A TEXT-BOOK OF MEDICINE VOL. I Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons- http://www.archive.org/details/textbookofmedic01dieu A TEXT- BOOK OF MEDICINE BY G. DIEULAFOY PROFESSOB OF CLINIC.UL MEDICINE AT THE FACULTE DE MEDECINE DE PABIS ; PHYSICIAN TO THE HOTEL DIEU ; MF.MBRE DE l'aCADEMIE DE MEDECINE AUTHORIZED ENGLISH TRANSLATION FROM THE FIFTEENTH EDITION OF "MANUEL DE PATHOLOGIE INTERNE" BY V. E. COLLINS, M.D. Lond., M.R.C.S., L.R.G.P. AM) J. A. LIEBMANN, PhD, M.A., LL.D. IN TWO VOLUMES VOL. I NEW YORK D. APPLETON AND COMPANY 1911 \ I- IIS" 7/ ^ LT^ s>l AUTHOR'S PREFACE TO THE ENGLISH EDITION. Having been asked for a preface to tlie English translation of my " Text- Book of Medicine," my first desire is to express tlie great satisfaction I feel at seeing my work translated into English, for that language is so widespread over both hemispheres that no other translation which has yet been made would have contributed to the same extent to the recognition abroad of this work of French origin. I must add that in writing my " Text-Book of Medicine," which has now reached its fifteenth edition, I have given much space to the works of my eminent English colleagues, since a number of them are of the very first importance. Thus will be found the illustrious names of Sydenham, Graves, Basedow, Corrigan, Addison, Bright, Stokes, Paget, etc., whose scientific researches are known and appreciated by everyone. Long ago my venerated master, the great Trousseau, popularized in his "Clinical Lectures" the valuable discoveries of English practitioners, and gave the names of their authors to the newly diagnosed diseases. I have followed the example of Trousseau, and have often dipped into English medical literature, so rich in precious documents. I shall lie satisfied if the medical profession in England will on their side give a good reception to the work which I am now presenting to them. G. DIKULAFOY. Paris, April 17, 1910. TRANSLATORS' PREFACE The " Manuel de Pathologie Interne," by Professor Dieulafoy, has passed through fifteen editions in France, and has been also translated into several European languages. The translators of the English edition have undertaken the work in the hope that English-speaking physicians may be afforded an opportunity of reading one of the most complete and helpful works on the practice of medicine that has appeared within recent times. The author's association with the late Professor Trousseau, combined with his own pro- found clinical knowledge, certainly makes his manual a safe guide to the practice of medicine. The author has throughout confined himself to established facts, avoiding useless discussions and sterile hypotheses. We have to thank Dr. A. N. Sinclair, for much kindly help in reading the proof- sheets. V. E COLLINS. J. A. LIEBMANN. April, 19J0. CONTENTS OF VOL. I u/ PART I DISEASES OP THE RESPIRATORY SYSTEM CHAPTER PAGE I. DISEASES OF THE NASAL FOSS^ --.... 1 I. CORYZA ........ 1 n. NASAL DIPHTHERIA -.-.... 4 in. NASAL SYPHILIS — SYPHILITIC RHINITIS .... 5 n. DISEASES OF THE LARYNX - - - - - - 23 I. GENERAL SURVEY OP THE ANATOMY AND PHYSIOLOGY OF THE LARYNX ------- 23 II. ACUTE CATARRHAL LuVRYNGITIS - - - - - 27 III. CHRONIC LARYNGITIS -••--- 29 IV. SYPHILIS OF THE LARYNX (SECONDAl^ LARYNGOPATHIES — TERTIARY LARYNGOPATHIES) - - - - - - 31 V. TUBERCULOSIS OF THE L.4RYNX — LARYNGEAL PHTHISIS - - 40 VI, LARYNGEAL DIPHTHERIA — CROUP - - - - - 47 VII. STRIDULOUS LARYNGITIS — FALSE CROUP - - - -56 VUI. (EDEMA OF THE LARYNX — (EDEMA IN BRIGHT's DISEASE - - 57 IX. SPASM OF THE GLOTTIS ------ C9 X. PARALYSIS OF THE MUSCLES OF THE LARYNX - - - 71 in. DISEASES OF THE BRONCHI --.-..- 76 -'l. ACUTE BRONCHITIS ----..- 76 _n. CAPILLARY BRONCHITIS — BRONCHO-PNEUMONIA — LOBULAR PNEU- MONIA .-..-.-- 79 -III. CHRONIC BRONCHITIS ...... 91 -IV. DILATATION OF THE BRONCHI — BROXCHIECTTASIS - - - 94 -V. PSEUDO-MEMBRANOUS BRONCHITIS - - - . - KX) VL TRA(rHEO-BRONCHIAL SYPHILIS ..... 102 VII. WHOOPING-COUGH ....... 104 VIII. ASTHMA ........ 109 IX. SUMMER ASTHMA — HAY-FEVER - - - - - 115 IV. DISEASES OF THE LUNG - - - - - - - 117 I. GENERAL SURVEY OF THE ANATOMY OF THE LUNG - - 117 — n. PULMONARY CONGESTION - - - - - - 118 Iir. INFLAMMATION OF THE CHEST - - - - - 119 IV. ACUTE LOBAR OR FIBRINOUS PNEUMONIA — PNEUMOCOCCIO INFEC- TION — PNEUMOCOCCIA - - - - - - 121 -V. CHRONIC PNEUMONIA — FIBROSIS OF THK LUNG - - - 139 -VL OCCUPATION PNEUMONIA — PNEUMOKONIOSI3 - - - 142 -VII. THROMBOSIS AND EMBOLISM OF THE PULMONARY ARTERY - 144 -VIU. GANGRENE OF THE LUNG — GANGRENE OF E.MBOLIO ORIGIN — GANGRENE OF AEKIAL OltlGIN .... - 149 ix CONTENTS OF VOL. I CHAPTER PAGE IV. DISEASES OF THE LUNG — Continued : IX. BRONCHO-PULMONARY HEMORRHAGE — HEMOPTYSIS - . 154 X. PULMONARY EMPHYSEMA ---... I59 XL CEDEMA OF THE LUNG — SUPERACUTE CEDEMA IN BRIQHT's DISEASE 161 XII. ON TUBERCULOSIS IN GENERAL — BACILLUS TOXINES - . 169 XIIL PULMONARY PHTHISIS — COMMON CHRONIC TUBERCULOSIS - - 176 Xn^ FIBROID PHTHISIS ---.-.. 195 XV. PNEUMONIC PHTHISIS — TUBERCULAR PNEUMONIA — CASEOUS PNEU- MONIA -------- 198 XVI. ACUTE GRANULAR TUBERCULOSIS — ACUTE GENERALIZED TUBER- CULIZATION ....... 203 XVII. FALSE TUBERCULOSIS OF THE LUNG - - - - 207 ■ XVni. CANCER OF THE LUNG --.... 213 XrX. BRONCHO-PULMONARY HTHIASIS - . . . . 216 XX. HYDATID CYSTS OF THE LUNG AND OF THE PLEURA - - 219 XXI. SYPHILIS OF THE LUNG - - - - • - 231 V. DISEASES OF THE PLEURA ---.... 248 I. ACUTE SERO-FIBRINOUS PLEURISY — TUBERCULAR SERO-FIBRINOUS PLEURISY ..---.. 248 II. HOW TO TELL IF AN ACUTE SERO-FIB«INOUS PLEURISY IS OR IS NOT TUBERCULAR — CYTO-DIAGNOSIS — SERO-DIAGNOSIS " • 268 III. HEMORRHAGIC PLEURISY ...... 284 rv. TRAUMATIC HEMOTHORAX ---... 295 V. PURULENT PLEURISIES OF THE GENERAL PLEURAL CAVITY • 305 VI. ASEPTIC PURIFORM EFFUSIONS IIs'TO THE PLEURA — INTEGRITY OP THE POLYNUCLEAR CELLS ..... 314 VII. PULSATING EMPYEMA - - - - - - 317 VIII. INTERLOBAR PLEURISY — VOMICE — INTERLOBAR HEMOPTYSIS - 325 IX. MEDIASTINAL PLEURISY — MEDIASTINAL SYNDROME - ■ 337 X. DIAPHRAGMATIC PLEURISY ---... 343 XL LOCULATED, AREOLAR, OR POLYMORPHOUS PLEURISY - 344 XII. SYPHILITIC PLEURISIES ...... 346 XIIL APPENDICULAR PLEURISIES — PYOPNEUMOTHORAX AND SUBPHRENIC EMPYEMA -.-.... 348 XrV. FCETID, PUTRID, AND GANGRENOUS PLEURISY - - - 357 XV. VOMICE -.-.-..- 367 XVI. CHYLIFORM AND CHYLOUS EFFUSIONS OF THE PLEURA . - 369 XVn. HYDROTHORAX ....... 372 XVIII. PNEUMOTHORAX — HYDROPNEUMOTHORAX .... 373 VI. DISEASES OP THE MEDIASTINUM ...... 377 I. TUMOURS OF THE MEDIASTINUM ..... 377 11. CANCER OF THE THORACIC DUCT ..... 382 PAET II DISEASES OF THE CIRCULATORY SYSTEM DISEASES OP THE PERICARDIUM . . . - I. ACUTE PERICARDITIS .... n. CHRONIC PERICARDITIS — ADHERENT PERICARDIUM - III. HYDROPERICARDIUM — HYDROPNEUMOPERICARDIUM 385 385 391 392 CONTENTS OF VOL. I XI CHAPTER PAOK II. DISEASES OF THE ENDOCAKDITM --.... 393 I. ACUTE ENDOCARDITIS ...... 393 n. CHRONIC ENDOCARDITIS ...... 404 in. VAL\njLAR LESIONS OF THE HEART .... 40.5 IV. MITRAL ORIFICE — INSUFFICIENCY AND STENOSIS . • - 410 V. AORTIC ORIFICE — INSUFFICIENCY AND STENOSIS - • • 425 VI. THE TRICUSPID ORIFICE — INSUFFICIENCY AND STENOSIS . . 427 VII. PULMONARY ARTERY — INSUFFICIENCY AND STENOSIS . . 429 VIII. MORBUS C.ERULEUS — CYANOSIS ..... 430 III. DISEASES OF THE MYOCARDIUM ...... 433 I. ACUTE MYOCARDITIS —FATTY DEGENERATION OF THE HEART • 433 II. FIBROSIS OF THE HEART --..-. 436 III. ANEURYSMS OF THE HEART — INFARCTS AND FIBROUS PATCHES, ETC. — RUPTURE OF THE HEART ..... 438 IV. SYPHILIS OF THE HEART ...... 441 V. TUMOURS OF THE HEART AND TUBERCULOSIS OF THE MYOCARDIUM 442 VI. HYPERTROPHY AND DILATATION OF THE HEART . - - 442 Vn. ASYSTOLE -...-... 446 nr. NEUROSES OP THE HEART ....... 447 I. PALPITATION ....... 447 n. PAROXYSMAL TACHYCARDIA ..... 449 III. PERMANENT BRADYCARDIA ---... 450 rV'. EXOPHTHALMIC GOITRE — BASEDOW'S DISEASE - . - 453 V. DISEASES OF THE VESSELS - " - . - - . . 470 I. PHXEBITIS — PHLEGMASIA ALBA DOLENS .... 470 II. SYPHILITIC PHLEBITIS ...... 47n in. ARTERITIS — ATHEROMA — ARTERIO-SCLEROSIS - • - 478 IV. SYPHILITIC ARTERITIS — ARTERITIS OBLITERANS — SYPHILITIC GAN- GRENE — ARTERITIS ECTASIANS — SYPHILITIC ANEURYSM - 486 V. ACUTE AND CHRONIC AORTITIS ..... 488 VI. ANEURYSMS OF THE THORACIC AORTA . • . - 491 VII. SYPHILIS OF THE AORTA — SYPHILITIC AORTIC ANEURYSMS - 502 VIIL DIAGNOSIS BETWEEN ANEURYSM AND NERVOUS PULSATION OF THE ABDOMINAL AORTA ...... 518 IX. CARDIO-AORTIC LESIONS VS TABES — TABETIC ANGINA PECTORIS - 519 X. ANGINA PECTORIS ....... 525 XI. ARTERIAL TENSION — HYPERTENSION — HYPOTENSION • - 530 PART III \/^DISEASES OF THE DIGESTIVE SYSTEM L DISEASES OF THE MOUTH I. ERYTHEMATOUS STOMATITIS 11. MERCURIAL STOMATITIS lU. ULCERO-MEMBRANOUS STO.AUTITIS IV. THRUSH ... V. APHTHA VI. GANGRENE OP THE MOUTH — NOMA VII. SYPHILIS OF THE LIPS 534 53 t 535 .537 539 543 .541 545 xii CONTENTS OF VOL. I CHAPTER PAQX I. DISEASES OF THE MOUTH — Continued : VIII. SYPHILIS OP THE TONGUE -..--- 546 IX. SYPHILITIC PERFORATION OF THE ROOF OF THE PALATE - • 551 X. TUBERCULOSIS OF THE MOUTH . . . - . 556 n. DISEASES OF THE THROAT AND PHARYNX ----- 559 I. ACUTE CATARRHAL ANGINA — ACUTE ERYTHEMATOUS ANGINA - 559 n. ACUTE TONSILLITIS — SIMPLE TONSILLITIS — SUPPURATIVE TONSIL- LITIS — ULCERO-MEMBRANOUS TONSILLITIS — VINCENT'S ANGINA 560 in. RETROPHARYNGEAL ABSCESS ..... 566 IV. CHRONIC ANGINAL CATARRH — GRANULAR ANGINA — CHRONIC TONSIL- LITIS ..-.---- 567 V. DIPHTHERIA - - - - - - - 569 VI. DIPHTHERITIC ANGINA ..---- 574 VII. PSEUDO-DIPHTHERITIC MEMBRANOUS ANGINA - . - 602 VIII. DIPHTHERITIC PARALYSIS - - - - ' - - 607 IX. HERPETIC ANGINA -.--.-- 612 X. GANGRENOUS ANGINA - - - - - -61.3 XI. CHANCRE OP THE TONSIL - - - - - - 614 Xn. SYPHILIS OP THE SOFT PALATE, THROAT, AND PHARYNX - - 020 XIII. TUBERCULOSIS OP THE BACK OP THE MOUTH AND OP THE PHARYNX 625 XrV. MASKED TUBERCULOSIS OF THE THREE TONSILS - - - 628 III. DISEASES OP THE CESOPHAGUS ..--.- 636 I. OESOPHAGITIS ....... 636 11. SPASM OP THE (ESOPHAGUS .... - 637 III. CANCER AND STRICTURES OF THE CESOPHAGUS ... 838 rV. DISEASES OF THE STOMACH ------- 644 I. GASTRIC DISTRESS — ACUTE CATARRHAL GASTRITIS -' - - 644 n. ACUTE GASTRITIS ------- 646 III. CHRONIC GASTRITIS ------- 647 IV. DYSPEPSIA -------- 649 V. GASTRALGIA -------- 654 VI. ULCERATION OP THE STOMACH — GENERAL CONSIDERATIONS - 656 VII. PNEUMOCOCCAL GASTRITIS WITH ULCERATION - - - 658 Vin. APPENDICULAR VOMITO NEGRO ----- 661 IX. EXULCERATIO SIMPLEX OP THE STOMACH - - - - 666 X. SIMPLE ULCER OP THE STOMACH (CRUVEILHIER's DISEASE) - 680 XI. PERFORATION OF SIMPLE ULCER OP THE STOMACH — SUPERACUTE PERITONITIS - - - - - - - 691 XII. PERFORATING ULCERS OF THE STOMACH AND DUODENUM CON- SECUTIVE TO APPENDICITIS - ... - 695 Xin. TRANSFORMATION OP SIMPLE ULCER OP THE STOMACH INTO CANCER 699 XrV. GASTRIC POLYADENOMA ------ 705 XV. CANCER OP THE STOMACH ------ 706 XVI. SYPHILIS OF THE STOMACH . . - - . 716 XVII. DILATATION OF THE STOMACH ... - - 720 XVIU. GASTRORRHAGIA — H^^MATEMESIS .... - 722 XIX. VISCERAL PTOSES ..----- 724 V. DISEASES OF THE INTESTINE -...-- 726 I. ACUTE ENTERITIS -.----- 726 II. INFANTILE GASTRO-ENTERITIS (INFANTILE CHOLERA) - - 728 CONTENTS OF VOL. I xiii CHAPTER PAGE V. DISEASES OF THE INTESTIJfE — Continued : III. APPENDICITIS — APPENDICULAR PERITONITIS— APPENDICULAR IN- TOXICATION — APPENDIC^MLA - - - . . 735 IV. MUCOUS, MEMBRANOUS, AND SABULOUS ENTERO-TYPHLOCOLITIS^ INTESTINAL LIATHISIS --.-.. 774 V. FALSE APPENDICITIS ---... 782 VI. INTESTINAL TUBERCULOSIS — TUBERCUL.\R ENTERITIS - - 788 VU. HYPERTROPHIC TUBERCULOJIA OF THE C^CUM — DIAGNOSIS OF THE TUMOURS OF THE RIGHT ILIAC FOSSA - - . - 792 VIII. ANO-RECTAL TUBERCULOSIS - - - - - 806 IX. SIMPLE ULCER OF THE DUODENUM — PERFORATION — SUPERACUTE PERITONITIS --..... 808 X. CANCER OF THE INTESTINE ..... 813 XL INTESTINAL OCCLUSION --.... 814 XII. CANCER OF VATER'S AMPULLA ..... 819 XIII. DYSENTERY ........ 821 XIV. INTESTINAL WORMS ..-..-- 828 VI. DISEASES OF THE PERITONEUM - .... 833 I. INTRODUCTION TO THE STUDY OF PERITONITIS - - - 833 n. ACUTE AND SUBACUTE TUBERCULAR PERITONITIS - - - 837 in. CHRONIC TUBERCULAR PERITONITIS - . . . 839 IV. PRIMARY PNEUMOCOCCAL PERITONITIS — ASSOCIATION OF THE COLI BACILLUS ---.... 846 V. PRUIARY STREPTOCOCCAl. PERITONITIS .... 854 VI. CANCER OP THE PERITONEUM — CANCEROUS PERITONITIS - - 860 VU. HYDATID CYSTS OF THE PERITONEUTM .... 862 VIII. ASCITES ........ 864 IX. CHYLOUS, CHYLIFORM, LACTESCENT ASCITES ... Sfio VII. DISEASES OF THE LIVER ....--. 870 X. ANATO>rY AND PHYSIOLOGY OF THE LIVES - - - 870 n. CONGESTION OF THE LIVER ..... 874 ni. PASSIVE CONGESTION — CARDIAC LIVER .... 875 rv. CIRRHOSIS OF THE LIVER IN GENERAL .... 878 V. VENOUS CIRRHOSIS — LAENNEC's ATROPHIC CIRRHOSIS — CIRRHOSIS BY GASTRO-INTESTINAL AUTO-INTOXICATION - - - 881 VI. HYPERTROPHIC ALCOHOLIC CIRRHOSIS — ^REGENERATION OF THE LIVER .-.-..-- 896 VII. CURABILITY OF CIRRHOTIC ASCITES AND CIRRHOSIS - - 899 VIII. HYPERTROPHIC CIRRHOSES . ..... 904 IX. PIGMENTARY UYPERTKOPHIC CIRRHOSIS — PIGMENTARY CACHEXIA 904 X. HYPERTROPHIC BILIARY CIRRHOSIS — HANOT's DISEASE - - 907 XI. MIXED CIRRHOSIS .... XII. TUBERCULOSIS OF THE LIVER XIII. CANCER OF THE LIVER AND BILE-DUCTS - XIV. SYPHILIS ..... XV. HYDATID CY.STS OF THE LIVER XVI. ALVEOLAR HYDATID CYST OF THE LIVER - XVII. FATTY AND AMYLOID DEGENERATION OF THK LIVEK - - 949 XViri. ABSCESS OF THE LIVER ..---- 9.")! XIX. APPENDICULAR LIVER ...-.- 9.").") 915 917 922 !»29 934 948 xiv CONTENTS OF VOL. I CHAPTER PAGE VII. DISEASES OF THE LiVEK — Continued : XX. GALL-STONES - - - - - - - . 964 XXL PERMANENT OBLITERATION OF THE COMMON DUCT — DIAGNOSIS OF THE CAUSE OF THE OBLITERATION - - - - 987 XXII. ANGIOCHOLITIS — CHOLECYSTITIS ----- 997 XXIII. ASSOCIATION OP APPENDICITIS AND CHOLECYSTITIS - - 999 XXIV. ABERRANT LOBE OF THE LIVER ----- 1004 XXV. ICTERUS — JAUNDICE — CHOL^MIA ----- 1004 XXVI. ICTERUS GRAVIS — ICTERUS AND THE PUERPERAL STATE - - 1011 XXVII. CATARRHAL ICTERUS — PROLONGED CATARRHAL ICTERUS - - 1021 VIII. DISEASES OF THE PANCREAS . - - - i - 1028 I. GENERAL SURVEY OP THE DISEASES OP THE PANCREAS - - 1028 IL CANCER OP THE PANCREAS ------ 1029 III. CYSTS OF THE PANCREAS --.--- 1029 IV. IL^MORRHAGE OF THE PANCREAS - ... - 1030 V. PANCREATITIS ---...- 1031 VI. PANCREATIC CALCULI ------ 1031 VII. RELATION BETWEEN PANCREATITIS AND GALL - STONES — PAN- CREATICO-BILIARY SYNDROME — CYTOSTEATONECROSIS AND PANCREATICO -PERITONEAL H-3EM0RRHAGE - - - 1032 TEXT-BOOK OF MEDICINE PART T DISEASES OF THE RESPIRATORY SYSTEM CHAPTER I DISEASES OF THE NASAL FOSSAE T. CORYZA. Coryza, or nasal catarrh, is the term applied to inflammation of the pituitary mucosa. I . Acute Coryza. Description. — Acute coryza shows itself by frontal headache and a feeling of obstruction and of tickling in the nasal fossae. At first sneezing is frequently repeated, and brought on again by the slightest impression of cold. The nasal mucosa, at first dry, soon secretes a clear and irritating liquid, causing erythema of the parts over which it flows. The nose is shiny and swollen ; the sen.ses of smell and of taste are blunted or abolished. The patient constantly keeps his mouth open, whilst his breathing is diflicult and noisy. Suction and deglutition are rendered difficult by the blocking of the nasal passages. These troubles are insignificant in the adult, but become serious in the infant, who cannot take the breast without suffocating. The inflammation spreads in various directions : to the frontal sinuses (sharp pains in the head) ; to the conjunctivae (injection of the eyes and lachrymation) ; to the mucous membrane of the Eustachian tubes (auditory troubles, buzzing noises). General malaise and transient fever may also be present. By the second or third day the cold is ripe : the nasal .secretion becomes thick and greenish, crusts form, the patient's nose is blocked up, his voice has a nasal twang, and her[)etic vesicles often appear round the nostrils or the lips. Towards the end of the first week the coryza ceases. When the inHammation reacht's the, laryn.x and the trachea, it produc^es laryngitis and tracheitis ; in vulgar parlance, " the cold has settled on the chest," 1 2 TEXT-BOOK OF MEDICINE ^Etiology — Diagnosis. — Cold and damp weather, the first sunshine of spring, chills of every kind, but especially of the feet, are the common causes of coryza. Influenza at its onset, measles during the period of invasion, and the iodides, produce a nasal catarrh which differs in nature from true coryza. Some asthmatics are suddenly seized with violent and repeated fits of sneezing. During the fit, which lasts from a few minutes to a quarter of an hour, the eyes are injected and watery and the nose runs freely; but after this fit, which precedes or replaces the attack of asthma, everything returns to normal. True coryza differs as much from this manifestation of asthma as it does from hay-fever, or spasmodic rliino-bronchitis. This malady, wliich in England has been described under the name of hay-fever, and in which there is a nervous element besides the catarrhal one, is often the ap- panage of gouty or asthmatic patients, and usually appears at the beginning of summer. It presents two chief forms, which may follow one another or be present together — on the one hand, nasal catarrh, with abundant secre- tion, uncontrollable sneezing, pricking sensations in the eyes, injection of the conjunctivae, violent headache and insomnia ; on the other hand, dyspnoea, resembling that of asthma and playing the chief part, while the nasal catarrh may be of secondary moment. Hay-fever will be discussed in detail under Diseases of the Bronchi, We must not confuse coryza with the nasal forms of diphtheria, of blen- norrhagia, and of glanders. When diphtheria attacks the nasal mucous membrane, it produces an abmidant secretion, wliich is sometimes san- guineous. On examining the nasal fossae, we can usually discern the diph- theritic membrane, and bacteriological examination shows the presence of Loffier's bacillus. Glanders likewise produces a specific coryza : the nasal mucous mem- brane is swollen, excoriated, and ulcerated ; nasal respiration is impossible, and sanious, foetid liquid flows from the nostrils. This discharge, wliich constitutes a sign of the liighest importance in animals, is much less profuse in man, and its presence would not suffice to establish the diagnosis if the cutaneous eruptions and the articular manifestations of glanders were absent. Treatment. — Inhalations of vapour of iodine and of ammonia have been extolled. In infants at the breast care must be taken to cleanse the nasal fossae of the secretions which hamper the movements of sucking and swal- lowing. Some rehef may be obtained from the following j)owder : SaHcylate of bismuth . . . . . . . . . . oiv. Powdered camphor . . . . . . . . . . 3i.ss. Cocaine hydrochlorate . . . . . . . , . . gr. i. DISEASES OF THE NASAL FOSS.E 3 The pricking sensations and the secretions are reHeved by the use of the following ointment twice daily : Menthol . . . . . . . . . . . . . . gr. ii. Lanoline . , . . . . . . . . . . gr. xlv. VaseUne (pure) . . . . . . . . . . . . 5ii. 2. Chronic Coryza. Description. — This form may follow attacks of acute coryza, or may be chronic from the outset. The sneezing, the frontal headache, and the fever of acute coryza are wanting, but there is no lack of other signs. The nose is stuffed up, so that the patient can only breathe with liis mouth open, especially at night. Respiration is embarrassed, noisy, and sometimes accompanied by a kind of snoring sound ; the voice is nasal ; the senses of taste and of smell are blunted ; the hearing is less acute, and buzzing in the ears is frec^uent. The nasal secretion may be scant or abundant. In clironic dry rhinitis, wliich is most conunon in adults, secretion is almost absent, and patients complain of a distressing feeling of dryness. More commonly, especially in young subjects, the nasal secretion is abundant, and the nasal nmcous membrane is covered with crusts and dried mucus. Chronic coryza has a slow course and an indefinite duration ; it is sometimes interrupted by acute attacks, and at other times more or less lengtliy remissions give some respite to the patient. We shall see later the frequency of ozaena in chronic coryza. On rhinoscopic examination, the mucous membrane appears red and hypertrophied, especially over the anterior part of the inferior turbinate bone (hypertropliic rliinitis). When the coryza is of very long duration, the nmcous membrane is indurated and fibrous, wliile the glandular elements show a tendency to disappear. Under the name of posterior coryza, Desnos has described a chronic inflammation of the naso-pharyngeal cavity. This variety is cliiefly asso- ciated with glandular angina ; the local lesions can only be discerned by rhinoscopy, and its chief symptoms are snuffling and hawking. In lymphatic cliildren a chronic herpetic coryza has been described. The orifice of the nostrils and the septum are covered by crusts like those of impetiginous eczema. After the crusts fall off, they leave bare slight ulcers, which become covered with new crusts, and the duration of the illness is indefinite. TJie changes in the so-called scrofulous coryza of infants arc character- ized by hypertrophy of the nasal mucous membrane which shows fungating vegetations, by deep ulcers wliich may attack the bones, by deformity and flattening of the nose. This old descri[)tion jnust be r(^vis«'(l, for niosi of these lesions are due to tubercular disease, or to early or late hereditary syphilis. 1—2 4 TEXT-BOOK OF MEDICINE Diagnosis. — In the following chapters we shall give the diagnosis ot chronic coryza from nasal syphihs and tuberculosis. It is enough for me to mention here that chronic coryza has many symptoms in common with adenoid growths of the naso-pharynx and with mucous polypi of the nose. Rhinoscopic examination will remove all doubts. Treatment. — The local treatment of chronic coryza consists in cleaning the mucosa by means of appropriate douches ; cauterization, powders, and snuffs are then employed. Lavage may be carried out by a siphon douche, the nozzle of wliich fits the nostril tightly ; the fluid, introduced without force, into one nostril, flows back through the opposite one without passing into the pharynx. These douches consist of lukewarm saline solutions, weak boric lotions, or solutions of chlorate of potash. The cures at Challes and Mont-Dore are of much service. As a snufE, one of the following preparations may be recommended : 1. Bismuth subnitrate ) -- t*" Venetian talc J * ' ' ' ' ' ' ' '•->•"• Precipitated chalk . . . . . . . . . . gr. v. 2 . Chlorate of potash . . . . . . . . . . gr. xlv. Powdered sugar . . , . . . . . . . 5v. Arsenical preparations, taken internally, are useful when the rhinitis is associated with the gouty diathesis. II. NASAL DIPHTHERIA. Description. — Nasal diphtheria is nearly always associated with diph- theria of the fauces, which it may precede or follow. It begins somewhat like a simple coryza, with redness of the nostrils and nasal discharge. There is but little sneezing. The nasal discharge is sanious, muco-purulent, or sanguineous, and contains membranes. Epistaxis is common, and usually precedes the formation of membranes. Repeated and profuse epistaxis was thought by Trousseau to be of evil omen. The patient's voice is nasal, and he can only breathe with his mouth open. The submaxillary glands are swollen. On rhinoscopic examination, the mucous membrane is swollen and coated with membrane, which is adherent, and usually localized to the posterior half of the nasal fossae. In some cases, especially in children with measles, the diphtheria may reach the nasal duct, and spread to the eyelids and the eyes. This oculo- palpebral variety shows itself by lachrymation, Avith redness and swelling of the conjunctiva and of the eyelids. Sero-purulent secretion appears, the eyelids and the ocular conjunctiva are covered with false membrane, and in some cases perforation of the cornea and destruction of the eye result when streptococcal infection is also present. DISEASES OF THE NASAL FOSS^ 5 Nasal diphtheria, described by the term " fibrinous rhinitis," may be of such duration as to be chronic. The diagnosis of diphtheritic coryza is easy wlien the patient is already suffering from pharyngeal or laryngeal diphtheria ; if coryza be the first symptom hesitation is pardonable. The diagnosis is very difficult, especially at the commencement, and I know only one way of settling the question — viz., by culture and bacteriological examination of the membrane or of the nasal mucus {vide Diphtheritic Angina). The prognosis is not very grave if the disease remain limited to the nasal fossae, and if the diphtheria bacillus be present alone without the strepto- coccus. If both organisms are present, the membranes usually present a different aspect, being diffluent and gangrenous, while the discharge is profuse, persistent, and accompanied by epistaxis. Such a coryza usually points to very severe diphtheria, and is one of the manifestations of Trous- seau's malignant diphtheria. Loffler's bacillus finds so favourable a soil in the nasal fossae that its localization in the nose appears to me to have great weight in determining diphtheritic paralysis. We often find virulent bacilli in the nasal cavities several weeks after tlie cure of diphtheritic angina. Diphtheritic coryza, like all thja varieties of diphtheria, should be treated mth injections of serum. The earlier the injection, the better the chance of success ; hence the importance of making a correct chagnosis from the very first. III. NASAL SYPHILIS— SYPHILITIC RHINITIS. In this chapter I shall review (1) the primary lesion, the chancre; (2) secondary troubles ; and (.'3) tertiary troubles. 1. Nasal Chancre. Description. — The study of nasal chancres comprises chancre of the skin of the nose and chancre of the nasal fossa\ Every sy{)hilitic chancre is composed of a mass of embryonif cells, and i'onns a small tumour (primary syphiloma), developed at the expense of the skin and of the subcutaneous tissue. The appearance of the chancre differs, however, on the skin and on the mucous membrane. On the skin it is covered by a crust, due to tiie j)resence of the horny layer, which does not exist in the nuico.sa ; the lesions of the mucous epithelium, soaked with fibrino-purulent licpiid, end, not in the formation of a crust, but of a false membrane, which is flaccid, greyish, and diphtheroid. 1. Let us first consider chancre of the skin. It is situated «tn the bridge of the nose, on tin* nostrils, on the ti[) of the nose, or on the 6 TEXT-BOOK OF MEDICINE nasolabial fold. On the bridge the chancre is flat ; elsewhere it is bulky, prominent, and spread out, forming a hypertrophic papule (Fournier). It runs the same course as all cutaneous chancres : at first it is a crack, or a reddish erosive papule, then it grows larger, becomes prominent and en- crusted, but always remains painless. This encrusted or pustulo-crustaceous chancre has the appearance of ordinary ecthyma. If the crust be raised, after having been first softened, the chancre appears with all its characteristics — viz., flat or slightly convex surface, erosive, but not ulcerated, smooth, reddish, often bleeding and covered with papillae. Sometimes a scanty purulent secretion may be noticed. The edges of the chancre are flat, not perpendicular ; strictly speaking, there is no edge, because there is no ulceration. Its base is indurated and parchment-like. Adenopathy is constant and may be uni- lateral or bilateral ; the condition is somewhat indolent, and is confined to the glands at the angle of the jaw, while one gland is often much larger than the 'others. After about two months the chancre heals without cicatrization ; the induration and the adenopathy, however, persist for a long while. The nasal chancre must not be confounded with a furuncle. From the first the part on which a boil is about to develop is swollen, painful, red, and shiny ; later it becomes purulent — characters which are quite different from those presented by a chancre. Chancre will not be mistaken for epithelioma, as the latter is a painful tumour, infinitely slower in its development, ulceration is delayed, the base is not indurated, and enlarged glands do not appear till much later. Epithelioma does not tend to spontaneous cicatrization, as chancre does. 2. Let us now consider chancre of the nasal fossae. This chancre always occurs on the anterior or posterior part of the nasal fossa. I merely mention chancre of the posterior orifice of the nasal fossa from accidental inoculation by an infected Eustachian catheter. Chancre of the vestibule usually arises on the cartilaginous septum. It develops as a greyish or reddish lump, wliich may be indurated or softened, and has rouglily the appearance of a mushroom. This chancre, in its hypertrophic form, partly fills the nostril and causes an ichorous or bloody discharge. The nose is red and swollen ; though it is deformed externally, no deviation of the septum is present. Eadiation of pain to the nose or the face is common. Enlarged glands at the angle of the jaw are always found. The chancre lasts from six weeks to two months, and then heals without cicatrization. The diagnosis between chancre and malignant tumour of the nasal fossa (sarcoma) must be based upon the following considerations : The evolution of sarcoma is much slower than that of chancre, nasal haemorrhage DISEASES OF THE NASAL FOSS.E 7 may be frequent and profuse, ulceration appears late, pain is acute, en- larged glands appear slowly ; lastly, sarcoma deforms the nasal fossaj and causes deviation of the septum. 2. Secondary Troubles — Syphilitic Coryza. I shall describe first cutaneous syphilides, and secondly those of the mucous membrane. 1. Cutaneous syphilides show here, as elsewhere, different forms, and may be dry, moist, or crusted. The dry syphilides are papular, papulo- lenticular, or papulo-squamous. They are frequent on the alse nasi, where they often present the granular form (Fournier). The moist, erosive syphilides, or mucous patches, appear as cracks and clefts in the ala nasi and the naso-labial fold. Sypliilides which are crus- taceous, papulo- or pustulo-crustaceous may invade the whole of the nose. All these syphilides are indolent in character and do not itch. They are rarely confined to the nose alone, and are generally found on the cheeks, the chin, or the forehead. 2. Secondary syj)hilis of the mucous membrane presents a different aspect, according to whether it attack the adult or the new-born infant, as early hereditary syphilis. In the adult we find bright red erythema of the mucous membrane and erosions, with muco-purulent or muco-sanguineous secretions, and with formation of crusts, which reform after they have been rubbed off. These crusts may block the nostrils, impede respiration, and simulate eczema. In the newly-born coryza is often the first sign of hereditary syphilis. It appears a few weeks after birth. The cliild breathes with great difficulty through the nostrils, and the movements of sucking are hampered ; but so far there is little distinction between syphilitic and simple coryza. Sero- purulent, and in some cases bloody, fluid exudes from the nose ; the secretion becomes more and more sanious, without being profuse, irritates the alae nasi and the upper lip, and produces ulcers covered by yellowish or greenish crusts, which may hide the upper lip. Nasal syphilis in the new-born, in contradistinction to what is seen at a later age, rarely results in tertiary le.sions and deformities (Trousseau). Specific coryza, however, may become chronic, with tliickening of the nmcous membrane, ulceration and swelling of the adenoid tissue. Perichondritis of the septum, destruction of the vomer, and obliteration of the lachrymal duct, have also been seen (Ziem). We must recognize sypliilitic coryza of the new-born in order to treat it without delay, and to avoid the possible contamination of the nurse from the child. Coryza rarely exists as the only manifestation of syphilis, and is usually accompanied or followed by other troubles which are an aid to diagnosis. We must, therefore, examine the child's body for skin cruption.s, 8 TEXT-BOOK OF MEDICINE roseola, erythema of an ashy tint on the neck, Imnds, or feet, and patches which are scalloped, do not itch, and are often scaly. We may sometimes find mucous patches round the anus or the navel, behind the ears, upon the scrotum or the labia majora, and Trousseau used to lay stress upon unhealthy fissures and ulcers of the folds of the skm. From this time many children with hereditary syphilis show changes in appearance : their bodies take on a brownish colour, the eyebrows fall out, and are replaced by the yellowish, scaly plaques of psoriasis. These marks of hereditary syphilis will aid in the diagnosis of syphilitic coryza. 3. Tertiary Troubles of Nasal Syphilis. The tertiary lesions of nasal syphilis which may result from the acquired or hereditary disease are in each case identical. As, however, syphilis may invade the nose or the nasal fossae, it is necessary to study each form. 1. Tertiary Syphilis of the Nose. — The skin lesion here is essentially the tubercle, which much resembles the chancre in structure, and is composed of a mass of embryonic cells. The syphilitic tubercle is a cutaneous gumma, and forms a small tumour of the size of a millet-seed, a small pea, or a cherry-stone. This gumma, which is, as it were, set in the skm, is at first firm and resistant, and projects above the surface of the skin. The syphilitic tubercle is rarely solitary, and variable numbers are seen in the same region ; they may be grouped in a mass, form segments of a circle, or sometimes fuse together and produce' a true gummatous infiltration, " a kind of plaque of hyperplastic integuments, studded or bordered by tubercular nodules." These dermatoses are common upon the face, but the nose is the " victim by choice " (Fournier). They are sometimes confined to one part of the nose ; at other times they invade the whole nose and spread to the face. The lesion, as we have said, appears as a tubercle (nodular syphiloma) or an infiltration (dilTuse sypliiloma). For several months the disease is in- sidious in its development ; pain, fever, enlargement of glands — in short, all signs — are absent. The nose, however, loses its normal aspect, becoming deformed and increased in size, while the affected skin is studded by dull red projections, and slight desquamation of the epidermis occurs. At a more advanced stage the dermatosis may present different aspects : in rare cases the tubercles, especially those which are isolated, spread, become indurated or almost horny, and end in atrophy. As a rule, however, both the nodular and the diffuse syphiloma, when untreated, end in softening, ulceration, suppuration, and formation of crusts. These syphilides are known as tuberculo - ulcerating and tuberculo-crustaceous, or as the gummatous ulcer which is serpiginous and perforating. Tliis phase, in which the gummatous tissue softens and ulcerates, is DISEASES OF THE NASAL FOSS.E 9 relatively rapid, and contrasts with the slowness of the preceding phase. At this period the nose is deformed, enlarged, budding out at one spot, ulcerated at another, sometimes gullied by purulent ulcers, and covered in places by brownish or greenish crusts, which are thick, stratified, and adherent. In spite of these lesions, we usually notice no functional trouble no fever, and little or no pain. When the lesions are deep, and especially when they have not beep treated in time, tertiary syphilis leaves indelible marks : the alae nasi are scalloped and destroyed ; the nose is deformed, flattened, thinned, and furrowed with hard, wliite, and honeycombed scars. 2. Tertiary Syphilis of the Nasal Fossae.— The lesions usually com- mence in the mucosa, and then invade the perichondrium, the cartilages. the periosteum, and the bone. The cartilage and the bone may be attacked from the outset. Sometimes the disease produces only superficial ulcers, which are not serious and readily recover, but at other times it destroys by invasion and perforation. It attacks the bony and the cartilaginous framework of the nose, lays bare the cartilages and the bones, gives risf to sequestra, and mutilates the organ, causing irremediable destruction. These lesions must be studied separately, for they present different symptoms according to the regioij. affected. (a) Hypertrophic Syphilitic Rhinitis. — The picture is one of chronic coryza : nasal respiration is incomplete or impossible, the patient wipes away thick mucus with crusts, and acute attacks sometimes supervene. On examination of the nasal fossa^, we find hypertrophy of the mucosa ; but this hypertrophy, which may be polypoid, must not be confounded with adenoid vegetations. The rhinitis is not always general, and may confine itself to one fossa, or to the inferior turbinate bone which fills the meatus. Ozaena often accompanies this syphilitic rliinitis. (6) Perforatiofi of the Septum. — The nasal fossae are separated by a bony and cartilaginous partition ; the bony part is formed, above by the per- pendicular plate of the etlimoid, below by the vomer, while the cartilaginous l)art is formed by the triangular cartilage, which fills up the gap left by the bony plates. The cartilage is usually first affected by syphilis : the lesion Itegins in the mucosa, reaches the perichondrium, which if lays bare, sets up necrosis of the subjacent cartilage, and then causes a round or oval perfora- tion of variable size. In some cases the lesion extends to the vomer na, other kinds being considered symptomatic. This malformation consists in a considerable enlargement of the nasal fossa;, with atrophy of the turbinate bones (especially the inferior ones) and thickening of the mucosa (Zaufal). This gaping of the nasal fossa; allows such a free passage to tiie current of e.\[)ired air that the secretions arc imperfectly swept away, the mucus becomes stagnant, and 2 18 TEXT-BOOK OF MEDICINE crusts form. In this alkaline medium a special micro-organism (a large diplococcus) has been described by M. Loewenberg, who considers it to be the specific cause of the foetor. Ozgena does not always develop in the same way. Its evolution is more or less rapid. True oza3na, which seems to be due to a congenital malforma- tion of the nose, generally shows itself during late infancy, when the nasal cavities are growing ; it takes months and years to develop. The foetor varies in different subjects, but is especially marked when crusts and mucus are expelled, and is so intense in certain patients that a whole ward may be tainted. As the sense of smell is lost, the patient is unconscious of the fcetor, but the disgust which he causes to those around him makes life miserable. The social consequences of this affection are terrible ; life in common with others becomes difficult, marriage is impossible for young girls, and the tendency to suicide is not rare. The patient often speaks with a nasal tone, which results from the resonance of the voice in the abnormally enlarged nasal cavities. The nose is often saddle-backed, the tip is tilted, and the nostrils gape. The infection which produces ozsena may be propagated in different directions, and give rise to dacryocystitis, conjunctivitis, keratitis, or sinusitis. M. Luc has described tracheal ozaena. The treatment of ozsena consists in the daily use of a nasal douche of bichloride of mercury (1 part of mercury in 10,000 of water). After the douche boric powder (Loewenberg) is carefully blown' into the nasal fossae and upper parts of the pharynx. Aspirations of very hot saline solution morning and evening for several months give excellent results (Bonnier). In the case of syphilis mercury as described in the preceding chapter must be exhibited. 6. Epistaxis. Description. — Epistaxis is hoemorrhage from the nasal mucosa. The bleeding, which is usually slight, consists in the flow of bright blood, drop by •drop, from one nostril, rarely from both.* If the bleeding be abundant, and especially if it occur while the patient is lying down with the head back, the blood flows through the posterior nares, and may then pass along the pharynx and oesophagus into the stomach, to be rejected by vomiting. A mistake may thus occur if the patient does not recognize the epistaxis, and is content with saying that he has vomited blood ; hence the rule to explore the nasal fossae carefully in doubtful cases of haematemesis. I have several times seen such errors in diagnosis. This year, at the Hotel-Dieu, one of my patients vomited fluid blood * Galen has noticed that the blood generally comes from the right nostril in diseases of the liver. DISEASES OF THE NASAL FOSSAE 19 and clots ; the hsematemesis resulted from nasal haemorrhage diverted into the stomach. On depressing the tongue we saw the blood flowing down the posterior wall of the pharynx, and examination of the septum revealed the source of the haemorrhage, which was at once arrested. The quantity of blood lost is very variable. In some cases the loss is slow, lasts from ten minutes to a quarter of an hour, and the subject does not lose more than one or two ounces of blood. In other cases the flow is rapid and profuse, appears from the nose and mouth at once, and may last several hours if efficacious treatment do not intervene ; the loss may then amount to more than a pint. Furthermore, as the bleeding readily recurs — ■ since any effort, such as blowing the nose or sneezing, is enough to detach the clots — it follows that in predisposed subjects (haemophilia) the loss of blood may assume large proportions. When the epistaxis is repeated and abundant, the patient becomes pale and weak, and is liable to fits of dizziness, vertigo, and syncope, as is customary after any great loss of blood. Nasal haemorrhage has a most irregular course ; it may appear daily, several times in the twenty-four hours, or months and years apart. It sometimes assumes an intermittent form, or returns at certain seasons of the year. etiology. — Epistaxis is very common at the age of puberty, but is more rare in old age. The abundance and the distribution of the vessels on the surface of the mucous membrane explain the frequency of these haemorrhages. Capillary aneurysips have been met with. Epistaxis may be active or passive. It is active when it is the result of an afflux of blood. I may quote, among other examples, the epistaxis favoured by the hyper- trophy of the heart in aortic insufficiency ; the supplementary epistaxis of the menstrual periods and of piles ; the haemorrhages which supervene after the suppression of a cutaneous affection, such as erysipelas (Sore) ; and those which are the result of sunstroke and of sudden changes of temperature or of atmospheric pressure. Epistaxis is frequent at the onset of typhoid fever and of measles, and is seen in the course of articular rheumatism (Trousseau) and of phthisis (Leudet) ; it is sometimes the herald of haemoptysis. Passive epistaxis is seen in blood stases, when the venous tension is increased (mitral and tricuspid lesions), or when the return of blood from the head is impeded (compression of veins by tumours of the neck and the mediastinum). Epistaxis in icterus simplex and icterus gravis, in the haemorrhagic forms of the eruptive fevers, in malarial infection, purpura, and Icucocytlurmia results from changes in the blood. Epistaxis is fre(]uent in diabetes and in Bright's disease ; indeed, diabetes predisposes to great bleeding. In the cliapter on Bright's Disease I shall dwell in detail on the epista.xis of chronic nephritis and on severe epistaxis, wliicii is sometimes one of tlie first symptoms of Bright's disease. Epidemics of epistaxis, which could only 2—2 20 TEXT-BOOK OF MEDICINE have been a larval fever, have been noted. The epistaxis which follows a fall upon the head sometimes indicates a fracture of the base of the skull, involving the upper wall of the nasal fossae. I must make special mention of epistaxis of local origin in ulcers of the mucosa, varices, angiomata, polypi, and vascular tumours of the septum. Epistaxis is rarely the result of haemorrhage from a wide area. Rhino- scopy shows in most cases that the rupture of the small vessels which gives rise to epistaxis occurs in certain defined regions — to wit, the antero-inferior and the central portion of the septum and the inferior turbinate bone, where erectile tissue exists. Diagnosis — Prognosis. — It is necessary to trace the cause of the bleed- ing to ascertain if it depend on some general state or on a purely local lesion (ulcer, varix, erectile tumour, angioma of the septum), to find out whether it be symptomatic of some affection of the liver, the heart, or the kidney, or whether it be supplementary to a suppressed haemorrhage, and to ask if it may not denote the onset of enteric fever, or if it be not the first sign of a hsemorrhagic form of some eruptive fever. The prognosis depends on the quantity of blood lost, the strength of the patient, and the cause of the bleeding. Each of these factors must be carefully considered. Epistaxis is sometimes a grave complication in measles and in typhoid fever. Treatment. — To arrest epistaxis the simplest measures, such as injection of very hot water (especially oxygenated water) into the nasal fossae or compression of the nose, sometimes suffice ; but in obstinate cases we must resort to plugging, which exerts direct pressure upon the seat of the haemor- rhage. It is first necessary to make out the site of the bleeding by direct examination. In twenty-five cases of epistaxis Chiarri has shown that the haemorrhage in twenty-two of them came from the anterior part of the septum. It is the " seat of election " in epistaxis, a seat easy to recognize, and we have only to look for it. " Raise the ala nasi, so that the orifice of the nostril is turned outwards as much as possible, follow an oblique line upwards and backwards, and at a distance of 1 inch the zone of bleeding will be found." We then apply a plug of wool at the point in question, and we can exert efficient pressure by keeping the plug in place •with, a stop- clamp applied astride the bridge of the nose, or by introducing into each nostril one jaw of the clamp forceps, previously wrapped with gauze (Range). If this plugging do not suffice, or if the seat of the bleeding be higher up or farther back, we introduce into the nostril, by means of forceps, a series of plugs of absorbent wool soaked in oxygenated water : percliloride of iron must not be used. After plugging, we survey the posterior orifice of the nasal fossae, so as to be certain that the blood does not continue to flow back- Avards into the pharynx. We can also perform plugging by means of a bladder of gold-beater's skin. For this purpose fix the bladder on a rigid DISEASES OF THE NASAL FOSS.E 21 urethral sound of small calibre, introduce the empty bladder into the nose, inject water througli the sound, so as to distend the bladder and plug the sound. This apparatus is easily kept in place, and has often yielded me the best results. If, in spite of these means, the epistaxis continue, posterior plugging must be employed. To plug the posterior nares use Belloc's sound, or a flexible uretliral bougie. Introduce the sound, smeared with vaseline, into the inferior meatus^, push it horizontally till it emerges behind the soft palate, seize it with forceps, and draw it out of the mouth. By means of a strong thread of sufficient length, suspend from this end of the sound a plug of wool smeared vnih boric vaseline, 1 inch long and half as broad. Next pull back the sound introduced into the nose. The gauze plug may be thus fixed in the posterior opening of the nose, while the index-finger, introduced into the mouth, helps the passage of the plug behind the soft palate. The thread is fixed to the cheek by means of diachylon or collodion ; it is kept in place by anterior plugging, which is usually combined with posterior plugging. The plug, however, soon becomes painful to the patient. The nose swells, breathing is impeded, and the patient can rarely tolerate the plugs for more than twenty to thirty hours. To withdraw them, moisten by injecting tepid water into the nostrils. The anterior plugs come out easily, while the posterior ones are detached by means of the injection, and are finally spat out by the patient. In some cases (erectile tumour, angioma) plugging is not the best treat- ment, and the bleeding surfaces must be cauterized with nitrate of silver, or preferably with the galvano-cautery at a dull red heat. By this means M. Luc was able at one sitting to arrest profuse epistaxis which threatened the life of one of my patients admitted for an angioma. Adrenalin must enter into the thera[)eutics of epistaxis. The bleeding mucosa is touched with a plug soaked in a solution of adrenalin (I in 1, ()()()). A plug of wool saturated with a weaker solution (say, 1 in r),()()() or I in 10,000) may also be left in situ. The vaso-constriction which results some- times produces paleness from the decoloration of the mucosa. When the haemorrhage has been abundant, give iced driidvs, use sub- cutaneous injections of ergotin, and administer, in tablespoonful doses, the following hnemostatic draught : 1^ Acid, sulphuric, dil. . . . . , , ll[ x. Tinct. ferri perchlor. . . . . . . ]]\x. Tinct. opii . . . . . . . . ii; v. A(|uam . . . . . . . . . . ad 7,ss. Employ injections of serum (see Appendix on Therapeutics). If these means fail to stop tlic blcfMJing, and if the patient's life be in 22 TEXT-BOOK OF MEDICINE danger, transfusion of blood muvst be employed. It is an operation which has often yielded me excellent results. Some years ago I performed transfusion upon two patients : the one was suffering from epistaxis of diabetic origin, the other from bleeding due to haemophilia. The former was an adult, the latter a child. In both cases the bleeding was exceedingly serious, on account of its amount and its persistence. The bleeding was at once arrested by transfusion. Periodic epistaxis, even though it is not due to a larval fever, is success- fully treated with sulphate of quinine. Lastly, it is necessary to remember that certain supplementary or critical bleedings must be respected, especially in old people, in whom they are often a safety-valve. CHAPTER II DISEASES OF THE LARYNX I. GENERAL SURVEY OF THE ANATOMY AND PHYSIOLOGY OF THE LARYNX. Vocal and respiratory troubles comprise nearly the whole of laryngeal pathology. As we cannot understand aphonia and dysphonia, with all their shades, and cannot grasp the mechanism of spasm of the glottis and the genesis of paralyses of the vocal cords, or diagnose changes in the recurrent and external laryngeal nerves, if we have not a mental picture of the normal functions of the laryngeal apparatus, I must briefly indicate the principal points in the physiology of the larynx. The skeleton of the larynx is formed l)y the cricoid, thyroid, and arytenoid cartilages. The cricoid is shaped like a ring, and is much broader behind than in front. The thyroid has been compared ta a sliield : it protects the vocal cords, which are inserted in the angle of its posterior surface. The arytenoids, which resemble a funnel in shape, play a most important part. They swing on their base at the crico-arytenoid articulation, and the opening or closing of the vocal cords is jiroduced by their different movements. Function of the Glottis. — The glottis is the space limited by the vocal cords (inter- ligamentous glottis) and by the arytenoid cartilages (intercartilaginous glottis). The inferior cords alone merit the name of vocal cords, for sound is produced at their level ; the superior vocal cords have usurped the term " cords," which must bo replaced by that of " ventricular bands." All the parts of the larynx, including its cartilages and joints (passive organs), its muscles and nerves (active organs), combine for one purpose — i.e., for the movements of tlio vocal cords and tlie different shapes of the glottis. The glottis plays two chief parts — the one, which concerns the individual's life, is the passage of air into the respiratory channels ; and the other, which is an attribute of species, is the emission of sound, from the simple cry to the modulations of the human voice. Respiration, therefore, on the one hand, and emission of sound on the other, are functions which show clearly the importance and gravity of diseases of the larynx. Muscles of the Larynx.— The muscles of the larynx may bo classified in several groups. The posterior crico-arytenoids form the first group. They are inserted into the i)osterior surface of the cricoid, and into the external and posterior process of the arytenoid. Their contraction draws the vocal processes outwards, especially if inspira- tion bo very deep. The posterior crico-arytenoids, then, are the muscles of respiration ; their r61e is to open the vocal cords, allow free passage to the air, and keep the glottis open durinij respir.-vtion. By their contraction they oppose the natural tendcnc^y of the lips of tJwj glottis to come together, like two valves, during the aspiration of uir iiitt> tlie liuig, an event which at once happens when they an^ [)aralyzod. 2:3 24 TEXT-BOOX OF MEDICINE Such is the isolated action of the posterior crico -arytenoid muscles as muscles of respiration. When they contract synchronously with the arytenoideus, they form a muscular band, which straightens the two arytenoid cartilages upon the cricoid. They thus become the antagonists of the thryo -arytenoid muscles, and free the arytenoids from the traction of the cords which would draw them forwards. They may also be looked upon as tensors of the vocal cords. This tension is effected by their means, and without them would be impossible. Furthermore, by acting in concert with the adductors, the posterior crico-arytenoids fix the arytenoid cartilages on the cricoid, make their movements firm, and thus allow the vocal cords at their posterior insertion to follow the movements of the cricoid. They are, therefore, muscles of inspiration, tension, and fixation. The second group is formed by the lateral crico -arytenoid muscles, which are the constrictors of the interligamentous glottis and the single ary-arytenoideus, which constricts the intercartilaginous and, consecutively, the interligamentous glottis. These muscles, )jy drawing the vocal cords together, shut the glottis, and place it in the desired position for the production of vocal efforts. For this act the glottis is quite shut, while in the production of the voice the cords do not. come quite in contact, but leave a space of variable shape and size between one another. By bringing the vocal cords together the constrictor muscles of the glottis assist in the production of sound — they jirepare it. Sounds can only be produced if the vocal cords be sufficiently approximated ; if they be too open, the expired air escapes, and is wasted without being used in the production of sound. This fact can easily be verified upon the larynx of a corpse. The third group comprises the muscles of phonation ; these are the thyro -arytenoid and crico -thyroid muscles. The thyro -arytenoid muscles are composed of two chief bundles, the one situated in the thickness of the vocal cord, the other outside it. This latter bundle, which is much the larger, is flattened against the thyroid cartilage, terminates at the outer edge of the arytenoid, and blends with the muscular loop, which the arytenoideus completes behind. The contraction of this muscular Ioojd shuts the glottis. The thyro-ary- tenoid is, then, a muscle of effort ; it is an adductor, like the lateral crico-arytenoideus, and it also plays a part in phonation, by bringing together the vocal cords, which the column of expired air seeks to open. It regulates the power of the voice by its opposition to the exjjiratory muscles of the thorax. The internal bundle of the thyro-arytenoldeus (the muscle of the vocal cord) draws the arytenoid and the thyi'oid cartilages together. It is not, therefore, a tensor of the vocal cord, neitlier does it stretch the cord at all ; it shortens the vocal cord and loosens, instead of stretching it ; but, as other muscles — the distensors of the vocal cords— begir to contract, it can no longer shorten, and as it cannot thicken or swell, it hardens and acquires a firmness and resistance which regulates the periodicity of the vibrations. The more tlie firmness is increased the greater become the vibrations and the higher the sound. This internal bundle is, then, the muscle of the diapason, as the external bundle is the muscle of the intensity of the sound. This muscle may thus be looked upon as a tensor of the cords, the word " tension " signifying the state of varying rigidity which results both from the passive distension of the cords and from their active retraction (Bonnier). The crico-thyroid muscle is the antagonist of the thyro -arytenoid, but it is only so by acting with the muscles which straighten the arytenoids upon the cricoid. The combined action of these muscles does not, properly speaking, produce the tension of the vocal cords, but only their distension. When the elevator muscles of the larynx draw the thyroid cartilage upwards and forwards, and with it the anterior insertion of the vocal cords, the latter, in their turn, pull on the arytenoids and the i^ostero- DISEASES OF THE LARYNX 25 cuperior part of the cricoid. The cricoid cartilage would then swing forwards, if the crico-thyroid muscle, taking the thyroid for its fixed point, did not straighten the cricoid by carrj'ing the posterior insertions of the cords backwards. In that case the cords can be stretched. The crico-thyroid muscle is, then, one of the distensors of the cords ; its paralysis, without producing complete aphonia, affects the voice and necessi- tates the assistance of the other distensor muscles. A fourth group forms the extrinsic musculature of the larjnix. Some are elevators of the larynx (mylo-hyoid, genio-hyoid, digastric, stylo-hyoid), and their action is con- tinued b}' the thyro-hyoid muscle. The others are depressors of the lar>nax, towards the sternum (sterno-hyoid and sterno-thyroid) and the shoulder-l)lade (scapulo-hyoid). Lastly, another muscle draws the lar\nix towards the vertebral column (inferior con- strictor of the pharynx) ; it is a retractor and completes the musculature of the apparatus of phonation. In fact, all these intrinsic and extrinsic muscles are simultaneously l)ut unequally in play during phonation. In intonation — that is, in the emission of voluntary sound — the thyroid prominence occupies a fixed level between the sternum and the chin. In modulation — that is, when the intonation is varied — the prominence rises for high sounds and descends for low ones ; as the neck and the head keep the same attitude, or as the chin remains at the same distance from the sternum, the pomum Adami always occupies tlie same level for the same intonation. When the head is bent or straightened — that is, when the relations between the chin and sternum vary — the levels occupied by the thyroid prominence vary equally, but a fixed height of the tliyroid prominence corresponds for eacli sound to a fixed attitude of the head. This prominence answers to the anterior insertion of the vocal cords. The functicm whicli we have just studied is due to tlie oombuied action of all the extrinsic muscles of the larynx. Phonation is in harmony with the act of expiration. In expiration the trachea, the cricoid, and with it the posterior insertion of the vocal cords, are raised, in proportion as the air escapes and the chest is emptied. It suffices to prolong a sound during the whole period of expiration to verify the ascent of the larynx. If the cricoid be raised, the thjToid must also be raised to maintain the same degree of tension of the cords, and it is only raised by the action of the elevators, which is modified by the depressgrs and the retractor. All the musculature, therefore, is in play. Wlien we modulate sounds (high sounds) up the scale, the cords are stretclu-d and the larynx is raised, while the contrary takes place when our intonation becomes lower. The elevators of the thyroid, drawing the anterior insertion of the cords upwards and forwards, are then^fore tensor muscles, just as the muscles which straiglitcn tht> arytenoids ujion the cricoid, and as the crico-thyroidcus. whicli diaws the posterior insertion of tlie cords downwards and backwards (Bomiicr). Nerves. — The muscles of the larynx are supplied by the re(rurn'nt and the external laryngeal nerves. The recurrent nerve, foriiicd by the spinal accessory and vagus nerves, supplies all the muscles except the crico-thyroidei ; tlic fibres from the vagus seem more esi)ecially reserved for the posterior crico-arytenoid muscles, which open the glottis, while those from the spinal a(;cessory supply the other muscular groups. The cricothyroid muscles, or indirect tensors of the vocal cords, are su|)plicd Ity llie external laryngeal brancdu-s of the superior laryngeal nerve, wlu'rli lakes origin from Ihe gangliform plexus of the vagus. The extrinsic musculatun^ is innervated by the motor branch of tin- trigeuiiuil. by th<' facial, the glosso- pharyngeal, and especially by the hyj)oglo.ssal nerve. Hcmnier has recorded seven cases of hysterical aj)honia in which the mu.sdes, inn(;rvated by the laryngeal nerves, were working perfectly. The want of tension in the cords was due to the inertia of the elevators supplied by the hypoglossal nerve. 26 TEXT-BOOK OF MEDICINE The larynx receives its sensory nerves from the vagus by the superior laryngeal nerve, which makes the upper part of the organ exquisitely sensitive, and by the external laryngeal nerve, which gives a more obtuse sensibility to the subglottic portion. Respiration — Voice — Effort. — Respiration goes on freely, thanks to the contraction of the posterior crico-arytenoid muscles, which dilate the glottis and keep it open during respiration. The laryngoscope shows that the glottis forms a triangle, with its base backwards, at the arytenoid cartilages. The production of the voice is much more complicated. The air in the ohest is expelled with a variable force, which is regulated by the contraction of the expiratory muscles on the one hand, and by the muscles of effort on the other, and differs in speaking or in singing. When the voice is to be produced, there is first accommodation on the part of the glottis — that is, the ary-arjrtenoid, lateral crico-arytenoid, and external thyro -arytenoid muscles draw the vocal cords together to the proper degree, so that they may vibrate under the pressure of the expired air. At this moment the glottis presents the appear- ance of a fusiform cleft, which may attain as much as 2 or 3 milUmetres in its greatest diameter. The external muscles fix the thyroid at a given level ; the crico-thyroideus carries the cricoid backwards and downwards ; the posterior crico-arytenoid muscles, assisted by the ary-arytenoideus, draw the arytenoids backwards ; and the cords would be extended, without being really stretched, if the internal bundle of the thyro-aryte- noideus did not struggle against the passive distension of the cords by their active retraction. The latter thus acquire a physiological aptitude for vibration, which may be looked upon as a tension peculiar to these organs. The height of the soimd is, then, produced by the tension of the vocal oords. In the chest-voice the sound is produced by the rapid periodic variations of pressure of the air at the glottis : the quicker the vibrations, the higher the sound ; the greater the resistance to expiration — that is, the greater the difference ,of pressure — the more intense the sound. The sound is not produced by the resonance proper of the vocal cords, but by the variations of tension which their vibrations give to the column of expired air at the level of the glottis. The mechanism of the production of the head-voice is still imperfectly known. According to some (Lermoyez), the mucosa of the cord is said to be the only vibra- tory part ; according to others (Bonnier), the larynx is said to act like a whistle of variable shapes, the column of air which comes out of the glottis breaking against the edge of the ventricular bands. The height of the soimd may be equally produced by the pressure of the expired air ; greater and greater pressure may thus raise the sound by a fourth, and even a fifth, the tension of the vocal cords remaining the same. Further- more, some authors admit that the tension of the vocal cords may be compensated, in a certain measure, by their approximation — that is to say, almost the same effect is obtained with the vocal cords when little stretched but close together and with the cords more open but very tense. Thanks to these different combinations of length, tension, opening, and pressure, the larynx gives the infinite shades and modulations of the voice in the acts of singing, lecturing, and conversing. The shape of the glottis, the vibrations of the cords, and the limits of these vibrations, can be verified by means of the laryngoscope. During the emission of a high soimd the anterior part of the vocal cords vibrate, and, in proportion as the sound becomes deeper, we see the glottis assume the ellipsoid shape, the vibrations being produced in the posterior parts of the vocal cords, and even in the interarytenoid glottis, which not only takes part in resjjiration, as was long supposed, but which also contributes to the production of low notes. These few remarks on the production of the luiman voice will help us to understand how a simple ulceration, the presence of a false membrane. DISEASES OF THE LARYNX 27 the paralysis of a muscle, the ankylosis of an articulation, or oedema of the arytenoid, reacts at once on such a delicate organ in different ways. The timbre of the voice varies in each individual, according to conditions which were unknown until the researches of Helmholtz. I will briefly recapitulate them. Every sound is formed of a fundamental note, and certain accessory notes, called harmonics, which have a fixed relation to the fundamental note. The harmonics are always higher in the scale than the fundamental note, ^\^len they do not bear a regular ratio to the fundamental note, the sound is simply a noise. WTien, on the contrary, they are in regular proportion, a musical note is produced. The timbre of the note, then, depends upon the grouping and the number of the harmonics. In the human voice the funda- mental notes and the harmonics are produced at the vocal cords, but other harmonics are also produced in the pharynx, the nose, and the mouth. Lesions of the mouth, the nose, and the pharynx, as well as those of the larynx, are therefore able to modify the timbre of the voice, which becomes throaty or nasal in different cases. The act of effort is only possible when the framework of the thorax, on which almost all the muscles of tlie trunk and some of the muscles of the upper Umbs are inserted, is firmly fixed. The thorax then becomes the fixed insertion -jjoint of the muscles which are to be brought into play in the effort. This initial fixation of the thorax is obtained by means of a deep inspiration, but on condition that the firmly closed lips of the glottis oppose the issue of the previously inspired air. In paralysis of the constrictor muscles of the glottis the effort is impossible. II. ACUTE CATARRHAL LARYNGITIS. Description.— Acute catarrhal laryngitis may occur as a distinct illness, or be secondary to some other ailment. In both cases it begins with a feeling of tickling in the larynx, and, as the sensiblity of the mucosa is increased, the inspired air appears too cold, and its passage into the respiratory channels is painful. The cough, which is at first dry and slight, becomes more severe as mucus accumulates on tlie lips of the glottis. Phonation and respiration soon become difficult ; the emission of sounds is painful, the high notes are lost, the voice is hoarse, altered in its low timbre, and almost inaudible, because the inflamed and paretic vocal cords are no longer in their normal state of tension and vibration. Trifling laryngitis only provokes hoarseness ; when it is intense, when the paralysis of the vocal muscles is very marked, and wlien the ventricular bands arc oedematous and cover the vocal cords, aphonia ])ecomes complete. The voice, which is deep and raucous, is sometimes interrupted by sliarp sounds, like those of the falsetto ; this phenomenon can be explained by the vibratory nodes which are formed on the cords, thickened and covered with mucus. Respiration is free in the adult. In the child, whose glottis is much narrower, dyspncea is frequent, and often complicated by suffocative attacks, which result from spasm of the glottis. The expectoration, insignificant at first, is compo.sed later of thick greyish sputum, wliich is less the result of the laryngeal inflamnjation than of the bronchitis and the tracheitis which are so often present. With the laryngoscope we sec that tlie mucosa has taken on ;i ilark colour 28 TEXT-BOOK OF MEDICINE at several spots; the epiglottis, the aryteno-epiglottic folds and the ar}i:enoids are red and swollen ; the vocal cords have lost their pearly, shining aspect, and are covered with rosy striations, though they escape the swelling which frequently attacks the ventricular bands. The secretion from the mucous glands is abundant ; it sometimes has a gummy aspect and coats the different regions. In the benign form the fever is insignificant. The illness does not last more than a week or a fortnight, and the different symptoms show rapid improvement, with the exception of the vocal troubles, which are much slower in their disappearance. We also see acute laryngo-traclieitis a frigore, which is more intense ; the fever is sliarp ; coughing and swallowing cause much pain ; the sputum is sometimes streaked with blood ; vocal troubles are very marked ; and the breathing is as much hampered as it is at the onset of oedema of the glottis, a fact which is explained by the swelling of the inflamed parts. With the laryngoscope we discover, in addition to the lesions previously described, ecchymoses, which are most marked on the anterior part and the free edge of the vocal cords, and which testify to the severity of the inflammation. etiology — Diagnosis. — Acute laryngitis is provoked by the direct contact of cold air with the larynx, and by its indirect action upon some other part of the body (cold to the feet). It is set up by irritant vapours, accom- panies tracheitis, bronchitis, or coryza, and is one of the chief symptoms of influenza. In measles it assumes a special type. The severe form may simulate oedema of the glottis ; the slight form, which is much more frequent, must not be confounded with nervous aphonia. Every individual who is seized with dysphonia or hoarseness, following a chill, has not perforce laryngitis ; he may have vocal paralysis (nervous aphonia) (Krishaber). In this case the laryngoscope reveals no trace of phlegmasia, and the vocal cords have kept their whiteness, but are incompletely stretched, and the paralysis, which is usually unilateral, causes dysphonia. These vocal troubles are due to paralysis of the external laryngeal nerve, which supplies the crico-thyroid muscle, by which the vocal cords are made tense.* Laryngitis, especially in children (laryngeal cough and hoarseness), is often the chief symptom of the invasion of measles ; the presence of pharyn- geal, ocular, and nasal catarrhs will settle the diagnosis. It must not be forgotten that laryngeal troubles of syphilitic origin, such as hoarseness and loss of voice, due to erythema and erosive sypliilides * This paralysis of the external laryngeal nerve is not more astonishing than that of the facial or radial nerves from the same cause. It is also curious to see that the same agent — cold — destroys the function of the motor nerves by causing paralysis, and exaggerates that of the sensory nerves by causing neuralgia (" Aphonic Nerveuse," These de Paris, 186.5). DISEASES OF THE LARYNX 29 of the larynx, have the closest resemblance to simple laryngitis. This fact has an important l^earing upon treatment. Prognosis — ^Treatment. — Acute catarrhal laryngitis, which is not for- midable in the adult, is more serious in children, because it produces suffo- cative attacks. It is subject to relapses, and is a serious misfortune in people whose larynx is a " professional instrument " (Peter and Krishaber), as in singers, barristers, or public speakers, who are sometimes obliged to abandon their profession because the voice is slow to regain its norm.al character, and is lost afresh under the influence of similar causes. Sweating, hot drinks, soothing gargles, powders, inhalations, blisters placed on the front of the neck, topical applications to the larynx, and, lastly, local blood-letting when the inflammation, is acute, form the general treat- ment. III. CHRONIC LARYNGITIS. I shall describe three varieties of chronic laryngitis — catarrhal, glandular, and hypertrophic. I would, however, remark that these varieties are not always distinct clinically ; in fact, they are often associated. Chronic Catarrhal Laryngitis.— This variety is hardly ever primary ; it usually succeeds one or several acute attacks, and, like every laryngitis, is kept up by the efforts of singing, by excess of tobacco, and of drink. Pain is absent, cough is moderate, and hoarseness is almost uniform, but rarely goes as far as aphonia. The laryngoscope shows redness and swelling of the mucosa, with varicose vessels and glandular projections. The inflam- mation is sometimes localized to certain spots, whicli are, in order of frequency, the posterior surface of the epiglottis, the aryteno-epiglottic ligaments, tlie ventricular bands, and the vocal cords. Gouty Laryngitis. — Gouty persons often suffer a form of chronic laryngitis with exacerbations, which are accompanied by rliinitis, tracheitis, and bronchitis. The bronchitis is at times limited to the bases of the lungs ; if it occupy the apices, the affection may be considered of a tubercular nature. This laryngitis is chiefly seen in singers during the first years of study, and is more frequent in summer than in winter. Most often it disappears spontaneously, when other manifestations of the diathesis appear, unless vocal strain has provoked definite iiypertrophy of tlie cords (Bonnier). Glandular Laryngitis.— Glandular or granular laryngitis is generally chronic from the outsfit, and does not, like the precetliiig form, follow attacks of acute laryngitis. It is often associated with granular pliaryngitis, which oj)ens the scene in many cases ; the condition might, therefore, be termed " graimhir pliaryiigo-laryngitis.'" Ilcrp('ti(; and artlirilic subjocls an* pre- dis[)()sed to it, but abuse of drink or lobacco, and especially the iinninderatc use of the voice, are its chief causes, 'i'lic inll,inini;ilit)n is liimictl, as a 30 TEXT-BOOK OF MEDICINE rule, to the clusters of glands on the posterior surface of the epiglottis, in front of the arytenoid cartilages, where the glands form a vertical ridge, and to those on the ventricular bands and on the vocal cords, where their mission is to moisten the papillary region of the vocal cord, and thus prevent loss of function. The inflammation attacks the glands of the arytenoids, of the base of the epiglottis, of the vestibule of the larynx, and of the vocal cords. The hypertrophy of the glands, together with the increased vascularity of the mucosa, alters the voice ; the singer can no longer sound the low notes, and soon loses the clear tone of the high notes. The loss of the high notes, which is one of the first symptoms of glandular laryngitis, is easily explained. In the normal state the high notes are produced as follows : The anterior processes of the arytenoid cartilages, by their approximation, bring the vocal cords into exact contact, and the lips of the glottis vibrate, especially in their anterior third, when a sound is emitted. The complete approximation of the vocal cords can no longer take place if the interarytenoid mucosa be swollen and thickened. The high sounds, therefore, are defective or sup- pressed. Later the patient loses the low notes, and the middle notes are also affected if the lesion reach the vocal cords. When the lesions are general, the laryngoscope shows the granular condition and the vascularity of the ventricular bands and of the vocal cords, in addition to the glandular hypertrophy described above. Erosions are sometimes seen at different points of the mucosa. Hypertrophic Laryngitis. — This form is usually associated with the preceding variety. The hypertrophy may be general or local, and, in the latter event, involves the epiglottis, the aryteno- epiglottic folds, and the vocal cords. Tiirck has described a variety of hypertrophy attacking the vocal cord, chorditis tuberosa. The hypertrophied parts are rigid, often deformed ; the epiglottis bends backwards, and partly hides the entrance of the larynx ; the aryteno-epiglottic folds are thickened and shortened ; the arytenoids resemble an irregularly shaped nipple ; and the vocal cords are much enlarged. Besides the various changes in the voice, hypertrophic laryngitis is some- times accompanied by dyspnoea, due to the swelling of the affected parts, which may obliterate the orifice of the larynx and gradually lead to asphyxia. In clu-onic laryngitis both local and general treatment are employed. The direct application of a 10 per cent., or even 20 per cent., solution of nitrate of silver, insufflations of bismuth, inhalations of iodine and sulphur vapour, and preparations of arsenic internally, are the therapeutic agents most employed. Good results are obtained from the cures of Eaux-Bonnes, Cauterets, and La Bourboule. Krishaber has successfully applied igni- puncture to the granulations of the larynx. DISEASES OF THE LARYNX 31 We must also prove that the nasal fossae are clear, and must restore nasal respiration. Gouty laryngitis often yields to hot local appHcations to the neck and to nasal douches of hot saline solutions. It is ameliorated by very warm gargles. The best of these gargles can be made with wine, adding infusion of cinnamon, which makes the gargle astringent ; the gargle must be used as hot as the patient can bear it. As a rule, all the symptoms yield very rapidly (Bonnier). IV. SYPHILIS OF THE LARYNX (SECONDARY LARYNGOPATHIES —TERTIARY LARYNGOPATHIES). The frequence and the importance of syphilitic lesions of the larynx deserve our careful attention. Lewin says : " Next to the skin and the throat, syphihs most frequently attacks the larynx." The epiglottis, the aryteno-epiglottic folds, the ventricular bands, the vocal cords, and the skeleton of the larynx, may show most diverse changes due to sypliihs. These changes may be superficial or deep. The superficial lesions, which comprise laryngeal catarrh, erythema, mucous patches, erosions and ulcers, with or without oedema, are seen in the secondary stage. The deep submucous infiltrations, which comprise diffuse or circum- scribed syphilomata, ulceration, hypertrophy, vegetations, changes in the cartilages, formation and elimination of sequestra, cicatricial retractions, progressive laryngo-stenoses, permanent deformities, and perilaryngeal phlegmon, are found in the tertiary period. Secondary Laryngopathies. Description. — The chancre has never been seen in the larynx. Tlie secondary lesions — erythema, catarrh, erosion, and ulceration — with or without oedema, first demand notice. Erythema appears a few weeks after infection, at the same date as the mucous or cutaneous syphilides, and is a very frequent trouble. Many people become hoarse within some weeks or months after infection, and ascribe the trouble to a chill, or speak of " loss of voice," when the mischief is really sypliilitic. With the laryngoscope the erythema is characterized by a rosy, ash-coloured, or reddish tint of the mucosa, and often coincides with erythema of the throat, which of is a vermilion colour, especially on the velum and the anterior pillars. Tlie voice becomes hoarse, and may be almost lost. The erythema disappears in a few months, but is prone to relapse ; slaty coloration of the vocal cords sometimes remains. In some cases erythema is accompanied by secretion, and laryngeal catarrh is found. Secondary syphiiides of the larynx may be erosive or ulcerative. The 32 TEXT-BOOK OF MEDICINE erosions are superficial ulcerations, which are opaline, rounded, or oval, and surrounded by a red border ; on the vocal cords they are usually elongated and situated on the free edge. Erosive syphilides sometimes coincide with erythema and provoke vocal troubles, but are not, as a rule, accompanied by oedema or dyspnoea. Swallowing is painful when the aryteno- epiglottic folds are involved. These erosive syphilides form part of the early secondary troubles, whilst the ulcerative syphilides appear later. The latter (and I do not allude to the deep ulcerations of the tertiary period) are much broader and more hollow than the erosive syphilides, their edges are sometimes prominent and of a vivid red, while the surrounding mucosa is oedematous ; they occupy the epiglottis, the arytenoid region, the ventricular bands, and the vocal cords. It must not be thought that the superficial lesions of the larynx belong solely to the first year after infection ; catarrh, erythema, erosions, and superficial ulcerations, with or without oedema, although they be slight and part of the " secondary troubles," may still appear many years after the primary infection. Most of these lesions, which may be called " benign," only cause vocal troubles. Pain is absent, and cough, so frequent in other forms of laryngitis, is often wanting in these cases. The voice is, however, altered and rough- ened ; this is the most constant symptom. Hoarseness, dysphonia, and sometimes aphonia, may supervene slowly or rapidly, and may be very obstinate. Persons suffering from sypliilis of the larynx are certainly more sensitive to the action of cold, and chills are no doubt to blame for first attacks, and also relapses, of these secondary troubles. Tliis knowledge will prevent us considering a laryngitis in which syphilis plays the chief part as a simple laryngitis a frigore. Dyspnoea is rare in these cases ; nevertheless, superficial and apparently benign lesions are sometimes accompanied by oedema of the larynx and respiratory troubles. This fact is very important ; Krishaber lays great stress upon it. Although dyspnoea may be exceptional in secondary laryngo- pathies, the oppression may rapidly increase, and tracheotomy would be necessary if the dyspnoea did not speedily yield to treatment. I have .several times proved this statement, and M. Mauriac, like Krishaber, affirms that " almost insignificant erosions may become a dangerous inflammatory centre, around which oedema of the glottis suddenly develojDs." In dealing with a laryngitis apparently due to chill, or with an apparently simple loss of voice, syphilis must always be thought of, and due investiga- tions made, to avoid an error in diagnosis. The discovery of the chancre and its satellite glands, the presence of syphilides of the skin (roseola), and of the mucosa} (mucous patches), headache, and alopecia, will all help to settle the pathogenic diagnosis. DISEASES OF THE LARYNX 33 Tertiary Laryngopathies. Description. — ^Tlie tertiary lesions are much rarer, but much graver, than the secondary ones. Though they do not appear, as a rule, witliin two years from the date of infection, they may be very early (during the first year) or very late (after the twentieth year). The tertiary laryngo- pathies coincide fairly often with specific lesions of the trachea and the lungs (" they are, as it were, the root "), while the secondary laryngopatliies are especially associated with specific lesions of the velum palati and of the throat. • 1. Ulcerative Syphiloma— Gummata.— The gumma may be super- ficial or deep, and may attack tlie soft parts or the skeleton of the larynx. In some cases it forms a small swelling, and is the gumma, properly speaking ; in others it infiltrates the tissues, and is the diffuse syphiloma (syphiloma en nappe). The Gumma is the most typical lesion of tertiary laryngeal syphihs. It may vary in size from a pin's head to a hazel-nut. Several isolated or confluent gummata in different stages of growth may be met with. As a rule, the gumma, seen with the laryngoscope, forms a rounded projection, which is of sombre hue and surrounded by reddish oedema. As softening takes place, it becomes yellowish at the centre, and in a few days an ulcer is formed, wliich shows little tendency to spontaneous lieahng. The edges of the ulcer are perpendicular, the floor is greyish, the surrounding tissues are hard and elastic. The area on which the ulcer is situated is oedematous. Tlie gummatous neoplasm is not always circumscribed ; it may infiltrate the mucosa and submucous tissue in a diffuse manner, and is then termed '■ syphiloma en nappe." This sypliiloma is often capricious, like the phagedaenic lesions, and produces serpiginous ulcers, wliich not only destroy the mucosa, but also attack the perichondrium, cartilages, and joints ; they may even reach the extralaryngeal tissues, producing inflam- mation of the neck (Mauriac). This diffuse syphiloma commences in the submucosa ; it may, however, start in the skeleton of the larynx. We see, lastly, other ulcerations which do not result from the necrobiosis of a gumma. In addition to the gummatous ulcers which I have just described, we may see tertiary ulcers, which at first look like a simple con- gestion of the mucosa or superficial erosions. We must not, however, trust to the " benign appearance," for this lesion, though apparently congestive, may be the prelude of severe phagedtena. The gummatous and ulcerative lesions which I have just described present the most varied pictures with the laryngoscope. The; <^|)i<:l<)ttis, which is so fre((uently attacked by syphilis, is thickened, hyperjilastic, oedematous, and deformed; it forms a dull red tumour, which obliterates the 34 TEXT-BOOK OF MEDICINE vestibule of the larynx to a variable extent. In other cases the epiglottis is indented, loopholed, or covered by ulcerations " from the slight erosion of its surface and of its edges to the serpiginous and gangrenous ulcers which reduce it to shreds " ; it is sometimes converted into an irregular stump. Phagedgena of the epiglottis is also frequent. The arytenoid region and the aryteno-epiglottic folds are deformed, cedematous, and hypertropliied by the gummatous tissue ; they block up the vestibule and hide the vocal cords. Vegetations are not rare. The folds are the seat of ulcerations with greyish floor and dark perpendicular edges. The vocal cords undergo the most varied changes : they are red, hyper- trophied, and ulcerated. The ulceration begins in the free border, eats into the cord, making it look like a saw ; the cord may be reduced to shreds, or the ulcer may end in vicious scars and adhesions. 2. Non-Ulcerating Syphiloma. — The diffuse infiltration does not always go on to ulceration ; it may run a very slow course, and may cause in the lar}mx (as in the lips and the prepuce) fibrous thickening which has no tendency to ulcerate. This thickening, which is rarely general, narrows the cavity of the larynx ; it affects the subglottic part of the organ, the epiglottis, the ventricular bands, and may be confined to one of these parts. The laryngoscope shows the affected part to be deformed and of a dull red ; its surface is granular, mammillated, and sometimes covered by vegetations. In an old syphilitic patient whom I have just seen hypertrophy of the left ventricular band and two vegetations in the arytenoid region were present. 3. Vegetations. — The neoplasm often takes the form of a vegetation. The vegetations are rarely solitary ; they may be isolated or confluent, sessile or pedmiculated, and may vary in size from a millet-seed to a pea. Their " seat of election " is the vocal cords and the ventricular bands. They develop on the surface, on the edges, and at the angle of the junction, but rarely invade the epiglottis, in distinction to ulcerations which have a marked preference for it. These vegetations, as a rule, develop in mucous membrane which is already diseased, and may, by reason of their number or of their size, narrow or block the glottis and the cavity of the larynx. 4. Lesions of the Skeleton. — The syphiloma may primarily attack the cartilages, or only invade them after the soft parts. The affected cartilages are, in order of frequency, the arytenoids and the cricoid. The thyroid is usually respected. The first result is calcification of the cartilage ; the calcified tissue then necroses, and the separation of the sequestrum is accompanied by suppuration, fistulas, and oedema. The necrobiotic process, which begins on the inner wall of the cartilage, may invade its whole thick- ness, and, after eating through it, set up inflammation in the front of the neck. DISEASES OF THE LARYNX 35 Dislocations and ankyloses of the joints result from the syphilomatous process. In some cases a fragment of cartilage, or an entire arytenoid, may be cast off through a fistula, be rejected by the mouth, or fall into the air- passages and provoke asphyxia. The changes in the cartilages of Wrisberg and of Santorini are perfectly visible \vith the laryngoscope. Crico- arytenoid ankylosis is almost always unilateral, and fixes the vocal cord on the affected side. 5. (Edema. — CEdema of variable colour often accompanies tertiary laryngopathies. Laryngeal oedema plays a considerable part in these cases ; it may be more or less extensive, and invades, in order of frequency, the epiglottis, the ventricular bands, the aryteno-epiglottic folds, the vocal cords, the parts below the cords, and the trachea. The symptoms present are stridor, sucking-in, and dyspncBa which borders on asphyxia. The laryngoscope reveals the deformity and the swelling of the cederaatous parts ; the epiglottis " is rolled up like a paper-twist, and swollen so as to resemble a chestnut or the cervix uteri," while the arytenoids form large pads, which obliterate the supraglottic region. Syphilitic oedema of the larynx will be studied in detail in Section 8. 6. Tracheo-Laryngeal Adenopathy.— The numerous glands which are present in the trachea and tlie larynx are sometimes attacked by syphilis, and we therefore find the symptoms which accompany lesions of the recurrent nerves (spasm of the glottis, or paralysis of the vocal cords). 7. Cicatrices — Laryngo-Stenosis.— Ulcerous lesions of the larynx some- times leave deformities, adhesions, and retractions, which affect both the voice and the breathing. The epiglottis may be displaced or deformed by the cicatricial bands, wliich draw it towards the aryteno-epiglottic folds or towards the lateral wall of the pharynx ; the result is complete deformity of the aperture of the larynx. The vocal cords may be converted into fibrous bands, which dislocate the vocal process ; the axis and the calibre of the laryngeal cavity are altered, and gradual laryngo-stenosis results. In some cases the stenosis arises from the welding of the ulcerated vocal cords, which then form a kind of diaphragm, and partially obhterate the glottis. 8. Paralysis. —The existence of syphilitic paralysis of the laryngeal muscles can only be recognized with the laryngo.scope. The paralysis is often unilateral, and chiefly affects tlie left cord. Paralysis of the posterior crico-arytenoid muscles is characterized by immobility of the vocal cords at the moment of inspiration ; the glottis, instead of being open during inspiration, tends to close, and asphyxia becomes imminent. When one lateral crico-arytenoid muscle is paralyzed, the cord on the corresponding side does not approach the other cord during phonation. Syi)l)ilitic para- lysis of the arv-arytenoidcus is very rare ; the laryngoscope shows that the intercartilaginous glottis remains open during the emission of sounds. 36 TEXT-BOOK OF MEDICINE Laryngoplegias are very often isolated. Their pathology is still imperfectly known : they may be due either to lesions of the glands adjoining the re- current nerves, or to an intracranial lesion, though it is far more likely that these partial paralyses have a peripheral origin. They may be compared with the paralysis of the oculo- motor nerves and with the various forms of facial paralysis which are seen in all stages of syphilis. Symptoms. — Vocal troubles are often the first to appear, and may vary from hoarseness to complete and persistent aphonia. Cough is rare and not important. Respiratory troubles, from shortness of breath to the most violent dyspnoea, are practically constant. Many patients suffer from breathlessness, to which they become accustomed by avoiding violent efforts. In some the attacks of dyspnoea are very severe ; in others the dyspnoea may improve for a while, only to return in a worse form ; lastly, in some cases, especially when oedema is present, the dyspnoea is so rapid in its onset that asphyxia becomes imminent, and intervention is imperative. Stridor and sucking-in accompany almost every case of severe laryngeal dyspnoea. This dj^spnoea is due to the stenosis of the larynx ; the narrowing may be rapid (acute laryngo-stenosis) or slow (progressive laryngo-stenosis). (Edema and abscesses are the commonest causes of acute laryngo-stenosis. Progressive laryngo-stenosis is due to many causes, such as develop- ment of gummata, diffuse hypertrophic syphiloma, presence of vegetations, oedema, abscesses, cicatrices, deformity of the aryteno-epiglottic region, dislocations of the arytenoids, and adhesions of the vocal cords. This enumeration explains sufficiently the diversity, the continuous or inter- mittent character, and the intensity of the respiratory troubles. I may remind the reader that asphyxia may follow the fall of a necrosed cartilage into the trachea. Swallowing is very painful, or almost impossible, in some patients, especially when the edges of the epiglottis and the arytenoids are inflamed and ulcerated. Sharp pains in the ear may accompany the dysphagia. Foetor of the breath is not so common as in cancer. Diagnosis. — There is often difficulty in diagnosis, because so many lesions of the larynx (hypertrophic laryngitis, syphilitic, tubercular, and cancerous disease, and oedema in Bright's disease) may cause the same vocal and respiratory troubles. Another difficulty in diagnosis results from the fact that such lesions as hypertrophic infiltrations, polypoid excrescences, ulcerations, and oedema may show an identical appearance with the laryngo- scope. The signs and symptoms which may help us in diagnosis demand mention. 1. Chronic Hypertrophic Laryngitis. — General health excellent, no loss of flesh, appetite good, dys^moea absent or trifling, obstinate cough, DISEASES OF THE LARYNX 37 and dryness of the throat ; for a long time past gradual change of the voice, loss of high sounds, hoarseness, and muffling of the voice. With the laryngoscope : Hypertrophy and granulations on the ventricular bands ; redness and granulations on the vocal cords, especially on their free border ; hypertrophy of the glands of the larvnx, chiefly in the arvtenoid region. Result : incomplete approach of the arytenoids ; insignificant erosions of the mucosa ; pharyngo-laryngeal catarrh, jvith abundant secretion. Gouty laryngitis presents during each acute attack marked erythema of the larynx, the pharynx, and the trachea. The periodicity of the crises, however, eliminates syphilitic erythema. The vocal cords have sometimes a blood-red appearance. 2. Tubercular Laryngopathy. — Wasting, loss of appetite, bronchitic cough, haemoptysis, or pre\'ious pleurisy, pulmonary lesions in course of development. In some exceptional cases primary laryngeal tuberculosis ; vocal troubles of every degree ; d3^spnoea absent or marked, according to the site and the severity of the lesions ; pain and dysphagia, which may be very acute. With the laryngoscope : Unusual pallor of the palate and of the vestibule of the larynx ; isolated -or combined lesions of the larynx, which present the following forms : (a) Tubercular infiltration, without ulceration, confined especially to the interarytenoid region, tlie epiglottic folds, and the ventricular bands ; hypertrophy and deformity of these parts, notably conical swelling of one or both arytenoids ; epiglottis enormous ; great swelling of the ven- tricular bands ; vocal cords dull and rough ; epiglottis asually healthy ; enlarged glands ; laryngeal catarrh. (6) Tubercular vegetations, which may be large, are found in the inter- arytenoid region. They are dull, livid, covered with purulent mucus, and often implanted upon an ulcerated base ; surrounding oedema pale. (r) Tubercular Ulcerations. — Their edges are jagged and Hat ; they are not deep, and the surrounding oedema is soft and pale. These ulcers in time destroy the ventricular bands, the vocal cords, and the folds of the epiglottis. By curetting the ulcers, li<|uid which sometimes contains the tubercle bacillus may be obtained. (d) Paralysis, or paresis of a vocal cord, a fairly frequent sign at the commencement of laryngeal tuberculosis (Libermann). 3. Syphilitic Laryngopathies. Health excellent ; no loss of appetite; no wasting ; cough absent or IrKling ; previous syphilis; vocal tr()ul)I('.s. from simple hoarseness to comj)l('te and persistent aphonia ; respiratory troubles, varying from shortness of breath to dyspnoj^i, with stridor and sucking-in ; pain on dculiitition and in the ears, according to the lesion. 38 TEXT-BOOK OF MEDICINE Examination with the laryngoscope : Pallor of the palate, the pharynx, and the larynx, so common in tuberculosis, is not seen. The laryngeal lesions, whether isolated or combined, are : (a) Rounded, prominent and reddish gumma, situated on the epiglottis, the folds, or the ventricular bands, projecting into the larynx and causing deformity. (b) Diffuse syphiloma of the hypertrophic form, situated in different regions, and often coinciding with excrescences and ulcerations. (c) Ulcerations. — Slightly different according as they are consecutive to gumma, diffuse syphiloma, or tertiary non-gummatous ulcerations. The syphilitic ulcer has generally thick perpendicular edges, whereas the edges of the tuberculous ulcer are jagged and flat. The syphilitic ulcer is usually deeper and more excavated than the tubercular one ; the oedematous tissues which surround the syphilitic ulcer are usually red and hard (in tubercular ulceration they are pale and soft). The syphilitic ulceration rapidly hollows out channels and perforates the tissues (tubercular ulceration is slOW in its progress). Syphilitic ulceration is found in every part of the larynx, but has a marked predilection for the epiglottis, and especially invades its laryngeal surface. Syphilitic ulcers are less numerous than tubercular ones, and leave scars behind them ; tubercular ulcers do not. (d) Vegetations. — They are rarer in syphilis than in tuberculosis. In syphilis vegetations are chiefly found on the base of the epiglottis, on the ventricular bands and the vocal cords (in tuberculosis they are usually found in the interarytenoid region). Syphilitic vegetations show a peculiar tendency to bud out ; they are usually associated with ulceration, tend to disappear and give place to a cicatrix. Tubercular vegetations continue to grow. If tuberculosis complicate syphilis, the diagnosis is exceedingly difficult. This association is not rare. It is remarkable that tuberculosi.s, if it be asso- ciated with syphilis, is less severe and less rapid than when it is present alone in the larynx. 4. Cancerous Laryngopathy. — The diagnosis is extremely difficult, becsuse cancer of the larynx may be almost latent for a year or two ; it does not affect the general health, the appetite remains good, the patient does not waste away, and the glands are not yet infectec'. Vocal troubles alone are present, but they have no distinctive character. Later, when the cancer has ulcerated, the nature of the lesion, the ready bleeding, the foetor of the breath, the acute pains in the throat and the ear, and the bloody expectora- tion, are signs in favour of cancer. But during the first period — and this period may be lengthy — how can a diagnosis be made ? In the first place, if the patient have no syphilitic nor tubercular taint, the question is somewhat simphfied. Cancer at the outset is always unilateral, and the lesion is clearly DISEASES OF THE LARYNX 39 circumscribed ; the " seat of election " is the ventricular band or the vocal cord. When the cancer is polypoid, it is distinguished from other vegeta- tions by the fact that the ulcer deepens in proportion as the tumour grows (Krishaber). The f ungating mass of cancer resembles a cauliflower ; it is ulcerated and bleeds easily. We find nothing similar in syphilis or tuber- culosis. 5. Polypi of the Larynx. — The polypoid growths of syphilis must not be confounded with the vegetations of tuberculosis and with papillomata. Tubercular vegetations are colourless, covered ^vith muco-pus, implanted on an ulcerated surface, and surrounded by more or less oedematous mucosa ; they are usually situated on the posterior part of the cord, or on the anterior process of the arytenoid. The papilloma may be as large as a millet-seed or a hazel-nut ; it may be pedunculated or sessile ; it is pearly, wrinkled, and sometimes covered by whitish mucus. Its " seat of election " is the anterior third of the free edge of the vocal cords, because this part is rich in papillfc and glands. These polypi cause vocal and sometimes respiratory troubles. G. (Edema of the Larynx. — Oedema of the larynx, due to many other causes, may simulate that due to syphilis. Dyspnoea, stridor, and sucking-in exist in both cases, and therefore careful examination should always be made as to the cause, in order to institute antisyphilitic treatment without delay if it be required. Treatment. — The recognition of syphilitic changes in the larynx is most important, because, except for certaui tertiary lesions and cicatricial stenoses, syphilitic affections of the larynx yield very readily to specific treatment. Local treatment is of only secondary importance ; specific treatment is imperative. Inunctions or solutions of mercury and iodide of potassium in large doses give very good results. The vocal and respiratory troubles disappear — sometimes slowly, at other times quickly — and in many instances specific treatment has averted troubles which seemed to demand tracheotomy. We must bear these facts clearly in mind. Krishaber has pul)lished some absolutely remarkable cases. For some years I have exclusively employed oily or aqueous injections of biniodide of mercury, and I find this preparation so superior that I treat syphilis by means of these injections alone, and hardly ever use iodide of potassium. This treatment will be found in the Appendix on Therapeutics. In some cases, however, this treatment does not at first succeed. We must persevere, and severe cases which have resisted treatment for twelve days or a fortnight begin to yield, provided we keep on. I have seen patients in a state of asphyxia from syphilis of the larynx. They had already taken mercury and iodides, but still the lesion had made progress, because the doses wcro neither sufficiently increased nor continued for a sufficiently long period. 1 have had the satisfaction of seeing these [Kiticiits recover. 40 TEXT-BOOK OF MEDICINE We must not be too ready to perform tracheotomy. Even when asphyxia appears imminent, death rarely occurs from syphilis of the larynx, and, if we push the treatment which I have just indicated, we shall generally succeed in averting the danger without operation. When tuberculosis and sypliilis are present together, it seems, according to the most recent statistics, that it may be advantageous not to treat the syphilis. Tonic treatment must especially be employed. In addition to the fact that mercury and iodides weaken a tubercidar patient, tuberculosis progresses in proportion as syphilis improves ; indeed, it appears to assume an exceptionally serious character. On the other hand, the two affections appear to neutralize one another to a certain degree — at least, for a time. Hereditary Syphilis of the Larynx. The larynx is no more secure from the lesions of early or late hereditary syphilis than other organs. " The laryngeal manifestations of hereditary syphilis are much more common in youth than we usually think. Mackenzie has met with a great number of cases, some in the first year (early hereditary), and others up to twelve and fifteen years (late hereditary)." The lesions attack the epiglottis (perichondritis), which is red, thick, ulcerated, and adherent to the neighbouring parts (larjnigeal atresia). The arytenoid regions and ventricular bands are infiltrated and covered with vegetations (Moure). The vocal cords are sometimes normal, at other times thickened and ulcerated. Vocal and respiratory troubles are the chief symptoms. The voice is husky or inaudible, and in the child who cannot talk the cry presents the same changes (Sevestre). Respiration is embarrassed from simple breathlessness to the most severe dyspnoea. I am convinced that many infants with laryngeal troubles which simu- late inflammation or oedema of the larynx are really suffering from heredi- tary syphilis. I saw, with Dr. Bonin, a young infant who had been seized with such severe attacks that tracheotomy was discussed. The attack yielded after some days, thanks to Van Swieten's liquor. M. Sevestre has reported several cases of the same kind. We cannot pay too much attention to the pathogenic diagnosis of laryngeal affections. V. TUBERCULOSIS OF THE LARYNX— LARYNGEAL PHTHISIS. Pathological Anatomy. — Each organ or each tissue reacts, in its own way, to the invasion of the tubercle bacillus. The large nasal tubercle, which might almost be taken for a sarcoma, and the small tubercular granulations scattered over the intestine or the meninges look quite different, and yet the same micro-organism is the cause in both cases. The larynx, too, has its DISEASES OF THE LARYNX 41 own peculiar kind of tuberculosis, and we find three varieties of lesion, either alone or in combination : infiltration, ulceration, and vegetations, are the usual lesions in tuberculosis of tlie larynx. In acute cases, and especially in acute pharyngo-laryngeal tul)ercu- losis, the miliary granulations are scattered over the surface of the larvnx ; but in chronic cases, which are much more frequent, the granulations are, so to say, hidden in the base or aroimd the ulcerations. The chief feature in tuberculosis of the larynx is infiltration ; ulcerations and vegetations may be present or absent. Tuberculous infiltration may attack all the layers of the lar^mx. It invades the glands, and develops at the expense of the connective tissue and of the epithelial cells ; it surrounds the vessels like a muff ; the tunica adventitia is involved, and the lumen of the vessel is obliterated. In the muscles it produces an interstitial myositis. Lastly, it becomes diffused throughout the different tissues, and provokes hypertrophic indurations, which, though bordering on fibrosis, only look like (edema (Doleris). In the cadaver the tuberculous infiltration appears as a greyisli or yellowisli swelling, with uniform or uneven surface ; it is firm to the touch, and fairly hard on cutting. For a long time tliis swelling was mistaken for oedema (Gougenheim). The interarytenoid region, the arytenoids — which stand out like sugar- loaves — the ventricular bands, the aryteno-epiglottic folds, and the epi- glottis, take part, separately or simultaneously, in the swelling, wliich may be considcra]>le. The vocal cords are more rarely swollen ; they are reddish, streaked with vessels, and sometimes resemble cushions in appearance. In some regions of the larynx, as in the vocal cords, the process is charac- terized by a fibrous or fibro-caseous condition, which closely resembles lupus. Laryngeal tuberculosis is often ulcerative. The ulcers begin in the superficial layer of the mucosa, often in a caseous gland. Small caseous foci are seen on the interarytenoid mucous membrane, the epiglottis, the folds, and the vocal cords. The lesion develops in the corium of the mucosa. First, congestion of the part, and, later, nniltiplication of the connective cells, are seen. This infiltration, which is primarily submucous, and especially active in the glandular acini, extends and undergoes caseous degeneration, followed by ulceration. These ulcers often become more extensive by the coalescence of secondary ulcers. The edges are jagged and infiltrated with tubercles ; the floor is covered with large polypoid vegetations, especially in ulcers of the interarytenoid region. The arytenoid region is generally first affected ; the ulceration may deepen and attack ihe crico-arytenoid articulation and the perichon- drium. The arytenoid and cricoid cartihiges are frequently attacked, while 42 TEXT-BOOK OF MEDICINE the thyroid cartilage usually remains free. In some cases the lesion starts in the perichondrium or in the joint, and forms a " tumor albus " con- taining bacilli. The invasion of the cartilage is preceded by calcareous infiltration and ossification, and is followed by necrosis, expulsion of the sequestrum, suppuration, fistula, and oedema. The sequestrum is reddish, dry, and situated at the bottom of a foul-smelling anfractuous cavity. The elimination of sequestra provokes migratory abcesses, and the pus finds its way into the larynx or the pharynx, or outwards through the skin. (Edema of the larynx, subcutaneous emphysema, and laryngeal fistulae result from this process. Tubercular ulcerations also attack the aryteno-epiglottic folds, and may destroy the ventricular bands, obliterating Morgagni's ventricles. The epiglottis is more rarely ulcerated. When it is attacked, the base and the laryngeal surface suffer, whereas syphilis usually affects the lingual surface. The vocal cords are often ulcerated, toothed like a saw, or completely destroyed. The vegetations in laryngeal tuberculosis may show two forms. In the first form the vegetation develops in an ulcer, and forms a bud, which is limited to the ulcerating surface and has a papillomatous appearance. These papillomata, wliich are chiefly found at the arytenoid region and the posterior part of the vocal cords, may grow to a large size. Sometimes they look like cauliflowers, partially obstruct the orifice of the glottis, and, as they are lacking in firmness, are easily detached. If they should fall into the respiratory passages, they may give rise to the gravest accidents. In the second form the vegetation does not begin in an ulcer, but develops on its own account, and is chiefly met with in primary tuberculosis of the larynx (Mandl). In tubercular laryngitis the peritracheal and bronchial glands are often attacked by inflammation, and cause lesions of the recurrent nerves. Symptoms. — Tuberculous infiltration may exist at certain points in the larynx without causing any symptoms. As a rule, the lesion is slow in its progress. At first it invades the arytenoid region, the ventricular bands, and the vocal cords, and for some time the only symptom is hoarse- ness and muffling of the voice ; neither respiratory troubles nor pain are present at this stage. In some cases, however, even from the first the patient experiences a tickling in the larynx, which is very disagreeable, and causes incessant jerky cough. The sufferer firmly believes that a particle of food has been arrested in the larynx. In some cases the voice remains almost normal, but the breathing is rather short and quick, and inspiration is more noisy than in the normal state, because the inspired air meets with resistance at the swollen glottis. DISEASES OF THE LARYNX 43 If tlie lar}Tix be examined at this stage, which may be of indefinite duration, we are struck by the unusual pallor of the velum palati, the pharynx, and the vestibule of the larjmx. We find swelling of the inter- arytenoid tissues, which are specially affected by tubercular lesions ; the cartilages of Santorini, the aryteno-epiglottic folds, the ventricular bands, and the epiglottis are all swollen. In some cases the vocal cords are greyish, or rosy and enlarged. At a more advanced stage these lesions are more marked ; the infiltration causes the arytenoids to stand out like sugar-loaves, and the interarytenoid space is covered with vegetations, while the ventricular bands are enormous and cover the subjacent vocal cords, which are no longer visible. The aryteno-epiglottic ligaments, which are fixed and swollen, narrow the aperture of the larynx ; the vocal cords are streaked with red, especially on their posterior third, have a skin-like appearance, and show erosions and indentations, while one cord is paretic and does not approximate well. Finally, the larynx as a whole is irregular, funnel-shaped, and covered with thick mucus. At this time the vocal troubles are very marked, yet aphonia may not be complete and dyspnoea may not be severe. The disease may remain for an indefinite period in the stage of tubercular infiltration without ending in ulceration ; if ulceration ensue, dyspnoea and acute pain supervene. The voice is almost completely lost ; sometimes the aphonia is complete, and it cannot well be otherwise, since the vocal cords are hypertrophied, ulcerated, covered by the enlarged ventricular bands, and fixed by the ankylosis of the arytenoids. The cough depends rather upon the changes in the lung than upon the lesions of the larynx ; it is stifled and belching (Trousseau and Belloc), so that the patient, when coughing, appears to be making attempts at belching.* Acute perichondritis is revealed by sharp pains, with respiratory embarrass- ment. If an abscess forms, the dyspnoea becomes excessive, and the abscess, which is situated in the arytenoid, opens into the pharynx or the larynx. Ulcers on the base of the epiglottis and on the aryteno-epiglottic folds are often associated with similar lesions of the base of the tongue and of the pharynx ; they render swallowing extremely painful. This dysphagia is so painful that in some cases the patient feels as though " a live coal had been swallowed." Not only is the pain made worse by the least attempt at swallowing, but in .some cases the patient experiences constant hvpor- sosthe.sia of the back of the throat. The saliva, which is abundant, cannot be swallowed, and drips from the mouth ; the patient, deprived of rest, sleep, * Thi.s phonnmcnon is easily oxplaincd. In iho. j)liy.'*i')l()gi<'al condition tin' smidcn opening of the vocal cords by a jerky (-xpirat ion gives llie coiigii its pciculiar tunc ; but in la^\^l<:(■al |)litliisis, as tlio wido-opon glottis no longer offers any resistance, tlio oxpinxl air is belched out. 44 TEXT-BOOK OF MEDICINE and nourishment, becomes marasmic and disheartened if relief be not forth- coming. Aural pain, which may be very intense in all laryngopathies, is sometimes present. Dyspnoea, which is so often seen in advanced tuberculosis of the larynx, is due to infiltration, swelling of the tissues, oedema of the larynx, polypoid vegetations, and to perichondritis, with its resultant abscesses. Every variety occurs : it may be slow or sudden in its appearance, and is sometimes accompanied by attacks of suffocation and spasms of the glottis. The breathing, which is harsh or noisy, sometimes takes a strident character. Laryngoscopic examination is often difficult by reason of the abnormal positions of the epiglottis, the swelling, the oedema, and the muco-purulent secretion which covers the larynx. The course and duration of the malady are very variable. In some cases the march of events is rapid, and life is threatened by an abscess following acute perichondritis, by oedema of the glottis, or by pulmonary phthisis, which complicates the laryngeal mischief and hastens events. The patient becomes marasmic, the wasting is extreme, and hectic fever closes the scene. Catarrhal Form. — I have just described the most common form of laryngeal tuoerculosis, which runs a slow course ; in some cases, however, the disease begins abruptly, like simple catarrhal laryngitis, with cough, sudden hoarseness, and aphonia, which may be complete and last for several days. Laryngoscopy reveals nothing but redness, swelling of the mucosa, and more or less abundant secretion. If the patient already have tubercular lesions in the lungs, though he have only slight signs, the laryngitis is open to discussion. Some writers say that it is tubercular, other writers call it " laryngitis in tubercular subjects." I do not say that tubercular patients cannot have catarrhal laryngitis, but I think that most cases of so-called catarrhal laryngitis in phthisical subjects are tubercular. They are more persistent than cases of simple catarrh, they are subject to relapses, they leave infiltration of the mucosa behind them, and though they are sometimes completely cured, yet they may end in infiltration and ulceration. This laryngitis, therefore, in a patient with haemoptysis, pleurisy, or tubercular lesions in the lungs, is really tubercular, even though it be apparently benign and catarrhal. Though it may be cured, and may rarely end in the other forms of laryngeal phthisis, I consider it as a manifestation of tuberculosis, just as are those cases of pleurisy or of haemoptysis which sometimes super- vene during excellent health. They are, nevertheless, the first sign of tubercular mischief that will be fully developed some months or years later. So-called catarrhal laryngitis presents in some cases frankly tubercular lesions, which prove that bacillary infection may occur, not only in the DISEASES OF THE LARYNX 45 depth of the tissues, but also in the superficial layers. Heintze, quoted by Hering, saw a trifling infiltration of the ventricular band, and found bacilli in it, between the epithelium, in the glands, and in the cylindrical epithelial cells of the glands. The bacillus, says M. Hering, may be introduced by the glands, and thus provoke an infection of superficial origin. Diagnosis. — Let us first establish the diagnosis at the start of the malady. The symptoms of laryngeal tuberculosis in its first period — namely, cough, hoarseness, and dysphonia — are common to every chronic laryngitis. These symptoms, therefore, cannot give sufficient data either Lor or against tuberculosis. Laryngeal tuberculosis may begin with paralysis of a vocal cord, the appearance of a papillomatous vegetation, or an attack of catarrh. An affirmative diagnosis, therefore, is difficult at the outset. Certain signs, however, are of very great importance. One of these signs is the unusual pallor of the velum palati and of the epiglottis. This pallor is sometimes as marked as in most characteristic anaamia ; the mucosa of the palate and the parts of the larynx which are usually pink take on a dull, greyish, and sometimes opaque tint in tuberculosis. This pallor is not seen in non- tubercular laryngitis, and is therefore a valuable sign. Another sign in laryngeal tube^rculosis is the initial localization of the lesions. The interarytenoid and the arytenoid regions are the seat of election in tubercular lesions ; swelling, granulations, and vascularization of the above regions, together with the anjemic appearance just described, are strongly in favour of tuberculosis. At a more advanced stage we must distinguish phthisis from syphilis and from cancer of the larynx. This question is fully discussed under Syphilis of the Larynx. Syphilis rarely attacks the vocal cords ; it seizes the parts which adjoin the pharynx — i.e., the epiglottis and the posterior surface of the arytenoids. Furthermore, syphilitic idceration is usually limited to one point, and does not invade the rest of the larynx. In tuber- culosis the ulcerations are multiple, and accompanied by more or less inteuso laryngitis. Tubercular ulcerations are frecpioiitly covered by p()ly[)()id growths, which are much rarer in syphilis. Syphilitic ulcerations are quickly imjiroved by treatment, whilst remedies have practically no effect on tubercular ulcerations. SyphiUs, like phthisis, may attack the cartilages, but in eighteen cases out of twenty necrosis of the larynx is of tubercular origin. By scraping the ulcer we can remove some particles of secretion and fitid the tubercle bacillus. Cancer of the larynx, and especially epithelioma, presents the peculi- arity of being almost indolent, and of having a very much slower course in the larynx than in other organs ; indeed, a patient with cancer of the larynx may live for two or three years after tracheotomy (Krishaber). \'ocal 46 TEXT-BOOK OF MEDICINE troubles are for a long while the only symptom, and when other local and general symptoms supervene, such as haemorrhage, foetor of the breath, dysphagia, pain, dyspnoea, etc., the laryngoscope generally reveals the cancerous vegetations. etiology. — According to Heintze, the larynx of adults who are suffering from pulmonary tuberculosis is aiTected in 50 per cent, of the cases. In some cases the laryngeal trouble is primary, and appears as the first mani- festation of tubercular infection. As a rule, laryngeal tuberculosis is secondary to pulmonary disease, and the infection of the larynx takes place either by the deep path of the vessels and lymphatics or by the superficial path along the surface of the mucosa, or through the excretory ducts of the glands. Louis supposed that the constant passage of infected sputum from the lungs infected the larynx. As for the other causes, they closely follow the aitiology of pulmonary phthisis. Males appear more predisposed than females, and the malady occurs in the former between twenty- five and forty years of age. In the child laryngeal tuberculosis deserves special mention : the younger the child the rarer the disease. Parrot found tubercular laryngitis in only 3 per cent, of autopsies on infants under two years. In the infant pul- monary tuberculosis is usually of the miliary form ; the child does not expectorate, and its larynx is not bathed in pus swarming with bacilli ; this factor, no doubt, helps to explain the rarity of tubercular laryngitis in children. In my experiments with Krishaber we studied the results of inoculation and contagion in the ape.* We were struck by the fact that animals which had been inoculated and had died from tuberculosis showed no tubercular changes in the larynx. Treatment. — Laryngeal tuberculosis is not incurable. It sometimes remains stationary, and several cases (Hering) prove that the tubercular ulcers may be cured. Every effort must be made to relieve the dysphagia and the hypersesthesia of the back of the throat, which cause such torture to the patient. For tliis purpose hypodermic injections of morphia should be given morning and evening. At meals the painful parts should be touched with a brush or a sponge, mounted on a curved handle and soaked in the following solution : Cocaine hydrochlorate . . . . 1 part. Water 50 parts. With a little practice, the patient himself can paint the painful parts with the solution, but he must avoid swallowing it. Inhalations and sprays of * Dieulafoy and Krishaber, Arch, de Physioloyie, March, 1881, No. 3. DISEASES OF THE LARYNX 47 water containing a little sulphur (AUevard) may render some service. Painting the ulcers with a 10 per cent, or 20 per cent, solution of lactic acid, and later with the pure acid, sometimes yields good results. Ruault employs phenol and sulphur in castor oil. The cough may be reUeved by careful intratracheal injections of menthol in oily solution, but this method demands much judgment. The gargles of very hot and astringent wine which Bonnier employs for gouty laryngitis are also of service, by soothing the cough and the pharyngo-laryngeal irritation. Bonnier prefers insufflations which the patient can use without the physician's aid, such as iodol, 1 part ; sodium benzoate, 6 parts ; tolu, 'J parts ; taimin, 1 part ; gum arable, 3 parts ; cinnamon, 020 part, to sprays of menthol or eucalyptus. Curetting the ulcers and cauterization has rendered good service in experienced hands. The " altitude cure " is not contra-indicated in cases of tubercular laryngitis. I have seen the larynx, as well as the lung, improve by the cure at Davos-Platz. VI. LARYNGEAL DIPHTHERIA- CROUP.* Definition. — Croup, or pseudo-membranous laryngitis, is charac- terized by tlie presence of membranes in the larynx and trachea. These membranes may exceptionally be due to a non- diphtheritic lesion, the diphtheria bacillus taking no part in the process. CUnical medicine had created a simple croup, said to be neither contagious nor infectious, and, indeed, clinical medicine was right. Bacteriology has shown that false membranes in the larynx and pharynx may be produced by microbes which have nothing in common with the diphtheria bacillus. A small diplococcus may give birth to membranes in the larynx or the pharynx, although it has none of the toxic properties of the diphtheria bacillas. We shall return to this point later. We fuid, then, diphtheritic croup, Avhich is the rule, and non-diphtheritic croup, which is the exception. History.t — In 1765 Home, a Scotch physician, published an interesting monograph on croup. He was the first to indicate clearly the characteristics of tliis malady, and to separate it from certain affections of the pharynx with which it had been previously confounded ; but he was doubly wrong in mistaking the identical nature of diphtheritic angina and of croup, which other observers had previously established, and in giving a single description for two distinct maladies — i.e., false croup and true croup. Bretonneau, * To avoid rcpelitions, seo articK'S on Diphtheria and Diplitlieritio Angina. t To complcto tho history, refer to the cliaptor on Diplithoria. 48 TEXT-BOOK OF MEDICINE in his memorable work on diphtheritis, re-established the identity which Home had failed to recognize. He applied the term " laryngite stridu- leuse " to a malady which simulates croup, but which has nothing in common with it. We know how brilliantly Trousseau completed the teachings of his master, Bretonneau, on diphtheria and croup, and with what success he made the operation of tracheotomy popular. The bacteriological researches of recent years have given valuable precision to the diagnosis and the prognosis of croup, while serotherapy has completely modified the treatment. Division — etiology. — Croup is primary when the diphtheria which engenders it attacks the patient while in good health. It is secondary when the diphtheria supervenes as a complication in the course of some other malady, such as measles, scarlatina, whooping-cough, or typhoid fever. Croup usually follows diphtheria of the pharynx, and statistics prove that the larynx is chiefly invaded from the second to the fifth day of the angina. Croup sometimes follows diphtheritic COryza — that is to say, the diphtheria begins in the nose and spreads to the larynx. Cases of croup secondary to diphtheria of the bronchi have been seen, and have been called " ascending " croup. Diphtheria may also invade the larynx before other parts, and the di-sease is then called primary. This form, however, is very rare, and, in order to vouch for this fact, we must be certain that the throat and the nasal fossae are normal. In some cases croup appears though false membranes in the throat are absent, and yet cultures made from the mucus on the tonsils may show the diphtheria bacillus. We see, therefore, how rare primary croup must be. The chief causes of croup are epidemicity and contagion. Contagion is only too well proved by the numerous examples of physicians who have contracted the disease from their patients. In certain parts — Paris, for example — croup is endemic Epidemic croup sometimes rages Avith terrible severity, as witness the epidemics which ravaged Europe in the sixteenth and seventeenth centuries — the enfermedal del garrotillo in Spain, the morbus strangulatorius in Italy. Croup spares no age, though it chiefly attacks infants between the age of two and seven years. Symptoms. —The present description refers to diphtheritic croup in children. Whether croup at once invade the larynx, or whether it be preceded by diphtheritic tonsillitis or coryza, the growth of membrane in the larynx and the trachea is immediately announced by vocal and respira- tory trouble. The false membrane may be said to sum up almost the whole history of croup, for its presence on the vocal cords and in the larynx alters the normal sounds, narrows the glottis, and hinders or prevents the entry of air into the lungs. r DISEASES OF THE LARYNX 49 The pathological role of the false membrane, however, is essentially a mechanical one. In some cases this mechanical role is of secondary importance, and the gravity of the illness does not arise from the obstruction of the larynx, but comes from the preceding angina, from the poisoning of the economy by the diphtheritic toxine, from the concomitant bronchitis and broncho-pneumonia, from the addition of secondary infections, from the association of the streptococcus with the diphtheria bacillus, etc. Cough is the earhest sign of croup. Slight and trifling at first, it returns in very short fits ; during the next few days it acquires a dull and muffled quality, and becomes as inaudible as the voice. As the disease progresses the cough becomes less frequent, and the fits only recur every quarter or half hour, and even at longer intervals (Trousseau). The voice is at first hoarse, but after some days it becomes inaudible, and the aphonia is com- plete. Vox nihil significat, said .\jet3eus. In the child the respiratory troubles are early and marked, because the larynx is narrower than in the adult. The dyspnoea, which is at first slight, begins at night, and is ushered in by shght whistling on inspiration ; it increases as the aperture of the glottis becomes narrowed by the false membrane, which forms chiefly on the aryteno-epiglottic ligaments and the vocal cords, and as the air meets. an obstacle, the inspiration is changed into a shrill and prolonged whistling. At the same time depression of the epigastric hollow and of the suprasternal fossse occurs. This " sucking- in " is due to the tendency each inspiration has to produce a vacuum in the chest, and to the compensatory ascent of the diaphragm. As the dyspnoea grows worse, the breathing becomes sawing, like the noise which a saw makes when it cuts stone (Trousseau). Every two or three hours at first, then every hour, and at yet more frequent intervals, we ob-serve terrible attacks of suffocation ; they result from spasms of the glottis, and resemble those seen in cEdematous or spasmodic laryngitis. This struggle may last several days, and, if the illness do not take a favourable turn, asphyxia ends the scene. " The bloated and cyanosed face, the hollow and shining eyes, express the most painful anxiety, and at length the death struggle begins, without there being from this time forward any attacks of suffocation, such as tho.se which have already occurred might lead one to expect " (Trousseau). Auscultation of the chest, when there is no pulmonary complication, reveals nothing but the echo of the laryngeal whistling. The respiratory rhythm is altered, and expiration becomes longer than inspiration, from the difliculty which the expiratory mascles experience in driving the air through the narrowed glottis. The expectoration is often characteristic, and about the third or the fourth day tiie patient coughs up shreds of membrane — Hat if they come from 4 50 TEXT-BOOK OF MEDICINE the larynx, tubular and branching if the bronchi be invaded. False membranes are coughed up in half the cases. The fever in croup is not, as a rule, high, and the temperature varies between 101° and 103° F. Albuminuria is frequent (See, Barbosa), and is due to nephritis, caused by the diphtheritic toxines. Multiple eruptions have often been noted in croup, as in diphtheritic angina (See) ; they show different forms and simulate the exanthems of measles and of scarlet fever. In adults the symptoms of croup present some differences, becau.se of the shape and size of the larynx. The modifications of the cough and voice are the same, but dyspnoea and asphyxia supervene slowly, and are not, as a rule, accompanied by stridor and attacks of suffocation. Course — Duration — Prognosis. — The course of croup may be divided into two periods — the first of dyspnoea, the second of asphyxia — while the two together may last from three days to a fortnight ; but many exceptions, especially during an epidemic, are seen in the course and the succession of symptoms, and the disease may be fatal on the third or even on the second day. Trousseau's lectures on diphtheria and croup will suffice to warn us against the surprises of tliis disease, and to show us how suddenly death may appear. These fulminant forms are chiefly seen in adults, and are due rather to the virulence of the infection than to the lesions in the larynx. A terrible attack of suffocation may occur, and be followed by continuous dyspnoea, or dyspnoea may come on without attacks of suffocation, and the patient succumb to the infection (malignant diphtheria). Abortive croup has been described. I have seen such an example in a little boy who, some days before, had been attacked by nasal diphtheria. In abortive croup the false membrane remains limited to the vestibule of the larynx, or, at least, the cords are scarcely affected. The vocal troubles are absent or insignificant, and the respiratory symptoms are not severe. The progress of croup varies a httle, according to the virulence of the infectious element. In general terms, when we see a relative calm between the attacks of suffocation, it means that the child is not yet threatened by the infectious element. If the little patient, however, be infected by the disease (malignant diphtheria), the truce is not complete : no lull is seen between the attacks, or after the expulsion of false membranes ; permanent dyspnoea, prostration, thready pulse, and marked albuminuria bear witness to the virulence of the infection and the gravity of the prognosis. Cases of prolonged croup must be recognized. M. Cadet de Gassicourt has cited cases of croup which lasted fifteen, twenty, or twenty-five days, and recovered ; there was no asphyxial stage, and tracheotomy was not per- formed. During the course of the disease remissions are sometimes seen : the DISEASES OF THE LAKYNX 51 voice regains its tone and the breathing its freedom ; but this improvement, which is due to expulsion of membrane, is too often transient, and must not be mistaken for recovery. Croup is an extremely serious malady, which formerly, even with surgical intervention, often ended in death. Injections of serum have recently improved the prognosis to a striking extent. Complications.— Diphtheria of the bronchi may precede or follow the laryngeal disease. In every case it increases the danger, because it adds a fresh obstacle to that already present in the larynx. The patient brings up membranes, which may be tubular, rolled up, or like coagulated mucus. Broncho-pneumonia is a still worse complication, which appears at all periods, both before and after tracheotomy, but, as a rule, from the third to the sixth day of the disease. It is sometimes accompanied by gangrene of the lung. Its onset is followed by a rise of temperature and violent dyspnoea, so that in a child the respirations may exceed sixty (Millard). Diphtheritic broncho- pneumonia is nearly always lobular, and not pseudo- lobar. Anatomically it is characterized by a large amount of fibrin and by hajmorrhages into the pulmonary lobules. Klebs' bacilli, and many other microbes — streptococci, pneumococci, and staphylococci — are found in the alveoli. In this variety, as in other kinds of broncho-pneumonia, these secondary infections play a most important part in the production of broncho- pulmonary lesions. Pleurisy is sometimes a complication, but is of moderate importance. Diphtheritic coryza, considered by Trousseau as of evil augury, is often present in the malignant form of diphtheria. In children tuberculosis is often associated with diphtheria of the respiratory tract. " The gravity of tuberculosis is such," says Variot, " that in fifty-four deaths which occurred in January and February at the Bretonneau Annexe, we found tubercular lesions in the thoracic organ? sixteen times." After croup, as after all the local manifestations of diphtheria, we some- times see paralysis ; but, as croup is rarely the only manifestation of diph- theria, these paralyses are chiefly due to the concomitant angina. Lastly, the eruptive fevers may appear in the course of croup, and give rise to serious complications. Diagnosis. — In cases where the diagnosis is difficult the laryngoscope must be employed, especially in adults. This method has often confirmed a doubtful diagnosis by revealing the presence of membranes in the larynx. Acute laryngitis, oedema of the larynx, and spasmodic laryngitis are the diseases which most resemble croup. In simple acute laryngitis the vocal and respiratory symptoms are not so severe, and do not gradually get worse, as they do in croup. In oedema of the glottis, which is very often but a part of some other disease, the antecedents at once enlighten us. In any 4—2 r,2 TEXT-BOOK OF MEDICINE case, the respiratory symptoms are worse than the vocal ; expiration is easier, less prolonged than in croup, and sometimes accompanied by a hruit de drapeau. The supraglottic oedema, which causes the dyspnoea, may also be visible. The diagnosis between croup and laryngitis due to hereditary syphilis demands special notice. The symptoms may simulate those of croap so closely that errors have been made. In my lectures at the Faculte I reported the case of a young child who was about to undergo tracheotomy for asphyxia set down to croup. Van Swieten's solution was given as soon as hereditary syphilis was diagnosed, and we succeeded in curing the child in a few days. M. Sevestre has reported several analogous cases. The possibility of laryngeal syphilis must always be considered in a young child who, in the absence of previous diphtheritic angina and of glandular en- largement, presents symptoms analogous to those of croup. The diagnosis between croup and false croup is somewhat difficult. The two diseases have a different onset. The invasion of croup is more insidious, and the respiratory symptoms gradually become intense. The invasion of false croup is more sudden. A cliild who has gone to bed in good health wakes suddenly, in the middle of the night, suffering from dyspnoea that reaches its height at once, and, this attack over, the patient appears next day to be in good health. In croup the cough and the voice are mufHed ; the presence of membrane on the vocal cords explains the aphonia. In false croup the voice and the cough are harsh and noisy, and resemble the barking of a dog. They are not muffled, as in croup, at any rate, between the attacks. During the attack of false croup, however, they may be muffled. Besides the signs peculiar to each disease which I have just enumerated, careful inquiry should be made into the antecedents of the patient : informa- tion should be sought as to whether diphtheritic angina have been recently present, and we must try to discover if some signs of it, such as enlargement of the submaxillary glands, do not remain ! we must not forget that croup is the only malady of the larynx which may be accompanied by the rejection of false membranes. Bacteriological Diagnosis. — The clinical diagnosis of croup is in many cases insufficient, and must be completed by the bacteriological examination of the membranes. Full details are given under Diphtheritic Angina, for diphtheritic angina and laryngitis are closely associated. I recapitulate here the points referring to croup. As I have already said, the diphtheria bacillus is not the only microbe capable of producing false membranes. Just as there are pseudo-diphtheritic anginoe, so there is a pseudo-diphtheritic croup. This form of croup is neither contagious nor infectious ; it is not accompanied by toxic symptoms, and is not marked by malignancy ; it is due to a small diplococcus (Brisou's coccus). DISEASES OF THE LARYNX 53 Martin records seven cases of croup due to this diplococcus, with mem- braneous angina of the same nature, and twelve cases of croup due to the same coccus, without previous angina. Non-diphtheritic croup, due to the diplococcus in question, is infinitely less serious than diphtheritic croup. It is not toxic ; recovery usually takes place without secondary infections and without tracheotomy. In these attenuated forms it may simulate stridulous laryngitis ; indeed, I am of opinion that certam cases of false croup are nothing else than a mild laryngitis, due to the diplococcus. In other cases the bacteriological examination of the membrane in croup reveals both the diphtheria bacillus and the small coccus. This association of the diplococcus and the bacillus is not usually grave, and M. Martin's monograph shows that these cases recover without secondary infections. On the other hand, when examination reveals the association of the diphtheria bacillus wdth the staphylococcus or the streptococcus, the prog- no.sis is bad. The same remark applies in the case of diphtheritic angina. The presence of the streptococcus in croup, as in angina, should make us fear grave results. In such a case the symptoms comprise marked glandular enlargement ("the proconsul's neck," Saint Germain), nasal discharge, diarrhoea, and albuminuria, which lead us to fear the death of the child as much from the general poisoning as from the croup. These few data, with which every physician must to-day be familiar, sufficiently indicate, in my opinion, the importance of bacteriology in the present question. If we cannot make a direct examination of the membranes from the larynx, the membranes and the mucus in the throat must be examined, and, even in the absence of membrane in the throat, the culture from a piece of mucus removed from the tonsil or from the pharynx may often allow accurate diagnosis and prognosis to be made. Secondary Croup, — This variety supervenes in the course of some other disease, such as measles, scarlatina, whooping-cough, or typhoid fever. The details will be found under these different diseases. In general terms, the secondary forms are less characteristic in their ways than primary croup and moro readily take on an infectious character. Croup in Measles.— Diphtheria has a liking for measles. Orouj) in measles is sometimes primary, and may appear about the same time as the rash. The disease is often mild, and the laryngeal symptoms are slight : yet the prognosis is extremely grave, because of the broncho-pneumonia which accompanies it, and of the double infection of meades and diphtheria. The membranes in the larynx are softer and more diffluent, and the lesions are more of the ulcerative type. Croup in Scarlatina. — Croup is much rarer in scarlatina than in measles ; it rarely occuirs alone, and more often coincides with diphtheria of the pharynx and the nasal fossae. 54 TEXT-BOOK OF MEDICINE Croup in Whooping-Cough. — Secondary croup in whooping-cough comes next to that of measles in frequency. Croup in Typhoid Fever. — Croup is excessively rare in the course of typhoid fever. Pathological Anatomy. — In croup the catarrhal inflammation of the mucosa, the congestion and the oedema of the submucosa, are of secondary moment ; the false membrane is the chief lesion. It covers the different parts of the larynx, and especially the aryteno-epiglottic ligaments and the vocal cords, either as a continuous membrane or in isolated patches. In colour it is a yellowish-white, sometimes tinted with minute haemorrhages. In some cases it is very thin, but in other cases its thickness may be as much as 2 millimetres, owing to the stratified layers which grow on its deep surface. The younger these layers are the greater their resistance, while the older layers, which are pushed towards the surface, have become friable. The false membranes are composed, not only of fibrin, but also of pus corpuscles and epithelial cells from the mucosa, which undergo a colloid infiltration, taken by Wagner for an albuminoid substance. These epi- thelial cells, converted into refractile blocks, are deformed and branched like a stag's horn (Wagner). Each stratum of the false membrane develops at the expense of the corresponding epithelial layer, and becomes more super- ficial as a fresh subjacent layer is produced. " It has been debated whether the false membrane is above or below the epithelium ; from what has been stated above, we see that it is formed exactly in the superficial layer of the epithelium, and partly at its expense. Its structure, too, seems to differ according to its age ; at the outset the epithelial network appears to be prominent, but a little later the fibrinous and purulent elements are in excess " (Leloir). The mucosa beneath the false membrane is usually intact, and rarely ulcerated. The diphtheria bacilh, the poison which they elaborate, and their association with other bacteria, are described in detail under Diph- theritic Angina. The diphtheria bacillus undoubtedly gives rise to the membranes, and to the poison which provokes intoxication and paralysis. Treatment. — I cannot here enter into all the details of serotherapy, and the reader is requested to consult the chapter on Diphtheritic Angina for further details. I shall here describe the application of serotherapy to croup. The results of treatment largely depend upon the previous performance of tracheotomy. The results are likewise very different, if the croup be due to the diphtheria bacillus alone, or if it be due to the bacillus associated with the staphylococcus or the streptococcus. Let us consider these results. DISEASES OF THE LAEYNX 55 1. A child who is suffering from croup has not yet been tracheoto- mized. The cough is raucous, the voice is inaudible, the breathing difficult, and the sucking-in well marked. Severe attacks of suffocation occur at brief intervals. At first sight tracheotomy seems unavoidable, but an injection of 20 centimetres of serum is given. Twelve hours later a second injection is given, and in the great majority of cases the injections of serum arrest the formation of fresh membranes, favour the r-.pid disappearance of those already formed, and recovery is rapid. " In 169 cliildreu admitted for diphtheritic angina, fifty-six showed lar}Tigeal trouble, and in twenty-five tracheotomy appeared unavoidable. Under the influence of injections of serum every twelve hours, the sucking-in decreased, and afterwards only returned in fits. The child brought up the false membrane, and after two or three days the breathing was natural, to the great astonishment of the house-physicians and attendants in the diphtheria pavilion, who, from their large acquaintance with children suffering from croup, quite thought the operation could not be avoided " (Roux and Martin). 2. In children suffering from croup who have undergone tracheotomy the success of serotherapy diminishes, according to the nature of the asso- ciated microbes. These associations are the same in croup as in angina, (a) The association of diphtheria with Brisou's small COCCUS is favour- able both in croup and in angina. In the statistics of Roux and Martin, the mortality was only one in ten cases, and this was due to broncho- pneumonia following tracheotomy. The quantity of serum injected amounted to 50 c.c. in divided doses. (6) The association of diphtheria with the staphylococcus is to be feared. It is not deadly in the case of angina, but is very fatal in cases of croup after tracheotomy, because it gives rise to pulmonary comphcations, such as broncho-pneumonia, which often follow the operation, and against which injections of serum are often impotent. In eleven cases Roux and Martin recorded seven deaths, a mortality of 63 per cent. The mean quantity of serum employed in divided doses amounted to 60 c.c. In these patients the membranes are pultaceoiLS and very extensive ; the temperature was always above 103° F., and the breathing was much quickened. (c) The association of the diplitheria bacillus with the streptoCOCCUS is most formidable, both in croup and in angina. In spite of serotherapy, the mortality in cases of croup which have been operated upon has b(^en 63 per cent., according to Roux and Martin. Broncho-pneumonia and pseudo- membraneous bronchitis are responsible for most of the deaths. Since many cases of secondary infection can be set down to tracheotomy, this operation must in future be replaced, when possible, by intubation. Intubation of the larynx was extolled by Bouchut, but his instrument rendered the results of intervention .so hazardous that physicians followed 56 TEXT-BOOK OF MEDICINE Trousseau's advice, and abandoned intubation, tracheotomy being infinitely superior. Great progress, however, has been made in the apparatus for intubation. The method has been so perfected, thanks to Collin's instru- ments and to Bayeux's technique, that hesitation is no longer possible. In the very great majority of cases intubation will replace tracheotomy. The -writings of Variot and Bayeux and of Martin give us the most com- plete information on this subject. As Bayeux says : " We run the risks of grave results — nay, even of the death of children — by delay. We risk nothing by intubation when carried out betimes." VII. STRIDULOUS LARYNGITIS— FALSE CROUP. JEtiology. — Stridulous laryngitis (Bretonneau), or false croup (Guersant), is simply an acute catarrhal laryngitis of infancy, which derives its spasmodic character from the tender age of its victims. In small children the intercartilaginous glottis is rudimentary, and the aperture of the glottis is short and narrow. Changes in the larynx are, therefore, readily accom- panied by dyspnoea, wliich in children takes the form of fits. This laryn- gitis is most frequent from two to six years, is often seen during the invasion of measles, and may be the forerunner of broncho-pneumonia. Description. — Trousseau has given so complete an account of this malady that I cannot do better than quote it in extenso ." " A child between the age of two and five years is seized in the middle of the night— about eleven, twelve, or one o'clock — with an attack of dyspnoea. He wakes out of his sleep in a very uneasy and feverish state. His cough is harsh and very frequent, but strong and noisy ; his breatliing is jerky, panting, and accompanied by inspiratory stridor. His voice, which is modified in its timbre, is inaudible during the fits, but rough and hoarse in the intervals. There is, however, one capital fact — it is never extinguished, as in true croup." Oppression and anxiety are sometimes excessive ; the face is congested, and the eyes express profound terror. This alarming crisis may last from half an hour to about three hours, but the attack then ends. The child becomes quiet, sleep returns, and the pulse-rate falls. The skin is slightly moist. Then the patient wakes up. The cough is still croupy, though looser. During the day it is still more catarrhal, the breatliing is less whist- ling, and the voice has almost regained its natural tone. As a rule, the attacks recur several nights in succession, but they always decrease in violence, while the days are good, the patient having but little fever or malaise, and suffering from a loose and less croupy cough. On questioning the parents we learn that the child went to bed quite well and fell into a peaceful sleep. Sometimes, on the contrary, we are informed that he had DISEASES OF THE LARYNX 57 been out of sorts for some days, that he had taken cold, but had retained his u^ual spirits. Lastly, if the throat be examined, the most careful examina- tion shows that false membranes and glandular enlargement are absent. This sudden onset, with symptoms wliich are more alarming in appearance than those at the commencement of croup, is in most cases characteristic of false croup. This malady results in cure, fatal cases being very rare. Diagnosis — Treatment. — The diagnosis of stridulous laryngitis is given under Croup. It is always necessary to think of hereditary syphilis of the larjTix, wliich simulates both croup and false croup. If the reader ^vill refer to Croup, he will see, under Bacteriological Diagnosis, that in some children the laryngeal troubles are due to the presence of a small diplococcus, and may resemble both true and false croup. I think that, even in a condition which has every appearance of false croup, we should not neglect bacteriological examination of the mucus or of the pharyngo-larpigeal secretions. A case which is taken for a false croup may be really laryngitis, or pharyngo -laryngitis, due to the diplococcus ; membranes may be present or absent. False croup recovers without active treatment. It is sufficient to apply blisters, or a sponge soaked in very hot water, to the child's neck (Graves). A moist atmosphere from a steam- kettle should be maintained around the patient's bed and emollient drinks given. Tracheotomy is only required in exceptional cases. False croup, however, has proved fatal. VIII. (EDEMA OF THE LARYNX— (EDEMA IN BRIGHT'S DISEASE. Syphilitic (Edema. Definition. — The terms "(Edematous laryngitis," '" oedematous laryngeal angina " (Trousseau), " laryngeal infiltration " (Jaccoud), and "oedema of the glottis," have been used to describe infiltrations of the larynx, which differ shglitly in nature, but present almost identical symptoms. Bayle, who first described oedematous laryngitis (1808), considered it, with good reason, to be dropsy of the larynx, analogous to dropsy of tlie celhilar tissue. Bouillaud and Cruveilhier, on the contrary, endeavoured to show that it had nothing to do with dropsy, but was really an inflammatory lesion, causing the formation of purulent fluid. Both opinions are true. In some cases it is a question of oedema in the true sense of the word, the inflltration being purely serous (nephritis, scarlatina, oedema from cold), but at other times the infiltration is sero-purulent (ulcerative laryngitis, laryngeal infections, erysipelas of the pharynx, tumours of the pliaryux and of tlie tongue, laryngo-typhus, etc.). In this chapter, however, I shall not consider purulent infiltrations of 58 TEXT-BOOK OF MEDICINE the larynx, or, at least, only in an incidental way. I have only in view oedema properly so-called — that is, infiltration of the larynx comparable to oedema of the cellular tissue. I have, therefore, headed this chapter " (Edema of the Larynx." I shall first give a general survey of the question and then discuss oedema as seen in Bright's disease and in syphilis. Site of the (Edema. — The laryngeal mucosa is not everywhere ad- herent to the subjacent fibro-elastic tissue. The adhesion is lax at the glosso- and aryteno-epiglottic folds ; in the arytenoid region it is quite slight, and it is not close on the vocal cords. Certain of these parts are rich in cellular tisssue, and therefore oedema readily forms there. According to its site, the infiltration may be supraglottic, glottic, or subglottic. The term " CBdema of the glottis " is therefore improper, and comprises but a small part of the question, because, in most cases, oedema affects parts other than the glottis. Supraglottic infiltration is the most frequent, because of the situation of the lesions which produce oedema, and especially because the submucous connective tissue is abundant in this region. The aryteno-epiglottic and glosso-epiglottic folds, the epiglottis, the ventricles of Morgagni, the interarytenoid tissue, and the pharynx itself, participate in the trouble, and the cushions of oedema can be felt by the finger. The oedema is said to be glottic when it occupies the vocal cords. When the infiltration is subglottic, the laryngoscope reveals a reddish swelling on the side of the trachea. Pathological Anatomy. — The mucosa which covers the oedematous parts is sometimes pale and anaemic, at other times red and injected. The vestibule is much infiltrated ; the aryteno-epiglottic folds, which, from the abundance and laxity of their connective tissue, present the chief lesion, are oedematous, and may be enormously swollen.* The epiglottis has lost its shape, and may be three times as thick as normal. These lesions readily explain the almost complete obliteration of the orifice of the larynx. The oedematous parts, on incision, are found to be infiltrated with serous fluid ; oedema sums up the whole lesion. When the infiltration of the larynx is secondary to deep ulcerations — perichondritis, necrosis of cartilages, or sequestra — we find, in addition to the serous or sero-purulent infiltration, the lesions described under Syphilis, Tuberculosis, and Cancer of the Larynx. etiology — Pathogenesis. — (Edema of the larynx may be primary, accidental, or secondary. Primary oedema exists as a distinct disease, and may be produced by a chill. Trousseau reports a remarkable case : " A * Sestier, by injecting water into the carotids of a cadaver, has produced artificial oedema of the larynx, studied its distribution and compared the size of each of the affected parts. Experimental research, in connection with pathology, shows that the aryteno-epiglottic folds are chiefly affected. DISEASES OF THE LARYNX 59 drunken man, who slept in the street one cold night, was seized by acute oedema of the larynx." The condition here was " true oedema " ; the swelling of the laryngeal mucosa is comparable to that of the nasal mucosa in coryza. I think, however, that laryngeal oedema a frigqre is very rare, and, on closer inspection, some other factor, such as Bright's disease or syphilis, is often found. Accidental oedema follows wounds and burns. Sestier has collected sixty-nine cases. Oedema secondary to some lesion of the lar5mx, or of a neighbouring part, is quite common. " Every inflammatory process," says Trousseau, " determines in its neighbourhood oedema which varies in direct ratio with the amount of loose connective tissue. In the eyelids, for example, and on the prepuce, where the connective tissue is abundant and loose, a pustule of variola, or a patch of erysipelas, may cause enormous swelling. This oedema, which Virchow called collateral, and which is some- times sero- purulent, finds a most favourable soil in the abundant lax cellular tissue of the supraglottic region. Laryngeal tuberculosis may cause oedema of the larynx. The condi- tion in some cases is a false oedema, and is really a tubercular infiltration which invades the folds, the ventricular bands, and the epiglottis ; these parts are hypertrophied and indurated by infiltration of tubercular tissue, and the condition is certainly not oedema. Nevertheless, true oedema may appear in the course of laryngeal tuberculosis ; it is provoked by ulceration, and especially by tubercular perichondritis and by lesions of the cartilages. The oedema in tuberculosis of the larynx chiefly occupies the arytenoid region ; it is asually soft and pale, because of the ana^niia of the mucous membrane. Cancer of the larynx causes oedema, which nearly always begins on one of the ventricular bands. It remains unilateral, reaches the arytenoid and the corresponding aryteno-epiglottic fold ; it rarely attacks the epiglottis, docs not spread far, and develops side by side with the cancer. LaryngO-typhus may determine severe oedema. In the decline of typhoid fever infiltration, due to the necrosis of the cartilages, appears; its onset may be slow or rapid. Scarlatina, especially during defervescence, may set up oedema of the larynx. Trousseau has reported several examples. Acute or chronic nephritis (including saturnine nephritis) may bring on oedema of the larynx. (Edema of the edge of the vocal cords is extremely frequent in young girls who are learning to sing. 60 TEXT-BOOK OF MEDICINE CEdema of the Larynx in Bright's Disease. The following example will give an exact idea of this condition :* A man was ad- mitted into my wards with symptoms of asphyxia. His chief complaint was noisy, laboured breathing, with stridor audible from one end of the ward to the other. Ex- piration little affected ; each inspiration required much effort. The inspired air finally entered the limgs, but caused a sa-nnng noise. Inspection showed considerable sucking- in, with depression of the suprasternal and epigastric hollows ; the diaphragm was apparently ch'awn upwards. The voice was tUghtly hoarse, a proof that the vocal cords were but httle affected. The man stated that he had been sick for the past month. The dyspnoea was not the first symptom, and the illness began with dysphagia, which gradually became so severe that the passage of food and drink was almost impossible. Ten or twelve days later the patient experienced a feeling of strangulation, which he compared to a foreign body blocking the entrance of the air-passages. The dyspnoBa was at first uniform, but later interrupted by paroxysms. These symptoms finally made life almost unbear- able. He was worn out, and could not take food. Breathing required the greatest efl'ort ; each inspiration was a struggle for life, and the prognosis was most alarming. Fig. 1. — CEdema of the Larynx. e, Epiglottis — very cedematous, irregular, and red. It forms an enormous eyebrow above the vestibule of the larynx, and is continuous with the aryteno-epiglottic folds, which are very cedematous. a, Arytenoid region — also swollen, deformed and retracted towards the oesophagus. h. Ventricular bands, which are very cedematous, and mask the vocal cords for the greater part of their extent. The anterior extremity of the vocal cords is visible. The obstruction was evidently in the larynx, but we had to ascertain its nature. M. Bonnier examined with the mirror. On opening the mouth, we at once noted a reddish oedema of the uvula, of the pillars, and of the velum palati. The uvula was bulky and tremulous, the pillars were cedematous, and the isthmus of the gullet was narrowed. Red oedema was visible at the base of the tongue and in the vestibule of the larynx. The epiglottis was bulky and much deformed, the aryteno- epiglottic folds were enormous, and the cedematous ventricular bands blocked the orifice of the glottis. The anterior part of the vocal cords could be seen momentarily, and their free edge was slightly cedematous. The illustration above represents the condition. It is now easy to follow the march of events. The dysphagia was caused by the oedema of the palate, the pharynx, and the epiglottis. The dyspnoea was due to oedema of the vestibule and of the ventricular bands ; these parts, by opposing the * " (Edeme Brightique du Larynx " {Climque Mtdicale de VHotel-Dieu, 1897, Sme Le9on, p. 49). DISEASES OF THE LARYNX 61 passage of the inspired air, made tlie breatliing difficult and stertorous. Spa-sms of the glottis, which are almost inseparable from such lesions, caused the fits of suffoca- tion. The diagnosis of oedema of the larpix was therefore established. The patient had neither tumour, laryngeal polj-pus, cicatricial stenosis, nor paralysis of the posterior cricoarytenoid muscles, which may all cause suffocation, stertor, and sucking-in, but was suffering from progressive oedema, which had started in the velum pahiti and the isthmus of the fauces, and had reached the larynx. The diagnosis, however, was not complete, for larjTigeal oedema, whether it be wliite or red, and local or diffuse, may be due to many causes. Cancer, tuberculosis, and, above all, sypliilis, may give rise to oedema of the larynx, while the existing lesion may be almost liidden. The oedema in this case was due to none of these causes ; it was not the result of cold, but of Bright's disease. The case was one of Bright's disease. It was riot a case in which oedema was severe and uriemic symptoms marked ; it was one of those cases of latent Bright's disease. In this patient we found all the minor troubles of " Brightism " — i.e., frequent micturition, cfamp in the calves, dead fingers, cryiesthesia, and itching. The arterial tension was exaggerated, the urine contained albumin, and the depuration was incomplete, as examination of the toxicity of the urine showed lowering of the toxic coefficient. We Fig 2. — Laryngeal (Edema. c. Epiglottis — still cedematous, but regaining its normal shape somewhat. a. Arytenoid regions still remain edematous and deformed. h. Ventricular bands. The swelling has diminished, the glottis is more patent, the vocal cords can be better seen, but their free edge is still irregular and swollen. had, then, to deal with redcma of the larynx, due to Blight's disease, and producing increasing asphyxia, which might well end fatally. His condition was so grave that I discussed the question of tracheotomy, or, belter still, of intubation. I was prepared, therefore, for any eventuality, but I began by applying several leeches to the front of the neck. The result was not long delayed. On the next day the improvement was manifest : the oedema of the palate had diminished, the dysphagia was less, the stertor was not so noisy, the breathing was easier, and the oed'ma of ihv larynx was on the road to recover, as may be seen from Fig. 2. .Milk diet was ordered from th(^ first, and two days later the improvement was still more marked. The annexed illustration (Fig. .3) gives a good idea of the im- provement which rapidly followed in the o-dematous parts. Six days later the patient was cured. (Edema may HujMirvene in the course of acute or of chronic nepliritis. When nephritis is very acute (as in scarlatinal and early syphilitic nephritis), ft produces oedema, which tends to become general, and the anasarca is often 62 TEXT-BOOK OF MEDICINE considerable. The serous cavities — notably the pleurae — contain effusions, and serous exudate may be present in the brain, the lungs, or o'ther organs. (Edema of the larynx is then associated with these various exudations. In chronic nephritis, on the contrary, the oedema has much less tendency to become diffuse ; it is more isolated and more localized to one region, such as the face, the lower limbs, or a single organ, and we see patients suffering from slowly progressive nephritis in whom pleural effusion or acute oedema of the lung supervenes, while oedema of the extremities is absent or slight. The same remark applies to oedema of the larynx in chronic nephritis. GEdema of the larynx may occur in the course of insidious Bright' s disease, while other parts of the body are free. This patient had never shown oedema in any other part before oedema of the palate and of the larynx appeared. In a patient of Fauvel's no trace of oedema had been seen, and the oedema of the eyelids only appeared after that of the larynx. Fig. 3. — Laryngeal (Edema. e, The epiglottis has lost all trace of ojdema. a, The arytenoid region has regained its normal aspect. h. The ventricular bands still hide the glottis to a slight extent, but they meet only during effort and phonation. The vocal cords are a little irregular along their free border, and the anterior half alone is visible during inspiration, but the air enters the larynx freely. In Jones's patient slight oedema of the lower limbs was present, when oedema of the larynx supervened. A patient of Fraenkel's had never had any oedema, so that in his case the oedema of the larynx was considered to be the first sign of nephritis. Hanot's patient had never shown the least trace of oedema, when oedema of the palate and of the larynx appeared. We see, therefore, that in the course of slowly progressive and more or less insidious chronic neplu-itis oedema of the larynx- (like that of the lung) may appear suddenly, without being preceded by peripheral oedema. Accordingly, several authors (Fauvel, Fraenkel) have stated that oedema of the larynx may appear unexpectedly as the first sign of Bright's disease. I do not hold this view. I admit that oedema of the larynx may appear as the first manifestation of oedema in a " Bright " case, but I cannot accept the statement that it may be the first symptom of Bright's disease. DISEASES OF THE LARYNX G3 In fact, at the present day we no longer look upon Briglit's disease as our ancestors did, and we do not wait for the appearance of oedema to make our diagnosis. We hunt out " Brightism," wliich may not be evident at first sight. We know that there is a mild form of uraemia which is insidious in its course, but yet perfectly recognizable. The study of the minor troubles of " Brightism," the estimation of the arterial tension, and the examination of the toxicity of the urine, reveal latent Bright's disease. We are thus able to affirm that, although an attack of epileptiform fits, of coma, of super- acute oedema of the lung, or of oedema of the larynx, may appear to be the first symptom of nephritis, it is in reality only the first apparent, and not the first real, symptom, and the nephritis has been already shown by signs which would not have passed unnoticed had trouble been taken to look for them.* I must insist on the fact that oedema of the larynx in Bright's disease is almost always preceded by oedema of the velum palati. It might truly be said that oedema commences in the throat and tlie uvula, and afterwards spreads downwards to the base of the tongue, the epiglottis, and the larynx. As a result, troubles in swallowing very often open the scene. At first the patient seems to have only a painful angina, but respiratory troubles soon appear. The oedema spreads downwards, causing a succession of com- plications which I have found in most of my cases. In a patient at the Hotel-Dieu dysphagia and cedema of the throat preceded oedema of the larynx and dyspnoea by ten or twelve days. In a patient at the Necker Hospital oedema of the throat and dysphagia occurred twenty-four hours before attacks of suffocation. In the cases reported by Abate and Jones cedema of the larynx and oedema of the palate, with dysphagia and suffoca- tion, appeared almost simultaneously. In M. Fauvel's patient the cedema of the palate preceded that of the larynx, and deglutition was impaired before respiration. In M. Hanot's patient the succession and tlie delimita- tion of tlie oedema was even more marked. In the first phase the cedema remained localized to the isthmus of the fauces and to the uvula, as an (edematous angina, causing acute dysphagia, which was cured by milk diet. Two months later, however, oedema of the palate reappeared, and also oedema of the larynx, causing acute attacks of suffocation. Hanot, in his notes on this case, has been careful to add : " Albuminuric oedema, limited to the uvula, may be the starting-point of oedema of the glottis." In a patient with painful angina the throat must be carefully examined, and if red or white (jedema of the uvula, of the pillars, or of the velum palati be present, nephritis must be suspected, the urine examined, the patient carefully questioned, search made for symptoms of " Brightism," and the * Diciiliifoy : " l^lude sur Ic Brightismc," Bulletin dc r Academic dc Medecinc, sdanco dcs G et 2U Juin, 1893. 64 TEXT-BOOK OF MEDICINE diagnosis of oedema of the throat due to Bright' s disease be made. TJiis oedema then becomes an important element in diagnosis, prognosis, and treatment. It is an element in diagnosis, because it helps us to trace Bright' s disease which at first might not be suspected ; it is an element in prognosis, for it leads us to foresee the probable extension of the oedema to the larynx ; it is an element in treatment, for it invites prompt action in order to check the disease and to avoid oedema of the larynx. CEdema of the larynx is one of the most formidable complications of Bright's disease. In some cases, it is true, it may remain limited, and for several days and weeks betray itself only by a trifling stridor during inspira- tion ; or, again, it may invade the larynx but slowly, so that complications may be averted. In other cases, however, the oedema may already be most acute, and the patient may rapidly succumb before help can be given. The situation is aggravated by the fact that oedema in Bright's disease does not always remain confined to the larynx, but invades the pleura and the lung. A patient of mine in the Charite had very extensive oedema of the lung, and succumbed some hours after tracheotomy — not so much from the laryngeal lesions as from the pulmonary oedema. Hanot's patient, who had both csdema of the larynx and of the lung, with 2 pints of fluid in the pleural cavity, died some hours after tracheotomy — not so much from the lesions in the larynx as Irom the pleuro-pulmonary mischief. It is often difficult, I grant, to gauge correctly the state of the lung in a case of oedema of the -larynx, because the extreme dyspnoea, and the echo of the " sawing sound "in the larynx do not always allow perfect auscultation of the lung. What treatment should we employ in this condition of oedema ? If death appear imminent, tracheotomy may give some chance of recovery. So many failures have been noted that I would rather advise intubation, which has been tried and proved. Scarification of the oedematous swelhngs does good. Bleeding is an excellent means of treatment. A dozen leeches are applied to the front of the neck, so as to produce copious bleeding. Hot compresses, warm gargles, and sprays are sometimes of use. If asphyxia be imminent, we can facilitate the entrance of air into the larynx by firm traction on the tongue. Do not forget that oedema of tlie lung or urajmia may also be present. Tracheotomy was unsuccessful in the three cases which I have reported, because two patients succumbed to pulmonary oedema, and the third to ursemic convulsions. If pulmonary oedema or ujsemia be present, both general and local bleeding are necessary. The nephritis must also be treated, and absolute milk diet is therefore prescribed. In place of milk by the mouth, we may give injections of lactose (150 grammes of water and 20 grammes of lactose). No chlorides should be taken, and injections of serum must not be given. DISEASES OF THE LARYNX 65 Syphilitic (Edema of the Larynx. (Edema is fairly rare in the course of secondary lesions of the larynx. Although they are superficial, and apparently benign, they are sometimes accompanied by oedema of the larynx and respiratory troubles. This fact is most important, and has been emphasized by Krishaber. Although dyspnoea may be exceptional in secondary lesions of the larynx (or, at least, it is very shght), yet in some cases the distress becomes suddenly acute, and tracheotomy would become necessary if the condition did not yield rapidly to appropriate treatment. I have often verified this fact, and Mauriac, like Krishaber, affirms that " quite trifling erosions may become a dangerous centre of congestion, around which oedema of the glottis rapidly develops." (Edema of different colours, with pallor or redness of the mucosa, often accompanies tertiary lesions. A red tint is sometimes the sign of sero- purulent infiltration. Laryngeal oedema plays a considerable part in the history of tertiary lesions, and is one of the commonest causes of dyspnoea and of threatening asphyxia. It may be more or less extensive, and may invade the aryteno-epiglottic folds, the epiglottis, the ventricular bands, the vocal cords, the space below the cords, and the trachea. The laryngo- scope shows the deformity and the swelling of the parts invaded. The epiglottis is twisted up and swollen fike a chestnut or the cervix uteri. The arytenoids form large cusliions, which obliterate the superglottic region. All tertiary lesions, etc., may at any moment cause oedema of the larynx, which may be Hmited, and not serious, or quite general. In the latter event, it may be slow or rapid in its progress, Krishaber and Mauriac have studied syphiUtic oedema of the larynx, and have shown that its intensity is not always in proportion to the severity of the exciting lesion. As a matter of fact, we meet with shallow lesions which, though scarcely appreci- able with the laryngoscope, may yet cause alarming oedema of the larynx. I have several times verified the correctness of these assertions. Iji my ward at the Necker Hospital, I had two patients with Laryngeal oedema. One of them had stridor and sucking-in, and was almost in a state of asphyxia. The danger was averted by energetic specific treatment. The other patient also had stridor, sucking-in, and feeling of strangulation, and with orthopncca, which left no doubt as to a laryngeal lesion. It wa.s of several weeks' duration, and had previously caused only vocal trouble. Bonnier found oedema of the larynx. The oedema had, in the case of one vocal cord, the polypoid appearance which can be seen in the subjoined figures. No suspicion of syphilis existed until I discovered on the right wrist a pustulo- crustaceous syphilide, which gave me the key to the case. I ordered active specific treatment, and in three weeks, as the Figs. 4, 5, 6, and 7 indicate, the oedema of the larynx disappeared, and with it all the troubles. 5 66 TEXT-BOOK OF MEDICINE Syphilis may produce oedema of the larynx in yet another way-— not by lesions limited to the larynx, but by setting up early nephritis, which is rapidly followed by peripheral oedema, anasarca, effusion into the serous membranes, and oedema of the lung and of the larynx. This sketch of the importance of syphilitic oedema of the larynx proves how carefully syphilis must be looked for, in order to give injections of biniodide of mercury without delay. Fig. 4. — CEdema of the Lakynx. December 21. — Day of patient's admission. Appearance of the glottis during forced inspiration. e. Swollen and turgescent epiglottis. a, (Edematous arytenoid region. h. Ventricular bands, which are markedly cedematous. A small portion of the vocal cords can be seen in front. Fig. 5. — (Edema of the Larynx. January 12.— e, Epiglottis, still swollen, but less flabby. a. Arytenoid region, which is less prominent. h, The ventricular bands have diminished in size, allowing the vocal cords and an cedematous polypoid mass to be seen. General Description. — I have given the special characters of certain varieties of oedema of the larynx, and will therefore recapitulate the general description. I would call attention to the fact that the march of events is sudden or slow, according to the cause. The palato -laryngeal infiltration, which is secondary to nephritis, sypliilis, scarlatina, or a cliill, may rapidly become general, and asphyxia soon appears, while the progress is much slower when the oedema is secondary to certain lesions of the larynx. In DISEASES OF THE LARYNX 67 the case of generalized cedema, respiration is rapidly compromised. The patient has the sensation of a foreign body wliich is strangling liim, and makes desperate efforts to get rid of it. During the com'se of the increasing dyspnoea attacks of suffocation supervene, " in which," says Trousseau, " the patient, with livid face, open mouth, gaping nostrils, eyes starting from the sockets, and skin running with sweat," grasps any support for his inspiratory muscles. These attacks last from ten to fifteen minutes, and are repeated in fatal cases at shorter intervals till death occurs. They are Fig. 6. — (Edema of the Larynx. January 16. — e, Epiglottis normal. a. Arytenoid region normal. b. Ventricular bands, which are still cedematous, though they allow the whole of the glottis to be seen. The polypoid swelling is implanted on the right vocal cord ; it is notably smaller. Fig. 7. — CEdema of the Larynx. January 18. — The larynx has resumed its normal appearance, with the exception of the right vocal cord, on which a remnant of the polypoid excrescence is seen. It may well have originated in a syphilitic papule. the result of spasm of the glottis, and are only seen in 60 per cent, of cases. Inspiration, wliich is noisy and accompanied ])y Stridor, is usually nuicli more painful than expiration, because the aryteno-e[)iglottic cusliions at the moment of inspiration are said to act as a valve wliich blocks the upper orifice of the larynx. These cushions, pushed back like floating bodies by expiration, produce a characteristic hruil dc drapeau (Sestier) in some cases. 5—2 68 TEXT-BOOK OF MEDICINE DyspncBa is not so rapid and so severe in many cases. In persons with syphilitic, tubercular, or cancerous lesions of the larynx, oedema supervenes as a complication, and increases gradually and slowly before compromising life. In some cases, however, dyspnoea due to oedema may be rapid and terrible. The voice and the cough are not greatly altered, as in croup, but still may be raucous or muffled if the vocal cords are involved, or if the oedematous parts come in contact. Deglutition is painful, because of the swelling of the laryngeal folds and epiglottis, and also because of the palato-pharyngeal oedema. The oedema of the pharynx and of the vestibule may be recognized both by sight and touch. OEdema, when consecutive to syphilitic, tubercular, or cancerous lesions, usually remains limited to the larynx, but oedema due to nephritis is often palato-pharyngo-laryngeal : the uvula looks like a lump of jelly, the mucosa of the throat is oedematous, and dysphagia precedes dyspnoea. Laryngoscopy is sometimes dangerous, for it may produce a severe fit of choking. The symptoms which I have' just enumerated readily explain the gravity of oedema of the larynx. Death often occurs unless we employ active inter- vention. QSdema of the larynx in nephritis is very dangerous. In ten cases of oedema appearing at the OUtset of nephritis, five died, two before and three after tracheotomy ; and in ten cases of oedenia supervening in the course of nepliritis, nine died, four before and five after tracheotomy (Amero). Diagnosis. — Foreign bodies and polypi in the larynx, spasms of the glottis caused by aneurysm of the aortic arch, croup and stridulous laryn- gitis, abscess of the pharynx, paralysis of the posterior crico- arytenoid muscles, and tumours of the mediastinum, may simulate oedema of the larynx, for all these conditions give rise to stridor and sucking-in. They have, however, the distinctive signs which I shall now enumerate. Polypi are easily recognized with the laryngoscope. The same remark appHes to paralysis of the posterior crico-arytenoid muscles. Aneurysm of the aortic arch shows dullness, blowing murmurs, and expansile pulsation if the tumour is large. With the laryngoscope, lesions of the larynx are absent, or limited to the paralysis of a vocal cord, from the compression of the recurrent nerve by the tumour. In croup we may note the presence or the remains of the diphtheritic angina which nearly always precedes it, the false mem- branes wliich are so often coughed up, the early and gradual alteration of the voice, the slow and difficult expiration, and often the glandular enlarge- ment in the neck. Stridulous laryngitis chooses early life, and appears suddenly. The dyspnoea at once reaches its limit, and after the suffocative attack, the relief is complete, and the voice and the breathing recover their DISEASES OF THE LARYNX 69 normal character. Retro-pharyngeal abscess is \asible on the posterior wall of the pharynx, and if the base of the tongue be well depressed, a swelling which may fluctuate and is of a deeper colour than the surrounding tissues is discovered. (Edema of the larynx being recognized, its cause must be diagnosed. The oedema may be primary, but before we admit the existence of primary oedema, or of oedema a frvjore, careful search must be made for any causes or the lesions which may, sooner or later, give rise to laryngeal oedema. It is important to exclude Bright's disease and syphilis, which are the two chief causes of oedema of the larynx. I shall not go into the treatment, which has already been studied in each special case. IX. SPASM OF THE GLOTTIS. Definition — etiology. — Spasm of the glottis results from tonic contrac- tion of the constrictor and tensor muscles of the vocal cords. It lasts some seconds, and causes suffocative attacks, which may result in death. The spasm is either symptomatic or idiopathic. The symptomatic spasm arises from stimulation of the recurrent nerves by a neighbouring tumour — e.g., aneurysm of the arch of the aorta, tuber- cular or cancerous glands, etc. How can excitation of one recurrent nerve alone provoke spasm of the glottis ? Krishaber has shown experimentally that stimulation of one recurrent nerve acts upon both lips of the glottis, just as stimulation of one vagus arrests or slows the heart-beat. Sympto- matic spasm is also seen in certain diseases of the larynx, such as croup, false croup, or oedema of the glottis, and it is remarkable that the spasm is intermittent, although the exciting cause is continvious. This intermittence is met witli in other spasmodic or painful actions of the nervous system (hepatic and renal calculi, neuralgia in cancer), though it is not easy to give the reason. Spasm of the glottis may appear alone, or be associated with other laryngeal troubles, as at the outset or during the course of locomotor ataxia. Idiopathic spasm of the glottis is not, like the preceding form, a symptom appearing in the course of another disease, but a real morbid entity which occurs in children from four to eighteen months old, and it is this form that cliiefly merits description here. This disease has been improperly called thymic asthma, because it was thought to be connected ^vith hypertrophy of the thymus. It is really a neurosis, which may be independent or related to dentition or to digestive troubles. Heredity may play some part, as several infants in the same family may be affected (Romberg). Description. — Tlie idiopathic spasm of infancy, whicli may or may not be preceded by prodromata, such as pains in the back and hands, or convul- 70 TEXT-BOOK OF MEDICINE sions, begins suddenly in the middle of the night, hke false croup. The glottis closes convulsively ; the breathing becomes more and more difficult, and is soon completely suspended, so that asphyxia is imminent. The distress is extreme ; the chest is immobile, and the vesicular murmur can no longer be heard. The face is cyanotic and bathed in sweat, the heart- beats are tumultuous, and we ask ourselves if the scene is not about to end in death. After fifteen or twenty seconds of complete apnoea, " the child takes a quiet breath again, and the attack ends by a high, sonorous inspira- tion that is quite characteristic, and does not resemble the croupy cough or the whoop in pertussis " (Tardieu). It is more like a shrill and very sharp hiccough (Herard), The attacks are not always complete, and the asphyxial period may be wanting. The usual duration is from a few seconds to two minutes, but in some cases they recur at very short intervals, and are prolonged for an hour or more (Gaspari). At first these attacks are only repeated once or twice a week ; later, they reappear daily, and as many as twenty- live to fifty have been counted in a day (Herard). Between the attacks the child's health is good ; fever, cough, and loss of appetite do not occur, and cachexia does not appear till late. The total duration of the malady is very variable, but its limits He between a few weeks and several months (Herard). The prognosis is most gloomy, and recovery is the exception. The symptomatic spasm in the adult presents some differences. The shape of the larynx and the resistance of the interarytenoid glottis explain why the spasms are less formidable than in the infant, and also why the inspiration is wheezing, some air being able to pass through the glottis. Diagnosis. — Stridulous laryngitis, wliich also results from a spasmodic contraction, resembles spasm of the glottis ; but the former attacks children from one to six years old, while the latter is seen between the ages of tliree and twenty months. The former is preceded or accompanied by catarrh, hoarseness, cough, and coryza ; the latter comes on so suddenly that asphyxia threatens in a few seconds. Hereditary syphilis often produces in young children laryngeal troubles which are so like spasm of the glottis that I am convinced that in many cases (treatment proves the point) syphilis is the cause. Treatment. — In the attack the face should be sprinkled with cold water and friction to the body should be employed. The spasm often yields when the child is forced to breathe through the nose. Antispasmodics are indi- cated. Change of air and a stay in the country are advisable. The possi- bihty of hereditary or acquired syphiHs must be thought of, and mercury and iodides employed. DISEASES OF THE LARYNX 71 X. PARALYSIS OF THE MUSCLES OF THE LARYNX. Laryngeal paralysis may be classed as of peripheral, bulbar, or cerebral origin, according to the seat of the lesion. Peripheral Lesions. — The laryngeal nerves may be directly injured by traumatism (Neumann), by surgical intervention, and by compression. Compression is more frequent in men than in women, and afEects the left recurrent nerve more often than the right (AvelUs). It may be due to tumours of the thyroid body or of glands, abscess, cancer of the oesophagus, aneurysms of the great vessels of the mediastinum and the root of the neck, pericarditis, and pleural effusions. Tumours of the base of the skull and fractures may compress or injure the vagus and the spinal accessory nerves. Tabes and diphtheria are accompanied by lesions of the laryngeal nerves, and the same holds good in certain intoxications and infections (alcoholism, saturnism, morphinism, syphilis, and diabetes). Finally, more or less lasting paralysis of the muscles of the larynx may be set down to extra- or intra- cervical action of cold. Bulbar Lesions. — The nuclei of the spinal accessory nerves may be affected by the following lesions : Syphilitic growths, tumours, caries, softening, hemorrhage, acute or chronic inflammation of the bulb, pachy- meningitis, disseminated sclerosis, amyotrophic lateral sclerosis, labio- glosso-laryngeal paralysis, and tabes. Cerebral Lesions. — The foot of the third frontal convolution (Garel), the subjacent white matter (Dejerine), the external part of the internal capsule (Garel and Dor), the caudate nucleus, and the claustrum (Picot and Hobbs), have been found diseased in cases of laryngeal palsies. The same troubles may be due to hysteria, or may be provoked by suggestion. The palsies may attack several groups, a single group, or a single muscle.* Paralysis of the Dilators. — Isolated paralysis of the posterior crico- arytenoid muscles is very rare (Ziemssen), though it has recently been noted in laryngeal phthisis (Gougenheim). When both muscles are paralyzed, the vocal cords no longer open, but fall together during inspiration from the action of the constrictor muscles, and, since very little air enters through the glottis, intense dyspnoea results. Vocal effort is possible, and tlie voice is slightly altered through imperfect fixation of the arytenoids. If the paralysis is unilateral, the immobihty of the vocal cord at the moment of inspiration may be seen with the mirror. Paralysis of the Constrictors. — Paralysis of the constrictors is much more common tlian the preceding form. It may be bilateral (hysteria and diph- theria), but is more often unilateral, and almost always consecutive to a * To complete this study, sco p. 23 et seq. 72 TEXT-BOOK OF MEDICINE direct lesion of the recurrent or of the spinal accessory nerves. The length of the course and the relations of the recurrent nerves explain the relative frequency of tliis palsy. The causes of the lesion include aneurysm of the carotid artery (Mackenzie), double paralysis from a cancerous tumour at the posterior lacerated foramina (Tiirck), cancer of the recurrent nerve (Heller), double paralysis by aneurysm of the subclavian and innominate vessels (Ziemssen), aneurysm of the arch of the aorta (numerous cases), cancer of the t Pig. 8. — Normal Larynx : Appearance of the Glottis dttring Deep Inspiration. E, Epiglottis ; L, base of the tongue ; B, ventricular bands ; V, ventricle of Mor- gagni ; R, aryteno-epiglottic fold ; A, interarytenoid region (distended) ; S, cartilage of Santorini ; W, cartilage of Wrisberg ; C, vocal cords, opened to their maximum ; F, hyoid fossa ; T, trachea, with superposed rings ; D, bifurcation of the bronchi. Fjg. 9. — Normal Larynx : Appearance of the Glottis during Phonation. The vocal cords are tense, and nearly touching in their anterior two-thirds. The cartilages of Wrisberg and of Santorini are approximated, and the interarytenoid region is partially effaced. The epiglottis is straightened, and the larjmx is elongated in the anteroposterior direction. oesophagus (Braune), chronic pleurisy of the right apex (Gerhardt), chronic 'pericardial effusions (Baiimler), and mediastinal tumours (Gueneau de Mussy). In paralysis of the constrictor muscles the glottis is constantly open, so that respiration is easy; but the voice is lost, and effort is incomplete. These symptoms are less marked when the paralysis is unilateral. The laryngoscope shows that both cords (or one of them, according to the case) remain immobile, and do not come together. DISEASES OF THE LARYNX 73 Paralysis of the Crico-Thyroidei. — These muscles are supplied by the external lar\nigeal nerve. The paralysis induces no respiratory trouble, because the dilator muscles are intact. Effort is complete, because the constrictors are healthy, and the voice is not completely lost, because the other muscles of phonation are intact ; but the voice is altered, and dysphonia is present, because the tension of the vocal cords is insufficient, and thei' Fig. 10.- -Paralysis of the Adductors dttring an Effort op Phoxation. The lateral cricoarytenoid muscles and the ary-arytenoid muscles are paralyzed. The vocal cords are relatively tense, but they cannot approximate to the middle line. The orifice of the glottis is triangular. Fig. 11. — Paralysis of the Tensors: Appearance of the Glottis dxtrinq an Effort of Phonation. The vocal cords appear curved, and sometimes beaded at their free edge, and the glottis gapes slightly. This appearance corresponds to paralysis of the cricothyroid muscle, or to paralysis of the elevator muscles of the larynx. vibration is incomplete during the emission of sound. This paralysis occurs in hysteria. It comes on after great vocal effort, and often follows a chill, like paralysis of the facial or of the radial nerve. Paralysis of the Elevators. — In order that the crico-thyroid muscles may produce the tension of the vocal cords necessary for phonation, the tiiyroid cartilage must be fixed above and in front by the elevators of the larynx — i.e., genio-hyoid, mylo-hyoid, digastric, stylo-hyoid, and thvro-hvoid muscles. If these muscles, wliich are chieHy ititiervated by the hypoglossal nerve, are paralyzed, the larynx remains depressed, the tension is incomplete, and the 74 TEXT-BOOK OF MEDICINE aphonia is almost absolute. The voice has a low, monotonous tone, due to the passive tension of the vocal cords under the strain of the expired air. Diagnosis — Prognosis — Treatment. — Laryngoscopic examination sim- plifies the diagnosis of paralysis of the larynx, and the discovery of the paralysis may give a clue to its cause. Mediastinal tumours may at first give no symptoms save vocal troubles due to paralysis of one vocal cord (compres- sion of the recurrent nerve). We are not liable, thanks to direct examina- tion, to mistake paralysis of the dilators for spasm of the constrictors, Fig. 12. — Paralysis of the Left Recttbrent Nerve: Appearance of the Glottis during an Effort of Inspiration. The left cord reaches beyond the middle line, being pulled over by the overaction of the muscles supphed by the right recurrent nerve. Fig. 13. — ^Paralysis of the Left Recurrent Nerve : Appearance of the Glottis during an Effort of Phonation, The left vocal cord remains in the cadaveric position. The right vocal cord passes slightly beyond the middle line, and is alone tense. although in both cases the respiratory troubles are almost similar. Again, paralysis of the muscles of phonation will not be confounded with atrophy of the vocal cords, or ankylosis of the arytenoid articulations, though the vocal troubles present great analogy. For similar reasons, laryngeal phthisis, cancer, and polypi of the larynx can be excluded. The diagnosis between paralysis of the crico-thyroid muscles and catarrhal laryngitis has been given in the description of the latter malady. DISEASES OF THE LARYNX 75 The prognosis is only grave in paralysis of the dilator muscles (pos- terior crico-arytenoidei), when dyspnoea may be so acute as to necessitate tracheotomy. Treatment varies with the cause of the paralyses. When they are primary, electricity is the best curative agent, especially in paralysis of the crico-th}Toid muscles. The voice often reappears at the first sitting. Cure is obtained by applying the electrodes over the region of the larynx, or even at any two parts of the body (Kjishaber). CHAPTER III DISEASES OF THE BRONCHI I. ACUTE BRONCHITIS Acute bronchitis is a catarrhal inflammation of the large and medium-sized bronclii. It is often associated with inflammation of the trachea, and, indeed, in some cases tracheitis is the chief trouble. Tracheo-bronchitis is often preceded by laryngitis, and " The cold has settled on the chest " is quite a common saying. Inflammation of the bronchioles will be studied later, under capillary bronchitis. Description. — Acute bronchitis shows different degrees of severity. Thus, the slight form, commonly called a cold on the chest, is almost apyretic, and is only accompanied by slight malaise and headache. The cough at first is painful, dry, and spasmodic, and the expectoration is serous and greyish ; but later the cough becomes loose, the sputum is thick, and in a week the illness is at an end. In the severe form bronchitis begins with general malaise, shivering, and fever, which rises at night. The patient complains of headache and loss of appetite. The breathing is wheezing and painful. The cough, which is at first dry, causes acute pain in the intercostal muscles and the diaphragm, and is often followed by the vomiting of mucus or of food. On percussion, the resonance of the chest is normal ; on auscultation, snoring and sibilant rhonchi are heard during inspiration and expiration on both sides of the chest (because bronchitis is always double), and are trans- mitted in different directions. These initiatory symptoms last from three to five days, and coincide with the immature stage. When secretion from the bronchial mucosa (called the mature stage) replaces the dry swelling of the immature stage, the fever falls, the breathing becomes easier, the cough is loose, the sputum thick and yellowish-green, and the column of air, instead of being broken up against the rough, dry mucosa, meets the liquid bronchial secretion. 76 DISEASES OF THE BRONCHI 77 As a result, the rhonchi change to rales, which acquire the timbre of bubbles bursting in a liquid, and are known as bubbling, mucous, or SUbcrepitant. Mucous rales in a large bronchus may simulate the gurgling of a cavity ; subcrepitant rales are finer, and have their origin in the smaller bronchi. Unlike rhonchi, the moist rales may disappear at certain spots after a fit of coughing has freed the bronchi from the obstructing mucus. The second stage lasts about a week, during which improvement gradually supervenes, and resolution is complete in about a fortnight. The urine now becomes abundant, and contains much sediment. Slight diarrhoea often completes the crisis. The disease may become chronic, or change to capillary bronchitis. In old people who cannot cough up the secretion bronchiti-; may turn to suffocative catarrh. ^Etiology. — Acute bronchitis is a disease of cold and damp weather, and in certain predisposed persons it appears on the least chill, or at the approach of winter. It is one of the chief elements in measles and influenza. It is less frank in whooping-cough, asthma, and hay-fever, where the nervous element is so much in evidence that the inflammatory element is much less marked. The broncliitis present at the commencement of typhoid fever is rather hypergemic than inflammatory, though it may turn to true catarrh, and become a troublesome complication. Bronchitis in Bright's disease is not a genuine one, and its special char- acters depend on pulmonary oedema or urajmic dyspnoea. The same remark applies to pseudo-bronchitis, which is associated with heart disease, and is especially characterized by signs of congestion and stasis in the lungs. Dust and irritating vapours may produce an inflammation of the bronchi, usually associated with lesions in the lungs. I make special mention of syphilitic bronchitis. The erythema and the catarrh, so frequent in the larynx during the first years of infection, also affect the trachea and the large bronchi. This subacute tracheo-bronchitis is Hable to relapse from exposure to cold. Many syphilitics, formerly immune to chills, complain that they take cold easily, and suffer from laryngitis and bronchitis. They are always liable to erythema and specific catarrhs of the larynx, the trachea, and the bronchi — catarrhs which are readily excited by chills. Bronchitis in young children deserves special mention. It seems some- times to be associated with teething and digestive troubles, and in this connection the Barillm coli has been said to play a prominent part. Even the most trifling forms of bronchitis in young children may be compUcated by congestion of the lung. The temperature rises, and we hear at the bases of the lungs fine rales, which lead us to fear the onset of capillary bronchitis. All symptoms subside, however, after one or two days (Cadet de Gassi- court). 78 TEXT-BOOK OF MEDICINE Diagnosis. — It is not enough to diagnose bronchitis, for that is quite simple ; but it must be distinguished from conditions which may simulate it ; above all, its cause must be made out, as the different forms require absolutely different treatment. SyphiUtic bronchitis, to wit, demands treatment with mercury and iodides ; bronchitis in Bright' s disease only improves with milk diet ; bronchitis in cardiac cases yields to the treatment suitable for heart diseases. Bronchitis in tuberculous patients cannot always be diagnosed by a study of the symptoms alone. Its tubercular origin is in some cases doubtful until bacilli are found in the sputum. Speaking broadly, apparent broncliitis which does not begin in a regular manner must be suspected ; a bronchitis which begins with fever is often spurious. On the other hand, we must be equally suspicious of so-called bronchitis in which cough is the cliief symptom, to the exclusion of fever and of expectoration. Because an individual coughs much, we must not at once suppose that he is suffering from tracheo-bronchitis. Hysterical persons suffer from frequent and incessant cough mthout having bron- chitis. We find people in whom the taenia and other worms provoke a cough that is quite wrongly styled bronchitis. After expulsion of the tsenia the cough disappears. Bacteriology. — Bacteriology cannot help us in classifying bronchitis. The microbes which inhabit the healthy air-passages, and include the Staphylococcus alhus and aureus, the Streptococcus pyogenes, the pneumo- coccus and the pneumobacillus, may all be found iii bronchitic sputa, and are in no way specific. Besides these microbes, the sputum in bronchitis often contains a bacillus identical with the Bacillus coli, a fungus of the genus O'idium, and microbes which give the sputum its yellowish or greenish colour. Treatment. — In sHght cases we should induce sweating by diaphoretic drinks. We must give soothing inhalations, and quiet the pain and the fits of cough by the following draught : R Orange-flower water , . . . . . . . . . iv. Syrup of chloral 1 oo -«• a c I,- " • • • • • • • • • . aa qV. feyrup or morphia j Cherry-laurel water . . . . . . • . . . §u. Dose : For an adult, a tablespoonful every two hours. In the severe form we should employ stimulating apphcations (mustard- plasters and bUsters) and dry-cupping to the chest. If the bronchi is much choked, especially in old people, emetics must be given. DISEASES OF THE BRONCHI 79 II. CAPILLARY BRONCHITIS— BRONCHO-PNEUMONIA— LOBULAR PNEUMONIA Discussion. — Should the temperature rise, the respiration become panting, and auscultation show fine subcrepitant rales on both sides of the chest, on the sixth, seventh, or eighth day, in a child sufiering from measles complicated by ordinary bronchitis, capillary bronchitis has set in. The thermometer soon registers 104° F., the dyspnoea becomes acute, and the respiration rate rises to 60, while dullness and tubular breathing are found over one lung or at both bases. Broncho-pneumonia has supervened. Another child has reached the stationary stage of whooping-COUgh without accident. In spite of the convulsive cough, fever is shght or absent, and but few bronchitic rales are heard in the intervals of the fits. Fever then appears ; the temperature rises ; the character of the cough changes, being more continuous and less convulsive ; the breathing becomes panting, and on auscultation fine scattered rfdes are audible on both sides of the chest. Capillary bronchitis has begun. The thermometer now registers 104*^ F., the cough becomes incessant, the dyspnoea is extreme, percussion and auscidtation show one or several pneumonic patches. Broncho-pneumonia has developed. In another cliild suffering from croup, who has or has not been operated upon, the situation appears quite favourable. The fever is very moderate, no toxic symptoms are present, and the prognosis is good ; but suddenly the temperature rises, the dyspnoea grows worse, and is no longer of laryngeal but of bronchial origin. Auscultation, although difficult, because of the laryngeal sounds, reveals fine rales in the chest. This condition means capillary bronchitis. Then the thermometer rises, and the dyspnoea becomes excessive. The dreaded broncho-pneumonia of diphtheria has set m. In an infant suffering from teething or from gastro-intestinal troubles a broncliitis, which may or may not be due to chill, begins. On auscultation, large broncliitic rales are heard, yet so far there is little fever or dyspnoea. The fever suddenly increases, the dyspnoea grows, the rales become fine and scattered. Capillary bronchitis is beginning. The temperature reaches 104° F. ; the intensity of the dyspnoea becomes acute ; auscultation shows tubular breathing at both bases. Broncho-pneumonia has supervened. In an adult who has had an apparently normal influenza, with moderate fever, broncliitis, and catarrhal expectoration, the temperature rises, the dyspiKjea grows worse, the expectoration becomes muco-purulent, and on auscultation rAles of all kinds are audible. These symptoms indicate influenzal capillary bronchitis. A step further, and bronchial breathing is 80 TEXT-BOOK OF MEDICINE perceptible in different spots — or at both bases. Broncho-pneumonia is present. These different examples prove that we find not a " single broncho- pneumonia," but " broncho-pneumonias," which, strictly speaking, may all follow bronchitis from cold, though they most often supervene in the specific infections of measles, whooping-cough, diphtheria, influenza, tuber- culosis, typhoid fever, erysipelas, etc. In some cases the capillary bronchitis is the trouble, especially in adults and the lobular pneumonia is of less importance. In other cases, on the contrary, the capillary bronchitis is not important, but has joined hands with broncho-pneumonia, which is then the chief lesion. Bacteriological research in broncho- pneumonia permits in some cases the isolation of such specific bacilli as those of diphtheria, typhoid fever, or tuberculosis, but these specific microbes alone are not sufficient to cause broncho-pneumonia. They are not always found in the foci of broncho- pneumonia, while other microbes normally present in the mouth or the air- passages are always found. These microbes, which are the true cause of broncho-pneumonia, are the Staphylococcus alhus and aureus, the Strepto- coccus, the Pneumococcus , the Pneumobacillus , and sometimes the Bac- terium coli. They increase the danger and make the prognosis worse. We can now begin the detailed study of capillary bronchitis and of broncho-pneumonia. Definition — History. — When inflammation affects the bronchioles, the bronchitis is said to be capillary. In ordinary bronchitis the larger bronchi are alone attacked, and therefore the air can circulate freely, in spite of the lesions present. In capillary bronchitis, on the contrary, where the small bronchi are inflamed, the narrowness of the tubes, the tliickening of their mucosa, and the obstruction by morbid products prevent the free passage of air, and produce dyspnoea, which too often ends in asphyxia. This dyspnoea is such a marked symptom that it gained for the malady the name of suffocative catarrh at a time when neither the seat nor the nature of the lesion was known Avith certainty. Under the terms " suffocative catarrh," " peripneumonia notha," and " false inflammation of the chest," Sydenham had confused bronchitis, asthma, and emphysema. His successors followed the same track, and Home, all through his work on membranous exudates, found the explanation of every kind of suffocative bronchitis in the false membranes. Laennec put an end to the confusion, and showed that suffoca- tive catarrh is a phlegmasia of the bronchi, but he attributed its extreme gravity only to the extent of the lesions. Andral substituted the more correct idea of the seat of the phlegmasia, and localized the lesions of capillary bronchitis in the bronchioles. The works of Gendrin, RilHet and Bathez, Fauvel, Legendre, and Barrier then appeared, and it may be DISEASES OF THE BRONCHI 81 said that capillary bronchitis, as now established, was the work of the French school. Capillary bronchitis, however, rarely exists in a pure form. More often in children — we might say always — the pulmonary lobules participate in the inflammation, and the disease takes the name of broncho-pneumonia (Seiffert), or of lobular pneumonia. This disease often follows measles, whooping-cough, and diphtheria. Pathological Anatomy. — In a child who has died of capillary bronchitis and broncho-j^neumoma we see, after opening the thorax, that the lungs do not collapse. The edges and the apices are emphysematous. The posterior and lower part of the lungs is bluish or brownish, and in these regions, which are dark and violet-coloured, isolated or confluent nodules of lobular pneu- monia are perceptible both to sight and to touch. Whether capillary bronchitis exist alone, which is rare, or be associated with inflammation of the pulmonary lobules, which is the usual condition, the inflammation of the small bronchi determines two kinds of lesions. The former affects the bronchi, the latter the corresponding pulmonary lobules. The mucosa of the bronchioles is swollen and smooth, instead of being folded longitudinally, as in the normal state. The vessels are engorged with blood, and allow the white corpuscles to pass out. The epitheUal cells lose their cilia, and become vesiculated ; they desquamate or become seg- mented, and give birth to new elements. The glands increase in size, and allow epitheUal cells and muco-pus to escape by their ducts. The sub- epitheUal connective tissue is infiltrated with leucocytes, and in the bron- chioles near the lobule the muscular fibres disappear, owing to the invasion of embryonic tissue. The inflamed bronchioles are enlarged in calibre. These acute dilata- tions cliiefly invade the smaller bronchi, and we see broncliioles which measure a centimetre instead of 1 to 2 millimetres in diameter. The dilata- tions are usually cylindrical, sometimes ampullary, and appear, when the lung is cut, as cavities which are filled with pus. They may be isolated or may communicate with one another. These dilatations are due partly to the mechanical action of secretions driven back by the inspired air, but chiefly to the diminished resistance of the inflamed tissue, which is deprived of its muscular elements. They exist in the broncho-pneumonia of young children, but may disappear with the cure of the disease. The inflammatory products, including cells, leucocytes, and fibrinous exudate, accumulate in the bronchi, which are " filled or almost obhterated from the branches of the second size to the smallest ramiflcations by a yellowish-white sub- stance " (Hardy and Behier). 'J'his obliteration of tli(! small bronchi induces changes in the corre- sponding pulmonary lobules. These changes have been explained as follows: G 82 TEXT-BOOK OF MEDICINE The inspired air cannot reach the lobules, because the small bronchi are choked with inflammatory products. During expiration, however, by the help of coughing, the air previously contained in the lobules can overcome the resistance of the plugs which act as valves, and close the lumen of the bronchi. As a result, the infundibula empty themselves of the contained air, and, as this air is not renewed, the lobules collapse, and cause the col- lapsed parts to look hke the lung of a foetus which has never breathed, whence the name of foetal state appUed to this lesion (Legendre). There is no proof of the absolute truth of this theory, and it may be asked if the air in the alveoli is not simply absorbed there. This fact would explain the production of the foetal state. The foetal state, also called atelectasis, or pulmonary collapse, is chiefly met with at the edges and the base of the lungs in young subjects with broncho-pneumonia. The collapsed parts are bluish, brownish, or violet- coloured, and do not crepitate on pressure. The cut section is smooth and miiform. They do not float in water, and although they may have this character in common with lobar pneumonia, they differ totally in that they can be blown out. Under the microscope, the alveoh are seen to be intact, but the vessels are gorged with blood. This stasis causes oedema, and atelectasis is often the first stage of splenization. So far, having in view only the changes proper to capillary bronchitis, I have described two lesions : the first active — that of the bronchus ; the second partly mechanical — the fcBtal state of the lung. Let us study the lesions of broncho-pneumonia. The diversity of the lesions complicates the description. There is not one lesion, as in pneumonia, and the morbid process is not homogeneous, but comprises bronchitis, congestion, hepatization, splenization, atelectasis, emphysema, etc. Sometimes splenization, at other times hepatization, is the chief factor, and as these expressions will often recur, it will be well to explain their meaning. We already know the signification of atelectasis, or the foetal condition. Hepatization, so called because of its coarse resem- blance to liver tissue, is the result of the inflammatory process which affects certain parts of the lung. Splenization, so called because of its coarse resem- blance to spleen tissue, results from lesions which are rather congestive than inflammatory, and is a kind of epithehal pneumonia. Carnlfication, so called because of its rough likeness to muscular tissue, is a condition of the pulmonary lobide described under Chronic Broncho-Pneumonia. More exact knowledge as to the structure of the lung has led us to abandon the idea that, as regards structure and circulation, the bronchiole was quite independent of the pulmonary lobule. Extension of inflam- mation from the one to the other, which was formerly supposed to be the exception, is really the rule, so that any lobular pneumonia may be pre- ceded or accompanied by capillary bronchitis. The bronchus, so to say, DISEASES OF THE BRONCHI 83 carries the inflammation to the lobule. Inflammation of the small bronchi sometimes precedes the outbreak of the lobular pneumonia ; at other times their appearance is almost simultaneous. Lobular pneumonia, or broncho- pneumonia, was called catarrhal when it was supposed to comprise only surface lesions. This designation is insufficient, for the lesions of lobular pneumonia are in some cases deep and parenchymatous. The lesions affect both lungs, and by choice the lower lobes and their posterior part. The islets of broncho -pneumonia may be diffuse or con- fluent. In the former event, they vary in size from a pea to a walnut, and contain one or several inflamed pulmonary lobules. They are scattered here and there in the middle of lung tissue, which may be healthy, con- gested, bluish, violet- coloured, collapsed, or emphysematous. This form is called disseminated lobular pneumonia. In the latter event, the lesion involves a large number of lobules, and may even affect an entire lobe. The disease then takes the name of confluent, or pseudo-lobar, pneumonia. Besides the principal lesion, some scattered islets are also found. In the disseminated form the nodules, which are of variable size, and often lozenge-shaped, are prominent, hard, and red in the congestive period ; they are greyish in the next stage, because of the pus cells in the alveoli, and finaUy become yellowish and caseous. The pseudo-lobar form differs from the preceding in the confluence of the nodules, which present various changes. Near a nodule in which pus is forming nodules which are simply congested or splenized may be seen ; consequently, the bulk of the lung presents diversity of colour and of consistence. The inflamed lobules are often superficial, and infundibula, fiiUed with beads of pus, which have been termed purulent graulations (Fauvel) and vacuoles (Barrier), are sometimes seen on their surface. These granulations are yellowish, rounded, as large as a pin's head, and most common on the surface of the lung. The vacuoles, which have the same origin, also contain pus, but are larger, because the alveolar septa are destroyed. On section, the cut surface presents a less granular appearance than in lobar pneumonia. As regards the minute structure, if we choose a well- inflamed lobule, and make the section at right angles to the intralobular bronchus, we see under the microscope — ■ 1. In the centre the bronchus is dilated and choked with cells and pus. The walls are in part infiltrated with embryonic cells, and have lost almost all their muscular tissue. These points are best seen in very young chiidi-en, but the lesion is curable. The bronchial dilatation, however, does not always disappear, and broncho-pneumonia may lead to chronic bronchi- ectasis. 6—2 84 TEXT-BOOK OF MEDICINE 2. Around the intralobular bronchus and its artery a zone of inflamed alveoli and ducts is found. This is the zone of hepatization, also called the peribronchial nodule (Charcot). In this nodule the phases of engorgement, and of red and grey hepatiza- tion, can be seen. The lesions of engorgement are as follows : Cut surface smooth, tissue spongy, red, and uniform ; crepitation has disappeared ; tissue sinks in water ; mider the microscope, the intralobular bronchus is seen surrounded by distended vessels, which are crammed with red cor- puscles ; the alveoH contain red corpuscles and fibrino-albuminous fluid. The lesions of red hepatization are as follows : On section, mottled surface ; around the bronchus, granulations hke those of lobar pneumonia ; under the microscope, alveoli filled with leucocytes and fibrino- purulent exudate ; walls of the alveoh infiltrated with leucocytes. The lesions of grey hepatiza- tion are : Nodule is less firm on section, dry, and mottled with red ; fibrinous exudate is replaced by pus ; intralobular connective tissue infiltrated with leucocytes ; tissue of the bronchus and the peribronchial nodule often blended in a puriform sheet, in the midst of which the pulmonary artery appears as a landmark. The peribronchial abscess, which is never peri- lobular, is formed in this way. 3. Around the peribronchial nodule is the zone of splenization, which is smooth on section. Splenization is characterized by lesions wliich are less inflammatory than those of hepatization. The alveoh contain a fibrinous exudate, with leucocytes and epithehal cells, derived from the alveolar walls, wliich have proliferated. This is the zone of epithelial pneumonia (Charcot). The walls of the alveoh at first undergo no change of structure. The peri- lobular spaces are well marked by the inflammation, but the suppuration does not affect them. I have just described splenization in its relations to hepatization of the pulmonary lobule, but splenization is sometimes the chief lesion in broncho- pneumonia, especially in the pseudo-lobar form, nodules of hepatization being absent. The splenized lung is red, cedematous, heavy, resistant, smooth on section, and filled with muco-pus, wliich comes from the bronchi. " This splenization, wliich is a kind of epithelial pneumonia, might well be consecutive to the obliteration of the bronchi " (Charcot). The epithehal cells of the alveoh swell and desquamate, the congestion is intense, albu- minous exudate occurs both inside and outside the alveoli, and if the lesion persists for some time the alveolar epithelium tends to become cubical, and the peri-alveolar connective tissue is thickened. Certain parts of the lung are affected by inflammation and congestion, independent of any pneumonic process. The peribronchial nodule, or zone of hepatization, is associated with phlegmonous inflammation of the intralobular bronchus, while the lesions DISEASES OF THE BRONCHI 85 of splenization are associated with obliteration of the bronchi in the splenized areas. Whatever be the form of the broncho-pneumonia, the congestion in generally intense in both sets of vessels, though it is most marked in the bronchial vessels. Hsemorrhage also occurs in the interior of the pneu- monic nodules. The entire lymphatic system may be involved, the bronchial glands are enlarged and congested, the intralobular spaces are thickened, and the lymphatic spaces are filled with white corpuscles. Visceral pleurisy is frequently met with over the superficial nodules of lobular pneumonia, and subpleural haemorrhages have often been observed by Parrot. Lastly, in those who have died from broncho-pneumonia emphysema is often seen, especially at the upper lobes and the anterior borders of the lungs. This lesion, joined with the congestion, explains why, post mortem, the lungs appear cramped in the thorax. Such, then, are the many lesions of broncho-pneumonia. Changes in the small bronchi, atelectasis, spleniza- tion, hepatization, haemorrhage, emphysema, combine in different degrees to produce the various anatomical types which I have just described. Experimental Broncho-Pneumonia. — While lobar pneumonia is difficult to reproduce in animals, broncho- pneumonia may be readily caused in them. The introduction of ammonia, essence of turpentine, and perchloride of iron through an opening in the trachea produces capillary bronchitis and broncho-pneumonia in animals. The same result is obtained by section of the vagi in the dog, an operation which favours the entrance of foreign bodies into the bronclii (Traube), and also that of pathogenic microbes. When the experiment has been quite successful, the lungs of the animal present all the lesions previously described : obstruction of the inflamed bronchioles, atelectasis, splenization, nodules of lobular pneumonia, and emphysema. Bacteriology. — Microbes are the active agents in broncho-pneumonia. It has been found possible to produce broncho-pneumonia in animals by injecting into the trachea cultures of different microbes. Several species of microbes may give rise to broncho-pneumonia in man. table gives their relative frequency in adults (Netter) : Pneumococcus Streptococcus Encapsuled bacillus Staphylococcus pyogenes . . These various microbes are often associated. The pneumococcus is most important in adults, the streptococcus in children. The following Per Cent. 38-47 30-77 2308 7-68 86 TEXT-BOOK OF MEDICINE Mosny believes that the anatomical varieties of broncho-pneumonia correspond to the particular microbe — streptococcus in the lobular, pneumo- coccus in the pseudo-lobar form. Netter does not hold this opinion. These different microbes are often found in the mouths, the nasal fossae, and the bronchi of healthy persons. Why do they become virulent at certain times ? I do not know, and I refrain from theories. In broncho-pneumonia, which supervenes in the course of diphtheria and of typhoid fever, the specific bacillus of these maladies may be found in the diseased lung, or may be absent, while the broncho-pneumonic focus always contains the other microbes previously quoted. The specific bacillus of diphtheria, of typhoid fever, and the as yet unknown microbes of other diseases, do not therefore appear to be capable 'per se of causing broncho- pneumonia. Their associates must be present, and these, the real cause of broncho-pneumonia, are the microbes of which I have spoken above. It has been asked if bacteriological examination of the sputum would not throw light upon the prognosis of broncho-pneumonia by establishing a scale of gravity according as the chief pathogenic agent be the pneumo- coccus, the pneumobacillus, or the streptococcus ; but the researches under- taken on this subject have as yet given no positive resu.lt. Symptoms — (a) Capillary Bronchitis. — The symptoms of invasion — i.e., the fever and the elevation of temperature — are more marked than in simple bronchitis. The fits of coughing are more painful, and are often followed by vomiting of mucus or of food. Dyspnoea, which is rapid in its appearance, is the chief symptom ; indeed, it is not seen with such severity in any other acute inflammation of the bronchi or of the lung. The dyspnoea is as severe as the suffocation produced by the false membrane of croup or by oedema of the glottis, and, indeed, the mechanism is much the same, for in both cases it is a question of foreign bodies which prevent the free passage of air : only in disease of the larynx " the obstacle occupies the common trunk of the air- passages ; in capillary bronchitis it is diffused in the terminal ramifications of the tree " (Jaccoud). The dyspnoea is con- tinuous and progressive. It is not interrupted by suffocative attacks and by remissions, as in the diseases of the larynx to which I have alluded, and soon reaches its acme, so that the respiration rate may be 50 in an adult and 80 in a child. The extreme distress, the small irregular pulse, the jerky voice, the working of all the inspiratory muscles, the violet tint of the Ups, the pallor of the face, and the coldness of the extremities, bear witness to the increasing asphyxia. During the asphyxial period the scene is heartrending. The patient sits up in bed ; his face is pale and covered with cold sweat ; his body is bent forward and propped up by his arms behind ; he tries instinctively to help his respiratory muscles, but yet, in spite of all Ids efforts, hsematosis is DISEASES OF THE BRONCHI 87 imperfect, and the blood is loaded with carbonic acid (anoxaemic poisoning). This toxic stage is characterized by cardiac weakness. The pulse is small and intermittent, the face becomes livid, the urine is scanty, and delirium appears. When capillary bronchitis ends favourably, recovery is announced by the ease in expectoration ; the sputum becomes more abundant, yellowish, and viscid ; the fever falls, and the dyspnoea gradually diminishes. Remis- sions, however, must be mistrusted, for they sue sometimes temporary, and may be followed by fresh inflammation. The physical signs are as follows : Percussion of the chest yields normal resonance. Auscultation, both during inspiration and expiration, gives fine subcrepitant rales scattered in front and behind over both sides of the chest. The large rales of ordinary bronchitis are often heard. Recamier gave the name bruit de tempSte to these sounds, which form a perfect tumult. The sputum is composed of the tliick purulent exudate from the small bronchi, and of a frothy secretion from the larger bronchi. In children there is no sputum. In some cases the secretion is so abundant that the patient repeatedly fills his spittoon with pus, as though he vomited it. It has been asked if capillary -bronchitis can be quite independent of broncho-pneumonia. It may be, especially in an epidemic. Whether the cause be cold, influenza, or measles, capillary bronchitis may be unaccom- panied by broncho-pneumonia. It is, however, always accompanied by emphysema of the antero-superior parts of the lung and by splenization of the postero-inferior parts. We may also find yellow granules, subpleural ecchymoses, and congestive foci which would have ended in broncho- pneumonia if death had not been so prompt. (6) Broncho-Pneumonia. — This malady behaves so differently, according to age, that it must be studied separately in adults and in children. Broncho- pneumonia in the adult presents some of the symptoms which have just been mentioned under capillary bronchitis. To this description the follow- ing symptoms must be added: The temperature rises to 104:° F., and the sputum may be streaked with blood, but is not rusty. If the inflammation only attack isolated lobules, the signs on auscultation are but little changed. If, however, tlio lesion occupy a large surface, and especially if it assume the form of pseudo-Iobar pneumonia, dullness, tubular breathing, and bronchophony appear simultaneously at the seat of the lesions, although these signs are not so severe as in lobar pneumonia. As the pneumonic lesions vary in intensity, rough bronchial breathing may be heard at one point and faint tubular breathing at another. These lesions are usually multiple, and invade in succession several regions in one, or both lungs, but es[)ecially the posterior and inferior parts. The sibilant 88 TEXT-BOOK OF MEDICINE and the mucous rales are more or less fine, numerous, and scattered, accord- ing to the concomitant changes in the bronchi. In children broncho- pneumonia is frequent, and is usually a very serious disease. As we shall see under ^Etiology, it is rarely primary, and usually supervenes in the course of simple bronchitis, or appears as a complication of measles, whooping- cough, diphtheria, or influenza. In infants it is very often tubercular. As a rule, high temperature, quick pulse, and severe dyspnoea indicate the invasion of broncho -pneumonia. Dullness and more or less harsh, tubular breathing indicate the part of the lung invaded. If the lesion is inflammatory, it takes some days to run its course ; if, however, it is congestive, it may disappear by the next day, and reappear at another point, which fact gives to broncho-pneumonia an appearance of mobility. Moreover, as the inflammatory and hypersemic lesions of the lung are differently combined, numerous clinical varieties may be observed. Broncho-pneumonia usually matures by successive outbreaks. Some- times one part of the lung is attacked before another part has cleared up ; at other times the new outbreak supervenes after two or three days of im- provement, which made recovery appear probable. On auscultation, the tubular breathing is in part masked by subcrepitant rales. It is not rare to find several foci of broncho-pneumonia. They are usually present on both sides, and more often at the base or the middle of the lung. The existence of a rub or of aegophony indicates concomitant pleurisy. The little patient, who is breathless and excited, utters plaintive cries, and the continual working of the alae nasi indicate the violence of the dyspnoea. The respiration rate may reach 50, 60, or even 80 a minute. The cough is constant and overpowering, the face is pale, the lips are blue. When broncho-pneumonia is of moderate intensity, it lasts from a fortnight to three weeks, and ends in recovery. We see, however, cases in which it carries children off in less than a week, and also fulminant forms wliich are fatal in two or three days. In the aged, broncho-pneumonia affects different forms. In the acute form, which much resembles the variety in an adult, we find violent cough, progressive dyspnoea, muco- purulent or muco-sanguinolent expectoration, with multiple rales and tubular breathing. In the suffocating form (suffoca- tive catarrh) the dyspnoea rapidly becomes alarming ; the expectoration is scanty, viscid, and sometimes quite airless ; the pulse is small and irregular ; the vital forces quickly fail ; the extremities become cold, a clammy sweat appears, and the patient dies in delirium or coma. Course — Duration — Prognosis. — The course of capillary bronchitis and of broncho -pneumonia has been divided into two periods — the one dyspnoeic, the other asphyxial — while the two together may last from one to three weeks. This division, however, is artificial. The prognosis is most grave. DISEASES OF THE BRONCHI 89 Death is common in children and old people, especially when the disease occurs in an epidemic form, and when it breaks out in a children's hospital as a sequel to whooping-cough, measles, and diphtheria. I have twice remarked that in children suffering from capillary bronchitis with measles the bronchitic symptoms improved on the appearance of pneumonia, as if under the influence of a natural revulsive. The fine scattered rales partly disappeared, as if the inflammatory process were about to concentrate itself at certain points. It seems at first sight as though the localized lesions could be easily controlled, but new foci of lobular pneumonia develop, and after several alternations in the course of events the termination is too often fatal. In favourable cases the dyspnoea mends, the fine rales disappear, and improvement is gradually established. Sometimes broncho-pneumonia shows a subacute course, and may finally become chronic. This course, although it be rare, is especially seen in the pseudo-lobar form, where splenLzation is the chief lesion, I shall refer to it under Clu-onic Pneu- monia. Diagnosis. — The diagnosis between capillary bronchitis and acute tuberculosis in the adult is given later,* Let us at present differentiate capillary bronchitis from simple bronchitis, pseudo-membranous bronchitis, pulmonary oedema, and congestion of the lung. The sonorous rhonchi and the mucous rales of simple bronchitis show no resemblance to the sharp, fine rales of capillary bronchitis ; the slight distress in the former is quite unlike the terrible dyspnoea of the latter. The appearance of these signs, however, in the course of a simple catarrh indicates the change from ordinary to capillary bronchitis. Pseudo-membranous l)ronchitis may occur without membranes in the larynx and the pharynx. The membranes which line the ramifications of the bronchi cause fits of dyspnoea, similar to those of capillary bronchitis ; but as the patient i)rings up long, branched membranes, tlie diagnosis is obvious. (Edema of the lung alone, or associated with passive congestion, is seen in Bright's disease, in mitral and tricuspid lesions, and in all cases where the pulmonary circulation is impeded. Auscultation reveals fine subcrepitant rales, which are most abundant at both bases ; fever is absent, the dyspn(JDa is intense, and the expectoration is frothy, albuminous, and rosy, when the case is one of superacute oedema of the lung. The diagnosis of broncho-pneumonia from lobar pneumonia is easy. Lobar pneumonia, as a rule, appears suddenly in healthy persons, and begins with stitch in the side and shivering ; while broncho-pneumonia most often develops in those wjio are already ill (measles, whooj>ing-r<»ugli, diphtheria, influenza). Lobar pneumonia is nearly always unilateral and * Vide Chapter IV., Section Hi. 90 TEXT-BOOK OF MEDICINE characterized by crepitant rales and tubular breathing, while broncho- pneumonia affects both sides of the chest at multiple centres, which are more or less extensive, and characterized by blowing breathing and multiple rales. In lobar pneumonia the cough is dry, and the sputum in adults is rusty ; in broncho-pneumonia it is loose, incessant, overpowering, and the sputum is muco-purulent. Genuine pneumonia usually ends from the fifth to the ninth day, and its termination is almost always favourable in children ; broncho-pneumonia is much more formidable, and lasts week» or even months. If the reader will turn to the chapter on Asthma, he will see that certain febrile forms of asthma, especially in children, may at first sight simulate capillary bronchitis. The diagnosis of broncho-pneumonia from acute tuberculosis is often very difficult. Both may supervene in the course of another disease (measles, whooping-cough) ; in both we find extreme dyspnoea, high tem- perature, early cyanosis of the face, with subcrepitant rales and blowing breathing. The predominance of the lesions at the apices and the presence of blood in the sputum are . presumptive signs in favour of tuberculosis, and the presence of bacilli is a certain sign. Sero-diagnosis gives valuable information. iffitiology. — Capillary bronchitis alone is hardly ever seen except in adults ; broncho- pneumonia is especially a disease of infancy and old age. Measles, whooping-cough, influenza, diphtheria, typhoid fever, erysipelas, cholera, and tuberculosis in infancy, are the affections in which broncho- pneumonia usually appears. I refer to these different diseases for the study of the special characters which broncho -pneumonia assumes in each. It often occurs after tracheotomy. It is more frequent in cold weather, and sometimes assumes an epidemic form. Suppurative and infectious lesions of the nasal fossae and of the tlu'oat may cause broncho-pneumonia by descending infection. The pathogenic agents pass through the larynx and the bronchi to the lungs ; in some cases the lung is affected, although the intermediary air-passages appear free. Simjile bronchitis may in some circumstances be followed by capillary bronchitis and broncho-pneumonia. Epidemics of broncho-pneumonia have been noted in workmen employed in crushing slag diu*ing the manufacture of steel. The dust and the microbes which are present both take their share in the pathogenesis. Let us also note the broncho-pulmonary lesions secondary to such con- ditions of the nervous system, as cerebral hsemorrhage, softening, general paralysis, mental affections, etc. Treatment. — In capillary bronchitis and broncho-pneumonia the indi- cations are identical. We must reduce the broncho-pulmonary inflamma- DISEASES OF THE BRONCHI 9J tion and favour the expulsion of the secretions which block the bronchi. The first indication will be attained by means of revulsives, blood-letting, dry- and wet-cupping, and application of leeches. Kermes, repeated emetics, ipecacuanha alone, or with tartar emetic, fulfil the second indication. For a child : I^t Syrup of ipecacuanha . . . . . . . . ^ii. Powdered ipecacuanha . . . . . . . . gr. xv. Give a teaspoonful or a dessertspoonful every five minutes till vomiting occurs. For an adult : I^ Ipecacuanha . . . . . , . . . . gr. xx. Tartar emetic . . . . , . . . . . gr. i. Divide into two doses, give at five-minute intervals, and make the patient drink tepid water to assist vomiting. For the fits of coughing and the pain the following draught will be useful : For an adult : J^ Orange -flower water . . . . . . . . 5iii- Syrup of chloral 1 byrup oi morphiaj Cherry-laurel water . . . . . . . . 3ii. A tablespoonful to be taken every three hours. Inhalations of oxygen are of some use in asphyxia. Lastly, the strength of the patient must be carefully supported by broths, tonics, and alcohol. A child two years old can take during the day a draught containing 25 grammes of sherry and 15 centigrammes of acetate of ammonia. Baths, both cold and hot, have been extolled (Renaut). This treatment cannot, and ought not, to be systematic. In a case with marked fever, very high temperature, and an ataxic tendency, baths at 75° F. are to be used. In a case with great broncliial embarrassment, much dyspnoea, and an adynamic tendency, hot baths are preferable. Injections of serum, in amount appro]iriate to the age of the patient, may be used with advantage {vide appendix on Therapeutics). Prophylactic treatment must not bo neglected, and children who are predisposed to colds and bronchitis must not be allowed to come near those suffering from broncho-pneumonia. III. CHRONIC BRONCHITIS. etiology — Description.— Altliough chronic bronchitis may be primary, it is often associated with constitutional maladies. In lymphatic and scrofulous subjects, in gouty persons, and those affected with skin Icsioas, 92 TEXT-BOOK OF MEDICINE and in old people, bronchitis may be chronic from the first, or follow upon more or less acute attacks. Clironic bronchitis is most prevalent during cold, damp weather, and chills provoke acute attacks, which have a very- bad effect upon the disease. Chronic bronchitis is characterized by long and painful fits of coughing, which are frequently repeated, especially in the morning and the evening. Animated conversation or a quick walk may bring on a fit which is often followed by abundant expectoration. The sputum is thick, greenish- yellow, and often mixed with froth. More rarely the expectoration is scanty, and the balls of sputum have the consistence of starch (dry catarrh). The breathing is wheezing and difficult. On auscultation, snoring and sibi- lant rhonchi and large bubbling rales are heard over both sides of the chest ; they may be so abundant as to simulate the gurgling of a cavity. There is no fever, the appetite is scarcely affected, and the dyspnoea is slight, apart from the fits of coughing. Chronic bronchitis has no fixed course ; it lasts several months, improves in fine weather, but reappears with the first cold. In artlu-itics subject to skin lesions, such as eczema or lichen, it is not rare to see a certain alternation between the cutaneous and the bronchitic troubles. Chronic bronchitis usually leaves behind it pulmonary emphysema, but the patient may live indefinitely till complications change the situation. These complications are of various kinds. Some, sudden in their appear- ance, comprise pulmonary congestions, which cause attacks of dyspnoea and acute broncho-pulmonary inflammations, which create immediate danger ; others, slow in their development, are pulmonary emphysema and lesions of the right heart, which give rise to increasing difficulty in breathing, cyanosis, and general oedema. Dilatation of the bronchi is also one of the consequences of chronic bronchitis. In feeble subjects, especially elderly ones, who have no longer strength to expel the secretion in the bronchi, clu-onic catarrh may change into a suffocative one. In the course of bronchitis the breath and the expectoration may some- times become foetid. This foetor, which may last weeks and months, is due to decomposition of the bronchial secretions, to the presence of butyric acid (Laycock), or to gangrene of the mucosa, which, however, is not so serious as gangrene of the lung. Certain persons suffering from chronic bronchitis may bring up for months and years branched, and often cylindrical, membranes. These may measure from 4 to 6 inches in length, are whitish, elastic, and chiefly com- posed of mucine. They must not be confused with diphtheria of the bronchi. DISEASES OF THE BRONCHI 93 Diagnosis. — Chronic catarrh of the bronchi must not be confounded with spurious bronchial inflammation, which is only an episode in the course of some other disease. In people suffering from cardiac disease (mitral lesions), the broncho-pulmonary circulation is easily impeded, and congestion and oedema of the respiratory passage are the result. Multiple rales are heard on auscultation, and the distress sometimes takes the form of fits. If the cardiac lesion is not recognized, these different troubles are set down to chronic bronchitis until other symptoms call attention to the true cause. The same remark applies to bronchitis in patients with Bright's disease. A patient complains of distress and suft'ocation, accompanied by cough and expectoration. On listening, we find mucous rales on both sides of the shest, usually most abundant at the bases. A superficial examination would readil} lead to the idea of subacute or chronic catarrh, but a minute interrogation reveals other important signs. The patient has frequent micturition, his eyelids are puffy, the heart is hypertrophied, and we find a gallop rhythm (Potain) ; the urine is albuminous ; and, in short, the so-called bronchitis is only an episode in Bright's disease. We shall see later that chronic bronchitis is often associated with asthma, dilatation of the bronchi, and emphysema. It precedes or follows them, and may, especially in asthmatics, become the chief trouble, so as to mask the real nature of the disease. Pathological Anatomy. — The diseased bronchi are thickened, and the connective tissue of the mucosa is mvaded by fibrous tissue, which some- times forms prominent vegetations. It is not rare to meet with superficial ulcerations at the glandular openings. Emphysema Ls often seen as a complication. Treatment. — The end in view is to dry up the secretion and modify the secreting parts. CVeosote (Bouchard), iodoform (See), aijd essence of turpentine give good results. These different medicaments may be ad- ministered by the respiratory passages as vapours (inhalation-rooms), and sprays (atomizers), or by the digestive tract. The following formulae relate to the adminLstration of these remedies : Capsules of creosote, each containing 1 minim. Dose, 4 to 8 with each meal. Perles of essence of turpentine, each containing 4 minims. Dose, 4 to G with each meal. Pills of iodoform, each containing 1 grain. One pill to be taken with each meal. Capsules, containing 4 minims of copaiba and 4 minims of tar. Dose, J to 8 with each meal. Terpenc may be employed, givhig daily G to 13 pills, each containing ] ^ minims, amounting to from 10 to 15 minims in twenty-four hours. 94 TEXT-BOOK OF MEDICINE Good results may be obtained with eucalyptol, given in doses of from 4 to 10 capsules daily. Arsenic and sulphur should be used with these different remedies. The sulphur cures of Saint-Sauveur, Luchon, and Cauterets, and the arsenical ones of Mont-Dore and La Bourboule, will be of much service. I often prescribe Labassere water, taken in the morning, fasting. The dose is 4 table- spoonfuls in hot milk. In old people especially the blocking of the bronchi by secretion must be carefully watched, and combated by means of repeated emetics. The patient who suffers from chronic bronchitis should avoid chills and pass the winter in a temperate cUmate. IV. DILATATION OF THE BRONCHI— BRONCHIECTASIS. Pathological Anatomy. — When we read the chapter which Laennec devoted to dilatation of the bronchi, and consider that this subject was previously untouched, we are astonished at his great accuracy. The lesions fomid post mortem are usually multiple, because dilatation of the bronchi is accompanied by chronic broncho-pneumonia, fibrosis of the lung, chronic pleurisy, with adhesions and pulmonary emphysema — lesions which are more or less marked according to the case. On openmg the chest, the lungs do not collapse ; in certain parts they are indurated, carnified, and hepati^ed, and their surface is mottled and cyanotic. In some cases a lobe is atrophied and cirrhotic. The lesions of recent acute broncho-pneumonia are not rare. In some cases the dilatations appear on the surface of the Imigs ; in others they are only seen on section in the depth of the organ. The large bronclii are rarely dUated ; bronchiectasis occurs chiefly in the third and fourth order of bronchi, which are 2 to 3 millimetres in diameter. The pathological anatomy of the dilated bronchi comprises their shape, structure, and situation. The shape is variable. Uniform dilatation, the rarest form, affects the whole length of the bronchus, the calibre alone being altered. Monili- form dilatation (Cruveilhier), by its successive swellings, gives the bronchus the appearance of a string of beads. Ampullary dilatation is the commonest form, and is made up of cavities which may be isolated, like a cyst, or commmiicate with neighbouring dilatations. In the latter case, the invaded area resembles the auricle of the heart, or an alveolar mass in which the septa are formed by the atrophied and fibrous lung tissue. Ampullary dilatation has different forms, accordmg as the enlargement invades the lateral parts of the bronchus, or an entire segment. These enlargements, or bronchial aneurysms, have been compared to aortic DISEASES OF THE BRONCHI 95 aneurysms — a comparison which is the more justified as it is the change in the bronchial wall which is chiefly responsible for the swelling. The dilatations vary in size from a pea to a pigeon's egg ; the peripheral portion of the bronchus, which is usually atrophied, terminates in a cul-de-sac, but it may in exceptional cases be dilated into a kind of cyst on the surface of the lung (Gombault). The different forms which I have described may be found combined in the specimen. The structure of the dilated bronchus varies according to the stage of the lesion. Where the lesion is but little advanced, the mucosa of the cavity is almost healthy, and is continuous with that of the bronchus ; the cylindrical epithelium remains ; the glands are atrophied ; the submucous connective tissue has lost some of its elastic folds ; and the muscular fibres are much separated, but rarely destroyed. When the lesion is very advanced, the bronchi have quite lost their normal structure ; the mucosa is no longer wrinkled, because the elastic fibres have disappeared ; the cylindrical epithelium (jjropulsive) is replaced by pavement (protective) epithelium ; the mucosa is covered with villi, wliich are composed of embryonic tissue and vessels. The muscular layer is converted into embryonic tissue with new vessels ; the cartilages also return to the embryonic state, and are infiltrated with calcareous salts. The elastic fibres of the connective tissue are broken up, and no longer form a complete ring around the bronchus. The connective tissue forms, so to speak, the skeleton of the diseased bronchi. The capillary vessels are number- less, tortuous, and dilated ; they present swellings of every shape, and project into the cavity of the bronchus. This capillary network is especially de- veloped in the villi and in the layers adjoining the lumen of the bronchus. The vessels anastomose in every direction and form a cavernous tissue. In the lesions of bronchiectasis there are, then, two kinds : the one — neo-formative — ends in the development of embryonic and vascular tissue ; the other — destructive — causes a loss of normal tissue (Hanot). In certain cases ulceration occurs, and the surface of the cavity may be attacked with " a superficial curable gangrene, which is analogous to the death of connective tissue in phlegmon." The liquid in the dilated bronchi is composed of mucus and pus in variable proportions ; it contains crystals of margarine and of cholesterine, and its mawkish odour becomes foetid in cases of gangrene. When a dilatation has lost its connections with the parent bronchus, it becomes filled with a caseous mass, and looks like an isolated cyst. Bronchiectasis chiefly affects the apex of the lung wlien the dilatation is nioniliform, while it more often occurs at the periphery when the swelling is anipullary. The dilatations are more frequent on the left side than on the right, and affect one lung only in the proportion of 20 to 4 (Bjirth). Bronchiectasis is always accompanied by clu'onic inflammation of the 96 TEXT-BOOK OF MEDICINE tissues — i.e., peribronchitis, fibrosis of the lung, and chronic pleurisy — but the origin of these tissues of new formation has not been completely eluci- dated. According to recent researches, the tissue of the chronic pneumonia which accompanies bronchiectasis is said to arise solely in the fibro- vascular framework of the lung, while the epithelium of the parenchyma takes no part, and the pulmonary tissue itself disappears by reason of the marked diapedesis which gives rise to the new fibrous tissue. " The parenchyma of the lung is transformed into granulation tissue, which finally forms adult connective tissue, more or less studded with vascular neoplasms, according to the age of the lesions. According to their more or less advanced organization into fibrous tissue, we may see the splenization, the carnification, and the areolar state of the parts of the lung which surround the dilated bronchus." Emphysema often accompanies bronchiectasis. Hypertrophy of the bronchial glands is sometimes seen, and tuberculosis, which was regarded as rare (Barth), appears to be fairly often associated with bronchiectasis (Grancher). etiology. — Bronchiectasis is a disease of middle and advanced age. It may result from acute bronchitis or broncho-pneumonia, but more often it follows clironic bronchitis, or broncho-pneumonia which has not cleared up, and is consecutive to measles, whooping-cough, mfluenza, or typhoid fever. In some cases the aetiology completely escapes our grasp. The chief theories of the pathogenesis of bronchiectasis are : Laennec : Accumulation of secretion in the bronchi, and consequent enlargement of these channels. Andral : Alteration in nutrition and diminished elasticity of the walls of the bronchi. Corrigan : Fibrosis of the lung, the retractile tissue of which puUs upon the walls of the bronchi. Stokes : Paralysis of the muscular fibres and diminution in the resistance of the bronchi. Mendelssohn: Pressure exerted by the air upon the diseased bronchi during fits of coughing. Gonbault admits the union of these different processes. Barth adds chronic pleurisy, acting, like pulmonary fibrosis, by its retractile tissue. Which of these theories are we to adopt ? Any morbid state capable of producing faulty nutrition of the bronchi (acute and chronic bronchitis), and any formation of extrabronchial fibrous tissue, might favour or produce bronchiectasis.* I admit the fact, but we must assign the proper value to each of these factors. * Paludism appears to act in this way in developing interstitial pneumonia. The cases of Frerichs, Lanceieaux, and Grasset, are quite conclusive (These de Grasset, MontpeUier, ISTi). DISEASES OF THE BRONCHI 97 It seems to me that we have exaggerated the role of chronic pneumonia and of pleurisy — in short, of fibrous tissues — when we look on them as retractile, and capable of producing bronchiectasis by mechanical action. There are cases, it is true, in which the action of the extrabronchial fibrous tissue appears evident ; perhaps, too, the bronchial and extrabronchial lesions develop on parallel lines, but the present tendency is to admit that the pulmonary lesion which accompanies the bronchial dilatation is most often the consequence, and not the cause, of the lesions in the bronchus. The phlegmasia begins in the bronchus ; it then extends around the bronchus, reaches the neighbouring pulmonary tissue, and thus gives rise to a systematic fibrosis. The proof that events mast follow this course is that chronic lobar pneumonia is not accompanied by bronchial dilatation, because the bronchus does not take part in the morbid process (Charcot), while bronchial dilatations are found in lobular or broncho- pneumonia, because the bronchus is always much altered. Therefore, whether there may or may not be pulmonary or pleural fibrosis, the lesion of the bronchus is the necessary fact that is indispensable to the production of bronchi- ectasis. By reason of the bronchial lesion the bronchus loses its normal elements, the elastic and muscular fibres give place to embryonic and vascular tissue which have no resisting power, and the bronchus dilates at its weak spot like an artery, the altered wall of which permits the formation of an aneurysm. It has been asked if there might not be some special condition capable of preparing the way for enlargement of the diseased bronchus, and arterio- sclerosis of the bronchial arteries has been suggested. In a case recently reported by Hanot arterio-sclerosis of the bronchial arteries was very marked. Symptoms. — Bronchiectasis shows itself by the following symptoms : The cough is fretjuent and spasmodic, as in chronic bronchitis, which often precedes dilatation. The expectoration becomes abundant, so that patients brmg up daily 4 to 12 ounces of muco-purulent fluid, with a mawkish and sometimes fcetid smell (bronchorrhoea). If the sputum is examined in the spittoon when its superficial layer alone is visible, it is frothy and aerated ; but if it is put in a measure-glass, it will be seen to have an opaque lower layer, which contains pus corpuscles, epithelial cells, and crystals of chole- sterine or oi margarine. The expectoration may be uniformly divided through the course of the day. Some patients, however, empty their dilated bronchi three or four times daily ; they are seized by fits of coughing or straining, like a fit of vomiting, and bring up each time 2 or 3 ounces of muco-purulent liquid. This fluid, which smells like fresh plaster, may become hxitid from decomposition of the fluid or from gangrene of the cavity. The breath then acquires such a stench that a whole ward may be tainted. 98 TEXT-BOOK OF MEDICINE This foetor, which is very tenacious, may exist, witli or without remissions, for months and years, and the unhapjjy sufferer avoids all company, and dare not show himself in public. HaBmoptysis is frequent m bronchiectasis. In some cases it can be set down to tuberculosis, which may be associated with bronchiectasis, but m a large immber of cases there is no question of tuberculosis. The haemoptysis depends solely on the bronchiectasis, and the bleeding is due to rupture of the tortuous, dilated capillaries (angiomata) which are present in the newly- formed bronchial and extrabronchial tissue. These forms of haemoptysis are a fresh source of difficulty in diagnosis. In some cases they have been the cause of death. In most cases dilatation of the bronchi exists on one side only, and affects the apex of the lung as often as the base. We find, on examination of the chest, a depression, which corresponds to the site of the dilatation, and is especially marked when bronchiectasis is associated with chronic pleurisy. This depression is frequently found at the middle and back part of the thorax. Percussion shows dullness, correspondmg to the diseased region. On auscultation the signs of a cavity are fomid, but the signs vary accordmg to the size and number of the cavities, and according as they are empty or full. They are sometimes masked by pleurisy, or by chronic pneumonia. Thus, m some patients the breathmg is blowing, cavernous, and even amphoric, and may or may npt be accompanied by gurglmg ; while bronchophony or pectoriloquy may be heard. Course — Duration — Termination. — When bronchiectasis is not asso- ciated with tuberculosis, the general symptoms are benign for a long while. There is no fever ; many patients ret am their appetite, and contmue to attend to their busmess, and m those who are not attacked by foetid bronchitis life is fairly comfortable, save that expectoration is abundant and dyspnoea may cause an mcreasing distress. In short, we are surprised, says Trousseau — and this is also Laennec's opinion — by the apparent innocence of the disease up to almost its final stage. In some cases death is the result of such complications as acute pneu- monia, acute broncho -pneumonia, gangrene of the lung, haemoptysis, cerebral abscess, purulent pleurisy, pneumothorax, tuberculosis, or pyaemia with articular and visceral abscesses. In other cases death comes more slowly, from the progress of the disease and from concomitant pulmonary troubles, which, after many years, are complicated by lesions of the right heart, or by consumption. The absorption of microbic products from the surface of the bronchial cavities produces a true septicaemia. The wasting, the hectic fever, the diarrhoea, the cachectic oedema, and the clubbed fingers, recall the picture of pulmonary phthisis. Bacteriology. — The fluid from the cavities contams numerous microbes, DISEASES OF THE BRONCHI 99 including the Streptococcus pyogenes,ihePneumococcus, and the Staphylococcus aureus, as well as saprogenic microbes, such as the Bacillus pyogenes fcctidus. These microbes perhaps play some part in the destruction of the bronchial tissues which favour dilatation, but they certainly play an im- portant one in most of the complications. These complications are not due solely to the toxines elaborated by the microbes, but also to the direct passage -of certain microbes into the blood and the organs. The acute septicaemia which sometimes supervenes m bronchiectasis, the suppurative artln-itis, the infarcts, and the cerebral abscesses are due to different strepto cocci {Streptococcus pyogenes, Streptococcus septic us liquefaciens) which have their original focus in bronchiectasis. Infective endocarditis with abscess in the liver and the kidney has been seen. It was consecutive to infection by the Staphylococcus aureus, from an infected bronchial dilatation. Diagnosis. — Pulmonary phthisis, foetid bronchitis, and pleural vomica have many signs in common with bronchiectasis. Let us first distinguish bronchial dilatation from tuberculous cavities in the lung, and let us take a well-marked case, in which bronchiectasis is not associated with tuber- culosis. The site of the lesion furnishes no distinctive sign, since bronchi- ectasis is as often unilateral as bilateral (twenty-six times m forty-three cases), and as frequent at the apex as at the base (Barth). Haemoptysis, cough, and clubbed fingers are also seen in both diseases. Lastly, cavernous breath- ing, gurgling, and pectoriloquy show in both cases the existence of cavities, but give no information as to their nature. Upon what points, then, can an affirmative diagnosis be based ? The expectoration in bronchiectasis is, it is true, more diffluent, more aerated and abundant than in phthisis ; but this distinction is not sufficient, and the true distinction lies in the different course of the two diseases. The patient affected only with bronchiectasis has for five, eight, or ten years suffered neither fever nor marked wastmg, but has simply coughed up abundant and sometimes foetid sputum, with or without dyspnoea. Such is not the course of tuberculosis. Fever, wastuig, dyspepsia, loss of strength, sweats, diarrhoea, are symptoms which coincide with the formation of cavities, and gradually increase with the spread of the lesion. Lastly, all doubts can be removed by examination of the sputum ; the presence of bacilli therein being a sure sign of tuberculosis. In foetid bronchitis, which is characterized by sloughing of the mucosa in the bronchioles (Lasegue), we find foctor of the breath and of the sputum, whi(;h is profuse, as in bronchiectasis ; l)ut the signs of a cavity are wanting. Between dilatation of the bronchi and vomica* of the pleui-a diagnosis is difficult. I am not referrbig to a vomica of the great pleural cavity occurring in piurulent pleurisy, the evolution of which we have followed out. It is ♦ Vide Chapter V., Section 15. 7—2 100 TEXT-BOOK OF MEDICINE evident that in such a case the abundance of fluid, its sudden appearance by way of the bronchi, and the signs of a large cavity replacing those of effusion, leave no doubt as to the diagnosis. I allude to those interlobar varieties (pleuro-pulmonary cysts) which differ from effusions of the great pleural cavity, in that the symptoms are obscure and the fluid is scanty. A patient coughs up for some time 10 to 15 ounces of foetid muco-purulent fluid daily. On inspection, the thorax is found to be flattened in the sub- scapular region. At the same level impaired resonance exists. On auscul- tation, the signs of the cavity may be recognized. The condition is just like dilatation of the bronchi. How, then, can we diagnose between this condition and a vomica ? We must investigate the course of events. Peter and I followed this course in a case similar to one described by Trous- seau.* The signs in bronchiectasis appear gradually, while the course of events is more sudden in interlobar pleurisy followed by vomica. The pleuritic phase is succeeded quite suddenly by the vomica, and the evacuated fluid is at first abundant, but diminishes during the next few days. Treatment. — The remedies employed to dry up the secretion from the dilated bronchi are practically those used in chronic bronchitis. Terpene may be prescribed, 6 to 10 pills daUy. Good results may be obtained with eucalyptol, given in doses of from 4 to 10 capsules daily. Turpentine, iodoform, and creosote will also find their indications. Inhalations and sprays of sulphurous and arsenical waters sometimes give go,od results. Revulsives, blisters, and the cautery must not be neglected. For the foetor of the breath and of the sputum, Paquelin's thermo-cautery should be employed. I have several times caused foetor to disappear for several days by multiple applications over the diseased region. As medical treatment too often fails, it is recognized that resort must be made to surgical measures. I am not speaking solely of antiseptic injections into the diseased bronchi. I allude to pneumotomy. I am well aware that the published results are not very encouraging, and the pul- monary haemorrhage which supervenes during the operation is a source of danger. Boswell Park, in his statistics, had nine deaths in twenty-five cases. These figures are not as yet very favourable to surgical attempts, but yet, when we thmk of the almost fatal prognosis of bronchiectasis, we confess that the hope of rational treatment lies in surgery. V. PSEUDO-MEMBRANOUS BRONCHITIS. This disease may have various origins. Sometimes the false membrane contains Loffler's bacillus, and mcreases the gravity of the prognosis in diphtheria of the larynx or pharynx ; sometimes the false membrane is * " Dilatation de Bronches " (" Le9ons de Clinique Medicale," tome i., p. 588). DISEASES OF THE BRONCHT 101 consecutive to pneumonia, especially massive pneumonia (Grancher), and the cause is the pneumococcus. Finally, in much rarer cases, we sometimes see after tuberculosis, measles (Jaeger), heart lesions, and ordinary bron- chitis, cases of pseudo-membranous bronchitis which are difficult to classify. Pseudo-membranous bronchitis does not always show a well-defined course. The bronchitis is only an episode of the disease which it happens to complicate. It is not so m the case of chronic pseudo-membranous bronchitis, in which the course and the symptoms are quite characteristic (Paul-Lucas Championniere). Chronic Pseudo-Membranous Bronchitis. etiology. — This form is chiefly seen in adult and elderly persons. It is more frequent in men than in women. Pulmonary affection and arthritism in the patient's ancestors appear to predispose to it. It may follow ordinary bronchitis, or be a complication of pulmonary tuberculosis. It is sometimes associated with the Aspergillus fmnigatus. Pathological Anatomy. — Post mortem the bronchial mucosa is seen to be slightly red and thickened. The false membranes are found in the trachea, the large bronchi, but especially in the smaller bronchi. The false membranes are branched like a tree or a piece of coral and form exact casts of the bronchi. These casts may be coughed up in small fragments, or in branching pieces 4 or 5 inches in length. The substance which forms them is white or rosy, and is often disposed in concentric lamina). In the large bronchi the membranes are hollow, and show a central lumen ; in those of small calibre the casts are solid. The structure of these membranes varies. They may be composed of firm mucus, coagulated albumin (Grancher), fibrin (Caussade), ur fat (Model). Charcot-Leyden crystals and eosinophile cells are at times found in them. In a case published by Claisse membranous bronchitis was associated with the streptococcus. In Griffon's case the pneumococcus was the pathogenic agent. Symptoms. — The affection generally begins as acute bronchitis, which may be accompanied by the expectoration of false membranes, and then gradually becomes chronic. The membranes may not appear till long after the disappearance of the acute bronchitis. In some subjects the affection is chronic from the start. The course is neither continuous nor progressive ; it is characterized by attacks. At more or less lengthy intervals the patients are seized with intense dyspncjea, retrosternal pain, and convulsive cough. At first they bring up abundant shreddy matter, and then false membranes, which may take the form of isolated fragments, or be rolled up in balls which unfold in water. In some cases an entire bronchial tree is brought up. Haemoptysis is very rare. After the expulsion of the membranes the dyspncca ceases. During 102 TEXT-BOOK OF MEDICINE the attacks the vesicular murmur is often diminished. We sometimes find a focus of crepitant rales which may be long persistent (Hyde Salter), or a hruit de drapeau, as in croup. The attack is generally apyretic. At the Necker Hospital I saw, in 1891, a man, fifty years of age, with pseudo- membranous bronchitis. For twelve months membranes were absent ; then he coughed them up every week for a month. The attack was preceded by certain symptoms the day before. He used to feel depressed, and would next day cough up large casts. He never had haemoptysis, and I found no signs on percussion and auscultation. He improved rapidly under iodide of potash, although he was not syphilitic. The duration of the disease is unlimited. A case of twenty-five years' duration has been quoted (Kirsch). The prognosis, not unlike that of simple chronic bronchitis, is only grave in a tubercular subject. Diagnosis. — The diagnosis rests entirely upon the examination of the sputum. When false membranes are discovered, histological and especially bacteriological exammations must be made, in order to ascertain if it be a case of diphtheria, pneumonia, or of chronic bronchitis, with or without tuberculosis. Rational treatment consists in the exhibition of iodide of potash, mercury, terpene, and creosote. VI. TRACHEO-BRONCHIAL SYPHILIS. As Mauriac justly remarks, the trachea and bronchi are simple con- ductors of air, and play a purely passive part, which cannot be compared with the many functions of the larynx. The symptoms of tracheo-bronchial syphiKs are therefore respiratory, but are more serious than in the larjmx, because tracheotomy is not applicable when the lesion is situated in the trachea or at its bifurcation. 1. Secondary Troubles. Description. — Erythema, catarrh, and erosions exist as secondary mani- festations in the trachea and the large bronchi ; but while vocal troubles and laryngoscopy readily reveal these secondary troubles if they are seated in the larynx, they can only be suspected when located in the trachea or the large bronchi. In certain cases, however, laryngoscopy may reveal them, although they are in the trachea. The symptoms are those of ordinary tracheo-bronchitis — viz., cough, slight dyspnoea, and expectoration. Their syphilitic origin may in many cases be affirmed, because they often coincide with mucous or cutaneous syphilides, and because they improve rapidly under treatment. Acute or subacute syphilitic tracheo-bronchitis is more common than we think. A case of tracheo-bronchitis which has lasted a long time, has been rebellious to other treatment, or has been set down to tobacco, artliritism, or chills, yields rapidly to mercury and iodide of potash. DISEASES OF THE BRONCHI 103 2. Tertiary Troubles. Pathological Anatomy. — In the trachea and the large bronchi, as else- where, the syphiloma may be circumscribed or diffuse. The lesion spreads either in the thickness of the mucosa or below it. Its action is not limited to the soft parts, and it invades the cartilages, the fibrous tissue, and the muscle. The gumma may be of large size, and the thickenings are more or less extensive. These tertiary growths usually end in circumscribed ulceration in the case of gumma, and serpiginous ulceration, which has a phagedaenic tendency, in the diffuse syphiloma. The ulceration may occupy a segment or the whole circumference of the trachea ; the phagedsena may attack the perichondrium and the cartilages, and perforate the trachea or furrow it from above downwards. In some cases the perichondritis and the chondritis are primary, the walls of the trachea bemg indurated and converted into a rigid narrow tube. Tracheo-stenosis and broncho-stenosis are the result of these lesions. The narrowing of the trachea may take place slowly or rapidly. The gummata and the ulcerations, with the resultmg oedema, narrow the trachea and the bronchi. The fibrous tissue forms longitudinal, oblique, transverse, or annular bands, and causes most marked constrictions. The fibrous scars produce two kinds of deformity in the trachea and bronchi, which diminish both in length and in breadth. The trachea, which is normally about f inch in diameter, is reduced to a third or a quarter of its size. The con- striction is rarely circular, like a diaphragm, but takes the form of an irregular, anfractuous channel, with superposed stages. The length of the trachea diminishes in proportion to the number of rings destroyed. The firmness of its framework is destroyed by the substitution of fibrous tissue for cartilage, and the consequent flattening during inspiration may cause asphyxia. The tracheo-bronchial syphiloma is nearly always accompanied or pre- ceded by pharyngeal or laryngeal syphilis. In sixty-five cases collected by Mauriac, in six only was the pharynx or larynx unaffected. The lower fourth of the trachea, with or without the participation of one or both bronchi, is the most frequent seat of syphiloma. The traclieo - bronchial glands iiTCi almost always enlarged. Description. — The cough and slight dyspnoea of the onset make us think at first of simple bronchitis, but otlier symptoms soon a|)pear ; obstinate spasmodic cough, the sensation of a foreign body, the feeling of constriction in the neck, pain behind the sternum, noisy breathing, stridor, continuoas and paroxysmal dyspnoea, indicate stenosis of the trachea. Respiration is often quiet when the patient is at rest, but movement brings on aruito 104 TEXT-BOOK OF MEDICINE dyspnoea ; attacks of oppression, due to reflex spasm of the glottis, super- vene night and day, and cause extreme distress. These attacks of oppression are one of the most salient characteristics of tracheal syphilis (Mauriac). I verified the truth of this assertion in a patient whom I saw with Dr. Poyet. The expectoration is frothy, but sometimes the patient brings up pieces of gummatous tissue, and even fragments of cartilage. The larynx, which normally rises during deglutition, is often fixed by scar-tissue in tracheal syphilis. Laryngoscopic examination may show the tracheal lesion even as far down as the bifurcation. When cure has not been obtained, or treatment has not been carried out in time, slow asphyxia, syncope, sudden death, perforation of the gullet, of the vessels, or of the mediastinum, with consecutive abscess, broncho- pneumonia and gangrene of the lung, are possible terminations. We must not mistake laryngo-bronchial syphilis for ordinary bronchitis, asthma, or tracheo-bronchial adenitis, lest we see the patient succumb for want of active treatment. Retrosternal pain, feeling of strangulation behind the sternum, tracheal stridor, immobility or lowering of the trachea during deglutition and preservation of the voice, together with the dyspnoeic troubles I have de- scribed, show that the trachea is stenosed. Several lesions in the larynx, as well as paralysis- of the posterior crico- arytenoid muscles, may cause similar dyspnoea ; but the stridor is laryngeal, the voice is generally affected, and the laryngoscope removes all doubts. The trachea may be compressed by an aortic aneurysm, in which case the signs of aneurysm are found. The trachea is sometimes depressed by tumours of the mediastinum, but other symptoms, such as dysphagia, oedema of the face and neck, deformity of the sterno-clavicular region, dullness, according to the extent of the tumour, and swelling of the supraclavicular glands, are usually present, and indicate the nature of the lesion. If syphilis of the trachea is recognized, or even suspected, mercury and iodide of potassium must be given in large doses. I prefer injections of bin- iodide of mercury. This treatment must be carried out thoroughly. Most active treatment may cause no improvement for a fortnight. VII. WHOOPING-COUGH. Description.— Whooping-cough is a contagious and epidemic disease, which is probably microbic, attacks the young especially, and confers almost absolute immunity. It is composed of a double element : the one inflammatory, catarrh of the bronchi ; the other nervous, the fit of coughing. It is customary to describe three stages in whooping-cough, but we may DISEASES OF THE BRONCHI 105 add the period of incubation, which extends from the moment of contagion to the outburst of the attack, and varies, according to Roger, from seven to ten days. In the first stage the catarrh resembles simple bronchitis. The child has fever and cough, as in ordinary catarrh ; but yet certain fine distinctions already indicate the specific nature of the disease : the cough is more obstinate and frequent, and the fever Ls more stubborn than in a simple cold. This stage lasts from three days to a fortnight, and passes insensibly into the stationary stage. In this stage— that of convulsive cough — the fever falls back, and the nervous element takes the lead. The cough is less incessant than formerly, but the expiratory jerks succeed each other so rapidly that the patient makes at first eight to ten, then fifteen to twenty, expirations without being able to take breath. The fit is now established, and the crisis shows the symptoms so graphically described by Trousseau that I cannot do better than repro- duce his picture : A child is at play. Some moments before the advent of the crisis he stops ; his mirth gives place to sadness. If he should be in the company of his playmates, he stands aside and tries to avoid them. He meditates his crisis, feels it coming, and experiences that pricking and tickhng in. the larynx which announces it. At first he tries to avert the paroxysm. Instead of breathing naturally and expanding his lungs to the full, as he was doing just before, he holds his breath, for it seems to him that the full current of air, by entering his larynx, •vvill produce the exhausting cough of which he has had a sad experience ; but, I repeat, whatever he may do, he T^-iU not prevent, and at most he will only be able to delay, the fit. The fit takes place. You at once see the patient look around for a support to which he may cling. If he is a child at the breast, he throws himself into the arms of his mother or of his nurse. If he is older and standing up, you notice him stamping, in a state of complete distress. If he is lying down, he sits up quickly and clutches hold of the bed-curtains or of the rails. The attack leaves him with a swollen face, and this swelling, which at times lasts for three weeks, may in some cases be quite enough to cause a practised physician to sus- pect the existence of whooping-cough. Let us return to the fit. The fit commences with a sudden, noLsy expiration, followed by a series of short, aphonic, convulsive, and more or less hurried expirations. At this moment a pause, which may last ten to fifteen seconds, occurs, and the chest remains motionless in the position of full expiration. During this phase of the fit the air expelled from the chest is not renewed , consequently, the patient, whose eyes are injected and streaming, lips cyanosed and face bloated, is in a state of distress bordering upon asphyxia. Then comes a long, singing, convulsive inspiration, whicli ends the fit, and brings a short spell of rest. A second fit, however, occurs at once, and is followed by several otiiers, which decrease in severity ; the inspiration, instead of being singing, be- comes aphonic, showing that the spasm of the glottis is less. The attack may then be said to be at an end. The series of fits constitutes the attack. 106 TEXT-BOOK OF MEDICINE During the fits the child brings up slireds of glairy mucus, which stick to the mouth. The end of the attack is often marked by the vomiting of glairy material or of food-stuffs. These attacks, which vary in duration from some seconds to ten or twelve minutes, are more frequent at night than in the day, and occur as often as sixty times in twenty-four hours. When this number is exceeded, the child's life is in danger (Trousseau). Between the attacks the patient has no cough to speak of ; the fit sums up the whole disease. During the catarrhal period, bronchitic rales are heard in the chest. As soon as the spasmodic period begins they disappear. In the third stage all the symptoms improve. The fits are less frequent, the inspiratory stridor is less marked, and the glairy mucus is replaced, especially in adults, by the thick sputum of bronchial catarrh. Herff examined the larynx both in himself and in others, after ansesthe- tizing the part with cocaine. He has shown that during the whole disease the mucosa, especially in the interarytenoid and arytenoid regions, is inflamed. During the attack mucus accumulates in this region. If this mucus is removed by a probe, the attack can be stopped ; but if the same region is tickled, the fits can be reproduced. Touching other parts of the larynx does not produce the same effect. The reflex which provokes the fit originates, therefore, in the interarytenoid region. Course — Duration. — Whooping-cough usually shows three stages. The convulsive cough very rarely appears at first, but is preceded by the catarrhal period. In some patients the fits are replaced by attacks of sneezing (Roger), and I have seen two examples of this in children of asthmatic parents. The fit, says Trousseau, sometimes ends by sneezing. AVhooping-cough has an average duration of six to eight weeks. Some patients, however, have fits of spasmodic cough for months, as though the malady had passed into a chronic state. The diagnosis of whooping-cough is indicated, even in the catarrhal stage, by the obstinacy of the cough and the tenacity of the fever. In the stationary stage the fit and the whoop are quite characteristic. Sometimes certain tumours of the mediastinum provoke a cough, termed " pertussoid " (Gueneau de Mussy), which somewhat resembles the true fit of whoopmg-cough. It is important m diagnosis to recognize the different forms of defaced* whooping-cough. I have already said that the fit may be replaced by attacks of sneezing. * The term " fruste " (defaced) was applied by Trousseau to cases of scarlatina, in which certain symptoms were absent. In archaeology it refers to an inscription, part of which is missing. DISEASES OF THE BRONCHI 107 At Chantilly I saw an olderly latly (her daughter had whooping-cough) who waa seized with spasms of the glottis and inspiratory stridor which lasted some seconds, and recurred repeatedly in the form of attacks, day and night. In tliis defaced form the fit of whooping-cough was reduced to an inspiratory spasm of the glottis, and the other elements were quite wanting. Similar cases have been published — two by Trousseau and one by Blache. Prognosis — Complications. — Whooping-cough per se is not a serious malady, and the gravity comes from the complications. Thus, the catarrh of the early period, which usually improves at the beginning of the spasmodic period, may invade the smaU bronchi. Fever then lights up, the dyspnoea becomes intense, and the tubular breathing of broncho-pneumonia or the fine rales of capillary bronchitis are heard in the chest. This serious com- plication, which may arise in all the stages, is chiefly seen in the stationary stage. The appearance of the inflammatory process often causes the nervous element to disappear — sfasmos febris accedens solvit. " When in a child with whooping-cough you find that the fits, which numbered fifty or sixty in the twenty-four hours, cease suddenly, although the disease may be still in the stationary stage, beware, for you will find yourself face to face with an inflammatory complication " (Trousseau). In an adult these inflammatory complications may take the form of pleurisy or lobar pneu- monia. Whooping-cough predisposes to tubercular disease of the bronchial glands and to tuberculosis. In some cases we find meningitis or miliary tuberculosis ; in others, it runs the course of chronic pulmonary tuber- culosis. The nervous element is connected with complications of another kind. Spasm of the glottis is frequent and very serious in children under four years of age. Convulsions may come on during the attacks or in the interval, and are very serious in infants. The fits cause a vesicular emphy- sema which in exceptional cases has become interlobular by rupture of air- cells in the lung. The repeated congestions excited by the fits induce epistaxls, haemoptysis, bleeding from the ear (rupture of the membrana tympani), subconjunctival ecchymosis, and cerebral congestion, with attacks of eclampsia. Furthermore, the vomiting of food is due to the fits of coughing, and leads to malnutrition if often repeated. The exaggerated contraction of the expiratory muscles causes involuntary evacuations and hemic©, and the rubbing of the tongue upon the incisor teeth causes ulccnitioit of tlie fr»num (Bouchut). etiology. — Whooping-cough is an epidemic and contagious disciisc which chiefly affects children between the ages of two and seven years. Tiie contagion is so virulent that an infant may be infected after being a few minutes in the company of a patient suffering from whooping-cougli. In 108 TEXT-BOOK OF MEDICINE the sporadic state it follows the usual course which we have described, but it assumes different characters in the epidemic form. Thus, in the epidemic of Dillingen, in 1811, patients were carried off by eclampsia ; in the Geneva epidemic, in 1850, capillary bronchitis was the chief complication (Rilliet) ; in other epidemics the catarrhal stage was very short, and the spasmodic one appeared almost from the start (Trousseau). Epidemics of whooping- cough and of measles sometimes follow each other so closely as to indicate a causal relation between them. Bacteriology. — Afanassief thought that he had discovered the bacillus of whooping-cough. This microbe — Bacillus tussis convnlsivcB — is said to be small, slender, and disposed in groups or colonies. Quite recently Bordet and Gengou claim to have obtained the specific organism of whooping-cough in pure cultures. It is a small bacterium of ovoid form, and presents the same appearance both in the sputum and in cultures. The presence of haemoglobin is necessary for its growth. It is specially abmidant in the exudate during the first fits. The broncho-pneumonia, however, which occurs as a complication is usually due to the streptococcus, the staphylococcus, the pneumococcns, etc. Treatment. — The indications must be directed to the inflammatory and the spasmodic elements. The former is relieved by emetics ; for the latter we employ opium, aconite, belladonna, and bromide of potash. The use of alkalies has been advised (Labadie-Lagrave). Revulsives and blisters should be reserved for the inflammatory complications. Anaesthesia of the interarytenoid region, induced by means of cocaine, has given good results. Fumigation with sulphur has been extolled. The patient enters the fumi- gating chamber, the windows having been opened after the fumigation. H. de Rothschild has obtained good results with chloroform. It should not be given in severe cases, where the patient is weakened by vomiting and insomnia. Acute bronchitis and broncho-pneumonia are, of course, contra- indications. It may be given till anaesthesia is complete, or may be inhaled during the fits alone. For inhalation 10 to 20 drops of the following mixture are sprinkled on lint : Anaesthetic chloroform . . . . . . . . . . 3iv. Essence of pine . . . . . . . . . . . . 3ii. Essence of eucalyptus . . . . . . . . . . 3ii. This measure has been curative in some cases and has caused great improvement in others. Hygiene plays a large part in the treatment of whooping-cough. The rooms should be as large as possible, and the child should not spend day and night in the same apartment. At the beginning of defervescence change of air is most useful in shortening the duration of the disease. DISEASES OF THE BRONCHI 109 Prophylactic treatment is essential. The patient should be isolated from other children. The things he has used and the room he has occupied should be thoroughly disinfected. Till. ASTHMA. The attacks of dyspnoea which constitute asthma are quite charac- teristic ; they appear suddenly, weeks, months, or even years apart. They may exist as a pure neurosis, without any inflammation of the bronchi, but in most cases they are complicated by a catarrhal element of variable intensity. Catarrh does not usually accompany first attacks of asthma, but is associated with them later. Sometimes it plays a minor part, and appears towards the end of the attack ; at other times it begins with the attack as a true febrile catarrh ; and lastly, in other cases, it is so marked that the nervous element is of secondary moment. These two elements, of which the nervous is constant and the catarrhal is variable, may finally give rise to chronic bronchitis and emphysema, and form a morbid cycle, which may be complicated by lesions of the right heart. Description. — The attack of asthma generally begins in the early hours of the night, without prodromata. ^ A patient who has gone to bed quite well wakes up suddenly with acute distress. He feels agonizing constriction in the chest, and his breathing is painful and wheezing. He gets up and opens the window to get air, putting every respiratory muscle into play. Hoping to make his breathing easier, he sits on his bed with his body bent, kneels upon a chair, with his head bent forward, or props himself up by leaning with his elbows on a piece of furniture. He strives hard, but the distress increases in spite of his efforts. Inspiration is imperfect ; expira- tion Ls slow, wheezing, and convulsive. His distress is extreme, and seeing the patient with face bloated and covered with sweat, with starting eyes and cyanosed lips, we might think that asphyxia was imminent. We should be wrong, for after this struggle has lasted for one or more hours the breatliing becomes easier, the air enters the chest better, the expiration is less con- vulsive and not so prolonged, and the crisis subsides. The end of the attack Ls sometimes indicated by a belching, by catarrhal expectoration, or the emission of dry, crepitant, or gelatinoas sputum, which takes the shape of vermicelli. The first urine voided is clear and abundant (nervous urine), and sleep returns. Next day the patient feels tired, and has a disagreeable sensation of thoracic constriction, with balloon- nig of the belly, and some tendency to breathlessness. An attack of asthma is rarely single ; we usually see a series of attacks, wliich are repeated for several days or weeks ; they often return at the same hour — usually at night. This series of fits forms an attack of asthma. 110 TEXT-BOOK OF MEDICINE The attacks do not always have the intermittent form just described. In some asthmatics the distress continues throughout the whole attack, and the paroxysms reappear day and night, or several times in the twenty-four hours, allowing no rest. Analysis of the attack of asthma shows that the dyspnoea presents peculiar characteristics. A respiration rate of 40 or 50 is not seen in asthma, as in broncho-pulmonary inflammations ; the number of respira- tions is, on the contrary, less than normal. The painful and wheezing inspiration only allows an insufficient quantity of air to enter the chest, and the expiration, which is still more painful, and three or four times as long as the inspiration, does not drive out the inspired air. Let me add that, even at the height of suffocation, we do not see sucking-in, as in croup, because in asthma the chest is always filled to its maximum with air. During the attack snoring rhonchi and mucous rales, which depend on the severity of the catarrh, are heard in the chest, or we may find total absence of the respiratory murmur in places. The chest is bulging and rounded, the diaplu-agm is depressed, and percussion gives the exaggerated resonance of acute emphysema. In the variety of asthma above described the nervous element is almost alone in play ; but when the catarrhal element is associated with it, the clinical picture is more or less modified. Some asthmatics during or towards the end of the attack suffer from fatiguing spasms of coughing, and bring up catarrhal sputum, which is also present between the attacks. The ex- pectoration is chiefly composed of gelatmous sputum, which is vermiform, and resembles fragments of vermicelli, or consists of rounded pellets, crepitant to the touch, and known as Laennec's paries. The sputum often contains Curschmann's spirals, octohedral crystals (Charcot-Leyden) and eosinophile cells (Miiller), which, however, are not characteristic of asthma. In some asthmatics the fever, the cough, and the nature of the sputum prove that bronchitis is present ; but the dyspnoea preserves its characteristic type, and appears in the form of paroxysms. In some persons, however, the bronchitis becomes clu-onic, emphysema appears, and from that time it becomes more difficult to estimate the nervous element. In some persons the attack of asthma is preceded or replaced by fits of sneezing. These spasmodic fits may occur thirty or forty times in a few minutes, and reappear night and morning for several consecutive days. During the attack of sneezing the eyes, which are injected and weeping, often itch acutely ; the face is congested, and the nose runs freely. Every- thing then returns to its normal state. This description would do well for hay-fever, as the reader will no doubt notice. In those affected with these sneezing fits it has been possible to predict asthma several months or years in advance. DISEASES OF THE BRONCHI 111 Pathological Anatomy. — The theories which hold that asthma is con- secutive to em^jhysema (Louis and Rostan), catarrh of the small bronchi (Beau), catarrh (Laennec), or pulmonary congestion (Bretonneau), are erroneous, as in the main they mistake the effect for the cause. The attack of asthma ls certainly produced by spasm of the muscles of respiration. A difficulty beguis when we try to decide which muscles are affected. Some authors (Biermer and Williams) would place the spasm in the bronchial muscles ; the contraction of the bronchi is said to prevent the circulation of the air and the lowering of the diaphragm to be consecutive to the exag- gerated fullness of the lung. According to others (See and Wintrick), the bronchi have nothing to do with asthma, and the spasm pervades m turn all the extrinsic muscles of inspiration, including the diapliragm, mtercostals, scalenis, trapezius, etc., which re mam convulsed tlirough the attack, keep the lung in a position of constant dilatation, and only permit a scanty renewal of the air m the pulmonary vesicles. A third opmion (Trousseau and Jaccoud) combines the two preceding ones, and admits spasm both of the extrinsic and of the intrnisic muscles of respiration. I share the last opinion, and believe that the number and the species of muscles involved depend on the severity of the attack. In violent attacks both extrinsic and intrinsic muscles, are involved ; in slight cases the spasm may well be limited to the muscles of the bronchi, or only encroach on the diaphragm. In all cases the sphere of nervous excitation does not remain localized to the muscles of inspiration; it also attacks the muscles of expiration, and the rhythmic spasm of the expiratory mascles explains the length and the mteasity of each expiration, which can only overcome part of the resistance of the inspiratory muscles. The renewal of the air in the lungs, therefore, is very incomplete, and dyspnoea is the result. When we see the swelling and secretion of the nasal and ocular mucous membrane in some asthmatics, we are tempted to admit that like swelling and secretion exist in the mucosa of the bronchi, and help to narrow their calibre. This hypothesis is the more probable in that Stark has seen swelling of the tracheal mucosa with the laryngoscope. The spasm of the respiratory muscles and the phenomena of vaso- dilatation and vaso-secretion are tliemselves due to a special condition of the nerves which govern these functions. This state of irritability Ls some- times spontaneous, or at least apparently so ; at other times it is due to a reflex act which starts in the terminals of the sensory nerves which supjily the bronchi or the nasal passages. Many theories now in .vogue woultl, indeed, assign the chief part to the nasal mucosa. I shall speak of this later, under ^Etiology. Course—Duration — Termination . — First attacks of asthma are generally benign, and leave no scquelic ; later, if catarrh also is present, and more 112 TEXT-BOOK OF MEDICINE especially if it predominate, the patient, even in the intervals, has a morbid condition, which is analogous to chronic bronchitis, and is the more tenacious because emphysema may also be present. The lesions of chronic bronchitis and of emphysema are especially seen in people who have at first suffered from asthma alone. Dilatation of the right heart and tricuspid insufficiency may finally be met with. Fortunately, the disease does not always follow the same course ; it may improve, without causing such complications, or may be cured by well-directed treatment. As a matter of fact, persons may have several attacks of asthma, which finally disappear. etiology. — Asthma presents all the caprices of a neurosis ; it may be provoked or reawakened by the most insignificant causes, such as a smell (Floyer), the fumes of a sulphur match, the dust of oats (Trousseau), or powdered ipecacuanha (Cullen). A man who suffers from asthma in the North remains well when he resides in the South. A patient has asthma in Paris, but not in Versailles. I know a man who is subject to severe attacks m Egypt ; he recovers as soon as he is at sea. Some asthmatics cannot enjoy a hearty laugh without being seized with a slight attack. A high altitude and life in the mountains are often prejudicial to asthmatics. Asthma is a neurosis, and, further, it is almost always a diathetic and hereditary neurosis, as Trousseau has clearly shown. " Skin diseases, rheumatism, gout, haemorrhoids, gravel, and migraine are affections which asthma may replace, and which, in their turn, may replace asthma. They are different expressions of the same diathesis." A gouty father begets children ; while young they have migraine or piles, and later gravel, asthma, or gout. The alternation of asthma and urticaria is a well-known fact, and asthma has been called " bronchial urticaria." The alternation of asthma with such neuroses as epilepsy, hysteria, hypochondria, and mania has also been noted. Asthmatics may have relapsmg or cychcal attacks of mania. Asthma is more frequent hi men than m women. It is a disease of all ages, and has been seen even in children, especially m the latter part of childhood. In children, asthma may behave as m adults, but it fairly often assumes the features of capillary bronchitis, suffocative catarrh, or broncho- pneumonia. The disease presents a grave appearance, and correct diagnosis is most important, because proper treatment gives excellent results. Trousseau and See report strikmg examples of this mfantile asthma, which must be recognized, so as to avoid serious mistakes. Diagnosii^. — Hay-fever closely resembles asthma, and belongs to the same family. Mediastmal tumours, enlargement of the bronchial glands, and aortic aneurysm produce attacks of dyspnoea, which must not be confounded with asthma. DISEASES OF THE BRONCHI 113 A form of pulmonary tuberculosis simulates asthma, and is known as pseudo-asthmatic. I am not speaking of acute miliary tuberculosis, which Andral compared to asthma because of the continuous or paroxysmal dyspnoea, but I allude to ordinary chronic tuberculosis. Certam tubercular patients at the outset, or during the course of their malady, suffer from attacks of asthma, and the tuberculosis may be overlooked if we forget this pseudo-asthmatic form. Diseases of the heart, especially mitral lesions, often provoke dyspnoea. In addition to this dyspnoea, the patient sometimes experiences attacks of oppression, which are more frequent at night. The attacks are as severe as those of asthma, and the dyspnoea has therefore been called *' cardiac asthma." The term is wrong. Mitral disease does not produce true asthma, and tiie paroxysmal dyspnoea of cardiac disease has not the char- acters of the dyspnoea in asthma. In a cardiac case the breathing is rapid and panting ; both inspiration and expiration are short and jerky ; palpita- tion is frequent ; the pulse is small ; the face is pale ; and the lips are cyanosed. Asthma presents quite a different picture. The breathing is not quickened, inspiration is slow and difficult, and expiration, which is wheezing and spasmodic, is three or four times as long as inspiration ; palpitation is absent, and the pulse remains regular. In some cardiac cases attacks of dyspnoea are the chief symptom, and mitral disease may show itself at first solely by attacks of cardiac dyspnoea, which are mistaken for asthma, just as in patients with Bright's disease the renal lesion shows itself by attacks of dyspnoea, wrongly called asthma. In any case, cardiac asthma and true asthma must not be confused. Lesions of the aorta are also accompanied by attacks of oppression, which bear some slight resemblance to those of asthma. These attacks of aortic dyspnoea, however, are more or less painful, like angina pectoris. In nowise have they the character of the true asthmatic attack, and the aortic lesion quickly decides the diagnosis. From want of care the dyspnoea of Bright's disease may be taken for asthma, and many patients with Bright's disease arc treated for asthma. This dyspnoea presents forms which are slightly different. In the first variety the patient is " short of breath," especially if he walks upstairs too quickly. The shortness of breath may be mistaken for asthma, but examination reveals pulmonary oedema, albumin in the urine, and other symptoms of Bright's disease. In the second variety the threatening asphyxia is due to superacute oedema of the lung. The fcdema rapidly invades the lung, the dyspnoea becomes acute, fine rales are heard all over the chest, and the patient coughs up frothy, rose-coloured, albuminous sputum, which is characteristic uf superacute oedema. 8 114 TEXT-BOOK OF MEDICINE In a third variety the dyspnoea is ursemic and toxic ; it may show thft character of Cheyne-Stokes breathing. This dyspnoea may appear in the form of attacks, which patients mistake for asthma. The attack comes on night and day, rapidly becomes acute, and reappears at the slightest move- ment It may recur several times in the twenty-four hours, or disappear and return after more or less lengthy intervals. Dyspnoea comes on at all periods of Bright' s disease, but we must never forget that it may be the first symptom. In some cases it appears suddenly, like an attack of asthma ; in others it establishes itself gradually, like a chronic bronchitis. A knowledge of these facts will prevent our sending patients to Mont-Dore or to Cauterets for bronchial catarrh, asthma, or emphysema, when they are really suffering from Bright's disease. Much attention has lately been paid to asthma following nasal lesions. Voltolini of Breslau in 1871 published cases of asthma in patients with nasal polypi. Removal of the polypi cured the attacks. Hack thinks that the pathological reflex has its origin in inflammation of the erectile tissue of the nose, and since then the nose has been accused (polypi, hypertrophy of the mucosa, deviation of the septum) of causing most cases of asthma, and also dyspnoea, migraine, cough, oedema, incontmence of urine, etc. The result was attempts to destroy the cause of so many ills by cutting and burning the nasal fossae. These statements are much exaggerated. It is quite true that the nasal mucosa plays a large part in asthma. Attacks sometimes appear after certain nasal stimuli. Sneezmg, nasal secretion, and swelling of the mucosa, are present in true asthma, in hay-fever, and in asthma following nasal polypi. It is therefore necessary to pay attention to the undoubted part which the nasal mucosa plays in the production of asthmatic attacks. It may occasionally be necessary to deal with this mucosa, but this is only one side of the question, and if in some cases the nasal mucosa, by its special excit- ability, be the origm of the reflex which provokes the asthmatic attack, this special excitability is often present elsewhere (bronchi, lungs, or centres in the medulla). Treatment. — We may first consider the treatment of the attack. The attack can be checked or much modified by prompt actioii. Inhalation of the fumes of Datura stramo7iium, nitrate paper, Espic cigarettes, hypodermic injections of morphia, inhalations of pyridine, and bromide of potash, are of service. Nitrite of amyl " is as dangerous as it is difficult to handle " (See). I constantly prescribe stramonium, smoked in a pipe. The dry leaves should be finely cut up and some small pieces of nitrate paper added. Pyridine may be used, either by inhalation of 10 or 12 drops on a hand- kerchief, or by allowing the drug to evaj)orate slowly near the patient. DISEASES OF THE BRONCHI 115 These remedies may be repeated two or three times a day, and when em- ployed for some time and between the attacks may cause marked improvement. Iodide of potash, however, is the best drug for asthma, both in the attack and in the intervals (Trousseau). The dose depends on the tolerance of the patient. We may begin with 10 grains daily, and increase to 30 grains, or even more (See, Jacc.oud). The drug should be continued for a long while, care being taken to suspend its use at mtervals. With iodide of potash Trousseau employed tmcture of lobelia in small doses. He also advises the use of belladonna and bromide of potassium, replaced, as the case may be, by preparations of arsenic. I usually advise the following regime between the attacks. During the first and third week of each month I prescribe 10 to 15 grams of iodide of potash daily, with 10 drops of tincture of lobelia. In the second and fourth weeks of the month I prescribe bromide of potash, 15 to 30 grains a day, and pills of extract of belladoima. This treatment should be continued for a very long while. Between the attacks iodide of codeine has been extolled. It is given in sjTTup (Labadie-Lagrave and Rollin), and the dose is | grain. The cure at Mont-Dore gives very good results (Tardieu). The local treatment in the attack consists m painting the nasal mucosa with a 5 per cent, solution of cocame. The nasal fossae must always be carefully examined, in order to remove polypi, or cauterize the mucous membrane, if necessary. IX. SUMMER ASTHMA— HAY-FEVER. This disease which in some respects resembles true asthma has been called hay-fever, summer asthma, or spasmodic rhino-bronchitis. The term " hay-fever " is not good, for fever is usually absent, and the disease occurs when there is no hay. The term " summer asthma " is preferable ; but as the disease is equally prevalent hi the autumn, the name " annual asthma " is better still. This disease, which is most common m the Anglo-Saxon race. Is not rare, and I have seen a good many cases. Description. — Annual asthma assumes two chief forms : the one is called oculo-nasal, the other oculo-naso-thoracic. The disease appears usually about the 15th or 20th of May, and almost at a fixed date. A person who Is not susceptible at other seasons is seized with a kind of " cold in the head." Sneezing, obstruction of the no.sc, and supra-orbital headache are present. The trouble is at first thought to bo a cold. The eyes, however, become the scat of pricking and intolerable itcliing, chiefly at the inner canthus. The patient rubs hia eyelids vigorously. The 8—2 116 TEXT-BOOK OF MEDICINE eyes are red, swollen, and weeping ; the conjunctiva is oedematous : th-Q tears are so abundant that they hamper vision, and flow over the cheeks ; the photophobia is intense, so that the patient avoids daylight. These troubles generally disappear or improve towards evening. In the nose we find the following symptoms : unbearable itching ; violent sneezing, repeated ten, twenty, or thirty times in succession ; profuse serous discharge from the nose, which runs " like a fountain." The nasal, like the ocular, symptoms are brought on agam or made worse by sunlight and heat ; they become less severe under the influence of shade and cold. Such is the oculo-nasal form of the disease. It persists for weeks, with alternating improvement and aggravation. The symptoms then improve, and recovery is complete till the followhig year. In the other variety, called oculo-naso-thoracic, in addition to the above symptoms, we find dyspnoea, like that of asthma. The dyspnoea begins about a fortnight after the ocular and nasal symptoms ; it becomes gradually worse, is marked by the occurrence of fits, and is complicated by catarrh, in which the patient coughs and brmgs up bronchitic sputum. Improvement now comes on, and recovery is complete in six weeks, till the next year. Patients have usually one annual attack. The prognosis is good, for this variety of asthma does not lead to chronic bronchitis or cardiac dilatation. In my opinion, annual asthma should be included in the family of true asthma. It forms part of the gouty diathesis, and is often hereditary. It may recur annually for a great number of years. This asthma is nothing but the spasmodic exaggeration of the defensive reflexes of the respiratory mucosa, which include sneezing, cough, and serous exudation from the mucous membrane. Its starting-point seems to be irritation of a submucous nerve filament belonging to the ethmoidal branch of the oplithalmic nerve, which is particularly sensitive in the angle formed by the nasal septum and the lateral wall at its upper part. Touching this pomt may provoke cough alone, sneeznig and laclirymation, or the com- plete crisis. This point must be burnt with the galvano-cautery, without troubling about the malformations or the various lesions of the nasal fossae. Partial or total relief is thus obtained. P. Bonnier, under the name of ** rhino -laryngitis sicca," has described an inverse form of hay-fever, which appears under identical conditions, but is characterized by painful dryness of the respiratory mucous membrane, producing aphonia. The various remedies employed are less efiicacious in this variety than in true asthma. A cool, shady room is a good measure. CHAPTER rv DISEASES OF THE LUNG I. GENERAL SURVEY OF THE ANATOMY OF THE LUNC4 The lung is made up of lobules of a polyhedral form, set one against the other, and separated by connective tissue. These lobules are well seen in the new-born, because at this age the network of connective tissue which surrounds them is much thickened. Later the dehmitation is less apparent, because the connective envelope loses its thick- ness. The dehmitation of the lobules, however, is readily seen on the surface of the organ, where the connective sheaths are infiltrated with dark material, and form a kind of mosaic. The pulmonary lobule represents the structure of the whole lung. It is a small and spongy polyhedral or conical mass, of about 1 c.c. in size, and joined to the rest of the organ by a short pedicle. This pedicle contains a bronchiole, which is given off at right angles from a large bronchial twig, and a pulmonary arteriole and vein, with lymphatics and nerves, the whole being ensheathed by connective tissue. The bronchus and the artery penetrate the interior of the lobule at the hilum, but the vein ramifies over the lobule, following the perilobular connective sheath. A transverse section of the lobule therefore presents two connective-tissue regions — a central one (the intralobular space, which contains the bronchus and the artery), and a peripheral one (the perilobular space), containing the vein. When the bronchus enters the lobule, it takes the name of intralobular, and parts company with the vein, but is accompanied by the artery as far as its farthest ramifica- tions. The intralobular bronchus traverses the lobule without diminution in size ; it forms the axis of tht; lobule, and in its passage gives off alternate branches, and ends by dividing dichotomously. Each branch derived from the intralobular bronchus passes into an acinus, and takes the name of " acinous bronchus." What is the acinus ? The lobule is formed by a number of acini, and each acinus, measuring 2 to 3 milli- metres in each direction, forms within its bronchus a small system, which has the following arrangement : On reaching the acinus, the branch, after a short course, spreads out like a funnel, and forms a kind of vestibule, whence^ arise three, four, or five alveolar ducts, which widen out to form infundibula. The infundibuluin may be considered as the expanded end of the alveolar duct. All these parts, except the acinous bronchus, are lined by the alveoli. The alveoli are air-cells in which liiiiuatosis goes on. They resemble shallow cups in the walls,* and in the; dried section of an acinus api)ear as oval or rounded cavities, separated by partitions, hke a beehive. The interalveolar septa form the skeleton of the acinus, and, like it, are composed of a connective membrane and elastic fibres. * Frey, " Traite d'Histologie," p. rA'.i. The opening of the alveolus into the infunclibulum is narrower than the: fundus of the alveolus. 117 118 TEXT-BOOK OF MEDICINE This fibro-elastic skeleton permits the extension and the retraction of the alveoli. supports the capillary network, and " gives a foundation to the pavement epithelium of the lung " (Ranvier). The capillary network of the lobule arises from the artery, and projects into the interior of the alveoli, when they are not too dilated. Lymphatic vessels are everywhere present, and surround the alveoli, infundibula, acini, and lobules (Grancher). Each disease of the lung alters the infundibulum, the acinus, and the lobule, in a particular way. In lobar pneumonia the lobule is filled with an exudate rich in fibrin, and the projection of the acini on the surface of the section explains the granular appearance of red hepatization. In disseminated or confluent broncho -pneumonia the inflammation spreads from lobule to lobule. The lobular bronchus is primarily invaded. Around the bronchus we find the peribronchial inflammatory nodule or zone of hepatization, and farther out the zone of splenization. The exudate is poor in fibrin, but rich in pus cells. In emphysema the lobule is distended to its maximum, and the alveolar septa are often atrophied or perforated. In pulmonary fibrosis the dense and fibroid interstitial tissue partly blocks the alveoli and the acini. In certain occupation pneumonias (miners, founders) the walls of the alveolus, the connective tissue, and the lymphatics are loaded with coloured particles (anthracosis). In tuber- culosis the walls of the alveoli, of the small vessels, and of the bronchial ramifications contribute to the formation of the tubercles. 11. PULMONARY CONGESTION. Congestion of the lungs may be divided into two chief classes — active, produced by afflux of blood ; passive, resulting from blood-stasis. 1. Active Congestion. Active congestion of the lung is caused by inhalations of irritant vapours ; by the sudden passage from a warm to a cold atmosphere, or vice versa ; by pathological neoplasms, especially tubercle. It accompanies the eruptive fevers — principally typhoid fever — in which it often makes the prognosis worse. It may be due to malaria, gout, and rheumatism, and is provoked by the suppression of normal or accidental haemorrhage (piles, menstruation). Some forms have a nervous origin (hysteria), arise from reflex action (large burns), and accompany cerebral lesions (haemorrhage and softening). The symptoms are in harmony with the severity and the extent of the hyperaemia. As a general rule, pulmonary congestion, if pushed to its extreme limit, may terminate in haemorrhage, with or without haemoptysis, and, indeed, cases of rapid death have been quoted (Devergie). Dyspnoea, cough, pain in the side, may be seen in the congestion of malarial, gouty, or rheumatic origin. In articular rheumatism this complication arises suddenly : the expec- toration is streaked with blood, the breathing is uneasy. On auscultation all the signs of broncho-pulmonary congestion, with oedema, are found, and death may occur in a few hours. DISEASES OF THE LUNG 119 2. Passive Congestion. Passive congestion is due to blood-stasis, caused by cardiac diseases (mitral and tricuspid lesions), degeneration of the cardiac muscle, and prolonged decubitus (hypostasis). Passive congestion is slow in its course, and is always accompanied by oedema of the lung. The capillaries allow the transudation of a highly coloured fluid, and pigmentation of the alveolar walls and of the epithelial cells is the result. Chronic hyperaemia often goes on to splenization — a condition in which the tissue of the lung is firm and reddish, like the pulp of the spleen. This morbid state has been called hypostatic pneumonia, although there is no pneumonia in the true sense of the word. The exudate is poor in fibrin and cellular elements. At the seat of the lesion percussion shows more or less complete dullness, and on auscultation the breathing is almost tubular. Treatment. — Bleeding and cupping should be reserved for acute con- gestion. The treatment of passive congestion forms a part of the treatment of the cardiac disease. When the congestion is hypostatic, the position of the patient should frequently be changed. III. INFLAMMATION OF THE CHEST. Discussion. — When I began to study medicine at Toulouse, my first teachers, former pupils of the Paris and Montpelier schools, and, con- sequently, rather eclectic than absolute, taught us that, besides pulmonary congestion and genuine inflammations of the broncho-pulmonary apparatus, there exist bastard phlegmasiae, called inflammations of the chest, wherein hyperemia and inflammation exist in irregular combinations. The term '' inflammation of the chest " has to-day almost ceased to exist. Treatises on pathology, the publications and the theses of our faculty, are for the most part silent on the subject. We speak of pulmonary congestion, pneumonia, and broncho-pneumonia, but not of " inflammation of the chest," which seems to have lost all its claims as a distinct morbid condition. I do not hold this view. I believe that inflammation of the chest should have a place in our nosology. Besides the genuine inflammations of the respiratory apparatus, such as pneumonia, broncho- pneumonia, pleurisy, and bronohitis. wo find othor bastard morliid stato>^. in which the hypersemic and inflammatory elements are differently combined, and whicli, by huit accord, have been called " fluxions." It is, moreover, remarkable that, while the plilogmasijin fix voluntarily upon certain parts of the respiratory apparatus so that they might he culled *• systematic," an epithet employed in diseases of the spinal cord (Vulpian), 120 TEXT-BOOK OF MEDICINE tlie fluxions, on the contrary, are naturally difEuse and multiple. Inflam- mation (fluxion) is rarely localized to the lung or to the pleura without affecting other parts of the respiratory apparatus. It may touch or strike the lung, the bronchi, the pleura, and the muscular layers of the thorax — in a word, all the superimposed layers of the chest, and hence custom termed it " inflammation of the chest." Cruveilhier was pertitient m describing pleurodynia, accompanied by fftver and pleural friction sounds, and Peter, in his " Clinical Lectures " tells us : " Inflammation, if it be intense, may not remain limited to the muscles, but may invade all the superposed planes of the thorax, including even the pleura." A step farther, and Peter would have come to inflamma- tion of the chest. Description. — Inflammation of the chest is a morbid state of variable intensity and nature. It is neither abortive pneumonia nor broncho- pneumonia, but another entity. Sometimes it spreads its action over all the parts of the respiratory apparatus ; at other times it leaves some parts almost untouched, and concentrates its action on the lung, the bronchi, or the pleura. As examples — An individual is seized with a sharp pain in the side ; he has slight rigors, cough, and fever. On examination, we find pleurodynia, w4th or without cutaneous hyperaesthesia. The pains affect not only the intercostals, but all the muscles of the part. The abdo- minal and lumbar muscles may also be involved. Friction sounds over the painful area, and bronchitic rales, scattered over both sides of the chest, are heard. In this case the skin, the muscles, the pleura, and the bronchi have been affected. The pleurisy is in the incomplete stage, and no effusion appears. The bronchitis is but shght, and the patient will be well in a few days. In another person the inflammation involves the bronchi and iung to a slight degree, but concentrates its action on the pleura, and effusion is found. To this category belong certain bastard pleurisies, obscured by the inflammation of the lung and of the bronchi. In another case the clmical picture presents some difference. The illness has commenced with fever ; the musculature of the thorax may or may not be painful. On auscultation we find fairly severe bronchitis and pleuritic rubs, and at one part of the chest we recognize dullness and blowing breathing, Mith broncho- phony, which are evidence of marked pulmonary congestion. From the onset the sputum is streaked with blood, the dyspnoea is fairly acute, and the temperature 102° F. or more. What name is to be given to this disease ? It is not pleurisy, for the pleural lesion is but incomplete. It is not bronchitis, although the bronchi have been attacked. It is not pneumonia in the true sense of the word. It is a case of inflam- mation of the chest which has concentrated its action upon the lung. Lastly, the pulmonary localization is yet more marked or extensive in some cases. The temperature reaches 104° F., the cough is painful, and the dyspnoea acute. Per- cussion reveals dullness, which shows the extent of the lesion. We might be tempted to call the disease pneumonia, and yet analysis of the signs and the symptoms proves that it is not a true case. The rale is neither so fine nor so dry as in pneumonia ; the DISEASES OF THE LUNG 121 tubular breathing is not so intense ; the bronchophony is not so marked ; the sputum, instead of being rusty, is rather streaked with blood. Bronchitic rales or friction sounds are scattered through the chest ; defervescence is not sudden ; and, although the inflammation may reach its maximum and be in excess of the hyperjemia, still, the disease is not true pneumonia. However, I must say that these forms are on the road to become lobar pneumonia. Pneumonia does not always present the classical type given for purposes of description. It often conforms to inflammation of the chest, and the barrier between the two is not insurmountable. Grasset regards inflammation of the chest as an attenuated pneumococcal in- fection. The prognosis varies according to the variety and intensity of the disease. Its aetio logical conditions are diverse. In some cases it forms the whole disease, and follows upon a chill (Woillez, Bourgeois) ; in others it is secondary to some general condition, such as influenza and catarrhal fever. Revulsives (dry-cupping, blisters), local bleeding (leeches, wet-cupping), emetics, quinme, and alcoholic drinks, should be employed, according to the nature and the severity of the malady. IV. ACUTE LOBAR OR FIBRINOUS PNEUMONIA— PNEUMOCOCCIC INFECTION— PNEUMOCOCCIA. Pneumonia is called lobar, when it invades a lobe, or part of a lobe, without healthy tissue intervening, in contradistinction to lobular pneu- monia, which causes isolated or confluent nodules. It merits the name fibrinous because, of all the inflammations of the lung, it Is the richest in fibrin ; the fibrinous exudate fills both the alveoli and the bronchioles. The alveolar walls and the connective tissue are almost completely unaffected by the process, and the parenchyma of the lung completely recovers its integrity after pneumonia. I shall first describe the disease as localized in the lung — that is, pneu- monia proper — and then leview its extra-pneumonic localizations, such as pleurisy, pericarditis, endocarditis, peritonitis, arthritis, gastritis, menin- gitis, nephritis, otitis, etc., finally discussing the different clinical types which the pneumonic infection may assume. Pathological Anatomy. — It Is customary to describe three stages in pneumonia ; engorgement, red and grey hepatization. The third stage is somewhat rare. Engorgement is characterized by intense congestion. The congested region, which is violet-coloured and increased in volume, crepitates a little, and pits on pressure ; it Is oedematous and infiltrated with a reddish scrum, which flows out on section. The capillaries are distended with blood, and allow plasma, red corpuscles, and leucocytes to pass out. The cells of the 122 TEXT-BOOK OF MEDICINE pulmonary epithelium become vesicular ; some fall into the interior of the alveolus, where they are enclosed by a fine network of fibrin. The stage of engorgement lasts from twenty-four to forty-eight hours. In the second stage, called red hepatization,* the lung is converted into a kind of solid block, which is red, mottled, and homogeneous through- out the whole extent of the lesion. The hepatized lung is heavy, and sinks in water ; it has become friable, and is easily torn or crushed by the finger. The cut section is practically dry, and studded with granulations. These granulations are about 1 millimetre in size, and are due to the fact that the infundibula are distended and moulded by the coagulated fibrin. The diseased lung is larger and heavier than the healthy one ; it may weigh as much as tlirice its normal weight. The hepatized tissue, after washing, becomes of a yellowish-grey colour, from the dissolution of the red corpuscles. Under the microscope the vessels are dilated and engorged with blood ; the alveoli are filled with a fibrinous network, which enmeshes epithelial cells and red and white corpuscles, f The alveolar arches and the epithelium are unaffected. Cells and fibrin are found in the small and sometimes in the large bronchi (fibrinous bronchitis). The pneumococcus is found in the granular cells and the fibrinous reticulum. After three to five days, the red hepatization gives place to resolution : the fibrin in the alveoli becomes granular, the pus cells grow large, and the liquefied and altered elements are reabsorbed in situ by the veins and lymphatics, or expelled in the sputum. In this way recovery results. When, however, pneumonia, instead of terminating by resolution, goes on to grey hepatization, the lung takes a greyish tint. Its cut section is granular ; the fluid which exudes is purulent ; the tissue becomes very friable, and finger-pressure produces a tear filled with pus. Under the microscope the alveoli appear full of pus corpuscles. Microscopic abscesses are frequently met with. The parenchyma, however, is seldom destroyed, and the pus is not, as a rule, collected so as to form an abscess. J Grey hepatization is not always a sign of pus (Rindfleisch). The grey colour of the lung tissue may indicate ordmary resolution. In this case the colour is brownish or yellowish-grey, and the tissue is fairly firm and granular, like that of red hepatization. The grey appearance is due to the small number of red corpuscles, the disappearance of the haemoglobin, and the abundance of migratory cells, which absorb the exudate. * TKis stage was called red softening by Andral. •f This exudate is very rich in granules of glycogen (Loeper, Arch. de. Med. Ex- 'perimentale, tSeptember, 1902). t The formation of abscesses is a very rare termination in pneumonia. In thirty- six cases collected by Grisolles (" Traite de la Pneumonic "), the abscess was situated twelve times in tlie ujjper lobe, nine times in the lower one, twice in the middle, and four times in several lobes at once. DISEASES OF THE LUNG 123 Pneumonia always induces lymphangitis. The lymphatic vessels of the inflamed region, like the pulmonary alveoli, contain fibrin, endothelial cells, and red and white corpuscles.* The corresponding lymphatic glands also participate in the process. Lobar pneumonia is found more often on the right than on the left side, in the proportion of 3 to 2 (Lebert). It is unilateral, or double, in the ratio of 8 to 1 (Grisolle) ; it affects the lower much more frequently than the other lobes. The blood is very rich in fibrin,! and contains two or three times the normal amount. Bacteriology. — Pneumonic infection is due to the pneumococcus. This organism was first isolated from the lung by Talamon (1883), and was thoroughly studied by Fraenkel. Netter has demonstrated its intervention in the complications of pneumonia. In health it is found m the saliva, where it was discovered by Pasteur ; and where Netter has found it to be patho- genic in one-fifth of normal persons, and Bezancon and Griffon have shown that it exists as a constant saprophyte on the surface of the tonsils. The pneumococcus resembles a candle-flame in shape. The organisms usually face each other by their tapering extremities, sometimes, however, by their other ends. In the hepatized lung the pneumococcus is present in pairs — i.e., as diplococci. In grey hepatization and in the pus from the complications it often forms short chains (Griffon). The pneumococcus stams readily with the aniline dyes ; the microbe stains by Gram's method. Staining with carbolic methylene blue shows a capsule which surrounds the elements. This microbe develops between 75° and 108°, but preferably at 98-5° F. On agar or on gelatinized serum it forms transparent colonies, like little drops of dew. The best culture medium is coagulated rabbit serum, and the best preservative medium is blood rendered uncoagulable, or blood - agar, in which the pneumococcus retains its vitality for several months (Bezancon and Griffon). The pneumococcus causes pathological results which differ according to its virulence and to the species inoculated. In the mouse little reaction is seen at the point of inoculation, but generalized infection occurs. In the rabbit the lesions differ according to the virulence of the injection — local and fibrinous if it is attenuated, general and haemorrhagic if it is virulent (Bezancon and Griffon, Fournier and Carnot). In the slieep and the dog, which are more refractory, the local reaction is very intense, and inocuhitiou of the lung produces hepatization. The blood contains a few microbes. * " It is impossible to aflfirm that a vaciiDlo filled with pneumonic exudalo is a transverse section of a lymphatic canal or of an alveolus " (Cornil and Ranvier, h>c. cil., p. G'JG). f This hyperinosis of the blond is explained by (he fact thai the blood is charged with fibrinogcaious mattMial from the iuHamed organ. 124 TEXT-BOOK OF MEDICINE In man the germ is found in all the pneumonic products : pneumonic secretion ; hepatized lung tissue ; fibrinous exudate in the bronchi ; glands of the hilum ; fibrinous inflammations of the pleura, the pericardium and the meninges ; vegetations of the endocardium, kidney, joints, and parotid glands. The pneumococcus may be obtained during the course of the affection by withdrawing from the lung a drop of exudate by means of aseptic puncture, or by isolating it from the sputum, or from the mucus in the throat. The pneumococcus may be found m the blood-stream ; but this infection of the blood does not imply a fatal ending, though it almost always coincides with grave pneumonia. To discover the pneumococcus in the rusty sputum or in the saliva, examination of stained films is not trustworthy, unless the prepara- tion literally swarms with encapsuled diplococci. Inoculation of mice is the best and most convenient method. These animals are so susceptible to the virus that death supervenes from general infection twenty-four to forty-eight hours after inoculation with the sputum, and post-mortem the pneumococcus is found in the blood and the organs. The toxine secreted by the pneumococcus has been studied by Klemperer, and quite recently by Fournier and Carnot. Agglutinative Reaction. — Pneumococcal infection causes an agglu- tinative reaction which is as follows : A little serum is obtained from the blood of a healthy individual or from a person suffering from some other disease (rheumatism, typhoid fever, tuberculosis, etc.). This serum is inoculated with a minute quantity of a culture of pneumococcus, and placed in the oven at 98° F. Next day this culture is as clean as though the serum had not been inoculated. Neither dust nor dots are visible, and if the tube is well shaken, the culture remains quite limpid. On the other hand, if a culture of pneumococcus is sown in the serum of patients suffering from pneumonic infection (pneumonia, pleurisy, peri- tonitis of pneumococcal origin, etc.), the culture, placed in the oven at 98° F., presents a characteristic appearance by the next day. Sometimes a dome-like false membrane is present at the bottom of the tube ; at other times we perceive several pseudo-membranous fragments. The culture in other cases contains dots resembling a coarse dust, which, on shaking, make the liquid turbid and then fall to the bottom of the tube. Without the aid of the microscope, by the comparative study of tube cultures, we can say whether pneumococcal infection is present or not. Under the microscope, if we examine a culture of pneumococci on healthy serum, or on serum from those with some other malady (rheumatism, tuberculosis, typhoid fever), we see that the pneumococci are isolated, and DISEASES OF THE LUNG 125 remain so, without any tendency to form chains or groups. No agglutina- tion occurs. On the contrary, if a culture of pneumococci on serum from patients with pneumococcal infection is placed under the microscope, we see that the microbes unite in long wavy chains, circumscribing clear spaces, in which, as a rule, free pneumococci are not present, and we can no longer distmguish the capsules of the pneumococcus. In some cases, especially in the experimental infection of the rabbit, the collections of pneumococci form masses. In human infection the formation of a true mass is exceptional at the outset of pneumonia, and wavy chains, separated by empty spaces, are more commonly seen. The chain therefore appears to be the first degree of agglutination, which later produces massing of the elements. Towards the end of the second stage the reaction becomes more intense. The pneu- mococcal sero-reaction gives equally positive results iia the primary extra- pulmonary localizations of the pneumococcus. Description. — In 25 per cent, of the cases lobar pneumonia is preceded by prodromata, which include lassitude, pains in the limbs, headache, epistaxLs, tracheitis, insomnia, and fever ; thoy last possibly one or two days. More often pneumonia begins suddenly with a single rigor, which is as prolonged as that of an intermittent fever, and is accompanied by a rise of temperature in the axilla to 103° F, This invasion is sometimes accom- panied by vomiting. By the end of the first day, or at the commencement of the second, dyspnoea, cough, and pain appear. The patient complains of a pain in the side, at the level of the nipple. This pain is increased by the res[)Lratory movements and fits of coughing. In some cases the pain is abdominal, or supraspinous, or may even be found on the healthy side. Distress appears from the first. The jerky and painful CO ugh is at first dry, but by the second day, or in the course of the third, the patient brings up sputum, which is tinged with blood, amber-coloured or rusty, aerated, and viscid. It sticks to the sputum-cup, and is pathognoTuouic of acute lobar pneumonia. The sputum, which is at first amber-coloured, like barley-sugar or apricot marmalade, and then rusty, may on the following days become of a brick- red colour. It represents the pneumonic exudate, which comprises white and red corpuscles, epithelial cells, surrounded by fibrin and some fibrinous filaments from the small bronchi. Pneumonic sputum is rich in mucus and chlorides. Th(; mucus renders it transparent and gelatinous. Tiie pneu- mococcus is found in abundance. Pneumonia does not cause anaemia, and the red blood-corpuscles an; little diminished in number. The blood-count shows a leucocytosis varyiu^f from 20,000 to 25,000, with considerable increase (85 per cent.) iji the poly- 126 TEXT-BOOK OF MEDICINE nuclear cells. Insufficiency, as well as excess of leucocytosis, may mean a bad prognosis. Percussion of the invaded area sometimes yields dullness ; at other times, according to Jaccoud, a transient tympanitic sound ; and auscultation reveals the driest and finest of all rales — i.e., the crepitant rale — which occurs in puffs towards the end of inspiration. It is not heard during expiration, and is often perceptible only after making the patient cough. The crepitant rale must at times be looked for in the axillary region. Durmg the following days (red hepatization) the functional symptoms increase, and though the pain in the side improves, the dyspnoea reaches such a degree that the respiration rate may rise to 40. The pulse, which is full, varies between 100 and 110 beats, and the temperature from 102° to 104° F., with a slight morning remission. At this time the aspect of the patient is characteristic — cheeks burning, face injected, eyes bright, tongue dry and coated, and voice short. The hurried working of the nostrils indi- cates the acuteness of the dyspnoea. The urine is scanty and high-coloured ; it is rich in urea and uric acid, but very poor in chlorides, which appear to be absorbed for the benefit of the exudate. Delirium, which sometimes appears at this stage, is quiet, but may be violent in drunkards. In the hepatized region the dullness is complete, and the vocal fremitus is increased, and, as the voice and the respiration are so well conducted by the solidified tissues, the voice is loud, but not articulate to the listener's ear. This condition is called bronchophony, and the breathing takes on the rough, blowing tone known as tubular. Further, as all the inflamed parts do not undergo their different changes at the same time, we may find tubular breathing and crepitations close together, just as later we notice redux crepitation and tubular breathing at the same time. The second stage lasts three or four days, or sometimes longer, after which recovery usually commences. The situation may, however, become worse. When pneumonia ends in recovery, the fever falls very rapidly with symptoms of crisis ; the wastmg ceases, and the patient enters on convalescence. This condition coincides with the liquefaction of the exudate ; the sputum becomes opaque and rich in fatty elements, the dullness disappears, and the tubular breathing gives place to a rale that is larger and more moist than the crepitation. This rale is the redux crepitation, which would better be called a subcrepitant rale. It is audible both during inspiration and expiration. If pneumonia passes into the third stage (grey hepatization), the sputum assumes a greyish or prune- juice tmt, the fever becomes adynamic m type, the pulse is small and irregular, the abdomen is distended, diarrhoea appears, clammy sweat covers the patient, and delirium is present at the end, which is almost always fatal. DISEASES OF THE LUNG 127 Extrapulmonary Localizations. The infection does not always spend all its force on the lung. In many- cases, even in frank pneumonia, but especially in epidemic pneumonia of a well-marked infectious type, the pneumococcus invades the pleura, peri- cardium, endocardium, meninges, stomach, peritoneum, joints, ear, etc. The invasion of these organs may be consecutive, parallel, or anterior to that of the lung ; it may, indeed, be independent of the pulmonary invasion. Let us study these forms. 1. Pneumococcal Pleurisy. — The pleura is almost always affected in pneumonia. The pleurisy is frequently dry, and limited to the production of false membranes, which vary in thickness, and cover the pleura to a variable extent, especially at the mterlobar fissures. In other cases we find pleurisy, with sero-fibrinous or purulent effusion. The pleural inflammation sometimes develops as a contact lesion from the pneumonic focus ; at other times it arises at a distance from the focus, the pneumococcus invading the pleura on its own account. Pleurisies with effusion often supervene in the decline of pneumonia or in full convalescence. They have, therefore, received the name of meta- or post-pneumonic. As a rule, they are not sero-fibrinous, but suppurative. Suppuration may be caused by the pneumococcus, without the aid of the usual pyogenic organisms (streptococcus and staphylococcus) ; and when these organisms are present, the infection is secondary. Meta-pneumonic pleurisy may invade the general cavity of the pleura, or else be encysted, i^iterlobar, diaphragmatic, or mediastinal (see Chapter V.), These forms may arise without pain, the fever may or may not return, and after three to six weeks they often end by vomica. Some eventually open in an intercostal space ; others, especially in children, termmate in absorption. The prognosis of these pleurisies Is, as a rule, not grave. Those which occupy the general cavity may exceptionally yield to thoracentesis, but in most cases operation for empyema is necessary. We also find early pleurisies in which the effusion occurs at the same time as pneumonia. Lemoine has given them the name of para-pneumonic. We must not forget that aseptic puriform effusions may also exist in pneumonia ; they must not be confused with septic purulent pleurisy.* 2. Pneumococcal Endocarditis. — Endocarditis is a fairly frequent complication of pneumonia. It aj)pears during the course of this affection (para-pneumonio), but most often during convalescence (meta-pneumonic). The pneumococcus itself is the cause (Netter), and is rarely found in associa- tion with other microbes, such as streptococci (Wcichsclbaum), or special bacilli (Lion). In exceptional cases endocarditis consecutive to pneu- monia is the result of the streptococcus alone (Jaccoud), und the uifection ♦ Vide Chapter V., Section 6. 128 TEXT-BOOK OF MEDICINE is secondary. Endocarditis is more frequent in certain epidemics of pneu- monia, in cases associated with influenza, and in the course of pregnancy. It is in general accompanied by other extrapulmonary infections due to the pneumococcus, such as purulent pleurisy, pericarditis, arthritis, etc. Suppurative meningitis iii particular is frequently associated with it. The invasion of the endocardium by the pneumococcus may be independent of pneumonia, and show itself in the course of certain affections caused likewise by the pneumococcus — viz., broncho-pneumonia, cerebro -spinal meningitis, inflammation of the great serous membranes, etc. Endo- carditis may develop in subjects who have no cardiac lesion, but previous valvular disease is singularly favourable to its appearance. Pneumococcal endocarditis usually attacks the left heart, and is found at the aortic more often than at the mitral orifice, in the proportion of 3 to 2 (Netter). Though it more rarely affects the right heart (one-seventh of the cases), it is, nevertheless, more frequent there than in endocarditis due to other microbes. Pneumococcal endocarditis causes vegetations rather than ulcerations. The vegetations are rounded, with a regular sur- face ; the largest are sessile, with a broad base, and very adherent. They are only detached in exceptional cases. Embolism is rare, and septic capillary emboli are not often seen. It is, therefore, exceptional to find emboli of the spleen, kidneys, etc., contrary to what is seen in streptococcal or in staphylococcal endocarditis, where the loosely attached vegeta- tions often give rise to these accidents. Destructive lesions may be seen — viz., little ulcers of the endocardium, tiny abscesses m the myocardium, followed by the production of valvular aneurysms. The virulent pneumo- coccus is found in the deep parts of the vegetations, just as in the blood. Pneumococcal endocarditis has been caused experimentally in the rabbit after previous injury to the valves, and even without traumatism. As a rule, endocarditis is silent when it develops at the same time as pneumonia, and passes unnoticed if the heart is not examined daily. Meta- pneumonic endocarditis, which supervenes some weeks after the onset of pneumonia, and often after a more or less complete period of apyrexia, may commence with a rigor and rapid rise of temperature. It commonly assumes the typhoid form of malignant endocarditis, with fever and grave adynamia. Auscultation may reveal blowing murmurs, variable in in- tensity and position at the different orifices. In some cases the symptoms of concomitant meningitis are the chief feature (Osier). The usual ter- mination is death, which occurs after a very variable period. Exceptional cases, followed by recovery (Traube, Lion), with or without persistence of the valvular lesions, are, however, recorded. 3. Pneumococcal Pericarditis. — This is another insidious manifesta- tion, only discovered by daily auscultation. This pericarditis, which is DISEASES OF THE LUNG 129 almost always accompanied by pleurisy, rarely begins before the fifth day of the pneumonia. Its frequency is variable, according to the epidemic. Abundance of fibrin is present, and the effusion is usually purulent. 4. Pneumococcal Meningitis. — Meningitis may supervene during pneumonia, or, later, during convalescence. In the former event it often passes unnoticed, the excitement and delirium being put down to fever or alcoholism. This is a common error. In the latter form the symptoms comprise fever, headache, quiet or violent delirium, pain in the nape of the neck, muscular rigidity, squint, contraction of the jaws, inequality of the pulse, Cheyne Stokes breathing, and coma. Post mortem the pia mater is infiltrated with greenish-yellow exudate, and the dura mater is converted into a thick cap. Bulbar and spinal menin- gitis are frequently met with. In some cases epidemic cerebro-spinal meningitis, due to the pneumococcus, has been observed. 5. Pneumococcal Nephritis. — The urinary troubles are various. Albu- muiuria, hsematuria, and anuria, have been noted. True nephritis, with ursemic symptoms, may occur. The renal changes have been minutely studied by Caussade. The kidney is large and ecchymotic. The nephritis is almost always haematuric. It may be caused by the pneumonic infection, for the pneumococcus has been found in the kidney or may be grafted upon existing lesions. G. Pneumococcal Gastritis. — The stomach, like other organs, may be infected Ijy the pneumococcus. I have quite recently seen this gastric infection in two patients suffering from pneumonia with generalized infec- tion — viz., peritonitis, pericarditis, endocarditis, meningitis, and arthritis.* These patients presented gastric symptoms of ])a,u\, nausea, vomiting, and abundant hsematemesis. Post mortem, the mucosa was studded with haemorrhagic erosions, due to acute necrobiosis. In one case pneumococci were swarming in the erosions. This form of gastritis is described in detail under Ulcers of the Stomach. 7. Pneumococcal Peritonitis.— I do not allude here to the primary form, I which will be described later. I am at present concerned with peritonitis which arises as a secondary condition in the course of pneumonia. Secondary peritonitis is rarer than the primary form. The symptoms aro abdomuial pain, tympanites, nausea, vomitiiig, and diarrhiea. This secondary peritonitis is not, in my opinion, as serious as the primary form. It was on the road to recovery in the two cases described. J * Diculafoy, " Gastrite ulcereuso pncumococciquo " {Clinique Medicale dc VILUd- Difii, 1S99, U"" le<,-on, p. 219). •j- Ditnilafoy, " rcritnnito primitive a I'ncumocoquca " {Clinique Medicale dc r/L'td- DIeu, 1S9G, 1S""= kvon, p. .390). J Vide " Ulcerative Gastritis." 9 130 TEXT-BOOK OF MEDICINE 8. Pneumococcal Arthritis. — Arthritis and synovitis may supervene during the course or the decline of pneumonia. In exceptional cases they may precede it, and, indeed, we see primary arthritis without pneumonia. It usually presents the same clinical aspect. The affected jomts are the seat of very acute pam, which is soon followed by swelling, oedema, and redness. It might almost be called a blennorrhagic arthritis, for the peri- articular synovial sheaths often participate in the process. Movement is very difficult, pressure is very painful, the temperature is raised, and the tongue dry, while the patient is prostrated and shows the signs of grave infection. The course varies somewhat in different cases. Sometimes it is rapid, and pus forms m a few days, but at other times its progress is slower. The prognosis of these joint lesions is usually grave not from the arthritis, but from the more or less general infection. The gravity of the prognosis can- not be based on the degree of virulence of the pneumococcus, for in a case ending favourably the pneumococcus was very virulent, while in one ending fatally its virulence was low. However this may be, the therapeutic indication is to let out the purulent fluid. Previous lesions (rheumatism., trauma) may favour articular infection by the pneumococcus. Experiments have given similar, but not constant, results. The lesions vary, accordhig to the intensity and the duration of the mfection. We may find serous or purulent effusion, thickenmg of the synovial membrane, and destruction of the articular cartilages and the ends of the bones. In one of my patients suffering from arthritis of the wrkt, the joints contained | ounce of pus, rich in pneumococci ; the articular surface was rough, and in places the cartilage had completely disappeared. 9. Pneumococcal Otitis. — Otitis is a fairly frequent complication of pneumonia. The disease has an acute course, and usually ends in recovery. Nevertheless, it may give rise to cerebral or cerebro -spinal meningitis, sinus plilebitls, or abscess of the brain and of the cerebellum. The enumeration of the complications of pneumonia, which include pleurisy, menmgitls, parotiditis, peritonitis, otitis, and suppurative arthritis, shows that suppuration plays a great part. The pneumococcus alone can cause suppuration, and the pus in such a case has special characters. It is viscid, rich m cellular elements, and of a greenish colour, like laudable J3us ; the serum does not separate out. In other cases, however, the usual organisms of suppuration — i.e, streptococci and staphylococci — cause secondary infection and suppuration. Varieties.— Pneumonia does not always show the same characters, but assumes somewhat different forms, accordmg to the age of the patient (old age), to the previous condition of health (want, alcoholism, pregnancy), to the numerous extra-pulmonary localizations, to the seasons of the DISEASES OF THE LUNG 131 particular year, or to other causes which are still imperfectly known (epidemic, or influenzal pneumonia) ; and, as Peter says, pneumonic conditions exist besides pneumonia ; in other words, there is a clinical as well as a patho- logical aspect. Varieties in Situation. Central Pneumonia. — Pneumonia sometimes remams localized hi the deep tissue of a lobe, and though the symptoms — i.e., rigor, high tempera- ture, dyspnoea, cough, and rusty sputum — point to pneumonia, yet the physical signs are wantmg ; dullness, rales, and tubular breathuig are absent, until the inflammation extends and yields the usual signs. Double Pneumonia. — A second attack of pneumonia may arise durhig the course of the first. This second attack. shows itself from the sixth to the eighth day. " Pneumonia is never double from the fn-st " (Grisolle). As regards site, every variety is possible, but most often the corresponding lobe of the opposite side Is affected. The second pneumonia ls generally less extensive than the first, and the inflammation is less severe. It does not begin with a fresh chill or pain in the side, and the appearance of the sputum is scarcely altered. Percussion and auscultation reveal the fresh focus which the symptoms had not almounced. The dyspncea, however, is more acute at the time of the fresh mvasion, and the temperature in the axilla affords valuable help. In unilateral j^neumonia the axillary tempera- ture is higher by some tenths on the affected side ; in double pneumonia the temperature is the same on both sides (Landrieux). Apical Pneumonia.— This form is justly regarded as very grave, and is often accompanied by collapse, adynamia, and a typhoid state. Suppura- tion is prone to occur, and delirium and jaundice may appear, while the usual signs of pneumonia — i.e., pain in the side, cough, and expectoration — are less marked. Apical pneumonia is a serious disease — first, because it ia more frequent m old age,* and also because alcoholism and general ill-health favour apical pneumonia. The reasons for this predilection are well dis- cussed by Peter, who regards the upper lobes of the lung as endowed with less vitality, and as " auxiliary and additional." Apical pneumonia is more frequent on the right side, and when the signs cannot be found m the clavicular region or in the supraspinal fossa, they miLst be looked for in the axilla. The situation of this variety might lead us to take it for a tubercular lesion. This error m diagnosis must be avoided. Massive Pneumonia. -In this form of pneumonia ((Jrancluu) the fibrmous coagulation extends throughout the whole bronciiial network of * VV<5 .SCO ill tlic statist ics uf iJiiiund Fiuilcl lliat in lliirty cjuscs of fatal pnouuionia thu apiucs wore aifuctud cigLtcun times (" Tiaitc ties Maladies dcs V'ioillurds," p. 4G0). y— 2 132 TEXT-BOOK OF MEDICINE the invaded territory, and reaches even the large bronchi. The air, there- fore, cannot enter the bronchial tubes, and most of the stethoscopic signs of pneumonia are wanting. Neither tubular breathing nor rales are heard ; expectoration is almost absent. It is therefore evident how difficult it may be to distinguish between pleuritic effusion and massive pneumonia. However, certam signs are of value in diagnosis. The dullness of pleural effusion is more complete and more fluid than that of pneumonia. Further, the displacement of organs (notably of the heart), which is absent in the case of pneumonia, is more or less marked in the case of effusion. Varieties of Pneumonia, according to Age. 1. Children are more subject to lobular than to lobar pneumonia ; still, lobar pneumonia is often seen, even as early as the first year. In young children the onset is often accompanied by convulsions, vomiting, and erythematous eruptions. The respiration is panting, and the pulse-rate may exceed 140. About the age of five years the dry, crepitant rale is heard ; below this age we find rather the subcrepitant rale. The other signs closely resemble those of pneumonia in the adult, but the child does not expectorate, and hence the absence of rusty sputum, which, however, is sometimes seen 'm. four- to five-year-old children. Under two years of age the cyclical course of the fever is really the only differential sign between lobar and lobular broncho-pneumonia. The prognosis is grave only in the very young ; a little later the disease is relatively benign. 2. In the aged, in whom there is little organic reaction, pneumonia is insidious ; the rigor is insignificant, and the pain in the side may escape notice. The colour of the face and the dryness of the tongue are sometimes the only signs. We wait m vain for rusty sputum, which does not appear. The crepitant rale is coarser than in the adult — in a word, pneumonia is altered by the age of the individual. At the Salpetriere ambulatory pneu- monia is sometimes seen ui old women, who contmue to eat and to attend to their occupations. They die almost suddenly, and suppurative pneu- monia is found post mortem. Clinical Varieties of Pneumonia. At the beginning of this article I described the ordinary form of lobar pneumonia, but it is clear that the extrapulmonary localizations in the pleuja, heart, meninges, and kidneys give a special aspect to pneumonia. On the one hand, some clinical varieties depend upon the predominance of the lesions in a certain organ, while in other cases the varieties depend on the general appearance of the morbid complex, and the disease assumes special features. 1. In the so-called inflammatory or sthenic form, often described by DISEASES OF THE LUNG 133 old writers, and frequent in the country, the chief characters are as follows : Redness of the face, epistaxis, violent headache, restlessness, severe inflammation of the lung, sputum which is sometimes bloody, speedy hepatization, rapid and quivering pulse. 2. The asthenic form is characterized by the following symptoms : Insidious onset, lassitude, early delirium, subsultus tendinum, prostration, stupor, soft and imequal pulse, tendency to adynamia, and collapse. 3. The nervous forms show several varieties. Delirium is common, especially in drunkards. It may not be associated with cerebral lesions, while in other cases delirium Ls caased by cerebral or cerebro-spmal menin- gitis, due to the local action of the pneumococcus. The paralyses consecutive to pneumonia show different forms. In the acute phase of pneumonia they nearly always affect the hemiplegic type, with or without aphasia, and with or without apoplexy. These pjiral3''ses, which are curable in the adult, but fatal in the elderly, are due to lesions of the cerebral vessels (Lepine). The paralyses which supervene during convalescence affect the para- plegic type, or the type of isolated paralyses, with or without muscular atrophy. These paralyses are in some cases due to meningo-spinal changes, in others to peripheral neuritis of 'toxic origin, like the palsies of diph- theria. 4. Biliary pneumonia comprises two very distinct forms. In the one there is pneumonia with jaundice, which is consecutive to catarrhal inflam- mation of the bile-ducts, or to perihepatitis produced by right basal pneumonia. These lesions are then purely local. In the other there is pneumonia with a biliary condition, which depends on a general morbid state. This condition is characterized by a subicteric tint, with al)sence of active reaction, soft pulse, headache, foul tongue, vomiting, and diarrhoea. The biliary condition accompanies the grave forms (apical pneumonia, alcoiiolism). It is connected with "the medical constitution of the season of the year." It forms part of what was called peripneumonic biliary fever, and explains tlie epidemics of biliary pneumonia. In some exceptional cases pneumonia is connected with a diffuse hepatitis, a variety of icterus gravis. 5. Malignant and Epidemic Pneumonia.— Every pneumonia, whether benign or malignant, is an infective dis(!ase, but clinically it is customary to reserve the epithets " infective " and "malignant " for the grave and abnormal forms. There is, first of all, the infectious pneumonia which has at different times appeared in epidemic form during epidemics of malaria, scurvy, and typhoid fever. Next, there is secoiidary pneumonia, supervening in tlio course of some general disease, and deriving its character and gravity from the surroundings in wliieh it develops. 134 TEXT-BOOK OF MEDICINE In many cases, however, pneumonia develops on its own account — ■ sometimes in an isolated form, but more often in the form of more or less circumscribed epidemics, which may be associated with those of influenza. It is accompanied by all the features of an infectious malady. The contagion is quite proved. The epidemic breaks out in a prison, in barracks, or in a small area, or confines itself to a house or to a family, tliree or four members being affected simultaneously or successively. In some cases this epidemic pneumonia differs but little from genuine pneumonia. As a rule, it presents special features, which have earned for it the names " typhoid," " asthenic," " adynamic," etc. Hepatization sometimes occurs at several foci. The sputum is bloody rather than rusty, and the disease is accompanied by swelling of the spleen, diarrhoea, albu- minuria, jaundice, pleurisy, pericarditis, vegetative endocarditis, menin- gitis, parotiditis, precordial distress, and prostration. The fever-chart does not resemble that of frank pneumonia. The histological lesions are somewhat special. The prognosis is not absolutely bad. The disease is benign m one epidemic, malignant in another. The prognosis, like the clinical picture, comprises every intermediate form. 6. Pregnancy and Pneumonia. — Grisolle maintained that lobar pneu- monia is formidable in pregnant women. At the present day the opposite opinion holds good. Many cases of pneumonia occurring at different stages of pregnancy have been published. The , disease was relatively benign for mother and child. Last year I saw tliree cases of pneumonia during pregnancy, one at a very late stage. The women recovered, and delivery took place without mishap. The transmission of pneumonia to the foetus is an established fact. In the published cases the child has succumbed a few days after delivery. The infant may succumb without showing any lesions in the lung. Post mortem we fbid lesions in the liver and the spleen, due to toxines which have traversed the placenta. Pneumonia in a nursing woman diminishes or suppresses the secretion of milk. As the pneumococcus can be transmitted by suckling, the mother should not continue to suckle her child. etiology. — Lobar pneumonia is a disease of adults. In the aged it assumes special features, and the child, though more subject to the lobular form, may contract the lobar variety. Changes of season — -as in November, March, and April— appear favourable to its development. Previous debility is not necessary as a predisposing cause, for pneumonia frequently attacks people in perfect health. Some persons have a special pre- disposition to recurrences and contract several attacks. Probably the pneumococcus is always present, awaiting a favourable opportunity for development. I have previously discussed epidemicity. Epidemics of pneumonia DISEASES OF THE LUNG 135- may be limited to a locality, or spread thsough a town, province, or country. They often coincide with influenza, and are due to unknown atmospheric or climatic causes, which increase the virulence of the microbe. The question of contagion demands notice. Pneumonia is contagious, and the sputum most often spreads contagion, which may be active long after recovery. The foetus may be infected by its mother, and may itself show the pulmonary and extrapulmonary lesions of the infection. The nature of lobar pneumonia has been interpreted in various ways, and till recently two chief theories were in evidence. One — the Hippo- cratic doctrine, upheld and defended by the Montpellier school — regarded the lesion of the lung as the local and secondary expression of a general state, called pneumonic fever. Pneumonia — that is to say, the lesion — would then be the result of pneumonic fever, which is the disease. The anatomo-pathological school of Paris has brought forward quite an opposite theory : The lesion in the lung represents the whole disease, and the local lesion Is the cause both of the fever and of the general symptoms. Between these extremes an intermediate opinion has found a place. It Is generally admitted that a chill is perhaps the commonest cause of pneu- monia ; for effective action, cold, or any other provoking cause, must find the system in a favourable condition of receptivity. Firstly, is it true that cold plays such a large part in the development of pneumonia ? According to some statistics, cold Is said to act as a pro- voking agent in only a half or a third of the cases. The cause of lobar pneumonia resides in the existence of an infectious organism — the pneumo- coccus — but the chill is tlie chief provokmg agent. The pneumococciLS being the cause of pneumonia, how are we to admit that its entrance into the lung may be followed, after such short delay, by the symptoms of acute pneumonia ? In answer to this objection, Jaccoud admits, with good reason, the possibility of auto -infection. " The human organism constantly lodges various microbes in large numbers. As long as its functions are normal, it Is a hostile medium, which wards off their noxious effects. However, let disturbance arise and alter the physiological functions, the hostile medium becomes friendly, and the affected organism is deprived of effective resistance against the very microbes which it but lately tolerated without being affected." The pneumococcus exists normally in the mouth (Pasteur), in the pharynx, and in the bronchi (Netter). Sliould it enter the lung in those who are not in a state of receptivity, its j)athogoiuc iiiHuonce is annihilated by the activity of the ])liagocytes. In the ojiposite condition pneumonia dcf^lares itself. The dissemination of the pneumococcus produces the extrapulmonary localizations above described. In opposition to the primary form just described, wc ^oo secondary ' 136 TEXT-BOOK OF MEDICINE infections which are less frank in evolution, and supervene in other diseases (diabetes, cachexias, gout, eruptive fevers, etc.). This variety of lobar pneumonia is somewhat rare, for the secondary form chiefly devolves upon lobular pneumonia. Course — Duration — Termination. — Lobar pneumonia has a mean duration of five to ten days. The period during which the temperature rises is short and rapid. By the second day it reaches its maximum (104° to 106° F.), remains stationary for some days, with a morning remission of J° to 1°, and in most cases defervescence is sudden and complete in twenty- four hours. This defervescence, which usually occurs between the fifth and the seventh days, is often accompanied by symptoms of crisis — viz., sweating, epistaxis, diarrhoea, and profuse secretion of urine contaming albumin and excess of chlorides.* This increase varies in proportion to the retention of chlorides m the tissues during the illness. It is remark- able that the defervescence is sometimes preceded by transient aggravation of the disease. This has been called the precritical phase. Labial herpes cannot be considered as a symptom of crisis, for it often appears at the onset of pneumonia. Suppuration in the lung is a frequent cause of death, which, however, may occur before the appearance of grey hepatization. Some patients are struck down by adynamia and fatal collapse during the stage of red hepati- zation, while others succumb through the extensive nature of the lesion, which invades several lobes, narrows the field of haematosLs, and induces asphyxia and cardiac paralysis. In some well-proved cases suppurative pneumonia has caused death by purulent infection, and the affected tissue may suppurate as a result of the pneumococcus alone. Diagnosis — Prognosis. — Let us first differentiate between lobar pneu- monia and other inflammations of the lung. 1. Lobar pneumonia is nearly always primary. It invades one or several lobes, remains confined to a definite area, and spares the rest of the organ. Onset, course, and termination are clearly marked : the crepitant rale, the tubular breathing, and the rusty sputum scarcely permit confusion ; suppuration is exceptional, and recovery is tlie usual termination when the infection does not involve other organs. These characters are distorted when the pneumonia is secondary, takes on an epidemic form, or develops in the aged. I would add, too, that even in its frank forms lobar pneumonia does not always present the complete picture sketched in this chapter. It has been my lot to see cases of lobar pneumonia which differ from the classical type. Many so-called lobar pneumoniae border on inflammation of the chest, * Up to defervescence the urine was scanty, dark, and in twenty-four hours con- tained 35 to 50 grammes of urea, instead of the normal quantity of 28 to 30 grammes. DISEASES OF THE LUNG 137 and are the intermediary forms which unite clinically the various inflamma- tions of the respiratory passages. 2. Lobular or broncho-pneumonia is especially frequent in children, and is often consecutive to some other malady (measles, diphtheria, whoop- ing-cough, influenza, tuberculosis, etc.). It deserves the name of " fibrinous " less than the preceding form. It Ls lobular — that is to say, it spreads by centres which are scattered tlirough both lungs, and may be isolated or confluent. The disease does not exhaust all its action on the inflamed centres. It progresses by successive outbursts.; its lesions and its course are irregular, and its description differs notably from that of lobar pneumonia. 3. Inflammation of the chest is not pneumonia, and, on the other hand, differs from simple congestion. It is a morbid condition in wliich the hyperaernic and inflammatory elements are differently combined. The inflammation affects one or several lobes, and does not spare the other parts of the respiratory system. The bronchi, the pleura, and the muscles of the thorax — in fact, all the superposed layers of the chest — may be affected in different degrees. 4. Spleno-pneumonia (Grancher) is thus defined by this author : " Between pulmonary congestion and lobar pneumonia, and side by side with broncho-pneumonia, there exists a morbid condition of the lung — a kind of subacute pneumonia, which simulates pleurisy with moderate effusion, and deserves its own description and denomination." Potain has described a variety of pneumonia which he has named congestive, and to which he says spleno-pneumonia may be likened. 5. Hypostatic pneumonia has not the anatomical attributes of a true pneumonia. It is a mixed condition, in which passive congestion and oedema play the chief part, and are accompanied by slight transudation of fibrin, and sometimes by hsemorrhage. This morbid condition, con- secutive to heart disease, hypostasis, and prolonged decubities, chiefly involves the posterior and lower parts of the lungs. 0. Pleurisy at first presents numerous analogies with pneumonia. In pleurisy, however, the chill is less violent, the initial temperature is not so high, the pain in the side is often more acute, expectoration is absent, and the friction soinid is more moist and diffuse tlian the dry, crepitant, and clearly localized rule of pneumonia. It is not sufficient to diagnose pneumonia : wc must also know whether it is inflammatory, biliary, or adynamic ; whether it is or is not complicated by pleurisy, endocarditis, ])ericarditis, meningitis, or otitis ; whether it is primary or secondary ; whether it is arc'f)in[)anied by alcoholism ; whether it is the first act in commencing typhoid fever ; whether it has developed in a diabetic or in a tubercular subject. Each of the.se points affects the prognosis and the treatment as mucli as the diagnosis. 138 TEXT-BOOK OF MEDICINE Treatment. — The treatment of pneumonia should be especially directed to the general condition. When pneumonia is regular and benign, we should be content with watchful expectancy, ordering acid drinks, laxatives, broths, and wine diluted with water. In the contrary case the indications must be acted on. Blisters are more harmful than useful in my opinion. Pain in the side may be relieved by leeches, antipyrin, injections of morphia, or by an ointment of vaseline 10 parts, methyl-salicylate 1 part. In sthenic pneumonia antiphlogistic treatment should be employed — i.e., blood-letting, cupping, leeches, and tartarate of antimony, or, better still, kermes, administered to Trousseau's prescription :. Kermes . . . . . . . . . . . . gr. xxx. Extract of digitalis . . . . . . . . . . gr. iii. Medicinal soap . . . . . . . . . . q.s. For 20 pills. Ten to fifteen pills are given in the twenty-four hours, and if vomiting or diarrhoea supervene, 1 drop of Sydenham's laudanum is given with each pill. Good results are also obtamed by infusion of digitalis, given at mtervals in the twenty-four hours (Hirtz) ; but I have never tried this remedy. Biliary pneumonia may be cut short by emetics, and especially by ipecacu- anha. Adynamic pneumonia should be treated with tonics and stimulants, such as quinine, tincture of coca, wine, or brandy. If the fever is severe, sulphate of quinine and antipyrin may be given. When pneumonia takes the ataxic form, with delirium, restlessness, and high fever, the following draught, in tablespoonfuls every hour, may be given with advantage : Orange-flower water . . . . . . . . . . gilL Cherry-laurel water . . . . . . . , . . Siii- Syrup of ether . . . . . . . . . . . . 3x. Bromide of potash . . . . . . . . . . 3ss. Cold baths have been extolled in the ataxic and hyperthermic forms of pneumonia. I have used this treatment' several times with success. I would advise giving the baths just as in typhoid fever. If pneumonia is accompanied by irregular pulse, feeble heart-action, and a tendency to syncope, subcutaneous injections of the following solution of caffein should be given : Distilled water . . . . . . . . . . 3ii. Benzoate of soda . . . . . . . . . . 3ss. Benzoate of caffeine . . . . . . . . . . 3ss. I would also advise in such a case injections of serum (8 to 16 ounces or more daily). For further details, see chapter on Therapeutics. The patient should drink plenty of milk, fresh water, and tisanes, with DISEASES OF THE LUNG 139 or without lactose, for it is essential to promote urinary secretion. Milk lias the further advantage of protecting the kidney — a fact not to be despised, especially as pneumococcal nephritis is now well recognized. Lastly, I must say a few words about the treatment of pneumonia by subcutaneous injections of essence of terebinth. Fochier (of Lyons) observed that in certain cases of puerperal infection, when no important lesion can be found, sudden improvement may coincide with the appearance of pus in the iliac fossa, the breast, a joint, or else- where. The appearance of a local abscess or cellulitis seemed to have a curative action. Fochier gave it the name of abscess of fixation. The question was then asked whether analogous abscesses could not be produced therapeutically. In women whose condition appeared desperate recovery was induced by subcutaneous injections of essence of terebinth. As Lepine had been successful in a case of pneumonia, I applied the treatment to two women suffering from severe pneumonia which was probably on the point of suppuration. Both patients recovered. The treatment is as follows : An injection of L5 minims of essence of terebinth — i.e., 60 minims for the four injections — is given by means of a sterilized syringe, in the subcutaneous tissue of the outer surface of each thigh and of the deltoid region of each arm. These injections produce extremely acute pain, lasting about two hours. The next day the injected regions present an oedematous, whitish, and diffuse thickening. The abscess which forms IS opened, and the pus in my two cases was amicrobic. Whether these phlegmons be called abscesses of fixation or abscesses of derivation matters little. What does matter is the therapeutical result. It deserves, I think, to be taken into serious consideration. This treatment, in my opinion, should be reserved for patients who are suffering from grave ])neumonia in which grey hepatization is imminent. Collargol has sometimes given good results (Netter). An ointment con- taining 13 per cent, of collargol is employed, and a piece about the size of a nut is daily rubbed into the skin. It is better to use intravenous injec- tion of ].") to .'}() grains of collargol. The prophylactic treatment of pneumonia should not be neglected. It must not be forgotten that, as pneumonia is contagious, proper precautions must be taken to isolate the sick, and to disinfect the sputum and articles of bedding or clothing used by the patient. V. CHRONIC PNEUMONIA— FIBROSIS OF THE LUNG. Chronic inflammation of the limg may affect the pareiu-hyina and liie con?u'ctive tissue. These lesions give rise to the varieties of chronic pneu- monia known as lobar, lobular, and cortical. 140 TEXT-BOOK OF MEDICINE The chronic pneumonia called caseous is really tubercular, and will be studied later, under Phthisis. Chronic Lobar Pneumonia. — The lobar form is much rarer than the lobular one. It may be primary, or may follow acute pneumonia. Malaria appears to play some part in its development. In our study of acute pneumonia we have seen that residual inflammation may still remain in the alveoli, and may take several weeks to absorb (Andral). This process, though it may be slow, rarely ends in chronic pneumonia, because the parenchyma of the lung is unaffected ; and if it do so end, it is because the parenchyma is affected by fresh inflammation. Two stages are described in chronic pneumonia — viz., red and grey induration. The lung tissue affected with red induration is firm and increased in size ; the cut section is less granular, and the tissues are less friable than in the red hepatization of acute pneumonia. The indurated part does not crepitate, and sinks in water. The walls of the alveoli and the perilobular connective tissues are invaded by fibrous tissue. The alveolar cavities are narrowed, and at times invaded by nodules of fibrous tissue which has replaced the wall of the alveolus. The fibrosis is intra- and extra-lobular. After several months red in- duration gives place to grey induration. The lung tissue, which has become impermeable, retracts and diminishes in volume. It is hard, creaks under the knife, and has all the attributes of fibrous tissue (Cruveilhier's fibrous metamorphosis). In this fibrous tissue excavations (ulcers of the lung) are sometimes met with, but no bronchiectasis is found, contrary to what is seen in chronic broncho-pneumonia. This chronic pneumonia extends in an uniform way tlirough a whole lobe or a part of the lung. It is more common at the base than at the apex. Dullness, deformity of the chest, muco-purulent sputum, tubular breath- ing, rales, and gurgling, are the signs of chronic pneumonia ; and if we add frequent hsemoptysis and cachexia, with fever, sweats, and wasting, it will be admitted that the diagnosis from phthisis would be very difficult if the existence of the latter were not confirmed by the presence of bacilli in the sputum. Chronic Broncho-Pneumonia. — Chronic broncho-pneumonia is more frequent than the preceding form, and usually follows acute or subacute broncho -pneumonia. It is most common in early life, and is caused by measles, diphtheria, whooping-cough, influenza, typhoid fever, and syphilis. In the chronic, as in the acute, form the lesions affect both the bronchus and the lobule. In a vertical section of the lobule, during the subacute phase the bronchus is dilated, and its normal elements are converted into embryonic tissue. The region of the alveoli which surrounds the bronchus DISEASES OF THE LUNG 141 is affected by hepatization ; the walls of the alveoli show embryonic infil- tration, and the alveolar cavities contain exudate, with epithelial cells and leucocytes. Around the hepatized area we find the splenized zone, which is the seat of congestion ; the epithelial cells desquamate and fall into the alveolar cavity. As the lesion becomes chronic the intra-alveolar elements undergo granulo-fatty degeneration, and the embryonic cells, which infiltrate the parenchyma, change into fibrous tissue. The fibrosis affects the peri- bronchial and perilobular connective tissue and the parenchyma of the lung atrophies. Chronic broncho-pneumonia chiefly afEects the lower lobes and the posterior part of the upper ones. The lung tissue is violet-coloured, dense, and dry ; the cut section is smooth, without granulations, and the divisions between the lobules are still perceptible under the low power. These lesions were called camification, by comparison with muscular tissue. In some cases the lung is fibrous and atrophied, and dilatations of the bronchi are found. They are due to changes in the bronchial walls, and as they are found before the lung atrophies (Charcot), it is hardly probable that they are consequent on the pulmonary fibrosis, as Corrigan supposed. The progress of chronic broncho-pneumonia is very slow, and the disease passes through a subacute stage, subject to periods of arrest. Dullness, rales, tubular breathmg, and sometimes gurgling, arc the most usual signs. Fever is common, the expectoration is muco-purulent, or at times blood- stained, and the disease usually ends in hectic fever. Chronic Cortical Pneumonia. — In some cases of pleurisy, when the absorption of fluid is very slow, the pleura becomes thickened, and forms a fibrous shell over the lung. The lobes are adherent to one another, and the parietal pleura is likewise adherent to the chest-wall. This fibro-plastic process does not always remain limited to the pleura, but reaches the lung probably along the lymphatics. The connective spaces between the lobules are transformed into fibrous arches, which surround the lobules, and finally involve the alveoli themselves. Pleuro-pulmonary fibrosis is thus brought about. These cases are somewhat rare (Brouardel, Tapret). I have seen one case in which bronchi- ectasis was also present. Pulmonary fibrosis as a secondary lesion is associated with diverse changes in the lung. It accompanies emphysema, tuberculous lesions, tumours, hydatid cysts, pneumokoniosis, etc. It is fairly common in elderly people. The fibroid regions arc indurated and pigmented, the fibrous framework of the lung is thickened, the walls of the vessels take part in the change, and the alveolar cavities are atrophied by the new tissue. Syphilitic fibrosis of the lung exists, and will be studied under Sypliilitic Legions of 142 TEXT-BOOK OF MEDICINE the Lung. The lesion called slaty induration of the apices, and frequent in the lungs of elderly people, is nothmg but a highly pigmented fibrous tissue. This tissue bounds the alveoli, which are atrojihied in some parts, emphysematous m others, and often contains small cysts of long standing, transformed into caseous or chalky material. VI. OCCUPATION PNEUMONIAS— PNEUMOKONIOSIS. The dust from coal, iron, steel, copper, and silicon, gives rise to chronic pneumonia, which we shall study under the names of anthracosis, siderosis, and chalicosis. Anthracosis. — Antliracosis may be physiological, most human lungs being normally mottled with black. When, however, the infiltration of carbon becomes excessive, the lesions cause special symptoms. Anthracosis occurs chiefly among miners, charcoal-burners, and moulders in copper, brass, or bronze, who use carbon dust m their work. The lesions seen are : at first emphysema, then a black coloration of the lung, which no longer crepitates, creaks under the knife, and sinks m water. On crushing the lung tissue, the fingers are coloured black, and also the water allowed to flow over its surface. The cut section may be mottled with black or be of an uniform black colour. The lung tissue is divided by large bands of connective tissue, which contam particles of carbon, heaped up at certam spots to form nodules. Histologically, we see fibrosis, which affects the connective tissue surrounding the lobule and its central bronchus. A fibrous mass, crammed with black grams, is found m these regions. Bronchi- ectasis is hardly ever seen ; on the other hand, obliteration of the bronchial arterioles is frequent, and hollow, irregidar ulcerations, containmg black, putrid material, are the result. The bronchial walls are intact. The pleura is adherent and thickened ; the glands are hard and black. Lesions of the right heart are sometimes seen. Does antliracosis predispose to tuberculosis ? Authorities are not in accord on this pomt. Oberthiir says positively that tuberculosis is rare in coal-miners. It may be admitted (Boulland) that if the damage to the lung favour the growth of the bacillus, this growth is arrested by the fibrosis, which isolates the foci and prevents their development. The symptoms display three periods (Tardieu). In the first period we see malaise, with loss of appetite, wastmg, and fits of coughmg, which are followed by blackened expectoration. On auscultation, the vesicular murnmr is feeble, the voice- sounds are exaggerated and sibilant and snoruig rhonchi are sometimes audible . In the second jDcriod the symptoms grow worse. Vomitmg appears, the distress mcreases, and the induration of the lung is complete. Muco-pus is often fomid m the sputum, and at times a little blood is present. The third DISEASES OF THE LUNG 143 period is characterized by the progress of the ansemia and by decline. The lung is hollowed out by cavities, and death supervenes, either by cachexia or by asystole. The duration may be several years. Chalicosis. — Infiltration of the lung by the dust of silica (chalicosis) is seen among stone-cutters (quarrymen, millstone sharpeners, flint-cutters, road labourers), needle sharpeners, glass, china, and earthenware workers, potters, and flax-combers (Greenhow). Post mortem the lungs are crammed with nodules, which are very hard and blackish, or at times grey, white, or yellowish. Histologically, we find lobular fibrosis, with narrowing of the alveoli and small crystalloid granules, which are strongly refractive to light, and composed of silica. Cavities, surrounded by grains of silica, may exist. The glands are hard and of a blackish-grey colour. Lesions of the right heart are common. The symp- toms, as in anthracosis, may present three periods. The sputum appears more abundant, and hsenioptysis is more frequent. The disease lasts three or four years. The phthisis of earthenware-makers (Porte) shows three forms — pneumonic, emphysematous, and suffocating. Siderosis. — Up to the present twenty-one cases of infiltration of the lung by particles of iron have been collected (Zencker and Merckel) ; they have been seen in workmen using red oxide of iron (looking-glass -makers, gold-beaters, and muTor -polishers). In one autopsy (Zencker) the surface of the lung was of an intense and uniform brick-red colour, streaked with darker lines, corresponding to the interlobular spaces. The pleura was covered with red patches. There were several cavities in the lung, without a trace of tubercles. The microscope showed fibrosis of the lung, with graimles of iron, which, on chemical exammation, gave its special reactions. The physical signs resemble those of anthracosis, and the red sputum is characteristic. The diagnosis is chiefly ba^cd on the characters of the sputum, which is black in anthracosis, red in siderosis, and without objective characters in chalicosis. Tlie diagnosis from pulmonary tuberculosis and from latent cancer of tlie stomach is most puzzling. In the first case inquiry as to the patient's profession, and examination of the sputum from the chemical and bacillary standpoint will be the chief points. In the case of latent cancer of the stomacli, where confusion is possible (Lctulle), error can only be avoided by careful study of the course of the disease. Treatment is, in the first place, propliylactic. Workrooms must be freely veutiluted, attempts at preventing the jjropagation of dust nuist be inaih-, and masks used. When piieuniokoniosis is present, change of profession should be advised. 1'liis radi(-al measure often arrests the disease. Revulsives, balsams, arsenic, anil iodide of potash are employed for the fibrosis. 144 TEXT-BOOK OF MEDICINE VII. THROMBOSIS AND EMBOLISM OF THE PULMONARY ARTERY. Thrombosis of the pulmonary artery is the obliteration of the vessel by a clot of blood formed during life. It has many causes, such as cachexia (tuberculosis, atlirepsia, malaria), compression of the artery by a mass of glands, or by a mediastinal tumour. Thrombosis is sometimes consecutive to extensive pneumonia, gangrene of the lung, and pleurisy (Vergely). Atheroma and fatty changes in the vessel are exceptional causes. Embolism is the sudden obliteration of the vessel by a body circulating in the blood; This body, or embolus, often arises from a thrombus. The results of embolism and the lesions to which it gives rise vary with the si2;e of the artery obliterated, and also with the nature of the embolus. It is therefore customary to study embolisms of the large, medium, and small branches of the pulmonary artery. To this last category belong the capillary embolisms ; to the two first, the lobular and lobar ones. The large embolus, which is arrested in an artery of large or of medium size, is generally caused by an mert body ; the embolism is then called mechanical. Capillary embolism may also be mechanical, but is more often infective and microbic. Mechanical Embolisms of the Pulmonary Artery. Pathogenesis. — The tlu-ombus may break up and give rise to emboli, which, however, arc much more rare than those which have their origin in the heart or in the great vems. 1. Embolisms of cardiac origin are chiefly seen in mitral lesions, and in mitral stenosis in particular (Duguet). Aortic affections, on the contrary, rarely give rise to them. Bucquoy has laid ^ress on pulmonary embolisms consecutive to arterio-sclerosis ; but as the affection is often accompanied by chronic myocarditis, this is, without doubt, a cause of embolism. In all these cases the process is as follows : On the walls of the right heart, and especially of the right auricle, masses of fibrin are deposited, and become interwoven with the muscular bmidles which project into the cavity of the auricle. The slowing of the stream and the change in the blood cause coagulation. The clot beaks down gradually, and its fragments escape to form embolisms m the branches of the pulmonary artery. Sometimes the embolus consists of the debris of the valves and chordae. 2. Phlebitis is a very frequent cause of embolism, especially in acute infectious diseases (typhoid fever, erysipelas, diphtheria, mfluenza, variola, etc.), because the clot develops rapidly, and its adhesion to the walls of the veins is very slight. A separate place must be given to pulmonary embolism. DISEASES OF THE LUNG 145 following puerperal phlegmasia. This accident usually appears within three weeks of the confinement ; beyond the fifth week puerperal embolism is exceptional. Phlebitis in chronic infectious maladies (tuberculosis, cancer) and cachexia (malaria, diabetes, gout, etc.) is more rarely followed by pulmonary em- bolism. Phlebitis consecutive to varices, fractures, or compression by tumour, may also give rise to embolism, especially if the lesion affect a vein in the lower limbs. In some cases phlebitis has a deep origin, as in phlebitis of the uterine and utero-ovarian veins (cancer of the uterus, uterine fibroma, cysts of the ovary, renal tumours, etc.), and yet in these different diseases embolism is to Ije feared. Pathological Anatomy. — In order to understand the lesions which result from pulmonary emboHsm, we must bear in mind that the lungs receive two kinds of arterial vessels — the bronchial arteries, charged with the nutrition of the organ, and the branches of the pulmonary artery, cliarged with assuring haematosis. These two systems remain independent. The branches of the pulmonary artery, like those of the spleen and kidney, are terminal (Cohnheim) — that is, each vessel occupies its own proper area, and does not ana.stomose with its 'neighbours. The result is a complete independence in their function and their diseases. In the case of throm- bosis there is, then, no reason to count upon the collateral circulation to remedy the effects of obstruction in the vessel. When the obstruction affects a lobar artery or the trunk of the pulmonary artery, anaemia is seen, or in case of sudden death, atelectasis of the terri- tory that is no longer irrigated is found post mortem. If, on the other hand, the patient has survived some hours, we find congestion, oedema, or perhaps an infarct, which may occupy nearly a whole lobe. As a rule, the obliterated vessel is much smaller — m most cases a lobular artery. The obstruction then shows itself by the formation of an infarct, which is called hamoptoic (Laennec), These infarcts may occur all over the lung, but are more frequent on the right side than on the left, and usually occur at the base, the posterior surface, and the edges of the lungs. They are sometimes single, at other times multiple, when their number may be unlimited, just like the number of embolisms which give rise to them. They have a blackisli, truffled colour, and a firm consistency, which permits their recognition by simple pressure, when they are situated deep in the paren- chyma of the lung. Their cut siu-f ace is shining, dry, and smooth, or granular if the blood distends the alveoli. Around tlie infarct the lung tissue is bright red, passing to yellow as the distance from the infarct increases. G?lderaa of the lung and pleurisy, which is generally quite limited, are frequently found. 10 146 TEXT-BOOK OF MEDICINE Under the microscope the alveoli are filled with red corpuscles, which are crowded together, and more or less deformed, according to the age of the infarct. The interalveolar spaces and the septa are packed with red corpuscles. In an old infarct the red corpuscles are no longer recognizable, and crystals of ha3matoidin and of hsematin, pigmentary granules infil- trating the alveolar walls, and fatty granulations predominate. The con- nective network is always thickened. This thickening is sometimes but slightly marked, and as the arteriole agam becomes permeable, restitutio ad integrum is favoured. Sometimes, on the other hand, fibrosis predommates and causes a fibrous cicatrix, which is retractile and prone to infiltration with calcareous salts (Pitres). The uifarct may be uivaded by various micro-organisms, whence the possible coexistence of suppurative or gangrenous centres. In other patients the embolus (phlebitis in puerperal women) contains the micro- organisms of suppuration or of gangrene. The chief factor in the production of infarcts is still surrounded by obscurity, in spite of experimental researches. Ranvier and Duguet have shown that some time elapses between the obliteration of the artery and the formation of the mfarct. The interval between these accidents is some- times as long as two or tlu"ee days, and it is then supposed that the walls of the artery become mflamed on the proximal side of the obliteration, break down, and fuially burst. The infarct is produced at this moment. This interpretation is to-day more generally admitted than that of collateral congestion (Virchow, Rmdfleisch). When the capillary embolisms (non-infectmg) are few in number, they are not, as a rule, accompanied by any change in the lung tissue, because the circulation is re-established by the anastomoses of the capillary network. If their number is considerable, they may give rise to grave results from the many capillaries obliterated. Experimentally, capillary embolisms are easily caused by the injection of finely-divided substances into the jugular vein. As these substances are irritant to the lung tissue, they determme pseudo- tuberculous granulations at the point where they are arrested. Symptoms — Diagnosis. — The large embohsms give rise to very dis- similar results. The patient may be struck down by syncope, and die suddenly ; he may survive some minutes or hours. Intense dyspnoea, rapid cyanosis, and cardiac troubles (angina and palpitations) are seen, though examination of the heart and of the lungs reveals no lesion. Lastly, in some cases the patient is seized with intense pain in the side, severe dyspnoea, and perhaps a rigor. Improvement soon occurs, and he sub- sequently coughs up more or less profuse blood-stamed sputum, provmg an infarct. In this form of embolism recovery may take place, but the patient often succumbs in a few days, after several attacks, with signs of acute asystole. DISEASES OF THE LUNG 147 The setiological conditions have a capital importance in diagnosis. The large embolLsms are due to phlebitis, while the medium ones usually arise in cardiac lesions. These same a?tiological indications will, in the case of sudden death, and hi the absence of an autopsy, justify the diagnosis of puhnonary embolism, and not that of angina pectoris due to aortic disease. Likewise the asthmatic attack, the sudden suffocations of uraemia, which arise under very different conditions, will hardly give rise to confusion. EmboUsms of moderate size — that is to say, those which always end in the formation of infarcts — have a more clear clinical history than the precedmg variety. We can diagnose an infarct in a cardiac patient whose heart begins to fail if we find sudden dyspnoea and intense pahi in the side, followed, some hours later, by the rejection of bloody sputum. The patient coughs up brownish or blackish viscid sputum, and not frothy blood, as m haemop- tysis. Auscultation, which is negative when the infarct is deep, reveals, in the case of a superficial uifarct, a silent or tubular area, around which subcrepitant rales are heard. Friction sounds, due to dry pleurisy or to slight effusion, may be heard. The early rales sometimes become moister and larger, while the vesicular murmur reappears ; sometimes cavernous breathing is heard when the infarct has been emptied tlu-ough the bronchi, leaving a cavity, which will finally be filled up. Li cases where some secondary uifection is grafted on the infarct, so as to produce suppiu-ation or gangrene, fever appears, and the expectoration takes special characters as regards appearance and odour. In elderly people the discovery of sudden effusion, which is preceded by pain in the side, often finds its explanation ia a latent uifarct (Vulpian). The repetition of complications and the coexistence of progressive cardiac weakness govern the prognosis. We have already shown the means of distinguishing between hsemoptysis and the bloody expectoration due to infarct ; in some cases, however, the Uifarct may give rise to true haemoptysis. The rusty sputum of pneu- monia is more viscid and aerated than that of pulmonary embolism, and again the clinical picture is quite different. Treatment. — To prevent, as far as possible, the formation of emboli every patient suffering from phlebitis should be kept in bed four or live weeks. When embolism occurs, we must treat symptoms : cupping, in- halations of oxygen, and sinapisms, (|uict the dyspnoea. The (juantity of blood brouglit up is rarely so abundant Jis to be formidable. The means recommended for hastening the absorjition of an infarct are practically futile. It is important to watch the condition of the heart, and to restore its tone by dijiitalis and caffeiu. 10—2 148 TEXT-BOOK OF MEDICINE Special and Infecting Pulmonary Embolisms. The name of special embolisms is given to the capillary obliterations due to inanimate foreign bodies, as opposed to microbic infecting em- bolisms. The first act mechanically ; the second, on the other hand, are endowed with vital properties, which cause suppuration, sloughing, and gangrene. The first group includes the debris of the fibrinous clot, broken up by disaggregation, as in old foci of phlebitis, fibrmous cysts in vems (Verneuil), and accumulations of cellular debris at a given spot (burns, frost-bite, certain intoxications). When the embolLsms occur at many points at once, they may end in death by suffocation, miless they pass mmoticed. More important are fatty embolisms, following fractures and osteo- myelitis. Dejerine thinks that the increase of the intramedullary pressure consequent upon inflammation causes the little oil-drops of the bony marrow to enter the capillaries. These embolisms cause sudden and ex- treme dyspnoea. The injured man has air-hunger ; his face and limbs are cyanosed ; he sometimes brings up blood-stained froth, and rapidly succumbs, with or without convulsions. Innumerable fatty droplets mixed with blood are found post mortem in the vessels of the lung, and some authors there- fore refer diabetic coma and suffocation in eclampsia to fat embolism. Gaseous embolisms belong rather to the domain of surgery, and usually follow the entrance of air mto the cervical veins. This accident shows itself by a characteristic whistlmg ; severe dyspnoea develops suddenly, and death usually follows. The infective microbic embolisms are daily becoming more numerous as the life-history of micro-organisms becomes better known. Some reach the lungs m the debris of clots ; others make up the embolus alone. The Streptococcus pyogenes is the most common ; then come the staphylococci, coli bacillus, and a host of other aerobic or anaerobic micro-organisms, which reproduce in situ most of their original processes. Miliary abscesses, suppurative and gangrenous infarcts, admit no other cause. This variety of embolism will be studied under gangrene of the lung. Pulmonary tuber- culosis and certam forms of pseudo-tuberculosis (tuberculosis due to Asper- gillus glaucus, fumigatus, etc.), frequently spread by the circulatory system, and can be reproduced experimentally (Renon).* The secondary cancerous nodules develojDcd in the lung are due to embolisms of cancerous origin, just as the white pulmonary infarcts of leucocytheemia are due to accumulation of hypertrophied leucocytes, and as the pigmentary embolisms of malaria are due to the arrest of pigment granules in the capillaries of the lung. * See the chapter on Aspergillary Pseudo-Tuberculosis. DISEASES OF THE LUNG 149 VIII. GANGRENE OF THE LUNG— GANGRENE OF EMBOLIC ORIGIN— GANGRENE OF AERIAL ORIGIN. We must first define the meaning of the word gangrene. Gangrene ia not simply the death of a tissue (necrosis or necrobiosis) ; it is death, with which putrefaction or fermentation is associated. This fermentation is due to anaerobic organisms (Pasteur). Gangrene, therefore, is not simply the death of a tissue ; it is the death of a tissue accompanied by putrid changes. " Sometimes gangrene pervades an already necrosed area, in which case it is secondary; at other times necrosis and putrefaction. of living tissues are caused by the same process, in which cases the gangrene is primary. Gaseous gangrene, symptomatic anthrax, noma, and some cases of pul- monary gangrene belong to the category of primary gangrenes." Two great processes are responsible for gangrene of the lung — ^gangrene of embolic origin, the germs reachmg the lung m the form of emboli by the venous channels ; and gangrene of aerial origin, the germs reaching the lung by the respiratory tract. 1. Pulmonary Gangrene of Embolic Origin. Pathology. — Whenever a purulent, putrid, or gangrenous centre exists somewhere in the economy (otitis, appendicitis, suppurative phlebitis, osteo-myelitis, etc.), this centre may give rise to specific emboli which end in the lung. Having reached the lung, the embolus provokes a like infection. If it contains germs of suppuration, the infarct suppurates ; if it contains those of putrefaction, the infarct becomes putrid ; if it carries the germs of gangrene, both these changes occur at the same time. Furthermore, puru- lent germs may sometimes start from an infected centre ; at other times, those of putrefaction and gangrene, as in the examples quoted l)elow. Let us take otitis, which I have compared to appendicitis, as it resembles the latter affection closely, in that the infection is elaborated hi a closed cavity and in the multiplicity of its complications. Whether the otitis be acute or chronic matters little ; it may at a given moment give rise to suppu- rative or gangrenous lesions. The former, such as cervical abscess, menin- gitis, abscess of the cerebellum, or of the cerebrum, will be studied later. Pulmonary gangrene consecutive to otitis will be studied here, and in order to judge of its importance I give a resume of cases. Case 1. — A young woman, who had excellent health in spile of a discharge from I lie ear for five years, wa.s seized suddenly with sharp pains in the right ear, fever, headache, and vomiting. A week later she came into hospital : prostration, severe headache on the right side, some right otorrhosa, no mastoid pain on pressure, tonguo dry, and breath ftetid. Some days later intense pain under li-ft hreast, suIk lepitant rules, high fever, acute dyspna'a, frequent cough, fa'tid sputum, albuniinuriu, and 150 TEXT-BOOK OF MEDICINE death. Post mortem several gangrenous infarcts in right Imig, and gangrenous pleurisy, with 15 ounces of fluid. The tympanic cavity, which was the starting-point of these troubles, contained a small quantity of foetid pus. Case 2. — A child, who for three years had discharge from the left ear, was suddenly taken ill with fever, mastoid pain, and vomiting. Brun opened the mastoid, and found foetid pus in the antrum. A diffuse gaseous phlegmon soon developed in the cervico-dorsal region ; breath foetid ; respiration panting ; death. Post mortem thrombo-phlebitis of left lateral sinus, and embolic gangrene of lung, both consecutive to otitis. Case 3. — Boy, affected for three years with apparently benign discharge from the right ear. High fever, with intense dyspnoea, rigors, and pain in chest, supervened. Auscultation showed mischief at right base. Pains in chest became most acute ; breath was foetid ; temperature rose to 104° F. ; death. Post mortem both lungs riddled with gangrenous centres "of various sizes and miliary abscesses consecutive to otitis. Appendicitis, like otitis (increased virulence of micro-organisms in a closed cavity), may also give rise to remote suppuration (liver, pleura, meningitis, etc.) and embolic gangrene of the lung. I shall here deal with gangrene of the lung. I saw the following case at the Hotel-Dieu : Man admitted for sharp pain at the right base. No expectoration. Signs of pneumonia found at the painful region. Temperature raised. Patient also complained of sharp pains below the right ribs in the flank and iliac fossa. Palpation gave a feeling of thickening and fluctuation. We therefore thought of an abdominal abscess, with consecutive pneumonia. Patient transferred to siu"gical ward and examined under cliloroform, but the abdominal effusion was not confiimed. Death two days later. On opening the abdomen we found a collection of foetid pus, 'with false membranes and adhesions. This collection was due to apjiendicitis. It started from the iliac fossa and tracked up below the liver, where a subphrenic pocket was found. At the base of the right lung a gangrenous centre as large as an orange. This centre was composed of two concentric layers — the outer reddish, the inner blackish, excavated, and foul- smelling. The examples above quoted give an idea of embolic gangrene of the lung. I have chosen my examples from otitis and appendicitis, but many other foci (bone lesions, bed-sores, puerperal lesions, endocarditis, etc.) may end in the same result. Pathological Anatomy.— This form corresponds to Laennec's circum- scribed gangrene, with the nearly constant addition of gangrenous pleurisy. The gangrenous centres vary from the size of a cherry-stone to that of an egg ; they are mostly present in both lungs, and are multiple ; some are superficial and sub pleural ; others are deep-seated. The subpleural centres have the conical shape of infarcts and a haemorrhagic tint. An arteriole is usually seen at the apex of the cone. The deep centres have the shape of blackish nodes, distinct from one another. Gangrenous infarcts show the following forms : " Small, firm infarcts, which appear to be quite recent, show on section a yellowish caseous nodule, purulent and ex- tremely foetid, in the centre of a brownish or greenish tissue engorged DISEASES OF THE LUNG 151 with blood. The older infarcts have in their centre softened inaterial of a chocolate-brown, surrounded by a scalloped collarette. Beneath the pleura, infarcts with a liquefied centre are found. The pleura is raised by- gaseous, foul-smelling bullae, forming little caverns, which do not appear to communicate with the bronchi. At its entrance into the infarct the arteriole is filled with blood and with bacteria in enormous numbers. At the centre of the infarct it has necrosed, and its wall is reduced to a shred. The bronchiole which accompanies it is flattened and full of desquamated cells and leuco- cytes (Guillemot). The gangrenous cavity contains a greyish pulp, composed of the following "elements : pus corpuscles, large cells infiltrated with fatty granules, masses composed of threads of connective or of elastic tissue and debris of capillaries, pigmentary granules, crystals of margarine, leucin, tyrosin, and various micro-organisms. All these elements are found in the sputum. The cavity is surrounded by a first layer, which serves as a wall and limits the loss of substance. This layer is made up of debris of lung tissue, elastic fibres, and obliterated vessels, which are continuous with the next layer. The second layer is formed of lung tissue in the condition of grey hepatization. It is friable and sanious ; the alveoli are filled with pus and large fatty cells, and the vessels are blocked by coagulated fibrin. The third layer, which is continuous with the healthy part of the lung, shows the lesions of catarrhal pneumonia. 2. Pulmonary Gangrene of Aerial Origin. Gangrene of aerial origin corresponds to the difluse form. It presents much the same changes as the circumscribed form, save that they are diffused and very extensive. In certain cases the well-marked nodules of circumscribed gangrene and the irregular lesions of the diffuse form are found together. Gangrene of the lung (circumscribed or diffuse) Is, as a rule, accompanied by pleurisy, which may be gangrenous, purulent, or sero-fibrinous. Pneumo- thorax Is not rare ; it may result from perforation or from putrefaction. Lastly, particles of sloughs may pass through the pulmonary vems into the left heart and the general arterial circulation, and set up lesions due to capillary oinbolisms. Pathogenesis.— Pulmonary gangrene of aerial origin may depend on various mechanisms. Since the cavity of the bronchi, bronchioles, and alveoli are, as it were, the prolongation of the bucco-pharyngeal cavity, it Is clear that microbes inhabiting this latter cavity may gradually reach and develop in regions when^ Ihoy do not normally exist. For their growth, however, the soil must be prepared ; the individual must be in a state of receptivity. 152 TEXT-BOOK OF MEDICINE For this reason this gangrene Ls not usually seen in robust people ; on the other hand, it is frequent in alcoholics, diabetics, and in sufferers from Bright's disease, malaria, mental disease, or chronic cerebral affections. It is sometimes met with in the course of acute infectious diseases — measles, variola, typhoid fever, etc. — or in subjects exposed to intense and pro- longed chill (Bucquoy). In other cases it may supervene as a complication in the course of various lesions of the respiratory tract — cavities of phthisis, cancer and sarcoma of the lung, chronic pneumonia, hydatid cysts, foreign bodies in the air -passages, perforation of the lung in chest wounds, foreign bodies carried in through such a wound (bullets, shreds of clothing, fragments of rib) ; opening of an abscess into the bronchi from the liver, spleen, kidney, etc. ; perforation of the oesophagus in cancer, whether spontaneous or due to forcible catheteri- zation. All the gangrenous or suppurative affections of the bucco-pharyngeal cavity — noma, diphtheria, bucco-pharyngeal abscess, laryngeal necrosis, operations ujDon the mouth and throat, removal of lingual cancer — may cause gangrene of the lung. It is probable in the latter cases that the obstruction to swallowing explains the entrance of infected particles mto the respiratory passages, an accident also seen in lunatics, patients suffering from labio- glosso-laryngeal and diphtheritic paralyses. A pulmonary infarct, resulting from non-infective embolism, may be invaded secondarily by micro-organisms. As regards lobar pneumonia, although gangrene is an exceptional ter- mination, and even denied by Laennec, yet some cases are found (Grisolle, Andral, Bouillaud, Lanceraux). Gangrene ls more frequent in lobular pneumonia ; but why tn any given case does the infection of the lung tissue end in gangrene ? To answer this question the patient's general condition has been called in question. It is said that in the insane, diabetics, and alcoholics the infectious process, instead of tending to resolution, finds in the general state of the subject, or perhaps in the then existing constitution (Graves, Leudet), a reason for ending in necrosis and putrefaction of tissue. On this account an individual already weakened by typhoid fever, or suffering from an eruptive fever (scarlatina, measles, variola), would run a risk of the pulmonary inflammation ending in gangrene. Syphilis sometimes determmes gangrene of the lung. Lastly, in certain cases a part must be assigned to overcrowding and to contagion, especially in hospital wards. Bacteriology. — The microbic origin of this affection was foreseen as early as 1849 by Virchow, but it is chiefly to Leyden and Jaffe that we are indebted for the first serious work on this subject. Without attributing to the Leptothrix pidmonalis — a microbe derived from the Leptothrix huccalis— DISEASES OF THE LUNG 153 as great an importance as tliese authors would do, we cannot hesitate to recognize that this micro-organism exists in most of the foci of gangrene, either alone or in association with the Monas lens, Cercomonas (Kannen- berg), Proteus vulgaris, Micrococcus tetragenus, and many other aerobic and anaerobic microbes. We may note the Bacillus ramosus (Veillon and Zuber), the Bacillus fragilis (Veillon and Zuber), and the Micrococcus fcetidus. " Upon the whole, in the centres of gangrene the aerobic flora is chiefly and sometimes uniquely represented by an almost constant species of streptococcus. In all cases this flora is less numerous than the anaerobic one. It may, indeed, be completely absent. The anaerobic species are, on the contrary, represented by various and very numerous kinds " (Guillemot). Symptoms.— Gangrene of the lung is sometimes ushered in by special symptoms, such as extreme rise of temperature, acuteness of thoracic pain, and adynamia ; but in other cases no hint may be given of the imminence of gangrene. I have seen two cases in which the course of events was as follows : An individual is taken ill with chills, nausea, and vomiting ; cough, dyspnoea, and pain are next added to the gastric symptoms. Auscultation shows slight pleural rub, scattered rales, and tubular breathing, due to pulmonary congestion or to broncho-pneumonia. The fever is moderate, and the general condition without special significance. At the commence- ment the disease simulates an ill-defined infection, but the Issue is not long in coming. The patient Is seized with dyspnoea and fits of coughing, and if there is a communication between the gangrenous centre and a bronchus (this is more rare in the case of embolic than of aerial gangrene), he brings up abundant blackish sputum, which Is mixed with blood and extremely foetid. It is then evident that a gangrenous focus has formed in the lung, and has just opened into a bronchus. As soon as the communication between the bronchus and the centre occurs, the expectoration and the breath become horribly foetid, and haemoptysis Is not uncommon. The sputum is very abundant, diffluent, greeuisli, or blackish ; it contains blood, pus, mucus, fat, crystals of mar- garine, elastic fibres, balls of filaments, and micro-organisms. When the expectoration Is abundant, if collected in a measure-glass, it usually presents three distinct layers. The top Is frothy and muco- j)urul(int ; the middle one, transparent and viscid, appears to be composed of thickened saliva ; lastly, at the bottom of the sputum-glass we find yellowish or greenish balls, giving off an offensive odour, and constituting what are usually called Dittrich's plugs. According to Charcot, foetor of the breath may be lacking in diabetic gangrene ; this feature is not absolute. When a gangrenous cavity forms, ])rovided it is superficial or of suflirioiit extent, auscultation yields the signs of a cavity — namely, cavernous breath- ing, gurgling, and pectoriloquy. Gangrene of the pleura, which beguis with 154 TEXT-BOOK OF MEDICINE intense pain in the side, acute dyspnoea, and the signs of effusion, is often associated with gangrene of the hmg. This aspect of the question will be studied under Putrid and Gangrenous Pleurisy. The existence of pneumothorax (by perforation or by putrefaction) is sometimes recognized. The general symptoms are usually marked — high fever, repeated chills, an earthy tint, loss of appetite, diarrhoea, and rapid wasting. Death usually ensues in gangrene of the lung. Kecovery may, however, take place, especially in the circumscribed form, either spontaneously or after operation. The diagnosis of gangrene from bronchiectasis has been already de- scribed. Gangrene should not be confused with foetid bronchitis, where the mucous membrane alone is attacked. Foetid bronchitis has special symptoms. In a person who suffers from bronchial catarrh the breath and expectoration become at certain times terribly foetid; but these troubles are transitory, intermittent, and perfectly curable, and auscultation shows the signs of bronchitis, not those of a gangrenous cavity. The mouth must be examined to make sure that the foetor of the breath is not due to some local affection, such as dental caries, ulcero- membranous stomatitis, gangrene of the tonsils, etc. The treatment of gangrene of the lung is very limited. The chief point is to support the patient's strength by means of tonics, quinine, wine, and alcohol. Creosote, balsams, hyposulphite of soda (Lanceraux) also find their indications. The patient should breathe an atmosphere loaded with the fumes of tar, and should be made to use sprays of carbolic acid. The gangrenous focus should be opened up, when it is clearly limited and superficial. Cases of pneumotomy have been followed by recovery, but successes are rare, judging from the cases which I have seen. IX. BRONCHO-PULMONARY HiEMORRHAGE— HEMOPTYSIS. I shall describe in the same chapter haemorrhages from the bronchi and from the lung. Haemorrhage from the surface of the bronchi is called bronchorrhagia ; that which occurs in the lung tissue itself — that is, in the alveolar cavities — takes the name of pneumorrhagia. This distinction is most often artificial. The term pulmonary apoplexy, which, by an abuse of language, was, and is still, used to designate haemorrhage of the lung, should be abandoned.* Spitting of blood after broncho-pulmonary haemor- * The term pulmonary apoplexy was created by Latour in 1815, and adopted by Laennec. This abuse of language was due to Rochoux, who in his wi'itings on cerebral haemorrhage had made wrong use of the term apoplexy, and employed it as synonymous with haemorrhage. Several authors have protested against this faulty term — for example, Gendrin, who coined the word pneumo-haemorrhage, and Trousseau, who called this lesion infiltration of blood. DISEASES OF THE LUNG 155 rhage, or hSBmoptysis, is only a symptom which serves to designate the rejection of blood which comes from the respiratory passages, just as hajma- temesis designates the vomiting of blood which comes from the digestive tract. etiology. — Bronchial haemorrhage (bronchorrhagia) is caused by con- gestion (strains, chills, hysteria). It is sometimes supplementary to a flux, or to an habitual haemorrhage (menstruation, haemorrhoids), and it is very often associated with pulmonary tuberculosis. According to circumstances, haemoptysis precedes or accompanies the hatching of tubercles ; later, it may be due to rupture of small aneurysms in the cavities. Bronchial haemorrhage may be associated with enlargement of the arterioles which accompanies bronchiectasis ; it very frequently accompanies the growth of hydatid cysts in the lung. Under interlobar plem-isy we shall see the cause of " interlobar haemoptysis." Haemophilia and purpura are sometimes accompanied by haemoptysis. Pulmonary haemorrhage (pneumorrhagia) is often passive (blood stasis), and due to diseases of the heart (especially mitral lesions). The occurrence of haemorrhage in heart affections has been variously inter- preted.* Some invoke the mechanical obstruction to the pulmonary circu- lation by the lesions at the mitral orifice ; others add to this cause the frequent hypertrophy of the right ventricle and the changes in the capillaries of the lung. A more recent theory attributes the haemorrhage to an em- bolism which, starting from clots in the right auricle, reaches the small branches of the pulmonary artery, and, after the fashion of capillary embolisms, provokes a haemorrhagic infarct. The eruptive fevers (black small-pox), icterus gravis, etc., provoke haemorrhage which appears to be connected with the alteration in the capillaries and a pathological state of the blood, named, for want of a better term, " state of dissolution." The causes of the haemorrhage associated with Bright's disease are ill understood. In the new-born, pulmonary haemorrhages connected with sclerema are seen (Hervieux). In some cases it is dilhcult to differentiate the origin of one haemorrhage from another : for example : the haemorrhages consecutive to broncho-pul- monary lithiasis, syphilis, hydatids of the lung, gangrene, cancer, inter- lo])ar pleurisy, etc. Pathological Anatomy. — The changes in bronchial haemorrhage are superficial ; the mucosa of the bronchi may be anaemic or congested, and coagula may be present in the lironchi. The lesions of pulmonary haMUorrhage are more important. If the haemorrhage, takes place by rupture, which is rare, the blood tears the lung * Athcromatoiis changos cannot bo accused in this case, as they arc cxtrciiicjy rare in (he pulnumary vessels (Roki(an.sky). 156 TEXT-BOOK OF MEDICINE tissue, collects in a diffuse fOCUS, as in the brain, and may burst into the pleural cavity. As a rule, however, the haemorrhage proceeds in a different way. The blood infiltrates the alveoli and the parenchyma without much destruction, and the infiltration takes the form of conical nodules, which show a centrally directed apex, recalling the distribution of the bronchi and vessels. These hsemoptoic infarcts, which vary in size and number, are clearly circum- scribed and deeply situated, as a rule, in the lower lobes. The cut section of the nodules is blackish and granular, like the hepatization in pneumonia, on account of the fibrinous coagula which make the infundibula prominent. The bronchi and the pulmonary vessels of the area near the infarct are obliterated by clots. The hsemoptoic nodule may undergo or provoke the following changes : It becomes indurated and retains its pigmentation ; it passes into fatty degeneration ; it causes secondary pneumonia at its peri- phery, or provokes limited gangrene. When it is subjacent to the pleura, it causes partial pleurisy. Symptoms. — The chief symptom in bronchial haemorrhage is haemop- tysis. When the haemorrhage is violent, the blood pours out of the nose and mouth ; it may also flow into the stomach, whence it is rejected by haematemesis. As a rule, the haemoptysis is more moderate, and the patient coughs up bright, frothy blood, which in the spittoon has the appearance " of the foam produced in a basin when an animal is bled " (Trousseau). It may cease in a quarter of an hour or half an hour, and recur some hours later, next day, or on succeeding days. The last sputum coughed up has not this frothy and bright red appearance, but is black and viscid. It is the remnant of the haemorrhage which has remamed longer in the bronchi. Haemoptysis is sometimes sudden, and the patient is as much surprised as scared by his spitting of blood. Sometimes it is preceded by a feeling of warmth m the chest and throat ; at other times it is preceded or ushered in by epistaxis. When supplementary to the menstrual flow, it is periodic, like the haemorrhage which it replaces. Bronchorrhagia has no physical signs. I am, of course, referring to signs directly related to the haemorrhage, and not "to those of the lesions which have caused the bleeding. When the haemorrhage is pulmonary, especially in cardiac cases, the clinical picture is very different. The blood which has infiltrated the lung tissue has not the same tendency to burst into the respiratory channels. Haemop- tysis is not, as in the preceding case, the chief symptom, but is often absent, and its characters distinguish it from haemoptysis in tuberculosis. The sputum in pneumorrhagia is neither bright red nor aerated ; it is blackish, viscid, and more or less mixed with mucus. The quantity of blood brought DISEASES OF THE LUNG 157 up is much less abundant than in bronchorrhagia. The hgemoptysis may last from ten to twenty days, and Grisolle considered this persistence as one of the best diagnostic signs. The differential signs are, however, not absolute, since the blood of bronchorrhagia, if it has remained long in the bro2ichi, may resemble that of pneumorrhagia. When the bleeding is abmidant or persistent, the patient presents the usual symptoms of great haemorrhage : pallor of the face, small pulse, tendency to syncope and to dyspnoea, which is proportionate to the extent of the lesion. If the nodules of j)neumorrhagia are large and superficial, percussion reveals dullness, and auscultation yields blowmg breathing and bronchophony. Broncho-pneumonia consecutive to pulmonary haemor- rhage is rare. Gangrene and perforation of the pleura are almost always fatal. Diagnosis. — The diagnosis of broncho-pulmonary haemorrhage has only one certain sign — that is, haemoptysis. Given haemoptysis, it is necessary to distinguish it from other haemorrhages (epistaxls, stomatorrhagia, haema- temesLs) which somewhat resemble it. We must, therefore, trace the cause, and for this purpose we inquire into the characters of the blood coughed up, the symptoms accompanying it, and the circumstances in which it super- vened. The larynx, the aorta, the' lungs, and the heart are subjected to a mmute examination. Cancers of the larynx sometimes provoke profuse h93moptysis. Aneurysms of the aorta may open into the trachea or into the bronchi, and cause sudden death from haemoptysis, or only slight bleeding, which recurs for several consecutive days or weeks. These cases are exceptional, but still they must be recognized, for both prognosis and diagnosis are involved. Spitting of blood, arising as a supplementary haemorrhage, must not be taken for haemoptysis of tubercular origin ; nor must we forget that hysterical patients have congestion and haemoptysis, which has nothing in common with tuberculosis. The diagnosis between the haemoptysis of pulmonary (tuberculosis) and that of cardiac origin (mitral lesion) is often made easy by the different characters of the blood and by the existence of the respective lesions in the lung or in the heart ; but the matter is not always so simple, and haemoptysis may appear as an early sign before the organic lesions are j^erceptible by our means of investigation. Furthermore, the distinctive characters of the bloody sputum are not absolutely rigid. Haemoptysis which has the appear- ance of a bronchorrliagia has, nevertheless, been caused by heart disease, as Trousseau has clearly shown. The diagnosis as to the nature of haemoptysis has been greatly simplified since the discovery of the tubercle bacilhis. Careful and repeated ex- amination of the sputum or of the blood in lucmoptysii in performed, and 158 TEXT- BOOK OF MEDICINE the presence of the bacillus sometimes allows us to state that the lesion is tuberculous. Although there is not absolute agreement between broncho-puhnonary haemorrhage and haemoptysis, it is difficult clinically to separate them, and the gravity of the prognosis often betrays itself by the persistence or the abundance of the haemoptysis. Fulminating haemoptysis is caused by the opening of an aortic aneurysm uito the trachea or hito the bronchi, or by the rupture of a small aneurysm in a tuberculous cavity (Kasmussen's aneurysm). Febrile haemoptysis m tuberculous patients is more grave than the apyretic form. The gravity of the prognosis depends also on the causes (pulmonary or cardiac lesions) which have produced the haemorrhage. Treatment. — Bronchial is more accessible to treatment than pulmonary haemorrhage. The initial haemoptysis of tuberculosis may be arrested by an emetic : Ipecacuanha . . . . . . . . . . gr. xv. Tartrate of antimony . . . . . . . . gr. ss. Give at once, as soon as the patient is seized with haemoptysis. The expectoration of blood is sometimes arrested before the complete effect of the emetic. Ipecacuanha may then be admmistered f grain every half-hour, or every hour. Good results are obtained with a mixture of perchloride of iron in a dose of 30 grains in 4 ounces of water. Iced and acid druiks are given, and a draught of the following compo- sition is prescribed : Distilled water . . . . . . . . . , §iv. Syrup of rhatany . . . . . . . . . . si. Rabel water . . . . . . . . . . . . 5ss. A tablespoonful to be taken every four hours. Pills of extract of thebaine, ^ gram in each, may be given nourly — from 4 to 10 pills in the twenty-four hours. Subcutaneous injections of ergotin may be used. Chloride of calcium, in drachm doses, may be prescribed. An ice-bag is kept in situ on the chest. Blisters applied to the thorax or to the actual seat of the congestion, revulsives to the lower limbs, dry-cupping and sinapisms, may also be employed. This treatment will be considered in detail in the chapter on Pulmonary Tuberculosis. Digitalis finds its indications in haemoptysis of cardiac origin. DISEASES OF THE LUNG 159 X. PULMONARY EMPHYSEMA. Definition. — Tlie name emphysema is given to the exaggerated dilatation ot the pulmonary tissue by air. When emphysema is limited to the alveoli or the lobules, it is said to be alveolar or intralobular ; but when the lobule is ruptured, and the air invades the interstitial tiasue of the lung, the emphy- sema is interlobular. Pathological Anatomy and Mechanism. — On opening the thorax, the lungs apjjear distended, and have but little tendency to collapse. The affected parts are greyish- white, crepitate a little, and have a downy feel- ing to the touch (Laennec). Emphysema usually involves the aj)ices and the anterior edges of the lungs. Spherical projections of different sizes, due to the emphysematous enlargements oi the infundibula, are seen on the surface. The vessels of these parts are for the most part obliterated, and the circulation is deficient, while it is increased in the neighbouring parts, which become the seat of oedematous congestion. On microscopical ex- amination of sections from an emphysematous lung which has been pre- viously inflated and dried, the alveolar walls are often found to be atrophied and perforated. The atrophy of the septa and of the elastic tissue permits dilatation of the alveoli and of the lobules. The dilatation is at first limited to some alveoli or to an infundibulum ; later, as the lesion spreads, the infundibula communicate with one another, and the dilatations, which are at first as large as millet-seeds, finally exceed a nut in size. In old people the apex of the lung is thus transformed into a lacunar tissue, in which the air circulates freely. How are the perforation of the septa and the communication between the infundibula brought about ? " Under a still unknown influence." The thinned septa are transformed ; in tlieii interior and on their surface they present ovoid masses of fatty granulations, which may come from the alveolar pavement epithelium or perhaps from the capillary vessels, and it is probable that this granular degeneration plays a large part in the perforations of the wall of the alveoli. The mechanism by which emphysema is produced has been varioursly explauied. Two orders of causes are admitted — mechanica'i ana trophic. Sudden efforts of expiration, the fits of whooping-cough, the cough of croup and of broncho-[)ncumoiiia, dilate the alveoli to excess, and produce acute emphysema. It is therefore not surprising that the same causes if often n^pcatod (usthma, chronic bronchitis), eventually cause emphysema by mechanical means. In other cases — in the aged, for example — faults in the nutrition of the lobule, atrophy and perforation of the alveoli, coincide 80 closely with the spread of emphysema that they appear to be the principal cause. It is therefore dilfirjult to say exactly what part corresponds to 160 TEXT-BOOK OF MEDICINE mechanical and what to trophic action, in the production of emphysema. In a good many cases this double process seems to exist. It is perhaps favoured by some special tendency of the lung tissue (heredity). Rupture of the emphysematous vesicles is a grave complication. If the perforation involves the pleural cavity, pneumothorax results. If the rupture occurs under the visceral layer of the pleura, or in the interstitial tissue of the lung (interlobular emphysema), the air travels along the con- nective tissue, reaches the mediastinum, and invades the subcutaneous tissue of the neck, the thorax, and other regions. Symptoms. — The shape of the thorax is peculiar. The chest is rounded and bulging in the clavicular regions, and when the emphysema is very ex- tensive, the intercostal spaces appear dilated, and the chest is enlarged at its base. In the affected regions percussion gives a more ringing sound than in health. This resonance may encroach upon regions which are usually dull, so that the area of cardiac dullness is replaced by hyperresonance. On auscultation, the vesicular murmur is feeble, the respiration has a harsh tone, inspiration is shortened, and expiration is prolonged. The obliteration of vessels produces blood stasis, which may extend to the right ventricle. Dilatation of the ventricle and tricuspid incompetence sometimes follow, and troubles m the cardio-pulmonary circulation may come on and increase the obstruction to respiration. The emphysematous patient has many reasons for his difficulty in breathing. The rarefaction of the lung tissue, the depression of the diapliragm by exaggerated distension of the lungs, the insufficiency of expiration, and the diminution in the field of haematosis, lower the respiratory capacity by 50 per cent., or even more, as shown by spirometry. Besides the continuous dyspnoea which is the result of the emphysema, we must also note attacks of suffocation, which often supervene, and are due to the various diseases, such as asthma, pulmonary congestion, or mitral lesions, that are so often associated with emphysema (Woillez). These various types of dyspnoea also exist when emphysema is associated with tuberculosis. The diagnosis is easy, but we must not forget that emphysema, instead of constituting the whole disease, is often only an episode in the course of another malady (asthma, tuberculosis, chronic bronchitis), which must also be diagnosed. Treatment. — The therapeutic indications are chiefly directed to the diseases which have produced the emphysema. As for the emphysematous lesions themselves, we have but little influence over them. Inhalations of oxygen and baths of compressed air are, however, generally recommended. DISEASES OF THE LUNG 161 XI. (EDEMA OF THE LUNG— SUPERACUTE OEDEMA IN BRIGHT'S DISEASE. (Edema of the lung is due to the transudation of blood-serum into the alveoli and the interstitial tissue of the lung. Congestion is sometimes present as well, and plays a more or less important part. In cases due to nephritis the oedema far outweighs the congestion, while in cases due to cardiac lesioas the congestion has the same importance as the oedema, and the lesion is called " congestive oedema," oi " cedematous congestion of the lung." On anatomical examination of the cedematous lung, congestion and atelectasis are found in association with oedema. The lung is heavy, and does not float. On section, abundant frothy, clear fluid exudes when oedema alone is the cause, but red-tinted when congestion is also present. Many causes provoke oedema of the lung. It may arise suddenly, following thoracentesis, when the operator has made the mistake of with- drawing a large quantity of fluid too rapidly or too completely. The opera- tion is scarcely finished when the patient is seized with suffocation, angina, and fits of coughing, and brings up a^rosy, albuminous, frothy liquid, which is the result of superacute oedema. It is fortunate if this terrible accident does not end in death. Congestive oedema of the lung is seen fairly frequently in the course of diseases of the heart, and during periods of asystole. Many persons suffering from ill-compensated mitral lesions are seized with dyspnoea, due to blood- stasis, elevation of the pulmonary tension, and resulting oedema. This con- gestive oedema chiefly occurs at the bases of the lungs. On auscultation, numerous fine moist rales are heard ; tubular breathing is heard if pleural effusion accompany the oedema. In certain cardiac cases congestive oedema of the lung exists, to the exclusion of lesions in other organs. The lung, which is the first to receive the recoil of the circulatory embarrassment, becomes congested, oedema appears, and dyspnoea is the first indication of the cardiac lesion. In other cardiac cases the oedema is associated with congestion of the liver (cardiac liver), of the kidney (cardiac kidney), or with oedema of the extremities — in short, it forms part of the asystolic syndrome. Appro- priate treatment may give good results, as we shall see in the chapter on Diseases of the Heart. Influenza (Teissier, Rendu) and aortic lesions (Huchard) may lead to OL'dema of the lung, but the chief cause is nephritis,* either acute or chronic. * SiipcracuUi (rdeiiiii of tlic liint^ may .suiMTvcno in tlio courso of iinyiiaiiry- Vinay (Li/on Mcdiad. IS!)7), whu ha-s Btudiid this complication, rightly cunsicK-LS it due lo ni'i^hritis gravidarum. u 162 TEXT-BOOK OF MEDICINE GEdema of the Lung in Bright's Disease : Slow Form— Acute Form— Superaeute Form. ffidema of the lung is very frequent in the course of acute and chronic neplu-itis. In many cases of acute scarlatinal or of early syphilitic nephritis, or nephritis a frigore, oedema of the lungs may be associated with dropsy of other parts. Sometimes the oedema affects the bronchi rather than the lungs, and is the old "albuminuric bronchitis of Lasegue"; at other titnes the lungs are oedematous, especially at the bases, and auscultation records a multitude of fine rales. Oldema as slight as this scarcely merits the name of a complication ; it forms part of the general dropsy, hampers the breath- ing, and brings on dyspnoea, but does not occupy the chief place in the course of the acute nephritis. The matter is very different in generalized oedema of the lung, and especially in the superacute from, which is a complication as sudden as it is terrible. The same remarks apply to oedema of the lung in chronic nephritis. In a dyspnoeic patient with Bright's disease we often hear at the bases the sub- crepitant rales of pulmonary congestion, which remains stationary for weeks and months. The patient who has attacks of dyspnoea and believes himself asthmatic is sometimes the victim of an error in diagnosis, and goes the round of the thermal cures in his search for the best treatment. In such a case the oedema is not of the first importance ; it is more or less extensive, more or less obstinate, takes its share in the respiratory embarrassment, but does not focus all the attention upon itself. It Is very different in the other variety of oedema— superacute pulmonary oedema— which may burst forth suddenly in the course of chronic nephritis, or more rarely in the com-se of the acute disease, and in a few hours endanger life. It is on this superacute oedema, then, that we shall fbc our attention. The following case gives an exact idea of it : A man of forty-five was seized with such acute distress that he was brought to hospital at once.* On admission, death appeared imminent : pale face, duU eyes, livid lips, bluish fingers and nails, hurried breathing, WTetched pulse — such was the con- dition of the moribimd patient. Any interrogation was impossible. The heart could not be examined, but both lungs were full of fine subcrepitant rales. At fu-st sight the condition recalled capillary bronchitis, suffocative catarrh, or acute phthisis. The diagnosis, although difficult, was not unpracticable. He brought up abundant frothy sputum, of a rosy colour. The eyelids were puffy, the legs slightly oedematous ; the temperature was subnormal, and the urine very albuminous. The o?dema and albuminuria pointed to nephi'itis ; the characteristic expectoration and the fine rales in the lungs indicated superacute oedema. The treatment was obvious. Charrier cupped the patient, and di-ew off 10 ounces * This case is taken from my lecture on Superacute CEdema of the Limg in Bright's Disease, in which I have quoted a large number of cases {Clinique Mcdicah de V Hotel- Dieu, 1897, p. 23). DISEASES OF THE LUNG 163 of blood. The effect was immediate. In less than an hour the breathing was easier, the expectoration was less profuse, the fine rales disappeared from the upper parts of the lungs, and death was averted. Strict milk diet and lactosed diinks were prescribed, and 5 teaspoonfuls of Trousseau's diuretic wine were given daily. Next day the breathing was easy, the temperature normal. The heart was ex- amined, and Ave heard a shglit bruit de galop. Rilles were no longer audible in the lungs except at the bases. The kidneys commenced to act ; and the urine, though almost supijressed the day before, amounted to 8 ounces, but was markedly albuminous. Two days later the patient was able to give us a complete history. He told us that for some time his health had been faulty, and he had suffered from pollakiuria, cramps in the calves, dead fingers, cedema of the eyelids and of the malleoh. Treatment produced rapid improvement. In a few days the situation had totally changed. Respiration became regular, except that some rales persisted at the bases of the lungs. The puffiness of the face and the cedema of the legs had completely disappeared, and the urine amounted to 50 ounces, although albumin wa^ still present and the depuration was imperfect, for the toxicity of the mine, as experimentally determined, was far from reaching its normal value. Symptoms. — The first point of importance is the suddenness of this cedema. Reference to the cases which I have collected shows that super- acute oedema does not, as a rule, result from bronchitis or some pulmonary condition which has gradually become more severe. The onset is nearly always sudden and unexpected ; the unforeseen accident comes on by day or by night. One patient was seized with superacute cedema while I was asking him questions, and on auscultation, I felt, so to say, the rising of the liquid in his chest. The same sudden onset occurred m tlu:ee of Girau- deau's patients. His first patient was seized while fast asleep, just as an attack of asthma comes on, although on the previous day she was quite well. Hls second patient was taken ill quite as suddenly in the night with superacute oedema dui-ing a period of apparently good health. The same remark applied to his third patient, who was stricken down two hours after dinner, although there was no premonition of such an accident. A sunilar thhig happened to Bouveret's patients. In one of them superacute oedema appeared suddenly, and death resulted ; in the other a first attack of cedema supervened, it is true, after a walk of tliree miles, but the two other attacks appeared without appreciable caiLse, when the patient was at rest. I do not say, of course, that events always have this course. In some cases superacute cedema is preceded by such prodromata as cough, dyspnoea, or rales. In such a case it seems that the soil is prepared ; it was so in my first case and in one of Giraudeau's cases. It is, however, an exception. Superacute oedema of the lung in Bright's disease is hardly ever the result of pro-oxistiug broncho-fjuimonary lesions. It bursts out suddenly, like an attack of asthma, all hough some hours previously no sus[)icion has been entertained. A second point is that superacute oedema of the lung is very often an isolated result uf Bright's disease, for, paradoxical as this may ap[)e;ir, it 11—2 164 TEXT-BOOK OF MEDICINE is hardly ever associated with the severe manifestations of uraemia, or with the marked oedema of Bright' s disease. Without knowledge on this point, it would appear that superacute oedema ought to supervene in the patient who is suffering from anasarca. This may be so, especially in acute nephritis. Giraudeau's patient was seized with superacute oedema of the lung in the course of acute nephritis with .anasarca. This, however, is a rare occurrence. Nearly all the cases which I have collected show that the mischief appeared as an isolated accident in the course of latent nephritis. It cannot be said, however, that this oedema attacks persons in perfect health. Close examination will show that they are more or less tainted with Brjghtism. If the " minor complications of Brightism " be carefully looked for, the evolution of an insidious nepliritis may be constructed. A group of symptoms, such as the sensation of dead fingers, cryaesthesia, auditory troubles, cramps in the calves, pollakiuria, itching, electric shocks, and epistaxis, will be found in their past history. We shall see that they were not exempt from such a trace of oedema as puffiness of the eyelids and of the alveoli. We shall find that their arterial tension is high, their tem- poral arteries are tortuous, the second sound accentuated, and a gallop rhythm is present. We shall find that these patients were subject to headache, which they styled migraine ; to suffocation, which they took for asthma ; and to colds, which they regarded as due to ordinary bronchitis. If their urine is analyzed, albumin will be found ; on testing the toxicity, it will be low. We shall find, in short, by a,n attentive and searching examination of this con- dition — which for a long time I have named Brightism — that the patient whose health appears to have been fairly good has in reality been suffering from mischief in his kidneys ; the urinary depuration has been affected, and he has been exposed to the risk of complications which gave more or less warning. After this digression as to the onset, let us resume our clinical analysis of the symptoms. The attack commences with a tickling in the larynx, jerky cough, and distress, which reaches its limit in some minutes, or perhaps some hours. These symptoms are due to sudden blocking of the pulmonary alveoli by sero-albuminous fluid. As a rule, the inundation begins in the bases, and may affect the whole of the lungs more or less rapidly. As the blood-serum transudes into the alveoli and the bronchioles under pressure, the patient is at once seized with fits of coughing, and then brings up the characteristic fluid, which is frothy and rose-coloured. Some patients may bring up as much as 2 or 3 pints in a few hours, or even more. It may be that the bronchi have not the power of expelling the fluid which has thus accumulated, and the asphyxia varies in indirect ratio to the amount of expectoration. As soon as dyspnoea appears, innumerable fine subcrepitant and sibi- lant rales can be heard over both sides of the chest, testifying to the 1 DISEASES OF THE LUNG 165 inundation of the alveoli and of the bronchioles. According to the rapidity and the extension of this inundation, the rales invade the whole, or nearly the whole, of the lungs. In proportion as the inundation increases, and if the expectoration is ever so slightly insufficient, dyspnoea increases rapidly ; the patient is pale, alarmed, and conscious of his extreme danger ; the pulse is small and quick, the lips are bluish, the nails livid, the limbs cold ; and the struggle may in a few moments end in death (fulminant forni), in a day (rapid form), or in three or four days (slow form). In some patients the condition is not absolutely perilous, so long as the sufferer can empty the inundated lungs. Paresis of the expulsive muscles may supervene, expectoration may be quite absent, and death from asphyxia occurs at short notice. In favourable cases the fluid is coughed up as soon as it forms, the inundation Ls arrested in time, and after a duration which varies from some hours to some days, the dyspnoea improves, the rales diminish, and the patient wins the struggle. We must, however, not be too sanguine, for the danger, though averted for a moment, may some hours or some days later recur and prove fatal. Sometimes convalescence requires several days ; at other times recovery comes on suddenly, and the patient is able to resume work on the next day. Superacute oedema of the lung in Bright's disease is made worse by the fact that not only may the patient succumb to an attack in a few hours, but that, although liLs lungs have recovered, he remains liable to fresh attacks. Several patients have had two or three repetitions of superacute oedema, months or years apart. Giraudeau's first case had three attacks in two years, and Bouveret's second case had three attacks in six months. Diagnosis. — The diagnosis of superacute oedema of the lung in Bright's disease follows from the description which has just been given. A patient with Bright's disease may have severe attacks of dyspnoea, but in this case it is a question of uraemic dyspnoea, which often exhibits the Cheyne Stokes type. It differs from that of pulmonary oedema in that we do not find rales and the characteristic sputum. Dyspnoea of toxic origin may, however, be combined with that due to oedema. We see a patient who is a prey to the most acute dyspnoea, but it is a case of genuine asthma, and the diagnosis will be easy. The number of respirations is not increased, but rather diminished. Everything points to spasmodic dyspnoea ; inspiration is painful, expiration whistling and very prolonged. The prominent fact on auscultation is not the innumerable rales of j)ulinonary rjedema, but the association of rales with signs of acute eni[)]iyKema. Expectoration is a})sent, or composed of shreddy, mucous, or pearly sputum, and in any case the frothy, albuminous, rosy expectoration of superacute oedema is not found. Prognosis and treatment are (piite 166 TEXT-BOOK OF MEDICINE different, for the attack of asthma is never grave, and blood-letting is unnecessary. I cannot review all the varieties of dyspnoea which may resemble that of superacute oedema. Such are the severe cases of dyspncea in suffocative catarrh, acute phthisis, cardiac asthma, and angina pectoris. Let us not forget that we can always make a correct diagnosis in superacute oedema from the following symptoms : Sudden onset of the dyspnoea ; fine rales over a large area of, or the whole:, chest ; incessant cough ; abundant frothy, albuminous, rosy expectoration ; frequent oedema of the face or of the legs ; albuminuria ; and previous symptoms of Brightism. Pathological Anatomy. — In a case reported by Bouveret both lungs, from base to apex, were oodematous. The fluid literally streamed out on cutting and squeezing a lobe between the fingers. The bronchi were full of the same frothy rose-coloured fluid. The kidneys were small, granular, and cystic. The heart was enormous, the aorta much dilated, but not atheromatous ; the sigmoid valves were healthy. The coronary arteries presented yellow patches of endarteritis. In Huchard's case nephritis was found post mortem, with small granular kidneys, weighing together 5| ounces, and pericarditis, with about 3 ounces of sero-fibrinous fluid in the pericardium. The lungs were so infiltrated with serous fluid that two pints of albuminous rose-coloured fluid were pressed out by gentle squeezing. At the autopsy on Giraudeau's patient the lungs were bulky and violet-coloured. On section and on pressure a large quantity of frothy rose-coloured fluid, like that brought up in the expectoration, flowed out. The kidneys showed acute congestive nephritis ; they were large and violet- coloured ; the capsule stripped easily, and in places subcapsular haemor- rhages were visible. The heart showed general hypertrophy, which was most marked in the left ventricle. The valvular and arterial orifices were healthy. The aorta presented no trace of aortitis, either at its origm or in the arch. Giraudeau observed the following lesions in the lungs of a young girl : The pulmonary alveoli were filled with coagulated fluid, which im- prisoned desquamated epithelial cells and some red corpuscles. The capillaries of the septa were gorged with red corpuscles. It seemed that certain septa were thickened by a true interstitial oedema. At these points the bloodvessels were less apparent, as if the circulation had been impeded by the compression of the vessels. Pathogenesis. — What is the explanation of superacute oedema m Bright's disease ? The undeniable clinical fact is that patients with Bright's disease are liable to slight oedema in any part — in the lungs, the larynx, and the cellular tissue — just as they are prone to effusion into the serous cavities. DISEASES OF THE LUNG 167 Why, then, this localization in the lungs ? I do not know. As Brouardel remarks, from a medico-legal point of view, cold and alcohol appear to have been important factors in many persons who have died from this cause. A drunken man sometimes falls asleep in the open air during intense cold. He dies, and post-mortem superacute oedema of the lung is found, with lesions of nepliritis, which are never wanting. Some authors (Huchard and Renaud) assign the jsrincipal, if not the only, part to the lesions of aortitis and peri- aortitis. According to Huchard, the needful intermediary between acute pulmonary oedema and Brightism is aortitis, and especially periaortitis, with its inflammatory or reflex reaction on the cardio-pulmonary plexuses. I am sorry to differ from this view. I do not deny, of course, that some aortic cases may have congestion and oedema of the lungs ; but what I main- tain, .supported by undoubted evidence, is that superacute oedema of the lung has been found in many cases of Bright's disease in which neither aortic nor periaortic lesions were found during life or post mortem. The subject on whom Bouveret made an autopsy had neither aortitis nor periaortitis ; Giraudeau's two cases showed neither of these lesions. My patient had neither aortitis nor periaortitis. Brouardel, who at the Morgue performed post-mortems on patients who died of superacute oedema of the lung, says that the aortic lesions are far from being constant, while the renal ones are never lacking. He noted, among others, the autopsy of a man who suffered from latent nephritis, and succumbed to superacute a^dema of the lung. The autopsy revealed the integrity of the aorta, but showed the lesions of nephritis. To the anatomical let us add the clinical proofs. Many patients with Bright's disease, whose cases I have reported, have neither before nor after their attacks of pulmonary oedema had any sign of aortitis. The question seems to me settled. We do not know by what mechanism superacute oedema in Bright's disease is produced. I do not, however, reject the idea of pulmonary vas- cular troubles of vasomotor origin, the return circulation being for the moment annihilated, and favouring considerable hypertension in tlie afferent vessels. Loeper blames the increase of the l)lood concentration ; Widal tlie increase f)f the clHoride of soda in the blood. Treatment. — The urgent indication is bleeding. In spite of the cokl- ncss of the patient and the threatening collapse, which would at first appear as contra-indications, there must be no delay, and, without losing an instant, 10 to 15 ounces of blood must be withdrawn. The marvellous results of bleeding must have been seen to make its imporfance clear. I do not exaggerate in saying that it produces in the patient a visible change. In a case at the Necker Hospital o^flema came on with such ra])i(lity that death 168 TEXT-BOOK OF MEDICINE would have speedily followed unless bleeding had been performed at once. The patient, who had not lost consciousness, told us that he felt himself dying and recovering in the space of a few moments. In my patient at the Hotel-Dieu blood-letting had such a marvellous result that imminent death was arrested, and the rales which filled his chest from apex to base disappeared as by magic, leaving only a residue at the bases. Bleeding gave a similar result in Giraudeau's first case.* Of all methods of blood-letting bleeding is, without doubt, the most favourable ; but, in default of bleeding, wet -cupping over the chest may be made, or, better still, two dozen leeches may be applied. Dry-cupping of the thorax and of the lower limbs is also useful. Subcutaneous injections of caffeine or ether are often indicated. We must remember, however, that the kidneys are inactive, and therefore use caffeine with caution. We may start with an injection of a grain, and be ready to repeat it several times during the following hours. Oxygen in large doses may also render some service. The patient's strength must be supported by milk and weak tea, with a little alcohol. We must also know what to avoid. Blisters must not be used, for the patient has Bright's disease, and the action of cantharides on the kidneys will rapidly make the situation worse. For the acute dyspncea our thoughts turn to morphia, but caution is necessary, for morphia in such conditions may cause grave mishaps. As Brouardel says : " These are cases which it has been my lot to see fairly frequently. A patient begins to choke. It is evening, and one of the physicians on night duty is called. He gives an injection of morphia, following an only too common rule ; the patient gets no relief. A second and third injection at length bring quiet ; some minutes or hours later the patient succumbs, and the family blame the physician who has given the injections. Autopsy and inquest follow. It is found that death was due to superacute oedema of the lung." Danger once averted, do not lose sight of the patient. Absolute milk diet must be prescribed, chloride of soda, which favours oedema (Widal), avoided, and the urinary secretion closely watched. In short, he must be treated as a case of Bright's disease, and be advised to avoid with the greatest care every cause of overwork and chill. * In my wards I have recently seen two more cases of superacute oedema, in which bleeding suddenly arrested asphyxia that was threatening the patient's life. DISEASES OF THE LUNG 169 XII. ON TUBERCULOSIS IN GENERAL— BACILLUS TOXINES. Local Tuberculosis. Nature of Tuberculosis. — By his immortal work on pulmonary phthisis, Laennec bequeathed to tlie medical world such an exhaustive description of this disease, with its lesions, its forms, and its signs, that we must all do homage to his genius. On December 5, 1865, Villemin read a paper before the Academic de Medecine, and upset all previous theories as to the nature of tuberculosis. By numerous and well-conducted experiments, Villemin showed that tuber- culosis is a virulent, infectious, and inoculable disease. As soon as Villemin's discovery was known, inoculation of tuber- culosis was repeated, and varied to infinity in France and abroad. The tuberculous material was introduced into the serous cavities of the pleura and of the peritoneum. Cohnheim practised inoculation, by means of a fine needle, mto the anterior chamber of the eye, and, owing to the transparency of the cornea, was day by day able to follow the evolution of the tubercular process, and in some cases show the generalization of tuberculosis m the animal under experiment. Chauveau produced tuberculosis in the bovine species by mixing tuberculous material with their food, and observed in several cases that the intestine, which had served as the point of entrance for the virus, was much changed by the lesion. Tappeiner and Wcichsel- baum produced tuberculosis in dogs by making them breathe the powdered s])utum of phthisical patients. Krishaber and myself have experimented upon the monkey, in order to deal with the animal which nearest approaches man, and in the numerous experiments made with my intimate and lamented friend I was struck at the autopsy with the severity of the infectious pror-ess. Three-quarters of our inoculated monkeys died of tuberculosis in a few weeks, while out of twenty-eight monkeys kept away from all con- tamination, and not inoculated, only one died of tuberculosis.* So great was the importance of Villemin's discovery that it completely changed our ideas of tuberculosis, and gave it a place in the list of infectious diseases. It had also the result of sanctioning, in irrefutable fashion, Laennec's doctrine of the identity and the unity of tuberculo-caseous l<'sions, and, at the same stroke, destroyed the German teaching, which, * Our comploto researches concern scventy-eiglit monkeys. Out of sixteen monkeys inoculated with human tubercle, twelve died with tubercular lesions ; out of Iwenfyfour monkeys win'eh were not inoculated, but wliieli livi-d witli the inoculated monkeys, live died from tuberculosis ; out of ten monkeys which wc^re inoculated with purulent matter, only one died tulwrculous ; out of twenty-eight nionki-ys which wen^ i.solatcd from ••v«'ry Rource of contamination, only one died from tubercular disease {Arch.de I'/ii/siologic, Mars, 1884, No. ."J). 170 TEXT-BOOK OF MEDICINE under the eminent patronage of Virchow and Niemeyer, differed from the work of Laennec, and looked upon tuberculous infiltrations of the lung as simple caseous degeneration, or so-called scrofulous phthisis. This latter part of the question, however, with its developments, will be treated in one of the following chapters. Bacillus of Tuberculosis.— The infectious nature of tuberculosis being demonstrated, the question was to discover the microbe of the disease. The work of Pasteur and his culture methods, which had given such marvellous results in the study of other diseases (antlu-ax), served as a guide. The work was begun, and in May, 1882, Koch discovered the bacillus of tuberculosis. This bacillus may be revealed in the sputum by the process described below.* It forms a very slender, straight, or bent rod, in length equal to the third part of a blood-corpuscle— that is to say, 2 or 3 //. The bacillus is of uniform size throughout its whole length, but ovoid swellings, which may be due to the presence of spores, are seen. The small, colourless, oval vacuoles in the interior of the bacillus have also been looked upon as spores. In order to stain Koch's bacillus, Ziehl's method is employed at the present day. It consists m leaving the slides for ten to twenty minutes in a solution of carbol-fuchsin which is prepared as follows : Fuchsin . . 1 gtamme Carbolic acid Absolute alcohol Distilled water . 5 grammes 10 90 The preparation is then decolorized, either with a 30 per cent, solution of nitric acid, or by a mixture of five parts of absolute alcohol with one of nitric acid. In order more clearly to define the bacilli, the slide is stained a second time with methylene blue in a solution of water and alcohol. By this process the bacilli are stamed red, while the tissue and other microbes are of a blue colour. These characters distinguish it from all other micro-organisms. It is analogous only with that of leprosy. The so-called pseudo-tuberculous, or acid-resisting bacilli, are more thick- set, and are less resistant to decoloration by acids, especially nitric acid.f * Some of the most purulent sputum is taken with a needle and spread out on a slide, which has previously been washed in diluted nitric acid, and afterwards in alcohol. A second slide is placed upon the first, and the two are rubbed together so as to form a film on each of the slides. The albumen is then coagulated by passing the slide three times through the flame of a Bimsen burner, or by placing upon it a few drops of a mixture of alcohol and ether in equal parts. The slides may then be put in the staining fluid. •1- Tlie tubercle bacillus is not the only one which remains stamed by Ziehl s method after decoloration with acids. A group of other baciUi possesses the same property ; DISEASES OF THE LUXG 171 The bacilli in tubercular sputum are usually free, and are rarely found enclosed in the leucocytes or the epithelial cells. They may be single or in pairs, or grouped en masse. In histological preparations the bacilli are found en masse in the giant 3ells. The discovery of the tubercle bacillus has been of the highest importance, for its presence is a sure sign of tuberculosis. The proof that the bacillus is indeed the active agent of tuberculosis, as the bacterium is the active agent of anthrax, is that the tubercle bacillus has been successfully isolated, cultivated, and inoculated. Koch, inspired by his culture methods, pro- ceeded in the following manner : He took a small piece of tubercular material, and placed it on sterile gelatinized serum, which was then put in an oven at 99^ F. Roux and Nocard have introduced glycerinated media, which are an excellent culture material. Good results are obtained by the addition of 1 to 2 per cent, of glucose to the glycerinated media. After twelve days or a fortnight the appearance of dry or scaly particles, "omposed of colonies of bacilli, is noticed. These colonies are whitish or yellowish, not shining, clearly isolated from one another, and but little adherent to the culture medium. The tubercular particles, transported to another culture medium, re- produce new colonies of barilji, and so on, through several successive cultures. Bezan^on and Griffon have extolled the use of glycerinated blood-agar and yolk of egg with agar, which give earlier and more certain cultures than other media. From the point of view of diagnosis, the discovery of the tubercle bacillus has had considerable influence. We know how difficult the diagnosis often is between pulmonary phthisis and other diseases, such as bronchitis, clu-onic catarrh, chronic pneumonia, bronchiectasis, chronic laryngitis, pulmonary Byphilis, hydatids of the lung, etc. In these different cases the presence of the bacillus in the sputum furnishes the proof of tuberculosis ; and its absence, after several sucx^.essive examinations, enables us to deny, in a more or less certain fasliion, the existence of tuberculosis. In cases where the search for the bacillus is fruitless recourse is had they aro tliorofon^ callod arid-re.v,stin/j, or p.s('iido-tul)frculniis. Thoy arc mot with in milk anrl in butter, and aro found in pianta, in earth, and manure. They may l)e patho- genic in animals. In man acid-resisting bacilli are found in the smegma, the cerumen, the nasal mucus, in certain affections of the eyes, of the uro-genital system, and of ii. At a more or less advanced stage in phthisis the menses become irregular, and 186 TEXT-BOOK OF MEDICINE may be suppressed, or at times replaced by Icucorrhoea. These troubles explain why pregnancy is rarer in phthisical women. The puerperal and nursing states have, furthermore, a bad influence on the course of the disease. The oedema seen in phthisis is of diverse origin : cachectic oedema, which begins in the lower extremities ; painful oedema, which is due to venous coagulation (phlegmasia alba dolens), and is generally limited to one limb ; and diffuse oedema, with lesions of the kidney and albuminuria, are seen. Lesions of Other Organs. — I have so far described the lesions of the lung, and discussed the most usual symptoms of pulmonary phthisis. There is hardly an organ which escapes tubercular infection. Whether tubercular infection be present alone, or whether it be aided in its work of destruction by secondary infections from the toxines of other microbes, many and varied troubles result, modifying the picture of the disease or hastening its course. The study of these complications will be discussed fully when dealing with the tuberculosis of each organ ; I shall here content myself with a rapid enumeration. 1. Digestive System. — The changes in the digestive system com- prise tubercular ulcerations of the tongue, the mouth, and the larynx ; tuberculosis of the tonsils ; gastritis, which is sometimes ulcerating ; all varieties of dyspepsia ; chronic enteritis ; ulceration and fistula of the anus ; tuberculosis of the mesenteric glands ; acute and chronic peritonitis. The lesions of the liver present the most diverse forms ; for the liver, like every other organ, has its own peculiar tuberculosis. The tubercular granu- lation is not the only lesion present. We find also tubercular lesions affecting the type of cirrhosis or of fatty or amyloid degeneration. 2. Circulatory System. — The troubles of the circulatory system in- clude palpitation, which is very frequent ; dilatation of the right heart ; tubercular pericarditis and endocarditis ; the formation of clots in the veins of the limbs ; and thrombosis of the pulmonary artery, which is a possible cause of rapid death. 3. Genito-Urinary System. — The testes, the prostate, the bladder, the kidney, the ovaries, and the uterus, may be affected by tuberculosis. It may remain as a local condition, or precede that of the lung. 4. Nervous System. — Here we find extensive or localized meningitis ; lesions of the cerebrum, with all their train of symptoms ; tubercular lesions of the mesoencephalon and the bulb, and those of the spinal cord (tuber- cular leptomyelitis), which do not differ in their clinical description from other varieties of myelitis. In opjjosition to these lesions of the nervous centres, I would mention peripheral neuritis, which has of late been carefully studied. Clinically, it shows itself by sensory (neuralgia, hypersesthesia, anaesthesia), motor (paralysis, paresis), and trophic troubles (amyotrophia, zona). DISEASES OF THE LUNG 187 5. Organs of the Senses. — Otitis in phthisical patients is a catarrh of the drum (otorrhoea), with perforation of the membrana tympani. The ulceration of the mucosa causes caries and necrosis of the petrous bone. This otitis may be consecutive to pharyngeal catarrh, which has spread to the drum through the Eustachian tube (Belliere). Tuberculosis of the nose and of the nasal fossse has been already described. Tuberculosis in Children. — I shall now mention tuberculosis in children and elderly people. Children may become tubercular at all ages, but the very young child (one from a few days up to two years old) presents a familiar form of tuberculosis. It has been summed up by Landouzy and Queyrat as follows : Infantile tuberculosis often appears as a broncho- pneumonia. It may show all the lesions of tuberculosis seen in adults, including cavities surrounded by fibrous tissue and aneurysms, which pre- dispose to fatal haemoptysis. Tuberculosis is transmitted to the new-born either by mediate contagion or by heredity. In elderly people tuberculosis is more frequent than is usually supposed, but it has not the cliaracteristics of phthisis in the adult. It is more torpid, and its symptoms are less marked. Course — Prognosis — Termination. — The course and duration of pul- monary phthisis are extremely variable. One individual, for example, may for many years bear the growth of tubercular products without passing into the third stage ; while another, after six or eight months' illness, is already a victim to sweating, wasting, diarrhoea, and hectic fever. Some people who have had apparently insignificant haemoptysis show no symp- toms of proved tuberculosis until ten or fifteen years later. Others may have had several attacks of haemoptysis and inveterate bronchitis, but yet have dragged out a more or less invalid existence, without ever reaching the third stage. Many causes hasten or retard the course of pulmonary phthisis. Firstly, there is the nature of the soil on which the disease has developed ; then there are the cares of every kind, hygiene, questions of climate, nourishment, and comfort, and hence the much quicker course of tuberculosis amongst the poorer classes, while among those in easy circum- stances we can often check or modify its progress. It has been said that when emphysema occurs in a tubercular lung, it arrests the progress of the tuberculosis for the time being. Between the local changes in the lung and the general condition of the patient there is, of nece.ssity, some parallelism. We see people with local .signs of advanced tuberculosis (softening and cavities), but they live on, without reaching the stage of consumption. These examples must be known in order to avoid grave errors in prognosis. The natural end of pulmonary tuberculosis is often death by i»hthisis ; yet cases of cure are frequent (({rancher). I have often s(!en recovery from 188 TEXT-BOOK OF MEDICINE pulmonary tuberculosis when it is treated at an early period. The tubercle may recover (cretaceous and fibrous condition), and the small cavities may cicatrize. In certain conditions death supervenes from complications, such as laryngeal phthisis, purulent pleurisy, pneumothorax, enteritis, perito- nitis, meningitis, etc. Syncope, embolism, or thrombosis of the pulmonary artery are causes of sudden death. iEtiology. — Heredity and contagion are the two great causes of pul- monary phthisis, and in this respect tuberculosis shows an analogy with syphilis. In both heredity may betray itself by early or by late manifesta- tions. The early ones are, in the one case, syphilis in the new-born ; in the other, tuberculous broncho -pneumonia of infancy, meningitis, and tuberculi- zation of the peritoneum and of the bronchial glands. The late manifesta- tions are, in the one case, the multiple lesions of hereditary syphilis ; in the other, pulmonary phthisis and the various local tubercular lesions till lately considered as scrofulous. Sometimes the parents are notably phthisical ; at other times they show only such imperfect evidences of tuberculosis as inveterate bronchitis or suppurating adenitis, wrongly regarded as scrofulous ; they drag out a more or less invalid existence, without going on to confirmed phthisis. They may be cured, or think themselves cured. These troubles favour tuber- culosis, and children born of such stock may, unfortunately, inherit the original taint. Sometimes, in a family where' tuberculosis or scrofula reigas (and they are identical), the parents in whom the germ is latent beget children who develop tuberculosis, while the parents themselves are only affected later. We may consider heredity in two ways : either the subject inherits the infectious principle — that is to say, the seed ; or he only inherits the predis- position to contract tuberculosis — that is to say, the nature of the soil which is favourable to its growth. Many authors mcline to this latter opinion. Peter says that people are not born tubercular, but tuberculizable. Bouchard says that the tuberculosis which parents transmit to their children is prospective, and not actual. This opinion is admissible, but it is none the less true that the hereditary lesion has been caught red-handed in the foetus. The inoculation of guinea- pigs with blood from a foetus conceived by a phthisical mother has caused tuberculosis analogous to that which a fragment of tubercular lung produces. We possess to-day undeniable cases of congenital tuberculosis. In two cases out of five, Koch's bacillus has been found in the blood of the umbilical vein of infants born of tubercular mothers (Bar and Renon). Tuberculosis has been recognized in the foetus at various ages. It may be, says Kuss, that the germs reach the foetus a little before delivery, or at the moment of birth (thanks to placental depletion, produced by the first DISEASES OF THE LUNG 189 inspirations), and only succeed in setting up appreciable foci at the end of several months. It is therefore reasonable to admit that hereditary tuber- culosis Ls transmitted directly by the germs. The whole question consists in recognizing what the conditions will be which, sooner or later, will favour the growth of the germs, which may long remain in a latent state. This latency of the bacilli is not at all surprising. The contagious nature of tuberculosis had been long supposed, but it was clearly established by Villemm. To-day it is based upon a consider- able number of cases. Cases of contagion between husband and wife are relatively frequent : a healthy husband becomes tubercular through contact with his wife who is dymg of phthisis. He marries again, and, in his turn, gives tuberculosis to his second wife, who was quite well. I could give many more cases ; the more intimate the living in common with phthisical persons, the more is contagion to be dreaded.* In the preceding chapter I describe the modes of transmission of tuber- culosis by experimental measures. How can we explam its transmission in the human species ? It is possible that the bacillus enters the digestive tract by means of food and drink, and in this connection milk, both from a tubercular animal and from a tubercular wet-nurse, has been incriminated. Calmette thinks that the intestinal tract is often the entrance-gate of pulmonary tuberculosis. Verneuil thinks that the contagion may take place through the genital tract. In some cases the bacillus has entered the economy through a wound in the skin. The respiratory passages are the usual entrance gateway of the infectious germ (spore or bacillus), and in most cases the lung Is the first organ attacked. The germs exist in abundance in the sputum of phthisical patients, and experience has proved that the sputum may be dried, powdered, and kept for several weeks without losing its virulence, since the dust, when uihaled by animals, causes tuberculosis (Tap}>einer). Transmission to man prob- ably occurs in this way : the debris of sputum, reduced to powder, floats in the air and enters the bronchi. In order that the germ may produce its noxious effect, the bronchus must have first lost its epithelium, and it may be asked if bronchitis and broncho-pneumonia (measles, whooping- cough) do not especially favour the entrance of the germ. In all cases the contaminated person must be in a condition of receptivity, for in case of con- tagion we find favourable soils and soils refractory to the growth of germs. Children of tubercular stock, patients with diabetes or convalescent from * These propositionH are general, and ajjply equally to animals and to man. Krid- haber and myself, in 1883, made exix-rimental researches upon tuberculosis in the ape, and lost only one monkey out of eighteen which were living together, but wen* kept isolated from every source of contaminatif)n, while we lost five monkeys from tuber- culosis out of twenty-four which lived with tubercular animals. They had cunt rated tuberculosis by contagion (Arch, de Fhysiulogie, 1883). 190 TEXT-BOOK OF MEDICINE acute diseases (measles, whooping-cough, typhoid fever) are in a state of receptivity. The soil is prepared by malnutrition, failing health, excesses of every kind, exhaustion, fatigue, trouble, and repeated pregnancies. " It may be said that tuberculosis is the common end of all constitutional degenerations in families as well as in individuals " (Jaccoud). Traumatism and contusions of the thorax may be placed in the category of predisposing causes, by tilling the soil in which the bacillus \$as in a latent condition. Since attention has been called to this point many cases have been collected, and I know of several in which injury to the thorax has been followed by tuberculosis. Tuberculosis is most common in youth ; it appears, however, at other periods. It is fairly common in advanced age and in children during earliest infancy. It is more common in warm climates, and is comparatively rare in high-lying countries. Diagnosis. — The diagnosis of pulmonary phthisis is sometimes difficult, not only at the onset of the disease, but even at more advanced periods. See divides the disease into latent, larval, and pseudo- phthisis. In latent phthisis we find ill-marked symptoms, such as pallor, wasting, with or with- out fever, catarrhal cough, or haemoptysis. The cases of larval phthisis are those which assume the mask of an acute affection of the respiratory tracts, such as bronchitis, pleurisy, broncho-pneumonia, or laryngitis. The cases of pseudo-phthisis are diseases such as bronchial dilatation, syphilitic gummata of the lungs, hydatid cysts of the lung, aspergillary tuberculosis, and neoplasms of different kinds that simulate phthisis, but are not of tubercular origin. In these different cases the diagnosis is not always simple, and the recognition of Koch's bacillus renders the greatest service. As regards diagnosis, I think it useful to state the following precepts : Every youth or adult who wastes much or rapidly, with or without fever, must be suspected of having tuberculosis, in the absence of diabetes or Basedow's disease. Every girl or young woman who has neither genuine chlorosis, Bright's disease, nor syphilitic anaemia, but yet has the apjjearance of chloro-ansemia, must be suspected of having tuberculosis. Every individual who has haemoptysis must be suspected of tuberculosis. The cases of so-called supplementary haemoptysis are very often tubercular ; but, on the other hand, we must remember that there is a group of non- tubercular cases, such as haemoptysis in bronchitis, hydatids, or syphilis of J the lung, false tuberculosis, etc. Koch's tuberculin has undoubted value in diagnosis, and may reveal even the most hidden trace of tuberculosis. It has therefore attracted the attention of hygienists, and has been employed in veterinary practice forj the early diagnosis of tuberculosis in cattle. DISEASES OF THE LUNG 191 In man great care must be taken in using injections of tuberculin for purposes of diagnosis. The amount must not be more than yV or t milli- gramme ; two or three injections may be made at intervals of two or tlu:ee days. In case of positive reaction, the temperature rises about 1° or more. The rise is often accompanied by lassitude and headache. The cuti-reaction does not give constant results. I have verified this fact at the Hotel-Dieu. Prognosis. — I shall not dwell at length on the prognosis of pulmonary phthisis. The preceding description sliows how serious the disease is. There is, however, a point to which I would call attention — viz., that tubercu- losis is cured much more often than we suppose. Not only is it curable at its onset, but it is still curable at an advanced period. In people who have died from quite another disease we often find old fibrous or cretaceous tubercular lesions, which prove that they have at some time been affected by tuberculosis. Treatment. — Let us first consider prophylactic treatment, the object of which is : (1) To modify as far as possible the evil results of heredity in a person of tubercular stock ; (2) to remove the causes of contagion. The individual should from infancy live in the open air, in the country, and in a high-lying locality, take much exercise, have abundant nourishment, and avoid all causes of contagion ; for, thanks to his origin, he is, above all others, in a state of receptivity. The means employed to avoid contagion are as follows : Choose for the child a nurse who has no tubercular taint ; never permit a child to sleep in a room with phthisical parents ; do not allow husband and wife to share the same room. Collect, as far as possible, the products of expectoration in a basin, which is emptied and washed several times a day ; and do not allow sputum to be left on linen, pocket-handkerchiefs, or on the floor, where it dries, is reduced to dust, and becomes a potent cause of contagion. Purify rooms and bedding after the death of a phthisical patient ; expose clothing which the patient has used, to steam at a temperature of 212°, or, better still, jjurn it. If these precautions were taken, the balance-sheet of phthisis would be much diminished. We may next consider the different medicines and their respective efficiency in phthisis. Cod-liver oil, in suflioient doses, builds up the constitution. Intolerance on the part of the stomach and diarrhoia are contra-indications. Tolerance may sometimes be established by giving the oil in increasing doses, after it has been well cooled in a freezing mi.xture. I have obtained excellent results with cod-liver oil in large doses — e.g., a tumblerful. Some patients take 10 to 15 ounces daily for several weeks. I repeat that the results obtained are often surprising. When the oil disagrees, I substitute fatty and oily foods : caviare, sardines in oil, tunny-fish, slices of bread and butter, pdte de 192 TEXT-BOOK OF MEDICINE foie cjras, etc. Excellent results are sometimes obtained. I would especially recommend eggs and raw meat in large quantities. Meat- juice has been used with benefit. The good effects of this regime do not rest solely upon pure and simple super- alimentation, but on the particular quality of the food. Glycerine is a very useful and economical drug, and is given daily in doses of 1 to 2 ounces, with a little rum, and flavoured with a drop of essence of peppermint (Jaccoud). Preparations of arsenic, because of their trophic action, are much indicated : arseniate of soda is given in doses of ^V to yV grain daily in distilled water ; or arsenious acid, in doses of -oV to yV grain daily, in the form of granules, each containing -^^ grain. Cacodylate of soda, in daily injections of about 1 grain or more, is an excellent medicine. (See Appendix on Therapeutics.) Creosote stimulates the appetite and lessens the bronchial secretion ; it is given in capsules or in pills, each containing 1 minim creosote. The patient takes as many as ten or twenty during his meals. Counter-irritation, by repeated blisters or by the cautery, is useful in dealing with inflammation and congestion. In my own practice I make much use of counter-irritants. It is well to use the cautery, and to allow suppuration to go on as long as possible. A good way is to apply the cautery-point 200 or 300 times a week, and to continue this treatment for a long period. The fever of tuberculosis, especially in the hectic form (absorption fever), may be checked by salicylic acid (Jaccoud's method). Twenty grains of salicylic acid are given during the morning in three cachets, at intervals of half an hour. According to circumstances, the dose is diminished, stopped, or repeated some days after. Aspirin (acetyl-salicylic acid) in 5-grain doses, repeated three or four times a day, is useful for the fever of phthisis (Renon) ; abundant perspiration limits its use. Cryogenin, in doses of two or three cachets, each containing 1 grain, has a remarkable antithermic action. Antip}Tin is efficacious, in daily doses of 30 to 40 grains. For the fever, I have often prescribed bathing with tepid water or cold baths, with great benefit to the patient. Haemoptysis should be dealt with in the following manner : If very abundant, it is sometimes arrested by an emetic, such as ipecacuanha (30 grains). If it is more trifling, ipecacuanha is prescribed in nauseating doses, and one or two of the following pills are administered every hour, or every two hours : Ipecacuanha . . . . . . . . . . . . gr. i. Extract of opium . . ... . . . . • • gr. uV DISEASES OF THE LUNG 193 Other means are also used for haemoptysis : subcutaneous injections of ergotin, solutions containing perchloride of iron, and counter-irritation to the chest by means of blisters. The patient should be kept absolutely at rest, given iced and acidulated drinks, and have abundant cold nourish- ment, which should be administered in small quantities. The following tbaught may also be prescribed, in tablespoonfuls, every three hours : Distilled water . . . . . . . . . . ^iv. Syrup of rhatany . . . . . . . . . . 51. Rabel water . . . . . . . . . . . . ni xlv. The sweats are relieved by white agaric (Trousseau), in doses of .'3 grains, taken every evening, in a cachet ; by atropin ( Vulpian), in doses of Jg grain ; or by cam}»horate of pyramidon, in doses of from 6 to 8 grains, in a cachet. Diarrhoea, which is often profuse, may be treated with chalk in largo doses ; by opiates (five to ten pills, each containing J- grain opium, given in the course of twenty-four hours) ; by methylene blue, given daily, in three cachets, each containing 3 grains of lactose and 1 grain of methylene blue. Vomiting may be relieved in some cases by 2 drops of laudanum, taken before a meal ; or by a tablespoonful of lime-water, with the addition of uV grain of hydrochlorate of cocaine ; at other times by lavage of the stomach, or, better still, by artificial feeding. This artificial feeding (super- alimentation, gavage), used by Debove, has often proved effective, not only in vomiting, but also in malnutrition. Milk, lentil-flour, and powdered meat are given through a tube. Some patients will swallow, without the help of the tube, 6 ounces of powdered meat in the twenty-four hours, the powder being suspended in milk or broth, given at short intervals. Super- alimentation sometimes produces remarkable effects. Koch's Tuberculin.— I must now give some details of treatment by K'--"-^^ When necrosis occurs, the cast-of5 tissue contams bacilli in more or les Isiderable numbers, and the ulceration ^^us produced -ay te - f^^^^^ into a simple wound, covered with fleshy granulations, which may form scat tissue. In a healthy man 1 c.c. of lymph is necessary to produce a rise of tem- perate to 100" F, In a tubercular man a dose of from 1 to 3 c.. o lymph is sufficient to produce, at the end of two or three hours, a r go , a tempe a ture of 104° F., cough, vomiting, acute pain, enlargement of the spleen, a^d Iht delirium. These symptoms last twelve to fifteen hours. In he c:lf:f lupus, local reaction can be made out at the site of the — ' lesions. At the end of five or six hours the lupoid areas swell ^^^^^'>^^^- and sometimes necrose. The redness diminishes after two or three days and is accompanied by scaling. Two or three -*s la the scha become detached, leaving in favourable cases a '-t'^g <=;^*^- J '^^ ^n thing happens in tuberculosis of the glands, bones, "'J^*^' *>"**"* J is less clear. In favourable cases of pulmonary tuberculosis, after sub- 1 talus injections of lymph in very small doses the cough is less re quent, the expectoration becomes mucous, the baolh diminish, and finally disappear, and the general condition improves. Such are the results of tuberculin in favomrable cases ; ^ut these cases are exceptional, and. after many well-conducted observatior. the infatuation first aroused has given place to the most profound '^^''f'- i„„eulati«ns Most serious accidents, and even death, have occurred after 'no™l''t»m of tuberculin Amongst these accidents, I would note meningitis endo- Xlema of thfglottis and of the l-S- ^™-'^°-P"--:"'j\:': After inoculations performed in my wards with the grea es care^ I have seen perforation of the tympanic membrane from 7ff'™.°*'*f , ,^,'^ f, gloomy results have caused the use of mjections of tuberculm m phthisis " \^"mtion of physicians at the St. Louis Hospita, which for two months'and a half tried tuberculin on thirty patients ^-^^^^-l^Z^^^l^' decided aoainst Koch's method of treatment. In some cases temporary reductt n °of the lupoid mass and temporary attenuation of the tuberculous lesion were seen, but cure was never obtained. In the course of these xT^iments no patient, fortunately, succumbed, >>-*-, gravyompa^ tions were seen in the heart, brain, and kidneys, as well as the most a a^n ^neral symptoms. In some cases tubercular centres m the lung, tUl the latlCwere reawakened, and it was very difiicult to arrest the lesion wh.cl had once more become acute. • • i o a,.r1 nlUa Tuberculocidin.-Klebs has separated the noxious principles and alka DISEASES OF THE LUNG 195 loids of Kocli's tuberculin from the active principle which is an albumose. This purified lymph, or tuberculocidin, does not give rise to febrile reaction ; it causes retrogression in the tubercular tissues, without necrosis, and brings about the destruction of the bacilli. The dose, at the commencement of treatment, is ^^ grain, and it may be raised to 7 grains later. The results are encouraging. C. Spengler (of Davos) has combined the action of tuberculin with tuber- culocidin. He injected a mixture of from 5^^^ grain of tuberculin with ^ grain of tuberculocidin. Injections were made several days following, and in some cases the fever yielded. Denys has used bouillon, freed from the tubercle bacillus by filteriug^ in the treatment of tuberculosis in man. He gives hypodermic injections in doses varying from 1 to 25 c.c. He has seen good results, but the value is not yet exactly known. Let us now consider thermal and climatic treatment in pulmonary tuber- culosis. Speaking generally, thermal cures are absolutely contra-indicated while the patient is suffering from haemoptysis or from fever. In patients affected with slow tuberculosis, who are but little prone to sharp reaction, haemoptysis, or broncho-pneumonia, Mont-Dore, la Bourboule, and the sulphur- waters, such as Cauterets, Luchon, Eaux Bonnes, etc., may be recom- mended ; but in patients suffering from pulmonary tuberculosis in the irrita- tive form, the warm alkaline springs of Royat and Ems, or the cold sulphur springs of Allevard, are advisable. A similar distinction should be made when choosing a place of residence for tubercular patients. In cases liable to febrile attacks and palpitations of the heart, high altitudes, such as Davos and Saint-Moritz, will be most beneficial. These elevated situations give wonderful results, as regards improvement and cure, from the purity of the air and the activity which they cause in the breathing. All forms of phthisis, however, are not suited to these high altitudes ; stations of moderate altitude, or the maritime ones of Cannes, Mentone, Arcachon, Algiers, Madeira, or Pan, are then to be considered. Surgical treatment of tubercular lesions of the lung, interstitial injections of drugs, and pneumotomy, are questions which are under consideration, and upon which it would be premature to pronounce an opinion. XIV. FIBROID PHTHISIS. The tubercles in the lung, instead of undergoing caseation, may be con- verted into fibrous tissue. They form isolated granulations, which aro proiniiicut and very hard to the touch ; thiur structure is completely niodilied by the fibrosis. Fibrous tubercles had already been noted by Baylc, but io— 2 jgg TEXT-BOOK OF MEDICINE Cruveilhier was the first to show the importance of this change : " Pulmonary tubercles are too generally considered as being inc^able; ^W -7 become cicatrized" He noted "granulations and tubercles of recovery -that inert granulations and tubercles-perfectly distinct from those m process of development, with which they had been confounded. Cruvem^ier a^^^^^^ noted that tubercular lesions may recover at any stage, ^^^^ "^ ^ granulation to the cavity, by a fibrous change ; and that, fiirthe , part of the Lg tissue around the tubercles may be converted mto fibrous tissue^ This change constitutes a means of isolation and cure of the tubercular centres The condition constitutes the curative phlegmasia, or dark slaty induration which we now call interstitial pneumonia in phthisical patients. Later Grancher and Charcot showed that this fibrous change is very common, and may occur at a very early stage ; it must be considered as one of the modes of evolution of the tubercle. Furthermore, the works of these authors, and those of Renaut, Bard, Cornil, and Thaon, made it plain that Cruveilhier' s dark f^^ ^^^^'[Z may end in true pulmonary fibrosis or fibroid phthisis ; and that while the fibrous change in the young tubercle is a true process of recovery, the puhnonary cirrhosis which surrounds the caseous tubercles has not always that happy result. Indeed, we now know that Koch's bacillus may remain aUve foTfvcry long time in caseous tubercles surrounded by fibrous tissues, and that pulmonary fibrosis of an invading character may cause disastrous results, and be in itself a serious condition. • n • Lastly Cruveilhier showed that large fibrous tubercles, especially in old people, may contain not only caseous substance, resembling dry putty but also stony granules. Very small calcareous granules have been noted by Schlippel and by Ziegler in the tubercular follicles, where they assume quite a special disposition, and are made up of concentric layers Metch- dkolf found calcareous bodies of the same character m the tubercles of Algerian gerbil {Meriones Shawi), an animal in which the infection spreads very slowly after inoculation. In the centre of these calcareous bodies we find tubercle bacilli, which in the early stages of the lesion appear perfectly normal, and are surrounded by a layer of amorphous substance. Later they lose their faculty for taking stains, degenerate, and disappear. According to Metchnikoff, the stratified layers are multiple cuticles, secreted by the bacillus for defensive purposes, and the phosphate of lime is probably deposited in this cuticle by the giant cell itself, in its reaction against the *'''' Although these facts are not applicable to the calcareous bodies in the tubercle of man, they are very interesting as reconciling the tubercles o^ recovery with the ideas we have concerning them. The histological changes are as follows : DISEASES OF THE LUNG 197 1. Fibrous Tubercle. — When the tubercle reaches its stationary stage, we find new connective fibres, which interpose themselves between the cells, and finally make up most of the granulation in which giant cells may still be met with at the centre or at the periphery. " These giant cells are often situated in a cavity which holds them exactly, and is made up of fibrous Dundles, forming a circle around them. The isolated fibrous tubercles, and the periphery of the large confluent tubercles of the same nature, have in their interior capillary vessels permeable by the blood. The wall of the vessel is often thickened, especially in the sclerosed tissues. While the tissue of the granulation becomes fibrous, " the septa of the pul- monary alveoli have a tendency to become thickened, and interstitial pneumonia develops around the granulations that have become fibrous." In the thickened walls of the alveoli, small round cells, which infiltrate the bundles of the connective tissue, are seen in large numbers. In the oldest, and especially the confluent, fibrous tubercles the giant cells disappear at the centre of the islet, which is now only formed of fibrillary connective tissue, without vessels and cellular infiltration ; fibrous tubercles, with giant cells and permeable vessels, are found at the periphery. The old fibrous tubercles may be infiltrated with black pigment. Those black granulatioiLS, composed of particles of carbon, and also of altered blood- pigment, may occupy the whole granulation, or only a part of it. They are then situated at the periphery, for they are found chiefly in the cells ; they may be seen in the giant cells. These fibrous tubercles, even when they contain giant cells, may be considered as absolutely arrested in their evolution. 2. Interstitial Pneumonia.— The fibrous, pigmented tubercles otten cause thickening of the septa of the lung, so that they may be situated in the middle of an indurated connective tissue which no longer presents alveolar cavities. Around these masses, where the lung structure has quite perished, the pulmonary tissues show the lesions of interstitial pneumonia : thicken- ing of the alveolar septa, which are made up of fibres of connective tissue and flat cells containing black pigment ; alveolar exudate, made up of leucocytes and pigmental epithelial cells ; alveolar septa covered with layers of large swollen epithelial cells ; narrowing of the alveoli, which may take an elongated form, while their direction is perpendicular to that of the thickened interlobular septa. In certain places distended vessels, which form a kind of cavernous tissue, are found in the connective tissue. Side by side with the lesions of interstitial pneumonia we sometimes see opaque formations, which to the naked eye resemble tubercles. This condition IS really one of venous thrombosis, surrounded by fibrous zones, possessing a rich collateral circulation (Cornil). This interstitial ])n('unioni:i may be found around caseous centres and healed cavities with thickened walls. 198 TEXT-BOOK OF MEDICINE This condition is seen in the lung, where the fibrosis has made slow progress. In these cases it is often found associated with chronic adhesive pleurisy and thickening of the subpleural connective tissue. In this way arises pulmonary fibrosis, which not only deprives a part or the whole of the lung of all function, but which may also result in deformity of the chest and dilatation of the bronchi. In other cases fibroid phthisis does not run the same course. The induration may affect a whole lobe, or even both lungs, in the form of islets, or of large masses around indurated or caseous miliary tubercles without or with merely small cavities. Interstitial pneumonia then presents a form of subacute phthisis, and at times matures fairly rapidly : m six months or in a year (Cornil). To sum up : the fibrous change may affect young, isolated tubercles, and thus bring about a true cure of these lesions. The interstitial pneu- monia which is often present, and the fibrous change in the more advanced lesions, are frequently of good omen. On the one hand, however, they do not always arrest the course of the lesions ; and, on the other hand, they may go beyond the mark, and give rise to pulmonary fibrosis, with its results. XV. PNEUMONIC PHTHISIS— TUBERCULAR PNEUMONIA- CASEOUS PNEUMONIA. Since Laennec traced the anatomical and clinical history of phthisis two chief schools of thought have arisen — the one affirming the unity, and the other the duality, of phthisiogenous lesions. According to the former, pulmonary tuberculosis and caseous pneumonia are one disease ; they are both traceable to heredity, go on to the same termination — i.e., phthisis— and if their lesions, tubercular granulations and caseous infiltrations present any difference, such difference concerns only the form of their morbid products, and not their nature. Laennec therefore bequeathed to us the doctrine of their unity, both from the anatomical and the clinical point of view. According to the dualists, on the other hand, pulmonary tuberculosis and caseous pneumonia represent two distinct diseases. In 1850 Reinhardt affirmed that the lesion described by Laennec as tubercular infiltration was nothing else than "caseous pneumonia." According to the dualists, the pathological anatomy, course, and prognosis were different in the two cases. Tubercular granulations and caseous infiltration had neither the same origin nor the same nature ; heredity was the chief element in the case of the tubercular patient, while in the case of the patient with caseous disease, he got off with a pneumonia which Virchow called scrofulous, he had not the ill-luck to become tubercular " (Niemeyer). DISEASES OF THE LUNG 199 You see, said the dualists, that this scrofulous pneumonia (Virchow's) has nothing in common with pulmonary tuberculosis, since there is a differ- ence in form, seat, origin, and nature between the two maladies — difference in form, becaiLse the tubercular granulation is nodular, while caseous pneu- monia Ls diffuse ; difference in situation, because the granulation arises outside the alveolus, while caseous pneumonia arises inside ; difference in origin, because the tubercular granulation develops at the expense of the connective tissue, and caseous pneumonia at the expense of the pulmonary endothelium. Such were the anatomical and histological arguments invoked by the duahsts, and it is on this ground that each of their conclusions has been vigorously attacked and successfully routed in various works, and notably by Grancher, in a thesis which forms an eloquent plea in favour of Laennec's work. But what definitely ruined the dualist doctrine and confirmed the triumph of the French school is Villemin's discovery, on the one hand, and Koch's discovery, on the other. Since Villemin made his memorable experi- ments, we know that all tubercular products are virulent and inoculabie, whatever their form may be ; and we know also, since Koch's great dis- covery, that all these products contain the specific bacillus of tuberculosis. The experiments of Auclair deserve quoting : In the rabbit caseous pneumonia follows the intratracheal injection of an ethereal extract of bacilli from tubercular patients ; interstitial pneumonia may be the result of inoculation with a chloroform extract of the same bacilli. The double fibro-caseous evolution of the tubercle appears, then, to depend upon a double toxine, whicli explains the incidence of the lesions to one or to the other process, or to both at once. There is no longer any reason for preserving the term " caseous pneu- monia." The infectious malady called tuberculosis, which runs an acute, sub- acute or chronic course in the lung and other organs, shows itself anatomically by products of a tubercular nature. The products are sometimes of small size and nodular in shape (grey granulations, miliary tubercles) ; at other times they are of large size (discrete or confluent nodules, tubercular infil- tration). The granular form may exist alone — i.e., acute granular tuber- culosis. The pneumonic form, whether discrete or confluent, may exist alone — i.e., caseous pneumonia, or, better, tubercular broncho-pneumonia, which may more or less quickly give rise to acute and subacute phthisis. Pathological Anatomy. — Tubercular ])neumonia is usually limited to one lung ; it may be; limited to a few lobules or invade a whole lobe. It attacks the lower as well as the upper lobe. The lung presents different appearances, according as the lesion is more or less advanced. In the more advanced stage the lung tissue resembles 200 TEXT-BOOK OF MEDICINE Roquefort cheese — hence the name " caseous pneumonia " — and the greyish areas form with the yellowish and brownish ones a kind of mosaic. The cut section does not present the granular condition of lobar pneumonia, but is more opaque, smooth, dry, homogeneous and angemic. The lesions of commencing tubercular pneumonia are seen side by side with the caseous masses. We find masses of rosy-coloured, quivering, and semitransparent substance, called by Laennec " colloid infiltration," but since termed " caseous colloid pneumonia " (Thaon) ; masses of greyish homogeneous substance are also seen : this is Laennec's grey infiltration. These tubercular infiltrations may go on to caseation. If we study caseous infiltration closely, we see that it is not disseminated at random through the lung ; it is composed of more or less confluent nodules, leaving between them lung tissue that is healthy, or showing the lesions of ordinary broncho-pneumonia. The caseous nodules have a special texture, and are, for the most part, developed around a small bronchus, which is the centre of their formation (peribronchial nodules). They are composed of (1) a central region, and (2) a peripheral zone. The older the central zone, the more caseous it is. Some vestiges of lung are seen — i.e., arterioles — rings and bands of elastic tissue, which represent the bronchioles and the alveolar walls. Around this central region, which comprises the caseous centre of the tubercular follicle, we see a zone that is well defined on the side of the central region, but irregular at the periphery. This embryonic zone (Grancher) is formed of embryonic cells, that infiltrate the walls of the alveoli and their cavities ; and giant cells that are irregularly disposed in the form of a crown (Charcot), and complete the analogy between the caseous nodule and the tubercular follicle. Here, as in the tubercle, the degeneration begins at the centre, and the lesion extends at the circumfer- ence. These caseous nodules which are seen in the different varieties of caseous pneumonia are collections of a tubercular nature ; the condition is Laennec's tubercular infiltration in its most absolute sense. The caseous inflammation is tubercular, and contains Koch's bacillus. The softening of the caseous substance, the ulceration that results, and the cavity, are produced by the process we have already described in the case of tubercle. Caseous pneumonia, however, may last a long while, without giving rise to ulceration of the lung ; considerable masses may long remain in the same condition, although the lung is impermeable to air and blood (Cornil and Ranvier). Chronic caseous pneumonia, like chronic tuberculosis, is always accom- panied by interstitial pneumonia (Grancher), and often by fibrinous pleurisy. We shall see later in what relation tubercular granulations are associated, mth it. Bacteriology. — The tubercle bacillus has always been met with ii DISEASES OF THE LUNG 201 caseous pneumonia. In the lobar form the bacilli are found in the centre of the infundibula, in the embryonic cells that fill the alveoli, and in the walls of the alveoli. A similar distribution obtains in the lobular forms. The tubercle bacillus, however, is not alone in evidence in the lesions of tubercular pneumonia and broncho-pneumonia. Mixed infections are present, just as in all broncho-pneumonias ; the pneumococcus, the pneumo- bacillus, and the streptococcus predominate in the diseased zone around the caseous masses. This peripheral zone represents the less advanced stage of the lesion, while the caseous centre represents its completion. The secondary or associated microbes predominate in the peripheral zone, and it is probable that they engender centres of broncho-pneumonia and start the lesion, which the bacillus finally casefies. Description. — Tubercular pneumonia may be lobular or pseudo-lobar (Vulpian). A lobar form has also been described, but, according to Charcot, tubercular pneumonia is never lobar, and the cases which have been called lobar are confluent lobular or pseudo-lobar. Tubercular pneumonia, whether it be lobular or pseudo-lobar, some- times resembles an acute phlegmasia, and at other times a chronic disea.se ; but all intermediate forms — notably the subacute variety — are found between these two extremes. The acute pseudo-lobar form begins suddenly with fever, chill, pain in the side ; and, indeed, the violence of the chill, the high temperature, the coloured and viscid sputum, may closely resemble the onset of true lobar pneu- monia. I saw, some years ago, a medical student who was carried off in a few weeks by tubercular pneumonia of the middle lobe ; his sister had died some time before from chronic tuberculosis. The acute lobular form, in its initial symptoms, resembles broncho-pneumonia. The acute forms may carry off the patient very quickly, within a few weeks, even before pulmonary ulceration has had time to develop. At other times cavities appear early, and auscultation allows us to follow the course of events. Wiieti thf progress of the disease is a little slower, the clinical picture of subacute tubercular pneumonia is seen. These acute and subacute forms answer to the terms " acute phthisis " and " acute pneumonic phthisis." Chronic tubercular pneumonia may follow the acute condition, or be ciirouic from tlie first. In the latter case the disease begins silently, preceded or not by some suspicious symptoms, such as laryngitis, bronchitis, or hffimoplysis. The patient coughs and complains of distress, which is often paroxysmal, and comparable to the dyspncea of heart disease, or of an attack of astliina. He loses strength and wastes. On auscultation, we find in one or in several lobes tubular breathing, subcrepitant rales, and marked diniinutioii of the vesicular ninrmur. These signs are sometimes predominant ; ihey remain stationary in the invaded regions ; but the 202 TEXT-BOOK OF MEDICINE lesion, in spite of its extent, may only canse moderate fever, and trifling, or purely catarrhal, expectoration. It is exceptional for caseous pneumonia to recover ; in most cases the chronic form leads to ulceration of the lung, cavities, slow consumption, and phthisis, in the true sense of the word. In other circumstances, and in spite of several months' duration, the patient succumbs without ulceration of the lung. He is carried off by asphyxia, with symptoms of hectic fever, sweating, and diarrhoea. I have seen two cases of this kind : one, with Tardieu, in a young girl whose brother died two months later of ordinary tuberculosis ; the other, with Krank and Leudet, in a young woman in whom caseous pneumonia complicated, as often happens, fibrinous pleurisy. In both patients almost the whole of the right lung appeared to be converted into a huge caseous block ; the dullness was absolute, and the absence of every normal and abnormal sound alternated in places with slight tubular breathing, or with subcrepitant rales. The growing dyspnoea and the asphyxia were the chief symptoms throughout the disease. During infancy, as I have said in the chapter on Pulmonary Phthisis, tuberculosis often shows itself as a broncho-pneumonia. Diagnosis. — The diagnosis of tubercular pneumonia is exceedingly diffi- cult at the commencement. The acute forms simulate broncho -pneumonia or genuine pneumonia, and it is soon evident that we are dealing with acute phthisis. It must be said, however, that cases of acute caseous pneumonia rarely show the symptoms of genuine inflammation. Thus, in the form which simulates lobar pneumonia the sputum contains more blood, or is accompanied by genuine haemoptysis ; defervescence does not occur ; wasting is rapid ; signs of cavities appear in some cases, and the patient is carried off by acute consumption. The chronic and subacute forms of caseous pneumonia are quite as in- sidious in their course. The inflammation is ill defined ; the stethoscopic signs, rales, and tubular breathing remain stationary ; secondary pneumonia is thought of, and the primary cause is sought elsewhere. The question is asked whether the patient may not be diabetic, or suffering from Bright's disease, or cardiac mischief ; but the appearance of further symptoms soon makes the diagnosis clear. In these doubtful and difficult cases too much information cannot be obtained. The patient's antecedents (haemoptysis, suspicious bronchitis), and the question of heredity (phthisis among forebears or relatives) will^ have great weight in diagnosis. The presence of tubercle bacilli in the sputum of patients with caseous! pneumonia is less frequent than in cases of common tuberculosis. Bacilli] may be wanting in the expectoration, although they may be found in the^ lung tissue at the autopsy. DISEASES OF THE LUNG 203 XYI. ACUTE GRANULAR TUBERCULOSIS— ACUTE GENERALIZED TUBERCULIZATION. The terms "galloping" and "acute," applied to phthisis and tubercu- losis, have been variously interpreted by authorities, and this confusion has certainly complicated the study of these diseases. We must abandon the term "galloping," and keep only the epithet "acute," in opposition to that of " chronic." Phthisis is chronic when the lesions slowly and gradu- ally end in ulceration of the lung, cavities, and consumption ; it is sub- acute or acute when these lesions run a rapid course, as in certain cases of tubercular pneumonia : the patient then passes through the stages of phthisis in a few months or weeks, instead of several years. These different forms — chronic phthisis, which is the most common, subacute and acute phthisis — have been described in the preceding chapters. I shall now give the description of another form of tubercular infection — viz., acute granular tuberculosis, acute granulosis, or granulia. In the different varieties of phthisis which we have already reviewed, the grey granulation was of minor importance, while the miliary tubercles and the diffuse or circumscribed tubercular inflammations almost entirely made up the lesion. In acute granular tuberculosis the chief lesion is the tubercular granulation, while the hyperaemia and broncho-pulmonary infection only occupy a second place. The tubercles are so confluent, asphyxia and death arc so rapid, that the secondary degenerations and the ulcerations of the lung that accompany phthisis have not time to develop. We must, however, remember that the different forms of tubercular infec- tion may exist simultaneously in the same subject, in which case we find post mortem the lesions of chronic phthisis or of acute tubercular pneumonia, and the confluent granulations of acute tuberculosis. Pathological Anatomy. — The lesions of acute tuberculosis differ accord- ing as the granulations are or are not accompanied by congestion, bron- 'liitis, broncho-pneumonia, pleurisy, or old tubercular lesions. 1. In some cases the granulations constitute the only lesion, or, at least, the neighbouring inflammation which accompanies them is insignificant ; the parenchyma of the lung is riddled with granulations, both on its surface and in its deep parts. On section, the lung appears riddled with granula- tions ; these are almost always quite young, grey, and somitransparont ; wlien they are older they undergo degeneration in the centre. In chronic tuberculosis (ordinary phthisis) the miliary tubercle develops chiefly around the bronchiole, which serves as its centre of formation ; but in acute tuberculosis the grey granulation develops chiefly around the l)loodvessels and the lymphatics. The structure of the granulations has been described elsewhere. 204 TEXT-BOOK OF MEDICINE 2. In other cases the granulations of acute tuberculosis are accom- panied by intense congestion, capillary bronchitis, broncho-pneumonia, and pleurisy. If the disease has lasted some time, the tubercular granulations and the broncho-pulmonary infiltrations have already undergone initiatory softening and caseation. 3. In a large number of autopsies we find both acute and quite recent crops of granulations, and an old tubercular lesion, or a caseous nodule of broncho-pneumonia. On these facts Blihl founded his theory, according to which the crops of acute tuberculosis are only secondary lesions, grafted on the chronic lesion which has favoured their develop- ment. Cases of secondary infection, well known from Laennec's time, are very frequent ; they demand serious consideration, and prove that an indi- vidual attacked by acute tuberculosis has been already in the power of the tubercular infection, because old silent lesions are found in the lung, the brain, or other organs. Cases of secondary acute tuberculosis have been noted in patients primarily affected with tuberculosis of the eye, or with tubercular infiltration of the spine, of the lymphatic glands, etc. Still, acute tabercu- losis may be primary, as has been noted, in a large number of cases. Acute tuberculosis does not, as a rule, remain limited to the respiratory system. It often invades other organs and systems, and then merits the name of acute tuberculization. Few organs escape ^ peritoneum, meninges, pericardium, endocardium, synovial membranes, liver, spleen, kidneys, choroid, thyroid gland, bronchial and mesenteric glands, etc., may be invaded by the tubercular granulations. The glands may rapidly reach an enormous size, and cause certain com- plications, such as " compression of the bronchi, with symptoms of asphyxia ; compression of the mesenteric arteries, with intestinal gangrene ; compres- sion of the common bile-duct, with jaundice." In acute tuberculosis the granulations are usually found in the vascular and lymphatic tissue. Giant cells and bacilli have been recognized in the internal coat of the meningeal vessels and in the fibrinous thrombi of the vessels ; they have been seen in the lining membrane of the pulmonary veins (Miigge) ; in the tunica intima of the endocardium of the right heart ; in the vegetations of the endocardium ( Weigert) ; in the walls of the veins ; in the tunica intima of the inferior vena cava ; in the blood ; in the wall of the thoracic duct (Ponfick) ; and in the walls of the lymphatic vessels : so that acute tuberculosis " results, in all probability, from the entrance of bacteria into the general circulation of the blood or lymph plasma." Description. — Acute tuberculosis shows such different forms that an attempt has been made to classify them, either by the anatomical lesion or by the leading symptom. Although the different classifications proposed DISEASES OF THE LUNG 205 may be purely fanciful and but little in agreement with the clinical data, I feel that they are necessary for a pathological description. 1. There is a catarrhal form, of benign appearance, in which acute and almost latent tuberculosis (Leudet) resembles a seasonal fever, with some pulmonary or gastric symptoms ; but the patient is rapidly carried ofi by attacks of suffocation or of syncope after a more or less lengthy illness, which did not appear serious, and was supposed to be bronchitis or influenza. These latent forms are the more insidious inasmuch as they may be apyretic. I have seen a case at the Necker Hospital. 2. The suffocative form, which Graves calls acute tubercular asphyxia, and which, says Andral, resembles an acute attack of asthma, is characterized by increasing dyspnoea and asphyxia, which come on without warning, or, at least, in the midst of trifling symptoms. Pain, cough, and expectoration are absent ; the fever is moderate, and auscultation shows only some rales. This form, which is often accompanied by broncho-pulmonary congestion, may carry off the patient in four or five days. If an}i:hmg can give a clue to the diagnosis, it is precisely the absence of sigas, or, at least, the disproportion between the gravity of the symptoms and the levity of the physical signs. 3. Acute tuberculosis may be 'associated with the infections of the respiratory system (diphtheria), and is then partly masked by them. Thus when it takes the form of capillary bronchitis, we find cough, dyspnoea, and expectoration. There are the same fine, sibilant and subcrepitant rales ; and if other symptoms, such as bloody sputum, enlargement of the spleen, abdominal or cerebral troubles, are not present, the diagnosis is most difficult. When acute tuberculosis is associated with broncho-pneumonia (acute phthisis), the difficulties in diagnosis are the same as in the preceding case. The disease runs its course in a few weeks, or in two to three months ; we see the rapid formation of ulcers in the lung and the consumption of the patient, and this variety is confounded with pneumonic phthisis. In some cases the broncho-pulmonary inflammations give place to pleural inflammation, and the sero-fibrinous or haemorrhagic pleurisy is so promi- nent that the acute tuberculosis passes unnoticed, until it shows itself by symptoms that have nothing in common with simple pleurisy. A. The typhoid form answers especially to acute generalized tubercu- lization, and closely resembles typhoid fever : headaciii^, insomnia, pul- monary congestion, epistaxis, abdominal and cerebral troubles, and lenticular rose spots, are present. There exist, nevertheless, some distinctive signs which may assist in the diagnosis. In acute tuberculosis the stupor Is less profound ; hypera3sthesia of the chest is acute (Bouchut) ; ophthalmoscopic examination sometimes reveals tubercles in the choroid (Bouchut); the stetho- fcicopic signs are more marked at the apex of the lungs, and the sputum l^ L 206 TEXT-BOOK OF MEDICINE sometimes mixed with red blood ; the patient has attacks of dyspnoea, and the temperature cm-ve presents some differences. While the febrile cycle of enteric fever is made up of three periods, in which the temperature successively ascends, remains stationary, and descends, the temperature in acute tuberculosis is much higher at night than in the morning, and scarcely deviates from this type during the whole disease. Sero-diagnosis (VVidal) will remove all doubts between enteric fever and acute tuberculosis, 5. The cerebral form may show itself suddenly by loss of consciousness, followed by coma and symptoms of meningitis ; these symptoms recall the description of acute hydrocephalus, and, indeed, abundant effusion is found post mortem m the ventricles. The cerebral symptoms do not supervene as a simple episode, as is seen in the other varieties of acute and chronic tuberculization ; here they draw all the attention to themselves. 6. Unusual Forms. — There are cases which are, indeed, more rare and insidious than the precedmg ones, in which tuberculosis shows itself by such imusual symptoms that the nature of the disease is not recognized at first. Colin has published the history of a patient in whom the miliary tubercles primarily appeared in the kidneys, and the disease was at first taken for acute nephritis. In a case of Laveran the tuberculosis first invaded the articular synovial membrane, and for the first few days the disease was looked upon as acute rheumatism. 7. In some cases the tubercular lesions are little marked, but the viru- lence of the bacillus is exaggerated, and the disease truly deserves the name acute tubercular infectious fever. The case looks like typhoid fever, but there is no stupor, and the fever may improve under the influence of antipyrin. Diagnosis — Prognosis. — I have indicated the difficulties in diagnosis with regard to each of the forms which acute granular tuberculosis may assume. A search for bacilli in the sputum should never be neglected. It is the most valuable method, and in many cases has cleared up a doubtful diagnosis. Acute tuberculosis and acute generalized tuberculization are nearly always fatal, and, indeed, some forms carry the patient off in a few days. There are exceptions to this rule. Sometimes the tubercular granulations occur m intermittent crops ; the disease is not very acute, and lasts several months. In other cases the acute attack gives place to a chronic state, and acute tuberculosis becomes ordinary pulmonary phthisis. In some cases, when the tubercles have not been confluent, they pass into the fibrous state ; the disease becomes chronic, and may then be almost harm- less, if the patient is not affected with other acute or chronic manifestations of tubercular infection. Acute tuberculosis especially attacks young people and soldiers, and DISEASES OF THE LUNG 207 the military medical officers have insisted on its quasi-epidemic character. It is not rare in very young children, up to the age of fifteen or eighteen months, and although in them it is nearly always generalized, the absence of local symptoms renders the diagnosis very difficult (Parrot). The treatment of acute tuberculosis varies, according to the form that the disease assumes : tannin, in daily doses of 15 grains, and iodide of soda, in daily doses of from 120 to 240 grams (Lepine), appear to have given good results. XVII. FALSE TUBERCULOSIS OF THE LUNG. The tubercle, which is a mode of reaction of the tissues against patho- genic agents, is not in any way specific to Koch's bacillary tuberculosis. It may be met with in different affections, characterized histologically by tubercles ; these are cases of pseudo-tuberculosis. The causes of pseudo-tuberculosis are multiple. I would mention certain animal parasites — the Strongylus vasorum, whose eggs produce in the dog a tubercular reaction in the pancreas (Laulanie) ; the Ollulanus tricuspis, and the Pseudalius ovis fuhnonalis, one of which produces pneumonia in the cat and the other m the sheep. At bther times bacterial parasites are seen — for example, the bacilli of Maiassez and Vignal's zoogloeic tuberculosis ; also tubercles are produced by fungi, such as Favus cladothrix (Sabraces and Dubreuilh), Eppinger's streptothrix (Picot, Riviere, and Sabraces), and the aspergilli, which include Asfergillus subfuscus (Olsen and Gade), Asper- gillus nidulans (Lindt), As-pergillus flavescens, and, above all, Aspergillus jumigatus. Pseudo-tuberculosis is especially due to the latter fungus, and as it is the only one that has been observed in anything like a complete manner in man, it is the only one we shall describe here, under the name of aspergillary pseudo-tuberculosis. Aspergillary Pseudo-Tuberculosis. In man aspergillary pseudo-tuberculosis (pulmonary aspergillosis) has been met with chiefiy in pigeon-feeders and hair-combers. I have seen it several times in my wards at the Necker Hospital.* Bacteriology. — The Aspergillus jumigatus, which belongs to the order of xVscomycctes and to the family of the Perisporiacea?, is composed, in the adult state, of a mycelium made up of short alternating liyphae, whicli are slightly dilated at their extremities, and give off sterile, sc[)tate, and colour- less branches, and colourless or slightly colom-ed fruit-bearing ones. These latter support the spores, which rest on the receptacle or spore-bearing head, * Diculafoy, Chantemesso ct Widal, " Uno rseudo-tubcic-ulujic .Myti.i.si(luo " {Congress do Berlin, 1889). 208 TEXT-BOOK OF MEDICINE from which they emanate by the strangulation of small cells having the form of quills, and called basidia. The spores of the Aspergillus fumigatus are green or brownish, accordiiig to the media. Their maximum development takes place at 98° F.— that is, at a temperature nearly the same as that of the human body. These spores grow very well on Raulin's liquid, on beer wort, and Sabouraud's maltose ; their colour is brown on the former and green on the latter culture medium. In certain cases they may take on a yellowish colour. Gelatine is liquefied by Aspergillus fumigatus. In animals the pathogenic action of this fungus is well marked. Pigeons die three or four days after inoculation of the spores in the axillary vein ; rabbits die in six or eight days, and guinea-pigs in four or five days, after injection into the veins of the ear. The ape is less sensitive ; and this patho- genic action, which is nil in the sheep, is present in the case of dogs and cats (Saxer). Inhalation into the trachea kills pigeons in from twelve days to a fortnight. The ingestion of spores produces exceptionally in the rabbit tubercular lesions of the intestine, which may go on to perforation (Renon). Spontaneous aspergillosis is fairly frequent in birds ; it may invade the eggs during incubation, and transmit the disease to the chick (Leucet). It^s fairly rare in Mammifera?, where it takes the form either of chronic phthisis or of superacute hgemorrhagic septicaemia (Leucet). The spores of the Aspergillus fumigatus are present in the air, -upon trees, in the most superficial layers of the soil, and are also found in the nasal mucosa and the saliva of persons who are healthy, or who are suffering from the most diverse affections. The surface of seeds is, however, theu- chosen haunt (Renon). The resistance of the spores is considerable, and their vitality is enormous. They still reproduce themselves after two or three years' sojourn in an old culture, but their virulence is, in consequence, found to be attenuated. Their vitality is weakened by a more or less prolonged sojourn in organic mem- branes (Renon). Heat kUls them, and they then become harmless to animals ; but the animal is none the less susceptible to the injection of viru- lent spores, and appears to succumb the more quickly, as the degree of heat necessary for the sterilization of the primarily injected spores has been high. By a progressive inoculation with virulent spores, rabbits can be made to stand considerable doses, that would rapidly kill the control animals. The Aspergillus fumigatus does not produce toxines. Neither culture fluids nor substances extracted from the mycelium possess any vaccinal powers (Kotliar, Renon). In the rabbit the spores traverse the placenta, and are directly transmitted from the mother to the foetus. ^Etiology— Pathogenesis.— It is interesting to consider how pigeon- feeders may take the disease. Infected pigeons present on the floor of the mouth a small tumour, or chancre, which may cause a mouth-to-mouth DISEASES OF THE LUNG 209 contamination. It is probable that more usually pigeon and feeder find the common cause of their disease in the spores of the AspergUlus fumigatus which are present on the grains of millet and vetch. Hair-combers may also contract aspergillary tuberculosis. They are infected from the flour which they rub on the hair to remove the grease This flour contams many spores, while the undressed hairs collected every mornino in the dirt-boxes by the rag-pickers of Paris scarcely contain any of them*' Jiirds livmg m this dusty atmosphere succumb in a fortnight to three weeks • pigeons that are made to inhale this dust die of aspergillary tuberculosis In some cases aspergillosis finds in man a soil perfectly prepared by previous mflammation of the broncho-pulmonary system. The affection IS then secondary ; its progress is slow, and almost alwavs masked by the symptoms of the primary disease ; it is not recognized, as a rule, until the autopsy. In other cases aspergillary pseudo-tuberculosis is a primary or autonomous affection that is identical with the disease seen in animals and It IS this form that I have especially in view in this chapter. The French conception of primary aspergillosis (Dieulafoy, Chantemesse and Widal lotam, Renon, Gaucher and Sergent), after having been actively attacked in Germany, ls now completely admitted ; it is indisputable, for it corresponds exactly with anatomical, experimental, and clinical facts (Renon) Cases have been multiplied during the last few years, and, according to Saxer primary aspergillosis is much more frequent than is usually supposed The only difference that stiU separates the French from the German school consLsts in the term " pseudo-tuberculosLs," which is applied in France to the primary aspergillary ulcerative process in the lun.^ If we remember that this affection, which destroys the lung tissue, presents all the clinical signs of tuberculosis, we see that we are very nearly in agreement, and that in every case the idea of aspergillosis as a primary disease receives a striking confirmation. Symptoms.-Asporgillary pseudo-tuberculosis presents various forms Ihe disease may begin with slight or with abundant haemoptysis followed m general by other attacks at intervals of several months, or of one or two years. At the same time, fatigue, loss of strength, with dyspepsia and anorexia appear. The cough is dry, and recurs in fits. The expectoration, at first fro liy becomes greenish and purulent, and the sputum is often streaked with blood. The signs of pulmonary tuberculosis in its first stage are found --namely, slight induration at one apex, with harsh breathing and some- times prolonged expiration. A rise of temperature to 102° F., with or without niglit sweats, may be noted; sometimes, also, pleurisy, with or without eftusion, may occur. In some patients haemoptysis is rare, and the signs "t l>ronchitis are most prominent. The cough is Licessant, and suffo- 14 210 TEXT-BOOK OF MEDICINE cation i. intense, especially during the night. Indeed, ;«->- °|;>;*; asthma " (Benon) are seen ; the breathlessness diminishes durmg the day, bnt 3y f the patient makes no active efforts. The .putum is greeni^. Z2nt and sometimes nummular. During the attaclcs a brmtd. tempete, wMi norh g sibilant and subcrepitant rales, is heard ; between the attacks, r™ptom of puhnonary induration at the apex of the lung may be found. nrrruK the other organs are healthy, the liver and spleen bemg '■^Ihe'ci" -the disease is not always progressive, and slight improve ment of variable duration may alternate with transient ^W^^f^^, ^^^ fe not as in ordinary tuberculosis, a gradual and progressive extensKin of the ons After a period of transitory cachexia, the patients regain tlieir good condition, and sometimes resemble tubercular patieii s ->}^f^l^l would not be considered sick if auscultation were not performed Retro Session is therefore nearly always the rule -the aspergiU,^ g-duaUy d^ Ippears from the expectoration, and a definite cure may be caused by fibrosis, as is seen in the case of animals. j ti,„ 1„„<,<, bv Koch's The most formidable complication is the mvasion of the lungs by K-och s bacUlus, which gradually takes the place of the f™S- ■ t^^^;-- ^^^^ that of an ordinary pulmonary tuberculosis, accompanied by local lesions, : aiialt^ulalrUaneouftuberculosis. Thisfibro-plast.^^^^^^^^^ asnerdUus however, helps the struggle against the new parasite but the cS access ma; overshoot the mark, and m one case Reiion and bergent h^ve notTd that fibrosis became, in its turn, the chief complication, and the patient died of dilatation of the heart, with asy.stole. The duration of aspergillary tuberculosis is very long ; it has lasted three six eight years and more in the cases that have so far been observed Th iSfc /««>«- niay not harm the lung, and may only mvade the bronchial system. The result is a peculiar --''-»- —^• which was essentially chronic in the two known case. J^'^^^^™ ' composed solely of mycelium and spores were situated in ^"^^ » «« ~ and expelled almost every month, with a crisis of acute dyspncea (Obici, ''"D^gTosUr-^^trLportant to make an early diagnosis, but this is im- possMe'by clinical methods alone. We should think of the asperg" ; hi a patient who has tubercular lesions, recognized as such by physical xam!:ation, the course of events is slow and the general heathremams goo ^ The probability will become much greater if the patient be exposed in hfs work to handlmg gram or flour (pigeon-feeders, hair-combers miller edimen. etc.) ; and it will become a certainty if Koch's bacillus be absent fromThe sputim and the mycelium be present. The diagnosis, thereforp entirely rests on bacteriological exammation. DISEASES OF THE LUNG 211 In searching for the bacilli, the Ziehl-Kiihne method should be employed. If the result ls negative, we must prove the absence of the bacilli by inocula- tion of a guinea-pig with the sputum. If thirty or forty days afterwards the animal presents no tubercular lesion (verified bacteriologically) at the point of inoculation, the question is decided : it is not a case of Koch's tuberculosis. The search for fragments of mycelium in the sputum should be made with an aqueous solution of safTranin, or, better still, by staining with thionin. If the search is negative, recourse may be had to cultures. If it is positive, the same procedure should be employed, to make certain that the fragments are really those of the aspergillary mycelium. The fresh sputum, collected aseptically, should be sown in tubes of sterilized Raulin's liquid, and placed in an oven at 98° F. If the sputum contains spores or mycelium, we shall, by the second day, see that isolated filaments, which are united into a tuft of mycelium, rise up from the sown particle ; the mycelium will rise gradually, and take from three to six days to reach the surface. Some hours later it will form a whitish, velvety, and absolutely characteristic carpet, which twenty hours later is covered with greenish spores, that assume a smoky-black colour in a few days. We must then verify the pathogenic action of the fungus thus found on the rabbit, and absolutely prove the Aspergillus fumigatus, since the two other species, Aspergillus niger and Aspergillus glaucus, which develop under these con- ditions, are non-pathogenic. The animal will succumb in a few days to a generalized aspergillary tuberculosis of all the viscera, but especially of the kidneys, and a fragment of the latter organ, sown in a tube of Raulin's liquid, will in five or six days reproduce a culture of the Aspergillus fumi- gatus. The cycle will be complete, and absolutely no room will be left to doubt the existence of the fungus in the sjiutum. We can thus eliminate asthma, chronic bronchitis, and Koch's tuber- culosis. The pseudo-tuberculosis produced by the Rhizomucor parasiticus (Lucet and Constantin) closely resembles aspergillosis ; minute examination of the parasite found in the sputum and cultures will alone prevent error. Actinomycosis of the apex of the lung is often accompanied by chocolate- coloured expectoration, which consists of a mixture of blood and pus ; the peculiar grains of the actinomyces arc found in it. In the exceptional cases of puhuonary mycosis, due to Eppinger's streptothrix, the form of the mycelium in the sputum is different, and cultures decide the question. Prognosis.— The prognosis of aspergillary pseudo-tuberculosis is rela- tively good ; this does not obtain in pseudo-tuberculosis complicated by Koch's bacillus. The remissions arc less frequent and less prolonged ; the puhuonary signs are more marked, and death may supervene at a distant date. 14-2 212 TEXT-BOOK OF MEDICINE Pathological Anatomy. — ^When aspergillary pseudo-tuberculosis is secondary, and occurs as a complication of chronic bronchitis or of previous pulmonary tuberculosis, it is, as a rule, a post-mortem discovery : small velvety, greenish, or brownish tufts, composed of adherent mycelium, are found. The cavity contains full-blown spores. Outside this infiltration of the walls of the cavities by the fungus we may see (Lichtheim, Cohnheim, Fiirbinger) tubercles of the size of a nut or of a millet-seed, which, under the microscope, show an abundant mycelium extending from the tubercle to the alveoli. The lesions of simple and primary aspergillary pseudo-tuberculosis have been studied in man (Ribbert, Boyce, Saxer), and also in animals (Dieulafoy, Chantemesse and Widal, Ribbert, Renon, Obici, Saxer). Microscopically there is no difference between the tubercle due to the aspergillus and that due to Koch's bacillus. In pigeons the lesions affect especially the lung and the liver ; in rabbits they affect the kidneys ; and pleurisy, enteritis with perforation of the gut, peritonitis, cystitis, and osteitis of the vertebrae, with congestive abscess, simulating Pott's disease, may be noted. All these lesions are tubercular in form. The mycelium is passed in the urine, when the renal changes are marked (Renon). The tubercles vary in size from a pin's head to a small pea ; they may undergo vitreous degeneration and calcification, with formation of true cavities ; at other times we find a tubercular infiltration en nappe. Asper- gillary tuberculosis may pass into a fibrous condition, which is one of its active modes of cure. This process is also seen in man, even when bacil- losis is present as a complication. At the autopsy of a pigeon-feeder, affected in succession by these two maladies, Renon and Sergent noted marked lesions of chronic pneumonia ; the fibrous tissue extended from the bronchi to the pleura, choking the lung tissue proper. " The histological lesions are in every way comparable with those of bacillary tuberculosis. In a section of the lung we see a large number of tubercular nodules, surrounded at their periphery by giant cells. The growth of these nodules can easily be followed. The young ones are formed by an agglomeration of leucocytes or of epithelial cells around one or several branches of mycelium. The older granulations present in their centra a feltwork of mycelium, the interlacing branches of which stain better at the periphery, in the immediate neighbourhood of the giant cells. In certain cases the tubercle is solely represented by a very large cell with multiple nuclei ; while the protoplasm contains a ramification of mycelium, either alive and well stained, or altered in structure: moniliform, unstained, and partly digested by phagocytes " (Dieulafoy, Chantemesse and Widal). In chronic cases we sometimes find in the tubercle tufts of abundant mycelium, presenting a great likeness to actinomycosis (Laulanie, Renoi DISEASES OF THE LUNG 213 Ribbert, Boyce) and to the actinomycotic forms of Koch's bacilhis (Renon). Indeed, according to the German school, the fungus plays the chief part in the production of the histological lasions in the human lung. The aspergillus is said to provoke foci of necrosis, which, by elimination of their con- tents, cause cavities. This process is said to be specific (Saxer). We see, however, that two at first irreconcilable opinions are almost brought into harmony, although the primary pathogenic action of the parasite has remained a subject of active discussion. Treatment. — ^The treatment is symptomatic and general. Haemor- rhage must be treated by the means given under Pulmonary Tuberculosis. Bronchitis may be alleviated with creosote and terpene, and tincture of lobelia, with iodide of potash, which has given fail- results in animals, should be employed for the attacks of suffocation (Rer.on). The general condition should be maintained by superalimentation and by large doses of cod-liver oil (.3 to 5 ounces daily), and residence in the country, at the seaside, or in a climate at high altitude should be advised. XVIII. CANCER OF THE LUNG. etiology. — Cancer of the lung may be primary or secondary ; the former is rare, the latter common. The growth is frequently secondary to cancer of the breast, which extends to the parietal pleura, when the subpleural lymphatics carry cancer cells to the lung. Tlie mechanism is the same in the propagation of cancers from tlie mediastinum to the lung. Cancer of the lung is sometimes secondary to that of tlie abdominal organs — glands, stomach, intestines, liver, and ovary. The spread of cancer from these organs to the lung takes place in different ways : by venous emboli, following the course of the portal vein, vena cava, right heart, and pulmonary artery ; by way of the lymphatics, the cancer reaching the peritoneum over the diaphragm and passing through this muscle by means of the lymphatic communication existing between the peritoneum and the pleura, and invading the visceral pleura and lung. When cancer is consecu- tive to that of the limbs or of tlie head, the propagation takes place by the venous (■Jianiicls. Pathological Anatomy. — Cancer of the lung may be lobar or diffuse. The lobar varirty forms a bulky mass, which may involve or comjjress the neighbouring organs (tracjiea, oesophagus, arteries, and veins); in tlir diffuse form th(! growth is (lissimiinated in the form of nodules in the deep layers, or on the surface of the organ. 214 TEXT-BOOK OF MEDICINE Lobar cancer is usually primary and unilateral. Diffuse or noaular cancer is nearly always secondary, and affects both lungs ; the cancerous nodules may be superficial (sub pleural) or deep (intrapulmonary). They are of all sizes ; some are no larger than a pin's head, and the condition is called miliary carcinosis, from its resemblance to tuberculosis ; other nodules are as large as a pea or a walnut. Primary cancer nearly always assumes the encephaloid form. Secon- dary cancer is a reproduction of the parent growth, which may be scirrhous, melanotic, colloid, or adenomatous (Marfan). The cancerous mass may finally become softened ; in some cases it forms a bloody pulp, the elimination of which may give rise to a cavity. Microscopic examination in primary cancer shows the alveoli blocked by spherical or polygonal cells, with large ovoid nuclei. The alveolar walls are usually normal. " There is no stroma of new formation in cancer of the lung, and it is the fibrous framework of this organ which takes its place." The epithelial origin has been definitely shown by Malassez. Cancer arises in the epithelium ; it is uncertain whether the bronchial or glandular epi- thelium may not give rise to it. All the structures in the mediastinum may be invaded by cancer of the lung. The lymphatic vessels and the corresponding glands (cervical and axillary glands), especially the bronchial ones, may show simple inflamma- tion or cancerous change. The pleura is usually i'nvolved in cancer of the lung ; the result is pleurisy, with effusion, which is very often haemorrhagic (see Haemorrhagic Pleurisy). Description. — In a description of cancer of the lung it is necessary to distinguish the symptoms which properly belong to it from those which depend on invasion of the mediastinum and of the pleura ; this distincstion, however, is very difficult, for cancer rarely remains confined to the lung without affecting the pleura or the glands of the mediastinum. The symptoms proper to cancer of the lung are somewhat limited. The patient complains of pain (pain in the side, which may or may not be radi- ating) of increasing intensity ; the pahi may be brachial, cervical, or inter- costal, and accompanied by zona. Cough is a usual symptom. Dyspnoea may be slight, severe, continuous, or paroxysmal, with or without stridor, depending on the multiplicity of its causes. Compression of the trachea and the bronchi, compression of the vagus and recurrent nerves, lesions of thejpleura, and pleural effusion, may all cause dyspnoea. Haemoptysis is fairly frequent, and some authors have given as charac- teristic the currant- jelly-like expectoration which contains cancer elements and elastic fibres from the lung. I have lately seen a typical case of tliis expectoration, with Dr. Marcano, in cancer of the lung, secondary to that of the breast. According as the cancer is lobar or diffuse, the dulhiess yields DISEASES OF THE LUNG 215 more or less precise information ; auscultation may sometimes show tubular breathing and bronchophony. When the bronchial glands are invaded by cancer, the symptom-complex, which we shall study under Tumours of the Mediastinum, is found. I shall here simply mention two of these symptoms : paroxysmal or intermittent dyspnoea (compression of the vagus and phrenic nerve) and cough, which is often analogous to the fits of whooping-cough. The cancerous mass may also cause compression of one recurrent nerve (dyspncea and spasm of the glottis), of the oesophagus (dysphagia), or of the venous channels (oedema of the face and neck and supplementary circulation). It sometimes happens that acute, subacute, or latent pleurisy masks the development of cancer of the lung ; the patient only complains when dyspnoea, due to effusion or to other causes, has become severe. Pleurisy is discovered ; thoracentesis ls performed, and fluid, which is most frequently blood-stained, is drawn of? ; and yet, in spite of the operation, pain, cough, and dyspnoea continue. I have seen several cases — one, among others, with Dr. Auburtin. The patient had a considerable pleural effusion. I evacuated seven pints of blood-stained fluid in four sittings. The im- provement was of short duration,^ and, though the effusion did not recur, the cancer continued its progress. In one of the following sections we shall see the importance ' of haemorrhagic pleurisy in cancer. After a duration of from one month to two years, cancer ends in death. Death which supervenes from increasing dyspnoea and asphyxia is terribly painful ; injections of morphia are in such cases the only palliative. Rapid or even sudden death has often been noted. In other cases the patient dies in a state of asystole, with general oedema, cyanosis, and coma. Some- times hectic fever supervenes and ends the scene. The diagnosis of cancer of the lung presents serious difficulties, especially when it is primary and runs an acute course. We are so used to the slow progress of cancer, to the gradual breaking-up of the individual, and to the characteristic colour of the skin, that the diagnosis is often at fault when cancer runs an acute course. This acute course is not rare in cancer of the lung. An individual in good health shows symptoms which might quite well be put down to acute phthisis. He dies in a few weeks, and cancer of the lung is found post mortem. In doubtful cases we must never omit to look for cancer in other organs — e.g., cancerous nodules under the skin, cancer of the liver, rectum, testis, or uterus. A previous operation or the presence of a scar (breast) may give a clue. I have twice seen cancer of the lung in patients wiio liad undergone operation — the one for disease of the left testis, the other for an osteo- 216 TEXT-BOOK OF MEDICINE sarcoma of the knee.* It is also necessary to make sure of the condition of the corresponding axillary or cervical glands ; this evidence of cancer, although inconstant, is none the less valuable when it exists. XIX. BRONCHO-PULMONARY LITHIASIS. Pathological Anatomy and Pathology. — " Lung stones," or broncho- pulmonary lithiasis, has been well described by Poulalion. From the histo- logical point of view, they may be divided into three categories — cartilagi- nous or cartilaginiform, bony, and calcareous bodies. We must also differ- entiate the growths and the changes which take place in the thickness of the broncho-pleuro-pulmonary tissues, and constitute parenchymatous, cartilaginous, bony, or calcareous concretions, from those which occur in the Ulterior of normal or accidental cavities in the respiratory system, and are always calcareous in nature, constituting calculi, properly speaking (broncholiths). 1. The cartilaginous or cartilaginiform growths are made up of carti- laginous or other dense fibroid tissue ; they may be situated in the walls of the bronchi, in the pleura, or in the lung tissue. They have the appear- ance of cartilage, and are resistant, elastic, whitish, opaline, and of a bluish sheen. 2. Bony growths are characterized by the existence of osteoblasts and the presence of newly-formed Haversian canals. These bony calculi arise in ossified bronchial cartilages (bronchial dilatation, pulmonary phthisis), in ossifications of the tracheo-bronchial mucosa, in ossifications of the pleura, developed in the fibrous shell of old pleurisies. 3. Calcareous growths result from calcification of the different tissues in the respiratory system, by incrustation with particles of tribasic phos- phate of lime and carbonate of lime. Among the lesions of the lung which may undergo calcareous transformation we must notice, m the first place, the caseous tubercle, then infarcts, broncho-pneumonic nodules, miliary abscesses, pseudo-tubercles of actinomycosis or of the aspergillus, and, lastly, cysts and tumours of the lung. The lung may only contain some isolated, calcareous concretions, as is the case in the caseous nodules of ordinary tuberculosis which is in process of cicatrization and cure. At other times, on the contrary, the concretions are in considerable number, and the lung tissue is, as it were, riddled by them ; this condition is called calcareous granulosis of the lung (Poulalion). The parenchymatous concretions may become stationary and remain latent, but in other cases they may undergo a process of enucleation which * This i:)atient, whom I saw with Dechambre, was suffering from cancer of the upper left lobe, which presented the appearance of encysted pleurisy. DISEASES OF THE LUNG 217 causes their migration into the tissues, and generally ends by their passing into the air-passages. Intracavitary calculi present the most marked analogy with biliary and urinary calculi ; they may, like the latter, have as their nucleus of origin foreign bodies from wathout, or parenchymatous concretions which have been set free ; they are formed in the bronchial channels, or in cavities accidentally developed. Symptoms. — In some cases broncho -pulmonary lithiasis, especially in its parenchymatous forms, may be latent, and only be discovered post mortem. As a rule, the presence of calculi in the respiratory passages pro- duces troubles similar to those which occur in the biliary or in the urinary tracts. True crises of bronchial and pulmonary colic occur. Sometimes the expulsion of the concretion takes place without the patient perceiving it, and he expectorates the calculus while coughing ; at other times, on the contrary, as happened to a patient in my wards, the expulsion is preceded by heaviness, dyspnoea, pain, constriction, anguisli, and a feeling of tearing, either in the sternal region or at the sides of the chest. Thene pains are almost always followed by obstinate, jerky cough, during which the patient suddenly experiences a sharp, tearing sensation in the larynx, and increase of the dyspnoea, followed immediately by the expulsion of a hard body, which may strike against the back of the incisor teeth. The expectoration of the calculas being accomplished, the bronchial COlic ends, and the cough and pain frequently yield at the same time. Sometimes it is only a case of abortive bronchial colic ; the patient, while coughing, experiences a painful sensation or feeling of a foreign body rising in the trachea, and then passing back again into the bronchi and lung. The duration of the crisis is very variable. It may last a few moments, or even some hours — as many as forty-eight (Poulalion). The number and size of the calculi brought up are also variable ; as many as 400 have been counted, and may be as large as a ])in's head, a millet-seed, or a nut. Tlie expectoration of calculi is often accompanied by Imemoptysis, which, tliough generally slight, is sometimes fulminant ; the bleeding may precede the expectoration of the calculus by some days, but as a rule accompanies it. We may see fever due to neighbouring inflammation, or to the action of the calculus on the altered mucosa, with consecutive absorption of septic products. PLxamination of the chest before, during, or after the crisis most often yields but trifling information ; bronchitic rales are heard, and it is only in obstruction of a large bronchus by a concretion that we can recognize behjw the obstacle more or less extensive absence of breath- sounds. Br()ncho-])ulnionary lithiasis may ofcur in the course of tnborculosis, and favour the development of the latter trouhle. 218 TEXT-BOOK OF MEDICINE In other cases the chronic course of lithiasis simulates phthisis, although absolutely no tuberculosis is present ; this is known as pulmonary pseudo- phthisis of calcareous origin (Poulalion). During a more or less lengthy period the patient suffers from cough, which is at first dry, but later is accom- panied by mucous or muco-purulent sputum. These symptoms become worse ; signs of induration, of pulmonary congestion, or of localized bron- chitis, aiad even those of small cavities, are often found. The general con- dition becomes bad ; wasting and night-sweats appear. Haemoptysis is common. The attention, however, is chiefly attracted to the dyspnoea and the pain ; both come on in more or less intense attacks, until in a more violent fit of coughing than usual the patient brings up the calculus, with or without haemoptysis. The symptoms now show marked improvement, when only one calculus exists ; but the relief is temporary when there are several calculi, and their expulsion is always preceded by a period of aggrava- tion. In this form Koch's bacilli are never found in the sputum. Cure is the rule when there are no complications. As complications, I may note acute bronchitis, which generally ends favourably ; pleuro- pneumonia, which is often fatal ; abscess of the lung, which sometimes opens up the bronchi, or ends in perforation of the pleura and pyopneumothorax. Sudden death from obstruction of a large bronchus by a calculus has been noted (Tice). Diagnosis. — The diagnosis is almost always impossible before expulsion of the calculus. Cough, dyspnoea, and pain in the chest are quite insufficient signs, and the rejection of the calculus must be waited for. We must then ascertain whether the patient is tubercular or not, and whether the con- cretion is of intraparenchymatous or intracavitary origin. Examination of the sputum for bacilli and inoculation of the guinea-pig will help to decide the first point ; as regards the second, histological examination of the cut section will establish it. The differential diagnosis must be made from fragments of bone that are coughed up, but do not come from the respiratory system ; from portions of the vertebrae in Pott's disease (Chenieux) ; from a sequestrum from the larynx ; calcareous concretions formed in the ventricles of the larynr (Pravaz) ; concretions from the crypts of the tonsils ; rhinoliths which have fallen into the pharynx ; and, lastly, foreign bodies which have reached the lung from without. The prognosis of calculous pseudo-phthisis is not grave when the patient brings up the foreign body ; yet apart from the complications mentioned above, the prognosis is much affected by the weakened condition of the lung and the possible development of tuberculosis. Treatment can only be symptomatic ; surgical intervention appear^ hardly possible, because precise indications are wanting as to the seat of the DISEASES OF THE LUNG 219 calculus. If calcareous change in tubercles is favourable to their cure we should assist this calcification by the use of soluble phosphates and by nourishment which contains much vegetable matter. XX. HYDATID CYSTS OF THE LUNG AND OF THE PLEURA. Pathological Anatomy. — In frequency hydatid cysts of the lung come next to those of the liver — that is to say, we see them fairly often. As I have described in detail (see Liver) the life history of the hydatid, I shall here notice only the characters peculiar to hydatid of the lung. The cyst usually affects the right base. It is sometimes associated with a cyst in the liver. The pulmonary cyst is unilocular, the alveolar cyst being extremely rare. In order to reach the lung, the embryo follows various routes. It may enter the respiratory tract by aspiration of dust ; it may be ingested with food and drink, pass from the intestine into the portal veins, traverse the liver, the subhepatic veins, the vena cava, and the heart, to be arrested in the lung. The embryo may perhaps enter the ha?morrhoidal veins, pass tlirough the pudic and the internal iliac veins, reach the inferior vena cava, without passing into the liver (Chachereau), and travel through the heart into the lung. In the case of coexistence of hydatid of the liver and of the lung, it may be asked if the embryo has not migrated directly from the one organ to the other. The adventitious covering of hydatid cysts of the lung is very thin ; it may be completely absent, and this fact will explain why the cyst so readily opens into the bronchi. Hydatid cysts of the pleura are rare, unless the pleura has been invaded secondarily by a pulmonary cyst. Description. — As the lung is less tolerant than the liver, the early growtli of the pulmonary cyst is rarely quite latent. In the liver, cysts may be present for a long while and may attain large proportions without pro- ducing symptoms or results ; enlargement of the right hypochondrium is sometimes the first sign of the hydatid cyst. In the lung, on the other hand, it is exceptional for the hydatid to remain quiet long ; indeed, its presence may be revealed early by important symptoms, of which haemoptysis is the most striking. Period of Onset. — Dry, jerky cough may be the only symptom for weeks. It is the result of a reflex, and simulates the cough of tuberculosis, with this difference, however — that the cough in tuberculosis is almost always followed by some ex})ectorati()n. The pain, which is rarely sharp at this stage, may simulate pleuritic pain or intercostal neuralgia ; in some cases it is obstinate, and radiates into the neck, the shoulder, and the epigastrium. 220 TEXT-BOOK OF MEDICINE Dyspnoea is present at an advanced stage of the malady, and in com- plications ; although it is rare during the early growth of the hydatid, it has been noted in some cases. Haemoptysis, from its importance and its frequency, deserves careful atten- tion, and, while it may be either slight or severe, and more or less repeated, plays a large part in the history of pulmonary hydatids. Early haemoptysis, arising at the onset of the malady — before any other symptom, indeed — and late haemoptysis, coincident with the opening of the cyst, are both seen. Early haemoptysis comes on as a precursory sign in this disease, as in many pulmonary affections. It is, indeed, remarkable that the first cry of revolt on the part of the lung against the invader is perhaps a means of defence. Since phagocytosis is insufficient to meet the attack, the vessels take part, and it may be said that the lung seeks to get rid of its adversary by the ejaculation of blood ; it sometimes succeeds, and the haemoptysis, having no ill results, is then termed " essential." I have named this early haemoptysis " defensive." It is very frequent in pulmonary tuberculosis ; tubercular haemoptysis may, indeed, arise in the course of apparently excellent health, when no suspicion of tuberculosis exists. Parents who have suffered from haemoptysis may beget tubercular children, although the former may have had no other sign of tuberculosis than the haemoptysis, which has left no traces. We also find early haemoptysis in false pulmonary tuberculosis ; I have seen it many times in pigeon-feeders affected with aspergillary tuberculosis {vide Chapter IV., section xvii.). Early haemoptysis is also seen in patients with broncho-pulmonary concretions, who are suspected of tuberculosis, until they bring up the concretions during an attack of bronchial colic. Hydatid cysts of the lung especially provoke early haemoptysis, as will be seen from the following examples, taken from my clinical lecture on the subject :*- A case sent to me by Dr. Leroy : On May 22, 1898, the first haemoptysis came on, without appreciable cause, and a so-called pleuritic pain appeared on the right side. Four months later fresh haemoptysis (about a pint of bright frothy blood) suddenly took place ; obstinate cough supervened, and the patient was convinced that he had tuberculosis. He was treated without success, for his strength gradually decreased. At intervals pain reappeared on the right side ; appetite diminished, and six months later he had lost 32 pounds in weight. Next year the same symptoms were present : frequent fits of coughing, and further spitting of blood. Four large hsemoptyses were recorded. On each occasion the haemoptysis was treated with ergotin, Rabel -water, and applications of ice, with absolute rest in bed. Each bleeding left the patient still more feeble ; though he had no fever, he coughed continually. The situation became worse, and the diagnosis of haemoptoic tuberculosis appeared no longer doubtful. * Dieulafoy, " Les Hemoptysies des Kystes Hydatiques du Poumon " {Clinique Medicale de r Hotel -Dieu, Paris, 1905), 16'"'^levon. I DISEASES OF THE LUNG 221 A decisive incident, however, revealed the true nature of the affection. On Novem- ber 12, 1899, the cough became more violent than ever, and he coughed up much blood- stained sputum and a large piece of hydatid membrane. The thoracic pain, the cough, the numerous haemorrhages, were due, not to tuberculosis, but to a hydatid cyst of the lung, which had previously given no definite sign. The expulsion of hydatid membranes and the attacks of haemoptysis recurred on several occasions. The .expulsion of hydatid membranes was almost always heralded, twenty-four hours in advance, by fits of coughing and by more or less abundant haemop- tysis. On the other hand, some of the haemorrhages were not followed by expulsion of hydatid membrane. From March 24, 1900, to the beginning of April, 1901, thirteen large hajmorrhages were counted, without expulsion of pus or of membrane. They con- tinued during May, but it was not till August 25 that pus and large membranes were brought up. During the last four months of 1901 the hcPmcrrhages recurred, and were always followed by the coughing up of hydatid membranes, with or without purulent sputum. In 1902 haemoptysis, membranes coughed up ; from May 22, 1898, to April 12, 1902, haemorrhage on sixty different occasions, and membranes coughed up on forty- three. He is now cured. Case published by Laveran : A soldier, twenty-six years of age, was in excellent health up to the end of October. He practised fencing a great deal, and in the latter part of October, during an assault-at- arms, he suddenly felt sharp pain in the chest, and brought up about a tumblerful of bright red blood. After a few days he resumed his duties, but soon felt pain on both sides of the chest, and had fresh hajmorrhage. On December 5 he was sent to a military hospital, where phthisis was diagnosed, and he was invalided out. Next April the cause of these haemorrhages was discovered : the patient coughed up pus containing hydatid membranes, and thus got rid of his hydatid cyst seven months after the first spitting of blood. A medical student has published his own case : After an attack of pleurisy the patient had slight haemoptysis, in April. The sputum was frothy and tinged with bright blood, while signs of congestion and crepitant rales, were found at the right apex. During May the patient was treated with quinine, creasote, etc. Fever app(;ared, and he lost his appetite. On May 25, fresh haemoptysis. Finally, after a series of troubles, thought to be tubercular, in January 1.3 of the next year, he found a piece of hydatid membrane, 2 inches square, in the sputum. Watelet relates the following case : A man of forty was taken ill with haemoptysis and wasting ; rales in tlic left lung ; tuberculosis suspected. F'our months later fresh haemoptysis, foetid sputujn, and expul- sion of enormous hydatid membrane. Landouzy writes : A woman had five ha-morrhages three months before the rupture of the pulmonary cyst. The blood was red and frothy ; the quantity about half a tumblerful on each occa- sion. She had been considered tubercular. Fenger and Hollister speak of a patient who had attacks of haemoptysis for twelve years. Later he brought up the cyst ; pncumotomy became necessary, and he recovered com})letely. In a case of hydatid of the lung reported by Delgrange haemoptysis, which was sometimes triHing, sometimes very profuse, persisted for five months. 222 TEXT-BOOK OF MEDICINE In his admirable lecture on hydatids of the lung Trousseau has been careful to say that hsemoptysis has been noted in almost every case, and, among other examples, quotes Mercier's case : A man was subject to haemoptysis for several years, but showed no other signs of tuberculosis ; he was suddenly seized with acute pain in the right side ; examination of the chest revealed hydropneumothorax. Post mortem hydatid of the lung was foiuid ; it had caused perforation of the pleura and ulceration of a bronchus. A gentleman from the Argentine Republic, thinking himself affected with pulmonary tuberculosis, consulted me at the beginning of 1902. He complained of obstinate cough for two months and frequent haemoptysis. No sputum. On auscultation, I dis- covered no trace of tuberculosis, neither rales nor dullness being present. Examination of the sputum failed us, because the patient brought up none. The appetite was bad, and the man was wasting. I left the diagnosis open. After an interval of some weeks I saw the patient a second and third time, and the most minute investigation revealed nothing. The haemoptysis continued. One day the patient brought me a bottle containing a cloudy liquid, with a quantity of hydatid shreds, which he had brought up during the night, after terrible fits of cough- ing and of breathlessness, which almost amounted to suffocation. The diagnosis was clear, and I took the offending body to the H6tel-Dieu, telling my pupils the history of this patient. Hearn, in his work, which comprises 144 cases of hydatid of the lung, gives prominence to the frequency of haemoptysis. " In less than a fifth of my cases," says he, " there is no mention of it." In Iceland, where hydatid disease is so frequent, Finsen says that it is almost possible to diagnose pulmonary echinococcus from spitting of blood. Vegar and Cranwell, in their monograph on hydatid cysts in the Argentine Republic, say that haemoptysis constitutes one of the most important symptoms in cysts of the lung. Widal has reported a case of hydatid cyst of the lung in which daily haemoptysis without fever and expectoration remained the chief symptom for four months. To sum up, haemoptysis, whether early or anterior to the rupture of the cyst, presents different forms. In some cases haemoptysis is reduced to a minimum. We see bloody, brownish, or reddish sputum of a gooseberry or currant colour. This sputum is coughed up, and may recur several times in the day for weeks or for months, with or without periods of arrest. Some- times bright red blood is brought up at more or less definite intervals for months or even years. On examining the cases, we see that haemoptysis may precede the other signs. I think that the embryo may, from the moment of its fixation in the lung, cause haemoptysis, and I believe that haemoptysis may be repeated when the hydatid cyst is only as big as a pin's head, a small pea, or a nut, and may go on during the growth of the cyst before its rupture. Such is the early haemoptysis. It is evident that we must recognize it. The above details will, I think, suffice as regards early haemoptysis] DISEASES OF THE LUNG 223 which accompanies the growth in the lung ; subsequently we shall have to study the late haemoptysis which accompanies rupture of the cyst. Let us now consider pleurisy — a very rare complication, it is true, but one which may nevertheless supervene from the first. It is important to remember that pleurisy may supervene at the onset of a pulmonary hydatid. I do not speak, of course, of hydatid of the pleura, which is extremely rare, as we shall see later ; I allude to those cases of pleurisy which develop in the ordinary way from the onset of the pulmonary cyst. I do not know its exact pathogeny, but it is certain that pleurisy may develop in hydatid of the lung, as in that of the liver — e.g. : A hospital attendant, who had been treated for a month for pleurisy, which was cured, coughed up four months later foetid sputum and hydatid membranes. A medical student, Marconnet, was taken ill "mith pleurisy, which preceded the other symptoms of hydatid. " The numerous attacks of pleurisy," says Marconnet, " from which I suffered during my disease were assuredly due to the formation of the cyst. They were, moreover, so strange that they puzzled my doctors. The effusions dis- appeared as if by magic. If it be admitted that my first pleurisy may have been primary, and that it was not the result, but the cause, of localizing the hexacanthus, how can the pleurisies wliich were consecutive to it be explained ? Is it not more rational to consider that they were all caused by the parasite ?" Another medical student, Chachereau, who also reported his own case, suffered at the age of twenty-three from pleurisy, which was the first symptom to appear. At the end of 1872 he suffered from left pleurisy, with much effusion. Dr. Leonard! recognized the gra%nty of his condition, and thought of puncture. The pleurisy showed a most insidious course. The effusion was absorbed rapidly, and the other symptoms of hydatid made their appearance much later. From the first, hydatid of the lung may excite general symptoms. Loss of strength, anorexia, and wasting have been noted in a large number of cases. In short, it is seen that, in its first period, hydatid of the lung shows its presence by symptoms which simulate pulmonary tuberculosis to such an extent as to be mistaken for it. A patient comes to us with haemop- tysis, and says that for some time past he has been coughing and wasting. It is quite natural to suppose the onset of tuberculosis. However, he does not bring up sputum, and the rales are not clearly localized to the apex of the lung, while the search for bacilli in the blood couglied up is negative. This is quite true, and yet, in the face of repeated hamoptyses, cough, anorexia, wasting, and attacks of pleurisy, we cannot eliminate the idea of early tuberculosis. Perusal of the reported cases shows that the mistake has almost always been made. In such cases the sero-diagnosis of tuber- culosis must not be neglected, for a negative sero-diagnosis is of great value. Radingraj)liy may sometimes be of use. Evolution of the Cyst. — We have studied the onset of hydatid of the lung ; let us now follow the other pliases of its growth. If the growing cyst reaches the size of the foetal or adult head, and spreads towards the walls 224 TEXT-BOOK OF MEDICINE of the thorax, they may become arched. According to the localization of the cyst, the arching occupies the lower, lateral, or upper part of the chest. It simulates in different cases intrathoracic tumour or encysted pleurisy. Sometimes the cyst, if it be very large, may simulate general pleurisy, Examples of these different varieties are as follows : Moutard-Martin says : " In a patient who had akeady had several attacks of ha?mop- tysis, arching of the lateral and inferior part of the thorax appeared on the left side. This arching rose as high as the seventh intercostal space. Over this area dullness was complete, tactile vibrations were abolished, and the normal vesicular murmur was replaced by tubular breathing. With all reserve, it was thought to be a case of encysted pleurisy. Thoracentesis was performed, and it was found that a hydatid cyst of the lung had been pimctured." " A patient," says Danlos, " presented arching of the lower lateral and posterior part of the thorax on the right side. This arching reached as high as the fourth inter- costal space. At this level the intercostal spaces bulged outwards. Percussion gave complete dullness, and auscultation showed abolition of the vesicular murmur. The patient had a hydatid cyst of the lung." In a case which was reported by Debove all the signs of encysted jjleural effusion on the left side were found — namely, abolition of the thoracic vibrations, dullness on per- cussion, absence of vesicular murmur, and displacement of the heart. The case was one of hydatid of the lung. Landouzy writes : " The patient, who had had violent haemoptysis, showed dijata- cion of the chest on the left side, ■v^dth bulging below the clavicle. Dullness on percus- sion, abolition of thoracic vibrations, tubular breathing, and marked deviation of the heart were found. Puncture confirmed the diagnosis, and 6 pints of liquid were drawn oil from a hydatid cyst of the lung." Large cysts may, then, produce bulging of the thorax, displace the heart, and simulate encysted or extensive effusion. In some cases they produce other symptoms, of which the most important are pain, dyspnoea, myosis 3n the same side as the cyst (Widal), and pressure signs, such as oedema of the lower and upper limbs. Diagnosis. — In the early stage hydatid cyst of the lung, especially if it be deeply situated, escapes our methods of investigation. It produces no dullness, no deformity, and no bulging of the thorax. Some rales, due to the pulmonary congestion around the cyst, may be heard, but they do not help us in diagnosis. Radiography may furnish some information. Haemop- tysis must be taken into careful consideration. If, in an individual suffering from repeated haemoptysis, there is no reason to suspect tuberculosis, asper- gillosis, calculosis, or bronchiectasis, hydatid cyst of the lung must be especially thought of. The diagnosis will be almost certain if the haemop- tysis is accompanied by urticaria, as in Chachereau's case. The diagnosis of hydatid cysts, when they produce deformity or bulging of the chest, is also very difficult. To facilitate the discussion, let us divide them into two categories. In some cases the bulging is so clearly limited that the cyst forms a tumour. If the bulging occurs at the tense and antero- lateral part of the chest, hydatid cyst of the liver is thought of ; if it deforms DISEASES OF THE LUNG 225 the upper region of the thorax, aneurysm or tumour of the mediastinum Nvill first enter our minds ; if it is posterior and lateral, the idea of an inter- lobar pleurisy presents itself ; if the thoracic deformity occupies the postero- inferior part of the chest, basal effusion is diagnosed. In other cases the cyst does not form a tumour, but by its large extent simulates pleurisy of the great pleural cavity, and presents most of its signs and symptoms, such as dilatation of the thorax, absolute dullness, abolition of the vibra- tions, tubular breathing, and deviation of the heart — in fact, everything tends to produce mistakes. Aspiratory puncture would remove all doubts. This is true, but we shall see later the mischief which may result from puncture. In making a decision, we must inquire carefully into the symp- toms which have marked the onset of the disease and have accompanied its progress. Haemoptysis occupies the chief place. Rupture of the Cyst.— All hydatid cysts of the lung do not grow towards the walls of the thorax, neither do they acquire a large size. Many cases are not large enough to betray themselves by any bulging of the chest ; but, whatever be the size of the cyst, be it large- or small, complications will certainly appear. They comprise inflammation of the neighbouring regions, infection and suppuration in the cyst, and its rupture into the bronchi or into the pleura. In many cases rupture of the cyst is preceded or accompanied by broncho- pulmonary lesions, which we must recognize. Pulmonary congestion, broncho-pneumonia, and pleuro-pneumonia have been observed either during the growth of the cyst or at the moment of its infection (Walske, Lorieux). This side of the question has been neglected by some writers on hydatid of the lung. I shall sum it up by describing a case under my care at the Necker Hospital : One of my attendants, wlio had had htrmoptysis several months before, was taken ill with fever, cough, pain in the chest, and blood-stained sputum. On examining the patient, we found subcrepitant mucous riiles and faint tubular breathing over the middle third of the chest behind on the right side. This condition simulated a bastard pneumonia, or pulmonary infarct. For several days these signs did not change, with the exception of some friction sounds which blended with the diffuse rales. The expectoration continued to be abundant, viscid, and hicmoptoic ; but then it changed in character, becoming muco-purulcnt, and one day the patient coughed up several shreds of hydatid membranes, which cleared up the diagnosis. The fever fell. The liydatid cyst had suj)purated, and tlu; neigliljouring lung tissue had I'ecomo aiTcct-ed by a bastard pneumonia. These pneumonic attacks (lesions of tli(! jmcumocoi'cus) may appear at different periods in the evolution of the cyst. They arc as important as the attacks of pleurisy mentioniMl at the hcsginiiing of this artich?. As long as the (;yst docs not su[)[)urat(; ru[)ture docs not occur. Kxctq)- tious to this rule arc extremely rare (Marconnet's case). The cyst may 15 226 TEXT-BOOK OF MEDICINE open into the bronchi (vomica), as most often happens, into the pleura, or into the pleura and the bronchi at the same time (pyopneumothorax). Let us study these different modes of rupture. Rupture into the bronchi is sometimes preceded by a febrile stage, with bronchitis, pulmonary congestion, incessant cough, and purulent, blood- stained, or foetid expectoration. At this time the cyst is fissured, but not yet freely open. If the cyst is small, or if the communication with the bronchus is of small size, the opening of the cyst does not quite take the characters of a vomica. The patient, after fits of coughing, brings up homogeneous, purulent, sputum, Kke currant jelly. Sometimes the expec- toration is genuinely blood-stained, and booklets, shreds, or hydatid vesicles, that prove the case, are found in the blood or in the expectoration, which is sometimes foetid. If the cyst ls large, and the communication with the bronchus is well established, the patient is seized with terrible fits of coughing, a feeling of tearing, and suffocation bordering on asphyxia, which is caused by the liquid and the membranes that block the ah-tubes. He brings up, as if by vomica, a large quantity of fluid, which is clear and transparent, like spring-water if the cyst is not suppurating (Marconnet's case), but muddy, sero- purulent, blood-stained, and of nauseous odour and taste, if the ruptured cyst has suppurated. In the fluid of the vomica hydatid vesicles are sometimes found, from the size of a pin's head to that of a walnut, but more often membranous shreds of various sizes are seen. The first vomica is generally the largest, but it is rarely the only one. We sometimes meet with a series of vomicge which are repeated for days, weeks, and months. In the space of a year Chachereau had fifteen vomicae, or at least hydatids were expelled fifteen times. As a rule, I repeat, the first vomica is the most severe, and the others are rather a purulent ex- pectoration with shreds of membrane. The breath and the expectoration are often foetid. So long as the hydatids are not all brought up, the purulent expectoration does not cease. In many cases rupture of the cyst is announced or accompanied by a more obstinate and abundant haemoptysis than the early attacks seen ni the first period of its growth. Chachereau had fifteen in eighteen months. They were trifling before the rupture of the cyst, abundant at the moment of rupture, and persisted for five months after the last vomica. Marconnet had slight hemoptysis before rupture of the cyst, but almost fatal haemor- rhage at the moment of rupture. In Habershon's case haemoptysis caused the death of the patient, and at the autopsy the pulmonary vein was foun4 cut tlu-ough, causing the haemorrhage. _ V Urticaria fairly often accompanies rupture of the pulmonary hydatid, like that of hydatids in every region. Arnault has cited a case of genera ' DISEASES OF THE LUNG 227 urticaria after rupture of the cyst into the bronchi. Chachereau had his first attack of urticaria some days before the cyst opened into the bronchi, and had ten attacks in succession, which were sometimes so severe that sleep became impossible. Delageniere quotes the case of a woman who was seized with urticaria after the cyst perforated the pleura. Urticaria is, therefore, a symptom which fairly often accompanies rupture of hydatid cyst of the lung. New sigas appear after rupture of the cyst into the bronchi. On auscul- tation, multiple rales and, at times, cavernous breathing are heard. As secondary infection often occurs in the cyst, fever is not rare, and with it the usual train of symptoms— viz., sweating, anorexia, wasting — appears. When we see these wasted, anaemic patients, who spit up pus and blood and have clubbed fingers (Trousseau), we would not be able to eliminate the idea of phthisis if bacteriological examination did not rectify the diagnosis. The diagnosis of the hydatid vomica is quite simple when membranes and shreds are found in the voided matter. In default of hydatid mem- branes that present a characteristic shape, it is necessary to search care- fully for booklets, because the presence of a single booklet makes a doubtful diagnosis certain. In many cases the vomica does not appear with charac- teristic symptoms, and we then lack a clue to the diagnosis. Most patients think they are suffering from bronchitis, and say that for a week, a fort- night, or longer, they have been coughing up muco-purulent or blood-stained sputum. They do not mention the shreds of hydatid, which may have passed unnoticed. These patients are examined, and in one we find signs of bronchiectasis ; in a second, those of chronic bronchitis, with bronchor- rh(jea ; in a third, sigas of pulmonary cavity, Avith repeated haemoptysis ; in a fourth, signs recalling the vomica which follows encysted interlobar pleurisy. So far it in sometimes difficult to make a diagnosis. Urticaria, when it exists, is a point of great value ; but the histological examination of the expectorated matter must never be neglected, for the presence of hydatid membrane and booklets can alone give positive information. Rupture of the cyst into the bronchi is sometimes a mode of cure, but often the pulmonary fistula, which is a centre of infection, becomes an inexhaustible source of purulent expectoration and haemoptysis. The patient continues to cough up membranes and much purulent foetid sputum. Fever supervenes, with its train of septic symptoms, including diarrhoea, loss of appetite, wasting, sweats. We sec next true hydatid phthisis pro- duced by secondary infections. Tuberculosis may also develop as a secon- dary infection in the cdursi; of hydatid of tlie lung. Rupture into the Pleura. — Lot us consider rupture of the cyst into the pleura. 15—2 228 TEXT-BOOK OF MEDICINE I must first, however, discuss an interesting question : Can the hydatid cyst develop primarily in ths pleural cavity ? Primary hydatid cysts of the pleura are extremely rare. Laennec, Cruveilhier, Davaine, and Trous- seau scarcely admit the possibility of the primary development of a hydatid cyst in the pleural cavity. Davaine, in twenty-five cases of thoracic hydatid, only once found a primary hydatid of the pleura. Dupuytren and Joffroy reported a case of pleural hydatid ; careful consideration, says Trousseau, shows that it was a cyst of the lung which opened into the pleura, because the patient had had haemoptysis. Vigla, in his work on hydatids of the thoracic cavity, quotes only one case of pleural hydatid, and it is a very doubtful case, as it lacks post-mortem verification. Maydl published in 1891 a memoir upon echinococci of the pleura ; after having analyzed in detail each of the cases contained in this work, I find that there is no case of primary hydatid of the pleura, but only of hydatids secondary to those of the lung or of the liver. Further, frequent as primary hydatid is in the parenchyma of organs, it is exceptional in serous cavities. The hydatid is found in the liver and the subperitoneal tissues, but very seldom in the peritoneum. The hydatid is found in the brain, but very seldom in the meningeal cavity ; in the heart, but very seldom in the pericardium ; in the lung, but very seldom in the pleura. Cysts of the serous and of the pleural cavities have in most cases penetrated these cavities by effraction. A cyst of the lung may work through the thickened pleura, and thus simulate a cyst of that tissue (Trousseau). From these facts we must conclude that hydatid of the pleura is nearly always secondary to one that starts in a neighbouring organ and per- forates the pleural cavity. The thickened pleura often opposes this inva- sion, and when perforation takes place it may consist of a simple slit or a large tear in the pleura. In some cases the invasion of the pleura may be insidious, but more often it is accompanied by dyspna3a and pain. We find signs of dry pleurisy (rub) or of pleural effusion. The following case is typical : A boy, of tubercular appearance, was suddenly seized with stabbing pain in the right lung. On auscultation, friction sounds were heard. The whole right side of the chest became enlarged, and was absolutely motionless during respiration. The dullness was absolute. Post mortem, the right pleura was found to be ruptured, and filled with sero-purulent fluid and membranes from a huge hydatid of the lung, which had burst into the pleural cavity. In other cases, which are the most frequent, the cyst of the lung shows two perforations, which communicate with the pleura on the one hand and with the bronchi on the other. I have carefully analyzed these cases, and have found that perforation almost always takes place first into the bronchus, while the other perforation occurs a little later. The perforation into the DISEASES OF THE LUNG 229 bronchus is generally a small fissure. It does not produce tlio large vomica with acute symptoms, and the patient appears to have only foetid bron- chitis or broncho-pneumonia with gangrene. He brings up purulent, foetid, blood-stained sputum. Perforation of the pleura now occurs, and pneumo- thorax appears. If the perforation of the pleura takes place before that of the bronchi, and the lung is adherent to the pleura, the symptoms of pneumothorax may not be violent ; in other cases the pneumothorax is accompanied by terrible pain, acute dyspnoea, and threatening asphyxia. The subjoined cases give a clear idea of these different modes of per- foration : In a case reported by Bucquoy, perforation of the pleura preceded that of the bronchi. The patient had a hydatid cyst of the right lung. Very abundant effusion into the right pleura (opening of the pulmonary cyst into the pleura) apjicai'ed. Later, signs of pneumothorax (opening of the cystic ca^^ty into the bronchi) supervened, and the patient brought up much foetid purulent fluid by repeated vomica?. The situa- tion became very serious. Thoracotomy was performed, and the incision gave exit to infectious, purulent fluid, and to a hydatid cyst as large as an orange. Danlos relates a case in which the perforation of the bronchi preceded that of the pleura. The onset of the pneumothorax was dramatic, and followed by death. In a man aged forty-five years deformity and bulging were present at the lower lateral and posterior part of the right side of the phest. Hydatid cyst of the lung was diag- nosed. The patient was seized with fits of coughing, and brought up purulent and ffjetid sputum (small opening of the cyst into the bronchus). Ten days later he felt terrible pain on the right side, with dyspncea. On auscultation, amphoric breathing was heard (perforation of the pleura and pneumothorax). The jiatient died, and the autopsy revealed a huge hydatid cyst at the base of the right hmg, causing the above complications. In a oa.se given by Fouquier the pneumothorax came on suddenly. The patient died, and the autopsy showed a hydatid cyst of the lower right lobe of the lung, com- municating on the one hand with two bronchi, and on the other with the pleural cavity by a rounded opening with raised edges, into which the end of the index-flnger could easily be introduced. Summary. — The diagnosis of hydatid of the lung is very difficult before perforation of the cyst and vomica. Haemoptysis, pleurisy, and attacks of pneumonia do not clear up the diagnosis. Bulging of the chest, dull- ness wliich is clearly defined, and previous or simultaneous hremoptysis not due to tuberculosis, are valuable signs in diagnosis. We know that great precautions are needed in exploratory punctures, which are, how- ever, tlie only means of clinclting the diagnosis before tlie rupture of the cyst. When a patient has cough, is wasting, and has repeated hfemoptyses and phniral complications, we think first of pulmonary tul)erculosis. Examina- tion for Imcilli is negative, and the diagnosis remains in doubt. The patient later brings up hydatid vesicles or membranes, and the diagnosis becomes certain. In some cases, however, even after purulent fluid lias been rejected 230 TEXT-BOOK OP MEDICINE through the bronchi, diagnosis is very difficult, because the membranous shreds may escape the patient's notice, and tlie lesion would pass unper- ceived if we did not find vestiges of membranes or booklets on microscopic examination. Lastly, in other cases the disease, at a given moment, assumes the appearances of broncho-pneumonia, as in my hospital atten- dant, and a hydatid of the lung would not be recognized if membranes and booklets were not found in the expectoration. The same remarks apply to the passage of the hydatid into the pleural cavity and to the question of pyopneumothorax. As I have discussed the diagnosis in regard to the different complica- tions which may arise in the course of hydatid of the lung, further reference is superfluous. Prognosis. — In this chapter I have reviewed the complications of hydatid of the lung, and we have seen its gravity. In exceptionally fortunate cases, the cyst may be cured spontaneously — that is to say, it may undergo necro- biosis, which is equivalent to cure. In some cases rupture of the cyst into the bronchi results in cure, but before recovery is definite the patient runs the risk of most grave complications — viz., at the moment of rupture haemoptysis, vomicae, and pyopneumothorax ; and later secondary infec- tions, hectic fever, and tuberculosis. Treatment. — As medical treatment has no effect on hydatid of the lung, surgical intervention must be resorted to. Certain authors have recommended expectant treatment, but this method has scarcely given good results, as the following statistics prove : Hearn, in 128 cases of pulmonary hydatid, left to run their own course, counts 82 deaths — a death-rate of 64 per cent. Madelung, in 19 untreated cases, records 6 deaths. Thomas Daviss records 31 deaths in 133 cases of pulmonary hydatid which opened into the bronchi. Such figures are not encouraging, and explain the necessity for surgical intervention. Aspiratory puncture is insufficient and frequently dangerous in hydatid cysts of the lung. Mirallie has collected 43 cases in which simple puncture was performed ; 1 1 cures, 22 deaths, and 10 negative results are recorded. Punctures are frequently followed by sudden or by rapid death. Thus, in the 22 fatal cases noted above, we find that they may be divided as follows : In 1 case the patient died after a blank puncture ; in 10 cases death was sudden — death came on in one minute (Acland, Philippe, etc.), in five minutes (Holden), in seven minutes (Bristowe), in half an hour (Lansdale and Holden), in two hours (Hector Mackenzie), in nine hours (Cornil and Gibier), in thirteen hours (Duffey). In almost all these cases the accident was accompanied by some attacks of coughing, with cyanosis and asphyxia, coldness of the extremities, and sometimes rejection of blood and fluid. DISEASES OF THE LUXG 231 Puncture, therefore, must be abandoned ; it is dangerous even for purposes of exploration. Pneumotomy is tlie best method, and is absolutely indicated. It gives such good results that the recoveries amount to 90 per cent. XXI. SYPHILIS OF THE LUNG. Discussion. — Syphilis of the lung is of the highest importance. Too many mistakes in diagnosis occur from want of care in looking for this malady. It endangers the patient's life ; but, on the other hand, it gives us an opening to score a therapeutic success, for we can sometimes restore health in a few weeks or in a few months to people who appear to be in the last stage of phthisis. The chief manifestations in the lung include broncho-pneumonia of tubercular aspect, cavities simulating phthisis, gangrene, fibrosis of the lung, and dilatation of the bronchi, without counting mediastinal adeno- pathies and pleurisy. Before we undertake the clinical study of these syphilitic lesions, we must consider an important point : At what date may syphilis attack the lung ? Is it soon or long after infection ? This division into early and late lesions is clearly marked in such organs as the brain, the spinal cord, the kidneys, etc. Take, for example, cerebral syphilis. Its lesions are sometimes late and at other times early. The late lesions, such as obliterating or dilating arteritis, and gummatous lesions of the bones, meninges, or brain (general paralysis), appear many years after infection. We also see early cerebral syphilis which is almost exclusively confined to the arteries of the circle of Willis. It may, some months after infection, give rise to endarteritis obliterans, with cerebral softening and hemiplegia, and to arteritis ectasians, with rupture of an aneurysm, meningeal haemor- rhage and death from apoplexy. This distinction between early and late lesions is nowhere more marked than in the kidneys. The tertiary disease usually takes the form of chronic nephritis, with or without gummatous, sclero-gummatous, and amyloid lesions, while early renal syphilis appears some months after the chancre, and causes acute or hyperacute nephritis, which Is sometimes most dan- gerous. It was formerly thought that syphilis only attacked the organs in the so-called tertiary stage. This view Ls incorrect. Some organs are aff(M'tod by syphilis at a very early stage, and the lesions, though early, are far from being benign. They are quite as serious as the lesions of the tertiary stage. I will, therefore, put the question afresh : Do we find in the lung early syphilis, that appears within the first few months after infection, and late 232 TEXT-BOOK OF MEDICINE syphilis, that appears only after a long interval ? The answer is categorical. Syphilitic lesions of the lung are, practically speaking, never early. I would ask you to remember that I am speaking of the lung, and not of the bronchi. Bronchitis may be one of the earliest manifestations of syphilis. Many people, when once infected, take cold with the greatest ease. They suffer from laryngitis or tracheo -bronchitis ; they cough and expectorate. On auscultation, sibilant and mucous rales are heard, and the trouble is put down to influenza or to an ordinary cold, and not to recent syphilis. Tracheo-bronchitis may recur several times, even during the early years of Infection, and sometimes arouses unjustifiable suspicions of tuberculosis. These so-called attacks of bronchitis lead us to send patients to take a cure at Mont-Dore, Cauterets, Eaux-Bonnes, and Luchon, when we should have begun by prescribing mercury. Laryngo-tracheo-bronchitis is, then, one of the early manifestations of syphilis. Lesions in the lungs, on the other hand, occur late, and not one of the other visceral determinations, as Mauriac rightly remarks, develops at a later period. This rule appears to me absolute, and, save for some exceptional cases, it may be said that syphilis of the lung only appears in the advanced tertiary stage. After these explanations, let us enter upon our subject. Syphilis of the lung, as of other organs, presents various forms — gumma (circumscribed syphiloma), diffuse syphiloma, and fibrosis. These different forms may be isolated or associated. For the clear arrangement of this question I propose the classification which I have followed in my clinical lectures at the Hotel- Dieu.* Syphilis of the lung may show the following forms : First Type. — Pulmonary syphiloma, with acute febrile course, simu- lating acute tuberculosis or tubercular broncho-pneumonia. Second Type. — Pulmonary syphiloma of slow course, simulating ordinary chronic tuberculosis and phthisis in the stage of cavity. Third Type. — Broncho-pulmonary syphiloma, with fibrosis or sclero- gummatous lesions, simulating chronic pneumonia and cirrhosis of the lung, with or without bronchial dilatation, pleurisy, and tracheo -bronchial adenopathy. Fourth Type. — Syphilitic gangrene of the lung. Fifth Type. — Syphilitic pneumopathy, complicated by pulmonary tuberculosis. Sixth Type. — Hereditary pulmonary syphilis. * Dieulafoy, " Syphilis du Poumon et de la Plevre " {CUnique Medicale de V Hotel- Dieu, 1898, lemons 18 et 19). DISEASES OF THE LUNG 233 1. Pulmonary Syphilis, with Acute Course, simulating Acute Tuberculosis. In some cases — which are rare, it is true — syphilis of the lung shows an almost faithful picture of acute tubercular broncho-pneumonia — i.e., fairly- sudden onset, acute fever, incessant cough, violent dyspnoea, muco-purulent expectoration, rapid wasting and profuse sweats, dullness on percussion, rales and tubular breathing on auscultation. The above symptoms may be common to syphilitic and to acute or subac-ute tubercular broncho- pneumonia. The following example was seen by Giraudeau in Hayem's wards : Patient, thirty-five years old. She had cough, and for a week fever was continuous. Temperature up to 104° F. On admission, dull zone, with tubular breathing and sub- crepitant rales over the middle part of the left lung. Nothing elsewhere. Right lung healthy. Frequent cough and profuse expectoration. During the next few days, rapid formation of a cavity. The breathing soon became tubular, and the expectora- tion muco-purulent. Later, in addition to tubular breathing, large mucous rales appeared, wasting was considerable, and night-sweats occurred. On February 21 — that is to say, in twenty days — a cavity had formed in the lung. Cavernous breathing, pectoriloquy, and bronchophony were audible over the greater part of the middle lobe. Gurgling was present ; the sputum was ruunmular, and streaked with blood. The patient appeared to be suffering from acute phthisis. On February 28 vaginal examination revealed in the right cul-de-sac a rounded ulcer, which was as big as a sixpence, punched out, and covered by a greyish, adherent layer. This gummatous ulcer showed the need for specific treatment. The lung trouble was then thought to be specific in nature, and Gibert's syrup given in doses of two tablespoonfuls daily. After some weeks, the situation improved, the appetite came back, the nummular sputum, sweats, and fever disappeared. The cavernous breathing and gurgling were replaced by rough breathing. The cavity had cicatrized. As the treatment had caused stomatitis, it was st02:)pcd. Ninety grains of iodide of potash were prescribed daily, and when the patient left the hospital she had regained her healthy look, and the gummatous ulcer in the vagina was undergoing cicatrization. A littl(! while after, this woman came back for treatment, not for the lung, which was healthy, but for ost(!op(!riostitis of the frontal bone, which yielded to sj)eeific treat- ment. It was, therefore, undeniable that this woman had been attacked in a short time with vaginal gumma, sy})hilis of the lung, and frontal ostefjporiostitis. .hidgitig by the rapid and excej)tionally serious course of the l<'si(in in the lung, she was doomed to die. She was saved by specific treatment. I have seen a similar case. I att<'nded a ])a(ient supposed t^ bo suffering from influenza. He coughed, had slight fever, and cfmii)lain<'d of j)ain in the chest, esjieciaiiy at the apex of tlu' left lung, where I found tubular breathing and rules, due to ]))ilmoiiary congestion. This man, who was up to then in robust health, asked for a blister, which i ijrcscribed, as well as n draught containing kermes. During the next few days the situation became worse. TIk- cough was incessant, and at niglit the dyspncea was unusually sc^vere. The spiitmn soon became muco-jiurulent and nummular. The early rales changed to guiniiiig. ilis strengtii failed, and I thought of acut<' lul)ereular pneumonia. The jjrognosis wius very grave. Incidentally, the jiatient told uw. that his left t<>ati3 iiad been affected for some days. I found it enlarged and painful. Orchitis wiw 234 TEXT-BOOK OF MEDICINE present, but not epididymitis. As he had no discharge, I thought at once of tertiary syphilis. I questioned the patient, who rephed that he had had a cliancre ten months before. This revelation threw Hght on the subject. Was it not possible that syphilis was at once the cause of the lesion in the Ixmg and in the testis ? I prescribed iodide of potash in large doses, and also asked the advice of Foumier. He considered the orchitis and the lung trouble to be syphilitic, and advised inunction of mercury in addition to the iodide of potash. The picture changed so rapidly that after a few nights the dyspnoea disappeared. A fortnight later the fever had subsided, the general condition was excellent, tubular breathing and gurgling had disappeared, and the only local sign remaining at the apex of the right lung was slight dullness with some rales, which finally disappeared. The lesion of the testis was also cured. The case was undoubtedly acute phagedsenic syphiloma, which rapidly caused breaking-down of the apex, and was clearly arrested in its course by specific treatment. I have never lost sight of this man, and I have treated him since that time for a syphilitic whitlow, but there has never been any further question of pulmonary lesions. In my clinical lectures, several cases of this acute and subacute broncho- pneumonic syphiloma with fever will be found. In nearly all these cases it has simulated acute tubercular broncho-pneumonia : onset fairly sudden, acute fever and dyspnoea, muco-purulent expectoration, rapid wasting, pro- fuse sweats, with dullness, rales, tubular breathing, and gurgling, are the signs common to acute broncho -pneumonic syphiloma and to acute or to subacute tubercular broncho-pneumonia. It has been said that syphilitic pneumopathy may occur without fever, wasting, or any sign of hectic. This is true in a certain number of cases of slow course, which we shall study later, but not of the acute forms, in which the diagnosis is extremely difficult. If we carefully think over the acute cases, we shall agree that patients who suffer from fever, accompanied by signs of pulmonary softening, purulent sputum, and night-sweats, and pass into rapid consumption within a few weeks, clinically resemble those who are suffering from acute phthisis. In them, it is true, dyspnoea is often severe and out of proportion to the lesion, but this symptom is not sufficient to decide the diagnosis. The physical signs — rales, tubular breathing, gurgling — are those of acute phthisis. It has been said that the localization of the lesions may reveal the true nature, because the syphilitic lesion is often situated in the middle part of the lung, and especially on the right side. This special topography is, indeed, worth remembering : it may lead us to think of syphilis ; still it is not constant, for in a case of Raymond, and also in one of my cases, the lesion was at the apex of the lung, which is the usual seat of tuber- culosis. Acute syphiloma and acute tubercular broncho-pneumonia have, there- fore, very many points of resemblance, and hence it is only possible to make a diagnosis of pulmonary syphilis if the patient present other syphilitic lesions, such as osteitis or painful periostitis, ulcerating gumma, specific eruption, or syphilitic testis. If we find some such stigmata of syphilis as DISEASES OF THE LUNG 235 an exostosis of the tibia, frontal periostitis, the presence of scars, and the repeated absence of Koch's bacilhis from the sputum, we can give a diag- nosis of acute syphilitic pneumopathy. In short, if pathognomonic symptoms of acute pneumonic syphiloma do not exist, it is at least necessary to collect all the information which may give a clue to the diagnosis. In one of my patients at the Hotel-Dieu pneumonic syphiloma was diagnosed, thanks to tertiary syphilis of the shoulder and the back. In the patient whom I saw with Fournier syphilis of the testis revealed the nature of the pul- monary lesion. In Giraudeau's patient an ulcerated gumma of the vagina led him to discern acute s}T)hilis of the lung. What is the cause of acute syphiloma of the lung ? The syphiloma may be circumscribed (syphilitic gumma) or diffuse (broncho-pneumonic syphi- loma). Gummata of the lung may be as large as a lentil or an egg. They are more or less numerous, and may be situated on the surface oithe lung, under the pleura, or in the deep parts of the organ. They are indurated anct greyish in an early stage of their growth, but finally soften and become converted into a yellowish pulp, which may pass into a bronchus, and leave in Its place a gummatous cavity, with fihrous walls. When cure sets in, the walls of the cavity become covered with granulations, the cavity con- tracts, and is replaced by scar tissue. Diffuse syphiloma of the lung assumes a special form, and causes a kmd of sypliilitic broncho-pneumonia, which may be acute, subacute, or clironic. The acute form, which has been discussed in the examples quoted above, is somewhat rare. Microscopic examination has given the following r.'^ults : ^ " Microscopic examination," says Remy, " shows that the tumour is composed of a number of nodules of broncho-pneumonia in various stages (catarrhal, fibrinous, and caseous). There is no well-marked general cap- sule formed by a zone of fibrous tissue, as in the case of gummata. At some pomte, however, this capsule is seen, but it is formed by the septum of the lobule, and not by newly-formed tissue. No central artery is found. The lesions are rather grouped around the l^ronchi, as in broncho-pneumonia. The lesion as a whole consists in several masses of caseous appearance, which are surrounded by more active zones. The caseous mass is composed of pulmonary alveoli, filled with cells, whicli have lost their shape and appear to be undergoing fatty degeneration. The envelope of the caseous mass is sometimes formed by a thickened interlobular septum, at other times by alveoli which are filled with leucocytes, and present thickened walls. Further- more, we find in the thickness of the broiu-lii, vessels or interlobular septa, masses of young cells which reveal an inflammatory condition." Syphilitic broncho-pneumonia has ho.o.n studied in the f not know of a more conclusive case than the following (Dubousquet- Laborderie and Gaucher) : A little girl, eight and a half years old, was wasted and cachectic. She coughed continually, her apjietite wjus gone, her tem|)erature was 102 ' F., and her pulse HO. Her general condition, in short, wa,s that of a patient in the last stage of phthisis. Cavemou.s breathing and gurgling were heard in the right supraspinous fossa. I^rge mucous rales were scattered throughout the whol(. chest. The diagnosis was pulmonary tuber- culosis in the third stage. Treatment gavgophony tl)o voice is bleating, while it is diffuse in bronchopliony, and clearly articulate in pectoriloquy. 252 TEXT-BOOK OF MEDICINE ("the bleating of a goat") ; and (4) aphonic pectoriloquy*— that is to say, the clear and articulate transmission of words pronounced by the patient in a Avhisper (Bacelli, Gueneau de Mussy). These signs are usually most marked at the lower angle of the scapula, and are of great importance, but yet not one of them is pathognomonic of pleural effusion. They may lose their purity and become disfigured if the lung be congested and re- sistant beneath the effusion (pleuro-congestion), I shall now say a few words on the correct method of percussion, and the means used in determining absence or diminution of the vocal fremitus. If percussion is to give reliable information, it must not be performad forcibly, as is too often done, for the sound then obtained destroys in a grsat measure the delicate shades of dullness, or of impaired resonance which indicate the presence or the absence of effusion. Care must therefore be taken to percuss as lightly and softly as possible, in order to give a true result. I may make a similar remark as regards the disappearance of the vocal fremitus. If the patient be made to count in a high voice, the vibrations are transmitted — less strongly, it is true — on the side of the effusion ; but they are still transmitted, and their presence may give rise to error. If, on the contrary, the patient be made to count in a slightly raised voice, the vibrations may still be transmitted to the healthy side, but are quite absent over the effusion. As the effusion increases (2 to 3 pints), certain signs are modified : the aegophony becomes less clear, and rather bronchophonic in character ; the soft tubular breathing on expiration takes a bronchial tone, and is also audible during inspiration ; auscultation reveals the exaggerated breathing, called " puerile," on the healthy side ; and the effusion, by its constant progress, displaces the neighbouring organs. The displacement of organs is of value in estimating the amount of the effusion. It has much less value in effusions on the right side, because the liver is much less mobile than the heart, and is only pushed downwards when the fluid amounts to at least 3 pints. On the other hand, in effusions on the left side, displacement of the heart is a sign on which I cannot lay too much stress. The displacement of the heart is shown by inspection, palpation, and auscultation. It is not only the apex of the heart which is displaced, but the whole heart itself, and with the change of position it also alters its relations to the chest-wall. In order to ascertain the displacement, we must look for the maximum point of the impulse. My numerous observa- tions lead me to conclude, aj^proximately, that this maximum point reaches the left border of the sternum in effusions of 20 ounces ; it reaches the right border of the sternum with an effusion of 40 ounces ; and lies between the * LatJnnec had already jjointed out this phenomenon, and Bacelh has given the conclusions which may be drawn from aphonic pectoriloquy as a sign of pleiu"al effusion. DISEASES OF THE PLEURA 253 sternum and riglit nipple with an effusion of 60 ounces. This is the moment at which thoracentesis must be performed. When these effusions are on the left side, dullness replaces the normal tympanitic sound in Traube's space. The semilunar, or Traube's, space, is situated at the left base, and corresponds in part to the pleuro-parieto- diaphragmatic cul-de-sac. Its upper limit is the fifth or sixth costal cartilage in front, and the ninth or tenth ribs behind, while its lower limit is the edge of the thorax. At its middle part — that is to say, in the nipple line — the vertical height is about 4 inches, and its width about 4-| inches. The costal wall and its pleura, the diaphragm and its pleura, the colon and the stomach correspond anatomically to the semilunar zone ; the lung only touches the upper limit (Jaccoud). In the normal state percussion cf this zone gives a tympanitic note ; on the other hand, m a large left effusion the diaphragm is pushed down, and dullness replaces resonance. It is true that normal resonance may also disappear, at least in its upper part, as the result of adhesions. When the effusion is very large (5 pints and more), the skodaic note in the clavicular region disappears, the dullness becomes absolute over all the affected side, the displacement of organs reaches its maximum, the whole mediastinum is pushed back, and the obstruction in the pulmonary cir- culation, without doubt, leads to pulmonary thrombosis, and perhaps to sudden death, which sometimes occurs in large effusions. On auscultation, we find total absence of all normal or abnormal sounds, or else tubular breathing, which may be so loud as to resemble cavernous or even amphoric breathing (Landouzy). Paresis of the thoracic muscles on the affected side is more or less marked, but constant. It is accompanied or followed by muscular atrophy, which may begin with the onset of pleurisy and may remain after it. These muscular atrophies affect the intercostal and pectoral muscles, the latis- simus dorsi, the serratus magnus, etc., and it is easy to appreciate them, either at first sight or by the respiratory troubles which they cause. These muscular changes explain in part the modifications in the respiratory type, the smaller amplitude of the chest (on the affected side), its relative im- mobility on inspection and palpation, and the respiratory restraint which results. They also enter largely into the external deformities, as well as into those of the skeleton which accompany and survive pleurisy. Functional Symptoms. — As soon as the fluid reaches a certain amount, the [)atient lies on the affected side, in order to give free play to the healthy lung. He experiences a sensation of distress or of heaviness, but dyspnoea Is rarely seen. Dys[)n(ra is not a usual symptom of pleurisy with effusion. 'i'hc ellusion, even when it amounts to '6 i)ints, causes little acceleration of the 254 TEXT-BOOK OF MEDICINE respiration rate. I do not speak, of course, of the early pain in the side, which is often accompanied by acute dyspnoea, and I make exception if congestion of the lung is also present. In all other cases of acute, subacute, or latent pleurisy, however, dyspnoea is not marked, even with an effusion of 3 pints ; and, as we shall see in a moment, when discussing the indications for thoracentesis, we should be quite wrong in waiting for dyspnoea to decide the prognosis and the treatment of pleurisy. The conclusion from this absence of dyspnoea, even when the fluid is considerable, is that dyspnoea indicates the presence of complications. When the respirations in pleural effusion exceed thirty, the reason is either that the fluid is very abundant, amounting to about 5 pints, or that com- plications are present. On careful search, we shall find that the pleurisy is secondary, and has appeared in the course of Bright's disease or cardiac mischief. Other inflammations, such as double pleurisy, bronchitis, pneumonia, pericarditis, inflammation of the chest, or congestion of the lung, will be discovered. I must dwell for a moment on congestion of the lung, which so fre- quently accompanies pleurisy. This fact has been emphasized by Potain. Congestion of a part of the lung often accompanies pleurisy, especially in its period of formation ; as a result, the signs of effusion are somewhat modified by those due to the affected lung — segophony is not pure, but becomes broncho-segophony ; tubular breathing, instead of being distant and muffled, becomes more harsh ; the quality of the dullness and the shades of the thoracic vibrations are modified. When we are not familiar with these points, we may miss an existing effusion and refer the signs to conges- tion of the lung ; or, on the other hand, we may fancy the fluid to be abundant when it is as yet scanty. I shall consider this point again, under Diagnosis. In acute pleurisy the fever is moderate and sometimes absent : the temperature does not exceed 102° F., as a rule ; the defervescence may be rapid or slow, and occurs at ill-defined times, in some cases with symptoms of crisis. Course — Duration — Termination. — Pleurisy is a disease of surprises. Its course is insidious, and the extreme irregularity of its habits is not the least important point in its history.* I was therefore very surprised, at the Academic de Medecine, to hear that pleurisy is a cyclical f disease. I have only to consult our case records to prove that pleurisy is quite the opposite of a cyclical malady. In pleurisy we cannot foresee the succession of symptoms, the temperature curve, the time of defervescence, or the moment when the effusion appears * Dieulafoy : " Des Irregularites de la Pleurisie Aigue," Ga^tte Hebdomad., 1878, No. 3. •j- Academie de Medecine, April, 1892. DISEASES OF THE PLEURA 255 or is absorbed. In one case pain and fever are marked, and the effusion appears between the twelfth and the fifteenth day. In another the disease is insidious, and effusion exists for a month or six weeks, when the patient comes to the hospital with some distress, which often scarcely merits the name of dyspnoea. I have several times seen fever persist, although the effusion diminished. Binet gives a remarkable example.* In many cases fever disappears with or without symptoms of crisis, the patient considers himself cured, and still the effusion increases. In fact, pleurisy is so irregular in its course that it pr^ents a different appearance in each patient. It is not possible to say whether the febrile period will be of long or of short duration, whether the effusion will be abundant or scanty ; at what time defervescence will occur, and whether it will coincide or not with absor2)tion of the fluid ; whether this absorption will be slow or quick ; and whether, in spite of the fall of the fever, the fluid will not continue to increase. Do not these clinical considerations justify the assertion that pleurisy proceeds in quite a different way to cyclical diseases ? We cannot, therefore, speak of a cycle in pleurisy. This question will be referred to under the Indica- tions for Thoracentesis. If the effusion is slow to absorb, the insufficiency of the haematosis and the lack of appetite often cause weakness and anaemia. In exceedingly rare cases sero-fibrinous pleurisy has ended by vomica. When pleurisy ter- minates favourably, the fluid is absorbed ; the displaced organs recover their former position ; the lung resumes its function ; and on inspiration and expiration we hear a grating friction sound, or hruit de cuir neuf, which indicates absorption of the fluid and presence of false membranes on the layers of the pleura. This redux friction may be heard at several spots in front and in the axilla. It is sometimes so marked that it may be felt on palpation. These signs remam long after the pleurisy. Impaired resonance and weak vesicular murmur often persist months after recovery. The immediate prognosis is not grave. We must, however, not forget that large effusions may determine thrombosis of the pulmonary vessels or cardiac embolism, and induce syncope, rapid asphyxia, and death. This important point will be discussed under Thoracentesis. Convalescence is usually protracted, and many patients, even though taken ill while in excellent health, remain weak, and for several months carry the stamp of their disease. Pleurisy at times leaves false membranes and adhesions, which affect the functions of neighbouring orgaiLS (diaphragm, lung, and pericardium), and may ultimately give rise to encysted effusions. Another important fact as regards prognosis is that the most frank pleurisy Is often the begimiing of tuberculosis, which becomes evident months or years later. ♦ Archives de Midecine, April, 188-4, p. 4UG. 256 TEXT-BOOK OF MEDICINE Diagnosis. — At first, before efEusion appears, diagnosis may be difficult. Pleurisy should not be confused with lobar pneumonia, for the latter begins with a violent rigor, very high temperature, intense dyspnoea, crepitant rales, and rusty sputum. The diagnosis, however, may be difficult, for the friction rale of pleurisy somewhat resembles the rale of pneumonia. Inter- costal neuralgia and hepatic colic may simulate the pleuritic pain in the side, but they differ in the absence of fever and of physical signs. Febrile pleurodynia shows more analogy with pleurisy, and it may coincide with a partial dry pleurisy. This question has been discussed under Inflammation of the Chest. Pulmonary congestion, massive pneumonia, and spleno-pneumonia (Grancher) have several signs in common with pleural effusion. In the case of pulmonary lesions, however, the dullness is less complete, the thoracic vibrations are less affected, the neighbouring organs are not displaced, and the aphonic pectoriloquy is less clear. In spite of all these distinctive signs, I admit that an early diagnosis is difficult in some cases. It is also important to recognize the diseases which may be associated with pleurisy — e.g., the coexistence of pulmonary congestion and pleurisy (pleuro-congestion), for the presence of the former modifies the signs of efEusion. In consequence of the congestion, the distribution of the fluid in the pleura is modified. The congested lung becomes more dense, and does not allow itself to be flattened. It sinks in t)ie fluid, raising the level, so that, without careful examination, the effusion would appear very abun- dant, when it may really be quite scanty. The limits of the dullness, the nature of the tubular breathing, the characters of the voice, and the fre- quent presence of bronchial rales are the most important jioints. We must distinguish between effusion due to pleurisy and that due to hydrothorax. Hydrothorax is not rare in the course of acute or chronic nephritis, and sometimes occupies both pleurae. It is sometimes associated with oedema of the extremities and of the lung. This is chiefly the case in acute nephritis. At other times hydrothorax is an isolated manifestation of chronic nephritis, just as oedema of the larynx or of the lung may be. The general rule is : hydrothorax due to nephritis causes more severe dyspnoea than pleuritic effusion does, because hydrothorax in Bright's disease is nearly always associated with oedema of the lung or with uraemic dyspnoea. The discovery of symptoms of " Brightism " and of albu- minuria will complete the diagnosis. It is still necessary to distinguish effusion due to pleurisy from hydro- thorax consecutive to heart disease. The diagnosis of effusions into the pleura presents other difficulties, as we shall see. For example, a patient suffers from dyspnoea. He is examinedj and on one side of the chest signs of a large effusion are found. The c DISEASES OF THE PLEURA 257 ness is complete, or nearly so, the thoracic vibrations are diminished, and aegophony, aphonic pectoriloquy, and tubular breathing, or even cavernous and amphoric breathing, are heard. A patient who presents these signs, or some of them, may have pleurisy with effusion, just as he may have a cyst in the liver, the spleen, or the kidney, which has pushed up the diaphragm and encroached on the thoracic cavity. Another patient may have cancer of the lung, or malignant hypertrophy of the thoracic glands, etc. Vergely has clearly shown these points in the case of a patient who presented all the signs of pleural effusion and in whom an adeno-carcinoma was found. yEgophony, aphonic pectoriloquy, and blowing breathing are certainly of great value, but these signs may exLst without any large effusion in the pleura. False membranes, tumours, flattening of the bronchi, and con- densation of the Imig tissue, may modify the normal conditions of ausculta- tion to an extent not yet well defined, and may sometimes simulate pleural effusion. In a doubtful case the surest sign of pleural effusion on the left side is displacement of the heart. When the effusion is on the right side, depression of the liver should be taken into consideration. We shall see, when we study hydatid cysts of the liver and of the spleen, upon what signs a diagnosis must be based if these cysts simulate pleural effusion. When pleurisy has been recognized, it is also necessary to diagnose its cause, to ascertain whether it is sero-fibrinous, hsemorrhagic, or purulent, and whether it is associated with tuberculosis which is latent or is already at work. We cannot say without exploration whether an effusion is sero-fibrinous or htcmorrhagic. We often expect to draw off scrum, and are surprised to find blood-stained fluid. Clinical Varieties. — Pleurisy presents numerous clinical varieties, a fact which it is important to remember. 1. Latent Pleurisy. — Acute pleurisy does not always begin witli the acute symptoms mentioned above. The pain is sometimes trifling, and the symptoms of onset are so slight tliat in hospital we frequently see people wh(j have been at work without Ijcing able to fix the start of their illness. It is not rare to see latent cases in which fever, pain, and dyspnoea are absent, while the effusion reaches considerable proportions unnoticed by the patient, but these cases may be accom[)anied by fever of the inter- mittent ty})e. It usually indicates infective changes in the fluid. '2. Rheumatic pleurisy may be dry, or accompanied by effusion ; it may be simple or double ; it appears, changes, and disappears with great mobility (see Rheumatism). In many cases })leurisy is provoked by a neighbouring or by a remote lesion (hydutid cyst of the lung, of the liver, etc.). Treatment. — In acute pleurisy two chief elements — pain and clTusion 17 258 TEXT-BOOK OF MEDICINE — demand relief. For pain, we employ wet-cupping, leeches, injections of morphia, antipyrin ; later, if the effusion makes rapid progress, what line of treatment must be followed ? Blisters have only a very limited use in the treatment of pleurisy. Many persons have three, four, and five blisters, and are exposed to the risk of cystitis, erysipelas, or of a crop of boils, without gaining the least benefit. As I believe that blisters have no real effect on the effusion, I abstain from prescribing them. I think that other medical means, such as bleeding, purgatives, diuretics, and sudorifics, have quite a secondary place in the treatment of pleural effusions. The more I see, the more I recognize that these means are useless and sometimes harmful. We may therefore discuss the value of, and the opportunity for, surgical intervention, or thoracentesis. Thoracentesis. — To my eminent teacher. Trousseau, belongs the honour of having clearly stated the indications and operative technique of thora- centesis. In spite of keen opposition. Trousseau so popularized this opera- tion, which had been previously neglected, that he may justly be con- sidered as its inventor. He only punctured the chest when the effusion threatened the patient's life, and the operation was performed with Rey- bard's trocar. In 1869, however, when I designed the aspirator and applied the method of aspiration to the treatment of pleural effusions, the technique of thora- centesis was so simplified that the old method was gradually abandoned, and it must be admitted the new one was soon abused. As thoracentesis by aspiration has been universally adopted, I shall describe my published method. Indications. — On the question of thoracentesis, the first point for dis- cussion is that of the indications. Should we operate in spite of fever, or wait for defervescence ? Should we employ aspiration in moderate effusions, or reserve it for large ones ? How far should we consider the complications which may arise ? These questions, which have been often debated and differently decided, are reduced to the following proposition, which sums up the question of opportunity : Given acute pleurisy with effusion, two cases may present themselves — in one thoracentesis is urgent, in the other it is debatable. When is it urgent, and when is it debatable ? The discussion should proceed on these lines. The urgency of thoracentesis must be based only upon the estimation of the quantity of fluid effused. The presence or the absence of fever or of dyspnoea are secondary considerations. We must, before all, con-j sider the amount of the effusion. We cannot rely upon dyspnoea, for it a faulty guide. Large effusions are sometimes associated with slight dis-j tress, and patients may have three or four j)ints of fluid in the pleura, anc still be able to walk about. DISEASES OF THE PLEURA 259 Trousseau says that a nursing woman, who carried her child, walked from Saint-Eustache to the Keeker Hospital without feelmg much fatigue. Six pints were drawn ofE by thoracentesis. A carman of whom Andral speaks went on driving his horses, and felt but slight discomfort, although he had a very large effusion. We see, says Landouzy, people who walk several miles to hospital, and complain of stomach-ache, or of attacks of fever, although they have enormous effusions. I have often seen similar cases. I have performed thoracentesis in a student who came regularly to the hospital, and felt very little distress, in spite of an effusion amomiting to 4 pints. Dyspnoea is quite deceptive. If we wait until dyspnoea appears before evacuating an effusion, we shall delay until the patient's life has long been in danger from the quantity of the effusion before our decision has been made. With still more reason, thoracentesis should not be delayed until the patient has cyanosis of the face and of the fingers, as some authors would advocate. The cases of sudden and rapid death caused by large effusions have not all been published. It is a pity, for we should perhaps be less severe on thoracentesis, and should see its indications better. Trousseau saw sudden death in the course of pleurisy on three occasions. One of his patients had such slight distress that thoracentesis was post- poned, but next morning the patient died. Landouzy has reported a case in which dyspnoea was absent. This fact did not prevent sudden death from jjleural effusion. Dujardin-Beaumetz's patient had neither dyspnoea nor cyanosis, and yet his death was sudden. Oulmont quotes the case of a man who was talking with some friends in his garden. He went to lie down, and fell dead from an effusion in the pleura. Two patients whose hLstories have been reported by Binet and Lcgrand had no dyspnoea. One suffered so little that he refused thora- centesis, and asked that it might be put off. Two hours later the effusion proved fatal. The other patient, who was in apparently good health, also died suddenly from the same cause. After such information, is dyspnoea a necessary indication for the urgency of thoracentesis ? And we know these mishaps are not the only ones ; the majority are never published. I have collected forty cases, which I brought before the Academic. How many would there be if we could make a complete list ? These cases are, for the most part, copies of one another. At every turn we see that the patient who dies suddenly has been suffering from an effusion, causing only insignificant dyspncca — so insignificant, in fact, that in many cases thoracentesis has been rejected, or imprudently put off till next day. I think that we must finally dismiss the inexact indications upon which the question of urgency in thoracentesis has been based. The duration of 17—2 260 TEXT-BOOK OF MEDICINE the pleurisy matters little. It is not a matter of importance whether such troubles as fever or dyspnoea be present or absent. The amount of the effusion is the key of the situation. At the risk of repeating myself on this important point, I say that dyspnoea is a false sign and a treacherous guide when we have to decide upon the urgency of thoracentesis. To wait for dyspnoea and, a fortiori, to wait for cyanosis of the face and of the fingers, is gratuitously to antici- pate a catastrophe. If we search in the hecatomb of patients who have died suddenly because puncture was not performed in time, we shall find many examples which show clearly that a large effusion may prove fatal, even though it has caused but slight dyspnoea. It is much more likely to kill if dyspnoea be intense, while precious time is lost in applying blister after blister. These cases of sudden or rapid death may result from various causes. Sometimes they are due to clots (thrombosis or embolism) which arise in the heart, the large vessels, or even in the lung itself. If the clot is formed in the large pulmonary veins, or in the left side of the heart, it often causes cerebral embolism, with its results — viz., apoplexy, hemiplegia, aphasia, etc. If the clot is formed in the right heart or in the pulmonary artery, it may produce rapid asphyxia and death, as in cases quoted by Paget, Smith, and Blachez. The patients suffered from left pleurisy, and died suddenly from syncope. At the autopsy the clot hat/ 'originated in the trunk of the pulmonary artery, and reached into the smaller vessels. In a certain number of cases death has supervened suddenly from syncope, the effusion being situated more often on the right side than on the left, but it is not easy to explain the reason. Louis was therefore wrong in stating that simple pleurisy is not a cause of immediate death, " A patient may die suddenly from acute pleuritic effusion " (Trousseau). These accidents can be set down to the effusion, and therefore, I repeat, the urgency of thoracentesis must be based solely upon the amount of the effusion. But, it will be asked, at what moment does urgency arise ? Is it when the effusion amounts to 4 or 5 pints ? And, further, how can the quantity be estimated ? How can we ascertain that it reaches 3 pints or more ? My analysis in cases of sudden death shows that death has never been caused by an effusion of less than 4 pints. Once only (Blachez) the pleura contained 3 pints of serous fluid. This exceptional case ought not to be included, and I estimate that, in a well-made adult, when the effusion reaches about 4 pints, the urgency of thoracentesis is clear. We must consider the estimation of the amount of fluid. Upon what signs and symptoms are we to rely ? Careful study of the signs of pleurisy shows that m small effusions tubular breathmg is muffled and limited to DISEASES OF THE PLEURA 261 expiration ; in moderate ones (2 to 3 pints) it has a bronchial tone, and is present during both inspiration and expiration ; in large effusions (4 pints or more) the breathing is in some cases cavernous, but in others it is inaudible. These auscultation data, however, are not absolute— that is to say, thev are insufficient for the estimation of the amount of fluid present. I would say the same concerning measurements with the cyrtometer (Woillez). This method, though excellent at times, is often faulty. We must, therefore, associate the preceding signs with the more exact informa- tion furnished by the extent of the dullness and by the displacement of organs. Let us take, for example, a left pleurisy. When the dullness and the absence of fremitus reach behind as high as the spine of the scapula, the resonance in Traube's space has disappeared, and a dull note replaces the skodaic note in the clavicular region, and especially when the heart is dis- placed, so that the maximum of the apex-beat is situated at the right edge of the sternum or between the sternimi and the right nipple, although at this moment the pleural cavity may not be filled to its maximum, such signs in an adult denote that the effusion is about 4 pints. Thoracentesis is then urgent. Operation is imperative, and we must not forget that pro- crastination is an unfortunate formula which costs patients their lives. When the effusion is situated on the right side, the problem is rather more difficult, because there is no displacement of the heart. Nevertheless, percussion and examination of the vocal fremitus give similar information to that which I have just mentioned. I may add that depression of the liver, when present, is a sign of great value. The liver is only pushed down by large effusions, which I estimate at about .3 pints. The estimation of the effusion is therefore rather more difficult on the right side, but it is quite as important, for the statistics given above show that sudden death is more frequent in right than in left pleurisies. The discussion so far has referred only to simple pleurisy. Tiie same principles are applicable to cases with complications. The direct or indirect compHcations of pleurisy, such as pulmonary congestion, okl adhesions, valvular lesions of the heart, or pericarditis— in short, all the lesions which impair the pulmonary circulation or narrow the field of lu-cma- tosis— are not a contra-indication to thoracentesis. On the contrary, they demand it as .soon as the effusion readies large proportions ; only the evacuation of the fluid in such a case demands precautions, which will be indicated later. The estimation of the quantity of fluid is sometimes dillicult, as witness the very numerous cases in which the more or less con- gested lung makes the amount of fluid appear larger than it really is. These facts have been emphasized by Potain. It ls really only by the moit delicate differences in auscultation and percassion that we can clinically 262 TEXT-BOOK OF MEDICINE distinguish the part due to congestion of the lung from that due to efEusion. The worst that could happen in such a case would be to overestimate the quantity of fluid. But where would be the harm ? Is it not better to withdraw 2 pints of fluid when the urgency is not absolute than to expose the patient to sudden death by not performing thoracentesis in time ? I have just discussed " thoracentesis of urgency." Apart from urgent thoracentesis, in which the surest guide is the quantity of fluid effused, the operation is disputable in all other cases. Some admit it, others reject it, and certain authorities, indeed, consider it harmful. Let us discuss these different opinions. As long as the temperature is raised — that is, as long as the acute stage of pleurisy exists — it is better to wait for defervescence before deciding. If the absorption of the effusion takes place naturally, and appears to be rapid, it is useless to intervene. If, however, the effusion remains stationary, or absorption appears slow and difficult, the fluid must be drawn off. Fluid cannot remain long in the pleura with impunity. The displaced organs become fixed in their vicious positions ; the flattened and adherent lung acts badly; two of the chief functions in the economy — i.e., hsematosis and circulation — are compromised, without counting the passage of the inflam- mation into a chronic state and the liability to purulent changes (Trous- seau). Thoracentesis, performed at the right moment, may shorten the malady by some weeks, and cause the fall of the residual fever which often accompanies effusions that are slow to absorb. Operation. — Up to 1869 only Trousseau's method was in use. He punctured in the sixth or seventh intercostal space, and 2 inches from the outer border of the pectoralis major — that is, in the axilla. A small incision was first made in the skin in order to prepare the way for the pas- sage of the trocar, which was at once thrust into the chest. The tube of the trocar was armed with goldbeater's skin, which, by acting as a valve, prevented the entrance of air into the chest during inspiration. The fluid escaped from the chest first in jerks, then in drips, and during the opera- tion the patient was generally seized with fits of coughing, which were dis- tressing, and sometimes " violent, irrepressible, and very sharp." Trousseau considered that this cough favoured the outward flow of the fluid, and in some persons it lasted for part of the day. Let me add that towards the end of the operation the fluid was commonly coloured red by admixture with blood. Thoracentesis thus performed, although not a very difficult operation^ required some skill, and at times some boldness, on the part of the surgeon,] and some resignation on that of the patient. It was, therefore, reservec for urgent cases, and performed by a restricted number of physicians. When I invented the aspirator, and performed aspiration for effusions DISEASES OF THE PLEURA 263 in the pleura, the old technique was replaced by a needle-prick so trifling that hardly any mark remained on the skin after the operation, and the fluid, instead of being forced out by jerks, with distressing attacks of coughing, passed into the aspirator from the thoracic cavity unknown to the patient. Thoracentesis was thus brought within reach of the least experienced physician. It became the most easy and the least painful of all operations, and the most junior student has to perform it in my wards. My method is as follows : The patient sits up in bed, with his arms held forward. I mark the exact spot upon the skin, which has previously been washed with a solution of sublimate, and insert the needle behind in the seventh or eighth inter- costal space, in a line with the inferior angle of the scapula. This point ls lower and more posterior than in the old procedure. It has the advantage of attacking the fluid in a more dependent position. Thoracentesis should be performed with an aseptic No. 2 or No. 3 needle, and not with a larger instrument. The permeability of the needle is proved by means of a silver wire. The needle is connected with the aspirator by indiarubber tubing ; a vacuum is created in the bottle, and the puncture is then made. For this purpose, the operator with his left index-finger finds the intercostal space, so as to define the rib above with the dorsal surface of the finger and the rib below with its palmar surface. He then uses the extremity of the index-finger as a guide, and holding the aspirating needle in the right hand, penetrates the chest wall witli a sure thrust. The needle is pushed in about 1 inch, the tap corresponding with the aspirator is opened, and the fluid flows through the indicator tube into the bottle. If the fluid does not appear, the needle has not been sufficiently pushed home. It is pushed on boldly, the previous vacuum indicating the exact moment at which it meets the fluid. The aspirator, once filled, is slowly emptied, and this temporary delay is beneficial to the lung, which does not lend itself to too rapid expansion. This manoeuvre is repeated several times, according to the capacity of the aspirator, and the flow is stopped after 2 pints of fluid have been drawn off. The needle is withdrawn, and the operation only takes eight or ten minutes. Scarcely any trace of the punc- ture is to be found on the skin, and no dressing is needed. When the operation is properly performed, the patient should suffer neitlier fits of coughing nor pain. If pleurisy is associated witli other lesions, and the field of haematosis is narrowed by cardiac or by pulmonary lesions, if pleural adhesions are thouglit to exist, and especially if during the operation the patient complains of a feeling of tearing or pain in the interior of the chest, it is better to stop the flow, and repeat the opera- tion next day. These precautions, however, which are rightly very neces- sary in pleurisy with complications, are rarely required in simple |)leurisy. 264 TEXT-BOOK OF MEDICINE What must be our line of action as regards the fluid remaining in the chest ? If the effusion is very large and exceeds 4 pints, we remove 2 pints next day or the day after, and so on until the effusion is drained. If, how- ever, the quantity of fluid has been primarily estimated at about 3 pints, and 2 pints have already been withdrawn, is it then necessary to repeat the operation ? I think that it is not advisable. In effusions estimated at about 3 pints I have often removed two-thirds only, and have found that recovery went on rapidly, the residue being more quickly absorbed after part of the fluid had been withdrawn. I think that a repetition is only indicated when the fluid remabiing in the pleura amounts to 2 pints or more. We must not forget that in some cases the fluid, after evacuation, reforms rapidly and obstinately. We must then perform thoracentesis as often as may be necessary, carefully examining the patient for some days after the operation, as the fluid may form again insidiously, and cause sudden death. If thoracentesis is performed in time, patients should not die from pleuritic effusion. In performing thoracentesis, the choice of the aspirator is indifferent. However, the rackwork aspirator appears to me the most convenient. The choice of the needle is important, and I recommend exclusively No. 2 needle, the calibre of which measures only r2 millimetres in diameter. Several objections have been made to this needle — that it permits but a slow flow of fluid, that it is easily blocked, and that its sharp point may injure the lung. What foundation is there for these objections ? The small bore of the needle retards the flow of fluid, but this is bene- ficial to the patient, for the slow flow allows the lung to expand gradually, and prevents painful fits of coughing. The hypothesis that so fine a needle may easily be blocked is hardly ever realized, and, supposing it does happen, we need only withdraw the needle and make a fresh puncture. Another objection to the needle is that its point may wound the lung. In order to prevent this accident, a special trocar has been invented (Castiaux). I have never seen the lung wounded by the needle. The lung, which is compressed and pushed back by the fluid, expands slowly, and does not meet the needle quickly. Further, a simple manceuvre prevents every chance of this. We need only withdraw the needle gradually as the fluid flows out, and to make it turn, so as to bring it almost parallel with the intercostal wall. Consecutive Accidents. — Congestion and oedema of the lung, albuminous expectoration, slow and sudden asphyxia, syncope, hemiplegia, apoplexy, more or less rapid death, and purulent changes in the fluid, have been seen after thoracentesis. DISEASES OF THE PLEURA 265 Aspiration has more than once been accused of these mishaps, an accusa- tion which Reybard's trocar did not escape. Let me at once say that these accusations have no foundation. The abuse of thoracentesis has arisen from aspiration. I know this fact, and regret it ; but as regards its abuse, there is at times a question, if not of inexperience, at least of imperfect knowledge of the technique. It is not sufficient to have in hand a needle and an aspirator ; it is also necessary to know how to use them. I shall analyze, therefore, the accidents imputed to aspiration, seek their cause, and discuss their worth, hoping to prove that, with precise indications and proper technique, thoracentesis by aspiration is the most innocent of all operations. 1. Albuminous Expectoration — Asphyxia. — Dyspnoea and asphyxia, which I place in the first group, arise as follows : Immediately or a little while after thoracentesis, the patient, who is seized with cough and distress, brings up frothy and blood-stained albuminous sputum, and the fine rales of pulmonary cedema are heard on auscultation. In mild cases the symp- toms rapidly improve, but in other cases the complication is very formid- able. The cough is paroxysmal, the dyspnoea increases, and the patient brings up as much as 3 or 4 pints of expectoration, which in the receiver is divisible into several layers, the upper frothy and yellowish, the lower more dense and albuminous. The intensity of the dyspnoea, the duration and the quantity of the expectoration, are variable, and the patient only regains his normal condition at the end of twelve or of twenty-four hours. Lastly, in some exceptional cases (I know only of six) the results have been fatal, and asphyxia has come on so rapidly after thoracentesis that patients have died in a few minutes. Since 1853 these cases of dyspnoea have been studied and variously interpreted. How can we explain the albuminous expectoration and the asphyxia ? No wound of the lung has been found post mortem, and sup- posing that puncture of tiiis organ may have allowed the fluid to pass into the bronchi, it would also have allowed air to pass from the bronchi into the pleura, causing symptoms of hydro-pneumothorax. Wounds or spon- taneous perforation of the lung, therefore, cannot be blamed. We must look to acute oedema of the lung as the cause of alltuminous (^\i)('(i()ruti()ii, dyspmjea, and asj)hyxia (llerard) ; but the cause of the acute oedema still remains to be explained. The method of aspiration has been blamed. It has been said that asjdration lowered the tension in the pleura, and allowed the fluid to liow out too quickly. How little foundation exists for this accusation is seen from the reports, which show that in sixteen cases of thoracentesis followinl by albuminous expectoration (Terillon's thesis), the operation had been 266 TEXT-BOOK OF MEDICINE performed twelve times with Reybard's trocar, and only four times by aspiration. In the six fatal cases, the operation was performed three times with the trocar and three times with aspiration. Aspiration, therefore, is not directly responsible, since most of the accidents have supervened apart from it. If these accidents have nothing to do with the operative procedure, to what, then, are they due ? In six cases in which operation was followed by death, five were cases of complicated pleurisy. In the first (Gombault), the opposite lung was partly fibrous and bound down by old pleuritic adhesions ; in the second (G-irard), the patient was suiTering from acute rheumatism with double pleurisy ; in the third (Behier), tubercular broncho-pneumonia was also present on the right side ; in the fourth (Dumontpallier), the patient had bronchitis and adhesions of the left lung, in addition to right pleurisy ; in the fifth (Bouveret), the asphyxiated patient had old tubercular pleurisy, with adhesions and 7 pints of fluid. Let us analyze the cases in which thoracentesis has been followed by oedema of the lung (Terrillon's thesis) and albuminous expectoration. Here also complications were present in most cases. Thus, in Cases 13 and 17 (Lasegue), the patients had aortic and mitral lesions, oedema of the lower limbs, etc. ; in Case 3 (Bucquoy), hypertrophy of the heart, with mitral and aortic murmurs ; in Case 15 (Lancereaux), the patient was four months pregnant, and subject to chronic bronchitis-, with night-sweats ; in Case 7 (Marotte), the patient was suffering from pleurisy as well as from pulmonary tuberculosis. I find that the accidents due to thoracentesis, when pleurisy was not associated with any complication, have been caused by withdrawing rapidly and at one sitting too large a quantity of fluid — 10 pints in Case 6 (Marotte), 7 pints (Worms), 5 pints in Case 18 (Faussillon), and 4 pints in other cases. The benign, grave, or fatal cases of pulmonary oedema and albuminous expectoration have, therefore, always been associated either with com- plications or with the immediate withdrawal of too large a quantity of fluid, and most often with these two causes combined. These accidents, then, are not directly referable to exaggerated lowering of the pleural tension produced by aspiration, since the same accidents supervene with Reybard's trocar wlien the tension is the same inside and outside the chest. When, however, aspiration is badly performed, trouble follows ; but it is not a question of the quality of the vacuum, but of the quantity. Acci- dents do not occur because 2 pints of liquid have been withdrawn with a proper vacuum, but because 4 or 5 pints Lave been drawn at once with an incomplete vacuum or with none at all. It is not aspiration which is at fault, but the way in which it is done. A patient has had 6 or 7 pints i DISEASES OF THE PLEURA 267 of fluid in his chest for five or six weeks. The heart and the pulmonary vessels are displaced, the lung is flattened, the circulation is hampered. These organs are suddenly deprived of 6 pints of fluid which has for a long time impeded their functions, and the blood at once rushes into the pul- monary vessels, the air into the alveoli, and yet we are astonished that accidents supervene. What astonishes me is that they do not occur more often. It is not aspiration, nor a too perfect vacuum, which must be blamed for these accidents. It is aspiration prolonged without measure, or the emplojTnent of too large a trocar. It is, in short, the ill-advised method, which, without holding to principles that should never be departed from, allows a large effusion to be drawn off too rapidly at one sitting. I repeat again that the secret of preventing accidents consists in using a No. 2 needle and in limiting the quantity of fluid withdrawn at a sitting to 2 pints. I have always carried out this plan, and in the 180 cases which served as a basis for my discussion at the Academic de Medecine, we find that the patients suffered no mishap. Pulmonary congestion, albuminous expec- toration, and threatening asphyxia were never seen. We may, then, draw the general conclusion that thoracentesis, properly done, never causes trouble ; while thoracentesis, if imprudently rejected or postponed, exposes every patient suffering from a large effusion to the risk of sudden death. 2. Early or Late Syncope. — In some cases patients die from synco23e one or two days after operation. Analysis of these cases proves that the acci- dents resulted from various causes which were in every case independent of thoracentesis, and included clots in the heart or the pulmonary vein, phlebitis, and thrombosis, and gangrene of the pleura (Besnier). 3. Purulent Changes. — The accusation that serous fluid may become purulent is certainly one of the gravest accusations which has been brought against thoracentesis. This accusation has been brought up durhig the last disciLssion at the Academic, but it has no foundation. If we puncture in the early stage of pleurisy, and do not examine the fluid carefully, we may conclude the effusion is benign, because the fluid is clear and citron-coloured ; then, if a fresh puncture is made later, thoracentesis is ^vrongly accused of having caused infection, because we forget that we have punctured at two different stages of the disease, and that thoracentesis has nothing to do witii this change. A similar remark holds good with regard to the pathogenic agents in the fluid of sero-fibrinous pleurisy. Fluid containing the pneumococcus or the staphylococcus may, on the first ]nincture, be scro-fibrinous, and may become purulent from the nature of the disease, and not from thoracen- tesis. The question of this purulent change in pleuritic effusion htllowing 2G8 TEXT-BOOK OF MEDICINE thoracentesis appears clear, in my opinion. Aseptic thoracentesis cannot cause sero-fibrinous fluid to become purulent, and if the change has occurred, it is not the operation which should be blamed, but the operator. II. HOW TO TELL IF AN ACUTE SERO-FIBRINOUS PLEURISY IS OR IS NOT TUBERCULAR— CYTO -DIAGNOSIS — SERO-DIAGNOSIS. Discussion. — As we have studied the symptoms, course, and treatment of acute pleurisy, let us now consider the tubercular nature of these cases. We are often consulted by patients who have been attacked while in good health by acute sero-fibrinous pleurisy. The case appears innocent, and it has the characters of primary pleurisy. The conditions under which it has developed appear to stamp it as pleurisy a frigore, and yet, learning from experience, we doubt the benignity of the disease, and ask ourselves whether the condition is not really tubercular — a fact which greatly modifies the prognosis. How can we solve this problem, which sometimes is very difficult ? Are we in a position to say that the case is tuberculous or not ? We must now discuss this question.* When I commenced my medical studies, acute pleurisies were classed as primary and secondary. The former class was said to result from chill, whence the name " pleurisy a frigore." It was called idiopathic, meaning by this that it was not secondary to any other pathological process. It was also called " frank pleurisy," which excluded the idea of any original taint. This primary form served as the general descriptive type of acute pleurisy. In opposition to this primary form, writers described secondary pleurisies which supervened in the course of some other disease, such as pneumonia, rheumatism, 3right's disease, etc., or were consecutive to neighbouring lesions of the thoracic and abdominal organs. In this incongruous group pleurisy due to tuberculosis occupied the chief place, but primary pleuro- tuberculosis was not yet well known, and tubercular pleurisy was chiefly considered as a complication of phthisis. The question of tubercular pleurisy has been gradually elucidated, and it is evident that all cases do not resemble one another. The first category includes cases supervening in phthisis when lesions exist in the lung and bacilli are present in the sputum. Pleurisy appearing under these condi- tions is almost certainly tuberculous ; but this fact is of minor importance in the present discussion, since we know in advance that the patient is tubercular. * Dieulafoy, Clinique Medicate de V Hotel- Dieu, 1905, le9ons 1 et 2. DISEASES OF THE PLEURA 269 In the second category let us place cases supposed to be tubercular. The lung appears free, it is true, yet the patient is suspected of tubercu- losis. One is of tubercular stock ; another has previously had obstinate bronchitis, haemoptysis, fistula in ano, or so-called rheumatism, which is only tubercular pseudo-rheumatism (Poncet). Some patients in their infancy have had suppurating glands in the neck, which have left scars ; coxalgia, which has left slight lameness ; or adenoid hypertrophy, with larval tuberculosis of the tonsils.* In short, the cases belonging to this category have been preceded at a more or less distant date by previous tubercular lesions. Sometimes they follow a prodromal phase that is of indefinite duration, and is characterized by loss of strength and wasting. Clinically, I repeat, these cases are suspicious of tuberculosis. Quite different are the cases of tubercular pleurisy which now require notice. We find no trace of tuberculosis, either in the past or in the present. The patient has been attacked with pleurisy while in good health, either without appreciable cause or following a chill, just as a patient is seized with tonsillitis or with coryza. The onset and course of the disease, the appearance of effusion, the results of thoracentesis (if it has been per- formed), and convalescence itself, recall the picture of so-called pleurisy a frigore. Appearances, however, are often deceptive, for we shall find that the man who recovers from pleurisy suffers some years later from more or less advanced pulmonary tuberculosis. The pleurisy from which he recovered was the initial manifestation of the tubercular infection which has developed later. Another patient who has been completely cured of pleurisy dies six months or a year later from tubercular meningitis. These cases, moreover, are not isolated. On the contrary, they are frequent, and have thrown douljt upon the existence of pleurisy a frigore. Landouzy in 1884 deprived pleurisy a frigore of its ancient privileges. " Every pleurisy," says he, " which does not stand the test is tubercular, although the patient may be robust." Kelsch and Vaillard sustained the accusation, and the course of events fitted in so well in this respect that pleurisy a frigore has lost part of its importance. Landouzy's opinion, however, aroused sharp protests, and facts in opposition to his opinion were sought for. Cases of acute pleurisy a frigore were published. It was said they had no connection with tuberculosis, since they recovered without sequelae. Partisans arranged themselves into camps, and pleurisy a frigore continued to be admitted by many physicians. We have to see on wliicli side the truth lies. Lot us carefully examine * Diinilafov, " 'i'lilxTCulosf! Ijiirvrt! dcs Trois Aniygflali-s " {Aradhnif de MCdecine, 8('anco du 'M Avril, 18SJ5 ; ut " Maiiuol de I'ttthologio lutorao," t. ii., p. l'J7). 270 TEXT-BOOK OF MEDICINE the evidence, for it is important in prognosis to know whether pleurisy is tubercular or not. Let us first consider the cases of sudden death in patients suffering from pleurisy a frigore, and see whether post-mortem examination discloses tubercular lesions. The following case (Landouzy) might be quoted as a type of pleurisy a frigore. A healthy baker went out while in a profuse sweat to buy some wine. Whilst walking he felt that he had. caught a cold, but continued his work. Pain in the side, respiratory distress, and fever appeared. The j)leurisy ran its course. Some months later he died suddenly, while under Landouzy's care. Post mortem, much serous fluid was found in the right pleura, and the right lung showed small foci of latent tuber- culosis. This case, although apparently one of pleurisy a frigore, was really tubercular. Kelsch and Vaillard have published the following cases : A healthy trooper was taken ill with acute pleurisy. He died suddenly while talking Avith his comrades, just as he was going to the Val-de -Grace Hospital. At the autopsy a large effusion was found in the right pleura, which was studded with tubercular granulations. Another soldier, who was suffermg from right pleurisy, was reading by his bed, when he suddenly fainted and died. A large right-sided effusion was foimd post mortem ; the pleura was studded with tubercular nodules. These cases of serous pleurisy, say Kelsch and Vaillard, " supervening in strong men without any tuber- cular taint and having only the usual signs of pleurisy, would certainly have been considered as inflammatory if sudden death had not revealed their true nature." In days gone by, at the Saint-Antoine Hospital, I saw the two following cases, which have been published by Binet and Legrand : A man in good health was taken iU with right pleurisy, which he attributed to a chill. For several days we followed the spread of the effusion, which finaUy reached about 4 pints. Although dyspncea was absent, we decided on thoracentesis about 11 a.m. The patient protested, and the operation was postponed tiU evening; but an hour later the man got up, and died from sjTicope before help could reach him. At the autopsy, as I wished to know the exact amount of the effusion, I performed thora- centesis on the corpse, and drew off 4 pints of yeUowish fluid. Latent tuberculosis had been present ; at the apex of the lung we foimd a cretaceous tubercle. The second of my cases refers to a robust man who had no tubercular history. His trade exposed him to sharp changes of temperature, and especially to local chiUs : he carried blocks of ice on his back. The pleura and the lungs were therefore much exposed to cold. He came under my care for pleurisy. At the right side we found an effusion, estimated at about 6 jjints. Two pints were dra-mi off by puncture on three successive days. He felt very well, but the hquid continued to reform. Some days later he got up, but had gone only a few steps when he fell down, his face cyanosed, his lips blue, and died in a few seconds. At the post-mortem, as I wished to know exactly the quantity of effusion causing his sudden death, I performed thoracentesis on the body, and drew off 71 ounces of fluid. I then discovered that the pleurisy, which appeared to be a frigore (contact with the ice-basket), was really tubercular; I found tuberculosis of the pleura and a tubercular nodule in the Ixmg. A person may apparently regain his health after acute pleurisy, but some months later he is carried off by acute phthisis or by menmgitis, show- DISEASES OF THE PLEURA 271 ing the tubercular nature of the pleurisy. In 1884 I saw the following case : A mechanic, aged twenty-eight, came imder my care for pleurisy a frigoie of three weeks' standing. There was nothmg to make me think of tuberculosis ; it was a typical case of pleurisy. On the left side I foimd a large effusion, which I estimated at 4 pints. 1 began by drawing off 2 pints of sero -fibrinous fluid. A few days later I drew off 2 pmts more. Everything went well — the patient regained his health ; bat six months afterwards he came imder my care with signs of meningitis, and died in a few days. At the i)Ost-mortem we foimd that the pleurisy was cured, only a few adhesions remain- ing, but tubercular meningitis and some tubercular granulations in tho lang were present. In his anatomical and experimental researches on tuberculosis of the pleura, Peron arrives at the following conclusions : " Acute pleurisy, called ' frank,' is usually tubercular in nature, and is in many cases due to dis- crete infection of the pleura." Clinical medicine teaches us that many patients who are a^jparently suffering from primary pleurisy are really affected with tuberculosis, because, although they may be cured of pleurisy, the tubercular infection invades the lung, meninges, peritoneum, or other parts of the body some months or years later. Clinical medicine, however, also teaches us that there are other patients in whoih acute pleurisy, with large effusion, may recover without leaving any tubercular taint ; the patient, after having recovered his health, lives for ten or twenty years, but yet neither he nor his descendants show any signs ol tubercular infection. Many statistics may be consulted on this subject. Fiedler, in Germany, reports 92 cases of sero-fibruious pleurisy which he punctured : of this number, 17 died in hospital from tuberculosLs, 8 died after leaving, 66 left the hospital either tubercular or suspected of tuberculosis, and 21 were in good health at least one or two years later. The statistics of Barrs and Bowditch in England, and those of Mayor and Ricochon in France, give results which are not in agreement, but still the tubercular element occupies the largest part. For some years I questioned my colleagues (Brouardel, Grancher, Vcrgely, Lepiiie, etc.), in order to learn their opinion and the result of their observations. Vergely sent me four reports, referring to patients with pleurisy who were punctured fifteen, twenty, and twenty-two years previously ; they remained in good health, as did their children. Lepine has furnished me with six cases, seen a great number of years ago, and never followed by tubercular miseliicf. Since my first work on thoracentesis by aspiration, which dates back more than thirty years, I have punctured a great many cases. I have lost sight of nearly all the hospital patients, but have been able to follow up many of those treated in ])rivatc, and I can quote cases of persons who suffered from acute pleurisy and recovered without any signs of tuberculosis. 272 TEXT-BOOK OF MEDICINE I owe the following notes to Dr. Lamarre (of Saint-Grermain) : The forage-store at Saint-Germain was formerly situated in the Rue d' Alsace, nearly a mile from the quarters. The square of the Chateau is about half-way on the road from the forage-magazine to the barracks. When Lamarre was appointed Assistant Physician to the Samt- Germain Hospital, the outer walls of the trenches of the castle had just been raised to the height of 3 feet. This wall became a natural lounge for the soldiers who carried forage on their backs. They used to come from the store, and, while in a sweat, they leant their backs against the wall, so as to rest their load on the top. Suddenly, however, an epidemic of acute pleurisy a frigore broke out in the regiment, while no cases were seen among the civil population. The mischief always affected the right side. The men made good recoveries, with or without aspiration, according to circumstances. They were clearly, says Lamarre, cases of pleurisy a frigore. The angle of the Chateau square where the soldiers rested was sheltered except from the cold north- east wind, which lashed the right side of their chests. At the request of Lamarre and of the Surgeon-Major of the regiment, the Colonel forbade the men to stop at this dangerous spot, and no more cases of pleurisy occurred. The regiments on guard duty, however, change every six months, and fresh cases of jjleurisy, due to the same cause, occurred in the regiment which had just marched in. It was again necessary to prohibit the men on fatigue duty from stopping and resting against the wall. This experiment (for this fact has the value of an experi- ment) occurred several times, ■with the same regularity. By confining ourselves to clinical facts we see, then, that the cure of acute pleurisy, without any residue of tuberculosis, is not so rare. These facts furnish an argument for those who defend acute pleurisy a frigore : " You see clearly," they say, " that these cases of pleurisy are not tuber- cular." Moreover, they add : " Since pleurisy a frigore exists in animals, why should it not exist in man ?" Trasbot, in an interesting paper, has shown that pleurisy a frigore is common in horses, dogs, and sheep, and may have nothing to do with tuberculosis. In support of this opinion, the following facts have been quoted : In 1871 a line regiment of Cuirassiers who had just been supplied with clipped horses were picketed in the open, often without blankets, and in a few weeks thirty cases of pleurisy, nearly all fatal, occurred among the animals. This fact was so striking that the military authorities at once prohibited the purchase of all clipped horses. Duvieusart saw 100 cases of pleurisy, with 60 deaths, in a flock of 400 sheep which had just been shorn during a very cold February. These animals were not tubercular, and the pleuritic fluid, injected mto guinea- pigs, never caused tuberculosis. Rousseau saw several healthy dogs attacked by pleurisy, after havuig in the depth of winter followed a stag in a pond for almost an hour. In all these cases, adds Trasbot, there was no question of tuberculosis. I quote Trasbot word for word : " The three domestic species — horse, dog, and sheep — in which pleurisy is most often met with are precisely those in which tuberculosis is most rare. . . . Thus, the facts drawn from extensive clmical observation in different species of animals are in J DISEASES OF THE PLEURA 273 formal contradiction to the idea that pleurisy may in these species be a form of tuberculosis. This proposition, which is derived from clinical data, is also absolutely confirmed by experiment. The injection of the fluid from sero-fibrinous pleurisy in horses or in dogs has never caused tuber- culosis in guinea-pigs or rabbits." It appears undeniable, then, that simple pleurisy a frigore is frequent in animals. Veterinary medicine shows the power of chills in causing pleurisy among animals. But let us limit our study to human medicine, and state the question afresh : Does there exist in man true pleurisy a frigore which is not tubercular ? and if it exists, by what means can it be distinguished from the tubercular form ? Laboratory Researches. — To answer this question, an appeal has been made to the multiple resources of the laboratory. Inoculations. — It was thought that the introduction of pleuritic fluid into the peritoneum of guinea-pigs would furnish important information, as the iiioculation would transmit experimental tuberculosis to the animal if the fluid were tubercular. The method of inoculation certainly gives valuable information, but in a fairly large number of cases it leaves the tubercular or non-tubercular nature of pleurisy in doubt ; its value Is abso- lute when the result is positive, but a negative result does not prove that pleurisy may not be tubercular. AH observers are agreed that tubercular pleurisy may give negative results after inoculation of pleural fluid. A negative result is easily understood, because the fluid may have very little virulence, and the bacilli may be so disseminated that the few organisms introduced into the peritoneum are rapidly destroyed. Injections of tuberculin furnish information of undeniable value. According to the official figures from the clinics in Prussia, patients suffering from apparently simple but really tubercular pleurisy are nearly as sensitive to injections of tuberculin as frankly tubercular patients are. Injection with tuberculin, even if carried out according to Grasset's rules, is not always exempt from harm. Cultures. — The application of culture methods to the search for the tubercle bacillus in effusions has only recently been successful. If we are to obtain positive results, a culture medium that is extremely favourable to Koch's bacilli should be employed. Glycerinated blood-agar, as used by Bezan9on and Griffon, is the best medium. The mixture of aseptic rabbit's blood with agar furnishes soil on which the microbes develop in abundance, although they will not grow on the usual media. If glycerine is previously added to the agar-agar, glycerinated blood-agar is obtained, on the surface of which it Is only necessary to place the suspected litpiid, whether it be pus, cerebro-spinal fluid, removed by puncture, pleuritic fluid, etc. 18 274 TEXT-BOOK OF MEDICINE We may use, in place of ordinary culture -tubes, Erlenmeyer's flasks, at the bottom of which a layer of the mixture of the blood and glycerine agar is allowed to settle. The tube is carefully sealed and placed in the oven at 37° C. After three or four weeks, colonies, which increase in number and have the following characters, are seen to appear. At first the colonies are smaller than a pm's head, but they soon become larger, growing in prominent mulberry- shaped masses of a chocolate colour. Under the microscope, preparations show bacilli, isolated or in clumps, which are usually of a twisted form. The number visible to the naked eye is proportionate to the amount of fluid sown, and especially to the richness of this fluid in bacilli. The results obtained by this procedure are not constant, but it is an excellent control measure, often used in our clinic. Sero-Diagnosis. — What may we expect from sero-diagnosis ? Let me first remind the reader that it is the sero-diagnosis of tuberculosis. Speaking generally, sero-diagnosis supposes two factors ; whether the case be one of typhoid, pneumonic, or tubercular infection we need : on the one hand, a homogeneous culture in a fluid medium, in which the microbes are separated one from another ; and, on the other hand, serum from the infected patient, which, on addition to the culture, produces agglutina- tion of the microbes. In 1898 Arloing tried to find a sero-diagnosis for tuberculosis, comparable with Widal's method in typhoid fever. The problem was solved when he obtained homogeneous cultures of Koch's bacillus in a fluid medium. In order to obtain the conditions most favourable to success, we must employ a culture of tubercle bacilli twelve days old. A small quantity of the culture is placed in a very small tube. This culture is mixed with blood- serum from the finger of a patient who is thought to be suffering from some tubercular lesion. The mixture is so made that it represents one part of serum to five parts of culture, or one part of serum to ten parts of culture, etc. The tube is then shaken, to favour mixing, and the effect is watched. If the result is positive, agglutination occurs after an interval of one to five hours. The upper layers of the mixture become clear, while flakes accumulate at the lower part of the tube and give to this layer a muddy aspect, contrasting with the limpid nature of the upper layers. Microscopic examination will confirm the result of the agglutination, and the Koch's bacilli appear in masses instead of being isolated. Sero-diagnosis is applicable in tubercular pleurisy. Courmont found that a positive reaction may be obtained by mixing cultures of Koch's bacilli either with blood-serum or with pleuritic fluid in dilutions of 1 to 20, 1 to 10, or 1 to 5. The agglutinating power of the blood is not always equal to that of the I DISEASES OF THE PLEURA 275 serum ; it may be more or less marked, and may exist while that of the serum is absent, or vice versa. Courmont in the following table has summarized the results of positive and negative reactions with pleuritic fluid and with blood-serum ; -r. .,. .. r>o I ^ case, 1 in 20 /■Positive reactions, 23 cases i\ In 31 cases with I "^ (74nercent) j 6 cases, 1 in 10 pleui-itic fluid 'I ^ V ■> [16 cases, 1 in 5 iNegative reaction 8 cases, 1 in 5 (26 per cent.). /Positive reactions, 18 cases (3 cases, 1 in 20 9 cases, 1 in 15, 1 in 10 6 cases, 1 in 5 INegative reactions 4 cases (19 per cent.) The results obtained at the Hotel-Dieu confirm the value of sero- diagnosis in tubercular pleurisy ; we must, nevertheless, remember that the procedure is sometimes at fault. Cyto-Diagnosis. — Cyto-diagnosis is based on the examination of the cellular elements found in the fluid of pleurisy and of serous effusions in general. A few words of explanation are necessary. Certain cells respond by an offensive and defensive reaction against the attack of the patho- genic agents, but the same cells do not always react to different provoking agents. The polynuclear neutrophUes, or microphages (Metchnikoff), engulf the streptococcus or the pneumococcus. The large mononuclear cells, or macrophages, have a more powerful action ; they absorb, and sometimes succeed in destro3dng, the tubercle bacillus ; they readily digest large cells, such as red corpuscles and polynuclears. It was therefore natural to suppose that the presence of a particular cell in the fluid would indicate the nature of the pathogenic agent. From this idea cyto-diagnosis has arisen. In 1900, under the name of " Cyto-diagnosis," Widal and Ravaut first published their valuable work, of which the chief features are as follows : In a case of pleurisy we desire to know the cellular elements in the fluid. For this purpose we draw off, with a sterile syringe, some pleuritic fluid, and centrifugalize it, A sediment forms at the bottom of the tube ; we pour off the fluid, so as to leave in the tube only a little liquid, which forms a cloudy emulsion with the cellular debris. A drop of this emulsion is placed on a slide and stained with thiouin, eosin - ]ia)inatin, or with Erlich's tri-acid mixture. On microsco])ical examination, we see cells of various kinds — red cor- puscles, polynuclear leucocytes, large mononuclear cells, lymphocytes, isolated endothelial cells, and endothelial plaques. These elements, how- ever, do not exist indifferently in all cases. A slide does not at the same time show numbers of polynuclears, lymphocytes, and endothelial cells. 18-2 276 TEXT-BOOK OF MEDICINE Except for the red corpuscles, which exist in most pleuritic fluids, one speci- men will contain chiefly lymphocytes, while the polynuclear and the endothelial cells are absent, or in very small numbers. Another specimen of fluid contains almost nothing but polynuclear cells, while the lymphocytes and endothelial cells are absent, or very few in number. Lastly, a third specimen contains chiefly endothelial cells and plaques — the lymphocytes and polynuclear cells are absent, or few in number. The preponderance of one or other variety of cell in the pleuritic fluid constitutes the cellular formula for this fluid, and leads to the cjrto-diag- nosis. From this point of view, Widal and Ravaut have described three kinds of pleurisy, each with its own cyto- diagnosis. The first variety comprises effusions in cardiac disease, Bright's disease, and cancer, as well as those due to irritation or to compression by neigh- bouring organs. No infective agents are present, and consequently we find no phagocytosis, but only the processes of transudation and desquama- tion ; the condition is a kind of congestive oedema. To use an old expression, it is here less a case of exudate than of transudate ; it is by transudation that the liquid carries away the endothelial cells from the serosa into the fluid. Accordingly, these so-called mechanical effusions have a special formula ; the fluid, as a rule, contains neither lymphocytes nor polynuclear cells (at any rate, in the first stage). Endothelial cells from the serosa are almost exclusively met with. These cells are very large in comparison with the size of the red cor- puscles and the leucocytes. They may be isolated or agglomerated, bilobed, trilobed, or fused in large endothehal plaques with polycyclical edges. After staining with eosin-ha^matin, the nucleus is seen to be much darker than the protoplasm. The outline of the cells is almost circular ; in the endothelial plaques, however, the outline of the cells disappears at the points where the protoplasm is fused. These plaques, which vary in size and in number, are characteristic of mechanical effusions. Widal and Ravaut met with them in twelve cases. The post-mortem examination of three patients with this variety of pleurisy, and the negative results of the intraperitoneal inoculations in guinea-pigs with pleuritic fluid from seven similar cases prove that tuberculosis is not in evidence. These endothelial masses are not only characteristic of mechanical pleurisy, but their presence in the fluid excludes the hypothesis of tuberculosis. They are not found in the fluid in recent cases of tubercular pleurisy, no doubt, " because the tubercular neomembrane prevents the patchy desquamation of the endothelium." Similar observations have been made in my wards : the fluid in every case of tubercular pleurisy, though very rich in lympho- cytes, did not contain endothelial plaques. A similar assertion may be made, especially with regard to the first stages of mechanical effusions, I DISEASES OF THE PLEUEA 277 but later the lymphocytes may abound. The presence of the plaques suffices, nevertheless, to specify the diagnosis. In the second variety of pleurisy the fluid has quite a different cellular formula. This variety includes acute infective pleurisies. The patho- genic agents, which . include the streptococcus, the pneumococcus, the Bacillus typhosus, etc., after causing cellular reactions of attack and defence, may no longer be present, but the phagocytes or polynuclear leucocytes exist in abundance. We also meet with large mononuclear cells, which may be large leucocytes, or may be derived from the serous membrane ; while we may also recognize the presence of endothelial cells, which are isolated or have remained absolutely normal. With regard to these cases, Widal and Ravaut give the following information : In three out of seven cases of pleurisy in typhoid fever, the relative abundance of large polynuclear leucocytes characterized the formula of the effusion. In a case of sero-fibrinous streptococcal pleurisy, there were only neutrophile polynuclears, with deformed nuclei. In sero- fibrinous pneumococcal pleurisy, the formula gives rather the impression of attack and defence. This formula is characterized by the presence of red corpuscles and of a few lymphocytes, but especially by the abundance of the polynuclears and by the presence of a greater or less number of large mononuclear cells, some of which are really macrophages and engulf the polynuclears. It is quite exceptional to meet with two or three endo- thelial cells fused together. Some odourless fluid was withdrawn by exploratory puncture from one of my patients who had pleurisy on the right side. The fluid was examined by Apert, and contained only polynuclears ; neither lymphocytes nor endo- thelial plaques were met with. The absence of lymphocytes excluded acute tubercular pleurisy ; the absence of endothelial plaques put mechanical pleurisy out of court. A few days later turbid foul-smelling liquid, like dirty water, was withdrawn. The fluid, which was rich in polynuclears at the first puncture, now contained only a few cells in the shape of granular masses, which did not stain well ; they were dead leucocytes in process of granulo-fatty degeneration. Aerobic and anaerobic cultures of the liquid revealed a varied microbic flora. In aerobic cultures the Staphylococais (dbus appeared. In anaerobic cultures, colonies in the form of whitish points, composed of a small micrococcus en masse, appeared. The leuco- cytic formula of this foetid pleurisy was the same as in other infectious varieties. In short, polynuclear and mononuclear elements characterize acute infective pleurisies ; lymphocytes, when met with, are less numerous, and it is exceptional to find endothcilial masses, with two or three nuclei, l^^ig. 14 represents the cellular formula. We see several polynuclear leucocytes and one large uninuclear cell. 278 TEXT-BOOK OF MEDICINE We now come to the third variety, which is the most important of all, and corresponds best to acute pleurisy a frigore. On micro- scopic examination of the pleuritic fluid, we see that the cellular formula is characterized "by the almost exclusive presence of lympho- cytes, which are confluent and mixed with a relatively large number of red corpuscles. At times we perceive here and there mononuclear cells, as well as lymphocytes, which at first sight seem to be the only leucocytes in the specimen." The polynuclears, when met with, are not numerous ; they are perhaps the result of secondary infection. The endothelial cells must be very rare, because in seventeen cases Widal and Ravaut never met with them. I have examined the cellular formula of these cases, employing prepara- tions made with fluid from seven patients in the Saint-Christophe and ^ ?$u Fig. 14. — PoLYNtr clear LEtrcocyTEs, Sainte-Jeanne wards. Numerous lymphocytes and some red corpuscles are met with ; neither polynuclears nor endothelial plaques are seen. This description corresponds to that given by Widal and Ravaut. This cellular formula, or pleural lymphocytosis with red corpuscles, indicates that the case is tubercular. Histological examination of the pleura and inoculation of the peritoneum in guinea-pigs with the pleuritic fluid confirm their tubercular nature. 'The following case was related to me by Widal, and is a strikmg example : A youth was taken ill with the symptoms of pleurisy a frigore — i.e., repeated rigors, stitch in the right side, and cough, but no expectoration. On the ninth day he was admitted under Widal, with the signs of abundant effusion on the right side. Thora- centesis was performed, and 4 pints of yellow liquid were withdrawn. The liquid showed a typical lymphocytic formula, indicating pleuro -tuberculosis. On the follow- ing day the temperature varied between 102° and 104° F. Four days after the puncture the patient suddenly sat up, choked, and died in a few seconds. Post mortem : The left lung looked like an infarct engorged with blood ; this conj dition seemed to depend upon an extensive pulmonary embolism. Tubercles were nol DISEASES OF THE PLEURA 279 present in either lung. The pleural cavity contained 3 pints of sero-fibrinous fluid. The pleura was much thickened. No tubercles were visible to the naked eye, but histological sections showed everywhere tubercular tissue. Many giant cells were seen in the fibroas tissue of the inflamed serous membrane. Fig. 15 represents these lesions. In this section of the thickened pleura tissue is infiltrated with numerous cells. We see a giant cell, containing numerous nuclei, arranged like a crown at the periphery of the cell. The entire pleura was really a tubercular membrane studded with giant cells, but the lung was unaffected. The condition was primary tuberculosis of the pleura. The fluid produced tuberculosis in guinea-pigs. This case sums up the whole question ; it would formerly have been con- sidered as a case of simple pleurisy a frigore, when it was really tubercular. The cytoscopic examination of the fluid was undertaken, but lymphocytes alone were found ; the diagnosis of tubercular pleurisy was verified by the Fio. 15, — Section of Pleura. histological examination of the pleura and by the results of inoculation of guinea-pigs with the pleuritic fluid. We have, therefore, several methods of ascertaining the tubercular nature of acute pleurisy, but I much prefer cyto-diagnosis, because it is simple and expeditious. In acute pleurisy (the patient being in good health) abundance of lympho- cytes and absence of endothelial plaques from the fluid point to tubercular mischief. Cytoscopic examination of the fluid is as necessary as bacterio- logical analysis of the sputum in a doubtful case of pulmonary tuberculosis. In every case of pleurisy cyto-diagnosis is necessary. Every report in which cyto-diagnosis is wanting is incomplete. In my wards this fact is never neglected. We must not be satisfied even though the diagnosis is clinically evident, because surprises may happen. Pleurisy, considered to be tubercular 280 TEXT-BOOK OF MEDICINE because it has supervened in the course of phthisis, may not be tubercular ; pleurisy, considered influenzal because it has occurred in the course of influenza, may be tubercular ; the influenzal infection has here favoured the development of pleurisy. Cases of traumatic pleurisy, which might have been referred to the trauma alone, are really tubercular, the injury having awakened the latent germs. I have so far considered tubercular pleurisy, which is acute or of recent date. The leucocytic formula of the fluid may be quite different in a case of tubercular hydropneumothorax, which results from gross tubercular lesions in the lung. Under such conditions the lympho- cytosis is not the chief point : " old deformed polynuclears with much divided nuclei are seen, as well as cells with vesicles in their protoplasm, and some- times also amorphous masses, which appear to be derived from the endo- thelium." The diagnosis in this variety depends chiefly on clinical research. Nattan-Larrier has devised an ingenious method, which consists in the injection of | c.c. of pleuritic fluid into the mamma of a female guinea-pig which is suckling. The mamma acts as a living culture medium. The bacilli begin to appear in the milk after five to ten days. When we wish to examine the milk, the animal is put on its back, and the mammary gland is squeezed with the fingers of the left hand ; a drop of milk exudes from the nipple. The drop is spread out over a slide in a thin layer. The films are fixed with alcohol, stained with Ziehl's fuchsin, and decolourized with 30 per cent, nitric acid ; the ground substance is stained with Kiihn's blue. We see even as early as the fifth day that some bacilli are engulfed by the macrophages, or are isolated between the leucocytes. A few days later the bacilli are more numerous, and their recognition is more easy. This method has been extended to other fluids (peritoneal effusion, cerebro-spinal fluid, etc.). It has been used in my wards at the Hotel-Dieu, and I have proved the correctness of the results. By this method the daily search for bacilli allows us to follow the course of the inoculation, and reveals tuberculosis as soon as it begins to develop in the gland. We also see that the glands become larger in a few days and that the inguinal glands swell ; the mamma is there- fore the starting-point of widespread lesions. Let us return to the origin of our discussion. The original question was : Are we in a position to know whether acute sero -fibrinous pleurisy is or is not tubercular ? The answer is an affirmative one. Henceforth it will be possible for us to estimate correctly the so-called " essential " pleurisy. We shall see from the first that most cases which answer to the description of so-called frank pleurisy a frigore are really tuber- cular ; cyto-diagnosis stamps them, and lymphocytosis unmasks their origin. We shall see, further, that there are infectious agents capable of causing acute pleurisies which have nothing to do with tuberculosis. An individual suffers from sero-fibrinous pleurisy with effusion, as he might from pneu- I DISEASES OF THE PLEURA 281 monia ; the pneumococcus is the provoking agent. Another person has acute pleurisy with effusion ; here the streptococcus is the pathogenic agent. In a third person, who also has acute pleurisy with effusion, we find fcetid or non-foetid infection of the pleura by aerobic, or by anaerobic, germs, etc. This group of acute pleurisies, which I might further enlarge, has nothing to do with tuberculosis. Bacteriology has classed them according to their pathogenic agents ; cyto-diagnosis includes them in the same cellular formula; they are cases of pleurisy with polynuclear and mononuclear cells. The pathogenic diagnosis of pleurisies which were formerly indefinite is now so clearly elucidated that we may ask what place can be assigned in medicine to " essential " pleurisy, in which cold was considered the only cause. Ought this variety of pleurisy to surrender its place in our nosology for ever, after having occupied the chief place ? Should it be definitely cut out, or should a place still be reserved for it ? The future will tell us. Curability of Tubercular Pleurisy. — Let us now approach another side of the question. How can we explain the fact that acute pleurisy, called a frigore, but recognized as tubercular, may recover without leaving any traces ? This very curability was the chief argument against tuberculosis. Our reply is that if these cases recover it does not say that they may not be tubercular. The disease is sometimes limited to the pleura (primary pleuro- tuberculosis), the lung is free, and the rest of the organism is healthy ; as the serosa is well armed for defence and the virulence is feeble, it is not surprising that pleurisy may recover without the infection of other parts. Further, recovery is not special to tuberculosis of the pleura ; other sero- membranes have the same privilege. Tuberculosis of synovial membranes, from simple arthritis to tubercular pseudo-rheumatism, is cured fairly often. Tuberculosis of the pericardium (Rendu) belongs to the same category. Cases of recovery from tubercular peritonitis with ascites are no longer reckoned. Cases of ascites, formerly catalogued under the terms "essential," or " a frigore," are certainly cases of tubercular peritonitis, which are attenuated and readily curable. Some recover under medical treatment without the help of surgical intervention, some after puncture, with or without consecutive injections, while others are cured by laparotomy. The cure of one of these cases formerly caused much stir. On March 20, 1840, at a time when no one dared to touch the peritoneum, my uncle, Paul Dieulafoy, of Toulouse, was bold enough to inject tincture of iodine into the peritoneal cavity after removal of the fluid. This operation was successful, and since then other cases have been reported. I have often recognized this curability in simultaneous tuberculosis of the pleura and the peritoneum. Tubercular pleurisy is therefore perfectly curable ; indeed, it may be said that it is sometimes quite benign in nature. Peron, who studied this question 282 TEXT-BOOK OF MEDICINE from the anatomical and experimental point of view, comes to the same conclusion : '* In tubercular sero-fibrinous pleurisy, which assumes the clinical bearing of acute tuberculosis, the infection is at its minimum ; the reaction of the organism is considerable." Griffon, in collaboration with Bezan9on, has just verified this idea experimentally by measuring the degree of virulence of the pleuritic fluid in several patients under my care. Their researches show that the effusion in frank pleurisy which tuberculizes the guinea-pig, a most sensitive animal, is generally benign in a more resisting animal, such as the rabbit. Only one of my patients had pleuritic fluid of sufiicient virulence to cause experi- mental tuberculosis in an inoculated rabbit. The affection was of long dura- tion, with high fever, and this patient has come back to my wards suffering from pulmonary tuberculosis, which is secondary to the pleurisy. The curability of tubercular pleurisy suggests some reflections. When we speak of cure in tubercular pleurisy, are not our thoughts limited to the pleura ? What will happen later to the lungs after the pleurisy is cured ? Is the patient destined to become tubercular ? This is the whole point of the question. The answer is somewhat difficult. It is said, with good reason, that definite cure without sequelae results when the disease is limited to the pleura and the lung is free. This statement is true, but how can we say that the lung is absolutely free in an individual who is, suffering from primary pleuro-tuberculosis ? Do we not know, as Potain has taught, that acute pleurisy is often accompanied by an inflammatory condition of the lung ? What is the nature of the pleuro-congestion ? A small focus of tuberculosis may exist in the lung without showing any symptom, and yet this latent focus may become the origin of tuberculosis. Rapidly fatal miliary tuberculosis of the lung may appear to be primary, though it is really consecutive (the autopsy shows this) to a small tubercular focus that was insidious in its growth. The same arguments apply to tubercular pleurisy. An individual while in good health is taken ill with acute pleurisy. Cyto-diagnosis shows that the disease is tubercular, and everything points to primary pleuro-tuberculosis ; the most minute examination, according to Grancher's scheme, reveals no lesions in the lung, and yet the apparently primary mischief in the pleura may well be consecutive to a small focus in the lung which has infected the pleura. We have the proof of this in the case quoted above. Landouzy's patient while in good health was seized with apparently primary tubercular pleurisy ; he died suddenly, and the autopsy revealed a small focus in the lung. My two patients who died suddenly had both been ] taken ill with apparently primary pleurisy. At the autopsy we found aj small focus in the lung, which had given rise to infection of the pleura. These cases prove that true primary pleuro-tuberculosis, associated with j no pre-existing lesions in the lung, and secondary pleuro-tuberculosis, setup DISEASES OF THE PLEUEA 283 by a small latent focus in the lung, may both assume the symptoms of so- called frank pleurisy. In many cases it is not possible to distinguish them ; clinically, they may show no differences, and cyto-diagnosis includes them in the same cellular formula. These two varieties of tubercular pleurisy, however, are not comparable as regards prognosis ; one is less grave than the other. In the primary form the lesion in the pleura may recover without producing general infection of the lung, or of the other organs. If the lung is already affected, although the lesion is small, the prognosis is not so good, for we have to cure tuberculosis, both of the pleura and of the lung. The prognosis in acute cases of long duration is evidently uncertain. Treatment. — I would refer the reader to the preceding section ; I have, however, some remarks to add. Acute pleuro -tuberculosis is generally accompanied by much effusion. Perhaps this effusion is a mode of defence ; perhaps the lung which is compressed by the fluid has less tendency to be infected from the pleura. If this hypothesis be true, it would be better not to perform thoracentesis too hastily ; but yet, on the other hand, we know how dangerous it is to allow too much fluid to accumulate in the pleura : sudden death may be the consequence, whatever be the theory employed to explain it. It is therefore necessary to perform thoracentesis in good time. There is another question which is also of importance. In the case of acute tubercular pleurisy the fluid may reform rapidly, even when it appears to have been drained away by thoracentesis. I have found that this rapid and obstinate reproduction of fluid is much less marked in acute infective pleurisies that are not tubercular. I have often in tubercular cases had occasion to draw off 4 or 5 pints of sero-fibrinous fluid by two or three successive punctures. The effusion seemed to cease for the moment, and the patient was considered cured ; but yet the fluid reformed without fever, dyspnoea, or pain, and in a few days amounted to 3 pints or more. The patient must be kept under observation, even if the acute phase appear to be ended ; and we must not forget that fluid may reform rapidly after puncture, and cause sudden death, if we be not forewarned. I have just given my recommendations in the acute phase of pleurisy, but treatment does not stop there. The patient is convalescent, but the tubercular lesion lies hidden, though health is apparently regained. What will happen in this case ? Will it be cured without leaving any scquolno, or may it not rather be the first stage of tubercular infection, which will later attack the lung or the other organs ? We know nothing of this, but we do know that the patient has tuberculosis, and we should place him under the best therapeutic and hygienic conditions. An individual who is convalescent from acute pleurisy should for a long while take care of himself, even though he be considered as cured of active 284 TEXT-BOOK OF MEDICINE disease. Tubercular infection lies in wait for him. Years must pass before he can be considered free from all risk of tuberculosis. Special attention must be paid to hygiene. The patient should avoid all causes of over-fatigue. Nourishment should be substantial and varied ; food and diink which excite the appetite should be chosen. As regards residence, preference should be given to high altitudes, and life should be passed in the open air. All kinds of exercise are permissible, provided they are never carried to excess. As regards tonic and constitutional remedies, cod-liver oil should be given in increasing doses — e.g., 2 to 4 ounces daily — if it is well tolerated ; many patients will swallow a tumblerful of cod-liver oil before meals. In order to render it less disagreeable, it may be cooled by placing the glass in ice. In patients who do not take cod-liver oil well we should recommend fatty foods, such as cream or bread and butter. Oysters, caviare, sardines in oil, tunny fish, smoked fish, and meat should form part of the diet. Raw meat and meat-juice are of benefit in cases of tuberculosis (Richet and Hericourt, Josias and Roux). Injections of cacodylate of soda should also be given. III. HEMORRHAGIC PLEURISY. General Considerations. — For many years while I was occupied with the histological examination of fluid from acute pleurisies, I had seen that my specimens contained some thousands of red corpuscles per cubic millimetre. With 1,500, 2,000, and 3,000 red corpuscles per cubic millimetre the colour of the fluid was not sensibly altered ; the colour only becomes rosy when the fluid contains 5,000 to 6,000 red corpuscles per cubic millimetre. I have called these pleurisies histologically hsemorrhagie, in order to differentiate them from true hsemorrhagic pleurisies, which are quite distinct. Fluid which is very rich in red cells may remain histologically hsemorrhagic without becoming hsemorrhagic in the true sense of the word. In this section I shall leave out hsemorrhage into the pleura from injury, and shall only take count of hsemorrhagic pleurisy from the medical aspect. It is customary to include various morbid conditions under the term " hsemorrhagic pleurisy." Hsemorrhagic effusions into the pleura which are consecutive to tubercular or to cancerous lesions are the most frequent. These effusions are sometimes only symptomatic, and develop as a complica- tion in the course of cancer, or of pleuro-pulmonary tuberculosis ; at other times they attract attention from the first, and appear as the prodromata of hidden tubercular or cancerous lesions. In some cases hsemorrhagic effusions into the pleura appear independent of tuberculosis or cancer ; they seem to be simple hsematomata of the pleura. This simple hsematoma, however, must be extremely rare, and the more I study the question the more DISEASES OF THE PLEURA 285 I believe that the hsematoma is only a benign or curable haemorrhagic tubercular pleurisy. We do not see therefore one, but several kinds of haemorrhagic pleurisy. The fluid is reddish or blackish, and contains fibrin, haematin, red cor- puscles, and dissolved elements ; the composition depends upon the nature of the pleurisy and on the abundance and the age of the fluid. I may say in advance that the haemorrhagic nature of the pleural fluid usually comes as a surprise ; thoracentesis is performed, and the fluid is found to be haemorrhagic. It is practically impossible to afflrm before thoracentesis that pleurisy is haemorrhagic. What are the signs and symptoms which would lead to such a diagnosis ? In the great majority of cases haemorrhagic pleurisy is just like the sero-fibrinous form ; I see no dis- tinctive signs between them : the course may in both cases be acute, sub- acute, or latent. On palpation the same modifications of the vocal fremitus ; on percussion, the same character of the dullness ; on auscultation, the same tubular breathing and aegophony, as well as aphonic pectoriloquy which has been given as a distinctive sign between sero-fibrinous and purulent or haemorrhagic effusions. I have found aphonic pectoriloquy in most of my cases, and it was very clearly marked in a case of haemorrhagic pleurisy described by Jaccoud, and hence I repeat the haemorrhagic nature of the fluid is a surprise. We perform thoracentesis, thinking to draw off sero- fibrinous fluid from the pleura, and we are often astonished to find it haemorrhagic. Under some conditions haemorrhagic pleurisy may simulate empyema ; the general symptoms which lead to this error in diagnosis are due to the tubercular or to the cancerous lesions which have set up pleurisy. The patient is feeble, has an earthy colour, and shows oedema of the lower limbs and of the chest-wall ; thoracentesis is, performed with the idea that pus will result, but here again we are much astonished to withdraw blood-stained fluid. We make this mistake because we are too accustomed to consider ffidema of the che.st-wall as a sign of suppuration ; it is, indeed, a valuable sign, but it is not limited to purulent effusions. It is also met with in haemorrhagic and even in some sero-fibrinous effusions. Htemorrhagic pleurisy may at times be suspected beforehand — e.g., when the trouble develops in a cancerous patient. Whether the cancer be primary or secondary, we may prophesy in such a case that the effusion k perhaps haemorrhagic. I say perhaps, for effusion of cancerous origin is sero-fibrinous in at least one-third of the cases. In short, the diagnosis of the haemorrhagic nature of the fluid rests upon no certain sign ; its existence may be suspected and reservations made as to the qualities of an effusion which shows unusual characters, but it is impossible to affirm the haemorrhagic nature. After these few remarks it will be 286 TEXT-BOOK OF MEDICINE evident that the study of haemorrhagic pleurisies is surrounded by difficulties ; therefore, in order to facilitate the description, I shall divide them into four groups : First Group. — These cases supervene in the course of hepatic cirrhosis and of Bright's disease, or appear as a pleural haemorrhage in the course of scurvy and the eruptive fevers. In this group I shall also place haemor- rhage from the opening of an aortic aneurysm, or from the rupture of an atheromatous aorta. This group, then, contains the most dissimilar varieties. Second Group. — This group comprises the tubercular pleurisies. Three varieties must be distinguished. In the first variety the condition forms part of an acute tuberculosis ; in the second variety pleurisy supervenes in the course of ordinary chronic tuberculosis ; in the third variety haemorrhagic pleurisy appears as the first symptom of tuberculosis : it is the result of local or primary tuberculosis of the pleura. Third Group. — To this category belong cancerous pleurisies, whether the cancer be j)rimary or secondary. Fourth Group. — Simple haematoma of the pleura forms the fourth group. First Group. Description. — The most dissimilar effusions are found in this group. Does cirrhosis of the liver deserve the place assigned to it in the pathogenesis of haemorrhagic pleurisy ? I think not. In Moutard-Martin's remark- able work two cases of haemorrhagic pleurisy are, in my opinion, wrongly con- sidered as dependent on cirrhosis of the liver. One of them is taken from Laennec's famous memoir, in which the lesions of atrophic cirrhosis were first described. A patient with atrophic cirrhosis had also haemorrhagic pleurisy on the left side. Laennec, however, did not say that the pleurisy resulted from the cirrhosis ; I am more inclined to believe that the pleurisy was tubercular in nature, for at the autopsy " the deep layer of the pleura contained innumerable greyish tubercles." The other case which has also been considered as dependent on cirrhosis of the liver may, I think, have been due to independent lesions of the pleura ; for if we look up the details of the autopsy we shall agree that it is difficult to admit atrophic cirrhosis in a liver of " normal size, which showed remarkable friability, and broke up on pressure with the finger into a pulp." I do not deny, of course, the haemorrhagic form of pleurisy in the course of hepatic cirrhosis, for I have seen several cases ; but I think that it is rare as opposed to the sero-fibrinous form, which is fairly common. I also regard haemorrhagic pleurisy associated with Bright's disease as exceptional, though Bright's disease predisposes on the one hand to effusion, and on the other to haemorrhage. DISEASES OF THE PLEURA 287 In pleuro-pulmonary inflammations of infectious origin (influenzal pleuro-pneumonia, typhoid fever), the fluid is sometimes hsemorrhagic. In the hsemorrhagic forms of the eruptive fevers haemorrhagic effusion is sometimes met with, but it is here a case of haemorrhage into the pleura rather than that of an inflammatory condition, properly speaking. Haemorrhagic effusion may also result from opening of an aortic aneurysm, or from the rupture of an atheromatous aorta. Several cases have been published ; the following case is given by Ribail : A man, thirty-five years of age, suffering from palpitation, breathlessness, and angina pectoris, came into the Beaujon Hospital, under Gombault. The diagnosis of aortic aneurysm, with aortic insufficiency, was made. A month later the patient felt a sharp pain on the left side. Pleural effusion was recognized, and punctures gave issue to 12 ounces of bloody fluid on the first, 16 ounces on the second and third occa- sions. The patient died suddenly from angina pectoris. Post mortem, the left pleura was found covered by a clot, which was continuous with the clot in an aortic aneurysm. Second Group. Description. — This group includes haemorrhagic pleurisies of tuber- cular nature. I shall divide them into three varieties. The first variety is associated with acute granular tuberculosis, or with acute tubercular broncho-pneumonia. The lesions in the pleura and in the lung appear together ; the general symptoms are usually very marked : fever is acute, temperature is very high, dyspnoea is severe and continuous, or sometimes paroxysmal. The estimation of the quantity of fluid is very difficult, because the signs of pleurisy are distorted by the subjacent lesions in the lung. The dyspnoea is sometimes so violent and the quantity of fluid appears so large that thoracentesis is performed ; 1 or 2 pints of haemorrhagic fluid are withdrawn, but practically no relief follows, because the dyspnoea, like all the other symptoms, is due rather to the lung trouble than to the effusion. The effusion, however, either from its early appearance or its abundance, sometimes appears to be the chief lesion. The patient experiences some relief after the evacuation of the fluid, and may even ask for a second or a third operation; but the severity of the general symptoms, the elevation of the temperature, the persistent or rapid reappearance of dyspnoea after evacuation of the fluid, the wasting and the signs found on auscultation, prove that the effusion is associated with acute tuberculosis of the lung and pleura. The sputum must be examined for bacilli. The prognosis is nearly always fatal in these forms. In the second variety haemorrhagic pleurisy is associated with tlio ordinary chronic forms of plitliisis, and I am surprised tliat Moutard-Martin has stated that it never coexists with chronic tuberculosis. I have collected several cases which, on the contrary, prove that the chronic as well as the acute forms of tuberculosis may cause haemorrhagic pleurisy. 288 TEXT-BOOK OF MEDICINE The pathogenic diagnosis is very simple. The patient presents both the symptoms of pulmonary tuberculosis and of pleurisy. Fever, pain, and dyspncBa may be absent ; the mischief may end after one or more punctures, because it has been only an incident in the course of the tuberculosis, just as sero-fibrmous pleurisy may be. In the third variety — and I draw special attention to this point — pleurisy appears as the initial symptom of tuberculosis. It is the result of primary tuberculosis of the pleura. Tuberculosis may commence in the pleura, just as it may in the synovial membrane, testis, prostate, eye, skin, pericardium, etc. ; remain localized for a lengthy period, and recover without becoming general. As we have seen in the section on sero-fibrinous pleurisy, it often happens that pleurisy is met with m an individual who recovers, but shows signs of pulmonary tuberculosis some months or years later. In this case pleurisy, though simple in appearance, was only the result of tuberculosis, which showed itself by effusion, and then became generalized throughout the Imig. Hsemorrhagic pleurisy, therefore, may result from local or from initial tuberculosis of the pleura ; and just as persons have haemoptysis long before other signs of tuberculosis, so others have hsemorrhagic pleurisy as the first symptom, and, if I may use the expression, these people " reject their hsemoptysis into their pleura." These cases may present all the signs of sero-fibrinous pleurisy, and the haemorrhagic nature of the fluid is only recognized on puncture ; thoracentesis is performed once, twice, three, or four times, the fluid is drawn off, the pleurisy cured, and the case thought to be one of simple hsematoma of the pleura ; but yet signs of pulmonary tuberculosis appear a few months later, and show the error in diagnosis. These considerations show that the pathogenic diagnosis of this variety may be fairly easy or very difficult. It is easy if the patient has signs of acute or of chronic pulmonary tuberculosis ; if the pleurisy arises during apparently good health, the diagnosis cannot be settled either by the quality or by the quantity of the fluid, or by the course of the pleurisy, which may be acute, subacute, or latent. In such a case the various methods of labora- tory research given above must be employed. In a patient under my care for diabetes and haemorrhagic pleurisy, the lymphocytosis demonstrated the tubercular nature of the pleurisy. This form of pleurisy, when accompanied by fever, becomes much more serious, and the gravity arises from the lesions in the lung. Nevertheless, the condition may recover perfectly after one or several punctures. Ii have pubhshed cases, and Lereboullet has quoted others. The patient is] sometimes definitely cured, in which case it is probable that the haemorrhagicj pleurisy was the result of local tuberculosis of the pleura ; at other times DISEASES OF THE PLEURA 289 the patient, after recovering from pleurisy, subsequently develops tuber- culosis in the lung. Pathological Anatomy. — The lesions show some peculiarities. Some- times the lesion is found at the same time in the lung, in the pleura, beneath the pleura, or in the false membranes ; at other times it is limited to the pleura or the false membranes. The walls of the vessels show coagulation necrosis, and Kelsch thinks that the haemorrhage is due to this change. Numerous vessels are obstructed by hyaline thrombi ; the vessel walls are no longer distinct, and are surrounded by fibroid networks. The newly-formed membranes are generally stratified and rich in vessels, friable if yomig, thick and firm if old. These membranes are composed of granulation tissue, and of deeper layers that are made up of lymphatic cells, connective bundles, and fibrous tissue (Malassez). Third Group. Description. — Pleurisy in the course of pleuro-pulmonary cancer is not always hsemorrhagic ; the fluid is sero-fibrinous in at least one-tliird of the cases, and this fact must carefully be borne in mind, for it would be wrong to reject the hypothesis of cancer because the effusion was sero- fibrinous. The haemorrhagic form alone, however, must now occupy our attention. Haemorrhagic pleurisy in cancer may arise quite suddenly, like acute pleurisy, or have an insidious onset, so that the patient finds some difficulty in fixing the date. These different varieties are found, moreover, in sero-fibrinous, haemorrhagic, purulent, tubercular, or cancerous pleurisy. From the clinical point of view I shall divide haemorrhagic pleurisy in cancer into two varieties. In the first variety, pleurisy appears in an individual who has obvious cancer. We find in one patient cancer of the stomach, oesophagus, intes- tines, rectum, omentum, liver, kidney, bladder, prostate, testis, eye, skin, or of one of the vertebrae ; in another patient we see cancer of the uterus or of the breast. Cough, thoracic pain, continuous or paroxysmal dyspnoea and currant- jelly expectoration, appear during the course of these cancers. Pleural effusion is then discovered, and thoracentesis gives vent to haemor- rhagic fluid. In such a case the pathogenic diagnosis is clear — viz., secondary cancer of the lung and of the pleura ; and it may be stated that the hajmor- rliagic pleurisy is of cancerous origin. In some cases we do not witness the evolution of tlie cancerous lesions, but the patient shows traces of a more or less recent scar, resulting from an operation for epithelioma of the nose or of tlie lip, for cancer of the breast or of the testis, or for osteo-sarcoma. Pleurisy then aj)pears and thora- centesis yields haemorrhagic fluid. The lung and the pleura have evidently been attacked by secondary cancer. 19 290 TEXT-BOOK OF MEDICINE . The pathogenic diagnosis, however, is not always so simple. In the cases wliich constitute the second variety, hsemorrhagic pleurisy is not preceded by otherwise appreciable cancerous lesions. Primary cancer may afEect the pleura and only give rise to symptoms of pleurisy, which may be acute or insidious in its onset. The pathogenic diagnosis is sometimes difficult. If hemorrhagic pleurisy, consecutive to mediastino-pulmonary cancer, were always accompanied by special symptoms, such as dysphagia, aphonia, oedema of the arm or of the face, and well-marked collateral circulation, which are so common in tumours of the mediastinum, and if the patient suffering from pleurisy showed supraclavicular glands, currant- jelly expectoration, and violent attacks of dyspnoea, which are seen in cancer of the lung, the patho- genic diagnosis of the pleurisy would be signally simphfied ; there are cases in which nothing leads us to suppose the existence of cancer of the mediastinum or of the lung. There are also cases in which cancer of the pleura is primary, or associated with early cancer of the lung, which may pass unnoticed ; the pleural effusion is then the chief feature, and we find hsemorrhagic pleurisy which presents much difficulty as to its origin. The following signs and symptoms helped me to make a diagnosis in a case of hemorrhagic pleurisy, consecutive to primary cancer of the lung, in a man twenty-two years old : Pain constitutes an important symptom; it is frequent, sometimes sharp, persistent, unhke the " stitch in the side " of common pleurisy. It may be worse at the base of the thorax, and radiate to the shoulder, the arms, and the wrists, so that patients beheve themselves to be suffering from rheumatism. Acuteness and radiation of the pain are fairly frequent symptoms in pleuro-pulmonary cancer. Neuralgia of the brachial plexus was the cliief symptom in one of Behier's cases. One of Lancereaux's patients complained of " a sharp pain in the left side of the neck, and in the shoulder on the same side," and later swelhng of the joints of the left arm supervened. In several of my cases I have noted pains in the joints, so that I have asked myself whether pseudo-rheumatism may not be one of the manifestations of cancer. These pains are not found in hemorrhagic tubercular pleurisy. Dyspnoea is one of the usual symptoms of cancerous pleurisy. It may be continual or paroxysmal, and is relieved by thoracentesis, but the relief is only of short duration. This dyspnoea is found in most of the cases of cancerous pleurisy, and I have seen it cause terrible agony on three occa- sions ; it depends chiefly upon the cancerous lesions in the mediastinum and the lung. Similar dyspnoea is not found in chronic tubercular hsemorj rhagic pleurisy. Some cases of hemorrhagic pleurisy, associated witr acute tuberculosis of the lung and of the pleura, may be accompanied bj DISEASES OF THE PLEURA 291 acute dyspnoea ; in these cases, however, the fever is liigh ; this does not happen in cancerous pleurisy. Permanent displacement of the heart is seen in left cancerous pleurisy, at first on account of the fluid, and later because the growth in the pleura and the lung may help to cause deviation. Further, the heart sounds are heard all over the chest, as though they were transmitted to the ear by soUd lung, which is a good conductor of sound. Acceleration of the pulse has often been observed, and the pulse-rate may be 100 or 120, although fever is absent. It may be asked whether this acceleration is not due to the pressure of the growth on the pnsumo- gastnc nerve. In one of my patients who had continuous tachycardia I found a cancerous nodule of the size of a hemp-seed in the interventricular septum of the heart. The nature of the fluid drawn off by thoracentesis may furnish evidence in favour of cancer. The fluid is often brownish or blackish, blood forming a tenth or a twelfth part. The fluid contains very httle fibrin, in contra- distinction to the effusion in tubercular pleurisy, which usually contains a large amount. In some cases (Fraenkel, Quincke) agglomerated or isolated polymorphous epithehal cells, with a large nucleus and vacuoles, have been found in the fluid. Nattan-Larrier has studied the cases of cancerous pleurisy in my wards, and has worked out their cytological formula. In addition to red corpuscles, two different types of cells may be met with : (1) Masses of cells which are large, thick, and have polycyclical outHnes ; masses of cells, disposed in layers, of variable size and indefinite outlines, protoplasm refracting and vacuolated ; irregular nuclei, which stain unequally. (2) Isolated cancer cells, which are easily recognized by their inequality in size, by the fact that they are larger than the leucocytes or the endothehal cells, by their ovoid or irregular shape, by their clear outUne, by their refracting protoplasm, which is studded with basophile granules and clear vacuoles, and by their multiple nuclei, which are irregularly placed and stain imequally. I have noticed the existence of polynuclear cells in cancerous pleurisy with much effusion. Eosinophile polynuclear cells are never met with in the fluid from these cases of hsemorrhagic pleurisy. Bard has laid stress on the characters of the serum after centrifugaliza- tion. The serum is said to remain coloured with hajmoglobin in cancerous pleurisy, while it is colourless in other hajmorrhagic affusions. This hajmo- lytic action, which is easily recognized with the naked eye, is made certain by the addition of tincture of guaiacum and turpentine (blue coloration of the laky serum by this reaction). These findings have been confirmed by all authorities. In some cases the pleuritic fluid is composed of nearly pure bloud. " 19-2 292 TEXT-BOOK OF MEDICINE Thoracentesis is performed, and fluid which has the aspect of arterial or of venous blood is drawn off. In one of my patients puncture gave exit to a fluid having the appearance of arterial blood, and caused me at first sight to think that it might be a case of intrapleural hgematoma, due to rupture of an atheromatous or a dilated aorta. Lymphosarcoma, colloid cancer, epithelioma, and endothelial carcinoma, may cause such intrapleural haemorrhages. The blood does not clot, but remains fluid. The rapid and persistent reproduction of haemorrhagic fluid after thoracentesis is common to tuberculosis and to cancer ; it is, however, much more marked in the case of cancer. Thus, in one of my cases thoracentesis was performed thirty-three times in five months, and 44 pints of haemor- rhagic fluid withdrawn. In one of Desnos' cases thoracentesis was per- formed thirty times in six months, in a woman with cancer of the pleura, and 80 pints of haemorrhagic fluid were withdrawn. I have, however, seen cases in which the fluid of pleuro-pulmonary cancer may dry up after a few punctures ; and, on the other hand, I have seen cases of tubercular haemor- rhagic pleurisy in which the fluid formed with such obstinacy that six, ten, and fifteen punctures were necessary. It would, therefore, be wrong to base an absolute opinion upon the drying up, or upon the obstinacy of the haemorrhagic fluid, in order to banish the idea of cancer. The youth of the patient is no argument agaujst the hypothesis of can- cerous pleurisy, for this lesion has been found in patients who were only eighteen years, twenty-four years, twenty-three years, twenty-two years, and ten years of age respectively. One of my patients was only twenty- two years of age. Fourth Group. Description.— Under the term " pleural haematoma " we must include cases of haemorrhagic pleurisy, which are not due to tuberculosis or to cancer. The anatomical process is in some points comparable to chronic hydrocele and to pachymeningitis ; the condition is a haemorrhagic pachy- pleuritis. In some cases the haematoma, according to Wintrich, is said to be genuine pleurisy, in which the intensity of the initial inflammation determines haemorrhage into the pleura. A typical case of simple haematoma may be thus described : A patient has haemorrhagic pleurisy. The symptoms sometimes resemble those of simple pleurisy, but at other times the appear- ance of the patient and the general symptoms may lead us to fear tuber- culosis or cancer of the jjleura. Thoracentesis is performed, and haemorrhagic fluid drawn off. In simple haematoma the liquid is fibrinous, and the ten dency to reaccumulation is shght. The condition sometimes yields to a single puncture, and we are rarely obUged to aspirate more than two or three DISEASES OF THE PLEURA 293 times. The relief is notable, and the general condition shows progressive improvement. The diagnosis of simple haematoma must not be hastily made, even though the conditions have yielded to thoracentesis. In some cases, as I have already said, hsemorrhagic pleurisy is the only indication of local or primary tuberculosis of the pleura. Hsemorrhagic pleurisy may recover after thoracentesis, when a favourable prognosis holds good ; on the other hand, a pleural hematoma is thought to have been cured, and the error is recognized some months later, when undoubted signs of tuberculosis appear. The more I see, the more I believe in the rarity of pleural haematoma ; the condition is nearly always tubercular. In my wards at the Necker Hospital I had a patient with every sign of pleural hsematoma. The fluid, which dried up after a single puncture, did not cause inoculation tuber- culosis in guinea-pigs. The patient, who had never had any sign of pulmonary tuberculosis, left the hospital in good health. If I had lost sight of him, I should have thought that it was a case of simple haematoma, but he came back to me a year later with pulmonary tuberculosis. The ao-called pleural haematoma was therefore haemorrhagic tul^ercular pleurisy. Treatment of Haemorrhagic Pleurisies. The treatment is very simple. Revulsives, bhsters, and other medical means, such as diuretics and purgatives, etc., give here no more benefit than they do in sero-fibrinous pleurisy. What line of treatment must be adopted in a case of haemorrhagic pleurisy ? One treatment alone is rational — viz., aspiration of the fluid. Pleurotomy, customary in empyema, should not be employed in these cases. The rules for aspiration laid down under simple pleurisy are in every way applicable to haemorrhagic effusions. The pleura is punctured with a No. 2 or No. 3 needle, care being taken never to withdraw more than 2 pints of fluid at one sitting. In this way we can avoid fits of coughing, attacks of dyspnoea, intrathoracic pain, and other much more serious troubles which sf)metinies ac(;ompa?iy thoracentesis when too large a quantity of fluid has wrongly been withdrawn at one sitting. As I have discussed the important question of thoracentesis fully, further notice is needless. The evacuation of 2 pints of fluid at a sitting, which represents the maximum amount in simple pleurisy, is usually too high in the haoniorrhagic variety. After evacuation of 20 to 30 ounces, the patient often experiences dragging pains, and I have been several times obliged to stop the flow after 10 or 15 ounces. The patient rarely experiences the marked relief which follows the evacuation of the fluid in simple pleurisy. This fact depends much on the condition of the pleura and of the lung, as well as of their respective lesions. 294 TEXT-BOOK OF MEDICINE I have always seen that the relief is more marked in cases of tuberculosis than of cancer. When the fluid reaccumulates rapidly, we are obliged to perform thora- centesis repeatedly, and the patient finally clamours for it, because the operation gives momentary relief to his distress. I recently treated a lady who had been sent to me from Lisbon. She begged me to perform thoracentesis every four or five days. I succeeded in lessening her terrible dyspnoea by means of repeated punctures and injections of morphia. Thoracentesis is only to be performed when there is necessity, and only the surplus in the pleura should be drawn off. As the fluid is sometimes very rich in blood cells, thoracentesis is a form of bleeding, and repeated punctures cause weakness. In certain cases of hsemorrhagic pleurisy the fluid yields after one, two, or three punctures ; this happens in simple haematoma of the pleura, and in some cases of tubercular pleurisy. In cancerous pleurisy the fluid is repro- duced with more obstinacy. In some malignant cases, however, we succeed in drying up the fluid. All hsemorrhagic pleurisies may, then, be curable. The tuberculosis is but little curable, the cancer is incurable. Under some circumstances the fluid which contained much blood at the first puncture contains less in the following ones ; it loses its tint and becomes serous. These changes are seen both in tuberculosis and in cancer, as I have reported. These very important facts show us that it would be wrong to take the drying up or the decoloration of a hsemorrhagic fluid as the basis of a favourable or of an unfavourable prognosis as to the cause of the haemorrhage. The evolution of hsemorrhagic fluids in the pleura gives us imperfect information as to the cause and the nature of the lesion which produces the haemorrhage. Hsemorrhagic pleurisies only become purulent (a change which is very rare) if organisms of suppuration produce secondary infection. In the contrary case, whatever be the number of the punctures, the fluid does not become purulent, either in simple hsematoma or in tubercular and cancerous pleurisy. I have performed more than thirty punctures on the same patient, but the hsemorrhagic fluid did not become purulent. Thoracentesis is the only means available in cancerous pleurisy. The dyspnoea is commonly so acute that we are obUged to give several injections of morphia daily. The commonplace treatment by tonics and constitutional remedies, such as arsenic, lecithin, and preparations of coca and kola remains. DISEASES OF THE PLEURA 295 IV. TRAUMATIC HiEMOTHORAX. Traumatic haemothorax demands the physician's attention, and therefore deserves notice in a text-book of medicine.* Resume of a Case. — On September 24, 1906, man, aged twenty-two, admitted to the Hotel -Dieu, under De Deuke, for a stab in the back. Pain in chest and dyspnoea were severe two days later ; he was therefore transferred to my care. The woimd, which had healed over, was in the fifth left intercostal space, about an inch from the spine. Inspection showed slight bulging, ynth absence of vibrations, and dullness at the left base. Traube's space was resonant. Soft tubular breathing on expiration, aegophony, and pectoriloquy pointed to pleural effusion. No signs of pneumothorax. Heart not displaced ; cough frequent ; dyspnoea somewhat marked ; temperature 103° F. (this fact attracted my notice). No haemoptysis ; no blood-stained sputum. Diagnosis : traumatic hasmothorax. Exploration in order to examine the fluid, and also to see if the pleura were infected . 20 c.c. of fluid, almost as red as pure blood, withdra^Ti. During the first week in October the only change was an increase in the amount of effusion, and during the next week it was clearly abundant. The dullness now extended higher, vocal fremitus was absent over the lower two-thirds of the chest, and the heart was displaced to the right. The increase in the effusion was not due to blood, but resulted from serofibrinous pleurisy, as proved by punctures. On October 18 the fluid had lost its former red tint. Friction sounds above the effusion proved pleurisy following hfemothorax. On November 1 the fluid had partially absorbed ; friction sounds wore present in the axillary region. The fluid, on puncture, was pale yellow and fibrinous. Patient's appetite was good, his general condition excellent, and he left for Vinconnes on November 11. He came back a week later for slight dyspnoea. There was a good deal of fluid, and on puncture 200 c.c. of sero-fibrinous liquid were drawn off. A fortnight later he went out well. The nature of the fluid withdrawn at the different punctures was determined in my laboratory. As aerobic and anaerobic cultures on solid and fluid media showed tho absolute sterility of the Hquid, the fever clearly did not depend on infection of the pleura. At the first puncture (September 27) the fluid, which was almost blood-red, contained 2,100,000 red and 4,000 white corpuscles. The fluid was put in a tube ; twenty-four hours later we found a red sediment, containing blood cells, and amounting to a fifth of the contents of the tube. The supernatant fluid was not laky, but pale yellow ; it was not fibrinous, and showed no trace of coagulation. No clot had formed in this tube on December 10. We were surprised that tho sediment formed one-fifth and tho serum four-fifths. Did this excess of serum come from clots in the pleura ? If this were so, some of the blood effused must have clotttid. Puncture, October 18 : the fluid was quite different. It was no longer red, and its rosy tint showed how quickly the red cells had been absorbed. The proportion of red to white cells was only 35,000 to 0,200. Eosinophiles Lymphocytes Macrophages Colls from tho pleura Nucleated red corpuscles : 1 or 2< Per Cout. . 35 . 35 , 20 , 10 * TiiewMoy, Clinique Medicale de V Hotel-Dieu, llUKi. I !">« et 12"'" l<'(M)n. 296 TEXT-BOOK OF MEDICINE The deposit, on standing, was not red, but of a rose colour, and its amount about one-thirtieth of the total contents. Flakes of fibrin were floating in the yellow fluid. On November 11 the fluid resembled that of an ordinary pleurisy, and contained 13,000 red to 8,500 white corpuscles. It was practically a " histologically hsemor- rhagic " pleurisy. No deposit appeared on standing ; a thin layer of sediment, with a rosy tint, appeared only after centrifugalization.- The fluid was sero -fibrinous, and clotted in the tube. Blood-counts showed : Red Corpuscles. White Corpuscles. November 1 .. .. 3,200,000 .. 5,000 November 11 .. .. 3,840,000 .. 4,400 November 22 .. .. 4,200,000 .. 6,000 The eosinophiles amounted to 10 per cent. Pathological Physiology. — Does the blood effused in hsemothorax remain fluid, or does it form clots ? Trousseau and Leblanc, from experi- ments on the horse, have shown that clotting occurs if blood be allowed to flow into the pleura after section of an intercostal artery. Trousseau hence concluded that similar coagulation might take place in haemothorax in man. This view has recently been opposed by Tuffier and MiUan, who state " the bloody effusion in the pleura does not clot in cases of traumatic hsemothorax." We can decide the point by consulting the pubUshed cases of traumatic haemothorax (C. de Gery). Case 1. — Very severe haemothorax on the left side. - Six pints of bright blood drawn off. Later, 4 pints of blood, " mixed with clots, which at times stopped the flow," drawn off by thoracentesis. Case 2. — Young woman wounded by a revolver bullet. Hsemothorax formed quickly ; repeated haemoptysis occurred ; weakness was extreme, and syncope im- minent. Two inches of the eleventh rib resected. Blood gushed out, and blackish clots, as large as oranges, were expelled on expiration. Cases 3 and 4. — Haemothorax, Resection of ribs ; fluid blood and clots removed. These quotations prove that Trousseau was right. The blood may clot in the pleura, just as it does in the peritoneum, the pericardium, the meninges, and the joints. This fact has an important practical apphcation ; the clot may plug the wound in the lung. The results of Trousseau's experiments may be stated as follows : Haemothorax was produced by making a penetrating wound of the lung in a horse. The animal was killed, and the wound in the lung examined. " A clot of fibrin filled up the wound in the lung like a sword in its scabbard." This protecting clot sometimes formed half an hour after the injury, and on attempting to draw the clot out it was necessary to break it, because it was embedded in the interlobular cellular tissue by numberless fibrinous radicles^ which broke on traction. If the post-mortem was not performed till forty-eight or seventy- two hours after the injury, the wound was closed by a remarkable process. DISEASES OF THE PLEURA 297 The woimd in the hmg was inflamed, and the pleura itself was also affected to a variable extent. A plastic exudate was adherent to the serous membrane, and blended with the fibrinous nucleus of the wound, intimately- adhering to it. The whole track of the injury was thus obhterated by fibrinous clot, and the edges were covered by a fibrinous disc, adherent to the pleura, to the lips of the wound, and to the plug of clot. The effusion of blood, therefore, in traumatic hgemothorax may form clots in the pleural cavity ; yet, strange to say, the same blood, when drawn of? and placed in a test-glass, does not clot, or at least coagulation is imperfect or delayed. The study of cases clears up this point. In my own case, the bloody fluid did not coagulate in the tube, which was kept in the laboratory for two months. In Sacquepee's case the fluid from the pleura was set aside, and behaved like de- fibrinated blood ; it did not clot, although it was kept for two months. Patel and Leriche ptmctured the pleura four days after a wound, and drew off 7 ounces of blood. The fluid had not clotted by night. In a case published by Gaultier and Fran^ais puncture was performed on the tw(mty- first day. Three pints of bloody fluid were drawn off. The fluid did not begin to clot till six hours later, and the clot did not retract till twelve hours later, while fresh blood from the patient's finger clotted normally at the end of half an hour. Milian quotes a case in which the fluid was drawn off sixteen days after the injury. It clotted at the end of an hour, and the retraction of the clot expressed yellowish senjm. These examples prove that we have not yet exact knowledge as to the properties of the fluid in heemothorax. As a rule, the fluid does not clot, though it may do so, and in the latter event coagulation is delayed. The blood in haemothorax remains aUve, haematolysis does not occur, and the serum does not become laky, but remains of a straw colour. All authori- ties agree upon this point, as the following examples prove : In my case, hsematolysis was quite absent, the red corpuscles were intact, and the exuded serum kept its yellow tint for six weeks. In Tufiier and Milian's case " it was not possible to find blood cells in process of mortification. The red corpuscles and the leucocytes preserved their normal shape and their usual reactions ; they took stains perfectly, and, in fact, remained alive. The serum exuded in vitro after retraction of tlie clot was yellowish, and did not show the least tinge of red. This fact shows that hiematolysis did not occur in the effusion, and that the intact red corpuscles wore d<^stin(;d to be absorlx^d." In Sacquepee's case " the serous fluid above the red sedi- ment had a vfiry marked ycillow colour ; it showed no colouring due to hyemoglobin, and Wius not laky ; \\w same characters obtained in all the samph^s taken." The, ])()int is therefore decided, and we may state that hcematolysis does not occur in traumatic haemothorax. C'ytological oxamiiKiiioii of tlu^ blood gives intor(^stiii<^' information. When I gav(^ the cellular forimila in my case, I mentioned that llie cftsino- philes were as high as 35 per cent. The eosinophiles in the hlood weri^ 10 per eont., while normal blood only shows 2 to 4 per cent. 298 TEXT-BOOK OF MEDICINE Other cases show this enormous predominance of the eosinophiles. In Sacquepee's counts they amounted to 33 per cent. I do not wish here to discuss eosinophilia in hsemorrhagic pleurisies, and in traumatic hsemothorax. Burnet thus writes on pleural eosinopliilia : " The affinities for stains between the eosinophiles and the red blood- corpuscles would lead us to suppose that the eosinophile is a polynuclear cell charged with red corpuscles. Klein describes a case of hsemorrhagic pleurisy, with marked eosinophiha in the exudate and in the blood. He holds that the eosinopliiles are not leucocytes normally charged with haemoglobin, but phagocytes which have ingested degenerated red corpuscles." Widal and Faure-BeauUeu arrive at the following conclusions upon pleural eosinophilia : " Our cytological findings lend support to Dominici's idea that the eosinophiles may be of lymphatic origin. We conclude from our researches that the pleural eosinophilia takes place in situ, and that the blood eosinopliilia results from the migration of cells which have their origin in the morbid focus." However this may be, it is certain that my patient had 35 per cent, of eosinopliiles in the effusion, and 10 per cent, in his blood. The absorption of the red corpuscles may be very rapid in hsemothorax. The colour may change from red to rose in a week or a fortnight. The number in my patient fell from 2,100,000 to 35,000 in three weeks. In Tuffier and Milian's case the red corpuscles fell from 390,000 to 22,500 in sixteen days. " As we know by blood-counts that the number of corpuscles diminishes daily in the effusion, and as, on the other hand, we know that these red corpuscles are not destroyed, they can only be absorbed." The method of this rapid absorption of the red corpuscles in hsemothorax has been repeatedly discussed. We can eHminate hsematolysis because the red corpuscles remain intact, and do not lose their haemoglobin, as the yellow tint of the serum proves. How, then, do they disappear ? Do the eosino- philes absorb the red corpuscles ? " It is probable that the polynuclear and mononuclear cells destroy the red corpuscles, and carry away the debris. On the other hand, the endothehal cells do not remain inactive ; we often find perfectly intact corpuscles in their protoplasm, while others are swollen, pale, and surrounded by a vacuole. A certain number disappear, therefore, by intracellular digestion. These two modes, however, do not appear sufficient to produce such a rapid effect. Other unknown causes doubtless play some part " (Sacquepee). It is strange that the number of white cells increases, while the number of red corpuscles rapidly diminishes. In my patient the white cells rose from 4,000 to 8,500. The polynuclears first disappear ; the lymphocytes are found in the fluid for a Ions while. I DISEASES OF THE PLEURA 299 Symptoms. — We may now commence our clinical study of traumatic hsemothorax. Gross injuries of the chest, the heart, and the great vessels demand surgical treatment, and are therefore foreign to our subject, which embraces only those forms of haemothorax that are amenable to medical science. We shall here consider the course of haemothorax apart from complica- tions, wliich will be dealt with later. A patient has been wounded in the chest. The injury may involve all the layers of the chest-wall, or may not be visible externally (fracture of ribs) ; the bleeding may come from some vessel in the wall or from a wound of the lung, but yet in each case the blood very readily finds its way into the pleura, and forms a haemothorax. The initial symptoms vary somewhat with the nature of the wound and with the amount of bleeding. The injured man may become pale, complain of pain and distress, and lose consciousness. The injury, however, may be almost unnoticed, and the only sign may at first sight be the external bleeding. The wound of the lung may show itself by early haemoptysis. In some instances the patient brings up blood-stained sputum, but in others we find frothy bright red blood, which is coughed up at intervals. One of my patients, with a bullet wound, had a severe attack of haemoptysis, which was followed by slighter attacks. In Sacquepee's case the haemoptysis lasted for several days. The case reported by Connelsville is exceptional : the patient died from haemoptysis in a few minutes, and it was found post mortem that a fragment of rib had pierced the lung. It would be reasonable to suppose that a wound of the lung would always be followed, if not by abundant haemoptysis, at least by blood-stained sputum. Our supposition does not hold good ; slight or profuse haemoptysis is far from being frequent. My patient who was stabbed in the chest did not bring up any blood. Haemoptysis was noted only eight or ten times in forty- four cases of traumatic haemothorax collected by de Gery. It is true that haemothorax is not always associated with a wound of the lung ; the blood in the pleura may come solely from the chest- wall, in which case the absence of haemoptysis is readily explained. When blood invades the pleural cavity, dullness, absence of vocal fremitus^ tubular breathing, and perhaps aegophony enable us to determine the presence and tlie amount of tlie effusion. Cough, dyspnoea, weakness, and Itallor vary with the severity of the case. Haemothorax may not be accompanied by fever, but in some rases, from the third to the fifteenth day, the temperature rises to 10.3° or 101° F., and remains high for some time. We may then ask whether the pleura has not been infected by the foreign body. The fever leads us to fear pneumonia or 300 TEXT-BOOK OF MEDICINE empyema, and we are the more anxious in that the injured man has more pain and more distress while the fluid in the pleura increases. Such an attack naturally awakens our attention, but fortunately it does not, as a rule, indicate any serious complication. When my patient had a temperature of 103° F. four days after the injury, we were not greatly sur- prised ; cultures of the fluid remained quite sterile, and we therefore con- cluded that the attack of fever indicated absorption of the blood and the onset of secondary pleurisy. We know that fever may last some time in cases of hsemothorax, quite apart from infection, and we now admit that absorption of the red corpuscles gives rise to fever, and to effusion of serous fluid in the pleura. The same condition obtains in subarachnoid haemorrhage, when blood passes into the ventricles of the brain and into the subarachnoid space of the spinal cord. The blood, as Prus says, may have a very irritant action upon the parts with which it comes in contact. " The recognition of Kernig's sign and the haematolytic reactions in subarachnoid haemorrhage show that the extravasated red corpuscles undoubtedly cause inflammatory changes." Further, whatever truth there may be in these hypotheses, it is certain that fever in haemothorax may coincide with absorption of the red corpuscles, with the gradual decoloration of the haemorrhagic effusion, with the appear- ance of serous fluid, and with the subsequent discavery of pleural friction sounds. The following cases prove this point : In my patient the temperature was 105° F. on admission, and the attack was of short duration. We found soon after an increase in the pleural fluid, which coincided with the rapid decoloration of the original effusion, the fibrinous condition of the newly-formed fluid, the marked diminution in the number of red corpuscles, and the appearance of friction sounds. In Sacquepee's case the fluid is said to have remained stationary for some time, although the number of red corpuscles diminished. " We must conclude that a large amount of serous fluid passed into the pleura, and thus compensated for the absorption of the solid part." In Tuffier and Mihan's case the patient had fever, the serous effusion increased in amount, and the specimens showed progressive diminution in the red corpuscles. Friction sounds were heard later in the axilla. Secondary pleurisy may appear early or late, but it is impossible to fix the exact moment of its onset, for the same signs (dullness, absence of fremitus, tubular breathing, aegophony) are common both to serous effusion and to haemothorax. Unless we are on our guard, we may wrongly suppose that more blood is being poured out into the pleura, when a serous effusion is really being formed. In order to gain information as to the relative importance of the bloody and of the serous effusion, we may take samples of the fluid, which DISEASES OF THE PLEURA 301 are placed in small tubes. On comparison of the samples, the presence of pleurisy is shown by the rapid attenuation of the red tint of the lowest layer, which coincides with the diminution in the number of red corpuscles, and by the appearance of fibrin in the serous layer. Friction sounds later make the diagnosis certain. We may fear that the fever is due to infection of the lung, or to com- mencing empyema ; we have, however, a simple means of deciding this point : " Make cultures of the fluid. If you find them sterile, you can eUminate any idea of infection." Complications. — I have first sketched the course of an uncomplicated case of traumatic hsemothorax. The prognosis is nearly always good, and recovery results in a few weeks, without the need for surgical intervention. Let us now pass on to the complications of haemothorax, and first consider the condition known as " hsemopneumothorax." Air may enter the pleural cavity either through a woimd of the chest- wall or of the lung. This double channel of entrance might lead us to suppose that pneumothorax would be a frequent comphcation of chest wounds. I am of opinion, however, that tliis complication is somewhat rare. It was not seen in the cases quoted above, and was found in only twelve out of forty-four cases collected by De Gery. It may perchance pass unnoticed, because we can only make a summary examination in a patient who is fainting from loss of blood. The presence of pneumothorax makes the situation worse : distress, suffocation, weakness of the pulse, and lipothymia are more marked when this complication is present. Consideration for the patient does not always allow us to make a complete examination, and we cannot try for a succussion splash ; yet the tympanitic note on Ught percussion over the upper part of the chest is usually sufficient, especially if amphoric breathing is also present. In some cases we may hear the air entering and leaving the chest at each respiration. Let us now consider suppurating haemothorax. In some patients the pleura is infected, and the fluid becomes purulent, as in the following examples : Haemothorax occurred on the right side from a bullet-wound (Grecnleaf). A little blood wa.s drawn oflf by thoracentesis. Empyema supervened ; P^stlander's opera- tion was performed, and the patient linally recovered. Case. rejHjrtcd by dhrisUnitch. — A boy was shot at close range with a revolver. He wius kept quiet for three, days. On the fourth day effusion, fever, and dyspnoea. On the sixth day ho nearly died from suffocation. Foul-smelling bloody Huid was with- drawn on jjuncture in the seventh space. Resection of the fifth and sixth ribs. On incision of the pleura and the lung much pus and blood came out, thd the empty focus. During the next few days pus was repeatedly brought up in large quantities. The fa-tor of the breath and of the s()utum continued, the dyspncea was very acute, the general condition became grave, and the patient died after an illness of nearly three months. A caN-ity was found between the middle and lower lobes on the right side. Tho fluid in it was horribly foetid. The walls of this interpleural cyst were irregular, soft, and covered with putrefying debris with a gangrenous odour. A blackish slough wa-s present. Multiple sections of the lung tissue around the cavity showed very marked fibrosis. There was no trace of tuberculosis. 334 TEXT-BOOK OF MEDICINE Case 2.— A woman, aged sixty-three, had been taken ill a month before with pain in the right side and shivering fits. Acute dyspnoea, cough, and abundant diarrhoea, accompanied the onset of the disease. As the situation did not improve in spite of treatment, she was admitted under Chauffard. She had extreme dyspnoea, ^the respirations were forty-five a minute, and the evening temperature was over 103° F. Examination of the thorax showed behind, on the right side, slight dullness over the lower two -thirds, abolition of the vesicular murmur, and. faint tubular breathing on expiration. These signs somewhat simulated those of pleural effusion, and yet punctures in different intercostal spaces gave no result. The diagnosis of pleurisy was, therefore, abandoned, and spleno -pneumonia was thought of. Some days later cavernous, breathmg was heard over the middle of the right lung ; mterlobar pleurisy was suspected, and aspiratory puncture gave exit to 3 ounces of foul sanious pus. Bacteriological examination of the pus revealed micrococci, streptococci, and rods. Some days later foul-smelling pus was brought up. The tubular breathing, recognized at the level of the interlobar space, took an amphoric timbre. Antiseptics were injected into the focus. The infection contmued its ravages, and the patient died in about two months. At the autopsy a gangrenous pocket was found in the interlobar fissure. This primary lesion was accompanied by secondary foci of suppurative broncho -pneumonia in the lower lobe of the lung. In these two cases immediate operation would probably have warded off these complications. In another list of complications I place those of long duration which supervene long after the interlobar vomica. In some patients the improve- ment which follows the vomica is neither genuine nor lasting ; we try several methods of treatment, and, fearing operation, we temporize. The patient continues to cough and to spit ; the interlobar cavity goes on secreting and does not fill up ; the fever reappears ; the breatliing is hampered ; the patient, who intoxicates himself in small doses, has no appetite, and wastes ; the fingers become clubbed, and, although he is not tubercular, he yet appears to be so. In this picture I allude especially to a patient under my care at the Laennec Hospital : . A man, thirty-five years of age, was admitted into Leprae's ward for left inter- lobar plem-isy, which was followed by vomica. For a long time he had brought up purulent and foetid expectoration, accompanied by cough and dyspnoea. He left the hospital and came under my care five months later. At this time he had fever, and brought up two spittoons full of foetid pus daily. I found a zone of dulhiess, which began at the spme of the left scapula, and extended obliquely from above downwards, and from within outwards, as far as the axilla. The resonance, above and below, was almost normal. Auscultation of this zone revealed the signs of cavity — viz., cavernous breathing and gurgling somids. I had to content myself with placing a trocar in the cavity, and daily gave injections of alcohol. The patient became worse and succumbed four months later. At the autopsy I found the left interlobar fissure converted into a cavity filled with foetid pus, the walls being thickened and fibrous. The fibrosis had reached the adjacent Imig tissue, and dilated bronchi were present in the fibrous and lardaceous parenchyma. No tuberculosis. This case proves that a cavity, if left to itself, in interlobar pleurisy may remain infected and cause fibrosis of the lung and bronchiectasis. Such a gloomy result would not happen to-day, as immediate surgical treatment would lead to cure. DISEASES OF THE PLEURA 335 Diagnosis. — Such may be the results and consequences of interlobar pleurisy if left alone ; it is necessary, however, to diagnose and to treat the condition in order to avoid the catastrophes of which I have just spoken. In my opinion the medical treatment of interlobar pleurisy is futile. Our part as physicians is to diagnose interlobar pleurisy, to follow out its course, to distinguish the cases in which it is spontaneously curable, when a vomica has occurred, to decide upon surgical intervention, and, lastly, to point out to the surgeon the exact field of operation. Our part is still considerable, for interlobar pleurisy is one of those numerous medico-surgical diseases in wliich the hfe of the patient is in our hands. It is not sufficient, during the first phase of the disease, to reUeve the pain, cough, and dyspnoea by sedative draughts, by injections of morphia, or other appropriate means ; we must endeavour to make a correct diagnosis, and once the disease is diagnosed we must come to an immediate decision. Diagnosis, however, is not easy in these cases. The disease begins ^vith pain in the right or left side, accompanied by fever, cough, and dyspnoea ; this onset is common to pneumonia, pleurisy, broncho-pneumonia, and inflammation of the chest. The first few days pass, and the diagnosis is uncertain ; the idea of lobar pneumonia is put aside, because rusty sputum, crepitant rales, and tubular breathing are absent ; the idea of pleurisy is practically ehminated, because neither friction sounds nor the later signs of effusion are found. Percussion, however, reveals regions in which the reson- ance is not normal. On auscultation, rales, friction sounds, and sometimes, too, ill-defined tubular breathing are heard, and we then fall back on the elastic diagnosis of pleuro-congestion. We feel, however, that this is not the truth, and we always hope that more definite signs will permit us to locahze the lesion. During the onset of interlobar pleurisy this indecision is by no means wrong, for, as I said above, we lack the exact elements for diagnosis. The pleuritic focus, which is deeply hidden between the lobes of the lung, cannot yet reveal itself ; the adjacent lobes of the lung take their part in the congestive process, and attract our attention by causing tubular breatliing, rales, and dullness. It is only about the eighth or the tenth day that the mterlobar effusion becomes more abundant, and takes its share in the symptoms. Fresh signs are now seen ; the dull zone is marked off from more resonant areas. If the disease occupies tlie horizontal part of the fissure, it is behind, towards the upper third or middle of the lung, that we find a band of dullness, suspended, as it were, between more resonant regions. If the mischief affects the obUque portion of the fissure, we find the band of dullness in the axilla, with more resonant regions above and below it. Theoretically, exploratory punctures should help us in the diagnosis. If aspiratory puncture in the suspected region gives exit to purulent fluid, the 336 TEXT-BOOK OF MEDICINE diagnosis is clear. This method has often been put into practice ; in several cases it has been performed six or eight times in the same subject, but most frequently to no purpose. The conditions are quite different when it is a question of puncturing a purulent effusion in the great pleural cavity, or an interlobar effusion. In the former case the aspirating needle, after passing through the walls of the chest, at once enters the fluid without encountering the lung in its passage. It is quite different in interlobar effusion ; the coUec- tion being fairly deeply situated, is surrounded by a more or less considerable thickness of lung, and the needle buries itself in the lung, when we expect it to enter the fluid collection. Read the cases again, and you will see that, in spite of several punctures at different levels, the focus is not found m many cases. Aspiratory punctures, therefore, in the case of interlobar pleurisy, do not give to the diagnosis the support which might be expected. Radio- scopic and radiographic (Tufiier) examination is a method which ought not to be neglected, for it may peld valuable information. In some cases the diagnosis of interlobar pleurisy can be made before the vomica ; in others it only becomes evident after the vomica. Moreover, at this time the symptoms given by auscultation change, and m place of a dull and silent zone we now find cavernous breathing, large rales, and curclino". " I have not finished with the inherent difficulties of diagnosis in interlobar pleurisy. The following case gives much information : A man, fifty-seven years of age, was admitted for fever, cough, and pneumonic expectoration, which was slightly fc^tid. He said that, after a chill, he had been taken ill two months ago .vith a violent rigor, chattering of the teeth, and pam m the right side. Had he had pneumonia ? I am not certain, for he had, so he said, no rusty sputum. However this may be, the disease went on, with fever, cough, pain in the chest, and expectoration. About twenty-five days after the commencement of the illness, at six o'clock in the morning, he felt something bui'st in 1^J^«1^«^*' ^^,^' j\^^'^ hours, brought up about 5 ounces of foul-smelling, puinilent fluid. He had had a vomica. During the next few days the cough and the expectoration contmued and three weeks after the vomica the patient, who was feverish and wasted, and was still bringing up 5 oimces of pus daily, came into hospital. , . ., i • ^„+^i Examination showed the locahzation of the lesion. At the level of the horizontal interlobar fissure, on the right side, we found a zone of dulhiess, limited above and below by more resonant regions. Over the dull zone, auscultation ^^^^^^f .^"^ular breathing and rales. We had no doubt as to the diagnosis, and concluded that our patient had emptied an interlobar pleurisy by vomica. As the fever and the general ill-health persisted, I asked Cazin to open the infected cavity. The operation was performed, and we were then convinced that the purulent focus in the interlobar fissure was but a lobar abscess of the lung, situated at the upper part of the middle lobe, m contact with the interlobar pleura. The admirable lecture of Trousseau on the diagnosis of lobar and interlobar vomica helps us to appreciate the difficulty in diagnosis. As Trousseau says, abscesses of the lung are extremely rare, and what some DISEASES OF THE PLEUEA 337 authors have taken for lobar are really interlobar abscesses. In any case, whether it be a question of vomicae consecutive to lobar abscess or inter- lobar pleurisy, the indications for treatment are identical. Treatment. — As I have abeady stated, medical treatment is purely illusory. There is an infected cavity filled with fluid, which must be evacuated. In the fortunate but rare cases the vomica itself accomplishes the evacuation of tliis focus, and in a few weeks spontaneous recovery occurs. It is, however, preferable not to wait for the vomica, and in every case, if the fever persists, and the compUcations of infection continue, in spite of the vomica, we should operate ; and if the operation is performed at the proper time, secundum arteni, we shall be on the road to success. Moreover, in the eight patients whose history I have traced in my chnical lectures, six who have been operated upon recovered ; the two who had not been operated upon succumbed. IX. MEDIASTINAL PLEURISY— MEDIASTINAL SYNDROME. Discussion. — Under some circumstances false membranes and adhesions shut off the pleura ; the pleurisy is then said to be partial or encysted. Encysted pleurisy m.ay occur in the great pleural cavity, which is divided up by septa ; it is, however, in the interlobar, diaphragmatic, and mediastinal regions that pleurisy finds conditions naost favourable to encystment. Speaking generally, there is absolute difEerence between pleurisy of the great pleural cavity and encysted pleurisy. This difference depends on several causes. When pleurisy develops freely in the great pleural cavity, the liquid spreads between the chest-wall and the lung. The lung escapes by allo\\ing itself to be depressed, thus averting the pressure, while the neigh- bouring organs are displaced ; the symptoms are slight, and dyspnoea only becomes severe when the effusion is considerable. The conditions in encysted pleurisy are quite different. When pleurisy develops in an interlobar space, between the contiguous surfaces of two pulmonary lobes, the latter, being in contact with a closed cavity, readily become infected, and for a time the pulmonary trouble masks the pleural miscliief. Later, when the effusion has formed, it is deeply hidden, and so partly escapes our means of investigation ; the symptoms, therefore, are not comparable with those of pleurisy of the great pleural cavity, in which the lluid is in direct contact with the chest-wall. When the pleurisy is diaphragmatic, the picture again changes, for the relation of the diaphragm and the endings of the phrenic nerve give rise to >i><''ial symptonLs. Ijastly, when pleurisy is confined to the mediastinal region, the clinical picture depends upon the importance of the organs compressed l)y the 338 TEXT-BOOK OF MEDICINE membranes and the mediastinal fluid. In order to grasp the cHnical course of events, I will recall briefly the chief anatomical points. The mediastinum is the region between the two lungs. It extends from before backwards, from the sternum to the vertebral column, and from above downwards, from the sternal notch to the diaphragm. This region, which corresponds to the median part of the thoracic cavity, may be divided into an anterior and a posterior mediastinum. This distinction, however, is fictitious, and this division into two mediastina " holds good only at the root of the lung, because above and below, between the sternum and the vertebral column, no such separation exists " (TiUaux). We find in this region the heart and the great vessels, the trachea and the large bronchi, the oesophagus, the pneumogastric, plirenic, splanchnic and recurrent nerves, the large azygos vein, the thoracic duct, the glands, etc. All these organs are covered by a layer of pleura, which separates them from the lungs. The mediastinal pleura, like other serous membranes, is therefore formed of two layers : one of which covers the organs in the mediastinum, whHe the other covers the contiguous surfaces of the lungs. It is in the virtual space which exists between these two layers that the false membranes and the fluid of mediastinal pleurisy are encysted. Mediastinal pleurisy may be situated on the right or on the left side ; it may be divided into several varieties, according as it affects the anterior or the posterior mediastinum, and the upper or the lower part of the mediastinum. These subdivisions are scarcely apphcable chnically ; in the few cases, however, which I shall relate, we shall see that we are deahng chiefly with posterior pleurisy. What happens when effusion and false membranes accumulate between the layers of the mediastinal pleura ? The membranes and the fluid form a tumour, and push back the lung and the organs of the mediastinum. The fact that the lung is pushed back matters httle— it is a common condition m all pleural effusions— but if the organs of the mediastinum are displaced or compressed, the condition is very difierent. The heart is but httle affected by mediastinal pleurisy, but tliis is not the case with the other organs. If the trachea is displaced or flattened, dyspnoea, stridor, and sucking-in result. In the case of the oesophagus dysphagia appears, solid foods can no longer pass, and Uquids can only be swallowed with difficulty. If the great azygos vein is compressed as it receives the small azygos and seven or eight right intercostal veins, blood-stasis results, and the collateral circulation shows itself by a network of distended veins over the chest. If the pneumogastric nerve is stimulated by the presence of fluid and of pleuritic membrane^ the patient is seized with fits of coughing and severe attacks of suffocatio^ If the recurrent nerve is hampered by the exudate, laryngeal troubles, such as hoarseness, dysphonia and spasms of the glottis, at once supervene. I propose to call this collection of symptoms the mediastinal syndrome, DISEASES OF THE PLEURA 339 which points to the existence of a tumour in the posterior mediastinum. This syndrome is apphcable to mediastinal pleurisy, and existed in two patients, whose history I will now sketch : Clinical Cases.— A young man admitted for intense dyspnoea, with stridor and 8ucking-in. Inspiration was accompanied by a loud scraping noise, while the sucking- in was evident in the supra- and substernal regions. Examination over the posterior mediastinum gave valuable information. We found pain on pressure and dulhiess on percussion ; we discovered that the stridor was most marked m the posterior mediastinum, from which point it spread to both lungs The disease had begun suddenly, five weeks before, with rigors and distress.' Some days later attacks of suffocation had supervened with fits of coughing, which resembled whooping-cough ; but expectoration was absent. The voice became raucous and dull, but not aphonic. About four weeks after the onset of the disease the patient noticed that solid food passed with difficulty • he said that " it seemed to stop on its way down.^' This dysphagia, joined to the' stridor proved that the trachea and the oesophagus were displaced, or compressed by a solid or a fluid tumour in the mediastinum. This hypothesis was confirmed by the collateral circulation over the upper thoracic region, proving that the great azyc^os vein was compressed in the mediastinum. We had, therefore, to find out what the lesion of the mediastinum was. It was not a glandular tumour, because enlarged glands were not present in the neck, the clavicular hollow, or the axilla ; and the patient had neither tuberculosis, syphilis! nor cancer. It was not an epithehoma of the oesophagus, compressing the trachea,' because the dysphagia had been preceded by attacks of suffocation and stridor. We could eliminate lymphadenoma, because the onset was acute and recent, while the examination of the blood was normal, the white corpuscles being in proper quantity and the red corpuscles as high as 4,800,000. .Alight it be a purulent collection in the mediastinum— /.e., abscess from congestion, phlegmon, or mediastinal pleurisy ? I ought to say that I thought of mediastinal pleurisy. On the night after admission he was seized with violent fits of coughing, and although there had previously been no expectoration, he brought up foul-smelling, purulent sputum ; and next morning I found in the sputum-glass about 2i ounces of greenish homogeneous pus, such as is caused by the pneumococcus. Although the bacteriological examination did not reveal pneumococci, Griffon, with serum taken from the patient, obtained a positive result : agglutination of the pneumococci in chains and in masses! The pus in the posterior mediastinum was probably the result of a pneumococcal pleurisy, going on to vomica. The patient was cured six weeks later. A woman, forty-four years of age, came under my care for obstinate cough. She had suffered for a week from attacks of suffocation and stridor, audible at a distance. Ilie cough was paroxysmal. \Vhen the cough came on after a meal, it provoked vomiting of food ; although it lasted only a short while, the distress was extreme, ihe stridor, as well as tho supra- and substernal sucking-in, were more marked during the cri.ses of dyspnoea. At times the voice was raucous and muffled. The disease appeared to have started from a chill. Cough and distress were the first signs. Stridor and attacks of dyspntea appeared later. Dysphagia supervened, and the patient had difficulty in swallowing hquids. '• Something shut up " as soon as she swallowed any food. Breathing was audible on both sides ; no abnormal sounds. Percussion showed aormal resonance. Heart and aorta normal. No fever. Temperature, 3ss was extreme, the temperature reached 1M°F., and the patient d,ed "Ttttfautopsy mechastinal pleurisy was found. The collection wa. situate, between tie irmer'aspect of the I'eft lung and the left wall o the -fd-tmum » nmited by false membranes, which were thick, tibrmous, -f ™Yb^dant hS 2 two layer's of the mediastinal pleura. The pus, wteh ™'' ""' f j""**"' ^, ,^„ ..lassicil featurc-s of pneumococcal pus, and spread downwards as fat as DISEASES OF THE PLEURA 341 diaphragmatic sinus, which was filled with false membranes, while it did not reach higher than the hilum of the lung. Mediastinal pleurisy here occupied the lower part of the mediastinal pleura. Further, the left interlobar fissure was joined together, and adhesions existed between the lower lobe and the costal pleura. The whole lower lobe was increased in size ; the cut section showed a typical areolar abscess, of a spongy appearance, the pockets of which were full of pus. The mediastinal glands were hyper- trophied. Bacteriological examination showed that the pus in the pleura and the lung contained only most virulent pneumococci. Description.— We may now discuss mediastinal pleurisy, which is a new chapter in pathology. We shall not consider pseudo-mediastinal pleurisy, which, from its situation on the left side, simulates pericarditis with large effusion (Grancher). Mediastinal pleurisy may be primary or secondary — primary when the pneumococcal infection is present only in the mediastinal pleura, secondary when it is consecutive to pneumonia. It appeared to be primary in my two patients, as well as in Bouveret's case ; it was associated with pneumococcal suppuration in the lung in Thoinet and Griffon's case ; Andral's patient was tubercular. Mediastinal pleurisy is unilateral, and is usually confined to the anterior, posterior, or inferior regions of the mediastinal pleura ; it may extend to other regions, such as the costo-diaphragmatic sinus, and coexist with adhesions of the interlobar fissure and, adhesions of the lung to the chest- wall. The liquid was purulent in the six cases quoted ; purulence is, indeed, common to encysted pleurisy of the mediastinum, the interlobar fissure, or the diaphragm. In three cases in wliich the infectious agent was looked for the pneumococcus was found. The onset of mediastinal pleurisy is not distinctive ; the pain in the chest, the fever, and the cough give no precise indication. When infection of the mediastinal pleura occurs, the adjacent lung is affected by the closed cavity, becoming inflamed and congested. The hidden focus is accessible neither to percussion nor to auscultation. The patient coughs, breathes with difficulty, has fever, and complains of distress ; sputum is absent or has no special feature, and we think of pneumonia or of pleurisy, but we cannot localize the lesion. Purulent fluid and false mem- branes accumuhite in the affected segment of the pleura, and form a kind )f tumour, the localization and the size of which determine tlie appearance )f symptoms. If the encysted collection travels toward the lung, and affects the niediasti- lum to only a slight extent, the signs ar(> uncertain, and the diagnosis emains indefinite. If the pleural collection travels towards the organs of the i.iediastinum and pushes them back, the mediastinal syndrome then ajipears. pyspiiffia, attacks of opjm'ssion, suck-ing-in and stridor, dyspiiagia, whoup- |iig-cough, displacement of the larynx and the trachea, recognized on 342 TEXT-BOOK OF MEDICINE laryngoscopic examination, vocal troubles, collateral circulation in the thorax, are the symptoms and signs which help us in diagnosis. Let me emphasize the value of stridor, which occupies the chief place in lesions of the mediastinum. What must be understood clinically by this word " wheezing " (cornage) ? It is a term employed in veterinary medicine. Some horses, whose breathing is almost normal as long as they are at rest, are seized while trotting or cantering with laboured breathing, accompanied by a rasping noise, which constitutes the " bruit de cornage " (roaring). A healthy man breathes silently both during inspiration and expiration, and we cannot, so to say, hear him breathe, because the air traverses the glottis, larynx, and trachea freely. If the air meets any obstacle to its passage, sonorous vibrations are at once produced, and the " bruit de cornage " becomes audible. The tone of this bruit varies some- what according to circumstances ; it may have a snoring, rasping, or sawing character. The lesion may be situated in the larynx or in the trachea, so that we find laryngeal and tracheal stridor. The former stridor is far from rare • oedema of the larynx, spasm of the glottis, paralysis of the posterior crico- arytenoid muscles, and cancerous lesions of the larynx — in short, any lesion which produces stenosis of the larynx — may determine stridor. When the stridor is of laryngeal origin, the vocal troubles and examination with the laryngoscope indicate the site of the lesion. The tracheal lesions that may cause stridor are intrinsic when they arise in the walls of the trachea (syphihtic gumma, polyjjoid excrescences, and stenosis), and extrinsic when they arise in the mediastinum (solid and fluid tumours) ; mediastinal pleurisy is of this nature. While the injury to the organs of the mediastinum caused by pleurisy shows itself by the symptoms just enumerated, the examination of the dorsal region, which corresponds to the posterior mediastinum, furnishes valuable signs. Pressure on the upper dorsal vertebrae and the corre- sponding costo-vertebral grooves is painful. In the same region more marked dullness is found on the right or left of the vertebral column, according to the side affected. The stridor is most marked at this spot, and diminishes as the distance from the mediastinum increases. Sonorous and moist rales may be heard in the lung near the mediastinum. They indicate congestion of the lung, are present in front and behind, and are more numerous on the affected side. Radiography may give useful information, as in one of my patients. Mediastinal pleurisy, like most encysted empyemata, tends to vomica. The vomica generally supervenes some weeks after the onset of the disease, and is scanty, as the pus, encysted in the mediastinal pleura, never reaches a large amount. The vomica of my patient at the Necker Hospital might DISEASES OF THE PLEUKA 343 be put down at 6 ounces ; in my patient at the Hotel-Dieu it did not exceed 3 ounces : it was fcBtid in both cases. Andral's patient had an abundant vomica, but the approximate quantity is not given. Diagnosis. — The diagnosis of mediastinal pleurisy is very difficult. The signs are insufficient and indefinite until the mediastinal syndrome appears. When this syndrome appears, percussion and auscultation of the dorsal region (which corresponds to the posterior mediastinum) give informa- tion as to the locahzation of the lesions. We can then by these signs and symptoms, aided by radiography, arrive at the topographic diagnosis ; the knowledge that the lesion occupies the mediastinum is the first step in the diagnosis. The nature of the lesion has then to be ascertained. Is it tuberculous, cancerous, or syphihtic adenopathy ? is it a lymphadenoma, or is it an aneurysm of the aorta ? is it an abscess or pleurisy ? As I have said, the onset and the course of the symptoms may give a clue to the diagnosis. Mediastinal adenopathies and tumours do not begin suddenly \Nith fever : the onset is insidious, and the course slowly pro- gressive ; moreover, the swelHng in the neighbouring glands (neck, axilla) aids in the diagnosis. Mediastinal pleurisy, on the contrary, arises suddenly, like an acute febrile disease ; fever, paiii, and cough mark the onset, dyspnoea is early, and vomica supervenes in at least half the cases. Furthermore, in the three cases in which laboratory researches have been made, bacteriological examination and sero-diagnosis iave demonstrated the pneumococcus ; sero-diagnosis would therefore be useful before the appearance of the vomica in order to ascertain the nature of the disease. Treatment. — The prognosis is not free from gravity. The disease is serious in itself, and also from the secondary infections which may reach the bronchi and the lungs. We must, then, be ready to operate if occasion arise. Thanks to the marvellous progress of surgery, the posterior mediasti- num has become fairly accessible to surgical investigations. Dr. Potarca (of Bucharest), in a work entitled " La Chirurgie Intramediastinale Pos- terieure," has collected several cases of operations for purulent collections in tlie posterior mediastinum, phlegmon, mediastinitis, suppuration from bony or from glandular lesions, and foreign bodies. Although in the memoir in question purulent mediastinal pleurisy is not studied (apart from Zimbicld's doubtful case), it is still true that the posterior mediastinum should be opened in mediastinal pleurisy if occasion arise. X. DIAPHRAGMATIC PLEURISY. Pleurisy of the diaphragmatic portion of the pleura may be primary or secondary, and dry or accompanied by effusion, which may be fibrinous or purulent, free or encysted. The dry form is the more frequent. Cirrhosis 344 TEXT-BOOK OF MEDICINE of the liver, peritonitis, nepliritis, the puerperal state, tuberculosis, and pneumonia are the common causes of diaphragmatic pleurisy. In pelvic peritonitis the inflammation is transmitted from the peritoneum to the pleura by the lymphatic vessels, especially by those which accompany the utero-ovarian vessels, and pass along the pillars of the diaphragm. As regards metapneumonic pleurisy of the diaphragm, the considerations enumerated in the case of interlobar pleurisy remain the same. The effusion is usually scanty, and sometimes encysted, wliile the lung is often the seat of acute congestion, which enters largely into the clinical picture of the disease. The symptoms of diaphragmatic pleurisy vary in severity ; they are sometimes moderate, but in acute cases the disease shows itself by sharp pain at the middle of the diaphragm (neuralgia of the phrenic nerve). The pain reaches as high as the shoulder, and can be provoked by compressing the insertions of the diaphragm into the tenth rib (diaphragmatic point) two fingers' breadth from the linea alba (Gueneau de Mussy), or by pressing on the phrenic nerve in its passage between the lower heads of the sterno- cleido-mastoid muscle. The inferior costal region is immobilized because of the paresis of the diaphragm (Andral), and the usual signs of pleurisy — viz. friction rub, dullness, tubular breathing, and segophony — only appear when the great pleural cavity is also affected. In the grave cases — which are, moreover, rarer than Andral's description would lead us to suppose— the symptoms are acute, and recall the crises of angina pectoris ; the breathing is short, and interrupted by hiccough ; the voice is "broken ; dyspnoea is excessive ; one-half of the diaphragm is immobiUzed, and if the other half is affected, the patient's life is in danger. Suppurative diaphragmatic pleurisy has no special symptoms, but behaves like the pleurisy which we have just described ; it is encysted, like partial pleurisies, and in some cases, especially in elderly people, it remains latent, being only found at the autopsy. It ends fairly frequently by vomica. The agonizing pains of diaphragmatic pleurisy may be reUeved by means of dry-cupping, fifteen or twenty leeches, or injections of morphia ; antipyrin may be prescribed, and an ointment of methylate of salicylate may be applied to the painful region. XI. LOCULATED, AREOLAE, OR POLYMORPHOUS PLEURISY. Pleurisy arising in the great pleural cavity may be loculated. Some- times it occupies a large pocket, which may contain several ounces of sero- fibrinous or purulent fluid (unilocular) ; at other times a series of small ones, when we speak of multilocular pleurisy. Unilocular Pleurisy. — I have recently had a case under ray care at the DISEASES OF THE PLEUKA 345 Hotel-Dieu. The pocket was encysted in the middle portion of the right pleural cavity behind. A woman, twenty-one years of age, had her first attack of pneumonia in 1898. The disease was situated on the left side. On May 21, 1900, pneumonia of the right apex, after a chill. Temperature was over 10-t° F. ; acute pain in the side ; tongue dry and red ; vomiting and diarrhoea ; condition of the patient very grave. On May 28 the temperature, which had varied from 103° F. to 10-4-5° F., showed some tendency to fall ; the vomiting and the pain in the side became less. Two days after, pain reappeared, but was now lower down ; and while auscultation revealed the existence of redux crepitation at the apex, very harsh breathing, accompanied by friction soimds and some crepitant rales, was already perceptible over the middle of the lung. From June 1 to 5, the temperature varied from 101° to 103° F., patient's condition was satis- factory, and pain in the side disappeared. On the 5th, examination showed dullness at the angle of the scapula, over an area of 2 inches in the vertical and 4 inches in the horizontal direction. This dullness was clearly limited above, where the apex had re- gained its resonance, while it gradually becami! less marked below. Vocal fremitus abolished only in the region where the dullness was absolute. Auscultation showed distant tubular breathing and very clear a^gophony over the dull zone, with slight aphonic pectoriloquy. Exploratory puncture blank, 1 inch above and 2 inches below the dullness. At the focus itself a green sero -purulent fluid, rich in leucocytes, and containing numerous pneumococci, mostly in chains of from five to ten elements, as well as some diplococci, was drawn off. The pneumococcus was inoculated into a mouse, and showed itself virulent, while it grew well on the different culture media, and preserved its chain-like form on agar. From the 31st to the 7th the condition remained stationary, and the pleurisy made slow progress, diffusing in a circle, and invading the base and the apex at the same time, the dullness being propagated towards them. The pleurisy remained, however, clearly " suspended," and on Jime 11 punctures yielded pus neither at the apex nor at the base. In the centre of the dull zone, however, the pus was greenish, thick, creamy, and rich in pus corpuscles and fatty granules. The pneumo- cocci in chains had become rare. On the 12th, operation for empyema was performed at the level of the angle of the scapula, with resection of a rib, and we found 10 ounces of pus, forming a focus limited above and below by false membranes. The patient recovered. This was veiy clearly a case of loculated pleurisy, with a large pocket, which had developed in the great pleural cavity, and not a case of interlobar pleurisy. Moreover, in interlobar pleurisy the signs (iegophony, souffle, and pectoriloquy) have never the clearness fovmd in the present case. Areolar and Polymorphous Pleurisy. — Loculated pleurisy may be chronic from the first, or be due to acute attacks affecting the pleura, which is already partitioned off by the false membranes of former inflammation. Loculated pleurisy may be sero-fibrinous, hsemorrhagic, or purulent ; indeed, it is not rare on performing thoracentesis to meet with serous fluid in some pockets and pus in others. Sometimes the loculation is simple, and the false membrane divides the efEusion into two pockets only ; more often the loculation is multiple, and the pockets are numerous ; lastly, in some cases the pleurisy is areolar, as if the false memljranes were themselves infiltrated with serous fluid. Areolar and polymorphous pleurisy usually present the following forms : W(^ find in a patient the signs of considerable effusion, and diagnose the 346 TEXT-BOOK OF MEDICINE presence of 4 or 5 pints of fluid in the pleura ; puncture is performed, and we are astonished at withdrawing very Uttle fluid, wliich is not in proportion to the signs present ; further, we note the persistence of the signs of effusion at the other parts of the thorax, either above or below the point of puncture. The exploratory needle shows that fluid is still present at these points, and we conclude that a membranous septum is interposed between two or more pockets of fluid. This form has been called " partitioned pleurisy." Sometimes the fluid is identical in the different pockets ; at other times it is serous in some and hsemorrhagic or purulent in others. In this case the pleurisy is called " polymorphous " (Galliard). The disposition of the false membranes wliich partition the pleura is, however, very variable. Sometimes a single horizontal, oblique, or vertical pseudo-membranous partition, which divides the pleura into two (bilobed pleurisy), exists ; at other times multiple and irregular adhesions divide the pleural cavity into numerous small and distinct cavities (multilocular or areolar pleurisy). In the latter case we often see pockets occupied by a gelatinous quivering mass that is formed of a fibrinous network impregnated with serous fluid, while the neighbouring pockets contain sero-fibrinous, sero-hsemorrhagic, or sero-purulent fluid. The partitioning has been attributed to the false membranes of ante- cedent pleurisies ; relapsing pleurisy is said to be more easily partitioned than pleurisy which affects an intact serosa. In these cases the pleurisy is said to be multilocular from the start. We may also observe the following varieties : encysted serous pleurisy, followed by adjacent empyema, or encysted em- pyema, complicated by adjacent sero-pleurisy. The latter cases are more common, because empyema is much more often encysted than serous pleurisy. Save in exceptional cases (Jaccoud), the diagnosis of loculated pleurisy can only be made after puncture. The attention is arousejd by the in- sufiicient quantity of fluid evacuated. Sometimes, also, the puncture may be blank, if the needle penetrate the septum. The diagnosis will be confirmed by methodical exploration of the pleural cavity, by means of an aspirator, which is provided with a long needle. The prognosis is especially serious when encysted suppurations escape notice, because this fact prevents treatment by free incision ; we only find them at the autopsy. We must remember that polymorphous pleurisy may be symptomatic of tuberculosis or of pleuro-pulmonary cancer. XII. SYPHILITIC PLEURISIES. Early syphihtic pleurisy occurs in the secondary stage, while late syphi • litic pleurisy is seen during the tertiary period. The early form has been well described by Chantemes^e and Widal, who DISEASES OF THE PLEURA 347 quote several conclusive cases. At the Hotel- Dieu I have seen a very clear example : A man, twenty years of age, came into the hospital with pain at the lower angle of the left scapula. Pleurisy without effusion was found. Friction sounds were heard, which extended behind and laterally as far as the axillary region. Other ortrans healthy. Auscultation of the lung showed no lesions, and we had to deal with apyi-etic, painful pleurisy of four days' duration. We could not incriminate tuberculosis, influenza, or rheumatism. This boy, how- ever, showed a well-marked syphilitic roseola. The syphilis was two months old. The cicatrix of a chancre was visible on the dorsal surface of the penis, and enlarged glands were present in the groins. He complained of headache and sore -throat, and we found syphilitic angina, with mucous patches. As pleurisy had appeared in a youth, who had for two months been infected with sj'philis, it seemed natural to consider the pleurisy as a secondary complication of syphilis, and I placed the patient on mercurial treatment. The pleurisy remained dry, and I found no effusion. The pain and friction sounds disappeared in ten days. Similar cases have been published, and the occurrence of syphilitic pleurisy in the secondary stage is therefore well proved. Why should we not see early syphiUtic pleurisy when we see nephritis, arteritis, icterus, and ]>ronchitis appear among the early manifestations of syphilitic infection ? Early syphiUtic pleurisy may be dry, or be accompanied by effusion. I do not beUeve that the efiusion is ever so abundant as to necessitate thora- centesis. An important difference between early and late syphilitic pleurisy is that the former is not associated with pulmonary lesions, while the latter, with which I am now dealing, forms part of the broncho-pulmonary syphi- loma discussed in the chapter on Syphihs of the Lung. I have been able to find only a small number of cases of tertiary syphihtic pleurisy. According to Mauriac, " this pleurisy is often seen, and is accompanied by effusion." Tertiary lesions of the pleura may be placed in one of the following categories : Either the pleural lesion is an unimportant complication of the pulmonary lesion, or the effusion is abundant ; the pleurisy is the chief feature, and the condition well merits the name of syphilitic pleurisy. As an epiphenomenon, mention must be made of this pleurisy in some cases of tertiary sypliihs of the lung ; it has been referred to by Carlier. In one, he says without further amplification, that the pleura on one side contained 300 grammes of a clear yellow fluid, and the visceral layer presented recent false membranes, which were very easily torn, while the parietal and diaphragmatic layer was also inflamed. In Jacquin's thesis Balzer's case of syphiUtic pleurisy with large effusion is described : A man, thirty-two years of ago, came to hospital with functional troubles and physical signs which led to the diagnosis of caseous pneumonia on the right side. A month later abundant effusion appeared on the right side. Ple\irisy, complicating f i]l)or- culosis of the lung, was then diagnosed ; but after four days the patient died, and the autopsy revealed a syphilitic liver liiat M'as studded with gummata and segmented by 348 TEXT-BOOK OF MEDICINE scars. The right lung was also full of gummata, the largest of which just involved the pleura. These gummata did not contain a single Koch's bacillus. The lesions in the right pleura were so characteristic that I give them in detail. " In the right pleura a much more considerable effusion exists than physical examination would have led me to suppose. There are about 4 pints of turbid blood-stained serum. The parietal and visceral layers of the pleura are considerably thickened over the whole extent of the effusion. They show a continuous fibrous covering, 1 or 2 millimetres in thickness, attaining at the base of the lung a thickness of nearly 1 centfmetre. This fibrous cap is sur- rounded by false membranes at several spots. At the points where the fibrous thicken- ing is most considerable we find, on section of the pleura, hard yellowish caseous masses as large as a pea or as a millet-seed." This case of tertiary syphilitic pleurisy, in which the effusion amounted to 4 pints, is most conclusive. I saw the following case : I was called to treat a man with terrible dyspnoea, which had recurred in more or less acute attacks for the past year. Tubercular broncho -pneumonia had been diagnosed. On my first examination I found signs of an effusion, which I estimated at 1^ pints. Although this quantity of fluid did not explain the patient's dyspnoea, I performed thoracentesis, but drew off only 21 ounces of slightly rose-coloured fluid. The patient experienced, however, no relief. I searched, wthout success, for the cause of the disease, when he finally confided to me that he had had syphilis. This avowal guided my treatment. I at once gave mercury and iodide of potash in large doses, and the dyspnoea improved so rapidly that at the end of a few weeks the breathing was almost normal. At my last visits no trace of pleurisy remained, though the broncho- pulmonary lesions were slower to improve. In this case, again, the syphilitic nature of the trouble was shown by the beneficial action of specific treatment. There exists, then, tertiary pleurisy, which is associated with syphilitic lesions of the lung, and the true means of diagnosing it is to think of syphilis. XIII. APPENDICULAR PLEURISIES— PYOPNEUMOTHORAX AND SUBPHRENIC EMPYEMA. In 1890 I read a paper before the Academic de Medecine* on "Appen- dicular Pleurisy," a name which is generally accepted at the present day. Later, in my clinical lectures at the H6tel-Dieu,f as I had seen how frequently appendicular subphrenic empyema precedes or accompanies infection of the pleura, I have united appendicular pleurisy and sub- phrenic empyema in a single description, and I shall do so in this chapter. I think that it will be useful to give a resume of some cases : Clinical Cases. — A man, twenty-six years of age, admitted to the Hotel-Dieu. He suffered from shortness of breath, was pale, had an anxious look, with simken eyes, and a wretched pulse ; he appeared moribund. He complained of a pain in the right side of the chest, and was so feeble that he could not raise himself on the stretcher. On * Dieulafoy, " La Pleuresie Appendiculaire " (commimication a 1' Academic de Medecine, seance du Mardi, 10 Avril, 1900). t Dieulafoy, " Pleuresie Appendiculaire et Empyeme Sous-phrenique " (C'linique Medicate de V Hotel-Dieu, 1903, vol. iv., 15""^ et 16™* letons). DISEASES OF THE PLEURA 349 the right side I found a large eflfusion, with absolute dullness, except at the apex, where the resonance was exaggerated. It is not common for pleural effusion, however abundant, to show such general symptoms. In this case it was not simply, dyspnoea, but adynamia, bordering on collapse, which dominated the scene. What, then, did this efEusion conceal ? Apert at once performed exploratory puncture, in order to ascertain the nature of this pleurisy, and drew ofi turbid fluid, which was of nauseous odour and not homogeneous. The case was therefore one of foetid, perhaps of putrid or of gangrenous, pleurisy. There was not time to make a pathogenic diagnosis, and the imperative indication was immediate surgical intervention. Marion therefore came to see the patient, but found him in his death agony, with thready pulse and cold, cyanosed limbs. Death occurred soon afterwards. Prom the information given by the family, it was possible to reconstruct the case. He was taken ill on November 10 Anth abdominal pains, which increased in severity during the night, chiefly on the right side. Next morning, as he felt easier, he went to his office. In the evening he passed a motion. The next night was more comfortable, but on Sunday evening (the third day) he was seized ^rith such severe pain on the right side of the belly " that he twisted and groaned in agony." During the exammation his wife remarked that the belly was particularly painful on the right side. An enema and poultices, with laudanum, were prescribed. Next day vomiting came on. Patient had fever and rigors ; he was constipated, and the abdominal pains were as severe as ever. During the next few days the situation did not improve. The hepatic region became painful, and a blister was ordered. Meanwhile the patient began to cough, and complained of pain in the right side of the chest. Pleuro -pneumonia was diagnosed. Fever retmrned ; violent pain in the chest, M-ith extreme dyspnoea, cold sweats, and tachycardia, supervened. On the morning of the 29th hydropneumothorax was found. He was then brought to the Hotel-Dieu. To sum up : The disease, which lasted nineteen days, was divisible into two stages : the first or abdominal stage was characterized by acute appendicitis, and treated by medical means; while the second or thoracic stage terminated with symptoms of pneumo- thorax and death. Let us now see what the autopsy revealed. Thoracic cavity first examined. Intercostal space perforated under water. As soon as the pleura was opened, a nauseous odour was noticed, and bubbles of gas came up through the water, showing the presence of foetid gases in the pleura, and confirming the diagnosis of pneumothorax, made during life by the physician who had sent up the patient. The case was one of j)neumothorax by putrefaction, and not by perforation. In the pleural cavity, were 7 pints of very foul greyish fluid. The left lung, which was pushed back against the spine, was reduced to a fifth of its normal size, airless, and no longer crepitant. No adhesions bound it down to the costal wall, but its base was adherent to the diaphragm. Pus was present between the two layers of the thickened diaphragmatic pleura. No sign of perforation or of gangrene found. The pleurisy was putrid, but not gangrenous ; putrefaction and formation of gas, but no mortifica- tion of the tissues, existed. Let us now pass on to the abdominal cavity. On the left side, nothing to notice ; no trace of peritonitis. On the right side, numerous adhesions from the abdominal wall to the organs, and, on tearing them through, 5 ounces of pus, quite as fa-tid as the pleural fluid, flowed out. The abdominal cavity was explored, j)us and membranes found ; some were spread out over the intestine and the liver, while others reached up b<'iiind the caicum and the colon. I'osterior surface of tiie ciecum bound down by membranes to the [)arietal peritoneum. The appendix was included in this mass. It was very long, of the vertical type, and passed up on the posterior surface of the c;eiuin ; it was free at its caical origin, but higher up it wits surrounded by adhesions and bathed 350 TEXT-BOOK OF MEDICINE in pus. Its walls, which were double their proper size, were becoming gangrenous, but liad not perforated. It was in this part of the apiaendix, wliich had been trans- formed into a closed cavity, that the acute toxi-infection was elaborated. The jiurulent track continued behind the colon, turned round the hepatic flexure, and spread out in front of the right lobe of the hver, setting up abscesses in its course. The liver was partly hidden by perihepatitis. The diaphragm was examined for a perforation ; as none was found, the infection had evidently been carried to the pleura by the lymphatic vessels. Other organs — i.e., liver, spleen, kidney, and heart — were healthy. The left lung, however, had been infected. The apex showed a splenized region as large as an egg, with several infarcts in different stages of evolution. The left pleura was healthy. Bacteriological and experimental researches were made by Apert with the jjua dra^\^l oiT by aspiratory puncture, and also the peritoneal pus removed at the autopsy. The result was as follows : Some of the micro-organisms were aerobic, while others were anaerobic. They had caused putrid pleurisy, as shown by the formation of gas within the pleura. With guinea-pigs and rabbits, inoculation of pus into the cellular tissue and in- jection of pus into the vein of the ear produced abscesses and infarcts, containing the same micro-organisms that were found in the specimens of pus. The patient had been taken ill with classical appendicitis. I do not know what the original diagnosis was, but I do know that the treatment was medical when it should have been surgical. The man would have been saved by early operation, just as we save all the patients who are operated on in good time, when no precious time is lost in medical treatment which is based on erroneous pathogenic concejjtions. This treat- ment is Avrong, for it apjjears to be doing something when it does nothing but give the toxi-infection time to strike a fatal blow. Enemata, sedatives, and rest were ordered, while infection of unusual \'irulence was brewing in the closed cavity of the appendix. Aerobic and anaerobic microbes then made their way through the walls of the appendix, and provoked the formation of purulent tracks, which took an ascending course, and in a few days reached up behind the caecum and colon, and spread to the anterior and upper surface of the Hver. The phrenico-pleural phase now appeared ; cough, dyspnoea, and pain were its signs. The diaphragm was not perforated, but, thanks to the lymphatic channels, was traversed by microbes of undiminished virulence. It might well be said of this process, Vires acquirit eundo. The pleural infection was so acute that the effusion rapidly reached 7 pints. Putrefaction was shown by the appearance of the pneumo- thorax. The lesions were so severe that events hurried on, and the patient died nine- teen days after the onset of appendicitis. The infection, which started from the appendix, had followed two courses — the one by the lymphatics, and the other by the blood. The lymphatic infection took place by extension ; though it started so far down and reached so high up, yet in a few days it spread across the abdominal cavity and invaded the pleura. The infection of the left lung was due to microbic emboli. But, it will be asked, is pleurisy a frequent complication of appendicitis ? It is certainly far from rare, and in proof I can quote many cases. I saw a very remarkable case. The patient was a lady, in whom I diagnosed appendicular jileurisy and subphrenic empyema. The double operation was j^erformed by Segond : he operated first on the pleura, and a fortnight later he attacked the subphrenic empyema. The patient recovered. In consultation with Brun and Jalaguier, I saw a youth with appenchcular pleurisy. On May 20 he was attacked mth appendicitis. Three days later Brun found severe peritonitis. Operation performed next morning. Appendix was gangrenous ; DISEASES OF THE PLEURA 351 peritoneal fluid was sero-purulent and foetid. Free drainage established. During the next few days, in spite of improvement in the peritoneal condition, situation was grave, and temperature very high. No cause could be found for the persistence of these alarming symptoms. On June 2 symptoms of right pleurisy were discovered, and exploratory puncture drew oil turbid fluid. On June -i operation for emjjyema ; a large quantity of dirty, horribly foetid fluid dra^mi off. Free drainage established. Next day diffuse inflammation at the edges of the thoracic wound, but no gaseous crepitation. During the following days the inflammation stopped ; the antiseptic irrigations of the pleura seemed to indicate that the pleural focus had been effectively treated, but yet fever persisted and the situation became worse. I then saw the patient, with Brun and Jalaguier. Minute examination revealed no fresh lesions in any organ. We were of opinion that the patient was suffering from a profound intoxication, and prescribed accordingly. About June 11 cerebral symp- toms (intoxication, or perhaps meningeal infection) of photophobia, strabismus, irregu- larity of the pulse, and stiffness of the neck supervened, and the patient died. Resume of two cases of appendicular pleurisy described by Terillon : A young man, seventeen years of age, had suffered from appendicitis. Belly dis- tended and painful ; on the right side a jjainful swelling, reaching from the ihac crest to the false ribs. Affection was of six days' duration. Temperature, 103° F., and pulse rapid. Intervention decided on. On opening the abdomen, caecum was adherent to the abdominal wall ; sharp gush of pus occurred. The abscess occupied the iliac fossa behind the caecum, and reached up towards the kidney. On the next day the temperature as high and the pulse as rapid as before operation ; general condi- tion worse. Two days later it was noticed that the respiration was embarrassed, and existence of a large right effusion was made out. Puncture yielded pus. After opera- tion for empyema, fever fell at once, improvement followed, and the patient was completely cured. Boy, fourteen years old, had suffered for five days from right iliac peritonitis. The temperature was 10-t^ F., and the gravity of the situation was e\adent. Terrillon pro- posed immediate operation, which was not agreed to. Ten days later he was sent for in a hurry. The child was sitting up in bed, having shown symptoms of asphyxia since the morning. Large effusion present on right side. About a pint of fcetid pus was dra-n-n off by puncture, but syncope came on suddenly, and the patient died. It is probable that in this case, as in the preceding one, prompt operation would have brought about a cure. The pleural complications of appendicitis have been studied in Germany since 1891. Here is a series of cases. Wolbrecht, in his thesis (Berhn, 1891) entitled " Pleural Complications in TyphUtis and Perityphhtis," quotes a few cases, two of wliich are personal. Case 1. — A joiner, twenty-four years of age, who some days before had experienced the symptoms of perityphlitis, came into his clinic. Signs of subphrenic abscess and of right pleurisy. Exploratory puncture drew off fujtid pus. Operation for empyema perforimd ; lifth rib resected ; 5 pints of nauseous fluid withdrawn. Two months later patient was cured. Case 2. — .\ num suffering from ])erityphlitis, with circumscribed peritonitis. Ten days later right pleurisy, witli rederaa of tlie chest-wall. Exploratory pum^ture showed turbid blood-stained cflusion. Three days later patient seized with violent coiigli, and brought up abundant foul-smelling pus. lie finally recovered, after a convalescence of three mouths. 352 TEXT-BOOK OF MEDICINE Larsen and Winge relate a case of appendicitis, with retrogression of the peritoneal symptoms at the end of the first week : Pain in the right hypochondrium appeared, and right pleurisy developed rapidly. The dyspnoea became very intense, and death followed. Post-mortem : pyopneumo- thorax on the right side ; perforated appendix buried in an abscess ; narrow purulent track ran up behind the Uver, and had perforated the diaphragm in two places. Grawitz, under the title of " Perforation of a Perityphlitic Abscess into the Pleural Cavity," has pubHshed the following case : A woman was taken ill a fortnight before, with pain in the right side of the belly, constipation, fever, and vomiting. Later the symptoms of right pleurisy supervened, and the patient died three weeks after admission to hospital. Post-mortem : the whole appendix was converted into a sac, and had perforated ; near its base was a calculus, the size of a haricot bean. The intestinal coils were adlierent in the right iliac fossa, and the pelvis contained pus. From the gangrenous appendix a sinuous cavity extended upwards behind the right kidney and the duodenum. A perforation, as large as a sixpence, was present in the posterior part of the diaphragm, and established com- munication between the subdiaphragmatic region and the right pleura. Three pints of foetid pus in the pleural cavity. Wollert has pubUshed similar cases : A young man, sixteen years of age, was taken ill with appendicitis. Thirteen days later sharp pains at the right base, and intense dyspnoea. Right pyopneumothorax, with metallic tinliling, found. Post-mortem : iDcritonitis, consecutive to appenchcitis. Sheet of pus over the ascending colon, the diaphragm, and the hver. The diaphragm was perforated, and the right pleura contained 8 pints of j)urulent Huid, with, foetid gas. Appendicular pleurisy is sometimes serous ; the infection is reduced to a minimum, and recovers with or without operation. Case seen with Larcher and Monod : Young girl suffering from appendicitis, diagnosed by Larcher, and operated upon by Monod on May 9. Everything went well until May 18, when pain appeared in the right hypochondrium and at the base of the chest. The temperature now rose to 103° F. Cough was frequent, though expectoration absent. This condition lasted for several days, without appreciable change. I was then called to see the patient, and found friction sounds and fluid on the right side. In this case we had to discuss the projjriety of surgical intervention. As the general condition was not bad, we agreed to see patient again before we decided. We had the satisfaction of witnessing the successive disappearance of the tubular breathing and the friction sounds, while the fever yielded and recovery ensued at the end of four weeks. A child, fourteen years of age, who had had several previous attacks, was again taken ill with appendicitis and pericsecal abscess. He was operated on by Jala- guier. The appendix, of the vertical t3rpe, had a bent extremity, which was adherent and communicated with the cfecum. Some days later dyspnoea came on ; dullness, with tvibular breathing on expiration, and aphonic pectoriloquy, were cUscovered at the right base. Some effusion formed, but was absorbed eight days later. Korte reports the case of a woman suffering from retrocsecal inflammation. In spite of incision, the infiammation passed through the diaphragm and reached the pleura. Resection of the eighth and ninth ribs ; patient recovered from the effusion, which, the author states, was serous. Another case of Korte's is that of a man, twenty- eight years of age, who was taken ill with sharp abdominal pains on the right side, DISEASES OF THE PLEUKA 353 fever, and shivering. A purulent collection necessitated surgical intervention, and a putrid phlegmon, which reached from the csecum to the diaphragm, was opened. An effusion, which was punctured, formed on the right side. The author describes it as serous. The patient finally recovered. Description. — The first point to note is the manner in which the appen- dicular infection reaches the pleura. How does a remote lesion like appen- dicitis attack the pleural cavity ? Why does appendicitis, which is a very small lesion, succeed in a few days in producing putrid pleurisy, with several pints of fluid ? Let us try to answer these questions. The infection, wliich becomes more virulent in the closed cavity of the appendix, causes the pathogenic microbes, Bacillus coli, and other aerobic or anaerobic germs to spread to the peritoneum. Sometimes perforation or gangrene of the walls of the appendix occurs, and the microbic pulp spreads widely over the peritoneum ; at other times the migration of microbes takes place through the imperforated wall, as we may see from specimens.* The infection, after reaching the peritoneum, behaves in different w^ays. It may only spread a short way from its seat of origin, being hmited or not by adhesions, or it may excite remote foci, wliich show no apparent relation to the original focus. These remote abscesses are due to microbes carried to a distance, but in what way we do not always know. Can these remote abscesses arise in the pleural, as in the peritoneal, cavity ? In other words, can remote pleurisy occur in the course of appendicitis ? Certainly ; but most often it is by proximity, through the peritoneal track, by way of the adhesions and of the lymphatics that extension to the pleura takes place. Under such circumstances the appendicitis is nearly always of the ascending type. The direction of the appendix is an essential factor. In appendicitis of the descending type the purulent collections and adhesions often form in the pelvis near the bladder and rectum, but in the ascending type the pus and membranes pass up towards the hver. The infection takes place from below upwards, because the initial focus, or 'primum movens, gives it this direction. It reaches the hypochondrium, passes through the diaphragm, and invades the pleural cavity, having marked its route by purulent tracts, so that it is possible to follow the infection from its small origin in the appendix to its full maturity in the thorax. Appendicular pleurisy nearly always occurs on the right side; there are very few exceptions to this rule. Let us now turn to the cUnical side of the question. At what moment may pleural com})lications ensue in appendicitis ? They appear about a week or a fortnight after the on.set of appendicitis. The infection, which starts from the appendix, does not begin its migration before the third or fourth day. Surgery has, therefore, time to intervene. By suppressing * Diculafoy, Clinique Mcdicalc del' Hutd-lJicu, 18'J7, pp. 345, .'>l(">, 347. 354 TEXT-BOOK OF MEDICINE the infecting focus at its commencement, the disease is cut off at the root. Let us not forget that appendicitis, whether slight or severe, may be fol- lowed by pleurisy, just as it may be followed by abscess of the liver ; in the case of appendicitis the benign nature is only apparent. Pleural com- pUcations are hardly hkely when the active process of appendicitis is extinct. The appearance of appendicular pleurisy is usually heralded by the symptoms which I have called abdomino-phrenic — viz., pain in the right hypochondrium radiating to the shoulder, dyspnoea, and apparent increase in the size of the liver. These symptoms are explained by the perihepatitis and the subphrenic empyema which often precede the stage of pleurisy. Pleural symptoms, pain in the side, and cough appear in their turn, and blend with the abdomino-phrenic ones. The abdomino-phrenic symptoms, which usually precede those of pleurisy, may themselves be preceded by abdominal symptoms of pain in the right flank, puffiness, and dullness ; they indicate the passage of purulent infection from the right iHac fossa to the hypochondrium. As appendicular pleurisy has not always the same course, we must study its various forms. As a rule, the pleurisy is putrid, with much effusion ; the fluid forms rapidly. The fever is variable ; dyspnoea, anxiety, loss of strength, weak pulse, sallow and earthy tint of the skin, bear witness to the gravity of the situation. It is true that the pleural infection is not the only cause : the peritoneal infection is responsible for its share. (Edema of the wall is not rare. We frequently find amphoric breathing and hippocratic succussion, which point to pneumothorax. At first we tliink of pleuro-pulmonary perforation, and do not admit the possibility of pneumothorax from putrefaction. In considering putrid right pleurisy, we must always think of appendi- citis, even though it has been so slight as to attract but Httle attention. We must reconstruct the appendicular and abdominal stages, which have preceded the phrenic-pleural stage by six or eight days. Whether there be pneumothorax or not, as soon as pleurisy develops suddenly, with grave symptoms, we should without delay investigate the nature of the fluid. Exploratory puncture is performed at once, and turbid, non-homogeneous, greyish or brownish foetid fluid is drawn off. In such a case, without waiting for the result of aerobic or of anaerobic cultures, operation for empyema must be performed immediately. The fluid, in a test-tube, divides into two layers ; the lower one forms a dense, dark- coloured deposit ; the upper has a serous or turbid appearance. Appendicular pleurisy has httle tendency to vomica; its course is so rapid and compUcations occur so quickly that the vomica has, doubtless, no time to occur. I know of only two cases : DISEASES OF THE PLEURA 355 One (Krokne) concerns a young girl with appendicitis and jjeripaecal peritonitis. Some weeks later subphrenic empj^ema occuri'ed, and was followed by fits of coughing and fcetid vomica. Laparotomy, performed forty-eight hours later, revealed a large subdiaphragmatic abscess, opening into the thoracic cavity. The condition might, perhaps, have been due to the opening of a subphrenic abscess without concomitant pleurisy. I would say as much conceriiiiig the following case, reijorted by Andre and Michel : A yoimg woman had appendicitis and peritonitis. Laparotomy evacuated a quantity of fcetid pus ; pleuro -pulmonary signs appeared later ; exploratory punctures made, in order to ascertain the nature of the fluid, gave no result, and an exploratory incision had no better success. The patient was seized with vomica and died. No autopsy was allowed. Such is the history of putrid appendicular pleurisy in its most common form. In some cases the fluid, as I have said, is serous, the infection is reduced to a minimum, and the condition resembles serous pleurisy, which absorbs spontaneously or yields to puncture. These benign cases of appen- dicular pleurisy are not accompanied by the grave symptoms of the preceding variety. Appendicular Subphrenic Empyema. — I have mentioned above how the infection ascends from the appendix to the pleura. In its course this infection marks its route by puridcnt collections, of wliich one is subphrenic empyema. The collection may be of Uttle or of serious import ; we may find from 1 to 3 pints of fluid. If the collection is small in amount the signs are difficult to recognize, but yet the subphrenic pain is a good guide. If the collection is abundant, we find, besides the pain, which may be made worse by pressure in the subphrenic region, deformity and bulging in the epigastric and right hypochondriac regions ; the Hver, which is pushed down by the effusion, appears enlarged, though it is only displaced, and, on the other hand, the dullness, wliich ascends towards the thoracic cavity, simulates a non-existent effusion in the pleura. Although the liver is surrounded by pus it remains free, and tliis point distinguishes it radically from appendicular infection of the organ, which is then riddled with abscesses. The reason is that the mode of infection is quite different in the two cases. In the former case the infection spreads by the peritoneum, and has nothing to do with tlie liver, while in the latter case, the infection is carried to the liver tissue by the portal vein. The infection, in its upward course, does not always reach the j)l<'ura, but is arrested in its progress and causes subplirenic empyema without consecutive pleurisy. Cases of tliis nature are not immerous ; they have been described by Leyden, by Mayal, Lang, and Greig Smith ; and in France have been treated in works which are reviewed in Lape}-re's monograph. Spillman has pubUshed the following case : 23—2 356 TEXT-BOOK OF MEDICINE ' A youth with appendicitis Avas, on the seventh day, seized with dyspnoea and very sharp pain between the nipple and the false ribs on the right side ; absolute dullness in the axilla and at the right base ; punctures were negative ; acute dyspnoea and death some days later. Post-mortem : purulent tracts and subphrenic collection, estimated at 4 pints, in addition to appendicitis ; the lungs were oedematous, but the pleura was free. Subphrenic empyema does, therefore, occur without concomitant pleurisy, but most often both lesions are present. Cases in which the abscess contains gas have been quoted, and deserve therefore the name of appendicular subphrenic pyopneumothorax. Speaking generally, pyopneumothorax is consecutive to perforation of a neighbouring organ, to ulcerations of the stomach and duodenum, to per- foration of the diaphragm, and communication with the thoracic cavity, etc. These cases of pyoj)neumotliorax are very rare, and when gas is found in the subphrenic focus it nearly always comes from perforation of a neigh- bouring organ, such as the stomach, intestine, but especially the diaphragm and air-passages. In a case published by Starcke, subphrenic pyopneumothorax was consecutive to appendicitis, but the presence of gas was explained by perforation of the diaphragm and communication with the bronchi. Greig Smith speaks of subphrenic pyopneumo- thorax following appendicitis. Here also the presence of gas was due to perforation of the diaphragm. Vanlair says a child presented an epigastric tumour (probably subphrenic empyema) after appendicitis. Three days later pneumothorax suddenly appeared on the right side ; the skin over the epigastric tumour became thin. An incision was made, letting out foetid fluid and gas. We may suppose that the gases in the sub- phrenic collection came from the concomitant pneumothorax. Case 1 (reported by Sallet). — A child had a swelling in the -epigastric angle, following appendicitis. At the same time abolition of vocal fremitus, segophony, and dullness were found at the base of the right side of the chest. Below the dull area amphoric resonance and bruit d'airain. Thoracentesis yielded foul pus. Next day lower ribs resected and the diaphragm incised. Pus and gas came out, and death supervened three weeks later. Post-mortem, the subphrenic pocket contained no pus, and the pleura only some serous fluid. Case 2. — A child had appendicitis ; eight days later painful swelling in the right hypochondrium ; diagnosis of subphrenic abscess, verified by operation ; death next day ; no autopsy. Eisenlohr writes : A youth had appendicitis ; symptoms of peritonitis supervened a week later. Some days afterwards tubular breathing at the right base, marked tym- panites and bulging of the hypochondrium. Patient died, and post-mortem, mild appendicitis, causing all these troubles, was found. Right side of the peritoneal cavity invaded by pus and adhesions. Between the liver and the diaphragm a pocket full of pus and gas. This pocket communicated through a perforation in the diaphragm with the right pleura, which also contained pus and gas. Appendicular subphrenic pyopneumothorax, therefore, exists. It is ushered in by the symptoms of subphrenic abscess, given above, with bulging, tympanites of the epigastrium or hypochondrium and acute dyspnoea. It may, therefore, be difficult to know whether pyopneumothorax is supra- or subdiaphragmatic. Does the gas in the subphrenic pocket come from a DISEASES OF THE PLEURA 357 communication with the air-passages, or can a putrid collection, as in putrid pleurisy, produce the gas ? The analysis of the cases which I have just quoted nearly always shows production of gas by effraction, perforation of the diaphragm, and communication of the subphrenic focus with the pleura or with a bronchus. In two cases only, tliis production by effraction has not been noted. It is possible that in subphrenic pyopneumothorax, as in putrid pleurisy, gas may result from putrefaction. Surgical intervention is the only treatment in subplirenic empyema. It must be early, and is often double ; it may be triple, and comprise the empyema, the pleurisy, and the appendicitis. In a case reported by Margery tliree successive operations were performed : first, laparotomy, to open the abscess in the ihac region and resect the appendix ; secondly, ten days later, opening of the subphrenic abscess ; and, lastly, operation for empyema some days afterwards. Remarkable to relate, the case terminated in recovery. XIV. FCETID, PUTRID, AND GANGRENOUS PLEURISY. This section is devoted to the pleurisy in which foid-smelling fluid is present. I propose to unite them under the general term of ozsenous pleurisies {S^eiv, to smell badly). The symptom which first attracts attention is the foul smell of the pleural fluid, whether it is evacuated by puncture, incision, or by vomica. A few drops drawn off by exploratory puncture are often sufflcient to exhale a foul odour. I, for my part, have seen several instructive cases Avhich I have described in my lectures at the Hotel-Dieu.* We have, therefore, material for clearing up the question of ozsenous pleurisy, which I shall divide into three groups — foetid, putrid, and gangrenous. Foetid Pleurisy. This name must be reserved for pleurisy in which the fluid is foul-smelling, while the stench is not due to putrefaction or gangrene. The term " foetid " implies that the pleurisy is neither putrid nor gangrenous. It is not putrid, for it has none of the characters of putrefaction and does not give off gas in the pleural cavity (the patient, therefore, has not pneumothorax) ; inocula- tion of the fluid does not cause gaseous inflammation, and the liquid, placed on a culture medium, produces neither fermentation nor l>ul)bles of gas in the test-tube. The pleurisy is not gangrenous, for we find neither sloughs in tlie fluid nor any trace of gangrene in the walls. This proves that the odour of the fhiid is not an index ftf pu< refaction * Dieulafoy, " Pleuresies Fetides, Putricles, Gangr^neusea " {Clinique Medicale de I'Hi'M-lJieu, \W:i, vol. iv.. IJ'"" et 4"'"' If9()ns). 358 TEXT-BOOK OF MEDICINE or of gangrene, in the same way as fcstor of the breath and of the expectora- tion does not always mean gangrene of the lung. Tliis important distinction had not escaped the notice of Laennec and Trousseau. The cases of sero-purulent or purulent pleurisy that are simply foetid, without putrefaction and gangrene, are so frequent that it would be common- place to publish them. The fluid was foetid in several of the cases reported in my lectures on interlobar pleurisy. It is to be noted that encysted pleurisy is more often foetid than putrid or gangrenous, while putridity and gangrene are common in pleurisy of the great pleural cavity. Pleurisy of the great pleural cavity may not be foetid, as is proved by the following case, which is, I believe, the only one of foetid pleurisy that has been closely examined by cy to- diagnosis and cultures, and confirmed by experimental research : A man, twenty-seven years of age, admitted for pain in right side, obstinate cough, and foetid expectoration. Disease began six weeks before. He was taken ill with shivering fits, fever, and sharp pain in the right side of the chest. Fits of coughing soon supervened, and he brought up much yellow but odourless expectoration. The pain, which extended all over the right side, had its maximum behind, below the scapula, and the expectoration became foetid. The man looked ill ; respiration rate increased, and his temperature was 103° F. The sputum glass was filled with diffluent fcetid expectoration of a greyish-yellow colour. It had never been blood-stained. The breath was also fcetid. The foetor was, however, not like that of gangrene. Examination of the sputum revealed neither blood, elastic fibres, nor Koch's bacilli, but numerous microbes. Thi'eads, bacilli, cocci, diplococci, and streptococci ; no pneumococci. Dullness behind most marked over middle and inferior part of chest. On ausculta- tion, subcrepitant rales above this zone, and at the level of the eighth intercostal space, 4 inches from the median line, cavernous breathing, but no gurgling — a fact which proves that the condition was due to consolidation of the lung, and not to cavity. Below this zone, on expiration, tubular breathing of a pleuritic tone. Exploratory puncture gave exit to a serous fluid, which was for the time being odour- less. Cy to -diagnosis showed polynuclear cells ; no lymphocytosis, no endothelial plaques. The absence of lymphocytosis ehminated acute tubercular pleurisy. The absence of endothelial plaques put mechanical pleurisy out of the question. We had to do with an acute infectious pleurisy, consecutive to a similar lesion of the lung. However, one thing puzzled us : the pulmonary lesion was foetid and the pleurisy was not. The lesion of the lung resembled neither pneumonia nor broncho -pneumonia. We might have considered hepatization of the lung, resembling somewhat the infarcts consecutive to septic emboli, but we found no suspicion of such an origin. The left side of the chest was healthy and the heart was normal, while the urine contained neither sugar nor albumin. During the next few days the situation changed. The patient looked ill, was pros- trated, and had an earthy tint. The cavernous breathing diminished and the foetid expectoration was less abundant, but the pleural effusion made rapid progress. The dyspnoea increased, the temperature rose to 103° F., and exploratory puncture yielded turbid fluid, like dirty water, and horribly foetid, although some days before it Avas yellowish and odourless. The absence of pneumothorax eliminated putrid pleurisy. The fluid was placed on culture medium and inoculated into a guinea-pig. As the case demanded immediate surgical intervention, Legueu resected the ribs. The incision let out 4 pints of fluid, which resembled muddy water, and had a very DISEASES OF THE PLEURA 359 marked fcetor. No gas, no membranes, no shreds of slough. The finger could only just reach the retracted lung. No adhesions. Result of operation excellent. In a ie^v days the sputum became less abundant and lost its foetid odour. Recovery complete in six weeks. Examination of the foetid fluid from the second puncture (Apert). The fluid was not purulent in the true sense of the word, but turbid and analogous to dirty water. On direct examination with the microscope, this fluid, which at the first puncture was rich in polynuclear cells, now contained only cellular elements in the form of granular masses, which stained badly and did not show nuclei. They were dead leucocytes, showing granular degeneration. Further, many different microbes were found, in- cluding long thin threads, thin and short bacilli, and small micrococci. All these microbes, except some micrococci, did not stain by Gram. On aerobic cultures (agar and broth), colonies of Staphylococcus cdbus. On anaerobic cultures (thick agar), colonies having the appearance of white lenticular points. No development of gas among these colonies, either upon glucose agar or on ordinary agar ; the cultures remained odourless. Microscopical examination of these colonies showed that they were composed of masses of a small micrococcus, which did not stain with Gram, and resembled Veillon and Zuber's Staphylococcus parvulus. A cubic centimetre of freshly-drawn fluid, inoculated under the skin of a guinea- pig, produced neither pus nor gas, and the animal remained in good health. Such was the history of tliis case. Let us discuss it. The patient showed two stages of infection — the one puhnonary, the other pleural. Although the expectoration and the fluid were foetid, there was no resem- blance to gangrene. Was this a case of putrid pleur-isy ?* At first sight it might have been thought so, but proof is absent. All the signs of putridity were wanting : no formation of gas in the pleura, no pneumothorax, no gaseous inflammation along the track of the aspirating needle, no bubbles of gas in the test-tubes, and no gaseous lesions in the tissues of the inoculated animal. Foetid pleurisy remained. This man evidently had had foetid pleurisy, set up by a similar lesion in the right lung. There is nothing to show that, had the pleurisy been left to itself, it would have become putrid. The fluid in footid'pleurisy is turbid or sero- purulent, and we find aerobic or anaerobic microbes in great variety, which, though little apt to produce putrefaction or gangrene, may give off a foul odour (that of asafcetida), just as other microbes (chromogenes) give off colouring substances. This variety is the least formidable of the group of ozsenoas pleurisy ; it does not rapidly cause grave symptoms (adynamia, tendency to collapse, and syncope), but it must be discovered as quickly as possible by exploratory puncture and operated on without delay. The differentiation of foetid from putrid and gangrenous pleurisy is not always easy at first, and the degree of foetor is not sufficient to make a diagnosis ; la])oratory experiments and operation are sometimes necessary to confinn it. * " La IMeuresie Medinstine " (('llni/ » ' ^^& A It V ^ 'v'^*'°V ($; ^ :::x ■ss- Fig. 18. — Temperature Chart. bacillus), which was isolated or disposed in pairs and masses, and stained with Gram. The other species showed itself in the form of yellowish muriform colonies, due to fine cocci in mass. Experiments were made upon animals. One guinea-pig received under the skin ^ c.c. of vaginal pus, and another ^ c.c. of pleural pus, without result. A rabbit received i c.c. of pleural pus in the veins, without any other result than serious indisposition, which yielded after two days. These researches allowed us to recon- struct the nature and the course of the infection. The disease occurred in two stages. The toxi-infection started from the fundus vagina?. Halle has shown that the vagina normally contains aerobic microbes in the form of a streptococcus, differing from the Streptococcus pyogenes, and strictly anaerobic microbes, which, after inoculation of animals in pure culture, cause abscesses and gangrene. The aero-anaerobic toxi- infection had therefore arisen in the plugged vaginal cloaca. The infectious germs had been carried by the veins to the right heart, thence to the lung, and had passed into the pleura. Infection of the lung showed itself by rigors, fever, and i^ain in the side. An ill-defined area of lung had been embohzed and converted into a putrid, but not gan- grenous, infarct. The pleural fluid, which was odourless at the first puncture, was putrid at the second one. We thus built up the vaginal, pulmonary, and pleural stages of the infectious process. In tliis series of infections tlie infection was putrid, but not gangrenous. It was DISEASES OF THE PLEUKA 363 putrid, as proved by the production of gas in the anaerobic cultures. It Tvas not gan- grenous, for we drew off from the pleura no sloughing shreds. An analysis of the sputum revealed neither fibres nor sloughs. Here the process of putrefaction was not associated with mortlGcation. The history of appendicitis furnishes us with many cases of putrid and of gangrenous pleurisy. I have discussed appendicular pleurisy in a pre- ceding section. It may, indeed, be said that appendicitis is one of the most frec^uent sources of purulent pleurisy. As a model let me mention the following case : A man came to us moribund, with extensive right pleurisy, complicated by pneumothorax, and died some hours before the operation. His history and the autopsy enabled us to reconstruct the morbid picture. The pleura contained 7 pints of foul- ameUing pus and gas. Pleurisy and pneiimothorax were the result of appendicular infection. The lesions, which started from the appendix, began in the right part of the abdomen, and reached the right thoracic cavity. The putrid infection here was not of embolic origin, as in the preceding case, but the lesions spread by continuity. I think it useful to quote cases of putrid pleurisy : Widal's Case. — Man suddenly taken ill with acute pain on the right side of the chest and violent dyspnora. Tiie pain, after rehef from an injection of morj^hia, reappeared. The dyspnoea increased, the cough became paroxysmal, the general condition grew worse, and the patient was admitted under Widal. At the left base, dullness and tubular breathing (effusion) ; above, tympanites and amphoric breathing (pneumothorax). The dyspncea was so acute that a puncture was at once made, and gave exit to 2 pints of puriform fluid of extremely foetid odour. No improvement. Next day the signs of hydropneumothorax were complete. Around the puncture a bright red swelling developed, which on pressure yielded gaseous crepitation. The gaseous inflammation commenced some hours after the puncture. Ojieration decided upon, but the patient died before the surgeon's arrival. Post-mortem : On opening the thorax, greyish, sanious, and extremely foetid fluid, mixed with gas, escaped from the left pleura. The pleur?e, after removal of the false membranes, were carefully examined. These membranes were fibrinous and not ad- herent. No trace of gangrene found on the serosa. The left lung was also examined with the greatest care : no tubercules, no foci of broncho-pneumonia, no gangrene. This case, then, is one of putrid pleurisy without gangrene. The pathogenic agent was the Proteus vulgaris. A guinea-pig was inoculated under the skin with 1 e.c. of pleural fluid. Next day a large pocket developed at the point of inoculation, and gave very evident gaseous crepitation on palpation. On the skin which covered tin's gaseous aliscess an ulcer soon formed, and gave exit to sanious and fcrtid fluid containing various microbes, chiefly tlie Proteus vuk/aris. Courtois-SufTlfs Case.— A man, twenty-three years of ago, who had had chills and pail) in tlic sifle at tlio right base, came into the Beaujeon Hospital. Kight pleurisy with eflusion, estimated at 2 pints. In a few days the dyspnoea was marked, the patient ])ecame cyanosed, and thoracentesis was necessary. The puncture gave exit to about 1 J l)ints of puriil(!nt fluid, which was extremely feet id. Next day, at the seat of puncture, an (edematous and reddish swelling appeared, which had the appearance of a phlegmon, and oxttmded as far as the base of the thorax. On paljiation, fine crepitation, due to gaseous inflltration. During the next few days the situation grew wor.sc: the temperature \\as about lO.T F., sweats were abundant and fcrtid, the face was bloated and earthy, and the dyspno'a acute. Thoracotomy gave exit to fluid pus, whicli was extremely fu'tid and of a brownish tint. Tiio pleural cavity was then washed out with a very 364 TEXT-BOOK OF MEDICINE weak solution of permanganate of potash. After some nps and downs the patient died. The results of the autopsy were : In the chest -wall a gaseous inflammation around the seat of the puncture, pleural cavity contained a little fluid, pleura thickened, but no trace of gangrene in the lung or the pleura. Boinet's Case. — Well-built man, twenty-four years of age, seized with rigors, cough, and acute pain at the lower part of the left side of the chest. Left pleural effusion, with amphoric breathing and metalhc tinkling (pyopneumothorax). The situation rapidly became worse. Puncture yielded sanious pus of extremely foetid odour. Next day operation for empyema gave exit to 4 pints of stinking pus and gas. "Patient died twelve days later. Post-mortem, Boinet found three pockets in the pleura, containing putrid fluid mixed with gas. No communication with the lung, no tubercular lesions, and no gangrene in the lung or the pleura. Netter's Case. — Child with pyopneumothorax. Puncture gave exit to foetid pus and gas. Subcutaneous emphysema then developed. Broca operated for empyema, and the child made excellent progress. With regard to these cases of putrid pleurisy, Netter says that he has found an anaerobic bacillus in the form of long, thin filaments, mixed with other micro-organisms. Description. — These cases give a clear idea of putrid pleurisies. They chiefly affect the great pleural cavity, unlike foetid pleurisy, which is usually encysted. The fluid is sero-purulent, turbid, greyish, and not homogeneous ; when placed in a test-tube, it divides into two layers — the lower dense and opaque, the upper more transparent. These cases frequently have an embohc origin ; the original focus may be in the vagina or the appendix, as was the case with our patients, in otitis, in osteomyehtis, in phlebitis, etc. In some cases putrid pleurisy results from neighbouring lesions (lung or mediastinum). It may be set up by abdominal mischief, renal or hepatic suppurations, subphrenic empyema, with or without perforation of the diaphragm. In other cases the cause and the origin remain unknown. The microbes, which are chiefly anaerobic, lead to the formation of gas (putrefaction) in putrid pleurisy. The appearance of pneumothorax without perforation of the pleural cavity is thus explained. This pneumothorax, formerly called essential, is quite different to pneumothorax by perforation. The latter is due to the introduction of air into the pleura, while the former arises without the presence of air. From the clinical point of view we find in both forms the same physical signs — viz., tympanites, amphoric breathing, metallic tinkling, and liippo- cratic succussion. Gas may form in the walls of the thorax and produce gaseous phlegmon. Simple aspiratory puncture sows the germs in the chest-wall, and a gaseous phlegmon with oedema follows in a few hours. Experimental research yields analogous results. The inoculation of a drop of pleural fluid in the cellular tissue of an animal provokes gaseous phlegmon (Widal). DISEASES OF THE PLEURA 365 Lastly, the development of gas may be abundant in anaerobic cultures ol the pathogenic agents of putrid pleurisy. The diagnosis of putrid pleurisy is impossible before puncture. Every case is accompanied by general symptoms, which rapidly becom,e grave, and comprise small, quick pulse, dyspnoea, prostration, and collapse — symptoms which are rarely found in other varieties of pleurisy. In such a case the additional presence of pneumothorax is in favour of putridity, but yet the putrid nature of the effusion can only be established by exploratory puncture. Accordingly, if we are in doubt, even though the effusion is scanty, we must confirm the diagnosis by early puncture. Furthermore, puncture should immediately be followed by thoracotomy, with or without resection of ribs, for the needle track may rapidly become infected, and diffuse gaseous inflammation may develop in a few hours. But it will be said puncture only shows us the foetor of the fluid ; it does not at once reveal putridity. To this I would reply that it matters Httle whether the pleurisy be foetid or putrid : every foul-smelling pleurisy should be operated on without delay. Gangrenous Pleurisy. The phenomena of putrefaction just described are common to putrid and to gangrenous pleurisy. These two varieties are distinguished, not by the foetor of the fluid, but by the shreds of slough which float in the effusion or are adherent to the walls. The description of putrid and gangrenous pleurisy present many similar points, yet the latter may assume two forms which are of importance : sometimes the lung is not involved; at other times the gangrene is pleuro- pulmonary, and is then far more grave. I shall here quote cases of the former variety : Comby and Vogt's Case. — Young girl, eleven years of age, taken ill with left pleurisy. Some days later she woke up with true orthopnooa. Next day Comby and Vogt found extreme dyspnoea, temperature 104 "" F., signs of effusion at the base of the left chest, and above those of pneumothorax. First diagnosis was pneumothorax from tubercular perforation of the lung. Four days later puncture gave exit to a pint of very foetid pus. The first diagnosis was then changed to gangrenous pyopneumothorax. Comby incised the seventh intercostal space, and came on a mass of false membranes, which he Ijroke up with the hnger. Four or five pints of horribly fcetid pus came out. The child finally recovered. Rendus Case.* — A man who looked phthisical was admitted for pncurao- thorux. He was wasted, cyanosed, and much distressed; cough frequent, breath had no odour, and temperature was normal. Pleural eftusion at the right base and above j)neumothorax. Succussion splash and metallic tinkling. This condition was said to have begun with violent pain in the right side. On the day after admission his condition * Meeting of February 3, 181)9. Althoiigli the author has entitled his papi r " Putrid Pleurisy," the putrid pleurisy was in reality gangrenous, because he found " a large lihrecl of sloughing tissue, in which elastic fibres were discovered under tlio niiiroscope. 366 TEXT-BOOK OF MEDICINE was alarming. Dyspnoea was acute, cyanosis was marked, and the heart was dis- placed ; puncture yielded extremely foetid pus. Rist at once operated. One and a half jjints of foetid pus came out, and the cavity was washed out with a solution of permanganate of potash. Two days later painful oedema -with emphysematous crack- ling was found at the right base. An incision was made, and very foetid serous fluid, mixed with bubbles of gas, let out. Later a phlegmonous patch of the same nature appeared on the left arm, at a spot which had been vaccinated some days before. The condition of the patient became very alarming. Restlessness and dehrium were acute ; the pus from the empyema again became very foetid, and washing-out of the pleura brought away a large slough of blackish gangrenous tissue, which was extremely foetid, and showed elastic fibres under the microscope. Patient finally recovered. Bacterio- logical examination showed the presence of anaerobes. Let us now turn to those cases in which we find gangrene of the lung and of the pleura ; it is usual for grangrene of the lung to precede that of the pleura. To avoid repetition, I would ask the reader to turn to the section on Gangrene of the Lung. Pleuro-pulmonary gangrene, hke that of the lung, may have an emboUc (otitis, appendicitis, etc.) or an aerial origin. As the points have been discussed under Gangrene of the Lung, I shall not repeat them. The descriptions of gangrenous and of putrid pleurisy in part blend. Acute pain in the side, fever, bad pulse, earthy tint of the skin, dyspnoea, prostration, and tendency to collapse, show the extreme gravity of gan- grenous pleurisy ; fcetor of the breath, stinking and blood-stained sputum, show the participation of the lung in the gangrenous process. As regards prognosis, the addition of gangrene marks a further step in the gravity of putrid pleurisy ; but in reahty these two varieties are so closely alhed that they almost come under one description. The same aero-anae- robic agents which produce pleurisy — that is simply putrid — may cause gangrene either in the patient or in animals used for experimental research. In Widal's case the gangrene was absent, but yet inoculation of the pleural fluid in a guinea-pig " produced a gaseous and gangrenous abscess in the animal, which died after extensive sloughing of the skin of the abdo- men and thorax." In Rendu's case the pleurisy was labelled putrid, but yet a gangrenous shred was found later in the thoracic cavity. The line of cUnical demarcation between putrid and gangrenous pleurisy is, therefore, not absolute ; putrefaction and mortification may appear together or in succession. The spread of gangrene from the pleura to the lung can only be recog- nized by foetor of the breath and of the expectoration, and by the presence of elastic fibres and sloughs in the sputum. Such is the history of stinking pleurisies and their tliree groups — foetid, putrid, and gangrenous : the foul smell of the effusion, which is the first step in diagnosis can only be revealed by early puncture, and immediate surgical intervention is the only method of treatment. DISEASES OF THE PLEURA 367 XV. VOMICA. Definition. — Considering only its etymology, the word vomica (from vomere, to vomit) is improperly applied to the symptom which we are about to describe ; custom, however, has consecrated it, and the word vomica serves to describe the rejection of pus by the respiratory channels, just as haemoptysis denotes the rejection of blood from the same passages. Custom has even gone farther, and, by an abuse of language, has finally included under one term the symptom and the lesion, so that we speak of pulmonary, pleural, or hepatic vomica — that is to say, a purulent collection in the lung, pleura, or in the liver, which has burst into the bronchi and has been coughed up. Description. — The complete study of vomicse comprises the diagnosis both of the symptoms and of the lesion. I shall here outhne the chief varieties. 1. Pulmonary Vomica. — Pneumonia suppurates fairly often (grey hepatization), but the pus very rarely collects in the form of an abscess. The works of Laennec, Graves, and Trousseau, show how rarely pulmonary abscesses occur in the course of pneumonia ; they are so rare, indeed, that Grisolle has only collected twenty-three proved cases. These abscesses sometimes form very rapidly, on the fifth day of pneumonia (Woillez), or on the twelfth, and are never rejected later than the twentieth day. The pus from the pulmonary vomica is scanty, phlegmonous, sometimes mixed with blood, and of a brownish colour. The pneumococcus is the pathogenic agent. Directly after the evacuation of the abscess the physical signs change, and where the signs of pneumonia have been present we now find cavernous breathing and splashing sounds. 2. Pleural Vomicae. — These vomicse are much more frequent and follow interlobar, mediastinal, or diaphragmatic pleurisy, or pleurisy of the great pleural cavdty. The vomica of interlobar pleurisy is the most frequent of all. Speaking generally, vomicse of the pleura appear much more slowly than those of the lung. Purulent collections in the pleura open into the bronclii after three to six weeks, and later still when the great pleural cavity is affected. As an exception to this rule, when purulent pleurisy develops in a child, or in a woman during the puerperal state, the vomica may appear from the second to the third week (Trousseau). The symptoms are different, according as the vomica is provoked by partial pleurisy, which only contains some ounces of pus, or by pleurisy of the great pleural cavity, wliich may contain several pints. In encysted dia[)iiriigniatic or interlobar pleurisy the quantity of usually fcEtid pus brought up at the moment of the vomica does not exceed some ounces ; it then gradually diminishes, and, in fortunate cases, the pleuro- 368 TEXT-BOOK OF MEDICINE bronchial fistula closes. This mode of cure is possible in metapneumonic interlobar pleurisy. I would refer the reader to the section on Interlobar Pleurisy. In the case of the great pleural cavity, when the pleura contains 4 or 5 pints of pus, the course is less simple. The bursting of pus into the bronchi often determines dyspnoea, bordering on asphyxia. Fatal cases have been quoted, and the patient, who has extreme distress, brings up streams of purulent fluid through the mouth and the nose. The first evacuation is generally followed by improvement, and then the patient, while changing his position or coughing, continues to bring up some ounces of pus. He no longer appears to vomit, but only to cough up the pus. As soon as a certain quantity of pus has accumulated in the pleura, the patient is seized with fits of coughing, and voids the pleuritic fluid five, six, or ten times a day. Sometimes the evacuation of pus stops, but is repeated one or more days later, and in some cases the breath and the fluid evacuated become horribly foetid. Unless the fistula is so constituted as to form a valve (Chomel), the inspired air enters the pleural cavity, and the signs of pyopneumothorax are found. Does pleurisy become purulent when the vomica has once formed ? Several modes of termination may occur ; one is recovery, which is rare in general but possible in interlobar pleurisy, especially in the metapneumonic variety. In some patients the improvement consecutive to the vomica is only transient ; the cavity becomes infected, and the fever does not cease, while the patient loses appetite, becomes cachectic, and finally succumbs. In other patients the cavity shrinks, but the pleura and the lung are invaded by fibrosis, with or without dilatation of the bronchi, which, sooner or later, compromises the individual's life. The preceding description will have made it apparent that the pleural vomica only occurs in empyema. There are, however, some extremely rare cases in which sero-fibrinous pleurisy is terminated by vomica. 3. Vomica with Hydatid of the Lung.— The pleural vomicae which I have just described are the most frequent ; there are, however, some rarer varieties, which I shall now review. Suppurating hydatids of the lung may cause vomicae which simulate pleural vomica, with this difference, however — that we find fragments of hydatid membranes and booklets in the rejected matter. 4. Vomica in Congestion Abscesses. — Chenieux's paper contains nine cases of vomicae, consecutive to congestion abscess, following Pott's disease. The pus often contains bony sequestrse. 5. Vomica from Suppuration of the Liver. — Abscesses and suppurating DISEASES OF THE PLEURA 369 hydatid cysts of the hver may result in vomica ; adhesions are estabUshed by the intermediary of the diapliragm, perforation follows, and the patient voids the Uver abscess through the bronchi. When the vomica has its origin in an abscess of the liver the pus is reddish, tliick, and sometimes fcEtid ; when the vomica is consecutive to a suppurating hydatid of the Uver, the purulent fluid is mixed with hydatid membranes. 6. Vomica with Suppuration of the Kidney. — Suppurating cysts of the kidney and pyonephrosis may terminate by vomica. It is not customary to consider as a true vomica the quantity of pus which may be brought up at one time by a patient with dilatation of the bronchi ; it is, however, a pseudo-vomica of which the distinctive characters should be well known. The treatment of vomica varies with its causes, and surgery gives the best results. XVI. CHYLIFORM AND CHYLOUS EFFUSIONS OF THE PLEURA. The pleura, Kke the peritoneum, may contain milky effusions which have the appearance of an emulsion. On thoracentesis we expect to find a sero- fibrinous or purulent effusion, but we draw off chyliform fluid. This fluid is odourless, and has no tendency to coagulate, because it is not fibrinous ; in a test-tube it forms no deposit in its lower part, and will keep for days or weeks without putrefaction ; under the microscope it shows some leucocytes, and in most cases contains a large number of fine fatty granules, soluble in ether, while chnical analysis reveals a large increase of fatty matter. The onset may be ushered in by acute pain in the side, but is more often unnoticed. The collection increases insidiously, Uke a subacute pleurisy. This latent period may last eighteen months. The effusion at length causes distress, displaces organs, especially the heart, and flattens the lung. It may become a cause of dyspnoea, but is not accompanied by the general symptoms of fever which are so frequent in purulent effusions. Chyliform effusion shows no tendency to absorption. After it has been evacuated, it recurs obstinately. Punctures relieve the patient, who thinks iiimself cured ; but the fluid slowly reforms, and fresh evacuation becomes necessary after a more or less extended period, during which every morbid symptom has apparently disappeared. ChyUform effusion at times gives way to empyema, in wliich case the staphylococcus is usually in evidence. Fever appears, with pain in the .'^idc ; the chest- wall becomes cedematous ; the effu.sion rapidly increases ; tiic fluid makes its exit by vomica, and death soon follows. More rarely chyliform effusion recovers after first becoming sero-fibrinous. 24 370 TEXT-BOOK OF MEDICINE The clinical picture just sketched is that of tubercular chyUform pleurisy ; indeed, tuberculosis is the cause in two-thirds of the cases. I have had a remarkable example. Patient admitted in May, 1899, to the Hotel-Dieu, with an effusion of 3 pints, which had Ijeen practically latent. His general condition appeared excellent : no wasting, no fever ; if he had not suffered Avith severe dyspncea, he would not have given up his work. About 40 ounces of characteristic chyhform fluid were drawn off. He felt better, and asked to go out. He was, however, persuaded to remain for some weeks. In three weeks 60 ounces were clra-«Ti off by successive pimctures. The effusion at length seemed to dry up, and the patient went out, persuaded that he -was cured. We saw him again five years lat«r, when he came to be treated for sciatica. He was work- ing without feeling any malaise. He looked well, did not cough, and only found that he readily became breathless, and at times felt some pain in the chest. The physical signs of effusion, however, were present, and thoracentesis yielded similar fluid to that dra^vn off five years before. His condition remained good for about a month, but then, mthout ajipreciable cause, his temperature ran up, and severe pain in the side developed. Exploratory puncture showed the chyhform effusion had been replaced by pm'ulent fluid, containing staphylococci. He died four months later. In other more rare cases the disease runs a rapid course, but the efiusion is r.ather lactescent than chyhform, and develops in the course of confirmed phthisis. I have recently seen such a case in which the fluid was in turn sero- fibrinous, serous, lactescent, and purulent. The patient died in ten months. While tuberculosis is present in two-thirds of these cases of lactescent effusion, cancer is only present in one-third. At times the patient has had a growth for a long wliile, and the chyhform effusion is only a secondary condition. At other times the pleuro-pulmonary cancer is primary. The onset of the malady is almost silent. Both acute dyspnoea and sharp pains attract the patient's notice, and we find a very large effusion, which, on puncture, shows all the characters of chyhform fluid. In some cases a few red corpuscles may be present. The fluid forms again with extreme rapidity, and we may find, after evacuation, that the resonajice does not return to normal. In a short while puncture gives no rehef : the aspirating needle has to travel through a much thickened wall. At last puncture yields only a little bloody fluid, and the signs of compression, the dyspnoea, and the pain still persist. The patient wastes and grows weak, and fever may appear. Such a picture is quite opposed to that of tubercular chyh- form pleurisy. It is always easy to recognize the nature of chyhform pleurisy by the appearance of the fluid, by its microscopical analysis, and by its chemical composition. It is, however, more difficult to ascertain its pathogenic cause. If the patient has proved phthisis or evident local tuberculosis, the diagnosis will naturally be in favour of tubercular effusion. On the other hand, the existence of visceral cancer, rapidly progressive course, signs of pressure in the mediastinum, with oedema and collateral circulation. DISEASES OF THE PLEURA 371 enlarged glands in the axilla, and the appearance of phlebitis, all point to cancerous effusion. The final appeal must always be made to laboratory methods. Cyto-diagnosis, as a rule, shows only a few cells in a case of can- cerous effusion. Nattan-Larrier found neoplasm cells, while endotheUal plaques were discovered in a case of lactescent effusion, which supervened in the course of leucocythsemia (Sicard and Monod). Inoculation into the peritoneum, or better, into the mamma, of the guinea-pig will often prove that the chyhform fluid is tubercular. This method was employed in two cases under my care. The causes of chyliform effusion in the pleura have been as much dis- cussed as the causes of chyliform effusion in the peritoneum, and are quite comparable in each case. The older writers thought that the effusion of chyle in the pleura followed rupture of the thoracic duct. Tliis opinion no longer holds good. In one of Debove's cases the thoracic duct was healthy, and a similar finding occurred in two of my cases. Granulo- fatty degeneration of the chronically thickened layers of the pleura (Quincke) has also been invoked. In Debove's case the pleura was covered with tissue some milhmetres in thickness, made up of several superposed layers, which showed numerous fatty granules under the microscope. In one of my cases Nattan-Larrier found very dense mature fibrous tissue, which had undergone hyaline degeneration in places. Every trace of fibrinous exudate had disappeared ; the cellular infiltration was but little marked ; the vessels, though scanty in the superficial layer of the neo-membrane, were numerous in the deep parts. Some giant cells were also present near the lung, which was sclerosed. Recent researches seem to show that the chyhform aspect of the fluid results from disintegration of its cellular elements (leucocytes or cancer cells). As the result of a cause which has so far escaped us, the cellulai elements in suspension in the fluid are said to degenerate, and give rise to fatty and albuminous fluid if the disintegration is incomplete, and to purely fatty fluid if the transformation is perfect. This hypothesis has been confirmed by Nattan-Larrier, who has seen in vitro the serous fluid from cancerous pleurisy change aseptically into lactescent fluid, while the number of cells rapidly diminished. Chylous Effusion. — Apart from the undoubted cases in wliich the effusion is not chyle, we find others which are true cases of chylothorax, the effusion being chylous. Shaw has collected twenty-cases. Traumatism was the cause in one-third of these cases. The others were said to result from an obstacle to the lymph-flow, with or without rupture of the thoracic duct, or of the great lymphatic vessels (cancerous glands or lymphadenoma in the mediastinum, obhteration of the thoracic duct, thrombosis of the sub- clavian vein). The diagnosis is easy when the effusion follows trauma. 24—2 372 TEXT-BOOK OF MEDICINE A man had his chest caught between the driving-wheel of a steam-engine and a wall. He was taken to the hospital, where the left clavicle and several ribs were found to be fractured. Two days later effusion was discovered in the left pleura. Exploratory puncture yielded milky fluid of a rosy colour. Chemical and microscopical examination showed the presence of chyle, mixed ^vith blood. Ten days later the red corpuscles had disajipeared, and the effusion had the appearance and composition of pure chyle. Absorption took place mthout complications, and the patient recovered fairly rapidly (Handmann). In cases of this nature the effusion results from rupture of the thoracic duct. It is situated on the left side (Wiesinger, Kummel), It has the histo- logical composition of chyle, but its chemical composition varies with the nature of the fluid and the time of digestion ; glucose and peptones may be found in it, and the proportion of fat will increase considerably after the ingestion of butter (Strauss). In cases of this nature, when the rupture is due to an injury, the prognosis is not bad. Let us now note a third group of cases, in which the lactescence of the effusion is not the result of a local infection, but the consequence of a general alteration in the fluids of the organism. It is in cases of this kind that we see the coexistence of identical effusions in the various serous cavities ; chyliform effusions have been seen at the same time in the peritoneum, the pleura, and the pericardium (Bramwell). The blood-serum (Achard), the serous fluid from blisters, and the liquid from oedematous areas may be opalescent. This opalescence of serous effusions is comparable to the opalescence of the blood-serum described by Widal. The prognosis depends upon the general condition. Finally, in some cases chyliform effusion into the pleura may result from the presence of the Filaria sanguinis (Lancereaux). XVII. HYDROTHORAX. Hydrothorax is hydrops of the pleura. Both pleurse are often affected, and the fluid is analogous to blood-serum, and very poor in corpuscles. The condition is a kind of serous transudation analogous to that of oedema. Hydrothorax is the result of mechanical causes, of which the most common are lesions of the mitral orifice, and of dyscrasise, of which the most usual are cachexia and Bright's disease. Hydrothorax is therefore only a symptom which supervenes as a com- plication in the various morbid states I have just enumerated. It estabhshes j itself in an insidious fashion, Avithout fever and pain ; its physical signs] resemble fairly closely those of pleuritic effusion. The cyto-diagnosis has been given under Pleurisy. DISEASES OF THE PLEURA 37^ XVIII. PNEUMOTHORAX— HYDROPNEUMOTHORAX. Pneumothorax (Itard) implies the presence of air or of gas in the pleural cavity ; if fluid is also present, the lesion takes the name of hydropneumo- thorax, and if this fluid is pus, the case is one of pyopneumothorax. Pathogenesis. — There are two chief varieties of pneumothorax : pneumo* thorax by perforation, and pneumothorax by putrefaction. The former is the more frequent, and results from the passage of air into the pleural cavity. Injury, wounds of the pleura and lung, tuberculosis, emphysema, strains, infarcts, superficial haemorrhagic nodules, general and interlobar purulent pleurisy, foci in the peribronchial glands, cysts, or abscesses of the hver and of the kidney, are the usual causes of these pleuropulmonary perforations. * 1. Strain and Emphysema. — Pneumothorax may appear suddenly, following a strain, whether the patient have emphysema or not. An emphy- sematous patient may also be suddenly attacked by pneumothorax, even though he has made no effort. In these various cases the rupture of the air- vesicles permits the air to reach the pleural cavity, the vacuum is destroyed, the lung shrinks and collapses, and pneumothorax is produced. Galliard has collected thirty-seven cases of pneumothorax from strain. A bugler was suddenly taken ill with pneumothorax while vigorously blowing his iastruraent. A clergyman was seized with pneumothorax during a fit of hearty laughter. A man was taken ill with pneumotliorax. while raising a chair with his arm extended. A student was seized ^vith pneumothorax while dancing vigorously. In this variety of pneumothorax the onset is sudden, with tearing pain in the thorax, and very acute dyspnoea. The classical signs are at once evident — tympanitic resonance and amphoric breathing. Although terrible at its onset, this form is not grave, for there were only tlu*ee deaths in thirty-seven cases (Galliard). The pneumothorax remains pure, the presence of fluid (hydrothorax) is very rare, and suppuration (pyothorax) is the exception. The perforation usually becomes obhterated, the air effused into the pleural cavity is absorbed, the lung resumes its function, and recovery follows in a few weeks. 2. Tuberculosis. — Tuberculosis is the most usual cause of pneumo- thorax. Perforation of the lung may supervene, either at an advanced stage (cavity and softening) or at the onset during the first stage. Cases have, indeed, been quoted, and I have seen them myself, in which pneumothorax * Sauasicr, who has collected 131 cases of pneumothorax, classifies them, according to their causes, as follows: Pulmonary phthisis, 81; pleurisy, 21; gangrene of tlie lung, 7 ; emphysema, 5 ; pulmonary apoplexy, 3 ; cancer, 1 ; abscess of the hmg, 1 ; liydatid of the lung, 1 ; hepatic abscess, I (" Recherchos sur Ic Pneumothorax," Paris, 1S41). 374 TEXT-BOOK OF MEDICINE occurred in an apparently healthy person, and was the precursor of tubercu- losis that had so far shown no symptoms. In such a case tubercular pneumo- thorax resembles that due to emphysema or to strain. The pathogenic diagnosis is extremely difficult. How are we to know whether pneumo- thorax, supervening suddenly in an apparently healthy subject, is or is not tubercular ? We may perhaps use, as a control measure, an injection ot 2 milligrammes of tuberculin. This means has been employed by Chauf!ard, and the absence of reaction in his patient proved that the pneumothorax was not tubercular. It was formerly held that purulent change in an effusion following tubercular pneumothorax was of necessity due to secondary invasion by other micro-organisms : Friedlander's bacillus. Staphylococcus aureus, Bacillus saprogenes, etc. (Netter). These conclusions are no longer admitted. Observations have shown that tubercular empyema may result solely from the infection of the tubercle bacillus without the presence of other micro-organisms. I have devoted a clinical lecture to " purely tubercular pyopneumothorax without super- added infection," and to the cases already observed I have added others which leave no doubt as to the pathogenesis of the pyopneumothorax. Speaking generally, pneumothorax is more frequent in adults than in children ; it has, however, been seen in children of all ages, even in those under two years of age ; " but the influence of age varies, according to the causes of the pneumothorax. Tubercles produce perforation at any age ; the rupture of the vacuoles of broncho-pneumonia determines it exclu- sively between the ages of two and four years." The presence of air in the pleural cavity is generally followed by hydro- thorax, and in 147 cases collected by Moneret the pneumothorax remained pure in sixteen only ; fluid formed in all the others. Some cases have been noted in wliich the fluid remained serous for a very long time. I had a patient' under my care in whom the fluid of a tubercular hydropneumothorax remained free from any micro-organism for eight months. These cases are exceptional ; most frequently the fluid becomes purulent, and contains the microbes of suppuration, especially when the perforation is consecutive to a tubercular cavity or to an abscess ; in some cases the fluid became purulent, although there was only simple rupture of the pulmonary alveoli (strain or emphysema). The gases in the pleura vary in quantity : nitrogen and carbonic acid predominate, oxygen being in the smallest proportion, while sulphuretted hydrogen usually accompanies pyopneumothorax. Post mortem one or several perforations are found ; their size, shape, and situation vary, according to the cause. When the perforation is not readily visible on the surface of the lung, it must be made so. For this purpose DISEASES OF THE PLEURA 375 the pleural cavity is filled with water, and insufflation through the trachea is performed. The bubbles which appear at the mouth of the fistula indicate its position ; the pleuro-pulmonary fistula, however, may be cicatrized or obhterated, and the corpus delicti passes unnoticed. I have elsewhere described the lesions which cause pneumothorax. Symptoms. — The invasion of pneumothorax is violent or quiet, ac- cording to the cause of the perforation. When the irruption of air affects a healthy pleura free from adhesions, the lung collapses, and the symptoms are sudden ; the pain in the side is severe, and the dyspnoea is excessive. Under other circumstances, when the lung is already fixed by adhesions, the onset is less violent, the pain and dyspnoea are slower to appear, and are less severe ; in some cases, indeed, the disease is latent. When pneumothorax results from the opening of a purulent collection into the bronchi (vomica), entrance of air into the pleura may follow the voiding of the pus through the bronchi. The physical signs of pneumothorax are as follows : Mensuration shows enlargement of the thorax, unless chronic pleurisy has already caused retraction. Percussion yields a clear and tympanitic sound, metallic in timbre (Trousseau's bruit d'airain).* The vocal fremitus is diminished or abolished, and the heart may be displaced by gas when the pneumothorax is situated on the left side. On auscultation the breath-sounds, the cough, and the voice-sounds become amphoric, and the rales change to a silvery sound, known as metallic tinkling. There is, furthermore, a sign which I have long pointed out : If the patient is made to drink small mouthfuls of fluid during auscultation, the swallowing of the fluid produces a gurgling sound of amphoric timbre. The above signs result from the presence of air in the pleura ; the simultaneous existence of fluid and of gas in the pleura shows itself by a splashing noise, audible on auscultation even at a distance, provided the patient be gently shaken. This symptom is called hippocratic succussion. The tension of the gaseous effusion is variable, according as the perfora- tion of the lung is obhterated or not. If it persists, the intrapleural pressure is practically the same as that of the atmosphere ; if it is obhterated, the intrapleural pres.sure varies from -7 during inspiration, to -f3 during expiration. In several patients I have found that these figures are variable. Simple pneumothorax may recover in three or four weeks, but the nature of the perforation and the formation of pus aggravates tiie prognosis. I have, however, often seen the cure of pneumothorax and of hydropneurao- thorax in tubercular patients. * If the poslcrior region of the pfili(!nt's chest is auBcnKated wliilo llio fronl is percussed, the percussion yields the hriiit d'airain. Tlii.4 bruit is still lid (or lieard if the percussion is made by moans of two coins. 376 TEXT-BOOK OF MEDICINE In some cases pneumothorax and hydropneumotliorax are localized to some portion of the thoracic cavity by previous adhesions ; tliis condition is partial pneumothorax. Diagnosis. — Large pleuritic effusions may give rise to amphoric breath- ing,* but the other signs are so different that mistakes are not possible between gaseous and fluid collections. Large cavities in phthisis may simulate pneumothorax, but are nearly always localized to the apex of the lung ; the rales become of a splashing nature, and the signs of amphorism are less marked. In some cases partial pneumothorax and hydropneumothorax are very difficult to diagnose, and it is essential to make a methodical examination, dividing the thorax into three regions — anterior, axillary, and posterior (Jaccoud). I have described a partial inferior pneumothorax with pleuro-peritoneal symptoms. It must not be confounded either with subphrenic abscess, which is an abdominal affection with pleural symptoms, or with certain cases qf subdiaphragmatic peritonitis. Pneumothorax, or hydropneumo- thorax, being recognized, it is still necessary to diagnose the cause, for the aetiology of the perforation is the principal basis of the prognosis. The treatment varies in j^neumothorax, hydropneumothorax, or pyo- pneumothorax. In a tubercular patient with hydropneumothorax it is, perhaps, preferable not to withdraw the fluid, for the spread of tuberculosis may be hindered in the lung thus compressed. In a case of pyopneumo- thorax Potain obtained striking success with injections of steriUzed air. I have treated tubercular pyopneumothorax by multiple punctures ; at each puncture only 2 ounces of fluid were withdrawn, and an intrapleural injection of solution of sublimate was given. Pneumothorax by Putrefaction. — I have so far dealt with pneumo- thorax by perforation. Essential pneumothorax, independent of perfora- tion and consecutive to exhalation of gas by the pleura, was formerly admitted. This view is no longer held, but some authors have stated that purulent fluid in the pleura may produce gas by decomposition, and give rise to pneumothorax. This latter form no doubt does exist, and is due to putrefaction, caused by anaerobic microbes. I have dealt with pneumo- thorax by putrefaction under Putrid Pleurisy. Pneumothorax by putre- faction is the opposite of pneumothorax by perforation ; wliile the latter is due to the passage of air into the pleural cavity, the former is due to the production of gas in a cavity into which the air has not penetrated. * These amphoric sounds are due to a cavity, filled with gas, which plays the j^art of a resonating chamber. Metallic tinkUng is only a rale which, in contact with this ca\-ity, assumes a special timbre, and it is not essential in order that the tinkling may be produced to have a communicatiou between the cavitj' and the bronchus in which the rale arises. CHAPTER VI DISEASES OF THE MEDIASTINUM I. TUMOURS OF THE MEDIASTINUM. Anatomy. — The organs of the mediastinum are so numerous, their lesions so fre- quent, and their disposition so important, by reason of the troubles which result from these lesions, that I Avill briefly describe the anatomy of this region. The name " mediastinum " is given to the irregularly shaped cav-ity which is filled by numerous organs, and occupies the space between the sternum, the vertebral column, and the inner surface of the lungs. To understand the construction of the mechastinal cavity, it is enough to know the relations of the pleurae in this situation. The pleur», after being in contact behind the sternum, open out, and in the interval which extends from the posterior part of the sternum to the root of the lung they circumscribe a space called the " anterior mediastinum." They continue their course from the root of the lung to the anterior surface of the vertebral column, and circumscribe a second space, known as the " posterior mediastinum." - The height of tlie anterior mediastinum equals the anterior vertical diameter of the thorax. Its shape may be compared to a triangular pyramid, two sides of which are lateral and one posterior. The anterolateral sides are formed by the layers of the pleura which are attached to the sternum ; they are in relation (the right especially so) with the lung. The posterior side, which is the smallest, is in relation with the oesophagus below and with the oesophagus and the thoracic cavity above. In this tri- angular space the following organs are contained : The pericardium, extending vertically from the xiphoid cartilage to the middle of the first piece of the sternum, and horizontally for about 4 inches to the left of the middle line of the sternum and 1 inch to the right. The heart, the apex of which corresponds to the sixth rib, is found about 4 inches from the median line of the sternum. The arch of the aorta, which corresponds to the middle and upper part of the sternum, contains the cardiac plexus in its concavity. On the same plane as these vessels we find, on the right side, the innominate artery and the superior vena cava ; on the left the common carotid and subclavian arteries, and more externally the recurrent and phrenic nerves. Behind these organs is the root of the lung, formed by (1) the bronchi situated on the same plane as the inner part of the second intercostal spaces ; (2) the pulmonary arteries ; (3) tlu! pulmonary veins. The posterior part ol the mediastinum is vrry didcrcnt from the anterior one. Its li'ngth is nearly equal to that of the dorsal column, and its shape that of a four-sided jjyraraid, with its apex below. The lateral sides are formed by the pleuras wliich open out above to receive the subclavian arteries. The posterior side corresponds to the vertebral column, while the anterior is limited by the bifurcation of the trachea in its ui)pcr fourth, and by the pericardium in its lower three-fourths. In this irregular quadrangular space the following organs are met with : 377 378 TEXT-BOOK OF MEDICINE The thoracic aorta and cesophagus, which are at first situated on the same trans- verse plane, but approach one another during their descent, so that the oesophagus is finally placed in front of the aorta, and helps to form the apex of the pyramid. The vena azygos major occupies the right side of the vertebral column, behind the cesophagus ; the vena azygos minor is placed on the left side of the dorsal column, behind the aorta ; while the thoracic duct is situated between the two azygos veins. We also find connective tissue, lymphatic glands, and twigs from the great sym- pathetic plexus and the pneumogastric nerves which surromid the oesophagus. The lymphatic glands have a special importance, from the numerous diseases that occur in them. As a whole, they receive the lymphatic vessels from the pleura, lungs, trachea, bronchi, heart, pericardium, and chest-walls. The groups of glands which deserve special attention have been described by Barety : (1) Right and left peri- tracheo-bronohial groups ; (2) right and left subbronchial groups ; and (3) inter bronchial groups. Pathological Anatomy. — Among the numerous tumours Avhich develop in the mediastinum, we shall consider : (1) Simple adenopathy ; (2) tubercu- lar adenopathy ; (3) cancerous adenopathy ; (4) degeneration of the thymus ; (5) aneurysm of the aorta ; (6) abscesses of the mediastinum ; (7) cancer of the oesophagus ; (8) glandular hypertrophy, ^v'ith or without leucocythaemia. 1. Simple Adenopathy. — Acute diseases of the lungs and of the bronchi produce engorgement and inflammation of the tracheo-bronchial glands, especially in children. Pneumonia, capillary bronchitis, and the catarrhs associated with measles, whooping-cough, or influenza, lead to adenopathy. The glands sometimes become much enlarged ; inflammatory congestion and oedema are present, and sometimes " hyperaemia and effusion of blood cause an increase in size, with red coloration of the whole gland tissue, which then resembles liver." Acute adenitis sometimes goes on to suppuration. 2. Tubercular Adenopathy. — The tubercles develop along the vessels in the cavernous or in the folhcular system of the gland, and present the same characters as in other tissues. The tubercle undergoes fatty change, and when the granulations are confluent, the parts situated between them may undergo caseous degeneration. In children tubercuhzation of the bronchial glands is never primary, but always consecutive to tuberculosis of the lung ; the lesion in the lung may be insignificant, while the glandular mischief is very extensive (Parrot). 3. Malignant Adenopathy. — Sarcoma and carcinoma of the bronchial glands are often consecutive to mahgnant disease of the lung ; lymph- adenoma, which is much more frequent than the preceding forms, is generally primary ; it develops in young healthy subjects, and at times assumes the more mahgnant form of lymphosarcoma. These malignant tumours grow large, invade the organs of the mediasti- num, the heart, the lungs, and envelop the vessels and nerves. In other cases the infection is carried to a distance, probably by way of the lym- DISEASES OF THE MEDIASTINUM 379 phatics, veins, or serous membranes, and secondary nodules are found in tlie kidney, liver, etc. 4. Degeneration of the Thymus. — The most contradictory opinions have been enunciated on the subject of tumours of the thymus ; their frequency has in turn been exaggerated and denied. It is certain that in children, and even in adults, we find sarcomata of different forms and slow evolution, which have arisen in the vestiges of the thymus. 5. Glandular hypertrophy, with or without leucocythsemia, will receive a separate description. 6. Syphilis may involve the mediastinal glands (see Syphilis of the Lung). Symptoms.— Besides the signs and symptoms special to the pathology of each of the organs in the mediastinum (cancer of the oesophagus, aneurysm of the aorta, lymphadenoma, glandular tuberculosis, etc.), certain signs are common to all tumours, and serve to give a complete picture of the pathology of the mediastinal region. This is what I have named the mediastinal syndrome. For example, the compression of a bronchus, of a venous trunk, or of a recurrent nerve, is always followed by the same effects, whether it be due to aneurysm of the aorta, glandulai hypertrophy, lymjahadenoma, or cancer. These common signs and uniform symptoms are nearly all tlie result of compression exercised by tumours upon the organs in the mediastinal region. They are as follows : 1 . Deformity. — This deformity affects the sternal region. The first piece of the sternum may be raised, or the bulging may predominate at the sterno- clavicular joints ; sometimes the bones are worn away, as in aneurysm of the aorta, and the expansile tumour takes the place of the bone. When the swelling is due to masses of glands (lymphadenoma, cancer), the glands in the supraclavicular hollow are often enlarged. Other signs are also present : normal resonance gives place to dullness, which varies according to the size of the tumour, and may often be found behind in the interscapular region (Gueneau de Mussy). Bronchophony and bronchial breathing are proper to changes in the glands near the trachea and the bronchi, while a double centre of pulsations marks the existence of aortic aneurysm. When the disease is of long duration, the retraction of the chest-wall, which has sometimes been observed, is probably due to the comj^ression of a large bronchus, with impaired activity of the lung. 2. Compression of the Bloodvessels. — This result is very common in tumours of the mediastinum. "' The arteries and the bronchial veins may be compressed by the suprabronchial and intertracheo-bronchial glands, the brachio-cephalic venous trunks, and the branches of the arch of the aortA by the retrosterno-clavicular glands " (Barety). 380 TEXT-BOOK OF MEDICINE The arterial vessels, being more resistant, suffer less from compression than the veins, and it is not rare to see an aneurysm of the aorta or a large mass of glands compressing the superior vena cava, the vena azygos major, and the innominate vein. When the superior vena cava is compressed, the passage of blood through this channel into the right auricle is difficult or impossible, and the result is blood-stasis in the areas which pour their blood into the tributaries of the superior vena cava — that is to say, in the head, the upper limbs, and the upper part of the thorax. Following the blood-stasis, we observe dilatation of the subcutaneous venules ; bluish networks show themselves on the thorax, shoulders, and arms, etc., while the jugular veins are dilated. This venous stasis is followed by tlie formation of a collateral circulation — that is to say, the blood which, as a rule, flows into the left auricle tlirough the superior vena cava, now takes another course, and seeks to reach the same goal by the inferior vena cava. The blood passes through its altered channel by means of deep and super- ficial anastomoses, which join the superior to the inferior caval system, and which from actual necessity become many times larger than the normal. These anastomoses are the large and small azygos, intercostal, internal mammary, deep epigastric, superficial epigastric, and circumflex ihac veins. By these altered channels the blood of the superior caval system attempts to pass into the inferior caval one in order to reach the right auricle. Hence in these abnormal cases the blood flows from above downwards in the cutaneous veins of the thorax and abdomen, and it is easy to prove the direction of the current by pressing back the blood in a dilated venous segment, and alternately removing the compression in the upper or in the lower end of the bloodless segment. If the vena azygos major participates in the compression, the re-estabhsh- ment of the circulation takes place only by the inferior vena cava. In the opposite case the azygos system which empties itself into the superior vena cava takes part in the re-establishment of the circulation. In short, the blood-stasis in the veins, the situation of these networks, and the direction of the blood-current give valuable information, which may point out the obstacle to the circulation in the mediastinum. When the collateral circulation is efficient, the symptoms are shght. In the opposite case, oedema of the hands and face is seen, the lips are violet- coloured, the eyes are injected, the patient suffers from giddiness, nose- bleeding, and headache — in short, from the signs of cephaUc congestion, due to venous stasis. When the subclavian artery or the brachio-cephahc trunk is compressed, the radial pulse diminishes in size. On the affected side compression of the pulmonary artery or of its branches has several times been noted ; ulceration of these vessels causes fulminant haemoptysis. DISEASES OF THE MEDIASTINUM 381 3. Compression of the Trachea and Bronchi. — The left bronchus is more often compressed than the right ; the vesicular murmur diminishes or disappears in the corresponding lung, but the thoracic resonance is pre- served. The union of these two symptoms — absence of breath-sounds and preservation of resonance — eliminates the idea of an effusion into the pleura, and can only be explained by narrowing or by compression of the bronchus. When the calibre is much diminished, we find inspiratory sucking-in, which is most marked in the supraclavicular and epigastric hollows (Gueneau de Mussy). Compression of the bronchi and of the trachea often produces rough and whisthng inspiration, which has received the name of stridor (Cayol). This sound is heard whenever stenosis affects the larynx, the trachea, or the large bronchi. 4. Changes in the Pneumogastric, Recurrent, Phrenic, and Sym- pathetic Nerves. — The symptoms, consecutive to changes in these nerves, difEer according as the nerve is irritated (symptoms of excitation) or destroyed (symptoms of paralysis). This is a very important distinction. Hoarse paroxysmal cough, resembling that of whooping-cough, has been noted in a great number of cases (Gueneau de Mussy) of bronchial adeno- pathy. " In children especially, when spasmodic cough shows itself at once or persists long after genuine whooping-cough, there is reason to suspect compression of the pneumogastric nerve by degenerated bronchial glands " (Verliac). Dyspnoea, with or without paroxysms, often results from compression of the vagus and the recurrent nerves. The attack may simu- late asthma (Herard), or may resemble angina pectoris. In one case the symptoms were due to irritation of the right vagus, which was congested and adherent to the swollen and degenerated glands (Barety). I have seen an analogous case. Laryngeal troubles betray themselves by the raucous nature of the voice (dysphonia), and by spasms of the glottis. The changes in the voice are explained by the paralysis of the vocal cord supplied by the affected re- current nerve. The diagnosis is readily verified by the laryngoscope. Spasms of the glottis are due to excitation of the recurrent nerve. Ex- citation of one nerve alone is sufficient to provoke spasm of the glottis (Krishaber). The change in the phrenic nerves determines diaphragmatic neuralgia and attacks of dyspnoea (Bazin). InequaUty of the pupils is often seen, and arises, doubtless, from changes in the great sympathetic nerve. 5. Dysphagia is due to the compression of the ccsophagus by media^ stinal tumours, tumours of the aorta, degeneration of glands, etc., and tu adherence of the oesophagus to neighbouring organs. Its perforation lias been noted five times (Barety). 382 TEXT-BOOK OF MEDICINE Diagnosis — Prognosis. — The diagnosis is often difficult. Sometimes the lesion betrays itself only by an isolated phenomenon — viz., per- manent contraction of one pupil, paroxysmal dyspnoea, analogous to attacks of asthma, aphonia simulating a malady of the larynx, spasmodic and paroxysmal cough resembling whooping-cough, or agonizing retro-sternal pain, which is nothing less than angina pectoris. Even when attention is directed to the seat of the disease, the difficulty is not entirely overcome, for many mediastinal tumours have symptoms in common, and it is then neces- sary to diagnose the nature of the tumour. If, however, they have characters in common, they also have some special characters which aid in the diagnosis. Thus, in aneurysm of the aorta we often find a movement of expansion, a double centre of pulsations^ and a double or single blowing murmur. Glandular affections of the media- stinum (lymphadenoma, leukaemia) are generally accompanied by glandular hypertrophy in other regions, as the neck, the axilla, or the groin. In tubercular adenopathy the condition of the lungs must be carefully inquired into. Cancerous degenerations sometimes involve the supra- clavicular glands. The prognosis is generally grave. Tumours, by their more or less rapid progress, compromise the respiration and the circulation, and the patient dies either slowly from asphyxia, or suddenly from syncope, or from attacks of suffocation. Rapid death generally depends upon changes in the vagus and recurrent nerves. Certain lesions of the mediastinum may be treated' surgically (Ziem- bicki). Dr. Potarca (of Bucharest), in a work entitled " Posterior Intra- mediastinal Surgery," has reported numerous operations performed for purulent collections in the posterior mediastinum, phlegmon, mediastinitis, suppuration in the bones or the glands, and abscesses from foreign bodies. II. CANCER OF THE THORACIC DUCT. The thoracic duct, which collects the lymph from the lower hmbs and the thoracic and abdominal viscera, extends from the receptaculum chyh to the left subclavian vein. It belongs, therefore, to the posterior media- stinum, where it passes up between the two azygos veins behind the oeso- phagus, until it crosses the posterior surface of the arch of the aorta and enters the cervical region. The thoracic duct carries matter absorbed by the digestive tract, but in pathological conditions it may transport microbes and cellular emboli to the right heart. Secondary cancer of the duct occurs when cancer cells are grafted on to its walls. Nattan-Larrier has described two cases of secondary cancer of the duct. The organs which usually give rise to secondary cancer of the duct DISEASES OF THE MEDIASTINUM 383 are the stomach, the uterus, and the testicle, because their lymphatics pass more directly to the duct ; then come the rectum, the pancreas, the kidney, and the ovary. The thoracic duct is invaded by vascular propaga- tion. The degeneration, affects successively the lymphatics from the can- cerous organ, the corresponding glands, their efferent lymphatics, and finally the thoracic duct. Invasion by effraction is quite exceptional. In one-half of the cases the entire duct is involved, in one-quarter the growth stops at some distance from the termination of the duct, wliile in more rare cases the lesion is hmited to the origin of the vessel. When the entire duct is invaded, it resembles a vessel injected with paraffin. " The receptaculum is as large as the thumb, and looks hke a flabby, nodular, whitish cord, wliile a granular mass exudes on puncture. Below the recep- taculum we find a network of cancerous lymphatics over the sides of the aorta. Higher up we find the duct, properly speaking ; it forms a trunk 3 to 4 milhmetres in diameter, wanding over the posterior surface of the aorta. At some points it divides into three or four branches, which remain separate for 3 or 4 inches, and then reunite to form a trunk as large as the primary vessel. After passing round the subclavian artery the cancerous duct reaches the vein, which it perforates at the junction of tliis vessel with the internal jugular vein." Sections show secondary cancer of the duct. The epithehomatous cells are fixed in the connective tissue, and form buds, which obhterate the lumen. At the termination of the duct we often find a cancerous vegetation which floats in the subclavian vein. The subjoined case is very typical : Woman who had suffered from dyspepsia for many years, admitted in July, 1900. Repeated melaena and hcematemesis, complete anorexia, and marked wasting. She complained of acute epigastric pain, and pali)ation revealed a large tumour at the level of the greater curvature of the stomach. She had cancer of the stomach, confirmed by a large gland in the left supraclavicular fossa. The left suVjcIavian vein soon became thrombosed. Fever appeared, and she died from streptococcal septicaemia. Post mortem, cancer of stomach and secondary growth involving the entire thoracic duct, which was completely obliterated, and showed all the features above described. Cancer of the thoracic duct shows itself by symptoms and signs which are at times difficult to distinguish from those due to the primary growth. Wasting and malnutrition are rapid. Yet, strange to say, obhteration of the duct is not, as a rule, accompanied by lymphostasis. In three cases only did milky effusion in the peritoneum coincide with cancer of the duct. In two cases the chyhform ascites was due to cancer of the ijcritoneum, and in the third case the chylous effusion was due to the spread of the growth to the subperitoneal lacteals. We must therefore admit that the lymph- flow is usually re-cstabUshed by the collateral channels. Phlebitis of the left arm is fairly common, and is due to thrombosis, which starts from the 384 TEXT-BOOK OF MEDICINE anastomosis of the duct with the vein. The phlebitis is seen in 25 per cent, of cases. The existence of glands in the left supraclavicular fossa has been noted in half of the cases. The discovery of a prelumbar tumom-, accompanied by double vari- cocele, would point to invasion of the thoracic duct, since the prelumbar glands are affected in all cases of epithelioma of this tube. Nevertheless, the prelumbar glands may be cancerous, while the duct is not invaded. No one of these signs has absolute value, but their appearance in cancer of the stomach or of the uterus would lead us to think of secondary growth in the thoracic duct. PART II DISEASES OF THE CIRCULATORY SYSTEM CHAPTER I DISEASES OF THE PERICARDIUM I. ACUTE PERICARDITIS. Pericarditis is inflammation of the pericardium. Senac (1783) was the first to separate pericarditis from other diseases of the heart. In 1806 Corvisart applied to it the signs given by percussion ; in 1824 ColUn, assistant to Laennec, discovered the pericardial rub (bruit de cuir neuf), and some years later Bouillaud created cardiac pathology. i^tiology. — The so-called primary (a frigore) pericarditis does not exist. The secondary form is sometimes associated with a neighbouring lesion (pleurisy, aneurysm of the aorta). It may follow injury, but usually occurs in infectious diseases and constitutional maladies. Pericarditis associated with pneumonia may be parapneumonic or metapneumonic. It may be dry, sero-fibrinous, hgemorrhagic, or purulent. The fluid does not contain much fibrin, and the pus is homogeneous. Pneumococcal pericarditis may be independent of any pulmonary lesion. The eruptive fevers, and especially scarlatina, may be accompanied by pericarditis. The fluid may be sero-fibrinous, htemorrhagic, or purulent, and almost always contains the streptococcus. Pericarditis in erysipelas is also associated with the streptococcus (Denuce). Pericarditis consecutive to influenzal broncho- pulmonary lesions is associated with several microbes, among which the streptococcus is the chief. Pericarditis in Bright's disease is said in some cases to be of toxic origin. Tubercular pericarditis is sero-fibrinous, ha3morrhagic, or purulent, and due to Koch\s bacillus, with which other organisms may be associated. Purulent pericarditis consecutive to pyaemia is duo to staphylococci or streptococci, but it is sometimes impossible to find the point of entry. 385 25 386 TEXT-BOOK OF MEDICINE The most frequent cause is acute rheumatism, which is probably a microbic disease. The pericarditis appears during the first and second weeks of articular rheumatism, but may appear at the same time as the articular lesions, or even apart from them. In some cases it is associated with endocarditis or with pleurisy. It attacks patients at any age, but by preference young children and infants. Pathological Anatomy. — Acute pericarditis has been divided, Hke pleurisy, into two varieties, according as it is dry or accompanied by effusion. In acute pleurisy, however, effusion is the rule, while in peri- carditis it is the exception. In ten patients suffering from rheumatic pericarditis, effusion is perchance found but twice. From an anatomical point of view, acute dry pericarditis does not exist, for a certain quantity of exudate is always found post mortem. CUnically, however, the effusion is not considered, unless it is sufficient to cause special signs, and from this point of view pericarditis with effusion is somewhat rare. Pericarditis may be partial or general. It is usually situated near the aorta and at the base of the heart. The visceral layer, or epicardium, is always the more affected. At first the congested vessels form a fine net- work on the surface of the serosa, which loses its polish and becomes covered with a fibrinous exudate, the papillary aspect of which (cor hirsutum) has caused it to be compared to a cat's tongue, or to sUces of bread and butter which have been pressed together and then quickly separated. The papillae are formed of fibrin, epithehal cells, and pus corpuscles. Their special form is due to the incessant movements wliich are given to the fibrin by the heart. The outer layer of the serosa takes no part. The connective tissue of the serosa shows embryonic infiltration, and the lymphatic vessels are crammed with fibrin and white corpuscles. The quantity of fluid varies from a few drachms to a pint or more ; it may be sero-fibrinous (rheumatism, pneumonia), haemorrhagic (tuberculosis, Bright's disease, scurvy, cancer, and cachexia), or purulent (scarlatina, pneumonia, typhoid fever, and puerperal conditions). The heart muscle often shows superficial myo- carditis. Tubercular pericarditis deserves special mention. It super- venes in the course of acute or of chronic tuberculosis, or occurs as a primary local tuberculosis. Effusion may or may not be present, and in the former case the fluid is often hsemorrhagic. In recent cases the tubercular tissue contains bacilli but they may be absent in old cases (Cornil and Babes). The mediastinal glands are indurated and enlarged, while the cellular tissue around them is adherent to the pleura and the lungs. Tubercular pericarditis sometimes ends in adherent pericardium. Description. — The invasion is very variable, and although this diversity of onset may not be solely imputable to its causes, pericarditis is usually insidious and latent (Stokes), and far more rarely acute and painful. DISEASES OF THE PERICARDIUM 387 The patient sometimes complains of more or less severe oppression, with palpitation and pain in the precordial or in the epigastric region, or between the shoulders. As a rule, especially in rheumatic pericarditis, these symptoms, and especially the pain, are absent or shght. In some exceptional cases, however, the symptoms of acute pericarditis are very marked : the face is pale ; the patient is anxious ; the pain may be terrible, accompanied by chill and Upothymia, and analogous to the pain of angina pectoris — a fact vrhich would prove that the cardiac plexus and the phrenic nerve are affected by the inflammation. Auscultation during the onset of the malady reveals a rub. This rub, which is at first systoUc, soon becomes systolic and diastolic. It is a sound that comes and goes — i.e., a "bruit de frou-frou.'* As the friction sounds are not absolutely synchronous with the heart sounds, it is preferable to say that the one is mesosystolic and the other mesodiastolic. The want of synchronism depends on the fact that for both layers of the pericardium to produce a friction sound it is necessary that " the displacement of the surface of the heart should have reached a certain degree, that the muscular contraction should have just commenced, and that, in consequence of the form and volume of the heart, the surfaces in contact be, so to say, relaxed, after having been dragged apart more or less suddenly " (Potain). The pericardial rub has special characters. It is more rasping than the cardiac murmur, and is not propagated in the direction of the blood-stream. It has its maximum intensity about the third intercostal space, where the anterior surface of the heart is more directly in relation with tlie chest, and increases in intensity when the jJatient bends forward or when the stethoscope is firmly appUed to the chest-wall. Lastly, it is not absolutely isochronous with the normal sounds of the heart. In some cases the rub is intense and general. It often happens that the systolic rub commences a little before the systole ; it is presystohc, and causes a triple sound, called the " bruit de galop " (Bouillaud). This bruit de galop has a special rhythm, and its three periods are divisible in the following manner : The first two sounds, which are short and hurried, are formed, one by presystohc friction, and the other by the normal sound of the heart, with or without friction ; while the tliird sound corresponds to the normal second sound of the heart, or to this sound covered by a friction sound. This bruit de galop, composed of two short sounds and one long one, must not be confounded with the sounds, called " l)ruit de caille " and " bruit de rappel," the rhythm of which is a sign of mitral stenosis, and is inverse to the bruit de galop, being made up of a long and two short sounds. The single or double rulj, witli or witliout bruit de gah»[), is therefore a sign of dry pericarditis ; but when oifusion is present, the fluid separates 25—2 388 TEXT-BOOK OF MEDICINE the layers of the pericardium, and the rub disappears. In some cases, however, the rub may still be perceptible towards the base of the heart, in spite of a large effusion. In proportion as the effusion forms, the fluid collects in the dependent regions of the pericardium. A small effusion passes unnoticed, but large ones cause the following signs and symptoms : On inspection and palpation, we find that the cardiac waves and the impulse of the heart against the chest-wall become gradually effaced. On auscultation, the heart sounds become faint and tend to disappear. Bulging of the precordial region, so characteristic in a child suffering from peri- cardial effusion, is less marked in the adult, because the ribs are more resistant, and the pericardium, distended by the effusion, finds room at the expense of the diapliragm, which it pushes down, and at the expense of the posterior mediastinum, which it pushes back. The most valuable sign of pericardial effusion is dullness. This dullness varies according to the quantity of fluid effused. Its shape and limits furnish valuable information. Pericardial dullness is triangular or conical in shape, with its apex reaching as high as the third rib, where the peri- cardium is reflected on to the great vessels ; its base blends with the dia- phragm. In large effusions, which amount to about a pint, the vertical line of dullness, which extends from the apex of the cone to its base, measures 6 or 7 inches, and the fine of horizontal dullness, which is close to the base of the cone, has nearly the same length. Percussion, therefore, rather than the other signs, shows the daily progress of the effusion. When the effusion is abundant, it gives rise to more or less marked symptoms, which include dysphagia, pallor and puffiness of the face, dyspnoea, which is sometimes acute and accompanied by fainting and angina, cyanosis and oedema of the peripheral parts, small intermittent pulse, and pulsus paradoxus. Some of these symptoms — namely, the smallness and irregularity of the pulse — may be due to compression of the auricles, which offer less resistance to the effusion than the ventricles. The pulsus paradoxus is found in cases of effusion and of pericardial adhesions, and consists of three or four pulsations, followed by suppression of the radial pulse for a like period, with no interruption of the heart-beats. The disappearance of the pulsations coincides with the end of inspiration. Dyspnoea, angina, attacks of suffocation, and threatening asphyxia, may be due to the pericardial effusion when it is associated with endocarditis, pulmonary congestion, and pleuritic effusion that often accompany peri- carditis, especially in the case of acute rheumatism. Several of these symptoms may also be present in the paralytic form of pericarditis, which is due to degeneration of the heart muscle. In such cases the patient may succumb from asystole. DISEASES OF THE PERICARDIUM 389 The course of pericarditis is irregular ; its duration is uncertain, and the fever cycle indefinite. The absorption of the fluid is followed by the gradual disappearance of symptoms, and the rub (frottement de retour) again appears. When the pericarditis has been slight, without effusion, as in rheumatic cases, the serous membrane returns to its normal condition, and recovery takes place in one or two weeks. Diagnosis — Prognosis. — Apart from the exceptional cases in which the symptoms are acute, pericarditis is a disease which must be carefully looked for, because it develops without warning. Repeated auscultation is necessary in patients who have one of the diseases enumerated under the setiology of pericarditis, especially in those who are suffering from articular rheumatism, and it will then be possible to recognize the rub at its onset. The diagnosis must be made in each form. The rub can be distinguished from cardiac murmurs by the signs indicated above. The diagnosis from the pleuritic rub is very simple, because the patient can at will stop breathing, and at the same time suppress the rub of pleurisy. I will briefly recapitulate the signs by which pericardial effusion may be diagnosed. The shape and situation of the dullness are the most valuable points ; then come the disappearance of the cardiac impulse, the faintness and disappearance of the heart sounds, and the pulsus paradoxus. Let us not forget that the pericardial rub may persist, in spite of a large effusion. Pericardial effusion and encysted effusion in the left pleura present some analogy, but the situation and the conical shape of the dullness in the precordial region, the weakening of the cardiac impulse, and the remote- ness of the heart sounds, are in favour of pericarditis. Hypertrophy of the heart and pericardial effusion have two signs in common — i.e., the extent of the dullness and the weakening of the heart sounds. In hyper- trophy the dullness coincides with the apex of the heart, while it descends lower than the apex in pericardial effusion (Gubler). In its common forms acute rlioumatic pericarditis is not a serious malady. The gravity of the prognosis depends on the abundance of the effusion, and on certain complications, such as endocarditis, pleurisy, congestion of the lungs, inflammation of the myocardium, and ventricular thrombosis, which causes sudden death. The prognosis also depends on the causes which have given rise to pericarditis. The rheumatic form, for example, is not nearly so grave as the tubercular one. Treatment. — If the inflammation is inteiLse, and especially if the pain is severe, blood-letting should be performed. We may prescribe leeches or f'U])j)ing to the precordial region, and employ blisters, or apply ice-bags, which are left in situ. When the heart muscle is weak, digitalis or caffeine is administered, and the pain is relieved by subcutaneous injections of 390 TEXT-BOOK OF MEDICINE morphia. If the efEusion threatens to bring on asphyxia or syncope, the fluid should be withdrawn without delay. The history of paracentesis of the pericardium and the operative technique have been minutely described by Trousseau ; but this opera- tion has been modified, and I may say much simpUfied, since I have employed the aspirator. I omit, therefore, the old procedure, and mention the conclusions given in my memoir on paracentesis of the pericardium (" Traite de 1' Aspiration "). Experiments performed on the cadaver give the following conclusions : 1. In an adult the pericardium may contain an amount of fluid, which in exceptional cases may exceed 2 pints. 2. Whatever be the degree of fullness, the pericardium reaches its greatest transverse diameter at the level of the fourth, or sometimes of the fifth, intercostal space. 3. At tliis level the pericardium is not covered by the left lung. The lung, on the contrary, forms a notch, simulating a crescent, which extends from the fourth to the sixth rib, and persists even when the lung is in- sufflated. This notch coincides with the maximum point of the transverse diameter of the distended pericardium, and consequently leaves a space free for the aspirating needle. 4. The pericardium, distended by fluid, extends beyond the left border of the sternum for as much as 4 or 5 inches. 5. I therefore recommend paracentesis in the fifth left intercostal space, about 2 inches from the left border of the sternum. For this purpose a No. 2 needle is employed. The aspirator is emptied of air, and the puncture is made at the proper spot. When the needle has gone J inch into the tissue — i.e., as soon as the needle is no longer in relation with the external air — the corresponding tap of the aspirator is opened, and a vacuum results in the needle, which becomes an aspirating one. With the vacuum, so to say, in hand, we then proceed to search for the effusion. The needle is pushed in slowly until the effusion flows through the glass index. For the dangerous operation proposed by Aran, Jobert, and Trousseau, I have substituted a simple needle-prick, which is absolutely harmless, and demands neither special skill nor exceptional surgical knowledge. Paracentesis does not give the good results of thoracentesis, because it has been chiefly employed in secondary pericarditis, which is often asso- ciated with tuberculosis, and is therefore incurable. In some cases, especially when the fluid is purulent, pericardotomy is indicated. DISEASES OF THE PERICARDimi 391 II. CHRONIC PERICARDITIS— ADHERENT PERICARDIUM. Pathological Anatomy. — Chronic pericarditis may be primary or conse- cutive to acute pericarditis. The aetiology is the same in both cases. The false membranes and the adhesions which are the chief lesions in clironic pericarditis present different aspects. The false membranes arise in the serosa, as vascular buds, which unite to form adhesions between the two layers of the serous membrane. The adhesions may be partial or general. When partial, they fix the apex of the heart, surround its base like a ring, or form septa and cavities, filled with fluid and degenerated cells. When general, they obliterate the cavity and lead to pericarditis obliterans (Stokes) or ankylosis of the heart (Bouillaud). If the inflammatory process also affects the external layer of the pericardium, this in turn forms adhesions with the neighbouring organs — viz., pleura, lung, diaphragm, and chest-wall. The false membranes may be an inch in thickness ; they are haemorrhagic, infiltrated with tubercles, or encrusted with calcareous salts. The ossiform patches in the pericardium are no more osseous tissue than the cartilaginiform patches are composed of cartilaginous tissue, for the latter do not possess chondroblasts, and are composed of lamellar con- nective tissue and elastic fibres (Cornil and Ranvier). When chronic pericarditis is accompanied by effusion, the fluid, which is variable in quantity, may be purulent or haemorrhagic, and contains shreds of membranes. The muscular fibre of the heart, which has become flabby and yellowish, is more or less affected by fatty degeneration, and we find, as the case may be, enlargement of the cavities, hypertrophy or atrophy of the heart, and insufficiency of the tricuspid and mitral valves. Description. — When chronic pericarditis ends in adhesions, it readily passes unnoticed. It is only evident if friction sounds exist, if the effused fluid is abundant, or, lastly, if the adhesions are very extensive. At the points where the false membranes are not adherent a rasping rub is audible. If the effusion is sufficiently abundant, it shows itself by the signs described under acute pericarditis. Adherent pericardium, if uncomplicated, may give no symptoms ; but if it is accompanied by degeneration of the myocardium and dilatation of tiie heart, it shows itself by the subjoined signs and .symptoms. In the first place the adhesions cause trouble in the cardiac circulation. In the normal condition the intrapericardial vacuum favours the filling of the cavities of the heart during dia.stole ; if, however, adliesions form, the expulsion of blood is hindered during the systole, and the cavities do not fill during diastole, because the vacuum is suppressed. Adherent pericardium causes the following symptoms : The patient is a prey to more or less acute and constant dyspnoea, which increases with the least effort. He experi- 392 TEXT-BOOK OF MEDICINE ences precordial pain, which may disappear during rest, but at times returns with the least exertion or fatigue. On pressure we find tenderness of the phrenic nerve in the neck and in the region of the diaphragm. On examination of the thorax, bulging of the precordial region is often seen. Percussion may show considerable increase in the size of the heart. On palpation the systohc shock is much less marked than in the normal condition. General adhesions produce signs which are most marked when the adhesions involve the chest-wall : these signs are — retraction of the inter- costal spaces during systole (Wilhams), systohc retraction of the epigastric angle, and reduphcation of the heart sounds. The muscle often degenerates, becoming less resistant, and, with the assistance of the false membranes, dilatation of the ventricles and con- secutive insufficiency of the valves result.* Congestion and oedema, asphyxia, asystole, and sudden death may follow. Ill . H YDROPERIC ARDIUM— H YDROPNEUMOPERICARDIUM. Hydropericardium is dropsy of the pericardium. It is not the result of an inflammatory process like pericarditis, but occurs in the course of other diseases. Hydropericardium is due either to mechanical causes which embarrass the circulation in the cardiac vessels, or to dyscrasiae and cachectic states which modify the composition of the blood. The signs of hydro- pericardium and most of its symptoms, except fever, are those of peri- carditis with effusion. Hydropneumopericardium denotes the simul- taneous presence of gas and fluid in the pericardium. Here, as in pleurisy, it has been asked if purulent fluid may, by decomposition of its elements^ produce gas. This view is no longer admitted. The common causes of hydro- pneumopericardium are injury, communication between the pericardium and an abscess of the Hver (Graves), the oesophagus (Chambers), or a cavity in the lung (Dowel). The presence of gas in the pericardium shows itself by a tympanitic sound in the precordial region. On auscultation the heart sounds assume a metallic tone, and if the fluid is in sufficiently large amount, the heart, striking the fluid and gas, produces a kind of gurghng, analogous to the noise of a windmill wheel (Laennec). * These secondary lesions affect not only the right ventricle and tricuspid valve, but also the left ventricle and mitral valve ( Jaccoud). CHAPTER II DISEASES OF THE ENDOCARDIUM I. ACUTE ENDOCARDITIS. Endocarditis is inflammation of the endocardium. Discussion. — It is customary to divide acute endocarditis into two groups : on the one hand simple, more or less benign endocarditis, and on the other infective endocarditis, which corresponds to the old name malig- nant. This division, though convenient for a theoretical description, is one which I consider artificial, as it is known to-day that every case of acute endocarditis is more or less of an infective nature, and dependent upon the presence of micro-organisms. Further, upon what are we to base our division of acute endocarditis ? Not on the nature of the lesions, for infective endocarditis, which so often causes vegetations and ulcerations, has not alone the privilege of causing these lesions. We find cases of simple endocarditis, which are so benign that they do not enter into the category of " infective," but yet they may be accompanied by vegetations which lead to embolism and to ulcerations of the valves or the chordae tendinese. Can the aetiology of endocarditis and the bacteriological knowledge acquired during the past few years serve as a basis of classification ? For example, can rheumatic endocarditis be considered as being characterized by its relatively benign course, by lesions that are limited to the heart, and by the absence of embolic complications ? And can endocarditis in the puer- peral state, in certain cases of pneumonia, of scarlet fever, etc., be infective and accompanied by cardiac and extracardiac lesions, by mechanical and septic emboli, and characterised by general characters and symptoms that are too often exceedingly grave ? Not so ; aetiology, althougli having a relative part in the anatomical and clinical evolution of endocarditis, cannot be the starting-poiiit of a division, for exceptions would be met with every moment. Endocarditis in the course of scarlatina, of smallpox, or of erysipelas, which are eminently infectious diseases, is often benign and almost latent, while endocarditis in the course of trut^ rhoumatisni may exceptionally assume a typhoid and iiuiiigiiant form. The nature of endocarditis, the variety of its lesions, the diversify of its 393 394 TEXT-BOOK OF MEDICINE micro-organisms, the benign or grave nature of its course, depend, as always, on the co-operation of certain causes which mutually support or oppose one another. We must especially remember the specific origin of the disease, the quantity and quality of the pathogenic agent, the previous condition of the endocardium, and the state of receptivity and of resistance of the individual. I shall, in order to faciUtate description, adopt the artificial division of endocarditis into two groups, first stating the fact that they are related cHnically by numerous intermediary forms. In the first group I shall describe simple acute endocarditis, and shall choose for my type the most common of all— rheumatic endocarditis ; in the second group I shall have to discuss the chief forms of infective endocarditis — viz., pneu- monic, pyaemic, puerperal, etc. In the course of this description we shall find that certain cases of endo- carditis do not merit the name " infective," for they show no symptoms of infection. On the other hand, they do not merit the name of " simple," for, in spite of the benign nature of their symptoms, they are sometimes accompanied by the formation of large emboli, which block the arteries of the limbs or of the brain. I call these cases emboligenous, this term being applied to emboU of a certain size, and not including, of course, capillary emboK and the formation of haemoptoic or of septic infarcts, lesions described under infective endocarditis. We may, therefore, see simple emboligenous, and infective or mahgnant, endocarditis. Simple Acute Endocarditis. /Etiology. — Many infectious diseases — blennorrhagia, scarlatina, diph- theria, variola, the setiologic importance of which has been too much ex- aggerated (Quinquaud), erythema nodosum (Trousseau), chorea (See), facial erysipelas (Jaccoud), pneumonia, and malaria — may cause endocarditis, which is often microbic, and from its characters and symptoms would in many cases deserve the name of simple endocarditis ; often, indeed, so simple that it would pass unnoticed without minute examination of the heart, and, in fact, several of these cases recover without leaving any sequelae. Such cases will not serve as the type in the present description. I would rather choose rheumatic endocarditis, which is the most common of all, but conforms to the type of simple acute or subacute non-infective endocarditis. Acute, subacute, or chronic articular rheumatism may provoke endo- carditis (Bouillaud), but it is chiefly in the course of acute articular rheu- matism that endocarditis develops. I refer the reader to the article on rheumatism, where this question is treated in detail. Endocarditis usually appears in the second week of the rheumatic attack, but in some exceptional DISEASES OF THE ENDOCARDIUM 395 cases it precedes the articular manifestations. Rheumatic endocarditis especially affects adults and children. Pathological Anatomy. — The inflammation nearly always chooses the endocardium of the left heart, affects the mitral more often than the aortic valves, the central face of these valves more often than the parietal one, and their free edge rather than other parts. This locahzation depends on several causes : (1) the mechanical effects of pressure and friction exercised at these points by the blood-current ; (2) the lessened resistance of the affected parts of the valves, which are, at the same time, more worn out and not so well organized (Peter). In order to understand the changes in endocarditis (acute or chronic), we must remember the structure of the endocardium, which much resembles that of the endarterium. The endocardium is composed of an endothelium made up of a single layer of flat cells ; a second layer, formed by flattened cells that are superposed and separated by lamellar substance ; and a tliird layer of elastic tissue and of bundles of connective tissue (Cornil). The first layer is not found post mortem ; the second layer is very thin at the level of the valves ; the third layer (fibro-elastic tissue), at the free edge of the auriculo-ventricular valves, gives origin to the tendons of the papillary muscles. The auriculo-ventricular valves may be consi- dered as a fold of endocardium, the two lips of which are united by fibrous connective tissue, insuring resistance (Ranvier). The arterial valves result from the folding back of the internal membrane of the arteries on the ventricular endocardium. When endocarditis is slight and transient, it is rather exudative than proliferative. The type of prohferative endocarditis is the rheumatic form, which we are now considering. The inflammation chiefly attacks the mitral valve, the edges of which are swollen, thickened, and much vascularized, while in the normal state the capillary vessels are few in number. These vessels are affected by endarteritis, and their lumen is almost obli- terated. The changes develop in the layer of flattened cells. Micro-organisms often cause the embryonic elements to proliferate and form granulations, which are so small and so numerous that they give to the endocardium a rough appearance. These granulations, which were at first taken for collections of fibrin, are really composed of embryonic tissue, covered by a thin layer of fibrin. They are friable, soft, and transparent in the acute stage, and some show at their centre vessels in process of formation. The granulations may invade fairly large surfaces of the parietal, ventricular, or auricular endocardium, but are usually found at a small distance from the free edge of the valves, where they form a wavy, maiuTnillatod line. The granulations, which sometimes reach the size of a pin's lioad or of 396 TEXT-BOOK OF MEDICINE a pea, may be villous, filamentous, nummular, warty, or raspberry-like, and surround the valves like a garland. They may give rise to emboli, which are carried in every direction. These complications, however, will be discussed later under Embohgenous and Ulcerative Endocarditis. Description. — The phenomena of invasion in acute endocarditis are, so to say, non-existent. Rigors, dyspnoea, and palpitation are not seen, or at least are so slight that endocarditis passes unnoticed in a case of articular rheumatism, unless the heart is examined daily. In valvular endocarditis we find blowing murmurs, which are related to the seat of the lesions and will be described under Valvular Lesions. All the orifices of the heart may be affected, but for the moment it is enough to say that the mitral orifice is most generally attacked, and the aortic orifice is next in frequency. The murmur that characterizes mitral endocarditis is heard at the apex of the heart — that is to say, below and outside the nipple ; this soft murmur is nearly always systohc, mitral insufficiency being the rule and stenosis the exception, during the acute stage of endocarditis (Bouillaud). The duration is rarely more than two or three weeks. After this time the trouble resolves and the murmur disappears, but the mischief may become chronic, when the murmur also persists. Endocarditis which is consecutive to such infectious diseases as ery- sipelas, mumps, erythema nodosum, etc., may recover without leaving any trace. Recovery, however, is not to be reUed on. A patient who has suffered from rheumatism or scarlatina, and been considered as cured because the murmur has disappeared, may yet suffer from chronic endocarditis, which is latent in its evolution. The morbid process is not extinct, but proceeds slowly and insidiously to alter the tissues wliich it has attacked, and often creates irremediable lesions, that may only appear after years. Simple acute endocarditis, however, presents no immediate danger, and its gravity results from the chronic valvular lesions wliich so often follow. Local blood-letting, leeches, cupping, blisters to the precordial region, and the preparations of digitahs form the basis of treatment. We must never lose sight of the frequent change from the acute to the chronic state. Bhsters and applications of the cautery must therefore be continued for a lengthy period when the disease has left some traces. Ulcerative, Infective, or Malignant Endocarditis — Emboligenous Endocarditis. Pathogenesis. — The acute endocarditis just described presents no imme- diate gravity ; it is only formidable in the future, because of the chronic valvular lesions which too often follow. We find, however, another form of acute endocarditis, called typhoid, ulcerative, infective, or malignant, DISEASES OF THE ENDOCARDIUM 397 wliicli at its onset or in its course may show a typhoid or septic character, and ends fairly frequently in death. We know to-day that there is, not one, but several varieties of infective endocarditis. Discussion of their pathogenesis is singularly simpUfied since the dis- covery of bacteria ; their aetiology is no longer given up to simple hypothesis, as was formerly the case, and we can Avith some method group the lesions and the symptoms that are peculiar to each variety. The nature and the degree of virulence of the micro-organisms, the previous condition of the endocardium, the conditions of resistance or receptivity of the individual, are all factors which have to be taken into account. This question may, I tliink, be stated as follows : The endocardium, whether healthy or previously injured so that it is in a State of receptivity, offers a favourable site for the arrest and development of certain pathogenic agents. These agents may have the most varied origins. Some enter the economy by the skin (abrasions, excoriated corns, boils, burns, wounds, erysipelas, injuries) ; others are introduced through the mucosa of the uterus (abortion and accouchement), through the genito- urinary mucosa (lesions of the urethra and bladder), and through the digestive mucous membranes (stomatitis, ton- silUtis, ulcerations of the stomach, the intestines and the bile-ducts) ; others, again, penetrate through the serous membranes (lesions of the peritoneum, pleura, and synovial membranes) ; some are introduced through the respiratory channels (broncho-pneumonia, ulcerative lesions of the lung, gangrene, and bronchiectasis) ; others may enter through bone lesions (osteomyelitis) ; finally, in some cases the entrance gateway cannot be found, in which event we invoke auto-infection, calling the endocarditis primary. Many microbes may cause infective endocarditis. I shall first cite the pyogenic microbes, streptococci and staphylococci ; then the pneumococcus, the bacillus of typhoid fever and of tuberculosis, the gonococcus, and other microbes not classified, or not yet found in other diseases (Weichselbaum, Gilbert and Lion). These microbes are chiefly aerobic, a fact which doubtless explains their preference for the left heart and for oxygenated blood. Endocarditis of the right heart is more rare. Cases have, however, been published. These microbes, after entering the economy by one of the gateways above enumerated, arc carried by the blood to the heart, and invade the endo- cardium, either superficially, through the crevices in the connective tissue, or deeply, by way of tiic small vessels. This invasion may be helped by previous changes in the serous membrane. After implantation on their culture medium, the pathogenic agents, either alone or in combination. 398 TEXT-BOOK OF MEDICINE crown their work of destruction, and the pathological process may assume several forms. In the first variety the lesion leads to the formation of vegetations which are more or less bulky and friable. These vegetations become detached from the endocardium, and are launched into the vessels in the form of emboh. If the embolus is of large size, it obliterates a fairly large artery, and causes secondary complications, which depend on the obhterated vessel (hemiplegia, aphasia, and gangrene). If the embolus is of smaller size, it causes infarcts in the kidney, spleen, intestine, or lung, and the symptoms depend on the organ invaded. In this first category of complications the embolus causes simple obstruction of the vessels. The embolism is called mechanical and may be formidable, but is not septic. In short, the cases of endocarditis which form this first variety are embo- ligenous, but do not deserve the name of infective, because they do not give rise to septic or infective emboli. In the second variety the morbid process goes on to necrosis and ulceration, and in most cases vegetations and ulcerations are present to- gether. These ulcerations may perforate the valves, tear away the pillars, and detach shreds of the chordae, giving rise to mechanical embolism. Here also the endocarditis may not be infective, but rather ulcerative, with vegetations. It is emboligenous and most grave, but the process may not be infective. Lastly, in the third variety I place the true cases of infective endo- carditis. Ulcerations and vegetations are as a rule present, but the impor- tant feature is that their products are septic and infective : they pour septic capillary emboh into the blood-stream, and their symptoms recall the picture of typhoid or purulent infection. From this rapid enumeration we see that we should be wrong in including all cases of severe or of fatal endocarditis under the term " infective." There is a place for intermediate cases, according as the morbid process is accompanied by infecting pathogenic agents or not. Pathological Anatomy. — At the onset of malignant endocarditis (I in- tentionally preservet his epithet " malignant," as it applies to every endo- carditis which is not of the simple type) under the influence of micro-organisms, we find in the valvular tissue infiltration of wandering cells, hypertrophy and multiplication of cells, and desquamation of the endothehal layer, which is replaced by fibrin. In the meshes of the fibrinous reticulum colonies of bacteria are found, which " penetrate by more or less large chinks into the interior of the valves." In cases of malignant endocarditis, the inflammation nearly always gives rise to large vegetations and deep ulcerations. In such a case we find on the sigmoid or on the mitral valves, on the chordae tendinese, on the papillary muscles, and on the median septum, a vegetation of the size of a DISEASES OF THE ENDOCARDIUM 399 pea or of a strawberry, or a collection of smaller vegetations, of which some are flattened, papilUform, or raspberry-hke, while others are pedunculated and ready to break of?. These vegetations, wliich are formed largely of embryonic tissue and are covered by a, mass of fibrin, are very rich in microbes, which are found either on the surface in the fibrinous layers or in the deep parts of the vegetations. It is probable, therefore, that the bacteria deposited on the valves by the blood-stream develop in the superficial fibrinous layers, and then penetrate tlirough the crevices of the connective tissues as far as the surface and the central parts of the valves. It is also possible that bacteria are primarily introduced by the vessels in the valves. In some cases the vegetations soften into a kind of atheromatous pulp, composed of granulations, cellular debris, fatty elements, and various septic micro-organisms. These different elements, when launched into the blood- stream, cause a source of emboh, which are sometimes mechanical, at other times septic, and affect the brain, hmbs, spleen, hver, intestines, kidneys, etc. The organs affected show hsemoptoic and suppurative infarcts, with miliary abscesses, abscesses of the sldn and the joints, suppuration of the cranial and spinal meninges ; diarrhoea, albuminuria, and enlargemeut of the spleei* are found, and the patient often succumbs to gangrenous, typhoid, toxic, or infectious comphcations, etc. The spleen is usually bulky, as happens, moreover, in many infectious diseases. During hfe the blood contains micro-organisms which can be cultivated. Let us now pass on to the ulcerations of mahgnant endocarditis. They commence as small superficial yellowish patches ; Httle by httle they become deeper and more extensive, and may perforate the valves, causing valvular aneurysms (Foerster, Pelvet). The aneurysms of the sigmoid valves are formed at the expense of the superior face of the valves, those of the mitral valves at the expense of the inferior face. This localization is regulated by the direction of the blood-current, the enlargement taking place on the side of the greater blood-pressure. These ulcerations also cause perforation of the intraventricular septum and rupture of a pillar, or of the chordjE tendineaB. This condition forms a new source of emboli. In many cases, let me repeat, mahgnant endocarditis is at first vegetative and ulcerative. If we analyze the cases and consult the results of autopsies, we shall find a double process of exuberant prohfera- tion and deep ulceration. These different processes explain the method of formation of (Mnboli and their multiple varieties. Experimental pathology has succeeded in producing infective endo- carditis. Ribbert, in 1885, by injecting | gramme of culture of Stdpluj- lococcus aureus into the ear of a rabbit caused embolic foci of carditis and of 400 TEXT-BOOK OF MEDICINE valvular endocarditis, with consecutive lesions of acute endocarditis. Wys- sokowitsch varied the experiments. By means of a silver sound passed into the right carotid he first injured the cardiac valves, and then introduced micro-organisms of different kinds {Staphylococcus pyogenes. Streptococcus septicus, etc.), producing not only parasitic foci of endocarditis, but he also found in the different organs emboU with infarcts and abscesses which contained the same microbes as in the endocardium. Description. — In infective endocarditis the general symptoms are, as a rule, much more important than the local signs. On auscultation, one or several murmurs may be recognized, depending on the severity of the lesion and on the orifice affected. In some cases the murmur is soft or masked by pericarditis, in other cases it acquires a musical tone called whining (Bouil- laud). This whining murmur, which is also met with in chronic valvular lesions, has a peculiar interest in ulcerative endocarditis. It may be due to the vibration of a body (pillar, cord, or vegetation) floating in front of an orifice, and has often given warning of the onset of embolism (Gubler, Potain). Embohsm, whatever its origin, may act in a mechanical way, obliterate a cerebral artery, such as the Sylvian artery, or its branches, and give rise to apoplexy, hemiplegia, aphasia, or softening of the cerebral tissues. The embolism may obliterate the artery of a limb and produce consecutive gangrene. These compUcations are very serious, but, I repeat, they are not infective, and the endocarditis which has given rise to them is purely emboligenous, causing compUcations of a mechanical and not of an in- fective nature. In other cases, on the contrary, the endocarditis is essentially infective, the general symptoms dominate the scene, and we see from the first that the patient is sufEering from an infective disease of a typhoid or pysemie type. When ulcerative endocarditis assumes the typhoid form, dryness of the tongue, prostration, rapid elevation of temperature, shivering fits, which appear during the first days of the attack, are symptoms that give the patient a "typhoid look"; add to this, broncho-pulmonary congestion, stupor, ballooning of the belly, enlargement of the spleen, albumin aria, and diar- rhoea, and we see the difficulty of diagnosis between this typhoid state and typhoid fever. However, the diagnosis of endocarditis is aided by the murmurs audible at the orifices of the heart, by the absence of lenticular rose spots, by the course of the symptoms, by examination and culture of microbes in the blood, and by negative sero -diagnosis. This endocarditis appears to depend on the presence of encapsuled lanceolated microbes (Jaccoud). The pyaemic form of ulcerative endocarditis closely resembles purulent DISEASES OF THE ENDOCARDIUM 401 infection. We find repeated chills and liigh temperature, and, indeed, the case is really one of infection, because the endocarditis throws septic emboK and specijBc bacteria into the blood-stream. These capillary emboli form ecchymotic spots on the surface of the skin and the serous membranes, suppurative infarcts, mihary abscesses, and superficial or deep foci of gan- grene, and provoke suppurative subarachnoid meningitis. The patient has a subicteric tint ; abscesses develop under the skin, and death follows in dehrium. This pysemic form is chiefly met with when the micrococci of suppuration are present in the blood (Jaccoud). When the valves of the right heart are affected, the lungs present ecchy- motic spots, haemoptoic, gangrenous, or suppurating infarcts and abscesses, varying in size from a pea to a nut. The diagnosis is based on auscultation of the heart, and on the finding of foci of suppuration or of phlebitis. For description I have chosen different types of infective endocarditis, but I would hasten to say that these types are not always so clearly marked clinically, and the different varieties just described are often combined. The course and duration of the disease vary in each case. Marked elevation of temperature is not always seen. The disease, instead of being continuous, may show successive attacks, with complete remissions of fairly long duration. The prognosis is not absolutely bad, and recovery has occurred in a fairly large number of cases (Jaccoud). The typhoid form may last several weeks, but the pysemic form is more serious and rapid. Varieties. — I shall now enumerate the chief varieties : 1. Rheumatic Endocarditis. — Rheumatism causes simple, euiboii- genous, or infective endocarditis. The simple form is much the most common, and has served as our descriptive type of acute endocarditis. Rheumatism, however, may give rise to embohgenous endocarditis, with large emboU in the cerebral arteries and in the vessels of the hmbs (Jaccoud). It may also caase infective endocarditis of the typhoid form. Infective endocarditis rarely arises during a first attack of rheumatism ; it usually shows itself in the individual whose endocardium is already the seat of chronic endocarditis. This, says Jaccoud, is the most usual cause of infective rheumatic endocarditis. The pathogenic agent of rheumatism is still unknown, but in some cases the lesions in malignant rheumatic endo- carditis are due to the association of microbes. 2. Pneumonic Endocarditis. — Pneumococcal endocarditis may be para- pneuuKjiiic or metapueumonic ; it may precede pneumonia (prepncumonic) or be quite independent. Tliis variety has a tendency to form vegetations rather than ulcers, and sometimes causes small abscesses in the endocardium. It affects the aortic more often than the mitral orifice, but has also been found in the light heart, affecting the tricuspid and pulmonary valves, rneumonic endocarditis is rarely emboligenous, because the vegetations 26 402 TEXT-BOOK OF MEDICINE are implanted upon a large base. It rarely gives rise to capillary emboli, but is sometimes infective and suppurative ; meningitis is fairly often asso- ciated with it. Pneumonic endocarditis may develop in patients who have had no previous cardiac defect. Old lesions of the valves are, however, singularly favourable to its development. The pneumococcus is not always the sole cause ; other microbes — streptococci and certain unclassified bacilh — are sometimes associated with it. This endocarditis usually passes unnoticed if we do not examine the heart in patients suffering from pneumonia. It fairly often assumes the simple form, and may recover without leaving any traces. Pneumonic endo- carditis has been produced experimentally in the rabbit (Netter), after the valves have previously been injured. 3. Endocarditis in Pregnancy and the Puerperal State.— In infective endocarditis associated with pregnancy it is necessary to distinguish endocarditis gravidarum, which supervenes during pregnancy, from endo- carditis which follows post-puerperal trauma of the uterus. The latter is only a variety of septicgemia, and is much more serious than the former. Non-puerperal trauma of the uterus may j)roduce the same result. Endocarditis gravidarum is less frequent than the puerperal form. Its origin is more difficult to study, for it does not appear to depend on an infec- tion of uterine origin. This variety cannot, however, be looked upon as a simple one supervening in the coujse of pregnancy. The gravid state makes the prognosis of the disease worse, and the foetus itself suffers from the maternal infection. The researches of Nattan-Larri-er have shown that maternal endocarditis causes important histological changes in the organs of the foetus. The toxines in the blood of the mother pass through the placenta, and determine reaction of the blood-forming organs ; while the liver and kidneys show lesions of degeneration which vary directly with the severity of the infection. The evolution of gravid endocarditis is, moreover, variable, and bacteriological examinations have shown that it may be produced by the pneumococcus, the streptococcus (Netter, Weichsel- baum), or by unclassified bacilh (Girode). Puerperal endocarditis shows vegetations and ulcers, and the resulting capillary emboli are septic in nature, and may lead to hsemoptoic or sup- purating infarcts. It is generally due to a streptococcus of extreme virulence. The chnical picture is habitually that of the pysemic form, and though the prognosis is very grave, recovery may take place. Some years ago, with Champetier de Eibes, I saw a case of post-puerperal endocarditis, with septicsemic symptoms, multiple abscesses, and mitral lesions. The patient recovered from the infection and the cardiac lesion — at least, the murmurs disappeared. DISEASES OF THE ENDOCARDIUM 403 These attenuated forms depend, doubtless, on a streptococcus of slight virulence. The streptococcus is not the only pathogenic agent which may- be met with in puerperal endocarditis. Other microbes may infect the uterine wound, and give rise to septicsemia with endocardial lesions. The staphylococcus (Ch. Leer), the pneumococcus (Schahl and Hergott), the coh bacillus (H. Rendu), have been found either in isolated cases or in epidemics of puerperal infection in which the streptococcus was not present. 4. Endocarditis of Septicsemic and Pyaemic Origin.— This form is very common, and is consecutive to a suppurating wound on the surface of the body or in the deep tissues of the organs (urethra, kidney, bladder). It is chiefly due to the entrance of the Streptococcus pyogenes and the Staphylo- coccus pyogenes into the blood, either alone, together, or associated with other microbes. When the mischief is due to the streptococcus, the ulcerations may be extensive, but the vegetations are usually small, soft, and greyish. Infarcts are very frequent, and suppurate rarely, unlike those caused by the staphylo- coccus, which suppurate frequently. When endocarditis is due to the Staphylococcus aureus, as in the case of boils, or of osteomyelitis, as well as of many central or peripheral sup- purative lesions, the disease more usually affects the left than the right heart. Vegetations are more common than ulcerations ; the vegetations are small and soft, while the infarcts are suppurative. Miliary abscesses are found in the spleen, kidneys, lungs, and brain. The cUnical picture recalls the description of purulent infection, with typhoid state, eruptions, and cutaneous suppurations. In the Necker Hospital I had a patient suffer- ing from mahgnant endocarditis of the typhoid form, caused by the Staphylo- coccus albus, which was found' in a pure state during life, and after death in the pus from the miliary abscess in the endocardium. Streptococcal endocarditis consecutive to erysipelas is extremely rare. Curable endocarditis, however, is found fairly frequently during the course of erysipelas. 5. Typhoid Endocarditis. — Primary typhoid endocarditis, due to Eberth's bacillus, is very rarely seen. Cases of secondary typhoid endo- carditis, due to tlie coli bacillus and other microbes, are more frequent. 6. Biliary lithiasis may provoke infective endocarditis, by reason of germs derived from the bile-ducts. The infection appears to be due to micro-organisms derived from the intestine. 7. Tubercular Endocarditis.— This form has only been seen in acute miliary tuberculosis. It appears either in the form of isolated granula- tions — i.e., miliary tubercles, which exist most often on the free edge or auricular face of the mitral valve- or in the form of vegetations. In certain cases Koch's bacilU have been fouuil in these lesions, which 26—2 404 TEXT-BOOK OF MEDICINE may therefore be considered specific. Further, tubercular endocarditis has been produced experimentally in the rabbit by intravenous injection with cultures of Koch's bacillus, preceded by injury of the aortic valves. The vegetations on the valves, produced at the same time as the general miUary tuberculosis, contained the tubercle bacillus. More rarely these lesions are caseous. Koch's bacilh are also present in them. These various lesions are latent, and do not produce special symptoms. Lesions of the endocardium in tubercular patients are not absolutely rare, but they are not always due to Koch's bacillus. The latter are cases of old endocarditis, independent of tuberculosis or of recent more or less vegetating lesions, which have nothing specific as regards histological structure, and in which bacteriological examination sometimes reveals other micro-organisms than Koch's bacillus. These recent lesions fomid post mortem in tubercular patients, most frequently upon the mitral valve, may therefore be considered as due to secondary infections (P. Tessier). 8. Blennorrhagie Endocarditis. — If the reader will turn to the chapter on Blennorrhagia, he will find cases of endocarditis due to the gonococcus. II. CHRONIC ENDOCARDITIS. >Etiology. — Chronic endocarditis arises from the same causes as acute endocarditis, rheumatism claiming the largest share. In alcohohc, sypliiUtic, gouty, or elderly persons it is sometimes secondary to fatty, fibrous, or atheromatous changes which invade the arterial system. The coexistence of tuberculosis and mitral endocarditis has been nqted by Potain and Tessier. Chronic endocarditis often follows the acute form, but at other times it is primary, and becomes estabhshed in an insidious manner. Its course is slow. The valvular lesions develop unknown to the patient, and in rheumatic cases many people, whose health is apparently excellent, only show the first symptoms of valvular mischief after a forgotten attack of acute articular rheumatism. Pathological Anatomy. — The vegetations, which are soft and friable in acute endocarditis, are here hard and fibrous, and the vessels that are so numerous in the acute stage over the swollen mitral valve disappear in proportion as the lesion becomes chronic. The inflammatory process, which commences in the layer of flattened cells, reaches the subjacent layer, which is rich in connective tissue, and gives rise to fibrous tissue. In this fibrous tissue we find islets undergoing fatty change, atheromatous centres and calcareous incrustations, lesions wliich present great analogy with endarteritis deformans. Tliis change in the endocardium, and the retractile property of the fibrous tissue explain the alterations in the valves and orifices of the heart. DISEASES OF THE ENDOCARDIUM 405 Every part of these orifices is invaded. The chordae tendineae and the auriculo-ventricular valves are shortened and indurated ; tlie fibrous zone which surrounds the orifices is hypertrophied. The musculi papillares are also affected. They are sometimes thickened and shortened — the valves may be three or four times larger than normal — or, on the other hand, atrophied or adherent. Their edges are fused, jagged, thickened, and covered mth granulations. The vegetations are chiefly situated on the auricular surface of the auriculo-ventricular valves and on the ventricular surface of the sigmoid valves. These lesions, in which adhesions, fibrosis, atheroma, and calcification are combined, finally cause deformity of the orifices, and impede the action of the valves ; insufl&ciency of the valves and narrowing of the orifices then follow. The muscular fibre of the ventricles and auricles hypertrophies because of the increased work, and compensation is established ; but later when the muscular fibre is also invaded by the morbid process, the columnse carnese and the ventricles show fibrous changes, and their vessels are affected by endarteritis, which causes mal- nutrition. The degenerated cardiac muscle no longer fights with the same efficiency. In some cases (old age, alcoholism) the lesions do not begin in an inflam- matory, but in a retrogressive process, which in its turn induces inflamma- tion. Atheroma plays the principal part. The atheromatous degeneration appears here, as in some cases of endarteritis, to be the primary lesion (Cornil and Ranvier). The symptoms of chronic endocarditis closely resemble those of valvular lesions of the heart, wliich will be studied in the following sections. III. VALVULAR LESIONS OF THE HEART. General Survey. — Whether endocarditis is of microbic origin, as in most acute and also in many chronic cases, or is consecutive to the athero- matous lesions of gout and old age, the lesion may cause transient or per- manent insufficiency and stenosis. An orifice is said to be stenosed, when instead of allowing ten parts of blood to pass at each beat of the heart, it only allows seven, five, or even less, to do so. Insufficiency is present when the valves which normally prevent all regurgitation of blood no longer plug the orifice, and hence allow the blood-wave to regurgitate. The four orifices of the heart (arterial or auriculo-ventricular) may be affected, but those of the left heart are much more often involved than those of the rigiit. Stenosis and insufficiency are often combined at the same orifice ; each of them may, however, show itself alone. This dissociation is chiefly seen iu insufficiency due to mechanical causes. Thus enlargement of the right ventricle brings with it dilatation of the tricuspid orifice and insufficiency 406 TEXT-BOOK OF MEDICINE of the valves, just as enlargement of the aorta, may bring with it dilatation of the aortic orifice and insufficiency of the sigmoid valves. Further, whatever be the mechanism of the lesion, whichever be the orifice affected, as soon as the distribution of the blood- waves is not regular, and one of the parts of the cardiac machinery is affected, the whole circula- tion feels the shock. It is true that the shock is felt more or less slowly according to the orifice damaged and to the efficacy of compensation, but the final result is the same, and, as Jaccoud has forcibly said, valvular lesions raise the pressure in the veins and lower it in the arteries, which is equivalent to saying that they finally cause passive congestion, oedema, dropsy, thrombosis, and haemorrhage, with all their train of functional troubles. Valvular lesions may, nevertheless, be neutralized, even for a long time, provided they are compensated. Compensation is a kind of substitution, due to dilatation of the cavities of the heart and to hypertrophy of its walls. Let us take, for example, aortic insufficiency : The left ventricle is subjected to an excess of pressure by the surplus of regurgitated blood, and its muscular fibre undergoes marked hypertrophy. This mechanism of compensation, which exists in different degrees, according to the orifices affected, renders the valvular lesions harmless for a period varying in duration with the nature and the seat of the lesion. A time comes, however, when the compensation is no longer sufficient. The cardiac muscle, which is badly nourished and invaded by fibrous tissue, wliile its vessels are damaged by endarteritis, has no longer the necessary energy to face the danger. The functional troubles bedome more marked ; congestion, blood-stasis, and dropsy progress ; malnutrition becomes general ; irremediable lesions develop in the organs ; cyanosis, dyspnoea, and coma gradually reach their maximum ; and the condition is summed up in a single word — asystole (Beau). While the heart is being worn out, the small vessels which form the peripheral and local circulation become affected and lose their resistance. Each organ becomes diseased in its turn, and the disease of the heart is changed into a disease of the whole organism. Asystole, however, may, under the influence of proper treatment, or even spontaneously, improve for a time ; but after some remissions, of an uncertam duration, the patient reaches the stage of cardiac cachexia (Andral). The disease is no longer confined to the heart, but affects the whole body. " Thus, when he has ceased to live, the patient has in reality only ceased to die " (Peter). In patients dying from cardiac cachexia we find general changes. The lungs are the seat of congestion, oedema, infarcts, and haemorrhage. The brain is congested; the cerebral sinuses are engorged with dark blood. DISEASES OF THE ENDOCARDIUM 407 The liver, which is large and indurated, presents the so-called " nutmeg change." The kidney, which is enlarged, shows multiple arborizations on its surface. The spleen is engorged with blood. The heart is generally- enlarged ; its muscular fibre is pale, degenerated, and studded with fatty and fibrous islets. It contains clots — some yellowish, fibrinous, firm and adherent, and consequently of old formation ; others soft, cruoric, and of recent formation. Diseases of the heart have not always this slowly progressive course. Some patients die suddenly (aortic insufficiency) ; others are stricken down by comphcations (pulmonary haemorrhage, cerebral embolism). In some the disease is rapid, and cachexia is established in a few months, while in others infective endocarditis is grafted upon an old valvular lesion, and is sometimes fatal. Signs and Symptoms. — The chnical account of diseases of the heart cannot be dealt with in a general survey, because the symptoms of mitral disease are very different from those of aortic disease. I refer the reader, then, to the separate study of each orifice. This statement does not hold good with regard to the signs of cardiac lesions, and notably to the abnormal sounds, the mechanism of which will be better grasped in a general survey. Mechanism of Abnormal Sounds. — Locally, the valvular lesions of the heart are shown by morbid sounds called murmurs and reduplications, the interpretation of which rests upon the previous knowledge of the physio- logical sounds. In the normal state two sounds are heard at the apex : the first is long and well marked, the second is duller and shorter. At the junction of the sternum and the second right intercostal space two sounds are also heard, but the rhythm is the inverse of that at the apex. The first or systolic sound is dull ; the second or diastolic sound is longer and more marked. As two sounds are produced at each orifice of the heart, and as there are four orifices, it follows that eight sounds are produced in each cardiac cycle ; but only four are perceptible (two at the apex and two at the base), because in the normal condition they blend and give rise to two sounds at the apex and two sounds at the base. To what are these sounds due ? Each of them is composed of a chief element, caused in situ, and an accessory or propagated element. First Sound. — At the apex of the heart the first sound has for its chief element the Knap})iiig of the valves (mitral and tricuspid), and for its accessory element the re-echoing of the first sound of the base, which is due to a sudden distension of the arterial walls (aorta and pulmonary artery) by the blood- wave. At the base of the heart the first sound is formed of the same elements, with tliis difference — tiiat the element which was accessory at the apex becomes here the cliicf one, and vice versa. 408 TEXT-BOOK OF MEDICINE Second Sound. — At the apex of the heart the second sound has for its chief element the passage of blood into the ventricles (Skoda's interpreta- tion), and for its accessory element the snapping of the sigmoid valves. At the base of the heart the second sound is made up of the same elements, with this difference — that the element which was accessory at the apex becomes here the chief one, and vice versa. In short, whether it be a case of valvular snapping or of sudden distension of the walls, all normal sounds of the heart are solid sounds (Monneret) ; that is to say, produced by the vibration of solid parts. In pathological conditions, however, the solid sounds undergo the following modifications : First, they are replaced by murmurs — that is to say, by fluid sounds, due to vibrations of a blood- wave traversing a diseased orifice ; secondly, they are reduplicated, the roduphcation occurring in the first or in the second period ; thirdly, they may disappear without other modifications, and without being replaced by any abnormal sound. The blowing murmurs are variable in tone and intensity. They may be softened and prolonged (aortic insufficiency), hissing like a jet of steam (mitral insufficiency), strident (aortic stenosis), or so little marked that they resemble rather a dull rumbhng than a blowing sound (mitral stenosis). In some cases the murmur is changed into a musical sound, called whining (Bouillaud). The whining is due either to the nature of the lesion of the orifice, or to some floating shred thrown into vibration in front of an orifice by the blood- wave. I cannot, however, too strongly insist on this point that the presence of a murmur or of a reduplication is not sufficient t6 prove an organic lesion. We find reduphcations and murmurs which have nothing to do with the lesion of an orifice. Such are the important extra-cardiac murmurs, so carefully described by Potain ; such are the normal reduplications, " resulting from transitory changes which the movements of respiration cause in the pressure of the blood contained in the heart and the great vessels " (Potain). Such, also, are the aortic and mitral murmurs due to chloro-ansemia. Let us, however, return to the organic murmurs of the heart and apply the preceding data to each of the valvular lesions. 1. Mitral insufficiency is characterized by a systolic murmur at the apex. During the ventricular systole in the normal condition the blood- wave from the left ventricle passes completely into the aorta, because the mitral valve plugs the auriculo -valvular orifice ; but in the pathological state, as the valve is not able to plug this orifice, part of the ventricular blood- wave flows back into the auricle, and a systolic murmur is produced. This murmur has its maximum near the apex of the heart, at the level of fche mitral orifice below or outside the nipple. DISEASES OF THE ENDOCARDIUM 409 2. Mitral stenosis is characterized by a diastolic murmur, by a pre- systolic murmur, or by reduplication of the second sound. In order to understand the mechanism and the value of these pathological sounds which are heard at the apex of the heart, we must briefly discuss the ventricular diastole. During diastole the ventricle is dilated, the auriculo-ventricular orifice opens widely, and the blood passes through the auricle into the ventricle. The passage of the blood is, however, somewhat slow. It begins gradually during the ventricular diastole, and terminates more suddenly during the pause, when the auricle is contracted. If, then, the murmur of stenosis is produced during the first part of the passage (which is very rare), it is diastohc (Herard) ; if it is produced during the second part of the passage, it corresponds to the pause, and is therefore presystolic (Gendrin). The murmur of mitral stenosis is not loud, because the blood-wave is feebly pushed through the constricted orifice, even when the auricle is hyper- trophied. Accordingly, this murmur is rather a presystolic booming or rumbling (Duroziez). Mitral stenosis is also characterized by reduplication of the second sound, and as the second part of this reduphcation may be blowing, we find a rhythm of three beats, composed of one long and two short periods. Several theories exist as to this reduplication of the second sound : the one supposes that there is a want of sjmchronism between the second sounds in the two ventricles ; the other holds that the want of synchronism exists between the second sound at the ventricular orifice and the second one at the arterial orifice (Jaccoud). While in the normal condition these two elements are blended, in mitral stenosis they are dissociated, the ventricular being behind the arterial sound. According to Potain, the dissociation depends on the closure of the aortic and pulmonary valves, the closure of the aortic valves being premature. However this may be, reduplication of the second sound, with or without a presystolic murmur, is a sign of mitral stenosis. 3. Aortic insufficiency is characterized by a diastolic murmur at the base. The reasons are : at the moment wlien the blood- wave has just been launched from the ventricle into the aorta, the backward movement finds, normally, an impassa])]e barrier in the sigmoid valves. When, however, these valves are unable to plug the orifice, some of the blood flows back into the ventricle, and a diastolic murmur is produced. 4. Aortic stenosis is characterized by a systolic murmur at the base. If the blood-wave tlirown by the ventricle meets with a coiistrictcd instead of an open orifice, a systolic murmur is produced. 410 TEXT-BOOK OF MEDICINE IV. MITRAL ORIFICE— INSUFFICIENCY AND STENOSIS. Mitral insufficiency is present when the mitral valve, which normally closes the Left aujiculo-ventricular orifice in order to prevent regurgitation of blood, does not plug this orifice, but allows the blood to flow back into the left auricle. Mitral stenosis is present when the lumen of the orifice has lost its normal dimensions. Stenosis and insufficiency are most often combined, and we then speak of mitral disease. If one only is present, we speak of pure stenosis or of pure insufficiency. In many cases the process begins with insufficiency, and stenosis occurs later. Lastly, in some patients stenosis appears to develop from special causes, and remains indefinitely in a pure condition. Pathological Anatomy. — Mitral stenosis may be due to concentric thickening and retraction of the fibrous ring. In most cases, however, the condition is due to lesions of the valves and their chordse. A welding of the free edge of the valves occurs at the level of the commissures. This welding might be compared to the narrowing of the aperture between the eyelids from adhesions of their commissures (Bouillaud). The tendinous pillars inserted on the edge of the valves participate in the cicatricial process. They become rigid, thickened, and retracted, and pull down the bicuspid valve, which takes the shape of a rigid and flattened funnel. In this manner stenosis is brought about, but as a rule neither the fibrous ring nor the vegetations of the auricular surface of the valve take any part. The mitral orifice, which normally is large enough to admit the thumb, becomes so narrow that it will scarcely admit a goose-quill. Dilatation and hypertrophy of the left auricle, followed by that of the right auricle and ventricle, are the consequence ; the left ventricle remains practically normal. The slowing of the blood-stream and the blood-stasis in the left auricle favour the formation of stratified clots, which are often adherent to its posterior wall. These clots, which pass into the left ventricle, and are launched into the blood- stream during systole, may become the source of more or less bulky emboli. On the other hand, the slowing of the blood-stream and the blood-stasis in the right auricle favour the forma- tion of clots, which are also fibrinous and adherent. These clots, which are launched from the right ventricle into the lungs, are the most common cause of pulmonary infarcts. Mitral insufflciency is the result of lesions which affect the valves or the fibrous ring. The lesions of the valves are thickening, induration and incrustations of the edges. There is no welding of the valvular com- missures. Under the influence of the retractile tissue the shortening and retraction of the valves oppose the complete adjustment of their auricular surface during systole, and insufficiency residts. The shortening DISEASES OF THE ENDOCARDIUM 411 of the chordae tendinese, which are also thickened and indurated, opposes the complete straightening of the valve during systole, and this helps to cause insuflEiciency. The papillary muscles, by their fibrous retraction, may act in the same manner. Rapture of the chordae tendineae may be a cause of insufficiency, and I would also mention valvular aneurysms and vegeta- tions. Mitral insufficiency, due not to a lesion of the valves and pillars, but to dilatation of the fibrous ring, does exist, but is relatively rare. In this case the left ventricle, during its dilatation, drags upon the papillary muscles and the tendinous pillars, and consequently produces abnormal tension of the valves and insufficiency. Dilatation of the left ventricle, which has previously lost some part of its contractility, is said, according to some authorities, to be a cause of pure mitral insufficiency, either transient or permanent. Mitral insufficiency induces dilatation and hypertrophy of the left auricle, the right auricle, and the right ventricle. The left ventricle, however, which is almost unaffected in stenosis, shows slight hypertrophy in in- sufficiency. Description. — We see persons among the leisured classes (rather than in hospital patients), who for many years have suffered from some mitral lesion, without having shown any symptoms, because the heart muscle is not overworked, and the lesion is well compensated. The functional hyper- activity of the muscle and the compensatory hypertrophy of the right ven- tricle struggle successfully against the evil distribution of the blood-waves, and undertake the maintenance of equilibrium. Dilatation and hyper- trophy of tlie right ventricle compensate as far as possible for the increase in the pulmonary arterio-venous tension, so that mitral insufficiency and stenosis may be latent for a long while. When, however, the cardiac muscle becomes feeble, or is attacked by some morbid change, such as fibrosis, end- arteritis of the small vessels, or granulo-fatty degeneration, which endangers its nutrition and its tone, we find visceral congestions, peripheral and splanchnic oedema, which result from the cardiac disease. Breathlessness and dyspnoea, with or without palpitation, are generally the first functional troubles in mitral lesions, because the pulmonary circula- tion, which is so close to the mitral lesion, is naturally the first to be affected; bronchial catarrh, congestion, oedema, and ha3morrhage of the lungs are among more or less remote results. These lesions produce increasing dis- tress, witli attacks of dyspnoea and haemoptysis. Breathlessness may for a long time be the only symptom of the mitral lesion. The patient is " short of breath " ; he does not notice it while at rest, but when he walks upstairs or makes an effort, distress appears. At this period the embarrassment of the pulmonary circulation docs not betray itself by any physical signs on auscultation. The slowing of the blood- 412 TEXT-BOOK OF MEDICINE stream and the marked pressure to which the flow in the pulmonary artery is subjected are two of the causes of this dyspnoea. On account of the mitral lesion the blood tarries or flows back into the left auricle, the blood-pressure increases in the auricle, the pulmonary veins and arteries, and the distension of the capillaries of the pulmonary alveoli provokes rigidity and swelling of the lung. Indeed, according to some authors, this rigidity and swelling is said to be the chief cause of cardiac dyspnoea. Later, as the result of pulmonary oedema, the dyspnoea becomes more persistent or intense, and auscultation reveals subcrepitant rales, which are usually present at both bases of the lungs. During this progressive dyspnoea, or even apart from it, the patient sometimes experiences attacks that are more frequent by night than by day, and similar to those of asthma, so that this paroxysmal dyspnoea has been called " cardiac asthma." This name is bad. Mitral disease does not produce true asthma ; the attack has not the characters of the dyspnoea seen in asthma. Let us analyze such an attack in a cardiac case. The breathing is rapid and panting, inspiration and expiration are short and jerky, palpitation is frequent, the pulse is small, the face is pale, and the lips are cyanosed. In asthma the picture is quite different : the breathing is not accelerated, inspiration is slow and painful, while expiration is whistling, spasmodic, and three or four times as long as inspiration ; palpitation is absent, and the pulse preserves its normal rate. In some cardiac cases the attacks of dyspnoea form the chief symptom, and the only sign of mitral disease may at first be attacks of cardiac dyspnoea, just as in ceitain cases of Bright's disease the renal lesion is heralded by attacks of ursemic dyspnoea. The mitral lesion also shows itself by such symptoms as palpitations and feeling of weight or of constriction in the precordial region. These symptoms are especially increased by strain or by active movements. Haemorrhage from the lung (known under the faulty term of pulmonary apoplexy) and haemoptysis, wliich accompanies it, are more common in mitral than in other lesions of the heart. These haemorrhages may be due to the mechanical obstruction of the pulmonary circulation, but are in most cases the result of small emboH, which arise from clots in the right auricle, are arrested in the pulmonary arterioles, and, like all capillary emboli, produce a haemorrhagic infarct. These infarcts, described under Pulmonary Embolism, are frequently followed by haemoptysis. Haemoptysis may be seen at different periods of mitral disease, more usually at a somewhat advanced one. According to the classical description, it appears in the form of blood- stained sputum of a blackish colour and alliaceous odour (Gueneau de Mussy), and lasts for days and weeks (Grisolle). Cardiac haemoptysis may, however, appear before any other symptom, and through a determinant cause (fatigue, excess, or pregnancy). DISEASES OF THE ENDOCARDIUM 413 Pulmonary infarcts, especially when they are cortical, cause sero-fibrinous or puriforni pleurisy, that is usually insidious and more frequent on the right side. Peripheral oedema, starting over the malleoh, is fairly often seen in mitral disease. At first the oedematous infiltration is absent in the morning after the night's rest, but later it becomes permanent, and may affect the thighs, the scrotum, and the trunk (anasarca). The skin of the legs and of the thighs is tliickened, red, and prone to erythema, erysipelas, and gangrene, especially after acupuncture. At an advanced period of heart disease the pleura, peritoneum, and pericardium often contain fluid. Deep-seated oedema affecting the cellular tissue of the splanchnic cavities is of great importance, as we shall see later under Treatment. Visceral congestions appear at different periods. I have already said that congestion of the lung, with or mthout pulmonary oedema, is generally the first to supervene. The obstacle to the pulmonary circulation has a double result : first, haematosis being incomplete, the general nutrition suffers ; second, the embarrassment in the lesser circulation gradually reachas the greater circulation, the right heart grows weak, and general circulatory distress follows. The liver often shows congestion (nutmeg or cardiac hver, with or without cirrhosis). The lesion shows itself by increase in the size of the organ, with acute pains in the hypochondrium, jaundice, and epistaxis. The cardiac liver is often accompanied by ascites. These lesions are most marked in cardiac patients who are also alcohohcs. Gastro-intestinal congestion provokes dyspeptic troubles, with indiges- tion, feehng of weight in the stomach, and somnolence. Congestion of the kidneys is shown by scanty urine, with sediment and albumin, lesions which rarely end in Bright's disease. Congestion of the encephalon and faulty oxygenation in the bulb produce insomnia (Peter), nocturnal delirium, maniacal excitement (Raynaud), and convulsions. Such are the lesions and symptoms of mitral disease. They usually run a slow course, and may last many years before they endanger life. The predominance of pulmonary, hepatic, or gastric troubles masks for a time the true cause of the disease. At length the affected muscle can no longer struggle against the obstacles at the periphery. The disease is no longer limited to the heart ; every organ is affected on its own account, and the entire organism is invaded. This progressive course is interrupted by periods of asystole. The patient, who very rarely dies suddenly (con- trary to aortic insufficiency), at length reaches the final stage of cardiac cachexia. Cerebral embolism may supervene at any period of mitral disease. It 414 TEXT-BOOK OF MEDICINE is more common in stenosis than in insufficiency, and produces troubles, such as cerebral softening, right hemiplegia, aphasia, etc., which will be discussed under Cerebral Embolism. In some cases the embolus follows another course — obUterates the peripheral arteries of the limbs and may produce gangrene. The preceding description refers to mitral disease as a whole — that is to say, the double lesion of insufficiency and stenosis. The functional troubles of mitral insufficiency in some respects resemble those of stenosis. Ausculta- cion, therefore, must differentiate between these two lesions. We find, however, a variety of pure mitral stenosis, which merits a separate description. It is much more frequent in women than men, and is seen in young girls and young women. It is independent of rheumatism and of the other causes which usually produce endocarditis. This stenosis is sometimes associated with chlorosis, and has also been looked upon as a lesion of evolution — i.e., an aplasia — analogous to the stenosis of the aorta and the arteries which, according to some authors, is said to be the anatomical characteristic of chlorosis. Potain, in fifty-five cases of pure mitral stenosis, with autopsies, has found pulmonary tuberculosis in nine of them. Fibrous endocarditis, which in tubercular patients goes on to mitral stenosis, is said by Teissier to be due, not to a bacillary infection, but to a tubercular intoxication. " This fibromatous process, resulting from the phthisiogenic intoxication, may be present in hereditary cases of tubercu- losis, and show itself by a like evolutionary tendency. Mild local tuberculosis (pulmonary, glandular, or osseous), as well as the attenuated hereditary forms (chlorosis, lymphatism, congenital debility), may be the actual factor or the hereditary caus^ of a pure mitral stenosis." Whatever may be its origin and its pathogenesis, this constriction causes such slight functional troubles that it may be latent for years ; but it is none the less serious, for it is frequently accompanied by cerebral embohsm, with hemiplegia and aphasia. Examination of the Heart and Pulse. — In mitral disease the apex is displaced, because of the cardiac hypertrophy, and the beat is in the sixth or seventh space, external to the nipple. The precordial dullness and bulging are less extensive in mitral than in aortic lesions, because the hypertrophy of the right heart is less considerable than that of the left heart. If the hand is applied over the heart, we often feel a systohc thrill. The pulse is small, because the mitral lesion diminishes the column of the blood-wave driven into the aorta. It is unequal and irregular, because the contractions of the left ventricle are not of equal strength and do not follow at equal intervals consecutively to the muscular change in the heart (Stokes), and perhaps also consecutively to the disturbance of the DISEASES OF THE ENDOCARDIUIH 415 cardiac innervation (Peter). These pathological characters of the pulse are revealed by the sphygmograph. The cardiac arrhythmia, perceptible on palpation and auscultation (G. See), is therefore characterized by irregular beats. This arrhythmia only shows itself at an advanced period of the disease ; it is sometimes excessive and is a kind of ataxia of the heart. Intermittences have been divided into true and false. True intermittence affects the pulse and the heart at the same time, the arterial pulsation being absent, because the ventricular systole is lacking. The so-called false intermittence would be better named " incomplete." The cardiac systole persists, but is too feeble to launch' a sufficient blood-wave, and the arterial pulsation is w^anting. Bouillaud has called this a stumble on the part of the heart. These intermittences are more marked in insufficiency than in stenosis, because part of the blood- wave passes back into the auricle instead of the whole wave entering the aorta. Mitral insufRciency shows itself by a somewhat rasping systolic murmur, which may be of a musical character and has its maximum below and external to the nipple. It is called the " apical murmur," in opposition to the basal murmurs, which are situated at the aortic orifice. Further, the maximum is not exactly at the apex of the heart, but rather at the middle part of the ventricle and at the level of the valvular vein (Peter). This murmur is sometimes soft and analogous to a bellows murmur ; at other times harsh and vibrating, like a jet of steam. It is propagated towards the axilla, and is very clear behind, between the scapulae. Mitral stenosis shows itself by various signs, which may be isolated or associated in the same patient. When the signs are complete, and the patient has not arrhythmia, we find a special rhythm of morbid sounds. Analysis shows that mitral stenosis may be characterized by a diastolic murmur (rare), by a rumbhng or presystolic murmur, or by a reduplica- tion of the second sound, while the second portion of this reduplication may be blowing. Mitral lesions are often accompanied by accentuation of tlie second pulmonary sound, from the exaggerated distension which the pulmonary vessels undergo. The coexistence of insufficiency and stenosis is shown by the simultaneous presence of the signs indicated under each of these lesions. Sometimes, on auscultation of a patient with symptoms of mitral disease, no morbid sound is heard, and the physical signs of the lesion only reveal themselves by a disturbance of tlie cardiac rhythm. It must be admitted in such a case that myocarditis is the chief lesion, and that the valvular miscliicf is of but s1i<,fht moment. Diagnosis — Prognosis. I n^jx^at here that the presence of a munuiir or of a reduplication is not enough to prove the existence of a mitral lesion. 416 TEXT-BOOK OF MEDICINE Some reduplications have nothing to do with the lesion of an orifice. Such are the normal redupUcations " resulting from transitory changes which the movements of respiration cause in the pressure of the blood contained in the heart and great vessels " (Potain). Certain murmurs do not depend upon any valvular lesion. Such are the murmurs of chloro- anaemic origin, the febrile murmurs, and the blowing sounds of extracardiac origin, described by Potain. It has been said that the murmur of mitral in- sufficiency is distinguished from other non-organic murmurs in that it alone is heard behind between the inner border of the scapula and the dorsal •spine. This is true with regard to the mitral murmur of a certain intensity, but this distinction loses its value when the murmur is shght. The form of mitral disease indicates fairly the gravity of the prognosis. Pure insufficiency or constriction is less serious than if the two lesions be associated. Intercurrent diseases, such as typhoid fever, eruptive fevers, influenza, and pneumonia, may have an evil influence on the mitral lesion, since they may sometimes graft terrible secondary infections upon it. I would repeat here that infective endocarditis usually supervenes in patients whose previously affected valves present a locus minoris resistentiae. Excess, fatigue, worry, and pregnancy have a deplorable effect upon diseases of the heart. It is opportune to recall Peter's aphorism relative to women suffering from cardiac lesions : " Daughters, no marriage ; wives, no pregnancies ; mothers, no nursing." Treatment. — The treatment of valvular lesions in general and of mitral lesions in particular is not confined to the lesion of the orifice or of the valves, but concerns the resulting compfications and also the concomitant changes hi the myocardium. In this' section I am deafing only with the treatment of " diseases of the heart " properly so called ; the treatment of cardio-aortic lesions will be given later. We have just seen that the symptoms consecutive to the nutral lesion only appear when the cardiac muscle is worn out. As long as the muscle is capable of facing the danger and the compensation is sufficient, all is well, or nearly so ; but when compensation becomes feeble, compUcations which in nearly all cases have a peripheral origin — i.e., visceral congestion and oedema — then appear. Imperfectly compensated valvular lesions lower the pressure in the cardio-arterial system, and raise it in the venous system of the lesser and greater circulations. Venous stases and oedema then appear. The stases affect the lungs, kidneys, brain, Uver, etc. ; the oedema affects the cellular tissue of the periphery and of the splanchnic cavities, the organs susceptible of becoming infiltrated (lung, brain), and the serous cavities (pleura, peri- cardium, and meninges). The tendency of diseases of the heart is therefore DISEASES OF THE ENDOCARDIUM 417 to change the patient into a kind of sponge ; liis organs are saturated with badly circulating blood, while his connective tissue is saturated with serous fluid. In such a medium the anatomical elements and the organs partially lose their function. Whether the disease shows itself by shght symptoms, such as trifling dyspnoea, malleolar oedema, and palpitations ; whether it betrays itself by more serious compHcations, such as orthopnoea, hepatic troubles, ohguria, anasarca, and arrhythmia ; or whether it finally produces the symptom- complex of asystole, the therapeutic indications are the same. It remains to be seen what drugs are most apt to answer to these therapeutic indications. Most authorities who have discussed this question say : Since the troubles in diseases of the heart arise from weakening of the heart muscle and from lowering of the arterial tension, restore the tone and the contractile power of the heart muscle, and at the same time you will raise the arterial pressure. For this purpose employ cardiac tonics. Further, as the lowering of the arterial pressure brings about the elevation of the venous tension, with oedema and congestion, lower this venous tension, and for this purpose employ blood-letting, purgatives, and diuretics. A table of these tonics and diuretic medicines has been drawn up. See has published several excellent papers on the question of cardiac drugs and of the therapeutic physiology of the heart, and I borrow the following classifica- tion from liis ^\Titings : Cardiac tonics : Strophanthus, strophanthin, spartein. Diuretic cardiac tonics : Digitalis, digitalin, Convallaria majalis, convallaraarin. Diuretic drugs : CafEein, theobromin, potash salts, lactose. Respiratory drugs : Iodide of potash, morphia. Our patient may be a prey to arrhythmia, dyspnoea, and oedema ; he may be in a condition bordering on asystole or be suffering from marked asystole. What medicine is to be given, and what indications are to be followed ? Is strophanthin superior to spartein ? is spartein superior to digitahs ? and is not the latter inferior to digitalin ? Is theobromin superior to caflfein, and cafEein superior to convallamarin ? I think that many physiciaas will hesitate, and I have experienced myself the doubts they will experience in making a choice. Such cardiac tonics as strophanthin and spartein had at one time some vogue, in Germany especially, so that it might truly be said that, prior to the discovery of these drugs, the therapeutics of diseases of the heart were in their infancy. CafEein and theobromin are so vaunted by some clinicians that it might be said that before the discovery of those drugs we could not cause diuresis in a cardiac patient, I have closely followed the action of tiicsc drugs, and I have succeeded in forming a clear opinion as to their worth. As far as 27 418 TEXT-BOOK OF MEDICINE I am concerned, I consider that the famous cardiac tonics are often medicines which weaken the contractile power of the muscle under the pretext of im- proving its tone. I have also found that theobromin, which is a valuable diuretic when properly handled, sometimes weakens the renal function under the pretext of exciting it. I am very far from contesting the worth of these drugs, but I think that most of them are far from possessing in asystole the value of digitahs, when it is well prepared and properly ad- ministered. Further, as I have neither the intention nor the pretension of undertaking here a comparative study of all the cardiac drugs, I shall simply give the results of my experience, and point out the treatment which I have employed for several years. Let us take first the most serious case — namely, a patient suffering from symptoms bordering on asystole or from complete asystole. The face is pale and covered with sweat ; the conjunctivae are yellowish ; the lips and ears are bluish ; the hands are swollen and cold, and the fingers cyanosed ; the pulse is small and irregular ; oedema has invaded the feet, legs, thighs, genital organs, and abdomen, and tends to spread higher ; the Uver is en- larged and very painful ; respiration is panting, interrupted by terrible attacks of suffocation, and asphyxia appears imminent. The patient seated in his chair or resting on his pillows, dare not move for fear of suffoca- tion. For a month he has not gone to bed, and sleep is impossible, save for snatches. The urine is scanty and contains much sediment. Auscultation of the heart is impossible ; auscultation of the lungs, thougli difficult, yet permits recognition of rales, due to oedema and pulmonary congestion. Such is the disease : what is the remedy ? I think we must consider both the heart and the periphery. It is uni- versally said that the condition is due to degeneration of the muscular fibre, which must be given fresh energy by means of the cardiac tonics. Letulle has shown that the muscular degeneration is not so great. If the heart is weakened, this degeneration plays only a small part. I am convinced that the most important part comes from the peripheral obstacles, from the blood which engorges the organs, from the serous fluid wliich impregnates the superficial and the splanchnic cellular tissue. In the presence of these obstacles the heart becomes weakened in pumping on the blood-wave, which advances with difiiculty. The arterioles fail to help it, the local circulations are at a standstill, and all the functions of the economy are in distress. I have often made the following comparison : When a cart is too heavily loaded and can advance no farther, the team will not move by whipping the tired horses, but it will do so if we Hghten the load. Similarly : in the case of the heart the desired effect will not be ob- tained by excessive stimulation of its already weakened muscle ; we shall obtain the result by hghtening its work, by diminishing the excess of venous DISEASES OF THE ENDOCARDIUM 419 tension, and by removing, as far as possible, the dam produced by congestion and oedema, and, above all, by improving the tone of the cardiac muscle, which is often rather exhausted than degenerated. To obtain these results I employ in a fairly systematic fashion the follow ing treatment : Six leeches are apphed to the precordial and hepatic regions, and some 5 or 6 ounces of blood are withdrawn. I cannot too strongly recommend the use of leeches, which is far too much neglected. I sometimes prescribe two or three leeches over the heart and over the liver, and I repeat this treatment several days in succession, with great benefit to the patient. At the same time I prescribe digitahs in the form of infusion or of Trousseau's diuretic wine. The drug has a direct cardio-vascular action and an indirect diuretic action. It stimulates the tone of the heart and the vasoconstriction of the peripheral arterioles. This combined action restores to the normal the inverted current of the interstitial exchanges. The arterioles and the heart muscle combine their energies to bring about a squeezing action on the parenchymata and the connective spaces. Digitahs, by its action on the heart and the vessels, restores to the cardio-vascular mechanism the functional energy wliich was lacking, and as Potain says ; " It is also an indirect diuretic, which causes the fluid of dropsy and of oedema to re-enter the circulation and be eliminated by the kidneys." The immediate result, as Loeper has shown, is a serous plethora of the blood, characterized by diminution in the total of albumin and in the red corpuscles, which are widely scattered through an increased quantity of fluid, and by increase of the chlorides and other principles wliich have accu- mulated in the tissues. The above is the first effect of digitalis, and iscalled the blood stage (Loeper) ; the urinary stage at once follows, and polyuria results. The polyuria varies directly with the amount of oedema due to asystole ; it often assumes the guise of a crisis which carries off in the urine the excess of chlorides, phosphates, and sulphates in the tissues. Improvement then follows. Digitahs alone, without other drugs, may yield the good results just mentioned. I feel, however, that it is preferable to add a true diuretic which acts on the kidney, wliile the digitahs acts upon the heart and the vessels. Trousseau's diuretic wine is a diuretic which does not exhaust the kidney and a cardiac tonic which does not exhaust the heart. The formula is ; White wine Alcohol (90 per cent.) Juniper berries Acetate of potash Digitalis leaves Sc^uill 7 pints 17 ounces 12 „ 7 „ -I j> 1 „ '>7 o 420 TEXT-BOOK OF MEDICINE I give 1 ur 2 tablespoonfuls daily for five or six days. One table spoonful contains 3 grains of digitalis, 10 grains of acetate of potash, 15 grains of jumper berries, and IJ grains of squill. We must note that Trousseau's formula has been altered, and that the wine in the Codex and hospital formulae contains 10 instead of 3 grains of digitaUs in a tablespoonful. A physician ignorant of this incomprehensible change would thus give his patient a far larger dose than he intended. I, therefore, ask for a return to the classical formula, wliich should never have been tampered with. For the diuretic wine we may substitute infusion of digitalis and theo- bromin given together. Make an infusion of digitahs leaves, 15 grains in 3f ounces of boiling water, filter, and add 8 drachms of syrup of currants. Give 1 ounce daily for a week ; stop the drug, and repeat if need be. At the same time theobromin is given in daily doses of 7 grains. It is absolutely necessary for the patient to take milk as a food and as a diuretic. He m.ay take it to his hking : boiled or fresh, hot, cold, or iced. The milk should be given every two hours in doses of 3 or more ounces, according to the tolerance of the patient. To alter its taste we may add orange-flower water or a spoonful of tea or of coffee, and we" may aerate it by aid of the sparklet. If the milk is badly digested, lime-water is added. In case of intolerance, cow's milk is stopped, and recourse made to goat's or to ass's milk, kephir. or koumiss. All other food is forbidden. Ices made with coffee, vanilla, citron, or with fruits are permitted. To produce active diuresis, I give lactose dissolved in Evian or in Vittel water. When lactose is simply tlirown into the water, the patient com- plains of the mixture, because the sugar does not dissolve well in cold water. The following solution must therefore be made : The lactose is first dissolved in a small quantity of hot water, and the solution poured into a bottle of Evian water, from which an equivalent quantity of fluid has previously been withdrawn. We have then a drink which, although not disagreeable to taste, may be rendered more agreeable by the addition of orange-juice, lemon- juice, or champagne. A cup of milk and a cup of lactose solution are taken alternately every one or two hours. In short, leeches, digitahs, diuretics, and especially Trousseau's wine, are used almost systematically for patients who come into hospital with asystole, or in a condition bordering on it. My cases are described in the hospital records, where they may be consulted, and I may say that, under this treatment, which is simple and easy, success is the rule and failure the exception. The urine, which has been as low as 6 ounces before treat- ment, amounts to 2 or 3 pints after a few days. A patient, for example, who drinks daily 4 pints of milk and 2 pints of DISEASES OF THE ENDOCARDIIJIM 421 lactose solution — that is to say, about 6 pints of fluid — sometimes passes about 8 to 10 pints of urine. The urine exceeds, therefore, the fluid ingested by 2 to 4 pints. This excess comes from the fluid which was enmeshed in the form of oedema in the superficial and in the splanchnic cellular tissue. When care is taken to weigh the patient daily, and to measure exactly the quantity of the fluid ingested and of the urine voided, we find that the weight of the patient diminishes by about 1 pound per pmt of urine excreted in excess. In a case of anasarca I have verified the fact that a patient may hold 20 to 30 pints of fluid in liis cellular tissue. The attention is as a rule only evoked by superficial oedema, but there is also hidden in the splanchnic cavities oedema which escapes notice and is most serious, because of the embarrassment it causes in the different functions. The subjoined chart shows the result in a woman who was moribund and cyanosed. The amount of urine was about 3 to 4 ounces. Under Weight of the Invalid in Kilos 60 Z5 ^0 65 60 55 50 Quantify of Urine in Litres. 7 6 5 2 1 Resuff oStainee/ in\ 16 eliPiys V s, ^ v.. ■^, T' IK y > \ ^ y^ x^ ^.N y r V. >k, "^ ^ \ y Y > ^:. IN < fe^ ^ ,/ r \ii> ^^< ^S/'^-J es •* -^ ^L ' ^//os Da''"'^'' 21 22 23 2a 26 26 27 26 / 2 3 a 5 6 7 6 9 rebruary March Fio. 19. — Weight and Ukine Chart. treatment the improvement was so rapid as to be a brilliant therapeutic success. In a fortnight she passed 100 pints of urine, and as the anasarca disappeared, she lost nearly 60 pounds in weight. The chlorides at the commencement of the urinary crisis amounted to 1 ounce. By the means just quoted the oedema disappears, the visceral congestion diminishes, the dyspnoea improves, and the heart-beats become regular. In place of distress, a delightful feehng of quiet obtains, movement is possible without attacks of suffocation, the broncho-pulmonary rales tend to dis- appear, and the patient can he down in bed and sleep. In some cases, however, disappointments occur. Some patients are refractory to treatment, others vomit the milk and solution of lactose, no matter what we do. The difficulty is surmounted by giving iced water in small amounts and by enemata composed of 6 ounces of the lactose solution. 422 TEXT-BOOK OF MEDICINE If, after some days of the above treatment, no improvement has accrued, and if the asystole becomes worse, we must lessen the work of the heart and reheve the patient's suffering by withdrawing the fluid from the pleura and the peritoneum. We must treat the oedema of the limbs and genital organs in the same way, and provide points of exit. We, therefore, make punctures, which are sometimes followed by lymphangitis, erysipelas, or patches of gangrene, in spite of antiseptic precautions, or else we apply the cautery once or twice to each hmb ; Vienna paste makes an issue which, once opened, acts like a fountain. In urgent cases, however, punctures are preferable. I have not yet spoken of morphia or of heroin ; not that I reject their use — on the contrary, I think that they are excellent adjuvants in severe dyspnoea, but they should be prescribed in very small doses. I must now mention certain accidents which may occur unless the case be carefully watched. The use of digitalis or digitalin, even in small doses, must not be too long continued, because the drug may be cumulative, and lead to sudden asystole. An inexperienced or careless physician mistakes the condition for obstinate asystole, and goes on with digitalis, being lucky if he does not increase the dose. " Characteristic pallor of the face and general coldness, with cyanosis, are signs of advanced poisoning, because they indicate vasoconstriction due to the predominant action of the sympa- thetic nerve. Tachycardia, arrhythmia, and pulsus bigeminus are symptoms of vasoparesis ; such a condition is asystole due to digitalis " (Huchard). Another matter deserves notice. During the treatment we must care- fully collect the urine passed in the twenty-four hours, and watch the parallel diminution in the weight of the patient. The reason is : Under treatment the oedema may be in part absorbed, without increase in the urine, or, in other words, the blood stage is not followed by polyuria. The serous fluid is absorbed and enters the circulation, but it is not eliminated by the kidneys in due course. Serous apoplexy may then follow, as pointed out by Andral. The symptoms are coma, convulsions, and dehrium. Cheyne Stokes breathing may or may not be present. We must add that these troubles are chiefly to be feared in patients whose kidneys are abeady affected. In any case, we see the reason for associating with the digitahs a true diuretic in order to favour the urinary as well as the blood stage. In addition to the troubles above noted, the patient may be seized with syncope and dyspnoea, which seem to herald early death. We may then ask whether sudden dilatation of the heart does not comphcate an already dangerous situation. In this case cardiac drugs must be handled with extreme care. Perhaps it is better to omit them. It has long been my practice to place an ice-bag over the heart, and patients feel such reHef that they will not dispense with it. Oxygen should be given in large doses. Ehxir of mate may be given in drachm doses. Injections of oil of camphor DISEASES OP THE ENDOCARDIUM 423 are useful, and strychnine may be given in the same way once or twice daily. When the patient has got over his asystole, when the excess of chlorides has been eliminated in the urine, when the dyspnoea, anasarca, and ar- rhythmia are better, he must not be considered as cured, for the cardiac lesion persists, and may at a given moment reproduce the same effects. For several weeks to come he should take only milk, or milky foods, eggs, stewed fruit, and a httle bread. Salt (chloride of sodium) should be proscribed, for we know that it favours the production of oedema (Widal, Merklen). Alcoholic drinks and tobacco should always be forbidden. Local treatment should not be neglected. It consists in an appUcation of Vienna paste to the cardiac region, and the issue is allowed to suppurate freely. Such is the treatment. It often dispenses with other cardiac tonics, such as strophanthin and spartein. It proves clearly that in the cardiac Btorm which we call asystole the true danger lies, not only in the heart, but in every organ and at the periphery, where congestion and oedema occur. The proof that the heart is worn out rather than degenerated is that, when the storm is over, it resumes its functions, and may do so sometimes for months and years before it becomes again enfeebled. We see daily such cases in hospital. Amongst other examples I would quote the case of a moribund woman treated in this manner. In spite of her mitral lesion, she has since remained in a very satisfactorj' state of health. I would mention, top, the case of a blacksmith, also cured of asystole for four years. In spite of a mitral lesion, he has been able to carry on his heavy work without any fresh mishap. He reports himself at the hospital every four or five months for a fresh issue to be made, because, he says, when the counter-irritation no longer acts, he experiences slight dyspncea and palpitation, which improve when the free issue is employed. I have thus seen a large number of asystolic patients resume their business for years. The attentive study of all these cases has inspired me with some thoughts on the subject of prognosis in diseases of the heart. When we have seen a certain number of cardiac patients triumph once or several times over the asystolic storms, and practically resume their work, we say that the mitral disease is too often considered as a very grave malady of almost fatal ter- mination, but it does not possess such a gloomy prognosis. The heart is a gallant organ ; it is the idtimum moriens. We have slandered it a little, since we have been willing to assign too large a part to the lesions of its vessels and its myocardium. We must treat it carefully when it is sick, assist it when its work is too difficult, but we must avoid forcing and weaken- ing it with cardiac tonics. I have just discussed the treatment during asystole, but what treat- ment should be used when the patient only complains of dyspnoea, oedema, or of cardiac angina ? In the first place, I recommend the treatment which 424 TEXT-BOOK OF MEDICINE I have just indicated, for it succeeds the better and quicker the less pro- nounced the comphcations. If dyspnoea is the cliief symptom, we may also employ iodide of potash, which is given in doses of 10 grains in the twenty-four hours. Lastly, at the onset of the mitral disease, if there is no notable com- plication, and if the disease only shows itself by palpitation, subcrepitant rales from pulmonary oedema, slight dyspnoea, or some oedema over the malleoli, the physician should not remain inactive, but should foresee and prevent the more serious complications, and attempt to stop the progress of the disease. It is useful to produce in the precordial region an issue which is allowed to suppurate, and which is renewed if there is occasion. Heavy meals, alcoholic drinks, and the use of tobacco should be forbidden. The professions which entail excitement, such as gambhng and the Stock Exchange, furnish a marked proportion of cardiac cases. Peter has seen many politicians in whom the disease made rapid progress. A life free from excitement and fatigue should be advised in these cases, and conduces to longevity. I employ the above treatment in a systematic manner, but I do not mean that other treatment may not give good results. Thus, digitalis may be given as a tincture or maceration. Digitalin is prescribed by Potain in an alcohohc solution (Nativelle's crystaUized digitahn, or Homolle's digitalin), of which 25 drops corre- spond to a demimilhgramme. This drug is taken at one dose in a little water, and three or four days should elapse before administering a fresh dose. The oily solution of Nativelle's digitalin may be given by subcutaneous injection in doses of | milhgramme per cubic centimetre. Strophanthus is chiefly indicated as a cardiac tonic. It does not slow the heart-beats, but it raises the contractile power of the myocardium. Five to twenty drops of the tincture are given. Caffein may be given in daily doses of from 7 to 30 grains, either in solution or by hypodermic injections. IjL Distilled water . . . . . . . . 5iii. Benzoate of soda . . . . . . . . 3i. Caffein . . , . . . . . . 3i. A Pravaz syringe of this solution contains 3 grains of caffein. That excellent diuretic theobromine is given in cachets, in doses of from 7 to 15 grains. The dose is increased or repeated if necessary. DISEASES OF THE ENDOCARDIUM 425 V. AORTIC ORIFICE— INSUFFICIENCY AND STENOSIS. Aortic insufficiency is present when the sigmoid valves which normally close the orifice, in order to prevent the backward flow of blood, do not sufficiently plug it to prevent the blood from flowing back into the left ventricle. Aortic stenosis occurs when the lumen of the orifice no longer has its normal dimensions. The aortic orifice, from its situation, participates in lesions of the aorta more than in other lesions of the heart. Thus, inflammations of the aorta and their most usual causes, especially syphilis, are, more often than rheu- matic endocarditis, the origin of lesions at the aortic orifice. According to circumstances, the lesions are sometimes those of chronic aortitis, at other times those of chronic endocarditis. Aortic insufficiency and stenosis are often combined. These lesions are due to adhesions, deformities of the sigmoid valves, vegetations, or calcareous incrustations of the valves or of the walls. Pure insufficiency is frequently associated with enlargement of the aorta, which, in its dilatation, pulls on the walls of the orifice. The stenosis is not always exactly at the orifice. Subaortic narrowing (Vulpian, Peter), arising from the contraction of the portion which is just in front of the opening of the aorta, has been described. Lesions of the aortic orifice, and especially insufficiency, cause enormous hypertrophy of the heart, in which the left ventricle takes so large a part (bovine heart). This hypertrophy, called providential, depends upon the hyperactivity of the heart muscle ; part of the blood- wave flows back into the left ventricle, and hypertrophy takes place because the work is ex- aggerated. Examination of the Heart and the Pulse — 1. Aortic Insufficiency. — In aortic insufficiency the precordial bulging and dullness are more extensive than in mitral lesions. The impulse may be diffuse and the apex- beat is in the sixth or seventh space. The pulse is characteristic, being regular, bounding (Corrigan) and falling (Stokes) : bounding, because the blood is violently propelled by the hypertrophied ventricle ; faUing, because the pulse vanishes directly after the beat, the aortic blood-wave being pro- pagated in two directions at the same time — towards the periphery and towards the- ventricle. These characters are seen in the sphygmographic tracing ; the line of ascent is sudden, because of the hypertrophy of tlie ven- tricle, and ends in a notch, wliich coincides with the return wave into tlio ventricle. The force of the systole communicates itself to the great arteries ; their pulsations are exaggerated, and often yield a thrill. It is in aortic insuificiency that we see best the changes of colour under the nails, iso- chronous with the cardiac systole. This phenomenon has been called the capillary pulse. 426 TEXT-BOOK OF MEDICINE We hear in the second right intercostal space a diastolic murmur, due to the propagation of a part of the blood-wave toward the left ventricle. Tliis diastolic murmur is heard in the great vessels of the neck and limbs. Thus, when the stethoscope is applied over the femoral artery, two murmurs (double crural murmur) are heard at the point compressed — a " souffle d'aller," which is not pathological, but due to the vibration of the blood- wave launched from the heart ; and a reflux murmur, which is much softer, and due to the vibration of the blood- wave, which tends to flow backwards. In order that the reflux murmur may be produced, the artery must be firmly compressed by the stethoscope, but not too much. The second murmur is sometimes replaced by a tone which has the same value (Skoda). The theory of flux and reflux in the arteries is hardly admitted to-day. The reflux remains absolutely true for the return of the blood- wave from the aorta into the left ventricle, but the backward return of the column of blood does not continue in the arteries. It is rather admitted that the phenomena described above result from the lowering of the arterial tension, which induces an exaggeration in the vibrations of the artery and a rapidity of the waves (Potain). The reflux murmur and the water-hammer pulse, which are sometimes so clear in pure insufficiency, are naturally less marked if stenosis is also present, because the blood- wave no longer finds so free a passage. Ausculta- tion at the aortic orifice also reveals the disappearance or the diminution of the second sound, which normally is due to the closure of the sigmoid valves. 2. Aortic Stenosis. — In aortic stenosis hypertrophy of the ventricle is also very pronounced, but the pulse is small, and shows in the sphygmo- graphic tracing an inclined up-stroke, because the blood-wave passes in a threadlike stream through the constricted orifice. Auscultation in the second right space reveals a systolic murmur, which is harsh and vibrating. This murmur is propagated into the great vessels which arise from the aorta, and often extends along the descending aorta to the interscapular region. General Symptoms. — These appear more slowly than those of mitral lesions, because aortic lesions are better compensated by the hypertrophy of the left ventricle, and because they have a less direct reaction upon the pulmonary and the general circulation. The patient looks anaemic, because the blood in part returns into the ventricle and does not all reach its destina- tion. He is also affected by cerebral congestion, due to the exaggerated ventricular contractions, and shown by epistaxis, pulsations in the tem- poral arteries, dizziness, ringing in the ears, etc. Some patients complain of angina pectoris, and are liable to faint. In this case the lesion of the aortic orifice is accompanied by aortitis, and DISEASES OF THE ENDOCARDIUM 427 the symptoms of aortitis are associated with those due to the insufficiency and the stenosis (Peter). The aortic lesions remain a local malady much longer than the mitral lesions, and it is only at a remote date (degeneration of the muscular fibre or mitral comphcations) that the invasion of the economy becomes general — • that congestion, cedema, and the symptoms, which precede or accompany asystole, appear. The patient may, however, be carried off suddenly before this stage. Sudden death is a fairly common termination in aortic lesions (Aran, Mauriac), while it is exceptional in mitral disease. Writers have attributed it to endarteritis obhterans, insufficiency of circulation in the coronary arteries (Mauriac), and angina pectoris, which is often associated with the aortic lesions (Peter). Treatment. — We cannot produce much action on the lesions of the aortic orifice. The cardiac erethism should be quieted by local (leeches, cupping, ice-bags) or general treatment. The iodides are absolutely indicated. We shall see in subsequent chapters the treatment for lesions of the aortic orifice associated with aortitis or sypliilis. VI. THE TRICUSPID ORIFICE— INSUFFICIENCY AND STENOSIS. .flStiology. — Inflammatory changes in the tricuspid valve are somewhat rare, except in foetal hfe. They nearly always affect the valves on both sides of the heart. Duroziez, however, maintains that they are less rare than is generally believed. The fibrous and atheromatous lesions of chronic endocarditis do not often attack the right heart. On the other hand, tricupsid insufficiency is often the result of a mechanical cause — namely, dilatation of the right ventricle. By reason of the exaggerated blood- pressure which occurs in chronic diseases of the lung, or in mitral lesions, the right ventricle allows itself to be distended. It also becomes distended through dystrophy of its muscular fibres, with or %vithout adhesions to tlie pericardium and the pleura, and drags with it the insertion zone of the tricuspid valve, which becomes incompetent. Some authorities, on the other hand (Potain and Rendu), refer this insufficiency to the increase in the capacity of the right ventricle. The direction of the ventricular pillars is altered ; the chordae tendinese are not long enough to permit the closure of the valves, and functional insufficiency results. Dilatation of the fibrous ring, correctly speaking, is quite exceptional. Reflex spasm of the pulmonary vessels (Potain and Franck) arising from gastro-hcpatic affections leads to dilatation of the right ventricle and fimctional insufficiency of the tricuspid valve. Lastly, acute and chronic 428 ■ TEXT-BOOK OF MEDICINE myocarditis and cardiac degenerations may end in like manner, by favouring paresis of the right ventricle. Pathological Anatomy. — In cases of inflammatory insufficiency the lesions are analogous to those of the mitral valves, and do not therefore require further details. In functional incompetence the valves are healthy, but the size of the right auriculo-ventricular orifice and ventricle is much increased. The ventricular walls are rather dilated than hypertrophied in insufficiency of inflammatory origin. The right auricle is dilated, and its walls are thinned. The venae cavse and the jugular veins are always much distended with blood. As regards the chief viscera, such as the Hver and kidney, more or less marked signs of blood-stasis are present. Description. — Tricuspid insufficiency is characterized by a systolic murmur, with its maximum at the xiphoid cartilage, while its tone is deeper and less whistHng than that of mitral incompetence. As the tricuspid valve is the " regulator of the venous circulation and of the general venous tension " (Raynoud), we must look for the cliief symptoms of this lesion in the venous system. Jugular pulsation first attracts attention. On inspection and with the sphygmograph, the external jugular vein shows an expansion and retraction, which is known as the venous pulse, and is explained in the following manner : During the systole, part of the blood- wave flows back into the right ventricle, and thence into the venous system. This pressure causes dilata- tion of the veins, and the valves of the external jugular veins become in- competent. Accordingly, at each ventricular systole the blood flows back into the venous system, and the jugular veins show a true systolic and sometimes dicrotic venous pulse, synchronous with the double auricular and ventricular systole. The reflux of blood in the inferior vena cava and the portal vein causes hepatic pulsations, which may be felt on palpation. The venous pulse may be present in the veins of the periphery, especially in the saphenous veins, when they are varicose. We know the gravity of tricuspid lesions, for " they form the bond of union between lesions of the lesser and the greater circulation " (Peter). Tricuspid insufficiency opens the door to asystole (Raynaud) ; so that the murmur has been rightly called the symptomatic murmur of asystole (Parrot). When equilibrium has been restored by appropriate treatment, the asystole disappears temporarily or finally, and with it the functional in- sufficiency. The latter may appear and disappear several times before being finally established. The disappearance and reappearance of the characteristic signs will serve as a guide in this respect. In some cases tricuspid insufficiency is certainly beneficial. It may DISEASES OF THE ENDOCARDIUM 429 eliminate or diniiiiish the excess of pressure in the lesser circulation, and thus prevent vascular ruptures. Indeed, the general condition some- times improves on the appearance of insufficiency. Hence the tricuspid valve has been called the safety-valve of the pulmonary circulation. Stenosis. — -Tricuspid stenosis may be congenital or acquired. Congenital stenosis is due to foetal endocarditis or to faults of development. Acquired stenosis is due to the adhesion of the valves, to stenosis of the tricuspid orifice, or to obstruction of this orifice by vegetations. Adhesions between the valves is the most usual cause, both before and after birth (Leudet). Perforation of the septa and stenosis of the pulmonary artery are frequent comphcations. Acquired stenosis is chiefly seen in women. It is usually due to rheu- matism, and nearly always coincides with stenosis of the mitral or other orifice. The chief symptoms are cyanosis, ascites, oedema, and curving of the nails. The venous pulse in the jugular veins is often absent, and a diastolic shock, with or without thrill, is found. The prognosis is very grave, and death usually occurs between the ages of twenty and twenty-five years. The diagnosis is possible when stenosis of the tricuspid orifice occurs without lesions of other orifices. VII. PULMONARY ARTERY— STENOSIS AND INSUFFICIENCY. Stenosis of the pulmonary ar-tery may be congenital or acquired. Congenital stenosis usually involves the sigmoid valves, which are adherent and enclose a more or less narrow cleft. As they are in close apposition, they obstruct the reflux of blood into the right ventricle. Hence insufficiency associated with congenital stenosis is rare. In some cases the stenosis affects the infundibulum, and has been called " prearterial " (C. Paul). The valves are often affected in such cases. The stenosis may involve the trunk of the artery in exceptional cases. Acquired stenosis, wliich is more frequent than is supposed, nearly always affects the valves, but cases of atheroma and of gummata (Schwalbe) affecting the pulmonary artery and causing constriction have been pubhshed. Apart from such exceptional cases, acquired stenosis of the valves often accompanies dilata- tion of the pulmonary artery beyond the obstruction, thus forming an exact opposite to the condition in aortic stenosis. Arterial dilatation is not seen in cases of congenital stenosis. The right ventricle is always hypertrophied and dilated. In congenital cases we often see perforation of the interventricular or interauricular septum, and sometimes persistence of the ductus arteriosus. Tiiis perfora- tion may also be seen in cases of acquired stenosis (C. Paul) resulting from myocarditis, wliich often accorapames endocarditis of the right heart. 430 TEXT-BOOK OF MEDICINE Congenital stenosis is certainly of inflammatory origin, but the cause of foetal endomyocarditis is generally obscure. In adults rheumatism, perhaps also traumatism, and especially infectious diseases, such as the eruptive fevers, puerperal conditions, broncho-pneumonia, etc., have been held responsible. Stenosis of the pulmonary artery may long pass unnoticed. In other cases the patient soon becomes breathless, and hable to frequent fits of coughing, which may be accompanied by bloody sputum. Chilliness of the extremities and sensations of numbness and anaesthesia in the hmbs are common. Cyanosis is much less constant, and its mechanism has received a different interpretation (see Morbus Caeruleus). It often appears at an advanced period of the disease, or as the result of some broncho-pulmonary complication. On auscultation, stenosis of the pulmonary artery is characterized by a systohc murmur, which is loudest in the second intercostal space, and can be traced towards the clavicle. Palpation sometimes reveals the existence of a systolic thrill at the same spot, and percussion shows more or less hypertrophy of the right ventricle. The sufferer rarely reaches adult age. Death frequently results from progressive asystole or from syncope, but the striking fact is that pulmonary stenosis appears to favour the development of phthisis in some cases. Insufficiency of the pulmonary artery rarely exists alone, especially when it is congenital. It is nearly always associated with stenosis. In the acquired form it results from the same causes as stenosis. It is characterized by a diastolic murmur, wliich is loudest in the second left space, and can be traced along the left border of the sternum. Functional troubles, chiefly in the lesser circulation, are present, and comprise dyspnoea and frequent haemoptysis. It is often accompanied by hypertrophy and dilatation of the right ventricle, and ends in death from asystole. On the other hand, the development of tubercles in the lung is exceptional when there is no coexistent stenosis. VIII. MORBUS CiERULEUS— CYANOSIS. This disease, which is most common in early life, is characterized by a bluish colour of the skin and the mucous membranes, with dyspnoea, attacks of suffocation, torpor, inertia, and tendency to chilhness. These symptoms result from cardiac and vascular lesions, which bring about the mixture- of the arterial and venous blood, and do not allow the venous blood to be sufficiently arterialized. Pathology. — The mixture of arterial and venous blood results from abnormal communication between the arterial and venous systems, and the abnormahties which make this communication possible affect the heart and DISEASES OF THE ENDOCARDIUM 431 great vessels. The abnormalities of the heart are represented by the persistence of Botallo's foramen (52 out of 69 cases, Gintrac), by communica- tion between the two ventricles (33 cases, Guillon), and by fusion of the cardiac cavities, so that the heart may show only one, two, or three cavities. The vascular abnormalities comprise abnormal origin of the vessels and per- sistence of the ductus arteriosus (30 cases, Almagro). Most of these mal- formations are congenital, and apparently due to arrested development of the heart, to endocarditis, and especially to stenosis of the pulmonary artery arising during intra-uterine life. Raynaud says of this mechanism : " When pulmonary stenosis is present, the consecutive changes in the heart are perfectly intelUgible. The right ventricle hypertrophies, because the obstruction demands increased work, but the dilatation is slight or absent, because the imperfect septum allows blood to flow back into the left cavities. The formation of the septum becomes arrested as a result of the reflux in question. If the lesion has arisen before the development of the ventricular septum — that is to say, before the end of the second month — -the two ventricles continue to communicate with one another, and the communication is the larger, as the pulmonary artery remains closed at a time more closely approaching that of conception. If, on the other hand, the ventricles are already shut off from one another when obhteration of the pulmonary artery takes place, the flow of blood from the right auricle into the corresponding ventricle is prevented, a powerful current is- established from the right to the left side of the auricular chamber, and Botallo's foramen remains open. As the aorta, howevei, is from this time the only channel open to the blood-stream, the blood can only reach the lungs through the ductus arteriosus, which therefore persists after birth as a permeable tube." These lesions, however, although they allow, more or less, the mingling of arterial and venous blood, do not always cause symptoms of morbus caruleus. Indeed, there are many examples (Gelau, Longhurst) showing that excellent health and absence of cyanosis have for many years been compatible with the mixing of the arterial and venous blood. Another factor is therefore reqilired to produce morbus caeruleus, and the lesions most favourable to tliis result are those wliich do not allow the mixed blood to be properly oxygenated in the lung. Examination of the blood has shown an increase in the number of red corpuscles (hyperglobulia), which may reach 8,000,000 or more. This hyperglobulia is often accompanied by an increase in the diameter of the red corpuscles (Vaquez). These phenomena have been compared to the hyperglobulia of higli altitudes, and have also been looked on as a means of defence on the part of the organism, which seeks to obtain compensation for the difficulty in oxygenation of the blood. 432 TEXT-BOOK OF MEDICINE Description. — The bluish coloration is most marked in the lips, the nostrils, the lobes of the ears, the ends of the fingers and toes, and the mucous membrane of the tongue and pharynx. The cyanosis is not always of the same intensity, and diminishes during sleep or after a long rest, while slight effort causes it to return. The fingers, in addition to the violet tint, show marked deformity, the last phalanx being swollen and rounded, while the nails are tliick, broad, and curved. Respiration is short and painful, the voice is shrill and jerky, and the patient cannot take exercise without feehng short of breath and suffering from palpitation, angina, and syncope. He is conscious of the lowering of his temperature (95° F., Tupper), and the slowness of his movements somewhat resembles those of cold-blooded animals. The cyanosis, dyspnoea, somnolence, apathy, and coldness are explained by the fact that the blood contains too much carbonic acid and not sufficient oxygen. The duration of life depends upon the nature and gravity of the lesion. Some patients die from asphyxia or syncope, while others become tubercular. Examination of the heart gives uncertain information as to the precise site of the lesion. The area of dullness varies with the hypertrophy of the ventricle, and palpation sometimes reveals a continuous thrill with rein- forcement. The murmurs heard on auscultation vary. Perhaps the systolic murmur, with its maximum at the fourth dorsal vertebra, indicates tiie persistence of a ductus arteriosus. CHAPTER III DISEASES OF THE MYOCARDIUM Myocarditis, or carditis, is inflammation of the heart. Virchow described two varieties : parenchymatous, or inflammation of the muscle ; and in- terstitial, or inflammation of the connective tissue. The former is usually found in acute cases, while the latter obtains in mo.st of the chronic cases. At the present day the general term of fibrosis of the heart is more often used. I. ACUTE MYOCARDITIS— FATTY DEGENERATION OF THE HEART. >Etiology. — Acute primary myocarditis is very rare (chill, injury). The causes of the secondary form are : (1) Rheumatism. The heart alone may be affected, or may be involved with the pericardium and endocardium. (2) Infectious diseases. Amongst these we must quote, as of primary impor- tance, typhoid fever, variola, scarlatina, diphtheria, erysipelas, puerperal fever, purulent infection, and ulcerative endocarditis. AlcohoUsm, syphihs, overwork, and previous cardiac lesions, also favour its development. In certain infectious diseases, such as diphtheria, the pathogenic agent does not enter the blood, and yet acute myocarditis is fairly frequent. In these cases toxines appear to play the chief part, just as in acute myocarditis, experimentally produced by injection of a filtered culture of the Bacillus pyoci/aneus into the veins. In other affections, however, such as typhoid fever, the pathogenic microbe has been found between the inflamed muscular fibres, and it may then be asked whether the micro-organism acts directly on the myocardium, or secondarily by its secretory products. The latter explanation is more generally accepted. In all these cases a certain role must be assigned to waste products which have accumulated in the blood, and, indeed, they alone (scurvy, experimental overwork) may be capable of affecting the vitality of the heart muscle. Pathological Anatomy. — The heart is generally enlarged, and its walls arc llabby and pale. (Ju section the dead-leaf tint of the muscular tissue 433 li.S 434 TEXT-BOOK OF MEDICINE is very clear. The tissue tears easily, explaining the ruptures of the musculi papillares and the intracardiac haemorrhages. Under the microscope the muscular bundles show more or less advanced changes : the striation is less clear than usual, and we find in the fibre fine fatty granules, which mask its structure. Vitreous or amyloid degeneration may be seen. The nuclei are swollen and sometimes increased in number. Metchnikoi!, however, says that this nuclear multiphcation is only apparent, and the increase is simply the result of the penetration of phagocytes into the inflamed fibres. In some cases the fibres are separated, and their anastomoses broken, as though the cement had been dissolved. The arterioles present clear traces of endarteritis and periarteritis. The question of inflammation or of degeneration has been much dis- cussed. Virchow, Zenker, and Hayem regard the condition as a parenchy- matous inflammation. Cohnheim, Cornil and Ranvier, and Rindfleisch, who base their opinion on the almost constant integrity of the interstitial tissue, hold that the lesions are degenerative. Hanot has cleared up the question by showing that the pathogenic agents may affect both the mucular and the comiective tissue. Each element reacts in its own way, but in both cases the condition is due to an inflammatory process. Suppurative myocarditis is rarer, and is chiefly seen in purulent infection and puerperal conditions. The pus may infiltrate the tissue, but is more often collected in the form of an abscess. The abscess may open into the pericardium or into the ventricles, and cause embohsms in the lesser or greater circulation. It may undergo caseous change and favour the forma- tion of an aneurysm. Description. — Acute myocarditis is not a self-evident affection, and its diagnosis demands careful search. Since it nearly always supervenes as a comphcation of some other disease, it often passes unnoticed. Weakness and irregularity of the heart-beats and of the pulse are the general signs. We also find disappearance of the first sound, while the second sound persists, but is muffled and distant. The second sound may, indeed, be replaced by a shght rusthng. When the myocarditis is less severe, the first sound may be replaced by a soft murmur, which is limited to the apex, and shows a marked tendency to alter from one moment to another. Under the same conditions we sometimes hear a " bruit de galop," due to a diastolic shock, indicating the ventricular dilatation which accompanies the change in the myocardium. Arrhythmia, which is often present, has been divided into regular and irregular. In the former the cardiac contrac- tion exists, but is so weak that it cannot be recognized either by ausculta- tion or by examination of the pulse. Sphygmographic tracings alone show that the arrhythmia is only ajDparent, and that an abortive pulsation really corresponds to the interval of silence. Lastly, the cardiac rhythm may DISEASES OF THE MYOCARDIUM 435 resemble that of the foetal heart, the condition being called embryo- cardia. The prognosis in these cases is very bad. Acute myocarditis is generally painless, although Peter has remarked that pain is caused by percussion of the third and fourth intercostal spaces, and radiates along the course of the phrenic nerve and the cardiac plexus. In some cases of typhoid fever painful crises resembhng those of angina pectoris have also been observed. In conjunction with the troubles affecting the power and rhythm of the heart-beats, we may note in some patients tachycardia, cyanosis, oedema, and chilhness of the extremities — in short, all the signs of algid collapse ; in others the phenomena of acute asystole predominate (cardiac form of typhoid fever). Lastly, we may see repeated attacks of syncope, wliich at times prove fatal. In typhoid fever in particular, some authorities, of whom I am not one, have attributed sudden death to acute myocarditis. This question will be treated in detail under Typhoid Fever. When recovery follows, Landouzy and Siredey think that the myo- cardium may preserve some rehcs of the profound change which it has undergone, and that this change may ultimately assist in the development of chronic mischief. Counter-irritation to the precordial region and cardiac tonics, such as digitaUs and caffein, are the measures generally employed for feeble action of the myocardium, but I would only recommend the use of these drugs with reserve. Degeneration is often irregular, especially when it is dependent upon a change in the nutrient vessels of the heart. In these cases the wall of the ventricle, especially at the apex, is often thinned. The symptoms of acute fatty degeneration of the heart resemble those of parenchymatous myocarditis. As regards chronic fatty degeneration, the symptomatology is practically that of fibrosis of the heart, with this differ- ence, however — that the phenomena of cardiac excitation are wanting. At first the striking fact is the weakness of the heat-beats, the increase in the size of the organ, showing its dilatation, and lastly, the phenomena of peri- pheral and visceral stasis. Accordingly, after some time asystole follows unless sudden rupture of the heart causes death. Fatty Degeneration. — Fatty degeneration of the heart has more in common with acute myocarditis. Ranvier, indeed, denies the latter disease, which would therefore be characterized solely by a fatty change in the muscles of the heart. Many conditions give rise to fatty degeneration. (1) Certain poisons (phosphorus, arsenic^^tc.) cause complete degeneration in a few days (acute degeneration) ; (2) alcoholism, lesions of the heart and of the valves which impede the circulation in the coronary arteries, gout, and old age cause chronic degeneration. 28—2 436 TEXT-BOOK OF MEDICINE In the second group we must also place cachectic conditions, resulting from chronic diseases, deep-seated suppuration, intense anaemia of long duration due to repeated loss of blood, chronic diarrhoea, and athrepsia. It is, however, important to distinguish between fatty degeneration and fatty overgrowth. The latter chiefly occurs in obese patients. It may exist alone for a long while before the malnutrition of the heart, due to accumulation of fat on its surface and between its muscular bundles, causes changes. Some causes (alcoholism), however, may produce simultaneous over- growth and degeneration. The macroscopic appearances are the same as in parenchymatous myo- carditis, but the microscope shows that the nuclei of the muscular fibres are intact, while the interior of the fibres is replaced by droplets of fat, which may be large, and which have taken the place of the sarcolemma. Frequently, also, a certain degree of granulo-pigmentary degeneration is seen. The coronary vessels, especially in chronic affections of the heart, are thickened, and their lumen is constricted or obliterated, proving the joermanent nature of the obstacle opposed to the nutrition of the myocardium. II. FIBROSIS OF THE HEART. Fibrosis of the heart, or inflammation of the connective tissue, corresponds in part to the old interstitial myocarditis of Virchow. It may be circumscribed or diffuse. When circumscribed it commences around foreign bodies in the walls of the heart — e.g^.,, hydatid vesicles or syphilitic gumma ta. It is also seen in areas of pericarditis or of endocarditis. In adherent pericardium the fibrosis may extend deeply and cause pericardogenous myocarditis (Brouardel, Poulain). Interstitial endocardogenous myo- carditis is much rarer. In children, however, we see constriction of the infundibulum due to tliis origin. The diffuse form constitutes fibrosis of the heart properly speaking. It has lately been the object of important work, which has profoundly modified our conceptions of the diseases of the myocardium. It nearly always begins with arterio-sclerosis of the arteries of the heart, and occurs chiefly in persons poisoned by alcohol, lead, and tobacco ; in arthritic, gouty, or syphilitic patients ; or in those who suffer from Bright's disease and malarial cachexia. It is also seen in elderly or overworked persons. It is important to remember that in all these cases more or less pronounced fibrous change is also present in most of the organs. Many are dependent upon atheroma or on arterio-sclerosis (Gull and Sutton, Debove, etc.). It may also be seen, as a secondary lesion, in patients suffering from valvular DISEASES OF THE MYOCARDIUM 437 affections. According to Du Pasquier, the large fibroid heart is associated with blood-stasis and ischemia. The fibroid heart is increased in size, of a brownish colour, and firm con- sistency. It cuts with difficulty, and we find at the most diseased points greyish-white patches, due to the inflammatory process. These patches are more frequent in the left than in the right heart, and more marked in the pillars of the interventricular septum, and especially near the apex. In some hearts these islets of fibrosis are only visible under the microscope ; they then appear to be composed of fibrillary connective tissue that is more or less dense, according to the age and interweaving of the elastic fibres (Letulle). Some develop around an artery affected by endoperiarteritis, while others are situated at a distance from the arteries. In the latter case we find no trace of periarteritis. Endarteritis exists alone, and shows itself at first sight by a narrowing in the calibre of the vessel. The second variety is the more frequent. Each may exist alone, but they are sometimes found together in the same patient, the fibrosis being mixed. The muscular bundles situated at the periphery of the fibrous islets are atrophied and broken up ; at the centre of the islet they have quite dis- appeared. Those situated externally to the inflammatory or degenerative process are enlarged, but their contents have often undergone fatty changes or amyloid degeneration (Letulle). These changes may lead to diminished resistance of the walls of the heart, with the formation of aneurysms, which generally develop at the spots where the pressure is most marked and the lesions in the muscle are most pronounced — namely, near the apex and in the left ventricle (Pelvet). Symptoms. — When the fibrosis has caused an aneurysm, sudden death may occur from rupture of the heart. In some cases very sharp precordial pain, due to the tearing of some deep muscle bundles, precedes the rupture by some days (Robin). Sudden death has also been noted in many cases of diffuse or circumscribed gummatous myocarditis (Mauriac). In general, fibrosis of the heart is of slow evolution and characterized by no pathognomonic symptoms. At the onset the patient complains of palpitation, breathlessness, dyspnoea, and sometimes of angina pectoris. The pulse is full ; the impulse is forcible. The apex of the heart is lowered and carried towards the axilla ; the first sound of the heart is dull ; the second, on the contrary, is ringing. The first sound is often reduplicated. This gallop rhythm, however, indicates arterio-sclerosis, rather than fibrosis of the myocardium. The pulse gradually becomes weak and irregular, the respiratory troubles increase, stasis-phenomena appear, and, after repeated truces, asystole finally results, just as in the case of uncompensated valvular lesions. The symptoms, due to the concomitant fibrous lesions in the kidneys, are often present as well, and these complex cases tax the 438 TEXT-BOOK OF MEDICINE skill of the physician in recognizing, from the symptomatology, the part belonging to each. Huchard says that it is possible to distinguish four chief forma of cardio-fibrosis : (1) A painful form, angina pectoris ; (2) an arrhythmic form, or " incurable claudication of the heart " ; (3) a tachycardiac form often associated with the preceding one ; (4) a myovalvular form characterized by mitral or aortic murmur, with evident fibrous lesions. Treatment. — At the onset we must employ means which lower the tension — e.g., milk diet, massage and passive movements, balneo-therapy at Bourbon-Lancy, Royat, or at Evian. An alcohohc solution of trinitrine, in doses of from 2 to 10 drops daily in water, may be prescribed. Tetra- nitrol has been advised in doses of y^ to ^ of a grain several times daily. Iodide of sodium is especially indicated. Later we may employ, but with great care, cardiac stimulants, such as caffein, digitahs, and strophanthus, for symptoms of asystole. We must never forget that cardio-fibrosis may be syphilitic in origin, in wliich case injections of biniodide of mercury are indicated. III. ANEURYSMS OF THE HEART— INFARCTS AND FIBROUS PATCHES, ETC.— RUPTURE OF THE HEART. Aneurysms of the heart affect chiefly the valves, the interventricular septum, and the apex. 1. Valvular aneurysms result from acute and especially from infective endocarditis. " The multiphcation of cells, their embryonic condition, the softening of the intercellular substance, and the disappearance of the elastic fibres — phenomena which are associated with endocarditis — deprive the valve of its power of resistance." As a result of this inflammatory process, two things may happen : the valve is perforated, or remains distended, and forms an aneurysm. Aneurysms of the sigmoid and mitral valves always have their opening at the side upon which the blood-pressure acts. A sigmoid aneurysm opens on the upper or arterial surface of the sigmoid valves, because the blood- pressure acts on this surface, while a mitral aneurysm opens on the inferior or ventricular surface, which supports the pressure of the blood during systole, when the valve is closed. Valvular aneurysms rarely preserve their spherical shape. They are more or less torn by the blood-stream, and the valve is converted into shreds. This rupture may show itself by a murmur which appears suddenly in the course of infective endocarditis. The murmur is due to insufficiency, and is therefore systohc if the mitral valve is affected, diastohc if the lesion affects the aortic valves. Apart from these exceptional cases, we find during hfe no indications of the rupture of the aneurysm. 2. Aneurysms of the interventricular septum usually have the same origin DISEASES OF THE MYOCARDIUM 439 as the preceding form, and are often simply the extension of a valvular aneurysm. As a rule, they are found by chance at the autopsy. When they burst by perforation, communication between the two ventricles allows arterial and venous blood to mix. 3. Aneurysms of the apex of the heart, also called partial, are quite different in their pathogenesis. They are due to fibrous myocarditis, or to simultaneous inflammation of the myocardium and endocardium. The fibrous spots have no reactive power, and readily yield to the blood- pressure ; dilatation and, later, aneurysm result. Some authors (Kundrat, Huchard) regard obUteration of the coronary arteries as important. The area, deprived of nutrient vessels, loses its resistance, and the aneurysm forms imperceptibly. As pericardial adhesions are frequently present near these aneurysms, the question has been asked whether these adhesions may not, by repeated traction, facihtate the production of a partial aneurysm. These aneurysms are, as a rule, situated in the left ventricle, near the apex. The tumour is so large that the size of the heart is doubled (coBUr en bissac). The aneurysm generally opens into the ventricle, and the blood-stasis within the sac is not sufficiently complete to bring about the formation of stratified clots. Cases have, however, been noted in which the aneurysmal cavity was filled with clots of this nature. The limiting wall is sometimes infiltrated with calcareous salts. There is, so to say, no symptomatology of these aneurysms. Sometimes one is found by chance post moYtem ; at other times the patient dies in asystole, or more often from rupture of the heart. The existence of a diastolic murmur at the apex, independent of aortic insufficiency, has, however, been noted, and also a diastolic sound heard over the middle portion of the heart, and differing from the gallop rhythm in Bright's disease by its clearer tone (Rendu). Infarcts and Fibrous Patches in the Myocardium. Post mortem, we sometimes find on the surface of the ventricles depres- sions resembling scars. On section of the ventricle we see that these de- pressions correspond to fibrous tissue which has replaced the myocardium to a more or less large extent. Sometimes, as in one of my patients, the muscle of the wall is replaced at the sclerosed patch by fibrous tissue, which is only one-third or one- fourth of the normal thickness. We find under the microscope simply connective tissue and dilated vessels. They are called fibrous patches in the myocardium. Thoy have long been known, but were until recent years looked upon as the result of chronic inflammation. We know to-day that these lesions are distinct from localized fibrosis of the myocardium, and are the result of an infarct ; they are true cicatrices. The myocardium may indeed Ijc the scat of an infarct, just as all organs 440 TEXT-BOOK OF MEDICINE and tissues in which the arterial anastomoses are not sufficiently numerous. The heart answers to this disposition, for the coronary arteries, which anastomose freely at the base, become terminal at the apex. The seat of election of these infarcts, caused by obstruction of one of the coronary arteries, is thus explained. This obhteration rarely occurs from embohsm. It is in the majority of cases a thrombosis, produced by the lesions of arteritis obliterans. The infarct may show itself either as a hmited yellow or red focus, the colour being due to necrosis of the damaged tissue, or as a haemorrhagic focus. In the latter case it has been supposed that the blood in the heart cavity secondarily inundates the focus of necrosis. The formation of some aneurysms of the heart may be thus explained. If the patient does not succumb, the infarct changes into cicatricial tissue, which may undergo calcification, and form the fibrous patch in the myo- cardium. When this scar is extensive, it forms a weak spot in the wall of the ventricle, and may lead to aneurysm and rupture of the heart. Although the production of an infarct may sometimes be revealed by precordial pain and tachycardia, the lesion has, as a rule, no clinical history. Rupture of the Heart. Rupture of the heart occurs in the course of some affections of the myocardium. Partial aneurysm of the heart, softening of the heart muscle by rapid obhteration of a coronary artery, fatty degeneration, and infective myocarditis, are the most frequent causes of these ruptures. The rupture may take place from without inwards-, but it more often occurs from within outwards, and is then due to the pressure of the blood upon the inner surface of the heart. In the former case, on the con- trary, the contraction of the affected muscle produces the tear. Both mechanisms may also occur together. In this case the two lines of rupture, instead of corresponding, are separated by unbroken muscular bundles. The rupture may be double or triple, but the apex of the left ventricle is the seat of election. At this point the wall is thinned, especially in cases of partial aneurysm, or of fibrous myocarditis. The pericardium is usually full of dark coagulated blood. The rupture is usually caused by a strain. Cases of rupture during sleep have, however, been quoted. It shows itself by inexpressible distress and acute precordial pain, which may radiate to the back and to the left shoulder. The patient utters a cry, his face becomes cyanosed, the beating of the heart is tumultuous, the pulse is small and cannot be counted, the breathing rapidly becomes embarrassed, and the patient dies within a few seconds. The rupture may be gradual, and may only become complete at the end of several days. We then see, in addition to the pain and vomiting which marked the onset of the rupture, the other symptoms just enumerated. DISEASES OF THE MYOCARDIUM 141 IV. SYPHILIS OF THE HEART. vEtiology. — Syphilitic lesions of the heart, first noted in 1859 by Virchow, are now becoming well kno^vn. They are chiefly seen during the tertiary period, about ten years after infection (JulUen), though they may appear earUer or later. Parrot has pubhshed several cases of hereditary syphihs of the heart in the new-born. Letulle and Nattan-Larrier have seen miliary gummata upon the valves in a syphihtic child who died at birth. Pathological Anatomy.— S}T)hihs affects the valves more rarely than the myocardium, especially the left ventricle. The interventricular septum and orifices are not often involved. Gumma or fibrosis is the usual lesion. The latter is recognized by its clear locahzation to one part of the heart, the other zones being free, and by the severity of the arterial lesions at this point, the arteries of the other regions being healthy. These characters, however, are not specific, and at most allow a suspicion of syphiUs, especially in the absence of other visceral manifestations. Syphilitic gummata in the heart, as in other organs, constitute the only real specific lesion. Their yellowish appearance, their elastic consist- ency, their well-defined hmits, their multiphcity, or the coexistence of miliary gummata in the neighbourhood, and the recognition of lesions in the liver, kidneys, etc., can hardly allow any mistake. In some cases they are surrounded by healthy muscular tissue, and project towards the endo- cardium, or towards the pericardium. The serous membranes are thickened ; the layers of the pericardium may be adherent. In other cases, on the con- trary, the endocardium is not thickened, but ulcerated, the gumma having emptied itself into the ventricular cavity, while the blood has entered the cavity, hollowed out at the expense of the myocardium. The possibihty of partial aneurysm is readily seen. Description. — The disease often remains latent, and is only discovered post mortem. In other cases we find all the .signs of a chronic affection of the myocardium — namely, increased precordial dullness, indistinct and irregular heart sounds (Semmola), arrhythmic pulse, retro-sternal pain, dyspnoea on effort, oedema, and cachexia. In short, we see the evolution of cardio-fibrosis or of progressive asystole. More .striking are the cases in which a syphilitic person previously exempt from cardiac trouble is taken ill with acute asystole, that proves fatal in one or two days (Tessier). Rapid death may be due to agonizing dyspnoea, recalling some pulmonary lesion rather than a cardiac affection. Lastly, sudden death may be consecutive to rupture of the heart, to syncope, or to embolism. The pathogenic diagnosis of cardiac syphilis is a matter of supposition. However, in a patient with old .syphilis, wlio suffers from symptoms of cardio-fibrosis, sypliilis should always be thought of, and daily injections of biniodido of mercury be administered. 442 TEXT-BOOK OF MEDICINE V. TUMOURS OF THE HEART AND TUBERCULOSIS OF THE MYOCARDIUM. Some rare cases of primary spindle-celled sarcoma are seen. Epithe- lioma naturally afEects the heart only as a secondary growth. Most cases of " cancer of the heart " are really secondary nodules of epithehoma, and are quite exceptional. These nodules are secondary to cancer of the ali- mentary canal, the lung, etc. ; in most cases they coexist with secondary nodules in the lung. They are situated in the myocardium, and chiefly in the right heart or in the interventricular septum. Cancer of the heart is not as a rule recognized during hfe. In some cases it may give rise to dyspnoea, tachycardia, precordial pain, etc. I have reported the case of a patient suffering from pleuro-pulmonary cancer, whose pulse-rate was ex- tremely quickened. At the autopsy I found a cancerous nodule as large as a hemp-seed in the interventricular septum. The other tumours are myxomata, forming pedunculated swelHngs on the auricular surface of the mitral valve, and hydatid cysts, which may be present in the myocardium as in other muscles. This affection is exceptional, and its sole clinical interest hes in the possibility of hydatid emboli, when the cyst opens into the cardiac cavity. Tuberculosis of the myocardium is a rare affection, which has no clinical history, and is found by chance post mortem. As a rule, it is coexistent with tubercular pericarditis, and frequently with tubercular lesions of the peritracheal glands. We may find miUary tuberculosis, but more often we see large isolated tubercles in which Koch's bacillus has been found. These large tubercles may be caseous or calcified. Koch's bacilli have been found by Peron even in the calcified lesions. Tubercular lesions of the myocardium are chiefly situated in the ventricles, and are most often seen in children. Tuberculosis of the myocardium is frequent in domestic animals which have become tubercular (dogs, bovine animals, and pigs), while it is rare in laboratory animals inoculated with tubercular products (Peron). VI. HYPERTROPHY AND DILATATION OF THE HEART. Pathology. — A muscle hypertrophies when it undergoes increased work. This general law includes the heart, which hypertrophies as the result of excessive or repeated contractions. The causes of this hypertrophy may be divided into two classes (Jaccoud) : (1) Simple or purely functional hypertrophy ; (2) hypertrophy from some mechanical obstacle. Simple Hypertrophy. — This form, which is also called primary, is due to nervous palpitation, and consequently to the causes producing this palpi- tation (adolescence, hypertrophy of growth, excesses of every kind, DISEASES OF THE MYOCARDIUM 443 abuse of drink, tobacco, tea, or coffee, hypertrophy in exophthalmic goitre). The whole heart is affected, and the hypertrophy does not as a rule, involve any special portion of the organ. Hypertrophy from Mechanical Obstacles. — The causes are : (1) lesions of the heart ; (2) lesions of the vascular system ; (3) lesions or abnormal conditions of more or less distant organs. 1. The mechanism by which valvular lesions of the heart cause hyper- trophy is readily understood. When an obstacle exists at one of the orifices, whether it is the reflux of the blood-wave, as in insufficiency, or whether this wave pass with difficulty through the orifice and the cavity, which is in front of the diseased opening, in order to overcome the excess of pressure, the walls of the cavity are subjected to exaggerated functional irritation, which finally produces hypertrophy. The h}T)ertrophy, which is at first locaUzed to the cavity in front of the diseased opening, finally extends to the other cavities. For example, lesions of the mitral orifice increase the blood-pressure in the left auricle, which hypertrophies ; the blood-stasis in the left auricle increases in its turn the blood-pressure in the pulmonary veins, the pulmonary artery, and the right cavities of the heart ; the right ventricle therefore is exposed to excess of work, as well as to exaggerated functional irritation, which, by its persistence, produces hypertrophy. This hypertrophy is, within hmits, compensatory to the mitral lesions, but the excess of blood-pressure in the right ventricle finally reacts on the venae cavse and the capillaries of the greater circulation. From the capil- laries the excess of tension reaches the arterial system, and finally the left ventricle shows hypertrophy. The lesions of the aortic orifice produce analogous effects, but different in degree. The power of the left ventricle and the enormous hypertrophy which accompanies aortic stenosis and incompetence protect the lesser circulation for a long while, so that the excess of tension in the pulmonary vessels and the right cavities of the heart appears later, and is less complete than in mitral lesions. 2. Aneurysm of the aorta or of the great vessels, acute or chronic aortitis, endarteritis, and general atheroma, are the lesions of the arterial system which may produce hypertrophy of the left cavities of the heart. How do such lesions determine hypertrophy of the left ventricle ? In the normal state the elasticity of the arteries diminishes the resist- ance experienced by the blood in passing from the heart to the vessels (Marey). Hence diseases which abolish or diminish this elasticity increase the resistance and raise the blood-pressure, the result being hypertrophy of the left ventricle. This pathology is perfectly applicable to chronic aortitis and to more or less general atheroma, though it does not sufficiently explain other cases. 444 TEXT-BOOK OF MEDICINE For instance, acute aortitis is nearly always accompanied by hypertrophy of the left ventricle, which must not be set down to a concomitant lesion of the aortic orifice, because it occurs in cases in which acute aortitis exists without comphcations. Aneurysms are often accompanied by hypertrophy of the left ventricle. In fifty-eight cases of aortic aneurysm hypertrophy of the ventricle was present in fifty-three. This hypertrophy cannot be set down to excess of pressure, for physiological experiments have proved that the presence of an elastic sac in the course of a vessel does not interfere with the circulation. Aneurysms of the arch of the aorta are by no means always accompanied by hypertrophy of the heart. In a certain number of cases (I have verified this fact three times post mortem) the heart was normal in size, although the aortic aneurysms were large. Arterial lesions of the lesser circulation cause hypertrophy of the right ventricle. Congenital or acquired stenosis of the pulmonary artery leads to hypertrophy and dilatation of the cavity of the right heart, Arterio-sclerosis of the heart, associated with sclerosis of the myo- cardium will be discussed under Bright's Disease. 3. The morbid condition of certain organs reacts upon the heart and determines hypertrophy. Chronic diseases of the lung react on the right ventricle, which dilates and hypertrophies ; chronic pleurisy and costo- vertebral deformities may produce the same result ; interstitial nephritis causes hypertrophy of the left ventricle (Traube, Potain). The mechanism in this case will be discussed under Bright's Disease. Transitory hyper- trophy of the left ventricle during pregnancy is generally admitted. Potain has reported cases of cardiac hypertrophy following lesions of the brachial plexus. Chronic lesions of the liver may favour dilatation and slight hypertrophy of the right ventricle (Potain). Cardiac hypertrophy following growth is said, to result from a want of parallel development between the heart and the other organs (See). Dilatation of the cavities of the heart nearly always accompanies hypertrophy (excentric hyper- trophy). It may be general or local, and as it depends on the lessened resistance of the walls, it is more marked in the right cavities of the heart. Often the chief lesion is dilatation, and is seen following diseases which lessen the resistance of the heart- wall. The dystrophies of the heart muscle, described under Degeneration and Myocarditis, belong to this class. Pathological Anatomy. — In true hypertrophy the size and weight of the heart are increased. The weight may reach as much as 1,000 grammes (the normal weight is 300 grammes). The thickness of the left ventricle reaches 3 or 4 centimetres (12 millimetres being the normal) ; the thickness of the right ventricle amounts to from 1 to 2 centimetres (3 millimetres bein» the normal thickness). DISEASES OF THE MYOCARDIUM 445 The structure has given rise to much discussion (LetuUe). Some hold that the hypertrophy is due to increase in the number of the primary bundles, while others admit increase in the size of the bundles, or both of these causes. Hypertrophy is not due solely to the change in the muscle. Lesions of the connective tissue, the endocardium, the pericardium, and the vessels are present in a hypertrophied heart. Nevertheless, the change in the muscular fibre is most important. There is no proof of the multiplica- tion of the primary bundles, while their hypernutrition is admitted by all authorities, and each primary bundle, instead of having the normal diameter of 15 to 20 fjb, reaches one of 25 to 30 /i. The muscular hypertrophy is dispersed through the affected regions, and in proportion as hypertrophy gives place to organic decay, the heart is invaded by diffuse fibrosis, by endoperiarteritis of the small vessels, and by disseminated fatty degeneration. In some cases more or less general cardiac cirrhosis is seen. The fibrous tissue appears to be localized around the small arteries in the heart muscle. The fibrosis of the myocardium is said to be consecutive to endo- periarteritis. The shape of the heart shows Uttle change when the hypertrophy is general, but is much modified in cases of partial hypertrophy. In this manner local hypertrophy of the left ventricle increases the longitudinal diameter of the heart, giving it an oval shape and an almost horizontal direction. The septum encroaches on the cavity of the right ventricle, and the papillary muscles are much enlarged. Hypertrophy of the right ventricle increases the transverse diameter of the heart, and tends to give it a spherical shape. Description. — As Jaccoud has observed, care must be taken to distinguish the symptoms proper to simple hypertrophy from those of hypertrophy, accompanied by cardio-pulmonary changes. As long as the muscle has not undergone fibro-fatty degeneration, hypertrophy of the heart produces neither blood-stasis nor dropsy. On the contrary, the hyper- trophied walls sometimes propel the blood with increased vigour, and cause congestion. Thus the enormous hypertrophy of the left ventricle in aortic insufficiency is often accompanied by cerebral congestion, with flushing, dimness of sight, ringing in the ears, headache, vertigo, and epis- taxis. The impulse of the blood-wave is shown tliroughout the whole arterial system by pulsation in the carotids, bounding pulse, dilatation and elongation of the arteries, and the patient complains of palpitation, precordial distress, and dyspnrjca. When, however, the hypertrophied and dilated muscles undergo fibro- fatty degeneration, and compensation begins to fail, the train of symptoms which we have enumerated several times in the last few sections appears. 446 TEXT-BOOK OF MEDICINE The physical signs of hypertrophy of the heart are as follows : The apex of the heart is displaced downwards and outwards, and the impulse has its maximum to the left of the sternum if the left ventricle is afiected, and in the epigastric angle if the right ventricle is involved. The pre- cordial bulging depends on the extent of the hypertrophy. The dullness is increased in the longitudinal direction by hypertrophy of the left ventricle, and in a transverse one by that of the right ventricle. Pure hypertrophy, apart from valvular lesions, does not show itself by any abnormal sound. The gallop rhythm present in hypertrophy of renal origin will be studied under Bright's Disease. Diagnosis — Prognosis. — The diagnosis of hypertrophy of the heart is made from the symptoms above mentioned. We must be on our guard in cases where the size of the heart is masked by the exaggerated percussion resonance of emphysema. The diagnosis between hypertrophy and peri- cardial effusions has been discussed under Pericarditis. Purely functional hypertrophy is not serious, and the compensatory form is favourable, in that it diminishes for a time the extreme gravity of the valvular lesions. The phenomena of congestion due to excessive cardiac contractions may produce troublesome results. In such cases it is necessary to diminish the tension in the arterial system, and to moderate the cardiac erethism. VII. ASYSTOLE. The word asystole must not be taken literally, for the absence of systole means death. In coining the word asystole, Beau supposed that, at an advanced period in valvular lesions of the heart, the contractions of the organ are so faulty that they open the road for congestion, oedema, and all the symptoms of cardiac cachexia. Beau's description remains true, but the interpretation of asystole must be modified. Asystole is produced by any cause which interferes with the contraction of the heart muscle. This class includes excessive fatigue, overwork, adherent pericardium, valvular lesions, imperfectly compensated dilatation, and especially degeneration of the muscular fibre (Stokes). It is proper to add that these causes of cardiac origin may be reinforced by those of peripheral or vascular origin, such as malnutrition and defective resistance of the small vessels. The symptoms and the course of asystole and of cardiac cachexia have been described under Valvular Lesions of the Heart and their Treatment, so that it is unnecessary to repeat them. CHAPTER IV NEUROSES OF THE HEART I. PALPITATION. According to many authors, palpitation is characterized by a change in the frequency, rhythm, and intensity of the heart-beats. This view of the question appears to me incomplete. The pulse-rate in fever exceeds 120, although palpitation is not present. The force of the heart-beats is much increased in some cases of hypertrophy of the left ventricle, but yet palpita- tion may be absent (Potain). Intermittence in mitral lesions certainly does not entail palpitation. Palpitation, then, is not absolutely associated with changes in the frequency, rhythm, and intensity : it often accom- panies, but is not the consequence of, such changes. " Palpitations," says Peter, " are spasms of the heart," and, I may add, distressing and painful spasms. We are not conscious of the action of the organs in life : when we are so, we recognize it by discomfort or by pain. In the normal condition the stomach and intestine execute their movements without our knowledge. When these movements change in character (spasms), they become painful. The heart follows the same law. In palpitation the heart- beats are distressing or painful to a variable extent, from simple discomfort to pain with angina and tendency to syncope. Pathogenesis. — Whatever is the initial cause of palpitation, some trouble in the nervous system of the heart must finally be acknowledged. In some cases this nervous trouble appears apart from any material change in the organ ; in other cases a material change is manifest. Between these two extremes many intermediate forms are found, but their classification is impossible. Nervous Palpitation. — The physiology of the innervation of the heart has been examined for an explanation of palpitation, and it is said that the pneumogastric and great sympathetic nerves are antagonists. Inhibi- tion of the pneumogastric or excitation of the sympathetic produces pnicti- cally the same effect — namely, the acceleration af the heart-beats. Hence all causes which lessen the action of tiie former or increase that of tlie latter 447 448 TEXT-BOOK OF MEDICINE may give rise to palpitation. Such a statement appears inexact, because acceleration is not sufficient to produce palpitation, and consequently it is not evident how causes which diminish the action of one of the antagonistic nerves may not at the same time enfeeble the action of the other. Ab- normal irritabihty of the nervous system, cerebro-cardiac neuropathy (Krishaber), exophthalmic goitre, excesses of every kind, abuse of drink, coffee, tea, or tobacco, are the usual causes of nervous palpitation. The so-called palpitations of growth and of reflex origin also enter into this class. Palpitation with Material Lesions. — In this class we find palpitation, which accompanies diseases of the heart, such as pericarditis and endocarditis, myocarditis, hypertrophy and dilatation, or valvular lesions. Acute inflammation, which at first sight would appear Ukely to irritate the nerve endings, is rarely accompanied by palpitation, while valvular lesions frequently are, and it remains to be seen what is the mechanism in these cases. Every case of stenosis, says Peter, is accompanied by spasm. Patho- logically constricted tubes, such as the uretlira or the oesophagus, and those normally constricted, such as the glottis or the biliary ducts, are subject to spasmodic contraction, and stenoses of the heart also provoke spasms called palpitations. But how are we to explain palpitation in aortic in- sufficiency, which is the exact opposite of stenosis ? Palpitation of Mixed Origin.— Marey has shown that lowering of the blood-pressure increases the rate of the heart-beats. The heart beats more quickly when its load is lessened. This experimental fact has been used to explain palpitation consecutive to haemorrhage, high temperature, or violent exercise, the blood-pressure diminishing as the result of haemor- rhage, or of dilatation in the peripheral vessels (vasoinotor nerves). A fresh element — namely, the quality of the blood, which is poorer in red corpuscles and in oxygen — is present in the palpitation of anaemia. Description. — The palpitations may be isolated or grouped in attacks. In sHght attacks the heart-beats are troublesome rather than painful, and are accompanied by precordial discomfort. In violent attacks the heart " beats as if it would burst the chest," its movements are sometimes tumultuous and disordered (arrhythmia), the pain is agonizing, the patient suffocates, his speech is interrupted, his face is pale and bathed in sweat, and his hands are cold ; he is threatened with faintness and syncope. Examination during an attack yields various results. In some cases the heart-beats are tumultuous and disordered, but in others they preserve their regularity. The pulse is not always in exact relation with the heart- beats. The pulsation in the radial artery may remain normal, in spite of the apparent intensity of the ventricular contraction. Palpitation is often brought on by trifling causes : emotion, movement, or a heavy meal. NEUROSES OF THE HEART 449 The diagnosis of the cause is the most important feature, and it is neces- sary to know whether the palpitations are purely nervous or are associated with some cardiac lesion. The treatment depends upon the recognition of the cause. The first indication is to eUminate anything which may produce palpitation (excesses of every kind — tea, coffee, tobacco, emotion, heavy meals). The preparations of digitaUs are the more indicated in proportion as the arterial tension is but little raised and the pulse is weak and com- pressible (Jaccoud). Bromide of potassium, valerian, the application of ice-bags to the pre- cordial region, and hydrotherapy yield good results. II. PAROXYSMAL TACHYCARDIA. Bouveret in 1889 applied the term " paroxysmal tachycardia " to a disturbance of the cardiac rhythm, characterized by crises during which the pulse beats from 180 to 220 times a minute. These crises come on suddenly without appreciable cause at various intervals, and cease just as suddenly, after a duration varpng from a quarter of an hour to some days. Since Bouveret's article many cases have been published, and I have had a patient under observation for two years. His history will serve as my type, because all cases of paroxysmal tachycardia are a replica of one another. One day, without apparent reason, he felt as though his heart were beating with extraordinary quicknes.a and violence. The attack, which lasted an hour and a half, wa.s painless, and passed otf suddenly. Next month a second attack. The crises have since recurred once or twice a month, and lately almost daily. The attack may be thus described : Something appears to get loose in the chest, and the heart beats violently. After a period, varying from a quarter of an hour to four hours, the attack ends as suddenly as it began. On examination during a crisis nothing special is to be noted in his appearance ; no distress, no angina ; he talks and is often able to carry on his work. During the attack a tremor of the chest- wall is seen, and on placing the hand over the heart, as many as 200 beats a minute may be counted. This condition lasts from one to three hours. At the end of the attack the patient feels a sudden shock due to a beat of exceptional force, and the normal rhj'thm is then re-estabhshed. It is curious that the patient can sometimes stop the crisis by fixing the chest in forced expiration and holding his breath ; he becomes cyanosed, and the jugular veins swell. He remains for a moment in this condition, and is sometimes obliged to take another breath without having strangled the crisis, but at other times he says: "It has stopped." The tremor ceases, and the pulse suddenly falls to 70 or 80. In all published cases the crisis has beeij practically identical. Sharp emotion, blows upon the epigastrium, abuse of cofEee or of tobacco, digestive, pulmonary, or uterine troubles, and physical or mental strain have been in turn invoked to explain this paroxysmal tachycardia. As a matter of fact, we do not know its aetiology. In the patient's previous history, hysteria, neurasthenia, and hereditary nervous diseases are wanting. 29 450 TEXT-BOOK OF MEDICINE As a rule, no valvular lesion is found, Bouveret accordingly called the disease " essential paroxysmal tachycardia," in order to distinguish it from ordinary tachycardia seen in cardiac affections. There are cases, however, in which the disease, while remaining identical from the semeiological point of view, coexists with mitral or aortic endocarditis. The patient of whom I have just spoken was suffering from aortic incompetence. The disease may last for an indefinite period. If the crisis only lasts a few hours, it is perfectly bearable. When it lasts several days, haemoptysis, indicative of pulmonary stasis, may occur. If the crisis lasts still longer, the hver becomes large and painful, the urine is suppressed, the right heart dilates, oedema and serous effusions form, and the patient appears dying. But as soon as the crisis ceases, the circulation is re-established, the oedema is absorbed, the urine becomes abundant, and the patient, who appears moribund, recovers. The prognosis, however, is grave, for the patient may succumb in a prolonged attack. The disease may remain stationary and be prolonged indefinitely, or it may improve and end in recovery. In my patient the attacks, which occurred daily, have become less frequent, and he has only one crisis every week or fortnight. Post-mortem examinations have been performed in fatal cases. Dilata- tion of the right heart and venous stasis in every organ have been found ; the lesions are evidently secondary and terminal. The primary lesions have not been found ; the neuromotor system of the heart has always appeared healthy ; the bulb, the spinal cord, the pneumogastric, and the sympathetic nerves are free from disease, and the heart itself only shows commonplace lesions. The characters of the disease are so specific that it is not necessary to dwell upon the diagnosis. The crises of paroxysmal tachycardia resemble neither the ordinary palpitation in heart disease nor the reflex palpitation of dyspeptic or hepatic origin, etc. Tachycardia in Basedow's disease may supervene in crises, but does not show the sudden passage from the state of crisis to that of absolute calm and vice versa. Treatment has so far been powerless to influence this disease. III. PERMANENT BRADYCARDIA. The pulse-rate in health is from 70 to 72. As a result of different in- fluences (intoxication, jaundice), the rate may fall below 50 ; but in this case the fall is transitory, while this section deals with permanent slowness of the pulse. The slowing is so great that the pulse falls to 20 beats, or even less. In one of my patients the pulse-rate fell to 14 per minute for some days. NEUROSES OF THE HEART 451 The pulse preserves its regularity. The sphygmographic tracing stows a short upstroke and a long-drawn-out downstroke. The arterial pressure is usually higher than normal. The heart-beats are well marked. The duration of the first pause is not increased, and it is the increase of the second pause that causes the slowness of the cardiac rhythm. In short, each heart-beat is normal, but the interval between the beats is much increased. This interval may not be completely silent. After the diastohc sound, muffled rumbhng sounds are heard. Vaquez has shown that they are due to an abortive contrac- tion of the auricles, and radiography has confirmed his interpretation. Bradycardia may be associated with perfect health, or may be accom- panied by morbid phenomena, caused in several ways. Any lesion that affects the cardiac innervation may result in brady- cardia, either by stimulating the system that slows the rate (bulb and vagus), or by inhibiting the system that quickens it (spinal cord and great sympathetic). Lesions may be present in the heart, and affect the intracardiac gangha (syphihtic gumma of the interventricular septum and upper part of the left ventricle, in Rendu and Massary's case). They may affect either pneumo- gastric nerve, which is compressed in its intrathoracic course either by the dilated aorta (Stackler's case) or by enlarged mediastinal glands (Lannois' case). The pneumogastric may also be injured in its intracranial course (compression by a gummatous tumour of the cerebellum). Many lesions may affect the cardio -inhibitory nucleus in the bulb (injury, cervical caries, syphihtic or tubercular tumours, infectious myelitis). Lesions of the accelerator system are less often in evidence, yet the presence of unilateral dilatation of the pupil has shown the lesion to be in the cardio-spinal centre, which is near the centre for dilatation of the pupil. All these cases of bradycardia depend upon such gross lesions that there can be no possible doubt as to their existence ; but the case is different in the syndrome which Charcot has called " Permanently slow pulse, with syncopal or epileptiform crises," and for which Huchard has proposed the name of " Stokes-Adams disease." The patients, who are of advanced years, often show signs of renal insufficiency ; their arteries are hard and tortuous, and the tension is high. They are subject to attacks of syncope, which in one of my cases had the following characters : The syncope was ushered in by a kind of aura : gonerai malaise, feeling of weight in tlie chest, buzzing in the ears, cold sweat, pallor, and chilliness. The patient lost consciousness and looked almost dead, with dull eyes and cadaveric tint. Aft«r two or three minutes the colour returned, the eyes opened, and she rapidly recovered con- sciousness. She had no involuntary emission of urine, no epileptiform movements. After the crisis she comi)laincd of feeling bruised, as though her body had been racked ; she sometimes felt sick, but did not vomit. 29—2 452 TEXT-BOOK OF MEDICINE The syncope may be immediately followed by an epileptiform attack. Whether the attacks are syncopal or epileptiform, they are often ushered in by very marked slowing of the pulse. The attacks succeed one another at variable intervals ; the more fre- quent they become, the more grave the prognosis. The patient finally dies during an attack of syncope which is more prolonged than the others, and the duration of the disease does not exceed three or four years. No grave lesions are found, as a rule. The kidneys and myocardium often show fibrous change ; the arteries of the nerve centres are atheromatous ; arterio-sclerosis of the vessels in the bulb appears to be the chief cause of the disease. No treatment has any efiect upon permanent bradycardia. Milk diet gives some benefit in cases of renal insufficiency (Debove). Rest is abso- lutely indicated (Hirtz). During an attack of syncope the patient must keep his bed. IV. EXOPHTHALMIC GOITRE— BASEDOW'S DISEASE. Medical and Surgical Treatment. ** Many patients will consult you for palpitation of the heart, but you will at once be struck by their strange look and their prominent eyes," and you will find hypertrophy of the thyroid gland. These patients are suffering from exophthalmic goitre, Graves' or Basedow's disease, characterized in a typical case by the following troubles, wliich are mostly of nervous origin : (1) cardiac troubles ; (2) ocular troubles ; (3) hypertrophy of the thyroid gland ; (4) motor troubles ; (5) psychical troubles. According to the case, these various symptoms may appear in succession or in combination. In some cases they are predominant ; in others they are indefinite. Description — 1. Cardiac Troubles. — Acceleration of the heart-beats is the essential symptom of Basedow's disease. This symptom is never lacking ; it is found in early cases, and even after all the other symptoms have disappeared, the acceleration of the heart-beats persists for some time longer. This symptom is due to paralysis of the nucleus of the vagus nerve. In some cases the patient does not notice the tachycardia, but in others the beats are distressing and cause palpitation. This palpitation becomes gradually more severe, and supervenes in the form of attacks ; 120 to 150 beats per minute may be counted during the paroxysms. The palpitation is often violent, and the cardiac impulse so strong that it raises the chest-wall, while the heart " beats as though it would burst." In spite of this disturbance, the beats may not be irregular. In another NEUROSES OF THE HEART 453 variety the beats are irregular ; the heart seems feeble, and its pulsations are hurried, uneven, and abortive. During the paroxysms the arrhythmia and cardiac weakness may lead to acute asystole, with dyspnoea, angina, and cyanosis. In some cases the symptoms of angina pectoris have been recorded. The symptoms of asystole disappear between the paroxysms. Lastly, in some patients the troubles of innervation are comphcated by hypertrophy, dilatation of the cavities, or insufficiency of the tricuspid and mitral valves. The hypertrophy is attributed to the functional hyper- activity of the heart, or to an excess of tension consecutive to lesions of the valves. These valvular lesions (insufficiency of the auriculo-ventricular and aortic valves) are sometimes entirely mechanical in origin. They may be caused by dilatation of the ventricles ; the heart muscle, weakened bv the strain, allows overdistension. These lesions are usually transient, and cease with the disease, though they may become permanent. The carotid arteries are tortuous and enlarged. The pulsation raises the tissues of the neck. These beats are not the contre-coup of the cardiac impulse, but the vessels in the neck, both arteries and veias, beat on their own account, and appear to participate in the overgrowth and pulsation which affect the vessels of the thjToid gland. The sphere of vascular excitation appears limited to this region, for violent pulsation is not found in the abdominal aorta, the radial artery, or elsewhere. In spite of these vascular troubles, the blood-pressure remains normal. Inequality of the two radial pulses has been found. 2. Ocular Troubles. — Spasms of the upper eyelid may precede or accom- pany the exophthalmos (Wecker). When the glance is directed downwards, the upper eyelid no longer follows the ball of the eye, but remains fixed above it (de Graefe). The exophthalmos is double, and may be so extreme that the eyeUds can scarcely cover the ball, giving to the physiognomy a strange expression of astonishment and terror, which Marchal de Calvi called the " tragic eye." This appearance is partly due to retraction of the levator palpebrse superioris, which causes considerable enlargement of the palpebral aperture (Stellwag). During the paroxysms the exophthalmos increases to such a degree that luxation of the eyeball has often been seen (Pain). The conjunctiva is often injected, and the cornea, being continually exposed, may become infected and ulcerated. The sight is unaffected, and it is rare to see myopia or j)resbyopia. The ophthalmoscope may reveal congestion of the choroid and dilatation of the retinal vessels. Galezowski and the wTitcr have seen retinal haemorrhages. In patients suffering from Basedow's disease, with or without hysteria, we sometimes see bilateral paralysis of the motor muscles of the eyeball, in which case the voluntary movements are chiefly affected, while the 454 TEXT-BOOK OF MEDICINE reflex ones are in part preserved. The whole external musculature — namely, the recti and the obHqui, innervated by the third, fourth, and sixth pairs — is paralyzed. In addition, the movements of the eyeball are abohshed, and only elevation of the upper eyehd is, as a rule, preserved. This inability to move the eyes gives a strange fixed look, and the patient cannot see an object to his right or his left without turning his head. The name " ex- ternal ophthalmoplegia '* has been given to this paralysis of the external musculature. The internal musculature, i^hich comprises the cihary muscles and the radial or circular fibres of the iris, and governs accom- modation and the dilatation or contraction of the pupil, is unaffected in Basedow's disease. External ophthalmoplegia maybe seen in patients suffering from both exophthalmic goitre and hysteria, or from either malady alone. 3. Thyroid Body. — The enlargement of the thyroid body results from dilatation of its numerous vessels. Auscultation of the gland therefore reveals simple or double blowing murmurs, which are louder during diastole, as in a cirsoid aneurysm. On palpation, we feel expansile pulsation, as in an aneurysm. The right lobe is more often invaded than the rest of the organ, and although the tumour is not as large as an ordinary goitre, it may, by compression of the trachea or by the excitation of the recurrent nerves, produce voice changes, spasm of the glottis, and paroxysmal attacks of suffocation. 4. Motor Troubles. — Tremors, paralysis, and choreiform movements may appear at the onset or during the course of Basedow's disease. Tremor is almost constant, but may be so shght that care is required to discover it. The tremor is most frequent in the upper limbs. The arms and hands, even during rest, show tremors, which hamper writing and all the delicate functions of the hand and fingers. In the lower hmbs the tremor is also present during repose, as well as in walking. During repose the limbs show a kind of pedal movement. In exceptional cases the tremor may invade the whole body, including the face and the tongue. Fibrillary movements are usually seen in all the muscles. In some cases tremor opens the scene, and attracts so much notice as to constitute a defaced form of Basedow's disease. On closer inspection, however, we usually find other symptoms, such as tachycardia, palpitation, peculiar look, pulsation of the carotids, diarrhoea, rapid wasting, diminished electrical resistance, etc. (Vigouroux). Although these symptoms may only be present to a partial extent, they assist in forming a diagnosis. The syndrome may be reconstructed from the recognition of some one symptom. Hence we are not liable to confound this tremor with that due to alcoholism, mercurial poisoning, neurasthenia, or morphinomania. Lastly, we may add that the tremor in Basedow's disease shows its special tracing (Marie), and gives about eight or nine oscillations a second. NEUROSES OF THE HEART 455 Paralytic troubles are manifold (Ballet). Without mentioning external ophthalmoplegia, the paralyses of Basedow's disease may show the most varied forms — monoplegia, hemiplegia (Teissier), weakness of the upper Umbs (Drejrfus-Brisac), diplegia, paralysis of the nuchal muscles (Chwos- teck), paresis of the lower Umbs (Heyden), and complete paraplegia (Charcot). These paralyses, whether shght and transient or severe and prolonged, have been set down to hysteria. As hysteria is sometimes associated with exophthalmic goitre, it is reasonable to admit that paralyses which are hysterical in nature may coexist with Basedow's disease. Due allowance, however, being made for the possible paralyses of hysteria, which, moreover, have their own characteristics, certain paralyses are inherent to Basedow's disease, without the need for invoking the intervention of another factor. Thus, my patient, who showed no signs of hysteria, was a perfect example of Basedow's paralysis. As regards the upper hmbs, the paralysis diminishes or aboHshes the functions of the hands. My patient could neither seize an object nor hold it. She was incapable of dressing herself, or of feeding herself, so that for some time she had to be fed by others. Paraplegia, varying in degree from paresis to total paralysis, is very common in Basedow's disease. Its prominent features have been given by Chevaher : " In the upright position, or in walking, although the patient experiences no feeUng of vertigo, the limbs give way and bend suddenly. Sometimes during a walk he may fall forward upon his knees. At other times, though more rarely, the motor weakness takes months to become complete, as in a case quoted by Charcot, where the impossibility of maintaining the upright position and of walking lasted nearly a whole year. These paraplegic troubles do not remain stationary ; they improve from time to time and grow worse again, and tliis relapse, which is followed by improvement, shows a certain analogy with the evolution of the disease. In the intervals the legs frequently collapse while walking, so that crutches may be needed." If we do not understand these cases, the idea of paraplegia consecutive to myeUtis at once enters our mind ; but we should not^ confound the para- plegia of Basedow's disease with myelitis, for in the former case bladder troubles are absent, the sphincters are intact, and we sen no trophic troul)les, no bed-sores on the sacrum. Moreover, we should not confound tliis para- plegia with that duo to hysteria, because, in addition to the numerous stigmata of hysteria, such as hemianajsthesia, narrowing of the \isual field, aboUtion of the pharyngeal and ovarian reflexes, hysterogenous zones, etc, hysterical paraplegia is soft, and accompanied by anaesthesia of tlio paralyzed parts, with complete loss of the muscular sense, while the muscles do not present the diminution of electrical resistance seen in Basedow's disease. 456 TEXT-BOOK OF MEDICINE Choreiform movements complete the triad of motor troubles in Base- dow's disease. They were very marked in my patient at the Hotel-Dieu, and a cursory examination revealed choreiform movements in the hands, arms, shoulders, trunk, neck, and face. It has been asked whether chorea and Basedow's disease are two associated maladies, or whether Basedow's disease may not be capable of causing choreiform movements, just as it causes tremors and paralysis. In 1864 L. Gros, comparing exophthalmic goitre with chorea, described a case of Basedow's disease, with choreiform movements which affected the upper and lower Umbs, the neck, and the face. In 1876, at the Congress of Clermont-Ferrand, Gagnon, while studying the rela- tions between exophthalmic goitre and chorea, quoted the case of a neurotic young girl who never had rheumatism. For a month this child had wasted, her character had changed, and she had palpitation. Tliis picture marked the onset of Basedow's disease. At this time the pulse-rate was 130, and hypertrophy of the thyroid body was evident. The disease followed its course, and two years later she showed choreic movements, which finally became general. In 1881 Gueneau de Mussy pubUshed a case of a young girl suffering from Base- dow's disease, with choreiform movements. For some weeks the locomotor functions had been so affected that the patient could not walk. She used to make some regular steps forwards or backwards, showing that the muscular power was much enfeebled, in addition to the incoherence of her movements. The cerebral functions were not spared. The young girl was strange, her memory was not reUable, she had troubled dreams, and even delirium. At the end of eight or ten months the choreiform and paralytic troubles disappeared, as well as the mental aberration. Raymond and Serieux, in a paper on Basedow's disease and mental degeneration, found in one patient permanent choreiform spasms of the external obhque muscle. Deleage, in 1894, communicated to the Societe des Sciences Medicales of Gannat a case of exophthalmic goitre with tremors, paralytic troubles, and choreiform movements. Is it a question of choreiform movements or of true chorea in these patients ? Kohler is incHned to look on this symptom as a choreiform motor trouble ; Dach states his opinion that it is only met with in children, which is wrong ; and Mobius thinks that it is a question of chorea super- vening as an accidental complication. For my part, I cannot compare this condition with Sydenham's chorea. I beheve that it is only a question of choreiform movements, and my reasons for this opinion are as follows : If exophthalmic goitre and chorea are indeed two associated diseases, as some authors think, why does Basedow's disease always precede chorea ? We do not see exophthalmic goitre during the course or during the decline of true chorea. Hundreds of children who are affected by chorea never develop exophthalmic goitre. I think, therefore, that choreiform move- ments are a part of Basedow's disease, just as are tremors and paralysis. The choreiform movements, with the tremor and paralysis, constitute a triad of motor troubles. The triad may be incomplete or complete, and we can understand how great is the disturbance in a muscular system affected at the same time by paresis, tremor, and choreiform movements. NEUROSES OF THE HEART 457 5. Other Nervous Troubles. — The sensory troubles in Basedow's disease consist in trigeminal neuralgia, intercostal neuralgia, racliialgia, and hemiansesthesia, which is usually associated with hysteria. In most patients vasomotor, trophic, and secretory troubles are seen. Albuminuria, glycosuria, and polyuria, which indicate disturbance in the bulb, have been noted. Many patients complain of an exaggerated sensation of heat. They open the windows, and often complain of being too heavily clad (Basedow, Teissier). This increase in temperature is appreciable with the thermo- meter, and sometimes reaches one degree higher than normal. Changes in the skin, sweating, purpura, pigmented patches, discrete or confluent vitiligo, alopecia, and chronic urticaria have often been observed, I have frequently seen pigmentation of the neck, shoulders, and arms, in the form of more or less large and discrete patches. (Edema is frequent, and chiefly affects the lower hmbs. Trousseau has seen hypertrophy of the breasts. We may also find the following series of symptoms : Dyspnoea, which may be associated with palpitation, is frequent. It may be continuous, intermittent, or paroxysmal, and is the chief symptom in some cases. It is probably due to changes in the nucleus of the vagus. The digestive functions suffer in Basedow's disease. I have found hypertrophy of the Uver and jaundice; bouhmia succeeds anorexia, and violent pulsations are seen in the epigastric angle. We may see vomiting and diarrhoea in the form of crises lasting one or more days. In spite of the increased appetite, patients waste and pass into a condition of exophthal- mic cachexia. The general wasting contrasts in a singular manner with the exaggerated development of the eyes and neck. Wasting may be the first apparent symptom. I have seen a patient who rapidly lost over a stone in weight ; wasting and tachycardia were here the only appreciable symptoms for some months. At first sight such wasting leads us to think of tuberculosis or of diabetes, and, as glycosuria is often present, the diagnosis must be carefully considered in order to avoid mistakes. Menstruation is nearly always affected. It may be irregular or sup- pres.sed, and the amenorrhoea is often accompanied by leucorrhoea. Re- estabhshment of the menstrual functions is one of the most favourable signs in prognosis. Pregnancy has sometimes a beneficial effect. In men im- potence is usually associated with Basedow's disease. Haemorrhages are sometimes seen. I have observed purpura, haemop- tysis, and retinal haemorrhages in the same patient. Cerebral hioniorrhago and death from apoplexy have been noted. I saw one case of this nature with Jaccoud. Vigouroux and Kohler have noted diminished resistance to electric currents. 458 TEXT-BOOK OF MEDICINE In some cases Basedow's disease and myxoedema have been associated ; no antagonism exists between them. 6. Psychical Troubles — Mental Condition. — As a general rule, few patients escape psychical troubles. Trousseau was the first to describe them : " The changes of character are such that Ufe becomes difficult for the entourage of these patients, who are irritable and exacting to such a degree that the disease forms their only excuse. In addition to these changes in character we may note insomnia — a cruel comphcation which reduces patients to extreme despair." Trousseau mentions psychical troubles in most of his cases, and assigns such importance to them that he gives them a prominent place in his wonderful description of exophthalmic goitre. All authors who have studied exophthalmic goitre have laid stress upon the psychical troubles. " In nearly all patients suffering from exophthalmic goitre," says Ball, " there exists a certain degree of exaltation. They nearly all have strange ideas, and these morbid manifestations may end in the most acute mania." According to JofEroy, " the patient is restless, often a prey to exaggerated activity, and yet incapable of methodical work or of prolonged mental effort. Among the first changes which exophthalmic goitre imprints upon the character of patients, we find in some cases depression ; or in others excitation." Boeteau thus describes the psychical troubles : " The chief symptom is profound melancholy, which more and more enters into every one of the patient's thoughts, so that he entertains ideas of suicide. At the same time the victims become impatient, surly, and remarkably emotional. Their will-power, when not quite absent, is often very feeble ; they are incapable of fixing their -attention upon any subject, even for a minute ; they cannot remember next day what they did the day before. They show complete indifference not only to what concerns them, but to everything which affects their family, even to those who are most dear to them ; and this indifference may sometimes amount to aversion." Psychical troubles may exist from the first — sometimes, indeed, as the initial symptom — so that the diagnosis remains in doubt until forcible beating of the heart, exophthalmos, goitre, tremors, etc., appear. The interpretation of the psychical troubles is not decided. Some authors consider them to be a direct part of the disease ; others, on the contrary, look upon them as due to hysteria and neurasthenia. To those who make these psychical troubles subordinate to hysteria, we may answer that there are cases of exophthalmic goitre in which hysteria is absent, and cannot, therefore, be the cause. Neurasthenia appears to be open to the same objections. It is undeniable that individuals may suffer at once from exophthalmic goitre and from neurasthenia or hysteria, but this is no reason to bring in neurasthenia in every case. NEUROSES OF THE HEART 459 It is perhaps more logical to admit that Basedow's disease, like chorea, awakens psychical troubles in predisposed persons. The psychical troubles of chorea show very great analogy with those of Basedow's disease. We find the same intellectual depression, the same inaptitude for work, lapses of memory, changes in character, melancholy, indifference, and irascibihty. Must we say that neurasthenia or hysteria has for some weeks been associated with chorea ? I think not. We must say (omitting cases in which the association does exist) that chorea can extend to the whole cerebro-spinal system, and excite slight or severe psychical troubles. The same reasoning appHes to Basedow's disease. Are we to say that, at the onset, neurasthenia comes to our rescue by bringing in its contingent of psychical troubles ? I think not. We must say that Basedow's disease can extend to the whole nervous system, and excite psychical troubles ju^t as it excites nervous troubles of every kind. Further, as Toulouse has remarked, " neuras- thenia has succeeded in donning the mental troubles which formerly belonged to exophthalmic goitre alone." These psychical troubles are usually transitory, and tend to recover. I shall now deal with certain serious mental troubles or true psychoses " running crescendo through the whole gamut from transitory or fugitive deUrium to inveterate mania " (Boeteau). These psychoses include acute and chronic mania, delirium with ideas of persecution, melancholia, irresistible impulses, and apprehensive madness, and have been repeatedly discussed (Raymond and Serieux, Joffroy). ' Resume of cases : Young woman, -without nervous antocedonts, taken ill with acute mania during Basedow's disease. She became violent and refused all food ; excitation gave way to depression ; her mental condition improved, but she died from cachexia. — A young woman, without personal or hereditary antecedents, had Basedow's disease compUcated by melanohoha. She refused food, tried to throw herself out of the window, and suffered from delusions. She recovered some months later. — A woman, suffering from typical exophthalmic goitre, was seized with irresistible impulses and delirium. She felt an impulse to kill her children, but she was able to resist the impulse, though she feared the greatest misfortunes. Her insomnia was persistent, and her distress was intolerable. A year later, however, recovery was complete. — My patient, with exoj)hthalniic goitre, had hallucinations of sight and hearing, was liaunted with ideas of persecution, and imagined that j^eople hid in her room in order to kill her. The psychosis in Basedow's disease, therefore, may assume very different forms. Difficulties begin when we have to interpret its intimate nature. Some authors say that these mental troul)les form an integral part of tlie disease. Whether the cerebral symptoms are slight, as is usually the case, or whether they are severe, with hallucinations, impulses, maniacal excitement, or delirium of every kind, it is none the less true tliat they are symptoms of a cerel)ral nature, and form part of Basedow's disease, in the same way as the other nervous troubles. This conception of Basedow's 460 TEXT-BOOK OF MEDICINE disease makes it a morbid entity, a neurosis, or a neuropsychosis, in which every part of the nervous system is more or less affected. Other authors enunciate a different opinion and divide up the disease. They say that the mental troubles, melancholia, delirium, or delusions — in short, every form of mental ahenation — must be set down as psychoses which do not spring directly from the disease, but are associated with it, just as the same authors would associate hysteria and neurasthenia with it. These morbid conditions which evolve in the same patient are not, therefore, hybrids in the true sense of the word ("in neuropathology," says Charcot, " hybrids do not exist "), but are associated, each association preserving its autonomy, characters, degree of gravity, and therapeutic indications. Tliis grouping of morbid conditions, neuroses, and psychoses, is said to have heredity as its cause. This opinion is seductive, although it is far from agreeing with the facts of heredity, and though it forms an incomplete explanation of the fact that heredity is sometimes direct, sometimes intermittent, and that there may be heredity of transformation, and also homologous heredity. According to some neuropathologists, persons affected with psychoses in Basedow's disease are really degenerates. " In many cases," say Raymond and Serieux, " Basedow's disease may be only a special locahzation of functional troubles which supervene in degenerates, or in predisposed persons, in some part of the cerebro-spinal axis. Magnan's theory of this failure of equiU- brium in the centres of the cortex or of the spinal cord (paralysis, or erethism of these centres) may be apphed to these different manifestations. Toulouse, in a critical review of the relations betw-een exophthalmic goitre and mental alienation, discusses this question, and shows us the defects of too hasty conclusions. " At this time," says he, " the tendency evident in psychiatry, thanks to the works of Morel and Magnan, is to refer mental diseases to some distant hereditary cause, and to overlook the closer causes. This psychopathic predisposition cannot be denied, but it is too general an idea, although it forms the basis of all mental ahenation. The hypothesis of predisposition does not suffice to explain the appearance of mental disorders in exophthalmic goitre, as in other maladies in which psychoses appear." The discussion, therefore, takes this form. There is a question of fact and of theory. Chnical facts show that many persons suffering from Base- dow's disease, especially women, may have psychical troubles and mental disorders as well as motor troubles (tremor, paralysis, choreiform movements) and nervous troubles of every kind (crises of diarrhoea, sweating, albuminuria, glycosuria, and visceral congestions), all of which depend upon the nervous system. Is it necessary to isolate these groups and claim for them an autonomous or hereditary origin in every case, independent of Basedow's NEUROSES OF THE HEART 461 disease ? I do not think that we need go so far. The question of soil and of acquired or hereditary disposition play, not only in neuropathology, but in the whole domain of pathology, too large a part for me to attempt to belittle their importance. I think, on the contrary, that heredity in all its forms is the conducting wire which helps us to assign things to their proper place ; but it does not furnish sufficient reason for cutting up a morbid entity and disjoining the pieces. Here, as elsewhere, I repeat, acquired or hereditary predisposition plays a leading part in' the production of psychical symptoms and mental troubles. These cerebral troubles, however, have undoubtedly arisen in persons who, neither in personal nor hereditary antecedents, have had anything which could explain the appearance of a psychosis apart from their Basedow's disease. Sometimes psychical troubles and mental disorders begin with this disease, increase during its paroxysms, and then disappear with the other symptoms, or even before them. There is, indeed, under these conditions, such affinity or agreement in the evolution of the different symptoms which comprise Basedow's disease, that it is very difficult in this case to see only the coupling of morbid conditions, and it appears to me more reasonable to admit the development of a series of nervous troubles of various kinds, assuming the form of neuroses or of psychoses, but having indeed a common origin. However this may be, the appear- ance of mental troubles is always of ill omen. Course — Termination. — Basedow's disease is rarely quite t5rpical. One of the cardinal symptoms may be absent or sHght, while other nervous troubles or symptoms are prominent. Sometimes the disease is more or less abnormal in appearance. The course is usually slow and progressive, and the disease may last for ten or twelve years, or even more. In some cases it runs an acute course. The symptoms follow one another rapidly, and the clinical picture is complete in a few weeks — indeed, it may be so in the space of twenty-four hours. My patient at the Hotel-Dieu, after terrible emotion, developed in a single night, tremor, paralysis, exophthalmos, hypertrophy of the thyroid gland and cardiac palpitation, and the mental condition appeared later. Trousseau quotes the following typical example of this sudden onset : A woman lost her father. She was much upset, and cried during the night. Next day she suddenly felt that her eyes swelled and the eyelids became raised, while the thyroid gland enlarged and showed unusual pulsation. She also felt violent palpita- tion of the heart. Four days later she came and consulted Desmarcs, who found ex- ophthalmic cachexia. Terrible paroxysms, described by Trousseau, may supervene in the course of the disease. After some prodromata, or, indeeti, suddenly, the patient has an acute attack of dysjmcea; the tliyroidghiiid bocoiiies eiihirged; palpitation is severe ; the eyes start from their sockets ; the face is bathed in 462 TEXT-BOOK OF MEDICINE sweat ; the vessels in the neck show rapid pulsation ; the dyspnoea is accom- panied by stridor and sucking-in, and death sometimes appears imminent. Quiet is, however, re-estabHshed, and the paroxysm ends. Acute paroxysms are much more serious than chronic ones. In a case quoted by Trousseau the patient was seized with such terrible attacks of suffocation that prepara- tions were made for tracheotomy. The paroxysms may only recur at in- tervals of months or years. They show infinite variation in their duration and gravity, and may even reappear every month or every few days. Exophthalmic goitre is a grave malady, for the mortahty amounts to 20 per cent. Death results from cachexia or from intercurrent trouble, such as paroxysms, pulmonary hsemorrhage, intestinal and ^cerebral haemor- rhage (Hirsch), multiple gangrene, mental alienation, angina pectoris, or pulmonary tuberculosis. etiology. — Exophthalmic goitre is a disease of the middle period of life. It is much more frequent in women than in men, and is often associated with a nervous temperament, hysteria, epilepsy, chorea, mental ahenation, diabetes, chlorosis, or pathological conditions of the genital system. It may appear after moral or physical shock, accident, emotion, fright, violent anger, or injury (De Graefe). Pregnancy has sometimes a beneficial influence on the progress of the disease, but, on the other hand, the goitre may appear during pregnancy. Heredity plays the chief part in its aetiology, and the parents may themselves be sufferers from goitre, or from one of the nervous diseases above quoted. As regards direct heredity, I do not know a more interesting or conclu- sive case than that of the family of Les , natives of a place near Soissons, where goitre is endemic. I have seen several members of this family, which in three generations has furnished six cases of Basedow's disease. I could quote cases in which the children of parents suffering from Basedow's disease were born with a goitre. For many years the goitre remained the only sign of the disease, and ten or fifteen years later other symptoms, such as exophthalmos and palpitations, appeared as the result of acute emotion, menstruation, or pregnancy. A more singular fact is that, in countries where goitre is endemic, we see goitre in persons who are not descended from parents affected with Basedow's disease, and yet at some period of their Uves exophthalmos and tachycardia appear in addition to the goitre. Diagnosis. — At first the diagnosis is very difficult, especially when the disease is abnormal, because we may only have a single symptom. Mistakes are rare when the chief symptom is goitre or exophthalmos ; but when the patient only complains of pulsation, tremor, rapid wasting, or attacks of dyspnoea, we must be able to reconstruct the disease by grouping certain NEUROSES OF THE HEART 463 symptoms, or traces of the more or less important symptoms above enumerated. In women the general symptoms may simulate chlorosis, but the accelera- tion of the pulse, the pecuUar look, the prominent eyes, the tremor of the hands and feet, the pigmented spots, the pulsation of the cervical vessels, and the shght sweUing of the thyroid body should indicate the diagnosis. As the exophthalmos in Basedow's disease affects both eyes, and is not accompanied by squint, it shows no resemblance to unilateral exophthalmos of orbital or of cranial origin. The prominence of the eyeball in myopic patients will be readily distinguished. The origin, appearance, and progress of exophthalmic goitre do not allow confusion with goitre, properly so called. Many cases will call for a minute inquiry into the symptoms present. Nature of the Disease. — Exophthalmic goitre is a cardio- vascular neurosis, resulting doubtless " from profound disturbance in the vasomotor nerves " (Trousseau). It is a neurosis of bulbar origin (See). We may, I think, be satisfied with Ballet's conclusions : The possible association of external ophthalmoplegia, of paralysis of the facial, the hypo- glossal or the motor branch of the trigeminal nerves, with exophthalmic goitre forms an argument in favour of the theory which refers Basedow's disease to some trouble in the central nervous system, and particularly in the bulb. The common troubles of the disease depend on nuclear paralysis of the vagus, wliich causes tachycardia, dyspnoea, and gastric troubles; and on paralysis of the vasomotor centres, which gives rise to flusliing of the face and neck. The goitre and the exophthalmos result from the coexistence of vasomotor paralysis and tachycardia. These paralyses do not depend upon a material lesion, but are simply functional troubles, capable of improve- ment, aggravation, recovery, or relapse. It follows from the preceding statements that Basedow's disease is especially a bulbar neurosis. Troubles of medullary or of cortical origin may also appear, and therefore Basedow's disease is often associated with other neuroses, such as unsoundness of mind, epilepsy, and especially hysteria. Treatment. — I will give here the treatment of Basedow's disease described in my lectures at the Faculte. Let us consider this treatment from two different points of view — (1) during the paroxysms, and (2) during the course of the disease. In dealing with an acute paroxysm, in which the thyroid and cardiac trouble are most severe, we must at once act because the paroxysm will last for half an hour or more, and may cause death, if we do not intervene immediately. Distress and dyspna^a are extreme. The excessive swelhng 464 TEXT-BOOK OF MEDICINE of the thyroid body compresses the trachea, causing stridor and preventing the free passage of air. In such conditions tracheotomy appears imperative, and, indeed, it would be indicated but for the danger arising from the dilatation of the vessels of the neck, which are gorged with blood, and the fatal haemorrhage which might result, as in a case quoted by Trousseau. How, then, are we to reheve the thyroid and cardiac troubles ? The first indication is fulfilled by the application of ice-bags to the thyroid until the crisis disappears. We should treat the cardiac excitation by digitahs, in large doses, as advised by Trousseau — e.g., 2 grains of the dried leaves in powder every half-hour for two or three hours, according to the severity and duration of the attack, while an ice-bag is applied to the precordial region. If this gives no relief, we must resort to bleeding, to the apphcation of leeches to the neck, and to careful inhalations of ether or of chloroform. The paroxysm ends more or less rapidly, and the patient is for the time being saved. We must, however, not forget that the disease remains, that it is dan- gerous in these cases, that other crises will appear, and that one or other of them will be fatal. Therefore we must be on our guard, and ready to act in a similar manner. It is, above all, necessary to prevent them^ — that is, to direct our attention to the disease itself. The physician must adopt the same course, although the patient has shown no paroxysms, because great improvement in the symptoms can be effected by rational and well- directed treatment. Many drugs have been extolled in exophthalmic goitre, and the chief among these are iodine and the iodides. Cheadle prescribes tincture of iodine, taken internally. This drug is certainly efficacious in simple goitre, but renders no service in exophthalmic goitre. Trousseau has even given his opinion against this method of treatment, and most writers agree with his advice. Bromides are indicated for the cardio- vascular excitation and erethism. Although this drug does not act directly on the disease, it at least has a favourable effect upon the symptoms, when given in large doses. Extract of valerian, or valerianate of ammonia, produces manifest improvement in the palpitation and the dyspnoea. All authors are unanimous in advising digitahs in the treatment of exophthalmic goitre. While it has the disadvantage of raising the blood- pressure, it has the advantage of slowing the heart-beat in severe tachy- cardia ; therefore its disadvantages must be passed over, and we must only think of reheving the patient. The dose varies according to the suscepti- bihty of the patient. In some patients 1 or 2 grains of the dried leaves will be sufficient, while in others it will be necessary to increase the dose, the NEUROSES OF THE HEART 465 whole point being to estimate the susceptibility of the patient. Except in rare cases, fligitalis is an excellent drug. The use of belladonna has in some cases caused improvement of all the symptoms, except the hypertrophy of the thyroid gland. Hydrotherapy, in spite of unfavourable criticism, is none the less an excellent method. The cold douche should not be given at first, but shower- baths at a temperature of 75° F. should be first given, and the temperature of the water should be gradually reduced. Electricity is certainly very efficacious. The continuous current appears to have given the best results. The following procedure is usually adopted : Two rheophores are applied on either side of the neck over the superior cervical ganghon, then over the vagi, and a current of from 3 to 8 miUi- amperes is allowed to flow for eight or ten minutes. A daily sitting is given for three to four weeks ; the treatment is then stopped and resumed at the end of a week. For some time past the faradic current has met with some credit (Vigouroux). This rapid survey of the different methods of treat- ment shows that digitahs, valerian, bromides, the continuous current, and hydrotherapy give the best results. As regards treatment with thyroid extracts, opinions are much divided. Voisin has quoted a case in which sheep's thyroid gland gave excellent results. In answer to Voisin's communication, Dreyfus-Brisac and Beclere declare that thyroid treatment for exophthalmic goitre has always, in their experience, increased the symptoms, and they are not alone in this opinion. For my part, I have for a long time used ipecacuanha. The idea of giving ipecacuanha in Basedow's disease occurred to me on seeing the success obtained in haemoptysis. These patients have erethism of the cardio- vascular and vasculo-pulmonary systems. The pulse is hard and vibrating during the haemoptysis. In such cases we give ipecacuanha in emetic doses if we desire to arrest abundant haemoptysis, or in fractional doses so as to cause nausea if we are treating more chronic bleeding. The pulse diminishes in frequency and force, and the haemoptysis improves or ceases. In Basedow's disease the treatment of cardio-vascular erethism is also one of the indications to be fulfilled. I have therefore given ipecacuanha with digitahs and opium in pills : I^ Powdered ipecacuanha . . . . • • gi'- iV Powdered digitalis leaves . . . . • ' S^- s^ Extract of opium . . . . • • g^- ^V To make one pill. Take four pills at equal intervals in the twenty-four hours. In giving ipecacuanha we should not cause vomiting, but only very shght nausea. We must then diminish the number of pills to three, or even 30 466 TEXT-BOOK OF MEDICINE two, in the twenty-four hours, and gradually increase the dose up to the limit of tolerance. With ipecacuanha I am fond of giving valerianate of ammonia in a daily dose of 2 or 3 teaspoonfuls, and I also employ hydrotherapy. I have treated many cases of exophthalmic goitre in this manner, and marked improvement, especially in the dyspnoea, has been the rule. It was particularly striking in two cases, and I do not think that any other method of treatment would have given a better result. The effect of this treatment is shown by the appreciable improvement after a few days, and very marked benefit after some months. The only inconvenience of this treatment is diarrhoea, which disappears as soon as tolerance conmaences. Surgical Treatment. — Surgical treatment consists in operations upon the goitre or upon the cervical sympathetic nerves. Let us first consider operations upon the goitre. The idea of partial or total removal of the gland or of enucleation by drawing it out of the wound and allowing it to waste (exothyropexia) arises from the somewhat erroneous conception that the hyperthyroidization is the chief cause of the symptoms and complica- tions of Basedow's disease. According to this theory, the goitre produces too much secretion, poisons the nerve centres, and produces auto-intoxication from functional hyper- activity. This theory, to be accepted, should be appHcable to every case. We find, however, nothing of the kind. The exophthalmos, tachycardia, etc., may be already marked, while the goitre is absent or slight. These defaced forms are far from rare, and we cannot, under such conditions, invoke primary hyperactivity of the thyroid gland. Abadie has quoted cases in which the exophthalmos was so marked that complete loss of both eyes had resulted, while the enlargement of the thyroid body was scarcely appreciable. In order to appreciate the question better, let us consider the operations upon the thyroid body and their results. Allen Starr gives statistics of 190 cases of thyroidectomy in Basedow's disease, with the following results : Recovery in 74, improvement in 45, failure in 3, and death in 33 cases. As a rule death was not expected, and occurred soon after the operation, or two or three days later. Whatever theory be used to explain the deaths, the patients succumbed with nervous symptoms — viz., excessive tachycardia (pulse-rate 180 to 200), sudden rise of temperature, angina, restlessness, profuse sweating, and collapse. Brissaud published a case in which Poncet performed exothyropexia, which is a benign operation, and consists in exposing the thyroid gland. The patient died without any warning. Lejars witnessed the following accident : NEUEOSES OF THE HEART 467 A girl eighteen years of age had tachycardia, slight exophthalmos, tremor, etc. The goitre was very moderate ; the right lobe of the thyroid body appeared to be the larger. It was firm, could be depressed, and showed neither nodules nor induration. The right lobe was removed en masse, after freeing the upper and lower cornua and ligaturing the vessels. The operation was satisfactory, and the patient rested well during the day. About eleven o'clock at night she was suddenly seized with intense dyspnoea and considerable acceleration of the respiratory movements. No flushing of the face, no asphyxia. She died in three-quarters of an hour. The autopsy revealed no operative lesion ; the recurrent, vagus, and sympathetic nerves, with their cervical branches, were absolutely intact. The fact, says Lejars, remains that a simple operation, performed A^ithout mishap, was followed by sudden death, which could not be explained at the autopsy, but appeared to be related to acute bulbar trouble. Jaboulay, in one of his cases, adds : Diminution of the mass remaining after partial extirpation of the goitre usually follows when the case is one of ordinary goitre. Section of the isthmus, for example, may cause atrophy of both the hypertroiahied lobes, and unilateral thyroidectomy produces diminution in the size of the remaining lobe. I have seen the opposite result in a case of Basedow's disease. Acting on the theory, which subordinates the other symp- toms to perversion of the secretion, I have several times operated upon her thyroid gland, and have left it exposed on two consecutive occasions. As each intervention was only followed by temporary improvement, I decided last year to remove the right lobe. Three months later the left lobe was enlarged, and quite recently the middle lobe formed a goitre as large as a small orange. After each operation upon the thyroid itself the symptoms showed genuine improvement, and the tremor in particular speedily disappeared ; but relapses occurred, with palpitation, tremor, and fresh goitre. Poncet sums up the matter thus : After various operations which I Have performed in exophthalmic goitre, including simple exothyropexia, I have seen a fatal result. Such results, and also the frequent return of symptoms which had yielded for a very short while before the operation, have made me very circumspect. For my part, I shaU not again meddle with the thyroid body in a case of Basedow's disease. It must be admitted that the results just quoted are hardly encouraging, but for a correct decision let us also take into account the successes obtained. Tillaux has reported a case of cure : At the Societe de Chirurgie, Tuffier presented two young women suffering from exophthalmic goitre, both treated by partial thyroidectomy, involving the right lobe and tlio isthmus. The first patient had been under medical treatment for two years at the Salpet^lere, with no result. After thyroidectomy the exophthalmos and the nervous troubles were cured. Later the tachycardia and the tremor ceased, so that two and a half years after the operation the patient was in good health. The left lobe of the th3Toid gland remained larger than normal, but had not increased in size since the operation. The second patient was a young woman whose condition was very grave when TufBer operated. She had taken tabloids of thyroid gland for six months, instead of tabloids of thymus glands. Symptoms of acute thyroidism, which demanded re- moval of the gland, appeared. Before the operation her contUtion was very grave : Enormous exophthalmos, violent dyspmca, incessant palpitation, pul.se 1-44, tliyroid gland double its normal size and showing marked pulsation, insomnia, tremor, (i-doma of the lower Umbs, and profuse diarrhrx-a. The results of the operation were remark- able. Next day the erethism of the vessels disappeared, the diarrha'a ceased, and tho 30—2 468 TEXT-BOOK OF MEDICINE pulse fell from 125 to 72. Condition quite satisfactory a month after operation. Ex- ophthalmos still present, although less, tremor cured, no trace of dyspncea, sleep good, no nervous symptoms. The future will show the ultimate worth of the operation. In spite of the successes above set down, as well as two other cases reported by Doyen, it is none the less true that operations in exophthalmic goitre expose the patient to very grave danger. We may therefore form a judgment upon the advantages or disadvantages of such operations in Basedow's disease. It seems, however, well estab- lished that the disadvantages outweigh the advantages. Operation, even when performed under the most favourable conditions, does not protect the patient from very grave risks, nor the surgeon from terrible surprises. The results obtained are temporary or incomplete. For these reasons I should be very loth to advise this operation. Another operation — viz., double section of the great cervical sympathetic — was first performed by Jaboulay. Trousseau had seen that the chief symptoms and vascular troubles in Basedow's disease do not extend beyond the area of the cervical sympathetic. The carotid arteries, with the thyroid vessels and their branches, are alone affected by the expansive pulsation, wliile the other vessels, such as the radial, the femoral, or the abdominal aorta, beat normally. Accordingly, the great sympathetic nerve has been considered as the cause, and theories, some based upon excitation, others upon paralysis of its branches, have been brought forward. None of these theories, however, were applicable to all the symptoms. The brilhant discovery of Dastre and Morat has thrown much light upon this ques- tion. These physiologists showed that the vasodilator fibres of the cervical sympathetic have a distinct origin, and upon this fact Abadie has built up an ingenious theory. Be this as it may, it is none the less true that double section of the great sympathetic nerve has given remarkable results. Out of six cases published by Jaboulay, one is absolutely characteristic : A woman fifty -five years of age had for three months suffered from exophthalmos, tachycardia, and tremor. Hypertrophy of the thyroid gland was absent. She had gained no benefit from thyroid extract. When she came under Jaboulay's care, " her look was indeed alarming from the exophthalmos, which had al&ost dislocated the left eye from the orbit, and the tremor was excessive. She suffered from tachy- cardia and from such intense dyspncBa that the possibihty of surgical intervention was discussed." Double ablation of the superior cervical ganglion was performed. The result was immediate. Three days later her face had lost its terrible expression, while the eyes, and the left eye in particular, had almost regained their normal position. Tremor, dyspnoea, and precordial pain completely disappeared, but the tachycardia persisted, and the pulse varied between 100 and 120. In his communication of October 21, 1896, at the Congres de Chirurgie, Jonnesco (of Bucharest) brought forward two cases of exophthalmic goitre, treated by double resection of the cervical sympathetic. NEUROSES OF THE HEART 469 Reclus and Faure's case is comparable to that of Jaboulay. The result of the operation was remarkable, but it is necessary to see, as Reclus says, what will become of the patient, for it may be only a case of transient improvement. The following case was pubUshed by Gerard-Marchant and Abadie : A young woman suffered from a defaced form of Basedow's disease, characterized chiefly by exophthalmos. Tachycardia absent ; thyroid body showed very slight hyper- trophy of the right lobe ; exorbitism was so marked that the lids did not cover the eye. Gerard-Marchant performed resection of both cervical sj'mpathetic nerves. The exophthalmos gradually diminished, but did not quite disappear. " This rdsult," say the authors, " was not maintained. Under the influence of emotion and fatigue, exophthalmos reappeared, although in a less degree than before the operation. It is right to add that there is no trace of goitre, and that her physical and moral condition has remained excellent." Chauffard and Quenu have published the following case : A man, aged twenty-five, admitted with the classical symptoms of Basedow's disease. Eyes very prominent, complete closure of the eyelids impossible. Goitre bilateral and pulsatile. Heart-beats very forcible, and rate 110 a minute ; dyspnoea and palpita- tion on the least effort. Carotids showed marked pulsation. Marked tremor of the hands and limbs. Patient irritable, unstable, and showed stigmata of hysteria. Quenu performed bilateral resection of the cervical sympathetic. After the operation, aggravation of the tachycardia and appearance of arrhythmia, which did not exist before, became manifest. Some days later heart showed a rate of 110. As regards the heart the benefit has therefore been nil, the goitre has been slightly affected, and the circumference of the neck, which before the operation was 38 centimetres, varies from 36| to 37 centimetres, since the operation. The eyes may be less prominent, but this is very doubtful. In short, the benefit obtained has been nil. We may, indeed, ask whether the patient has not rather suffered than profited by operation, since in two months he has lost 6 pounds in weight. In short, the results obtained by bilateral resection of the cervical sympathetic are so far too much at variance to yield definite information as to the value of this intervention. Besides the truly remarkable results (Jaboulay and Reclus' cases) there are others in which the good results are doubtful (Gerard-Marchant and Abadie's cases) or absent (Chauffard and Quenu's case). It is therefore impossible at present to give surgical treatment the preference over medical means. Both of them show defects and are often ineffectual, but medical treatment at least does not endanger the patient's life (I allude to operations on the goitre), and may result in recovery. CHAPTER V DISEASES OF THE VESSELS I. PHLEBITIS— PHLEGMASIA ALBA DOLENS. Phlebitis is inflammation of a vein. This question is in part surgical ; thus phlebitis consecutive to injury of veins, operations, inflammation, etc., is of traumatic or external origin. This variety was thoroughly described by Hunter (1795), Ribes (1816), and Dance (1828), who divided the condition into suppurative and adhesive phlebitis. This side of the question does not concern us, and, further, it is no longer of interest, since aseptic procedures are employed in surgery. The phlebitis which now occupies our attention arises from internal causes, and infectious phlebitis figures in the first rank. Sometimes the deep tissue of organs is the seat of phlebitis, at other times the miscliief develops in the veins of the trunk and the limbs. Phlebitis may pass unnoticed when deeply hidden in the splanchnic cavities, or show itself by symptoms depending upon its locahzation (portal vein, sinuses of the meninges) ; at other times it produces embolisms described under pulmonary embolisms. When phlebitis affects the veins of the limbs, it shows itself as phleg- masia alba dolens. The word phlegmasia is derived from (f)\iyfjia, (^Xe'yixaro'i, which in old-time medicine signifies phlegm (oedema). The literal translation of phlegmasia alba dolens is painful white oedema. I shall here describe the different kinds of phlebitis and phlegmasia alba dolens. Pathological Anatomy. — We have to study a double lesion : the one affecting the walls of the vein, or phlebitis ; the other affecting the blood, which forms a clot inside the vein — i.e., the obturator clot or thrombus. The name thrombosis is given to the process which ends in obliteration of the vein by a thrombus. 1. Phlebitis — Mechanism of Thrombosis. — A vein, when affected by phlebitis, is often obliterated by a blood-clot. Ancient theories considered phlebitis the initial phenomenon, and thrombosis the consecutive one. Later, at the instigation of Virchow, an entirely opposite theory has been admitted : thrombosis is the initial phenomenon, and phlebitis the secondary 470 DISEASES OF THE VESSELS 471 one. In spite of the infatuation for German researches, Vulpian fought against the too exclusive doctrine of Virchow, and taught that the coagula- tion of blood in the veins is preceded by a change in the vascular epithelium. Modern researches prove that Vulpian was right. In some cases the primary lesion of the vein is self-evident (varices, injury) ; in other cases it is at first sight less apparent. What do histology and bacteriology teach us ? In the great majority of cases phlebitis, Uke endocarditis, is due to microbic agents. Widal has found the streptococcus of puerpural infection in the clots of phlegmasia. Bacteriological examination must be made with material from the uterine veins, because coagulation starts in them, and gradually reaches the femoral veins, although we may not be able to find any trace of characteristic streptococci in the clot which ob- literates them. Chantemesse and Vaquez have found Koch's bacillus in phlebitis among tubercular patients. More often in the lesions of phlebitis we find not one specific bacillus, but the ordinary micro-organisms of sup- puration — viz., staphylococci or streptococci. In the latter case phlebitis supervenes as a secondary infection. In this manner the cases of phlebitis in influenza, typhoid, cancer, tuberculosis, cachexia, and possibly also chlorosis, are explained. The microbic agents are often present in the vessel wall and in the clot. Whether these agents penetrate the walls of the vein by the vaso vasorum, or whether the microbes circulating in the blood directly cause irritation of the vascular endothelium, matters Httle. The essential fact is that phlebitis precedes thrombosis. How does tluombosis arise ? Different interpretations have been given as to the formation of the thrombus : (1) An increase of the plasmin (spontaneously coagulable fibrin) ; (2) sloAving of the blood-stream. In- crease of plasmin is associated with cachectic conditions (cancer and phthisis), the puerperal state, and chlorosis. Slowing of the blood-stream is due to the pressure of aponeurotic laminae, situated in the course of certain veins (crural), to compression caused by the foetus, to degeneration of the heart muscle, and to cardiac paresis (Jaccoud) in severe fevers and cases of p}Texia. According to Hayem and Bizzorero, the haematoblasts, or blood- platelets, play a considerable part in the coagulation of the blood. However this may be, the lesion commences with granulo-fatty degenera- tion of the endothelial cells; the tunica intima becomes thickened, and granular and stratified layers of fibrin are deposited upon this granular tissue. This is the origin of the thrombus. The fibrinous clot is adherent. " All attempts to break down this adhesion are useless, and it is difficult to delimit exactly the wall of the vein which undergoes progressive thicken- ing. At the central point of the clot the wall presents a reddish bud, which arises from the deep tissue of the vein, and becomes lost in the 472 TEXT-BOOK OF MEDICINE coagulum " (Vaquez). After these preparatory changes the partial or total obUteration of the vein by coagulation of the blood is readily understood. 2. Thrombus. — We may now consider the clot itself. The clot fills the cavity of the vein more or less, and may be parietal or obhterating. The portion in contact with the vein is whitish and very adherent — " the clot of pulsation " (Hay em) — while the portion which obhterates the vessel is reddish, " the clot of stasis." The central end of the clot sometimes ends in a tapering manner. This end, struck by the current of blood, or detached by the stream from a collateral vein, may become an embolus. The thrombus may undergo one of the following changes : (1) Its elements may become disaggregated and disappear by absorption ; (2) it may be invaded and broken up by vasculo-connective vegetations of the tunica intima, and the vein is sometimes converted into a cord of cavernous tissue ; (3) the peripheral portions of the clot may alone undergo fibrous change and retract, so that the circulation is re-estabUshed through the centre; and (4) the thrombus may be broken up, and the detached fragment may cause embolism in the right heart or in the lung. The clot sometimes softens at its centre, and presents a puriform appearance which has been wrongly taken for suppuration, but is really a disintegration of the clot with granulo-fatty change. If the particles enter the blood-stream, they may cause infarcts in the lung ; and if bacteria are present in the thrombus, the capillary embohsms are also septic, and lead to septic infarcts and miUary abscesses in the lungs or in the heart. Description. — I shall give a general description of phlegmasia alba dolens, and return later to the pecuharities which each phlebitis may present, according to the cause which has given rise to it. Phlegmasia alba dolens may affect the veins of the upper and lower limbs, the neck and the face, but shows a remarkable predilection for the veins of the leg, and usually begins in the veins of the calf. It has an insidious onset, which is rarely febrile, and shows itself by pain, which is at first diffused through the whole Kmb, and later is locaHzed in certain points. In the leg, wliich is the ordinary seat of the lesion, the pain is more marked in the calf and the groin ; the limb is heavy and swollen, and the hypersesthesia is at times excessive. In some cases the patient complains of joint pains, simulating rheumatism ; in other cases pain may be completely absent. The bluish network under the skin shows that the circulation is impeded in the deep veins, and tends to re-estabhsh itself by the superficial ones. The deep veins are sometimes transformed into a hard, tortuous cord, which may be felt in the calf and followed up- wards, as far as the ring of the adductor magnus. The knee-joint is some- times filled with fluid ; the movements of the leg are difficult, as though the muscles were affected with paresis. Transient loss of power in the Kmb, with or without muscular atrophy, has also been noted. DISEASES OF THE VESSELS 473 The obliteration of the veins causes oedema which has special charac- ters : white, because the skin is bloodless ; smooth and hard, because the areolae of the skin are distended by serous fluid ; painful, from the com- pression of the nerve endings. It does not, therefore, resemble the oedema of cachexia, or of diseases of the heart and kidney. In some cases, however, it may be shght, or its absence may make an error in diagnosis easy. It may only appear days, or even weeks, after the pain. In some patients it is almost the only symptom of the lesion. The oedema often begins in the foot and leg, and later reaches up to the thigh. In puerperal phlegmasia, however, the oedema often begins at the root of the Hmb, and spreads from above downwards. Phlegmasia has a variable duration. We see sUght forms, as in a tuber- cular patient in whom the trouble only lasted about twelve days ; as a rule, it lasts four or five weeks. Patients feel the effects of the disease for a long time. For months and years walking tires them, and severe exercise causes the oedema to reappear. The cellular tissue and the skin are often the seat of ill-defined induration. Venous thrombosis fer se very rarely causes gangrene, which more usually supervenes in the course of phlegmasia, because the inflammation extends from the vein to an artery. In rare cases the clot breaks up, and is carried away by the blood-current ; the thrombus becomes an embolus, which gets stranded in the right heart, or passes through into the lung. Disastrous complications are the result : cardiac emboUsm may produce fatal syncope, while pulmonary embolism, according to its extent, produces rapidly fatal asphyxia, attacks of dyspnoea, pulmonary gangrene, and mechanical or septic infarcts in the lung. These complications, described under Pulmonary Embohsm, show how great may be the gravity of the prognosis. It is of interest to know at what period embolism is most to be feared. It is rightly admitted thar the accident in question is no longer to be feared six weeks after the appearance of phlebitis. The exceptions, however, must be reckoned with, as in the case quoted by Trousseau, where fatal embohsm supervened three months after the onset of phlebitis. The diagnosis is generally easy. It must not be forgotten, however, that pain and oedema, which are the chief symptoms, may be absent. Cases have been quoted in which the disease was almost latent, and yet the patients succumbed rapidly from pulmonary embohsm. On the other hand, phleg- masia may be of value in diagnosis. When we hesitate, for example, between ulcer and cancer of the stomach, the appearance of phlegmasia confirms the existence of cancer. Trousseau, who brought this fact so clearly to hght, was able to apply the senieiological value of phlegmasia to his own case. The appearance of painful oedema 474 TEXT-BOOK OF MEDICINE in the leg led him to diagnose the gastric cancer from which he died six months later. Varieties. — After this general description, let us consider special cases : 1. In puerperal women phlebitis appears some days after accouche- ment, rarely later than two weeks. It is often ushered in by fever. Puer- peral phlebitis is usually absent when the accouchement has been normal, and is generally seen only in cases in which the patient has shown some infectious phenomenon, foetid lochia, difficult or artificial deUvery, slight fever, etc. In other cases, after accouchement or miscarriage, no sign of infection may occur, and yet phlegmasia develops three or four weeks later. Phlegmasia of puerperal origin improves after three or four weeks, but may last much longer. I cannot direct too much attention to a variety of phlebitis which also has a uterine origin, although it may not be puerperal. I allude to the cases of deep phlebitis or of phlegmasia alba dolens which supervene after operations for diseases of the ovaries and uterus, and especially fibroids. 2. Phlegmasia in typhoid fever usually supervenes during the decline of the disease or during convalescence. Its onset is often febrile. It may afEect the veins of the upper Hmbs and the neck, and may be associated with arteritis. 3. Painful phlebitis occurs in influenza, and recent epidemics have provided material for its careful study. In the pubhshed cases the phlebitis affected the veins of the lower hmbs or of the arm. 4. Phlegmasia is frequently associated with tuberculosis. It usually supervenes in the cachectic stage. In some cases, however, it may appear early. 5. I would make the same remark concerning cancer. In most cases phlegmasia supervenes in the stage of cachexia, but in other cases (Trousseau was himself a memorable example) it appears during the first stage of cancer, before other positive symptoms. It is therefore a typographical error which states that Trousseau diagnosed cancer of the stomach a month before his death, on the appearance of phlegmasia. It was several months before liis death that the appearance of phlebitis in the calf led Trousseau to diagnosw cancer, although no other positive signs of organic disease were present. 1 am able to state this fact because I saw the case. 6. Phlegmasia associated with chlorosis presents pecuhar interest. Possibly this phlebitis, hke so many other cases, is due to a superadded infection. Certainly phlegmasia of chlorotic origin is far from being rare, and in some cases has been followed by pulmonary embohsm and death. In several cases death has supervened from phlebitis of the pulmonary veins. 7. Phlebitis has been noted in acute articular rheumatism and in pneu- DISEASES OF THE VESSELS 475 raonia (Obrecht). The importance of gouty phlebitis will be considered under Gout. 8. Phlebitis of the limbs may occur in the course of blennorrhagia. 9. Appendicular phlebitis is not uncommon. I have seen it in a woman suffering from appendicitis, which was operated on later by Segond. The phlebitis usually affects the left leg. It may appear as an infectious com- pUcation, even though the appendicitis be slight. Treatment. — In a patient suffering from phlegmasia we must avoid massage, and movement of every kind which may favour the displacement of a clot and the formation of an embolus. The affected hmb should be placed in a trough-spHnt in order to obtain complete immobiUty. The pains may be reheved by the following ointment : VaseUne, 10 parts ; methyl saHcylate, 3 parts. Salt must be excluded from the diet. Since Widal showed that the oedema in Bright's disease disappears by excluding salt, Chantemesse has apphed this treatment successfully to phlegmasia in enteric fever. I have seen the good effects of milk diet in women suffering from post-operative phlebitis. The cure at Bagnols (Department of Orne) is of much service. II. SYPHILITIC PHLEBITIS. Description. — Although sj^hiHtic phlebitis may not appear tiU some one or two years after infection, i€ is usually a much earUer manifestation of the disease. In one of Roussy's cases it appeared five months after the chancre. In one of my cases it supervened two and a half months after the chancre. Thibierge has recorded phlebitis of the internal saphenous and cephahc veins two months after the chancre. Fournier noted its appear- ance in the internal saphenous, median basiUc, and median cephaUc veins six months after the primary sore. Phlebitis, therefore, may appear witliin a few weeks or months of the chancre ; it may precede or coincide with the roseola and the mucous patches. Le Noir and Girdwood state that the sldn rash may not appear until several days after the onset of superficial phlebitis. Fournier and Loeper have recorded the fact that in one case phlebitis appeared two days before the papules in the skin. The disease does not always begin in the same way. A sensation of weight, formication, or cramp may be noticed in the Umb ; on the other hand, prodromata may be absent, the pain is acute from the first, iind oedema appears. In one patient the phlebitis had a sudden onset. He was returning liome when he felt acute pain in the left thigh, along the course of the saphenous vein, in the popliteal space, and in the leg. Next day the wliolc limb was oedematous. Mauriac's patient was in hospital when he felt a sharp pain in the right calf ; phlebitis had just commenced. Charcot speaks 476 TEXT-BOOK OF MEDICINE of a syphilitic patient who felt acute pain on the inner side of the left thigh ; phlebitis had just begun in the internal saphenous vein. Fever is exceptional or slight, and throughout the disease " the symp- toms," as Fournier says, " begin Hke those of a subacute phlebitis, which almost at once becomes of the apyretic variety, in which the affection com- prises simply a plastic induration of the venous trunk." The veins of the leg are more often affected than those of the arm. We find, in order of frequency, the internal saphenous, the external saphenous, the basihc, and the cephahc veins. The vein is not always involved along its whole course : the phlebitis is often partial. In one of Fournier's cases induration was noticeable over the internal malleolus, and did not appear again until above the knee, whence it extended to the groin. This segmentation has often been noted in the median cephahc and basihc veins. It is also common in syphihtic arteritis, where healthy and diseased segments alternate. We must note the multipUcity of phlebitis in the same patient. Other diseases besides syphihs cause multiple phlebitis, but this pecuHarity is, I think, nowhere more marked than in sypliihs. In thirty-six cases twenty-two patients had multiple phlebitis. In my patient both legs were affected. In Fournier's patient the left leg, the right leg and arm were involved. In Fournier and Loeper's case phlebitis was present in the left leg and in the right leg and arm. Syphihtic phlebitis is fairly often symmetrical. It is prone to relapse. A patient who thinks he is cured has a fresh attack some weeks or months after the first attack. Phlebitis is far more common in the superficial than in the deep veins. Mauriac, however, has seen a case of deep phlebitis with thrombosis. Andry and Constantin have seen phlebitis of the pophteal vein, resembhng in every way phlegmasia alba dolens. Pain and oedema are not as a rule as severe in the syphihtic as in the other forms of phlebitis. Nevertheless, when my patient was admitted to the Hotel-Dieu, the oedema extended from the foot to the trunk. Recovery occurs in a few weeks, and the veins regain their elasticity. This is the reason why specific phlebitis does not leave behind it, as the other forms do, interminable oedema, which reappears on the least provoca- tion, and obstinately resists all treatment, including massage and the cure at Bagnoles. We must not, however, suppose that syphihtic phlebitis is always of short duration ; in some cases the disease lasts five or six months, owing to the multiplicity of the lesions and to the relapses which occur. But a capital difference, which would alone suffice to distinguish the syphilitic from the other forms of phlebitis, is that it is not complicated DISEASES OF THE VESSELS 477 by emboKsm. In phlebitis due to puerperal or typhoid fever, to pneumonia, influenza, appendicitis, cancer, tuberculosis, gout, etc., the chief danger lies in emboHsm and infarcts. Nothing of the kind is found in syphihtic phlebitis, fatal embolism or infarcts having never been noted. The diagnosis comprises two stages. We must diagnose phlebitis and prove that it is syphilitic. The signs of phlebitis include pain in the course of a vein, the transformation of the vein into a rigid and at times indurated cord, and the appearance of oedema, which may be sUght, in the subjacent region of the Umb! We must not, however, confuse it with syphihtic lymphangitis, which also forms a superficial rigid, painful cord, with or without reddish tracks in the skin. Lymphangitis gives rise to enlarged and painful glands. Further, the rigid cord in lymphangitis does not coincide with the course of the vein. The decision as to the specific nature demands a survey of all the causes which may engender phlebitis. If we find no such cause, and if, on the other hand, the phlebitis appears a few weeks or months after the chancre, but especially at the same time as the secondary symp- toms, the lesion is specific. I have so far coasidered early phlebitis. The tertiary forms are (^uite exceptional. They may appear as gummatous tumours of the vein, or as generalized phlebosclerosis with dilatation of the veins. Pathological Anatomy. — This question has been worked out upon the living subject, because no one has died of the malady. Mendel reports a case in which Lion found a clot totally obhterating the resected segment of the vein. Darier and Civette have published the following conclusions on the pathological anatomy of phlebitis. Among the manifestations of severe secondary syphiUs we may find hard, movable nodules under the skin. Their anatomical situation is in the walls of the subcutaneous veins, their structure is that of a syphiloma, and they give rise secondarily to ordinary thrombo-phlebitis. Mercurial treatment brings about their disappearance, with an apparent return of the tissues to their normal integrity. The recognition of the spirochsete in the lesions of the vessel wall is the specific hall-mark of syphihtic phlebitis. Benda has outUned the findings in a case of syphihtic arteritis, while Nattan-Larrier and Brindeau have given a complete description of the lesions in a case of specific arteritis and phlebitis. These authors systematically examined eighteen syphihtic placentae, which showed such multiple vascular lesions as endophlebitis and endarteritis obliterans aut vegetans. In five placenta) they found stainable spirochaetae in the vascular layers of the veins and arteries, which correspond to the tunica media. This finding shows the importance and the action of the spirocha}tc. The first point in treatment is to immobihze the hmb. I know that this 478 TEXT-BOOK OF MEDICINE procedure may appear somewhat umiecessary after the statement that syphiUtic phlebitis has never caused embohsm. I would not, however, depend on it, because the unexpected may happen, and I therefore kept my patient at absolute rest in bed in the Saint-Christophe ward. Specific treatment must be employed. Iodide of potassium is not of much use in my opinion, and I prefer injections of a watery solution of biniodide of mercury daily for ten days, the dose being | grain. The treat- ment can be suspended, and then repeated if occasion arise. III. ARTERITIS— ATHEROMA— ARTERIO-SCLEROSIS. Anatomy. — Before undertaking the important question of diseases of the arteries, I will briefly describe their normal structure. The arteries are made up of elastic, muscular, and connective tissue, an endotheUal layer, nutrient vessels, and nerves. These tissues vary in extent according to the size of the artery and its functions, just as the arterial lesions vary according to the size of the vessel. An artery is composed of three coats : (1) The tunica externa, or adventitious coat, is composed of bundles of connective tissue, mixed with elastic fibres, and receives the vaso vasorum, which do not penetrate into the tunica media, except in pathological conditions. (2) The tunica media is the characteristic portion of the artery. In the large arteries (aorta, carotid, pulmonary arteries) the elastic tissue predominates, and the muscular elements are scanty. The elastic fibres and laminae form, as it were, a felting, whence the name fenestrated membrane. These elastic elements are supported upon the internal elastic lamina, which is more important than the external one. In arteries of medium size the tunica media is less rich in elastic tissue and more rich in muscular tissue ; the elastic felting is less impor- tant ; the internal lamina persists, but the external lamina has disappeared. The smooth muscle fibres form bundles which are transverse in direction,, and are inserted into the network of the tunica externa. In the arterioles the elastic tissue is only represented by the internal elastic lamina, which appears festooned in transverse sections, because the muscular fibres contract and the elastic lamina undergoes retraction. The connective tissue has disappeared. The nerves of the artery belong to the tunica media. (3) The tunica intima varies according to the artery : the endothelial layer, formed by endotheUal cells, is everywhere the same ; but in the large arteries of the elastic type we find a fibro- elastic layer, which is divided into two — the one showing longitudinal, the other trans- verse striation (the lesions of atheroma begin in the fibro-elastic layer). In arteries of the muscular type the longitudinal layer alone persists ; in the arterioles the tunica intima is formed by the endothelium alone. History — Discussion. — Since the commencement of the century, arteritis has been more or less intimately allied with questions of doctrine, Pinel, in his classification of fevers, gave the name of angiotenic to a tran- sient fever which originated, as he thought, in inflammation of the arteries. He said that this inflammation was shown post mortem by the redness of these vessels. Bouillaud did not agree with Pinel's narrow classification. In his opinion inflammation of the vessels and of the heart is not only a cause of fever, but represents fever taken in its widest sense. This forms the famous DISEASES OF THE VESSELS 479 angiocarditic fever, the anatomical proof of which Bouillaud also found in the redness and phlogosis of the hning membrane of the heart and vessels. At this time, moreover, medicine was dominated by the doctrine of inflam- mation, gastroenteritis according to Broussais, angiocarditis according to Bouillaud, or, in other words, gastro-intestinal inflammation, on the one hand, and cardio-vascular inflammation on the other ; but it was always inflammation causing slightly different types, according to the intensity of the inflammatory process. Two renowned men had been brought to this pass by adhering to system. Reaction, however, occurred. Trousseau and Rigot had abeady shown that the redness of the arteries, the so-called phlogosis, was only the result of cadaveric imbibition, and Bretonneau, in his memorable work, partly destroyed the doctrine of inflammation, and replaced it by the admirable doctrine of specificity, which has in our day been rejuvenated and confirmed by the discovery of microbes. Whilst medicine was led astray as to inflam- mation of the arteries and its consequences, surgeons pubhshed excellent works, and Frangois proclaimed that arteritis causes obhteration of the arteries and spontaneous gangrene. The German school next took the field with the doctrine of embohsm (Virchow), and from that time two causes of arterial obliteration were recognized — the one by thrombosis, the other by embolism. From this time two fines of study were estabfished : the one studied chiefly arterial degeneration, and it appears that the active process was rather neglected ; atheroma was found in every case — " this vital rusting," according to Peter's happy expression ; " a man is as old as his arteries," according to the dictum of CazaUs. On the other hand, the active process was especially studied, endarteritis and periarteritis, obliterating endar- teritis and dilating arteritis, being described. Small mihary aneurysms of the brain, associated with cerebral haemorrhage, were discovered (Bouchard, Charcot), and descriptions were given of the small aneurysms in pulmonary cavities, resulting in fulminant lia3moptysis (Rasmussen), while ectasia of the vessels in bronchial dilatation and the profuse haemorrhage which they jjroduced, were proved (Hanot). Our knowledge of these lesions has gradually progressed up to the present time, when we consider chiefly the pathogenesis of arteritis and the part played by infectious diseases and their agents. I must now, however, deal with another important question, that of arterio-sclerosis. In 1S72 Gull and Sutton described a kind of fibroid change in tlio arterioles and capillaries under the name of . arterio-capillary fibrosis. They showed that the change in the kidneys which results in atrophy ia simply the extension of a morbid process which has begun in tlic small vessels of this organ. The doctrine of arterio-sclerosis was thus created. 480 TEXT-BOOK OF MEDICINE What, then, is arterio-sclerosis ? It is arteritis of the arterioles, and especi- ally of the visceral arterioles. Endarteritis results in fibrous thickening of the tunica intima, in constriction of the arterioles, and in fibrous change in its walls. Atheroma and arterio-sclerosis, which are so unlike at first sight, result from the same causes, except that the result is atheroma in the large arteries or in those of medium size, and arterio-sclerosis in the visceral arterioles. Atheroma of the large arteries is said, therefore, to be the result of arterio- sclerosis of their vasa vasorum. The characteristic point is that the process commences in the small vessels, but as it does not remain limited to them, the process becomes extravascular, and extends to the connective tissue and the elements of the organ, which are replaced by newly-formed fibrous tissue. The change arises in the arterioles, and extends to the neighbouring regions in the form of bands and islets of fibrous tissue. Arterio-sclerosis, when once present, shows no Hmit. According to some authors (Martin, Huchard, Weber), it sums up the pathogenesis of nearly all the chronic affections of the viscera. Certain forms of nephritis, formerly considered as having an inter- stitial or epitlielial origin, including senile nephritis, which has been looked on as epithelial (Charcot and Gombault), would therefore be cases of renal sclerosis of vascular origin. Arterio-sclerosis of the coronary arteries would embrace the whole of cardiac pathology. The heart in Bright' s disease, the senile heart, the fatty heart, hypertrophic fibrous myocarditis, and myocarditis associated with valvular lesions, would all depend on arterio-sclerosis. Valvular lesions of the heart would depend upon the primary vascular lesions, and without arterio-sclerosis of the coronary arteries angina pectoris would not exist. The lesions of the aorta and the large arteries are also secondary to arterio-sclerosis. Atheroma only shows itself in arteries provided with vasa vasorum, and is the result of endarteritis and arterio-sclerosis of these vasa vasorum. The proof lies in the fact that the vasa vasorum, which correspond to the atheromatous patches, are always affected by arteritis obliterans (Martin). In the nerve centres arterio-sclerosis plays a considerable part, so that tabes, general paralysis, many syphilitic lesions, etc., may have their origin in arterio-sclerosis. The genito-urinary apparatus is also under the ban of arterio-sclerosis, which causes fibrous hypertrophy of the prostate and the bladder. I shall describe later the lesions of the kidneys. The stomach and spleen present changes due to arterio-sclerosis. The DISEASES OF THE VESSELS 481 portal vein, too, may be affected by phlebo-sclerosis (Laennec's atrophic cirrhosis). Such are the chief local manifestations of arterio-sclerosis. In different cases it may remain localized to a single organ, such as the kidney, heart, or lung ; it may attack several organs at once, or even become general and be asso- ciated or not with lesions of the large arteries, and especially with atheroma. These views of arterio-sclerosis are of much interest, but it must be admitted that for some years arterio-sclerosis has been singularly abused. It has become all-invading, and has been held to explain everything, so that when any difficulty is experienced in finding a pathogenic or chnical interpretation, the reply is : '"' It is arterio-sclerosis !" Does such a constant relation between the cause and effect really exist ? Is the arterio-sclerosis always the primary lesion, and are the fibrous lesions in the viscera always secondary to sclerosis of the small arteries ? When these visceral lesions are not in the immediate neighbourhood of the dis- eased arteriole., the partisans of this doctrine say that we must then admit either capillaritis or pericapillaritis ; but then we have reached the confines of the capillary network in the innermost layers of the tissues. Why, then, may it not be admitted that the irritant sclerogenous substance, whether bacillus or toxine ; whether animal, vegetable, or mineral ; whether alcohol or lead, may be able to act upon the cells of the connective tissue and of the organs ? The desire to reduce all visceral scleroses to arterio-sclerosis appears to me exaggerated. Reaction is taking place in this matter. Bard and Phihppe, in their interesting paper, have shown, as regards the heart, that side by side with vascular sclerous hypertrophic myocarditis there is room for interstitial myocarditis, in which the arterio- sclerotic lesion is secondary. In general paralysis, according to Joffroy, encephalitis is much more probably of parenchymatous than of vascular origin. Some authors, confounding the lesions and its effects, find it a simple matter to set down to arterio-sclerosis the symptoms of " Brightism," which are really symptoms of toxicity. The result is the confounding of the vascular lesions of the kidneys with the multiple effects of intoxication from insufficiency of the urinary depuration. After this general discussion, let us pass to the detailed study of arteritis and arterio-sclerosis. Arteritis may develop under the most varied con- ditions, and may have almost identical results, although its origin is very different. It is therefore necessary to divide up arteritis. Traumatic Arteritis. These cases belong chiefiy to the domain of surgery. Some, however, are of interest both to the physician and the surgeon, such as tlioso which develop in the neighbourhood of superficial or of deep ulceration of the 482 TEXT-BOOK OF MEDICINE skin, or of a viscus. In this case the walls of the artery do not escape the inflammatory and destructive process which affects the surrounding tissues, and, accordingly, two eventualities may happen. If the inflammatory process predominates, the walls of the artery become thickened and pro- liferate, the cahbre of the vessel is diminished, the blood coagulates, and the artery is gradually converted into an impermeable fibrous cord, which may ultimately be destroyed, without untoward consequences. If, on the other hand, the ulcerative process is rapid (ulcerative or suppurative arteritis), the walls of the artery are destroyed from without inwards, before coagula- tion of the blood can take place, lose their resistance, and finally give rise to an aneurysm. This sometimes happens in the interior of tubercular cavities or on the surface of gastric ulcers. If, at a given moment, the arterial tension increases, the resistance of the walls is insufficient, the aneurysm bursts, and fulminating haemorrhage occurs. The arterial lesions which occur when an artery is obliterated by em- bolism are also related to traumatic arteritis. The irritation produced by the foreign body, whatever may be its point of departure and its nature, leads to inflammation of the tunica intima and to lesions analogous to those which we shall describe later. Infective Arteritis. Pathogenesis. — This group comprises those cases which supervene during or after general diseases. They have been verified by pathological anatomy and by bacteriology, and their existence is indisputable. They are most often seen in acute diseases, such as typhoid fever, etc. (Taupin, Potain, Vulpian, Hayem) ; diphtheria (H. Martin) ; puerperal conditions (Simpson) ; scarlatina, measles, variola (Brouardel) ; malaria, rheumatism (Lancereaux, G-ueneau de Mussy), etc. Among the more chronic diseases which may cause arteritis, tuberculosis and syphihs specially deserve mention. The data acquired as regards the evolution of the tubercle bacillus show that propagation occurs both by the bloodvessels and by the lymphatics. If it is arrested in an arteriole, a colony of microbes develops at this point. The irritation thus produced in the walls of the artery, whatever be its size, suffices to cause specific inflammation. In this manner the starting-point of most tubercular granulations is explained. Syphihtic arteritis will be studied in the next section. As regards infective arteritis, developing in the course of the maladies enumerated above, it is probable that the arterial lesion is directly caused by the micro-organism which produces the infection, unless the toxines secreted by it can be also incriminated. These cases of arteritis would, therefore, in their mechanism resemble another class — namely, the toxic class of arteritis. They have, however, this distinguishing point— namely, that DISEASES OF THE VESSELS 483 in infective arteritis the number of diseased arteries and the extent of the lesions are always hmited, while toxic arteritis affects a large number of vessels, and involves each vessel to a large extent. Pathological Anatomy. — The following lesions are found in infective arteritis : (1) When a large artery, such as the aorta, is affected, the inner wall is red, rugose, and in places glazed, while other parts are depressed in a cuplike form, and resemble the pustule of variola {vide Aortitis), and the external surface shows a close network of capillary vessels filled with blood. (2) In the small arteries and in those of medium size the lesions are not visible to the naked eye, but under the microscope they are identical with those found in the large arteries. They comprise an increased thickness of the tunica intima (endarteritis), wliich projects into the lumen of the vessel — sometimes at one point only (parietal arteritis, Barie), at other times around the whole circumference of the vessel. When the artery is affected upon one side only, the granulation rarely projects sufficiently to ob- literate the lumen, which is simply constricted. If, on the other hand, the arteritis is circumferential, the lumen of the vessel rapidly disappears (obliterating arteritis), and the circulation is interrupted in the whole area suppHed by this artery, unless the collateral circulation supphes the defect. The thickening of the tunica intima depends on the multiphcation of the anatomical elements, and on the infiltration of leucocytes between these new-formed elements. Endarteritis may exist alone, 'but as a rule there is also some periarteritis. In this case the tunica externa is thickened, and pushes aside the structures in contact with it. In this case also the inflammation is characterized by the appearance of embryonic cells between the connective and elastic bundles of the tunica externa. All the elements show great tendency to undergo fibrous change. Symptoms. — The symptoms of arteritis in acute diseases vary according to the cahbre of the vessel, and to the organs which it supplies. 1. If the aorta is affected (syphiUs, variola, puerperal state, and malaria), the severe symptoms of acute or of subacute aortitis will appear. 2. If the artery is of medium size, as in a limb (typhoid fever), the patient experiences very acute pain along the artery, or at the extremity of the Umb, and the pain is increased by pressure and movement. At the same time the pulse diminishes or disappears completely, and the limb becomes cold, blue, and insensitive. A hard cord which rolls under the finger is felt along tlie course of the artery. If the obliteration is complete and the collateral circulation is not re-established, pustules form, livid patches appear, and the limb is affected by dry or moist gangrene. In some cases the results are not always so serious : the pulse gradually returns, the hard cord disappears, and the cyanosis only remains in the form of violet-coloured patches. Walking 31—2 484 TEXT-BOOK OF MEDICINE may cause oedema, lasting several months, but gangrene is averted, and recovery, although slow, is the usual termination. In some cases arteritis makes very rapid and acute progress, as we shall see under Typhoid Fever. If arteritis affects a cerebral artery (typhoid fever, syphilis), the resulting troubles depend on the functions of the area supphed by the diseased vessel. As the arteries of the motor zone are most often affected, the symptoms are nearly always very grave, and include hemiplegia, aphasia, contracture, etc. In the case of syphilitic arteritis, however, these troubles often improve and even disappear under antisyphiHtic treatment, when the artery recovers its permeabihty, as in a case of syphilitic arteritis of the temporal arteries pubhshed by Leudet. For further detail I refer to the section on Cerebral Syphilis. 3. If the diseased arteries are of small calibre, such as those of the muscles or of the viscera, the lesions are identical with those already described. In some cases the nutrition of the invaded tissues is severely compromised. If a muscle is affected, the myositis may cause softening, and end in rupture. If the arteritis arises in the heart, for example, inflammation of arterial origin, which may give rise to all the lesions and chnical signs of myocarditis, results. As a general rule, these inflammations are transient. Lately, however, cases of chronic myocarditis (Landouzy and Siredey), encephahtis, myelitis (Marie), and nephritis, originating in infective arteritis, have been published. Toxic Arteritis— Atheroma— Arterio-Sclerosis. We shall include in this group arterial lesions consecutive to pathogenic agents, to their toxines, and to vegetable or mineral poisons. The arterial lesions in alcohohsm may be taken as our type. Still, plumbism, gout, rheumatism, diabetes, old age, and the infectious diseases, may give rise to them. In some cases the irritative element differs, but the inflammatory processes are identical. They may be reduced to two chief groups : 1. As in the preceding case, the artery may be affected by endoperi- arteritis, which diminishes its cahbre and changes it into a fibrous tube. We then say that arterio-sclerosis is present (Gull and Sutton). 2. The tunica intima may be affected, but only in the layers subjacent to the endothehum. At this level yellowish cupHke patches are formed, having the dimensions of a lentil and filled by a fatty pulp, atheroma, which flows out when the endothehal covering is punctured. If the fluid as well as the fatty matter is reabsorbed, the calcareous salts only remain, and then give to the patch a rigid consistency. These atheromatous centres, which may exist in great numbers in the same vessel, may finally fuse, and give to the artery a cartilaginiform or ossiform rigidity. Accordingly, the name DISEASES OF THE VESSELS 485 of ossification of the arteries has been given to this disease, although it is not a correct term. The affected vessel loses its elasticity, bursts easily, and allows distension (aneurysm), while the irregularity of its internal surface favours coagulation of the blood (tlirombosis). These lesions, which are sometimes isolated, sometimes contiguous, occur almost exclusively in the arteries of the greater circulation. They are usually diffuse and always run a very slow course. When the whole arterial system is invaded, atheroma cliiefly affects the large arteries, while arterio-sclerosis develops by preference in the visceral arterioles. Arterio-sclerosis causes changes of two kinds in the viscera : (1) Peri- arterial inflammation which proceeds by foci, in the centres of which adiseased artery is always found (inflammatory sclerosis) ; (2) a lesion of degenera- tion, in which foci of sclerosis are also formed, but are always at a very long distance from the diseased vessel (dystrophic sclerosis, H. Martin), showing, therefore, the exact opposite of what occurs in the preceding case. Some- times these two kinds of change are found side by side (mixed sclerosis). Of the symptoms of atheroma and arterio-sclerosis, some are due to the arterial lesions themselves, while others depend on the visceral changes which they produce. Among the former (atheroma) we will cite the tor- tuous course and rigid character of the arteries and the increase of arterial tension, which is shown with the sphygmograph by a sharp line of ascent, followed by a flat top and a wavy line of descent ; the second sound, wliich is accentuated, and has a. ringing character; and the frequency of purpura and gangrene of the extremities. Among the troubles consecutive to the visceral changes we may note cerebral troubles, such as vertigo, loss of memory, giddiness, successive attacks of hemiplegia and aphasia, and faihng intelligence, which may result in complete dementia. In some patients the heart is cliiefly affected by arterio-sclerosis, palpitation, hypertrophy of the heart, angina pectoris, and paroxysmal dyspnoea are frequent. In other patients the digestive functions are first affected — loss of appetite and frequent indigestion. Lastly, in a fair number of cases renal changes open the scene and cause insufficiency of urinary depuration, and the numerous symptoms of Brightism, which must be carefully elucidated before the appearance of the grave symptoms of confirmed uraemia. The treatment of atheroma and arterio-sclerosis is based on the use of iodides, milk diet, and remedies which will lower the arterial tension (Huchard). 486 TEXT-BOOK OF MEDICINE IV. SYPHILITIC ARTERITIS— ARTERITIS OBLITERANS— SYPHILITIC GANGRENE— ARTERITIS ECTASIANS —SYPHILITIC ANEURYSM. In the course of syphilis the arterial vessels maybe affected alone, without any lesion of the neighbouring tissues. These cases only have a special clinical history. Sypliihtic arteritis of the brain, spinal cord, aorta, etc., is dealt with under syphiMs of these organs. I shall deal at present only with peripheral arteritis, and in particular with arteritis of the limbs, which forms a distinct and very interesting pathological group. The process (either in the arteries of the Umbs or in the cerebro-meningeal ones) may result in two different kinds of lesions : on the one hand, more or less complete obliteration of the vessel ; on the other hand, ectasia of the vessel or aneurysm. Arteritis Obliterans — Gangrene. — I do not know of a more typical case than that presented by Leudet (of Rouen) at the Blois Congress in 1884. The patient -was syphilitic, and suffered from painful obliterating arteritis of the anterior frontal branch of the left superficial temporal artery. This primary arteritis obliterans, limited to an arterial segment, was soon followed by symmetrical arteritis obliterans of the right side. Leudet was able to follow all its phases, including indura- tion, obliteration of the artery, diminution and cessation of the pulse ; then, under the influence of antisyphilitic treatment, he was able to follow the re-establishment of the arterial circulation, return of the pulse, permeability of the artery, and finally cure. SyphiUtic arteritis obhterans of the limbs may be followed, just as atheromatous arteritis, by mummification of the extremities, which is in every way comparable to ordinary senile gangrene. Here is a case : An old woman came under my care for gangrene of the right leg and foot, which had come on suddenly with sharp pain two months before. The toes were blackish and shrivelled ; the dorsum of the foot was li\id. A large slough had invaded the lower part of the limb. The pulse was absent in the dorsahs pedis and in the tibial arteries, the skin was cold and insensible, and the picture was, in a word, that of senile gangrene. One thing, however, struck us : Over the forearm and abdomen there were irregular pigmented scars, mth polycyclical outUnes, and on the left upper eyelid a large copper-coloured papule, with scalloped edges. These lesions were syphiUtic. I at once concluded tliat the gangrene of the leg was due to syphiUtic arteritis obhterans. The patient was given injections of biniodide of mercury, but the treatment came too late, and amputation became necessary. The patient soon succumbed. Examination of the amputated hmb showed that the gangrene had invaded most of the posterior muscles, in the form of huge lardaceous infarcts of a waxy-yellow colour. The femoral artery was healthy ; the branches of the pophteal, the tibio-peroneal trunk, and the posterior and anterior tibial arteries were obUterated in segments. At these spots the wall of the artery showed a ring-like thickening, and the lumen was obhterated by adherent thrombus. Between the segments the lesions were absent or very slight. Everywhere else, as was found later at the autopsy, the arteries were healthy and free from atheroma. Microscopical examination showed that this process DISEASES OF THE VESSELS 487 originated in the deep part of the subendothelial layer of the tunica intima, above the internal elastic limiting layer, and the organization of a thrombus had rapidly com- pleted the obhteration. Cases of this kind are relatively rare. Aune, however, has collected seven, and several analogous ones have been pubhshed. Syphihtic arteritis attacks the lower hmbs (Charcot, Fournier, Podres, Hutcliinson) as often as the upper ones, and may. be bilateral, symmetrical, or multiple, as shown by Magrez's case, in which arteritis obhterans invaded in succession the right arm and the legs, with gangrene of the left leg. The onset is sometimes progressive, with functional troubles, loss of muscular power, and intermittent claudication ; at other times sudden, with very sharp pain. Numbness, formication, coldness, cyanosis, and oedema then appear. The arterial pulsations disappear in the affected segment, and if the artery is superficial a painful cord may be felt. The slow forms may be arrested by treatment ; the permeabiUty of the vessel becomes re-established, and the threatening symptoms disappear, although a fresh attack of arteritis may show itself in some other part. In cases of sudden onset and rapid course the obhteration results in dry gan- grene. Accordingly, when a patient suffers from sharp pain, intermittent claudication, chiUiness, cyanosis, and gangrene of the foot, syphihtic arteritis must be thought of, and careful search made for other stigmata of syphilis. From the anatomical point of view our patient showed the chief characters of syphihtic arteritis. We see cases of departmental arteritis affecting a limited area of a limb. In this region the lesions do not show the same intensity at all points ; one segment of the artery is respected, while another is obliterated. In the limbs, as in the brain, arteritis obliterans is chiefly segmental, and at times symmetrical (Magrez's case affecting the lower limbs, and Leudet's case affecting the temporal arteries). When these anatomical characters are clear, it is easy to distinguish between syphilitic and athero- matous lesions, which are diffuse and general ; but there are exceptions, and syphihtic arteritis may be also more or less general, and result in similar lesions to those of atheroma (Cornil). The histology of syphilitic arteritis obliterans shows nothing specific. At a late period the three coats of the artery are thickened and infiltrated, with or without miliary nodules, resembUng microscopic gummata (Joffroy). The lesions frequently commence with endarteritis, rarely with periarteritis. Obliteration may occur as the result of two processes. Sometimes we find only endarteritis vegetans, which obliterates the artery more or less com- pletely, and converts it into a fibrous cord, without any appreciable throm- bus ; at otlier times (this is the more frequent) there is thrombo-a^-teritis obliterans : the endothelium desquamates, or becomes necrosed, and the thrombus contributes very largely in obhterating the vessel. In both cases 488 TEXT-BOOK OF MEDICINE the arteritis may be chronic or subacute. It appears possible to differentiate it from ordinary atheroma by the greater activity and the more rapid course in the direction of obUteration, as well as by the lessened tendency to degenerative lesions. Syphilitic Aneurysm. — The second type of syphiHtic arteritis in the limbs results in dilatation and aneurysm. The dilatations result from the same process of embryonic infiltration of the coats of the vessel ; the middle coat, wliich is much infiltrated, has lost all power of resistance, and yields at one or at several points. We may see upon some vessels buds of endarter- itis and aneurysmal dilatations. Here, as in the brain, these dilatations may be cyhndrical and extensive, or circumscribed and aneurysmal. Aneurysms sometimes develop in several arteries (pophteal and innominate trunks, Croft) ; they chiefly affect the femoral, popliteal, subclavian, brachial, and radial vessels. I have seen syphilitic arteritis of the left radial artery at the wrist, which had resulted in the formation of an aneurysm. The patient had been previously treated for a large serpiginous ulcer on the right arm. I saw him again two years later for a syphiUtic cavity in the right lung. Under mercury and iodide of potassium, in large doses for a long period, all symptoms were cured. When he came to me some years later for cerebral troubles, I noticed that he wore a wrist-strap. He informed me that for some weeks past faii'ly firm pressure had been employed for a painful aneurysm of the left radial artery, and that an operation had been decided upon, as no benefit accrued from the compression. I asked to see the aneurysm, which was as large as a small nut, and said that this aneurysm might be the result of syphiUs. I commenced treatment with large doses of mercury and iodides. The aneurysm gradually diminished in size, and three months later had quite dis- appeared. Treatment is very efficacious when commenced early, before the lesions are irremediable. It consists in giving daily an injection of the solution of biniodide of mercury. Iodide of potassium may be given in addition to the mercurial treatment. V. ACUTE AND CHRONIC AORTITIS. ^Etiology. — Both acute and clironic aortitis occur. Primary acute aortitis does not, however, exist. " In the immense majority of cases the lesions of acute aortitis develop in those vessels which have previously been attacked by chronic affections." Accordingly, these different varieties of aortitis should be described in the same chapter. Consequently, all causes which favour the development of atheroma, including old age, gout, and alcohohsm, find their place in the aetiology of aortitis. Syphilis has a pre- eminent place in the pathogenesis of aortitis and aortic aneurysms. Injury, blows, and contusions may be held guilty. Infectious diseases, typhoid fever, rheumatism, tuberculosis, variola, scarlatina, and influenza may the more excite attacks of acute aortitis in proportion as the aorta has already DISEASES OF THE VESSELS 489 been the seat of chronic lesions. It is probable that bacteriological researches will finally discover the pathogenic agents of these acute attacks. Cuzzatini has found the pneumococcus in a case of aortitis set down to cold. Pathological Anatomy. — When aortitis is frankly acute the aorta is dilated, and its inner surface is uneven. The lesion commences in the sub- endothelial coat of the tunica intima (Cornil and Ranvier). The tunica intima shows prominent patches, which vary in size from a pin's head to that of a small coin ; they have been named gelatiniform patches, on account of their transparent and gelatinous appearance. These patches are formed of spherical, nucleated, embryonic cells, and some branched, flattened cells, which normally are found' in the hning membrane. The patches may be a hundred times as thick as the normal membrane, and the inflammatory process, which is more active in the layers bordering on the endothelium when the aortitis is acute, especially affects the deep layer when it is chronic. These patches are sometimes of a dark brownish colour. Small fibrinous clots may be deposited on these patches, and at times become the origin of emboli. The middle coat is but httle altered, while the external coat is thickened and vascular. In some cases acute aortitis is ulcerative, or may even be suppurative. The lesions of acute aortitis may spread around the vessel, and cause pericarditis, pleurisy, lesions of the cardiac plexus, and consecutive angina pectoris, a comphcation which plays a large part in the symptoms of aortitis. Chronic aortitis, Uke chronic - arteritis, which is frequently associated ^vith it, is often called atheroma; but these two words, arteritis and atheroma, have not the same signification, for the word atheroma, which means a " pulp," denotes only one stage of chronic arteritis. Atheroma, " this vital msting " (Peter) and chronic arteritis may produce such changes in the artery that these lesions have been differently called deforming and nodular endarteritis, or arterial atheromasia. The lesions of chronic aortitis are characteristic. The aorta is nodular and dilated ; it is rigid to the touch and hard on section ; on its inner surface we find yellowish, calcareous, atheromatous patches, and dilatations of different shapes. The inflammatory process in chronic aortitis is analo- gous at the onset with that of the acute disease. The lesion begins in the subendothelial layer of the tunica intima, and forms patches which later undergo fatty and calcareous change— that is to say, atheroma. These degenerations, however, are not always the result of an influm- matory process, for cases occur in which fatty degeneration of the arterial walls is the primary lesion in point of time ; this lesion may affect all three coats, and may in its turn produce slow irritation and foci of chronic aortitis, so that these various lesions resemble one another, or are complete in themselves. According to some authors, these atheromatous lesions, 490 TEXT -BOOK OF MEDICINE which are apparently primary, are the result of arterio-sclerosis of the vasa vasorum (Martin). Whatever be their origin, the lesions of chronic aortitis are always accompanied by atheromatous centres and calcareous patches. The gela- tiniform patches of the tunica intima, by their fatty change, finally form an atheromatous centre, composed of fatty detritus, cholesterine, and crystals. The fibrillary groundwork which surrounds these foci takes on a chondroid appearance, and becomes infiltrated with calcareous granules. If the wall of the vessel is intact the focus projects into the artery as an atheromatous pustule, but if the endothelial layer bursts the contents of the focus are carried away by the blood-stream ; the blood enters the focus, and the blood-pressure at this point may cause dilatation and aneurysm. In some cases atheroma prepares the way for spontaneous rupture of the aorta, especially of its intra- pericardial portion. The blood filters between the atheromatous patches, dissects the tunica externa, and rupture occurs into the pericardium, pleura, or cellular tissue. In chronic aortitis the tunica media in turn undergoes change, and disappears in places, as the result of fatty degeneration ; it loses its resistance and elasticity, while the tunica externa often becomes fibrous, so that the whole vessel is invaded ; endarteritis, mesarteritis, and periarteritis are all present (Peter). The aortic orifice and valves often par- ticipate in the process of aortitis. In some cases chronic aortitis is associ- ated with generalized atheromasia. Description. — I shall first deal with acute aortitis, or at least with acute attacks which supervene in the course of a chronic process that is often latent. Acute aortitis behaves differently, according ,to the case ; it may pass unnoticed, just as acute endocarditis may do, or it may be accompanied by a feeHng of weight and oppression in the precordial and epigastric regions, or, lastly, it may give rise to the symptoms of angina pectoris. Pain and dyspnoea are sometimes the chief symptoms. The pain is retrosternal, stabbing, continuous or paroxysmal, and radiates to the arms, neck, back, intercostal spaces, larynx, oesophagus (dysphagia), stomach (gastric crises), or liver (false hepatic coUc). The dyspnoea is also continuous or paroxysmal, but the respiratory rhythm is not increased. During the attacks of pain and dyspnoea we see pulsation of the carotid and subclavian arteries, and the patient is sometimes seized with fits of cougliing, and brings up bloody expectoration. On auscultation, fine rales, indicating congestion and oedema of the lung, are found over a somewhat limited area. These attacks of congestion are not solely hmited to the lungs ; they affect the liver, which becomes enlarged and painful, and also cause intestinal dilatation and ballooning of the belly (Rendu). Sometimes acute infective aortitis results in the formation of a purulent collection, which opens into the vessel, and presents the clinical picture of pyaemic endocarditis. DISEASES OF THE VESSELS 491 Let us now consider chronic aortitis. The signs of chronic aortitis vary with the situation of the lesion ; let us take the most frequent case — namely, that of atheroma of the arch of the aorta. In the normal state the transverse dullness of the aortic and pulmonary trunks together is about 2 inches (Peter) ; in chronic aortitis the dullness may exceed 3 inches, according to the dilatation of the vessel. The aorta by its expansion raises the subclavian arteries, so that we can easily feel them in the supraclavicular hollows. Auscultation may reveal differences of tone or blowing murmurs (Potain). The first aortic sound, which in the normal state depends on the sudden tension of the aorta, may become exaggerated, harsh, and blowing as the result of the atheromatous roughness of the vessel wall. The second sound, which in the normal con- dition depends on the closure of the sigmoid valves, may be echoing and metalhc if the valves have lost their suppleness. A diastolic murmur, due to concomitant aortic insufficiency, may also be heard. The pulse is hard, while the radial artery, which often participates in the atheromasia, is tortuous and indurated. Atheroma of the aorta, hke general atheromasia, is always accompanied by hypertrophy of the heart. The chnical picture varies according as chronic aortitis comprises the whole disease, or as it is associated with a lesion of the aortic orifice, aortic aneurysm, nephritis, more or less extensive atheromasia, or local arterio- sclerosis. In short, chronic aortitis alone may remain silent for a long time, and is usually revealed by attacks of acute aortitis, while several of the symptoms which accompany it are borrowed — viz., hypertrophy of the heart, aortic insufficiency, angina pectoris, Bright's disease, etc. Aortic aneurysm and chronic aortitis present many common signs and symptoms ; among other distinctive signs there is one which has some worth — namely, that chronic aortitis does not form a tumour as aneurysm does, and consequently does not produce symptoms of compression. Blood-letting with leeches or cupping, blisters, the actual cautery, sub- cutaneous injections of morphia and antipyrin, form the general plan of treatment. Iodide of potassium should be administered in large and con- tinuous doses in acute and chronic aortitis. VI. ANEURYSMS OF THE THORACIC AORTA. etiology. — Aneurysm of the aorta is very rare before the age of thirty- five years, and its aetiology is closely related to that of acute and clironio aortitis. In the enumeration of its causes heredity should not be forgotten. Injuries of the thoracic region and heavy manual labour have an influence on aneurysm, but syphihs is tlie chief cause. 492 TEXT-BOOK OF MEDICINE Pathological Anatomy. — Aneurysm of the thoracic aorta affects, in order of frequency, first, the ascending aorta ; second, the convexity of the arch ; third, the descending aorta. The aneurysm varies in size from a small nut to that of the foetal head, and its shape is extremely variable ; it is said to be sacciform when the dilatation is limited to a part of the circumference, hke a sac hanging from the vessel ; it is said to be fusiform when the dilata- tion is equally distributed over the whole circumference of the invaded segment. The small hemispherical aneurysms found chiefly at the origin of the aorta are called cupuliform; the name dissecting is given to the aneurysm which results when the blood infiltrates between the internal and middle coats, and separates them to a certain extent. Two or three aneurysms in the course of the aorta are sometimes found in the same patient. There has been lengthy discussion upon the way in which the sac forms, and, according to the part assigned to the different coats of the vessel, the classification of aneurysms into mixed internal, mixed external, etc., has been proposed, but the question should be simphfied. When an artery is affected by chronic arteritis, the tunica media disappears, and the sac of the aneurysm is formed by the joined internal and external coats ; often, indeed, the walls of the sac are formed by the internal coat alone, which has been modified by the inflammation. " The newly-formed tissue which, wholly or in part, constitutes the sac is made up of flat cells, separated by a fibrillary substance, and undergoes fatty change, atheroma, and petrification ; we may also see old sacs formed of an inextensible calcareous shell " (Cornil and Ranvier). These lesions explain the formation and development of the aneurysm ; the tunica media disappears as the result of endarteritis and periarteritis, and the resistance of the vessel becomes insufficient, so that the artery yields to the blood-pressure, and the vulnerable points permit distension. The distension of the vessel does not necessarily induce thinning of its walls, for the growth of the morbid tissue continues ; at some points, however, thinning may result and favour the rupture of the sac. When the sac is opened, blood-clots and laminated fibrin are found. The clots are soft and recent, the layers of fibrin are elastic and greyish ; the older ones are found nearer the walls of the sac and are resistant, but no trace of organization is seen. Aneurysm of the aorta is not always associated with extensive athero- masia or with arterio- sclerosis ; indeed, atheroma may be only present in the aorta and nowhere else — that is to say, the aorta may be diseased on its own account, independently of any other arterial lesion. The heart, which some authors regard as being always hypertrophied in cases of aortic aneurysm, often preserves its normal size, as I have several times found. DISEASES OF THE VESSELS 493 The neighbouring tissues and organs in contact with the aneurysm undergo important changes ; the bones show excavations : this is not the result of mechanical wear and tear, due, as was first supposed, to the move- ments of the aneurysm, but is the result of an irritative process, or osteitis, which brings about the absorption. In other cases the sac is bound dowai to the neighbouring organs, and spreads the inflammatory process, which leads to softening, ulceration, and perforation of the invaded tissue or organ. The fact is thus explained that the aneurysm may open into the pleura, pericardium, oesophagus, trachea, pulmonary artery, superior vena cava, or right auricle. The communication between the aortic aneurysm and the veins gives rise to an arterio-venous aneurysm. Patients suffering from aneurysm of the aorta are frequently tubercular — e.g., eighteen times in forty-six cases. Various interpretations of this secondary phthisis have been given ; it has been supposed that the disease is brought about by the compression of the pulmonary artery, and it has been compared to the tuberculosis that accompanies constriction of this vessel. In one of my patients suffering from an enormous aneurysm of the aorta, death resulted from left tuberculai broncho-pneumonia, which had developed consecutively to compression of the bronchus and of the left pulmonary artery by the aneurysm. Symptoms. — Aneurysm of the thoracic aorta is sometimes latent, and the person affected may be suddenly carried off without any previous warning. I do not know a more conclusive case than one published by Roux of a young soldier, twenty-two years of age, who died suddenly from an aneurysm which opened into the pericardium. As a rule, events do not take this course, and the aneurysm shows itself by certain symptoms and signs ; their frequency and value I shall now discuss. 1. Pain.— Pain may be the first symptom. Its situation and its nature depend on the nervous network affected by the tumour, so that we see spinal pain and intercostal neuralgia (lesions of the spinal nerves at their point of exit from the vertebral column), pains in the arms or in the hands, and cubital neuralgia (lesions of the brachial plexus), the agonizing pains of angina pectoris (lesions of the cardiac plexus), diaphragmatic pain and phrenic neuralgia (lesions of the phrenic nerve). These pains may be continuous, intermittent, or paroxysmal, and many persons who have aneurysm of the aorta think that they are suffering from simple intercostal neuralgia, or from angina pectoris. 2. Dyspnoea. — The respiratory troubles vary much. One patient may have spasm of the glottis, with attacks of suffocation ; another has paralysis of the posterior crico-arvtonoid muscles, which open the glottis ; while a third suffers from hiccough, accompanied by angina and thoracic 494 TEXT-BOOK OF MEDICINE constriction (phrenic nerve). The dyspnoea is sometimes continuous, or nearly so, being excited and increased by the least efiort ; inspiration is painful, and accompanied by stridor (compression of the trachea or of a large bronchus). Stridor, whether it is complete or incomplete, is a symptom of great value ; when the patient is at rest, the stridor is but Httle marked, and only a slightly prolonged and rough inspiration is audible, but, as the result of effort, true stridor appears. When a large bronchus is compressed, auscultation reveals abolition or diminution of the vesicular murmur in the corresponding lung. Some patients have fits of coughing which resemble whooping-cough. 3. Vocal Troubles. — We find, according to the case, dysphonia or bitonal voice (Jaccoud), hoarseness of the voice, and aphonia. These vocal troubles may be intermittent or continuous, and depend on paralysis of the vocal cords, and especially of the left cord, as may be readily seen with the laryngoscope. 4. Dysphagia. — The trouble may be continuous or intermittent, and depends upon many causes : compression of the oesophagus by the aneurysm, paralysis or excitation of the vagus and the recurrent nerve, which supply the constrictors of the oesophagus and pharynx. Physical Signs. — On examination of the thorax we find dullness which is in direct relation to the size of the tumour, and we may sometimes discover bulging in the aortic region. If the tumour is visible externally, it shows pulsation, so that we might say there are two hearts in the chest (Stokes). The pulsation of the tumour may be single or double ; the first beat is due to the blood-wave which enters the aneurysm; the second beat has been differently interpreted : it may be due to the return of the blood- wave into the sac, or to the reflux of blood from the collateral arteries. Perhaps the two beats only represent the distension of the aneurysmal tumour at two different periods (Franck). The beats which occur later than the cardiac systole are expansile, and are sometimes accompanied by thrill. Auscultation over the sac reveals splashing and blowing sounds, which may be single or double, and audible in the anterior thoracic region, and sometimes in the interscapular region. The first splashing sound is due to the shock of the blood-wave upon the walls of the aneurysm, while the second is due to the closure of the sigmoid valves. The first blowing sound is due to the roughening of the aorta from atheroma, or its compression by the aneurysm ; the second sound {souffle de retour) is due to the return of the blood-wave into the sac, or to the aortic insufficiency wliich sometimes accompanies aneurysm. The radial pulse presents peculiar characters, the fines of ascent and descent being practically of the same length, because the jerky movement of the arterial pulse is converted into an almost continuous movement by DISEASES OF THE VESSELS 495 the presence of an extensible sac in the course of the arterial tree (Marey). If the aneurysm is proximal to the origin of the large arteries, the radial pulse is isochronous on both sides ; if the aneurysm is situated between the left sub- clavian artery and the innominate trunk, the left radial pulse is delayed. This retardation of the pulse depends chiefly upon the extensibility of the walls of the aneurysm ; the blood-wave is weakened and delayed. If, however, the sac of the aneurysm is but httle extensible, and covered with stratified or calcified clots, it loses its extensible properties, and then the conditions change. The signs given by the expansile pulsations in the tumour, the double beats, the splashing and blowing sounds, and the characters of the pulse, all depend on the degree of extensibihty in the walls of the aneurysm. In some cases total suppression of the radial pulse has been noted. It may depend on obHteration of the subclavian artery by clots in the sac, or on a patch of atheroma that has developed at the orifice of the collaterals of the aorta, in which case the pulsation of the subclavian artery can no longer be felt ; the suppression of the radial pulse may also depend on arterial obhteration, caused by an embolus detached from the fibrinous clots in the aneurysm, in which case the symptoms appear suddenly ; it may, lastly, depend upon constriction of the artery from endarteritis obliterans, in which case the symptoms of obHteration are much more gradual. Compression of a venous trunk (vena cava or innominate vein) may cause oedema and collateral venous circulation, as described under Tumour of the Mediastinum. When the circulation in the superior vena cava is inter- rupted, the head, upper limbs, and trunk — that is, the regions drained by the superior caval system — are cyanotic, oedematous, and show a network of dilated veins, while the abdomen and lower limbs are of normal colour. Condition of the Pupil. — The presence of a tumour may cause in- equahty of the pupils, the one being smaller or larger than the other ; if the sympathetic nerve is destroyed by the aneurysm, the pupil on the corre- sponding side is contracted (myosis), because the paralysis of the dilator fibres permits the free action of the constrictor fibres which arise from the common oculo- motor nerve. If the sympathetic nerv6 is irritated but not destroyed by the aneurysm, the pupil on the corresponding side may be dilated (mydriasis) from over- action of the dilator fibres. In any case the light reflex is not abolished. Inequality of the pupils is an important sign of aneurysm, and may help to distinguish aneurysm from aortitis in which a tumour is absent. InequaUty, however, does not always indicate the presence of a tumour ; it may be found, according to Babinski, in syphilitic persons who have neither aneurysm nor mediastinal tumour. They may have mydriasis or myosis, but the important point is that the light reflex is lost (Robertson's 496 TEXT-BOOK OF MEDICINE sign). The inequality of the pupils is due to syphilis of the nervous system; and is associated with lymphocytosis in the cerebro- spinal fluid. Inequality of the pupils in an aortic case may therefore have no direct relation to aortitis or aneurysm, but may be a functional effect of syphilis if the patient has that disease. Babinsld has pubhshed cases in support of his opinion ; Vaquez, Widal, and Lemierre have confirmed his view, and I have seen the following case at the Hotel- Dieu : A man, tliirty-six years of age, who had had a severe attack of angina pectoris, was admitted under my care. He had been picked up moribund and brought to the hospital. Some hours elapsed before he could give us exact information. He gave a clear history of angina pectoris ; for months past he had had similar attacks. His heart was hypertrophied, and a to-and-fro murmur was heard in the second»right space. The attacks of angina pointed to suprasigmoid aortitis. Eight pupil much dilated. If we had been unable to push investigations farther, we might have stopped at aortic enlargement. The hght reflex, however, was also absent. Syphilis of the nervous system was showTi by lymphocytosis of the cerebro-spinal fluid. He had had syphiUs twenty years before. The inequality of the pupils was therefore dependent upon syphilis, and it was possible to exclude a tumour. The autopsy showed the accuracy of this diagnosis : aortitis, no enlargement, no tumour of the aorta ; the lesion in the nervous system was posterior spinal meningitis. Inequality of the pupils in disease of the thoracic aorta may depend on two different causes : it may be due to interference with the sympathetic nerve by an aneurysm, or it may depend on a specific lesion of the nervous system coexisting or not with syphihtic aortitis ; in the latter case we find Argyll-Robertson's sign and lymphocytosis. Inequahty of the pupil in lesions of the aorta does not therefore of necessity imply the existence of an aneurysm. Topographical Diagnosis. — The existence of an aortic aneurysm will be recognized by the signs and symptoms just enumerated. Its exact position must also be diagnosed as accurately as possible, because it appears to me that its gravity depends more upon the situation than upon the size. It is generally beUeved that the largest aneurysms are the most for- midable ; there is some truth in this assertion, but it is far from being the rule. Some aneurysms of small size are more formidable than large aneurysms. An aneurysm which grows towards the exterior may exist for many years, in spite of its great size, before compromising the patient's Hfe, while small aneurysms, in relation with a bronchus or the trachea, may produce rapidly fatal haemorrhage in patients who have been almost ignorant of the lesion. Careful study of symptoms will help us to locahze the exact situation of the aneurysm. Aneurysms which develop in the convex portion of the arch and those of the anterior portion may reach a very large size, without causing ulceration and perforation of the trachea, with which they are in no immediate relation. DISEASES OF THE VESSELS 497 These aneurysms grow forwards and upwards towards the sternum and ribs, which become eroded by rarefying osteitis. They show themselves by dulhiess, blowing murmurs, and expansile pulsation : signs most marked over the tumour ; while their intensity is in relation with the prominence of the aneurysm, and the more or less complete disappearance of the chest-wall. Rupture into the trachea is not to be feared — at least, as long as the tumour does not affect the whole cahbre of the artery, including its posterior wall, and does not cause ulcerative mischief in the direction of the trachea. On the other hand, these mishaps are relatively frequent when the aneurysm is close to the loop of the left recurrent nerve. This variety merits special recognition ; I have called it aneurysm of the recurrent type. In this region the aorta beyond the bifurcation of the pulmonary artery is placed in front and a little to the left of the trachea, and proceeds towards Fig. 20. — Aneurysm of the Aorta, Recurrent Type. A, Section of the aneurysm of the aorta ; b, bronchus; r, recurrent nerve ; ce, oesoph- agus ; t, trachea ; I, larynx ; p, pneumogastric nerve ; c, common carotid artery. the loft bronchus, around which it passes from before backwards, and from right to left. At this point the aorta is in immediate relation with the lower part of the trachea and the origin of the left bronchus ; it is contiguous to the air-passages on its concave side and its anterior segment. Accordingly, from the point of view of prognosis, aneurysms are here formidable, even when they are of small dimensions, because experience proves that opening of the aneurysm into the trachea or into the bronchi, with most terrible liyL'morrhages, occurs most often in this region (Ordonneau). How can the situation of these aneurysms be recognized ? Dysphagia, a3sophagism (spasms of the oesophagus), pharyngism (spasms of the pharynx), and fits of suffocation and of strangulation (spasms of the glottis), vocal troubles (want of synergy of the vocal cords), and attacks of precordial pain, are among the symptoms which help us in the topo- graphical diagnosis of aortic aneurysm of the recurrent type. '62 498 TEXT-BOOK OF MEDICINE These symptoms are nearly all due to the close relation of the loop of the left recurrent nerve, which serves as a guide to the troubles it occasions. The importance of this variety of aneurysm wiU justify tiie following details : The two recurrent or laryngeal nerves which arise from the vagus and from the internal branch of the spinal accessory have different relations. The recurrent nerve on the right side arises at the level of the subclavian artery, which it embraces, forming a curve with its concavity upwards. It has no thoracic portion, and therefore usually escapes in tumours of the mediastinum and in aortic aneurysms. The left re- current nerve, on the contrary, has a thoracic portion, that corresponds to the first two dorsal vertebrae. It arises to the left of the fibrous cord, that represents the obliterated ductus arteriosus, turns round the lower and posterior portion of the arch of the aorta, which it embraces, forming a curve with its concavity upwards, and is therefore exposed to pressure from mediastinal tumours and aortic aneurysms. Fig. 21. — Recuekent Nerves : Posterior View. A, Arch of the aorta ; ce, oesophagus ; c, common carotid artery ; I, larynx ; t, trachea ; h, b, bronchi ; j3, p, pneumogastric nerves ; r, r, recurrent nerves, one of wliich (the left) coasts the arch of the aorta, and ascends along the oesophagus and the trachea towards the larynx ; the other, in a hke manner, coasts the innominate trunk on the right side. The recurrent nerves give off the following branches (Hirschfeld) : 1. Cardiac branches, which arise from the loop of origin of the recurrent nerves, and pass either directly to the cardiac plexus or by their union to the cardiac branches of the great sympathetic and vagus. 2. (Esophageal branches, which arise from the left recurrent nerve, and are dis' tributed to the coats of the upper portion of the oesophagus. The lower portions of this tube receive their nerves directly from the vagus. 3. Pharyngeal branches, to the inferior constrictor of the pharynx. 4. Tracheal branches, which arise in part from the right recurrent nerve. 6. After the recurrent nerves have passed through the inferior constrictor of the pharynx, their terminal branches supply all the muscles of the larynx, except the crico- thyroid muscles, which are innervated by the external laryngeal branch of the superior laryngeal nerve. The recurrent nerves send motor iibres to the laiynx, but furnish mixed fibres to the oesophagus, pharynx, and trachea. These different organs, further, receive a direct and indirect innervation from the spinal accessory and vagus nerves. The indirect DISEASES OF THE VESSELS 499 innervation is supplied through the intermediary tract of the recurrent nerves ; the direct innervation is supplied by branches arising directly from the spinal accessory and vagus. The researches carried out by French physiologists have established the following conclusions (CI. Bernard, Chauveau), as regards the respective part played by the spinal accessory and vagus in the compUcated movements of these organs : The vagus is the motor nerve of the oesophagus, either by its direct branches or by the intermediary of the recurrent nerve. The vagus and spinal accessory in part supply the larynx. The inferior constrictor receives fibres from the vagus through the recurrent nerve, and the upper part of the superior constrictor receives a direct branch from the spinal accessory. Among the muscles of the larynx the larger number, including the constrictors of the glottis and the vocal muscles, properly speaking, are innervated from the spinal accessory through the recurrent nerve. The other muscles arc innervated by the pneumogastric, and include the crico-arytenoid muscles, which make the vocal cords tense, and receive their nerve supply directly from the vagus by the exterior laryngeal nerve ; and the posterior thyro-arytenoid muscles, which dilate the glottis, and are consequently respiratory muscles, suppUed by the vagus tlirough the recurrent nerves. It is now easy to understand the production of the symptoms present in aortic aneurysm of the recurrent type. 1. The attacks of dysphagia and the spasms of the oesophagus and of the pharynx are exjjlained by excitation of the recurrent nerve, some branches of which pass to the upper part of the oesophagus and to the inferior constrictor of the pharynx. They are accorchngly symptoms of excitation, and not of paralysis, for dysphagia due to paralysis of a recurrent nerve would be incomplete, and would produce continuous embarrassment. There would not be paroxysmal attacks of pain, which are proper to muscular spasms. 2. The attacks of suffocation and strangulation, as well as the vocal troubles, are also explained by excitation of the recurrent nerve. For a long while these troubles, due to dyspnoea, were not clearly understood. The authorities, Avho considered them due to lesions of the recurrent nerve, were near the truth, though they were wrong in referring them to paralysis of the nerve and to consequent relaxation of the vocal cords. Krishaber, in 1866, in a paper " On the Occasion for Tracheotomy in Aneurysms of the Aortic Arch," was the first to give the true interpretation of this dyspnoea. This monograph, in which the author shows himself to be equally expert as an experimenter and as a clinician, deserves to be quoted in extenso. The attacks of suffocation that supervene in persons suffering from aneurysm of the aorta, are not due to paralysis of the recurrent nerve, as had been supposed. The nerve, instead of being paralyzed, is stimulated by its close relation to the aneurysmal sac. The muscles of the larynx are in a state of contraction as a result of this stimulus, instead of being relaxed. The glottis is in consequence narrowed spasmodically, and the embarrassment in breatliing is due to this naiTowing. This statement has been confirmed by experiments and Vjy laryngoscopic examination. Section of one recurrent nerve in an adult animal produces relaxation of the corre- sponding vocal cord, with dysphonia, but the respiration is in no way affected. In a similar manner, paralysis of one recurrent nerve in man produces relaxation and immobility of the corresponding vocal cord, but suffocation does not follow. Paralysis of the recurrent nerve is sometimes seen in aortic aneurysm, and Potain has iiublishod a case in which paralysis of the vocal cord, recognized with the laryngoscope, confirmed the diagnosis of an aneurysm of the aorta. When, on the contrary, the recurrent nerves of the animal are stimulated, tlio intrinsic muscles of the larynx enter into action, and as the constrictor muscles act 32—2 500 TEXT-BOOK OF MEDICINE chiefly upon the single dilator muscle, the glottis becomes constricted, and the animal is suffocated. A similar phenomenon occurs in man. How, then, can stimulation of one recurrent nerve affect both vocal cords at once, and produce spasms of the glottis ? How can unilateral excitation produce a bilateral effect ? Paralysis of one recurrent nerve causes paralysis of the corresponding vocal cord. Why, then, does excitation of a single nerve, such as occurs in aortic aneurysm, or in any other mediastinal tumour, produce spasm of both lips of the glottis and attacks of suffocation ? Krishaber has given us an explanation of this interesting fact by studying the role of the arytenoid muscle. This muscle, which is single and inserted on the two edges of the thyroid cartilages, always has the effect of bringing its two insertions together when it contracts. It is the only muscle in the economy which exerts its action simultaneously on both sides of a symmetrical organ. Accordingly, excitation of one of the recurrent nerves deter- mines, on the one hand, constriction of the interhgamentous glottis by the action of the lateral crico-arytenoid muscles and of the thyro-arytenoid muscle on the corre- sponding side, and, on the other hand, the complete occlusion of the respiratory glottis by the bilateral action of the arytenoid muscle. Respiratory and vocal troubles result from this action. These experimental results have been verified with the laryngoscope in a patient during an attack of suffocation caused by an aortic aneurysm. The whole left cord (side on which the recurrent nerve was stimulated) was drawn over to the middle line. The right vocal cord remained in its normal position, as regards its anterior two-thirds, but the space between the arytenoid cartilages — that is to say, the respiratory glottis — was completely closed. Extreme embarrassment of respiration resulted from this spasm of the glottis, and the voice was altered in character. The alteration of the voice was due to the tetanization of one vocal cord, to the forced approximation of the arytenoid cartilages, and to the respiratory distress. In another case the left vocal cord was paretic, while the voice was hoarse and bitonal. During the attacks of suffoca- tion, however, the laryngoscope showed that the two cords were in a condition of spasm, and almost completely obliterated the glottis. The spasm affected both vocal cords, although the left nerve (as was verified at the autopsy) was alone affected by the aneurysm. This research explains the attacks of suffocation, strangulation, dysphonia, aphonia, pharyngism, and oesophagism which often accompany aneurysm of the recurrent type. These symptoms may appear alone, in succession, or in combination. It is difficult to explain why the presence of a tumour in the region of the recurrent nerve produces at one time paralysis and at another time excitation. It would seem, theoretically, that the nerve would be excited at first, while its fibres are still intact, and paralyzed later, when the fibres are in part destroyed by the pressure of the tumour. Nothing of the kind, however, occurs. In some cases the paralytic stage is not preceded by a phase of excitation, and in other cases almost complete destruction of the recurrent nerve has been found post mortem, although the patient has shown no recurrent symp- toms. It is also difficult to say why the symptoms of excitation, suffocation, and strangulation come on in the form of intermittent attacks, wlien the determining cause is in continuous action. Such an occurrence is fairly common in troubles of the nervous system, which frequently assume an intermittent form, although the provoking cause is continuous. However this may be, the symptoms allow the localization of an aneurysm in the neighbourhood of the left recurrent nerve — that is to say, in the region where aneurysm is most grave, because it so often opens into the trachea and the bronchi. The aneurysm may not be as large as an egg or a nut, but it is very serious when situated in this region. DISEASES OF THE VESSELS 501 Termination. — Aortic aneurysm takes several years to develop ; recovery is unfortunately the exception, and death occurs in various ways. In about half the cases death supervenes without rupture of the aneurysm : the patient dies from pneumonia, for suppurative pneumonia is frequent in aortic aneurysm, from pulmonary phthisis ; from asphyxia, consecutive to compression of the trachea and bronchi ; from complications caused by compression of the pulmonary vessels or of the vena cava ; or sometimes from attacks of angina pectoris, as in two cases which I have recently seen. When death results from rupture, the opening involves, in order of frequency, the trachea, the bronchi, the pleura, the pericardium, the lungs, the oesophagus, and, very rarely, the skin.* When an aortic aneurysm opens into the trachea or a bronchus, the result- ing haemoptysis is sometimes so severe and sudden that death occurs in a few minutes. I have seen sudden death on two occasions. In other cases, however, the aortic aneurysm, whatever the point of rupture, may cause a series of small haemorrhages, that lasts for days and weeks before inducing death. In a certain number of cases the patient, for several days and on several occasions, brings up bloody sputum, which is the prelude of fatal haemoptysis. Rupture into the pleura is fairly frequent ; the blood may filter slowly into the pleura producing a pleural haematoma, the origin of which is sometimes misunderstood. Thoracentesis is performed once or twice, and when the patient dies, we are surprised to find post mortem an effusion of blood into the pleura consecutive to the opening of an aortic aneurysm. Rupture into the pericardium is not rare, as Godart has collected forty-seven cases. * The relative frequency of these perforations is as follows (Ball and Charcot, " Dictionnaire des Sciences Medicales," tome v., p. 546) : Right auricle Pericardium Pulmonary artery Pleura -; . , (right Anterior mediastinuiii Left lung Trachea [left Bronchi J right (both Gilsophagus Duodenum Peritoneum SuVjperitoneal tissue Cellular tissue of the anterior thoracic wall Rupture externally . . Death without rupturu 1 8 2 11 8 8 6 3 3 1 3 3 1 2 5 2 4 54 502 TEXT-BOOK OF MEDICINE Rupture of the aneurysm through the skin takes place under different conditions ; the perforation may occur externally, or may be subcutaneous and cause wide effusion of blood. Diagnosis. — Aneurysm of the thoracic aorta and chronic aortitis, with atheroma and general dilatation of the aorta, have many symptoms in common : pain, dyspnoea, attacks of angina pectoris are seen in both cases, as well as rupture of the aorta and consecutive heemorrhage. An aneurysm, however, forms a prominent tumour, which gives rise to distinctive signs ; the tumour alters the character of the radial pulse, gives the sensation of two hearts beating in the chest, and determines compression of the trachea with stridor ; compression of the veins with oedema and varicose dilatations ; and compression of the recurrent nerve with the symptoms already described. Tumours of the mediastinum also cause pressure symptoms, but they do not present a double impulse beat, the murmurs of aneurysm, or the inequality and want of synchronism in the two pulses. It is also necessary to make the diagnosis from arterio-venous aneurysm, for the aorta may communicate with the superior vena cava, the auricles, the pulmonary artery, and the right ventricle ; but diagnosis is sometimes very difficult, for the symptoms are, as a rule, simply an exaggeration of those already produced by compression of a venous trunk — i.e., oedema, cyanosis, collateral circulation, and tendency to coma. On auscultation a continuous blowing murmur, with systohc reduplication, may be heard. Lastly, the diagnosis between aneurysm of the aorta and that of the innominate artery must be made. In the latter case the distinctive signs are as follows : Prominence of the right clavicle ; bulgi'ng and dullness in the right clavicular region ; pulsation and murmurs in this region ; compression of the veins on the right side, with stasis in the right jugular vein, cervical and tracheal pains, which are more marked on the right side. Treatment. — The treatment of aneurysm of the aorta is general and local. Local treatment of the sac by electro-puncture has given good results, and this means, which is still on trial, has appeared to be of some efficacy. A definite opinion as to injections of gelatine caimot yet be given (Lancereaux). Mercurial treatment will be considered under Syphihtic Aneurysms. VII. SYPHILIS OF THE AORTA— SYPHILITIC AORTIC ANEURYSMS. At the Hotel-Dieu* I have devoted three lectures to this important question ; they will serve as my material for this section. Discussion. — Syphihtic infection may cause numerous lesions, including subacute and chronic aortitis, atheromatous and gummatous degeneration, * " Syphilis de I'Aorte," Clinique Medicale de V Hotel-Dieu, 4"^^ 5^% et 6™^ le§ons, 1897. DISEASES OF THE VESSELS 503 lesions of the aortic orifice and sigmoid valves, large aneurysms, sacciform aneurysm of the recurrent t}^e, small aneurysms which may be multiple and cupuhform, coronaritis obhterans, and coronaritis with miliary aneurysms. Aortic syphihs does not always show itself by diffuse lesions ; in many cases the lesions are locahzed to a segment of the vessel, forming a kind of segmentary aortitis, which is somewhat analogous to syphihtic segmentary arteritis. Distinct cUnical types result, and show a special group of signs and symptoms. It is therefore not enough to describe as a whole the syphi- htic changes in the thoracic aorta ; it is necessary, as far as possible, to divide them into certain forms, and I shall make an effort to do so in this section. It must, however, be understood that the aortic lesions which we are about to study, are syphihtic in nature, and no doubts must be left in the mind as to this fact. The recognition of syphihtic arteriopathies is of recent date. Not long ago savants doubted the action of syphihs upon the arteries, and authorities are still found whose opinions differ from those which I shall now state as to the action of syphihs on the aorta. That syphihs may attack the arteries, just as many infectious diseases do, need cause no surprise, and it is clear that syphihtic arteritis must enter into the hst of infectious diseases of the arteries. The proof is, however, wanting, both as regards the pathogenic agent of syphihs, which we do not know,* and also as regards the character of the arterial lesions which often have no special nature ; but, on the other hand, we find conclusive proofs and arguments in the efl&cacy of specific treatment, and also in other considerations. When a patient suffering from tertiary lesions is at the same time affected by syphihtic arteritis, whether it be obUterating or dilating, in parts which are accessible to the sight (hmbs and face), and when under specific treatment he recovers from the tertiary lesions and from the arteritis, it is evident that the arteritis in question was of a syphihtic nature. When an individual who is still young, and has no other cause for arteritis or for atheroma, contracts syphihs, and in the early months of his infection is affected by cerebral arteritis, which sometimes results in obliteration of the artery, with all its consequences, or at other times in aneurysm, with rupture (see section on Cerebral SyphiUs), a direct relation between the syphilis and the lesion of the artery cannot be denied. Now, syphihs, which has a marked predilection for the cerebral arteries, and also injures the peripheral arteries — i.e., the temporal, radial, pophteal, femoral, or in- nominate trunks — has no reason for sparing the aorta, and, in fact, it does not do so. When aortitis, with aneurysm, occurs in a young man about six years after syphihtic infection, and no other causes capable of explaining the aortitis can be found, it is rational to consider the lesion of the aorta as due to syphihs (case of Kalindero and Babes). When an individual is seized four, six, or ten years after infection with agonizing pains, due to aortitis, which is cured by specific treatment, it is natural to consider both the angina pectoris and the lesion of tlio aorta as due to syphilis (cases of Hallopeau, * Cf. p. 477, where mention is made of the spirochaeta. — ^Tkans. 504 TEXT-BOOK OF MEDICINE Rumpf, Vicenzo Vitone, and. personal case). When obliterating arteritis of the Syhian artery occurs in a syphilitic patient, and yields to specific treatment, it is rational to attribute this cerebral arteritis to syphihs, and if this individual some years later suffers from aortitis with aneurysm, it is also natural to attribute the aortic lesion to syphilis (personal case). When aortitis, with its train of symptoms, appears in an individual suffering from pustulo-crustaceous syphilides, it is very difficult not to doubt that there are two tertiary manifestations, which occur simultaneously or in succession, affecting the skin on the one hand and the aorta on the other (personal cases). When syphilitic perforation of the roof of the j^alate is seen in a woman suffering from aortic aneurysm, it is only right to admit that in such a patient the tertiary manifestations of syphilis have attacked successively the aorta and the roof of the palate (Jaccoud's case). When aneurysm of the aorta supervenes in a syphilitic patient who has lesions of the parietal bone, liver, and testis, it may be affirmed that the aortic lesion is also of syphilitic origin (Buehle's case). These arguments appear to me to be decisive. The aorta is not immune to syphihs. It may be added that these effects are generally tardy. In this respect there is some difference between syphihs of the cerebral arteries and syjjhilis of the aorta. In short, while syphihs may affect the arteries of the brain at a very early stage — even five or six weeks after infection — I do not think that such an early onset has ever been seen as regards the aorta, ^\^len I recall, one by one, my cases of syiihilitic lesions of the aorta, I find that these lesions have appeared only at a very advanced stage. In three of my patients at the Hotel-Dieu, syphilis of the aorta supervened from fourteen to twenty years after the chancre ; in two of my patients at the Necker Hospital, the aorta was infected only at an advanced period ; in one patient at the Saint-Antoine Hospital the first signs of aortic aneurysm appeared eighteen years after infection ; in one of Duguet's patients the aortic lesions supervened twenty years after infection. Mauriac considers that aortic lesions appear, as a rule, about twelve years after the chancre, and I place among the earliest the case of KaUndero, in which syphiUtic aneurysm of the aorta came on seven years after, and the cases of Rumpf and Vicenzo Vitone, in which syphilitic aortitis supervened four years and six years after infection. These facts are of importance, and serve to emphasize the fact that, if cerebral arteritis is to be feared during the first year of infect^on, there is no fear of aortitis for many years. Division. — We are now clear as to the existence and the time of appear- ance of syphilitic lesions of the aorta ; let us discuss in detail each of these lesions and their localizations. From the pathological point of view they differ but little from the lesions of common aortitis : atheroma is found in its different forms and stages ; the same deformities of the vessels and the same tendency to dilatation and to aneurysm are seen. There is notliing, either in the anatomical or in the histological picture, that can serve to difEer- entiate the lesions of chronic syphihtic aortitis from those of aortitis due to other causes. An interesting point, however, is that the aorta is sometimes the seat of true gummata, which may give rise to small cupulif orm aneurysms, regarded by some authors as characteristic of syphihs. These various lesions, including thickening, induration, atheroma, gum- mata, dilatation, aneurysms, etc., are sometimes diffuse and indefinitely dis- tributed over the thoracic aorta ; at other times they are localized to a clearly defined region, and present the following anatomical and clinical types : DISEASES OF THE VESSELS 505 1. Suprasigmoid syphilitic aortitis. 2. Sypliilis of the aortic orifice with incompetence. 3. Large aneurysms of the aorta. 4. Aneurysm of the recurrent type. 5. Small multiple cupuhform aneurysms. 6. Obhterating coronaritis and miliary aneurysms of the coronary arteries. This classification is far from being final, and does not include diffuse aortitis of the thoracic trunk, but it is perfectly applicable to a fairly large number of cases in which the aortitis is locahzed to a circumscribed region of the aorta. 1. Suprasigmoid Syphilitic Aortitis. In this type the lesion is confined to the first portion of the ascending aorta, thus forming a kind of segmentary aortitis, that may be called supra- sigmoid. In this form we find pain and angina (angor pectoris). • The pain, which may be slight or violent, transient, continuous or paroxysmal and acute, with suffocation and a sense of constriction in the chest, radiates hke the pain of angina pectoris, and has its maximum in the sternal or in the pre- cordial region, which is painful on pressure. In a patient with these symptoms the attention is at once called to the aorta. On percussion, no enlargement of the vessel can be made out ; on auscultation, no murmur is heard. Under such circumstances, and in tlie absence of any appreciable lesion, every possible supposition is considered, including neuralgia of the cardiac plexus, smoker's heart, hysteria, cardialgia of tabes — in short, all the causes that are capable of producing cardiac neuralgia ; while sufficient consideration is not paid to syphilis, because it may date back ten, twelve, or fifteen years, and, it may be added, because this suprasigmoid aortitis has not yet been sufficiently recognized. For my part, I consider it one of the most frequent manifestations of aortic syphilis. The situation and nature of the pains which it excites are sufficient to attract attention and lead to the diagnosis. These pains should cause no surprise, and no elaborate theories are necessary to explain them. Let us not forget that syphiUtic arteritis is sometimes extremely painful. One of Leudet's patients had very severe pain in the temporal arteries, which were affected by syphilitic arteritis ; one of my patients suffered much pain in the radial artery, which was the seat of a syphilitic aneurysm ; persons suffering from syphiUs of the cerebral arteries (basilar and Sylvian arteries) have at times fearful headache due to the arteritis. The same remark appUes to syphiUtic aortitis. Why should it not be extremely painful when the aorta adjoins the nerves of the cardiac 506 TEXT-BOOK OF MEDICINE plexus, whicli is always ready to produce the syndrome of angina pectoris ? Tlie agonizing sternal or retrosternal pain wliich radiates to the neck and left arm may be the result of syphilitic aortitis, especially when the supra- sigmoid segment is affected. The following cases prove the truth of this view : About fifteen years ago Potain and myself saw a woman, still young, with angina pectoris. The pains had been coming on for some weeks past, and had finally become very severe. They were continuous, yet broken by agonizing paroxysms, Uke those of angina pectoris. The aortic orifice was healthy ; the aorta showed no dilata- tion. She was too young for atheroma ; tobacco, hysteria, and tabes, were out of the question. Treatment proved unsuccessful, though an ice-bag gave some rehef. A tertiary ulcer appeared on the right thigh. Specific treatment was at once employed ; the ulcer was soon cured, and the pains of angina pectoris completely disappeared. I ask, WTiat could this case be, except an attack of syphilitic aortitis which had left the aortic orifice intact ? Some years ago, with Duplay and Ramond, I saw a gentleman suffering from serpiginous ulceration, which had destroyed part of the right thigh. He was finally cured. Five years later, very sharp j^ain in the cardio-aortic region. Auscultation revealed no lesion o£ the aortic orifice. I thought of suprasigmoid aortitis. Remember- ing the serpiginous ulceration, I prescribed specific treatment, which he did not take. Some months later Ramond was called out to see him. He was suffering from most terrible precordial pain, and died in a few hours. Hallopeau has published a very interesting memoir on this subject, in which he describes syphilitic angina pectoris : A man of thirty-six years of age, ten years before had had benign syphiUs, which was properly treated. He was taken ill one night with acute precordial pain, radiating to the left shoulder. During the next few days the pain recurred several times in the twenty-four hours, and radiated as far as the left elbow and the end of the last three fingers. The symptoms of angina pectoris disappeared completely under treatment with mercury and iodide. In the monograph to which I have just alluded, Hallopeau has collected the three following cases : The first, reported by Rumpf, concerns a man, twenty-nine years of age, who, six years before, had had chancre, followed by secondary symptoms, when he felt violent pain in the precordial region, radiating into the back and the left arm. The pain came back in the form of attacks, and was accompanied by a feehng of thoracic constriction and palpitations. The attacks at first were some days apart ; later they occurred daily. Auscultation revealed no abnormal sign at the aortic orifice, proving that the supra- sigmoid aortitis had not encroached upon it. The age of the patient excluded atheroma, and syphilis could alone be held guilty. Treatment confirmed the diagnosis, and recovery finally occurred. The other two cases are given by Vicenzo Vitone. One of his patients, thirty-four years of age, was, four years after infection, taken ill with headache and vertigo, and later with crises of angina, suffocation, and precordial pain, which radiated to the left arm. These attacks occurred several times a day. On auscultation no lesion of the aortic orifice was found, doubtless because the aortitis was confined to the suprasigmoid segment. The condition was due to syphilis, because subcutaneous injections of mer- cury arrested the attacks. DISEASES OF THE VESSELS 507 The other patient suffered from attacks of angina pectoris, which recurred several times a day, although on auscultation it was impossible to discover the slightest lesion ol the aorta or of the heart. In this case too the angina pectoris, which certainly depended on suprasigmoid aortitis, was cured by subcutaneous injections of calomel. These cases prove that syphiUtic aortitis may be extremely painful, and, just as arteritis in cerebral syphilis shows its presence by headache, so aortitis shows its presence by the symptoms of angina pectoris, from the most mild to the most severe forms. As long as the lesion remains hmited to the suprasigmoid segment of the aorta, the valves are not invaded, and the orifice remains healthy ; the symptoms of angina pectoris are the only evidence of the lesion, but they are quite sufficient to indicate the diagnosis. I cannot lay too great stress on suprasigmoid aortitis, which is a favourite locahzation of sypliihs of the aorta. In a patient suffering from angina pectoris without atheroma, lesions of the aortic orifice, or dilatation of the aorta, we are too often incUned to diagnose neuralgia due to tobacco, hysteria, or arthritis, and to mistake the true nature of the disease ; we accuse the patient of smoking or of drinking too much, cut off his tobacco, tea, and alcohol, and then consider our treatment sufficient. We are wrong. We are not sufficiently familiar with the idea that aortitis may arise ten, twelve, or fifteen years after infection, at a time when the patient himself no longer thinks of it, and we do not remember that aortitis, when it is confined to the suprasigmoid segment, may excite no other symptoms than those of angina pectoris. It is the more important not to make a mistake, because syphilitic aortitis, when taken in time, is curable ; if it is left to itself, it may lead to invasion of the sigmoid valves and coronary arteries, dilatation of the aorta, formation of cupuliform aneurysms, or rupture of the vessel. 2. Syphilis of the Aortic Orifice — Aortic Incompetence due to Syphilis. After having described suprasigmoid aortitis, let us consider the changes caused by its extension to the aortic orifice and the sigmoid valves. To give an idea of this process I have only to sketch the history of one of my patients at the Hotel-Dieu : A strong policeman, who was forty-five years of age, had for some time experienced such acute cardiac pain that he was unable to work. He could not wear his tunic buttoned, because the least pressure over the sternum was unbearable. Moreover, crises of angina pectoris, with all their train of symptoms, appeared on the least move- ment, sometimes even without any apparent cause. For some time life had been intolerable. He could not clean his room, and could only walk very slowly from one tree to another, as policemen are wont to do on their beat, without being seized with angina and suffocation, which pulled him up short. Percussion of the sterno-costal region caused fairly sharp pain. Auscultation showed that the angina pectoris was associated witii aortitis and aortic incompetence. Having made the first step in the diagnosis, it was necessary to find the cause of 508 TEXT-BOOK OF MEDICINE the aortic lesion and of the angina. He was not suffering from arterio -sclerosis, in the true sense of the word, and had no renal disease, for he had no albuminuria and no symijtoms of Bright's disease. He was an aortic case, with incompetence of the orifice and hypertroi)hy of the heart. The aortic incompetence was consecutive to a lesion of the aorta, and not to one of the heart. The sigmoid valves had been invaded from the side of the endarterium, and not of the endocardium. This distinction was established by the fact that aortic insufficiency, consecutive to lesions of the endocardium, and most commonly seen in rheumatic cases, is rarely painful, and may pursue its course for a long while without causing symptoms of angina pectoris. On the other hand, aortic insufficiency consecutive to lesions of the aorta is preceded or accompanied by symptoms of angina. It was not sufficient, however, to diagnose aortitis and aortic insufficiency ; it was also necessary to know what was the cause of these lesions. He was free from any infectious disease which might cause aortitis, but seventeen years before he had had a chancre, followed by enlargement of the inguinal glands, mucous patches in the mouth, etc. I was justified, therefore, in making a diagnosis of syphilitic aortitis with valvular incompetence. The treatment confirmed the diagnosis. I gave fifteen injections (oily solution of biniodide of mercury), and later a fresh series of twelve injections. The improvement was so marked that six weeks after admission he returned to duty. He came back every year for treatment with mercury, and the acute symj)- toms never reappeared. This case is a typical one of aortic insufficiency, associated with syphilitic aortitis. The lesion of the orifice was not improved by the treatment; the diastolic murmur did not diminish, because the lesion of the orifice was irremediable ; but, at any rate, the treatment was very effective, as regards the symptoms of pain and dyspna?a, so that we may hope that the lesion will not be fatally progressive, and that it may be arrested. For seven years I heard nothing of him, but in September, 1905, he came to the Hotel-Dieu, when I inquired as to his health. " Sir," said he, " for seven years I have had no jsain. I do my own work, and also do day-work for others. My health is gi-and, and there is not a better worker for miles round. I dig all day, and in summer I do harvesting from four in the morning till eight at night." Such was his statement. Seven years ago he had been under treatment for such severe angina that death appeared imminent. Fortunately, the angina was due to syphihs, and injections of biniodide of mercury worked a wonderful cure. The valvular lesion will always remain as marked as it was seven years ago, but we may say that it has become harmless. He has gone back to Ardeche to work. Perhaps I shall find him still in good health in yea.rs to come. 3. Syphilitic Aneurysms of the Aorta. My opinion is that aneurysms of the aorta are in most cases of syphiUtic origin. I recognize more than ever that syphihs has a marked predilection for the aorta. Too much importance cannot be given to early diagnosis. All treatment depends upon it. Syphihtic aortitis may result in dilatation of the vessel and in aneurysms of every size. They may assume considerable proportions, as in a man suffering from aneurysm of the arch. The first warnings were of two years' duration. He felt acute pain in the left cervical region and the left arm, without any symptom of angina pectoris. He had DISEASES OF THE VESSELS 509 so little distr&ss that he could, without the least breathlessness, ascend several stories, while carrying heavy weights. The pains which he experienced were not like those seen in cases of aortitis of the preceding type. It must be added that the localization of the lesion was quite different ; and while, in the other patients, the suprasigmoid aortitis reacted on the branches of the cardiac plexus in the form of angina pectoris, here the aneurysm of the terminal portion of the arch left the cardiac plexus intact, but affected the branches of the brachial plexus. \Mien this cer\'ico- brachial neuralgia appeared, he consulted Fournier, who diagnosed syphilitic aneurysm of the aorta. He had had a chancre, followed by secondary symptoms. In 1884 he was treated for syphilitic endarteritis obliterans of the left Sylvian artery at the Saint-Antoine Hospital. At this time, after violent headache, right hemiplegia with aphasia, appeared. I saw the patient some days later, and at once prescribed mercurial inunctions and iodide of potassium. The aphasia and hemiplegia tinally ended in complete recovery. Ten years later he suffered from aortitis of the same nature, which ended in aneurysm. These details were known to Fournier, who at once recognized the mark of syphilis, which, ten years apart, affected the Sylvian artery and the aorta. The proof that the aortitis was really syphihtic is that mercury and iodide of potassium, prescribed by Fournier, cured the cervico-brachial neuralgia, which no other treatment had been able to assuage. The aneurysm underwent no change, for it was the result of two lesions which do not retrocede, but the extreme pain caused by the aneurysm yielded to the specific treatment. He came to see me for the neuralgia, which had again become intolerable. Under the influence of specific remedies the pains and insomnia disappeared. A patient, thirty-six years of age, was admitted into the Saint-Antoine Hospital for an enormous syphiUtic aneurysm of the aorta. At the age of fifteen he had con- tracted syphilis, which was followed later by tertiary ulcerations, Avith indelible scars and painful exostoses. Sixteen years after the chancre, paias appeared in the right shoulder, and were more intense at night. Later they spread over the whole arm and right side of the chest. Six months later, oedema of the chest-wall on the right side and venous dilatation. Millard, finding pulsation to the right of the sternum, diagnosed a syphilitic aneurysm of the aorta, and prescribed Gibert's syrup, A^ith iodide of potassium. The redema and the collateral circulation disappeared, but the severe pains soon returned, and the patient was taken into my ward. At the right of the sternum, in place of the upper ribs, wliich had disappeared, I found a large aneurysm. The pains in the arm and shoulder were so sharp that the patient could get no rest. It was clear that he had suffered from a series of syphilitic troubles, ending in aneurysm of the aorta. I ordered mercurial inunction and iodide of potassium. The pains diminished, the nights became better, but no evident change in the aneurysm could be seen. He died sud- denly from fulminating haemoptysis. The autopsy revealed enormous dilatation of the ascending aorta and of the arcli, the walls of which were thickened. The sac was studded with small secondary aneurysms ; some were hollowed out like a cup, while others projected in the form of nodes, due to the stratified layers of fil)rin which filled the cup and were raised above the wall of the artery. Indeed, the sac contained a crop of small aneurysms, due to circumscribed gummata, as has been described by LetuUe, Kalindero, and Babes. These tumours may occur at any point of the thoracic aorta. The lesions found post mortem show sliglit difTerciices. In some cases the process is disseminated over the aorta, whicli is dilated, thickened, and studded with atheromatous patches at different spots ; in other cases the aortitis is limited to a segment upon which the aneurysm develops later, and the vessel is almost normal in the rest of its extent. 510 TEXT-BOOK OP MEDICINE 4. Aneurysm of the Aorta of the Recurrent Type. Let us noAv consider the lesion which I have named aneurysm of the recurrent type. I have employed this name because the aneurysm develops in the region of the aorta contiguous to the loop of the left recurrent nerve, and because its most prominent symptoms depend upon the close relation of this nerve. The anatomical, clinical, and experimental details of this variety of aortic aneurysm have been described in the preceding chapter, to which I refer the reader. Dysphagia, attacks of pharyngism, oesophagism, suffocation and strangu- lation, and vocal troubles, locahze the aneurysm in the neighbourhood of the recurrent nerve. This situation is especially serious, because rupture into Fig. 22. — Aneueysm of Rectjreent Type. i. Larynx ; p, p', vagus nerve ; A, aorta ; r, r', recurrent nerves. the trachea and bronchi most frequently occurs here. The aneurysm may not be larger than a nut, but it is very serious when situated in this region, as the following cases prove. The first of these cases is taken from Ordonneau's thesis. A man, fifty-eight years of age, came into the H6tel-Dieu at Nantes for violent pain in the neck and upper part of the chest. His respiration was embarrassed, and inspiration was characteristic of spasm of the glottis. The voice was hoarse ; swallow- ing was painful. As he felt better, he left the hospital, but returned soon after in a much worse state. He was cyanosed, the aphonia was complete, the dysphagia was more severe, and the attacks of oppression were terrible. As he was syphihtic, we thought of laryngeal syphihs, with consecutive oedema. Tracheotomy was performed. He succumbed during the night. At the autopsy the larynx was found free from disease. At the lower part of DISEASES OF THE VESSELS 511 the trachea, on its left side, there was an aneurysm of the arch of the aorta, no larger than a nut. The aneurysm was adherent to the trachea, and was skirted laterally by the left recvirrent nerve. The portion of the trachea which was not in contact with the aneurysm showed on its inner surface an ulcer a few milhmetres in diameter. At this point the aneurysmal sac was partly formed by the trachea, and was so thin that it would certainly have opened into the air-passage in a short time. This case is an exact reproduction of the statements made above. The syphiUtic aneurysm was of small dimension, and did not compress the trachea or the cesophagus. The dyspncea and dysphagia, therefore, were not produced by pressure on these tubes. Its existence was revealed by aphonia, dysphagia, spasms of the glottis, and asphyxia, due to the close relation of the recurrent nerve. Even if the patient had survived these complications, he was threatened by fatal haemorrhage, for the aneurysm was on the point of bursting into the trachea. Savard has published a similar case : A soldier, forty-four years of age, who had contracted syphihs, was many years after taken ill with vocal troubles and dyspnoea. Later the aphonia became complete, and the difficulty in breathing was compUcated by terrible attacks of suffocation and 8ucking-in. As auscultation of the chest, the heart, and the aorta, gave negative results, the possibihty of syphihs affecting the bronchial glands was thought of, and iodide of potassium prescribed. The situation, however, continued to grow serious, and on the second day after admission he died from haemoptysis in less than a minute. The autopsy revealed an aneurysm of the size of a nut, forming a diverticulum, attached to the aorta. The aneurysm, which was adherent to the left bronchus and to the trachea, compressed the left recurrent nerve. After the trachea and bronchi had been opened, Savard found at the origin of the left bronchus a perforation, establishing com- munication between the bronchus and the aneuiysm. The haemoptysis had taken place through this oi^ening. This case> which is absolutely typical, proves the gravity of aneurysms, even of small size, when they are near the loop of the recurrent nerve. It further proves that these aneurysms may reveal themselves by none of the usual signs, and may only betray their presence by the signs special to aneurysms of the recurrent type. When the aneurysm develops in this region, it almost completely escapes our methods of investigation, especially if it is of small size ; it causes no expansile pulsation, no double impulse, no dullness, and no murmurs ; its presence is not always shown by pain. In some cases nothing can be seen, heard, or felt, but yet we can arrive at the diagnosis of the aneurysm by the symptoms I have indicated. Kalindero and Babes have well brought out the role of gummatous aortitis and circumscribed gumma in the pathogenesis of syphihtic aneurysm of the aorta. Among their cases there is one wliich absolutely conforms to the recurrent type. A physician, twenty-nine years of age, had contracted sypliilis seven years previously. Treatment had for a long time kept him free from any manifestations of sypliiUs, when, six years after the infection, he was taken ill with dyspliouia, cough, ami severe dyspnrpa. Tlio physicians at Bucharest, after laryngoscopic examination, wore of opinion tliat tlic tradu-a and recurrent nerve were being compressed l)y asiiuill aneurysm or by enlarged glands, lu a few months the laryngeal symptoms disappeared, the 512 TEXT-BOOK OF MEDICINE attacks of suffocation were averted, he resumed his work, and his liealth appeared perfect. One day, without any warning, he died from fulminating haemoptysis in a few minutes. Before his death, however, he had still the time and the astonishing presence of mind to -svrite a few lines to Babes, begging him to make a post mortem and preserve the specimen. The autopsy demonstrated the existence of patches of syphiUtic aortitis and of a sacciform aneurysm as large as a nut, which had developed in the concavity of the arch of the aorta. The aneurysm rested on the left bronchus, and pushed the lower end of the trachea sUghtly to the right side. The aneurysm had opened into the left bronchus by a perforation 5 milhmetres in diameter. It is easy to reconstruct the different stages in this case. We have a young man who contracts syphihs. Seven years later syphilitic aortitis supervenes, and is chiefly locahzed to the aortic segment which is in relation with the loop of the left recurrent nerve. At this point an aneurysm of small size develops, and shows its presence by symptoms due to the proximity of the recurrent nerve — Aaz., dyspnoea, spasm of the glottis, and vocal trouble. After this warning everything becomes normal, but the aneurysm pursues its insidious course, without pain, pulsation, or any visible signs. One day rupture occurs, and is accompanied by fulminating hsemoptysis. I have seen a similar case, which shows how aneurysm of the recurrent type behaves. I saw, with Dr. Woelcker, a gentleman, fifty years of age, who for some months had experienced suffocation, with vocal troubles and difficulty in swallowing. Swallowing was painful and almost impossible during the attacks, while the aphonia was complete, and the suffocation so marked that the patient repeatedly thought that he was dying. Between the attacks the voice remained hoarse, deglutition was difficult, and the breathing was far from being normal. Examination of the cardio-aortic region yielded negative results. As the patient was syphilitic, I thought of some mecUastinal lesion, and aneurysm of the recurrent type came into my mind. I told his family of the possibility of fulminating haemoptysis. In order to gain further informatioD, however, I asked for a laryngoscopic examination by Dr. Bonnier. When Woelcker and Bonnier arrived at the house to examine the patient, the servants told them that he had just died of fulminating haemoptysis. This catastrophe verified the diagnosis, and I have not the shghtest doubt that this patient, hke those of KaUndero and Savard, died from rupture of the aneurysm into the left bronchus or the trachea. Such cases prove that aneurysm of the recurrent type has its special symptoms : dysphonia, aphonia, and attacks of sufEocation, of strangulation, of pharyngism, or of oesophagism, with or without precordial pain, are therefore found more or less in every case. These symptoms may occur in succession or in combination. They appear in the form of attacks, and though they may last only a short while as a kind of warning (Kahndero's case), they are none the less of the highest importance. They allow us to locaUze the aortic aneurysm in the neighbourhood of the recurrent nerve — that is to say, in a region which is especially serious, and in wliich opening of the aneurysm into the trachea or into the bronchi most usually occurs. It would therefore be wrong to consider that the largest aneurysms are the most formidable. An aneurysm which develops towards the exterior, and sometimes reaches considerable size, as in the case described above, may last DISEASES OF THE VESSELS 513 for several years, in spite of its size, before compromising the patient's life ; while small aneurysms which are in relation with the bronchus or with the trachea may cause fulminating haemoptysis in persons who scarcely suspect the existence of an aortic lesion. By careful study of the symptoms, which I have tried to put clearly, and by laryngoscopic examination, we can as accu- rately as possible define the topography of aortic aneurysm of the recurrent type. 5. Cupuliform Aneurysms— ^Gummata of the Aorta. Let us now consider syphilitic aortitis with circumscribed gummata, which result in multiple cupuliform aneurysms, varying in size from a pea to a nut. Several of these small aneurysms may be counted at intervals in the course of the thoracic aorta ; we might, indeed, speak of an eruption of small aneurysms. These aneurysms sometimes develop upon an aorta which is neither deformed nor dilated ; at other times they are set on the waUs of a large aneurysmal dilatation. According to several authors, these small aneurysms are absolutely special to syphilis. The subjoined cases will give an exact idea of this variety. On November 9, 1892, a man, forty-three years of age, was admitted for precordial pains, with angina and suffocation, which used to come on suddenly after a walk, or after some rather sudden movement, or, indeed, -vnthout apparent cause. On several occasions the crisis had been so violent that the patient thought he was dying. The l)ain started in the i)recordial region, and. radiated into the left arm and hand. The duration was variable. The first crisis 'had been short, but the later ones came on in rapid succession, and then lasted several hours, practically without any respite. The I)atient did not dare to walk or to go upstairs : he dreaded lying do\\Ti, because he was afraid of a reappearance of the crisis. He evidently had angina pectoris, and it behoved us to search for the cause. When he uncovered for examination, we noticed above the left clavicle a large and absolutely characteristic pustolo-crustaceous syphihde, and learnt that he had been syphilitic for ten years. Percussion and auscultation of the cardio-aortic region gave negative results. The aorta was not increased in size, and the aortic orifice was absolutely healthy. The patient had neither lead-poisoning, gout, diabetes, tabes, nor hysteria, and was not a smoker. As tertiary syphilis was in full activity, it was permissible to diagnose syphiUtic aortitis. On the evening of admission he refused to he down, so much did ho dread a crisis. He was seized with a terrible attack of angina pectoris. He was undressed and put to bed, but he had scarcely lain down, when he jumped up in agony, said that he was dying, and passed away in a few moments. At the autopsy my first care was to examine the aorta. It was not dilated, but on the surface we saw four small aneurysms, at intervals, from below upwards. The first aneurysm was of the size of a large pea, and situated at the level of the right auricle. The second aneurysm, of the same size, was 4 centimetres above the })receding one, in front and to the right of the aorta. The third aneurysm, of the size of an almond, formed a prominence, aljout a centimetre higher up, at the junction of the ascending and horizontal portions of the aorta. A fourth aneurysm, of the size of a cherry, wiis situated on the anterior part of the aorta, at the origin of tlio innominate trunk. The aorta was opened, and the integrity of the aortic orifice and sigmoid valves was proved. The vessel was thickcuod 33 514 TEXT-BOOK OF MEDICINE and studded with patches of gummatous and atheromatous aortitis. The first and third of these aneurysms were excavated in the form of a thin transparent cup, which would soon have ruptured. The second and fourth aneurysms formed a hard prominent projection, composed of fibrinous clots, adherent to the wall. On histological examina- tion of the thirmest portion of the aneurysm, the tunica media had almost disappeared. The coronary arteries were incised and carefully examined. Their walls showed arteritis at different points, but their orifice was absolutely free, and the lumen was not ob- literated. He had been attacked by acute syphiUtic aortitis, which had rapidly caused multiple aneurj^sms. The aortic orifice and the sigmoid valves had been spared, and death had supervened in an attack of angina pectoris, consecutive to aortitis. Let us remark, in passing, that death was not attributable to cardiac ischemia, consecutive to obhtera- tion of the coronary arteries, for the heart was not ischemic, and the coronary arteries were permeable at every point. A man, fifty-eight years of age, was admitted for agonizing dyspnoea, which had begun about two years previously, and had soon been followed by precordial pain, radiating into the left arm. Although the pain and the dyspnoea were present together, the latter was the chief trouble. On auscultation of the heart, I found a diastohc murmur of aortic insufficiency, and a systolic one of mitral insufficiency. I therefore made the following diagnosis : Angina pectoris, consecutive to aortitis which had encroached on the aortic orifice, \\'ith aortic and mitral incompetence. We had still to discover the cause of this aortitis, and as, after revie'vnng the probable causes, I could only find one — syphiUs, which the patient had had nine years before — it appeared to me natural to put the aortitis down to syphihtic infection. I prescribed mercurial in- unctions and iodide of potassium. A few days later the patient was seized with a terrible attack of dyspnoea and pain, which during the preceding days had recurred at closer and closer intervals, and he succumbed in a few minutes. At the autopsy our attention was first directed to the aorta. It was dilated with patches of chronic aortitis. We counted seven small aneurysms at intervals, from below upwards. The first aneurysm w^as as large as a plum-stone, and situated in front and to the right of the aorta, on a level with the apex of the right auricle. The second aneurysm, of the same size, was situated above the preceding one. The third aneurysm was smaller, and situated higher up. The fourth was situated on the anterior part of the aorta, near the innominate trunk. The fifth aneurysm occupied the anterior part of the aorta, near the left carotid. The sixth was situated close to the left subcla\"ian artery. The size of each of these last three aneurysms was equal to a cherry-stone. Lastly, a seventh aneurysm, of the size of a walnut, occupied the ascending and lateral portion of the aorta. Some of these aneurysms were cupuliform ; others were covered by fibrinous clots, wliich projected, fike nodes, into the lumen of the vessel. Histological examination of the more affected parts revealed complete disappearance of the tunica media. The coronary arteries were carefully examined, but were not obliterated either at their orifice or in their course. We found only some atheromatous patches 1 centimetre from the orifice of the i:iosterior coronary. The heart muscle was much hypertrophied, especiall_y in the left ventricle. Bands of fibrous tissue were found on histological examination. These two cases are very instructive. They prove that aortic syphiUs may take the form of circumscribed gummata, with or without other lesions of the vessel. In these cases, as in most syphihtic lesions of the ascending aorta, the angina pectoris was so severe that both our patients died from it. They died, although there was no inflammation of the coronary arteries, DISEASES OF THE VESSELS 515 proving that obliteration of the coronary arteries is far from being the only cause of fatal angina pectoris. The multiplicity of syphihtic aneurysms was shown by Jaccoud in 1886 in his clinical lectures at the Pitie, where he quotes several well-known cases. These include : the case published by VcaUin, of a man forty-fiv'e years of age, who was syphihtic, and died suddenly from haemorrhage into the pericardium. At the post mortem four aneurysms were found on the thoracic aorta. — The case of Orlebard, of a syphihtic j^atient,. twenty-nine years of age, at whose autopsy three anemysms of the thoracic aorta were found, the first being situated above the posterior sigmoid, the second a httle higher, and the third below the origin of the innominate trunk.— Malecot's case of a man, fifty-eight years of age, who was both alcohoUc and syphihtic ; post mortem three aortic aneurysms were found : one at the origin of the aorta, the second on the arch, and the third just above the diajDhragm. Nalty's case (Verdie's thesis) deals with a man who had had sj^phihs five years before. One day he noticed a beating at the root of the neck. Six months later a pulsating tumour appeared in the same region, below and a httle to the right of the sterno- clavicular articulation. This tumour was an aneurysm. As the patient had tertiary ulcers on the thigh and knee, it was reasonable to ascribe the aneurysm to syphihs, and treatment was presci'ibed. After transient improvement the situation tjocame worse, and the patient died. At the autopsy two aneurysms were found — one at the level of the innominate artery, the other in the aorta. The latter compressed the trachea behind, and in front projected into the sterno-cIa\'icuIar region. Besides these two large aneurysms there were upon the aorta several small aneurysms, characterized, says the author, by erosions of the walls of the vessel and gummatous I^rojections. Further, numerous guramata, varying in size from a pin's head to a cherry- stone, were scattered over the surface of the heart and the endocardium. Jonas has reported the case of a man, thirty-three years of age, who had had syphilis for nineteen years, and three months before was attacked by cardiac and aortic troubles. He died, and at the autopsy enlargement of the whole ascenchng part of the aorta was found. Its surface was irregular and partly calcified, and 4 centimetres above the aortic orifice eight or nine aneurysms, var^'ing in size from a pea to that of a filbert, were counted. In syphilitic aortitis, which has been carefully studied by I^rault and LetuUe, the whole of the arterial wall is infiltrated at a circumscribed spot by embryonic lesions. " Round cells, united at different spots into confluent nodules, have a suspicious appearance. We are generally right at some period or other, if not in recognizing, at least in suspecting, the formation of miliary gummata." Kalindero and Babes are still more explicit on the presence of syphilitic gummata in the aorta. According to these authors, the multiple small aneurysms are due to gummata of the walls of the aorta. These authors say that, in addition to aneurysm of the aorta due to sclerous aortitis, we see small circumscribed aneurysms, due to the development of syphilitic gum- mata in the walls of the vessel. Sy|)liilitic Icsiotis of the aorta arc, liise bacilli, which are non-virulent in the case of the guinea-pig, kill small })irds that are protected by a preventive injection of antidiphtheritic serum. Martin has further proved that these non-virulent bacilli can secrete the diphtheritic toxine in suitable media. Finally, several experimenters have been able to increase the virulence of these originally inoffensive microbes. These facts show tiiat, before creating a group of j)seudo-diphthcria l)acilli, very doHned characteristics have to be found, which will enable us to diiTerontiate tlu^m from the dij)lithcria bacillus. Tho diphtlieria bacillus has no tendency to ponotrato the organs ; Barbicr and ToUoraer maintain, however, that they have discovered the bacillus in the 572 TEXT-BOOK OF MEDICINE cervical and bronchial glands, the spleen, and in tlie medulla (post-mortem researches). Experiments. — The diphtheria bacillus is readily cultivated in alkaline veal broth. Half a cubic centimetre of culture injected into the cellular tissue of a pigeon kills it in less than sixty hours. A rabbit dies in a few days from an injection of 2 to 4 c.c. of culture. The guinea-pig is usually selected, and dies in less than thirty -six hours from a very small injection. In a few hours local oedema, with a h?emorrhagic patch, develops at the seat of inoculation. The bacilU remain confined to the cedematous region ; they do not enter the bloodvessels, the lymphatics, or the organs, and, in spite of their rapid diminution in the inoculated region, the disease continues its course, by reason of the toxine which has been formed in situ. After death the inoculated animals present identical lesions : general dilatation of the small vessels, congestion of the suprarenal capsules and the kidneys, swelling of the glands, pleurisy in the guinea-pig, and degeneration of the liver in the rabbit. By means of pure cultures, it is possible to reproduce the diphtheritic membrane on the trachea, the conjunctiva, or the pharynx of pigeons and hens, and on the vulva of the female guinea-pig ; all that is required is to paint the mucous membrane, which has been previously excoriated. It is possible to cause lesions and symptoms re- sembUng croup in the trachea of the rabbit. Diphtheria of the skin may likewise be produced in animals, provided the epidermis has been previously removed. Diphtheritic Membranes. — In tlie pathological condition the membranes invade the mucous membrane and the skin, provided always that the skin has been denuded of its epidermis and the mucous membrane of its epithelium. The membranes appear spread out, and reform with extreme facility. The membranes are much less common on the skin than on the mucosa ; they may develop on the surface of blisters, leech- bites, herpetic vesicles, cracks in the nipple — in short, wherever the integument is denuded of its epidermis. Cutaneous diphtheria (for example, diphtheria which develops after a blister) pre- sents the following characteristics : The invaded part becomes painful, red, and covered with a firm, greyish membrane, which is difficult to detach. ' The edges of the wound swell and take on an erysipelatous tint. Pustules form ; the epidermis falls off, and the bared skin is, in its turn, invaded. The false membranes fall off and reform, but finally disappear ; the cutaneous surface, however, has a feeble tendency to cicati'iza- tion, and may remain red, bleeding, and painful for a long time. Cutaneous diphtheria is usually grave, because it is often associated Math secondary infections (streptococci), and is sometimes followed by gangrene, but esj^ecially because it is prone to be the starting-point of general intoxication and malignant diphtheria (Trousseau). The membranes invade the mucous membranes of the pharynx, nasal fossae, larynx, bronchi, conjunctiva, eyelids, cornea, vulva, prepuce, anus, gums, mouth. Eustachian tube, and oesophagus. These various locaHzations of diphtheria, however, are far from being frequent ; the usual locaUzations are in the nasal fossae (diphtheritic coryza), the back of the mouth, the pharynx, which we shall study under the name of Diphtheritic Angina, and in the larynx, which we have described elsewhere under the name of Croup. The false membranes are only, as I have just said, local manifestations of diphtheria ; they are the most frequent and formidable manifestation, for the mem- branes in the larynx and respiratory passages may choke young patients who are not treated in time. Diphtheria, however, reveals itself also by toxic manifestations caused by a poison which we shall stud^ later. Diphtheritic Toxine. — The pathogenic microbe, so plentiful in diphtheritic mem- branes, does not enter the blood or the organs of patients who have fallen victims to diphtheria. How are we to explain the fact that colonies of bacilli, localized to some part of the mucous membrane or the skin, can cause the organic lesions (kidney, liver. DISEASES OF THE THROAT AND PHARYNX 573 nerves), the poisoning and the paralysis which so often occur ? "In diphtheria the infection is not produced by microbic invasion of the tissues, but by diffusion within the body of a toxic substance formed on the surface of the mucous membrane outside the body, as it were." This poison, discovered by Roux and Yersin, " has been the subject of a series of researches, considered even to-day as the best monograph which has ever appeared in bacteriology, and rightly so." Funk, in speaking thus, echoes the general opinion. Roux, by discovering the diphtheritic toxine, prepared the way for the discovery of the antitoxin. The toxine is obtained by cultivating the virulent diphtheria bacillus on broth, in contact with air. In order to prepare an active toxine, it is necessary to make use of a very virulent culture. It is also necessary to secure the exact alkalinity of the broths ; for this purpose the peptonized broth must be made alkaline, until it no longer reddens blue Utmus paper. The broth is placed in Fernbach flasks with a flat bottom, so that the layer of liquid may be shallow. After sterihzation in the autoclave, fresh virulent bacilli are sown in the broth, and heated in the stove to 37° C. Roux, liaving proved that the diphtheritic poison was produced more rapidly and in greater quantity when the cultures were made in contact with air, invented an ingenious method of passing a current of moist air into the culture. For this purpose, he connected the side aperture of Fernbach's flasks with a tube, so as to make a vacuum. In three or four weeks a culture rich in virulent toxine is obtained. A layer of whitish sediment, like a crust of ground-glass, is deposited at the bottom of the flask. This is a deposit of bacteria, and on the surface of the broth a whitish-looking scaly veil, composed of younger bacilU, is formed. The liquid between those two layers is turbid at the commencement of the culture, but gradually becomes more and more clear. The finished cultures are filtered through a Chamberland candle, and the clear liquid is stored in well-filled corked flask^, and kept in the dark at the ordinary tem- perature. The toxine thus prepared generally kills a guinea-pig of 500 grammes in forty-eight hours after a dose of -i. c.c. The inoculation of the toxine into certain animals, such as the guinea-pig, rabbit, etc., produces symptoms and lesions similar to those seen in patients who have suc- cumbed to toxic diphtheria. Subcutaneous injection in these animals produces a fibrinous sanguinolent oedema at the point of inoculatioii, followed by swelling of the glands, diarrhoea, and hurried, shallow breathing. The post-mortem lesions are : congestion of the intestine and bloody fluid in the bowel, hsemorrliagic congestion of the suprarenal capsules and the kidneys, yellow staining and fatty degeneration of the liver, pleuritic effusion, very marked dilatation of the vessels, myocarditis, and imperfect coagulation of the blood. Injections of toxine not only produce the acute intoxication just described, but also paralysis (and this is one of the most interesting sides of the work of Roux and Yersin), that closely resembles diphtheritic paralysis, which we shall discuss in one of the following sections. The diphtheritic toxine is closely related to the diastases and the venoms. Microbic Associations. — We have just studied the products of the diphtheria bacillus — i.e., the membranes and the toxine — but the secondary infections play a great part in the symptoms of diphtheria. The streptococcus, the staphylococcus, other cocci, the pneumococcus, and the bacteria of putrefaction assist in the morbid process. Tlicso microbes, and especially the streptococcus, give rise to suppurative adenitis, bronclio- pulmonary complications, otitis, and gangrene. Clinical observation has taught us that the membranes play quite a secondary part in some cases. From the very onset the malady has all the syni|)t()nis of the most septic and infectious diseases ; it is accompanied by all)Uininuriii and lia'inonliage, an(i iuviides the entire economy, causing adynamia and often killing by syncope. 574 TEXT-BOOK OF MEDICINE Trousseau, on account of its extreme gravity, gave to this disease the name of toxic or malignant diphtheria. Bacteriology has confirmed clinical research in every point ; it has given us the reasons and taught us the causes of the different forms of diphtheria. The production of the membranes is due to the presence of the bacillus. The symptoms of intoxication are due to the poison elaborated by the bacillus. The infectious symp- toms are due principally to the associated microbes. We shall study later the associa- tion of the diphtheria bacillus with the streptococcus — an association which reciprocally increases the virulence of the pathogenic agents, and causes malignant and fatal diph- theria. VI. DIPHTHERITIC ANGINA. Diphtheritic angina does not always show the same course and symptoms. In its most common and favourable form, which has been called since Trousseau's time normal diphtheritic angina, the intoxication and the infec- tion are, fortunately, of secondary importance. The disease invades the throat to a greater or less extent ; it often reaches the larynx, especially in children, and sometimes engenders severe paralysis, especially in adults. This proves that the disease is not without danger ; but, after all, the course and comphcations of the so-called normal angina can be nearly always cured with serum, and the rapid and fatal comphcations that are so frequent in the malignant form need not usually be feared. In the latter form, which is rightly known as toxic infective angina, and which I shall continue to call malignant, the general symptoms are far more important than the local ones. From the outset the malady has the appearance of a grave infectious disease. The entire economy is invaded in a few hours or in a few days. It is not the false membrane nor death by croup that is to be feared, but the rapid poisoning and collapse, to which patients often succumb. Some authors have attempted to classify diphtheritic angina according to bacteriological examination. Normal diphtheritic angina would thus be a monomicrobic angina, in which the bacillus exists in a pure state. On the other hand, malignant angina would be a polymicrobic angina, in which the diphtheritic bacillus is associated with other microbes — notably the streptococcus. There is some truth in these assertions, and these mono- microbic and polymicrobic forms will be described in this section, but I would hasten to say that such a radical bacteriological classification would be erroneous. I admit that the normal angina is often monomicrobic, but in many other cases it may be associated with cocci, diplococci, staphylo- cocci, and even streptococci (as I have just proved), and yet the angina does not lose its characteristics as a frank or normal angina. Per contra, it is not only a polymicrobic angina which can be malignant. I shall quote fatal cases of diphtheritic angina which were not polymicrobic, the diph- theria bacillus being present in a pure state (Roux, Martin). DISEASES OF THE THROAT AND PHARYNX 575 It is therefore best to retain the cUnical classification, and describe normal angina, which is but little toxic, and a malignant angina, which may be subdivided bacteriologically into angina with toxic symptoms and diphtheritic angina witli infective symptoms. And yet these two cUnical forms— normal and mahgnant angina — are not always clearly defined, and we find mixed forms. The disease may commence with mild symptoms, and yet after a few days it becomes mahgnant. Here, as in all toxic and infectious diseases, the poison and infectious agents show degrees and reserve surprises for us. Without affecting the truth of the description, it Ls possible to conform to the custom established by Trousseau, and to describe separately the two varieties. 1. Normal Diphtheritic Angina. Description. — While normal diphtheritic angina spares no period of hfe, it is much more frequent between the ages of three and seven years. Its onset is usually insidious and less acute than that of acute tonsilhtis. It installs itself by stealth. The fever is moderate, and may fall in three or four days ; the sore tlixoat is not severe, and the patient may feel hardly any pain on swallowing. While the above statement is practically true, we find many exceptions, since bacteriology has taught us not to be deceived by the multiple disguises of diphtheritic angina. The disease (in my description I borrow from Trousseau) commences with more or less vivid redness of the pharynx and swelhng of one tonsil ; in some cases both are involved. A well-defined white spot is soon visible on the affected organ. This spot at first consists of a layer resembling coagulated mucus, which rapidly becomes thickened and of a membranous consistency. At the commencement this exudate is readily detached from the surface, to which it is adherent by filaments penetrating the follicles of the tonsil. The underlying mucous membrane is healthy, except for the destruction of the epithcUum. The mucosa may appear to be hollowed out because it is swollen, and forms a kind of pad around the exudate. Ulceration is exceptional. After some hours the pseudo-membrane is more prominent, and covers the greater part of the tonsil. It becomes more and more ad- herent at the points first invaded, and takes on a yellowish or greyish-white tint. As a rule, the roof of the palate commences to become inflamed. The uvula swells, and is often covered with membrane witliin twenty-four hours. The membrane now appears on the other tonsil and the pliarynx. We find, however, many exceptions, since bacteriology has taught us not to be misled by the polymorphism of diphtheritic angina. We often see, not membranes, but erythematous, pultaceoiis, lacunar, or herpetic angina. From the first, or in a short while, we notice enlargement of the glands 676 TEXT-BOOK OF MEDICINE at the angle of the jaw on the same side as the affected tonsil. This adenitis is of great importance, because it is rarely absent. The glands are hard and movable, the periglandular tissue being unaffected. The adenopathy is due to the diphtheritic toxine, and we shall see that it changes in character in the streptococcal forms. The symptoms of angina are more pronounced by the second or third day ; the dysphagia is more severe, but the fever is shght, and may even disappear at this period. The child often has an ansemic look, due to diminution in the haemoglobin, as Quinquaud has shown. On examining the throat, the uvula, the pillars of the fauces, both tonsils, and the pharynx are in some cases covered with false membranes, which may have a lardaceous aspect. The membranes are produced so readily that they reappear in a few hours upon an area which has been entirely cleaned. This rapid development is often seen in young subjects. The throat may be completely covered with false membranes in thirty-six hours in a child of three years, whilst several days are necessary in an adult. The patches grow thicker from the addition of new layers, which are formed below the old ones. The most superficial layers are readily detached, but the deeper ones adhere to the mucous membrane, and cannot always be removed without causing slight bleeding. Some patches are, as it were, let into the surrounding mucous membrane, which projects, and gives the false impression of an ulceration. The membranes do not long preserve their whitish or yellowish aspect, because their colour is altered by liquids, vomited matter, drugs, or blood, which has come from the nasal fossse. They then take on a greyish or blackish tint, wliich, joined to the foetor present, leads to the wrong idea of gangrene. This gangrenous appearance is common in the adult, but rare in children, and explains the name gangrenous sore throat given to diph- theritic angina by several authors. Gangrene is exceptional in diphtheria. Bretonneau was loath to admit it, but it may be seen in grave cases and in certain epidemics. Normal diphtheritic angina is often accompanied by albuminuria. This symptom is not of serious import. In favourable cases the disease is not of long duration. After eight to ten days the glandular swelhng diminishes, the membranes no longer reform, the mucous membrane becomes clean, and the difficulty in swallowing disappears. If the patient has not been treated in time with serum, con- valescence is long, and may be comphcated by serious troubles. In the adult extension of the angina to the larynx is rare, but croup consecutive to the angina is very common in children when serum has not been used. Tliis terrible comphcation occurs when the angina has scarcely terminated — in fact, croup often arises while membranes are still DISEASES OF THE THROAT AND PHARYNX 577 present in the throat. It is announced by changes in the voice and by fits of dry cough at short intervals (see Croup). The frec[uency of croup in children makes diphtheritic angina much more serious in them than in adults. When, however, croup occurs in the adult, it is more dangerous than in the child. The termination of the disease with syncope, which is so common in mahgnant forms, is unusual in normal diphtheritic angina. Angina is not always the initial manifestation of diphtheria. It often follows diphtheria of the nasal fossse, which has been latent for some days. It may also follow diphtheria of the mouth, larynx, or skin, but this sequence is very rare. Prognosis. — Normal diphtheritic angina is generally benign. It may, indeed, be said that, apart from the comphcations of croup and broncho- pneumonia, which are much more common in children than in adults, normal diphtheritic angina is almost exempt from danger. It is, therefore, im- portant to distinguish it from the grave toxic variety. When the angina is normal, the fever is slight, and abates in a few days. The submaxillary adenitis is moderate, and rarely appears early. The colour is not from the first pale and leaden. Albuminuria is transient or absent. The pulse is of good quality. The bacteriological examination does not, as a rule, reveal the long, curved bacilh, and when other microbes are associated with the diphtheria bacillus, they are unimportant (Brisou's coccus), or are present in very small numbers (staphylococci, streptococci). Nevertheless, although normal diphtheritic angina excludes up to a certain point the idea of toxicity, it is none the less true that in the most normal case of diphtheritic angina some toxic symptoms exist. The glandular swelling, the albuminuria, and the decoloration of the tissues are evidence of poisoning by the diphtheria toxine. These toxic symptoms, which are sUght, I admit, I shall call primary, because they are contemporary with the angina. Diphtheritic angina, however, may be normal and benign in appearance, and yet excite secondary toxic symptoms. The poison accumulates insidiously in the system, and causes diphtheritic paralysis. Lastly, in very rare cases an angina which seemed to be normal may become grave, or even fatal, if not treated in time with serum, as the cases cited by Roux and Yersin and by Chaillou and Martin prove. We see, then, that, for different reasons, diphtheritic angina, even when normal and but slightly toxic, is not exempt from danger. There is, therefore, all the more reason to diagnose and treat the disease without delay. When we discuss the treatment, there is one point on which I siiall lay stress. It is not sufficient to treat diphtheria with injections of scrum. The earlier the treatment, the better it succeeds. 37 578 TEXT-BOOK OF MEDICINE 2. Toxic or Infective Diplitlieritic Angina — Trousseau's Malignant Diphtlieria. In the preceding section I described the action of the bacillus in producing false membranes which are harmless in the throat, but dangerous in the respiratory passages, where they may produce croup and asphyxia. Normal diphtheritic angina is the most common form, and is generally seen in sporadic cases. It may be seen, however, in certain epidemics, even when mahgnant diphtheria is raging. " In fact," says Trousseau, " in a family of whom four, five, or six individuals are stricken with the disease, normal diphtheritic angina, with or without croup, will be the general rule. The malignant form, which poisons patients in the same way as septic diseases do, will be the exception." In principle, as I stated above, the most normal case of diphtheritic angina is always accompanied by some toxic symptoms. The pallor of the face, the rise of temperature, the swelling of the cervical glands, and the albuminuria, are symptoms due to absorption of the diphtheritic poison. These symptoms do not entail danger when they are moderate ; they are more or less a part of the common description of many cases of normal diphtheritic angina, and do not afEect the prognosis. In some cases, however, the toxic symptoms are so acute that the patient hterally dies of infective poisoning, or, as Trousseau said, of malignant diphtheria. The following examples will show how rapid the evolution of mahgnant diphtheria may be. Description. — " One of my colleagues, Walleix," says Trousseau, "was in charge of a child suffering from diphtheritic angina, which was improving. While he was examining the child's throat, she coughed up some sahva, which entered his mouth. He took the disease. Next day he noticed a small pelhcular concretion on one of his tonsils. Fever developed, and in a few hours the tonsils and the uvula were covered with false mem- branes. Serous Hquid began to flow from the nose. The glands and the cellular tissue of the neck swelled considerably. He became delirious, and died forty-eight hours later, without any laryngeal complication." A country practitioner was attending a child suffering from croup, for which trache- otomy became necessary. During the operation the entrance of blood into the trachea caused fears of suffocation. The anxious physician apphed his mouth to the wound in the throat in order to suck out the fluid which was entering the trachea. He inocu- lated himself with the disease, and died forty-eight hours later of mahgnant diphtheria. Henri Blache was in charge of a child who had undergone tracheotomy. At the end of the third night he complained of slight sore throat. Acute fever was present, and false membranes on the tonsils. In a few hours enormous swelhng of the neck and continuous discharge from the nose. In twenty-four hours deUrium, and death seventy-two hours later from malignant diphtheria, without having sho\\Ti the slightest symptom in the respiratory passages. Some years ago Potain asked me to see a family suffering from diphtheria. On my arrival, I was told that the two children had died from diphtheritic angina. The mother had been taken the previous day with sore throat and prostration. My examination gave me a very bad impression. She was deadly pale ; her lips were blue ; her pulse wretched. The cervical glands and the DISEASES OF THE THROAT AND PHARYNX 579 cellular tissue formed a brawny mass. Marked albuminuria. Throat covered with diffluent fcetid membranes ; sanious nasal discharge. She was quite lucid, and had no illusions as to her condition. " Whatever you do," said she, " I shall die of the disease which has just killed my two children." She passed away next day. The respiratory passages were quite free from any infection. The fulminant form is, fortunately, very rare. In other cases the disease runs its course in eight or ten days, as in the following example from Trousseau's writings : A child, twelve years of age, had been attacked by slight angina three days previously. She was taken to the hospital. On examination, the fcetor of the breath was very striking. Putrilaginous membranes at the back of the throat and on the roof of the palate. On the right side much swelling of the cervical and maxillary glands. This glandular swelling, which from the first meant a grave prognosis, increased during the next few days, and involved the cellular tissue of the cervical and submaxillary regions. A most alarming phenomenon supervened — viz., erysipelatous redness of the skin, pointing to deep inflammation of the parts. On the third day diphtheritic coryza and profuse epistaxis made the outlook very gloomy. With such formidable symptoms, although the respiration remained normal, the prognosis was most grave. She grew cold, just like a cholera patient. She had a ten- dency to syncope. Her pulse was extremely feeble and slow. The respiration remained free, and the respiratory passages were not affected by the diphtheria. She refused to take any nourishment. The glands became smaller, the nasal lesions improved, and the erysipelatous redness disappeared ; but yet, in spite of this deceptive improve- ment in the local signs, the child died on the tenth day, " poisoned by the diphtheritic venom which had infected her." She died of syncope whilst turning round and refusing to take a drink. The picture of malignant diphtheria is not always as complete as it was in the above case. The horrible fcetor of the breath, the brauTiy induration of the cellular tissue of the neck, and the erysipelatous tint, on which Trousseau and Borsieri have laid such stress, may be absent ; in spite of the absence of these symptoms, however, the excessive pallor, the weak pulse, the obstinate refusal to take food or drink, the diarrhcea, the severe and early albuminuria, the rapid loss of strength, point to malignant diphtheria of most grave prognosis, although the respiratory passages are absolutely free. We may now ask how bacteriological researches can explain these malignant cases. 1. Toxic Malignant Diphtheria. — In some cases the grave or fatal eomphcations are due to the diphtheria toxine alone, and other microbes are absent. Roux and Yersin report half a dozen cases in their monograph of 1888. Cases 1, 3, 5, 6, 7, 10, concern young patients who died of toxic angina. Bacteriological examination yielded pure cultures of the diphtheria baciUus. Martin lias collected twenty-eight cases of fatal toxic diphtheria, in wliich bacteriological examination showed only the existence of long and curved diphtheria bacilli, without other microbes. Chaillou and Martin (in their memoir, July, 18()4) have collected ten fatal cases of toxic diph- theria, in which pure cultures of diphtheritic bacilU were found, without other microbes. The long curved bacillus was most frequently present. In the above ca.ses clinical observation was always confirmed by bacterio- logical examination. It is therefore possible for us to give an exact clinical 37—2 580 TEXT-BOOK OF MEDICINE description of this pure toxic angina, which constitutes one of the varieties of mahgnant angina. Tlie temperature is higher than in normal diphtheritic angina. It oscillates between 102° and 104° F., and remains at this point for some days. It is a bad sign if the temperature does not fall after the fourth or fifth day (Martin). The changes in the pulse follow the oscillations of the tempera- ture. The false membranes are thick, adherent, and of a greyish-white colour. They generally cover the tonsils, the uvula, the pillars, and the back of the throat, leaving no intervals of healthy mucosa. In some cases, however, the false membranes are discrete. The swelling of the cervical glands is more rapid and more marked in toxic than in normal diphtheria. Nevertheless, it is rare to see such marked swelhng as in diphthero-streptococcal angina. Albuminuria is more constant in toxic than in normal diphtheria, though it does not usually appear before the third day, and it does not disappear when the disease is about to end fatally. In toxic diphtheria the colour is more pale and leaden. The Ups are at times cyanosed, even though there is no danger of asphyxia. Diarrhoea is frequent. Distaste for food and drink is usually present. Rapidly increasing weakness, compressible pulse, and tendency to syncope, which do not exist, or are only slight in normal diphtheria, are a marked feature in these cases. Bacteriological examination, without being quite conclusive, shows that numerous colonies of long curved bacilH belong to toxic diphtheria. Experimental cultures on broth furnish valuable information as to the degree of toxicity. Brieger and Wasserman were able to extract from the blood of a child who died of toxic diphtheria, with collapse and cardiac failure, a quantity of diphtheria toxine, and to prove its specific action by inoculation of guinea-pigs. Martin has obtained similar results. Let us now compare the experimental lesions due to the injections of diphtheria toxine with those found in patients who have died from toxic diphtheria. They are quite similar : heart flabby and yellow, parenchy- matous and interstitial myocarditis, ecchymotic pericarditis, congested Hver, dilatation of the capillaries, and fatty infiltration of the hepatic cells ; infiltration of the tubuli contorti of the kidney and dilatation of the glomerular vessels ; enlarged spleen and hypertrophy of the Malpighian corpuscles ; swelhng of Beyer's patches and of the follicles ; infiltration of the intestinal mucous membrane. The symptoms and the lesions explain the action of the toxine in the case of toxic diphtheria. Let us now see how malignant diphtheria behaves when other organisms are also present. 2. Malignant Diphtheria with Microbic Associations. — In most cases the mahgnant forms of diphtheria are both toxic and infective. They are DISEASES OF THE THROAT AND PHARYXX 581 due to the reciprocal exaltation of the diphtheria bacillus and of the microbes which are associated with it. The streptococcus plays the principal part, as the following experiments of Roux and Yersin show : Prepare a weak culture of diphtheria baciUi, so that inoculation produces sUght local oedema in a guinea-pig. Prepare another culture of virulent streptococci, so that 1 c.c. will kill a rabbit in twenty-six hours. Prepare Ukewise a broth culture containing a combination of attenuated diphtheria bacilU and virulent streptococci. Take two guinea-pigs and inoculate them \vith ^ c.c. of the attenuated diphtheria culture ; take two others and inoculate them with | centimetre of the streptococcus culture, and two more Anth 1 c.c. of a mixture containing equal parts of the two cultures. In a few days the guinea-pigs inoculated \\-ith the weak culture show slight oedema and a little scab at the point of inoculation, but no other compU- cations. The guinea-pigs inoculated with the streptococcus show an abscess at the point of inoculation, but the guinea-pigs which have been inoculated with the mixture die two days later. At the point of inoculation false membranes and oedema containing diphtheria bacilh and streptococci appear. The lesions found post mortem comprise dilatation of the vessels, congestion of the suprarenal capsules, and effusion into the pleurae. Tubes of serum are inoculated with the oedema fluid. Next day the diphtheria colonies are well developed, while the streptococcus has only grown to a ,very small extent. It is, therefore, easy to separate the two microbes. We can now see how much the harmless diphtheria bacillus has been reinforced by contact with the streptococcus. For this purpose two cultures are made — one with the inojffensive diphtheria bacillus, and the other with the reinforced bacillus. The cultures are heated in the oven for a fortnight at 35° C. in a current of air, filtered through porcelain, and injected into the veins of four rabbits. Two rabbits are given 10 c.c. of the cultures of the reinforced bacillus. They die in thirty hours, so virulent is the culture. The other two rabbits are each given twice as large a dose of the culture of the weakened bacillus, and Uve two months. It is only after a long time that they grow thin and succumb to paralysis. The streptococcus and the diphtheria bacillus, when separated, are incapable of killing guinea-pigs ; when associated, they kill rapidly, owing to the lesions of diphtheria. When we compare the cUnical and experimental facts (Roux, Yersin, T'arbier, Martin, Chailh)u), we find in both instances identical results. In angina, which is both diphtheritic and streptococcal, either of the two microbes, isolated and cultivated separately, is rarely virulent, as animal inoculation shows. The two microbes together reciprocally increase their virulence, and hence the exceptional gravity of diphthero-streptococcal angina. 582 TEXT-BOOK OF MEDICINE The following figures indicate the gravity of these cases : According to Martin's statistics, 8 deaths in 10 cases ; Chaillou and Martin give 13 deaths in 14 cases ; Tezenas had 3 deaths in 3 cases. To this variety of mahgnant angina belong the fulminating cases which I referred to at the commence- ment of this article. Their symptoms have been admirably described by our predecessors, and bacteriological studies have in part explained their patho- genesis. At the onset of mahgnant angina the face is pale, leaden, and bloated ; the lips are cyanosed, though there is no danger of suffocation. The neck is enormous and " proconsular " (Saint-Germain) from the swell- ing of the glands and the oedematous infiltration of the cellular tissue. The skin of the face and neck is often shiny and erysipelatous in appearance (Borsieri, Trousseau). The breath is excessively foetid, especially when the exudates are invaded by the bacilU of putrefaction. Deglutition is very painful. The false membranes of the throat have often a gangrenous appear- ance. The temperature is usually high, and the pulse is rapid, tliready, and irregular. Albuminuria comes on early and is persistent ; diarrhoea is frequent ; haemorrhage is common (epistaxis, bleeding gums, purpura). In such cases, the nasal fossse being often invaded by both microbes, there is a copious purulent or bloody discharge, with rejection of false membranes. Be the angina rapid or slow, its gravity is considerable. Extreme rest- lessness with or without delirium, and prostration bordering on coma, are present, while collapse or syncope ends the scene. Death sometimes supervenes from certain comphcations, such as infective croup, purulent bronchitis, or streptococcal broncho -pneumonia. If recovery takes place, convalescence is long, and at times accompanied by ulceration of the throat, mouth, or nose, and by suppurative adenitis. This description differs, as will be seen, from that of purely toxic angina. In the latter the diphtheritic poison is the chief factor ; in diphthero- streptococcal angina, infection by the streptococcus claims a large share. This fact is made quite clear in Barbier's paper, in which he shows that the streptococcus enters the blood. It reaches the blood of the pulmonary veins, and thence affects the lungs, the bronchi, the mitral valve, the articulations, the pleurae (purulent pleurisy), the middle ear (purulent otitis), the tissues of the neck (adeno-phlegmon), the walls of the pharynx (retropharyngeal abscess), the spleen, etc. What I have just said of the streptococcus is in part apphcable to the staphylococcus. Although diphthero-staphylococcal angina is not so grave as diphthero-streptococcal angina, it still claims a place in the group of mahgnant anginae. The truth thereof is evident on consulting the statistics pubhshed on this subject. Conclusions. — We can now formulate the following conclusions as to the pathogenesis of diphtheritic angina : DISEASES OF THE THROAT AND PHARYNX 583 1. Diphtheritic angina is called normal or benign when it is neither toxic nor infective. Its benign nature is due to the feeble virulence of the diphtheria bacilli, or to the feeble receptivity of the soil in which they develop. It is also due to the absence of other microbes, or to the feeble power possessed by the associated microbes to increase in virulence. Nevertheless, normal angina, in spite of its benign appearance, is not always free from danger. It may be accompanied by asphyxia, especially in children (croup), or be followed by paralysis. 2. Diphtheritic angina is called malignant when it is toxic and in- fective. It is rather toxic than infective when the predominating features can be ascribed to the virulence of the diphtheria toxine ; it is rather infective than toxic when the predominating features are due to other microbes, especially the streptococcus. We must never forget the part played by the soil, which favours more or less the development of the poison. 3. The normal, toxic, and infective forms of diphtheritic angina occur with their distinctive characteristics, according as the bacillus limits its action to the production of membranes, or elaborates the poison in every degree of toxicity, with or without secondary infections. We find, however, mixed cases in wliicli these varieties are associated, and it cannot be otherwise, because it is always the same disease, which may present different aspects, but forms, after all, only one species. Diphtheritic angina, therefore, may start with benign symptoms, and then assume the characteristics of the toxic or infective form, with a fatal result. Polymorphism of Diphtheritic Angina — Herpetic, Lacunar, and Pultaceous Varieties. Diphtheritic angina is not always characterized by the formation of false membranes. Eor a long time, until bacteriological examinations were made, writers were loath to admit that membranes might be absent in diphtheritic angina. Non-diplitheritic membranous angina was well known, but few believed that membranes were ever absent in diphtheritic angina. For some years past bacteriological researches have shed light on the chaos of angina. Thick and adherent membranes are certainly the most common clinical feature in diphtheritic angina, but in a large number of cases — more numerous than we think — membranes are absent. It resembles catarrhal, erythematous, pultaceous, lacunar, or follicular angina. In other cases diphtheritic angina assumes the guise of herpetic angina. These herpetic, erythematous, pultaceous, or lacunar varieties are more frecjuent ia adults than in children. Of 137 cases of diplitheritic angina in adults, Roche found but 42 instances of the membranous variety. I shall review, therefore, these various kinds of diphtheritic angina, which, as will 584 TEXT-BOOK OF MEDICINE be seen, is essentially polymorphous, and I shall first describe the herpetic variety, as given in my lectures at the Faculte de Medecine in December^ 1894. 1. Herpetic Variety of Diphtheritic Angina. I will begin with the classical description of simple herpetic angina. Whether we speak of herpetic angina (Gubler) or of membranous angina (Bretonneau and Trousseau), or whether we follow other authors, and designate it " herpes of the pharynx," it is not less admitted that the characteristic feature of herpetic angina is the presence of herpetic vesicles on the mucous membrane of the throat. A child or adult is taken ill with symptoms of fever. The rigors and the fever are accompanied by lassitude and headache. Dysphagia appears. We find diffuse redness of the tliroat ; the tonsils are enlarged, and small swelUngs, wliich have been likened to sudamina, appear on different parts of the isthmus of the gullet or the pharynx. This condition is known as herpetic angina. In some cases the disease has the appearance of an erythematous angina, and the exudate is shght. In other cases we find vesicles on the mucous membrane of the throat and also a whitish pultaceous exudate. At times, indeed, we find not simply a pultaceous layer, but thick and extensive fibrinous membranes, simulating diphtheria so closely that Trousseau called this variety of herpetic angina by the name of " common membranous angina," the epithet "common" here ehminating all idea of diphtheria. Every medical man has seen more or less frequently these erythematous, pultaceous, or membranous forms of herpetic angina. When we are able to witness the actual, but sometimes fugitive, evolution of the herpetic vesicles, no room for doubt exists, and the diagnosis of herpetic angina is clear. The diagnosis often receives considerable support when the herpes, instead of remaining confined to the tliroat, invades other regions, such as the labial commissure, the lips, the nostrils, the chin, the cheeks, the con- junctiva, etc. If a patient has acute painful angina, with false membranes, which may even simulate diphtheria, and if at the same time herpes is present on the tonsils, the roof of the palate, the pharynx, and the face, we may diagnose herpetic angina, but we cannot exclude diphtheria. Tliis view is at least generally admitted, and is borne out by experience. The description of angina with herpes, therefore, must be revised. Bacterio- logical research in the last few years has shown, and is showing every day that angina, whether erythematous, pultaceous, or membranous, cannot be diagnosed for certain, except by bacteriological examination. Herpetic angina, like every othei variety, cannot escape bacteriological control. DISEASES OF THE THROAT AND PHARYNX 585 My researches on this subject, communicated to the Academie de Medecine,* have enabled me to place the matter on a firm basis. I have been able to prove that so-called herpetic angina is fairly often of a diph- theritic nature. I found it easy to verify the inconstancy and the insuffi- ciency of the symptoms furnished by clinical observation, and I cannot state too forcibly the fact that the eruption of herpes, which was formerly said to ehminate the idea of diphtheria, only serves to deceive us. It inspires us with false security, as the following cases show : Case I. — In 1895 a man, fifty-two years of age, admitted for severe herpetic angina, which had commenced suddenly four days before with rigors, fever, dysphagia, headache, lassitude, coryza, and slight epistaxis. Axillary temperature, 103° F. Ex- amination of the throat revealed diffuse redness and marked swelling of the tonsils, and on the roof of the palate herpetic vesicles irregularly disposed. A crop of herpetic vesicles was also present on the lips and on the right labial commissure. The maxillary glands were moderately enlarged. The natural diagnosis was herpetic angina. Next day a pultaceous deposit appeared on the right tonsil. This deposit on serum and agar showed staphylococci and diphtheria bacilli. The bacteriological finding reversed the former diagnosis. Nasal diphtheria, clinically suspected a few days previously from slight epistaxis and coryza, now appeared. The patient had nasal discharge and epistaxis, and voided false membranes from the nose. The pillars of the fauces and the uvula were also covered with patches of membrane. In spite of injections of serum, which were given too late, acute paralysis of the soft palate appeared a few days later. The paralysis invaded in turn the lower and upper limbs and the bladder. This case of angina showed all the cUnical features of herpetic angina, and it was only by bacteriological examination that we discovered the diphtheria, which was confirmed a few days later by generalized paralysis. Case II. — A girl, eighteen years of age, was admitted under Gouguenheim for sore throat, accompanied by headache, lassitude, and temperature of 104° F. Generalized redness of the pharynx and the tonsils. Herpetic vesicles, whitish and slightly adherent membranes on both tonsils ; herpetic vesicles also present on the lips and the com- missures. No glandular enlargement. The clinical diagnosis pointed to herpetic angina. Cultures made from the membranes on the tonsils yielded diphtheria bacilli, but no other microbes. An injection of 10 c.c. of serum was immediately given. Case III. — In 1892, at the Necker Hospital, the matron's son was taken ill with angina. The throat was so red that my house-physicians, Charrier and Renon, took it to be an early symptom of scarlatina. Next day herpetic vesicles appeared on the tonsils, and the diagnosis was herpetic angina. At the end of two or three days he was admitted to the hospital, and the existence of the herpetic variety of diphtheria was recognized. I also discovered diphtheritic coryza, which had commenced with epis- taxis. Very severe paralysis followed. The velum palati was first affected, and then the muscles of the head and the neck, the lower limb.s, and finally the upper limbs, were attacked in turn. He recovered two months later. Case IV. — Kelsch was asked to make a bacteriological examination in a case of angina which presented aM the clinical characteristics of herpetic angina. The culture revealed the diphtheria bacillus, and also the pneumococcua. Case V. — Huchard reported the following case to me : He was called upon to give bis opinion as to an angina in a child. Relying on the severity of the fever, the sudden- * Dieulafoy, " Angine Diphtherique a Forme Herpotirnio " (Academie de Medecine, Blanco des 11 Juin, 2 et 3 Juillet, 1895). 586 TEXT-BOOK OF MEDICINE ness of the onset, and the simultaneous appearance of herpes, he diagnosed herpetic angina, which was confirmed by Brocq. The case, which had every appearance ot herpetic angina, was really diphtheritic, and carried off the child in a few days. Description. — We are in possession of several cases which prove that the herpetic forms of diphtheritic angina are fairly common. What, then, becomes of the classical description and chnical diagnosis of the old herpetic angina ? The suddenness of its onset, the severity of the fever, the acute- ness of the general symptoms, the sharp pain in the throat, and the appear- ance of the herpetic vesicles on the tonsils, the velum palati, and the Hps, formed a symptom-complex, on which it appeared possible to base the diagnosis of herpetic angina. And in the differential diagnosis from diphtheritic angina great care was taken to accentuate the difference between the acute inflammation of herpetic angina and the more insidious and less painful onset of diphtheritic angina. This erroneous idea must be abandoned. The cases abeady quoted show that the herpetic variety of diphtheria may be as sudden and acute as the most classical so-called herpetic angina. In Huchard's case the angina began with very acute fever. The tonsils were red and swollen ; herpes was present ; and a most toxic diphtheria was masked by these acute symptoms. My httle patient in the Necker Hospital was taken ill with acute fever and severe sore throat. Herpes appeared, but here again the acute symp- toms masked diphtheria, wliich was followed by severe paralysis. In a case reported by Roux and Martin, a child was suddenly taken ill, with a temperature of 104° F., pulse of 160, and delirium.' The sore throat was severe ; the tonsils were much enlarged, red, and pultaceous ; herpes appeared on the lips. This picture is typical of herpetic angina, and yet it is quite deceptive, since it apphes equally to diphtheritic angina with herpes, I therefore propose to abolish the so-called herpetic angina, as it has been bequeathed to us by our predecessors. It can no longer retain its quasi-intangible place in our nosology. If we retain herpetic angina in the old sense of the word, we must remember that it is less a case of herpetic angina than of angina with herpes. We see streptococcal, staphylococcal, or pneumococcal angina with herpes, and, of most interest, a group of diphtheritic anginse with herpes,* as I hope I have clearly proved. Nevertheless — and tins is the question wliich redoubles the interest- it will be easy for us to connect the actual state of science with the tra- ditions handed down to us by one of our greatest clinical physicians. For * Jes (of Krakow) has found the diphtheria bacillus in the liquid of the vesicles of labial herpes in a patient stricken with diphtheritic angina (1896). DISEASES OF THE THROAT AND PHARYNX 587 this purpose let me quote from Trousseau's report, wliich was presented by him to the Academie, on behalf of the Conmiission on Epidemics, on November 22, 1859. The opinions given in this report are stated some years later in his " Chnical Lectures at the Hotel-Dieu " : " The characteristic of the epidemics of the year 1858," says Trousseau, " was the concomitance of herpes of the pharynx and diphtheritic angina. The former, though reduced to simple herpes of the pharynx, did not always run a regular course. Some cases were very prolonged ; at other times the membranous affection degenerated in situ. The physician ought anxiously to put the question to himself whether he is justified in maintaining a favourable prognosis. The two affections not only occurred one after the other (herpetic angina and diphtheritic angina), but in each partial epidemic the two pathological forms were found to be more or less closely associated." I might multiply these quotations, which prove that Trousseau had seen and described in detail the relations which may exist between diph- theria and the so-called herpetic angina. The bacteriological researches wliich I have already mentioned are a striking confirmation of the ideas of the greatest chnical physician of our French school. Trousseau not only discovered the herpetic variety of diphtheria, but also formed a clear idea of the gravity of the prognosis. We should be wrong to imagine that herpetic diphtheria is always benign. The cases above mentioned are convincing on this point. The child at the Necker Hospital was seized with severe diphtheritic paralysis, which placed its life in danger. Another of my patients similarly suffered from severe paralysis, lasting four months. Huchard's patient died within a few days. Trousseau, then, was accurate when he wrote : " Fatal diphtheria often commences with an eruption of herpes." Conclusions. — Diphtheritic angina may assume the appearance of her- petic angina. It is impossible clinically to affirm that a so-called lierpetic angina is or is not diphtheritic. Bacteriological examination enables us to decide the nature of the case. 2. Diphtheritic Angina of a Follicular Appearance. Let us now consider diphtheritic angina that simulates follicular tonsillitis. Here again the clinical picture; of the disease is deceptive. Chnically, a case appears to be tonsillitis, and bacteriology corrects the mis- take. To quote the proofs : In 1891 Jacobi showed bacteriologically that follicular tonsilUtis, especially in adults, is often dii)htheritic. During an epidemic of diphtherio in a boarding-school, Mouillot found amongst eiglaeen })atients eight cases of membranoua angina and ten cases of follicular tonsillitis. All were diph- 588 TEXT-BOOK OF MEDICINE theritic. One of the latter cases was followed by diphtheritic paralysis. Escherich has found the bacillus of diphtheria in several cases of so-called follicular tonsillitis. Koplik, in 1892, reported numerous cases of follicular diphtheritic angina. Chaillou and Martin have quoted eight cases of diphtheritic angina, presenting white points on the tonsils, and simulating follicular tonsilhtis. Gouguenheim says that in eighty-three cases of adults suffering from diphtheritic angina at the Lariboisiere Hospital, he found forty cases of follicular diphtheria. Diphtheritic angina, therefore, assumes, especially in the adult, the guise of folhcular tonsillitis, and bacteriological examination alone can decide the diagnosis. This follicular diphtheritic angina, although generally benign, may in exceptional cases be toxic and dangerous, as the cases of Chaillou and Martin show, as weU as Case CXII. in Martin's monograph. 3. Diphtheritic Angina of the Pultaceous Variety. This form is the rarest and most benign of all. The patient has angina presenting all the appearances of catarrhal, erythematous, pultaceous angina, and bacteriology reveals the bacillus of diphtheria. Feer reports three cases. One child showed at first moderate rednees of the throat, with a temperature of 103° F. The next day the thermometer registered 105" F. The tonsils were swollen and red, with some pultaceous deposit. Glandular enlargement was present on one side. The child was cured in a few days. The cultiire revealed the presence of diphtheria bacilli. Inoculation with a pure culture of these diphtheria bacilli killed a guinea-pig in ten hours. Concetti, in 1894, reported two cases of pultaceous diphtheritic angina, arising by contagion from children suffering with fatal pharyngeal and nasal diphtheria. The tonsils were enlarged, and covered with a layer which in nowise resembled diphtheria, but had rather the coarse appearance of a pultaceous exudate. The condition was diphtheritic. Clinical Diagnosis. — In a case of acute angina two mistakes may be made. The first error consists in diagnosing diphtheritic angina when it is not present. The converse mistake consists in mistaking a case of diph- theria for a non-diphtheritic angina. In the latter case we fail to recognize an existing diphtheria. The result is that the patient is not isolated and spreads the disease. Moreover, a patient who has not been treated early with serum Avill be more exposed to the immediate or remote consequences of diphtheria, including croup, early or late poisoning, and paralysis. These cases, wliich are too numerous, prove that it is imperative to recognize diphtheritic angina from the first, under the penalty of the gravest mishaps. CHnical resources, however, are very often insufficient. What signs and symptoms are to be looked for ? Can we rely upon the manner in which the angina commences ? It has been truly said that diphtheritic angina at its commencement is more insidious and accompanied by less DISEASES OF THE THROAT AND PHARYNX 589 fever than other forms of angina, which are more clearly inflammatory. If the reader \\all refer to the cases quoted in the preceding section, he will see that the herpetic form has often a most sudden onset, with marked sjTnptoms of fever. Can the severity of the dysphagia be rehed on ? It has been said and repeated— not without some truth — that deglutition is rektively easy in diphtheria, whilst it is, as a rule, very painful in non-diphtheritic angina. Tliis statement is often true, but yet we find many exceptions. The cas3S of herpetic diphtheria enumerated above showed early and severe dys- phagia. Can the character and the growth of the false membrane be relied on ? Here again the clinical characteristics of the diphtheritic membranes which were classical before bacteriological examination — viz., colour, thickness, adherence, elasticity, and reaction to chemical agents — are common both to diphtheritic and non-diphtheritic membranes. Is not the ready reproduc- tion of false membranes at least a characteristic inherent in diphtheria ? It was formerly beheved to be so, but since bacteriological examinations have been made, we know that membranes caused by Brisou's cocci, streptococci, staphylococci, or pneumococci, may be reproduced with the same readiness as the diphtheritic membrane. Is not the tendency which the membranes possess of invading the nasal cavities and the larynx at , least in favour of diphtheria ? In the section on Pseudo-diphtheritic Membranes we shall see that many of them, though due to streptococci or to Brisou's coccus, may invade the nose and the larynx. Cannot the glandular enlargement, which has been looked upon as a valuable sign, be of some help to us ? On the one hand, enlargement of the submaxillary glands may be almost wanting in pure diphtheria, and very marked in pseudo-diphtheritic angina. Baginski has reported sub- maxillary adenitis in five out of six cases of streptococcal angina. Tezenas speaks of similar swelling four times in four cases of streptococcal and staphylococcal angina. Jaccoud found adenitis in a case of pneumococcal angina. Martin has repeatedly noted marked adenitis in membranous angina due to Brisou's coccus. I have often made the same observation. Submaxillary adenitis is, therefore, of little assistance in diagnosis. Is albuminuria a sign of diphtheritic angina ? Pseudo-diphtheritic angina, caused by various microbes — notably streptococci — is frequently accompanied by albuminuria. This critical study of the signs and symptoms of diphtheritic angina sliows thatcHnical signs alone are insufficient for diagnosis. Several cases regarded by eminent physicians as diphtheria have been proved by bacteriology to be not so. I need only refer to pseudo-diphtheritic angina due to the strepto- cocci, Brisou's coccus, the pncuniococcus, or the staphylococci, which we 590 TEXT-BOOK OF MEDICINE shall discuss in the next section. Per contra, several cases considered as being non-diphtheritic have been proved by bacteriology to be diphtheria. I need only refer to the numerous cases of polymorphous diphtheria (her- petic, lacunar, and pultaceous forms). I am well aware that even at the present day many practitioners make their diagnosis in the case of angina solely by the chnical signs, and reserve bacteriological examination for doubtful cases. Bacteriological examina- tion, carried out systematically, is, in their oj^inion, unnecessary. After my communication to the Academic de Medecine, I was taken to task in the Premier-Paris of one of our medical journals, where I read the following sentence : " According to Dieulafoy and all bacteriologists, it is no longer permissible to make a diagnosis of angina without bacteriological examina- tion. Is there not some exaggeration in this proposition ?" That is the very word : we are taxed with exaggeration. We are given to understand that bacteriological examination is only useful in a case where chnical examination may be at fault. I cannot too strongly contradict such assertions. We are told that great clinical physicians in the past did not await the aid of bacteriology in order to diagnose cases of angina. I apologize to those who speak thus, but we must speak the whole truth. No one respects tradition more than I do, and I place great reUance on chiiical investiga- tion, but evidence must be accepted. I would refer my critics to the diagnosis made in his own case by Gillette, physician to the Children's Hospital, and one well versed in the diagnosis of diphtheria. Gillette thought he was suffering from herpetic angina. He congratulated himself on the severity of the inflammatory symptoms, the whiteness of the mem- branes, the bright redness of his throat, and the pain which he felt ; and yet the angina was diphtheritic, and proved fatal in a few days. I would ask my critics what they think of the diagnosis of Gubler, who was a man well versed in the study of angina. He taught that herpetic angina causes general paralysis, as diphtheria does, thus committing an error which he would never have made if bacteriology had enhghtened his diagnosis. I would refer my critics to the classification of Lasegue, who did not know exactly where the group of diphtheritic anginse began or ended, and in- vented the name diphtheroid angina. This name created the greatest confusion, wliich only bacteriology has been able to dissipate. In the subject under discussion chnical observation must give way to bacteriology. I know that it is hard to give up deeply-rooted convictions, but, at the risk of repetition, evidence must be accepted. A knowledge of the bacteriological work of the last few years shows the innumerable errors committed when the diagnosis of angina rested on chnical observation alone. In order to convince my readers, I think it useful tc point out the errors corrected by bacteriology. DISEASES OF THE THROAT AND PHARYNX 591 In the third report of the Pasteur Institute, Roux and Yersin state that out of 52 cases of membranous angina of diphtheritic appearance 19 were not diphtheritic. Morel, in his thesis on diphtheria, states that in 86 cases of membranous angina simulating diphtheria 20 were not diphtheritic. The most important paper pubKshed in France on this subject is that of Martin, who says : " Of 112 patients admitted to the Hospital for Sick Chil- dren for diphtheritic angina 36 had not diphtheria at all." He takes care to add : " CUnical study gave no information as to the nature of these 36 cases. Physicians had taken them for diphtheria, and yet bacteriological examination proved the absence of the diphtheria bacillus. They gave rise, therefore, to 36 diagnostic errors which it was cKnically impossible to avoid, and which, consequently, exposed to contagion 36 children who were in a state of receptivity." Baginsky, in 1891, published a series of 93 cases of membranous angina of diphtheritic appearance ; bacteriological examination proved that 25 of these cases were not diphtheria. In 1892 Baginsky published a second series of 154 cases of angina of diphtheritic appearance, in which bacteriology revealed 36 errors in diagnosis. WiUiam Hallock Park says : " In 159 cases of membranous angina of diphtheritic appearance, 89 cases — that is to say, more than half — were not diphtheritic." In 1892 Kophk reported 33 cases of membranous angina of diphtheritic appearance ; Loffler's. bacillus could not be found in 16 of them. Errors are more numerous in the case of secondary anginse supervening in the course of the infectious fevers, and notably in scarlatina. We have, therefore, a series of cases in which hundreds of errors have been made, because certain microbes — namely, Brisou's little coccus, streptococcus, staphylococcus, etc. — gave to these cases of angina the clinical appearance of diphtheria. Another series of errors consists, as we have said, in mistaking diph- theria for simple, lacunar, pultaceous, or herpetic angina. As this question has been fully discussed in the previous section, I shall not reopen the discussion. This polymorphism was a very frequent cause of error before bacteriology established the facts. Practitioners were too much accus- tomed to the idea of membranous diphtheria. We know to-day that herpetic, lacunar, and pultaceous forms of diphtheria exist. We must there- lore eliminate a partially correct diagnosis. In the case of angina the only way to arrive at an absolute diagnosis is by bacteriological examination. Jaccoud expressed this opinion in 1891, and Landouzy made an important communication to the Academie de Medecine on the same subject in 1895. The above discussion apphes equally to syphilitic angina. Chancre of 592 TEXT-BOOK OF MEDICINE the tonsil, whicli is covered with greyish false membranes and accompanied by dysphagia and glandular enlargement, somewhat resembles diphtheria ; but in the case of the chancre the lesion is unilateral, the tonsil is indurated, the disease runs a slow course, the ulcerated surface is readily cleaned, and the detritus is pultaceous rather than membranous. Mucous patches of the throat and of the tonsils are sometimes covered with false membranes, which simulate diphtheria. These membranes are whitish or greyish, of a gangrenous appearance, adherent to the mucous membrane, and accom- panied by submaxillary adenitis. These forms of syphilitic angina closely resemble diphtheria. These two lesions may, indeed, appear simultaneously, and are so much alike that the diagnosis can only be made by bacteriological examination. Ulcero-membranous angina, described in Section 2, is accompanied by diphtheroid membranes, and may simulate diphtheria. The absence of diphtheria bacilli and the presence of fusiform bacilH and spirilla (Vincent) prove the diagnosis. Phlegmonous tonsillitis itself may present difficulties in diagnosis from certain forms of diphtheritic angina. In both cases the pain is very severe, deglutition is difficult, the swelhng of the neck may be considerable, and the pulpy, sanious, diffluent coating sometimes present in malignant angina closely resembles the diphthero-streptococcal coating which covers the throat in phlegmonous tonsilhtis. Albuminuria may exist in either cask On what symptoms can the clinical diagnosis be based ? In phlegmonous amygdalitis the pain is more acute and more general, the dysphagia is excessive, and the patient can scarcely turn his head, which is rendered immovable by the contraction of the muscles of the neck ; he cannot open his mouth without acute pain, and can scarcely move his tongue. These symptoms are not so severe in diphtheria. In both cases the neck is puffy and swollen, but the swelUng appears earlier and is more marked in the glands than in diphtheria. In both cases respiration may be interfered with on account of the contraction of the isthmus of the gullet, but this symptom is much more prominent in phlegmonous tonsillitis, and gave to it the name of quinsey. In both cases examination of the throat may be difficult, but the patient suffering from diphtheria is the better subject, because he feels less pain. One essential feature is absent in diphtheria — viz., the tonsil and the velum palati are not pushed back and depressed by the peritonsillar phlegmon. Certain cases of suppurative tonsilhtis, how- ever, may be associated with the diphtheria bacillus and other microbes. I saw a case of diphthero-streptococcal angina which simulated suppurative tonsillitis. Bacteriological examination is therefore indisiDensable. Bacteriological Examination. — In a case of angina, what is the correct technique in a bacteriological examination ? A piece of membrane may be DISEASES OF THE THROAT AND PHARYNX 593 stained and examined under the microscope ; this method, however, is not trustworthy, and I therefore prefer to make cultures. A small piece of membrane is placed in a tube of gelatinized serum, as described in the pre- ceding section. Diphtheritic Angina. — In the case of diphtheria, either pure or asso- ciated with ocher microbes, it is possible, after an incubation of eighteen hours, to make out diphtheria colonies, which are the more characteristic the more spaced they are. The rapidity with which the first colonies appear is almost pathognomonic of diphtheria ; it is only in membranous angina due to Brisou's coccus that we find equally rapid growth. Typical colonies of the diphtheria bacilh are rounded, whitish, and more opaque at the centre than at the periphery. They project shghtly above the surface of the serum, and I have therefore called them papular. A fragment stained with Roux's blue shows the Klebs-LofHer bacillus (Section V.). Membranous Angina due to Brisou's Coccus.— A patient is sufiering from membranous angina which might easily be considered diphtheritic ; it has all the characteristics of a case of normal diphtheritic angina. I have seen such a case at the Necker Hospital, and the resemblance to diphtheria was such that bacteriology alone could decide the diagnosis. On making a culture, after eighteen hours colonies appear in the gelatinized serum ; they closely simulate diphtheria colonies. They appear early ; they are rounded and whitish, but their centre is not opaque. They are transparent through- out their whole extent, and have a humid appearance ; moreover, they are flat, and I have therefore called them macular, to distinguish them from the diphtheria colonies which are papular. On examining a stained fragment under the microscope we find no diphtheria bacilli, but only a small coccus, which is often paired hke a diplococcus. We know, therefore, the nature of the angina which at first sight so closely simulates diphtheria. We know that it is neither toxic nor infective, that it will not be followed by paralysis, and that even if croup is present, tracheotomy will not be required. Membranous Angina due to Streptococci.— These cases simulate diph- theria so exactly that in Martin's report we find an account of eight patients who were sent to the diphtheria ward when they had streptococcal angina. This angina will be studied in the next section. I will here content myself with giving the distinctive bacteriological signs. When membrane from the pharynx is placed on the culture medium, the colonies of streptococci make their appearaiic(>. somewhat later than those of diphtheria. We find immerous small punctiform colonies, which I call powdery ; they show but little tendency to grow larger, and the microscope reveals the streptococcus in straight or bent chains of three, four, five, or six elements. Primary or secondary streptococcal angina is frequent in the early stages of scarlatina, 38 594 TEXT-BOOK OF MEDICINE whilst the angina which appears during the dechne of scarlatina may be diphtheritic. Membranous Angina due to Staphylococci. — Membranous angina due to staphylococci has been taken for diphtheria. The colonies {Staphylo- coccus alhus and aureus) usually develop in twenty-four hours, and the bacteriological examination is so characteristic that a mistake is impossible. Membranous Angina due to Pneumococcus. — This variety of angina (see Section VII.) has been described by Jaccoud. The diagnosis from diph- theritic angina is absolutely impossible without bacteriological examination. This variety of angina, wliich is due to the pneumococcus, is not toxic, and does not spread to the larynx. Prognosis. — The prognosis of diphtheritic angina depends upon the chnical and bacteriological examination. Clinically, we must beware of cases of angina preceded or accompanied by nasal diphtheria. The nasal cavities are an excellent soil for the growth of the diphtheria bacillus ; it elaborates its toxine under the most favourable conditions, for it finds an even temperature and an incessant renewal of air by nasal respiration, just as in the method devised by Roux for the manufacture of the toxine. In mild diphtheria, early and grave comphcations need not be feared, but yet the poison is made on such a surface that sufficient toxine to cause diphtheritic paralysis may penetrate it. In mahgnant diphtheritic angina the presence of nasal diphtheria is of evil omen, as Trousseau rightly in- sisted. Early pallor, leaden and puffy face, abundant albuminuria, and tendency to prostration are bad symptoms. When thQ submaxillary glands are much enlarged from the first, the prognosis is usually grave. In some cases the inflamed glands behave like buboes — " they reek of the pest " — and form abscesses. The glandular suppuration may not be discovered, because the patient succumbs before the formation of an abscess. Early suppuration is a fatal sign : this statement does not hold in late suppuration. If the adenitis commences to suppurate when the angina is at an end, recovery may follow. These cases of adenitis are due to the association of the strepto- coccus with the diphtheria bacillus. Bacteriological examination furnishes valuable information as to the prognosis. A culture which shows discrete colonies of medium bacilli indicates less grave diphtheria than if the culture produce confluent colonies with long curved bacilH. As regards the prognosis, it is very important to know whether the bacillus of diphtheria is associated with other microbes. Bacteriological examination is, as we shall see, an indispensable element in the prognosis. Angina in wliich the bacillus of diphtheria is present alone is generally normal, with firm and elastic fibrinous membranes. It may be followed by croup, especially in children, and by paralysis, but it rarely assumes the maUgnant form. Diphtheritic angina which is associated with DISEASES OF THE THROAT AND PHARYNX 595 Brisou's coccus, is generally benign. Diphtheritic angina with which the staphylococcus is associated, is far more serious than the preceding forms. In the most serious or malignant form the streptococcus is also present. It is in such cases that the membranes may have a putrilaginous aspect and foetid odour, while the enlarged glands lead to the condition known as " the proconsular neck." MaUgnant angina is fairly frequently met with as a secondary affection in the dechne of scarlatina or during the course of measles and whooping-cough. etiology. — Diphtheritic angina is especially common in young subjects. It is endemic in certain countries, and when it rages in an epidemic form, the epidemic is often relatively benign or mahgn in a family, a town, or a district. In countries visited for the first time by diphtheria the angina and the other manifestations of the disease are generally severe. For example, in Bessarabia, where the scourge made its appearance for the first time in 1872, it carried o£E more than 12,000 victims in eight years. " In 1875 it appeared in the Province of Kerson, where the mortality varied from 27 to 62 per cent." Diphtheria is contagious, and the contagion may be direct or indirect. Inoculation of diphtheria, tried by Trousseau and Peter upon themselves, did not succeed ; it was a lucky failure, which only proves that the subjects were not in a state of receptivity. Direct contagion is only too well proved by the numerous examples of parents and physicians who have contracted the disease from a patient. I need only cite the case of Walleix, already mentioned, and of Herpin, who from a piece of membrane which entered his nostril, contracted coryza, angina, and paralysis. The cases of Blanche, Clozel de Boyer, Armango, and many others, whose memory we revere, will suffice. The contamination may be contracted from patients who have recovered from the attack because virulent bacilli are present for weeks in their oral and nasal cavities. After the disappearance of the membranes, virulent bacilli may exist for a fairly long time, although the mucous membrane appears quite healthy (Roux). Tezenas, who studied the duration of the contagious period in convalescent patients, furnishes us with the following information : He made cultivations daily in sixty cases after the disappearance of the membrane from the throat. In five cases bacilli were present for a variable period. In eleven cases the bacillus was present in the nose, while it was absent from the mouth and pharyjix. It was found in the nose for fifty- five days, and while it was present, it gave rise to a clear nasal discharge, that was generally unilateral. Centres of contagion may thus result. In other cases the contagion is indirect, and spreads through the interme- diary of the membranes, or of the dried sputum which has fallen on l)e(l(ling, clothing, toyy, or toilet articles. Cases of diphtheria occurring si.x months or 38—2 596 TEXT-BOOK OF MEDICINE a year later in previously infected surroundings are thus explained. These chnical cases agree with experimental researches, Roux having found that a particle of diphtheritic membrane, wrapped in a piece of Hnen and placed in a wardrobe, kept its virulence for more than five months. In other cases the diphtheria bacillus exists in the naso-pharyngeal cavity without causing the shghtest comphcation (Loffler). If, however, the virulence of the bacillus is increased, diphtheria occurs, and appears to be spontaneous. A first attack does not confer immunity ; diphtheritic angina may occur a second time. In some cases the angina is secondary — that is to say, it supervenes in the course of some other disease (scarlatina, measles, typhoid fever). These cases will be described under the primary disease. Do fowls suffer from diphtheria, and can they transmit it to human beings ? Saint- Yves Menard denies, with good reason, the identity of human and avian diphtheria. The latter is a pseudo-diphtheria which is not transmissible to man. Pathological Anatomy. — I described under Diphtheritic Angina the ap- pearance of the false membranes. These fibrinous membranes adhere more to the chorion when the mucous membrane is covered with stratified epithehum than when it is covered with simple epithelium, as in the air- passages. The membranes may acquire great thickness (^ millimetre to 2 milhmetres) from the stratified layers which are formed on the deep surface in contact with the mucous membrane. The younger the layers the more resistant they are, whilst the older ones are pushed towards the surface and became friable. Each layer of the false membrane is developed at the expense of the corresponding layer of the epithelium, and becomes more superficial as a new layer is pro- duced beneath. " A discussion has been raised as to whether the false mem- brane is situated above or below the epithelium. From what has gone before, we see that it is formed in the epithelial lining, and partially at the expense thereof." The false membrane replaces the epithehum. On post-mortem examination the diphtheritic membranes have in part disappeared, but examination during hfe shows that they are composed of a more or less dense network of fibrin, that encloses in its meshes altered epithelial cells, lymphocytes, red corpuscles, and micro-organisms. Many of the cells are dead, and their nuclei do not stain with picro-carmine. The epithelial cells are infiltrated with colloid substance, lose their nucleus, and are converted into homogeneous refracting blocks with pro- longations which branch like a stag's horns (Wagner) — Weigert's coagula- tion necrosis. A haemorrhagic exudate is sometimes found under the false membranes, and gives rise to ecchymoses. The structure of the false membrane changes somewhat at different periods of its growth. At first DISEASES OF THE THROAT AND PHARYNX 597 fclie epithelial changes are most marked and the fibrinous network is less important. Later the membrane becomes epithelial, fibrinous, and purulent, and in the last stage the fibrin is in excess (Leloir). The behaviour of the diphtheria bacilli was described in the previous section. The mucosa on which the membranes are about to develop is intiamed and swollen. After the membranes have disappeared, the mucosa has a dull look from the absence of epitheUum. Ecchymoses may be seen, but ulcers are rare. Ulceration, haemorrhage, and gangrene are chiefly seen in malignant diphtheria. When attacked by diphtheria, the tonsil undergoes changes, the description of which I borrow from Cornil. In a section we see the following features from the surface to the deep tissue : The false membrane which has replaced the epithehum burrows into the tonsillar crypts. In its deepest part it seems to blend mth the mucous chorion. The connective tissue of the mucous membrane is infiltrated with red and white corpuscles, its capillary vessels are filled with white corpuscles, and the inflammation which affects the reticular tissue and the folhcles of the tonsils explains the marked swelhng of these organs. The pharynx is the seat of similar lesions ; inflammatory hypertrophy of the lymphatic follicles is seen. The lymphatic glands of the neck are swollen and infiltrated with a turbid, "»erous, or purulent fluid. The membranes on the skin closely resemble those on the mucous mem- brane. They are in part formed at the expense of the modified epidermal layers, and are adherent to the papillae. Gangrene of the derma is some- times found. Ecchymoses have been found in the sulci of the cerebral convolutions. Pulmonary lesions (bronchitis, broncho-pneumonia) are very common, especially when croup complicates angina. They are gener- ally the result of secondary infections, the staphylococcus and streptococcus being responsible in many instances. The kidneys are almost always affected in severe diphtheria. We find hypera?niia and haemorrhage in the cortical layer, with cloudy swelUng of the epithelium of the tubules. The changes in the kidneys, hke those in the liver (fatty degeneration of the cells), are due to the diphtheritic toxine. The heart muscle is affected, and the papillary muscles in particular show granular degeneration. Interstitial myocarditis is at times fairly well marked. The valvular endocardium shows changes described by Labadie-Lagrave as endocarditis. They are rare, and result from secondary infections. In malignant angina the blood is fluid and sepia- coloured (Millard), and the number of rod corpuscles is diminished. This condition of dissolution is met with in certain infectious diseases. Treatment. — Since Roux's communication at the Buda-Pesth Congress, the treatment of diphtheria by serotherapy has replaced otlier methods. 598 TEXT-BOOK OF MEDICINE Behring first thought of applying serotherapy to the treatment of diphtheria, but it was Roux who, by discovering the toxine, rendered the discovery of the antitoxine possible. Roux selected the horse as the animal to produce the serum, and, while the labours of Behring gained few adherents in Germany, Roux's reports and results of his labours and those of his collaborators were sufficient to insure universal employment of the new method. The method consists in making horses immune against diphtheria, and in making use of the serum from an immune horse as a preventive and curative agent in diphtheria. The animal is inoculated under the skin of the neck and shoulders with progressively increasing doses of diphtheritic toxine. We start with very weak doses — less than 1 c.c, with or without the addition of iodine — and in a few weeks it is possible to inject at one sitting doses which are 200 and 300 times as large. In less than three months the horse is immune. As suggested by M. Nocard, some 10 pints of blood are taken from the jugular vein, yielding about 5 pints of serum. The same horse, if he continues immune, can supply the above quantity of antidiphtheritic serum every three weeks. Antidiphtheritic serum does not quite deserve the name antitoxine. The serum is not antitoxic in the true sense of the word, as it does not destroy the toxine. It does not affect the toxine, but acts on the cells of the organism, making them, for the time being, insensible to the poison. The toxine destroys the activity of the cell, while the anti- toxine revives and stimulates it (Roux). The serum restores to the cells of the organism a part of the phagocytic activity which they have lost through the action of the poison (Metchnikoff). Experiments. — The following method is used in studying the action of the serum on infected animals : Vulvar diphtheria is induced in a female guinea-pig. A few hours after inoculation we find, first, redness of the vulva, with swelhng and oedema of the mucous membrane, and later the appearance of diphtheritic membranes, vaginal discharge, fever, and loss of appetite. Some animals die in a few days from diphtheritic poisoning, some recover, and others suffer from paralysis. If, however, these animals receive a prophylactic dose of serum equal to one ten-thousandth part of their weight, the diphtheritic membranes disappear by the second day ; fever is less severe, and recovery always follows. If, instead of giving the antitoxine as a prophylactic, we inject it twelve hours after inoculation with diphtheria, curative results are obtained. The diphtheritic membranes disappear on the second day, and do not reform ; the bacilh disappear, and the animals recover. In any case, the curative dose of antitoxine used (after inoculation of diphtheria) must be very much larger than the prophylactic dose. DISEASES OF THE THROAT AND PHARNYX 599 Curative experiments give similar results in croup. If croup is pro- duced in rabbits, these animals die in a few days, the respiratory troubles and laryngo-tracheal lesions resembhng those found in croup in children. Rabbits which have been inoculated in the trachea after injection of serum. " do not take diphtheria, or, at least, it does not show itself by any apparent malaise." If the serum is injected into animals after tracheal inoculation, it may arrest well-marked diphtheria. These experiments, then, are very conclusive, and prove the eflS.cacy of antitoxic serum, provided the injection is not given too late. The serum, however, does not produce the same benefit in diphtheria associated with the streptococcus. " The association of the two microbes (diphtheria bacillus and streptococcus) produces in the rabbit rapid diph- theria, such as we see in young children. The pathological picture is the same." These two microbes reciprocally increase their virulence, and injections of antidiphtheritic serum have not the same efficacy. Let us now consider the treatment in a case of diphtheria. A sterilized syringe of a capacity of 20 c.c. is used, and the serum is injected under the subcutaneous tissue of the flank, the skin being first rendered aseptic. To a child under fifteen years of age 10 to 15 c.c. of serum are given; above fifteen years of age 20 to 25 c.c. are injected at one sitting. In some cases it is necessary to repeat the injection on one or more occasions. Let us analyze the results — (1) in pure diphtheria ; (2) in diphtheria with other micro-organisms. Pure Diphtheritic Angina. — Recovery is the rule after the serum has been injected. Fresh membranes do not appear twenty-four hours after the injection, and those already present become detached in two days. The temperature falls abruptly (Martin) and the general condition speedily improves. Furthermore (tliis point is very important), complications and croup are very rare, or, at least, if croup appears, it is very mild. The follow- ing quotation deserves consideration : " In 169 children admitted into hospital with, diphtheritic angina, 36 showed laryngeal troubles, 31 had croupy cough, and 25 had lost their voice and showed marked sucking-in, 80 that tracheotomy appeared advisable. Under the influence of the serum (and an injection may be given every twelve hours) the sucldng-in diminished, and only returned at intervals. The child coughed up the false membranes, and at the end of two or three days the respiration was normal, to the great surprise of the house-physicians and the nurses, who, from their experience of croup, were convinced that operation could not be avoided- Let us now see the action of serum in a case of diphtheritic angina when other microbes are present. The association of the diphtheria bacillus with Brisou's coccus is benign, and recovery is the rule after injections of serum. 600 TEXT-BOOK OF MEDICINE The association of the bacillus with the staphylococcus causes more severe angina ; nevertheless, recovery almost always follows after injections of serum, and this association is not as serious in the case of angina as it is in the case of croup after tracheotomy. The presence of the streptococcus gives rise to grave angina, in which injections of serum are not so effectual. The mortaUty has been 25 per cent. In diphthero-streptococcal angina, antidiphtheritic serum and Marmorek's antistreptococcic serum have been used together, but the results so far obtained with the latter serum have not been encouraging : " There is no reason to expect a positive action. We can only look for a modification of the condition of the throat and of the glands ; we cannot rely on any anti- toxic action " (Sevestre). I need not refer here to the treatment of croup by injections of serum {vide Croup), but, taking all the cases of diphtheria (angina or croup) as a whole treated with antitoxic serum, we obtain the following figures : The statistics of Roux, Martin, and Chaillou refer to 446 cases. Death- rate, 24*5 per cent. The statistics of Moizard refer to 231 cases. Death-rate, 14'7 per cent. The statistics of Le Gendre refer to 16 cases. Death-rate, 12' 5 per cent. The statistics of Lebreton refer to 242 children. Death-rate, 12 per cent. The statistics of Variot for the year 1895 give a total death-rate of 14" 5 per cent. " The year 1894," says Bayeux, " divides the therapeutics of diph- theria into two distinct epochs : the first, in which 55 per cent, of the cases died, and the second, when the mortality fell to 16 per cent., thanks to the use of antitoxine. This figure (16 per cent.) is supported by my own returns of more than 200,000 cases." The rate of mortaUty is diminishing continually, and will diminish still further, in proportion as cases of broncho-pneumonia are isolated, and tracheotomy is replaced, as far as possible, by intubation, and serum is in- jected without a moment's loss of time. We have Uved to see a thing hitherto unknown — that is, a week passing in Paris without a single case of diphtheria being notified ! A condition of success is to make the injection as soon as possible after the outbreak of the disease. Diphtheritic paralysis only supervenes, as a rule, when injection of serum has been delayed. I hold, therefore, that in a suspicious case of membranous angina, before bacteriological examination has decided the nature of the disease, we should begin by giving an injection. DISEASES OF THE THROAT AND PHARYNX 601 No one will ever repent having done so, even though the angina is not diphtheritic, whilst delay till the next, day may cause regret. As for local treatment in diphtheria, we must be satisfied with irrigations containing chlorinated soda (Roux). Painting with poisonous or caustic substances, such as carbohc acid and subhmate, must not be prescribed. I asked myself whether local painting of the throat with serum might not be beneficial. I therefore conducted some experiments with my house- physician, Marion. Female guinea-pigs were inoculated with vulvar diphtheria, and, when the disease appeared, the parts were painted several times a day with serum. No result was obtained. This conclusion, how- ever, refers only to ordinary serum obtained by the injection of toxine into animals. Martin, by injecting the bodies of the bacilli themselves into animals, obtained a serum which was no longer antitoxic, but anti-infective. Rist has shown that the bodies contain a poison differing from the soluble toxine. Martin's anti-infective serum can be made up in pastilles, which dissolve in the mouth and seem to have an action in situ on the diphtheria bacillus. Injections of antidiphtheritic serum sometimes cause cutaneous erup- tions, urticaria, and articular pains, which are less frequent in proportion as the technique has been perfected. Other complications for which the serum has been blamed (albuminuria, tachycardia, arrhythmia, muscular pains) must be set down to diphtheria or to streptococcal infections. It is important however, to make use of properly prepared serum ; bad serum might lead to trouble. Prophylactic Treatment. — As serum injections have a prophylactic action, it may be beneficial to inoculate the contacts, especially children and nurses. This prophylactic application of serum has given most satis- factory results (Mewim, Schiiler), and is a means of stamping out epidemics or of preventing their spread. Netter and Guinon have made systematic use of this prophylactic power. Every child admitted into the Trousseau Hospital receives 5 c.c. of antidiphtheritic serum, subject to reinoculation every three w^eks. Internal cases of diphtheria in the wards have become unknown. Patients must be closely watched, even after complete disappearance of the membranes, because the bacilU may remain for weeks in the throat or nose. Tezenas has published a very interesting work on this sul)ject. In sixty cases of diphtheria he found diphtheria bacilli in the Jiasal cavity, although the angina was completely cured and the bucco-pharyngeal cavity was free from them. This persistence of the bacillus in the nasal cavity is always associated with a limpid nasal discharge, whi(;h generally comes from one nostril. " As long as this discharge lasts, Loffler's bacilli arc found in the nasal cavity. The bacillus disappears with the discharge." 602 TEXT-BOOK OF MEDICINE The most minute precautions must be taken with regard to things that have been in contact with a diphtheritic patient. Linen or bedding must be baked in a steam-oven under pressure, for the diphtheria bacillus is very resistant, and persons have contracted diphtheria in a bed which a patient suffering from diphtheria had used several months, or even a year, previously, no antiseptic precautions having been taken. VII. PSEUDO-DIPHTHERITIC MEMBRANOUS ANGINA. Before the discovery of bacteriology it was well known that certain cases of mem- branous angina simulated diphtheria, though they were not diphtheritic. Bretonneau had expressed this view, and Trousseau wrote a most remarkable chapter on this subject. Returning to the familiar question of specificity, Trousseau reviews the forms of mem- branous angina which are not diphtheritic : membranous angina following cauteriza- tion of the pharynx with nitrate of silver and ammonia, and membranous angina due to the abuse of mercury. He teaches us that in scarlatina membranous angina is rarely diphtheritic (and bacteriology has proved that he is correct), and quotes cases of angina in the course of enteric fever which have been wrongly taken for diphtheria. Finally, following Bretonneau, he separates diphtheria from herpetic membranous angina, which he calls common membranous angina. The distinction made by these great masters, as a result of clinical observation, between diphtheritic and pseudo-diphtheritic membranous angina, has been clearly established by bacteriological researches. Bacteriology is responsible for this section, which is only the continuation and the complement of the two preceding sections. Bacteriology has enabled us to classify and to enumerate the nature and the character- istics of pseudo-diphtheritic membranous angina. The different microbes which will be referred to in the description of pseudo-diph- theritic angina, include Brisou's coccus, the streptococcus, the pneumococcus, the staphylococcus, and the Bacillus coli ; they may be associated in all the varieties of angina, whether catarrhal, pultaceous, herpetic, or suppurative. In some cases, however, they are associated with the formation of membranes, and the angina then simulates diphtheria, and merits the name " pseudo -diphtheritic." Pseudo-Diphtheritic Angina due to Coccus.— A child four or five years of age has, two days before, been taken ill with moderate fever, headache, loss of appetite, and sore throat. The temperature has been about 103° F. On examining the throat the mucous membrane is found to be red and covered with patches of membranous exudate. If the angina be of two or three days' duration, the tonsils, the uvula, and the pharynx may be covered with false membranes which simulate diphtheria. No distinction is possible between these membranes and those seen in certain cases of diphtheritic angina, as they are similar in appearance and structure. In each case they show the same power of adhesion, mode of invasion, and reproduction after removal. In addition, glandular enlargement is often found, though in a moderate degree. These signs and symptoms, therefore, are those of normal diphtheria. They were complete in a case at the Necker Hospital. My diagnosis of normal DISEASES OF THE THROAT AND PHARYNX 603 diphtheria, which seemed obvious, was proved to be incorrect by bacterio- logical examination. This variety of angina wliich simulates diphtheria so closely is due to Brisou's coccus, and was thus named from the child in whom Roux and Martin first observed this kind of angina. As it is absolutely impossible to make a diagnosis between this false and true diphtheritic angina by clinical observation alone, bacteriological examination is necessary. For tliis purpose we make a culture. A particle of the membrane is removed on a platinum loop and sown on a tube of gelatinized serum, which is placed in the oven at a temperature of 36° to 37° 0. Colonies appear on the surface of the serum after about eighteen hours ; they have, when well developed, the greatest analogy to those of diphtheria. In the first place they appear early — in fact, almost as early as those of diphtheria ; they are also rounded and whitish. They differ, how- ever, in some points. Their centre is not opaque ; they are transparent throughout their whole extent, and present a humid appearance. In addition, they are flat, for which reason I have named them macular, in order to distinguish them from the diphtheritic colonies wliich are papular. A stained fragment of the culture under the microscope shows no diph- theria bacilU, but only Brisou's coccus, the elements of which are often paired. We know, therefore, the nature of this angina, which at first sight closely simulates diphtheria, and we may be satisfied as to the prog- nosis, because angina due to Brisou's coccus does not give rise to toxaemia and is not followed by paralysis. In some cases it has been followed by croup, but in a very mild form. This pseudo-diphtheritic angina most often simulates diphtheria. It is liable to recur. It has been met with three times by Roux and Yersin. Martin's returns give twenty-five times in 200 cases of membranous angina ; Chaillou and Martin's figures give eleven times in ninety cases. Streptococcal Pseudo-Diphtheritic Angina.— The streptococcus may be found in every variety of angina. We are here concerned with mem- branous angina simulating diphtheria, for in the throat, as elsewhere, the streptococcus readily produces membranes (Widal). This angina, though generally benign, may be in some cases of excep- tional gravity. The disease sets in with rigors, fever, headache, and lassi- tude. The dysphagia is acute, and, on inspection of the throat, the mucous membrane is found to be red and inflamed, and the tonsils are sometimes enlarged. In some cases the exudate is pultaceous, but in otliers we find thick adherent membranes on the tonsils, the posterior wall of the i)liarynx and the velum palati ; they may even extend to the tongue and the lips. It has been rightly said that the streptococcal membranes are less elastic and 604 TEXT-BOOK OF MEDICINE more friable, yellowish, and cedematous than the diphtheritic membranes, which are whiter and more nacreous, as well as more firm and dry. These differences are more easy of description than recognition. As a matter of fact, some streptococcal membranes so closely resemble diphtheritic mem- branes that we cannot tell the difference. Inflammation of the submaxillary glands is said to appear earUer in streptococcal than in diphtheritic angina. Here again there are constant exceptions. As a clinical resemblance between streptococcal pseudo-diphtheria and true diphtheria, let me add that we often find rhinitis and laryngitis in both cases. The nasal discharge in each disease may be mucous, blood-stained, or puriform, with rejection of membranous shreds. In both cases the cough and the hoarseness indicate the invasion of the larynx by the streptococcus or by the diphtheria bacillus. In some cases streptococcal angina brings about such grave infection that erythema, polymorphous eruptions, albuminuria, and rheumatic pains may be noticed, just as in diphtheria, and such a grave general condition that death may result. Streptococcal angina is often secondary (grippe, measles, typhoid fever) ; it is most common at the commencement of scarlet fever. These secondary forms may be grave. We see, however, primary cases which prove fatal. The above description shows that the clinical diagnosis between tliis pseudo-diphtheria and true diphtheria is quite impossible. Streptococcal angina simulates diphtheria so closely, that in Martin's monograph we read that eight patients who were sent to the diphtheria ward were really suffering from streptococcal angina. Chaillou and Martin mention eight cases of streptococcal angina simulating diphtheria. I had quite recently at the Necker Hospital a case of streptococcal mebranous angina which simulated diphtheria so closely that a diagnosis would have been impossible without bacteriological examination. This xanaination is carried out in the manner already described. The strepto- coccus colonies appear rather later than those of diphtheria and of Brisou's coccus. After some twenty-four hours they appear in the form of a whitish stipphng, wliich never shows much increase in size. I have, therefore, thought it advisable to call these colonies dusty, and thus distinguish them at first sight from the macular colonies of Brisou's coccus and the papular colonies of the diphtheria bacillus. Even after fourteen to fifteen hours, stained fragments of the colonies on the surface of the serum show under the microscope little chains of mature streptococci. The cocci are arranged in chaplets, and in straight or wavy chains. Four or more cocci may be seen in each fragment of the chain. The streptococcus may be found in the mouth in the normal or patho- logical state under different conditions. Widal and Bezanfon have found DISP:ASES of the throat and pharynx 605 it in pseudo-membranous, diphtheritic, pultaceous, phlegmonous, and tubercular angina. Staphylococcal Pseudo-Diphtheritic Angina. — Staphylococci also may- be present in every variety of angina. I shall here discuss only the pseudo- diphtheritic variety. Tliis form is very much rarer than those previously described. I have, however, found four cases in Martin's paper, and four in that of Chaillou and Martin. I have seen three cases in adults. The patient shows the symptoms common to acute angina : febrile onset, dysphagia, inflammatory redness of the palato -pharyngeal mucous membrane, and sweUing of the submaxillary glands. The membranes then appear, but they are not as thick, adherent, and extensive as in diphtheria. It is, however, quite impossible to diagnose the condition from true diph- theria by chnical methods alone. Recourse must therefore be had to bacteriological examination. The staphylococcus forms, in less than twenty-four hours, wide, flattened, and irregular colonies on the serum, which at once indicate the diagnosis. The same culture, if allowed to remain in the oven, will soon give rise to much larger colonies, and after suitable staining the Staphylococcus alhus and aureus are readily found. The slide shows a heap of grains which do not form Uttle chains like the streptococcus, but are collected in grapehke bunches. Pneumococcal Pseudo-Diphtiveritic Angina. — This variety has been described by Jaccoud. It is very rare in children, and Chaillou and Martin have only seen one case. This disease has a sudden onset, with rigors, general malaise, and rapid rise of temperature to 103° or 104° F. On the first day the dysphagia is acute ; the mucous membrane of the throat is red and shiny ; the tonsils are swollen and purple. On the next day false membranes are seen in the throat. They commence in the form of white points, become confluent, and then spread and thicken hke diphtheritic membranes. The angina is usually accompanied by marked swelhng of the glands. If to these symptoms we add albuminuria, it is evident that this chnical picture closely resembles diphtheria. In the few cases which have so far been pub- hshed, the disease has not the shghtest tendency to invade the nasal fossae and the larynx. In such a case it is impossible for clinical observation alone to decide whether the angina is diphtheritic or not. Bacteriological examination is necessary, and reveals the presence of the pneuraococcus. Membranous Angina due to the Coli Bacillus. — This variety of pseudo- diphtheritic angina is very rare. The pathological agent is the coh bacillus, which has been found as an accessory organism in several cases of angina ; in some cases, however, pseud()-dij)hthoritic angina is due to the coli i)acillus alone. Martin and Chaillou mention two cases, while Lemioycz has pubhshed a most conclusive case. 600 TEXT-BOOK OF MEDICINE Herpetic Angina. — Herpetic angina (common membranous angina, Trousseau) will form the subject of a special section. Angina due to the Micrococcus Tetragenus. — In some cases tliia organism gives rise to an angina which somewhat resembles diphtheria. I give three cases which I have observed : Case I. — A healthy man was taken with fever, malaise, and pain in the right side. Pleural effusion was found on the right side. When I saw him some days later the effu- sion had almost disappeared, but the throat was covered with a pecuUar white layer, Avhich extended over the back of the pharynx, the velum palati, the jDillars, and the uvula. In places there appeared a multitude of prominent isolated granules, which gave the throat the appearance of having been sprinkled with sand. I have therefore proposed the name " sandy angina " for this variety. Tonsils not swollen ; no hyper- trophy of the submaxillary glands. Apert sowed two tubes of coagulated ox serum and two tubes of peptonized agar with the exudate ; he also made preparations by crushing one of the granules between two shdes, on which he found present, almost exclusively, encapsuled cocci, arranged in groups of four or in pairs. The serum culture showed no growth till the fourth day, but the tubes of agar from the first day showed a large number of prominent whitish colonies, which were glue-like, and formed threads when a fragment was lifted with the platinum wire. On microscopic examination, they were composed of tetrads, having all the characteristics of the Micrococcus tetragenus. Case II. — The patient had been under my charge for a fortnight with pleurisy, and the effusion had dried up, when he was seized with angina. On each tonsil five or six lenticular points of a clear white ; it had the appearance of a folUcular angina, but resembled the form which diphtheria also assumes. The serum culture gave within twenty-four hours streptococci and some colonies of staphylococci. The tubes of agar gave an almost equal number of tetrads and staphylococci. The Micrococcus tetra- genus, on being isolated, was cultivated in broth. A few di-ops of this broth, injected into a mouse, killed it in twenty-four hours ; the encapsuled tetrad was found in the blood. Case III. — A man was admitted to the Hotel-Dieu with symptoms of influenza, accompanied by rales, due to pulmonary congestion and pleural friction sounds ; some whitish exudate on the throat. The serum culture gave a negative result as regards diphtheria, but on agar there were mysterious colonies, including streptococci, small cocci, alone or in pairs and heaps, and about a dozen colonies of the Micrococcus tetragenus. This coccus, cultivated on broth, proved harmless on injection of a mouse with doses of J c.c. In these three cases " the tetragenic angina was accompanied or preceded by pleurisy. In the cases of tetragenic septicaemia hitherto observed (Chauffard and Ramond, Castaigne) pleurisy was present. Netter, Faisans, and Le Danamy have found the tetragenus in the fluid from sero-fibrinous pleurisy. The Micrococcus tetra- gemis shows a liking for the pleura." Syphilitic Membranous Angina. — In the previous section I said that the mucous patches on the throat and tonsils are at times covered with adherent greyish membranes which simulate diphtheria, the more as the glands at the angle of the jaw are generally enlarged. The diagnosis is easy if specific lesions are present in the mouth and pharynx, or if cutaneous or mucous syphihdes have been found. In cases of doubt, or even in cases where the two infections are superposed, bacteriological examination can alone confirm the diagnosis. The absence of Loffler's bacillus excludes the DIPHTHERIA. Plate I. Fig. 23 Fig. 24. \/ n/\ /\ •v^- \\V, Fig, 2 3. Fig. 23. — Culture ok Diphtheria on Gelatinized Serum. Discrete Colonies. When the colonics of diphtheria are well developed, they are characterized by round whitish snots, more opaque in the centre than at the circumference. I call these colonies papular, because they project from the surface of the serum. Some resemble little grains or semolina. Fig. 24. — Colonies of Diphtheria. Fig. 25. — Bacilli ok Diphtheria. They are as long as, hut thicker than, the bacilli of tuberculosis. They are swollen at their extremities, and are straight or slightly curved inwards. They are often disposed in groups of three or four, arranged in parallel lines, imitating the letters V, X, L, or simulating the acute (') or the circumllex ("i accent. They are never placed end-(jn. They look sometimes like short square needles which have been allowed to fall on a table in little heaps (Martini. To face p. 6or> SMALL COCCUS, BRISOU'S COCCUS. Plate II. ^*eL^, Fig. 27. ^ Sb cP CO