominate vein, the jugular venous pulse is often stronger on the right side than on the left. We must state, however, that the jugular venous pulse is not an absolutely certain sign of tricuspid insufficiency, since it may arise in hypertrophy of the right side of the heart without any insufficiency of the tricuspid, from the closure of the valves. If there is pulsation in the bulb of the jugular vein and the jugular valve is still capable of closing, a low, audible, venous, valvular sound may be produced by its closure. A sound may also arise in tricuspid insufficiency, as has been already said, from the tension of the valves in the femoral vein. A visible pulsation in the larger veins of the extremities is very rare, but in tricuspid insufficiency we quite frequently feel a venous pulsation in the liver, which organ is usually en- larged by passive congestion. This may be quite apparent even in many cases in which the jugular venous pulse is absent, because the veins in the liver are without valves. [It is best appreciated by means of bimanual palpation. — V.] Auscultation over the right side of the heart gives a systolic murmur in insuffi- ciency of the tricuspid, arising from the regurgitating blood-current. This may be heard loudest over the lower part of the sternum, or at the sternal end of the right fifth rib. The significance of this murmur in diagnosis, however, is im- paired by the fact that it can not always be separated from the systolic mitral murmur that often co-exists. 6. Stenosis of the Tricuspid Orifice Stenosis of the tricuspid orifice is an extremely rare disease, and hence it is without practical significance. It has usually been observed, up to the present time, as a congenital form of heart disease, almost always combined with other anomalies of development in the heart. The physical signs of tricuspid stenosis can easily be constructed theoretically. The first result must be a marked dilatation of the right auricle, and the occur- rence of a diastolic or presystolic murmur over the right side of the heart. From VALVULAE DISEASE OF THE HEART 323 the rarity and complex character of the cases, however, we have so far seldom had an opportunity to confirm these theories at the bedside. The prognosis of this form of heart disease is veiy unfavorable, since a long- continued compensation by increased labor on the part of the right auricle is scarcely conceivable. [Seventy cases of tricuspid stenosis have been collected by Bedford Fenwick, whose analysis affords good grounds for thinking that the lesion is often ac- quired. In fifty per cent, of the cases there was a clear history of rheumatism, and nearly all of the patients were more than twenty years of age at the time of death. This lesion is never found alone, but invariably combined with mitral stenosis ; all but eight of the cases were in women. Fenwick thinks that the influence of sex lies in the less onerous nature of the work of women than of men, the granu- lating edges of the valves being kept more in apposition, thus healing with adhe- sion and causing obstructions at the orifice.] 7. Insufficiency of the Pulmonary Valve Insufficiency of the pulmonary valve is also a very rare form of heart disease. It occurs as a congenital anomaly, often combined with other failures of develop- ment, or as a disease acquired after birth. The anatomical changes in the valve, which lead to insuificiency, are precisely analogous to those which cause insuffi- ciency of the aortic valve. The physical signs of this form of valvular disease consist chiefly of a marked dilatation and hypertrophy of the right ventricle, to be made out by percussion, and of a loud diastolic murmur over the pulmonary valve. These signs are explained in just the same way as the precisely analogous signs in the left ven- tricle in aortic insufficiency. In general, pulmonary insufficiency, like aortic insufficiency, seems to be com- pensated quite well for a long time by hypertrophy of the right ventricle. In many cases a co-existing patency of the foramen ovale also seems to be of favor- able influence, as it lessens the stasis in the right auricle and the veins of the body, while it renders easier the filling of the left ventricle. 8. Stenosis of the Pulmonary Orifice (Pulmonary Stenosis) and the other Congenital Diseases of the Heart 1. Congenital Pulmonary Stenosis.— While the stenosis of the pulmonary orifice acquired in later life is so rare that it has only slight practical signifi- cance, the congenital pulmonary stenosis is of far greater importance. It is, on the whole, the most frequent of the congenital forms of heart disease. Its origin is to be referred either to an endocarditis of the pulmonary valves during fcBtal life, or to anomalies in the development of the heart. The stenosis is often situated not merely at the pulmonary orifice itself, but farther back in the conus arteriosus, which seems to be narrowed by the formation of myocardial cicatrices. The pulmonary artery is often also narrowed as a whole. In the majority of cases we find, in addition, other anomalies of development in the heart, espe- cially patency of the foramen ovale, great defects in the ventricular septum, and. in about half the cases, patency of the ductus Botalli, etc. The symptoms of congenital pulmonary stenosis sometimes appear soon aftet the birth of the child. The first thing that strikes us is the marked cyanosis, which is constant, or else comes on with crying, or with movements of the body. Many children, however, reach a fair age, five or ten years, or even fifteen. In some cases the heart disease may be so perfectly compensated that the child may 324: DISEASES OF THE CIECULATOEY OEGANS be comparatively well for a time, and severe disturbances may not appear for several years. As a rule, children with congenital pulmonary stenosis present a very strik- ing appearance. The cyanosis is especially noticeable in the face, the lips, the nose, and the hands and nails. The parts mentioned feel cool. The eyes are often somewhat prominent, and there is a slight cedematous swelling about them. The peculiar club-like thickening of the terminal phalanges of the fingers and toes, a result of stasis, as seen also in many cases of bronchiectasis, is very char- acteristic. The nails also present a characteristic claw-like curvature. The whole development of the child is remarkably retarded. It often seems several years younger than it is. The muscles and fatty layer are slight. The gums are sometimes very spongy and disposed to bleed. In severe cases the child suffers from faintness, vertigo, etc. On physical examination of the heart, we usually find the cardiac region rather prominent. Percussion gives an increase of the heart's dullness, especially toward the right. This extension of the dullness is due to the hypertrophy of the right ventricle, which must arise in the same way as hypertrophy of the left ven- tricle in aortic stenosis. On auscultation, we hear a loud systolic murmur, which is perceptible over the whole heart, but which has its greatest intensity at the sternal end of the second left intercostal space. The eddies of blood, which pro- duce the murmur, may also often be felt by the hand as a systolic thrill. In some cases, however, we miss the murmur in pulmonary stenosis, just as in mitral ste- nosis. The pulmonic second sound is weak or inaudible, or it is replaced by a murmur if there is also insufficiency of the valve. The course of congenital pulmonary stenosis is always unfavorable. As has been implied, few children get beyond the age of fifteen years. Death ensues, either with general disturbances of compensation evidenced by dyspnoea and dropsy, as in every other form of heart disease, or from complications. Among the latter, we may mention especially the very frequent development of phthisis. 2. The Remaining Congenital Lesions of the Heart. — Inasmuch as other con- genital lesions than pulmonary stenosis have but slight clinical importance, we will limit ourselves here to a brief review of the same.* (a) Patency of the foramen ovale is a comparatively frequent lesion, whether alone or combined with others. Physical signs are mostly absent. In a few cases a presystolic murmur has been heard. When mitral insufficiency co-exists with a patent foramen ovale, venous pulsation may be caused. (&) Defects in the septum between the ventricles. These are most frequently situated in the posterior section of the anterior septum, and they likewise are associated with other anomalies, such as abnormal distribution of the arteries, pulmonary stenosis, or defects in the septum between the auricles. Sometimes the patency of the septum gives rise to a systolic murmur, but a diagnosis of the con- dition during life is scarcely ever possible. (c) Persistence of the ductus Botalli. Inasmuch as this contributes blood from the aorta to the pulmonary circulation the pressure in the latter is raised, hence there is to be observed accentuation of the second pulmonic sound and hypertrophy of the right ventricle. There is sometimes also a loud systolic murmur. (d) We have already spoken of congenital stenosis of the tricuspid valve. Congenital narrowing of the mitral valve and of the aortic valves may also occur, but they are extremely rare. * A more extensive ^j . ntation of the subject can be found in the article by Eauehfuss in Ger- hardt's " Ilandbuch dor Kinderlvrankheiten," vol. iv, and in text- books on pathological anatomy — for example, Orth's. VALVULAR DISEASE OF THE HEART 325 9. Combined Valvular Diseases of the Heart Although in what has preceded we have dealt with the several forms of valvu- lar disease of the heart separately, in order to present them in a general way, yet in reality combinations of them often occur in great variety. We find especially, as has already been mentioned, stenosis of an orifice co-existing with insufficiency of the accompanying valve; but diseases of two or more different valves are not infrequent, combined in the most diverse manners. The physical signs of these " combined forms of heart disease " may, of course, be inferred from the signs of anomalies of single valves, but the phenomena are often so compli- cated that the diagnosis of combined heart disease is generally much harder than that of the simple forms. Sometimes the single forms neutralize one another in their action. For example, the left ventricle is usually small in pure mitral ste- nosis, but, if aortic insufficiency be also present, it is nevertheless found dilated, at least to a certain degree. The influence of an absolute or relative tricuspid insuf- ficiency on the action of mitral disease, especially the decrease in tension in the pulmonary vessels caused by it, and also the diminished accentuation of the pul- monic sound, have been mentioned above. In reference to the clinical symptoms of combined heart disease we may say, on the whole, that, in a large number of cases, the disease of o?ie valve stands out as predominant in the whole picture of the disease. The other anomalies are only slightly noticeable, and often of later date. Hence, we may find at the autopsies of patients, who during life have shown the symptoms of disease of only one particular valve, unimportant changes on the other valves, which have been with- out clinical significance. General Comparison of the most Important Physical Signs in Valvul.aji Disease OF THE Heart Form of Heart Disease 1. 3Iitral in- sufficiency. 2. 3Iifral stenosis. 3. Aortic in- sufficiency. Inspection. 4. Aortic stenosis. Strong apex-beat, often somewhat displaced out- ward. Area of cardiac im- i Diastolic pulse enlarged, ! at the epigastric pulsa- tion. Palpation. Systolic thrill at the apex. Quite strong radial pulse. ■" thrill Apex - beat very strong, displaced downward and to the left. Visible pulsation of the medium - sized and smaller ar- teries. Apex - beat dis- placed to the left. apex. Small and oft- en irregular pulse. Very strong, heaving apex- beat. Pulsus celer. Heart's action not very strong. Pulse small, in- frequent, some- times slow. Percussion. Hypertrophy of the left, later of the right ventricle. Hypertrophy of the right ven- tricle. Marked hyper- trophy of the left ventricle. Hypertrophy of the left ven- tricle. Auscultation. Loud systolic murmur at the apex. Pul- monic second sound accentuated. Diastolic or presys- tolic murmur at the apex. First sound sometimes loud. Pulmonic second sound accentuated, and sometimes dou- ble. Loud diastolic aortic murmur, especially over tlie upper part of the sternum. Sounds in the ar- teries (femoral and brachial sounds, etc.). Sometimes a double sound or double murmur in the femoral. Loud systolic aortic murmur, transmitted to the right. 326 DISEASES OF THE CIKCULATOEY OEGAl^S [Bramwell reports that of 131 cases with macroscopic valvular lesion, the tri- cuspid was implicated in 33.58 per cent.; in all but 12 per cent, of these the changes were recent. Hence he thinks that tricuspid endocarditis is generally recovered from, and this he attributes to the relatively small strain to which that valve is subjected. The obvious therapeutic deduction is the importance of rest in mitral endocarditis.] General Sequels and Complications of Valvular Disease op the Heart After having discussed, in what precedes, the mechanism of the single forms of valvular disease, and the physical signs derived from it, we must now describe a number of symptoms and sequelae which may be present to a greater or less degree in all forms of valvular disease. With them we must also mention certain pecul- iarities of the individual forms. 1. Subjective Symptoms. — Fully compensated heart disease may exist, at least for a long time, without any subjective symptoms. This is especially the case in aortic insufficiency, more rarely in mitral insufficiency. Stenosis of the mitral or of the aortic valves almost always causes subjective symptoms. These symp- toms often do not exist so long as the patient keeps perfectly quiet physically and mentally, but they develop under appropriate circumstances, especially upon bod- ily exertion. The existing subjective symptoms in heart disease are by no means always referred, in the first place, to the heart itself. It sometimes happens that the patient comes to the physician complaining of various digestive disturbances, or in other cases of headache, vertigo, etc. The physical examination alone leads us to recognize the heart disease. As a rule, the patient's first and chief complaint is directed toward his difficulty in breathing. The shortness of breath, which increases on any physical exertion, comes on quite early in many cases. In the later stages it is almost always the most distressing symptom. The causes of dyspnoea in heart disease are manifold. In the first place dyspnoea results from congestion of the pulmonary circuit, with consequent slowing of the circulation in the lungs, and limitation of the exchange of gases in those organs. In later stages the anatomical changes in the lungs contribute also to an increase of the dyspnoea (vide supra, the chapter on brown induration of the lungs). Basch ascribes special importance to the fact that the distended capillaries encroach upon the alveoli, as a result of the passive congestion. This broadens the alveoli ("swelling of the lungs"), but at the same time impairs the mobility of the lungs (" rigidity of the lungs "), and thus embarrasses the exchange of gases in the lungs, just as in emphysema. Further investigations are necessary in order to determine the clinical importance of these conditions. The secondary bronchitis of heart disease is a very great factor in the dysp- noea. This bronchitis is a frequent result of the pulmonary stasis. Often the respiratory distress increases and decreases simultaneously with corresponding variations in the bronchitis. A purely mechanical cause of dyspnoea is the com- pression of the lower portion of the left lung by great cardiac hypertrophy. The highest grade of dyspnoea is reached when finally hydrothorax, hydropericardium, and pulmonary oedema are developed. From what has already been stated, it is easy to see why lesions of the mitral valve which directly impair the pulmonary circulation lead sooner to shortness of breath than do lesions of the aortic valves. Finally, it is self-evident that the condition of the heart has the great- est influence upon the degree of dyspnoea present, for all the phenomena of pulmonary congestion must increase or diminish, according to the functional integrity of the heart, and particularly of the left ventricle. If the contractile power of the left ventricle grows less, dyspnoea must at once increase. ISTot infrequently conditions of cardiac weakness develop with considerable sud- VALYULAE DISEASE OF THE HEART 327 denness, and occasion attacks of dyspnoea which, are termed cardiac asthma. Palpitation is the first subjective symptom to be mentioned of those which are referred directly to the heart.' It is not yet accurately determined under what circumstances the action of the heart is perceived by the patient himself. We sometimes see an uncommonly strong action of the heart, as in aortic insuffi- ciency, which is not perceived at all subjectively. In other eases, where objec- tivelj" the heart is not especially active, palpitation forms the patient's chief complaint. It usually first appears when the heart disease ceases to be fully compensated. It is increased or first excited by physical exertion or mental excitement. In many patients attacks of palpitation occur without any discover- able external cause, due apparently to nervous disturbance. They are sometimes associated with a striking acceleration of the pulse, the so-called tachycardia. Pain in the cardiac region is only rarely present in heart disease. The patients more frequently complain of an indefinite feeling of pressure and oppression in the chest, but still there do occur, particularly in aortic insufficiency, attacks of violent pain in the front part of the chest and the region of the heart, radiating to the shoulders and arms, and associated with a general feeling of extreme anx- iety and weakness. Such conditions are termed angina pectoris, or attacks of stenocardia (vide infra). Pains in the epigastrium and abdomen, which some- times form the chief annoyance of the patient, usually depend upon passive con- gestion of the liver (vide infra), or upon the tension of the abdominal walls from ascites, oedema, etc. We must finally mention here the rheumatoid pains in the joints and muscles, from which many patients with heart disease suffer. The greatest subjective distress occui's in the last stages of heart disease, when general dropsy develops. The patient's helplessness usually culminates. All motions of the body are difficult, the dyspnoea and oppression in the chest con- stantly increase, until death finally releases the patient from his mournful con- dition. 2. Sequelae in the Heart Itself. — We have already discussed the most impor- tant sequelse of valvular disease in the heart itself, its hypertrophies and dilata- tions. It remains for us to describe the influence of the cardiac disease on the frequency and regularity of the heart's action, and also to discuss some secondary diseases of the cardiac muscle and of the pericardium. In every well-compensated heart disease the heart's action may for a long time be of approximately normal frequency and regularity. We often find a constant and moderate acceleration of the pulse, which is easily increased from temporary causes. Obviously this increase in the number of heai't-bcats is often compensa- tory. If the left ventricle receives during diastole less blood than normal — for example, in stenosis — there is such an increase in the frequency of the cardiac contractions that the same amount of blood reaches the various organs in a given interval of time as before. Diminution of the pulse-rate (bradycardia) is ex- ceptional in valvular heart disease, except when it is artificially caused by large doses of digitalis. It is most frequent in aortic stenosis, and here perhaps it has a compensatory effect (vide supra). Marked changes in the rate of the pulse are due to severe disturbances of the nervous apparatus of the heart, and hence they are often associated with arhythmia. Under such circumstances, the pulse- rate may be as high as 120-140 beats per minute. A rare but interesting symptom is the sudden onset of attacks of enormous rapidity of the pulse, up to 160-200 beats and more (tachycardia). This is especially connected with mitral lesions. In the intervals the action of the heart is quiet, with approximately complete compensation of the cardiac lesion. The acceleration of the pulse occurs rather suddenly, and is usually associated with a subjective sensation of palpitation and 328 DISEASES OF THE CIRCULATORY ORGANS distress. It may last several Lours and then vanisli, -usually with the same sudden- ness. The exact cause of these attacks is unknown. They suggest a temporary paralysis of the inhibitory apparatus of the heart. Very often a well-marked acute dilatation may be demonstrated by percussion, during the attack of tachy- cardia. Arhythmia of the heart is of still greater importance than anomalies of the pulse-frequency. It always points to a severe disturbance of the nervous appa- ratus of the heart. The general circulatory disturbance which follows every valv- ular disease must of course make itself felt in the heart itself, and the nerves and ganglia of the heart can not remain undisturbed by it. Hence we generally see marked variations in the frequency and rhythm of the heart's action along with the other signs of beginning disturbance of compensation; but daily clinical experience teaches us that there is not a perfect parallelism between the two symp- toms. We find often enough in heart disease a considerable irregularity of the pulse without any of the other signs of marked disturbance of compensation, and, on the other hand, we see in many patients an almost perfect regularity of the pulse up to death. In mitral disease, especially in mitral stenosis, arhythmia of the heart is much more frequent than in aortic disease. We can not enter here into a complete discussion of the special varieties and symptoms of arhythmia. A distinction is made between the irregular pulse, in which the successive beats are separated by irregular intervals, and the unequal pulse in which the sepai-ate waves are of unequal height. In reality, both phe- nomena are often associated, for when the pulse is more rapid the left ventricle is imperfectly filled during diastole, and the pulse is consequently smaller. The irregularity of the cardiac activity may be extreme (delirium cordis) ; or it may be so modified as to have a certain pe- riodic regularity of its own (allorhythmia). One of the most important and frequent forms of allorhythmia is the pulsus higeminus (see Fig. Fig. 42.— Pulsus bigeminus. 42). In this there is first a vigorous systole and then, before the ventricular diastole is completely finished, a second weaker contraction, followed by a pause. We feel alter- nately a strong and quite weak pulse. The latter may be imperceptible, so that it can be made out only by the sphygmograph. In such cases, with co-ex- isting tricuspid insufiiciency, we sometimes find the number of the venous pul- sations twice as great as the number of the radial pulsations, because the sec- ond weaker contraction of the heart produces a visible venous pulse, but not an appreciable radial pulse. It is possible that in such cases we may have to do with an unequal contraction of the two halves of the heart, the right ventricle contracting vigorously, and the left feebly. If we listen to the heart when there is a pulsus bigeminus we hear four sounds in quick succession, the first two corresponding to the distinct radial pulse, the next two to the close- following systole of the heart which does not give rise to a distinguishable pulse. Continuous and regular pulsus bigeminus, as depicted in the preceding figure, is an infrequent phenomenon, but we very often have a few beats of this character at brief irregular intervals. It is certainly the most frequent cause of the inter- mittent ptilse. The fingers on the radial artery from time to time fail to distin- guish any pulse whatever, or else they perceive it merely as a short wave, closely following the preceding pulse ; but if we listen to the heart at the same time, we recognize that four audible heart sounds correspond to every intermission of the pulse. On the whole, the pulsus bigeminus is a bad sign, since it always points to a marked disturbance of the cardiac innervation ; but it may also pass away again and give place to a regular action of the heart. VALVULAE DISEASE OF THE HEART 329 Chronic valvular disease of the heart is often combined with anatomical changes in the cardiac muscle, and sometimes in the pericardium. Among the changes in the cardiac muscle, cloudy swelling, and especially fatty degeneration of the muscular fibers, are the most frequent. The fatty degenera- tion of the muscle occurs either in a diffuse form, or in little yellowish spots, which are plainly visible on the papillary muscles and trabeculse. The opinion has often been expressed that fatty degeneration of the muscles is the cause of the disturbance of compensation; that the cardiac muscle performs its increased work until fatty degeneration ensues and reduces its strength. This theory does not entirely correspond to the facts. We have often seen the greatest disturbance of compensation in valvular disease when section of the cardiac muscle showed no fatty degeneration ; and, on the other hand, we have seen great fatty degenera- tion of the heart, as in pernicious ansemia, when there were no signs of cardiac weakness during life. Anatomically, with our present aids to research, we can hardly ever decide with certainty whether the cardiac muscle is still capable of performing its normal functions or not. The usual state of the case is probably this, that fatty degeneration of the cardiac muscle is a result of the disturbance of compensation, and especially of the deficient supply of arterial oxygenated blood to the muscle (see the chapter on ansemia). There is as truly a passive congestion of the heart as there is a passive con- gestion of the liver and kidneys. The circulatory disturbance in the heart itself is the chief cause of cardiac insufficiency, and the phenomena of disturbed com- pensation. A frequent affection of the cardiac muscle in valvular disease is the presence of cicatricial changes and so-called myocarditic nodules in the substance of the heart. Chronic endocarditis may directly invade the subjacent parts of the car- diac muscles and set up a chronic inflammation there, but the cardiac cicatrices usually have another origin. The connective-tissue thickening beneath the endo- cardium is the result of a simple atrophy of the superficial muscular fibers due to the increased internal pressure of the blood, as in mitral or aortic insufficiency. The connective-tissue nodules within the cardiac muscle, however, depend in part upon a deficiency in the local supply of arterial blood. Simple sclerotic thickening of the coronary arteries, or complete embolism or thrombosis of a small branch of one of them, is the evident cause of these circumscribed cicatrices. On the other hand, it is also probable that disease of the myocardium is associated with the endocarditis, and is referable to the simultaneous action of the same causes, such as the infection of articular rheumatism, diphtheria, and syphilis. On care- ful microscopic examination we find, in almost all cases of valvular disease, quite extensive changes in the myocardium (Krehl), and in many cases these may cer- tainly impair the functional powers of the^heart. Still, we often find cicatrices of myocarditis without any signs of a previous disturbance in the compensation of the heart. A fuller discussion of this subject will be found in the next chapter. Pericarditis is not very rare as a result of chronic valvular disease. It is always a dangerous complication, and it may cause death. Regarding its origin, we have found that almost all the cases of heart disease complicated with peri- carditis show changes in the aortic valves. Hence it does not seem improbable to us that the secondary pericarditis in such cases is sometimes due to a direct invasion of the pericardium, by the excitants of inflammation passing from the aortic valves through the walls of the blood-vessel. 3. Symptoms of Stasis in the Different Organs of the Body. — As has fre- quently been mentioned in what precedes, the results of stasis of the blood make themselves manifest in heart disease in various organs. We have already spoken of the important results of blood stasis in the heart itself and the lungs. It re- mains for us to discuss the symptoms of stasis in the systemic veins. 330 DISEASES OF THE CIECULATORY ORGA^Tg As soon as the flow of venous blood into tlie right side of the heart is hindered, the venous stasis is shown by the cyanotic appearance of the patient. This cyanosis may exhibit any degree. In heart disease which is still, on the whole, well compensated, it is recognized only by the practiced eye of the physician as a slight bluish tinge of the lips, the alse of the nose, the cheeks, or the nails. With the increase of the disturbance of compensation the cyanosis increases, if it be not modified by the co-existence of general anaemia. In mitral disease, especially in mitral stenosis, the cyanosis is usually more marked than in aortic disease. The large veins, also, become plainly visible as a result of their complete filling, especially the large external jugulars. A further important symptom which follows the venous stasis is the oedema, the dropsy of heart disease. As we know from general pathology, every venous stasis, if it reaches a certain grade, leads to a transudation of the fluid of the blood from the capillaries. If the lymphatics can no longer carry this transuda- tion away, it collects in the meshes of the tissues and leads to cedema. The oedema of heart disease, therefore, does not appear until the venous stasis has reached a certain degree, and the compensation of the heart disease has become impaired. It first appears in those parts where there is a particularly loose tissue, as in the scrotum, or where mechanical conditions favor its development. The legs usually swell first, especially about the ankles, because here the stasis of the venous blood is increased by gravity. At first, slight cedema appears only temporarily and by day, and disappears again while the patient is in bed at night ; but, as the disturbance of compensation increases, the oedema also constantly grows worse, especially in the dependent parts of the body, until finally it may reach the highest degree of dropsy. Besides the cedema of the skin, transudations into the internal cavities occur, especially into the abdomen and the pleural cavity. The relation between the degree of cutaneous oedema and the amount of drop- sical transudation is variable ; thus, in particular, we may have a large amount of ascites, with only moderate swelling of the legs. This is probably occasioned in most cases by special secondary changes in the liver {vide infra) . The patient's distress is decidedly increased by marked oedema, as has already been said. All the motions of the swollen extremities are considerably impeded. Hydrothorax and ascites increase the dyspnoea, the former by compression of the lungs, the latter by upward pressure on the diaphragm. The passage of urine may be rendered very difficult by oedema of the prepuce. Besides that, we must men- tion that the skin, when very oedematous, is quite apt to become the seat of furuncular and erysipelatous inflammations. The .results of stasis in the internal organs may be best seen in the liver, spleen, and kidneys. Passive congestion of the liver is manifested by quite a considerable increase in the size of the organ. The lower boundary of the liver dullness extends several fingers' breadth beyond the edge of the ribs, and the anterior surface and lower border of the liver may often be plainly felt. The liver may also be enlarged in cases in which there are no other marked signs of passive congestion, such as dropsy. Quite severe pain in the hepatic region sometimes arises from the tension of the capsule of the liver. In later stages the liver may grow smaller again through a partial atrophy of the liver cells (atrophic nutmeg-liver). In- deed, there may even develop, as a result of the chronic congestion, a secondary cirrhosis of the liver, with a distinctly granulated surface. These are the cases in which marked ascites is especially apt to occur (vide supra). Slight jaundice often develops in heart disease, as a result of passive congestion of the liver, or perhaps sometimes from a secondary duodenal catarrh. The peculiar mixture of a cyanotic and slightly jaundiced hue of the skin is very char- acteristic in many cases, especially in mitral disease. It should be added that VALVULAR DISEASE OF THE HEART 331 the yellowish discoloration of the skin in heart disease is probably not always a genuine icterus, but it may be occasioned by the deposit of other pigments in the skin. Passive congestion of the spleen arises if the stasis of the blood extends to the splenic vein. The spleen increases in size and becomes firm and dense. It is often hard to make out the congestion from the increase of the splenic dullness, because percussion of the spleen is uncertain if there be also ascites, hydrothorax, etc. We can often, however, plainly feel the enlarged spleen under the edge of the ribs on the left. In the kidneys we find .passive congestion, with the final development of " cyanotic induration." The slowness of the circulation and the diminution of the arterial tension in these organs lead to marked changes in the ui'ine. In particular, there is a diminution in the quantity, especially if the patient is at the same time dropsical. The amount of urine falls as low as 800-500 cubic centi- metres (27-17 ounces), or even less, in twenty-four hours. It becomes dark, con- centrated, of high specific gravity, and abnormally acid, and hence it usually has an abundant sediment of urate of sodium. In marked degrees of stasis there is albumen in the urine as a result of the damage done to the glomerular epithe- lium. The amount of albumen is usually slight, but it may equal one third or one fourth of the volume of urine. Under the microscope we find, in the urine of simple passive congestion, only an occasional hyaline cast, and a few red and white blood-corpuscles. Careful examination of the urine in cases of severe heart disease is of the greatest practical importance, for the character of the urine as shown by the color, specific gravity, and amount of albumen, is an excellent index of the vigor of the heart and the condition of the circulation. Any change for the worse in the circulation is directly shown in a diminution of the amount of urine, and an increase in its specific gravity, or, it may be, in the appearance of albuminuria. Any improvement in the circulation, whether spontaneous or due to remedies, is shown first and clearest by an increase in the daily excretion of urine, and a cor- responding diminution in its specific gravity. We not infrequently meet with acute and chronic nephritis, particularly arterio-sclerotic nephritis, complicating heart disease. It is often no easy matter clinically to form a correct opinion about such cases. We may in part refer the numerous gastric and digestive disturbances, such as loss of appetite, vomiting, constipation, and diarrhoea, from which such pa- tients often sufl^er, to the stasis in the blood-vessels of the stomach and intestines; but of course there are not infrequently diseases such as acute and chronic catarrh of these organs, which are to be regarded as complications. 4. Embolic Processes. — The slowing of the circulation, and the disturbances in the nutrition of the walls of the vessels, which result from it, often give rise in heart disease to the formation of thrombi. These are situated in the heart itself, on the diseased valves, in the recesses between the trabeculse, in the auricles, etc., or else they form in the veins, especially in those of the lower extremity. From these thrombi fibrinous plugs may easily be set loose and enter the circu- lation, and thus give rise to embolic processes in distant organs. Some of the embolisms, whose clinical relations are especially important, have been more fully described elsewhere, and will be mentioned only briefly here. Embolism of the pulmonary arteries, proceeding from venous thrombi or from thrombi in the right side of the heart, gives rise to hasmorrhagic infarction of the lungs. Its pathogenesis and symptoms have already been discussed in a pre- vious section (see page 273). Embolism of the cerebral arteries is a common cause of apoplectic attacks, which are not infrequent in heart disease, and usually lead to hemiplegia. The 332 DISEASES OF THE CIECULATOEY OKGANS anatomical cause of the hemiplegia in these cases is the embolic softening of the brain which ensues. The details of this are given in the section on cerebral diseases (see page 1103). Embolism of the larger arteries of the extremities, such as the femoral and the brachial, is much rarer than the forms mentioned. It leads to embolic gangrene of the extremities, unless an adequate collateral circulation can be established. The skin of the peripheral parts, the fingers or toes, first becomes cool, bluish, and at last, if the circulation be wholly checked, almost black. The gangrene advances slowly, usually occupying weeks. Ulcerations develop as the necrotic portions are thrown off. The affection is extremely painful. The patient soon becomes very miserable from the pain and the septic fever that usually attend the ulcerations, and extensive gangrene almost always ends fatally. Sometimes there is embolism of the abdominal aorta. This is usually located at its bifurca- tion, and occasions a sudden and almost complete paraplegia, speedy disturbance of sensation, abolition of the reflexes, and loss of electrical excitability. No pulse can be felt in the peripheral arteries; the feet are pale and cold, and soon there are signs of gangrene in both legs. The condition is probably invariably fatal. Embolism of the renal arteries, with consequent anaemic or haemorrhagic in- farctions in the kidneys, may have no clinical symptoms at all, but it is sometimes indicated by sudden pains in the region of the kidneys and marked hsematuria (see page 644). Embolic infarction of the spleen is often marked by swelling of the spleen and by severe perisplenitic pains. In other eases it is wholly without symptoms. Embolism of a mesenteric artery is a very rare event. Its symptoms consist of a sudden intestinal haemorrhage, of severe colicky pains, general collapse, and peritonitis. 5. Complications on the Part of the Nervous System. — The most important complication on the part of the nervous system — embolic softening of the brain — has already been mentioned. We must also state that cerebral haemorrhage may occur in heart disease. It is especially frequent in aortic insufficiency, either as a result of co-existing atheroma of the cerebral arteries, or perhaps of the ab- normally high tension of the vessels during systole. Mental disorders have been repeatedly observed in chronic valvular disease. They are the result of the disturbance of the circulation, and the consequent im- pairment of nutrition in the brain. Hence they usually make their first appear- ance in the last stages of heart disease, at the same time with the other disturb- ances of compensation. The psychoses in heart disease most frequently have the character of melancholia, but conditions of confusional insanity and excitement also occur. 6. Secondary Affections of the Joints are not rare in heart disease. As acute endocarditis develops in the course of acute articular rheumatism, so, on the other hand, rheiimatic pains in the muscles and joints, and even acute swelling of the joints, associated with fever, appear in the course of chronic heart disease. Some- times we have the complete picture of acute articular rheumatism. Probably no fresh infection from without is requisite for the development of these second- ary lesions in the joints, but under certain circumstances there is an unusual development of infectious germs (staphylococci?) on the diseased valves, and large numbers of them passing into the circulation occasion a fresh constitutional infection. Y. Constitutional Symptoms. Fever. — In congenital and early acquired val- vular disease, the general development of the child is ordinarily much retarded. In heart disease in adults, however, we by no means always see an injurious influ- ence on the general nutrition. In many patients we even find a remarkably good development of fat. A marked general disturbance of nutrition, such as great VALVULAR DISEASE OF THE HEART 333 ansemia and general emaciation, often develops in the later stages, especially in aortic insufficiency. The wasting is of course often hidden by the oedema. In general, chronic heart disease runs its course without fever, but periods often occur in the course of the disease when there is a moderate and usually irregular fever. Marked disturbances of the general condition may or may not be associated with it. The basis of the fever is probably an acute exacerbation of the endocarditis, except, of course, in accidental complications. All variations occur, from a mild febrile movement without further symptoms to a severe acute recurring endocarditis (q. v.). In other cases the fever is connected with second- ary swelling of the joints, or with embolic processes. General Course and Prognosis of Valvular Disease of the Heart The course of valvular disease of the heart is in most cases very chronic. It may last for years. So long as there is a complete compensation, the patient feels almost perfectly well; sometimes he even has no misgivings as to his trouble. The slight difficulty in respiration and the incapacity for physical exertion are noticed, but little attention is paid to them, because the patient is used to them. In other cases there is a moderate disturbance for a long time, but it may be borne quite easily if the patient is rational and prudent in his conduct. We can not make any general statement as to the length of the stage of com- pensation, because cases differ very greatly in this resjject. It depends in part upon the intensity of the heart disease, in part upon the external conditions under which the patient lives, and in part, certainly, upon the different indi- vidual capacity for work and power of resistance of the heart. Thus it happens that many cases last for decades, while in others severe sequelae appear within a few months. External injurious agencies, acting on the patient, are of great influence on the course of heart disease. Severe physical exertion, an injudicious manner of living, intercurrent febrile disease, mental distux'bances, care, and anxiety are often followed by unhappy consequences. If the first signs of disturbed compensation appear, if severe dyspnoea, slight cedema of the ankles, etc., develop for the first time, these symptoms may disap- pear again completely under proper treatment. Severe disturbances of compen- sation even, great general dropsy, associated with very weak and irregular action of the heart, may abate, after a few weeks' duration, and the patient may feel quite well again. Exacerbations of the disease may come on several times and as often improve. Finally, of course, the improvement is incomplete. Persistent oedema and the other results of venous stasis ensue, the symptoms constantly increase in severity, especially the dyspnoea, until the patient dies after a long and distressing illness. Immediately before death in heart disease, certain irregu- larities in the innervation of the heart and in the respiration sometimes develop. Among these the so-called Cheyne-Stokes phenomenon deserves especial mention. It consists in a peculiar periodical variation in the respiratory movements. There will be, first, a complete pause in the respiration (apnoea), and this will be suc- ceeded by feeble breathing gradually becoming stronger, then gradually abating, and finally ending in another complete cessation of the respiration. The patient usually becomes more comatose during the cessation of respiration; his pupils contract. During the hard breathing the patient recovers somewhat, and his pupils dilate again. The chief cause of this rhythmical breathing is probably to be sought in the decided lowering of the excitability of the respiratory center. During the apnoea a considerable amount of carbonic acid collects in the blood before the respiratory center is sufficiently stimulated to resume its activity. We have seen the heart behave in a precisely analogous manner, but independ- ently of any Cheyne-Stokes respiration. There was a series of rapid but regular pulsations, alternating with a series of slower contractions. 334 DISEASES OE THE CIRCULATOEY OEGANS In regard to the particular forms of valvular disease, aortic insufficiency gener- ally gives the best prognosis, inasmuch as it may be very perfectly compensated for many years, but if severe disturbance of compensation once occurs in this form of heart disease, it gives a very unfavorable prognosis, since, as a rule, we can not reinvigorate the heart. Mitral insufficiency is also quite a favorable form of heart disease, which may be compensated for a long time. Mitral stenosis is de- cidedly inore unfavorable in its prognosis, and is associated with more disturb- ance ; but in all mitral diseases very severe conditions may improve once or even repeatedly. Aortic stenosis is also capable of quite good compensation, and in this respect it is even more favorable for the patient than mitral stenosis, but it often causes persistent cerebral symptoms, such as headache and vertigo, depending on anaemia of the brain, or very likely upon simultaneous changes in its blood-vessels. Whether established valvular disease of the heart is curable is a question which can not be answered unconditionally in the negative. Of course in the great majority of cases it is in itself incurable; only its sequelae can be prevented or removed to a certain degree. In children and young people, however, cases some- times do occur, as we ourselves have seen, in which there are all the signs of a pronounced heart disease, but after a long time recovery is complete. Of course it is very hard to decide whether we really have to do with a valvular disease that has been cured, because simple dilatation of the heart, relative insufficiency of the valves, anaemic cardiac murmurs, etc., may easily be confounded with pure valvular disease of the heart. Among the dangerous intercurrent accidents in valvular disease we must make especial mention of embolic processes, which may occur suddenly and without warning. The different forms of embolism have been mentioned above, and also the possibility of cerebral haemorrhage in heart disease. Intercurrent acute dis- eases, such as typhoid and pneumonia, often, but not invariably, take a very severe and dangerous course in patients with heart disease, because they make increased demands upon the heart. Treatment of Valvular Heart Disease 1. Prophylaxis. — Our means for preventing the development of heart disease are very limited. To avert endocarditis in articular rheumatism by the present method of treating acute rheumatism with salicylic acid is impossible. The proba- bility of the onset of endocarditis may be lessened only so far as the whole dura- tion of the disease is often considerably shortened by salicylic acid. We can also do little in the way of prophylaxis against the development of heart disease that is chronic from the start, since the cause of the disease is in many cases wholly unknown to us. Those injurious influences deserve the most attention which may favor the development of arterial atheroma and its conse- quent chronic valvular disease. The chief factors in this connection are exces- sive physical exertion and high living, including the use of too much alcohol and tobacco; but the role which these play in the development of genuine val- vular disease is certainly much less important than their influence upon certain myopathic and nervous diseases of the heart (see the following chapter). [There is evidence that the alkaline treatment of acute rheumatism lessens the danger of cardiac complications (see page 686).] 2. Treatment of Compensated Heart Disease. — If we have to treat a heart disease which already exists, but which is at the same time fully compensated, our treatment must be chiefly hygienic. The patient must be made aware of his heart disease without making him needlessly anxious. He must be told that his further good health depends in great part upon his own conduct, his discretion, and his perseverance. The patient must avoid everything which makes great demands upon the heart, or which may have a directly injurious influence on it. All VALVULAR DISEASE OF THE HEART 335 violent bodily exertion, too intense mental work, and also all excesses in eating, drinking, smoking, etc., must be avoided. That the physician's directions will often collide with the demands of. the patient's occupation, as well as with his favorite amusements and his habits, should not deter the physician from demand- ing the fulfillment of his prescriptions, at least so far as possible. Treatment by drugs is usually unnecessary in compensated heart disease. We do not know a remedy which has a directly favorable action on heart disease. The protracted use of iodide of potassium, Fowler's solution, arsenite of antimony ("granules of antimony"), etc., has been recommended. The efficacy of these remedies is very questionable. We can always try them, if a mild disturbance makes a prescription desirable and other remedies are not especially indicated. Beyond this, the physician is usually contented with an endeavor to improve the appetite and nutrition of the patient by means of iron, quinine, and bitters. If there is a suspicion that the heart disease may be due to syphilis, a trial of iodide of potash may be made, but a brilliant result from the employment of anti- syphilitic measures is hardly to be expected, because the mechanical imperfections of the valves, leading to regurgitation and stenosis, can scarcely be remedied. The employment of baths in heart disease deserves special consideration. ISTu- nierous experiences go to prove that they are not only well borne by patients with heart . disease, but that they exercise a peculiarly beneficial and invig- orating influence upon the action of the heart. In this regard, the greatest reputation is possessed by the warm mud baths, which are rich in carbonic diox- ide, particularly those at Nauheim. Even where there is incipient failure of compensation, there will be marked improvement upon the use of these or similar baths (e. g., Kissingen). Patients may also employ at home either simple, or, still better, salt baths, at a temperature of 88°-90° (25°-26° R.). Where there is no marked disturbance of compensation, the methodical employment of gymnastic exercises, the so-called Swedish movements, has a certain value in the treatment of heart disease. Regular muscular movements certainly promote the circulation of the blood, and thus lighten the task of the heart. If they are carried out cau- tiously and with a proper consideration of the individual case, they are not infre- quently beneficial. The best measure for the amount of bodily exercise for pa- tients with heart disease seems, to the author, to be the subjective sensation of dyspnoea. Any patient who has no special signs of failing compensation may walk at a slow pace until he experiences distinct dyspnoea. As soon as this hap- pens he must stand still and rest. The author regards it as a great mistake to encourage patients to persist in their efforts regardless of difficulty in breathing. We should not forget that any disturbance of the circulation which occurs must involve the myocardium itself in its influence. That a change of climate may prove beneficial is self-evident. It is particularly appropriate that patients with a tendency to bronchitis or rheumatism should spend the winter South. 3. Treaiment of Ruptured Compensation. — As soon as the compensatory activity of the heart, in a case of valvular trouble, begins to be impaired, as soon as there is marked dyspnoea, diminution in the excretion of urine, and oedema, we must promptly lighten the burden of the heart by complete bodily rest. Many cases, particularly of mitral disease, are completely restored, even when there are marked symptoms of cardiac embarrassment, by mere rest in bed with simple diet and without any other therapeutic measures; but if the disturbance of com- pensation is more marked and persistent, the physician must have recourse to digitalis, a remedy which possesses undoubted value when the powers of the heart are impaired. Digitalis has the properties of making the separate beats more powerful, of lowering the pulse-rate by lengthening the diastole, and above all of heightening the arterial tension. Digitalis is thei'efore indicated in every case of heart disease when there is persistent disturbance of compensation, and if the 336 DISEASES OF THE CIECULATOKT OKGANS pulse is small, of low tension, and, above all, frequent and irregular; tlie desired effect of digitalis is to make the pulse slower, more regular, and especially of higher tension. Under the influence of the increase in tension thus produced and of the acceleration of the circulation, the disturbances of compensation often disappear in a surprising fashion; there is more abundant diuresis, the scanty, dark, concentrated urine of passive congestion disappears, the daily amount of urine increases, and the urine therefore becomes clear and of lower specific grav- ity. The oedema then disappears, the dyspnoea ceases, the head becomes free, the general condition improves, and, in brief, there may again ensue a complete com- pensation of the heart disease. This change is sometimes accomplished in a com- paratively short time, in a few days or weeks. It is very important to prescribe digitalis in a correct manner in order for it to be efficient. Much experience has shown that it is best to give it at regular intervals of two hours, in doses of one grain and a half (gramme 0.1) of the powdered leaves, either in capsules or simply in water ; so that the patient receives in the course of a day some five or six powders — that is, eight or ten grains (gramme 0.5-0.6) of digitalis. If the remedy is well borne we may continue it in this manner, but usually it is omitted during the night, to be resumed in the same way on the next day. As a rule, the distinct specific influence of digitalis is evident after the employment of ten to fifteen powders in the course of two or three days. This is recognized by the marked diminution in pulse-rate, the in- creasing strength and regularity of the pulse, and the improvement in the general symptoms. Instead of the powder we may employ an infusion of the strength of 1 or 2 parts to 150 of water. Of this a tablespoonful must be given regularly every one or two hours. In some cases, particularly if the patient has already become accustomed to the remedy, we may prescribe still larger doses, up to thirty or forty-five grains (grammes 2-3) and even more, daily. But in every case digitalis should be given in regularly repeated doses, so as to obtain by their com- bined action the full effect of the drug. It is entirely useless to prescribe digitalis in small doses at long intervals. The remedy must never be prescribed unless we can accurately watch the pulse and the heart's action, for only thus can we obtain clear indications as to the further employment or the omission of the drug. Often some unpleasant incidental effects appear simultaneously with the bene- ficial influence upon the heart's action. Among these are nausea, vomiting, and specks before the eyes. If the digitalis is omitted these symptoms usually cease, while the beneficial effect upon the heart may last for a long time. "With regard to these incidental and disagreeable symptoms, different patients vary greatly. Many bear digitalis very well, others very ill. From a therapeutic point of view it is particularly embarrassing if the nausea, vomiting, and other disagreeable symptoms appear before the digitalis has produced an effect upon the heart ; but in such eases we should not be too hasty in abandoning the drug, especially if it is urgently indicated. If the patient can not bear the infusion we should administer the digitalis in powders, or vice versa. If the drug absolutely can not be given by the mouth, it should be injected into the rectum in the form of an infusion of the strength of 1 or 2 parts to 100 of water. This should be warmed to the temperature of the body and given, after a cleansing enema has been em- ployed, once or twice a day. The subcutaneous employment of digitalis has also been recommended, in the form of an. infusion of the strength of 3 parts to 100, of which two or three syringefuls may be injected daily (lU 25-40), but with this we have had no personal experience. Sometimes, especially if the patient has not been carefully watched, the cumulative effect of digitalis is shown in severe symp- toms of poisoning, such as collapse, very frequent pulse, disturbance of vision, and dilated pupils. Then such stimulants must be employed as camphor, ether, wine, and strong black coffee. How often digitalis is to be used in the case of heart VALVULAE DISEASE OF THE HEAET 337 disease can be determined by experience alone. Many patients, particularly cases of mitral disease, may undergo treatment with digitalis twenty to thirty times or more, with the best results. Eve-ry time that signs of impaired compensation return, we must try digitalis again. It must be confessed that it will often be necessary gradually to increase the dose. As is the case with so many other rem- edies, the patient becomes habituated to the drug. There is no maximum dose, and we must find out by experience in each case what the satisfactory amount may be. Some patients become at last genuine " digitalis eaters," and are unable to exist without large doses of digitalis. We have ourselves seen a patient take seventy-five grains (grammes 5) of the powder daily. In very many cases, how- ever, the beneficial effect of digitalis even in the larger doses fails at last to appear. The remedy is no longer borne and it must be abandoned. This usually marks the last stage of the disease. JSTot infrequently we see patients with distinct symptoms of passive conges- tion, in whom the character of the pulse seems at first to contraindicate the administration of digitalis : the pulse is perhaps frequent, but regular and strong ; in other cases it is not rapid at all, but yet somewhat irregular; or it may be even infrequent and regular. Particularly in cases of aortic insufficiency is it often very difficult to determine whether we should give digitalis or not. With all patients of this sort it is, in general, worth while to make a proper trial of digitalis, since it may often be beneficial, and yet we should exercise especial caution and vigilance with regard to its effects. The attempt to employ the active ingredients of digitalis in a pure form (viz., digitaline, digitaleine, and digitoxine) instead of the drug itself, have not yet proved very successful. We should admit that we ourselves, in common with other observers, have seen good results follow the use of digitoxine. This has been introduced quite recently, and is to be given in tablets containing j^-q of a grain (one quarter of a milligramme) every one or two hours. It has no special advan- tages over digitalis, but certainly deserves to be recommended as a substitute for digitalis when that drug is ill borne or ineffectual. Tincture of digitalis, vinegar of digitalis, and other preparations are far less efficient than digitalis leaves, and, in our opinion, may be disregarded. The best opportunity for their employment is when patients with slight disturbance of compensation need to take small amounts of digitalis persistently. [Digitalis is used more commonly in this country in the form of the tincture. The urine affords a good guide as to the safety of the continuance of the drug ; as long as the renal secretion is sufficient in quantity, and increasing rather than diminishing, th,ere is no danger of the toxic effects. It is, consequently, a good plan to follow carefully the twenty-four-hour quantity of urine when this can be done. There are cases in which digitalis must be taken for long periods, but it should then be given only twice a day, with twelve hours' interval between the doses, unless the patient has ready access to his physician; there is then less risk of toxic symptoms. In mitral cases, with or without secondary tricuspid regurgitation, where the cyanosis and other symptoms show that the right heart is engorged with blood which it can not propel onward, the relief afforded by venesection, or by a dozen leeches in the hepatic region, may be very great. Until the veins are relieved either in this way or by free purgation,' digitalis and stimulants iire useless, and a resort to them results merely in a loss of time, and perhaps in the loss of a life which might be saved.] Caffeine deserves the first mention among the substances having a similar action, which have of late been recommended as substitutes for digitalis by Le- pine, Riegel, and others. Given in repeated small doses, a total of fifteen to 22 338 DISEASES OF THE CIECULATOKY OEGAl!TS twenty grains a day (gramme 1.0 to 1. 5), it often slows, regulates, and strength- ens the activity of the heart, and also increases the arterial pressure. The salicy- late of caffeine and sodium is chiefly used, three to five grains (gramme 0.2 to 0.3) of the powder, and also the benzocitrate of caffeine in the same or smaller doses. The latter is also given subcutaneously. Besides caffeine, we may also mention here adonis vernalis, convallaria majalis, and sulphate of sparteine; but none of these drugs is as reliable as digitalis. On the other hand, in cases of simple acute or chronic weakness of the heart, the tincture of strophanthus sometimes proves decidedly beneficial. It is given in doses of ten drops several times a day. In many cases it is an excellent way to combine digitalis with some of the drugs already named, or with others, par- ticularly diuretics. Thus, for example, we may often with advantage add one or two parts of the tincture of strophanthus to the infusion of digitalis, or we may prescribe powders containing a grain and a half (gramme 0.1) of digitalis and of diuretine fifteen grains (gramme 1.0) in each dose, or digitalis and calomel (vide infra) ; or digitalis and caffeine. A combination of this sort which is often very efficient is the following: Infusion of digitalis, 30 grains to 5 ounces of water (grammes 2 to grammes 150) ; sodio-salicylate of caffeine, 30 grains (grammes 2) ; tincture of strophanthus, 1 drachm (grammes 4) ; liquor potassii acetatis, 2 ounces (grammes 60); syrupi aurantii, 1 ounce (grammes 30). M. S. A table- spoonful every two hours. 4. Symptomatic Treatment. — Some symptoms which often occur in heart dis- ease demand a special description. Dropsy is a symptom of venous stasis, and disappears if compensation be restored spontaneously or by the use of digitalis. Complete rest in bed and eleva- tion of the swollen parts serve as the chief aid in removing the dropsy. Dropsical patients ought also to change their position in bed frequently, if possible, that there m'ay not be too much oedema collected in the dependent portions of the body. It is a good plan to wrap up the swollen arms and legs with flannel bandages under gentle pressure. Mild massage of the oedematous parts may sometimes be of advantage. The amount of liquid ingested is to be limited, if possible. Of in- ternal remedies, besides digitalis, which should invariably be first employed, and drugs of similar action, the true diuretics are to be considered, such as acetate of potassium, acetate of sodium, and diuretine. They are sometimes ordered in combination with digitalis and sometimes alone, particularly when digitalis can not be borne or it is not indicated. Calomel is sometimes especially efficient in cardiac dropsy. Its diuretic influence has lately been emphasized by Jendrassik and others. It is prescribed in powders of three grains (0.2 gramme) three to flve times a day. Often a very marked diuresis will be caused after one or two days, with rapid abatement of the dropsy. The administration of the remedy is stopped as soon as the diuresis begins. It is also omitted if stomatitis develops. We have already mentioned the advantageous combination of calomel wifh digitalis (digitalis, one grain and a half, gramme 0.1; calomel, three grains, gramme 0.2), five such powders daily. In the last stages of heart disease the patient's condition may be particularly distressing from the severe general oedema. It is then justifiable to remove the ascites or hydrothorax by puncture, or to let the oedema drain out by scarifica- tion of the skin — long incisions into the subcutaneous cellular tissue— in order to procure relief for the patient. The scarification of the skin, however, is dan- gerous, and is not to be employed without urgent indications, because erysipel- atous inflammation, etc., is apt to ensue at the point of incision. We can recom- mend little silver capillary trocars (the so-called Southey's trocars), to which a thin rubber tube is attached. By the aid of these trocars we can drain off large amounts of serum. We must always use great cleanliness, however, and the utmost VALVULAE DISEASE OE THE HEAKT 339 disinfection of the skin, wrapping the parts in sterilized gauze. In patients with heart disease it is not, as a rule, advisable to attack the dropsy by sweating, by hot packs, or pilocarpine. The dyspnoea of heart disease is usually the most distressing symptom of all. Here, too, our chief task is of course to restore the compensation; but this failing, we must try to relieve the dyspnoea symptomatically. Morphine is most efficient in this respect. In general, morphine is, next to digitalis, the most indispensable remedy in the treatment of severe heart disease. It is usually well borne, and procures great relief, especially if given subcutaneously. If we have to do with the last stage of the disease, we need not spare large doses. Otherwise, of course, caution is necessary. Chloral hydrate should be cautiously employed in heart disease. It is often, however, well borne and gives the patient rest and comfort. We have also pre- scribed chloralamide in cardiac cases, with good results. In practice we must often prescribe external applications to the chest, mus- tard-plasters, hot poultices, and also hot foot-baths with mustard, ashes, etc. In severe cases their action is slight. Acetate of lead in large doses sometimes seems to have a favorable influence in severe dyspnoea, especially with threatening pulmonary oedema. We give the powder, up to a grain and a half (gramme 0.1), every two or three hours, and it is often a good plan to add half a grain or a grain (gramme 0.03 to 0.05) of opium. We can also frequently obtain decided relief for the patient, particiilarly if constipated, by a vigorous drastic purge, with com- pound infusion of senna or gamboge. Inhalations of nitrite of amyl seldom have a beneficial effect. Palpitation, constant or paroxysmal, is treated by applying ice to the cardiac region; the "heart-bottles," made of tin, act very well. In patients with aortic insufficiency and very excited action of the heart, we may recommend the pro- tracted use of ice. Hot poultices also are sometimes beneficial. The narcotics are the most efficient internal remedies, especially morphine, which,' of course, we should reserve for severe cases. If the palpitation is of a lesser degree, we may try bromide of potassium, or bitter-almond water. The subcutaneous use of morphine is again by far the most potent remedy in the anginous attacks, associated with pain and a feeling of distress. We may also use cutaneous irritation, mustard-plasters, etc., hot compresses or poultices, and perhaps strophanthus, nitrite of amyl, or nitroglycerine. We may prescribe bitter remedies — tinctura amara (P. G.), or compound tinc- ture of cinchona — and muriatic acid for the loss of appetite, in case this is not improved by regulating the activity of the heart. In addition, we must always endeavor to get a regular evacuation of the bowels. For the attacks of f aintness and vertigo, occurring especially in aortic stenosis, as a result of cerebral anaemia, we may prescribe a horizontal position, and stimu- lants — wine, ether, and Hoffmann's anodyne. If the cerebral symptoms depend upon venous stasis, we try to remove it by ice, mustard-plasters to the neck, and thorough derivation to the intestines. Especial accidents and complications, like pulmonary oedema, infarctions, or apoplexy, are to be treated according to the usual rules. 340 DISEASES OF THE CIECULATOET OEGANS CHAPTEE III DISEASES OF THE MYOCARDIUM: Preliminary Remarks.— In valvular disease of the heart a disturbance of the circulation takes place because of the functional impairment of the valves, or the obstruction of the orifices of the heart ; but in the diseases which we are now to consider we have to deal with impairment of the structure and functional activity of the cardiac muscle itself, while the valvular apparatus of the heart remains in- tact. The expression myocardial diseases of the heart, in a strict sense, is too narrow, inasmuch as we probably have diseases of the ganglia and nerves of the heart associated with the muscular diseases. Indeed these nervous lesions may often be the essential change, but as yet our knowledge with regard to the patho- logical changes in the nervous apparatus of the heart is extremely limited; and, on the other hand, most of the organic diseases of the cardiac nerves probably in- volve some secondary changes in the cardiac muscle. We may therefore, in the classification and consideration of these conditions of the heart, limit ourselves provisionally to the disturbances of the cardiac function observed during the life of a patient, and the anatomical changes in the muscle of the heart found after death. It remains to be discovered later what is the part which the degenerations of the nerves and ganglia of the heart have in the development of these disturb- ances. We must also point out that in what follows we shall consider merely the primary muscular diseases of the heart, in which the change in the heart is the cause of all the essential symptoms. We shall quickly find how difficult it is in these matters invariably to draw a sharp distinction between secondary and pri- mary disease. 1. Interstitial Myocarditis {Fibrinous Degeneration of the Myocardium. Sclerosis of the Coronary Arteries) .31tiology and Pathological Anatomy. — The anatomical changes of inter- stitial myocarditis result in irregular-shaped spots of a whitish luster, often very numerous, interspersed through the cardiac muscle and corresponding to a par- tial or complete destruction of the muscle-fibers and the substitution for them of a firm, fibrinous, cicatricial connective tissue. These places, which are best found by making horizontal sections of the myocardium, occur particularly in the left ventricle, and especially at its apex and in its anterior wall; but they may also be found everywhere, and especially in the papillary muscles. Often we may observe them as somewhat glistening retracted spots on the endocardial or pericardial surface of the heart. The origin of this interstitial myocarditis was explained by the researches of Weigert, Ziegler, Tluber, and others. In a great majority of cases, though perhaps not in all, the changes just sketched are directly associated with changes in the coronary arteries and their branches. In almost every case we find in these vessels marked changes due to endarteritis, or arterio-sclerosis. In places where this change in the vessel causes marked diminution of its lumen, the corresponding portion of the myocardium is imper- fectly supplied with arterial blood, and in consequence the muscular fibers grad- ually degenerate, lose their nuclei, and change into a friable, cheesy detritus. In place of the destroyed muscular fiber there is a new growth of connective tis- sue. With ordinary endarteritis these processes are slow and gradual, but under certain circumstances there may be a somewhat rapid occlusion of the branches of the coronary arteries, because of thrombosis or embolism of proximal origiii. In such cases we have a genuine cardiac infarction, presenting a spot of ansemic necrosis, or sometimes a rather fresh brownish-yellow haamorrhagic infiltratic«l. INTEESTITIAL MYOCAEDITIS 341 Of course, this limited necrosis and interstitial new growth will not occur if, in spite of the existence of arterio-sclerosis, the direct supply of blood remains suflficient, or, if insufficient, is eked out by the collateral circulation. If the formation of connective tissue is extensive, the entire heart wall may become decidedly thinner, so that it yields to the internal pressure of the blood. This sometimes occasions in the left ventricle the bulging of a limited portion of the wall of the heart, so-called cardiac aneurism. A cardiac aneurism of this sort, and also an extensive fresh infarction, may exceptionally result in rupture of the heart with escape of blood into the pericardium, and sudden death. Of still greater importance, because far more frequent, is the formation, in places where the fibrinous process reaches to the endocardium, of parietal thrombi inside the heart. These sometimes give rise to embolism in distant organs. As to further pathologic changes in the heart we find that certain portions of the heart are not infrequently dilated or hypertrophied. The dilatation may, at least in part, be due to the diminished resistant power of the cardiac walls, but in case of hypertrophy we must always seek for special causes, inasmuch as sclerosis of the coronary arteries as such can not lead to hypertrophy of a portion of the heart. As a rule, the cause is easily discovered, either in an associated arterio- sclerosis, or in those factors, such as dissipation, which may occasion, simultane- ously with arterio-sclerosis, an idiopathic hypertrophy of the heart. Of course, we must also bear in mind the possible but exceptional presence of such compli- cating diseases as interstitial nephritis, or pulmonary emphysema. With regard to the right ventricle we know, also, that this portion of the heart must hyper- trophy as a result of congestion in the pulmonary circuit, when the left ventricle is permanently weakened. The causes of this most important, and by no means rare, fonn of myocarditis which we have just described, and which is due to sclerosis of the coronary arteries, must be the same as the causes of this latter affection. Often the sclerosis of the coronary arteries is merely a part of a general arterio-sclerosis, but we sometimes find comparatively marked changes in the poronaries, although there are no specially extensive atheromatous changes in the other arteries of the body, and again, when there is well-marked arterio-sclerosis elsewhere, the coronary ar- teries may show slight symptoms of disease, if any. In general, howevei% we have the same setiological factors to explain sclerosis of the coronary arteries as arterio- sclerosis in general. Often we shall find the cause in high living, and particularly in chronic alcoholism. In other cases, habitual muscular overstrain seems to favor the development of arterio-sclerosis, and clinical experience shows that an important cause of sclerosis of the coronary arteries, particularly, lies in great mental effort and excitement, which indeed are not infrequently combined with the above-mentioned factors — for example, in the case of extraordinarily active business men, speculators, high officials, and physicians. All these considera- tions go to explain the fact that sclerosis of the coronary arteries is seen far more often in the male than in the female sex. That age plays an important part is uni- versally aclaiowledged. It is true of interstitial myocarditis, as of arterio-sclero- sis in general, that, as a rule, persons are attacked in the second half of life, from forty years of age on. Finally, we must add that hereditary tendencies to the development of arterio-sclerosis in general, and sclerosis of the coronary arteries in particular, can not be denied. That form of disease of the coronary arteries deserves special mention which is of syphilitic origin, and therefore somewhat distinct from ordinary arterio- sclerosis, although the number of proved cases is not great. It is scarcely possible to doubt that there is a specific syphilitic endarteritis of the coronary arteries, giving rise to almost exactly the same symptoms as ordinary arterio-sclerosis. At 342 DISEASES OF THE CIECULATOET OEGAifS any rate, tliis point should in every ease be considered, for tlierapentic reasons if for none other (vide infra). Finally, it is to be added that there may be another form of chronic myocar- ditis not associated with primary chronic disease of the arteries, but ^vith an antecedent acute myocarditis as a sequel of severe constitutional infectious dis- ease, such as typhoid, diphtheria, sepsis, or scarlet fever. The careful histological examination of the myocardium by Krehl, Romberg, and others, in eases of dis- ease of this sort, has demonstrated acute inflammatory processes in the cardiac muscle. It might very well be that chronic interstitial myocarditis, with all its results, should gradually develop from acute processes of this sort. Still, the matter needs further clinical study. There is a secondary chronic myocarditis as a sequel of chronic endocarditis (valvular disease), but this is only exceptionally of any importance in itself. The endocarditic process may extend directly to the neighboring muscular layers of the heart, or there may occur, especially in association with aortic endocarditis, embolic infarctions, the development of which is the same as of the previously described thrombotic infarctions of the heart. Finally, there is the possibility that myocarditis and endocarditis might appear simultaneously. It has been maintained that myocarditis may develop as a sequel of acute articular rheuma- tism. The development of myocarditis in this way, if it ever occurs, is probably very exceptional. Clinical History. — ^We must first mention that sometimes quite extensive cica- tricial formation may be found in the cardiac muscle post mortem, without the occurrence of any manifest symptoms referable to the heart during life. We see, then, that the heart may, under some circumstances, undergo quite a considerable loss in its contractile substance without injury. In many other cases, however, the heart's capacity for work suffers so much that the same s\T3iptoms arise as in valvular disease. The course of such cases may be very chronic. The symptoms begin quite gradually. The patient first has a slight dyspnoea or palpitation, and a feeling of distress in the chest, but only from external causes, such as slight physical exertion. Sometimes there is marked general weakness and languor. The patients have an unhealthy sallow look. They become easily tired, feel depressed, and scarcely capable of any great bodily or mental exertion. The symptoms gradually increase, and just the same results of disturbance of the circulation appear as in all the other forms of heart disease. The difficulty in breathing becomes more marked, oedema occurs, signs of stasis in the liver, intestines, and kidneys appear — in short, the well-known type of general circulatory disturbance develops. Physical examination of the heart shows marked anomalies of the heart's action in all severe cases. The pulse is often irregular in regard to its rhythm and the intensity of its single beats, but the arhytlnnia may also be wholly absent in spite of the degeneration of the myocardium, as we have often convinced our- selves. The pulse is at first quite strong and full, later it becomes weaker, of lower tension, and at last sometimes very small and scarcely perceptible. It may be increased in frequency, but we quite often notice in chronic myocarditis, espe- cially in the early stages, a very characteristic and persistent slowing of the pulse to 60, 50, or even less, in a minute. With this slowness of the pulse there is also frequently irregularity of the heart's action, especially the appearance of occa- sional double beats (pulsus bigeminus). Percussion usually shows an increase of the heart's dullness, due to dilatation or hypertrophy of the heart, the increase being either general or chiefly on one side. Auscultation shows the absence of any murmur, and hence the absence of valvular disease. The heart-sounds are distinctly audible, and sometimes quite loud and valvular, but in the later stages often low and obscure. The pulmonic second sound is accentuated, when there INTERSTITIAL MYOCAEDITIS 343 is stasis of the pulmonary circulation. In several cases we found the second sound for a long time very plainly divided — reduplicated. We must also mention that sometimes in pure myocarditis a sj^tolic murmur is heard at the apex which is due either to a relative insufficiency of the mitral valve, or to its incomplete closure, as a result of defective musciilar action of the left ventricle. We must make particular mention of one symptom of sclerosis of the coronary arteries, which, although it is not pathognomonic, is by far most often seen in association with it and therefore has an important diagnostic significance. We refer to the attacks of so-called angina pectoris (stenocardia, heart-pang). These attacks of genuine angina pectoris (compare also the following chapter) consist in the sudden occurrence of pain in the region of the heart, extending into the back, the left shoulder, and the left arm even to the tips of the fingers. In severe cases the pain is extremely violent. It is as if the chest were squeezed in a vise. At the same time there is a decided feeling of anxiety and oppression, as well as complete loss of strength — a sense of impending death. The patient seeks some support, he can scarcely move, scarcely utter a few words in a whisper; the ex- tremities grow cool, the brow moist and cold. The attack may be directly fatal, but this is the exception. As a rule, the symptoms pas away in a few hours, and the patient gradually recovers. In many cases of sclerosis of the coronary arteries attacks of this sort occur very often, in varying severity. ISTot infrequently an attack may be due to some special cause, such as the bodily exertion of a long walk or climb, errors in diet, or mental excitement. In such cases bad news may cause death. With regard to the true essence of angina pectoris, we are confined to hypoth- esis. The ordinary supposition of a sudden paralysis of the left ventricle explains many symptoms, but not all. The intense pain indicates irritation of the sensory nerves. Sometimes during an attack the pulse grows small and irregular, but often also, as we have learned by experience, it may not be very greatly disturbed. There may or may not be, during an attack, acute dilatation of the heart. Besides genuine angina pectoris, attacks of cardiac asthma are not infrequent in chronic myocarditis. This differs from angina pectoris in that the peculiar pain and constriction are not present, while the distress for breath, the parox- ysmal dyspncea, is prominent. In most cases of this sort we probably have really to do with sudden weakness of the heart. Another symptom that has been re- peatedly observed in sclerosis of the coronary arteries is simple syncope, due to acute anaemia of the brain, and perhaps also referable to simultaneous sclerosis of the cerebral arteries. The general course of the disease varies considerably in different cases. Much depends upon the patient — e. g., upon his ability to take good care of himself. Sometimes dyspncea, a-dema, and other general symptoms of passive congestion are prominent, and in such cases the patient is alternately better or worse. Other cases are characterized by attacks of angina pectoris. The termination is in- variably unfavorable. It may either occur gradually with increase in the circu- latoiy disturbance, or with complete suddenness like a stroke. This important clinical fact of sudden apoplectiform death ("paralysis of the heart ") in patients with sclerosis of the coronary arteries, demands consid- eration. It usually happens in elderly persons in comfortable circumstances and good livers, who up to that time have not regarded themselves as really ill; but they have repeatedly had slight attacks of vertigo, of oppression, etc. Suddenly a sort of apoplectic attack comes on, often after some definite cause, after a ban- quet, or after some physical exertion or mental excitement. Death follows in a few moments, or after a deep coma that lasts for several hours or even days. The diagnosis often remains in doubt in such cases, especially if we have not known the patient previously. The autopsy shows, as the sole pathological lesion, 344 DISEASES OE THE CIRCULATOEY OEGANS a sclerosis of the coronary arteries, with a more or less extensive cicatricial f orma-'^ tion in the heart. Apparently in these cases the moment must suddenly arise when the supply of blood to the heart is insufficient, and thus death is caused. Experiments upon artificial closure of the coronary arteries, by Cohnheim and others, agree perfectly with the clinical facts above mentioned. Artificial narrow- ing of the coronary arteries may also be well borne for a long time, until suddenly both halves of the heart stand still in a condition of diastole. In such cases, also, the heart seems to stop suddenly, but sometimes there are frequent anginous at- tacks, and death occurs in one of them. Finally, it should be mentioned that sud- den death in sclerosis of the coronary arteries may also be caused by embolism of the trunk of the coronary artery, or, as in one case seen by the author, by the bursting of a focus of myocarditis with haemorrhage into the pericardial cavity. Diagnosis. — The diagnosis of chronic myocarditis is by no means always easy and certain. We must first determine that there is a cardiac lesion of some kind. This is usually evident from the secondary symptoms of stasis, the condition of the pulse, the area of cardiac dullness, etc. Then the question arises whether we have to do with a valvular disease or with a myopathic disease of the heart. Here auscultation must chiefly decide. The absence of a heart murmur, in spite of other definite signs of heart disease, speaks against valvular disease, but not with complete certainty. All murmurs may be absent in the last stages, especially with a high degree of mitral stenosis, and hence we may easily confuse mitral stenosis with myocarditis, particularly when there is marked arhythmia of the heart. On the other hand, we have already stated that in pure myocarditis, with the valves intact, functional murmurs may be present, which may lead to an erroneous opinion as to valvular disease. If continued study of the case has en- abled us to exclude valvular disease, it remains to distinguish between chronic myocarditis or sclerosis of the coronary arteries on the one hand, and the other diseases of the myocardium (vide infra) on the other. We regard it as impos- sible to make this distinction with absolute certainty. All the diseases named present the same clinical picture of cardiac insufficiency, but what the anatomical conditions may be which occasion this cardiac insufficiency we can at present only conjecture with more or less probability, during life. The following symp- toms are most characteristic of coronary sclerosis : persistent inf requency (slow- ness) of the pulse, particularly if associated with arhythmia; attacks of genuine angina pectoris; and the evidence of arterio-sclerosis in the brachial, radial, tem- poral, and other peripheral arteries. Persistent rapidity and arhythmia of the pulse occur in interstitial myocarditis, just as in other myopathic diseases of the heart; but arhythmia is, in general, far more common when there is actual myocarditis than when there is simple muscular weakness of the heart. There is self-evident difficulty in the diagnosis of cases with sudden apoplectiform paralysis of the heart, and in distinguishing them from apoplexy, embolism, pan- creatic haemorrhage, and similar causes of sudden death. Prognosis. — The prognosis is evident frora what has been already said. Re- covery is impossible, but even extensive cicatricial formation in the heart may probably last for years without causing much disturbance. We must always be prepared for disturbances of compensation, and the manifold sudden accidents to which patients with myocarditis are exposed, but we can not foretell the time of their occurrence. Treatment. — The treatment of chronic myocarditis must be directed first to the dietetic and hygienic care of the patient. This is of the greatest importance. Eor obese persons accustomed to high living, a moderate, simple diet must be accurately prescribed. Alcoholic beverages must be greatly limited or wholly forbidden, and not more than two or three cigars allowed per diem. Moderate bodily exercise is beneficial, and indeed necessary, for the promotion of the circuia- SO-CALLED IDIOPATHIC HYPERTROPHY OF THE HEART 34:5 tion and the more rapid diminution of the obesity, but the patient must be ear- nestly warned against too violent exertion, nor can great mental effort be per- mitted. In summer, a quiet life injhe country or some mountain region is to be advised, or, under suitable circumstances, the cautious use of the waters of Carls- bad, Kissingen, Marienbad, or ISTauheim. Frequent tepid baths or mud baths may usually be employed even at home with advantage. Of internal remedies, iodide of potassium has been specially recommended to be used persistently, in the amount of eight to fifteen grains (gramme 0.5-1.0) or more daily. Iodide of potassium enjoys a reputation for an especial specific action upon arterio-sclerosis in general, and ought therefore to have a beneficial effect upon arterio-sclerosis of the coro- nary arteries. We have ourselves seldom seen very striking results from its use. Probably iodide of potassium is of benefit in cases of syphilitic origin, and we therefore recommend it particularly when there is any suspicion of a syphilitic taint. With disturbance of compensation, and with abnormally frequent, weak, and irregular action of the heart, digitalis and similar remedies are indicated, just as in valvular disease. In cases with an abnormally slow pulse, we may use them, provided great caution is exercised, but we must also be governed by the other pre- vailing symptoms. In attacks of angina pectoris (see the following chapter) the subedit aneous injection of morphine is by far the most efiicient, and often an in- dispensable remedy. Also, the frequently enumerated cardiac stimulants, such as strophanthus, camphor, ether, and wine, ought to be borne in mind, and, finally, one may make trial of nitro-glycerine (-^V to ^V oi a grain, gramme 0.001-0.002) in alcoholic solution, and of nitrite of sodium (two or three teaspoonfuls daily of a solution containing 1 or 2 parts to 120 of water). The inhalation of a few drops of nitrite of amyl is also sometimes beneficial, but more often it has no effect. In cardiac asthma, stimulants are indicated, but often narcotics as well. Mus- tard-plasters, the application of cold and of heat, hot foot-baths, etc., are also employed. Sometimes even in the worst cases we see good results from the use of digitalis. With regard to regimen and mechanical treatment compare the following section on idiopathic hypertrophy of the heart. 2. So-called Idiopathic Hypertrophy of the Heart (Mechanical Strain of the Heart) .^Etiology and Greneral Pathology. — ISTot infrequently cases during life pre- sent all the symptoms of an uncompensated cardiac lesion, and yet the autopsy discloses merely hypertrophy of the heart with a greater or less degree of accom- panying dilatation. There is no lesion of valves, coronary arteries, or myo- cardium. The cardiac hypertrophy, which involves the left ventricle chiefly, but often both ventricles, can not be regarded as secondary in the ordinary sense of the word, for in the heart itself and in the other organs we find nothing which can call forth a secondary hypertrophy of the cardiac muscle — no valvular disease, no chronic nephritis, no general arterio-sclerosis, and no pulmonary emphysema. Hence we term these cases " primary idiopathic " cardiac hypertrophy, in the sense that we can not discover any other primary disease. Notwithstanding, we must in these cases also seek the cause of the cardiac hypertrophy in some excessive demand upon the cardiac muscle, and as there are no macroscopic anatomical or mechanical changes involving an increase in the cardiac activity, we must seek other circumstances occasioning a functional over- strain of the heart. Careful observation and investigation of cases of this sort have taught us a number of such causes. Among the most frequent is habitual embarrassment of the circulation by excess in eating and drinking. There can be no doubt that every time food is 346 DISEASES OF THE CIECULATOEY OKGANS taken in large amount there is a temporary increase in the activity of the heart, the frequency of the pulse, and the tension in the arteries. This is in part because the specific gravity of the blood is temporarily increased by the material taken into it, and in part because the products of metabolism in the blood have a direct stimulating action upon the heart or the blood-vessels, and finally, because an ex- cessive ingestion of liquids temporarily increases the total amount of blood. In brief, there are numerous persons of the more favored classes who indulge too freely in eating and drinking, and for years go to excess in the pleasures of the table; and in the case of such persons there is, during a great part of their life, although not all the time, that condition which the older physicians termed plethora. All these circumstances which we have mentioned occasion an increase in the demands upon the heart, especially its left ventricle. The heart performs this extra work laid upon it, and consequently becomes gradually hypertrophied. Erom what has been said, it is easy to understand why this form of cardiac hypertrophy is especially frequent in the obese, and particularly in men from forty to fifty years old, though sometimes much younger. We have seen by far the most frequent examples of it in great beer-drinkers, and so in persons whose business tempts them to excessive indulgence in beer, such as landlords, brewers, hop-dealers, butchers, and many others. Persons of this sort often drink for years, almost daily, four or five, or even eight or ten, litres (quarts) of beer. Let the reader consider what an amount of liquid, and at the same time of nourishment (for one litre of beer contains about fifty or sixty grammes [two ounces] of carbo- hydrates), is in this way alone introduced into the blood. This explains the great frequency of cardiac hypertrophy which Bollinger has shown to exist at Munich ; but the " Munich beer-heart " is seen with unfortunate frequency in other towns than Munich. The alcohol is probably not a factor in the development of the hypertrophy of the heart, but we may well suppose that it promotes, or at least hastens, the degenerative changes in the cardiac muscle, and particularly in the cardiac nerves, which at last render the heart's action inadequate and the circulation imperfect. Eor the development of cardiac hypertrophy in itself is a circumstance which does not impair the health, but rather preserves it ; only, ex- perience teaches us that no heart can uninterruptedly perform an amount of work which is physiologically excessive, and escape final exhaustion — the point of time depending upon the individual vigor and other associated factors. A second cause of idiopathic hypertrophy is persistent muscular strain. Every muscular exertion increases the demands upon the cardiac activity. There is an increase in the frequency of the pulse and in the amount of blood passing through the heart. If excessive bodily exertion is habitual for a considerable period of time, there finally develops hypertrophy of the heart, usually affecting both ven- tricles, but especially the left. Thus is explained the hypertrophy sometimes seen in blacksmiths, locksmiths, baggage-carriers, laborers in vineyards (" Tiibingen heart"), and soldiers after severe campaigns. Why this hypertrophy should sometimes occur and sometimes be absent, under apparently similar conditions, must be explained by the difference in the physiological capacity of the individ- ual. Here, too, the abnormality of the condition does not become evident till the functional ability of the heart begins to fail (" heart overstrain," " irritable heart"). In the third place, it seems that in some few cases of idiopathic hypertrophy of the heart, in which none of the causes yet named are operative, it is abnor- mal nervous irritation of the heart which increases its activity, and hence, finally leads to its hypertrophy. This is perhaps the explanation of many cases of cardiac hypertrophy in persons Avho have long been exposed to many sorts of psychical excitement. The cardiac hypertrophy of exophthalmic goitre (q. v.) may also be put in this category. ISTot infrequently we may conjecture in an SO-CALLED IDIOPATHIC HYPERTEOPHY OF THE HEAET 347 individual case that several of the causes mentioned have been operative simul- taneously in the development of the hypertrophy. Thus, idiopathic hypertrophy of the heart is seen particularly oft.en in individuals who have to undergo great mental strain and excitement, and at the same time are heavy drinkers. There is usually associated with the hjiDcrtrophy a dilatation, referable to the persistent over-distention of the ventricles during diastole. The weaker and more yielding the myocardium becomes with the course of time, and the more passive congestion affects the heart itself (particularly the auricles and right ven- tricle), the more the dilatation increases; and with it comes degeneration of the cardiac muscle, or, at any rate, functional weakness of the same, giving rise to symptoms of cardiac insufficiency. Clinical History. — Idiopathic hypertrophy of the heart may certainly exist for a long time without causing the patient any subjective disturbance. We have already emphasized the fact that it is precisely the cardiac hypertrophy which protects the patient for a time from the onset of marked symptoms. Prodromata may occur for a long time before severe disturbance sets in. Among these are palpitation, a certain sense of discomfort in the cardiac region, and slight dyspnoea. The symptoms begin when the heart can no longer respond to the de- mands made upon it, and when it begins to fail. Then all the symptoms of cardiac insufficiency arise, in just the same way as in valvular disease and in chronic myocarditis. Hence we need not go into the details of the disturbances of compensation again. The whole series of symptoms of stasis, as well as the attacks of angina pectoris and cardiac asthma, described in the preceding chapter, also occur in idiopathic hypertrophies and dilatations of the heart. Another subjective disturbance is the peculiar and often very annoying feel- ing of " fluttering " of the heart — that is, a momentary feeling of fluttering con- traction of the heart. This symptom indicates, probably, abnormal conditions of contraction, and must by no means be confounded with the numerous sensations which hypochondriacal and neurasthenic patients refer to the heart. If the action of the heart is irregular, and especially if there is a tendency to bigeminal pulsa- tion, many patients feel every bigeminal contraction as a jolt or stopping of the heart. The general course of the disease differs considerably in individual cases. Sometimes there is moderate difficulty in breathing for a long time, especially on any physical exertion. The patient often complains of great languor, or nervous irritability, and sometimes of attacks of vertigo and faintness, and a tendency to perspiration. The appetite is poor, and there is very apt to be constipation. The condition may become quite suddenly worse after any marked injurious influence, especially after great physical exertion or mental excitement. Physical examina- tion discloses all the signs of hypertrophy of the heart. In the first place, the left ventricle is usually enlarged, corresponding to the direct causes of the con- dition. This enlargement is often better appreciated by accurate observation of the apex-beat than by percussion. Later the right side of the heart also becomes hypertrophied ; dullness on percussion then extends over the lower part of the sternum, with epigastric pulsation and undulatory movements in the veins of the neck. The heart-sounds are pure, at first valvular, later sometimes muffled and feeble. We lay especial value on the characteristics of the first sound of the heart. A dull, indistinct sound is probably a sign of considerable dilatation, while a normal valvular sound indicates a vigorous systole. In general, there is per- sistent frequency of the pulse, at least in patients Avho are led to seek the physician because of beginning symptoms. Infrequency of the pulse probably indicates, in most cases, co-existent sclerosis of the coronary arteries (vide supra). The fre- quent pulse may for a long time remain regular, but it is not always so. So long as the left ventricle does its work well the pulse may be tense, and the second 348 DISEASES OF THE CIECULATOET 0KGA:N"S aortic sound valvular; but if the heart becomes insufficient the pulse grows small, feeble, often irregular; the heart-sounds grow faint, and not infrequently that bad sign appears which is known as hruit de galop or gallop rhythm, and con- sists in a peculiar reduplication of the first sound of the heart ; * for each beat of the pulse we hear three sounds over the heart. At the same time the dyspncea and oppression in the chest increase, the amount of urine diminishes, and oedema appears in the legs. We now have the complete picture of an uncompensated heart disease. With proper treatment the symptoms may disappear again; but, sooner or later, they return. Death finally ensues from general dropsy or from some complications or intercurrent attacks, among which we may mention em- bolic processes. Cases of sudden death (paralysis of the heart) from heart-failure occur not very infrequently, as we know from experience, in idiopathic hypertrophy of the heart independently of chronic myocarditis. Diagnosis. — It is by no means an easy task for the physician to make an absolute diagnosis of idiopathic hj^pertrophy of the heart. Sometimes, when the subjective symptoms suggest an examination of the heart, it is easy to make out an increase in the cardiac dullness and a displacement of the apex-beat; but in other cases the presence of emphysema, or obesity, or even of dropsy, makes the physical examination very difficult. If an enlargement of the heart has been demonstrated, we must then exclude valvular disease, especially mitral stenosis, and also secondary hypertrophy, as a result of chronic interstitial nephritis, or other causes. It may be difficult to rule out nephritis if the patient is suffering from passive congestion when he first comes under observation, for then it is often hard to say whether the albuminuria which may be present, is to be referred to actual renal disease, or to passive congestion. Even if we can exclude nephritis we have still to determine whether there is simple hypertrophy of the heart, or an interstitial myocarditis. To settle this question is, as we have already said (page 344), very difficult. ^Etiology is always important — for example, if there has been an excess in beer, or in muscular exertion. Frequent attacks of angina pectoris, arhythmia, and a lowering in the rate of the pulse, suggest sclerosis of the coronary arteries. Xot infrequently diseases of the myocardium are eon- founded with chronic obliterative pericarditis. When we consider this latter con- dition we shall refer again to the differential diagnosis. Treatment. — The main points in the treatment of idiopathic hypertrophy of the heart are, in general, exactly the same as for valvular disease and interstitial myocarditis. We may, therefore, refer the reader for these to the preceding chap- ters. There is, however, one point which we would like to discuss in more detail here, because it is especially prominent in the treatment of diseases of the myo- cardium. We refer to the so-called dietetic and mechanical treatment of circu- latory disturbances. Much of what we shall say here applies also to other forms of chronic heart disease. Efforts have long been made, but with fresh zeal of late years, because of Oertel's recommendation, to promote and improve the circulation by mechanical means as well as by such internal remedies as digitalis. The following considera- tions lead one to regard such an influence as possible : 1. Diminution of the Amount of Fluid in the Body, and particularly in the Blood {^^ Desiccation^^). — This is the point upon which Oertel lays the greatest * This sign is not infrequently found in idiopathic hypertrophy of the heart, iu myocarditis, and particularly in secondary cardiac hypertrophy following chronic nephritis. It has not yet been fully and definitely explained. Perhaps we have to do with an audible muscle-sound originating in the auricle, perhaps with peculiar irregularities in the contraction of the heart [for example, the contraction of the right and left ventricles not being simultaneous. — V.]. SO-CALLED IDIOPATHIC HYPEETEOPHY OF THE HEAET 349 Stressi He believes that he can diminish the amount of blood in the body by with- drawing liquids, and thus lighten the task of the heart and restore the normal cir- culation. On this view rest the proscription of excessive drinking and the limita- tion of liquid nourishment, such as soup. We must confess that it is difficult for us to decide upon this point. Numerous well-known physiological experiments prove that the body maintains its amount of blood with great tenacity at a cer- tain constant ratio. Inasmuch as the body is able by means of numerous ways (secretion and absorption of liquids) to make speedy compensation for variations arising through changes in the amoiint of water ingested, it is by no means proved that the total amount of blood in patients with circulatory derangements is in- creased; and if actually there is a retention of fluid in the body (as indeed is certainly the case where oedema has developed), yet the liquid does not collect in the vessels, but in the lymph-spaces of the interstitial tissue, or possibly in the cells of the parenchyma itself. That the total amount of water in the system may be subjected to great variations must certainly be admitted; but this assumption, that in circulatory disturbances there is an increase in the amount of water con- tained in the blood, is not proved. On the other hand, there are facts which con- tradict it, such as the actual number of blood-corpuscles and the specific gravity of the blood. That there should be any increase in the labor demanded of the heart, requires that a large amount of fluid should be added to the blood in a relatively short space of time, so that an actual, although extremely temporary, hydrsemic plethora should exist. If this process is very frequently repeated, it "will surely result in a permanent hindrance to the circulation. These circum- stances are, however, actually found only in certain patients, particularly in great beer-drinkers. In them, of course, to forbid the ingestion of fluid means to forbid the drinking of beer, and is therefore of the greatest benefit ; and we can not in- sist too strongly upon the necessity of this injunction in the case of corpulent beer-drinkers who are beginning to have some dyspnoea. It is not, however, in our opinion, permissible to apply this rule about liquids, as is sometimes done, to every patient without individualizing. For those who live temperately and are of spare figure, the amount of fluid ingested needs no special attention from the physician. 2. Strengthening of the Cardiac Muscle and Promotion of Compensatory Hypertrophy ty Increased Physical Exertion. — That the fulfilling of this indica- tion may be of great importance is certain, and Oertel lays the greatest stress upon inciting the heart to more vigorous contractions by means of suitable bodily exertion, and especially by methodical mountain-climbing, in order by these means to promote as much as possible the development of cardiac hypertrophy. This view is probably fully justified and of obvious utility in many cases of simple muscular cardiac weakness. If, however, we apply it to those cases of circulatory disturbance in Avhich there is valvular disease, or some other actual mechanical hindrance to the circulation, or in which the heart is already suffering from func- tional strain, the matter seems to be entirely different. For we must consider that we can not transfer unreservedly to the cardiac muscle our current views relating to the voluntary muscles of the body with regard to exercise and invigoration. The functional activity of the heart is minutely regulated by means of an especial reflex apparatus, independently of our volition. We know that every increased demand upon the heart's activity is in most cases directly fulfilled by an increased cardiac effort. Under proper conditions the most marked cardiac hypertrophy may develop in a completely bedridden patient. We must therefore consider carefully whether, in cases of this sort, the further increase of the demands upon the heart is judicious; whether it may not, on the contrary, contribute to a pjemature exhaustion of the myocardium. It certainly seems to us, and our opinion is fortified by practical experience, that the prescription of increased 350 DISEASES OF THE CIECULATOEY OKGAITS bodily exertion, such as mountain-clinibing', should always be given with great caution, and with consideration of the individual circumstances, if the physician desires to avoid unhappy consequences. It may indeed be claimed that a cer- tain measure of bodily exercise is very suitable for many patients with valvular and other similar cardiac lesions, but we hold that the benefit lies less in the re- sultant " invigoration of the cardiac muscle " than in the promotion of the venous circulation occasioned by the motion of the extremities and the deeper inspirations; or, in the obese, in the increased metabolism of fat occasioned by the increased muscular effort. Nevertheless, the inconsiderate prescription of muscular exertion has worked much harm. Long mountain trips have a great and unique value for those circulatory disturbances alone which are occasioned by obesity, or associated with simple weakness and slight dilatation of the heart. 3. Promotion of the Circulation hy Massage, Passive Movements, Gymnastics, and Baths.- — It can not be doubted that the first three of these are siiitable means for the promotion of the circulation, especially in the veins. We ought not to overestimate their value, but we are fully justified in the assertion that they may sometimes be employed with decided benefit in circulatory derangements. There are patients whom we dare not permit to take general bodily exercise, and for these there is sometimes great benefit in Swedish movements methodically and regularly pursued, especially in the form of what is called resisted movements with the arms and legs. The employment of massage is likewise useful in appro- priate cases, in which there are such symptoms as slight oedema and moderate dyspnoea. Thermic stimulation and baths are considered to have a strengthening influ- ence upon the heart. About this we have as yet little physiological knowledge, but we can not ignore the fact of the beneficial influence upon many cardiac patients, from the use of lukewarm, or warmer baths, and in particular the salt baths and natural brine baths, containing carbonic-dioxide gas, as employed at ISTauheim and Kissingen, and other places. To sum up what has been said, we must, in every case of beginning impairment of the circulation, give full weight to the considerations just enumerated. We must find out the patient's mode of life, and determine and regulate his diet and exercise according to the individual circumstances. In this we must always pay great regard to the patient's constitution, whether he is obese or spare; whether he is full-blooded or angemic ; whether his muscular strength is great or small. It scarcely seems necessary to go into every detail in this place, since all the points are repeatedly discussed in other portions of this book. We would refer particularly, however, to the chapter on obesity. 3. Hypertrophy of the Heart, Associated with Congenital Smallness of the Systemic Arteries {Hypoplasia of the Aorta) For a considerable time, physicians have occasionally noticed cases, of the sort to be described, in which weakness of the heart and disturbance of the circulation appear at a comparatively early age. The patient complains of palpitation, dysp- noea, and slight oedema. On examination we usvially observe ansemia, combined with more or less cyanosis. The cardiac dullness is extended toward the left, and the apex of the heart is displaced in the same direction. There is no marked dila- tation of the right ventricle till the later stages of the disease. The heart-sounds are perfectly clear, unless there may be a murmur due to relative insufficiency of the mitral valve, or due to imperfect muscular contraction. The heart's action is usually regular, but considerably accelerated; the pulse small and the arteries contracted, but often of high tension. We observe the ordinary symptoms of in- HYPOPLASIA OF THE AOETA 351 creasing circulatory disturbance, and finally death. Upon autopsy we find the heart hypertrophied and usually dilated. The valves are normal, but the entire aorta and, in most cases, probably, the other large arteries, are hypoplastic, though otherwise of normal structure. Such cases are termed congenital hypoplasia of the systemic arteries, and it is believed that the hypertrophy of the heart is due to the increased effort to drive the blood through these small vessels. In our opinion, this condition of the blood-vessels deserves full consideration in forming an opinion about idiopathic hypertrophy of the heart ; but, ordinarily, still other factors are potent at the same time, for we sometimes find this hypo- plasia at the autopsy of persons who showed no material disturbance of the cir- culation during life, and in whom the heart is of normal or even less than normal size. Virchow has called special attention to the fact that this sort of hypoplasia of the aorta and its branches is sometimes found in association with chlorosis, or, perhaps more correctly, with constitutional anaemia. In these cases the smallness of the reservoir diminishes the volume of blood* contained in it, but it does not have any marked influence upon the heart, which indeed has a less than normal burden rather than an excessive one ; so that we believe that in those instances of congenital hypoplasia of the aorta in which there is severe circulatory disturbance there is either coincident smallness and feebleness of the heart itself (vide infra), or an association of the hypoplasia with other influences unfavorable to the heart. There have been repeatedly observed cases of cardiac hypertrophy due to muscular strain (for instance, in soldiers), or due to excessive drinking, in which congen- ital hypoplasia of the aorta and its branches has been found in association with the hypertrophy of the heart ; and in the cases which we have ourselves seen and in which the diagnosis was confirmed by autopsy, there have almost always been some Other factors unfavorable to the heart besides this congenital abnormality of the blood-vessels. Indeed, one can easily understand that the same injurious influences which a normal circulatory apparatus might endure for a considerable time without much damage, would occasion premature symptoms if the vascular system were abnormally developed. The recognition of hypoplasia of the systemic arteries during life is probably in every case difficult, and scarcely ever absolutely certain. Important factors would be the existence of anaBmia and a tendency to shortness of breath and palpi- tation from early youth; and also the discovery by palpation that the circum- ference of the arteries was less than normal. The condition of the heart is to be determined in the ordinary manner. Prognosis and treatment must likewise be governed by the same principles as in other forms of heart disease. 4. Primary Weakness of the Myocardium (Congenital Weakness of the Heart; Weakened Heart; Acute Muscular Strain of the Heart; Toxic Weakness of the Heart) If there is a myopathic heart disease, and the heart is at the same time hyper- trophied, this indicates that for a considerable time the heart has done an un- usual amount of work. In such cases, therefore, it can not be that the heart has been feeble from the start. It must indeed have been able to do more than is normally demanded of it. It is not until a later period, when its power is impaired, that we can say that the heart is relatively or finally absolutely feeble. There are cases, however, in which the heart is originally feeble — that is, its functional powers are below normal. This weakness is certainlj^ in many in- stances, congenital. It may be expressed in the structure of the heart, the organ being tmusually small with thin walls, or merely in physiological incapacity, the organ being apparently of normal structure. In either case the heart can not 352 DISEASES OF THE CIECULATOEY OEGAI^S satisfy even the ordinary demands made upon it. Patients of this sort complain, upon the least exertion, of palpitation, shortness of breath, and a sense of pres- sure over the heart. The pulse is usually frequent or, at any rate, very easily accelerated; a short but rapid walk, for instance, may raise the pulse-rate to 120 or 140 beats per minute. In many cases there are never any severer symptoms. The patient remains through life feeble, and " with a weak heart " ; but if his mode of life is favorable the heart manages to maintain the circulation. Not so, however, if unusual demands are made upon it — as, for example, in the course of military service, or in mountain climbing, or in unsuitable raodes of life. Then more threatening symptoms of cardiac insufficiency appear, either suddenly or gradually, and ex- press themselves objectively in dilatation (or stretching) of the heart. In some cases the heart is not able permanently to satisfy even the ordinary demands made upon it. We observe all the symptoms of circulatory disturbance, and at last upon autopsy find a heart which is dilated, but not much hypertrophied. Cases of this sort are not very frequent, but they certainly do occur ; their recognition dur- ing life, however, is not easy, for it is difficult to distinguish simple dilatation from insufficiency which is subsequent to hypertrophy. We shall probably be able to determine that there is some muscular heart disease because of the increase in cardiac dullness, the smallness and frequency of the pulse, and the ordinary tokens of disturbed circulation, such as dyspnoea, palpitation, osdema, and the urine of passive congestion. If we consider carefully the history of the case and the presence or absence of special ^etiological factors, we may be able while the patient is still alive to make a probable diagnosis of simple dilatation of the heart, as a result of muscular weakness. Acquired muscular weakness of the heart should be distinguished from the con- genital variety. It is occasioned by the action upon an originally normal heart of influences which damage the myocardium or its nervous apparatus. We often see temporary conditions of muscular weakness of the heart in anajmia, or fol- lowing severe attacks of acute disease. Even in these cases there are such differ- ences as to indicate a difference in the original vigor of the heart. The same is true of acute muscular strain of the heart. Acute attacks of cardiac weakness are seen in the case of soldiers at maneuvers, or in laborious mountain climb- ing, such as has of late been so often undertaken in an ill-considered manner; and these attacks are usually associated with acute dilatation. There is a sudden and enormous increase in the demands made upon the heart; the amount of blood which, in a given period of time, must pass through the muscles is increased; and the heart is unequal to the task. It yields to the increased tension and dilates. The pulmonary circulation becomes congested, the pressure in the arteries falls, and we have all the clinical phenomena of cardiac insufficiency, including dyspnoea, cardiac asthma, and sometimes angina pectoris. If there is prompt cessation of the effort and medical assistance, the condition may be restored to normal and so remain. This, for example, we lately saw in the case of a young and healthy person who escaped drowning only by desperate efforts. But sometimes there re- mains behind a permanent weakness of the heart, whether because the single ex- cessive strain caused a permanent damage to the heart, or because the heart was already of less than normal vigor, and betrayed its weakness for the first time when this excessive demand was made upon it. Certain forms of chronic intoxication are among the causes which frequently lead to acquired weakness of the myocardium, or its nerves. The most important of these, from a clinical standpoint, is chronic alcoholism, the noxious influence of which upon the heart is universally recognized. Less frequent, but still of practical importance, is chronic nicotine poisoning, or, to speak in a more general and perhaps more correct manner, the influence of excessive smoking. This is FATTY HEAET 353 especially evident in persons who have smoked many strong-flavored Havana cigars. The symptoms consist of an unpleasant subjective sensation in the re- gion of the heart (fluttering, pressure, or palpitation), of slight dyspnoea, and ob- jectively of a frequent, irregular, or intermittent pulse. Other objective cardiac signs are not present, at least at first; but there may be still other symptoms of chronic nicotine poisoning, such as specks before the eyes, disturbance of vision, and dyspepsia. If smoking is stopped in due time, the symptoms may vanish. Otherwise, there follow severer disturba.nces of the heart, although in most cases there are other etiological factors also present, such as alcoholism and mental strain. With regard to prognosis and treatment, there are few special statements to be made. If there are signs of congenital weakness of the heart we must strengthen the constitution in every way possible, and we must seek to give the patient, on the one hand, the proper amount of protection, and, on the other hand, cautious and moderate exercise of the cardiac muscle, by means of medical gymnastics; and in other respects regimen and hygienic precautions are of first importance, from a prophylactic and therapeutic point of view. The treatment of acute and chronic weakness of the heart by such remedies as cardiac stimulants and digitalis is controlled by the ordinary rules. Finally, we may mention in this connection that obliteration of the pericardial sac by chronic pericarditis, or as a sequel of antecedent acute pericarditis (vide infra), sometimes occasions atrophy of the myocardium, with resultant feebleness and dilatation of the heart. Oases of this sort may readily be confused with primary cardiac dilatation. 5. The So-called Fatty Heart .^Itiology and Pathological Anatomy. — By the name of " fatty heart " we often mean, at present, two quite distinct conditions of the heart — the one an abnormal deposit of fat in the heart, and the other a fatty degeneration of the muscular fibers of the heart. Fatty overgrowth and fatty infiltration of the heart are usually merely symp- toms of great general obesity. At the autopsy of very fat people we sometimes find the heart entirely inclosed in a thick capsule of fat. The fat is situated chiefly in the external pericardium and beneath the visceral pericardium. It is usually abundant along the course of the larger vessels within the grooves of the heart, but in marked cases the fat also involves the muscular substance, so that many groups of fat-cells are interspersed between the muscular fibers. The heart itself is otherwise quite normal or somewhat hypertrophied or dilated. There are in some instances also present sclerosis of the coronary arteries and indurations due to myocarditis. We have already mentioned fatty degeneration of the muscular substance of the heart as a frequent result of valvular disease. In myocarditis and idiopathic cardiac hypertrophy, and in the hypertrophy secondary to chronic nephritis and pulmonary emphysema, we also meet with fatty degeneration. We often find fatty degeneration of the heart, as well as of other organs, in severe acute infec- tious diseases, in phosphorus poisoning, and in all marked primary and secondary anaemias. Under the microscope we find the muscular fibrillse studded with little drops of fat, which may be so numerous that the nuclei and the transverse stria- tion of the fibers are quite concealed by them. We often find, besides the fatty granules, albuminous granules, which disappear on the addition of acetic acid ("cloudy swelling" of the cardiac muscle). If the fatty degeneration is of high degree, we can easily recognize it with the naked eye. Beneath the endocardium, especially on the trabeculae and papillary muscles, we see very fine and delicate yellow points and strife. With great fatty degeneration, as in phosphorus poison- 23 354 DISEASES OF THE CIECULATOEY OEGAl^TS ing and pernicious anaemia, the whole cardiac muscle is manifestly yellow, and also soft and flabby. It is claimed that rupture of the heart may occur as a result, of marked fatty degeneration. In fatty degeneration of .the heart the fat comes from the decomposition of albumen in the muscular cells. The occasion of it is probably a defective supply of oxygen, which has either a general cause, as in ansemia and phosphorus poison- ing, or a local cause, as disturbed circulation in the heart in heart disease. The details of this are given in the chapter on ansemia (page 708). Clinical Symptoms. — Fatty degeneration of the heart has no characteristic clinical symptoms. In the conditions under which we know it is apt to occur, we can usually suspect it during the lifetime of the patient, but we can not diagnos- ticate it. We must also mention that the frequently expressed opinion, that fatty degeneration of the heart invariably occasions general cardiac weakness, is very often incorrect. In pernicious anemia there may be quite a strong and a per- fectly regular pulse up to death in spite of the most marked fatty degeneration,, and many pei-sonal observations lead us earnestly to dispute the view that fatty degeneration of the heart is to be regarded as the regular cause of cardiac insuf- ficiency, and the consequent disturbances of compensation. We have made micro- scopic examinations in many cases, and failed to find any sign of fatty degenera- tion in the myocardium, although during life the signs of cardiac insufliciency were well developed. In general, with our present knowledge, it is impossible- to establish definite relations between the histological condition of the muscular tissue of the heart and its functional activity during life. We can not say much that is certain in regard to the clinical synaptoms of a deposit of fat in the heart. " Fatty degeneration of the heart " always plays a far larger part in popiilar speech than it does in reality. It is certainly a fact that difficulty with the heart and respiration is very often observed in fat people. Ex- amination of the heart, which, however, is decidedly impeded by the thick pannicu- lus adiposus, often shows in such cases an increase of the cardiac dullness, a small and sometimes irregular pulse, and faint but clear heart-sounds. The disturbance- may be very considerable, attacks of angina pectoris and cardiac asthma may come on, and death may follow with increasing dyspnoea and general oedema. If one has opportunity to make an autopsy in such cases, there will be found no single, constant anatomical change as the cause of the cardiac disturbance, but usually idiopathic hypertrophy (vide supra), or, less often, myocarditic changes with sclerosis of the coronary arteries, and the like. Sometimes, but by no means invariably, there is, of course, a marked deposit of fat upon the heart itself, but the question arises whether this can directly and seriously embarrass the cardiac- activity. The fact is that we often have seen similar well-marked cases of fatty heart which during life presented no special cardiac symptoms. There would be- more reason in ascribing an unfavorable influence to the fatty infiltration of the cardiac muscle; but in such cases there is almost always a coincident atrophy of the muscular structure, so that it is questionable whether the fatty infiltration is to be regarded as actually the primary pathological process. We ourselves are far more inclined to the view that there is primary atrophy of the myocardium, with this fatty infiltration as a secondary phenomenon, similar to the frequent and well-known occurrence of secondary lipomatosis of atrophic voluntary mus- cles. At any rate, we are as yet entirely unable to recognize cases of this sort of fatty heart during life, and it is certain that they are much less frequent than the other myopathic diseases of the heart. Therefore we can not associate with the term " fatty heart " any uniform- anatomical and clinical conception. It would be better to speak of the " heart- of obesity" — that is, of all the manifold injuries to which the heart of obese per- sons is exposed. CAEDIAC IsTEUEOSES 355 According to our experience, simple idiopathic hypertrophy of the heart is certainly the most frequent of these conditions, and it would be very desirable if physicians would have more reg^ard to the facts of pathology, when they are inclined to make an off-hand diagnosis of fatty heart. Treatment. — A great part of the disturbance of respiration in fat people de- pends not upon the cardiac weakness, but on the corpulency itself. The great bulk of the body, and the hindrance to the activity of the respiratory muscles, are very important factors. Treatment directed against the respiratory disturbance must hence attack the obesity chiefly, and thus in many cases we also assist the action of the heart. The detailed description of the hygienic methods of cure to be employed here is to be found in the chapter on obesity (page 784). In regard to the special treatment of the cardiac symptoms in the obese, this does not differ from the rules that obtain in other forms of heart disease. CHAPTER lY CARDIAC NEUROSES 1. Angina Pectoris (Stenocardia). — Angina pectoris is not an independent disease, but a group of symptoms, to which we have had frequent occasion to re- fer already; but for a considerable time this symptom-complex may be the only sign of disease. It is the paroxysmal occurrence of an extremely violent pain below the sternum and in the region of the heart, associated with a feeling of the greatest distress and oppression (" prjecordial anxiety," " sense of impending death"). The pain is usually described as cramp-like, boring, and constricting It not infrequently radiates from the heart into the shoulders and the left arm, sometimes as far as the tips of the fingers. The beginning of the attack is usually absolutely abrupt. It may last a few minutes or half an hour, or longer. The attacks may be infrequent with intervals of weeks or months, or they may be repeated several times a day. Respiration during the attack is often unaffected, in which point genuine angina pectoris differs from cardiac asthma. Many patients indeed seek to lessen their pain by holding the breath, and sometimes even in angina pectoris the respiration is hurried and irregular. It must be pointed out that the symptoms of " pure " angina pectoris and the symptoms of cardiac asthma may be clinically much intermixed and confused. The pulse is usually rapid and small during an attack, and not infrequently irregular. Some- times, however, we find that, in spite of the most violent pain and distress, the pulse remains strong, quiet, and apparently normal. If the hand is placed upon the heart a peculiar wavy motion and " fluttering " is felt in a few cases, and this symptom the patient also perceives subjectively. The countenance is usually pale during an attack; the hands feel cool. Toward the end of an attack there is often abundant perspiration. We are as yet entirely ignorant as to the internal processes which are the foundation of angina pectoris. The condition is often compared Avith neuralgia, and spoken of as " cardiac neuralgia." Other investigators suspect that there is a painful contraction of the blood-vessels of the heart. It is certain that angina pectoris rarely occurs as an independent disease, or pure neurosis. Xothnagel described a vaso-motor form of angina pectoris (" angina pectoris vasomotoria "), in which there were at the same time distinct signs of vascular contraction in the extremities, as indicated by pallor, cyanosis, and parsesthesife. In the case of excessive smoking, also, angina pectoris sometimes appears as a result of 356 DISEASES OF THE CIRCULATORY ORGAl^S chronic tobacco poisoniBg, without any other demonstrable change in the heart. Similar attacks may occur after strong mental excitement, but these have more or less connection with certain forms of hysterical and neurasthenic attacks, bearing a merely superficial resemblance to angina pectoris. The true angina pectoris is most often seen as a symptom in association with certain diseases of the heart and aorta, particularly sclerosis of the coronary arteries, insufficiency of the valves, aneurism of the root of the aorta; less often, idiopathic hypertrophy of the heart, and hypertrophy secondary to interstitial nephritis. The way in which the other symptoms of these conditions may be conjoined with the anginous attacks is sufficiently clear from their presentation in a previous chapter. We can not speak of the prognosis of angina pectoris as a distinct entity. In general angina pectoris is certainly of evil omen, and occasionally death may occur during the attack. With regard to the symptomatic treatment of angina pectoris, there is no doubt that in severe cases the greatest relief is obtained from a subcutaneous in- jection of morphine. We confess that the employment of morphine in severe heart disease always demands the greatest caution, but yet experience shows that in numerous instances this remedy is excellently borne, and most beneficial. Among other remedies should be named chloral and chloralamide, which also are to be employed with caution, but which sometimes have a good effect ; nitroglyc- erine to the amount of A to A of a grain (gramme 0.001-0.005), which is highly praised by many physicians; also nitrite of sodium, and inhalations of amyl nitrite, ether, or chloroform. If there are decided signs of cardiac weakness, camphor, strophanthus, and alcohol are to be employed as stimulants. An ice- bag may be placed over the heart, and sometimes, also, hot applications are of benefit; mustard-poultices, hot foot-baths, and the like are also frequently pre- scribed in practice. We must always bear in mind the general treatment of the underlying condi- tion, as well as the employment of purely sym.ptomatic remedies. Special atten- tion should be directed to any setiological factors, such as muscular strain, men- tal excitement, alcoholism, or excessive smoking. If we have to do with the " purely nervous " form of angina pectoris, without any physical signs of change in the heart, we must of course avoid the use of the stronger narcotic remedies so far as possible, and lay the main emphasis upon the general treatment of the nervous system by means of electricity, cold-water cures, and psychical influences. [In well-marked angina sudden death during a paroxysm is not very rare. In Dr. Arnold, of Rugby, the first attack proved fatal. The patient may, however, live for years — cases of survival for upwards of twenty, and one even of thirty, years being recorded. Flint has known recovery to occur. The prognosis depends somewhat on the condition of the cardiac valves and walls; but changes, espe- cially in the latter, may escape detection by any save a very skillful observer. Walshe states that in every one of twenty-four cases he examined during life he found physical signs of changes either in the heart, the aorta, or both. The experience of Balfour and Latham is similar.] 2. Nervous Palpitation. — By " palpitation " we understand the subjective perception of the movements of the heart. It is usually excited by increased ac- tion of the heart, but there is no constant relation between the intensity of the cardiac pulsations and the subjective feeling of them. We sometimes observe that patients with aortic insufficiency do not perceive the very strong action of their hypertrophied hearts, while in other cases a patient complains of a trouble- some feeling of palpitation, although the action of the heart does not appear objectively to be especially increased. We term cases " nervous palpitation " if the patient complains of palpita- tion when a physical examination of the heart shows no anatomical change in it. CAEDIAC NEUROSES 357 As a rule, in these cases we really have to do with a heart whose action is increased by abnormal nervous influences. In many cases the palpitation arises from slight external causes, which may give rise to little or no palpitation in a healthy per- son, as, for example, after the slightest mental excitement, after any slight phys- ical exertion, after taking food, after indulging in certain drinks, such as tea, coffee, wine, or beer, or after assuming certain positions, as in lying on the left side. Here, then, we have to do with an abnormal sensitiveness of the heart to external irritation. Usually the increase in vigor of the heart's action is associ- ated with a decided increase in its frequency. We have often seen patients with nervous palpitation who had a pulse-rate of 140 to 160 beats a minute after com- paratively slight exertion; but in other cases there is apparently a sort of hyper- sesthesia of the patient w^ith regard to the motions of the heart, so that contrac- tions of normal strength and rapidity give rise to disagreeable sensations. The patient rarely complains of continuous palpitation; it usually occurs in more or less sharply defined paroxysms. Very commonly in pure nervous palpi- tation we have to do with persons who, in general, suffer from nervous, hysterical, and neurasthenic symptoms, or they are anaemic persons, chlorotic girls, etc. ; but, on the other hand, nervous palpitation may occur in very full-blooded, " plethoric " subjects. Often hypochondriasis plays an important part, and dread of heart disease and the thought of its possible consequences excite a palpitation which confirms the patient in his delusion. The diagnosis of nervous palpitation can be made only when repeated careful examination shows no objective abnormality in the heart. In many cases, as when there are anaemic murmurs, the decision may be quite difiicult. We must always pay particular attention to the whole constitution and the general impres- sion which the patient makes. It is often especially difficult to distinguish between purely nervous palpita- tion in a heart otherwise functionally normal, and conditions of congenital or acquired weakness of the heart (vide supra). The prognosis is so far favorable in that the disease is not dangerous. In many cases improvement and final recovery may be effected, but other cases, of course, resist all therapeutic efforts very obstinately. The treatment must first be directed to improving the patient's general con- stitution. The antemic are to be given iron, quinine, and strengthening diet. We put full-blooded persons, however, on scanty fare, and prescribe for them bitter waters, or a bath cure at Marienbad or Kissingen. When there is hysteria or neurasthenia, it requires special treatment. If the patient is hypo- chondriacal, of course the main thing is for the physician to reassure him. We should avoid all the influences which seem to excite palpitation. As a symptom- atic indication during an attack we should recommend the patient especially to keep quiet. The use of cold to the cardiac region — cold compresses and ice-bags — often acts beneficially. On the other hand, however, it is to be noted that a tendency to palpitation associated with cardiac weakness may often be allayed by methodical exercise and the invigoration of the cardiac muscle consequent thereupon (see the preceding chapter). Among internal remedies we must employ nervines, and in severer cases even narcotics. Among the former we would men- tion especially ethereal tincture of valerian and bromide of potassium, which have repeatedly done us good service. Digitalis is lasually of little value in pure nevi- roses of the heart, but we may give it as an experiment, say fifteen to twenty drops of the tincture with the same amount of cherry-laurel water. 3. Tachycardia (Paroxysmal Tachycardia). — A peculiar and quite rare neu- rosis of the heart, tachycardia, consists of an enormous frequency of the pulse, coming on in paroxysms, up to 160-200 beats and more a minute. 358 DISEASES OF THE CIRCULATORY ORGAN'S We have already mentioned these attacks as a rare symptom in mitral and aortic valvular disease and in diseases of the myocardium, but precisely similar attacks occur as a pure neurosis without demonstrable lesion of the heart, particu- larly in anaemic, nervous, or obese individuals. We saw one very well-marked case in a lady with extreme neurasthenic melancholia. The attacks occurred many times a day, each lasting only a few minutes. We were often able while feeling the pulse to notice that it suddenly became extremely rapid, and then in a brief time almost with equal suddenness resumed its approximately normal rate. We have seen many similar attacks of genuine tachycardia, although not so extreme, in young and neurasthenic individuals, following muscular exertion — for example, in soldiers. Similar states develop sometimes after diphtheria {q. v.), and after other acvite infectious diseases ; but in such instances the tachycardia is usually more continiTOUS and not so distinctly paroxysmal. In men we must consider the possibility of the action of injurious habits, such as drinking and smoking. The individual attack usually begins quite suddenly, by day or by night, sometimes without any cause, but often it is apparently pro- duced by certain exciting causes, especially at times by overdistention of the stomach. The patient feels that the attack is coming, he becomes anxious and restless, and looks pale ; but there are not, as a rule, at least according to our experience, any symptoms like precordial anxiety, dyspnoea, or attacks of faint- ness. We notice in the heart itself, during the attack, chiefly a great acceleration of the heart-sounds. We sometimes hear indefinite, functional murmurs. The action of the heart is often quite regular, but there is not infrequently manifest arhythmia during the attack. Acute increase of the heart's dullness has been observed during the attack. We have repeatedly been able to verify a marked temporary dilatation of this sort, particularly in patients with heart disease, and also in one case of paroxysmal tachycardia affecting a sufferer from cirrhosis of the liver. In other instances and especially when the tachycardia is a mere neu- rosis, no such dilatation of the heart can be made out. We know little that is definite as to the nature of the attacks. The affection is usually regarded as a temporary paralysis of the vagus. We may also state here that paroxysmal and constant tachycardia have also been repeatedly observed in anatomical lesions of the cardiac nerves and their centers, in tumors and other affections in the vicinity of the medulla oblongata, and in compression of the vagus in the neck from new growths, and aneurisms. The prognosis of tachycardia depends first upon the nature of the underlying disease. We do not know whether a permanent recovery is possible in idiopathic cases, but we can always succeed in improving the condition. The treatment dur- ing the attack consists in enjoining complete bodily rest, and in applying ice to the heart. Such sedatives as bromide of potassium, water of bitter almonds, and tincture of valerian are particularly beneficial in the '•' purely nervous " cases. Sometimes the physician may even be consti^ained to the cautious injection of small amounts of morphine. In other respects our treatment is determined mainly by the underlying condition, if known. [If there is reason to think that the stomach is overloaded, gentle measures should be taken to empty it. — V.] The best way to guard against the return of the attacks is to give precise hygienic directions, suited to the patient's constitution and manner of life. The contin- ued use of iodide of potassium has sometimes seemed to us to be of service. PERICARDITIS 359 SECTION II Diseases of the Pericabdiuai CHAPTER I PERICARDITIS {Inflammation, of the Pericardiu7)i) etiology. — Pericarditis seldom appears as a primary idiopathic disease. It is usually merely a sequel or a complication of other diseases. Thus, it is observed with particular frequency in the course of acute articular rheumatism, where it appears sometimes alone, sometimes in combination with acute endocarditis. It is not impossible that some few cases of apparently primary acute pericarditis belong, from an setiological standpoint, to acute articular rheumatism — that is, they are excited by the same pathogenic factors which exceptionally attack the pericardium alone, without simultaneous participation of the joints in the disease. This supposition is rendered probable from the later course of many such cases. Eor instance, arthritis may ensue. Cases of secondary pericarditis, unassociated with articular rheumatism, occur, although much less often, in other acute infec- tious diseases, among which scarlet fever, measles, and septico-pysemic processes, as well as scurvy and purpura haemorrhagica, deserve especial mention. In sepsis and pyaemia the pericarditis is purulent, and in purpura, hsemorrhagic. Among the chronic diseases in the course of which pericarditis sometimes appears we must mention especially chronic nephritis. We have seen hsemorrhagic peri- carditis in association with leukaemia. Pericarditis sometimes occurs also in the victims of carcinoma, but here it is probably dependent upon a secondary septic infection. Finally, it should be mentioned that severe hsemorrhagic pericarditis is seen comparatively often in alcoholic subjects, and apparently as a primary •disease. Often it is really tubercular, but by no means always; and if not, the author is inclined to regard it as a primary hsemorrhagic inflammation, analogous to hsemorrhagic pachymeningitis or hsematoma of the dura mater. A large number of cases arise from an extension of the inflammation from the vicinity. Thus we not infrequently see pericarditis as a result of pleurisy, espe- cially on the left side, and in pneumonia complicated with pleurisy. New growths and ulcerative processes in the oesophagus, in the vertebrse, in the bronchial glands, or in the lungs, also lead at times to perforation into the pericardium and a con- sequent inflammation. It is not settled whether the pericarditis, which appears in the course of chronic valvular disease, is also to be regarded as arising from ex- tension by contiguity. We have thought of this possibility, because we have been struck with the fact that secondary pericarditis is especially frequent in valvular disease of the aorta, suggesting a direct propagation of the inflammatory genus through the aortic wall to the pericardium. Still, it must of course be allowed that this form of pericarditis may have an independent origin, particularly in cases of mitral disease. Pericarditis may also develop as a result of myocarditis, abscess of the heart, etc. Tuberculosis plays a very important part in the setiology of pericarditis. No small number of apparently primary cases of pericarditis turn out at the autopsy to be tubercular. This seems to come on in quite an isolated way, or as one symptom of a special localized form of tuberculosis, which we term tuberculosis of the serous membranes. In many cases we can discover the origin of a tuber- cular pericarditis in the direct extension of a tubercular pleurisy. In apparently primary cases the occurrence of the infection may sometimes be explained bj^ the 360 DISEASES OF THE CIECULATOEY OEGANS discovery of a tubercular lymph-gland, which has broken through into the peri- cardium. Pericarditis is usually a disease of youth and middle life, but it may also occur in advanced age. Pathological Anatomy. — Ordinary pericarditis involves the internal surface of the pericardium in either a circumscribed or diifuse manner. Inflamma- tion of the outer surface of the pericardial sac is distinguished as external pericarditis (vide infra). The anatomical processes in pericarditis are precisely analogous to those in inflammations of the serous membranes in general, especially of the pleura. We usually divide pericarditis into fibrinous, sero-fibrinous, hsemorrhagic, and purulent (or ichorous) forms, according to the character of the exudation. The fibrinous and sero-fibrinous forms, with an abundant fluid effusion into the peri- cardial cavity, are the most frequent, occurring in articular rheumatism, in valvu- lar disease of the heart, etc. Both layers of the pericardium are covered with masses of fibrine, which often show a reticular or villous arrangement (cor villosum). Besides this, we find more or less of a fluid effusion which distends the pericardium. The fluid is of a serous nature, contains more or less numer- ous flakes of fibrine, and is turbid from the admixture of cells — pus-corpuscles, and, in part, desquamated endothelium. A purulent pericarditis is always the expression of a specific infection of the pericardium. It is seen in pysemic dis- eases, as a result of empyema, and in perforation of abscesses, cancers of the oesoph- agus, etc., into the pericardium. A hsemorrhagic effusion is seen chiefly in tuber- cular pericarditis. In this we flnd miliary tubercles, and little cheesy nodules in the inflammatory new growths, besides all the signs of inflammation. The specific tubercular changes are sometimes recognizable with the naked eye, but at other times we have to use the microscope to find them. Hsemorrhagic pericarditis also occurs in general hsemorrhagic diseases, such as scurvy, and in weak and debili- tated persons, especially drunkards (vide supra). In long-continued pericarditis the cardiac muscle almost invariably undergoes changes. The heart is usually flabby and dilated, and the muscle often shows fatty degeneration. After the pericarditis has lasted a long time there is often considerable atrophy of the cardiac muscle, which is partly replaced by fat tissue. We have already mentioned the occurrence of pericarditis in connection with valvular disease and degenerations of the myocardium. In favorable cases of pericarditis we may have a perfect recovery. The so- called maculcB tendinece sometimes remain in the pericardium as residua of a past circumscribed pericarditis. In some cases the pericarditis leads to an adhe- sion of the two layers of the pericardium to each other, and obliteration of the pericardial cavity (vide infra). In many cases a chronic pericarditis finally de- velops from the acute form, or the whole affection takes a more chronic course from the outset. In this way chronic adhesions of connective tissue arise, and great thickening of the pericardium, but the amount of fluid is usually small. Sometimes the chronic pericarditis is interrupted by an acute exacerbation of the disease. Clinical Symptoms. — 1. SuhjecUve Symptoms, General Symptoms, and Fever. — Mild forms of pericarditis may develop, as in the course of an acute articular rheumatism, without causing any subjective symptoms. They are discovered only by a careful physical examination of the heart. In severe cases, however, the peri- carditis causes violent subjective symptoms, which of course have in themselves little that is characteristic. On careful questioning we often find that there is pain in the cardiac region, or not infrequently in the epigastrium. This pain is of decided diagnostic impor- tance, but it does not always exist. PEEICAEDITIS 361 A general feeling of constraint and distress is almost constant in all acute cases of any severity, and so is a feeling of dyspnoea, which may increase to the highest degree of orthopnoea. The patients, often complain of headache. In severe cases they become stupid and comatose. It is easy to understand that extensive pericarditis must impede the motions of the heart. Probably the most important way in which it does this is by in- creasing the tension in the pericardium, and thus embarrassing the diastole of the ventricles, so that the cavities of the heart are not normally filled and general dis- turbance of the circulation ensues. Furthermore, the pericarditic deposits and adhesions, and such changes in the myocardium as may occur, interfere with the cardiac systole. Thus are explained the early signs of diminution in the amount of blood received by the arteries, as shown by pallor and cerebral anaamia; the distention of the systemic veins, as shown by cyanosis ; and the disturbance of the pulmonary circulation, causing dyspnoea. The dyspnoea is also increased in large pericardial effusions by the mechanical pressure of the distended pericardium on the left lung. Acute pericarditis is usually associated with fever. This has no special type, and usually keeps at a moderate height— 102° to 103.5° (39°-39.8°C.)— but it often exhibits considerable variations. In cases of recovery the fever declines by lysis. Chronic pericarditis may run its whole course without fever. 2. Physical Signs — Inspection. — The general hne of a patient with severe pericarditis is pale, but also more or less cyanotic. He has an anxious expression. He lies with the upper part of the body raised, or he sits up in bed. The breath- ing is usually rapid, labored, and somewhat irregular. The veins in the neck are swollen and prominent. We very often see marked undulating or pulsating movements in the jugular veins, as a result of stasis. The cardiac region seems unusually prominent in all cases with much effusion, and the intercostal spaces there are flattened out. We sometimes detect a slight oedematous swelling of the chest-wall itself. If the action of the heart is powerful and the exudation small, the heart's movements may be distinctly visible. In other cases they are seen only faintly, and they may be noticeably diffuse. If the exudation is abundant, or if adhesions occur (vide infra), they may disappear altogether. Palpation in the milder cases shows the apex-beat in its normal position and of about normal strength ; but if the amount of the pericardial effusion increases, the heart is pushed away from the chest-wall by it, and hence the heart-beat grows weaker until it disappears entirely. In such cases it is sometimes to be felt again if the patient bends forward or lies on his left side. In the rest of the car- diac region we sometimes feel the movements feebly, but they entirely disappear as the effusion increases. There is diagnostic importance in the contrast between the great extent of cardiac dullness (inde infra) and the faintly distinguishable motions of the heart, with absence of a distinct apex-beat and any marked epi- gastric pulsation. In some cases, by laying the hand flat on the chest, we can feel the rub of the rough pericardial surfaces against each other. The pulse is usually accelerated, and in severe cases it becomes irregular. In every large effusion, as we have already said, the tension and height of the pulse are diminished. In severe cases the pulse sometimes becomes very small and weak, but, when the heart is otherwise normal and strong, it may also remain quite strong — and indeed this condition of the pulse, in contrast to the gi'eat weaken- ing of the heart-beat, is sometimes of diagnostic significance. In some eases with a large pericardial effusion we have seen a manifest pulsus paradoxus — that is, a diminution or a complete disappearance of the radial pulse on every inspiration. Changes in percussion-resonance are evident as soon as the pericardial sac is distended with exudation. The so-called triangular shape of cardiac dullness is 362 DISEASES OF THE CIECULATORY ORGANS regarded as especially characteristic of large pericardial exudations. The blunt apex of the triangle is found above in the second or third left intercostal space, near the edge of the sternum. The lateral boundaries run obliquely to the right and downward to about the right parasternal line, and to the left and downward to the left mamniillary line, or beyond. The broad base of the triangle which lies below is usually not to be defined by percussion, on account of the adjacent left lobe of the liver. On the border of the dullness we often find a tympanitic reso- nance due to the retraction of the adjacent lung. In general, the author's personal experience forces him to say that we must not be too dogmatic in the establishment of special shapes of cardiac dullness, as peculiar to pericarditis. The fact of enlargement of the area of cardiac dull- ness, and the marked sense of resistance upon percussion, are important signs, but there is a considerable variety in the shapes of the dull area, although extension of the dullness upward and to the right may be regarded as particularly frequent. According to Ebstein's observations, the first change in percussion in incipient •exudation is usually an extension to the right of the heart's apex, in a triangle between the heart and the liver. The area of the dullness depends, of course, in the first place, upon the amount ■of the effusion, but we must take special notice that in regard to this the relation is not constant. In old cases of pericarditis especially we sometimes fijid the cardiac dullness very extensive, while the autopsy detects only a little fluid in the pericardium. This is explained partly by a secondary dilatation of the heart, and partly by a persistent retraction of the lung. It is an often-mentioned but seldom available diagnostic sign of pericarditis that in many cases the still perceptible apex-beat lies within the cardiac dullness, since the pericardial effusion extends farther to the left than the heart itseK. It is also worthy of note that the dullness in pericarditis often shows very great changes when the patient changes his position. The dullness is more extensive when the body is erect than when lying down, and when the patient lies on his side it sometimes shows a lateral displacement of several centimetres. The same changes, however, though rarely so marked, also occur in a hypertrophied heart. The characteristic pathognomonic auscultatory sign of pericarditis is the peri- cardial friction-rub. This arises during the movements of the heart from the rubbing of the rough and inflamed pericardial surfaces against each other. The friction-rub is absent in pericarditis if the rough surfaces of the two layers of the pericardium are separated from each other by a considerable fluid effusion, or if they can no longer rub against each other from an adhesion of the layers of the pericardium. We usually hear the friction-rub loudest in the neighborhood of the base of the heart, but it may also be heard at other parts of the heart. In general the adventitious sounds of pericarditis are not transmitted to any great ■distance. The quality of the sound is described as rubbing, grating, or scratching. The friction-rub may be heard chiefly either during the systole or during the diastole of the heart, but it is in general not often closely associated with the phases of the heart's action. We sometimes find it intermitting frequently, and jerky. The intensity of the friction-rub sometimes varies with the phases of the respiration. It is usually louder on inspiration, but sometimes on expiration. If the patient changes his position, the intensity of the sound is sometimes altered. It is louder when sitting up than Ijing down, etc. The friction-rub often sounds louder if the stethoscope is pressed fimily against the chest, since in this way the layers of the pericardium are approximated to each other. The heart-sounds, when the valves are intact, may sometimes be heard as well as the friction-rub, or they may be completely drowned by the loud rub, at least in some parts of the heart. In general, they are faint in every case of pericardial effusion, since their conduction to the ear is impaired. In large effusions where PERICAEDITIS 363 no friction-rub is to be heard, we hear the heart-sounds, especially the first, but only very faintly and obscurely. This condition, in connection with the increase of the cardiac dullness, is of diagnostic importance. If there is also valvular dis- ease with the pericarditis, the pericardial and endocardial murmurs are some- times hard to distinguish from each other, but usually the former greatly pre- ponderate. 3. Sequelce of Pericarditis. — A large pericardial effusion may excite special symptoms from pressure on the neighboring organs. Thus we have already said that compression of the left lung must increase the dyspnoea. In many cases we also notice a moderate dullness over the left lower back, from compression of the left lower lobe. Not infrequently there is a combination of pericarditis and left- sided pleurisy with effusion. In rare cases difficulty in deglutition has been ob- served as a result of pressure on the oesophagus, and paralysis of one vocal cord from pressure on the recurrent nerve. In cases of long-continued pericarditis the same sequelae may develop as in any