A TEXT-BOOK t** OF PRACTICAL MEDICINE, WITH PARTICULAR REFERENCE TO PHYSIOLOGY AND PATHOLOGICAL ANATOMY. BY EELIX VOX NIEMEYER, u* ' PROFESSOR OF PA'. AND THERAPEUTICS, DIRECTOR OF TIIE MEDICAL CLINIC OF THE UNIVERSITY OF TUBINGEN. TRANSLATED FROM THE EIGHTH GERMAN EDITION, BY SPECIAL PERMISSION OF TnE A UTHOR. BY GEORGE H. HUMPHREYS, M. D., ONE OF THE PHYSICIANS TO TRINITY INFIRMARY, MEMBER OF THE NEW YORK COUNTY MEDICAL SOCIETY, FELLOW OF THE NEW YORK ACADEMY OF MEDICINE, ETC., AND CHARLES E. IIACKLEY, M. D., ONE OF THE PHYSICIANS TO THE NEW YORK HOSPITAL AND TRINITY INFIRMARY, MEMBER OF TIIE NEW YORK COUNTY MEDICAL SOCIETY, ETC., ETC. REVISED EDITION. VOLUME II. NEW YORK: D. APPLETON AND COMPANY, 1, 3, and 5 BOND STREET. 1881. Entered, according to Act of Congress, in the year 1869, by D. APPLETON & CO., In the Clerk’s Office of the District Court of the United States for the Southern District of New York. Entered, according to Act of Congress, in the year 1880, by D. APPLETON & CO., In the Office of the Librarian of Congress at Washington. TABLE OF CONTENTS OF VOL. II. DISEASES OF THE URINARY ORGANS. DISEASES OF THE KIDNEYS. PAGE Chap. I.—Ilyperaemia of the Kidney 1 II.—Haemorrhage from the Kidney 7 III. —Acute Bright’s Disease 10 IV. —Chronic Diffuse Nephritis—Chronic Bright’s Disease ... 14 Y.—Nephritis Vera—Interstitial Nephritis—Renal Abscess—Metastatic Deposits in the Kidney ......... 36 YI.—Perinephritis........... 40 VII.—Amyloid Degeneration of the Kidney 41 VIII.—Granular Degeneration of the Renal Epithelium .... 43 IX.—Carcinoma of the Kidney ......... 46 X.—Tuberculosis of the Kidney 46 XI.—Parasites in the Kidney 47 XII.—Deformities of the Kidney—Irregularities of its Shape and Position 48 XIII.—Addison’s Disease—Bronzed Skin 49 SECTION I. DISEASES OF THE PEL VIS OF THE KIDNEYS AND URETERS. Chap. I.—Dilatation of the Pelvis of the Kidney, with Atrophy of the Renal Substance—Hydronephrosis 54 II.—Inflammation of the Pelvis of the Kidney—Pyelitis ... 66 III. —Stony Concretions in the Pelvis of the Kidney 59 IV. —Carcinoma and Tuberculosis of the Pelvis of the Kidneys and of the Ureters 64 SECTION II. SECTION III. DISEASES OF THE BLADDER. Chap. I.—Catarrh of the Bladder—Cystitis Catarrhalis 66 II.—Croupous and Diphtheritic Cystitis *72 III.—Pericystitis *72 IV TABLE OF CONTENTS OF VOL. II. PAGE Chap. IV.—Tuberculosis and Carcinoma of the Bladder . . . . 73 V.—Hemorrhage from the Bladder—Hematuria Vesicalis ... 74 VI.—Stony Concretions in the Bladder 75 Neuroses of the Bladder 79 VII.—Hyperesthesia of the Bladder ....... 80 VIII.—Anesthesia of the Bladder . . . . . . . .80 IX.—Hypercinesis of the Bladder—Spasm of the Bladder—Cystospas- mus . . . .' 82 X.—Acinesis of the Bladder—Vesical Palsy—Cystoplegia ... 84 Additions to the Revised Edition of 1880 87 SECTION IV. DISEASES OF TIIE URETHRA. Chap. I.—Virulent Catarrh of the Male Urethra—Clap—Gonorrhoea ... 88 II.—Non-virulent Catarrh of the Urethra 98 DISEASES OF THE SEXUAL ORGANS. A.—DISEASES OF THE MALE SEXUAL ORGANS. Chap. I.—Nocturnal and Diurnal Pollutions—Spermatorrhoea .... 100 II.—Impotence and Irritability, with Weakness of the Male Sexual Organs 104 B.—DISEASES OF THE FEMALE SEXUAL ORGANS. SECTION I. DISEASES OF THE OVARIES. Chap. I.—Inflammation of the Ovary—Oophoritis (Ovaritis) .... 109 II.—Ovarian Cysts Ill III.—Complicated Neoplasia and Solid Tumors in the Ovary . . . 120 SECTION II. DISEASES OF THE UTERUS. Chap. I.—Catarrh of the Uterus and Catarrhal Ulcers of the Cervix Uteri. . 122 II.—Parenchymatous Metritis—Acute and Chronic Infarction of the Uterus 131 III. —Perimetritis and Parametritis . 135 IV. —Contractions and Closures of the Uterus—Ilsemometra, Ilydrometra . 137 V.—Curvatures of the Uterus—Flexions and Infarctions . . . 140 VI.—Changes of Position of the Uterus 144 VII.—Fibroid Tumors of the Uterus—Fibromyomata, Fibroids, Dermoids 147 VIII.—Cancer of the Womb. . . . . . . . . .154 IX.—Anomalies of Menstruation 158 X.—Retrouterine Hematocele—Ilaunatoma Retrouterinum—Pelvic Hema- tocele 165 TABLE OF CONTENTS OF VOL. II. V SECTION III. DISEASES OF THE VAGINA. PAGE Chap. I.—Virulent Catarrh of the Vagina 170 II.—Non-virulent Catarrh of the Vagina 171 III.—Croupous and Diphtheritic Inflammation of the Vagina . . . 173 DISEASES OF THE NERVOUS SYSTEM. SECTION I. DISEASES OF THE BRAIN. Chap. I.—Hyperaemia of the Brain and its Membranes . . . . .175 II.—Partial Hyperaemia and Partial (Edema of the Brain . . . 198 III. —Anaemia of the Brain and its Membranes 195 IV. —Partial Anaemia and Partial Necrosis of the Brain—Thrombosis and Embolism of the Cerebral Arteries—Softening .... 201 V.—Cerebral Haemori’hage—Apoplectic Stroke—Apoplexia Sanguinea . 215 VI.—Haemorrhages of the Cerebral Membranes—Apoplexia Meningea— Haematoma of the Dura Mater 230 Inflammations of the Brain and its Membranes .... 233 VII.—Inflammation of the Dura Mater—Inflammation and Thrombosis of the Cerebral Sinus 233 VIII.—Inflammation of the Pia Mater, with Puro-fibrinous Exudation—Menin- gitis of the Convexity—Meningitis Simplex .... 236 IX.—Basilar Meningitis, Tuberculous Inflammation, and simple Miliary Tu- berculosis of the Pia Mater—Acute Hydrocephalus . ’ . . 240 X.—Epidemic Cerebro-spinal Meningitis 247 XI.—Inflammation of the Brain—Encephalitis 254 XII.—Partial Sclerosis of the Brain 260 XIII. —Tumors of the Brain and its Membranes 262 XIV. —Serous Effusions in the Mature Skull—Hydrocephalus Acquisitus . 275 XV.—Serous Effusions in the Incomplete Skull—Hydrocephalus Congenitus 278 XVI.—Hypertrophy of the Brain 280 XVII.—Atrophy of the Brain 282 XVIII.—Aphasia—Asymbolia 285 Additions to the Revised Edition of 1880 287 SECTION II. DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. Chap. I.—Hyperasmia of the Spinal Marrow and its Membranes . . . 289 II.—Haemorrhage of the Spinal Marrow and its Membranes—Spinal Apo- plexy 290 III. —Inflammation of the Membranes of the Spinal Marrow—Meningitis Spinalis............ 292 IV. —Inflammation of the Spinal Marrow—Myelitis .... 295 VI TABLE OF CONTENTS OF VOL. II. PAGE Chap. V.—Growths and Parasites of the Spinal Medulla and its Membranes . 299 VI.—Hydrorhachis Congenita—Spina Bifida 300 VII.—Consumption of the Spinal Cord—Tabes Dorsualis—Ataxie Loco- motrice Progressive {Duchenne)—Gray Degeneration of the Pos- terior Columns of the Spinal Cord (Leyden)—Locomotor Ataxy . 302 Additions to the Revised Edition of 1880 310 DISEASES OF THE PERIPHERAL NER VES. Chap. I.—Inflammation of the Nerves—Neuritis 313 II.—Neuroma 315 III.—Neuralgia 317 IY.—Neuralgia of the Trigeminus—Prosopalgia—Tic Douloureux—Foth- ergill’s Faceache 327 V. —Hemicrania—Migraine 331 VI. —Cervico-occipital Neuralgia ....... 333 VII. —Cervico-brachial Neuralgia 334 VIII. —Intercostal Neuralgia 336 IX.—Mastodynia—Irritable Breast (Cooper) 337 X.—Lumbo-abdominal Neuralgia ....... 338 XI.—Neuralgia Ischiadica—Iscliias—Ischias Nervosa Postica Cotunnii— Sciatica—Hip-Gout . 338 XII.—Crural Neuralgia—Ischias Antica Cotunnii .... 342 XIII. —Anaesthesia of the Cutaneous Nerves 342 XIV. —Anaesthesia of the Trigeminus 348 Spasm involving particular Peripheral Nerves . . .349 XV.—Spasm of the Facial Nerve—Mimic Spasm of the Face—Tic Con- vulsif 351 XVI.—Spasm in the region of the Spinal Accessory Nerve of Willis . . 353 XVII.—Scriveners’ Spasm—Mogigraphia 355 XVIII.—Idiopathic Cramp of the Muscles of the Extremities—Arthrogryposis 357 XIX.—Peripheral Palsy 359 XX.—Palsy of the Facial Nerve—Mimic Facial Palsy—Bell’s Palsy . 366 XXI.—Palsy of the Serratus Muscle e 370 XXII.—Progressive Palsy of the Cerebral Nerves, Tongue, Velum Palati, and Lips ........... 372 XXIII.—Essential Palsy of Children—Spinal Infantile Palsy {Heine) . 373 Additions to the Revised Edition of 1880 ..... 377 SECTION III. SECTION iv. GENERAL NEUROSES, OF UNKNOWN ANATOMICAL ORIGIN. Chap. I.—Chorea—Chorea St. Viti—St. Yitus’s Dance 378 II.—Lockjaw—Trismus—Tetanus . . . . ... . 384 III. —Epilepsy—Falling Sickness 390 IV. —Eclampsia Infantum ......... 405 Y.—Hysteria ........... 409 VI.—Catalepsy 424 TABLE OF CONTENTS OF VOL. II. VII PAGE Chap. VII.—Hypochondriasis 426 VIII.—Paralysis Agitans—Shaking Palsy 431 IX.—Delirium Tremens—Mania a Potu 432 X.—Morphine Habit—Opium-Eating 435 Additions to the Revised Edition of 1880 437 DISEASES OF THE SKIN. I. —Hypertrophy of the Skin 440 Chap. I.—Diffuse Hypertrophy of the Papillary Layer and of the Epidermis— Ichthyosis 444 II.—Diffuse Hypertrophy of the Skin and Subcutaneous Connective Tis- sue—Pachydermia—Elephantiasis Arabum .... 446 II. —Atrophy of the Skin 447 III.—Hyperemia and Anemia of the Skin .... 460 IY.—Inflammation of the Skin 462 HI.—The Slighter Form of Acute Inflammation of the Skin without Vesi- cation—Erythematous Dermatitis—Erythema . . . 463 IY.—Erysipelatous Dermatitis—Erysipelas ...... 456 V.—Herpes—Acute Superficial Dermatitis, attended by Formation of Groups of Vesicles upon the Skin 462 YI.—Urticaria—Nettle-Rash—Acute Superficial Dermatitis, with Forma- tion of Weals .......... 464 VII.—Eczema—Diffuse Superficial Dermatitis, with Serous Exudation upon the Free Surface, and without Typical Course . . . . 466 VIII.—Impetigo—Diffuse Superficial Dermatitis, with Formation of Small Pustules 479 IX.—Ecthyma—Dermatitis, with Formation of Large, Isolated, Permanent Pustules .... - 481 X. —Pemphigus—Pompholyx—Superficial Dermatitis, with Formation of Large Isolated Blebs 482 XI. —Itupia—Dermatitis, with Formation of Isolated Flat Vesicles, from which Scabs of a peculiar Shape are formed .... 484 XII.—Psoriasis—Chronic Dermatitis, with Infiltration of the Corium, and Abnormal Growth of Epidermis 485 XIII. —Lichen—Dermatitis forming Groups of Persistent Conical Nodules 489 XIV. —Prurigo—Dermatitis with Small, Scattered, Itching Nodules . 490 XV.—Acne, Acne Vulgaris, Acne Disseminata—Inflammation and Suppura- tion of Obstructed Sebaceous Follicles 493 XVI.—Mentagra—Sycosis—Inflammation and Suppuration of the Sebaceous Glands and Hair-Follicles of the Beard 495 XVII.—Acne Rosacea—Gutta Rosacea—Chronic Inflammation of the Seba- ceous Glands of the Face, with Dilatation of the Blood-vessels and Growth of the Connective Tissue about them .... 497 V.—Hemorrhages of the Skin—Purpura . . . 498 VI.—Growths in the Skin 500 XVIII.—Lupus—Lupus Exedens 600 VIII TABLE OF CONTENTS OF VOL. II. PAGC VII.—Parasites in the Skin 505 Chap. XIX.—Favus—Porrigo Favosa, Lupinosa 505 XX.—Herpes Tondcns 608 XXI. —Pityriasis Versicolor . . . . . . . 510 XXII. —Scabies—Itch 510 VIII.—Derangements of Secretion in the Skin . . . 515 APPENDIX TO DISEASES OF THE SKIN. Scleroderma 521 Leprosy—Elephantiasis Grsecorum 522 Additions to the Revised Edition of 1880 . . . . . 523 DISEASES OF TIIE ORGANS OF LOCOMOTION. Rheumatism 526 Chap. I.—Acute Articular Rheumatism—Rheumatismus Artieuloruin Acuta— Rheumarthritis Acuta—Flying Gout 527 II.—Chronic Articular Rheumatism—Rheumatismus Articulorum Chronicus —Rheumarthritis Chronica . 535 III. —Deforming Articular Inflammation—Arthritis Deformans, Arthritis Nodosa, Arthritis Pauperum—Arthrite Chronique Seche . . 540 IV. —Muscular Rheumatism—Rheumatismus Muscularis . . . 542 V. —Gout—Podagra—Arthritis . 545 VI. —Rachitis—Rickets 557 VII.—Osteomalacia 565 VIII.—Progressive Muscular Atrophy—Atrophie Musculaire Graisseuse Pro- gressive—Paralysie Musculaire Progressive Atrophique . . 567 IX.—Progressive Muscular Paralysis as a Result of Hypertrophy of the In- terstitial Fatty Tissue 570 Additions to the Revised Edition of 1880 571 CONSTITUTIONAL DISEASES. ACUTE INFECTIOUS DISEASES. Chap. I.—Measles—Morbilli—Rubeola—Rougeole . . . . . .673 II.—Scarlet Fever—Scarlatina 685 III. —Rose-Rash—Roseola Febrilis 595 IV. —Small-Pox—Variola—Petite Verole . . . . • • 596 V.—Cow-Pock—Vaccina .......... 608 VI.—Wind-Pox, Water-Pox, Sheep-Pox, Varicella, Chicken Pox . . 612 VII.—Typhus Fever—Exanthematic Typhus—Petechial Typhus—Spotted Fever ............ 614 VIII.—Abdominal Typhus—Ueotvphus (Typhoid Fever) .... 623 IX.—Febris Recurrens—Relapsing Fever 654 SECTION I. TABLE OF CONTENTS OF VOL. II. IX PAGE Chap. X.—Epidemic Diphtheritis—Malignant Pharyngitis—Angina Maligna— Diphtheria 664 Malarial Fevers 669 XI. —Intermittent Fever 669 XII. —Remittent and Continued Malarial Fever ..... 687 XIII. —Yellow Fever 690 XIV. —Sudor Anglicus — Suette Miliaire—Sweating-Sickness — Friesel Fieber 694 XV.—Cholera Asiatica . . . . . . . 699 XVI.—Bloody Flux—Dysentery ........ 722 XVII.—Trichina Disease—Trichinosis ....... 731 Additions to the Revised Edition of 1880 738 SECTION II. CHRONIC INFECTIOUS DISEASES. Chap. I.—Syphilis ............ 742 Appendix.—The Glandular Chancre—The Virulent Acute Bubo 750 II.—Congenital and Hereditary Syphilis 784 Appendix.—Infectious Diseases transmissible from Brutes to Hu- man Beings 788 Chap. I.—Human Glanders 788 II.—Hydrophobia—Lyssa—Rabies 793 GENERAL DISORDERS OF NUTRITION WHICH DO NOT DEPEND UPON INFECTION. Chap. I.—Chlorosis 802 II.—Scorbutus—Scurvy 810 III. —Purpura Hmmorrhagica—The “Morbus Maculosus” of Werlhof . 815 IV. —Progressive Pernicious Anaemia 817 V. —Haemophilia (Haemorrhagic Diathesis) 819 VI. —Scrofula 820 VII.—Diabetes Mellitus—Mellituria 832 VIII.—Diabetes Insipidus. 843 Additions to the Revised Edition of 1880 847 SECTION III. DISEASES OF THE URINARY ORGANS. SECTION J. DISEASES OF THE KIDNEY. CHAPTER I. HYPEREMIA OF THE KIDNEY. Hyperemia of the kidney and its consequences are not to be con- founded with inflammation of the kidney, although during life it is some- times quite impossible to distinguish between the two, and notwith- standing that similar symptoms appear in both disorders, such as the presence of blood and albumen in the urine, as well as the appearance in it of peculiar objects, generally called fibrinous casts (although it is probable that they are not composed of fibrin, and certainly are not pure fibrin, but consist in great part of mucin). Etiology.—A thorough knowledge of the normal circulation of the kidney is indispensable to a proper understanding, not only of the physiology, pathogeny, and etiology, but also of the symptoms of hy- pereemia of this organ. To Virchow the credit is due of having cor- rected some of our former ideas upon this subject, and of having ren- dered others more complete. According to the result of his researches, the branches oi one par- ticular portion of the renal artery (that, namely, which belongs to the middle and outer part of the cortical substance) go exclusively to form the afferent vessels, and, entering the Malpighian capsules as such, these divide to form the vessels of the glomeruli. Then, leaving the Malpighian capsule as efferent vessels, they again break up into branches, once more to reunite as renal veins. On the boundary be- tween the cortical and pyramidal substances there is a sort of “ neutral ground.” Here there are arteries from which branches arise, some forming afferent vessels, glomeruli, and efferent vessels, with long off- 2 DISEASES OF THE KIDNEY. shoots running into the cortical and medullary substance, and others which act directly as nutrient vessels for the medullary substance. Finally, the renal artery has branches upon which there are no glome- ruli at all, and whose function is simply nutrition of the medullary substance. The resistance encountered by the blood which passes through the glomeruli is far greater than that met by the blood which merely flows directly from the arteries into the capillaries. Even under normal conditions the blood-pressure in the renal arteries is a very consider- able one, that vessel being both short and of disproportionately large calibre. When the pressure within these arteries is increased, hyper- aemia of course will first arise in that portion of the kidney where the blood encounters the greatest resistance, namely, in the cortical sub- stance, and, above all, in the glomeruli. Where the resistance is less, as in the medullary substance, although the circulation is accelerated there, the actual amount of blood which the part contains is not ma- terially increased. It is very different, however, when the escape of the blood from the renal veins is impeded. In such a case the quan- tity of blood in the veins and capillaries is augmented, but the en- gorgement cannot extend through the narrow efferent vessels into the glomeruli; and, as the contents of the arteries are abnormally reduced in most of the disorders in which there is an obstruction of the renal veins (as in cardiac and pulmonary diseases), the reason at once be- comes apparent why, even in cases of extreme obstructive hyperasmia of the kidney, the glomeruli are scantily supplied with blood, and the secretion of urine is proportionately small. Perhaps, too, nervous in- fluence may not be without effect in bringing about this condition, since it is possible that in the kidneys, just as in other organs, the ar- teries of the various vascular systems are not subject to the same land of innervation. The causes which induce fluxion to the kidney are: 1. The transient plethora induced by every copious draught of liquid. This hypersemia is most pronounced in the secretory portion of the kidney, and the profuse transudation which takes place out of the overloaded glomeruli is the principal step in the process by which the general plethora of the system is relieved. 2. There is a second cause of renal hyperaemia, which is closely analogous to the first, and which occurs when the left side of the heart is hypertrophied, and which also is confined to the arterial system, in- cluding the glomeruli. 3. Collateral fluxion to the kidney may result from compression of the abdominal aorta, or iliac arteries, by a tumor or gravid uterus, as well as from derangement of the circulation in the capillaries of the HYPERAEMIA OF THE KIDNEY. 3 skin in the cold stage of intermittent fever. In the second stage of Bright’s disease, compression of the vessels of the cortical substance, by the distended urinary tubules, also gives rise to collateral fluxion in the medullary substance of the kidney ( Virchoic). 4. Dilatation of the afferent vessels, from palsy of their muscular elements, seems to be the principal cause of that arterial hyperaemia of the kidney, the existence of which is revealed by the discharge of a large quantity of limpid urine in certain spasmodic diseases (urina spastica). 5. Fluxionary hyperaemia is found in the vicinity of inflamed regions and deposits of morbid product. This form of hyperaemia we have already endeavored to account for, in treating of an analogous condi- tion in other organs, ascribing it to a loss of tone in the tissues, and to a dilatation of their capillaries, whose walls are ill supported by the surrounding relaxed parts. 6. Renal hyperaemia complicates inflammatory disease of the urinary passages, especially disease of the pelvis of the kidney. 7. The renal hyperaemia which sometimes attends the use of can- tharides, balsam of copaiba, and similar drugs, as well as that which accompanies certain infectious diseases, especially scarlatina, measles, typhus, and cholera, seems to be of similar origin. However, the affec- tions of the kidney which arise from the diseases above named cannot all be attributed to hyperaemia. Many of them belong to the class of maladies which we shall describe as parenchymatous degeneration of the kidney, in Chapter VII., and which, undoubtedly, are capable of de- veloping without the occurrence of hyperaemia. This io equally true of the renal affections which so often accompany pregnancy. Obstructive engorgement of the kidney arises from causes similar to those which induce engorgement of the liver (see Volume I.), so that the two diseases often accompany one another; but it will readily be understood, from what has already been said as to the peculiar character of the hepatic circulation, that engorgement of the liver usually is of earlier occurrence and greater intensity than engorgement in the kidneys. Engorgement of the kidney arises: 1. In uncompen- sated valvular disease of the heart; 2. In structural disease of the heart, which depresses the functional energy of the organ; 3. When the vigor of the heart is impaired by a condition of marasmus; 4. In disease of the lungs, which causes compression or wasting of the pul* monary capillaries; 5. In conditions in which the aspiration of the blood to the thorax is arrested; 6. In rare instances, contraction and closure of the vena cava or emulgent veins, by compression or throm- bosis, give rise to engorgement of the kidney, but the hyperaemia arising in such cases is of very great intensity. 4 DISEASES OF THE KIDNEY. Anatomical Appearances.—A kidney in a state of recent hy- pergemia is of a more or less dark-red color. Sometimes it is enlarged, owing either to dilatation of its vessels or to serous infiltration. The oedema of its parenchyma and subcapsular connective tissue renders the hypergemic organ unnaturally moist and soft, and loosens its capsule. When cut into, and when the vessels of the glomeruli are much dis- tended by blood, the Malpighian coils dot the surface of the section, as dark-red points. When the hypergemia is of long standing, particularly when there is habitual engorgement, as occurs in chronic disease of the heart and lung, the changes which arise are of a different kind. The kidney is then but little enlarged, or remains of its normal magnitude, or may even be somewhat smaller than natural. It is more resistent in texture, and is of a uniform red color. Upon microscopic examination, the epithelium of the urinary tubules of the cortical substance is found to be swollen, the contour of the cells is ill-defined, and they are filled with finely-granular contents, which clear up upon the addition of acetic acid. Sometimes there is a desquamation of the degenerated epithelium here and there; and the tubules collapse after the epithe- lium is expelled, causing the surface of the kidney to become uneven by depressions of varying depth. Traube and Beckman have called particular attention to the difference between this condition and the degenerative chronic inflammation of the kidney, which we shall de- scribe in Chapter IV. as chronic Bright’s disease. While the alterations above described are going on in the epithe- lium of the cortical substance, the straight tubules of the medullary substance are usually found filled with a material which is sometimes transparent and pale, and sometimes of a more yellow color. By mod- erate pressure upon the pyramids, a large quantity of an opaque creamy liquid is discharged from the papillge, which contains a great deal of epithelium and a few of those casts of the tubuli, in the form of homo- geneous transparent tolerably firm cylinders. Symptoms and Course.—The kidney has so few nerves of sensa- tion, and its capsule is so distensible, that hypergemic swelling of the organ is never accompanied by pain. As the amount of urine secreted depends chiefly upon the degree of pressure within the vessels of the glomeruli, its secretion necessarily becomes more profuse in that form of renal hypergemia which involves the arterial system of the kidney, including the vessels of the Malpighian tufts. This is almost the only symptom caused by fluxion to the kidney, which arises from copious drinking, hypertrophy of the left heart, compression of the aorta o: inac arteries, and dilatation of the renal arteries. The urine is copi- ous in quantity, dilute in quality, of low specific gravity, and of a pale HYPERAEMIA OF THE KIDNEY. 5 x»lor. In such cases, the pressure in the glomeruli hardly ever is suf- ficient to occasion transudation of albumen, or to rupture the vessels, and cause extravasation of blood into the Malpighian capsules. This fact is in accordance with the results of physiological experimenta- tion. Ligation of the abdominal aorta below the origin of the renal arteries, in spite of the increase of pressure which ensues in those arte- ries, never results in albuminuria. A very different train of symptoms follows upon a moderate de gree of obstructive engorgement of the kidney. Since, as we have just shown, in almost every case of obstruction of the renal veins the degree of tension within its arteries is very small, there is a diminution instead of an increase of the secretion of urine. On the other hand, the strain upon the capillaries becomes exceedingly severe, since they cannot discharge their contents into the already overloaded veins until the pressure within them exceeds that within the veins. Hence, not only does the plasma of the blood readily escape from the capillaries into the urinary tubules, so that the scanty, concentrated, dark-colored urine contains albumen, and the so-called fibrinous casts (or, more properly speaking, exudation casts), but the delicate walls of the capil- laries give way before the strain, so that the urine is also full of blood- corpuscles. According to the recent observations of Liebermeister, the simultaneous appearance of blood and albumen is so usual in obstruc- tive hyperaemia of the kidney, that the appearance of albumen alone, without a trace of blood, almost excludes the idea of simple engorge- ment from the diagnosis, and indicates the existence of inflammation. This fact in pathology, which may be verified in almost every case of chronic disease of the heart, and traced through all its phases, agrees with the results of physiological experiment. Albuminuria and hsema- turia are the never-failing consequence of ligation of the renal veins, or of the vena cava above their point of entrance. The escape of plasma from the capillaries of the kidneys, in obstructive congestion, into the uriniferous tubules is analogous to the extravasation from the pulmonary capillaries into the air-vesicles, which occurs in engorgement of the lungs, and which is there called hypostasis. The so-called hypostatic pneumonia is quite as independent of genuine inflammatory action as is the disorder of the kidney at present under consider- ation. The form of renal hyperaemia which apparently proceeds from re- laxation of the tissues of the kidney and consequent dilatation of its capillaries, has no effect either in augmenting or diminishing the quan- tity of urine secreted. It is attended, however, by a more or less pro- fuse transudation of blood-plasma, as well as by a greater degree of shedding, and probably too by a more active reproduction of the cel- 6 DISEASES OF THE KIDNEY. lular contents of the uriniferous tubules. Hence, when, after the abuse of irritating diuretics, or in disease which we know to be frequently complicated with this form of renal hyperemia, we find the urine to be albuminous and full of casts thickly studded with epithelial cells, our diagnosis may be renal catarrh. This name, which has been applied to the form of hyperaamia in question by most modern pathologists, is not quite appropriate, it is true, as the tubules have no mucous mem- brane, and as the term catarrh itself means an affection peculiar to such a membrane. However, it is quite as appropriate as is the term catar- rhal pneumonia. (See Vol. I.) The course of both fluxionary and obstructive hypersemia of the kidney, when the exciting cause is of a transient character, usually is favorable, and the disease in itself probably never causes death. Al- though, during the last few weeks of a case of heart-disease, this affec- tion appears in its most intense form, yet it is not renal hyperasmia of which the patient finally dies, but the respiratory derangement, the dropsy, and other symptoms which proceed immediately from the cardiac disorder. However, it cannot be denied that the albuminuria aggravates the dropsy and hydrmmia, and aids in undermining the strength of the patient. The renal catarrh also runs a favorable course as a rule, and, when the primary disease tends toward recovery, usually terminates in complete restoration to health. Far more rarely, diffuse parenchymatous inflammation of the kidney may develop from renal catarrh. Treatment.—The measures called for in treatment of the cause of hypersemia of the kidney may be inferred from the account above given of the causes themselves. When the hypersemia of the kidney is but a symptom of a more wide-spread and grave disease, it is to the latter rather than to the hyperaemia to which the treatment should be directed Where it has arisen from the abuse of irritating diuretics, their employment must be discontinued, and all application of vesi- cants, and use of irritating salves upon suppurating surfaces (a very common cause of fluxion to the kidney), must be abstained from.. Be- sides this, large quantities of drink must be administered, in order as much as possible to dilute the acrid matter which has been secreted in the kidneys. Pure water or the dilute acids are the most suitable for the purpose. The old practice of using barley-water, linseed-tea, milk of almonds, and the like mucilaginous or oleaginous liquids, must be regarded as obsolete, as it is well known that such articles have no effect upon the character of the urine. General and local blood-letting, and derivatives to the skin or intes- tines, are only to be resorted to in fulfilling the indications from the disease itself, when such remedies are indicated for other reasons, oi HAEMORRHAGE FROM THE KIDNEY 7 ivhen the hyperaemia is extreme, and there are no counter-indications against blood-letting. CHAPTEE II. HAEMORRHAGE FROM THE KIDNEY. Etiology.—The causes of haemorrhage from the kidney are: 1. Wounds, contusions, and other injuries of the organ. The presence of calculi in the pelvis of the kidney is one of the most common sources of such injury. Hayer tells about a patient with renal calculus who had haematuria whenever he was compelled to ride. 2. Haemorrhage from the kidney may proceed from intense hyperaemia, and rupture of the overloaded renal capillaries, and especially from that form of hyperaemia which accompanies the first stage of inflammation of the kidney, and which ensues after the employment of irritating diuretics, as well as in that form of the affection which follows scarlatina, small- pox, typhus, malarial fevers, and other infectious diseases. The hyper- aemia which exists about the seat of a parasite, or a neoplastic growth, especially cancer, often gives rise to haematuria. Finally, the exces- sive obstructive engorgement of the kidney, produced by disease of the heart and lungs, often results in an escape of blood from the ienal capillaries. 3. In rare instances renal haemorrhage depends upon a hcemorrhagic diathesis, that unknown disorder of the olood-vessels from which scorbutus and purpura haemorrhagica proceed. 4. In the Isle of France, Brazil, and some other tropical regions, haemorrhage from the kidney is endemic, there being no known cause for the disease. A peculiar form of renal haemorrhage, haemorrhagic infarction, arises under conditions similar to those in which haemorrhagic infarction takes place in the spleen. This can be traced in most cases to embolism. Genuine renal apoplexy is usually the result of severe injury, but in children may also proceed from severe hyperaemia (Rokitans/cy). Anatomical Appearances.—In haemorrhage from the kidney, the blood may be effused into the normal interstices of the tissues without detriment to the latter. In this way ecchymoses arise, in which there are spots of varying size stained of a deep red, and from which blood flows freely when they are cut into. They are situated sometimes under the albuginea, or within the tissues of the kidneys themselves. In variola and diseases of that class, besides ecchymoses in the renal tissue, the mucous membrane lining the pelvis of the kidney is usually of an even, dark-red color, decidedly thickened (haemorrhagic, infiltration), and rough on the surface. When recent, haemorrhagic infarction has the appearance of a dark- red deposit of a cuneiform shape, the point of the wedge being directed toward the hilus of the kidney. When of longer standing, the deposit’ 8 DISEASES OF THE KIDNEY. loses its color, beginning at the middle, and becomes converted into a yellow, caseous mass, or else breaks down, forming a renal abscess, with yellow puruloid contents, which at first consist of detritus alone, but afterward are mixed with pus. Finally, these caseous or purulent masses also are reabsorbed, and at the site of the former infarction there is left a cicatricial contraction. The seat of renal apoplexy is generally the medullary portion of the kidney. Collections, of varying size, form in the lacerated paren- chyma, their contents consisting partly of clotted blood, and in part of crushed and broken-down debris of the tubules. It would seem that the contents, both of apoplectic extravasations and of haemor- rhagic infarctions, may undergo fatty degeneration and absorption, and that recovery may take place, leaving a depressed cicatrix. Part of the blood effused into the tubules coagulates, forming cylinders, which are densely studded with blood-corpuscles. Sometimes we find pig- ment in the tubules and Malpighian capsules, as the residue of some former extravasation of blood. Symptoms and Course.—The occurrence of renal haemorrhage does not become recognizable unless the blood be effused into the tubules, and discharged with the urine. Hence it not unfrequently happens, in post-mortem examinations, that haemorrhagic infarctions and apoplectic extravasations are discovered, which were quite undis- coverable during life, because the blood did not enter the uriniferous tubules. If the amount of blood mingled with the urine be very small, the color of the latter is a peculiar dirty red when viewed by reflected light, while by transmitted light it is a pure red of greater or less depth. After standing for some time, a somewhat characteristic, slightly flocculent, brownish sediment is precipitated. When urine containing blood is exposed to the action of heat and nitric acid, the albumen of the serum of the blood coagulates. If the sediment be examined microscopically, blood-corpuscles are found, some of which are well preserved, while others are somewhat altered. There are also the casts above described, studded with blood-corpuscles, which are peculiarly characteristic of renal haemorrhage. I strongly recommend Seller's test for blood as very simple and convenient, and by means of which the faintest trace of blood may be discovered. Heat the urine, then add caustic potash and heat anew. The phosphates are thus precipitated, taking with them the coloring matter of the blood, which imparts a dirty yellowish-red color to the sediment viewed by reflected light, and, when seen by transmitted light, gives a splen- did blood-red color. Neither the coloring matter of the blood nor that of the bile is precipitated with the phosphates, so that color- ation of urine which shows this reaction cannot be ascribed to the presence of the latter pigments. When the quantity of blood in the HAEMORRHAGE FROM THE KIDNEY. 9 urine is very large, it is of a dark or brownish red, and, after standing, forms a cake of blood at the bottom of the vessel. Not unfrequently, a partial coagulation of the blood takes place in the bladder, and the coagula thus formed can only be got rid of after great suffering on the part of the patient. Sometimes the blood coagulates while in the ureters. In such instances, the symptoms of renal colic, hereafter to be described, may arise, and long, worm-like coagula (casts of the ureters) may be voided. The course of renal haemorrhage necessarily depends upon the na- ture of the disease which causes the haemorrhage. When induced by renal calculus, bleeding occurs regularly after every violent exertion. Haemorrhage arising from the presence of a tumor, especially cancer, is usually very profuse and persistent. The bleeding which accompa- nies inflammation of the kidney and the infectious diseases, or which results from venous obstruction or scorbutus, is not often very severe Tn the endemic hasmaturia of the tropics there are periodical profuse flows of blood from the kidneys. In haemorrhagic infarction, if there be haematuria at all, it is always slight. It is usually ushered in by a chill, and is attended by pain in the region of the kidney, and by violent sympathetic vomiting. The occurrence of such a train of symptoms—a chill, lumbar pain, vomiting, and haematuria—in a case of heart-disease, would warrant the diagnosis of a rrtnal infarction, which otherwise generally escapes detection. Renal apoplexy is marked by similar symptoms, which, however, are of much greater intensity. The results of renal haemorrhage cannot be described in detail until after a more thorough discussion of the diseases whereon they depend. The hasmaturia arising from cancer, from renal calculus, and from the tropical disease, acts chiefly by producing exhaustion from loss of blood. Treatment.—The main point in the management of a case of renal hasmorrhage is the treatment of ,any hyperaemia, inflammation, or other constitutional disease from which it proceeds. In most instances, when the main disease is susceptible of efficient treatment, the haemorrhage does not require any especial attention. Sometimes, however, the danger of exhaustion arising fr om repeated attacks of profuse and per- sistent haemorrhage, such as occur in cancer and renal calculus, may require relief. Cold, in the form of a bladder of ice laid over the re- gion of the kidney, cold sitz-baths, or cold injections, should then be resorted to. Internal administration of styptics has been recommended, and the whole list has been given seriatim in many cases, each failing in its turn. Articles containing tannin, especially tannic acid itself, which is eliminated through the kidneys in the form of gallic acid, and thus is enabled to act directly upon the bleeding point, deserve the 10 DISEASES OF THE KIDNEY. greatest amount of confidence. Next to it, secale cornutum, or ergotine may be given, but the doses must be large. The only effect to be ex- pected from the preparations of iron is the beneficial action which they exert upon the deterioration of the blood. CHAPTER III. ACUTE BKIGHT’s DISEASE. Etiology.—The name Bright’s disease is generally applied to two forms of inflammation of the kidney. The first, which is the subject of the present chapter, is closely allied to croup of the larynx and air- vesicles, not only in its anatomical lesions—consisting of a coagulating exudation, containing epithelial cells, and often extravasated blood- cells, and which fills up and occludes the urinary tubules—but in its course, which is always acute, like that of the other croupous diseases above mentioned, and nearly always terminates either in recovery or death within a few days. It is rare for the disease to pass into the second form of Bright’s disease, which we shall describe in the next chapter, under the name of “ parenchymatous nephritis.” This latter circumstance, indeed, seems to me to indicate that it is both right and practical to regard acute and chronic Bright’s disease as independent and distinct affections. I attach little value to the term “ croupous nephritis,” applied to acute Bright’s disease, in the previous editions of this work, as I must acknowledge that it is a matter of doubt whether the exudation which fills up and obstructs the uriniferous tubules consists of fibrin like the exudation of croupous laryngitis and croupous pneumonia, and as it cannot be denied that the epithelium of the uriniferous tubules takes a more active part in the nutritive disor- ders attending acute Bright’s disease than is taken by the epithelial cells of the larynx and air-vesicles in croupous laryngitis and croupous pneumonia. 1. Acute Bright’s disease is a frequent complication of scarlatina. There is a prevalent notion among the laity that a child who dies of dropsy, after scarlet fever, “ has not been well taken care of; ” and many an unhappy mother, who has lost her child from this cause, re- proaches herself for years for having changed its linen too soon, or im- prudently opened a door, and thus brought about her child’s death. It is possible that chilling of the skin during scarlet fever may sometimes favor the occurrence of croupous inflammation, and may even actually produce it, but it is certainly not the case in the majority of instances. Besides the disturbance of the skin which it occasions, scarlatinous virus constantly induces disorders of the fauces and kidneys. In most ACUTE BRIGHT’S DISEASE. 11 epidemics they are of a hypersemic nature, and give rise to the weli- known symptoms of catarrhal angina in the throat, and in the kidneys cause renal catarrh, as described in the foregoing chapter. There are malignant epidemics of scarlatina, however, which give rise to much graver disorder of these organs. Instead of simple catarrh, there is nearly always a diphtheritic inflammation of the fauces, and, instead of a simple renal hyperaemia, the urinary tubules are attacked by croupous inflammation. In such epidemics, many children die of dropsy who have received the best possible care, while many, who have been actually neglected, escape unscathed. The virus of measles, typhus fever, and the poison of malaria, may also induce croupous nephritis, but they are far less frequent causes of the disease than is scarlatina. 2. Acute Bright’s disease arises during the typhoid stage of chol- era, and by many is regarded as a constant complication, if not the actual cause, of this very common and obscure sequel of cholera. Although we cannot subscribe to this latter opinion, having witnessed the death of many patients from cholera typhoid, whose urine was abundant and free from albumen, yet the frequence of croupous ne- phritis, as a sequel to cholera, cannot be denied. It remains an open question whether the vascular engorgement and inspissation of the blood, which take place in the algid stages of cholera, induce obstruc- tion of the renal capillaries from crowding together of the blood-cor- puscles, and extravasation of plasma and blood into the tubules, or whether the inflammation of the kidneys, like the other inflammatory affections of the typhoid stage of cholera, be ascribable to infection of the blood. It, undoubtedly, is very rare for croupous nephritis, in healthy subjects, to proceed from contusions, the misuse of irritating diuretics, exposure to cold, or other unknown exciting causes. Anatomical Appearances.—The anatomical alterations found post mortem after croupous nephritis are identical with those* so ad- mirably described by Frerichs as the first stage of Bright’s disease, the “stage of hypermmia and incipient exudation.” The kidney is often enlarged to twice its proper size, and its surface is smooth. The tunica albuginea is opaque, injected, and is easily detached. The cortical substance, to whose swelling the increase in volume of the kidney is mainly due, is of a more or less dark-brown color, soft, and easily torn. When cut into, a bloody adhesive liquid bathes the face of the section. Both the superficial and deeper parts of the cortical substance are dotted with dark-red points. The pyramids also are hy- peraemic and striped with red, and an opaque and often bloody liquid is usually found in the calices and pelvis of the kidney, which like- wise are injected with blood. Microscopic examination does not 12 DISEASES OF THE KIDNEF. exhibit any important change in the texture of the kidney. The glomeruli, being overloaded with blood, are very distinct. Extravasa tions of blood are almost always found in the Malpighian capsules and tubules, which account for the blood-red points above alluded to. There are likewise extravasations between the albuginea and the tu- bules. The uriniferous tubules, especially those of the cortical sub- stance, are filled with coagulated exudation. Upon microscopic ex- amination of the liquid expressed from the cut surface of the diseased kidney, we find the cylindrical masses of exudation covered with epi- thelium and blood-corpuscles, forming casts of the tubules. The epi thelium is not materially altered, only moderately swollen and clouded. Symptoms and Course.—Sometimes croupous nephritis is ushered in by a rigor, followed by fever and a sharp pain in the region of the kidney. In addition to this, there is almost always more or less violent (sympathetic) vomiting; indeed, vomiting is a more constant token of incipient disease of the kidney than either fever or pain, and it is well to warn parents of children with scarlatina of the serious nature of this symptom, and to require them to seek medical aid should it arise. The patient feels a constant inclination to pass water, but is unable to expel more than a few drops with each effort. The suppression of urine may be so complete that the whole amount se- creted in course of a day may not exceed an ounce or two. Its spe- cific gravity is high. Sometimes, and for a short time, it may be of the color of pure blood; more usually it is opaque, and of a peculiar dirty reddish-brown hue, and looks as though it really contained dirt. Both urine and sediment have this dirty appearance, which alone, to the eye of an expert, is a tolerably sure sign of acute Bright’s disease. There is a very large quantity of albumen in the urine, and, upon the application of heat and nitric acid, the half or even three-quarters of the liquid will coagulate. Upon microscopic examination of the sedi- ment, we find large quantities of epithelium from the tubules and urinary passages, as well as many blood-corpuscles, and casts stud- ded with blood-corpuscles. [Exact observation has taught us that the vascular walls, when inflamed, become permeable to substances which normally would not pass through them. Hence we may pre- sume that it is not the effect of mere pressure upon the Malpighian tufts, but rather of some change in their filtering power which gives rise to the albuminuria in acute Bright’s disease.] Dropsical symp- toms set in, and in most cases the dropsy soon becomes very se- vere. The face, hands, legs, and scrotum swell up, and the skin is so tensely swollen that an impression made upon it by the finger is soon effaced. The dropsy of croupous nephritis, like that of pa- renchymatous nephritis, as we shall presently see, shows a great ACUTE BRIGHT’S DISEASE. 13 tendency to shift its position, the swelling increasing in one part of the body, while it diminishes in another. When the progress of the disease is favorable, the coagula which block up the uriniferous tubules are washed away, the urine be- comes freer and more abundant, and the albumen diminishes. At the same time there is an abatement of the dropsy, which, in this disease, seems rather to depend upon suppression of the secretion of urine than upon that lack of the albumen in the blood which takes place in acute hydraemia. In the most fortunate cases, the dis- ease may terminate in from eight to fourteen days, recovery being- complete and without sequelae. In very many instances the nephri- tis is accompanied by acute inflammation of the lung, pleura, peri- cardium, or peritonaeum, and it is to one of these complications that the patient usually succumbs in fatal cases. It happens much more rarely that croupous nephritis, instead of terminating in the above manner, gives rise to the so-called uraemic intoxication. It is easy to comprehend that, in consequence of the suppression of the urinary secretion, substances may accumulate in the blood which act perniciously upon the nutrition and functions of the various organs. It used formerly to be supposed that the urea, which is the most abundant of the solid constituents of the urine, and which is the best known of all its organic ingredients, by accumulating in the blood, induced convulsions, coma, and ultimate palsy of the entire nervous system ; and when such symptoms ac- companied suppression of urine, they were called uraemic symptoms, or uraemic poisoning. Frerichs afterward supposed that this toxic effect was due to the presence of carbonate of ammonia, resulting from decomposition of the urea, rather than to the urea itself. This the- ory, however, cannot by any means be regarded as proved, and we must acknowledge that we are unacquainted with the excrementitious material retained in the blood, which exerts so pernicious an in- fluence upon the organism in cases of suppression of urine. How- ever, notwithstanding the rarity of uraemic poisoning in croupous nephritis, yet it is of great importance, as regards both the prog- nosis and treatment of the disease, not rashly to ascribe any con- vulsions or stupor which may arise to inflammation and exudation in the brain. Cases occur in which the convulsions and coma subside as the free secretion of urine is reestablished, and the attack termi- nates favorably. (For further details of the so-called uraemia, and of the frequent dependence of cerebral symptoms upon oedema of the brain, see Chapter IV.) I should finally state that cases of croup- ous nephritis occur in which the disease improves somewhat, but does not subside completely ; the albuminuria continues, and the 14 DISEASES OF THE KIDNEY. character of the acute croupous nephritis (acute Bright’s disease) runs into that of chronic diffuse nephritis (chronic Bright’s dis- ease). I have never seen such a case, and they must be very rare. Treatment.—In recent cases, and in tolerably robust subjects, it is advisable to resort to local depletion over the region of the kid- neys, by means of leeches or cups. The effect of the first applica- tion will decide as to the propriety of its repetition in case of recur- rence of the symptoms. General blood-letting should be rejected, as liable to aggravate the already existing tendency to deterioration of the blood. The use of calomel and other so-called antiphlogistics is equally improper. Warm baths, followed by envelopment of the body in woollen blankets, are much preferable to the internal ex- hibition of diaphoretics. In treatirg of chronic Bright’s disease, we shall go more into detail upon this subject, and upon the brilliant results which are sometimes obtained from diaphoresis. If the bow- els be confined, a few powerful doses of drastic medicine should be given—jalap, senna, or even colocynth. The profuse serous tran- sudation into the intestine caused by these medicines may have a beneficial effect upon the dropsy ; but it sometimes happens that the patient has a violent diarrhoea, and yet the dropsy continues to in- crease rapidly. Mineral waters containing carbonic acid are the most suitable beverage. We should not be too sparing in their adminis- tration, as the increase of pressure in the glomeruli, and the aug- mented transudation, may assist in washing away the obstructing coagula. On the other hand, drastic diuretics are contraindicated, owing to the inflamed condition of the kidney. During convales- cence, and in tedious cases even prior to convalescence, the ten- dency to deterioration of the blood must be combated by the administration of quinine and iron, and a plentiful supply of albu- minous food. CHAPTER IV. CHRONIC DIFFUSE NEPHRITIS CHRONIC BRIGHT’s DISEASE. [Pathology and Etiology.—The following synopsis may serve to give the reader an insight into the present state of knowledge regarding Bright’s disease. We have long made use of Frerichs’s classification of the anatomical stages of the disease : 1st, the stage of hyperaemia ; 2d, that of exudation and of commencing conversion of the exudation ; 3d, the stage of retrogression and atrophy. But it has been found that the first of these conditions properly belongs only to acute diffuse nephritis ; so that for chronic nephritis there CHRONIC BRIGHT’S DISEASE. 15 remain only the stage of inflammatory swelling and that of atrophy and shrinkage. But even the connection between these two stages has been denied by certain authors—Johnson and other English writers—who maintain that these conditions, instead of being phases of one and the same disease, are the products of totally different pathological processes. The very great diversity of opinion regarding the histology of Bright’s disease may be summed up as follows : For some authors the essential primary lesions in all forms of the malady originate in the renal epithelium (Johnson) ; for others, the disease begins only in the interstitial connective tissue (Traube). Others again believe that it may commence in both or either of these tissues. Hence they recognize an intertubular or interstitial, and an intratubular or parenchymatous form of the malady ; but they admit the coex- istence of the two forms. Johnson first pointed out a hypertrophy of the muscular coat of the small arteries, not only of the kidney, but of other organs, and showed that under such circumstances the epithelium cannot remain intact ; and he traces back the hyper- trophy of the left ventricle of the heart, so often met with in Bright’s disease, to the greater resistance opposed in that affection by the hypertrophied vessels. Latterly there has been great controversy upon the views of Gull and Sutton, according to whom, in the con- tracting form of the disease, the primary lesion is not in the kidney at all, but the atrophied kidney is merely one of the lesions which accompany a general disorder of the minute arteries and capillaries, and which consists in a deposit of hyaline lymph in the adventitia of the arteries (seldom in the intima), and in the outer coats of the capillary walls. It must be admitted that shrinking of the kidney and degeneration of the arterial walls often coexist; but further research has shown that such coexistence of the two lesions is by no means constant.] In Bright’s disease the epithelium of the uriniferous tubules exhibits the alterations which we have repeatedly described as char- acteristic of all parenchymatous inflammations. Its cells first in- crease considerably in bulk, through imbibition of an albuminous liquid ; their contents then undergo fatty metamorphosis, by which the epithelial cells gradually become converted into cells of fatty granules. Finally, the cell-membrane perishes, and the fat-globules emerge free into the urinary tubules. While these are the essential changes which the kidney under- goes, in the majority of cases coagulating exudations are also formed in the tubules, and in many instances proliferation of the interstitial connective tissue occurs. Atrophy of the kidney, which sets in 16 DISEASES OF THE KIDNEY. afterward, is the natural and necessary consequence of the inflam- matory process above described. Bright’s disease is a very common affection. Predisposition to it is far less in childhood than in more advanced life. Men are attacked by it somewhat more frequently than women ; persons of debilitated and depressed constitution more readily than those who are robust. Hence the poorer part of the community are more afflicted by the disease than the well-to-do class, being more ex- posed to the evils which produce it. 1. Chief among the predisposing causes of Bright’s disease is the temporary, and in a still greater degree the continual exposure of the skin to the effect of cold and moisture. This accounts for the great frequence of the disease in England, Holland, Sweden, and on the German coasts ; and not only upon that of the North Sea, as Frerichs has assumed, but also upon the eastern shore. In the very moderate number of beds in the Greifswald clinic, there used always to be many cases of Bright’s disease. 2. It would seem that the misuse of irritating diuretics and the incautious exhibition of cubebs and copaiba may sometimes lead to Bright’s disease, although, perhaps, this does not occur very fre- quently. 3. On the other hand, the abuse of ardent spirits unmistakably plays a most important role in the etiology of the disorder, so that Bright’s disease appears almost as frequently among hard drinkers as does cirrhosis of the liver. We have no physiological explanation of this circumstance ; but as recent researches have proved that alcohol taken into the system is not all consumed in the blood, as used formerly to be supposed, but that at least a portion of it, pass- ing through the urinary organs, is eliminated from the system unal- tered, it is conceivable that the alcohol may act locally upon the kidney, just as we have shown it to act in cirrhosis of the liver. 4. Bright’s disease very frequently is associated with tedious suppuration, with caries and necrosis of the bones, the surgical wards of the hospitals always furnishing a rich contingent of this malady ; although the latter causative agents lead to amyloid degeneration of the kidney with equal if not greater frequence. The connection between these exhausting affections and Bright’s disease is obscure. However, just as in other cachectic conditions, so the appearance of inflammation in the most diverse organs is so common an occurrence in these depressing maladies, that it becomes a question whether nephritis holds a closer relationship to such con- ditions than is held by pleuritis, pericarditis, peritonitis, and the like. CHRONIC BRIGHT’S DISEASE. 17 5. Finally, Bright’s disease often accompanies conditions of dys- crasia, resulting from gout, rachitis, syphilis, scrofula, and malarial cachexia, in which, however, besides the inflammatory degeneration, the lardaceous metamorphosis hereafter to be described is often observable. I agree with Traube, that it is improbable that simple obstructive hyperaemia from disease of the heart and the like gives rise to in- flammation of the kidney ; and I believe that, hitherto, there has been a great deal of confusion of this malady with that described in the preceding chapter. Nor can I regard pregnancy as one of the remote causes of Bright’s disease. The albuminuria so com- mon among pregnant women is not generally a result of inflamma- tion, but is rather due to a parenchymatous degeneration of the kidney, to be described in Chapter VIII. [Malarious poison predisposes to Bright’s disease, and, according to Bartels, is one of the most prominent of its causes. But an albuminuria arising during an acute febrile disorder has never been observed to terminate in chronic renal disease. On the other hand, chronic suppuration with continued fever may be followed not only by amyloid degeneration, but also by chronic inflammatory swell- ing of the kidney. Those observers who regard parenchymatous and interstitial ne- phritis as distinct diseases naturally ascribe each of them to differ- ent causes. The causes of that form which develops so insidiously and so very gradually in the interstitial substance are extremely obscure ; and Bartels remarks regarding these so-called “ contracted kidneys,” which he looks upon as a separate disease, that in scarcely one of his cases could his patients even guess at any cause for their malady over and above the influences which always more or less be- set them. English writers ascribe shrunken kidney largely to gout and to lead-poisoning. Dickinson states that twenty-six out of forty-two persons with lead-poison had died of shrunken kidney. While this form of renal disease is more common in advanced age, the other occurs more often between the ages of twenty and forty. In childhood it is rare, if we except cases of acute diffuse nephritis following scarlatina. Pathological Anatomy.—According to the present views of many, the term chronic Bright’s disease must be regarded as em- bracing two distinct forms of nephritis, the interstitial and the pa- renchymatous. The former, according to Klebs, begins with intense hyperaemia, with exudation of a lymph-like liquid throughout the whole cortical substance of both kidneys, which dilates the lymph- spaces of the interstitial tissue, and is accompanied by a constantly 18 DISEASES OF THE KIDNEY. increasing emigration of the white blood-corpuscles. Under favor- able conditions these cells may undergo fatty degeneration, and a complete resolution of the process may ensue ; otherwise they may convert themselves into fibrous tissue, causing permanent thicken- ing with or without shrinkage of the intertubular substance. In such a case as this, the process drags on for years ; and we find after death both kidneys shrunken, sometimes even to a third of their normal size, and the capsule thickened and opaque, and firmly adherent to the parenchyma. The surface of the organ is of a dull brownish-red, here and there of a dirty-yellow hue. The atrophy being complete in some parts of the kidney and less ad- vanced in others closely adjacent to the first, the surface becomes studded with small nodules, some of the size of a pin’s head, and some as large as a pea. Hence the term granular kidney. Such a kidney is very hard and tough. Upon section, the cortical substance is often found to be so much wasted that the secreting parenchyma only forms a narrow rim around the pyramids, while the latter are often but little reduced in size, being but sligthly affected by the disease. Certain whitish stripes sometimes observed correspond to the straight tubules which have become obliterated for want of sup- ply of secretion. The general diminution of the kidney, with atro- phy of many of its glomeruli and tubules, is always in the main as- cribable to the compression exerted by the contracting newly-formed connective tissue ; but other factors also contribute to this, such as wasting of the epithelium and urinary tubules. It is sometimes found that the process of thickening of the tissues is much more pronounced in the Malpighian capsules and their vicinity ; or, on the other hand, the greatest change may be in the tunica propria of the tubules and in the connective tissue between them. Accord- ingly, Traube distinguishes two forms of interstitial nephritis, the circumcapsular and the intratubular, each of which presents certain peculiarities from a clinical point of view. Not unfrequently, in the cortical substance we find numerous small cysts having clear contents, and vai'ying in size from that of a millet-seed to that of a pea. These probably are the product of constriction and dila- tation of parts of a uriniferous tubule, particularly of one of the convoluted tubes. The chronic parenchymatous form is regarded by some observ- ers as an inflammation which occurs exclusively and entirely in the secretory cells of the tubules. We do not hold it proved that there is such a form, and think that there may be confusion with the so- called “opaque swelling” of the kidney epithelium (Chapter VIII.). But we find that in some cases the elements of the tubules take CHRONIC BRIGHT’S DISEASE. 19 little part in the inflammatory process which is going on in the in- tervening tissues, while in others it is the prevailing seat of the dis- order. We believe that it depends upon the degree of the inflam- mation whether the secretory or merely the interstitial part of the organ shall be invaded. We shall see by and by that chemical ob- servation also teaches that cases of a very tedious insidious course betoken an interstitial disease, w7hile, on the other hand, chronic cases of a more active and less protracted form indicate the exist- ence of the parenchymatous disease. In the acute diffuse nephritis above described, the implication of the renal parenchyma proper is most apparent both from a clinical and anatomical point of view. If we trace back the difference between the parenchymatous and interstitial forms to a gradual variation in grade of the inflamma- tion, the existence of many intervening forms will be easy of com- prehension. In the chronic parenchymatous form, the kidney, in consequence of swelling of the epithelium and of deposits of exudation in the tubules, becomes very soft and swollen, sometimes to double its nor- mal size. The vessels of the cortical substance are bloodless (in the cadaver at least), the capsule is opaque and easily detachable, and beneath it the renal surface looks pale or yellowish, except where one or two venous trunks remain filled with blood. Upon section it is seen that the enlargement is all due to swelling of the cortical substance, which is sometimes an inch thick ; and that the pyramids take no part in the pallid coloring of the cortical sub- stance, but often form a marked contrast with it by their deep-red hue. Here and there a Malpighian body still remains like a red point on the pale field. The chief seat of the morbid process is in the convoluted tubules of the cortical substance, while the straight tubules of the pyramid rarely, and in but small degree, exhibit the exudation which causes the swelling and softening of the cortical substance. The cylindriform deposits, which occlude and render varicose many tubules, consist partly of swollen fatty epithelium, partly of lymphatic elements (pus) and blood-corpuscles, but espe- cially of hyaline or granular cylindrical masses. Many observers assume that, after a certain duration, the en- larged kidney gradually shrinks and atrophies, and suppose the atrophy to arise from the perishing of the glomeruli, by pressure of the intracapsular exudation, and the collapse of their tubules which have lost their epithelial lining. Even admitting the occurrence of such obliteration of some of the tubules, it may be questioned whether atrophy of the kidney can really be brought about through such a process alone, and without the concomitant thickening of 20 DISEASES OF THE KIDNEY. the intertubular tissue by interstitial nephritis. In fact, even the eminent authorities who believe in the distinct nature of the two forms of nephritis, nevertheless admit the possibility of the exist- ence of many intermediate or combination forms between the two. {Bartels.) To conclude our description of the pathological anatomy of this affection, it may be well to remark that in many instances the morbid changes which take place in the kidney are by no means easy of recognition by the naked eye. When the inflammation is of moderate extent, we often find merely a few pale-gray streaks lying in the renal tissue, which in all other respects looks perfectly healthy. Sometimes, when the disease is diffuse and scattered, it would be impossible without the aid of the microscope to de- termine with certainty its presence in the tubules and interstitial tissue. The numerous consecutive changes which chronic diffuse nephritis is apt to bring about in other organs and tissues will be duly mentioned when we come to discuss the symptoms of Bright’s disease.] Symptoms and Course.—Pain in the region of the kidney, which has been reckoned by most authors as among the most constant symp- toms of morbus Brightii, according to my observation, is wanting in the majority of cases throughout the entire course of the disease. It is true, that if we press with great force upon the kidney, the patients complain that the procedure is uncomfortable and distressing, but we shall hear a like complaint from well folk, whom we may subject to similar infliction. It is as unusual for the attention of the patient to be called to the grave nature of his disease by any marked diminution in the amount of urine which he passes, as it is for* him to suffer pain in the renal region. After the dropsy and the albuminuria have placed the diagnosis beyond a doubt, most patients, if asked whether they have passed too little urine in the course of their disease, will not only deny it, but will even declare that throughout the entire duration of their dropsy they have made a great deal of water. Such an account as this, from a patient with chronic dropsy, is in itself suggestive of the probable dependence of the dropsy upon chronic renal disease. On the other hand, if a patient assert that his dropsy has developed grad- ually, and that since its commencement he has always passed remark- ably little urine, there is a certain amount of presumption that the dropsy is of cardiac or pulmonary origin, and that it does not proceed from disease of the kidney. However, we must not ignore the fact that such statements from patients, as to their passing an unusual quantity of water, are often the result of a delusion upon their part. An inclination to pass water frequently, a symptom due to sympathy of CHRONIC BRIGHT’S DISEASE. 21 the urinary bladder, and common both to chronic and to acute Bright’s disease, but which is never very severe, impresses the patient with the idea that, in his frequent acts of micturition, he has discharged a large quantity of water. Accurate measurement of the amount passed in twenty-four hours shows that, in many cases, it does not quite reach the normal flow. In others it is normal; while in others, again, the proper quantum is really exceeded. A considerable diminution of the normal secretion or actual suppression of urine seldom occurs, and then merely forms, as it were, a short episode in the disease. This peculiar behavior of the urinary secretion, in chronic Bright’s disease, is alto- gether enigmatical. The slighter degree of suppression, which is the most frequently observed, admits of the easiest explanation; as the obstruction of numerous tubules by swollen and degenerated epithe- lium would obviously impede the outflow of the urine, and the com- pression of many of the glomeruli must effect a diminution in the amount of urine secreted. But how shall we explain the fact that, in many instances, in spite of this hinderance to the discharge, and in spite of the limitation of the secreting surface, the flow of urine still remains normal, or even is abnormally profuse ? Plow account for the fact that the increase in this secretion is peculiarly common in the third stage of the disease, at a period when the kidney is atrophied, and when many of its tubules and Malpighian capsules have collapsed and wasted away ? We admit that the hypertrophy of the left ventricle of the heart may perhaps assist in augmenting the secretion of urine bv increasing the pressure within the glomeruli, which still remain intact, thus hastening the filtration of liquid through them; but its influence is by no means to be so highly rated as to suppose that the absence of many defunct glomeruli can be more than compensated for by in- crease of internal pressure upon those which remain. Nor does the collateral fluxion to the remaining glomeruli, induced by obliteration of the blood-vessels in the affected portion of the kidney, do more than to explain why there is not a material decrease in the secretion of urine, and by no means accounts for its augmentation. There is some probability that privation of the blood of its albumen may have some effect in increasing the secretion from the kidney. As is well known, a liquid will pass more freely through an animal membrane from a dilute solution of albumen, than from a solution which is more concen- trated, the pressure being the same. But even this does not seem tc account for the increased production of urine which we so often observe in the third stage of Bright’s disease. Although, as before said, neither pain in the region of the kidney, nor any unusual flow of urine, calls attention to the grave disease which is going on, yet its recognition is no longer difficult, since it has 22 DISEASES OF THE KIDNEY. become the practice of the better class of physicians to make careful examination of the urine. Hospital patients do not generally apply for aid until the dropsy has appeared. Exclusion of other causes of dropsy will establish a strong presumption that we have a case of Bright’s disease to deal with. Examination of the urine places the diagnosis beyond a doubt. In private practice, the observant and ex- perienced .practitioner will have recognized the disease before the dropsy sets in. The history of the case is almost invariably as follows : The patients have long remarked a failure of their strength, and a pallor and anaemic aspect of their skin, and visible mucous membranes. As all their functions are apparently normal, they are unable to ac- count for this paleness and debility. The physician, after careful ex- amination of all other organs, can find no appearance of disease to which the loss of strength and impoverishment of the blood can be ascribed. He examines the urine, and finds it to be loaded with albu- men, and the symptoms are accounted for. No elaborate demonstra- tion is required to show that, in addition to the other expenditures of the blood, a daily loss from the blood of large quantities of albumen, which may amount to from twelve to twenty grammes in the twenty- four hours, cannot be made good by the daily supply of nourishment; or, in other words, a person subject to a daily drain from his blood of from twelve to twenty grammes of albumen necessarily becomes pale, bloodless, and enfeebled. As an examination of the urine reveals the existence of the disease before the occurrence of the dropsy as well as after it, it will be well to give a more detailed account of the charac- teristics of the urine secreted in parenchymatous nephritis. It is gen- erally of a pale-yellow color, and often exhibits a somewhat opalescent reflection. As it is more viscid than common urine, on account of the albumen which it contains, it is more easily made frothy than urine free from albumen, and the froth lasts longer. When there is no in- tercurrent febrile disease, its specific gravity is remarkably low, and may sink to 1005. This is principally on account of a decrease in its urea, and in a lesser degree owing to a diminution of the salts, especial- ly the alkaline chlorides. The reduction in the amount of urea cannot at first be ascribed to its retention in the blood. It would seem rather that, just as in other hydraemic conditions in which the urine is abnormally light, the metamorphosis of material in the body is going on more slowly than is natural, thus retarding the production of urea. The explanation of Schmidt as to the decrease in the saline constitu- ents of the urine, especially its alkaline chlorides, is less satisfactory, namely, that the saline ingredients of the blood augment as its albu- men diminishes, and vice versa. When the patients are already drop- sical, the transfer of the chlorides into their dropsical effusion is a CHRONIC BRIGHT’S DISEASE. 23 phenomenon of far greater importance. The significance of this cir- cumstance consists in the fact that, as long as the dropsy keeps in- creasing, the saline contents of the urine are very small, but whenever any rapid diminution of the effusion takes place, the salts are elimi- nated into the urine more freely, much more freely, indeed, than under normal conditions. If a portion of the urine be heated, after addition of a few drops of acetic acid, in case its reaction should be alkaline, or if nitric acid be added, the albumen coagulates. According to Frerichs, its quan- tity ranges from about 2.5 to 15.0 p. M. This presence of albuminuria, which usually persists throughout the whole course of the disease, and only disappears now and then, for short periods, unfortunately cannot be satisfactorily accounted for. One might be led into mistaking the albumen and the exudation cylinders for the products of inflammation, excreted from the free surface of the tubules, were it not that, in other and non-inflammatory diseases of the kidney, the urine contains both tube-casts and large amounts of albumen. I believe the presence of albumen in the urine to depend upon the destruction or degeneration of the epithelium. That normal urine should not contain albumen is confessedly extremely perplexing to the physiologists. They are al- most forced to suppose that the albumen does transude into the kidney, together with the water and salts; and they are reduced to the hy- pothesis that its absence from normal urine is in some way connected with the epithelial lining of the uriniferous tubules, the transuded albumen either becoming assimilated for the nutrition of the epithe- lium, or else its diffusion into the tubules, receiving some other modifi- cation, as yet unknown to us, from the epithelium. The observation that albuminuria exists in all diseases of the kidney, in which its epi- thelium is either degenerated cr destroyed, fully confirms this physio- logical hypothesis. After the urine has been allowed to stand for a while, a light, whitish, flocculent precipitate falls to the bottom of the vessel. If this sediment be placed under the microscope (for this purpose it is best to let it deposit in the bottom of a pointed champagne-glass), the well- known casts are found. At the commencement of the disease they are covered by epithelium, in a state of fatty metamorphosis ; at a later period, they seem quite bare, or are merely covered with granules and globules of fat. Besides this, the sediment contains common epithe- lial cells from the urinary passages, and smaller round, slightly-gran- ular cells. [By many the so-called urinary cylinders are supposed to be a product of the blood ; others ascribe their origin to alteration of the epithelium. They probably originate in various ways. The 24 DISEASES OF THE KIDNEY. cylinders should he distinguished from those so-called epithelial tubes formed by separation of long pieces of the lining of the straight tubes, and recognizable under the microscope as oblong rolls of epithelial cells. Such casts appear in the less serious dis- eases of the kidney ; hence their temporary presence warrants a favorable prognosis unless gainsaid by other signs. The cylinders proper belonging to the graver malady are solid plugs of exudation which have filled portions of tubes. There are two typical forms of them, with intermediate varieties : 1. Hyaline casts, which, though well defined, are transparent as glass, and hence are apt to be over- looked unless foreign matter adheres to them ; 2. Granular casts, more or less closely studded by minute fat-globules. Hyaline casts are probably formed by the exudation of a fibrogenous substance, which becomes fibrin within the tubules. Some ascribe their ori- gin to colloid metamorphosis of the epithelium. Another special modification of the hyaline cast is the waxy cast, which proceeds from the former, and is to be distinguished from it by its greater consistence, its yellowish color, and its more distinct outline. By many, granular casts are supposed to be the product of fatty meta- morphosis of hyaline cylinders ; others regard them as the result of croupous degeneration of the tubular epithelium. Other objects are often found adhering to the casts, such as pus, white blood-cor- puscles, blood-disks, degenerated epithelium, and clusters of fat- globules, vestiges of broken-down cells ; likewise the various crys- tals which are found in the urine. All the above-named objects are also found free in the urine of Bright’s disease. During an in- flammatory relapse an exceptionally large number of casts will appear in the urine ; otherwise they are not numerous, and some- times can only be found after filtering the urine and examining the dregs. Urinary casts are not a pathognomic sign of Bright’s disease, for they are found, as we shall see, in other renal affec- tions ; nor can we positively determine the form or stage of the disorder from the character of the casts. Nevertheless, the discov- ery of many casts, both hyaline and granular, with here and there an adhering lymph-cell or granular epithelial cell, favors a diagno- sis of an active progressive inflammation (a parenchymatous ne- phritis) ; while, if the casts are few, small, and hyaline, or if they are absent altogether, the urine being profuse, clear, and scant of sediment, we may suppose the disease far advanced, and that the kidney is shrunken (interstitial nephritis).] Dropsy is one of the most characteristic signs of Bright’s disease, excepting in a few rare instances, in which it has been absent through- out the entire course of the malady. It generally begins as anasarca. CHRONIC BRIGHT’S DISEASE. 25 At first the face and feet swell, the upper extremities, abdomen, and scrotum not becoming affected until a later period. The oedema often shifts its position in a peculiar manner, so that at one time the face or upper extremities may be the more swollen, at another the feet, ab- dominal walls, or scrotum, while the tumefaction subsides in the region at first affected. Moreover, if the patient be out of bed, the feet gen- erally show the greatest amount of swelling in the evening, while in the morning the feet are smaller again, and the swelling involves the hips, back, and hands. The more slowly the anasarca develops, so much the more does the skin lose its elasticity, and so much more slowly is the imprint of the finger effaced from the oedematous surface. The addition of ascites and hydrothorax to the anasarca does not take place until a more advanced period. In one exceptional instance, I have witnessed the appearance of hydrothorax and oedema of the lungs early in the disease, where previously there had only been a slight oedema of the integument, a condition of apparent security thus sud- denly becoming one of great danger. In cases which advance rapidly, the dropsy may attain great magnitude in a few weeks. I have seen a patient who weighed a hundred kilogrammes (i. e., two hundred and twenty pounds), who affirmed that, eight weeks before, he did not weigh fifty. Such extreme dropsical swelling, from the strain which it exerts, may be the cause of inflammation and gangrene of the skin, especially of the scrotum and labia majora. In the worst cases, the skin often bursts at several points, and the liquid trickles copiously from the rents. The pathogeny of the dropsy of parenchymatous nephritis is ex- ceedingly difficult of explanation. As is already stated, the dropsy often develops in the midst of a copious excretion of liquid from the kidneys, and hence cannot be ascribed to any increase of pressure upon the veins of this organ, although this must be regarded as the main cause of the dropsy of acute croupous nephritis, in which disease there is always a suppression of urine. It is true that, during any check to the secretion of urine which may occur in this disease, the dropsy makes rapid headway; and when the urine is scanty through- out the entire course of the malady, the dropsy soon becomes exces- sive, and the malady runs a subacute course. There is no doubt but that a “ hydraeinic crasis,” a lack of albumen in the blood, favors the occurrence of dropsy. Owing to the continual loss of albumen, which the blood is suffering, in Bright’s disease, a liquid which contains but little albumen flows through the capillaries of the system. Hence, an abnormal transudation takes place from the capillaries into the inter- stices of the tissues, and hence, too, the amount of serum returned to the veins is abnormally small. It is not to be doubted that the al> 26 DISEASES OF THE KIDNEY. sorption of liquid from the interstices of the tissues into the vessels is more active, in proportion as the difference in concentration in the liquid contained in the vessels and that without them is greater. Now, as, in parenchymatous nephritis, this difference is abnormally small, it follows, of course, that not only more liquid should leave the vessels, but that less should return to them. I have observed cases at my clinic which confirmed the correctness of this in the most strik- ing manner. A girl, who had been suffering for a year from paren- chymatous nephritis, stated that, some time before the appearance of the oedema, she had felt exceedingly dull and miserable. Being con- sidered plethoric, she was advised to get bled. A week after the blood-letting, the first symptoms of anasarca showed themselves, and since then have never entirely disappeared. It may be inferred in this case that the hydrasmia, which, though extant in moderation, still had not as yet produced dropsy, was so much aggravated by the blood- letting as to cause the dropsical symptoms to appear. In another case, the patient became anasarcous after a haemorrhage, but the ana- sarca afterward disappeared for a while, and set in anew after the es- tablishment of profuse suppuration. Nevertheless, hydraemia is not the sole cause of Bright’s disease, and probably not even its chief cause. Dropsy, as severe as that seen in Bright’s disease, is hardly ever observed in any other form of hydnemia. It often occurs early, but does not keep pace with the privation of the blood of its albumen. The peculiar manner in which the oedema shifts from one region to another is another argument against its dependence upon simple hydraemia. If we abstract blood from an animal, and inject a corre- sponding amount of water into its veins in its stead, the animal does not become dropsical. Finally, the dropsy is so very often accompa- nied by attacks of inflammation as to indicate that, besides the thin- ning of the blood, there is another source both of the transudation and exudation, consisting in some disorder of the tissues as yet unknown to us. It sometimes happens that the continual aggravation of the symp- toms above described, and the excessive dropsy, which finally may in- volve the serous sacs and alveoli of the lungs, cause death without further complication. In most cases, however, remissions occur, in which the condition of the patient improves, the albumen in the urine diminishes, and the dropsy subsides. After a while he grows worse again, perhaps once more to improve at a later period, and thus the disease will fluctuate. In such protracted cases the above symptoms are seldom the only ones, but are accompanied by others which arise in part as complications of the main disease, and in part are immediate consequences of it. CHRONIC BRIGHT’S DISEASE. 27 Of these, inflammation of the lungs, of the pleura, pericardium, perito- naeum, and meninges, deserve the first mention, as they are extremely frequent complications of Bright’s disease, and because it is of these intercurrent affections that the patient most frequently dies, far more frequently, indeed, than of the so-called uremic symptoms—to be de- scribed presently—or even of excessive dropsy. Such inflammations of the lungs, pleura, etc., do not differ from similar inflammations in other conditions of anaemia. The patient seldom succumbs at once to the first attack; and we not uncommonly find vestiges of previous inflammation, such as adhesions of the pleura, pericardium, and peri- tonaeum, besides the marks of the final seizure. Parenchymatous nephritis is often complicated by catarrh, particularly by catarrh of the bronchi and intestine. There is nothing peculiar about the for- mer, although in some cases the secretion is tolerably copious. The latter, however, is almost always characterized by a very abundant serous transudation, and by its extreme obstinacy. It would seem that the same cause which induces the escape of such large quantities of liquid into the subcutaneous connective tissue also gives rise to this immense transudation upon the free surface of the bronchial and in- testinal mucous membrane. Nevertheless, since the dropsy is not in- variably accompanied by catarrh, it must be admitted that its origin is somewhat obscure. According to my experience, chronic oedema of the lung is of very common occurrence in Bright’s disease. It gives rise to great dyspnoea, to a tormenting cough, and, at the climax of the coughing-fit, not unfre- quently induces vomiting. I have had repeated opportunity of observing, whenever the vomiting caused the patient to eject much secretion, that his breath became freer for a while, his cough ceased, and that the fine subcrepitant rales subsided. Paroxysms of so-called urinous asthma, which are said to occur in Bright’s disease, are probably de- pendent in a great degree upon oedema of the lung. Many patients with parenchymatous nephritis suffer from disease of the heart. Besides the adhesions of the heart and pericardium from former pericarditis, and the valvular derangement resulting from endocarditis, none of which are uncommon in Bright’s disease, we very often find a hypertrophy of the heart, and more especially a hypertrophy of its left ventricle. Traube has advanced the theory that this hypertrophy is a result of derangement of the circulation of the kidney, which he claims should augment the labor of the heart. This theory is disputed by Bamberger and others, who reply that the hypertrophy develops in a stage of the disease when no obstruction of any importance to the circulation of the kidney ex- ists. A more extensive collation of facts will be necessary to decide 28 DISEASES OF THE KIDNEY. this disputed point; but, at all events, enormous hypertrophy of the heart sometimes occurs even in the second stage of Bright’s dis- ease, and assuredly the circulatory disturbance of the kidney is not the sole cause of it. As is well known, the signs of the enlargement are not very striking, but, by paying attention, we can often detect an augmented heart-shock, or, in its absence, hear remarkably loud car- diac sounds. In a great number of cases, the symptoms of the so-called uraemic poisoning do not appear at all throughout the entire course of the com- plaint. Sometimes they develop slowly and gradually; sometimes they come on very suddenly. At times (but not always), the attack is preceded by a decrease in the secretion of urine, and in rare instances it has happened that, during or immediately prior to the appear- ance of the uraemic phenomena, the normal flow of urine has been largely exceeded (Liebermeister). It is a suspicious sign when pa- tients complain of severe headache, and become languid and apathetic, and still more so, if these symptoms be accompanied by vomiting, which occasionally is so very obstinate as to awaken apprehension of serious disorder of the gastric mucous membrane. All these sym{>- toms may subside again, without evil consequence; in other cases, however, the drowsiness increases to a deep stupor, or convulsions of an epileptic or more rarely of a tetanic character may arise. Even when the convulsions have not been preceded by drowsiness, they are usually followed by a condition of deep coma with stertorous breathing. The fits recur at longer or shorter intervals, the stupor meanwhile con- tinuing to grow deeper; and the patient may finally succumb to gen- eral paralysis. It is not at all rare, however, for the fits gradually to become less frequent, the intervening stupor less profound, and for the signs of “ uraemia ” to disappear, perhaps not to recur for weeks or months. In a previous section, we have already acknowledged that we are unacquainted with the nature of the poison causing uraemic intoxication. There is a. second difficulty in explaining the uraemia of parenchymatous nephritis, since certain well-attested cases of uraemic poisoning have been observed, in which there was no suppression of urine. If the urea and other material to be eliminated from the blood pass into the tubules by a process of pure endosmosis, it remains in- explicable how these materials can accumulate in the blood when the urine is secreted freely; hence we must assume that the epithelium of the urinary tubules has some important influence over the secretion of urine, and therefore that its disease or death may occasion an ab- normal state of the blood, even though the kidneys continue to dis- charge a sufficient quantity of liquid. Moreover, I think that it would be going too far to attribute all the grave nervous symptoms which CHRONIC BRIGHT’S DISEASE. 29 arise in parenchymatous nephritis—the headache, the convulsions, the coma, etc.—simply to a poisoning of the blood; and for many cases at least I agree to the equally one-sided views of Traube, according to whom the so-called uraemic symptoms depend upon oedema of the brain and cerebral anaemia. Since the first appearance of my text- book, I have been much gratified at the steady advance made by the doctrine which I propounded long ago, that the symptoms of the so- called cerebral pressure, due to encroachment upon the cavity of the cranium, whether by a depression of the skull, haemorrhage, tumor, abscess, inflammatory exudation, or serous transudation, all depend upon an arrest or obstruction to the flow of blood to the ganglion-cells and nerve-fibres of the brain. But, in spite of the experiments of Munk, I hold it to be unproved, and even improbable, that the acute oedema of the brain in Bright’s disease should have an origin different from that of oedema of other regions, or that it should be ascribable to an increase of pressure within the cerebral arteries. Moreover, it seems to me to be extravagant to endeavor to ascribe all cases of so-called uraemia to compression of the cerebral capillaries, and to anaemia of the brain. My position in this question is as follows: In chronic parenchymatous nephritis, various organs are subject to oedema, the precise cause of which is unknown. It is characteristic of this oedema, that it shifts its position. It may attack the lungs at any period, either early or late in the disease, sometimes causing death, and sometimes subsiding again after a short duration. In a manner precisely similar, and for the same unknown reason, the brain may become the seat of an acute or subacute oedema, to which many succumb, while in others the oedema changes its position, and the patients are restored to a state of tolera- ble comfort for a period of variable duration. Many cases of so-called uraemic intoxication, but by no means all, are the result of oedema of the brain, and consequent anaemia of the cerebral capillaries. We may infer that an attack of this kind depends upon such an oedema, and not upon blood-poisoning: 1. When the seizure takes the form of deep coma, with intercurrent eclamptic spasms. 2. When, at the time of its occurrence, the secretion of urine is normal or increased. 3. When the attack is accompanied by marked oedema of the face. 4. When the carotids pulsate strongly during the attack. As we shall see directly, this is a valuable but often ill-appreciated sign of repletion of the cranial space with blood, and of impediment to the exit of the blood from the same. [The temperature in uraemia may be either increased or dimin- ished. According to Bourneville, the average temperature is re- duced, but rises during the fits, and remains high during the inter- vals. In fatal cases it is very high, but it sinks gradually to the 30 DISEASES OF THE KIDNEY. normal when the outlook is favorable. According to prevalent modern views, the cause of the uraemic symptoms is due to insuf- ficient elimination by the kidneys of certain products of the body which, when sufficiently concentrated in the tissues, have a poison- ous action upon them, especially upon certain parts of the brain. This poisonous effect is exercised chiefly by the urea and its prod- uct of decomposition, carbonate of ammonia. According to JRosenstein, however, poisoning by carbonate of ammonia alone induces but one of the trains of symptoms, that of epilepsy, while the agent which produces the uraemia occasions not only epilepsy, but coma, convulsions, and delirium. Moreover, we must remember that in cases of uraemia, even when the presence of carbonate of ammonia in the blood has been demonstrated, the de- pendence of the uraemic symptoms upon its presence has not been proved. The quantity of urea excreted in the course of a day is generally diminished in Bright’s disease. This diminution of the daily quantum of excretion is often considerable at the very time when the secretion of urine is also reduced ; while in patients with extreme polyuria, whose health is as yet unshaken, the quantity of urea excreted, in spite of the small percentage contained in the urine, may even exceed the normal. If the daily excretion of urea is very small, we are justified in fearing that the disproportion be- tween production and excretion may lead to uraemia.] In many cases of Bright’s disease, the patients observe a grad- ual failure of their power of vision ; in others, blindness, more or less complete, sets in suddenly. I have heard a patient, upon com- ing to himself, after a uraemic convulsion followed by coma, ask to have the gas lit, although it was burning brightly at the time. This partial or total extinction of vision, too, used formerly to be re- ferred to uraemic intoxication, and was called uraemic amblyopia or amaurosis. Latterly, however, the real source of this disorder has been found to be an extravasation into the retina, accompanied by inflammation. A diagnosis of Bright’s disease has repeatedly been made by means of the ophthalmoscope alone. In one case which I have watched, the impairment and subsequent improvement of vis- ion which occurred manifestly coincided with the formation and absorption of such extravasations. [This disturbance of vision is not to be confounded with another —urazmic amaurosis—which appears sometimes superadded to an already existing retinitis, and sometimes comes on suddenly with the other uraemic signs, without previous derangement of the sight. In a few days, or even in a few hours, the sight fails so that a light cannot be distinguished ; but should the uraemia subside, vision may CHRONIC BRIGHT’S DISEASE. 31 soon be completely restored again. The speedy abatement of this form of blindness argues against its dependence upon permanent lesions. Somewhat more rarely, deafness and roaring in the ears have been noticed in uraemia. Course.—The course of chronic diffuse nephritis varies greatly. In one class of cases the disease may last for ten or even for twenty years, and may be so latent that the patient is scarcely aware that he is ill, and so that a careless physician who neglects to examine the urine can make but little out of his patient’s persistent but vague complaints of loss of strength and energy, of impaired appe- tite and digestion. When the inflammatory process runs this slug- gish course, the urinary tubules take but little part in the changes which are going on in the interstitial connective tissue. There are but slight and merely transient inflammatory exudations into the tubules, whose epithelium suffers but little direct damage ; hence, in such a case, but few if any casts or other characteristic forms are found in the urine. This languid process results merely in thicken- ing of the renal connective tissue, followed by shrinking. It is this grade of inflammation, according to our view, which marks the dis- tinction, both anatomically and clinically, between the forms of Bright’s disease. Sometimes the disease maintains this insidious character throughout its course. The patient then preserves a tol- erable appearance of health for years. His urine, which is copious and pale, shows but little albumen ; but late in the disease he gen- erally presents signs of a hypertrophy of the heart. In such a death may take place suddenly in a ursemic convulsion, before there has been any dropsy whatever. In other cases attacks of eclampsia recur at irregular intervals. Still other patients die of apoplexy in consequence of the hypertrophy of the left heart and of the accom- panying disease of the arterial walls. In another and larger class the course of the disease is less slug- gish and insidious. The inflammation is more active, and involves the tubules directly, so that dropsy soon develops. In some instances, which nevertheless are rare, the disease progresses steadily and with unabated activity to the end, causing the death of the patient in a few months by dropsy, secondary inflammations, or uraemia. Much more commonly there are marked fluctuations in its intensity. There will be periods, sometimes long ones, in which the urine re- tains its normal volume, is but moderately albuminous, and show's few casts or none at all. The dropsy abates and disappears ; in a word, the symptoms of parenchymatous nephritis fade awray or dis- appear. But between these intervals come exacerbations, during which, in spite of the most urgent and incessant efforts of the 32 DISEASES OF TIIE KIDNEY. patient to micturate, the daily secretion of urine is decreased, the percentage of albumen augments, numerous casts and cellular forms appear in the urine, and the dropsy makes further progress. Dur- ing these long remissions of the malady the diagnosis may be difficult; or beyond a moderate albuminuria, which alone affords no proof of Bright’s disease, the patient presents but vague symptoms, such as gastro-intestinal disturbance, anaemia, and loss of flesh. A patient is thus not unfrequently supposed to be convalescent, or even cured, until, sooner or later, relapses occur ; so that, after an average dura- tion of about two years, he succumbs to dropsy, to secondary inflam- mation of vital organs, or perhaps to uraemia. Should he escape all these dangers for a considerable time (as may happen exception- ally), then the active symptoms of the parenchymatous form of Bright’s disease may give place to that of shrinking and atrophy. There will be a very profuse pale urine, of low specific gravity, containing a moderate quantity of albumen (sometimes, though very rarely, absent), and but few or no casts. Prognosis.—While recovery from acute diffuse nephritis is by no means uncommon, the prognosis in the chronic form of the mal- ady is far less favorable ; and indeed it becomes almost absolutely bad as regards old or neglected cases, or when, from the condition of the heart and of the urine, an irreparable atrophy of the kidney can be made out. Nevertheless, even in some of these cases, though incurable, a hope may be held out of a tolerably comfortable exist- ence for some years, or at least so long as the dropsy is moderate and transitory, as the serous cavities are free, and as the secondary lesions and the uraemia do not appear, and while the patient main- tains his digestive powers. When the disease is recent and has been well and promptly treated, the prospects of complete cure are a little better. Sometimes the malady seems to run a medium course between that of the acute and chronic forms. The immedi- ate danger is then much increased, but the hope that, after many weeks or even months, a complete recovery may take place, is much more warrantable than in the chronic form. In a diffuse nephritis which is secondary to some other grave disorder, such as an old malaria or a tedious suppuration, the nature of the primary affection must be considered in the prognosis.] In respect to the duration and results of Bright’s disease, it may be said that there are cases which run their entire course in a period of from six weeks to three months, and others in which the malady drags on for years. I used to know a physician of large practice in Altmark, who only died within a few years, although he had all the symptoms of Bright’s disease as long as twenty years CHRONIC BRIGHT’S DISEASE. 33 ago. We have already alluded to the fluctuations in the intensity of the symptoms which take place in protracted cases. The most frequent termination of Bright’s disease is death ; although patients more commonly die of the intercurrent inflammations than directly of the disease itself. Complete recovery may possibly take place, but it is extraordinarily rare. The longer the duration of the mal- ady, so much the less is a favorable result to be looked for. In re- cent cases, the question always arises whether we have not to do with a croupous nephritis, which, as we have explained, admits of a better prognosis. Treatment.—The causal indications require that a patient with parenchymatous nephritis should wear flannel next his skin, and ex- change his dwelling, if damp and cold, for a dry and warm one ; and that he should be forbidden to go out at night or in bad weather, even during any temporary improvement. Well-to-do people, who dwell in bleak, damp, windy, seaside neighborhoods, should be in- duced to change their abode. Excesses in spirituous liquors, and the use of diuretics, cubebs, copaiba, and spices, are to be strictly prohibited. The discovery that Bright’s disease is an inflamma- tory affection has done but little toward an efficient treatment of it. The so-called antiphlogistic method is inapplicable to any of its stages. [The practice of blood-letting, the application of cold com- presses, and the use of calomel no longer find advocates. We possess no means of extinguishing this obstinate and refractory disorder. Our task is therefore by no means simple, nor can any uniform plan of management be adopted for all cases. Its treat- ment must be chiefly a treatment of symptoms. The main disor- der can only be attacked indirectly, by seeking to combat the indi- vidual pernicious or dangerous manifestations as they arise, and by striving to remove all influences tending to irritate the kidneys. From this point of view the scope and value of therapeutics in the varying phases of Bright’s disease, as tending to prolong the life and to ameliorate the condition of the sufferer, should not be underrated.] In fulfilment of the indications from the disease itself, derivation from the intestines by drastics, and from the skin by diaphoretics, has been proposed. We shall recur to the employment of this measure while treating of the management of the symptoms, as it often acts favorably upon the dropsy ; but we do not believe that the inflammation of the kidney can be arrested or allayed by such deri- vation. Frerichs speaks favorably of tannic acid, which he gives three times daily, in doses of from two to six grains, in combination 34 DISEASES OF THE KIDNEY. with aloes and in the form of a pill. The elimination of tannic acid through the urine in the form of gallic acid and pyrogallic acid, to which we have alluded elsewhere, warrants this treatment from a theoretical point of view. French# himself admits that, although he has observed a diminution in the quantity of albumen excreted, yet, in chronic cases, he has but seldom seen a complete disappear- ance of it. My own experience does not speak at all in favor of tannic acid. Bad as we have represented the prognosis of parenchymatous ne- phritis to be, we have often succeeded quite brilliantly in palliative treatment, and, in fulfilling the symptomatic indications, the therapeu- tics of Bright’s disease are by no means to be regarded as powerless. We have recognized the loss of albumen from the blood as the imme- diate cause of most of the symptoms of the disease, and hence our most important task by far is to cover the loss of albumen by a diet rich in protein substances, and by appropriate medication. Soft-boiled eggs, milk, strong meat-broths, and roast-beef, in as large quantity as the patient is able to digest, are probably the best preventives of the dropsy; and, while patients in comfortable circumstances often with- stand the loss of albumen with impunity for years, the poor, on the other hand, succumb to it far more speedily, because the former have better means than the latter to supply the daily losses which they suffer. Besides this, a moderate amount of beer or good wine should be prescribed, as by the use of these articles the waste of tissue is retarded and the nutrition promoted. Quinine and iron are the most suitable medicines. The former was thrown overboard by many phy- sicians during the time of a generally prevailing nihilism in therapeu- tics, and its supposed tonic action upon the fibres has been much de- rided. But, in these days of reaction against such nihilism, tonics, and especially the preparations of quinia, have once more come into repute, and, indeed, it would seem that they do exert a beneficial action upon the state of nutrition by diminishing the consumption of material. Preparations of iron are equally appropriate, since their effect upon the formation of blood is most decided, and it is not the albumen of the blood alone but also the red blood-corpuscles which are reduced in quantity in this disease. Neglect of such directions as the above, a blind groping in search of a specific remedy, and a vague, planless ex- hibition of diuretics after the dropsy has set in, are merely so many tokens of incapacity on the part of the physician. In a series of cases, which have been described by Dr. Schmidt, in his inaugural thesis, I have obtained most brilliant results where all other treatment had failed, by putting the patients upon an exclusive diet of milk. The patients did not take a grain of any medicine whatever, but drank CHRONIC BRIGHT’S DISEASE. 35 from five to six pints of cows’ milk daily. After the “ cure ” had beeD continued in this manner for about four weeks, some of the patients who, prior to the treatment, had been in the most wretched condition, had got rid of their dropsy, recovered an appearance of health, and re- gained so much of their strength as to be able to resume their business and even to perform hard labor. The albuminous character of the urine, however, has disappeared in but one case; in all the others it persisted. I am unable to account for the eminently beneficial action of milk upon Bright’s disease. I propose to try whether it be possible to obtain a physiological explanation of these results by a careful analysis of the phenomena attending an exclusively milk diet, during health as well as disease, especially by careful weighing of the body and by taking accurate account of every thing taken into and ejected from the system. If the above measures prove unsuccessful in averting the dropsy, or in allaying that which already exists, the establishment of active dia- phoresis is strongly to be recommended. No benefit, however, is to be expected from the use of spiritus mindereri, the antimonials, and other so-called diaphoretics. I have known patients in an advanced stage of dropsy to rid themselves of it completely, in a few weeks, by the daily use of a hot bath, of a temperature of 80° to 100° F., fol- lowed by sweating for two hours in woollen blankets. The diaphoresis was so great in one case, that as much as 800 cubic centimetres of the sweat which had soaked through was collected in a wash-basin placed undei the bed. All these patients were weighed before and after the sweating, and the clinical journals show that, during the sweating, they had lost two, three, and even four pounds in weight. However, it cannot be denied that, in some cases, this procedure also failed, nor that debilitated patients sometimes suffered so much from the process that I was obliged to desist from it. Finally, I may state that, in one instance, the abatement of the patient’s dropsy was coincident with the first appearance of uraemic convulsions. The profuse drain of liquid from the skin naturally makes the blood more concentrated, and this accounts for the absorption of the interstitial effusion. Since, however, in parenchymatous nephritis, the effusion contains urea and perhaps other salts, it is readily conceivable that an active abstraction of liquid from the system would have the effect of overcharging the blood with these materials, and might thus give rise to uraemia. However, a closer investigation of the cases above mentioned has led to the con- clusion that the supposed connection between diaphoretic treatment and the uraemic symptoms is improbable. Whatever the theoretical objections against the employment of diuretics may be, yet, in desperate cases, recourse should always be 36 DISEASES OF THE KIDNEY. had to them. Squills and other stimulating diuretics must not be em- ployed without the utmost caution, on account of the irritating action which they exert upon the kidneys; but there are certain salts, espe- cially cream of tartar, and the tartarus boraxatus (soluble cream of tartar), which are decidedly beneficial in their effect. The physician above alluded to has repeatedly freed himself of his dropsy through the free use of buttermilk, and the employment of cream of tartar and small doses of Dover’s powder. We have yet to mention the drastics as remedies against the drops}?-. Observations upon cholera have taught us that a heavy drain of water from the intestinal capillaries will render the blood more concentrated, and thereby promote absorption of dropsical collections. There was a very instructive case at the clinic of Tubingen, which has been de- scribed by Liebermeister, wdiere a patient with Bright’s disease was attacked by dysentery and died. In consequence of the thin, copious diarrhoea, the extensive general dropsy, from which this patient had long suffered, was reduced to a minimum a few days before his death. It may also be said in favor of the drastics that, during their employ- ment, the kidneys are saved from irritation. Nevertheless, we should never have recourse to them save in time of extreme need, since the patient is liable to be intensely affected by them, and since, by their persistent use, the digestion becomes impaired. The drastics most frequently employed in treatment of Bright’s disease are, elaterium, gr. I—colocynth, in form of decoction, 3 j— 3 ij, to water, § vj, or else in the form of tincture. As remedies against urasmic intoxication, Frerichs, who ascribes this condition to surcharge of the blood with carbonate of ammonia, has proposed the acids, especially benzoic acid, in order to form harm- less ainmoniacal combinations. In the cases observed by me, I have not been able to perceive any effect from this treatment which is based purely upon theory; whereas strong drastics, and iced applications to the head, always seem to produce a favorable impression. CHAPTER y. NEPHRITIS YERA INTERSTITIAL NEPHRITIS RENAL ABSCESS METAS- TATIC DEPOSITS IN THE KIDNEY. Etiology.—While in acute and chronic Bright’s disease the chief pathological changes take place in the uriniferous tubules, the altera- tions which occur in the intervening substance being altogether of a subordinate and secondary charactei, in the variety of renal inflamma- tion which forms the subject of the present chapter, the disease lies INTERSTITIAL NEPHRITIS—REN AL ABSCESS. 37 mainly in tlie scanty connective tissue which binds the tubules together. The most common causes of true nephritis are as follows: 1. Wounds and contusions. The kidney is seldom subjected to external violence, owing to its sheltered position. It is far more liable to injury from the presence of stones within the pelvis of the kidney. 2. Collections of decomposed ammoniacal urine in the pelvis of the kidney, the result of urethral stricture, enlargement of the prostate, palsy of the bladder from injury of the spine, and so forth. Here the irritation to which the kidney is subject is of a chemical instead of a mechanical nature. 3. Propagation of inflammation from the urinary passages to the kidney. It is easy to comprehend that an inflammation of the pelvis of the kidney, a pyelitis, might readily extend into the parenchyma of the organ, and cause nephritis; but the fact that nephritis is sometimes associated with gonorrhoea, but is not a result of extension of the latter disease by contiguity, and where there is no accumulation of urine in the pelvis of the kidney, is altogether enigmatical. 4. Propagation of the inflammation from the connective tissue of surrounding parts, the peritonaeum and other organs. This is the rarest of all the modes of origin. 5. Embolism of small arteries of the kidney, and the introduction of septic or miasmatic material into the blood. This is the source of the so-called metastatic nephritis, observed in endocarditis, valvular disease of the heart, and in the various disorders classed under the general title of pyaemia, as well as in the infectious diseases. There is usually no doubt as to the embolic origin of the cuneiform deposits, which, in the disease of the heart above alluded to, ocour almost as frequently in the kidney as in the spleen ; but it is sometimes extremely difficult to trace the origin of the small metastatic deposits which form in the kidney during the later stages of septicaemia, puer- peral fever, typhus, etc., to the action of embolism. It is questionable whether interstitial nephritis ever arises from the effect of cold, or from that of acrid diuretics. Anatomical Appearances.—In traumatic nephritis, or in ne- phritis arising from an extension of inflammation from the pelvis of the kidney, or from other organs, the kidney at first is enlarged, and is of a deep-red hue, which is either diffused over its whole substance, or else is confined to single spots in the cortical or medullary portion. Its consistence is much less firm. The albuginea is injected, thickened by infiltration, and easily detached. Upon section, the structure is indistinct, and the boundary between the cortical and pyramidal sub- stance is effaced. A bloody, thick liquid can be expressed from the surface of the cut. At a more advanced stage the redness subsides. 38 DISEASES OF THE KIDNEY. The color of the renal substance becomes of a dirty brown or gray, owing to compression of its vessels by the interstitial exudation, which already, here and there, contains pus. The discoloration usually begins at detached points, of the size of a hemp-seed. As it increases, these spots soften, until they finally break down into a purulent liquid. In this way small abscesses form, by the melting down of the renal substance, under the pressure of the con- stantly-accumulating pus-cells. In the cortical substance, the form of the abscess is more rounded; in the pyramidal, more elongated. The abscesses enlarge and coalesce, finally forming a great sac of matter, which may occupy one-half or even two-thirds of the kidney. Such an abscess may become incapsulated, and long remain embedded in condensed cellular tissue. In other cases, the deposits discharge in various directions, as into the pelvis of the kidney, the cavity of the abdomen, externally through long fistulous tracks, into neighboring parts of the intestine, which have become adherent to the wall of the abscess, or even, through the diaphragm, into an adherent portion of the lung. When the disease runs a more chronic course, it sometimes terminates differently. In such cases the interstitial substance of the kidney undergoes proliferation, while the peculiar tissues of the organ perish. At the close of such an attack of chronic interstitial nephritis, the kidney is irregular, and nodulated in shape. The elevations are more marked than those of the third stage of Bright’s disease, and the albuginea is firmly adherent in the sulci between them. Upon cutting into one of these depressed spots, instead of renal-tissue proper, we find nothing except the indurated substance of a cicatrice. The metastatic nephritis, which accompanies disease of the heart, shows no tendency to suppuration. In recent cases, distinctly circum- scribed, dark-red cuneiform spots are found in the kidney. The base of the wedge lies toward the periphery of the organ, the apex toward its hilus. Microscopic examination shows an intense engorgement of the vessels with dark masses of blood, blood being also effused into and between the tubules. Haemorrhagic infarction of the kidney, when of longer standing, undergoes metamorphosis similar to that already described as occurring in haemorrhagic infarction of the spleen. A dis- coloration commences in the middle of the point of infarction, which, having undergone a complete fatty metamorphosis, and all the fat having been absorbed, cicatrizes, leaving a depressed scar. The me- tastatic deposits which form in the kidney in infectious disease, and in consequence of the absorption of putrid matter into the blood, are generally much smaller, and far more numerous, than the infarctions which occur in disease of the heart. Moreover, their tendency to break down is very great, so that, upon examination, it is not usual to find INTERSTITIAL NEPHRITIS--REN AL ABSCESS. 39 solid spots, but merely abscesses in the kidney, surrounded by an area of redness. Symptoms and Course.—When not of metastatic origin, acute in- terstitial nephritis, like acute inflammation of other important organs, sometimes commences with a rigor. At the same time there are vio- lent pains in the region of the kidney, and, in this form of renal in flammation, there is a pain, which is hardly ever absent, which becomes almost intolerable upon the most moderate pressure, and shoots along the ureters to the bladder, and toward the testicle and thigh of the affected side. The sympathetic vomiting, which we have described as an almost constant accompaniment of acute parenchymatous nephritis, is nearly always present also in this form of nephritis. Owing to com- pression of the urinary tubules and Malpighian capsules by the inter- stitial exudation, the secretion of urine is repressed. That which is passed is concentrated, dark, and is often mingled with blood. The fever which accompanies this disease from the outset is very apt to assume a typhoid character. The patients become disturbed in mind, delirious, somnolent, and fall into a state of stupor, with convulsions; symptoms which are to be ascribed to a suppression of the urine, and to a surcharge of the blood with excrementitial matter. The disease may terminate fatally, in the course of a few days, through general pa- ralysis of the nervous system. The occurrence of suppuration in the kidney may be suspected when the disease continues without remission, and when its course is marked by numerous chills, and, above all, when pus is discharged with the urine. When an abscess forms in one part of the kidney, the rest of which has not been affected, or has regained its healthy condition, the disease takes a more chronic course; but the fever continues, and consumes the patient gradually, who almost always dies sooner or later of a phthisis renalis. To detail the various modi- fications of symptoms which arise from the complications of pyelitis, cystitis, and the bursting of renal abscesses in various directions, would lead us too far. The different courses which the matter may take have already been mentioned above. There is a form of inter- stitial nephritis, which is very difficult of recognition, in which the substance of the kidney gradually perishes, and is replaced by a new growth of connective tissue. A permanent derangement of the urinary secretion, a constant desire to pass water, dull pains in the region of the kidney, dropsy, great listlessness, which gradually increases to coma, with other indications of the so-called uraemic poisoning, are the symptoms of this form of disease, but they are very rarely properly interpreted. Metastatic interstitial nephritis, not having any characteristic symp 40 DISEASES OF THE KIDNEY. toms, is usually overlooked during life. However, I have sometimes noticed that the formation of a large haemorrhagic infarction in the kid- ney is accompanied by a chill, that the patient complains of severe pain in the kidney affected, and that the urine is scanty and contains blood. When we encounter symptoms like these, in a case of disease of the heart, we may confidently diagnosticate the existence of an in- farction of the kidney, particularly wThen there is or has been evidence of embolism elsewhere. Renal metastases, which form during septi- caemia, puerperal fever, etc., are usually mere “accidental” discov- eries upon the dissecting-table. We cannot even suspect their exist- ence during life. Treatment.—As, in most cases of interstitial nephritis, it is im- possible to meet the causal indication when the affection proceeds from the presence of a stone, or from a collection of putrid urine in the pelvis of the kidney, or from embolism or infectious disease, we must confine our efforts to an antiphlogistic treatment, which is much more appropriate in this case than in those heretofore described. The repeat- ed application of leeches, cut cups, and of cold over the kidney, with the subsequent use of long-continued warm baths and warm poul- tices, and the exhibition of drinks containing carbonic acid, are the most approved measures. The sequelae, especially the abscesses and fistulas which may form, must be treated according to the symptoms. CHAPTER YI. PERINEPHRITIS. Etiology.—In rare instances tlie adipose tissue, in which the kid- ney is enclosed, becomes the seat of a primary, independent inflamma- tion, which is usually the result of an injury, or, as has been claimed now and then, of exposure to cold. Much more frequently the inflam- mation is secondary to a suppurative action within the pelvis or sub- stance of the kidney. I have seen one case in which a pericystitis extended along the ureter to the fat around the kidney. Anatomical Appearances.—As a rule, inflammation of the areolar envelope of the kidney soon results in suppuration. The tis- sues then become discolored, and their meshes are filled with pus. The small collections of pus coalesce and an abscess forms, often of very considerable magnitude, and which may point in almost any direction. In other cases there is no suppuration, but the loose cellular tissue be- comes condensed and indurated, and is converted into a thick fibrous rind. Symptoms iND Course.—When perinephritis is acute, its symp- PERINEPHRITIS. 41 toms bear a strong similarity to those of acute interstitial nephritis. A violent fever, which sometimes is ushered in by one or more rigors, and by severe pain in the region of the kidney, which becomes intoler- able whenever the adjacent muscles of the body contract, or are sub- jected to any strain by movement of the body, is a symptom common to both diseases. There is one important distinctive point between the two; in pure uncomplicated perinephritis, there is no suppres- sion of urine, nor does the urine contain either blood, albumen, or pus. If the disease goes on so as to give rise to a large abscess, a tu- mor appears in the renal region, which fluctuates with greater or less distinctness. If the abscess break into the cavity of the abdomen, it occasions an acute peritonitis, which speedily terminates in death. Recovery may take place where the abscess discharges into the intes- tine, or where it points externally, or is opened artificially. External opening of the abscess generally occurs in the back, below the false ribs, and is usually preceded by an excessive aggravation of the pain upon movement of the body, and by a more or less extensive oedema of the skin over the region affected. In other cases the pus descends along the psoas muscle, giving rise to a symptomatic abscess, which usually makes its appearance below Poupart’s ligament. Treatment.—The most appropriate treatment of a recent case of perinephritis is local blood-letting, and, in a later stage of the disease, the systematic .application of cataplasms and, the use of lukewarm baths. Abscesses must be opened as soon as possible, according to surgical rules, and should be kept open for a while. CHAPTER YII. AMYLOID DEGENERATION OP THE KIDNEY PARENCHYMATOUS NE- PHRITIS, WITH AMYLOID DEGENERATION. The kidney, like the liver and the spleen, not unfrequently under- goes a degeneration, by the deposit in the elements of its tissues of a material whose reaction against iodine and sulphuric acid resembles that of the cellulose of plants, but whose chemical constitution is more like that of the protein substances. Amyloid degeneration of the kid- ney takes place under conditions similar to those under which it oc- curs in the liver and spleen, its causes being severe chronic disease, such as syphilis, mercurial poisoning, rachitis, consumption of the .ungs, and long-standing suppuration, such as occurs in caries and necrosis. The degeneration probably always commences in the walls of the blood-vessels, particularly in those of the glomeruli, to which it usually 42 DISEASED OF THE KIDNEY". remains limited; while, at the same time, the epithelium of the tubules undergoes the changes already described in Chapter IV. The name u parenchymatous nephritis, with amyloid degeneration,” is, therefore, more appropriate for this form of disease than the term “ amyloid or lardaceous degeneration of the kidney.” Even microscopic examina- tion is not by itself sufficient to enable us to distinguish between the affection in question and simple parenchymatous nephritis. But, if a thin slice of the specimen be treated for a few moments with a solution of iodine, the red color of the glomeruli becomes so distinct even to the naked eye, that, even before resorting to the microscope, the appear- ance of a multitude of small red dots, standing out in contrast to the surrounding yellow ground, makes the diagnosis almost certain. Under the microscope the loops of the glomeruli seem remarkably large, and present a peculiar dead lustre. The Malpighian capsules, too, often ex- hibit a broad, homogeneous, dull outline. If, prior to the examination, the preparation have been laid for a time in a dilute solution of iodine, the bodies above described will assume the characteristic yellowish- red color. Upon the subsequent addition of a few drops of sulphuric acid, they become of an indistinct violet or dark blue. It is very un- usual for the tunica propria, and still more so for the epithelium of the urinary tubules, to participate in the amyloid degeneration. When an individual, who hitherto has enjoyed good health, is affected by albuminuria, dropsy, and deterioration of the blood, it is so very improbable that he is suffering from amyloid degeneration of the kidney, that that disease may confidently be excluded from the diagnosis. On the other hand, the appearance of similar symptoms in a person who has long been afflicted by syphilis, consumption, tedious suppuration, or any other exhausting malady, makes it extremely prob- able that we have to deal with an amyloid degeneration of the kidney, or, more properly speaking, with a parenchymatous nephritis with amyloid degeneration of the walls of the renal vessels. If the patient also have an enlargement of the liver and spleen, and if the portions of these organs accessible to palpation present the characteristic resistance of amyloid degeneration, the diagnosis is still more sure. In distinguishing between amyloid degeneration and simple parenchy- matous nephritis, Traube lays great stress upon the high specific grav- ity and dark color of the urine in the former disease. My own obser vations fully confirm the truth of Traube’s views, and I may add that 1 have been struck, not only by the darkness of the urine, in amyloid renal degeneration, but also by its unnatural, yellowish-brown color; moreover, my colleague, Hoppe-Seiler, has shown that such urine con- tains extraordinary quantities of indican. There is nothing in the quality of the exudation-casts, or in the degree of frequence of uraemic GRANULAR DEGENERATION OF THE RENAL EPITHELIUM. 43 symptoms, whereon to base a differential diagnosis between a sim- ple parenchymatous nephritis and one which is complicated by amyloid degeneration. Moreover, the difference between the two conditions is a matter of but little practical interest. The treatment recommended for amyloid degeneration of the liver and spleen is equally appropriate in amyloid disease of the kidney. It is questionable whether a retrogression of the disease be possible. The preparations of iron and iodide of iron may act beneficially upon the primary disease, but can hardly cure a degen- eration of the kidney. CHAPTER VIII. GRANULAR DEGENERATION OF THE RENAL EPITHELIUM. [Frequently on autopsy we find the kidneys flabby, bloodless, of a pale, dirty, grayish-red color, somewhat enlarged, or of normal size. From their cut surface we may scrape off a cloudy grayish pulp. This pulp consists of epithelial cells swollen by albuminous infiltration and dotted with numerous fine granules, which render the nuclei indistinct, but which vanish in the presence of potash and acetic acid (thus showing that they consist of albuminous particles). At a later period fat-granules may appear. When the disorder is intense, the kidney becomes tender and flabby, and the epithelium falls off ; but, if of only a moderate degree, the cells may undoubt- edly be restored to their normal condition. Proliferation of the epithelium occurs, but very rarely, and then only late in the disease. Granular degeneration is not peculiar to the kidney, but is often found simultaneously in the cells and tissues of the most diverse organs, particularly in the liver, the heart, and the muscles. This widespread appearance of the disease shows that its cause must be a general one. In the bodies of persons who have died of infectious diseases—pyaemia, typhus, or acute miliary tuberculosis—more or less marked granular degeneration is found, as a result either of some abnormity of the blood, or perhaps as a consequence of the persistent elevation of the temperature which attends these diseases, and which, according to Schultze, exercises a most pernicious in- fluence upon cellular formations. But the disorder also is found when there has been no fever, in chronic anaemia, chronic disease of the heart or lungs, and in poisoning by phosphorus, sulphuric acid, and carbonic oxide. Sometimes the cause of the granular de- generation is purely local, and is limited to the kidney where it is found, supplementing other morbid conditions. Very important 44 DISEASES OE THE KIDNEY. results are ascribed to the more intense grades of this lesion. Thus it is supposed in acute forms often fatally to cripple the action of the heart. The condition is also found in the bodies of pregnant and puer- peral women. At present we have no definite knowledge as to how pregnancy affects the minute structure of the kidney and other or- gans in these cases.] The most common and frequently the sole symptom of parenchym- atous degeneration of the kidney is the presence of albumen in the urine. We may say, too, that whenever there has been albuminuria during pregnancy or during grave disease, the renal epithelium will be found to be in a more or less advanced state of degeneration after death. How often the question is asked by the anatomist during the autopsy, whether the patient had albuminous urine! On the other hand, I will not venture to state positively that the albuminuria, which so often accompanies the conditions above referred to, is always the result of degeneration of the epithelium of the kidney, or that degen- eration of the renal epithelium is always attended by albuminuria. The quantity of albumen which the urine contains is probably never so great in parenchymatous degeneration as in amyloid degeneration, and parenchymatous inflammation of the kidney. When it arises after acute febrile disease, it never produces dropsy. This symptom is often absent, too, during pregnancy accompanied by parenchymatous renal degeneration and albuminuria. Sometimes, however, there is a mod- erate degree of dropsy, and in rare instances a very large one. When it accompanies pregnancy, it is sometimes a source of danger, owing to the eclamptic attacks which it provokes during and immediately after parturition, and of which we shall have more to say when we come to treat of diseases, of the nerves. If the original disease terminate in recovery, the nutritive disorders of the renal epithelium to which it has given rise are also completely repaired. Soon after delivery the albuminuria and dropsy disappear in almost all cases, another proof that the malady in question is not to be confounded with interstitial nephritis. We are quite ready to admit that in most cases of eclampsia puerperarum there is renal dis- ease ; but we deem it quite inadmissible to attribute the albuminuria, dropsy, and eclampsia to “ Bright’s disease.” After what has been said already regarding parenchymatous degen- eration, further discussion of its treatment becomes superfluous. We shall treat hereafter of the proper management of the eclampsia. CARCINOMA OF THE KIDNEY. 45 CHAPTER IX. CARCINOMA OR THE KIDNEY. Op the malignant neoplastic growths, carcinoma is the one most frequently seen in the kidney. Renal cancer is sometimes primary; sometimes it accompanies carcinoma of other organs, as a secondary formation. Young persons, and even children, are quite frequently at- tacked, although it is somewhat more common in advanced age. Cancer of the kidney generally assumes the medullary form. Scirrhus and colloid are far more rare. The former sometimes de- velops in the form of circumscribed nodules of varying size, which gradually replace the parenchyma of the kidney. Sometimes the can- cerous degeneration spreads farther and farther into the surrounding tissues from its original point of development, so that the kidney gradually becomes transformed into cancer (Rokitansky, infiltrated cancer). A carcinomatous kidney may attain an enormous bulk some- times, forming a nodular tumor of the size of a child’s head. The de- generation often involves the lymphatic glands in the hilus of the kid- ney, whence it spreads to the retroperitoneal and mesenteric lym- phatics, and to the ligaments and periosteum of the spinal column; or else it may grow inward into the cavity of the organ, and thence into that of the adjoining veins. The frequency with which cancer of the kidney is complicated with cancer of the testis is a matter of impor- tance, which calls to mind the still more common coincidence of tuber- culosis of these organs. Haemorrhages both within the tumor and on its periphery are very apt to occur. In the latter case, the blood is effused either into the peritonaeum or else into the urinary passages. The disease often remains latent for a long time. It is usually by the gradual advance of a marasmus, for which no other cause can be assigned, that suspicion is awakened of the existence of a malignant tumor in a region inaccessible to palpation. There may be no pain at all in the lumbar region, and, when it does exist, it is not character- istic. The renal secretion may go on undisturbed, and the urine may be quite free of blood and albumen. As the disease advances, the tumor formed by the cancerous kidney, which is often of enormous size, can generally be felt through the abdominal walls, especially when the latter have become wasted and relaxed. The form of the tumor, and especially its immobility, will prevent our mistaking the enlarged kidney for an enlargement of the liver or spleen. It cannot be moved from side to side, nor does it follow the motions of the diaphragm. Very large cancers of the right kidney sometimes produce a remarkable and peculiar displacement of the liver inward, causing it to turn upon its 46 DISEASES OF THE KIDNEY. long axis, so as to bring a large part of its convex surface in contact with the abdominal wall. ILematuria and albuminuria are absent about as frequently as they occur. As already stated, part of the bleeding proceeds from the vessels of the growths which push into the urinary passages, while another part is the result of excessive hyper- cernia of the surrounding tissues. Owing to the large quantity of blood thus discharged, the hsematuria often forms one of the most prominent symptoms of this disease. The complexion of the patient assumes the dirty hue so common in cancer, and he dies of exhaustion which progresses all the more rapidly when the haemorrhages are frequent and profuse; unless, indeed, death ensue in consequence of some intercurrent disorder, or from the invasion of other vital organs by secondary cancer. Treatment is ineffectual, and must be limited to husbanding the patient’s strength, repression of the haemorrhages, and removal of coagula from the bladder, according to surgical rules. CHAPTER X. TUBERCULOSIS OE THE KIDNEY. Rokitansky recognizes two forms of renal tubercle. The first form is symptomatic of a tuberculosis involving several or even the majority of the organs. In acute miliary tuberculosis, gray nodules, sim- ilar to those found studding the lungs, pleura, peritonaeum, etc., are also found in the albuginea and parenchyma of the kidney. In extensive chronic tuberculosis, tolerably large, yellow, cheesy deposits of tubercle are sometimes met with in the kidneys, but they rarely contain collec- tions of softened tubercular matter or tubercular cavities. The first of these forms has but little effect upon the action of the organ. It is unrecognizable during life, and is of more moment in a pathological than in a clinical point of view. The second form of renal tubercle is generally complicated with tuberculosis of the testicle, prostate, seminal vesicles, and urinary pas- sages. It is not constantly preceded by pulmonary tubercle; but this disease almost always sets in at a more advanced period of renal dis order. In this second form the deposit is very copious, and the indi- vidual nodules soon coalesce into large tubercular masses. The organ becomes enlarged, assumes an irregular, knobby shape, and within it we find large cheesy collections, some of which are filled with tubercu- lous pus. This form of renal tuberculosis, too, would likewise frequently escape observation, were not the diagnosis almost always aided by the complications above mentioned. The longer a chronic disease of the urinary passages has coexisted with the admixture of pus, and now and PARASITES IX THE KIDNEY. 47 then of blood in the urine, the tuberculous character of which is in- dicated by the coexistence of an enlargement of the testicle, so much the more likely will it be that the lddney itself has become involved in the disease. The diagnosis receives further confirmation if we are able to feel an uneven tumor in the region of the kidney, through the flaccid walls of the abdomen. CHAPTER XI. PARASITES IN THE KIDNEY. The echinococcus is the parasite most frequently found in the kid- ney, although even there it is met with less frequently than in the liver. Its presence in this prgan is originally due to the existence of the embryo of the tenia echinococcus in the intestinal canal (see Yol. I.). We have no knowledge as to why the young brood, in their emigra- tion from the bowel into the other organs of the body, should some- times enter the kidney. The echinococcus sacs, which occasionally attain the size of a fist or of a child’s head, are quite like those found in the liver and spleen. They are embedded in a fibrous capsule be- longing to the kidney. They may atrophy and burst, discharging their contents in different directions. They may also occasion inflammation and suppuration in the parts about them, and the renal abscess thus re- sulting may burst into the peritonaeum, intestine, or pelvis of the kidney. The development of echinococci in the kidney may be entirely un- attended by symptoms. In some instances, however, the patients com- plain of a dull pain in the lumbar region, which we cannot well account for. A tolerably sure diagnosis may be made out if we can feel an i rregular nodular tumor in the region of the kidney, and at the same fime can exclude carcinoma, tuberculosis, and hydronephrosis, to be treated of hereafter. Certainty is only possible when cysts of the echinococci or traces of them are discharged with the urine. The hyaline walls of the daughter cysts, consisting of concentric layers, distinctly recognizable under the microscope, are not easily mistaken. Symptoms of renal colic may arise during their passage through the ureters, and their discharge from the bladder is often attended by the utmost distress, especially in men. [The strongylus gigas is the largest of known round worms. The female may attain the length of half a yard or more. Its mouth is bordered by six wart-like projections. The male is smaller, and at his tail-end has a cup-shaped appendix, at the bottom of which is the genital opening with the penis protruding from it like a hair. The method of development of this parasite has not been ascertained. 48 DISEASES OF THE KIDNEY. Schneider found worms in certain fish which seemed to represent the early forms of a strongylus ; and the fact that the strongylus species most generally infest fish-eating animals argues in favor of this view. Its occurrence in man is very rare indeed. According to Davaine, but seven well-authenticated cases have been collected. We know, however, that in brutes the creature usually occupies the pelvis of the kidney, more rarely descending the ureter into the bladder, and that its presence causes symptoms similar to those of calculus, and may cause retention of urine and hydronephrosis.] CHAPTER XII. DEFORMITIES OF THE KIDNEY IRREGULARITIES OF ITS SHAPE AND POSITION. Absence of one kidney usually is accompanied by abnormal magnitude of the other, and the secretion of urine remains normal. Union of the two kidneys, which then are generally connected by a narrow bridge of renal substance at their lower ends—the so-called horseshoe kidney—is a matter of mere anatomical interest, and of no clinical importance. The same is true also of lobulation of the kid- ney, which depends upon a persistence after birth of the foetal con- dition of the organ, and is distinguishable from an acquired lobular state of the kidney by the healthy condition of the renal parenchy- ma and capsule at the depressed points. Irregularity of position is most common in cases of horseshoe kidney ; the united organs then usually lie much deeper than natural, sometimes as low down as the last lumbar vertebrae. But, even without the coexistence of this malformation, an unnaturally deep position of the kidneys is not an uncommon congenital deformity, and is usually accompanied by irregularity in the origin and number of the renal vessels, as well as by anomaly in the lengths of the ureters. Misplacement of the kidney, with abnormal mobility, is a mat- ter of greater importance. Quite a considerable number of cases of this anomaly have been observed since attention was first called to it. In Greifswald alone I know of three cases of movable kidney. The kidney (and almost always the right one) lies embedded in a loose areolar tissue. Its vessels are elongated, and have a sort of mesentery formed out of the reduplication of their peritoneal coat. Such anomalies are most common among women whose abdominal integuments have become greatly relaxed by repeated child-bearing. According to Ilayer, it may also result from violent concussion of ADDISON’S DISEASE. 49 the body—as from a fall from a great height. In other cases there is no other anomaly, nor is there any apparent cause for the mobility of the viscus. When the patient stands erect, the movable kidney may be felt usually below the liver, or even still deeper. Its char- acteristic bean shape is distinctly recognizable, and it often can be pushed a considerable distance to the right or left, but more easily upward and downward. A patient in my ward, by moving and shaking his body, was able to get his kidney into a great variety of positions. There are either no evil results whatever attending the affection, or they depend upon complications, although colics and slight, inflammations of the peritonaeum may result from pressure of the movable organ upon the other viscera. The knowledge that she has a tumor in her abdomen often acts very injuriously upon the spirits of the patient, who sometimes becomes hypochondriac. Little can be done by way of treatment for a movable kidney ; but the patient (particularly if she have very flabby abdominal walls) generally feels better when she wears an clastic bandage of gum elastic or knit cotton. CHAPTER XIII. addison’s disease—bronzed skin. [This disease, first described by Addison, still presents an obscure problem, notwithstanding the laborious researches of many of our most acute observers (Virchow, Meissner, Averbeck, Klebs, Eulen- burg, Guttmann, Risel, and others). All former doubts as to the real existence of such an independent affection are now dissipated ; but it has been shown that the lesions which used to be thought fundamental and characteristic of it, namely, the morbid state of the suprarenal capsules and the dark stain upon the skin, though commonly present, are not its essential features. The original as- sumption that Addison’s disease depends upon a degeneration and destruction of the suprarenal capsules is contradicted by the nega- tive results of experiments made in seeking out the hitherto un- discovered functions of these organs, as well as by the fact that the capsules have been found destroyed or in a state of disease in bodies of persons who during life presented none of the symptoms of the malady. Attention was thus directed to the sympathetic plexus of nerves adjacent to the capsules, the implication of which in this affection Addison himself had already pointed out; and the opinion was gradually reached by a number of English, French, and German observers that a morbid state of the abdominal sympathetic, par- 50 DISEASES OF THE KIDNEY. ticularly of the coeliac plexus and semilunar ganglia, and of the nerves connecting them with the suprarenal capsules, is of essential importance in the disease. The circumstance which speaks most in favor of this view is, that in most of the cases in which the sympa- thetic has been examined, besides the suprarenal lesion usually present, there has been also found either redness, swelling, thickening, fatty degeneration, atrophy, pigmentation, or wasting of the ganglia. But out of twenty-nine cases collected by Guttmann and Eulenburg the sympathetic was found more or less altered in nineteen and nor- mal in ten. This negative result, though of only a minority of cases, reduces the above attempt at explanation to a mere theory ; the more so when we read that experiments by Adrian Schmidt, Lamanshy, Schiff, and others upon the abdominal ganglia give rise to no symptoms suggestive of Addison’s disease. A further hy- pothesis was then advanced, that the disorder depended upon derangement of the central nervous system and not upon that of the sympathetic ; and Rossbach describes it as a hitherto undefina- ble functional disturbance of the nervous system lying in close re- lation to, but not inseparable from, the suprarenal capsules, and characterized by psychic disorder, intense antemia, debility, and very often by a dark staining of the skin. In order to account for a connection between a nervous disturb- ance and a morbid stain upon the skin, the cases of albinism have been invoked in which the anomaly is very distinctly limited to a district of skin corresponding to a certain nerve-district, as have also the cases of sudden turning gray of the hair under the influence of mental emotion. The deposits of pigment which form in the skin of pregnant women, and in many who suffer from menstrual and uterine disease, have also been pointed out in support of the view that staining of the skin may proceed from disorder of the supra- renal capsules. The anatomical changes of the suprarenal capsules found in Addison’s disease are not always the same. In most cases there is a caseous fibrous degeneration resulting from chronic inflammation of the organ. The capsules are often of two or three times their normal size, sometimes even as big as a hen’s egg, and are converted into masses of dense connective tissue containing cheesy or calcare- ous nodules. Their surface is irregular and knotty, and often adhe- rent to adjacent structures. Their consistence is tough and hard. The inflammation, instead of being general, may however be only partial and limited to single spots. The disease is generally bilateral. The many cases in which both capsules have been found totally destroyed argue against the theory that the suprarenal capsules are ADDISON’S DISEASE. 51 secreting organs, and Addison’s disease a result of over-production of deleterious chemical matters in the blood (particularly tauro- cholic acid), which partially dissolves the blood, thus causing the anaemia, while a precipitation of the pigment of the blood occasions the bronze color. In rarer cases, instead of this degeneration, we have found carcinoma, extravasation of blood in the tissues of the capsules, and sometimes simple atrophy ; hence it must be concluded that the bronze color is not due to any special process. The imme- diate cause of the brown skin is a deposit of pigment in the rete Malpighii ; but pigment-cells are also to be found in the true skin, and are to be distinguished from those in the rete Malpighii by their containing iron. There are sometimes no lesions whatever of other important or- gans ; but more frequently there will be found enlargement of the spleen and of the intestinal follicles, cheesy degeneration of the mes- enteric glands, and sometimes caries of the vertebrae.] Symptoms Course.—The darkening of the skin, whence the malady derives one of its names, although it is by no means its most important or most dangerous symptom, occurs gradually. If the patient die before it has become very pronounced, it is apt to be overlooked entirely. Such cases, however, do not disprove the con- nection between disease of the suprarenal capsules and the deposit of pigment in the rete Malpighii. It is only by degrees that the discoloration of the linea alba and nipples' in pregnancy acquires a sufficient degree of intensity to become conspicuous, and indeed there are many persons in whom it is never very marked even at term ; and yet no one denies the existence of a connection between pregnancy and such pigmentary deposit. t In some instances the skin becomes so dark as to resemble that of a mulatto or negro. One of my patients, a baker, from Ileil- bronn, used to be generally known as “ Black R .” The color sometimes is a pure gray, inclining to black, like plumbago. At other times it has a brown or yellowish tinge. It generally com- mences upon the exposed parts of the body, but, although more in- tense upon those regions, is by no means confined to them, a cir- cumstance which might save us from errors of diagnosis in dealing with sailors, field laborers, and others whose hands and faces are often of an exceedingly dark grayish-brown tinge. The roots of the nails also remain white. The palms of the hands and soles of the feet are spotted here and there, but are not uniformly discolored. The sclerotica never participates in the discoloration, and its pearly hue often forms a marked contrast with the dark color of the face. Black spots upon the lips and mouth seem to me to be pathogno- 52 DISEASES OF THE KIDNEY. monic of the affection. At all events, no mention is made of them in any of the negative reports of bronzed skin without disease o' the capsules. Its more serious symptoms consist in an extreme debility, ofter combined with deep depression of spirits. In some instances this debility increases from time to time into profound and long-con- tinued swoons. Sometimes the adynamic symptoms are so promi- nent as to remind one of a severe attack of typhus, or of some other acute affection, with so-called typhoid symptoms. Mistakes for typhus, however, may always be avoided if all the elements of the case be attentively considered, especially if the temperature be ob- served. If, however, the case has not been long under observation, and if the discoloration of the surface be not very distinct, it may be impossible to make a positive diagnosis. The great lassitude and insurmountable sense of weakness, unattended by any apparent cause of exhaustion, would seem to proceed from a disorder of in- nervation. The richness of the suprarenal capsules in nervous ele- ments, and the numerous communications existing between them and the various nervous plexus, especially the solar plexus, rather confirm such a supposition. Pain in the back, and still more frequently pain in the epigas- trium, is a very fi*equent but not a constant symptom. In one of my cases the pain was so violent that the patient for weeks was treated with poultices. In a second, severe pain in the epigastric region was one of the most conspicuous symptoms, wdiile in the third the patient never complained of pain at all. Dyspepsia and vomiting are reported as occurring in nearly every case ; yet even these symptoms are sometimes absent. The vomiting of Addison’s disease may be regarded as a so-called sym- pathetic vomiting ; since, in disease of other organs adjacent to the stomach, and even in such as contain fewer nerves than the suprarenal capsules, and whose nervous connection with the stomach is much less obvious, such sympathetic vomiting occurs. Diarrhoea has been observed in many cases. In two of my three cases the dirrahoea was very obstinate. It would be easy to account for this diarrhoea, could it be proved post mortem that the coeliac ganglion always was diseased ; since, according to the experiments of Budge, all the rabbits whose coeliac ganglia he removed suffered from diarrhoea. But independently of this, there is nothing sur- prising in the occurrence of diarrhoea in disease of the suprarenal capsules, these organs being richly endowed with nerves, and stand- ing in intimate relation with the nervous plexus of the abdominal ADDISON’S DISEASE. 53 organs, and since, too, there is no doubt as to the dependence of liquid discharges upon disturbance of innervation. The convulsions and other grave nervous disorders which some- times occur are difficult to account for. One of my patients had repeated epileptic attacks. Post-mortem examination usually affords no clew as to the origin of these symptoms. The temperature of the body is not increased, unless there be some complication of a febrile character. The beat of the heart and the pulse is accelerated, and toward the close of the malady is often extremely feeble. The great fre- quence of the pulse stands in striking contrast with the lowness of the temperature, and, if no note be taken of the latter, it is liable to cause an erroneous impression that there is fever. The progress of the disease is almost always chronic. There are but two or three known cases where the process has run an acute course, speedily terminating in death. Although there are a few cases in which a temporary improve- ment has been observed, yet we have no well-authenticated instance of complete recovery ; and death must be regarded as the most fre- quent, and probably, indeed, as the sole termination of this malady. Treatment.—Of course, the treatment of Addison’s disease must be a mere treatment of symptoms. In one of my cases it was very evident that good nourishment and careful nursing were not without a beneficial effect upon the course of the disorder. The patient, a poor servant, was repeatedly received at the clinic, in a state of extreme emaciation/and unfit for any labor. He always gained considerably in weight in the course of a few weeks, and so far recovered his strength that he could be employed in a variety of occupations ; until, three years and a half after his first recep- tion at my clinic, he suddenly and unexpectedly died in one of the above-mentioned epileptiform attacks. SECTION II. DISEASES OF TIIE PELVIS OF THE KIDNEYS AND URETERS. CHAPTER I. DILATATION OF THE PELVIS OF THE KIDNEY, WITH ATROPHY OF THE RENAL SUBSTANCE HYDRONEPHROSIS. Etiology.—Whenever the flow of the urine, through the ureters, into the bladder, becomes permanently obstructed, the urine accumu- lates in the pelvis and calyces of the kidney. If the pressure of the urme within the pelvis of the kidney be very great, the openings in the tubuli recti and papillae are closed, and the papillae themselves be- come compressed. The urine then ceases to flow from the kidney into it« pelvis, and distention of the latter would progress no farther were it not that the pelvis and calyces possess a mucous membrane, and still continue to produce mucus, which is mingled with the accumulated urine. Hence more and more liquid collects in the renal pelvis, dis- tending the latter, till finally the pressure flattens out the papillae, and induces a gradual atrophy, which may terminate in the total loss of the substance of the organ. Closure of the ureter may proceed from the impaction into it of a stone. Far more frequently, hydronephrosis depends upon compres- sion of the ureter by a tumor, or by a callous contracting cicatrix in the peritonaeum which covers it, or by a growth, especially by a cancer, of the subperitoneal connective tissue. In other cases, closure of the ureter is the result of inflammation, which has induced swelling of its mucous membrane, or adhesion of its walls. The lower and the closer to the bladder the obstruction is, so much the larger is the portion of ureter which takes part in the dilatation. Moderate degrees of dilatation of the uriniferous apparatus some- times arise from an impediment to the discharge of urine, which exists DILATATION OF THE PELVIS OF TIIE KIDNEY. 55 in the urethra or bladder, but, in such cases, the affection being bilat- eral, the dilatation of the renal pelvis can never become so great as to close the mouths of papilke of the kidneys without involving danger to life. It seems strange that, on autopsy, hydronephrosis of both sides, which seems to have existed a long time, is frequently found. Anatomical Appearances.—According to Rokitansky, in the milder degrees of hydronephrosis, the papillae are shrunken, hardened, and leathery. Gradually the papillae disappear in the concavity of the dilated calyx, while above it the renal substance diminishes, its tissues becoming compressed, leather-like, and tough. In extreme cases, the substance of the kidney is only a line or two in thickness, finally dis- appearing, leaving a membranous sac, of a lobulated appearance exter- nally, and cellular within. The cells communicate with each other, their wTalls having burst or atrophied ; they contain a urinous liquid, clear and serous, or turbid and containing a sediment, varying greatly in character. These sacs may attain the size of a child’s head, or even that of a man’s. A dilated ureter may attain almost any conceivable size, its calibre equalling or even exceeding that of the small intestine. The walls of the ureter are thickened, and the tube itself, instead of running straight to the bladder, is tortuous and convoluted, like a gut. Symptoms and Course.—Hydronephrosis cannot be detected, ex- cept in its most intense form, and, of course, this cannot exist when both ureters are obstructed. The secretion of urine is not diminished, as the active kidney acts vicariously for the disabled one. There may not be any pain in the lumbar region. Diagnosis is solely based upon the discovery of a somewhat soft and indistinctly-fluctuating tumor in the region of the kidney. If there be any temporary abatement of the obstruction to the escape of urine from the organ, the tumor may diminish from time to time, and such an occurrence sometimes aids the diagnosis. When the sac becomes inflamed (as has sometimes been observed), there is much pain, accompanied by severe rigors. The pus which forms may point in various directions, thus giving great diversity to the character of the symptoms. Should the impediment which has obstructed one ureter extend so as to prevent the flow of urine into the bladder from both kidneys, all secretion of urine wall cease, and the patient will speedily perish, under symptoms of uraemia. Treatment.—If the obstruction lie in the urethra only, diligent catheterization may prevent dilatation of the urinary passages, or arrest such dilatation when it has commenced. It is out of our power, how- ever, to arrest or to allay the graver forms of dilatation with atrophy of the renal substance, which proceed from obstruction of a ureter unless the obstruction of the ureter be caused by a tumor, susceptible of relief by medical or surgical interference. 56 DISEASES OF THE PELVIS OF THE KIDNEYS AND URETERS. CHAPTER II. Etiology.—In rare cases, the pelvis of the kidney is the seat of a croupous or of a diphtheritic inflammation. This is usually accompa- nied by similar inflammation of other mucous membranes, and is usually a concomitant of infectious disease. It is most commonly observed in the typhoid stage of cholera, but may also proceed from catarrhal in- flammation, especially that arising from calculous pyelitis. Catarrhal pyelitis, in the great majority of cases, is the result of an irritation of the mucous membrane, induced by the presence of calculi in the pelvis of the kidney. In similar manner, the ammonia of stagnant and putrid urine may provoke a most intense catarrh of this region. Much more rarely, catarrh of the urinary passages is caused by acrid substances, such as cantharides, the balsams and resins, which have been taken into the .system, and excreted with the urine. Again, we frequently find pyelitis as the result of severe gonorrhoea, the inflammation having extended to the bladder and ureters. A mild form of catarrhal pyelitis is a common complication of Bright’s disease. It sometimes appears during pregnancy, and during the later stages of typhus, as well as during the desquamative period of the acute exanthemata. A hasmorrhagic form of this affection sometimes accompanies scurvy, and the morbus maculosus of Werlhof. Anatomical Appearances.—In croupous or diphtheritic inflam- mation of the pelvis of the kidney, its mucous membrane is found either to be covered by membranous exudation, or else is converted into diphtheritic eschars, which, upon separation, produce irregular losses of substance. In recent cases of catarrhal pyelitis, the mucous membrane is red- dened bv injection, and (especially in the scorbutic form) by ecchy- mosis. At the same time, it is relaxed, and covered by purulent mucus. When of longer standing the redness disappears, or becomes discol- ored, the tissue of the mucous membrane is swollen, and, in some cases, is incrusted with urates, or with salts of lime. The pelvis of the kidney usually is dilated, and its walls are thickened. Not unfrequently, the renal parenchyma has suffered atrophy, as in hydronephrosis. In cases of long-continued mechanical irritation, there often is ulceration of the mucous membrane, which may terminate in its perforation, followed by infiltration of urine into the surrounding areolar tissue, with suppurative destruction of the latter. The resulting abscesses may point in various directions, as into the cavity of the peritonaeum, or externally, forming long fistulous openings; or, previously forming adhesion, it may burst INFLAMMATION OF THE PELVIS OF THE SIDNEY PYELITIS. PYELITIS. 57 into some neighboring organ (such as an intestine). Now and then the liquid contained in the pelvis of the kidney is gradually absorbed. The pelvis shrivels into an indurated tissue, which incapsulates its in- spissated contents, the ureter becoming obliterated and converted into a tendinous cord. Symptoms and Couese.—Croupous and diphtheritic pyelitis are scarcely ever recognized during life, as in the majority of cases they are only partial manifestations of those grave and wide-spread disor- ders which attend the malignant infectious diseases, septicaemia, scar- latina, small-pox, or the typhoid stage of cholera. Sometimes wThen ca- tarrhal calculous pyelitis becomes aggravated into the croupous or diph- theritic form, shreds and lumps of fibrin are discharged with the urine Acute catarrhal pyelitis may commence with a rigor or with re- peated chills, and be attended by febrile symptoms. The patients complain of pain in the region of the kidney, which radiates along the ureters, toward the testicles, and which is increased upon pressure. When the inflammation has been severe, I have also repeatedly observed vomiting, even in the cases where the disease had spread from the urethra to the pelvis of the kidney. A frequent and sometimes pain- ful inclination to pass water is a constant symptom. According to Oppolzer, the secretion of urine increases ; this may to some extent be due to hypermmia of the kidney, in the parts supplied by the vasa afferentia; but if the pyelitis be complicated with interstitial nephritis, the secretion of urine may be diminished in amount. Very often at the outset the urine contains blood, in greater or smaller quantity; and it always contains pus, and in some cases, but not in all, tesselated epi- thelium, lying row upon rowr, detached from the pelvis of the kidney. If the disease be of long duration, still more pus appears in the urine. When recently passed, the latter is opaque; after standing a w hile, a wrell- defined sediment is deposited, of a yellowish-white color. Owing to the pus serum which it contains, the supernatant liquid shows the characteristic coagulation of albuminous urine upon the application of nitric acid and heat. The microscope shows the sediment to con- sist of innumerable pus-cells. In pyelitis calculosa, affecting one side only, the impaction of a calculus sometimes causes a temporary but complete arrest of the flow of urine from the pelvis of the kidney. Any urine which is then discharged from the bladder must, therefore, proceed from the healthy kidney. Hence, as long as the obstruction continues, the urine is usually quite limpid, although the symptoms are all aggravated. When the obstruction is removed, the urine again be- comes turbid. One patient, whom I have seen, had learned, by ex- perience, that her suffering would be more severe as long as her urine remained clear; and she used to long for the time when pus would be- gin to pass again. 58 DISEASES OF THE PELVIS OF THE KIDNEYS AND URETERS. Owing to persistent suppuration, and to the slow fever which gen- erally accompanies it, chronic pyelitis may lead to marasmus and dropsy, terminating in death. When due to stones in the renal pelvis, the chronic disease is liable to acute exacerbations, particularly after any jolting of the body; or else periodical haemorrhages occur, which accelerate the exhaustion of the patient. Violent pain in the back, difficulty of motion of the spinal column, pain on drawing up the thighs, aggravation of the fever, and repeated chills, are indicative of threatening perforation of the wall of the renal pelvis. After per- foration has actually occurred, and when an abscess has formed in the surrounding tissues, the disease assumes the characteristics of perine- phritis. A tumor which fluctuates more or less distinctly is found in the region of the kidney, etc. (see Sec. I., Chap. VII.). When the ab- scess bursts into the peritoneal sac, the patient speedily perishes, with the symptoms of acute peritonitis. If the pus burrow downward, a cold abscess forms, which makes its appearance in the lower part of the back, beneath Poupart’s ligament, or in the perinasum. If the perforation take place into the intestine, masses of pus are discharged with the stools; the tumor which had formed diminishes or disappears entirely, and a more or less permanent recovery takes place. It is not always easy to decide if a pyuria originate in the bladder or in the pelvis of the kidneys. In a pyelitis without implication of the bladder, the desire to micturate may be very troublesome, and the act of urinating may be accompanied by pain in the urethra. In chronic pyelitis as well as in chronic cystitis, the urine contains quantities of pus-cells, which render it cloudy, and when it stands for some time they sink to the bottom as a whitish-yellow sediment. The idea that the acid reaction of such urine indicates a pyelitis, while alkaline reaction speaks for a cystitis, is not absolutely correct; for in chronic vesical catarrh even when of long standing it is generally acid, and only becomes alkaline in the bladder under certain circumstances, of which we shall speak when treating of catarrh of the bladder. Another criterion also, which I formerly considered valuable in the diagnosis of pyelitis from cystitis—namely, that in inveterate vesical catarrh the purulent sediment was usually mixed with quantities of mucus, while in chronic pyelitis the urine did not contain a trace of mucus—is not always true. The mucous masses evacuated in the urine in some cases of chronic vesical catarrh are the result of mucous trans- formation induced in the purulent secretion from the vesical mucous membrane by alkaline fermentation of the urine. If the urine does not undergo this decomposition in the bladder, when freshly passed, it will contain no mucous masses; but, if we leave urine with a simple purulent deposit (wnether it come from the bladder or the pelvis of STONY CONCRETIONS IN THE PELVIS OF THE KIDNEY. 59 the kidney) in an open vessel till it undergoes alkaline fermentation, the sediment will become tough and mucous. We can only be sure of disease of the pelvis of the kidney, when we find connected groups of spindle-shaped flat epithelium in the urine, especially after violent exercise. But, even in cases where the patient com- plains of pain in the region of the kidneys, extending thence to the pelvis and testicles, we must not be misled, by any existing dysuria, into the diagnosis of pyelitis. Treatment.—For acute catarrhal pyelitis we may refer to what has been said already concerning acute interstitial nephritis. At the outset, the application of leeches, cut cups, as well as of cold, over the region of the kidney, is advisable; and, when the pain and strangury are very severe, the exhibition of opium and the subcutaneous injection of a solution of morphine. In order to dilute the urine as much as possible, the patient should drink freely of liquids, avoiding the use of salted or spiced food or beverage. The employment of alkalines, and the alkaline-saline mineral waters of Vichy and Karlsbad is deserv- edly in repute in the treatment of pyelitis. If the malady assume a tedious form, let the patient use long-continued warm baths, and apply hot poultices to the lumbar region. The acratothermae are coming more and more into use in the treatment of pyelitis and its kindred complaints. At the baths and springs of Wildbad, I have seen the utmost benefit result from making the patient spend as long a time in the bath as possible, and causing him to drink as much of the pure lukewarm water of the springs as he could take without inconvenience. We do not attempt to decide whether camphor, which enjoys so high a reputation as a remedy for all irritations of the urinary passages, really exerts the beneficial action ascribed to it. Where there is tedious suppuration, astringents should be employed, especially tannin, for reasons already given. In order to diminish the production of pus, we may also try whether the patient will bear the exhibition of the balsams, especially copaiba. For this purpose, Oppolzer recommends the patient to drink lime-water and milk (aquae calcis, milk, aa lb. £ to lb. ij. daily). CHAPTER III. STONY CONCRETIONS IN THE PELVIS OF THE KIDNEY. [Etiology and Pathology.—Stony concretions may form in any part of the urinary passages, from the uriniferous tubules to the bladder. They may assume the shape of a fine powder (sand or 60 DISEASES OF THE PELVIS OF THE KIDNEYS AND URETERS. gravel), or form masses varying in size from that of a mustard-seed to that of the fist. They are classified, according to their composition, into—1. Those composed of pure uric acid, or of uric-acid salts ; 2. Those composed of oxalate of lime ; 3. Stones of phosphate of magnesia and ammonia and phosphate of lime ; 4. Stones of car- bonate of lime ; 5. Cystine calculi; 6. Xanthine stones. Besides these, there are stones of several components, which are often so formed that around a nucleus alternating strata are superimposed, which vary as the conditions for the excretion of the different ma- terials have varied from time to time. The most common of these stratified stones are composed of a nucleus of uric salts or of oxa- late of lime covered by shells of phosphatic matter. The causes of urinary calculus are many, and in part still un- known. The formation of uric-acid stones is ascribed to the long- continued over-acidity of the urine, due either to the actual increase in the quantity of the acid in the body as a result of imperfect oxy- genation, to a sluggish mode of life, to a diet too rich in flesh, or to lack of the supply of oxygen, or else to such an increase of the free acids of the urine that the soluble uric salts which it contains are decomposed, and the uric acid separated. This may proceed from an acid fermentation within the organ, in which the coloring and extractive matter of the urine turn into lactic acid, or else an acid- ification in the primary passages favors such an excretion. Con- ditions which produce a concentrated urine, as abstinence from water, persistent diarrhoea, or badly-compensated heart-disease, may also give rise to such excretion. Oxalate-of-lime stones, generally called mulberry calculi, have likewise various modes of origin. Sometimes, when the urine is alkaline, the acid forms in the urine itself, probably through decom- position of the uric acid. Sometimes the stone forms when the diet has been exclusively vegetable, from excessive use of sorrel, tomatoes, and the like. Again, these calculi may appear under con- ditions of body not fully understood ; but, as we know, the charac- teristic crystals of oxalate of lime are found in the urine of many patients of sluggish habit, disordered digestion, or derangement of the respiratory or nervous apparatus. Stones of phosphate of lime or ammonia, or of a mixture of the two, are apt to form wherever a long-continued alkaline condition of the urine produces alkaline precipitates in it. Such decomposi- tion of the urine may proceed from chronic inflammation or other diseases of the urinary tract, due to retention of urine. It may be caused by the use of foul catheters, or by the presence of a foreign body, such as a uric-acid or oxalate-of-lime calculus, which thus may STONY CONCRETIONS IN THE PELVIS OF THE KIDNEY. 61 furnish a nucleus for a phosphatic shell. From the experiments of Studensky, who inserted foreign bodies into the bladders of dogs and put lime into their food, it would seem that an excess of lime in the food predisposes toward phosphatic calculi. Even the phos- phates which properly exist in the body may by morbid and exces- sive transformation produce stones in the urine, as sometimes hap- pens in osteomalacia. Gravel and stones form at all ages of life. In childhood, how- ever, the disposition toward stones—perhaps through uric-acid in- farction of the new-born—seems the greater ; and in old age it is also common. That men should suffer more often than women would seem to be because of their different modes of life. How much geological and climatic influences have to do with endemic tendency to stone in certain countries, as England, Holland, and parts of Germany, has not been made clear. Concretions rarely form in the kidney-substance proper ; but cases like those of uric-acid infarction of the new-born have been seen in the adult, in which uric acid was found after gout, hsema- toidin crystals after haemorrhage, and bile-pigment after jaundice. Carbonate of lime, too, has been met with. Real stones are also found as very great rarities in the kidney proper, or rather in por- tions of the dilated uriniferous tubules. The ordinary seat of gravel and of stone is in the calyces or pelvis of the kidney. The smaller stones are roundish ; larger ones mould themselves to the shape of the region which they occupy, so that stones of the calyx acquire a pyramidal form.] Stony concretions form in the pelvis of the kidney, probably xmder the same conditions which cause them to form in the bladder. When treating of vesical calculus, we shall discuss the pathogeny and etiology of these calculous formations more fully. Many, and perhaps the majority of stones in the bladder, originate in the pel- vis of the kidney, and pass thence through the ureters into the blad- der, where they increase in size by precipitation from the urine. Anatomical Appearances.—In cases of uric-acid infarction, upon section through the pyramid, we see delicate yellowish-red stripes running in the direction of the tubules. Upon microscopic examination, these tubules are found to be filled with a blackish, coarsely-granular material. Upon the addition of an acid, these masses disappear, and are replaced by crystals of uric acid. Ac- cording to Virchow, dilatation of the tubules and the formation of cysts in the kidney of the foetus may arise from permanent obstruc- tion of the efferent tubules. In the luemorrhagic-pigmentous in- farction we also see red streaks, with a tinge of yellow in them, in 62 DISEASES OF THE PELVIS OF THE KIDNEYS AND URETERS. the pyramidal substance ; and, under the microscope, the tubules are seen to be filled with granular, or globular, or lumpy masses, and with the well-known hsematoidin crystals. In calcareous in- farction, whitish-yellow stripes are found in the pyramids ; and, under the microscope, black masses are visible in the tubules, which dissolve with effervescence upon the addition of acid. The deposits of triple phosphate, which also produce yellowish-white stripes in the pyramids, sometimes coalesce into stones of the size of a hemp- seed, and may cause suppuration and destruction of the renal pa- renchyma. Calculous concretions which form in the pelvis and calyces of the kidney have the same chemical composition as vesical calculi. There is great variety in their size, shape, and number. The smaller ones are no larger than a grain of sand, and are of a rounded form, or else have the shape of a calyx of the organ. The larger ones, which may be of the size of a pigeon’s or hen’s egg, fill up the whole renal pelvis, often forming a complete cast of its shape, and of that of the calyces. Symptoms and Course.—Red gritty deposits upon the napkins of newly-born infants, which cease to appear in the course of a few weeks, constitute the sole and not very trustworthy sign of the ex- istence of uric-acid infarction. That of calcareous infarction and the presence of phosphatic deposit in the tubules cannot even be suspected during life. In many instances stony concretions in the pelvis of the kidney give rise to no symptoms whatever. We often enough see small urinary calculi, which certainly must have formed in the kidney, voided with the urine, the patient never having suffered the slight- est inconvenience prior to their discharge. In other instances there is renal haemorrhage, and in others the signs of pyelitis calculosa. (See Chapter II.) Some persons experience a sense of weight and of pain in the lumbar region whenever the body is jolted. As these symptoms are very ambiguous, we are not warranted in in- ferring even the probable existence of a renal calculus from them, unless from time to time the pain grow worse, with slight attacks of fever, and unless, after such exacerbations, the urine contain fine granular sediment, or small fibrinous clots incrusted with crystals, and a few blood-corpuscles, or perhaps perfect calculi. In two of my cases, the diagnosis of renal calculus wras strength- ened by the fact that, on examining some flocculi which swam in otherwise limpid urine, groups of connected epithelial cells, of the characteristic form of epithelium of the pelvis of the kidney, were recognized ; and they showed no signs of fatty metamorphosis, and STONY CONCRETIONS IN THE PELVIS OF THE KIDNEY. 63 bad sharp outlines and distinct nuclei, which rendered it probable that they had been detached by some mechanical force. The passage of a calculus through the ureter is sometimes at- tended by symptoms to which the term renal colic has been applied. Clots of blood and parasites passing through the ureter may like- wise give rise to renal colic ; and it is not impossible, though very improbable, that a mere spasm of the ureter may sometimes have like effect, but such cases are comparatively rare. It is incompre- hensible why large stones often pass unnoticed through the ureter, while much smaller ones (which are not always rough or angular) may cause intense anguish. In this affection, the patient (often after a severe jolting) suddenly feels a frightful pain darting from the kidney toward the bladder, and thence to the thigh and testicle. He screams and writhes with agony, and grows cold, prostrate, and demoralized. Though constantly striving to micturate, but little water flows. Vomiting is frequent, so that the seizure is apt to be mistaken for biliary colic or enteralgia. In irritable subjects there may be convulsions. Sometimes temporary remission interrupts the torment of the patient—soon, however, to be followed by renewed and violent exacerbations. In other cases the pain increases stead- ily, and then ceases as suddenly as it commenced ; and, unless the calculus give rise to fresh trouble by its presence in the bladder, a complete recovery ensues immediately. Such attacks may pass off in a few hours, and rarely last over twenty-four hours ; and, in spite of the formidable aspect of its symptoms, life is hardly ever en- dangered by renal colic. Sometimes, though not often, the im- provement is incomplete ; the pain diminishes, but does not cease entirely, the symptoms of colic becoming complicated with those of pyelitis. Treatment.—The treatment of uric-acid and calcareous infarc- tions is, of course, out of the question. In discussing the treat- ment of vesical calculus, we shall speak of the procedures theoreti- cally proposed for the purpose of dissolving stones, and shall then point out their inefficiency. In treating renal colic, it is merely necessary that the physician be sure of his diagnosis, in order to obtain the happiest results. He must not content himself by applying leeches, giving restora- tives for the small pulse and cool skin, or with other useless half- measures, but should boldly order opium every hour or two. The anaesthetic action of the opium alone is insufficient to account for the relief which usually follows this treatment. It is much more likely that the muscular fibres of the ureter, which have been thrown into a state of contraction by the irritation of the stone, 64 DISEASES OF THE PELVIS OF THE KIDNEYS AND URETERS. which they have spasmodically grasped, are relaxed by the narcot- ism induced by the opium. If the opium given internally be vom- ited, a subcutaneous injection of morphine may be used. Inhala- tion of chloroform vapor seems to have an action similar to that of the opium, and is the next best remedy. In like manner, a copious blood-letting may be of service, from the relaxation to which it gives rise ; but in most cases this may be dispensed with. The patient, however, who is demoralized by pain and terror, will not be satisfied by the mere hourly administration of a powder and the inhalation of chloroform. He will loudly demand that something more be done for him, and, as a matter of humanity, we should yield to his entreaty. If circumstances permit, let him make use of a warm sitz-bath or complete bath. It has also often been recom- mended to seat the patient naked upon a stool, and to lay his bare feet upon a cold floor. As a beverage, copious draughts of some mineral wTater, containing carbonic acid, should be prescribed, in order, if possible, that the urine pressing after the stone may drive it before it into the bladder. CHAPTER IV. CARCINOMA AND TUBERCULOSIS OF THE PELVIS OF THE KIDNEYS AND OF THE URETERS. Carcinoma of the urinary passages is rare. It scarcely ever occurs except where cancer of other organs, especially of the kid- ney, extends into the walls of the renal pelvis. In rare instances, independent nodules of cancer appear in the pelvis of the kidney and ureters, accompanying carcinoma of the bladder or kidney. Tubercle of the uriniferous apparatus has already been alluded to in treating of tuberculosis of the kidney, and was there stated to be a partial manifestation of a general disposition to tubercle, in- volving the testicle, prostate, seminal vesicles, and kidney. The diffuse caseous decomposition, which the mucous membrane of the urinary passages presents, cannot always be referred to the forma- tion and softening of discrete tubercular granulations ; although sometimes nodules as large as a millet-seed, either in groups or dis- crete, and (where these have broken down) round or irregular ulcer- ations, are found upon the mucous membrane. Sometimes the uni- form proliferation of cells and their caseous metamorphosis convert the inner wall of the ureter and of the pelvis of the kidney into a yellow pultaceous mass. In other places the degenerated mucous CARCINOMA AND TUBERCULOSIS OF THE KIDNEY. 65 membrane is fissured and broken down, containing extensive losses of substance. Under sucb circumstances the urinary passages are always much dilated, and their wall thickened. Tuberculosis of the uriniferous apparatus is easy of diagnosis, when it can be ascer- tained by palpation that the prostate and testicle also are diseased, and when the urine is alkaline and mingled with pus and debris. Extension of tuberculosis from the bladder to the ureters is so com- mon an occurrence that it may always be anticipated in such cases. SECTION III. DISEASES OF THE BLADDER. CHAPTER I. OATAltRH OF THE BLADDER CYSTITIS CATARRHAL1S. Etiology.—Catarrh of the urinary bladder may arise: 1. From direct irritation of the vesical mucous membrane. Unskilful injections in gonorrhoea, frequent or rude catheterization, foreign bodies, espe- cially calculi, may also produce the affection. The admixture of acrid substances in the urine, or the formation of irritating matter in the bladder, owing to decomposition of the urine, may give rise to a most intense form of catarrhal cystitis. To this class the vesical catarrhs belong, which are induced by the misuse of cantharides and of balsam copaiba, as well as those which arise in cases of spinal disease, typhus, stricture, and enlargement of the prostate, and other conditions caus- ing retention of urine. In the same way, drinking of new beer will occasion a very transient catarrh of the bladder.* 2. In other cases catarrhal cystitis arises from the extension of an inflammatory irrita- tion from other organs to the bladder. First under this heading stands the cystitis which accompanies inflammation of the prostate, and in many cases of gonorrhoea, and which often long outlasts the original disease. 3. Chilling of the skin, especially of the feet and abdomen, not unfrequently results in catarrh of the bladder. 4. Finally, a symp- tomatic vesical catarrh is one of the concomitants of growths and other grave disorders of the bladder. Anatomical Appearances.—In acute cases the mucous mem- brane of the bladder is reddened, swollen, and relaxed. Its surface is covered with mucus, mixed with detached epithelium and young cells in variable quantity. In chronic catarrh of the bladder this redness of the mucous mem- brane fades, and the color sometimes becomes a dirty gray. The mu- cous membrane is swollen and thickened. The submucous and inter- * Or is this annoying but harmless and transient malady due to acute irritation of the urinary passages by large sharp crystals of oxalate of lime, which may appear after drinking bad beer containing much carbonic acid ? I have often urged my students (but hitherto in vain) not to miss an opportunity of examining microscopically the urine passed during such an attack. CATARRH OF THE BLADDER—C OSTITIS CATARRHALIS. 67 muscular connective tissue, and the muscular fibres themselves, are also thickened and hypertrophied. Upon the inner surface of the blad- der there lies a gray puriform mucus, or a yellowish purulent secre- tion. The urine contained in the bladder is often decomposed, is of an acrid ammoniacal odor, and alkaline reaction. Chronic catarrhal cystitis rarely terminates in recovery. Far more frequently, as the malady advances, the proliferation of cells upon the free surface of the bladder is complicated with a vast cell-growth in the tissues of its mucous, submucous, and muscular coats. In this way catarrhal mucous ulcers and submucous abscesses are formed. Perforation of the vesical wall sometimes takes place. Should this occur after the bladder and its neighboring organs have become con- solidated by pericystitis, abscesses may form around the former, which, under favorable circumstances, may open either externally, or into the rectum, or vagina, and, in unfavorable ones, may break into the ab- dominal cavity. Another, but not a very common, result of vesical catarrh is diffuse suppuration. This generally occurs in cases of reten- tion of urine, and arises from the corrosive action of the putrid contents of the bladder upon its mucous membrane. The mucous membrane is then found to be extremely soft, discolored, and of a brownish-red or blackish hue. It is covered with dirty exudation, or broken down into a ragged, pultaceous substance, infiltrated with fetid pus. The mus- cular fasciculi are pale and tear easily. The submucous and intermus- cular tissue is infiltrated with ichorous matter; within the bladder there is a blackish-brown, chocolate-like liquid, of an intensely ammo- niacal odor, consisting of decomposed urine, blood, pus, and shreds of detached mucous membrane. In the worst cases the destruction at- tacks all the coats of the viscus, whose contents escape into the al> dominal cavity. An enormous thickening of the walls of the bladder, a common result of the hypertrophy of the muscular fasciculi already referred to, may be mentioned as a third termination of chronic vesical catarrh. This condition, however, sometimes arises in cases of long-standing impediment to the passage of the urine, without vesical catarrh. In such cases the wall of the bladder attains a thickness of from several lines to half an inch or more. The muscular fasciculi have grown into rounded bars, and form rib-like projections upon the interior, the ap- pearance of which has been compared with that of the right ventricle of the heart (vessi'e d colonne). According as the capacity of the bladder is increased or diminished by this hypertrophy, it is called ex- centric or concentric. In the former case the bladder may rise into the abdomen as far up as the navel; in the latter it may be shrunken to the size of a walnut. In some cases of chronic vesical catarrh, es- 68 DISEASES OF THE BLADDER. pecially when associated with impediment to the exit of urine, the mucous membrane, pressing asunder the muscular fasciculi, is forced in between them, forming diverticuli. At first small and round, these latter ultimately expand into large bottle-shaped pouches, of the size of a fist. Their communication with the bladder is at first a narrow chink, which afterward becomes round and sphincter-like. Owing to the incompleteness with which these diverticuli are evacuated, they often become the seat of urinary deposit, and of incapsulated calculi. Symptoms and Course.—Acute catarrh of the bladder is some- times accompanied by febrile symptoms. As a rule, however, there is neither elevation of temperature nor acceleration of pulse. In quite recent cases, the patients complain of an undefined pain in the hypo- gastric region and perinaeum, which extends upward toward the kid- ney, and along the urethra toward the glans penis. In the more severe forms of vesical catarrh, pressure exerted upon the region of the bladder gives rise to pain. The hyperaemic and irritable vesical mucous membrane evinces the utmost intolerance against its contents. The collection of a few drops of urine in the bladder occasions the most urgent desire for its expulsion. The sphincter vesicas also is in a constant state of spasm, thus causing a vesical tenesmus quite analo- gous to that of the rectum already described in catarrhal rectitis. The patient scarcely has the urinal out of his hand, micturition is ex- tremely painful, and the few drops of urine which are expelled in short spirts from the urethra produce a feeling as though molten lead were running through the penis. As in all recent catarrhs, at first the quantity of mucus formed is small, so that but a few flocculi are scattered through the urine. Afterward the urine passed becomes turbid, and lets fall a mucous sediment in greater or less profusion. The disease may run its course, and get well in a few days; and that form caused by drinking fresh beer usually passes off within a few hours. In other cases it is more protracted, or passes into the chronic form. Sometimes the spasmodic contraction of the sphincter vesicae, which occurs in acute vesical catarrh, gives rise to complete retention of urine, and in old persons especially, owing to secondary diseases (oedema and fatty degeneration of the muscles of the bladder), a my- opathic palsy of the detrusors arises, which also causes retention. It is this circumstance which renders simple vesical catarrh a dangerous disease to old persons. In chronic catarrh of the bladder, the pain usually abates after a while, but the intolerance of the viscus against its contents and the constant inclination to urinate continue. The quantity of mucus increases considerably. At first a somewhat trans- parent stratum of mucus sinks to the bottom of the vessel, after- ward the urine becomes thick and turbid, and its sediment is more CATARRH OF THE BLADDER—CYSTITIS CATARRIIALIS. 69 Dpaque, and of white or yellow color. If the urine undergoes the so-called alkaline fermentation in the bladder—the secretion of the diseased mucous membrane, full of pus-cells and disintegrating epi- thelium, suffers a peculiar transformation (already mentioned when treating of pyelitis) forming a gelatinous coherent mass, which, when poured from one vessel to another, holds together, and can be drawn into long threads. In previous editions of my text-book I have stated that this pro fuse secretion of mucus often acted as a ferment upon the urine, giv- ing rise to an “ alkaline fermentation; ” that in this alkaline fermen- tation the urea was decomposed into carbonate of ammonia, and that new ammoniacal combinations formed, namely, urate of ammonia and phosphate of ammonia and magnesia (triple phosphate). I was compelled to add that the mucus contained in the urine did not al- ways act as a ferment; and that, in many cases of protracted vesical catarrh, I had constantly found the reaction of the urine to be acid. In the course of the last year, from observations made by Traube, as well as from investigations and experiments of my own, which have Deen published by Teuffel, in the Berliner Klinischen Wochenschrift, I have become convinced that this alkaline fermentation is not pro- duced by the mucus, but is owing to the presence in the urine of or- ganisms of a low grade, which probably usually find their way thither through the introduction into the bladder of dirty catheters. A high- ly interesting observation, made in my clinic, upon a young girl with palsy of the bladder, affords striking evidence of the correctness of this opinion. In the bladder of this patient, who for weeks had been catheterized with an ill-cleansed instrument, there had developed a most typical alkaline fermentation. Her urine, which was of a pun- gent ammoniacal odor and alkaline reaction, contained the thorn- apple-like crystals of urate of ammonia, large coffin-lid-shaped crystals of ammonio-magnesia-phosphate, with many vibriones and fungi of a low order; but it contained neither cellular elements nor large quan- tities of mucus. A careful research into the history of the case showed that the patient never had had any symptoms of vesical catarrh. Chronic vesical catarrh drags on for weeks, months, and even for years. It is a remarkable fact, and one difficult to explain, that it usu- ally is accompanied by loss of appetite and by derangement of diges- tion. The longer the disease has lasted, se much the less are the chances of a perfect recovery. Ulceration of the vesical mucous membrane is to be suspected when the sediment of the urine grows more and more purulent, when, from time to time, blood is discharged with the urine, and when a slow fever arises, which consumes the strength of the patient. He then 70 DISEASES OF THE BLADDER. ultimately dies of vesical-phthisis, especially if it be associated with abscess about the bladder, or tedious suppuration from fistulous pas- sages. When catarrhal inflammation of the bladder passes over into dif- fuse suppuration, the patient becomes collapsed, his countenance ap- pears sunken, the pulse is small and thready, and the skin cold. The urine is discolored, of a brownish or blackish hue, contains shreds of mucous membrane, and exhales a fetid odor. Even though the wall of the bladder be not completely destroyed, and though there be no escape of its contents into the abdominal cavity, yet malignant peri tonitis soon develops, and the patient dies within a few days, of gen- eral prostration. Thickening of the wall of the bladder, from hypertrophy of its mus- cular fasciculi, may be detected when the viscus also is dilated, by the appearance above the symphysis pubis of a firm tumor, which some- times extends as high as the navel, or even higher, and which in fe- males is apt to be mistaken for a distended womb. Generally speak- ing, patients are unable to empty a bladder thus thickened and dis- tended, even though there be no obstacle to its evacuation in the vesi- cal neck or urethra. It is only the excess of urine (for which, so to speak, there is no room left in the already enormously overfilled blad- der) that is passed by the patient, or which runs from him involuntari- ly if the sphincter be palsied. Thus it may happen that, in the course of twenty-four hours, he may pass a normal amount of water, and still retain from two to six pounds or more in his bladder, which can only be removed by means of the catheter. In concentric hypertrophy, the bladder can be felt through the wall of the vagina or rectum, as a hard tumor, which may give rise to all sorts of blunders. In these cases, the bladder being incapable of distention, there is a constant desire to pass water, wrhich does not give the patient a moment’s rest; and, when the sphincter is relaxed, there is an incessant dribbling of urine. Treatment.—The causal indication, first of all, demands the pro- tection of the vesical mucous membrane from the injuries which have occasioned the disease. This is most difficult of accomplishment where rude catheterization or careless injections into the urethra have provoked catarrh of the bladder; as well as where the exhibition of cantharides and the like, or the long-continued use of fly-blisters, or of irritating ointments, or where persistent retention and decomposition of the urine are the irritants which are acting upon the mucous mem- brane. When it proceeds from the extension of an inflammation of the urethra or 'svoinb, the application of a few leeches upon the pcrinceum, or portio vaginalis, is advisable. If the apparent cause be cold, we should resort to a diaphoretic course of treatment. It is onlv when CATARRH OP THE BLADDER—CYSTITIS CATARRHALIS. 71 quite recent and of great intensity that the indications from the dis- ease itself call for local blood-letting, which then is better performed upon the perinaeum than above the symphysis. In most cases of acute catarrhal cystitis, hot poultices upon the abdomen, and general warm baths, suffice to relieve the symptoms and to bring about a favorable termination. Besides this, we must take care that the urine enter the bladder in as dilute a condition as possible; but, if we strictly forbid the use of all salt and spices, it will be useless to mix oleaginous or mucilaginous materials in the patient’s drink. It is best to let tlm patient drink the artificial or natural mineral waters—the Seltzer, Wildunger, Fachinger, or Gailnauer waters, or soda-water, or lime- water, mixed with equal parts of milk. The semina lycopodii have a peculiar reputation as a remedy for vesical catarrh (sem. lycopod. 3 ss—to mel. despumat. 3 jss. f. elect, s. 3 j every two hours), as has also camphor, where the complaint arises from the abuse of cantharides (camphor pulv. gr. vj, emulsion of almonds, § vj). The employment of small doses of opium in the form of Dover’s powder, given at night before bed-time, or in the form of tinctura thebaica, in divided doses, is not only harmless, but a most efficient remedy against pain and vesical tenesmus. The more the pain abates, and the more copious the admixture of mucus and pus in the urine, so much the more ur- gently are the astringents indicated. The astringent most commonly employed is a decoction of the folia uva ursae ( \ ss. to 3 vj, a table- spoonful every two hours). The continued use of tannin is still more efficacious: I have obtained some most happy results from it in cases which seemed almost desperate. In the later stages of acute vesical catarrh, and still more in the chronic form of the disease, the balsams and resins, which are of such striking benefit in catarrh of the urethra, also do excellent service. To this class belong the oil of turpentine, tar-water, Peruvian balsam, and, above all, balsam copaiba, which may be given in capsules of gelatine. If these remedies fail, we should have recourse to local treatment. I have repeatedly made injections with lukewarm water, the temperature of which I gradually bring down to 65° F. after the manner recommended by Civiale, and cannot sufficiently praise their efficacy, especially in treatment of women. Astringent injections, among which solutions of nitrate of silver, sul- phate of zinc, and tannic acid, are recommended, should be used wit! greater caution; so too with injections of emulsion of balsam copaiba ( 3 j to | j), the efficacy of which is greatly extolled by some phy- sicians. No modification of this treatment is demanded where ulcera- tion of the bladder is detected. Suppurative destruction of the vesical mucous membrane is quite insusceptible of treatment. In excentric hypertrophy, the bladder must be emptied by the catheter regularly 72 DISEASES OF THE BLADDER. every eight or twelve hours, and an elastic bandage should be fitted to the abdomen. In concentric hypertrophy, on the other hand, the patient must be charged to retain his water as long as possible, in order gradually to dilate the bladder. It has also been proposed to introduce an elastic catheter, closed by a cork, into the bladder, by which i he urine may be evacuated every two or three hours. CHAPTER II. CROUPOUS AND DIPHTHERITIC CYSTITIS. Croupous and diphtheritic cystitis scarcely ever occur, excepting tn cases of severe infectious disease—in septicaemia, typhus, small-pox, and scarlatina—and are accompanied by similar inflammation of other mucous membranes. Far more rarely it arises after the abuse of can- tharides, after difficult labor, or in consequence of very intense irrita- tion of the bladder from decomposed urine. In this form of inflam- mation a coagulating exudation of variable thickness and consistence is formed, a portion of it infiltrating the tissues of the mucous mem- brane, while another portion lies upon its free surface. The process rarely extends over the entire surface of the bladder. More usually it is confined to detached streaks and spots of a rounded form. After separation of the diptheritic slough, there remain losses of substance in the mucous membrane. The disease can only be recognized when whitish membranous coagula are discharged with the urine, with symptoms of severe tenesmus. In the croupous cystitis which some- times follows the abuse of cantharides, or difficult forceps deliveries, we occasionally see large tenacious false membranes discharged with the urine. The treatment of croupous and diphtheritic cystitis should be similar to what we have already advised in cases of violent and acute catarrhal cystitis. CHAPTER III. PERICYSTITIS. Besides the inflammation induced by perforation of the bladder, and by abscesses and suppuration of its walls, another and independent inflammation, which we call pericystitis, sometimes involves the connec- tive tissue which surrounds this organ, and connects it with the adja- cent parts. It is of far less frequent occurrence than the inflammation which takes place about the rectum, and is hardly ever observed excepting as an accompaniment of infectious disease, typhus, the acute exanthemata and septicaemia. As a still greater rarity, it arises idio TUBERCULOSIS AND CARCINOMA OF THE BLADDER. 73 pathically without known cause, in persons previously in good health. This inflammation shows great tendency to pass into suppuration, and to destroy the parts involved; it is very apt to spread into the tissues which attach the bladder to the other pelvic viscera, and to the sides of the pelvis. The pus may ultimately penetrate into the bladder, rectum, vagina, or externally into the perinaeum. There is also a form of chronic pericystitis, which not unfrequently accompanies chronic vesical catarrh, and vesical ulceration, and which creates induration of the surrounding connective tissue, and causes firm adhesion of the bladder and surrounding parts. Sometimes this also results in the formation of an abscess. The affection is generally difficult of recognition, as the resulting painful tenesmus of the bladder, the dull, continuous pain in the pelvis, the repeated chills, and the complete retention of urine, which occur when the urethra or the ureters are obstructed by an abscess, furnish insufficient data for a diagnosis. A diagnosis can only be in some de- gree certain when an abscess projects above the pubis from the ante- rior surface of the bladder, presenting a spherical prominence, which does not disappear when the bladder is emptied; or else when we can feel a tumor in the perineum, or through the rectum or vagina. The treatment of pericystitis belongs to the province of surgery. CHAPTER IY. TUBERCULOSIS AND CARCINOMA OP THE BLADDER. Tuberculosis of the bladder usually appears as a complication of tuberculosis of the ureters, renal pelvis, and kidneys. Discrete and conglomerate tubercles also form in the bladder sometimes, which, upon breaking down, produce rounded or irregular excavated ulcers. Some- times (but more rarely than in the ureters and pelvis of the kidney) there is a diffuse caseous' degeneration of the mucous membrane, which .occasions wide-spread destruction. The symptoms of tuberculosis of the bladder are very similar to those of chronic vesical catarrh and vesical ulceration. The copious admixture of mucus and pus in the urine, which is often in a state of ammoniacal decomposition, the tormenting desire to urinate, the fre- quent haemorrhages from the bladder, which are the signs of excentrio and concentric vesical hypertrophy, also attend vesical tuberculosis. Our only positive data for a differential diagnosis are the coexistence of degeneration of the prostate or testicle, and the appearance of elastic fibres, or of larger bits of tissue in the urine, from which we may infer the destructive nature of the process which is going on. In a female 74 DISEASES OE THE BLADDER. patient of mine, suffering from tuberculosis of the bladder, urinary passages, and kidneys, I found an irregular eroded ulcer, with peculiar edges, in the vulva, surrounding the orifice of the urethra. The treatment of tuberculosis of the bladder is identical with that of chronic vesical catarrh, but is generally quite unavailing. Carcinoma of the bladder is not common. Sometimes it is primary, sometimes it occurs secondarily to similar disease of the uterus or rec- tum. It assumes the form of scirrhus, more often the medullary form, but the villous cancer is more frequent than either. The former twt sometimes produce diffuse degeneration of the wall of the bladder, which, upon breaking down, forms communicating openings with the vagina, uterus, or rectum. Sometimes they take the shape of circum- scribed and even pedunculated growths. The villous cancer forms soft tumors, consisting of thin, delicate villous excrescences, which float in water, and which often become detached during life, giving rise to haemorrhage. The most prominent symptoms of cancer of the bladder are, like- wise, those of chronic vesical catarrh. Haemorrhage is still more com- mon than in tuberculosis. Diagnosis must depend upon the continuance and constant aggravation of the symptoms, the early appearance of a bad cachectic condition, in the discovery of cancer of other and espe- cially of neighboring regions, and, above all, upon microscopic exami- nation of the detached particles of the growth discharged with the urine. Treatment is in vain, and should be limited to a repression of the haemorrhage, the relief of any retention of urine which may arise, and the combating of intercurrent symptoms. CHAPTER V. HAEMORRHAGE FROM THE BLADDER HEMATURIA VESICALIS. Haemorrhage from the vessels of the bladder is often of traumatic origin. Sharp-edged stones, or foreign bodies, which have entered the viscus, are the usual causes of the bleeding. In hysterical women, we must be prepared for the most extraordinary devices. Not at all un- frequently, they introduce foreign bodies into their genitals, or into their urethra, which may be the cause of the haemorrhage. In other cases, ulcers of the bladder cause erosion of its vessels, and consequent bleeding. Neoplastic formations also, tubercle, carcinoma, but espe- cially the villous cancer, give rise to losses of blood. Very rarely, such haemorrhages depend upon the misuse of cantharides (haematuria toxica), or upon a haemorrhagic diathesis. Finally, an excessive dila- tation ,>f varicose veins of the part may result in their rupture, with STONY CONCRETIONS IN THE BLADDER. 75 an effusion of blood. Haematuria from this cause, however, is very rare, although the laity are much inclined to ascribe all haematuria to “ haemorrhoids of the bladder.” The conditions producing impedi- ment to the circulation and dilatation of the vessels are far less favor- able in the bladder than in the rectum; and, as a rule, this last and rarest of the causes of vesical haemorrhoids is not to be thought of, unless, after a scrupulous review of all the symptoms, all other forms of the disease can be excluded from the diagnosis. In haemorrhage into the bladder, the blood and urine are less inti- mately mixed than when the bleeding comes from the ureters, renal pelvis, or kidneys. The clots which form are also of larger size. Nev- ertheless, both these signs may prove fallacious, and hence diagnosis of the region whence the bleeding proceeds is often a matter of great difficulty. The attendant symptoms furnish the most trustworthy aids lo diagnosis of the source of the haemorrhage. Vesical haemorrhage is almost always accompanied by evidence of change of structure in the bladder. During the intervals between the bleedings the urine contains mucus and pus, and there is dysuria, etc. Our main task in the treatment of vesical haematuria should be to combat the original disease. In severe cases, cold should be applied to the region of the bladder, and large doses of tannin should be given. Where the bleeding threatens to exhaust the patient, we must have recourse to injections of cold water, with a solution of alum, sulphate of zinc, or nitrate of silver. In vesical haemorrhoids as well as other forms of vesical haemorrhage, cold injections have the best effect. CHAPTER VI. Etiology.—The manner in which stones form in the kidney and bladder is obscure. None of the current explanations of the process have shown themselves proof against the various objections made to them. Especially is this the case with the theory that these concre- tions are the result of a peculiar derangement of assimilation, of a diathesis, wherein uric acid, oxalic acid, the phosphates, etc., form so profusely in the system, and are eliminated from the blood through the kidneys in such quantities, that they are precipitated in the urinary passages. The explanation of Scherer is very plausible. He believes that the substances deposited in the urinary passages, and which sometimes form stones, are not eliminated from the kidneys in their present shape,, and only form through the decomposition which the urine undergoes STOUT CONCRETIONS IN THE BLADDER. 76 DISEASES OF THE BLADDER during its abode in the urinary passages. This decomposition is similar to that which takes place in urine when allowed to stand exposed to the air. There is at first an acid fermentation. The coloring and ex- tractive matter of the urine become converted into lactic acid, so that the urea is liberated from its soluble combinations, and is precipitated. The acid fermentation is followed by an alkaline one. The urea is converted into carbonate of ammonia, and, by a combination of the ammonia with the phosphate of magnesia, an ammonio-magnesian phosphate is formed—the so-called triple phosphate. The ferment which excites this decomposition in the urine, while yet in the bladder, is the mucus resulting from vesical catarrh; but, according to Scherer, besides this, the mucus plays another and most important role in the formation of calculi, by forming a cement to hold the sediment together, since coagula of mucus form the nuclei of most stones, to which the deposits afterward adhere by accretion. According to the theory of Scherer, the formation of stones, which consist of a nucleus of uric acid enclosed in layers of phosphates, is as follows: As long as the acid fermentation of the urine continues, uric acid is precipitated; when, however, the catarrh has continued for some time, and, perhaps, has become aggravated by the presence of a calculus in the bladder, alka- line fermentation sets in, and the phosphates are thrown down. According to a very brilliant hypothesis of Mechel, the formation of precipitates is not requisite for the production of a urinary calculus. He claims that almost all stones consist originally of oxalate of lime, and are formed as follows: The mucous membrane of the urinary pas- sages becomes the seat of a specific catarrh, called by Mechel the “stone-forming catarrh” (stein-bildenden catarrh). In this catarrh a tough adhesive mucus is secreted, which has a tendency to acid fer- mentation, and in which oxalate of lime appears when such fermenta- tion occurs. At first this oxalate-of-lime mucus is of a gelatinous con- sistence. Gradually, however, it takes up more and more oxalate of lime from the decomposed urine, and thus, growing more and more firm, finally becomes stony. As long as the urine remains decidedly acid, the stone enlarges, from the accretion and petrifaction upon it of fresh layers of oxalate-of-lime mucus. If the urine afterward become alkaline, the stone no longer grows from “ apposition,” but from “ in- tussusception,” combined with a “ metamorphimus,” that is to say. the oxalate of lime is at first displaced by uric acid, and urate of am monia, and afterward by the phosphates. In this manner an oxalic calculus becomes converted into a phosphatic calculus. To attempt to point out all the flaws in each of these theories, and the various objections which might be advanced against them, would take too long. Among other matters, the fact still remains unex- STONY CONCRETIONS IN THE BLADDER. 77 plained, I hat hereditary tendency should play so decided a part in the formation of stone in the bladder. All the different generations of one family have been observed to suffer from the same sort of stone. Males are attacked by stone more frequently than females. The age of childhood is by no means exempt; indeed, children are rather liable to the formation of calculi and gravel in their urinary passages. In some countries, as in England, the malady is much more common than in others. Drinking-water which contains lime seems to have some influence in the production of stone, and the use of fermenting bever- ages containing carbonic acid is quite decided, at least as to its effect in producing oxalate-of-lime calculi. Any irritation which occasions catarrh of the urinary passages may give rise to stone in the bladder ; but it is quite enigmatical why many catarrhs last so long without forming concrements, while others give rise to their formation very soon. Anatomical Appearances.—Urinary calculi vary in size, shape, and chemical composition. The smaller, which are usually extremely numerous, we call “ gravel.” Their form and color depend mainly upon their composition. They may be classified as follows : 1. Stones consisting chiefly of uric acid and its salts. . They are round or oval; usually of a reddish-brown color, very hard and heavy, and with a smooth or nodular surface. 2. Stones of oxalate of lime. They usually present a nodulated, gland-like surface, whence their name, “ mulberry calculus.” They are very hard, and of a dark-brown or blackish color (through the admix- ture of transformed hasmatine). Yet some oxalate-of-lime stones are small and pale, and in form bear a strong resemblance to hemp-seeds. 3. Stones consisting of ammonio-magnesia phosphates. They are of a whiter or grayer color; have a round or oval shape; are light in weight, and are of friable, chalky consistence. 4. Calculi of cystine. These are rare. They are usually of a yel- lowish-white color. Their surface is smooth, more rarely nodular. 5. Stones formed of xanthin, which are more rare even than the cystine calculi. They are very hard, of a yellowish-red color, and usu- ally have a smooth surface. 6. Stones, consisting of various layers and strata of diverse com- position, are very common. Sometimes, the nucleus is of uric acid and the outer layers of oxalate of lime; more rarely, the contrary arrange- ment obtains. The most common form of stratified calculus is that in which a nucleus of uric acid or of oxalate of lime is enclosed in a hull of phosphates, or in which there are several alternate layers of these substances. Stones often lie free in the bladder, changing their position as the 78 DISEASES OF THE BLADDER. attitude of the body is varied. Quite frequently, too, they are lodged and embedded in pouches and diverticuli in its wall. The mucous membrane is either in a state of catarrh or of catarrhal ulceration. The muscular tunic is usually hypertrophied; yet, if the calculus be smooth and light, all of these appearances may be absent. Symptoms and Course.—Sometimes, but not very often, patients with “ stone ” have a distinct perception that there is a foreign body in their bladder which changes its place as the posture of the patient is altered. A more important and constant symptom is pain about the bladder, which is aggravated by walking, driving, or riding, and which is relieved by lying upon the back. The pain darts along the penis to the glans, and causes the patient, especially if he be a child, to pull upon the prepuce, so that in children an oedematous thickening or ab- normal length of the prepuce is to be regarded as a characteristic, or, at least, as a suspicious sign of vesical calculus. During micturition, the stream of urine is often suddenly interrupted, owing to obstruction of the neck of the bladder by the stone. If the patient change his attitude, his ability to pass water is frequently restored. Even though the beginning of the act of micturition be easy and painless, yet, tow- ard its close, there is usually the most acute suffering. This is com- bined with aching in the testicles, thighs, and lumbar region, with spasmodic contraction of the anus, and even with general reflex phe- nomena. The whole of these symptoms, however, together with occa- sional haematuria, are insufficient to establish a diagnosis; and we should make it a rule never to pronounce a positive opinion until the presence of a stone has been reduced to a certainty by means of the sound. Treatment.—The possibility of dissolving large vesical calculi, by means of internal medication, must be pronounced as hitherto un- proved, although theoretically such possibility cannot well be denied Means have been proposed of rendering the urine alkaline, or else of increasing its acid reaction, according to the chemical constitution of the stone. The former task, as is well known, is far easier of accomplish- ment than the latter, as the carbonates and vegetable salts supplied to the system are discharged with the urine as alkaline carbonates, while it is quite difficult to augment the quantity of acid in the urine. Theoretically, the benzoic acid, which is excreted in the form of hippu- ric acid, is adapted for the solution of a phosphatic calculus. But the continued exhibition of this remedy in large doses is forbidden, owing to its pernicious action upon the digestive organs. The administration of tartaric and citric acid might also have a good effect in the solution of phosphatic calculi; but these harmless articles have never come into use. Indeed, as soon as a stone in the urinary passages has been STONY CONCRETIONS IN THE BLADDER. 79 diagnosticated, it is usual to administer alkaline carbonates, quite re- gardless of the chemical nature of the stone, and to send well-to-do patients to Vichy or Karlsbad, those springs having a world-wide reputation as remedies against lithiasis. Perhaps the benefit derived from this mode of treatment depends upon the effect of the remedies upon the vesical catarrh, which is one of the main causes of the affec- tion. According to Meckel's theory, the exhibition of the alkaline carbonates and salts of the vegetable acids is indicated, because the urine is thereby rendered alkaline, and the metamorphosis of a stone, consisting of oxalate of lime, or of uric acid, into a softer and more friable phosphatic calculus, is promoted. At all events, we strongly advise that the old method of treatment be adhered to, and that no new “ cures ” be adopted, based merely upon a priori reasoning. Be- sides the alkaline carbonates, and the basic phosphate of soda, of which about two drachms may be taken daily, the carbonate of lithia has of late obtained a great reputation as an antilithic, and is warmly recommended by many. I should attach little weight to such recom- mendations, were they based solely upon the theoretical ground that the carbonate of lithia has a solvent power of uric acid six times as great as that of bicarbonate of soda. But, as we have some reports, upon good authority, of good clinical results obtained by its use, I admit the propriety of making further experiment with this drug (lithiae carb. gr. j — v t. d.). The Wildunger, Vichy, or Karlsbad waters may also be used as a beverage. We have already discussed the mode of treating the catarrh and haemorrhage of the bladder to which calculus gives rise. The opera- tion for stone in the bladder is a matter for the surgeon. NEUROSIS OF THE BLADDER. We are still in need of considerable physiological light as to the normal innervation of the bladder, and to the process of micturition. It is difficult satisfactorily to account for the well-known facts that a healthy man is often unable to pass water when required to do so in the presence of a stranger who watches him, and that the first attempts of a novice to make water while on horseback or in a wagon are often attended with difficulty, while these things are easy enough to one who is accustomed to them. Nevertheless, our comprehension of the nervous disorders of the bladder will be facilitated if we classify them into motor and sensory neuroses, and subdivide the latter class into hyperaesthesia and anaesthesia, the former into hypercinesis and acinesis. 80 DISEASES OF THE BLADDER CHAPTER VII. hyperaesthesia of the bladder. Hyperaesthesia of the bladder is most commonly seen in indi- viduals addicted to sexual excess, especially to onanism—a very mod- erate degree of fulness of the bladder causing in them a most intense desire to urinate—“ castus raro mingitIf they have not opportunity to indulge their inclination to pass water, they suffer pain over the bladder and along the penis. The power of retaining the urine is not generally impaired in such cases, the hyperaesthesia being pure and uncombined with motor disturbance. Sometimes, however, this irri- tability of the bladder is accompanied by a diminution of power in the detrusors; and it is not without reason that a strong stream of urine passes for a sign of chastity among the laity, and a languid dribbling one for a token of the reverse. Extreme hyperaesthesia of the bladder sometimes follows gonorrhoea. Patients are sometimes met with who are quite unfitted for their previous occupation, being unable to hold their water for over a quarter of an hour at a time, and are thereby reduced almost to desperation. This form of hyperaesthesia, perhaps, is always accompanied by a slight catarrh. The intolerance of the bladder against its contents is the most prominent symptom of this form of catarrh; and I have never noticed any excessive production of mucus. For the milder form of hyperaesthesia of the bladder, such as affects dissipated persons and onanists, I recommend cold river and sea baths, cold sitz-baths, and cold douches. The more severe forms, which re- main after cure of a gonorrhoea—the cold-water-cure, injections into the bladder, and other active procedures, proving ineffective—I have in some instances seen disappear rapidly and without trace under large doses of balsam copaiba. There are no well-authenticated observations of neuralgia of the bladder, that is, of painful excitement of the sensory nerves, which cannot be traced to irritation of their peripheral extremities. CHAPTER Y 111. Some persons can suffer the accumulation of a very large amount, of urine in their bladder without feeling an urgent inclination to evacu- ate it. This condition, however, is hardly to be regarded as a morbid one. On the other hand, it seems to me admissible to ascribe tlx1 ANAESTHESIA OP THE BLADDER. ANAESTHESIA OF THE BLADDER. 81 enuresis nocturna (nocturnal wetting the bed) to an imperfect anies- thesia and diminished irritability of the vesical sensory nerves. This extremely distressing affection, for which the patient not unfrequently is subjected to the most abominable treatment, and which often de- stroys the happiness of families whose older children are afflicted by it, is usually classed with palsy of the bladder. Many cases of enu- resis nocturna as I have seen, however, I have never been able to per- ceive that the sphincter vesica failed in its duty during the day, or that the children had any dribbling of urine, nor when the inclination to urinate came upon them were they ever in great haste to reach the urinal. Indeed, there are only two possible ways of accounting for enuresis nocturna. Either the sensation to which a full bladder gives rise is too feeble to awaken the child from his normal sleep, or else the sensation is of its normal intensity, but the sleep is unusually pro- found. In the latter case it would seem as though nocturnal incon- tinence of urine occurred somewhat as do those well-known cases in which children sometimes fall out of bed in their sleep without awak- ening. In the cases which I have seen, especially in adult patients, I have not been able to discover such unnaturally profound sleep. For- tunately, it is rare for enuresis nocturna (which usually affects chil- dren, and often lasts up to the time of puberty) to continue after the twentieth year. Knowledge of this fact is of importance, the best means of comforting the patient and his relatives in their distress be- ing the communication of this intelligence. It is customary to deprive children, suffering from this affection, of all drink or liquid food during the evening hours, and to waken them during the night once or twice to make them pass water. There is no objection to be made to these measures, excepting that they scarcely ever do the least good. I must protest most earnestly, however, against the cruelty of whipping or otherwise punishing a patient with nocturnal incontinence, unless the wettings of the bed manifestly be the result of laziness. In families, but still more in boarding-schools, orphan asylums, poor-houses, and prisons, punishment for this offence is inflicted all the year long, generally without effect; and if we only take the trouble to listen to the shocking stories of “ piss-a-beds ” of the lower classes, it will be clear to any one that the inefflcacy of the punishment was not due to its want of severity. Without attempting any explanation of the fact, I will merely call to mind that the dread of going to sleep often has a soporific effect, the desire to do so the op- posite, and that, if one wishes to awake at a certain hour, the fear of oversleeping is injurious, while the confidence that one will awaken in time is beneficial. In the same way, we find that children with noc* fcurnal incontinence, who have been severely chastised the day before, 82 DISEASES OF THE BLADDER. and who go to sleep in dread of further punishment, still awake in the morning with their bed wet through. On the other hand, if we can excite confidence in the use of some entirely inert medicine, for which, however we promise great things, so that the patient can go to bed hopefully, and without fear, he is often awakened in the night by the inclination to micturate, and remains for some time, or even perma- nently, cured of his affection. From time to time secret remedies for nocturnal incontinence, with testimonials as to their efficacy, are adver- tised in the newspapers. That such testimonials are not all inten tionally false, is certain; but it is equally certain that the success of the remedies is due more to the psychical impression made by the confident commendation of the article, than upon the medicinal effect of the article itself. We must never tire of again and again exciting the hopes of the patient, and of writing harmless prescriptions for him, of the value of which he must be assured. Even in little children, and still more frequently in grown persons, I have seen at first a tem- porary and afterward a permanent effect produced in this way, which amazed both the patient and his friends. I have usually ordered small doses of carbonate of potash, and recently, according to a suggestion of Trousseau's, one-fifth to one-third of a grain of pulv. herb, bella- donna, with equal parts of the extract. Other remedies, such as strychnine, cantharides, large doses of syrup, ferri iodidi, and injec- tions of irritating matter into the bladder, are objectionable. It is of importance, however, to pay attention to any indications which may arise from the special condition of the patient.1 CHAPTER IX. IIYPERCINESIS OF THE BLADDER SPASM OF THE BLADDER CYSTO- SPASMUS. Violent contraction of the muscles of the bladder frequently arises in consequence of the irritation which foreign bodies, especially stones, create within it. Such spasm is usually accompanied by organic dis- ease of the viscus. However, since abnormal irritability of the motor nerves of an organ arising as a reflex symptom, in consequence of ex- citement of the sensory nerves of that organ from structural disease, is not usually counted among the neuroses, the term spasm of the bladder is not to be applied to such symptomatic contractions of the vesical muscles, but should be reserved to designate the abnormal con- dition of the motor nerves, which exists independently of any struc- tural alteration in the wall of the bladder. SPASM OF THE BLADDER. 83 Romberg divides the causes of spasm of the bladder into cerebral, spinal, and reflex. With regard to the first, I would call to mind the fact that the irritability of the sympathetic nerve, though independent of the influence of the will, is by no means entirely independent of the irritability of the fibres and ganglia of the brain. Mental emotions have a distinct action upon the sympathetic system; and just as the muscles of the skin contract under the influence of terror, producing a “ goose-skin,” so we often, under like circumstances, see violent con- traction of the detrusor urinae muscles, with intense inclination to pass water. So, too, in inflammation of the spinal marrow and in struc- tural disease of the brain, spasm of the detrusors occurs, according to Romberg—a fact which is not easy to explain, as the innervation of the detrusor is derived from the sympathetic; although, indeed, we see an analogous condition in the occurrence of vesical spasm from mental emotion. Vesical spasm is generally of reflex origin. In an irritable subject the impression upon the sensory nerves of the urethra, pro- duced by the introduction of a catheter, will provoke spasm of the sphincter vesica. In other cases, irritation of the rectum and, very fre- quently, irritation from the womb give rise to spasmodic contraction of the bladder. Finally, there are cases of vesical spasm which are merely local manifestations of a general neurosis, and must be ascribed to a morbidly exalted irritability of the entire nervous system, which we usually call hysteria. The symptoms of spasm of the bladder vary according as the af- fection involves the detrusor urinse or sphincter vesicse muscles. In the former case, a very slight degree of fulness excites intense desire to urinate. The patient can scarcely prevent a constant escape of water by closure of the sphincter; or else he is quite unable to do so, so tha t the urine is constantly flowing away—a condition generally termed enuresis spastica. On the other hand, when the sphincter muscle is in a state of spastic contraction, the patient can only pass water drop by drop, or in a very fine stream, and with great effort (dysuria spastica). Sometimes the closure of the sphincter is absolute, and there is com- plete retention of urine (ischuria spastica). Finally, the antagonistic muscles, both detrusor and sphincter, may be attacked simultaneously. A condition of great distress then ensues, in which, in spite of violent desire to void the urine, there is inability, more or less complete, to satisfy such desire. In these cases the spasmodic affection sometimes extends to neighboring organs, giving rise to spasm of the rectum, to tremors of the entire body, and occasionally to general convulsions. One characteristic of spasm of the bladder is the alternation of violent paroxysms and intervals of exemption. The former often last but a minute or two, although sometimes they last half an hour or more. 84 DISEASES OF THE BLADDER. They recur at longer or shorter intervals, and usually cease as suddenlj as they have begun. Diagnosis of spasm of the bladder in its stricter sense demands caution, as its occurrence is somewhat rare, and as it is often extremely difficult to distinguish it from other maladies of that viscus. It is only when the latter can be excluded from diagnosis, after careful examina- tion of the urine, and scrupulous attention to the attendant symptoms of the case, and after we have assured ourselves by repeated sound- ing that there is no foreign body lodged in the bladder, that we are warranted in supposing tne existence of a pure vesical hypercinesis. Treatment of spasm of the bladder, first of all, demands removal of the exciting cause. In some instances, the cure of a fissure of the anus, or of a chronic hyperaemia or inflammation of the womb, consti- tutes the chief, or, indeed, only remedy, for vesical spasm. In other cases, it will subside if we can succeed in altering the nutritive con- dition of the patient, by a thorough modification of external relations, and thus quiet the morbid irritability of the nervous system. For the paroxysms themselves we should have recourse to warm baths, clys- ters of camomile or valerian tea, with the addition of a narcotic; and, above all, to the internal exhibition of opium. In addition to this, Pitha warmly recommends the cautious and gentle introduction of a wax bougie into the bladder. CHAPTER X. ACIHESIS OP THE BLADDER VESICAL PALSY CYSTOPLEGIA. Palsy of the bladder may involve the sphincter muscle, the detru- sor urinrn, or both of these muscles simultaneously. Contraction of the detrusor is not dependent upon volition, but arises reflexly from the stimulus of the urine collected in the bladder. Contraction of the sphincter, on the other hand, is subject to the will. Up to a certain point of distention, the tone of the sphincter suffices to counteract the action of the detrusor, which presses upon the contents of the bladder and strives to open its outlet. If this point be exceeded, the tone is overcome, and the sphincter requires the action of volition to keep it closed. From these physiological facts, the causes of vesical palsy be- come somewhat more comprehensible. In the first place, it is quite plain, both in structural disease of the brain and in grave febrile consti- tutional disease, in which the function of the brain is overthrown, why palsy of the sphincter should be a very common symptom, and why palsy of the detrusor should be somewhat more rare. In apoplexy and in typhus, the number of patients who wet their bed is greater PALSY OF THE BLADDER. 85 than that in which the use of the catheter is required. If, however, the paralysis finally extend from the cerebro-spinal system to the sym- pathetic; if the power of involuntary movement be also impaired; if the patient can no longer swallow; if the abdomen become tympa- nitic from palsy of the intestinal muscles ; the detrusor urinae also takes part in the paralysis, and the distended bladder rises above the sym- physis. There is another very common circumstance, however, which also contributes to the occurrence of incontinence of urine in cases of disease of this kind, namely (as happens in a variety of conditions of other peripheral organs), the overfilling and overflowing of the bladder (Kohlrausch) make no impression on the consciousness, and hence no impulse is derived from the will to contract the sphincter and to close the bladder. At the same time, however, it must be admitted that, in some cases of apoplexy and of severe typhus, palsy of the detrusor sets in early, and before there is any general palsy, and without our being able to account for this phenomenon. In disease of the spinal marrow, likewise, palsy of the sphincter is of far more common occurrence than palsy of the detrusor. Most paraplegic patients have to wear a urinal, in order not to wet themselves, because the conducting power of their spinal marrow is iftterrupted. The use of the catheter, on the other hand, is but seldom necessary, on account of palsy of the detrusor. However, the fact that such necessity does sometimes occur, perhaps is owing to the locality of the lesion. It seems to be the ganglia which transmit the impression from the sensory nerves of the bladder to the motor nerves. It is possible that, if that portion of the spinal cord be destroyed at which this transmission takes place, the detrusor will be palsied; on the other hand, that, if the lesion of the spinal marrow be above this point, transmission of impressions from the brain to the sphincter will be interrupted, while that from the sensory nerves of the bladder to the motor fibres of the detrusor continues unimpaired. The result of comparison of a large number of cases of this kind, which I have examined within the last few years, fully supports this hy- pothesis. Besides this form of vesical palsy, the cause of which is central, there are others in which the peripheral expansions of the nerves have suffered lesions, through which they are deprived of their function; although, indeed, it is generally out of our power to furnish anatomical proof of such structural disorder. Finally, there is a myopathic palsy of the bladder arising from dis- ease in the minute texture of the muscular fibres of the organ, and in the nerve-tips which terminate in them. The most common cause for this form of vesical palsy is the severe stretching of the vesical mus- cles, and their participation in the affections of the mucous membrane. 86 DISEASES OF THE BLADDER. A distention of the bladder, which perhaps has occurred but once, and to which a mechanical obstacle to the discharge of the urine, or a false shame in some over-modest person, has given rise, may result in perma nent vesical paralysis. It may also proceed from a vesical catarrh, especially in aged persons, from implication of the vesical muscles in the disease. The symptoms of vesical palsy vary according to the muscles affected. When the palsy is complete and is confined to the sphinc- ter, the urine flows away involuntarily as soon as the bladder has be- come full enough to overcome the tone of the sphincter. When the paralysis is incomplete, the patient is able to resist the pressure of a somewhat fuller bladder, but he must hasten to find some befitting place to pass water, as his sphincter will fail of its office if he wait too long and the pressure increase. This incomplete palsy of the sphincter is of very common occurrence in conjunction with partial paralysis of the lower extremities, and is attributable to an incomplete interruption of conducting power of the spinal marrow. In palsy of the detrusor, the tone of the sphincter is not overcome by such a degree of tension of the bladder as, under normal conditions, would excite contraction of the detrusors sufficient to overcome it. Unless artificially emptied, the bladder is distended excessively, and it is only after the distention has reached an extreme point, or by the action of the abdominal muscles (where they are not paralyzed also), that a portion of the contents of the bladder is expelled. If the palsy be pure and uncomplicated, the patient can arrest or postpone the outflow of urine. When incomplete, the bladder does not become so full before evacuating a portion of its contents as it does in complete palsy. The patient, however, endeavors to assist the action of the detrusor, by bringing his abdominal muscles into play, so that he often breaks wind while passing water. In spite of all his efforts, he cannot eject a strong arched stream, but the urine dribbles verti- cally down between his feet. This form of incomplete palsy of the detrusor is chiefly seen in marasmic subjects, and individuals weakened by sexual excess. Finally, in patients in whom both sphincter and detrusor are pal- sied, the bladder is in a state of permanent over-distention, the tone of the sphincter yielding later than it normally should do. Every ad- dition made to the contents of the bladder induces a corresponding out- flow from it, and the patient is unable to hinder or to arrest this flow. The patient usually, indeed, is quite unaware that his bladder is full, and only seeks medical aid on account of the continual enuresis, and generally is greatly surprised when we evacuate the urine from the 1,ladder, which often contains an enormous quantity of it. TALSY OF THE BLADDER. 87 In treatment of palsy of the bladder, the causal indication can rarely be met. Especially is this the case in the forms of it arising from dis- ease of the brain or spinal marrow. When it is due to immoderate distention of the organ, it is of importance to use the catheter assidu- ously, partly in order to prevent further distention, which might aggra- vate the palsy, partly to excite more vigorous contraction of the de- trusor, by the irritation which the catheter induces. In cases of in- complete palsy, instead of passing a catheter, JPitha recommends the introduction of a solid wax bougie as far as the neck of the bladder, claiming that “ the catheter ” relieves the muscles of all exercise, and thus encourages “ their indolence.” The indications from the disease call for the use of cold baths, douches, and clysters. If these fail, and if the source of the palsy be peripheral, we should proceed with due precaution to the injection of water into the bladder, which at first should be lukewarm, and afterward should gradually be reduced in temperature. If this be of no avail, the application of electricity, as recommended by Duchenne, will also prove ineffectual. We shall hardly find a well-authenticated case of cure of vesical palsy by the use of strychnine, which has also been recommended. ADDITION TO THE REVISED EDITION OF 1880. SECTION III. DISEASES OE THE BLADDER. 1.—P. 82. I have now and then earned the thanks of an adult by recom- mending to him a contrivance which has been advertised in the newspapers. A bit of leather or caoutchouc, of the size of a bean, is to be pierced through its middle by a fine opening, through which the loop of an elastic band is to be drawn, so as to slide stiffly. Upon going to bed, the prepuce, having been stretched over the glans, is to be inserted into this loop, which must then be tightened just enough to close its orifice, but not closely enough to cause discomfort, and so that upon urinating the prepuce will be put on the stretch by the water which is held back. The patient will be awakened by 'the distention of the prepuce if he passes water during sleep, and may then take off his apparatus, confident that for that night his bed will not be soiled. One young man tells me that only since obtaining this contrivance has he ever dared to sleep awav from home. SECTION IV. DISEASES OF THE URETHRA. According to the plan of our book, we omit without notice all affections of the urethra pertaining to the department of surgery, and which are treated of in detail in surgical works, and shall merely de- scribe the inflammation of the urethra. CHAPTER I. VIRULENT CATARRH OF THE MALE URETHRA CLAP GONORRIKEA. Etiology.—The urethral mucous membrane does not undergo any specific change in gonorrhoea. The process which takes place in it is identical with that which arises in any other mucous membrane, under the action of other irritants, and bears the name of catarrh or blen- norrhoea. Nevertheless, gonorrhoea is a specific disease. Its course distinguishes it plainly from all other catarrhs which affect the urethral mucous membrane, or that of other regions. The difference is all the more especial in an etiological point of view, for a gonorrhoea never arises otherwise than by contagion, in spite of the persistent denial of some authorities, and the lying assertions of shame-faced patients. Of the nature of the virus of gonorrhoea we know as little as we do of that of small-pox or other infectious matter; but we do know that the matter exerts a specific influence upon the system—that it always produces a clap, never a chancre or syphilitic ulcer. True, opinions are still divided as to whether this disease is followed by secondary disorders, and by a general implication of the system; but even authors who still believe in metastatic gonorrhoea and gonorrhoeal constitutional infection now agree that the consecutive diseases are altogether different from the sequelae of syphilis, with which they have nothing in common. The gonorrhoeal virus is a contagium jixum, its vehicle is the secretion of the diseased mucous membrane, and it is GORORRIKEA. 89 only by contact of this secretion with a mucous membrane susceptible of infection that the complaint can be transmitted from one person to another, or from the mucous membranes of one organ to that of another in the same individual. As in other infectious disorders, between the time of infection and that of the outbreak of the disease there is a certain interval, known as the period of incubation. The length of this period is from three to eight days. The appearance of a gonor- rhoea as early as twenty-four hours after an impure coitus, or as late as three or four weeks afterward (Simon), if it occur at all, is to be regarded as a rare exception. Credulous persons will hit upon cases where the period of incubation has lasted longer still. Every physician who has had much to do with venereal patients, especially with patients from the better classes of society, will have found out that it is much easier for a patient to confess to excesses perpetrated six or eight weeks ago than to those of which he has been guilty but recently. The more reason he has to be ashamed of himself, so much the more is he disposed to antedate his delinquency. Least of all are married people to be trusted in this respect, and their assurance that “ they would just as lief confess to sins of a week’s standing as those of six weeks ” is not to be relied upon. Contact of a mucous membrane with gonorrhoeal virus does not always result in infection. Indeed, the susceptibility to contagion varies greatly in different individuals. Daily experience teaches us that two men may have intercourse with a woman having virulent fiuor albus, one of whom may contract gonorrhoea, while the other may escape. We do not know by what causes this predisposition to gon- orrhoeal infection is increased or diminished. It cannot be attributed either to the greater or less degree of venereal excitement during coitus, nor to incomplete introduction of the penis, nor to the degree of “ acclimatization ” of the exposed individual to the person of the other. It is idle to indulge in unsupported theories upon this question. We do not even know why it is that, of all the various mucous membranes of the human body, only that of the urethra, those of the female gen- itals, the eye, and in some degree those of the rectum, are susceptible of gonorrhoeal inflammation, while all others are quite proof against the infection. Even different portions of one mucous membrane ex- hibit different degrees of susceptibility to gonorrhoeal poison. Al- though the infecting secretion acts first upon the orifice of the urethra, the gonorrhoea is most apt to develop in the fossa navicularis. Anatomical Appearances.—Opportunities of making post-mor- tem examination of patients with gonorrhoea are rare, and it was long ere we could obtain positive knowledge that the seat of gonorrhoea was the urethra. In recent cases of the disease the mucous membrane 90 DISEASES OF THE URETHRA. is reddened, injected, swollen, and coated with punform secretion. It is a matter of importance for the prognosis and treatment of gonorrhoea to know that, in the first and second week of the complaint, the ana- tomical changes only involve the anterior portion of the urethra— the fossa navicularis—which is very richly endowed with glands; and it is not until afterward that the lesions extend to the mem- branous and prostatic portions of the urethra. In very severe cases, the inflammation of the mucous membrane is accompanied by inflam- mation and infiltration of the corpora cavernosa, which not only dimin- ish the calibre of the urethra, but render a uniform enlargement of the penis during erection impossible. Far more rarely submucous abscesses form in severe gonorrhoea, or, what is a much more serious accident, inflammation and suppuration of the prostate occur. The lymphatics of the penis may also become implicated in the inflamma- tion, and sympathetic swellings of the inguinal glands are not unfre- quent complications of the disease, although suppuration in such cases is quite exceptional. The most common complications of gonorrhoea are inflammation of the epididymis and catarrh of the bladder. These affections both make their appearance about the end of the first or second week, that is, at the time when the pars prostatica becomes involved in the in- flammation, and when opportunity is afforded for the extension of the inflammation to the vasa deferentia and neck of the bladder. In chronic gonorrhoea the mucous membrane is swollen and stud- ded here and there with fungous granulations. Its follicles are en- larged and its secretion is more mucous. In many cases, circumscribed spots, and sometimes extensive tracts of the submucous tissue, are hypertrophied, indurated, and firmly attached to the mucous mem- brane. It is to this that most urethral strictures are due. Symptoms and Cottkse.—The commencement of a clap is an- nounced by an itching sensation at the mouth of the urethra, which does not amount to pain, accompanied by a scanty secretion of a trans- parent, clear mucus. At the same time the meatus seems slightly reddened, and its lips are usually agglutinated by the dried secretion, a thin scale of which is also spread over the tip of the glans. An in- creased desire to pass water then sets in; the patients often have noc- turnal pollutions, and during the day suffer from frequent erections, which often induce thoughtless persons to indulge in further excesses. Gradually, generally in the course of a day or two, the sense of itch- ing in the urethra gives place to a burning pain, extending from the meatus to the fossa navicularis. This pain increases, and, during the act of micturition, is extremely severe. The inclination to pass water becomes more frequent than before, so that -with each effort a few GONORRHOEA. 91 drops only are voided, and those with the utmost suffering. The se- cretion, formerly scanty, tenacious, and transparent, gradually becomes more copious, thicker, and purulent, making yellow, stiff stains upon the patient’s linen. The lips of the meatus are red and swollen ; the entire penis also, especially the glans, is more or less swollen, and the urethra throughout its entire length is sensitive to pressure. At this period, the prepuce, irritated by the discharge, or else owing to propa- gation of the irritation, often becomes excoriated and oedematous ; so that the product of a balanitis is added to the secretion which flows from the urethra. If the outlet of the prepuce be small, a phymosis is very apt to occur, or paraphymosis, if the patients imprudently re- tract the prepuce behind the glans. At this stage erections occur with still greater frequence than at the outset of the disease; but the stretching and expansion which the organ undergoes during the pro- cess cause the most intense pain to the patient, deprive him of his rest at night, and induce him to resort to the wildest expedients to arrest his suffering. All these symptoms, the painful micturition, the flow of thick, yellowish-green pus, the redness and swelling of the urethra, and the painful priapism, usually continue to increase for a period of about eight or fourteen days. After attaining their acme, the pain upon micturition usually begins to abate, the redness and swelling of the meatus gradually subside, the erections are less fre- quent and less painful; but at this time the discharge is often more profuse than ever, so that the laity regard this as a favorable sign, and think that the “ clap must be made to run ” in order to relieve their suffering. After a lapse of a week or two the discharge gradually diminishes, becomes mucous, and may finally cease altogether in the course of five or six weeks without any treatment whatever, as has been proved by the results of homoeopathic practice. Much more frequently, however, there remains a stationary scanty mucous discharge which may last for months and years. During the day, if the intervals between the acts of micturition be long, this secretion glues the lips of the urethra together. When the patient awakens in the morning, a tolerably large drop of it has collected, and runs out between the adherent lips of the meatus as soon as they are separated. The stiff stains upon the linen are now of a more grayish color, although generally there is a small but distinct yellow spot in their middle. A discharge of this kind is called “ gleet ” or “ goutte militaire.” If, while it lasts, tho patient exposes himself to further exciting cause, the gonorrhoea not unfrequently breaks out again; that is, the pain does not return but the discharge once more becomes abundant and more purulent. Excess in wine or sexual intercourse is the most apt to cause such 92 DISEASES OF THE DRETI1RA. relapses, but exposure to cold and over-exertion seem to have a similar effect. The symptoms and course of gonorrhoea present a good deal of variation. First of all, they vary in the degree and duration of the in- flammatory symptoms, and the pain, redness, and swelling of the ure- thral mucous membrane. A classification of the affection into various species, such as the erysipelatous, synochal, erethetic, and torpid, has been based upon this variation, without, however, any practical advan- tages being derived from such arrangement. Generally the inflam- matory symptoms of a first clap are far more severe than those of the second and third, but there are exceptions to this rule. In severe gonorrhoea, with intense hyperaemia, rupture of small blood-vessels with haemorrhage often occurs, imparting a reddish or brownish hue to the discharge. Although this haemorrhage is not at all dangerous, yet the “ bloody,” or “ black,” or “ Russian clap,” has a terrible reputation among the laity. The flexion which the penis undergoes during erec- tion (known as chordee) is of greater moment. These flexions result from a loss of elasticity on the part of the inflamed portion of the cor- pus cavernosum, which prevents it from participating in the enlargement of the penis. It sometimes happens that the inflamed portion of the corpus cavernosum undergoes permanent atrophy, and that thenceforth the penis when erect is distorted. Sometimes, too, when the atrophy extends entirely through the corpus cavernosum at one point, ever afterward erection is only practicable from the root of the organ up to that point. Among the less serious accidents which may occur during gonorrhoea, is the formation of small abscesses about the urethra. Severe pain, increased by pressure, and a hard circumscribed swelling about the urethra, are the characteristic signs of the formation of such abscesses. They nearly always run a favorable course, whether they perforate externally or into the urethra. A much more dangerous but also a more rare complication of gonorrhoea is inflammation of the prostate. We may infer that the prostate is the seat of hyperaemic swelling, from the unpleasant sense of pressure in the perinaeum of which the majority of patients with gonorrhoea complain, as well as from the enlargement and induration of the prostate so often seen in old persons, chiefly in those who have had gonorrhoea in their youth. If the prostate be much inflamed, there is an extremely unpleasant sense of pressure, or a dragging, throbbing pain in the perinaeum, extend- ing into the bladder and rectum, which is greatly aggravated upon the passage of the urine or the faeces. Both in the perinaeum and through the rectum we can feel a tumor of varying size. Micturition becomes more and more difficult, and the dysuria may increase to absolute retention of urine. If the inflammation go on into suppuraf ion, an al> GONOKREKEA. 93 scess forms, which may point either externally or else inwardly, giving rise to symptoms of the most serious and varied character, for further description of which we refer to the text-books of surgery. Gonor- rhoeal lymphangitis and lymphadenitis present no extraordinary features. Resolution is the more frequent termination of a gonorrhoeal bubo. Suppuration of such a bubo indeed is so rare an occurrence, that it always should excite suspicion of the existence of a glandular chancre. Finally, gonorrhoeal orchitis, the most common of all the complications of this disease, is undoubtedly the result of propagation of the inflam- mation from the urethra to the seminal vesicles and vas deferens. At first the pain in the cord, testicle, and epididymis is not very severe, the patient complaining rather of a sense of weight in the testicle. Soon, however, the pain augments, and the epididymis, which is the chief seat of the inflammation, becomes very sensitive to the slightest touch. To the hard irregular tumor formed by the inflamed epididymis there is soon added an effusion into the tunica propria tes- tis, so that in a few days the testis may become as large as a goose- egg or fist, or even larger. The enlarged testicle is less movable than before, as the thickened and indurated spermatic cord has become less flexible than when healthy. The greater the effusion into the tunica vaginalis becomes, so much the more does the tenderness, upon pressure of the swollen organ, concentrate itself at the point where the epididymis is situated. Generally the disease terminates in resolution, but a slight induration of the epididymis almost always remains for some time, or even during life, occasionally proving an object of groundless hypochondriacal anxiety to the patient. Some- times, especially in persons suffering from varicocele, the gonorrhoeal orchitis recurs several times. The discharge from the urethra almost invariably subsides during the continuance of the inflammation, but as invariably reappears when the orchitis abates. Far more rarely, the affection terminates in suppuration, tuberculous degeneration, or in- duration. For some time the term gonorrhoeal metastasis has been applied to a variety of morbid processes affecting individuals who had had gon- orrhoea. In the majority of cases, it cannot be proved that there is any relation of cause and effect between these affections and the dis- ease in question. Gonorrhoeal ophthalmia and the well-known inflam- mation of the joints known as gonorrhoeal rheumatism, or gonorrhoeal gout, are the only ones of these maladies in any sense of the word entitled to such name. The former proceeds from a direct transfer of the virus to the conjunctiva, and is one of the most dreadful con- sequences of the disease. I have seen an instance in which a married man, having contracted a clap, abstained from all sexual intercourse 94 DISEASES OF THE URETHRA. with his wife, but communicated a gonorrhoeal ophthalmia to her and to his child, whereby both mother and child lost their sight, the man escaping. That the inflammation of the joints above referred to ac- tually stands in genetic relation to gonorrhoea may be inferred from the fact that it occurs in individuals who have not been exposed to any other cause of disease; that it attacks patients who have never suffered from such symptoms before, and who never have them after- ward, and that it sometimes recurs with every gonorrhoea which the patient contracts, and disappears as the gonorrhoea subsides. This arthritis has no particular effect upon the progress of the main disease, nor do the anatomical lesions of the affected joint, or the symptoms and termination of the affection, present any peculiarity. The seat of gonorrhoeal arthritis is almost always in the knee, more rarely the foot or hip-joint, never in the joints of the upper extremity. Treatment.—The only reliable prophylactic measure which I can recommend is the avoidance of all danger of infection. I do not feel called upon to make further suggestions for the benefit of dissolute men, who merely desire to continue their irregularities unpunished. We shall spare ourselves any detailed enumeration of the various methods and means employed in the treatment of gonorrhoea, and con- fine ourselves to a description of the most important and desirable ones. The best therapeutic results are to be obtained in a perfectly recent gonorrhoea before the symptoms have become severe, as it then gen- erally can be cured in a few days. In order that the number of trac- table cases of this kind may be increased—for it is only now and then that we see one—we should make all our patients aware that the dis- ease is continually increasing in extent and violence, so that each day of delay only makes it worse. Such opinions, delivered by physicians who have the confidence of that portion of the public among whom gonorrhoea is most common, have marked effect. It is scarcely credible how coolly and with what cynicism these people talk of their debaucheries and their consequences, what an extensive knowledge of the subject is shown by some of the laity, and how much one can learn from them. For instance, in Magdeburg, where the innumerable com- mercial travellers of the various mercantile houses meet annually at the hotels, report is always made as to whose pox has relapsed, and who remained cured, and wThat injections have answered the best for gon orrhoea, etc. Only a short time after I had begun to prescribe injec tions of tannin in recent claps, where the symptoms were still trifling (and I had been very successful with this treatment), the number of recent gonorrhoeas which sought my aid multiplied considerably. 1 usually ordered three powders, each of which contained half a drachm GONORRH(EA. 95 of tannin. One of these was to be dissolved in a half pint of red wine, and the solution was to be used as an injection. If the result was un- satisfactory, the two other powders were to be put into the same quan- tity of wine, and the injection to be continued with this doubly-strong solution. It has repeatedly happened to me that a patient has pulled one of these very powders out of his pocket which I was about to pre- scribe for him, and which he had obtained from a friend, and has asked whether he might try that first. In order that these injections may be of service, we must give them once or twice ourselves, or let a skilled assistant give them. If we neglect this precaution, it often happens that the liquid does not enter the urethra at all, or perhaps is merely thrown under the prepuce, and flows back past the syringe. Gon- orrhoea syringes must be so small that they will not hold more liquid than the urethra is capable of containing. It is then unnecessary to compress the posterior end of the canal. The best plan is to have a sup- ply of suitable syringes at some particular instrument-maker’s, and to give them some unobjectionable name, since many patients, feeling too much embarrassed to ask for a “ penis-syringe,” get an “ ear-syringe,” or other unsuitable article instead. I have cut short a large number of recent virulent gonorrhoeas in two or three days by injection of tannin. Even where the disease is not quite recent, but where the in- flammation is not very violent, I have often used the tannin, and ob- tained excellent results, although the cure was less rapid. I have no idea of claiming especial qualities and merits for tannin; but I have employed this article much more often than nitrate of silver, sulphate of zinc, sugar of lead, and other astringents. I have never had occa- sion to prescribe the strong solution of nitrate of silver (gr. x—xv. to § j), for its effects can hardly be better than those obtained from tan- nin, and since even its introducers admit that it sometimes causes severe and even violent symptoms, such as I have never seen in my treatment. When the inflammation is very severe, it is well to wait for its abatement before resorting to injections. A restricted but not over-restricted diet and a strong cathartic of calomel and jalap art' also advisable in such cases. The customary prescription of milk ol almonds makes the patient unnecessarily conspicuous, without being of the slightest benefit to him. When there is extreme tenderness to pressure along the urethra, but only then, we should apply from ten to fifteen leeches to the perinaeum. Cold applications are also service- able ; but, to do good, they must be kept up continuously. Cold com- presses must be changed industriously, or the patient must be allowed to sit for a long time in a sitz-bath. Compresses which are allowed to remain until they grow warm, and sitz-baths continued for a short period only, merely increase the tendency to erection, and aggravate 96 DISEASES OF THE URETHRA. the pain. After the inflammation has subsided somewhat, we should proceed to the use of injections of tannin in these cases also. The fact that their .action is less certain in this stage of the disease is probably because, when of long standing, the inflammation is no longer confined to the more accessible anterior portions of the urethra, but has spread into the posterior regions, where an injection can reach it less easily. In tedious cases, in which injections of tannin are more apt to fail, I have often made use of the other astringents above men- tioned, without, however, obtaining any better success. When astrin- gent injections remain without effect, it is time to have recourse to cu- bebs and balsam of copaiba. There is no doubt but that these articles are also efficacious in the earlier stages of the disease, and that many a clap has been “ aborted ” by their use in free doses. If, however, we can succeed without them, it is better to do so, rather than to subject the stomach and intestine to the action of these noxious substances. It not unfrequently happens that protracted gastric and intestinal catarrhs result from the abuse of cubebs and balsam of copaiba. More- over, the abortive action of these remedies, according to my experience, is often merely temporary—much oftener than is that of injections— so that patients, who have supposed themselves well of their disease, in a few days have as free a discharge again as they had before using the medicine. The idea, that strictures are more liable to occur under the use of injections than where gonorrhoea is treated by internal medication, is based upon an error. It is true that formerly a great many patients who were treated by injections had strictures after- ward ; but the reason of this was, that injections were only resorted to in very chronic cases of the disease, while cubebs and copaiba were given in the more recent ones. The long duration of a gonorrhoea is the most frequent cause of strictures. The early use of injections, and consequent speedy stoppage of the blennorrhoea, is the best preventive of their occurrence; just as permanent thickening of the conjunctiva is best averted by the early and active applications of astringents. Where cubebs and copaiba are used, it should be in full doses, which, however, must not be kept up too long; that is, not longer than three or four days after the discharge has ceased. Large doses are relatively better borne than is the long- continued administration of smaller ones, while the latter do not ac- complish the object better, even when kept up for weeks. Cubebs alone can be taken very well, if finely powdered and stirred up in soda-water. Four or five heaped teaspoonfuls of the powder may be given in the day. Balsam of copaiba is best prescribed in gelatine capsules, four, six, or eight of which may be taken daily. Should we wish to combine the two articles, we recommend the pills of cubebs. GONOERHffiA. 97 3 ss., bals. copaibas 3 ij, cera alba q. s. u. f. pil. 120. About three boxes of such pills will be required; ten of the pills to be taken at first three times a day, and afterward four times a day. The gelatine capsules, containing extract of cubebs and balsam of copaiba in com- bination, are also to be recommended. If there should be a diarrhoea, with severe scalding pain about the anus, or if an eruption—spots of roseola—appear upon the face and body (which is not uncommon), the use of the medicine must be suspended. The results of treatment in a recent gonorrhoea are most satisfac- tory; that of an old inveterate gleet, however, is quite the reverse, and the longer it has lasted so much the worse will the prognosis be. Before all else, we must satisfy ourselves, by the introduction of a catheter, as to the existence or non-existence of an urethral stricture. When there is such a stricture, the inflammation often lurks just be- hind it, and no benefit is to be expected from the use of injections which cannot well reach the affected point, until the stricture has been relieved by the use of bougies. Where there is no stricture, or where the existing stricture has been dilated, we should inject a strong solu- tion of tannin or of nitrate of silver, and, when this fails, should intro- duce a sound, smeared with an ointment of lunar caustic, into the ure- thra. Guthrie’s unguent, opthalmicum magicum may also be employed (arg. nit. gr. ij—g. x, ung. cetacei 3 j, liq. plumb, gtt. xv.) The haemorrhage which sometimes occurs during gonorrhoea scarcely ever requires particular attention. If it be exceptionally profuse, we may apply cold, or endeavor to stanch the bleeding by compression of the point whence it proceeds. In order to prevent the painful erec- tions which occur chiefly during the night, the patient should eat but very little food toward evening, and, above all, should avoid drinking. If, nevertheless, his rest be disturbed, and if the customary popular remedies fail of effect (such as walking barefoot about the room or jumping from a chair), we may give a Dover’s powder in the evening. I have no personal experience of the effect of lupuline, which has also been recommended. If chordee develop, apply leeches (but rather to the perineum than to the penis), and give an opiate at night. Ab scesses forming in the urethra require poultices, and the prompt punc- ture of any fluctuating point. Upon the first signs of inflammation of the prostate, apply a large number of leeches to the perinmum, and, after the leeches have fallen off, encourage the bites to bleed, by the application of hot stupes. Sometimes the leeching has to be repeated. Internally give calomel with opium, in divided doses. Whether this last prescription really be of service I do not venture to say. The catheter is never to be applied without the utmost caution, and in some cases it must be laid aside altogether for a while. If the 98 DISEASES OF TIIE URETHRA. retention of urine be absolute, puncture of the bladder may be neces- sary. Fluctuating abscesses of the perinseum are to be opened promptly. For further information regarding inflammation of the prostate, we refer to the books of surgery. The lymphangitis and lymphadenitis usually subside quickly under simple rest in bed. If, after the gonorrhoea has entirely abated, there still remain a swelling in the inguinal region, we should resort to com- pression, a practice which has often and very improperly been applied to syphilitic buboes. If the patient be walking about, let him wear a hernia truss with a large pad. If he be confined to his bed, a heavy bag of shot, which, not being quite full, yields and makes a uniform pressure over the tumor, is the best means of compression. In order to avert gonorrhoeal orchitis, it is desirable to cause all patients with gonorrhoea to wear a suspensory bandage, to which suitable appliances may be attached to save their linen from becoming soiled. This latter precaution is necessary, as the envelopment of the penis in rags, made fast with bandages, does harm. We should select and apply the sus- pensory ourselves, so as to make sure that it does not “ bind ” any- where. Badly-fitting ones, of course, do more harm than good. Upon the first sign of orchitis the patient must betake himself to bed, and there remain, with a wedge-shaped cushion between his thighs, upon which the scrotum is to be so arranged that there shall not be the slightest strain upon the spermatic cord. Besides this, a large number of leeches should be applied to the cord, the after-bleeding from which should be encouraged. The pain almost always subsides after the depletion. When this has been accomplished, hot poultices must be applied night and day to the scrotum, and, should there be any fresh attack of pain, the leeching must be repeated. Much benefit has also been ascribed to the internal exhibition of calomel combined with opium in this affection. Compression of the testicle, by means of which abatement of the pain and rapid subsidence of the tumor are sometimes effected, is a procedure which often fails, and which, accord- ing to my experience, generally can be dispensed with. CHAPTER II. NON-YIKULENT CATARRH OF THE URETHRA. Simple non-virulent catarrli of tlie urethra is a somewhat rare af- fection. Local irritation of the urethra by foreign bodies, irritating injections, sexual excess, especially coitus practised during the men- strual period, are its most usual causes. A symptomatic catarrh also accompanies urethral ulcers, particularly urethral chancres. In other XOX-YIRULEXT CATARRH OF THE URETHRA. 99 instances, tlie inflammation of other organs, as the prostate or bladder, spreads to the urethra. The symptoms of non-virulent urethral catarrh are swelling and redness at the meatus, painful burning along the urethra, especially during micturition, and the discharge of a scanty mucous secretion. All this usually subsides in a day or two without medical aid. The more intense and protracted catarrh which accompanies a urethral chancre however, is attended by purulent discharge, and may easily be mistaken for a gonorrhoea. We shall have more to say as to the distinction between the two conditions, in treating of urethral chancre. Avoidance of the causes from which the affection proceeds, and removal of the conditions by which it is kept up, are the sole treatment requisite for this unimportant and mild disease. Occasionally a simple catarrh of the urethra only shows itself by adhesion of the lips of the urethra in the morning. Then the patient, annoyed at the idea of having a gleet, presses and squeezes the penis till he brings out a little mucous discharge. This may be relieved by warning him against thus irritating his urethra. DISEASES OF THE SEXUAL ORGANS. A.—DISEASES OF THE MALE SEXUAL ORGANS. In this section we shall speak only of spermatorrhoea and impo- tence, leaving the other diseases of the male sexual organs to surgery. CHAPTER I. NOCTURNAL AND DIURNAL POLLUTIONS SPERMATORRHOEA. From the occurrence of puberty till the virile power has been lost, most men have occasional nocturnal emissions, without our being able to say that they are a sign of disease. If the emissions are repeated at unusually short intervals, if they come without lascivious dreams, if mey are accompanied by incomplete erections, or if they occur during the waking state (diurnal pollutions), the condition is a pathological one. The persons who consult physicians on account of pollutions are chiefly young men from seventeen to twenty-five years of age. They complain of having emissions of semen one or more nights each week, which weaken them greatly, and that they feel particularly dull and list- less the day after an emission. We should not have too much confidence in these patients, or rather we should mistrust that they are concealing some important fact. The first glance at these confused and embar- rassed young men usually shows that they have a bad conscience; in many cases we may tell what the trouble is from the mysterious letters in which they request a consultation. It is not generally difficult to obtain from these patients a confession that they have previously mas- turbated, and some even appear to be relieved by making the acknowl- edgment. We must not be satisfied with this confession, however, but should carefully seek to find out if they do not still continue the practice. This confession is generally far more difficult for them ; but 1 shall not exaggerate in saying that full two-thirds of the patients SPERMATORRHOEA. 101 a ho have consulted me for their pollutions have at last acknowledged that they still masturbated. These persons seek aid because they have been frightened by reading the miserable books which give such overdrawn pictures of the results of onanism. They hope that it will only be necessary to tell of the frequent occurrence of the emissions, and that they may be silent concerning the cause. The case is somewhat different with a second class of persons who seek medical aid for their pollutions. These also have masturbated during youth, but have subsequently ceased to do so; they also, how- ever, have come across some bad book describing the terrible results of the habit, and they have been greatly terrified, and have become very hypochondriacal. They do not have nocturnal emissions oftener than healthy persons, but each recurrence gives new stimulus to the hypochondriasis; they are considered very dangerous, and the patients imagine they are experiencing the evil effects of which they have read. The letters that such patients write often form a wonderful contrast to their personal appearance. From the account of their case as given in the letter, we may be prepared to meet a deplorable-looking being, instead of whom comes in a hearty, robust man, that it is difficult to recognize as the writer of the letter. A third class of persons who consult the physician for their pollutions do suffer from general debility, are badly nourished and anaemic. They have never been given to onanism; nor do the emissions occur fre- quently, but the day after their occurrence the patients feel peculiarly dull and relaxed, and are inclined to refer the cachexia from which they are suffering to their pollutions. It is well known that, in dis- eased, exhausted persons, the excitability of the nervous system is more apt to be abnormally increased than it is in strong and healthy ones, and that inclination to pollutions, as one symptom of erethism, is more frequently seen in the former than in the latter. We often find that persons, who have never suffered from pollutions while in health, are afflicted with them when attacked by severe disease or during con- valescence. Besides the last class of persons, in whom the pollutions are not the cause but the result of the diseased and exhausted constitution, and in whom this exhaustion with its causes must be the objects of treat- ment, there are patients in whom the repeated pollutions are the only reasons we can find for a feeling of great debility and an unconquer- able lassitude. Such patients are very peculiar: they cannot think acutely, are sad, cannot work; they are cowardly, easily frightened, complain of trembling, noises in the ears, dizziness, neuralgic pain in the back of the head, etc. Their complaints remind us most strikingly of those of hysterical women, and it is perfectly justifiable to designate 102 DISEASES OF THE MALE SEXUAL ORGANS. this collection of symptoms as hysteria. It is difficult to understand why pollutions should have so injurious an effect on the organism in a few persons, while by most they are borne without observable harm. We cannot consider the loss of semen as the cause of the exhaustion and nervous disturbance. The sexual excesses to which young husbands generally give way very rarely have any injurious effect on their health; even if they have daily intercourse, most of them remain just as strong as they were previously while perfectly continent. In such persons the loss of seminal fluid is so very much greater than in those who suffer from occasional pollutions, that injurious results would occur much more frequently in them if the loss of the fluid were the cause of the injury. From the favorable results that I have had of late years in treating this affection, and patients with spermatorrhoea by repeated cauterizations of the caput galinaginis, I believe that the hysterical symptoms occurring in it are exactly analogous to those occurring in women who have erosions of the os uteri; or in other words, that they do not depend on loss of semen, but that morbid irri- tability of the sexual organs may excite extensive disturbances of innervation in men just as it does in women. When speaking of hys- teria I shall explain more in detail that erosions of the os uteri do not necessarily induce hysteria, but that this is only apt to occur where there is a decided predisposition for it. The case is just the same in men who masturbate or who have pollutions or spermatorrhoea from irritation of the genital organs. I must, however, warn my readers against taking it for granted that all men who have hysterical symp- toms masturbate or suffer from pollutions or spermatorrhoea. Hys- teria does not depend exclusively on affections of the sexual organs, either in men or women. By spermatorrhoea, in the strict sense, is understood a condition where the semen is not regularly ejected during a complete or incom- plete erection, but where it is washed out by the urine, or flows out slowly while the bowels are being evacuated. The statements of Lallemand and several other authors, concerning the frequency of spermatorrhoea, are exaggerated. Increased excretion of prostatic fluid is often mistaken for spermatorrhoea. In the white, frothy, or transparent viscous fluid which sometimes collects in considerable quantity at the mouth of the urethra after sexual excitement without coitus, there are usually no spermatozoa or they are very few in number. Frequently also the frothy fluid secreted from the urethral mucous membrane during a gleet, or the mucous filaments in the urine when there is catarrh of the bladder, are mistaken for semen. The microscope alone can render the diagnosis positive. The causes of true spermatorrhoea are obscure. Relaxation or SPERMATORRHOEA. 103 dilatation of the excretory ducts of the vesicular seminales and other morbid but not well-known changes (probably catarrh and erosions), in the caput galinaginis, appear to be at the root of the disease. Lallemand and others have exaggerated the injurious results as well as the frequency of spermatorrhoea. I knew a railroad agent in Magdeburg who, for at least ten years, lost a considerable quantity of semen with every stool, without any observable bad effect on his gen- eral health. He was married, and his wife had several children by him while he was affected with the spermatorrhoea; he also acknowl- edged that, during his daily trips to Leipzig, he not unfrequently committed sexual excesses. In some persons, it is true, the same symptoms occur that we described when speaking of pollutions. Treatment is comparatively powerless against a morbidly-increased inclination to pollution. The best results are attained by paying par- ticular attention to the constitution of the patient, and seeking to rec- tify any thing that is out of order. This may be the reason why fer- ruginous preparations and the natural chalybeate baths are so popular for pollutions, and why some patients are improved or cured by sea- bathing, others by the cold-water treatment. Cold sitz-baths and washing the genitals with cold water have the reputation of strength- ening the sexual organs and arresting pollutions; but these should not be used in the evening, especially just at bedtime, for, if used at that time, they absolutely favor the occurrence of pollutions. Heavy suppers and drinking freely of. tea, etc., just before bedtime, should be forbidden. It is improper to prescribe camphor, lupulin, and sim- .lar medicines. Greatly as cauterization of the caput galinaginis, by means of Lallemand’s porte-caustic, was esteemed for a time, it has since gone out of fashion. When Lallemand"'s work first became known, every practitioner considered it necessary to have one of his instruments, but most of them have been laid on the shelf for years. However, where the emissions of semen are abundant, and the constitution of the patient undermined, and where, by excluding other anomalies, we may regard relaxation or dilatation of the ducts of the vesiculae semi- nales, or chronic inflammation in the back part of the urethra, as the probable causes of spermatorrhoea, we may cauterize the caput galina- ginis, lege artis. In other cases we may confine ourselves to prevent- ing constipation, ordering the genitals to be washed in cold water, and treating any existing complications. 104 DISEASES OF THE MALE SEXUAL ORGANS. CHAPTER II. IMPOTENCE AND IRRITABILITY, WITH WEAKNESS OF THE MALE SEXUAL ORGANS. During the period of manhood, complete and permanent inability of performing coitus successfully is rarely seen. Even some deformi- ties of the penis, loss of one testicle, or disease of both, often will not cause absolute impotence. On the other hand, cases of diminished power and of temporary impotence are very frequent, and it is of the utmost importance for the practitioner to be thoroughly acquainted with the various and peculiar forms under which these states may occur. Unhappy marriages, barrenness, divorces, or perhaps an occa- sional suicide, may be prevented by an experienced physician, who has the entire confidence of his patient, if he can give him comfort and consolation when consulted concerning impotence. The persons that come to the physician for counsel are chiefly young husbands, filled with despair at the discovery that they cannot cohabit with their wives. Not only sensual women, but all, without exception, feel deeply hurt, and are repelled by the husband whom they may previously have loved dearly, when, after entering the married state, they find that he is im- potent. The more inexperienced and innocent they were at the time of marriage, the longer it often is before they find that something is lacking in their husband; but, once knowing this, they infallibly have a feeling of contempt and aversion for him. And it is not the lost pleasure or the fear of remaining childless that brings the young hus- bands to the physician, but a sense of shame, and the knowledge that they are becoming contemptible and disgusting to their wives. This sad secret is often concealed from the nearest relatives, and confided only to the physician, in whose art and discretion the patient has full confidence. The next most frequent class of persons that consult the physician for impotence are young men engaged to be married, who, previous to their wedding-day, have experimented w'th lewd women to see whether they were impotent, and who have not succeeded on that occasion. Impossible and disgusting as this may sound to the student, when he acquires a moderate practice he will often encounter persons who will relate such things to him with perfect unconcern. Under proper treatment the great majority of these cases terminate well, so that, when the desperate spouses fall into the right hands, in the course of time they almost always become happy husbands and fathers. The most frequent cause of temporary impotence is lack of self-confidence, and a consequent straining of the mind for the success IMPOTENCE. 105 of the coitus. Erections not only come without the influence of the will, but the ardent desire for them interferes with their occurrence. The more unconcerned the individual, the less attention he pays to the erections, the more certain and permanent they will be when there is sexual excitement. The patients usually volunteer the information, that they have powerful and continued erections at times when they are of no use, but have none when there is an opportunity for coitus, or that, if erections occur, they pass off even during the coitus, before the ejaculation has taken place. Even when such patients have re- gained their self-confidence by one successful coitus, and have then re- tained their virile power for some time, they often have long relapses of their impotence from a single failure of the act. There arc also cases where the virile power of the patients returns perfectly when they have intercourse with their wives, and they can even visit them at very short intervals ; but it always fails if they make the attempt with some other women with whom they have not previously had con- nection. The most frequent cause of this diminished power is onanism; sexual excess or repeated pollutions far more rarely cause it. But the diminished power of the onanist is usually first increased to temporary impotence by reading popular and medical treatises on the results of masturbation. In those writings the loss of manhood is described as the inevitable result of onanism, and the readers are thus robbed of all self-confidence. If both the depressing effect of onanism and the despondency from reading these papers act on the same person, the first attempt at coitus almost always fails. But, as we have already said, the effect of this first failure is to induce subsequent ones for a long time. Other persons, not debilitated by onanism, and under- taking coitus with perfect confidence, fail in the act from being intox- icated at the time; but even such persons may become temporarily impotent from the disturbance of self-confidence by the failure, and from paying too much attention to the success of the next attempt, for fear it also will fail. In still other cases the only causes for the failure of the first coitus are excessive excitement and a certain embarrassment and anxiety. Such persons have often led an unusually chaste life, and, with a rare innocence after marriage, they have attempted coition, being perfectly ignorant of the process. In the first weeks of their married life they are greatly depressed and troubled by their sad experiences. If we meet them a few years subsequently, when they have healthy, bloom- ing children, they laugh freely over the mishaps of their honey-moon. Besides the numerous cases of deficient power and temporary im- potence under the above classes, we must mention the rarer cases, 106 DISEASES OF THE MALE SEXUAL ORGANb. where the impotence depends on actual functional debility of the sexual organs during the age of manhood. They are distinguished from the above by the fact that, during sexual excitement, even when there is no psychical impediment, there are no erections; nor do these oc- cur, as they usually do even in children, without a feeling of desire, when the patient wakes up with a full bladder. Occasionally examination of the genitals in such cases shows something abnormal: the testicles are atrophied, small, and soft; the scrotum hangs relaxed, or else the penis is flabby and cool, or very small and hard. In other cases the most careful examination of the genitals shows nothing abnormal. Some years since, a farmer consulted me for his impotence. As he was somewhat over thirty years old, and a strong, muscular man, without excess of fat, and as I found nothing wrong about his gen- itals, the penis being well-developed, the testicles large and hard, I considered it certain that his impotence was of the first variety, and consequently gave a good prognosis. But the case turned out differ- ently from what I had expected; and, after being married a year, the man was divorced, the impotence having continued all this time. This second form of impotence must also remain unexplained until our knowledge of physiology and pathological anatomy advance beyond their present state. We shall pass over the cases where congenital malformations, cas tration, or other imperfections, are the cause of the impotence, as well as those where it is only one symptom of general debility in exhaust- ing diseases, especially in diabetes, and shall only add a few words concerning irritability with weakness of the male sexual organs. Some authors include the form of impotence first described under the head of irritable weakness, and, in fact, the persons there described are on the one hand irritable, as they are very readily excited by con- tact with women or other causes; and, on the other hand, they are weak, for the erections are not strong and do not last long. But by irritability with weakness, in the strict sense, we understand a condi- tion where, during sexual excitement, the ejaculation occurs before actual copulation has taken place, or even before the erection is perfect. This weakness also occurs chiefly among persons who have previously masturbated. As long as strong erections still take place occasionally, the prognosis in these cases is almost always good. Even when, from masturbation, this affection has lasted for a long time be- fore marriage, and continues during the first weeks of wedded life, it generally disappears if the mode of life be regulated, and the sexual desire be moderately gratified, but not artificially excited. In the first form of impotence the causal indications require chiefly i psychical treatment. It is often enough to tell the patient of the IMPOTENCE. 107 nappy results in similar cases that we have treated, and to assure him that, according to all experience, his disease is unimportant and only temporary. Others are cured by having coitus forbidden. The non- chalance that they thus acquire during sexual excitement and the in- attention to the strength and duration of the erections render co- habitation possible, and they have the first successful coitus during the time it was forbidden, while previously it had always failed. For ignorant persons we may order some harmless substance, and promise the best results from it, but, at the same time, forbid coitus for a sea- son. In such cases the patients will often come back in a few days and confess deploringly that they could not abide by the restriction. We should particularly warn all persons, suffering from impotence, against artificial excitement, especially against fingering and rub- bing the genitals, and thus attempting to excite erections ; we should represent to them most earnestly and continuously both the injurious effects and the indecency of such a procedure. All the so- called aphrodisiacs are useless and injurious. Washing the genitals with cold water, cold hip-baths, and cold douches, occasionally appear beneficial, and we should employ these remedies in the second form of the affection also. In some cases of impotence, and particularly in cases of irritability with weakness, cauterization of the prostatic por- tion of the urethra, by means of LallemancTs porte-caustic, has been remarkably beneficial. Probably in these cases the disease depended on spermatorrhoea due to relaxation and dilatation of the ducts of the vesiculae seminales; occasionally, also, the operation may have had a favorable psychical influence. In the latter cases, reading LallemancPs book would greatly aid the cure, for there the result of the cauteriza- tion is pictured in such glowing colors that the description must re- store courage to the most faint-hearted. Recently some electro-thera- peutists have strongly recommended electricity for impotence; and this treatment (besides which these men, according to their own ac- counts, advise the impotent husbands to refrain from seeing their wives, and to try coitus with lewd women [!]) is said to be very beneficial. In men of full virile power I have often induced erections by faradisation of the inner surface of the thigh, but, where there was impotence even after using electricity for weeks, I have seen no re- sults worth mentioning. But, as my own observations have not been very numerous, I will not pronounce decidedly on the subject, and shall simply give a short account of the plan of treatment advised by Benedict and Schultz. According to Benedict we should place the copper pole of a constant battery over the lumbar vertebras, and pass the zinc pole forty or fifty times in the direction of the spermatic cord, then transversely over the different zones of the upper and lower sur- 108 DISEASES OF THE MALE SEXUAL ORGANS. faoe of the thighs, and then lengthwise in the perineum. Such a sit- ting should last two or three minutes. Moreover, about three times a fortnight the copper pole should be applied, by means of a catheter- shaped rheophore, to the vicinity of the ejaculatory duct, and passes should be made with the zinc pole in the direction of the spermatic cords. If there are any particularly insensible places, Benedict uses Faraday's galvanic brush, and, if the testicles are peculiarly insensible, he passes a strong current through them. The sittings should take place every day, and be continued for some time, as improvement did not take place for months in some cases: Schultz, in Vienna, has for a long time used the induced current for pollutions and impotence. Under this treatment the success was very poor; but he claims that it is much greater since he has com- menced using a constant current. He places the positive pole over the fifth dorsal vertebra, the negative over the sacrum or to the peri- naeum. Each sitting lasts from one to three minutes, and they are re- peated three or four times a week. Schultz employs a battery with twenty or thirty DanieVs elements of medium size. B. —DISEASES OF THE FEMALE SEXUAL ORGANS SECTION I. DISEASES OF TIIE 0 VARIES. CHAPTER I. INFLAMMATION OF THE OVARY, OOPHORITIS [OVARITIS], Etiology.—The Graafian follicle, the stroma of the ovary, and its serous coating, may become the seat of inflammation. The first two forms occasionally lead to suppuration of the parenchyma, the last almost always leaves thickening- of the serous coat and adhesions to neighboring organs. Parturition, with its sequelae, most frequently causes oophoritis; but, as we exclude the diseases caused by pregnancy, delivery, or child- bed from discussion in this section, we shall here pass by puerperal oophoritis. Next to childbed, the disease appears to begin most fre- quently at times when the ovary is hyperasmic, and is the seat of a physiological injury from the rupture of a Graafian vesicle. The best- known causes of non-puerperal oophoritis are injurious influences act- ing on the body at the time of menstruation, such as catching cold, getting the feet wet, coitus during menstruation, etc. One attack of the disease predisposes to another. Anatomical Appearances.—Ovaritis attacks only one ovary. If the inflammation start from the follicles, we find one, or more rarely several, of the Graafian vesicles swollen to the size of a pea or a cherry, filled with a variegated exudation, and their external envelopes reddened by capillary injection. At the same time the ovary is usu- ally but little enlarged; except a slight oedema, the stroma appears normal; the serous covering usually participates in the inflammation. In most cases the disease runs a favorable course; the exudation is 110 DISEASES OF THE OVARIES. reabsorbed and the follicle atrophies; in other cases it degenerates to a serous cyst, and exceptionally ends in suppuration and formation of an abscess. If the inflammation start from the stroma of the ovary, the process is usually limited to a decided hyperaemia, an inflammatory oedema, and a proliferation of the connective tissue, which subsequent- ly leads to thickening and shrinking of the ovary. Suppuration and formation of abscesses, or diffuse destruction of the ovary, rarely occurs in these cases. In non-puerperal ovaritis, Kiwisch has only twice seen this rare termination. Inflammation of the peritoneal covering is sometimes primary, sometimes secondary to that of the parenchyma. In recent cases the ovary is usually covered by a scanty fibrinous ex- udation, which unites it loosely to the neighboring parts, particularly to the broad bands of the uterus and the Fallopian tubes, whose peri- toneal covering usually participates in the inflammation. Subsequent- ly firm adhesions, by means of fibrous bands and filaments, readily form between these parts ; not unfrequently these closely envelop the ovary and openings of the tubes. Exceptionally, peritoneal ovaritis causes abundant exudation, and encapsulated foci are formed in the pelvis. Symptoms and Course.—The symptoms of a partial peritonitis in the neighborhood of one of the ovaries are the only signs usually furnished by ovaritis. If the peritoneal covering be not inflamed, the disease almost always remains latent. The ovary lies so deep in the pelvis, and is so completely covered by intestines, that pressure downward from above the symphysis pubis does not affect the ovary, unless the abdominal walls are very much relaxed and distensible. Hence it is important to decide, by vaginal examination, whether the ovary be really the origin of the pain. Occasionally the diseased ovary may be reached through the rectum. The etiology, also, may confirm the diagnosis. If we meet the above symptoms in a patient who has caught cold, or received injury in some other way at the menstrual period, and the menses have suddenly ceased, the presump- tion that the partial peritonitis starts from the ovary is more tenable than that it depends on disease of some other organ, covered by peri- tonaeum. The symptoms may be modified by an extension of the in- flammation to neighboring organs. Uterine blennorrhoea and bloody or bloody serous discharge from the uterus, pain in passing water 01 faeces, neuralgic pains or numbness in the corresponding extremities may accompany ovaritis, while in other cases they do not occur. Oophoritis is only exceptionally accompanied by fever. The course ot the disease varies greatly. In favorable cases the symptoms pass off in a few days, without leaving a trace. Probably the combination of symptoms called colica scortorum (colic of prostitutes) depends on OVARIAN CYSTS. slight ovaritis, which runs a rapid course, and terminates favorably. At least, in women of suspicious character, I have often seen severe pain in the lower part of the abdomen, which appeared to originate in the ovaries, and was increased by slight pressure, rapidly dis- appear after the application of leeches. If the disease lasts long; if it causes adhesion of the ovary with neighboring parts, and thick- ening of the peritoneal covering, the symptoms of ovaritis will fre- quently recur periodically for a long time, particularly at the men- strual periods. As the opening of a Graafian vesicle, even under nor- mal circumstances, is accompanied by symptoms like those of inflam- mation, it may be readily understood that, under the above-described normal circumstances, it is often accompanied by those of actual inflam- mation. I know a lady who was treated over ten years ago by a cele- brated gynecologist for severe ovaritis, and who has had returns of her disease several times a year ever since. The copious exudations in peritoneal ovaritis, and the perforation of abscesses in the parenchym- atous forms, may cause the above-described encapsulated effusions in the pelvis, or even diffuse peritonitis, with rapid course and fatal results. Treatment.—In acute ovaritis we should apply ten to fifteen leeches in the inguinal region, or, where it can be done readily, we may apply a smaller number to the neck of the womb. Cataplasms and warm baths aid their action. We should also secure copious evacuations from the bowels; but should avoid drastics, and limit our- selves to giving castor-oil and enemata. Calomel and mercurial oint- ment are not needed in the treatment of ovaritis. If the disease be protracted, the blood-letting should be repeated occasionally. The systematic use of brine-baths and the internal administration of prepa- rations of iodine and iodine mineral waters also appear beneficial. CHAPTER II. OVARIAN CYSTS. [There are various forms of ovarian cyst. 1. Hydrops follicularis. Here one or more Graafian vesicles are transformed into cysts, which is proved by the fact that in young cysts of this kind the ovulum is still to be found. It is sup- posed that such cysts owe their origin to an abnormal thickness of the walls of the ripe follicles, which, under the influence of the menstrual afflux, swell up to the size of a pea, but do not burst, as physiologically they should do. But the appearance of these cysts before puberty, and even in newly-born children, proves that a mere 112 DISEASES OF THE OVARIES. indisposition to burst is not the sole cause of their formation, and that a morbid state of the secretion within the follicle may be the real cause. Sometimes these cysts are solitary ; sometimes they exist in great numbers. They are generally small, and hence often remain undetected until after death. Exceptionally, a cyst or a cluster of cysts makes a tumor of the size of a fist, very rarely of the size of the head. Such a cyst has thick walls, is smooth within, and contains a yellow, serous liquid. In young cysts traces of fresh or altered blood can be perceived. Communication between several cysts due to atrophy of the intervening tissues is rarely seen. 2. The so-called cystomata, or cystoids—that is to say, prolifer- ating cysts—are by far the most common and important form of ovarian tumor. By most new authors the histogenesis of a cystoma is sought in the epithelial components of the ovary. According to Waldeyer's graphic account, a cystoma does not originate from the ordinary egg containing a Graafian follicle, but rather from the more rudimentary forms of the epithelial portion of the ovary, from the rounded balls of epithelium, and from the tubular struc- tures, the so-called llPflilyer,s tubes” which have probably origi- nated at the embryonal period of the organ. Instead, however, of normally developing into Graafian follicles, from the very commence- ment they have developed into cystomata ; or else the follicle is converted into a cystoma by repeated proliferation of the epithelium of its inner surface. As in all mixed tumors in their later periods, there is in a cystoma an intergrowth of epithelial, dermoid, and vesicular structures, out of which the various types of tumor are built. This growth by proliferation of the interior of the cyst the author classifies in two groups, glandular and papillary. In the glandular form sections through the cyst-wall everywhere exhibit small, simple, tubular epithelial pits (almost always cylinder-epithe- lium) in the substance of the wall, which present the character of a glandular formation. The mouths of these tubes soon become stopped up by tough secretion, and then, almost exactly as other “ retention-cysts ” form, they become first distended pouches and then small sacs. Upon the interior of the walls of these sacs new depressions form, which in their turn deepen and form pouches and cysts, and so on ; thus a honeycomb appearance is produced. In the papillary cystoma the proliferation of the connective tissue of the cyst-wall is the main feature. From their inner surface numer- ous ramifying, shaggy, highly-vascular vegetations sprout. Some- times these are circumscribed, growing only within a certain limit; sometimes they increase incredibly, filling the whole sac. There are many intermediate forms. OVAKIAN CYSTS. 113 Many of the smaller, more recent cystomata are of a more solid structure, and upon section show numerous vesicles filled with gelat- inous matter. Older tumors, which are often as large as the head, and which sometimes widely distend the whole abdomen, and con- tain fifty litres or more of liquid, consist mainly of a principal cyst, in which the accessory cysts grow, and, as their walls become thin- ner, finally hurst. Thus the multilocular cysts tend to become uni- locular. The contents of a cystoma are not always the same, but consist generally of a stringy, thick, dirty-brown or yellowish-green liquid, of specific gravity 1018 to 1024. More rarely, it is a thin liquid or a stiff jelly. According to E. Eichwald, the chemical contents con- sist of two series of organic substances : 1. Mucous matter, derived from direct conversion of the cell-protoplasm of the epithelium. Mucin is gradually converted into what is known as colloid matter, and further is changed into mucopeptone {Eichwald), a substance analogous to the albuminpeptone of albumen. 2. Albumen appears either free or combined with soda. The latter is converted into paralbumin (which then no longer coagulates upon heating), and further into metalbumin, which will not precipitate with nitric acid. Finally it becomes albuminpeptone, the last of the series. TVal- deyer considers paralbumin and metalbumin as of value in a diag- nostic point of view. The former is never wanting in ovarian cysts, and never present in ascites. A more convenient test of the liquid obtained from the abdomen by puncture is by the microscope, under which the discovery of cylinder-cells is of the greatest importance. Colloid globes (degenerate, swollen cells), blood, pigment, and cho- lesterin-crystals are often found. Wandering cells are not found unless the cyst-wall suppurates, which, however, is not very uncom- mon. The liquid of ascites is usually of a clear, light-yellow color, of specific gravity 1010 to 1015, and contains amoeboid corpuscles and pavement-epithelium ; and upon standing exposed to the air, if any blood has become mingled with it during the puncture, it often, after a lapse of twelve or twenty-four hours, throws down a clot of fibrin, which never occurs in ovarian liquid. If a viscid substance of a somewhat dark color and a specific gravity of about 1018 or 1024 be drawn from an abdominal puncture, it is hardly necessary to seek any further proof that ovarian cyst is its source. Ovarian cysts are attached by a pedicle, which is sometimes long and narrow, sometimes short and thick, and which includes the ovarian ligament, the tube, and the broad ligament of the womb. Sometimes the seat of the tumor is upon the side of the womb it- self. The main cyst-wall embraces the entire tumor, and in the 114 DISEASES OF THE OVARIES. larger cystomata adhesions more or less extensive to the neighbor- ing serous sui’faces are often found—a matter of great importance in a question of ovariotomy. Regarding the causes of ovarian cysts little that is trustworthy is known. In exceptional instances such growths are met with even in childhood, and it is probable that many which are not detected until adult age have existed during youth. Of three hundred and forty-eight cases observed by Lee, West, Scanzoni, and Schroeder, ninety-seven were prior to the thirtieth year, one hundred and forty-five between the thirtieth and fortieth years, seventy between the fortieth and fiftieth years, thirty-one between fifty and sixty, and two between seventy and eighty. Both ovaries are very often found diseased (fifty out of ninety-nine times, /Scanzoni); but the changes in the less affected ovary are usually stationary, and both ovaries are seldom found simultaneously in such a state of cystic degeneration as to form large tumors, and it is equally rare for the extirpation of one ovary to be followed by the growth of a tumor upon the other. 3. Dermoid cystomata are always congenital. From the sketch given by His and Waldeyer of the embryonal development of the so-called axischord, from which the rudiments of the genitals de- velop, it will be seen that in this part, in which the different ele- ments of the embryonal rudiments grow into one another, and in which especial germinal lamina) are no longer distinguishable, ele- ments of skin, fat, nerves, muscle, and bone might stray into the sexual sphere. Dermoid cysts do not. usually become developed until after puberty ; they are rare during childhood. As a rule, they are relatively small (about the size of an apple or fist), but sometimes grow as large as the head. The structure of the interior wall of the cyst closely resembles that of the skin. There is an epidermic covering, beneath which is a layer of connective tissue resembling the cutis, and in which irregularly-arranged papillae can sometimes be found. A layer of fat (panniculus adiposus) is very constantly found beneath the cutis. Sometimes deposits of true bone are found in the connective tissue, which may even contain rudimentary teeth embedded in alveolar processes. More rarely a growth of gray nerve-substance or of transverse striped muscular fibres is made out. The wall of the cyst, like the skin, contains sebaceous hair-follicles, sometimes even sweat-glands ; and the cav- ity of the cyst is filled with the products of these organs, a mixture of epidermic cells, sebaceous secretion, masses of fat and choles- terin, and of hair either still growing or cast off and rolled into a ball.] OVARIAN CYSTS. 115 Symptoms and Course.—In some few cases the symptoms as- cribed to ovaritis in the last chapter precede hydrops ovarii. More frequently there are no premonitory symptoms, and even the cysts themselves excite no symptoms as long as they are small and do not press against any neighboring organ. It depends on the position of the cyst whether it will cause trouble on attaining some size, and as to what the nature and amount of this trouble will be. Cysts of even moderate size, situated behind the uterus in Douglas’s cul-de- sac, and pressing the uterus against the bladder, may cause severe urinary difficulty ; this may be either strangury or dysuria, accord- ing to the part of the bladder pressed upon. Defecation may also be hindered by small tumors ; and pressure on the nerves running along the posterior wall of the pelvis may cause pain in the small of the back, or signs of pressure on the nerves of the extremities; these are sometimes pains, sometimes a feeling of numbness. Last- ly, oedema and varices of the lower extremities sometimes result from pressure of an ovarian cyst on the venous trunks in the pelvis. Besides the above symptoms, there are sometimes changes in the breasts, particularly swelling, discoloration of the areola, and even secretion of colostrum. Occasionally, too, there is sympathetic vomiting, and a general disturbance like that which takes place at the commencement of pregnancy. As the tumor gi-ows and rises out of the pelvis, the symptoms of pressure on the pelvic organs usually subside. Many patients then feel quite well, and the disease can only be recognized by ex- amination, of which we shall speak hereafter. In some cases, how- ever, the inconveniences continue. For instance, in spite of the enlargement of the other parts, the wedge-shaped, thin portion of the cyst may extend far down into the pelvis, and continue to cause the symptoms of pressure on the pelvic organs. On the other hand, as it rises, the cyst may stretch the bladder, and thus induce more trouble with the urine. As the tumor continues to enlarge, the space in the abdomen is gradually lessened ; the movements of the diaphragm are hindered, and it is pressed upward. Then we have the symptoms of com- pression of the abdominal viscera and of the lower lobes of the lungs. Even a moderate fulness of the stomach, or a slight disten- tion of the intestines by gas, becomes very annoying ; vomiting is easily excited ; the patient becomes short of breath, and bronchial catarrh results from the collateral fluxion to the upper lobes of the lungs. Even the secretion of urine maybe interfered with by com- pression of the kidneys and their vessels. Finally, the general nu- trition, which has usually been unimpaired up to this time, suffers 116 DISEASES OF THE OVARIES. from the various disturbances of the organs engaged in the forma- tion of blood. Anaemia and hydraemia are developed ; the patient loses strength and emaciates ; the menses, which have previously been regular, cease ; even where there is no compression of the veins, the lower extremities become cedematous as a result of the hydraemia ; finally, the patient dies, with the symptoms of general marasmus. The duration of the disease before its fatal termination varies greatly. It often continues for years ; some patients, however, die much sooner from intercurrent diseases, and not a few as the result of their treatment. The tumor does not usually grow steadily, but increases at intervals. Scanzoni has observed cases whei'e the liquid in the cyst increased and decreased periodically. Just before men- struation, the tumor increased in size, as a result of increased secre- tion from the wall; when the menses ceased, it diminished again. Some cysts only attain a moderate size, and then remain stationary. In one case that I saw, an ovarian cyst, which developed when the patient wTas eighteen years old, and rapidly attained a considerable size, remained for twenty years without growing any more. It has not been clearly proved that ovarian cysts can entirely disappear from reabsorption of their contents, but a diminution in size seems to occur occasionally from metamorphosis of the walls, such as ossification. Among the complications that may arise during the disease, we shall first mention the peritonitis which is so frequent; this some- times occurs spontaneously when the cyst grows very rapidly, some- times it is the result of operation. It is characterized by more or less pain, which is increased by pressure, and by fever. Since it causes adhesion of the ovary to the neighboring parts, it is very im- portant for the prognosis of ovariotomy. Inflammations of the inner surface of the cyst-wall are rarer and more difficult to recognize than inflammation of the external surface. They are usually caused by tapping, and induce a change in the quality of the contents of the cyst. This inflammation is generally painless, and a slight fever is usually its only symptom. Occasionally ovarian cysts burst from excessive distention, or from the action of external forces, and their contents enter the abdominal cavity. This accident may be favor- able, or the reverse, according to the quality of the contents. There have been cases where purely serous fluid was evacuated into the abdomen, and was quickly absorbed, and the cyst did not fill again for a long while, and in some cases it never filled. But even in such cases the escape of the fluid into the abdomen is accompanied by severe pain and constitutional disturbance. Where the ruptured cyst OVARIAN CYSTS. 117 contained a more irritating liquid, or fat, hairs, etc., death resulted from severe peritonitis. In the case above mentioned, rupture of the cyst was caused by concussion of the body twenty years after the formation of the cyst. At first only a moderate peritonitis was induced by the escape into the abdomen of the thick, almost pulpy, contents of the sac, which contained quantities of cholesterin. It seemed as if the fall the woman had was really a piece of good luck. The abdomen was entirely collapsed just after the rupture, and only filled slowly ; but the fulness increased steadily, and, after a few weeks, the abdomen was more distended than ever before. It was evident that the inner wall of the ruptured cyst continued to secrete liquid, which was emptied into the abdomen ; and, besides this, there was peritoneal exudation. Tapping was repeatedly nec- essary. At the first tapping there were drawn off twenty thousand cubic centimetres of a mixture of the secretion of the cyst and of peritoneal exudation, which weighed fifty-one pounds, being one- third the entire Aveight of the patient before tapping. Death from exhaustion took place a few weeks after the fourth tapping. Au- topsy entirely confirmed the diagnosis made during life. Lastly, instead of rupturing suddenly, ovarian cysts may be gradually opened by inflammation of their walls, and their contents may be evacuated into the abdomen, unless the cyst has pre\Tiously become adherent to some neighboring organ, in which case they are emptied into it. Such perforations most frequently occur into the rectum, and atrophy of the cyst has been observed in a few cases as a con- sequence of this. Not unfrequently ovarian cysts may be recognized by physical ex- amination, even before they have risen out of the pelvis. If situated in Douglas’s cul-de-sac, or between the uterus and bladder, or even to the side of the uterus, a distinct, sharply-bounded, and more or less movable tumor may usually be felt through the vagina ; it displaces the uterus in various directions, according to its position. Occa- sionally, also, we may feel the tumor through the rectum. The more distinctly we can perceive that the tumor does not perfectly follow the movements of the uterus, the more certain is the diag- nosis. If the ovarian cyst rises out of the pelvis, it usually forms a round, movable, painless tumor, with a distinct upper border, and there is more or less evident fluctuation. If Ave move the tumor with one hand, while the other is in the vagina, we find that the uterus only moves Avith the tumor Avhen the movements are very extensive, and vice versa. [When the tumor is adherent to the uterus, this test, of course, fails ; and then, unless its want of hardness gives the right clue, it 118 DISEASES OF THE OVARIES. is liable to be mistaken for a fibroma of the womb. It is also diffi- cult sometimes to distinguish between such a growth and a cyst of the ligament, or dropsy of the tube. Parametritic and perimetritic exudations, especially 'when situated in Douglas’s space, can be felt through the vagina as rounded masses ; but under conjoined manip- ulation, it can be ascertained that they are not well-defined ball- like tumors. Moreover, they are accompanied by the symptoms of an inflammation of which they are the product, and after abatement of the inflammation increase no further, but rather tend to diminish. Faecal masses which are often to be felt through the vagina can be indented like putty by the finger, and disappear after unloading the bowel. As it grows, the tumor rises out of the pelvic cavity, unless held down by adhesions in Douglas’s cul-de-sac, in which case vio- lent symptoms arise like those which are presented by the retro- flexed gravid womb in a case of incarceratio uteri. The tumor first appears as a round body in one or other iliac fossa, recognizable by percussion and palpation, sharply marked above, and painless. It may be confounded with sundry other pelvic tumors. From a distended bladder it may be distinguished by the introduction of a catheter. From haemometra, from inter- stitial fibroid, and from pregnancy, it may be distinguished by care- ful palpation per vaginam, showing that the latter tumors are all directly in connection with the vaginal portion of the womb, besides possessing other peculiarities. As the tumor grows larger it rises in the belly, assuming a mid- dle position, so that when the pedicle is long it is difficult to decide whether the growth springs from the right or left side of the pelvis. Since the bowels are attached to the back of the abdomen, they necessarily yield backward as the tumor mounts in the cavity, so as to lie behind and beside it, although sometimes a coil of bowel lies in front of it. Upon making the patient lie upon her back, the tumor may be grasped more or less distinctly, and fluctuation sooner or later becomes perceptible, notwithstanding the fact that these growths are generally multilocular, because many of the small cysts gradually coalesce so as to form large ones. The tumor may present a uniform surface, or its multilocular character may be disclosed by the distinct ball-like prominences on the abdomen. Its consistence is sometimes uniform, and sometimes elastic and fluctuating in one portion, while at others solid masses may be felt, consisting of papillary growth or extensive proliferation of the cellular tissue. It is easy to distinguish an ovarian cystoma from corpulence of the abdomen and from meteorism. In such cases the percussion- sound is tympanitic. An ovarian sac with its walls not very tightly OVARIAN CYSTS. 119 distended, and lying closely in contact with a large part of the ab- dominal wall, may be so difficult to feel, and its fluctuation is some- times so marked, that it may be mistaken for an ascites ; of course, only with that extreme grade of ascites in which the tympanitic sound of percussion is extinguished even in the very highest part of the belly, and in which therefore the patient cannot by sudden changes of attitude cause dull and tympanitic sounds to be heard alternately upon percussion, a very characteristic mark of ascites of moderate degree. The distinctive signs usually given—that when the patient lies upon the back the abdomen is rounded when there is a cyst and flattened in-ascites ; and that when there is a cyst, the percussion in the lumbar region will be tympanitic because the bowels are displaced downward and backward, but that in ascites the percussion-sound is dull—deserve attention, but may cause error. The vaginal portion of the cervix often gives no positive informa- tion, since the tumor cannot always be touched from below through the vagina. The womb, although at times grown fast to the tumor and dragged up with it into the belly, and at others pushed down, displaced, or bent, now and then presents no change of position. The state of the lower extremities deserves great attention in the diagnosis. If but little swollen, then the fluctuating abdominal tumor is probably a cyst. In obscure cases exploratory puncture and aspiration, although not quite free from risk, give valuable aid, both by rendering an exact palpation of the tumor practicable, and by furnishing the material for chemical and microscopic tests. The diagnosis of a dermoid cyst is based chiefly upon its small size and slow growth. Not unfrequently it remains undiscovered during the life of the patient. If, however, it continues to grow, it may lead to perforation into the bladder, intestine, or vagina, or else through the abdominal wall. The discharge of its peculiar contents will then reveal its character. In one or two instances a complete recovery has followed such an evacuation of a dermoid cyst. Malignant degeneration sometimes occurs.] If the tumor grows, it usually approaches the median line. Very large ovarian cysts, which rise to the costal cartilages on both sides, and fill both sides of the abdomen, can no longer be distinctly bounded and distinguished as separate tumors. The abdomen, which is enormously distended and very tense, is usually more prominent than broad, and changes its shape very little with change of the position of the body. At the same time both inspection and palpa- tion show the irregular shape of the distended abdomen, which is due to the fact that these large tumors do not consist of one tumor, but of a union of several cysts. Wherever the tumor comes in con- 120 DISEASES OF THE OVARIES. tact with the abdominal wall, percussion is absolutely dull. Since the intestines are pushed upward and to the side by ovarian tumors, the dulness becomes most decided at the prominent parts of the abdomen, where it is full in ordinary ascites ; at the most dependent lateral portions, on the contrary, the tone is less dull and is tympa- nitic. The uterus may be dislocated in various directions by large ovarian cysts. Hence the result of vaginal examinations varies greatly in different cases. The uterus may be pushed downward so much as to constitute a prolapse ; it may be displaced forward, or the vagina may be elongated, and the uterus elevated, so that the os uteri cannot be reached by the finger. Treatment.—The treatment of ovarian cysts belongs almost exclusively to surgery. All absorbent remedies are useless, and, as most of them are active, they are injurious. This is particularly true of the preparations of iodine and mercury. Occasionally we may retard the growth of the cyst by laxatives and derivatives ; but, as we can only carry out this treatment for a short time, the effect is only temporary, and it is no advantage to the patient to have the tumor remain stationary for a few weeks, and then con- tinue its growth. But we cannot hope by internal remedies to cause a change in the inner wall of the cyst that shall deprive it of its expansibility. In spite of the slight prospect of benefit from medicinal treatment of ovarian cysts, humanity requires us to give the patients a chance at the renowned baths and springs in Kreuz- nach, Tolz, etc. [When the tumor threatens life, ovariotomy should be performed. The success of certain specialists of late years is remarkably good. Out of five hundred ovariotomies, Spencer Wells has saved three hundred and seventy-two patients, and lost one hun- dred and twenty-eight.] CHAPTER III. COMPLICATED NEOPLASIA AND SOLID TUMORS IN THE OVARY. From the excessive formation of new connective-tissue cells that accompanies the development of cysts, we have cystosarcoma. This forms tumors which rarely attain the size of those described in the last chapter. Fibroid tumors, unaccompanied by the formation of cysts, rarely develop alone in the ovary, but they have occasionally been obsei’ved of very large size. For several years past I have been treating a patient, aged fifty-five years, who has a very hard, nodular fibroid SOLID TUMORS IN THE OVARY. 121 tumor, as large as a child’s head, in the right ovary ; it can he moved to the right or left, and is easily rotated on its axis. Carcinoma of the ovary is of somewhat more frequent occur- rence, but it also is rare. Medullary carcinoma is almost the only form that occurs here ; scirrhous and colloid cancer of the ovary are very rare. From complication with formation of cysts, carci- noma of the ovary may form immense tumors. This neoplasm almost always extends over large portions of the peritonaeum. Occasionally we may decide with more or less certainty that there is not a simple cyst of the ovary, from the hardness of the tumor, and from the course of the affection differing from that usual to ovarian cysts. In most cases the diagnosis is obscure. If ascites accompany a nodular tumor of the ovary, and we can discover no other cause for it, the chances are that there is cancerous degenera- tion. In one case of excessive ascites I made the diagnosis of car- cinoma of the peritonaeum starting from the ovary, even before feeling the nodular tumor of the ovary (which was rendered very perceptible by tapping), by excluding other causes of ascites, and from the account the patient gave of having had pain in the lower part of the right side of the abdomen and right thigh, as well as of varicose veins of the right leg that had preceded the abdominal dis- tention . The treatment of these ovarian tumors is the same as that of ovarian cysts ; but the hope of success is even less than it is in the latter disease. SECTION II. DISEASES OF THE UTERUS. CHAPTER I. CAT A RKTI OF THE UTERUS A XI) CATARRHAL ULCERS OF THE CERVIX UTERI. Etiology.—During menstruation the hyperasmia of the uterine mucous membrane is so excessive that the overfilled vessels are ruj>- tured. Before the hyperaemia attains this grade, and when it is di- minishing, the mucous secretion from the uterus is increased and changed. This catarrh, which is physiological as it were, becomes pathological if the hyperaemia of the uterine mucous membrane and the change of the secretion last beyond the normal duration of men- struation, or come at a time when no ripened ovum has been detached. Remembering this, we may readily finderstand why catarrh of the uterus is among the most frequent of diseases, being at most excelled in frequency by catarrh of the stomach, an organ subjected to the same conditions. The tendency to uterine catarrh varies greatly with the age. It is rare in childhood, when periodical recurrence of physiological conges- tion of the uterus does not yet exist; during the age for child-bearing it is very frequent; in old age the predisposition is decidedly less. Among the exciting causes are : 1. Congestion in the vessels of the uterus ; in diseases of the heart and lungs, where the return of blood to the right heart is impeded, the hinderance to the flow of blood from the veins of the uterus usually ap- pears as catarrh of the mucous membrane, and is analogous to cyanosis and dropsy of other parts of the body. Still more frequently the ob- struction to the escape of blood is nearer the uterus. In many cases, compression of the hypogastric veins by tumors, or, more often, by col- lections of hardened fasces in the rectum or colon, are the causes of UTERINE CATARRH. 123 catarrh of the uterus ; we have before said, that some patients suffer- ing from uterine catarrh, dissatisfied with the treatment of their phy- sicians or even of celebrated gynecologists, fall into the hands of charlatans, or use Morrison’s pills, and for a certain time are benefited by the continued use of these laxatives that are vaunted as panaceas. 2. Many cases of uterine catarrh are caused by direct irritation of the uterus, and, from what was said above, it is evident that any nox- ious influence acting on the uterus, when in a state of congestion, will prove more injurious than at other times ; hence that imprudence during menstruation most readily induces uterine catarrh. The uterus is directly irritated by too frequent or too energetic coitus, by mastur- bation, or by wearing pessaries, etc. The uterine catarrh accompany- ing other diseases of the uterus, such as parenchymatous inflammation, neoplasia, etc., and which is usually called symptomatic catarrh, also depends on the direct irritation. 3. Like other catarrhal affections, this also may depend on consti- tutional disease. Acute catarrh of the uterus occurs in typhus, cholera, variola, and other infectious diseases; chronic catarrh usually accompa- nies chlorosis, scrofula, and tuberculosis. As we have often said, the connection between the local disturbance and these general diseases is not understood. 4. When we read of the epidemic appearance of uterine catarrh, it simply means that, without any known cause, the disease occurs more frequently at one time than at another. Anatomical Appearances.—Acute catarrh of the uterus is rarely seen post mortem. The changes of the mucous membrane of the uterus in acute catarrh do not differ from those of other mucous membranes in the same disease. There are hyperaemia, swelling, succulence, and relaxation of the tissue; the secretion of mucus is diminished at first, but subsequently increased; in the first stages this mucus is clear and deficient in solid constituents; subsequently it becomes yellowish, and contains quantities of young cells. In chronic catarrh the mucous membrane is more swollen and hy- pertrophied ; it is brownish red or slate gray; the secretion from the cavity of the uterus appears more or less purulent, and is often mixed with blood. The secretion from the cervix uteri, on the other hand, is usually tough, coherent, and forms gelatinous plugs. Where the pro- cess has lasted a long while, the structure of the mucous membrane is changed. The ciliated epithelium is replaced by cells without cilia. Part of the glands is destroyed, while others swell up like cysts. In many cases the surface of the uterine cavity, particularly of the poste- rior wall, is covered with granulations that bleed readily, or with poly- poid growths. The swollen and granulated mucous membrane often 124 DISEASES OF THE UTERUS. projects from the gaping os uteri, particularly when a large speculum is introduced [noser’s ectropion of the os uteri). The ovula Nabothi are very frequently found. These are round translucent nodules, from the size of a millet-seed to that of a pea, and tilled with liquid, which are seated in the cervical canal and about the os uteri. They are the distended follicles of the portio vaginalis, whose excretory duct is closed, but whose secretion continues. Both forms of catarrhal ulcers that come on other mucous membranes also occur very frequently in catarrh of the uterus, and are very readily observed, as they occur chiefly at the os uteri. Diffuse catarrhal ulcer or catarrhal erosion is most frequently found at the posterior lip of the uterus; it may thence spread to the anterior one. The loss of sub- stance is very superficial, irregular in shape, has a dark-red base, and is usually covered with puriform secretion. Follicular ulcers, which re- sult from the suppuration or rupture of obstructed follicles, form small round losses of substance, which show no inclination to spread laterally. Granulating ulcers of the os uteri are almost as frequent accompani- ments of uterine catarrh as are the ovules of Naboth, simple erosions, or follicular ulcers, and are more important than these. They are dis- tinguished from simple erosions, from which they appear to proceed, by their irregular, granular, readily-bleeding surface. The softness of the granulations prevents our mistaking them for simple erosions oc- curring over a thick group of ovules of Naboth, which have a nodulated granular appearance. Symptoms and Course.—If we except the virulent form, of which we shall hereafter speak, severe catarrh of the uterus running an acute course is rare. The disease usually begins with symptoms of severe congestion of the pelvic organs, -with pains in the sacral and inguinal regions, with a feeling of fulness and weight in the pelvis, often also with dysuria and tenesmus. Pressure on the lower part of the abdo- men gives the patient pain, although we cannot feel the uterus. When the disease is mild, these symptoms usually appear without fever; when it is more severe, especially in irritable subjects, they are not unfrequently accompanied by fever. After three or four days, the patients notice a discharge from the genitals; this is at first transparent and somewhat glutinous; it leaves gray spots on the underclothes; subsequently it becomes cloudy, more or less purulent, and leaves yel- low spots on the clothes. If we introduce the speculum (a measure which causes great pain if the vagina participate in the disease), we find the portio vaginalis swollen, dark red, and the secretion above described is escaping from the os uteri. While the reaction of the vaginal secretion is acid, this is alkaline. In most cases the pain and any accompanying fever disappear in from eight to fourteen davs. CHRONIC UTERINE CATARRH 125 The discharge also generally becomes less copious about this time, 01 a little later; it loses its purulent appearance, and finally disappears entirely. In other cases these symptoms of acute catarrh are followed by those of chronic catarrh of the uterus. The latter cases, where chronic uterine catarrh is developed from the acute form, are far rarer than those where only the symptoms peculiar to the former were developed at first. In these cases the commence- ment of the disease can rarely be recognized with certainty. As long as it is not abundant, the patients do not usually attach much importance to the discharge, which is the most prominent, and for a long time the only, symptom of their disease. If asked how long they have had it, they are almost always unable to tell exactly. The daily amount of the discharge varies: sometimes it is slight; in other cases the patient must change the underclothes daily, and must even lay folded napkins under her at night. The dependence of the discharge on catarrh of the uterus may be inferred when glairy plugs are evacuated from time to time, or if we find in the underclothes the gray, stiff spots that this form of secretion leaves. It is uncertain whether a discharge that leaves yellow spots comes from the uterus or vagina. The more readily it chafes the inner surface of the thighs, the more probable that part of it at least is vaginal secretion. Later in the disease it not unfrequently happens that the secretion from the uterine cavity is retained there by- swelling of the mucous membrane, and by tough plugs of mucus that obstruct the canal. The retained secretion collects in large quantities, and distends the uterus. Under these circumstances, there are occa- sionally pains like labor-pains, very painful contractions of the uterus, that are usually called uterine colic. The longer the catarrh lasts, and the more change it has caused in the mucous membrane, the more fre- quently we see abnormal symptoms accompanying the physiological congestions of the uterine mucous membrane that occur during men- struation. Among these, the most frequent are severe xnolimina before the occurrence of menstruation, and pain while it lasts, dysmenorrhoea. In other cases there is too much blood lost, or, on the contrary, too little or none at all. Conception is not always prevented; the fact, that occasionally women with very obstinate and excessive catarrh of the uterus conceive, appears to indicate that it is not the uterine catarrh, but the extension of the disease to the oviducts and their closure by the secretion of the mucous membrane that lie at the root of the sterility which is so common in the disease. When women with chronic catarrh of the uterus do conceive they abort easily, and are in- clined to placenta praevia. Veit believes that both the deep seat of the placenta in the uterus and the sterility common in this disease are due to the circumstance that it is difficult for the ovum to become em 126 DISEASES OF THE UTERUS. bedded in the uterine mucous membrane. In the former case the ovule does not become attached near the opening of the ovary, but at a deeper point; in the other case it is not even arrested at the os uteri, but falls through and is lost. The symptoms of uterine catarrh are not much altered by the development of the ovules of Naboth, and catarrhal and follicular ulcers at the os uteri. Granulating ulcers, on the contrary, cause pain, and bleed readily during coitus, and are most apt to induce the nervous symptoms of which we shall hereafter speak. The influence of chronic uterine catarrh on the general health varies greatly. Some women bear even high grades of the complaint well; their nutritive condition, strength, and blooming appearance is all that could be wished for. But some soon emaciate, become dull, relaxed, and pale or dirty-colored, with blue rings around the eyes. From the anaemia and hydraemia, but particularly from irritation of the nerves of the uterus having a reflex action on other nerve-trunks, we find anomalies of innervation in many patients with chronic uterine catarrh. Most frequently there is general hyperaesthesia; but neuralgic and spasmodic affections, and decided hysteria, not unfrequently accom- pany chronic uterine catarrh. Proving the frequent association between these so-called “ hysterical ” symptoms and catarrh and other diseases of the uterus, and carefully studying them up, were certainly steps in advance; but recently there is great tendency to fall into the error of referring all hysteria to uterine disease without due examination, thus neglecting the other causes of hysteria. Since in this disease the whole attention has been paid to the portio vaginalis, and both laity and physicians have almost exclusively given over the treatment to gynecologists, it cannot be denied that many cases are cured which would formerly have remained uncured; but many also remain uncured now, which would formerly have received aid. Hence it is important that every physician should have a certain acquaintance with “ the diseases of women,” and particularly that he should understand the use of the speculum. If he do not wish to enter on the local treat- ment, he may turn the case over to a gynecologist; but he should be able to determine whether local treatment is advisable or not. The fact, that the objection women have to the use of the speculum is almost overcome, is due to the specialists. In the upper classes the women and their husbands consider it as a matter of course that, when there is fluor albus, the speculum must be introduced; but among the middle classes also, a physician who has the confidence of his patients will find but little difficulty if he says that it is necessary to make a careful examination with the speculum. It is only by introducing this instrument that we can attain any certainty as to the source of the discharge, and concerning most of the changes of the os uteri above CATARRH OF THE UTERUS. mentioned. Exploration with the finger alone can, at most, decide that there is swelling of the portio vaginalis, which, as we shall here- after see, accompanies most cases of uterine catarrh, and that the ovules of Naboth are present. Catarrh of the uterus generally runs a very tedious course. The disease may drag on for years, and it often defies all treatment. In the proper place we shall speak of chronic paren- chymatous metritis, flexion and closure of the cervical canal, as the frequent results of this disease, which, in other cases, is due to this closure, and is kept up by it. Treatment.—In the treatment of catarrh of the uterus it is most important to fulfil the causal indications. Grateful as we should be for the labors of recent gynecologists, and brilliant as the results of their treatment of uterine catarrh appear when compared with the results of former treatment, still some of them are not free from the reproach of neglecting the causal indications while attending to the indications from the disease. Where catarrh of the uterus is one of the symptoms due to general venous congestion, dependent on disease of the heart or lungs, very often the causal indications cannot be fulfilled, and the remedies that have a beneficial effect on catarrh of the uterus are not employed for the uterine disease, but for some other disturb- ance. If the congestion of the uterine mucous membrane be due to habitual constipation, proper treatment of this disease, as previously advised, has the best results. We do not treat catarrh of the rectum, which depends on congestion of the hemorrhoidal veins due to habitual constipation, with local remedies till we have tried whether “ sublata causa cessat effectus; ” nor should we employ local treatment for catarrh of the uterus till we are satisfied that removal of the existing constipation is not sufficient for the cure. Then the peculiar conditions, of which we shall hereafter speak, will preponderate. After active local treatment, laxative mineral waters are often prescribed as after-treat- ment ; and these do more good than the actual treatment, because they fulfil the causal indications. A woman named Graff‘ living in Thurin- gen, has an enormous practice among patients with leucorrhoea. They all drink complicated infusions of manna, rhubarb, senna, and other laxative remedies, and many bless the result of this treatment, to which they were driven by the lack of success of all previous treatment. Plrysicians, who do not pay sufficient attention to the causal indications in treating catarrh of the uterus, deserve the blame for this. Of course, any thing, that could have induced or can keep up irritation of the uterus,, must be carefully removed and kept away. Hence the causal indications may require the removal of tumors of the uterus, or the cure of other changes of structure which induce the catarrh of the uterus Where the uterine catarrh depends on constitutional disease, it is noi 128 DISEASES OF THE UTERUS. always possible to remove the cause; but frequently the original dis- ease is so important, or other dangerous results of it are so prominent, that we cannot attend to the uterine catarrh. This is particularly true of tuberculosis. Finally, it is not always possible to say whether anaemia aud chlo- rosis are the results or cause of this disease. If we think that the sequence in which the symptoms occur and other causes justify us in the latter supposition, we may often obtain the best results from the use of iron, quinine, a moderate amount of wine, and nutritious diet. Moreover, the good result of cold-water treatment, sea-bathing, and different mineral waters in uterine catarrh, is due to the fact that they have fulfilled the causal indication. Any practitioner will bear witness that the constitution suffers in many cases without our being able to discover the cause; and that anomalies of the constitution, which show themselves by a change in the secretion and function of different or- gans, cannot always be cured by preparations of iron and nourishing diet, even if there are evident coexistent signs of anaemia and hydrae- mia. Under such circumstances, all we can do is, to change and im- prove the constitution by placing the patient under the most different circumstances, changing the entire mode of life, and particularly by modifying as much as possible the exchange of tissue by baths and douches, by giving quantities of water with or without the addition of salts, and by other means. Among the anomalies of secretion that occur in the different organs of such patients, catarrh of the uterus is very frequent; and it often disappears very quickly when we succeed in improving the constitution, while it does not yield to exclusively local treatment. I have seen the most surprising results from such treatment in the Greifswalder clinic, where the arrangements to some extent replaced the treatment by mineral waters and baths, and where Professor Liebermeister, at that time assistant physician of the medi- cal clinic, kept account of the effect of the changed diet, increased ex- ercise, and copious supply of salty liquids, of the baths and douches, by weighing the body and examining the urine. The indications from the disease may be far more readily fulfilled in catarrh of the uterus than in catarrh of other organs that are less accessible. The uncertainty of internal remedies for catarrh has been repeatedly mentioned. They may be dispensed with in the treatment of uterine catarrh, and muriate of ammonia (which many physicians consider just as efficacious foi bronchial catarrh as for gastric and in testinal catarrh) is not used in uterine catarrh because we have bettei and more certain remedies for it. I should be entirely misunderstood, if it were supposed that I considered the local treatment of uterine catarrh as superfluous, or underrated its results; in what was said CATARRH OF THE UTERUS. 129 above, I only intended to show that one indication should not be followed to the neglect of the othei’s. In all cases where the cause of the catari’h cannot be discovered, as is most frequently the case, local treatment must be used ; and where it has existed for a long time, and is complicated with ulcers, particulai'ly granulating ulcers, local treatment should be ixsed with that for fulfilling the causal indications. Among the local remedies we shall fii*st mention in- jections into the vagina. It is not long since these constituted the only local treatment for “ leucori’hoea,” no matter whether it came from the uterus or vagina. They aid the treatment and are re- quired for cleanliness, although they are of far less use than the procedures to be hereafter mentioned. In acute catarrh we inject lukewarm water ; in chronic catari'h, at first lukewarm, and after- ward cold water, or solutions of sulphate of zinc, tannin, or alum. [Thomas, Emmet, and other eminent gynecologists of America prefer to' employ vaginal injections of water, of as high a temper- ature as the patient can comfoi’tably bear, the action of heat upon the tissues being more enduring than that of cold.] Instead of using an enema syringe with a uterine nozzle, it is well to employ a clysopompe (Davison’s syringe), so that we may throw in a large amount of liquid without irritating the vagina by frequent intro- duction of the nozzle. The application of leeches to the os uteri in acute catarrh is indicated when it begins with great severity, and in chronic catarrh when the substance of the uterus pai’ticipates in the inflammation, or when there is acute exacerbation of the disease with symptoms of severe congestion in the pelvis. Scanzoni also recommends them when there are granulating ulcers on the os uteri. We should apply leeches to the os uteri ourselves, or have it done by a nurse skilled in the operation. Gynecologists of the pi’esent day are refraining more and more from the use of leeches in the treatment of catarrh of the uterus and ulcers of the os, while formeily they were used far too often. The local application of nitrate of silver, in substance or in strong solution, is by far the most effective treatment of chronic uterine catarrh, and particu- larly for catan'hal erosions and follicular ulcers of the vaginal por- tion of the uterus. To prevent the caustic from breaking off in the cervical canal, we should employ sticks of double-annealed nitrate of silver, or have it hardened by the addition of a few grains of niti’ate of potash. When thus prepai’ed, we may push it boldly into the ceiwical canal. If cautei’izations with solid nitrate of sil- ver cause haemorrhage, which is often the case even in simple ulcer, we should use in its place concentrated solutions (one part to two or four of water), which should be poured in through the speculum 130 DISEASES OF THE UTERUS. rather than used on a brush. I should employ these solutions much oftener, if it were not so difficult to protect the fingers and clothes from being soiled. The application should be repeated once a week or oftener, till the discharge diminishes and the portio vaginalis has regained its normal appearance. The result of this treatment is so striking, that touching the os uteri and its cervical canal, in chronic catarrh of the organ, must be classed among the most grati- fying operations in medicine. The pain induced by the cauteriza- tion is usually very insignificant, but in some cases it is quite se- vere. If the nitrate of silver be passed far into the cervical canal, some women will have painful contractions of the uterus, that may continue for hours. Besides nitrate of silver, the remedies most frequently used for catarrhal erosions and follicular ulcers of the os uteri are pyroligneous acid, liquor hydrargyri nitrici, and cuprum aluminatum (lapis divinus). Pyroligneous acid is particularly bene- ficial where the ulcers have a great tendency to bleed ; the liquor hydrargyri nitrici, and still more the lapis divinus, are to be tried when the nitrate of silver has failed. In such cases the actual cau- tery is a very effective remedy, and the opposition to its use is ascribable to its psychical effect rather than to the pain or danger accompanying it. Pyroligneous acid poured through the speculum is an invaluable remedy for the granulating ulcers of the os uteri that bleed readily. In most cases it arrests the haemorrhage more certainly than sesquichloride of iron or alum ; the latter is applied to the os uteri in substance more readily than in solution. We should only use injections into the cavity of the uterus in cases of absolute necessity, i. e., only when the above treatment fails, and we are forced to believe that the cavity of the uterus chiefly is dis- eased. In such cases we should use the ordinary solutions of nitrate of silver (3 ss. to water f j). The effect of these injections is much more severe than that of touching the os uteri with nitrate of silver ; they not unfrequently induce severe inflammatory symp- toms ; where the cervical canal is contracted, they should never be employed. [Injections into the cavity of the uterus are never to be prac- tised except in cases of the utmost urgency, when other treatment fails, and when the chief seat of disease is known to be within it. For this purpose nitrate of silver (0’5 to 30‘0) may be employed, or, when there is a tendency to bleed in consequence of prolifera- tion of the mucous membrane, the liq. ferri chloridi, tincture of iodine, alum, tannin, or carbolic acid. It is well known that the liquid injected may possibly pass through the tubes into the peri- tonaeum ; but aside from this danger, the operation not only excites PARENCHYMATOUS METRITIS. 131 severe uterine colic, but in many instances has induced a fatal metritis or peritonitis. Hence the operation demands the utmost precaution. A ready escape for the liquid injected must be secured by dilating the cervix by means of sponge-tent, and the quantity of liquid used must be very small. When the womb is tender to the touch, and when we suspect that there is a parenchymatous metri- tis or other complication, intrauterine injection must not be at- tempted.] C II A P T E E II. PARENCHYMATOUS METRITIS—ACUTE AND CHRONIC INFARCTION OF THE UTERUS. Etiology.—The changes of the substance of the uterus in acute and chronic parenchymatous inflammation rarely go beyond exces- sive hyperaemia, inflammatory oedema, and proliferation of its con- nective-tissue elements, in which the muscular elements usually par- ticipate but little or not at all. There is rarely suppuration or for- mation of abscesses. We do not include the puerperal form here. For the etiology of parenchymatous metritis we may refer to that of the catarrhal form. The injurious influences there men- tioned sometimes cause inflammation of the substance of the uterus ; at others, of its mucous membrane ; but most frequently of both. These influences also cause parenchymatous metritis more readily if they act while the uterus is in a state of physiological congestion. Lastly, the parenchymatous metritis of an unimpregnated uterus must often be regarded as the continuation of a puerperal metritis ; or at least a large number of cases date from the period of a con- finement or of an abortion. Anatomical Appearances.—In acute parenchymatous metritis, we find the uterus increased in size, particularly in thickness. It may attain the volume of a hen’s egg or larger. The over-filling of the blood-vessels causes its substance to appear more or less dark, and usually irregularly reddened. These changes are most marked in the layers lying next the mucous membrane. Occasion- ally there are effusions of blood into the parenchyma. The mu- cous membrane almost always shows the signs of acute catarrh. The serous coat also often participates in the inflammation, and is covered with deposits of fibrin. In chronic infarction, the uterus is often enlarged to three or four times its normal size ; its cavity increases, particularly in the long diameter ; its walls may become an inch thick. The hyperse- 132 DISEASES OF THE UTERUS. mia which is at first present subsequently disappears, as the vessels are compressed by the neoplastic shrinking connective tissue. Then the substance appears very pale and dry, and becomes denser and harder, often to such an extent that it creaks under the knife. In rare cases we find hypersemic spots and veins that have become dilated as a result of the obstructed flow of blood. If the vaginal portion be chiefly affected, the os uteri is greatly swollen, and occa- sionally elongated like a snout. The mucous membrane almost in- variably shows the changes described in the previous chapter. On the peritoneal surface we often find firm adhesions to neighboring organs. Symptoms and Course.—Acute parenchymatous metritis begins with a chill more frequently than the catarrhal form does, and is more apt to be accompanied by symptoms of fever in its subsequent course. The pain in the sacral and inguinal regions, the feeling of pressure in the pelvis, the sensitiveness of the lower part of the ab- domen, the dysuria and tenesmus, are present in the former as well as in the latter, and almost always attain a higher grade than they do in the simple catarrh. The uterus can rarely be felt above the symphysis pubis, but through the vagina we may usually detect en- largement and tenderness of the inferior segment, and a moderate shortening and thickening of the portio vaginalis. There are also anomalies of menstruation. If, as is commonly the case, the dis- ease begins during menstruation, the bleeding usually ceases sud- denly ; if the time for menstruation occurs during the progress of the disease, we either have metrorrhagia (metritis haemorrhagica), or, as more frequently occurs, there is no bleeding. Except during the period of menstruation, the discharge characteristic of uterine catarrh (the constant companion of parenchymatous metritis) is present. In favorable cases the disease runs its course in from eight to fourteen days, the symptoms subside gradually, and the disease ends in perfect recovery ; in unfavorable cases, chronic in- farction remains. There have been some very rare instances where an abscess formed and perforated into the abdomen, and the dis- ease thus terminated fatally. Except at the menstrual periods, the symptons of chronic in- farction of the uterus are often not very prominent. Frequently the patient complains only of a feeling of weight in the pelvis and a sensation of “ bearing down.” The pressure of the enlarged uterus on the rectum and bladder usually causes constipation, as well as a frequent and annoying inclination to go to stool and to urinate. At the commencement of the disease, menstruation is often free and prolonged ; but the more the vessels of the uterus PARENCHYMATOUS METRITIS. 133 are compressed by the neoplastic connective tissue, the more diffi- cult menstruation becomes and the scantier the flow. Finally, the menses are often absent for months or years, while the regularly recurring molimina seem to indicate that the ripening and throwing off of the egg takes place at normal periods. In this form of me- tritis also—which, moreover, is always accompanied by the catarrhal form—the nutritive state of the patient usually suffers after a time, and the hypersesthesia and other disturbances of innervation, men- tioned in a previous chapter, usually develop. On physical exami- nation we may often feel the enlarged uterus through the abdominal walls above the symphysis pubis, particularly if we push it up a lit- tle with the finger introduced into the vagina. On vaginal exam- ination, we also discover that the vaginal portion is enlarged, indu- rated, and more or less painful. On introducing the uterine sound (which should not be employed unless the practitioner is skilled and experienced in its use), the increase in the long diameter may be ascertained. Although not dangerous, the disease is very obstinate and tedious. Even in its advanced stages it cannot be regarded as absolutely incurable ; the decrease after confinement of the uterus, which had been greatly enlarged during pregnancy, renders it not improbable that there may also be a retrocession of the pathologi- cally increased tissues of the uterus. Occasionally improvement and cure of infarction of the uterus have been seen directly after pregnancy, and in such cases it seemed as if, with the involution of the uterus after confinement, there had been at the same time a diminution of the physiologically and pathologically increased tissue. Treatment.—According to the variety of the exciting cause, the causal indications are fulfilled by the different rules prescribed in the preceding chapters. In many cases the continued use of slight laxatives is very beneficial, particularly the laxative waters of Marienbad, Franzenbad, Kissingen, etc. The indications from the disease are best answered by the repeated application of leeches (four to six) to the portio vaginalis. Although I have seen a most favorable effect from this treatment, in my own practice and in that of others, where the disease was recent, it has seemed of little use in protracted cases. Theoretically, also, we may expect better results from abstraction of blood while the connective- tissue formation is still new, and the catamenia are plentiful and con- tinued, than when the capillaries have been compressed, the uterus deprived of blood, and the menses have ceased. Before convincing ourselves by personal observation of the brilliant results of abstraction of blood in the first stages of parenchymatous metritis, and finding how well the patients bear the loss, it is usually difficult to make up 134 DISEASES OF THE UTERUS. our minds to increase the copious loss of blood by applying leeches to the vaginal portion of the uterus every week or two. A more irritating treatment, particularly the continued use of warm douches to the uterus, seems preferable in the later stages of the disease. These douches should be used about ten minutes every day ; the water employed should not be over 99° or 108° F. It is also worth while trying the use of Kreuznach and other saline baths, as well as the baths and waters of Krankenheil. The internal administration of iodide of potassium and of bromide of potassium, as recommended by Simpson, is also beneficial. [Acute metritis demands absolute rest in bed, the pelvis being kept somewhat elevated. When, from the tenderness of the belly, we suspect a complication with peritonitis, leeches should be applied to the abdomen and followed by cold compresses. When the inflam- mation seems limited to the womb, local depletion of that organ should be practised by leeching the vaginal portion of the cervix, unless the virgin condition of the patient forbids it. Scarification by means of Mayer’s lance-knife has, however, in a great measure supplanted the leech applied to the womb. It has the advantages over leeching that the procedure is quite painless, and that the amount of blood to be drawn can be nicely regulated by making the incisions deeper or shallower. Moreover, many observers believe that the suction of a leech may set up an irritation which tends rather to augment the fluxion toward the affected part than to check it. According to Schroeder, scarification should be repeated about every third or fourth day, not more than half an ounce of blood being drawn at one operation as a rule ; but if the patient is ple- thoric and the womb enlarged, an ounce may be taken. Syringing the parts with cold water is a practice which should never follow scarification ; for, although the cold produces a momentary con- traction of the vessels, a relaxation quickly follows, which brings with it a renewed congestion and thwarts the purpose of the op- eration. The demonstration by Emmet, of New York, that the majority of so-called ulcerations of the womb are really the effect of laceration of the cervix, is an important advance in the pathology and thera- peutics of this subject. He holds that lacerations occur during labor more often than has been hitherto supposed. They occur most fre- quently in the median line, and then heal readily, and generally escape notice. But if the rent is extensive, and runs in a lateral direction, the weight of the womb tends to force the lips of the wound asunder, so that union by first intention cannot take place. When the woman assumes an erect posture, the flaps diverge still PERIMETRITIS AND PARAMETRITIS. 135 further, and the mucous membrane of the cervical canal becomes everted and chafes against the vaginal walls. Through the irritation thus set up, the angle of the laceration becomes the seat of an ero- sion, which may spread over the everted surfaces. Such an ulcer heals with great difficulty, and only by granulation and by the for- mation of a dense cicatrix. The womb usually suffers subinvolution with all its consequences, and the cicatrices are a fruitful source of neuralgia and other forms of uterine irritability. As long as the fissure remains open, the ulceration is most refractory to all treat- ment. It is necessary to close the laceration by a surgical opera- tion. This i» judicious hands is neither difficult of accomplish- ment nor dangerous, and yields most satisfactory results.] CHAPTER III. PERIMETRITIS AND PARAMETRITIS. Inflammations of the parts about the uterus occur very fre- quently just after confinement, and not unfrequently at other times. In the latter case they usually depend on disturbance of the menses. If the inflammation starts from the serous coat of the uterus and its appendages, and the case is one of partial peritonitis, the disease is called perimetritis ; if, on the contrary, the inflammation is in the subperitoneal connective tissue, it is called phlegmon periuterina, or, according to Virchow, parametritis. Perimetritis leads to more or less copious exudation on the free surface of the peritonseum. Scanty fibrinous exudations cause adhe- sions with the neighboring organs. Even large fluid exudations are usually encapsulated by adhesions at their edges. After absorption of the exudation, adhesions to the pelvic organs often remain. In parametritis there is infiltration of the subperitoneal tissue, which is firm from the first. The infiltration may be reabsorbed ; but a firm induration often remains as the result of connective-tissue pro- liferation. In other cases the inflammation goes on to suppuration, and abscesses form, whose contents may perforate into the rectum, vagina, bladder, or abdomen. It is often difficult to distingnish between perimetritis and para- metritis during life ; they begin and run their course with more or less severe subjective and objective symptons of fever. The patients complain of pain deep in the pelvis, which is increased by pressure on the lower part of the abdomen. Generally, also, there are symptoms of compression of the pelvic organs, the bladder, rectum, 136 DISEASES OF THE UTERUS. and, according to my experience, of the nerves along the walls of the pelvis. The presence or absence, and the degree of severity and obstinacy of dysuria and difficult defecation, as well as of the pain extending along the sacral, sciatic, and crural nerves, depend in each case on the seat and amount of the exudation. Where there has been extensive exudation, on examination we may find a tumor of variable size above the pubis. Examination through the vagina or rectum usually shows that the uterus is displaced and firmly wedged in. Intraperitoneal exudations usually fill Douglas’s cul- de-sac, and may be readily felt. Subperitoneal infiltrations and abscesses are generally somewhat higher, but they aiso can mostly be reached by the finger. [Unless the two conditions should happen to coexist, the results of physical exploration show differences in many respects which can be made out by bimanual palpation. A peritoneal exudation sinks into Douglas’s space, as being the lowest level in the abdominal cavity. The cul-de-sac becomes distended and pushed downward. If the exudation has coagulated, or when a liquid exudation is incap- sulated so that it cannot yield to the finger, we can feel a more or less voluminous tumor, such as a retrouterine hasmatocele presents, lying behind the uterus and vagina, displacing the one upward and forward, and bulging the other forward and downward. On the other hand, the extraperitoneal exudation of parametritis is found as a rule toward the side of the womb, sometimes on both sides ; and through the vagina it feels at first like a resisting infiltration, and afterward like a hard, sharply-defined tumor, which seems to spring from the lateral edges of the womb, the boundary-line between the two being sometimes difficult to determine. In exceptional cases— as when Douglas’s cul-de-sac is closed by adhesions—a perimetritic exudation may likewise form in a more lateral region of the pelvic peritonaeum, and bulge downward ; and conversely, there have been rare cases of parametritic exudation into the areolar tissue, behind and even in front of the uterus and the upper vaginal region. In such instances, when the intra- and extra-peritoneal exudations exist together, a diagnosis becomes extremely difficult.] The disease may continue for weeks, and greatly exhaust the patient by the accompanying fever. [Extraperitoneal abscesses tend by preference to find an outlet at the surface of the body, especially in the groin, or from the iliac fossa, or after passing under Poupart’s ligament to appear upon the front surface of the thigh, or else to perforate backward through the ischiatic foramen and muscles of the buttock. On the other hand, intraperitoneal abscesses open moi’e often into the cavities of CONTRACTIONS AND CLOSURES OF THE UTERUS. 137 the body, particularly into the intestine and vagina. As a diagnos- tic hint, we will here mention that pain in a limb, really caused by pressure of an exudation upon a nerve, has now and then been mis- taken for a pure sciatica. Schultze also describes a latent parametritis posteriori, of insidi- ous, tedious course, usually due to mechanical causes, and said to produce a shortening of Douglas’s folds, and to be a most important factor in the production of anteflexion and anteversion.] The perforation of subperitoneal abscesses or of intraperitoneal exudations into the intestines or bladder is marked by the sudden decrease in size of the tumor, and by the evacuation of purulent masses with the stools or urine ; perforation into the abdomen causes severe general peritonitis, which quickly proves fatal. Even in favorable cases the patients generally recover slowly. In many of the patients under my observation the neuralgic pains lasted for months. Treatment.—[Treatment of an acute recent perimetritis de- mands absolute confinement to the bed, leeching to the groins, the application of ice-bags to the abdomen, mercurial inunction, confine- ment of the bowels by opium—in short, the treatment of a peritoni- tis. A recent parametritis calls equally for complete repose, but in other respects the treatment may be less active. The bowels should be gently moved, while cleansing and disinfecting injections should be frequently repeated, to clear away all putrid secretions, which are the common exciting cause of this form of inflammation.] Local abstraction of blood and the application of cataplasms to the lower part of the abdomen act well in the treatment of recent cases of perimetritis and parametritis. We should continue the use of the latter as long as there is any swelling left, even if there be no pain. In protracted cases I have found great benefit from the use of warm salt baths, with an addition of mother-liquid, and the internal administration of iodide of iron. At the same time, we must keep up the nutrition and strength by proper diet, and treat any existing fever by antipyretics. CHAPTER IV. CONTRACTIONS AND CLOSURES OF THE UTERUS—HJ)MOMETRA, HYDROMETRA. In young persons who develop late, moderate degrees of contrac- tion of the os uteri are quite frequent. They hinder conception, 138 DISEASES OF THE UTERUS. without rendering it impossible. Moreover, they impede the escape of the menstrual blood, and cause it to collect temporarily in the uterus, and to be expelled by painful contractions (uterine colic). I have frequently known women to menstruate without difficulty after their first confinement, who, during their maidenhood and the first years of married life, had severe uterine colic during menstrua- tion. Great flexions and angular curvatures cause contraction of the cavity of the uterus at the point of flexion, which also impedes conception, and occasions uterine colic during menstruation. Final- ly, neoplasia, Avhich encroach on the calibre of the uterine cavity and the cervical canal, have the same effect. Perfect closure, atre- sia of the uterus, is very rare. It is sometimes congenital, some- times the result of erosions and ulcers, which, in cicatrizing, have caused adhesions. The seat of congenital closure of the uterus is usually at the external orifice, that of the developed form at the internal orifice. As long as the women continue to menstruate, the menstrual blood collects behind the point of closure, causing hcemometrci. If the closure does not take place till the menses have ceased, the catarrhal secretion from the mucous membrane occasionally collects in the closed cavity, and distends the uterus. Sometimes this secre- tion resembles serum or synovia, doubtless because the excessive ten- sion destroys the secreting glands in the mucous membrane, and the latter becomes like a serous membrane. The above state is called hydrometra. In hcemometra, which, moreover, depends upon atresia of the vagina oftener than upon atresia of the uterus, the uterus may be gradually distended till it becomes as large as it does in the later months of pregnancy, and the blood contained in it, which is usually black and tarry, may amount to eight or ten pounds. According to the observations of Scanzoni and Veit, when the distention takes place rapidly, the walls of the uterus are thinned ; if it comes on slowly, they are thickened by hypertrophy. In the early stages it is difficult to diagnose liEemometra. During childhood closure of the uterus or vagina is hardly ever discovered. The first morbid symptoms occur about the commencement of puberty. At intervals of four weeks there is severe uterine colic, with a feeling of pressure and weight in the pelvis, and signs of severe congestion of the other pelvic organs, or of perimetritis. At first the patients feel well again after these symptoms have continued a few days ; but after four weeks there is a relapse. After a time the intervals are no longer free from pain. The abdomen increases in size ; the uterus rises above the symphysis pubis, and may rise as high as the navel. CONTRACTIONS AND CLOSURES OF THE UTERUS. 139 In the monthly attacks the pains become very severe. The patients emaciate, and may become marasmic ; or, if no mode of escape be furnished for the blood, the uterus may rupture, or they may die of peritonitis. The latter disease is particularly apt to occur if the tubes be also filled with blood, and their contents escape into the abdomen. Haemometra cannot be recognized with certainty, or distinguished from other forms of amenorrhoea or dysmenorrhcea, particularly at its commencement, without a careful local examina- tion. If, at the commencement of puberty, there be uterine colic at regular intervals of four weeks, while there is no escape of blood, and if there be, at the same time, a distention of the abdomen, which periodically increases slightly, wTe should suspect the develop- ment of a hcemometra, and urge an examination. If the haemome- tra depend on atresia of the vagina, we find the latter distended to a tense tumor, whose lower end extends into the vestibide. If the external os uteri be closed, the vaginal portion is often entirely obliterated, and the position of the os uteri may not be recogniza- ble. If, on the other hand, the internal os uteri be closed, the vagi- nal portion may retain its normal length. Besides this, we find the uterus distended to a considerable size ; sometimes, but not always, there is fluctuation. The treatment of hsemometra is purely sur- gical. It is rarely that a hsemometra terminates favorably without the intervention of skilled assistance. In such exceptional cases the blood finds a way either through the normal passages or else into one of the abdominal cavities. Sometimes menstruation ceases pre- matux-ely, or the climacteric arrives, when the symptoms abate, and the bloody contents of the uterus assume the character of hydro- metra. The treatment of haemometra is purely surgical, and con- sists in opening the sac between two menstrual periods. The mode of operation must necessarily vary greatly according to the circum- stances of the case. The procedure is a somewhat dangerous one, and demands attentive study in the books of surgery and gyne- cology. Of course, hydrometra can only result from acquired closure of the os uteri or vagina, and after the menses have ceased. Mild cases of the disease are seen quite often ; severer cases, where the uterus is distended to the size of a head or larger, are rare. The most important symptom of hydrometra is an enlargement of the uterus, which usually occurs gradually, and without exciting atten- tion, while in some few cases it is quite rapid and decided. This may be detected on physical examination, and is often even per- ceived by the patient. If the walls of the distended uterus be 140 DISEASES OF THE UTERUS. thinned, there is occasionally distinct fluctuation ; if they be hyper- trophied, we do not find this most important sign for distinguishing hydrometra from almost all other uterine tumors. Occasionally there is uterine colic, particularly during severe congestions of the uterus. If the closure be incomplete, these contractions sometimes force out the collected fluid, and, according to Scanzoni, occasion- ally also gases that have formed from them. The treatment of hy- drometra consists in surgically making a passage for the liquid, and in attempting, by astringent injections, to limit the secretion of the mucous membrane. CHAPTER V. CURVATURES OF THE UTERUS FLEXIONS AND INFARCTIONS. Etiology.—[Any abnormal change between the directions in the axis of the neck of the womb and that of its body is called a flexion; but it must be borne in mind that when the bladder is empty the womb is normally bent slightly forward. The bend or angle is nearly always at the internal os. When the deformity is such that the fundus inclines forward, and the curve or angle included be- tween it and the cervix is anterior, wre have an anteflexion ; the con- trary constitutes a retroflexion. There may also be lateral flexions, but they are rare.] There are various views regarding the pathogeny of these dis- tortions. Most authors think that the causes of the flexure lie in the uterus itself, and support their view on the fact that, at the point of distortion, the wall of the uterus is always flattened, and its parenchyma loose and reflexed. Virchow considers the changes at the point of flexion as secondary symptoms, due to the pressure on the walls of the uterus at this point, and to the amemia of the parenchyma caused by this pressure. It is his opinion that most distortions of the uterus, particularly anteflexions, are caused by congenital or developed shortening of the ligament of the uterus, and by its consequent fixation on distention of the bladder and rectum. It is most probable that the causes of the flexions are not always the same—that they are sometimes within, sometimes outside of the uterus. [Schultze believes that a posterior parametritis of insidious course and somewhat frequent occurrence causes a shortening and rigidity of the fold of Douglas, thereby producing a displacement backward and upward and fixing of the cervix, which is the com- monest cause of anteflexion as well as of anteversion.] Hetroflexions, the most frequent form in women who have had CURVATURES OF THE UTERUS. 141 children, are, on the other hand, rare in those who have had none ; they almost always date from the time of a confinement or an abor- tion. If the involution of the uterus go on slowly after its contents have been evacuated, if it remain enlarged and relaxed, the fundus readily sinks down on account of its weight, or is pressed down by the other contents of the abdomen. As the greater part of the ute- rus remains in the posterior wall after delivery, it is natural that it should most frequently sink backward ; but we cannot wonder if there are deviations from this, as they may readily be induced by different positions of the distended intestines in the vicinity, and by other accidental causes. At this period a complete return to the normal state is certainly possible. The bending of the uterus is straightened out when it contracts early. But, if this do not take place soon, the parenchyma, at the point of curvature, becomes anaemic and atrophied from the continued pressure, or the fundus uteri forms some abnormal attachment. In either case we have a permanent anomaly—a distortion in the strict sense. Scanzoni men- tions, as the most frequent cause, the slow and incomplete involu- tion of the uterus, and, as the most important etiological factors of the retroversion, early marriages, frequent and quickly repeated pregnancies, abortion, artificial delivery, etc. Anteflexions chiefly occur in those who have had no children. In young persons the most frequent cause seems to be a relaxation of the substance of the uterus by chronic catarrh ; in aged persons it is a senile atrophy of the uterus, at the point wrhere these distor- tions always occur, that is, near the internal os uteri. It is easy to understand that anteflexion should be the more frequent form of distortion in women who have had no children, if we remember that a virgin uterus has normally a slight inclination forward. In this case also, it seems to me, there is no doubt that the flattening of the wall of the uterus, and the atrophy of the tissue at the point of flexion which takes place after a time, are due to the pressure and anaemia. Besides these flexions, caused by anomalies of the substance of the uterus, there are others which are undoubtedly caused by short- ening of the uterine ligaments, as is proved by the cases observed by Virchow, where there were flexions without any structural change in the parenchyma. In the same way, distortion may result from fibroid tumors in the anterior or posterior wall of the uterus, from tense adhesions, or from the pressure of tumors. The more securely the lower portion of the uterus is held in place by a rigid vagina, the more readily flexions occur; the less firmly it is held, the more often displacements will occur instead. 142 DISEASES OF THE UTERUS. Anatomical Appearances.—On autopsy, flexions of the uterus may be readily recognized, as part of the anterior or posterior wall of the body, instead of the fundus, forms the highest part of the uterus. Generally we may readily restore the sunken fundus to its position, but it sinks back again to its former place when we let go of it. In some cases it cannot be restored to its normal position on account of peritoneal adhesions with the surrounding parts. Be- sides the flexion, there is almost always a slight anteversion or re- troversion. If we cut the uterus out of the body, and hold it erect by the vaginal portion, the fundus sinks down, either anteriorly or posteriorly ; if it be held horizontally, it not unfrequently holds its weight if the flexed portion be upward, but it bends together if we reverse it. The point of flexion is always near the internal os uteri. Here the flexion is sometimes slight, sometimes at right angles, or even at an acute angle. The os uteri is almost always moderately open, even in women who have had no children ; this is a natural result of the tension on the anterior lip in retroflexion, on the pos- terior lip in anteflexion. The internal orifice, on the contrary, is contracted partly by the flexion itself, partly by the swelling of the mucous membrane. In older women, we occasionally find complete atresia of the internal os uteri. The contraction or closure of the internal os uteri causes more or less hydrometra. The disturbance of circulation at the point of flexion sufficiently explains the almost constant complication with catarrh of the uterus, ulcers of the os, and parenchymatous metritis. Symptoms and Course.—The most constant symptoms of flexion depend on the impeded escape of the contents of the uterus. Hence the patients usually suffer severely from dysmenorrhoea as long as they continue to menstruate. Small clots of blood that has coagu- lated in the uterus are often mixed with the menstrual blood, which is evacuated with severe uterine colic. Uterine colic may also be caused, in the interval between the menses, by the impeded escape of the mucous and serous secretions, retained above the point of flexion. In many cases there are also the symptoms of uterine catarrh, as described in the first chapter, the fluor albus uterinus, decided loss of blood during menstruation, etc. Difficult and pain- ful evacuation of the rectum, desire to urinate and pain while doing so, the signs of ana3mia and bad nutritive condition, and finally the disturbances of innervation that have been so often mentioned, com- plete the description given by many women suffering from flexion of the uterus. But we must add that sometimes women with very decided flexions of the uterus never have any, or have but few, of these symptoms ; or, if they do occur, they soon pass off without CURVATURES OF THE UTERUS. 143 the disappearance of the flexion. Sterility itself, although very fre- quent, does not constantly accompany flexions of the uterus. Hence it appears that it is not the flexions, but the other anomalies of the uterus, which complicate them, that cause the symptoms above de- scribed. These complications are so frequent that their absence is an exception. This is partly because the same injurious influences that induce the flexions also excite the different forms of metritis ; partly because the disturbances of circulation at the point of flexion cause hyperfemia and exudation in the parenchyma, mucous mem- brane, and serous covering of the uterus. The course of flexions is very tedious. The disappearance of the condition is exceedingly rare, if it ever takes place. Flexion can only disappear completely if new parenchyma is formed in place of the flattened and atrophied uterine tissue. When, with advancing years, the periodical recur- rence of physiological congestion of the uterus ceases, all the symp- toms usually moderate ; and when, in aged persons, the uterus and part of its blood-vessels become atrophied, the patient may feel pretty well. On physical examination, the finger introduced through the va- gina first feels a dislocation, anteriorly or posteriorly, of the portio vaginalis, caused by the coexistent anteversion or retroversion. We also generally find the os so patulous that the point of the finger may be readily passed into it, even in women who have had no chil- dren. From the vagina, either before or behind the vaginal portion, wTe may find the body and fundus of the uterus, forming a round, firm, movable tumor. Usually, also, we may reach the point of flexion. The fact that the opposite part of the vagina is empty prevents our mistaking a flexed uterus for one that is enlarged, or diseased in some other way. The introduction of the uterine sound aids the diagnosis ; but when the uterus is flexed this operation is peculiarly difficult, and we again repeat that, in the hands of an unskilful physician, or even in those of a skilful one, the uterine sound is a dangerous instrument, which should be used as little as possible. Treatment.—We have already said that total disappearance of a flexion must to a certain extent be considered as a physiological impossibility, as it is almost always accompanied by atrophy of the parenchyma of the uterus at the point of flexion. “ Flexion instru- ments,” sounds, redressers, and intra-uterine pessaries, which were for a time much used for flexions, do actually no good, but much harm. Scanzoni has stated plainly that in his large gynecological practice he has never cured a flexion, and that he considers the use of flexion instruments as of no use, and dangerous. Tonics also, 144 DISEASES OF THE UTERUS. whether used locally or internally, promise no benefit. The advice that patients with anteflexion should hold their urine as long as possible, so that the distended bladder may raise up the fundus, and that patients with retroversion should retain the fieces for the same reason, is given from theoretical grounds, and has not proved correct. ( Virchow says that anteflexion results from great distention of the bladder while the uterus is fixed.) Most gynecologists advise wear- ing a firm girdle around the pelvis and lower part of the abdomen, and many patients praise the results of this treatment. It is diffi- cult to understand that, even in retroflexion, pressure on the lower part of the abdomen should relieve the patient. Perhaps their greater ease may be due to the compression of the uterus and its consequent bloodless state. Little as we can do to remove the flexions, we may do much to relieve the sufferings of the patient if we treat the catarrh and pa- renchymatous inflammation of the uterus, which first call attention to the flexion, according to the rules laid down in previous chap- ters. Occasional abstractions of blood from the portio vaginalis are peculiarly beneficial, and are almost always effective in cases of flexion. [To allay the distressing menstrual colic caused by retention of clots at the constricted point of flexure, most gynecologists resort to mechanical dilatation of the cervical canal. According to the expe- rience of Sims and others, bloodless dilatation by means of bougies is less beneficial than, and fully as dangerous as, incision of the neck by the metrotome.] CHAPTER VI. CHANGES OF POSITION OP THE UTERUS. The uterus, which is very movable, may be dislocated in any direction. The most important deviations in position are antever- sion, retroversion, descent, and prolapse. Anteversion most frequently occurs in women with strongly curved pelvis. The natural inclination forward of the uterus may be increased by the pressure from above of fluids in the peritoneal sac or of tumors, and anteversion may thus be caused. More fre- quently the uterus sinks forward from its own weight ; hence al- most always moderate degrees of anteversion accompany infarc- tions and new formations in the fundus uteri. Anteversion rarely becomes excessive, since each distention of the bladder restores the uterus to place, if some peculiar circumstance does not interfere with CHANGES OF POSITION OF THE UTERUS. 145 the reposition. Corresponding to this, the annoyance caused by the disease is usually slight, and it is only when the uterus is otherwise diseased and enlarged, or when it swells up at the menstrual period, that compression of the pelvic organs and tension of Douglas’s liga- ments cause pain in the small of the back, pressure in the pelvis, difficult micturition, desire to go to stool, and pain during defeca- tion. On vaginal examination, we find the portio vaginalis directed backward toward the hollow of the sacrum, and passing the finger forward we come without interruption upon the body and fundus, which lie against the anterior part of the vagina. Retroversion depends on the same causes as anteversion. A con- tinued pressure from before backward, tense adhesions on the pos- terior surface of the uterus or tumors in its posterior wall, cause a sinking of the fundus uteri into Douglas’s space, and a prominence of the vaginal portion toward the symphysis pubis. The retrover- sion that occurs independently during the first months of preg- nancy, and soon after confinement, is a very important disease ; that occurring at other times is generally only a subordinate result of other diseases of the uterus or other pelvic organs. The symp- toms of retroversion are analogous to those of anteversion, and they also depend on the pressure of the horizontally-displaced uterus on the pelvic organs, particularly on the rectum and bladder. Descent and prolapse of the uterus depend chiefly on relaxation of the parts that maintain the uterus in position, particularly its ligaments, the pelvic fascia, and the vagina. If, during this relaxa- tion, a stronger pressure from above downward act on the uterus, the latter is pressed down, inverts the vagina, and passes deeper into it, and the result is a descent. If part of the uterus protrude from the vulva, we speak of a prolapse ; when the entire uterus lies outside of the vulva, it is called a prolapsus completus. Relaxation of all the parts that should maintain the uterus in position occurs most frequently in the puerperal state ; and it is the abdominal pressure that most often presses the uterus downward. Poor wo- men, who cannot take care of themselves after confinement, but are obliged to do hard work that causes abdominal pressure a few days subsequently, are peculiarly liable to descents and prolapses. As every descent of the uterus inverts the vagina, and each prolapse of the uterus induces prolapse of the vagina, so, on the other hand, prolapse of the vagina may give rise to descent or prolapse of the uterus. If the lower end of the vagina be prolapsed, as a result of rupture of the perinseum during delivery, or from some other cause, the upper end exercises traction on the uterus, which either results in elongation of the vagina or descent of the uterus. De- 146 DISEASES OF THE UTERUS. scent or prolapse of the uterus only exceptionally occurs in women who have had no children. When they do occur, it is because the same conditions exist as after confinement, and particularly because the vagina is relaxed by blennorrhoea and venereal excesses, or the uterus is pressed downward by heavy tumors in the pelvis. If prolapse of the uterus take place suddenly, as occasionally happens from lifting heavy weights, from severe coughing, or strong bear- ing-down efforts, the stretching of the ligaments causes severe pain in the abdomen, and great general disturbance, fainting, nausea, etc. If the descent or prolapse develop slowly, there is usually but little annoyance at first ; this consists chiefly in an undecided feel- ing of pressure downward, and in stretching pain in the lower part of the abdomen and small of the back. The deeper the uterus de- scends, the more annoying these symptoms become ; they increase when the patient stands up, Avalks, coughs, etc ; they diminish dur- ing rest, and in the horizontal position. There are also inconven- ience and pain during urination and defecation, and there are con- stipation, colic, and other symptoms due to dislocation, pressure, and tension of the abdominal organs. If the uterus project from the vulva, it at first forms a round or oval tumor, as large as a wal- nut, which may be easily replaced ; but soon the uterus covered by the vagina advances, the tumor rapidly increases in size, and is re- placed with difficulty ; it feels doughy, but on firm pressure we may distinguish a hard body more deeply seated. If, with the anterior wall of the vagina, the fundus and posterior wall of the bladder be drawn through the vulva (cystocele), on the anterior wall of the prolapse we may see a tense and sometimes fluctuating tumor, which swells and subsides again several times during the day, and into which, by exercising some skill, we may introduce a male catheter through the urethra. On introducing the finger into the rectum, we find it bulged forward. The os uteri gapes open, because the vaginal portion is averted ; it is reddened and covered with glairy mucus. The prolapsed vagina is dry, parchment-like, thickened ; the epithelium resembles epidermis ; frequently it is ex- coriated by the friction of the clothes and the irritation of the urine that trickles over it, and not unfrequently deep ulcers form in it. The treatment of dislocations of the uterus is purely surgical ; and it would lead us too far to speak even of the choice of certain pessaries, and of the rules for their introduction and employment. FIBROID TUMORS OF THE UTERUS. 147 CHAPTER VII. FIBROID TUMORS OF THE UTERUS FIBROMYOMATA, FIBROIDS, DERMOIDS. [Pathology and Anatomical Appearances.—These growths are to be regarded as partial hyperplasias of the uterine parenchy- ma, and consist of masses of smooth muscular fibres intermingled in varying proportion with connective tissue. In their original form they always present rounded, sharply-defined tumors. They are non-malignant in their character, and are far more common than any other form of uterine growth. They rarely appear before pu- berty, and their liability to develop increases up to a certain point with the age, so that they are most commonly found in persons from thirty to fifty years old, while beyond this age they are compara- tively rare. They are met with both in the married and unmarried, and are often associated with menstrual disorder and sterility, which, however, must be looked upon as consequences rather than as causes of the disease. Nothing certain is known regarding their cause. Fibromyomata vary greatly in size. They may be no larger than a pea, or may form a tumor as large as the head, and may weigh several pounds ; but this is somewhat rare. They are sometimes solitary and sometimes multiple, and in the latter case they are usually small. The constitution of a fibromyoma varies. Sometimes the fibrous element preponderates, giving it more the character of a pure fibro- ma ; sometimes (but rarely) the growth consists almost purely of unstriped muscular fibres, thus approaching the true myoma in na- ture. Upon section, their structure is found to consist of more or less regular concentric layers of wTavy connective tissue, between which the finer bundles of muscular fibres are arranged. The more the firm, tendinous, fibrous tissue preponderates, so much the harder is the tumor and the paler its cut surface. When the muscular ele- ment prevails, the section presents more of the grayish-red coloring of the normal uterine tissue. As a rule, fibromyomata are but spar- ingly vascular, and very seldom contain large blood-vessels. There is, however, one form in which these tumors consist, either partially or totally, of enormously dilated blood-vessels. Sinuses filled with blood may even form, giving to the tumor a likeness to the erectile tissue of the corpus cavernosum, and also its capacity to swell and shrink ; so that sudden changes of volume in such a tumor can be observed ( Virchow's telangiectatic or cavernous myoma). 148 DISEASES OF THE UTERUS. Fibromyomata often exist in a conglomerated form. The tumor is then irregular and knobby in contour, instead of l’ounded. This shape is sometimes attributable to the blending of several indepen- dent tumors ; but more commonly the self-same morbid process which causes the original growths in their simpler form again re- peats itself in the substance of the new growth. Each vessel, with its appertaining connective tissue and muscular fibres, proliferates, and begets, as it were, a second generation of nodules within the older ones. Although the fibromyoma springs from the uterine paren- chyma, yet at a later stage it no longer remains closely connected with it, but lies within the uterine substance, though quite isolated from it by a layer of loose areolar tissue, so that it can very easily be enucleated. Sometimes, however, old fibroids of large size main- tain their connection with the womb by a pedicle, or even by a broad fibromuscular band. Such an attachment usually contains large blood-vessels. The womb is usually hypertrophied, but in advanced age it is atrophied. Now and then it is elongated and thinned, and it is often out of place. Fibromyomata rarely spring from the cervix, but rather from the fundus or body. Their classification according to their more su- perficial or deeper seat in the uterine wall is of great practical im- portance. Thus we distinguish (1) the subserous, (2) the submucous, and (3) the interstitial fibroids, although many tumors present in- termediate forms. In the subserous fibroma, the tumor, which usually has originated in the outer layers of the womb, tends to- ward the abdominal cavity, into which it projects in strong relief. Its base, at first wide, may by degrees grow narrower, and ultimately even present a mere stalk of the peritonaeum. Total detachment, indeed, has been observed ; but in such cases the growth has soon formed new adhesions, either in the vicinity of its point of origin or in Douglas’s cul-de-sac. Subserous fibroids are often multiple, and usually are small ; but if their vascular connection with the uterine parenchyma, by which they are nourished, should happen to be kept up, they may attain a great size, and rise into the abdo- men. By these large subserous tumors the womb is misplaced, distorted, and stretched ; but it is almost never hypertrophied. When springing from the side of the womb, they may penetrate between the two folds of the broad ligament, forcing them asunder so as eventually to lie quite outside of the peritonaeum. The sub- mucous fibroid, on the contrary, tends to grow inward, toward the cavity of the womb, into which it juts like a globe, distending it, and displacing it to the side opposite to that whence it springs. Its surface is covered either by mucous membrane alone, or by a thin FIBROID TUMORS OF THE UTERUS. 149 layer of parenchyma. The womb itself is usually hypertrophied as if pregnant, and the portio vaginalis is soon obliterated. Practically it is of great importance to distinguish between submucous growths having a broad attachment to the womb, and those which project into it so completely as to be held by a mere pedicle. The latter, the so-called fibrous polypi, are a subject for surgical treatment. The interstitial, intraparietal, or intramural tumors tend less to project from the uterine wall; but, where they become large, they cause a bulging of both inner and outer wall, thus taking an intermediate position between the two extraparietal forms of fibromyoma. The same variation as to seat holds good with regard to the far rarer fibromyomata of the neck and vaginal portions of the womb. Submucous fibromata of the cervix usually appear as fibrous polypi. These must not be confounded with the more common mucous poly- pus, which is merely a product of catarrhal relaxation of the mu- cous membrane with cystic enlargement of the follicles (ovula Na- bothi). The latter are easily distinguishable from the fibromyomata by their softness and smallness, rarely exceeding a hazel-nut in size. Uterine fibromyomata may undergo many further transforma- tions. The commonest one is an accumulation of liquid in the lymph- spaces, which dilates them, causing an oedematous softening of the tumor, and sometimes a cystic metamorphosis. In the latter case we find either numerous small cysts, or else a large cavity whose ragged sides and trabeculae announce it to be the product of the blending of several smaller cysts. Heteroplastic action may also arise, such as myxomatous or colloid degeneration, sarcoma, or cystosarcoma. True cancer probably does not occur, except as a secondary disease, by metastasis or by propagation in continuity from a cancer of the uterus proper. Symptoms and Course.—The symptoms of a fibromyoma vary greatly, according to the size and seat of the tumor. Small subse- rous growths, or those which are completely extraparietal, and which, being merely attached by a thin stem, have ceased to grow, often give no symptoms at all. Sometimes a small growth flexes or upsets the womb by its weight, either backward or forward, accord- ing as its .seat is in the front or back wall of the organ. A large extraparietal tumor, on the other hand, displaces the womb in the direction away from its seat, or sometimes draws the womb up with it into the abdomen. The pressure exerted by a dislocated womb or by a voluminous tumor upon adjacent parts may cause various evils—backache, incontinence or retention of urine, obstruction of the rectum, swelling of the feet, neuralgia, or even paresis of a leg. The irritation often causes local peritonitis, with consecutive incap- 150 DISEASES OF THE UTERUS. sulated exudation, or with adhesions ; and these latter may by and by hinder the tumor from lifting itself as it grows out of the pelvis, so that the pressure upon the other pelvic organs may give rise to the symptoms of incarceration. All these pressure-symptoms usu- ally grow worse during the menstrual period. The submucous fibromyomata also soon create serious distress. In this form the distended and hypertrophied womb itself forms the tumor, and when large it naturally produces the same pressui’e-symp- toms as those caused by subserous tumors. But the growth, being enclosed in muscular masses, excites the latter to strong contraction. The tumor, projecting into the womb, stretches and irritates its mu- cous lining, thus inducing leucorrhoea and haemorrhages of great frequence and severity. These metrorrhagias occur even when the tumor itself is very poor in blood-vessels, and proceed entirely from the mechanically overladen vessels of the mucous membrane. At first the bleedings seem to attend the menstrual periods, which are then excessive and followed by a mucous discharge. By and by the haemorrhages recur irregularly, and with ever-increasing frequence and severity, so that the patient’s life may be jeoparded by sheer loss of blood. Great suffering during menstruation also arises in this form of fibroma. There is pain, which is sometimes continuous, and sometimes an intermittent uterine colic, like labor- pain, due to the obstruction by the tumor to the menstrual flow. If the catamenial function ceases permanently—and this is apt to take place quite late in life in these cases—this distress is abated or ceases entirely. Interstitial tumors occupy a middle posi- tion both as regards seat and symptoms. Being well surrounded by uterine tissue, and being under more favorable conditions for growth than the subserous and submucous tumors generally are, their de- velopment is often quite rapid, and they sometimes attain colossal dimensions. The existence of a fibromyoma cannot be made out without man- ual examination, and even then it is sometimes very difficult. The subserous tumor is felt as a hard ball-like or nodular lump, which, if it spring from the fundus, can be felt more easily through the ab- dominal wall, and if from the lower part of the womb, is best found through the fornix vaginae. The examination should aim to prove that the tumor really proceeds from the womb, and does not merely lie next to it. Sometimes an ovarian cyst or an old parametritic or perimetritic exudation adheres so closely to the uterus that nothing will shed light upon the case but a due weighing of other facts, such as the consistence of the mass, which, if a fibroma, should be hard, and never is soft unless it be in a state of cystic degeneration, FIBROID TUMORS OF THE UTERUS. 151 when it is more like an ovarian cyst in consistence ; or else the his- tory of the case would show a preexisting pelvic inflammation, had any occurred. Subserous fibroids attached only by a thin fibrous stem are often thought not to belong to the womb, and, although too hard to be mistaken for ovarian cysts, may be difficult to distin- guish from a solid ovarian growth. The examination should further determine that the object felt is not the womb itself, displaced and enlarged. An anteflexed or retroflexed womb may simulate a tumor lying in the uterine wall; but conjoined manipulation will demon- strate that beside the tumor in question a second one exists, which, in situation, form, and consistence, corresponds to the womb ; and, if necessary, the introduction of a sound will show by its direction that it does not enter the tumor, but takes an entirely normal course. Sometimes by means of the sound we can tell that the uterus, al- though distorted and displaced, by no means corresponds in length with the volume of the tumor. Submucous fibroids lie hidden within the womb, and distend it; hence they may be confounded with other conditions which cause uterine enlargement—above all, with pregnancy, uterine infarction, and hfemometra. Unless the history of the case and other circum- stances distinctly preclude the supposition, the tumor may be mis- taken for a gravid womb, because the same general disorders which characterize pregnancy, as well as the changes in the breasts which then arise, may likewise be met with now. The condition of the vaginal portion is of great value in the diagnosis. In pregnancy it is remarkably soft and flabby. In a case of fibroma the cervix rapidly disappears, and the os uteri will gape so that the tumor within it can easily be found. The uterine souffle so regularly heard in pregnancy is, nevertheless, not a sure sign of that condi- tion ; for it also is heard in cases of fibroma, and in rare instances where there is an ovarian growth. In chronic metritis the tender- ness of the womb to pressure stands in contrast to the insensibility of a fibroma. Moreover, in infarction the vaginal portion is thick- ened and not obliterated, and the sound enters easily ; whereas a fibroma opposes an obstacle to its passage, not always readily over- come. After excluding pregnancy, the diagnosis may be sometimes facilitated by the introduction of a sponge-tent into the cervix. The canal being thus dilated, it becomes practicable to examine precisely the tumor with the finger and sound, and particulai-ly to determine whether the tumor is attached by a broad base or by a slender pedicle—a matter of the utmost importance as regards therapeutics and prognosis. Interstitial tumors bulge less distinctly 152 DISEASES OF THE UTERUS. into the uterine cavity, and the enlargement of the organ is not so general and uniform. Very large interstitial fibromata, which rise into the abdomen, may be mistaken for other abdominal growths ; not for ovarian cysts, however—which, though hard in places, also as a rule present elastic, fluctuating portions to the touch—but rath- er for solid ovarian tumors and for subserous fibromata. But in these two cases the womb itself does not form part of the tumor, but is merely displaced by it; and we must strive to ascertain if the two bodies can be made to move independently of one another. If so movable, the growth is probably ovarian ; if attached, it is most likely a subserous fibroid ; but no absolute certainty of this can be attained, because an ovarian growth may be bound fast to the womb, and a subserous fibroid with a long pedicle may float freely. When the uterine sound 'passes deeply into a tumor, or when its tip can be felt through the walls of the growth, we may infer that the mass is not merely attached to the uterus, but is the uterus itself. An expert with the sound can also determine that the enlargement of the organ is not uniform, but chiefly affects one or other wall. This decidedly points toward the presence of an interstitial fibroid. Fibromyomata of the cervix, which are more rare, are easy of diagnosis. They present either rounded, hard, circumscribed lumps, which distend one of the lips of the os, or else appear as fibrous polypi protruding from the cervix. Prognosis.—The prognosis of uterine fibromyomata has its good and its bad points of view. The fact is well attested that such tumors have now and then shrunk away and disappeared, but such good fortune must never be counted on ; the more so, because these rare cures seem never to be due to treatment, but rather to favor- able accidental conditions—parturition, the climacteric, or the like. The affection is generally to be regarded as incurable ; yet the prognosis is so far favorable that life is seldom immediately imper- illed by it. Sometimes, indeed, the envelope of the tumor suppu- rates, causing peritonitis or pyaemia ; and the general nutrition has been known to suffer seriously through the pressure of an enormous fibrous tumor upon adjacent abdominal organs. The tumor some- times ceases to grow so early as never to cause any symptoms ; while others by their development render life a burden, until the attainment of the climacteric brings about an arrest of development, or until a sort of imperfect retrogression takes place by calcification of the tumor. Spontaneous expulsion of the growth through the uterine canal has been observed in a series of cases. A few times it has been known to be expelled into the abdomen or into the blad- der, and even to be discharged through the abdominal walls. Such FIBROID TUMORS OF THE UTERUS. 153 an event is either the result of sloughing and suppuration of the capsule, with subsequent bursting of the resulting abscess, in which case the danger to life is very great, or else the extrusion conies to pass by the less dangerous method of spontaneous enucleation. A tumor juts from the os ; at its apex an opening forms by sloughing of the mucous membrane, and through this opening, which enlarges more and more, the tumor is gradually pushed by the uterine con- tractions. It sometimes happens that, pregnancy occurs notwith- standing the presence of a fibromyoma. Childbed in such a case is beset with peculiar dangers. Treatment.—Very little reliance is to be placed upon medical treatment of a fibromyoma with a view to its dispersion, arrest, or atrophy. Iodide of potassium, bromide of potassium (first proposed by Simpson), chloride of calcium (Rigby), arsenic and phosphorus (Gueniot), seem to effect very little ; while the brine-baths, particu- larly those containing bromine and iodine (Kreuznach, Munster am Stein, and Adelheidsquelle in Bavaria), seem sometimes to bring about a certain reduction in bulk of the tumor. Hildebrand claims that by means of subcutaneous injections of ergotine, employed originally to control the bleeding, not only the haemorrhage, but also the tumor, was made to disappear; but, in spite of other corroborative testimony, the value of this treatment is not yet es- tablished. Some fibromyomata are curable by surgical treatment ; and by following nature’s suggestion of spontaneous enucleation, not only submucous tumors, but even interstitial ones, have been removed through the vagina by a surgical operation, though at considerable risk to life. As a last resort, indeed, to save life, when the rapid growth of the tumor was obviously about to kill the pa- tient, extirpation of the tumor, either with or without the womb, has been successfully accomplished. The surgical treatment of pedunculated submucous tumors is more satisfactory ; and we not seldom meet women, who have been brought almost to death’s door by persistent haemorrhage from fibrous polypi, restored in a few months after their removal to a state of blooming health. As a rule, however, we must renounce the expectation of actually curing a fibromyoma, and content ourselves with enjoining a quiet mode of life, with little physical exertion or excitement, forbidding frequent sexual intercourse, and with practicing small local blood-let- ting upon the vaginal portion, with regulation of diet; also with the recommendation of a treatment during the summer-time by baths calculated to retard the growth of the tumor. Regarding the treat- ment of the bleeding, we refer to the article upon menorrhagia.] 154 DISEASES OF THE UTERUS. [CHAPTER VIII. CANCER OF THE WOMB. Etiology and Anatomical Appearances.—Primary cancer appears more frequently in the womb than in any other organ of woman, not excepting the breast. Secondary cancer of the womb, on the other hand, is rare. Nothing certain is known as to the cause of this miserable disease, and its assumed hereditary trans- missibility is not proved. It is met with chiefly among married persons, especially among multipara, and with increasing frequency from the thirtieth year up to the climacteric period, which age fur- nishes the most victims. Beyond it cancer is common enough still, and does not become a rarity until the seventieth year. The point of origin of primary cancer is almost always in the neck of the womb, very rarely in its body. According to Waldeyer, all forms of cancer spring from the true primordial epithelium of the organism, and hence are to be regarded generally as epithelial growths ; and even the smootli and papillated cancroids formerly distinguished as carcinomata are to be included in this category. The development of cancer of the cervix is as follows : The super- ficial epithelium of the mucous membrane proliferates, throwing offshoots into the connective and muscular tissue beneath it. These sprouts, ramifying in all directions, everywhere form new nests of cancer-cells, and encroach more and more upon the normal tissues, which finally break down and ulcerate through pressure and arrest of circulation. The cancerous infiltration meanwhile continues to invade new tissues around it, which in their turn ulcerate. This is often accompanied by considerable development of the papillae of the mucous membrane, and this is in the beginning liable to be confound- ed with the non-malignant papillary outgrowth due to catarrh. In- deed, it has been assumed that papillomata, originally simple, might change into cancer by consecutive ingrowth of their epithelium into their basement-tissue. At a later period the malignant papilloma is distinguishable from the simple form by the rapidity and luxuri- ance of its growth, and by its early ulceration. At other times, in- stead of papillae, there develops a smooth, knotty group of swellings in one or other lip, or perhaps throughout the whole circumference, of the os. These nodules, unless they prematurely break down by ulceration, may form a tumor which fills the upper part of the va- gina. But there are cancers which do not begin at the surface, but originate deep in the interior of the neck, and develop as circum- CANCER OF THE WOMB. 155 scribed knots pushing toward the surface. Even this form of can- cer, however, must derive its origin from preexisting epithelium, probably from isolated cervical glands, and from abnormally dis- tributed vestiges of the primordial epithelial germ. Sometimes the disease takes the form of a firm scirrhus, but more commonly it assumes that of a soft medullary cancer, with a predominance of epithelium and with scanty connective tissue. The infiltration and ulceration travel upward to the internal os, and sometimes even in- vade the body of the womb. Thus not the neck alone, but a large part of the body of the organ, may disappear. An extension of the disease to the vagina imparts to the latter a hard, puffed-up, brawny quality, so that the finger can no longer recognize the os uteri. Still later, the cancerous infiltration of the ureters often causes obstruc- tion of the urine and hydronephrosis (even to the extent of fatal uraemia), and, by invasion of the bladder and rectum, with conse- quent destruction of the septa separating these cavities, large fistulae are formed ; and it has even happened that all three cavities have been blended into one horrible cloaca. The tubes, ovaries, and other pelvic organs, and the muscles, areolar tissue, and even the bones, are finally attacked, either by contiguity or by metastasis ; so that at last the womb is, as it were, walled up by cancerous in- filtration and peritoneal adhesions. More distant regions finally arc invaded—the inguinal and retroperitoneal glands, the peritonaeum, omentum, mesentery, intestine, liver, and perhaps even the breast. Symptoms and Course.—In the earliest stages of uterine can- cer there is slight pain in the back and abdomen, the menstrual flow is augmented, and there is leucorrhcea, which is not at first profuse, except in a case of malignant papilloma. So little is pre- sented to distinguish it from the more unimportant disorders of the sexual organs, that in the beginning the malady is rarely recognized. It would seem, indeed, that that form of it wdiich commences by deep-seated nodules presents no symptoms whatever so long as the mucous membrane remains intact. In many cases no serious symp- toms arise until the cancerous mass begins to ulcerate and break down ; so that the period for operative interference has already passed ere the nature of the malady has been recognized. Indeed, even in the earlier stages, while the mucous membrane remains sound, a local examination will not always reveal the existence of cancer, and the most experienced gynecologists admit that the dis- tinction between a cervix enlarged by cancerous infiltration and a simple hypertrophy of the neck may at first be impossible. Schroe- der describes a condition of the mucous membrane as characteristic of cancer even before the period of ulceration. The membrane is 156 DISEASES OF THE UTERUS. tightly adherent to the tissues underlying it. As Waldeyer has it, the mucous membrane seems to be tacked down by the ingrowing epithelial sprouts, which penetrate the tissues beneath them like so many brads. After' it has attacked the vagina and surrounding connective tissue, the recognition of cancer is easy. When the period of ulceration sets in, a series of grave and often very distressing symptoms arise. The leucorrhcea becomes more profuse, and somewhat sanguinolent (like meat-washings), and final- ly, by admixture of gangrenous particles, acquires an ichorous char- acter, and assumes a darker dirty-brown or greenish-black color, and emits so foul and putrid an odor as to disgust not only the neighbors but the patient herself. Haemorrhage is rarely absent. In the beginning there is merely an augmentation of the menstrual flow, but the bleeding afterward becomes irregular, and is often the first symptom which alarms the patient. Elderly women, how- ever, are prone to ascribe such bleedings to the irregularities com- mon at the menopause, and hence give themselves little concern over it. Only in cases of hard cancer is haemorrhage ever absent. It is most profuse in the papillary form. Notwithstanding its fre- quence and abundance, which often reduces the patient to the low- est stage of anaemia, a fatal haemorrhage is rare. The abdomiqal and lumbar pains are sometimes insignificant throughout the disease ; while at other times the patient suffers in- describable agony, especially during the night. This violent pain does not depend upon the ulceration, but upon extension of the can- cerous growth into the connective tissue and other parts of the body, and appears to be due to pressure of the indurated mass upon the nerve-twigs which it encloses. Besides this, there may be sharp pain from pressure set up by a secondary peritonitis, arising from the irritation of the cancerous nodules. Finally, the pain may as- sume a paroxysmal form—-a uterine colic—in consequence of an ob- structed outflow of blood and secretion from the womb. Incessant and painful urinary irritability indicates invasion of the bladder, while a suppression of the urine makes it probable that the ureters are occluded by the growth. Obstinate constipation, followed by tenesmus, haemorrhoids, and diarrhoea, indicates an implication of the rectum. Prior to the stage of ulceration the general health of the patient is fairly comfortable ; afterward she grows pale, anaemic, cedema- tous, and emaciated, and the countenance often presents that dirty- yellow coloring so commonly seen in cancer, although not a trust- worthy sign of it. The more frequent trie bleedings, the more profuse the discharge, and the more constant and severe the pain, CANCER OF THE WOMB. 157 so much the sooner does the general health of the patient give way. There is also almost always a derangement of the stomach, with loss of appetite and loathing of food, and a tendency to nausea which contributes to break down the strength ; and it is often hard to determine whether the vomiting is due to a sense of disgust, or arises from gastric catarrh or gastric irritation reflected from the genital organs, or from the effect of uraemic poisoning. Ulceration usually first attacks the inner surface of the lips of the os. After this has once begun and loss of substance has taken place, the diagnosis by digital and ocular examination is no longer difficult. One source of error might be the destruction of the va- ginal portion of the cervix by that very rare form of ulcer {ulcus phagedoznicum corrodens) first described by Clarice, and identified with certainty in a few instances only by Klebs and JCoerster, and the cause of which is still unknown. In a doubtful case, nothing hut the microscopic examination of an extirpated portion of the cervix can determine whether the base of the ulcer contains traces of carcinoma or not. But, after all, the prognosis of a corroding ulcer is scarcely better than that of cancer; for our experience has shown that neither by the strongest caustics, nor even by the hot iron itself, can the ravages of the latter he checked and the ulcer healed. As we do not generally know how long the latent stage of cancer has existed, its duration can rarely be stated with certainty. Dating from the time of first discovery, Gusserovj estimates that most pa- tients succumb in about a year or a year and a half. Yet there are examples of a rapid course of only a few months, and others again of several years’ duration. Death usually takes place from exhaus- tion, or else the patient dies of complications. These are acute or chronic uraemia, gradual or perforative peritonitis, miliary carci- nosis of the peritonaeum, septicaemia, dysentery, diphtheritic inflam- mation of the vagina or bladder, pneumonia, or (what is more rare) embolism of the pulmonary artery, embolic gangrene of the lungs, fatty degeneration of the heart, pyelonephritis, or pylephlebitis as a consequence of putrid thrombosis of the portal vein. Treatment.—The treatment of cancer of the womb is essen- tially surgical, and an operation, although it very rarely cures the patient, yet affords the only chance of effecting even a temporary improvement. Unfortunately, the malady is seldom brought under treatment until the vagina has become implicated, or until so much of the cervix is involved that an amputation can no longer he made through healthy tissue. Yet even then the operation is justified as affording a last chance for prolonging life. This is best done by 158 DISEASES OF THE UTERUS. removing all parts which seem affected by knife or scissors, and by scooping away the less accessible portions by means of Simon’s sharp spoon, and then by cauterizing the wound with the hot iron, or by means of the alcoholic solution of bromine first recommended by Mouth, and approved by Schroeder and Ilenneberg. Otherwise the escape of cancerous offshoots which often exist in parts seem- ingly healthy, or of remnants of the ulcer which often extend up to the inner os, may render the operation abortive. The relief of pain is the most important duty in treatment of the symptoms. Hypo- dermic injections of morphine and opiate enemata are often quite indispensable. When the flow is profuse, copious astringent vagi- nal injections are demanded ; and for the foul odor we must employ disinfectants, such as carbolic acid, permanganate of potash, and chloride of lime. The haemorrhage is to be combated by the use of ice, or of cold or very hot injections, or of dilute liquor ferri ses- quichloridi; or else we must tampon with sponges, or plugs of cot- ton charged with strong liquor ferri cliloridi. For the insomnia which is so common, chloral furnishes an invaluable remedy.] CHAPTER IX. ANOMALIES OF MENSTRUATION. [It has generally been assumed that the menstrual flux is inti- mately connected with the ripening and bursting of a Graafian ves- icle, and with the escape therefrom of one or more eggs ; but this view of the subject has latterly been contested, and the complete independence of ovulation and menstruation has been asserted (Bei- get). According to our present information upon the subject of ovulation, the uterine mucous membrane at puberty undergoes cer- tain periodical metamorphoses, the nature of which has been ascer- tained by the researches of Kundrat and Engelmann. They find that at the menstrual period the uterine mucous lining swells up and develops ; its glands elongate and dilate, and a proliferation of the round cells of its basement-tissues takes place. This process is fol- lowed by a retrogressive one, based upon a fatty degeneration of the upper layers of the mucous membrane, so that the bleeding is caused, not, as is generally supposed, by a menstrual fluxion and hy- peraemia, but by destruction of the mucous membrane through fatty degeneration. The purpose of the increased development of the mucous membrane is that the egg may be received into it, and only at this time of so-called nidation is the growth of a fructifying egg ANOMALIES OF MENSTRUATION. 159 possible ; while in the remaining period, that of so-called denida- tion,, during the menstrual flow and during the exfoliation of the mucous membi’ane, any egg which may reach the uterus will perish. Hence it would at first seem as though conception could only take place after a coitus immediately preceding menstruation, and never from coitus following it ; but we should bear in mind that the ripened egg which leaves the ovary at the menstrual epoch re- quires a certain period of time, not precisely known, for its passage through the tube, at the end of which period the state of denidation may have passed over. According to the newest views, those of John Williams, based upon examination of twelve wombs, the re- generation of the fatty mucous lining begins immediately after ces- sation of the bleeding, and progresses steadily until the next retro- gressive period commences. Thus the womb would seem never to be at rest, but to be either in a state of evolution lasting about three weeks, or of involution lasting about one week. Only at the period of involution would implantation and fixing of the ovum (as far as the womb is concerned) seem to be impossible, while impregnation might take place at any part of the period of evolution. Bischoff\ however, doubts if an egg be capable of fructification during the latter part of the period of evolution. More probably the egg must receive an impulse toward further development from the seminal fluid while still in the tubes, and only in the improbable event of an egg’s requiring three weeks to traverse the tube would there be no period of intermenstrual unfruitfulness.] Anomalies of menstruation are not independent diseases, but are symptoms of affections of the sexual organs, or of other diseases impairing the general health. Hence the discussion of amenor- rhcea, dysmenorrhcea, menorrhagia, etc., does not properly belong to a text-book of special pathology and therapeutics, but to a work on semeiology and diagnosis. Following the example of most au- thors, for practical reasons, we will give a short account of the most important menstrual disturbances. Too early menstruation—menstruatio prcecox—is not frequent, if by this term we mean only those cases of haemorrhage from the female genitals before puberty that are accompanied by the expul- sion of a ripe ovum. As we have no certain means of finding out whether this complication exists or not, we must note whether the haemori’hage recurs at regular intervals ; whether it is accompanied by disturbance of the general health, by pains in the back, and other symptoms which almost always accompany menstruation proper. Haemorrhage occurring once, or at irregular intervals in the course of acute diseases, particularly of acute infectious dis- 160 DISEASES OF THE UTERUS. eases, as well as in chronic dyscrasia and venous congestions, has nothing to do with menstruation. If, in our climate, menstruation begins between the twelfth and fourteenth years, instead of the fourteenth and sixteenth, it is only a morbid symptom if the girl he undeveloped. Many girls at this age, who still go to school and wear short clothes, have full breasts and hair on the pubes. We may say that they have developed too early, but not that they have any anomaly of menstruation ; in them the absence of the menses would be pathological. But, besides these cases, we not unfre- quently find apparently undeveloped girls, aged eleven or twelve years, with regularly-recurring haemorrhages from the genitals, and such characteristic symptoms of congestion in the pelvis that we cannot doubt there is a case of early ovulation—a true menstruatio praecox. Experience shows that almost all such girls subsequently suffer from obstinate chlorosis. Cases where menstruation has been observed in small children are only partially reliable. It is very rare indeed for menstruation to cease several years too late. Among us, women usually menstruate till forty-five or forty-eight years old. If menstruation has begun early, it usually ceases somewhat sooner ; if the reverse, it continues a few years longer. Scanzoni has seen only one case, in his practice, where an unmistakable menstrual haemorrhage continued to the age of fifty- two years. Even very old women are inclined to regard all haemor- rhage from their genitals as menstrual. Of course, we can only speak of amenorrhoea when the menses are absent in a woman who lias attained the age of puberty, and has not passed the climacteric, and who is not pregnant or nursing. [Above all, be it observed that the absence of menstrual flow does not warrant the inference that ovulation has ceased. We know, in- deed, that conception may take place during amenorrhoea. On the other hand, the cessation of ovulation after destruction of the ova- ries is not always followed by absence of the menses. In excep- tional cases menstrual bleeding has been observed to continue for some time after the sexual function has been destroyed.] Tardy menstruation is one form of amenorrhoea ; too early ces- sation is another form. If a girl sixteen or eighteen years old be no more developed than one of ten or twelve years, she can no more be said to have retarded menses than a fully-developed girl of twelve or thirteen who menstruates can be said to have menstru- atio prrecox. Except in cases of tardy menstruation or too early cessation of the menses, amenorrhoea more frequently depends on constitutional disease than on local affections of the genitals. It is chiefly chlorosis, scrofula, and tuberculosis that retard the occur- ANOMALIES OF MENSTRUATION. 161 rence of menstruation, or cause its arrest. It is not always easy to determine, in these cases, whether the ovum does not ripen, or whether only the haemorrhage that usually accompanies the expul- sion of the ovum is absent. If, at intervals of four wTeeks, we no- tice more or less decided molimina, accompanied by swelling of the breasts and increased discharge of mucus from the genitals, it would seem as if only the haemorrhage were wanting ; in the reverse cases, we may suppose that ovula do not ripen. Among the dis- eases of the sexual organs, degeneration of the ovaries rarely causes amenorrhoea, and only does so when both ovaries are at the same time the seat of organic disease. Among the various diseases of the uterus, chronic catarrh, and especially chronic infarction, in which the blood-vessels are compressed by the shrinking connective tissue, most frequently induce this disease. Amenorrhoea occasion- ally occurs in strong, healthy girls, in whom the genitals have not developed so rapidly as the rest of the body. Lastly, Scanzoni concludes, from the cases where the menses (which had previously been normal) ceased on the occurrence of paraplegia, that amenor- rhcea may result from abnormal innervation. The sudden arrest of the menstrual flow—suppressio mensium— is most frequently the symptom of acute metritis. It depends on the same injurious influences that we mentioned in the etiology of that disease, and is accompanied by the same symptoms. More rarely the menses cease suddenly, if the amount of blood in the uterine vessels be lessened by a diminution of the entire amount of blood in the body by venesection, or by excessive fluxion to some other organ. [Sometimes, at the period when the menstrual flow should appear, instead of it a bleeding occurs from some other region, from a haemorrhoid, from a wound or ulcer, from the nose, the bronchi, or the stomach. Such bleeding, it would seem, might properly be called “ vicarious ” so long as it was supposed that the menstrual flux had the effect of evacuating effete matter from the system. It might then have been inferred that refuse which was not voided by legitimate methods might be advantageously got rid of by un- usual processes. Nowadays, however, with our present conceptions of the nature of menstruation, it is difficult to And a reason for a vicarious menstrual haemorrhage. When we remember that the amount of the flow in all is only from about eight ounces to (at the utmost) about thirty ounces, the theory that the omission of an habitual menstruation can give rise to a general plethora must seem very rash. Most probably vicarious haemorrhages stand in close relation to a very active general nervous and circulatory excite- 162 DISEASES OF THE UTERUS. ment, accompanying ovulation, under the influence of which bleed- ings may take place at points predisposed to it, both when the menses are absent and when they are present. The direct treatment of amenorrhoea by emmenagogues has un- dergone great limitation of late years. Many of the ancient physi- cians (mistaking cause and effect) were disposed to ascribe divers disorders to amenorrhoea as a cause, and to consider the reestablish- ment of the menstrual flow a matter of great importance ; where- as, in many a broken-down subject, it is rather to be wished that she may not be still further prostrated by loss of blood. Some- times, however, in exhausted, bloodless patients, the growth of the Graafian vesicle is arrested, and the periodical ovulation with its uterine hyperoemia does not take place. Such amenorrhceas, arising from defective nutrition and anaemia, can only be successfully treated by allaying the main disease by tonics, iron, strengthening diet, fresh air, and the like. All the different emmenagogues pos- sess in common the property of inducing hyperaemia of the pelvic organs, and especially of augmenting a congestion which already exists, and thus of producing a haemorrhage. This object is most certainly obtained at the time when the menses should naturally return. This period is not, however, invariably one of twenty- eight days ; for it may vary by several days in the same woman. Accepting the results of recent researches, that menstrual flow does not proceed from engorgement alone, but is also the effect of a fatty degeneration and exfoliation of the uterine mucous membrane, it becomes impossible to admit that the flux can be induced by em- menagogues at any other time than that of nidation. Artificial induction of the menstrual flow may be called for when certain disturbances (pain in the back, local congestion, and the like) which normally accompany menstruation indicate a con- gestion of the pelvic organs, and that the haemox*rhage which should promptly relieve them has failed to arise. Measures calculated still further to augment the hyperscmia of the womb may then be re- sorted to to bring on the bleeding. These are irritating foot-baths, w'arm sitz- or full-baths, dry cups or mustard-plasters to the thighs, a hot or even a cold douche to the sacrum, clysters of aloes, or direct irritation of the womb by irritating vaginal douches. More rarely, painting the os with iodine, passage of a sound, or electricity may be tried ; but we should be slow to resort to the internal exhibition of aloes or of savin, on account of their undesirable secondary ef- fects. We must bear in mind, too, that, if we fail to induce the flow by these means, we may nevertheless so augment the uterine congestion as to aggravate the existing distress. Hence the use of ANOMALIES OF MENSTRUATION. 163 emmenagogues is only proper when the amenorrhoea is due solely to feebleness of the uterine congestion. In other cases the conges- tion is to be relieved by local depletion, leeches, or scarification of the vaginal portion, or in virgins by cups applied to the inner side of the thighs.] Menorrhagia, or too copious menstrual hajmorrhage, has been already mentioned as a symptom of various structural changes and of tumors in the uterus. But it also occurs without perceptible dis- turbance of nutrition, where the escape of blood from the uterus is hindered in heart and lung diseases, etc., as well as in fluxions in- duced by irritation of the uterus from sexual excess, perhaps also by sensual excitement. In very rare cases menorrhagia depends on a haemorrhagic diathesis, being a symptom of scurvy, purpura hsemorrhagica, acute infectious diseases, such as haemorrhagic small- pox or measles,- or of typhus, etc. Where it is due to obstructed efflux or increased afflux of blood to the uterus, it is usually pre- ceded by symptoms similar to, but more marked than, those with which normal menstruation usually begins. Part of the blood passes off in a fluid state, part coagulates in the vagina, forming irregular clots ; rarely it coagulates in the uterus, and there forms so- called fibrinous polypi, such as frequently appear after abortions. Plethoric patients often bear very decided loss of blood without injury ; anaemic patients have the symptoms of increased anaemia. The treatment of menorrhagia requires great attention to the origi- nal disease. The occasional application of leeches to the cervix is often of surprising benefit in those cases dependent on chronic in- flammation of the uterus. As soon as the loss of blood is decided and threatens to impair the strength, it is important to prevent all bodily exertion and mental excitement, and to keep the patient in a horizontal position during menstruation. At the same time we for- bid all stimulating food and drink, and order mineral or vegetable acids. It will only rarely be necessary to employ cold water or ice- compresses, or to have recourse to styptics. In some cases, how- ever, the bleeding threatens life, and then it is necessary to act energetically, and even to inject hot-water solutions of chloride of iron, etc., into the uterus. [The term dysmenorrhcea is applied to the conditions under which, instead of the trifling disorders which are almost normal, grave and distressing symptoms arise, especially violent pain in the back, belly, groins, and thighs, and sometimes sympathetic derange- ment of remote organs, such as cramp in the stomach, vomiting, diarrhoea, numbness, headache, dizziness, and convulsions. The causes of dysmenorrhcea are numerous. It has been assumed that 164 DISEASES OF THE UTERUS. a menstrual congestion of extraordinary activity might give rise to pain in the womb and ovaries, by irritating the nerves of those or- gans (congestive dysmenorrhoea). In other cases we are reduced to assuming that an unnatural irritability of the nerves—either gen- eral and combined with hysteria, or else local and limited to the gen- ital region—is the cause of the suffering (nervous dysmenorrhoea). But there is no doubt that we more often have to do with organic disease of the womb or ovaries or other pelvic organs, or with a fibromyoma, an infarction, a dislocation, or a degeneration of the ovaries. One form of dysmenorrhoeal pain proceeds from spasmodic contractions which the womb sets up in order to expel some foreign body from its cavity—a polypus, a blood-clot, or a collection of liquid blood. The obstacles to the menstrual outflow are stricture of the cervical canal, either congenital or acquired, acute flexion of the womb, and growths blocking up the channel; perhaps also spasm of the internal os (obstructive dysmenorrhoea). In this form the pains present a characteristic intermitting type, like those of colic or like labor-pains, the spasms corresponding with the periods of uterine contraction (uterine colic); and these attacks, which are more severe before the flow begins, subside after the contractions have expelled the stagnant blood from the uterine cavity. Membranous dysmenorrhoea is a special form of obstructive dysmenorrhoea. Under normal conditions at the period of deni- dation, the outer layers of the proliferating mucous lining of the womb undergo fatty degeneration, and are cast off impercepti- bly and in minute particles. Sometimes, however, by a morbid exaggeration of this process, there arises an exfoliation more or less profound of the mucous membrane, which then comes away in sheets. Indeed, the entire menstrual decidua may be cast off, in the form of a complete three-cornered sac corresponding to the form of the uterine cavity, with its smooth inner surface riddled by holes (mouths of the uterine glands), and its outer surface rough and rag- ged. Microscopic examination of the connective tissue of the mu- cous membrane, and the finding of the glands embedded in it, will prevent confusion of such an object with a mere fibrinous clot ; while the more difficult distinction between this process and that of an early abortion will be aided by the circumstance that the expulsion of menstrual decidua is seldom confined to a single menstruation, but is often repeated for months and years, even up to the climac- teric period. The chronic metritis and endometritis which often accompany this form of exfoliative menstruation are regarded by many as the cause of the process. The affection is attended by colic of greater RETROUTERINE HEMATOCELE. 165 or less violence, according as the expulsion of the membrane and blood is retarded or accelerated. The diagnosis depends upon dis- covery of the membrane. The prognosis and treatment of dysmenorrhoea must of course depend mainly upon a true understanding of its cause. Obstructive dysmenorrhoea is best treated by artificial widening of the cervical canal, either by bloodless dilatation, or else by incision or divulsion, which give far better results. For details we refer to the text-books on surgery. In membranous dysmenorrhoea, the objects of treatment should be the metritis and endometritis, regarded by some as the causes of the symptoms. When no complication forbids it, after subsidence .of the period we may resort to applications of nitrate of silver, liquor ferri sesquichloridi, carbolic acid, or tincture of iodine in the cavity of the uterus, always observing the precautions given elsewhere. Although the result will probably not be perfect, yet a thinning or temporary arrest of the membranous formation may be obtained. Here, too, in obstinate cases, dilatation of the uterine neck may facilitate the escape of the decidua, and thus diminish the uterine colic. Violent pain is to be allayed by opiates, either by the mouth, rectum, or hypodermic injection, and by hot compresses to the belly. If there be fever, and the pain assume an inflamma- tory type, an acute metritis or perimetritis is to be feared, and proper steps should be taken to meet it.] CHAPTER X. RETROUTERINE HEMATOCELE HEMATOMA RETROUTERINUM PEL- VIC HEMATOCELE. [The French were the first, and Nelaton was the foremost, who investigated the subject of retrouterine hsematocele, and fixed its position as a form of disease. The seat of a hsematoma may be either within or without the peritoneal sac. The latter is very rare, occurring from haemorrhages into the areolar tissue surrounding the cervix and vagina, and into that between the folds of the broad ligaments of the womb. These extravasations do not present any very definite symptoms, but merely form a tumor of variable char- acteristics. As regards the intraperitoneal haBmatoma, of wThich alone we now treat, let us premise that it is not every free accu- mulation of blood in the peritoneal sac that is included under this term ; for a free collection of blood, like a free effusion of serum, cannot at first present to the touch a well-defined tumor. We limit 166 DISEASES OF THE UTERUS. the term to those bloody effusions which are cut off from the peri- toneal sac above them, and which are completely enclosed by inflam- matory exudation and adhesion, so that they may exhibit all the qualities of a tumor. It is true that a free extravasation, after the blood has coagulated, may present to the examiner’s touch an object of a certain solidity and firmness ; but it does not offer the resist- ance opposed by the tensely-stretched walls of the encapsulated blood-tumor, into the cavity of which more and more blood is es- caping, nor does it displace the neighboring organs. The effused blood usually collects in the most dependent part of the peritoneal cavity, the deep pouch between womb and rectum knowm as Doug- las’s cul-de-sac. It pushes the womb forward and upward, and the rectum backward. Douglas’s fold is forced downward upon the posterior vaginal fornix, thus forming a large tumor, which may even extend upward above the brim of the pelvis. An anteuterine haematocele, which is a very great rarity, con- sists in an encapsulated blood-tumor situated in the shallow anterior pouch between the bladder and the womb. An intraperitoneal haematoma may form in one of two ways : Either the haemorrhage takes place within a closed pouch already formed by previous peri- tonitic adhesions, or else the bleeding may come first, and the encap- sulation follow as a result of adhesive peritonitis which the contact of the effused blood excites in the peritonaeum of the superimposed coils of intestine. The capsule once closed, a further extravasation may distend the sac and gradually displace the neighboring organs. The sources of pelvic haemorrhage are many and diverse, and during life they can, as a rule, only be conjectured. The bleeding proceeds most often from the ovarian vessels, and the insignificant physiological loss of blood which accompanies rupture of a Graafian vesicle may be aggravated into a profuse and alarming haemorrhage. This may take place as a consequence of an excessive hyperaemia of the sexual organs, caused by violent exertion, or by blows, falls, mental excitement, masturbation, or coitus. Various diseases of the ovary, such as inflammation with abscess, bursting of a haemor- rhagic cyst, or rupture of a superficial varicose vessel, may have a like effect. In certain disorders of the tubes, so large an accumula- tion of blood or of inflammatory exudation may form in them as to result in rupture or perforation of their walls. It is less pi’obable that the blood can accumulate in the tubes (as it does in the womb in haemometra), and thence can pass through the abdominal opening into the peritonaeum in sufficient quantity to form a tumor. It has long been known that by the bursting of a tubal or extrauterine preg- nancy, if the resulting haemorrhage is not speedily fatal, a haematoma RETROUTERINE HEMATOCELE. 167 may form. ' Rupture of varicose veins of tlie broad ligaments may lead to intra- or extra-peritoneal hsematoma, according as the blood passes into the pelvic cavity or into the areolar tissue between the serous folds. Finally, the pelvic peritonaeum itself is a not unfre- quent source of the bleeding. Dolbeau first announced that the blood might flow from vessels in a pseudomembrane, the product of a slow peritonitis. Virchow shares his views, which are in some measure supported by the fact that in a slighter degree a similar process may take place in men. The predisposing factors in pelvic haemorrhage are the catamenial periods, the disorders giving rise to the so-called haemorrhagic diathesis, scurvy, purpura, icterus gravis, and the haemorrhagic exanthemata. Gynecologists differ greatly as to the frequence of the affection. Schroeder found it in five per cent, and Seyfert in seven per cent, of his cases. Beigd thinks that mild cases are very common, but that they run their course un- detected except by accident. The disease is liable to arise at any time throughout the whole period of sexual activity ; it is most common between the ages of twenty-five and forty, and in women who have borne children. The formation of a pelvic hasmatocele is usually preceded by symptoms arising from the remoter fundamental disturbance which causes the haemorrhage. The establishment of the hsematoma itself is in most cases attended by unmistakable signs of internal bleeding, sudden pain in the belly, faintness, pallor, feeble pulse, coldness of the extremities, nausea, vomiting, and the like. Sometimes these symptoms recur again and again, whenever, as may happen from time to time, the bleeding is renewed. The history of an obscure case of this kind may furnish important data toward forming a diagnosis. The hajmorrhage having taken place, there ensues a more or less severe peritonitis, excited by the presence of the effused blood. This has the effect of encapsulating the effusion, unless in- deed it be already included within an envelope, the result of ancient adhesions. Then follow the symptoms of pressure and crowding of neighboring organs by the tumor, tenesmus or impediment at stool, vesical pressure, and neuralgia from pressure upon the nerves of the lower extremities or engorgement of the dislocated womb, some- times of such intensity as to cause metrorrhagia. The most impor- tant diagnostic test is by vaginal and rectal touch, whereby we may detect a retrouterine tumor of rapid growth, which often rises above the pelvic brim, but which also bulges downward into Douglas’s cul- de-sac, and more or less against the posterior vaginal wall. The tu- mor is soft, elastic, even fluctuating to the touch, but grows more firm after a few days, when the blood has coagulated. Should re- 168 DISEASES OF THE UTERUS. absorption take place as the weeks or months go by, it becomes very hard and uneven, and at the same time shrinks, becoming smaller and smaller, until it finally vanishes altogether, save a small lump close to the hack of the womb. In unfavorable cases, as when the haematoma is very large, the size and tension of the tumor continue to increase ; the fever, the tenderness upon pressure, and other signs of local peritonitis are aggravated ; so that a distinction between an inflammatory exudation and a haematocele may at this period be very difficult, unless the sudden onset of the attack and the precur- sory signs of internal haemorrhage can he taken into account. In such cases the blood is generally discharged spontaneously through the rectum or vagina, and the sac may finally close up after grad- ually evacuating its black, grumous, tarry contents. In exceptional cases a haematoma proves fatal through sloughing of the sac-wall and blood-poisoning, or through general peritonitis after bursting of the sac into the abdominal cavity ; for it would seem that the altered blood is far more irritating to the peritonaeum than that which is recently effused. Long-continued suppuration of a fistu- lous sac may finally wear out the patient. The treatment of a haematoma requires, above all, perfect and continued rest, and avoidance of anything which can accelerate the circulation. If the bleeding persists or recurs, we must apply ice to the abdomen or insert it into the vagina, at the same time giving the liquor ferri sesquichloridi internally, and injecting ergotin be- neath the skin. Should the symptoms of haemorrhage threaten life itself, transfusion of blood or milk is indicated, as in all other haemorrhages. Pain is best allayed by hypodermics of morphine. The inflammatory symptoms and local peritonitis are to be met by striving, by full doses of opium, to arrest movement of the bowels, and thus to favor the adhesions by which the haematoma is becom- ing enclosed. Only after the inflammation has abated should the bowels be cautiously moved by enemata or by irrigation [Ilegar's method). Gynecologists differ as to the merit of evacuation of a haematoma by puncture. Since opening the sac entails the danger not only of renewal of the bleeding, but also of putrefaction within the sac and its consequences, it should not be lightly attempted, nor until all hope seems lost of resorption, or else until violent symp- toms make it seem hazardous to await spontaneous evacuation. The sac is to be punctured with a small trocar—or, better still, by the aspirating needle—the entrance of any air being carefully pre- vented. Puncture is most commonly made through the vagina or rectum. Should the contents prove to be suppurating or putrid, the opening must be freely enlarged, and the putrescent matter as RETROUTERINE HEMATOCELE. 169 completely as possible removed by disinfectant irrigation, in order to prevent the consequences of septic absorption. When the symptoms of a haematoma are mild, and it seems in- clined toward absorption, the patient is merely to be kept at rest, with a light, nutritious diet, and impediments to the stools or urine are to be properly relieved.] SECTION III. DISEASES OF THE VAGINA. In this section we shall only treat of the inflammations of the vagina, leaving the congenital anomalies, tumors, and other diseases of that organ, to the text-books on obstetrics and surgery. CHAPTER I. VIRULENT CATARRH OF THE VAGINA. Etiology.—For the pathogeny and etiology of gonorrhoeal catarrh of the vagina, we may refer to what we have said of virulent catarrh of the male urethra. Anatomically, it is not distinguishable from non- virulent catarrh, but its course and origin are different. The disease is not induced by sexual excess, or any other cause than infection with gonorrhoeal matter. Anatomical Appearances.—In women the chief seat of virulent catarrh is the mucous membrane of the vulva and vagina; more rarely it extends to that of the uterus. But in almost all cases the catarrh extends to the urethra, and this is important in the diagnosis. The affected mucous membrane at first shows the changes peculiar to the most severe form of acute catarrh; subsequently those of chronic ca- tarrh. The secretion, which, in the beginning, is usually scanty, sub- sequently becomes very copious, purulent, irritates the vulva and inner surface of the thighs, but is only peculiar in that it is the bearer of the contagion. Symptoms and Course.—The first symptoms of gonorrhoea in the female, a feeling of itching and warmth in the sexual organs, and a scanty mucous discharge, are not very characteristic, and are often un- noticed. A few days after the commencement of the disease, there are severe burning pain in the genitals, swelling of the vulva, ardor urinoc. ; but these troubles rarely become so severe as to interfere greatly with NON-VIRULENT CATARRH OF THE VAGINA. 171 walking, sitting, and moving the body. The secretion, which in this stage is yellowish-green, thick, and purulent, often oozes up in large quantities between the labia; in the vulva and its vicinity, even to the anus, we find shallow ulcers, which are not to be confounded with chancres. We may almost always press pus out of the urethra. Af- ter the disease has lasted a fortnight or three weeks, the pain abates and ceases; the discharge loses its purulent appearance, but continues a long while till the secretion, which constantly becomes more mucous, dries up, and loses its power of inoculation. Treatment.—The local treatment, which we preferred to internal remedies for gonorrhoea in men, is almost exclusively used for the dis- ease in women. Considering the different seats of gonorrhoea in the two sexes, it may be readily understood that copaiba or cubebs, whose active constituents are excreted with the urine, may have an effect on gonorrhoea in the male urethra that it cannot have on the disease in the female, where the vagina is chiefly affected. While there is se- vere pain, we prescribe scanty diet, laxatives, long-continued sitz- baths, during which a speculum should be left in the vagina, if its in- troduction be not too painful. If there be no symptoms of inflamma- tion, or if they have been allayed, we may employ injections of solu- tions of tannin, nitrate of silver, alum, sulphate of zinc, acetate of lead, etc. Injections of plumbi acet. crystall. 3 iij.—Aqua? conj. j, as recommended by Ricord, are very efficacious; instead of being inject- ed, this solution may be poured in through a speculum, and the latter slowly withdrawn, so that the fluid shall come in contact with all parts of the vagina. In very obstinate cases we may introduce wads of charpie, sprinkled with alum, into the vagina, or touch the parts with solid nitrate of silver. CHAPTER II. NON-VIRULENT CATARRH OP THE VAGINA. Etiology.—JKbllik&r and Scanzoni, who have carefully examined the secretion from the vaginal mucous membrane, both in health and disease, found perfectly healthy secretion in very few women, and only in those who had had no children, and had not frequently indulged in coitus. It was so scanty that the surface of the mucous membrane was <*nly lubricated by it; it was nearly as clear as water, fluid, only viscid, white or yellowish in spots; it was almost always acid, and, besides a small amount of pavement epithelium, it contained no noticeable solid constituents. Shortly before and after menstruation the secretion was more copious, always fluid, and almost always acid; at this time if 172 DISEASES OF THE VAGINA. contained more epithelial cells, and, after the cessation of the menses, as long as it retained its red color, there were more or less blood-cor- puscles in it. In catarrhal affections they found the secretion either milky and thin, or more yellowish and thicker. The more opaque, white, or yellow, the secretion appeared, the more numerous were its pavement epithelium and young cells (mucous and pus-corpuscles), often also the infusoria discovered by Donne (trichomonas vaginalis), and some few fungous filaments and vibriones. Hence we see that these observers rarely found a perfectly normal secretion, and that catarrh of the vagina is one of the most common of female diseases. Irritation of the vagina, by sexual excess, is the chief cause of catarrh of that part, it is true; but it is often induced by other causes, which were mentioned when speaking of uterine catarrh. It is particularly to be borne in mind that catarrh of the vagina, like that of the uterus, depends as often on constitutional as on local causes. A consideration of the exciting causes shows that this disease must be rare during childhood; and this is true, except in the cases where oxyuris have passed over the perinaeum from the anus to the vagina, and have there caused great irritation. Anatomical Appearances.—In acute catarrh we find the mucous membrane bright red, swollen and relaxed; in many cases we see small prominences on it, which give the membrane a granular appear- ance, and which are not, as was formerly supposed, due to distention of the follicles, but to swelling of the mucous papilke. Sometimes these changes affect the entire vagina, at others only parts of it. At first the secretion is scanty, but, after the disease has lasted a very short time, it becomes more copious and more or less opaque. [The inflammation usually spreads all over the vagina, and over the vulva as well. Sometimes, however, a portion only of the va- gina is involved. For instance, at the beginning of a vaginal gon- orrhoea the lower part only will be attacked, while a catarrh caused by disease of the cervix or uterus will be confined chiefly to the up- per part of the canal. Hildebrand describes a peculiar ulcerous form of inflammation of the upper vagina, caused by loss of the epithelium and slight hypertrophy of the papillae, and finally adhesion of the vaginal por- tion to the vaginal walls, so that the fornix vaginae is obliterated, and the os uteri is to be felt at the top of a funnel-shaped tube. Schroeder has also seen this disease, which in one case resulted in complete atresia, in another in partial closure of the vagina below the vaginal portion, and in a third case in complete contraction (stenosis) of the entire upper vaginal region.] In chronic catarrh the walls of the vagina appear distensible and NON-VIRULENT CATARRH OF THE VAGINA. 173 flaccid. The membrane is more bluish red and its surface more fre- quently granular than in the acute variety ; the secretion is some- times more milky, sometimes more yellow and thick. Not unfre- quently the relaxation of the vagina induces prolapse, particularly of the anterior wall. Symptoms and Course.—In non-virulent catarrh also, if it begin acutely, the patient complains of prickling and burning in the pri- vate parts ; but, as the mucous membrane of the urethra is unaffect- ed, she has no pain on urination. In chronic catarrh the discharge of the abnormal secretion, the leucorrhoea (fluor albus vaginalis), is often the only symptom of the disease. The chief means of decid- ing whether the discharge be from the vagina or uterus is by exam- ination with the speculum. Many women bear the drain without any injury ; in others it induces anaemia, pallidity, weakness, and emaciation. Treatment.—In treating non-virulent vaginal catarrh, just as in uterine catarrh, we must first attend to the causal indications. But we cannot often cure the disease without accompanying local treatment. We would chiefly recommend the hip-baths and injec- tions mentioned in the last chapter ; in obstinate cases, the introduc- tion of a tampon sprinkled with alum, and even the application of solid nitrate of silver. CHAPTER III. CROUPOUS AND DIPHTHERITIC INFLAMMATION OF THE VAGINA. Croupous and diphtheritic inflammations of the vaginal mucous membrane are common during puerperal fever, but are rare except in the puerperal state. They either depend on local irritation or on constitutional disease. Thus, the discharge from a sloughing can- cer of the uterus, the urine constantly flowing through a vesico-vag- inal fistula, a bad pessary, or a large uterine polypus projecting into the vagina, may induce croupous or diphtheritic inflammation of the vaginal mucous membrane ; while the disease is also often observed in the later stages of typhus, cholera, measles, and small-pox, and accompanying similar affections of other mucous membranes. Usually only certain spots of the vagina are covered with croup- membrane, or changed to diphtheritic sloughs. In the vicinity of these spots the mucous membrane is dark red ; after the slough has been thrown off, irregular losses of substance remain ; these are sometimes superficial, at others deep. Our attention is called to the disease by severe pain in the parts, and by a fetid, often bloody 174 DISEASES OF THE VAGINA. discharge, which begins in a few days. Local examination is the only means of certain diagnosis. Where a large or putrefied pes- sary has caused the inflammation, its removal, and the use of luke- warm, and later of cold and astringent, injections, ordinarily suffice to cure the disease. The affection usually disappears readily also if a large polypus, that has forcibly distended the vagina, be removed. On the other hand, where sloughing cancer or ve'sico-vaginal fistula has caused the disease, we must limit ourselves to a palliative treat- ment. In those cases occurring in the course of infectious diseases, it is usually sufficient to attend to cleanliness, as the secondary dis- ease generally passes off with the primary. DISEASES OF THE NEKVOUS SYSTEM. SECTION I. DISEASES OF THE BRAIN. CHAPTER I. HYPERAEMIA OP THE BRAIN AND ITS MEMBRANES. Etiology.—For a time the fact was ignored that on autopsy the nlood-vessels within the skull were sometimes found distended and at others empty, and it was supposed that the amount of blood contained m the closed cranium of an adult could neither increase nor diminish, but was constant; and that anaemia or hyperaemia was only supposable when the brain-substance was increased or diminished, that is, when there was hypertrophy or atrophy of the brain. This view was based on the following reasoning: The brain is not compressible, at least not by the pressure to which it is subjected from the contents of the blood-vessels; and it is surrounded by walls which do not expand; consequently only the same amount of blood can enter the skull as passes out from it, and conversely only as much blood can pass out ot the skull as enters it. This reasoning is false, as it starts with the supposition that the contents of the cranium consist only of the mem- branes of the brain, the brain-substance and the blood-vessels with their contents; it leaves the cerebrospinal fluid out of consideration. This, which is a simple transudation, can rapidly increase or diminish, and can at least partly pass into the spinal canal, which is not entirely enclosed by rigid walls. In almost all autopsies it may be seen that the amount of blood contained in the vessels and the amount of cere- brospinal fluid are in inverse proportion ; that a distention of the ves- sels of the meninges is accompanied by a decrease of arachnoid fluid, and conversely that, when the vessels are less full, the meshes of the 176 DISEASES OF THE BRAIN. textus cellulosus subarachnoidealis contain a greater amount of serum. Only when the brain is atrophied do we find oedema of the membranes with overfilling of the vessels ; and only when an effusion of blood, a tumor, or a collection of fluid in the ventricles, has contracted the space in the skull do we find, along with anaemia, dryness of the membranes, and disappearance of the sulci between the cerebral convolutions. The division of cerebral hyperaemia into active and passive, or, to retain the expressions previously used, into fluxionary and congestive, is practically valuable not only on account of the consideration being easier, but because the symptoms of one form differ from those of another. Fluxionary hyperaemia results—1. From increased heart-action. It is true that, in this case, while the arteries are fuller than usual, the veins are less so; hence the entire amount of blood in the vessels of the brain and its membranes is not increased by the stronger action of the heart. But the increased lateral pressure induces increased ful- ness of the capillaries, and it depends chiefly on these (not on the amount of blood in the large vessels) whether or not the brain acts normally and is normally nourished. This form of cerebral hyper- emia occurs temporarily from augmented energy of contraction of a healthy heart, as in fever and great bodily or mental excitement; it is habitual in the permanently increased activity of a hypertrophied heart, but only when the hypertrophy is an independent disease, or in case it accompanies an obstruction to circulation, when it has become greater than is necessary for the compensation. Simple, non-com- plicated hypertrophy of the heart is not frequent, and occurs almost exclusively in topers and persons who continually do hard work. On the other hand, hypertrophy that has become greater than was neces- sary to compensate the obstruction to the circulation is quite frequent. Examples of this are the occasional enormous hypertrophies of the left ventricle when there is insufficience of the aortic valves, and perhaps also the hypertrophy of the heart in morbus Brightii. 2. Fluxionary hyperaemia of the brain results from too slight resist- ant power of the afferent blood-vessels, whether this be congenital or acquired. When the cerebral arteries have delicate, thin walls, so that they yield to an increased pressure of the blood sooner than the other arteries of the body do, and hence, when the action of the heart is only moderately increased, fluxionary hyperaemia of the brain is in- duced, it is customary to say that the person so affected has a tendency to “ rush of blood to the head.” 3. Fluxionary hyperaemia to the brain results from an increase of the lateral pressure in the carotids as a consequence of obstructed escape of blood from the aorta into other branches. As a type of this HYPERAEMIA OF THE BRAIN AND ITS MEMBRANES. 177 “ collateral fluxion ” to the brain, we may mention the habitual cere- bral hypermmia where there is contraction or closure of the aorta at the point where the arterial duct terminates in the aorta (Volume L, page 363). It frequently results from compression of the abdominal aorta and its branches, by the distended intestines and by exudations. In the same way obstruction of the cutaneous circulation during the cold stage of intermittent fever, and from the action of severe cold, induces collateral fluxion to the brain. According to Watson, in cold nights many unfortunates are arrested in the streets for being drunk, when they are only suffering from cerebral hyperaemia as a result of disturbance of the cutaneous circulation. It is not improbable that severe muscular exertion may also induce increased fulness of the carotids and fluxionary cerebral hypenemia, by the pressure of the con- tracted muscles on the capillaries. 4. A fourth cause is paralysis of the vasomotor nerves of the cere- bral vessels. Physiological experiments show that, if the cervical por- tion of the sympathetic nerve be divided, the vessels on the correspond- ing side of the head become dilated. The cerebral vessels appear to be similarly affected by the use of spirituous liquors, by some poisons, as well as by great emotions and excessive mental activity. I would particularly call attention to the last cause, as I have frequently seen dangerous hyperaemia of the brain after too prolonged mental labor, which resulted fatally from the occurrence of oedema. We can hardly give any other explanation for these cases, than that the walls of the vessels are paralyzed by the above influences, their calibre dilated, and the supply of blood consequently increased. 5. Lastly, fluxion to the brain results from atrophy of that organ. The space left in the skull by the disappearance of the brain-substance is partly filled by the dilatation of the vessels. We shall find this dilatation of the vessels to be a frequent cause of their rupture; and, as atrophy of the brain often follows apoplexy, it is also a cause of returns of apoplexy. We shall not attempt to say whether or not the fluxionary hyperaemia of the brain, occasionally observed during con- valescence from severe disease, is the result of atrophy of the sub- stance of the brain or of the neuroglia and consequent dilatation of the vessels. Passive hyperaemia, congestion of blood in the brain, depends— 1. On compression of the jugular veins and vena cava descendens. As a type of this form, we may mention the excessive cerebral con gestion caused by strangulation. The jugular veins are most fre quently compressed by enlarged thyroid or lymphatic glands, the vena cava descendens by aneurisms of the aorta. 2. Congestion of the brain results from energetic expiratory move- 178 DISEASES OF THE BRAIN. ments while the glottis is contracted. In coughing, straining, playing wind-instruments, etc., as we have often shown, the flow of blood into the thorax is hindered; the pulmonary circulation contains too little, the general circulation too much blood. Under such circumstances, the brain must sufler fai more from hyperaemia than other organs sup- plied by the general circulation, particularly the liver, spleen, and kidneys; because the passage of blood through the upper aperture of the thorax is more impeded than it is through the lower, since these abdominal glands undergo the same compression from the abdominal muscles that the veins of the thorax and the heart do. 3. We have cerebral congestion in all those diseases of the heart where the function of that organ is impaired, if they are not compli- cated by other anomalies of opposite effect, and so compensated. In non-compensated valvular disease of the left ventricle, the whole amount of blood in the vessels of the brain and its membranes is not increased, it is true, since, while the veins are overfilled, the arteries are less full; but the overfilling of the veins obstructs the flow of blood from the capillaries, thus inducing capillary hyperaemia, which, as we have shown, is the most important cause of the cerebral hyperaemia. The affection caused by valvular disease of the right heart is far greater than that from valvular disease of the left heart; for, in the former case, not only is the escape of venous blood from the brain impeded, but the entire amount of blood in the skull is increased. 4. The same state of affairs occurs in extensive compression or atrophy of the vessels of the lungs as in pleuritic effusions, emphy- sema, or cirrhosis of the lungs. In these diseases also, when the right ventricle is not hypertrophied in proportion to the impediment to the circulation, the systemic circulation is overloaded at the expense of the pulmonary, and the amount of blood in the skull is increased. Since the contents of the cerebral veins and sinuses cannot pass into the overfilled jugular veins, the same excessive cyanosis occurs in the brain that is so evident in the skin, and which is almost pathognomonic of the diseases in question. The last stage of emphysema gives us an excellent opportunity of studying the gradual development, steady in- crease, and, finally, the severest symptoms of congestion of the brain. Lastly, we must mention a form of cerebral hyperaemia which is neither fluxionary nor congestive, and which is peculiarly important, as it should be very carefully avoided by persons suffering from disease of the blood-vessels, and having a tendency to apoplexy; I mean those cases of hyperaemia that appear as one symptom of temporary general plethora induced by a very free supply of food and drink. Anatomical Appearances.—On post-mortem, examination, it is often difficult to decide whether the vessels of the cerebral membranes HYPERH2MIA OF THE BRAIN AND ITS MEMBRANES. 179 and still more so whether those of the cerebral substance, have been more than normally filled with blood during life. Mistakes in the account of the autopsy are frequent. The mistakes regarding the amount of blood in the cerebral mem- branes depend partly on the fact that, when unaccustomed observers find the vessels much distended at the dependent parts of the surface of the brain, they diagnose a hyperasmia of the cerebral membranes, even if the blood has only sunk downward, and the vessels in the upper part be empty. Still more frequently another error is committed even by practised observers: that is, from a similar distention of the vessels on the convex surface of the cerebrum, hypermmia of the cerebral membranes is decided on without looking further. It should be borne in mind that the arteries supplying the cerebral membranes with blood lie at the base of the brain, and that only very fine arterial twigs reach the convexity of the greater hemispheres. All the large blood-vessels usually seen on the surface of the brain, when the skull is opened, are veins. Distention of these veins is a normal appearance, if the indi- vidual has died of an acute disease by which his blood was not con- sumed, or, if he has died suddeidy from suffocation, acute poisoning, or from some other accident involving no loss of blood. Hence it is entirely wrong, in such cases, to decide, from the overfilling of the veins, that there has been hypermmia of the brain or its membranes during life, and to connect this pretended hyperaemia with the symp- toms that have been observed. In the history of the post mortem, accounts of excessive hyperaemia of the brain and its membranes are often combined with others of a similar excessive hyperaemia of the lungs, liver, kidneys, etc. If there were no mistake here, did we not have to suppose that, in the body of a previously healthy person, who had died neither from exhausting disease nor loss of blood, the normal amount of blood was often considered pathological, these accounts of post mortem would only convey the absurd idea that the entire amount of blood in the body was increased by poisoning, suffocation, etc. We must make it a rule to consider hyperaemia of the cerebral membranes as proved only in those cases where the finest vessels also are injected, and where the overloading of the cerebral vessels is not at all in proportion to the amount of blood in other organs. The great difficulty of detecting, in the cadaver, a hyperaemia of the substance of the brain, that has existed during life, depends chiefly on the fact that the first fine ramifications of the vessels supplying the brain take place in the pia mater, and that the vessels passing thence to the substance of the brain are mostly capillary (I/uschka). As these can scarcely be recognized with the naked eye, it is customary to use the size and number of the drops of blood oozing up on a cut 180 DISEASES OF THE BRAIN. surface of the brain as a means of determining the amount of blood contained in the cerebral vessels. I do not deny that this sign has some value, particularly in judging of passive cerebral hyperasmia; but I must add that the size and number of these drops of blood de- pend far more on the fluidity of the blood than on the fulness of the vessels. At all events, in cases where there can be no doubt of death having resulted from increased flow of blood to the head, or from its obstructed escape thence, on a section through the brain, its substance is often found very pale, and on its cut surface only a few small blood- drops ooze up. This circumstance, and the symptoms of paralysis occurring in the severer cases of cerebral hyperaemia (of which we shall speak more fully in the next paragraph), cause it to appear to me very probable that, when there is increased lateral pressure in the small arteries and veins of the brain, a transudation of serum from them into the perivascular spaces and interstices of the brain may very readily take place, and cause compression of the capillaries. It is only in yielding and distensible organs and tissues, which are not enclosed by firm envelopes, that any considerable oedema can coexist with a normal fulness of the capillaries. In all tissues enclosed by fascia or other firm capsule, oedema causes ansemia of the capillaries. If the size of the brain be not diminished by atrophy, and if the skull be closed, or, it remaining opened, if the dura mater be tense, there is no doubt that a slight transudation of serum will suffice to completely compress the capillaries of the brain. It is true, we cannot be sure, from post-mortem examination, that there is such a secondary oedema; but the supposition that such is the case appears to us perfectly justi- fiable when a patient has died with the symptoms of cerebral paralysis, and if, on autopsy, we find that the very white hue of the brain-sub- stance and the slight number of small blood-points appearing on its cut surface contrast strongly with the distention of the large vessels in the meninges. Where the hyperasmia is often repeated, atrophy of the brain and decided dilatation of the vessels result. The vessels of the meninges, which are unmistakably dilated, run a tortuous course; on section through the brain, we may distinctly see the gaping mouths of the vessels; the dilatation may even be observed in the capillaries on microscopical examination. There is plenty of serum in the sub- arachnoid spaces, the brain-substance is moist and shining. This ap- pearance, which is frequent in topers, is readily understood, if we remember that, in atrophy of the brain, the fluid contents of the skull must increase so as to fill the cavity. It is doubtful whether the de- velopment of the Pacchionian bodies can also be considered as a result of repeated hyperaemia; they are sometimes solitary, sometimes HYPER.EMIA OF THE BRAIN AND ITS MEMBRANES. 181 grouped as whitish, opaque excrescences of the arachnoid, coming par- ticularly along the sides of the longitudinal sinus. The pressure that they exercise on the dura mater separates its filaments, so that they perforate it; by further pressure they also cause atrophy of the bone, and they are then found embedded in little fossae in the skull. Micro- scopically, they consist of connective tissue; occasionally they contain fat and chalky salts. Symptoms and Course.—Before taking up the symptomatology of hyperaemia of the brain, I shall warn against the wide-spread error, so injurious to ihe patient, of considering all cases of disturbance of function of the brain, where severe structural changes can be excluded, as due to hyperaemia (or anaemia). Thus, the disturbance of the cerebral functions in fever is not due to increased afflux of blood to the brain from excited action of the heart; but, as we have repeatedly pointed out, it depends partly on the high temperature of the blood in the cerebral vessels, partly on its abnormal quality, the “ feverish state,” a necessary result of the in- creased transformation of tissue during the fever. Delirium and other severe cerebral troubles are most common in the so-called asthenic fevers, just where the increase of bodily temperature and the produc- tion of warmth attain the highest grade, while the heart’s action is hastened, but weakened, and there is no fluxion to the brain. According to the observations made during the last war, as well as from the valuable investigations and experiments of Obernier, the symptoms of sun-stroJce, or insolatio, do not, as was formerly sup- posed, depend on hyperasmia of the brain, induced by the action of the sun’s rays on the head. The symptoms of this disease consist in a paralysis of all the functions of the brain, occurring either suddenly or gradually. In the latter case the paralysis is preceded by excite- ment, delirium, and other symptoms of cerebral irritation. It has been determined that, in our zone at least, the action of the sun’s hot rays is not alone sufficient to induce these severe attacks, but that they only occur when individuals are subjected to great fatigue, on a very hot day, particularly if, at the same time, they sweat very little, be- cause they do not drink enough. We may assume that, under such circumstances, while the radiation of heat is limited on account of the high temperature of the surrounding atmosphere, while the production of heat is increased by the active muscular exercise, and the coolness induced by free perspiration is limited, there is an overheating of the body, an increase of the bodily temperature to a height incompatible with life. We have already sufficiently explained the significance of the fulness of the veins of the meninges, which is found on autopsy ic cases of sun-stroke. 182 DISEASES OF THE BRAIN. [The condition known under the term “ sunstroke,” or better, “ heatstroke ” (for the direct action of the sun’s rays is by no means essential to it), used formerly to be ascribed to a hypersemia of the brain ; a belief which has now been conqjletely exploded by experi- ments upon animals and by post-mortem examinations. It is now known, from the researches of Obernier, that in this disease there is a serious derangement of the heat-producing function and a great rise in the bodily temperature, which in extreme cases may reach 109° or 110° Fahr. Absolutely nothing as yet is known, however, of the anatomical lesions upon which sunstroke depends. It was formerly ascribed to grave alterations in the blood, to its over-acidity by overloading with carbonic and lactic acid, to destruction of its red corpuscles, to accumulations in it of urea, and the like. Koester in one case has found a hemorrhage in the right superior sympa- thetic ganglion, and in the right sympathetic itself, as well as smaller extravasations about and in the two vagi, and thinks we should look for the derangements in the vasomotor and respiratory nervous systems. Arndt seeks for an anatomical basis for the disease in the so-called “turbid swelling” (triiben Schwellung) developed in the brain, liver, kidneys, and other tissues, under the influence of the enormously high temperature, just as it occurs in high fever from other causes. The different symptoms presented during life may depend upon the degree in which the turbid swelling has at- tacked individual organs. In milder cases the temperature is below 104° ; the mind is muddled, the chest oppressed and uneasy, the pulse very frequent, the heat great, the skin moist, and there is a general but moderate feeling of languor. If relief cannot be gained through water-drinking and quiet, graver symptoms appear. The temper- ature then rises above 104°, the pulse to 130 or 140 ; the sweating becomes profuse and the thirst distressing. The patient loses con- trol over himself, and is oppressed by fulness of the head, dizziness, sensory delusions, and precordial distress. He is forced to sit down, or else sinks suddenly unconscious, and lies with flickering imper- ceptible pulse and sunken features. Sometimes there are epilepti- form fits. Although under proper treatment many very severe cases recover, yet the number which end fatally, particularly during the marches of armies in hot weather, is sometimes large. Many pa- tients improve at first, and then relapse unexpectedly. This fact, as well as the experience that recovery after sunstroke is slow, that it has many sequelae, such as vague pains, disposition to faint, indi- gestion, unnatural drowsiness, and the like, which are often obsti- nate, and the circumstance that sometimes there remains a psychical irritability or a permanent impairment of intellectual function, all HYPERJGMIA OF THE BRAIN AND ITS MEMBRANES. 183 indicate that the disorder has a definite material basis, which in bad cases is not always repaired.] Lastly, the symptoms of acute alcoholic poisoning, as well as that from opium and other narcotics, do not depend at all, or at any rate depend to a very small extent, on over-fulness of the cerebral vessels, although in them the brain is liyperaemic. The case appears to be different in the symptoms induced by the immoderate use of liquor for a length of time, or the continuous misuse of narcotics, a practice which has greatly increased since the introduction of subcutaneous injections of morphine. In such cases cerebral hyperaemia plays a more important part, at least, than it does in the symptoms of intoxi- cation and of acute opium-poisoning. [Abnormal fulness of the brain and its membranes is a common enough affection. Its symptoms may vary greatly. Not unfre- quently they are so insignificant as to attract little or no attention ; so that many persons with habitual plethora about the head are fa- miliar with the sensation which it causes, and do not consult a phy- sician. But there are other cases in w7hich hyperaemia causes symp- toms of the utmost gravity ; and between the mere sense of giddi- ness after stooping which one man may feel, and the formidable— nay, fatal—apoplectiform seizure which may befall another, there is a long series of interchanging types, whose differences, however, by no means always correspond to differences in grade of the hyperae- mia. Most of the symptoms bear the character of a morbid nervous excitement with exaltation, although others take on the form of depression and paresis. The psychical, the sensory, or the motor functions may be especially disturbed, according to the seat of the hyperaemia and to the receptivity of the individual. One might at first suppose that the symptoms of an active hyperaemia of the brain should be widely different from those of a passive congestion ; since in the first there is an increased afflux to the brain of arterial blood, the constant supply of which is so essential to the continuance of the brain-function, whereas in the latter this arterial supply must be more or less diminished, and the symptoms of carbonic-acid poison- ing should also be present. But in reality the two forms of hyperae- mia bear a close resemblance ; and this is due to the fact that a lack of blood in the brain is capable of causing like symptoms with those from overloading of the brain with arterial blood ; and it is well known to the practitioner that the distinction between cerebral hy- peraemia and cerebral anaemia may present obstacles at the bedside only to be surmounted by prolonged observation of the patient. The symptoms of the mildest grade of hyperaemia of the brain consist in a feeling of pressure and weight in the head, or of an 184 DISEASES OF THE BRAIN. actual headache, often accompanied by dizziness and an extraordi- nary susceptibility of the special senses. There is a buzzing in the ears, and a dazzling light before the eyes. This latter usually be- gins at a spot in the eccentric field of vision, with a quivering as though smoke were rising. It advances to the middle of the field, obscuring the whole, and renders accurate seeing impossible. The part first affected begins to clear, and in half an hour all is over. The arteries of the eyeball are branches of the internal carotid, and would naturally participate in an intracranial hyperasmia. Hence, in an obscure case the ophthalmoscope should aid us.] Hyperasmia of the brain is marked partly by symptoms of increased excitability of the nerve-filaments and ganglion-cells and by their mor- bid excitement (symptoms of irritation), partly by symptoms of dimin- ished or lost excitability of these nerve-elements (symptoms of depres- sion). Usually the -symptoms of irritation precede those of depression, in other cases the former do not occur, and the latter begin from the outset. It is commonly supposed that this difference of symptoms depends on difference of pressure on the brain from the more or less distended blood-vessels, and reference is made to the analogous action of the peripheral nerves, which are also irritated by a moderate pressure and paralyzed by a stronger one. This explanation appears very suit- able as regards the symptoms stances, and consequently affect the production of typhus germs. The susceptibility to typhus poison varies greatly with the individ- ual. There is one very interesting point, which is also seen in other infectious diseases, that persons who have lived for some time in a place peculiarly liable to the disease (as Munich), without being at- tacked, are in less danger when epidemics occur than those who have recently come to the place. It can scarcely be supposed that this is because the former were originally less disposed to the disease than the latter, but because, after a long absence from their native place, on iheir return to it, they are just as liable to the disease as new-comers who have only been there a short time. This fact probably depends on some unexplained accommodation to typhus poison. Statistics concerning the influence of age, sex, condition of life, and constitution, on the susceptibility for typhus, have shown that infants and old people are rarely attacked by abdominal typhus ; persons of middle age are most liable to it; males are attacked oftener than females; strong, well-nourished persons, oftener than weak, badly-nourished ones; and that the disease is proportionately more frequent among the poor than among the well-to-do classes. Formerly, it was generally believed that tuberculous patients were never attacked by abdominal typhus ; this is not absolutely true, although it rarely occurs. The same is true of patients with heart-disease, carcinoma, and other chronic or acute diseases, and of pregnant or nursing women. Pregnancy gives almost absolute immunity to the disease. Except in rare cases, one attack removes the susceptibility. Since 1820-1830, during which time exanthematic typhus has become more rare, abdominal typhus has become more frequent. With the exceptions mentioned in the pre- ceding chapter, it is the common form of typhus throughout Europe, TYPHOID FEVER. 627 It occuis far north in Russia and Denmark; in middle Europe, espe- cially in Germany, France, and the Netherlands; and even in the south—in Italy, Syria, and Turkey—it is not rare. In Great Britain, exanthematic typhus is the common form, but abdominal typhus also occurs, especially in the country towns, and the parts of England not visited by Irish emigrants (Hirsch, Griesinger). Anatomical Appearances.—It will be most convenient to speak first (as Ilcimernik does) of the post-mortem appearances when death has occurred early in the disease, before the typhus process proper has set in, and then to give a description of the lesions that are found when death has occurred later, during the repair of the changes induced by the typhus. The bodies of persons who have died early in the disease do not appear greatly emaciated; rigor mortis is very marked; we find ex- tensive hypostatic congestion in the dependent parts of the body, and occasional bed-sores commencing over the sacrum. The nostrils often appear smoky, and the teeth and gums are covered with a black coat- ing. There are often numerous sudamina on the skin. On opening the body, the muscles appear very dark red, hard, and dry. The blood in the heart and large vessels is thick, dark colored, and contains little, loose, blackish-red coagula, rarely a small amount of discolored fibrin. Chemical and microscopical examinations of typhus blood have so far given negative results as regards the actual anomalies, that is, as to those which depend directly on the infection with typhus poison. The decrease of fibrin occurs in other infectious diseases also; the increase of blood-corpuscles, on which the dark color chiefly depends, seems to be only relative, and to result from the thickening of the blood, caused by great perspiration, and loss of water by diarrhoea. After the typhus nas continued some time, the blood is consumed, and becomes poor in albumen and blood-corpuscles. The brain and spinal medulla show no constant changes corresponding to the severe functional disturbances of these organs during life. They sometimes contain more, sometimes less blood, and vary in consistence. We find changes in the respira- tory organs in all cases; the typhous laryngeal ulcer already described (Yol. I.) is not unfrequently found, especially in certain epidemics. There are always signs of an extensive catarrh, even in the smallest bronchi, marked by dark redness of the mucous membrane, and scanty, tough secretion. At the dependent parts of the lungs there is more or less hypostatic congestion, sometimes only great hypostatic hyper- aemia and condensation of the pulmonary tissue from swelling of the alveolar walls (splenization); sometimes hypostatic oedema; sometimes the so-called hypostatic pneumonia (Yol. I.). Besides the above, more or less extensive portions of lung are not unfrequently collapsed, or in 628 ACUTE INFECTIOUS DISEASES. a state of atelectasis, from collections of secretion or swelling of the mucous membrane of the bronchi leading to them having rendered the passage impervious. In some cases also we find lobular and lobar pneumonia, not affecting the dependent part of the lung, and not de- pending on hypostasis, even at the height of the disease, although it is more common after it has run its course. The bronchial glands are swollen, vascular, and occasionally have a medullary appearance, such as we shall describe for the mesenteric glands. The heart is usually relaxed, its muscles pale, sometimes of a dirty-red color; the endocar- dium and lining membrane of the vessels are infiltrated, red, and dis- colored. The spleen is greatly enlarged, occasionally twice, or even six times its normal size; its capsule is tense, its parenchyma pulpy, and of a dark-violet or blackish-red color. In rare cases we find the capsule of the spleen ruptured, and blood poured through the rupture into the peritoneal sac. In the great curvature of the stomach, some- times only the large vessels are distended, sometimes the mucous mem- brane appears dark red, from injection of the finer vessels, and relaxed from infiltration after death. The most important changes occur in the small intestine; to these ileotyphus owes its name. PoMtansJcy, on whose unsurpassed description of the “typhous affection of the mucous membrane of the ileum” we base our description, divides it into four stages. In the first or congestive stage, the mucous membrane of the small intestine is the seat of great hyperasmia. It appears swollen, relaxed, cloudy, covered with mucous and epithelial masses. This condition extends over all the membrane of the intestine, it is true, but it is most marked in the lower part, near the valvula JBauhini. The mesenteric glands are moderately swollen, soft, vascular, and dark colored. In the second stage, or that of typhous infiltration, the gen- eral redness and swelling of the mucous membrane increase, and con- centrate on the parts around the solitary and Peyer’s glands in the lower part of the ileum. In these tissues there are very peculiar changes, which are pathognomonic of typhus. More or less of the glands, and parts around them, swell so as to rise half a line or a line above the surrounding mucous membrane. These prominences are rather hard, and show through the mucous membrane with a gray or yellowish-red color; they have flat or steep edges; they are seated firmly on the muscular coat, and are intimately connected with the mucous membrane covering them. The size of the swollen solitary glands varies from that of a millet-seed to that of a pea. Peyer’s patches, on the conti ary, form patches from the size of a silver gros- chen to that of a dollar; they are generally oval in shape, and in the vicinity of the valve they usually coalesce, so that at this point they often cover a strip of intestine several inches long. On the cut surface TYPHOID FEVER. 629 it looks as if the diseased intestinal glands were infiltrated with a soft, grayish-white, or pale-reddish encephaloid mass; and although it has of late been found that in typhus disease the intestinal glands are not infiltrated with amorphous exudation, but that there is an increase of their cellular elements which, even under normal circumstances, are peculiar; still the expression “ medullary infiltration ” has almost uni- versally been preserved. Occasionally the degeneration extends be- yond the follicles, and there is a “ medullary infiltration ” of the con- nective tissue of the mucous membrane in their vicinity, a cellular neoplasm, originating from the connective-tissue corpuscles ( Virchow). In this stage the mesenteric glands are swollen to the size of a bean, or a hazel-nut, are of a grayish-red color, and quite hard. In the third stage, which* Rokitansky calls the stage of relaxation, softening, and breaking down, the changes in the affected glands vary greatly in dif- ferent cases. Not unfrequently the process becomes retrogressive, without the occurrence of destruction of the wall of the follicle or of the mucous membrane covering it; the swelling of the glands subsides, while their contents are reabsorbed after the cellular elements have been destroyed by fatty metamorphosis. These cases appear chiefly to correspond to the so-called abortive typhus. In other cases, the covering of the follicles is changed to a dry, friable slough, colored yel- low by the feces; this slough sometimes extends over the whole of the gland, so that its form and size correspond to those of the plaque; sometimes it is limited to part of the covering, and the slough has an irregular, angular, or roundish form. In still other cases, the individual glands composing Peyer's patches rupture, and empty their contents outwardly, without the covering sloughing. As a result of this, the surface of the plaque looks as if full of holes, or has a net-like appear- ance (plaques d surface reticulee). The mesenteric glands are most swollen in this stage; some of them attain the size of a pigeon’s or even of a hen’s egg. Their covering is usually bluish or brownish red, while their substance has a grayish-red, medullary appearance. In the fourth stage, or that of ulceration, the sloughs formed on the plaques or solitary glands are either thrown off in mass, or, after precedent dis- integration, and a loss of substance, a typhous ulcer remains. PoJci- tanslcy gives the following as the most important characters of the typhus ulcer: According as it has resulted from a solitary follicle or from a Peyer's patch, it is round or oval, and, if there has only been a partial slough on the Peyer's patch, it is irregular; it varies in size from that of a hemp-seed or a pea to that of a dollar; its seat is in the lower part of the small intestine, and the ulcers proceeding from Peyer's patches are of course opposite to the insertion of the mesentery. The long diameter of the elliptical ulcer corresponds to the long axis of the 630 ACUTE INFECTIOUS DISEASES. intestine; the margin of the ulcer is formed by a bluish-red, later slate- gray border of mucous membrane, about a line broad, which is movable over the surface of the ulcer. The floor of the ulcer is a delicate layer of submucous connective tissue, which covers the muscular coat. As soon as the slough is detached, the swelling of the mesenteric glands begins to subside, but they long remain larger and more vascular than normal. There are many deviations from this customary course of the disease on the mucous membrane; we shall briefly mention the more important of them: Occasionally, in the second and third stage, the hyperaemia of the mucous membrane over the swollen glands, and in their vicinity, becomes excessive. The mucous membrane is dark red, covered with ecchymoses; the patches resemble spongy, vascular, polypous proliferations, and the contents of the intestines are often mixed with a quantity of blood. A very serious event in the third, or sloughing stage, is the perforation of the intestine, which results from gangrene, not only of the mucous covering, but also of the correspond- ing part of the serous and muscular coats. The perforation is followed by severe peritonitis. Milder peritonitis also occurs without perfora- tion. The deviations of the intestinal affection in typhus, as regards extent, are very marked; sometimes only a few Peyer’s and solitary glands are affected; sometimes the ileum is almost covered with them. In the latter case we usually find the process further advanced in the vicinity of the valve than in the upper part of the intestine, and oc- casionally the difference of the stages in the different points is so marked as to lead us to suspect a succession of attacks. Not unfre- quently the colon participates in the disease (colotyphus), then the solitary glands of the colon undergo the same changes as those of the small intestines. Far more rarely the process extends to the jejunum, and even to the pyloric portion of the stomach (gastrotyphus), the solitary glands, and certain portions of the mucous membrane, which usually correspond to the folds, undergoing the changes characteristic of typhus. Where death occurs during the recovery of the ulcer and the other results of the disease, after the proper typhus process has run its course, the post-mortem appearances differ from those above described, and we must not limit ourselves to describing the processes which precede the healing of the ulcer, but must give a short glance at the state of the other organs, particularly as they show certain anatomical changes which never or very rarely occur during the first weeks of the disease. The bodies of patients who have died during the third or fourth week of the disease, or later, are more or less emaciated; the skin is pale, rigor mortis moderate, and, if there be decided anaemia, there is but little hypostatic congestion. In many cases the teeth and gums are TYPHOID FEVER. 631 still covered with a blackish coating. Over the sacrum, trochanters, and elbows, we usually find bed-sores; there may be destruction of the skin only, or of the other soft parts also, extending to the bones. In many bodies there is slight oedema of the lower extremities, and, if one or other femoral vein be obstructed by a thrombus, there is very marked oedema of the corresponding limb. Lastly, on the skin we often find petechiae, miliary vesicles, ecthyma pustules, and, in some cases, abscesses in the subcutaneous and intermuscular connective tissue, and suppuration of the parotid glands. On opening the body, the muscles no longer appear red and dry, but are pale and infiltrated. The blood in the heart and great vessels has lost its dark color, is fluid, and not unfrequently contains fibrinous clots, particularly when there has been inflammation of any organs. The brain is usually pale, moist, and the blood-points appearing on its cut surface are lighter, and contrast less with the white brain-substance than they did earlier in the disease. In the lungs, besides extensive hypostasis, we often find lobar or lobular pneumonia, and occasionally there are inflamma- tory exudations in the pleural sac; any laryngeal ulcers extend deeply and reach or destroy the perichondrium. In rare cases we find peri- chondritis laryngea without ulceration of the mucous membrane (Vol. I.). The heart is very relaxed and flabby, the endocardium and tunica intima of the vessels are greatly infiltrated. The swelling of the spleen has subsided, its capsule is often wrinkled, its tissue relaxed and pale; occasionally it contains haemorrhagic infarctions. The distention of the vessels and capillary hyperaemia of the stomach have disappeared at the same time as the swelling of the spleen. The ulcers of the intestine are on the road to recovery, or are already cicatrized, especially in those cases where death was due to other causes. Rokitansky describes the healing and cicatrization of typhus ulcers as follows: The loose border of mu- cous membrane, forming the edge of the ulcer, becomes attached to the floor of the ulcer gradually from the periphery toward the centre, at the same time it becomes more pale and less thick; the delicate connective- tissue layer, which covers the muscular coat in the floor of the ulcer, be- comes whitish, thickened, and is finally transformed into a serous plate, into which the adherent border passes imperceptibly, thinning as it ap- proaches the centre. The mucous membrane gradually extends over this plate toward the centre of the ulcer, but, at the same time, be- comes thinner, from the tension to which it is subjected. When the edges of the mucous membrane come together and adhere, the healing is complete. From the thinning of the mucous membrane, the cicatrix forms a slight depression; it is often somewhat pigmented, it is smoother than the parts around, and studded with a few tufts. Cica- trization of typhus ulcers never causes stricture of the intestines. As 632 ACUTE INFECTIOUS DISEASES. the ulcers heal, the mesenteric glands return to their normal size, and often shrink to small, firm, slate-gray bodies. Some, also, become case- ous and subsequently calcareous. Typhus ulcers do not always heal up, as above described. Occasionally the healing is delayed, but does finally occur. In other cases there is ulceration at the edges and base of the ulcer, which may cause erosion of vessels and abundant intes- tinal haemorrhage or perforation of the intestine. It is difficult to de- termine whether rupture of the serous coat in these slow ulcers finally results from suppuration of its tissue, from extensive gangrene, or, after destruction of the muscular coat, from simple rupture of the thin wall. The fact, that, not unfrequently, errors of diet and mechanical causes, such as compression of the abdominal contents by vomiting, precede the perforation, seems to show that the perforation of the serous coat is often induced mechanically. When death occurs late in the disease, besides the remains of the typhus processes, we occasionally find the evidences of croupous and diphtheritic inflammation of the mucous membrane of the intestinal canal, especially of the large intestine, and very rarely in the gall-bladder also. Lastly, we must add that more or less extensive nephritis, as well as thrombi in the veins, is among the changes not unfrequently found after the typhus proper has run its course. Symptoms and Course.—In many cases, the evident commence- ment of the disease is preceded for days or weeks by indefinite pre- monitory symptoms, which do not at the time enable us to determine the nature of the malady, but are of diagnostic importance after the disease has developed, as in doubtful cases they aid us in distinguish- ing typhoid fever from other affections that begin suddenly, without premonitory symptoms. These prodromata are feelings of general illness, mental disquiet, great dulness and relaxation, loss of appetite, indigestion, restless sleep disturbed by dreams, headache, dizziness, wandering pains in the limbs, which are usually considered rheumatic, and repeated epistaxis. These symptoms may last from a few days to several weeks. We generally consider that the disease proper begins when the first chill occurs during the premonitory symptoms, or, if there has been no prodromal stage, when a chill notifies the patient of his illness. This chill is rarely so severe and continued as in intermittent fever or pneumonia; there is usually no shivering or chattering of the teeth. Frequently there is not a single chill, but several, and cases do occur without any chill. Hence, especially in inattentive patients, we cannot always tell whether the disease is at the seventh or eighth, or at the thirteenth or fourteenth day. The pathologico-anatomical changes in the intestines during ty- TYPHoID FEVER. 633 phoid fever do not correspond to any marked clinical stages, so as to enable us accurately to distinguish the symptoms corresponding to the stages of congestion, typhus infiltration, sloughing, and ulceration, and to give the symptoms of these different phases of the intestinal dis- ease. Nor does the time that has elapsed since the first chill give any definite clew to the pathologico-anatomical stage of the bowel affec- tion ; but, on the other hand, we may suppose that, at the end of the third, or, at latest, at the end of the fourth week, the true typhus pro- cess has terminated, and that any existing morbid symptoms are only its remains, and belong to the secondary diseases of the blood and of different organs, induced by the typhus infection. Therefore Hamer- nik makes “ a first and second period of the typhus blood-crasis; ” in his communications from the Pfeufer’s clinic, Vogel speaks of two groups of symptoms, the “ intoxication ” and the “ reaction ” symp- toms ; Griesinger makes a “ first and second period of the disease.” We also shall divide the symptoms into two classes, and shall speak first of the symptoms of the disease itself afterward of the symptoms of the sequelae. As we mentioned above, the former occur in the first three or four weeks of the disease, the latter later in its subsequent course. Even during the first week the patient becomes very weak and much prostrated; but few can leave their beds during the first days; at the same time they complain of headache, which is chiefly in the forehead; of vague pains in the extremities, of buzzing in the ears, flashes before the eyes; of dizziness, which is particularly severe when they rise in bed, or attempt to walk. The sleep is restless and broken by dreams, in which the patients often speak single words, or whole sentences, in a loud voice. During the first week, while awake, the patient is usually perfectly conscious, but shows little interest in things around, and answers slowly and unwillingly to questions. There is great thirst, no appetite; there is a slimy or bitter taste in the mouth ; many patients ask for an emetic, because their stomach is out of order. Occasionally there is diarrhoea, but at first the bowels are usually constipated, and it is not till the end of the week that the patient has several pulpy or even fluid stools daily; in still other cases, the bowels remain constipated throughout the week, and induce imprudent physicians to prescribe laxatives. If these or an emetic be given at the commencement of the disease, they almost al- ways induce severe diarrhoea, which it is difficult to arrest. The pas- sages are rarely accompanied by much pain. During the first week of typhoid, there is often repeated epistaxis, which is not apt to be abundant, and which relieves the headache. In most, but not in all oases, cough and mucous expectoration betray the bronchial catarrh, 634 ACUTE INFECTIOUS DISEASES. vhich may be discovered by physical examination even during the first week. Among the objective symptoms comes next the changed appearance of the patient. While in bed, the face, especially the the cheeks, appears red; but, if he has been sitting up for some time, lie looks pale and meagre. At first the tongue is rarely thickly coated, moist and broad, showing impressions of the teeth along its sides ; it usually has a thin, whitish, epithelial coating, through which some papillae project as red points ; it is covered with a tough, slimy mucus, and appears narrow and pointed. The thin, epithelial coating usually falls off, gradually leaving, as Vogel aptly describes it, “ a moist, red, smooth tongue, that looks as if covered with gold-beater’s skin, or else is already inclined to dryness. If there be at first a thick, adherent coating on the tongue, it is usually detached from the point posterior- ly, and from the sides toward the middle, so that the wThitish yellow fioating appears enclosed in a very red border, which constantly in- creases in width ; but in some cases the detachment begins centrally, so that in the middle of the tongue there is a red stripe, that has a pe- culiar tendency to become dry, and at the sides two whitish-yellow, moist, slimy stripes. The central stripe is often broad anteriorly, and disappears posteriorly, so that on the point of the tongue we see a red triangle, with the apex posteriorly.” In spite of this peculiar disturb- ance of nutrition on the surface of the tongue, and of the diminution of secretion in the mouth, on microscopical examination of the coating of the tongue, Vogel could find nothing characteristic. Palpation and percussion do not show any anomaly of the heart or lungs, but on auscultation even at first, and always by the end of the first week, we find a more or less extensive whistling sound (rhonchus sibilans), due to catarrh of the smaller bronchi. Even during the first days the ab- domen is usually somewhat puffed up and tense; deep pressure over it is generally painful, and this sensitiveness to pressure exists not only in the ileo-coecal region, but also about the navel and in the epigastrium. On pressure in the right iliac region, particularly if there has already been severe diarrhoea, we notice a gurgling sound, the so-called ileo- coecal gurgling, whose diagnostic importance was formerly much over- estimated. Toward the end of the first week, the enlargement of the spleen is ordinarily marked. The enlarged organ usually has a horizon- tal position; it rarely projects beyond the ribs, and is pressed upward and backward against the spinal column by the distended intestines. Hence, the typhus spleen is rarely to be reached on palpation, and, even when it caii be touched, it is so soft that we are unable to define its outlines. But, if we lay the patient on his right side, with his left hand on his head, on percussing the lower ribs of the left side, we find a dull space, which may be six inches long by four wide, and which, TYPHOID FEVER. 635 corresponding to the eighth, ninth, and tenth ribs, nearly reaches the spinal column posteriorly, and the margin of the ribs anteriorly. An increase or decrease of the spleen-dulness, to the extent of a centime- tre or so, cannot be made out with certainty, in spite of what enthusi- asts in physical diagnosis assert. Even when the dulness has undoubt- edly increased or decreased slightly, we must bear in mind that this may depend not only on diminution or enlargement of the organ, but also on changes of its position. A greatly enlarged spleen may in- duce but little dulness when it is pressed into the hollow of the dia- phragm by the distended intestines, and only a small part of it lies in contact with the thoracic wall. Toward the end of the first week, on careful examination, we often find a few pale-red, roseola spots, about the size of a lentil, on the epigastrium and neighboring portions of the abdomen and breast. Finally, the most important objective symptom is the fever. The temperature rises very regularly, in a manner al- most pathognomonic of abdominal typhus. During the first week, the evening temperature is nearly two degrees higher than that of the morning; the morning temperature of the next day is about one degree lower than that of the preceding afternoon. For instance, a patient who has a temperature of 104°. 6 this evening, will, as a rule, have a temperature of 103°.7 to-morrow morning, and to-morrow even- ing a temperature of 105°.5. Toward the end of the first week, oc- casionally there is no increase of evening temperature; but even then the morning temperature is almost always about one degree lower than that of the evening (Wunderlich). During the first week, the pulse usually increases to ninety or a hundred, or even higher. Its fre- quence does not by any means always correspond to the temperature of the body, for, besides this, there are other causes, not always evident, that influence the heart’s action. Among other things, the pulse is ac- celerated from twenty to thirty beats in the minute, if the patient sits up in bed awhile, strains himself, or becomes excited in any way. Regarding the quality of the pulse, the blood-wave is usually quite large, but the artery remains soft during its diastole, and we often no- tice that the first pulsation is followed by a second, weaker one, that the pulse beats double. The double pulse, which does not occur exclu- sively in abdominal typhus, but is more frequent here than in any other disease, and consequently is not without diagnostic importance, is probably due to deficient activity of the contractile elements of the arterial walls, which are in a sub-paralytic state, as it is called. At least it may be shown that, if the arterial walls possessed no contractile filaments, but only elastic elements, the first pulsation, caused by the blood-wave, would be followed by a second evident pulsation (“ Nachschwingung ”). During the first week, in accord- 636 ACUTE INFECTIOUS DISEASES. ance with the severity of the fever, the urine is concentrated, high colored, and of increased specific gravity (1020 or more). If the pa tients replace the water they lose in perspiration and diarrhoea by drinking freely, the absolute amount of urine is not diminished ( Vogel). The production of urea, which is increased in proportion to the supply of nourishment, as shown by Vogel, corresponds to the elevation of temperature, which depends on the increased transformation of tissue. Later in the disease, when the fever disappears, the increased produc ■ tion of urea also ceases, and, like the temperature, falls below the nor- mal amount. The chlorides are diminished in the urine of typhus pa- tients. The explanation of this is less simple than that of the increase of urea. It partly depends on less salt being eaten with the food, partly on increased excretion of the chlorides by the bowels, partly perhaps because, while the blood is deficient in albumen, it retains more salts. However, neither the increase of urea, nor the decrease of chlorides, nor, finally, the slight albuminuria, is characteristic of typhus, as it also occurs in other diseases accompanied by severe fever and copious exudations. In the second week of the disease the complaints of pain in the head and limbs cease, but the dizziness becomes worse and the noises in the ears are accompanied by deafness, which, however, does not depend on disturbance of innervation, but, on a propagation of the typhous oral and pharyngeal catarrh to the Eustachian tube and cavity of the tympanum. The expression becomes more stupid, the inatten- tion greater; the intellect, which was usually clear during the first week, becomes cloudy, and the patient gradually falls into a somnolent, stupid state, from which he can only be aroused with difficulty, and for a short time. In spite of the dry mouth, he manifests no desire for water, but drinks with avidity when a glass of water is placed to his lips. It is often necessary to urge the patient repeatedly, to make him show his tongue, and when he has at length, after several unsuccessful attempts, succeeded in protruding the trembling organ, he occasionally forgets to draw it back, and must be reminded and urged to do this act also. Toward the end of the second week particularly, the stools and urine are often passed in bed, because the patient does not per- ceive the necessity of evacuating the distended rectum or bladder, oi because he neglects to contract the sphincters energetically by an ac tion of his will. Many patients lie unconsciously on their backs ; if placed on the side, the body and limbs follow their own weight, with- out the patient making any attempt to change his position, even if it be uncomfortable. The occasional trembling movements of the lips, or a few incomprehensible words that the patients mumble, alone show that the mental activity is not all lost (febris nervosa stupida): Othei TYPHOID FEVER. 637 patients, who are just as insensitive to the external world, who denude themselves without any modesty, do not answer questions, and scarcely react to the strongest irritants, show by their whole manner that they are living in an excited dream; they are constantly agitated, throw off the bed-covers as fast as they are replaced; thrust first one foot, then the other, out of bed, attempt to stand up or run away, talk loud or disjointed words, gesticulate, speak unknown tongues, and become morose and angry when they are held or in any way restrained (febris nervosa versatilis). It is astonishing what energy and persist- ence such patients often show in attempting to carry out their morbid impulses. Occasionally, during the entire disease, a certain circle of hallucinations recurs; the patients pursue any object that they can- not attain, are grieved by any sorrow that they are constantly combat- ing, etc.; in other cases the phantasms alternate confusedly with others having apparently no connection with them. Occasionally this alternation is so great that during the day the case appears to be a febris nervosa stupida, while during the night it seems to be a febris nervosa versatilis. In some cases the patients are constipated, even during the second week of typhoid fever; but, as a rule at this time, there are several watery evacuations daily. They vary in number from three to six, or even to twenty or more in twenty-four hours, but we cannot, from their frequence, decide the number and extent of the typhus ulcers, as the diarrhoea does not depend on them, but on the catarrh accompanying them; it is exceptional for the stools to be ex- cessively frequent, and it is most common to have only three or four passages daily. The dejections have the color and appearance of badly-cooked pea-soup, in which the meal is not thoroughly mixed, but has sunk to the bottom. They have an alkaline reaction, contain only traces of albumen, and have no microscopic elements or chemical constituents peculiar to typhus. The upper watery layer contains chiefly salts, and owes its alkaline reaction to the large amount of car- bonate of ammonia in it. The lower stratum consists of remains of food, detritus, epithelium, mucous corpuscles, numerous crystals of triple phosphates, and small yellow flocculi and globules, of whose origin and character we know nothing definite. Respiration is hastened and superficial. In some cases, in spite of the extensive catarrh, there is neither cough nor expectoration; in other cases the patients cough a good deal, and expectorate quantities of tough mucus. The objective symptoms also have changed to some extent in the second week. The cheeks are now more brownish red or bluish, the eyelids are half- closed, there is dried mucus at their corners, the conjunctiva is injected, the nostrils smoky-looking. A brown, tough mucous, fuliginous coating clings to the teeth and gums, and the tongue is covered with a browr 638 ACUTE INFECTIOUS DISEASES. crust, which gradually becomes blackish by admixture with blood from small fissures in its mucous membrane. Decomposition of the coating of the tongue and teeth causes a very disagreeable, penetrating odor; movement of the tongue is much impaired, so that speech be- comes indistinct, chewing of hard substances often impossible, and even drinking difficult. Physical examination of the thorax almost always shows more or less extensive condensation of the dependent portions of the lungs; on both sides of the spine the percussion-sound is less intense; on ausculting over the back, we find a weak vesicular or undecided breathing and fine mucous rale, rarely bronchial respira- tion, and at other parts of the chest there are numerous loud rhonchi. The belly is usually puffed up by the excessive meteorism of the intes- tines, which has never been explained. Its sensitiveness to pressure continues, as does the ileo-csecal gurgling in many cases. The en- largement of the spleen has increased; and that organ is pressed still farther backward and upward by the inflated intestines. In some cases the roseola spots have become quite numerous, and have spread from the epigastrium and lower half of the thorax to the back; suda- mina frequently occur. Among the objective symptoms of fever, the bodily temperature in the evening is usually 104° to 106°; in the morning there is only a slight remission. The pulse, which is less full, soft, almost always double, is often as high as 110 to 120, ox- more. In many cases the urine contains traces of albumen. In the third week of typhoid fever, the patient becomes excessively weak; he cannot sit up; and, if the bed be inclined, he slides down toward the foot of it, as often as he is lifted up. In the relaxed mus- cles we may often see and feel contractions of single fasciculi, the so- called subsultus tendinum. The somnolence and stupor reach the highest grade; the noisy delirium ceases, and the restlessness gives place to increasing stupor; some patients make automatic motions with the hands, or pick at the bedclothes, and almost always pass their feces and urine in bed. Occasionally the detrusor urinrn is also paralyzed, and the bladder excessively distended. The coating on the tongue and teeth becomes thicker, crusty, and fetid; the stammering speech grows unintelligible; drinking is very difficult. The chest and abdominal symptoms, also the frequency of respiration, rhonchi and mucous rales, dulness along the back, diarrhoea, and meteorism, become very decided. The spleen does not enlarge any more, but its swell- ing begins to subside. In the third week the roseola spots also begin to grow pale, while the sudamina increase, and petechfe some- times appear. In most patients there is erythema about the sacrum and detachment of the epidermis, and the exposed cutis sloughs. At the commencement of the thi~d week there is also apt to be an in- TYPHOID FEVER. 639 crease of the temperature and of the pulse. The morning remissions are indistinct. Fatal termination is most common in the third week, if not induced by some peculiar accident, death results from oedema of the lungs, after the prostration, weakness, temperature, and pulse have reached the highest grade. The more the respiration is affected, the sooner and more readily paralysis of the heart occurs. In favorable cases there is a subsidence of the symptoms about the middle of the third week. The state of deep sopor, during which the patient lives a dream-life, gives place to natural sleep. While awake, the expres- sion of the patient shows that he pays some attention to the things about him, which, at the height of the disease, had no existence for him; he also recognizes his attendants. The first glance in which affection and gratitude again appear may be regarded as an advance, although the danger is not yet over, and although the hopes awakened by this and other signs are often blasted. The more quiet and con- tinued the sleep, the clearer the intellect usually is during the waking state. The patients begin to complain of the bed-sores, and to lie on the side, so as to avoid pressure on the sore parts. They no longer pass their urine and feces in bed, but call for the bed-pan when they wish to have a stool, or empty the bladder. The number of respirations decreases, the patients cough oftener, and more strongly, and easily expectorate the mucus collecting in the bronchi, which has become less tough, and is usually yellowish. The passages are less frequent, and contain some consistent matter. The blue, sodden appearance of the patient disappears, the face becomes paler. The tongue grows moist at the edges and tip, its coating is gradually thrown off; speech becomes more intelligible; there is less difficulty in drinking. We hear moist rales in the chest, the dulness along the spine disappears ; even at these points the respiratory murmur becomes distinct, mete- orism decreases, the spleen dulness grows less, the roseola spots dis- appear. With the abatement of the other symptoms, the difference between the morning and evening temperatures becomes remarkable ; while the thermometer placed in the axilla still rises to 104° to 106° in the evening, in the morning it is often only 101° to 103°, or even less. These lower degrees are not observed in the evening for some time yet. As the temperature decreases, the pulse also falls, although the two do not keep pace. At the same time the pulse becomes fuller, and loses its rebounding character. This general improvement, which often does not occur till the fourth week, while the symptoms have maintained their intensity, or even increased till the end of the third week, often passes directly into convalescence, and the slow recovery alone shows that remains of the typhus process, especially intestinal ulcers, still exist; in other cases, the improvement is only temporary; 640 ACUTE INFECTIOUS DISEASES. the symptoms grow worse, and the patients die of paralysis of the heart and suffocation. In some cases, finally, the above symptoms are followed by those of retarded repair of the typhous local affections and sequelae. The appetite, which often becomes wolfish during con- valescence, may prove fatal, if the physician be careless, or the patient intractable. We shall again refer to the danger accompanying this symptom. Almost all convalescents lose their hair. But, as the hair- follicles have undergone no permanent disturbance of nutrition, a new growth of hair sprouts up soon after the old has fallen out. We have attempted to give as comprehensive a view as possible, and, at the same time, a tolerably complete one, of a severe “ normal ” case of typhus.* But it would lead us too far to describe with equal fulness the numerous and varied deviations that it presents in differ ent cases, and we must satisfy ourselves with noting the most impor- * Wunderlich, who has made a very large number of measurements of tempera- ture in typhoid fever, gives the most important results of his observations about as follows: The course of the fever is typical and perfectly characteristic; it distin- guishes abdominal typhus from any other disease. Besides the cases Avhich exactly follow the regular type, there are others which deviate from it—irregular cases. The causes of the irregularities cannot be recognized in every instance. The course of the disease shows two sharply-bounded, distinct periods, which correspond to the deposi- tion and rcabsorption of the infiltrations and exudations. These periods agree with certain portions of time, and in regular or nearly regular cases they respectively correspond to the first and last half of the disease. In mild forms, the first period lasts only a week, or a week and a half; the entire disease lasts three or four weeks. In severe cases, the first period lasts two, three, or three and a half weeks ; the en- tire disease lasts five, six, or occasionally from eight to ten weeks. In the first week, it is such an absolute rule for the temperature to rise two de- grees toward evening, and to fall one degree before the next morning, that, if the temperature on the second or third day be 104° or over, we may exclude typhoid ; the same is true, if between the fourth and sixth days the evening temperature do not rise to 103°, and, lastly, if the evening temperature begins to decrease again as early as in the second half of the first week. A decided increase of temperature during the first week is generally an unfavorable sign, while a slight increase is favorable. In the second week we may exclude typhoid, if the temperature be below 104° on one or mere evenings between the eighth and eleventh day, and, conversely, on the evenings of the second week, scarcely any other acute disease shows repeated rise of the even- ing temperature to 104°. A favorable course of the disease during the second week renders it probable that the third week will be still milder, while, on the contrary, a severe and unfavorable second week may lead us to expect that the subsequent course of the disease will be unfavorable. Among the favorable indications during the sec- ond week are: an evening temperature between 104° and 105°; a morning tempera- ture one or two degrees lower; late occurrence of the exacerbation (not before 10 a. m.) ; early occurrence of the remission (before midnight); regular and daily moder- ate decrease of temperature, as compared with that of the preceding day. Among the unfavorable indications are: continued elevation of the morning temperature; in crease of the evening temperature to 105°.5, or more; early occurrence of the daily TYPHOID FEVER. 641 *ant modifications of its course, and the severest and most dangerous accidents that present themselves. First, there are many cases which are not characterized by any re- markable lack of intensity of the symptoms, or by any other peculiari ties during the first week; but in the second week the symptoms do not grow worse and prove dangerous, as in “normal” typhus, but they decrease, and toward the end of the second or third week have all disappeared. Lebert has proposed the name abortive typhus for these cases, and it seems to me preferable to other names, such as “ febricula,” “ febris typhoides,” etc., because it better expresses the fact that these cases are only modified, benign, brief forms of typhoid, and not a peculiar variety of disease. After what we have said, it would be a useless repetition to give a description of the course of abortive typhoid during the first week; so we shall only remark, that many of the cases which former writers call “ gastric fever ” or “ mu- cous fever ” are to be regarded as abortive typhus. The old customary precaution, of waiting till the ninth day of the disease before saying whether the case was “ one of gastric or nervous fever,” was and still is very justifiable. The designations “ gastric fever ” and “ nervous fever,” in common use, exactly correspond to what modern physicians mean by “ abortive typhus ” and “ normal typhoid,” and since the laity do not understand precise scientific terms, it would be well to keep up this old custom. As in the first week the thermometer is the most certain means of distinguishing typhoid from a genuine febrile gastric and intestinal catarrh (Yol. I.), so in the second week it is the most certain means of deciding whether the disease will be an abortive ty- phus or not; the other symptoms are far more deceptive. If we find thvd on the eighth or ninth day of the disease the temperature ceases to rise, but gradually falls, and especially if we find decided morning remissions at this time, we may be almost certain that the case is one of abortive typhus. Cases where the temperature rises again exacerbations; late occurrence of the daily remissions ; and very high temperature at any time. In the third week, in mild cases, there are great morning remissions, so that the morning temperature may be three to three and a half degrees lower than the even- ing temperature, and may become normal toward the end of the week. And from the middle of the week the evening temperature also decreases. Iu severe cases, on the other hand, the temperature sinks but little during the third week, or else it maintains the same height, or even rises. In the latter case, we may almost posi- tively expect a severe fourth week, and not look for a decided decrease of the fever before the fifth week. We may look for the approach of death, if the temperature remain for some time at 107J ; if it suddenly rise to lOY.S or 108°, or when it suddenly falls very low, say to 94°. We must not expect perfect convalescence till the temperature is normal in the evening also. 642 ACUTE INFECTIOUS DISEASES. toward the end of the second week, and the subsequent course of the disease is as above described, are rare. Even in abortive typhus, the sleep is restless and disturbed by dreams, and patients talk in their sleep during the second week; but when awake their mind is clear, and only a moie or less marked apathy reminds us of the coma vigil of severe cases. The bronchitic symptoms are moderate; the daily evacuations are few in number, or there is no diarrhoea. The patient looks pale and worried rather than blue and sodden. The tongue is inclined to dryness, but is not covered with a firm crust. There is either no deafness, or else it is only slight, like the oral and pharyngeal catarrh. The abdomen is soft and only moderately promi- nent. Frequently there is no ileo-cascal gurgling or sensitiveness of the abdomen to pressure. The spleen-dulness is but little increased. Only exceptionally a few roseola spots occur on the epigastrium. During the morning, and while the patient remains in bed, the pulse is only moderately hastened. In the third week, or toward the end of the second, the temperature is usually normal, and is only elevated moderately toward evening; the tongue remains moist, and the patient begins to have some appetite. The morbid symptoms of the thoracic and abdominal organs have disappeared, particularly the diarrhoea. Many patients are anxious to get up; but, on attempting to rise or move about the room, are usually surprised at their feebleness, of which they were not aware while in bed. The strength returns slowly, and this tardy convalescence shows the severity of the disease that the patient has had. The conjecture above advanced, that in abortive typhus there is no sloughing of the diseased intestinal glands, is not founded on post-mortem examination, for which the favorable course ef the disease gives no opportunity, but on the early cessation of the diarrhoea, and the absence of the sequelae, so common in severe and tedious cases of typhus, especially of those depending on retarded cica- trization of the intestinal ulcers, and on the ulceration occurring in their place. There is a second modification of typhus which differs materially from that above described ; it is usually termed typhus ambulator ius. It is not very rare for persons who have only suffered from a slight amount of weariness and depression, loss of appetite and slight diar- rhoea, but have still been able to attend to business, or go on a jour- ney, to die suddenly of perforation of the bowel or intestinal haemor- rhage. On autopsy of such cases, we may find numerous intestinal ulcers along with sloughing patches and medullary infiltration of the mesenteric glands; in short, the anatomical changes of advanced ty- phous disease of the intestines. It is difficult to explain this peculiar form of disease, except on the supposition that, under some circum- TYPHOID FEVER. 643 stances, the infection with typhous poison may give rise to local changes in the intestines, but induce so little alteration in the blood and nutrition as to cause no noticeable functional disturbance. While in typhus ambulatorius the constitutional disturbance and fever are so slight as to be scarcely observable, some other cases of typhoid are characterized by unusual intensity of the constitutional disturbance, and especially by the height of the fever. In these cases the disease usually runs a “ tumultuous ” course. Even in the first week the temperature rises to 106° or more, and the pulse beats 120 to 130 per minute. During the day, the patients lie in a state of deep somnolence, and look stupid; at night they have high delirium, and can scarcely be kept in bed. Subsultus tendinum, picking at the bedclothes, and occasionally convulsive movements, begin early. The ntensity of the local symptoms usually corresponds to that of the gen- eral disease. The tongue becomes dry and crusted early; even during the first week the bronchitic symptoms, the signs of condensation of the lungs, the meteorism, diarrhoea, and the enlargement of the spleen, attain as high a grade as they usually do by the end of the second week. Toward the end of the first or the beginning of the second week the patient is greatly prostrated, slips down in bed, has a small, irregular pulse, and very rapid superficial respiration. Such patients often die early of paralysis of the heart and oedema of the lungs. In other patients, after a tumultuous course during the first week, the symptoms moderate and show no marked peculiarities during the second or third week. Between typhus of great intensity and tu- multuous course, and typhus of moderate intensity, and between this and typhus ambulatorius, there are numerous intermediate forms, which we shall not fully describe. Many cases, treated for weeks as “ gastric ” or “ mucous ” fever, and finally recovering without any affec- tion of the intellect or dryness of the tongue, are mild cases of ty- phoid ; but it is certainly going too far to scratch gastric and mucous fevers entirely out of the list of diseases. As we have shown above, the height of the bodily temperature is more important than the roseola or the enlargement of the spleen in diagnosing between typhoid, that is, an infectious disease, and a genuine intestinal catarrh. The appearances are also modified when the typhous intestinal disease is very slight, or, to use the customary expression, when the typhus localizes itself very slightly, if at all, in the intestines, and “ runs almost exclusively in the blood.” Since, in the first weeks espe- cially, the distinction between abdominal typhus and other acute in- fectious diseases is based chiefly on the intestinal symptoms, an exact diagnosis is entirely impossible in such cases, and we must occasionally content ourselves with a probable diagnosis, by the exclusion of other 644 ACUTE INFECTIOUS DISEASES. infectious diseases. If the intestinal symptoms fail entirely, or if there are only slight indications of them, while the bronchitis is severe and is early complicated with collapse and hypostasis of the lung or with decided pneumonia, we have the disease which, especially in those fatal cases where autopsy has shown medullary infiltration of the bronchial glands, has been called pneumo-typhus or broncho-typhus. It is evident that these cases, where the patients have a very cyanotic look and hastened and painful respiration, belong to the malignant forms. While the severe fever increases the production of carbonic acid, the disease of the bronchi and lungs impedes the excretion of the extensively formed deleterious gases. The formation of typhous ulcers in the larynx is not usually accompanied by any characteristic symp- toms, and modifies the appearance of the disease so little that we are less justified in making “ laryngotyphus ” a separate class than we should be in so considering broncho- and pneumo-typhus. But while, during the first weeks of the disease, laryngeal ulcer is not usually recognized, and is accidentally found on autopsy, it plays a very important part in the sequela? of typhus. Among the accidents that interrupt the normal course of the dis- ease during the first weeks, the most important are perforation of the bowel, intestinal haemorrhage, and the abundant epistaxis which occasionally occurs during the second or third week. The perforations of the intestine, which occur during the first weeks of the disease from the formation of a slough not only in the mucous coat covering the patches, but also in the muscular and serous coats at the affected parts, induce intense peritonitis; but since, pre- vious to the perforation, there has occasionally been adhesion between different loops of intestine, from inflammation of the peritoneum, this inflammation is sometimes partial, not total, at first. The first signs of perforation are a severe pain in the abdomen, which usually arouses the patient even from deep stupor, and which becomes excessive on the lightest pressure over the abdomen; the patient collapses sud- denly, the face becomes distorted, the pulse small, the extremities cool, and death usually occurs in from twenty-four to thirty-six hours, with the symptoms that we have described (Yol. I.) as indicative of peri- tonitis from perforation of the bowel. The most certain point in the diagnosis of perforation of the intestine is the escape of air into the peritoneal cavity, which is shown by the liver being pressed away from the abdominal wall and a consequent disappearance of the liver-dul- ness. If this symptom be absent, there is at least a possibility that the peritonitis is not due to perforation of the intestine. Intestinal hemorrhages, occurring in the first weeks of typhus, from erosion of the vessels on the detachment of the slough, or from rupture 1YPH0ID FEVER. 645 of the overfilled capillaries in the spongy elevations of the mucous membrane over the plaques above described, if abundant, often betray themselves before the appearance of blood in the dejections, by the collapse of the patient, which is accompanied by a sudden fall of his temperature, and occasionally by a clearing of the intellect. The loss of blood is often very considerable, but patients rarely die as a direct result of the haemorrhage; the bleeding usually ceases, the typhus pursues its course, but the strength of the patient does not carry him through, and most patients die, sooner or later, after the haemorrhage, from the exhaustion that is completed by the fever and diarrhoea. The abundant haemorrhages from the nose during the second and third weeks are far less dangerous than the intestinal haemorrhages; they are due to an acute haemorrhagic diathesis, which frequently occurs from excessive debility. They may be so severe as to require the tampon, they exhaust the patient, and at least retard convalescence. In women there is often haemorrhage from the genitals also, which does not always occur at the menstrual period. Although the loss of blood is not great, those haemorrhages which are greeted by the laity as favorable signs are usually mail ominis. If we bear in mind that most typhus patients recover very slowly even when the intestinal ulcers heal, the fever disappears, and the ap- petite returns immediately after the disease has run its course, and do not fully regain their strength for five or six 'weeks, it is not difficult to understand that retarded healing of the intestinal ulcers, and the continuance of even a moderate fever by the bowel-disease, should in- crease the danger to the patient. In these cases we find the typhus proper followed for weeks by symptoms of an asthenic fever, or of a fever in debilitated and anrnmic persons. The intellect remains cloud- ed, although the violent delirium usually disappears; the patient be- comes weaker, and slips down in bed more frequently than before. The tongue does not again become moist, or else becomes dry again, the bronchitic symptoms disappear, but the hypostases extend; en- largement of the spleen and roseola spots can no longer be found, but the meteorism and diarrhoea continue more or less marked. The bed- sore over the sacrum spreads, increases in depth, and may cause fright- ful destruction. Bed-sores also develop over the trochanters, elbows, and on the knees also, if the patients be laid on the belly. Petechias and ecchymoses form at different parts of the body, especially where there has been any temporary pressure. Emaciation becomes exces- sive ; the pallid skin is constantly bathed in perspiration. The visible mucous membranes also become pale and bloodless. There is often slight oedema of the lower extremities, or excessive oedema of one leg from thrombosis of the femoral vein. Many patients die in the sixth 646 ACUTE INFECTIOUS DISEASES. 3r seventh week, or even later, of this slow form of typhoid In other cases the diarrhoea ceases, the intestinal ulcers heal; but the bed-sores nduce fatal exhaustion; at least, we not unfrequently find deep de- struction of the soft parts and exposure of the bones, and recently- healed intestinal ulcers, as the only post-mortem appearances in cases that have proved fatal late in the disease. The pneumonias, pleurisies, suppurations of the parotid, diphtheritic inflammations of the intestines, nephritis, and other sequela) of typhoid above mentioned, show them- selves, just as in other debilitated persons, by objective rather than by subjective symptoms. Chills, and renewed increase of the bodily tem- perature, should excite the suspicion of one of these consecutive diseases and induce a more careful examination. Repeated chills, very high temperature, quick collapse, generally depend on pyaemia, induced by absorption of ichor from the bed-sores. The occurrence of severe pain in the larynx, hoarseness, aphonia, and the signs of acute laryngeal obstruction, indicate perichondritis laryngea, which is caused by ty- phous laryngeal ulcers penetrating deeply, but also occurs indepen- dently of this as a sequel of typhus. Lastly, we must mention that in some cases perforation of the in- testine occurs in the fifth or sixth week, not only while the patient is debilitated by the fever, induced by sluggish ulcers, but even while convalescence is going on perfectly well. Far more rarely haemor- rhages occur at this time, from slowly-healing ulcers. Recovery is the most frequent termination of typhoid fever; it takes place in about three-fourths of all cases; but some epidemics are far more malignant, while in others the mortality is much less. In most fatal cases death occurs in the second or third week of the dis- ease, that is, at its height; but we have already stated that, where the course is very rapid, the disease may prove fatal in the first week, and, in protracted cases, not till the fifth or sixth week, or even later. The different causes of death have been sufficiently described when speaking of the symptoms and course. Sometimes typhoid ends in incomplete recovery; sequel®, such as disturbances of innervation, neuralgias, partial paralyses, partial anaes- thesias, or mental disturbances, remain; occasionally typhus leaves a tabes and a lasting anaemia and hydraemia, which are not thoroughly understood. The material changes on which these disturbances of in nervation depend have not been discovered on post-mortem examina- tion. The supposition, that the remaining sickness and the deficient formation of blood depend on destruction of the intestinal glands and impermeability of the mesenteric glands, is incorrect. Pulmonary con- sumption not unfrequently develops during convalescence from severe typhoid fever. TYPHOID FEVER. 647 Treatment.—Prophylaxis requires that, in large cities, where typhoid fever is endemic, there should be sanitary police rules to pre- vent the soil from becoming soaked with putrid decomposing materials. Of late, many attempts have been made, by drainage in cities, to re- move the moisture of the soil, which greatly favors the decomposition of animal substances, and, consequently, the occurrence of typhus and cholera germs. Should the drainage succeed, and should it decrease the number of typhus and cholera cases, as the drying up of swamps sometimes does that of intermittent fever, the still youthful science of hygiene would boast of a brilliant triumph. Some physicians still doubt the contagiousness of abdominal typhus, or, at least, consider it as not proved. But such views must not be brought to the bedside of the patient; here the fact, that the non-contagiousness has not been proved, must make us act as if its contagiousness had been de- monstrated. The sick should be isolated from the well, and only those attendants required in caring for the patients should be allowed in his vicinity. It is just as important that all healthy persons, who can be spared, should be removed from the locality where the infection of one or more persons has occurred. I have learned of one very sor- rowful instance in Rheinland during the past few years, where, ap- parently, from the neglect of this precaution, almost all the members of one family, one after another, died of abdominal typhus. Lastly we must take care that the dejections of patients be not thrown into privies used by other persons. We know no prophylactic remedies that protect from infection by typhoid. When abdominal typhus has once begun, we may, under some cir- cumstances, attempt to cut short its course. It is now generally recog- nized that this cannot be done by emetics or venesection, which, for a time, were recommended for this purpose; in fact, these measures al- most always have an injurious influence on the course of the disease. Only when there is undigested food in the stomach, should we give a dose of ipecac.; in all other cases we must remain immovable to the senseless and often annoying requests of the laity for the administra- tion of an emetic. The case is very different with a few large doses of calomel. After the accurate observations of Wunderlich, we can scarcely doubt that by this remedy we may, in some few cases, cut short the disease (according to Wunderlich, one or two five-grain doses are enough), and that in the great majority of cases where this remedy is given during the first week, and before the occurrence of much diarrhoea, the course of the disease is rendered milder and shorter. The experience of Pfeufer’s clinic, as well as my own, perfectly agrees with Wunderlich'1 s. We shall not attempt to say whether the calo- mel has a favorable influence on the typhous intestinal disease, by op- 648 ACUTE INFECTIOUS DISEASES. posing the sloughing and ulceration, and whether, consequently, we can only expect benefit from it in the first weeks of the disease, when these changes have not yet taken place. TVillebrand has lately rec- ommended iodine as a specific in typhoid, and the results published by him, Liebermeister, and others, urge us to make more trials with the preparations of iodine in this disease, although the treatment is not a new one. Willebrand dissolves six grains of iodine and twelve of iodide of potassium in one drachm of water, and gives three or four drops of this solution in a wineglassful of water every two hours. It is said that, even after one, two, or three days of this treatment, there is a decided remission of the temperature; sordes do not come on the gums, or they disappear early; the fever ceases in an unusually short time. In most cases of typhus, the indications are to protect the patients from all injurious influences, to combat dangerous symptoms, and to maintain the strength of the patient by dietetic rules. In the first place, wherever circumstances permit, we should see that the sick- room be not too small, and be very careful to have it well ventilated. Fresh, pure air is very necessary for all typhus patients, and they do not catch cold nearly so readily as the laity imagine. The tempera- ture of the room should be regulated by the thermometer, and should be kept as nearly as possible at 60° to 65°. In North Germany there is a belief that a vessel of water under the bed prevents bed-sores. If it do not fulfil the expected end, this practice is probably useful in maintaining a certain degree of moisture in the room. We should also attend carefully to the patient’s bed. The coverings should not be too heavy, and the sheet should have no creases in it. The bed and body linen should be changed as often as soiled. We should not neglect to see that the body of the patient is kept scrupulously clean through- out the attack. Even among the neatest persons this is not super- fluous, for they are often prejudiced, or else fear to injure the patient by exposure, or do not carefully inspect the parts about the anus and sexual organs, so as to cleanse them from any excretions. Neglect of this precaution frequently cannot be subsequently made good. The most insignificant erythema on the nates, which might have been avoided, may prove very dangerous late in the disease, by forming the commencement of an extensive bed-sore. If the pa- tient be too weak to clean his own mouth, we should have it washed out regularly with a linen rag wet with cold -water, or, still better, with cold soda-water. Particular care should be paid to washing ff the sticky mucus clinging to the teeth and gums, before it dries and decomposes. Even when the patient is in a state of stupor, he usually shows some signs of pleasure and gratitude after this proceed TYPHOID FEVER. 649 ,ng. The best article of drink is pure spring-water or soda-water; if there be severe diarrhoea, we may give oat or barley water. All addi- tions of fruit-juices, vegetable acids, toasted bread, etc., to the drinks, soon become objectionable to the patient. The patient must drink freely, in order to replace the loss of water induced by the copious perspiration. If, during the advanced stages of typhoid, they do not ask for drink, because they do not perceive the want of it, it should be offered to them. Badly-instructed or thoughtless nurses sin a great deal against this rule. Shall we give the patient nourishment, or place him on absolute diet ? Views vary greatly on this point. Most German and French physicians consider the administration of meat- broths, eggs, and other nutritious substances in fevers generally, as so decidedly injurious, that they regard “ fever-diet ” and water-soup as identical. From England, there is an accusation against the German physicians particularly, that their dietetic rules cut off from the patients the supply of material by which the consumed portions of the body might be replaced, and that, consequently, the mortality is greater in Germany than in England, because the patients are starved, as it were. There is some truth in this assertion. I have no hesitation in saying, that the aggravation of a fever by giving the patient milk, eggs, and meat, has not been proved by actual observation, and I be- lieve that much injury may be done by blind faith in the correctness of this hypothesis. There is no doubt that in every fever the con- sumption of the constituents of the body is greatly increased, and that no sort of exercise will use up the body so rapidly as a fever does. While continued bodily exertion is usually borne with impunity, be- cause the increased consumption is hidden by increased supply, most fatal cases of fever are due to insufficient material being furnished for the replacement of that used up. Regarding typhoid fever, particu- larly, we find that in this disease the bodily temperature is above the normal for several weeks, and the consumption of tissue, by which this calorification is induced, is greatly increased. We see that in the most favorable cases, during convalescence, the greatly debilitated pa- tients, who have often lost ten to twenty pounds in weight, recover very slowly; and we must agree, that these facts urge us to give meat, milk, eggs, etc., rather than water-soup, until it shall be proven that such diet increases the fever. But, on the other hand, it cannot apparently benefit the patient if we give him this nourishment, and he is not able to assimilate it; on the contrary, it would hurt him to fill his stomach with food that will not be digested, but will decompose and cause irritation of the gastric and intestinal mucous membrane. We have before seen that dyspepsia is a constant accompaniment of all fevers. If we do not attend to this fact in regulating the diet of 650 ACUTE INFECTIOUS DISEASES. typhoid cases, but expect that their stomachs will supply plenty of gas trie -juice to digest large quantities of protein substances, we shall not increase their strength, but shall add a complication which will aug- ment the danger. From this we have the rule, supported by ex- perience, that at first we should give typhoid patients small quantities of milk and strong broth several times daily, whenever they desire it. The longer the disease continues, and the greater the exhaustion of the patient, the more untiringly we must attempt to supply nourishing food, but always in small quantities and in fluid form. In addition to these di- etetic rules, we should have typhoid patients washed all over with pure cold water, or with a mixture of three parts of water to one of vinegar. This should be repeated several times daily, and should be done very carefully, so that its beneficial and soothing effects may not be an- nulled by the fatigue induced by the act itself. In a mild, regular course of typhoid, we need give no medicine; but probably the old prescription of dilute chlorine-water (aqua oxymuriat. 3 ij, aqua des- till. § vj, det. ad vitr. nig., tablespoonful every two hours), or of mu- riatic acid in mucilage (acid, muriat. cone. 3 ss, mucil. salep § vj, syr* simp. 3 j, tablespoonful every two hours) is at least of palliative ser- vice ; and, as there are few patients that can be treated entirely with- out medicine, we should prescribe the above mixture, and it deserves the preference over other more active prescriptions. We may also follow the old custom of giving the muriatic acid in a weak infusion of ipecac, (gr. viij to § vj), instead of in simple mucilage, during the second week, if the diarrhoea and bronchitic symptoms increase, and in a weak decoction of Peruvian bark during the third week. The above treatment answers for most cases; but there are many others which require a different procedure, and in which threatening danger can only be averted by energetic treatment. In abdominal as in exanthematic typhus and other infectious diseases, the greatest danger is from the severity of the fever. But against this we hav6 a most efficient remedy. The danger from the fever is a double one. On the one hand, the increase of bodily warmth above a certain point induces paralysis of the heart and renders life impossible; on the other hand, continued increase of the production of heat, or, what is the same thing, protracted increased transformation of tissue, on which the feverish over-heating depends, induces consumption of the body of the patient. In fevers of proportionately short duration, as in the acute exanthemata, exanthematic and abdominal typhus, the danger from increase of the bodily temperature is, of course, more to be feared than that accompanying the increased production of heat. But, in combat- ting the former, we should not lose sight of the latter, or else we may injure the patient instead of benefiting him. Without fear of being TYPHOID FEVER. 651 misunderstood, I may give this warning before urgently advising the abstraction of heat in treating either exanthematic or abdominal ty- phus ; because, so far as I know, the hydrotherapeutic treatment of typhoid fever was first introduced and carefully observed in my clinic. Until within a few years, when the bodily temperature had risen to a dangerous height, and there was occasion to lower it, I have had the patients wrapped in cold, wet sheets, and the proceeding repeated at intervals of ten to twenty minutes, until the desired end was attained. After satisfying myself that the patients were unnecessarily annoyed by the repeated transportation from one bed to another, which was unavoidable in this operation, I have used cold baths in its place, and they are much more convenient. I found that they had the same effect, and were better borne by the patient than was the repeated envelop- ment of the body in wet sheets. But I could not hide from myself that, immediately after the bath even, there was occasional exhaustion along with the retardation of the pulse, sinking of the temperature, and clearing of the intellect. This exhaustion usually passed off quickly, and the disease finally terminated in recovery; but, along with such cases, others occurred where the exhaustion continued longer after the baths, and where early death made me doubt if I had actually benefited the patient, or if, while removing one danger, I had not in- duced another. Perhaps this anxiety was overstrained, but, after the careful observations made at my clinic by Liebermeister and Immer- mann as to the amount of heat passing from the patient into the water, the possibility of this danger cannot be denied. It is true we reduce the temperature of the body by cold sheets and cold baths, but we at the same time increase the production of heat. If this were not so, the patient would be cooled much more. I think it would be proper to compare the action of an energetic abstraction of heat to that of excessive exercise; then it will be asked if it be advisable to subject an already exhausted patient to this action. The question, is it not possible, by hydrotherapeutic means, to reduce the temperature of the body without exhausting the patients by an excessive increase of the production of heat ? which I consider a very important one, has been solved by Obernier and especially by Ziemssen. I consider the dis- covery, that a far less energetic and less sudden abstraction of heat than was accomplished by the methods formerly employed by myself and others will reduce the temperature of a typhoid patient two degrees or more, is a very important advance in the therapeusis of the disease I have not observed the above-mentioned state of exhaustion, which formerly alarmed me, since I have ceased to wrap patients in cold, wet sheets, or place them in cold baths, but have employed the following plan, recommended and tried by Ziemssen: As often as his tempera- 652 ACUTE INFECTIOUS DISEASES. ture rises above 104°, the patient is placed in a bath, whose tempera- ture is about 10° below that of his body, or about 94°. While the body and limbs are gently rubbed, we add cold water gradually till the temperature of the bath is reduced to about 68°. The patient is to remain about twenty or thirty minutes in the bath, till he is slightly chilled, and then to be placed quickly in a warm bed. At first, four or five baths daily are necessary, subsequently two or three. The method of Ziemssen has one great advantage, that in private practice there is no great objection made to it. The laity consider it much less objec- tionable to place a patient in a lukewarm bath than to wrap him up in wet sheets, or to pour cold water over him, etc. For moderating the fever in exanthematic as well as in abdominal typhus, next to the ab- straction of heat, the administration of quinine deserves most confidence. This remedy has been repeatedly recommended in abdominal typhus, and almost as often it has been given up, because it did not equal the expectations of the employers. The only effect of quinine on the disease is to moderate the fever. If the temperature of a typhoid pa- tient rise above 102°, I give quinine, but of late do not give such large doses as formerly, when I prescribed ten-grain doses and during the day gave as much as thirty grains. Now I usually prescribe one or two grains at a dose, in solution with dilute sulphuric acid. If we use quinine at the same time with the abstraction of heat, we are not obliged to repeat the latter so often, which is a decided advantage. Wunderlich has recommended digitalis as an antipyretic in abdominal typhus, and the results claimed by this trustworthy observer, in cases with frequent pulse and continued high temperature, urge us to further trials of this remedy, of whose antipyretic action, in the treat- ment of pneumonia and other inflammatory diseases, we have already spoken. Next to the fever, the most dangerous symptoms, when extensive, are the disturbances of the respiratory organs, the bronchial catarrh, hypostasis, and collapse of the lung; but, unfortunately, we are far more powerless in regard to these dangers than in regard to that in- duced by the fever. The advice of most authors to give lukewarm, instead of cool drinks, when there is severe bronchitis, is based rather on theory than practice ; when feeling the burning skin of a typhoid patient, no one would think seriously of combating the bronchitis by warm infusions. In severe typhous bronchitis, the most customary prescriptions are wet or dry cups, warm compresses, sinapisms, and blisters to the chest, and the internal administration of an infusion of ipecac, (gr. vij to § vj), or of an infusion of senega ( 3 ss to § vj), to which may subsequently be added liquor ammonia* anisat. ( 3 ss— 3 j). None of these prescriptions do much good, though the occasional ap- TYPHOID FEVER. 653 plication of wet and dry cups most frequently causes temporary allevia- tion, and in most cases the cutaneous irritants are even injurious. If we hear extensive moist rales in the chest, while the expectoration is arrested, we may give a few doses of flores benzoes (gr. ij—iv), and, if they fail, give a certain emetic, which will be of service here, and, avert the threatening danger, if any remedy can. To prevent the ex- tension of hypostasis, we may attempt to preserve the patient from constantly lying on the back, by changing him from one side to the other; but, unfortunately, this good advice cannot always be carried out continuously. The treatment of collapse of the lung and of pneu- monia is the same as that of the bronchitis. In profuse epistaxis, we should not try mineral acids and cold applications too long, but apply a tampon early. Among the intestinal symptoms, moderate diarrhoea requires no especial treatment. If the evacuations become very profuse, we may give astringents, especially solutions of alum (3 j to 3 vj), or of tannin (3j — 3 ss to 3 vj), with an addition of tinctura opii (3j— 3 ss). For the tenesmus, which is occasionally very annoying, starch injections containing ten to twelve drops of laudanum are almost al- ways beneficial. Where there is much meteorism, we may attempt to evacuate the gas by passing a stomach-tube up the anus. Constipa- tion is to be overcome by injections, or by castor-oil. In intestinal haemorrhage, we should apply cold or ice compresses to the abdomen, and renew them frequently, at the same time giving alum internally in the form of serum lactis aluminatum. In perforation of the intes- tines, we should also employ cold compresses to the abdomen, but especially should give opium in quickly-repeated large doses (a grain every hour or two). At the same time, the patient may take small quantities of ice-water, or small portions of ice, to quench his thirst, but should have no food at all for several days. If peritonitis occur, independently of perforation of the bowel, cold compresses over the abdomen still deserve the preference to leeches. If there be paralysis of the detrusor vesica?, which, to the great injury of the patient, is often overlooked by inexperienced and careless physicians, the bladder should be evacuated at least twice daily by the catheter. It has already been stated that scrupulous cleanliness greatly aids in preventing bed-sores. On the first appearance of erythema, we should protect the reddened spot from further pressure by an air-cushion, and wash it several times daily with lead-water, dilute brandy, or with red wine. Eroded spots should be covered with lead or zinc salve, or with ungt. tannicum (ungt. contra decubitum Autenreithii), and lightly touched with nitrate of silver. If there be a deep loss of sub- stance, with unhealthy base, it should be treated, according to the 654 ACUTE INFECTIOUS DISEASES. rules of surgery, with cataplasms, stimulating salves, red precipitate, or nitrate of silver. If, in spite of all our care, the strength of the patient sink more and more, if the pulse become small, the collapse and prostration dangerous, we should boldly give strong wines, such as madeira, port, etc., or strong beer (Pfeufer). No analeptic or roborant medicine in the pharmacopoeia has an effect equal to that of a strong wine. The fear of increasing the fever by administering alcoholic liquors is un- grounded ; and it is best not to wait for great exhaustion before giv- ing wine, but, in all cases where the patients begin to grow weak toward the end of the second or commencement of the third week, to give them half a pint of light wine daily. Lastly, during convalescence, the diet of the patient should be most carefully watched. The number who die during convalescence from typhoid fever, from the fault of the physician, because he has neglected to say exactly what and how much they may eat, or from their own, because they have not followed the rules laid down for them, is proportionately large. It is best to let the patient eat fre- quently, but only a little food at a time, so that the slight amount of gastric juice secreted by the convalescents may suffice for its com- plete digestion. All indigestible food, which forms large amounts of fasces, should be strictly forbidden. An apparently insignificant indi- gestion, a moderate diarrhoea, or slight vomiting, should be regarded as a very dangerous occurrence, because it may induce perforation of an ulcer that has not yet cicatrized.3 CHAPTER IX. FEBRIS RECURRENS RELAPSING FEVER. Etiology.—Relapsing fever is among the acute infections about whose propagation by contagion there is no doubt; but we hesitate to proclaim this as a purely contagious disease, such as the acute exan- themata, measles, scarlatina, and small-pox, which never occur in a person who had not been infected by a measles, scarlatina, or small- pox patient. There are certain points in favor of the view that the infecting substance, which induces relapsing fever, is not only pro- duced in the body of the patient, but that it may be produced outside of the human body. The mere fact, that certain regions, whose telluric conditions give rise to a pure miasm, malaria, are also subject to epi* demies of relapsing fever, can hardly be made to agree with the ex- RELAPSING FEVER. 655 tension of the disease by contagion alone; this is still more true of the fact taught by experience, that, in places where relapsing fever has not been seen for years, if a famine occur, and, from lack of proper food, people are obliged to eat bad or spoiled provisions, the disease will not unfrequently break out. On the other hand, there are grave objections to this double mode of origin and extension. The same reasons that satisfied us that the contagion in other infectious dis- eases consists in low organisms, are just as valid in relapsing fever; and, although we cannot say it is impossible, we are still very averse to supposing that organisms which reproduce themselves in the human body may also develop and increase outside of it under such different conditions. The great resemblance in the mode of extension of relapsing fever and in its symptoms to the forms of typhus already treated of, cannot escape notice. On the other hand, there are some points indicating a difference between relapsing and typhus fevers, and a certain relation- ship to intermittent fevers. This circumstance, as wrnll as the fact that there is no case known where a patient with typhoid or typhus fever has communicated relapsing fever to another person, and vice versa, has decided the best authorities to rank febris recurrens as a third form of typhus after abdominal [typhoid] and exanthematic [typhus] typhus fever. Now, if, after typhoid and typhus fevers had long reigned, relapsing fever occurred with them or in their place, this might probably be simply due to a modification of the low organ- isms forming the contagion of typhoid or typhus fever, induced by the vicinity of a marsh or the effect of bad food; in other words, to the development of a new species allied to but differing from the former ones. I believe generally that the history of epidemics strongly supports the correctness of Darwin's theory of the origin of new species. For my part, I have no doubt that, in the course of centuries, new infec- tious diseases have developed and taken the place of others that for- merly prevailed. In the writings of the ancients we find wonderfully- accurate descriptions, even of forms of disease, whose recognition and distinction offered the greatest difficulties. There can be no doubt that the regular and easily-recognized combination of symptoms char- acterizing measles, scarlatina, typhoid fever, etc., would not have es- caped the sharp observation of Hippocrates, if it had existed then as it does now about the native place of the great Asklepiad.* If the correctness of this hypothesis be accepted, and the depen- * But in the writings of Hippocrates there is one place which seems to indicate that febris recurrens occurred even in his day. 656 ACUTE INFECTIOUS DISEASES. dence of contagious diseases on an infection of the body from low or- ganisms be regarded as certain, the appearance of new infectious dis- eases must seem a proof of the development of new species of organic beings. Should not the varied malignity shown by epidemics of the same disease at different times, and certain peculiarities of the indi- vidual epidemics, be most simply referred to slight modifications, and the gradual passage of certain phases of infectious disease in other forms as extensive modifications of the low organisms ? The susceptibility to relapsing fever seems very general, and it has often been noticed that almost every dweller in even large houses exposed to the contagion was attacked by the disease. No age es- capes the affection; but most cases are among the young and middle- aged. The predisposing influence of bad dwellings and insufficient food is not to be mistaken. Poor people furnish so large a contin- gent of the cases of relapsing fever that this cannot be explained solely by their numerical preponderance over the well-to-do classes. Peo- ple in good circumstances have no immunity from this disease, and nurses and physicians attending patients with it are not unfrequently infected. One occurrence of relapsing fever does not seem to remove the liability to it, as it does in other forms of typhus. Anatomical Appearances.—The result of autopsies made in epi- demics of febris recurrens of different intensity and malignity, together with symptoms observed during life, justifies the following conclusions: The infection of the organism by contagion not only induces high fever running a peculiar course, but also pathological changes in vari- ous organs, especially in the spleen, liver, and kidneys. Usually these pathological changes consist only of disturbances of the circulation and in such changes of structure as may be readily removed. But in malignant epidemics more extensive structural changes develop in the above organs, bearing partly the character of parenchymatous, partly of suppurative inflammation. The disturbances of nutrition due to relapsing fever have not a specific character, and do not differ from those induced by other injurious influences. The corpses long retain a rigor mortis which occasionally begins very early. The skin is usually light yellow, sometimes typically jaundiced. At the dependent parts of the body there is extensive post-mortem hypostatic congestion. The muscles are not so dark as in other forms of typhus. On mi- croscopical examination a more or less extensive degeneration of the muscular fibrillm will be found; they appear cloudy, indistinctly trans- versely striated, filled with molecular fine granules, which disappear on the addition of acetic acid, while the filaments become pale, and show neither transverse nor longitudinal strife (Kilttner). This degen REnAPSING FEVElt. 657 eration is not confined to, or even chiefly localeu in muscles, which, during life, were the seat of severe pain, but, when found at all, usu ally extends to all the muscles of the body. In recent cases the blood is dark cherry-red, and contains but few fibrinous clots. In protracted cases the blood is watery and without a trace of coagulation. When death occurs at the height of the disease, the brain and meninges are vascular and dry, the ventricles empty. If death does not result till the later stages of the disease, the meninges are slightly injected, the brain itself bloodless and pale, the subarachnoid spaces and lateral ventricles containing quantities of serous fluid. Some observers (Kremianshy) found haemorrhagic pachymeningi- tis very often, partly in its commencing stage, partly as an extensive haematoma of the dura mater. The bronchial mucous membrane presents no constant changes; the lungs are more or less congested, especially at the dependent parts; in protracted cases they sometimes contain haemorrhagic in- farctions or extensive pneumonic infiltrations. The heart is flabby, pale, and friable. On microscopical examina- tion, Ruttner found it infiltrated with an albuminous or fibrous mass. If the disease has lasted long, the walls of the heart are occasionally much thinned. As a rule, the gastric and intestinal mucous membrane is reddened by injection and ecchymosis. The intestinal glands are sometimes enlarged, but never sloughing. The ductus choledochus is occasion- ally closed, by swelling of its mucous membrane, and obstructing masses of mucus. In such cases the contents of the intestine are but little colored, while the gall-bladder is distended. The liver is considerably enlarged, apparently from the increased amount of blood in it. According to KiXttner, it sometimes has a mar- bled appearance, distinct, yellowish-white, wax-like spots appearing in the normal parenchyma; .when far advanced, these resemble nodules of medullary cancer. At such points the individual acini are not rec- ognizable. The liver-cells have lost their polygonal form; the nuclei are perceived with difficulty, and filled with homogeneous contents. In cases beginning with icterus, and proving fatal in the first attack (bilious typhoid), the same author found the liver smaller, the paren- chyma jaundiced, much relaxed, and broken down. There were the same microscopical appearances as in acute yellow atrophy of the liver. The spleen also is enlarged; it may attain five or six times its normal size and weigh four pounds or more; its parenchyma is only exceptionally as soft and fluid as in the first stages of the other forms 658 ACUTE INFECTIOUS DISEASES. of typhus; usually it is hard and friable, and on section the Mal- pighian bodies project as grayish-white or jaundiced points the size of a pin’s head. Occasionally in the spleen we find yellowish-white foci, roundish or irregular in shape, from the size of a hemp-seed to that of a hazel-nut, at first quite firm, but later breaking down into pus. KUttner considers these as ruptures in the cavernous venous meshes of the spleen, which subsequently, as in phlebitis after venous throm- bosis, induce inflammation, suppuration, and putrefaction of the parts around. The kidneys also are enlarged, sometimes to double their normal size; this is due solely to swelling of the cortical structure. It is difficult to detach the capsule, and, when this is done forcibly, small portions of the renal tissue remain adherent to it. On microscopical examination we find the epithelium of the uriniferous tubules swollen and filled with fine molecules; in the later stages the epithelial cells have been destroyed, and the tubules are filled with fine granular de- tritus. Rarely there are numerous small abscesses scattered through the kidneys. Symptoms and Course.—The length of the period of incubation is not yet accurately determined. Many patients feel perfectly well from the inception of contagion till the outbreak of the disease, while others complain, a few days before the actual commencement of the malady, of ill-defined and uncharacteristic disturbances of their general health, of great weariness, pain and heaviness in the head, increased thirst, and occasionally of migratory pain in the extrem- ities. Whether the above prodromata have occurred or not, the disease itself almost unexceptionally begins with a chill of variable duration and intensity, followed by a persistent feeling of great heat. With the commencement of the fever the patients become very weak, complain of pain in the head, especially in the forehead, often also of dizziness and tinnitus, and of severe muscular pains almost characteristic of the disease, which affect chiefly the neck and limbs, and are among the most annoying symptoms of the disease. A slight amount of psychical excitement, usually present at first, generally passes off. The feeling of illness is unmistakable, the patients show- ing no interest in their surroundings. Delirium and deep sopor are exceptional, even where the fever is very high, which is a strong argu- ment against the exclusive dependence of psychical disturbances, in acute infectious diseases, on the height of the bodily temperature. At first, the face is slightly flushed, the skin hot and dry, rarely is it covered with slight perspiration. We must beware of regarding this moisture of the skin at the height of the disease as a favorable sign. RELAPSING FEVER. 659 (I have already stated that, of two patients with equal bodily temper- ature, the one whose skin is moist is the more feverish.) There is great thirst, but no appetite, although the patients do not obstinately refuse food. The tongue is broad, rounded anteriorly, and bears the imprint of the teeth along its sides; it has a thick, white coating, the edges and point are red. Even where the fever is high the tongue usually remains moist, and is scarcely ever covered by the dry, black coating visible on the small pointed tongue, and on the teeth, and gums, in typhoid fever. The pharynx also is affected by catarrh, usually mild, but some- times very intense, characterized by more or less injection of the mu- cous membrane and secretion of a tough mucus. In some cases bil- ious vomiting occurs at the commencement. As a rule, there is con- stipation ; far more rarely, diarrhoea, perhaps from excessive drinking. The respirations are increased in proportion to the fever, and, without any complication of the lungs or bronchial tubes, may attain to thirty or forty, or even more, in a minute. There may be symptoms of bron- chial catarrh or not. The abdomen is neither distended nor depressed; the regions of the liver and spleen are sensitive to pressure, and some- times spontaneously painful. Physical examination early shows con- siderable enlargement of the liver and spleen. Not unfrequently the former extends almost to the navel and far into the left hypochon- drium. The latter is also perceptible to the touch when it extends beyond the angles of the ribs. According to the careful researches of Obermejer, in most cases the urine shows the peculiarities of parenchymatous nephritis. Be- sides more or less albumen, blood-corpuscles and dark epithelial cyl- inders were found in about two-thirds of his patients; later in the course of the disease the cylinders were covered with granular epi- thelial detritus, and finall}” perfectly pale cylinders were passed. As a rule, during the fever the amount of urine passed is diminished; its specific gravity is 1012 to 1020. A slight degree of icterus, sometimes accompanying the above symptoms and depending on catarrh of the ductus choledochus, is readily recognized to be hepatogenous by the diminished color of the feces and the discovery of bile-acids in the urine, and is to be distin- guished from the icterus hereafter described, which is probably htema- togenous and renders the disease malignant. From the above description it is evident that, apart from the se- vere muscular pains, the patient’s symptoms resemble those accompa- nying intense fever; and in fact we may regard the fever as the most prominent and characteristic symptom of this disease. This fever shows not only the peculiarities to which the disease owes its name, but it 660 ACUTE INFECTIOUS DISEASES. has others which enable a certain diagnosis, even in the first at- tack. From the observations of Obermejer, who has taken accurate meas- urements of temperature during the chill, with which the later at- tacks also usually begin, we may assume that the bodily tempera- ture is elevated even during the initial chill, and that this is even preceded by a slight elevation of temperature. The bodily tempera- ture attained is very unusual; it is not at all rare for it to reach 107.3°, and in some cases 109°, or an elevation that never occurs in other diseases, and at which many regard the continuance of life as impossible. This, like typhoid fever, has a remittent type. The daily variation is usually about one degree, the greatest differences being in the morning and evening. The pulse also is more frequent in relapsing fever than in almost any other disease. In nearly every case it rises to 110 or 120, not unfrequently to 120 or 130 and even to 150 beats per minute, without being in itself of very evil import. The frequency of the pulse corresponds far less than in other diseases to the bodily temperature. As a rule, the pulse is at first hard and tense, later, from paresis of the muscular coats of the vessels, it becomes soft, undulat- ing, and not unfrequently dicrotic. With slight modifications the dis- ease goes on thus for from five to seven, rarely longer than eleven or twelve days; then there is a sudden change. After a transient increase of all the symptoms, in which the bodily temperature reaches its highest point, the peripheral arteries pulsate strongly, and abundant epistaxis often occurs ; the previously-dry skin breaks into a copious perspiration, and there is an alleviation of all the symptoms. Accord- ding to Obermejer, the duration of defervescence is usually eight or nine hours, during which time the body cools off about 9°, so that, if before the crisis the temperature was 106.4°, afterward it will be 96.8°, or less than normal. I have no doubt that the excessive loss of warmth, caused by the evaporation of the perspiration, contributes materially to this rapid fall of temperature. During a critical sweat, the active flow of blood from the interior of the body to the surface will almost equalize over the body the loss of warmth that is induced by evaporation of the perspiration. Such a sweating must induce cooling, such as could not be attained in the same length of time by any hydropathic procedure. It does not lessen the loss of heat by conduction and radiation ; and to this is added the great loss due to evaporation of the perspiration. I would call attention to the im- mense amount of heat withdrawn by evaporation of the abundant perspiration during a Turkish bath; for there, in spite of the sur- rounding air being 40° or more warmer than the body, and the con- tinued heating from within, there is no considerable elevation of its RELAPSING FEVER. 661 temperature. I should like to know if such a rapid defervescence of the fever is seen in cases where, instead of sweating, there is critical diarrhoea. In the days following the crisis, the bodily temperature, which had almost always fallen below the normal, rises one to two degrees. The pulse varies from 48 to 50 beats a minute, the appetite returns, the tongue cleans off, the muscular pains subside, the patients feel stronger, and many of them wish to leave their beds. But only in rare cases, where the disease is incorrectly termed re- lapsing, does this very agreeable condition (which, to the uninitiated, must seem a commencing convalescence) actually form the beginning of recovery. In most cases, in from six to eight days, rarely less, or from twelve to fourteen, there is a new attack, closely resembling the first. This second attack also usually begins with a chill of variable duration and intensity; the subsequent feeling of heat, debility, de- pression, and thirst, attains about the same degree as in the first stage of the disease. The muscular pains also recur, but are less severe ; the tongue, which had cleared off, is again coated, the appetite is lessened. The spleen and liver, which during the interval had some- what decreased in size, again swell, and occasionally become even larger than in the first attack. During this second paroxysm, the bodily temperature rises just as high as, in many cases higher than, in the first, but the pulse is usually less frequent. The second attack is commonly shorter than the first, lasting only three or four days. The crisis terminating it has about the same symp- toms as that closing the first attack. The disease generally ends with the second attack. Far more rarely it is followed by a third, fourth, or even fifth, which have essentially the same symptoms. By far the most common termination is in recovery; the very slight mortality, which in most epidemics is only two or three per cent., and rarely higher than six or eight per cent., is in great con- trast to the severity of the symptoms, especially to the temperature. If the disease prove fatal, death results either during the attack, from collapse and general paralysis, or more rarely during the interval, from exhaustion, or lastly as a result of secondary diseases and complications, among which pneumonia is the most important. JPastau, as well as Obermejer, has given us valuable investigations as to the weight of the body in relapsing fever. These show that during the disease the body loses from a tenth to a fifth of its weight, and that this cannot be solely referred to the diminished supply of nutriment. Exact investigations prove again the correctness of the doctrine that increased transformation of the constituents of the body plays the most important part in the elevation of temperature during 662 ACUTE INFECTIOUS DISEASES. fever. It is very interesting to me to find that Obermejer lias proved that there is a steady decrease of the weight of the body during the attack, but that it is far greater and more rapid on the critical days. These observations agree perfectly with those which were made in my clinic by Dr. Steiner even before the Leyden investigations, and which led to the following conclusions: Where the bodily tempera- ture is only moderately increased, the loss of weight may be less than that observed during the same length of time in healthy persons. This is because during fever the function of the perspiratory glands, as well as of other secretory organs, is suspended, and the loss of bodily weight from evaporation depends chiefly on evaporation of the per- spiration. But, if the bodily temperature rise to 102° or 104°, the loss of weight is always greater than in healthy persons under circum- stances as nearly as possible the same. When the temperature of the body is so high, even if the secretion from the sweat-glands be entirely arrested, more fluid is evaporated from the mucous membrane of the respiratory passages than is usually evaporated from the surface of the body and the air-passages together of persons with normally-acting sweat-glands. The most rapid decrease of bodily weight occurs at the defervescence of the fever, for then the sweat-glands again act, while the still-elevated temperature is accompanied by accelerated evapora- tion. I believe in the correctness of the idea that, at the height of the fever, there is only a relative retention of water in the body, but do not think it necessary to refer this retention to diminished action of the sweat-glands. Under certain influences still unknown, possibly merely as a re- sult of the action of a particularly intense contagion, relapsing fever assumes a very malignant character. The appearance of the disease is especially modified by excessive participation of the biliary appara- tus, and in most cases death appears with severe symptoms. Grie- singer describes this malignant form of relapsing fever, from his obser- vations made in the East, and terms it bilious typhoid. The St. Peters- burg epidemic of 1864 to 1866, where, besides simple recurrent fever, there were numerous cases of bilious typhoid, especially at its com- mencement, fully confirmed Griesinger's description of the disease, as well as his opinion that it was a severe form of recurrent fever. At first the symptoms vary little from those of simple recurrent fever, except that there are more depression and headache, and greater mental sluggishness, bilious vomiting is more frequent, and the tongue shows a tendency to dryness, while in simple recurrent fever it is apt to remain moist during the whole course of the disease. Usually, after a few days there is diarrhoea, with evacuation of bilious looking masses; or else the passages have a dysenteric appearance RELAPSING FEVER. 663 Often also there is bronchial catarrh of variable intensity; and gen- erally from the fourth to the sixth day of the disease, after the liver and spleen have swollen considerably, and become painful, there is severe icterus without discoloration of the feces. About this time the prostration of the patients is very great; they are perfectly apathetic and somnolent or delirious. The tongue is dry and crusted, pulse slow, the hot skin loses its turgescence; and, in this state, many die with the symptoms of sudden collapse. In others, at about the same time as in simple recurrent fever, there is a more or less complete crisis, followed by a rapid improve- ment of all the symptoms. The patients seem to be convalescing, tiL a relapse occurs with the former symptoms, and they generally soon succumb. Finally, in other cases there is no crisis, and in the second week, except for the intense icterus, we are reminded of severe and protracted cases of other forms of typhus. According to Griesinger’s description, this period of the disease is characterized by more or less profound sopor, delirium, great sensitiveness of the abdomen, involuntary pas- sages of dark, thin feces, or markedly dysenteric dejections, or occa- sional large evacuations of clotted blood, difficulty of swallowing, croupous coating on the pharynx, bronchitis, extensive lobular pneu- monia, occasional pericarditis, petechia and miliaria of the skin, and irregular chills. It almost always terminates with slight convulsions, sometimes by sudden collapse, internal haemorrhages (rupture of the spleen), or secondary disease of the thoracic organs. Rarely, the patient recovers either with a rapid change, or slowly and irregularly —the latter is especially the case if there has been extensive disease of the thoracic or abdominal organs, such as pneumonic infiltration or dysentery. Treatment.—The prophylactic rules for preventing the spread of or protecting one’s self against relapsing fever appear at once from what we have said of its etiology. Improvement of the condition of poor people, care for healthy nourishment, and roomy dwellings, ne- cessary as they are for prophylaxis, will probably never be fully car- ried out, as it is so much easier to separate the healthy from the sick, as is required by the contagiousness of the malady. The slight mortality contraindicates an energetic treatment of the disease. Thus far attempts to cut short the process and prevent relapses by quinine have failed. In the same way digitalis did no especial good in the Berlin epidemic. By cold baths, in recurrent fever also, we may almost always lower the temperature from one to five degrees; but this usually continues only a short time, the bodily temperature soon rising again to its 664 ACUTE INFECTIOUS DISEASES. previous height or even higher (Obermejer). I have repeatedly said that I consider energetic abstraction of heat by cold baths quite a he- roic remedy. If the high temperature in recurrens were accompanied by great danger to life, of course we should have no hesitation in com- bating the exhaustion of the body, from the increased production of heat, by the energetic and continued use of cold baths; but, since, in spite of the high temperature, relapsing fever has a low mortality, scacely three per cent, of the patients dying, I do not consider cold baths indicated in this disease. It will be well to limit ourselves to sponging the body with cold lotions, and, if the cerebral symptoms be severe, to the application of ice to the head. At the same time we should attend most carefully to the patient’s cleanliness and supply of fresh air, and internally give dilute mineral acids. Obermejer recom- mends the administration of lemon-juice when the kidneys are much affected. We should carefully give the patients nourishment early, and, if there be much debility, prescribe some wine. From the ten- dency to diarrhoea, they should not drink much water. During con- valescence, iron and quinine may be given. Griesinger recommends large doses of quinine (gr. x-xxx daily) in bilious typhoid. He says it is just as useful here as in intermittent fever ; but it is well not to begin the quinine treatment till after the administration of a mild purgative of salts, oil, or cream of tartar, at the commencement of the disease. CHAPTER X. EPIDEMIC DIPHTHERITIS MALIGNANT PHARYNGITIS—ANGINA MALIGNA DIPHTHERIA. Etiology.—Epidemic diphtheritis belongs among the infectious diseases, and even among those that are most typically contagious. The miasmatic origin of the disease is doubtful, at least in our coun- try, where it has only occurred during the past ten years, and has ap- peared almost exclusively as more or less extensive epidemics which occasionally spread around from one place to another. The contagion is contained in the false membrane and shreds of tissue detached from the fauces, and in the air breathed out by the patient. Physicians are in great danger of being infected by the morbid products coughed out by the patient when they are painting or cauterizing his throat, or per- forming a tracheotomy. Science has to mourn the loss of a series of excellent physicians and observers who fell victims to diphtheria while DIPHTHERIA. 665 in the line of their duty. The numerous cases of infection of persons who have been in the same room with diphtheritic patients, without coming in their immediate vicinity, prove that the air exhaled by the patient, which does not contain shreds of exudation or tissue, is a ve- hicle for the contagion, Further observation must decide, if, besides the above vehicles for the poison, there be still others; how tenacious the infection is; whether persons who do not themselves take the dis- ease may carry it to third parties, etc. The predisposition to diphthe- ria is unmistakably very extensive. The greater frequency of the dis- ease among children than adults does not seem to me due to greater predisposition of the former, but to their being more exposed to infec- tion than adults are. Anatomical Appearances.—Just as in other infectious diseases, in diphtheritis also certain organs are chiefly subjected to the disturb- ances of nutrition, and (to employ our former mode of expression) diphtheritis is constantly localized in the fauces, less constantly in the upper portion of the air-passages, in the kidneys, spleen, and in some very obscure manner in the nervous system. The disturbances of nu- trition in the above organs do not anatomically correspond. In the pharynx we find the form of diphtheritic inflammation to which the disease owes its name, and which we have often described. The fauces, and especially the tonsils and soft palate, are covered with grayish-white pseudomembrane, which is not easily removed, and which leaves an ulcerated loss of substance, when it finally breaks down into a discolored fetid mass, and falls off. The diphtheritic pseudomembranes, or, to speak more precisely, the diphtheritic sloughs, result from superficial gangrene of the mucous membrane, which again depends on compression of its nutrient vessels by an interstitial fibrin- ous exudation, or from swelling of the tissue-elements, which are filled with a cloudy substance. If the larynx and trachea participate in the disease, the croupous, not the diphtheritic, form of inflammation of the mucous membrane occurs; that is, the surface of the mucous membrane is covered with a more or less tough and consistent false membrane, which may readily be removed, and leaves no loss of substance after its removal. This circumstance has induced some physicians to iden- tify primary genuine croup, which is due to catching cold, etc., with croupous laryngitis caused by infection with diphtheritic contagion. I consider this a false view. The division of diseases, according to the pathologico-anatomical changes they induce, is only a make-shift. In all cases where, as in genuine and diphtheritic croup, we find that two anatomically similar disturbances of nutrition depend on very different causes, we should consider them as distinct. A small-pox pustule may very much resemble one induced by rubbing antimonial ointment 666 ACUTE INFECTIOUS DISEASES. into the skin; a pemphigus bleb may resemble a blister induced by a circumscribed burn, but no one would assert that these scarcely-dis- tinguishable disturbances of nutrition were due to the same disease. The previously-described parenchymatous degeneration of the kidneys is found in about half of the cases. The spleen is usually enlarged and soft. The anatomical changes of the nerve centres, or peripheral nerves, on which diphtheritic paralyses depend, have not yet been dis- covered. We know as little about the anomalies of the blood in diph- tlieritis as in other infectious diseases. Symptoms and Course.—The disease almost always begins with apparently insignificant and harmless symptoms. In some cases the general health is disturbed a few days before the disease breaks out; the appetite is less; the patients complain of dulness, depression, and chilliness. More rarely the disease begins with a severe chill, ac- companied by nausea and vomiting. At the same time the patient complains of difficulty of swallowing; but in most cases this is no greater than it usually is, in simple catarrhal angina. If the fauces be not yet covered with false membrane, but only somewhat reddened and swollen, at this stage we can only suspect or recognize the disease, when we know that diphtheritis is epidemic, or that persons about the patient have or have had the disease. A very suspicious, and usually a very early, symptom is a hard swelling of the lymphatic glands lying at the bifurcation of the carotid artery, which, as Luschka especially insists on, are directly connected with the lymphatic vessels of the soft palate. Not unfrequently the persons about the patient have their attention first called to the disease by swelling of these glands, the complaints of slight difficulty of swallowing having passed unnoticed. It is far more common for us to find more or less extensive grayish- white patches in the fauces at our first examination, than to have the opportunity of examining the throat at the commencement of diphthe- ritis, before the formation of false membranes has begun. And then we can have no doubt about the dangerous and malicious foe with which we have to deal. Even in cases where the disease has begun without a chill, where the fever is slight, or entirely absent, where the general health is excellent, so that the patient can hardly be kept in bed, even where the difficulty of swallowing is very insignificant, and where the deposits are very slight, are thrown off without putrescence, and leave a scarcelv-perceptible loss of substance, we are not at all sure that the disease will run a favorable course, that the dangerous accidents, of which we shall hereafter speak, will not occur, and that there will be no paralysis during convalescence. The fact, which I have fre- quently observed, that albuminuria occurs during the above cases, which run their course without fever, shows that the parenchvmatous DIPHTHERIA. 667 degeneration of the kidneys in diphtheritis is not due to excessive in crease of the bodily temperature, but is a direct result of the infection with diphtheritic poison. If the disease has begun violently, if a chill and repeated vomit- ing have been the first symptoms, the subsequent course of the dis- ease also is usually more severe. It is true, the difficulty of swallow tr- ing generally remains moderate, and the fever does not become very high, but the patient grows pale, the eyes become dull, the pulse small, and usually frequent, rarely retarded; the patients are very sluggish and apathetic. In many cases the putrefaction of the false membrane causes a penetrating, foul breath. If the nasal mucous membrane participate in the disease, a discolored, fetid fluid flows from the reddened and eroded nostrils. The swelling of the cervical glands becomes more marked; the enlarged glands are very hard and resistant, but have no tendency to suppurate. In about half the cases, examination of the urine shows the presence of a considerable amount of albumen. Even, after a few days, death may occur from general paralysis, while the intellect remains clear. Some patients, whose state had not excited any anxiety, and whose general condition was previously very satisfactory even, die unexpectedly with the symptoms of general collapse, without our being able to find any explanation for the occurrence. Sometimes also attacks of deep syncope occur, and pass over, till finally a new attack ends in death. Even the last- mentioned severe cases may terminate favorably. Then the false membranes are detached, and no new ones are formed; the remaining ulcers clean up and cicatrize. At the same time the difficulty of swallowing disappears, the glandular enlargement subsides, the de- pression of the patient disappears, and, if there be no sequelae, perfect convalescence follows in two or three weeks; but it is usually a long time before the patients recover entirely. The disease, as above described, is greatly modified when the diphtheritic inflammation of the fauces is accompanied by croupous in- flammation of the larynx and trachea; for then the above symptoms are complicated with hoarseness, aphonia, excessive dyspnoea, and other symptoms described when speaking of genuine croupous laryn- gitis. This complication occurs in the mild, as well as in the severe cases. Frequently, examination of the fauces and the epidemic occur- rence of diphtheria alone enable us to decide to which form of croup- ous laryngitis the case belongs. Even such cases may end in re- covery ; but most of the patients die, some with the symptoms of col- lapse, some with those of insufficient respiration, and poisoning of the Dlood with carbonic acid. Even when the disease apparently ends in recovery, it is often fol 668 ACUTE INFECTIOUS DISEASES. lowed by paralysis. The not unfrequent occurrence of diphtheritic paralyses after very mild cases, as well as the curious fact that they never follow the disease immediately, but come on from two to four weeks after its disappearance, sufficiently explains why the connection between the paralyses and the diphtheritis so long escaped recogni- tion. Paralysis of the soft palate and pharynx is the most frequent form of diphtheritic paralysis, and generally precedes the other forms; when the soft palate is paralyzed, the patients have a nasal voice; on at- tempting to swallow fluids, they enter the nose. If the pharynx also be palsied, the act of swallowing is greatly impaired, and we are some- times obliged to nourish the patient through a stomach-tube. This paralysis of the muscles near the seat of diphtheritic inflammation is most frequently accompanied by that of the muscles of the eye, by which the power of accommodation is lost, and the patients begin to squint. The extremities also, especially the feet, are occasionally at- tacked by more or less complete paralysis. In a very small epidemic I saw two cases of total paralysis of all the extremities. The progno- sis of diphtheritic paralysis is generally favorable; almost all cases re- cover sooner or later. The various attempted explanations of these cases are unsatisfactory. We do not even certainly know whether they are of peripheral or central origin. It has been suggested that the paralyses after diphtheria are analogous to those occasionally ob- served after other severe diseases, especially after severe typhus. But this suggestion is opposed by the great frequency of diphtheritic paral- ysis compared to that after other diseases, as well as by the marked disproportion between the intensity of the malady and the consequent paralyses, distinguishing diphtheritic paralyses from those remaining after other diseases. Treatment.—Prophylaxis requires that the physician should pro- tect himself from contact with the false membrane and shreds of tissue that are coughed up, and that he should warn the attendants on the patient of the danger of this contact. When circumstances permit, those who have nothing to do with the care of the patient should keep out of the sick-room. The recommendations of the varied internal and external remedies that are said to have proved efficacious against diphtheritis, have usu- ally originated in the last stages of epidemics, at which time the cases are usually milder, and recoveries more frequent, even without treai ment. Almost all physicians, experienced in the treatment of diph theria, agree that, in severe attacks, the most prized remedies are per fectly useless. In recent cases I deem it advisable to remove the false membrane carefully, and touch the dried bases with nitrate of silver, concentrated muriatic acid, or liquor ferri sesquichlorat., but not to re- DIPHTHERIA. 669 peat this operation more than once or twice daily, and not to continue t too long. Besides this, as long as the mucous membrane is still very red and swollen, I let the patient swallow small pieces of ice slowly, and prescribe a solution of chlorate of potash ( 3 i to § vi), with directions to take a tablespoonful in the mouth every two hours, and to keep it in contact with the pharyngeal tissues for some time before swallowing it. I have no personal experience about the local application of chlorine-water, or the solutions of sulphite of soda ( 3 i to the | j), or of permanganate of potash, which are said not only to remove the fetid odor, but also to arrest the putrefaction. On account of the threatening collapse, we must avoid all debilitating treatment, especially abstraction of blood; on the contrary, we should, from the first, attend to keeping up the strength of the patient by tonics, quinine, and iron, and by wine and nutritious diet. If collapse occur, we should give analeptics, camphor, musk, and particularly plenty of strong wine. Croupous laryngitis coming on during the disease requires about the same treatment that we advised in the first volume for idiopathic croupous laryngitis; only I do not employ ab- straction of blood or calomel even in recent cases. Tracheotomy should not be deferred too long, if we hope to have it succeed, which it rarely does. Short, cold ablutions, cold douches, and sea-bathing, have obtained the most confidence in diphtheritic paralysis. The induced and con- stant currents have also been advised. I have subjected many cases to long-continued treatment by electricity without benefit. In one case, where the patient was paralyzed in all her extremities, and was treated at my clinic by electricity, without benefit, for four weeks, she completely recovered, without any treatment, a short time after be- ing dismissed from the hospital.4 [Diphtheria so often occurs without our being able to detect the source of contagion, that we may very strongly suspect its occa- sional spontaneous origin. Some authors regard general blood-infection as the first step, and say the throat-affection is only a local expression of this, as the bronchitis is of measles or pharyngitis of scarlatina ; while others say the affection is at first local, and may remain so or may become a general disease. Numerous vegetable organisms (micro- cocci) have been found in the diphtheritic membranes and even in the blood of the patients. The transmissibility of diphtheria to the lower animals by inoculating in the muscles, trachea, cornea, etc., has been proved, and the excessive multiplication of bacteria at these points has indicated them as the bearers of the contagion. In favor of the first view is the fact that at the commencement of 670 ACUTE INFECTIOUS DISEASES. the disease there may be high fever, but no change perceptible at the point where the diphtheritis subsequently appears ; also that in scarlatina, which is a primary blood-disease, diphtheria often occurs. The claims for the local origin of the disease are supported by the results of inoculation, which tend to show that the disease starts from the point of inoculation and spreads through the body. It has been asserted that these experiments prove nothing certainly, and that inoculation of other decomposing substances may induce the same changes as the diphtheritic membrane causes. If the diph- theritic poison entered the lungs and was thence transferred to the blood in some cases, and located and was propagated in the pharynx in others, it would perhaps explain both classes of cases. Some English observers consider it as established that milk is frequently an infectious agent; whether the poison is generated in the cow itself, or whether the milk is merely a carrier of germs taken in the cow’s food, is not decided. Persons in the vicinity of a diphtheria patient may have a catar- rhal angina due to the poison. A second form is croupous diph- theritis, with a membrane which may be readily detached from the subjacent mucous membrane. The third and severest form is where the fibrinous deposit is both on and in the membrane ; between the fibres are pus- and blood-cells, micrococci, etc. ; the mucous mem- brane is quickly destroyed, leaving gray or brown sloughs, which render the breath very foul; this slough may extend to the sub- jacent cartilage or bone. Deeper in the air-passages, diphtheria is croupous in nature ; the ulceration of the mucous membrane does not usually extend below' the larynx, that is, where pavement changes to cylindrical epithelium. In persons who have died of diphtheria, the blood is generally imperfectly coagulated, dark, and tar-like. Changes in the kidneys are very common. The latent stage of diphtheria is usually short, though cases occur w'here it is possibly of some weeks’ duration. The catarrhal form has the same symptoms as ordinary angina, and it may be only the surrounding circumstances that would lead us to suspect diph- theria ; it may run its course in this way, or become a severe dis- ease. Croupous diphtheria is usually accompanied by high fever; there may be burning in the throat or pain on swallowing ; if these symptoms be absent, the disease may for some time escape recogni- tion. Inspection shows the mucous membrane to be dark red and swollen, with deposits of false membrane, which develop rapidly, and may even cover the whole pharynx and extend into the nares or middle ear, but especially into the larynx, or else may remain confined to the pharynx. The latter cases are apt to terminate INTERMITTENT FEVER. 671 favorably, the false membranes being detached and the fever sub- siding in a few days. Such cases are common in youths and adults, but advance of the disease to the larynx is more to be dreaded in infants. As the first deposits clear off, others may take their place. In septic or putrid diphtheria there is infiltration and mortifica- tion of the mucous membrane itself, with consequent ulcers and gangrenous loss of tissue. The detached fragments putrefy and give a foul odor to the breath ; the submaxillary and lymphatic glands are swollen ; there is fever characteristic of septicaemia ; and usually the patient dies in a few days. But a line of demarcation may form around the necrosed parts, and recovery take place. If the disease attacks the nose, it causes a running, which may be mistaken for cold in the head till the discharge becomes bloody or sanious. Diphtheritic paralysis may not occur till four or five weeks after the disease ; it is peripheral in character, as is shown by the diminu- tion of electro-muscular excitability ; it lasts several weeks or even months ; it most frequently affects the muscles of the pharynx and eye ; the prognosis is usually favorable. In the treatment, various disinfectants, such as chlorine one part to six of water, weak solutions of carbolic acid, salicylic acid, per- manganate of potash, also alcohol, etc., may be employed locally in conjunction with hot vapors, wdiich hasten suppuration, and possibly the pus may wash off the micrococci; these hot vapors may be tried every half hour or so. We should avoid rough or frequent cauter- izations, for fear of increasing the inflammation. In diphtheria of the larynx we may use sprays of lime-water and salicylic acid. Tracheotomy has rarely proved a successful operation in this dis- ease. Internal administration of chlorate of potash and tincture of muriate of iron, properly diluted, and in doses suited to the age, every half hour to two hours, is perhaps one of the most favorite methods of treatment.] MALARIAL FEVERS. CHAPTER XT. INTERMITTENT FEVER. Etiology.—Intermittent fever results from infection of the body with a poisonous substance called marsh miasm, or malaria. Malaria is not a product of decomposition (see below), but the decomposition of vegetable substance has an unmistakable influence on the devel- opment or excessive increase of this poison. I shall only adduce the following circumstances in support of this fact: Malarial fevers are 672 ACUTE INFECTIOUS DISEASES. endemic chiefly in marshy regions, and in such places the number of persons affected increases or decreases according as circumstances favor or do not favor the decomposition of dead vegetable matter in the marshes. If it grow very cold, so that the marshes freeze up, the in- termittent fever ceases. The same thing occurs when, in dry seasons, the marshes entirely dry up, or if, in very wet seasons, a thick layer of water protects the mouldering bottom of the marsh from the action of the sun and air. On the other hand, in marshy regions, hot seasons, if not too dry, so that the sun’s rays can act freely on the exposed but still moist bottom of the marsh, are characterized by the great preva- lence of intermittent fever. It is uncertain whether the decomposi- tion of certain vegetables, or a peculiar quality of the water, favors the development of malaria more than other causes. A mixture of sea- water with spring and rain water—which occurs in marshes near the ocean, from high tides or heavy winds forcing the sea-water into the marshes—so-called brackish water, appears to be peculiarly injurious, because many fresh-water plants, as well as many marine plants, con- tained in the mixture, cannot thrive in it, and consequently die and decompose. Malarial fever is endemic in low lands near rivers, which are flooded yearly, just as in marshy regions. No especial explanation is necessary to show that this flooding also causes the death of quantities of vegetable matter, which subsequently decomposes when exposed to great heat. Intermittent fever occurs where land has lain for a long time uncultivated, and is then broken and tilled again, from the same causes as it does in marshy regions; for here, too, quantities of dead vege- table matter are brought up and undergo decomposition. Lastly, in some cases where intermittent fever occurs under apparently opposite circumstances, that is, when it is very dry, it has been shown that the soil was rich in subsoil water, and that, under a dry, porous sur- face, parched by the summer heat, there were subterraneous swamps. These common peculiarities, which appear in most of the regions where malarial fever prevails, do not, however, as was before said, justify us in concluding that malaria is a chemical body, an organic or inorganic, a solid or gaseous product, formed by the decomposition of vegetable substances. On the contrary, the non-occurrence of intermittent fever, in some typically swampy places, and its appearance in some places where extensive or specific putrefaction would be most unlikely to take place, seem to indicate that while the conditions peculiar to swamps, marshes, etc., favor the development of malaria, they are not a sine qua non, nor do they alone suffice to induce the disease. This view is even more strikingly supported by the observations that all the persons drinking water from a certain swamp were taken sick with intermittent fever, as these observations contrast with a large number INTERMITTENT FEVER. 673 of others, where the water of other marshes was drunk without this effect. If the morbific power were simply the product of chemical de- composition, this exclusiveness would be entirely inexplicable. I have no hesitation in saying decidedly that marsli miasm—malaria—must consist of low vegetable organisms, whose development is chiefly due to the putrefaction of vegetable substances. It is true these low organisms have not actually been observed. No one has seen “ mala- ria spores,” but the facts above mentioned, as well as many other causes, urge us to believe that the poison exhaled by marshes, as well as that given off by a patient with measles, is an organic living sub- stance. There is, however, an important difference between the mias- ma vivum, which is the specific cause of intermittent fever, and the jontagium vivum by which the acute exanthemata, exanthematic ty- phus, and other infectious diseases, spread. The latter reproduces itself in organisms infected with it; malaria, on the other hand, is not reproduced in the body, of a patient with intermittent fever. There is no soil in the human body favorable to its development or increase. Intermittent fever is never introduced into other places by patients w ho have caught it in a svrampy region. While a short residence in a malarious district is often enough to give intermittent fever, one may share the same v7ard with a large number of intermittent patients in a hospital, at some distance from such a place, without danger. Hence, in distinction to the “ contagious ” diseases, malarial fever is termed “ miasmatic contagious ” or “ purely miasmatic.” There are extensive sections of country where the circumstances for the formation of malaria exist everywhere, in all parts of which in- termittent fever occurs; but there are also small circumscribed mala- rial foci, where numerous cases of intermittent are seen every spring and summer, wdiile the whole surrounding country remains free. In these last-mentioned circumscribed malarial foci, in towns lying near marshes, in certain sections or streets of cities, where intermittent fever is endemic, some very interesting observations have been made about the extension of malaria: among other things, it has been shown that, from its point of origin, miasm spreads more readily in a horizontal than in a vertical direction, it is often arrested by insignificant obsta cles, such as groves, stone walls, etc., and rarely passes the boundaries thus formed, unless the wind be in a particular direction. The extensive epidemics of intermittent fever which occasionally appear are very remarkable. During such epidemics, while the cases are unusually frequent in places where the disease is endemic, they also occur in places where either no cases or only sporadic ones had been seen for years. These epidemics do not always come in very hot, moist seasons, so that they might be referred to the circumstances 674 ACUTE INFECTIOUS DISEASES. being very favorable to decomposition of vegetable substances, and hence uncommonly favorable for the development of malaria, and for its spread from places where it always exists to others that are gen- erally free from it; but they appear to be due to other unknown causes, which also favor the development of malaria, or to an extension of the disease from its point of origin to distant places by currents of air. We do not know why, but great epidemics of intermittent have often preceded epidemics of Asiatic cholera. In hot countries, cholera and intermittent, and, still oftener, dysentery and intermittent (see next chapter) frequently prevail at the same time. The sporadic occurrence of intermittent is most curious. Those cases where persons affected with malaria move from places where ma- laria is prevalent, and continue to present the symptoms of infection for a time after settling in their new home, are not to be counted as sporadic. But, both in city and country, cases occur where the persons could not have been infected elsewhere. There is no explanation for these cases, except the supposition of very limited foci, which are harmless for persons outside of them, or of a very diluted miasm, which only affects a few persons who are peculiarly disposed. There is not the least ground for the supposition that, under some circumstances, intermittent may result from other causes than from infection with malaria. Every age, both sexes, and all constitutions, have a predisposition to intermittent fever, and the greater or less tendency to the disease, in various persons, does not depend on the constitutional differences to which it has been referred, but to other only partially understood in- dividual peculiarities. Exhausting exercises, and other debilitating influences, errors of diet, and particularly catching cold, increase the predisposition so much, that persons, who have long been exposed to malaria with impunity, are not affected by it till one of these causes has acted on them. The same explanation must answer for those cases where persons who have escaped the disease in malarious places are attacked by it after leaving them. Then the infection has evi dently taken place earlier, but has not shown its effects in the person who was little disposed to the disease, and has not caused injurious results till the necessary predisposition was induced by other noxious agents. Among the influences that increase the predisposition to intermittent, the most evident is one or more previous attacks of the disease, which is just the opposite of the case in the acute exanthe- mata and typhus. There is only an accommodation of the organism to the poison to the extent that persons who have been exposed tc it for some time have a chronic disease with enlargement of the spleen, without fever, instead of having intermittent fever. The INTERMITTENT PETER. 675 geographical extension of intermittent fever is immense; in the torrid zones the disease is especially frequent, and it prevails in most places that are not very dry: in the temperate zones it chiefly affects certain more or less extensive districts; in the frigid zones it does not occur. For further information, we refer to Griesinger’s work and to the very exhaustive treatise of Hirsch on the geography of intermittent fever. Anatomical Appearances.—Autopsies of persons who have died of simple intermittent fever are rare. They show no characteristic changes beyond those that we have already described (Vol. I., Dis- eases of the Spleen). If simple intermittent fever depends on infection with malaria, the anomalies of the blood dependent on the infection have so far escaped chemical and microscopical examination. The im- poverishment of the blood in red corpuscles and albumen, which always results from long-continued intermittent, depends on consumption from high fever, and perhaps also on degeneration of the spleen. On autopsy of persons who have died of pernicious intermittent, we often find signs of melanremia and occasionally remains of inflammation, effusions of blood, or excessive hypereemia in different organs. Symptoms and Course.—I. Simple Intermittent Fever.—The pe- riod of incubation of the malarial infection is not exactly known. It is probable that, at most, two weeks may pass from exposure to the miasm till the first symptoms appear; in some cases the latter seem to follow the former immediately. Before the intermittent character of the disease, to which it owes its name, becomes very evident, before attacks of fever (paroxysms) and intervals of exemption from fever (apyrexias) alternate, the infec- tion with malarial poison not unfrequently evinces itself by a con- tinued, only more or less remitting and exacerbating, disturbance of the general health and various functions. This constitutional disturb- ance, which is called the prodromal stage of intermittent, has no char- acteristic peculiarities, and can only be rightly interpreted and distin- guished from the prodromal stage of other infectious diseases by bear- ing in mind the endemic and epidemic circumstances. After the pro- dromal symptoms have lasted several days, or in other cases without their appearance, the first fever paroxysm occurs. A paroxysm of intermittent fever consists of three stages: chill, fever, and sweating. The chill begins with a fit of weakness, and great faintness; the patients gape, and stretch their limbs. These symptoms are soon accompanied by a subjective sensation of cold, at first consisting of cold sbiverings over the skin; afterward, of continued chilliness, so that the patient wants to wrap up as warmly as possible. When the chill increases, the limbs tremble involuntarily, the lips quiver, the teeth chatter, and the whole body is often shaken around 676 ACUTE INFECTIOUS DISEASES. ill bed. When the chill begins, there is also more or less headache, oppression of the chest, and hurried respiration; the latter, and the quivering of the lips, render speech indistinct and interrupted; there is often vomiting also, especially if the chill comes soon after eating. Objective examination first shows the altered appearance of the pa- tient ; he looks like a person exposed to severe cold, without sufficient clothing, and who is consequently thoroughly chilled. The size of the body appears diminished; the face is sunken; the nose pointed, the rings are too large for the fingers. As the flow of arterial blood to the skin is impeded, the latter appears pale, and, as the blood collects in the veins and capillaries, the lips, ends of the fingers and toes, look blue. The flow of blood to the fingers is often entirely arrested; they look waxy, have no feeling, and do not bleed if wounded. The skin of the extremities and body has the appearance known as goose-flesh (cutis anserina). The pulse is very frequent, small, and hard; the se- cretion of urine is usually increased; the urine passed is limpid, and of low specific gravity. Physical examination generally shows en- largement of the spleen. While the diminished supply of warm blood during the chill causes the periphery of the body to assume more and more the temperature of the surrounding atmosphere, and to actually sink several degrees, the temperature of the blood and internal organs rises rapidly. This rise, which begins even before the chill, reaches two or three degrees, and, in severe cases, still more. The above symptoms are mostly to be ascribed to spasmodic contraction of the muscles of the skin and peripheral arteries during the cold stage. The immediate results of this spasm are the goose-flesh, the small, hard pulse, and the deadness of the fingers. The contraction of the muscles of the skin and peripheral blood-vessels secondarily in- duces the apparent diminution in size, the dryness and pallid ap- pearance of the skin, the collection of blood in the veins, and the fall of temperature on the surface of the body. The chilly feeling of the patient is too decided to be referred exclusively to the fall of temperature of the periphery; on the other hand, the contin- ued coolness of the surface, even under thick feather-beds (which is peculiarly remarkable, because the body gives off but little heat to the parts around), is certainly due to the fact that, during the chill, there is less warmth supplied to the surface, on account of the diminished supply of blood. Lastly, the disturbance of the peripheral circulation increases the lateral pressure in the vessels of the internal organs. But, as we do not know whether the spasm of the muscles of the vessels is limited to the peripheral arteries, and does not extend tc the internal ones, it is doubtful whether the headache, oppression, ao celerated respiration, vomiting, increased secretion of urine, swelling of INTERMITTENT FEVER. 677 the spleen, etc., can be referred to collateral fluxion to tlie organs impli- cated in these symptoms. At all events, as we have before said, col- lateral fluxion to the spleen is not the sole cause of enlargement of that organ. The cold stage lasts from half an hour to three hours; in the first paroxysms, it is usually shorter and less severe than subse- quently ; and its intensity and duration generally decrease again if the disease last a long time. The hot stage does not begin suddenly, but gradually; at first the chill is only interrupted by temporary flashes of heat, and a permanent feeling of warmth only comes on by de- grees. The headache becomes more severe; the patients grow rest- less, and not unfrequently slightly delirious or somewhat stupid; the feeling of oppression on the chest increases, while the breathing almost always becomes deeper, freer, and slower. Thirst is greatly increased. The appearance of the patient changes. The size of the body ap- parently increases, the color returns to the skin, the pale, livid look, the goose-flesh, the cyanotic hue of the lips and ends of the fingers disappear; the face becomes flushed, and herpetic vesicles often come out on the lips; the previously small pulse grows full and strong, the carotids throb, the urine becomes more saturated, and the enlarge- ment of the spleen increases. In the hot stage, the bodily temperature is increased at the periphery also; at the commencement of this stage, the temperature of the blood reaches its highest point, and remains there till toward its termination, when it gradually begins to fall. All these symptoms show that the spasm in the muscles of the skin and vessels has disappeared and given place to a subparalytic state. The relaxation of the cutaneous tissue and of the walls of the vessels suf- ficiently explains the increased entrance of blood into the previously bloodless tissues, and their consequently increased color and warmth. The severe headache, the oppression of the chest, which are often accompanied by catarrhal symptoms, and finally the continued enlarge- ment of the spleen, render it very probable that the arteries of the brain, bronchi, and spleen, are in the same condition as those of the periphery. The duration of the hot stage varies; sometimes it is only a few hours, in severe cases the dry heat continues six, eight, or even twelve hours before a pleasant perspiration breaks out on the skin. The sweating stage begins with moisture in the armpits and on the fore- head ; but soon the perspiration, at first moderate, but later very copi- ous, extends all over the body. The patients feel greatly relieved, the headache remits and gradually disappears, the mind becomes clear, the oppression passes off, the depth and frequence of the respiration be- come normal, the thirst is less annoying, the pulse is full, soft, and less frequent. The dark urine generally deposits rich sediments of urates; this depends on the great concentration resulting from the loss 678 ACUTE INFECTIOUS DISEASES. of water bj evaporation and sweating; it does not occur ii the patients replace the loss of water by drinking freely. During the sweating stage, the bodily temperature gradually falls, and toward its end be- comes nearly normal. When the paroxysm is over, and the apyrexia begins, most patients fall into a deep sleep, from which they awake much fatigued and dull, it is true, but feeling relatively wrell. When all the stages of the paroxysm are well marked, the disease is called an intermittens completa; if one or other stage fails or is indistinct, it is called incompleta. In rare cases, the stages of the fever are said not to follow the regular order; for instance, the cold stage closes the paroxysm instead of opening it (typus inversus). After the first paroxysms of intermittent, the apyrexia is rarely “ pure.” The patients have no fever, it is true; in some cases the temperature is even low and the pulse slow; but the appetite is often poor; the tongue coated, digestion disturbed; the patients are sensitive to changes of temperature, and complain of an indefinite feel- ing of illness. After a few paroxysms the disturbances usually sub- side, and during the apyrexia the only symptoms we notice are steadily-increasing debility and more evident impoverishment of the blood. If intermittent fever is very protracted, the apyrexias often become impure again, and the intermittent type approaches the remit- tent (febris intermittens subcontinua). According to the rhythm in which the paroxysms follow each other, we distinguish intermittens quotidiana, tertiana, and quartana. In the quotidian, the paroxysms recur in nearly or exactly twenty-four hours ; in the tertian, in twice twenty-four hours; in the quartan, in three times twenty-four hours after the commencement of the last one. It is less certain if there be also a five, six, or seven day rhythm, or if the intervals be even longer. The most frequent varieties are the tertian and quotidian. If the paroxysms recur at an earlier hour than it did the last fever-day, the disease is called anticipating, in the oppo- site case it is called retarding. By continued anticipation or retarda- tion, the rhythm of the fever may change, and a tertian may become a quotidian, or the reverse. If a paroxysm last almost till the com- mencement of the next one, we have a febris intermittens subintrans. When the apyrexia of a quotidian, tertian, or quartan intermittent is interrupted by a weak, short paroxysm, -which often occurs at a differ- ent time of day, it is called febris intermittens duplicata. In quo- tidiana duplicata there are two attacks each day, one severe, the other mild; in tertiana duplicata there is one attack each day, but one day it is mild, the next weak, etc.; in quartan duplicata, parox- ysms occur on two successive days, while the third day remains free. Intermittent fever never begins double ; this rhythm usually develops INTERMITTENT FEYER. 679 after the disease has lasted a long time, or particularly after numerous relapses. The course of intermittent is so often modified by the administra- tion of medicines, especially of quinine, that few physicians have actually observed a case left to itself, or, as is generally said, the nor- mal course of an intermittent. On this point also we are indebted to the homoeopaths for some important information. In the first place, there is no doubt that the peculiar fever paroxysms and apyrexias, which characterize infection with malaria, almost always continue for a time, even if the patient be removed from further action of the poison. Among other cases, I know of a young sailor who suffered from intermittent fever in Greifswald, and who had a relapse while at sea, four weeks after his last attack. It is also certain that, when a long time has passed since the action of the poison, the symptoms of malarial poisoning almost always disappear without medical aid. To avoid illusion, we must bear in mind that it is not only those who fly from the malarious region after acquiring intermittent fever, but also those who remain in the place till the malaria has disappeared, that finally escape the action of the poison. At a time when no new cases are observed in a place which has been visited by intermittent, it would be foolish to regard the final cure of a case, which had previous- ly been treated ineffectually, as a proof of the peculiar efficacy of the remedy last used. As the prevalence of the malaria among us only lasts a few months, the number of spontaneous cures is certainly much greater than is usually supposed. Another question is, whether, from continued action of the poison, the organism becomes so blunted to its injurious influence, that the symptoms of intoxication cease. At all events, such cases are rare, and it is more frequent to find those where continued action of the malaria has only modified the symptoms of intoxication, so as to change a pure intermittent into an intermittens subcontinua, or chronic malarial illness without fever. As was stated, when speak- ing of the individual paroxysms and apyrexias, after a prodromal stage but little characteristic, most cases of intermittent begin as tertian or quartan fevers, the apyrexias being at first imperfect, but becoming pure after a while. When the disease has lasted even a very short time, the patient appears very pale and cachectic, and this symptom is the earlier and the more marked, the greater the en- largement of the spleen. If the spleen remain small, from rigidity of its capsule, or from other unknown causes, the patient does not have this peculiar pale and sickly appearance until later. From this fact, which may be observed in most cases, as well as from the second fact, that the healthy color quickly returns when we can rapidly reduce the 680 ACUTE INFECTIOUS DISEASES. size of the spleen, we have concluded that the great pallor of the patients after the first attacks of intermittent does not solely, and, at all events, does not exclusively, depend on general impoverishment of the blood, but mostly on the lack of blood in the skin, which must be induced by its collection in the spleen. While Junod's boot is applied to one extremity, there is great hypersemia of that limb, and consequent anaemia of the rest of the body; if the boot be removed, the normal distribution of blood is soon reestablished. We do not, however, mean to say that the fever of intermittent differs from other fevers in regard to the consumption of the body; on the contrary, intermittent fever would be one of the most dangerous of diseases, if those inex- plicable pauses did not occur between the paroxysms, during which the consumption is interrupted, and the tissues of the body restored by plentiful supply of nourishment, more than in any other feverish disease. From the high temperature (106° Fahr. or more), reached in intermittent fever, the consumption of the body is very marked. This is evident, not only from the increased production of urea, but also from the emaciation and hydrasmia that occur in protracted cases. There is no doubt that the production of urea is only increased during the paroxysm, and not during the apyrexia; on the other hand, in two cases of quartan intermittent, I found that the excretion of urea was increased during the apyrexia also, or, in other words, that the in- creased amount of urea produced during the paroxysm was not all ex- creted till some time during the following apyrexia. If the paroxysms be not temporarily or permanently arrested by the administration of quinine, or if they do not soon cease spontaneously, the hydrsemia at length becomes so excessive, that in many cases more or less dropsy oc- curs, without the urine being diminished in quantity, or containing albu- men. This dropsy is analogous to those occurring during other exhaust- ing diseases, although it is probable that the organic and functional disturbances of the spleen accompanying protracted intermittent fever add to the degree of hydrsemia, and to the frequency of the dropsy. The longer the affection lasts, the more reason there is to fear the devel- opment of permanent organic change in the spleen, liver, or kidneys • this usually assumes the form of lardaceous degeneration, with coinci dent deposit of pigment, and leads to incurable disease. Continued intermittent fever often induces chronic parenchymatous nephritis also, and, in other cases, a haemorrhagic diathesis. These severe sequelae of simple intermittent fever are generally prevented by proper treat- ment ; and, even where intense malaria is endemic, under careful man- agement, excessive dropsy, fatty degeneration of the abdominal or- gans, and cachexia, rarely occur. It is true, neither quinine, nor any other known remedy is so certain an antidote for malarial poison as INTERMITTENT FEVER. 681 to cut short the entire disease; but, for the most important and dan- gerous symptom, the fever, quinine is almost infallible. After giving proper doses of quinine, the patient almost always escapes a series of paroxysms; and, as the cachexia and impoverishment of the blood, and, to some extent, the spleen-affection also, probably depend on the fever, the patients not only do not grow worse during the administra- tion of the quinine, but they improve and pick up even if the disease be not entirely extinct. Although, for the sake of brevity, we may designate as relapses the many cases where paroxysms recur shortly after stopping the quinine, strictly speaking, it is incorrect; for the cases where these so-called relapses occur, even after moving into a region free of malaria, prove that the disease was not cured, but only one of its symptoms removed. The homoeopaths assert that under their treatment there are no relapses : there is some truth in this as- sertion ; for, when the paroxysms have ceased under homoeopathic treatment, the disease is certainly all gone. The fact, that, after the administration of quinine in sufficient doses, relapse does not occur in many cases, rather favors the view that, besides its palliative action on the paroxysms, this medicine has also a favorable influence on the entire disease caused by the malarial infection ; but it is also possible that in such cases the palliative action continues till the disease passes off spontaneously. When the action of quinine is only palliative (as it is in the majority of cases), usually about seven, fourteen, or twenty- one paroxysms are missed, and the next one occurs in about two, three, or four weeks, rarely sooner. According to my own observation, the assertion, that the relapses almost regularly take place the fourteenth, twenty-first, or twenty-eighth day, is exaggerated; I have far more frequently seen relapses a few days before or after these dates. It is not at all rare for relapses to occur three or four times, or oftener, and for the disease to run on interruptedly for months, before actually ceasing. I deem it proper to speak of the modification of the course of intermittent fever by quinine under symptomatology, because, as we have already said, most physicians have no opportunity of ob- serving intermittent fever without this modification of its course. Much that is said in the text-books on medicine, about the course of intermittent fever, certainly does not refer to the disease when left to itself. II. Pernicious Intermittent Fever.—Intermittent fever may prove dangerous to children, to the aged, and to very debilitated or sickly persons, without being of unusual intensity or duration, or having any complications. Children inclined to convulsions not unfrequently have an epileptiform attack during the cold stage, as they also have in the initiative chill of inflammatory diseases. This is not usually danger- 682 ACUTE INFECTIOUS DISEASES. dus, but occasionally it passes into general paralysis, ending in death. In very old or broken-down persons, the danger from a simple par- oxysm lies chiefly in the threatened exhaustion of the still remaining strength. Such cases, which only take on an acute course from indi- vidual peculiarities of the patient, are not usually called pernicious. Some cases of intermittent acquire a pernicious character, from the usual symptoms becoming very intense, or being protracted a long time. In this class belong the cases where the liyperaemic swelling of the spleen is so great that its capsule is ruptured, or where the chill is so severe as to cause dangerous obstruction of the circulation, as well as those cases where the paroxysms do not cease in from six to ten hours, but continue for twenty-four hours, or longer, and leave the patient very much exhausted, or where only certain stages con- tinue beyond the usual time. It seems to me very probable that some forms of the so-called pernicious fever also should come under this head, as it is probable that they are not complicated, only that the customary symptoms are greatly increased. Even in simple normal intermittent there is an increase of the temperature, such as is ob- served in scarcely any other disease; and the short time that this increase lasts is the only reason that it does not prove dangerous to the patient. In all diseases where the bodily temperature becomes excessive, or remains high for a long while, we have the symptoms of great adynamia, and finally of paralysis of the heart, and these are the most prominent symptoms of pernicious fever. The deep stupor of patients with febris intermittens comatosa, as well as the delirium preceding the coma, reminds us strongly of the symptoms in severe typhus, malignant measles, and other infectious diseases accompanied by high fever. When these cases terminate fatally, we do not gen- erally find any anatomical changes in the brain. In febris algida the heart’s action grows feebler, the pulse smaller; the blood collects in the veins; there is cyanosis; the temperature of the periphery closelj approaches that of the surrounding air, because the loss of warmth due to the obstructed circulation is not replaced by a supply of warm blood; the patients grow cool; in short, we have the symptoms of acute paralysis of the heart, which may even result from the intensity of the fever without complications. There is no doubt that, in these severe forms of intermittent fever, there is often pigment in the blood; but the coincidence of melanaemia with severity of intermittent fever does not justify us in regarding the latter as a result of the former. On autopsy of several cases of intermittent fever that died with severe brain-symptoms, Frerichs found melanaemia, it is true, but he found no pigment in the capillaries of the brain; and I have observed simi lar cases. INTERMITTENT FEVER. 683 Under the head of congestive, pernicious intermittent, in the strict sense, we must class those cases where the malignant course of the disease is caused by hyper®mia, effusions of blood, inflammations, and, perhaps, also by obstructions of the circulation in different organs, in- duced by stoppage of the capillaries with pigment. Probably these disturbances of nutrition and circulation in the central organs of the nervous system are the origin of the maniacal, apoplectic, epileptiform, and tetanic convulsions, which occasionally complicate the paroxysms, and have led to the designations febris intermittens perniciosa, mani- acalis, apoplectica, epileptica, tetanica. A rather frequent but rarely dangerous complication of intermittent fever-is a severe bronchitis, which exacerbates with every paroxysm and remits with each apyrexia. Febres intermittentes comitat® pneumoniacac and pleuritic®, or cases of intermittent h®moptysis, are rare. In many cases of congestive in- termittent, there is jaundice. Copious watery transudations from the intestinal canal, violent vomiting, and profuse diarrhoea, may cause thickening of the blood, and give the paroxysm a great resemblance to the algid stage of cholera. In some cases there are also profuse inter- mittent intestinal h®morrhages. (Among fifty-one cases of pernicious intermittent, observed by Frerichs, there was profuse diarrhoea seven- teen times, profuse intestinal h®morrhage three times.) The serous transudations and h®morrhages into the intestinal canal may depend on acute congestion due to obstruction of the hepatic capillaries by pigment, but this has not been proved in all cases. Lastly, we have to mention the complications of intermittent with diseases of the kidneys. They evince themselves by albuminuria, h®maturia, and in severer cases by the suppression of urine. (In the fifty-one cases of Frerichs, albu- minuria was seen twenty times, suppression of urine five times.) Pernicious intermittent fever occurs chiefly in tropical-fever regions, it is true, but even with us, in places where intense malaria prevails, it is not rare, and individual cases are seen in every large epidemic of intermittent fever. The malignant character either appears at the Start, or does not manifest itself till the second or third paroxysm, or even later. After malignant congestive symptoms have appeared, the apyrexias are often so imperfect that the diagnosis is very difficult or even impossible. In the epidemics observed by Frerichs, most patients were sent into the hospital with the diagnosis of a typhus. III. Concealed Intermittent Fever.—While, as a rule, intermittent fever results from infection with malaria, we not unfrequently see ex- ceptional cases where, instead of fever-paroxysms, there is neuralgia, the attacks of neuralgia being separated by regular intermissions, cor- responding to the apyrexias of a simple intermittent. These deviations from the rule are inexplicable, it is true, but this is also true of regular 684 ACUTE INFECTIOUS DISEASES. simple intermittent fever, which we do not in the least understand. The intermittent neuralgias resulting from malaria, which chiefly bear the name of intermittentes larvatas, most frequently affect the supra- orbital, more rarely other branches of the trigeminus or other nerves. We may omit a description of the attacks, as they are about the same as those of neuralgic attacks from other causes. They are accompa- nied by a slight elevation of temperature, perceptible by the thermom- eter. In rare cases, other anomalies of excitement of the cerebro- spinal and vaso-motor nerves appear to result from malaria. Among these are intermittent anaesthesia, paralysis, spasms, psychical dis- turbances, and hyperaemia or oedema of different organs. Treatment.—Prophylaxis requires that the State should attempt to remove by sanitary laws (which do not come in our province) the injurious influences which notoriously favor the development of mala- ria ; that it should drain the marshes in whose vicinity intermittent fever is endemic, and should protect by dikes those lands that are overflowed yearly. Moreover, persons obliged to reside temporarily or permanently in malarial regions should observe certain rules, which afford more protection than any prophylactic medicines. ITauschJca, who has apparently had great experience, gives very precise and prac- tical rules for life in malarial regions. In his special pathology and therapeutics, he advises: 1, on going to a dangerous place, to assume at once the peculiar mode of life of the inhabitants; on the Weichsel to drink schnaps, in Banate slivovitz, in Hungary only to eat melons and pickles with plenty of pepper, in Italy to drink plenty of lemonade and black coffee, and avoid eating at night, also to drink water pre- pared as is customary at different places ; 2, to suit the clothing to the temperature of the time of day, especially to protect the person by warmer clothes against the cool evening air, and to keep the windows closed at night; 3, to seek a dwelling high and dry above the marshes, etc.; 4, to avoid getting wet through, errors of diet and other excesses, so as not to bring on any other disease by which the tendency to ma- laria will be increased; 5, to avoid certain things, such as the use of vegetables, milk, and bathing in rivers or the sea, especially after sun- down. Sleeping in the open air seems to be most dangerous. Treatment of the paroxysm may almost always be dispensed with, except as regards directing the regimen. As soon as the first symp- toms of chill are observed, the patient should go to bed; but we should warn the attendants against piling on too many bed-clothes, as they do not warm the skin, and only interfere still more with the cir- culation in the peripheral parts, and with the impeded respiration. If the chill be very severe, the skin may be rubbed with warm woollen cloths, and warm bottles placed in the bed. Hot drinks neither re- INTERMITTENT FEVER. 685 aeve tne feeling of chilliness nor increase the temperature in the pe- ripheral parts, which is diminished in spite of the increased temperature of the blood; but we may yield to the generally urgent entreaties of the patient for warm drink, so far as to allow him a few cups of tea, if we are certain that he will be moderate. If there be severe vomiting during the cold stage, w'e may give effervescing powder, and, if this fail, a few drops of laudanum. If the patient become so collapsed as to alarm us, we may give analeptics, strong coffee, wine, camphor, ether, and opium, have the patient rubbed, and apply sinapisms. In the hot stage we may try cooling treatment, light covering, plenty of cold drink in small quantities; where there is severe congestion of the brain, use cold water or ice-compresses to the head, and sometimes local blood-letting. Venesection is only to be practised in the most urgent cases, as it rarely does good, and may cause dangerous collapse; in its place, in attacks of pernicious fever, besides local blood-letting and derivatives, the use of opium has proved the most efficient treat- ment. The sweating stage must be awaited in bed. Especial treat- ment to increase the sweating is unnecessary, as there is no advantage from its being very profuse. The patients should not change their underclothes till this stage has terminated. The treatment during the apyrexia aims at preventing the return of paroxysms by the adminis- tration of quinine, unless there be some peculiar objection to giving that medicine. The formerly common idea, that it was advantageous for the patient to have a certain number of paroxysms, and that the fever should not be arrested till after the third, fifth, or even seventh attack, was based on false premises. The sooner he is freed of his paroxysms the better for him. A morbid state of the gastric mucous membrane, however, which occasionally occurs after the first paroxysm of intermittent, contraindicates the administration of sulphate of quinine, and, in mild cases at least, this morbid state should be re- moved before ordering the irritating salt. In treating intermittent fever, the diagnosis of gastric catarrh, or foul stomach, is not made very exactly, and emetics are used too freely; some physicians begin the treatment with an emetic, as a matter of course; others prescribe muriate of ammonia till the tongue is thickly coated, and then give an emetic to prepare the patient for quinine. Unless certain indications, that we have given for the administration of emetics in gastric catarrh, be present, we consider it improper, or at least superfluous, to open the treatment of intermittent with one. But if, at the commencement of the fever, the patient has made great errors of diet, especially if, just before the paroxysm, he has filled his stomach with food which has remained undigested, and by decomposing has irritated the gastric mucous membrane, there is just cause for giving an emetic. We have 686 ACUTE INFECTIOUS DISEASES already described the difference between gastric catarrh due to indi gestion and the slignt dyspepsia accompanying most fevers which re- quires no emetic, and does not prevent our giving quinine. Pfeufer'k recommendation, to give quinine in one large dose instead of in several smaller one sduring the apyrexia, has very rightly become popular. Usually, in adults, one dose of ten grains of sulphate of quinine suffices to arrest the chills; in children, five grains suffice, in still smaller chil- dren, two or three grains answer. Another slight chill often occurs, and the attacks then cease. It is best to give this dose of quinine some hours before the expected chill, so that we may be sure of its acting during the apyrexia. Small doses should only be preferred when large ones are vomited by the patient; in such cases we may give two grains every two hours, till twelve or fifteen grains have been taken during the apyrexia. Quinine is most frequently given in pow- der or pill (quiniae sulphat. gr. x, ext. gentian, q. s. ut f. pill. no. iv). Solution of bisulphate of quinine (quiniae sulph. gr. x, aquae meliss. § iij, acid, sulphur, dilut. 3 ss, syrup. § ss) is said to be particularly effective, but it is unpleasant to take, especially in large doses. If quinine is not borne by the stomach, it may be given by injection, as it acts just as well by the rectum (or by hypodermic injection). Other salts of quinine have no advantage over the sulphate; quinoidine and tincture of quinoidine are cheaper, and hence may be preferably used in poor practice ; of the latter remedy we may give twelve or fifteen drops every two hours, or give a teaspoonful a short time before the expected chill. According to Wunderlich, this is quite as effica- cious as quinine. If the patient has escaped one chill under the above treatment, he almost always escapes a second and third, or even a number; but it is advisable to continue small doses of quinine for a few days longer, unless the spleen has distinctly and steadily de- creased in size. The more perfectly the spleen returns to its normal bulk, the greater is the probability that there will be no relapse. I have already given my ideas about the custom of repeating the qui- nine on the seventh, fourteenth, twenty-first, and twenty-eighth days. When this is being done, the chill often occurs on the day just pre- ceding the one when the medicine was to be given. I think it much safer to tell the patient that he will probably have a relapse toward the end of the second, third, or fourth week, and that at these times he must watch carefully for any premonitory symptoms, and on the slightest suspicion of a chill he must take a full dose of quinine. By careful attention to the rudimentary attacks which almost always pre- cede perfect relapses, most patients of moderate intelligence may pro- tect themselves from the latter. The belief, that, in cases of relapse, the patient must daily take an ounce of tincture of Peruvian bark ir REMITTENT AND CONTINUED MALARIAL FEVER. 687 stead of quinine, is antiquated. Besides the administration of quinine or its repetition, we should urge the patient to adopt all the rules spoken of under prophylaxis. When the circumstances of the patients permit, we should have them leave the affected place for six or eight weeks. We have already explained that this does not render the ad- ministration of quinine superfluous. If chronic malarial dyscrasia develop, besides a nutritious and strengthening diet, the patient should twice a day take half a glass of bark and wine (tine, cinchonas 3 i, tine, cinnamom. 3 i, acid, sulph. aromat. 3 ij to a bottle of Rhine wine), or three or four teaspoonfuls daily of tine, cinchonas comp., combined with large doses of iron. In most cases the benefit of this treatment is very evident: even advanced dropsy usually disappears in a short time without any diuretic reme- dies ; should it unexpectedly fail, we ought to absolutely insist on a temporary change of residence, even if it be very inconvenient. The above treatment is almost always successful in simple inter- mittent. Experiments with substitutes for quinine, such as salacin, piperin, salt, etc., have led to negative or doubtful results. The only febrifuge, except Peruvian bark and its preparations, that deserves con- fidence, is arsenic, in the form of Fowler’s solution (four to six drops three times daily during the apyrexia). In view of the far more cer- tain and safe action of quinine, I consider the use of arsenic as only justifiable in those rare cases where quinine fails, even in large doses. In pernicious intermittent, our first object is to prevent the occur- rence of the next attack. While carrying out the treatment required by the congestive symptoms during the attack, we should not wait for a complete intermission before giving quinine; but, as soon as there is the slightest abatement of the symptoms, we should give large doses of quinine (3 j to 3 ss. or more), and, if the patients cannot swallow, give it by enema [or, better, by hypodermic injection, giving about one-third the dose by the mouth, perfectly dissolved]. In the concealed form of intermittent, quinine is almost as effica- cious as in the simple form ; but even here its action appears only pal- liative and symptomatic, as it does not prevent relapses. CHAPTER XII. REMITTENT AND CONTINUED MALARIAL FEVER. Etiology.—Remittent malarial fevers occur chiefly in the tropics, it is true, but they are occasionally observed among us also, in places where malarial diseases are endemic, and at other places also when epidemics of intermittent are prevailing. Hence I cannot class remit 688 ACUTE INFECTIOUS DISEASES tent malarial fever among the exotic diseases and pass it by, but 1 shall follow the excellent description of Griesinger in my short ac- count of it, as I have but little knowledge of the affection from per- sonal observation. The dependence of remittent fever on malarial infection is shown, first, by its exclusive occurrence in places where we know, from the quality of the soil and climate, and from the occurrence of numerous cases of intermittent, that there is an intense malaria ; secondly, from the many cases where remittent fever becomes intermittent. We do not know whether the change of symptoms be due to a modification of the poison, and, if so, in what this modification consists. The more severe the cases of intermittent, the more frequent are the remittent cases. Anatomical Appearances.—As regards the melanaemia, the post- mortem appearances of remittent fever correspond with those of per- nicious intermittent. At least, in almost all places where remittent fever is endemic, in the rare cases of autopsy it has been noticed that the cortical substance of the brain is of a dark, ashy hue, and the spleen and liver are blackish. Besides these changes, which are not constant, traces of more or less severe icterus are often found, some- times with, again without, obstruction of the gall-ducts; as well as the remains of catarrhal and diphtheritic inflammation of the intestines, and, more rarely, haemorrhages into the stomach, haemorrhagic infarc- tions in the lungs, or lobular pneumonia. Symptoms and Course.— Griesinger distinguishes three forms of remittent fever. According to him, the first and mildest form begins with a sudden feeling of severe illness, high fever, and foul stomach. These are soon accompanied by enlargement of the spleen, mild jaun- dice, irregularity of the bowels, discoloration of the faeces, and herpes labialis. The depression of the patient, the pain in the head and limbs, the dizziness, noise in the ears, and not unfrequent bronchitis, remind us of a commencing typhus; but from the first the fever shows a decided remittent character. Irregular exacerbations, which subse- quently become regular, and usually have a quotidian type, are fol- lowed by distinct remissions. These gradually pass into perfect inter- missions, the patient sweats freely, and feels well; the remittent becomes a simple intermittent. In other cases, even without this change, the disease terminates in recovery, by a gradual decrease of the symptoms; it lasts from a few days to three weeks. In the severer form the fever is very high, the remissions are well marked only at first; the disease reminds us of a severe typhus; the patients become stupid and delirious; the tongue grows dry, and the spleen is enlarged. Generally, also, but not always, there is icterus; REMITTENT AND CONTINUED FEVER. 689 other cases are complicated with pneumonia, dysentery, etc., and still others have indications of the so-called pernicious attacks. The dis- ease usually lasts from eight to fourteen days. If it ends in recovery, it usually first becomes intermittent. Death may occur suddenly with the symptoms of a pernicious intermittent. The severest forms run their course with the symptoms of an indis- tinct and irregular exacerbating and remitting fever of very adynamic character. The patients collapse quickly, and soon fall into deep apathy. There are also various but not constant disturbances of func- tion and nutrition in almost all the organs, so that the symptoms of the disease vary greatly. Many patients become jaundiced. There is often epistaxis, vomiting of blood, and hsematuria; in other cases there is albuminuria, or suppression of urine; in others, symptoms of cholera or dysentery; the spleen and liver enlarge considerably, and often become the seats of inflammation and suppuration. Inflamma- tory exudations not unfrequently form in the serous membranes and lungs also, and in the skin there are petechias, bed-sores, and gangrene. Death usually occurs in this stage, with coma or convulsions, or with the symptoms of febris algida. Treatment.—According to Griesinger, in the milder forms of re- mittent fever, the acute affection of the gastro-intestinal mucous mem- brane should be combated by absolute diet, acids, and, if requisite, by emetics and laxative medicines. We should give quinine as soon as the remissions and exacerbations become decided, and the latter begin with a chill. Any complications should be treated separately, as quinine alone does not answer for them. In the severer and severest forms, the most important indication is the early and continued use of quinine in large doses, till improvement begins. At the same time, the congestive symptoms are to be treated symptomatically, just as in pernicious intermittent fever. [At present malarial poison is by many supposed to consist of microscopic vegetable parasites, in algse cells and spores, from the decomposition of vegetable substances. IlarJcness asserts that the algae cells, which Salisbury found in the sputa of patients and re- garded as the active principle of malaria, are found not only in malarial regions, but on the highest Alps, and occur in the sputa and other secretions of healthy persons. Intermittent fever is a wide-spread disease. It is especially frequent in the tropics at places which are not particularly dry ; in the temperate zones it occurs at certain places ; but the frigid zones escape. It is very common in Western Africa, the West Indies, Mexico, and our Southern States, but occurs to some extent in all the States. 690 ACUTE INFECTIOUS DISEASES. The period of incubation for malaria is uncertain. Patients sub- jected to the poison for a long time, or suffering from the disease, look pale and cachectic, probably from changes in the blood, per- haps partly due to fever,, partly to affection of the blood-forming organs. The red blood-corpuscles are less numerous ; the remains of those destroyed appear as pigment in the blood and some of the organs. This diminution in number is greatest at first, but goes on till recovery begins ; but at the same time it is said they increase in size. Kelsch says the white corpuscles decrease in number faster than the red do, but in the interval increase gradually, and that at the time they are least numerous the spleen is largest. If after the intermittent paroxysms have ceased the spleen or liver remain enlarged, the patient cannot be regarded as cured. Chronic enlargements of the spleen may attain an enormous size ; or there may be amyloid degeneration of the spleen, the liver, or the kidneys. Where in the treatment of malarial diseases the preparations of cinchona prove ineffectual, we may try eucalyptus globulus, of which we may give 3 ss-3 ij of the tincture, or 10-20 drops of fluid extract, several times daily. Another substitute for quinine is arsenic, either as pills of arsenious acid or as Fowler’s solution. In cases of malarial neuralgia, or where there is gastric disturbance, the Fowler’s solution may be used hypodermically. Faradization of the splenic region is said often to diminish the size of the spleen, as also the use of cold douches over that organ while the patient is in a tepid bath.] [CHAPTER XIII. YELLOW FEVER. Without discussing the question as to when and where yellow fever originated, we may say that in the United States its different epidemics seem to come from the West Indies, and to start among us from New Orleans ; thence its course of travel is along rivers or by the seaports. The cause of the disease is not certainly known, but it is sup- posed to be in the nature of germs. The affection is not conta- gious ; i. e., a patient having it, if stripped of his clothing and dis- infected, may be placed among other patients without spreading the disease. So, the germs do not develop and multiply in the YELLOW FEVER. 691 patient, but they do so in articles about him (fomites) ; germs may be carried in clothes and other articles, or in ships, especially in the bilge-water. These germs are deprived of activity by a freez- ing temperature, but may be awakened by a heat of 90° Fahr. ; they are destroyed at 250° Fahr. It has been maintained that yellow fever is only a variety of malarial fever, but the evidence seems to be very strongly against this view. The National Board of Health (United States, 1879) reaches conclusions about as follows : The essential cause of yellow fever is a “ germ ” wThich is capa- ble of growth and propagation outside of the human body, and which flourishes especially in decaying organic matter. Disinfec- tion must attack the germ and that on which it grows. Disinfec- tion is a poor substitute for cleanliness ; it is best done by sulphate of iron, carbolic acid, fresh quicklime, fresh charcoal-powder, chlo- rides of zinc and aluminium, and permanganate of potash. The disinfectant must be brought into actual contact with the germ ; when the germ is dry, it must be moistened or else subjected to a dry heat of 250° Fahr. While the infected articles are dry, move them as little as possible ; moisten them with boiling water or some disinfectant solution. The Board advises moist cleansing, followed by fumes of sulphur, using about 18 ounces of sulphur to 1,000 cubic feet of the space to be disinfected. The removal of an unpleasant odor is no proof of disinfection. Textile fabrics which have been exposed to yellow-fever infection should be placed in boiling water or in an oven ; rooms and houses which have been occupied by yellow-fever patients should be disinfected as soon as possible. Lastly, they suggest that “ every suspicious case of sick- ness should be at once isolated, and every possible precaution taken to prevent infection, by providing attendants who have had the disease, and thorough disinfection of all discharges from the sick. If the disease proves to be yellow fever, all articles of clothing and bedding used about the sick should be burned, the house should be vacated, and every room tightly closed and fumigated with burning sulphur.” Yellow fever only occurs when the temperature is high ; in the northern part of the United States most of the epidemics have be- gun in July and August. A frost suddenly checks the spread of the disease. Susceptibility to this affection is greatly influenced by race and acclimation ; in many epidemics negroes escape ; acclimation may 692 ACUTE INFECTIOUS DISEASES. cause some change in the tissues that impedes absorption of the germs. It is said that acclimated persons are not troubled by mosquitoes, which are usually very plentiful in yellow-fever re- gions. Anatomical Appearances.—Rigor mortis is early and decided. The skin is more or less jaundiced. The heart is often pale and relaxed ; its muscles may have undergone fatty degeneration. The greatest changes are seen in the abdomen ; there is acute catarrh of the mucous membrane of the alimentary canal; rarely there may he ulcers in the stomach, and there is usually more or less dark blood (black vomit is blood mixed with the fluids of the stomach). The liver is but little changed in size, but is of uneven yellow color (more marked in the left lobe), and its cells are filled with fat; it looks like the fatty liver of drunkards. The spleen is not especially changed. The cortical substance of the kidneys is often swollen, and there are signs of inflammation in all parts of them. Symptoms and Course.—The period of incubation is not set- tled, but probably is from a few hours to three days. The first symptoms are chilliness alternating with fever, or perhaps a severe chill, great restlessness, red face and eyes, headache (“ the most characteristic symptom of the disease is the p>eculiar pain in the forehead and eyeballs, with the drunken appearance of the eye”), pain in the joints, fever (102° Fahr. or more), frequent respira- tion, and frequent pulse. Severe cases sometimes have a cadav- eric odor early in the disease. The tongue is coated and swol- len, the pharynx reddened ; the gums swell and bleed readily. The epigastrium is very sensitive, and there is usually vomiting. The kidneys are affected, and albuminuria is common ; it is said that if the albumen disappears gradually, it is a favorable sign, while its continuance or increase is ominous. The symptoms in- crease till the second or third day, the temperature rising to about 105°. Then there may be jaundice of the skin and conjunc- tiva ; the urine contains bile ; the faeces retain their color, show- ing that the jaundice is haematogenous. There is frequent haemor- rhage from the nose, or more rarely from the stomach ; the latter is of evil import. After increasing in severity for about two or three days, the symptoms subside ; the temperature may fall to normal in twelve hours, but does not usually go below 100° ; the patient may feel so much better as to think he is well; but the nausea and sensitiveness of the epigastrium remain. This stage of remission may last one or YELLOW FEVER. 693 two days, or it may be the commencement of convalescence. In the third stage the symptoms again grow worse, the temperature rising to 104° ; the patient is usually apathetic, though he may completely retain consciousness. Now come the jaundice and haem- orrhages from the alimentary canal ; that from the stomach con- stitutes the “ black vomit ” which has given one name to the dis- ease. While this “ vomit is thick and pasty, being raised in small quantities, and thrown up mixed with natural mucus, the physician does not despair of his patient. The thin black fluid with the coffee- ground sediment is always, in Mobile, a fatal symptom.” If the disease continues, the kidney trouble may grow worse, and entire suppression of urine occur. If this third stage is severe, it mostly terminates in death (“from syncope, uraemia,-apoplexy, or asphyx- ia”) ; but sometimes the temperature falls suddenly, the patient sweats freely, and the severe symptoms all subside. Convalescence is slow, and for a long time the stomach remains weak. In severe cases- the strength of the patient may not be “ reestablished sooner than from ten to ticenty days after the cessation of the febrile symp- toms,.” “ The average duration of fatal cases is less than a week.” The Treatment of yellow fever, as of other epidemic diseases, has varied greatly with different epidemics. Bleeding, salivation, purging, sweating, etc., have each had their advocates ; but at pres- ent the most favored plans may be considered—first, that of ad- ministering at the start a large dose (gr. xx each) of calomel and quinine, followed after a few hours by a purge, and subsequently to treat symptoms ; and, secondly, the treatment by laxatives, such as cream-of-tartar and tamarind-water, followed by tonics, and, if the disease goes on, by active stimulants. It is considered very desirable to keep the patients well covered in bed, and in moder- ate perspiration; the latter may be aided by hot foot-baths under the bed-clothes and by warm aromatic teas. Possibly frequent small doses of jaborandi or its active principle, piloearpin, might prove beneficial.] 694 ACUTE INFECTIOUS DISEASES. CHAPTER XIY. SUDOR ANGLICUS.—SUETTE MILIAIRE.—SWEATING-SICKNESS.— FRIESEL EIEBEE. A large number of authorities, especially the Germans, deny the existence of sudor anglicus as a peculiar disease. Thus Hebra ignores the well-known fact that the prevalence of this malady is restripted within extremely narrow geographical limits, and that, between the various epidemics of it which have arisen long intervals have elapsed ; so, having never met with a case of it himself, he concludes that there is no such disorder. His remarks that there is no febrile affection in which fever-vesicles may not appear, and that the invasion and course of malaria are never accompanied by symptoms which accord with those of sudor anglicus, prove nothing, save that the exanthema is not patho- gnomonic of this disease, and by no means disprove the fact attested to by many trustworthy authorities, that, besides typhus, acute ar- ticular rheumatism, puerperal fever, and many other febrile com- plaints, there also exists a peculiar sickness characterized by sweating and a miliary eruption more profuse than is often observed in any other disease. That suette miliaire, or the sweating-sickness, should be named after one of its prominent symptoms, is quite consistent with the ordi- nary practice in the case of a disorder not referable to some simple pathological state of a special organ. Etiology.-1—Sudor anglicus, beyond a doubt, is an infectious dis- ease. Its exclusively epidemic appearance, its independence of the action of the weather, and other assignable antihygienic influences, as well as the results of the few autopsies which have been made, sufficiently warrant our classing it with typhus, the acute exanthe- mata, and other disorders which we believe to proceed from infection of the organism by a specific and probably organic poison, and which diseases are certainly more numerous and varied than they are said to be in the schools. Whether the specific poison of the sweating sick- ness be reproduced in the person of the patient, and thence be trans- mitted to others; or, in other words, whether it be a contagious dis- ease, is doubtful. All inoculations with the contents of the miliary vesicles, hitherto made, seem to have afforded negative results. This fact, as well as its narrow territorial confines, make it seem more prob- able that sudor anglicus is not contagious, but that it proceeds from a SWEATING SICKNESS. 695 miasma, tliat is, a poison which originates without the body, and which is not reproduced within it. Regarding the geographical range of sudor anglicus, and the influ- ence of the seasons, and other causative agents upon its epidemic oc- currence, Hirsch, who has made it the subject of a most thorough historical, geographical, as well as pathological study, speaks as fol- lows : “ But few diseases have so limited a geographical range. Its home is in France, southwest Germany, and Italy, while in the Neth- erlands, middle and northern Germany, and latterly in Spain, it has only been met with in occasional epidemics. In other parts of Europe, and the continents of either hemisphere, it is quite unknown.” Of the recorded epidemics, five-sixths broke out in the spring or summer. In autumn they were rare, in winter somewhat more frequent, but never very extensive. The appearance of sudor anglicus does not seem to depend upon any particular atmospheric conditions, and arises as often in mild spring weather as during hot summer. Most fre- quently epidemics broke out during weather characterized by a moderate temperature and remarkably moist atmosphere. Swampy ground seemed less favorable to its development than a dry, sterile soil. In contrast with many other infectious disorders, sudor anglicus is less frequently seen in large, densely-populated cities, than in small rural communities, country market-towns, and other similar localities. Of the older physicians, Lancisi, and more recently Schonlein, accuse the water in which hemp has been steeped, of favoring the develop- ment of the sweating-sickness. With regard to the conditions in life which, during an epidemic of this disorder, have been found to predispose to it, it has everywhere been observed that vigorous persons of middle age are peculiarly liable to be attacked, and that women, especially those who are preg- nant, or in child-bed, or suckling their children, are more prone to it than men are. In other respects the mode of life seems to have no effect upon the predisposition to the sweating fever. The poor, who usually afford the greatest number of victims to epidemics, do not suffer from sudor anglicus more than the rich. Anatomical Appearances.—Nearly all authorities speak of the early appearance and rapid progress of putrefaction of the corpse. There are no fibrinous clots in the blood, which is thin and dark of color. The cerebral veins and sinuses are full of blood, and the serum in the ventricles is sometimes increased in quantity. The mucous membrane of the air-passages appears reddened. Somewhat rarely pneumonic infiltration is found in the lungs. The assertion that vesi- cles similar to those of the skin are found upon the mucous membrane of the intestine as yet lacks confirmation. The spleen is swollen and 696 ACUTE INFECTIOUS DISEASES. soft; the liver filled with blood ; the general appearance corresponds with that usually revealed upon the autopsy of an exanthematous patient. Symptoms and Course.—In a few instances the disease is pre- ceded by languor, headache, soreness of the limbs, loss of appetite, indigestion, and other premonitory but non-characteristic symptoms. Much more commonly the disorder breaks out suddenly, without any precursory signs whatever. The patient goes to bed feeling per- fectly well, and awakes in the night bathed in sweat, the flow of which in a few cases is preceded by a slight chill. He complains of a painful sense of constriction about the precordium, and of an indescribable ter- ror and restlessness. The countenance is reddened, the skin hot, pulse frequent, and urine scanty and concentrated; strange to say, thirst is not always much augmented. Most patients further complain of head- ache, of a feeling of stiffness and tension about the nucha; many also suffer from mental confusion, dizziness, roaring in the ears, palpita- tion of the heart, and painful spasms of the extremities, like those of cholera. These are accompanied by a more characteristic symptom, a sense of numbness and pricking of the skin, particularly in the fingers and over the regions where the eruption afterward breaks out most profusely. The sweating is so copious as to saturate the clothing and bedding, and sometimes even the mattress. A peculiar odor has been ascribed to this perspiration by some, who compare it to the smell of rotten straw or musty vinegar; but more probably the odor proceeds from decomposition of the sweat which soaks the bedding. At the end of about three or four days, the eruption appears, pre- ceded by an aggravation of all the above symptoms, but particularly by an increase of the perspiration, and the prickling of the skin. Scattered here and there among the spots of the eruption, solitary sudamina appear—limpid vesicles filled with sweat, beneath which the skin seems so normal that one might mistake them for drops of water.* The greater part of the eruption, however, is of the miliary form and should rank with the eczemas, since the elevation of the cuticle is not the result of mere perspiration, but of an inflammatory effusion. The vesicles at first are tolerably transparent, but soon be- come pearly and turbid; and according as they are or are not surround- ed by an intensely reddened areola they are described as miliaria rubra or miliaria alba. Sometimes the effusion accompanying the hyperaemia of the sudoriparous glands in miliaria rubra is so slight that there are apparently no distinct vesicles, but merely solid nodules * To guard against misunderstanding, the term miliaria crystallina should be disused. SWEATING SICKNESS. 697 {eczema papulatum). The eruption then bears a great resemblance to measles. When the effusion is very profuse beneath the cuticle the vesicles become so large as to suggest a varicella.—The first ap- pearance of the exanthema is upon the sides of the neck and the upper part and front of the chest. Thence it spreads to the belly, back, arms, and legs; it rarely attacks the face or hairy scalp. The erup- tion breaks out either all at once, the whole body becoming cov- ered with vesicles within a few hours; or else it comes out in crops, one part of the body after another being assailed. The latter is a very common form of the eruption. The fresh outcroppings of the rash are always preceded by an aggravation of the other symptoms, espe- cially of the sweating and pricking of the skin. Sometimes there is no eruption at all. Such instances are not to be regarded as analogous to the rare cases of scarlatina with- out exanthema and of abdominal typhus without intestinal lesion. Here the rash seems to depend upon mere sweating; and the latter is the real pathognomonic sign of sudor anglicus. Whether or not there be also a miliary eruption depends a good deal upon the degree of susceptibility of the skin of the individual, just as in cases of sun-burn or of mercurial inunction, it depends in part upon the activity of the irritant and in part upon the sensitiveness of the skin whether or not an eczema solare or eczema mercuriale shall ensue. When the disease takes a favorable type, the fever and other symptoms assume a remittent and sometimes even an intermittent form, and about the sixth to the tenth day the sweating begins to abate, and no more fresh crops of the vesicles arise. The restlessness also ceases, as well as the headache, prickling, and loss of appetite; the fever subsides, sleep is tranquil, urine copious, the vesicles dry up, and convalescence is established; during which the macerated and loosened cuticle exfoliates, sometimes in large sheets, sometimes in bran-like scales. Occasionally a relapse interrupts convalescence, and runs a course like that of the original seizure. The malady may thus drag on for weeks, and greatly exhaust the patient, rendering his recovery very slow. While in many epidemics the favorable type is so much the rule, that the majorit}T or even all patients recover, yet there are others in which the sudor anglicus, without especial complication, makes many victims. It may terminate fatally at any period, death taking place suddenly and without warning, either with symptoms of excessive dyspnoea, or else of cerebral and cardiac palsy. Sometimes the end is preceded by a cessation of the sweating and a fading of the exam 698 ACUTE INFECTIOUS DISEASES. thema. This has been accounted for upon the obscure hypothesis of a metastasis of the disease to internal organs. The most common complications of sweating-sickness observed in the more accurately described epidemics are angina and a diphthe- ritic stomatitis, generally termed aphthae. More rarely it is compli- cated with bronchitis and pneumonia. In a few of the epidemics dysentery was observed instead of the usually obstinate constipation. When of very protracted duration, or unusual intensity, then, like other tedious and very severe infectious disorders, it develops a haemorrhagic diathesis with abundant epistaxis and the appearance of petechia, and in women by abnormal bleedings from the genitals. Unfortunately, no accurate measurements of the bodily tempera- ture during sudor anglicus have as yet been taken. This circumstance greatly embarrasses our estimate of the physiological value of the symptoms. How, for instance, is the peculiar restlessness to be ac- counted for ? Is it due to inspissation of the blood through enormous sweating, and upon consequent impediment to its circulation through the capillaries of the lungs, as in cholera, with which sudor anglicus has been compared ?—Or, is the calorification so much heightened during the fever as to occasion a surcharge of carbonic acid which cannot be neutralized by respiration ? Indeed, we are forced to the inference (owing to the considerable cooling which the skin must suffer through evaporation of the profuse perspiration) that the pro- duction of heat is much more active in sudor anglicus than in infec- tious diseases in which the skin remains dry, always supposing the temperature of the diseases to be equal. Cooling of the body by evaporation of the sweat may protect the patient from the perils aris- ing from too high a temperature of the blood, but not from its over- charge with carbonic acid—one of the necessary results of excessive calorification; at all events, this would account for the apnoea of sweating-sickness. Again, does the supposed danger of checking the sweating depend upon the fact that, without the cooling effect of rapid evaporation of the sweat, the temperature will reach a point at which the brain and heart are palsied ? Such questions must be de- ferred until our knowledge of the temperature in sudor anglicus shall be made as exact as that of typhus and other disorders. Treatment.—Until we shall have more thoroughly investigated the conditions upon which the sweating-sickness depends, prophy- lactic measures against its invasion and extension are out of the question. At the outset of the attack an emetic is urgently recommended by many. From all reports, however, it is by no means clear that the disease has ever been cut short by this means; and we shall CHOLERA ASIATICA. 699 therefore do well to confine its exhibition to cases which commence with well-marked gastric disturbance. Its administration, however, at the beginning of a sudor anglicus, during which the bowels are generally confined throughout, is not so hazardous a step as it would be at the commencement of a typhoid fever, when an emetic might seriously aggravate the diarrhoea which always sets in. The various drugs which have been deemed specifics in certain epidemics have invariably failed in others, and quinine alone seems to have maintained its reputation as an antipyretic. It may be given in doses of twelve or fifteen grains daily, not only when the type of the malady is decidedly remittent or intermittent, but even when the type is continued and the temperature exceeds a certain height. The fact that the danger of the sweating-fever is greatly dependent upon the height of the temperature has already forced itself upon the attention of the best observers, even without the use of the thermometer. When there is no occasion to use quinine, it is best to prescribe acids, especially muriatic or phosphoric acids properly diluted. An important step in the treatment of sudor anglicus dates from the time when the practice ceased of keeping the patients immod- erately warm, for fear that the sickness should “ strike in.” If my opinion be correct, namely, that the production of heat is intensely active, but that the danger of an overheating of the body is averted by evaporation of the sweat, then it is plain that it would be danger- ous to envelop the patient in thick blankets, beneath which the air is so saturated with moisture as to impede further evaporation. Light clothing and free ventilation are imperatively indicated. At the same time the patient must not be set in a draught, lest he take cold, the danger from which is greater in sudor anglicus than in kindred affec- tions, owing to the profuseness of the perspiration. CHAPTER XV. CHOLERA ASIATICA. Etiology.—It is possible, and even probable that, where cholera is endemic, it results from miasm. Whether this miasm, the cholera germ, develop in India, on diseased rice or not, and whether or not the disease rage in India, more especially in years when circum- stances particularly favor the increase of these vegetable germs, among us, it is not indigenous; but all the cholera epidemics occurring among us are due to the exotic parasite being brought to us by cholera pa- tients, and finding for a time a suitable soil and favorable circum- 700 ACUTE INFECTIOUS DISEASES. 3tances for increasing; with us cholera is never miasmatic. (I shall not dwell on the question whether Hallier and Klobb, who have found numerous fungi in the dejections of cholera patients, have actually discovered the cholera germ, for I do not feel competent to decide it.) Cholera is not contagious in the strict sense of the word, for a healthy person never takes cholera from contact with a patient having that disease. (My experience in the first cholera epidemic that I saw, where I wrapped many naked patients in blankets, and often held them in my arms for some time, made me a decided anti-contagionist, and I took this ground in my first publication, some twenty years since.) But, as the word contagion is universally used in the sense, that diseases which are transferred from sick to healthy persons are contagious, and as this is very decidedly the case in cholera, we must class cholera among the contagious diseases. The vehicle of conta- gion is not, as in the acute exanthemata and exanthematic typhus, the exhalation from the skin and lungs, but the dejections of cholera pa- tients. It has been certainly proved that fatal cholera epidemics have broken out in places previously free from it, because some traveller, having cholera germs in his intestines, has used a privy, or that the dejections of a cholera patient have been emptied into a privy, fre- quented by other persons. In 1848, a transport of recruits from Stet- tin, where cholera was raging, came to Magdeburg; two of these re- cruits sickened of cholera the night of their arrival. They were imme- diately taken from their quarters to the military hospital, which was some distance off, without coming in contact with the inhabitants. A few days after, the cholera broke out in the house, and in the street where they had passed the night. The fatal epidemic did not spread to the rest of the city for some weeks. In large, thickly-populated cities, where there are numerous cases of the disease, the extension of an epidemic is more difficult to follow than it is in small, thinly-settled towns where the number of cases is limited. A small epidemic in Greifs- wald gave me an excellent opportunity for observing the spread of cholera. In almost every case I could find that the patient had used the privy of some house containing cholera patients, or one whose cess- pool communicated with that of the privy of affected houses, or that they had used a privy in common with persons from these houses who had diarrhoea. Since it has been known that cholera is only trans- ferred to healthy persons through the dejections of cholera patients, a series of previously enigmatical and apparently contradictory observa- tions, concerning the spread of the disease, have been satisfactorily ex plained. "YVe may readily understand that cholera should spread from place to place more rapidly than it formerly did, since in these days of railroads and steamboats people travel more quickly than thev used to CHOLERA ASIATICA. 701 do. It is no longer surprising that cholera should follow the routes of travel, that it should spread sometimes with the wind, sometimes against it; sometimes from west to east, again from east to west. The long leaps that cholera epidemics often make are simply due to the fact that travelling cholera patients only infect those places where they leave their dejections, while all intervening places escape. If the cholera germ were contained in the dejections of those patients only who suffered from the severest form of the disease (cholera as- phyxia), as they cannot travel, long springs of cholera epidemics could only occur when persons infected with cholera poison travelled during the period of incubation, and the disease did not fully develop in them till they had reached some place distant from their previous residence. But besides such cases, among which are the cases in Magdeburg above mentioned, numerous examples show that a person suffering from simple choleraic diarrhoea, and who does not feel very sick at the time, nor even become so later, contains the germs of cholera, so that he may infect a privy, and thus start an epidemic. Against the view that cholera was spread by the evacuations of the patients, it has been urged among other things that in some cases persons who had swallowed the dejections of cholera patients escaped the disease, and that attempts to give animals cholera, by introducing into their bodies the contents of the intestines of patients who had died of cholera, or the evacuations of cholera patients, had generally failed. These facts cannot be denied. To make them agree with those above mentioned, it has been suggested that the recent dejec- tions of cholera patients do not contain the cholera germ in the stage of development necessary to infection, nor in the necessary amount, but that the dejections only become dangerous when the germs of the dis- ease are placed under circumstances favorable to their development and increase, by admixture with decomposing animal substances. This hypothesis is very plausible, and has been generally accepted, as it is supported by numerous facts ; for, while, according to the observations of Thiersch, recent cholera dejections were not dangerous for animals, feeding them with old dejections of the same sort induced cholera. Experience has taught that persons who wash the clothes of cholera patients, after they have lain for some time, and persons who change the bed-clothes a few days after the death of the patient, are more apt to be infected than those who place the bed-pan under the patient, oi replace the wet sheets by dry ones. It is most dangerous for the per- sons in a house, if the evacuations of a cholera patient are emptied into a privy filled with excrement, into a cess-pool, or thrown on a dung-hill. At such places the cholera germ seems to find circum- stances most favorable to its development and increase. 702 ACUTE INFECTIOUS DISEASES. When cholera has been introduced into a place, it sometimes hap- pens that only those persons are attacked who live in the same house, or use the same privy. It has even been observed that, in certain cities where cholera has been repeatedly introduced, it has always been limited to these house epidemics. But, in other cases, the dis- ease spreads from the house where it was introduced, to neighboring streets, large portions of the city, or even over the whole vicinity. This may either happen every time the cholera visits the place, or only in certain epidemics, while in others this extension does not occur. We are indebted to Pettenkofer for the discovery that porosity of the soil, enabling the contents of the privies and cess-pools containing the cholera germs to freely permeate and soak the ground for some dis- tance around with this dangerous mixture, favors the rapid extension of the disease, while the opposite quality to some extent protects from such an extension. We are also indebted to Pettenkofer for the dis- covery that the occasional predisposition of a place to an extension of cholera depends on the excrements containing the germs, and per- meating the soil, being exposed to circumstances favorable to decom- position. As we have already shown, when speaking of the etiology of typhus, moisture of the soil plays a very important part among these circumstances, but it is not the only one. There is no doubt that the conditions for decomposition may be peculiarly favorable when a very moist soil suddenly dries to a certain extent; and it can- not be denied that the sudden fall of the water of the soil may prove very dangerous for the spread of cholera. The opposing facts, which have also been proved, show that the number of cholera cases may in- crease independently of the sudden fall of the water in the soil, and that it is one-sided to regard the fall of the water as the sole cause for favoring decomposition of the excretory matters, mingled with cholera germs, which have soaked through the soil. The cholera poison is rarely taken into the system by drinking water containing it. As a rule, it undoubtedly enters the nose and mouth with the air, and is swallowed with the saliva. Using infected privies is so dangerous, because they are the favorite lurking-places for cholera germs, and the gases arising always contain dust-like par- ticles. The poison passes from the privy into the atmosphere of the house, and we must agree with Piermer in considering the dwellings as more liable than the inhabitants to infect. Next to the soaking of tne infecting substance through the soil, the disease appears to spread from one house to another, chiefly through the gutters and drains. The susceptibility to cholera poison is very extensive. No age, sex, or constitution, escapes it. When the cholera poison spreads over the whole city, almost every one suffers from it; even those not a6 CHOLERA ASIATICA. 703 feoted with the severer forms have some troubles, apparently depend- ing on the weaker action of the poison. Certain influences appear to increase the predisposition to the severer forms of the disease, or to diminish the resisting power of the organism to the action of the poi- son. Chief among these are errors of diet, emetics, and laxatives, catching cold, and other debilitating influences. It is true, foolish people seek to excuse their excesses at the time of cholera epidemics by saying that the mode of living can have no effect in inducing cholera, because persons who lead the most proper lives are attacked by and die of the severest forms of the disease. Even if this reasoning was meant in earnest, it does not require refutation. Whoever is exposed to a poison, whose action kills many persons, while others recover from it, is foolish to subject himself to injurious influences which lessen his chances of recovery, even if the avoidance of these injurious influ- ences gives no guaranty for a favorable termination. The number of cholera patients taken into the Paris hospitals is said to be one-eighth greater on Monday than any other day. In the Magdeburg epidemics, the commencement of a fair, which gave opportunity for excesses of all sorts, has repeatedly been observed to have a very unfavorable influence on the number of cases and deaths. For the numerous important historical and geographical data that have been collected concerning cholera, since 1830, when it first ap- peared in Europe, I must refer to special works where the principal epidemics are fully described; for imperfect extracts from them would be unsatisfactory. Anatomical Appearances.—Bodies of patients who have died of cholera remain warm a long time; a post-mortem increase of the bodily temperature has sometimes been observed. A second pecu- liarity of these bodies is the occasional contraction of certain muscles after death, by which the extremities, especially the fingers, are moved, and change the position they had just after death. The movements of the fingers that I have actually seen, and the changed position in which I have found the bodies a few hours after leaving them, have always made a very disagreeable impression on me. If death has occurred at the height of the disease, the appearance of the body is characteristic. We usually find it in a position to which the clinched hands, variously bent limbs, and swollen muscles, give a peculiarly threatening appearance (“ fighting attitude The rigor mortis is hard to overcome. The face is often so distorted as to be hardly recognizable. The eyes are deep in the orbit, and are sur- rounded by wide, blue rings; the eyelids are half closed; the uncov- ered portions of the eyeballs are dry as parchment, the nose is pointed and projects far bejmnd the sunken cheeks. The lips are bluish, 704 ACUTE INFECTIOUS DISEASES. sometimes deep blue. The other parts of the body also have a more or less marked cyanotic appearance. This is most apparent in the ter- minal phalanges of the fingers and toes. The skin of the fingers is often shrunken, and wrinkled like that on the fingers of a washer- woman who has had her hands in the suds all day. On opening the bodies we remark the hardness and dryness of the subcutaneous con- nective tissue, and the dark-red color of the muscles. The blood is thick, of the color of huckleberry-juice, and contains a small amount of soft, black clots; it is collected in the right heart and veins, while the arteries and left heart are often perfectly empty. The cerebral sinuses and veins of the meninges are distended with dark blood, while the cerebral substance is dry and hard. The pericardium does not con- tain a trace of serum, its inner surface feels pasty, and is often covered with ecchymoses; the muscular substance of the heart is contracted, hard, and of a dirty-red color. The surfaces of the pleura, like those of the pericardium and other serous membranes, are covered with an adhesive layer. They also often contain small ecchymoses. On open- ing the thorax, the lungs collapse very quickly and completely, appar- ently because the empty, dry bronchi offer no opposition to the escape of air from the alveoli. On cutting into the lungs, we find them re- markably dry, and free from hypostasis and oedema. The relaxed, baggy small intestine has a peculiar rosy appearance, even before it is opened, while the large intestine preserves its natural color. On open- ing the intestines, quantities of a colorless or faintly-colored fluid, con- taining white flocculi, often escape ; this liquid exactly resembles the “rice-water discharges” of cholera patients, which we shall more minutely describe. I have found the greatest amounts of transuda- tion in the intestines, in cases of so-called cholera sicca. The mucous membrane of the small intestine is finely injected, especially near the valve, and growing less so as we pass upward. The vascularity is occasionally accompanied by greater or less escape of blood into the tissue, and on the free surface of the mucous membrane. Then the mucous coat shows numerous, often extensive, ecchymoses, and the con- tents of the intestines appear reddened from the admixture of blood. Sometimes the small intestine is pale, and neither vascularity nor ecchy- moses can be found; but since we find the intestines filled with watery transudations even in such cases, and as these transudations come from distended, not from empty vessels, it follows that the pale hue of the mucous membrane is to be regarded as a post-mortem appearance. It is a matter of daily experience for visible mucous membranes that have been very hyperasmic, and secreted abundantly during life, to become pale after death. The mucous membrane and whole intestinal wall are swollen and relaxed from oedematous infiltration. As a rule, also, the CHOLERA ASIATICA. 705 solitary and Payer's glands are swollen and distended. The individual follicles may attain the size of a hemp-seed. In consequence of this swelling of the intestinal glands, the inner surface of the bowel looks as if sprinkled with isolated and conglomerated granulations. Occa- sionally certain follicles of the patches burst, and then the surface has a sieve or net like appearance {plaques d surface reticulee). The most important appearance in the intestine is the great loss of epithelium The intestinal villi are stripped of their protecting envelope; occa sionally, at certain spots, the epithelial covering is only elevated by a serous effusion, and is still loosely adherent to the villi; but in most places it is already detached, and lies on the intestinal Avail as shreds of mucus, or forms the whitish flocculi already spoken of as floating in the transudation. The comparison of the intestine in cholera to a por- tion of the skin from which the epidermis has been removed by a blis- ter, or by boiling water, is very correct; and, if it be remembered thai the denuded portion of intestine is quite extensive, it will be diflScuH to understand why some observers speak of a “ disproportion ” be- tween the anatomical changes in the intestinal canal and the severe symptoms observed during life. The large intestine does not show any constant changes, and there is but little alteration in the jejunum. The gastric mucous membrane is more or less reddened by hypenemia and ecchymosis; its tissue is swollen and relaxed from serous infiltra- tion. The liver is of normal consistence and pale; on being incised, only a small amount of thick, huckleberry-colored blood flows out slowly from the large vessels. The gall-bladder is almost always dis- tended with thin, brownish or greenish bile. The spleen has no con- stant change. In the first stages of cholera the kidneys are appar- ently normal, except an excessive venous liyperaemia; in other cases, even at this time, certain places, especially in the pyramids, are whit- ish ; and at these points, on microscopical examination, we find the uriniferous tubules filled with cloudy, swollen epithelium and fibrous exudation. The mucous membrane of the urinary passages is covered with mucous and epithelial masses, the bladder is contracted, and almost always entirely empty. Hence we see, when death occurs at the height of the disease, the characteristic changes consist chiefly in extensive catarrh of the intestines, accompanied by detachment of the epithelium and copious transudation, in decided thickening of the blood and excessive venous liyperoemia of the kidney. When death occurs during the stage of reaction, or so-called cholera typhoid, the anatomical appearances differ in some respects from the above. Then the limbs are less constantly contracted, rigor mortis is less marked; the teeth and gums are often covered with a dirty coat- ing, the cyanosis has disappeared or is slight. The subcutaneous con- 706 ACUTE INFECTIOUS DISEASES. nective tissue and muscles are moister; the blood is more fluid and less dark. The cerebral membranes are usually injected; not unfre- quently there is a considerable amount of fluid in the meshes of the pia mater and m the lateral ventricles; the cerebral substance itself is moister ; the right heart is usually overfilled, the endo- cardium and lining membrane of the large vessels is greatly infil- trated. In this stage the lungs are no longer dry, but are vascular, and are often the seat of extensive oedema and hypostasis, and not unfrequently also of lobular or lobar pneumonia, or of haemorrhagic infarctions. The outer surface of the small intestine has lost its rosy tint; the contents are colored with bile. In some cases the epithelium is replaced, and no disturbances of nutrition are discoverable in the mucous membrane; but it is often the seat of a typical diphtheritic inflammation, which changes more or less extensive patches of the mucous membrane into brown, dry sloughs. This secondary diphthe- ritis occurs not only in the small intestine, but often extends to the large intestine ; it may also attack the gall-bladder, vulva, and vagina. The liver and spleen are not always changed, but are usually very hyperaemic. Not unfrequently rupture of the spleen has been found. The kidneys also are vascular, and often show the signs of acute croupous inflammation. The bladder contains more or less urine, which is usually albuminous. Symptoms and Course.—Almost every one exposed to cholera poison complains of light oppression in the prcecordium, rumbling in the bowels, and a feeling of impending diarrhoea. These symptoms of slight indigestion, which unmistakably result from the action of the poison, apparently only increase where the infection is rather intense, or the organism inclined to a more or less severe disease. It has also been attempted to refer the feelings of terror, the fainting-fits, cramps in the legs, and other disturbances of innervation occurring during a cholera epidemic, to the action of cholera poison ; and among the laity the idea has become so firmly implanted, that the fear of cholera is very dangerous, or is even the commencement of the disease, that during a cholera season there are plenty of persons who dread having a fear of the cholera (!). I regard this belief as groundless, and think that the above symptoms are solely the result of the psychical impressions induced in excitable persons, by the terrible disease, the accounts of sickness, the numerous and unexpected cases of death. The same, or very similar symptoms are experienced by the inhabitants of a bom- barded town; and, although timid persons show no immunity to chol- era, they are not more frequently attacked than unterrified persons are. According to my observation, cholera attacks never begin with a feeling of terror, fainting, cramps in the legs, etc., although it often CHOLERA ASIATICA. 707 happens that these symptoms urge the patient to seek medical aid. If we examine such cases carefully, we always find that they have been preceded by diarrhoea, to which the patient paid no attention. Some observers estimate the period of incubation at from one to three days; others say from eight to fourteen. We rarely have the opportunity of exactly determining the time between the action of the poison and the outbreak of the disease. In a few cases that I observed in Greifswald, in 1859, as well as in a number observed by Dr. Grttttner, then assistant physician in the Medical Polyclinic, in a small town on the Mecklenburg boundary, where the limits of the in- fection could be pretty accurately determined, the period of incubation was certainly not less than thirty-six hours, and not more than three days. The mildest form of cholera is a simple diarrhoea, which is not ac- companied by colicky pains or tenesmus, and causes no constitutional or other disturbance, except a moderate degree of depression and re- laxation. The evacuations follow each other more or less closely; they are very copious and watery, but have neither lost their odor nor color. These cases do not appear on the official lists as cholera; but, although the police do not consider them as such, science should do so. This is shown: 1. By the large number of cases of diarrhoea occurring in cholera times, although almost all sensible people carefully avoid errors of diet, catching cold, and other sources of injury. 2. The great obstinacy of these diarrhoeas, and the slight efficacy of opium against them. 3. The well-known transportation of cholera by persons suffer- ing from these diarrhoeas. 4. But especially the numerous transfor- mations of simple “ cholera-diarrhoea ” into the severest forms of the disease. Many patients, especially of the poorer classes, worried by a diarrhoea that would not give way to domestic remedies, go to the doctor’s house for a prescription at noon, and in the evening lie cold, pulseless, and cyanotic, in an almost hopeless state. The investiga- tions concerning cholera, made during the late epidemic, especially in the hospitals, which are otherwise very serviceable and valuable, have made some believers in the false views concerning the significance of the intestinal affection in cholera, which I combated twenty years ago It has again been forgotten that very many cholera patients, who do not seek admission into hospital, have no symptoms but the profuse diarrhoea. I consider it much more important to determine the fre- quent occurrence of a gradual transformation from simple cholera diar- rhoea to cholerine, and to malignant cholera, and to prove the iden- tity of these three forms, than to seek for pathognomonic signs of epi- demic cholera. The transformation from the mildest forms of cholera to the severest 708 ACUTE INFECTIOUS DISEASES. is formed by those cases where violent vomiting accompanies the diar- rhoea, where the discharges acquire the well-known “ rice-water ” ap- pearance, but without the occurrence of the paresis of the heart and thickening of the blood, which constitute the terrible symptoms of cholera asphyxia. This still mild form, or, rather, these comparatively low grades of the disease, which, however, often increase to the highest grades, have been distinguished from cholera diarrhoea on the one hand, and from cholera asphyxia on the other, by the names “ erethitic chol- era,” or “ cholerine.” The discoloration of the dejections depends chiefly, or entirely, on their excessive dilution by the quantities of fluid transuded into the intestine; hence the more copious the pas- sages, and the more rapidly they succeed each other, the more com- pletely and speedily they lose their brown color and fecal odor. Oc- casionally all the contents of the intestine are passed at the first evac- uation. In such cases, even after the second movement, the dejections consist of an almost colorless and odorless fluid, holding in suspension more or less white flocculi. We must not conclude, from the lack of color in the passages, that the formation or excretion of bile has ceased; for even if the bile be produced in normal amount, and poured into the intestines, it can have no great effect on the color of the large quantity of liquid. Chemical and microscopical examinations of chol- era stools have shown that the serum, transuded from the intestinal capillaries, contains little albumen, but plenty of salts, especially of chloride of sodium, and that the white flocculi floating in the serum rarely consist of perfect cylindrical epithelium, but generally of its re- mains, in the shape of fine, loose nuclei, with coarse and fine granular masses embedded in a mucous basement substance, and of round, nu- cleated, coarse, or finely-granulated cells (Bruberger). Cholera-stools occasionally contain crystals of triple phosphate, remains of food, para- sites, vibriones, and fungi. Lastly, the dejections sometimes contain blood-corpuscles; then the fluid is somewhat richer in albumen, which has escaped from the capillaries along with the blood. These charac- teristics of cholera-stools, which all authors consider pathognomonic, fully explain the symptoms of cholera. We are justified in comparing the effects induced in the bowels by cholera poison, with those pro- duced on the skin by a blister. In both cases the protective covering is removed, and there is an excessive transudation from the capillaries. It only depends on the intensity, and particularly on the extent, of the process, whether symptoms of paralysis of the heart develop, and whether the loss of water from the blood shall prove dangerous. Case? where the heart’s action is but little weakened, and where the loss of water from the blood is to some extent replaced, correspond to chole- rine. When the characteristic cholera stools begin, the thirst already CHOLERA ASIATICA. 709 caused by the simple cholera diarrhoea is decidedly increased. This torturing symptom hardly requires explanation, as it always follows loss of water from the blood, whether induced in fevers by the increase of insensible perspiration, by sweating, or by increased excretion of urine. In cholerine the loss of water from the blood is greater, and consequently the thirst is more intense than in cholera diarrhoea. The characteristic evacuations, severe thirst, weariness, and depression, are usually accompanied by a very annoying symptom, which it is difficult to explain; there are occasional spasmodic contractions of certain mus- cles, especially of the calves of the legs, which last from half a minute to a minute, and are very painful. These cramps are not pathognomo- nic of Asiatic cholera, however, for they also occur in severe attacks of cholera morbus. In favorable cases, the discharges gradually be- come less frequent and copious; the bile poured into the intestines again suffices to color the passages. Finally, the diarrhoea ceases, and the patient begins to recover; but convalescence is always slow. In other cases the disease relapses after it appeared to be doing well, and then becomes dangerous. Lastly, in still other cases there is no im- provement, the cholerine changes to cholera asphyxia. Cholera asphyxia depends on the highest development of the intes- tinal affection. At least all its characteristic symptoms may be directly referred to the severe and extensive disease of the intestinal mucous membrane and to the copious exudations from the intestinal capil- laries. The accounts of persons dying during cholera epidemics with the symptoms of pulselessness, cold skin, cyanosis, etc., who had had neither diarrhoea nor vomiting, and in whose intestines no characteristic changes were found, have become more rare in late epidemics; so that at present almost all experienced physicians deny the occurrence of “ cholera sicca,” which was generally considered as proved in the first cholera epidemics. But the case is different in regard to the views about the dependence of the other symptoms of asphyctic cholera on the intestinal disease. Many physicians, who consider the latter as constant, do not refer the other symptoms of cholera to it, but think that the intestinal disease in Asiatic cholera has no more effect on the general appearance of the disease than the bowel lesion in abdominal typhus has on the symptoms of that affection. We shall again refer to the erroneousness of this view. In many cases asphyctic cholera develops from a cholera diarrhoea or a cholerine that has existed for several days; but, fully as often, the symptoms to which this form owes its name come on a few hours after the first cholera passage. By this all the contents of the intestines seem to be evacuated; the patients are astonished that the vessel which they used is nearly filled, but do not suspect that they are in great danger and neglect to seek aid for 710 ACUTE INFECTIOUS DISEASES. the simple and painless diarrhoea, while previously they have perhaps worried the physician about every insignificant colicky pain. The first passage is soon followed by a second, this by a third, and so on till a great number have occurred at short intervals. The evacuations are very copious and fluid, and, as they lose their fecal odor and become colorless, they soon acquire the rice-water appearance. Even after the second or third passage, many patients feel very weak and depressed, or they may be so faint as to be unable to move from the close-stool to the bed without assistance ; at this time, also, painful contractions of the muscles of the leg usually begin, and a longing for drink, which increases with every passage. The more the patients drink, the sooner the diarrhoea is accompanied by vomiting, by which at first merely the contents of the stomach, but, after a time, large quantities of a pale, yellow liquid, are evacuated. The patient rapidly grows weak, the voice loses its power (vox cholerica), the evacuations are passed in- voluntarily, the secretion of urine ceases, the painful muscular cramps increase and return more frequently; the torturing thirst cannot be allayed, and these symptoms are accompanied by a feeling of great anxiety and oppression, which, together with the cramps in the legs, forms the most painful symptom of cholera. Meantime the appearance of the patient has become frightful; the eyes are sunken, the nose pointed, the cheeks hollow (facies cholerica); the skin of the hands is wrinkled like that of a washerwoman who has washed all day; if it be picked up in a fold, the fold remains for a time and disappears slowly. The lips, extremities, and genitals, grow blue; the whole surface some- times assumes a bluish or grayish look. The radial pulse, which be- comes smaller after the first passages, frequently cannot be felt an hour after the commencement of the cholera attack. Finally the pulse dis- appears from the carotids also, the impulse and sounds of the heart become indistinct, and, while the circulation grows more imperfect, while less warm blood reaches the periphery, the temperature becomes corpse-like, particularly at the uncovered parts (stadium algidum). Rarely the patients complain of headache, more frequently of black spots before the eyes, noises in the ears, or dizziness. The mind is not cloudy, but most patients are apathetic; while they complain of pain and oppression they are indifferent to the danger, and answer in- attentively and slowly. Reflex excitability is diminished; in severe cases even irritating vapors induce neither coughing nor sneezing; the patients do not wink if the finger be approached to the conjunctiva, and do not wince if we dash water on them. It cannot be wondered at, that in the first cholera epidemics even those physicians who re- garded rice-water passages as pathognomonic of cholera, who ordered careful anti-diarrhceic regimen for their patients, and treated every diar- CHOLERA ASIATICA. 711 rhcea energetically, should not have gone a step further, and recognized the intestinal lesion as the starting-point of the other symptoms and as the true source of danger. The rapidity with which the patients changed, the great disturbance of all the functions, the pulselessness, coldness, suppression of urine, vox cholerica, facies cholerica, lack of contractility in the skin, and the fact that many patients were received into the hospital in this state, who had no diarrhoea or vomiting after their reception, and who did not always tell that they had previously had violent evacuations, led to untenable hypotheses. It is true it was acknowledged, that cholera poison led to an affection of the intestinal canal; but at the same time it was accused of having a directly per- nicious effect on the blood, nervous system, and more or less on all the organs and tissues, the intestinal canal escaping altogether sometimes. Cases where the algid stage develops in a few hours are certainly less suited to explain the dependence of all the symptoms on the intestinal affection than are those where it develops in the course of several days. From the identity of the symptoms that finally result, however, we cannot doubt that the rapid cases are to be explained in the same way as the others. The immediate result of acute intestinal catarrh, of the excessive transudation from the intestinal capillaries, and of the diminished absorption of the fluid drank, is a thickening of the blood, its sudden impoverishment in water and salts. As long as the disease is moderate, it has no particular effect on the circulation and distribu- tion of blood through the body; only the thirst is increased and the secretion of urine diminished. But, as a burn of the second order is free from danger as long as it affects only a limited portion of the sur- face, while it becomes very dangerous if widely extended, and as we dare not deprive the entire surface of its epidermis by blisters, so an extensive and intense choleraic affection of the intestines induces the severe and threatening symptoms that characterize the algid stage. The heart’s action is palsied, the blood, deprived of its water, eagerly takes the fluid from the interstices of all the tissues. Hence the tis- sues all become dry and diminished in size; the nose becomes pointed, the cheeks hollow, the eyes sink into the orbit, the skin of the fingers shrivels, and, when pinched up, stands in folds. Even pathological collections of fluid, which had previously resisted all treatment, effu- sions in the pleura, joints, etc., are absorbed. Moist eruptions and ulcers acquire a parchment-like surface. In spite of the patient’s drinking constantly, the loss of fluid so far exceeds the supply that he may lose one-fifth of his weight in a few hours. The thicken- ing of the blood explains the drying up of all the secretions of the saliva, tears, sweat and urine, just as well as it does the absorption of the interstitial fluids; the blood actually does not contain the material 712 ACUTE INFECTIOUS DISEASES. for these secretions. In the suppression of urine, however, the stag- nation of the circulation also plays an important part. The feebleness of the heart’s action, which causes the weakness and indistinctness of the impulse and tones of the heart, the diminution and disappearance of the pulse in the radial arteries, and even in the carotids, appear to depend chiefly on the depressing influence that severe acute disease, especially of the abdominal organs, has on the organic nervous system, and particularly on the nerves of the heart. Immediately after the perforation of an ulcer of the Stomach I have often seen loss of pulse* cyanosis and coldness of the extremities, and in one case, already men- tioned, perforation of the duodenum, was diagnosed as cholera sicca. Such cases, where there could not be the slightest suspicion of an in- fection, show that the hypothesis that the cholera-poison poisons the sympathetic, is untenable. On the other hand, it is not improbable that the stagnation of blood in the capillaries of the heart’s substance has something to do with the paralysis of that organ. We know that blood can only pass freely through the capillaries wrhen the blood-cor- puscles are separated from each other by a sufficient amount of inter- cellular fluid. Hence a loss of wrater from the blood, such as occurs in cholera, must hinder or even arrest the circulation in the capillaries; and, if the blood in the capillaries of the heart stagnate, according to all physiological and pathological experience, paresis of the heart is the inevitable result. The cyanosis that occurs in the algid stage of cholera depends on the same cause as that occurring in other diseases, on an abnormal distribution of the blood—the arteries, which receive no blood from the heart, contract and press their contents into the capillaries and veins; but the collection of the blood in these vessels causes very great cyanosis in cholera, because the blood is so concen- trated, and hence is relatively rich in colored corpuscles, and because, from the retardation of the circulation, it has become so venous in character, and consequently very dark. If an attempt be made to bleed in the algid stage, as was often done in the first epidemics, a thick, dark stream springs from the swollen vein, but no more blood follows the first spirt, the stream soon ceases, and then it is difficult to bring out even a few drops by pressure and rubbing. As the circula- tion is reestablished, the cyanosis rapidly disappears, although the blood still remains of a dark, huckleberry color. As early as 1848, in my pamphlet, “Die Symptomatische Behandlung der Cholera,” I showed that the cyanosis and asphyxia did not depend exclusively on the thickening of the blood, but was mostly due to the paralyzing influence of the extensive intestinal disease on the sympathetic nerve. The correctness of this view is supported by the frequently rapid dis- appearance of the cyanosis, etc., by its ceasing before the thickening CHOLERA ASIATICA. 713 of the blood could possibly be remedied by the absorption of liquid. The stagnation of blood in the capillaries of the lungs, induced by the paralysis of the heart and thickening of the blood, explains one symp- tom, for which I could give no explanation in 1848, that is, the feeling of anxiety and oppression, which is rarely absent in the algid stage. The change of the blood in the pulmonary capillaries is just as neces- sary for the respiratory act as the change of air in the air-cells ; and stagnation of the circulation induces the feeling of want of air and oppression, just as is done by obstructions in the bronchi and alveoli, which impede the entrance and exit of air. The very slight amount of carbonic acid in the air expired by cholera patients shows that, in spite of the extensive movements of the chest and the unimpeded en- trance of air to the air-cells, respiration is imperfectly performed. Lastly, the complete arrest of the secretion of urine in the algid stage, and its diminution even in cholerine and cholera diarrhoea, are easily explained. "We know that the amount of urine secreted depends chiefly on the amount of lateral pressure in the glomeruli of the Malpighian capsule; we have already explained, that in heart and lung diseases, which induce imperfect filling of the heart and arteries, the secretion of urine is diminished; hence it is not strange that the urine should be suppressed in the algid stage of cholera, where the heart’s action is reduced to a minimum, and the pulse cannot be felt even in the large arteries. The low temperature of the periphery of the body appears partly due to the diminished production of warmth, partly to the diminished supply of warm blood to the skin (from the weakened ac- tion of the heart). Cholera asphyxia runs a very acute course. Many patients die in six, twelve, or twenty-four hours. The algid stage rarely lasts longer than two days. The evacuations often cease some time before death, and we must be careful about regarding this as a favorable sign, as it is not due to cessation of the transudation, but to paralysis of the in- testinal muscles. On the contrary, patients in whom the evacuations continue for a long time recover more frequently than those in whom they cease suddenly. It would be wrong to decide from this fact that an excessive and long-continued transudation into the intestine had a favorable influence on the course of the disease, or was at least unim- portant. It would be much more correct to interpret the fact thus: In cholera, the occurrence of paralysis of the intestines is one of the most unfavorable symptoms, and the continuance of the evacuations shows that the intestines are not yet paralyzed, and so justifies a more favorable prognosis. The death of the patient is a gradual “ going out; ” the rattling in the throat especially, which takes place shortly before death in most diseases, is absent. In favorable cases the pas- 714 ACUTE INFECTIOUS DISEASES. sages become fewer and less copious, and the liquids taken into the stomach are no longer vomited. The first signs of improvement, which always introduce the change in the disease, are soon followed by symp- toms which show that part of the liquid taken is absorbed, and that the blood is consequently thinned. The capillary circulation is re- stored, the pulse returns to the carotids, then to the radial arteries; the cyanosis disappears; the skin resumes its color, and the face loses its distorted appearance; the disease passes from the algid stage to that of reaction. Occasionally, this stage offers no peculiarities, and forms the beginning of convalescence; then, when the asphyctic symp- toms have ceased, there are a few more copious passages, with dis- tinctly fecal odor. Even on the second or third day there are pulpy or formed stools, or else constipation. Every thing indicates that the lost epithelium has been regenerated. We may compare these cases to those where a superficial dermatitis from a blister has been entirely removed in a few days by regeneration of the epidermis. When the stage of reaction forms the commencement of convalescence, even the stagnation in the capillaries during the algid stage has not led to considerable disturbance of nutrition in any organ; only there is ex- ceptionally albumen in the first urine evacuated, on account of the stagnation in the veins that precedes the reestablishment of the nor- mal circulation. In other cases, where the damage to the intestine is less quickly and completely repaired, the violent evacuations cease dur- ing the stage of reaction, but a moderate diarrhoea, with fluid, badly- smelling greenish stools, continues; the pulse remains small; the tem- perature of the extremities low, and the patients are in great danger of dying from exhaustion on an exacerbation of the intestinal disease. But there is not generally a return of the algid stage with disappear- ance of the pulse, cyanosis and coldness of the body; the incomplete reaction is more apt to pass into the so-called typhoid stage of cholera, but not unfrequently it ends in protracted convalescence, after the diarrhoea has ceased. Sometimes after the algid stage the pulse not only returns, but becomes unusually full and strong, the previously sunken temperature rises above the normal height, the cheeks turn dark red, the eyes are injected, and the signs of fluxionary hypereemh to the brain and other organs appear. These violent reactive symp toms are difficult to interpret. They most probably depend, at least partly, on the abnormal quality of the blood, and the consequent im- pediment to the capillary circulation. The symptoms of violent reac- tion also pass imperceptibly into those of the typhoid stage, or into convalescence. The opinion, which I advanced from my observations of the first cholera epidemics, that the temperature was only dimin- ished at the periphery while it was elevated within the body, has been CHOLERA ASIATICA. 715 proved to be correct on the whole. From numerous careful observa- tions of the temperature in cholera patients, J:lterbogTc arrived at the following results: 1. In the algid stage, the head, extremities, etc., are colder than in almost any other disease. 2. In the algid stage, the temperature of the cavities of the body, such as the vagina and rectum, is the highest (that can be measured) in the body, and it should always be taken for measurements. 3. In the algid stage, whether the case be favorable or fatal, the temperature within the body is usually in- creased, more rarely normal, most rarely diminished, although no cause for this has ever been found in the pathological symptoms during life, or on autopsy. 4. In the algid stage, the temperature of the whole body usually rises with the approach of death, but does not appear to increase afterward. But there are cases where this rise does not take place without our being able to find any reason for this deviation. 5. The commencement of reaction is not accompanied by any elevation of temperature, but the interior of the body usually cools off, while the outer parts warm up. 6. In cases of protracted reaction, the tempera- ture of the whole body generally sinks below the normal. 7. The in- flammatory sequelae generally, if not always, cause a decided eleva- tion of temperature. 8. During perfect convalescence, an abnormal elevation of temperature is often seen, without any pathological cause for it being discoverable. The general name of “ cholera typhoid ” has been given to the secondary symptoms that often follow the proper cholera attack. From the fact that these sequelre follow cholera asphyxia almost exclusively, never simple cholera diarrhoea, rarely cholerine, and do not constantly follow the first form of the disease, we may conclude that they do not directly depend on infection with cholera poison, but are based on the pathological processes during an attack of cholera, par- ticularly of the severest form. As we have already seen, the same state of affairs occurs in typhus, where also the proper symptoms of poisoning are often, but not always, followed by secondary affections due to the typhus. It may be readily seen that the stagnation of the thickened blood in the capillaries, and the consequent interruption of nutrition, if they last for several hours, a day, or more, may have a very injurious effect on the nutritive condition and functions of the organs; and we have already mentioned a series of inflammatory symptoms whose remains were found in the bodies of persons who died after the termination of the actual cholera attack. This view of the origin of the secondary diseases (the cholera typhoid) also agrees with the fact that they most frequently occur when the algid stage has been very marked and protracted. The fact that the secondary inflammations remain more or less latent, and often betray them- 716 ACUTE INFECTIOUS DISEASES. selves only by symptoms of excessive adynamia (“typhous symp- toms”), is a peculiarity shown also by other inflammations when they attack debilitated persons. We shall only call attention to the fact that in old, decrepit persons, if physical examination be neglected, the outward resemblance and the subjective symptoms often cause pneu- monia to be diagnosed as catarrhal fever, nervous influenza, typhus, etc. According to my experience, acute croupous nephritis, with the retention of urine that it causes, by plugging up the uriniferous tubules, is the most frequent sequel of cholera asphyxia, but is by no means the constant cause of cholera typhoid, as is often asserted. If the se- cretion of urine remain suppressed after the disappearance of the symp- toms of collapse, or if the scanty urine contain quantities of albumen and fibrinous casts for days, if vomiting recommence, and the patients complain of severe headache, and become comatose, or have epilepti- form convulsions, we may make a diagnosis of acute croupous nephri- tis and so-called uraemic intoxication. In such cases the skin has oc- casionally been found incrusted with crystallized urea. The first or second day after the cessation of the asphyctic symptoms many pa- tients pass a normal or even very large amount of urine; and the albu- men, which is at first constant in it, usually disappears after a few days, nevertheless they fall into a state of great apathy and stupor, or mut- tering delirium, the tongue becomes dry and crusted, the pulse fre- quent, and often double; the temperature is elevated; the patients slip down toward the foot of the bed, and the disease so exactly re- sembles a severe typhoid, that there is no doubt the name cholera typhoid wTas intended for these cases. Besides the above symptoms, there is usually diarrhoea, with fetid evacuations mingled with shreds of epithelium; and, while the patients can scarcely be aroused from their comatose state by loud cries or other irritants, they twitch the face or recover consciousness, and complain of pain, if strong pressure be made on the abdomen. In these cases there is diphtheritic inflam- mation of the intestines, which often succeeds the catarrhal or proper choleraic enteritis, and which is perhaps induced by the irritation of the denuded intestines by their contents; most patients who fall into this state die of exhaustion. If, instead of diphtheritic inflammation of the intestine, there be a similar affection of the genitals, a pneumonia, pleurisy, or some other inflammatory sequel of cholera, the appearance of the patient does not materially differ from the above description. The typhoid symptoms due to the fever prevail, and the subjective symptoms of the local disease fall into the background, or disappear entirely. Lastly, in some cases, neither during life nor on autopsy can we find any local disease to which to refer the exhausting fever, of which many patients die after the cholera proper has run its course CHOLERA ASIATICA. 717 Peculiar importance has been attached to the fact that, during the so- called cholera typhoid, a maculated, papular, or erythematous exanthe- ma has been observed ; and the “ cholera-exanthema ” has even been compared to the “ typhus-exanthema,” and its occurrence regarded as a proof of the similarity or relationship of cholera typhoid and typhus. The exanthema is not, however, so constant a symptom of cholera ty- phoid as to be pathognomonic, and according to my observation it oc- curs chiefly in those cases where sinapisms have been applied repeat- edly or continuously to the extremities during the algid stage, or where the extremities have been rubbed energetically. The exanthema, which chiefly affects the limbs, often extends to the trunk, hence its occur- rence seems to me to be due to continued stagnation of the circulation, and consequent interruption of the nutrition of the skin, and to be favored by precedent irritation of the skin. Moreover, attention has recently been called to the fact that the diagnostic importance of the exanthema of typhoid fever has been overvalued, and that roseola spots and erythema also occur in many other feverish diseases. Treatment.—We shall not discuss the sanitary police regulations by which we may hope to arrest the progress of cholera epidemics; and shall only call attention to the fact that, in the Mecklenburg epi- demic of 1859, it was shown that the quarantining and locking up, which, from the experience of previous epidemics, were declared to be utterly useless, were found to afford full protection when energetically and perseveringly followed out. Since a person, suffering from an ap- parently simple and harmless diarrhoea, may carry the cholera-poison to a previously healthy place and there induce a fatal epidemic, places that would be protected must cut themselves off from all communica- tion with the rest of the world. It would be very satisfactory if the attempts to dry the soil of cities by drainage, and by improving the erection of privies, should have the desired result of lessening the pre- disposition of the affected places for extensive cholera epidemics. It would also lead us too far, were we to treat fully of the police regula- tions that physicians, in places where the cholera has appeared, must require of the proper authorities, and here we can only make certain suggestions. Since the privies, cess-pools, dirty gutters, etc., favor the development of the cholera-poison, they should be energetically cleaned and disinfected. Stools of cholera patients should never be thrown into the common privy. One of my pupils, Dr. Reich, while still a student at Greifswald, was cholera physician at Tribsees, a small town on the Mecklenburg border, where he succeeded in urging the police to empty all the privies and have a certain quantity of solu- tion of sulphate of iron poured into them. Large tanks, filled with this fluid, were placed before each house to facilitate this procedure, 718 ACUTE INFECTIOUS DISEASES. which was strictly enforced on the inhabitants. But it has not been proved, on the contrary, it is much doubted by competent authority, whether sulphate of iron, which so well removes the unpleasant smell from privies, also interferes with the development and increase of the cholera germs. The epidemological section of the Berlin Academy of Medicine recommend the disinfection of body and bed linen by boiling in water; for the disinfection of privies, chloride of lime (ten parts, in solution, to one hundred of feces); for bed-pans, night-stools, etc., they recommend a mixture of two parts of permanganate of soda, forty-five parts of sulphate of iron, and fifty-three parts of water (ten parts to one hundred of feces, or a wineglassful for each person); for the disinfection of dwellings where cholera patients have been sick, chlo- rine gas. Physicians should also persuade the proper authorities to have prepared sufficiently large and properly-constructed lazarettos, well supplied with nurses, where patients with suspicious diarrhoea may be separated from those with well-marked cholera; they should urge the supply of healthy nourishment to the poor by soup and eating houses, and that the people may be informed, by temperate and simple publications, of the danger they run by neglecting an ordinary, pain- less diarrhoea. Lastly, where it is possible, places should be arranged where the inhabitants of houses that have been attacked may find shelter. The prophylactic rules for physicians to recommend to their own patients, on the outbreak of a cholera epidemic, are as follows : since there is far more danger in a city where cholera is prevalent, and still more in a house where it has broken out, than in other places, it is sensible for persons, who can make a long journey without great incon- venience, to fly from the disease. Such persons should be sure—1, to start on their journey soon enough; 2, to go off as far as possible; 3, not to return till the last trace of the disease has disappeared. We should strictly forbid those who must remain from using a strange privy. It is remarkable that this important and certainly not super- fluous advice is not given in the cholera regulations published by Griesinger, JPettenTcofer, and Wunderlich. If I were writing regula- tions for the cholera, before treating of disinfection of privies, I should urge not to rely on it, and not to visit even a carefully-disinfected privy that is used by strangers. There are many heads of families who would not object to buying a night-stool for themselves and family during a cholera epidemic. We should also let our patients be careful about their diet; i. e., avoid all food that is difficult of diges- tion, and all articles of diet and drink that tend to produce diarrhoea. Complete and sudden change of the mode of life is not advisable, and wc should allow the moderate use of good red wine and strong beei CHOLERA ASIATICA. 719 that is not too new and has not become sour. On the other hand, all excess should be carefully shunned. The foolish assertion, that these rules are useless, as many persons who are careful of their diet are taken sick, while others who live carelessly escape, should be an- swered with rational arguments, and persons who are susceptible to reason should be shown that no one knows that he is not already in- fected with cholera, and that the impending attack will certainly have a very severe course, if some other injurious influence besides the cholera-poison be acting on the intestinal canal. Lastly, the patients should be advised to send for a physician as soon as they are attacked by a diarrhoea, and to remain in bed till the physician comes, to drink a few cups of hot coffee or peppermint-tea, and to take some “ cholera drops ” which they should have on hand. It cannot be denied that energetic diaphoresis occasionally averts an attack of cholera. At least, in every cholera epidemic, we see persons that have been at- tacked by copious diarrhoea, great debility, cramps in the legs, and even vomiting, and who, on account of these symptoms have drunk large quantities of hot liquids (usually coffee with rum), buried in the bed-clothes and reeking with perspiration, while the passages, which were often discolored and beginning to resemble rice-water discharges, and the vomiting also, have ceased. Experience also teaches that in such cases, if the sweating be arrested too soon, a true cholera attack not unfrequently comes on, and that it is well not to let a cholera patient leave his bed till he has had a formed stool. The cholera drops, usually named after some well-known physician, that are sold by the apothecaries during cholera epidemics, consist of laudanum, generally with the addition of some ethereal tincture, which is super- fluous and often detracts from the efficacy. Their use without medical advice should be recommended, because opium is one of the most efficient remedies against cholera diarrhoea, and because its success is the more certain the more recent the case. The so-called Russian cholera drops are particularly celebrated: I>. tinct. valer. aeth. 3 ij; vin. ipecac. 3i; tinct. opii 3j; ol. menth. pip. gtt. v. Hi. S. twenty to twenty-five drops every hour or two. While the most careful prophylactic treatment often fails, vre are still less able to fulfil the indications from the cause or from the dis- ease, after cholera has once broken out. In almost every epidemic, especially tovrard its close, when the malignancy of the disease has abated, and the number of recoveries is greater than that of the deaths, certain specifics are recommended both by physicians and quacks. But their reputation has never lasted through the first weeks of a sub- sequent epidemic. Radix sumbul, carbo trichloratus, and other rem- edies recommended as panaceas in cholera, have very justly been 720 ACUTE INFECTIOUS DISEASES. thrown aside. Hence we must content ourselves with striving1 to ful fil the symptomatic indications, and we shall do this the more success- fully, the more closely we attend to and combat those symptoms on which the others depend. The symptomatic treatment which, in the first epidemics, consisted in attempts to elevate the fallen temperature by vapor-baths, and by having the patient drink hot teas during the algid stage, but not allowing them a drop of cold water, and in at- tempting to draw blood from all cases of cholera asphyxia, was cer- tainly incorrect. Depression of the temperature of the body is a late occurrence in the series of symptoms induced by the cholera infection; warm tea, which is more readily vomited than any other drink, is not nearly so well borne as small quantities of cold water; venesection cannot raise the depressed action of the heart, on which the venous congestion depends. The symptomatic treatment of cholera requires, first of all, attention to the intestinal disease, the arrest of the acute catarrh and extensive transudation of serum from the intestinal capil- laries, the source of all the other symptoms and of the danger. The second symptomatic indication is, to replace the water lost from the blood. If we succeeded in making a cholera patient sweat while the transudation into the intestines continued, we should injure him by the increased abstraction of Avater. Lastly, the third indication, Avhich we must bear in mind from the first, is to combat the threatening paralysis of the heart. We shall not discuss whether opium (the most frequent prescription in genuine intestinal catarrh, and the last refuge in all other diarrhoeas), besides retarding the movement of the intes- tines, also lessens the secretion of the intestinal mucous membrane, and the increased transudation from the intestinal capillaries; at all events, it OAves its frequent use in cholera to its antidiarrhoeic action. Even after satisfying themselves that, in many cases, opium has had no effect on cholera diarrhoea, most physicians seek its aid in new cases, because they have sometimes found it of undoubted benefit even in this affection. I fully agree Avith this treatment, and, before trying other methods, I give opium for cholera diarrhoea, although not in the form of cholera drops but in the shape of Dover’s poAvder, or as tinc- ture in mucilage, Avithout the addition of any ethereal substance. If the patient has taken a number of doses of opium (half a grain to a grain) in the course of a feAV hours, and the diarrhoea has improved, it is Avell to continue it in smaller doses till a formed stool shows that the excessive transudation into the intestines has ceased. If, on the other hand, in spite of the repeated doses of opium, the diarrhoea continues or groAvs Avorse, if the patient collapses visibly, if his skin groAvs cool, and the dejections lose their color, I regard the continuation of opium as contraindicated; Avhile, in such cases, I haATe had the best results from CHOLERA ASIATICA. 721 cold compresses frequently applied to the abdomen, and from the ad- ministration of calomel (a grain every hour). In regard to the speedy favorable effect of this treatment, especially of the application of cold compresses to the abdomen, on most patients, in regard to its favor- able influence on the entire disease, and the principles which induced me to employ it, I refer to my brochure already mentioned, “Die Symptomatische Beliandlung der Cholera,” Magdeburg, 1848, and would only mention that, in 1854, when Ifeufer was commissioned to instruct the Bavarian physicians in the treatment of cholera, he recommended my method as being the most successful, according to his experi- ence. Nitrate of silver, which has been recommended by many per- sons, especially by Levy of Breslau, and which I have frequently em- ployed, because, a priori, it seemed the most efficient, did not succeed with me. The second indication, to replace the loss of water from the blood by supplying water, is best attained by giving the patient small portions of ice-water, or small pieces of ice to swallow at short inter- vals. Large quantities of liquid, especially of warm drink, are usually vomited at once. At all events, since cholera patients have been almost universally allowed to drink cold water, they suffer less than when, in spite of the torturing thirst, they were allowed no drink, or, at most, warm tea. As the paralysis of the heart disappears, as the transudation from the capillaries ceases, and the normal functions of the stomach and intestines are restored, the circulation usually becomes normal at once, and, without the use of any stimulant, the action of the heart, even where reduced to a minimum, may become greater than normal within a few hours. But this does not prove that stimu lants are useless or unnecessary in the treatment of cholera; in the earlier epidemics, they were almost exclusively employed. As soon as the pulse grows small and the patients are evidently in collapse, stimulants should be given from time to time, to try and prevent com- plete paralysis of the heart, until the termination of the acute disease in the intestines. Among the stimulants, champagne that has stood on ice is preferable to most others, especially to the ethereal oils, car- bonate of ammonia, etc., because, along with its stimulant action on the nervous system, it has no irritant effect on the gastric and intes- tinal mucous membrane. In poor practice, rum or arrack, diluted with water, is best. In some cases it is well to alternate the administra- tion of ice and ice-water with a few cups of hot strong coffee. It is often vomited again, but frequently not till the pulse has become fuller, and the temperature somewhat elevated. If the evacuations upward and downward have ceased, while the continuance of the symptoms of collapse shows that paralysis of the intestinal muscles, and not arrest of the transudation, has induced this change in the disease, stimulation 722 ACUTE INFECTIOUS DISEASES. is the proper treatment, and the return of the evacuations is the best evidence of its success. Frictions of the skin with tincture of mustard often relieve the painful cramps in the muscles; but I would warn against the very common application of mustard-plasters. For, even if they be left on a long while, the patients rarely complain of their burning, and the attendants are so excited by the fearful appearance of the patient that they lose their presence of mind, and forget the sinapisms, and I have seen them left on half a day, and during conva- lescence the patient has been troubled by obstinate and painful inflam- mations of the skin induced by the mustard. Of course, nourishment cannot be given to cholera patients during the actual attack; but, even after the attack is over and reaction has begun, we should be very careful about the food, and in order to protect the diseased intestine from injury, we should give nothing more irritating than diluted milk, meat-broth, and biscuit. Nutritious and solid food should not be allowed till pulpy and consistent stools appear. Infringement of this rule is generally severely punished. No general rules can be given for the treatment of the stage of re- action, and still less for the sequelae of cholera comprised under the name of cholera typhoid, for the treatment must be based on a careful analysis of the symptoms in each case. The former custom of bleed- ing for violent reaction should be discontinued. If there be evidences of great fluxion to the brain, we should apply ice compresses to the head and leeches behind the ears. But we must take care not to mis- take the hydroceplialoid that often occurs in children after an attack of cholera with hyperacmia and oedema of the brain. If the severe symptoms of cholera typhoid depend on uraemic intoxication, we may employ the treatment already laid down, little as is the prospect of success. If the attack be followed by an asthenic fever with typhoid symptoms, and the belly be puffed up and painful, and thin but colored and badly-smelling evacuations are passed from time to time, we may cover the abdomen with cataplasms, and order small doses of calomel and opium. In the same way, when treating inflammations of the different organs occurring after cholera, we must bear in mind the ex- haustion of the patient. BLOODY FLUX—DYSENTERY. CHAPTER XVI. Etiology.—Dysentery is an infectious disease (when treating of diseases of the intestinal canal, in the first volume, we spoke of “ca- tarrhal dysentery,” which does not depend on infection) ; but it differs from typhus, and other infectious diseases, in that the infection with dysenteric poison induces perceptible pathological changes in the in- DYSENTERY. 723 testinal canal only. The anomalies observed in other organs, and in the blood, during dysentery, as well as the more or less severe fever accompanying the disease, are secondary symptoms, induced by the intestinal affection. Dysentery is thus closely allied to cholera, where the infection also causes, first, a severe disease of the intestinal mucous membrane, and, secondarily, as a result of this primary disease, changes in the composition of the blood, in the circulation, and in the nutrition of the various organs. Of course, the intestinal affection is not the same in dysentery as in cholera, and consequently its influence on the blood differs from that of cholera. Dysentery poison cannot be directly observed, as an organic, living substance, any more than the poisons inducing other infectious diseases can, but the reasons so often repeated, especially when speaking of typhus, induce us to refer dysentery also to an infection of the body by a certain species of low vegetable organism, and to speak of a “ dysentery germ,” as we have already spoken of a “ typhus germ ” and a “ cholera germ.” From this point of view, we may, to some extent, understand the facts which have been determined by thorough observation concerning the spread of the disease. Dysentery results, although not exclusively, from a miasm; or, in other words, the dysentery germ grows, flourishes, and increases, out- side of the human body, and persons staying near its locality are in danger of being attacked by it. The circumstances favorable to the increase and propagation of dysentery poison, among which a high temperature and a certain amount of moisture are prominent, exist in the tropical regions; there the disease is endemic through large por- tions of country. According to the classical work of Jlirsch, in Europe only the peninsulas, as the south of the continent, and the islands about them, constantly offer such favorable conditions for the increase of the dysentery germ as to cause the disease to be endemic there. But, through almost all Europe, the conditions for the increase and propagation of dysentery, which is endemic with us also, are occasion- ally so favorable, especially late in the summer, that the disease be- comes epidemic. The circumstance that dysentery is not endemic or epidemic in all regions where high temperature and moisture con- stantly exist, justifies the conclusion that these are not the only things necessary for the growth of the germ, or else that it is not so widely spread as to be found everywhere that conditions favorable to its de velopment exist. The coincident epidemic or endemic occurrence of dysentery and intermittent is frequent, but not at all constant, accord- ing to the recent observations of Ilirsch. Dysentery exists where the requirements for malaria, marshes, etc., are not present. It attacks the open country oftener than the city. 724 acute INFECTIOUS DISEASES. The dysentery germ appears to reproduce itself always, or un- der favorable circumstances, in the body of the infected person, and it would seem that the dejections of the patient contain the contagion thus formed, or its components; for, while it has not been proved that one person catches dysentery from another, it is more than probable that the disease may be communicated to healthy persons through the dejections of dysentery patients, or by the night-stools, bed-pans, or enema syringes that have been used by them. This causes dysentery to resemble cholera, while it speaks against the asserted connection between it and malaria. Why should not the same or similar influ- ences, such as high temperature and moisture, favor the development of various specific low organisms, just as it does the increase of differ- ent varieties of higher plants and animals ? Catching cold, getting wet, great fatigue, the use of unripe vege- tables, and other injurious influences, have been advanced as causes of dysentery, and it cannot be denied that persons exposed to these influ- ences are more readily affected than others. Nevertheless, infection with a specific poison is the sole cause of this disease, and the part that the above influences play in the etiology is only to render the organ- ism more sensitive to the action of the poison; in other words, they increase the predisposition to dysentery. Anatomical Appeakances.—The anatomical changes found in the intestines of dysentery patients, on autopsy, are a type of diph- theritic inflammation. The diseased portions of mucous membrane are infiltrated with a fibrinous exudation, and, as a result of their compres- sion by the exudation, are necrosed and changed to a slough. If the slough be cast off, a loss of substance in the mucous membrane re- mains. According as this loss of substance is superficial and of slight extent, or deep and extensive, the destruction of the mucous mem- brane is, or is not, capable of complete repair. In the former case only can the intestine become perfectly well, while in the latter, in place of the membrane destroyed, there is a callous cicatricial tissue, which not unfrequently constricts the intestine. In the mildest grades of dysentery we find the mucous membrane of the large intestine, especially the summits of the folds projecting inward, deeply reddened by ecchymosis and injection, and to some extent infiltrated by a grayish-white, soft exudation, covering the epi thelial coating. In these cases, it looks as if the diseased part wyere covered by a bran-like coating; but if we scrape off this coating with the handle of a scalpel, tlfere remains a superficial loss of substance, which shows that the exudation did not lie on the mucous membrane, but entered into it. The submucous connective tissue is infiltrated with serum, and swollen. The serous coat appears cloudy and dull DYSENTERY. 725 from oedema. This change occurs chiefly, and generally exe.usively, in the large intestine, and it is rare for the dysenteric affection to ex- tend to the lower portion of the small intestine. In higher grades of the disease, more glutinous, or more hard, membranous gray-white layers cover large portions of the interior surface of the intestine; they are removed with difficulty, and only along with the mucous mem- brane. If they are already detached, the submucous tissue lies exposed. The whole intestinal wall appears thickened by the excessive oedema of the submucous tissue, and of the muscular and serous coats, but cer- tain parts, corresponding to the spots formed by the exudation, are especially swollen, so that they form nodular prominences on the inner surface of the intestine. When dysentery is of this high grade, the serous coat of the intestine usually participates in the inflammation, and is covered with a thin layer of fibrin, which unites it to the sur- rounding parts. The diseased intestine is evidently dilated, and is filled with epithelial masses, shreds of exudation, and with an albumi- nous fluid mixed with more or less blood; it usually contains no feces. In the highest grades of dysentery, according to Rokitansky, “ large portions of the mucous membrane are changed to a black, rotten, friable, charred mass, which subsequently is not unfrequently thrown off and passed as tubular pieces; the submucous tissue either appears infiltrated by charred-looking blood and by a bloody serous fluid, or else pale, and the blood in its vessels is consumed to a black, stiff, powdery mass; but later, as a result of the throwing off of the dead parts by a reactive inflammation in the deeper layers, it appears infil- trated with pus. Besides a dirty-grayish discoloration and loss of lustre, the peritoneal coat is in some places injected by dilated capil- laries, and covered by a brownish, discolored, ichorous exudation. The foul-smelling intestine, containing a blackish-brown fluid, like coffee-grounds, is either in a state of passive dilatation, or it is collapsed, and, when the process has lasted a long time, the muscular coat is shrunken, pale, faded, and readily torn.” The glands of the mesocolon belonging to the diseased portion of intestine are more or less vascular, swollen, and relaxed. The liver is nyperasmic, and in the malignant dysentery of the tropics it is not un- frequently the seat of abscesses, which are doubtless due to the intes- tinal veins carrying ichor or emboli from the diseased intestine to the liver. If death do not occur at the height of the disease, the dysenteric process either subsides, or a slow inflammation (“ chronic dysentery ”) remains, which subsequently carries off not a few of the patients. In the former case, the edges of the loss of substance are approximated, by the contraction of the connective tissue which forms their base, till 726 ACUTE INFECTIOUS DISEASES. they finally come in contact, if the loss has not been too great. Then, as in cicatrizing ulcers of the stomach, there is sometimes stricture, sometimes not. If, on the other hand, the opening be very large, its edges do not come together, and we find more or less extensive patches of the inner surface covered, not by mucous membrane, but by callous connective tissue. According to Rokitansky’s apt description, this tissue not unfrequently forms “ fibrous bands and striae, which project in the shape of seams into the intestine, cross each other in various directions, and often form valvular or ring-shaped duplicatures in the intestine, thus inducing a very peculiar stricture of the colon.” If, on the other hand, the intestinal disease takes a chronic course or tends to recovery, the losses of substance become chronic ulcers, and those changes occur in the intestine which we described as follicular ulcera- tion. In the thickened, strongly pigmented, mucous membrane, the inflamed follicles become ulcers, at first round, afterward irregular; occasionally, also, in the thickened submucous tissue, abscesses and fistulous passages form, and subsequently perforate the muscular coat and induce peritonitis or abscesses about the rectum. Symptoms and Course.—Occasionally, premonitory symptoms precede the actual outbreak of the disease for several days; these consist in an undefined constitutional disturbance and irregularity of digestion, especially loss of appetite, thirst, slight colicky pains, and inclination to diarrhoea. The commencement of the disease is rarely characterized by a chill, and not often by rigors even, or other symp- toms of fever. But in most cases dysentery begins with an apparently innocent diarrhoea, during which the faeces passed are not suspicious- looking, which is preceded by very moderate colicky pain, and is ac- companied by very little, if any, of the tenesmus which afterward be- comes so painful. But the more frequently the passages succeed each other, the more severe and continued become the colicky pains (tor- mina ventris) which begin some time before each evacuation, and shortly before its occurrence attain great severity. The evacuations are accompanied by a very torturing and painful bearing down of the rectum, to which is often added strangury. In spite of the severe and long-continued straining, proportionately slight, non-feculent, mucous, gray-colored masses (dysenteria alba) or muco-bloody masses (dysen- teria rubra), 'and occasionally pure blood, are evacuated. In some cases a few hard scybala are from time to time passed with the mucous or muco-bloody masses. Immediately after an evacuation the patient feels relieved, and usually has pain only on hard pressure against the abdomen, especially in the region of the colon; but soon, often even in a few minutes, the tormina begin again; the patient writhes ana groans, and, when the pains have attained the highest grade, tenesmus DYSENTERY. 727 recommences, and again a small quantity of dysenteric dejections of a sickening odor is passed. Sometimes this scene is repeated twenty or thirty times in twenty-four hours. If at first absent, febrile symptoms always come on in the course of the disease. Where the intestinal le- sion is moderately intense, the fever has an erethetic or synochal char- acter ; the pulse is moderately frequent, full, and hard. But in the high- est grades of the disease the fever acquires an asthenic character very early; the pulse becomes small, and very frequent. According to the character of the fever, dysentery has been divided into inflammatory, adynamic, and putrid, or typhous. This classification corresponds very nearly with the different grades that we described above. Even in the mildest grades, and when the fever is moderate, the patients are greatly run down by the loss of albumen, the pain, and the loss of sleep; they become pale; the pulse, at first full, grows small; there is great mental depression; the dulness and want of spirits are very marked. If we filter the dejections, and add nitric acid to the filtrate, we shall find that the albumen in it is sufficient to stiffen almost the whole contents of the reagent-glass, even where the dejections scarcely have a reddish tinge, and only solitary blood-corpuscles are found un- der the microscope. This great loss of albumen also explains why, in favorable cases—where, after four to eight days, the tormina and tenes- mus grow less and gradually disappear, and where, often by the end of the first, or the beginning of the second week, the masses passed again become feculent—the convalescence is almost always slow. The character of the blood of a convalescent from dysentery is, as Schmidt aptly remarks, very similar to that of a person with Brights disease; and I can confirm, from my own experience, the observation that gen- eral dropsy follows slight cases of dysentery far more frequently than it does other diseases of equally short duration. In the higher grades of dysentery, the evacuations succeed each other at very short intervals, the colicky pains scarcely cease, and oc- casionally become unbearable; the abdomen is sensitive to even a light pressure. The tenesmus also is more continued and severe than in the milder forms. The dejections contain a great deal of blood, nu- merous flocculi and shreds, and occasionally large membranous masses. In many cases large quantities of pure blood are evacuated. At first the pulse is more frequent and full; later it becomes very frequent, while its fulness usually diminishes rapidly. There are also great con- stitutional disturbance, loss of appetite, dry tongue, deep physical and mental depression, and frequently dulness of the mind and slight delir- ium. If the disease runs a favorable course, the symptoms gradually subside, the intervals between the evacuations become longer, the dejections again grow brownish and feculent; the epithelial and exu- 728 ACUTE INFECTIOUS DISEASES. dation masses, as well as the blood, which long continues to be mixed with them, diminish; the pulse rises, the tongue grows moist, the mind clearer ; but convalescence is always slow, and, in the most favorable cases, weeks elapse before the patient can leave his bed. If the dis- ease is to prove fatal, the pulse becomes smaller, the apathy increases, consciousness is lost, the complaints of pain and tenesmus cease, the evacuations are involuntary, and the patient dies, as in other rapidly- exhausting diseases, of general paralysis. If the disease pass from the acute to the chronic form, as is very often the case in the higher grades, the fever disappears, and we have the symptoms of follicular ulcera- tion of the intestines. Diarrhoea generally alternates with constipa- tion ; occasionally normal feces, with muco-bloody masses clinging to them, at other times only a puriform fluid from the ulcerating mucous membrane, is evacuated; the patients become very much emaciated, and, after languishing for months, usually die of marasmus and dropsy. If the losses of intestinal mucous membrane heal, leaving a cicatricial stricture, the symptoms of protracted dysentery of high grade are fol- lowed by those of stricture of the intestine. For the rest of his life the patient suffers from habitual constipation, and the various incon- veniences accompanying this state. On carefully inquiring into the causes of chronic abdominal diseases, we can frequently trace them to a dysentery that existed several years previous^. In the highest forms of dysentery, the putrid or septic forms of authors, after the disease begins as above described, the passages as- sume a discolored, brownish-red or blackish color, and a carrion-like odor; and large, black, sloughy shreds of mucous membrane are not unfrequently mixed with them. The pulse soon becomes small and very frequent, the extremities cool, and the body burning; the patients are collapsed, the countenance distorted, the tongue and gums are cov- ered with dry sordes, and the mind is very dull. Tormina and tenes- mus cease very early in the disease; the discolored, thin, fetid passages are passed involuntarily, owing to the relaxation of the sphincter, and they excoriate the parts with which the}'’ come in contact. In such cases, to the symptoms of adynamia are often added those of an acute haemorrhagic diathesis, bleeding from the nose, petechia, etc. During the first days even, the patient may die of septic dysentery; and re- covery is very rare in this form of the malady, which occurs chiefly in camps, besieged towns, or under other unfavorable conditions. Dysen- tery patients with the higher and highest forms of the affeetion do not often die of peritonitis or pyaemia ; in the tropics not a few probably die later from the hepatic abscesses which develop during the disease. Treatment.—Prophylaxis demands that the circumstances which experience shows to favor the development and propagation of dysen- DYSENTERY. 729 teiy poison be removed as much as possible; the rules for obtaining this end are, according to what was said above, partly the same as those treated of in the prophylaxis of intermittent fever, partly those of typhus and cholera. Since the dejections of dysentery patients are very probably the bearers of the poison reproduced in the infected or- ganism, prophylaxis further requires that the bed-pans, enema syringes, etc., of dysentery patients should never be used for other persons, and that the dejections should not be thrown into the common privy, but into a separate pit, and disinfected with a solution of sulphate of iron. Lastly, prophylaxis requires the avoidance of all those causes which increase the tendency to dysentery by rendering the body more sus- ceptible to the action of the poison. Little probability as there is of a person acquiring dysentery by eating unripe fruit, sleeping on the wet ground, etc., if he be not at the same time exposed to the dysen- tery poison, it is still certain that, during an epidemic, these causes favor the outbreak of the disease. We cannot fulfil the causal indications, or those from the disease in dysentery, as we know no antidote that counteracts the poison. The attempt to arrest the disease by active treatment with bleeding, emetics, purgatives, large doses of opium, etc., has very properly been abandoned, and, at present, the treatment is limited to combating the symptoms. But the symptomatic treatment of dysentery only prom- ises good results, if we bear in mind the dependence of the diarrhoea, tormina, tenesmus, and other symptoms, on a diphtheritic inflammation of the intestinal mucous membrane. If we do not attend to this fact, but give opium to arrest the diarrhoea even in cases where hard masses of faeces are collected above the inflamed portion of intestine, we shall render the disease worse, for impacted and decomposed faeces alone are enough to excite a diphtheritic inflammation. In the milder grades of dysentery it is well to begin the treatment with a mild laxative, such as castor-oil or decoction of tamarinds, and to return to this rem- edy every time that the dejections contain no faecal matter for a day or two. The reason for this treatment has just been explained. It is only advisable to give an emetic, of ipecac, or tartrate of antimony, in cases where the stomach is filled with undigested substances. Even in the mildest grades of dysentery, the patient should carefully keep in bed, and eat nothing solid, but live on soup diet. If he be strong and full-blooded, mucilaginous water-soup is sufficient; but, if he be weak and anaemic, it is well to attend to keeping up the strength from the first and to advise concentrated meat-broths. Most patients are relieved by the application of warm poultices to the abdomen. If the tormina be very severe, and be not relieved by the cataplasms, or if the abdomen be unusually sensitive to pressure, we shall find great 730 ACUTE INFECTIOUS DISEASES. benefit from the application of leeches to the abdomen (in adults ten to twenty), and allowing the bites to bleed for a time under the poul- tices. Internally we may give an emulsion, and at evening a moderate dose of opium. This treatment is enough for many cases of mild dys- entery ; but in others, in spite of it, the passages increase in number, the tormina and tenesmus are more severe, and the fever augments greatly. In such cases, as well as in the higher grades of dysentery where local abstraction of blood is almost always indicated, the ad- ministration of calomel with opium is the most trustworthy treatment. It is customary to give one grain of calomel with a quarter of a grain of opium every two hours; and I think this treatment, especially when combined with five to ten grains of Dover’s powder at bed-time, de- serves the preference over large doses (gr. x) of calomel, which have also been recommended. If salivation result from the continued use of calomel, we must stop it, and continue the opium alone, then it is best to give the tincture in mucilage, or in a weak infusion of ipecac. In just such cases a combination of opium and acetate of lead is highly spoken of. But I always consider it best, besides the small doses of opium given during the day, to give a full dose at night. If this treat- ment also fail, we have still less to expect from the internal adminis- tration of nitrate of silver and the vegetable astringents, especially tannin. According to my experience, the employment of the latter remedy in the form of enema, which is praised by many authors, is objectionable on account of the difficulty of giving a clyster when the tenesmus is so great, and on account of the increase of the tenesmus caused by the most careful injection as well as by the medicament itself. Moreover, if the remedy is to come in contact with the whole of the diseased surface, the enema must be very large; the contents of a simple enema syringe do not pass much above the rectum. In the highest grades of dysentery, treatment is almost always with- out benefit. The great prostration of the patient, the threatening paralysis forbid the abstraction of blood as well as the administration of calomel and opium, and we must limit ourselves to maintaining the strength of the patient as well as possible, and preventing general paralysis, by the administration of tonics and stimulants. In chronic dysentery, especially when the tenesmus has abated, enemata of solu- tions of nitrate of silver or sulphate of zinc deserve most confidence. If there be no collection of faeces above the seat of disease, or if the muco-purulent and bloody masses are accompanied by the passage of thin faecal matter, we may give astringents internally also, and in such cases I prefer catechu ( 3 ij to § vj water and § ss gum-arabic, a table- spoonful every two hours) to tannin and nitrate of silver, as it is doubtful if the latter reach the intestines in a very efficient form. If TRICHINOSIS. 731 stricture of the intestine remain after dysentery, it is to be treated as previously described. CHAPTER X Y 11. TRICHINA DISEASE—TRICHINOSIS. There may be some doubt in what division of special pathology trichina disease should be considered; whether it should be treated of among the diseases of the stomach, as the first seat of the disease is there, or among the diseases of the organs of motion, as the trichinae pass from the intestinal canal into the muscles; or among the infec- tious diseases. In the present edition I have decided to treat of tri- chinosis among the infectious diseases, as I here uphold the depend- ence of the infectious diseases on the presence of a lower organism, more strongly than I did in former editions. The origin of trichinosis from a contagium vivum is proved. The symptoms have the greatest resemblance to those of the infectious diseases. Even the period of incubation is common to both. "VVe may go still further and say that there is far less doubt about trichinosis being an infectious disease than about any other disease belonging to this class. Etiology.—For more than twenty years numerous punctate, white bodies had occasionally been seen in the muscles, on autopsy, which the microscope showed were small cysts containing a thread-like worm, wound up spirally. This worm, the trichina spiralis, showed no sexual organs, and it was altogether obscure whence it came, how it reached the muscles, and whether it was capable of further development. We have already shown that the supposition, according to which the muscu- lar trichina was the undeveloped state of the tricocephalus dispar, was soon found to be erroneous. From experiments, by Virchow, Leuck- art, and others, of feeding animals with flesh containing trichina?, it was shown that the muscular trichinae become free in the stomach and intestines of the animals fed, during the digestion of the meat; in a few days they attain the length of three or four millimeters, and form male and female perfect animals, intestinal trichinae. In the female, which is far more numerous and about two-thirds larger than the male, innumerable eggs develop, and from these young ones escape, living, from the body of the mother, even in from five to eight days, and move freely in the intestines. The young brood of the intestinal trichinae now soon perforate the Avail of the intestine, part of them passing into the abdominal cavity, part betAveen the folds of the mesentery to the spinal column, thence to the diaphragm, abdominal muscles, and fol- lowing the intermuscular connective tissue to the other muscles of the body. The number of these Avandering trichinae is innumerable. They 732 A.CUTE INFECTIOUS DISEASES. are particularly numerous about the ends of the muscle, where it be- comes tendinous, probably because their further progress is obstructed at these points. Trichinae have a particular preference for the muscles of the loins, diaphragm, the intercostal and cervical muscles, and for those of the eye and larynx. In the extremities, as a rule, “ the fur- ther from the trunk, the fewer tricliinas in the muscles” (Reny). In the human Being, at least, they seem never to enter the muscles of the heart. The wandering of trichinae induces parenchymatous and inter- stitial myositis. The free, emigrating trichinae, which gradually attain the length of one-third of a line, are not visible to the naked eye. At the point where they finally become attached, the irritation they induce leads to a development of the sarcolemma, and thus to the formation of a capsule, which is egg or lemon-shaped. This capsule grows thicker; calcareous salts are deposited in it, and it is the trichinae enclosed by such calcified capsules that are visible to the naked eye. At least two months are required for the formation of a perfect capsule. The etiology of the trichina disease in animals is still obscure. Of course the solution of the question, whence come the trichinas in pork ? is very interesting, and of great practical importance. It is probable that they acquire them chiefly or solely by eating tricliinous rats. It is well known that pigs not unfrequently eat live and dead rats, and it is also known that rats not only frequently have trichinas, but that they often die of them. In the human being the trichina disease results solely from eating tricliinous pork. The raw flesh is the most dangerous, hence the dis- ease is proportionately more frequent and more severe in those who have the bad habit of eating raw meat than in others. More fre- quently than in the raw form, pork is eaten prepared in a manner that does not kill the trichinae. Even large pieces of well-boiled or baked pork, which do not show any red spots on being cut, and into which we may easily pass a fork without a feeling of grating, never contain tricliinas. But they may exist in roast pork, whose external portion only has been exposed to a temperature of 55° R. [156° F.], while the inner part has not been heated so much, looks bloody, and is somewhat hard and coherent. . And even in small pieces of meat, and in the various forms of sausages, if they be cooked for only a short time, the trichinas remain alive in the parts distant from the surface. Trichinas are found especially often after the use of so- called fresh blood and meat sausages, of meat-balls, and similar preparations. Long-continued salting (pickling) of pork, without the addition of water, kills the trichinas even in large pieces ; on the other hand, numerous trichinae may survive in pickled meat that has onlv TRICHINOSIS 733 remained a short time in a weak solution of salt. Smoking the meat only kills those trichinae that are near the surface. The so-called quick smoking, where the ham is painted with pyroligneous, acetic acid, or creasote, and left in the smoke only a short time, or not at all, affords the least protection. Poisoning by raw hams, chitterlings, brain pud- ding, chopped sausage, and other slightly-smoked varieties of sausage, is often seen. The fact that smoked trichinous flesh is repeatedly eaten without injury, is partly because it has been carefully pickled for a long time before smoking, and partly because the meat in ques- tion had been kept for a long time, and completely dried, which also kills the trichinae. Very few cases of encapsulated trichinae, and not a single one of acute trichina poisoning, have been observed in southern Germany; this is because the people there dislike raw flesh, even when pickled and smoked. Since all persons who eat living trichinae are not equally affected, and as the severity of the disease is not by any means always in pro- portion to the number of trichinae probably introduced into the stom- ach, we may speak of a greater or less predisposition to trichinosis. But the causes on which this predisposition depends are not yet known. We can only assert that it is connected with the condition of the gastric and intestinal mucous membrane, or with the character of the contents of the stomach and intestines, and that, after the use of trichinous meat, severe diarrhoea, by which the still undigested por- tions of flesh, with the trichinae contained in them, are evacuated, is to be regarded as favorable. Children have a certain immunity to trichinosis; at least children recover from trichina poisoning, from which they certainly are not exempt, more readily than adults, per- haps because they do not digest a part of the meat. Anatomical Appearance.—On autopsy of the lower animals that have been poisoned with trichime, if they have died or been killed dur- ing the first weeks, besides the numerous intestinal trichime and young ones that have already entered the muscles, we find in many cases the remains of enteritis and peritonitis. On the other hand, on autopsy of human beings who have died in the first week or two after accidental poisoning by trichime, we never find exudation in the intestine or peri- tonaeum, but only the signs of a more or less intense intestinal catarrh, and often a decided swelling of the mesenteric glands. This is doubt- less because, on intentionally poisoning, a much larger number of trichinae is given them than is swallowed by a person accidentally so poisoned, consequently a much larger number of the trichinas pass through the intestinal walls, and the lesion caused by them is far more intense. After the fifth week, distinct signs of interstitial and parenchymatous inflammation appear in the muscles as fine, grayish- 734 ACUTE INFECTIOUS DISEASES. red striae. The microscopic examination of such spots shows that in them the muscular fibrillae have broken down to a granular detritus mass, while the interstitial connective tissue is increased by fresh pro- liferation. The number of trichinae in the muscles is the greater, and the parts affected more extensive, the longer the disease has lasted. In protracted cases we find even the muscles of the extremities con- taining quantities of trichinas. This circumstance, and the experience that even in the seventh and eighth week we find living intestinal trichinae, filled with eggs and embryos, render it not improbable that the intestinal trichinae bear young not only once but repeatedly, and that they pass into the muscles at different times. The other changes found in the bodies of trichina patients are not pathognomonic, and cor- respond with those found in the bodies of persons who have died of other diseases, accompanied by high fever and rapid exhaustion. Ac- cording to Cohnheim, even the muscles have no constant and charac- teristic appearances, except the above-mentioned anomalies, and a cer- tain density and toughness, but in regard to their color and moisture vary greatly, just as they do in typhus. In many cases there are signs of extensive bronchitis, and of hypostasis in the lungs, or pneumonic infiltration, and sometimes thromboses in the veins. Lastly, when the disease has lasted a long while, and the fever has been very severe, in some bodies we find the parenchymatous degenerations of the liver, kidneys, and heart, which we have already mentioned. Symptoms and Course.—Since Zenker, in 1860, made the impor- tant discovery that the entrance of trichinas into the human body caused a severe and even fatal disease, a number of violent epidemics of trichinosis have been so carefully observed and described, that the symptomatology of the newly-discovered disease is now as well de- termined as that of most other maladies that have been known a long time. Before the trichinas which have entered the stomach are set free by the digestion of the flesh in which they are embedded, the patients have no trouble. In some cases, which Henz calls insidious trichino- sis, even when the trichinae have become free, when they have mated and are rearing their young, and when the young brood perforate the intestinal canal, there are no signs of an intestinal disease. Such pa- tients have a good appetite, regular bowels; they feel fatigued and depressed, and complain of travelling pains, and a certain stiffness in the limbs, it is true, but they can go out and attend’ to their business. Gradually the vague pains are localized in certain muscles: these swell, become hard and rigid; oedema, fever, and other symptoms characteris- tic of trichinous myositis are developed. It is most probable that, when the disease runs this course, onlv a few trichinae have reached the stom< TRICHINOSIS. 735 ach, or remained there, and that consequently the development of the intestinal trichinae and their passage through the walls have only slightly interfered with the functions of the stomach and intestines, while suc- cessive broods and repeated emigrations of young trichinae have filled the muscles with the parasites. It is difficult to explain the occasional sudden change of insidious trichinosis into dangerous forms, unless it be due to an extensive emigration of a new generation of trichinae into the respiratory muscles. This insidious commencement of the disease, with its total absence of gastric disturbance, is in striking contrast with the very trouble- some intestinal symptoms observed at the commencement of some cases. The first cases in the famous Hederleben epidemic were re- garded as cholera, because the patients were attacked with severe vomiting and purging, which could not be checked. Three of them died on the sixth day of the disease, with the symptoms of paralysis and thickening of the blood. For the diagnosis between “trichinous cholera ” and Asiatic cholera, and cholera morbus, Kratz and Ruprecht lay particular stress on the peculiar stretching, muscular pain, which is located chiefly in the flexors of the extremities, and is increased both by movement and pressure. The commencement of trichinosis with cholera symptoms, which is not frequent, shows that an unusually large number of living trichinae have reached the stomach, and that consequently the gastric and intestinal walls have suffered more than usually. This idea is supported by the fact that cholera symptoms have hitherto been observed only in cases of poisoning with raw meat. The absence of all intestinal symptoms, as well as severe attacks of vomiting and purging, is only exceptionally observed after the use of trichinous flesh. Far the greater number of patients complain in a few hours, or not till a few days after the poisoning, when the young brood has been hatched, of severe pressure in the stomach, of eructa- tion and nausea, combined with a feeling of great heaviness and de- pression. There is almost always diarrhoea, the passages being at first brownish, subsequently yellow, thin, and accompanied by more or less severe colicky pain. These gastric symptoms are soon accompanied by those of the entrance of the trichinae into the muscles, vague pains, and a feeling of stiffness, as well as a peculiar oedema of the face affecting chiefly the eyelids, in which the conjunctiva also participates occasion- ally, so that there is chemosis. The movements of the patient are now sometimes very much impaired, partly because their muscles be- come more rigid and less supple, partly because every attempt to stretch them is very painful. The different muscles swell considerably, become tense and as hard as caoutchouc, just as in the rigor mortis. According to Cohnheirri’s description, in severe cases the constant and 736 ACUTE INFECTIOUS DISEASES. characteristic position of the patient is as follows: “ He lies on the back with the shoulder and elbow-joints sharply bent, and the hands slightly flexed; on the other hand, the knee and hij> joints are but slightly bent, or nearly straight; so that the patient is unable to lift the arm, extend the forearm, sit up, or bend the knees.” Cohnheim explains this position correctly, by ascribing it to the patient’s attempt to assume a position where the different groups of muscles are the lease extended; with the swelling of the muscles there is oedema extending from the arms toward the hands, from the thighs toward the feet, but not affecting the scrotum or labia. Besides the above symptoms, from the third to the fifth week of the disease, there are frequently attacks of severe dyspnoea, which subside again in the sixth week; they doubt- less depend on trichinous disease of the respiratory muscles. Where the disease attacks the muscles of the glottis, the voice is sometimes lost; sometimes affection of the masticatory muscles causes trismus; participation of the glossal and pharyngeal muscles induces impaired movement of the tongue and dysphagia. Trichinosis is accompanied by high fever, with slight morning remissions. Although this fever is unmistakably not of zymotic origin, but depends on the extensive dis- ease of the muscles, and is to be regarded as a symptomatic inflamma- tory fever, it very closely resembles the fever observed in the course of typhus and other infectious diseases, and occasionally the tempera- ture curves can scarcely be distinguished from those of typhus. The evening temperature sometimes reaches 106°, that of the morning re- mains somewhat lower. The bodily temperature does not become normal for a long time, often not till the sixth or seventh week. The frequency of the pulse corresponds with the temperature, and in severe cases reaches 120 to 140 beats a minute. Copious perspiration, with a miliary eruption, is somewhat characteristic of the fever accompany- ing trichinosis. The constitutional influence of trichinous fever, the effect that it has on the sensoriuin and other functions, is just the same as that from great elevation of the bodily temperature in other dis- eases. The pulse becomes small and weak, the thirst painful, the tongue dry, the patients sink into apathy, or become delirious; occa- sionally there are twitching and trembling of small groups of muscles, bed-sores over the sacrum, and with these symptoms the patients may die of exhaustion. The usual symptoms of trichinosis are more or less modified by the occurrence of extensive bronchitis, hypostasis, or pneumonic infiltration; but the pneumonic infiltrations alone (which are frequent) betray their presence by subjective as well as objective symptoms, by piercing pain in the side, cough, dyspnoea, etc. If the disease takes a favorable course, as not unfrequently happens in severe cases, the muscles gradually become less rigid and painful, the bodih TRICHINOSIS. 737 temperature and tlie pulse lower, the perspiration less copious, the thirst abates, appetite returns, but the exhausted patients are confined to bed for a long time, and regain strength very slowly. Just as after other severe diseases, oedema often occurs during convalescence, affect- ing even the scrotum and labia. Treatment.—Prophylaxis.—When the flesh of a slaughtered hog is carefully examined microscopically, and no trichina; can be found, it may be used, even raw, without danger. There is no doubt that, if competent microscopists examined the flesh of all the pigs killed, new epidemics of trichinosis might be avoided with certainty. I do not think it would be at all difficult, either in the city or country, to find competent persons, who could be so instructed, by microscopical courses and popular theoretical teaching, that they could tell certainly whether specimens of meat referred to them contained trichina? or not. My brother, by his trichina catechism, and by practical courses, has fully qualified a large number of the laity for the microscopical examination of pork for trichina?. Nevertheless, in opposition to celebrated author- ities, I must say that I regard the introduction of an obligatory micro- scopical examination of meat as no guaranty against new epidemics of trichinosis. I have not sufficient trust in the conscientiousness of the persons to whom this would be intrusted, especially in the rural dis- tricts, to believe that, after they had examined for trichina? in vain for years, they would continue their examinations with the necessary ex- actness. It is evident that a microscopical examination, if not carefully conducted, might prove dangerous, because persons relying on it might carelessly eat uncooked meat. The only certain protection against trichina-poisoning is, to eat no pork that has not been prepared in a way that would kill any trichina? present. Whoever wishes to eat uncooked pork, smoked ham, sausage, etc., should previously inform himself that the pig from which they came contained no trichina?. I advise my students to warn their patients (even those living in places where the flesh is examined) against the use of all dishes prepared from pork, which we mentioned under Etiology as being dangerous. Treatment of the Disease.—From what we have said of the tenacity of life of muscular trichina?, there is little hope of finding a remedy by which they may be killed without injury to the patient in whom they exist. Friedreich's proposal, to use the very bitter nitropicrate of pot- ash in trichinosis, has not proved serviceable; it certainly permeates all the tissues of the body, but the views regarding its anthelmintic action differ. It is also doubtful whether benzine, as recommended by Mosler, has any effect. There is far more hope that, some time, we shall find a remedy to kill intestinal trichinae, or remove them from the bowels. This indication exists, not only in recent cases, but must be remem- 738 ACUTE INFECTIOUS DISEASES. bered later in the disease, since it is proved that, after Aveeks, liv- ing intestinal trichinae, filled AATith embryos, may exist in the bowels, and consequently it is not improbable that there may be neAV emi- grations of trichinae into the muscles. The presence of diarrhoea should not deter us from beginning the treatment Avith a few doses of calomel or castor-oil, and, if necessary, repeating this treatment occasionally, as advised by Huprecht. It does not seem to me to be proved that benzine, of which Master gives 3 j to 3 ij in gela- tin capsules, is inefficacious against intestinal trichinae, so that we should cease using it. The rest of the treatment is symptomatic. For the fever, quinine is advised ; for progressive prostration, stim- ulants ; for the subsequent anaemia, the preparations of iron. Mos- ler proposes, as the most efficacious remedy for the painful SAvelling of the muscles, the use of long-continued Avarm baths. [The origin of the trichinae in SAvine is an interesting question. The assertion that the disease originates in the rat is doubted, for it is said that trichinous rats come from slaughter-houses, where they may have fed on hogs’ flesh. It is at least as probable that trichinae are original with sAArine as that they are so with rats ; and they may be propagated by pigs which eat offal of other pigs containing intestinal trichinae and embryos, or by their eating the flesh itself, as sometimes happens.] ADDITIONS TO THE REVISED EDITION OF 1880. SECTION I.—ACUTE INFECTIOUS DISEASES. 1.—P. 586. Bacteria have been found in the blood of scarlatina patients, as in that of measles and small-pox patients ; when rabbits were inoc- ulated with this blood, the bacteria were found in their blood. Dr. Carpenter thinks that scarlatina is sometimes caused by decompos- ing blood from slaughter-houses. It has been variously stated that cases occur from defective seAverage. The sources of contagion are so \raried and often so obscure that in a large city at least it is dif- ficult to exclude this mode of origin from any case. Among the complications of scarlatina, acute nephritis is proba- bly the most common. Its symptoms usually begin in the desqua- mative stage during the third Aveek. In this stage also comes a rarer complication, viz., acute articular rheumatism ; this lias the same symptoms and endocardial complications as simple rheuma- ADDITIONS TO TIIE REVISED EDITION OF 1880. 739 tism, but it is more apt to be accompanied by severe joint-disease and suppuration. Besides these, there may be inflammations of serous membranes, pleuritis, pericarditis, or meningitis, also pneu- monia, etc. The prognosis is less favorable than in measles ; mild epidemics are less frequent, and even mild cases often become complicated ; this is justly called a treacherous disease. In not a few epidemics the mortality will reach one-third. Cases in children under five years or in old persons, those with high fever, intense and long-con- tinued eruption, or with any of the severe complications, are unfa- vorable. 2.—P. GOT. Some persons are so susceptible to the poison that it acts ever when very dilute, as coming through the windows from the next house, or by letters, paper money, etc. The nature of the poison is. not understood. Minute spherical bodies (bacteria) have been found in the contents of the pustule, in the shin around it, and in the in- ternal organs ; but it is not certain that these bacteria are the vehi- cles of the contagion. The results of the experiments of Chauveau, Burdon-Sanderson, and others, in removing the bacteria from vac- cine lymph, do not agree with those of M. Wolff and Hillier. Weigert believes that the first changes, which occur in the cells of the rete Malpighii, are not of inflammatory nature, but are analogous to changes caused by diphtheritis in the epithelium. The cells of the rete are transformed into translucent flakes of irregular shape and size, and without nuclei; they cause an irritation, which induces an effusion of lymph that separates the affected cells, forming small interspaces in a sort of mesh-work made by the remains of the epi- dermis. About these interspaces there is active cell-proliferation, and numerous pus-corpuscles escape from the vascular loops lying under the swollen papillse of the skin, which gradually fill the meshes as the efflorescence ripens. In regard to the central excavation in many pocks, it is not sc constant appearance, and is said by Bind- ffeisch to occur where the pustules develop around a hair-follicle or sweat-gland, and to be caused by the covering of the pustule being held down by the epidermis projecting into these depressions. On the mucous membranes variola is often accompanied by catarrhal redness and swelling ; but where these membranes are exposed to the air, there is a pustular eruption like that on the skin. When patients die in the eruptive stage, the spleen is usually much enlarged. When delirium occurs in small-pox, it may be due to the fever, 740 ACUTE INFECTIOUS DISEASES. and partly perhaps to the inflammation of the scalp causing liyper- semia of the brain. Delirium is more apt to occur in those who have previously been drinkers. A stage of great excitement is often followed by one of weakness with feeble heart-action, which may end fatally. As the pocks dry up the parts around become pale and less swol- len, and the patients are again recognizable ; the inflammatory pain gives place to excessive itching, and probably many of the resulting cicatrices may be due to scratching. Small-pox has numerous complications, such as bronchitis, pneu- monia, pleurisy (often with purulent effusion), diseases of the larynx, meningitis, uterine haemorrhages, abortions, and affections of the eye and ear. Some observations seem to show that the protection from vacci- nation does not begin till twelve or thirteen days after the opera- tion ; but it should be resorted to even after exposure, in hopes it may at least render the course of the disease milder. Inoculation, which was formerly in vogue, usually induced very light cases, but deaths sometimes occurred. It is a question how long a patient convalescent from small-pox continues to produce contagion, and how long he should be isolated. He should be isolated till the stage of desquamation is entirely past—say fourteen days after the disease is over. Dr. Waters, in the London “ Lancet,” says if sun-light be ex- cluded from the room, the disease is arrested at the papular or vesicular stage, and the pain, itching, and smell are less annoying. Constant applications of emulsion of bitter almonds seem to have the same effect. 3.—P. 654. If the fresh dejections of a typhoid patient spread the contagion, persons immediately about him would be most apt to contract the disease, but this does not seem to be the case ; so the stools proba- bly undergo some change which render the germs in them more active. Some authors believe that typhoid may develop spontane- ously, others that it is always due to contagion ; the poison from the patient reaching some place favorable to its development, and thence again entering the human body. Most epidemics of typhoid begin after the heat of summer, when the soil is dried to the greatest depth ; but others occur indepen- dently of the time of year or of the dryness. Their extent is usually limited, perhaps to a town or one part of a city, or perhaps to a single house, in which case it must be referred to infected drinking-water ADDITIONS TO THE REVISED EDITION OF 1880. 741 or defective drainage. Typhoid is relatively rare during pregnancy, but doubts are rising against the-old view that it hardly ever occurs in the puerperal state. The period of incubation probably varies, but seems to average about fourteen days. The parenchymatous degeneration of the muscles of the heart may result in passive dilatation ; the feeble action following the de- generation may induce disturbances of the circulation, especially emboli, particularly if the weakened contractions favor coagulations in the heart, and particles from these coagula pass from the right heart into the lungs or from the left into the aorta, and reach the spleen, kidneys, etc., causing haemorrhagic infarctions and possibly abscesses. Venous thrombosis, especially of the crural vein, not unfrequently follows the impairment of circulation. Among the nervous symptoms, besides the febrile delirium or stupor, there may be others referrible to cerebral cedema or haemor- rhage, meningitis or embolism ; mental disturbances, which usually recover ; paralyses of the facial, ocular, or vocal muscles, or para- plegia. If these paralyses cannot be attributed to severe changes in the nervous centres, they usually recover. Besides the albuminuria, which disappears with the disease, there are sometimes haemorrhagic infarctions or even diffuse ne- phritis. In severe cases of typhoid, bed-sores are not uncommon in spite of the greatest care, and as a sequel of the disease there may be numerous furuncles. According to JOiebermeister, from 7 p. m. to 8 a. m. is the best time for baths ; this being the natural period for remission, if the patient can be kept for several hours at a temperature approach- ing normal, he may better stand a brief increase of temperature. Another good time for the bath is about noon, at which time also most patients show a tendency to remission. Menstruation, which usually comes in typhoid at its regular time, is customarily regarded as a contra-indication to baths ; but in severe cases they may be continued, as they may with almost any of the complications, such as diarrhoea, meteorism, etc. Even in threaten- ing paralysis of the heart, some stimulant may be given, and fol- lowed by short tepid baths. SECTION II. CHRONIC INFECTIOUS DISEASES. CHAPTER I. SYPHILIS. Of late years the study of syphilis has undergone a complete revolution, and the new doctrines have been adopted with remarkable readiness by almost all prominent writers upon the subject, even by those who a few years ago were their most zealous opponents. In previous editions of this work I have expressed a disbelief in the an- cient views, according to which inoculation by one and the same poison at one time acts locally, and at another induces infection and disorder of the entire system; and I there declared my preference for the modern theory, according to which there are two poisons, one of which merely induces local disease, namely, an ulcer at the point of inoculation, ac- companied in some instances by inflammation and suppuration of the neighboring lymphatic glands; while the other always gives rise to constitutional disorder, with extensive derangement of nutrition. At that time, however, I did not declare myself so unreservedly in favor of the doctrine of the duplicity of the virus (or duality, to use another common expression) as I now do. I think that it will be to the advantage of my readers if I devote a few lines to a brief analysis of the belief which a short time ago was universally current, regarding the relation of the chancre, or primary syphilitic ulcer, to constitutional syphilis, or lues venerea. It was sup posed that the secretion of the ulcer possessed virulent properties, whereby, when brought in contact with an excoriated surface, or upon penetrating through a thin coating of epidermis, it induced a specific dermatitis, and a primary syphilitic ulcer. At this stage, it was be- .ieved that the noxious power of the virus often became exhausted; and that, if we could succeed in destroying or in healing the ulcer be- fore the infection from it could involve the constitution, the disease TIIE CHANCRE. 743 would remain local; if the attempt failed, then a series of affections of remote parts of the body, resulting from constitutional implication, fol- lowed the local ulcer, the secondary and tertiary syphilitic diseases. The formation of an induration upon the base or edges of the primary sore was considered an ominous sign, proving the almost certain infec- tion of the system. Hence the attempt was usually made to destroy recent non-indurated ulcers with strong caustics, while older and in- durated sores were nearly always treated constitutionally, especially with mercury, which was almost universally regarded as the antidote for syphilis. Finally, the majority of syphilologists, following the teach- ing of Hicord, supposed that syphilis could only be propagated by the primary sore, or chancre, or, in other words, that the secretion of the chancre was the only vehicle of contagion; and that it was not con- tained in the discharge of secondary affections, nor in the blood, or secretions of syphilitic persons, a theory which was never fully credited by practising physicians. It would take too long to relate in detail how each of these propositions in turn first was doubted, then was re- futed, until at last the whole theory was abandoned as false, or, at all events, as based upon erroneous observation. We shall touch upon some of these errors in laying down the tenets of the modern doctrine. In the present chapter we shall treat first of the chancre, and of the glandular chancre or acute bubo/ after which we shall describe constitutional syphilis, the first manifestation of which consists in syphilitic induration and the primary syphilitic ulcer. To the latter we shall not apply the term chancre, according to the usage of most modern authors. As the chancre is not a constitutional disease, it might, perhaps, have been entirely separated from the subject of syphilis, and classified with gonorrhoea, and other affections of the genitals; but, although such an arrangement would be more systematic, yet, considering the extremely frequent coexistence of the chancre with syphilitic indura- tion, it does not seem so practical. The chancre often is called the w soft chancre,” in contradistinction to the sore of primary syphilis, the “ hard chancre.” Other authors call it the “chancroid,” reserving the term chancre for the primary syphilitic ulcer. Other syphilologues apply the epithet “ virulent ” to the chancre, and call the ulcer of primary syphilis the “ infectious ’ ulcer. It is very desirable that authors should agree as to the names of the two diseases, in order to allay the confusion arising from a diver- sity of nomenclature. Etiology.—We shall not discuss the question as to the origin of A.—THE CHANCRE. 744 CHRONIC INFECTIOUS DISEASES. the chancrous virus, since we have no means of deciding it; but there is no doubt that at the present time it never develops spontaneously, and that no one nowadays contracts a chancre who has not been in- fected with its virus. The chancre, then, belongs to the class of purely contagious diseases; and we are fully entitled to employ the term chancre-contagion instead of chancre-virus. Unlike the contagion of measles, scarlatina, and small-pox, the con- tagion of the chancre is not volatile, nor capable of poisoning the at- mosphere about the patient, and of infecting individuals within its reach. It is of a fixed nature, and is only found in the secretion of the sore, and in the contents of a chancrous bubo. The poison itself can- not be detected in either of these vehicles, either under the microscope or by means of chemical examination. The matter which covers the sore, and the contents of a glandular chancre, do not differ perceptibly, either morphologically or chemically, from the discharge of an ulcer of any other kind, or from the pus of other suppurating glands. The predisposing conditions for the chancre are usually more gen- eral perhaps than those of any other disease. Neither age, sex, nor constitution, seems capable of modifying the susceptibility to its infec- tion. It is true that individuals in the prime of life are more often af- fected than children or old persons; that men suffer oftener than wo- men, the vigorous and healthy more frequently than the feeble and sickly; but this is simply because the former expose themselves to contagion more than the latter, and not because they are more sus- ceptible to its influence. Hence persons with a thin epidermis are more liable to infection, because slighter injuries suffice to produce solution of continuity of their skin, thereby enabling the poison to act upon the corium. The results of sypliilization, that is, the artificial production of chancres by inoculation, seem to show that such inocula- tions, when repeated a great many times, have the effect of extinguish- ing the susceptibility to contagion. By far the most common mode of transmission of the chancre is by coitus with a person who is already diseased. Infection also some- times results from lewd embraces, from kisses, and from the use of water-closets, tobacco-pipes, tumblers, and similar articles, impregnated with the chancre-virus. Physicians and midwives are sometimes in- fected in making vaginal examinations, and conversely, women are now and then inoculated by nurse or doctor; but these and all other modes of origin of the chancre, often as they are assigned by patients, are extremely rare in comparison with that of impure intercourse. Excoriation of the cuticle or epithelium, at the point where the poison comes in contact with the genitals, favors transmission of the disease, but it has not been proved that an abrasion of the surface is essential TIIE CHANCRE. 745 to infection. On tlie contrary, chancres are often observed to develop upon parts of the genitals where the most careful search immediately after coitus had failed to detect any breach of continuity of the epider- mis. Upon other parts of the body, too, tvliere the epidermis is thin, such as the lips or the nipples, infection may occur without wound of the cuticle, while upon the hand or other region thickly covered with cuticle, as long as there is no breach of continuity, the contact of the poison produces no effect. The seat of the chancre, therefore, is most generally upon the genitals, far more rarely upon the anus, between the breasts, in the mouth, or upon the hands. Symptoms and Course.—According to the concurrent belief of all trustworthy observers, the period of incubation of the chancre-virus is a very brief one. Iticord goes so far as to declare that it has no incubative period, but that changes arise at the point of contact of the poison immediately upon its implantation, although they are not com- monly noticed at first, owing to their apparent insignificance. Course of an Inoculated Chancre.—Upon introducing some of the secretion of a chancre beneath the epidermis, through a puncture from a lancet-point, no change takes place at the point of inoculation during the first twenty-four hours. At about the thirty-sixth hour a slight redness appears, and in forty-eight hours there is a distinct, bright-red macula. In the course of the third day the macula rises into a flatfish papule, and upon the fourth day the epidermis is raised, forming a vesicle, sur- rounded by a reddened areola. In the next day or two its contents become more yellow and purulent, the vesicle transforming into a pus- tule, which bursts between the fifth and eighth day; or else, together with its contents, dries up into a scab. After rupture of the pustule, or after removal of the scab, we see an ulcer of the size of a pin’s head, or perhaps as large as a pea; it is almost circular, and penetrates into the corium in a manner disproportionate to its size. Its edge, which is oedematous from inflammation, has a puckered appearance. In the next few days, the base and edges of the sore are attacked, by a diphtheritic process, and it begins to enlarge. As the elements of the tissues are necrosed, and broken down into detritus, the base of the sore assumes a grayish, dirty, lardaceous appearance. As the diph- theritic destruction goes on irregularly at its periphery, the borders of the ulcer acquire a gnawed, ragged form. If the point of inoculation be destroyed by caustic within the first four days, the destructive pro- cess may generally be cut short. After the fourth day this is scarcely ever possible. A chancre of accidental origin begins either by a macule or papule, upon which, after repeated exfoliation of the cuticle, an excoriation and loss of substance takes place, or else a vesicle or pustule forms 746 CHRONIC INFECTIOUS DISEASES. first and bursts; or, what is more common still, the chancre proceeds from infection of a laceration, which, instead of healing immediately, becomes covered with a dirty-looking exudation. The characteristics of a sore arising in this way are not always so well marked as to admit of its ready distinction from other forms of ulceration. In doubtful cases, therefore, it is very advisable to inoculate the thigh of the patient with some of the secretion of the sore; two or three such punctures should be made, and should be covered with a watch-glass attached by adhesive plaster. As we shall hereafter learn, the inoculation of a patient having a syphilitic ulcer with some of his own matter results negatively. When the inoculation takes place, and the changes de- scribed above occur, there can be no further doubt of the chancrous nature of the ulceration. For the present, we shall merely describe the more common forms of simple uncomplicated chancre; then, after giving an account of the primary syphilitic ulcers, we propose to treat of the modifications of the chancre which arise from its complication with syphilitic induration. The common diphtheritic chancre is characterized by ragged and detached edges. The loss of substance looks as if it were made by a punch. Its most common seat in men is upon the inner surface of the prepuce, the surface of the glans and sulcus between the prepuce and glans, and, above all, the fraenulum ; less frequently, it is upon the outer surface of the prepuce, or the integument of the penis. Ulcers of the feenulum are nearly always deep and excavated, and the framulum itself is perforated. When the sore is situated in the sulcus, between the prepuce and glans, the ulceration is apt to extend, by spontaneous inoculation, over a large portion of the corona glandis. If it penetrate deeply at this point, the loose subcutaneous tissue becomes infected by the secretion, and gives rise to a virulent abscess. When seated upon the glans, it usually penetrates more profoundly than when upon the prepuce, although perforation down to the urethra, with the formation of a urethral fistula, is rare. The urethral chancre is not common. It usually begins at the mouth of the urethra, and a small loss of substance which extends inward is visible upon its swollen and deeply-reddened lips. At other times the urethral chancre is more deeply situated, and only betrays its existence by the purulent flow from the meatus and by pain in the urethra, situated at some particu- lar point, and which is increased by pressure or by making water. If a concealed urethral chancre be not complicated with gonorrhoea, it is easy to recognize it, as the scantiness of the purulent flow will attract attention, and prevent its being mistaken for a clap. Successful inocu- lation, however, is the only means of making the diagnosis sure. It is hardly ever detected, though, when accompanied by a gonorrhoea. THE CHANCRE. 747 as, owing to the copiousness of the discharge, and to the absence of other conspicuous symptoms, inoculation is almost always neglected In women, the most frequent seat of the common chancre is the vulva upon the posterior commissure, and at the entrance to the vagina. In very rare instances it appears in the vagina, and even upon the vaginal portion of the neck of the womb. When the common chancre begins to heal, the destruction ceases, and the lardaceous appearance of the base of the ulcer disappears (“the chancre cleans up”), granulations appear upon the base and edges of the ulcer, which gradually fill up the loss of substance. After the chancre has healed, there remains a cicatrix, more or less distinctly stellated, according to the depth of the ulcer. The period at which the process of repair commences is very variable. Some chancres become covered with granulations, and trans- form into simple sores, which do not secrete inoculable pus in a week or two, while others go on extending for months, and retain all their characteristics; that is, ragged edges, lardaceous base, and virulent discharge. The superficial chancre occurs most frequently upon the glans and prepuce in men; and between the labia and nymph®, and at the en- trance to the vagina, and on the neck of the womb, in women; and it appears in both sexes with equal frequence on the skin. When situ- ated upon the glans, an exact counterpart of the ulcer is usually found upon the corresponding inner surface of the prepuce. The form of the ulcer is irregular, and its surface looks as if the cuticle had been scald- ed off. At its edge there is a white border. The destructive process never extends deeply. When situated at the orifice of the prepuce, cracks occur in its folds, which render retraction of the prepuce very painful. The superficial chancre often results in phimosis and para- phimosis. In the former instance it is almost indistinguishable from balanitis, excepting by means of inoculation. When a superficial chancre is situated upon the external integument, the scanty secretion soon dries up into a thin crust, and it is not until after it has been treated with a wet dressing that its raw, reddish-yellow surface, spar- ingly covered with secretion, becomes visible. The follicular chancre develops from a sebaceous gland. Its sur- face is very small, disproportionately deep, and long retains its regular round form. The phagedenic chancre usually originates from the common chancre. Its secretion is thin, ichorous, and very offensive; its form is irregular, its base is of a grayish-white or greenish color, consisting of necrosed tissue and of infiltration; its edges are livid, and sur- rounded by coppery-red areola. It spreads rapidly, and in men it sometimes destroys a large portion of the prepuce, glans, skin of the 748 CHRONIC INFECTIOUS DISEASES. penis, and scrotum; and in women, eats away the labia, perinseum, and parts about the anus. The phagedenic ulcer only appears in broken-down, cachectic subjects, and loses its malignant character as the constitution improves. Then the devastation ceases; the diphthe- ritic coating upon the base of the ulcer is castoff; healthy granulations form, and the malignant, eating sore changes into a simple ulcer, with a tendency to cicatrize. If the constitution of the patient does not improve, or if it becomes still more depraved by the further exposure to noxious influences, especially by the use of mercury, the destructive jwocess, which continues without stopping, finally becomes complicated by a slow fever which consumes the patient. The gangrenous chancre is sometimes a modification of the phage- denic chancre, while at other times it develops from the ordinary form of the disease; in either case, the base of the ulcer and the parts about it become bluish, and are afterward converted into a black, insensi- ble moist slough. There is a dusky redness immediately around the eschar, which is encircled by a somewhat extensive and severe oedema. The disease may advance until it has destroyed a large portion of the penis, or labia and perinaeum, and life itself may be imperilled by the constitutional disturbance which accompanies the gangrene. At other times the destructive process ceases sooner; a line of demarcation forms, the sloughs separate, and the disease recovers, leaving a more or less extensive loss of substance behind it. We do not always know why chancres become gangrenous. Now and then, owing to the action of unknown causes, gangrenous chancres become of very frequent occurrence, or, at least, are more common than usual. In many in- stances, however, mechanical action, such as straining or tension of the inflamed part (as, when the chancre is complicated with phimosis or paraphimosis), chemical agents, or irritation of the sore by the putre- faction of retained secretion, may be regarded as causes of the malady. Treatment.—In proportion as the opinion has gained ground that the chancre never leads to constitutional syphilis, the old and erroneous practice of treating chancres by mercury has died out. The progress of knowledge has speedily borne fruit in this instance, the importance of which cannot be sufficiently prized. We have only to consider that, but a few years ago, at least one-half of the physicians used to subject all patients with chancres to a course of mercury, and thus often enough ruined their health by means of this pernicious poison, under the mis- taken impression that they thereby averted induration of the ulcer, and prevented constitutional contamination. Nowadays, a physician who treats a simple chancre with mercury makes a gross blunder. On the other hand, I do not think it judicious to make the treatment of a sim- ple chancre a purely local one. It will heal much more rapidly if the THE CHANCRE. 749 patient be brought under favorable hygienic influences, and if he be de- fended from all noxious agencies throughout the course of the disease. If the circumstances permit, it is well to confine him to his chamber, or, at all events, to forbid all unnecessary walking. Moreover, since the majority of this class of patients are young and vigorous, living more or less freely, and drinking spirituous liquors, it is generally advisable to place them upon a rigid diet (gruel morning and evening, with broth and a little meat at mid-day), to forbid coflee, beer, wine, or spirits, and now and then to give small doses of some saline cathartic (one or two glasses of Friedrichshaller, or Piillnaer bitter water), which may be taken in the morning, fasting. Although a chancre usually heals much more quickly under this treatment than when a strict regulation of the diet is neglected, it is merely because of the luxurious mode of life led by most patients who have exposed themselves to the infection of the chancre. The above directions are not applicable, and indeed might do great mischief, and retard the healing of the sore, if applied in the case of a badly-nourished, cachectic patient. In such a case, the diet must be nutritious and rich; the use of wine and beer is indicated, and often exerts a favorable effect upon the healing of the ulcer. The local treatment of a chancre must be similar to that of any other atonic ulcer, of which the chancre may be regarded as the proto- type. Until after the fourth or seventh day, it is advisable to de- stroy the ulcer by caustics. For this purpose, it is best to make use of the potassa fusa, the Vienna paste (quicklime, five parts; caustic potash, six parts), or the chloride of zinc, which makes a dry eschar (I*, zinci chlor., butyr. antim., aa 3 ij, f. c. pulv. alth. past, mollis). After the seventh day it is not advisable to cauterize, as then the pro- cess of healing is retarded rather than promoted thereby. As a rule, ointments should not be used, and the sore should be dressed with warm camomile-tea, or other mild, stimulating liquid. The most common applications are the aromatic wine, the black-wash (calomel 3ss; aquae calcis § ij), the yellow-wash (hyd. chlor. corrosiv. gr. j; aquae calcis § ij). The blue-wash (cupri sulp. gr. j ; aquae § j), which is almost exclusively used by Von JBarensprung, is also highly to be recommended. When the chancre is very painful, and when its dis- charge is very profuse, compresses, wet with lead-water and cold sitz- .baths, are of benefit. It is generally sufficient to dress the wound twice a day, after previously washing it or bathing the part in camo- mile-tea. Too frequent dressing does harm. If, in spite of this treat- ment, the floor of the ulcer retains its lardaceous aspect, it is advisable to sprinkle the surface now and then with a thin layer of red precipi- tate. After the sore has lost its specific character, and nevertheless is slow in healing, it may be touched lightly with lunar caustic, or dressed 750 CHKONIC INFECTIOUS DISEASES. with a wash of zinc or lead. When the fraenulum has been perforated, it is best to divide the remaining bridge of mucous membrane at once. Where a phimosis prevents the proper treatment of the chancre, injec- tions beneath the prepuce must be practised methodically, in order to remove the accumulated secretion. It is sometimes necessary to operate for phimosis; but this is never to be done excepting in urgent cases, as the entire wound generally becomes converted into a chancre. In the treatment of the phagedenic chancre, the general health of the patient must receive our first attention. Ilis strength is to be husbanded rather than reduced; and a nourishing diet, and sometimes wine, bark, and iron, are indicated. The utmost cleanliness is to be observed. As a topical application we recommend dressings of dilute so- lution of acetate of lead, or of chloride of lime ( § ss— § j to water % vj). Treatment of the gangrenous chancre is to be conducted upon simi- lar principles, paying due attention to the surgical rules for the treat- ment of mortification. APPENDIX. THE GLANDULAR CHANCRE.—THE VIRULENT, ACUTE BUBO. Etiology.—We have seen that the virus which the chancrous mat- ter undoubtedly contains (although we are unable to isolate it or to de- monstrate it to view) may be transferred to other parts of the body, and that it will cause inflammation and ulceration at its point of implanta- tion. In a similar manner the virus is very often taken up by the lym- phatic vessels, and conducted to the neighboring lymphatic glands, in which it also gives rise to specific inflammation and suppuration. A lymphatic gland thus inflamed and suppurating from absorption of the chancre-poison is called an acute, virulent bubo, or, what is better, a glandular chancre. All chancres do not cause virulent adenitis with equal frequency. It is most apt to accompany an ulcer of the frasnu- lum. Neglect of cleanliness and a too irritating mode of treatment seem to favor absorption of the virus, and the production of the viru- lent bubo. Cases seem to occur now and then, in which the virus reaches the corium through the epidermis without producing any lesion at its point of entry, but is there taken up by the lymphatics, carried . by them to their glands, where it gives rise to specific inflammation and suppuration. Such a bubo, which has not been preceded by a chancre, is called a “ bubon d’embl^e.” Symptoms ixd Course.—A virulent bubo generally makes its ap- pearance in the second, third, or fourth week, more rarely in the fifth or sixth week, and it sometimes develops immediately after the forma- THE GLANDULAR CHANCRE. 751 tion of the chancre. The first symptom of this troublesome complica- tion consists in a feeling of pain at a circumscribed point in the groin, not far from the genitals. Upon examination, we find a small lump, which, already even, is sensitive to the slightest pressure, and which corresponds to a moderately enlarged inguinal gland. The dispropor tion between the severity of the pain and the smallness of the swell- ing, the proximity of the latter to the genitals, the fact that one or two only of the glands are enlarged and never a large number of them, make us aware, even thus early, that we have to deal with an acute virulent bubo, and not with the so-called sympathetic bubo, or with the syphilitic glandular enlargements hereafter to be described. The further course of the virulent bubo varies. In very rare instances the inflammation is resolved, and the pain and swelling of the affected gland gradually subside. In such cases it is not improbable that it is merely the inflammation which has spread along the lymphatic vessels to the gland, but that the chancrous virus has not been absorbed with it, or, in other words, that the bubo is a sympathetic one. The process above alluded to, namely, the extension of an inflammation along the lymphatics to the lymphatic glands is a very common occurrence also among non-specific ulcers. Far more frequently, and probably always, in the case of a virulent bubo, the inflamed gland suppurates. In favorable cases the pus soon perforates the capsule of the gland and the adherent skin which covers it. In other instances, the connective tissue about the gland becomes the seat of an extensive inflammatory exudation, the tumor becomes much enlarged, and is no longer mova- ble. It becomes very difficult for the patient to walk, and, in spite of the efforts which he usually makes to conceal it, we can perceive that he favors the affected side as he steps. In persons with a tendency to fever, there is also an elevation of temperature, acceleration of the pulse, general malaise, and other febrile symptoms. Considerable time elapses thus, ere the skin begins to redden, and ere the circumscribed point of fluctuation makes its appearance. If a puncture then be made at this point, or if the skin assume a dark-red hue and grow thinner and thinner, until the matter is discharged spontaneously, a small portion only of the swelling subsides, and it is often as large as a man’s fist, and of an irregular, knobby form. By-and-by fluctuation, followed by escape of matter, occurs at other points; but, in spite of the numerous abscesses, weeks and months often pass by without any diminution in the size of the tumor in which they form. The course of a virulent bubo is equally tedious and intractable, if the matter which has escaped from the inflamed gland into the surrounding areolar tissue have formed sinuses and fistulous tracts, as well as when the accumulation of matter within the gland is slow to point and 752 CHRONIC INFECTIOUS DISEASES. does not discharge itself until the inflammation of the surrounding tis- sues has also resulted in numerous abscesses. After breaking of the abscess and discharge of the matter, the resulting ulcer shows the properties of a chancre and discharges inoculable pus. Its edges are ragged, bluish red, and generally somewhat undermined; its floor is covered with false membrane, and it is very slow to heal. A chancre thus produced from a virulent bubo may become phagedenic or gan- grenous, and may give rise to wide-spread destruction, which some- times terminates in erosion of the femoral vessels, or in peritonitis. Treatment.—It matters little whether a virulent adenitis be ac- companied by a chancre or not; in either case, the probability that the inflammation of the gland will not end in suppuration is so small, that we may spare the patient the applications usually recommended to discuss a bubo, such as leeching, inunction of blue ointment, method- ical bandaging, and the like. I usually cover a bubo with a simple plaster, generally the emplastrum fuscum (emplas. galbani. co.), and make it fast with a spica bandage. Under such treatment the bubo now and then subsides; in other instances, it suppurates without causing the patient much annoyance. Should fluctuation appear at a point which unmistakably corresponds to the gland, I immediately let out the matter through one or more punctures; but if the surrounding areolar tissue be already in a state of phlegmonous inflammation, and if fluctuation appear, which does not seem to be in a gland, but to proceed from a phlegmonous abscess, I am not so hasty in opening it, but prefer to wait until the parts about the softened spot are also in a state of suppuration, and until the hardness has disappeared under the pressure of the pus. As soon as this occurs, and after the skin over the point of fluctuation has become well thinned, I convert the entire top of the abscess into an eschar, by persistent rubbing with caustic potash. During this process (which I learned at the Hamburg hospital) the adjacent parts must be protected from contact with the liquefying potash. This treatment is, no doubt, painful, but has this great advantage, that no fistulous track nor sinuses ever form, and that, the day after the separation of the eschar, the bottom of the abscess presents the aspect of a healthy ulcer. According to my experience, also, this cure is much more rapid than when we have to make punc- ture after puncture, as fresh points of fluctuation show themselves, to lay open fistulae as they form, and to remove the undermined edges of the ulcer. Latterly, I have often had recourse to another mode of treating virulent buboes, and with striking effect. I put a vesicatory upon the tumor, cautiously open the resulting blister, and then allow a new cuticle to form under a simple dressing. I then immediately blister CONSTITUTIONAL SYPHILIS. 753 again, and repeat the procedure until the infiltration about the gland, which usually begins to resolve after the first vesication, disappears entirely. Then, if a fluctuating point appear, I puncture it, or destroy its covering with caustic paste. In none of the cases thus treated by me have any sinuses or fistulas formed B.—CONSTITUTIONAL SYPHILIS The question as to the origin of the syphilitic poison is quite as obscure as is that of the origin of the chancre-virus. At the present day, syphilis is a purely contagious disorder. Its venom reproduces itself in the organism which it infects, and the transplantation to an- other person, of the virus thus reproduced, is the only manner in which syphilis can be propagated. The exact nature of the syphilitic virus, or, as we may say with equal propriety, the syphilitic contagion, is unknown, since we are un- able to obtain it in an isolated form, and to test its chemical and phys- ical properties. Like the chancre-virus, however, it is of a fixed char- acter, and does not pervade the atmosphere around the patient; but its habitat is by no means confined to the secretion from the syphilitic ulcer, and to the contents of syphilitic tumors, for it is also contained in the blood. It does not seem to exist in the natural secretions of the body, such as the saliva or urine, nor in pathological exudations produced by intercurrent disease. Thus, if we inoculate a healthy child with pure vaccine lymph, obtained from a syphilitic subject, the child thus vaccinated does not become syphilitic; but, if the lymph contain a little blood, which is a vehicle for the syphilitic poison, the latter will also be implanted upon the patient. It has not yet been determined whether the virus exists in the milk of a syphilitic woman. The frequence with which the disease is transmitted to infants, from wet-nurses, may be due to the existence of bleeding excoriations upon the nipples of the nurse. In the following chapter we shall treat of its propagation during the act of generation. Liability to syphilis is so general, that an immunity to its virus, if it exist at all, is certainly very rare. The fact that healthy persons, adults, and men, are more frequently infected than invalids, women, or children, is simply because the former are more apt to be exposed to the disease than the latter. Like the chancre-virus, the syphilitic poi- son is more difficult of inoculation when the cuticle is thick and resist- ing than when it is the reverse, a circumstance which argues in favor of the practice of circumcision. Infection is also more likely to occur when the genitals are strongly developed than when they are small. Eczema of the glans and prepuce, likewise, greatly increases the dan- ger. Notwithstanding this very general susceptibility to the syphilitic 754 CHRONIC INFECTIOUS DISEASES. virus, however, the system once contaminated by it obtains an immu- nity almost absolute against subsequent infection. This very interest- ing fact is analogous to the freedom from further attacks of scarlatina, measles, and small-pox, enjoyed by persons who have once suffered from those diseases. If we inoculate the discharge of a syphilitic sore, or any other vehicle of syphilitic contagion, upon a person who has a primary syphilitic induration or syphilitic ulcer, at the moment of in- oculation, or who has already had one, we shall obtain negative results, It is this fact which has given rise to such gross errors. For a long time experimental inoculation was only practised upon individuals who were already syphilitic, and, from the negative results which followed, when blood or the secretion of secondary sores was employed, it was inferred that blood and secondary secretions were not contagious. It was not until it was determined to inoculate healthy, or, at least, non- syphilitic persons with these vehicles that it was ascertained that the want of result of the former experiment was simply due to the immunity of syphilitic persons to further infection, and that their blood, and the discharge from secondary syphilitic ulcers, were quite as infectious as the secretion of a primary sore. Exceptions to this rule seemed to oc- cur ; inoculation of the secretion of a primary sore upon the person having the sore resulting sometimes in another sore. It is now deter- mined that in such cases the syphilitic ulcer is complicated by the chancre. The ulcer which follows the inoculation is a chancre, and not a syphilitic ulcer. Contamination of the system with syphilitic virus affords no protection against infection by the chancre, any more than does the preexistence of one or several chancres secure the pa- tient from further action of the chancrous virus. Since even a person having a primary syphilitic ulcer or induration, but who has no secondary symptoms, is already secure from further syphilitic infection, we may regard the primary induration and ulcer as a sign of contamination of the system, and as the first symptom of con- stitutional syphilis. Since, however, the above-named affections stand first in the series of disorders which occur, and as the first sign of con- stitutional infection always appears in the form of an ulcer or indura- tion at the point of entry of the virus, the terms “ primary induration ” and “ primary sore ” may be regarded as perfectly appropriate. The immunity against fresh infection, which contamination with poison affords, accounts for the interesting and formerly very perplex ing fact that infants are infected by syphilitic nurses more frequently than by syphilitic mothers. Generally, a child sucking at the breast of its nurse is not at first syphilitic, and, therefore, is liable to infec- tion, while the child which sucks the breast of a syphilitic mother i? nearly always syphilitic itself, and hence can not be inoculated. CONSTITUTIONAL SYPHILIS. 755 By far the most frequent exciting cause of syphilis is coitus with an infected individual; but there are many well-authenticated cases where infection has been conveyed by the hand of a physician or mid- wife, by using a pipe, or tumbler, or privy, polluted by the venereal virus. There is no doubt, moreover, that the disease has often been propagated by vaccination, and another series of cases is known to have sprung from the use of dirty lancets, and in bleeding and cupping, by careless surgeons. Symptoms and Course.—I. The Primary Syphilitic Indura- tion, and Primary Syphilitic Ulcer.—The period of incubation of the syphilitic virus is from three to four weeks. A correct knowledge of this fact is of recent date. Prior to this discovery, which was made by inoculating healthy subjects with syphilitic virus, we were unable to account for the phenomenon that, in a large number of cases, a chan- cre (chancroid), after lasting for some weeks, would become indurated at its base and edges; and this it was which caused the false impres- sion that a soft chancre could assume a pernicious character, and change into a hard one. Experience has taught that the indurated chancre is almost always the precursor of secondary symptoms. The following is the correct interpretation of these facts: Both poisons, the chancrous, as well as the syphilitic, act simultaneously upon one and the same point; in a few days the chancre forms; the period of incubation of its virus being a very short one. Three or four weeks afterward, the time of incubation of the syphilitic contagion having ex- pired, the syphilitic induration develops at the base and edges of the ulcer. It may happen that the chancre has healed before the incuba- tive stage of the syphilis has terminated. In such a case an indura- tion forms in the scar of the chancre. The conversion of a syphilitic induration into a chancre, by the implantation of chancrous virus, may also take place. [Some observations seem to indicate that the poison of chancre and chancroid may be present on the same sore, giving a “ mixed ulcer ; ” so that an apparently soft chancre may become indurated and be followed by constitutional symptoms, and, on the other hand, inoculation from an apparently hard chancre on the bearer of it may induce a chancroid. It has, however, been asserted that inoculation of pus of any hind in a syphilitic patient may induce an ulcer re- sembling a chancre. Even on this point, where so many observa- tions have been made, opinions are not undisputed ; and we may consider that the relation of chancre and chancroid to each other, and to syphilis, is not absolutely determined in all details. After exposure to the disease, some time elapses before the de- velopment of the indurated sore, then some weeks longer before the 756 CHRONIC INFECTIOUS DISEASES. appearance of the other symptoms of constitutional syphilis. There is considerable regularity in the succession of these symptoms, re- minding us of the course of the acute exanthemata. There may even be premonitory fever and enlargement of the spleen. The so-called “secondary” symptoms affect the skin and mucous mem- branes ; in the “ tertiary ” stage there are changes in the subcu- taneous and submucous connective tissue, the bones, fibrous and serous membranes, and internal organs. This division into stages is not always accurate, as they may extend into each other ; but usu- ally they are separated by an interval of latency more or less long. Chancroid sometimes occurs in the anus and rectum from un- natural coitus, or from the pus of a neighboring chancre. A care- less physician may mistake syphilitic ulcerations of the anus for haemorrhoids ; they may cause stricture of the rectum. If syphilitic iritis be accompanied by much dimness of vision, this may be due to cloudiness of the vitreous or to retinitis. "When the periosteum and bones are diseased, the joints may become affected from the same cause ; but other joint-affections may occur incidentally, and be called syphilitic rheumatism. Even in these cases, iodide of potassium is very useful. All authors do not agree that treatment of the primary sore is useless ; but some claim that where it is recent and favorably situ- ated (on the prepuce, etc.), it may be excised and sequela? be thus prevented. Fournier says, in treating syphilis, he gives one or two grains of iodide of mercury daily for two months, then discontinues for one month ; a second treatment for two months is followed by an interval of three months, and a third treatment for one or two months. This treatment with increasing intervals is continued for two years. The second year iodide of potash is combined with the mercurial.] After inoculation of a suitable subject with syphilitic virus, whether accidental or intentional, that is to say, of a subject who is not syphi- litic, and who has never been so, and after expiration of the term of in- cubation, there arises, not a vesicle nor pustule which breaks, leaving a sore—as occurs after infection from the chancre—but a hard papule, or nodule of variable size and thickness. The smaller syphilitic indu- rations are of the size of a lentil or pea, the larger attain the size of a bean, or of a small hazel-nut. Microscopic research shows the indura- tion to be the product of profuse proliferation of cells and nuclei, which have no characteristic peculiarities, and which lie embedded between the normal elements of the parts, in the scanty connective tissue. The epidermis, or epithelium, over this lmi'd infiltration, at first does not ex- hibit any lesion; but soon the epithelial covering begins to exfoliate, CONSTITUTIONAL SYPHILIS. the new coating becomes thinner, the surface shows a peculiar glitter- ing, dirty redness, and, after repeated exfoliations, the epithelial coat is not renewed, but the surface remains raw, and gives off a scanty secretion. In other instances the surface forms a scab, which, after separation, leaves an ulcer with a hard base. The primary syphilitic ulcer may be called the ulcerative induration of syphilis. Its most common situation is upon the genitals; in men, upon the inner surface of the prepuce, and in the coronary fossa; in women, between the nymphse, at the posterior commissure, and at the entrance to the vagina. Sometimes, however, it appears upon the nipples, at the angles of the mouth, upon the tongue, and not unfrequently upon the fingers. No part of the body is exempt, and a syphilitic induration will arise wherever the virus touches a spot where the cuticle is thin, or where it has been abraded. The localities above mentioned, how- ever, are the ones most favorable to the occurrence of infection. When but a single follicle is implicated, the induration assumes the form of an upright cylinder, and, if a series of them lying close together be in- volved, the confluence of these indurations forms a hard elevation. When the induration is situated upon the lips of the meatus urinarius, that orifice forms a somewhat gaping, rigid funnel, which feels carti- laginous to the touch. Not unfrequently, when the mouth of the pre- puce is somewhat narrow, its anterior border becomes fissured during coitus. If this point becomes indurated in consequence of syphilitic infection, the prepuce can no longer be drawn back, its outlet having been converted into a hard ring. A phimosis of this kind will subside after the induration has been resolved. The bottom of a syphilitic ulcer is not lardaceous, its edges are not eroded, nor does it show any tendency to spread. All these charac- teristics are peculiar to the chancre (chancroid), nor is a syphilitic sore painful, like a chancre, being usually very indolent. It is also soli- tary, as a rule; and it is only as an exception, when several points are infected simultaneously, that several syphilitic sores are ever seen to- gether. Until the induration ulcerates, it is often overlooked; and it is not until the sore is established, that the attention of the patient or physician is drawn to it. Sometimes, the induration is so slight, that the sore may be mistaken for a chancre. In such cases all doubt may be dispelled by inoculation. The following are the more important forms recognized among syphilitic ulcers: The superficial ulcer (Ricord's chancre parchemine). In this Variety the induration forms a thin cake. An attempt to pinch up a spot of this kind between the fingers imparts a feeling as though a bit of parchment had been slipped beneath the ulcer. Its surface secretes 758 CHRONIC INFECTIOUS DISEASES. a scanty thin liquid, in which no pus-cells can be found under the micro- scope, but only a granular detritus. It often heals quickly, but the secondary symptoms follow this form of sore quite as surely and promptly as any other variety. The elevated sore (ulcus elevatum) presents an excoriation which is almost void of discharge, seated upon an indurated base of varying thickness and consistence, by which it is elevated above the surround- ing level. From time to time it is coated by a thin layer of epithelium, which generally soon exfoliates in fine scales, leaving a new excoriation. The Hunterian chancre (ulcus vallatum) not only has a hard base, but is surrounded by an elevated, hard, callous border, so that it is deeper in the middle than at the periphery. It rarely heals in less than five or six weeks. All the different forms of syphilitic sore may become phagedenic, that is, they may be attacked by a rapidly-extending diphtheritic pro- cess. The destruction then often spreads beyond the limit of the in- duration, largely involving the skin or mucous membrane. When the syphilitic induration is associated with the chancre, the operation of both poisons upon the same point results in a modification of the ulcus vallatum, that is, the border of the chancre becomes hard and callous, and surrounds it like a wall. At a later period the induration likewise appears in the bottom of the ulcer. The duration of a syphilitic induration or a syphilitic sore varies. Three months, at least, nearly always elapse ere the hardened spot recovers its normal consistence. The induration often lasts half a year, and even longer. It is remarkable that, as the secondary symptoms begin to appear, the induration begins to dissolve, and then soon sub- sides, leaving behind it a brown pigmented spot. The pigment marks the former site of the disease for a tolerably long time. When it finally disappears, the spot remains whiter than the adjacent parts, like the cicatrix of a neoplastic growth. Unless the indurated spot has also been the seat of a chancre, there is no depression. II. The Indolent Bubo and Extended Syphilitic Disease of the lymphatics,—An acute enlargement of the lymphatic glands occurs in many of the acute infectious diseases and in syphilis, the prototype of the chronic infectious maladies, the lymphatic glands always parti cipate in the disorder induced by infection of the system by this per nicious poison. The changes which take place in the glands consist ir a cellular hyperplasia, and they are but seldom the seat of actual in flammation or suppuration. More frequently, especially when the dis- ease lias been of long standing, caseous metamorphosis occurs here and there in them, and this is afterward followed by a calcification. In a few days after its development, the primary syphilitic induration CONSTITUTIONAL SYPHILIS. 759 almost always gives rise to a painless or else to a very slightly pain- ful enlargement of the inguinal glands—to indolent buboes. The number of the glands implicated is always somewhat large, and they are seldom very greatly swollen. Each gland usually attains the size of a bean or almond; and it is exceptional, and only in scrofulous sub- jects, that it becomes as large as a walnut. The surrounding con- nective tissue is not affected; the glands remain isolated, and, even when their number and the degree of tumefaction are such as to pro- duce a large lump, it is always of an irregular nodulated shape, and it can readily be perceived that it consists of a conglomeration of iso- lated glands. Sometimes a thickened and indurated chain of lymphat- ic vessels can be detected between the primary sore and the indolent bubo. In the rare instances in which indolent buboes suppurate, the skin becomes adherent to the glands beneath it, and gradually reddens, and the tumor becomes painful; some time elapses, however, before fluctuation appears. If, finally, the purulent contents escape, or if they be evacuated artificially, they leave sinuous and tedious fistulous ulcers behind them. Involution of an indolent bubo proceeds very slowly. Several months always elapse ere the swelling of the glands dimin- ishes, and often the last trace of the enlargement does not disappear for years. Whenever cheesy metamorphosis with calcification has oc- curred, small hard elevations remain for life. The usual seat of pri- mary induration being upon the genitals, indolent buboes are generally found upon the inguinal region; and it is almost without exception the glands which lie above the fascia lata, on the side corresponding to the seat of the primary sore, which are affected. In primary affections of the mouth and fingers, it is respectively the submaxillary and axil- lary glands which are involved. About five or six weeks after the formation of the indolent buboes, upon careful investigation, we shall find numerous enlarged lymphatic glands, lying far away from the point of infection and from the indolent bubo, and situated in various regions of the body. This enlargement is most frequent and conspicuous in the cervical and axillary glands, the inguinal glands of the opposite side, and the cubital and submaxil- lary glands. The size attained by these enlargements varies from that of a pea to that of a bean or hazel-nut. They are quite painless; and. even when pressed upon, are not more sensitive than other parts of the skin. These diffuse glandular swellings often last for years; and, as long as they continue to exist, the syphilis is not extinct, even though no other manifestation of lues be discoverable. Inflammation and suppuration of such glandular swellings are quite exceptional, and are then always the consequence of a complication. HI. Condylomata.—The only condylomata which are of syphilitic 760 CHRONIC INFECTIOUS DISEASES. origin are the broad ones covered by a thin coat of epidermis, 3m which, if seated upon the skin, are usually in a state of superficial ulceration, and bathed in a slimy, ill-savored secretion. The dry, pointed condylomata, which are covered by a thick layer of epidermis, are the result of local irritation, and most commonly appear at points moistened by gonorrhoeal discharge. The syphilitic condyloma is one of the most frequent symptoms of general infection of the system, and it rarely fails to appear in the series of morbid processes which gradually develop under the influence of the venereal poison. As a rule, too, the condyloma is the first symptom which succeeds the pri- mary affection and the enlargement of the lymphatics. Its external aspect and histological character have already been described. Upon the skin, the most frequent seat of the soft condylomata is between the nates; in women, between the labia; and in men, upon the scrotum and outer surface of the penis. Sometimes they spread over the inner surface of the thighs. Their appearance at the angles of the mouth is quite common; they are more rare at the commissure of the eyelids, between the toes, and under pendulous breasts. They often become fissured, especially when they have coalesced so as to form extensive growths, and in this way painful and obstinate ulcers often form. Fissures and cracks (rhagades) frequently appear in the skin about the condylomata. They are attended by severe pain and heal slowly. We have already treated of the condylomata of the mucous membrane, of the mouth and fauces (plaques muqueuses), and of the condyloma- tous growths which accompany syphilitic laryngeal ulceration. IV. Syphilitic Disease of the Skin—Syphilides—Syphilitic Ex- anthemata.—Syphilitic affections of the skin depend partly upon hy- peraemia and exudation, and partly upon the development and meta- morphoses of the “ gummy tumor ” (tubercular syphiloma) of the skin. In the former class the exudation is sometimes thrown out upon the surface of the skin, sometimes within the tissues, and sometimes in both together. A classification of the syphilides into many species has been based upon the modifications thus induced, and upon the variety in extent and magnitude of the eruption. Since, however, the classification of all other non-specific hyperoemic and inflammatory cutaneous affections is also founded upon similar data, we may be brief in our discussion of the syphilides, and confine ourselves to a description of the differences by which the syphilitic exanthemata may be distinguished from the non-syphilitic ones. The general peculiarity of syphilitic eruptions, upon which most weight has always been laid, is their color; and, indeed, all syphilitic exanthemata, when of somewhat long standing, are of a peculiar coppery-red hue ; and chronic eruptions which do not present this color, CONSTITUTIONAL SYPHILIS. 761 even though the}7 appear upon notoriously syphilitic subjects, ought not to be regarded as of syphilitic origin. This proposition, however, does not admit of inversion. A rash need not be syphilitic because it has a coppery color, as is sufficiently proved in cases of psoriasis and of acne rosacea (commonly known as “ copper nose,” on account of its appear- ance). The origin of this color is to be attributed to the addition to the redness, caused by the capillary hyperaemia, of yellow, blue, and brown pigment, the result of minute extravasations of blood, and the metamorphoses of the hsematin thus set free. In very recent cases the coppery hue is not observable, no extravasations having as yet oc- curred, or because the effused blood has not yet undergone change of color. Another characteristic of the syphilitic exanthemata (which is closely related to the foregoing one, as it also depends upon gradual transformation of the coloring matter of extravasated blood into pig- ment) is, that, after they have recovered, stains of pigment are almost always left in the skin. Syphilitic eruptions may be further distinguished from non-syphilitic ones, from their type being still less distinctly marked than that of the latter. In the same subject we almost always find patches which be- long in part to one and in part to another species, and here and there a spot about w7hich wTe shall be in doubt what category to assign it to For instance, there are often red spots which we hesitate to call roseola/ because they are covered with scales of epidermis; but, on the other hand, we cannot regard them as psoriasis, because their coat of epi- dermic scales is so much thinner than in the non-syphilitic psoriasis. The situation of the efflorescence is also of great importance in dis- tinguishing between the simple and the specific eruptions. The spe- cific exanthemata are most apt to appear upon parts of the skin which are exposed to the air, and upon • such as lie immediately above the periosteum. It is a very suspicious circumstance, when a rash which has a peculiar predilection for certain localities—as psoriasis has for the knees and elbows—appears elsewhere, upon some unusual region instead of upon its favorite seat—as when psoriasis affects the palms of the hands. Another peculiarity of a syphilitic eruption is, that the various efflorescences generally take the form of circles, or of segments of circles. It is to be borne in mind, however, that it is only -when this circular arrangement is the result of grouping, and not when it proceeds from healing of a disease in the middle while it continues to spread at its edges, that it is characteristic of syphilis. Finally, it may be added, that syphilitic eruptions scarcely ever itch. In order to determine the question of the syphilitic origin of a doubtful case, it is of importance to ascertain whether it has been preceded by a primary 762 CHRONIC INFECTIOUS DISEASES. ulcer, and whether there be any other concomitant syphilitic disease. The crusts and scabs which form in syphilis are distinguishable by being much thicker, as a rule, than those of non-syphilitic origin. This is generally because, beneath the dried, purulent contents of a syphilitic pustule, there is usually an ulcer, the product of which also thickens and dries into a scab. The kidney-shape or horse-shoe shape of specific ulcers of the skin is also somewhat characteristic. This is due to the healing of the sore at one edge while it spreads at another. The most common form of syphilitic cutaneous disease is the macu- lous exanthema, the roseola syphilitica. This is an eruption of small, irregular round spots of roseola, which here and there are often con- fluent ; and its appearance is often preceded by a febrile disturbance. The favorite seat of the rash is upon the belly, on the sides of the chest, and upon the flanks. The face is hardly ever affected beyond where the forehead and scalp join. At first the spots are bright red, but afterward become livid and coppery. Some of them are level with the skin, while others rise slightly above it. In the latter case they re- semble the wales of urticaria, although, unlike the latter, they do not itch. After lasting a long time, the roseola spots assume a dirty brownish-red appearance, and, when they finally fade, they leave a grayish-brown stain behind them. Sometimes the eruptions extend to the glans penis. In the latter situation, the epidermis over the efflo- rescence soon separates, leaving a bright-red, moist erosion, which bleeds readily, and which is not to be confounded with the superficial chancre. The roseola is one of the earliest symptoms of constitutional infection. It is never seen in inveterate cases. When treated by mercury, it usually subsides within four weeks. When neglected, it passes over into the papulous, squamous, and pustulous forms of syphi- lide. The papulous syphilide (lichen syphiliticus) is characterized by its coppery-red, and frequently, in old cases, by its brownish-red color. The papules are sometimes no larger than a millet-seed (miliary pap- ules) ; sometimes they attain the size of a lentil (lenticular papules); sometimes they are solitary; sometimes they form groups, which latter usually assume the form of circles, or the segment of a circle. Their most common seat is the junction of the forehead with the hairy scalp, although they also appear upon the trunk and extremities. When of long standing, they are usually covered with scales of detached epider mis. If, instead, small pustules form upon the apices of the papules, the eruption is generally called acne syphilitica. Like the maculous syphilide, the papulous exanthema appears early in the disease, although it is sometimes observed in its later stages. In such cases, the points of efflorescence are less numerous, and evince a still more marked ten- dency to form circles or arcs of circles. The papulous sjqflnlide is CONSTITUTIONAL SYI HILTS. 763 more intractable than the maculous, and several weeks usually elapse before it yields even to an energetic treatment. The scaly syphilitic eruption (psoriasis syphilitica) often com- mences as a syphilitic roseola or lichen. The spots are discrete, and rarely become large, although they may be very numerous. The color of a specific psoriasis is generally darker than non-specific, and the scaly layer is usually thin. Not unfrequently cracks form in the infil- trated skin, which lead to ulceration. As we have already remarked, the knees and elbows are hardly ever affected in syphilitic psoriasis. Palmar and plantar psoriasis, which always is of syphilitic origin, begins with the formation of small, round, or oval callous spots of a pale-red or yellowish color. After the thickened cuticle has become detached from these spots, or has been scratched off by the patient, the copper-colored, infiltrated cutis is exposed to view, surrounded by concentric circles of dried desquamating epidermis. This circle en- larges, while sometimes the centre begins to heal, or covers itself afresh with a coat of horny cuticle. Now and then the efflorescences, which at first were separate, afterward coalesce, causing great thick- ening of the epidermis, which cracks readily, forming extremely painful fissures or rhagades. The pustulous syphilide is called impetigo, or ecthyma, according as it produces small and pointed or large and flat pustules. They are sometimes solitary, sometimes formed in groups, and appear upon the face and scalp as well as upon the body and extremities. They are surrounded by a coppery areola, and dry up into scabs, which, when situated upon the scalp, are very annoying, owing to their liability to be torn off by the comb. Beneath the scabs of the ecthyma pustules, and more rarely under those of impetigo, there are ulcers, which eat more or less deeply into the cutis. The color of the scars, which always remain after the healing of ecthyma, is at first a coppery-red, and afterward remarkably white. Syphilitic impetigo and ecthyma are more serious affections, and appear at a later stage of the disease than any of the exanthemata hitherto described. In spite of the most careful treatment, many months often elapse ere they begin to heal. The pustulous syphilides are quite intractable, and sometimes outlast all the other symptoms of the disease. There is an eruption known as varicella syphilitica, and which, in- deed, bears a great resemblance to varicella. It is almost always pre- ceded by febrile disturbance. The vesicles, which are numerous, and scattered more or less over the whole body, spring from red maculae. The liquid contained in them is at first slightly turbid, afterward purulent, and finally dries up into round, blackish crusts, which, when they fall, leave brownish stains behind. This, also, is an obstinate 764 CHRONIC INFECTIOUS DISEASES. variety, and often drags on with repeated relapses for weeks and months. Rupia syphilitica, like ecthyma, originates in a destructive derma- titis. Its mode of development is as follows: Upon a livid, red spot, of the size of a pea or bean, there rises a flabby bleb, containing a dirty, turbid, and sometimes bloody liquid. The contents of the bleb dry up into a scab, which gradually is built higher and higher by the product of the ulceration, which is constantly eating deeper into the skin beneath it, while a ring of new vesicles forms around its border, the drying of whose contents makes the scab wider. If we detach one of these oyster-shell-like crusts, we find beneath it a foul, ulcerated surface, secreting a thin ichor. Sometimes large portions of the body are studded with numerous rupia scabs, which here and there are con- fluent. In other instances, there are only a few, which then are very large. Like ecthyma, rupia belongs to the graver affections, and only appears at an advanced stage of the disease. They heal very slowly. Not unfrequently, only one side of the ulcer beneath the scab heals, while on the other it continues to spread. In this way, horseshoe- shaped, or kidney-shaped ulcers form. The scars, which always result from rupia, are like those of ecthyma, only larger. While the syphilitic cutaneous affections hitherto described are the result of irritative and inflammatory processes, syphilitic lupus depends upon the development and degeneration of a neoplasm peculiar to this disease, which arises in the form of nodules (“ tubercula syphilitica ”) not merely in the skin, but in a variety of other organs. These syphi- litic tubercles (called “ gummata,” or “ gummy tumors,” by Virchow, even when they are of a hard consistence, and remain so while they exist, and which are called “ nodular syphiloma ” -by Wagner) have nothing in common with tubercle in the common sense of the word. Virchow counts them in the class of “ granulation tumors,” that is, tumors which even at their fullest stage of development contain no mature connective tissue, nor any analogue of it, but consist mainly of elements of a transitory nature, and in which degeneration, death, softening, and ulceration is the regular and necessary consequence of existence. Wherever the syphilitic tubercle appears, it consists of nests of very numerous small cells, with large nuclei, which are lodged in the interstices of the affected tissue, and from which they have sprung through profuse multiplication of its cellular elements. The recent nodules are soft, of a grayish-red color, and infiltrated with a scanty juice. After lasting for some time, they either soften and ulcerate, or else undergo an incomplete cheesy metamorphosis. The most frequent seat of the syphilitic cutaneous tubercle is upon the face, especially upon the forehead (corona veneris), and, next in frequence, upon the CONSTITUTIONAL SYPHILIS. 765 region of the shouider-blades, and the dorsal surface of the extremities. Some of the nodules are superficial, while others are deeply seated. The more superficial ones are smaller, while the deeper seated ones are larger. At first a small, movable tumor, somewhat sensitive to pressure, appears in the skin, which gradually reddens above it, and rises into a dark-red hemispherical nodule, which rather resembles a boil. Sometimes the covering of the tubercle remains unbroken, and, its contents becoming absorbed, its surface gradually grows paler, sinks in, and a scar forms without there ever having been any ulcera- tion. If the tubercle breaks, a turbid, serous liquid escapes under the cuticle, and, thickening, forms with it a scab. Beneath this scab the ulcer continues to penetrate more and more profoundly. Not unfre- quently one common, broad crust covers a cluster of nodules. The ulcer may retain the circular shape of the tubercle, but it more com- monly happens that the sore extends at one edge, while it granulates and cicatrizes at the other. Thus, like the rupia, the tubercle produces horse-shoe and kidney-shaped ulcers. The scars, which remain after healing of a syphilitic lupus, long retain a brownish-red stain, and, after the disease has subsided, become remarkably white. The hair often falls out, in syphilis; but, as a rule, this is merely a defiuvium capillorum, unless the scalp be the seat of an eruption. The hair-bulbs do not perish, and, after the disease has abated, the growth of the hair is as luxuriant as ever. The syphilitic exanthemata, on the other hand, usually destroy the hair-follicles, and cause permanent baldness or alopecia. The nails, also, undergo changes from implication of their matrix in the cutaneous disorder. In the simple infiltration of the matrix of the nail, which often accompanies psoriasis syphilitica, the nails de- generate, becoming misshapen, fissured, and homy. In the more rare ulceration of their matrix, they often become detached. V. Syphilitic Disease of the Mucous Membranes.—Next to the external integument, the mucous membranes are the most common seat of syphilitic disease, although all of them are not affected by con- stitutional syphilis with equal frequence. The lining of the mouth, fauces, nose, and larynx, and, next to these, the mucous surface of the rectum, are the regions upon which the malady is most prone to local- ize itself. The mildest form of syphilitic disease of the mucous membrane, and at the same time the one which appears soonest after the primary infection, is syphilitic catarrh. In special instances, it is not always easy to distinguish between a catarrh depending upon syphilis, and one arising from other causes. A remarkably deep, bluish redness, an abruot line of demarcation between the affected spot and the sound 766 CHRONIC INFECTIOUS DISEASES. parts, and a milky, turbid appearance of its epithelial coating, are sus- picious, but not pathognomonic signs. In most cases the diagnosis depends mainly upon the history of the case, and upon the coexistence of other syphilitic symptoms, particularly enlargement of the lymphatic glands, and maculous or papulous exanthemata, and above all upon the refractoriness of the catarrh to simple treatment, and its speedy disappearance when treated by mercury. The appearance of mucous papules, with their transformation into condylomata, erosions, and ulcers, is one of the earlier symptoms of syphilitic infection. Their mode of development is as follows : A spot of mucous membrane of about the size of a pea rises above the sur- rounding level, and seems firmer, and somewhat reddened. If it does not heal after reaching this stage, the epithelium covering the flattened nodule becomes opaque, and assumes a milky, or pearly appearance. After separation of the thickened epithelium, a bright-red erosion re- mains, which bleeds easily. This is followed by a sore, with an un- even, whitish-gray bottom, the product of molecular disintegration, or else plaques muqueuse and mucous condylomata form, from augmented vegetation and development of connective-tissue fibres. We have al- ready treated of the syphilitic mucous papule, and of the ulcers and condylomata of the mouth, fauces, and larynx, to which they give rise. We rarely obtain an opportunity of observing the earlier stages of syphilitic disease of the rectum. The ulcers which arise from mucous papules of the rectum, and the scars which they leave after healing, bear a close resemblance to dysenteric scars. A distinction may be based in some measure upon the seat of the sore, and resulting cicatri- cial stricture, the syphilitic ulcers being situated in the cloaca of the gut, or else close to the anus, while the dysenteric ones are found in the sigmoid flexure. The gummata and tubercular syphilomata of the mucous membranes have the same character and mode of development as those of the skin. A nodule of the size of a shot forms in the mucous membrane, and gradually grows until it projects above the surrounding level. If not made to resolve itself by judicious treatment, it softens, bursts its epithelial cover, and turns into a sore. Wide-spread destruction of the nose, palate, fauces, and larynx, may thus occur. Not unfrequently the disease spreads to the submucous tissue, and the cartilage, perios- teum, and bones. The ulcers often produce contractions in healing. YI. Syphilitic Iritis.—The syphilitic contagion not unfrequently gives rise to inflammation of the iris and the choroid coat of the eye. This is a very common complication of the syphilitic exanthemata. Modern ophthalmologists deny the existence of any specific mark of distinction between the syphilitic and non-syphilitic inflammations of CONSTITUTIONAL SYPHILIS. 767 these membranes—such as distortion of the pupil inward and up- ward. Besides the simple syphilitic iritis, there is another form, known as “ gumraous” iritis. For a description of the very character- istic symptoms and course of this affection, we must refer to the text- books upon ophthalmology. VII. Syphilitic Disease of the Periosteum and Bones.—One of the common symptoms of syphilis consists in a pain along the bones, unaccompanied by any appreciable objective manifestations. At first these pains are vague and ill-defined. Afterward they are fixed at certain points, particularly in the bones lying close beneath the skin, such as the tibirn and the cranial bones. They are increased by pres- sure, and usually remit during the day and recur at night. These osteocopic pains are probably dependent upon a slight disease of the periosteum, capable of complete and speedy recovery, and which prob- ably consists in moderate hyperaemia with an inflammatory oedema. The severe strain which the naturally-unyielding periosteum suffers, even when but slightly infiltrated by serum, fully accounts for the vio- lence of the pain. In bad cases of inveterate syphilis, swellings form here and there upon the bones, accompanied by great suffering, which becomes excru- ciating at night. Such swellings, when of a boggy consistence, are called “ gummata; ” if their consistence be somewhat hard, they are colled “tophi” (nodes). Like all other syphilitic affections of the periosteum and bones, they are most apt to appear upon the skull, the shins, the sternum, and other bones lying close beneath the skin. Gummata receive their name from the viscid-looking liquid which flows from them when punctured. They consist of cells and nuclei, with very little connective tissue, and a great deal of liquid intercel- lular substance, their elements corresponding closely to those of the recent succulent syphiloma. These tumors may decrease and disap- pear entirely, the liquid and cells both being absorbed, the latter first undergoing fatty degeneration. In other instances pus forms in them, and they turn into abscesses, which, when opened, either naturally or artificially, discharge their contents. Tophi, although their consistence is very hard from the outset, so that they are apt to be mistaken by ignorant persons for excrescences from the bone, are circumscribed neoplastic thickenings and elevations of the periosteum by inflammatory exudation. The periosteum whence they spring has but little tendency to suppuration, and by means of an early and appropriate treatment we can often bring about their resolution. When of longer standing, bone forms in the thickened tis- sue ; the tophi are thus converted into exostoses, and are then no longer capable of reabsorption. Besides the form of exostosis just mentioned. 768 CHRONIC INFECTIOUS DISEASES. which proceeds from ossification of the periosteum, there is another, dependent upon inflammation and proliferation of the bone itself Tophi and exostoses by pressure upon neighboring1 nerves may cause neuralgia, anaesthesia, or palsy, and when situated upon the inner sur- face of the skull may occasion serious disorder of the brain. Syphilitic caries and necrosis are sometimes the consequence of purulent periostitis, where the pus effused between the bone and peri- osteum has cut off the portion of bone affected from its nutrient blood- vessels. At other times it proceeds from an ulceration, originating in the soft parts, and which has destroyed the periosteum, and laid bare the bone; while, in still another series of instances, the periosteum, at first, is healthy, and the caries and necrosis are the result of a simple or gummy syphilitic inflammation. The question why the denuding of the bone of its periosteum and the ostitis sometimes cause an ul- ceration of the bone, or caries, while, at others, it induces the death and separation of large pieces of bone, or necrosis, we shall leave un- discussed, as being a question belonging to general surgery. When bone exfoliates from syphilitic necrosis, the loss of substance is seldom filled up by new bone. A depressed spot almost always remains, or, if the bone has been perforated, there will always be a hole in it with smooth edges. Syphilitic caries and necrosis occur more frequently upon the bones of the face and skull than upon those of the trunk and extremities, although the latter, especially the sternum, tibia?, and clavicles, do not always escape. The most dreadful devastation occurs in the bones qf the nose and hard palate. The vomer and the vertical plate of the ethmoid usually go first, so that the two nostrils commu- nicate by an orifice of variable size. Afterward the entire bony sep- tum perishes, and the turbinated bones, the walls of the ethmoid cells and frontal sinus, the nasal and lachrymal bones, are also destroyed. The nose thus loses its support, and sinks in behind its apex, which then points upward. If the disease attack the floor of the nostrils, after perforation of the hard palate, a communication is established be- tween the cavities of the mouth and nose; so that food and drink can enter the latter. More rarely, destruction of the hard palate com- mences in the mouth, although I have seen a piece of bone as large as a florin exfoliate from the lower surface of the hard palate, without any syphilitic ozeena. When caries and necrosis of the nasal bones arise from ulceration of the mucous membrane which has penetrated and destroyed the periosteum, the patients suffer long from an ill-smell- ing ichorous and often bloody discharge from the nose, which, at a later period, also contains bits of blackened bone. The septum of the nose is often perforated in such cases without its external covering exhibiting any particular change; but, if the destruction of the nasal bones be CONSTITUTIONAL SYPHILIS. 769 preceded by syphilitic periostitis, the skin soon becomes reddened, and the face grows cedematous upon the affected side. Sometimes the integuments are perforated by the pus and fragments of bone, and thus a fistulous opening is established in the back of the nose. Syph- ilitic ozasna, often causing a more or less extensive destruction of the bones of the nose, may recover completely. Some time ago, at the autopsy of a syphilitic person, besides an extensive recent anostosis excentrica (see below), I found a complete absence of the bony sep- tum, the turbinated bones of the nose and the inner walls of the antra of the upper jaws. But there was no bare bone to be found, the huge cavity which represented the nose being everywhere lined by a smooth cicatricial membrane. Besides caries and necrosis, a third destructive disease of the bones occurs in syphilis, which was first accurately described by Bruns, although Virchow first pointed out how frequently it originated from a syphilitic taint. Bruns describes this peculiar form of consumption of bone, to which he gives the name anostosis excentrica, as a dissolution and liquefaction of the bone, beginning excentrically, proceeding from the medullary canals and medullary cells, and marked by swelling and redness of the tissues contained in these spaces, but never accompa- nied by suppuration. The calibre of the canals is first enlarged at the expense of their walls, the progressive absorption of which ultimately causes the canals to blend into irregular cavities. The effect of this process is to render the diseased bone porous, and spongy, like carious bone, and in a macerated specimen it is impossible to tell whether the destruction is the result of caries or of anostosis excentrica. When the disease commences upon the exterior of the skull, its surface first assumes the worm-eaten, rough appearance of superficial caries; but afterward the loss of substance extends more deeply, and here and there may even perforate the cranial wall. The inner surface of the pericra- nium is said to be reddened, swollen, and granulated over the whole diseased region, and the medullary tissue within the diseased bone is converted into a red vascular mass, intimately connected with the peri- cranium. Not a trace of pus is anywhere to be found. The adjacent bone is either unaltered, or else a reproduction of bony matter takes place on the edges of the seat of disease, which is thus surrounded as by a wall. When the process attacks the outer surface of the cranial wall, an extensive growth of new bone may also occur on the interior of the vault of the skull. This description of anostosis excentrica, which has been taken almost word for word from the text-book of Bruns, agrees so closely with Virchow"'s account of “ caries sicca,” or the inflammatory atrophy of the bones of syphilitic persons, that it can hardly be doubted that both observers have described one and the 770 CHRONIC INFECTIOUS DISEASES. same disease. From microscopic examination of the soft tissue and of the more solid and resisting masses, the points of which contain a yellowish-white and very dry substance, Virchow has satisfied himself that the conical or spindle-shaped contents of the cavities, resulting from the loss of bone, consist of the specific neoplastic product of syphilis, to which he gives the name of gummata even when it is not soft, and which Wagner calls the syphiloma. YIIL Syphilitic Sarcocele.—Syphilitic contagion sometimes gives rise to an inflammation of the testicle, distinguishable from other forms of orchitis by certain peculiarities, particularly by its seat, and the tediousness of its course. The disease begins in the tunica albuginea and its continuations, and induces a proliferation of young cells and new connective tissue upon the interior of the tunic, and be- tween the seminal tubules. Under the pressure caused by this tumor, which afterward contracts and indurates, the proper substance of the gland disappears. Besides this simple syphilitic orchitis, there is a second form, distinguished by the formation of dry, whitish-yellow, homogeneous nodules in the affected organ, in addition to the prolif- eration of the albuginea. Virchow calls the former disease simple syphilitic orchitis, and the latter, gummy orchitis. Wagner believes that there is no essential difference between the nodular syphiloma, or gummy tumor, and the diffuse syphiloma. According to his views, the form first mentioned is the diffuse syphiloma, while the latter con- stitutes the nodular syphiloma of the testicle. The symptoms of syphi- litic sarcocele consist in a slowly-progressing enlargement of one or both testicles, which develops either without any pain at all, or else is accompanied by occasional lancinating twinges. The testicle becomes very hard, loses its regular shape, and may grow to the size of a fist. Sarcocele is often accompanied by a serous effusion in the tunica vagi- nalis propria. Sometimes the disease, after making some progress in one testicle, attacks the other. Virchow describes a syphilitic periorchitis: This may commence as a hydrocele, but soon occasions thickening of the albuginea and tunica vag- inalis propria, causing adhesions, or even complete synechia of the latter. IX. Syphilitic Disease of the Connective Tissue, Muscles, and Viscera.—In cases of inveterate syphilis, tumors presenting the char- acteristics of the gummy tumor, or syphilitic tubercle, are also found in the subcutaneous and submucous connective tissue, and in the inter- stices of the muscles (Virchow). When properly treated, they sometimes disappear, while at other times they suppurate, producing abscesses and intractable ulcers. The muscles also, especially those of the upper extremity, the throat and neck, are sometimes the seat of syphilitic disease. Virchow CONSTITUTIONAL SYPHILIS. 771 describe? a simple and a gummy myositis. The former depends upon proliferation of the interstitial connective tissue, producing an indura- tion of the latter, while the primitive muscular fasciculi suffer atrophy, and perish. In the latter form, tumors, often of considerable size, arise in the muscles, and upon section show reddish-white or yellowish- white, slightly striped deposits, which are usually not absolutely dry. Microscopic examination reveals a finely-cellular, dense granulation of the intramuscular substance, with premature fatty degeneration, in which the cells perish, leaving a granular, fatty, and apparently struc- tureless mass. Similar masses are sometimes found in the substance of the heart. Perhaps some cases of induration of portions of the car- diac muscles depend upon simple syphilitic myocarditis. Among the syphilitic diseases of internal organs, syphilitic hepatitis has been described in detail. TVagner and other authorities have ob- served syphilitic lesions in other organs, the spleen, the kidney, and even the pancreas, wThich closely corresponded w'ith those found in the liver, sometimes inducing thickening in the envelope of the viscus, some- times diffuse induration of its substance, and sometimes producing cir- cumscribed nodules in it. Dittrich has already recognized the occur- rence of syphilitic disease of the lung, in the form of nodular, firmly-re- sisting indurations, either of a white color, cr else stained black, by deposit of pigment, and which enclosed dry, cheesy accumulations. It would also seem that, besides this gummous pneumonia, an interstitial syphilitic pneumonia also occurs. It may sometimes be very difficult, or even quite impossible, to decide whether a disease of the lung de- pends upon syphilis or not. Syphilitic affections of the encephalon consist in part of chronic in- flammation of the meninges, which may involve the pia mater, the arachnoid, or the dura mater, in the form of a pachymeningitis externa (endocranitis) or interna; and, among other symptoms, sometimes give rise to palsy of one of the cerebral nerves. Sometimes, syphilitic de- posits occur, which formerly were often mistaken for inspissated ab- scesses, or for caseous tubercles. (See “Diseases of the Brain.”) It follows, from this brief enumeration of the various syphilitic dis- eases of the tissues and organs, that the points on which the disease localizes itself are far more numerous than was formerly supposed; and that Wagner’s statement, that syphilis attacks all the tissues which contain vessels, is fully warranted. The General Course of Syphilis.—It is a remarkable fact that, while the syphilitic taint at times gives rise to palpable symptoms, at others no sign of the persistence of the infection can be detected, ex- cepting the enlargement of the lymphatic glands After the healing of the primary ulcer, a period of several weeks usually elapses before 772 CHRONIC INFECTIOUS DISEASES condylomata, exanthemata, or other consequences of the infection, ap pear; and, after the latter have subsided, another interval of exemption usually ensues, ere a second series of disorders disturbs the apparent good health of the patient. For these alternations, which usually re- cur again and again during the course of the disease, no satisfactory explanation has as yet been furnished. The time which intervenes between the healing of the primary ulcer and the appearance of the secondary symptoms, as well as that between the various outbreaks of the secondary manifestations themselves, varies greatly in different cases. The causes of this difference, and the influences which shorten or prolong the period of latency, are likewise in a great measure un- known. It seems, however, that in vigorous constitutions, and in per- sons who live luxuriously, the secondary symptoms set in sooner, and recur at shorter intervals, and that the length of the period of latency is somewhat dependent upon the treatment adopted. Rarensprung, relying upon a large experience, affirms that, when mercury is not employed, a period of latency of several months, or even years, never occurs, and that the secondary symptoms and their re- lapses appear within six weeks at latest, after the healing of the in- durated ulcer, or after the subsiding of the outbreak last treated. He does not hesitate to declare a patient treated without mercury to be safe and permanently cured, who continues free from constitutional symptoms three months after treatment has been discontinued. If this assertion could be substantiated, the well-authenticated cases of latency of syphilis, during a period of ten or twenty years, would be attributable entirely to mercurial treatment. Such protracted periods of latency, however, if they really do occur, are at all events extremely rare, be the treatment non-mercurial or mercurial. It is equally rare, also, for secondary symptoms to arise prior to the healing of a recent primary sore. As a rule, they do not make their appearance until from eight weeks to three months after infection, and the relapses usually follow one another at similar intervals. A certain degree of regularity can be recognized in the manner in which the various manifestations of the disease succeed one another After the healing of an indurated ulcer, there is a great probability that in a few weeks or months it will be followed by condylomata, a maculous exanthema, or by a syphilitic angina; but, at this stage, the patient is quite secure against rupia, syphilitic lupus, or disease of the bones. Conversely, an individual, who for years has suffered repeated relapses of syphilis, is in danger of destructive disease of the skin and subcutaneous areolar tissue, of caries and necrosis of the bones, but not of broad condylomata, or of sypnilitic roseola. The disorders and complications of disorders which stand first in order in the series of CONSTITUTIONAL SYPHILIS. 773 syphilitic affections are called secondary affections; others, which are ikewise frequently combined one with another, but which appeal* later, are called tertiary affections. The former are usually considered to include indolent buboes, the condylomata, the exanthemata with the exception of rupia and lupus, the superficial ulcers of the mucous mem- brane, and iritis; while lupus, rupia, disease of the bones, and the gummy tumors of the submucous and subcutaneous areolar tissue, and the disorders of the muscles and viscera, belong to the tertiary class. Upon comparing the two classes, it will be found that the secondary diseases are less malignant, that is, are less destructive than the ter- tiary; and that they usually are limited to the superficial tissues, to the skin and mucous membrane ; while the tertiary affections attack the deeper-seated, “ more noble ” organs. This mode of classification, however, makes it impossible to draw a sharp boundary between the two forms, and it is idle and unprofitable to dispute as to whether the intermediate varieties rank as secondary or tertiary, such as sarcocele, which, though not one of the earlier consequences of infection, still usually precedes lupus and disease of the bone, and which, in respect to its malignity and to its locality, occupies an intermediate position. In rare and exceptional instances, disease of the bones forms one of the early symptoms of general syphilis. The opponents of the treatment by mercury attribute this early appearance of the so-called tertiary accidents to the mercury, and even go so far as to assert that the em- ployment of mercurials, by aggravating the pernicious influence of syphilis upon the organism, actually is the cause of the tertiary mani- festations ; and that, under non-mercurial treatment, syphilis does not affect the bones. Although both statements, in their fullest accepta- tion, are decidedly untrue, yet neither of them is quite without foun- dation ; for, if the disease be not subdued, while the constitution has been ruined by immoderate and reckless dosing with mercury, perni- cious forms of syphilis, such as lupus and disease of the bones, are more liable to arise than when it still lurks in the system of a robust indi- vidual. It would almost seem, indeed, that the constant increase in malignancy which shows itself in each succeeding attack, in cases of syphilis where mercury has not been employed, is the result of deterio- ration of the constitution induced by the previous attacks. At all events, the contrary effect is seen in robust constitutions, in whom, when the disease is not completely extinguished at first, each relapse is less severe than the preceding one. While, with the exception of a slight fever, which usually precedes and accompanies the secondary symptoms, the disease is borne for a con- siderable length of time without constitutional disturbance, yet, when the attacks recur constantly, when the patient’s rest is continually dis- 774 CHRONIC INFECTIOUS DISEASES. turbed by nocturnal pain, when protracted suppuration consumes his strength, and, above all, if an active mercurial treatment be superadded, a general marasmus, the so-called syphilitic cachexia, sets in. This term is not exactly appropriate, since it does not proceed directly from syphi- litic infection, but indirectly from the nutritive disturbance to which it leads, or from the method of treatment adopted. Accordingly, the syphilitic cachexia has no peculiar features by which it may be distin- guished from other non-specific forms of cachexia. Even amyloid de- generation of the liver, spleen, kidneys, and other organs, which often accompanies the syphilitic cachexia, is not peculiar to this disease, but also develops in the course of other non-syphilitic diseases of bone as well as in malarious affections, scrofula, and rickets. Treatment.—The treatment of the primary syphilitic induration and primary syphilitic ulcer must be directed mainly against the con- stitutional disease, the first manifestation of which we have found it to be. Abortive treatment is out of the question, save when we have to treat an excoriation produced during a suspicious coitus ; but in such a case, after destroying the affected part, we cannot tell whether the absence of induration and of subsequent symptoms is the result of the treatment or not, as we have no criterion for distinguishing an in- fected excoriation from a non-infected one. The extirpation of an in- duration, or its destruction by means of caustics, is altogether useless. As a general rule, a new induration forms upon the edges of the wound thus produced. Besides the use of constitutional remedies, the primary syphilitic sore should be treated according to the principles already laid down for treatment of the chancre. First of all, the utmost clean- liness must be maintained. Washes, mild or strong, according to cir- cumstances, should be used, together with gentle applications of lunar caustic, or sprinklings with red precipitate, and the like. Internally, unless contraindicated by special circumstances, I treat the primary ulcer and primary sore with mercurials. I am wTell aware that the in- duration is capable of disappearing without their use, and that this treatment affords no guaranty against the appearance of consecutive symptoms ; but the indisputable fact, that the secondary symptoms are fewer and later in appearing when treated by mercury than when treated without it, induces me to prefer the former treatment to the latter. Besides, a cautious employment of this drug is far less liable to be followed by mischievous results than is asserted by its opponents. In the first year of my practice I did not employ mercury in syphilis, but in my second I commenced to use it upon almost every indurated sore, and in all cases of secondary disease. The number of patients which I have treated in this manner cannot of course be compared with that treated in the course of a year or two in the syphilitic ward of one CONSTITUTIONAL SYPHILIS. 775 of the great hospitals, but it is large enough to prove that the mis- chief produced by mercurial treatment has been greatly overestimated. As I have kept most of the patients, whom I have treated for syphilis, under observation for some time afterward, and since, after the marriage of many of them, I have become their family physician, it would have been more difficult for the pernicious effects of a course of mercury to escape my notice, than that of many a chief of a large syphilitic ward, who loses sight of his patients as soon as they are discharged. A se- ries of observations, many of them very close ones, and now continued for over eleven years, of a by no means inconsiderable number of per- sons who have undergone a careful mercurial treatment, has converted me from an opponent into a decided advocate of mercury. It lies out of the plan of this work to recount all the celebrated modes of treatment by mercury, or to detail the minute directions en- joined in the different methods, the number of pills to be taken daily, the manner of raising and reducing the dose, etc. I admit that I re- gard all sharply-defined routines not only as useless, but as absolutely dangerous, as it induces inexperienced or careless physicians to treat all varieties of constitution by the same formula. Experience has taught that the efficacy of mercury, as a remedy against syphilis, does not depend upon the form in which it is administered, whether as a suboxide, an oxide, a basic salt, a chloride, or an iodide. It is equally immaterial, as regards its efficiency as a remedy, how the mineral enters the blood, whether it be by the intestinal mucous membrane or through the skin. Hence our choice of a preparation of the drug should fall upon one which, while an effective remedy, does the least possible harm to the constitution. Since, however, the pernicious influence wffiich this mineral exerts upon animal life is susceptible only of a par- tial explanation, we can merely diminish or avert the more subordinate mischief to the intestinal mucous membranes, to which the use of mer- curials gives rise, by choosing preparations which are the least irritat- ing to them, or by not introducing the drug through the intestines at all, but through the skin. If we deemed the action of calomel and iodide of mercury upon the intestine, when cautiously administered, to be very great or very pernicious, we should regard the reintroduction of the “ inunction-cure ” as a most important step in the therapeutics of syphilis; but, believing as we do, that these disadvantages are trifling, and nearly always temporary, we cannot concur in the ecsta- sies of those who see the beginning of a new era in the reestablish- ment of the treatment of syphilis by mercurial inunction. I do not mean by this that I look upon mercurial inunction as an improper method of treating syphilis; indeed, I very often make use of it myself, especially in clinical practice, for it does all that mercurial treatment is 776 CHRONIC INFECTIOUS DISEASES. capable of doing; and I know of no objection to it, excepting that salivation sometimes occurs more suddenly and with greater severity m this than in other cures. As a rule, I follow the directions laid down by Sigmund for this mode of treatment (which, compared with the notorious and dangerous “grand inunction-cure” of Louvrier, scarcely deserves the name of inunction), but I do not pedantically hold myself strictly to Sigmund'1 s precepts. The patient having taken several daily warm baths, I cause a half drachm of blue ointment to be rubbed into the skin, and, where there seems to be danger from delay, I rub in a whole drachm. Upon the first day I apply it to the legs, the second to the thighs, the third to the arms, the fourth to the back, the fifth to the legs again, and so on. The precise order in which the rubbings succeed one another is of course unimportant. At points within the patient’s reach he can rub the ointment in for himself; at others, an attendant must do it. Each inunction should continue from ten minutes to a quarter of an hour, and, before rubbing again, the surface previously rubbed is to be washed with soap and water. The temperature of the room should not be above sixty-five or seventy de- grees Fahrenheit, and must be ventilated daily. There is no objec- tion to the patient’s changing his linen. It is useless to combine the hunger-cure with the inunction-cure; and it may even do harm. As soon as the least trace of salivation shows itself, the treatment must be suspended; and any of the ointment still adherent to the skin should be carefully removed by a bath, or by a thorough washing. Should the healing of the ulcer or resolution of the induration come to a stand-still after cessation of the salivation, or, in cases of secondary disease, should the improvement not continue after the salivation abates, I recommence the mercurial frictions, one or two of which then almost always perfect the cure. I observe the rule of always suspend- ing the treatment upon the occurrence of salivation, not only when the mercury is employed in the form of ointment, but in all other forms of mercurial treatment, and simply because I regard salivation as a sign that a sufficient quantity of the mineral has been absorbed. It mat- ters not whether the mercury be applied upon the skin, or to the in- testines ; in either case a part only of what is administered is absorbed, and the rest either remains upon the skin or else is expelled in the stools. Hence, even if we could tell how large an amount of it must be introduced into the system in order to effect a cure of a syphilitic affection, we should still be ignorant of the number of inunctions of ointment, or of internal doses of calomel, corrosive sublimate, or iodide of mercury, requisite to produce the desired result. Salivation, of course, affords no criterion of the amount of mercury absorbed, but it certainly indicates that enough of the drug has been taken up to pro CONSTITUTIONAL SYPIIILIS. 777 duce a decided impression upon the system. That the one effect, namely, the salivation, is almost always accompanied by another, the improvement of the syphilitic lesion, follows even from the erroneous belief entertained by many old physicians, that salivation is a beneficial crisis. Notwithstanding that I regard salivation as a valuable guide in the treatment of syphilis by mercury, just as I regard dilatation of the pupil as valuable in treatment of epilepsy by atropin, showing that the dose administered is sufficient, and although I do not regard the appearance of slight traces of salivation as an objection to such method of cure, yet I consider it extremely unsafe when we have not the op- portunity to suspend the treatment before the salivation has made any considerable progress. Salivation has no curative effect whatever, and I always seek to allay it by administration of chlorate of potash, either in solution ( 3 j to water § ij), a tablespoonful of it to be taken every two hours, or else in the form of pastilles. If, when in doubt whether to continue the cure or to discontinue it, we decide to give one or two more doses of calomel, corrosive sublimate, or iodide of mercury, we run far less risk, by so doing, of producing a severe sore mouth, than if we rub in another half drachm of mercurial ointment. The great objection to the inunction treatment, that in it we cannot say how much of the mercury enters the body, does not exist in using subcutaneous injections of corrosive sublimate. In this treatment, which of late has run a strong opposition to the inunction treatment, and has to some extent supplanted it, we may even more certainly control the dose than we can in internal adminis- tration, and we save the gastric and intestinal mucous membrane just as completely as we do by the inunction treatment. I acknowledge that I began the employment of subcutaneous Injections of corrosive sublimate with a certain distrust, and that I did not resort to it till it had been urgently recommended to me by various persons. I feared that the pain and inflammations, with partial necrosis of the skin that it must cause, would be out of proportion to any possible benefits arising from its use; indeed, it seemed doubtful to me if this inflammation and necrosis of the skin would not interfere with or entirely prevent the absorption of the remedy. Experience soon taught me better. If sufficiently dilute solutions are employed, the pains are perfectly bearable and of short duration ; by the same precaution, severe inflammations and necrosis of the skin may be avoided. The absorption of corrosive sublimate appears to follow subcutaneous injection just as quickly as that of morphine does; in short, the advantages seem to outweigh the objec- tions so much, that any practitioner, who has treated his syphilitic patients for a short time with subcutaneous injections of corrosive 778 CHRONIC INFECTIOUS DISEASES. sublimate, will acknowledge that we are much indebted to Lewin for its introduction. In my clinic, we at first used Letter's syringe, which holds twelve grains of fluid, and with this injected twelve drops of a solution of corrosive sublimate (gr. j to 3 j). Later, with the best results, we injected a solution (gr. j to § ss) with one of PaikrVs syringes, holding half a drachm (that is, the eighth of a grain of cor- rosive sublimate in a solution one fourth the strength of the former) once or twice daily. We obtained this syringe also from Letter in Vienna, but, as the canula was rather thick, and consequently the puncture pained and bled, we had a canula made like that on the ordinary hypodermic syringe. Nevertheless, the conviction, that the internal administration of mer- curials, cautiously conducted, does not produce any lasting injury to the mucous membranes, has caused me, in spite of the general commenda- tion of injections and the inunction-cure, to adhere to the internal ex liibition of mercury in private practice. The article I generally employ in cases of primary induration and primary sore, is calomel. Of all mercurials, this one is the least open to the charge of causing serious or permanent detriment to the mucous membranes when given in mod- erate doses. If it really were injurious, considering how universally it is employed, especially in diseases of children, the number of persons suffering from its effects would be very large. I will only call to mind that the Plummer's powders, used in ophthalmia and other scrofulous complaints, the minute doses of calomel used in infantile diarrhoeas, the larger ones, pushed almost to salivation in croup, pleurisy, and other inflammations, still are among the most common of prescriptions, and that ten or twenty years ago they were even more generally ad- ministered than now. An exceedingly rich experience has taught us, that the innumerable multitude of persons who have used calomel more or less, for other purposes than antisyphilitic treatment, have not suffered any permanent injury to their digestion or their general health, but are now as healthy as they were before. Calomel, how- ever, has no great reputation as an antisyphilitic (at least, in Ger- many), and the corrosive sublimate is preferred to it by most prac titioners, as a means of treating primary and secondary symptoms The reasons for this are twofold: firstly, it often causes diarrhoea; secondly, it soon produces salivation. I do not regard either of these objections as valid. I have never found that the diarrhoea which nearly always sets in at the beginning of a course of calomel (but which usually subsides in a few days) interferes materially with the cure, and, as salivation soon occurs in spite of it, we may confidently infer that the medicine is not all evacuated, but that a sufficient amount of it is absorbed and taken into the blood. With regard to the second objec- CONSTITUTIONAL SYPHILIS. 779 lion, for reasons given above, I rather look upon the early appearance of salivation as an advantage, insomuch that, in cases where, owing to idiosyncrasy of the patient, salivation occurs later than I had expected, oi where it fails to appear at all, I have been anxious lest I might ad- minister too large a quantity of mercury, not having this valuable guide to inform me when to discontinue the remedy. To adult patients I usually give a grain of calomel twice daily, or half a grain three times a day. When given in the form of powder, I have it wrapped in a wafer, in order to screen the mucous membrane of the mouth from contact with the drug. Generally, however, I have it made up with liquorice into pills, each of which contains half a grain. Next to calo- mel, I have most frequently made use of the protiodide of mercury. I am not aware that this article possesses any advantage over calomel, and I have generally noticed that its exhibition oocasions severe pain in the bowels, which scarcely ever occurs in the diarrhoea induced by calo- mel. On account of these annoying symptoms, Ricord (to whose au- thority the protiodide of mercury mainly owes its reputation and exten- sive adoption) combines it with narcotics ; but, even with Ricord’s pills (hydrarg. protiodid., lactucar. gall., aa 3 iss, ext. opii aquaeos. gr. ix, ext. guaiac. aquasos. 3 j, f. pil. no. xxxvj), I have often been obliged to give opium, on account of severe pain in the bowels, so that I have now been induced to abandon the use' of the protiodide. I shall now merely add a few words about corrosive sublimate, for, although I am by no means one of its admirers, and consider it as far inferior to other preparations of mercury, yet it probably is more generally employed in syphilis than any other. The corrosive properties of the drug forbid its ad- ministration in large doses, and I believe a gradual increase of the dose to be improper. Can one expect the stomach to accustom itself to the action of the medicine so as to tolerate large quantities without becoming corroded ? and why should we increase the dose when it is of importance to be able to suspend the treatment at precisely the right moment, in order to avoid introducing too much mercury into the sys- tem ? Corrosive sublimate is valued principally because, in the first place, it is slow to produce salivation, and because, under its use, less mercury is taken into the system than under other mercurial treat- ment. I cannot regard it as an advantage that the chemical proper- ties of corrosive sublimate should compel us to administer it in such doses that the object aimed at, the introduction of a certain amount of mercury into the system, is only very slowly attained; and I can- not admit that much more mercury is taken up in a treatment by cal- omel, if discontinued when salivation commences, than in a treatment by corrosive sublimate when pushed to the same point. It cannot be denied, however, that many people are cured of their syphilis by cor 780 CHRONIC INFECTIOUS DISEASES. rosive sublimate, and especially by the very injudicious method of Dzondi. If we employ this article, it must not be given on an empty stomach, and is best administered in the form of pills; but they should not be made up with bread-crumbs and sugar, according to Dzondi/s formula, but with powdered extract of liquorice; and the dose should not be raised, as is done in Dzondi1 s treatment, from the fifth of a grain to a grain and a half, but from half to three-quarters of a grain should be given daily, in divided doses. In order to protect the gas- tric mucous membrane from the corrosive action of the sublimate, it has been proposed to give the albuminate of mercury, and thus at once to furnish the combination which, when the pure bichloride is used, eventually forms in the stomach, at the expense of the gastric mucous membrane, and experience shows that double doses of this preparation can be tolerated without detriment. If it were not that I am already perfectly satisfied with the medicines already spoken of, [ should have recourse to the albuminate. Ddremprung proposes the following formula: 5 Hydrarg. bichlor. corrosiv. gr. ij, ovum uuum, aqua destillat. 3 vj, ammon. muriat. 3 j, misce exactissime. Filtra. D. S., a tablespoonful every two hours. The dietetic rules to be observed during internal mercurial treatment must be regulated according to the condition of the patient. As a general rule, it is ad- visable to restrict his diet, without going so far as to let him sulfer from hunger; but now and then it may become desirable to feed the patient upon the most nutritious food, under conditions already de- scribed in treating of the chancre. The common practice of administer- ing large quantities of “ decoction of woods ” is superfluous. Finally, while we subject the patient to an active treatment, in order not to expose him to other prejudicial influences, we must regulate his habits and carefully watch over his general health. For this reason it is ur- gently advised that syphilitic patients, who are undergoing a course of mercury, should keep their room, particularly in winter, and that they should be visited daily. We have said above that the primary ulcer and primary sore would heal without the use of mercury; but that under such treatment the recovery was slower, and the secondary attacks came on more fre- quently and earlier. This is equally true of the privation-cure (En* tziehungs-cur), and the hunger-cure, the methodical use of cathartic salts, and of Zittmunn's decoction, and other compound decoctions, the object of which is to throw the skin, kidneys, and intestine, into a state of increased activity, the supply of nourishment, meantime, being re- duced to a minimum. If this kind of treatment be very energetically conducted, and if the state of nutrition be depressed by a severe course of simple or double Zittmann's decoction, we may, no doubt, succeed CONSTITUTIONAL SYPHILIS. 781 ra accelerating the healing of the primary affection. But, frequently, just as the patient is beginning to recover from his eleven or twenty- two days of fasting, purging, and sweating, the first crop of secondary symptoms begins to develop. The preparations of iodine are altogether useless against the pri- mary affections; although certain physicians, who only practise in the country, or in the smaller towns, and who, rarely having occasion to treat syphilis, have an exaggerated dread of the effects of mercury, place great confidence in iodine. During my practice in Magdeburg, I remember many cases, w’here travellers visiting the small towns, and consulting the physician of the place for indurated chancres, afterward came under my hands, suffering from the worst iodine eruptions that I have ever seen. From the recipes which they brought with them, it was often quite evident that the iodic exanthema had been mistaken for a syphilide, and the worse it grew, the larger were the doses of iodine prescribed. The secondary and tertiary symptoms of syphilis must always be treated with the utmost circumspection and care, since there is no dis- ease in which therapeutic errors can do such serious harm as in consti- tutional syphilis. Mercurial treatment is nearly always of signal bene- fit in the secondary and tertiary forms of the disease, and frequently not only relieves and allays the symptoms as they arise, but some- times brings about a complete and permanent cure. If, however, it be administered again and again in unsuitable cases, instead of mitigating the malady, it renders it still more pernicious, causing destruction of the bones, degeneration of internal organs, and even endangering life itself. The fact that horrible forms of syphilis are more rare than they used to be, probably is partially because the “ grand inunction- cure ” and other methods of over-treatment are being banished more and more from the therapeusis of the malady, and that our employ- ment of mercury is now more cautious and restricted. The indications for mercurial treatment of constitutional syphilis have generally been summed up as follows: The secondary affections alone call for mer- cury, while the tertiary accidents demand the exhibition of iodine. Although this formula is somewhat inexact, yet, upon the whole, it is perfectly true. Mercurials are indicated in nearly all cases where the affection belongs to the secondary group, while, in cases of a manifestly tertiary character, they are generally contraindicated. To this rule an- other is very properly added, that even in secondary affections mer- cury is contraindicated, when it has already been used repeatedly with- out success. The principles upon which the mercurial treatment of syphilis is based may be deduced from what I have said above, re- garding the course of the disease, and from the same remarks it will 782 CHRONIC INFECTIOUS DISEASES. also become apparent why I have spoken of the customary formulary of indications as inexact, although right on the whole. When an in- dividual, sooner or later after his recovery from an indurated chancre, begins to suffer from condylomata or from eruptions, I do not hesitate to prescribe mercury, either by inunction with blue ointment, or in the form of calomel, to be taken-internally, without regard to whether the indurated ulcer has already been treated by mercury or not, for at this period it very seldom happens that, owing to the state of the patient’s general health, or to the form of the syphilitic outbreak (then usually a lupus or an affection of the bones), or from both the causes combined, the constitution of the patient has suffered much either from the effects of mercury or from the disease itself. It is only in these very excep- tional instances that I consider a mercurial treatment contraindicated at the period when signs of constitutional infection first appear, for we may be almost certain that, if the syphilis cannot be successfully eradi- cated by means of mercury, its next attack will be of a most pernicious character. On the other hand, where the constitution is still unim- paired, the good effect of mercury in allaying secondary symptoms is most striking. The condylomata, exanthemata, and sore throat, dis- appear much more rapidly than an indurated ulcer does, when treated by mercury, and it often happens that not only are the immediate symptoms allayed, but a permanent cure is effected. There are other cases, however, in which the disease only becomes latent and not ex- tinct ; and where it reappears some time after the subsidence of the first set of symptoms, or relapses, to use the common expression. The maAagement of these relapses varies greatly, according to their character. When the disorder is slight, as when plaques muqueuses appear upon the tongue, or when a few scattered pustules form upon the scalp, the attack is manifestly of a less serious character than the previous mani- festations have been, and it is not advisable to renew the mercurials. Syphilis never subsides suddenly, but usually dies out slowly and gradually, and we may always hope for this favorable termination when the new symptoms are of a less serious nature than their prede- cessors. Although I do not advise a repetition of the mercurials in such cases, yet the patient should be most carefully watched, kept upon a reduced diet, and preserved as far as possible from all othei noxious influences, until the last traces of the disease have disappeared. The “privation-cure” (“ Entzieliungs-cur”), and even the Zittmami’s decoction, are suitable remedies for such cases. At the height of the disease, the action of these methods of treatment is merely palliative, but when it is beginning to decline, they really seem to accelerate its complete disappearance. On the other hand, when the relapse shows that the disease has not assumed a milder character, if the new mani- CONSTITUTIONAL SYPHILIS. 783 festations are as severe as tlie former ones, or even more severe, but still retain the nature of the secondary disorders, and if, as is generally the case, the patient’s constitution still seems to be unimpaired, I re- commence the mercurial treatment, and, indeed, under oertain circum- stances (for instance, in case of rapidly-spreading ulceration of the fauces, liable to become complicated with- syphilitic laryngitis), I even make the treatment more energetic than before. I order daily inunc- tions of a drachm of blue ointment, or else give daily, or every other day, two doses of calomel, of ten grains each, after the method of Weinhold. It has often been objected, regarding TVeinholcVs treat- ment, that its only action is a laxative one; that it does not salivate, and that it exerts no important influence upon syphilitic affections. These a priori view's stand in direct opposition to the results of my own experience in many cases where I have given half-scruple doses of calomel. If the relapse be unmistakably of a tertiary character, or if it be merely of an intermediate nature between the secondary and tertiary forms; or, if the constitution of the patient have begun to suffer, wheth- er from the disease or the treatment, then mercury is not only contra- indicated, but even dangerous. Never use a grain of it under such cir- cumstances, and I am certain that by such precautions the evil effects of mercurial treatment may be averted. I may be brief in stating the indications for the use of iodine in the treatment of syphilis. In all cases vdiere the spontaneous and speedy extinction of the malady is not to be calculated on, and in which the employment of mercurials is contraindicated, the exhibition of iodine is urgently indicated, and then affords the utmost benefit. If we limit the administration of the medicine to the above class of cases, and are as methodical in its employment as we have been with mercury, we shall find that its value in the treatment of syphilis is by no means in- ferior to it. The preparation of iodine most generally employed is the iodide of potassium, from ten to thirty grains of which are usually given daily, in the form of a watery solution. Some physicians give larger doses, or strengthen the solution, by adding one or two grains of iodine to it, but apparently do not thereby augment its effect. According to my experience, Bdrensprung to the contrary notwithstanding, I have found the iodide of iron to be a very efficient preparation, especially where there is advanced anaemia. I usually employ it in the form of 6yrup of the iodide of iron syr. ferri iodid. 3 ij, syr. simpl. 3 ij. m,. S. 3 j every twro hours), and by its means have often produced iodic eruption and catarrh. The appearance of this symptom, like that of mercurial salivation, requires a suspension of the remedy. If the sus- pension be followed by an arrest of improvement in the symptoms, the 784 CHRONIC INFECTIOUS DISEASES. iodine must be resumed after the catarrh or eruption has subsided. The diet should not be reduced; not on account of the remedy, how- ever, but because of the condition of the patient’s general health. On the contrary, his food should be nourishing, and he should be allowed a little wine or beer. For persons of broken-down constitution I not rmfrequently prescribe iron, quinine, and cod-liver oil, besides the iodine. The local treatment of the secondary and tertiary symptoms should be restricted to the extirpation of old condylomata (wdiich, though they always dry up under mercurial treatment, do not always disappear en- tirely), to the application of atropine in iritis, to local blood-letting, and to occasional surgical procedures, which may be demanded on ac- count of destructive inflammation of the skin, caries, or necrosis. The majority of the secondary and tertiary affections do not require local treatment. S}rphilization, wdiich, during the last ten years has been much lauded as a certain means of eradicating syphilis, and of protecting the system against further infection, has again fallen into disrepute, or at all events is now merely practised by its introducers, and by the enthusiastic disciples of their new doctrines. The process of syphiliza- tion consists in the production of chancre pustules upon the skin of a person afflicted with constitutional syphilis, which process is continu- ally to be repeated, until the inoculation ceases to act. Apart from the fact that some persons do not become proof against the chancre- virus, after suffering several hundred and even as many as two thou- sand inoculations, it has not by any means always followed that, the immunity once attained, the syphilitic affection has healed; and, where recovery lias taken place, it remains more than doubtful w hether it has been in consequence of the syphilization. CHAPTER II. CONGENITAL AND HEREDITARY SYPHILIS. Etiology.—We shall pay no attention to the forms of infantile syphilis, arising from the infection of a child during birth by syphilitic ulcers upon the genitals of its mother, or upon the nipples, lips, or other parts of the body, of its nurse, for these forms of syphilis do not differ, either in point of origin, or of course, from the syphilis of adults. By the term congenital hereditary syphilis, of which alone we now propose to treat, wre mean a form of that malady occurring in newly- born children, and originating in the embryo, from constitutional dis- ease existing in the father at the time of begetting the child, or in the CONGENITAL AND HEREDITARY SYPHILIS. 785 mother during the period of pregnancy. The manner in which the contagion is transmitted to the embryo from the father or mother is altogether unknown, and we shall, therefore, confine ourselves to a statement of a few known and authentic facts, without attempting any explanation of them. If a woman who has secondary syphilis becomes pregnant, the foetus nearly always dies prematurely, and is expelled by an abortion or miscarriage. In such cases, the foetus is generally so much putre- fied that it cannot be determined whether it bears traces of syphilis upon it or not. In like manner, a woman who is healthy at the time of conception, but who subsequently contracts syphilis, usually aborts or miscarries, giving birth to a decomposing foetus. In other cases, the child is carried to term, but dies either at the time of its birth or shortly before. It then either bears distinct evidence of syphilis upon its wasted body, or else there is no anomaly beyond its extreme emacia- tion. In rare instances the child is born alive, and lives for a longer or shorter period of time. In such cases, the syphilis may appear im- mediately after birth, or else may remain latent, and develop weeks or months afterward. Inasmuch, then, as constitutional syphilis of the mother exerts so pernicious an influence upon her offspring, that it usually perishes either long before or else during birth, it will be readily understood that the majority of cases of congenital syphilis, which become the object of clinical investigation and medical treat- ment, are the progeny of syphilitic fathers. It is an extraordinary but well-established fact that syphilis may be thus transmitted from father to child, without infecting the mother who bears the infected offspring in her womb. Hereditary syphilis, derived from a syphilitic father, sometimes manifests itself immediately after birth, while at other times the characteristic symptoms do not appear until later. Symptoms and Cotjese.—The symptoms of congenital syphilis consist principally of affections of the skin and mucous membranes; and it is only in rare instances, when the disease drags on incurable, Dut without killing the child, that it causes disease of the bones. When children are born with evidence of the disease upon them, or when it makes its appearance a few days after birth, it usually proves to be of a more malignant nature than when it remains latent for some weeks. The former class, in which the malady assumes the character of a bullous or pustulous syphilide, occasionally accompanied by a coryza (see below), was for a long time misunderstood, and used to bear the name of pemphigus neonatorum. When the child does not come into the world with the disease already upon him, it usually commences upon the palms of the hands and soles of the feet, and afterward 786 CHRONIC INFECTIOUS DISEASES spreads to the arms, legs, and body, and sometimes to the face. Roundish spots, as large as a pea or bean, and of a dirty-red color, are first observable. In a short time the cuticle which covers them is elevated into a bleb by the effusion of a turbid liquid. These blebs burst, leaving excoriated, moist spots upon the skin, which show no tendency to heal, and new blebs form upon the toes and fingers. Not unfrequently some of the nails fall off, The later crops of blebs be- have like their predecessors, and, as, day after day, new ones arise, the unhappy child becomes excoriated at innumerable points. I have even seen the blebs form in the mouth and nose. The malady may last from a week to a fortnight; more rarely three or four weeks, and al- ways terminates fatally. Some of the cases occurring in my private practice, in which the mother, with touching patience, daily cleansed and bound up the fingers and toes of her babe, never suspecting that its dreadful disease was the consequence of the excesses of its father, have made an indelible impression upon my mind. When syphilis remains latent for a few weeks, it presents another aspect. (The bullous syphilide never commences latei than the first week of infancy.) The child is often born in apparently good condi- tion, and does not seem to differ in any respect from a healthy child. About a fortnight after birth, and in some instances as late as a month, or even two months after birth, it grows restless and thin, and its sur- face assumes a remarkable dirty color. The skin also becomes ex- tremely dry, rough, and shrivelled; and, in particular, the hands and feet look as if covered by a delicate husk, like that of an onion. It soon be- comes difficult for the child to nurse, the nasal mucous membrane being swollen, and the nostrils always filled by a thin secretion. This swell- ing of the mucous membrane, and the profusion of the discharge, give rise to a peculiar snorting and snuffling, which is almost pathognomonic of congenital syphilis; so that, in the absence of other signs, we can hardly err in diagnosticating the disease from this symptom, together with the peculiar condition of the skin. In most cases, the coryza is accompanied by an eruption, which, beginning in the region of the anus, spreads to the genitals, thighs, and loins, as well as to other parts of the body, particularly to the face. This eruption is generally of a character intermediate between that of the maculous, papulous, and squamous forms. The separate maculae are rounded, of the size of a pea or bean. Their color is a coppery or yellowish red, which be- comes actually yellow when pressed upon by the finger. They may be either distinct or confluent. At first they are level with the skin, afterward they project somewhat above it; then their surface is not rounded, but flattened, as if the top had been shaved off. As the affection advances, the maculae are often covered with scales of epider* CONGENITAL AND IIEREDITxVRY SYPHILIS. mis, or with a continuous coating of thin desquamating layers of cuticle, and, where the surface is habitually soiled by urine or the ex- crements, it becomes excoriated. Another constant symptom of con- genital syphilis consists in the formation of rhagades at points where the skin changes into mucous membrane, especially upon the mouth and anus. It can often distinctly be perceived that the lips of the child are incurved and bleed readily upon the slightest movement, and that it dreads to use them either in suckling, laughing, or crying. The act of defecation cannot be accomplished without great suffering, so that the child cries and moans whenever the bowels are moved. The rhagades are often accompanied by condylomata, and in neglected cases large ulcers, of a peculiar irregular, angular figure, form between the nates, and sometimes in the flexures of the thighs, and in other regions where intertrigo is apt to arise in healthy children. The dis- charge from these sores is scanty, and readily dries up into a scab, which is of a blackish color, owing to its containing an admixture of blood. We have already stated that it is rare for congenital syphilis to attack the bones. Cases are reported now and then, however, in which the usually slight ulceration of the nasal mucous membranes causes destruction of the bones of the nose, and depression of that feature in the first year of childhood. In other equally rare instances, congenital syphilis of early infancy either is overlooked or becomes latent in consequence of treatment, and breaks out again at the period of puberty in the pernicious form of syphilitic lupus, or disease of the bones. , In the autopsies of children who have died of congenital syphilis, or who have been born dead by syphilitic mothers, the characteristic lesions of the disease are sometimes found in the internal organs, especially the liver and lungs, more rarely in the brain. In the former it consists merely of a diffuse, uniform induration, the sequel of a simple non-gummous hepatitis. In the lungs, nodules, with cheesy centres of the size of a pea or walnut, are formed, as well as a form of diffuse condensation, first described by Virchow, who calls it “ white hepatiza- tion,” and which consists of a filling up of the air-vesicles with epithelial cells in a state of partial fatty degeneration. In the brain, Schott, in one case, has found gelatinous tumors of the size of a hazel-nut situ- ated beneath the lower surface of the two anterior lobes of the cere- brum. Finally, the thymus gland is sometimes considerably enlarged, and contains abscesses. Treatment.—Hitherto, the treatment of the bullous syphilide has always been in vain. On the other hand, in the second form of con- genital syphilis just described, comparatively good results may be ob- tained by means of appropriate medication. The most common and best method of cure consists in the exhibition of small doses of calomal (gr. £} 788 CHRONIC INFECTIOUS DISEASES. morning and evening, and the inunction of five or ten grains of mercurial ointment daily, or every other day. The treatment must not be pushed to salivation, but should be suspended as soon as a decided improve- ment in the symptoms begins to manifest itself, and renewed again whenever the improvement seems to flag. It is very important that the strength of the child should be supported by the most nutritious diet possible. It would be wrong, however, to intrust it to a wet- nurse, since this would expose the latter to the danger of infection. That a syphilitic child, although it rarely infects its mother, often does so to its nurse, is simply because the mother is generally syphilitic already, and hence is proof against further contagion. APPENDIX. INFECTIOUS DISEASES TRANSMISSIBLE FROM BRUTES TO HUMAN BEINGS. We shall merely discuss the subjects of glanders and hydrophobia in the following chapters. Regarding the malignant pustule, though this is likewise an infectious malady, communicable from the lower animals to man, yet, as it is more especially a matter of surgical inter- est, I refer to the text-books of surgery. CHAPTER I. HUMAN GLANDERS.—MALLEUS HUMIDUS ET FARCINOSUS. Etiology.—There is an infectious disease which attacks animals possessing an undivided hoof, especially horses, asses, and mules, and which is called glanders or farcy, according to the locality in which the lesions induced by the virus develop themselves. The virus of glanders, which is identical with that of farcy, repro- duces itself within any organism which it has infected, and the trans- mission of the virus thus reproduced in one individual to another is the most frequent, and indeed probably the only manner in which the malady is propagated. In other words, glanders is a contagious dis- ease, and probably is a purely contagious one. Its virus, like other contagions, is insusceptible of demonstration under the microscope, or by means of chemical analysis, and we only recognize its presence by its effects. It is contained in the discharge of the farcy-buttons pres- ently to be described, in the flow from the nostrils, the blood, and ( Viborg) in the excretions, the saliva, urine, and sweat. Whether it is volatile, and capable of pervading the insensible perspiration of the .nfected oerson, is doubtful. The fact that the disease may be traus- GLANDERS. 789 mitted at a distance of ten or twelve paces, might be dependent upon the circumstance that particles of nasal secretion might be thrown that distance by a horse, or because the snorting of the animals produces small bubbles of the secretion capable of floating for some time, and of being propelled by the faintest current of air. The glanders may be communicated from the horse, ass, or mule, to various other mam- malia. Man is likewise susceptible to it, so that coachmen, grooms, cavalry-soldiers, horse-doctors, and other persons having business among diseased animals, are not unfrequently infected by it. In rare instances, and probably during post-mortem, sections only, the disease has been transmitted from man to man. The virus of glanders seems to be capable of penetrating the epidermic and epithelial coats, since most cases of infection by it have not been preceded by any wound of the skin. Anatomical Appearances.—The lesions induced by infection with the poison of glanders consist in peculiar nodules in the mucous membrane of the nose, the lymphatic glands, the skin, the muscles, the lungs, and other organs. At first they are hard, but afterward soften, disintegrate, and form abscesses and ulcers. According to Virchow, whose description of glanders we follow, these nodules are the product of a proliferation of cells. In the more recent nodules the cells are young, small, and delicate, and there are many free nuclei; in the older ones the cells are large, distinctly nucleated, lie closely together, and make up almost the entire mass of the tumor. As they progress, the older cells degenerate, and become partially filled with fat globules ; they then lose their sharply-defined contour, and break down, so that the nodule finally contains only a mass of detritus, with a few isolated elements. Virchow calls attention to the similarity in thp progress of development of the farcy and glander nodules, and that of tubercle; but remarks, pointedly, that no inference ought to be drawn from the coincidence of these processes, as the transformation of cells into caseous material is not peculiar to tubercle, and occurs not only in that disease, but also in pus, cancer, and sarcoma. The nodules which develop upon the nasal mucous membrane of horses, asses, and similar brutes, and which constitute glanders par excellence, are of the size of a hemp-seed or pea. The ulcers which re- sult from their bursting are at first solitary, or grouped, but gradually coalesce, imparting to the mucous membrane a peculiar worm-eaten look. The destruction then extends by the development and burst ing of new nodules upon the edges of the ulcer, as well as upon its floor, and upon the surrounding parts, and by gangrenous disintegra- tion of large portions of its surface. The ulceration also strikes deeply laying bare the cartilages and bones, which die and are dis- 790 CHRONIC INFECTIOUS DISEASES. charged. The eruption of nodules is attended by a nasal catarrh which is very intense around the ulcers, and is at first accompanied by a thin transparent secretion. The discharge subsequently becomes thick, tenacious, and purulent; and when the ulceration is far ad- vanced, it is discolored by the admixture of blood, and becomes acrid and fetid, and contains the debris of the necrosed tissues. In farcy, a disease which develops in the skin and lymphatics of horses and similar animals, the tumors are larger than the genuine tubercles of glanders. They contain a greater quantity of caseous mat- ter, are discrete, or else congregate in clusters, or chains and wreaths. After bursting, they form rounded ulcers, with elevated or everted edges, with a foul, irregular bottom, furnishing a profuse ichorous dis- charge, which often glues the surrounding hairs together, drying up with them into hard crusts. Both glanders and farcy appear in man. The latter form, however, is the more common, and usually attacks the skin, upon which it gen- erally produces an eruption of tubercles, which are larger and more numerous than those occurring in brutes. The lesions of the nasal mucous membrane are exactly like those found in the horse. Those of the skin, subcutaneous areolar tissue, muscles, and lungs, are puru- lent rather than caseous; so that in the skin they look like pustules, and in the connective tissue, muscles, and lungs, they bear a great similarity to metastatic abscesses. The lymphatics and their glands are likewise often implicated in the disease in man, and, as in horses, they sometimes produce a chain of farcy-buttons. An inflammation not unfrequently extends from the lymphatics to the neighboring skin, which thus becomes the seat of a malignant erysipelas, with a ten- dency to gangrene. Symptoms and Course.—The period of incubation of glanders or farcy is of very variable duration. Where the virus has been im- planted upon a wound, the first symptoms generally appear within three or four days; but, when infection occurs where there has been no breach of surface (as when the virus is inhaled), the malady often does not break out for months. The course and magnitude of glan- ders also differ in the two cases. When the poison acts upon an abrasion, the first symptoms which appear are usually local; the wound inflames ; the lymphatics of the part form knotted chains, and their glands swell painfully. The inflammation assumes an erysipela tous character, and is attended by an intense oedema. Blebs form, and pustules, having discolored ichorous contents, and sometimes real gangrenous bullae, arise upon the skin, and abscesses often develop, or diffuse phlegmonous destruction takes place in parts about the in- flamed lymphatics. Sometimes the disease seems to go no furthei GLANDERS. 791 than this, its effects remaining confined to the lesions about the wound just described, and to a fever of an intensity corresponding to the severity of the case. Signs of a general implication of the system often accompany the above symptoms, however; and indeed they usher in the disease whenever it has not been preceded by a wound. The term prodromal stage, or stage of invasion, is usually applied to the period during which, although none of the lesions characteristic of glanders or farcy have as yet appeared, still the fever, constitutional disturbance, and certain subjective symptoms, announce a general in- fection of the system. Sometimes a single rigor occurs at the beginning of the attack, in others the rigor is repeated several times. The skin grows hot, the thirst augments, the pulse is accelerated, the patient feels depressed and languid, complains of pain in the head, sleeps badly, has no appe- tite ; in brief, exhibits a series of symptoms such as accompany other infectious diseases or local disorders which are accompanied by fever. These manifestations, however, are accompanied by another constant, and somewhat characteristic phenomenon, namely, a violent pain in the joints and muscles. The seat of this pain is usually in the vicinity of the greater articulations. It is generally augmented by motion or pressure, and is sometimes, although not always, attended by moderate swelling of the painful part. Although these articular and muscular pains often cause the disease to be mistaken for rheumatism, yet, when they occur in an individual whose history is suspicious, they may aid us in an early and correct interpretation of the symptoms. The first stage of the disease lasts for a longer or shorter period (and it may continue for three or four weeks, or more) ; the symptoms either increase steadily all the time, or else gradually grow milder, so as to subside almost completely when the second or eruptive stage, the stage of localization of the malady, sets in. The aspect of the dis- ease at this period presents many varieties, according as the malady selects one or other tissue as its seat. If it attack the nasal mucous membrane as glanders in the stricter sense of the term, an erysipela- tous inflammation makes its appearance upon the exterior of the nose and its vicinity. The nose, the eyelids, and the forehead swell, as- suming a dusky redness, and are covered by blebs, the precursors of gangrene. The patient cannot breathe through his nostrils, from which there flows a liquid, at first scanty, thia, and mingled with streaks of blood; afterward foul, bloody, and sanious. If the patienl lie upon his back, the discharge flows through the posterior nares into the pharynx, and provokes him to hawk and cough. The discharge causes erosion of the lining of the mouth, soft palate, and tonsils, which are of a deep-red hue, and are covered with ulcers and sloughs 792 CHRONIC INFECTIOUS DISEASES. [n addition to these manifestations of glanders, or independently of them, when the nose is not attacked, characteristic lesions usually are found upon the skin, which were formerly regarded as a pustulous eruption, until Virchow demonstrated that in glanders there was no elevation of the epidermis by an exudation thrown out from the sur- face of the cutis, but that the skin suffered a circumscribed disintegra- tion, above which the cuticle for some time remained intact. Accord- ing to Virchow, the affected portions of skin at first are intensely red- dened, and very small, almost like flea-bites; they then change into papules, and the little elevations afterward assume the aspect of pus- tules. Beneath their epidermis we find a tolerably thick, yellow liquid, filling up a hole in the corium. The contents of the glanders- pustules, enormous numbers of which often appear upon the body, sometimes grow bloody, and dry up into small blackish or brownish crusts. Besides this scattered eruption, Virchow describes clusters of larger “ farcy-buttons,” which lie deeper in the skin, in the form of large, flat, hard, red tumors, from which the cuticle is finally separated by an effusion of blood, so as to form bluish bullae. The upper por- tion of the cutis, which covers these clusters, is also infiltrated by a haemorrhagic exudation, and afterward breaks down into a pulpy detritus. The “ farcy-buttons ” of the subcutaneous areolar tissue and mus- cles arise either with diffuse inflammatory infiltration of the adjacent parts and all the symptoms of a severe phlegmon, or else small cir- cumscribed, hard, or boggy tumors form, which are quite painless, and then may develop unobserved. Sometimes the contents of the nodules are absorbed; more commonly the skin either ulcerates or sloughs, and great destruction, occasionally extending even to the bones, is the con- sequence. Participation of the lungs and bronchial mucous membrane in the disease is announced by shortness of breath, cough, and rales. The deposits are too minute to admit of detection by physical examination. The larger the number of these symptoms simultaneously pre- sented by the case, and the more rapidly they progress, so much the sooner will the patient succumb with all the signs of the most intense adynamy, and of the so-called typhous or putrid fever, the malady always ending fatally. Death may occur as early as the first day or two, while other cases drag on until the third week. In chronic glanders and chronic farcy the characteristic lesions of the nasal mucous membrane, muscles, and areolar tissue, are more sparing and less speedy of development than in the acute form, which is of far more frequeut occurrence. The skin usually remains intact, while the lungs and bronchial lining are soon affected. Pauses not HYDROPHOBIA. 793 unfrequently occur in the'eruption, so that the disease seems to have subsided until another cold abscess begins to form or a new eruption breaks out. In chronic glanders and farcy also, the majority of pa- tients finally perish of marasmus, and there are very few instances in which the disease is reported to have ended in recovery. Tkeatmeot.—One of the important tasks of a sanitary police should be to diminish the opportunity for the propagation of the virus as much as possible, by the enforcement of strict regulations. Such precautions alone can be productive of certain results, while the utmost vigilance and care will not furnish security, when, either from carelessness or selfishness, the regulations are neglected. Prevention of constitutional infection, by vigorous destruction of the point of inoculation of the glanders, can only be hoped for imme- diately after contact of the virus with the wound. The remedies proposed for the cure of pronounced glanders, calomel in large doses, iodine, Fowler’s solution, injections of a strong solution of creosote into the nostrils, and the cold-water cure, are all productive of but little benefit, according to our present experience. A treatment of the symptoms, in which local disturbance, fever, and the strength of the patient, are taken into account, is the one most to be commended. CHAPTER II. HYDROPHOBIA—LYSSA—RABIES. Etiology.—The difficult question about the nature of rabies and its proper position in the nosological system remains unsettled. The fact that the poison, the absorption of which induces the disease, is reproduced in the body of the patient, goes far toward proving that it is infectious. This view is also favored by the symptoms occurring among certain classes of animals. The two chief forms of rabies in dogs, the quiet and raging, remind us of the febris nervosa stupida and febris nervosa versatilis of old authors. On the other hand, there are certain objections to classing lyssa among typhus fevers, the acute exanthemata, and other acute infectious diseases. I would especially call attention to the variable duration of the period of incubation in different persons. We do not certainly know the length of time between the action of the contagion and the outbreak of the malady in all infectious diseases, but we suppose that the difference of this interval is only slight in different persons. In lyssa the period of incubation varies weeks and months, even if we do not consider 794 CHRONIC INFECTIOUS DISEASES. extreme cases. Moreover, there is an essential difference between the character of the fever in this and other acute infectious diseases. In lyssa, among the symptoms are some nervous ones, slightly analo- gous to the neuralgias which occasionally occur, instead of the fever in malarial infection. Lyssa lxumana most resembles tetanus, although I cannot understand how it is possible to deny the occurrence of lyssa as an independent disease, and to identify it with tetanus. In the well-observed cases, neither continued tension of the spinal muscles nor pain in the contracted muscles has been mentioned, while neither is ever wanting in true tetanus. The difference between lyssa and tetanus is, that the spasms, which may be termed tetanic, only occur in some paroxysms, and are limited to certain nerves, and more par- ticularly to those which are by no means chiefly affected in traumatic or rheumatic tetanus. When Romberg terms lyssa a toxoneurosis, he says all that we actually know of the nature of the disease. Without the experience that the poison is reproduced in the body of the patient, we might most reasonably suppose that a toxic neuritis, or a toxic neuropathia, spread from a peripheral nerve, on which the poison had worked, to the medulla oblongata and cerebrum; and, since in many cases changes in the wound or in the cicatrices precede the outbreak of the malady, and the time between these changes and the outbreak is very short, it would be most probable that the poison had remained latent at the seat of injury, but afterward had rapidly spread in a centripetal direction. This latency would most remind us of that of syphilis between the different outbreaks of the disease. However, all this reasoning lacks a solid foundation. Lyssa, or rabies, in its stricter sense, is a disease which origi- nates in animals of the dog kind, and which indisputably is propa- gated, in most instances, by infection of one animal by another. We shall not discuss the question whether this be its only mode of propagation, or whether, under certain circumstances, it may develop spontaneously. The rabies of other races of animals and the hydro- phobia of human beings are purely contagious maladies. This poison, which exists in the saliva, blood, and perhaps in other fluids of the body, is not volatile, but fixed in character; it cannot pass through the epidermis, and hence does no mischief, unless brought ir contact with an ulcerated or excoriated surface. The most common cause of human rabies is the bite of a mad dog. More rarely the disease originates in the bite of some other rabid animal, such as the wolf, the fox, the cat, or the ox. The possibility of infecting a healthy man by the bite of a man suffering from hydro- phobia has not yet been proved positively; but the inoculation of the disease from human beings to brutes has reoeatedlv been successful HYDROPHOBIA. 795 Bites of rabid animals upon bare portions of tlie body are far more dangerous tlian if the part bitten be covered by the clothing; as, in the latter case, the poisonous saliva is not so readily conveyed to the wound, being wiped off from the teeth by the clothing. For the same reasons, there is no danger from the licking, or otherwise moistening, of the sound skin by the saliva, blood, or other fluids of a rabid animal, unless there should happen to be an abrasion or fissure upon its surface,. The virus, when implanted upon an excoriation of the skin, does not lead to hydrophobia unless there be a certain degree of predispo- sition to the disease. Inoculations of the saliva of rabid animals, as practised by Jlertwig, succeeded only in twenty-three per cent, of the animals operated upon, seventy-seven escaping; and, according to Fa- ber's statistics, out of one hundred and forty-five persons bitten by rabid animals, in Wiirtemberg, only twenty-eight had hydrophobia. Anatomical Appearances.—No lesions characteristic of the dis- ease are found in the bodies of those who have died of hydrophobia. The most common conditions consist in intense rigor mortis, extensive post-mortem hypostasis, early putrefaction (so that, soon after death, blebs full of gas begin to arise), intense staining of the endocardium and walls of the vessels, hypermmia and serous exudation in the brain and its membranes, in the spinal marrow, in some of the sympathetic gan- glia and nerves; hypersemia and swelling of the mouth and fauces, both of which contain a collection of tenacious mucus; hypostasis and oedema of the posterior parts of the lungs ; engorgement of the walls of the stomach, and great abdominal glands. All these lesions, espe- cially the injection of the nervous centres and nerves, upon which, at times, great stress has been laid as explanatory of the nature of the disease, are not constant, and, for the most part, seem to arise just prior to dissolution, in consequence of the disturbance suffered by the functions of respiration and circulation during the attacks presently to be described. In the cases which I have seen, autopsy showed a decided swelling of the tonsils and follicular glands at the root of the tongue and the posterior wall of the pharynx, exactly corresponding with Virchow's observations. Symptoms and Course.—Most cases of lyssa that have been well observed and described closely resemble each other. One that I have seen corresponds closely to the dreadful picture which Romberg drew from his own and other cases. As it is universally assumed that morbid processes due to the action of a specific poison run their course with symptoms which only vary through personal idio- syncrasy and the variable intensity with which the poison has acted, those reports of lyssa humana differing from our description, in which the characteristic symptoms and their peculiar sequence are not 796 CHRONIC INFECTIOUS DISEASES. mentioned or really did not occur, must arouse the suspicion that they were badly observed, or that there was an error of diagnosis. Opinions differ as to the length of its period of incubation. The statements that hydrophobia has made its appearance twenty or thirty years after the bite of a rabid animal, as well as those according to which the disease has broken out as early as the second or third day, are probably dependent upon imperfect observation. The shortest term of incubation appears to be about eight or ten days; the longest, twelve or thirteen months. In the majority of instances, the malady breaks out in about forty days after the reception of the bite. The reasons for this inequality of the period of incubation are obscure. The assertions of Marochetti, who claims that, during the incubative stage, vesicles form beneath the tongue, and that, by destroying these vesi- cles, the outbreak of the disease can be averted, have not been substan- tiated. But there are numerous instances in which, toward the end of the stage of incubation, and a day or two before the onset of the malady, peculiar alterations have been observed in the wound or its scar, for the wound has generally healed by this time. The bite as- sumes a livid color, grows painful, and discharges a yellow ichor. The scar, which has generally soon formed without remarkable symp- toms, grows bluish red, swells, and sometimes breaks out afresh. The patient also complains of painful sensations, shooting centripetally from the wound or scar, or of a sense of numbness in the bitten mem- ber. These disturbances at the point of entry of the virus are very often wanting. The first or prodromic stage of the disease is marked by a peculiar depression of the patient’s spirits, amounting to an acute melancholy, and which has caused the term stadium melancliolicum to be applied to this period of the disorder. The patient seeks solitude, is timid and apprehensive, and either sits motionless and plunged in deep ab- straction, or else is unable to rest at all. Some complain of an indefi- nite feeling of dread and oppression, and sigh repeatedly without any reason for so doing. Some are preoccupied with sad forebodings, or, if aware of their perilous condition, are incessantly tormented by dread of the onset of the malady. Sleep is restless and broken by frightful dreams. The precursory signs of the spasmodic disturbance of respiration, afterward to attain so terrible an intensity, soon super- vene. The patient complains of pressure in the proecordium, draws profound, sighing inspirations, the diaphragm is depressed, the epi- gastrium bulges, and the shoulders are drawn upward. This spas- modic breathing is the first token of the tonic spasm of the muscles of inspiration which causes such frightful torments in the second stage of the disease. HYDROPHOBIA. 797 The prodromic term having lasted two or three days, the second or furious stage begins. Its onset is marked by a fit of choking, sud- denly induced by an attempt to drink, which renders the patient in- capable of swallowing a drop. The moment the fluid enters the mouth and the motion of swallowing is made, spasmodic inspiratory motions begin; the thorax rises inter- ruptedly, and remains in the position of deepest inspiration for ten or twenty seconds. During this time the features betray anxiety and terror, the eyes protrude, head and shoulders are thrown back, then comes an expiration, with which the attack passes off. I have satisfied myself that the inspiratory muscles, as well as those of the pharynx, are implicated in these seizures. This combination of spasmodic con- tractions in both of these sets of muscles is a frequent symptom; it always appears in the straining preceding vomiting, as well as in the retching following irritation of the pharynx by the finger, etc. Retch- ing is always accompanied by a feeling of suffocation, from the contrac- tion of the inspiratory muscles complicating the spasm of the pharynx; and we are justified in giving the name of retching-fits to these spasms, which form the pathognomonic symptom of lyssa, and are given in every well-recorded case. The dread of water is entirely due to the dreadful experience of the patient on trying to drink. This was so, not only in my case, where the patient, an energetic and courageous man, voluntarily made repeated attempts to drink, before he rejected with terror any sugges- tion of the kind, but it is the same in all cases of undoubted lyssa that have been well observed and accurately described. Reports of cases where hydrophobia is given as a primary symptom are worthy of no credence. It is a curious fact that, at first, the act of swallowing solid food is not followed by spasms. Even a draught of air on the skin, or touching any thing cold, sudden irritation of the eye by dazzling light, even sudden mental excitement or surprises, may induce attacks. According to my observation, the pharyngeal muscles do not partici- pate in the reflex spasms induced by irritating other parts, as the mouth or palate. On suddenly arousing my patient, he opened his mouth widely, threw the head back, the thorax was raised as in full inspiration, the epigastrium became prominent, but there was no actual retching. At the height of the disease, it looked as if attacks occurred from time to time, even without cause ; but I think that even these apparently spontaneous attacks must be regarded as reflex spasms, and be referred to collections of tough mucus in the pharynx or to the trickling into it of saliva. This supposition is based on the haste and abandon with which the patients eject saliva and mucus, 798 CHRONIC INFECTIOUS DISEASES. and their attempts to introduce the finger far into the throat, for the purpose of removing mucus and sputa. Various authors name tetanic or epileptiform spasms among the symptoms of lyssa ; but, on careful examination, I have not been able to discover a case where the detailed description of the spasms fully convinced me that they were tetanic or eclamptic. It is nowhere stated that the muscles of the back were tense, except during the attacks, or that consciousness was lost during the general convulsions. In my patient, there was also opisthotonos—he threw his hands and feet about, and pitched around, so that he frequently fell on the floor. But these symptoms reminded one far more of hysterical spasms, or of the actions of a tortured, despairing man. The above symptoms are soon accompanied by attacks of boundless rage, in which the patients are hard to manage, destroy all fill at comes in their way, strike, kick, scratch, and bite, if held fast— and, not unfrequently, kill themselves, if they are carelessly watched. The biting, inarticulate howling, and barking sounds, are not made more frequently by a hydrophobic patient than by another madman in the maniacal stage of chronic cerebral disease.* The patient often warns his attendants between the fits, which seldom last longer than a quarter or half an hour, and begs pardon for his misbehavior toward them, and sets his worldly affairs in order, in perfect consciousness of the near approach of his end. The paroxysms of madness and convul- sions, having steadily grown more frequent for two or three days, now begin to diminish in violence as the patient loses strength. Rarely, it happens that death occurs at the height of the malad}T, during a severe and long-continued choking-fit. The exhaustion and collapse usually augment from hour to hour; the voice grows hoarseand feeble, the respiration shallow, the pulse small, irregular, and very frequent, and death ensues with the signs of a general paralysis, which is some- times preceded by a deceptive amelioration of the symptoms. It might be supposed that the attacks of madness occurring in lyssa were simply a result of the despair that would affect even a person not having this disease, if he suffered from retching at short intervals for a day or two. I once attended a patient suffering from severe pharyngitis, who, when I asked him to try to drink, hurled the glass from him, and acted like a madman. We find something like this, too, in patients with croup or oedema glottidis. The fact, also, that sometimes patients of very temperate * 7iomberg says that a great inclination to bite, along with the absence of charac- teristic reflex spasms, is one of the diagnostic points between true lyssa and those hypochondriacal and maniacal conditions that fear of the disease not unfrequently develops in persons that have been bitten. This state might be termed lyssophobia. HYDROPHOBIA. 799 and resigned natures do not become maniacal would also favor this view. But there are some objections to it, especially the fact that, even in persons the most resigned, the absence of mania is one of the rarest exceptions, as well as the excessive height that the madness usually reaches in lyssa patients. It is certainly more probable that the madness in lyssa is not due to moral grounds, but is caused by a propagation of the excessively increased morbid excitability of the motor-central apparatus of the pharyngeal and respiratory nerves to the central organs of the psychical functions. The symptoms of the mania have many analogies to reflex spasms. Trifling mental excitement causes severe outbreaks, violent motions, and excited actions in manaical patients, just as slight irritation of the skin causes severe reflex spasms in patients with tetanus. Treatment.—We shall only make the following brief remarks about the sanitary measures by which the state should try to protect its subjects. The only prophylaxis is by confinement of dogs. No attention should be paid to the lovers of dogs. Any one who expends sympathy on the “ poor dog,” and petitions against his being tied up, or wearing a muzzle, should be made to watch a patient with hydrophobia for half an hour, and he would soon be cured. Most muzzles that dogs wear do not prevent their biting, and they are only protective when they do so. It is very important not to kill dogs suspected of madness, but to shut them up and observe them closely. Death, which soon takes place spontaneously, and the symptoms under which it occurs, are far more important in deter- mining that the dog was mad, than are the results of autopsy; for, from the latter, especially if the dog was killed by violence, it cannot be said with certainty whether the dog was mad or not, and harm has been done by such unreliable, demonstrative assertions. The most we can say is that negative results of an autopsy, where no changes have been found in any organ of a dog suspected of rabies, to explain the symptoms and death, go to prove the probability of the diagnosis—especially if we find hair, straw, rubbish, etc., in the stomach ; for, while a healthy dog would not be apt to swallow them, a mad one would. If a man has been bitten by a dog suspected of rabies, prophy laxis requires a destruction of the spot with which the poison may have come in contact; and every dog that has bitten without pro- vocation, or without previous inclination to bite, should be sus- pected. The object of prophylactic treatment should be to destroy the por tions of skin which have come in contact with the virus. It consists in excision of the wound, and in the vigorous cauterization of the part 800 CHRONIC INFECTIOUS DISEASES. with the hot iron, or with a deliquescent caustic, such as caustic potash, butter of antimony, and the like. It is also advisable not to permit the sore, resulting from detachment of the eschar thus made, to heal too rapidly, but, if practicable, to keep it suppurating for months. These measures are all the more likely to be successful, the earlier they are applied, but they should never be neglected, even though weeks have elapsed since the infliction of the bite. As a further precautionary treatment, the exhibition of mercury to the point of salivation, large doses of belladonna, and a series of other so-called antilyssa, are employed; but it is very questionable whether the disease has ever been averted by the use of any of these articles, and whether the cases in which hydrophobia has not followed upon the bite after the use of anagallis arvensis, gentiana cruciata, rosa canina, genista luteo-tinctoria, cantharides, or may-worm, did not belong to the seventy-seven per cent, of subjects in whom the predisposition to rabies did not exist, and without which hydrophobia never occurs. Inasmuch as, after the establishment of the disease, these measures do not pro- duce even the slightest palliative effect, their prophylactic virtue is more than doubtful; hence, I by no means regard it necessary to subject a man, who has been bitten by a mad dog, to the baneful in- fluence of mercury, although I should not hesitate to resort to any procedure, be it never so severe or dangerous to the life of the patient, if, according to actual experience, any benefit were to be expected from it. If the disease has broken out, there is little hope of curing it, or even of alleviating the sufferings of the patient, for hitherto there has been no accurately observed case of lyssa having any other termi- nation than a painful death. Even the waiting and nursing are very difficult, and should only be trusted to persons who are humane as well as fearless and energetic. Every thing that can induce return of the spasms, and, later, of the paroxysms of madness, should be carefully avoided. To relieve the thirst, small enemata of cold water may be given from time to time. In the case I saw, these were well borne and quickly absorbed. In recent cases, where the patient is young and vigorous, we may bleed, as in some cases this has proved of undoubted benefit. If the patient will bear it, we may also let him inhale chloroform from time to time, and give subcutaneous injections of a strong solution of morphine. The favorable results said to have been attained in some cases of tetanus, by the use of curare, decided me to try it in a case of lyssa under my care. At first later •|th of a grain of carefully-tested curare was subcutaneously injected at intervals of three to four hours. Distrustful as we were about the result, this treatment still seemed of palliative benefit, and seemed HYDROPHOBIA. 801 to afford greater relief than the morphine injections. The patient repeatedly prayed for the continuance of the curare injections, as he was firmly persuaded that they relieved him. This experience is enough to make me urge injections of curare in any case of lyssa humana; and, as nothing can be lost by it, to give it even more boldly than we did. SECTION III. GENERAL DISORDERS OF NUTRITION WHICH DO NOT DEPEND UPON INFECTION. CHAPTER I. CHLOROSIS. Etiology.—The subjects of anaemia and hydraemia belong rather to the province of general pathology, since such anomalies of the quan- tity and quality of the blood never arise as independent affections, but always appear as an accompaniment or consequence of other diseases. The state of the blood which gives rise to the condition known as chlorosis differs from that which induces hydraemia. In chlorosis, only the cellular elements of the blood are diminished in number, while its quantum of serum, albumen, and saline constituents, is generally nor- mal. In hydraemia, on the other hand, not only is the blood poor in cellular elements, but its serum is deficient in albumen, and it probably is overcharged with salts. A chlorotic state of the blood (oligocytliae- mia, Vogel) often develops with a certain degree of independence; or, to speak more accurately, it frequently arises without our being able to perceive any morbid condition which, by augmenting the consump- tion of the blood, or by diminishing its production, might induce chlo- rosis, and which generally can be discovered in anaemia and hydraemia. In the present chapter it is the former class of cases alone with which we have to do, and we shall not notice those rare instances in which oligocythaemia develops as a symptom in certain diseases. In females between the ages of fourteen and twenty-four, chlorosis is one of the most common of disorders. It is very natural, then, to ascribe the disease to the effects of those processes which are going on in the bodies of young girls at the period of puberty; but we are still ignorant as to what physiological connection exists be- tween the two conditions. We know equally little of the causes CHLOROSIS. 803 winch favor the occurrence of chlorosis at the time of puberty; for, al- though it is not improbable that the development of this affection is often encouraged by a want of fresh air and exercise, by improper nourishment, mental excitement, improper reading, masturbation, or by a generally unhealthy mode of life, yet the disease arises often enough under conditions precisely the opposite of these, in girls who work all day in the open air, who are well fed, do not read novels, and are not addicted to any secret vice. I may add that, according to my observation, obstinate chlorosis attacks all young girls without excep-' tion, in whom the menses have appeared in the twelfth or thirteenth year, and before the development of the breasts and pubes. Far more rarely chlorosis—oligaemia without assignable cause— appears in children and in pregnant women, and sometimes even in males. The number of instances of chlorosis in this class is very limited. Ax atomical, Appearances.—The lesions characteristic of chloro- sis lie mainly in the blood, which, with Virchow, we may regard as a tissue consisting of cells with a liquid intercellular substance. As has been said already, this intercellular substance, the serum, does not present any constant anomaly. Its composition generally is normal; more rarely there is a diminution of its albumen. In other cases, again, the amount of albumen of the blood-serum seems to be increased, so that, besides the oligocythaemia, there is hyperalbuminosis. In the first two instances, the whole volume of the blood is probably reduced, while in the latter the possibility cannot be denied that, in spite of the diminished number of the blood-corpuscles, the absolute bulk of the blood is augmented, adding a serous plethora to the oligocythaemia. In pronounced chlorosis, the disease in the red-blood corpuscles may be so great that a thousand parts of blood may contain but sixty or forty parts of dried blood-cells, instead of the normal average of one hundred and thirty parts. Upon the autopsy of a chlorotic person, who has died of intercurrent disease, the viscera are all found to be remarkably pale. In some cases, the signs of simple fatty degenera- tion are found in the tunica inthna of the great vessels.1 Symptoms axd Course.—The most striking symptom of chlorosis consists in the pallor of the skin and visible mucous membranes. When the skin contains but little pigment, as is the case in blondes, the sur- face of the body is of a pure white; while, when the pigmentation is intense, as in black-haired persons, it is more of a dirty-gray or yel- lowish hue. The pallor is often most distinctly pronounced upon the ears, while in the mucous membranes the loss of color is most remark- able in the conjunctiva and the gums. The reason for this blanching of the complexion is manifest. The number of red-blood corpuscles 804 GENERAL DISORDERS OF NUTRITION. upon which the blood itself depends for its redness, and the tissues through which it circulates for their tints, is reduced one-half, or one- third, or even lower. The exceptions to this rule, namely, the occa- sional instances of chlorosis in which the cheeks retain their redness, are easy of explanation, when we come to know that the color of the blood is but one of the causes upon which the tint of the cheek de- pends ; another consisting in the filling and distention of the capil- laries. Just as there are persons whose cheeks are pale, in spite of the deep hue of their blood, because their capillaries are inadequately filled, so there are other chlorotic persons who, notwithstanding that their blood is pale, always have red cheeks, because their capillaries are filled to bursting, and are varicose. The transient flush observed in almost all chlorotic persons when excited or heated, and to which we shall refer hereafter, is also to be ascribed to a momentary disten- tion of the capillaries wTith blood. The fat in the subcutaneous areolar tissue of chlorotic persons is often normal in amount, and is sometimes even in a state of exuberant development. This condition furnishes an important distinctive marie between chlorosis and the chronic anaemia which often manifests itself in latent consumption, and in other concealed disorders which affect the quality of the blood. In a symptomatic anaemia or hydrasmia of this kind, which is frequently confounded with chlorosis, the subcutane- ous fat soon vanishes as the color of the skin fades. CEdematous effusion into the subcutaneous cellular tissue is rare in this disease. Hence a moderate paleness of the surface, accompanied by oedema of the feet, warrants the suspicion of hydraemia and not of chlorosis; and conversely, when the lips, cheeks, and ears are white as wax, and yet there is no sign of oedema, it is probable that the serum of the blood retains its normal composition, and that the case is a pure oligocythae- mia and not a hydraemia. Chlorosis is always accompanied by more or less shortness of breath, owing to a diminution in the number, sometimes amounting to one-half or more, of the bodies which take up oxygen, and give out carbonic acid. The normal number of respiratory acts is insufficient to supply oxygen to the lungs in quantity adequate to the wrants of the system. Every bodily effort, by increasing the consumption of tissue, and augmenting the production of carbonic acid, aggravates the dysp- noea, and multiplies the patient’s breathings to a distressing degree. Hence patients with pronounced chlorosis scarcely ever fail to com- plain that they “ get out of breath ” when they walk fast, or mount the stairs. The diminution in the interchange of gases, and especially the impediment to oxygenation of the blood, also accounts for a second series of symptoms peculiar to chlorosis. The strength of the muscles, CHLOROSIS. 805 which, to be vigorous, calls for a supply of well-oxygenated, blood, is greatly reduced. The patient is easily fatigued, and complains of a sense of weight in his limbs, and not unfrequently (pseudo-rheumatic) muscular pains are induced by the slightest effort, such as only are felt by healthy folk after unusual and excessive exertion. Important as it is to the normal function of the muscles that a free supply of well- oxygenated blood should circulate within them, this is equally essen- tial to the proper action of the nerves. In treating of the neuroses, in almost every instance, we have referred to the state cf the blood in chlorosis as an important point in their etiology. Hence, neuralgia is extremely common among chlorotic patients, that of the trigeminus being especially frequent among the peripheral neuralgias, while in the internal organs cardialgia is more common. Anaesthesia, convul- sions, and palsy, are rarer, and are seldom observed excepting when (as sometimes happens) hysteria develops during the disease. There are nearly always signs of hysteria in chlorosis, which consist of general bodily and mental hyperaesthesia, a troubled, irritable temper, a dis- position to weep, perverted appetite (for instance, a craving for coffee- beans, slate-pencils, etc.). The organs of circulation present numerous deviations from the normal. The patients nearly all complain of palpitation. I have already declared that this symptom is not altogether due to an aug- mented or accelerated action of the heart, being also in some degree dependent upon a general hyperesthesia, whereby the impulse of that organ is rendered distressingly perceptible, whereas it is not felt at all by most persons, even when its beat is enormously intensified by hypertrophy (Vol. I.). Upon auscultation of the chest, over the heart and great vessels, we hear the blowing sounds so often alluded to, and which are known as “ blood murmurs,” to distinguish them from the morbid murmurs depending upon alteration of the structure of the heart. This name is inappropriate, however, as the sounds are not caused directly by the altered condition of the blood. They most probably arise from an abnormal tension of the valves and arterial walls. Far more frequently, upon listening over the jugular vein, a pecu- liar humming, singing murmur is heard, known as the “Nonnen- gerausch,” or “ bruit de diable.” The name is derived from the sound of the humming-top, called “ Brummkreisel ” in North Germany, and “Nonne” (nun) in other places; while in France it is called the 4 diable.” The sound is more intense upon the right side than upor. the left, and subsides when the patient assumes a horizontal attitude or draws a forced breath. The mode of origin of the “ bruit de diable ” seems to be as follows: The lower part of the internal jugular veins 806 GENERAL DISORDERS OF NUTRITION. lying behind the sternoclavicular articulation is attached upon all sides, so that it cannot collapse, like other veins, when the stream of blood is reduced in volume. When the jet of blood which enters this large space is too small, it can only fill it by forming an eddy. This whirling current throws the walls of the veins into sonorous vibration. If the neck be turned to one side so as to compress the jugular of the opposite side between the omohyoid muscle and the cervical fascia, the bruit de diable becomes audible in the majority even of full-blooded, healthy persons. When the sound is perceptible without such a turning of the neck, it may always be inferred that the patient’s blood is impoverished and that his veins are scantily filled. The excessive nervous irritability arising from inadequate oxygenation of the blood also involves the vasomotor nerves; whence the sudden flushing and paling of chlorotic persons. Besides the cardialgia already alluded to, other serious disorders of the digestive system arise in chlorosis, which, unless watched with patience and attention, might give rise to dangerous mistakes. The appetite is nearly always diminished; after eating, there is a sense of pressure and fulness in the epigastrium, with acid eructations and other symptoms of dyspepsia, which, in most patients, depend on “ atonic weakness of digestion ” (Vol. I.), and generally disappear as the state of the blood improves. Affections such as these are not dangerous, and nearly always get well under proper treatment; unfortunately, however, the chronic ulcer of the stomach is also a very common occur- rence in chlorosis, and often develops undetected. In treatment of a chlorotic patient, it must never be forgotten that the cardialgia and dyspepsia may be dependent upon this grave lesion of the stomach, and all suitable means must be invoked to aid us to a correct diagnosis. Neglect of such precautions may terminate in an unexpected and tragic denouement by haamatemesis, or even by perforation. The urine of a chlorotic patient, unless there be intercurrent fever, is remarkably limpid and light. The lowness of its specific gravity is probably owing to the small amount of urea which it contains, and its light color to a deficience in coloring matter. Reduction in the supply of oxygen sufficiently accounts for the decrease in the destructive assimi- lation, and consequently for the diminution of the urea in the urine. We know but little regarding the formation of its coloring matter, but it can scarcely be doubted that it is derived from that of the blood; lienee, when the number of the blood-corpuscles, which contain the red matter, is diminished, it is not surprising, caeteris paribus, that the coloring of the urine should decrease. The sexual function nearly always suffers derangement, generally in the form of amenorrlioea, more rarely in the form of excessive men- CHLOROSIS. 807 struation or of dysmenorrhoea (Yol. II.). When amenorrhoea occurs, it is almost always because the ovules do not mature; for, generally, all the other signs which attend ripening and expulsion of the ovum are absent, besides the bleeding. By the laity, and even by some physicians, amenorrhoea is supposed to be a constant symptom of chlorosis, an error which may sometimes be productive of the utmost mischief, by inducing the premature suspension of remedies still urgently required, on ac- count of the presence or appearance of the menses. Indeed, owing to this erroneous idea, that chlorosis is always attended by amenorrhoea, it not unfrequently happens that chlorotic girls, suffering from dysmenor- rhoea or menorrhagia, and complaining of headache and palpitation, are supposed to be “ too full-blooded,” and are therefore purged and bled. Finally, in many chlorotic patients, besides the irregular menstruation, there is a catarrh of the uterus and vagina (Yol. II., pp. 123, 171). The course of chlorosis, unless cut short by proper medication, is almost always slow and tedious. This disease, if not detected, or if treated homoeopathically, often lasts for months, and sometimes for many years. It generally terminates in recovery, although, in very young persons, one or more relapses are apt to occur. More rarely, chlorosis passes over into other disorders, such as tuberculosis. It never endangers life, excepting through its complications, particularly the very common one of chronic ulcer of the stomach. The stories about acute febrile chlorosis terminating in death are the result of erroneous diagnosis ; although it is true that unimportant febrile dis- eases, when they attack chlorotic patients, are often accompanied by typhoid symptoms and assume a malignant type. Treatment.—Attempts to fulfil the causal indication in chlorosis are very seldom followed by benefit, a proof that the causes to which the disease is generally ascribed are not relevant ones. Chlorotic girls are often restored to health in a few weeks, by the fulfilment of the indications from the disease itself, although they had been long and carefully, though fruitlessly, protected from pernicious agencies, had passed months in the country, lived on the best of food, exercised daily, and taken a course of German or Swedish gymnastics without bringing color to their lips and cheeks, relief to their shortness of breath, or improvement to their irritable and fretful temper. The reputation which dietetic treatment enjoys, as a remedy for chlorosis, is mainly attributable to the circumstance that not only does pure oligo- cythaemia bear this name, but it also is given to a great variety of anaemic conditions, in which such treatment is indispensable, while the use of iron is but of secondary importance. Experience teaches daily that brilliant cures of pure chlorosis may be made under the most un- favorable external conditions. 808 GENERAL DISORDERS OF NUTRITION. The indications from the disease itself demand the exhibition of iron. If any medicine ever deserved the name of a specific, iron does, as a remedy in this disease. The surer our diagnosis, so much the more certain may we be of succeeding; and when, contrary to our expecta- tions, we fail of success, there will be reason for suspecting that the case is not simple chlorosis, but an anaamia depending upon some other unperceived or unrecognizable disorder. The progress of a chlo- rosis, which, developing in a young girl at the period of puberty, has defied all treatment, often proves it to have been but the initiatory stage of a tuberculosis, or the anaemia consequent upon a chronic gastric ulcer. We are ignorant of the manner in which the iron improves the defective state of the blood. The existing red-blood corpuscles are not wanting in iron, but there is a deficiency of the red corpuscles themselves, into whose chemical composition iron enters to a slight extent. Perhaps the iron stimulates the activity of the region where the red corpuscles are formed, or perhaps it regulates the digestion, and thus promotes the supply of material for the forma- tion of blood-corpuscles. But there is no sound foundation for any of these hypotheses, the number of which might be materially increased. Opinions vary greatly as to the proper form and dose of iron. Iron- filings are much prized by certain well-known and fortunate practition- ers ; others, equally celebrated and successful, prescribe one or other of its salts, to the exclusion of all the rest, claiming its effects to be more certain, and better borne. Others, again, begin treatment with the “ mildest ” of the ferruginous preparations, as the mallate or lac- tate of iron, proceeding thence to the “ stronger ” ones, the chloride and sulphate, winding up the treatment with the filings. Besides the limatura ferri, which may be given in three to six grains as a dose, generally with an addition of powdered cinnamon, the tinct. ferri pomat. (gtt. xv-xxa), the lactate of iron (gr. ij-v), the ferri carb. saccliarat. (gr. iv-x), the tinct. ferri chlor. (gtt. x-xxx), ferri sulph. (gr. j-iv), are the preparations of iron in most common use. From the estimate in which these various preparations are held by different established authorities, and from the fact that nearly every practitioner has his “ pet article,” which he uses in the majority of cases, it may be in- ferred : 1. That the efficacy of iron in chlorosis does not depend upon the form in which it is administered. 2. That nearly all ferruginous preparations are well borne in chlorosis. 3. That special indications for the exhibition of one or other of them cannot be laid down. Foi more than twenty years I have used BlaucVs pills almost exclusively in chlorosis, and have witnessed such brilliant results from them in a large number of cases, that I have never found any opportunity to ex- periment with other articles. Instead of the forty-eight huge boli, CHLOROSIS. 809 according to Bland's original prescription (fiE, Ferri sulp. pi.lv., potass, carb. pur®, aa § ss, tragacanth. q. s. u. f. pil.), I have ninety-six pills made. Nor am I so timid in increasing the dose according to Bland's formula, but order three pills thrice daily, and sometimes four or five if they are well borne, which they almost always are. Three boxes of Bland's pills nearly always suffice to cure the most persistent chlorosis. At Magdeburg and Greifswald I often had to send my re- cipe for the pills to a great distance, my good fortune in the treatment of chlorosis—to which, by-the-by, I owe the rapid growth of my prac- tice—having given me a groat reputation as the possessor of a sover- eign remedy against that disease. I do not suppose that Bland's pills excel all other ferruginous preparations in virtue; indeed, I have repeatedly satisfied myself that colleagues who made use of other recipes obtained equal results, pro- vided only that they gave doses of equal size; but I also believe that the efficacy of Bland's pills cannot be surpassed, simply because they can be administered in very large doses without distressing the patient. I had an opportunity to test the truth of this some ten years ago. I was asked for my recipe by one of my colleagues, and at first referred him to the Canstatt text-book, which contained the well-known formula for Bland's boli; but, as he did not have that book, I told him the formula, adding, that I began with three boli, raising the dose one bolus every three days. Some time afterward my colleague took occa- sion to thank me, extolling the excellent effect of the medicine, and stating how well it had been borne by the patient. As it turned out, however, he had misunderstood me, and, instead of raising the dose every three days, had added one bolus at every dose. It has been maintained that the treatment of chlorosis does not require large quantities of iron, because the amount of it taken up by the blood is very small, and since, even when small doses are given, a large portion of the metal always passes off in the stools as superflu- ous, and further, because the efficacy of the chalybeate springs in this disease proves that a minimum of iron will suffice. Without going into groundless theoretical discussions, I will admit that the disease will also recover (although somewhat slowly) under the use of smaller doses of iron, and may be cured by chalybeate waters; but the numbej of patients who have recovered in my practice through the employment of Bland's pills, and under that of my colleagues under the use oi carbonate of iron (pil. ferri carb.), or of lactate of iron in large doses, after they had taken small doses of tincture of iron and wine of iron for years without positive effect, and had repeatedly visited Pyrrnont and Driburg, is large enough to warrant the assertion that we shall cure chlorosis most speedily and surely by means of those ferruginous 810 GENERAL DISORDERS OF NUTRITION. preparations which can be tolerated in the largest doses, and of these Bland's pills stand highest on the list. A very common error in the treatment of this affection consists in the attempt to relieve the erethism, digestive disturbance, and other troubles due to the state of the blood, by means of mineral acids, bit- ters, and other medicines; while iron, from which alone, or at least from which the greatest benefit is to be anticipated, is neglected. Such preparatory treatment almost always retards the recovery un- necessarily. I will finally observe that, as long as my chlorotic patients continue languid, indisposed to exertion, and void of appetite, I do not urge them to walk or to eat, generally to their great satisfaction; but I make them promise that they will exercise assiduously as soon as they feel the strength and inclination to walk, and that they will take food freely whenever they gain an appetite to eat, the acquirement of which is seldom long withheld. I have already said that relapses of chlorosis cannot be averted, especially when it sets in at the commencement of the period of evolution; hence I always take the precaution of suggest- ing the possibility or even the probability of a relapse, and have often found that the patient and her relatives do not take the prospects much to heart, when I assure them that the second attack will be as speedily curable as the first. Although, as I have said, I consider the chalybeate springs super- fluous, and far less effective than iron given in large doses, yet, when a convalescent from chlorosis fears a relapse, I would recommend the springs of Pyrmont, Driburg, Cudowa, Altwasser, St. Moritz, in Swit- zerland, and Imnau, in Swabia. CHAPTER II. Etiology.—The abnormal changes in the quality of the blood t( which chlorosis is due can be detected by microscopic and chemical in vestigation; these aids fail us in our researches upon scurvy. It has been stated, indeed, that, in scorbutic blood, the fibrin is diminished, or has lost its coagulability; or that the salts of soda are abnormally increased, while those of potash are diminished; but, after repeated in- vestigation, the truth of none of these statements has been established. Nevertheless, the . commonly adopted opinion, that scurvy is a disease dependent upon a derangement in the composition of the blood, is probably correct. Independently of the fact that the disease arises under conditions unfavorable to a normal composition of the blood, we SCORBUTUS SCURVY. SCURVY. 811 shall see, while discussing its symptoms, that these depend upon a disease of the capillary walls, extending throughout so large a portion of the system that wTe must infer that the starting-point of the malady is an imperfect state of nutrition of the capillary walls resulting from improper nourishment. With regard to the etiology of scurvy, we shall limit our remarks to a statement of the conditions which are found to favor the develop- ment of the disease, since, until we know in what the scorbutic state of the blood consists, all theoretical reasoning upon its connection with these pernicious conditions is idle. Scurvy is so common an occurrence during long voyages at sea (sea-scurvy), where the crew live almost entirely upon hard bread and salt meat, and are entirely deprived of potatoes and fresh vegetables, that the disease has been attributed sometimes to the over-supply of salt in the food, sometimes to wTant of fresh meat and vegetables, and sometimes again to both causes com- Dined. The theory, that in scorbutic blood there is an undue prepon- derance of the salts of soda over the salts of potash, seems to find support from the frequence of this affection among seamen who are deprived of vegetables, while profusely supplied with salt. Neverthe- less, although it cannot be denied that the food of sea-faring people during long voyages furnishes one of the conditions which favor the occurrence of scurvy, yet this is by no means to be regarded as the sole cause of the disease. Scurvy has been known to break out early, and with great virulence, in ships where the crew have been greatly exposed to cold, particularly to moist cold, as well as in ships which have been detained by protracted calms at the equator. It has also been observed that immoderate fatigue and a despondent, melancholy state of mind favor the development of the disease, while a crew who work moderately, and keep up their spirits and courage, retain their health much longer, in spite of the badness of their food. That scurvy does not depend exclusively upon the use of salt food, and want of fresh provision, is proved still more forcibly, and moreover, the hypoth- esis regarding the preponderance of the salts of soda over those of potash in scorbutic blood is overthrown by the fact, that it also appears among people whose diet is almost entirely vegetable, but who suffer from destitution, and live in cold, moist cellars, as is the case m north- ern countries, especially in Russia (land-scurvy). The repeated outbreaks of scurvy among the inmates of garrisons and prisons, and other humanely and conscientiously kept institutions, is a remarkable fact, and one which cannot always be ascribed to the influences above mentioned. Anatomical Appearances.—The bodies of persons who have died of scurvy, if the disease has been of long duration, exhibit ex- 812 GENERAL DISORDERS OF NUTRITION. treme emaciation and a moderate oedema, particularly of the lower extremities. The integuments are of a dirty, ashy hue, and are gen- erally covered by dry detached epithelium. Here and there extrava- sations of variable size are found in the tissue of the cutis as well as in the subcutaneous and intermuscular connective tissue. Besides the liquid effusions of blood, hard coagulated infiltrations, stained red by an admixture of blood, are almost always found beneath the skin, be- tween the muscles ; more rarely within the muscles themselves. The blood is remarkably liquid and dark in color. The walls of the vessels and the tissues about them are deeply stained by it. In the cavities of the pleura, pericardium, peritonaeum, and articular capsules, there is almost always a serous or serofibrinous effusion, with an admixture of blood. The lungs are more or less compressed by the pleural effusion, while the uncompressed portion is the seat of a bloody oedema. The liver, spleen, and kidneys, are studded with ecchyinoses, and appear relaxed and filled with blood, which also is extravasated, and infiltrates the tissues. Ecchymoses also exist between the serous and muscular coats of the intestine. The mucous membrane of the intestine is red- dened, swollen, and relaxed, and sometimes is in a state of follicular ulceration. Symptoms and Course.—The first signs of scurvy are usually those of a general cachexia; the patients complain of great debility and lassitude, and particularly of a sense of excessive weight in their lower limbs. Their spirits are deeply depressed, they can no longer devote themselves to the slightest work, and are excessively sad and despondent. At the same time the face of the patient loses its bright hue and grows pale and muddy, the lips acquire a bluish, livid tinge, the eyes sink into their sockets, and are surrounded by a blue ring. These symptoms are usually accompanied by darting or piercing pains in the limbs and joints, which might easily be mistaken for rheumatic pains. It is not usual for the characteristic local manifestations of scurvy to show themselves until the precursory symptoms have con- tinued for some days or even for some weeks ; although CejJca has often observed the disease to commence locally, the signs of cachexia not appearing until the gums had grown very sore, and all the body was covered with scurvy-spots. In our first volume we have described the scorbutic sore mouth in detail. It is the most common and generally is the first of the local symptoms of the disease. There are exceptions, however, to this rule also. CejJca mentions instances in which sugillations, tense oedema of the feet, and hard, painful infiltration of the connective tissue, pre- ceded the bloody oedematous relaxation of the gums. The effusions of blood into the tissue of the skin, mentioned above, sometimes take SCURVY. 813 the form of small round petechias, sometimes of vibices, and sometimes of extensive ecchymoses. They almost always appear first upon the lower extremities, and afterward spread over the rest of the body. Regions exposed to the action of trifling mechanical violence are espe- cially liable to become the seat of the ecchymoses. In the epidemic in the house of correction at Prague, described by Cejka, the influence of mechanical action was strikingly apparent. In most patients the hol- lows of the knees were most affected, but, in wood-cutters and in per- sons who worked at the spinning-wheel, the right arms were attacked. Wool-combers and laundresses suffered in their forearms; women in the place where their garters pressed. The spots which at first were violet, and of almost a blackish brown, pass through the well-known changes of color peculiar to extravasations, blue, green, yellow, etc. When new spots appear, while the old ones are fading, dark-blue and green- ish-yellow spots are found simultaneously upon the skin. Sometimes circumscribed effusions beneath the epidermis give rise to blebs filled with a bloody liquid (purpura bullosa, pemphigus scorbuticus), which, if they burst and are treated carelessly, may result in obstinate ulcers. Ulcers also form in some patients after the receipt of trifling injuries. They are characterized by the flabby, spongy, bleeding granulations which cover their surface. The hard infiltration of the subcutaneous and intermuscular areolar tissue forms rounded tumors beneath the skin, varying in size from that of a hazel-nut to that of a fist, situated usually upon the lower, more rarely upon the upper extremities, and upon the belly, throat, and cheeks; they cause more or less pain, and are covered by a skin which either retains its normal color or else is suffused by blood. Sometimes the indurations are extensive and dif- fuse, covering the hams, the calves of the legs, and the inner surface of the thighs. They are hard as a board, and, owing to the pressure which they exert upon the muscles, they render all movement of the affected limb impossible. The cutis. remains immovable above this diffuse induration, and is either of normal appearance or is suffused with blood. Besides the bleeding from the gums, which, though not always very profuse, is seldom absent, haemorrhage from other mucous membranes occurs in some patients, especially epistaxis, haemoptysis, metrorrhagia, and bleeding from the bowels. Ecchymosis of the con- junctiva and effusions into the chambers of the eye, with malignant ophthalmia, have occasionally been noticed. The inflammations of internal viscera, particularly scorbutic peri- carditis and pleuritis, do not differ in any characteristic or peculiar man- ner from primary inflammation. Voluminous effusions are often rap- idly deposited, putting the patient in danger of suffocation; but I have also witnessed the rapid and unexpected reabsorption of large collec- 814 GENERAL DISORDERS OF NUTRITION. tions in the pleura and pericardium of scorbutic persons. Owing to the variety and irregularity in the succession of the symptoms of this disease, the few cases which have come under my observation have presented very different aspects. Its course is chronic, and, if the pernicious influences under which it has arisen be not allayed, it is often extremely tedious. In these pro tracted cases the prostration of the patient becomes excessive; some- times he faints with every attempt to sit upright; he complains of a distressing palpitation and great dyspnoea; the action of the heart grows very weak and rapid, extensive oedema arises in the subcuta- neous connective tissue, while the soreness of the gums, the ecchy- moses, the brawny infiltration of the areolar tissue, and the other local affections, increase greatly in extent and intensity. A marked feature of the disease consists in the rapidity of its abatement and the sudden transformation from a condition of the utmost distress to one of rela- tive convalescence, often terminating in full recovery, when the patient is rescued from noxious influences, and placed in a condition favorable to a cure. It is true that, under such circumstances, their recovery is very slow, and they always retain a great tendency to relapse. A fatal termination of scurvy occurs either late in the disease from extreme exhaustion and general dropsy, or else it takes place earlier and before the prostration has acquired much intensity from pleurisy, pericarditis, profuse bloody diarrhoea, or other complications. Treatment.—In modern days the sea-scurvy has become rare, owing to the shortening of voyages, and to the better supplying of ships, especially by the provision now made of lemon-juice, sauer-kraut, and hermetically sealed vegetables. Land-scurvy also, which formerly was of much more common occurrence, has become a rare disease in this country, from the wholesomeness of the dwellings and the improved diet which paupers now enjoy, thanks to the progress of modern cul- ture, so that a prophylaxis against scurvy is no longer talked of. In- deed, precautionary remedies are now superfluous, excepting when several cases of scurvy break out in a barrack, or workhouse, or similar institution, causing apprehension of an epidemic appearance of the dis- ease. These precautions consist in the most scrupulous attention to cleanliness, warmth of clothing, ventilation of apartments, exercise in the open air, a sufficient allowance and proper choice of food, which should consist of fresh meat, and, if possible, also of fresh vegetables, and salad. Good beer should also be provided, and, where this is un- obtainable, brandy-and-water should be administered. The cost of such attentions is amply compensated for, if we succeed in putting a check upon the disease. In cases of pronounced scurvy, the freshly-expressed juice of eertaiu PURPURA HEMORRHAGICA. 815 plants, especially that of the order of crucifera, such as water-cresses, cabbage, mustard, radishes, horse-radishes, spoon-wort (scurvy-grass), and the like, is extremely beneficial, while the extracts of the same plants are quite useless. The healing effect of a fresh vegetable diet upon scurvy is much more positively ascertained than is. the depend- ence of the disease upon a want of such nourishment. Next in virtue is the juice of certain acid fruits, especially that of lemons and oranges, although that of cherries, currants, apples, and the like, is also serviceable. The mineral acids are of no benefit whatever. The bitters and aromatics, also, are of a questionable and certainly of a very secondary value. The barm of beer, also, has a great reputation as an anti-scorbutic, when given to the amount of six or eight ounces daily. It is very important that the rules as to diet and regimen, laid down above, in treating of the prophylaxis, should be carefully ob- served. The local treatment of the sore mouth has been discussed already. For the ecchymoses and infiltrations, lotions and compresses wet with aromatic vinegar, spirits of camphor, and the like, may be applied. The haemorrhages and internal inflammations are to be treated upon general principles, due regard always being had to the prostrate condition of the patient. CHAPTER III. PURPURA HJEMORRHAGICA—THE MORBUS MACULOSUS ” OP WEKLHOF. Etiology.—The symptoms of the spotted disease of Werlhof re- semble those of scurvy, as far as regards the appearance of extravasa- tions of blood from the capillaries of the skin and mucous membrane; but the haemorrhages are not accompanied by any affection of the mouth, nor by the peculiar subcutaneous and intermuscular infiltra- tions, nor the haemorrhagic inflammations of the serous membranes, which we know to be symptoms of scurvy. The reason for the tenderness of the capillaries in Werlhof's dis- ease is obscure. The extension of the haemorrhages over various parts of the body, its frequent occurrence among feeble and debilitated per- sons, and among convalescents from severe illness, and its appearance m those who dwell in damp, unwholesome lodgings, or in other unfa- vorable conditions, make it probable that the disease of the blood- vessels depends upon an improper state of this nutrition, or upon insufficient or bad nutriment. On the other hand, robust, powerful .ndividuals, living under the most advantageous circumstances, and 816 GENERAL DISORDERS OF NUTRITION. who do not offer the slightest reason for a defective state of blood, aie also sometimes attacked. Symptoms and Course.—Sometimes the first symptoms of Werl- hof's disease consist in the appearance of numerous purpuric spots upon the skin; in other instances the haemorrhages are preceded for some days or weeks by digestive derangement, languor, debility, but never by the signs of severe cachexia, such as generally precede the onset of scurvy. The purpuric spots, though small, are generally nu- merous. Their most common seat is upon the extremities and body, although the face is often speckled by numerous petechiae. While the first set of petechiae are passing through the blue and green stages, new blood-red ones make their appearance. Now and then haemor- rhages from the surface are observed ; but such phenomena cannot prop- erly be called bloody sweat (p. 453). Minute, punctiform ecchymoses are also found upon the mucous membranes, especially those of the mouth and fauces. Epistaxis, haematemesis, haematuria, and bloody evacuations from the bowels, are of far more common occurrence in this disease than in scorbutus. When it attacks an otherwise healthy and vigorous individual, and when the haemorrhages do not recur too fre- quently, the undisturbed condition of the patient’s general health often forms a marked contrast with the objective symptoms. Very numer- ous and oft-repeated haemorrhages may result in intense anaemia, a tendency to syncope, dropsy, and even death. In previously healthy persons, however, such a termination of the disease is rare. As a gen- eral rule, the affection ends in recovery after a duration of between two and four weeks. Treatment.—The customary treatment of IVerlhof's disease, which originated with Werlhof himself, consists in the administration of sulphuric acid and quinine. Although there is no proof that the use of these articles exerts any decidedly beneficial influence upon the course of the disease, yet, not to be too skeptical, and for want of more certain remedies, it is advisable to give the dilute sulphuric acid or the elixir of vitriol in doses of ten or twelve drops every two hours in the beginning of the disorder, followed at a later period by a decoction of bark with an addition of sulphuric acid. In cases of profuse epis- taxis which do not readily subside under the application of cold, the tampon must be employed promptly, since the longer the bleeding is allowed to last, so much the more obstinate does it become. For the haematemesis, bits of ice, alum-curds, and cold compresses to the abdo- men, should be employed; for haematuria, large doses of tannin. In ex- treme anaemia it is of importance that the patient should preserve a horizontal attitude as a precaution against swooning. PROGRESSIVE PERNICIOUS ANAEMIA. 817 [CHAPTER IY. PROGRESSIVE PERNICIOUS ANAEMIA. The old names of “ essential,” “ idiopathic,” “ fatal anaemia,” etc., probably referred to the disease now called “ progressive per- nicious anaemia.” Little is known of the causes of this gradually progressing disease, which is nearly always fatal. It is most fre- quent in middle age, but occurs later, as well as in childhood. It is more frequent in females, especially after confinement or during pregnancy, in which case it is apt to induce miscarriage, followed quickly by death. Sometimes the disease can be ascribed to no cause ; at others it may be referred to bad nourishment, repeated losses of blood, diarrhoea, etc. The onset is usually insidious, with great paleness of the skin and mucous membranes ; if there is no fever, the nutritive condition of the patient may be little disturbed. The patients are very feeble, with great tendency to faintness, dyspnoea, palpitation, blood-murmurs, and gastric disturbances, vomiting being very common. The spleen and lymphatic glands are not swollen, wherein it differs from leueluemia, nor does the skin have the brownish color of Addison’s disease. There is no regular fever curve ; indeed, there is no fever till the disease is far advanced ; autopsy has revealed no sufficient cause for the fever. Often, especially late in the disease, there may be epistaxis, pe- techise, ecchymoses on the legs, and haemorrhages from the female genitals, from the stomach, air-passages, etc., or into the tissue of the heart, the pericardium, dura mater, brain, retina, etc. ; the lat- ter are said to be quite frequently discoverable on ophthalmoscopic examination of the region of the papilla as reddish spots or radiat- ing stria3 ; it is said that these spots are characterized by peculiar gray or white specks. These haemorrhages are not, however, lim- ited to this disease ; they may occur in various other forms of anae- mia ; they may be due to the retinal vessels being diseased and being ruptured by vomiting. As pernicious anaemia begins very gradually, and is not at first detected, its duration cannot be determined; it may prove fatal within a few weeks from the time of its discovery, but usually runs on for months or even years. All cases do not prove fatal. The diagnosis is difficult in the commencement. It is said that even in the early stages some of the blood-corpuscles are very small, but this is a disputed point. The anaemic symptoms cause it to re- semble leuchaemia, but in the latter there is marked increase of the 818 GENERAL DISORDERS OF NUTRITION. white corpuscles, and in pseudo-leuchaemia there is swelling of the spleen and lymphatic glands. Cases occur where it is impossible to make an accurate diagnosis, especially when an enlargement of the spleen accompanies the pernicions ansemia. There seem to be cases of transition between this and other diseases. Litten says that changes of the medulla of the bones are found in pernicious anae- mia, just as in medullary leuchaemia; and time must teach us how far this is a constant process, and whether the real lesion in this affection is a disease of the medulla of the bones, as that of the spleen and lymphatic glands is in pseudo-leuchaemia. Cases where cachectic states accompany undiscovered cancers may be mistaken for pernicious anaemia. Treatment has proved unsatisfactory ; even the cases ending in recovery seem to have done so spontaneously. We can do little more than remove injurious influences, and give good diet, air, and tonics, especially iron. It has been claimed that great benefit has followed the adminis- tration of phosphorus, but other observers deny the efficacy of this remedy. In some of these forms of anaemia the employment of arsenic by the mouth and subcutaneously is reputed to be very efficacious, but it has not yet been sufficiently tried to enable us to say in which cases it will do good and in which it will fail. It seems quite certain that some patients who are not benefited by administration of iron, will improve if the iron is continued while inhalations of oxygen gas are given in doses of two or three gallons diluted with air several times daily.] HEMOPHILIA. 819 CHAPTER Y. HAEMOPHILIA (HAEMORRHAGIC DIATHESIS). Etiology.—The names haemophilia, hmmorrhapliilia, are applied to a congenital haemorrhagic diathesis distinguished either by the un- usual obstinacy of traumatic haemorrhage or a tendency to sponta- neous bleedings. Hitherto no abnormity capable of accounting for the symptoms has been detected either in the blood or the vascular walls of the patient, although in a small number of cases the walls of the blood-vessels have been found to be remarkably thin and delicate. In most cases of haemophilia the disease is hereditary, that is, the patient descends from a family one or more of whose members in preceding generations have suffered from the same affection. There are instances in which it has been transmitted through four generations; others in which a generation has been “ skipped,” the grandchildren having haemophilia, but not the children. It is rare for every member of a family to inherit this dangerous disorder, and the daughters seem to remain free from it with especial frequerice. There also are well- authenticated observations which leave no doubt of the occurrence of congenital haemophilia not dependent upon hereditary predisposition. Symptoms and Course.—Until the discovery is made that a tri- fling wound will give rise to an irrepressible and dangerous loss of blood, there is no symptom to warn the patient of his perilous con- dition. Some observers, indeed, claim that this class of patients are distinguishable by the remarkable delicacy of their complexion, their superficially situated and conspicuous veins, blonde hair, and blue eyes, and, in one family that I know of, this description is equally applicable to the whole of them, including the female members, who are exempt from the disorder. Other observers, again, state expressly that the patient’s appearance presents no perceptible characteristics. The accidents which give rise to these alarming haemorrhages are generally extraction of a tooth, a puncture, a small cut or laceration, and it would almost seem as if such injuries were more dangerous than severe wounds. The blood oozes out as if from a sponge, al- though no bleeding vessel is discoverable ; all attempts to stanch the bleeding are in vain, and it persists for days. The blood, which at first is normal, gradually growls thin and wTatery, forming small, loose coagula. At last the complexion of the patient acquires a waxy pallor, the lips lose their color; syncope and other signs of exsanguinity oc- cur, and the patient may perish in a few days. More commonly, how- ever, the bleeding ceases, and the patient, in a state of utter exhaus- tion, slowly recovers from the effects of his enormous loss of blood. 820 GENERAL DISORDERS OF NUTRITION. which often amounts to many pounds. Besides these dangerous ex- ternal haemorrhages, extensive extravasations occur beneath the skin, in consequence of the slightest contusion. Wunderlich tells of a boy, who, after receiving a flogging at school, came home black and blue, and so covered with stripes and welts that a charge was preferred of cruelty. It afterward appeared that he had the haemorrhagic dia- thesis. Spontaneous bleeding cr haemorrhages without assignable cause do not generally take place until after the patient has suffered repeatedly from traumatic haemorrhages. They generally proceed from the nose: but likewise arise from the bronchi, stomach, intestines, and kidney, and may also occur in the substance of the skin and subcutaneous areolar tissue. They are generally preceded by molimina, such as palpitation of the heart, stupor, signs of cerebral congestion, pain in the limbs, and, in some cases, painful tumefaction of the joints, particularly those of the knee and ankle. There have been instances in which the bleed- ing from the navel-string could not be stanched, but more usually it is not until the period of dentition, and sometimes after the sixth or eighth year of life, or later, that the diathesis betrays itself by a dan- gerous haemorrhage. Most patients die young—few surviving the period of childhood. Cases are known, however, in which the patient has lived to a good old age, the tendency to bleed diminishing, or ceasing altogether, as life advanced. Treatment.—No remedy is known likely to prove efficacious in congenital haemorrhagic diathesis, and we must therefore confine our efforts to a careful regulation of the habits, and the removal of all nox- ious agencies; so that, perhaps, by improving the general condition of the constitution, this dangerous diathesis may subside. Of course, all wounds must be scrupulously avoided. When the bleeding occurs in spite of such precautions, besides the ordinary haemostatic articles, among which steady pressure and the actual cautery are the best, glauber salts in cathartic doses should be prescribed, and, when the bleeding threatens life, two to five grains of secale cornutum every half-hour. These two prescriptions have been of great benefit in some instances. CHATTER VI. SCROFULA. Etioi.ogy.—The term scrofula signifies a morbid (cachectic) con- dition of the system, manifested by a remarkable liability to certain forms of nutritive disorder of the skin, mucous membranes, joints, bones, organs of special sense, and, above all, the lymphatic glands. SCROFULA. 821 A person having merely a tendency to such diseases may also be called scrofulous, although not actually suffering from any one of the above symptoms. The hypothesis that scrofula depends upon a faulty composition of the blood (dyscrasia), and that the lesions found in scrofulous persons were due to the deposit in the tissues of a matter circulated by the blood, and called a “ scrofulous material,” is almost universally aban- doned. The alterations which take place in the skin, mucous mem- brane, joints, bones, and organs of special sense, are of an inflamma- tory nature, and cannot be distinguished from similar affections of a non-scrofulous character, excepting by their intractability and the tediousness of their course. It is impossible to point out any charac- teristic features in a scrofulous eruption or arthritis, or to find any dif- ference between them and similar non-scrofulous affections. Even the caseous metamorphosis, to which the inflammatory products are so prone, is by no means pathognomonic of scrofula, but is common to all diseases of a chronic character which have a tendency to disintegra- tion or destruction. Notwithstanding, however, that such inflamma- tion presents no distinguishing mark whereby its scrofulous nature may be recognized, yet there will rarely be any doubt as to whether or not a case of this kind is entitled to the name. If its exciting cause have been so slight as to be overlooked ; if we are informed that “ the disease came on of itself; ” if this attack, or other similar ones, have arisen repeatedly without assignable cause; if it be accompanied by a series of other disorders, especially chronic inflammation and persistent enlargement of lymphatic glands, it is to be called scrofulous. If, on the contrary, there be known external conditions, whose action upon the system sufficiently accounts for the occurrence and the obstinacy of the affection, without necessitating the supposition that there is any special morbid tendency; if it exist independently, and be uncompli- cated with chronic enlargement of the lymphatics, then it is not to be called scrofulous, notwithstanding the great similarity, nay, the abso- lute resemblance, of its external symptoms to those of a scrofulous disorder. In its origin, scrofula, perhaps, is quite as often a congenital mal- ady as an acquired one after birth. Congenital scrofula is particularly common among offspring of scrofulous parents. There are families, nearly or quite all the children of which inherit the disease. This hereditary form of scrofula is close- ly allied to that in which parents were tuberculous at the time of be- getting the child, or in which the mother was so during pregnane}7, or else suffered from cancer, tertiary syphilis, or some other malady, as well as that form of scrofula occurring in children begotten of aged 822 GENERAL DISORDERS OF NUTRITION. parents. As we know that many of the bodily and nental traits of parents are transmitted to their progeny, it will not seem extraordi- nary that children of feeble, sickly fathers or mothers should have a greater tendency to disease than those whose progenitors are vigorous and healthy; but we are totally unable to account for the fact that scrofula is also very prevalent in the children of parents who are too closely related to one another by blood. It must be added, moreover, that it is not every child of scrofulous, sickly, feeble, or superannuated parentage, and not all of the issue of the marriages of near relatives, who suffer from congenital scrofula. Indeed, many children thus born are healthy, and without any decided tendency to disease; and, on the other hand, this malady often attacks the offspring of parents entirely exempt from the action of any of the above predisposing agencies. Acquired scrofula generally arises as a result of pernicious in- fluences which have impeded the healthy development of the system during the first years of life. First of all, among these, stands im- proper nourishment; a coarse diet, containing but little nutriment in comparison with its bulk, being very properly held in especially evil repute. The earlier this injudicious feeding of an infant commences, so much the greater is the danger that it will become scrofulous; hence, the children fed on pap furnish a very important contingent to the army of scrofulous persons. Want of fresh air and exercise exerts an influence as baneful as that of improper food. Hirsch has collected a large number of facts, proving that, in foundling hospitals, orphan asylums, boarding-schools, factories, and similar institutions, the con- tinual abode in a badly-ventilated atmosphere, saturated with steam, and poisoned by animal effluvia and the products of putrefaction, is in the highest degree favorable to the development of scrofula; and that, according to the experience of these institutions where there is no lack of cleanliness, good food, and warm clothing, the above pernicious agents alone suffice to induce the disease. It springs most frequently, however, from the combined effects of all these different anti-hygienic influences. Although we have declared the chief cause of scrofula to be the impairment of the normal develop- ment of the system during childhood, through the action of the above- mentioned noxious agencies, yet it must be added that, in prisons, poor- houses, and workhouses, the disorder also breaks out among adults subjected to the simultaneous effects of bad nourishment and want of fresh air. The development or reestablishment of scrofula is, like- wise, a not unfrequent sequel to certain acute and chronic diseases; and this is all the more likely to be the case, the younger and the more undeveloped the subject of disease happens to be. Among SCROFULA. 823 the diseases of childhood, measles is especially mischievous in this way. Anatomical Appearances.—Having already stated that scrofu- lous inflammation has no peculiar characteristics, it would now be ab- surd to attempt to describe the anatomical alterations of the skin and mucous membranes, induced by scrofulous eruptions and catarrh. And, indeed, we may refer altogether to the article upon cutaneous diseases for a description of the anatomical alterations of the skin; and to other parts of this work, for an account of the lesions found in the various mucous membranes, merely adding that in scrofula the inflammatory products are generally richly provided with young cells, which accounts for their tendency to caseous metamorphosis. A description of the esions of the bones, joints, and organs of special sense, particularly those of the eye, observed in scrofulous subjects, and which, likewise, are not marked by any distinctive peculiarity, belongs to the province of surgery and ophthalmology. The latter science has anticipated the others by the discovery of the illusory nature of the oft-described symptoms of scrofulous ophthalmia. The alterations which take place in the lymphatics of scrofulous subjects require further attention: first, because the disorders of these organs as yet have received but cursory notice, no special section of this work having been devoted to their consideration; secondly, be- cause, in persons thus afflicted, disease in the lymphatics is so common that, among the laity, scrofula is commonly spoken of as having “ en- larged kernels,” or simply “ having kernels.” In the first place, it happens more frequently in scrofulous persons than in non-scrofulous ones, that the lymphatic glands around an inflam- mation of the skin or mucous membrane become the seat of an inflam- matory process, which has extended along the lymphatic vessels from the skin, and has involved the glands. The connective tissue around the gland next participates in the inflammation of the glandular parenchy- ma, and abscesses and ulceration ensue, which, like all abscesses and ulceration of glandular substance, are very intractable, and often heal, leaving an irregular, ragged, unsightly scar. Owing to the extreme frequence of scrofulous eruptions upon the face and scalp, and of scrofulous otorrhcea, the lymphatic glands of the neck are the most common seat of this form of inflammation and ulceration. Besides these, however, a chronic non-inflammatory enlargement of the lymphatic glands is so often observed in scrofulous subjects, that their presence may almost be regarded as pathognomonic. They may attain a very considerable size, and, when several of them are clustered together, they form huge, knotted cords, or shapeless lumps. The individual tumors are regular in form, smooth of surface, and of a tol 824 GENERAL DISORDERS OF NUTRITION erably firm consistence. No foreign elements can be detected in them under the microscope. They are the product of simple hypertrophy, or, rather (since it is the cells that are multiplied, and not the tissue of the stroma), of a “ cellular hyperplasia.” But, as the number of cellu- lar elements contained in a lymphatic gland, even during health, is a very variable one, the complete subsidence of the enormously enlarged glands of scrofulous subjects, which enlargement is entirely due to an excessive accumulation of cells, will not seem extraordinary. Never- theless, the gradual diminution of, the tumor, with its final return to its normal dimensions, is not the sole termination of this form of glandular affection. Sometimes the tumors, which at first were the result of mere hyperplasia, sooner or later become inflamed. The surrounding areolar tissue takes part in the inflammation, after which, it is no longer practicable to distinguish the individual glands in the general mass. The skin becomes adherent to the tumor, and cannot be made to glide over it. Suppuration and the formation of abscesses generally follow slowly and gradually upon the inflammation, and the skin, hav- ing become extremely attenuated, is perforated by the pus, leaving a sinuous ulcer, with undermined edges. In other instances, inflamma- tion and suppuration only take place at a solitary point in the tumor; and the matter formed at this spot does not burst through the capsule of the gland, but thickens, and undergo escaseous metamorphosis. In such a case, if the swelling subside, the caseous mass projects above the surface of the gland, giving it an irregular shape. A partial or complete caseous degeneration may also take place in the hyperplastic mass, without any previous inflammation or suppuration, the over- crowded cells drying up, and suffering “ anaemic necrosis ” (necn> biosis). Such an occurrence at circumscribed points likewise renders the contour of the gland irregular and angular. The caseous deposit may subsequently become calcified, but, since it acts as an irritant upon surrounding parts, like any other foreign body, it may subsequently give rise to an obstinate inflammation and suppuration. When an entire gland underwent caseous metamorphosis, the process used for- merly to be called infiltrated glandular tuberculosis. If, on the other hand, the deposit of caseous matter was limited, the gland was sup- posed to be affected by miliary tuberculosis, although there wTere no miliary tubercles to be found in it. The most frequent seat of scrof- ulous hyperplasia of the lymphatic glands, like that of scrofulous in- flammation, is in the neck, especially behind the ear, and under the lower jaw, extending thence to the shoulder. The bronchial and me- senteric glands are also very often the seat of scrofulous hyperplasia, with all its consequences, as above described. The terms scrofulous catarrh of the bronchi or intestines is perfectly appropriate to bronchial SCROFULA. 825 and intestinal catarrhs, accompanied by enlargement or caseous de- generation of the bronchial or mesenteric glands. Symptoms ayd Course.—In many instances the scrofulous ca- chexia betrays itself by the patient’s habit of body, which will often arouse suspicion of his delicacy and of his feeble power of resistance against disease, long before any actual morbid tendency (diathesis) is, as it were, officially announced by the occurrence of frequent and ob- stinate attacks of illness induced by causes so insignificant as to have escaped observation. The “ scrofulous habit ” is marked by a deficience of blood and by a bad nutritive state of the more important and more highly-organized tissues; sometimes accompanied by an accumulation of fat in certain regions, especially in the ■ upper lip and nose. When the imperfect nutrition is accompanied by an over-production of fat, there seems to be an indolent state of the processes of constructive and destructive assimilation; but when not only the skin and the muscles, but also the subcutaneous fat, is in a state of imperfect development, it is probable that these processes are in a condition of unnatural activity. Based upon these differences, in the patient’s bodily habit, a classifica- tion of scrofula into the torpid and erethitic forms has been made. Canstatt very aptly describes the torpid scrofulous habit in the follow- ing words: “ An unusually large head, coarse features, a thick chin, swollen abdomen, enlarged cervical glands, and flabby, spongy flesh; ” and depicts the habit of erethitic scrofula as follows: “ A skin of re- markable whiteness, with a tendency to redden easily, and through which the rose-pink or bluish subcutaneous veins are visible, a deep redness of the cheeks and lips, blueness of the thin and transparent sclerotica, which imparts a swimming and languishing look to the eyes. The muscles of such persons are thin and soft, and their weight is light in proportion to their stature, indicating a slightness of their bones. The 4eeth are handsome, and of a bluish lustre, though long and narrow; the hair is soft.” There is no lack of examples of either of these forms of disease, and though it may not be possible immediately to assign every case to one or other category, yet in practice it will be well to adhere to the classification into torpid and erethitic scrofula, since, as we shall find by-and-by, we thereby obtain valuable data for the estab- lishment of therapeutical indications. Scrofula, although principally a disease of childhood, rarely declares itself in the first year of infancy, excepting through a few faint tokens. At the period of puberty scrofulous diseases usually subside, and with them the scrofulous habit more or less completely disappears. More rarely, exposure of the body to pernicious influences at this time excites the subsiding scrofulous tendency to renewed activity, or even induces a 826 GENERAL DISORDERS OF NUTRITION. relapse of disease which has been dormant for years. We have already stated that, under such circumstances, persons, who during childhood did not suffer from the disease, are attacked by it later in life. It is impossible to describe scrofula briefly, and at the same time comprehensively; for its various manifestations combine in the most diverse manner: in one case, this group of symptoms, in another, that one assuming prominence ; and since many patients, notwithstanding the tedious course of their malady, remain free from symptoms which form the most important feature in other cases. And although it is little to be doubted that the localization of scrofulosis (if we may use the term) depends either upon the action of causes which are especially hurtful to the organ attacked, or else upon the morbid susceptibility of the organ to influences whose effect is universally injurious, never- theless we can seldom tell why it should be marked in one case by a scrofulous exanthema, in another by an ophthalmia; why, in a third, a disease of bone should prevail; and it is equally inexplicable why the inflammation and hyperplasia of the lymphatic glands should be more extensive and obstinate in one case than in another. It has not been determined even whether there be such a thing as primary hyperplasia of the glands, or if this process, like the inflammation, be always of a secondary character, proceeding from irritation transmitted to the gland from some neighboring focus of inflammation. As the reality of the latter fact is susceptible of proof in a great majority of instances, it is not improbable, where it cannot be proved, that the irritation for- merly existed at the point of origin of the lymphatic vessels involved, but that it has already subsided; for it is a rule that glandular enlarge- ments long outlast the morbid process which has induced them. The cutaneous eruptions which are the most common, and often the earliest symptoms of the diathesis, are usually situated upon the face and scalp. They generally belong to the form of dermatitis, in which an exudation, more or less fdled with cells, is effused upon the surface of the cutis, and which nowadays are known as eczema and impetigo, and used formerly to be called tinea and porrigo. The more destruc- tive affections of the skin—such as lupus—do not usually appear until a later period of life. Scrofulous inflammation of the mucous membrane is most apt t< appear in the vicinity of the natural orifices of the body, where if readily implicates the neighboring skin, especially if it be moistened by the superabundant secretions. Thus scrofulous coryza is usually complicated with eczema of the upper lip ; inflammation of the exter- nal auditory passage with eczema about the ear; catarrhal conjuncti- vitis with eczema of the cheek ; conversely, the cutaneous eruptions about ail orifice often spread to its mucous membranes, thus inducing SCROFULA. 827 coryza, otorrhcea, conjunctivitis, or ulceration of the cornea. Catarrhs of the intestine and bronchi, and the rarer affections of the genito- urinary apparatus by their obstinacy, may readily excite a suspicion of a more malignant destructive process; and indeed scrofulous catarrh of the bronchi, by extending into the air-cells of the lung, and by in- ducing caseous metamorphosis, with subsequent destruction of the pneumonic deposits, not unfrequently terminates in pulmonary con- sumption. Besides, it often happens that enlarged bronchial glands soften and break down, forming vomicas, which discharge their con- tents into the bronchi. Scrofulous ulceration of the bowels has already been described in detail. Scrofulous inflammation of a joint sometimes takes the form of a simple hydrarthrosis, sometimes that of a so-called tumor albus, while at others it assumes the nature of a malignant arthrocace, accompanied by suppuration, caries of the articular surfaces, burrowing of pus, and the establishment of fistula. The disease of the bones sometimes begins in the periosteum, sometimes in the bone itself, now presenting the character of periostitis and ostitis, and now that of caries, necrosis, or of the two combined. As long as the existence of cheesy masses was regarded as char- acteristic of the tuberculous nature of a disease, it was of course neces- sary to ascribe many of the inflammations of the joints and bones of scrofulous persons to a complication of scrofulosis with tuberculosis. Among the organs of special sense, the eyes and more particularly their superficial tissues, the Meibomian glands, the conjunctiva palpe- brarum, the conjunctiva bulbi, and the cornea, are often afflicted by obstinate inflammation. Indeed, in doubtful cases, the presence of opacity or of scars upon the cornea, has been accepted as important evidence that a patient has been scrofulous during childhood. In the nose, excepting the rare instances in which that organ is destroyed by lupus, scrofulous inflammation merely takes the form of an obstinate coryza, which, however, is hardly ever absent. In the ears, besides the inflammation of the external auditory canal, already alluded to, caries of the petrous bone, with all its mischievous consequences, is apt to ensue. The objective symptoms of scrofulous disease of the lymphatic glands have been described above. The adenitis and the phlegmonous inflammation of the parts about them may be attended with great pain and by more or less of fever, with evening exacerbations. In consequence of this, not only does the patient’s general health suffer, but, if the inflammation and its attendant pain continue for weeks and months, as they often do, his strength is consumed, and his nutritive condition is greatly impaired. After the abscesses which form have 828 GENERAL DISORDERS OF NUTRITION. burst spontaneously, or liave been lanced, and if no new centre of in flammation have formed meantime, the fever gradually abates, the patient’s strength returns, the emaciation ceases, often long before the ulcers have begun to heal, and while they still secrete large quantities of pus. Glandular tumors depending upon cellular hyperplasia are not attended either by pain or fever; but, when very voluminous, particu- larly when seated upon the neck, they not only produce great deform- ity but hinder the mobility of the head. Hitherto it has not been ascertained whether scrofulous enlargement of the lymphatic glands exerts any detrimental influence upon the composition of the blood, whether the cellular elements destined for the blood are retained in the gland, or whether scrofulous glands affect the quality of the blood as the glands of leucaemia do, but in a far slighter degree. The progress of scrofula is tedious and treacherous, and nearly always is marked by periodical alternations of improvement and aggra- vation. Either the same series of symptoms recurs again and again with renewed severity, or else, the former set having abated, or sub- sided, new ones arise. Complete recovery from scrofula is a very com- mon occurrence, especially if we include the cases in which no trace of the disease remains excepting a peripheral speck upon the cornea, an unsightly cicatrix, or other mark, which does not disturb the general health and comfort. Death rarely results from the lesions to which the epithet of scrofulous is usually given. Of these, tedious disease of the bones and joints, and suppuration of the bronchial glands, are the only ones which endanger life. On the other hand, a large num- ber of scrofulous children die of croup, hydrocephalus, and other acute maladies, for which such subjects have a predisposition quite as decided as for the affections to which the term scrofulous usually is applied. Finally, it should be mentioned that lardaceous disease of the liver (BudcTs scrofulous tumor of the liver), spleen, and kidneys, often de- velops during scrofulous disorders, particularly in tedious cases of suppuration and disease of the bones. Regarding the relationship of scrofula to tubercle, we have already stated that no doubt many scrofulous children afterward become tuberculous; but also that a large number of them escape tuberculosis, especially those in whom the constitutional delicacy, upon which the former affection depends, subsides in after-life, and in whom no caseous deposits remain as residua of scrofulous disease. Treatment.—The prophylaxis against congenital scrofula lies almost beyond the sphere of the physician. It is devoutly to be de- sired that scrofulous, tuberculous, sickly, and superannuated persons should not marry at all, and that healthy and vigorous individuals SCROFULA. 829 should not wed their near relatives. But the representations of the physician, that the issue of such alliances are likely to be scrofulous, will rarely deter a man from marrying. On the other hand, it is not only an imperative, but a grateful task to the physician, to endeavor to provide, by proper precautionary measures, against the extension of acquired scrofula. How to fulfil this duty becomes apparent from what has already been said regarding the causes of acquired scrofula. Above all, it should be borne in mind that the development of this disease is promoted, not by one particular noxious influence merely, but by every condition incompatible with health, to which the system, especially during childhood, can be exposed. It often happens that, from the moment when the first tokens of scrofula appear, or even as soon as the parents begin to dread its attacks, the child is carefully deprived of every particle of bread and butter, potato, and the like, and dosed with huge prophylactic spoonfuls of cod-liver oil, while at the same time he is suffered to sit all day long in a close chamber, or upon the benches of an overcrowded school-room. A sufficiency of fresh air and muscular exercise are prophylactic measures of quite as much importance as regulation of the diet is; and we shall here call attention to an error upon this subject, to which we have referred once before while discuss- ing the prophylactic treatment of consumption: namely, the belief that the use of bread and potatoes favors the development of scrofula and tubercle, and the consequent complete privation of children of this kind of food; while in reality the mischief is due to an insufficient supply of animal food—a diet of potatoes and other articles, containing little nourishment in proportion to their bulk, not being injurious unless it forms their sole or at least their principal subsistence. This error is so prevalent, that the discovery that the child has surreptitiously eaten a potato has cost many an anxious mother a sleepless night, and many a child has uselessly been sent to bed hungry on this account. The treatment of pronounced scrofula, where the prophylaxis has been neglected or unsuccessful, requires, first of all, a careful regulation of the regimen upon principles already laid down. Children wfitli con- genital scrofulosis must not be the subjects of experiment with artifi- cial food; but, if the mother have not milk enough, or if she be sickly or feeble, so that, both in her own interest and in that of the babe, she must be forbidden to suckle it, a good wet-nurse must be selected with the utmost care. There is no substitute for the mother’s or nurse’s milk, and the first year of infancy is perhaps the most important to the constitution of the whole life. When the child is older, the directions as to the diet and the mode of life must be given with the utmost pre- cision. It is not advisable to order that “the patient shall eat but little bread, and a good deal of meat, soup, milk, and the like;” and 830 GENERAL DISORDERS OF NUTRITION. that “he must not work too long,” and should take “plenty of out- of-door exercise.” To be successful in our object, the quantities of food and drink must be prescribed definitely, as well as the number of hours allotted to each form of occupation. Cod-liver oil has a special and well-merited reputation as a remedy against scrofula, and there are plenty of instances where it has done good service. On the other hand, perhaps no remedy has ever been so much abused as this one. Whosoever supposes that the mere pres- ence of a thick nose, a sore upper-lip, or a bunch of enlarged cervical glands, affords sufficient ground for the prescription of this medicine, will often fail to benefit his patient, and sometimes will do him harm. Daily experience teaches, however, that such is the general belief, and that he who seeks to combat it does not merely fight a windmill. Let any one ask a patient whose scrofula has outlasted his childhood, and who has passed again and again from one practitioner to another, how often he has had cod-liver oil prescribed for him since the time of its first failure during childhood; how many months or years he has taken it; and how much the whole aggregate quantity would amount to; and he will be surprised at the answer. Nevertheless, in all proba- bility, the next physician whom the patient consults will prescribe it again. A most serviceable means of distinction, between the cases in which cod-liver oil is indicated and those in which nothing is to be ex- pected from it, is afforded by the symptoms of the torpid and erethitic forms of scrofula. When the patient’s slender frame, the lack of fat beneath his skin, and his accelerated pulse, warrant the belief that his nervous system is in a state of over-activity, cod-liver oil is generally of the most signal benefit. Under its use the plumpness of the body increases, while the general susceptibility of the system, and the dis- eases consequent upon it subside. These are the cases to which this article owes its name as an anti-scrofulous remedy. But if the patient be clumsy and thick-set; if the nose and upper-lip be enlarged, and the adipose layer over the rest of the body strongly developed; if the action of the heart be retarded rather than accelerated; if the irrita- bility of the nervous system seem unusually obtuse; in short, should there be reason to suppose that the waste of the system is diminished rather than increased, we cannot hope to relieve the disease by means of the oil. Nevertheless, it is precisely this class of patients who in vain have taken such enormous quantities of it in the course of their lives. Besides the oil, and as a corroborant of its effects, so to speak, articles containing a little tannin, such as parched acorns, “ acorn-coffee,” and home-made infusions of walnut-leaves, are very often prescribed. Such a practice is greatly to be commended whenever there is a chronic catarrh of the intestines embarrassing the digestion and the absorption SCROFULA. 831 of cliyle, and where apprehensions are entertained that the oil may aggravate the intestinal disorder. When used in appropriate cases, we prize the efficacy of cod-liver oil, with acorn-coffee, and walnut-tea, most highly, although we strongly deprecate its indiscriminate employment in every form of scrofula; but, as it is requisite that its exhibition should be long continued in order to produce favorable results, certain rules for its administration must be laid down. The disgust for the oil, which in adults is sometimes invincible, is soon overcome by chil- dren, who generally speedily cease to fight against the customary dose of two teaspoonfuls daily, and even ask for it themselves when the period for its administration has expired. But, if the treatment be kept up for months without occasional intermission, an unconquerable, and theh too generally a permanent aversion to the disgusting medi- cine will arise, even among children, so that vomiting and retching ensue after every attempt to force it down. This awkward occurrence, which often renders further treatment futile, may nearly always be avoided by interrupting the “ cure ” for a week or a fortnight after continuing it for four or six weeks. In order to make children take the acorn-coffee as willingly as real coffee, it is sufficient to add a few coffee-beans to the acorns before roasting them. It is far more difficult to furnish definite instructions for the use of the brine-baths, whose anti-scrofulous virtues enjoy a reputation almost as great as that of cod-liver oil. We know too little about the action of these baths, and about the effect which they produce upon nutri- tion, and the advantages derived from the salt, iodine, and bromine, which they contain, to enable us to determine upon theoretical princi- ples where they are indicated and where they are unlikely to do good. A calm analysis of the positive and negative effects of brine-baths in scrofula, which would be the best means of obtaining fixed indications for their use, has not, as yet, been made; and the doctors at the baths, who certainly ought to be the best judges of the extent and limits of their healing powers, rarely send away a scrofulous patient as unfit to use the brine. Hence, there is no resource but to send persons, who have in vain tried cod-liver oil and other anti-scrofulous remedies, to Kreutznach, Isold, Kosen, or Wittekind, or some similar watering- place, in the hope that they may be among those to whom the baths will exhibit their anti-scrofulous virtues, which are by no means illu- sory ; and, if the circumstances of the patients do not admit of this, they must use artificial brine-baths at home. In recent times the cold-water cure has earned for itself a most favorable reputation as a remedy for scrofula; and, indeed, a series of cases is on record in which complete and perfect cures have been ob- tained by these means, after all other modes of treatment had been 832 GENERAL DISORDERS OF NUTRITION. applied in vain. We certainly are justified in asserting that cod-liver oil treatment cannot be substituted for the water-cure, nor vice versa; but we may go still further, and declare that the oil is not only useless in a case adapted for the water-cure treatment, but is absolutely per- nicious ; and the same holds good regarding the hydropathic treatment in a case where large doses of cod-liver oil are indicated. When we consider that formerly the “ decoctions of woods,” laxative tisanes, an- timonials, mercurials, and other drugs intended to stimulate the emuno tories into activity, were much employed in scrofula, and when, after weeks of such treatment, a profuse flow of urine or of sweat was final- ly induced, or, when the patient began to purge copiously, very good results were sometimes obtained, it will be plain that this treatment (the effect of which is to cause an intensely active destructive assimi- lation and consumption of the tissues) can only benefit the class of patients in whom these processes are in a state of indolence and inac- tivity. The hydropathic treatment has a similar though far less per- nicious influence, and is of signal benefit in the torpid form of scrofula, that is, in that form where cod-liver oil is powerless, as I have repeat- edly had opportunity of satisfying myself. Iodine and the mercurials are also generally regarded as good anti- scrofulous medicaments. It is impossible to hold such views while believing scrofula to consist in a cachexia, marked by a peculiar prone- ness to disease, and evinced by a series of nutritive disturbances; for one cannot well suppose that the use of iodine or mercury can aug ment the power of the system to resist noxious influences. I therefore consider it improper to prescribe these articles solely on account of the scrofula, and without fixed indications arising from the peculiarities of the case. At the same time I will not deny that the cases are pretty numerous in which the preparations of iodine and of mercury are indi- cated. For further details, I refer to the books of local pathology and therapeutics, surgery and ophthalmology, merely alluding to the great benefit derivable from the internal and external exhibition of iodine in the chronic hyperplasia of the fymphatics. In particular, where chronic indolent enlargements of the lymphatic glands form the sole remaining vestige of a former disease, astonishing advantage is often gained by the use of the Adelheid springs and the Krankenlieil waters.2 CHAPTER VII. DIABETES MELLITUS—MELLITURIA. Etiology.—The pathogeny of diabetes still remains obscure. The discovery of the physiologists, that sugar appears in the urine of animals after puncture of the floor of their fourth cerebral ventricle, has not as DIABETES MELLITUS. 833 yet thrown light upon the mystery. We know that the presence of sugar in the urine, whence diabetes mellitus derives its name, does not depend upon functional abnormity of the kidneys; that the sugar is not formed in them, and that it is excreted from the blood ; but we are altogether ignorant wherein the constitutional anomaly consists, in consequence of which a diabetic patient’s blood contains sugar, and a healthy person’s none. As the various hypotheses offered to account for diabetes are of little practical value, we shall mention a few merely of those most generally entertained. In the first place, diabetes has been ascribed to an insufficient de- gree of transformation of the sugar in the blood. Indeed, if the sugar into which the amylaceous substances that have been eaten are con- verted, and that which is formed in the liver, were to circulate in the blood without undergoing further alteration, and if this substance did not disappear again from the blood during its passage through the lungs, it would necessarily form one of the normal constituents of the urine; hence it cannot be denied that the pathological presence of sugar in the urine may possibly depend in some cases upon a failure of the conditions under which the normal transformation of the sugar takes place. However, as long as we are ignorant as to what these conditions are, we obtain but little aid from the hypothesis that their absence is the cause of diabetes. The assertion, that the non-assimila- tion of sugar in the circulation of diabetic persons is due to a want of alkalies in the blood, has been disproved. The theory of the existence in the blood of healthy persons of a certain unknown ferment, which induces the assimilation of sugar, but which is absent in the blood of diabetic persons, is untenable. Others have sought to trace the origin of diabetes to an abnormal- ly accelerated conversion of amylaceous matter into sugar, this being due to a diseased condition of the digestive juices. To this theory there are still greater objections than to the preceding ones. It seems that even in healthy persons the amylaceous ingesta are all changed into sugar (Trommer has proved this to be the case even in geese that have been “crammed”), and yet we know that healthy urine never contains sugar even after the ingestion into the system of very large quantities of amylaceous matter, or of pure sugar. But the re- sult of the treatment based upon these hypotheses has afforded the best evidence of their unsoundness. Were the source of diabetes an over-active and immoderate conversion of amylum into sugar, the dis- ease should cease upon the stoppage of the supply of amylum. Ex- perience, however, teaches us the contrary; as, even where for weeks and months the food of the patient has been exclusively animal food, the sugar rarely disappears from the urine. Finally, since Claude 834 GENERAL DISORDERS OF NUTRITION. Bernard has shown that the liver produces glycogenous substances and sugar, the hypothesis that diabetes depends upon a disease of the liver has gained ground, although the theory is not supported either by pathological or clinical observation. Claude Bernard himself thinks that the diabetes induced experimentally in animals, by the “ diabetic puncture,” depends upon the nervous derangement of the liver to which the operation gives rise. As a consequence of abnormal innervation, not only is the production of glycogenous matter aug- mented, but its conversion into sugar is also hastened. He believes, too, that in the human subject, diabetes mellitus likewise is due to an over-activity of the nerves which stimulate the function of the liver, and considers it probable that, “ if it were in our power to galvanize the sympathetic nerve,” this would be the best possible mode of treat- ing diabetes symptomatically; the function of this nerve being weak- ened by the undue activity of its antagonists. The possibility cannot be denied that more glycogenous matter is formed in the liver of a diabetic person than in that of a healthy one ; but it is neither proved nor even probable that this anomaly constitutes the only or even the essential lesion of the disease. It is not to be supposed that the pound of sugar which some patients discharge in the course of every twenty- four hours is only a small portion of the sugar which they produce daily, and that a larger portion undergoes that transformation in the blood which, normally as we know, is undergone by very large quan- tities of sugar, while a smaller portion of it remains, as it were, super- fluous, and passes away in the urine. In conclusion, I will present another very specious hypothesis, which really accounts better than any other for the origin of diabetes. According to Tscherinoff\ the liver-sugar is not made from the glycogen, but, on the contrary, the glycogen is formed from the sugar which arrives in the liver. Hence, instead of glycogen (sugar-former), it should be called glycoplithin- ium, or sugar-consumer. If the liver loses its capacity to convert the sugar into glycophtliinium, the sugar remains in the blood, and thus causes diabetes. Regarding the etiology of diabetes, our knowledge is equally vague, for although we learn from the history of many cases that the disease has arisen sooner or later after the exposure of the patient to certain noxious influences, yet these influences are so general in their character, and act so often upon the system without being followed by diabetes, that it becomes questionable whether the disease be at- tributable to their action at all. Griesinger, after collecting a large number of foreign and domestic cases, has come to the following conclusion: Diabetes occurs much more frequently in males than in females, the proportion being about DIABETES MELLITUS. 835 three to one. During childhood and old age it is rarer than dining the prime of life, the period of greatest frequence being between the ages of thirty and forty in males, and in females between ten and thirty. The disease sometimes appears to depend upon hereditary predisposition. The most commonly recognized exciting causes are: exposure to cold and wet, external violence, concussions of the whole body being a more fertile source of the disease than injuries to the brain and spinal marrow; also immoderate eating of sugar, new wine, and “ fruit-must,” unfermented juice of fruit, indulgence in immoderate mental exertion, mental depression, intoxication, etc. Anatomical Appearances.—No constant lesion is found post- mortem in the bodies of those who have died of diabetes mellitus. The most common appearances are the following: extreme emacia- tion, the integument often presenting remains of bed-sores, boils, car- buncles, and sloughs. There is no remarkable lesion in the brain ; in the lungs there are almost always tuberculous, or caseous deposits, of variable age, and not unfrequently pneumonia, or gangrene. The heart is flabby and atrophied; the liver usually normal, though sometimes hyperasmic. Hypertrophy of the pancreas occurs with remarkable fre- quence, considering how seldom this organ is the seat of disease. The walls of the stomach are moderately thickened, through muscular hy- pertrophy, probably the result of distention. The kidneys are en- larged by hyperremia, and sometimes are in a state of chronic paren- chymatous inflammation (Bright's disease). Symptoms and Course.—The most conspicuous and remarkable symptom of diabetes mellitus consists in the evacuation of enormous quantities of pale urine, whose high specific gravity, contrasted with its limpid aspect and sweetish taste, often alone suffices to place the diagnosis beyond a doubt. It is by no means rare for a diabetic pa- tient, in the course of twenty-four hours, to pass from five to ten thou- sand cubic centimetres of urine (from five to ten quarts), and, in some instances, the daily discharge has been much larger. No credence should be given to the stories of diabetic patients passing six or eight times this amount, or even more. It is maintained by some that the quantity of urine discharged exceeds the amount of liquid which has been drunk during the meals. If this were true, and unless there were a corresponding waste of the body, we should be compelled to assume that, instead of exhaling liquid through the skin and lungs, the patient actually imbibed moisture in this way from the surrounding atmos- phere. Since, as long as the temperature of the body remains higher than that of the air about it, such an occurrence would be incompatible with physical laws, I think it most likely that the observations have been erroneous in the instances where individuals have been reported, 836 GENERAL DISORDERS OF NUTRITION. for long periods together, to evacuate a larger weight of urine and feces than they had taken in of food and drink, without losing in weight. Every investigator and experimenter, who has given his at* tention to the subject of diabetes, has to suffer from the strong in elination on the part of the patient to deceive him, and to conceal a portion of the liquid that he drinks. In the researches and experi- ments of Reich and Liebermeister at the Greifswalder clinic, the re- sults of which have been published by Dr. Reich, at first, the quantity of urine and feces, evacuated by both of the patients under observa- tion, seemed to exceed the amount which they ate and drank. But after they began to watch the patients so closely that they were never left alone for a moment, nor withdrawn from immediate observation, the quantity of ingesta began to exceed that of excreta of urine and feces. With regard to the cause of the immense increase in the secretion of urine in diabetes, Liebermeister and Reich have proved by their experiments that the very large quantity of liquid which they imbibe is not of itself sufficient to account for it. For a number of days, and with great care, they measured out equal portions of food and drink to two patients with diabetes, and a similar portion to a perfectly healthy and trustworthy man (Mr. Hoffmann, student of medicine), and meas- ured the flow of urine for every twenty-four hours, from each of them, with the same accuracy. The result showed, that in Candidate Hoff mann the secretion of urine was considerably augmented by the very large quantity of liquid which he had swallowed in the cause of science, but that it was far less than that passed in the same time by the sick men. Hoffmann passed from five thousand to six thousand cubic centimetres (five to six quarts), while the patients passed from seven thousand to ten thousand. It is possible that the presence of sugar in the blood may increase the power of filtration through the glomeruli of the Malpighian capsules, thereby augmenting the amount of urine secreted. However, this hypothetical explanation of the polyuria of diabetes is superfluous, since it is fully accounted for by Vogel, in his classical work upon this disease, as follows: “ What- soever may be the source of the sugar contained in the blood in dia- betes, the necessary consequence of its presence is, that the saccharine serum of the blood greedily attracts to itself, by endosmosis, all the liquids from the parenchyma, and all the water of the food and drink which enters the alimentary canal. The more the blood attracts water, so much the more does it increase in volume, and augment the intravascular pressure. The increase of pressure in the glomeruli of the Malpighian capsules of the kidneys then produces polyuria.” The high specific gravity of diabetic urine, which in mild cases DIABETES MELLITUS. 837 ranges from 1020 to 1030, and in severe ones from 1030 to 1050, de- pends almost exclusively upon the quantity of sugar in it; for although the common belief has not proved true, that the absolute amount of urea and salts is reduced in diabetic urine, yet, owing to the enormous quantity of water in which they are dissolved, their relative quantity is very small indeed. Liebermeister and Reich found that the produc- tion of urea of their patients not only was greater than that of healthy persons moderately supplied with mixed food, but that it also exceeded that of a healthy man, who ate as much food as the diabetic patients did. The amount of urea fluctuated in the patients from thirty-two to fifty-five grammes, and in a healthy subject from twenty-nine to thirty- two grammes. Although the profusion of the urine, its high specific gravity, and its sweetish taste, are decidedly indicative of the presence in it of sugar, yet its positive existence can be easily proved by means of one of the many “ sugar-tests.” Although it is important to select the most delicate and surest of these, when we wish to determine the presence of very minute quantities of sugar, and although the supposed discov- eries of traces of sugar in healthy urine, and in many other pathologi- cal and physiological conditions, are in a measure due to our mistaking other substances, having similar reaction, for sugar, yet, when it appears in large quantities, as it does in diabetic urine, Trommels test is quite sufficient to settle the diagnosis. An excess of liquor potassae is to be mingled with a portion of the urine to be examined; a dilute solution of sulphate of copper is then to be added, drop by drop, as long as the precipitate which first forms will redissolve when stirred. The liquid (which, if sugar be present, will show a blue color) is then to be filtered and warmed. The precipitation of red oxide of copper in the liquid, while still below the boiling-point, furnishes absolute proof that the solution contains sugar. If albumen also be present, it must pre- viously be separated by boiling and filtration. Another more simple test consists in warming the urine after adding a solution of potassa. The presence of sugar is indicated by the liquid’s assuming a yellow color, which gradually deepens into a dark brown. If this color does not appear, the non-existence of sugar is certain; but, even when visi- ble, it is always advisable to try Trommer’s test also. For the details of the somewhat elaborate fermentation-test, and the other tests for sugar, we refer to the text-books upon organic chemistry. Felding’s “ liquid ” furnishes a very sure means of determining the percentage of urea, and also of the sugar, if the quantity of urine passed in twenty- four hours be measured. Aiebermeister and Reich, who, in their many experiments, examined each portion of the urine separately, only noting as reliable those observations which agreed, hardly ever had 838 GENERAL DISORLERS OF NUTRITION. occasion to repeat the process in the same portion of urine, aftei they had conducted their researches for a few days. The polarizing apparatus of Soldi- Ventzlce is a more convenient and rapid method of ascertaining the percentage of sugar in the urine. The cheaper polarizing apparatus of Iiobiquel, though less accurate, is also appli- cable to this purpose. In low grades of the malady, the quantity of sugar is not more than from one to two per cent.; in more intense forms, it is as much as six or seven per cent., or more. In well-pro- nounced instances, the entire amount excreted daily may exceed a pound. The proportion of sugar, however, varies greatly during the progress of the disease, sometimes even fluctuating perceptibly in the course of a day. The causes of these fluctuations are in a great meas- ure unknown, and we are acquainted with a few only of the agents which are capable of increasing or diminishing the percentage of sugar in the urine. Of the former, large draughts of liquid, heavy meals, especially eating large quantities of sugar or of amylaceous matter; of the latter, the exclusion of sugar from the food and drink, particu- larly the removal of amylaceous matter and similar glycogenous food. The influence of a meal upon the percentage of sugar voided continues for several hours, and then is replaced by a similar discharge of a much more gradual character. Dr. Moritz Traube infers, from the great de- crease in the elimination of sugar which takes place after several hours’ fasting, that, at a certain period during the night, there must be none at all. Had Dr. Traube but tested the truth of his conclusion (and he states expressly that he has not done so), had he merely examined a little of this urine of the last few hours of the night, which he supposes should not contain sugar, he would probably find himself to be in the wrong. Among the cases under observation at my clinic, one of which was of quite recent origin, affecting a young, vigorous man, still capa- ble of work, and in the fourteen cases investigated by Seegen in Karlsbad, the urine passed in the latter hours of the night and those of early morning invariably contained sugar. Hence Dr. Traube1 s proposed “ law ” is undeserving of credit until it shall have been proved that cases do occur in which it is as he supposes. The parching thirst which distresses the patient day and night is easily accounted for, as it has been proved that the polyuria of diabetes is not merely a consequence of much drinking, but rather that the patients drink much because they suffer an excessive loss of water through the kidneys. Claude Bernard ascribes the thirst of diabetic patients to the elevated temperature of the liver, which undoubtedly induces an increased absorption in the intestinal canal. This hypoth- esis, like the others, is idle. A diabetic patient is thirsty on account of the thickening of Ins blood, much of whose water has been dis- DIABETES MELLITUS. 839 charged from his kidneys, just as another one thirsts who sweats pro- fusely, or who suffers a great evaporation from his skin from fever, or like a cholera patient who is discharging water through the capillaries of his intestines. A second factor consists in the desiccation of all the tissues as a result of intense endosmotic action from the parenchyma into the vessels. Sugar may be employed as well as salt for the pur- pose of drying meat in order to preserve it. It is by no means rare foi a patient to drink from ten to fifteen quarts of water during the day. The thirst is most intense an hour or two after meals, that is, while the formation of sugar is most active and the production of urine the most copious. This immense waste of water through the kidneys likewise accounts for the complete arrest of perspiration, and for the decrease in the in- sensible evaporation from the skin, which have been observed at my clinic. The antagonism between the secretions of the skin and kid- neys is as well shown in the dryness of the surface of diabetic people as in the reduction of diuresis, which usually accompanies profuse per- spiration. Griesinger reports an interesting case, in which sugar was present in the urine and sweat alternately, and in which, whenever the sweat became strongly saccharine, the percentage of sugar in the urine sank one-half. In the aforementioned researches of Liebermeister and Reich, it was found that a diabetic patient scarcely perspired a third of the quantity given off by a healthy person. Finally, according to the experiments of Kundc and JDj/mhorn, who, by artificial abstraction of water from frogs and mammalia, have induced opacity of the crys- talline lenses of these animals, it seems not improbable that the cataract which often accompanies diabetes is a consequence of the excessive loss of water, although indeed the ophthalmologists have raised many objections to this explanation. An insatiable hunger is a symptom of diabetes, quite as constant as is the unquenchable thirst. It is almost incredible how much food such a patient will consume during a day, often quite regardless of its quality. This voracious hunger, as well as the steadily increasing and finally extreme emaciation, manifestly are due to the fact that a large part of the food eaten is of no profit to the system, because, instead of being devoted to the repajr of used-up constituents of the body, it is immediately excreted. Moreover, the consumption of the nitro- genous components of the body is considerably increased in diabetes, as is shown by the augmentation in the quantity of urea produced. Of course there can be no elevation of the bodily temperature, a large part of the heat-producing material passing off from the blood unused. The impotence, which is nearly always observed in this disease, is probably dependent upon a general decline in the patient’s strength 840 GENERAL DISORDERS OF NUTRITION. and nutriiivt condition; nevertheless, the attempt has been' made to ascribe diabetic ipipotence to the drying up of the sperm for want of water, and to a saccharine condition of the semen, supposed to deprive it of its power of inducing nervous excitement. Finally, we have to mention a series of phenomena, which, al- though less constant than those heretofore described, still often accom- pany them and serve to complete the picture of the disease. Caries of the teeth is a symptom which sets in early in the majority of cases. Falk explains this phenomenon by supposing that the teeth are ex- posed to the action of a free acid, formed by decomposition of saccha- rine secretion within the mouth. Then, again, phymosis and excoria- tions of the prepuce and glans in men, and of the parts about the meatus urinarius in women, are very distressing occurrences, due prob- ably to wetting of these parts with saccharine urine. Finally, there is often a great tendency to inflammation, ending in necrosis and mor- tification, exhibited in the very frequent occurrence of furuncles, car- buncles, lobular pneumonia, and pulmonary abscesses and gangrene. Consumption of the lungs develops as a terminal symptom in many diabetic persons. According to Griesinger, nearly one-half of all pa- tients die in this way. Now and then albuminuria is associated with mellituria, thereby augmenting the exhaustion and accelerating the demise of the sufferer. It is not improbable that the parenchymatous nephritis, upon which the albuminuria depends, is a consequence of the constant irritation of the kidney by the presence of sugar in the urine, thus forming a sort of analogue with diabetic balanitis. The course of diabetes is always chronic, lasting for months and years. In but a very small number of the cases reported, the disease has been acute, terminating fatally within a few weeks, or even sooner. We have scarcely any trustworthy observations of the incipient stages of the malady. Nearly all patients only come under treatment at a period when the profuse urination, tormenting thirst, insatiable hun- ger, and steadily advancing emaciation, have awakened the suspicion of the existence of serious disease; and they are scarcely ever able accurately to state when the present symptoms first arose, or by what others they had been preceded. Even in the few examples in which the malady has developed quickly, an augmented hunger, thirst, and an unnatural diuresis, were the first manifestations which attracted the attention of the patients and their friends. Diabetes usually lasts from one to three years. More than sixty per cent, of the cases collected by Griesinger terminated fatal I3 within that period. It must, however, be recollected that statistics usually refer to cases treated in hospital, while the majority of those treated in private practice are never published. There is no doubl DIABETES HELLITUS. 841 that patients in comfortable circumstances, and who possess the means of taking1 good care of themselves, hold out against diabetes much longer than those who are obliged to seek refuge in hospitals. A complete and permanent recovery from diabetes (if it ever occur at all) is extremely rare; although plenty of cases have been recorded in which a pause in the symptoms, of longer or shorter duration, has been observed. Death, when not the result of some intercurrent com- plication, usually takes place with the signs of extreme marasmus. Sometimes nervous symptoms arise shortly before death, calling to mind the characteristics of uraemic intoxication. Treatment.—Numerous remedies and “ cures ” have been recom- mended for diabetes; unfortunately, most of them have been devised upon principles based on purely hypothetical views as to the nature of the disease, and very few of them rest upon facts established by ex- perience. We shall not discuss procedures such as that whose object is to hinder the conversion of amylum into sugar by exhibition of acids; or that in which nitrogen is to be supplied to the system by adminis- tration of ammonia; or in which it is sought to allay irritability of the kidneys by means of opium ; or to act upon the liver by means of ox- gall, or gallic acid, or any of the other purely theoretical suggestions. We are indebted to Griesinger for a positive experimental demonstra- tion of the inefficacy, and in some cases even the detrimental character, of some of these modes of treatment, such as that by alcohol, rennet, yeast, sugar—intended to supply the place of that lost from the blood. Experience has also established the fact of the beneficial influence of certain dietetic rules, the first hints of which, however, were derived from theoretical reasoning. It is of the utmost importance that dia- betic patients should live principally upon animal food, and that they should eat but very little starchy or saccharine matter. The absolute prohibition of food containing starch and sugar has been abandoned of late; experience having taught, in the first place, that although the loss of sugar might undergo temporary diminution by this procedure, yet it could not cure the diabetes ; and besides, it has been found that there are very few patients who for years can endure a diet consisting exclusively of meat, eggs, fish, oysters, crabs, salad, and JBouchardafs bran-bread. It relieves the patients greatly, in carrying out the rest of the treatment, to allow them to eat a small portion of bread daily; and it does them no material harm. If we do not allow them this in- dulgence, we run the risk of their soon becoming so impatient, at the excessive restraint, as to refuse further obedience, and make up for lost time by eating copiously of bread and fruit, for which they almost always have a great desire. Besides the meats, the patient ma}r be allowed such vegetables as do not contain either sugar or starch, oi 842 GENERAL DISORDERS OF NUTRITION. but very little of them. Bouchardat has proved, by the comparison of the articles of food which a diabetic may take without prejudice, that it is quite possible to keep up a sufficient degree of variety in the character of the meals. The list of articles which he permits is about as follows: All sorts of meats roasted, stewed, and even dressed with spices, but not with flour; fresh water fish and marine fish, in eating which the want of bread is less felt than in eating meat; oysters, mus- cles, crabs, lobsters, etc. ; eggs in all the forms known to the culinary art; rich, good cream, but no milk; of the vegetables, spinach, arti- chokes, asparagus, green beans, the different varieties of cabbage; of the salads, water-cresses, endives, lettuce; of fruits, strawberries and peaches. Although the loss of sugar is augmented by very free sup- ply of liquid, and decreased by a privation of it, yet it is not advisable to forbid the patient to quench his thirst. Griesinger, who has ex- perimented upon this subject also, concludes that there is no rapid or considerable decrease in the loss of sugar until the thirsting has been pushed to the point of general disturbance of the system; and, as such a condition can only be endured for a very short time, he allows the patient just enough liquid to slake his thirst. Besides spring- water, acidulated water may be allowed as a beverage, as well as coffee, well-fermented beer, and wine, if not too new, especially red wine. Inasmuch as diabetic persons are very liable to take cold, and show a predisposition to pneumonia, and the like, directions regarding their clothing must also be laid down, and especially must they be urged to wear flannel next the skin. ' Besides these dietetic rules, under the conscientious oDservation of which diabetes, although incurable, is often tolerated for a great length of time without appreciable decline (as can be proved by many well-attested instances), there are certain medicinal remedies whose effects in diabetes are very decided. In private practice, no credit should be given to the claims of any drug based upon the bare asser- tion that it has benefited or cured a case of diabetes, particularly when it has been known to fail in other instances. But even those remedies which only exert a slight influence upon the course of the disease (proved, however, by accurate and •continuous measurement of the urine, sugar, weight of the body, etc.) should be urgently recom- mended to private patients by their physicians. At present, however, the alkaline carbonates are the only medicines whose beneficial action upon diabetes can be claimed with certainty. In Griesinger1 s clinic, the exhibition of doses of bicarbonate of soda effected a distinct al- though slight improvement in the disease. The equally well-estab- lished success of the springs of Carlsbad and Vichy have been much DIABETES INSIBIDUS. 843 more marked. The old reputation of the Carlsbad waters, as a cure for diabetes, has vindicated itself most brilliantly, according to the ob- servations of Seegen. According to him, there can no longer bo any doubt that in many cases of diabetes mellitus, a course of several weeks at these springs results in an abatement of the thirst, a decrease in the urination, a gain in weight, and in a disappearance of the sugar from the patient's urine. Whether or not these results be per- manent, or merely transitory, still, in our present state of knowledge, a course of waters at Carlsbad is the measure which should deserve the chief reliance as a remedy for diabetes mellitus.3 CHAPTER VIII. DIABETES INSIPIDUS. Diabetes insipidus and diabetes mellitus, in spite of the agree- ment of their most conspicuous symptoms, polyuria and unquenchable thirst, are altogether distinct diseases. In the former, the urine does not contain any foreign ingredients, the presence of which might ac- count for the symptoms. It is true that not long since, in the urine of a patient with dia- betes insipidus, Mosler discovered inosite, which is not among the normal constituents of urine, and he advanced the hypothesis that inosite played the same part in diabetes insipidus (inosuria) that sugar does in diabetes mellitus (mellituria). But the very slight amount of inosite excreted in the urine of Mosler’s patient would render this idea improbable, and it is entirely refuted by one of my pupils, Dr. Strauss, who wrote an excellent monograph on diabetes insipidus.* After finding inosite in the urine of two cases of diabetes insi- pidus—in one case 0.14-74 grm. in 6,700 ccm. of urine, in the other 1.508 grm. in 9,600 ccm. of urine—Strauss caused three healthy persons, in whose urine there was no inosite, to drink large quan tities of water (about ten quarts in twenty-four hours); after this . inosite was found in the urine of all three patients, in about the same proportion as in the patients with diabetes insipidus. These beautiful experiments show that a body which normally exists in the kidneys, liver, lungs, and muscles, but, as it undergoes changes in the body, is not found in normal urine, may be excreted through the kidneys by giving large quantities of ■water. * Die einfache zuckerlose Hamruhr, von Dr. F. Strauss. Tubingen, 1870. Terlag der Lauppschen Buchhandlung. 844 GENERAL DISORDERS OF NUTRITION. The most specious of the hypotheses, as to the pathogeny of insipid diabetes, is that which ascribes the polyuria to derangement of innervation of the blood-vessels of the kidney. If the afferent vessels of the Malpighian capsules were to become dilated, in conse- quence of paralysis of their walls, the pressure within the glome- ruli would increase, and with it the rate of filtration of the urine would augment, thus giving rise to polyuria. This primary symptom would be accompanied secondarily by polydipsia. When large quan- tities of water are withdrawn from the blood, as a consequence of pro- fuse urination, then (just as also occurs after profuse sweating, or intense liquid diarrhoea) the fluids from the interstices of the tissues are greedily absorbed by the now concentrated blood, thus giving rise to an increased need for liquid, and to a sense of severe thirst. Al- though I regard this as probably a true explanation, and although it acquires further support from the discovery of Bernard, that polyuria may be induced in animals by wounding their medulla oblongata at a point somewhat farther up than that at which the so-called “ diabetes puncture ” is performed, yet I am by no means inclined to regard it as absolutely correct. With regard to the somewhat obscure etiology of diabetes insipi- dus, we must confine ourselves to the announcement of the following facts : The disease is more common in males than in females, and in youth than during middle age. I cannot confirm the assertion that old age is exempt from it, as I have seen a case in a patient fifty years old. Its exciting causes have so often been referred to mental affec- tions, to the drinking of cold beverages while the body was over- heated, to cold, to over-exertion, to abuse of spirituous liquors, and other agencies, of a nature so various, and of such common occurrence, that the dependence of the malady upon their influence must be regarded as questionable. It is different with the observations of cases where diabetes insipidus has occurred after injuries of the skull, and in the course of acute and chronic diseases of the brain. These cases, in con- nection with the above-mentioned experiments of Bernard\ are peculiarly interesting. Anatomical Appearances.—The results of the small number of autopsies held upon persons who have suffered from diabetes insi- pidus agree so imperfectly, that nothing positive can be affirmed regarding the anatomical lesions from which the malady originates. Thus, in a case described by Neujfer, the kidneys, contrary to all expec- tation, were found small and atrophied, while in another, mentioned by Lebert, they were enlarged and hypertrophied. Symptoms and Course.—The amount of urine discharged by a DIABETES INSIPIDUS. 845 patient with diabetes insipidus is as great as, or even greater than, that passed in diabetes mellitus. In twenty-four hours it often amounts to from 10,000 to 15,000 com. (ten to fifteen quarts), and sometimes even more. A little girl, ten years old, with diabetes insipidus, who was very undeveloped, and only weighed twenty-three pounds, during her stay in the Tubingen clinic, passed daily an amount of urine that weighed about one-third as much as her body. The urine is very limpid, and, in contradistinction to diabetic urine, of low specific gravity. It rarely rises above 1.005, and often sinks to 1.001 or 1.0005. The relative amount of urea and salts in the urine is low, but the absolute amount of urea excreted in twenty-four hours is usually normal or somewhat increased. In one case that I observed, where the patient consumed a moderate quantity of nitrogenous material, he passed 9,000 ccm. of urine, containing 38 grm. of urea, in twenty-four hours. Rarely the amount of urea passed in the twenty- four hours is diminished. Thus, in one of the cases in my clinic, published by Strauss, where the patient weighed about 114 pounds and had good diet, he passed only 23.42 grm. of urea in the twenty-four hours.* The excretion through the skin and lungs seemed to be consider- ably reduced, judging by the relative quantities of the liquid drank and urine voided. Doctors Schrrddtlein and Spaeth, who for some time ate and drank exactly the same quantities of food and drink taken by a patient with diabetes insipidus at my clinic, in twenty-four hours excreted from two thousand to twenty-six hundred grammes through their lungs and skin, while the patient only lost from five hundred and forty to six hundred and forty grammes by the same way and in the same time. Strauss's observations also led to the result that, taking the same amount of fluid, the patients passed from five hundred to two thousand centimetres more urine than healthy persons, while, in the latter, the loss of weight by insensible perspiration was considerably more than in the former. * In some cases of diabetes insipidus the urine is said to have a very high specific gravity, and to contain an abnormal amount of urea. In this form of disease, about which the observations are very scanty, the original disease would consist of an increased destruction of tissue; the great thirst, as well as the increased secretion of urine, would be very insignificant as compared with the severe con- stitutional disturbance, and would be explained as in diabetes mellitus. The serum of the blood is abnormally concentrated, and, on endosmotic principles, draws water from the tissues. We shall not further consider this obscure and problematical form of diabetes insipidus. 846 GENERAL DISORDERS OF NUTRITION. Strauss |ustly regards this as another proof that polydipsia is not the cause ol polyuria, but the reverse. He writes as follows: “ What reasonable and satisfactory grounds are there for assuming that the cutaneous and pulmonary exhalations of a polydiptic person should differ from those of a healthy person who voluntarily drinks copiously of water ? ” But if we suppose a polyuria with consequent concentration of the blood, and decrease of water in the tissue, there would be nothing strange in a diminished gaseous excretion of water by the skin and lungs. In our cases, as in most others, among the symptoms referring to the skin, we find mentioned dryness, harshness, and frequent itch- ing, while profuse perspiration is not mentioned in a single case. The quantity of liquid imbibed daily, including that contained in the food, is said to have amounted sometimes to sixty or eighty pints. Of course, such a quantity could never permanently be less than that of the urine secreted, without the occurrence of a corresponding de- crease of the weight of the body. All cases, wherein it is claimed that the quantity of urine secreted exceeded that of the liquid imbibed, must have been inaccurately observed. In my case, the sense of hunger was considerably augmented. Trousseau also tells of a patient who ate such enormous quantities that, at a certain restaurant where bread was furnished d discretion, they paid him to stay away. In this disease (unlike diabetes mellitus, in which a part of the food consumed, instead of going to repair the used-up constituents of the body, is voided unused), this unnatural hunger—which, moreover, is not a constant occurrence—can only be accounted for by supposing that the exaggerated consumption and dis- charge of water accelerate the waste of the nitrogenous elements of the body. It may be accepted as a law that, during an accelerated flow of the juices of the parenchyma through the organs, a larger quantity of albuminous material is consumed. In some patients the general health and vigor long remain undis- turbed. A girl twenty years of age, with insipid diabetes, who remained under observation at my clinic for a considerable time, retained her blooming aspect, and could even do hard work without special effort. In other patients, signs of digestive derangement, cardialgia, vomiting, irregularity of the bowels, emaciation, and an un- accountable sense of debility, set in early. In the instance reported by Neuffer, the patient died with these symptoms, no appreciable cause of death being discoverable upon autopsy. The course and duration of the disease vary. In some cases it develops gradually, in others it sets in suddenly. Not unfrequently a transient improvement in the symptoms is observed. It may also happen that, during the attack ADDITIONS TO THE REVISED EDITION OF I860. 847 of some intercurrent disease, the daily flow of urine becomes normal, and returns to its former profusion after the attack has terminated. As a rule, the malady lasts for years without imperilling life. It is only in rare instances, as in that of Neuffer, already alluded to, that death takes place without the intervention of some other disease. Complete and permanent recovery from diabetes insipidus is likewise an ex- tremely rare event. Treatment.—It is always suspicious when numerous remedies are recommended for a disease; in such cases, usually, none of them have any special effect on the course and termination of the affection. This is also true of the recommendations of saltpetre, in the shape of sal prunelke, of valerian, belladonna, opium, ergotine, creosote, and other remedies in diabetes insipidus. They are not based on the results of experience, but on theoretical grounds. I have not used any of these remedies persistently and energetically, as my patients bore their disease pretty well—so that there was no necessity for energetic treatment. On the whole, I would advise you, in treating simple diabetes, to limit yourselves to preventing the bad results induced by the disease, or to combating them if they have already appeared. Especial attention should be paid to the disturbances of digestion and nutrition, which are not uncommon. Rational diet, combined with cod-liver oil, malt extract, and iron, improved the con- dition of the little girl above-mentioned, without diminishing her thirst, or the secretion of urine; and, although her early death had been expected, she was discharged from the clinic considerably increased in weight and much improved in health. ADDITIONS TO THE REVISED EDITION OF 1880. SECTION III. GENERAL DISORDERS OF NUTRITION. 1.—P. 803. According to Virchow, in obstinate cases of chlorosis there is defective development and small size of the aorta and vessels gen- erally. The aorta may be so small as not to admit the little finger, while its walls may be uncommonly thin ; they, however, retain their elasticity, unless there has been fatty degeneration of the inner and middle coats. This failure of vascular development is sometimes accompanied by stunted growth of the whole body. The heart is sometimes small, but is usually normal, or slightly di- lated ; exceptionally it is hypertrophied. There is an inclination 848 GENERAL DISORDERS OF NUTRITION. to endocarditis of the left ventricle. In women with this trouble of the heart and blood-vessels, child-bearing may induce ulcerous endo- carditis. Feverish diseases ai’e more dangerous in chlorotic persons than in others. In giving iron in chlorosis, it is well to administer it after eating. Mineral waters containing pyrophosphate of iron may be drunk at meal-times. This drug may have to be discon- tinued when there is gastric disturbance or fever. Iron is to be aided by good, easily digestible diet, and residence in a healthy locality. In chlorosis and ansemia generally, alcoholic beverages may be useful by impeding transformation of tissue, but should be avoided if they induce excitement, palpitation, rush of blood to the head, etc. Trial must decide whether wine or beer answers the best purpose. 2.—P. 832. Of late it has been considered possible that the use of milk from cows with murrain might have an injurious effect, because forma- tions similar to those in tubercles in men have been found in the an- thrax-nodules of cattle, and because experiments have shown that feeding other animals on the milk of these cows will give them tuberculosis and diseases of the lymphatic glands of the mesentery and neck, similar to those in scrofula. Hence the use of such milk may be suspected as a cause of the trouble, but has not yet been proved to be so. In the treatment of scrofula considerable reputation is enjoyed by the mud-baths of Nauheim, Kreuznach, etc., in Germany ; they increase the transformation of tissue, and prove advantageous for the glandular enlargements, as well as for the affections of the mu- cous membrane and skin. When cod-liver oil is given, it is some- times better borne when not taken on an empty stomach, but half an hour or so after eating. Pale, anaemic children often require some preparation of iron. When the patient is not anamiic or fee- ble, at proper seasons it is often well to order a laxative mineral water, such as a continued moderate use of Carlsbad water. The waters containing iodine have so very small a percentage of it, that it is doubtful if it has any special effect. 3.—P. 843. There have been numerous disputes as to the glycogene builders ; among them are grape, cane, milk, and fruit sugar, inulin, glycerin, etc. Amylaceous food has the greatest effect on the formation of sugar ; under its use the portal vein is always rich in dextrin. It ADDITIONS TO TEE REVISED EDITION OF 1880. 849 is not known just how sugar is made from the food ; it normally exists in the blood in such slight quantity that it does not transude into the urine ; in the blood of diabetic patients Cantani found it as high as 8 parts in 1,000. Artificial mellituria may be induced by dividing the inferior cer- vical ganglia, or by irritating the floor of the fourth cerebral ven- tricle (which at the same time induces polyuria) ; division of the splanchnics has no effect. Schiff induced diabetes by destruction of the spinal medulla before and behind the origin of the brachial nerves, etc. Artificial diabetes may also be induced by injections of curare, solutions of common salts, some of the salts of soda, nitrite of amyl, morphine, etc. ; this effect is prevented by previous division of the splanchnics. Diabetes is a disease of the vasomotor nerve-system ; on au- topsy the liver is found normal, but there are frequently changes in the brain (tumors, etc.). Possibly the sugar formed during digestion of amylaceous substances, being taken up by the lymphat- ics and portal vessels, enters the blood directly. Cantani regards sugar in the blood as necessary to life, and thinks it is one source of strength ; it appears as grape-sugar, and is broken up by some ferment; if the organs furnishing this ferment (the pancreas ?) be diseased, the sugar appears in the urine. In the first stages of diabetes, by withdrawing amylaceous food, the collection of sugar in the blood and its excretion by the urine may be prevented, and by continuing this treatment for some time the disease may perhaps be entirely cured ; even later in the disease, the excretion of sugar may be arrested, but it is doubtful if the disease can be cured. Although the above theories are not universally accepted, the treat- ment advocated is probably the most successful of the many that have been tried. Possibly diabetes may depend on a variety of causes, having as a common result the non-consumption of sugar and its excretion by the urine. Senator divides it into neurogenous, gastro-enteroge- nous, and hepatogenous forms. . The first wrould include the cases caused by injuries, tumors, etc., affecting the nervous system ; the second, the Cantani cases ; and the third class, cases where, as a result of hyperaemia of the liver, hepatic sugar passes more rapidly into the blood. There would seem to be either two forms of dia- betes, or else two stages of the same disease, in one of which exclu- sion of amylaceous substances from the diet prevents the appearance of sugar in the urine. Diabetic urine often has a peculiar odor, which is ascribed to aceton. Bottcher tests for sugar by adding to urine m a test-tube 850 ADDITIONS TO THE REVISED EDITION OF 1880. a small quantity of nitrate of bismuth ; then freely adding a con- centrated solution of carbonate of soda, or some potash lye ; then heating to the boiling-point. If sugar be present, the bismuth turns gray, then black. This test may be used in addition to others, but is less delicate than the copper test. IIDEX. A. Abscess of the Brain, ii., 255; of the Heart, i., 355 ; of the Kidneys, ii., 36; of the Liver, i., 669; of the Lungs, i., 169; of the Ovaries, ii., 110; of the Spleen, i., 752; metastatic of the Liver, i., 668; metastatic of the Lungs, i., 158. Abscess, retropharyngeal, i., 476. Acarus scabiei, ii., 510. Acholia, i., 677. Achroma, ii., 448. Achromatopsia, ii., 310. Acinesis, ii., 359. Acne, ii., 493. Acne rosacea, ii., 497; syphilitica, ii., 762. Acorn Coffee, ii., 830. Addison’s Disease, ii., 49. yEgophonv, i., 186. Agenesis, ii., 283. Ageustia, ii., 349. Agraphia, ii., 286. Akinesis, i., 491. Albino, ii., 448. Albuminate of Mercury, ii., 780. Albuminuria, Origin of, Test for, ii., 22; after Scarlatina, ii., 592. Alcoholic Poisoning, ii., 184, Alopecia circumscripta, ii., 449 ; syphi- litica, ii., 765; anata, ii., 525. Amaurosis in Bright’s Disease, ii., 30. Amenorrhcea, ii., 160, 807. Amylea, ii., 300. Anaemia et Cachexia splenica, ii., 817. Anaemia, progressive pernicious, ii., 817. Anaesthesia dolorosa, ii., 345 ; of the cu- taneous Nerves, ii., 342 ; of the Trige- minus, ii., 348. Analgesia, ii., 345. Aneurism, true and false, i., 418; dis- secting, i., 426; cylindrical fusiform, i., 419; cardiac, i., 346; of the Aorta, i., 417; of the cardiac Valves, i., 393. Angina catarrhalis, i., 463 ; Ludovici, i., 477; membranacea, i., 15; paren- chymatous, i., 465 ; pectoris, i., 384; syphilitica, i., 467; maligna, ii., 664. Anidrosis, ii., 518. Anostosis excentrica, ii., 769. Anteflexion of Uterus, ii., 141, Anteversion of Uterus, ii., 144. Anthracosis, i., 201. Antiperistaltic Motion of the Bowels, i., 594. Aorta, Aneurism of, i., 417; Calcification of, i., 415; Atheroma of, i., 415; fatty Consumption of, i., 415; Rupture of, 1., 426 ; Inflammation of Coats of, i., 413; Stricture and Obliteration of, i., 427. Aortic Valves, Constriction of, i., 359. Aphasia, ii., 285. Aphonia paralytica, i., 54; ii., 438. Apneumatosis, i., 130. Aphthae, i., 437. Apomorphia, i., 563. Apoplectic Stroke, ii., 215; Cicatrix, ii., 218 ; Cyst, ii., 218. Apoplexia meningea, ii., 230 ; sanguinea, 11., 215; serosa, ii, 278. Apoplexie foudroyante, ii., 227. Apoplexy, cerebral, ii., 215, 320; pulmo- nary, i., 139. Appetite, perverted, ii., 805. Ai’ea Celsi, ii., 449. Argyria, ii., 403. Arsenic, i., 339. Arteriosclerosis, i., 430. Arthritis, ii., 545; deformans, ii., 540. Arthrogryposis, ii., 357. Arthropathia, ii., 226, 414. Artificial Anus, i., 589. Ascaris lumbricoides, i., 623. Ascites, i., 649. Asthma acutum Millari, i., 51; convul- sive, i., 88; humid, i., 74; laryngeal, i., 51; thymic, i., 51; urinous, ii., 27. Asymbolia, ii., 286. Ataxie locomotrice progressive, ii., 302. Atelectasis Pulmonum, i., 130. Atheroma, i., 415, ii., 520; of the Ar- teries, i., 359. Aubree’s Specific, i., 94. Aura epileptica, ii., 394. 852 INDEX. B. Bacteria, ii., 738. Balanitis, ii., 91. Baldness, ii., 448, 765. Barbadoes Leg, ii., 446. Basedow’s Disease, i., 388. Basilar Meningitis, ii., 240. Bath Itch, ii., 468. Baths in Bronchitis, i., 82; Rheumatism, ii., 535; Scarlatina, ii., 594; Typhoid Fever, ii., 651. Belladonna, ii., 402. Bile Fever, i., 631; Test for, i., 708. Black Vomit, ii., 692. Bladder, Acinesis of, ii., 84; Anaesthe- sia of, ii., 80; Cancer of, ii., 73; Ca- tarrh of, ii., 66; distended, ii., 70; Haemorrhage from, ii, 74; Hyperaes- thesia of, ii., 80 ; Ilypercinesis of, ii., 82; Neuroses of, ii., 79 ; Palsy of, ii., 84; Spasm of, ii., 82; Stone of, ii., 75 ; Tuberculosis of, ii., 73. Bladder-worm, i., 624. Blaud’s Pills, ii., 808. Bleeding at Nose, i., 305. Blepharospasm, ii., 352. Blindness from Tumors of Brain, ii., 269. Blood-murmurs, ii., 531, 806. Blood Test, ii., 8. Bloody Flux, ii., 722. Bloody Sweat, i., 160; ii., 498. Bothriocephalus latus, i., 623. Brain, Abscess of, ii., 255 ; Anaemia of, ii., 195 ; partial Anaemia of, ii., 201; Atrophy of, ii., 282 ; Aneurisms in, ii., 262, 287 ; gummy Tumor of, ii., 264; Hyperaemia of, ii., 175; partial Hy- peraemia of, ii., 193 ; Haemorrhage into, ii., 215 ; Hypertrophy of, ii., 280; Inflammation of, ii., 254; Softening of, ii., 201; yellow Softening of, ii., 204; white Softening of, ii., 206; Sclerosis of, ii., 260; syphilitic Disease of, ii., 771; Tumors of, ii, 262. Brayera anthelmintica, i., 628. Breast, irritable, ii, 337. Bright’s Disease, acute, ii., 10; chronic, 11., 14. Brine Baths, i., 13 ; ii., 831. Bromide of Potassium in Epilepsy, ii., 403. Bronchi, Diseases of, i. 61; Catarrh of, 1., 61; Catarrh of, in the newly-born, i., 72; Croup of, i., 86; Dilatation of, i., 65, 202 ; Haemorrhage from, i., 145; Hyperaemia of, i., 61; Spasm of, i., 88. Bronchial Asthma, i., 88; Respiration, i., 140, 185. Bronchiectatic Cavities, i., 199. Bronchitis, capillary, i., 70. Bronchophony, i., 185. Bronchopneumonia, i., 194. Bronchorrhoea, chronic, i., 76. Bronzed Skin, ii., 49. Bruit de Diable, ii., 805. Bubo, acute, ii, 750; indolent, ii., 758. Bulbar Palsy, ii., 372. Bullrich’s Salt, ii., 554. Buttermilk, i., 519, 564. c. Cacotrophia, ii., 561. Calcareous Infarction, ii., 62. Calculus, ii., 77; renal, ii., 60. Callosities of Skin, ii, 441. Calomel as an Anti-syphilitic, ii., 778. Calori,' ii., 468. Calvities, ii., 448. Cancrum Oris, i., 439, 462. Capillary Bronchitis, i., 70. Caput obstipum, ii., 354. Carbonic-acid Poisoning, i., 23. Cardialgia, i., 551. Carlsbad Water in Diabetes, ii., 843. Catalepsy, ii., 424. Cataract in Diabetes, ii., 839. Catarrh, i., 1; syphilitic, ii., 765. Catarrhal Fever, i., 631. Cerebral Arteries, Aneurisms of, ii., 262, 287; Thrombosis of, ii., 201; Sinus, Inflammation of, ii., 233. Cerebrospinal Meningitis, epidemic, ii., 247. Chancre, ii., 743; glandular, ii., 750; parcliemine, ii., 757; inoculated, ii., 745 ; phagedenic, ii., 747 ; gangrenous, ii., 748; diphtheritic, ii., 746; Hun- terian, ii., 758. Chancroid, ii., 743. Chicken-pox, ii., 612. Chloasma, ii., 441; uterina, ii., 442. Chloride of Sodium and Gold, ii., 422. Chlorosis, ii., 802, 847. Cholaemia, i., 677, 720. Cholelithiasis, i., 733. Cholera Asiatica, ii., 699; infantum, i., 504 ; morbus, i., 501; quarantine, ii., 717 ; typhoid, ii., 715. Cholerine, ii., 708. Cholesteatoma, ii., 264. Chorda Tympani, ii., 327. Chordae tendincae, Adhesions and .Rup- ture of, i., 393. Chordce, ii., 92. Chorea, ii., 378. Cirrhosis of Liver, i., 670. Clairvoyants, ii., 419. Clap, ii., 88. Clavus hystericus, ii., 414. Cliquetis metallique, i., 325, Club-foot, ii., 375. INDEX, 853 Cod-Liver Oil in Scrofula, ii., 830. Cold Applications in Inflammation, i., 28, 282. Cold Beverages as Causes of Consump- tion, i., 220. Colic, i., 617; biliary, i., 734 ; Painters’, 1., 619; of Prostitutes, ii., 110; renal, 11., 63. Comedones, ii., 493, 520. Compressed Air, Respiration of, i., 92. Conception, ii., 159. Condyloma of Larynx, i., 37; syphilitic, ii., 759. Constipation, habitual, i., 571, 590. Consumption, galloping, i., 253; pulmo- nary, i., 212, 235. Convulsions, ii., 189. Coqueluche, i., 95. Cor taurinum, i., 318. Corns, ii., 441. Corona veneris, ii., 764. Coryza, i., 299. Cosme’s paste, ii., 524. Cough, induced by irritation, i., 767. Cow-pox, ii., 608. Cracked-pot Sound, i., 238. Cramp, ii., 350; idiopathic, of Extrem- ities, ii., 357. Craniotabes, ii., 560. Crepitant Rale, i., 185. Critical Eruption, ii., 468. Croup, i., 15; Membrane, i., 17; false, spasmodic, i., 7. Crusta lactea, ii., 471. Curare in Chorea, ii, 383; in Tetanus, 11., 389. Cyanosis, acute, i., 123, 133; in Croup, 1., 23 ; in Disease of the Heart, i., 205, 376, 382; of Hunchbacks, i., 133 ; of Cholera, ii., 712; in congenital Mal- formation of the Heart, i., 382. Cysticercus cellulosus, i., 624 ; of Kid- ney, ii., 47 ; of Brain, ii., 205. Cystitis, catarrhal, ii., 66; croupous and diphtheritic, ii., 72. Cystoplegia, ii., 84. Cystospasm, ii., 82. D. Darwin’s Theory, ii., 655. Deafness, from Tumors of Brain, ii, 269 ; from Uraemia, ii., 31. Death-rattle, i., 69. Decubitus, ii., 453. Defluvium Capillorum, ii., 449. Deglutition, Disturbance of, ii., 514. Delirium, ii., 1S6; tremens, ii., 432. Derangement of Secretion in the Skin, 11., 217. Dermoid Cyst, ii., 114. Dextro-cardia, i., S80. Diabetes mellitus, ii., 832 ; insipidus, ii., 843. Diachylon Ointmemt, ii., 475. Diapedesis, i., 160. Diaphoresis, ii., 35. Diaphragm, Movements of, i., 120. Diarrhoea serosa stercoralis, i., 569; lienterica, i., 572 ; ablactatorum, i., 572, ii., 561. Diet of Infants, i., 505. Digestion, Diseases of Organs of, i., 431. Digitalis in Heart Disease, i., 329, 371, 406. Diphtheria, epidemic, ii., 664. Diuretics in Heart Disease, i., 372. Diverticuli of (Esophagus, i., 488. Dizziness, ii., 187 ; from Tumors of Cere- bellum, ii., 213, 273, 561. Dropsy of Kidney, ii., 12, 24; malarial, ii., 680. Duodenal Ulcer, i., 583. Dura Mater, Inflammation of, ii., 233. Dysentery, epidemic, ii., 722; chronic, ii., 725 ; catarrhal, i., 570. Dysmenorrhoea, ii., 125, 164. Dyspepsia, i., 502, 555. Dysphagia, i., 480, 491. Dysphagia inflammatoria, i., 480. Dysphonia, i., 54. Dyspnoea, i., 229, 283, 290. Dysuria spastica, ii., 83. E. Ecchymomata, ii., 498. Echinococci of Liver, i., 697; of Kidney, ii., 47 ; of Brain, ii., 262. Eclampsia Infantum, ii., 405; Puerpe- rarum, ii., 44. Ecthyma, ii., 481. Ectropion of Os Uteri, ii., 124. Eczema, ii., 466. Eczema solare, mercuriale, ii., 468. Electricity in Chorea, ii., 383 ; in Consti- pation, i., 596 ; in Diagnosis of Paraly- sis, ii., 312, 363, 377; in essential in- fantile Palsy, ii., 376 ; in facial Neu- ralgia, ii., 370; in facial Palsy, ii., 370; in Neuralgia, ii., 322; in Impo- tence, ii., 108; in Torticollis, ii., 354; in Sciatica, ii., 341; in Scriveners’ Spasm, ii., 356. Elephantiasis Arabum, ii., 443, 446; Grsecorum, ii., 522. Embolism, renal, ii., 7, 37; cerebral, ii., 292. Emphysema of the Lung, i., 110. Emphysematous Thorax, i., 125. Emprosthotonos, ii., 386. Empyema, i., 268, 272. 854 INDEX. Encephalitis, ii., 254. Endarteritis deformans, i., 314, 414. Endocarditis, i., 342 ; ulcerative, i., 346, 392. Enteralgia, i., 617. Enteritis catarrhalis, i., 565. Enuresis, ii., 306 ; spastica, ii., 83 ; noc- turna, ii., 81, 87. Ephelides, ii., 441. Epididymitis, ii., 93. Epiglottis, tuberculous Ulcer of, i., 40. Epilepsy, ii., 390; simulated, ii., 399. Epileptiform Convulsions, ii., 259, 271. Epistaxis, i., 305 ; ii., 816. Erysipelas, ii., 455 ; ambulans, ii., 460. Erythema, ii., 453; nodosum, ii., 323, 455. Eucalyptus globulus, ii., 690. Eustachian Tube, Closure of, i., 475. Exanthemata, syphilitic, ii., 760. Expectorants, i., 83. Expectoration, Absence of, in Senile Pneumonia, i., 179; in Abscess of Lung, i., 182; in Bronchial Croup, i., 87; in Bronchial Dilatation, i., 204; in Bronchorrhcea, i., 76 ; cocta, i., 6 ; of Croup, i., 21; cruda, i., 6 ; elastic Fi- bres in, i., 233 ; of Empyema, i., 269; gangrenous, i., 182; globosa fundum petentia, i., 233 ; mucopurulent homo- geneous, i., 67; in (Edema of the Lungs, i., 140; of Pneumonia, i., 173; of Pulmonary Abscess, i., 182 ; of Pul- monary Consumption, i., 233. F. Facial Palsy, ii., 225, 366. Facies Cholerica, ii., 710. Faeces, i., 636. Fallon Palate, i., 468. Falling Sickness, ii., 390. Farcy, ii., 788. Fauces, chronic Catarrh of, i., 463. Favus, ii., 505. Fecal Fistula, i., 589. Fever, bile, or catarrhal, i., 631 ; essen- tial, i., 633; typhus, ii., 614; ship, jail, camp, lazaretto, ii., 616 ; gastric, mucous, nervous, ii., 641; hectic, i., 234; spotted, ii., 614; typhoid, ii., 623; intermitting, ii., 671; malarial, ii., 671 ; remittent and continued, ii., 687; relapsing, ii., 654; pernicious, ii., 681; concealed malarious, ii., 683 ; yellow, ii., 690. Flea-bites, ii., 498. Fluor albus, ii., 126, 173. Formication, ii., 294. Fothergill’s Face-ache, ii., 327. Freckles, ii., 442. Fremissement cataire, i., 424. Friction Sounds, endocardial, extraperi- cardial, pericardial, i., 404; pleuritic, i., 278. Friesel Fieber, ii., 694. G. Gall-bladder, Dropsy of, i., 731. Gall-ducts, Catarrh of, i., 726 ; Croup and Diphtheritis of, i., 729 ; Dilatation of, i., 730. Gall-stones, i., 733. Galloping Consumption, i., 253. Gangrene of Lung, i., 207. Gangrenous Sore Mouth, i., 451. Gastric mucous Membrane, acute Catarrh of, i., 493 ; chronic Catarrh of, i., 511; Croup and Diphtheria of, i., 524. Gastric Influenza, i., 64. Gastricismus, i., 499. Gastritis phlegmonosa, i., 524. Gastrodynia neuralgica, i., 545. Gastromalacia, i., 497. Genu valgus, ii., 375. Gin Liver, i., 671. Glanders, ii., 788. Gleet, ii., 91. Glioma, ii., 264. Globus hystericus, i., 490; ii., 417. Glossitis, i., 449. Glossopharyngeal Palsy, ii., 372. Glottic Muscles, Palsy of, i., 20, 54. Glottis, G'ldema of the, i., 45. Gluge’s Inflammation Globules, ii., 254. Gonorrhoea, ii., 88; in the Female, ii., 170. Gonorrhoeal Abscess, ii., 92; Gout, Or- chitis, Ophthalmia, Rheumatism, ii., 93. Gout, ii., 545 ; flying, ii., 527 ; atonic or anomalous, ii., 550; internal, ii., 551. Goutte militaire, ii., 91. Grape-cure, i., 142, 329. Gravedo, i., 299. Gravel, ii., 607. Graves’s Disease: see Basedow’s Dis- ease. Grayness, ii., 450. Green Soap, ii., 476. Grippe, i., 64. Gummata, or gummy Tumors, ii., 764. H. Hematocele, retro-uterine, ii., 165. Hematoma of Dura Mater, ii., 230. Hematuria toxica, ii., 74. Ilemometra, ii., 137. Hemophilia, Hemorrhagic Diathesis, ii., 819. Hemoptysis, i., 150; from Inhalation of Astringents, i., 13. INDEX. 855 Haemorrhoids, i., 609 ; of Bladder, ii., 75. Hallucinations, ii., 186. JIaut mal, ii., 390. Headache, ii., 1S5. Heart, Abscess of, i., 355 ; acute Aneu- rism of, i., 346 ; chronic Aneurism of, i., 356 ; Atrophy of, i., 339 ; Ausculta- tion of, i., 380 ; congenital Anomalies of, i., 351; Cancer, Tubercle, and Par- asites of, i., 376 ; Degeneration and Growths of, i., 375; Dilatation of, i., 330; fatty Metamorphosis of, i., 375 ; fibrinous Deposits in, i., 379; Hyper- trophy of, i., 371, ii., 28 ; Neuroses of, 1., 384; Percussion of, i., 324; Palpita- tion of, i., 384; Rupture of, i., 378; valvular Disease of, i., 358 ; Immunity- of Persons with Heart Disease to Phthisis, i., 222. Heat-stroke, ii., 182. Hectic, i., 234. Heim’s Pill’s, i., 250. Helminthiasis, i., 622. Hellor’s Test for Blood, ii., 8. Helmerich’s Ointment, ii., 514. Hemicrania, ii., 331. Hemiplegia, ii., 225, 286. Hepar adiposum, i., 685. Hepatitis, chronic, i., 670 ; metastatic, i., 666 ; suppurative, i., 665 ; syphilitic, i., 681. “ Herdsymptome,” ii., 194, 206. Herpes, ii., 462 ; rodens, ii., 502; ton- dens, tonsurans, ii., 449, 508 ; circina- tus, ii., 463 ; zoster, ii., 463. Hip Gout, ii., 338. Hoarseness, i., 5, 232. Hodgkin’s Disease, i., 767. Hump-backed Persons, i., 133. Hunger in Diabetes, ii., 839. Hydatids, i., 697. Hydroa febrilis, ii., 462. Hydrocephalic Softening, ii., 276. Hydrocephaloid, ii., 199. Hydrocephalus acquisitus, ii., 275; acute, 11., 242 ; chronic, ii., 277 ; congenitus, ii., 278 ; externus, ii., 275; ex vacuo, ii., 276 ; senilis, ii., 276. Hydrometra, ii., 137. Hydronephrosis, ii., 54. Hydropathy in Scrofula, ii., 831. Hydropericardium, i., 408. Hydrophobia, ii., 793. Hydrops vesicas Fellas, i., 731 ; Ovarii, ii., 115. Hydrorachis acquisita, ii., 293; congen- ita, ii., 300; rheumatica, ii., 294. Ilydrothorax, i., 284. Hyperaesthesia, ii., 413. Hyperidrosis, ii., 516. Hyperinosis, i., 171. Hyperkinesia, i., 490; ii., 350. Hypertrophy: see various organs. Hypochondria, i., 515. Hypochondriasis, ii., 426. Hypostasis, i., 136. Hysteria, ii., 126, 409, 438. I. Ichthyosis, ii., 444 ; scbacea, ii., 579. Icterus, i., 705 ; catarrhal, i., 726 ; hsema- togenous, i., 714 ; in Relapsing Fever, 11., 659 ; in Cirrhosis, i., 675 ; from Gall- stones, i., 735 ; in Pneumonia, i., 175 ; spasticus, i., 714. Idiocy, ii., 283. Idiosyncrasies, ii., 414. Ileus, i., 574. Illusions, ii., 186. Impetigo, ii., 479 ; figurata, ii., 50S. Impotence, ii., 104. Infantile Palsy, ii., 373. Influenza, i., 64. Inhalation of nebulized Liquid, i., 12. Injections of hot Water, ii., 129. Inoculation of Tubercle, i., 39. “ Insanity of the Muscles,” ii., 380 Insolation, ii., 181. Intestine, Catarrh of, i., 565 ; Carcinoma of, i., 604; Contraction and Closure of, 1., 586; Haemorrhage from, i., 609, ii., 644 ; Invagination of, and Intussuscep- tion of, i., 587; Perforation of, ii., 644; Rotation of, upon axis, i., 587; Scrofulosis of, i., 598; stony Concre- tions in, i., 588 ; Strangulation of, i., 587 ; Tuberculosis of, i., 598. Iritis, syphilitic, ii., 766; gummous, ii., 767. Iron in Chlorosis, ii., 807. Irritable Breast, ii., 337. Ischias, ii., 338. Ischias antica, ii., 342. Ischuria spastica, ii., 83. Itch, ii., 510. J. Jail Fever, ii., 616. Jaundice, i., 705. Joints, hysterical, ii., 414. Jugulars, Pulsation of, i., 374. Junod’s Boot, i., 135. K. Keloid, ii., 443. Kidney, Diseases of, ii., 1 ; Abscess of, 11., 36; amyloid Degeneration of, ii., 41 ; Bright’s Disease of, acute, ii., 10; chronic, ii., 14; contracted, ii., 17: 856 INDEX. Carcinoma of, ii., 45 ; Carcinoma and Tubercle of Pelvis of, ii., 64 ; Deform- ities of, ii., 48 ; Dilatation of the Pel- vis of, ii., 54 ; Diseases of the Pelvis of, ii., 54; granular, ii., 18; Haemor- rhage from, ii., 7 ; Horse-shoe, ii., 48; Hypcraemia of, ii., 7 ; Infarction of, ii., 9 ; Irregularities of Position of, ii., 48 ; metastatic Deposits in, ii., 36; Mobil- ity of, ii., 48; pain in, ii., 4; Para- sites of, ii., 47; parenchymatous De- generation of, ii., 43 ; stony Concre- tions in Pelvis of, ii., 59; Tuberculosis of, ii., 46. Kummerfeld’s Lotion, ii., 495. Kussmaul’s Treatment, i., 522. L. Laryngismus stridulus, i., 51. Laryngitis, croupous, i., 15; catarrhal, i., 1. Laryngo-stenosis, i., 8. Larynx, acute Catarrh of, i., 1; chronic Catarrh of, i., 7 ; Cancer of, i., 43 ; Croup of, i., 15; Fistula of, i., 40; Growths and Polypi of, i., 43 ; nervous Affections of, i., 57; Ossification of, i., 40; Perichondritis of, i., 49 ; Syphi- litic Disease of, i., 35; typhous and variolous Ulcers of, i., 33 ; tuberculous Disease of, i., 38 ; Ulcers of, i., 31. Lead Colic, i., 617. Lead Palsy, ii., 361. Lebenswecker, ii., 545. Lentigincs, ii., 441. Lepra maculosa, ii., 522. Lepra vulgaris, ii., 486. Leprosy, ii., 522. Leuchasmia, i., 756. Leucocythsemia, i., 756. Lcucorrhoea, ii., 173. Lichen, ii., 489 ; circumscriptus, ii., 508 ; lividus, ii., 498. Lilion&se, ii., 442. Lipomata, ii., 264. Liver, Abscess of, i., 668; acute yellow Atrophy of, i., 717; Anatomy of, i., 722; Budd’s scrofulous Tumor of, ii., 828; Cancer of, i., 692 ; Cirrhosis of, i., 670; Degeneration of, amyloid, lar- daceous, waxy, i., 690; fatty, i., 685; granular, i., 670; Hydatids of, i., 697 ; Hypersemia of, i., 657; Inflammation of, suppurative, parenchymatous, i., 665; interstitial, i., 670; Metastasis of, i., 666 ; nutmeg, i., 659 ; physical signs of Enlargement of, i., 662; Syphilo- ma of, i., 681 ; Tuberculosis of, i., 696. Lockjaw, ii., 384. Locomotor Ataxia, ii., 302. Lumbago rheumatiea, ii., 543. Lungs, Abscess of, i., 109 ; Apoplexy of, i., 165; Atrophy of, i., 109 ; Atelectasis of, i., 130; Cancer of, i., 257; catar- rhal Inflammation of, i., 194; croupous Inflammation of, i., 166 ; chronic inter- stitial Inflammation of, i., 199; cheesy Infiltration pf, i., 1*70; Cirrhosis of, 1, 170; Collapse and Compression of, i., 130; Consumption of, i., 212; Em- bolism of, i., 158; Emphysema of, i., 110 ; Gangrene of, i., 169, 207 ; Haem- orrhagic Infarction of, i., 157; Ilmm- orrhage into, i., 157 ; Hepatization of, 1., 168 ; Hyperemia of, i., 134; Hyper- trophy of,i., 108; Induration of, i., 199; Metastasis into, i., 157; miliary Tuber- culosis of, i., 253; Gldema of, i., 134, 258; permanent inspiratory Expan- sion of, i., 69 ; syphilitic Disease of, i., 771; acute miliary Tuberculosis of, i., 253 ; chronic Tuberculosis of, i., 210 ; tubercular Infiltration of, i., 212. Lupus, ii., 500 ; syphilitic, ii., 704. Lyssa, ii., 793. Lyssaphobia, ii., 798. M. Magnctizers, ii., 419. Malarial Fever, ii., 671. Malignant Pustule, ii., 788. Malleus hmnidus et farcinosus, ii., 788. Malt Extract, i., 252, 536. Malum Coxe senile, ii., 540. Mania, ii., 190. Mania a Potu, ii., 432. Marasmus, i., 572. Mastodynia, ii., 337. Measles, ii., 573. Meeglin’s Pills, ii., 331. Melanemia, i., 761, ii., 682. Melasmata, ii., 441. Mcllituria, ii., 832. Membranous Croup, i., 15. Meningite foudroyantc, ii., 251. Meningitis simplex, ii-, 236 ; spinalis, ii., 292 ; rheumatic, ii., 532. Menorrhagia, ii., 163. Mentagra, ii., 495. Menstruation, Anomalies of, ii., 158; Absence of, ii., 159; precocious, ii., 158; vicarious, ii., 161; difficult, ii., 163; excessive, ii., 163; irregular, suppression of, ii., 161. Mental Depression, i., 515. Mercurial Stomatitis, Sore Mouth, i., 431 ; Eczema, ii., 468 ; mercurial Inunction, 11., 776; mercurial hypodermic Injec- tion, ii., 777. Mercury in Syphilis, ii., 773. INDEX. 857 Mesenteric Glands, scrofulous Disease,of, 1., 598. Metalbumen, ii., 113. Metallic Click, i., 325. Metritis, ii., 131 ; haemorrhagica, ii., 132. Metrorrhagia, ii., 132. Miasm, ii., 625, 671, 689. Migraine, ii., 331. Miliaria rubra et alba, ii., 468, 517. Miliary Tuberculosis, acute, i., 253. Milium, ii., 520. “ Milk Cure,” i., 435. Mimic Spasm of Face, ii., 351 ; facial Palsy, ii., 366. Miserere, i., 574. Mistura solvens, i., 81. Mitral Valve, Insufficience of, i., 385; Constriction of, i., 370. Mogigraphia, ii., 355. Molluscum simplex contagiosum, ii., 443. Monopathophobia, ii., 426. Morbilli, ii., 573 ; confluentes, ii., 576. Morbus maculosus of Werlhof, ii., 815. Morbus sacer, ii., 390. Morphine Poisoning, chronic, ii., 183; hypodermic Injection of. ii., 326; Habit, ii., 435. Mother’s Marks, ii., 443. Mouth, Catarrh of, i., 431; Excoriations and ulcers of. i., 441; syphilitic Affec- tions of, i, 444 ; scorbutic Affections of, i., 445. Mucor muado, ii., 574; racemosus, ii., 506. Muguet, i., 447. Mulberry Calculi, ii., 60. Mumps, i., 453. Muscular Atrophy, progressive, ii., 570. Muscular Rheumatism, ii., 542. Myelitis, ii., 295. Myocarditis, i., 354. Myxoma of Brain, ii., 263. N. Naevus, ii., 441. Nasal mucous Membrane, Catarrh of, i., 299 ; Haemorrhage from, i., 305 ; Poly- pus of, i., 301. Nasal Tone of Voice, i., 466. Nebulizer, i., 12. Nephogene, i., 12. Nephritis, croupous, ii., 16 ; parenchyma- tous, ii., 40 ; vera, ii., 86; interstitial, 11., 36. Nerves, Inflammation of, ii., 313. Nervous Cardialgia, i., 551. Nervousness, ii., 413. Nettle-rash, ii., 464. Neuralgia, ii., 314, 317, 376; cardiac, i., 385; coeliaca, i., 619; cervieo-occipi- tal, ii., 333; cervico-brachial, ii., ' 834; crural, ii., 842; intercostal, ii., 338 ; isehiadica, ii., 336 ; lumbo-abdo- minal, ii., 338 ; of tlic Trigeminus, ii., 327. Neuritis, ii., 313. Neuroma, ii., 315. Neuromantia, ii., 316. Neurotomy, ii., 330. Nictitatio, ii., 352. Night-sweats, i., 253. Nodding Spasm, ii., 353. Nodes, ii., 767. Noma, i., 451. Norwegian Itch, ii., 512. Nosebleed, i., 305. 0. Gldema of the Brain, ii., 191 ; in Blight’s Disease, ii., 25 ; of Lungs, i., 134 ; of Glottis, i., 45; hypostatic, i., 137. Oesophagitis, i., 480. Oesophagus, Auscultation of, i., 485 ; Di- latation of, i., 486; morbid Growths of, i., 488 ; nervous Affections of, i., 490 ; Perforation of, i., 4S9 ; Rupture of, i., 489; Strictures of, i., 482 ; spas- modic Stricture of, i., 490. Oidium albicans, i., 447 ; Schonleinii, i., 505. Oligocythaemia, ii., 802. Omodynia rheumatica, ii., 544. Onanism, ii., 105. Oophoritis, ii., 109. Ophthalmoscope in Brain Lesions, ii., 270. Opisthotonos, ii., 386. Opium-eating, ii., 435. Optic Nerve, Atrophy of, ii., 306. Orchitis, ii., 93; syphilitic, ii., 770. Orthotonos, ii., 386. Ossification, deficient, in Rachitis, ii., 557. Osteocopic Pain, ii., 767. Osteomalacia, ii., 565. Otorrhcea, a cause of Brain Disease, ii., 255. Ovaritis, ii., 109. Ovary, Abscess of, ii., 110; Cysts in, ii., Ill; Dropsy of, i., 652; Inflamma- tion of, ii., 109; Inflammation of, in Parotitis, i., 456 ; Tumors of, ii., 120. Ovula Nabothi, ii., 124. Oxalic Diathesis, i., 559. Oxaluria, i., 560. Oxyuris vermicularis, i., 623. Ozaena, i., 303; syphilitica, ii., 73S. P. Pacchionian Bodies, ii., ISO. Pachydermy, ii., 443. Pachymeningitis, ii., 230; externa, ii., 233. 858 INDEX. Palpitation of Heart in Chlorosis, ii., 805. Palsy of Bladder, ii., 84; central, ii., 268 ; of Deglutition, i., 491 ; diptli- theritic, ii., 668; essential, of Chil- dren, ii., 373; facial, ii., 366; hys- teric, ii., 360; of Insane, ii., 239; intermitting, ii., 684; peripheral, ii., 268, 359 ; of Pharynx, ii., 372; pho- nic, of the Glottis Muscles, i., 54; phonic, of the Glottis-closers, i., 56; progressive, of the cerebral Nerves, 11., 372; psychical, i., 55; spinal, ii., 373 ; shaking, ii., 431. Papules, ii., 489. Paracentesis Thoracis, i., 284, 298. Paralbumen, ii., 113. Parametritis, ii., 135, Paraplegia, ii., 298. Parasites in the Skin, ii., 505. Parenchymatous Nephritis, with amyloid Degeneration, ii., 35. Paresis, ii., 360. Parotitis, i., 453. Pai’s vagum, Section of the, i., 20. Pathophobia, ii., 426. Pectoral Fremitus, i., 183. Pectoriloquy, i., 186. Peliosis rheumatica, ii., 499. Pelvis of Kidney, Cancer of, ii., 64 ; Dila- tation of, ii., £4 ; Inflammation of, ii., 56; stony Concretions in, ii., 59 ; Tu- berculosis of, ii., 64. Pemphigus, ii., 482; foliaceus, ii., 484. Penicillum glaucum, ii., 506. Pericarditis, i., 394 ; scorbutic, ii., 753. Pericardium, Adhesion of, to Heart, i., 406; Cancer of, i., 412; Tuberculosis of, i., 412. Perichondritis laryngca, i., 49. Pericystitis, ii., 72. Periencephalitis, ii., 239. Perimetritis, ii., 135. Perinephritis, ii., 40. Periostitis, syphilitic, ii., 767. Periproctitis, i., 607. Peritonaeum, Air in, ii., 644 ; Cancer of, 1., 654 ; Dropsy of, i., 649; Tubercu- losis of, i., 654. Peritonitis, i., 638. Perityphlitis, i., 568, 574, 607. Pertusds, i., 92. Petechiae, ii., 498. Petit mal, ii., 397. Pharyngitis, catarrhal, i., 463 ; croupous, i., 462; diphtheritic, i, 479; follicu- laris, granulosa, i., 465 ; phlegmonous, i., 471; syphilitic, i., 474. Pharynx, Catarrh of, i., 463; gummy Tu- mor of, i., 475. Phlegmasia alba dolcns, i., 430. Phonetic Paralysis, i., 54. Phthisis pituitosa, i., 76 ; tuberculosa, i., 212 ; renalis, ii., 39. Pia Mater, simple Inflammation of, ii., 236; tuberculous Inflammation of, ii., 240. Piles, bleeding, blind, i., 609. Pills, Asiatic, ii., 48S; Blaud’s, ii., 80S; Heim’s, i., 250; Martini’s, ii., 422; Ricord’s, ii., 779. Pine-needle Bath, i., 80. Piss-abed, ii., 81, 87. Pityriasis of the Mouth, i., 448; rubra circumscripta, ii., 508; tabescentium, 1., 220, ii., 448; versicolor, ii., 510. riaques muqucuses of Larnyx, i., 36. Pleura, Cancer of, i., 295 ; Inflammation of, i., 264; Tuberculosis of, i., 294. Pleurisy, Pleuritis, acute, i., 264; fibrin- ous, i., 266 ; purulent, i., 268 ; rlieu- matica, i., 265; scorbutic, ii., 813; sero-fibrinous, i., 266; sicca, i., 269. Pleuritic Effusion, i., 274. Pleurodynia rheumatica, ii., 544. Pleurosthotonos, ii., 386. Pneumogastric Nerve, Neuralgia of, i., 551. Pneumonia, i., 166; bilious,?., 175; ca- tarrhal, i., 194; caseous, i., 212; chronic, i., 199; croupous, i., 166; hy- postatic, i., 137; interstitial, i., 199 , lobular, i., 131; metastatic, i., 162; migratory, i., 261; notha, i., 69. Pneumopericardium, i., 410. Pneumorrhagia, i., 150. Pneumothorax, i., 287. Podagra, ii., 545. Poisons, Effect of, on Stomach, i., 525. Pollutions, diurnal and nocturnal, ii., 100. Polypi of the Skin, ii., 443. Polypus of Nose, i., 301; of the Womb, 11., 152. Pompholyx, ii., 482. Porrigo asbestina, ii., 508; favosa, ii., 505; larvalis, ii., 471; lupinosa, ii., 505. Portal Vein, Inflammation of, i., 683. Progressive fatty muscular Paralysis, ii., * 570. Progressive muscular Atrophy, ii, 567. Progressive pernicious Anaemia, ii., 817. Prosopalgia, ii., 327. Prostate, Inflammation of, ii., 92. Prune-juice Expectoration, i., 87. Prurigo, ii., 490; Pudendorum, ii., 492. Psammoma, ii., 263. Pseudo-Croup, i., 60. Pseudoleuchaemia, i., 767. Psora, ii., 518. Psoriasis, ii., 452, 485 ; annulate, con- ferta, diffusa, grcllata, gyrata, etc., ii., 486 ; inveterata, ii., 486 ; of the Mouth, INDEX. 859 1., 449; Palmaris and Plantaris, ii., 486, 763; syphilitica, ii., 763. Ptyalism, i., 458. Pulmonary Artery, Diseases of, i. 428; Aneurism of, i., 429 ; Contraction of Mouth of, i., 373. Pulmonary Diseases : see Lung?. Pulsation, epigastric, i., 126 ; of the Ju- gulars, i., 3.74. Pulse, diehrotic, ii., 635 ; jerking, i., 364 ; small, of Pneumonia, i., 191; slow, of Icterus, i., 710. Pulsus celerrimus, i., 364. Punaisie, i., 303. Pupil, Contraction and Dilatation, ii., 187. Purpura, ii., 498 ; bullosa, ii., 813; huem- orrhagica, ii., 815; papulosa, ii., 198; pulicosa, ii., 499; rheumatica, ii., 499; senilis simplex, ii., 499; urti- cans, ii., 498. Pustules, atheromatous, i., 415. Pyelitis, ii., 56. Pylephlebitis, i., 683, 723. Pylorus, Stricture of, i., 513, 516. Pyothorax, i., 268. Pyuria, ii., 58. Q. Quinia as an Antiperiodic, ii.,686. R. Rabies, ii., 793. Rachitic Pelvis, ii., 560. Rachitis, ii., 557, 572. Rales, crepitant, i., 785 ; moist, in Phthi- sis, i., 238; subcrepitant, i., 69 ; tra- cheal, i., 69. Rectum, Cancer of, i., 604. Relapsing Fever, ii., 654. Renal Abscess, ii., 36. Renal Colic, ii., 69; Apoplexy, ii., 7; granular Degeneration of Epithelium, 11., 43. Respirators, i., 248. Respiratory Muscles, Spasm of, i., 94. Retro-uterine Ilaematocele, ii., 165. Retroversion of Uterus, ii., 145. Ilevelenta Arabica, ii., 572. Rheumatic Callosities, ii., 542. Rheumatism, ii., 526, 571; acute articu- lar, ii., 527 ; chronic articular, ii., 535 ; deforming articular, ii., 540; gonor- rhoeal, ii., 93 ; muscular, ii., 542. Rhonchi, sibilant, i., 68; sonorous, i., 68. Rickets, ii., 557. Ricord’s Pills, ii., 779. Risus caninus, sardonicus, ii., 352. “ Rose,” the, ii., 460. Roseola aestiva, autumnalis, ii., 451; febrilis, ii,, 595 ; idiopathica, infan- tilis, symptomatica, ii., 451; syphi- litica, ii., 762; typhosa, ii., 638. Rose Itasli, ii., 595. Rougeole, ii., 573. Rubeola morbilosa, ii., 573. Rupia, ii., 484; syphilitic, ii., 764. Rush of Blood to the Head, i., 364 ; ii., 175. Russian Clap, ii., 92. s. Saint Vitus’s Dance, ii., 378. Salaam Convulsions, ii., 353. Salivation, i., 458; in Syphilis, ii., 716. Salt-rheum, ii., 467. Sand-tumors of Brain, ii., 263. Sarcina, i., 514, 542. Sarcocele, syphilitic, ii., 770. Sarcoptes Hominis, ii., 510. Scabies, ii., 510. Scarlatina, ii., 585. Scarlet Fever, ii., 585, 738. Schneemann’s Treatment, ii, 594. Sehroth’s Treatment, i., 522. Sciatica, ii., 338. Scleroderma, ii., 521. Sclerosis, ii., 569. Scorbutus, ii., 810. Scriveners’ Spasm, ii., 355. Scrofula, i., 217; ii., 820, 848. Scrofulous Habit, ii., 825. Scurvy, ii., 810. Seborrhoea, ii., 519. Semilunar Valves, insufficience of, i., 359, 373. Serous Effusions in the immature Skull, ii., 278; in the mature Skull, ii., 275. Serratus Muscle, Palsy of, ii., 370. Sheep-pox, ii., 612. Shingles, ii., 419. Ship-fever, ii., 616. Siderosis, i., 202. Skin, Diseases of, ii., 440; Hypertrophy of, ii., 440; Atrophy of, ii., 447 ; Hy- peraemia of, ii., 450; Anaemia of, ii., 450; Inflammation of, ii., 452. Small-pox, ii., 596. Snuffles, i., 303. Soor, i., 447. Spasms, clonic and tonic, ii., 350; of the facial Nerve, ii., 351; of the spinal Accessory, ii., 353 ; hysterical, ii., 416 ; idiopathic, ii., 357;. intermitting, ii., 684; psychical, ii., 422; nodding, ii., 353. Spasmus Glottidis, i., 51. Spermatorrhoea, ii., 100. Spina bifida, ii., 300. Spinal Marrow, Apoplexy of, ii., 290; Atrophy of, ii, 302 ; Carcinoma of, ii., 860 INDEX. 300; Consumption of, ii., 302 ; Cysti- cerci and Echinococci in, ii., 299; gray Degeneration of, ii., 302 ; Growths in, 11., 299 ; Haemorrhage into, ii., 290; Ilypcraemia of, ii., 290 ; Inflammation of, ii., 295; Inflammation of Mem- branes of, ii., 292 ; Irritation of, ii., 290; Tubercle of, ii., 300. Spleen, Diseases of, i., 739 ; Abscess of, 1., 752; amyloid Degeneration of, i., 750; Carcinoma of, i., 754; acute Enlargement of, i., 740; chronic En- largement of, i., 745; haemorrhagic Infarction of, i., 347, 751 ; Hydatids of, i., 754 ; Ilypcraemia of, i., 739 ; Hy- pertrophy of, i., 746; Inflammation of, i., 751 ; lardaceous, i., 750 ; Size of, i., 743; Tuberculosis of, i., 754; En- largement of, in Typhoid Fever, ii., 628; wandering, i., 754. Spotted Fever, ii., 614. Sprue, i., 447. Sputa: see Expectoration. Status gastricus, i., 499. Stenosis, i., 358. Stiekhusten, i., 95. StoYnacace, i., 439. Stomach, Catarrh of, i., 493 ; Cancer of, i., 538; Cough, i., 123; Dilatation of, i., 522 ; Haemorrhage from, i., 516, 545; Position of, i.. 542; Softening of, i., 497 ; Spasm of, i., 551; Ulcer of, i., 516, 528. Stomatitis, i., 431; croupous, i., 437. Stone in the Bladder, ii., 77. Stricture, cardiac, i., 356. Strychnine in Palsy, ii., 366. Sudamina, ii., 576. Sudor anglicus—suette miliaire, ii., 694. Sugar, Test for, ii., 837, 849. Sunstroke, ii., 181. Suppressio Mensium, ii., 161. Supraclavicular Region in Croup, i., 19. Suprarenal Capsules, Disease of, ii., 49. Sweat, ii., 516. Sweating of Hands and Feet, ii., 517; Sweating in Phthisis, i., 253; Sweating Sickness, ii., 694. Sycosis, ii., 495. Syphilides, ii., 760. Syphilis, ii., 742; congenital, ii., 784; constitutional, ii., 753 ; hereditary, ii., 784. Syphilitic Acne, ii., 762; Alopecia, ii., 765; Catarrh, ii., 765; Disease of Bone, ii., 767; Disease of Muscle and Viscera, ii., 770; Disease of Perios- teum, ii., 766; Disease of mucous Membranes, ii., 765 ; Exanthemata, ii., 760; Iritis, ii., 766; Lupus, ii., 764; Roseola, ii., 762; Rupia, ii., 764; Sarcoccle, ii., 770; primary Ulcer, ii., 750; Varicella, ii., 762. Syphilization, ii., 784. ►syphilomata, ii., 264. T. Tabes dorsualis, ii., 302. i Ta?nia mediocanellata, solium, i., 622. | Tape-worm, i., 622, 630. j Tarentism, ii., 425. Telangiectasis, ii., 443. Temperature of Body, i., 637; in Cholera, 11., 703 ; Danger from high, ii., 650; in Typhoid Fever, ii., 640 ; in Sudor anglicus, ii., 608; in Ileat Fever, ii., 182; in spinal Diseases, ii., 387. Temporal Bones, Caries of, ii., 235. Testicle, Inflammation of, in Parotitis, i., 456. Tetanus, ii., 384; Neonatorum, ii., 388. Thrombosis, i., 430. Thrush, i., 447. Tic convulsive, ii., 351. Tic douloureux, ii., 327 Tinea favosa, ii., 505 ; furfuracca, ii., 470. Tongue, parenchymatous Inflammation of, i., 449; Deviation of, ii., 36S. Tonsils, Inflammation of, i., 474, 479. Tooth-rose, ii., 455. Tophi, ii., 767. Torpid Indigestion, i., 558. Torticollis, ii., 354; rheumatica, ii., 543. Trachea, Diseases of, i., 61; Croup of, 1., 86. Tracheotomy, i., 594. Trembling, ii., 261. Trichina Disease, Trichinosis, ii., 731. Trichomonas vaginalis, ii., 172. Tricoccplmlus dispar, i., 624. Tricuspid Valves, Disease of, i., 374. Trismus, ii., 384. Trychophyton tonsurans, ii., 508. Tubercle, i., 214; syphilitic, ii., 764; painful, ii., 316 ; Inoculation of, i., 262. Tubercula dolorosa, ii., 316. Tuberculosis of the Bladder, ii., 73; in Emphysema and Heart Disease, i., 222; of the Intestines, i., 598; of the Kid- neys, ii., 46 ; of the Larnyx, i., 38; of the Liver, i., 696; of the Lungs, i., 212 ; of the Pleura, i., 294. Typhlitis stercoralis, i., 581. Typhoid Fever, ii., 623 ; Poison, ii., 740. Typhus, abdominal, ii., 623; abortive, 11., 641; ambulatorius, ii., 642; ex- anthematic, ii., 614; ileotyphus, ii., 623 ; Sequela? of, ii., 646 ; Observation of Temperature in, ii., 637. INDEX. 861 u. Ulcer of the Cervix Uteri, ii., 157; of the Duodenum, i., 553 ; of the Larynx,' i., 40; of the (Esophagus, i., 489; of the Pharynx, i., 464 ; of the Stomach, i., 528, ii., 806; of the Endocardium, 1., 346. Umbilication of Vaccine Vesicle, ii., 610. Uraemic Amblyopia, ii., 30; Intoxication, 11., 28. Ureters, Cancer of, ii., 62; Closure of, ii., 54; Diseases of, ii., 54; Tubercu- losis of, ii., 62. Urethra, Abscess of, ii., 92 ; non-virulcnt Catarrh of, ii., 98; virulent Catarrh of, ii., 8S. Uric-acid Infarction, ii, 62. Urina spastica, ii., 418. Urinary Organs, Diseases of, ii., 1. Urine, Amount of, ii., 4. Urine in Bright’s Disease, ii., 20. Urticaria, ii., 464. Uterine Colic, ii., 125, 133. Uterus, Anteflexion of, ii., 141 ; Antever- sion of, ii., 144; Cancer of, ii., 154; Catarrh of, ii., 122; Curvature and Flexions of, ii., 140; Descent and Pro- lapse of, ii., 145; Displacements of, ii., 145; fibrous Polypi of, ii., 147; Infarction of, ii., 131 ; Eetroflexion of, ii., 140; Stricture of the Mouth of, ii., 137; Ulcers of, ii., 122, 124; Injec- tions into, ii., 130; lacerated Cervix, ii., 134 ; Tumors of, ii., 147. Y. Vaccina, ii., 508. Vaccination, ii., 605. Vaccinoid, ii., 608. Vagina, croupous and diphtheritic In- flammation of, ii., 173 ; non-virulent Catarrh of, ii., 171; virulent Catarrh of, ii., 170. Valves of Heart, Aneurism of, i., 393; Hypertrophy of, i., 358; Vegetations upon, i., 345. Valvular Disease of Heart, i., 358 ; com- pensating Hypertrophy of the Ven- tricles in, i., 360; Origin of, i., 351. Varicella, ii., 612; syhilitica, ii., 763. Variola, ii., 595. Varioloid, ii., 604. Veins, Diseases of, i., 429. Venesection in Apoplexy, ii., 228; in acute (Edema of the Lungs, i., 149; in cerebral Hyperaemia, ii., 192; iu acute Pneumonia, i., 188, 190; in En- docarditis, i., 854. Venous Trunks, Diseases of, i., 429. Veratria in Pneumonia, i., 192, 2G2. Vermiform Appendix, Perforation of, i., 575. Vcrtige (ipileptique, ii., 397 ; stomacale, i., 561. Vertigo it Stomacho laeso, i., 561. Vesical Palsy, ii., 82; Catarrh, ii., 58; Phthisis, ii., 70. Vesie k Colonne, ii., 59. Vichy Water in Diabetes, ii., 842. Virus, venereal, Duality of, ii., 74S. Vitiligo, ii., 448. Vleminckx’s Solution, ii., 488. Vocal Chords, Palsy of, i., 55. Vomiting in gastric Catarrh, i., 501, 523 ; ' in Disease of Brain, ii., 187 ; in Penal Disease, ii., 12. Vomitus Matutinus, i., 514. Vox cholerica, ii., 710. w. Warts, ii., 440, 442. Water-brash, i., 514. Water-canker, i., 451. Water on the Chest, i., 2S4; on the Heart, i., 409. Water-pox, ii., 612. Werlhof’s Disease, ii., 815. Whey-cure, i., 11. Whooping-cough, i., 95. 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