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STATE VETERINARY COLLEGE. 1897 Digitized by Microsoft® Cornell University Library RB 25.0333 1897 A handbook of pathological a ni Digitized by Microsoft® This book was digitized by Microsoft Corporation in cooperation with Cornell University Libraries, 2007. You may use and print this copy in limited quantity for your personal purposes, but may not distribute or provide access fo it (or modified or partial versions of if) for revenue-generating or other commercial purposes. Digitized by Microsoft® Digitized by Microsoft® Digitized by Microsoft® Digitized by Microsoft® Digitized by Microsoft® A HANDBOOK OF PATHOLOGICAL ANATOMY AND HISTOLOGY « & With an Introductory Section on \e oa Ge! POST-MORTEM EXAMINATIONS AND THE METHODS OF PRESERVING AND EXAMINING DISEASED TISSUES BY FRANCIS DELAFIELD, M.D., LL.D. Professor of the Practice of Medicine, College of Physicians and Surgeons, Columbia College, New York AND T. MITCHELL PRUDDEN, M.D. Professor of Pathology and Director of the Laboratories of Histology, Pathology, and Bacteriology, College of Physicians and Surgeons, Columbia College, New York fifth Loition ILLUSTRATED BY THREE HUNDRED AND SIXTY-FIVE WOOD ENGRAVINGS PRINTED IN BLACK AND COLORS NEW YORK WILLIAM WOOD AND COMPANY Digitized by {Aigrosont® ae Qaarr, | Lf by ‘ x i oe XE as —r a " Co CHT BY : WILLIAM WOOD & COMPANY, 1896. KE No Fd Le Dota (8697 PRESS OF ‘THE PUBLISHERS? PRINTING COMPANY 132-136 W. FOURTEENTH eT. NEW YORK, Digitized by Microsoft® PREFACE TO THE FIFTH EDITION. THE aims followed in the preparation of this the fifth edition of this work are identical with those which were kept in view in former editions. It has been the intention of the authors to give to students and practitioners of medicine, first, the knowledge neces- sary for the making of autopsies, the preservation of tissues and their preparation for microscopic study, and to outline the methods of study of pathogenic micro-organisms; second, to describe con- cisely, with such illustrations as seem necessary, the lesions of the acute infectious diseases and, so far as they are known, the micro- organisms concerned in their causation, the various phases of de- generation and inflammation, the character of tumors, the special lesions of different parts of the body, of the general diseases, of poisoning, and of violent deaths. All of the sections of the book have been revised, and some of them largely rewritten in the light of recent contributions to science. Many new cuts have been added. The section on the blood has been rewritten for us by Dr. James Ewing. FRANCIS DELAFIELD, T. MITCHELL PRUDDEN. Digitized by Microsoft® Digitized by Microsoft® CONTENTS. PART FIRST. THE METHOD OF MAKING POST-MORTEM EXAMINATIONS AND OF PRESERVING AND EXAMINING PATHOLOGICAL TISSUES. The object in making post-mortem examinations.—Causes of death, 3.—Ex- TERNAL INSPECTION, 4.—Cadaveric lividity, 5.—Putrefactive changes, 5.— * Cooling of the body, 6.—Rigor mortis, 7.—Contusions, 7.—Wounds, 8.— Fractures, scars, and tattoo marks, 9. INTERNAL EXAMINATION, 9.—The Head. Removal of calvarium, 10.—The dura mater, the pia mater, the brain, 11.—Methods of opening the brain, 11-18.—Base of the cranium, 18. —The Spinal Cord, 19. Preservation of cord and membranes, 21.—The Thorax and Abdomen, 22. General inspection of abdominal cavity, 23.—. The heart, 25.—The pleural cavities, the lungs, 28-29.—Pharynx, larynx, and cesophagus, 29.—The Abdomen, 30. Kidneys, 31.—Suprarenal capsules, 32.—The spleen, 33.—Intestines, 34.—Stomach and duodenum, 35.—Liver, 36.—Pancreas, 37.—Genito-Urinary Organs. Male organs, 38.—Female or- gans, 39. AUTOPSIES IN MEDICO-LEGAL CASES AND OF SUSPECTED POISONING, 41. EXAMINATION OF THE BoDIES OF NEW-BORN CHILDREN. General Inspection, 42. —Internal Examination, 46. GENERAL METHODS OF PRESERVING TISSUES AND PREPARING THEM FOR STUDY, 50. —Fresh tissues, 50.—Decalcifying, 51.—Hardening and preservation, 52.— Miiller’s fluid, 53.—Formalin, osmic acid, Fleming’s osmic-acid mixture, 54. —Corrosive sublimate, Long’s solution, 55.—Embedding and section cutting, 56.—Staining, 60.—Preservation of museum specimens, 638. PART SECOND. CHANGES IN THE CIRCULATION OF THE BLOOD.—CHANGES IN THE COMPOSITION AND STRUCTURE OF THE BLOOD.—HYPERTROPHY, HYPERPLASIA, REGENERATION, DEGENERATION, ETC.—INFLAM- MATION. — ANIMAL AND VEGETABLE PARASITES.—INFECTIOUS DISEASES.—TUMORS. CHANGES IN THE CIRCULATION OF THE BLoop. Hypereemia and anemia, 69.— Hemorrhage and transudation, 69-71.—Thrombosis and embolism, 72-75. CHANGES IN THE COMPOSITION AND STRUCTURE OF THE BLoop. Coagulability of the blood, 76.—Anhydrzmia, hydreemia, heemoglobinemia, anemia, 76-77. Changes in the Red Blood Cells, '77.—Changes in the White Blood Cells, 82-86. Digitized by Microsoft® vi CONTENTS. Melanemia, 86.—Method of examination of the blood, 86-89.—Foreign Bod- tes in the Blood, 89. HYPERTROPHY, Hyperpiasia, REGENERATION, METAPLASIA. Hypertrophy and hyperplasia, 91.—Regeneration, 91. Direct cell division.—Indirect cell di- vision, 92.—Metaplasia, 95. DEGENERATIVE CHANGES IN THE TISSUES. Necrosis, coagulation necrosis, 96.— Cheesy degeneration, 97.—Parenchymatous degeneration, 98.—Fatty degen- eration and fatty infiltration, 98.—Amyloid degeneration, 100.—Glycogen degeneration, Mucous degeneration, 102.—Colloid degeneration, 103.— Hyalin degeneration, 104.—Calcareous degeneration, 105.—Pigmentation, 106. INFLAMMATION, 107.—Degeneration and necrosis, 107.—Congestion, transuda- tion, and emigration, 108.—Production of new cells and tissues, 109.— Phases of inflammation, 110.—Exudative inflammation, 110.—Productive inflammation, 117.—Necrotic inflammation, 119.—Repurative Production of New Tissue.—Healing of wounds, 120.—Healing of fractures, 125. PARASITES. Animal Parasites. Protozoa, 127.—Worms, 130.—Arthropods, 141.— Methods of study and preparation of animal parasites, 142. Vegetable Parasites. Bacteria, 143.—Morphology and physiology of bacteria, 144-153.—Classification of bacteria, 153.—Methods of studying bacteria. 154.—Cultivation of bacteria, 158.—Bacterial examinations of post-mortem specimens, 167.— Yeasts and Moulds, 168.—The Relation of Bacteria to Dis- ease, 171.—Infection and Immunity, 177. THE InrecTious Diseases, 183.—INFECTIOUS DISEASES INDUCED BY THE PYO- GENIC BACTERIA, 188.—ERYSIPELAS, 194.—PY4MIA AND SEPTIC/ MIA, 196.— ACUTE CEREBRO-SPINAL MENINGITIS, 199.—ACUTE LOBAR PNEUMONIA AND THE INFECTIOUS DISEASES INDUCED BY THE DIPLOCOCCUS PNEUMONIA, 201.—IN- FECTIOUS PSEUDO-MEMBRANOUS INFLAMMATION OF MUCOUS MEMBRANES, 204.— GONORRH@A, AND OTHER INFLAMMATORY LESIONS INDUCED BY THE MICRO- COCCUS GONORRH@Z, 206.—ANTHRAX, 209.—TUBERCULOSIS, 213-216.— Lupus, 227.—LEPROSY, 229.—SYPHILIS, 231.—GLANDERS, 235.—RHINOSCLE- ROMA, 238.—BUBONIC PLAGUE, 239.—TYPHOID FEVER, 240.—DIPHTHERIA, 250.—TETANUS, 255.—INFLUENZA, 257.—BACTERIA WHICH MAY BE OCCASIONAL INCITERS OF INFECTIOUS DISEASE IN MAN, 259.—ACTINOMYCOSIS, 262.—ASIATIC CHOLERA, 265.—RELAPSING FEVER, 269.—VARIOLA, 271.—SCARLET FEVER, 273.—MEASLES, 274.—TYPHUS FEVER, 275.—HYDROPHOBIA, 276.—YELLOW FEVER, 279.—THE MALARIAL FEVERS, 280.—PHARYNGO-MYCOSIS, 284.—IN- FECTIOUS DISEASES OF ANIMALS, 285. Tumors. SECTIONI. GENERAL CHARACTERS, 286.—Cause of tumors, 290.—Classi- fication of tumors, 293.—Cysts, 296.—Various lesions sometimes described as tumors, 297.—Nomenclature of complex tumors, 297.—Preservation of tumors, 298. SeEcTION II. Special forms of tumors, 299-348. PART THIRD. MORBID ANATOMY OF THE ORGANS. THE NERVOUS SYSTEM. THE MEMBRANES OF THE BRAIN.—The Dura Mater, 34’. Heemorrhages, 347.—Thrombosis.—Inflammation, 348.—Tumors, 351.—The Pia Mater, 352. C&dema, hyperemia, and hemorrhage, 358.—Tuberculous Digitized by Microsoft® CONTENTS. vii meningitis, 359.—Syphilitic meningitis, 362.—Tumors, 362.—The Ventricles of the Brain, 365.—Acute and chronic ependymitis, 365.—Congenital hydro- cephalus, 867.—Secondary hydrocephalus and primary hydrocephalus in adults, 368.—Tumors, 368.—Pineal Gland and Pituitary Body, 369. THE Brain. Thrombosisand embolism, 370.—Hyperemia, anzemia, and cedema, 373.—Heemorrhage, 374.—Changes in ganglion cells in toxemia, 376.—Sec- ondary degenerations, 377.—Hypertrophy and atrophy, 378.— Wounds, 379. Holes or cysts in the brain, 380.—Inflammation of the brain, abscesses, 380. —Chronic interstitial encephalitis (sclerosis), 382.—Encephalitis in new- born, 383.—Syphilitic and tuberculous encephalitis, 384.—Lesions of brain in chronic paresis of insane, 885.—Pigmentation, tumors, 386.—Malforma- tions, 387. SpinaL Corp. Dura Mater Spinalis. WHeemorrhages, inflammations, 389.—Pa- rasites, 390.—Pia Mater Spinalis. Hzemorrhages, inflammations, 390.—Tu- mors and parasites, 391.—The Cord. WHeemorrhage, 391. Heematomyelia and hematomyelopore, 391.—Injuries, secondary degenerations, 393.—Progres- sive spinal muscle atrophy, bulbar paralysis, amyotrophic lateral sclerosis, 396-397.—Poliomyelitis anterior, 399.—Chronic myelitis, multiple sclerosis, 400.—Posterior spinal sclerosis, 402.—Solitary tubercles, gummata, cysts, and tumors, 403.—Syringomyelia, 404.—Malformations, 404. THE PERIPHERAL NERVES. Changes after division, acute and chronic neuritis, 408.—Tumors, 409.—Acromegalia, scleroderma, 410.—Preparation of nerve tissue for microscopical study, 410. THE RESPIRATORY System. Larynx and Trachea. Malformations, inflamma- tion, 413.—CEdema glottidis, tumors, 416. The Pleura. Uydrothorax, hemorrhage, inflammation, 417.—Pleurisy with production of fibrin, pleurisy with production of fibrin and serum, 418.— Pleurisy with production of fibrin, serum, and pus (empyema), 421.—Chronic pleurisy, 423.—Tuberculous pleurisy, 424.—Tumors, 425. The Bronchi. Inflammations, 426.—Bronchiectasia, 429.—Tumors, 481. The Lungs. Malformations, injuries, congestion, and oedema, 482.—Hzamor- rhage, 433.—Emphysema, 434.—Atelectasis, 486.—Gangrene, 437.—Inflam- mation, classification, acute lobaf pneumonia, 438.—Broncho-pneumonia, 443.—Secondary and complicating pneumonia, 448.—Pneumonia of heart disease, 449.—Interstitial pneumonia, 451.—Tuberculous pneumonia, 452. —Acute miliary tuberculosis, 453.—Subacute miliary tuberculosis, 456.— Chronic miliary tuberculosis, 457.—Acute pulmonary phthisis, 459.—Ex- perimental phthisis, 460.—Chronic phthisis, 469.—Syphilitic pneumonia, 475.—Tumors, 476.—Parasites, 477. The Mediastinum, 477. Inflammation, 481.—Tumors, 478. THE VASCULAR SYSTEM. —FPericardium. Injuries, dropsy, hemorrhage, pneumo- natosis, 480.—Inflammation, tumors, 483. The Heart. Malformations, 483.—Abnormal size and positions of heart, 485.— Wounds and ruptures, 486.—Atrophy, hypertrophy, 487.—Dilatation, 489.— Degeneration, 490.—Fatty infiltration, atrophy of pericardial fat, 492.— Myomalacia, fragmentation of endocardium, 493.—Inflammation, simple acute endocarditis, mycotic endocarditis, 494.—Chronic endocarditis, 496.— Chronic ulcerative and tuberculous endocarditis, myocarditis, 498.—Changes in heart valves, aneurism of the heart, 500.—Thrombosis of the heart, 501. --Tumors and parasites, 502. Digitized by Microsoft® Vili CONTENTS. The Blood Vessels. Atrophy and hypertrophy, 502.—Degeneration, 503.—The Arteries. Inflammation, acute arteritis, 503.—Chronic arteries, 504.—Dila- tation and aneurism, 5V9.—Aneurism of the different arteries, 512.— Stenosis, 513.—Ruptures and wounds, 514.—Tumors, 516.—The Veins. Dilatation, 517. —Wounds and ruptures, inflammation, 518.—Tumors and parasites, 520.— The Capillaries, 520.—The Lymph Vessels, 520. Inflammation, 521.—Lym- phangiectasis, tumors, 522.—The Lymph Nodes, 522. Inflammation, 523.— Pigmentation, 526.—Inflammation with cheesy degeneration, 527.—Tuber- culous inflammation, 528.—Syphilitic inflammation, 529.—Degenerations, 530.—Hyperplasia, 531.—Tumors and parasites, 532. Tar ALIMENTARY CanaL. The Mouth. Malformations, 5383.—Hypertrophy of cheeks and lips, inflammation, stomatitis, stomatitis ulcerosa, 583.—Syph- ilitic and tuberculous stomatitis, gangrene, 584.—Tumors, 535.—The Tongue. Malformations, hypertrophy, 536.—Inflammation, tumors, 537.—The Phar- ynx and Gisophagus. Malformations, 538.—Inflammation, 540.—Ulcera- tion, 541.—Dilatation of cesophagus, 541.—Stenosis, 542.—Tumors, 543. The Stomach. Malformations, post-mortem changes, injuries, heemorrhage, 546. —Inflammation, 547.—Ulcers, 550.—Dilatation, 553.—Tumors, 554.—Degen- erations. The Intestines. Malformations, 557.—Incarceration, 558.—Intus- susception, 559.—Transposition, wounds, and ruptures, 560.—The Small In- testine. Inflammation, lesions of solitary and agminated nodules, 561.— Emboli, 562.—Large Intestine. Inflammations, 563.—Tumors, 575.—Con- cretions, parasites, 577. THE PERITONEUM. Malformations, 578.—Inflammation, 579.—Tumors, 587.— Parasites, 589. Tue Liver. Malformations, acquired changes in size and position, 590.—Ane- mia and byperemia, 591.—Wounds, rupture, and hemorrhage, lesions of hepatic artery, lesions of portal vein, 598.—Lesions of hepatic veins, atro- phy of liver, degenerations, 599.—Pigmentation, 599.—Acute yellow atro- phy, 600.—Inflammation, acute hepatitis (abscess), 601.—Chronic intersti- tial hepatitis (cirrhosis), 604.—Syphilitic hepatitis, 605.—Tuberculous hepatitis, 609.—Perihepatitis, 611.—Hyperplasia of lymphatic tissue in the liver, 611.—Tumors, 612.—Parasites? 641. The Biliary Passages and Gall Bladder. Catarrhal inflammation, suppurative and croupous inflammation, 617.—Constriction, occlusion, and dilatation, 618.—Biliary calculi, 619.—Tumors, 614. THE SPLEEN. Wounds, rupture, and hemorrhage, 621.—Disturbances of the cir- culation, 612.—Inflammation, 624.—Perisplenitis, 628.—Alterations of spleen in leukemia and pseudo-leukemia, 628.—Degenerations, 629.—Pigmenta- tion, tumors, 528.—Parasites, 630.—Malformations and displacements, 631. THE PANCREAS. Hemorrhage and inflammation, 632.—Degenerations, 633.—Fat necrosis, 634.—Tumors, 635.—Malformations and displacements, 636. THE SALIVARY GLANDS. Inflammation, 637.—Tumors and parasites, 638. THE THYROID GLAND. Hyperemia, inflammation, degenerations, and tumors, 639.—Parasites, malformations, myxcedema, 641.—Exophthalmic goitre, 643. Tue THYMUS GLAND, 643. THE SUPRARENAL BopiEs. Malformations, hemorrhage, thrombosis, inflamma- tion, 644.—Degeneration, tumors, 645. Digitized by Microsoft® CONTENTS. ix THE URINARY APPARATUS. The Kidneys. Malformations and changes in posi- tion, 646.—Bright’s disease, classification, acute congestion, 647.—Acute degeneration, 648.—Acute exudative nephritis, 650.—Acute productive ne- phritis, 655.—Chronic congestion, 658.—Chronic degeneration, 659.—Chronic productive nephritis, chronic Bright’s disease, 660.—Suppurative nephritis, 671.—Ureteritis, 672.—Pyelo-nephritis, 672.—Tuberculous nephritis, embo- lism, and thrombosis, 673.—Hydronephrosis, 674.—The cystic kidneys, 675. Perinephritis, 676.—Renal calculi, tumors, 677.—Parasites, 680. The Urinary Bladder. Malformations, 680.—Changes in size and position, 681. Rupture and perforation, 682. Disturbances of circulation, inflammation, 688.—Tumors, 685.—Parasités, calculi, 687. The Urethra. Congenital malformations, and changes in size and position, 688. —Wounds, ruptures, and perforations, 689.—Inflammation, 690.—Tumors, 691. THE ORGANS OF GENERATION. FEMALE.—The Vulva. Malformations, heemor- rhage, and hyperemia, 692.—Inflammation, 693.—Tumors and cysts, 694. The Vagina. Malformations, changes in size and position, 695.—Wounds, per- forations, inflammations, 696.—Tumors, 697.—Parasites, 698.—The Uterus. Malformations, 698.—Changes in size, 699.—Changes in position, 700.—Rup- ture, perforation, hyperemia, and hemorrhage, 702.—Inflammation, 704.— Puerperal inflammation, 708.—Ulceration, degeneration, tumors, 709.— Parasites and cysts, 718.—The Ovaries. Malformations, changes in size and position, hypereemia, hemorrhage, 719.—Inflammation, 720.—Tumors, 722. The Fallopian Tubes. Malformations, changes in position and size, 730.— Hemorrhage, inflammation, 731.—Tumors, extra-uterine pregnancy, 782. The Placenta. Hemorrhage, 733.—Inflammation, degenerations, 784. The Mamma. Malformations, hemorrhage, inflammation, 735.—Tumors, 738. ORGANS OF GENERATION. Mae. The Penis. Malformations, 741.—Inflamma- tion, tumors, 743.—The Scrotum, 744.—The Testicles. Malformations, hydro- cele, 745.—Heematocele, 746.—Spermatocele, inflammation, 747.—Tumors, 750.—The Seminal Vesicles, '51.—The Prostate. Hypertrophy, 751.—In- flammation, 752.—Parasites, concretions, 753.—Cowper’s Glands, 753.— The Male Mamma, 753. Tue Bones. Disturbances of circulation, injuries, 754.—Inflammation, perios- titis, '755.—Osteitis, 757.—Osteomyelitis, 763.—Necrosis, '765.—Caries, rachitis, 766.—Osteomalacia, 769.—Alterations of the bone marrow in leu- keemia and anemia, 770.—Atrophy, tumors, 771. DISEASES OF THE JOINTS. Inflammation, 775.—Tumors, 778. Muscie. Hemorrhage, infarction, wounds and ruptures, inflammation, 780.— Degenerations, atrophy, pseudo-hypertrophy, 783.—Tumors, 787.—Para- sites, 788. PART FOURTH. THE LESIONS FOUND IN THE GENERAL DISEASES, IN POISONING, AND IN VIOLENT DEATHS. DISEASES CHARACTERIZED BY ALTERATIONS IN THE COMPOSITION OF THE BLOOD. CHLOROSIS, 791.—PERNICIOUS ANAMIA, 792.—LEUKa&MIa, 794.—PsEUDO-LEU- KIA (Hodgkin’s Disease), 796. Scorsutus, PurPuRA, 798.—HMATOPHILIA, 799. Digitized by Microsoft® x CONTENTS. ADDISON’S DisEAseE, 800. Gout, 802. ACUTE RHEUMATISM, 803. DIABETES MELLITUS, 804. SUNSTROKE, 806. DEATH FROM BURNING, 807. DEATH FROM ELECTRICITY, 808. DEATH FROM SUFFOCATION, ASPHYXIA, 809.—Death from Stranguiation, Hang- ing, 810.—Death from Drowning, 811. DEATH FROM POISONING, 814. Digitized by Microsoft® Ry co ot Bowed 10. 11. 12, 13. 14. 15. 16. 1%. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27, 28. 29. 30. al. 32. 33. 34. 35. LIST OF ILLUSTRATIONS. . View-of the base of the brain, with the temporal lobes furasd backward Distoma hepaticum, . Digitized by Microsoft® 7 Paae . Side view of the human brain, showing its fissures and convolutions, . 12 . Method of opening the brain, first incisions, 13 . Method of opening the brain, final incisions, 14 and outward, : 16 . Drawing of the brain axis, Seuacaled from thes fiaies veantla, 16 . Brain mantle, seen from below, 17 . Outlines of spinal cord sections, - i ‘ ‘ . 21 PLATE. —Blood cells, . ; ‘ é : - opposite 80 . Phases of mitosis, or indirect eel diciaibas 92 . Cheesy degeneration (coagulation necrosis) in miliary iibonele of dive, 97 Fatty degeneration of heart muscle, 98 Fatty infiltration of liver cells, ‘ 99 Amyloid (waxy) degeneration of dapillaries of a « plomneniiie 5 in the kidney, - 101 Corpora amylacea, : . 102 Mucous degeneration of epithelial golly ‘ . 102 Mucous degeneration of fibrous tissue of mamma, . 103 Colloid degeneration of epithelial cells, . 104 Hyalin degeneration of capillary blood vessels, . 104 Pigmentation of connective-tissue cells of the lungs, és - 105 Emigration of white blood cells in inflamed bladder of frog, . 11 Exudative inflammation—pneumonia, . 118 Exudative inflammation—appendix, . 113 Pus cells from catarrhal inflammation of brovohial mucous arenibkane, 116 Omentum of dog, showing peritonitis on fourth day, . 116 Developing blood vessels in new-formed tissue, . 121 Granulation tissue from wound of skin, . 122 Fibroblasts from granulation tissue, 122 Cicatricial tissue, : . 128 Exuberant granulations, . 124 New-formed cartilage and osteoid tissue from callus after feabuiee of the femur, . 125 Amoeba coli, . 127 Coccidium oviforme, . 128 Balantidium coli, . 129 Cercomonas intestinalis, . 129 Trichomonas vaginalis, . 129 . 130 Xii LIST OF ILLUSTRATIONS. Fic. PaGE 36. Head of Tenia solium, . . . . : . 131 37. Head and proglottides of Tania edledendilate:, . . ° . . 131 88. Cuticula of echinococcus cyst, . 3 i F . ° ° . - 138 89. Scolices of Tania echinococcus, $ B . e ° ‘ . 183 40. Hooklets from scolex of Tenia adhinceneeak, 7 s s . a . 184 41. Ascaris lumbricoides, F , ‘ ‘ ° ° ° : . 135 42. Oxyuris vermicularis, 3 3 . 7 ‘ - . . . . 136 43. Eggs of nematode worms, * 3 . . . . . . . 137 44, Trichocephalus dispar, . . . . . . . . . 137 45. Trichinee encysted in muscle, . : . . . . . . - 139 46. Filaria sanguinis hominis, : . : . . . ° s . 140 47. Sarcoptes hominis, . 2 ‘ 3 ‘ * . . . < . 141 48. Pediculis capitis, . . . . . ‘ . 141 49. Drawing of three typical fois. of henotenia, 3 . . ° . . 143 50. Bacilli showing flagella, . ‘ é 3 . . . . 7 . 144 61. Growth aggregates of bacteria, : : . . . . « 145 52. Leptothrix buccalis with micrococcus eclonies: . . . . - 145 53. Sarcina, . 3 : : 7 : . . . . . 146 54. Bacteria with capenle, ‘5 ‘< - ; ° . . e é . 146 55. Bacilli showing spores, . j fs . . . . . 147 56. A tube of solid transparent auivient dln. . a . . . - 160 57. Pure culture of bacteria on nutrient agar, . : . . . - 161 58. A culture of bacteria on potato, oe : . ° s “i S . 161 59. A Petri gelatin plate culture of bacteria, < . ° . . . 163 60. A Petri gelatin plate culture of bacteria, c 7 fs e ‘ . 164 61. Petri’s agar plate culture of bacteria (mouth), . i ° . - 165 62. Sterilized cotton swab in sterilized tube, i 7 ‘ 5 : . 166 63. Yeast—saccharomyces, . , - ij , : 5 Ganglion cells of the spinal cord, . $ . 377 Atrophy of a circumscribed portion of brain convolutions ina abate. . 879 Syphilitic obliterating endarteritis of a cerebral artery, é > . 383 - Solitary tubercle of cerebellum, ° é : . ‘“ ‘ . . 384: Hemorrhage in spinal cord, . 7 . . . . . . . 392: Heematomyelopore, . 5 3 S é ‘ a : . 892 Descending degeneration, spinal goed, 5 . ‘ . 7 7 . 395 Ascending degeneration, spinal cord, . 7 : : . ‘ - 895° Ascending degeneration, spinalcord, . : . . ; : . 396 - Amyotrophic lateral sclerosis, . . 3 7 . . . . . 397: Degenerated tissue, spinal cord, . i. 3 ; . : % . 898 Poliomyelitis anterior, . . . 7 0 ‘ é . 399° Poliomyelitis anterior, . . . . . ‘i ‘ é ‘ . 399 Multiple sclerosis, spinal cord, . . ‘ ‘i : : 5 . 401 Posterior spinal sclerosis, . ; : . ‘ . 7 A . 401 Posterior spinal sclerosis, ‘ - 5 ‘ . . . A . 402 Syringomyelia, > . : : . a 2 . < - « 404 Hydromyelia, . 3 é 2 * . ‘ : . ‘ ‘ . 406 False heterotopia, 2 . ‘ A . a . : . 7 . 406 Multiple neuritis, is . . . s . . . i: . . 408 Ulcer of larynx, 3 ¢ 5 . S . . . . 7 . 414 Tuberculous laryngitis, . ‘ ‘ é é . . : - . 415 Pleurisy in dog, 7 . ‘ ° . . . . * . - 420 Tuberculous pleurisy, . . . . ° . . . ° « 425 Catarrhal bronchitis, ls A . a < . . é ‘ . 427 Croupous bronchitis, ‘ a ¢ A ‘ e 7 . 3 ~ 428 Bronchiectasia, . ‘ % . S m 5 . < . 5 . 480° Adenoma of bronchi, é ; é : . . < * ‘ . 431 - Emphysema, ‘ é is . . . . . 5 : s . 485 | Emphysema, i . ‘i 5 7 7 . . . . é . 436 Acute lobar pneumonia, . ° . . . é . 489 Acute lobar pneumonia with denned Gaus: ‘. : : ; . 440 Acute lobar pneumonia with organized tissue, . : ; ‘ . 441 Acute lobar pneumonia with organized tissue, ° . is : . 442 Broncho-pneumonia, child, ‘i . . . . . ° . . 443 Broncho-pneumonia, child, ‘ $ 7 . . . . $ . 445 Broncho-pneumonia, adult, 4 a ‘ * * . . 3 . 446 Broncho-pneumonia, persistent, . . e ss ‘ 3 . 447 Broncho-pneumonia, persistent, . 5 . . . . . . 448 - Broncho-pneumonia, in diphtheria, . . . . s - . 449 Lung of heart disease, 3 : . . e . E - ‘ . 450 Interstitial pneumonia, - . . . . . . . . 451 Miliary tubercle, lung of child, 7 5 . . . . : . 454 - Peribronchitic miliary tubercle, . . . ‘ . . . . 455° Aggregation of miliary tubercles, . : . . . : . . 456° Miliary tubercle, ‘ . : ‘ - : . . i ‘ . 457°: Digitized by Microsoft® xvi LIST OF ILLUSTRATIONS. Fia. PAGE 224. Miliary tubercle, : : : ‘i : ‘ . is 7 . 458 225. Miliary tubercle, s . . 7 : : . 459 226. Experimental pulmonary gine rabbit, . "i i ; . 460 227. Experimental pulmonary tuberculosis, rabbit, . . é : - 460 228. Experimental pulmonary tuberculosis, rabbit, . : . : . 462 229. Tuberculous broncho-pneumonia, . ‘i . . . . : . 463 230. Coagulation necrosis and pneumonia, . 5 ‘ e ‘ ; . 464 231. Acute phthisis, : ; 3 7 : . : . ° . 465 282. Acute phthisis, ‘ 3 ‘ : ‘ ‘ : - : . 467 233. Acute phthisis, F : : : : ‘ . . . 468 234. Chronic phthisis, . : ‘ . . . i : . 469 235. Tuberculous jutiemiviation of fang, . : . . : : ‘ . 470 236. Chronic phthisis, : : 7 < 7 . - ‘ : ‘ . 470 237. Chronic phthisis, . 7 : . . . . Fi . 2 . 471 288. Chronic phthisis, . , 3 : . ‘ . . F : . ATL 239. Chronic phthisis, ; 7 ‘< . 3 3 ‘ 3 : 3 . 472 240. Healed phthisis, . : 3 . Fi : ’ . ‘ ‘ . 478 241. Tubercle tissue, . F ‘ ‘ é . * a % . ; . 474 242. Syphilitic pneumonia, ‘ 3 ‘ 5 . : ‘ ‘ . 475 248. Adenoma of lung, ‘i ‘ : . . . . 7 é A476 244. Obliteration of partcardfal sac, . : ‘ . . - r 482 245. Fatty degeneration of heart, . : 4 . 3 ‘i 3 3 . 490 246. Fatty infiltration of heart, 5s 5 m a ‘ é . . . 491 247. Atrophic pericardial fat, . é ° e . : . . $ . 492 248. Vegetation on heart Valve, 4 re ee ‘ : : ‘ . 495 249. Mycotic endocarditis, 2 . . . . . . . ‘ . 496 250. Chronic endocarditis, . i ;: : . : . . ‘ . 497 251. Chronic endocarditis, . ‘ . . s . . ‘ . 498 252. Chronic interstitial swoearditia, a . . 5 ‘ ‘ ‘ . 499 253. Chronic arteritis, ‘ ‘ 5 ‘ . . . . 2 ‘ . 505 254. Chronic arteritis, ' : ‘ . ‘ é ° é * ‘ . 506 255. Chronic arteritis, . ‘ ‘ . . . . . = ‘ . 507 256. Chronic arteritis, e . ; < . je . . . . . 508 257. Chronic arteritis, : : 7 . . . . . . ‘ . 509 258. Atheroma of aorta, . * 4 . . . . . . . . 510 259. Atheroma of aorta, . ‘ ‘5 removed, when necessary, without cut- ting the scrotum, by enlarging the inguinal canals from within and crowding the glands through them and cutting them off. The average weight of the adult testicle with its epididymis is, accord- ing to Krause, from 15 to 24.5 gm. (about } oz.). Inflammatory lesions, tuberculosis, abscesses, and tumors are the most frequent lesions. Preservation.—The urethral canal and bladder may be pinned open and hardened in strong alcohol, or in formalin solution, or in Miiler’s fluid. The prostate, vesic- ulee seminales, testicles, and tumors may be hardened in the same fluids. Digitized by Microsoft® POST-MORTEM EXAMINATIONS. 39 The Female Organs.—The position and general condition of the pelvic organs should first be determined by inspection. Abnor- mal adhesions of the ovaries, broad ligaments, Fallopian tubes, and uterus ; malpositions of the uterus ; subserous tumors of the uterus, and ovarian tumors, are frequently observed. Hemorrhage into the posterior cul-de-sac is sometimes found. The urine should be collected, if necessary, as above directed ; the organs should be dis- sected away laterally, as in the male, care being taken not to injure the ovaries and Fallopian tubes. The bladder is then drawn strongly backward and upward, and dissected away from the symphysis and the pubic arch, and, the point of the knife being carried forward and downward, the vagina is cut off in its lower third, the rectum severed just above the anus, the remaining attachments cut, and the pelvic organs taken out together. If it be necessary to remove the external generative organs, after freeing the lateral surfaces of the internal organs and the bladder, the legs are widely separated and the vulva and anus circumscribed by a deep incision. The tissues close beneath the pubic arch are now dissected away from below and the vulva thrust back beneath the symphysis; it is now seized above the bone, and together with the anus dissected away and removed with the other organs. The Bladder is first opened and examined. The vulva may now be examined for hypertrophies, inflammatory lesions, ulcers, cica- trices, cysts, and tumors. The vagina is opened along the anterior surface ; its more common lesions are inflammations, fistula, ulcers, tumors, and rarely cysts. The Uterws.—Before opening this organ its size and shape should be determined. The adult virgin uterus is a pear-shaped body, flattened antero-posteriorly ; the upper portion, or body, is directed upward and forward, whilst the lower portion, the cervix, is directed downward and backward. It is covered anteriorly by peri- toneum to a point a little below the level of the os internum ; pos- teriorly, to a point a little below the level of its junction with the vagina. The peritoneal investment separates from the organ at the sides to form the broad ligaments. The uterus is held in position by the broad and round ligaments and by its attachments to the bladder and rectum and vagina. The upper end, the fundus, does not extend above the level of the brim of the pelvis. Its average length is about 7.6 cm. (3 in.) ; its breadth about 5.1 cm. (2 in.) ; its thickness about 2.5 em. (1 in.) ; its average weight is about 31 to 46 gm. (1 to 14 oz.). During menstruation the uterus is slightly enlarged and the mucous membrane of the body becomes thicker, softer, and its vessels engorged with blood ; while its inner surface is more or less thickly covered with blood and cell detritus. A descrip- Digitized by Microsoft® 40 THE METHOD OF MAKING tion of the complicated changes in the uterus which pregnancy entails may be found in the works on obstetrics. After pregnancy the uterus does not return to its original size, but remains somewhat larger ; the os is wider and frequently fissured. We not infrequently find in the mucous membrane of the lower part of the cervix small transparent, spheroidal structures, called ovula Nabothi ; these are small retention cysts caused by the closure of the orifices of the mucous glands of the part. The more common lesions observed in the uterus are malpositions, malformations, lacerations, ulcerations of the cervix, acute and chronic inflammation of the mucous membrane or muscularis, or both, thrombosis and inflammation of the veins, and tumors. In the infant the uterus is small, the body flattened, the cervix disproportionately large. During childhood the organ increases in size, but the body remains small in proportion to the cervix. At puberty the shape changes and the body becomes larger. The Ovaries are flattened, ovoidal bodies, situated one on each side and lying nearly horizontally at the back of the broad ligament of the uterus. Their size is variable and they are usually largest in the virgin state. Their average weight is from 3.9 to 6.5 gm. (3 to 5). They measure about 3.8 cm. (13 in.) in length, 1.9 cm. (2 in.) in breadth, and nearly 1.3 cm. ($ in.) in thickness. The sides of the ovary and its posterior border are free; it is attached along the anterior border ; to its end is attached the ovarian ligament ; to its outer extremity one of the fimbriz of the Fallopian tube. The ovary is covered on its free surface by cylindrical epithelium, and its surface is less glistening than the general peritoneum. The surface of the ovary is smooth in the young, but becomes rougher and depressed in spots as the process of ovulation goes on. In adult females we usually find corpora lutea in their various stages. We should seek for evidences of acute and chronic inflammations, for tumors and cysts. The Fallopian Tubes, lying in the upper margin of the broad ligaments, are from 7.6 to 10 cm. (3 to 4in.) in length. The length often differs considerably on the two sides. ‘They commence at the upper angles of the uterus as small perforated cords, which become larger further outward and bend backward and downward toward the ovary. They terminate in an expanded fimbriated extremity about 2.5 cm. (1 in.) beyond the ovary. They are covered by peri- toneum, and the mucous membrane lining them, continuous with that of the uterus, is thrown into longitudinal folds. Malpositions by adhesions, closure, inflammations, and cysts are the more common lesions. The possibility of tubal pregnancy should be borne in mind. Digitized by Microsoft® POST-MORTEM EXAMINATIONS. Al Preservation.—All of these organs and their tumors may be hardened in Miiller’s fluid, or in formalin solution, or in strong alcohol. The vagina should be stretched flat on cork and the cavity of the uterus laid wide open. Great care should be taken not to touch either the internal surface of the uterus or the external surfaces of the ovaries, since in both the epithelium is very easily rubbed off. It is better, after opening them by a transverse incision, to suspend the ovaries by a thread in a jarof the preservative fluid than to let them lie on the bottom, since the epithelium is thus less liable to be rubbed off. Larger eysts of the ovary for exhibition purposes should be distended with preservative fluid (see p. 64). AUTOPSIES IN MEDICO-LEGAL CASES. While every autopsy should be made as carefully and completely as circumstances will permit, it should be always borne in mind that in examinations which may have medico-legal bearings it is of the highest importance to examine thoroughly both macroscopically and microscopically every part of the body from which light may be derived as to the cause of death, for in medico-legal cases it is not infrequently as important to be able by a complete examination to declare the absence of lesions which could cause death as to deter- mine the presence of those upon which the opinion as to the actual cause of death in a particular case rests. Bearing this in mind, the technique of autopsy making is essentially the same whatever the ends which the facts elicited may be destined to serve. AUTOPSIES IN CASES OF SUSPECTED POISONING. It is always best, in cases of suspected poisoning, to preserve for the chemist not only the stomach and intestine, but the entire liver and brain; or, if portions of these only can be saved, these portions should be carefully weighed, as well as the entire organs, and the relative amount of tissue reserved carefully noted at the time. It is even well, particularly in cases in which the administration of the readily diffusible poisons, such as arsenic, strychnia, etc., is sus- pected, to preserve the whole of all the internal organs, together with a large piece of muscle and bone; since with large quantities of tissue the results of the chemical analysis depend less upon calcula- tions, and are hence more comprehensible to the average jury. In all such cases jars should, if possible, be procured which have never been used before, and these should be carefully washed and rinsed with distilled water. They should have glass stoppers and be sealed at once and carefully labelled before leaving the hands of the operator. If they can be delivered to the chemist without much delay, no preservative fluid should be added. If they are to be kept for a considerable time, pending the action of a coroner’s jury or for some other reason, a small quantity of pure strong alcohol may be Digitized by Microsoft® 42 THE METHOD OF MAKING poured over them. In this case the operator should be particular to ‘preserve a quantity, at least half a pint, of the specimen of alcohol used, in a clean, sealed, and labelled bottle, so that this may be tested by the chemist and be proven to be free from the poison. It is better in all cases, however, to avoid, if possible, the use of alcohol. In all autopsies which may have medico-legal importance full notes should be taken by an assistant as the operation proceeds, carefully read over immediately afterward, and dated and kept by the operator for future reference. The labelling and disposition of the jars should be recorded in the notes. The specimens should not for a moment be out of the sight of the operator until they are placed under lock and key and seal, or are delivered to some authorized person, so that there may be no question of their identity should the case come into court. EXAMINATION OF THE BODIES OF NEW-BORN CHILDREN. In examining the bodies of new-born children we may have to determine, besides the ordinary lesions of disease, the age of the child, whether it was born alive. how long it has been dead, what was the cause of death. GENERAL INSPECTION, The Size and Age.—Caspar’ gives the following description of the foetus during the different months of intra-uterine life : At the fourth week the embryo is 8 to 13 mm. (,% to #5 in.) long. The cleft of the mouth and two points indicating the eyes can be recognized in the head. The extremities are represented by little wart-like projections. The heart can be distinguished ; the liver is disproportionately large. The umbilical vessels are not yet formed. The entire ovum has about the size of a walnut. At the evghth week the embryo is 2.3 to 4 em. (8; to 1,5; in.) long. The head forms more than a third of the entire body ; the mouth is very large; the nose and lips can be distinguished, but not the ex- ternal ear. The hand is longer than the forearm ; the fingers are formed, but joined together ; the toes look like little buds ; the soles of the feet are turned inward. The position of the anus is indicated by a point. The abdomen is closed. All the viscera can be recog- nized. Centres of ossification are formed in the apophysis of the first cervical vertebra, the humerus, radius, scapula, ribs, and cranial bones. There are rudimentary external genitals, but the sex can 1 Caspar, ‘‘ Handbook of Forensic Medicine.” Revised German Edition by Liman, or Sydenham Society Translation. Digitized by Microsoft® POST-MORTEM EXAMINATIONS. 43 hardly be distinguished. The ovum has about the size of a hen’s egg. At the twelfth week the placenta is formed. The embryo is 5 to 6.5 cm. (2 to 2$ in.) long and weighs about 31 gm. The head is separated from the thorax by a distinct neck. The eyes and mouth are closed. The nails can be perceived on the fingers. The sex can be recognized. The umbilical cord is inserted near the pubes; the muscles begin to be recognizable. The thymus and suprarenal cap- sules are formed. The cerebrum, cerebellum, medulla, and the cav- ities of the heartcan be recognized. The humerus is 1.7mm. long: the radius 5.5 mm.; the ulna 6.6 mm.; the femur and tibia 4.4 to 6.6 mm.; the fibula 5.5mm. The ovum is as large as a goose’s egg. At the sixteenth week the embryo is 13 to 15 em. (5 to 6 in.) long and weighs 77 to 93 gm. (24 to 3 oz). Theskin is of a rose-red color and has considerable consistence. The formation of fat in the subcutaneous tissue has begun. The scrotum and labia are formed. The face begins to assume its characteristic appearance. There is whitish meconium in the duodenum. The liver is not so dispropor- tionately large, and the gall bladder is formed ; the anus is open. The length of the humerus, radius, and ulna is 1.7 cm. ; the femur and tibia 8.8 toilcm. The calcaneus begins to ossify at the middle of the fourth month. At the twentieth week the embryo is 26 to 28 cm. (10 to 11 in.) long ; it weighs from 225 to 320 gm. (73, to 100z.). The nails are quite perceptible. There is a thin down on the head. The head is still disproportionately large, occupying about one-fourth of the body. ‘There is as yet none of the vernix caseosa. The secretion of bile has commenced and stains the meconium. The insertion of the umbilical cord is still further off from the pubes. The liver, heart, and kidneys are large in proportion to the other organs. The convolu- tions of the brain cannot be recognized. The humerus is 2.8 to 3 cm. ‘ong; the radius 2.6 cm.; the ulna 2.8 em.; the femur, tibia, and fibula, each 2.6 cm. The astragalus and the upper part of the sternum begin to ossify. From this time on the length of the foetus forms an approxi- mately accurate basis for the estimation of itsage. From this pe- riod till tts maturity the length of the foetus, determined in centimetres, corresponds to about one-fifth of the number of months of its age. From this time on the weight exhibits marked individual differences, and is therefore a less reliable criterion of its age than is the length. At the twenty-fourth week the embryo is 31 to 34 cm. (12 to 13 in.) long and weighs 750 to 875 gm. (24 to 28 oz.). The lanugo and vernix caseosa are formed. The skin is of a dusky cinnabar-red Digitized by Microsoft® ‘ 44 THE METHOD OF MAKING color. The meconium is darker. The scrotum is empty, small, and red ; the labia majora are prominent and held apart by the project- ing clitoris. The pupillary membrane is present and readily recog- nized. The length of the humerus and radiusis 3.5 em. ; of the ulna, femur, tibia, and fibula, each 3.7 cm. Atthe twenty-eighth week the embryo is 36.4 to 39 cm. (144 to 15} in.) long and weighs 1,500 to 1,750 gm. (48 to 57 oz.). The hair is more abundant and longer. The great fontanelle measures about 4 cm. (1£in.) in diameter, and all of the fontanelles are readily per- ceived. The skin is of a dirty-reddish color and abundantly beset with the lanugo and vernix caseosa. The large intestine contains much meconium. The humerus is 4.5 to 5 cm. long; the radius 3.7 cm.; the ulna 4 cm.; the femur, tibia, and fibula, each 4.2 to 4.6 cm. At the thirty-second week the embryo is 39 to 41.5 em. (154 to 163 in.) long and weighs 1,500 to 2,500 gm. (48 to 81 oz.). Theskin is lighter in color; the pupillary membrane has disappeared. The testicles are in the scrotum or the inguinal canal ; the labia are still widely apart and the clitoris prominent. The nails reach nearly to the ends of the fingers. The humerus is 5 to 5.2 cm. long; the ra- dius 4 to 4.2 cm.; the ulna 4.8 to 5 cm.; the femur 5.2 cm.; the tibia and fibula, each 4.8 to 5cm. The last sacral vertebra begins to os- sify. At the thirty-sixth week the embryo is 44.2 to 46 em. (17.4 to 18 in.) long and weighs about 3,000 gm. (97 oz.). The scrotum begins to become wrinkled and the labia to close. The hair becomes more abundant, while the lanugo begins to diminish in amount. At the fortieth week the foetus is fully developed and the term of its intra-uterine life accomplished. The fresh corpse of a new-born child at term no longer resembles that of the immature foetus. The skin is firm and pale, like that of an adult. The lanugo has disappeared except on the shoulders. In the majority of cases the hair on the head is 1.5 to 2 cm. (% to # in.) long. The great fontanelle is, in the average, 2 to 3 cm. (,8; to 175 in.) long. As determined by an analysis of 661 cases, the average length is 50 cm. (20 in.), the weight 3,256 gm. (105 oz.). The nails are hard and reach to the tips of the fingers, but not to those of the toes. The cartilages of the ears and nose are hard. The labia are more nearly closed. An ossification centre in the lower epiphysis of the femur should be sought for, as its presence is one of the most reliable signs of the maturity of the foetus. If it is absent the footus is, as arule, not more than thirty-seven weeks old ; but in rare cases it may be absent at term. A centre of ossification 1 mm. (.039 in.) in diameter indicates an age of 37 to 38 weeks, if the child was born Digitized by Microsoft® POST-MORTEM EXAMINATIONS. 45 dead or died soon after birth. Rarely it is no larger than this at term. A diameter, at birth, of 1.5 to 9 mm. (.058 to .351 in.) indi- cates an age of 40 weeks. A diameter of less than 9 mm. (.351 in.) indicates, as a rule, that the child has lived some time after its birth; a less diameter than 7 mm, (.273 in.), however, does not prove the contrary. Twenty-four hours after the birth of the child the skin is firmer and paler. The umbilical cord is somewhat shrivelled, although still soft and bluish in color. From the second to the third day the skin has a yellowish tinge and the cuticle sometimes appears cracked. The umbilical cord is brown anddry. From the third to the fourth day the skin is yellower, and the cuticle is apt to separate from the skin. The umbilical cord is of a brownish-red color, flattened, semi- transparent, and twisted. The skin around its insertion is red and congested. The head should be examined for the marks of injuries. Very commonly some portion of the scalp will be found swollen and infil- trated with blood and serum. This may be the caput succedaneum formed during delivery. The mouth and nose should be examined for the presence of any foreign bodies which might have caused suf- focation. The neck should be examined for marks of strangulation. The umbilical cord may be twisted around the child’s neck and strangle it. The mark left by the cord is usually continuous, broad, not ex- coriated, sometimes accompanied by ecchymoses in the skin. The entire body should be examined for the presence of vernix caseosa, blood, marks of injury, and the existence of putrefaction. It should be remembered that putrefaction is apt to commence ear- lier in the bodies of young children than in those of adults. The umbilical cord may be cut or torn. It usually separates by the fifth day, sometimes not until thetenth. If the umbilicus is cica- trized and healed the child has probably lived for three weeks. A zone of redness around the insertion of the cord may exist previous to birth. Redness and swelling (which may disappear after death) with suppuration can only be found in a child which has lived for several days. The drying and mummification of the cord may take place as well in dead as in living children. It is possible for a child to die by hemorrhage from a cut or torn cord, either before or after it has breathed. The extremities may exhibit fracture of the bones. These may occur during intra-uterine life, from injuries to the woman or from unknown causes ; or may be produced by violence in delivery, or by injuries after birth. Digitized by Microsoft® 46 THE METHOD OF MAKING INTERNAL EXAMINATION. The Head.—The fontanelles and sutures should first be examined as to their size and for penetrating wounds. Anincision should then be made through the scalp across the vertex, and the flaps turned backward and forward as in the adult. With a small knife the edges of the bones should be separated from the membranous sutures and the dura mater, beginning low down in the frontal and going back into the lambdoidal suture on either side. The bones are then drawn outward and cut through around the skull with strong scis- sors. The brain is removed and examined as in the adult.’ Effusions of blood—cephalheematoma—may be formed, soon after birth, between the pericranium and bone, or, more rarely, between the dura mater and bone. Clots are also found between the dura mater and skull ; between the dura and pia mater; more rarely in the substance of the brain, as the result of protracted or instrumental deliveries, or of injuries after birth. The cranial bones may be malformed, or exhibit the lesions of rickets or caries, or be indented, fissured, or fractured. These latter lesions may be produced during intra-uterine life by injuries to the mother, by unknown causes, by difficult deliveries, or by direct vio- lence after birth. In cases of chronic internal hydrocephalus in young children, in which the ventricles are much dilated and the brain substance thinned over the vertex, the brain is very apt to be torn in removal, and the amount of dilatation thus becomes difficult of determination. It is, therefore, better in such cases to place a pail of water beneath the head, or even immerse the latter in it, and remove the brain in the water. In this way it floats after removal, supported on all sides. It may now be opened in the water and the extent of the lesion deter- mined at once, and parts saved for microscopical examination. If it be desired to preserve the brain for demonstration of the le- sion or for a museum specimen, it should be transferred unopened to a large jar containing a mixture of equal parts of alcohol and water. A portion of the ventricular fluid should now be removed with a syringe provided with a small canula, and replaced by strong alcohol. This may be done by puncturing the ventricles from below. The fluid in the jar, as well as in the ventricles, should be changed in forty-eight hours and then gradually increased in strength until the organ be- comes hard. The brain may then be cut transversely. across, when the degree of dilatation of the ventricles, etc., will be revealed. The brain, of course, shrinks considerably by this process, but the rela- tive proportions are approximately preserved. The brain is normally much softer and pinker than in the adult, 1 Or an incision through the bones with a fine saw may be made as in the adult. Digitized by Microsoft® POST-MORTEM EXAMINATIONS. 4” the pia more delicate; both may be much congested or anzemic with- out known cause. The ventricles contain very little serum. Malfor- mations, apoplexies, hydrocephalus, simple and tubercular inflamma- tory lesions, are to be looked for. Spinal Cord.—Extravasations of blood between the membranes of the cord may occur from the same causes as those in the brain. Spina bifida is the most frequent malformation. The Thorax and Abdomen.—These are opened as in the adult. The peritoneal cavity contains a very little clear serum. cut them off from the wooden blocks, since alcohol extracts from these a dark resinous material which colors the specimen and inter- feres with the staining of sections made later. The severed speci- men can be readily refastened to fresh bits of wood by a drop of celloidin when more sections are to be made.’ Paraffin.—For some purposes, especially when extremely thin though not large sections are required, paraffin embedding is almost, indispensable. The sections of tissues thus embedded may be cut exceedingly thin (2-3 mic.) and when these are fixed to the slide and appropriately stained the conditions for the study of cytological details are more favorable than by any other method. For the paraffin technique the specimen should be small, say } ¢.c. as a maximum limit. The specimen is freed from the preservative fluid by washing in water and then is transferred to a series of graded alcohols as follows: thirty per cent, fifty per cent, and seventy per cent, and finally ninety-five per cent. The specimen remains in each of these alcohols for two or several hours and is then placed in abso- lute alcohol. Complete dehydration of the specimen in absolute alcohol is indispensable for the success of this method, for if the slightest trace of water be left in the specimen shrinkage or other artificial changes in the tissues are produced, when the specimen is transferred to the clearing media preparatory to immersion in the melted paraffin. When the specimen is thoroughly dehydrated by absolute alcohol it may be transferred to xylol, remaining in this until it sinks and becomes clear, which takes place in an hour or two. It is then im- mersed in a small dish or glass box of melted paraffin, kept in a con- stant temperature bath held at 52° C., where it remains until com- pletely permeated by the paraffin. It is best to use paraffin which has a melting point of 50° C. After the specimen has remained for a while in the first dish of melted paraffin it is transferred to a second dish of the same in order to remove any traces of xylol remaining in the specimen, for traces of xylol are lable to make the paraffin soft or cohesive after the specimen is embedded. The length of time of the paraffin immersion depends upon the size and density of the specimen; as a genneral rule one-half hour is sufficient for small, soft, or porous fragments. An hour or one-and-a-half hours at the utmost is sufficient for the melted paraffin permeation. A longer period of 1 Small squares of thick glass or small cubes of hard rubber, though somewhat more expensive than the “deck plugs,” are cleaner and more convenient, since the embedded tissue can be preserved in alcohol, fastened to the block and ready for cutting at any time. Digitized by Microsoft® PATHOLOGICAL SPECIMENS. 59 immersion may interfere with the finer structural details of the tissues. A small paper box considerably larger than the specimen itself is filled with melted paraffin, and with a warm needle or forceps the specimen is transferred to the paper box and set in its proper position in the bottom so that the surface to be cut lies against the bottom of the box. In order to avoid the slow cooling of the paraffin around the specimen in successive layers, which prevent the forma- ‘tion of a homogeneous mass, the paper box with its contents is quickly cooled by being put into cold water, even iced water. When the paraffin block is hard it is fastened with paraffin on to one of the various disks belonging to the paraffin microtome, trimmed so as to have exactly a rectangular cutting surface, and sections are cut with adry knife. In order to stain these sections the paraffin must be removed from the interstices; this may be done with xylol. But when the supporting paraffin is removed from the sections they are liable to fall to pieces during the further staining and other manipu- lations. The only practical plan therefore with the great majority of paraffin sections is to affix them to a slide and carry them in this way through the various staining and mounting procedures. The best way of affixing delicate paraffin sections to a slide is by means of a thin film of “albumen fixative.” This is a mixture of albumen and glycerin. Equal parts of white of egg and glycerin are thoroughly stirred together, filtered through paper, and a small amount of carbolic acid added to prevent the growth of micro- organisms. A very small drop of this albumen mixture is placed on one end of the slide, and with the ball of the finger or a fold of cloth it is spread over the rest of the slide in as thin a film as possible. While this scarcely perceptible film of albumen fixative is still moist, the paraffin sections or the ribbons of serial sections divided into proper lengths, are laid upon the film and gently tapped down flat with a small camel’s-hair brush or the finger-tip.' 1 Not infrequently very thin paraffin sections will curl or become corrugated as they leave the knife, so that it is difficult to place them flat upon the fixative film. Should this occur, a few drops of water may be spread out in a thin layer over the fixative film while it is still moist on the slide, and the whole slide, with the layer of water upon its surface, is very gently heated over the flame—just sufficiently to soften but not to melt the paraffin. If the sections are then floated out on the warm layer of water they will uncurl and flatten out. The layer of water is then drained off, when the flattened sections will lie flat upon the fixative film and remain fast- ened there. All traces of the water are now allowed to evaporate in the air; or, the evaporation of the water may be hastened by exposure to a temperature four or five degrees below the melting point of the paraffin. A convenient plan is to place such slides on top of the paraffin bath where the temperature is not sufficient to melt the paraffin and yet expedites the evaporation of the water. The slides must be ab- solutely dry before going on with subsequent procedures. Digitized by Microsoft® 60 GENERAL METHODS OF PRESERVING The slide with the attached paraffin sections is now heated over a flame, warmed just sufficiently to begin to melt the paraffin; this is a very delicate point in the operation. Just enough heat must be used to melt the paraffin and no more. If the slide be heated beyond this point the sections may be shrunken or completely ruined. While the slide is still warm it is plunged into a jar of xylol, oscillated to and fro for a few seconds, then placed in a jar of absolute alcohol, then passed through a series of jars containing different strengths of alcohol—say ninety-five per cent, seventy per cent, fifty per cent, and thirty per cent, remaining a few minutes in each, and finally into water. Now the sections upon the slide may be stained in whatever ‘way desired, carried up through the graded alcohols to absolute alcohol, then cleared in xylol or other clearing media, and mounted in balsam. Tightly covered cylindrical jars or wide-mouthed bottles are used for the better manipulation of paraffin sections, the whole slide being dropped into a bottle for staining as well as for the dehydration and clearing. Section Cutting may be done in an emergency by the free hand with a razor ground flat on the lower side, but better sections can be obtained by means of a microtome, and practically all section cutting for microscopical purposes is done by some form of this instrument. One of the most useful of these is Thoma’s, which is made in three sizes, the intermediate or the larger one being the more useful. The Schanze microtome is also well adapted for general work, as are some of the American instruments made on the same plan. For cutting sections of tissues embedded in paraffin, and especially for serial sec- tions, the Minot microtome of the improved form is excellent. Methods of Staining.—Sections of hardened tissues may be stained for microscopical study in a variety of ways, but for routine work the double staining with hematoxylin and eosin is most gene- tally useful and is applicable to nearly all cases. Hematoxylin solution (Delafield’s) is prepared as follows: To 100 c.¢. of saturated solution of ammonia alum add 1 gm. of heema- toxylin crystals dissolved in 6 c.c. of ninety-five-per-cent alcohol. This solution is exposed to the light for three or four days, the color meanwhile changing from a dirty red to a deep bluish-purple color. Then 25 c.c. each of glycerin and wood naphtha are added. This mixture is allowed to stand for a day or two and is then filtered, and the filtration is repeated at intervals until a sediment no longer forms. The solution is now ready for staining, and should be consider- ably diluted with water as it is used, the best results being obtained by diluting the fluid with from ten to twenty times its bulk of water. The sections are immersed in the fluid, and allowed to remain until Digitized by Microsoft® PATHOLOGICAL SPECIMENS. - 61 they have acquired a distinct purple color which persists after rinsing in water. They are now placed for a moment in a dilute alcoholic solution of eosin, and then mounted in glycerin which has been colored lightly with a alcoholic solution of eosin. In this way the nuclei of the cells will be stained of a purple color, while the cell bodies, and to a certain extent the intercellular substance, will be colored a light rose-red. If specimens are to be mounted in Canada balsam, they are stained with hematoxylin as before, and the eosin staining is done by tinging with a saturated alcoholic solution of eosin the alcohol with which the final dehydration of the specimen is accomplished. A similar result may be obtained by tinging the oil of cloves or origanum with which the clearing of the sections is effected. Gage’s hematoxylin is more dilute than the above, and chloral hydrate is added as a preservative in place of the wood naphtha. Its formula is as follows: Sterilized Distilled Water..................4. 200 c.c¢ Potash or Ammonia Alum................... 7.5 gm Chloral Hydrate... sisseuvas yeaa kee aes 4.0 Hematoxylin crystals. ..... 0... 0... ee eee eee O.1 “ Add to the mixture of water and chloral hydrate the hematoxylin crystals dissolved in 10 c.c. of ninety-five-per-cent alcohol. The proper color is developed after a few days’ standing (“ripening”). This stain keeps rather better than Delafield’s, which occasionally reddens and precipitates. It may be diluted for use. fron Hematoxylin (Hetdenhain’s).—Sections are soaked for an hour in a two-per-cent solution of ammonia sulphate of iron, then rinsed with water and put for an hour in a one-half-per-cent aqueous solution of hematoxylin (prepared by heating); again rinsed and put again in the iron solution, in which the color gradually fades. The section must be watched during the process of the differentiation which takes place in the iron solution, and when this is accomplished to a proper extent the section is thoroughly washed in running water and mounted in the usual way. This method is especially valuable for the study of nuclear structures, the color of these ranging from blue to black, depending upon the length of time of immersion in the stain and the grade of differentiation. ; By the use of this method micro-organisms may be stained black, and in this condition are, as Leaming has shown, well fitted for the purposes of photomicrography. Picro-Acid Fuchsin (Van Gieson’s).—This double stain, first suggested by Van Gieson,' especially for the nerve tissue, has wide 1 Van Gieson, Laboratory Notes, etc., New York Med. Jour., July 20th, 1889. Digitized by Microsoft® 62 GENERAL METHODS OF PRESERVING applications in both normal and pathological histology, and is most useful when following a deep hematoxylin stain. It colors the fibrillated connective-tissue fibres and the neuroglia in general a bright or garnet red, and also the axis cylinders and ganglion cells. Myelin, muscle fibres, and certain other cells are stained yellow, while the nuclei after the hematoxylin stain are brownish-red in color. Van Gieson’s stain is also of value, although its limitations in this particular are not yet fully determined, as a coloring agent for hyalin amyloid colloid and mucin in the tissues. As a differential stain for fibrillated connective-tissue fibres it is of value in the study of various tumors and especially of the sarcomata. It is commonly prepared in two strengths, the stronger for use especially in nerve tissue staining, the weaker for general purposes. The formule and method of using as suggested by Freeborn! are as follows: Picro-acid Fuchsin. Stronger solution— One-per-cent aqueous solution Acid Fuchsin.. 15 c.e. Saturated aqueous solution Picric Acid and Water ci vedas te eerreneine oat each 50 “ Weaker solution— One-per-cent aqueous solution Acid Fuchsin... 5 Saturated aqueous solution Picric Acid........100 “ oc The tissues may be hardened either in alcohol, Miiller’s fluid, or formalin, but Miiller’s fiuid is preferable. Sections are first stained deeply with hematoxylin, washed in water, and put into the staining fluid, in which they remain for vary- ing periods, depending upon the tissue and the strength of the stain, but in general from one to five minutes. The sections are now rapidly dehydrated by alcohol cleared with oil of origanum and mounted in balsam. Golgi’s Silver Stain.—While this well-known method has com- mended itself most highly to morphologists for special and largely for topographical purposes, it has not as yet taken so definite a posi- tion in the armamentarium of the pathologist as to bring it within the scope of this handbook. There are many methods of staining and numerous slight modi- fications of old and approved methods. While some of the special staining methods are useful in the attainment of certain ends, the few simple methods which have been here described will suffice for most of the routine morphological work of the pathologist. 1 Freeborn, Transactions New York Path. Soc., 1893, p. 73. Digitized by Microsoft® PATHOLOGICAL SPECIMENS. 63 Methods of Preserving Specimens for Gross Demonstration and for Museums.—When specimens of diseased tissues or organs are to be preserved entire for exhibition in jars in a museum, it is in most cases desirable first to get rid of the blood. This may be accomplished, as a rule, by putting them for twenty-four hours in running water, after they have been sufficiently opened so that the water can get to them. They are now brought into proper condition by the removal of superfluous parts and the requisite dissections. Then they are carefully brought into the position and form which it is wished to preserve by stuffing with horsehair or absorbent cotton and by the use of thread. When thus carefully adjusted they are either suspended or laid on a wad of absorbent cotton in sixty- to eighty-per-cent alcohol. In this they usually become hard, and are finally, after the removal of the temporary stuffing and braces, trans- ferred for permanent exhibition to fresh, clear eighty-per-cent alcohol. This description applies especially to such specimens as have cavities to distend or display. The more simple specimens, such as the solid viscera, tumors, etc., may be freed from blood in the same way and hardened in sixty-per-cent alcohol. In many cases an excellent hardening is obtained by injecting the preservative fluid through the blood vessels. The lungs are well hardened by pouring the fluid through the trachea into the air spaces. Methods have been from time to time suggested for the preserva- tion of gross specimens so as to show in part at least their natural colors. None of these methods have proved very satisfactory. On the whole a recent method devised by Jores’ is the most promising, for in many specimens the color of the blood is in a measure preserved. This method is summarized as follows. The fresh speci- mens arranged in proper position for display are put for twenty-four hours in the following solution: Formalina¢ sc. 2aiat, ay vedeaietaatiey eas 5 parts. Sodium Chlorid...........0esce ee eee seer eee 1 part. Magnesium Sulphate............... 0.000005 2 parts. Sodium Sulphate................00. cee eee 2 Wrateniensccs Sadist aa Se a eating ty 100.“ The quantity of the solution should be liberal, and if the speci- mens be large they may remain for two days in the solution, the latter being renewed at the end of the first day. The specimens, rinsed off with alcohol, are now put into strong 1 See Jores, Centbl. f allg. Path. u. Path. Anat., February 29th, 1896. Digitized by Microsoft® 64 GENERAL METHODS OF PRESERVING alcohol (ninety-five per cent), where they remain until they are per- meated by the fluid (usually twenty-four to forty-eight hours). The color of the specimens, lost in the formalin, is partially restored by the alcohol. They are now placed for permanent preser- vation in equal parts of glycerin and water. Formalin (two-per-cent solution) and alcohol alone are useful for preserving gross specimens either for demonstration or museum pur- poses. The fresh specimen should be placed directly, without removal of blood, into an abundant quantity of the solution which is renewed at the end of forty-eight hours. After three or four days the hardening is completed with sixty-per-cent and eighty-per-cent alcohol. Certain color features of gross specimens are often fairly well preserved in such formalin specimens. Firm-walled cysts of various kinds are well preserved in a natural condition of distention by drawing off the natural contents through a fine canula and refilling with and immersing in the following solu- tion, known as Flemming’s Chromic and Acetic Acid Mixture: One-per-cent Chromic Acid solution.......... 20 parts. - 7 Acetic Acid solution............10 “ NWALOT sirscceiboiie h oy dua 0 aie goanictad Wacoal De ave tee tee pee fo « After soaking for forty-eight hours in this mixture the tissue, as far as it has penetrated, becomes firm and stiff and of a greenish-gray color. The specimen is now washed thoroughly in running water and preserved in eighty-per-cent alcohol. Cysts, such as echinococcus cysts, small embryos in their mem- branes, cystic kidneys, etc., may be preserved in a nearly natural con- dition by placing them in a five-per-cent aqueous solution of chloral hydrate, and after a week replacing this by a ten-per-cent solution of the same, in which they may be permanently preserved. Such specimens may be preserved in a saturated aqueous solution of chloroform, or in formalin (two per cent). We would most urgently commend to the reader the importance of putting pathological specimens which are to be hardened and sub- sequently examined microscopically, at the earliest possible moment into the preservative fluids, which should always be abundant. And, furthermore, when specimens are large it is very desirable to cut them open, so that the fluids may come into direct contact with the tissues. It should be borne in mind that immediately after death or the removal of parts from the body, especially in warm weather, changes commence in the tissues and progress very rapidly, so that in some cases a few hours’ or even a few moments’ delay will not only render subsequent microscopical examinations difficult and un- Digitized by Microsoft® PATHOLOGICAL SPECIMENS. 65 satisfactory, but may lead to serious errors. As above stated, Miiller’s fluid, alcohol, and formalin are the most generally useful agents. Carbolic acid and glycerin should not be used, even for the temporary preservation of fresh tissue. They not only do not harden and preserve the tissue elements, but they—especially glycerin —render them almost wholly useless for microscopical examination. The not uncommon practice of wrapping a specimen ina cloth soaked in alcohol or carbolic acid, and permitting it to remain in this for hours or days, is of no use whatever in preserving specimens of which microscopical examinations are to be made. Almost equally useless is the too common practice of placing a specimen in a bottle which it nearly fills, and pouring a little preservative fluid around it. Not only should the proper fluid be used, but it should be abundant, and the specimen so prepared and arranged that it may come into direct contact with it. 6 Digitized by Microsoft® Digitized by Microsoft® PART I. CHANGES IN THE CIRCULATION OF THE BLOOD. CHANGES IN THE COMPOSITION AND STRUCTURE OF THE BLOOD. HYPERTROPHY, HYPERPLASIA, REGEN- ERATION, DEGENERATION, ETC. INFLAMMATION. ANIMAL AND VEGETABLE PARASITES, INFECTIOUS DISEASES. TUMORS. Digitized by Microsoft® Digitized by Microsoft® CHANGES IN THE CIRCULATION OF THE BLOOD. HYPER MIA AND ANAIMIA, There is an important series of changes in the character of the circulation during life which may, when death ensues, either alter considerably in appearance or disappear altogether. Among the more important of these changes are hypercemta—excess of blood in apart; and ancemia—deficiency of blood in a part. These condi- tions and the causes which lead to them will not be described in de- tail in this book, which has chiefly to do with alterations of the tissue which persist and may be studied after death. Tissues which have been the seat of a temporary, and sometimes of a prolonged, hyperee- mia, may show to the naked eye nothing abnormal after death, or they may look redder than normal; they may be oedematous, and more blood than usual may flow from them when incised. On micro- scopical examination the blood vessels may be normal in appearance, or more or less distended with blood. Long-continued hyperzinia may lead to hemorrhage and transudation, to pigmentation, to hyperplasia of tissue, or to an atrophy of tissue through pressure, or even to death of tissue. The paleness which is characteristic of ancemic tissues may not be evident after death. Anzemia may lead to no recognizable micro- scopical changes. On the other hand, if long continued it may in- duce atrophy and fatty degeneration, and, if excessive, may lead to death of tissue. HAMORRHAGE AND TRANSUDATION. Hemorrhage is an escape of blood from the heart or vessels. It may occur from a rupture of the walls of the vessels, and is then called hemorrhage by rhexis. The rupture may be occasioned by injury, by some disease of the walls of the vessels which renders them too weak to resist the blood pressure from within, or it may occur from the blood pressure in the thin and incompletely developed walls of new-formed vessels in ae tissue, tumors, etc. Digitized by Microsoft® 70 CHANGES IN THE Under other conditions, without recognizable changes in the walls of the vessels, all the elements of the blood may become extravasated by passing, without rupture, through the walls of the vessels. This is called hemorrhage by diapedesis. These hemorrhages are usually small, but may be very extensive. They usually occur in the smaller veins and capillaries, the cells and fluids of the blood passing out through the cement substance between the endothelial cells. Consult Goldscheider, “Klin. u. Bak. Mitth. u. Sepsis Puerperalis, ” Charité- Annalen, Jahrgang 18, p. 237. Digitized by Microsoft® 198 THE INFECTIOUS DISEASES. tion; post-mortem staining of the tissues; congestion of the lungs, stomach, intestines, and kidneys; extravasations of blood in the serous membranes; swelling of the solitary and agminated lymph nodules in the small intestine; swelling of the spleen and parenchy- matous degeneration of the liver and kidneys. 3. In some cases there are localized inflammations. The joints, the connective tissue around the joints, the pleura (Fig. 74), the pericardium, the peritoneum, the pia mater, and the connective tissue in different parts of the body may be inflamed. These local inflammations are of a purulent character, except in the serous mem- branes, where the principal inflammatory product may be fibrin. 4. There are cases in which the veins in the neighborhood of the wound contain softened, puriform thrombi; without infarctions in the viscera, there may be inflammation of the joints and serous mem- branes. 5. In other cases the veins contain thrombi; there are infarctions and abscesses in the viscera; local inflammations of the joints and serous membranes may be present or absent. The thrombi are formed regularly in the veins near the wound, but they may be sit- uated in veins at a distance, and sometimes, although infarctions and abscesses are present, no thrombus can be discovered. The veins may be distended by the thrombi or only contain small coagula. The different kinds of thrombi, and the varieties of emboli and in- farctions which they produce, are described in the article on Throm- bosis, page 72. Various lines of research on minute changes in cells which bac- terial and other poisons may induce justify the expectation that more and more we shall be able to associate characteristic groups of symp- toms in septicemia, for which there is now no morphological basis, with well-defined cell alterations. Digitized by Microsoft® ACUTE CEREBRO-SPINAL MENINGITIS. This is usually defined as an acute infectious disease of which the characteristic lesion is an exudative inflammation of the pia mater of the brain and cord. It may, however, be regarded as an infec- tious inflammation of the pia mater accompanied by constitutional symptoms. At all events, there are inflammations of these mem- branes, which occur both as isolated cases and also in epidemics, with similar symptomsand similar lesions, and which are not apparently caused by traumatism nor by infection from other foci of inflamma- tion. As a rule the inflammation of the pia mater results in a large pro- duction of serum, fibrin, and pus, which infiltrate the pia mater and accumuiate in the ventricles, so that the gross appearance of the brain is ckaracteristic. The exudation is especially abundant at the base of the brain and over the posterior surfaces of the cord. In children the distention of the lateral ventricles with purulent serum may be a marked feature, while in adults the quantity of serum is apt to be small. It is important to remember that a meningitis which induces marked cerebral symptoms, continues for a number of days, and causes death, may produce so little change in the pia mater that after death this membrane upon gross examination looks normal. This is especially common when the disease is not epidemic, but occurs in the sporadic form. When, however, we look at the pia mater in these cases with the microscope we find a slight infiltration with pus and fibrin, or a growth of new cells resembling the cells of the pia mater. While the above are the characteristic lesions of this disease, there are a number of secondary or associated changes in different parts of the body which are not constant, but which occur with suffi- cient frequency to render their mention necessary. There may be subserous punctate hemorrhages in the endocardium; petechize in the skin; hyalin and granular degeneration in the voluntary striated muscle; occasional multiple abscesses in various parts of the body; suppurative inflammation of the joints; parenchymatous degenera- tion of the heart, liver, and kidneys; and swelling of the gastro- intestinal lymphatic apparatus and of the spleen. Digitized by Microsoft® 200 THE INFECTIOUS DISEASES. Cerebro-spinal meningitis may occur by itself or in connection with some other acute infectious disease, such as acute lobar pneu- monia, mycotic ulcerative endocarditis, pyeemia, multiple suppura- tive arthritis, otitis media, puerperal fever, typhoid fever, etc. The Jesions are essentially the same in epidemic and in sporadic cases of acute cerebro-spinal meningitis, and in both modes of occur- rence the disease is probably caused by bacteria. Numerous careful studies have been made on the bacteria occur- ring at the seat of lesion in sporadic cases occurring both with end without complicating lesions in other parts of the body. The Streptococcus pyogenes has been demonstrated in a few cases, occurring in connection with suppurative inflammations elsewhere. The Diplococcus lanceolatus (pneumococcus) (see page 201) has been found in several cases, and in some of these without any lung lesion. Weichselbaum has described the occurrence in several cases of adiplococcus not known to occur elsewhere, which was found largely confined to the pus cells, and which he called Diplococcus entracellularis meningitidis. Animal experiments with this as well as the pneumococcus would indicate that they may stand in a cau- sative relation to the disease. Some other scattering forms of bacteria have been described, but not with sufficient frequency and definitive- ness to enable us to judge of their significance. It seems probable, therefore, from what we know at present, that several forms of bacteria are capable of causing acute cerebro-spinal meningitis. Which is the most frequent and important, it remains for further researches to show. Bacterial studies of the cases in epidemics of cerebro-spinal meningitis have not been numerous since the development of the new technique. But there is reason to believe that the Diplococcus lanceolatus plays here also an important réle.’ The close topographical relationships which the nasal cavities and the middle ear bear to the meninges is significant in this connection on account of the possibility of the transmission to the brain mem- branes of bacteria not uncommonly present and usually harmless in the former situations. ' For literature and a study of cases consult article on “Epidemic Cerebro-Spinal Meningitis, ” by Ferner and Barker, American Journal of the Medical Sciences, 1894. Also Jiiyer, Zeitschrift f. Hygiene, etc., Bd. xix., p. 351. Digitized by Microsoft® ACUTE LOBAR PNEUMONIA AND OTHER INFECTIOUS DISEASES INDUCED BY THE DIPLOCOCCUS LANCEOLATUS. (Pneumococcus : Diplococcus pneumonice.) This germ is frequently spoken of as the pnewmococcus of Frdnkel, because its significance and life history in connection with acute lobar pneumonia were first demonstrated by him.’ During their development these germs are distinctly spheroidal. But in their mature condition they are apt to become slightly elongated and often a little broader at one end than at the other, assuming a lanceo- late form. They are very apt to occur in pairs, and frequently are seen in short chains, rarely in long chains. Very frequently, when o c @ % 2p eo @ Fie. 75.—DipLococcus LAaNcEOLATUS (PNEUMOCOCOUS) WITH CAPSULES. Stained by Welch’s method. growing in the living animals, the pneumococcus is surrounded by a distinct, homogeneous capsule of varying thickness (see Fig. 75). This capsule does not, as a rule, develop in artificial cultures. The coccus itself is readily stained; the capsule is not easily demonstrated except by special staining methods. The pneumococcus has no spontaneous movement and grows but feebly at ordinary room temperature. It grows much better at the temperature of the body, forming on the surface of very slightly alkaline agar’ plates faint grayish, dewdrop-like, inconspicuous ‘It was discovered by Sternberg in saliva, and its pathogenic power demon- strated, some years before its full significance was understood in connection with pneumonia. * The growth of the pneumococcus is less certain and abundant on the ordinary agar than on Guarnieri’s gelatin agar mixture or on Welch’s modification of this. The formula for this modification is: 950 gm. meat infusion, 5-10 gm. pepton, 6-8 gm. agar, on gm. gelatin. The gelatin and agar are boiled separately in 50 1 Digitized by Microsoft® 202 THE INFECTIOUS DISEASES. colonies, somewhat similar to those of Streptococcus pyogenes, but usually more delicate. In beef tea it forms at body temperature a faint whitish sediment with slight turbidity of the fluid. As a rule, the cultures are prone to soon lose their virulence and to die off early, but the virulence may be maintained by successive inoculations in the rabbit. The pneumococcus injected, while virulent, subcutaneously into mice and rabbits induces a rapidly fatal septiceemia, often with little marked anatomical change, save enlargement of the spleen. Some- times there are necrotic foci in the liver, fibrin in the glomeruli of the kidneys, fatty degeneration of the heart. Suppurative inflam- mation at the seat of inoculation and elsewhere may follow. The blood and viscera may show under these conditions numerous cocci, mostly with capsules, or they may be confined to the seat of inocula- tion. Cultures which have been reduced in virulence, so as not to cause early death by septicemia, may, when introduced into the trachea of rabbits, induce a fairly typical lobar pneumonia. Different species of animals show marked differences in vulner- ability to the ravages of the pneumococcus. This germ is the exclu- sive inciter of typical acute lobar pneumonia in man. It appears to act, in part at least, by the development of an albuminous poison which has been tentatively called pnewmotoxin. It would seem to be the pneumotoxin which induces the symptoms in acute lobar pneumonia indicative of systemic poisoning, since the bacteria them- selves are usually confined to the lungs.’ For a more detailed description of these lesions of pneumonia, and an account of other bacteria which may be present, see page 438. In addition to its more common effect in inducing lobar pneu- monia, this diplococcus has been very frequently found in, and stands apparently in a causative relation to, some forms of exudative inflammation of the serous membranes, either in connection with or without a primary lobar pneumonia. Thus it has been repeatedly found in pleuritis, otitis, meningitis, empyaema, pericarditis, endo- c.c. of water before mixing. The reaction should be made distinctly but feebly alkalin. The mixture solidifies at room temperature. It should be used in Petri plates, and though it softens the colonies remain separate at 35° C. (see Johns Hopkins Hospital Bulletin, December, 1892). It is especially important in pre- paring culture media for the pneumococcus to use the most exact tests available for fixing the reaction, since the vigor of the growth is, as 7. C. Janeway has shown, closely dependent upon this. The observations of the Klemperers suggest the possibility that at a certain period of the disease the blood or body juices are capable of developing a substance antidotal to this pneumotoxin, the advent of the former being signalized by the so-called “crisis.” Satisfactory applications of this alleged “pneumonia antitoxin’ in therapeutics have not yet been made. Digitized by Microsoft® THE INFECTIOUS DISEASES. 203 carditis, and in peritonitis. It has also been found in abscesses of the viscera and in exudative inflammation of the joint. The Diplococcus lanceolatus is a frequent inhabitant of the mouth, even in health. It has been found in the mouths of about twenty per cent of healthy persons examined. It is thrown off in the sputum in lobar pneumonia, and no doubt from these sources in the dried condi- tion, as dust, furnishes the infectious agent which in favoring con- ditions of the body lights up the inflammatory process in the lungs. For staining the pneumococcus with its capsule the method suggested by Welch! gives the most satisfactory result. The exudate containing the germ is dried and fixed upon the cover glass in the manner described on page 154. It is uow treated with glacial acetic acid, which is at once drained off and replaced by anilin-gentian-violet solution (page 156) this being drained off and renewed several times until the acetic acid is displaced. The speci- men is now washed with a two-per-cent solution of sodium chlorid, in which it may be covered and studied. Such specimens are not usually suited for permanent preservation, although occasionally after drying and mounting in balsam the capsules retain their color. Annoying color precipitates frequently interfere with full success by this method. The pneumococcus may be stained in sections by Weigert’s modifications of Gram’s method with preliminary contrast stain (see page 157). By this method the fibrin in the pneumonic exudate is also stained. 1 Welch, Johns Hopkins Hospital Bulletin, December, 1892, p. 128. Digitized by Microsoft® INFECTIOUS PSEUDO-MEMBRANOUS INFLAMMATION OF MUCOUS MEMBRANES. (Pseudo-Diphtheria: Diphtheroid-Angina ; Membranous Angina.) ; Under a variety of conditions, as during scarlatina and measles, whooping-cough, typhoid fever, etc., or entirely apart from any complicating disorder, an acute exudative inflammation of the mu- cous membranes, especially of the upper air passages, occurs, which Fie. 76.—PsEUDO-MEMBRANOUS INFLAMMATION OF TRACHEA. In this case there is purulent infiltration of the mucosa and submucosa, and of portions of the mucous glands. u, false membrane; b, portion of intact epithelium; c, infiltration of the mucosa with fibrin; d, portion of mucous gland infiltrated with pus. is associated with, and is apparently caused by, the growth of a streptococcus (Fig. 77) which in morphological and biological characters seems to be identical with the Streptococcus pyogenes. There may be much or little fibrinous exudate; there may in early stages, or even throughout, be none at all. The pellicle when formed may be loose or adherent, sharply circumscribed or tending to spread. The submucous tissue may show little change, or may be congested Digitized by Microsoft® THE INFECTIOUS DISEASES. 205 and oedematous, or may be the seat of suppurative inflammation {see Fig. 76), necrosis, or gangrene. The process may be confined to the tonsils. While under these varying conditions the inflammatory process is usually a local one and runs its course with or without the symptoms of septiceemia, occasionally the streptococcus finds access to the blood and may induce the lesions of pyemia. On the other hand, it may by aspiration gain access to the lungs and induce varying phases of complicating broncho-pneumonia. The Staphylo- coceus pyogenes is not infrequently associated with the streptococcus in these lesions, but is not apparently of primary significance. Sim- Be SS aie a> SA BES i See BS Oj st nee: 58 PGS BEE Se Pee eS Se AEE Ss ee 0) bk Ra Fe Y LHe ey aE IRO, Bee — , yaoes ay Vee eS ES {7 S$" Bip Ps 9 hd 2M, LOGI La, Fic. 77.—InFEcTIous Croupous INFLAMMATION OF THE TRACHEA. Section through the pseudo-membrane and underlying tissue, showing large numbers of strep- tococci. \e @ \ X ulating very closely, as it does in many cases, both the local and general phenomena of diphtheria, this disorder has formerly been confounded with it, and has been only recently recognized as a distinct phase of disease. It is now most frequently called pseudo-diphtheria. It seems in part to cover the condition formerly known as croup, in part those cases formerly thought to be mild diphtheria.’. In many phases of acute angina, in many cases of follicular tonsillitis, strepto- cocci have been found in large numbers. 1 For a general consideration of the relationship between this form of pseudo- membranous inflammation and diphtheria, with original studies and bibliography, consult Park, “Diphtheria and Allied Pseudo-Membranous Inflammations, ” Medical Record, July 30th and August 6th, 1892. Digitized by Microsoft® GONORRH@A AND OTHER INFLAMMATORY LESIONS INDUCED BY THE MICROCOCCUS GONORRH@:Z (GONOCOCCUS). The Micrococcus gonorrhes is most commonly found in the exudate of gonorrhceal inflammation of the mucous membranes, especially of the urethra. It may be found free or enclosed in leu- cocytes or other cells within or between the superficial epithelial cells. It is also often present in the exudate in arthritis, and in tubal, ova- rian, perimetritic, and other inflammations, arising as complications of gonorrhea. Under these complicating conditions the gonococcus may occur alone or in association with the pyogenic cocci. It is generally most abundant during the acute stage of the inflammation. The gonococcus is apt to occur in pairs, the apposed sides being more or less distinctly flattened (Fig. 78). It stains readily with the Fie. 78.—Micrococcus GoNORRH@#& (GoNococcUS). anilin dyes, and differs from most known cocci which might be mistaken for it in that it is decolorized by the iodin solution in the Gram’s method of staining. If after the use of the iodin solution in Gram’s method the cover glass be rinsed with alcohol to complete the decolorization and then with water, and the specimen be stained for afew minutes in a dilute aqueous solution of Bismark brown, rinsed and mounted in balsam, the gonococci will appear of light-brown color, while most other germs will retain the violet color (see Fig. 79). In exudates a con- siderable part of the gonococci are usually contained in the bodies of pus cells. The gonococcus thrives best at about the temperature of the body (37° C.); and has been artificially grown ona variety of culture media which contain considerable albuminous material in solution. Human Digitized by Microsoft® THE INFECTIOUS DISEASES. 207 blood serum—squeezed from the placenta—and mixed with pepton- ized agar in accordance with the method of Wertheim, has been in the past most commonly employed for cultures. Heiman’ has found the clear exudate or transudate from the pleural cavities in man (“chest serum”) to form a convenient and ex- Fie. 79.—A Cover GLASS PREPARATION OF GONORRH@AL ExupatE. Stained by Gram’s method with gentian violet; contrast stain with Bismark brown. The gonococci have been decolorized by the iodine solution and restained by the brown; while other bacteria cocci and bacilli which were mingled with them still retain the original violet color. cellent substitute for blood serum. This is sterilized by the discontin- uous or fractional method? (or it may be filtered through an unglazed porcelain filter), and then mixed with two-per-cent agar—containing Fie, 80.—Pus CELLs conTAINING Gonococcr. From a case of gonorrhceal urethritis. one-per-cent pepton and one-half-per-cent salt—in the proportion of one part of the serum with two parts agar, melted at about 40° C. ' Herman, “ A Clinical and Bacteriological Study of the Gonococcus,” etc. New York Medical Record, June 22d, 1895, contains bibliography. > Tn fractional or discontinuous sterilization, the serum, filled into tubes, is exposed for an hour on five successive days to a temperature of from 65° to 68° C., standing in the interval at the ordinary temperature of the room. In this way the serum may be rendered sterile without coagulation, which seriously interferes with its value as a culture medium for the gonococcus. Digitized by Microsoft® 208 THE INFECTIOUS DISEASES. In this chest-serum agar the surface growth of the gonococcus is in the form of small circular, sharp-edged, slightly raised, grayish-white colonies, coarsely mottled in the central portion, finely granular toward the borders. The lower animals are not, asa rule, susceptible to inoculations of the mucous membranes with the gonococcus, but suppurative inflammation has been induced in mice and guinea-pigs by intraperitoneal injections. Inoculations- of pure cultures of the gonococcus upon the urethral mucous membranes of man is followed by a characteristic catarrhal inflammation. ¢ The evidence is now complete that the gonococcus stands in a causative relationship to the characteristic inflammation with which it is so constantly associated. But in what measure this germ, in what measure the strepto- coccus and staphylococcus may be responsible for the complicating inflammations when both germs occur together, is yet to be deter- mined. Inasmuch as one or more forms of cocci and diplococci occurring in the normal and in the inflamed urethra are morphologi- cally similar to the gonococcus, great caution should be exercised in doubtful cases in pronouncing upon the nature of suspicious germs. But the pronounced tendency of the gonococcus to gather within cells; the sometimes conspicuous but often ill-defined flattening of the apposed sides of the gonococci; the decolorization by Gram’s method, which leaves most other germs apt to be associated with the gono- coccus still stained, and whenever practicable the artificial culture characters—these all should be considered in the summary of evi- dence.* 1 Yon Hibler, Centralbl. f. Bakteriologie, etc., Bd. xix., p. 120, 1896. For sum- mary of current work on the gonococcus with bibliography consult Nedsser and Schaffer, “ Ergebnisse der allg. Aetiologie der Menschen- u. Thierkrankheiten, ” 1896, p. 477. Digitized by Microsoft® ANTHRAX. (Splenic Fever; Malignant Pustule; Charbon; Carbuncle.) This disease, which is much more common in the lower animals, especially the herbivora, than in man, is widely prevalent in Europe. It is rare in the United States, but seems in certain regions to be more common than formerly. It is induced in man by accidental inoculation with the Bacillus anthracis, which causes the disease in the lower animals. Inocula- tion may occur through the skin by the agency of flies and other insects which have been feeding on animals infected with this disease; by handling their carcasses or hides, or in other ways. Following Fic. 81.—ANTHRAX—MALIGNANT PUSTULE—OF THE SKIN. From a man in New York who had been handling foreign hides. Bacilli stained with gentian violet. this skin inoculation a pustule is apt to develop—“ malignant pustule” —and varying phases of an acute exudative inflammation, which may be hemorrhagic, sero-fibrinous, purulent, or necrotic, accompany the local proliferation of the germs (Fig. 81). From this local source a general infection may ensue. In some cases general infection may occur without evident external lesion. Infection with anthrax may occur through the lungs, most often among those who handle infected wool or hides, the dust from which is inhaled (“wool-sorter’s disease”). Under these conditions there may be cedema, lobular pneumonia with involvement of the pleura, Digitized by Microsoft® 210 THE INFECTIOUS DISEASES. mediastinum, and other adjacent structures. Infection through the gastro-intestinal canal occurs through the ingestion of food contain- ing anthrax spores, and is apt to be accompanied with inflammatory and necrotic changes, which are described in detail among lesions of the intestine. ‘When general infection occurs the post-mortem appearances vary. Decomposition, as is usual in acute infections, generally sets in early. The blood is frequently not much coagulated and dark in color. Heemorrhages and ecchymoses are frequently found in the serous and mucous membranes and in various other parts of the body. The lungs may show small hemorrhages and cedema, and the Fic. 82.—BacILLUS ANTHRACIS GROWING IN THE BLOop VESSELS OF THE LIVER OF A MovusE INOCULATED WITH A PURE CULTURE OF THE BACILLUS. bronchi may be deeply congested. The pleural cavities may contain serum. The intestines may exhibit the lesions of the so-called ¢ntes- tinal mycosis, The bronchial and other lymph nodes may be swollen. The spleen may be swollen, very dark in color, and soft, sometimes almost diffluent. The bacillus which causes the disease may be found, usually in large numbers, in the spleen and in the capillary blood vessels, especially in the liver (see Fig. 82), lungs, kidneys, and intestine. The Bacillus anthracis is from 5 to 20 » long and about 1 +. broad, and is often uneven along the sides. The ends of the bacilli are not rounded, but square or slightly concave, and the bacilli often hang together end to end, forming thread-like structures (see Fig. 83). Digitized by Microsoft® THE INFECTIOUS DISEASES. 211 While the bacilli in the vegetative condition are easily killed, they develop spores, outside of the body only, and these are very invulner- able to the action of the ordinary germicidal agents and to heat, resisting often for many days the action of from two to five-per-cent carbolic acid and defying for some minutes the action of live steam. Anthrax bacilli are immobile and are easily stained by the anilin dyes. A capsule may be demonstrated upon them. They grow readily on artificial culture media at ordinary room temperatures, fluidifying gelatin and usually growing out, before they do so, in a network of delicate filaments into the solid medium. These linear or thread-like outgrowths from a central colony give in puncture inoculations in gelatin tubes a brush-like appearance which is quite characteristic. Surface colonies on agar and gelatin plates show a delicate, felt-like outgrowth from the central mass. The growth on potatoes is volu- minous. Subcutaneous inoculations of the anthrax bacillus into various species of animals—white mice, guinea-pigs, rabbits, sheep and cattle—induce anthrax. White mice are especially susceptible, a = A g i mm Cee eX # Fie. 83.—BacILLus ANTHRACIS CONTAINING SPORES. usually succumbing to the anthrax septicemia in from two to four days. In the blood of the diseased animals multitudes of the bacilli are found, showing their proliferation in the blood vessels and else- where. The anthrax bacillus is of especial interest and importance, because it was this bacterium which was first absolutely demon- strated to be the cause, and the only cause, of a well-defined disease in man, and because we know more of its life history than of almost any other of the bacteria. If cultures of the anthrax bacillus be made at a temperature of about 42°C. growth occurs, butit is meagre. Spores are not formed as they are at body temperature, and the virulence of the germ dimin- ishes day by day, so that at last the most susceptible animals are not affected by large inoculations of the living organisms (page 179). If fresh cultures of these organisms be made in various stages of their diminishing virulence and maintained at their optimum tem- perature, spores will again form, the growth will become vigorous, and in morphology quite characteristic; but the physiological quali- ties which determine virulence will remain more or less in abeyance. Digitized by Microsoft® 212 THE INFECTIOUS DISEASES. By inoculation of animals with anthrax cultures, beginning with those which, having been maintained at 42° C. for from fifteen to twenty days, and thus possessing but feeble virulence, and passing to those cultivated at 42° C. for a shorter time and which were therefore more virulent, Pasteur was able to secure immunity from anthrax in a series of the lower animals. Based upon these experiments a method of protective vaccination has been practised on a large scale among sheep and other animals in some parts of Europe and has been of great economic value. According to some authorities the death rate from anthrax has under these preventive inoculations been reduced in sheep from ten per cent to about nine-tenths of one per cent, and in cattle from five per cent to less than four-tenths of one per cent. Digitized by Microsoft® TUBERCULOSIS. Tuberculosis is an infectious disease characterized by inflammatory and necrotic processes in the body due to the presence and growth of the Bacillus tuberculosis (tubercle bacillus). The most distinctive morphological feature of tuberculosis is the development under the influence of the tubercle bacillus of larger and smaller gray or white or yellow, firm or friable masses of tissue called tubercles. The Bacillus tuberculosis is a long, slender bacterium varying in length from 3to 4» (from one-quarter to one-half the diameter of a red blood cell) and in breadth from 0.2 to 0.5 4. It is frequently Fic, 84.—TUBERCLE BACILLI IN SPUTUM FROM A CASE OF PULMONARY TUBERCULOSIS. Showing the bacilli in pus cells. more or less curved, and the individual bacilli may cling together end to end, forming threads or chains. The bacillus (Fig. 84) is stained with difficulty by the anilin dyes (see below), and when stained often presents an irregular beaded or knobbed appearance, due to an un- evenness in the coloring of the protoplasm, or to involution changes. It is immobile and spores have not been demonstrated in it. At the temperature of the body it can be grown on many of the artificial culture media, such as coagulated blood serum, five-per-cent glycerin-agar, five-per-cent glycerin-nutrient broth, on potato, and. in a variety of organic and inorganic mixtures. Digitized by Microsoft® 214 THE INFECTIOUS DISEASES. The growth of the tubercle bacillus in cultures is very slow in comparison with that of most of the pathogenic micro-organisms. After several weeks’ growth it forms dry, scaly masses or thin, wrinkled pellicles on the surface of the media (Figs. 85 and 86). It requires a certain amount of oxygen for its growth, and thrives best in the dark. It is killed by an exposure of a few hours to direct | ; | | | EEE IEEE TM MES ania Fig. 85. Fig. 86. Fig. 85.—CULTURE OF TUBERCLE BACILLUS ON GLYCERIN AGAR.—From tuberculosis in the bird. Fic. 86,—CULTURE OF TUBERCLE BACILLUS ON GLYCERIN AGAR.—From tuberculosis in man. sunlight, or if moist is killed by an exposure of from ten to fifteen minutes to 70° C. On the other hand, it may long retain its vitality in the dried condition. Cultures can be continued indefinitely from generation to genera- tion with a slowly diminishing virulence which finally is largely lost. Under certain conditions the virulence may be restored or enhanced by successive inoculations into susceptible animals. Certain modified forms or varieties or races of the tubercle bacillus are Digitized by Microsoft® THE INFECTIOUS DISEASES. 215 known, notably that which is concerned in inducing the lesions of fowl tuberculosis. The tubercle bacillus does not, so far as we know, grow in nature outside of the bodies of men and certain warm-blooded animals. It is thus strictly parasitic. Tuberculosis is a very common disease not only of man but also of many of the lower animals, especially of cattle, and inasmuch as the victims of this disease, both men and animals, are apt to throw off enormous numbers of the bacilli in the sputum and other excreta, the germ is very widely dispersed in inhabited regions, especially in buildings frequented by uncleanly tuberculous persons or by infected cattle. It may be conveyed by the milk and milk products of tuber- culous cows. Among the lower animals, guinea-pigs, rabbits, monkeys in con- finement, and cattle are particularly susceptible to the action of the tubercle bacillus. Although tuberculosis is widespread in man, he is not, as compared with some of the lower animals, particularly sus ceptible. While the tuberculous process presents some special dif- ferences in different animal species in rate of development, amount of necrosis, tendency to softening, calcification, etc., the fundamental effects are similar in man and in the lower animals. The effect on the body cells of the presence and growth of the tubercle bacillus varies considerably, depending upon the number and virulence of the germs present, the character of the tissue in which they lodge, and the vulnerability of the individual. In general, it may be said that tubercle bacilli may stimulate the connective-tissue cells in their vicinity to proliferation; or they may excite emigration of leucocytes from blood vessels and lead to the production of other exudates; or they may cause death of tissue. Thus the phases of inflammation which are excited by the tubercle bacillus are produc- tive, exudative, and necrotic. The tubercle bacillus may produce these effects separately or simultaneously, in the sequence just indi- cated or in some other; and now one, now another of them may pre- ponderate. Tuberculosis manifests itself most often in the form of an inflam- mation affecting some one part of the body, as the lungs (the part most frequently involved in adults), the gastro-intestinal tract or the skin—“ localized tuberculosis.” While the lungs are most frequently involved in tuberculosis in adults, in children it is the lymph nodes which are most commonly affected,’ and very often the bones and joints. Such a localized tuberculosis may retain through- out the characters of a local inflammation, or it may be accompanied by the clinical evidences of systemic infection. It may give rise 1 See Northrup, New York Medical Journal, February 21st, 1891. Digitized by Microsoft® 216 THE INFECTIOUS DISEASES. through metastasis to the successive development of tuberculous inflammation in other parts of the body, or to a sudden development of tuberculous inflammations in many parts of the body at the same time—general miliary tuberculosis. A general infection may be caused by the diffusion through the body of bacilli derived from a local tuberculosis, such as tubercular phlebitis or arteritis, or from the breaking into a vessel of a tuber- culous lymph node, or by the inspiration into the lungs of large numbers of bacilli. In a considerable proportion of cases the local lesions produced by Fig. 87.—A Miiary TUBERCLE From A LyMPH Nopz, x 850 and reduced. The giant cells are enclosed by the basement substance. the tubercle bacillus are in the form of circumscribed nodules or masses of new-formed cells or tissues which are called tubercles, or if small melzary tubercles. In many cases, however, the lesion is not circumscribed but diffuse, and more or less widely infiltrates or replaces the tissues involved. This is called diffuse tuberculous inflammation (dif- fuse tubercle). Miliary Tubercles.—Miliary tubercles are small nodules of irreg- ularly spheroidal shape (Figs. 87, 88, 90, 223 and 224), the smallest Digitized by Microsoft® THE INFECTIOUS DISEASES. 217 hardly visible to the naked eye, the largest as large as a pea.’ The smaller tubercles are gray and translucent; the larger are usually, especially in the central parts, opaque and white or yellow on account of the necrosis which is apt to commence here. In studying the effects caused by the tubercle bacillus on living tissues it should be always borne in mind that while as a whole the lesions produced are quite characteristic, there is still no one structural feature or combination of features of tubercles or tuberculous inflam- mation which is absolutely distinctive of the action of thisgerm. In The branches of the giant cells form part of the basement substance. doubtful cases the demonstration of the presence of the germ itself may be necessary for the establishment of the character of the lesion.’ 'The term mildary tubercle, which arose from the crude coincidence in size be- tween small foci of tuberculous inflammation und some forms of millet seed, is now very liberally applied to tubercles which are very much larger as well as to those which are very much smaller than millet seeds. It is convenient to designate a spheroidal mass of new tissue formed under the influence of the tubercle bacillus, whatever its minute structure, as a tubercle granulum (see Fig. 188). Very fre- quently two or more tubercle granula are joined together by a more diffuse forma- tion of tubercle tissue to form larger or smaller miliary tubercles—conglomerate tuber- cles (see Fig. 189). 2 The term tubercle tissue, which is in common use, indicates a tissue formed Digitized by Microsoft® 218 THE INFECTIOUS DISEASES. The experimental studies in animals, as well as the morphological data gathered from the examination of tuberculosis in man, show that when tubercle bacilli in moderate numbers lodge and develop in the living body one of the early local effects is a proliferation of the con- nective tissue and endothelial cells. These become larger and poly- hedral, with conspicuous nuclei. These new cells are often called epithelioid on account of their approach in form to the epithelial cell type (Fig. 87). A. new reticulum or stroma may form hand-in-hand with the Fic. 89.—TuBERCULOUS TissuE. Showing giant cells. Photograph from a miliary tubercle. growth of these new cells (Fig. 88), or the old stroma may persist, adapting itself in form and arrangement to the new conditions. Hither after the connective-tissue cell proliferation or hand-in- hand with it, or preceding it, or altogether independently of it, emi- gration of leucocytes and extravasation of serum may take place from blood vessels in the vicinity of the germs. During the more or less active cell proliferation which occurs under the stimulus of the tubercle bacillus multinuclear cells'—giant cells—may be formed under the influence of the tubercle bacillus rather than a tissue which is morpho- logically characteristic of tuberculosis in distinction from other forms of new tissue. ' For an account of giant cells, which are found under various conditions and are by no means confined to tuberculous inflammation, consult Marchand, Virchow’'s Archiv, Bd. -xciii., p. 518. Digitized by Microsoft® THE INFECTIOUS DISEASES. 219 (Fig. 89), either by persistent nuclear division in growing proto- plasmic masses which do not divide into separate cells, cr by the coalescence of the bodies of cells already formed. More or less new tissue with numerous small spheroidal mono- nuclear cells and little stroma may form in and about the tuberculous foci. Blood vessels are not apt to develop under the influence of the tubercle bacillus. Old blood vessels are, on the other hand, usually obliterated as the new tissue forms. Sooner or later the tubercle bacillus is apt to associate with its Fic. 90.—A NoDULE oF TUBERCULOUS INFLAMMATION (MILIARY TUBERCLE) IN THE LUNG. Showing polyhedral cells, small cells, giant cells, and coagulation necrosis at the centre. stimulative a destructive action, which leads to coagulation necrosis in the new-formed tissue as well as in the old tissue of the infected region. This necrosis is more apt first to manifest itself in the central portions of the tuberculous foci (Fig. 90) and may progress outward; the nuclei become fragmented or disappear, or fail to stain in the usual way, the protoplasm becomes more homogeneous, and cells and stroma form at last a structureless mass of tissue detritus which tends to disintegrate (coagulation necrosis or cheesy degenera- tion), forming cavities or, if on free surfaces, ulcers. As coagulation necrosis progresses, the tubercle masses lose the Digitized by Microsoft® : 220 THE INFECTIOUS DISEASES. gray translucent appearance which in their early stages they are apt to present to the naked eye and become more opaque and of yellowish- white appearance at the centres. Finally dense fibrous tissue may form in and about foci of tuber- culous inflammation, encapsulating or sometimes entirely replacing the more characteristic new-formed structures. It is in this way—by the formation of connective tissue—that such repair as is possible after local tuberculous inflammation, is brought about. Before the discovery of the tubercle bacillus and while our knowl- edge of the lesions of tuberculosis was largely limited to their mor- phology, it was natural that much stress should be laid upon the variety in structure which the nodular growths called tubercles pre- sented, and that elaborate classifications and groupings of tubercles were often deemed important. With an exact knowledge of the inciting cause of the new growths and of the varying phases of their development in the body, the mor- phological peculiarities of tubercles are not now to be regarded as of such extreme significance, since they for the most part indicate simply variations in the local effect of a definite poison. These vari- ations are due to differences in the amount and intensity of the poison, to the degree of susceptibility of the individual, to the struc- ture of the particular tissue or organ involved, and to the extent and variety of local complications caused by other agencies. It is, however, usually convenient and sometimes important to recognize structural types in miliary tubercles. Thus they may be composed wholly of small spheroidal cells—“ lymphoid tubercles,” or of larger polyhedral cells—“ epithelioid-celled tubercles” or of both forms of cells together and with or without a new-formed stroma; or of any of these combinations with giant cells. Then coagulation necrosis, which may occur in tubercles of any type; development of new dense connective tissue; association with various phases of simple exudative inflammation—all of these contribute to the variety in the structural types of miliary tubercles. Diffuse Tuberculous Inflammation (Diffuse Tubercle).—1. If the infection with tubercle bacilli be extensive, or if step by step the bacilli are distributed in the tissues about the primary seat of infec- tion, considerable amounts of tubercle tissue of one or other form may develop and pass into the condition of coagulation necrosis, so that at length large necrotic masses, with a comparatively small amount of well-defined tubercle tissue, either diffuse or in the form of granula, may alone remain to indicate the character of old and slowly progressive local infection. This form of lesion is found in the large tuberculous masses in the brain, in the mucous membrane Digitized by Microsoft® THE INFECTIOUS DISEASES. 221 of the bronchi, in large flat masses of the serous membranes, and in the diffuse, cheesy infiltration of the lymph nodes, kidneys, ureters, bladder, prostate, testicle, and uterus. These large areas of tuberculous inflammation are apt to be white or yellow in the central and necrotic portions, which are sometimes dense, compact, and hard, sometimes soft and friable. These areas are not infrequently surrounded by an irregular gray zone of tubercle tissue or by a dense fibrous tissue capsule. 2. In marked contrast with the phase of diffuse tuberculous in- Fig. 91.—Min1ary TUBERCLE IN LuNG oF CHILD. Showing the Bacillus tuberculosis—stained with fuchsin—in the contents of the air vesicles and in their thickened walls. (The sizeof the bacilli relative to other elements isslightly exaggerated.) flammation just described, though often associated with it, is that in which the formation of inflammatory exudates is a prominent feature. This exudative form of tuberculousinflammation is best exemplified in the lungs by some of the forms of acute phthisis (see page 466). The tubercle bacillus is under certain conditions markedly pyogenic aud when it rapidly develops in the air spaces of the lungs or sud- denly gains access to them in large quantities pus, serum, fibrin, and exfoliated or proliferated epithelial cells may collect in and largely fill the air spaces, and then the whole new exudate and the old lung tis- Digitized by Microsoft® 222 THE INFECTIOUS DISEASES. sue may,:over larger or smaller areas, rapidly undergo coagulation necrosis. Thus in one phase of tuberculous inflammation the intensity and rapidity of the local poisoning by the bacillus do not permit of the formation of organized new tissue at all, but only of exudative prod- ucts (Fig. 91). Less intense degrees of exudative inflammation are liable to develop in the vicinity of miliary tubercles anywhere in the body, but especially in the lungs. It has been found that tubercle bacilli which have been killed by boiling or otherwise, when introduced into the body of the rabbit Fic. 92.—INFLAMMATORY NODULE (PSEUDO-TUBERCLE) IN THE LIVER OF THE RABBIT PRODUCED BY THE INTRAVENOUS INJECTION OF DEAD TUBERCLE BACILLI. Most of the dead bacilli have disintegrated, setting free the bacterial proteid peculiar to this germ, which has stimulated the new cell growth, A few fragments of the bacilli, however, still remain. either beneath the skin, into the serous cavities, or into the blood vessels and the air spaces of the lungs, are capable, as they slowly disintegrate, of stimulating the cells of the tissues where they lodge to proliferation, and to the production of new tissue morphologically identical with tubercle tissue in its various phases (Fig. 92). Coag- ulation necrosis, however, does not occur. Dead tubercle bacilli are also markedly chemotactic and capable of causing local suppuration and abscess.’ i For further details concerning the effects of dead tubercle bacilli in the body see Prudden and Hodenpyl, New York Medical Journal, June 6th and 20th, 1891, and Prudden, ibid., December 5th, 1891. Digitized by Microsoft® THE INFECTIOUS DISEASES. 2k: It would seem probable then that while the power of the tubercle bacillus to induce necrosis and the fever which in many cases indi- cates a systemic intoxication, may be due to metabolic products of the living germ, the local lesions characteristic of exudative and pro- ductive inflammation may be due to a peculiar bacterio-protein which is set free by the disintegration of the bacilli in the tissues. The number of bacilli which are present in the lesions of tuber- culosis is subject to great variations. They are usually abundant in the walls and contents of phthisical cavities, and in tubercle tissue which is undergoing cheesy degeneration and disintegration. In these situations they may be found in myriads, forming sometimes a large part of the disintegrated mass. They are found in cells and scattered among them. Sometimes they are present in considerable numbers in the giant cells of miliary tubercles. In the acute general tuberculosis of children they are often present in large numbers, par- ticularly in the lungs (Fig. 91). They may be found in tuberculous in- flammation in any part of the body, and have been seen in the blood. The bacilli are almost constantly discharged in the sputa of patients suffering from pulmonary tuberculosis, often in enormous numbers— from one to four billion in twenty-four hours, according to Nutall’s estimate—and their presence sometimes affords valuable diagnostic aid in early stages of obscure forms of the disease. Under a variety of conditions, especially in the older tuberculous lesions, the bacilli may not be demonstrable. This apparent occa- sional absence of the bacilli is probably due either to their disappear- ance as the process grows older, or to some unknown changes which interfere with the ordinary staining procedures. In human beings cases of direct local inoculation of tuberculosis in the skin and accessible mucous membranes have been reported, but they are not very common. There is no doubt that the bacilli may be introduced into the ali- mentary canal by infected milk and meat of tuberculous cattle. They may be transmitted from the sick to the well by means of the sputum, which is allowed to dry and becomes pulverized and which is inhaled as dust, and this, under the ordinary conditions of modern life, is the chief means of infection. Whether the tubercle bacillus can enter the tissues of the body through intact mucous membranes, or whether a lesion, however minute, is a necessary condition is not yet fully determined. The observations of Loomis and others on the occurrence of tuberculous bronchial lymph nodes in persons exhibiting no appreciable tubercu- Jous lesions elsewhere would indicate the probability of access of the ba- cilli to the lymph channels without primary lesion at the portal of entry. Tuberculin.—When the tubercle is grown on glycerinated nutri- Digitized by Microsoft® 224 THE INFECTIOUS DISEASES. ent broth certain metabolic products are formed and pass into solution in the fluids. If after some weeks of vigorous growth the germs are separated by filtration and the broth concentrated by evaporation, a dark-brown fluid results which is called tuberculin. This substance —at one time believed by many, and still by a few observers, to pos- sess distinct curative properties in certain forms of tuberculosis—has assumed great economic importance on account of its value as a diagnostic agent in bovine tuberculosis. For it is found that if administered subcutaneously in small quantity to cattle, a definite and marked temperature reaction follows in tuberculous animals, while those which are sound are unaffected. The existence of even very slight lesions may be detected in this way. In man also tuber- culin has proved of value in cases in which the efforts to establish a diagnosis by the usual method have proved futile. Concurrent Infection in Tuberculosis.—A. concurrent infection with the tubercle bacillus and other pyogenic micro-organisms is of extreme significance in that phase of tuberculous inflammation of the lungs commonly called phthisis (see page 459).’ While the so-called cold abscesses may be caused by the tubercle bacillus alone, this germ is not infrequently found under these conditions to be associated with other pyogenic micro-organisms, especially the streptococcus and staphylococcus. METHODS OF STAINING THE TUBERCLE BACILLUS. In Fluids.—Yor the examination of fluids, such as sputum,’ ete., the material should be spread in a thin layer on a cover glass, dried in the air, and then passed thrice through the flame (see page 155). While, as has been said above, the tubercle bacillus is stained much less easily with the anilin dyes than are most bacteria, it can be deeply colored by the use of accessory agents which intensify the stains or render the protoplasm of the bacilli more accessible to them. But when once stained the tubercle bacillus clings with great tenacity to its color in the presence of the usual decolorizing agents. A variety of methods are in vogue for staining the tubercle bacillus, most of them being more or less unessential modifications of the original process formulated by Koch and Ehrlich. The stain- ing fluid which we have found most generally useful is known as Ziehl’s solution. This is made by adding to a five-per-cent aqueous 1 Consult Spengler, Zeitschrift f. Hygiene, etc., Bd. xviii, p. 342, 1894 (Bibliog- raphy. Tt is well in obtaining sputum for examination in cases of suspected pulmonary tuberculosis to secure that which has been raised during several hours, including the early morning discharge. Digitized by Microsoft® THE INFECTIOUS DISEASES. 225 solution of carbolic acid about one-tenth its volume of saturated alcoholic solution of fuchsin. This carbolic fuchsin will keep un- changed for a long time. The prepared cover glass is floated in a watch glass or porcelain capsule—specimen side down—on this coloring fluid, and gently heated almost to boiling for from three to five minutes. The entire specimen is thus completely stained, tubercle bacilli, tissue elements, and other bacteria which may be present, all in the same way. The next step is to remove the color with acid from all the structures which may be intermingled with the tubercle bacilli; the later, owing to the tenacity with which they retain the color, being but slightly affected. This is done by dipping the cover glass into an aqueous or alcoholic solution of five-per-cent sulphuric acid, and shaking it about for a few seconds. The acid may be even a little more dilute than this. Under the influence of the acid the specimen on the cover glass loses its red color and becomes gray or colorless. It is then thoroughly rinsed in three or four successive portions of alcohol, and finally in water. By this manipulation the red color may be to a slight extent restored. Care should be taken not to expose the specimen too long to the action of the acid, because then the bacilli may be also partially or completely decolorized. A little experience will enable the experi- menter to judge of the proper time for the action of the acid. The specimens may be studied in water with the use of an oil immersion and the Abbé condenser, or they may be dried in the air and mounted in balsam. Inasmuch as not infrequently some other bacteria besides the tubercle bacilli retain a slight red color, it is well, after the specimen is rinsed in water, to float the cover glass for a few minutes in a dilute aqueous solution of methylen blue, which will replace the red color in all of the bacteria except the tubercle bacilli and which might be mistaken for it, forming a marked color contrast between them. The contrast stain should not be intense. Various other anilin dyes may be used instead of the fuchsin, and there are various minor modifications of the process which are often employed; but, on the whole, for routine sputum examinations we recommend the method here given. In Sections.—Thin sections of tuberculous tissue which has been hardened in alcohol are stained in the same way, except that instead of drying and fixation by heat the sections should be fixed to the cover glass by means of the albumen fixative (see page 59), and then cover glass and section are manipulated together. When differentiation is complete the section is cleared in oil of cloves or cedar or origanum and mounted in balsam. 19 Digitized by Microsoft® 226 THE INFECTIOUS DISEASES. For purposes of simple recognition of the bacilli in sections it szems to the writer usually better to have no color in the preparation other than that which the tubercle bacilli possess. But it is often convenient to demonstrate the nuclei of the cells at the same time, and this may be accomplished by staining lightly afterward with a dilute solution of some color which will contrast with that of the bacilli, such as Bismark brown or methylen blue. In the examination of urine for the presence of the tubercle bacil- lus it is well to collect the sediment by means of a centrifugal machine. In the examination of milk, or other fat containing fluids for tubercle bacilli, it is well, after the film has been formed upon the cover glass and before staining, to rinse with chloroform followed by alcohol, and this by water. Occasionally one finds in urine acicular crystalline bodies con- siderably resembling the tubercle bacillus in size and shape, and retaining a red color after the decolorization of the specimen. A careful study of the form, however, will suffice to prevent mistakes. The only other bacilli which are liable to be mistaken for the tubercle bacilli are the bacillus of leprosy and the so-called smegma bacillus which sometimes occurs beneath the prepuce. The lepra baci- lus may be distinguished from the tubercle bacillus by the following differential staining process: If the lepra bacillus be stained for ten minutes in a dilute alcoholic solution of fuchsin (five drops of saturated alcoholic solution of fuchsin to 3 c.c. of water), and then rinsed for a few seconds in a solution of nitric acid (1 part) in alcohol (10 parts), it will retain a red color, while under the same treatment the tubercle bacillus remains uncolored. The smegma bacillus is readily decolorized by alcohol after stain- ing by Ziehl’s solution, and is thus to be distinguished from the tubercle bacillus. The bacillus described by Lustgarten as occurring in syphilitic lesions resembles the tubercle bacillus inform, but after staining with Ziehl’s solution is said to be decolorized by sulphuric acid. So little certainty exists, however, as to the existence or significance of the so-called syphilis bacillus that differential staining methods are not now to be considered as trustworthy (see page 234).’ ' The announcement of the discovery of the Bacillus tuberculosis by Auch was’ made in the Berliner klin. Wochenschrift, 1882, No. 15. A most elaborate and valu- able article on the same subject by Auch is contained in the “ Mittheilungen aus dem Kaiserlichen Gesundheitsamte, ” vol. ii. The very voluminous literature on the subject of the tubercle bacillus which bas accumulated since 1882 is for the most part scattered through the German, English, and French journals. It may be best obtained by consulting files of the Index Medicus of dates since April, 1882, or Banmgarten’s “Jahresbericht ttber die Fort- schritte in der Lehre von den pathogenen Mikroorganismen. ” Digitized by Microsoft® LUPUS AND OTHER FORMS OF TUBERCULOSIS OF THE SKIN. Local tuberculous inflammation of the skin may occur in the form of small nodules or wart-like thickenings, as the result of accidental inoculation. Local skin infection may occur about the orifices of the Fic. 93.—Lurus oF FACE. ‘ody in tuberculous persons from contact with secretions or excretions containing the tubercle bacilli, or about sinuses leading to tuberculous abscesses, joints etc., or in the vicinity of tuberculous lymph nodes. Finally, a chronic form of tuberculous inflammation which presents Digitized by Microsoft® 228 THE INFECTIOUS DISEASES. special clinical features has long been known under the name of lupus. Lupus.—This form of inflammation most frequently occurs in the skin of the face, but also in the mucous membrane of the mouth, pharynx, conjunctiva, vulva, and vagina. The lesion consists of small, multiple nodules of new-formed tissue, somewhat resembling granulation tissue, in the cutis or mucosa and submucosa. By the formation of new nodules and amore diffuse cellular infiltration of the tissue between them, the lesion tends to spread, and by the conflu- ence of the infiltrated portions a dense and more or Jess extensive area. of nodular infiltration may be formed. There may be an excessive: production and exfoliation of epidermis over the infiltrated area, or an ulceration of the new tissue. Microscopical examination shows the lesion to consist of small spheroidal cells intermingled with variable numbers of larger, so- called epitheloid cells and cell masses, and in many cases contains. giant cells (Fig. 93). In some cases a well-marked reticulum is present between the new cells, and these are often grouped in masses. around the blood vessels. In some cases there is, without previous. ulceration, a formation of new connective tissue in the diseased area, and a well-marked cicatrization; in other cases the cells and inter-. cellular substance undergo a disintegration which leads to ulceration. The morphological characters of the lesion long ago led to the conjecture that lupus was in reality a form of tuberculous inflamma- tion. This view has now become established by the numerous obser- vations which show the very constant presence of the tubercle bacillus. in small numbers at the seat of inflammation. In the clinical group of diseases called lupus there are other forms. of lesion which are not caused by the tubercle bacillus. Digitized by Microsoft® LEPRA (LEPROSY). This disease is very common in India and in other hot countries. It is not common in America, but in the Gulf States, in Mexico, among the Norwegians in the Northwest, and in the eastern British provinces a considerable number of cases are grouped. Isolated cases are, however, encountered now and then in various parts of the United States. Leprosy is characterized by the development of nodular and some- times diffuse masses of tissue, consisting of larger and smaller cells of various shapes—spheroidal, fusiform, and branched, with a fibrous stroma—the whole somewhat resembling granulation tissue. The Fic. 94.—THE BaciuLi or LEpRosy. Stained with gentian violet. From a nodule in the skin. new tissue is most frequently formed in the most exposed parts of the skin, as the face, hands, and feet, but it may occur in the skin of any part of the body. It is formed more rarely in the subcutaneous con- nective tissue, in intrafascicular connective tissue of nerves, in the viscera, and in the mucous membranes. The mucous membranes most frequently affected are those of the eye, nose, mouth, and larynx. The nodules may be very small or as large as a walnut, and may be single or joined together in groups or masses. The tissue of the part in which the new formation occurs may be atrophied and replaced by, or may remain intermingled with, the leprous tissue, or it may be hypertrophied. The nodules may persist for a long time without Digitized by Microsoft® 230 THE INFECTIOUS DISEASES. undergoing any apparent change, or they may soften and break down, forming ulcers; but ulceration, except in the mucous mem- branes, is said usually to occur as the result of injury or unusual exposure. The leprous tissue may change without ulceration into cicatricial tissue, or cicatrization may follow ulceration. Various secondary lesions and disturbances of nerve function are associated with the formation of leprous tissue in the nerve and central nervous system, but these we cannot consider here. In all the primary lesions of leprosy, bacilli are said to be present, mostly in the cells, and particularly in the larger transparent sphe- roidal forms, but sometimes free in the intercellular substance. The bacilli have been found in the skin, mucous membrane of the mouth and larynx, in peripheral nerves, in the cornea, in cartilage, in the testicles, and in lymph nodes. Sometimes the cells contain but few bacilli, but they are frequently crowded with them. The bacilli are from 4 to 6 » long and very slender, being usually less than 1 » in thickness. They are sometimes pointed at the ends and sometimes present spheroidal swellings (Fig. 94). In their comportment toward staining agents, as well as in general morphological characters, they considerably resemble the Bacillus tuberculosis, but they are more readily stained. They may be stained with fuchsin or gentian violet by the ordinary method, or by the method employed for staining the tubercle bacillus (see page 224). According to Neisser, the lepra bacillus may be artificially culti- vated at body temperature on blood serum and on boiled eggs. Bordoni-Uffreduzzi claims to have grown it on glycerinated blood serum. It is said by Byron to grow on glycerin-agar with two per cent of sugar, in tubes sealed to retain the moisture.’ But these reports of success in the artificial cultivation of the lepra bacillus have not yet received the seal of experimental confirmation. Lepra is communicable from man to man by direct inoculation. Under modern and proper sanitary conditions the disease is not readily communicable. In a few cases animal inoculations have been made with what appears to be positive results. The structure of the new tissue growth, the absence of coagulation necrosis, and the peculiar grouping of the bacilli in the large trans- parent cells are characters which usually clearly distinguish the lesions caused by the leprosy bacillus from those of tuberculosis. 1 Byron, New York Pathological Society, January 27th, 1892. Digitized by Microsoft® SYPHILIS. The lesions of this form of infectious disease are in many respects morphologically similar to those of tuberculosis, and are unquestion- ably due to the presence in the body of some form of micro-organism. Fia. 96.—NEW-FORMED TISSUE IN SYPHILITIO INFLAMMATION. From a ‘‘ hard chancre,”’ showing swollen endothelium in a small blood vessel. Digitized by Microsoft® 232 THE INFECTIOUS DISEASES. That this is so, however, we do not know by direct observation and experiment, but by inference. The characteristic lesions of syphilis consist in a more or less circumscribed formation of new tissue. This new tissue may be made up largely of small spheroidal cells (Fig. 95), or of these with polyhedral cells and of occasional giant cells. All of these new cell Fie. 97.—SECTION FROM A PRIMARY SyPHILITIC NODULE OF THE Mucous MEMBRANE OF THE MOUTH. Showing collections of cells about the blood vessels in the submucous tissue. undergo coagulation necrosis and to disintegrate at the centres. They may be converted into cicatricial tissue. The new tissues in syphilitic inflammation contain, as a rule, few blood vessels. It may form diffusely or in circumscribed masses. The endothelial cells of the blood vessels near the inflammatory foci in syphilitic inflammation are not infrequently swollen and may proliferate (Figs. 96 and 98, B). The vessels may otherwise undergo extensive changes. Digitized by Microsoft® THE INFECTIOUS DISEASES. 233 In the primary lesion, which is called chancre, there may be obliterating endarteritis, a small spheroidal cell infiltration of the connective tissue (Fig. 97), proliferation of connective-tissue cells, swelling of the vascular endothelium, and an occasional development of giant cells. This new tissue may become fibrous or necrotic and may ulcerate. Following the primary lesion there may be inflammation of the , ives t ve N gop @ gf oe Se ig UCAS Fig. 98.—SEcTION oF A PorTION OF a SYPHILITIC CoNDYLOMA OF THE Mucous MEMBRANE. A, GEdematous papilla; B, swollen endothelial cells in small blood vessels of a papilla; C, pus cells in the submucous connective tissue; D, pus cells in the epithelium ; E, disintegration of the epithelium in the superficial portion of the mucous membrane. lymph nodes, of the skin and mucous membranes, of the bones and viscera. One of the most characteristic phases of the secondary intamma- tions of syphilis results in the formation in the periosteum or the viscera of masses of new tissue called gummata. The smaller gummata consist of a mass of small spheroidal and epithelioid cells (see Fig. 95). As these cell masses grow larger they Digitized by Microsoft® 234 THE INFECTIOUS DISEASES. are apt to become necrotic at the centre, and we may then have, as seen by the naked eye, a grayish-white, usually firm mass, with a more or less dense and irregular cheesy centre and a translucent, often radially striated border of dense fibrous tissue (see Fig. 247). A bacillus closely resembling the tubercle bacillus in form and size has been described by Lustgarten and others as occurring in the lesions of syphilis. It isfound in very smallnumbers. A distinctly characteristic mode of staining is not known, and it has never been cultivated on artificial media; so that the evidence that this bacillus is the cause of syphilitic inflammation does not appear to us at all convincing. It is not always easy to distinguish on morphological grounds between the lesions of syphilis and those of tuberculosis, but the greater variety in the developmental stages of the tuberculous foci which may be found in a single individual; the grouping of the lesions in a manner indicative of progressive local infections, and in the last resort the demonstration of the presence of the tubercle bacillus, will usually suffice to distinguish the tuberculous from the syphilitic lesion, even without recourse to the clinical history. For further details regarding syphilitic lesions see Changes in the Viscera, Part ITI. Digitized by Microsoft® GLANDERS. Glanders is an infectious disease caused by the presence and growth in the body of a bacillus called the Bacillus mallei. It is most common in the horse, affecting the mucous membrane of the nose (when involving the skin the disease has been called farcy), and can be communicated to man and to certain other of the domestic animals by direct or accidental inoculations. The disease is most frequent in those who come much into direct contact with horses. The seat of primary local infection in man is most often the skin, more rarely the mucous membranes about the noge and mouth. The local lesions are similar in man and the lower animals. In the presence of the Bacillus mallei there is usually a circumscribed or more rarely a diffuse infiltration of the tissue with small spheroidal cells—leucocytes—with which new connective-tissue cells (epithelioid in form) may be mingled. These whitish foci of cells accumulation may be small and to the naked eye resemble miliary tubercles; or, they may be larger and nodular. The tissues about them may be infiltrated with blood. But the accumulated cells are apt in the presence of the bacilli to become necrotic and disintegrate and thus lead to smaller and larger abscesses, or, if near the surfaces, to ulcers. If occurring on mucous membranes these lesions are often accom- panied by intense diffuse catarrhal inflammation. As the glanders nodules soften, the bacilli are apt to diminish in number or in the capacity to stain, so that it may be possible to detect their presence only by inoculation or culture methods. The disease may begin at a single point, so that it may be mis- taken for a carbuncle or gangrenous erysipelas. But the infection is apt not to remain local; the bacilli, finding their way along the lymph channels into various parts of the body, set up fresh foci of inflammation and necrosis. Then the skin may be covered witha pustular eruption; furuncles, carbuncles, and abscesses may form beneath the skin and in the muscles. Nodules are found in the nasal mucous membrane, the lungs, kidneys, testes, spleen, and liver. The joints may be inflamed, and there may be osteomyelitis. The glanders infection may, however, pursue a more chronic course, with hard, persistent nodules and sluggish ulcers. Under Digitized by Microsoft® 236 THE INFECTIOUS DISEASES. these conditions the detection of the bacillus in the tissue by a simple morphological examination may be difficult. While some forms of glanders nodules somewhat resemble in gross and microscopic appearance certain forms of miliary tubercles, the absence in the former of coagulation necrosis and of giant cells, and the tendency to rapid disintegration and softening in the latter will usually suffice for the distinction between the two sets of lesions. But the demonstration of the bacilli characteristic of each is in all cases decisive. The Bacillus mallei is a slender bacillus proportionately thicker than the tubercle bacillus, with rounded ends, occurring singly or in pairs (Fig. 99). It stains easily with the anilin dyes, but readily gives up the color in presence of even feeble decolorizing agents such as dilute alcohol or acids._ It is left decolorized by Gram’s method. When stained, uncolored areas are apt to remain in the body of Ai Fic. 99.—Baci~tLus MAuuet. the germ. Whether these are spores or not is not yet definitely determined. In the tissues the bacilli may be stained with Léffler’s alkaline methylen blue, or with Ziehl’s solution, great care being taken not to stain too deeply lest in the decolorization which is to follow the bacilli as well as the tissue elements may lose their color. It is well to decolorize in very dilute acetic acid (1:300), then wash carefully in water, dry the section on the slide with blotting paper and very gentle heat, clear with xylol, and mount in balsam. The glanders bacillus grows readily on almost all of the ordinary artificial culture media, and best at blood heat. The growths on solid media are apt to be viscid. On potatoes it forms in two or three days an abundant yellowish pellicle which in a few days darkens and finally becomes brown in color. It gradually loses its virulence in successive generations of artificial cultures. The germ is easily killed by moist heat, but may remain alive in a dried state for months. Field mice and guinea-pigs are very susceptible to infection with the Bacillus mallei, and after inoculation develop highly char- acteristic local and general lesions. In cases in which an early diagnosis is imperative it is well, | in Digitized by Microsoft® THE INFECTIOUS DISEASES. 237 addition to the morphological examination and cultures of the sus- pected exudate, to inject a small amount into the peritoneal cavity of amale guinea-pig. If the virulent glanders bacilli be present, within two or three days the testicles will swell and develop an intense sup- purative inflammation. As the glanders bacillus grows in nutrient broth a proteid sub- stance—or substances—develops, which when concentrated by evapo- ration of the broth is called mallein. This substance prepared and administered to horses suffering from glanders, as tuberculin is pre- pared and administered to tuberculous cattle (see page 224), gives a similar temperature reaction, and is thus an important diagnostic agent, Digitized by Microsoft® RHINOSCLEROMA. This disease, which occurs especially in eastern Europe and occa- sionally in other parts of the world, is a chronic inflammation of the nasal, pharyngeal, and laryngeal mucous membrane. In this inflam- mation a diffuse or nodular formation of new tissue, somewhat re- sembling granulation tissue, occurs, which tends to assume a dense cicatricial character. Constantly associated, it is said, with this lesion is a bacillus called Bacillus rhinoscleromatis. This bacillus in most of its morpho- logical and biological characters closely resembles the pneumobacillus of Friedlander, growing readily on the common culture media and developing a capsule, and it may be identical with it. The relationship of this bacillus to the lesions of rhinoscleroma do not appear to be as yet definitely established, since inoculations in men and animals have not given positive results. Digitized by Microsoft® BUBONIC PLAGUE. (Oriental Plague; Black Death.) This readily communicable and extremely fatal infectious disease is especially characterized morphologically by an acute inflammatory swelling of the lymph nodes, most often those of the inguinal region, which are apt to suppurate or to become gangrenous. Hemor- rhages are common. Carbuncles may occur. This disease, formerly not uncommon, has gradually become ex- tinct in Europe. In the early summer of 1894 a severe epidemic occurred at Hong-Kong, and both Kitasato and Yersin discovered that the disease is caused by a short, thick, motile bacillus with rounded ends, staining more deeply at the ends than in the middle. It grows readily on the ordinary culture media at blood heat, and on inoculation into mice, rats, guinea-pigs, and rabbits effects are pro- duced similar to those of the disease in man. The bacilli are present in the blood, in the lymph nodes, and in the viscera. The germs appear to gain entrance to the body through the abraded skin, the lungs, and the gastro-intestinal tract.’ 1 Consult Yersin, Calmette and Borrel, Aunales de l'Institut Pasteur, July, 1895, p. 589. Digitized by Microsoft® TYPHOID FEVER. Typhoid fever is an infectious disease constantly associated with a bacillus called the Bacillus typhi abdominalis. The lesions of typhoid fever are usually well marked and con- stant. They may conveniently be divided into two classes: I. Those lesions which are characteristic of the disease. To this class belong the hyperplasia and ulceration of the lymph nodules (lymph follicles) of the intestine; the hyperplasia of the mesenteric lymph nodes (lymph glands), and of the spleen. II. Those lesions which frequently occur with this fever and yet are not peculiar to it. To this class belong the parenchymatous degenerations in the viscera, especially in the liver and kidney; hyalin degeneration of voluntary muscles; suppurative inflammation in various parts of the body; endarteritis and thrombosis, infarctions, complicating pneumonitis, etc. I. The Intestines.—The lesions of the intestines consist of an inflammatory enlargement (hyperplasia) of the solitary lymph nodules and of the agminated lymph nodules (Peyer’s patches). Necrosis of the nodules with ulceration frequently follows the hyper- plasia. The process appears to begin with a catarrhal inflammation of the mucous membrane, accompanied or immediately followed by changes in the lymph nodules. The lesions in the lymph nodules begin early ; they have been observed in persons who have died forty-seven hours after the commencement of the disease. The increase in size of the agminated and solitary nodules may be rapid or gradual. The nodules may be only slightly enlarged, or may project so as to fill up the cavity of the intestine. The enlarge- ment is usually more marked in the agminated than in the solitary nodules. Usually the whole of a Peyer’s patch will be enlarged, but sometimes only a part of it. If the enlargement is gradual the dif- ferent nodules which make up a Peyer’s patch are enlarged, while the septa between them remain but little changed and give the patch an uneven appearance. The patches which are only moderately enlarged are of reddish or reddish-gray color, are soft and spongy, and their edges blend grad- ually with the adjoining mucous membrane. The patches which are Digitized by Microsoft® THE INFECTIOUS DISEASES. R41 more intensely affected are of gray or brownish color, of firm consist- ence, and rise abruptly from the surrounding mucous membrane, or even overhang it like amushroom. The largest patches are some- times more than three-eighths of an inch thick. The enlargement and intiltration may spread from the patches to the surrounding mucous membrane, so that the patches appear very large; a number of them may become fused together, and there may be even an annular infiltration entirely around the lower end of the ileum. The infiltration of the Peyer’s patches may also extend outward into the muscular coat, and even appear beneath and in the peritoneal coat as small, gray, rounded nodules. This condition is usually found only with a few patches in the lower end of the ileum; some- times in the cecum and appendix vermiformis. These little gray nodules usually correspond to diseased patches beneath them; some- times they appear to excite an inflammation of the peritoneum, accompanied by the production of numbers of similar nodules all over that membrane. Hoffmann describes a case in which the inflamma- tion extended to the pleura, with the production of similar nodules there. . The solitary nodules are affected in the same way as Peyer’s patches. They may be hardly enlarged at all, or be quite prominent, or may be affected over a larger portion of the intestine than are the patches. Very rarely the solitary nodules are enlarged, while the patches are not at all or but slightly affected. The inflammation and enlargement of the agminated and solitary nodules may be followed by a healing process. The character of this process varies according to the intensity of the previous inflam- mation. 1. If the disease was mild and the enlargement of the nodules moderate, the enlargement gradually disappears and they resume their normal appearance (resolution). 2. In moderate enlargements resolution proceeds first in the nodules, leaving the septa between them for a time still swollen and prominent. This gives to the surface of a patch a reticulated ap- pearance. After a time, however, the entire patch becomes flat- tened and uniform. 3. The solitary nodules or the separate nodules of a patch soften, break down, and their contents are discharged with some attendant hemorrhage. ‘This leaves a bluish-gray pigmentation, due to altered hemoglobin, in the situation of each nodule, and this may remain for years. 4. In more severe types of the disease the enlargement of the nodules ends in ulceration. This takes place in two ways: Digitized by Microsoft® 242 THE INFECTIOUS DISEASES. (a) The enlarged nodules soften, break down, and discharge into the intestine. In this way are formed small ulcers. These ulcers increase in size by the same softening process, which gradually attacks their edges, and in this way ulcers of large size. may be formed. The ulcers may extend outward only to the peritoneal coat, or they may involve the peritoneal coat also and perforate. (b) In the severest forms of the disease considerable portions of the enlarged patches may slough and become detached, leaving large ulcers with thick, overhanging edges. The slough may involve only the nodules, or it may involve also the muscular and peritoneal coats. These ulcers also may afterward increase in size, and several of them may be joined together. If the patient recover the ulcers cicatrize, their edges become flattened, their floors are converted into connective tissue covered with cylindrical epithelium. Both forms of ulceration sometimes end in perforation. This is effected by the extension of the ulcerative process through the perito- neal coat or by the rupture of the floor of the ulcer. Peritonitis and death are the usual result. In rare cases, however, the patient recovers and the perforation is closed by adhesions. The minute changes which take place in the development of the intestinal lesion are as follows: At first the blood vessels around the nodules are dilated and con- gested, while the nodules are swollen and the epithelium falls off. Then the nodules increase in size, largely from a growth of new cells. The new cells are, in part, similar to the lymphoid cells which nor- mally compose the nodules; in part are large, rounded cells, some of which contain several nuclei. The production of new cells is not confined to the nodules, but extends also to the adjacent mucous mem- brane. In many cases also little foci of the same cells are found in the muscular, subserous, and serous coats. This increased number of cells compresses the blood vessels and the parts become anzemic. Soon the cells degenerate, either by granular degeneration of indi- vidual cells or by gangrene of part of a nodule. In either case the degenerated portion is eliminated into the intestine and leaves an ulcer of which the floor and edges are infiltrated with cells. After this the cell growth goes on and the ulcer enlarges, or the cells are gradually replaced by connective tissue and cicatrization follows. The lesions which we have described are found most frequently and are most pronounced in the lower part of the ileum. They are not always, however, confined to this situation. Enlarged and ul- cerated nodules may be found over the entire length of the ileum and even in the jejunum. They may also extend downward and be found Digitized by Microsoft® THE INFECTIOUS DISEASES. 243 in the colon, even as far down as the rectum. The same changes may also take place in the appendix vermiformis.’ Besides the regular typhoid lesions of the intestines which have . been described, we occasionally meet with others of a secondary and more accidental character. Gangrene of the intestinal wall sometimes occurs. It most fre- quently involves a portion of the wall corresponding to an ulcer, but may also affect other portions where no ulcer exists. The process may terminate in perforation or in healing. Croupous Inflammation may attack the mucous membrane of either the large or small intestine. The mucous membrane between the typhoid ulcers is then more or less covered and infiltrated with an exudation of fibrin and pus. Perttonitis of a mild type is a frequent accompaniment of the intestinal lesions. It appears to have but little influence on the course of the disease. Severe peritonitis is usually due to perforation, less frequently to ulcers which reach the serous coat but do not perforate. When there is infiltration of the serous coat with the typhoid new growth, the peritonitis may be accompanied by a production of little gray nodules of the same character throughout the peritoneum. Infarctions of the spleen, inflammation of the ovaries, and per- foration of the gall bladder are sometimes the cause of peritonitis. Hemorrhage from the intestines may be slight and due to the inflammatory swelling and congestion of the mucous membrane; or it may be due to the ulceration of the follicles and opening of the blood vessels, and is then often profuse. Mesenteric Lymph Nodes.—The mesenteric nodes undergo changes similar to those in the nodules of the intestines, and are usually affected in a degree corresponding to the intensity of the intestinal lesion. The nodesare at first congested and succulent; then there isa pro- duction of lymphoid cells and large cells (Fig. 262), as in the intes- tinal nodules, and the node becomes enlarged. When the enlarge- ment has reached its full size the congestion diminishes and the cells begin to degenerate. The degeneration may take place slowly, and then the node gradually returns to its normal condition; or more rapidly, and then little foci of softened, purulent matter are formed. If the patient recovers the small foci are absorbed, leaving a fibrous 1 Owing to the frequent involvement of Peyer’s patches the larger intestinal ulcers in typhoid fever are apt to have their longest diameter lengthwise of the gut in contrast to spreading tubercular ulcers, which, owing to the extension of the local in- flammation along the encircling lymph channels, are apt to have the longest diameter crossing the gut. But exceptions to this general rule are common. Digitized by Microsoft® 244 THE INFECTIOUS DISEASES. cicatrix; the larger foci may become dry, necrotic, and enclosed in a fibrous capsule. The inflammation of the nodes may produce a local or general peritonitis. Intense exudative inflammation may occur in the nodes, which may be densely infiltrated with serum, fibrin, and pus. The Spleen.—In nearly every case of typhoid fever the spleen is enlarged. This enlargement begins, as a rule, soon after the com- mencement of the disease, increases rapidly until the third week, remains stationary for a few days, and then diminishes. The organ is congested, of dark-red color, and of firm consistence while it is increasing in size. After it has reached its maximum size its con- sistence becomes soft and there is a considerable deposit of brown pigment. The enlargement appears to be due to congestion and hyperplasia (compare page 624), In rare cases the softened spleen ruptures, with an extravasation of blood into the peritoneal cavity. There may be infarctions of the spleen, which sometimes soften and cause peritonitis. II. The second class of lesions comprises those which are fre- quently found with typhoid fever, but are not peculiar to it. The Mouth.—A number of changes are found about this .region. The follicles at the root of the tongue and the tonsils may be enlarged ; the muscles of the tongue may undergo waxy and granular degen- eration; gangrenous ulcers may attack the floor and sides of the mouth and destroy large areas of tissue. The Pharynx may be the seat of catarrhal or croupous inflamma- tion, producing superficial and deep ulcers. The Parotid is, in a moderate number of cases, the seat of an inflammation which tends to suppuration. In this process both the glandular acini and the connective tissue between them are involved. Which of the two has the larger share in the process is still in dis- pute. A slight enlargement and induration of the parotid and submax- illary glands is said by Hoffmann to be a frequent lesion, and to depend on increase of the gland cells and dilatation of the acini with their secretion. The Pancreas undergoes changes similar to those in the salivary glands. It becomes at first swollen and red, then hard and grayish, then yellow. The vessels are at first congested, afterward there is increase of the gland cells, and lastly degeneration. The Liver may preserve its normal character or may present changes. In many cases the organ will be found swollen, pale, soft and flabby. Minute examination then shows that the liver cells have Digitized by Microsoft® THE INFECTIOUS DISEASES. 245 undergone parenchymatous degeneration. They are filled with fine granules and small fat globules, and the degeneration may go on so far that the outlines of the hepatic cells are lost and nothing but a mass of granules can be seen. Less frequently we find in the liver very small, soft, grayish nodules. They are situated along the course of the small veins, and there is at the same time a diffuse infiltration of lymphoid cells along the small veins. The nodules consist of lymphoid cells; they are often too small to be distinguished with the naked eye.’ Small necrotic foci are sometimes present. The Heart.—In a considerable number of cases the muscular tissue of the heart is altered by granular, fatty, or hyalin degenera- tion or by pigmentation. Myocarditis, endocarditis, and pericar- ditis are of occasional occurrence. Thrombi in the cavities of the heart and vegetations on the valves are sometimes found. Detached fragments of these may be lodged as emboli in the different arteries. The Artertes.—There may be an acute inflammation of the ar- teries, especially at the commencement of convalescence. There are two varieties: an obliterating and a parietal arteritis. In the oblit- erating arteritis there is infiltration of all the coats of the artery, with roughening of the intima and the formation of a thrombus within the vessel, and this may be followed by dry gangrene of the part supplied by the artery. In the parietal variety the wall of the artery is infiltrated with cells, but the intima is not roughened and no thrombus is formed. The Veins.—Thrombosis of the larger veins, especially of the femoral vein in the third and fourth weeks of the disease, is not un- common. The Larynx is very frequently the seat of catarrhal inflammation, with or without superficial erosions. Less frequently there is croup- ous inflammation, followed in some cases by destructive ulceration. The Lungs.—Catarrhal inflammation of the large bronchi is very common. Broncho-pneumonia occurs in two forms. There may be a severe inflammation of most of the bronchi of both lungs, with cellular infiltration of the walls of the bronchi and zones of peribron- chitic pneumonia; or there is an intense general bronchitis, with lobules of the lung corresponding to obstructed bronchi, either col- lapsed or inflamed, or both. From the long-continued recumbent position of the patients the posterior portions of the lungs become congested, dense, and un- 1 Reed, “ An Investigation into the so-called Lymphoid Nodules in the Liver in Typhoid Fever,” American Journal of Medical Sciences, November, 1895. Johns Hopkins Hospital Report, vol. v., p. 379. . Digitized by Microsoft® 246 THE INFECTIOUS DISEASES. aérated. Sometimes, in addition to this, irregular portions of the lungs become hepatized. Less frequently there is a regular acute lobar pneumonia. There may be infarctions. Gangrene of the lungs occasionally occurs, either associated with lobular pneumonia or with infarctions, or as an independent condition. Fibrinous pleurisy and empyema occasionally occur. The Kidneys very frequently present the lesions of acute degen- eration, and occasionally those of acute inflammation. Small collec- tions of lymphoid cells and small abscesses may be found in the kidney. Catarrhal and croupous inflammation of the bladder may occur. The Ovaries.—Hemorrhage and gangrenous inflammation have been observed in rare cases. The Testicles.—Orchitis has been described.’ It is usually de- veloped during convalescence; is unilateral; and usually affects the testicle alone, less frequently: the epididymis; it may terminate in suppuration. The Brain.—Acute meningitis is rare. Thrombosis of the venous sinuses, and obliterating endarteritis of the cerebral arteries, are occasionally observed. The Voluntary Muscles, especially the abdominal muscles, the adductors of the thigh, the pectoral muscles, the muscles of the dia- phragm and of the tongue, frequently undergo the hyalin degenera- tive changes described under muscle lesions. The Skin.—Gangrenous inflammation of the skin frequently occurs in the form of bed sores, affecting especially the skin over the sacrum and trochanters, where it is subjected to the constant pres- sure of the bed. There may be suppurative inflammation in almost any part of the body. Perhaps the most important of these local suppurations is that which results in retropharyngeal abscess. The post-typhoid bone lesions are important.’ In the secondary bone lesions after typhoid as well as elsewhere the bacillus may remain alive for long periods, even several months. THE BACILLUS OF TYPHOID FEVER. The presence of a bacillus in various parts of the body in typhoid fever, in a considerable proportion of the cases examined, has been well established by a large number of observers. This bacillus does not occur in the body, so far as is known, except in connection with this disease. 1 Ollivier, Rev. de Méd., November and December, 1883. 2 Parsons, Johns Hopkins Hospital Reports, vol. v., p. 417. Digitized by Microsoft® THE INFECTIOUS DISEASES. 247 In the early stages of the disease the bacillus may be found in the lymphatic structures of the intestines and in the mesenteric lymph nodes and the spleen. It may be present in the bone marrow, kidney, liver, bile, lungs, and in the blood, and it may be found, though not in such abundance as was formerly assumed, in the intestinal con- tents after the disease had become well established. In the viscera it is apt to occur in larger and smaller masses or clusters (see Fig. 100). It has been repeatedly found in the urine. The typhoid bacilli may be present alone or in association with other germs in the foci of suppuration which so frequently complicate typhoid fever, also in the exudates in inflammations of the serous membranes and in the endo- cardial vegetations.’ The typhoid bacillus is usually about three times as long as broad, being about one-third as long as the diameter of a red blood cell. Fic. 100.—CLusTER oF TYPHOID BACILLI IN THE SPLEEN. But it varies considerably in size when growing on different media. It is rounded at the ends, and frequently contains rounded structures which have been regarded as spores, but which further researches have led us to believe are not spores but vacuoles. The bacillus is beset with flagella. The typhoid bacillus can be readily cultivated on the ordinary culture media at room temperature. It forms delicate, bluish-white, sinuous-edged, spreading colonies on the surface of nutrient gelatin, which it does not fluidify. Several other bacteria grow in a similar way on gelatin. The growth of the typhoid bacillus on boiled potatoes, 1 See Flerner, Journal of Pathology and Bacteriology, April, 1895, and Johns Hopkins Hospital Reports, vol. v., p. 3438. Also for full consideration of the pyo- genic powers of the typhoid bacillus consult Dmochowski and Janowski, Ziegler’s Beitr. z. path. Anat., etc., Bd. xvii., p. 221. Digitized by Microsoft® 248 THE INFECTIOUS DISEASES. in a nearly invisible pellicle, is a marked culture characteristic. If, however, the potato be slightly alkaline the surface growth becomes evident. In cultures the typhoid bacilli often cling together end to end, forming long, thread-like structures (Fig. 101). The bacilli in fluids are actively motile.’ Inoculations of the typhoid bacillus into animals, while not pro- ducing a disease in all respects like that in the human subject, may cause death with symptoms and lesions as closely resembling those in man as we are often able to produce in animal experimentation. Although similar effects may be induced in animals by the inocula- tion with other germs, the evidence that typhoid fever in man is produced by the typhoid bacillus, and by this alone, is altogether so strong as practically to amount to a demonstration. It is probable that the usual symptoms and lesions of typhoid fever are largely due to the absorption of toxic substances which are produced as the result of the life processes of the bacteria at the point of their greatest accumulation and activity. Fia. 101.—BaciLLus TypPHosvus. From a gelatin culture. During artificial cultures in nutrient broth a poisonous albuminoid product or products are formed and have been named typhotoxin. Injection into rabbit may in addition to general toxic symptoms induce hyperplasia of the intestinal lymph nodes. Some of the inflammatory complications which occur in typhoid fever are due to the growth of the bacillus in unusual places in the body, but many of them are due to a secondary infection with other germs, notably with the pyogenic cocci. Infection with the typhoid bacillus seems to occur largely through the gastro-intestinal canal. In a large proportion of cases the disease is communicated by means of food, and especially of milk and drinking-water which have been polluted with the excretions of persons suffering from the disease. Many serious epidemics of typhoid fever have been traced 1 Several bacilli are known which considerably resemble the typhoid bacillus in form and general biological characters under cultivation. Most noteworthy among these is the Bacillus coli communis, which is a constant resident of the gastro- intestinal canal. This germ, which in the past has no doubt been frequently mis- taken for the Bacillus typhosus, may now be differentiated from it. Digitized by Microsoft® THE INFECTIOUS DISEASES. 249 to pollutions of milk and drinking-water from such sources.’ Oysters which have been taken from grossly polluted waters, as near sewer openings, have been the means of conveying the germs.” In milk the typhoid bacillus not only remains alive for long periods but undergoes active multiplication. It may remain long alive in water and even for a time multiply. In the soil and when dried it may remain alive for months. Frozen in ice it has been found alive after more than three months. It is readily killed by exposure to strong sunlight. METHODS OF STAINING THE TYPHOID BACILLUS. The bacilli, when taken from cultures, stain readily with the ordinary anilin dyes, such as fuchsin and gentian violet (see page 130.) In sections of the organs they do not take the stain so readily. They are decolorized by Gram’s method. One of the most satisfactory solutions for this purpose is that of Ziehl, which is made as follows: Filtered saturated aqueous solution of Carbolic Acid, 90 Saturated alcoholic solution of Fuchsin............. 10 The sections are soaked for half an hour in this solution and then ‘decolorized by alcohol, cleared in oil of cedar, and mounted in balsam. The decolorization should be done carefully, the section being ex- amined from time to time as it proceeds, so as to avoid the removal of too much color. The nuclei should remain faintly colored, but not so much so as to conceal the clusters of more deeply stained bacilli.® 1 Freeman, New York Medical Record, March 28th, 1896. 2 Foote, Medical News, March 238d, 1895. 3 For recent summary of studies on the typhoid bacillus and typhoid fever, with bibliography, consult Dunbar, “Ergebnisse der allg. Aetiologie der Menschen- u. ‘Thierkrankheiten, ” 1896, p. 605. Digitized by Microsoft® DIPHTHERIA. Diphtheria is an acute infectious disease caused by the Baczllus diphtheric (Loffler), and usually characterized by a pseudo-mem- branous inflammation on some of the mucous membranes or occa- sionally on the surface of wounds, and by immediate or remote effects of absorbed toxic substances. The mucous membranes which are the most frequently affected in diphtheria are those of the tonsils, pharynx, soft palate, nares, larynx, and trachea; less frequently those of the mouth, gums, con- junctiva, cesophagus, and stomach. The local inflammation in mucous membranes may present various phases, which represent clinical types of the disease. Thus there may bea simple redness of the affected surfaces which leaves no trace after death, or a catarrhal inflammation. On the other hand, in the more marked forms of the lesion there may be a fibrinous exudate which infiltrates the mucous membrane, or, intermingled with pus cells, epithelial cells, red blood cells, bacteria, and granular material, forms a thick or thin pellicle on the affected surfaces. This pellicle may undergo coagulation necrosis, and hand-in-hand with this there may be superficial or deep coagulation necrosis of the mucous mem- brane. The false membrane in diphtheria is thus formed by a combination of inflammation and necrosis, the extent of the necrosis and the amount of inflammatory products varying in the different cases. The pseudo-membrane may disintegrate or exfoliate, with or without loss of tissue in the underlying mucous membrane. Phleg- mon, abscess, and cedema are liable to occur as local complications. Adjacent and distant lymph nodes are apt to be swollen, and often show, on microscopical examination, small foci of cell necrosis and disintegration. Similar necrotic foci and areas of small spheroidal- cell accumulation with fatty degeneration may be found in the kidney, spleen, and liver. Acute nephritis and degeneration of the heart muscle are not infrequent.‘ The exact nature of the nerve lesions which may be associated with the late paralyses of diphtheria is not yet clear. ' For a study of heart lesions in diphtheria consult Schamschin, Ziegler’s Beitr. z. path. Anat., Bd. xviii., p. 64, 1895. Digitized by Microsoft® THE INFECTIOUS DISEASES. 251 Catarrhal bronchitis and broncho-pneumonia or lobular pneumonia frequently complicate diphtheritic lesions of the upper air passages and fauces. Bacteria of various forms are commonly present in the false membrane, and some of the forms may penetrate deeply into the underlying tissue. The germ, however, which stands in a causative relationship to this disease is the Bacillus diphtheriz of Léffler. In man the diphtheria bacilli are largely confined to the seat of local lesion, and sometimes occur in enormous numbers (see Fig. 102), especially in the older layers of the pseudo-membrane. But they may become widely distributed through the blood. The systemic effects in diphtheria appear to be due to the absorption into the body of toxic material elaborated by the germs. The very frequent association of the pyogenic cocci with the diph- Rudy Fic, 102.—DIPHTHERITIC INFLAMMATION OF THE TONSIL. Showing Léffler’s bacilli in the pseudo-membrane. theria bacillus give rise to a complicating series of results which make the clinical picture and the lesions of diphtheria sometimes very complex. Thus the complicating bronchitis and broncho-pneu- monia, as well as pyeemic symptoms and lesions, may be due to the presence in the pseudo-membrane, and the entrance into the deeper air passages and the blood, of the Streptococcus pyogenes and the Staphylococcus pyogenes, the Diplococcus lanceolatus, Bacillus coli communis, and others. The Bacillus diphtheriz, first described and definitely associated with this disease by Loffler, is from 2.5 to 3 » in length and 0.5 to 0.8. » in thickness, and is characterized morphologically by marked irreg- ularities in its form (Fig. 103). While the typical form is that of a Digitized by Microsoft® 252 THE INFECTIOUS DISEASES. moderately stout, round-ended, straight, or slightly curved bacillus, it is very apt—perhaps as a result of degeneration—to appear club- shaped or pointed at the ends, irregularly segmented, and to develop at the ends or elsewhere a strongly refractile material which stains more deeply than the rest of the protoplasm. The diphtheria bacillus is immotile, grows slowly and scantily at room temperature, but at body temperature develops rapidly in bouil- lon and on agar, glycerin-agar, and blood serum. On glucose-broth serum (Léffler’s blood-serum mixture) the growth is particularly vigorous (see page 162). On glycerin-agar plates it grows in the form of moderately small, grayish-white, slightly spreading, rough-edged colonies. According to Welch and Abbott, it grows abundantly in an invisible pellicle on potatoes. It does not form spores. Welch and Abbott have found that in fluids it may be killed by an exposure of ten minutes to a temperature of 58° C. But it may remain alive for weeks, or even months, in fragments of dried membrane.’ Fig. 103.—Bacituus DIPHTHERIA. From exudate in the throat of a case of diphtheria; showing irregularities of the bacilli in shape and size and coloration. It may be stained with Léffler’s alkalin methylen-blue solution or by Gram’s method. The diphtheria bacillus is subject to extreme variations in viru- lence, forms being met with in which all the usual cultural character- istics are not in the slightest degree virulent. These are sometimes inadvisably called pseudo-diphtherva bacilli. The name pseudo-diphtheria bacillus is more wisely limited to such germs as, though resembling the diphtheria bacillus, still present distinct cultural peculiarities. * TInoculations of virulent cultures subcutaneously in guinea-pigs are regularly followed by a localized hemorrhagic cedema with a variable amount of whitish exudate. Death usually follows the inoculation in from two to five days. In addition to the local lesions there may be—but this is not constant—swelling of the adjacent and 1Consult Park and Beebe, ‘‘ Report on Bacteriological Investigations ; Diagnosis of Diphtheria,” Bulletin No. 1, Health Dept., New York City, 1895; Studies and Bibliography. Digitized by Microsoft® THE INFECTIOUS DISEASES. 253 of the abdominal lymph nodes, serous effusions into the pericardial, pleural, and peritoneal sacs, swollen spleen, and acute parenchy- matous and fatty degeneration in the liver, kidney, and heart muscles; congestion and sometimes hemorrhage of the suprarenals. Micro- scopical examination shows, in a considerable proportion of cases, fragmentation of nuclei and other evidences of cell death at the seat of inoculation and in the viscera.’ Animals which survive the inoculations may later develop paralysis, and a similar result may follow the injection into rabbits of culture fluids. The bacilli do not gain access to the body at large, but may be found at the seat of inoculations. Inoculation into the mucous membranes of rabbits, pigeons, and certain other animals may result in the development of a pseudo-membrane somewhat resembling that of the disease in man.” During the growth of the diphtheria bacillus in nutrient broth an albuminous toxic substance is developed which mingles with the broth. This is called diphtheria toxin, and subcutaneous injections of this toxin in animals—guinea-pigs, for example—proves fatal, in appropriate dosage, with symptonis and lesions similar to those caused by inoculation with the living germ. It has been found that by repeated injections of the diphtheria toxins in susceptible animals, at first with small], then with gradually increasing doses, the animal may at length become so insusceptible to. the action of the poison that many times the usually fatal dose is borne without sensible reaction. Similar immunity can be conferred in certain animals by the use of the living cultures of the diphtheria bacillus either fully virulent or with reduced virulence (see page 179), administered at first in small doses which are gradually increased. In whichever way immunity be conferred it has been found that the blood of the artificially immunized animal contains a substance, or substances, called diphtheria antitoxin, which on being intro- duced with the blood serum into other susceptible organisms, may not only confer a quickly established immunity, but, without destroy- ing the diphtheria germ, may protect against its toxic effects when the disease is already under way. Thus through the artificial im- munization of horses the so-called “serum therapy” has assumed a ' For a detailed description of minute cell changes in animals following inocula- tion with diphtheria bacilli, see Welch and Flevner, Bulletin of the Johns Hopkins Hospital, August, 1891; also Abbott and Ghriskey, ibid., April, 1893. 2 It is important from the prophylactic standpoint to remember that the Bacillus diphtherie may remain alive in the mouth of the human subject for many weeks after recovery from the local lesions of the disease, and also that healthy persons. when the disease is prevalent may harbor the bacilli in their mouths. Digitized by Microsoft® 254 THE INFECTIOUS DISEASES. very important and beneficent réle in the prevention and management of diphtheria. Although there is no differential stain for the diphtheria bacillus, its morphological peculiarities are, as above indicated, so marked that when occurring in considerable numbers in the membranes or when examined from serum cultures definite conclusions as to its identity can usually be arrived at without recourse to complete biological analysis. But this as well as animal inoculations will often be necessary when the morphological characters are doubtful, and when the degree of virulence is to be determined. For the practical ends of early diagnosis it has been found that if a smear of material from the local lesion be made over the surface of a “slant tube” of Léffler’s blood-serum mixture, and placed in an in- cubator at blood heat for twelve hours, the diphtheria bacilli, if present, will usually have outstripped in growth most of the other germs which were present in the exudate. If now cover-glass preparations be made of a considerable quantity ef the new growth which is dotted in scarcely visible colonies over the surface of the serum, the presence or absence of the diphtheria bacillus can, in a large proportion of cases, be determined from its peculiar morphological features (Fig. 105). This method, elaborated by Park* and put into practice on a large scale by the Health Department of New York, has now become an almost indispensable factor in the control of diphtheria by health officials in many parts of the world, and is of especial importance in connection with the use of diphtheria antitoxin serum, whose highest promise lies in early administration. ' Consult Biggs, Park and Beebe, ‘‘ Report on Bacteriological Investigation and Diagnosis of Diphtheria, ” Bulletin No. 1, Health Dept., City of New York, 1895. Digitized by Microsoft® TETANUS. (Lockjaw.) This disease is caused by a bacillus—Bacillis tetani—which is rather widespread and in some places very abundant, occurring with other germs in the soil, especially in manured soil, and gaining entrance to the body through wounds, which are often very slight. The Bacillus tetani is a rather long, slender, motile germ, often growing in pairs or threads and prone to develop a spore in one end (Fig. 104), under which condition the bacillus swells at the end and becomes club or racket-shaped. It is readily stained. At the room temperature it grows on artificial culture media, and is strictly anaérobic, flourishing in an atmosphere of hydrogen. It fluidifies gela- tin after sending out into it irregular-shaped, ray-like outgrowths. 2NA\% AFA aN ae Fie. 104.—BaciuLus Teranti. From a culture. The spores of the tetanus bacillus are very resistant to drying, to heat, and to various chemical disinfectants. Characteristic tetanic symptoms followed by death may be induced in mice, guinea-pigs, and rabbits by subcutaneous inoculation of cultures. Man and the horse are markedly susceptible to tetanus; birds are as a rule insusceptible. The local lesion in tetanus is usually slight and not characteristic, often consisting in a slight suppuration. The morphology of the lesions of the nervous system to the exis- tence of which the symptoms of tetanus so directly point is yet obscure. Overfilling of the blood vessels, cellular exudate into the perivascular spaces, and rather indefinite changes in the ganglion cells have been recorded. The bacillus remains at the seat of local Digitized by Microsoft® 256 THE INFECTIOUS DISEASES. lesion and produces its effect by the elaboration of a most intense poison or toxin, called tetano-toxin. The action of this toxic sub- stance appears sometimes to continue in the body after the death of the organisms which have elaborated it. This infectious disease affords a most typical example of toxzemia. If the tetanus bacillus be grown in nutrient broth at blood heat out of contact with oxygen the toxin is developed and mingles with the Huid. This toxin when freed from living germs is capable of producing all the symptoms of the disease. Broth cultures may after some weeks have acquired such an ex- treme intensity that the dried poisonous material, separated from the inert Huids and partially purified, may be fatal to a mouse weighing 15 gm. in a dose of 0.00000005 gm. Estimating according to the relative weights of the subjects, the minimal] fatal human dose would be about 0.23 mgm. This toxin is rendered inert by a temperature above 65° C. and by light. By procedures similar to those described in diphtheria immuniza- tion (page 253), the tetanus toxin has been used to secure artificial immunity in dogs, goats, and horses, and here also the blood serum of the immunized animals has been prepared in a dried state and employed in man for therapeutic purposes with some degree of suc- cess. The theoretical promise of the tetanus antitoxin for therapeutic purposes in man is, however, in practice rendered in large measure futile, because the existence of the disease is not recognizable until the toxzemia is sufficiently marked to produce the nervous symptoms, at which time an enormous and not easily determined dosage is required to neutralize or counteract the effects of the already elabo- rated poison. Statistics are as yet too meagre to justify a definite opinion as to _ the practical value of serum therapy in tetanus. For purposes of diagnosis it may be necessary to inoculate a white mouse at the base of the tail with suspicious material at the same time that morphological examination and anaérobic cultures arel made. Should tetanus develop in the mouse within a few days con- trol cultures may be made from the exudate at the seat of inocula- tion. Digitized by Microsoft® INFLUENZA. (Epidemic Catarrhal Fever; La Grippe.) This is an infectious disease characterized by fever, physical and mental prostration, and inflammations of different parts of the body. It differs from the other infectious diseases in that, instead of a single characteristic lesion, there is a disposition to acute exudative inflam- mation of either the pia mater, the sheaths of the peripheral nerves, the conjunctiva, the ears, the nose and throat, the larynx, the bron- chi, the lungs, the pleura, the stomach, or the colon. Hither one or several of these inflammations may be developed at the same time, or successively in one individual. It is, however, not uncommon to see cases of influenza in which no one of these inflammations is present. The numerous bacterial studies which up to 1892 had been made on epidemic influenza had failed to reveal any micro-organism which could fairly be regarded as of etiological significance, although some of the complicating inflammations of the lungs had been shown to be very frequently associated with the pyogenic cocci—Staphylo- coccus pyogenes and Streptococcus pyogenes and the Diplococcus pneumoniz.’ Karly in 1892 Pfeiffer, Kitasato, and Canon’ described the occur- rence in the bronchial exudate and in the blood of influenza patients of avery small bacillus, hitherto unknown or possibly noted earlier by Babes. This bacillus was sometimes present in the bronchial exudate in enormous numbers, and often with little contamination with other germs. In the blood it was sometimes abundant, some- times scanty. It stains with some difficulty with the simple anilin dyes; but by Ziehl’s solution (page 224); or by warmed Léffler’s methyl blue (page 158); or by Czenzysnki’s fluid (page 283), heated with the specimen at body temperature for from three to six hours, it is readily colored. The bacilli are very slender and short (one to one and a half times as long as broad), sometimes lie singly, some- times in pairs or short chains or heaps, and are not motile. This so-called influenza bacillus grows best at body temperature. On glycerin-agar it forms very small, scarcely visible dewdrop-like 1 Consult Finkler, “Die acuten Lungenentziindungen, ” 1891, p. 452. 2 Deutsche medicinische Wochenschrift, January 14th and May 26th, 1892. 21 Digitized by Microsoft® 258 THE INFECTIOUS DISEASES. colonies; these, although growing close together, do not tend to coa- lesce, as many germs do. According to Pfeiffer the growth is more voluminous if the sur- face of the agar be smeared with blood—best of mau or the pigeon— since the hemoglobin appears to favor the growth. It does not grow at a temperature at which nutrient gelatin remains solid. In beef tea it forms a scanty, cloudy growth. It has been cultivated through several generations, but is prone to die. Animal inoculations have given diverse and not very marked results. The earlier observations have been in general confirmed by later studies of others.’ On the whole, we can only say at present that while the occur- rence of the above-described bacillus in influenza, and exclusively here, is interesting and apparently significant, we cannot yet definitely regard it as of established importance in the etiology of the disease. The observations of the writer upon this germ have been too limited to permit of an independent opinion. ‘For bibliography and later data consult Beck, “Ergebnisse der allg. Aetiologie der Menschen- u. Thierkrankheiten, ” 1896, p. 742. Digitized by Microsoft® * BACTERIA WHICH MAY BE OCCASIONAL INCITERS OF INFECTIOUS DISEASE IN MAN. Bacillus edematis malignt.—This bacillus, which is frequently present in dust, in putrefying substances, and in garden earth, con- siderably resembles the anthrax bacillus in form, but is more slender and has rounded ends. When it develops spores the bacillus is swollen or bellied at the middle. It is strictly anaérobic, growing readily in gelatin-agar and blood serum. It fluidifies gelatin. Gas is developed in its growth on blood serum. Several times this bacillus has been found in persons who have received dirty wounds, and it has been associated with hemorrhagic cedema, gas formation in the tissue, and gangrene. Similar lesions are produced by inoculation of the pure cultures in animals. This bacillus is readily stained by any of the common anilin dyes." Bacillus pneumoniee (Friedltnder).—In a small proportion of cases of lobar and lobular pneumonia, and in a few cases of exuda- tive inflammation of the pleura, pericardium, meninges, and middle ear, this bacillus has been found. It is sometimes found alone, but in pneumonia is frequently associated either with the Diplococcus pneumonie or with the pyogenic cocci. It has been found in the nasal secretion and mouths of healthy persons. While belonging definitely among the bacilli, it so frequently occurs in the form of very short rods or ovals or short chains that it was formerly thought to belong among the cocci. The bacilli, whether longer or shorter, single or in short chains, in cultures as well as in exudates, are sur- rounded by a narrow hyalin capsule. It grows readily, at ordinary room temperature, in gelatin, which it does not fluidify, forming a white mass, which, heaping itself upon the surface and less markedly along the puncture line, forms a rather characteristic “nail-like” growth. It grows abundantly on other culture media. It is moderately pathogenic for mice. It seems highly probable rather than proven that it may be at least: partially responsible for the lesions with which it is infrequently associated inman. This germ was formerly believed to be of great importance 1 Consult Novy, Zeitschrift f. Hygiene, etc., Bd. xvii., p. 209 (bibliography). Digitized by Microsoft® 260 THE INFECTIOUS DISEASES, in connection with acute lobar pneumonia, and for a time was gener- ally spoken of as the pneumocccus of Friedlander. It is now known not to be a coccus, and is certainly of subordinate if at all of serious importance in the induction of inflammation of the lungs. Its identity with the so-called Bacillus rhinoscleromatis (page 238) is claimed by some observers. If it be not identical with them it is closely related to capsulated bacilli found by Nicolaier’ in pus, by Abel*® in ozcena and found under various conditions and described under various names by Bordoni-Uffreduzzi, Pfeiffer, Mori, and others. Bacillus colt communts (“colon bacillus”).—This germ, which is of constant occurrence in the intestinal canal of man, is commonly reckoned among the saprophytes. It is both morphologically and biologically very similar to the typhoid bacillus, to which it appears to be closely related. It is dis- tinguishable from the typhoid germ by several well-marked cultural features, as well as by its pathogenic power. The points involved in the differential diagnosis of the colon from the typhoid bacillus are too intricate and numerous to be considered here. Recent studies, especially those of Welch, have shown that not infrequently when the Bacillus coli communis finds access to the peri- toneal cavity or other parts of the body where it does not belong, it is capable of inciting serious and even fatal disease. It may induce local suppurative inflammation, necrosis, and toxeemia. In the kidney, in the gall passages, in hemorrhagic pancreatitis, in appendicitis, and repeatedly in peritonitis, as well as in other lesions, it has been found either alone or in association with other germs. It would appear from the observations of Welch,* who found it in one or more of the organs of the body in thirty-three out of about two hundred autopsies, that lesions of the mucous membrane of the intes- tine, hemorrhage, ulceration, perforation, catarrhal and diphtheritic inflammation, strangulation, injury, etc., may open the way for its access to various parts of the body. In some cases its presence was associated with lesions, in some not. On the whole, it would seem that we are justified in regarding the colon bacillus as of occasional pathogenic importance in man. The limitations of its significance must be determined by further studies.* 1 Nicolater, Centralb. f. Bak., October 18th, 1894, p. 601. ® Abel, ibid., Bd. xiii., Nos. 5 and 6, 1893. 3 Welch, “The Bacillus Coli Communis: The Conditions of its Invasion of the Human Body, and its Pathogenic Properties, ” Medical News, December 12th, 1891. * For résumé of properties of the Bucillus coli communis, with bibliography, consult Darling, Boston Med. and Surg. Jour., November 15th and 22d, 1894. Digitized by Microsoft® THE INFECTIOUS DISEASES. 261 Micrococcus tetragenus.—This coccus growing in tetrads has been repeatedly found in cavities in the lungs in pulmonary tubercu- losis and in abscesses elsewhere. While its usual significance is not yet clear, it has been shown to be pyogenic. Bacillus pyocyaneus.—A pyogenic organism producing a green- ish fluorescence in culture media, is of occasional occurrence in sup- purative inflammation. It has been found in peritonitis and pericar- ditis, in broncho-pneumonia, in phlegmon, and under a variety of conditions in the gastro-intestinal canal.’ Bacillus proteus.—This germ is common in putrefying sub- stances, is frequently present in the intestinal contents; it grows in bizarre and irregular forms on gelatin and agar, and may apparently under certain conditions be pathogenic. Bacillus aérogenes capsulatus.—Several observers have de- scribed an anaérobic, gas-forming bacillus occurring in emphysema- tous phlegmons, in gangrene, in peritonitis, and also after death in cases with early and abundant post-mortem gas formation in the tissues, especially in the blood vessels and in the liver (see page 614). It is probable that the gas-forming anaérobic bacillus above named, which was first described by Welch and Nuttall in 1892, is identical with some of those which under different names has been since described by various observers.” 1 Kossel, Zeitschrift f. Hygiene und Inf. Kr., Bd. xvi., p. 368; also Jakowski, ibid., p. 474. 2 For a full consideration of thisimportant micro-organism see Welch and Fleaner, Journal of Experimental Medicine, vol. i., p. 5, 1896. Digitized by Microsoft® ACTINOMYCOSIS. This disease is due to the growth in the body of a micro-organism whose botanical position is not quite clear, but which seems to belong among the bacteria. This micro-organism, the actinomyces, appears to belong to one of the more complex groups of bacteria called the Cladothricacese, which develop in the form of branching filaments. These filaments in actinomyces frequently separate into longer and shorter rod-like or almost spheroidal segments. It may be grown on artificial culture media, flourishing best at body temperature. It at first develops in the form of delicate, Fie. 105.—ActTinomyces Bovis. Showing one of the yellowish masses of the parasite separated from the surrounding tissue. branching threads, the older cultures showing segments which resemble bacilli and cocci, and various bulbous, flask-like or club- shaped forms which appear to be the result of degeneration (“involu- tion” forms) (Fig. 105). Successful inoculations of cultures have been made in animals. This micro-organism grows in radiate masses, especially in the jaws of cattle, but is of occasional occur- rence in man. The fungous mass may form a large tumor in the jaw, by its own growth and by the formation of granulation tissue, which is apt to slough and spread, so that not only may the tissues of the tongue, pharynx, larynx, etc., be involved, but nodules of similar character may form in the gastro-intestinal canal, lungs, skin, etc. In man suppuration with necrosis and the formation of abscesses, Digitized by Microsoft® THE INFECTIOUS DISEASES, 263 ulcers, and fistulee may be the marked accompaniments of its growth in parts near the surface of the body. In the Jungs the lesions may be essentially those of an acute general bronchitis or in the form of broncho-pneumonia (Fig. 106), with the formation of new tissue. Abscesses and cavities may form which extend into adjacent parts. The characteristic masses of the micro-organism may be found in the sputum in these cases of actinomycosis of the lungs.’ In intestinal actinomycosis nodular masses of new tissue with Fic. 106.—ACTINOMYCES GROWING IN HumAN BRONCHUS. Tne bronchus is filled with a purulent exudate and its wall is becoming involved. ulceration may develop in the mucosa and submucosa. Metastases have been described. The fungus forms little yellow masses as large as a millet seed or smaller, which are scattered through the new-formed granulation tissue or mingled with the pus, giving the growths a very character- istic appearance. It is the peculiar radiate grouping of the filaments of the growth (Fig. 106) which gave rise to the name “ray fungus.” ' For a detailed description of the lung lesions in actinomycosis, with general bibliography, see Hodenpyl, “ Actinomycosis of the Lung,” New York Medical Record, December 18th, 18M gitized by Microsoft® 264 THE INFECTIOUS DISEASES. The disease is propagated from one animal to another by inoculation or by contact of the growth with a wound or an abrasion of the mucous membrane. The fungous masses may become calcareous. In the examination of sputum, feces, pus, etc., for the presence of actinomyces, the naked-eye appearances may be of value, since the yellowish-white granules are often quite visible, especially ona black background. Suspicious masses may be teased ‘and studied unstained, or stained by Gram’s method. Sections of tissue contain- ing actinomyces may be hardened in alcohol, and sections stained by Gram’s method with contrast eosin stain. Digitized by Microsoft® ASIATIC CHOLERA. In some cases of cholera there are no marked changes to be found after death. In no case are the lesions distinctive of this disease. If death occur during the invasion of the disease or in the stage of collapse, the appearances may be as follows in the more marked cases : The bodies remain warm for some time, and the temperature may rise for a short time after death. The rigor mortis begins early and lasts for an unusually long time. The muscles sometimes exhibit a peculiar spasmodic twitching before the rigor mortis sets in, especially the muscles of the hand and arm. The Skin is of a dusky gray color, the lips, eyelids, fingers, and toes of a livid purple. The ends of the fingers are shrivelled, the cheeks and eyes fallen in. The Brain.—The sinuses of the dura mater are filled with dark, thick blood. The pia mater may be normal, or edematous, or ecchy- mosed, or infiltrated with fibrin. The brain is usually normal, but may be dry and firmer than usual. The Lungs are retracted and anzemic, the pleura may be dry or coated with fibrin. The Heart is normal. The Peritoneum may be dry or coated with a layer of fibrin. The Stomach is usually unchanged, but may be the seat of ca- tarrhal inflammation. The Small Intestine.—There may be ecchymoses in the mucous membrane; the mucous membrane may be soft and cedematous; there may be general congestion, or the congestion may be confined to the peripheries of the solitary and agminated nodules, and these nodules may be swollen; or there may be croupous inflammation and superficial necrosis. All these changes are regularly most marked at the lower end of the small intestine. There is apt to be post-mortem desquamation of the epithelium. The characteristic rice-water fluid may be found in the intestines after death, or instead of this dark- colored, bloody fluid. The Large Intestine is usually normal, but in some epidemics croupous inflammation occurs in a considerable number of cases. Digitized by Microsoft® 266 THE INFECTIOUS DISEASES. The Spleen may be soft. The Liver may show small areas of granular or fatty or hyalin degeneration. The Kidneys are often increased in size, with white and thick- ened cortex and congested pyramids. The epithelium of the cortex tubes may contain coarse granules and fat globules, or be necrotic. The tubes may contain cast matter and broken-down epithelium. These changes may be looked upon as being simply of a degenerative character or as the results of an acute degeneration from absorbed toxins. The Uterus and Ovaries may be congested and contain extra- vasated blood. If the patient do not die until the stage of reaction, the body does not preserve the same collapsed appearance, and there are often inflammatory changes in different parts of the body, especially in the larynx, the lungs, the stomach, and the intestines. According to the researches of Koch, which have been abundantly confirmed by others, there are constantly present in the small intes- phe, MAE oy Fic. 107,—SPIRILLUM CHOLER# ASIATIC, From a culture. tines of cholera patients, during the early and active stages of the disease, characteristic curved rods which are not known to occur in the body under any other conditions, and which have been proved to cause the disease. These rods are from 0.8 to 2.0 » long, and are sometimes slightly, sometimes considerably curved (see Fig. 107). When growing under suitable conditions, the individual rods are apt to cling together by their ends, forming S-shaped figures or spirils of considerable length. From the curved shape of the individuals they are also often called “comma bacilli;” but the organism appears to belong among the spirilla and is therefore called Spirtllum cnolercee Asiatice (or “Cholera vibrio”). The spirilla may be present in moderate numbers in and beneath the mucous membranes of the intestine, and in very large numbers in the intestinal contents and in the dejections in the acute forms and early stages of the disease. In the process of their growth and multiplication in the intestinal canal they apparently produce a poisonous substance, the local action and absorption of which into the body fluids produce the symp- toms and lesions of the disease. The systemic effects appear to be in Digitized by Microsoft® THE INFECTIOUS DISEASES. 267 the nature of a septic intoxication. Thecholera bacillus may retain its vitality for a considerable period in water, and on moist substances, such as damp linen, earth, and vegetables, it may increase in num- bers with great rapidity. A temperature of from 30° to 40° C. is most favorable for its growth. At about 16°C. proliferative activities cease, but the germs are not killed by —10° C. They are readily killed by drying, and the presence of acids is very inimical to their growth. There is not sufficient evidence that they form spores, and their period of life is short. The cholera bacillus is readily cultivated on artificial culture media, such as gelatin, agar, milk, beef tea, potatoes, etc. In fluids it is capable of performing active movements and is furnished with flagella. While it may be readily stained by the ordinary methods when present in the dejecta, its morphological characters are not absolutely distinctive, since several forms of curved bacilli belonging to the same group and closely resembling the cholera vibrio have, undir varying conditions, been found in the dejecta and in the mcuth. It is often of the highest importance to determine, at the earliest possible moment, whether or not a suspected case be one of Asiatic cholera or some other form of acute intestinal disorder, so that in the former case the proper measures may be instituted to prevent the spread of the disease. The characters which are developed in cultures of the cholera bacillus enable an expert biologist to distin- guish this organism from all other known forms. But the scope of this work does not permit a detailed description of the cultural peculiarities of the germ. Nor should the responsi- bility of such determinations be assumed without adequate prelim- inary laboratory experience. By taking together the morphological and biological characters, it is possible, usually on the second or third day, to determine whether the intestinal contents of a suspected case do or do not contain the bacillus of Asiatic cholera. The cholera vibrio, both in the dejecta and in pure cultures, is readily stained by the ordinary anilin dyes. The results of animal experiments with the cholera germ are not in themselves decisive in determining its relationship to this disease, since animals do not react in its presence as man does. However, the constant occurrence of this organism in Asiatic cholera, its absence under other conditions from the body, and the accidental laboratory infections which have several times occurred in men handling pure cultures of the germ, leave no doubt as to its instrumentality in the causation of the disease. Digitized by Microsoft® 268 THE INFECTIOUS DISEASES. The disease is communicated from one person to another by the pollution of food or drink with the discharges which contain the virulent germs. The results of a large amount of work which has been done, look- ing toward a practical artificial immunization of man against Asiatic cholera in the East have not yet been sufficiently definitely formulated to permit a final judgment as to its value.’ 1 For the details of his researches on Asiatic cholera, see Koch’s report, “ Arbeiten a. d. kaiserlichen Gesundheitsamte, ” Bd. iii., 1887. Consult also Shakespere’s “ Re- port on Cholera in Europe and India, ” 1890. For bibliography of recent studies see Dunbar, “Ergebnisse der allg. Aetiologie der Menschen- u. Thierkrankheiten, ” 1896, p. 804. Digitized by Microsoft® RELAPSING FEVER. (Typhus recurrens; Famine Fever; Spirillum Fever; Seven Day Fever.) The lesions which may be present in this disease are not distinc- tive of it. Its distinguishing feature, apart from symptoms, is the presence in the blood at certain periods of the specific micro-organism. Fie. 108.—SprrocHX2TE OBERMEIERI IN THE BLOOD IN A CASE OF RELAPSING FEVER, The Skin may be jaundiced; it may be mottled by extravasations of blood. The Brain and Spinal Cord are unchanged. The Pharynx and Larynx may be the seat of catarrhal or croup- ous inflammation. The Lungs.—There may be bronchitis, broncho-pneumonia, lobar pneumonia, hypostatic congestion, and pleurisy. The Heart is often soft and flabby, with degeneration of its mus- cular fibres. There may be ecchymoses in the pericardium. Digitized by Microsoft® 270 THE INFECTIOUS DISEASES. The Stomach and Small Intestine may be congested; there may be ecchymoses in the mucous membrane; there may be catarrhal inflammation. The Colon may be the seat of catarrhal or croupous inflammation. The Mesenteric Nodes may be swollen. The Liver is often enlarged and the hepatic cells are swollen and granular. The Spleen is large and soft. The change in its consistence is so marked that the spleen may rupture spontaneously during life. The spleen may also contain infarctions of different sizes; some are red, some yellow, some necrotic. Those which are necrotic may give rise to a local or general peritonitis. The Kidneys show the lesions of parenchymatous degeneration. Degenerative and hyperplastic changes in the medulla of the bones have been described. Bacteria.—In the blood of all parts of the body during the febrile attacks may be found, in very large numbers, a long, slender spiril- lum called from its discoverer Spirocheete Obermeieri. It disappears from the blood during the afebrile intervals. The organism is from 14 to 40 » in length, and performs rapid, undulating movements (Fig. 108). The inoculation of healthy men and of monkeys with the blood of relapsing-fever patients which contains the bacteria induces a similar disease. Pure cultures have not as yet been made of these bacteria, but for the reasons indicated, and since the organism has never been found except in connection with the disease, there is every reason for believing that the Spirochete Obermeieri is the cause of relapsing fever. Digitized by Microsoft® VARIOLA. (Small-pox.) Small-pox is an acute, readily communicable, infectious disease, especially cuaracterized anatomically by an inflammation of the skin which passes through a series of more or less distinctive phases of papule, vesicle, pustule, with a final drying of the exudate and necrotic tissue constituting the crust. _Various phases of the exanthem are used to designate forms of the disease. Secondary lesions are diffuse suppurative inflammation of the skin, inflammations of the mucous membrane, hemorrhages in various parts of the body, and acute degeneration of the kidney, liver, and spleen. The skin lesion shows in general at first circumscribed areas of inflammation above the ends of the papille, with the development of a fluid-filled reticulum, so that vesicles are formed (Fig. 109). These at first contain a clear fluid, but by the gathering of pus cells the fluid becomes turbid and accumulates to form a pustule. Hand-in-hand with these changes the papille and adjacent layers of the corium may become infiltrated with cells. The contents of the pustules and the necrotic tissue above dry and form the crusts. When the changes are largely confined to the epidermis the lesion may leave no deform- ity. But if the changes in the cutis are considerable, cicatricial Digitized by Microsoft® 272 THE INFECTIOUS DISEASES. tissue may form, leaving scars. The association of local hemor- rhage with the above changes gives rise to the hemorrhagic form of exanthem. Various micro-organisms, both bacteria and protozoa, have been described as occurring in the local skin lesions of small-pox, but the cause of the disease is still unknown. The protection conferred by a successfully weathered attack of small-pox is one of the most striking examples of this form of ac- quired immunity (see page 179). The more recent views of the im- munity conferred by vaccination against small-pox is based upon the demonstration that the disease variola in man and the disease vaccina in the bovine species are the same, and not different, as was formerly believed; that the disease in the cow is only a modified form of the human disease. The effect of the passage of the unknown but cer- tainly existing micro-organisms through the insusceptible bovine— thus runs the rationale in the new light—is to so diminish the viru- lence of the germ that by its subsequent inoculation in man im- munity is produced without the profound disturbance which infection with a germ of unmitigated virulence would involve. Digitized by Microsoft® SCARLET FEVER. (Scarlatina.) This is an infectious, readily communicable disease characterized by a diffuse skin eruption, and frequently accompanied by inflam- mation, either catarrhal, croupous, or gangrenous, of the tonsils, pharynx, and larynx. There may be acute hyperplasia or suppuration of the cervical lymph nodes. There is very frequently an acute exudative or an acute diffuse nephritis. The spleen may be enlarged. Broncho- pneumonia, endocarditis, and pericarditis may occur. The exanthem or skin eruption in scarlatina is a simple dermatitis, as the result of which the papille and subpapillary stratum become infiltrated with fluid or leucocytes, or both, the leucocytes being gathered especially about the blood vessels. There may be small hemorrhages, and the acute phase of the inflammation is followed by an increased production of epithelium and an exfoliation of the super- ficial layers. These lesions of the skin are, excepting the hemor- rhages, very slightly marked after death. That the disease is due to some form of micro-organism there can be no doubt. The exact nature of this organism is not yet known. The acute nephritis so often present appears to be due to some poison produced in the body during the disease. One of the most marked features of the disease is the predisposition which it entails to the incursions of pathogenic germs other than those which we believe to cause the disease itself. Thus an infectious croupous inflammation in the mouth, tonsils, pharynx, larynx, and trachea, due to a strepto- coccus (see page 205), is a frequent complication. True diphtheria due to the Léffler bacillus is also prone to establish itself upon the vulnerable inflamed mucous membranes. So also the frequently associated pneumonia, the inflammatory hyperplasia and suppuration of the lymph nodes, suppurations in various parts of the body, the endocarditis and pericarditis which are not uncommon, may all be due to a secondary infection with the pyogenic cocci. 22 Digitized by Microsoft® MEASLES. A readily communicable infectious disease, the most prominent features of which are an intense hyperemia with inflammation of the skin, associated with catarrhal inflammation of the mucous mem- brane of the air passages. The inflammation of the skin is anatom- ically of thesame general type as that in scarlatina. Acute degener- ation of the kidney or acute exudative nephritis may follow. The more common secondary lesions are broncho-pneumonia, pseudo- membranous inflammation of the pharynx and larynx, suppurative inflammation in various parts of the body, and diphtheria. These complications, as in scarlatina, are doubtless, in part at least, due to secondary infection with other germs than those causing the disease itself. The micro-organism causing measles is not known.’ 1 Canon and Pieliche in 1892 (Berliner klin. Wochenschrift, April 18th, No. 16) recorded the discovery in the blood in fourteen cases of measles of a very small bacillus, about as long as the radius of a red blood cell, but varying considerably in size. It is best stained with Czenzynski’s solution (p. 68), or with a solution containing one-half the amount of eosin. Sometimes the staining is uniform, some- times the middle portion is paler. These bacilli were sometimes abundant, some- times scanty in the blood, lying singly or in heaps. Meagre cultures were obtained in three cases in beef tea. They did not seem to grow on the ordinary solid media. Bacilli similar in form were found in the exudate from inflamed mucous membrancs in measles. The observations of these writers are interesting and suggestive, but until they shall have been confirmed by others and been greatly extended nothing can be regarded as established regarding the etiological significance of the germs. Digitized by Microsoft® TYPHUS FEVER. (Hospital Fever; Spotted Fever; Jail Fever; Ship Fever; etc.) This disease has not, so far as we know, any characteristic lesion save the petechial skin eruption; but yet after death we may finda number of morbid conditions, such as are common to many of the infectious diseases. The entire body has a tendency to rapid putrefaction. The blood is often darker and more fluid than in other diseases. The voluntary muscles may undergo waxy and granular degener- ation. The brain and its membranes may be congested. The mucous membrane of the pharynx and larynx may be the seat of catarrhal or croupous inflammation. In the lungs there may be bronchitis, broncho-pneumonia, or hy- postatic congestion. The walls of the heart may be soft and flabby. The agminated nodules of the ileum, and the mesenteric nodes may be a little swollen. The spleen is often large and soft. The kidneys and liver are frequently the seat of parenchymatous degeneration. The nature of the infective agent in typhus is unknown. Several observers have recorded the finding of micro-organisms of one kind or another in the disease, but proof that any of these have causative relationship to the disease has not yet been furnished.' 1 Brannan and Cheesman, “A Study of Typhus Fever, ” Medical Record, June 25th, 1892. Digitized by Microsoft® HYDROPHOBIA. (Rabies.) The lesions which have been found in this disease are not constant nor are they characteristic. Though well marked in some cases, they are but very slightly developed in others. The lesions, when present, are apt to be most marked in the medulla oblongata and pons, but they may be present in the cord (Fig. 110). They consist of small hemorrhages, accumulation of Fie. 110.—Section oF SPINAL CorD FROM A CASE OF HYDROPHOBIA. Showing large accumulation of leucocytes about the blood vessels, both in the gray and in the white matter, (From a specimen prepared by Van Gieson. ) leucocytes about the blood vessels in the perivascular lymph spaces and around the ganglion cells, and of thrombi in the smaller blood vessels, and of degeneration of the ganglion cells especially in the spinal cord.’ None of these lesions are, however, pathognomonic of this disease. 1 Babes, Annales de |’ Institut Pasteur, April, 1892, and August, 1895. For an account of lesions in experimental rabies consult Golgi, Berliner klin. Wochenschrift, April 2d, 1895. Digitized by Microsoft® THE INFECTIOUS DISEASES, 277% While there is every reason for believing that hydrophobia is due to the introduction into the body of some special form of micro- organism, and while the recent researches of Pasteur and others have brought to light many interesting and important facts regarding the general nature and distribution in the body of the infectious agent, nothing is yet definitely known about the particular organism which induces the disease. It is known that the infectious agent is in the saliva and salivary glands of rabid animals, and that it may be present in the saliva of the dog two or three days before the symptoms of the disease are manifest. It is not present in the blood, but seems to be especially Fig. 111.—HypropHosiA, TRANSVERSE SECTION OF SMALL BLooD VESSELS IN THE SPINAL CorD. From the same case as Fig. 110, more highly magnified. Showing accumulation of leucocytes and proliferation of connective-tissue cells in the adventitia of the vessels. concentrated in the central nervous system and particularly in the medulla oblongata. Notwithstanding the total ignorance of the micro-organism con- cerned in inciting hydrophobia, his genius in wise experiment en- abled Pasteur to discover and to establish a method for artificial immunization against the disease which has proved most beneficent. After obtaining a virus of definite intensity, which was accom- plished by a series of inoculations beneath the dura mater in rabbits of portions of the spinal cords of rabid animals, it was found that by drying spinal cords of definite and high virulence in the air, with due protection against aérial contamination, the virulence diminished Digitized by Microsoft® 278 THE INFECTIOUS DISEASES. day by day. With virus thus obtained of virulence ranging from that which is practically inert to that of the utmost potency, it has been found possible to safely accustom both animals and men to the presence of amounts of hydrophobia virus contained in the spinal cord emulsion, which under ordinary conditions would prove speedily fatal. In other words, it has been found possible to confer artificial immunity against the disease. This process occupies several days, and immunization must be completed before the disease has begun to manifest itself; but as the incubation period in hydrophobia is a long one, it has been possible, in a large and increasing number of cases, to save the lives of persons bitten by rabid animals. In view of the importance of diagnosis, in dogs which have died or have been killed under suspicion of rabies, the spinal cord and medulla should be saved. Portions of the fresh medulla in emulsion water should, if possible, be inoculated beneath the dura mater of two healthy rabbits and the development of rabic paralysis and other symptoms observantly awaited. Other portions of the medulla and cord should be hardened in Miiller’s fluid and alcohol, and carefully examined especially for small perivascular accumulations of leucocytes. The existence of these in the medulla and cord of an animal suspected of rabies will go far toward confirming the suspicion. Digitized by Microsoft® YELLOW FEVER. This infectious disease is without characteristic lesions save for the hemorrhages and pigmentation in the skin. The following con- ditions are, however, frequently present after death: Rigor mortis is marked and occurs early. The Brain and its meninges are usually congested. The Skin is of a yellow color from the presence of bile pigment, and may be mottled by ecchymoses. The Heart is of a pale or brownish-yellow color. Its muscular fibres may be the seat of fatty degeneration. The Lungs may be congested. The Stomach often contains the characteristic black fluid due to altered blood pigment which is vomited during life. Its mucous membrane may be congested, softened, and is sometimes eroded. The Intestines are dark-colored, often distended with gas, and sometimes contain blood. The Liver in the earlier stages of the disease may be intensely congested. More frequently it contains but little blood, is of a light- yellow color, and the hepatic cells show the changes of an intense acute degeneration, much more marked than are found in any other disease except acute yellow atrophy of the liver. The gall bladder is apt to be contracted. The Spleen shows no marked changes. The Kidneys present the lesions of an intense form of parenchy- matous degeneration. Tubules usually contain masses of hyalin material. While its mode of occurrence and the characters of its symptoms and lesions afford a strong presumption that yellow fever is an acute infectious disease, none of the various studies which have been made upon its etiology have as yet revealed the presence of any micro- organism to the action of which it can be fairly attributed.’ 1 The studies of Sternberg on the “Etiology and Prevention of Yellow Fever, ” published in the form of a Government report in 1890, contain the result of a great deal of research by modern methods, and should be consulted for a full exposition of this disease and its lesions. Digitized by Microsoft® THE MALARIAL FEVERS. The characteristic lesions of malarial poisoning are certain changes in the blood, the spleen, and the liver. In the more intense and acute form of malarial poisoning the blood contains numerous particles of black or brown pigment, which are either free or embedded in cells resembling the white blood cells or in the endothelium of the blood vessels. After death this pigment is found in the blood vessels throughout the body, but is most abun- dant in the blood vessels of the liver (see Fig. 293) and spleen. These organs are then usually of large size and of a peculiar brown or black color. In some of these severe cases there are also extravasations of blood from the mucous membranes and in their substance. There may also be general jaundice. Focal necroses in the viscera similar to those occurring in other infectious diseases have been described. In the milder and more protracted cases of malarial poisoning the composition of the blood is altered and the patient may become pro- foundly anemic. The spleen may become the seat of chronic inter- stitial inflammation with pigmentation (see Fig. 305). The liver may exhibit the changes of chronic interstitial hepatitis. The attempts to establish a causative relationship between the various forms of bacteria which from time to time have been found in the bodies of persons who are the victims of malarial poisoning, and the symptoms and lesions of the disease, have all been unsuc- cessful. On the other hand, a large number of careful studies by various observers have led to the general belief that the disease is due, not to vegetable, but to intercellular animal organisms which are very constantly found in the blood of affected persons. These organisms, which belong among the protozoa, may be ap- propriately called the hematozoa of malaria. They are, however, often called the Plasmodia malariz. In brief, the facts upon which this belief rests are as follows: The blood of those suffering from malarial poisoning may contain, which the blood under other conditions does not, one or more of the structures which are shown in Fig. 112. Digitized by Microsoft® THE INFECTIOUS DISEASES. 281 1. Inside of the red blood cells may be found colorless bodies, sometimes occupying a small part, sometimes nearly filling the cell. These bodies may or may not contain pigment granules. They may exhibit amceboid movements (a and b). They are called the ame- boid bodies. 2. Colorless discoidal bodies, usually a little larger than the red blood cells, which contain pigment particles, sometimes scattered irregularly, sometimes grouped toward the centre. These are be- lieved by some observers to be the later developmental stages of the Fig. 112.—TH&t Hamatozoon or MauaRia (PLASMODIUM MALARL®) IN THE BLoop. a, unpigmmented amoeboid body ina red blood cell; b, pigmented amveboid body; ¢, colorless discoidal body with pigment; d, segmenting body; e, fragments of segmenting body; f and g, crescentic bodies; h, flagellate body. a,b, d,e,f,gare drawn from specimens of malarial blood prepared by Dr. Walter James; c and h are drawn after sketches by Dr. James. amceboid bodies, which have increased in size at the expense of the red blood cells. A grouping of pigment granules indicating segmen- tation is sometimes seen in these bodies. These are called the en- cysted bodies (c). 3. Bodies, about the size of a red blood cell, which are composed of a congeries of irregularly rounded structures grouped about a central mass of pigment. These are called segmenting bodies or rosettes (d). 4. Smaller isolated or clustered structures which are apparently 2: : Digitized by Microsoft® 282 THE INFECTIOUS DISEASES. the result of the breaking apart of the segmenting bodies, as seen at e. Often called spores. 5. Crescentic bodies containing a central mass of pigment (f and g). 6. Bodies, smaller than a red blood cell, which are actively mobile und are furnished with one or more flagella at one side—h, flagel- late form. These are the main forms which have been described. The amceboid forms are apt to occur in the acute stages of the disease, the crescentic forms in the chronic stages. The segmenting bodies are apt to be present immediately before or during the chill; the pigmented amceboid bodies, according to James, are present at all {imes, but are most numerous during and before the paroxysms. In general, it may be said that the number of these bodies is proportional to the gravity of the case. The amceboid forms disappear shortly after the administration of quinine, while the crescentic bodies often persist for a considerable time under the same conditions. It is believed that these various forms represent phases in the clevelopment of one or more varieties of the parasite. The cycle of «levelopment appears to be brief—in the organism of tertian fever about forty-eight hours—in that of quartan about seventy-two hours —and quickly recurrent; so that paroxysm may follow paroxysm, the height of each corresponding to the sporulation or segmentation of the parasite. If the body be infected with a single brood or growth of the para- sites the paroxysm will be apt to recur regularly, in accordance with a simple type; but should two or more broods or groups, reaching the period of sporulation at different times, be present, the paroxysm will recur with greater frequence and at less regular intervals. While much is known about the hematozoa of the various phases of malarial fever, much study is still necessary for the completion of their life histories, and much more light is needed on the way in which the parasites produce their effects in the body, aside from the destruction of the blood cells, to which pigmentation is due. All attempts to cultivate the organisms under artificial conditions have thus far failed. While by the direct transference of malarial blood from animal to animal and from man to man the disease may be induced, under the ordinary conditions of life it is not communicable; nor do we know the habitat of the organism in nature or its portals of entry to the body. Whatever its full etiological significance or its life history, its discovery in the blood, even with our present knowledge, since it is unknown except in malarial disease, is of great diagnostic value in doubtful cases.’ ' For bibliography and a résumé of the work already done on this subject con- Digitized by Microsoft® THE INFECTIOUS DISEASES. 283 Method of Examination.—The fresh blood taken from a finger prick may be examined in thin layers on the warm stage with one- twelfth oil immersion. For stained preparations the method described on page 88 may be followed, or, after spreading and fixing the blood film as above, the cover may be floated, specimen side down, for from ten to fifteen minutes in Czenzynski’s fluid: Aqueous Methylen Blue, saturated solution...... 20 ¢.¢. One-half-per-cent solution of Eosin in seventy- per-cent Alcohol.................00. Soat babys elo Water............ Dra. Wah dea Get mete oe om Me Fia. 178.—GANGLION CELLS OF THE SPINAL CoRD. Stained by Nissl’s method with methylene blue. Showing, A, normal ganglion cells; B, gan- glion cells in acute myelitis with marked changes in the chromophy lic masses of the cell bodies. interpretation of appearances in a field in which the morphological norm has been as yet so inadequately investigated and in which nutritional and functional changes are still so obscure.’ SECONDARY DEGENERATIONS. Lesions of the brain which involve the destruction of motor gan- 1 An interesting consideration of the relation of infectious processes to diseases of the nervous system, by Putnam, may be found in the American Journal of the Medical Sciences, March, 1895. For a résumé of the recent observations on the degenerative and regenerative proc- esses in the nervous system, with bibliography, consult Stroebe, Centralbl. f. allg. Path. und Path. Anat., December 15th, 1895. Consult also Berkley, Medical Record, March 7th, 1896. 31 Digitized by Microsoft® 378 THE NERVOUS SYSTEM. glion cells or nerve fibres are regularly followed after a time by de- generative changes in these nerve fibres below the seat of lesion. It is particularly lesions in the central convolutions, the internal cap- sule, portions of the corona radiata, and the pes pedunculi, which destroy the motor fibres passing through these parts, and are followed by degenerative changes in the fibres below. The most important and frequent lesions followed by this effect are those involving the anterior two-thirds or three-fourths of the internal capsule. It will suffice merely to mention these changes here, as they are considered more in detail in the section devoted to lesions of the spinal cord (page 393). HYPERTROPHY AND ATROPHY OF THE BRAIN. True Hypertrophy of the brain is rare, and probably always con- genital. An increase in the size of the brain from the proliferation of the neuroglia sometimes occurs in children either before or after birth, less frequently in youth, and very seldom in adults. The white substance of the hemispheres is increased in amount. If it take place before the ossification of the cranium, the bones are sep- arated at the sutures and fontanelles; if after this, the inner table of the skull may be eroded and thinned. When the cranium is opened the dura mater appears tense and anemic, the convolutions of the brain are flattened, the brain substance is firm and anzemic, the ven- tricles are small, the ganglia and cerebellum are either of normal size or compressed. The disease is usually very chronic, and destroys life with symp- toms of compression of the brain. There may, however, be acute exacerbations. Atrophy.—This may occur as a senile change, or, in adults, in chronic alcohol, opium, or lead poisoning, in chronic insanity, and in chronic meningitis or from local interference with the circulation. In children who are much reduced by chronic diseases atrophy of the brain may accompany atrophy of the rest of the body. The atrophy affects principally the cerebral hemispheres, and may be uniform or more marked in some parts than in others, involving the whole of a hemisphere or of a lobe or only single convolutions or groups of these (Fig. 179). The convolutions are small, the sulci broad, the ventricles usually dilated, the brain tissue firm, the gray matter discolored, the white substance grayish in color; the blood vessels may be dilated. The basal ganglia may be small. Serum accumulates in the pia mater and the ventricles; the pia mater, and often the skull, become thickened; the brain tissue may be cedema- tous or contain small hemorrhages. The nerve elements of the brain Digitized by Microsoft® THE NERVOUS SYSTEM. 379 tissue are those most involved in the atrophy, the diminished areas being usually harder and firmer than normal. WOUNDS OF THE BRAIN. The brain may be directly wounded by a foreign body, or indi- rectly by fragments of bone driven into it, or it may be lacerated by severe contusion without fracture or solution of continuity of the skull. It is very difficult to estimate the degree of injury which must cause death, since persons frequently die from slight, and may Fic. 179.—ATROPHY OF A CIRCUMSCRIBED PorTION oF BRAIN CONVOLUTIONS IN A CHILD. From a lesion of the corresponding blood vessels. (From a specimen loaned by Dr. Freeman.) recover from very severe, wounds of the brain. In incised wounds of the brain more or less hemorrhage occurs at the seat of lesion, and the brain tissue in the vicinity soon undergoes degenerative changes. These may be comparatively slight or extensive. Inflammatory re- action may occur in the vicinity, and the adjacent brain tissue, as well as the hemorrhagic and degenerated area, become infiltrated with pus cells. After a time the injured and degenerated area may become surrounded by new-formed connective tissue, and the de- composed extravasated blood and detritus of brain tissue, more or less fatty, may be absorbed, and thus after a time the part heals by Digitized by Microsoft® 380 THE NERVOUS SYSTEM. a more or less pigmented cicatrix. The healing is in most cases very slow and may occupy months or even years. The pia mater may participate to a marked degree in the inflammatory healing process. Abscesses may form near the seat of injury. After wounds which involve the removal of portions of the cra- nial bones, it is not uncommon after a few days to see a bleeding fungous mass project through the opening. This mass, some- times wrongly called hernia cerebri, consists of degenerated brain tissue, blood, and granulation tissue, with more or less pus. The brain tissue below itis degenerated, broken down, soft, and puru- lent, and there is often abscess in the adjacent brain tissue. Such wounds may finally heal by the absorption of the broken-down brain tissue and blood, and its substitution by granulation tissue. Lacerations of the brain tissue without fracture may appear shortly after the injury as simple more or less circumscribed areas of capillary hemorrhage ; the brain tissue about these may degene- rate, pus may form, and abscesses be developed ; or the degenerated and lacerated tissue may be gradually replaced by granulation tis- sue which finally forms a cicatrix. The process of degeneration and softening and of healing in such lacerations of brain tissue may occur very slowly indeed, even occupying years, and not infre- quently the degenerative changes are very extensive and progres- sive. In many cases, of course, the injury is so extensive, or in- volves such important parts of the organ, that very little or no inflammatory or degenerative change takes place before death. HOLES OR CYSTS IN THE BRAIN (PORENCEPHALUS). Larger and smaller holes may be found in the brain tissue from dilatation of the perivascular lymph spaces, or well-formed cysts may exist from hemorrhage, inflammatory softening, hydatids, etc. There are, however, cases in which one or several holes of varying size are found in the brain which cannot be determined to have either of the above modes of origin. They may lie deep in the brain substance or close under the pia mater, or may communicate with the ventricles. This condition is sometimes called porencephalte, and may co-exist with various mental aberrations, hydrocephalus, etc." INFLAMMATION OF THE BRAIN (ENCEPHALITIS). It has been already mentioned that the brain tissue about heemor- rhages and areas of embolic and thrombotic softening may undergo 1 Consult v. Kahiden, “Ueber Porencephalie,” Ziegler’s Beitr. zur Path. Anat., etc., Bd. xviii., p. 231. Digitized by Microsoft® THE NERVOUS SYSTEM. 381 inflammatory changes leading to the formation of new connective tissue. There is a class of cases in which localized areas of the brain undergo softening, with more or less extravasation of red and white blood cells and hyperzemia of the blood vessels, so that the softened material consists, as seen under the microscope, of detritus of brain tissue in a condition of fatty degeneration, with more or less pus cells or pigment. When such areas are red in color from inter- mingled blood cells or pigment the condition is called red inflam- matory softening. When fatty degeneration prevails, and the red blood cells or their derivatives are not abundant, the softened area looks yellow or yellowish-white, and this is often called yellow in- flammatory softening. The origin of these processes is very ob- scure and their inflammatory nature not well defined. Abscess of the Brain.—The small multiple abscesses of the brain which occur with pyemia form part of that disease and require no separate description. The large single abscesses occurring under different conditions are those to which the name of ‘“‘abscess of the brain” is usually applied. These abscesses occur in two forms : The non-capsulated abscess, an irregular cavity containing thin pus and softened brain tissue. The walls of the cavity are ragged and infiltrated with pus, and outside of the walls is a zone of cede- matous and softened brain tissue. If the abscess is near the pia ma- ter it may set up a meningitis; if itis near the lateral ventricles it may rupture into them ; if it is near the sinuses of the dura mater it may cause thrombosis. The encapsulated abscess has a capsule of connective tissue, and contains thin or cheesy pus. Abscesses of the brain are usually single ; they may attain a con- siderable size. They are most frequent in the cerebral and cere- bellar hemispheres, rare in the central ganglia, the pons, and the medulla oblongata. The most common cause of this disease seems to be chronic sup- purative otitis (42.5 per cent, Gowers), while acute otitis is a com- paratively rare cause. With the otitis there may also be caries of the temporal bone, suppuration of the mastoid cells, and inflamma- tion of the dura mater. The abscess is usually situated deep in the brain ; only rarely is it continuous with the inflamed dura mater and bone. When the abscess is deeply situated, and the bone and dura mater are not diseased, it is difficult to tell how the infection travels from the ear to the brain. Abscesses due to this cause are situated in the temporo-sphenoidal, the frontal, the occipital, and the parie- tal lobes, or in the cerebellum. Digitized by Microsoft® 382 THE NERVOUS SYSTEM. Another frequent cause of abscess of the brain is traumatism— blows or falls on the head (24 per cent, Gowers). Such injuries may not hurt the skull, or may produce fractures or necrosis. There is often a considerable interval between the time when the injury is inflicted and that when the symptoms of the abscess are developed. When the cranial bones are uninjured the abscess is situated deep in the brain ; when there is necrosis of the bones the abscess may be superficial ; when the bones are fractured the abscess may be either superficial or deep. The abscess is regularly situated beneath the point of injury, rarely in the opposite side of the brain. Chronic disease of the nose, either the mucous membrane or the bones, has been the cause of a few abscesses in the frontal lobes. Disease of the orbit has also given rise to abscesses in the same position. In a few cases the abscesses have been due to caries of various portions of the cranial bones. In a considerable number of cases (one-sixth, Gowers) no cause for the abscess has been discovered. Very frequently in acute meningitis there is an infiltration of pus cells along the walls of the vessels which enter the brain from the pia mater ; and under a variety of conditions which we do not un- derstand, as in some cases of typhoid fever, delirium tremens, ery- sipelas, and under many other conditions, there are numerous and sometimes very large numbers of leucocytes scattered through the substance of the brain, sometimes around the ganglion cells, some- times along the vessels in the perivascular sheaths. Chronic Interstitial Encephalitis—Sclerosis.—This lesion of the brain tissue may occur diffusely, occupying an entire lobe or more or less of the whole brain, or in circumscribed small areas. It consists essentially in an increase of the connective-tissue elements, the neuroglia, and an atrophy of the nerve elements, particularly the ganglion cells and the medullary sheaths of the nerves. With these changes are usually associated the formation of Gluge’s corpuscles, corpora amylacea, granular and fatty degeneration of the nerve ele- ments, and thickening and proliferation of cells of the walls of the blood vessels. The areas of sclerosis may be very dense and hard, or gelatinous in consistence. The diffuse form of sclerosis is most frequently seen in general paresis of the insane, and not infrequently in the brains of drunk- ards, The circumscribed form of sclerosis, multiple sclerosis (sclérose en plaque), is much more coramon than the diffuse form, and may occur in the brain alone, or may be associated with a similar lesion in the spinal cord. It is almost entirely confined to the medullary substance, and the areas of sclerosis vary in size from that of a pea Digitized by Microsoft® THE NERVOUS SYSTEM. 383 to that of an almond. They may be few or numerous, they may be white, grayish, or grayish-red in color, and are usually, but not always, sharply outlined against the unaltered brain tissue. Al- though in many cases the increase in the connective-tissue elements seems to be the primary lesion, and the degeneration of the nerve elements secondary to this, it is quite possible that in some cases the increase in connective tissue may be secondary to a degeneration of the nerve elements from loss of nutrition or from other causes. Fic. 180—SyYPHILITIC OBLITERATING ENDARTERITIS OF A CEREBRAL ARTERY, X 50 and reduced. There is reason for the belief that multiple sclerosis may be the re- sult of disseminated local necrotic lesions of acute infectious diseases —scarlatina, for example—occurring at an early period of life.’ Encephalitis in the New-born.—This condition, first described by Virchow, is said to consist in the formation of circumscribed col- lections of cells of various sizes containing many fat granules (granu- lar corpuscles) and forming yellowish masses, from 1 mm. to 6 mm. i See Oppenheim, Berl. klin. Wochenschrift, March 2d, 1896. Digitized by Microsoft® 384 THE NERVOUS SYSTEM. in diameter, in the brain tissue. A more diffuse occurrence of granu- lar corpuscles is also described, but this is said by some observers to be physiological. The nature of this lesion is but little understood and is still the subject of controversy. Syphilitic Inflammation of the Brain sometimes results in the formation of so-called gummy tumors. These are most frequently found near the periphery of the brain, not infrequently connected with the meninges, and may be sharply circumscribed. The central portion of the tumor is usually in a condition of cheesy degeneration, and in the periphery we see fibrous tissue or a dense infiltration of small spheroidal cells. Syphilitic inflammation of the brain very frequently occurs in a diffuse form, characterized by the formation of a gelatinous, grayish Fig. 181.—Sotirary TUBERCLE oF CEREBELLUM. a, a, miliary tubercles with giant cells; b, b, miliary tubercles without giant cells; c, diffuse tubercle tissue; d, central cheesy mass; e, nerve tissue of the cerebellum. tissue consisting of a more or less homogeneous or granular base- ment substance, with numerous small spheroidal cells. The nerve elements are atrophied. Obliterating endarteritis may occur as a re- sult of syphilitic poisoning (Fig. 180). : Tuberculous Inflammation of the brain substance usually mani- fests itself in the formation of circumscribed masses of new tissue Digitized by Microsoft® THE NERVOUS SYSTEM. 385 from 0.5 cm. to 1 cm. in diameter, or larger. These may be single or multiple, are most common in young persons, and very fre- quently occur in the cerebellum. They are apt to occur in connec- tion with tuberculous inflammation of other organs. They are fre- quently called solitary tubercles, and usually consist of a dense central cheesy mass, around which is a grayish zone containing tubercle granula, numerous small spheroidal cells, with occasionally , larger polyhedral cells and giant cells (Fig. 181). They do not, as a rule, seem to be formed by an aggregation of miliary tubercles, although these may be present in the periphery. Tubercle bacilli have been found in these solitary tubercles. They sometimes suppurate and break down, and then may simu- late simple abscesses. Conglomerate and scattered miliary tubercles of the ordinary form sometimes occur in the brain, usually in connection with tuber- cular inflammation of the meninges or ependyma. LESIONS OF THE BRAIN IN GENERAL PARESIS OF THE INSANE. The changes in this disease are in the main those of chronic dif- fuse encephalitis, but the appearances vary greatly and depend to some extent upon whether the brain is examined in early or late stages of the disease. According to Meyer, in the early stages of the disease the convolutions, particularly of the anterior cerebral lobes, are swollen, the gray matter congested and softened in places. The brain tissue is more or less infiltrated with leucocytes. Fatty de- generation of the walls of the capillaries, and punctate hemorrhages, are also common. In later stages of the disease a great variety of changes may be observed: hemorrhagic pachymeningitis, thickening of the dura mater, and close adhesions to the skull; thickening and opacities of the pia mater, adhesions of the latter to the dura mater and to the brain tissue. The brain tissue is apt to be atrophied, and the ventri- cles dilated and filled with fluid. The pia mater may be cedematous, the ependyma thickened and roughened. On microscopical exami- nation the neuroglia is found to be increased in amount, the ganglion cells shrunken and sometimes pigmented ; the nerve fibres may also be atrophied, and the blood vessels in a condition of fatty or hyalin degeneration. There may be an accumulation of fatty and granular cells along the walls of the blood vessels. Secondary degenerations in the spinal cord are not infrequently observed. It is very difficult to make positive and definite statements regard- ing many such lesions of the brain as those just indicated, or in general of brain lesions whose nature must be revealed by microsco- pical study, because our technical procedures in the study of the Digitized by Microsoft® 386 THE NERVOUS SYSTEM. brain, even in normal conditions. are still quite unsatisfactory and incomplete. The brain tissue is so delicate and liable to post-mortem changes, and the effects of different preservative agents are so liable to variations, that great caution is necessary in arriving at conclu- sions regarding the minuter lesions affecting the nerve tissue of the brain. PIGMENTATION. This may occur in any portion of the brain or its meninges from the decomposition of extravasated blood. In persons affected by malaria the gray matter of the brain has sometimes an unusually dark or even blackish appearance. This color is due to the presence of black pigment granules within the capillary blood vessels. The obstruction to the vessels by masses of these pigment granules may cause capillary apoplexies. The pigment may also be found in the walls and in the twmina of the vessels of the pia mater. Pigmented patches of congenital origin are not infrequently seen in the pia mater. They may be due to the presence of branching pigmented cells. TUMORS OF THE BRAIN. Neuroglioma ganglionare.—This is a form of tumor probably due to disturbances in the development of the brain. It occurs in the form of circumscribed tumors or of diffuse enlargements of por- tions of the brain. The pia mater over these tumors is unchanged and the convolutions retain their shape. The tumors are formed of neuroglia, in which are contained little groups of ganglion cells (Ziegler). Glioma.—This is the most common tumor of the brain. It occurs with especial frequency in children and young adults. Such tumors occur in all parts of the brain, but they are found most frequently in the cerebrum. There may be a single tumor, or there may be sev- eral such tumors in different parts of the brain ; some of them attain a large size. These tumors may be sharply circumscribed, or merge imperceptibly into the brain substance ; sometimes the tumor is ar- ranged so as to form the wall of a cyst which contains clear serum. They may be white and hard; gray, soft, and gelatinous ; infiltrat- ed with small hemorrhages; or partly degenerated and softened. The brain tissue around these tumors may be inflamed or necrotic. The tumors are composed of neuroglia, the relative quantity of neu- roglia cells (Fig. 137) and of fibrils (Fig. 136) varying in the different. tumors. If the cells are very numerous, with but little basement sub- stance, the tumor is called a glio-sarcoma. Digitized by Microsoft® THE NERVOUS SYSTEM. Sarcomata occur in any part of the brain. They are single cr multiple. They are composed of round or fusiform cells with more or less basement substance. Endotheliomata are found in the substance of the brain. They are of the same types as have been described as occurring in the pia mater. . Myxoma, fibroma, lipoma, and osteoma are rare forms of brain tumor. Angioma.—Small collections of dilated vessels are found in the substance of the brain. They seem to be congenital, like the nevi of the skin. The cysts of the cerebellum are very curious bodies. They are found in young persons and in adults. They occur in any one of the lobes of the cerebellum. They may be as large as a hen’s egg. They contain clear serum or colloid matter, and their walls are formed of thickened neuroglia. We are ignorant of their mode of origin. They give marked clinical symptoms and are regularly fatal. PARASITES. Cysticercus and, more rarely, echinococci are found in the brain. MALFORMATIONS. Cyclopia.—This malformation consists in an arrest of develop- ment affecting the cerebrum, which, instead of separating into two hemispheres, remains single, with one ventricle, and the rudiments of the eyes usually become joined and form one eye. This single eye is in the middle of the face, near the place of the root of the nose, in a single orbit. Over this is an irregular body representing the nose. The rest of the face is well formed. Or the eyeball may be wanting entirely, or there are two eyes joined together, or, more seldom, two separate eyes. The orbit is surrounded by rudiments of four eyelids. The frontal bone is single, the nasal bones unde- veloped ; the ethmoid, vomer, and turbinated bones are absent. The optic nerve is double, single, or absent. There may be hydrocepha- lus. Such children are incapable of prolonged existence. Anencephalia.—This malformation may be of various degrees. The brain may be entirely absent, and the base of the cranium is covered with a thick membrane, into which the nerves pass. Or the membranes may form a sort of cyst containing blood and serum, or portions of brain. Of the cranial bones, only those which form the _ base of the skull are present (Acraniza). The scalp is usually partly or entirely absent over the opening in the skull; the eyes stand prominently out, and the forehead slopes sharply backward. This malformation may occur in otherwise well-developed children. Digitized by Microsoft® 388 THE NERVOUS SYSTEM. Aydrocephalus.—This lesion has been already considered on page 367. It is probable that in some cases hydrocephalus internus is due toa primary partial anencephalia, and that the accumulation of fluid is of secondary occurrence. In rare cases, only part of one lateral ventricle is hydrocephalic, giving to the head a protuberance on one side. The viability of the foetus depends upon the degree of the hydrocephalus. Hydrocephalus externus is an accumulation of serum beneath the pia mater, or, according to some authors, between the pia and dura mater. It causes dilatation of the cranium and compression of the brain. It is of very rare occurrence, and may also be secondary to partial anencephalia. Cephalocele, or Brain Hernia.—When abnormal openings exist in the skull from malformation, the contents of the cerebral cavity are apt to protrude in the form of larger or smaller sacs. This may occur in cases of well-marked anencephalia or in cases in which the brain is well developed. The protruding sac formed of the meninges may or may not be covered with skin. If the contents of the sac are simply fluid, the lesion is called hydromeningocele ; if composed of brain substance, encephalocele ; if the sac contain both fluid and brain substance, it is called hydrencephalocele. The sacs may be very small or as large as a child’s head. They may protrude from the top of the skull in acrania. They most frequently protrude through openings in the occipital bone, often hanging down in large sacs upon the neck ; also at the root of the nose, along the line of the sutures, at the base of the skull, and elsewhere. Microcephalia.—This is an abnormally small size of the brain, with a correspondingly small cranium. The diminution in size af- fects principally the cerebral hemispheres, though the other parts of the brain are also small. The convolutions are few and simple, the cavities often dilated with serum ; on the membranes there may be traces of inflammation. The cranium is small, the face large, the rest of the body small. The malformation is ir some cases caused by inflammation or dropsy of the brain during foetal life. It is en- demic in some countries, but single cases may occur anywhere. The foetus is viable. Absence or incomplete development of portions of the brain may occur, not only in idiots, but in persons whose minds are perfect. * 1 For a general consideration of malformations of the central nervous system con- sult Thoma, “Text-Book of Pathological Anatomy, ” vol. i., p. 206 et seq. Digitized by Microsoft® THE SPINAL CORD. THE MEMBRANES OF THE SPINAL CORD. A.—THE DURA MATER SPINALIS. The dura mater spinalis, unlike that of the brain, does not serve as periosteum to the bones forming the cavity, so that the lesions of the two membranes differ somewhat. HAMORRHAGE, Hemorrhage may occur, as the result of injury, between the dura mater and periosteum, or it may occur in tetanus, asa result of circu- latory changes induced by muscular spasm, or in the asphyxia of new-born children. Small hemorrhages on the surfaces of the mem- brane may occur as the result of inflammation. Serous fluid may accumulate outside of the dura mater as a re- sult of post-mortem changes, or in connection with circulatory or inflammatory changes in the membranes. INFLAMMATION. Acute external pachymeningitis is usually secondary to dis- ease or injury of the spinal column, and may result in collections of pus between the dura mater and periosteum, usually most abun- dant posteriorly. Hcemorrhagic pachymeningitis occurs in the dura mater spinalis, with the formation of products similar to those observed in the brain, in the chronicinsane and in drunkards. S7vm- ple chronic pachymeningttis interna, with the formation of new connective tissue containing brain sand, is not infrequent. The new tissue may form minute projections or roughness of the sur- face, or, when more abundant, the psammomata. Tuberculr in- flammation of the dura mater spinalis may occur in connection with tubercular meningitis, or be secondary to tubercular inflammation of the vertebree, Digitized by Microsoft® 390 THE SPINAL CORD. TUMORS. Fibromata, lipomata, chondromata, myxomata, endothe- liomata, and adeno-sarcomata’ occur in the dura mater spinalis as primary tumors. Carcinomata and sarcomata may occur as secondary tumors. Small plates of new-formed bone are rarely found in the dura mater spinalis. PARASITES. Echinococcus developing outside of the spinal canal may perfo- rate the dura mater ; or the cysts may lie between the dura mater and the pia mater. It is obvious that even small tumors in the spinal canal may give rise to serious results from compression. B.—THE PIA MATER SPINALIS. It is almost impossible in most cases in the pia mater, as well as in the dura mater spinalis and in the spinal cord, to judge with cer- tainty, from the appearances after death of the blood contents of the vessels, of these parts during life. The same is true of abnormal quantities of serum found after death. The veins of the pia mater, especially in the posterior region, may be greatly distended with blood after death, without pre-existing disease ; and the intermen- ingeal space may contain much fluid under the same condition. HAMORRHAGE. Hemorrhages may occur from injury in connection with severe convulsions, or general diseases such as the hemorrhagic diathesis, scurvy, small-pox, etc. The hemorrhages under these conditions, except from injury, are not usually extensive. But in some cases of injury or cerebral apoplexy ; from the bursting of aneurisms of the basilar or vertebral arteries ; or in cases in which we cannot find a cause, a very large quantity of blood may collect between the dura and pia mater, and in the meshes of or beneath the latter. INFLAMMATION. Acute exudative spinal meningitis occurs under essentially the same conditions and with essentially the same post-mortem ap- pearances as acute cerebral meningitis, though it is less frequent. The exudations are apt to be most abundant in the posterior por- tions. It may be associated with a similar inflammation of the pia ' Hodenpyl, American Journal of the Medical Sciences, March, 1888. Digitized by Microsoft® THE SPINAL CORD. B91 mater cerebralis, and the inner surface of the dura mater may be involved. The disease may be circumscribed, but usually affects the entire length of the membrane. Tuberculous inflammation is usually most marked, when asso- ciated with a similar condition of the pia mater cerebralis, in the up- per portions of the cord ; but it may extend over the entire membrane. The conditions under which it occurs and the character of the le- sions are similar in both. Chronic spinal meningitis is not infre- quent, manifesting itself in the formation of larger or smaller patches of new connective tissue or thickenings of the pia mater. The pia and dura mater may thus be firmly united in places by ad- hesions, or the pia mater may become closely adherent to the sub- stance of the cord. Not very infrequently large numbers of pigment cells are found in the pia mater spinalis,, sometimes giving it a distinct gray or blackish color. TUMORS. Small plates of cartilage and bone are sometimes found in the pia mater. Fibromata, myxomata, sarcomata, and endotheliomata have been found. PARASITES. Cysticercus sometimes occurs in the meshes of the pia mater. THE SPINAL CORD. HAMORRHAGE, This is much less frequent than in the brain, but may occur either as capillary apoplexy or as larger apoplectic clots. Capil- lary hemorrhages, similar in appearance to those of the brain, may occur as the result of injury, or near areas of softening or tumors, or may accompany severe convulsions, as in tetanus. Apoplectic clots, which are comparatively rare in the spinal cord, are usually small, commonly not more than one cm. in diameter, and are similar in their appearances, and in the changes subsequent to their forma- tion, to.those of the brain. They are usually the result’ of injury ; but they may occur spontaneously, probably in most cases as a result of inflammation, and are then most apt to occur in the gray matter. Sometimes, however, hemorrhagic foci are found in the spinal cord without traumatism or evidence of inflammatory change. HAMATOMYELIA AND HHZMATOMYELOPORE. Several cases have_been descr ed_in 5 ich long tubular canals Digitized by Microso 392 THE SPINAL CORD. were found in the spinal cord. These have been considered the result of central necrosis, myelitis, etc., varieties of syringomyelia, and variously named. These long cavities have no well-defined Fig. 182.—SecTIon oF THE SPINAL CoRD SHOWING H&MORRHAGE INTO THE GRAY MaTTER AND ExrenDING LENGTHWISE OF THE CorD. Showing an early phase of hematomyelopore. (Van Gieson.) Fig. 1883.—H@MATOMYELOPORE. (Van Gieson.) The section shows at one point a cyst-like cavity in the spinal cord, originating in a hemor- rhage in the posterior root and extending nearly the eutire length of the cord. The sides of the cavity are now covered with tissue detritus. wall and no distinct lining membrane. They are filled with blood and tissue detritus. Van Gieson has shown that they correspond to columnar hzemor- Digitized by Microsoft® THE SPINAL CORD. 393 rhages within the cord, usually following traumatisms in which the blood forced its way lengthwise of the cord, forming columnar masses. On the absorption of this blood the long cavities or canals are left. This condition Van Gieson has called hematomyelopore. INJURIES. The spinal cord may be compressed or lacerated by penetrating wounds, by fracture or dislocation of the vertebrae, or by concussion without injury to the vertebree. The spinal cord is found simply disintegrated, or there may be much hemorrhage and the disinte- grated nerve tissue be mixed with blood. If life continue, the nerve elements may degenerate; Gluge’s corpuscles and free fat droplets may form; blood pigments may be formed; and when inflammation supervenes more or less pus may be intermingled with the degen- erated detritus. There may be marked changes in the minute structure of the cord, without any change being evident to the naked eye. SECONDARY DEGENERATIONS IN THE SPINAL CORD. The modern conception of the structural elements of the nervous system is that they are complex cell units called newrons, which may extend over long distances, and although without direct anastomoses stand in intimate topographical and functional relationships with one another. The neuron consists of a cell body, an axis-cylinder process, the neuron, and protoplasmic processes of the cell called dendrites. A destruction of the cell body or a separation of the processes from the cell body is accompanied by a degeneration of the processes. The cell bodies are grouped together in the gray matter of the brain and cord and in the ganglia situated along the peripheral nerves. Through the dendrons impulses are conducted to the ceil bodies; through the axis-cylinder processes they are conducted from the cell body. : When the cell bodies of the neurons of certain parts of the brain and of the spinal cord are destroyed, or when the motor nerves lead- ing from them are severed or seriously injured, that portion which is deprived of or separated from its cell body degenerates. After a time—frequently two to four weeks—the medullary sheath and axis cylinder disintegrate, becoming granular and fatty. These products of degeneration may be in part absorbed at once, or may collect in cells, forming the so-called compound granular corpuscles. After a still longer time—sometimes several months—the degenerated 32 Digitized by Microsoft® 394 THE SPINAL CORD. areas become gray in color from the absorption of the degenerated myelin, harder, and somewhat shrunken. These changes are partly due to the formation of new connective tissue which takes the place of the degenerated nerve fibres. Since the affected portion of nerve tissues becomes gray or trans- Jucent after the myelin is broken down and absorbed, and the new connective tissue is formed, this is often called Gray Degeneration, or, as the degenerated areas are harder than normal, it is sometimes called Sclerosis. Now, it is found that this secondary degeneration takes place in the direction in which the fibres conduct—in centripetal or sen- sory fibres, upward; in centrifugal or motor fibres, downward. Thus we have Descending Secondary Degeneration (Descending Sclerosis), and Ascending Secondary Degeneration (Ascending Sclerosis). Descending Secondary ‘Degeneration.—This change affects chiefly the motor nerve fibres, and may reach but a short distance from the seat of lesion, or may extend for a long distance, depending upon whether the severed fibres run a short or long course befvre reaching their termination. Lesions of the brain, such as embolic softenings and apoplectic clots, which destroy or interrupt any of the motor nerve fibres originating in the central convolutions, may be followed by degeneration of the portion of the fibres situated periph- erally to the lesion. These fibres pass through the corona radiata, anterior portion of the internal capsule, pes pedunculi, pons, and thence to the anterior pyramids, where most of them decussate and pass to the posterior part of the lateral columns of the opposite side. Those which do not decussate form a narrow band at the inner part of the anterior columns of the same side, constituting the columns of Tiirck. These fibres which convey motor impulses from the brain to the cord form a system called the pyramidal tract. Now, a lesion in the brain separating the motor nerve fibres of one side from their cells of origin in the motor cortex will be followed by areas of degeneration in the posterior part of the lateral column of the opposite side, and in a narrow band near the anterior longitu- dinal fissure of the same side (see Fig. 184). A lesion below the medulla, involving the fibres of the pyramidal tract on one side, will be followed by degeneration of the fibres on the same side below the point of lesion. If a part only of the fibres in any of these regions is interrupted the amount of degeneration is of course proportion- ately small. Ascending Secondary Degeneration.—Any lesion interrupting the course of the centripetal (mostly sensory) nerve fibres in the cord is followed by degeneration of the central ends of the involved fibres, Digitized by Microsoft® THE SPINAL CORD. 395 because these are separated from their cells of origin either in the spinal ganglia or in the gray matter of the cord itself. Part of these sensory fibres—some of which are short, others long— Fie. 184.—DescenpiInG SECONDARY DEGENERATION. Section of cord in cervical region. Degeneration of the column of Tiirck and of the crossed pyramidal tract. are situated in the posterior columns and form communications be- tween different parts of the gray matter. Fig. 185.—AscENDING SECONDARY DEGENERATION IN THE SPINAL CoRD (UPPER CERVICAL REGION). After fracture of the spine destroying the eighth cervical segment; the lesion involves the columns of Goll, the direct cerebellar tract, and the columns of Gowers, Others of the sensory fibres are grouped in anarrow band near the posterior longitudinal fissure, forming the columns of Goll, Digitized by Microsoft® 396 THE SPINAL CORD. while other sets, forming the so-called direct cerebellar tract and the columns of Gowers, are situated in the periphery of the lateral columns. A lesion of the cord involving the severance or destruction of: these centripetal fibres will be followed by ascending degeneration of the direct cerebellar tract and of the columns of Golland Gowers and. of the entire posterior column, just above the lesion (Fig. 185). The: degeneration may be traced along the columns of Goll to the resti- form bodies, and in the cerebellar tract to the cerebellum. Lesions involving the entire thickness of the cord will produce bilateral. degenerations. Following the secondary degeneration of the nerve fibres, whether: ascending or descending, new connective tissue may form, filling the: space formerly occupied by the nerve elements (Fig. 186). This new connective-tissue development was formerly looked upon as the primary factor in various forms of sclerosis in the central nervous system to which the nerve changes were secondary; but the Fie. 186.—AscenpiIng Gray DEGENERATION. A small portion from edge of degenerated region of cord shown in Fig. 185, more highly magnified. A, normal nerve fibres; B, degenerated area. new knowledge on the subject makes it evident that the connective tissue should be looked upon not as a chronic interstitial inflamma- tion, but as the result of a replacement fibrous hyperplasia. PROGRESSIVE SPINAL MUSCLE ATROPHY. Degeneration or atrophy of the anterior nerve cells of the spinal cord and their neuraxons may be associated with varying degrees of atrophy of the corresponding muscles—progressive spinal muscle. atrophy. BULBAR PARALYSIS. Similar changes in the cells of the motor nuclei of the medulla may be associated with paralysis of the tongue, lips, anc larynx, and constitute the so-called bulbar paralysis. AMYOTROPHIC LATERAL SCLEROSIS. Under obscure conditions there may be degenerative changes. ef Digitized by Microsoft® THE SPINAL. CORD. 397 ‘both the central motor neurons from the brain to the cord and of the peripheral motor neurons from the motor cells of the cord to the ‘muscles. These conditions determine a replacement fibrous hyper- plasia (sclerosis) in the lateral column and also in the anterior cornua of the spinal cord. If small groups of neurons are involved the ‘sclerosis may be slight. This condition has been called amyotrophic lateral sclerosis (Fig. 187). It should be borne in mind, in looking for these secondary lesions, that they are not developed until considerable time has elapsed since the development of the primary lesion, and that when small areas Vie. 187.—SecTIoN oF SPINAL CorD IN AMyoTROPHIC LaTERAL ScLEROsIS. Shows degeneration of the crossed pyramidal tracts on both sides. are involved they are usually inconspicuous. In any event, the Jesions are apt to be more evident to the naked eye in specimens hardened in chromic fluids than when fresh, and microscopical examination is often necessary for their recognition. INFLAMMATION, Acute Myelitis. This lesion of the spinal cord, which is sometimes distinctly in- flammatory in character and sometimes of a degenerative nature, as usually confined to a comparatively limited longitudinal extent of the cord, and hence is sometimes called transverse myelitis. When the cord is removed and laid upon the table, if the lesion is marked, a flattening of the cord at its seat may be observed ; or on passing the finger gently along the organ the affected segment -will be found softer than the rest of the cord. On making a section through the diseased portion the nerve tissue may be white or red Digitized by Microsoft® 398 THE SPINAL CORD. or yellowish or grayish; it may be quite firm, but is usually more or less softened and sometimes almost diffluent.’ Microscopical examination shows different appearances, depend- ing upon the stage of the inflammatory or degenerative process. There may be much blood, or, if the lesion has existed for some time, blood pigments ; also fragments of more or less degenerated nerve fibres and ganglion cells (Fig. 188), myelin droplets, free fat granules, and larger and smaller cells filled with fat granules (Gluge’s corpus- cles), pas cells, granular matter, neuroglia cells, and sometimes cor- pora amylacea. The various combinations of these elements give rise to the different gross appearances which the diseased part pre- sents. In earlier stages of the lesion the blood vessels may be dilated, the nerve fibres and cells swollen; or the walls of the blood vessels may be thickened or fatty, or surrounded by a sheath of leu- Fig. 188,—DEGENERATED Tissuz FROM ACUTE MYELITIS. cocytes and cells derived from the connective-tissue cells of the ad- ventitia. The lesion is apt to commence in the gray matter or at its edge, and then extend first laterally and afterward upward and downward. In a certain number of cases the degenerated material may be absorbed and a cicatrix or cyst formed. In the least extensive forms of the lesion there is apparently a regeneration of the nerve fibre, and a restoration of the functions of the cord. Secondary gray degeneration, both ascending and descending, may occur in the form of myelitis, varying in extent according to the size of the primary lesion. Acule disseminated myelttis runs a rapid course, and proves fatal in a short time. The inflammation may involve nearly the whole length of the cord, but is more intense in some places than in others. The cord is swollen and congested, it is infiltrated with pus ‘Tt should be remembered that a mechanical injury to the cord in removal, such as crushing or bruising, may reduce the injured portion to a pulpy consistence and thus produce appearances somewhat similar to those of some forms of inflammator softening (see p. 381). re Digitized by Microsoft® THE SPINAL CORD. 399 cells, the connective-tissue framework is swollen, and the nerve ele- ments are degenerated (see Poliomyelitis). Poliomyelitis Anterior (Myelitis of the anterior horns).—This Fig, 189.—POLIOMYELITIS ANTERIOR. Showing degenerated area in anterior cornua, with atrophy of gray matter. A, Atrophic region. Specimen prepared by Dr, Ira Van Gieson, name is applied to a group of cases which are characterized py clini- cal symptoms indicating changes in the anterior gray cornua. The disease occurs both in children and in adults, and varies in the Fig. 190.—PoLIOMYELITIS ANTERIOR. Showing portion of Fig. 189 at edge of affected area, more highly magnified. A, normal ganglion cells surrounded by nerve fibres ; B degenerated ganglion cells; C, granular masses at place of ganglion cells; D, small cavity containing fluid Digitized by Microsoft® 400 THE SPINAL CORD. severity, acuteness, and duration of its symptoms. In many cases there is complete recovery, and then we must suppose that the changes in the nervous tissue were not destructive in their character. In other cases the symptoms are more permanent, indicating a destruc- tive lesion. From the autopsies so far recorded we learn that the lesion is most frequent at the lumbar and cervical enlargements of the cord, but may occur anywhere, and is often in scattered patches (Fig. 189). There is degeneration, shrinkage, pigmentation, and atrophy of the ganglion cells in the anterior gray cornua (Fig. 190). The chromophyllic masses in the ganglion cell bodies may be disin- tegrated and in various ways altered (see page 376). There may be an increase of connective tissue in the gray cornua and in the anterior and lateral columns. There may be degeneration and destruction of a considerable part of the anterior cornua; there may be atrophy of the anterior nerve roots. The cord may be considerably distorted as the result of the lesion. There is evidence that the lesion in many of the cases of so-called Landry’s paralysis are those of acute myelitis or of poliomyelitis, involving important changes in the ganglion cells.’ 4 CHRONIC MYELITIS. Chroyic Interstitial Myelitis.—-Under this heading are em- braced a variety of lesions which probably differ from one another somewhat in the nature of the changes involved, but more in the seat of the disease. We shall consider without special classification the most important forms. Chronic Transverse Myelitis.—In certain cases of pressure on the spinal cord from a tumor or from displacement of the bones of the vertebral column, etc., instead of becoming softened or under- going acute inflammatory changes, the cord becomes the seat of a localized formation of new connective tissue, with consecutive atro- phy of more or less of the nerve elements in the gray and white matter. The cord becomes in this way harder, and sometimes shrunken at the seat of lesion, and grayish in color. This change may be followed by ascending and descending gray degeneration. Multiple Sclerosis.—This lesion, similar in its nature to multi- ple sclerosis of the brain, often occurs with it. It consists in the formation, in more or less numerous scattered, circumscribed areas, of new connective tissue, apparently derived from the neuroglia. The formation of new connective tissue is preceded or accompanied by degeneration and atrophy of the nerve fibres and ganglion cells. The new connective tissue consists of the characteristic branching 1 Consult Batley and Ewing, New York Medical Journal, July, 1896. Digitized by Microsoft® THE SPINAL CORD. 401 neuroglia cells, surrounded by a more or less dense network of fine fibrille, many if not most of which seem to be branches of the neu- roglia cells. Corpora amylacea and sometimes fat droplets, either free or contained in cells, may be present in the sclerosed areas. Fie. 191.—MvuLTIPLE SCLEROSIS IN SPINAL CoRD. Showing larger and smaller areas of atrophy of nerve elements with formation of connective tissue. The areas of sclerosis may involve both gray and white matter, and may be very small or large (Fig. 191). If very small or in early stages of formation, they may not be recognizable by the naked eye, Fig. 192.—PosTERIoR SPINAL SCLEROSIS (TABES DORSALIS). Section of the spinal cord in the cervical region. but when visible they are grayish, translucent, and firmer than the surrounding tissue, and may or may not present a depressed sur- face; they sometimes project above the general level. The cause of Digitized by Microsoft® 402 THE SPINAL CORD. this, as of other forms of so-called idiopathic interstitial myelitis, is very obscure. Posterior Spinal Sclerosis (Locomotor Ataxia; Tabes Dor- salis).—The lesions of this condition consist essentially of degener- ation in the peripheral sensory neurons, especially in the spinal gan- glia and posterior roots. This change involves degeneration and atrophy in greater or less degree of the nerve fibres in the posterior columns of the spinal cord and an associated replacement fibrous hyperplasia or sclerosis (Fig. 192). Not infrequently the posterior portion of the lateral columns are also involved. Exceptionally a large part of the lateral columns is involved, and also the anterior cornua. The change usually com- ( & ») a 2 PEAY. say os TNS (Sine i) ee ie yA Fie. 195.—PosTERIOR SPINAL SCLEROSIS. A portion of sclerosed area in the posterior columns of the spinal cord. a, New formed con- nective tissue; b, blood vessels; ¢, nerve fibres; d, atrophied nerve fibres. mences in that portion of the posterior columns bordering on the posterior cornua, but may involve, as above stated, the adjacent parts. It is usually most marked in the lower dorsal and lumbar regions. The sclerosis may extend upward to the restiform bodies, but in the cervical region it isapt to beconfined lagely to the columns of Goll, although there are exceptions to this. When the lesion is well developed the pia mater over the affected area is usually thickened and adherent to the cord. In its early stages there may be no change evident to the naked eye; but when advanced the posterior columns may appear somewhat depressed, and grayish and firmer than the rest of the cord. The microscopical ap- pearances vary, depending upon the stage and extent of the lesion. Digitized by Microsoft® THE SPINAL CORD. 403: The walls of the blood vessels may be thickened; there is more or less new connective tissue consisting of neuroglia cells and very numer- ous interlacing, delicate fibrils. There may be numerous corpora amylacea and fat granules, either free or collected in cells. The nerve fibres may be numerous, but separated more or less widely by the new connective tissue, or they may be very few in number and irregularly scattered through the new tissue (Fig. 193). The atrophy may involve the fibres of the posterior nerve roots and cornua, and even the ganglion cells of the latter. The peripheral nerves and the cells of the spinal ganglia may be degenerated. According to the researches of Lisauer,‘ the columns of Clarke in the dorsal region show in this disease a very constant and marked diminution in the number of delicate fibrils which under normal conditions surround the ganglion cells. In the rare cases in which the sclerosis extends to the lateral columns and to the anterior cornua, the minute characters of the lesions are the same. There is much reason for the belief that the formation of connective tissue in tabes is not the primary factor in the disease but is secondary to degeneration of the nerve fibres in the involved portion cf the cord, and is thus in the nature of a replace- ment connective-tissue hyperplasia or fibrosis. Solitary tubercles and gummata may occur in the spinal cord, but are not common. TUMORS. Cysts may occur as a result of softening or from unknown causes. Sometimes very long, narrow canals are found in the spinal cord, even reaching nearly its whole length. Some of these are evidently the dilated central canal, as they are lined with epithelium. Others, however, doubtless originate in hemorrhages (see Hzematomyelo- pore, p. 391). In the pia mater of the cord are sometimes found small fibromata, osteomata, and lipomata. Endotheliomata, of the same types as have been described as existing in the pia mater of the brain, are much more rarely found in the pia mater of the cord. A fatty sarcoma’ of the pia mater, which infiltrated the cord, formed a tumor as large as a filbert, and had for twelve years caused gradually increasing paraplegia, has been described. Two curious cases* of diffuse sarcoma and one of endothelioma of the pia mater of the whole length of the cord are recorded. They 1 Fortschritte der Medicin, Bd. ii., No. 4, 1884. 2 Trans. Lond. Path. Soc., xxxix. % Trans. London Path. Soc., xxxviii.; Arch. fiir Psych., 1885. Digitized by Microsoft® 404 THE SPINAL CORD. occurred in girls of 44, 16, and 22 years of age. In each case the pia mater of the whole length of the cord was diffusely thickened and studded with nodules. In two of the cases the growth was composed of round cells, in the third case of large endothelial cells arranged in alveoli. In two of the cases the clinical symptoms lasted only for about three weeks, in the third case for five months. The acuteness of the symptoms was such as to indicate the existence of spinal men- ingitis. In the spinal cord itself gliomata, fibromata, sarcomata, glio-sar- comata, and angio-sarcomata occur, but are rare. When gliomata or glio-sarcomata do occur in the spinal cord, the new growth is apt to extend for some distance lengthwise in the cord and to be attended with the formation of a cavity; this condition is usually described under the name of syringomyelia. Fia. 194.—SYRINGOMYELIA. Transverse section of cord. A, white substance of cord, distended by tumor; B, B, dis- torted and atrophied gray substance of anterior cornua; C, tumor mass (glio-sarcoma); D, cavity in cord. Drawn from specimen prepared by Dr. Van Gieson. SYRINGOMYELIA. This lesion of the spinal cord consists in the formation of glio- matous or glio-sarcomatous tissue in the vicinity of the central canal, and its subsequent partial disintegration with the formation of one or more cavities within the substance of the cord (Fig. 194). These cavities, which are filled with fluid, vary greatly in size, shape, and extent, and, while usually situated in the central region of the cord, they may involve the anterior and posterior cornua and invade the posterior columns. There nay be two communicating cavities, and these may, but usually do not, open into the central canal. The lon- gitudinal extent of these cavities varies greatly. The lower cervical and upper dorsal regions are most frequently involved. The cavity is usually lined with tissue somewhat denser than that which makes Digitized by Microsoft® THE SPINAL CORD. 405 up the bulk of the tumor. The gliomatous or glio-sarcomatous tissue which forms the basis of the lesion in syringomyelia probably origi- nates from the layer of neuroglia which surrounds or extends away from the central canal. Syringomyelia is frequently mistaken for hydromyelia (see below), which is a congenital malformation, and in which the longitudinal cavity in the cord is at some period lined with epithelial cells. Syringomyelia has also been confused with heematomyelopore (see page 392). There seems, furthermore, to be a class of lesions of the cord, usually classed as syringomyelia, in which cavities of various forms co-exist with a tumor in the vicinity of the central canal. But these cavities do not appear to be formed by a breaking down of the tumor tissue, but in some other way as yet little understood. MALFORMATIONS. The malformations of the spinal cord may be conveniently classed as follows (Van Gieson) :’ I. ConGENITAL DEFORMITIES ASSOCIATED WITH MOoNSTROSI- TIES, AND INCOMPATIBLE WITH ExtTra-UTERINE LIFE. These may be divided into: 1. Amyelia, or absence of the spinal cord. This is almost in- variably associated with absence of the brain. 2. Atelomyelia, or partial development of the spinal cord. This is often seen in the anencephalous or acephalic monsters, where, cor- responding to the incompletely developed brain, there may be various degrees of defective development in the length of the cord. 3. Diastematomyelia, a condition in which a portion of the whole of the cord is split into two lateral halves. Each half of the cord, being enveloped in its own membranes and giving rise to its own nerve roots, may fuse together to form a single cord at some region. 4. Diplomyelia, or a formation of two spinal cords—a duplication of the spinal cord. This happens in the various kinds of double monsters. II. Minor ConGEnitAL MALFORMATIONS NOT INCONSISTENT WITH THE MAINTENANCE OF LIFE. 1. Hydrorrhachis interna is a defective closure or arrangement of the divisions of the primary fcetal central canal often resulting in the dilatation of the central canal by fluid (Hydromyelia) Fig. 195). This dilatation may bé moderate, or so extreme that but little of the substance of the cord is left as a thin shell around the central cavity. 1 Van Gieson, “ Artefacts of the Nervous System,” New York Medical Journal, 1892. Digitized by Microsoft® 406 THE SPINAL CORD. When they have not been destroyed by atrophy, epithelial cells may be found lining the cavity. This condition may be accidentally found after death. Its pres- ence may also be indicated by its association with spina bifida.’ Fig. 195.—HYyDROMYELIA. In the section from which this drawing was made, the epithelial cells surrounding the di- dated central canal were well preserved, 2. Heterotopia, or misplacement of the substances of the cord. (a) There may be misplaced portions of the gray matter. (b) Portions of the white matter may be arranged in an unusual manner. 3. Anomalies of the Spinal Nerve Roots. “0d YP KASS T A ae fed eR AN pees Ge OS \ aa nu ¥ic. 196.—Fause HETERoTopIA. SECTION FROM CERVICAL REGION OF SPINAL CoRD. Showing artificial displacement of the structures by an experimental bruise (‘‘ false hetero- topia’’) after the removal of the cord from the body. (Van Gieson.) * Under this subdivision the condition known as hydrorrhachis externa may be conveniently alluded to, which consists in an abnormal congenital accumulation of fluids between the meninges of the cord, causing more or less diminution in the volume of the iatter. Digitized by Microsoft® m8 THE SPINAL CORD. 407 4. Asymmetries of the Spinal Cord. III. MALFORMATIONS OF THE SPINAL CORD ACQUIRED DURING Extra-UTERINE LIFE OR SECONDARY TO DEFECTIVE DEVELOP- MENT IN OTHER PaRTs OF THE Bopy. 1. Distortions following other cord lesions. 2. Asymmetry of the cord due to arrested development after birth or to secondary atrophy of portions of the cord in association with defective development or absence of some other part of the body. 3. Asymmetry of the cord with congenital defects of the extremities or muscles, such as intra-uterine or other amputations, clubfoot, ete. 4, Variations in the volume of the cord as a whole. False Heterotopia.—Congenital displacement of the gray or white matter of the spinal cord—heterotopia—has been frequently de- scribed. Van Gieson’ has shown, however, that in a large propor- tion of cases the so-called heterotopia is an artefact (Fig. 196) and has been caused by bruises or careless handling of the cord during its removal from the body or in the process cf examination or hard- ening. Spina bifida.—In the majority of cases hydrorrhachis is ac- companied by a more or less complete lack of closure of the spinal canal posteriorly, so that the collections of fluid within may pouch outward through the opening in the form of asac. The sac may be covered by skin, or this may be absent, either from the begin- ning or as a result of thinning and rupture. The walls of the sac may consist of the dura mater and the pia mater, or, in cases of hydrorrhachis externa, of the dura mater alone; when both are present they are usually more or less fused together. Inside of the membranes of the sac there may be a shell of distended nerve tissue of the cord ; or the spinal cord may be split posteriorly and the sides crowded sideways ; or there may be a rudimentary fragment of the cord suspended in the sac or attached to the walls ; or the cord may be but little changed and remain inside the spinal canal. The openings in the spinal canal may be due to the complete or partial absence of the vertebral arches, or more rarely the sac may protrude through openings between the completely formed arches. Spina bifida most frequently occurs in the lumbar and sacral regions, but it may occur in the dorsal or cervical regions, or the canal may be open over its entire length. Very rarely it is open on the anterior surface. The protruding sac may be very small or as large asa child’s head. The fluid in the sac is usually clear, but may be turbid from flocculi of degenerated nerve tissue, 1 Van Giteson, loc. cit. Digitized by Microsoft® 408 THE SPINAL CORD. THE PERIPHERAL NERVES, CHANGES IN NERVES AFTER DIVISION. ‘When nerves are divided or a portion destroyed by injury, the nutrition of certain parts of the fibres is interfered with, apparently because of the separation of these from their neurons, and they suffer degeneration ; but after a time, if the conditions be favorable, they may undergo regeneration and restitution of function. The degene- ration not only affects the entire severed portion, but it occurs at nearly the same time in all parts. The degeneration consists in the breaking-up of the medullary sheaths into variously shaped droplets, and the decomposition of these, with the formation of fat, which may remain for some time either free or enclosed in cells, and. finally be absorbed (see Fig. 197). The axis cylinder, too, is, in many cases at least, more or less completely destroyed. The neurilemma. and its nuclei do not seem usually to undergo degeneration, but may persist and take part in the regeneration of the nerve when restitu- tion occurs, After a variable time, if the conditions are favorable, the divided Fic. 197,—DEGENERATION OF NeRVE FIBRES IN MULTIPLE NEURITIS. From a case of alcohol poisoning. Specimen stained with osmic acid. The broken-down medullary sheath and fat droplets are stained deep black. ends of the nerve may be united, and a regeneration or new forma- tion of nerves in or about the severed portions may occur, so that the function may be resumed. Considerable time is required, frequently months, for the completion of the regenerative process. Degenera- tion of the nerves not only follows mechanical injuries, such as inci- sion, crushing or tearing, and compression, as from a tumor or dis- location of the bones, but it may result from disease of the special nerve centres with which the nerves communicate, or from inflam-- mation of the nerves themselves. INFLAMMATION, Acute Hxudative Neuritis.—Primary acute inflammation of the nerves may occur as the result of injury, or it may be secondary to an inflammatory process in its vicinity, although, owing to the dense lamellar sheaths and the special blood supply, the nerve trunks. may escape participation in even very severe inflammatory processes. Digitized by Microsoft® THE SPINAL CORD. 409 in surrounding tissues. The inflamed nerve may be red and swollen and infiltrated with serum and pus cells. The process may undergo resolution or terminate in gangrene and destruction of the nerve, or it may become chronic and result in the formation of new connective tissue. Degeneration and regeneration of the nerve fibres, similar to those above described as following division of nerve trunks, may oc- cur in acute neuritis. Chronic Interstitial Nenritis.—This is essentially a chronic in- terstitial inflammation resulting in an increase of connective tissue in the nerve sheath and intrafascicular bands. Asa result of this the nerve fibres undergo atrophy from pressure ; the medullary sheath, and finally the axis cylinder, being, in more or less of the fibres, par- tially or completely destroyed. Multiple Neuritis.--Under a variety of conditions, such as ex- posure to cold and wet, overexertion, poisoning by alcohol, arsenic, lead, etc., and in connection with the acute infectious diseases, a de- generation of the nerve fibres in various parts of the body may occur (Fig. 197), which may be accompanied with or followed by prolifera- tive changes in the neurilemma cells. Regeneration of the affected nerve fibres may occur under these conditions, as after experimental division of the nerves, leading to their restitution." In some forms of multiple neuritis the inflammation is exudative in character, and new cells of various forms are found within and between the nerve fibres. The exact part which the neurilemma and other intrafasci- cular cells play in the inflammatory and regenerative changes of nerves is not yet very fully made out. Syphilitic and Tuberculous Inflammation of the nerves is not common except at their central ends, in connection with similar in- flammations of the meninges, or when they are secondarily involved in connection with these inflammations in neighboring tissues. Leprous Inflammation.—This consists in the formation within the nerve of masses of new-formed tissue somewhat resembling granulation tissue, in whose cells multitudes of characteristic bacilli are uniformly found (see Leprosy). It constitutes the variety of leprosy known as lepra anesthetica. TUMORS. The tumors of the nerves are such as consist largely of or con- tain new-formed nerve tissue—frue neuromata ; and the so-called 1Consult Starr, ‘‘ Multiple Neuritis.” “The Middleton Goldsmith Lecture for 1887. Trans. New York Pathological Society, 1887, p. 1. 33 Digitized by Microsoft® 410 THE SPINAL CORD. false neuromata (Figs. 141 and 142), which are for the most part fibromata or myxomata of the connective tissue of the nerve. Myzxo-sarcomata are less common, and primary sarcomata rare. The nerves may be secondarily involved in sarcomata or carcino- mata, though not infrequently nerves pass through these tumors without being in the least involved in their peculiar structure. Pal- tauf has described as endotheliomata rare tumors of the glandula carotica.’ ACROMEGALIA. This rare disease is especially characterized by an overgrowth of the terminal portions of the extremities and of the bones of the face. Butthere may be a general involvement of the skeleton. This excessive growth is in the diameter and not in the length of the bones, accompanied by local exostoses, and is associated with an overgrowth of the soft parts composing the involved extremities. A marked enlargement of the pituitary body has been found in some of the cases, and this has been claimed to be the causative factor in the nutritional abnormality leading to the hypertrophic lesions of the bone.” SCLERODERMA. Under little understood conditions a sharply circumscribed or widely extended hardening of the skin may occur as the result of a swelling of the old and formation of new connective tissue in the skin. This is associated with thickening of the walls of the blood vessels. The new-formed tissue may contract, it may continue to form so that the lesion is progressive; or, cessation of the process and recovery may occur.° METHODS OF PREPARATION OF NERVE TISSUE FOR MICROSCOPICAL STUDY. The general methods of hardening have already been given on pages 18 and 21. For minute study there is no one method of staining and mounting upon which we can rely exclusively for the study of all lesions. A. preliminary examination of areas of tnflammatory soft- ening, or of the disintegrated tissue in apoplectic clots, or of the new-formed tissue in chronic hemorrhagic pachymeningitis inter- 1 Paltauf, Ziegler’s Beitrige zur path. Anatomie, etc., Bd. xi., p. 260, 1882. 2 For a careful description of a case and a discussion of its relationships to similar abnormalities consult Arnold, “ Acromegalie, Pachyacrie oder, Ostitis,” Ziegler’s Beitr. z. path. Anat., Bd. x., 1891. 3 Lewin and Heller, “Die Sclerodermie, ” Berlin, 1895, bibliography. Digitized by Microsoft® THE SPINAL CORD. 411 na, may bemade by teasing portions of the affected tissues in one-half- per-centsalt solution. Or the tissues in these lesions, or in any others in which fatty degeneration is suspected, may be placed for twenty- four hours in one-per-cent aqueous solution of osmic acid, and then washed and teased in glycerin. In this way the myelin and the fat will be stained brown or black. Secondary and other degenerations of medullated nerves may be studied by soaking the nerves for twenty-four hours In one-per-cent solution of osmic acid, and then staining with picro-carmin and teasing and mounting in glycerin. Suppurative inflammation of the central nervous system and its membranes, or the connective-tissue changes in general, may be studied in sections from the tissues hardened in Miiller’s fluid and alcohol, stained double with hematoxylin and eosin (see page 60), and mounted in Canada balsam. A very useful method of staining sections of nerve tissue, espe- cially of the brain and cord, is that known as Weigert’s hematoxy- lin method. The tissue is first well hardened in Miller’s fluid. Blocks of the hardened tissue are embedded in celloidin and sec- tions made in the usual way. The sections are first soaked for twenty-four hours in a saturated aqueous solution of neutral cupric acetate diluted with an equal bulk of water. They arenow thoroughly washed twice in water, then in alcohol, and then are tiansferred to the hematoxylin solution, made as follows : Hematoxylin crystals ..............22 0005 1 gm. Alcohol,. 97 per céntic. esccs sea ccae dees ee cons 10 cc. Waterasegacds Garicesiar esas cided ana 90 * Saturated aqueous solution Lithium Car- DONALO were enews sabe aoa ee Te In this solution the sections remain for two hours. (If the finer fibres of the cerebral cortex are to be brought out the sections must remain for twenty-four hours in the hematoxylin solution.) The sections are now thoroughly washed in two or three waters and transferred to the bleaching solution, composed as follows : Potassium Ferricyanid................. 2.5 gm. Sodium Biborate................2. 200. Re W ater iow seat sede wenee eeu ate soca 200- Ee In this fluid the sections discharge a brownish color, and they remain in it until the gray matter has a distinct yellow color and the white matter is bluish-black. The time required to produce this effect varies considerably, and is usually from half an hour to an hour. The sections are now washed, dehydrated with alcohol, Digitized by Microsoft® 412 THE SPINAL CORD. cleared up in oil of cloves or oil of origanum, and mounted in bal- sam. The sections may be stained in alum carmine before dehy- dration, to bring out the nuclei. In sections stained by this method the gray matter, connective-tissue elements, and ganglion cells have a yellow or yellowish-brown color, the axis cylinders are uncolored or have a slight yellowish tint, while the medullary sheaths are bluish- black or black. To demonstrate the presence of miliary aneurisms in or about apoplectic clots, it is usually necessary to macerate the brain tissue in water until the nerve elements disintegrate, and they may then be washed away under a stream of water, leaving the blood vessels with their aneurisms exposed. Nissl’s Staining Method.—There are several variations of this method, but the following gives good results in most cases: The essential feature of the so-called Nissl’s method is the appli- cation of the anilin dyes to the staining of certain structural elements in the nucleus and cytoplasm, which are distinguished from the other structures of the cell by a differentiating decolorization with alcohol. Methylen blue is the most generally useful of the anilin dyes for this purpose. The specimens should have been carefully hardened in sublimate solution or in alcohol or in formalin. Very thin sections are stained in one-per-cent solution of methy- len blue. The staining may be effected on a slide on which the sec- tions are floating in the blue solution by gently heating over a lamp until the fluid steams. The sections are now transferred to a mixture of absolute alcohol 90 parts, with anilin oil 10 parts, in which the differentiation is effected by the use of successive fresh portions of fluid until slight but distinct differentiation in color is seen between the gray and white matter of the nerve tissue. The exact degree of decolorization which gives the best pictures will be learned by practice of the method. The sections are now freed from the bulk of the alcohol upon the slide, cleared in xylo], and mounted in dammar varnish, in which the color is apt to be preserved better than in balsam. By this procedure the chromosomes and the chromphylic bodies in the cytoplasm of ganglion cells are sharply differentiated, and thus abnormal condi- tions may be detected in them (see Fig. 178). The applications of this method of staining to other cells than those of the nervous system are wide and of great promise. Digitized by Microsoft® THE RESPIRATORY SYSTEM. THE LARYNX AND TRACHEA. MALFORMATIONS, The larynx and trachea may be entirely absent in acephalic mon - sters. The larynx may be abnormally large or small. The epiglot- tis also may be too large or too small, or may be cleft. There may be communications between the trachea and the cesophagus, and then the pharynx generally ends in a cul-de-sac, and the cesophagus opens into the trachea. There may be imperfect closure of the original branchial arches, so that there are fissures in the skin leading into fistulee which open into the pharynx or trachea. The fissure in the skin is small and is situated about an inch above the sterno-clavicu- lar articulation, usually on one or both sides, more rarely in the mid- dle line. Individual cartilages, as the epiglottis, or one or more rings of the trachea, may be absent, or there may be supernumerary rings. The trachea may divide into three main bronchi instead of two, and in that case two bronchi are given off to the right lung and one to the left. The trachea may be on the left side of the cesophagus or behind it. INFLAMMATION. Acute Catarrhal Laryngitis.—This cecurs as an idiopathic in- flammation, as a complication of the exanthemata and the infectious diseases, and is produced by the inhalation of irritating vapors and of hot steam and smoke. The inflammation varies in its intensity in different cases. The mucous membrane is at first congested, swol- len, and dry ; then the mucous glands become more active and an increased quantity of mucus is produced. There is an increase in the desquamation of the superficial epithelial cells and in the pro- duction of the deep cells. A few pus cells are found in the mucus and in the stroma of the mucous membrane. For some reason in- flammation of the larynx is frequently attended with spasm of its Digitized by Microsoft® 414 THE RESPIRATORY SYSTEM. muscles, thus producing attacks of suffocation. In severe cases cedema of the glottis may be developed. After death the congestion of the mucous membrane frequently disappears altogether. Chronic Catarrhal Laryngitis.—The surface of the mucous membrane is dry or coated with muco-pus. The epithelium is thick- ened in some places, thinned in others, or in places entirely destroyed. The stroma is somewhat infiltrated with cells, diffusely thickened, or forming little papillary hypertrophies, or thinned, or necrotic and ulcerated (Fig. 198). The mucous glands are swollen and prominent. The inflamma- Fie. 198,—An Utcrr oF THE LARYNX IN CHRONIC CaTARRHAL LARYNGITIS, X 850 and reduced. tion may extend to the perichondrium of the cartilages and thus cause their necrosis. The most severe forms of chronic laryngitis are those associated with pulmonary phthisis. Some forms of chronic laryngitis with thickening of epithelial and submucous tissue are called Pachydermia laryngis. Acute Suppurative Inflammation may attack the posterior sur- face of the epiglottis and the aryepiglottidean ligaments. The stroma of the mucous membrane is swollen and infiltrated with serum and pus. Abscesses may be formed in the stroma, which rupture internally, or extend outward into the neck, or into the wall of the pharynx or of the cesophagus. Suppurative inflammation may accompany catarrhal, croupous, tubercular, and syphilitic laryn- Digitized by Microsoft® THE RESPIRATORY SYSTEM. 415 gitis, inflammations and injuries of the pharynx and tonsils ; it may complicate typhoid fever and the other infectious diseases. Croupous Laryngitis occurs most frequently as one of the le- sions of diphtheria ; it complicates the exanthemata and the infec- tious diseases. It is produced by the Bacillus diphtherix, by strep- tococci, by the inhalation of irritating gases, hot steam or smoke, and by the introduction of foreign bodies. The mucous membrane is swollen and congested. Its surface is coated with fibrin and pus, and its stroma is infiltrated with fibrin and pus. The epithelial cells undergo coagulation necrosis. It is not often that there is necrosis of the deeper tissues. Fig. 199.—TuBERcULOUS LARYNGITIS. Syphilitic Laryngitis.—Syphilis often causes laryngitis. The inflammation may have the ordinary characters of an acute or chronic catarrhal inflammation, or it is a productive inflammation with the formation of new tissue in the stroma of the mucous mem- brane. This new tissue is principally composed of small cells, which often degenerate and die. In this way the mucous membrane of the larynx and the tissues beneath are thickened in some places and de- stroyed in others, these changes being especially marked in the upper portion of the larynx. If the perichondrium is involved by these changes there may be necrosis of the laryngeal cartilages. Tuberculous Laryngitis in its simplest form consists of a catarrhal inflammation, a growth of new cells in the stroma, and the forma- Digitized by Microsoft® 416 THE RESPIRATORY SYSTEM, tion of tubercle granula in the stroma without necrosis. The mu- cous membrane is thickened ; it is coated with a layer of mucus, pus, and desquamated epithelium. From the epithelial layer out- ward the stroma is infiltrated with cells and with tubercle granula (Fig. 199). ‘When there are added to the production of tubercle tissue an ex- cessive formation of cells and a tendency to necrosis, the conditions become much more serious and complicated. The catarrhal inflam- mation is intense, with the production of large quantities of pus and mucus. The necrosis results in the formation of ulcers of different sizes and shapes; the inflammation and necrosis extend from the mucous membrane to the wall of the larynx. The epiglottis, the vocal cords, and the adjacent mucous membrane are coated with muco-pus ; their surfaces are ragged and irregular. In places the mucous membrane is destroyed, so that ulcers are formed ; in places itis thickened and infiltrated with cells and tubercular -tissue ; in places it is necrotic. In the most severe cases the entire thickness of the wall of the larynx, with its cartilages, is involved. CGidema of the Glottis is the name given to serous infiltrations of the mucous membrane of the upper part of the larynx. The swelling is most marked on the posterior wall of the epiglottis, in the aryepiglottidean ligaments and the false vocal cords. In these places the cedema of the stroma of the mucous membrane may be sufficient to close the larynx. Acute cedema is due to an inflammatory exudation of serum, and accompanies inflammations of the pharynx, larynx, and neck. Chronic cedema is of dropsical character and is caused by disease of the heart, pulmonary emphysema, and compression of the veins of the neck. TUMORS. Retention cysts of the mucous glands of the larynx may reach such a size as to form sacs projecting into its cavity. Papilloma is the most frequent form of tumor of the larynx. The tumors grow most frequently from the vocal cords. They con- sist of a connective-tissue stroma arranged so as to form papillae covered with epithelium. They are sometimes congenital. Fibromata, lipomata, myxomata, and angiomata are occa- sionally met with. Chondromata grow from the normal cartilages and are usually multiple and sessile. They may project into the cavity of the larynx. Sarcomata of the larynx have been seen in a considerable num- ber of cases. They occur both in children and in adults. They are composed of fusiform or round cells, with a stroma which varies in quantity in the different cases. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 417 Carcinomata may invade the larynx from the tongue or the pharynx, or may originateinit. They are composed of flat epithelial cells packed together in the usual way. In the trachea tumors are of rare occurrence, but occasional examples of growths similar to those in the larynx have been met with. Cheesy and otherwise altered bronchial lymph nodes may by ul- cerative processes enter and obstruct the trachea. THE PLEURA. HYDROTHORAX, Non-inflammatory accumulations of clear serum in the pleural cavities are of frequent occurrence. They are produced by the same causes which effect dropsy in other parts of the body—le- sions of thd heart, liver, and kidneys, and changes in the circulation and in the composition of the blood. If the amount of serum is small it is of little consequence ; if it is large it may compress the lower lobes of the lungs and interfere with respiration. There may be changes in the endothelium of the parietal pleura. Instead of the regular endothelium, large and small flat cells of ir- regular shape are found. HASMORRHAGE., Extravasations of blood in the substance of the pleura are found in persons who have died after suffering from the infectious dis- eases ; and as the result of injuries to the wall of the thorax. Blood in large quantity in the pleural cavities is found after rup- ture of an aneurism of the heart with rupture of the pericardium. Bloody serum in the pleural cavities is not often found with ordi- nary pleurisy. But with tubercular pleurisy and traumatic pleurisy it is not infrequently present. INFLAMMATION. The inflammations of the pleura are all spoken of by the common name of pleurisy, or pleuritis. All the different inflammations of the lung are capable of being accompanied by pleurisies, which begin in the pulmonary pleura and extend to the costal. Besides these, however, there are many pleurisies which belong primarily to the costal pleura and extend from there to the pulmo- nary pleura. Such pleurisies occur as idiopathic inflammations, as complica- Digitized by Microsoft® 418 THE RESPIRATORY . SYSTEM. tions of various diseases, as the result of injuries, or are produced by the inflammation of adjacent parts. We can distinguish : I. Pleurisy with the production of fibrin. IJ. Pleurisy with the production of fibrin and serum. III. Pleurisy with the production of fibrin, serum, and pus. IV. Chronic pleurisy with the formation of adhesions. V. Tuberculous pleurisy. All the varieties of pleurisy can best be studied in the lesions which are developed in and on the costal pleura. The lesions can be observed in the human subject, and can be produced artificially in the lower animals. It isin these artificial pleurisies especially that we are able to see the early changes produced by the inflammation and to watch the process step by step. The free surface of the costal pleura is covered with a single layer of flat cells—the endothelium. The pleura itself is formed of planes of connective tissue reinforced by elastic fibres. Connective-tissue cells with large bodies and branching processes are present in con- siderable numbers, being most abundant in the layers beneath the endothelium. In the connective tissue are embedded blood vessels, lymphatics, and nerves. I. Pleurisy with the Production of Fibrin—Dry Pleurisy— Acute Pleurisy. This form of pleurisy is apt to involve circumscribed areas of the costal, mediastinal, diaphragmatic, or pulmonary pleura, less fre- quently the entire pleura of one side of the chest. While the inflammation is going on the affected portion of pleura is coated with fibrin, the surface of the opposite portion of pleura is coated in the same way, and bands of fibrin join the two together. After the inflammation has run its course we find the affected portion of pleura thickened by the formation of new connective tissue, while bands of connective tissue extend between the opposed pleural surfaces. As an exceptional condition there is inflammation of the entire pleura of one side, with the production of such an enormous amount of fibrin as to compress the lung and cause death. IT, Pleurisy with the Production of Fibrin and Serum—Pleurisy with Effustion—Subacute Pleurisy. This is the most common form of pleurisy. Asa rule, it involves the greater part of the pleura of one side of the chest. Sometimes, however, the pleura of both sides of the chest is involved, and then the pericardium also is often inflamed. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 419 While the inflammation isin progress the surface of the affected pleura is coated with fibrin, and bands of fibrin stretch between the ‘ parietal and pulmonary pleura. In the pleural cavity is serum in. variable quantity. This serum is clear, or turbid from the presence of pus cellsand flocculi of fibrin. The lung is compressed in different degrees and positions, according to the quantity of the serum and the character of the adhesions. If the patient recover the serum is absorbed, the fibrin disappears, and there are left behind connective-tissue thickenings of the pleura and adhesions. These two forms of pleurisy, although different in their clinical histories, are yet anatomically essentially the same. In both of them we find a regular sequence of changes. First, the production of fibrin and a few pus cells, either with or without serum. Second, a gradual-absorption of the serum and fibrin. Lastly, the formation of permanent new connective tissue in the form of adhesions or of thickenings of the pleura. Throughout the whole process the tissue of the pleura is but little changed ; the products of inflammation, although they originate in the tissue of the pleura, do not infiltrate it, but make their way to its surface, there accumulate, and there undergo their different changes. Variations from the regular course - of the inflammation are effected by the excessive formation either of the fibrin, the pus, or the serum, and by the manner in which these inflammatory products are absorbed. If we endeavor to follow out the successive-changes by which the fibrin, pus, and serum make their appearance and then disappear, and the way in which permanent new connective tissue takes their place, we encounter several difficulties. It is difficult to obtain autopsies which will give the lesions belonging to each successive day of the disease ; the pleura does not really show well if the pa- tient has been dead more than two or three hours before the autopsy; and in most cases the inflammation is too intense, its products are too abundant, to be easily studied. To obviate these difficulties we must resort to experiments on the lower animals. By injecting a solution of chlorid of zinc into the pleural cavities of dogs we can excite pleurisies closely resembling those which we see in the human subject. By varying the amount of fluid injected we can obtain pleurisies of different degrees of intensity. By using a number of animals we can observe the course of the inflammation from hour to hour and from day to day. In such an artificial pleurisy the first change is congestion. The pleura is of a uniform bright-red color, its surface moist and shining. There is as yet no serum and no fibrin. Already, however, the en- dothelial cells have fallen off in patches, the superficial connective- Digitized by Microsoft® 420 THE RESPIRATORY SYSTEM. tissue cells are swollen and increased in number, and a few pus cells are present. These are all the changes for from half an hour to six hours after the irritant has been applied to the pleura. The next step in the inflammatory process is the production of serum and fibrin. The serum collects in the bottom of the pleural cavity, the fibrin coats the pleura. As the fibrin is produced the pleura loses its natural moist and shining appearance. The fibrin appears first in the form of little granules, knobs, and threads be- tween the edges of the endothelial cells and overlying them. A few pus cells are entangled in the fibrin and infiltrated in the superficial layers of the pleura. The swelling and new growth of the connec- Fie. 200.—AnN ARTIFICIAL PLeuURISY IN THE DoG, OF TwENTY-FouR Hours’ Duration, xX 750 and reduced. Swelling and growth of connective-tissue cells in the pleura. ' tive-tissue cells are now well marked. The bodies of the branching cells are swollen, and small polygonal, nucleated cells, arranged in rows between the fibres of the basement substance, make their ap- pearance. By the end of twenty-four hours these changes are fully developed (Fig. 200). After this the production of fibrin, serum, and new connective- tissue cells continues, and by the third or fourth day the new connec- tive-tissue cells are present, not only in the superficial layers of the pleura, but also in the layer of fibrin coating its surface and forming adhesions. By the fourth or fifth day the cells in the fibrin are still more Digitized by Microsoft® THE RESPIRATORY SYSTEM. 421 numerous ; blood vessels make their appearance, which can be in- jected from the arteries of the pleura. After this the serum is gradually absorbed. The layer of fibrin and cells on the surface of the pleura exhibits a constant decrease of fibrin and increase of cells, and becomes more intimately connected with the surface of the pleura. By the fourteenth day the fibrin has disappeared and a basement substance has been formed between the cells. Of the new cells the superficial ones are changed into endothelium, the deeper ones into branching cells. The changes in the adhesions between the pulmo- nary and costal pleura are the same as those in the layer of fibrin coating the costal pleura. The lesions of human pleurisy seem to be essentially the same as those of the artificial pleurisy just described. But the inflammatory products are formed in larger quantities, a much longer time is re- quired for their absorption, and the formation of new connective tissue follows more slowly. In these forms of pleurisy, therefore, two distinct processes take place : 1. The blood vessels are congested, and through their walls trans- ude the plasma of the blood and a few white blood globules. 2. The superficial connective-tissue cells are increased in size and number. The products of the first of these processes, the fibrin and serum, are regularly reabsorbed. The product of the second of these processes, the new connective- tissue cells, regularly increases until a layer of new connective tissue is formed. The natural termination of such a pleurisy is the recovery of the patient, with thickenings of the pleura and adhesions. The irregular terminations are: The death of the patient, the protracted existence of the fibrin and serum, and the change of the character of the inflammation so that pus is produced. In aconsiderable proportion of cases the examination of the exu- date in a simple uncomplicated case of sero-fibrous pleurisy fails to reveal the presence of micro-organisms. ITT, Pleurisy with the Production of Fibrin, Serum, and Pus— Empyema. This form of pleurisy may occur under several different condi- tions. 1. The infammation is at the very outset of severe character, with the formation of pus. Digitized by Microsoft® 422 THE RESPIRATORY SYSTEM. 2. A pleurisy with the production of fibrin and serum, either gradually or suddenly, changes its character and pus is formed. 3. Phthisical areas of softening, or abscesses of the lung, abscesses in the wall of the thorax, or in the liver, or in the abdomen, rupture into a pleural cavity and set up an empyema. 4. The inflammation may be not only purulent but also gangre- nous in character. The fluid in the pleural cavity, the fibrin and pus coating the pleura, and the pleura itself, may putrefy, with the proliferation of bacteria and the evolution of gases. This may take place either in a closed pleura or in one which has been opened. 5. If there is an opening into a pleural cavity, either through the lung or through the wall of the thorax, there is air in the pleural cavity, in addition to the inflammatory products. Such a condition is called pyo-pneumothorax. In all these different cases the pleural cavity is partly or com- pletely filled with purulent fluid, and the lung is either compressed against the vertebral column or partly adherent to the chest wall. Sometimes, however, the purulent fluid is shut in by adhesions, either between parts of the lung and the thoracic wall, or between the lung and the diaphragm, or between the lung and the pericar- dium, or between the lobes of the lung. The fluid in the pleural cavity is usually a thin, purulent serum, composed of serum, pus globules, endothelial cells, and pieces of fibrin. But sometimes this fluid is very thick and viscid. In empyema in its earlier stages the lesions are the same as those in pleurisy with effusion, with the addition of pus in the serum, the fibrin, and the superficial layers of the pleura. In children the inflammation may remain in this condition for a long time, but in adults other changes in the pleura are soon devel- oped. These changes consist in the growth of a large number of small polygonal and round cells, the basement substance is split up, and the pleura is changed into a tissue resembling granulation tissue. The pleura is thus considerably thickened. Its surface is coated with fibrin and pus, or is bare like the surface of an ulcer. In this condition the pleura may remain for months or years, its inner layers formed of granulation tissue, its outer layers of dense connective tissue. Sometimes the cell growth is more active, necrotic changes are added, and sothere is a conversion of portions of the pleura into pus. Such a suppuration may extend from the pleura to the. fas- cie, the muscles, the skin, the diaphragm, or the lungs. Thus the pus may find an exit, through the wall of the thorax, into the peri- toneal cavity or into the lungs. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 423 If the empyema becomes gangrenous the pleural cavity contains foul gases, the purulent serum is dirty and stinking and swarms with bacteria. The fibrin coating the pleura is of green or brown color. Portions of the pleura itself may also become gangrenous. In old cases the thickening of the pleura may reach an enormous degree and it may become calcified.‘ The perichondrium of the car- tilages and the periosteum of the ribs may become inflamed, with ne- crosis of the cartilages and ribs or a production of new bone. Empyema is, therefore, a very much more serious lesion than the two forms of pleurisy just described. The lesions involve not merely the surface of the pleura, but its entire thickness. When the pleura has thus been converted into granulation tissue it is hardly possible for it to return to a normal condition. It is important to remember that in children the changes in the pleura itself are less profound, and that in adults they become more and more marked, according to the duration of the disease. Bacteria’ are present in the exudate in a large proportion of cases of empyema. The Streptococcus pyogenes, Staphylococcus pyogenes, Diplococcus lanceolatus, and the Bacillus tuberculosis are the most common inciters of suppurative inflammation of the pleura. Interlobular Lymphangitis.—Inflammations of the pleura with the production of pus and fibrin may extend to the lymphatics in the interlobular septa, around the bronchi, and around the blood vessels. This occurs with pleurisies due to septic poisoning and with those which occur without discoverable cause. It is seen more frequently in children than in adults. The lymphatics in the interlobular septa, and those around the bronchi and blood vessels are distended with pus cells, the septa are much thickened, and the lobules separated from each other. IV. Chronic Pleurisy with the Formation of Adhesions. This form of pleurisy may follow one of the varieties of pleurisy just described, it may be associated with emphysema and chronic phthisis, or it may occur by itself. After death the pulmonary and costal pleura are found thickened and joined together by numerous adhesions. These changes may involve only a part or the whole of the pleura on one or both sides of the chest. 1For a résumé of our knowledge of various calcifications in the lungs, and allied conditions oiten called ‘‘lung stones,” consult Polaiilon, ‘Les Pierres du Poumon,” etc., Paris, 1891 ; or Legry, Arch. gen.de Méd., March and April, 1892. 2 Consult “ Ztiology of Exudative Pleuritis, ” Prudden, New York Medical Jour- nal, June 24th, 1893. On the relationship between empyzema and subphrenic ab- scess, consult Meltzer, New York Medical Journal, June 24th, 1893. Digitized by Microsoft® 424 THE RESPFRATORY SYSTEM. The thickened pleura is covered with endothelial cells, which are increased in sizc and number; the connective-tissue cells in the pleura are also increased in number, and the blood vessels are more numerous. The adhesions are formed of connective tissue resembling that of the costal pleura, containing blood vessels and covered with endo- thelium. V. Tuberculous Pleurisy. In acute general tuberculosis miliary tubercles are often present in the pleura. In acute and chronic phthisis, besides the fibrin, pus, serum, and new connective tissue so often produced, there may also be miliary tubercles or larger, flat, cheesy nodules. There are, however, cases of tuberculous pleurisy which have the characters of a local tubercular inflammation. Tubercles are either absent altogether from the rest of the body or of secondary import- ance to the pleurisy. This form of pleurisy involves the pleura of one side of the tho- rax only. It may be rapidly developed, the patient dying at the end of two weeks ; or it may continue for months. It seems to be very fatal. The inflammation may be confined to the costal pleura or may in- volve also the diaphragmatic and pulmonary pleura. The gross ap- pearance of the lesion varies. 1, The pleura is thickened, its surface is bare of fibrin ; it is of a bright-red color from the congestion of the blood vessels, and this red surface is mottled with white dots—the miliary tubercles. In the pleural cavity is bloody serum. 2. The pleura is thickened ; it is thickly coated with fibrin ; no tubercles are visible to the naked eye; the pleural cavity contains clear serum. 3. The pleura is thickened and the pleural cavity contains puru- lent serum. In all the cases the changes in the pleura itself are essentially the same. The thickened pleura is infiltrated with new connective-tissue cells. Scattered through its entire thickness are tubercle granula, either single or joined together by diffuse tubercle tissue (Fig. 201). The smaller blood vessels show a growth of their endothelial cells. In the exudate of tuberculous pleuritis the tubercle bacillus may frequently be detected by simple staining, especially if the solid ele- ments be brought together from a considerable quantity of the fluid by a centrifugal machine. But in suspicious cases of exudative pleurisy which give nega- tive results on morphological examination of the fluid, the inocula- Digitized by Microsoft® THE RESPIRATORY SYSTEM. 425 tion of guinea-pig with a considerable amount of the exudate or with the material concentrated by the centrifuge is more decisive and may reveal the nature of the lesion when the simple morphological tests have failed. TUMORS. Fibroma.—tittle white or pigmented fibromata, of the size of a pin’s head and scarcely raised above the surface, are often present in the pulmonary pleura. Fig. 201.—TuBercuLous Pieurisy, X 90 and reduced. Drawn from a vertical section of the costal pleura. Larger fibrous tumors are formed in the deeper layers of the cos- tal pleura, and project into the pleural cavity. They may become de- tached and are then found loose in the pleural cavity (Lebert). Lipoma.—Fatty tumors are formed beneath the costal pleura and project into the pleural cavity (Lebert). 34 Digitized by Microsoft® 426 THE RESPIRATORY SYSTEM. Carcinomata, sarcomata, and lymphomata are usually second- ary to similar tumors in other parts of the body.’ A peculiar form of primary new growth in the pleura has been described by several observers.’ It is associated with a pleurisy with the production of fibrin and serum. There is a diffuse thickening of the costal pleura, or circumscribed nodules of different sizes. The new growth seems to begin in the lymphatics of the pleura, which are distended with flat, nucleated cells. I (Delafield) have seen two of these cases. The first case was a woman, fifty-three years old, who was ill, with the symptoms of pleurisy with effusion, for four months. After death the left pleural cavity was found to be full of bloody, purulent serum. The costal pleura was moderately thickened and coated with a layer of fibrin and pus. Beneath the fibrin and pus was a thin layer of granula- tion tissue. In this tissue and in the pleura were anastomosing tu- bules filled with flat, nucleated cells. The tubules looked like lym- phatics. The second case was a man, sixty-three years old, who had symp- toms of pleurisy with effusion, for four months. After death the right pleural cavity was found half-full of bloody serum. The cos- tal, diaphragmatic, and pulmonary pleura were coated with fibrin and contained numerous white nodules, some of them as large as a pigeon’s egg. These nodules were formed of a connective-tissue stroma enclosing irregular spaces and tubules filled with flat, nu- cleated cells. While these tumors are often puzzling, and the observer may be in doubt whether they should be called endothelioma or carcinoma or sarcoma, recent studies seem to indicate that they are, for the most part at least, endotheliomata (see page 312). THE BRONCHI. INFLAMMATION. Acute Catarrhal Bronchitts is a disease of very common occur- rence, but one which seldom proves fatal. Our knowledge of its lesions is derived from severe cases, from experiments on animals, from cases which are complicated by other diseases, and from the symptoms which we observe during life. The inflammation involves regularly the trachea and the larger and medium-sized bronchi, less frequently the smaller bronchi also. Asa rule, the bronchi in both lungs are equally affected. 1 For description of ciliated cysts of the pleura, consult Zahn, referred on p. 548, 2 Birsch-Hirschfeld, “Path. Anat.,” p. 768. #. Wagner, Arch. d. Heilkunde, xi. R. Schulz, Arch. d. Heilkunde, xv. Thderfelder, “ Atl. d. path. Hist.,” 4 Lief. Frankel, Berliner klin. Woesbnseu' By Wicrasoke- 3 THE RESPIRATORY SYSTEM. 427 The first change seems to consist in a congestion and swelling of the mucous membrane, with an arrest of the functions of the mucous glands. This is attended with pain over the chest, a feeling of op- pression, sometimes spasmodic dyspnoea, and a dry cough. After this the mucous glands resume their functions with increased activity, the congestion diminishes, there is an increased desquamation of epi- thelium, an increased formation of the deeper epithelial cells, and a moderate emigration of white blood cells. Sometimes the red blood cells also escape from the vessels. The patient now has less pain and oppression ; the cough is accompanied with an expectoration of mu- cus mixed with epithelium, pus, and sometimes blood. Fia. 202.—AcuTE CATARRHAL BRONCHITIS, X 850 and reduced. After death the only lesions visible are the increased amount of mucus, the growth of new epithelium, mucous degeneration of the epithelial cells, a few pus cells infiltrating the stroma, and the gene-., ral congestion of the mucous membrane. The whole process is a superficial one, not producing any changes in the walls of the bron- chi beneath the mucous membrane (Fig. 202). ‘When the inflammation involves the smaller bronchi also they may be full of pus, but their walls are unchanged. The filling of the small bronchi may result in the collapse of the groups of air vesicles to which they lead, and thus are produced areas of atelectasis, which may be further changed by inflammatory pro- cesses. Digitized by Microsoft® 428 THE RESPIRATORY SYSTEM. Chronic Catarrhal Bronchitis.—This form of bronchitis may be the sequel of one or more attacks of acute bronchitis. More fre- quently it is associated with emphysema, heart disease, interstitial pneumonia, phthisis. pleuritic adhesions, or the inhalation of irritat- ing substances. There is in most cases a constant production of mucus, pus, and serum in considerable quantities, and these inflammatory products may have a very foul odor. Less frequently these products are very scanty—dry catarrh. Fig, 203.—Croupous (Fisrinous) BRONCHITIS. Fibrinous casts of the bronchi, similar to those shown in the photographs, were coughed up at irregular intervals for several years. In examining the bronchi in these cases after death we are often struck by the want of proportion between the symptoms and the lesions. The same bronchi which during life were constantly pro- ducing large quantities of inflammatory products and injuring the patient’s health, after death may be but little changed from the nor- mal. In other cases, however, the lesions are more marked. The bronchi contain mucus and pus; they may be congested ; their walls are often trabeculated. The epithelium is deformed and desquamating, with_a peed Hon of new cells in the deeper layers. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 429 the mucous glands are large or atrophied. The connective-tissue stroma is thickened and infiltrated with cells. The coats of the ar- teries in the walls of the bronchi may be thickened. There may be cylindrical dilatation of one or more bronchi. The muscular coat may be thickened or thinned. Very frequently the epithelial cells of the air vesicles and air passages are increased in size and number. Acute Croupous Bronchitis occurs as a lesion of diphtheria, as associated with croupous laryngitis, as the result of the inhalation of hot steam, with lobar pneumonia, and sometimes as an idiopathic disease. The bronchi are lined or filled with a mass of fibrin, pus, and de- squamated epithelium. Fibrin and pus may also be found beneath the epithelium and infiltrated in the stroma. Chronic Croupous Bronchitis is attended with the formation in one or more bronchi of masses of fibrin which are expectorated by the patient in the form of branching casts of the bronchi (Fig. 203). The disease is a very chronic one, and is often associated with phthisis. After death the bronchi are said to be found but little altered from the normal. Curschmann ‘has described under the name of “ bronchiolitis exudativa” a form of bronchitis in which small threads and bands of gray or yellow, partly transparent, coagulated matter are formed in the small bronchi. Vierordt’* has found similar formations in lobar pneumonia. Leyden and Levi have found them in broncho-pneu- monia. In different forms of bronchitis, especially in those associated with asthma, the exudation may contain small, octahedral bodies, probably composed of mucin. They are accidental formations, prob- ably formed from cells, and may be found in the sputa. BRONCHIECTASIA, Dilatation of the bronchi presents itself under three forms: the cylindrical, the fusiform, and the sacculated. The cylindrical dilatation is a uniform enlargement of one or more bronchi for a considerable part of their length. It is found in bronchi of every size, but most frequently in the medium-sized. The fusiform dilatation is a mere variety of the cylindrical. The bronchus is uniformly dilated for a short distance, and then resumes its natural size. Several such dilatations may be found in the same bronchus. The sacculated dilatations form the largest cavities. These cavi- 1 Deutsch. Arch. f. klin. Med., xxxii. ?Berl. klin. Wochensch., 1883. B. Levi, Zeitsch. f. klin. Med., ix. Leyden, Virch. Arch., Bd. Ixxiv. at 3s . Digitized by Microsoft® 430 THE RESPIRATORY SYSTEM. ties communicate with one side of the bronchus; the peripneral por- tion of the bronchus may be obliterated. The bronchus leading to the cavity may be of normal size, or dilated, or stenosed, or even completely obliterated. Such sacculated dilatations may reach a very large size and may communicate with each other. Any inflammatory process which involves the thickness of the wall of a bronchus seems to be capable of producing dilatation of that bronchus. In acute general bronchitis and broncho-pneumonia in children, cylindrical dilatation of a number of the medium-sized bronchi is often produced. Fig, 204.—SECTION OF THE WALL OF A BRONCHIECTASIA, < 850 and reduced. In the persistent broncho-pneumonia of children such dilatations reach a still greater development. In acute and chronic phthisis tubercular inflammation gives rise to sacculated dilatations, which expand with time and are made still larger by the destruction of the adjacent lung tissue. Chronic bronchitis may lead to cylindrical or sacculated dilata- tions, sometimes of great size, Occlusion of some of the bronchi, consolidation of portions of the lung, and extensive pleuritic adhesions, may also produce bronchi- ectasia. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 431 The walls of these dilatations may preserve the characters of the wall of the bronchus, more or less altered by inflammation (Fig. 204), or these characters may be altogether lost. The dilatations may contain mucus and pus, or they may be empty. TUMORS, Ossification of the walls of the bronchi is sometimes found. Lipoma in the submucous connective tissue has been described by Rokitansky. Fibroma and chondroma have been described. Sarcomata of the walls of the bronchi occur as secondary growths, and as extensions of similar growths in the mediastinum. Primary Fic. 205,—ADENOMA OF THE BRONCHI. From a specimen loaned by Dr. Stewart. sarcoma of the bronchi’ seems to be rare. Hesse describes a form of lympho-sarcoma forming nodules around the bronchi as of common occurrence among the miners in some cobalt and nickel mines. Adenoma of the bronchi is of rare occurrence (Fig. 205). Primary carcinoma of the bronchi is described by several authors, but it is not common. Langhans describes a primary carcinoma of the lower end of the trachea and the large bronchi in a man forty years old. The lower end of the trachea and the large bronchi showed a general thickening of their walls, with flat tumors projecting inward. The new growth 1 Hesse, Archiv d. Heilkunde, xix., p. 160. Digitized by Microsoft® 432 THE RESPIRATORY SYSTEM. was composed of a stroma enclosing cavities filled with cells. The cells were small, nucleated, polygonal or cylindrical in shape, and packed closely together. Apparently the new growth originated in the mucous glands. : Carcinoma of the walls of the bronchi may occur as a secondary lesion. It may be formed in the large or small bronchi, follow the course of the bronchial tree, or extend to the lung tissue or to the trachea. THE LUNGS. MALFORMATIONS. One or both lungs may be entirely wanting or only partially de- veloped. In some of the cases with only one lung the patients have grown up to adult life. A peculiar degeneration, by which the lung is converted into a number of sacs containing air and serum, the sacs communicating with the bronchi, has been seen in a few instances. The lobes may be subdivided by deep fissures. An accessory lobe, separated from the lung, between the base of the left lung and the diaphragm, has been described by Rokitansky. There may be hernia of the lung, with absence of part of the wall of the thorax. There may be transposition of the lungs, with similar changes in the position of the heart and the abdominal viscera. INJURIES—PERFORATIONS. Severe contusions of the thorax may produce rupture of the lungs, with extravasations of blood into the pleural cavities. The lungs may be wounded by a fractured rib and by penetrating weapons and projectiles. Such injuries often produce bleeding into the lung tissue and inflammatory changes. The lungs, however, exhibit a considerable degree of tolerance for such injuries, and the patients often recover. Collections of pus in the pleural cavities, the mediastinum, the liver, the spleen, the kidneys, and the peritonal cavity may perforate the lungs. Abscess of the lung may be secondary to liver abscess from amceba coli. CONGESTION AND CEDEMA. These two conditions are regularly associated with each other in the lungs, although one or the other of them may preponderate in ditferent cases. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 433 A moderate degree of congestion and cedema of the posterior por- tions of the lungs is often found as a result of post-mortem changes. In persons who have been comatose from any cause for some hours before death, congestion and cedema of the lungs are regularly developed. With disease of the heart, kidneys, and lungs the congestion, and especially the cedema, may be excessive. The lungs may be so com- pletely infiltrated with serum as to be unaérated. Such a solid cedema of the lungs is sufficient of itself to cause death. It has been asserted by Welch’ that the cause of such an excessive cedema is a paralysis of the left side of the heart, while the force of the right heart is unimpaired. Such an explanation seems to be plausible.’ Patients confined to bed for a considerable length of time may develop congestion of the dependent portions of the lungs—hypo- static congestion. The affected portion of lung is shrunken, con- gested, and imperfectly aérated. HAIMORRHAGE. Extravasations of blood within the air cavities are found with the general diseases which produce a disposition to bleeding in different parts of the body. Blood from the bronchi or from cavities may be inspired into the air vesicles. Valvular lesions of the heart, especially of the mitral valve, are often accompanied by the production of hemorrhagic infarctions in thelungs. These infarctions are circumscribed, of rounded or wedge- shaped forms, from the size of a walnut to that of an orange. They are of dark-red color, unaérated, the air passages distended with blood, and are often surrounded by a zone of pneumonia. They may be situated in any part of the lungs, but are most common in the lower lobes. When they are near the surface of the lungs a circum- scribed pleurisy is often produced. Such infarctions may produce death; they may become gangre- nous, or the blood may become absorbed, or they may be gradually changed into a smaller mass of pigmented fibrous tissue. These infarctions are usually produced by emboli or by thrombosis of branches of the pulmonary artery. Infarctions of smaller size, and with more disposition to be sur- rounded by inflammatory changes, are produced by emboli from the right side of the heart and from thrombi in the veins of pyzemic 1 Virchow’s Archiv, Bd. 72. ° For bibliography, etc., of pulmonary cedema consult Léwit, Ziegler’s Beitriige zur path. Anat., etc., Bd. xiv., p. 401, 1893. Digitized by Microsoft® 434 THE RESPIRATORY SYSTEM. patients. These infarctions are usually situated near the surface of the lung.’ Hemorrhages with rupture of the lung tissue are produced by severe contusions, by penetrating wounds, and by the rupture of aneurisms. EMPHYSEMA. Emphysema is of two kinds—interlobular and vesicular. Interlobular Emphysema is produced by the rupture of air spa- ces and the escape of air into the interstitial tissue of the lung. Or the pulmonary pleura may also be ruptured and the air escape into the pleural cavity, or into the mediastinum and from thence into the neck. Such a rupture of the air spaces is most frequently caused by broncho-pneumonia with consolidation of portions of the lungs. Vesicular Hmphysemcais adilatation of the air passages and vesi- cles of the lungs. A temporary emphysema can be produced in a variety of ways. The bronchi may be obstructed in such a way that the air can enter the air spaces, but cannot escape from them. A portion of the lungs may be consolidated or compressed, and then the air spaces of the rest of the lungs will be dilated. Death may take place, with a dilatation of the lungs which remains after death. Permanent emphysema may change an entire lung if the other lung becomes permanently unaérated ; it may change portions of a lung if other portions are consolidated. “Substantive emphysema” is a term which is now used in a clinical rather than in an anatomical sense. It is used to designate a group of cases in which there are regularly developed changes in -the shape of the thorax, certain characteristic physical signs, a lia- bility to bronchitis, to constant and spasmodic dyspneea, to venous congestion of the viscera and of the skin. In patients who present such symptoms during life, we find after death diffuse changes of both lungs, of which dilatation of the air spaces may form a part (Fig. 206). If the dilatation of the air spaces does exist, the term “substantive emphysema” is appropriate; if it does not exist we employ a term which contradicts itself. The real lesion of substantive emphysema is a chronic productive inflammation of the lung with the formation of new connective tis- stuie—a process analogous to similar chronic inflammations of the en- docardium, arteries, and kidneys, and one which, like them, may constitute a formidable disease or an unimportant senile change. Both lungs are moderately or considerably increased in size. Very often they are partly covered by connective-tissue pleuritic adhesions. 1 Recent studies on lung infarctions have been made by Grawitz, “Festschrift” for Virchow’s 71st birthday, 1891. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 435 The mucous membrane of the bronchi may be coated with mucus or with muco-pus. The muscular coat of the bronchi may be thick- ened ; their entire wall may be thickened or thinned and infiltrated with cells; they may be narrowed or dilated ; they may be sur- rounded by zones of pneumonia. The cells which line the walls of Fie. 206.—PuLMonaRy SUBSTANTIVE EMPHYSEMA. Blood vessels injected, showing dilatation of the air spaces and new growth of interstitial connective tissue. the air spaces are increased in size and number. The walls of the air spaces are more or less thickened, except in the case of some of the air spaces which are dilated. In the walls of some of the air spaces, those which are thickened as well as those which are thinned, are formed small holes (Fig. 207) which may later reach a large size, so that adjacent air spaces become fused together. In some cases of substantive emphysema no dilatation of the air spaces exists. In many of the fatal cases the dilatation is but moderate ; in some cases it is very marked. The dilatation may Digitized by Microsoft® 436 THE RESPIRATORY SYSTEM. involve the air passages alone, or both the air passages and the vesicles. It is not uniform, but involves some parts of the lungs more than others. The arteries throughout the lungs and in the walls of the larger bronchi may have their coats thickened. The capillaries in the walls of the air spaces which are but little dilated are unchanged. Those of the dilated air spaces are separated by wider intervals ; they may be smaller ; it is said that they may be obliterated. The right ventricle of the heart may be dilated or hypertrophied, or both. There may be venous congestion of the pia mater, the Fig. 207. EMPHYSEMA, SHOWING HoLes IN THE WALLS OF THE AIR VESICLES, X 850 and reduced. From a case of chronic miliary tuberculosis. stomach, the small intestine, the liver, the spleen, the kidneys, and the skin. There may be dropsy. ATELECTASIS. A collapsed and unaérated condition of portions of lung tissue is either congenital or acquired. 1. In congenital atelectasis portions of the lung are firm, non- crepitant, of a dark-blue or purple color, depressed and smooth on section. These portions can usually be artificially inflated, and then Digitized by Microsoft® THE RESPIRATORY SYSTEM. 437 cannot be distinguished from the surrounding pulmonary tissue. This condition is produced by the inability of the child after birth to fully inflate its lungs, either from want of sufficient vitality or from obstruction of the bronchi. If the child lives for some time, and the collapsed lobules are not inflated, they become hard and dense. 2. In young children the smaller bronchi may become ob- structed by the inflammatory products of bronchitis and the corre- sponding air vesicles will then collapse. We then find scattered through the lungs collapsed lobules like those in the new-born child. Inflammatory changes may be subsequently developed in the col- lapsed lobules. 3. In adults, large or small portions of lung tissue may become collapsed as the result of bronchitis, of stenosis of a large bronchus, of compression of a bronchus, of paralysis of the pneumogastric, of compression of the lungs by fluid or by new growths, and of long- continued feebleness of the act of respiration. GANGRENE OF THE LUNGS. It is customary to distinguish two forms of gangrene of the lung, the circumscribed and the diffuse ; yet both can occur together. Circumscribed gangrene occurs in the form of one or more rounded or irregular masses of variable size. The gangrenous por- tion of lung is at first brown and dry. The surrounding lung tissue is congested or cedematous, or infiltrated with blood, or inflamed. If the gangrenous focus is near the pleura the latter will be coated with fibrin. Gradually the gangrenous portion of lung assumes a dirty-green color and a putrid odor. It becomes soft, broken down, and separated from the surrounding lung. The blood vessels may be obliterated by thrombi, or eroded, so that there are profuse hemor- rhages. Such a gangrenous process may extend to the adjacent lung tissue, or a zone of gray or red hepatization or of connective tissue may be formed. The fluid from the gangrenous lung may pass into the bronchi and be expectorated; or it may run from one bronchus into another and set up new gangrenous foci or diffuse gangrene. The pulmonary pleura may be perforated and a gangrenous pleur- isy produced. Gangrene may follow lobar or broncho-pneumonia, especially such phases of the latter as result from the inspiration of foreign material containing micro-organisms from the mouth; it may arise from infectious emboli in the lungs, or by an extension of a gan- grenous process from an adjacent part. Diffuse gangrene may follow the circumscribed form; it may Digitized by Microsoft® 438 THE RESPIRATORY SYSTEM. complicate lobar pneumonia or occur as an idiopathic condition. A large part of a lobe or of an entire lung becomes greenish, putrid, and soft, and the pulmonary pleura is inflamed. There may be hem- orrhages from eroded vessels. There may be general septiceemia. Various forms of bacteria may be present in gangrenous areas of the lungs. Among those frequently present is the Staphylococcus pyogenes, Streptococcus pyogenes, pneumococcus, and various sapro- phytic micro-organisms. PNEUMONIA. The inflammations of the lungs, as distinguished from those of the bronchi and pleura, are called “ pneumonia.” In the present state of our knowledge the classification of the different forms of pneumonia must be an arbitrary one. We describe separately : I. Acute lobar pneumonia. II. Broncho-pneumonia. III. Secondary and complicating pneumonia. IV. The pneumonia of heart disease. ", Interstitial pneumonia. VI. Tuberculous pneumonia. VIL. Syphilitic pneumonia. I. Acute Lobar Pneumonia. This is an acute exudative inflammation, which involves regularly the whole of one lobe, or the larger part of one lung, or portions of both lungs. It is an infectious inflammation, caused by the growth in the lung of the Diplococcus lanceolatus (Diplococcus pneumonize of Frankel) (see page 201).' The inflammation is of pure exudative type, characterized by con- gestion, emigration of white blood cells, diapedesis of red blood cells, and exudation of blood plasma, while the tissue of the lung itself is but little changed. During the first hours of the inflammation, only irregular por- tions of the lobe which is to be inflamed are involved; later the entire lobe. The lung is congested, cedematous, tough, but not consoli- dated. The air spaces contain granular matter, fibrin, pus cells, red 1 There are occasional irregular forms of pneumonia attended with the growth of other species of bacteria, and which involve whole lobes. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 439 blood cells, and epithelial cells (see Fig. 208). The epithelium re- maining on the walls of the air spaces is swollen; there are large numbers of white blood cells in the capillaries. The larger bronchi are congested, dry, or coated with mucus; the small bronchi contain the same inflammatory products as do the air spaces. The pulmo- nary pleura, as a rule, is not coated with fibrin. This is called the stage of “congestion.” The stage of congestion regularly only lasts a few hours, but it may be protracted for several days. When the exudation of the inflammatory products has reached ‘Fig. 208,—AcuTE LoBAR PNEUMONIA—ReED AND GRAY HEPATIZATION, x 850 and reduced. Showing the pneumococci of Frankel in the exudation, stained violet. its full development the presence of these products within the air spaces and bronchi causes the lung to be solid, and at this time the lung is said to bein the condition of ‘‘red hepatization.” The lung is now consolidated, red, its cut section looks granular, the granules corresponding to the plugs of inflammatory matter within the air spaces. For some time after death the inflammatory products re- main solid and the cut section of the lung dry ; but later, with the commencement of post-mortem changes, these products soften and Digitized by Microsoft® L400 THE RESPIRATORY SYSTEM. the cut section is covered witha grumous fluid, The air vesicles, the air passages, the small bronchi, and sometimes the large bronchi, are filed and distended with fibrin, pus cells, red blood cells, and epithe- lium, and may contain large numbers of bacteria (Fig. 208). In spite of the pressure on the walls of the air spaces the blood vessels in their walls remain pervious. The pulmonary pleura is coated with fibrin and the interstitial connective tissue of the lung is infil- trated with fibrin. The hepatized lobe is increased in size, some- times so much so as to compress the rest of the lung. About one- fourth of the fatal cases die in the stage of red hepatization at any time from twenty-four hours to eleven days after the initial chill. Fig. 209.—AcuTE LoBparR PNEUMONIA WITH THE PRODUCTION OF ORGANIZED TISSUE IN THE AIR Spaces, < 130 and reduced. The section shows a number of air vesicles containing organized tissue. After the air spaces have become completely filled with the exu- dation, if the patient continues to live, there follows a period during which the exudate becomes first decolorized and then degenerated. This is the period of ‘‘gray hepatization.” The lung remains solid, its color changes, first to a mottled red and gray, then to a uniform gray. The coloring matter is discharged from the red blood cells and the exudate begins to degenerate and soften. The lung is found passing from red to gray hepatization at any time between the Digitized by Microsoft® THE RESPIRATORY SYSTEM. 441 second and the eighteenth day of the disease. It is found com- pletely gray at any time from the fourth to the twenty-fifth day. About one-half of the cases die in the condition of mottled red and gray hepatization ; about one-fourth in the condition of gray hepa- tization. If the patient recovers the exudate undergoes still further de- generation and softening and is removed by the lymphatics. This is the stage of ‘‘resolution.” It should commence immediately after Fic. 210.—ORGANIZED TISSUE IN AN AIR VESICLE, X 850 and reduced. defervescence and be completed within a few days. But it may not begin until a number of days after defervescence, or it may be un- usually protracted, The pneumococcus of Frankel (often also called the Diplococcus pneumonie of Frankel) is the bacterium most often present in the lungs in acute lobar pneumonia, and the form which there is much reason to believe, in the large proportion of cases, to be the cause of the disease. The germ is described on page 201. There is a form of lobar pneumonia in which the inflammation is not ee an exudative ongeb tt hpeeds ASP a growth of new con- A442 THE RESPIRATORY SYSTEM. nective tissue in the walls of the air spaces and in their cavities (Fig. 209). This condition has been usually described as a chronic inflam- mation following an ordinary lobar pneumonia. It seems really to be from the outset a special form of pneumonia. For we find, in patients who have not been sick for more than a few days, that the pneumonia already has its characteristic form. Still further, even in its earlier stages the clinical history is somewhat different from that of an ordinary lobar pneumonia. Fie. 211.—Arr VESICLES CONTAINING ORGANIZED TISSUE IN LoBAR PNevumonI4A, < 350 and reduced. The blood vessels are injected. If the patient dies within three weeks of the commencement of the pneumonia we find one or more lobes consolidated but not much enlarged. The hepatization is smooth and dense. The walls of the air spaces are thickened and coated with an increased number of epithelial cells. Some of the air spaces contain only fibrin and pus, but in others there is new connective tissue, basement substance and cells (Fig. 210). In this new tissue there may be new blood vessels, which can be artificially injected from the vessels of the lung (Fig. 211), Digitized by Microsoft® THE RESPIRATORY SYSTEM. 443 If the patient lives for several months we find the lung very dense and smooth. The growth of new connective tissue is more ex- tensive, the air spaces are completely filled, their walls are much thickened, and in some places the lung tissue is completely changed into smooth connective tissue. Fic. 212.—BRoNCHO-PNEUMONIA FROM A CHILD. The walls of the bronchi thickened with zones of peribronchitic pneumonia, IT, Broncho-pneumonia (Capillary Bronchitis, Lobular Pneu-- monia, Catarrhal Pneumonia). This is the ordinary pneumonia of young children; it is frequent. also in young persons, but not as common in adults. In children it seems to be usually due to causes similar to those: which produce lobar pneumonia in adults—that is, to micro-organ- isms, especially the pyogenic cocci, and sometimes to the inhalation. or inspiration of inorganic irritating substances. In adults the disease may present itself to us in a variety of ways. 1. The patients have au ordinary attack of catarrhal bronchitis. lasting for several days. Instead of getting well promptly, how-- Digitized by Microsoft® 444 THE RESPIRATORY SYSTEM. ever, the patients continue to cough and to feel sick, and on examin- ing the chest we found a circumscribed area where there is dul- ness on percussion and loud, high-pitched voice. This consolidation of the lung does not, however, last very long, and the patients make a good recovery. 2. The patients are suddenly attacked with a very severe and general broncho-pneumonia. There are chills, a rapid rise of tem- perature, headache, pains in the back and chest, vomiting, great prostration, a rapid pulse which soon becomes feeble, very bad breathing—rapid, labored, and insufficient—venous congestion of the skin and of the viscera, cough, at first dry, then with profuse mucus and blood-stained sputa, sleeplessness, restlessness, and delirium, and albumin in the urine. There are coarse subcrepitant and crepi- tant rales over both lungs, sibilant and sonorous breathing ; the per- cussion note is normal, or exaggerated, or dull. The disease lasts for from seven to fourteen days, and is very apt to prove fatal. 3. There is a form of broncho-pneumonia in adults which re- sembles lobar pneumonia. There is a general catarrhal bronchitis, with broncho-pneumonia and consolidation of one or more lobes. The symptoms and physical signs are like those of lobar. pneumonia, but with some difference. The invasion of the disease is not as sud- den, the pulse is more rapid, the cerebral symptoms are more con- stant, the expectoration is like that of bronchitis, the physical signs are more slowly developed, the duration of the disease is rather longer and resolution is slower. 4, Thereis a form of broncho-pneumonia which resembles acute phthisis. The patients have a cough with expectoration, at first mucous, afterward muco-purulent. There is a moderate fever, with evening exacerbations and sweating at night. The patients steadily lose flesh and strength. The physical signs are those of bronchitis and of consolidation of parts of the lung. The disease is protracted, continuing as long as ten weeks, and is apt to prove fatal. With substantive emphysema there may be developed a subacute or chronic broncho-pneumonia. The essential or constant lesion of broncho- Jpmewmiauial is an in- flammation of the walls (not the mucous membrane) of the bronchi and of the air spaces immediately surrounding the inflamed bronchi. The walls of the bronchi are thickened and infiltrated by a growth of new cells. The walls of the air spaces are thickened, their cavi- ties are filled with fibrin, pus, and epithelium or with new connec- tive tissue. The inflammation, involves the medium-sized and smaller bronchi of both lungs, but.is not everywhere equally severe ; in some parts of the lungs the lesions are much more marked than in others. In some of the cases there are no other changes except some general congestign gb dba iRero obpather cases there may be THE RESPIRATORY SYSTEM. 445 added a catarrhal inflammation of the mucous membrane: of the bronchi, diffuse consolidation of parts of the lung, pleurisy, dilata- tion of the inflamed bronchi, areas of atelectasis, simple or tubercu- lar inflammation of the bronchial glands. The trachea and the larger bronchi are congested and coated with mucus. The smaller bronchi contain pus, their walls are thickened and infiltrated with cells, and they may be dilated. Around many 7 i Nt Fic, 213,—BRONCHO-PNEUMONIA IN 4 CHILD, X 750 and reduced. Air vesicles in diffuse hepatization. of the small bronchi are narrow zones of congestion or hepatization The rest of the lungs is congested and cedematous. Or the zones of peribronchitic pneumonia are larger, so that a sec- tion of the lung is mottled with little whitish nodules, each nodule corresponding to a cut bronchus surrounded by its zone of pneumonia. Or between these zones of peribronchitic pneumonia are areas of diffuse hepatization which render portions of the lung completely solid (Fig. 213). Or there may be areas of atelectasis corresponding to occluded bronchi. Dera Digitized by Microsoft® 446 THE RESPIRATORY SYSTEM. There is often a thin layer of fibrin on the pulmonary pleura. The bronchial glands are the seat of simple or tubercular inflamma- tion. The dilatation of the bronchi ig not constant. “When present it is of the cylindrical character and involves the medium-sized bronchi for a considerable part of their length. Such dilated bronchi are each of them surrounded by a narrow zone of pneumonia ; the inter- vening lung tissue may be still aérated or hepatized. In these peribronchitic zones of pneumonia the thickening and cellular infiltration which exist in the walls of the bronchi extend Fig. 214.—BRONCHO-PNEUMONIA IN AN ADULT, X 850 and reduced. An air vesicle containing organized tissue in a zone of peribronchitic pneumonia. also to the walls of the air spaces. These walls are thickened and infiltrated with cells, while the cavities of the vesicles are filled with pus and epithelium or with tissue resembling granulation tissue (Fig. 214). In the diffuse hepatization the air vesicles are filled with epithelium, pus, and fibrin in varying proportion and quantity ; the walls of the air spaces remain unchanged. The portions of lung which are not hepatized are congested and cedematous. The cavities of the vesicles are diminished by the en- larged capillaries, the epithelium is swollen, and in many vesicles a. few pus or epithelial cells are to be found. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 447 Such a broncho-pneumonia differs from the ordinary lobar pneu- monia very decidedly. The inflammatory process is not a superfi- cial one, resulting only in filling the bronchi and air spaces with in- flammatory products, but it affects also the tissue of the lung, infil- trating the walls of the bronchi and of the air spaces. This interstitial character of the inflammation seems to be the reason why the disease is often protracted and sometimes succeeded by a chronic inflammation. This chronic condition we will call ** Persistent Broncho-pneumonia.” FiG. 215,—PERSISTENT BRONCHO-PNEUMONIA. The original acute broncho-pneumonia is succeeded by a chronic inflammation involving especially the interstitial tissue. This inflammation may involve only some of the smaller bronchi and small zones of vesicles around them, and then a section of the lung will seem to be studded with fibrous nodules (Fig. 215). Or all the bronchi of some part of the lung will be inflamed, the peribron- chitic zones of pneumonia will become continuous, and so part of a lobe or an entire lobe become converted into a dense mass of con- nective tissue. The air vesicles are obliterated by the new connec- tive tissue, the interlobular septa and the pulmonary pleura are thickened (Fig. 216), and the inflamed bronchi may be dilated. The blood vessels, however, are, for the most part, not obliterated, so Digitized by Microsoft 448 THE RESPIRATORY SYSTEM. that the lung does not become necrotic or degenerated, although occasionally areas of cheesy degeneration exist. IIT. Secondary and Complicating Pneumonia. Inflammation of the lungs occurs frequently as a complicating condition with lesions of the brain and spinal cord, with pyeemia, with the continued fevers, after injuries and surgical operations, and in patients who are confined to bed for a long time from any cause, The pneumonia developed in these cases may follow one of two ifferent types. Fig. 216.—PERSISTENT BRONCHO-PNEUMONIA. _ 1. Part of the lung, usually the posterior portion, is congested, leathery, only partly aérated, and mottled by irregular patches of red or gray hepatization which have no relation to the bronchi. In the hepatized portions of the lung the air spaces are filled with pus and fibrin. 2. The inflammation has the characters of a broncho-pneumonia. The small bronchi are filled with pus, their epithelium is altered, their walls are infiltrated with pus, and around each bronchus is a zone of air vesicles filled with pus and fibrin. The lung is mottled with little whitish nodules, corresponding to the bronchi and the Digitized by Microsoft® THE RESPIRATORY SYSTEM. 449 peribronchitic zones, and between these there may be a diffuse hepa- tization. In children suffering from diphtheria, with pseudo-membranes containing pathogenic bacteria in the fauces and upper air passages, a secondary pneumonia may apparently occur as the result of the entrance into the lung spaces of the germs from above (Fig. 217).? Although the pyogenic bacteria are the most frequent inciters of secondary and complicating pneumonia, other forms of germs are capable of inducing it. Fic. 217,-BRONCHO-PNEUMONIA IN a CHILD, COMPLICATING DIPHTHERIA. Air vesicle showing inflammatory products and large numbers of bacteria (streptococci) stained with methy] violet. IV. The Pneumonia of Heart Disease, Lesions of the aortic and mitral valves, and dilatation of the left ventricle, often produce a diffuse, chronic inflammation of both lungs of a peculiar character. This condition is often called pigment in- duration, or brown induration, but it is really a chronic pneumonia. The lungs are diminished in size and of a peculiar yellow-pink color, mottled with spots of black or brown pigment. They are not congested, but are of a dry, leathery consistence ; or portions of them 1 Consult Prudden and Northrup, ‘‘Studies on the Etiology of Pneumonia com- plicating Diphtheria in Children,” American Journal of Medical Sciences, June, 1889. 36 Digitized by Microsoft® 450 THE RESPIRATORY SYSTEM. may be in the condition of a smooth red hepatization. The appear- ance of these lungs may be modified by the presence of haemorrhagic infarctions, by the pre-existence of emphysema, or by cedema. Minute examination of these lungs shows four separate pathologi- cal conditions. 1. A change in the capillaries in the walls of the air spaces. These capillaries are dilated and tortuous, so that they project into the cavities of the vesicles (Fig. 218). The degree of the dilatation varies in the different lungs; in some itis very marked, in others but light. 2. A thickening of the walls of the air spaces, due partly to the Begs Bh. , Fic. 218.—Lune@ or Heart DISEASE. Showing dilated capillaries of the walls of the air vesicles and the presence of hematogenous pigment in the exfoliated epithelial cells of the air vesicles. dilatation of the capillaries, partly to a growth of smooth muscle, and partly to a growth of connective tissue. The degree of the thickening varies very much in different cases. 3. A formation of black or brown pigment in the shape of gran- ules and small masses. This is deposited in the walls of the vesicles, in the interstitial connective tissue, and in the new cells within the vesicles (Fig. 218). 4, A formation of cells within the air spaces. The walls of the vesicles are coated with a layer of flat, nucleated cells. Similar cells, or swollen and granular cells, are present in the cavities of the Digitized by Microsoft® THE RESPIRATORY SYSTEM. 451 vesicles (Fig. 218). If these cells are numerous the cavities of the vesicles are filled, and there results a smooth red hepatization. V. Interstitial Pneumonia. This name is given to a chronic productive inflammation, which involves the connective-tissue framework of the lung and the walls of the air spaces, and results in the formation of new connective tissue and the obliteration of the air spaces (Fig. 219). Such an interstitial pneumonia may follow acute lobar pneumonia Sia Fic. 219.—INTERSTITIAL PNEUMONIA, X 90 and reduced, From a case of chronic phthisis. with the production of new connective tissue; broncho-pneumonia; chronic pleurisy; chronic bronchitis; or be caused by the inhalation of the dust of coal or of stone. The condition of the lung varies with the cause of the interstitial pneumonia. If it follows acute lobar pneumonia with the production of new connective tissue, one lobe, or the whole of one lung, is covered with pleuritic adhesions. The lobe or the lung is small, smooth on sec- tion and dense. The air spaces and small bronchi are obliterated ky the new connective tissue. If it follows broncho-pneumonia, one or more lobes are studded Digitized by Microsoft® 452 THE RESPIRATORY SYSTEM. with fibrous nodules, which correspond to the inflamed bronchi; or the whole of a lobe is converted into dense fibrous tissue. The pleura is thickened, the bronchi are inflamed and often dilated. If it follows thickening of the pleura, bands of connective tissue extend from the pleura into the lung, the bronchi are inflamed and often dilated. If it follows chronic bronchitis, there are fibrous nodules around the bronchi, with more or less diffuse connective tissue. If it is due to the inhalation of coal or dust, we find in both lungs fibrous peribronchitic nodules and diffuse connective tissue. When only one lung is involved the other is apt to be emphysem- atous. Suppurative interstitial pneumonia is sometimes produced in cases of septicemia. The pulmonary pleura is coated with fibrin, the bronchi contain pus, portions of the lung are hepatized, and the in- terlobular septa are infiltrated with pus. VI. Tuberculous Pneumonia. We employ the name of “ tuberculous pneumonia” to designate the inflammations of the lungs which are caused by the introduction of tubercle bacilli into these organs. Such tuberculous inflammations of the lungs may be confined to them, or they may be accompanied by tuberculous inflammations of other parts of the body. For the development of a tuberculous inflammation there seem to be necessary the irritation of the tissues caused by the tubercle bacilli and a predisposition on the part of the individual. The development of such an inflammation in any part of the body is also favored by the conditions which favor or the causes which induce other phases of inflammation. The tubercle bacilli are capable of setting up different anatomical forms of inflammation, either separately or together. They may give rise to exudation from the blood vessels, to the production of new tissue, or to necrosis (see page 218). The introduction of tubercle bacilli into the lungs, therefore, may produce: an exudative inflammation with fibrin and pus cells in the air spaces; a productive inflammation with the growth of epithelial cells, or of round-celled tissue, or of a tissue composed of basement substance, large and small cells, and giant cells, called tubercle tissue (see page 217); or there may be added necrosis of the new tissue and of portions of the lung. The character of the inflammation in each case seems to be gov- erned by the number of bacilli which are introduced into the lungs and the way in which they are introduced, as well as by the suscepti- Digitized by Microsoft® THE RESPIRATORY SYSTEM. 453 bility of the individual. If a large number of tubercle bacilli are inhaled through the bronchi, both productive and exudative inflam- mations may be set up in a considerable portion of the lungs. If, on the other hand, but a small number of bacilli are inhaled, or if these find their way into the lungs through the blood vessels or lymphatics, then there are small foci of productive inflammation with but little exudation. There are two ordinary ways in which the lungs are infected: (a) The bacilli which float in the air are inhaled and irritate the small bronchi and the air spaces; (0) the bacilli contained in a focus of tuberculous inflammation in some other part of the body are carried by the blood vessels to the lungs, become lodged there and set up small areas of inflammation. The changes in the lungs may also be modified by an infection with other pathogenic micro-organisms. As the gross appearance of the lungs varies with the character, extent, and development of the different phases of inflammation excited by the tubercle bacilli, a number of arbitrary names have been given, which may still be conveniently used. We describe, therefore, Acute Miliary Tuberculosis; Subacute Miliary Tuberculosis; Crronie Miliary Tuberculosis; Acute Phthisis and Chronic Phthisis. Acute Miliary Tuberculosis.—The acute development of miliary tubercles in the lungs is usually only part of general tuberculosis, although the lesion may be most extensive in the lungs. Both lungs are apt to be involved, but the distribution, number, size, and character of the miliary tubercles differ in different cases. The larger bronchi are the.seat of catarrhal inflammation; the lung tissue is congested; the air spaces contain epithelium, pus, and fibrin in small quantity. The tubercles are found in the parenchyma of the lung, in the connective tissue forming the septa, along and in the walls of the bronchi and blood vessels, and in the pulmonary pleura. They are scattered singly through the lungs, or aggregated in groups. They may be separated by considerable interspaces, or so close together that the lung is rendered nearly solid. Some are so small and transparent that they can hardly be seen with the naked eye; others are larger and more opaque. In children’s lungs large masses are found of the same structure as miliary tubercles. In many cases it seems evident that the lungs are infected through the blood vessels, or perhaps through the lymphatics, for the general tuberculous infection is secondary to a localized tuberculosis of some other part of the body. But in other cases no such localized primary focus can be found, so that infection by inhalation is possible. The Digitized by Microsoft® 454 THE RESPIRATORY SYSTEM. whole picture of acute tuberculosis is such, however, as to give the impression that the infection usually takes place through the blood vessels and lymphatics. The anatomical forms of miliary tubercles are as follows: 1. Miliary tubercles composed of a group of air vesicles contain- ing amorphous granular matter, with a few shrunken cells and an external zone of pus cells. The walls of the air spaces may be still visible, and may be infiltrated with exudate, or they may be necrotic Fig. 220,—M1m1ary TUBERCLE IN LuNG oF CHILD. Showing the Bacillus tuberculosis—stained with fuchsin—in the contents of the air vesi¢les and in their thickened walls. (The size of the bacilli relative to other elements is slightly exaggerated.) and lost in the mass of granules. The only changes are exudation and necrosis (Fig. 220). In adults such tubercles are usually small, but in children they may reach a large size. 2. Miliary tubercles formed by the infiltration of the wall of a bronchiole or air passage with tubercle tissue or granulation tissue. This infiltration is apt to involve only one side of the bronchiole or air passage (Fig. 221). It may be confined to this or it may extend to the walls of the adjacent vesicles. These vesicles may remain Digitized by Microsoft® THE RESPIRATORY SYSTEM. 455 empty, they may be dilated, or they may be filled with tubercle tissue or with epithelium, fibrin, and pus. In these tubercles we see productive inflammation by itself in some cases, combined with exudation in others. The inflammation seems to begin in the walls of the small bronchioles and to extend: from them to the adjacent air spaces. Fig. 221.—A PERIBRONCHITIC MILIARY TUBERCLE. In all miliary tubercles there is often cheesy degeneration of the central portions. Although all miliary tubercles are caused by the presence of tubercle bacilli, it may be quite difficult to demonstrate the bacilli in each. These tubercles are formed by a combination of productive and exudative inflammation which involves groups of air spaces. 3. Miliary tubercles composed of a group of air spaces of which the walls are infiltrated and the cavities filled (Fig. 222) with granu- Digitized by Microsoft® 456 THE RESPIRATORY SYSTEM. lation tissue or tubercle tissue; as the infiltration progresses the blood vessels are obliterated (Fig. 223). Such an infiltration may involve symmetrically the whole of the wall of an air space, or only a por- tion of the wall. The cavities of the air spaces are filled with tuber- cle tissue, or with epithelium, fibrin, and pus. In some of these tubercles the tubercle tissue, both in the walls of the air spaces and in their cavities, is well developed (Fig. 224); then they look like little tumors replacing the lung tissue. In others the outlines of the walls of the vesicles are preserved, granulation tissue predominates, the cavities of the vesicles contain pus, epithelium, fibrin, and less tubercle tissue (Fig. 225); then the tubercle look, like little areas of a composite hepatization. esas, Subacute Miliary Tuberculosts.—The disease usually involves only the apex of one lung, or one lobe, or portions of both lungs. The inflammation may continue for weeks or months, then stop and the patient recover. Or the patient may have a number of attacks, from each one of which he recovers. Or the disease may con- tinue, extend, and cause death within a few months. Or it may be succeeded by chronic miliary tuberculosis. The miliary tubercles are small. Most of them are formed within the air spaces or around the bronchioles. They are composed princi- pally of tubercle tissue or of round-celled tissue. In the portion of lung where the tuberculous inflammation is going on there may also be localized catarrhal bronchitis and pleurisy. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 457 It seems evident that the infection is produced by a small number of bacilli, and that the principal effect of their presence is a produc- tive inflammation of the walls of the air spaces and of the small bronchi. It is much to be regretted that we are still uncertain as to the method of infection in these cases. There is no demonstration as to whether the bacilli are usually introduced through the bronchi or the blood vessels. Fig, 223.—A Miniary TUBERCLE, X 3800 and reduced Involving only two air vesicles, of which the walls are infiltrated and the cavities filled with tubercle tissue. The blood vessels of the air vesicles are injected. Chronic Miliary Tuberculosis.—The morbid process is apt to begin at the apex of one lung and then slowly extend, either pro- gressively or in attacks, until a large part of the lungs is involved. The whole course of the disease is such as to give the impression of an infection through the blood vessels and lymphatics and not by inhalation. The: inflammation excited is of the productive form running a slow course. Digitized by Microsoft® 458 THE RESPIRATORY SYSTEM. In the simplest form of the disease the only change in the lungs is the formation of miliary tubercles. These tubercles are harder and denser than those found with general tuberculosis or with subacute pulmonary tuberculosis. They are composed of tubercle tissue, or round-celled tissue, or connective tissue, or are in the condition of cheesy degeneration. Usually, however, in addition to the miliary tubercles there are other changes in the lungs. These additional lesions begin in the eT as te Wiliaya se Pia, 2244.—A Miuiary Tupercie, < 3380 and reduced. Formed of several air vesicles filled with tubercle tissue and surrounded by a zone of tissue resembling granulation tissue. same part of the lung where the tubercles are formed, and accompany the development of the tubercles in fresh parts of the lungs. There may be a localized catarrhal bronchitis. There may be an inflammation of the walls of the bronchi, with partial destruction of these walls and the formation of cylindrical or sacculated bronchiectasie. The walls of the cavities thus formed may be converted into connective tissue, or they may remain suppu- rating and necrotic. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 459 There may be an interstitial pneumonia with the production of new connective tissue, the obliteration of the air spaces, and the con- solidation of portions of the lungs. There may be dilatation of the air spaces of the portions of the lungs which are not consolidated. There may be thickening of the pulmonary and costal pleura, with connective-tissue adhesions. While the morbid process begins as a localized tuberculous inflam- mation of the lungs, and often retains throughout this local charac- ter, yet it may also happen that from this local lesion other parts of the body may be infected. Tuberculous laryngitis, and tuberculous Fig. 225.—A Minrary TUBERCLE, < 300 and reduced. Formed of a number of air vesicles. some containing tubercle tissue, others pus and epithelium. inflammation of the solitary and agminated lymph nodules of the small intestine, often complicate the pulmonary lesion, and some- times even acute general tuberculosis is produced. Acute Pulmonary Phthisis.—This name is used to designate the tuberculous inflammation of the lungs in which exudative inflamma- tion preponderates, but is associated with productive inflammation. It seems evident that this feature of the inflammation is due to the large number of bacilli introduced by inhalation through the bronchi, or which rapidly grow in the lung, and to the frequent association of an infection with other bacteria, especially streptococci. The changes produced in the lungs by the introduction into the bronchi of tubercle bacilli can be well studied in animals. One of us Digitized by Microsoft® 460 THE RESPIRATORY SYSTEM (Prudden)' by the injection of tubercle bacilli alone and associated with streptococci into the tracheze of rabbits has been able to repro- duce very closely the lesions of acute phthisis. Fig. 226. Fig. 227. Fic. 226.—EXPERIMENTAL TUBERCULOUS INFLAMMATION (MILIARY) IN THE LuNG OF a RABBIT. The rabbit's lung shows miliary foci of tuberculous inflammation, twenty-two days after the: injection through the trachea of a small quantity of broth culture of the tubercle bacillus. Fic. 227.—EXPERIMENTAL TUBERCULOUS INFLAMMATION IN THE LunG oF A RaBBit. Large areas of solidification in the lung twenty-eight days after the injection through the: trachea of a considerable quantity of a pure culture of the tubercle bacillus. The lesions resem- ble those of acute phthisis in man. If asmall quantity of a pure culture of the tubercle bacillus in very minute flocculi is mixed with a considerable quantity of salt 1 New York Medical Journal, July 7th, 1894. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 461 solution and introduced into the lungs through the trachea a number of small areas of consolidation are produced which have the gross appearance of miliary tubercles (Fig. 226). These small areas of consolidation are composed of epithelial cells and leucocytes. After the development of these cell masses, which may occur within a few hours, they may remain with little apparent change, or become more or less infiltrated with leucocytes, or become cheesy, or be surrounded by a dense zone of small spheroidal cells. When larger quantities of the tubercle bacillus are introduced into the lungs through the trachea large areas of consolidation are formed (Fig. 227), which may involve whole lobes or whole lungs. The first effect upon the lungs is the collection about the bacilli, in the air spaces where they have lodged, of dense masses of leucocytes. These cell collections immediately about the germs form the centres of the inflammatory foci which develop later. They correspond in shape to the shapes of the small bronchi and the connecting air spaces in which the bacilli have lodged. The walls of these cell-filled spaces may soon become necrotic, even within twenty-four hours. The blood vessels about these intra-alveolar masses of small cells and tubercle bacilli are intensely congested, and within forty-eight hours a considerable proliferation of alveolar epithelium has occurred in the zone of air spaces surrounding the primary foci. Giant cells may form in the air spaces, apparently by the fusion of the new-formed epithelial cells. The changes of a productive inflammation may begin in the walls of the air spaces about the primary small-celled foci as early as the third day. The smaller bronchi belonging to the involved air spaces may also be densely packed with small spheroidal cells. Within the first three days, if the quantity of injected tubercle bacilli be large, the air spaces about the involved areas may be the seat of an exudative inflammation, so that they are closely filled with fibrin and leucocytes as well as with epithelium. Almost as soon as they have collected a large part of the leucocytes about the tubercle bacilli may die, so that within three days after the intro- duction of the bacilli these cell masses are converted into a granular mass—coagulation necrosis—in which only the nuclei can be distin- guished. The tubercle bacilli are confined to these central cell masses, so that both the epithelial cell proliferation and the exudative inflam- mation appear to result from some soluble product of the tubercle bacillus which may be diffused. As time passes the naked-eye distinction is maintained between a larger or smaller irregular-shaped central white area of consolida- tion, the seat of lodgment of the bacilli, and a surrounding translu- cent zone of consolidated lung which contains few bacilli. The cen- tral mass of necrotic cells and lung tissue gradually undergoes Digitized by Microsoft® 462 THE RESPIRATORY SYSTEM. coagulation necrosis and increases in size by encroachment on the surrounding zone of consolidation. The translucent border zone of consolidation grows wider, the air spaces in it are filled with epithe- lium, fibrin, and leucocytes. There is a growth of new tissue in the walls of the air spaces. Giant cells are often abundant in this zone. The changes thus far indicated are such as may occur within the first two weeks after the injection of the bacilli. From this time on Fic. 228.EXPERIMENTAL TUBERCULOUS INFLAMMATION IN THE LUNG OF A RABBIT, WITH THE FORMATION OF CAVITIES. The lung was injected with a considerable quantity of tubercle-bacillus culture through the trachea, followed after twenty-eight days by the injection of the broth culture of the strepto- coccus pyogenes. Animal killed seven days after the streptococcus injection. The specimen shows Jarge areas of consolidation with cavities. The lesions resemble those of acute phthisis with cavities in man. up to the seventh week the changes are quantitative rather than qualitative. The central necrotic mass may become fully cheesy, and may grow slowly larger by encroachment upon the surrounding zone of epithelial cell proliferation and productive and exudative in- flammation. The areas of consolidation may coalesce so as to render whole lobes or lungs solid, so that to the naked eye the cut surface Digitized by Microsoft® THE RESPIRATORY SYSTEM. 463 presents an irregular mottling with large or small white masses and more translucent intervening areas. The intima of the large blood vessels near the involved areas may be thickened and smaller trunks may be obliterated. In the presence of the tubercle bacillus alone the cheesy areas but rarely soften and break down so as to form cavities. If, however, after the tuberculous inflammation of the lung has been produced and allowed to continue for a number of days, a culture of Streptococcus ec aae Fie, 229. TUBERCULOUS BRONCHO-PNEUMONIA. The walls of the bronchi are thickened and surrounded by zones of pneumonia. pyogenes be introduced into the trachea in a rabbit, within twenty- four hours the cheesy areas begin to soften. The softening may be- gin at the centre of a cheesy area, or may surround a central portion of the necrotic mass. The softening is soon followed by absorption, and go cavities are formed of varying sizes and shapes (Fig. 228). Tt will thus be seen that in the rabbit a concurrent infection with the tubercle bacillus and the streptococcus has an important bearing Digitized by Microsoft® 464 THE RESPIRATORY SYSTEM. upon the breaking down of lung tissue which leads to the formation of cavities. While it would not be wise to assume from these ex- periments on the rabbit that a similar condition exists in man, it will be seen presently (page 467) that in fact a similar concurrent infection in man in acute phthisis actually does often exist. The tuberculous inflammation of the lungs in human beings pro- Fig. 230.—An AREA oF CoAGULATION NECROSIS SURROUNDED BY A ZONE OF PNEUMONIA, x 40 and reduced. duced by the inhalation of a large number of tubercle bacilli pre- sents five varieties which have well-marked anatomical and clinical characteristics. I. In one or more lobes there are miliary tubercles in considerable numbers, and a diffuse hepatization. The miliary tubercles have the structure already described under the head of acute tuberculosis. The diffuse hepatization is like that of lobar pneumonia—the air spaces are filled with fibrin, pus, and epithelium. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 465 This form of acute phthisis is not of common occurrence. I=f an entire lung is consolidated the patients usually die within a short time. If only one lobe is involved, it is possible for them to recover, for the fibrin, pus, and epithelium to be absorbed, and only the miliary tubercles left as a permanent change. II. There is a general catarrhal bronchitis and a tuberculous in- flammation of the walls of some of the bronchi and of small zones of air spaces immediately surrounding them, but there is no diffuse con- solidation. The inflammation of the walls of the bronchi is produc- tive with the formation of tubercle tissue and round-celled tissue. Fig. 231.—TusercuLous INFLAMMATION OF THE LuNG WITH CHEESY DEGENERATION ABOUT THE BRONCHI IN A SINGLE LoBULE OF THE LUNG—ACUTE PHTHISIS. That of the surrounding zone of air spaces is partly productive, partly exudative. Some of the air spaces are filled with epithelium or with fibrin and pus, some with tubercle tissue. In these patients the only physical signs are those of the general bronchitis. If the lesion is not too extensive recovery is possible. III. There is acatarrhal bronchitis, a tubercular inflammation of the walls of the bronchi and of the air spaces surrounding them, and a diffuse consolidation of rather complex character. One or more lobes are competely consolidated, while in other parts of a lung there are little whitish nodules, but no general con- 8 Digitized by Microsoft® 466 THE RESPIRATORY SYSTEM. solidation. The consolidated portion of lung is not of uniform appearance. It is evidently made up of white or yellow areas of different sizes and shapes, surrounded by zones of red or grayish hepatization. The blood vessels of the white and yellow areas are occluded and cannot be injected, the vessels of the surrounding zones of hepatization are pervious. The white and yellow nodules are formed in three different ways. 1. One or more air passages with the air vesicles belonging to them have their cavities filled with fibrin, pus, epithelium, and tubercle tissue, while their walls are more or less infiltrated with tubercle tissue. The tubercle bacilli find their way into these air passages and excite an inflammation which is principally produc- tive. 2. There is an inflammation of the walls of the small bronchi and of the air spaces around them so that on section these bronchi and associated air spaces look like nodules. These little bronchi are inflamed in three ways: (a) The bronchus contains pus and epithe- lium, its wall is infiltrated with round cells, the surrounding air spaces are filled with epithelium, pus, and fibrin. (0) The wall of the bronchus is infiltrated with tubercle tissue and the surrounding air spaces contain tubercle tissue. (c) There is no change in the wall of the bronchus, but the surrounding air spaces contain tubercle tissue. The tubercle bacilli lodge in the small bronchi and set up exudative or productive inflammation in their walls and in the air spaces which surround them. 3. There are small or larger areas of the lung in the condition of coagulation necrosis or of cheesy degeneration. These areas are sur- rounded by zones of exudative or of productive inflammation. They correspond exactly to the changes produced in the lungs of rabbits by the injection of tubercle bacilli into the trachea. It is from the rabbit’s lungs that we can learn the early stages in the formation of these areas of coagulation necrosis. The tubercle bacilli lodge in’ groups of air spaces and set up in them an exudative inflammation. These air spaces are quickly filled with pus and epithelium, and the blood vessels in their walls become obliterated. Then follow degen- eration, coagulation necrosis, and cheesy degeneration. At the same time these necrotic areas seem to act as irritants and around them are set up zones of exudative or productive inflammation. In the diffuse hepatization between the nodules the blood vessels remain pervious and can be readily injected. The air spaces are more or less com- pletely filled with inflammatory products. The inflammatory prod- ucts are: pus cells, fibrin, large epithelial cell, minute shining granules, and a peculiar transparent substance. Some air spaces are entirely filled with granules, others with fibrin, others with epithelial Digitized by Microsoft® THE RESPIRATORY SYSTEM, 467 cells, and still others with pus cells, while in still other air spaces these products are combined in different proportions. IV. In acertain number of the cases of acute phthisis, with the Fia, 232,—AcvTE Prrnisis—CAVITIES FORMED BY SOFTENING OF AREAS OF COAGULATED NECROSIS. changes in the lungs just described, within a short time the areas of coagulation necrosis soften and form cavities. Then the lung is honeycombed with irregular, ragged holes of different sizes (Fig. 232). Digitized by Microsoft® 468 THE RESPIRATORY SYSTEM. The conditions are the same as those seen in the rabbit’s lung when infection with tubercle bacilli is followed by infection with strepto- cocci. It seems probable that in the human lung the softening of the areas of coagulation necrosis is due to a secondary infection with streptococci. Numerous observers have in fact found that the Streptococcus pyogenes is present often in enormous numbers both in the consoli- dated areas and in the walls of the cavities in acute phthisis in man. It is probable, furthermore, that in this concurrent infection with Fic. 233.—AcuTE PHTHISIS—TUBERCULOUS INFLAMMATION OF THE LUNG AND DILATATION OF BRONCHI. the tubercle bacillus and the streptococcus the latter may play a most important part not only in the local lesion, but in the systemic poi- soning of which the hectic fever is so frequent a symptom.’ V. There are cases of acute phthisis in which the changes in the walls of the bronchi are especially marked. (a) The walls of the small and larger bronchi are infiltrated with tubercle tissue which undergoes cheesy degeneration. The cavity of the bronchus is dilated and contains inflammatory products also in a condition of ! Citation of the earlier studies on concurrent or mixed infection in pulmonary tuberculosis will be found in the study by Prudden, New York Medical Journal, July 7th, 1896. Consult also Petruschhy. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 469 cheesy degeneration (Fig. 233). The adjacent air spaces may be unchanged, or may contain tubercle tissue, pus, fibrin, or epithelium. The necrosis may extend to the surrounding lung. In this way, partly by dilatation, partly by necrosis, cavities of considerable size are formed. (6) There is a general dilatation of the bronchi in a considerable portion of the lung without any marked change in their walls, and regina iy nt Hie Net vate Fig. 234.—Curonic Paruisis, x 850 and reduced. An air vesicle filled with fatty epithelium. with only a moderate quantity of inflammatory products in their cavities. This change is especially apt to affect the medium-sized and small bronchi. The lung tissue between the bronchi is usually consolidated. When such a lung is cut it looks as if it were honey- combed with small cavities, but these cavities are only sections of the dilated bronchi. Chronic Pulmonary Phthists.—The lesions are of the same Digitized by Microsoft® 470 THE RESPIRATORY SYSTEM. Fig. 235.—Dirruse TUBERCULOUS INFLAMMATION PRODUCING DirrusE CONSOLIDATION OF THE Lune, X 300 and reduced. Fig. 236.—CHRonic PHTHISIS—INTRA-ALVEOLAR PNEUMONiA. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 471 Fic. 237,—CHRONIO PHTHISIS, X 850 and reduced. Showing growth of connective tissue within an air vesicle. Fic, 238.—-CHRONIO PHTHISIS, < 850 and reduced. rowth of connective tissue within an air vesicle. igitized by Microsoft® Showing 472 THE RESPIRATORY SYSTEM. nature as those of acute phthisis, but are modified by the long con- tinuance of the inflammation. 1. The air spaces: (a) The air spaces are filled with swollen and fatty epithelium (Fig. 234), or with fibrin and pus, while their walls are unchanged and their blood vessels remain pervious. (b) The air spaces are filled and distended with compact fibrin and shrivelled pus and epithelium. Their walls are compressed and thin, or thickened and infiltrated with cells. The blood vessels can be only f EG Wi y p Ly 4 Fig, 239.—InTERsTITIAL PNEUMONIA oF CHRonic Puruisis, x 850 and reduced. very imperfectly injected. This condition may be succeeded by com- plete cheesy degeneration. (c) The walls of the vesicles are thickened, their cavities are filled with new connective tissue often containing new vessels (Figs. 235, 236, 237, and 238). This new connective tissue may look like an out- growth from the wall of the vesicle, or as if it was formed free in its cavity. (d) There is a diffuse interstitial growth of fibrous tissue and granulation tissue in the walls of the air spaces, the bronchi and the blood vessels, and in the septa. By this new tissue the air spaces are compressed and deformed or completely obliterated (Fig. 239). Digitized by Microsoft® THE RESPIRATORY SYSTEM. 473 2. The nodules: These, as in acute phthisis, consist of areas of coagulation necro- sis, peribronchitic nodules, and miliary tubercles. The tubercles may preserve their characteristic structure, or un- a cheesy degeneration, or be changed into fibrous tissue (Fig. 240). The areas of coagulation necrosis undergo cheesy degeneration, or soften and form cavities. They are surrounded by tubercle tis- sue, or granulation tissue, or connective tissue (Fig. 241). Fic. 240.—AN OLp MILIARY TUBERCLE CONVERTED INTO Fiprous TIssvE (‘‘ HEALED TUBERCLE”), < 90 and reduced. The peribronchitic nodules are much the same as in acute phthisis. 3. The bronchi: The changes in the bronchi in chronic phthisis form a very im- portant part of the morbid process. (a) The larger bronchi may be the seat of a chronic catarrhal inflammation, accompanied by the production of large quantities of mucus and pus. (6) The bronchi of all sizes may be inflamed, with the production of new cells in their walls, in addition to the inflammatory changes of their inner surfaces. Such a cellular infiltration of the walls of the bronchi is often followed by dilatation—either fusiform or saccu- lated. (c) Tubercle granula and granulation tissue are found in the Digitized by Microsoft® 44 THE RESPIRATORY SYSTEM. walls of the bronchi. These tissues may degenerate, soften, and thus form ulcers. (d) The entire thickness of the wall of a bronchus may become the seat of inflammation of a peculiar character. The surface of the mucous membrane is coated with pus, the epithelial layer can no longer be seen, the wall of the bronchus is infiltrated with cells. The inflammatory products undergo cheesy degeneration, so that we find the inner surface of the bronchus coated with cheesy matter, while its wall is also changed into cheesy matter. Such a condition of the bronchus is usually followed by sacculated dilatation. Fig. 241.—TuBERCLE TissUE AROUND AN AREA OF CoAGULATION NECROSIS, 850 and reduced. The cavities of chronic phthisis, therefore, are formed by the dilatation of inflamed bronchi, by the softening of areas of coagula- tion necrosis, or by the combination of both these processes. When cavities are once formed they are apt to continue and to become larger as the disease goes on. Their walls may be converted into granulation tissue, which ulcerates in some places and prolife- rates in others ; or portions of the wall become necrotic ; or all ac- tive processes cease and the wall of the cavity is formed of new connective tissue. The lung tissue between the cavities becomes compressed and altered in various ways. As the cavities increase in Digitized by Microsoft® THE RESPIRATORY SYSTEM. 475 size they touch and open into each other. In this way large portions of the lung may be converted into a dense mass honeycombed with cavities, VII. Syphilitic Pneumonia. Persons suffering from inherited or acquired syphilis sometimes develop inflammations of the lungs which seem to be due to the syphilitic infection. The lungs may then be affected in several dif- ferent ways. Fig. 242.—INTERSTITIAL SyPHILITIC PNEUMONIA, X 170 and reduced. 1, There is an interstitial pneumonia, beginning around the lar- ger bronchi and blood vessels at the root of the lung, and extending to the walls of the air spaces and interstitial ccnnective tissue, so that the central portions of one or both lungs are converted into a dense mass of connective tissue (Fig. 242). 2. There is an interstitial pneumonia, with the formation of gum- my tumors, 3. There is an inflammation of the wall of the trachea and of the larger bronchi. There are ulcers in the mucous membrane, their walls are very much thickened, and their cavities are narrowed or dilated. 4, There are circumscrived areas of interstitial inflammation Digitized by Microsoft® 476 THE RESPIRATORY SYSTEM. around the smaller bronchi, forming small, hard peribronchitic nodules. 5. There is a diffuse hepatization, involving lobules or an entire lobe. The affected portion of the lung is red or white or grayish. The walls of the air vesicles are infiltrated with cells, and their cavi- ties are filled with epithelial cells. 6. There may be a broncho-pneumonia, like the ordinary broncho- pneumonia of children ; or a lobar pneumonia, like that of adults. 7. There may be an obliterating endarteritis of branches of the Fig. 243.—PrimarRy ADENOMA OF THE LuNG, X 300 and reduced. pulmonary artery, with the formation of white infarctions sur- rounded by zones of connective tissue.’ TUMORS. Dermoid cysts have been found in the lungs in a few instances. Fibromata have been described by Rokitansky. Enchondromata may occur both as primary and secondary tu- mors. The primary tumors are small and are believed to originate in the cartilages of the bronchi. The secondary tumors often attain a very large size. 1 Filler, Charité Annalen, 1834, p. 184. Digitized by Microsoft® THE RESPIRATORY SYSTEM. 477 Osteoma is very rare. A. case is described by Luschka.’ Sarcomata as secondary tumors are of not infrequent occurrence. A primary adeno-sarcoma is described by Weichselbaum.’ Lymphomata are found in cases of leukemia and pseudo-leu- keemia. Adenoma of the lungs is of rare occurrence as a primary tumor (Fig. 243). Carcinoma as a secondary growth may have the form of nodules or of diffuse infiltration. Primary carcinoma of the lung has been described by a number of authors. The new growth is in the form of small nodules surrounded by pneumonia. As the result of the new growth and the pneumonia a considerable part of both lungs may be rendered solid. The bronchial glands may be infiltrated, and there may be secondary nodules in the pleura. The new growth may originate in the walls of the air spaces or in the walls of the bronchi.* PARASITES. E'chinococct occur in the lungs in their ordinary cystic form. The sacs may suppurate and discharge through the pleura, the bronchi, the wall of the chest, or the diaphragm. In bronchiectasiz and in gangrenous cavities in the lungs vege- table parasites of various kinds have been described—both moulds and bacteria. The Bacillus tuberculosis is regularly found in the walls and con- tents of cavities in acute and chronic phthisis, sometimes in enor- mous numbers. It is also often present in great numbers in the nodules of tubercular inflammation, particularly when these are softening and beginning to break down to form cavities (see Tuber- culosis). THE MEDIASTINUM. The anterior mediastinum is situated in front of the pericardium, between it and the sternum. At its superior part the two layers of pleures separate somewhat to enclose the vestiges of the thymus gland ; behind the second piece of the sternum they are in contact, but below this the left pleura recedes from its fellow toward the left side, leaving an angular space of some breadth. The triangularis sterni muscle bounds this space in front. 1 Virch. Archiv, Bd. x., p. 500. 2 Tbid., Bd. Ixxxv., p. 559. 3 On the diagnosis of malignant tumors of the lungs, consult Betschart, Virch. Archiv, Bd. exlii., p. 86, 1895; also Adler, New York Medical Journal, February 8th and 15th, 1896. Digitized by Microsoft® 478 THE RESPIRATORY SYSTEM. The posterior mediastinum, stretching from the pericardium to the bodies of the vertebree, encloses between its layers the lower part of the windpipe and gullet, the thoracic duct, the descending aorta, the azygous vein, the pneumogastric nerve, and some lymphatic glands. INFLAMMATION. Suppurative inflammation may occur either in the anterior or posterior mediastinum. It may be caused by fractures, caries, or necrosis of the sternum and vertebrz, by perforation of the cesopha- gus, by suppuration of the lymphatic glands, by pleurisy, or may occur without discoverable cause. The pus may infiltrate the connective tissue, or may form ab- scesses which may attain a large size. The inflammation may ex- tend to the pleura or the pericardium , the abscesses may displace the heart, the lungs, or the sternum ; or they may perforate through the skin into a pleural cavity, the cesophagus, the trachea, or a bronchus. TUMORS, The most common form of new growth in the mediastinum is that known by the names of lymphoma, lympho-sarcoma, and lymph- adenoma. These tumors are confined to the mediastinum, or they are asso- ciated with similar growths in other parts of the body in the disease called ‘‘ pseudo-leukzemia.” Persons between the ages of twenty and thirty years seem to be the most liable to the growth, but it is also not uncommon in chil- dren. The growth begins in the lymphatic glands in the mediastinum, and at the root of the lung. It increases at first slowly, then more rapidly, and gradually infiltrates the adjoining tissues. In this way the walls of the trachea, bronchi, and aorta, the pericardium, the pleura, and the lung, become infiltrated with the growth. The tumor also compresses the surrounding organs. The growth is composed of a connective-tissue stroma infiltrated with small round cells, the relative quantity of cells and stroma vary- ing in the different cases. Besides this form of tumor there may also occur in the medias- tinum tumors similar to those which grow in the pleura and behind the peritoneum—tumors which resemble both the sarcomata and carcinomata, and which it is difficult to classify. Aberrant thyroid- gland tissue may be found in the mediastinum. Complex tumors belonging among the fcetal inclusions or terato- Digitized by Microsoft® THE RESPIRATORY SYSTEM. AUD mata are of occasional occurrence in the anterior mediastinum. They may contain bone, cartilage, connective tissue, muscle, hairs, skin, etc. Cysts sometimes lined with ciliated epithelium may form in such tumors.’ 1 Consult Hare, “Tumors of the Mediastinum, ” Philadelphia, 1889; also Zahn, Virchow’s Archiv, Bd. cxliii., pp. 170 and 416, 1896. Digitized by Microsoft® THE VASCULAR SYSTEM. THE PERICARDIUM. INJURIES. The pericardium may be wounded by penetrating weapons, by gunshot wounds, and by fragments of bone. It may be ruptured by severe contusions of the thorax, and by rapid extravasation of blood into the pericardial sac. Perforations may be produced by empyema, by mediastinal ab- scesses, by abscesses of the chest wall and of the liver, by aneurisms of the aorta, and by suppurative inflammation of the pericardium. DROPSY. In most post-mortems we find a little serum, from one-half ounce to one ounce, in the pericardial sac. This serum is usually clear and of a light-yellow color; if decomposition has commenced it may be of a reddish color, or it may be slightly turbid from the falling-off of the pericardial epithelium. Large accumulations of serum are found as part of general drop- sy from heart disease, kidney disease, etc. The serum is clear and of a light-yellow color. Hydro-pericardium is usually moderate in comparison with the accumulations of serum in the other serous cav- ities; sometimes, however, there is a very large amount of serum, which hinders the movements and interferes with the nourishment of the heart. HEMORRHAGE. Extravasations of blood in the cavity of the pericardium are pro- duced by wounds and rupture of the heart, rupture of the aorta and of aneurisms, and occur with pericarditis. Small extravasations in the substance of the pericardium are found with scurvy, purpura, fevers, etc. PNEUMONATOSIS. Air or gas in the pericardium is sometimes found as a post-mor- Digitized by Microsoft® THE VASCULAR SYSTEM. 481 tem appearance, accompanied with drying of portions of the pericar- dium. Wounds or paracentesis of the pericardium ; the perforation of ulcers of the stomach, cavities of the lungs, and ulcers of the ceso- phagus, may admit air into the pericardial cavity. In purulent peri- carditis with foul, decomposing exudation, gases may be evolved. INFLAMMATION. Pericarditis is very rarely a primary lesion. It is most frequently associated with rheumatism and Bright’s disease, but is also found with pneumonia, pleurisy, phthisis, endocarditis, pyeemia, and may be produced by injuries. The inflammations of the pericardium resemble those of the pleura. They usually begin acutely or subacutely, but may be- come chronic. There is a greater disposition to the escape of blood from the vessels than in pleurisy, so that the inflammatory products are often mixed with blood. The inflammatory process usually be- gins at the base of the heart and from there extends over the rest of the pericardium. Haudative Pericarditis. We may distinguish : 1. Pericarditis with the Production of Fibrin.—In the milder examples of this form of pericarditis the pericardium is congested, or also studded with minute hemorrhages ; its surface is roughened by the deposition of a thin layer of fibrin. In the more severe cases the entire surface of the pericardium is covered with a thick layer of fibrin, and there are fibrinous adhesions between the visceral and parietal pericardium. If the inflammation continues for any length of time the pericardium itself becomes thickened and infiltrated with cells, and the wall of the heart may also undergo inflammatory changes. If the patient recovers the fibrin may be absorbed and the pericar- dium return to its normal condition. Or, instead of this, as the fib- rin disappears there is a growth of new connective tissue which forms permanent thickenings and adhesions of the pericardium, which may afterward become calcified. 2. Pericarditis with the Production of Fibrin and a good deat of Serum.—In these cases the pericardium is coated with fibrin, but, in addition, there is a large effusion of serum into the pericardial sac. This serum accumulates at first between the floor of the pericardium and the lower surface of the heart, and, as it increases, distends the pericardial sac in all directions, pushing the heart upward and for- ward. The pericardial sac may be so much distended as to compress 39 Digitized by Microsoft® 482 THE VASCULAR SYSTEM. the trachea, the left bronchus, the cesophagus, or the aorta. If the patients recover the serum is absorbed, and permanent adhesions and thickenings are left. 3. Pericarditis with the Production of Fibrin, Serum, and a good deal of Pus.—This variety may have the purulent character from the outset, or it may begin as one of the forms just described and afterward assume the purulent character. These latter cases are apt to run a chronic course. In the chronic cases the pericardial sac contains a large amount of purulent serum. The pericardium is coated with fibrin and is itself thickened and infiltrated with cells. The walls of the heart Fic. 244.—OBLITERATURE OF THE PERICARDIAL SAC IN a CHILD. Showing blood vessels growing from the visceral pericardium into the blood clot filling the sac. Transverse section. A, Heart; B, pericardium; C, new-formed vascular tissue extending above to the unorganized clot. A similar layer of new vascular tissue was present over the parietal pericardium, and in places the two layers had coalesced, obliterating the sac. (Specimen loaned by Dr. Freeman.) may be the seat of interstitial myocarditis. In some cases the pro- ducts of inflammation undergo putrefactive changes ; in some cases the serum is absorbed and the fibrin and pus undergo cheesy degene- ration ; in some cases extensive connective-tissue adhesions and cal- cific plates are formed. The pathogenic bacteria most frequently found in the above va- rieties of pericarditis are the Streptococcus and Staphylococcus pyo- genes and the Diplococcus pneumoniz. Obliteration of the Pericardial Sac.—As the result of the for- mation of vascular new connective tissue between the pericardial walls, the sac may be partially or wholly obliterated. Digitized by Microsoft® THE VASCULAR SYSTEM. 483 This may be the conclusion of an acute inflammatory process or it may result from the organization of a blood clot (see page 73) following heemorrhage into the sac. It may occur as the result of the latter process early in life. Tuberculous Pericarditis. This lesion may occur by itself, but is apt to be associated with other tuberculous inflammation in the vicinity of the heart. There may be miliary tubercles scattered diffusely, or limited to certain regions in the pericardium, which is otherwise little changed. Not infrequently, however, there is a considerable thickening of the pericardium, either visceral or parietal, or both. In such cases the new-formed tissue consists of fibrous tissue and of tubercle tissue which has undergone extensive cheesy degeneration. The thickened visceral and parietal pericardium are often more or less grown together, so that the pericardial sac may be partially or almost completely obliterated. An inflammatory exudate often ac- companies the tuberculous process. TUMORS. Fibromata sometimes are developed in the pericardium. They are often of polypoid form, and from atrophy of the pedicle may be- come free in the pericardial sac. Sarcomata and carcinomata occur as secondary growths either from continuous infiltration or as metastatic tumors. : Cysts of the visceral pericardium have been described. We have seen a pedunculated cyst, containing about 6 c.c. of clear fluid, hanging into the pericardial sac from its attachment near the pulmonary artery. The origin of these cysts is obscure. . Endotheltoma.—There may be a growth of flat cells arranged in anastomosing tubules which look like lymphatics, in the pericar- dium, resembling similar growths in the pleura. THE HEART. MALFORMATIONS. The malformations of the heart are usually closely connected with malformations of the aorta and pulmonary artery. They de- pend on arrest of, or abnormal, development; on endocarditis, myo- carditis, thrombosis, or mechanical causes. I. The common arterial trunk is only partially, or not at all, separated into aorta and pulmonary artery. The divisions between the heart cavities are at the same time defective : Digitized by Microsoft® 484 THE VASCULAR SYSTEM. 1. There is one ventricle and no auricle. 2. There is one ventricle and one auricle. 3. There is one ventricle and two auricles ; the aorta is alone or incompletely separated from the pulmonary artery. Ii. The trunk of the pulmonary artery or of the aorta is ste- nosed or obliterated, and from the obstruction to the current of blood the development of the septa between the heart cavities is pre- vented. 1. The aorta, at its origin, or in the ascending portion of the arch, is stenosed or closed. The pulmonary artery gives off the de- scending aorta, and supplies the carotids and subclavians. The fora- men ovale remains open, or there is no septum between the auricles. The ventricular septum is also usually defective. The right ven- tricle is hypertrophied. 2. The pulmonary artery is stenosed or closed. Its branches are supplied by the aorta, through the ductus arteriosus. The ventricu- lar septum is defective, the foramen ovale is open, or the auricular septum defective. III. The malformation affects the aorta and pulmonary artery after they are more fully developed. 1. There is stenosis of the aorta between the left subclavian and ductus arteriosus, or just at the opening of the ductus arteriosus. The descending aorta is then a continuation of the pulmonary artery. 2. The aorta gives off all its branches from the arch, but the de- scending aorta is a continuation of the pulmonary artery; or the carotids may spring from the aorta, the subclavians from the pul- monary artery. 3. The vessels are transposed ; the pulmonary artery arises from the left, the aorta from the right ventricle ; the pulmonary veins empty into the left, the venee cave into the right auricle ; or the veins also may be transposed. The septa are defective. IV. The aorta and pulmonary artery are normal, but the cardiac septa are defective. 1. The foramen ovale remains partly open. This condition may continue through life without giving an; trouble. 2. The ductus arteriosus may remain open for many years ; this also may cause no disturbance. 3. There is a small or large opening in the ventricular septum. This may give rise to no symptoms, unless disease of the heart or lungs be superadded. V. Hither of the auriculo-ventricular orifices may be entirely closed. The foramen ovale remains open, and the ventricular sep- tum is defective. Digitized by Microsoft® THE VASCULAR SYSTEM. 485 VI. The valves of the different orifices of the heart may be ab- sent or defective. The arteries or the ventricles are usually defec- tive at the same time. The aortic and pulmonary valves may consist of two large or four small leaves, instead of the usual three. The edges of the semilunar valves may be fenestrated. These alterations are usually of no significance. Generally speaking, the existence of openings between the two auricles or the two ventricles, admitting some admixture of venous and arterial blood, produces no marked change in the circulation. If, however, the passage of the current of venous blood into the right heart is in any way interfered with, the consequences are very serious. Cyanosis is produced, the skin is of a bluish color, the small veins and capillaries are dilated, exudation of serum and hypertrophy of connective tissue take place, especially in the fingers and toes. Besides the malformations already mentioned we may find : Entire absence of the heart. Abnormal septa and chordze tendinex in the heart cavities. Abnormal shapes of the heart. Abnormal positions of the heart. (a) There is a smaller or larger defect in the walls of the thorax, so that the heart projects on the outside of the chest; the pericar- dium is usually absent. (b) The diaphragm is absent, and the heart is in the abdominal eavity. (c) The heart is in some part of the neck or head ; this occurs only in foetuses very much malformed. (d) The heart is transposed, being on the right side. ABNORMAL SIZE OF THE HEART. (a) The heart may be abnormally large in connection with ob- structive anomalies of the great vessels. (b) The heart may be abnormally small (hypoplasia). This most frequently occurs, according to Virchow, in chlorotic individuals and those who are the victims of the hemorrhagic diathesis. In these cases the aorta and other large arteries are apt to be unusually small and thin-walled. Very rarely two more or less perfect hearts are found in the same thorax. CHANGES IN POSITION. Changes in the position of the heart are congenital or acquired. The congenital malpositions have already been mentioned. Digitized by Microsoft® 486 THE VASCULAR SYSTEM. The acquired malpositions are caused by: 1. Hypertrophy of the heart; its long axis approaches the hori- zontal direction. 2. Changes in the thoracic viscera. Emphysema of both lungs pushes the heart downward. Emphysema, pleurisy with effusion, or pneumothorax of one side pushes the heart to the other side. Pleurisy or chronic pneumonia, producing retraction of one side of the thorax, draws the heart to that side. New growths, aneurisms, and curvatures of the spine displace the heart in various directions. 3. Changes in the abdomen. Accumulations of fluid and new growths in the abdomen, and tympanites, may push the heart up- ward. WOUNDS AND RUPTURES. Wounds of the heart are produced by penetrating instruments, by bullets, and by fragments of bone. The right ventricle is the more frequently wounded ; next the left ; rarely the auricles. The wound may penetrate into the cavities of the heart or only pass partly through its wall, or a bullet or the broken end of a weapon may be embedded in the wall. If the wound penetrate a cavity and be gaping, death may follow instantly and the pericardium be found filled with blood. If the wound be small and oblique, the blood may escape gradually and death may not ensue for several days. In rare cases adhesions are formed with the pericardium and the wound cicatrizes. Wounds which do not penetrate may cause death by the inflammation which they excite, or may cicatrize. Bullets and foreign bodies may become encapsulated in the heart: wall and remain so for years. Ruptures of the heart wall occur in various ways : 1. Severe contusions of the thorax may produce rupture, usually of one of the auricles. 2. Spontaneous rupture occurs usually in advanced life. Rupture is most frequent in the left ventricle, and, in a considerable proportion of cases, near the apex. There is usually one rupture, but sometimes more. The rupture is usually oblique and larger internally than ex- ternally. The heart wall, near the seat of rupture, may be infiltrated. with blood, or blood may infiltrate the subpericardial fat. The heart: wall may be of normal thickness, or thin ; it is usually soft and ina condition of fatty infiltration or degeneration. The rupture very frequently takes place when the patient is quiet. Death may be almost instantaneous or may not ensue for several hours. Fatty degeneration leading to rupture of the heart may be gene- ral, or itis frequently circumscribed and due to obliterating endar- teritis, atheroma, thrombosis, or embolus of one of the coronary arteries, whereby a portion of the heart wall is deprived of nourish- Digitized by Microsoft® THE VASCULAR SYSTEM. 487 ment and degenerates. Or rupture of a branch of one of the coronary arteries may induce rupture of the heart wall. Acute and chronic myocarditis, with or without the formation of abscess or cardiac aneurism, or the presence of tumors in the heart wall, or hydatids, may lead to the rupture.’ 3. In very rare cases rupture is produced by stenosis of the aorta and dilatation of the heart cavities. 4, Rupture of the papillary muscles and tendons may be produced by fatty degeneration or inflammatory or ulcerative processes. ATROPHY. Atrophy of the walls of the heart may be accompanied with no change in the size of its cavities ; or with dilatation (the same as pas- sive dilatation); or, more frequently, with diminution in the size of the cavities. The atrophy involves most frequently all the cavities of the heart, but may be confined to one or more of them. The muscular tissue appears normal, or brown from the presence of little granules of pigment in the muscular fibres, which are some- times present in large numbers—brown atrophy ; or the muscular fibres may undergo fatty degeneration ; or there may be an abnor- mal accumulation of fat beneath the pericardium ; or there may be a peculiar gelatinous material beneath the pericardium—this con- sists of fat which has undergone mucous degeneration. The heart ‘may be so much atrophied as to weigh four ounces, The causes of atrophy of the heart are : 1. It is a congenital malformation ; the heart of an adult then looks like that of an infant. 2. Any chronic and exhausting disease, repeated hemorrhages, old age, typhus fever, dysentery, etc., may produce atrophy. 3. Chronic pericarditis, with large serous effusion, or with thick- ening of the pericardium, producing constriction of the coronary ar- teries. 4, Stenosis, atheroma, calcification, or thrombosis of the coronary arteries may produce partial or total atrophy. 5. Myocarditis, with fatty or fibrous degeneration. 6. Mitral stenosis may cause atrophy of the left ventricle. HYPERTROPHY. All the cavities of the heart may have their walls hypertrophied, or the thickening may involve one or more. While the wall of a 1 Consult Councilman, “On Sudden Deaths due to the Heart, ” Boston Medical and Surgical Journal, November 9th, 1893, Digitized by Microsoft® 488 THE VASCULAR SYSTEM. ventricle is thickened, its cavity may retain its normal size—simple hypertrophy ; or be dilated—eccentric hypertrophy ; or it may be contracted—concentric hypertrophy. Cure should always be exercised in judging of this condition, for a firmly contracted heart seems to have a small cavity and thick walls. The existence of such a condition as concentric hypertrophy is denied by some authors. Eccentric hypertrophy is the most com- mon form. Simple hypertrophy is not common, but may occur in connection with the atrophied kidneys of chronic diffuse nephritis. The muscle tissue in hypertrophied hearts is firmer and denser than normal, and is apt to have a darker color. Fatty degeneration may, however, be associated with it, giving the walls a lighter appear- ance. It is probable that the increase of tissue in the hypertrophied heart wall is the result of increase both in size and number of the muscle fibres. Hypertrophy of both ventricles increases both the length and breadth of the heart. Hypertrophy of the left ventricle (alone) in- creases its length. The apex is then lower and further to the left. than usual. Hypertrophy of the right ventricle (alone) increases the breadth of the heart toward the right side; but sometimes the right edge of the heart retains its normal situation and the apex is displaced to the left. With large hypertrophy of both ventricles, the base of the heart may sink, so that its long axis approaches a horizontal direction. Hypertrophied hearts may weigh from forty to fifty ounces, or even more. Hypertrophy of the heart may depend upon a variety of causes : 1, Changes in the valves; either insufficiency or stenosis in the valves leading from a cavity, and insufficiency in valves leading to a cavity, may induce hypertrophy of its walls. 2. Obstruction to the passage of blood through the arterial sys- tem, as in atheroma and other diseases of the intima ; congenital or acquired stenosis of vessels, pressure of tumors, etc., on vessels ; certain forms of chronic diffuse nephritis, especially atrophied kid- neys, lead to hypertrophy of the left ventricle, and sometimes sec- ondarily to hypertrophy of the right ventricle. 3. Obstruction to the passage of blood through the pulmonary artery by stenosis or by certain diseases of the lungs, particularly emphysema and chronic phthisis, may lead to hypertrophy of the right ventricle, and, secondarily, of the right auricle and left ven- tricle. . 4, Any cause, whether muscular or nervous, which increases the rapidity and force of the heart’s contractions, may produce hyper- trophy. Digitized by Microsoft® THE VASCULAR SYSTEM. 489 5. Dilatation of the ventricles, from any cause, is frequently fol- lowed by hypertrophy. 6. Pericarditis may produce hypertrophy by inducing softening and dilatation of the ventricles, or by leaving adhesions which ob- struct the heart’s action. Chronic myocarditis also may lead to hy- pertrophy. Finally, for some cases of hypertrophy no satisfactory cause can be found. Howard’s table of 105 cases of cardiac hypertrophy shows its association with arterio-sclerosis in 59 per cent; with ne- phritis in 13.4 per cent; with valvular lesion in 12.4 per cent.’ It should be borne in mind that an increase in the amount of fat in and about the heart may make the organ appear larger, when there may be actually a considerable decrease in the amount of mus- cle tissue. DILATATION. Dilatation may be combined with hypertrophy—active dilata- tion ; or there may be no increase of muscle tissue, but a thinning of the walls proportionate to the dilatation of the cavity—passive dilatation. Either one or all of the heart cavities may be dilated, the au- ricles most frequently ; next the right ventricle ; least often the left ventricle. Active dilatation has been considered under hypertrophy. Passive dilatation may be produced by : 1. Changes in the valves, Mitral or aortic stenosis or insuf- ficiency may produce dilatation of the auricles and right ventricle. Pulmonary stenosis or insufficiency may produce dilatation of the right auricle and right ventricle. Aortic insufficiency, with or without stenosis or mitral insufficiency, may produce dilatation of the left ventricle. Dilatations from these causes are often succeeded and compensated for by hypertrophy of the heart walls. 2. Changes in the muscular tissue of the heart walls. Serous infiltration from pericarditis, myocarditis, fatty degeneration and in- filtration, atrophy of the muscle fibres, may all lead to dilatation. 3. A heart which is already hypertrophied may, from degenera- tion of the muscle, become dilated. 4. Acute exudative inflammations of the lungs and acute pleuritic exudations, by rendering a large number of vessels suddenly im- permeable to the blood current, may produce sudden stasis in the pulmonary artery and dilatation of the right heart. 5. There are curious cases of acute and chronic dilatation of the 1 Howard, Johns Hopkins Hospital Reports, vol. iii., p. 265. at Digitized by Microsoft® 490 THE VASCULAR SYSTEM. ventricles for which no mechanical cause can be found and which are very fatal. DEGENERATIONS, Acute Degeneration ; Parenchymatous Degeneration of the Heart Muscle.—This lesion frequently occurs in typhoid and typhus fever, pyzemia, erysipelas, and other infectious diseases, as well as in the exanthemata, as a result of burns, and under a variety of other conditions. It is characterized by the presence in the muscle fibres of the heart of greater or less numbers of albuminous gran- ules of various sizes, most of them very small. They are not as re- fractile as fat droplets, and are insoluble in ether, while swelling up and becoming almost invisible under the influence of acetic acid. Sometimes they are so abundant as to conceal the striations of the fibres. The degeneration is usually quite uniformly diffused through Fic, 245Farty DEGENERATION OF THE Heart Mvscug. Teased. the heart, whose walls are softer than normal and of a grayish color. This lesion may be associated with or followed by fatty de- generation. Fatty Degeneration of the Heart Muscle.—This consists in the transformation of portions of the muscle fibres of the heart into fat, which collects in the fibres in larger and smaller droplets, sometimes few in number, sometimes so abundant as to entirely destroy or conceal the normal striations (Fig. 245). These droplets are soluble in ether, and remain unchanged on treatment with acetic acid. This degeneration is sometimes quite universal, but is more apt to occur in patches, giving the heart muscle a mottled appearance. This mottling may usually be best seen on the papillary muscles. The degenerated areas have a pale-yellowish color, and the muscle tissue is soft and flabby ; but when moderate or slight in degree the gross appearance may be little changed, and the microscopical ex- amination be necessary for its determination. This degeneration may lead to thinning of the walls, or to rupture of the heart, or to Digitized by Microsoft® THE VASCULAR SYSTEM. 491 inability to fulfil its functions. It is not infrequently the cause of sudden death. It may be secondary to hypertrophy of the heart, to inflamma- tion of the heart muscle, or to pericarditis ; to disturbances of the circulation in the coronary arteries by inflammation, atheroma, etc. It may be due to deteriorated conditions of the blood in wasting dis- eases, excessive hemorrhages, exhausting fevers, leukemia, etc., to poisoning with phosphorus and arsenic and to the toxins of mi- crobic origin developed in infectious diseases, such as diphtheria, scar- latina, typhoid fever, etc.‘ It may occur in otherwise apparently healthy persons. Fatty Degeneration of the Endocardium.—lIt is not uncommon to find, especially in elderly persons, fatty degenerations occurring Fig. 246.—Farty INFILTRATION OR LIPOMATOSIS OF THE HEART. The lesion is excessive, the heart muscle being to a large extent atrophied. (The fat cells are represented in the drawing, for the sake of clearness, of relatively too large size.) in patches, especially on the valves, but also on the general endocar- dium. They may also occur in ill-nourished and anemic individuals. Small, or even considerable, areas of fatty degeneration appear, asa rule, to be of little or no clinical significance. They are at least not inconsistent with perfect health. In these areas of fatty degenera- tion the connective-tissue cells are more or less completely filled with larger and smaller fat droplets. almylotd Degeneration of the endocardium or the walls of the 1 Consult Flexner, Johns Hopkins Hospital Bulletin, March, 1894; also Scham- schin, Ziegler’s Beitrage zur path. Anat., etc., Bd. xviii., p. 64, 1895. Digitized by Microsoft® 492 THE VASCULAR SYSTEM. blood vessels and intermuscular connective-tissue septa is a not very infrequent, but usually not very important lesion. Hyaiin Degeneration sometimes occurs. Calcification of the products of inflammation in pericarditis, or of connective-tissue membranes in chronic pericarditis, sometimes occurs, and in the latter case the heart may be more or less enclosed by a caleareous shell. The muscle fibres of the heart wall may, though rarely, become densely infiltrated with salts of lime. Fatty Infiltration or Lipomatosis of the Heart.—This lesion, which should be clearly distinguished from fatty degeneration, con- sists of an unusual accumulation of fat about the heart and between its muscle fibres (Fig. 246). The subpericardial fat, which may be present in considerable quan- Fic. 247 —ATRopHIC PERICARDIAL Fat. From young person dead of carcinoma of the stomach and peritoneum, Stained with osmic acid and teased. tity under normal conditions, may be so greatly increased in amount as to form a thick envelope enclosing nearly the entire organ. Some- times the accumulation of fat extends into the walls of the heart, between the muscles, causing atrophy of the latter, frequently to a very great extent, so that the function of the heart is seriously in- terfered with. This occurs sometimes in general obesity, or as a re- sult of chronic pericarditis, or in drunkards, or in debilitated or old persons. Atrophy of the pericardial fat tissue not infrequently occurs in persons emaciated by chronic disease, and then the usual situations of the fat are occupied by a tissue resembling mucous tissue in its gross characters. Microscopical examination shows that in this atrophic fat the fat cells have largely lost their contents, and the Digitized by Microsoft® THE VASCULAR SYSTEM. 493 whole tissue has undergone a partial reversion to its original embry- onic form (see Fig. 247). Myomalacia.—When, through obliterating endarteritis, athero- ma, thrombosis, or embolus of a branch of the coronary arteries, the blood supply is cut off from a circumscribed portion of the heart wall, the tissue in the affected area may undergo fatty degeneration, lead- ing to rupture. Or, instead of extensive fatty degeneration, the muscle fibres may break down into a granular detritus and the con- nective tissue about them suffer retrograde metamorphosis, so that the whole affected area may be soft and yellowish-white or grayish in color. If, as not infrequently occurs, there is considerable extra- vasation of blood, the degenerated area may be of a dark-red color. Under these conditions the wall may rupture; or acute inflammatory processes may occur; or the degenerated tissue may be gradually absorbed, and replaced by new connective tissue which gradually grows dense, shrinks, and assumes the characters of cicatricial tissue. This may occur in any part of the heart wall or in the papillary muscles, but is most common in the region supplied by the anterior coronary arteries. When the heart wail is involved the new-formed connective tissue nay yield to the blood pressure from within and aneurism of the heart be formed. Impaired nutrition of a portion of the heart wall as the result of narrowing or obliteration of the coronary arteries or their branches is of great significance, whether it lead to such extreme lesions as those just described, or to fatty degeneration, or to atrophy of the muscle cells with a production of new connective tissue, because it is the dominant factor in many cases of sudden death. According to Sternberg’ the right coronary artery supplies the following regions of the heart: most of the right auricle; the poste- rior part and most of the anterior part of the right ventricle; most of the interauricular and interventricular septa; the posterior part of the left ventricle and the posterior papillary muscles. The re- mainder of the heart is supplied by the left coronary artery. Fragmentation of the Myocardium.—Attention has been called by a number of observers to a condition of the heart muscle sometimes observed, it is said, in acute infectious diseases, in acute and chronic diseases of the central nervous system, and in sudden death from a variety of causes. The muscle tissue is soft, friable, opaque, and often yellowish. Examination shows a loosening of the muscle cells from one another, as if by some change in the cement substance.” It is still questionable whether this may not be a post-mortem change. 1 Tnaug. Diss., Marburg, 1887. 2 Oestreich, Virchow’s Archiv, Bd. cxxxv., p. 79, bibliography ; also Dunin, Ziegler’s Beitrige zur path. Anat., etc., Bd. xvi., p. 134, 1894. Digitized by Microsoft® 494 THE VASCULAR SYSTEM. INFLAMMATION. Endocarditis. The endocardium is a connective-tissue membrane which lines the cavities of the heart and forms its valves. Its inner. surface is covered with a layer of endothelial cells. It is but poorly supplied with vessels, and the inflammations which attack it are of the cel- lular variety. The ordinary products of inflammation, pus, fibrin, and serum, are scanty or absent altogether. The connective-tissue cells and basement substance are principally concerned in the inflam- matory processes. The new tissue thus produced is prone to de- generation and calcification. The roughening of the endocardium due to the inflammation often causes a coagulation of fibrin on the inflamed surface. In foetal life it is the endocardium of the right heart, in extra- uterine life that of the left heart, which is usually inflamed. The endocardium which forms the valves is that which is most frequently inflamed, but the other portions of it are by no means exempt. 1. Simple Acute Hndocarditis.—This is most apt to occur in connection with rheumatism, but may occur under other conditions. It may attack a heart which was previously healthy, or one in which the lesions of chronic endocarditis already exist. In some cases the only lesion is a simple swelling of the valves. They are thick and succulent, but their surfaces remain smooth. The basement substance is swollen, and there is a moderate pro- duction of new connective-tissue cells. In other cases the growth of connective-tissue cells is very much more marked, the basement substance is split up, and little cellular fungous masses, called vegetations, project from the free surface of the endocardium. On these roughened surfaces the fibrin of the blood is deposited, and so vegetations of considerable size may be formed (see Fig. 248). In still other cases the cell growth, while in some places it forms vegetations, in other places degenerates, and thus portions of the valves are destroyed. This is stmple acute ulcerative endocar- ditis. In some cases of this disease the patients recover and the valves seem to return to a normal condition ; in other cases the valves are left permanently damaged ; and in still others chronic endocarditis follows the acute form. 8, Mycotic or Malignant Endocarditis (malignant ulcerative endocarditis). The direct inciting cause of simple acute endocarditis of the forms Digitized by Microsoft® THE VASCULAR SYSTEM. 495 described above is unknown. But in a considerable number of cases of acute endocarditis bacteria have been found in and about the vegetations (see Fig. 249), and proved, by careful experiments, to stand in a causative relation to the lesion. Those cases of acute endocarditis in which the lesions are in- duced by the direct action of bacteria are called mycotic or malig- nant endocarditis ; or, since the new-formed as well as the old tissue about the bacteria is apt to become necrotic and thus lead to larger or smaller losses of substance, the lesion is often called wlcera- tive endocarditis. Cases of multiple aneurism in connection with mycotic endocarditis have been reported. Cultivations of the bacteria occurring in the heart lesions in ‘ ; t ugh ae oa HOS ytd See ua aban ef id iy coe nin ee ind TaN) ‘pled Bie es Pa) YD. byte a! Ss 2 ( SBN! P %) bisa A an bls ifeas ASS Fie, 248.—VEGETATION ON AORTIC VALVE IN ENDOCARDITIS. Showing granular thrombus over the surface. malignant endocarditis have shown that, while various species of bacteria may occasionally act as an inciting cause, it is most com- monly induced by the Staphylococcus pyogenes aureus and the Strep- tococcus pyogenes. The Diplococcus lanceolatus, B. typhosus, B. tuberculosis, B. anthracis, Micrococcus gonorrhcese and others have been occasionally found. It has been, furthermore, found ‘that a lesion or injury of the en- docardium, either on the heart valves or elsewhere, predisposes to the lodgment and growth upon them of the disease-producing bacteria when once they have gained access to the circulating blood.’ ' For a detailed consideration of the relationship of bacteria to malignant endo- carditis, with experiments and literature, see Prudden, Am. Jour. Med. Sciences, January, 1887; Weichselbaum, Ziegler’s Beitrige zur path. Anat., Bd. iv., 1888, p. 127; Thayer and Blume, Bull, Johns Hopkins Hospital, April, 1896. Digitized by Microsoft® 496 THE VASCULAR SYSTEM. Mycotic endocarditis is frequently a secondary complicating le- sion, but may occur as a primary disease. It is most apt to be asso- ciated with the acute infectious diseases, and in many cases may be regarded as one of the local manifestations of pyeemia. In some cases there is a formation of new tissue in the form of organized vegetations on the valves or general endocardium ; in other cases necrosis either of the new-formed or the old tissue is the most marked feature. Blood clots are apt to form on the affected surfaces and often largely make up the so-called vegetations. The mitral and aortic valves are frequently the seat of the lesion, but it may occur elsewhere. Detachment of bacteria containing fragments of the vegetations or clots may give rise to single or multiple infectious emboli (see p. 73) and abscesses in various parts of the body, such as the spleen, kid- Fig, 249.—Mycotic ENDOCARDITIS. Schematic drawing of a section of vegetation, showing colonies of micrococci stained with methyl violet. neys, brain, skin, heart wall, etc. Bacteria similar to those in the heart lesion may be found in these secondary abscesses (see Fig. 66). It is probable that these abscesses in ulcerative endocarditis do not always arise from cardiac emboli, but may precede the heart lesion. 3. Chronic Endocarditis may succeed acute endocarditis, or the inflammation may be chronic from the outset. It affects most fre- quently the aortic and mitral valves, and the endocardium of the left. auricle and ventricle; similar changes in the right side of the heart. being much less frequent. There are two main anatomical varieties of chronic endocarditis, which may occur separately or together. (1) The endocardium is thick and dense, its surfaces are smooth or covered with small, hard vegetations or ridges; it is often infil- trated with the salts of lime. (Fig. 251). Digitized by Microsoft® THE VASCULAR SYSTEM. * 497 (2) There is a growth of connective-tissue cells in the endocar- dium, with a splitting-up of the basement substance. Some of the new cells continue to live, others degenerate. By the combination of such a cell growth and destruction the endocardium is in some places destroyed, in others changed into projecting vegetations. Fibrin is deposited on the roughened surfaces (Fig. 250). After a time the condition may be further complicated by the shrink- age and deposition of the salts of lime in the new tissue and Fic. 250,—CHRONIc ENDOCARDITIS. Showing ‘‘ vegetation’ on heart valve with large blood clot—mitral valve. in the endocardium. All these changes may extend to the wall of the heart beneath the endocardium. The most important result of chronic endocarditis is its effect on the heart valves, producing insufficiency and stenosis. The changes in the valves are followed by changes in the walls and cavities of the heart, and disturbances of the circulation throughout the body. 41 Digitized by Microsoft® 498 ® THE VASCULAR SYSTEM. 4. Chronic Ulcerative Endocarditis.—Large ulcers or perfora- tions of the valves may be formed in chronic endocarditis, upon which clots may form, so that in gross appearance a great similarity exists between this and malignant ulcerative endocarditis, particu- larly if the latter have been engrafted upon an already chronically diseased endocardium. The microscopical and biological examina- tions must usually be resorted to in order to determine the exact sig- nificance of the lesion.. 5. Tuberculous Endocarditis may occur in connection with tu- bercular pericarditis or general miliary tuberculosis. The tubercles Fie. 251.—Curonic EnpocarDImTis. Thickening of the aortic valve. may be small and single, or grouped in masses, and show the usual degenerative changes. Myocarditis. The inflammatory changes in the walls of the heart involve pri- marily the interstitial tissue and blood vessels, the muscle fibres being secondarily affected by atrophic and degenerative changes. Interstitial Myocarditis may be acute and purulent, or chronic with the formation of new connective tissue. Acute Purulent Myocarditis may be diffuse, infiltrating the wall of the heart with pus. This may occur as a complication of scarlatina and from unknown causes. More frequently the purulent inflammation is circumscribed, pro- ducing abscesses. These occur with pyeemia, mycotic ulcerative en- Digitized by Microsoft® THE VASCULAR SYSTEM. 499 docarditis, and other infectious diseases. They are of different sizes and either single or multiple. They are produced by the lodg- ment of infectious emboli in small vessels. The contents of the ab- scesses consist of pus, broken-down muscle tissue, and bacteria. These abscesses may open into the pericardial sac and set up a pu- rulent pericarditis ; or into a heart cavity, giving rise to thrombi in the heart and emboli in different parts of the body ; or the wall of the heart is weakened by the abscess so that it ruptures, or an aneu- rismal sac is formed ; or an abscess in the interventricular septum may establish an opening between the ventricles ; or the suppura- tive process may extend upward and form an abscess in the connec- tive tissue at the base of the heart. In rare cases the patients recover, the contents of the abscesses become dry and hard, and enclosed by a wall of fibrous tissue. Fia. 252.—Cuaronic InrerstTit14L MyocarDIris. Showing transverse section of a portion of a papillary muscle. Chronic Interstitial Myocarditis may be associated with chronic pericarditis or endocarditis or myomalacia, but in a large proportion of cases it occurs in connection with lesions of the coronary arteries. Occasionally, however,.there is a formation of new connective tissue in the myocardium as well as in the endocardium without evident lesion of the coronary arteries or the above-mentioned conditions. There is a growth of new connective tissue or of granulation tissue between the muscular fibres, with atrophy and degeneration of the muscle. This growth may be in the form of circumscribed patches (Fig. 252), or diffused over a considerable part of the wall of the heart. Such an interstitial inflammation is often followed by dilata- tion of the cavities of the heart, by the formation of aneurisms of the wall of the heart, and of thrombi in the cavities of the heart. It is believed by many observers that the new connective tissue which develops in the heart in connection with atrophy of the muscle fibres, as a result of impaired nutrition due to a narrowing of the Digitized by Microsoft® 500 THE VASCULAR SYSTEM. lumen of the coronary arteries, is not in the stricter sense inflamma- tory in its nature, but is rather a fibrous hyperplasia, the new- formed connective tissue forming secondarily, to replace the muscle fibres which have atrophied. It is interesting in this connection to note that under these conditions the muscle fibres immediately be- neath the endocardium and close around the blood vessels where the nutritive supply is most abundant are often not atrophied, nor is the growth of connective tissue marked. Syphilitic Myocarditis is accompanied by the growth of ‘cone nective tissue or granulation tissue in the wall of the heart between the muscular fibres. The pericardium and endocardium may also be thickened, and pericardial adhesions may be formed. Gummata of the heart are of rare occurrence.' CHANGES IN THE VALVES. Fenestration of the valves is usually a change productive of no bad consequences. It occurs very frequently in the aortic and pul- monary valves. The valves may be thinner than usual, and close to their free edges are small slits extending from the centre to the attached edges of a leaf. Aneurisms of the valves are produced in two ways: 1. They are the result of endocarditis. One of the lamelle of the leaf of a valve is destroyed, and the other lamella is converted into asac filled with blood. These aneurisms are found in the aortic valve, projecting into the ventricle ; and in the mitral valve, project- ing into the auricle. Not infrequently the wall of the aneurism gives way, so that there is a rupture entirely through the valve. 2. The entire thickness of a leaf of a valve is converted intoa sac filled with blood. This occurs in the aortic, mitral, and tricus- pid valves ; its cause is unknown. Heemorrhage in the substance of the valves is sometimes found in very young children. It does not appear to have much clinical importance. ANEURISM OF THE HEART. Sacs filled with blood, situated in the walls of the heart and com- municating with its cavities, are formed in several different ways. 1. In consequence of inflammatory processes in the endocardium and muscular tissue, a small or large portion of the wall is converted into fibrous tissue. The portion thus changed no longer resists the pressure of the blood from within, and is driven outward. Sucha pouch may be a circumscribed sac communicating with’ the heart 1 For consideration of gonorrheal myocarditis consult Councilman, Am. Jour, Med. Science, September, 1893. Digitized by Microsoft® THE VASCULAR SYSTEM. 501 cavity by a small opening, or may look like a dilatation of part of the ventricle. The wall of such an aneurism becomes thinner as the sac increases in size. It is composed of the endocardium, new fibrous tissue, visceral pericardium, and sometimes the adherent parietal pericardium. The walls may calcify, or rarely they become so thin as to rupture externally or into the right ventricle. The sacs may contain fluid blood or be filled up with fibrin. Such aneurisms are usually situated in the wall of the left ven- tricle ; rarely in that of the left auricle. If they are in the septum they may project into the right ventricle. They are usually single, but sometimes two or three are found in the same heart. 2. Fatty degeneration of the heart wall may reach such a point that the wall yields and is pouched out into an aneurismal sac. 3. Endocarditis and myocarditis, or fatty degeneration, may so soften a portion of the heart wall that the endocardium and part of the muscular tissue are ruptured and a ragged cavity is formed. This form of aneurism usually does not attain a large size, but soon ruptures externally and causes the death of the patient. THROMBOSIS OF THE HEART. Itis very common to find after death, in the heart cavities, yellow, succulent, semi-translucent masses. They are most common and of firmest texture in persons who die of acute inflammatory diseases. They may adhere quite firmly to the walls of the heart, and may ex- tend in long, branching cords into the vessels. They are formed in the last hours of life and just after death. They have no clinical or pathological importance. Coagulations of the fibrin of the blood in the heart do, however, occur during life, and may exist for years. If the fibrin adheres to the valves in small masses these are called vegetations ; if it coagu- lates in the heart cavities in larger bodies they are called thrombi or heart polypi. Such thrombi are found in all the heart cavities. They form flattened masses firmly adherent to the endocardium; or rounded bodies in the spaces between the trabecule; or have a polypoid shape and are attached by a narrow pedicle, or very rarely are globular and free in the cavity of the auricle. They are usually found in connection with some valvular lesion which prevents the free circulation of blood through the heart. They are firm, dry, and of a whitish color; they may soften and break down at their centres, so as to look like cysts filled with pus, or they may calcify. They are usually entirely unorganized, consisting simply of fibrin, but may become organized. One of us (Delafield) has seen an organized thrombus in the heart Digitized by Microsoft® 502 THE VASCULAR SYSTEM. of a man, whose history was unknown, who was found dead in the street. Wilson presented before the New York Pathological Society, 1892, a large thrombus of the auricle which was partly organized. Cases are reported of organized thrombi in the auricles, which were the seat of tuberculous inflammation, which sometimes does not in- volve the heart wall.’ Sometimes sarcomatous and carcinomatous tumors in different parts of the body are accompanied by the formation of thrombi in the heart cavities, which are composed partly of coagulated blood, partly of tissue like that of the primary tumor. TUMORS.” Primary tumors in the heart are rare, but sarcomata, myxomata, fibromata, and lipomata may occur. Rhabdomyomata, probably congenital, may occur in the heart wall as circumscribed nodular masses.” A cavernous tumor of this kind has been described. Sec- ondary tumors, as a result of metastasis or of continuous growth from adjacent parts, are not very infrequent. These are usually carcinomata or sarcomata. Secondary chondromata have been observed. Syphilitic gummata may occur in the heart wall.’ PARASITES. Echinococcus sometimes occurs in the heart wall and may per- forate into the cavities. Cysticercus cellulose has been observed. THE BLOOD VESSELS. ATROPHY AND HYPERTROPHY. Atrophy of the blood vessels may involve the entire trunk or some of its elements. It may occur as a part of general malnutrition of the body, or in connection with atrophy of particular organs, or aS an accompaniment of various diseases of the vessels them- selves, Hypertrophy, which is especially seen in the arteries, may occur in the establishment of a collateral circulation upon the closure of arterial trunks; or it may occur as the result of increased blood pres- sure, as in some forms of hypertrophy of the heart. ! Kotlar, Rev. Centralblatt f. Bakteriologie, April 7th, 1894, p. 498. ° For bibliography of heart tumors consult Berthenson, Arch. de Med. exp., vol. v., p. 3886. 3 Justt, Centralblatt f. path. Anat., etc., January 18th, 1896. 4 Loomis, Am. Jour. of the Med. Sciences, October, 1895, bibliography. Digitized by Microsoft® THE VASCULAR SYSTEM. 503 DEGENERATION. Fatty Degeneration.—This may occur in the walls of otherwise unaltered vessels, or in those which have undergone a variety of in- flammatory or degenerative changes. It may occur either in the in- tima or media, or both, and may be so extensive as to form a very prominent gross lesion, or so little developed as to require the micro- scope for its recognition, When marked, especially if occurring in the intima of large vessels, smaller and larger spots or stripes or patches may be seen, of ‘a yellowish-white color, usually sharply cir- cumscribed, and sometimes smooth, sometimes roughened on the surface. It is most apt to occur in the aorta, but may be found in any of the vessels. In moderate degrees of the lesion we find on section that the cells of the intima contain fat droplets in greater or less number. When further advanced, not only are the cells crowded with fat droplets, but the intercellular tissue also may be more or less densely infiltrated with them. Sometimes the infiltration is so dense that the tissue breaks down, and there may be an erosion of the sur- face, forming a so-called fatty ulcer. When the media is involved the muscle cells contain fat droplets. It may lead to the formation of aneurism or to rupture of the vessels. Calcification usually occurs in vessels otherwise diseased, and may involve either the intima or media. It consists in the deposi- tion of salts of lime either in the cells or intercellular substance. The lime may be in the form of larger or smaller granules or in dense translucent plates. Amyloid Degeneration, which may affect all the cvats of the ar- teries, but especially the intima and media, will be considered under the lesions of the organs in which it most commonly occurs. Hyalin Degeneration may cause thickening of the intima of the blood vessels by its conversion into or infiltration with a homoge- neous material somewhat similar to amyloid (see page 84). Or it may involve the entire wall of smaller vessels, converting them into irregular lumpy cords. The lumen of vessels thus changed may be obliterated or occluded by thrombi. THE ARTERIES. INFLAMMATION. Acute Arteritis. Acute inflammation of the walls of the arteries is, in the major- ity of cases, the result of injury, or of an inflammation in the vicin- ity of the vessel, or of the lodgment within it of some foreign body of an irritating or infectious nature. The inflammatory process may Digitized by Microsoft® 504 THE VASCULAR SYSTEM. be largely confined to the inner layer of the vessels—endarteritis; or it may commence in the outer layers—periarteritis ; or it may involve the entire wall. The blood vessels in the outer layers may be congested, the tissue cedematous and infiltrated with pus cells, and the entire wall may become necrotic. The intima, if this layer is involved, loses its natu- ral gloss, looks dull and swollen. It may become infiltrated with pus from the outer layers, and it may become necrotic. Under these conditions thrombi usually form, and in these may occur the various changes which have been already described on page 60 Chronic Arteritis. Since the publication of the studies of Gull and Sutton on arterio- capillary fibrosis, attention has been every year more and more di- rected to morbid changes in the arteries as one of the most frequent of diseased conditions. It is evident that these morbid changes are caused by alcohol, lead, gout, and syphilis; that the disposition to them is hereditary in some families ; that they constitute one of the regular senile changes ; that they are often associated with chronic diseases of the viscera ; that the patients can be unconscious of their existence, and that, on the other hand, they can cause most distressing symptoms, and even death. At the present time it is customary to speak of these morbid con- ditions under the names of arterio-sclerosis and atheroma, and to accept the conclusions drawn by Thoma from an extended series of studies. Thoma teaches that : 1. Every long-continued slowing of the blood current causes con- traction of the middle coat of the aorta, and, if this is not sufficient to accelerate the blood current, to a growth of connective tissue in the intima. 2. Primary diffuse and nodular arterio-sclerosis depends upon a weakening of the wall of the blood vessel due to constitutional con- ditions. This is followed by dilatation of the vessel, slowing of the blood stream, and then the growth of connective tissue in the intima. 3. Secondary arterio-sclerosis is caused by slowing of the blood current produced by changes of the circulation in the capillary vessels. It appears to me (Delafield) that the most practical view of these morbid changes in the arteries is to consider them the results of a combination of chronic productive inflammation and of degeneration occurring in connective tissue. We shall then think of the arteries as we do of the heart or the liver or the kidneys, as a definite part of the body, liable to become the seat of chronic inflammation from Digitized by Microsoft® THE VASCULAR SYSTEM. 505 the same causes as those which produce similar changes on other parts of the body. In all the arteries the wall is composed of an outer connective-tis- sue coat supplied with blood vessels, of a middle coat formed of smooth muscle, and of an inner connective-tissue coat not supplied with blood vessels. Inthe small arteries inflammation simply causes the formation of new tissue; in the large arteries and in the aorta, besides the formation of new tissue, there is also the death and de- generation of tissue. There is sufficient difference between the changes in the small arteries, the large arteries, and the aorta to make it convenient to described them separately. Fic. 253.—CHRoNIC ARTERITIS—CERRBRAL ARTERY. Inner coat thickened; degeneration and softening (atheroma) of a part of the thickened area. 1. The Small Arteries.—(a) The simplest change in the small arteries is an increase in the size and number of the endothelial cells. This is best seen in the arteries in miliary tubercles and in small gummata. (b) There is a growth of new connective tissue from the endothe- lium which encroaches upon the lumen of the artery and finally oc- cludes it. The growth is composed of large branching cells, small round cells, and basement substance ; later the cells become smaller and less numerous, the basement substance denser. The growth forms a ring on the inside of the intima which is notsymmetrical, but is thicker in some one place. This change always narrows the calibre Digitized by Microsoft® 506 THE VASCULAR SYSTEM. of the artery, and, when far advanced, occludes it. It is seen very frequently in the small arteries in every part of the body. It is often called ‘‘ obliterating endarteritis ” (Figs. 253 and 254). (c) There is a thickening of the inner coat beneath the endothe- lium. The change begins by a growth of cells and a splitting-up of the basement substance in the intima immediately beneath the endo- thelium. Then there is a growth of basement substance, with but a moderate number of cells, which renders the inner coat thicker and Fig. 254.—CHRonic OBLITERATING ENDARTERITIS—KIDNEY. thicker until the lumen of the artery is considerably narrowed, but yet the artery is not occluded. The endothelial cells may remain in place and unchanged over the thickened intima. This change is of very frequent occurrence, so that it is easy to see all the stages of the growth, from the first splitting-up of the intima until it is changed into a dense thickening. (d) The thickening of the inner coat just described, instead of occurring by itself, may have joined with it either a thickening of Digitized by Microsoft® THE VASCULAR SYSTEM. 507 the muscular coat alone or a thickening of both the muscular and outer coats (Figs. 255 and 256). (e) There is a thickening of the intima, a replacement of the mus- cular coat by connective tissue, and a thickening of the outer coat. This can properly be called a “sclerosis” of the artery. Periarteritis Nodosa.—A few cases have been described in which many of the small arteries in the muscles and in the viscera were beset with small white knobs projecting from inside or sur- rounding the vessels. These circumscribed thickenings of the vessel wall are apt to involve all the layers of the vessel and may encroach Fig. 255.—CHRoNIc ARTERITIS. {nner and middle coat thickened—radial artery. upon the lumen. The thickened portions are infiltrated with small spheroidal cells. Multiple aneurisms may develop at the seat of the local thickenings.’ 2. The Large Artertes.—In the large arteries altogether the most frequent change is the thickening of the intima. This is often pres- ent in arteries which look normal to the naked eye. But besides the thickening of the intima there is often in addition a thickening of 1 Consult v, Kahiden, Ziegler’s Beitrage z. path. Anat., etc., Bd. xv., 1894; also Graf, ibid., Bd. xix., p. 181, 1896. Digitized by Microsoft® 508 THE VASCULAR SYSTEM. the middle and outer coats, or a replacement of the muscular coat by connective tissue. When all the coats are thickened in this way the arteries often become elongated and tortuous. Occasionally there are areas of degeneration in the thickened wall of the artery, or even in- filtration with the salts of lime. The Aorta.—The changes in the aorta differ from those in the arteries by reason of the combination of degeneration and necrosis with the growth of new tissue due to the chronic inflammation, by Fig. 256.—CHRonICc ARTERITIS. With sclerosis of all the coats of the vessel—kidney, the frequency of calcification, and by the liability of the outer coat to purulent infiltration. We find, therefore, in the aorta: (a) Simple thickening of the inner coat by new connective tissue. (b) Degeneration and softening of the inner and middle coats. (c) Calcification of the inner and middle coats. (d) Infiltration of the outer and middle coats with pus cells. (e) Thinning and atrophy of the inner and middle coats. (f) The formation of thrombi on the roughened surface of the inner coat. Digitized by Microsoft® THE VASCULAR SYSTEM. 509 Inflammatory changes in the aorta associated with degeneration, calcification, etc., are often called “atheroma” (See Figs. 258 and 259). Tuberculous Inflammation of the Arteries. In tuberculous inflammation the walls of the arteries, particularly the smaller ones, may be thickened and their Jumina obliterated (Fig. 260). Fic, 257.—Curonic ARTERITIS. With thickening of all the coats of the vessel—kidney. DILATATION AND ANEURISM. 1. Cirsoid aneurism consists in the dilatation and lengthening of large or small arteries. The walls of the artery are thinned, the vessel is tortuous and in places sacculated. These changes are most frequent in small arteries, especially the temporal and occipital. Digitized by Microsoft® 510 THE VASCULAR SYSTEM. Fig, 258.—CHRonto INFLAMMATION OF THE AORTA, WITH DEGENERATION oF NEW-FoRMED Tissuz (ATHEROMA). a, adventitia; 6, media; c, new tissue developed in the intima; d, degenerated area; e, area of softening; g, fat droplets in softened area, Fig. 259. Inner coat thickened and necrotic; mi Bigitize fH iV WIPO SORES: and breaking down (atheroma). —CHRoNIc INFLAMMATION OF THE AORTA, THE VASCULAR SYSTEM. 511 They involve the trunk of the vessel and its branches, or may extend to the capillaries and small veins. They form larger or smaller tumors beneath the skin. Rarely they are found in the larger arteries, and even in the aorta. 2. The ordinary aneurism is a dilatation of the coats of the artery over a larger or smaller part of its course. Such dilatations are usually due to chronic endarteritis and atheroma. The blocking ro “ “eee Fic. 260.—TuBERCULOUS ARTERITIS IN THE LuNG. Showing the encroachment of an area of tuberculous inflammation upon the wall of the artery and the formation of a mass partly occluding the lumen of the vessel. This section shows how the generalization of the tubercular inflammation through the body may occur by the sweeping -away of the tubercle bacilli by the blood and the establishment of new foci in various parts of the ‘body. From specimen prepared by Dr. J. 8. Ely. of a vessel by an embolus may lead to the development of an aneur- ism. According to their shape we may distinguish two varieties of aneurism: the diffuse and the circumscribed. (a) The diffuse, cylindrical, or fusiform aneurism consists in a uniform dilatation of all the coats of an artery, so that it assumes the shape of a fusiform or cylindrical swelling. In the walls of the dilated portion of the vessel there are often smaller, circumscribed dilatations. The wall of the aneurism is atheromatous or calcified ; the middle coat may be atrophied. The arch of the aorta is the most common seat of this form of aneurism, but the entire length of the aorta, or parts of any other arteries, may be dilated in the same way. Digitized by Microsoft® 512 THE VASCULAR SYSTEM. (6) The circumscribed or sacculated aneurism consists either in a dilatation of the entire circumference of an artery over a short por- tion of its length, or in a dilatation of only a small portion of one side of the wall, so that the aneurism looks like a swelling attached to one side of the artery. The aneurism commences as a dilatation of all the coats of the vessel ; but as soon as it attains any consider- able size the middle coat atrophies, so that the wall is composed of the inner and outer coats; or the inner coat is destroyed by endar- teritis, so that the outer coat alone forms the wall of the aneurism. As the aneurism increases in size it presses upon and causes the de- struction of the neighboring tissues and viscera, and portions of these tissues and viscera become incorporated with, or take the place of, the wall of the aneurism. The cavity of the aneurism is filled with fluid or clotted blood, or with layers of fibrin which adhere closely to its wall. The communication between the aneurism and the artery may be small or large. If arterial branches are given off from the aneu- rism they may remain open or become plugged with fibrin ; or their walls are thickened and their cavities narrowed by endarteritis. Death is produced by the pressure and interference of the aneurism with the adjoining viscera, or by rupture. The rupture may allow enough blood to escape to destroy life, or the blood may be held in by the soft parts and a second false aneurism formed about the original one. Dissecting aneurisms are those in which, owing to a solution of continuity of the inner layers of the artery, the blood gets between the media and adventitia, and forces its way for a greater or less distance between them. Or it may separate the media into two layers. ANEURISMS OF THE DIFFERENT ARTERIES. The aorta may be dilated over its entire length, or there may be diffuse or circumscribed dilatations at any portion of its course; or there may be several aneurisms, situated at different points. The ascending portion of the arch of the aorta may be uniformly dilated in a fusiform shape, or there may be circumscribed dilatations on its anterior wall, or, more rarely, on its posterior wall. The sacculated aneurisms may be of all sizes and may rupture within the pericar- dium ; or they may form a cavity in the upper part of the ventricular septum and communicate by openings into the pulmonary artery and left ventricle ; or they may dilate downward between the visceral and parietal pericardium, in front of the heart, pushing that organ backward. They may perforate into the right or left auricle or right ventricle, the superior vena cava, or the pulmonary artery ; or they may reach a large size, press on and erode the right side of the Digitized by Microsoft® THE VASCULAR SYSTEM. 513 sternum and adjoining ribs, project under the skin, and even rup- ture externally. The transverse portion of the arch may be dilated in a fusiform shape, or there may be sacculated aneurisms at any point in its wall. The sacculated aneurisms usually reach a considerable size. They press on the sternum and ribs in front, or on the esophagus, trachea, and bronchi behind. The large arteries given off from the arch may be occluded. They cause death by pressure on the air passages, the cesophagus, and the vena cava; or may rupture externally or into the cesophagus, trachea, bronchi, pulmonary artery, or pleural cavi- ties.’ On the abdominal aorta we usually find aneurisms sacculated. If they are situated high up they may project into the pleural cavities; if lower down, into the abdomen. They may compress and displace the viscera, vessels, and nerves, and erode the vertebre. They may rupture behind the peritoneum, into the peritoneal cavity, the pleural cavities, the inferior vena cava, the bronchi, the lungs, the duodenum, the colon, the pelves of the kidney, or the posterior mediastinum. The coronary arteries may be dilated throughout, or may be the seat of small sacculated aneurisms. These may rupture into the pericardium, or may cause rupture of the heart wall. The pulmonary arterves are rarely the seat of aneurisms. Dif- fuse and circumscribed dilatations, however, sometimes occur on the main trunk and on the two principal branches of the artery. They do not usually reach a large size, but may cause death by rupture. General dilatation of all the branches of the pulmonary artery is more common. It is found in connection with stenosis of the mitral valves and with compression or induration of the lung tissue. Of the other arteries of the body there is hardly any one which may not become the seat of an aneurism, but those of the popliteal artery are most common. A very few cases of multiple small aneurisms have been described, involving many of the smaller arterial trunks (see Periarteritis nodosa,” page 507). STENOSIS. Stenosis and obliteration of the aorta, at the point of entrance of the ductus arteriosus, have been described in a considerable number of cases. The situation of the stenosis is either exactly at the entrance of the ductus arteriosus or close on either side of this point. The de- 1 For an analysis of thirty-four cases of aortic aneurism consult Biggs, Am. Jour, of the Med. Sciences, March, 1889. 2 Graf, Ziegler’s Beitrige zur path. Anat., etc., Bd. xix., p. 181, 1896. 42 Digitized by Microsoft® 514 THE VASCULAR SYSTEM. gree of stenosis varies. The aorta may be entirely closed and con- verted into a solid cord for a length of half an inch; or there may be a circular constriction through which there is a larger or smaller opening—the constriction is uniformly circular ; or there is a septum springing from the concave side of the vessel at the opening of the ductus arteriosus ; or there is a cicatricial-like contraction of the aorta. The walls of the aorta at this point may be thickened and sclerosed. The ductus arteriosus may be closed or open. Above the constriction the aorta is usually dilated ; below it, it is normal, dilated, or ste- nosed. Stenosis of the aorta produces hypertrophy of the left ventricle, and, later, of the right ventricle, with venous congestion through- out the body ; or there may be a collateral circulation developed be- tween the arteries given off above and below the constriction ; or there may be rupture of the aorta, the right ventricle or auricle. This condition is found at all ages, but is produced during feetal life or in the first year of extra-uterine life. Itis probable that it may be caused after birth by an abnormal closure of the ductus ar- teriosus. This vessel normally becomes closed without the forma- tion of a thrombus. If a thrombus is formed it may extend into the aorta and obstruct it; or the ductus arteriosus is filled with a throm- bus, but increases fora time in size ; afterward, as the thrombus is ab- sorbed, the vessel contracts and draws the walls of the aorta together. Stenosis of the aorta and of some of the other arteries has been observed, in a few rare cases, without any known cause. Endarteritis, with the production of atheromatous and calcareous patches, may obstruct or entirely obliterate the smaller arteries. This is especially seen in the arteries of the leg, foot, and brain, and in the coronary arteries. The writer has seen a case in which the subclavian was completely occluded in this way. Narrowing of the aorta and of all its branches, with thinning of the arterial coats, is found as a congenital condition. It usually oc- curs in females, in connection with imperfect development of the whole body. Stenosis from thrombosis or embolism is treated of elsewhere. RUPTURES AND WOUNDS. Rupture of arteries may occur under the following conditions: 1. Fatty degeneration or endarteritis, with atheromatous changes, may so soften and destroy the inner and middle coats of an artery as to admit of its rupture. Rupture of the aorta in connection with tuberculous inflammation of the vessels has been described. The aorta, just above the valves, is the most frequent seat of this lesion. The rupture may run in any direction; its edges are irregular and Digitized by Microsoft® THE VASCULAR SYSTEM. 515 jagged. The blood may burst through all the coats of the aorta at the same point; or more frequently the external coat remains and the blood is infiltrated in the middle coat and between it and the external coat. In this way a dissecting aneurism is formed, which may extend along the aorta for a considerable distance. After a short time the external coat usually gives way at some point, and the blood escapes. In rare cases life is prolonged for some time, the rupture being closed by a new membrane. We also find ruptures from fatty degeneration and atheroma in the arteries of the brain and lungs; in the coronary arteries, the coeliac axis, the mesenteric arteries. and in the arteries of the ex- tremities 2. In rare cases stenosis of a portion of the aorta may cause rupture at some point between the seat of stenosis and the heart. 3 Contusions, wrenchings, and severe falls may rupture the walls of an artery, either partially or completely, producing trau- matic or dissecting aneurisms, or completely severing the vessel. 4, Penetrating wounds may injure or entirely sever an artery. If the vessel be large and the injury severe, death from hemorrhage is the usual result. A small artery may become closed or be the seat of a false aneurism. In the healing of a wounded artery two conditions co-operate. The vessel retracts and contracts, and a thrombus is formed within it. The contraction may be alone sufficient to close the vessel ; its coats thicken, and the inner surfaces finally are fused together ; or the blood coagulates and forms a thrombus in the vessel near the wound. This thrombus later becomes organized and the vessel is converted into a fibrous cord. Spurious or false aneurisms are found most frequently con- nected with vessels of the extremities. When an artery is wounded the blood escapes into the surrounding soft parts, and a cavity is formed filled with blood and broken-down tissue. This condition may terminate in several ways. (a) The wound in the artery may heal and the effused blood be absorbed. (b) The effused blood and broken tissues may become gangrenous and the surrounding soft parts be inflamed. (c) A sort of sac wall may be formed by the soft parts, while the wound of the artery remains open, so that we have an aneurismal sac through which the blood is constantly pouring. 5 If an artery be wounded, and at the same time the vein which accompanies it, we have as the result the conditions called aneu- rismal varix and varicose aneurism. In aneurismal varix the artery and vein become adherent at the seat of injury, so that the arterial Digitized by Microsoft® 516 THE VASCULAR SYSTEM. blood passes directly into the vein. There is a smooth, rounded opening between the two vessels, the vein is dilated into a sac, and the veins emptying into it are dilated and tortuous. In varicose aneurism the artery and vein do not communicate di- rectly, but a false aneurismal sac is formed between the vessels, into which the blood is poured before passing into the vein. Varicose aneurism may also be produced by the spontaneous rup- ture of an aneurism into a vein. The aneurism presses against the vein, becomes adherent, and finally ruptures into it. This condition has been observed between the aorta and pulmonary artery ; the aorta and inferior and superior vena cava ; the popliteal artery and vein ; the femoral artery and vein ; the splenic artery and vena azygos ; thein- ternal carotid and sinus cavernosus. Even in cases of perforation by aortic aneurisms life is usually prolonged for some time. 6. Destructive inflammation or tumors of the surrounding tissues may invade and destroy a portion of the wall of an artery. Thus ulceration of the trachea, bronchi, bronchial glands, and cesophagius, or tumors of these parts, may perforate the aorta; gangrene of the lungs, the pulmonary arteries; ulcer of the stomach, the gastric arteries, etc. TUMORS. Secondary tumors, chiefly carcinomata and sarcomata, may occur in the walls of the arteries by continuous growth from without, involving first the external layers. To these layers they are usually confined, for the density of the inner layers affords such marked resistance to the infiltration of the tumor cells that they are apt to pass intact through the tumor, which grows around them. More frequently the arteries become secondarily involved in the growth of malignant tumors by the occurrence within them of emboli formed by larger and smaller masses of tumor cells. — These emboli are usually of small size, and are apt to get into the circulation by growing through the walls of the veins into their lu- mina. Large embolifrom tumors are most apt to occur in the branches of the pulmonary artery. The emboli, formed as they are for the most part by cells capable of growth and proliferation, are apt to soon form connection with the walls of the vessels, and, by the growth into them of blood vessels from the vasa vasorum to find the condi- tions necessary for their development, and they may thus soon in- volve the entire wall of the vessel and grow out into adjacent parts. Digitized by Microsoft® THE VASCULAR SYSTEM. 517 THE VEINS. DILATATION. Dilatation of the veins, or phlebectasia, presents itself under a va- riety of forms. 1. Simple Dilatation.—The vein is uniformly dilated in a cylin- drical or fusiform shape ; its length is not increased ; its walls are of nosmal thickness or thinned ; the valves increase in size, or are in- sufficient, or atrophic, or are torn. 2. Cirsoid Dilatation.—The vein is uniformly cylindrically di- lated, but is also increased in length, so that it assumes a very tor- tuous course. The walls are normal, thickened, or thinned. 3. Varicose Dilatation.—A circumscribed portion of the wall of the vein is dilated so as to form a globular sac. The sac communi- cates with the vein through a large or small opening. The wall of the sac is formed of the coats of the vein, which preserve their nor- mal thickness, are thickened or thinned ; the middle coat may dis- appear entirely. There may be only one such dilatation, or there may be a number on the same vein, or a number of veins may be af- fected at the same time. The vein may be otherwise normal, or, more frequently, is dilated in the cirsoid form. 4, Anastomosing Dilatatvon.—A number of contiguous and anastomosing veins are dilated, both in the cirsoid and varicose forms. The vein then looks like a series of cavities separated by thin partitions. The dilatations of the same vein become adherent to each other and to those of the adjoining veins; portions of the wall of the dilated parts may disappear, and we find a number of cavities containing venous blood and separated from each other by thin partitions. The course of the vein can no longer be followed out. Spontaneous cure of dilatations of the veins is not common, and usually occurs only in the lesser degrees of the lesion. Most phle- bectasiz increase steadily in size and extent. Very frequently thrombi form in the dilated veins, and either partially or completely fill them ; and these in rare cases may become organized, or the clots may dry and become calcified, forming phleboliths (see page 60), and, by the formation of new connective tissue in the walls, they may become enclosed in a fibrous capsule, with the oblitera- tion of the vessel. The wall of the dilated sac may become so thin that it finally ruptures, and the blood is discharged externally. Sometimes inflammation is set up in the tissues surrounding the vein, and we find both the surrounding tissues and the wall of the Digitized by Microsoft® 518 THE VASCULAR SYSTEM. vein the seat of purulent infiltration or fibrous thickening. The parts of the body from which the dilated veins draw their blood may exhibit the results of chronic venous congestion, cedema, hyperzemia, and hypertrophy or ulceration. When occurring in mucous membrane, dilated veins are usually associated with persistent catarrh. There is hardly one of all the veins of the body which may not be dilated. The hemorrhoidal veins ; the veins of the leg and thigh ; those of the pelvis and pelvic viscera ; those of the spermatic cord, scrotum, and labia; those of the abdominal wall; those of the neck and arms—are the ones most frequently found in this condition. The causes of dilatation are principally some mechanical obstruc- tion to the passage of the blood through the veins toward the heart ; but changes in the walls of the vessels from inflammation or injury, etc., are not without influence. WOUNDS—RUPTURE. Wounds of the veins usually heal by a simple contraction and an adhesive inflammation of their walls ; sometimes by the forma- tion of athrombus. Rupture of the veins may be produced by se- vere contusions and crushings of the body and by violent falls. Perforation of a vein may be produced by suppuration of the soft parts and the invasion of the walls of the vessel ; by the pressure of an aneurism or of a new growth; by the thinning of the wall of the vein in phlebectasia. INFLAMMATION. Inflammation of the veins, phlebitis, may involve chiefly the ex- ternal layers—periphlebitis ; or the internal—endophlebitis ; or, as is very frequently the case, the entire wall may be affected. Phlebitis may be caused by the presence of a thrombus, by injuries, or by an infectious inflammation of the surrounding tissues. Throm- bosis of the vein, either primary or secondary, is a very constant accompaniment of phlebitis. Acute Phlebitis may commence as a suppurative periphlebitis or as a result of inflammatory processes about the vessel. The outer layers of the venous wall are congested, swollen, infiltrated with serum and pus. The inner coats may become infiltrated with pus; they may become necrotic and disintegrate. A thrombus is con- stantly formed under these conditions, which may for a time stop the circulation and keep the products of inflammation and degenera- tion from mixing with the blood ; but the thrombus itself is prone to Digitized by Microsoft® THE VASCULAR SYSTEM. 519 disintegration, and thus the exudations and decomposing fragments of tissue may enter the circulation. On the other hand, owing to the presence of irritating or infec- tious material within the vein and the formation of a thrombus, the inflammatory process may be at the commencement an endophlebi- tis, but usually, if the inflammation be at all severe, the entire wall of the vessel will eventually be involved. The pus cells in both eases doubtless come from emigration from the vasa vasorum. Acute phlebitis may terminate in the absorption of the thrombus and the return of the vein to its normal condition ; in the obliteration of the vein ; or portions of the thrombus may become detached and find their way as emboli into various parts of the body. The most im- Fig. 261.—TuBERcULous PHLEBITIS. The section is from one of the pulmonary veins in a child dead of acute general miliary tuber- culosis. Specimen loaned by Dr. W. P. Northrup. portant results of phlebitis are usually those which depend upon the introduction into the blood of these emboli or of septic material (see Thrombosis and Embolism, page 72, and Pyzemia).' Chronic periphlebitis produces thickening, principally of the outer coats of the veins, but the inner coats may also be involved. The surrounding tissue may be also thickened and coalesce with the walls of the vein. There may or may not be thrombosis. Chronic endophlebitis is a not very common lesion, of the same general character as chronic endarteritis. More or less circum- scribed patches of new connective tissue are formed in the inner coats, which may undergo fatty or calcareous degeneration. Tuberculous Inflammation of the walls of the veins may occur as an extension of the process from without or from a lodgment of the tubercle bacilli in the blood current on the intima (Fig. 261). 1 Consult Freudwetler, “Experimental Phiebitis,” Virch. Arch., Bd. cxli., p. 526, 1895. Digitized by Microsoft® 520 THE VASCULAR SYSTEM. This is not infrequent in the pulmonary veins, and Weigert has called attention to the fact that in acute miliary tuberculosis the growth of tubercle tissue into the lumina of these veins from tubercular lymph: nodes is of frequent occurrence and readily explains the topography and mode of occurrence of the general disease. The tu- bercle bacilli which are present in the tubercular tissue growing into the lumen of the veins find thus an easy distribution. Syphilitic Inflammation may involve the walls of the veins either as gummy tumors or as more diffuse thickenings. TUMORS. Primary tumors of the veins are rare. Small lecomyomata have been described in the saphenous and ulnar veins. A myo-sarcoma as large as a man’s fist has been described, situated in the dilated vena cava inferior, The veins are not infrequently secondarily in- volved by sarcomata and carcinomata, and sometimes by chondro- mata, The thin walls of the veins offer comparatively little resist- ance to the encroachment of malignant tumors, which thus gain access to the circulation and may form metastases in various parts of the body. PARASITES. Echinococcus is sometimes found in the veins, having either de- veloped there or perforated from without. Two species of distoma (liver fluke) occur in man. D. hepati- cum occurs rarely in man, and, while usually found in the bile ducts, may occur in the vena cava. D. hematobium is very common in man in Egypt and in other parts of Africa, and usually occurs in the portal vein or its branches, and frequently in other veins. THE CAPILLARIES. The walls of the capillaries are so thin and so intimately con- nected with the surrounding tissues that their lesions are studied most appropriately among the diseases of the several organs. Dila- tation of the new-formed capillaries in tumors, granulation tissue, etc., and fatty and hyalin degeneration of their walls, may be mentioned here as readily observed lesions occurring under a variety of conditions. The changes which we assume to occur in the walls of the smaller veins and capillaries in exudative inflammation, by reason of which fluids and blood cells pass through them, are not yet sufficiently understood to be described with definiteness. THE LYMPH VESSELS. The smaller lymph vessels can hardly be treated as independent Digitized by Microsoft® THE VASCULAR SYSTEM. 521 structures, since their walls are so closely joined with the tissues through which they pass ; the lymph radicles, indeed, being nothing more than the spaces in the connective tissue in which the variously shaped connective-tissue cells lie. In the larger lymph vessels we find a moderate number of more or less independent lesions. INFLAMMATION. Lymphangitis. Inflammation of the larger lymph vessels is usually secondary and connected with some wound or injury. Owing, it is believed, to the entrance into the lymph trunk of some septic material or bac- teria, the vessels, sometimes for a considerable distance away from the wound, become red, tender, and painful. Under these condi- tions the microscopical appearances which the vessels present vary. In some cases the redness disappears after death and we find no ar- preciable alteration. In other cases we find the walls of the lymph vessels more or less densely infiltrated with pus cells, and the lumen may contain variable quantities of pus and fibrin and desquamated endothelium. The tissue about the vessels may also be infiltrated with serum and pus. These lesions may undergo resolution and the vessel be restored to its normal condition ; or the vessel wall and sur- rounding tissue may die or become involved in abscess ; or new con- nective tissue may form in and about the vessel, sometimes with obliteration of its lumen. The lymph nodes may participate in the inflammatory process. Inflammation of the lymph vessels may occur as the result of dis- section and other wounds, and the bites of venomous reptiles. It may occur in the uterine lymphatics in the phlegmonous form of puer- peral fever, and under other conditions. Tuberculous Lymphangitis.—Tuberculous inflammation occurs both in large and smalllymph vessels. Miliary tubercles and diffuse tubercle tissue may form in the walls and project into the lumen of the larger trunks ; or in the smaller vessels the new growth may en- tirely fill the lumen, and grow in this, with more or less involvement of the walls. This may occur independently, but it is most fre- quently seen in connection with tubercular inflammation of adjacent tissues. Thus from tubercular lymph nodes in the vicinity of the thoracic duct there may be a direct extension of the tubercular in- flammation, an involvement of the walls of the duct, and a growth of tubercle tissue into its lumen. Such growths in the thoracic duct have been shown by Weigert to be frequent in acute general miliary tuberculosis, and very satisfactorily explain the dissemination of the tubercle bacilli. In the vicinity of tubercular ulcers in the intestines. Digitized by Microsoft® G22 THE VASCULAR SYSTEM. furthermore, we often see the subserous lymph vessels, which pass from the vicinity of the ulcers, distended with the products of tuber- cular inflammation and looking like dense white knobbed cords. Syphilitic Inflammation of the lymph vessels not infrequently occurs in the vicinity of syphilitic ulcers in the primary stage. In later stages there may be thickening of the walls of the vessels and the development of gummy tumors in and about them. LYMPHANGIECTASIS. Dilatation of the lymph vessels occurs under a variety of condi- tions. It may be congenital, or it may be due to some hindrance to the flow of lymph onward—as by pressure from any cause, or from the occlusion of the vessels by inflammation—or it may be produced by unknown causes. If the dilated vessels form a circumscribed mass, this is often called a lymphangioma (Fig. 127). In certain forms of elephantiasis and in macroglossva the dilatation of the lymph ves- sels is an important factor. Its occurrence is not infrequent in the labia, prepuce, and scrotum. TUMORS. The relation of the endothelium of the lymph vessels and spaces to endotheliomata has been already mentioned in the section on Tumors. The dissemination of malignant tumors through the lymph chan- nels is of frequent occurrence, and is particularly marked in the case of carcinoma. In the vicinity of carcinomata the lymph vessels are not infrequently crowded with the tumor cells, forming white, irreg- ular cords; or small masses of the tumor cells may be found in the lymph vessels, either near to or remote from the tumor. White, irregular networks are often formed in this way beneath the pleura in carcinoma of the lung (Fig. 131), or beneath the capsule of the liver. Transverse sections of lymph vessels thus distended show sometimes swelling and detachment of the endothelium and a crowd- ing of the lumen with tumor cells. Whether or not the endothelium participates in the new formation of the characteristic carcinomatous cells is not known. THE LYMPH NODES (Lymph Glands).! It is well, in studying the lesions of the lymph nodes, to remember that they are structures so placed in the course of the lymph vessels 1 What we call lymphatic tisswe embraces not only the so-called lymph glands and the less complex but still well-defined structures found in the stomach, intestines, tonsils, and elsewhere, and called lymph follicles, but also the less well-defined, Digitized by Microsoft® THE VASCULAR SYSTEM. 523 that the lymph, in flowing toward the larger central trunks, passes through them, undergoing a sort of filtration as it percolates through the trabeculze of the lymph sinuses. If this simple fact be borne in mind the diseases of the lymph nodes, which are in the majority of cases secondary, are much more readily understood. Particles of pigment which in any way get into the lymph vessels are carried along until a lymph node is reached, and here they are, in part at least, deposited among the trabecule of the sinuses, while the lymph passes on and out of the efferent vessels (Fig. 264). The same thing occurs when cells from malignant tumors, bacteria of various kinds, etc., gain access to the lymph vessels; and also, as there is good reason for believing, in the case of many poisonous materials which our present knowledge does not enable us to associate with bacteria. These various materials, filtered out of the lymph by the glands, may act in a variety of ways to produce lesions in them. INFLAMMATION. Acute Inflammation of the lymph nodes usually occurs in con- nection with some inflammatory process in the region from which its lymph is gathered. The nodes are in the majority of cases swollen, reddened, and softer than normal, and often the seat of smaller and larger hemorrhages. Sometimes one, sometimes several nodes of a cluster are affected. The microscopical examination shows the most prominent change to be a great increase in the number of cells in the follicles and cords, as well as in the lymph sinuses. These cells are, in part, small and spheroidal, and similar to those normally filling the meshes of the follicles ; in part large polyhedral or variously shaped cells with prominent nuclei; the latter cells are most abundant in the lymph sinuses. In addition to this there is swelling of the endothelial cells of the reticulum of the sinuses (Fig. 262). The blood vessels may be distended with blood, or there may be blood, in greater or less quantity, free in the sinuses and follicles. The origin of the large irregular masses of tissue resembling that of lymph follicles, which, as Arnold has shown (Virchow's Archiv, Bd. lxxx., p. 315; Bd. Ixxxii., p. 394; Bd. Ixxxili., p. 289; Bd. lxxxvii., p. 114), is widely disseminated in variable amounts in different parts of the body; in the lungs, beneath the pleura, and elsewhere ; in the liver, kidneys, etc. Although the exact nature of these more diffuse masses of lymphatic tissue is too little understood, as indeed is that of the lymph follicles and glands themselves, there is reason to believe that they are analogous structures and prone to be affected by similar deleterious agencies. It seems better, in view of the fact that the so-called lymph glands are not glands at all, in the ordinary sense of the word, to call them lymph nodes, and the smaller masses of lymphatic tissue scattered through various parts of the body lymph nodules instead of ‘‘ iymph follicles.” Digitized by Microsoft® 524 THE VASCULAR SYSTEM. number of new cells which may form in a very short time is not yet definitely known. They may be emigrated leucocytes or their de- rivatives ; they may be derivatives of the endothelium of the reti- culum ; or they may be in some cases, at least in part, cells which have been brought into the node, through the afferent trunks, from some external inflammatory focus. The capsule of the nodes, and not infrequently the connective tissue about them, may also be in- filtrated with round cells. Acute inflammation may terminate in resolution, the new cells disappearing either by fatty or other degeneration, or by being car- ried off in the lymph, and the node return to its normal condition. Gay AR Ee ie i oh ey s/s ee es 262.—ACUTE INFLAMMATION OF LympH NopE IN TYPHOID FEVER. Showing a portion of one of the mesenteric nodes. A, capsule; B, perifollicular space or lymph sinus, containing in its meshes many large cells; C, portion of one of the follicles, with large and small cells in the meshes of its reticulum. This is the rule in the less intense forms of inflammation. On the other hand, the inflammatory process may become purulent and so intense as to lead to the formation of abscess, usually with a greater or less involvement of the tissue about the nodes. Fibrin and fluid exudate may be present in considerable quantity. There may be at first numerous small abscesses, which coalesce to form larger ones. These abscesses—buboes—may open externally or internally, or they may become dried and converted into cheesy masses which may calcify and, by a chronic inflammation in their periphery, become Digitized by Microsoft® THE VASCULAR SYSTEM. 525 enclosed by dense connective tissue. Sometimes, instead of abscess being formed, the tissue of the inflamed nodes becomes necrotic and breaks down, inducing more or less severe inflammatory or necrotic changes in the tissues in their vicinity. Small necrotic foci alone may form. In still other cases acute inflammation of the lymph nodes passes into the chronic form. Moderate degrees of inflammation in the lymph nodes are very common in connection with various forms of inflammation in neigh- boring parts. Thus simple pharyngitis, gastro-enteritis, erysipelas, simple purulent inflammation, etc., are often associated with this lesion of the nodes. The lymph nodes of children are, as arule, more easily affected by moderate inflammations in neighboring parts than Fic. 263.—CaRoNICc INFLAMMATION OF BRONCHIAL LyMPpH Nopg. Showing obliteration of the lymph sinuses and atrophy of the lymph follicles by the new-formeq connective tissue. are those of adults. Purulent inflammation of the lymph nodes is most frequently associated with severer forms of inflammation of adjacent or related parts, especially those of an infectious character, syphilitic inflammation, poisoned wounds, pyemia, etc. In a cer. tain number of cases we find bacteria in the inflamed lymph nodes, either singly or in zodgloea colonies, which have presumably some- thing to do with the lesion. In many cases the lesion of the lymph nodes appears to be in- duced, not by bacteria in the nodes themselves, but by poisons pro- duced elsewhere by the action of bacteria and brought to the nodes by the lymph. The swelling of the lymph nodes in typhoid fever Digitized by Microsoft® 526 THE VASCULAR SYSTEM. and diphtheria is probably induced in this way. Necrotic urea in the lymph nodes may result from the presence of bacterial poison. Chronic Inflammation.—This is characterzed by the increase of the connective-tissue elements of the node, with a gradual and com- mensurate disappearance of the lymphoid cells. The reticulum of the follicles and sinuses becomes thickened and fibrous, and in the trabeculee and capsule new connective tissue is formed, until, in ad- vanced cases, the entire node may be more or less completely con- verted into a mass of connective tissue. This condition is very fre- quently seen in the lower tracheal and in the bronchial nodes, apparently as a result of the lodgment in them of respired pigment particles ; but it may occur in any nodes, either as a result of re- peated moderate degrees of inflammation or from causes which we Fic. 264,—PIGMENTATION OF BRoNcBIAL LympH NopDE. The pigment is largely in the lymph sinuses and enclosed in cells. A, capsule of node; B, lymph follicle; C, perifollicular lymph sinuses. do not know. In some cases the nodes are greatly enlarged and the new tissue contains many large cells, while in other cases the con- nective tissue is dense and contains but few cells (Fig. 263).* Pigmentation.—The pigment which is very frequently found in lymph nodes may be derived from the hemoglobin of the blood, either in the nodes themselves or in remote parts, or it may be formed of various materials introduced into the body from without, ‘such as the pigments used in tattooing, respired dust particles of va- 1 Consult Ribbert, ‘‘ Ueber Regeneration und Entziindung der Lymphdriisen,” Ziegler’s Beitriige zur path. Anat., Bd. vi., 1889, p. 187. Digitized by Microsoft® THE VASCULAR SYSTEM. 527 rious kinds—coal, stone, iron, etc. (Fig. 264). The pigment particles, which usually first lodge in the lymph sinuses, may collect here in large quantities, either in the reticulum or the cells lying in its meshes , they may penetrate the follicles and cords and find perma- nent lodgment there. They usually induce a greater or less degree of chronic inflammation, so that in extreme cases, such as are fre- quently seen in the bronchial lymph nodes, nothing is finally left of the node but a more or less deeply pigmented mass of dense connec- tive tissue. The function of the node is, of course, in this way par- tially or entirely destroyed. The pigment in these cases appears to reach the node, in part by being carried along free in the lymph cur- rent, in part by becoming enclosed in leucocytes and being trans- ported by them. Pigmentation of the nodes is most marked in those about the root of the lungs, which are frequently of a mottled gray ora black color, but it may occur in the mesenteric and other nodes. Under similar conditions the diffuse lymphatic structure in the lungs and liver may be similarly pigmented. Inflammation of the Lymph Nodes with Cheesy Degenera- tion.—This lesion of the lymph nodes, which is distinct from the above-mentioned comparatively infrequent cheesy degeneration of the contents of old abscesses, commences with changes similar to those above described in simple inflammation. The node in this con- dition is swollen and feels harder than normal; on section it has a uniform reddish-gray color. Microscopical examination reveals a great increase in the number of parenchyma cells, some small and spheroidal, others large and polyhedral. Sometimes the larger cells are multinuclear, and not infrequently the reticular framework and the capsule are thickened. As the process advances the characteris- tic necrotic changes make their appearance. We may find at first a greater or less number of the cells converted into a strongly refrac- tile material, and the nuclei no longer capable of being stained. Then larger and smaller masses of cells undergo cheesy degenera- tion, with complete destruction of the blood vessels, reticulum, and the spheroidal and other cells, and their conversion into a granular material. A section through the node in this condition shows the cut surface mottled with irregular-shaped, larger and smaller opaque white patches, which indicate the areas of cheesy degeneration. These patches may increase in size and coalesce, so that a large part of, or even the entire gland may be converted into a more or less dense, cheesy mass which may be surrounded by the thickened capsule. In this condition they may remain for a long time, and not infre- quently, owing to the involvement of a series of associated nodes, either simultaneously or one after another, and the increase of con- Digitized by Microsoft® 528 THE VASCULAR SYSTEM. nective tissue about them, we find large, irregular nodular masses made up of a congeries of similarly affected nodes. On the other hand, the cheesy material may soften and break down, and, by the establishment of purulent and necrotic inflamma- tion about them, abscesses may form which may open externally. These abscesses may heal; but usually the healing is difficult and slow, and long-continued suppurations, frequently with the develop- ment of fistule, are very common. Under these conditions the in- flammation may assume a tubercular character. Instead of soften- ing, the cheesy material in the glands may become dry and hard and undergo calcification. Cheesy inflammation of the lymph nodes is most common in the cervical, bronchial, and mesenteric groups, but may occur anywhere. Itis most apt to occur in badly nourished young persons, who, in addition to the lesion of the lymph nodes, are very liable to suffer from chronic inflammations of the mucous membranes, skin, perios- teum, joints, and the subcutaneous and other connective tissues. This general condition is known as scrofula, and the lesion of the nodes is sometimes called scrofulous inflammation. It is not in- frequently associated with tuberculous inflammation of the nodes, either as an independent lesion or as a part of a general tuberculosis, and by some writers tuberculous and scrofulous inflammation of the lymph nodes are considered to be identical. In a considerable pro- portion of cases, however, of so-called scrofulous inflammation of the lymph nodes, there is no formation of tubercle tissue and we find no tubercle bacilli, so that we must consider this class of cases as sim- ply inflammatory, with a tendency to cheesy degeneration. Tuberculous Inflammation may occur in connection with simple inflammatory changes in the lymph nodes, or with the form of in- flammation which tends to cheesy degeneration. It may be local, confined to the nodes, or it may occur in connection with general acute miliary tuberculosis or with tuberculous inflammation of single organs. It may occur in single nodes, or in several nodes of the same group, or in groups situated in different parts of the body. In its simple and acute form there may be no evident change to the naked eye in the appearance of the nodes, or they may be besprinkled with small, grayish-white, translucent spots. Under these conditions the nodes may be reddened and soft, or swollen and denser than normal. In more adwanced forms of the lesion the tubercles coalesce and un- dergo a greater or less degree of cheesy degeneration. Under these conditions the cheesy areas are evident to the naked eye as more or less sharply circumscribed, opaque, whitish areas, frequently sur- rounded by an irregular, more translucent, grayish zone of tubercle tissue which merges insensibly into the adjacent tissue. The entire Digitized by Microsoft® THE VASCULAR SYSTEM. 529 node may become involved, and more or less completely converted into a cheesy mass, in the periphery of which a zone of tubercle tis- sue may or may not be evident. Microscopically the small nodules or miliary tubercles are seen to consist of more or less circumscribed collections of small spheroidal, or more frequently larger polyhedral cells, with or without well-de- fined giant cells. They usually commence to form in the follicles and lymph cords of the nodes, and from these may spread and involve the entire surrounding tissue. The cheesy degeneration, which here as elsewhere is apt first to involve the central portions of the tuber- cles, presents the usual appearances. Tubercle bacilli may be found in the edges of the cheesy areas or in the tubercle tissue about them. Simple inflammatory changes regularly occur in the periphery of the tubercles. There is an increase of cells in the lymph sinuses and. follicles, and a more or less marked swelling, and apparently a pro- liferation of the cells of the reticular tissue of the node. In cases in. which the process is chronic there is often marked increase of the connective tissue of the nodes, the reticular tissue becomes dense and fibrous, and the trabeculze and capsule are thickened. The. tubercles themselves, instead of undergoing cheesy degeneration, may become fibrous or be converted into a hyalin material. The cheesy material may dry and shrink, and become enclosed by a capsule of dense connective tissue and become calcified ; or it may soften, and thus cavities be formed in the glands, filled with grumous material ; or inflammatory changes may be induced in the vicinity of the nodes, leading to abscesses. On the other hand, hy- perplastic inflammation in the periphery of the affected nodes may result in their becoming bound together into a dense nodular mass. When cheesy degeneration has occurred, to the naked eye tuber- culous lymph nodes may not be distinguishable from those in scrofu- lous inflammation, but in some cases the nodular character of the new tissue around the cheesy centres is evident. The process 1s usually a slow and chronic one, except when occurring in connection with acute miliary tuberculosis in other parts of the body. It may occur in any of the nodes, but is most frequent in those of the bron- chial, mesenteric, and cervical regions. ’ Syphilitic Inflammation. — The lesions of the lymph nodes which occur in connection with syphilitic poisoning vary greatly, depending upon the stage of the disease. In the primary stage the lymph nodes in the region of the seat of infection are apt to pre- sent the lesions of an ordinary acute inflammation, with a tendency to the assumption of the purulent form. 1 For a consideration of the significance of tuberculous bronchial lymph nodes in children, consult Northrup, New York Medical Journal, February 21st, 1891. 43 Digitized by Microsoft® 530 THE VASCULAR SYSTEM. In the secondary stage of the disease the nodes of other regions, neck, elbow, axilla, etc., are frequently swollen and hard. On microscopical examination there may be an increase of connective tissue in the capsule and trabecul, but the chief change is in the accumulation in the follicles and lymph sinuses of larger and smaller spheroidal and polyhedral cells. The reticular tissue may be thick- ened and the walls of the blood vessels infiltrated with cells. In this condition the nodes may remain for a long time, not tending to form abscess; or they may undergo resolution through degenera- tion and absorption of the cells. In the tertiary stage of the disease the nodes may be the seat of chronic inflammation characterized by the formation of gummy tumors. Under these conditions they may form large, firm nodular masses by the growing together by new connective tissue of several altered nodes. The gross and microscopical characters of gummata of the lymph nodes are, in the main, similar to those in other parts of the body. There are important changes in the lymph nodes which occur as local manifestations of general diseases, such as typhoid fever, leprosy, etc., which will be considered under the headings of these diseases, Degenerative changes in the lymph nodes, with the exception of those above described, are not of great frequency or significance. Atrophy is a very regular occurrence in old age. In this con- dition the nodes are small, hard, and, unless pigmented, white. Microscopical examination shows a marked diminution in the num- ber of parenchyma cells, while the reticulum and the capsule and trabeculee may be thickened. There may be an accumulation of fat around the node in connection with senile atrophy. It should be remembered, in this connection, that the lymph nodes, as well as the lymphatic tissue in general, in children are more voluminous and contain a greater number of parenchyma cells than in adults. Amyloid degeneration of the blood vessels and reticulum of the lymph nodes occurs under the conditions which favor this change in general. It may occur in connection with amyloid degeneration of other parts of the body, or by itself. It may occur in nodes other- wise normal, or in those which are the seat of other lesions—thus in simple chronic or tubercular inflammation. It is frequently found in the mesenteric lymph nodes, in connection with waxy degenera- tion of the intestinal mucous membrane. Hyalin degeneration of the external layers of the smaller arteries and the capillaries of the lymph nodes, and also of the parenchyma cells, occurs occasionally in old age or in connection Digitized by Microsoft® ‘ THE VASCULAR SYSTEM. 531 with wasting diseases. The vessels and cells are swollen and con- verted into a translucent, strongly refractile substance resembling amyloid optically, but not responding to its micro-chemical tests. By the accumulation of this material the uninvolved parenchyma of the nodes may be compressed and atrophied. HYPERPLASIA OF THE LYMPH NODES (Lymphoma). In addition to*the considerable enlargements of the lymph nodes in inflammation which have been described above, they become en- larged under a variety of conditions which we do not understand. This lack of knowledge of the etiology, together with our ignorance of the function of the lymph nodes, and the morphological similarity, or even identity, which these enlarged nodes present, render it very difficult to decide upon the exact nature of the change, and in many cases to distinguish one form from another. In the first place, there is a class of cases in which, sometimes slowly, sometimes with great rapidity, the lymph nodes of certain regions, especially the abdominal, axillary, cervical, and inguinal, enlarge not infrequently to an enormous extent. They may be either hard or soft, even almost fluctuating ; the individual nodes may be distinct or merged into one another. Sometimes the nodes in nearly all parts of the body are affected. Microscopically we find that the enlargement is due, in the soft varieties, to an enormous increase of small spheroidal and polyhedral cells and a growth of the reticular tissue. It is a new formation of lymphatic tissue, but the normal relations of follicles, cords, and lymph sinuses are not pre- served. In the harder varieties there is a thickening of the reticular tissue in addition to an increase of cells. In very rare cases portions of the nodes may become cheesy. Sometimes larger and smaller hemorrhages occur in the nodes, especially in the softer forms. In addition to these changes in the lymph nodes there is, in a consider- able proportion of cases, a new formation of lymphatic tissue in greater or less quantity in other parts of the body, in the spleen, in the gastro-intestinal canal, in the marrow of bones, in the liver, kid- neys, etc., and the number of leucocytes in the blood and in other parts of the body is increased. This general condition is known as leukcemia and will be considered under the general diseases. The enlarged lymph nodes in this disease may be called, for convenience, leukcemic lymphomata. In the second place, there is a form of disease in many respects, particularly in the lesion of the lymph nodes, resembling leukaemia. There is, however, usually a less prominent involvement of the spleen and other lymphatic structures, and, what is more striking, no increase in the number of iF leuieoey tee in the blood. Thisis called Hodg- Digitized by Microsoft® 532 THE VASCULAR SYSTEM. . kin’s disease, or pseudo-leukcemia, and the enlarged lymph nodes may in this case be called pseudo-leukeemiclymphomata. The lesions of the lymph nodes are similar in both diseases, and it is convenient to assign different names to them simply because, for reasons which we do not at all understand, they seem to arise under different condi- tions and to be associated with a constant difference in the character of the blood (see page 794). TUMORS. Sarcomata occur in the lymph nodes as primary and second- ary tumors, and these may be of various forms: spindle-celled, large and small round-celled, and angio-sarcomata. It is not easy in many cases to distinguish morphologically between the small round-celled sarcomata and the above-described lymphomata. /1- bromata, myxomata, and chondromata occur in the lymph nodes, but are rare. Hndotheliomata are described, but are not common. Secondary carcinomata are of frequent occurrence, the form of the cells and the nature of their growth depending upon the seat and character of the primary tumors. PARASITES. Aside from various forms of bacteria which are not infrequently found in the lymph nodes—thus in diphtheria, splenic fever, typhoid fever, tuberculosis, etc.—filarta, trichince, and pentastomum have been described. Digitized by Microsoft® THE ALIMENTARY CANAL. THE MOUTH. MALFORMATIONS. Malformations of the lip and cheeks are usually associated with defective formation of the bones of the mouth. The entire process is generally due to an arrest of development. 1. The lower jaw is absent ; the upper jaw and hard palate small and imperfectly formed; the temporal bones nearly touch in the median line. The lower part of the face is, therefore, wanting ; the mouth is absent, or small and closed posteriorly; the tongue is absent. Such a malformation is rare ; the foetus is not viable. 2. The face remains in its early fcetal condition of a large cleft ; the mouth and nose form one cavity ; the orbits may be united in the same cavity. The fcetus is not viable. 3. There isa cleft in the upper lip, upper jaw, and hard palate. The cleft corresponds to the point of junction of the processes of the superior maxilla with the intermaxillary bone. There may be one cleft or two, one on either side of the intermaxillary bone. The cleft involves the lip alone, or the lip and superior maxilla, or the lip, maxilla, and palate. There may bea single or a double cleft in the palate, and the cleft may involve either the hard or soft palate, or both. If there are two clefts of the lip and maxilla the portion of lip and bone between them may be small, or entirely absent so as to leave a large open space. The soft palate may be entirely absent. This is a common malformation and does not endanger life. 4, Rarely we find a cleft involving the middle of the lower lip, and sometimes extending into the inferior maxilla. 5. Either the inferior, the superior, or both maxillary bones may be abnormally small. 6. The edges of the lips may be partly or completely joined to- gether. The opening of the mouth may be only a round hole. 7. The lips may be absent or imperfectly developed. 8. The corners of the mouth may be prolonged by clefts in the cheeks nearly to the ears. Digitized by Microsoft® 534 THE ALIMENTARY CANAL. HYPERTROPHY. The skin of the cheeks and lips may be hypertrophied in connec- tion with elephantiasis of the face. There may be a thickening of the lips alone, so that they appear double. This thickening may be due to an increase of all the ana- tomical elements of the lips; or there may be an increase and dilata- tion of the lymphatic vessels, giving to the growth a soft, oedematous character. INFLAMMATION, Catarrhal Stomatitis is found most frequently in children. It is produced by a great variety of local and constitutional causes. Of the conditions which are seen during life, the congestion, increased production of mucus, and swelling of the mucous membrane, but little remains after death. During life the congestion and swelling of the mucous membrane are well marked. There are often white patches, produced by the death of the superficial epithelial cells. There may be an increased production of mucus, which runs constantly from the mouth, or, in- stead of this, the entire mucous membrane is unnaturally dry. The only structural changes which can be demonstrated are the degenerative changes of the epithelial cells and the production of pus cells, which infiltrate to a moderate degree the stroma of the mucous membrane and appear upon its surface. Small clear vesicles may form beneath the epithelium from the collection of serous exudate. Croupous Stomatitis is produced by local irritants, by extension of the same form of inflammation from the pharynx, and it occurs with the exanthematous fevers and with diphtheria. Portions of the mucous membrane are swollen and congested, and covered with a false membrane. This false membrane is composed of a thickened layer of epithelium in the condition of coagulation necrosis, and of fibrin and pus in variable relative quantity. The stroma of the mucous membrane may be infiltrated with pus and fibrin, and portions of it may become necrotic. STOMATITIS ULCEROSA’ (Stomacace ; Stomatite Ulcero-mem- braneuse). This form of stomatitis occurs in children betweer the ages of four and eight years, and in adults between the ages of eighteen and twenty-five years. It is apt to occur in localized epidemics, in hos- pitals and asylums, and among soldiers and sailors. Some of the forms of mercurial stomatitis seem to be identical with this form of inflammation. 1 Bergeron, **Stomatite pleerosa,” Union. Médic 1859. Bohn, ‘‘ Mundkrank- heiten der Kinder,” 1880. th d by Microson® THE ALIMENTARY CANAL. 535 The inflammation begins at the margin of the gums of the lower jaw. The gums are swollen and coated with a grayish, soft matter composed of bacteria and detritus. Then follows destruction of tis- sue; the gums are destroyed around the teeth, and these fall out; the inflammation extends to the lips, cheeks, and tongue. The ulcers are coated with a thick, soft, gray membrane. The surround- ing soft parts are swollen, and there may be necrosis of the jaws.’ Syphilitic Stomatitis.—As a result of syphilis there may be pro- duced either the so-called mucous patches or gummy tumors. In the mucous patches we find at first the epithelial layer thickened and the papille of the stroma swollen and infiltrated with cells. This may be followed by desquamation of the epithelium and ulce- ration of the stroma. The deeper gummy tumors may also soften and form ragged ulcers of some size. Tubercular Stomatitis commences with the formation of miliary tubercles or of larger tubercular masses in the stroma of the mucous membrane. These masses soon degenerate, soften, and form ragged ulcers resembling very closely syphilitic ulcers. GANGRENE. Gangrene of the lips and cheeks, or noma, is most frequent in ca- chectic children as a consequence of the abuse of mercury. Much more rarely it occurs in adults after typhus and other exhausting diseases. The disease begins in the mucous membrane of the cheeks near one of the corners of the mouth. The mucous membrane be- comes black and gangrenous; the gangrene extends rapidly through the entire thickness of the cheek and produces perforation ; it ex- tends laterally in all directions. TUMORS. Adenomata are formed in the mucous membrane covering the mouth, lips, and soft palate. The tumors are rounded, usually small, sometimes as large as a hen’s egg. They may be situated in the thickness of the mucous membrane, or project in a polypoid form. They are formed by an hypertrophy of the normal mucous glands. The glandular acini are increased in number and size, the epithelial cells are increased in number and may undergo colloid degeneration. Papillomata occur most frequently at the edges of the lips, but are also found on the gums, the floor of the mouth, and the cheeks. "R. Volkmann, Virch. Arch., Bd. 1., p. 142, describes five cases of inflammation of the mucous glands of the lower lip. The lip was swollen and hard, the mucous glands and their ducts were dilated. Digitized by Microsoft® 536 THE ALIMENTARY CANAL. They are formed of hypertrophied papille, covered with thickened ‘epidermis. They very often ulcerate. Carcinomata are of frequent occurrence. They may be found ‘at any part of the mucous membrane of the mouth, but as a rule be- gin in the edge of the lower lip. They may orginate in an ulcerating papilloma, or as a flat, super- ficial growth from the deeper layers of the epithelium, or as deep nodules starting in the mucous glands. They are composed of large masses of epithelial cells, closely packed together, often forming nests, and arranged in anastomosing tubular masses. The stroma surrounding these masses is infiltrated with cells. Ina few cases the infiltration of the stroma with small round cells may be very marked, so marked that the epithelial growth may be obscured. The new growth increases in size, ulcerates, infiltrates the adjacent tissues, and may give rise to metastatic tumors. Angtomata are found in the lips. They may be congenital or developed after birth. Fibromata, lipomata, and enchondromata have been seen in a few cases in the lips. When they appear in the mouth they usually grow from the bones. THE TONGUE. MALFORMATIONS. Absence of the tongue is found in connection with the extreme defects of development of the face already mentioned. The anterior portion of the tongue may be absent while its base remains. The lower jaw is then small. The tongue may be partly or completely adherent to the floor of the mouth. The frenulum may be abnormally short, or may extend to the tip of the tongue. In rare cases the sides of the tongue are adherent, or its upper surface may be adherent to the roof of the mouth. HYPERTROPHY. Macroglossia, or hypertrophy of the tongue, is almost always a congenital lesion, and is especially common in cretins. The tongue is so large that the cavity of the mouth cannot contain it; it is pro- truded through the lips and displaces the jaws. The lips may also be hypertrophied in the same way. There is an hypertrophy of all the anatomical elements which make up the tongue, and in addition to this there may be a dilatation of the lymphatic vessels. Digitized by Microsoft® THE ALIMENTARY CANAL. 537 INFLAMMATION. Inflammations of the tongue may be associated with similar changes in the mouth, or may occur by themselves. Superficial Glossitts.—Inflammation involving only the mucous membrane of the tongue may occur as an acute or chronic process. The acute forms present no marked lesions. The chronic forms result in an increased production of epithelium and an hypertrophy of the papille of the tongue. A moderate development of such an inflammation is not infre- quently associated with derangements of the stomach. The tongue is large, its surface is irregular from the hypertrophy of the papilla. There may be no change in the epithelium, and then the surface of the tongue is clean and red; or the epithelium is increased and the tongue is covered with a white fur. More severe forms of the disease also occur, especially with syphilis. The hypertrophied papille and increased epithelium then alter very decidedly the appearance of the tongue. Parenchymatous Glossitis may be produced by mercurial poison- ing, by injury, or by unknown causes. The tongue is swollen, the muscular and connective portions are congested and infiltrated with serum and pus. The inflammation may stop at this point or it may go on to the formation of an abscess. Syphilitic Glossitis.—In persons suffering from constitutional syphilis there may be mucous patches on the surface of the tongue ; or gummy tumors in its stroma, which often soften and form deep ulcers; or a diffuse, chronic inflammation of the surface of the tongue, with hypertrophy of the papille. Tubercular Glossttis.—There may be a tubercular inflammation of the connective tissue of the tongue just beneath the epithelial layer, resulting in the formation of tubercle granula and granulation tissue. In this way tumors of some little size are formed, which may remain unchanged for some time, or may degenerate, soften, and form ulcers. TUMORS. Cysts.—The most common forms of cysts are the sacs beneath or partly in the substance of the tongue (ranula). They are formed by dilatation of the ducts of the submaxillary and sublingual glands, or make their appearance in the connective tissue beneath and in the tongue. Angtoma.—Cavernous vascular tumors are found in the sub- stance of the tongue and projecting from its surface. Lipoma and fibroma are rare. They form nodules in the sub- stance of the tongue or project in a polypoid form. Composite Digitized by Microsoft® 538 THE ALIMENTARY CANAL, tumors, composed largely of fat, are found on the tongue as a con- genital condition. Lupus occurs in the form of nodules and ulcers at the base of the tongue. Sarcomata are not common in this situation, but they may occur both in children and in adults. Carcinoma.—This form of new growth may begin in the tongue ot may extend to it from the adjacent tissues. The growth is com- posed of large, flat epithelial cells packed closely together in anas- tomosing tubular spaces and surrounded by a connective-tissue stroma. Amyloid tumors of the tongue have been several times reported. Micro-organisms of various forms; bacteria, moulds, and yeasts, are always present in the mouth, often in enormous numbers. They are for the most part not of significance save for the putrefactive pro- cesses which they initiate and maintain in mouths not properly cleansed. On the other hand, Staphylococcus and Streptococcus pyo- genes and the pneumococcus are of frequent occurrence in the mouths especially of those who live in towns and crowded dwellings. The tubercle bacillus may be present in the mouth as well as in the nose of those who care for uncleanly consumptives. The fungus of aphthe (soor), and leptothrix, which under usual conditions are not harmful, may incite serious local disease. The so-called Mycosis pharyngis is apparently due to the growth in susceptible persons of a form of leptothrix not yet thoroughly studied, on account of the technical difficulties in the way of its arti- ficial cultivation ' (see page 284). THE PHARYNX AND THE CSOPHAGUS. MALFORMATIONS. When, as not infrequently occurs, the embryonal gill clefts do not properly close, fistule may remain. These may in rare cases be complete, so that an opening exists from the pharynx, larynx, or trachea to the side of the neck. More frequently, however, these fistulee are incomplete and shallow, and open either inward into one of the above-named organs or outward on to the neck. Small portions of the gill clefts may persist without external openings, and .from these subcutaneous cysts of the neck are often developed. Or a por- 1For the results of systematic studies on the bacteria of the mouth consult the works of Miller and of David. For bibliography and studies on micro-organism asso- ciated with acute angina see Stoos, Mitth. a. d.klin. med. Inst. der Schweiz, 3. Reihe, Heft 1, 1896, and for membranous rhinitis, Abbott, Medical News, May 13th, 1893; for ozena, Abel, Zeits. f£. Hygiene und Infectkr., Bd. xxi., p 89. Digitized by Microsoft® THE ALIMENTARY CANAL. 539 tion of the cleft may be cut off, forming a cyst, while the fistula per- sists with its external opening. The walls of these fistula and cysts may be covered with mucous membrane having cylindrical or flattened or ciliated surface cells. Fig. 265.—SecTion oF THE WALL OF a Cyst oF THE NECK. Formed from imperfect closure of embryonal gill cleft—diffuse lymphatic tissue, Fig. 266.—SECTION OF THE WALL oF a Cyst oF THE NECK. Formed from imperfect closure of embryonal gill cleft—nodules of lymphatic tissue. Or, when formed from the outer gill clefts, they may be lined with skin.’ ‘Schmidt, Virch. Arch., Bd. cxliii., p. 369. Literature of amyloid tumors in general. Digitized by Microsoft® 540 THE ALIMENTARY CANAL. Not infrequently the walls of these cysts and fistula are embedded in lymphatic tissue, which may be diffuse or gathered in nodular form (see Figs. 265 and 266). The cesophagus may be entirely absent, or its lower portion may be present and joined to the pharynx by a solid cord; or the pharynx, or the lower part of the cesophagus, may be continuous with the trachea; or the entire esophagus may be represented by a solid cord. Diverticula of the pharynx, dilatations of the cesophagus, and di- vision of the middle portion of the cesophagus into two branches have all been observed. INFLAMMATION. Catarrkal and Croupous Pharyngitis are usually associated with the same forms of inflammation in the mouth and have the same characters. In catarrhal inflammation involving the tonsils and those portions of the pharynx richly supplied with the so-called submucous adenoid tissue, leucocytes may penetrate in considerable numbers the peculiar thin epithelium.” These may, on exposed surfaces, form a part of theexudate and be removed; or in thecrypts of the tonsils they may, with epithelium and various forms of bacteria, form those whitish plugs characteristic of follicular tonsillitis. In chronic inflammation of the tonsils and pharynx there may bea large and permanent hyperplasia of the adenoid tissue, with more or less dense fibrous tissue, leading to enlargement of the tonsils and to diffuse or circumscribed nodular or pedunculated masses of vas- cular new tissue in the vault or elsewhere in the pharynx. The ton- sils, on the other hand, may atrophy. Submucous Pharyngitis may occur with inflammations of the mucous membrane, with caries of the cervical vertebre, with inflam- mation of the cervical and parotid glands, with periostitis of the cranial bones, or may be idiopathic. It may result in swelling and cedema, in induration, or in suppuration. It is most important when it affects the posterior wall of the pharynx and forms retro- pharyngeal abscesses. Such abscesses may cause death by suffo- cation. Catarrhal Gisophagitis may be either acute or chronic. The chronic form may produce ulceration, or relaxation and dilatation of the walls, or hypertrophy of the muscular coat. 1 Consult Dobrowolski, “Lymph Nodules of the Larynx, CAsophagus, etc.,” Ziegler’s Beitriige z. path. Auat., Bd. xvi., p. 48. 2See Hodenpyl, ‘‘ Anatomy and Physiology of the Faucial Tonsils,” Am. Jour, Med. Sciences, March, 1891. Digitized by Microsoft® THE ALIMENTARY CANAL. 541 Croupous Césophagitis is found with croup of the pharynx, and after the exanthemata and other severe diseases. Irritating and caustic acids and alkalies destroy larger or smaller portions of the mucous membrane. The necrosed portions are of a black or whitish color, surrounded by a zone of intense congestion. If the patient recover the patches of membrane which have been destroyed slough, fall off, and leave a granulating surface. In this way dangerous stenosis of the esophagus may be produced. Foreign bodies which are swallowed and become fixed in the ceso- phagus cause inflammation of the mucous membrane and of the ad- joining soft parts. The inflammation may go on to produce ab- scesses around the cesophagus, or to destroy the wall of the canal, and the foreign body finds its way into the trachea, aorta, or peri- cardium. Inflammation of the submucous tissue of the oesophagus, apart from the cases just mentioned, is not common. It may cause the formation of abscesses, or of fibrous tissue, which may produce stenosis. ULCERATION, Ulceration of the pharynx occurs in rare cases as the result of catarrhal inflammation. More frequently it is produced by syphilis, either in the form of superficial ulcers or of deep and extensive de- structions of tissue from the softening of gummy tumors. Lupus also sometimes attacks the upper part of the pharynx and produces extensive ulceration. Ulceration of the cesophagus is not common, but a few cases of simple perforating ulcers have been described.’ Foreign bodies in the cesophagus may perforate its wall, as al- ready mentioned. Perforation of the cesophagus from without may be produced by inflamed bronchial glands, by cavities and gangrene of the lungs, by abscesses in the mediastinum, by abscesses ac- companying caries of the vertebre, and by aneurisms of the aorta. Cases have been described of rupture of the wall of the cesophagus by violent coughing and vomiting, but it seems probable that there was really some previous disease to account for the rupture. DILATATION.” Simple cylindrical dilatation of the cesophagus is usually the re- sult of long-continued stenosis of the cesophagus or of the cardiac end of the stomach, although not nearly all the stenoses are fol- lowed by dilatation. These dilatations are formed at first immedi- 1 Graefe u. Walther, Jour. fir Chir. und Augenheilk., Bd. xix. Med. Chir. Trans., vol. xxxvi. Rokitansky, ‘‘ Path. Anat.” 2 Ziemssen, ‘* Cyclopedia of Medigpeitascne” 542 THE ALIMENTARY CANAL. ately above the stenosis and then extend upward. Only in rare cases does the dilatation involve the whole length of the tube. The entire wall of the dilated portion of the esophagus is thickened, and there may be polypoid growths from the mucous membrane. In rare cases there is cylindrical dilatation of part or of the whole of the cesophagus without a stenosis or any discoverable cause. In these cases the dilatation is usually greatest near the middle of the cesophagus and diminishes upward and downward, so that the ceso- phagus has a fusiform shape. The dilatation may reach a very con- siderable degree, the walls of the cesophagus are thickened, its mucous membrane may be covered with papillary outgrowths or ulcerated. The Sacculated Dilatations of the oesophagus are of two kinds : those due to pressure, and those due to traction. The dilatations due to pressure are situated in the posterior wall of the pharynx, just at its junction with the cesophagus. The smaller sacs are from the size of a pea to that of a hazelnut; the larger sacs may reach an enormous size and hang down between the cesophagus and the vertebral column, the opening into the cesopha- gus remaining comparatively small. It is supposed that a limited area of the wall of the cesophagus loses its power of resistance against the pressure exercised upon it in each act of swallowing ; it then is forced outward by the pressure, and so there is formed first a protru- sion and then a sac. When a sac is formed the food enters it, accu- mulates there, and so the sac becomes larger and larger. The dilatations due to traction are situated on the anterior wall of the cesophagus, at a point nearly corresponding to the bifurcation of the trachea. They are of funnel shape, with the small end outward. Their length varies from two to twelve millimetres ; the width of the opening into the cesophagus is from six to eight millimetres. These dilatations are due to inflammation of the parts adjoining the oesophagus, especially of the bronchial glands, followed by ad- hesions to some part of the anterior wall of the cesophagus. These adhesions then contract and draw the wall of the cesophagus out- ward, and in this way the dilatations are formed. Ata later time these sacs may perforate into the bronchi, the lungs, the pleural cavity, the pericardium, the aorta or pulmonary artery. STENOSIS. Congenital Stenosis.—Besides the defects of development of the cesophagus which are incompatible with life, there may be a congen- ital stenosis of some part of it which causes difficulty in ewallovans, but yet does not destroy life. Stenosis by Compression is not uncommon. Tumors of the Digitized by Microsoft® THE ALIMENTARY CANAL. 543 neck and mediastinum, and aneurisms of the aorta are the usual causes. Stenosis by Obstruction.—Foreign bodies may be lodged in the cesophagus. Tumors may hang down from the pharynx into the cesophagus, or may be situated in the wall of the cesophagus. In- flammation of the esophagus, due to the ingestion of irritating poi- sons, produces cicatricial stenoses. A few cases of stenosis due to syphilitic inflammation have been reported. TUMORS. The veins of the cesophagus may be enormously dilated. They may rupture and so give rise to heemorrhage.' Cysts.—Small retention cysts of the follicles of the mucous mem- brane are sometimes found. Larger cysts of the cesophagus lined with ciliated epithelium have been described.” Papillomata of small size may be found in considerable numbers throughout the entire length of the cesophagus, or may occur singly. Large papillary tumors are more rare. Fibromata grow from the periosteum of the bones at the base of the skull, and project into the cavity of the pharynx and posterior nares in the form of large polypoid tumors. Small fibrous tumors are formed in the submucous connective tissue of the cesophagus. Tumors, which attain a very large size, originate in the submucous connective tissue on the anterior wall of the lower part of the pharynx, and as they grow hang down into the cesophagus. Soft polypoid tumors consisting largely of loose succulent connective tissue and lymphatic tissue are often called “adenoid polyps” (see Fig. 267). Hairy polyps of the pharynx have been described by Arnold * and others. The occurrence of cartilage and bone in the tonsil has been described by Stoeltzner.* Lipomata of small size are sometimes found in the walls of the cesophagus. Myomata composed of smooth muscle may grow in the muscular coat of the cesophagus and attain a considerable size.* Adenoma.—A polypoid adenoma composed of tubules lined with cylindrical epithelium, and growing from the anterior wall of the cesophagus, has been described by Weigert.* 1 Bristowe, Trans. London Path. Soc., 1856. 2 Zahn, Virch. Arch., Bd. exliii., p. 171. 3 Arnold, Virch. Arch., Bd. cxi., p. 176. Bibliography. 4 Stoeltzner, Virch. Arch., Bd. cxli., p. 446. ’Vireh. Arch., Bd. xliii., p. 187. Med. Times and Gazette, November 28th, 1874. Glasgow Med. Journal, February, 1878. 6 Virch Arch., Bd. lxvii., p. 516. Digitized by Microsoft® 544 THE ALIMENTARY CANAL. I (Delafield) have seen one tumor, the size of a chestnut, growing in the soft palate, which was composed of a stroma of connective and mucous tissue in which were irregular, anastomosing tubules filled with small, polygonal, nucleated cells. It should be called an ade- noma or a carcinoma. Another composite tumor grew from the mucous membrane of the pharynx behind the left tonsil. It filled the pharynx below the level Fic. 267.ADENOID PoLyP oF PHARYNX. of the palate. It had the gross appearance of a myxo-sarcoma, the central portions being very soft. It was composed of connective tissue, mucous tissue, fat, sarcomatous tissue, and irregular tubules lined with small, polygonal, epithelial cells. Some of the tubules were distended with masses of hyalin matter. The whole structure re- sembled that of the tumors so often found in the parotid region— tumors which can be called ‘‘ adenoid myxo-sarcomata.” Carcinomata may originate at any part of the wall of the pharynx and cesophagus. They are composed of flat epithelial cells closely packed together in masses in the usual way. In the eso- Digitized by Microsoft® THE ALIMENTARY CANAL. 545 phagus the new growth begins in the deeper layers of the mucous membrane, and grows so as to encircle the tube for a length of one or more inches. The tumor remains as a flat infiltration, or it ulcer- ates, or it projects inward in large, fungous masses. The growth may extend up and down the cesophagus, and even involve the pharynx or stomach. The ulcerative process may extend outward so as to produce perfo- ration into the air passages, the lungs, pleure, pericardium, and large blood vessels. The new growth may extend outward and infiltrate the surround- Fig. 268.—DirruseE SARcoMA oF THE PHaArynx, X 850 and reduced. ing soft parts, so that the cesophagus is surrounded by large, solid, cancerous masses. Metastatic tumors are also sometimes formed. Sarcoma.—lI have seen one case in which there wasa diffuse growth involving both the tonsils, the posterior and lateral walls of the pharynx, the base of the tongue, and the epiglottis. Thenew growth replaced the mucous membrane, infiltrated the soft parts for a short distance, and projected inward in polypoid masses. It was composed of small, polygonal, nucleated cells contained in a very delicate nucleated stroma’ (Fig. 268). 1For literature of malignant disease of the tonsils, consult Newman, American Journal of the Medical Sciences, May, 1892. Houwsell, Beitr. zur klin. Chirurgie, Bd. xiv. AA Digitized by Microsoft® 546. THE ALIMENTARY CANAL, THE STOMACH. MALFORMATIONS. ' Malformations of the stomach are not common. The organ may be entirely wanting in acephalous foetuses. It may be of various de- grees of smallness, sometimes no larger than the duodenum. It may be divided into two halves by a deep constriction in the middle. The pyloric orifice may be stenosed or entirely closed. The stomach may be outside of the abdominal cavity from a hernial protrusion through the diaphragm or at some point in the abdominal wall. It is found on the right side, instead of the left, when the other viscera are transposed, and the position of the cardiac and pyloric orifices is correspondingly inverted. POST-MORTEM CHANGES. In adults the stomach after death is of a grayish or pinkish color, sometimes mottled with red ecchymoses. The mucous membrane is soft and the epithelium easily brushed off. At the fundus the food is usually found collected, and here the mucous membrane is the softest. It is very common to find the epithelium removed from the entire fundus of the stomach, so that all that portion of its wall is grayer and thinner, there being a sharp dividing line between the two por- tions. Sometimes this post-mortem softening process goes on to de- stroy all the coats of the stomach, and even the adjoining portion of the diaphragm. In this way the contents of the stomach may be emptied into the pleural cavity by a large, ragged opening in the stomach and diaphragm. When the softening affects all the coats of the stomach the softened portion is not sharply limited. The entire thickness of the affected portion of the wall is converted into a gray or yellow semi-transparent jelly, or into a blackish, broken-down pulp. This softening is most frequent in children, but also occurs in adults, usually in connection with severe and exhausting diseases. INJURIES. Perforating wounds of the stomach usually give rise to a fatal peritonitis, It is possible, however, for the wound to heal, or a gas- tric fistula may be formed. Rupture of the stomach may be produced by severe blows or falls. HAMORRHAGE, Small extravasations of blood in the wall of the stomach are fre- quently found in persons who have died from one of the infectious diseases. Digitized by Microsoft® THE ALIMENTARY CANAL. 547 Hemorrhage into the cavity of the stomach may be produced in a variety of ways. In ulcers of the stomach there may be bleeding from the small vessels of the ulcer or from the perforation of a larger artery. In cancer of the stomach there may be bleeding from the tumor. Some cases of chronic gastritis are characterized by general bleed- ing from the mucous membranes of the stomach. Cirrhosis of the liver is not infrequently attended with large hemorrhages from the mucous membrane of the stomach. Small aneurisms of the arteries in the wall of the stomach may rupture internally. In yellow fever and some of the other infectious diseases there is hemorrhage into the cavity of the stomach. Patients may vomit biood during life, and after death no lesion to account for the bleeding be found. INFLAMMATION. Acute Catarrhal Gastritis, as we see it after death, is usually due to the ingestion of irritating substances, or forms part of the lesions of cholera morbus. If we can judge from clinical symptoms, it occurs during life as a temporary condition from a variety of causes. After death the mucous membrane is found congested and swollen, or the congestion may have disappeared. The mucous membrane is coated with an increased amount of mucus, especially at the pyloric end of the stomach. Sometimes there are a number of minute white dots in the substance of the mucous membrane. The structural changes in the mucous membrane consist simply in a swelling of the cells of the gastric tubules, a slight infiltration of the stroma with pus cells, and a swelling of the patches of lym- phatic cells. The little white dots, when they are present, are com- posed of small foci of pus between the gastric tubules, with degene- ration and destruction of some of the tubules. Chronic Catarrhal Gastritzs is a very common disease. There is, however, no very close relation between the severity of the symp- toms during life and the extent of the lesions found after death. In some cases chronic alcoholism, or the abuse of drugs, or the mode of life of the patient seems to be the cause of the lesion. Chronic phthisis, chronic Bright’s disease, cirrhosis of the liver, and fatty liver are often accompanied by chronic gastritis. Organic dis- ease of the heart, or pressure on the ascending vena cava, produces a form of chronic gastritis characterized by intense general congestion. After death the stomach is found either empty or still containing food. It is of normal size, or dilated, or small, sometimes hardly larger than the duodenum. Its inner surface is coated with a thick Digitized by Microsoft® 548 THE ALIMENTARY CANAL. layer of tenacious mucus, most abundant at its pyloric end. The mucous membrane is congested, or white, or slate-colored, or mottled with small white spots. It is of normal thickness, or thinned, or thickened, or there are little polypoid projections from its surface, or there is cystic dilatation of the gastric tubules (Fig. 269). The con- nective tissue and muscular coats remain unchanged, or they are Fig. 269.—CHRONIC GASTRITIS, Showing changes in the glandular coat. A small cyst formed by dilatation of a tubule. thinned and relaxed, or they are hypertrophied. The hypertrophy may be diffuse, or it is confined to the pyloric end of the stomach and may then produce stenosis of the pylorus. The minute lesions consist principally in changes in the mucous membrane. The cells of the gastric tubules are swollen, degenerated, and broken down. The tubules are atrophied and deformed, or di- lated into cysts. The patches of lymphatic tissue about the blind Digitized by Microsoft® THE ALIMENTARY CANAL. 549 ends of the tubules are increased in size. The connective tissue be- tween the tubules is infiltrated with cells and increased in quantity. Croupous Gastritis is of rare occurrence. It is found in chil- dren with croupous inflammation of the pharynx and cesophagus, and is then usually in small patches. In adults it is almost always secondary to typhus, pyzemia, puerperal fever, cholera, dysentery, the exanthemata, and irritating poisons. The false membrane is in small patches, or may line a large part of the stomach. The disease is usually not diagnosticated during life, the symptoms of the pri- mary disease diverting attention from the gastritis. I (Delafield) have seen one case of idiopathic croupous gastritis in an adult. A man, forty-six years old, was in good health until eight days before his death. At that time he caught cold, had pains over his bowels, tenderness over the liver, constipation, cough with mu- cous expectoration, temperature 1024°, pulse 120. On the day of his death, the eighth day of the disease, the temperature was 100°, pulse 112, tongue dry, abdomen tympanitic and tender, and he died in a prolonged attack of syncope. At the autopsy all the viscera were ex- amined. Excepting evidences of bronchitis in the lungs, there were no lesions save in the stomach. About two-thirds of the internal surface of the stomach, including the lesser curvature and anterior and posterior walls, appeared to be covered with a thick false mem- brane, which did not quite reach to the cardiac or pyloric orifices, Minute examination showed that there was a layer of exudation on the internal surface of the mucous membrane. This exudation con- sisted of fibrillated fibrin and lymphoid cells dipping into the mouths of the follicles. Beneath the exudation the mucous membrane was thickened and altered. A large number of lymphoid cells separated the follicles, and even replaced them entirely. The submucous layer was very much thickened by the presence of lymphoid cells, fibril- lated fibrin, and fibrous tissue. The muscular coat was separated into layers by groups of lymphoid cells. Wilks and Moxon mention a similar case in a man with chronic Bright’s disease, and a case of both croupous gastritis and colitis with abscess of liver. Suppurative or Phlegmonous Gastritis.—A formation of cir- cumscribed collections of pus may occur in the connective-tissue coat of the stomach, as it does in other parts of the body, in puerperal fever and the infectious diseases. Idiopathic suppurative gastritis is a disease of rare occurrence. Leube’ has collected thirty-one cases, of which twenty-six were males and five females. In some of the cases the inflammation was 1 Leube, “ Ziemssen's Cyclopedia, ” vii., p. 157. Digitized by Microsoft® 550 THE ALIMENTARY CANAL. ascribed to the excessive use of alcohol, in others to a wound in the region of the stomach, in others to some error in diet. Fagge’ describes a case in a male of fifty-one years of age, with- out discoverable cause. Silcock * describes a case in which the gastritis followed the ope- ration of gastrostomy. I have seen one case occurring in an adult male, without any known cause. The suppurative inflammation seems to begin in the connective- tissue coat of the stomach. From thence it may extend to the glan- dular coat and produce perforations, or outward to the muscular and peritoneal coats. In some cases there is added a local or general peritonitis. The inflammation may involve one or more circumscribed areas and so produce abscesses, or it may be a diffuse process involving the whole extent of the wall of the stomach. Toxic Gastritis.—The mineral acids, the caustic alkalies, arse- nic, corrosive sublimate, and the metallic salts, phosphorus, camphor, and all other irritating materials, cause different lesions of the stomach, according to their quantity, their strength, and the length of time that has elapsed before death. In large quantities they destroy and convert into a soft, blackened mass both the mucous membrane and the other coats, so that perfo- ration may take place. In smaller quantities they produce black or white sloughs of the mucous membrane, surrounded by a zone of in- tense congestion. If death does not soon ensue the ulcerative and cicatricial processes which follow such sloughs may contract and deform the stomach in various ways. If the poisons are of less strength they produce a diffused con- gestion of the mucous membrane, with catarrhal or croupous exuda- tion on its surface and serous infiltration of the submucous coat (see chapter on Poisons). ULCERS OF THE STOMACH. The Chronic Perforating Ulcer.—This form of ulcer is often seen ; according to Brinton, in five per cent of persons dying from all causes. It occurs in females nearly twice as frequently as in males. As regards theage, Brinton concludes that the liability of an individual to become the subject of gastric ulcer gradually rises, 1 Trans. Lond. Path. Soc., 1875, p. 81. 2 Tbid., 1883, p. 90. Digitized by Microsoft® THE ALIMENTARY CANAL. 551 from what is nearly a zero at the age of ten, to a high rate, which it maintains through the period of middle life; at the end of which period it again ascends, to reach its maximum at the extreme age of ninety. Lebert gives one hundred and ninety-eight cases in which the ulcers were found at the autopsy, as follows : AGE. NUMBER OF CASES. AGE. NUMBER OF CASES. 15 to 20 years.......... 20 50 to 60 years . Be 29 20 to 30 years. ........ 48 60 to 70 years.......... 19 30 to 40 years.......... 28 70 to 80 years.. ...... 5 40 to 50 years...... ... 43 Hauser’ gives thirty autopsies from Erlangen of ulcers which were still open, as follows : | AGE. | NUMBER OF CASES. AGE, NUMBER OF CASES. 20 to 30 years....,. ... 3 50 to 60 years.. ...... 7 30 to 40 years.......... 3 60 to 70 years... ...... 8 40 to 50 years.......... 3 70 to 80 years.......... 6 Moore’ gives the following table of the fatal cases of ulcer of the stomach occurring at St. Bartholomew’s Hospital from 1867 to 1879 : SEX. AGE. POSITION. CAUSE OF DEATH. M. 36 Near pylorus...... .-... 2.06. Perforation. M. 19 Greater curve near pylorus. . .|Hzmorrhage. M. 47 Near pylorus..........ceeeees Exhaustion. M. 47 PH OMS) fase erie see Fase AE Phthisis. M. 41 SES tated Golarnla tasers eharssate af M. 52 fe Ree ee bas eialsttnlaroe wean Exhaustion. M. 46 Lesser curve near pylorus...... Perforation. F. AUN a aaimy aisileleler eset thaniavn tutest enachie are Si Sinus in liver to lung. M. 57 Cardiac end.... .....s+00s . |Heemorrhage. M. 19 Near pylorus..... .. ....e..0- Perforation. M. 40 ME Me cream — AedttnnSsadsaddasers “e F. 46 Posterior wall. .. ....... ... i. Goodhardt’ describes an ulcer of the stomach, which proved fatal, from hemorrhage in an infant at birth. The situation of these ulcers, according to Brinton, is as follows: In 43 per cent, the posterior surface ; in 27, the lesser curvature ; in 16, the pyloric extremity ; in 6, both the anterior and posterior sur- faces ; in 5, the anterior surface only ; in 2, the greater curvature ; in 2, the cardiac pouch. Thus about 86 ulcers in every 100 occupy the posterior surface, the lesser curvature, and the pyloric sac. The analysis of 793 hospital cases by Welch shows that the ulcers 1“Das chron. Magengesch., ” 1883. 2 Trans. Lond, Path. Soc., 1880, p. 110. Ibid., 1881, p. 79. Digitized by Microsoft® dd2 THE ALIMENTARY CANAL. were on the lesser curvature in 288, in the posterior wall in 235, at the pylorus in 95, on the anterior wall in 69, at the cardia in 50, at the fundus in 29, on greater curvature in 27. As regards the number of ulcers, two or more are present in about twenty one per cent; there may be two, three, four, or even five ulcers. In cases of multiple ulcers the ulcers are often developed successively. In size the ulcers vary from one-quarter of an inch to five or six inches. They are usually of circular shape, sometimes oval; sometimes two or more are fused together. The perforation is largest in the mucous membrane. It may re- main confined to this, cr extend outward and involve the connective tissue, muscular and peritoneal coats, its diameter becoming smaller as it advances. The ulcer looks like a clean hole punched out of the wall of the stomach. Its floor shows no active inflammatory changes. Its edges may be in the same condition, or they may be thickened by the growth of connective tissue and cells. The rest of the mucous membrane of the stomach is apt to be ina condition of chronic ca- tarrhal inflammation. The ulcer may perforate directly through the wall of the stomach, and the contents of the latter are discharged into the peritoneal cav- ity ; or adhesions are formed between the wall of the stomach and the neighboring viscera, so that the bottom of the ulcer is closed ; or if the liver, the intestines, or the abdominal wall become adherent, they may be invaded by the ulcerative process, and cavities or fistu- le are formed communicating with the stomach ; or, if the adhe- sions are incomplete, a local peritonitis and collections of pus may be developed. During the progress of the ulcer there may be repeated small hemorrhages from the erosion of small blood vessels, or large hem- orrhages from the erosion of large arteries. In many cases these ulcers cicatrize, and such a cicatrization may produce various deformities of the stomach. It is very difficult to understand how these ulcers are produced. It seems probable that the nutrition of a circumscribed part of the wall of the stomach is interfered with, and that this portion is then destroyed by the action of the gastric juice. But we are still igno- rant of the way in which the obliteration of the arteries is effected. It has, indeed, been demonstrated in animals that an artificial em- bolism of the branches of the gastric arteries will produce ulcers of the stomach ; and in the human stomach we occasionally meet with cases of embolism of the branches of the gastric artery and ulcers. But the clinical history of most cases of ulcer of the stomach will Digitized by Microsoft® THE ALIMENTARY CANAL. 553 not correspond with such a method of causation. A chronic oblite- rating endarteritis would seem to be a more probable cause. Hemorrhagic Erosions occur as rounded spots or narrow streaks, formed by a loss of substance of the mucous membrane. The mucous membrane at these points is congested, soft, and cov- ered by small blood clots. The destruction of the mucous mem- brane is usually superficial, but may involve its entire thickness. The number of these erosions may be so great that the entire inter- nal surface of the stomach is studded with them. They give rise to repeated hemorrhages, and are accompanied by catarrhal inflamma- tion of the rest of the mucous membrane. They occur at all periods of life, even in infants. Their usual seat is the pyloric portion of the stomach. Fic. 270.—SuPerFiciaL Necrosis oF THE Mucous MEMBRANE OF THE STOMACH—CBILD. They may be idiopathic. Usually, however, they occur in con- nection with some serious general disease. Follicular Ulcers somewhat resembling the ulcers of the small intestine are occasionally met with. They are produced by changes in the aggregations of lymphatic tissue which are situated about the blind ends of the gastric tubules. I have seen in the stomach of a child numerous small ulcers formed by a superficial necrosis of the glandular coat. There were similar ulcers in the colon. There was no clinical history (Fig. 270). DILATATION. . Very considerable degrees of dilatation of the stomach are found at autopsies, without stenosis of the pylorus or any other mechanical cause tu account for them. It is usually difficult to determine how Jong these dilatations have existed and how much effect they have in causing death. Nine such cases are recorded by Goodhardt.’ Acute Dilatation of the stomach, with vomiting of very large 1Trans. Lond. Path. Soc., 1883, p. 88. Digitized by Microsoft® 554 THE ALIMENTARY CANAL. quantities of thin fluid, has been observed in a few cases.’ It is a very curious condition, the dilatation of the stomach being developed suddenly and without discoverable cause. Of the mechanical causes which produce.dilatation of the stomach, a stenosis of the pylorus is the most common. Such a stenosis may be effected by a tumor, by chronic inflammation and thickening, and by the cicatrization of ulcers. Less frequently obstructions of the small and large intestines act in the same way. Some forms of chronic gastritis are attended with dilatation of the stomach without stenosis. Fic. 271.—FIBRoMa IN THE WALL OF THE STOMACH OF A CHILD, There were several of these small tumors in the wall of the stomach. In rare cases circumscribed, sacculated dilatations are produced by the presence of foreign bodies—portion of wood, metal, etc. TUMORS. Paptlloma.—It has already been mentioned that in some cases of chronic gastritis there are small, polypoid hypertrophies of the mucous membrane. Besides these we find polypoid tumors which may reach a considerable size. They are composed of a connective- * tissue stroma arranged so as to form tufts covered with cylindrical epithelium. In some cases there are also tubules lined with cylin- drical epithelium, so that the tumor has partly the structure of an adenoma. Fbromata of small size are sometimes found in the con- 1Tbid., vol. iv. and vol. xxxiv., p. 82. Hughes Bennett, “Practice of Medicine.” Fagge, Guy’s Hospital Reports, vol. xviii., p. 1. Andral, Clinique Médicale. Digitized by Microsoft® THE ALIMENTARY CANAL. 555: nective-tissue coat. Lipomata are formed in the submucous con- nective tissue in the shape of rounded or polypoid tumors. They usually project inward, but sometimes outward beneath the perito- neum. They may also appear in the form of numerous yellow nod- ules beneath the mucous membrane. Myomata occur in the form of rounded tumors which originate in the muscular coat, but may gradually separate themselves from it and project inward or outward. The submucous myomata are at first small tumors lying loosely attached in the submucous tissue. As they grow larger they push the mucous membrane inward and take the shape of polypoid tumors. Lymphomata in the wall of the stomach are seen in some cases of leuksemia. Sarcomata are said to occur in the wall of the stomach in rare in- stances. It must be admitted that in some of the tumors of the wall of the stomach, which are ordinarily called cancerous, the structure .is not well defined, and it is possible that some of them are sarco- mata. A myo-sarcoma growing outward from the greater curvature of the stomach is described by Brodowski.’ The tumor weighed twelve pounds. It was composed largely of smooth muscle cells. There was a secondary tumor in the liver. Adenoma.—It has been already mentioned that in some of the papillary tumors of the mucous membrane there is a considerable growth of tubules lined with cylindrical epithelium. Besides these we find in the submucous coat circumscribed tumors composed of tubules like those of the gastric mucous membrane. Small tumors resembling the pancreas have also been seen in the submucous and subserous coats. Carcinoma of the stomach is almost always primary. But very few secondary cases have been recorded.’ Primary carcinoma of the stomach is of the colloid variety, or common cancer, or cancer with cylindrical epithelial cells, or it is pig- mented. Colloid cancer is composed of a connective-tissue stroma, arranged so as to form cavities of different sizes, which contain colloid matter and polygonal cells. It infiltrates first the submucous connective tissue and then extends inward and outward. In this way there is formed a diffuse thickening of the pyloric end of the stomach rather than a circumscribed tumor. Sometimes the whole of the wall of the stomach is changed in this way. Secondary tumors are usually situat- ed in the peritoneum. 1Virch. Arch., Bd. lxvii., p. 227. *Tbid., Bd. xxxviii. and Ixxxvi., p. 159. Trans. Path. Soc., J.ondon, 1876, p. 264. Digitized by Microsoft® 556 THE ALIMENTARY CANAL. Carcinoma with cylindrical epithelial cells. These tumors are formed of a connective-tissue stroma, which may contain numerous round cells, and of tubules lined with cylindrical epithelium like that of the mucous membrane of the stomach. In these tumors the new growth seems to begin in the gastric tubules. As the arrangement of the tubules is more or less regular, these tumors may be called adenomata or carcinomata, (see Fig. 147). Common cancer is formed of a connective-tissue stroma enclosing rounded and tubular spaces filled with small, polygonal, nucleated cells. In some cases this structure is well marked. In others the stroma is abundant and filled with round cells, the spaces are very small, and the epithelial cells few ; it may then be difficult to distin- guish between inflammatory thickening, sarcoma, and carcinoma. . Both these forms of carcinoma, common cancer and cancer with cylindrical cells, run the same course as regards their gross appear- ance, their situation, and their development of metastatic tumors. About sixty per cent of these tumors are situated at the pyloric end of the stomach, on the lesser curvature or on the posterior wall. The cardiac end of the stomach, the greater curvature, or nearly the entire wall of the stomach may also be the seats of the new growth, but not as frequently. The new growth usually follows one or other of three types. 1. There is a circumscribed, flat tumor formed in the deeper layers of the mucous membrane and pushing this membrane inward. After a time the mucous membrane over the centre of the tumor dies, the destructive process involves the tumor also, and so an ulcer with thickened edges is formed. In some cases the new growth ex- tends laterally and outward, while the central destruction still con- tinues ; then the ulcers reach a large size, their walls and floor are thick, and peritoneal adhesions are formed over them. In other cases the ulcer perforates completely through the wall of the stomach, un- less the opening is closed by adhesions to the neighboring viscera. 2. Large rounded tumors are formed, often several inches in dia- meter, which project into the cavity of the stomach. 3. There is a diffuse, flat infiltration of the deep layers of the mu- cous coat, of the connective-tissue coat, and sometimes of the muscu- lar coat, which does not ulcerate and hardly forms a tumor. This infiltration may be confined to the pyloric end of the stomach, or may involve nearly the whole of its wall. There is in most of the cases a good deal of chronic catarrhal in- flammation of the mucous membrane. If the pylorus is obstructed the stomach is often dilated. The new growth may extend from the stomach to the cesophagus, but it very seldom involves the duodenum. Digitized by Microsoft® THE ALIMENTARY CANAL. B57 Metastatic tumors are very common. The liver, the lymphatic glands, and the peritoneum are the parts most frequently affected, but such metastases have been seen in nearly every part of the body. DEGENERATIONS., Calcification of the mucous membrane of the stomach some- times occurs as a metastatic process in connection with extensive diseases of the bones. Waxy Degeneration sometimes involves the blood vessels of the mucous membrane. FOREIGN BODIES. Among the various foreign bodies which by accident or design may be present in the stomach may be mentioned hairs, thread, string, etc., which having been swallowed from time to time, usually by hysterical women. These may be closely packed together into a large mass nearly filling the cavity of the stomach, to which in shape it may correspond. Such a specimen of gastric hair ball, men- tioned by Osler, is in the museum of McGill University, and another, reported by Findler, isin the museum of the College of Physicians and Surgeons, New York. THE INTESTINES. MALFORMATIONS. Diverticula of the intestines occur in several different ways : 1. The abdominal walls are cleft asunder at the navel. The ileum opens through this cleft by a narrow aperture in its wall. The lower portions of the ileum and the colon are small or entirely closed. 2. There is an opening in the abdominal wall as before, but there is not a direct opening into the ileum. There is along diverticulum of the ileum, with an open end projecting into the opening in the ab- dominal wall. 3. The abdominal wall is closed. There is a diverticulum of the ileum, connected with the navel by a solid cord. 4, There is an unattached diverticulum of the intestine. This is much the most common form. The diverticula occur only in the lower part of the ileum. They usually spring from the convex sur- face of the intestine, more rarely from its attached border. In the latter case they are joined to the mesentery by a fold of peritoneum. The diverticulum forms a pouch, one to six inches long, of about the same diameter as the intestine, smallest at its free extremity. Such diverticula do not interfere with the functions of the intes- tines. They sometimes form. pant ofja,yhermia, Sometimes the remains 558 THE ALIMENTARY CANAL. of these intestinal diverticula—called Meckel’s diverticula—form soft, projecting tumors at the umbilicusin children. Microscopical exam- ination of such tumors often shows the structure of the intestinal mucosa and muscularis. If they remain attached by a fibrous cord to the navel, this cord may be the cause of incarceration of a portion of the intestines.! Cloacee consist in the union of the rectum, bladder, and organs of generation in a common outlet. 1. Simple Cloace are : (a) Complete, and consist in the common opening of the urethra or ureters, the vagina, and the rectum into the closed bladder, or into a sinus opening outward which represents either the vagina or the rectum. (6) Incomplete. Therectum opens into the vagina, the bladder, or the urethra, while the lower part of the rectum is closed or absent. 2. Cloace combined with Cleft Bladder.—(a) The simple cleav- age of the intestines is combined with cleft bladder. The anterior abdominal wall from the umbilicus to the symphysis, the symphysis, and the anterior wall of the bladder are absent ; the gap is filled with a membrane which represents the posterior wall of the bladder. On to this membrane open the ileum, ureters, and vagina. (6) Theintes- tine is perfectly formed, but the rectum opens into a common sinus with the ureters and vagina; or the ureters open into the cleft blad- der, and the rectum and external genitals are united ; or the ureters open into the rectum, and the latter terminates normally. 3. Cloace combined with Abdominal Hernia.—There is a her- nial sac containing all the abdominal viscera. At the lower end of the sac is an opening leading into a sinus in which open the lower end of the ileum, the bladder or urethra, and the ureters. The rec- tum is absent. Atresia Ant consists in a deficient development of the colon or rectum. The entire colon may be absent ; the rectum may be absent, or represented by a solid cord ; or the upper or lower part of the colon may be absent, or separated by a solid cord. More rarely blind terminations of the small intestines are found, and sometimes a narrowing so complete as to close the canal. The intestines are also found abnormally shortened in various de- grees. A colon of unusually large size has been described as of occasional occurrence.’ INCARCERATION. 1. The most common form is that in which a portion of intestine is strangulated by a fibrous band. Such fibrous bands are produced t so false Te, diverticula, see p. 577. * Formad, University. Medical, Magazine, June, 1892. Bigiized by iCrOSOR® THE ALIMENTARY CANAL. 559 by peritonitis or the remains of foetal growth. They pass from the intestines to the abdominal wall, or from one part of the intestines to another. The intestine becomes in some way caught under one of these bands and is compressed by it. The stricture thus produced may cause a gradual accumulation of feeces in the intestine above it, and may last for along time before death ensues. In other cases the stricture interferes at once with the circulation of the blood ; the in- testine is intensely congested, becomes gangrenous, and death takes place with the symptoms of general peritonitis. 2. A portion of intestine becomes caught in some abnormal open- ing in the mesentery or omentum, or in the foramen of Winslow, or between the two layers of the mesentery. We have seen a case in which twelve feet of intestine had passed through a small opening in the mesentery. 3. A coil of intestine makes half a turn at its base, so that the two sides of the loops cross at its base. In this way the lumen of the intestine is completely closed and the vessels are compressed, so that congestion, peritonitis, and gangrene result. This form of in- carceration is most frequent in the ascending colon. In the small intestine it only occurs when the gut is fixed by old adhesions. 4. A portion of the intestine, with its mesentery, makes one or more complete turns on itself, closing the canal and compressing the vessels. 5. A portion of the intestine makes a half or entire turn about its longer axis. This is very rare, and only occurs in the colon. 6. The mesentery of a part of the intestine is long and loose, in ‘consequence of a dragging down of the intestine by a hernia or by habitual constipation. The portion of intestine thus permitted to hang down is habitually filled with feces, and by its pressure on some other part of the mtestine produces an incomplete stricture. INTUSSUSCEPTION. This change of position consists in the invagination of one por- tion of intestine in another portion. Usually this takes place in the direction of the peristaltic movements, from above downward ; more rarely in the opposite direction. The parts are found in the following condition: There are three portions of intestine, one within the other. The inner portion is continuous with the intestines above the intussusception ; its peritoneal coat faces outward. The outer portion is continuous with the intes- tine below ; its peritoneal coat also faces outward. The inner portion is turned inside out, its mucous membrane is in contact with the mucous membrane of the outer portion. In rare cases the intus- susception is complicated by the invagination of a second portion of Digitized by Microsoft® 560 THE ALIMENTARY CANAL. intestine in the inner tube, and even by a third intussusception into the second one. These changes occur both in the large and small intestine ; most frequently the lower part of the ileum is invagi- nated in the colon. The invaginated portion may be from a few inches to several feet in length. The lesion is most frequently found in early childhood. The intussusception, by the dragging and folding of the mesen- tery which it produces, causes an intense congestion of the parts, and even large hemorrhages between the coats of the intestine. The congestion may induce fatal peritonitis, or gangrene of the intestine, or chronic inflammation and adhesions, and the patient lives for a considerable time with symptoms of stricture. In other cases the invaginated portion of intestine sloughs, the outer and inner portions become adherent, and the patient recovers, with or without some de- gree of stricture. Besides this grave form of intussusception we often find, es- pecially in children, one or more small invaginations not attended with congestion or inflammation. These are formed during the death agony or immediately after death. TRANSPOSITION. The position of the intestines may be the opposite to that which is usually found. The transposition may affect all the abdominal viscera, or only a single viscus is transposed. WOUNDS—RUPTURES. Penetrating wounds of the intestine usually prove rapidly fatal, either from shock or from peritonitis. Sometimes, however, the wound becomes closed by the formation of adhesions with the neighboring parts. Sometimes the wound in the intestines becomes adherent at the position of the wound in the abdominal wall, and an intestinal fistula is formed. Rupture of the small intestine is not infrequently produced by se- vere blows on the anterior abdominal wall. It is noticeable that such blows may not produce any marks or ecchymoses of the skin. Such ruptures usually prove fatal very soon, but sometimes the patient lives several days and the edges of the rupture undergo inflamma- tory changes. Strictures of the intestine are sometimes followed by rupture of the dilated intestine at some point above the stricture. Digitized by Microsoft® THE ALIMENTARY CANAL. 561 THE SMALL INTESTINE. INFLAMMATION, Acute Catarrhal Inflammation of the greater part of the small intestine is developed as part of the lesion of cholera morbus, and after the ingestion of irritant poisons. Acute inflammation of the duodenum accompanies gastritis, and occurs as an idiopathic condition. Acute inflammation of the ileum occurs as an idiopathic condi- tion, and accompanies inflammation of the colon and of the solitary and agminated lymph nodules. In many of these cases we infer the existence of the inflamma- tion from the clinical symptoms. After death the most marked lesions are the increased produc- tion of mucus and the congestion. In very severe cases the inflam- mation may extend to the peritoneal coat. Chronic Catarrhal Inflammation of the small intestine accom- panies heart disease, phthisis, emphysema, cirrhosis of the liver, and Bright’s disease. The intestine is coated with an increased amount of mucus; it is often congested ; there may be a general thickening of all its coats. Croupous Inflammation is produced by irritant poisons; it is associated with croupous colitis, and it occurs as an idiopathic disease. The mucous membrane is coated with fibrin, its stroma is infiltrated with fibrin and pus, and this infiltration extends to the connective tissue, muscular and peritoneal coats. Suppurative Inflammation of the submucous connective-tissue coat is said to occur in rare cases. It is usually metastatic. It takes the form of purulent foci of variable extent, which perforate either inward or outward. THE SOLITARY AND AGMINATED GLANDS (LYMPH NODULES). It is not uncommon to find in healthy adults who have died from accidental causes a considerable swelling of the solitary and agmi- nated glands (lymph nodules) of the ileum, without any reason which we can discover to account for this swelling. Extensive burns of the skin may be followed by a very marked swelling of the solitary and agminated nodules. In persons who have died from the infectious diseases it is not uncommon to find these nodules swollen. In children, swelling of these nodules, often followed by softening and the formation of ulcers, accompanies many of the catarrhal in- flammations of the large and small intestines. a Digitized by Microsoft® 562 THE ALIMENTARY CANAL, In pulmonary phthisis we very frequently find changes in the solitary and agminated nodules of the small intestine, less frequently in the solitary nodules of the colon. The changes seem to be of the same character as those which take place in tubercular inflammation of lymphatic nodules in other parts of the body. The nodules become swollen, their elements are multiplied, tuber- cle granula are formed, the central portions of the nodules become cheesy. The cheesy degeneration extends ; it is followed by soften- ing and by death of the mucous membrane over the nodules ; the softened tissue is discharged into the intestine, and ulcers are formed with overhanging edges. After this the ulcer shows no tendency to heal, but, on the contrary, becomes larger, usually extending late- rally so as sometimes to nearly encircle the gut. After death we find, in different patients, these ulcers in all their stages of develop- ment. They vary much as to the proportion between the tubercular and the ordinary inflammatory changes. In some the tubercle granula are numerous, in others they are few or even absent alto- gether. The tubercle bacilli are very constantly found in them. There is also usually a tubercular inflammation of the peritoneum over the ulcers, and sometimes of the lymphatics and nodes of the mesentery. Although these ulcers often reach a large size, it is but very seldom that they perforate into the peritoneal cavity. Ulcers of the Duodenum.—A. few cases have been recorded in which extensive burns of the skin have been followed within a few days by the formation of deep ulcers of the duodenum. It is still uncertain how these ulcers are produced. Chronic perforating ulcers, resembling the chronic ulcers of the stomach, are found in the duodenum. They are associated with similar ulcers in the stomach or occur by themselves. Some curious ulcers of the upper part of the small intestines are described by Israel.’ There were five ulcers, from two and one-half to ten centimetres long, encircling the intestine, with irregular, granulating surfaces. Syphilitic ulcers produced by changes in the solitary and agmi- nated glands of the small intestine are sometimes found in infants. EMBOLI. Emboli have been found in the superior mesenteric artery in a number of cases ; in the inferior mesenteric artery they are less fre- quent. They produce an intense venous congestion of the entire wall of the intestine, with hemorrhage into its cavity and its wall. 1 Charité-Annalen, 1884, p. 707. Digitized by Microsoft® THE ALIMENTARY CANAL. 563 THE LARGE INTESTINE. INFLAMMATION, The mucous membrane of the large intestine is very frequently the seat of acute and chronic inflammatory processes. The larger number of these belong to the condition which is described clinically under the name of dysentery. The inflammation affects most fre- Fic. 272.—AcuTe CATARRHAL COLITIS. With mucus on the surface of the mucous membrane, distending the tubules and filling some of the cells (beaker cells). quently the rectum, sometimes the entire length of the colon, some- times only the upper part of the colon. Acute Catarrhal Colitis.—The lower end of the colon is the por- tion most frequently involved in this form of inflammation, but it may be its upper end or the entire length of the gut. The name ca- Digitized by Microsoft® 564 THE ALIMENTARY CANAL. tarrhal colitis is the only term used at the present time to designate three morbid conditions of the colon, which differ from each other both in their anatomical and clinical features. 1. The inflammation is of simple exudative type. It is usually confined to the lower end of the colon, runs its course within a week, and is not fatal. The glandular and connective-tissue coats of the colon are swollen and congested, with more or less infiltration with Fig. 273.—SuPPURATIVE COLITIS. The inflammation is confined to the connective-tissue coat, causing destruction of large por- tions of this coat, thus undermining the glandular coat. The photograph is from a vertical section through the whole wall of the colon, and shows a separation of the glandular from the vascular coat. serum and pus cells. There is an increased production of mucus (Fig. 272) which coats the surface of the colon and comes away with the stools in the form of membranes or cord-like shreds." There may be bleeding from the surface of the inflamed mucous membrane. 1 Numerous observations have been made and a large bibliography has been gathered on what is called membranous enteritis or colitis, for which the reader may consult Butler, New York Medical Journal, December 28th, 1895, or Akerlund, Arch. f. Verdauungs Krankheiten, Bd. i., p. 396, 1896. Digitized by Microsoft® THE ALIMENTARY CANAL. 565 2. The inflammation is of exudative type, but with an excessive production of pus cells. It may involve any part of, or the entire Fie. 274,—CaTARRHAL CouirTIs. Showing swollen lymph nodule. Fig. 275.—CATARRHAL COLITIS, PRODUCTIVE AND NECROTIC. length of, the colon. It may cause death within a few days or con-. tinue for several weeks it zd Ph Msn is swollen and con- 566 THE ALIMENTARY CANAL. gested. The stroma between the tubules, the connective-tissue coat, and sometimes the muscular and peritoneal coat are infiltrated with large numbers of pus cells (Fig. 273). The solitary nodules may be swollen (Fig. 274). There is an increased production of mucus. 3. The inflammation is of the productive type with exudation. It may involve any part, or the entire length, of the colon. It may cause death within a few days, or continue for several weeks, or be Fig. 276.—Crovpovus Couiris. False membrane in patches. followed by chronic colitis. The wall of the colon is swollen and congested. There is an increased production of mucus. There is a growth of new connective tissue with an excess of cells, confined to the stroma between the tubules or also involving the connective- tissue coat. 4. There may bealso a considerable production of pus cells, which are found adherent to the surface of the mucous membrane and infil- trating the glandular and connective-tissue coats. In addition we Digitized by Microsoft® THE ALIMENTARY CANAL. 567 find numerous small ulcers in the glandular coat. The ulcers are often so small that they cannot be seen with the naked eye. They seem to be formed by necrosis of small areas of the glandular coat (Fig. 275). Croupous Colitis.—This form of inflammation may involve the rectum alone, or the entire length of the colon, or only its upper por- tion. The mucous membrane is congested and swollen, and coated — TE. IE pra Fia. 277.—FoLiicuLtarR (NoDpULAR) COLITIs. with a layer of false membrane ; the connective tissue between and beneath the glandular tubules is infiltrated with fibrin and pus, and in severe cases the inflammation involves the muscular and peri- toneal coats also. The inflammation is usually more intense at some places than at others, so that the surface of the mucous membrane shows the false membrane in isolated patches (Fig. 276). Less fre- quently there is a uniform coating with the false membrane. In mild cases, as the inflammation subsides, the products of inflammation are Digitized by Microsoft® 568 THE ALIMENTARY CANAL. absorbed and the wall of the intestine returns to its normal condition In more severe cases the quantity of the inflammatory products is so great that portions of the wall of the intestine become necrotic. This necrosis may involve only the glandular coat, or it may extend deeper into the wall of the intestine. The necrosed tissue after a time sloughs away, leaving behind ulcers of different sizes and depths. After this the ulcers may cicatrize, or their floors and walls may remain in the condition of granulation tissue for an indefinite length of time. When Fie. 278.—AM@BIC COLITIS. Connective-tissue coat of the intestine infiltrated with new cells and with amcebee. The larger spherical structures in the section are sections of blood vessels; the smaller darker nuclei belonging to the new-formed tissue cells; the spheroidal nucleated structures of intermediate size are the amoebee. the latter is the case there is added a chronic inflammation of the wall of the intestine between the ulcers, with changes in the mucous membrane and thickening of the connective-tissue and muscular coats. Follicular Colitis (Nodular Colitis). —In many cases of catarrhal and croupous inflammation of the colon the solitary follicles (lymph Digitized by Microsoft® THE ALIMENTARY CANAL. 569 nodules) become more or less swollen and necrotic. Besides these cases, however, there are others in which the changes in the nodules form the principal part of the lesion, while the catarrhal or croupous inflammation is but slightly developed. The nodules are first swollen, then necrotic, then slough away and leave little circular ulcers with overhanging edges (Fig. 277). These ulcers are usually numerous and extend over a large part of the colon. The patients have diarrhceal rather than dysenteric passages. The ulcers are apt Fig. 279.—Ameasric CoLiris. Showing amcebze in connective tissue. Magnified 1,000 diameters and reduced. to show but little disposition to heal, and the acute colitis often be- comes chronic. It seems probable that some of the cases which look like follicular colitis are really examples of amcebic colitis. ' Ameebic Colitis.—This form of colitis is caused by the presence in the wall of the intestine of amcebee. These organisms were first recognized by Lambl in 1859. Since then they have been described by a number of observers, most fully by Kartulis and by Councilman (see page 128). Digitized by Microsoft® 570 THE ALIMENTARY CANAL. The amcebex are found in the little, gelatinous masses which are found in the stools. They are of rounded shape, and, when alive, change their position and shoot out and retract little projections (pseudopodia). Their outer portion is composed of a pale hyalin or homogeneous substance; the inner contains vacuoles and is more refractive (see Fig. 30). In the colon the amcebee are found in the connective-tissue coat and in the floors of the ulcers (Figs. 278 and 279). The principal Fia, 280.—Ama@sio CoLitis—twelve days’ duration. A deep ulcer with overhanging edges formed by circumscribed necrosis. effect of the presence of the amceba seems to be to cause the death of tissue. The addition of inflammatory changes seems to depend upon an additional infection with streptococci, or other micro-organisms. As an ameebic colitis may last for many months and as the same pa- tient may have a number of attacks, by the time of death the changes in the colon are very considerable. The cases which have come under our observation have followed one of these anatomical types. (a) There is a diffuse inflammation of exudative and productive Digitized by Microsoft® THE ALIMENTARY CANAL. 571 type which involves a considerable part of the colon. The cnanges. are confined to the glandular and connective-tissue coats. In the glandular coat there is a growth of new connective tissue and an infiltration of pus cells between the tubules. In the connective-tissue coat we find new connective-tissue cells, pus cells, and amcebe. The ulcers are superficial and involve only the glandular coat. We find also in many places portions of the glandular coat which are necrotic, but have not sloughed away. (6) There are foci of circumscribed exudation and necrosis scat- Fig. 281.—Ama@sic Couitts. Showing diffuse necrosis of glandular coat. tered through the colon. These foci begin in the connective-tissue coat, but may be so large as to involve all the other coats of the colon. The exudation forms a sort of nodule which soon becomes necrotic and sloughs away, leaving a deep ulcer with overhanging edges (Fig. 280). The amcebe are found in the walls and floors of the ulcers. The glandular coat between the ulcers shows various changes due to catarrhal and productive inflammation. (c) Considerable areas of the glandular, connective-tissue, and muscular coats are necrotic. The dead tissue is found still in place, or has sloughed away, leaving very large and deep ulcers (Fig. 281). Digitized by Microsoft® 572 THE ALIMENTARY CANAL. In some cases of amoebic colitis necrotic and inflammatory changes of the same character are found in the liver and in the right lung. Necrotic Colitis.—There is a form of inflammation of the colon in which considerable areas of the connective-tissue coat become necrotic, leaving the glandular coat undermined and separated from the muscular coat. In this way large ulcers with overhanging edges are formed. ‘This form of colitis is very fatal. There is another very fatal and obscure form of necrotic colitis in which the symptoms are rather of septic poisoning than of inflam- Fig. 282.—NEcRoTIC CoLiris. Circumscribed congestion and necrosis of the glandular and connective-tissue coats. mation of the colon. After death the inner surface of the colon is found studded with little blackish swellings. In these swellings the blood vessels are gorged with blood. The glandular and connective- tissue coats are infiltrated with pus cells and there is a superficial necrosis (Fig. 282). Various forms of micro-organisms have been found in connection with suppurative and necrotic lesions of the colon: Streptococcus pyogenes, Staphylococcus pyogenes, Bacillus coli communis, Ba- cillus proteus, Bacillus pyogenes, and others. Digitized by Microsoft® THE ALIMENTARY CANAL. 573 The exact significance of these germs is yet obscure.’ Chronic Colitis.—If a chronic inflammation of the colon has continued for any length of time, the wall of the gut is found to be very much changed. The glandular coat may be uniformly thick- ened, or thrown into the form of polypoid tumors, or atrophied, or destroyed by ulcers of various sizes and shapes. The connective- tissue and muscular coats may be thickened or thinned. Apparently chronic colitis may follow any of the forms of acute colitis. The Ceecum.—Catarrhal inflammation of the caecum is not un- common. It is usually produced by an habitual accumulation of feeces in this part of the intestine. The course of the inflammation is chronic, but marked by acute exacerbations. At first the mucous membrane undergoes the ordinary changes of chronic catarrhal in- flammation; then there is a slow suppurative inflammation which extends through the wall of the intestine and produces ulcers and perforations. Through these perforations the faeces may pass into the peritoneal cavity, or the perforations are partly closed by adhe- sions, and abscesses are formed, or sinuses into the surrounding soft parts. The Rectum.—Besides the inflammatory changes already de- scribed as existing in the colon, we sometimes find a suppurative inflammation of the connective tissue which surrounds the rectum, either associated with lesions of the mucous membrane or occurring by itself. In adults the lower end of the rectum is the part of the intestine which is the most frequent seat of syphilitic ulceration. Most of these ulcers seem to be the result of unnatural coitus, or of infection from specific sores of the vulva; but some of them seem to be due to the softening of gummy tumors. The Vermiform Appendix.—The appendix is given off from the inner and posterior aspect of the lower end of the caput coli. It is from two to six inches in length. It may be turned upward behind the caecum, or it may hang downward free in the peritoneal cavity. It is composed of peritoneal, muscular, connective-tissue, and glan- dular coats. 1. The mucous membrane may be the seat of acute catarrhal in- flammation. This is of mild type and short duration, with conges- tion, swelling, and an increased production of mucus; or it is of severer type, of longer duration, and the cavity of the appendix is distended by large quantities of mucus and pus. 2. The entire thickness of the wall of the appendix may be the seat of an acute exudative inflammation. The appendix is very 1See Kruse and Pasguale, Zeits. f. Hygiene und Infkr., Bd. xvi., p. 1, 1894; also Oérenville, Tavel, and others, Ann. Suisses des Sc. Méd., sér. ii., p. 581, 1895, Digitized by Microsoft® 574 THE ALIMENTARY CANAL. much increased in size, sometimes to the size of a man’s finger. This « increase in size is due, not to a dilatation of the cavity of the appen- dix, but to a thickening of its walls. The walls are congested, swollen, infiltrated with fibrin and pus, the peritoneal coat covered with fibrin. There is no necrosis and no perforations. If the appen- dix is behind the caecum, or if adhesions are formed early, there is only a localized peritonitis. If the appendix projects freely into the peritoneal cavity and no adhesions are formed, a general peritonitis is soon established. Fic. 283,—AcUTE SUPPURATIVE APPENDICITIS. Appendix removed by operation twelve hours after first symptoms. Streptococcus was found in the exudate. (Specimen prepared by Dr. Van Gieson.) 1, Mucous membrane of the appendix; 2, lymphatic nodules in the mucous membrane; 3, submucosa; 4. muscularis; 5, mesentery of the appendix; 6, pus and fibrin covering the appendix; 7, dense infiltration of the wall of the appendix with pus. 3. At one or more points in the wall of the appendix there is an exudative inflammation with necrosis. In this way small or large portions of the wall of the appendix are destroyed, large or small perforations are formed, and the contents of the appendix escape into the abdominal cavity. In these cases the appendix usually contains a feecal concretion. Such perforations are regularly followed by the formation of an abscess around the appendix (Fig. 283). The pus may extend from this abscess in any direction and for long distances, so that we find abscesses deep in the pelvic cavity, or under the diaphragm, or at other remote points. Digitized by Microsoft® THE ALIMENTARY CANAL. 575 4, The entire appendix becomes gangrenous within one or two days, with the formation of an abscess, or general peritonitis. This is the most fatal form of appendicitis; its etiology is obscure. 5. In catarrhal or croupous colitis the inflammation may extend to the appendix. 6. In typhoid fever there may be changes in the wall of the ap- pendix of a character similar to those in the wall of the small intes- tine. 7%. There may be a tuberculous inflammation of the appendix, with the formation of ulcers. As the result of chronic inflammation in the appendix strictures or obliteration of the lumen of the appendix may occur. The lumen of the appendix frequently contains concretions of faecal material which have often been mistaken for foreign bodies. For- eign bodies, such as grape and apple seeds, and various small objects which have been swallowed, sometimes, though rarely, find their way into the appendix. Both the fecal concretions and the foreign bodies may act as important predisposing agents of inflammation and per- foration of the appendix, through pressure, erosion, etc., of the mucous membrane, affording portals of entry to various forms of ‘pathogenic micro-organisms. The Streptococcus pyogenes, Staphylococcus pyogenes, the Ba- cillus coli communis, and Bacillus proteus are the bacteria most commonly found associated with the lesions of acute appendicitis and its accompanying peritonitis.’ TUMORS. Myomata.—Tumors composed of smooth muscle and connective ‘tissue grow in the muscular coat and project inward. They may be large enough to obstruct the intestine, and may then give rise to ‘intussusception. In the duodenum such tumors may obstruct the ‘common bile duct. Less frequently these tumors project outward into the peritoneal cavity. Lipomata may be developed from the submucous coat and grow ‘inward, or from the subserous coat and project outward into the peri- toneal cavity. Polypoid Tumors, projecting into the cavity of the intestine and composed of connective tissue and covered with epithelium, are fre- -quently found. They are associated with catarrhal inflammation or 1 Hodenpyl, ‘Etiology of Appendicitis,” New York Medical Journal, December 30th, 1893. Consult also, Kelynack, “The Pathology of the Vermiform Appendix, * 1893. Berry, Jour. of Path. and Bact., vol. iii., p. 160, 1895 (bibliography). _Ribbert, Virch. Arch., Bd. cxxxii., p. 66. Digitized by Microsoft® 576 THE ALIMENTARY CANAL. occur by themselves. They are found throughout the intestinal tract and may be single or multiple. They grow from the submucous coat and project inward. Some of them are small, solid, connective-tissue tumors, covered by the mucous membrane which they have pushed inward. Others are of the same character, but of large size. In others the connective tissue is arranged in branching tufts, covered with cylindrical epithelium; and in these last tumors there may also be tubules lined with cylindrical epithelium, giving to the growth the characters of an adenoma. Adenomata are found in the duodenum and colon. They form flat infiltrations of the wall of the intestine, or project inward as poly- poid tumors. They are composed of tubular follicles, like those of the intestinal mucous membrane, and of a connective-tissue stroma. In some of these tumors the tubules have a tolerably regular shape and arrangement; there is no infiltration of surrounding tissue; the tumor is of benign nature. In other tumors the tubules are irregular in shape and arrangement, and the growth infiltrates the surrounding parts. There is no sharp dividing line between these tumors and the carcinomata. Carcinomata are found in the colon and the duodenum, and are of three varieties. 1. The new growth is composed of tubules lined with cylindrical epithelium. It begins asa flat infiltration of the submucous coat, which soon surrounds the intestine, infiltrates the whole thickness of the wall of the gut, and may extend to the surrounding soft parts. Fungous masses project into the cavity of the intestine, while at the same time ulcerative and destructive processes are going on. Ac- cording to the exact arrangement of the growth, there is more or less stenosis of the intestine. 2. The growth has the characters of colloid cancer and forms a diffuse infiltration of the intestinal wall, completely surrounding it and often extending over a length of several inches. 3. In the rectum there is sometimes a carcinomatous growth, with flat epithelial cells (epithelioma), like similar growths in the skin.’ Lymphoma.—Tumors composed of tissue resembling that of the lymphatic glands originate in the solitary and agminated nodules, and in the intestinal wall in cases of leukemia and pseudo-leukzemia. Similar tumors are found as an idiopathic lesion both in the large and small intestines. These tumors are irregular, diffuse growths infiltrating the wall of the intestine, the mesentery, and the neigh- boring lymph nodules, and reaching a considerable size. They often 1Consult Bohm, Virch. Arch., Bd. cxl., p. 524 (bibliography). Digitized by Microsoft® THE ALIMENTARY CANAL, 577 ulcerate internally and produce dilatation or stenosis of the intes- tine. It is hard to tell whether some of these tumors should be called lymphomata or sarcomata.’ CONCRETIONS (ENTEROLITHS). There are sometimes found in the intestines round, oval, or irreg- ular masses of firm consistence. They are usually small, but may reach the size of a man’s fist. They are composed of fecal matter, mucus, bile, the carbonate and phosphate of lime, and triple phos- phate. They may produce inflammation, ulceration, and perfora- tion. FALSE DIVERTICULA OF THE INTESTINE. Not infrequently one finds at autopsies either in the small or large intestine diverticula or herniz, consisting of the mucous mem- brane which has been crowded through the muscularis and is covered by the serosa, which project from the exterior of the gut usually near its mesenteric attachment. These so-called “false diverticula” may be large, but are usually not larger than a pea; they may be single or numerous. They usually cause no functional disturbance, but may, through the accumulation of feecal material within them, be the seat of perforation.” ANTHRAX INTESTINALIS (MYCOSIS INTESTINALIS). The anthrax bacillus may find lodgment in the intestinal mucous membrane either by the ingestion of food containing the germ or by metastasis through the blood from some other seat of infection, especially the skin. The intestinal lesions are most apt to occur in the small intestines and in the upper part of the colon. The mucous membrane is studded with larger and smaller brown or black frequently elevated patches, or areas of local congestion, or hemorrhage, or necrosis. The mucous membrane near the inflam- matory and necrotic foci may be edematous. Hyperplasia of the spleen and lymph nodes is apt to accompany the intestinal anthrax. The anthrax bacillus may be found about the seat of local lesion in the intestine, in the associated lymph nodes, and when secondary to local infection elsewhere it may be found in the primary lesion and in the blood. It is believed that other forms of bacteria may cause 1For study of congenital tumors of the intestines consult Huetes, Ziegler’s Beitr. z. path. Anat., Bd. xix., p. 391, 1896. 2Consult Edel, Virch. Arch., Bd. cxxxviii., p. 347; also Hanseman, ibid., Bd. exliv., p. 400. 46 Digitized by Microsoft® 578 THE ALIMENTARY CANAL. intestinal lesions somewhat similar to those of anthrax, but the researches in this direction are not yet sufficiently numerous to per- mit of very definite statements. Ascaris lumbricotdes is found in the small intestine, either singly or in considerable numbers. In rare cases a number of worms may form a mass which produces inflammation, ulceration, and perfora- tion. Oxyuris vermicularis is found in large numbers in the rectum. Tricocephalus dispar is found in the ceecum. Ankylostomum duodenale is found in the duodenum and may give rise to considerable hemorrhages. Trichina sptralis is found in its adult condition in the small in- testine. Pentastomum denticulatum occurs in the submucous tissue of the small intestine in an encapsulated condition. Cysticercus cellulose has been seen, in a few cases, on the mu- cous membrane. Tenia solium, Toenia mediocanellata, and Bothriocephalus latus are all found in the small intestine. Very large numbers of various forms of bacteria are regularly found in the intestinal cavity, intermingled with its contents and clinging to its walls. Among the most common of these is the Bacillus coli communis (see page 260). THE PERITONEUM. The free surface of the parietal peritoneum is covered with a single layer of flat, polygonal, nucleated cells. Beneath these cells are succes- sive planes of connective tissue extending down to the muscles and fascie. These planes are formed of a fibrillated basement substance reinforced by elastic fibres, and of branching cells. Embedded in the connective tissue are the nerves, blood vessels, and lymphatics. The lymphatic system is very extensive. The omentum consists of fibrillated connective tissue arranged so as to form a meshwork. The trabecule of the meshwork are com- pletely covered by large, flat cells. In the basement substance, be- neath the endothelium, are branching cells. In the larger trabeculs are blood vessels, lymphatics, and fat. Sometimes we find on the larger trabeculz little nodules formed of polygonal or branched cells. MALFORMATIONS. Arrest of development of the peritoneum occurs in the shape of fissures in the mesial line or external to it; in the case of the dia- phragm being absent, of a fusion with the pleura; and as defective Digitized by Microsoft® THE ALIMENTARY CANAL. 579 development of the mesentery, the omentum, and the other folds of the peritoneum. Excess of development occurs in the shape of unusual length of the mesentery, the omentum, and the other folds of the peritoneum ; or of supernumerary folds and pouches. These are chiefly found in the hypogastric, iliac, and inguinal regions and near the fundus of the bladder. There is access to these sacs by a well-defined fissure or ring, which is frequently surrounded by a tendinous band lying in the duplicature. They may give rise to internal incarceration of the intestines. INFLAMMATION. The very great extent of the peritoneum, and the readiness with which its lymphatic system absorbs foreign matters from the perito- neal cavity, render peritonitis a most severe and dangerous form of inflammation. If the greater part of the peritoneum is inflamed we call the lesion a general peritonitis. If only a circumscribed area is involved it is a local peritonitis. The course of the inflammation may be rapid or slow, so that we speak of acute and chronic inflammation. The inflammation may be attended with the production of tubercle tissue, and then it is a tubereular peritonitis. I. Acute Peritonitis. The acute inflammations of the peritoneum may occur as idio- pathic lesions without discoverable cause ; but much more frequently they are directly due to some appreciable cause. ‘Wounds and contusions of the wall of the abdomen ; wounds, ulcers, new growths, incarcerations, intussusceptions, ruptures, perforations, and inflammations of the stomach and intestines ; inflammation of the vermiform appendix ; injuries, ruptures, and inflammations of the uterus, ovaries, and Fallopian tubes; rupture and inflammation of the bladder ; inflammation of and about the kidneys ; abscesses and hydatid cysts of the liver; inflammation of the gall bladder and large bile ducts ; thrombosis of the portal vein ; inflammations of the spleen, pancreas, lymphatic glands, retroperitoneal connective tissue, vertebre, ribs, and pelvic bones; septicemia and the infectious dis- eases, and chronic Bright’s disease—are all ordinary causes of acute peritonitis. According to the exact cause of the inflammation, the peritonitis is at first either local or general. A local peritonitis may remain cir- cumscribed, or it may spread and become general. We can distinguish two anatomical forms of acute peritonitis. 1. Cellular Peritonitis.—This form of peritonitis may be fro- duced by any irritant Bish S98; t act too,energetically. It can be 580 THE ALIMENTARY CANAL. excited in dogs by injections of very small quantities of a solution of chloride of zinc. In the human subject we find it with perityphlitis, with circumscribed abscesses in the peritoneal cavity, and in cases of puerperal fever which die within forty-eight hours after the devel- opment of symptoms. After death we find the entire peritoneum of a bright-red color from the congestion of the blood vessels ; but there are no fibrin, no gerum, no pus, no other lesions visible to the naked eye. Minute examination, however, shows a very marked change in the endo- Fig. 284.—AcuTE CELLULAR PERITONITIB. Human omentum, x 750 and reduced. thelial cells. They are increased in size and number, and the new cells coat the surface of the peritoneum and project outward in little masses (Fig. 284). 2. Hxudative Peritonitis.—The ordinary form of acute perito- nitis is attended with the production of serum, fibrin, and pus, and with changes in the endothelium and connective-tissue cells. If we inject a solution of chloride of zinc or of some other irri- tant into the peritoneal cavity of a dog, we find that by the end of one or two hours inflammatory changes are evident. There is alit- tle serum in the peritoneal cavity, a general congestion of the peri- Digitized by Microsoft® THE ALIMENTARY CANAL. 581 toneum, and little knobs and threads of fibrin on its surface. There are no marked changes in the endothelium or connective-tissue cells, but pus cells are present.in moderate numbers in the stroma just be- neath the endothelium, and white blood cells in the vessels. After the lapse of twenty-four hours the lesions are more marked. The congestion of the peritoneum is much more decided, there is more serum in its cavity and a thicker layer of fibrin and pus on its surface. Minute examination shows that two distinct sets of chan- ges are going on at the same time : (1) a production of fibrin, se- rum, and pus ; (2) a swelling and multiplication of the endothelial cells. Ifthe inflammation is very intense the pus and fibrin are most abundant ; if the inflammation is milder the changes in the endothelium are more marked. The fibrin coagulates on the free surface of the peritoneum. The white blood cells collect in large numbers in the blood vessels, and as pus cells infiltrate the stroma and collect on its surface. There is no special change in the con- nective-tissue cells. The endothelial cells may remain in place, although their edges and corners are separated by pus cells and knobs of fibrin ; or the endothelium falls off in large patches ; or the sur- face of the peritoneum is covered with numerous cells which look like endothelial cells more or less deformed. But few dogs survive the third day of an acute artificial peritonitis. In the human subject, if death takes place before the third day, both the gross and minute changes are the same as those seen in the dog. There are present the same general congestion, the pus, fibrin, and serum, the desquamation and multiplication of the endo- thelial cells (Fig. 285). In many cases of peritonitis, however, death occurs between the sixth and fourteenth days of the disease. The appearance of the peritoneum at this period of the inflammation is not always the same. Thecongestion of the blood vessels may persist, it may be very intense and accompanied with extravasations of blood, or it may be entirely absent. There may be a thin coating of fibrin and pus gluing together neighboring surfaces of peritoneum, or this layer may be very thick. Theaccumulation of pus may be superficial, or it may infiltrate the whole thickness of the peritoneum and the sub- peritoneal connective tissue. The quantity of purulent serum in the peritoneal cavity may be small or large, and this serum may contain few or many pus cells, or the serum may be of a dirty-brown color and filled with bacteria. When the puruient serum is shut in by adhesion it is often thick and yellow, like the pus of an abscess. The minute appearances diifer from those seen at an earlier stage, rhiefly in the larger amount of inflammatory products and in the changes in the fixed connective-tissue cells. During the first three Digitized by Microsoft® 582 THE ALIMENTARY CANAL. days of an acute peritonitis the connective-tissue cells are but little changed, but by the seventh day there is a marked increase in their size and number. Acute peritonitis may prove fatal by the fourteenth day ; or it may be succeeded by chronic peritonitis ; or the patients recover and permanent connective-tissue adhesions and thickenings of the peri- toneum are left behind. Recovery is most common when the peri- tonitis has been a local one. Many species of bacteria have been found in the exudate in acute exudative peritonitis, but the significance of many of them is very Fic. 285.—Acuts ExupatTivE P&Rrronitis, EIGHT DAYS’ DURATION. Human omentum, x 850 and reduced. uncertain on account of the liability to contamination of the exudate, either before or after death, by the germs in the intestinal contents. Streptococcus pyogenes, Bacillus coli communis, Staphylococcus pyogenes, Micrococcus lanceolatus, Bacillus pyocyaneus, Bacillus aérogenes capsulatus, and many others have been reported. The Strep- tococcus and the Bacillus coli communis appear to be most frequently present. Very often two or more micro-organisms are associated in the exudate. ‘Consult Tavel and Lanz, “ Peritonitis, ” Mitth. a. Kl. u. Med. Inst. d. Schweiz, 1 Reihe, Heft i., p. 1, 1893; also Avlverschmidt, ibid., Heft 5, p. 432. Digitized by Microsoft® THE ALIMENTARY CANAL. 583 The probability of the passage of bacteria without visible perfor- ation through the intestinal wall should be borne in mind.’ IT. Chronic Perttonitis. We find the following varieties of chronic peritonitis : 1. Cellular Peritonitis.—This form of peritonitis is found as a complication of chronic endocarditis, of cirrhosis of the liver, of chronic pulmonary phthisis, and of acute general tuberculosis. Neither fibrin nor pus is present, but there may be clear serum in the peritoneal cavity. The peritoneum may look normal to the naked eye, or it may be studded with very minute, translucent nodules. JTL IM WW My Mt ravi Le ph aS WC — Fie. 2&6.—Oaronic Cr~tLuLar PERITONITIS OCCURRING WITH PULMONARY PHTHISIS. Human omentum, x 750 and reduced. Minute examination shows changes in the endothelial cells and the connective-tissue cells. These cells are everywhere increased in number and altered in shape ; or, to speak more guardedly, the sur- face of the peritoneum is covered with cells which look as if they were derived from the endothelium and the connective-tissue cells (Fig. 286). Some are large, flat cells; some smaller, polygonal cells ; some irregularly fusiform ; some large, granular masses con- 1 Arnd, ibid., Heft 4, p. 395. Digitized by Microsoft® 584 THE ALIMENTARY CANAL. taining a number of nuclei. Although these new cells are found over most of the surface of the peritoneum, yet they are more nu- merous in little patches which are scattered here and there. 2. Peritonitis with Adhesions.—There may be a formation of permanent adhesions without the production of fibrin or pus. It is often, indeed, difficult to tell whether old peritoneal adhesions are due to the form of chronic peritonitis of which we are now speaking, or whether they are the result of an acute peritonitis. But there are some cases in which the mode of development of the adhesions seems evident. If, from perityphlitis or some other cause, a collection of pus is shut in in some part of the peritoneal cavity, we may find the rest of the peritoneum smooth and shining; no serum, fibrin, or pus, no thickening ; but the neighboring surfaces of the peritoneum are at- tached to each other by adhesions. These adhesions are in the shape of threads and membranes, often ‘of the most extreme tenuity. They are formed of a fibrillated basement substance, the fibrils crossing each other in all directions. In the basement substance are cells, some fusiform and stellate, but most of them look like large branch- ing cells, of which the cell bodies have become fused with the base- ment substance while the nuclei remain. Close to these adhesions the peritoneum may appear normal to the naked eye, but if it is put in water very fine threads and membranes" will float upward from its free surface. Minute examination shows that the connective-tissue cells are increased in size and number, that the endothelial cells are replaced by cells of a great variety of shapes, and that the thin little threads and membranes on the surface are formed of large branching cells (Fig. 287). Such a peritonitis with adhesions appears to be a more advanced stage of the cellular peritonitis just described, but the inflammation, instead of stopping at the production of cells alone, goes on to the formation of membranes. We sometimes find in the same patient chronic pleurisy with adhe- sions and chronic peritonitis with adhesions. 3. Chronic Peritonitis with Thickening of the Peritoneum.— This form of peritonitis occurs quite frequently as an idiopathic lesion. It may involve the greater part of the peritoneum or be con- fined to the capsules of the liver and spleen. The most marked feature of the lesion is the thickening of the peri- toneum—a thickening which may reach as much as an inch. The outer portions of the thickened peritoneum are composed of dense connective tissue, the inner layers of granulation tissue. The surface of the peritoneum is smooth or covered with fibrin. There may also Digitized by Microsoft® THE ALIMENTARY CANAL. 585 be connective-tissue adhesions between different parts of the perito- neum. The peritoneal cavity contains clear and -purulent serum. In some cases the parietal peritoneum is principally involved ; in others the peritoneum of the stomach, intestines, liver, and spleen. The thickening of the capsule of the liver is attended with a diminu- tion in the size of that viscus. 4. Chronic Peritonitis with the Production of Fibrin, Serum, and Pus.—This form of peritonitis may follow acute peritonitis, may be due to lesions of the abdominal viscera, or may occur without known cause. The abdominal cavity contains purulent serum, either free or shut SAN we WS REA Fic. 287.CHRonic PERITONITIS WITH ADHESIONS, X 750 and reduced. Parietal peritoneum. LN SUN in by adhesions. The surface of the peritoneum is coated with fibrin and connective-tissue adhesions. The coils of intestine, and all the neighboring surfaces of the peritoneum, are matted together partly by fibrin, partly by permanent adhesions. 5. Hemorrhagic Peritonitis.—This occurs most frequently as a local inflammation. It involves the peritoneum behind and around the uterus in the female, and that covering the recto-vesical excava- tion in the male. The affected portion of the peritoneum is covered Digitized by Microsoft® 586 THE ALIMENTARY CANAL. with layers of new membrane infiltrated with blood. The membranes are formed of connective tissue containing numerous blood vessels and infiltrated with blood. The extravasations of blood may form tumors of considerable size. General hemorrhagic peritonitis is described by Friedreich. In two cases of ascites, which had been frequently tapped, he found the visceral and parietal peritoneum covered with a continuous mem- brane of a diffuse yellowish-brown color, mottled with extravasations of blood. The membrane was thickest over the anterior abdominal wall. It could be separated intoa number of layers. These layers were composed of blood vessels, masses of pigment, branching cells, and fibrillated basement substance. In many places the extravasated blood was coagulated in the shape of round, hard, black nodules. The entire new membrane could be readily stripped off from the peritoneum. 6. Tuberculous Peritonitis.—This occurs as one of the lesions of acute general tuberculosis, with chronic pulmonary phthisis, with tuberculous inflammation of the genito-urinary tract, and as a local inflammation. The gross appearance of the lesion varies. When tuberculous peritonitis occurs as one of the lesions of general tuberculosis, there are numerous small miliary tubercles, increase in the size and number of the endothelial and connective-tissue cells, and sometimes a little fibrin. Some of the miliary tubercles are com- posed of tubercle tissue, others of round and polygonal cells. Asa complication of tuberculosis of the genito-urinary tract we find the peritoneum studded with miliary tubercles, coated with fibrin, and serum is also present in the peritoneal cavity. As a complication of chronic phthisis there are miliary tubercles in the peritoneum of the small intestine immediately over the tuber- cular ulcers of the mucous membrane. There may also be thickening of the peritoneum and permanent adhesions. The anatomical forms of primary tuberculous peritonitis are: 1. The peritoneum is everywhere studded with miliary tubercles, its surface is coated with a thin layer of fibrin. 2. The peritoneum is studded with miliary tubercles, or with larger cheesy nodules; in its cavity are large quantities of serum. 3. The peritoneum is studded with miliary tubercles or with cheesy nodules. Its cavity contains large quantities of fibrin, which not only coat the peritoneum but fill up the spaces between the viscera. 4. In addition to the presence of miliary tubercles in the perito- Digitized by Microsoft® THE ALIMENTARY CANAL. 587 neum its apposed surfaces are fastened together by connective-tissue adhesions. The coils of small intestine especially are fastened to- gether in this way. 5. The tuberculous inflammation is confined to the omentum. By the formation of tubercle tissue and of connective tissue the omentum is converted into a hard tumor, which occupies the upper part of the abdominal cavity. 6. There are miliary tubercles in the peritoneum, connective- tissue adhesions, and collections of serum and pus. In this way the abdominal cavity becomes divided up into cavities of different sizes, each cavity containing more or less serum and pus. TUMORS. Fibromata are developed from the subperitoneal connective tis- sue and project inward into the peritoneal cavity. They are found beneath the parietal peritoneum and that covering the intestines. Such tumors may reach a very considerable size. Papillary fibromata of the peritoneum may be secondary to papillary fibroma of the ovary. Lipomata.—Circumscribed tumors composed of fat tissue are formed beneath the intestinal and parietal peritoneum and in the mesentery. These tumors may become changed into fibrous tissue or calcified. Their pedicles may become atrophied so that they are left free in the peritoneal cavity. When they grow beneath the parietal peritoneum they may form fat hernia. At the umbilicus, in the inguinal canal, along the vas deferens, in the crural ring, and in the foramen obturatorium, fatty tumors may grow, project outward under the skin like herniz, and, by drawing the peritoneum after them into a pouch, may open the way for a future intestinal hernia. Plexiform Angio-Sarcoma.—Very large tumors, resembling in their gross appearance colloid cancer, have been described by Wal- deyer.’ They are formed by a new growth of blood vessels, with a production of gelatinous tissue from their adventitia. Carcinoma of the peritoneum is either secondary or primary. The primary tumors assume the character of colloid cancer or of common cancer. The colloid form frequently involves the greater part of the peri- toneum and forms a large mass which distends the abdomen. The omentum is changed into a large, gelatinous mass; the subjacent muscles, the lymphatic glands, and the liver are infiltrated with the new growth, and soft, gelatinous masses project into the peritoneal 1Virch. Arch., Bd. lv., p. 134. Digitized by Microsoft® 088 THE ALIMENTARY CANAL. cavity. The umbilicus is sometimes invaded, so as to project out- ward in the form of a semi-translucent tumor. The appearance of the new growth is that of a soft, jelly-like mass embedded in a fibrous stroma. The minute structure is that of a connective-tissue Fie. 288.—Cystic PaPILLoMA OF THE OMENTUM. Secondary to papilloma of the ovaries (Freeborn). stroma, arranged so as to form cavities of different sizes. These cavities are filled with a homogeneous, gelatinous basement substance and with polygonal cells. Common carcinoma appears in the form of numerous small Digitized by Microsoft® THE ALIMENTARY CANAL. 589 nodules scattered everywhere in the inner layers of the peritoneum. These nodules are small, firm, and white, and are composed of a fibrous stroma enclosing cavities filled with polygonal cells. With the formation of these nodules there are often associated a general thickening of the peritoneum, an accumulation of serum in the peri- toneal cavity, and adhesions. Sarcomata appear in the form of solitary, slowly growing tumors behind the peritoneum or between the folds of the mesentery. These retroperitoneal sarcomata are found both in children and adults. They usually originate behind the peritoneum covering the posterior part of the abdominal wall. The retroperitoneal sarcomata may be of the small spheroidal- celled type (lympho-sarcoma) or of the fusiform-celled type. They are often very vascular. At first they grow slowly inward, pushing forward the peritoneum and abdominal viscera. After a time they assume a more noxious character, infiltrating the soft parts with which they come in contact, and forming metastatic tumors in the omentum, mesentery, intestinal wall, liver, lungs, and in other viscera. Endotheliomata similar in structure to those originating in the pleura are of occasional occurrence in the peritoneum. They may form single well-defined tumors or flattened masses in the thickened peritoneum. Cuboidal or polyhedral cell masses often grouped along the side of anastomosing channels in the new-formed or old connective- tissue stroma sometimes lend a glandular character to the type of growth.’ Cysts of the mesentery are of occasional occurrence. They may be filled with chyle, with blood, or with serous fluid,’ or may be due to the echinococcus. Lipomata of the mesentery are recorded. Multiple cysts of the omentum may form by transplantation of papillary cyst-adenomata from the ovary (see Fig. 288). PARASITES. Echinococct can be formed in their regular way at any part of the visceral and parietal peritoneum, or be free in the peritoneal cavity. These cysts may be small, or so large as nearly to fill the abdominal cavity. Cysticercus cellulosce may also be developed in the subperitoneal connective tissue. 1See Endothelioma, p. 312. 2 Regarding cysts of the mesentery consult Wetchselbaum, Virchow’s Archiv, Ba. lxiv., p. 145; Bramann, Archiv fir klin. Chirurgie, Bd. xxxv., p. 201; Hahn, Berliner klin. Wochenschrift, June 6th, 1887, p. 408; Robinson, British Medical Journal, January 31st, 1891. : Digitized by Microsoft® THE LIVER. MALFORMATIONS. Congenital malformations of the liver are not common and are of little practical importance. The organ may be entirely wanting ; the lobes may be diminished or increased in number ; its form may be altered, so that it is rounded, flattened, triangular, or quadrangular. ° The gall bladder or gall ducts may be wanting; the ductus choledo- cchus may be double, both ducts emptying into the duodenum, or one emptying into the duodenum, the other into the stomach. The single ductus choledochus may also empty into the stomach. Owing to abnormal openings in the diaphragm or the abdominal parietes, the liver may suffer displacement upward or forward. In congenital transposition of the viscera the liver is found on the left side, the stomach and spleen on the right side. Small, isolated bodies, having the same structure as the liver, have been afew times found in the suspensory ligament and in the lesser omentum. ACQUIRED CHANGES IN SIZE AND POSITION. As a result of tight lacing very marked changes are sometimes produced in the shape of the liver. By the narrowing of the base of the thorax the organ is compressed from side to side, and its convex surface is pressed against the ribs. In consequence of this there are found ridges and furrows on its convex surface. In consequence also of the circular constriction, a part of the right, and usually of the left lobe also, becomes separated by a depression. Over this depressed and thinned portion of the liver the capsule is thick and opaque. In extreme cases the depressing and thinning reach such an extent that there is only a loose, ligamentous connection between the separated portion and the liver. AA series of depressions are sometimes found on the upper surface of the right lobe of the liver, running from front to back, apparently caused by folds of the organ. Structural changes in the liver may induce changes in its size and shape. Itmay be increased in size by tumors, hydatid cysts, abscesses, Digitized by Microsoft® THE LIVER. 591 fatty and amyloid degeneration, by congestion, and sometimes by cirrhosis, etc. It may be diminished in size by atrophy, by cirrhosis, by acute parenchymatous degeneration, etc. Changes in the position of the liver are produced by alterations in its size, by pressure downward from the thoracic cavity and upward from the abdomen, by the constriction of tight lacing, by tumors or circumscribed serous exudation between the liver and diaphragm, by curvature of the spine. The liver is readily turned, by pressure from above or below, on its transverse axis. The transverse colon may be fixed above the liver so as to push it backward, downward, and to the right. There are a few cases recorded of dislocated and movable livers. These occarred in women who had borne children and whose abdominal walls were lax. With ascites it is not uncommon to find the liver quite movable. ? ANZ MIA AND HYPERAMIA. Ancemia of the liver may be general or partial. It may be due to general anzemia or to local disturbances of the circulation, such as swelling of the cells in parenchymatous or other degeneration, pres- sure of tumors, etc. Theorgan appears pale, often of slightly yellow- ish or brownish color. It may be harder than usual, and smaller. Hypercemia of the liver is either an active or a passive process, In health the amount of blood in the liver varies at different times, being regularly increased during the process of digestion. When the digestive process is unduly influenced by the ingestion of spirits, Spices, etc., the hyperemia assumes abnormal proportions, and when this is often repeated it may lead to structural changes in the organ. Severe contusions over the region of the liver sometimes cause a hyper- gmia, which may result in suppurative or in indurative inflammation, In hot climates and in malarious districts active and chronic hyper- zemia of the liver are frequent and often cause structural lesions. In scurvy, also, the liver is sometimes congested. Cessation and Suppression of the menses and of hemorrhoidal bleeding may cause hyperemia of the liver. In all these varieties of active congestion the liver is enlarged, of a deep-red color, and blood flows freely from its cut surface. The passive congestions of the liver are produced by some obstruc- tion to the current of blood in the hepatic veins. Valvular diseases of the heart, emphysema and fibrous induration of the lungs, large pleuritic effusions, intrathoracic tumors, angular curvature of the ‘pine, aortic aneurisms pressing on the vena cava, and constrictions 1Consult Graham, “ Displacements of the Liver,” Trans. Assn. Am. Phys., vol. ., p. 258, 1895 (bibliograp}yH)tjzed by Microsoft® 592 THE LIVER. of the vena cava and of the hepatic veins, may all produce a chronic hyperzemia of the liver. In all these cases, as the congestion affects principally the hepatic veins, we find the centre of each acinus con- gested and red while its periphery is lighter in color. This gives to the liver a mottled or nutmeg appearance (nutmeg liver). The liver cells in the centre of each acinus are frequently colored by little gran- ules of red or black pigment, and the cells at the periphery become fatty, so that the nutmeg appearance is still more pronounced. A liver in this condition is usually of medium size, but may be smaller or larger than normal. Fic. 289.—Curonic CONGESTION OF THE LiveR (nutmeg liver). This section shows complete atrophy of the liver cells at the centre of the lobule. a, dilated vena centralis; b, dilated capillaries filled with blood; c, portal vein surrounded by connective tis- sue; d, gall duct; e, atrophied liver cells; g, nearly normal liver tissue. When the congestion is long-continued the veins at the centre of each acinus may become permanently dilated, the hepatic cells in their meshes become atrophied (Fig. 289), so that the centre of each acinus consists only of dilated capillaries or of theseand new connec- tive tissue ; or the dilatation and atrophy of the liver cells may, in circumscribed portions of the organ, involve the entire acinus. In long-continued congestion the liver is usually smaller than normal, and may be slightly roughened or uneven on the surface; but it is Digitized by Microsoft® THE LIVER. 593 sometimes enlarged. The peculiar nutmeg appearance may be very: well marked, or it may not be evident, the organ being of a dark-red color. WOUNDS, RUPTURE, AND HAMORRHAGE. Wounds of the liver may induce hemorrhage, which, if life con- tinue, is followed by inflammation. Serious wounds of the liver are usually fatal, but recovery may occur even after the destruction of a considerable portion of the organ, Rupture of the liver may be produced by severe direct contusions or by falls. It may be produced in children by artificial delivery. The rupture usually involves both the capsule and a more or less con- siderable portion of the liver tissue. It is commonly accompanied by: large heemorrhage, and is usually fatal. Heemorrhage.—Extravasations of blood in the substance of the liver, or more frequently beneath the capsule, are found in new-born children after tedious or forcible labors. In adults hemorrhage, except as the result of injury, is uncommon. LExtravasations of blood are sometimes seen in malignant malarial fevers, especially in tropical climates; in scurvy, purpura, and phosphorus poisoning ; and bleeding may occur in and about soft tumors, abscesses, and echinococcus cysts. It may also occur as a result of thrombosis of the hepatic vein. LESIONS OF THE HEPATIC ARTERY. The hepatic artery is in rare cases the seat of aneurisms which may attain a large size. Such aneurisms may displace the liver tis- sue, compress the bile ducts so as to cause jaundice, and may rupture into the stomach or abdomen. Owing to its abundant anastomoses, emboli of the branches of the hepatic artery usually induce no marked lesions, but they sometimes result in hemorrhagic infarctions. LESIONS OF THE PORTAL VEIN, Thrombosis, Embolism, and Inflammation.—Thrombosis of the branches of the portal vein may be produced by weakening of the cir- culation from general debility—marasmatic thrombi ; by pressure on the vessel from without, as in cirrhosis, tumors, gall stones, dila- tation of the bile ducts, etc. ; by injury ; by the presence of foreign materials within the vessel; and as a result of inflammation of its wall, or of embolus. The thrombus may form in the vessels in the liver or be propagated into them from without. It may partially or 4 q Digitized by Microsoft® 594 THE LIVER. entirely occlude them. The clot may become organized as a result of endophlebitis, and a permanent occlusion of the vessel ensue. If the clot be a simple, non-irritating one, leading to occlusion, the conse- quences are usually more marked in the abdominal viscera than in the liver itself. The branches of the hepatic artery form sufficient anastomoses to nourish the liver tissue and prevent its necrosis, even in complete occlusion of the portal vein ; and if occlusion occur slow- ly the organ may continue to perform its functions. But this oblite- rative form of thrombosis is usually attended by ascites, enlargement of the spleen, dilatation of the abdominal veins, and sometimes by hemorrhage from the stomach and intestines. In another class of cases, in addition to the local and mechanical effects of a thrombus, there may be necrotic changes and suppurative inflammation in the walls of the vessels or in the liver tissue about them. The thrombi are apt to soften and break down, and the frag- ments may be disseminated through the smaller trunks of the portal vein. In this way, by the distribution through the smaller vessels of a disintegrated thrombus from a large trunk, or by the introduc- tion into the branches of the portal vein of purulent or septic material from some of the abdominal viscera or from wounds, multiple foci of purulent inflammation in the portal vein, and multiple abscesses in- volving the liver tissue, may be produced. In many cases the pre- sence of bacteria may be detected in the inflammatory foci. These soft thrombi of the portal vein and the accompanying pyle- phlebitis and abscess may be caused in a variety of ways. Ulcera- tion of the intestines and stomach, abscesses of the spleen, suppurative inflammation of the mesentery and mesenteric glands, inflammation and ulceration of the bile ducts from gall stones, inflammation of the umbilical vein in infants, may all induce thrombi in their respective veins, which may be propagated to the portal vein or may give rise to purulent or septic emboli. Two cases are recorded in which a fish bone in the portal vein induced suppurative inflammation in that vessel. One of these cases, occurring in Bellevue Hospital in 1867, was reported by Dr. E.G. Janeway. Male, 47 ; dying, after a four weeks’ illness, in a typhoid condition, with lesions of sero-fibrinous peritoni- tis and chronic diffuse nephritis. There were numerous small ab- scesses in the right lobe of the liver, two in the left lobe. The left division of the portal vein contained a firm red and white clot over an inch long ; the right division was lined with a firm thrombus. The walls of the vein were thickened and contained purulent fluid. A fish bone, two inches long, its centre covered by a thrombus, lay half in the mesenteric and half in the portal vein. In infants inflammation of the umbilical vein may not oaly induce inflammation of the portal vein and abscesses in the liver, but multiple Digitized by Microsoft® THE LIVER. 595 abscesses in various parts of the body, and acute peritonitis may be induced. Rupture of the Portal Vein, with fatty degeneration of its walls, has occurred in a few instances. Chronic Endophlebitis, with atheroma and calcification, may occur in the walls of the portal vein, giving rise to thrombosis. Dilatation of the Portal Vein, either uniform or varicose, may occur in various parts of the vessel or its branches. It may be caused by destruction of the liver capillaries in cirrhosis, or by occlusion of the vein by thrombi, tumors, etc. THE HEPATIC VEINS. The hepatic veins present lesions similar to those of the portal vein and its branches, but they are much less frequent. They may be dilated by obstruction to the passage of venous blood into the heart. They may be the seat of acute and chronic inflammation, and soft thrombi and suppurative inflammation may be produced by abscesses in the liver. ATROPHY OF THE LIVER. Atrophy of the liver may affect the entire organ or be confined to some part of it. General atrophy may occur in old age as a senile change, or may be induced by starvation or chronic exhausting dis- eases. The organ is diminished in size, is usually firm, and the acini appear smaller than usual. Microscopically the change is seen to be due to a diminution in size of the liver cells, and hand-in-hand with this there occurs frequently an accumulation of pigment granules within the atrophied cells. The cells may entirely disappear over circumscribed areas, leaving only shrivelled blood vessels and con. nective tissue; or, in some cases, there may be an increase of con- nective tissue in connection with the atrophy of the cells. When much pigment is formed in the cells the lesion is often called pigment atrophy. Essentially the same changes may occur in circumscribed portions of the liver, as the result of pressure from new connective tissue in cirrhosis, from tumors, hydatids, amyloid degeneration, gall stones, etc. In atrophy from pressure the liver cells are apt to become very much flattened and squeezed together as they diminish in size. DEGENERATIVE CHANGES. Acute Degeneration ; Parenchymatous Degeneration (Cloudy Swelling).—In a variety of acute and infectious diseases—pneumo- nia, typhoid and typhus fevers, scarlatina, variola, diphtheria, ery- sipelas, yellow fever, septicemia, and in certain cases of acute ana- Piecaen * ‘Digitized by Microsoft® 596 THE LIVER. mia and phosphorus poisoning—the liver is somewhat swollen and, on section, of a dull yellowish-gray color, looking somewhat as if it had been boiled. It contains less blood than usual, and the outlines of the lobules are indistinct. Microscopical examination shows the ‘lesion to consist of a swelling of the liver cells and an accumulation in them of moderately refractile, finer and coarser albuminous gran- ules. Those granules may disappear and the cells return to their normal condition, or, as is frequently the case, they may pass into a condition of fatty degeneration. Very frequently fatty and paren- chymatous degenerations are associated together. Small areas of necrosis of liver cells may be found in certain acute infectious diseases (see Fig. 67). Fatty Infiltration.—In the normal human liver there is usually a certain amount of fat in the liver cells, and this amount varies con- siderably under different conditions. The gross appearance of pathological fatty livers varies a good deal, depending upon the amount and distribution of fat and its as- sociation with other changes. If the lesion is uncomplicated and considerable the organ is increased in size, the edges rounded, the consistence firm, the color yellowish, and the cut surface greasy. The lobules are enlarged and their outlines usually indistinct, and the blood content diminished. The liver isincreased in weight. If the amount of infiltration be moderate the outlines of the lobules may be more distinct than usual and the centres appear unusually red. This is due to the fact that the accumulation of fat usually commences in the periphery of the lobules and progresses toward the centre, so that the centre appears darker by contrast with the fatty periphery. The lesion may be uniform throughout the organ or it may occur in patches. In the latter case the liver has a mot- tled appearance, irregular yellowish patches alternating with the brownish-red, unaffected portions. Fatty infiltration is often associated with chronic congestion (nut- meg liver), with cirrhosis and amyloid degeneration ; the picture may then present considerable complexity. Fatty livers may be stained brown or greenish with bile pigment. Microscopically the liver cells are seen to contain larger and smaller droplets of fat (Fig. 290), and frequently large drops of fat occupy nearly the entire volume of the cell, so that the protoplasm may be visible only as a narrow, nucleated crescent at one side, or it may disappear altogether (Fig. 291). The microscopical appear- ances of course vary, depending upon the degree of infiltration and the association with other lesions. Fatty infiltration of the liver may occur as a result of excessive ingestion of oleaginous food: in chronic alcohol, phosphorus, and Digitized by Microsoft® THE LIVER. 597 arsenic poisoning ; in certain exhausting diseases accompanied by malnutrition, as in pulmonary phthisis, chronic dysentery, etc.; and under a variety of conditions which we do not understand. Fatty Degeneration.—In this condition, which in many cases cannot be morphologically distinguished from fatty infiltration, the fat is believed to be formed by a transformation of the protoplasm Fig. 290.—Fatty INFILTRATION OF LiveR CELLS. of the liver cells. The fat droplets are, for the most part, very small and abundant, though this is not constant. Fatty degenera- Fig. 291.—Farty InFivtraTIoNn oF LIVER. Portion of the periphery of a lobule. tion of the liver cells frequently follows, and is associated with, cloudy swelling under the varying conditions in which this occurs, or it may appear in profound anemia and in acute phosphorus and arsenic poisoning. Amyloid Degeneration (Waxy Liver).—In the liver amyloid degeneration may be general or local ; so extensive as to give the Digitized by Microsoft® 598 THE LIVER. organ very characteristic appearances, or so slight as to be unrecog- nizable without the aid of the microscope. It may be associated with other lesions. When the change is extensive and general the liver is enlarged sometimes to more than twice its normal size; the edges are thickened and rounded; the surface smooth; the tissue tough, firm, inelastic, more or less translucent, and of a brownish- yellow color. The lobular structure may be more or less indistinct, or it may become very evident by an associated fatty degeneration of the peripheral or central cells of the lobules. The translucency and peculiar appearance of the tissue may be best seen by slicing off a thin section and holding it up to the light. When the lesion is Fruaden Fie. 292.—Amy.Lorp DEGENERATION OF THE Liver. The degenerated walls of the vessels are stained red. less considerable the liver may be of the usual size, and may feel harder than normal, and here and there a translucent mottling may be evident, or the degeneration may be apparent only on the addi- tion of staining agents. When, as is frequently the case, itis as- sociated with cirrhosis, the liver may be small and nodular, and the appearance of the cut surface will vary greatly, depending upon the character of the cirrhotic change and the presence or absence of fat. This degeneration usually commences in the walls of the intra- lobular blood vessels, causing them to become thickened and translu- cent. The liver cells are squeezed by the thickening of the vessels and may become partially or completely atrophied (Fig. 292). Digitized by Microsoft® THE LIVER. 599 It is stated by some observers that the liver cells may also become waxy, but we have been unable to find them unmistakably thus changed. The liver cells not infrequently undergo fatty metamor- phosis. Amyloid degeneration may also involve the interlobular ves- sels, and in advanced stages larger and smaller areas of liver tissue may be nearly or completely converted into the dense, refractile sub- stance which in its arrangement but obscurely represents the group- ing and structure of the affected lobules. Not infrequently atrophic or fatty liver ceils are seen scattered singly or in clusters through the amyloid masses. In the affected regions the blood content of the liver is considerably diminished, or it may be nearly entirely absent. Amyloid degeneration of the liver is usually associated with a similar lesion of other organs, such as spleen, kidneys, intestines, etc., although it may occur in this organ alone. It usually occurs in cachectic conditions, as in chronic phthisis ; in chronic suppurations, especially of the bones ; in syphilis, and sometimes in malarial poison- Fic. 293.—PIGMENTATION OF THE LIVER IN MALARIAL FEVER. The pigment in this specimen was contained in cells lying within the liver capillaries. ing. It occasionally occurs unassociated with any of these con- ditions. PIGMENTATION OF THE LIVER. As a result of severe malarial poisoning a variable amount of brown, black, or reddish pigment is often found in the blood. This is usually mostly taken up by the leucocytes and deposited in various parts of the body, chiefly in the liver, spleen, and marrow of the bones. In the liver it is usually found enclosed in variously shaped cells which lie especially in the blood vessels, but sometimes in the tissue between them (see Fig. 293). The liver cells frequently con- tain bile pigment, but usually are free from the melanotic pigment characteristic of this malarial condition. As the result of this ac- cumulation of pigment the liver may have a dark reddish-brown, an olive-brown, or black color (sometimes called bronze liver). This condition may be associated with various other lesions of the liver, depending upon the najure and, extant of wach the organ will present 600 THE LIVER. a great variety of appearances. Thus there may be fatty or waxy degeneration, cirrhosis, chronic congestion, etc. Pigment may be found in the connective tissue along the portal vessels similar in character to that which occurs in the lungs from the inhalation of coal dust. This inhaled pigment, according to the researches of Weigert, doubtless finds access to the blood and is de- posited in the liver as it is in the spleen and hepatic lymph nodes. Pigmentation of the liver cells, which is to a certain extent nor- mal, may be greatly increased as a result of atrophy, localized heemor- rhage, and of obstructive jaundice.’ ACUTE YELLOW ATROPHY OF THE LIVER. This disease is characterized anatomically by a rapid diminution in the size of the liver as the result of a granular and fatty degenera- tion and disintegration of the liver cells. The liver, sometimes with- in a few days, may be reduced to one-half its normal size. On open- ing the abdominal cavity the organ may be found lying, concealed by the diaphragm, close against the vertebral column. The amount of diminution and the general appearance of the affected organ de- pend to a considerable extent upon its previous condition—7.e., whether or not it was the seat of other lesions—as well as upon the degree of degenerative change. In general, if the lesion is well marked, the liver is small, flabby—sometimes almost fluctuating— and the capsule wrinkled. On section the cut surface may show but little trace of lobular structure, but presents an irregular mottling with gray, ochre-yellow, or red; sometimes one, sometimes another color preponderating. Microscopical examination shows varying degrees of degeneration and destruction of the liver cells. Most evidently in those parts which have a grayish appearance, the outlines of the cells are preserved and the protoplasm is filled with larger and smaller granules. In the yellow portions the outlines of the liver cells may be preserved, and they may contain varying quantities of larger and smaller fat droplets and granules of yellow pigment. Or the cells may be com- pletely disintegrated, and in their place irregular collections of fat droplets, pigment granules, red and yellow crystals, and detritus; only the connective tissue and blood vessels of the original liver tis- sue remaining. The red areas may show nearly complete absence of liver cells and cell detritus, and sometimes irregular rows of cells which are variously interpreted as being new-formed gall ducts or proliferated liver cells. In these areas it appears to be, in part at ' The distribution and amount of the pigment may be well seen by staining thin sections with eosin and mounting in eosin-glycerin or balsam. Digitized by Microsoft® THE LIVER. 601 least, the blood contained in the vessels which imparts the red color. Sometimes the interstitial tissue is infiltrated with small spheroidal cells resembling leucocytes. Crystals of leucin and tyrosin are sometimes found intermingled with the cell detritus. In some cases the liver is not diminished in size. These lesions of the liver are frequently associated with enlarge- ment of the spleen and parenchymatous degeneration of the kid- ney and of the heart muscle. Multiple hemorrhages may occur in ‘the gastro-intestinal canal, kidneys, bladder, and lungs. There is usually marked jaundice. Rod-shaped bacteria and micrococci have been found in the liver, but their significance is doubtful ; we have not been able to find them in the cases which we have examined. The cause of the disease is unknown, and it is doubtful whether it is a disease primarily of the liver or an acute infectious disease with local lesions. It is not unlikely that more than one form of lesion is grouped under this heading. INFLAMMATION OF THE LIVER. Acute Hepatitis (Purulent Hepatitis ; Abscess of the Liver).— Purulent or suppurative inflammation of the liver may be the result of injury ; it may be secondary to inflammation of the gall ducts or the branches of the portal vein. It may occur as the result of the presence of tumors, parasites, or from propagation of an inflam- matory process from without, as in ulcer of the stomach with ad- nesions to the liver and secondary involvement of the latter. It is often directly due to the introduction into the organ, through the blood vessels or gall ducts or otherwise, of bacteria. Purulent in- flammation in the liver almost always results in abscess. Large abscesses of the liver may be traumatic, but are often due to unknown causes. They are not infrequently associated with dys- entery, and may then be due to the conveyance of micro-organisms through the veins, or lymph channels, or peritoneum, or gall ducts from the intestinal ulcers. They may be due to the presence of the amceba coli. They occur most frequently in tropical climates, but are not very uncommon in the temperate zone. They are usually single, but there may be several of them. They are sometimes so large as to occupy a large part of the lobe. They are most frequent in the right lobe, but may occur in any part of the organ. They tend to enlarge, and as they do so they approach the surface of the liver. Here the contents of the abscess may be discharged into the perito- 1For an account of a bacterial study of a case of Infectious Febrile Icterus (Weil’s disease) consult Jaeger, Zeits. f. Hygiene u. Infectkr., Bd. xli., p. 525, 1892, = Digitized by Microsoft® 602 THE LIVER. neal cavity. More frequently, however, as they approach the sur- face, a localized adhesive peritonitis ensues, so that the liver becomes bound to adjacent parts, and thus the abscess may open into the pleural cavity, or, owing to a secondary pleurisy with adhesions, into the lung tissue. They may open into the pericardium. They may open externally through the abdominal wall; into the stomach, duo- denum, colon, or pelvis of the right kidney; into the hepatic veins, portal vein, vena cava, or gall bladder or gall ducts. The early stages in the formation of large abscesses of the liver are but little known. It is probable, however, that in many cases they are the result of the confluence of smaller abscesses. Their contents, usually bad smelling, may be thick and yellow like ordi- nary pus, but more commonly they are thin, reddish-brown, or green- ish in color from admixture with the pus of blood, gall pigment, and broken-down liver tissue. Microscopical examination shows the con- tents to consist of fluid with pus cells, more or less degenerated blood, degenerated liver cells, fragments of blood vessels, and pigment granules and crystals. The walls of the abscess are usually ragged, shreds of necrotic liver tissue hanging from the sides. Microscopical examination of the liver tissue near the abscess shows infiltration with pus, flattening of the liver cells from pressure, cloudy swelling, and necrosis of those lying along the cavity. Bacteria or the amceba coli or both may be present. Liver abscesses due to the presence of the amceba coli have certain peculiarities, concerning which reference is made to the studies of Councilman and Lafleur, “ Amcebic Dysen- tery,” Johns Hopkins Hospital Reports, vol. ii., p. 490, 1892. The amecebic abscesses are usually free from bacteria. Other ab- scesses may contain the Bacillus coli communis, or the Streptococcus pyogenes or Staphylococcus pyogenes. Notinfrequently, however, especially in old abscesses, examination both morphological and cultural fails to reveal the presence of micro- organisms. After the discharge of the contents of the abscess or without this if it be not very large, granulation tissue may form in the wall of the cavity and a fibrous capsule be produced, enclosing the contents, which become thickened and often calcareous, and in this condition may remain for a long time. Or the connective-tissue walls may approach one another and join, forming a fibrous cicatrix at the seat of the abscess. Several large abscesses may, one after another, heal in this way after evacuation of their contents, with little diminution in the size of the liver.’ | Hdebohis, “ Dysentery and Hepatic Abscess with Amoeba Coli,” Proceedings of the New York Pathological Society, 1892. Digitized by Microsoft® THE LIVER. 603 \bscesses of the liver accompanying inflammation of the portal vein and gall duct are considered elsewhere in this section. Small multiple metastatic abscesses are not infrequent in pye- mia, and are called pycemic abscesses. In these abscesses we can readily study the various stages of formation. Suppurative processes in any part of the body—in the head, upper and lower extremities, ete.—may act as distributing centres for micro-organisms.’ These, entering the circulation, may pass the heart and pulmonary capil- laries, with or without inducing lesions in the lungs, and, lodging in the vessels of the liver, induce circumscribed necrosis of the liver Fig. 294.—SMALL ABSCESSES IN THE LIVER CONTAINING BACILLI. Associated with a suppurative inflammation of the gall bladder and gall ducts, tissue (see Fig. 294) and suppurative inflammation. Under these conditions we may find on a section of the liver larger and smaller yellowish or grayish spots, the larger of which may be soft and _pre- sent the usual characters of abscesses. The smaller, which may not be larger than a pin’s head, may present the usual consistence of liver tissue with the lobular structure still evident; others may be softer, more yellow, and surrounded by a zone of hypereemic liver tis- sue. Microscopical examination of the earlier stages often shows the blood vessels filled with micrococci, scattered and in masses. Around 1 Kruse and Pasquaic, Zeits. f. Hygiene u. Infkr., Bd. xvi. Digitized by Microsoft® 604 THE LIVER. these the liver cells are found in various stages of necrosis; in many the nuclei do not stain and the bodies are very granular, or the entire cell is broken down into a mass of detritus. About these necrotic islets of liver cells pus cells collect and often form a zone of dense infiltration. Thus, by the increase of pus cells and the necrosis of liver tissue, small abscesses are formed whose contents are inter- mingled with greater or less numbers of bacteria, which seem to in- crease in number as the process goes on. By the confluence of small Fig. 295.—Curonic INTERSTITIAL HEPATITIS. a, new-formed connective tissue; 6, dilated blood vessels of the new tissue; c, gall duct; d, parenchyma of liver. abscesses larger ones may be formed. Death usually ensues, how- ever, before the abscesses attain a very large size. Chronic Interstitial Hepatitis (Cirrhosis).—The most marked result of chronic interstitial hepatitis is the formation of new connec- tive tissue in the liver. The character, amount, and distribution of the new tissue vary greatly in different cases. Secondarily there are usually marked changes in the liver cells and in the blood vessels and gall ducts. The new tissue is most commonly formed and most Digitized by Microsoft® THE LIVER. 605 abundant in the periphery of the lobules along the so-called capsule of Glisson, but it may extend into the lobules between the liver cells. It may surround single lobules, or more frequently larger and smaller groups of lobules (Fig. 295). It may occur in broad or narrow, ir- regular streaks or bands. It is frequently more abundant in one part of the liver than in another. The new-formed tissue tends to con- tract, and thus compromise by pressure the enclosed islets of liver tissue, causing them to project, in larger“and smaller nodules, from the surface of the organ. The liver cells may be flattened or atro- phied from pressure; or, from interference with the portal circula- tion, they may atrophy or become fatty; or they may become colored with bile pigment. The varied appearances with cirrhotic livers present to the naked eye depend largely upon the amount and distri- Fia. 296.—HYPERTROPHIC .CIRRHOSIS OF THE LIVER. Showing formation of connective tissue bet ween the liver cells, bution of the new connective tissue and upon the secondary changes in the liver cells. In some cases the liver is enlarged, sometimes so much so as to weigh nine or ten pounds, the surface smooth or slightly roughened —hypertrophic cirrhosis : in other cases it may be finely or coarsely nodular on the surface. It may be smaller than normal, sometimes _ very small indeed, so as to weigh only one or two pounds—atrophic cirrhosis. The surface may then be very rough and uneven from the projection of larger and smaller nodules of liver tissue, or it may be quite smooth; or the organ may be greatly distorted by the con- traction of large bands or masses of new connective tissue. In sec- tion through cirrhotic livers the new tissue may not be visible to the naked eye, or it may appear as grayish, irregular streaks, or bands, or patches, often sharply outlined against the dark-red, or brown, or Digitized by Microsoft® 606 THE LIVER. yellow, or greenish-yellow parenchyma. When, as is often the case, fatty infiltration is associated with atrophic cirrhosis the liver, may not only not be diminished in size but may be larger than normal. On microscopical examination the new connective tissue is found in some cases loose in texture and containing many variously shaped cells; or it may be dense and contain comparatively few cells; it is usually quite vascular. In some forms of hypertrophic cirrhosis there may be a very general and extensive growth of new fibrous tis- sue in and along the capillaries between the liver cells (Fig. 296). In other cases of hypertrophic cirrhosis the new growth of connective BM ie ‘a XS fi ay os. ‘ We rye \ e, err ees SN] f) ; Wiia a5 a A pat 4) Fic. 297.—Curonic INTERSTITIAL HEPATITIS. Showing a portion of the section shown in Fig. 244, but more highly magnified. a, portions of liver lobules; 6, new-formed connective tissue; c, gall ducts, apparently new formed; d, blood vessels in the new tissue. tissue is abundant between the liver lobules and along the smaller gall ducts, without encroaching materially upon the parenchyma. Not infrequently, when occurring largely between the lobules, it will _ be found to have encroached more or less upon their peripheral por- tions. Very frequently there are found in the new connective tissue cylindrical ducts lined with cuboidal cells, and resembling gall ducts (Fig. 297, c); or irregular rows of more or less cuboidal or polyhedral cells, which look somewhat like the lining cells of the medium-sized gall ducts, or like altered liver cells. The branches of the hepatic Digitized by Microsoft® THE LIVER. 607 and portal veins, particularly the latter, often become obliterated by pressure from the new connective tissue or from chronic thickening of their walls, so as to seriously interfere with the functions and nutrition of the liver cells. The bile ducts also may become obliter- ated, or there may be catarrhal inflammation, especially of the larger trunks. The branches of the hepatic artery are much less liable to alterations than the other vessels. The capsule of the liver is usually thickened, either uniformly or in irregular patches; or its surface may be roughened by larger and smaller papillary projections. The liver is frequently bound to the diaphragm or other adjacent organs by connective-tissue adhesions. Amyloid and fatty degeneration may be associated with cirrhosis. Cirrhotic livers frequently show an unusual number of leucocytes in the blood vessels. The obstruction to the portal circulation induced by cirrhosis usually gives rise to a number of secondary lesions, since collateral circulation is rarely established in sufficient degree to afford much relief. The hemorrhoidal and vesical veins may be greatly enlarged, and also veins of communication between Glisson’s capsule and the diaphragmatic veins. In rare cases a very peculiar dilatation of the cutaneous veins about the umbilicus is observed. Theenlarged veins form a circular network around the umbilicus, or a pyramidal tumor alongside of it, or all the veins of the-abdominal wall, from the epigastrium to the inguinal region, are dilated. This condition is said to be produced by the congenital non-closure and subsequent dilatation of the umbil- ical vein and its anastomoses with the internal mammary, epigastric, and cutaneous veins. According to Sappey, it is not the umbilical vein which is dilated, but a vein which accompanies the ligamentum teres. There is very frequently also a dilatation of the veins of the abdominal wall, which has a different cause. It is produced by the pressure of the fluid of ascites on the vena cava, and is found with ascites from any cause and with abdominal tumors. Ascites is the most common secondary lesion of cirrhosis. It usually begins at an early stage of the disease, and is apt to increase constantly. It usually precedes cedema of the feet, but both may appear at the same time. This fluid is of a clear yellow or brown, green or red ; it is sometimes mixed with shreds of fibrin, and more rarely with blood. The peritoneum remains normal, or becomes opaque and thick, or there may be adhesions between the viscera. The spleen is very frequently enlarged, and the enlargement may be very considerable. When itis not increased in size this seems usually due to previous atrophy of the organ, or to fibrous thickening Digitized by Microsoft® 608 THE LIVER. of its capsule, or to hemorrhages from the stomach and bowels occur- ring just before death. The stomach and intestines are often secondarily affected by the obstruction to the portal circulation. Profuse hemorrhage from the stomach and intestines may occur and sometimes cause sudden death. The mucous membrane is then found pale, or congested, or with hemorrhagic erosions. Sometimes the blood is infiltrated in the coats of the stomach and intestines. The mucous membrane of the stomach, and of the entire length of the intestines, is frequently the seat of chronic catarrhal inflammation, and is sometimes uniformly and intensely congested and coated with mucus. In other cases both the mucous and muscular coats are pale, but very markedly thickened. Cirrhosis of the liver is not infrequently accompanied by chronic diffuse nephritis. The causes of cirrhosis are imperfecly understood. Itisa disease of adult life, but exceptionally occurs in children. In adults it seems in many cases to be directly dependent upon the continued ingestion of large quantities of strong alcoholic liquors. It very rarely occurs as a result of beer drinking. There are many cases of cirrhosis for which no cause can be discovered. Itis probable that in certain cases a degeneration of circumscribed areas of liver parenchyma precedes and probably determines the new formation of connective tissue. Welch’ has described the occurrence of small circumscribed areas of fibrous tissue in the liver, replacing liver cells and containing coal pigment. This rare lesion he has called cirrhosis hepatis anthra- cotica. Syphilitic Hepatitis.—Chronic interstitial inflammation of the liver very frequently results from syphilitic infection, either congeni- tally or in the later stages of the acquired form. It may occur in a diffuse manner, new connective tissue being formed either between the lobules, or within them between the rows of liver cells. The new tissue may be rich in cells, or dense and firm. This form is fre- quently seen in children, and cannot be distinguished, either macro- scopically or microscopically, from similar forms of interstitial he- patitis from other causes. In other cases, particularly in children, there may be numerous small gummata (so-called miliary gummata) scattered through the liver, together with more or less new connective tissue (Fig. 298). In adults gummata are usually larger, varying.in size from that of a pea toa hen’s egg, and may be surrounded by larger and smaller irregular zones of ordinary connective tissue (Fig. 299). In still 1 Welch, ‘‘ Cirrhosis hepatis anthracotica,” Johns Hopkins Hospital Bulletin, Febru- ary and March, 1891. Digitized by Microsoft® THE LIVER. 609 other cases in adults we find larger and smaller dense, irregular bands or masses of connective tissue running through the liver, drawing in the capsule and often causing great deformity of the organ. These bands and masses of new tissue may or may not en- close gummata, either large or small. These deforming cicatrices, either with or without gummata, are very characteristic of syphilitic “inflammation of the liver. This, like the simple interstitial inflammation of the liver, may be i ee 4 Fie. 298.—Sypuinitic Hepatitis. A so-called miliary gumma from the liver of a child with congenital syphilis. associated with fatty and waxy degeneration, and with atrophy of the parenchyma from pressure. Tuberculous Hepatitis.—This lesion, which is usually secondary to tubercular inflammation in some other part of the body, or a part of acute general miliary tuberculosis, is most frequently characterized by the formation of larger and smaller miliary tubercles, which may be either within or between the liver lobules or in the walls of the bile ducts. Many of the tubercles are too small to be seen with the naked eye; others may be just visible as grayish points ; still others may be from one to three mm. in diameter, with distinct yellowish- white centres. Microscopical examination shows considerable varia- 49 Digitized by Microsoft® 610 THE LIVER. tion in the structure of the tubercles in different cases, as well as in the same liver. Some of them, usually the smaller ones, consist simply of more or less circumscribed collections of small spheroidal cells, which are not morphologically distinguishable, so far as the form and arrangement of the cells are concerned, from simple inflam- matory foci, or from the diffuse masses of lymphatic tissue which occur normally in the liver. In other forms we find a well-marked reticulum with larger and smaller spheroidal and polyhedral cells, with or without giant cells. In still other forms there is more or less extensive cheesy degenera- tion. The larger forms are conglomerate, being composed of several tubercle granula joined together to form a single nodular mass. The Fig. 299.—Gumma oF LIVER. a, cheesy centre; 6 fibrous periphery; c,small-celled peripheral infiltration; d, portions of live lobules. liver cells at the seat of the tubercle are destroyed, and the interstitial tissue and blood vessels either destroyed or merged into the tubercle tissue. In the periphery of the tubercles the liver cells may be in a ‘condition of coagulation necrosis, and the tissue round about may be infiltrated with small spheroidal cells. There is in some cases a new formation of gall ducts or of structures which resemble these, and which in transverse sections look considerably like giant cells. Tu- bercle bacilli, frequently in small numbers, but often in great abun- dance, may be found within the tubercles. Tuberculosis of the liver may be associated with cirrhosis, waxy and fatty degeneration. Much more rarely than the above form there are found in the liver Digitized by Microsoft® THE LIVER. 611 more or less numerous scattered tubercular masses from the size of a pea to that of a walnut or larger, with cheesy centres and usually a new growth of connective tissue in the periphery. These so-called solitary tubercles of the liver may be softened at the centres. Tu- bercular inflammation of the gall ducts may give rise to numerous scattered, cheesy nodules, as large as a pea or larger, which may be softened at the centre and stained yellow with bile. This lesion is rare and seems to be more frequent in children than in adults. Perihepatitis.—Acute inflammation of the serous covering of the liver, with the formation of fibrin, may occur as a part of acute general or localized peritonitis, and over the surface of abscesses, tumors, hydatids, etc., of the organ, when these lie near or approach -the surface ; or it may be secondary to acute pleurisy. Chronic perihepatitis, resulting in the thickening of and forma- tion of new connective tissue in and beneath the capsule of the liver, may be secondary to an acute inflammation of the capsule, or it may be chronic from the beginning and associated with chronic pleurisy, chronic peritonitis, and cirrhosis. In this way more or less exten- sive adhesions of the liver to adjacent structures may be formed ; or, by contraction of the new-formed connective tissue, consider- able deformity of the liver may be produced. The capsule is some- times uniformly thickened, sometimes the new tissue occurs in more or less sharply circumscribed patches. The surface is sometimes roughened from little, irregular projecting masses of connective tissue. Microscopically the new-formed tissue is usually dense and firm, but it may be loose in texture and contain many cells. Not in- frequently bands or masses of connective tissue run inward from the thickened capsule between the superficial lobules, causing local- ized atrophy of the parenchyma. Hyperplasia of Lymphatic Tissue in the Liver.—In some forms of leukemia and pseudo-leukeemia the liver is not infrequently enlarged and soft and besprinkled with small white spots, or streaked with narrow whitish, irregular bands, or of a diffuse grayish color. Microscopical examination shows this change to be due to an accu- mulation of cells resembling leucocytes, either along the portal vein, or diffusely through the liver tissue, or in small circumscribed masses. The amount of accumulation of these small cells varies much, but is sometimes so great as to seriously compromise the liver cells. The origin of these new cells is not yet definitely known. They may be, and doubtless in part are, brought to the organ through the portal vein; but they may, in part at least, be formed in the liver itself, possibly from the capillary endothelium. In typhoid fever, small-pox, scarlatina, diphtheria, and measles small circumscribed sses of ,cells rese ing leucocytes are some- mS Ot by hagescanes S y 612 THE LIVER. times found in the liver, lying in the meshes of a delicate reticular tissue. These are sometimes called miliary lymphomata ; but it should be remembered that small masses of lymphatic tissue nor- mally occur in the liver, and that as, under the above conditions, an hyperplasia of the lymph nodes and spleen is wont to occur, these so-called lymphomata are very probably normal structures, which have become more prominent under the conditions of disease owing to an acute inflammatory condition induced by absorbed ptomaines. TUMORS OF THE LIVER. Tumors of the liver may be primary or secondary ; the latter are most common. Cavernous Angiomata.—These tumors, usually small, from five to fifteen mm. in diameter, are most common in elderly persons and are of no practical significance. They may be situated at the surface or embedded in the organ, and are of a dark-red color ; sometimes sharply circumscribed by a connective-tissue capsule, sometimes merging imperceptibly into the adjacent liver tissue. Microscopically they consist of a congeries of irregular cavities (Fig. 144, page 327) filled with blood and frequently communicating freely with one another. The walls of the cavities consist of connective tissue, often containing small blood vessels, and are sometimes thick, sometimes thin. They are believed to be formed by dilatation of the liver capillaries, with subsequent thickening of their walls and atrophy of the adjacent liver cells. Small fibromata and lipomata have been described, as also fibro- neuromata of the sympathetic. Adenomata of the liver are of not infrequent occurrence. They are sometimes small and circumscribed, sometimes very large and multiple. They present two tolerably distinct types of structure. In one form the tissue presents essentially the same structure as nor- mal liver tissue, except that the arrangement of the cells is less uni- form and the cells are apt to be larger. They look like little islets of liver tissue, sometimes encapsulated and sometimes not, lying in the liver parenchyma. In the other form the cells are less like liver cells, are frequently cylindrical, and are arranged in the form of irregular masses of tubular structures with more or less well-de- fined lumina. These tumors are sometimes large and multiple, and in one case described by Greenfield there were metastatic tumors in the lungs. These tubular adenomata are in some cases so closely similar to some of the carcinomata as to be scarcely distinguishable from them, and seem, indeed, to merge into them. Cysts may de- velop in adenomata.’ 'See Dimochowshi and Jang celery Meio sG ree Anat., Bd. xvi., p. 102. THE LIVER. 613 Carcinomata are the most common and important of the liver tumors, and may be primary and secondary. Primary carcinomata of the liver are probably developed from the epithelium of the gall ducts, and in some cases are arranged along the larger trunks. Their cells are usually polyhedral, sometimes cylindrical, and may be ar- ranged irregularly in alveoli or form more or less well-defined tubular structures. Secondary carcinomata of the liver, which are by far the most common, are most frequently due to the dissemination in the organ of tumor cells from carcinomata of the stomach, intestines, pancreas, or gall bladder. But they may be the result of metastases from the mamma, cesophagus, uterus, and various other parts of the body. In secondary carcinomata the cells resemble more or less closely the type of those forming the primary tumor. The form in which the carcinomatous nodules in the liver present themselves is subject to considerable variation. Sometimes they are single, but more often multiple ; they may be very large, or so small as to be scarcely visible to the naked eye ; very frequently numerous small nodules are grouped in the periphery of a larger cancerous mass. They are sometimes deeply embedded in the liver, sometimes they project from the surface. The liver is frequently enlarged, sometimes enormously so. The nodules are usually whitish or yellowish or pink in color, but they are often the seat of hemor- rhages, and may become softened at the centre, forming cysts filled with degenerated tumor tissue which is often mixed with blood. The nodules are sometimes hard, sometimes soft and almost diffluent. Fatty degeneration is frequent, and may be evident to the naked eye in the form of yellowish streaks or patches on the cut surfaces. Owing to the degeneration and partial absorption of the central por- tions of the tumors, the nodules on the surface frequently present a shallow depression at the centre. The tumors may be sharply out- lined against the adjacent liver tissue, or may merge imperceptibly into it. They may be so large or numerous as to occupy the greater part of the enlarged organ. The liver tissue in their vicinity shows flattening and atrophy of the liver cells from pressure, and there may be infiltration with small spheroidal cells. The tumors may press upon the portal vein or its branches, or upon the gall ducts, and thus seriously interfere with the functions of the organ. Sometimes, how- ever, the tumors are very large and abundant without causing any apparent detriment to the liver functions. They are not infrequently stained with bile. Melanotic carcinomata sometimes occur in the liver, most frequently as secondary tumors. In some cases, instead of forming separate, distinct nodules, the cancerous growth develops in the form of a diffuse infiltration of the Digitized by Microsoft® 614: THE LIVER. organ, so that the often greatly enlarged liver is irregularly mottled with white and reddish-brown masses, and may then somewhat resemble some forms of chronic interstitial hepatitis. Sarcomata.—Spindle-celled, melanotic, and telangiectatic sarco- mata may occur in the liver as secondary tumors. Secondary myxo- mata and chondromata have also been described, but they are very rare. Angiosarcoma may occur as a primary tumor.’ Cavernous lymphangiomata have been described in a few cases. Cysts, usually of small size, may occur by dilatation of the bile ducts. They may be multiple and contain serum, mucus, and degenerated epithelium. Single cysts, apparently unconnected with the gall ducts, are occasionally found in the connective tissue of the-liver. They may be lined with ciliated epithelium. The liver is sometimes the seat of larger and smaller multiple cysts, varying from microscopical size up to that of a pea, and some- times larger. They do not appear to communicate with the gall ducts. They are sometimes associated with multiple cysts of the kidney. Their origin and nature are not understood.’ Occasionally the liver is found at the autopsy, even if this ba made but afew hours after death, more or less completely riddled with small, irregular-shaped cavities, from the size of a pin’s head to that of a pea. These holes are due to the accumulation of gases in the liver, and are frequently associated with the presence of the Bacillus aérogenes capsulatus (see p. 261). PARASITES. Echinococcus.—This parasite is the most common and impor- tant of those which occur in the human liver. It forms the so-called hydatids of the liver. These represent one of the developmental stages of the small tapeworm of the dog, Tenia echinococcus (see page 108). The cysts in the liver may be very small and multi- ple, but they may be as large as a man’s head or larger. The liver may be greatly increased in size, and the tissue about the cysts atrophied. The liver itself furnishes a connective-tissue capsule, within which is the translucent, lamellated membrane furnished by the parasite. On the inside of this we may find a layer of cells, granular matter, and a vascular and muscular system belonging to. the parasite. Projecting from this inner capsule are the brood cap- sules and heads or scolices of the immature tapeworm. The sco- 1 Arnold, Ziegler’s Beitr. z. path. Anat., Bd. viii., p. 128. * Consult Pye-Smith, “‘ Cystic Disease of Liver and both Kidneys,” Trans. London Path, Soc, vol, xxxii., p. 112, 1881, Digitized by Microsoft® THE LIVER. 615 lices may become detached from the wall and lie free in the cavity, which is filled with a transparent or turbid fluid. Not infrequently the cysts are sterile, and are then simply filled with clear or turbid fluid ; or the embryos may have died and disintegrated, and their detritus, including the hooklets, may be intermingled with the fluid contents of the cysts. The contents of the cysts may be mixed with fat, cholesterin crystals, pus, bile, or blood; or form a grumous mass, in which we may or may not be able to find the hooklets of the scolices or fragments of the lamellated wall. The connective tissue of the walls of the cysts may be greatly thickened, or they may be calcified. In other countries the lesion is much more common and fre- quently more formidable than in the United States. The cysts reach an enormous size, the veins of the liver may be compressed and filled with thrombi, the bile ducts compressed and ulcerated. So much of the liver tissue may be replaced by the hydatids that the patient may die from this cause alone. Very frequently there is local peritonitis, and adhesions are formed between the liver and the surrounding parts. In some cases the cysts rupture, and their con- tents are emptied into the peritoneal cavity, the stomach, the intes- tines, the pleural cavity, or the lung tissue. Sometimes the cysts perforate the bile ducts, the vena cava, or some of the branches of the portal or hepatic veins. Sometimes the abdominal wall is per- forated and a fistula formed between the cavity in the liver and the surface. In cases in which we do not find the scolices entire, a careful ex- amination of the inner cyst wall or of its contents will frequently establish the diagnosis by revealing single hooklets (see Fig. 40, page 134) or fragments of the characteristically lamellated wall (see Fig. 38, page 133). Echinococcus multilocularts, which is apparently an abortive form of the above species (see page 132), is very rare indeed in the United States. The writer (T. M. P.) has examined a specimen sent to him by Dr. Edward J. Ill, of Newark, N. J., and which is now in the museum of the College of Physicians and Surgeons, New York. The patient was a male, age thirty-one, German, sin- gle, farmer. He had been in the United States five years. For a year previous to his death he had been out of health, and jaundiced and somewhat emaciated. A. large, indistinctly fluctuating tumor was evident in the right lumbar and umbilical regions, and appa- rently connected with the liver. Aspiration of the tumor gave a. milky fluid believed to be pus. An opening was made into the tu- mor by one of the surgeons attending the case, and death occurred, hage. after ten hours, from Bigeed by Microsoft® 616 THE LIVER. The liver was found adherent to the abdominal walls, and about one-fourth of the right lobe of the liver was occupied by an irregu- lar cavity with very rough, ragged walls. These walls were in some places from one to two inches in thickness, and appeared to the naked eye to consist of dense connective tissue in irregular bands and fascicles, which enclosed very irregular, mostly small cavities. Microscopical examination showed that the cavities were lined with the delicate, lamellated cuticula characteristic of the echi- nococcus cysts. No hooklets were found. Fig. 300 is a drawing from this specimen. Fig. 300,—EcHINococcus MULTILOCULARIS OF THE LIVER. Distoma hepaticum, D. sinense, D. lanceolatum, may occur in the gall ducts and gall bladder. D. stnense occurs especially in the East, and has been found in great numbers in the bodies of China- men. D. hematobtum is very common in Egypt and Abyssinia, occurring in the blood vessels of the liver. Pentastoma denticulatum is the undeveloped form of Penta- stoma, teenioides, a parasite which inhabits the nasal cavity of dogs and some other animals. In the liver of man it usually occurs in the form of small, rounded, calcified cysts. The cysts may contain fat, calcareous matter, and the remains of the dead parasite, among which the hooklets may be found. Ascaris lumbricoides sometimes finds its way from the intestines Digitized by Microsoft® THE LIVER. 617 into the bile ducts. It may cause no disturbance here, but in some cases the worms have been present in large numbers and caused occlusion, dilatation, and ulceration of the biliary passages, and have led to the formation of abscess of the liver. Psorospermia, the very common parasite in the rabbit’s liver, has been found a few times in the liver of man. THE BILIARY PASSAGES. Catarrhal Inflammation most frequently attacks the lower por- tion of the common duct and the gall bladder. In the acute form it usually leaves but few changes appreciable after death. An ab- normal coating of mucus, and sometimes congestion of the blood vessels, are almost the only post-mortem lesions. Owing to the swelling of the mucous membrane and the accumulation of mucus in the lumen, the ducts may be temporarily occluded, but this occlusion may not be evident after death. If, however, the inflammation be- comes chronic, the walls of the bile ducts may become thickened and their lumina more or less permanently obstructed. In consequence of this, dilatation or ulceration of the bile ducts may ensue. Tem- porary obstruction of the bile ducts may produce marked pigmenta- tion of the liver, owing to the accumulation of pigment granules in the liver cells, particularly in the vicinity of the capsule of Glisson, and jaundice of the entire body. The gall bladder may be inflamed by itself—cholecystitis—or in connection with inflammation of the biliary passages. If the disease is chronic the wall of the bladder may be thickened; polypoid growths may occur in the mucosa; the duct may be occluded; dila- tation, ulceration, the formation of gall stones, calcification, and atrophy may ensue. Inflammation of the stomach and duodenum, hyperzemia and inflammation of the liver, concretions, and parasites are the usual causes of catarrhal inflammation of the biliary passages, but it may occur without these. SUPPURATIVE AND CROUPOUS INFLAMMATION OF THE BILE DUCTS (ANGIOCHOLITIS). The walls of the ducts may be covered or infiltrated with a fibrin- ous or a purulent exudate; they may ulcerate. These lesions occur most frequently in connection with obstruc- tion of the bile ducts by gall stones or otherwise, and in typhoid and typhus fever, pyeemia, cholera, or they may be due to the extension of inflammatory processes from without. They also occur under un- known conditions. Digitized by Microsoft® 618 THE LIVER. In many cases of inflammation of the gall ducts, the Bacillus coli communis, in fewer, the pyogenic streptococcus and staphylococcus are apparently concerned. Suppurative inflammation may produce perforations of the ducts or bladder, with escape of bile and peritonitis; or fistulous openings between the gall bladder and the duodenum, colon, and stomach, or through the abdominal wall. Or the inflammation may extend to the liver tissue and produce abscesses. Under the latter conditions we may find a series of small abscesses ranged along the walls of the suppurating gall ducts. In more advanced stages the abscesses may become large and communicate with one another, so that a con- siderable portion of the liver may be occupied by a series of com- municating cavities with ragged walls, containing pus and detritus of liver tissue more or less tinged with bile. Such abscesses may become more or less completely enclosed by conective-tissue walls. The portal vein may also become inflamed, and perforations may be formed between it and the bile ducts. Constriction and Occlusion may be produced by inflammation of the ducts themselves, by new growths in their walls, by calculi or parasites in their lumina, by changes in the hepatic tissue in chronic and acute hepatitis, by aneurisms, or by pressure on the duct from without, as by tumors in the head of the pancreas, etc. The obliteration of the smaller bile ducts produces no marked lesions. When the ductus communis or the hepatic duct is ob- structed, the ducts throughout the liver are frequently dilated and the liver tissue bile-stained. The liver may undergo atrophy and the whole body be intensely jaundiced. When the cystic duct is ob- structed the gall bladder is dilated. Dilatation of the bile ducts is usually produced by strictures in the ways just mentioned, or by calculi. When calculi have pro- duced the dilatation this condition may sometimes continue after they have found their way into the intestines. Sometimes, however, we meet with very marked dilatation of the bile ducts without being able to make out any present or past obstruction. The dilatation may affect only the common and hepatic ducts, or it may extend to the smaller ducts in the liver, which are then dilated uniformly or sacculated. They may contain bile, mucus, or calculi. The liver is at first enlarged, but may afterward atrophy. The gall bladder may be dilated in consequence of obstruction of the common or the cystic duct. In the latter case it may reach an immense size and form a large tumor in the abdominal cavity. The dilatation is generally uniform, the bladder retaining its normal shape ; sometimes, how- ever, there are diverticula, which are usually produced by calculi. If the obstruction to the hepatic duct is incomplete or movable the Digitized by Microsoft® THE LIVER. 619 gall bladder may contain bile, and often calculi. If the obstruction is complete the contained fluid may gradually lose its biliary char- acter and become a serous or mucous fluid of a light-yellow color— hydrops cystidis felle. The walls of the bladder may be of nor- mal thickness, or thinned, or thickened, or calcified. If the obstruc- tion is due to a calculus, this may pass into the intestine and the gall bladder be suddenly emptied. Usually the bladder fills again, owing to its loss of contractile power. Biliary Calculi.—These bodies are of common occurrence. They are found usually in the gall bladder, sometimes in the hepatic, cystic, and common ducts ; less frequently in the small ducts of the liver. In the gall bladder from 1 to 7,800 calculi have been counted, as FG Fig. 301.—ADENOMA OF THE GALL Duct. This section isfrom a small tumor growing within one of the larger gall ducts within the liver. Prepared by Dr. Larkin. They vary in size from that of a pin’s head to that of a hen’s egg, or they may belarger. Single gall stones are usually spheroidal or ovoid- al; when multiple they are usually flattened at the sides or faceted. They may be composed : 1. Principally of cholesterin, and may be of pure white color, or tinged with various shades of yellow or brown by bile pigment. The fractured surface shows a radiating crystalline structure. 2. Of cholesterin, bile pigment, and salts of calcium and magnesium. These are usually dark-colored, brown, reddish-black, or green, and may be spheroidal or faceted, smooth or rough on the surface ; the fracturedsurfageis yguallyxadiating crystalline. This is the most common form, 620 THE LIVER. 3. Principally of bile pigment. Such calculi are rare, usually small, very dark-colored, and not numerous, 4, Of calcium carbonate. These are rare, have a nodular surface, and a clear crystalline, not radiating fracture. Most calculi are formed around a central mass, sometimes called the nucleus, which may consist of cholesterin, bile pigment, mucus, or epithelium, or more rarely of some foreign body. Thus a dead parasite, a needle, and fruit seeds may serve as nuclei. The body of the calculus may be homogeneous, or lamellated, or crystalline. Biliary calculi in the gall bladder may produce no symptoms and only be discovered after death. In the hepatic and common ducts they may obstruct the flow of bile and produce fatal jaundice ; or they may pass from time to time into the intestine, producing biliary colic. If they are impacted in the cystic duct they may produce dila- tation of the gall bladder. They may get into the duodenum by ulceration through the walls of the ducts or gall bladder, or in the same way into the peritoneal cavity. Gall stones which get into the intestinal cavity usually pass off without doing any further injury, but very large calculi may cause occlusion of the gut with fatal results. TUMORS OF THE GALL BLADDER AND LARGER GALL DUCTS. Small fibromata have been described in the gall bladder and in the common duct, but they are very rare. The most common tumors are carcinomata., These may be primary or secondary, and present the usual structural variations. The cells may be cylindrical, poly- hedral, or they may present the characteristics of colloid cancer. Primary carcinomata of the gall bladder and larger gall ducts are not uncommon. Not infrequently the pancreatic and common ducts are both involved, and it is difficult to say whether the tumor is primary in the head of the pancreas or in the gall duct. The bladder and ducts may also be secondarily involved in carcinomata of the stomach, liver, and duonenum. Adenoma of the gall ducts is of occasional occurrence (Fig. 301). Digitized by Microsoft® THE SPLEEN, In studying the alterations produced in the spleen in disease it is important to bear in mind the peculiar relations in which this organ stands to the blood vessels and to the circulation. After passing through the various branches of the splenic artery and the limited systems of capillaries which are associated with it, the blood is not received at once into venous trunks, as in other parts of the body, but is poured directly into the pulp tissue. In this it circulates, un- der conditions which render it liable to stagnation and undue accu- mulation, before it is taken again into well-defined vessels through the open walls of the cavernous veins. Moreover, these conditions, naturally unfavorable to undisturbed and vigorous circulation, are reinforced by the association of the splenic with the sluggish and often interrupted portal circulation. Bearing these considerations in mind, it will be in a measure plain why, asis in fact the case, the spleen should be more liable to alterations in size than any other or- gan in the body, and why, serving as it does as a sort of blood filter, it should be especially susceptible to the influence of deleterious ma- terials of various kinds which in one way or another gain access to the blood. In this respect the relations of the spleen to the blood, and of the lymph nodes to the lymph, present suggestive analogies, WOUNDS, RUPTURE, AND HAMORRHAGE. Wounds of the spleen are usually accompanied by extensive hemorrhage and are commonly fatal. Death usually occurs as the result of this hemorrhage, but it may be due to secondary inflam- matory changes. Healing and recovery may, however, occur. Rupture of the spleen may be traumatic or spontaneous. In the former case it may be due to direct violence in the region of the or- gan or to injury to the thorax, falls, etc. In certain diseased condi- tions the spleen is more liable to rupture than when it is normal. The rupture usually involves not only the capsule, but a more or less considerable portion of the parenchyma, and of course leads to Digitized by Microsoft® 622 THE SPLEEN. hemorrhage. Spontaneous rupture is rare, but may occur as the result of excessive enlargement of the organ, as in typhoid fever, malaria, ete.—see below—or as the result of abscess. Hemorrhage.—Aside from the extensive hemorrhages from in- jury and rupture, the spleen may be the seat of small circumscribed hemorrhages in various infectious diseases, although, owing to the peculiar distribution of the blood, it is often very difficult to distin- guish between a moderate interstitial hemorrhage and hyperemia. DISTURBANCES OF THE CIRCULATION. Anemia.—This may be associated with general anemia, but it is not always present in this condition When marked and unasso- Fid. 802.—CoNGESTION OF THE SPLEEN. b, dilated cavernous veins; c, trabecule of pulp tissue compressed between dilated cavcrnous veins; d, glomerulus. ciated with other lesions the spleen is apt to be diminished in size, the capsule more or less wrinkled, the cut surface dry and lighter in color than normal, the trabecule unduly prominent. In this, as in other alterations simply of the blood content of the spleen, neither the gross nor microscopical appearances are constant, because of the redistribution of blood which is apt to occur in the viscera after death. Hyperceemia.—This may be passive, occurring when some ob- struction to the portal circulation exists, most frequently in cirrho- sis of the liver, but also with certain valvular lesions of the heart, emphysema, etc. The spleen is enlarged, but usually only to a moderate degree. The capsule is apt to be tense, and on section the Digitized by Microsoft® THE SPLEEN. 623 pulp is dark-red and may be soft or firm. The cavernous veins are dilated (see Fig. 302). Usually, when the lesion has existed for some time, there is a thickening of the trabeculae and reticular framework of the spleen, so that they are prominent on section. In other words, there is a chronic interstitial splenitis following the chronic congestion. : Active Congestion of the spleen, which in most cases is scarcely to be differentiated from some forms of acute inflammation, and probably in many cases is associated with it, very frequently occurs in a great variety of acute and infectious diseases, such as typhoid fever, pneumonia, diphtheria, pyeemia, the exanthemata, etc. The spleen is enlarged, the capsule tense; on section the pulp is soft, dark-red in color, often swelling out from the cut surface and con- cealing the glomeruli and trabecule. Under these conditions we may find the cavernous veins distended with blood and the inter- stices of the pulp infiltrated with a variable, sometimes large quan- tity of red and white blood cells. Or wemay find, in addition to this, an increase in cells, which characterizes acute inflammation or hy- perplasia of the spleen (see below). Infarctions of the Spleen.—Kmbolic infarctions of the spleen are of frequent occurrence. They may be single or multiple, small or very large, sometimes occupying half of the organ. They are in general approximately wedge-shaped, corresponding to the area of tissue supplied by the occluded artery. They may be hemorrhagic, z.e., red, or they may be white (see page 62). Infarctions, originally red, may become white after a time from changes in the blood pig- ment. They may usually be seen as dark-red, reddish-white, or white, hard, sometimes slightly projecting areas on the surface of the organ. Not infrequently the centre of the infarction is light in color, while the peripheral zone is dark-red. A layer of fresh fibrin is sometimes seen over the surface of the infarction. The general as well as the microscopical appearances which they present depend largely upon the age of the infarction. In the earlier stages the hemorrhagic infarctions present little more under the microscope than a compact mass of red blood cells, among which may be seen the compressed necrotic parenchyma. The white infarction may show at first ina general way the usual splenic structure, but the entire tissue is in a condition of coagulation necrosis. The tissue may disintegrate and soften, and be more or less completely ab- sorbed, with or without fatty degeneration. A zone of inflamma- tory tissue may appear around the infarction and upon the capsule, and this tissue, becoming denser, assumes the characters of cicatri- cial tissue and contracts around the unabsorbed remnant of the in- farction, so that finally nothing may be left but a dense mass of Digitized by Microsoft® 624 THE SPLEEN. fibrous tissue, which frequently draws in the surface, causing more or less distortion of the organ. This cicatrix may be pigmented or white. If the embolus be of an infectious, irritating nature, in addition to its mechanical effects there may be suppuration, gangrene, and the formation of abscess. There may be perforation of the capsule and fatal peritonitis. INFLAMMATION. Acute Hyperplastic Splenitis (Acute Splenic Tumor).—The conditions under which acute inflammation of the spleen occurs have already been mentioned under active hyperemia, with which it is usually associated. Itisa frequent though not a constant ac- companiment of the acute infectious diseases, and seems in all cases to be a secondary lesion. The spleen is enlarged, sometimes to two or three times its normal size. On section the pulp is soft, often almost diffluent, and projects upon the cut surface. The color is sometimes dark-red, sometimes grayish-red, or mottled red and gray. The trabecule and glomeruli are usually concealed by the swollen and softened pulp, but the glomeruli are sometimes unusually promi- nent. Microscopical examination shows the marked increase in size to be due in part to the hypereemia; in part to a swelling and increase in the number of cells, sometimes of the pulp, sometimes of the glomeruli, or of both. We find large, multinucleated cells; cells resembling the ovoidal and polyhedral cells of the pulp, but larger and with evident division of the nuclei. Cells resembling leuco- cytes may be present in large numbers, and larger and smaller cells in a condition of fatty degeneration, or containing pigment, are often seen. The elongated cells lining the cavernous veins may be swollen or increased in number. Not infrequently larger and smaller cells are found which contain structures looking like red blood cells or their fragments. In some cases, particularly in scar- latina, hyperplasia of the glomeruli is a prominent feature. In some cases, particularly in typhus and recurrent fevers, the cells of the glomeruli undergo marked degenerative changes, so that they may form small softened areas looking like little abscesses. Small ne- crotic areas, often associated with localized suppuration, are some- times found in typhus and typhoid fever, scarlatina, etc., and may be due to infectious emboli. As the primary disease runs its course the swelling of the spleen subsides, the capsule appears wrinkled, the color becomes lighter, and sometimes the organ remains for a long time, or permanently, small and soft. The cause of these marked changes in the spleen in infectious diseases is not understood. It seems probable that they are due to Digitized by Microsoft® THE SPLEEN, 625 the lodgment in the organ of some deleterious materials which have found access to the blood. Whether these materials are bacteria, or products of the life processes of bacteria, or something entirely apart from these, we do not in many cases know. Bacteria have, indeed, in many cases been found in the organ under these condi- tions, but by no means with the frequency and abundance which the commonness and prominence of the lesion would lead us to expect if it were in all cases due to their presence. Suppurative Splenitis (Splenic Abscess).—Small abscesses may be found in the spleen as the result of minute infectious emboli, and these may coalesce to form larger abscesses ; but larger and smaller abscesses may form in the spleen without evidence of their embolic origin. Sometimes the entire parenchyma is converted into a soft, necrotic, purulent mass surrounded by the capusle. Itis rare for simple infarctions to result in abscess, but it does occasionally occur. Abscess of the spleen may occur from the propagation of a suppu- rative inflammation to the organ from adjacent parts ; from peri- nephritic abscesses, ulcer and carcinoma of the stomach, ete. Ab- scesses of the spleen may open into the peritoneal cavity, inducing fatal peritonitis, or, owing to an adhesive inflammation, the opening may occur into the post-peritoneal tissue, into the pleural cavity, lung, stomach, intestines, or it may open on the surface. On the other hand, the contents of the abscess may dry, shrink, and be- come encapsulated and calcified. Abscesses may occur in ulcera- tive endocarditis, pyeemia, typhoid fever, and more rarely in inter- mittent fever, and under a variety of other conditions whose nature is unknown to us. Chronic Indurative Splenitis (Chronic Splenic Tumor).—There may be, as we have already seen, a new formation of connective tissue in the spleen as a result of chronic congestion or infarctions, or about abscesses, But there is a more diffuse formation of con- nective tissue, usually in the nature of an hyperplasia, which oc- curs under a variety of conditions, and is now marked and exten- sive, and again comparatively ill-defined. It is always associated with more or less extensive changes in the parenchyma. In its most marked form it is found in chronic malarial poisoning, and under these conditions it may be found not only in persons who have suffered from repeated attacks of intermittent fever, but also in those who have not thus suffered but have resided in malarial regions. The enlarged spleen is often called ‘‘ague cake.” Similar condi- tions, though usually less marked, may occur in congenital and ac- quired syphilis, from prolonged typhoid fever, and as a result of acute hyperplastic splenitis from various causes, and also in leukeemia Anse ati louie: ae. Digitized by Microsoft® 626 THE SPLEEN, The gross appearance of the spleen in chronic indurative splenitis varies greatly, both in the size of the organ and in the appearance of the section. The spleen may be enormously enlarged or it may be of about normal size. Itis usually, however, enlarged. The cap- Fig. 303.—Curonic InpURATIVE SPLENITIS. Showing swelling or proliferation of the lining cells of the cavernous veins. sule is usually more or less thickened, frequently unevenly so. The consistence is usually considerably increased, but this is not always the case. The color and appearance of the cut surface present Fia. 304.—CHronic INTERSTITIAL SPLENITIS. a, thickened capsule; b, thickened trabecule; c, dilated cavernous veins; d, dense pulp tissue with obliterated cavernous veins. much variation. It may be nearly normal or it may be grayish, or dark-brown, or nearly black. The color may be uniform or the sur- face may be mottled. The glomeruli may be scarcely visible or Digitized by Microsoft® THE SPLEEN. 627 ‘very prominent ; the trabecule are in some cases nearly concealed by the pulp ; in others they are large, prominent, and abundant, so that the surface is crossed in all directions by an interlacing network of broader and narrower irregular bands, between which the red or brown or blackish pulp lies. Not less varied are the microscopical appearances of the spleen sander these conditions. In one class of cases there is more or less uniform hyperplasia of both pulp and interstitial tissue. The paren- chyma cells are increased in size and number ; there may be swell- ing and proliferation of the lining cells of the cavernous veins (see Fig. 303). The reticulum of the pulp, as well as that of the glome- ruli, and also the trabeculw, are thickened. In another class of cases the thickening of the reticular and trabecular tissue, either uni- formly or in patches, is the prominent feature (Fig. 304), while the changes in the pulp are rather secondary and atrophic. In both forms irregular pigmentation is frequent, the pigment particles being Fig. 305.—_MauariaL SPLEEN. ‘Showing thickening of the trabecular network of the pulp, with pigmentation of the pulp cells. deposited either in the cells of the pulp or glomeruli, or in the new- formed interstitial tissue (Fig. 305). Finally, there are all interme- diate forms of induration between those described, and the changes are by no means uniform in the same organ. When these spleens are large they are liable to displacement. Syphilitic Splenttis.—This lesion may present itself as an in- durative process due to the formation of new connective tissue, and present no distinct morphological characteristics. In rare cases, however, gummata may be present in connection with the new fibrous tissue; then the nature of the lesion becomes evident. Tuberculous Splenitis.—This lesion is secondary, either to tuber- cular inflammation in some other part of the body, or is the result of the general infection in acute general miliary tuberculosis. The tuber- cles may be very numerous and still invisible to the naked eye, or they may be just visible, or as large as a pin’s head or thereabouts, and very thickly strewn through the organ or sparsely scattered. In other Digitized by Microsoft® 628 THE SPLEEN. cases the tubercles are larger, sumetimes as large as a pea, and they are then usually not very numerous. Microscopically they present the usual variety of structure, sometimes as simple tubercle granula, sometimes as conglomerate tubercles ; they may consist simply of a collection of small spheroidal cells, or there may be larger polyhedral cells and giant cells with a well-defined reticulum. Cheesy degene- ration occurs under the usual conditions. Tubercle bacilli are usu- ally present, particularly in the more acute forms, sometimes in small, sometimes in enormous numbers. They seem to be especially abundant in acute general miliary tuberculosis of children. These tubercles may be formed in the glomeruli, in the walls of the smaller arteries, in the pulp tissue, and in the trabecule and capsule. Owing to the peculiar character of the spleen tissue the earlier stages are not readily recognized, since simple collections of small spheroidal cells are not distinctly outlined against the normal tissue. There is frequently a moderate swelling of the spleen, owing to hyperemia and hyperplasia of the parenchyma. Perisplenitis.—Acute inflammation of the capsule of the spleen may occur as a part of a general or localized peritonitis, or as a re- sult of lesions of the spleen itself, such as infarctions, abscesses, and acute hyperplastic inflammation. Under these conditions a fibrinous pellicle, with more or less pus, may be formed on the surface of the organ. Chronic perisplenitis, resulting in the production of new connective tissue, either in patches or as a more or less general thick- ening of the capsule, is of frequent occurrence. It may follow acute inflammation of the capsule, or be a part of general or localized chronic peritonitis. It is common in connection with chronic indura- tive splenitis, and it may occur from unknown causes. Sometimes the capsule is three or four mm. in thickness over a considerable area; sometimes very small nodular thickenings or papillary projec- tions occur. Asa result of this process adhesions, sometimes very extensive, may form between the spleen and adjacent parts. The thickened capsule is sometimes more or less extensively calcified. Alterations of the Spleen in Leukemia and Pseudo-Leukcemia. —The lesions of the spleen are essentially the same under both of these conditions. They consist, in general, of an hyperplasia, some- times most marked in one, sometimes in another of the structural elements of the organ, but usually they all participate in the altera- tions. The changes which occur in the earlier stages are but little known. The gross appearances of the spleen, as we find them in persons dying of either of the above diseases, present considerable variation. They are usually enlarged and sometimes are ten or fifteen times the normal size. They are usually hard, but are some- times of the ordinary consistence, or softer. The capsule is usually Digitized by Microsoft® THE SPLEEN. 629 thickened and rough. The section of the spleen may be of a uniform dark-red color, but it is more frequently mottled red and gray. Sometimes the glomeruli are inconspicuous, but they are very often enlarged and prominent. They may be two to four mm. in diameter, and, owing to an infiltration of the arterial sheaths with lymph cells, may appear to the naked eye as grayish, round or elongated bodies, arranged along branching, interrupted, grayish streaks. The trabe- cula may be greatly thickened, as also the reticulum of the pulp, so as to be evident to the naked eye. Brown or black pigment may be collected around the glomeruli or in the pulp. Hemorrhagic infarc- tions or circumscribed extravasations of blood may further compli- cate the picture. Microscopically the appearances are essentially the same as those above described in acute hyperplasia and in chronic interstitial sple- nitis, depending upon the stage and variety of the disease. Owing to the great size which some of these spleens attain they are liable to displacement, and they may interfere by pressure with the functions of neighboring organs. DEGENERATIVE CHANGES IN THE SPLEEN. Atrophy.—The spleen may become atrophied in old age; as a result of prolonged cachexia, and in connection with profound and persistent anemia; or, more rarely, from unknown causes. The capsule may be wrinkled and thickened, the color pale, the trabecula prominent, the consistence increased. The change is largely in the pulp, whose parenchyma cells are decreased in number. Amyloid Degeneration.—This degeneration may affect the glo- meruli or the pulp tissue, or both together. When confined to the glomeruli the spleen may or may not be enlarged, and the cut sur- face is more or less abundantly sprinkled with round or elongated, translucent bodies resembling considerably in general appearance the grains of boiled sago. These are the waxy glomeruli. Such spleens are often called ‘‘sago spleens” (Fig. 306). Microscopical examination shows that the degeneration is confined to the walls of the arteries, capillaries, and reticulum of the glomeruli, with atrophy and disappearance of the lymphoid cells. In other cases, either with or without involvement of the glo- meruli, there is waxy degeneration of the blood vessels and reticu- lum of the pulp, which may occur in patches or be general and more or less excessive. If the alteration is general and consider- able the spleen is enlarged, its edges rounded, its consistence in- creased. On section it appears translucent, and the distribution of the degenerated areas may be readily seen by holding a thin slice up to the light. The SREB FB RS Bhar tected, or there may be 600 THE SPLEEN. similar degenerations in other organs. The general conditions under which this lesion occurs, and the methods of staining and studying, are given on page 100, Pigmentation of the spleen may occur as the result of the de- composition of hemoglobin in the organ under a great variety of conditions: thus after hemorrhagic infarctions, small multiple haem- orrhages, acute hyperplastic splenitis, ete. Or the pigment may be anthracotic and be brought to the organs from the lungs or bronchial glands (see page 106). Bile pigment may also be deposited in the spleen in jaundice. The pigment may lie in the walls of the smaller arteries, in the cells and reticulum of the pulp, or free in the latter tissue, or in the follicles. It is usually quite unevenly dis- Fia, 306.—AMYLOID DEGENERATION OF GLOMERULI OF THE SPLEEN—‘“‘SaGo SPLEEN.”’ The ‘“‘ waxy ” portions are stained pink. tributed. The pigment may be red, brown, or black. According to Weigert anthracotic pigment may be sometimes seen with the naked eye in the periphery of the glomeruli as dark crescents. Primary tumors of the spleen are rare. Small fibromata, sar- comata, and cavernous angiomata sometimes occur. Sarcomata and carcinomata may occur in the spleen secondarily either as me- tastatic tumors or by extension from some adjacent part, as the sto- mach. Dermoid cysts are described, but are rare. Other larger and smaller cysts, whose mode of origin is in most cases obscure, not infrequently occur. PARASITES. Pentastomum denticulatum is not infrequently found in the spleen, usually encapsulated and calcified. Cysticercus is rare. Digitized by Microsoft® THE SPLEEN. 661 Echinococcus is occasionally found, and, if the cysts are large or numerous, may cause more or less extensive atrophy of the organ. Various forms of bacteria have been found in the spleen. Micro- cocct have been found in pyemia, small-pox, ulcerative endocar- ditis, diphtheria, and under other conditions. The Bacillus anthra- cis occurs here in anthrax ; the Bacillus tuberculosis in tubercular inflammation; and bacilli have been described in typhoid fever. Spirochete Obermeiert may be found in relapsing fever. MALFORMATIONS AND DISPLACEMENTS, The spleen may be absent in acephalous monsters, and with de- fective development of other abdominal viscera. Very rarely it is absent in persons who are otherwise perfectly developed. Small accessory spleens, from the size of a hazelnut to that of a walnut, are not infrequent. They usually lie close to the spleen, but-may be considerably removed from it; thus they have been found em- bedded in the head of the pancreas. Two spleens of about equal size have been observed. The form of the spleen is subject to con- siderable variation. It may be made up of several distinct lobes. It may be displaced congenitally or as the result of disease. It may be on the right side in transposition of the viscera. As the result of congenital defects in the diaphragm the spleen may be found in the thorax ; or in deficient closure of the abdominal wall it may, together with other abdominal viscera, be found outside of the body. The spleen may be pressed downward by any increase in the con- tents of the thorax. It may be fastened by adhesions to the concave surface of the diaphragm,.so that its long axis is nearly horizontal instead of vertical. It may be displaced by changes in the contents of the abdominal cavity. If the organ is increased in size it fre- quently becomes tilted, so that its lower border reaches the right iliac region. If the ligaments are too long congenitally, or if they are lengthened by traction, and if the organ is at the same time in- creased in weight, it may become very movable. It may sink down- ward, with its hilus turned upward ; or it may be rotated on its axis, and, owing to torsion of the vessels thus produced, the organ may atrophy ; or the pressure of the ligaments and vessels across the duodenum may cause occlusion of the gut. Digitized by Microsoft® THE PANCREAS. The diseases of the pancreas appear, so far as we know, with a few exceptions, to be of little practical importance ; that is, they do not often give rise to symptoms of disease or cause death, but the lesions are found in the bodies of persons dead from other diseases. It is probable, however, that in many cases their apparent insignifi- cance is due to our lack of knowledge of the interference with func- tions which lesions of the gland induce, and to the incomplete exami- nation of the pancreas which is so common at autopsies. Hemorrhage into the substance of the pancreas may occur as the result of injury’; in the hemorrhagic diathesis ; in connection with valvular diseases of the heart or interference with the portal circula- tion; or in connection with extensive fatty degeneration and fat necrosis of the organ. Such hemorrhages may be minute or exten- sive. Several cases of sudden death are recorded in which the only discoverable lesion was an extensive hemorrhage into the substance of the gland’ and the tissue about it. In these cases it has been as- sumed that death was caused by interference with the heart’s action, through pressure on the solar plexus and semilunar ganglion, but it may be due to other causes (see below, Fat Necrosis). The hemor- rhage may be moderate and limited to the pancreas, or it may ex- tend into the subperitoneal tissue for a considerable distance, Hemorrhage of the pancreas may be associated with acute in- flammatory changes and with more or less extensive gangrene of the organ. The gangrenous pancreas may be more or less encapsu- lated ; it may lie, bathed in pus, in the abdominal cavity ; it may, by ulceration of the intestinal wall, get into the gut and be dis- charged with other intestinal contents. INFLAMMATION. In some cases of typhoid fever, pyeemia, yellow fever, and other acute infectious diseases, the pancreas is red, swollen, and cedema- tous. Microscopically the most prominent lesion is a swelling and 1Consult Leth, “Rupture of Pancreas, ” Lancet, September 28th, 1895, Digitized by Microsoft® THE PANCREAS. 635 undue granulation of the glandular epithelium, and hyperemia. This condition is known as Parenchymatous Pancreatitis. Suppurative Pancreatitis is not very common, and may be primary or due to the extension of a suppurative inflammation from adjacent or distant parts of the body. There may be a diffuse infil- tration of the organ, with pus cells or larger and smaller abscesses. The abscesses may open into the gastro-intestinal canal or into the peritoneal cavity. The causes of primary suppurative pancreatitis are often most obscure. It may be associated with fat necrosis and with hemorrhage and gangrene of the pancreas. Chronic Interstitial Pancreatitis (Cirrhosis of the Pancreas).— This lesion consists in an increase of interstitial connective tissue, which may be general or confined to some particular portion of the gland. The organ is sometimes enlarged, sometimes smaller than normal. It is usually dense and hard ; secondary atrophy of the parenchyma regularly occurs. It may be due to chronic inflamma- tory processes in the vicinity of the organ. Syphilitic Inflammation.—Chronic interstitial pancreatitis is frequently found in congenital syphilis of the new-born, and the gross and microscopical lesions are similar to those above described. It is not definitely established whether or not a similar lesion may be caused by acquired syphilis. Gummata are very rare in the pan- creas, but have been described in congenital syphilis in very young children. Tubercuious Inflammation.—Larger and smaller tubercles and tubercular, cheesy nodules are occasionally found in the pancreas in connection with acute general miliary tuberculosis or with tubercular inflammation in some other organ, particularly with that of adjacent lymph nodes, the lungs, and the intestine. DEGENERATIVE CHANGES IN THE PANCREAS. Atrophy of the pancreas may occur in old age and as a result of pressure from tumors or other adjacent structures. Marked atrophy of the pancreas is found in a certain proportion of cases of diabetes mellitus, but it is not constant. Fatty Degeneration of the parenchyma cells may occur, and in some cases is so extensive as to lead to nearly complete destruction of their protoplasm. Fatty Infiltration, which should be distinguished from fatty degeneration, consists in the accumulation of fat in the interstitial tissue of the gland. This may be so excessive as to cause nearly entire destruction of the gland structures. Under these conditions the outline of the organ may be preserved, the fat being enclosed by hi le, ees Digitized by Microsoft® 634 THE PANCREAS. Amyloid Degeneration.—This usually occurs in connection with similar degeneration in other organs, and is confined to the walls of the blood vessels and the interstitial tissue. Fat Necrosis.—A very peculiar lesion of the fat tissue, most frequently seen in the fat tissue about the pancreas or between its lobules, but sometimes in fat tissue in other parts of the body, has been a few times described and called fat necrosis. White or yel- lowish nodules, varying from the size of a pin’s head to that of a pea or larger, are seen embedded in the fat, the central portion being often soft and grumous and readily squeezed out. They are some- times calcified and sometimes surrounded by a connective-tissue Fie. 307.—Fat NECROSIS IN THE PANCREAS. Drawn from a specimen prepared by Dr. Ira Van Gieson and reported to the New York Patho- logical Society, 1888. capsule. Microscopical examination shows degeneration and dis- integration of the fat tissue (Fig. 307). They are most frequently found in marasmatic persons. When the lesion is extensive, accord- ing to Balser, it may cause death, either directly or by inducing hemorrhage. Some of the extensive hemorrhages about the pan- creas, above mentioned, may be caused in this way.’ 1 Fora detailed consideration of acute inflammation, hemorrhage, gangrene, and fat necrosis of the pancreas, with bibliography, consult Witz, Middleton Goldsmith lecture for 1889 on ‘‘ Acute Pancreatitis,” Transactions New York Pathological Society, 1889. For special studies on fat necrosis consult Langerhans, Virchow’s Archiv, Bd. cxxii., p. 252, and in the “‘ Festschrift ” for Virchow’s seventy-first birthday, Digitized by Microsoft® THE PANCREAS. 635 TUMORS. Carcinomata are the most common and important of the tumors of the pancreas. They may be primary or secondary. Primary carcinomata are most frequently found in the head of the organ, but may occur in other parts. The hard or scirrhous form is most com- mon, but occasionally soft and succulent and colloid forms are found. They are liable to involve adjacent parts by continuous growth, and may form metastases in the liver, adjacent lymph nodes, etc. Secondary carcinoma in the pancreas may occur in carcinoma of the stomach, duodenum, and the gall ducts and gall bladder. Asa result of carcinoma of the pancreas, aside from the extension of the growth, there may be pressure on the ductus chole- dochus, with jaundice ; or on the pancreatic duct, with cystic dila- tation ; or pressure on the duodenum, with stenosis of the gut; or pressure on the vena cava, or portal vein, or superior mesenteric vein, etc., with disturbances of the circulation. Concretions of carbonate and phosphate of lime are frequently found in the pancreatic ducts. They are usually multiple, small, whitish, smooth, or of rough and irregular shape. Sometimes, how- ever, they reach a diameter of more than an inch. They consist chiefly of calcium phosphate and carbonate. Besides these free con- cretions the walls of the ducts are sometimes encrusted with salts of lime. Such concretions may produce dilatation of the pancreatic ducts and large cysts, or more rarely abscesses. Foreign Bodies.—Gall stones sometimes find their way into the pancreatic duct. Ascarides have been found in the ducts in a con- siderable number of cases. Cysts.—These are mostly due to dilatation of the pancreatic ducts. 1. The entire duct may undergo a uniform cylindrical dilatation. With this cylindrical dilatation we sometimes find associated small sacculi. 2. There may be sacculated dilatations at some points in the ducts. These dilatations form cysts of large size, as large even as a child’s head. Their walls frequently undergo degeneration and calcification. These cysts often become filled with blood, and may then be mistaken for aneurisms. 3. The small branches of the pancreatic duct may be dilated so as to form a number of small cysts. These cysts are filled with serum, mucus, pus, or a thick, cheesy material. Cysts of the pancreas may result from old areas of necrosis or hemorrhage, and in other ways.’ 1 Consult Tilger, “ Cysts of Pancreas, ” Virch. Arch., Bd. exxxvii., 848 (bibliog- aphy). ee Digitized by Microsoft® 636 THE PANCREAS. MALFORMATIONS AND DISPLACEMENTS. The pancreas may be entirely absent in anencephalous and double monsters, and in congenital umbilical herniw. The pancreatic duct may be double; it may open into the duodenum at some distance from the biliary duct, or into thestomach. The head of the pancreas may be unduly developed, and sometimes even completely separated from the rest of the organ, opening into the duodenum with a duct of its own. Occasionally there is a small accessory pancreas situated beneath the serosa of the duodenum or stomach. The pancreas is so firmly bound down that its position is not often changed. Sometimes, however, it is found pressed downward by tight lacing, displaced by aneurisms, or contained in umbilical and diaphragmatic hernia. Digitized by Microsoft® THE SALIVARY GLANDS. THE PAROTID, SUBMAXILLARY, AND SUBLINGUAL. INFLAMMATION, This condition is most frequent and important in the parotid. The lesions of the epidemic disease known as mumps are most fre- quently confined to the parotid gland of one side, but the submaxil- lary and sublingual may be at the same time involved. The gland is swollen and there is often cedema of the mucous membrane of the mouth and pharynx. Very little is known of the actual minute changes which the gland undergoes in this disease. Acute parotiditis occasionally occurs as a secondary lesion in a variety of diseases, as in typhoid and scarlet fever, pyzemia, pneu- monia, etc., and by propagation of inflammation from the mouth. Under these conditions the inflammation is usually suppurative and frequently results in abscess or sloughing. The interstitial tissue of the gland is more or less densely infiltrated with pus cells, and the parenchyma cells may undergo fatty degeneration and disin- tegration. The inflammation may be confined to the gland or it may spread to adjacent parts, sometimes causing much destruction of tissue, and may give rise to inflammation of the brain or of the inner ear, or even to metastatic pyzemic abscesses in different parts of the body. Healing may occur, with the formation of salivary fistulee. The submaxillary gland may be involved with the parotid in the suppurative inflammation. Acute suppurative inflammation of the connective tissue about the submaxillary gland is sometimes of serious import. Sloughing and gangrene may occur and are apt to spread to adjacent parts. Septiczemia, cedema of the glottis, or pneumonia may complicate the process and cause death. The sublingual gland is not often the seat of inflammation. Chronic inflammation, leading to the formation of dense inter- Digitized by Microsoft® 638 THE SALIVARY GLANDS. stitial tissue, sometimes occurs in the salivary glands. This may occur by itself or follow an acute inflammation. The Excretory Ducts of the salivary glands may become inflamed from the presence of foreign bodies or of concretions formed in them. They may become occluded from the presence of calculi or as the result of inflammation, and may thus become widely dilated both in the main branches and in the finer ramifications. The dilatation of Wharton’s duct to form larger and smaller cysts containing salivary fluid, sometimes gives rise to very large and troublesome tumors which constitute one of the forms of ranula. TUMORS. Fibromata are of occasional occurrence in the parotid. Chon- dromata, endotheliomata, sarcomata and fibro-sarcomata, and myxomata; or more frequently mixed tumors formed of varied com- binations of these, are of frequent occurrence in the parotid and of occasional occurrence in the submaxillary gland. These complex or mixed tumors are of more frequent occurrence in these glands than in any other part of the body, except possibly the ovary. They are sometimes rendered still more complicated in structure by the forma- tion of cysts, and what has been regarded usually as an atypical glandular growth, lending them an adenomatous character. The more recent studies upon the mixed tumors of the salivary glands, however, have led to the belief that a large part of these complex growths are endotheliomata, which are especially prone in these regions to undergo secondary degenerative or metaplastic changes.’ Carcinomata of the salivary glands are rare. Fibro-sarcoma and melano-sarcoma have been described. Pri- mary carcinoma of these glands is very rare. A case of rhabdomyoma of the parotid gland, with evidences of atypical development of portions of the gland, has been described by one of us.” PARASITES. Echinococcus has been observed in the parotid gland. ' Volkmann, Deutsche Zeits. f. Chir., Bd. xli., p. 61. ” Prudden, ‘‘Rhabdomyoma of the Parotid Gland,” American Journal of the Medical Sciences, April, 1888. Digitized by Microsoft® THE THYROID GLAND.’ Hypereemia of the thyroid gland, often accompanied by consider- able enlargement of the organ, may be the result of valvular disease of the heart; it occurs in Basedow’s disease; it may be temporary or permanent, and in the latter case may give rise to the formation of new connective tissue. Hzemorrhages may occur, causing pigmen- tation of the organ. Inflammation of the thyroid gland is not very common and may occur from a variety of causes. It may result in the formation of larger and smaller abscesses or in the production of new connective tissue. Tuberculous inflammation, with the formation of miliary tubercles, is of infrequent occurrence. Syphilitic inflammation, with the formation of gummata, has been described, but is rare. Degeneration.—Colloid degeneration of the epithelial cells of the gland, and the filling of the alveoli with colloid material, is of common occurrence, and when occurring in moderate degree may be regarded as a normal event, since a certain amount of this change is found in many otherwise apparently normal glands. It may occur, however, to such an extent as to constitute a lesion (see below). Amyloid degeneration, particularly of the blood vessels, is of in- frequent occurrence. Hyaline degeneration of the stroma of the thyroid may occur. Inflammation (Thyroiditis).—Suppurative inflammation of the thyroid is of occasional occurrence. Chronic interstitial inflamma- tion, and tuberculous and syphilitic inflammation are rare. TUMORS. Among the most important of the lesions of the thyroid is the en- largement of the organ commonly known as the gottre or struma. The enlargement of the gland may occur in several different ways, and in only a part of the cases is to be considered as a tumor. Thus, a simple hyperemia may, as above stated, cause considerable en- largement of the organ, and this is sometimes called struma hyper- 1 For a study of the normal and pathologic histology of the thyroid, with bibli- ography, consult Muller, Ziegler’s Beitr. z. path. Anat., etc., Bd. xix., p. 127, 1896. Digitized by Microsoft® 640 THE THYROID GLAND. cemica. The true goitre, however, consists in the enlargement of the old and the formation of new gland alveoli, while with these changes there is very frequently associated a greater or less amount of colloid degeneration. When there is new formation of gland tissue the growth has the character of an adenoma. The hyperplasia may occur diffusely, so that the whole gland is more or less enlarged; or it may occur in the form of circumscribed nodules. When the col- loid degeneration is prominent, so that the tumor has a gelatinous look, it is called colloid struma (Fig. 308).’ Accumulations of fluid, blood, colloid, etc., in the old or new-formed alveoli, may cause dilatation and atrophy of the walls of the alveoli, so that cysts, some- Fig. 308,—CoLttom Struma—GoitRe. The colloid materia) filling the alveoli is stained red, times of large size, are formed. Thus occurs the cystic struma. Again, the blood vessels may undergo marked dilatation, so that we may havea telungiectatic struma,; or cavernous angiomata may form within them. Very frequently all these varieties of lesions are present in the same goitre. The appearances may be rendered still more complex by the occurrence of haemorrhages and pigmentation, calcification, purulent or indurative inflammation (strumitis), and by the not very infrequent association with carcinoma and sarcoma. The cause of goitre is not well understood. The growth is, asa rule, 'For a consideration of the nature of colloid and its formation in struma see —einbuch, Ziegler’s Beitr. z. path. Anat., etc., Bd. xvi., p. 596 (bibliography). Digitized by Microsoft® THE THYROID GLAND. 641 slow, but occasionally a very rapid enlargement occurs as the result of a sudden increase of the colloid degeneration. In many cases even ‘very large goitres give rise to but moderate inconvenience, but they aay assume great significance by encroaching upon neighboring parts. ‘Thus death may be caused by pressure on the trachea, cesophagus, or on the large vessels. Sarcoma, either spheroidal or spindle-celled, may occur as primary ‘tumors in the thyroid, either in otherwise normal glands or in con- nection withstruma. Melano-sarcoma hasbeen observed. Second- ary sarcomata are rare. Primary carcinoma, both glandular and scirrhous, occurs in the thyroid, and, particularly in the softer forms, may spread to adja- -cent parts and occasionally form distant metastases. PARASITES. Echinococcus cysts have been found in the thyroid. MALFORMATIONS. The thyroid gland is sometimes very small, either as the result of atrophy or as a congenital deficiency. This is most marked in the -condition called myxcedema (see below). It'may be irregularly lobulated. There may be small accessory glands situated at some distance from the normal position, as in the mediastinum or pleura. MYXC@DEMA. This disease occurs most frequently in middle-aged women, and its cause is unknown. The skin of the face is apt to be swollen and waxy, causing a peculiar and rather characteristic appearance of the features. The skin of the body is apt to be dry and rough, and the hair may fall out. Perspiration is, as a rule, diminished. The men- tal condition is dull, and loss of memory and insanity may occur. Bodily movement and speech are apt to be impaired. The fat tissues may be atrophic, and the subcutaneous tissue has ‘been shown in some, though not all, of the cases to contain an un- usual amount of mucin. In some cases the fibres of the upper layers of the corium are crowded apart by fluid. The most marked and constant lesion in this disease is an atrophic condition of the thyroid gland. The parenchyma of the gland is more or less completely replaced by fibrillar connective tissue and by -‘new-formed reticular tissue resembling the lymphatic tissue of the lymph nodes. The general appearance of the atrophied thyroid gland is shown in Fig. 309. In a case reported by Hun, which one of us has examined, the 51 Digitized by Microsoft® 642 THE THYROID GLAND. lobes of the thyroid measured less than one-half of an inch in dia- meter, and the entire gland weighed only about 7.2 gm. (112 grains). In addition to the lesion of the thyroid there are apt to be chronic endarteritis and chronic diffuse nephritis. In some cases there is an accumulation of small spheroidal cells about the smaller blood vessels in various parts of the body, and also petechial hemorrhages. While the atrophy of the thyroid is the most marked and frequent lesion in this disease, our lack of knowledge about the function of this gland prevents a definite conception as to the relationship of this change to the symptoms. By the destruction of the thyroid from disease, or as the result of its removal in men and animals, a condition considerably resembling myxcedema is apt to be induced. Fie. 309.—SEcTION OF THE ATROPHIED THYROID GLAND IN MYxX@DEMA. a, interstitial tissue; b, atrophied lobules with small spheroidal-celled or lymphatic tissue in their peripheries. Myxcedema appears to be identical with that condition which has been described as cachexia strumipriva.' The relationship of an atrophied thyroid to sporadic cretinism is worthy of investigation.’ 1 For detailed descriptions of myxcedema, and the literature, see Hun and Prud- den, “ Myxeedema,” Am. Jour. Med. Sciences, July and August, 1888, and “Report on Myxedema” in Supplements to the Clinical Society Transactions, vol. xxi., London, 1888. 2 Consult Osler, “Sporadic Cretinism in America, ” Trans. Assn. Am, Phys., vol. v., p. 880, 1898, and yes, N. Y. Med. Jour., March 14th, 1896. Digitized by Microsoft® THE THYROID GLAND. 643 EXOPHTHALMIC GOITRE. (Basedow’s Disease, Graves’ Disease.) The characteristic lesions of this disease are unilateral or bilateral enlargement—largely hypereemic—of the thyroid and protrusion of the eyeballs. These lesions are apt to be associated with functional disturbance of the heart.’ THE THYMUS. Small accessory thymus glands are occasionally found near the thyroid. The thymus occasionally but not usually persists until youth or middle age instead of undergoing the usual developmental atrophy. Small heemorrhages are described in the thymus of young chil- dren as the result of venous congestion in asphyxia, etc. They may also occur in the hemorrhagic diathesis. Suppurative inflammation of the thymus is of occasional occur- rence, and is usually secondary to a similar inflammatory process in some other part of the body. Tubercular and syphilitic inflammation of the thymus are de- scribed. The sarcomata are the most common tumors of the thymus.’ 1 On the relationship between the thyroid and Basedow’s disease consult Hulen- berg, Deutsche med. Wochensch., October 4th, 1894; also Edmunds, Jour. of Path- ology and Bacteriology, vol. iii., p. 488, 1896; Fwrner, Virchow’s Archiv, Bd. exliii., p. 509, 1896 (bibliography) ; Kénnteutt, Med. Record, April 18th. ? On the relationship of hyperplasia in a persistent thymus to Hodgkin’s disease consult Brigidt and Piccoli, Ziegler’s Beitr. z. path. Anat., etc., Bd. xvi., p. 388. Digitized by Microsoft® THE SUPRARENAL BODIES—ADREN ALS,’ MALFORMATIONS. In acephalic and other monsters the suprarenal capsules may be atrophied or entirely absent. Sometimes in well-formed adults these organs cannot be discovered. There may be little rounded nodules loosely attached to the surface of the capsules and having the same structure. Accessory and misplaced adrenals are not uncommon. If one of the kidneys is absent or in an abnormal position its suprarenal capsule usually retains its proper position. HAMORRHAGE, In children, soon after birth, it is not very infrequent to find large heemorrhages in one of the capsules, converting it into a cyst filled with blood. The same lesion has been observed in a few cases in adults. THROMBOSIS. Klebs describes a case of capillary thrombosis of the cortex in both capsules in a woman after excision of the knee joint. INFLAMMATION. Suppurative inflammation, with the formation of abscesses, has been seen in a few cases. The most frequent lesion of the suprarenal capsules is tuberculous inflammation. They are usually increased in size, their surfaces are smooth or nodular. The normal structure of the gland is lost, and is replaced by tubercle tissue, connective tissue, and cheesy matter (see Addison’s Disease). Syphilitic inflammation, with and without the development of gummata, is of occasional occurrence. 1 For consideration of relatio.ship of adrenals to nervous system see Alexander, Ziegler’s Beitr. z. path. Anat., Bd. xi., p. 145 (bibliography). Digitized by Microsoft® THE SUPRARENAL BODIES—ADRENALS. 645 DEGENERATION. Fatty degeneration of the cortical portion of the capsules is the rule in the adult. It sometimes occurs in nodular areas. In chil- dren under five years of age it is a pathological condition. Amyloid degeneration may involve both the cortical and medul- lary portions. In the cortex it usually involves only the walls of the blood vessels; in the medulla both the blood vessels and the cells of the parenchyma may undergo this degeneration. The capsules are usually firm and of a grayish, semi-translucent color. Pigmentation of the inner cortical zone is frequent in old persons. TUMORS. Carcinoma of the adrenals is not common. It may be primary, but is much more frequently secondary. Either one or both of the capsules may be the seat of the new growth. Sarcoma occurs as a primary and secondary growth. Probably many of the older cases described as cancers were really sarcomata. Cylindroma.—Klebs describes a growth of this character in one of the adrenals, secondary to a tumor of the same kind in the supra- orbital region. He gives to such tumors the name of lymphangioma cavernosum. The exact character of these growths is still obscure. They consist of irregular follicles and cavities, lined with epithelium, and containing peculiar hyalin, structureless bodies. Cysts are found, both single and multiple. They are usually situated in the cortex. Neuroma.—Ganglionic neuromata have been described by Weich- selbaum and Freeman. Glioma has been described as occurring in the medullary region. An hyperplasia of the gland tissue (adenoma or struma lipoma- tosa suprarenalis) with fatty degeneration in the form of circum- scribed nodules, is described by Virchow and others. Some of the so-called adenomata of the kidney are probably ade- nomata of displaced accessory adrenals.’ 1Consult Ulrich, Ziegler’s Beitr. z. path. Anat., Bd. xviii., p. 589, 1895. Digitized by Microsoft® THE URINARY APPARATUS. THE KIDNEYS. MALFORMATIONS. Entire absence of both kidneys is sometimes associated with great malformation of the entire body. Such foetuses are not viable. Absence of one kidney is not uncommon, the left kidney being more frequently absent than the right. The absence of the kidney may be complete, the ureter being also absent ; there may be an ir- regular mass of much-atrophied kidney tissue with connective tissue and fat, or there may be only a little mass of connective tissue and fat representing the kidney, and a ureter running down to the blad- der. The single kidney which is present is usually much enlarged. It may be in its natural position or displaced downward. Since the extirpation of the kidney has been practised by sur- geons it has been found that absence of one kidney is more common than was formerly believed. ‘When both kidneys are present one of them may be much larger than the other. Sometimes one kidney will have two pelves or two ureters. A rather frequent malformation is the so-called horseshoe kidney. The lower ends of the kidneys are joined together by a commissure. The commissure is usually composed of kidney tissue, but some- times of connective tissue. The two kidneys may be normal, except for the commissure ; or their shape, the arrangement of the vessels and ureters, and the position, may be unnatural. The two kidneys may be united throughout so as to look like a single misshapen kidney with two or more pelves and irregular blood vessels. The united kidneys may be both situated on one side of the vertebral column or in the pelvis. CHANGES IN POSITION. The kidneys may be placed in an abnormal situation, in which they are either fixed or movable. Digitized by Microsoft® THE URINARY APPARATUS. 647 _ The change in position is either lateral or downward. When displaced downward the kidney may be over the sacrum or below this in the cavity of the pelvis. The vessels also have an irregular, origin and distribution. The kidney is firmly attached in its abnor- mal position. Movable or wandering kidneys are found in adult life as a result of tight lacing, of pregnancy, of overexertion, and of unknown causes. They are more frequent in females than in males. The right kidney is the one more frequently affected. The blood vessels oe lengthened and the attachments of the kidney longer and ooser. BRIGHT’S DISEASE. This name is used as a convenient term to group together a cer- tain number of diseases of the kidney. This group may be subdi- vided as follows : I. Acute Bright's Disease. . Acute Congestion of the Kidney. . Acute Degeneration of the Kidney. . deute Hxudative Nephritis. alcute Diffuse Nephritis. II. Chronic Bright’s Disease. Chronic Congestion of the Kidney. Chronic Degeneration of the Kidney. Chronic Diffuse Nephritis with Exudation. Chronic Diffuse Nephritis without Exudation, He to wo et hwo ACUTE CONGESTION OF THE KIDNEYS. Acute congestion is caused by the ingestion of certain poisons, by extirpation of one of the kidneys, by severe injuries inflicted on any part of the body, by surgical operations, especially those on the bladder and urethra, and by over-exertion. We are rarely able to obtain human kidneys in the state of acute congestion, for the condi- tion is not usually a fatal one. In animals, however, the condition can be produced experimentally by cantharidin. It is found that the kidneys are enlarged, that the veins, capillaries, and Malpighian tufts contain an increased quantity of blood, and that the epithelial cells of the cortex tubes are flattened. There may be an exudation of serum and an escape of red blood cells from the vessels. Digitized by Microsoft® 648 THE URINARY APPARATUS. ACUTE DEGENERATION OF THE KIDNEYS. (Acute Bright’s Disease; Parenchymatous Nephritis; Parenchy- matous Degeneration.) The introduction of certain poisons into the body is regularly fol- lowed by changes in the cells of the viscera. The poisons which exert this effect may be mineral poisons, such as arsenic, mercury,, and phosphorus; or the poisons of infectious diseases, such as diph- theria, typhoid fever, etc. According to the quantity and virulence: of the poison received into the body, there are more or less marked. changes produced in the cells of the viscera. Fia. 310.—AcvuTH DEGENERATION OF THE KipNeY (Acute Parenchymatous Degeneration). From a case of yellow fever. a, the swollen and granular epithelium peeling off and disinte- grating; b, hyalin material in the lumen of the tubule. Small doses of such poisons, acting only for a moderate length of time, produce simple swelling of the cells. The cells are swollen, more opaque, more coarsely granular (Fig. 310). They are not dead, nor broken down, nor do they contain any new substances; the change: in their appearance is due to the swelling of the network which forms. a part of every cell. Under these circumstances there are either no changes at all in the blood-vessels of the viscera, or a slight conges- tion, with, perhaps, a little exudation of serum. Larger doses of such poisons, or more virulent poisons, or a longer’ Digitized by Microsoft® THE URINARY APPARATUS. 649 duration of the action of a poison, are attended by the deposition in the cell bodies of granules of albuminous matter and gloubles of fat. At the same time there is a change in the nutrition of the cells, and they are often broken and disintegrated. Under these conditions there may be considerable congestion of the vessels and an exudation of serum. Very large doses of such poisons cause the death of the cells of the viscera, a death which may take the form of coagulation necrosis or of disintegration and breaking down of the cell. With these changes there will often be an excessive congestion of the vessels and a large exudation of serum and the formation of casts. As the kidneys are excreting organs it is rather natural to think that the substances which cause degeneration of the renal epithelium do so because they are excreted by the kidneys. But, as the same poisons produce similar degeneration in many other parts of the body, it seems more probable that the effect of the poison is produced in the same way that it is in the nerves, the muscles, the liver, and the spleen. The well-known fact that temporary cutting off of the arterial blood from the kidneys in animals is followed by degeneration or death of the renal epithelium, has led to the idea that degeneration of the kidneys, especially in cholera, is due to ischemia. This seems possible, but it is a theory not at all applicable to most cases. of acute degeneration. It is a question of much importance whether the same toxin pro- duces degeneration or nephritis according to its dose, or whether two or more different toxins are necessary. In scarlatina and diphtheria, for example, the rule is that acute degeneration comes in the early days of the disease, acute exudative nephritis in the late days of the disease, and acute productive nephritis just after the close of the disease. Does this mean three different toxins, or that the same toxin varies at different stages of the disease, or that the only differences is in the dose? For clinical purposes the recognition of the fact that acute degen- eration is the ordinary lesion of the infectious diseases is of much practical importance. The gross appearance of the kidney varies with the extent of the degeneration. In the ordinary mild cases, such as accompany pneu- monia, the kidney is a little larger, the cortical portion a little thicker and paler. In the severe cases, such as accompany acute yellow atrophy of the liver, the kidney is considerably enlarged and more or less congested. Digitized by Microsoft® 650 THE URINARY APPARATUS. ACUTE EXUDATIVE NEPHRITIS. (Acute Bright’s Disease; Parenchymatous Nephritis; Tubal Nephritis; Desquamative Nephritis; Catarrhal Nephritis; Croupous Nephritis; Glomerulo-Nephritis.) Acute exudative nephritis is frequently a primary inflammation, occurring either after exposure to cold or without discoverable cause. It may complicate any one of the infectious inflammations Fig. 311.—AcuTe ExupDATIVE NEPHRITIS. Showing cortex tubes containing coagulated ma‘ter and with flattened epithelium. or diseases, but is especially common with scarlet fever. It is one of the forms of nephritis which ara apt to accompany pregnancy. The infectious diseases are often complicated with inflammations of different parts of the body. The probable causes of these are the chemical poisons produced by the growth of the pathogenic bacteria belonging to each disease. It seems also that the poison of each dis- ease has a preference for particular portions of the body. In rheuma- tism the joints and heart are regularly inflamed; in measles the bronchi; in scarlet fever and diphtheria the throat and the kidneys. Digitized by Microsoft® THE URINARY APPARATUS. 651 As regards the presence of bacteria in the kidneys themselves as exciting causes of inflammation our knowledge, save for certain phases of suppurative lesion, is incomplete. Whether nephritis in puerperal women and after exposure to cold is due to disturbances of circulation or to some poison in the blood, is not certain. The nephritis has the ordinary characters of an exudative inflam- Fie. 312.—Acute ExupDATIVE NEPHRITIS. Showing tubes with flattened epithelium aud containing red-and white blood cells and casts. mation: congestion, an exudation of blood plasma, an emigration of white blood cells, and a diapedesis of red blood cells; to which may be added swelling or necrosis of ‘the renal epithelium and changes in the glomeruli. In the milder cases we find the inflammatory products—serum, casts, white and red blood cells—in the urine. But in the kidneys after death we find no lesions, unless it may be afew casts in the straight tubes. The morbid process is confined to the blood vessels Digitized by Microsoft® 652 THE URINARY APPARATUS. of the kidney, and its only result is the exudation into the renal tubules. In the more severe cases we find the kidneys large and smooth, the cortex thick and white, or white mottled with red, or the entire kidney intensely congested. If the stroma is infiltrated with serum the kidney is succulent and wet; if the number of pus cells is very great there will be little, whitish foci in the cortex. There are, besides the exudation, changes in the tubes, the stroma, and the glomeruli. All the changes are most marked in the cortical portion of the kidney. Fig. 313.—Acuts Nrepuritis, X 850 and reduced. Paris green twenty hours before death. In the tubes the epithelium may be flattened, or swollen, opaque, and detached from the walls of the tubes. There may be a uniform, symmetrical dilatation of all the cortex tubes. The tubes may be empty or they may contain coagulated matters in the form of irregu- lar masses and of hyalin cylinders. The irregular masses are found principally in the convoluted tubes; they seem to be formed by a coagulation of substances contained in the exuded blood plasma, and are not to be confounded with the hyalin globules so often found in normal convoluted tubes. Digitized by Microsoft® THE URINARY APPARATUS. 653 The hyalin cylinders are more numerous in the straight tubes, but are also found in the convoluted tubes. They are also formed of matter coagulated from the blood plasma, and are identical with the casts found in the urine. The tubes may also contain red and white blood cells. The hyalin casts, the coagulated matter, and the red and white blood cells may be all found in the urine while the nephritis is going on. In some cases there is an excessive emigration of white blood cells. This excessive emigration is not necessarily attended with Fie. 314.—AcUTE NEPHRITIS OCCURRING WITH ACUTE GENERAL TUBERCULOSIS, X 850 and reduced. exudation of the blood serum, and so the urine of these patients may contain no albumin. The white blood cells are not found equally diffused throughout the kidney, but are collected in foci in the cortex. These foci may be very minute or attain a considerable size. They do not resemble the suppurating foci seen with embolism or with pyelo-nephritis. In the glomeruli we find considerable changes. The cavities of the capsules may contain coagulated matter and white and red blood cells, just as do the tubules. The capsular epithelium may be Digitized by Microsoft® 654 THE URINARY APPARATUS. swollen, sometimes so much so as to resemble the tubular epithelium, and this change is most marked in the capsular epithelium near the entrance of the tubes. The most noticeable change, however, is in the capillary tufts of the glomeruli. These capillaries are normally covered on their outer surfaces by flat, nucleated cells, so that the tuft is not made up of naked capillaries, but each separate capillary throughout its entire length is covered over with these cells. There are also flat cells which Fia, 315.—AcuTz ExupatTrve NEpgRItis. Showing a glomerulus with growth of tuft cells and thickening of the capsular epithelium, line the inner surfaces of the capillaries, but not continuously as in the case with capillaries in other parts of the body. In exudative nephritis the swelling and growth of cells on and in the capillaries change the appearance of the glomeruli. They are larger, more opaque; the outlines of the main divisions of the tufts are visible, but those of the individual capillaries are lost. This change in the appearance of the glomeruli is due to the swelling and growth of the cells on and in the capillaries (Fig. 316). Digitized by Microsoft® a THE URINARY APPARATUS. 655 In very severe cases the growth of the cells on the tufts is so con- siderable that they form large masses of cells between the glomerulus and its capsule. The walls of the arteries in the kidneys may be thickened by a swelling of their muscular coats. Acute exudative nephritis is regularly a transitory lesion. It may, indeed, be so severe as to destroy life in a short time. But, as Fig. 316.—AcutTe NEpPHRITIS. Showing the swelling and growth of cells in and on the capillaries of a glomerulus in a case of scarlatina, a rule, if the patients do recover from it they recover completely and the kidneys return to their natural condition. ACUTE PRODUCTIVE (OR DIFFUSE) NEPHRITIS. (deute Bright’s Disease, Parenchymatous Nephritis; Croupous Nephritis; Glomerulo-Nephritis.) This is an acute inflammation of the kidneys, characterized by exudation from the blood vessels, a growth of new connective tissue jn the stroma, and changes in the evithelium and the glomeruli. Digitized by Microsoft® 656 THE URINARY APPARATUS. The kidneys are increased in size, the capsules are not adherent, the surfaces are smooth. The cortical portion is red, or white, or - mottled. The mucous membrane of the pelvis is sometimes con- gested. Of the tubules in the cortex, in some the epithelium is flattened, in some there is coagulated matter or casts, in some the epithelium is swollen, degenerated, or contains globules of fat. In those parts of the cortex in which there is a growth of new connec- tive tissue, the tubes may be atrophied. The tubules of the pyramids show but little change except that they may contain casts. In the stroma of the cortex there is a growth of new connective tissue, Fic. 317.—AcuTE PRopuctIvE NEPHRITIS. A vertical section of the cortex, showing the wedge-shaped growth of connective tissue. varying in different kidneys as to the relative proportion of cells and basement substance. This new tissue in many of the kidneys follows the line of the arteries which run up into the cortex in the form of elongated wedges (Fig. 317). But in other kidneys the new tissue is diffuse, or in irregular patches. Many of the glomeruli show only an increase in the size and number of the cells which cover the capillaries, with some swelling of the capsule cells. But in others there is an extensive new growth of capsule cells which compresses the tuft of vessels. This growth of new cells from the capsule cells must not be confounded with ac- Digitized by Microsoft® THE URINARY APPARATUS. 657 cumulations of white blood cells within the capsules, nor with the growth of new cells on the walls of the capillaries. The glomeruli which are changed in this way are in groups, each group correspond- ing to some one artery. The whole picture of the nephritis is that of a combination of exudative and productive inflammation. When such a nephritis becomes chronic it is often possible to fol- low its course for many years, and to see at the end of that time that i (aa ess pe et \eess de < oe hi SS = Nee Re , ie a Fic. 318.—Sus-acuTeE PropucTivE NEPHRITIS. Glomerulus showing the growth of capsule cells. the anatomical changes in the kidneys are of the same kind, but much more extensive. This is the most serious and important of the forms of acute ne- phritis, for the reason that its lesions are from the first of a perma- nent character. It does not follow exudative nephritis, nor is it merely a modification of it; from the very outset it is a different form of inflammation. In the kidneys of persons who have been sick only a few days, the characteristic lesions are already evident. Pro- ae Digitized by Microsoft® 658 THE URINARY APPARATUS. ductive nephritis is governed by the same law as that which belongs to productive inflammation in other parts of the body—the disposition of the inflammation to continue as a subacute and chronic condition. It is of importance to recognize that in exudative nephritis the lesions are temporary, and after their subsidence the kidneys return to their normal condition, just as the lungs do after a lobar pneumonia. In productive nephritis, on the other hand, some of the lesions are per- manent, the kidneys can never return to their normal condition, just as in an interstitial pneumonia the lung never gets rid of the new connective tissue. Post-scarlatinal nephritis is nearly always of the productive form. Nephritis complicating diphtheria or developed during pregnancy is very frequently of this type. A primary nephritis in a person over twelve years old, if of subacute form, is almost invariably a produc- tive nephritis. On the other hand, this form of nephritis very sel- dom complicates any of the infectious diseases except scarlatina and diphtheria. These facts assist very much in making the diagnosis between the two forms of acute nephritis. It is easy to remember that post-scar- latinal nephritis and primary nephritis of subacute type are nearly always of the productive form; and that nephritis with diphtheria and pregnancy is often of the productive form; while acute nephritis under all other conditions is regularly of the exudative form. CHRONIC CONGESTION OF THE KIDNEYS. There are a number of morbid conditions which interfere with the circulation of the blood in the aortic system in such a way that the blood accumulates in the veins and is diminished in the arteries. The most common of these conditions are: chronic inflammation of the aortic and mitral valves, dilatation of the heart, aneurism of the arch of the aorta, pulmonary emphysema, and large accumulations of fluid in the pleural cavities. In pulmonary emphysema the disturbances of circulation are con- fined to the cases in which there is obstruction to the passage of blood through the lungs, dilatation and hypertrophy of the right ventricle, and then venous congestion of the aortic system. More or less dropsy is regularly developed at about the same time as the conges- tion of the kidneys. Large accumulations of fluid in the pleural cavities, if they re- main for any length of time, may produce well-marked chronic con- gestion. By far the most common cause of chronic congestion of the kid- neys is disease of the heart. So long as a heart with chronic endo- Digitized by Microsoft® THE URINARY APPARATUS. 659 carditis, or myocarditis, or dilatation, is able, in spite of its dam- aged state, to carry on the circulation fairly well, no secondary changes in the kidneys are produced. But as soon as the blood ac- cumulates in the veins to any considerable extent the kidneys may suffer. One of three things regularly happens to them: either chronic congestion, or chronic degeneration, or chronic nephritis is developed. It is also necessary to remember that chronic endocar- ditis and chronic nephritis often exist in the same person, although neither one of them is secondary to the other. The kidneys are of medium size, or rather large. Their weight is Increased, somewhat out of proportion to the increase in size. The color is dark-red, the consistence is very hard, the surfaces are smooth, the capsules are not adherent. The congestion is most marked in the veins of the pyramids; these contain an increased quantity of blood, and are often dilated. The capillaries of the cor- tex are also congested, but it is rather exceptional to find them dilated. The epithelium of the convoluted tubes is swollen, and the separate cells of which it is composed are more evident. Or, instead of this, the epithelium is much flattened so that the lumen of the tube is larger. The most constant and characteristic change is in the glomeruli. The capillaries which make up the glomerulus are dilated, with more or less thickening of their walls. This change in the glomeruli is usually, if not always, present and persists, even if the congestion is succeeded by a true nephritis. While the congestion often persists up to the time of the patient’s death, it may, instead of this, be followed by a chronic nephritis. If that is the case the specific gravity of the urine falls and the excre- tion of urea is diminished. The nephritis follows the anatomical type of a chronic nephritis without exudation, but the dilatation of the capillaries of the gomeruli persists. CHRONIC DEGENERATION OF THE KIDNEY. (Chronic Bright’s Disease; Chronic Parenchymatous Nephritis; Fatty Kidney.) The same mechanical obstructions to the circulation—heart disease, pleuritic effusions, ete.—which produce chronic congestion, can, instead of this, produce chronic degeneration of the kidney. It is said that anemia of the kidneys produces degeneration of the renal epithelium. Experiments upon animals show that this view is possible. It may be that the degeneration of the kidneys seen in old and feeble persons is due to a diminished blood supply, but we can hardly speak with certainty on this point. Chronic Digitized by Microsoft® 660 THE URINARY APPARATUS. diseases, such as phthisis and cancer, are followed by chronic degen- eration of the kidneys. There is a group of cases in which, although the health of the patients is not good, it is not easy to fix on a defi- nite cause for the chronic degeneration. Apparently, many of the authors who describe a “chronic parenchymatous nephritis” include under this head both chronic degeneration and chronic nephritis. The matter is further complicated by the fact that kidneys may be in the condition of chronic degeneration for some time, and then become further altered by a chronic nephritis with exudation, and by waxy degeneration of the glomeruli. If the degeneration follows heart disease the kidneys are large, and together may weigh from sixteen to twenty ounces. Their sur- faces are smooth; the cortical portion is thickened, of pink or white color, the pyramids are red. The gross appearance is that of the so- called large white kidney. The epithelium of the cortex tubes is swollen and coarsely granular. The capillaries of the glomeruli are dilated, with more or less thickening of their walls. The veins in the pyramids are congested. There are no changes in the stroma, or in the arteries. If the degeneration follow phthisis, cancer, or any wasting dis- ease, the kidneys are usually large, with a white or yellowish cortex. There are no changes except in the cortex tubes. In these the epithelial cells are either coarsely granular, or infiltrated with fat. If the degeneration occur in old people, or without discoverable cause, the kidneys may be either large and white, or of the size and appearance of a normal kidney, or small and red. There are the same degenerative changes in the epithelium of the cortex tubes, with no lesions in the stroma or the glomeruli. CHRONIC PRODUCTIVE (OR DIFFUSE) NEPHRITIS WITH EXUDATION. (Chronic Bright’s Disease; Chronic Parenchymatous Nephritis; Chronic Glomerulo-Nephritis; Waxy Kidney; Large White Kidney; Chronic Diffuse Nephritis; Chronic Desquamative Nephritts.) This is a chronic inflammation of the kidney attended with a growth of new connective tissue in the stroma, permanent changes in the glomeruli, degeneration of the renal epithelium, exudation from the blood vessels, and sometimes changes in the walls of the arteries. It has been customary to hold that in these kidneys the primary and most important changes are in the renal epithelium, while in another set of kidneys the primary and important changes are in the Digitized by Microsoft® THE URINARY APPARATUS. 661 stroma. In other words, that the cases of chronic nephritis can be divided into two classes—parenchymatous nephritis and interstitial nephritis. I (Delafield) do not think that this classification is supported ‘by facts. - In all the forms of chronic nephritis changes are to be found in’ the renal epithelium, the glomeruli, and the stroma. Whether the changes in the stroma, the glomeruli, or the epithelium are the more marked makes no difference in the clinical symptoms. But the presence or absence of exudation from the renal blood vessels does correspond to a marked difference in the symptoms. The existence of the exudation from the renal vessels is easily shown by the presence of serum albumin in the urine. In this way we readily distinguish two forms of chronic nevhritis, one with exudation and one without. The way of looking at the matter, then, is this: We find after death from chronic nephritis a great many varieties in the gross appearance of the kidneys. Some are large, some are small, some are red, some are white, etc. There is no regular corre- spondence between these different gross appearances of the kidneys and the clinical symptoms. We find in these same kidneys changes in the renal epithelium; in the stroma, in the glomeruli, and in the arteries. Sometimes one, sometimes the other of these elements of the kidneys is the most changed. There is no regular correspondence between the predomi- nance of the changes in one of the kidney elements over the other and the clinical symptoms. The easiest working scheme is to admit that in chronic nephritis all the elements of the kidney are more or less changed, but that the cases vary as to whether there is or is not an exudation of serum from the blood vessels. The presence or absence of such an exuda- tion does correspond to a well-marked difference in the clinical symp- toms. In the present state of our knowledge and for clinical purposes, we divide all the cases of nephritis into two classes, chronic nephritis with exudation and chronic nephritis without exudation. It is admitted that it is easy to divide up these kidneys according to their anatomical changes, into a number of fairly well-marked classes. But as this division does not correspond to clinical divisions it is valueless for clinical purposes. Although it is convenient to describe two forms of chronic ne- phritis--one with much albuminuria and dropsy, and one with little or no albuminuria, or dropsy—yet it must be remembered that these are not separate lesions of the kidneys, but varieties of the same lesion. For in all these kidneys two changes are constant—produc- Digitized by Microsoft® 662 THE URINARY APPARATUS. tive inflammation of the glomeruli and stroma, and degeneration of the renal epithelium. The only real difference between the kidneys is whether, besides the growth of new tissue and degeneration of renal epithelium, there is or is not an exudation of serum from the blood- vessels of the kidneys. In speaking of the exudation of serum from the vessels and its presence in the urine, we speak of it as it occurs during the whole course of the disease, and not as it occurs for short periods. We mean that in an exudative chronic nephritis there is usually a large quantity of albumin in the urine, but that there may be periods during which the albumin diminishes or entirely disappears. In the same way, in a non-exudative nephritis there may be periods during which albumin is present in considerable quantities. Generally speaking, the character of the clinical symptoms will vary with the presence or absence of the albumin. A considerable number of cases of chronic nephritis follow an attack of acute or subacute productive nephritis. The conditions of chronic congestion and chronic degeneration of the kidney are not infrequently followed by a true nephritis. Syphilis, chronic tubercular inflammation of any part of the body, chronic endocarditis, and chronic suppurative inflammations are often complicated with chronic nephritis. It is very difficult to find a satisfactory cause for the primary cases. There are many of these, especially in young and middle-aged adults. The nephritis is developed in a slow, insidious way in per- sons whose previous health had been good, and in whom no exciting cause is discoverable. Gross Appearance of the Kidney.—There is considerable vari- ety in the gross appearance of the kidneys. The types which I (Delafield) have seen most frequently are as follows: 1. Large white kidneys, weighing together sixteen ounces or more, the capsule adherent or not, the surface smooth or nodular, the cortex thick and white, the pyramids large and red. 2. Large mottled kidneys. These resemble the large white kid- neys in every respect except that the cortex, instead of being white, is mottled in a variety of ways with white, yellow, red, and gray. 3. Kidneys which resemble types one and two, but are not en- larged, the kidneys together not weighing over nine ounces. 4+. Small kidneys, weighing together not more than five ounces, the capsules adherent or not, the surfaces nodular, the cortex thin, atrophied, white, the pyramids rather large and red. These kidneys belong to persons who have had symptoms of kidney disease for many years, with periods of apparent recovery. 5. Kidneys which have the ordinary appearance and consistence Digitized by Microsoft® THE URINARY APPARATUS. 663 of the chronic congestion due to heart disease, but in addition the capsules are adherent and the surfaces finely nodular. 6. Kidneys of different sizes—large, medium-sized, and small, with adherent capsules and nodular surfaces. The cortex is gray, or gray mottled with red. The kidneys do not look at all like the large white kidneys. This is a type of frequent occurrence. 7. Kidneys which in their size, color, and general appearance are Fig. 313.—CHRronic NEPHRITIS WITH EXUDATION. Cortex with flattened epithelium and containing coagulated matter. hardly to be distinguished from normal kidneys, except that their capsules are adherent. 8. Kidneys of small size, weighing together not more than four ounces, with adherent capsules. The cortex is atrophied, red, and ir- regular. These kidneys are found in persons who have given symp- toms of kidney disease for a number of years. It might naturally be supposed that such marked differences in the gross appearance of the kidneys would correspond to equally marked differences in the clinical histories and minute lesions. Digitized by Microsoft® 664 THE URINARY APPARATUS. This, however, is not the case. The clinical histories are practically interchangeable, and the minute lesions are essentially the same. Microscopical Appearances.—I£ we make vertical sections of the cortex of all these kidneys, no matter what their size or color, we get with a low magnifying power the same general picture. Instead of the uniform and orderly arrangement of tubes and glomeruli which we see in the normal kidney, the tubes seem to be obliterated in some places and dilated in others. There is a growth of fibro-cellular Fie. 320.—CHronic NEPHRITIS WITH EXxuDATION. A glomerulus, showing growth of the tuft cells. tissue in regular wedges, in irregular patches, or diffuse between the tubules. If we examine the different constituents of the kidney in detail we find: The tubes are in some places of normal size, in some places atro- phied, in some places dilated. The atrophied tubes are in the patches of new connective tissue. The dilated tubes are not very large, nor do they form cysts. Digitized by Microsoft® THE URINARY APPARATUS. 665 The epithelium of the tubes is in some places merely flattened. These tubes are empty, or contain coagulated matter, casts, and red and white blood cells. In other tubes the epithelium is more or less swollen, sometimes so much so as to completely fill the tubes. In still other tubes the epithelial cells are swollen, their reticulum is very coarse with large meshes, and they are infiltrated with fat. The kidneys vary as to which of these changes in the epithelium predominates, but all of them may be found in the same kidney. Fia. 321.—Crronic NEPHRITIS WITH ExupaTIon. Glomerulus showing a growth of the tuft cells. The new connective tissue is in the form of wedge-shaped masses in the cortex which follow the line of the straight arteries and veins, or itis in irregular masses, or it is arranged diffusely so as to sepa- rate the tubes from each other. The longer the nephritis lasts, the greater is the quantity of new connective tissue. The relative pro- portion of basement substance and cells and the density of the base- ment substance vary in the different kidneys. The new tissue is well supplied with blood vessels. Digitized by Microsoft® 666 THE URINARY APPARATUS. The glomeruli are changed in several different ways: 1. They resemble the glomeruli in acute exudative nephritis. They are large, the convolutions of the capillaries are seen with difficulty, there is a very great increase in the number of the cells which cover the capillaries, but these new cells are not of large size. Wealsosee glomeruli, which apparently have been of this type, small and atrophied. . 2. There is an increase not only in the number, but also in the Fig, 322,—CaRonic NEPHRITIS, WITH EXUDATION. Glomerulus showing a growth of capsule cells. size, of the cells which cover the capillaries. These cells are so large that they project outward from the surface of the glomerulus. There is also an increase in the size and number of the cells within the capillaries. These glomeruli are found in all stages of atrophy. 3. The capillaries are changed in the same way by a growth of large ceils on their outer surfaces and within them. In addition there is a very extensive cell-growth beginning in the cells which line the capsule. The mass of new cells produced in this way may be so Digitized by Microsoft® THE URINARY APPARATUS. 667 great as to compress the capillaries (Fig. 322). The glomeruli also become atrophied, the capillaries are shrunken, and the capsule cells changed into connective tissue. 4. If chronic congestion of the kidneys is followed by chronic nephritis, the dilatation of the capillaries due to the congestion con- tinues, and there is added an increase in the size and number of the cells which cover the capillaries. 5. The walls of the capillaries are the seat of waxy degeneration, while the cells which cover them are increased in size and number (Fig. 323). Fig. 323.—Waxy DEGENERATION oF TUFT CAPILLARIES. a, the tuft is completely transformed into a waxy mass; ), portions of tuft waxy; c, tuft ca- pillaries normal; d, convoluted tubule with disintegrating epithelium. 6. Besides the atrophied glomeruli already described, there are others which are small and shrunken, with comparatively little new growth of cells. The arteries are not infrequently much altered by inflammatory changes. There is a growth of cells and basement substances from the inner surface of the artery which obstructs its lumen; or there is a thickening of each of the three coats of the artery; or all the coats of the artery are thickened and converted into a uniform mass of dense connective tissue; or the wall of the artery undergoes waxy degeneration. Digitized by Microsoft® 668 THE URINARY APPARATUS. CHRONIC PRODUCTIVE NEPHRITIS WITHOUT EXUDATION. (Chronic Bright’s Disease; Cirrhosis of the Kidney; Granular Degeneration; Interstitial Nephritis; Chronic Indurative Nephritis; The Artervo-Sclerotic Kidney.) While this form of nephritis is especially common in persons over forty-five years old, itis by no means rare in young adults, and is occasionally seen in children. Fig. 324.—CHRONIC NEPHRITIS WITHOUT EXUDATION. Atrophied glomerulus. It seems to be caused by chronic alcoholism, lead poisoning, gout, and by the same conditions as those which cause emphysema, endo- carditis, and cirrhosis of the liver. It follows chronic congestion of the kidney, hydro-nephrosis, and chronic pyelitis. The larger number of the affected organs are found after death to be diminished in size; the two kidneys together may not weigh more than two ounces. The capsules are adherent; the surfaces of the Digitized by Microsoft® THE URINARY APPARATUS. 669 kidneys are roughened or nodular, the cortex is thin and of a red or gray color, A. considerable number of these kidneys, however, do not differ in their sizo or appearance from normal kidneys, except that their capsules are adherent and their surfaces roughened. Occasionally the kidneys are large, weighing together from 16 to 32 ounces, with smooth or nodular surfaces, and a cortex of red, gray, or white color. Fic. 325.—CHronic NEPHRITIS WITHOUT EXUDATION. [ Showing an atrophied glomerulus. If the nephritis follows chronic congestion, the kidneys remain hard, but the cortex becomes thinned, the capsules adherent, and the surface roughened. , There is a growth of new connective tissue in the cortex and also in the pyramids, which becomes more and more extensive as the disease goes on. In the cortex the new tissue follows the distribution of the normal subcapsular areas of connective tissue, is in the form Digitized by Microsoft® 670 THE URINARY APPARATUS. of irregular masses, or is distributed diffusely between the tubes. In the pyramids the growth of new connective tissue is diffuse. The tubes, both in the cortex and pyramids, undergo marked changes. Those included in the masses of connective tissue are diminished in size, their epithelium is flattened, some contain cast matter, many are obliterated. The tubes between the masses of new Fig. 326.—Caronio NEPHRITIS WITHOUT ExuDATION. An atrophied glomerulus. connective tissue are more or less dilated; their epithelium is flat- tened, cuboidal, swollen, degenerated, or fatty. The dilatation of the tubes may reach such a point as to form cysts of some size, which contain fluid, or coagulated matter. These cysts follow the lines of systems of tubes, or are situated near the capsules. Of the glomeruli a certain number remain of normal size, but with the tuft cells swollen or multiplied. Many others are found in all stages of atrophy and of change into connective tissue (Figs. 324 and 325). The atrophy seems to depend partly on the growth of Digitized by Microsoft® THE URINARY APPARATUS. 671 tuft cells and intra-capillary cells, partly on the thickening of the cap- sules, partly on the occlusion of the arteries. If the chronic nephritis follow chronic congestion of the kidneys the glomeruli remain large, with an increased growth of tuft cells, or they become atrophied, but with the dilatation of the capillaries still evident. The capillaries of the glomeruli may be the seat of waxy degeneration (Fig. 326). The arteries exhibit the same changes as have already been described in speaking of chronic exudative nephritis. SUPPURATIVE NEPHRITIS. Suppurative inflammation in the kidney may follow injuries to the organ, the lodgment in its vessels of infectious emboli, and may accompany pyelitis and cystitis. 1. Suppurative Nephritis from Injury.—Gunshot wounds, in- cised or punctured wounds, falls, blows, and kicks are the ordinary traumatic causes. If the injury be a very severe one it usually causes the death of the patient in a short time; if it is less severe, suppura- tive inflammation is developed. The inflammatory process may be diffuse, so that nearly the whole of one or of both kidneys is converted into a soft mass composed of pus, blood, and broken-down tissue; or it is circumscribed and one or more abscesses are formed in the kidney. 2. Abscesses.—In pyemia and in malignant endocarditis small infectious emboli find their way into the arteries of the kidneys and produce necrosis of small areas of tissue, with surrounding zones of suppurative inflammation. The entire kidney is enlarged and con- gested, and is dotted with little white foci surrounded by red zones. The foci are formed by an infiltration of pus cells between the tubes, with more or less degeneration of kidney tissue. Sometimes ab- scesses of one or both kidneys are met with which have existed for a long time and for which no cause can be discovered. After death the kidney may be changed into a sac of pus surrounded by fibrous tissue. The pelvis and calyces may be dilated and their walls thick- ened. The connective tissue around the kidney, and its capsule, may be also thickened. Suppurating sinuses may extend from the kidney into the surrounding soft parts. Whatever the form in which it may manifest itself, suppurative inflammation of the kidney may be induced by some one or combina- tion of the pyogenic micro-organisms which may lodge within it under favorable conditions. Thus Streptococcus pyogenes, Staphlococcus pyogenes, Bacillus coli communis; the pneumococcus, the typhoid bacillus, and others may be found in the suppurative foci. Sometimes, however, espe- Digitized by Microsoft® 672 THE URINARY APPARATUS. cially in the more chronic processes, the technical procedures at our command fail to reveal the presence of micro-organisms. When the suppurative inflammation is consecutive to similar pro- cesses in the bladder or ureters the processes are usually due to the same infective agent (see page 684). Suppurative Pyelitis is often associated with suppuration of the kidney substance on the one hand, and on the other hand, and more frequently, with a similar process in the bladder or ureters, or both on the other. But it may occur by itself. It is incited by the same micro-organisms as are concerned in the induction of the associated lesions in the kidney and bladder. In the latter case, it is most often the Bacillus coli communis, the Streptococcus pyogenes, and Staphy- lococeus pyogenes which are concerned. The mucous membrane of the pelvis may be congested, thicker and more opaque than normal, and coated with pus or with patches of fibrin. The presence of pelvic calculi is to be regarded as a predis- posing rather than as a direct inciting agent in suppurative pyelitis. SUPPURATIVE URETERITIS. The conditions under which suppurative inflammation of the ureter occurs are similar, as is the general appearance of its mucous membrane, to these just indicated in the pelvis. SUPPURATIVE PYELO-NEPHRITIS WITH CYSTITIS. (“Surgical Kidney.”) In this grouping of lesions, which is usually initiated by the inflammation of the bladder, the affection of the kidneys is usually bilateral. The suppurative areas in the kidney may be in the form of small abscesses scattered through the kidneys, or in the form of elongated whitish streaks or wedges between the tubules. The purulent foci are often surrounded by a red zone of congestion. The kidney tissue in the vicinity of the abscesses may be necrotic, the outlines of the cells being preserved but their nuclei absent or not revealed by the usual staining agents (see Fig. 68). The infective agent may traverse the ureters in the passing from the inflamed bladder to the kidneys without leaving the mucous membrane of the ureter intact. CHRONIC PYELO-NEPHRITIS. Chronic cystitis or calculi in the pelvis of the kidneys may set ug Digitized by Microsoft® THE URINARY APPARATUS. 673 a chronic inflammation which involves both the pelvis and calyces and the kidney tissue. The mucous membrane of the pelvis and calyces is thickened, the epithelial layer is changed, there is a growth of granulation tissue beneath the epithelium, and there may be little polypoid outgrowths. The surface of the mucous membrane is coated with pus or fibrin, or the cavity of the pelvis is dilated and distended with purulent serum. The kidney itself is the seat of a chronic interstitial inflamma- tion with the production of new connective tissue, and sometimes of pus, with obliteration of the renal tubules. TUBERCULOUS NEPHRITIS. This lesion is usually, though not always, associated with tuber- cular inflammation in other parts of the genito-urinary tract. It is usually unilateral, occurring most frequently on the left side. The process may commence in the kidney or in some other part of the genito-urinary tract. If only one kidney is involved the other is apt to become the seat of chronic diffuse nephritis with waxy de- generation of the walls of the arteries. The tubercular inflamma- tion may occur in a kidney already the seat of chronic inflammatory changes. The lesion is apt to begin in the mucous membrane of the pelvis and calyces, and extends from thence first to the pyramidal and after- ward to the cortical portion of the kidneys. In the mucous mem- brane of the pelvis and calyces there is a growth of granulation tissue studded with tubercle granula in the stroma, while the epithe- lial cells proliferate, become deformed, and desquamate. This pro- cess is often rapidly succeeded by cheesy degeneration of all the in- flammatory products. In the kidney there is the same production of granulation tissue and tubercle granula, which soon undergo cheesy degeneration, the degeneration involving the adjacent kidney tissue. In addition to this there is in the rest of the kidney chronic interstitial or suppura- tive inflammation. So the entire kidney is enlarged, portions are in the condition of cheesy degeneration or have sloughed away, while the rest of the kidney is dense and hard. Or, if suppuration takes place, the kidney is hollowed out into cavities filled with cheesy mat- ter and pus. Sometimes the process comes to a standstill, and then the cheesy portions are infiltrated with salts of lime. EMBOLISM AND THROMBOSIS. Acute and chronic endocarditis affecting the left side of the heart, and chronic endarteritis of the aorta, frequently result in the forma- 53 Digitized by Microsoft® 674 THE URINARY APPARATUS. tion of vegetations, portions of which become detached and lodged as emboli in the branches of the renal artery. The occlusion of an artery in this way produces in the kidneys wedge-shaped infarctions, varying in their size with the size of the obstructed artery. The infarction loses the natural red color of the kidney and becomes first yellow and then white. The renal epithe- lium degenerates and disappears, the tubes become collapsed and shrunken ; around the infarction is a zone of congestion and of infil- tration with pus cells. After this the infarction becomes shrunken, dense, and changed into connective tissue. The kidney is then left deformed by the cicatricial depressions and contractions. It is pos- sible, however, for the infarction to become gangrenous, or to be surrounded by a zone of purulent infiltration, and break down so as to form an abscess. Rarely the infarctions are of the hemorrhagic variety. Embolism of the trunk of the renal artery produces complete ne- -crosis of the kidney. Infectious emboli are small and produce little purulent foci (see above). Thrombosis of the renal vein and its branches may occur in pa- tients suffering from chronic Bright’s disease.’ It can also be pro- duced by tumors pressing on the veins, by thrombi of the vena cava, and occurs as a primary lesion dependent on the general con- ‘dition of the patient. HYDRONEPHROSIS. Dilatation of the pelvis and calyces of the kidneys is found as a ‘congenital condition. In some cases other malformations, such as -club-foot, hare-lip, and imperforate anus, are also present. The pel- ves and calyces of both kidneys, and the ureters, are distended with urine ; the bladder is also distended and its wall may be hypertro- phied. The urethra may be closed, or no obstruction can be demon- ‘strated. In these latter cases it is supposed that there does exist some membranous obstruction, which is broken by the probe or ‘catheter used to explore the urethra. In adult life hydronephrosis is produced by mechanical obstruc- tion of the urethra or ureters, due to inflammation, tumors, or calculi. According to the position of the obstruction, either one or both kidneys are involved. The pelvis and calyces are dilated, sometimes enormously, and filled with urine alone or urine mixed with pus. The kidney tissue is flattened and thinned over the distended cavities. Its texture may ' Moxon, Trans. Lond. Path. Society, 1870, p. 248. Digitized by Microsoft® THE URINARY APPARATUS. 675 remain unchanged, or there may be developed suppurative pyelo- nephritis or chronic diffuse nephritis. THE CYSTIC KIDNEY. Cysts are formed in the kidneys, both during intra-uterine and extra-uterine life. The congenital cystic kidney is a very remarkable pathological condition. Hither one or both kidneys are enormously enlarged and converted into a mass of cysts. The cysts are of all sizes and are separated from each other by fibrous septa or compressed kidney tis- lll io. Fia. 827.—Cysts or KipNey—Curonic NEpuHRITIs. sue. They contain a clear yellow, acid fluid holding in solution the urinary salts. Or the fluid is turbid and brown, and contains blood, uric acid crystals, and cholesterin. The cysts are lined with a single layer of flat, polygonal cells. They seem to be formed by a dilatation of the tubules and of the capsules of the Malpighian bodies. As causes for such dilatations are found obliteration of the tubes in the papillee, and stenosis of the pelvis, ureters, bladder, or urethra. Other congenital malformations are often associated with this one.’ In adult life we find three varieties of cystic kidney : 1. In kidneys which are otherwise normal there are one or more _ | Virch., Ges. Abhandl. Digitized by Microsoft® 676 THE URINARY APPARATUS. cysts filled with clear or brown serum or colloid matter. These cysts do not appear to interfere at all with the function of the kid- neys. 2. In chronic diffuse nephritis, especially in the atrophic form, groups of tubes are dilated. Apparently one or more of the larger tubes in the pyramids is obstructed, and this causes dilatation of a corresponding group of tubes. Sucha dilatation may be moderate in size, or it may form cysts visible to the naked eye. 3. Both kidneys are very much enlarged and converted into a mass of cysts containing clear or colored serum or colloid matter. The nature of these cysts is uncertain. It is possible that they are congenital. They are sometimes associated with similar cysts in the liver. They seem to produce no renal symptoms until shortly before the patient’s death, unless chronic nephritis also exists, and then there are the ordinary symptoms of chronic Bright’s disease. PERINEPHRITIS. The loose connective tissue which is situated around and beneath the kidney may become the seat of suppurative inflammation, and in this way abscesses of considerable size are formed. Such a perinephritis may be either secondary or primary. The secondary cases are due to extension of the inflammation from ab scesses in the vicinity, such as are formed with caries of the spine, pelvic cellulitis, puerperal parametritis, perityphlitis, and suppura- tive nephritis. The primary cases occur after exposure to cold, after contusions over the lumbar region, and after great muscular exertion ; or no cause can be discovered. Complicating cases occur in the course of typhus and typhoid fevers and of small-pox. Most of the reported cases have been in persons between the ages of twenty and forty years. Less frequently children and older per- sons are affected. In the idiopathic cases the connective tissue behind the kidney seems to be the point of origin of the inflammatory process, and it is here that the pus first collects. After the abscess has formed the suppuration extends and the pus burrows in different directions : backward through the muscles ; downward into the iliac fossa, the perineum, the bladder, the scrotum, or the vagina; forward into the peritoneal cavity or the colon ; upward through the diaphragm. The kidney itself is simply compressed by the abscess, or its tis- sue becomes involved in the suppurative inflammation. Digitized by Microsoft® THE URINARY APPARATUS. 677 RENAL CALCULI. In the kidneys of new-born children, from the first to the four- teenth day after birth, the large tubes of the pyramids often con- tain small, brownish, rounded bodies composed of the urates of am- monium and sodium. Similar masses may also be present in the calyces and pelves. In still-born children these masses are usually absent. The carbonate and phosphate of lime may be deposited in the tubes of the pyramids, in the form of white linear masses, in the kidneys of old persons and of those who have suffered from destruc- tive diseases of the bones. Urate of soda in the form of acicular crystals is deposited both in the tubes and stroma of the kidneys of gouty persons. Concretions of the urinary salts are often formed in the pelves of the kidneys. They may remain there as rounded masses, or they may attain a large size and be moulded into the shape of the pelvis and calyces. Smaller calculi may pass into the ureter and either become impacted there or pass through it into the bladder. The most common form of calculus is that composed of uric acid. But they may also be formed of uric acid with a shell of oxalate of lime, or of oxalate of lime alone, or of the phosphates, or of cystin. The most serious result of the presence of these calculi is the oc- clusion of the ureters or the production of pyelo-nephritis. TUMORS. Fibroma.—Small, hard, white fibrous nodules are frequently found in the pyramids. They are of no special importance. They may be mistaken for miliary tubercles. Large fibromata are very rare.’ Lipoma.—Small fatty tumors are found in the cortex of the kid- ney just beneath the capsule. They are composed of fully devel- oped fat tissue. The fat is developed in the stroma so as to replace the kidney tissue.’ Papilloma.—Villous tumors, formed of tufts of connective tissue covered with epithelium, may grow from the mucous membrane of the pelvis.“ A peculiar form of papillary and cystic growth of the ureter is described.‘ Myxo-Sarcoma.—Large tumors may grow from the pelvis of the kidney. They are not simple myxomata, but are composed of mu- cous tissue, fat, and sarcomatous tissue. 1 Wilks, Trans. Lond. Path. Soc., xx. 2 For bibliography of fat tumors of the kidney pena Ulrich, Ziegler’s Beitr, z. path. Anat., Bd. xviii., p. 603. 3Trans. Lond. Path. Soc., 1870, p. 289. 4Virch. Arch., Bd. Is Bjgiz89-by Microsoft® 678 THE URINARY APPARATUS. Myoma.—Small tumors composed of smooth muscular fibres and. of round cells are found in the cortex close to the capsule. A tumor composed of striated muscle and round cells is described by Cohnheim.’ A tumor composed partly of smooth muscle, partly of striped muscle, and partly of sarcomatous tissue is described by Eberth.’ Angioma cavernosum occurs in the form of small nodules situ- ated in the cortex. Lymphoma.—Small white tumors composed of tissue like that of the lymphatic glands are found in cases of leukemia and pseudo- nc coeanttits RETO oy EON? See ‘a ew gow s'0 Evstieyee ur Os Besar Gres Fic. 328.—ADENOMA OF THE KIDNEY. Papillary form. leukemia. Less frequently they are found with typhoid fever, scar-. let fever, and diphtheria. Adenoma.—This form of tumor is situated in the cortex of the. kidney and may invade the pyramidal portion also. Usually there is. only a single tumor, but sometimes two or more, or they may even occur in both kidneys. They vary in size; some are not larger than a pea, others are as large as a hen’s egg. They are of rounded form of whitish color, and separated by a capsule from the kidney fissue: The tumors are most frequent in persons over forty years of age. 1Virch. Arch., Bd. lxv., p. 64. ?Tbid., Bd. lv., p. 518. Digitized by Microsoft® THE URINARY APPARATUS. 679 There are two principal varieties of these tumors, the papillary and the alveolar, which are, however, closely related. 1. The Papillary Adenoma.—There are cavities of different sizes, from the walls of which spring branching tufts covered with cylin- drical or cuboidal epithelium (Fig. 328). These tufts nearly fill the cavities. : 2. The Alveolar Adenoma.—There is a connective-tissue frame- work enclosing small round, oval, or tubular alveoli, lined or filled with cells (Fig. 329). The cells are usually large and may be cylindrical, cuboidal, or polyhedral, and may be pigmented in a manner similar to the cells of the adrenals. Fig. 329.—ADENOMA OF THE KIDNEY. Glandular form. Fatty degeneration of the epithelium may be excessive and glyco- gen may form in the cells. In these tumors the stroma may be present in considerable quantity, or the blood vessels may form con- spicuous features, or a cystic distention of the alveoli may occur. Large areas in these tumors may become necrotic. Many of these tumors appear to have developed from adrenal cells. estray in the kidneys. They may form metastases. The relationship between true adenoma of the kidney, adenomata which appear to develop from strayed adrenal elements, and similar tumors which are regarded by some observers as endotheliomata or Digitized by Microsoft® 680 THE URINARY APPARATUS. endothelial sarcomata, and certain forms of angio-sarcoma, is not yet altogether clear.’ Carcinoma.—Besides secondary carcinoma of the kidney there is also a primary form. Our knowledge of this has been much ob- scured by confounding with it adenomata and sarcomata. There seems to be, however, a real epithelial growth, originating in the kidney tubules, which forms tumors of large size and malig- nant character. Sarcoma.—Tumors formed of connective-tissue cells may origi- nate either in the pelvis of the kidney or in the kidney itself. They form tumors of large size and malignant character. Those which grow from the pelvis are usually myxo-sarcomata. Those which originate in the kidney tissue reach a large size and are soft and hemorrhagic. Their stroma forms irregular alveoli filled with small round cells. PARASITES. Echinococcus, in its ordinary form of mother and daughter cysts, is sometimes found in the kidney. The cysts may open into the pel- vis of the kidney, into the pleura, or through the wall of the abdomen. Cysticercus cellulosce is of very rare occurrence. Pentastomum denticulatum has been seen once by E. Wagner. Filaria sanguinis hominis is found in the arteries, veins, lym- phatics, and stroma. Strongylus gigas has been found several times in the pelvis of the kidney. THE URINARY BLADDER. MALFORMATIONS. Exstroversion of the bladder is one of the most frequent mal- formations, and may occur in either sex. It presents several varie- ties : 1. The umbilicus is lower down than usual, the pubic bones are not united at the symphysis, the pelvis is wider and shallower than it should be. Between the umbilicus and pubes the abdominal wall is wanting. In its place is a projecting, ovoid mass of mucous mem- brane, in which may be seen the openings of the ureters. The penis is usually rudimentary ; the urethra is an open fissure (epispadias) ; the clitoris may be separated into two halves. The ureters usually ‘Consult Paoli, Ziegler’s Beitr. z. path. Anat., Bd. viii., p. 140; Askanazy, ibid., Bd. xiv., p. 83, 1893; 0. Hahiden, ibid., Bd. xv., p. 626; Sudeck, Virch. Arch. and Ulrich, Ziegler’s Beitr. z. path. Anat., Bd. xviii., p. 589, 1895; Lubarsch, Virch. Arch., Bd. exxxv., p. 149. Digitized by Microsoft® THE URINARY APPARATUS. 681 open normally; sometimes their openings are displaced or are multi- ple. They may be dilated. 2. There may bea fissure in the abdominal wall, filled up by the perfectly formed bladder. 3. The umbilicus may be well formed, and there is a portion of abdominal wall between it and the exstrophied bladder. 4, The external genitals and urethra may be well formed, and the symphysis pubis united, while only the bladder is fissured. 5. The genitals, urethra, and symphysis may be well formed, the bladder closed except at the upper part of its anterior wall. The bladder is entirely or in part inverted and pushed through the open- ing in the abdominal wall. The Urachus normally remains as a very small canal, five to seven cm. long, with a small opening into the bladder, or entirely closed at that point. If there is a congenital obstruction to the flow of urine through the urethra, the urachus may remain open and the urine pass through it. Or the bladder may present, even in the adult, a slender distention reaching close to the umbilicus as the result of a persistent urachus.’ Absence of the Bladder is of rare occurrence. The bladder may be very small, the urine passing almost directly into the urethra. The bladder may be separated into an upper and a lower portion by a circular constriction. It may be completely divided by a vertical septum into two lateral portions. Diverticula of the wall of the bladder are sometimes found in new-born children. Partial or com- plete closure of the neck of the bladder may occur. This may lead to hydronephrosis, or the urine may be discharged through the open urachus. CHANGES IN SIZE AND POSITION. Dilatation.—This may be general or partial, leading to the formation of diverticula. General dilatation of the bladder is produced by the accumulation of urine in consequence of some mechanical obstacle to its escape, or of paralysis of the muscular walls of the organ. The dilatation is usually uniform and may be very great, so that the bladder may reach to the umbilicus. If the walls of the bladder are paralyzed, or the obstruction occurs suddenly or is complete, the wall of the blad- der is thinned. When an incomplete obstruction exists for some time the walls of the bladder are apt to hypertrophy, so that, al- though the bladder is larger than normal, the walls may not only be of the usual thickness, but even very much thicker. In the fetus 1 Bly, Trans. N. Y. Path. Soc., 1893, p. 64. Digitized by Microsoft® 682 THE URINARY APPARATUS. dilatation of the bladder may reach such a size as to interfere with delivery. The retained urine in dilated bladders is liable to decomposition, leading to inflammation or gangrene of the mucous membrane. Diverticula of the bladder may be produced by the pouching-out of circumscribed portions of the wall of the bladder, the wall of the pouch containing all the layers of the bladder wall. More frequently, however, they are produced by a protrusion of the mucous membrane between hypertrophied bundles of muscle fibre. They may be very small, or they may be as large as a child’s head. They may com- municate with the bladder by a large or a small opening. The de- composition of stagnant urine in diverticula is apt to induce inflam- mation. Calculi may be formed in them or may slip into them from the bladder. Hypertrophy of the muscular coat of the bladder is usually pro- duced by mechanical obstructions to the outflow of urine, such as stricture of the urethra, enlarged prostate, calculi, new growths, etc. The muscular coat is thickened uniformly or assumes a trabeculated appearance. The organ retains its normal capacity, or is dilated, or becomes smaller. The mucous membrane is frequently the seat of chronic or acute inflammation. Dilatation of the ureters and hydro- nephrosis frequently accompany this condition. Hernice of the bladder sometimes accompany intestinal herniz through the inguinal and crural canals and the foramen ovale. The changes in position of the bladder, produced by displacements of the vagina and uterus, will be mentioned with the lesions of those organs. In the female the base of the bladder may press downward, caus- ing protrusion of the vaginal wall (vaginal cystocele) ; or there may be inversion and prolapse of bladder through the dilated urethra. RUPTURE—PERFORATION,. Penetrating wounds of the bladder may permit escape of urine into the abdominal cavity, or infiltration into the surrounding con- nective tissue, or permanent fistule. Such wounds are always seri- ous and frequently fatal, owing chiefly to the severe and often gangrenous inflammation which decomposing urine sets up in the connective tissue, or to the peritonitis induced by the same cause. Rupture of the bladder may be produced by severe blows and falls when the bladder contains urine. More rarely rupture takes place from overdistention. Death may occur from rupture of the bladder with escape of urine into the peritoneal cavity, without evi- dences of peritonitis. Digitized by Microsoft® THE URINARY APPARATUS. 683 Perforations of the bladder are produced by ulceration and gangrene, by abscesses from without, and by cancerous ulceration from the adjoining organs. Fractures of the pelvic bones may pro- duce laceration of the bladder. Perforations of the bladder may lead to the establishment of fistulee, communicating with the rectum, vagina, uterus, or opening externally. DISTURBANCES OF CIRCULATION. Hypereemia.—Aside from active hyperemia of the mucous mem- brane in acute inflammation, the bladder is not infrequently the seat of chronic congestion from obstruction to the venous circulation. Under these conditions there may be chronic catarrhal inflamma- tion, or a marked dilatation of the veins (vesical hemorrhoids), which may give rise to hemorrhage or to obstruction of the opening of the ureters. Hemorrhage.—Extensive hemorrhages into the bladder are com- monly due to injury or to the presence of calculi or tumois. Small hzemorrhages into the substance of the mucous membrane may ac- company inflammation, the hemorrhagic diathesis, scurvy, purpura, small-pox, etc. Ifthe hemorrhage is considerable and occurs rapidly in an empty bladder, a clot is apt to form; but when the blood mixes with urine as it is extravasated it more commonly remains liquid and is discharged as a reddish-brown fluid. INFLAMMATION. Acute Cystitis.—This may be incited by the presence of urine which has decomposed under the influence of bacteria; by cantha- rides or other drugs; by the presence of foreign bodies and calculi; or if may be due to an extension of gonorrhceal urethritis or vagi- nitis; or it may occur without assignable cause. The mucous mem- brane is swollen and congested, although these alterations may not be very evident after death. Thesurfaces may be coated with mucus containing red blood cells and pus. The epithelium is apt to be loosened and in some places peeled off, so that superficial or deep ul- ceration may occur. We may find mixed with the urine in the organ shreds of mucus, pus cells, epithelial cells of various shapes, usually more or less swollen and granular, or fragments of such cells; red blood cells and bacteria. Resolution may occur from acute ca- tarrhal cystitis, but it very frequently assumes a chronic character. Chronic Cystitis.—In this form the mucous membrane may be swollen, succulent, grayish, or mottled with spots of congestion or extravasation, and covered with a layer of mucus and pus. Micro- scopically the membrane, may be, more ora!es8 infiltrated with pus 684 THE URINARY APPARATUS. cells, and pus may be constantly produced and thrown off into the ‘urine. Later the mucous membrane may become thickened either diffusely or in the form of tufts or polypi. In some cases it becomes atrophied. Owing to decomposition of the hemoglobin in the extra- vasated blood the mucosa may become pigmented, brown, or slate- colored. The mucous membrane frequently becomes eroded, espe- cially on the most elevated portions, or deep ulcerations may occur. The muscular coats may become paralyzed and the bladder dilated; or the submucosa or the muscularis, or both, may become hypertro- phied. The mucous membrane may become encrusted with urinary salts. In another class of cases the inflammation assumes a more intense and necrotic character. Larger and smaller shreds and patches of the mucosa die, become brown or gray in color, loosen or peel off, and become mixed with the urine and exudations. The gangrenous process may extend to all the coats of the bladder, so that perforation and fatal peritonitis may occur. The gangrenous form of cystitis is more apt to occur in paralytics. In still another class of cases the inflammation assumes a suppurative character. The submucosa, the intermuscular connective tissue, and the adjacent parts become infil- trated with pus, either diffusely or in the form of larger and smaller abscesses, which may open externally or internally, forming deep ulcers. In all these cases the inflammation may extend to the ureters and kidneys; it may skip the ureters and involve the kidneys. The small nodules of lymphoid tissue in the mucous membrane of the bladder, especially near the neck, may become enlarged and prominent in cystitis, and may then be mistaken fur miliary tubercles (nodular cystitis).’ . Croupous Inflammation.—In connection with any of the above lesions the mucous membrane of the bladder may be covered, in patches or sometimes over a considerable portion of its surface, with a layer of fibrin, either granular or fibrillar, enclosing pus and epi- thelial cells and bacteria. The mucosa may be infiltrated with fibrin. This form of inflammation may occur in connection with severe infectious diseases—measles, diphtheria, scarlatina, typhoid fever; in connection with similar inflammation of the external genitals, in puerperal fever, noma, and sometimes in the presence of foreign bodies. It is rarely an idiopathic disease. Various forms of bacteria have been found in the urine in connec- tion with the various phases of inflammation of the bladder. Aside from the tubercle bacillus which is always concerned with 1 Alexander, Journal Cutaneous and Nervous Diseases, July, 1893. Digitized by Microsoft® THE URINARY APPARATUS. 685 tuberculous lesions, the most common micro-organisms are the Bacil- lus coli communis, Streptococcus pyogenes, and Staphylococcus pyo- genes and Bacillus proteus. Many other forms are of occasional occurrence. While the exact significance of the germs named in connection with cystitis is not yet fully clear, there is much reason to attribute serious importance especially to the Bacillus coli communis.’ Tuberculous Inflammation.—This disease commences by the for- mation of miliary tubercles in the mucous membrane of the bladder. By the coalescence of the tubercles and the degeneration of tissue about them, ulcers are formed, and it is most frequently in the ulcer- ative stage that the lesion is seen. The ulcers, which may be large or small, are usually most abundant at the base of the organ. Their edges may be cheesy, and miliary tubercles in greater or smaller numbers are usually found in the mucosa about them. Not infre- quently large shreds of tissue are loosened and cast off. The mucosa about the ulcers is apt to be infiltrated with small spheroidal cells. Tubercle bacilli are present in many of the tubercles and in the edges and base of the ulcers. They may also be found in the urine, and are then of diagnostic significance. Catarrhal inflammation is a very constant accompaniment of this lesion. Tubercular cystitis may occur in connection with tubercular inflammation of the lungs, intestines, or of the kidney, uterus, prostate, etc. TUMORS. Fibromata have been described, occurring as small nodular tu- mors in the submucosa, but they are rare. Aside from the polypoid thickenings of the mucosa occurring in chronic cystitis, soft vascular paptllomata are of frequent occur- rence. These tumors vary in size from that of a pea to that of a pigeon’s egg or larger. They consist of a fibrous, often very vascu- lar stroma, and are covered on the surface with numerous small, closely set, villous projections, over which are irregular layers of elongated or cylindrical cells. These tumors are very liable to bleed, are often accompanied by vesical catarrh, and may be covered by a precipitate of urinary salts. The epithelium is liable to peel off from the surface of the villi and appear in the urine. Sarcoma of the bladder has been described. Carcinoma,.—Carcinoma of the bladder is most frequently sec- ondary, and is then rarely due to metastasis, but usually to an ex- 1Consult Schmidt and Aschoff, “Die Pyelonepbritis, ” Jena, 1893; also Barlow, Arch. f. Dermatologie u. Syphilis, 1893, p. 855; also Melchior, “ Cystitis and Urinary Infection,” 1895 (bibliography). Digitized by Microsoft® 686 THE URINARY APPARATUS. tension of the growth from neighboring parts, as the uterus, vagina, or rectum. Primary carcinoma of the bladder may occur : 1. As a diffuse scirrhous infiltration of the entire wall of the bladder, usually with ulcerations of its inner surface. 2, As a circumscribed nodule which grows inward and out- ward, ulcerating on its inner surface, and sometimes producing per- forations. 3. As villous or papillomatous growth. The tumor grows from one or more points of the inner surface of the bladder. It is Fig, 330.—PaPILLOMA OF THE BLADDER. formed of tubular follicles lined with cylindrical epithelium, and, on its inner free surface, of tufts covered with cylindrical epithe- lium. The new growth may involve the entire thickness of the wall of the bladder. 4. A few cases of carcinoma have been described in which the stroma contained a varying quantity of smooth muscle tissue.’ Cysts.—Dermoid cysts of the wall of the bladder have been de- scribed, but are rare. Small cysts with serous contents sometimes occur in the mucous membrane; a part of them, at least, are be- lieved to be due to faulty embryonal development. ' The literature of tumors of the bladder may be found in Stein’s ‘‘ Study of the Tumors of the Bladder,” 1881. Digitized by Microsoft® THE URINARY APPARATUS. A87 PARASITES, ETC. Among the animal parasites occasionally found in the bladder may be mentioned Echinococcus, Distoma hematobium, Filaria sanguinis, Ascarides, and Oxyurides. A great variety of foreign bodies may be found in the bladder, particularly in the female. If their stay is long they are apt to be- come encrusted with urinary salts. CALCULI. Vesical calculi may occur singly or in great numbers, and vary greatly in size, ranging from small, sand-like particles up to masses four or five inches in diameter, but the usual range is from the size of a pea to that of a hen’segg. They are usually oval, spheroidal, or elongated ; or, when several are present, they are apt to be faceted. The surface may be smooth or rough. They are usually more or less distinctly lamellated, and are frequently formed around a central body called a nucleus, which may either be formed of urinary salts or some foreign body. Their most common constitu- ents are phosphates, uric acid and urates, and calcium oxalate, or various combinations of these. Uric Acid Calcult.—These are the most common of vesical cal- culi. In the form of small brownish-red, crystalline aggregations they may be passed as “‘ gravel.” The larger uric acid calculi are not commonly of very great size, are frequently finely nodulated on the surface, but may be smooth. The color varies from light yellow to dark reddish-brown ; they are usually dense and lamellated. Calcult formed of Urates.—Calculi composed of pure urates are rare, these salts being more commonly combined with uric acid and the phosphates to form the complex calculi. Sodium urate, in the form of small spined, more or less globular crystalline masses, forms one of the varieties of ‘‘ gravel.” Phosphatic Calcult.—Pure calcium phosphate calculi are, rarely, found as whitish, usually smooth, and small lamellated concretions. Mixed or Triple Phosphate calculi are common, and frequently attain large size. These calculi are sometimes pure, but the deposit is more frequently associated with other salts, either as encrusting or intercalated lamelle. Triple phosphate calculi are usually rough on the surface, of grayish-white color, lamellated, and frequently very friable. Small gray or white, hard, and usually smooth calculi of pure calcium carbonate occur rarely. Calcium carbonate is sometimes passed as gravel in the form of minute spheroidal bodies, either singly or in clusters. Calcium Oxalate calculi (mulberry calculi) are comparatively Digitized by Microsoft® 688 THE URINARY APPARATUS. common, either pure or in combination with uric acid or the phos- phates. Calcium oxalate may occur in the form of very small, hard, smooth concretions, or as larger, heavy, hard, finely or coarsely nodulated brown or blackish lamellated masses. The nucleus or some of the lamella, or both, are often composed of uric acid. Cystin Calculi are usually ovoidal in shape, of waxy consistence, of clear or brownish or greenish-yellow color, with mammillated surface and crystalline fracture. Cystin may be associated in a variety of ways with other calculi. Xanthin Calcult, which are very rare, are usually of moderate size, smooth, of a cinnamon or cinnabar-red color, lamellated, and oval or flattened in shape. Solid masses of fibrin and blood sometimes occur in the bladder, and may exist as independent structures, or form nuclei for the de- posit of urinary salts. For a detailed account of calculi, the conditions under which they form, modes of analysis, etc., we refer to special works on this subject. THE URETHRA. CONGENITAL MALFORMATIONS. Some of the malformations of the urethra are described with those of the penis. The urethra may be impervious or may open at the root of the penis. More commonly there is partial obliteration or stricture of some part of the canal. The entire urethra may be dilated into a sac full of urine. There may be a canal on the dorsum of the penis, formed by the fusion of the spermatic cords, and opening in the glans above the urethra. There may be two or more openings of the urethra. The canal may be dislocated so as to open in the inguinal re- gion. A number of cases have been reported in which a valve in the urethra has produced hypertrophy of the bladder, dilatation of the ureters, and hydronephrosis.’ Owing to its narrowness, greater length, and peculiar connec- tions with the internal generative organs, the male urethra is much more liable to disease than the female. CHANGES IN SIZE AND POSITION. Dilatation of the urethra may be produced by strictures, or by !Virch. Arch., Bd. xlix., p. 348. Digitized by Microsoft® THE URINARY APPARATUS. 689 calculi or other bodies fixed in its lumen. The dilatations are fusi- form or sacculated in shape, and may reach the size of an orange or be even larger. Strictures of the urethra are usually produced by inflammation of its walls. The stricture may be temporary, produced by a diffuse inflamma- tory swelling of the mucous membrane, or by the raising of the re- laxed membrane into a fold or pocket. Permanent strictures are produced by structural changes in the walls of the urethra. 1. The mucous membrane and submucous tissue are left hard and unyielding by the preceding inflammation. Subsequently the new fibrous tissue contracts and narrows the canal. 2. Ulceration of the mucous membrane leaves cicatricial tissue, which contracts, and also produces adhesions and bands of fibrous tissue. 3. There is fibrous induration of the corpus spongiosum and con- sequent constriction of the urethra. The most frequent position of strictures is at the junction of the membranous and spongy portions of the urethra, or close to this point. They also occur at the fossa navicularis and the meatus, but frequently in the prostatic portion. There may be one stricture or several. The consequences of stricture are dilatation of the urethra, the bladder, the ureters, and hydronephrosis ; inflammation and ul- ceration of the urethra behind the stricture, with perforation, infil- tration of urine, or the formation of fistulee.’ The urethra may also be obstructed by folds of the mucous mem- brane ; by muscular valves at the neck of the bladder ; by wounds ; by polypi and swollen glands ; by new growths ; by changes in the prostate and perineum ; by calculi, mucus, blood, and echinococci coming from the bladder ; by foreign bodies introduced from with- out. Prolapse and inversion of the mucous membrane is seen in young girls and womenin rare cases. There is a bluish-red swelling, from. the size of a pea to that of a walnut, at the meatus. In the male invagination of the mucous membrane of the urethra has been seen after injuries of the perineum WOUNDS—RUPTURE—PERFORATION, Wounds of the urethra are produced in many ways, but most commonly by catheters and bougies. The wounds may cicatrize, or 1 For literature of stricture of urethra, and plates illustrating several forms, see article by Dzttel in Pitha and Billroth’s “Handbuch der allg, Chirurgie,” Bd. iii., bth. 3. ore j4 Digitized by Microsoft® 690 THE URINARY APPARATUS. there may be infiltration of urine or the formation of fistule or false passages. Ruptures of the urethra are produced by severe contusions and by fracture of the pelvic bones. Extravasations of blood and urine, and gangrenous inflammation of the surrounding soft parts, are the ordinary results. Ulceration and perforation of the urethra may lead to the forma- tion of fistulee, which open in various directions through the skin. INFLAMMATION. Catarrhal Urethritis may be simple and due to the action of chemical irritants, to the extension to the urethra of inflammation from other parts, and to unknown causes ; but it is most frequently due to the action of the gonorrheeal poison. In its acute form it in- volves either a portion or the whole of the urethra. The mucous membrane is red, swollen, and covered with muco-pus. The inflam- mation may extend to the fibrous wall of the urethra, the corpora spongiosa and cavernosa. This may result in the formation of new connective tissue or of abscesses, especially near the fossa navicula- ris. The inflammation may also extend to the bladder, the glands of Cowper, the prostate, the spermatic cord, and the testicles. The inguinal glands also may be swollen and inflamed, and the lymphatic vessels on the dorsum of the penis may be involved in the same pro- cess. Chronic inflammation of the urethra may exist fora long time with the production of a muco-purulent exudation, but without the occurrence of marked structural lesions. In other cases it leads to ulceration, to fibrous induration of the wall of the canal, to indura- tion and swelling of the mucous follicles, to polypoid thickenings of the mucous membrane. The exudation in gonorrhceal inflammation of the mucous mem- branes, not only of the urethra but also of the vagina and of the eye, constantly contains, in greater or less numbers, a form of micrococ- cus which is said by some observers—although this is denied by others—to present characteristic morphological characters. The Micrococcus gonorrhcezee—called gonococcus—which is spher- oidal or ovoidal in shape, usually occurs in pairs or in groups of four or more, and may be contained in the pus cells (Fig. 80) or lie on their surfaces‘or free in the fluid. The pus cells sometimes contain very large numbers of the micrococci. The gonococcus may be stained by drying the exudation on a cover glass and using Gram’s method. For details as to the biology of the gonococcus see page 206. Digitized by Microsoft® THE URINARY APPARATUS. vyl Croupous Inflammation is sometimes seen in children. Fibrin- ous casts of a small or large portion of the canal may be formed. Syphilitic Ulcers may be situated at the meatus or as far back as the fossa navicularis. They are apt to produce strictures. Tubercular Inflammation rarely occurs in the mucous mem- brane of the urethra in connection with tubercular inflammation of the bladder, prostate, or testicles. TUMORS. Aside from the polypoid outgrowths from the mucous membrane of the urethra as the result of chronic inflammation, fibrous polyps may occur congenitally, or polyps containing glandular structures or cysts rarely occur. Carcinoma may occur as a result of local extension from adjacent organs or metastasis from the bladder. Cysts may occur in the mucous membrane as a result of the dilata- tion of the mucous glands. Circumscribed masses of dilated veins occasionally occur in the urethra, forming the so-called urethral hemorrhoids. The sinus pocularis may be dilated in children by the retention of its secretion, so as to form a tumor which may obstruct the exit of urine, cause hypertrophy of the bladder and dilatation of the ureters. Digitized by Microsoft® THE ORGANS OF GENERATION. FEMALE GENERATIVE ORGANS. THE VULVA. MALFORMATIONS. The external genitals may be entirely absent or imperfectly de- veloped. The fissure between the labia may be unformed, or the la- bia may grow together, with or without obstruction of the urethra. The clitoris and nymph may be abnormally large, or the nymphz may be increased in number. The clitoris may be abnormally long, resembling a penis ; at the same time the vagina is narrow, the ute- rus small and undeveloped or malformed ; the ovaries small, some- times situated in the labia ; the mamma small, and the body of a masculine character. Such cases are sometimes called pseudo-her- maphrodites. The clitoris may be perforated by the urethra or may be cleft and apparently double. The hymen frequently exhibits various anomalies. It may be entirely absent. The opening may be very large or in unusual pla- ces ; there may be several openings ; the free edge may be beset with papillary projections ; there may be no opening at all.’ HAEMORRHAGE, HYPER-EMIA, ETC. Heemorrhage may take place from wounds or ulcers of the vulva, but the most important form of hemorrhage is that which occurs in the connective tissue of the labia majora. This is produced during labor or from external injury. One of the labia may be swollen and distended by the extravasated blood until it isas large as a child’s head. The blood may be gradually absorbed, or it may decompose with suppuration or gangrene of the surrounding tissue. The puru- 1 For description and illustrations of anomalies of the hymen, which may be use- ful for medico-legal purposes, see Courty’s ‘‘ Diseases of Uterus, Ovaries, Fallopian Tubes,” Trans, by McLaren} Bo By Microsoft® THE ORGANS OF GENERATION. 693 lent matter may escape through the skin and the patient recover, or the suppuration may extend into the pelvis and cause death. » A varicose condition of the veins of the labia is not infrequent. Gidema may occur in acute form in pregnant and puerperal women, and may terminate in suppuration or gangrene. (CHdema of the la- bia majora frequently accompanies disturbances of the venous cir- culation, as in certain heart and lung diseases ; or it may occur in chronic diffuse nephritis or other wasting diseases, or as a result of thrombosis or other disturbances of circulation in the uterine or peri- vaginal venous plexuses. This may be excessive, leading to the transudation of fluid through the skin, to the formation of vesicles, to superficial erosion, or even to gangrene. INFLAMMATION. The skin, mucous membrane, connective tissue, and glands of the vulva may be the seat of inflammation. Acute catarrh of the mucous membrane may be caused by a variety of irritating influ- ences, but is most frequently due to gonorrhceal infection. The mucous membrane is swollen and red and covered with a muco-pu- rulent exudation. The labia may be swollen, the glands of Bartho- lin are liable to be involved, and abscesses of the labia may be de- veloped. Chronic catarrhal inflammation may lead to superficial or deep ulceration of the mucous membrane, or to papillary outgrowths, or to thickening of the labia. Suppurative inflammation of the tis- sue of the labia may occur in connection with a similar process in neighboring parts. Erysipelatous inflammation of the skin of the vulva is frequent in young children and may cause death. Inadults itis less common. Inflammation of the vulvo-vaginal glands may be acute and produce abscesses, or chronic and produce induration of the gland. Gangrene may follow erysipelatous inflammation, may occur after parturition, may accompany severe exhausting and infectious dis- eases, or may occur as an epidemic disease, especially anzong chil- dren. It may be the result of bruises or other injuries. In some forms, such as those known as noma and hospital gangrene, the destruction of tissue proceeds with extreme rapidity. Herpes, eczema, lichen, prurigo, etc., may be found on the skin of the vulva. Syphilitic inflammation and ulceration are of frequent occurrence on the vulva, particularly on the mucous surfaces, and frequently lead to considerable destruction of tissue and cicatricial contractions. Simple Croupous Inflammation may occur, with or without diphtheria and a similar lesion of the fauces or elsewhere, and is fre- ted with gangrene. quently associa Digitized by Microsoft® 694 THE ORGANS OF GENERATION. Lupus.—This form of inflammation, usually with more or less destructive ulceration, occasionally occurs in the vulva. TUMORS. Fibroma.—Circumscribed fibrous tumors are found in the con- nective tissue of the labia, mons veneris, perineum, clitoris, and entrance to the vagina. They may attain a large size, and, attached only by a pedicle, may hang far down between the legs. The skin is usually movable over the surface of these tumors. Fibroma diffusum (elephantiasis).—This usually involves the clitoris or the labia, or both, and may extend to surrounding parts of the skin. It consists essentially of a diffuse hypertrophy of the skin and subcutaneous tissue, with or without involvement of the papillae and epidermis. The surface may be smooth or rough. Sometimes when the new growth is circumscribed, rough or smooth polypoid growths, often of large size, are formed. When the papillz and epidermis are much involved, larger and smaller cauliflower-like excrescences may cover the hypertrophied parts and the surface be very rough and scaly. Paptllomata.—These growths consist of hypertrophied papille covered with thick layers of epithelium. They vary in size from that of a pea to that of an apple, and have a cauliflower appearance. Syphilitie Condylomata.—In one form, the so-called mucous patch, there is an infiltration of the papillary layers of the skin or mucous membrane with variously shaped cells and fluid, so that the tissue has a gelatinous appearance. In other cases there is an hypertrophy of the papille, so that larger and smaller wart-like ex- crescences are formed. This is called the pointed condyloma. Inpomata, fibro-myomata, and fibro-sarcomata are of occasional occurrence in the vulva. A few cases of melano-sarcoma are re- corded. Chondroma of the clitoris has been described. Carcinoma of the vulva may be primary, usually in the form of epithelioma of the clitoris or labia, or it may be secondary to cancer of the uterus, vagina, etc. Cysts are found in the connective tissue of the labia majora and minora. They are from the size of a pea to that of a child’s head. They may contain serum, colloid material, purulent or bloody fluid, or they may have the characters of dermoid cysts or atheroma cysts. Their origin is in many cases obscure. In some cases they are doubtless due to dilatation of lymph vessels. Cysts may be formed by a stoppage and filling with fluid of the canal of Nuck, or by adila- tation of the ducts or acini of the vulvo-vaginal glands. Digitized by Microsoft® THE ORGANS OF GENERATION, 695 THE VAGINA. MALFORMATIONS. The vagina may be entirely absent, and the internal organs of generation also absent or imperfectly developed. Hither the upper or the lower portion of the canal may be absent while the remaining portion is present. The vagina may be closed by an imperforate hymen or by fibrous septa at any part of its canal. The canal may be abnormally small without being occluded. . The vagina may be double, in connection with a double uterus ; or, while the uterus is normal, the vagina may be incompletely di- vided by a longitudinal septum. CHANGES IN SIZE AND POSITION, Dilatation of the vagina is produced by tumors, by the prolapsed uterus, and by the accumulation of blood and mucus behind con- strictions or obliterations of the canal. Lengthening of the vagina is produced by any cause which draws the uterus upward. Nar- rowing of the vagina is found asa senile change ; is produced by tumors and by ulceration of the wall of the canal. Extensive ulcers may even cause entire obliteration of the canal. Prolapse of the vagina occurs by itself, usually as a result of thickening or laxity of its walls, or in connection with prolapse of the uterus. As an idiopathic process it usually takes place soon after parturition. A larger or smaller portion of the canal is in- verted and projects through the vulva. The entire circumference of the canal may be inverted and prolapsed, or only the anterior or pos- terior wall. The prolapse is at first small, but may afterward grad- ually increase in size and may drag down the uterus with it. In other cases prolapse of the uterus is the primary lesion, and the vagina is inverted by the descent of that organ ; or the body of the uterus may retain its normal position, while an hypertrophy and lengthening of the cervix alone drag down the vagina. Hernia vesico-vaginalis—cystocele—may be either the cause or effect of a prolapse of the vagina and uterus. If the cystocele is the primary lesion, it begins as a small projection of the wall of the blad- der into the anterior part of the vagina. As the urine accumulates in this sac it increases in size, projects through the vulva, draws down the vagina and the anterior lip of the cervix, and finally the entire uterus. If the cystocele is the secondary lesion, it is simply produced by the dragging-down of the posterior wall of the bladder by the inverted vagina. Digitized by. Microsoft® 696 THE ORGANS OF GENERATION. Hernia intestino-vaginalis.—A portion of the intestines may be- come fixed in Douglas’ cul-de-sac between the rectum and the uterus. This portion of intestine gradually becomes larger, pushes forward the posterior wall of the vagina, inverts and fills up that canal, and finally projects through the vulva. It may drag with it the pos- terior wall of the vagina and the uterus. Rectocele vaginalis.—A_ sac is formed by the projection of the anterior wall of the rectum and the posterior wall of the vagina. This lesion is of rare occurrence and does not reach a large size. When the vagina is prolapsed there is usually an inflammatory condition of the lining membrane or a thickening of the epidermis. WOUNDS—PERFORATIONS. Wounds of the vagina are made by penetrating instruments, by forceps and other obstetrical weapons, and by the foetus during delivery. Such wounds may heal, may give rise to large hemor- rhages, may suppurate, may produce abscesses in the surrounding tissues, may leave fistulous openings into the vagina or may cause constriction or obliteration of its canal. Vesico-vaginal Fistulce are usually produced by injuries from instruments or from the foetus during delivery ; less frequently by ulceration of the vagina, bladder, or adjacent connective tissue, or by abscess in the surrounding parts. The fistule form an opening between either the bladder or the urethra and the vagina. They allow the urine to pass into the vagina. Spontaneous cure does not take place. Recto-vaginal Fistule are formed in the same way as the last- mentioned. They allow the passage of gas or faeces into the vagina. They sometimes heal spontaneously. INFLAMMATION. Catarrhal Inflammation of the vaginal mucous membrane may be acute or chronic. It is most frequently caused by gonorrhceal infection, but may be due to local irritation or depend upon general causes. It not infrequently occurs in the new-born. In the acute form the mucous membrane is swollen and frequently covered with a muco-purulent or a purulent exudation. In the chronic form the mucous membrane may be swollen, covered with a purulent exuda- tion ; there may be an exfoliation of epithelium, shallow or deep ero- sions, or ulcers. Sometimes large shreds or membranes are cast off from the va- gina which consist wholly of exfoliated, flat epithelium (Fig. 331). In other cases the mucous membrane is thickened, dense, and some- Digitized by Microsoft® THE ORGANS OF GENERATION. 697 times pigmented, or it may be roughened, covered with papilla, or it may be relaxed and prolapsed. Croupous Inflammation may occur after parturition, in dysen- tery, in typhus and typhoid fever, diphtheria, scarlatina, measles, and other infectious diseases. The mucous membrane is swollen and covered with a: grayish layer of fibrin and pus. The mucosa and submucosa may be infiltrated with fibrin and pus. The infiltrated portions of the mucosa and submucosa may die and become gangre- nous, and thus deep and extensive ulcers be formed. Suppurative Inflammation of the fibro-muscular coat of the vagina may occur after injuries or in pregnant and puerperal wo- men. Abscesses may be formed which penetrate into the labia or into the pelvic connective tissue. In other cases the intense phleg- Fie. 331.—VacrnaL EpiItHeLium A fragment from a large exfoliated mass. monous inflammation may lead to the death and casting-off of por- tions of the vaginal wall, or even of the entire wall. Gangrene of the vagina may occur as a result of croupous or intense suppurative or syphilitic inflammation, or from unknown causes. In the form of noma it may be very extensive and rapidly destructive. Tuberculous and Syphilitic Inflammation, usually leading to more or less extensive ulceration, may occur in any part of the vagina. Tuberculous inflammation is secondary to tuberculosis of other parts. Syphilitic ulcers may heal, sometimes leaving marked cicatrices, and sometimes not. TUMORS. Fibroma, fibro-myoma, sarcoma, myoma levicellulare, are of Digitized by Microsoft® 698 THE ORGANS OF GENERATION. occasional occurrence in the vagina. Myoma striocellulare is of rare occurrence. Papillomata are of frequent occurrence as a result of chronic inflammation. Carcinoma of the vagina is usually secondary to cancer of the uterus. It may be primary as a circumscribed nodular tumor, or more frequently it occurs in a papillary and ulcerating form and often spreads to neighboring parts. Cysts.—These are not very common and may be small or as large asa hen’segg. They may be lined with flattened epithelium, and contain serous or viscid, dark-colored or transparent fluid. PARASITES. Among the animal parasites Oxyurts and Trichomonas vagina- lis are of occasional occurrence. Among the vegetable forms Oidium albicans, Leptothrix are occasionally seen, while micrococct and various other forms of bacteria are common. Staphylococcus and Streptococcus pyogenes have been found many times in the normal vagina. The pathogenic significance of the bacteria in the vagina is not yet established. THE UTERUS. MALFORMATIONS. The uterus, up to the third month of intra-uterine life, consists of two large cornua, which by the fusion of their lower ends form the uterus. The uterus, tubes, and vagina may be entirely absent, with or with- out absence of the external genitals. Or the uterus alone, or the upper part of the vagina also, may be absent. The uterus may be only rudimentary while the vagina is normal. It then appears as a flattened solid body with solid cornua. Or there are two cornua joined at their lower extremities so as to form a small double uterus. Or the uterus is represented by a small sac, which may or may not communicate with the vagina. Or there is a very small uterus, with thin muscular walls and two large cornua. Only one of the cornua which should form the uterus may be developed while the other is arrested in its growth. The uterus is then a long, cylindrical body, terminating above in one tube. On the side where the other horn should have been developed there is no tube, or only a rudimentary one. Both ovaries are usually present. The two cornua may be fully developed, but their lower ends remain separated and form a double uterus. An entire separation into two distinct uteri and vagine is very rare. More frequently the uterus consists of one body, divided by a septum into two cavities. Digitized by Microsoft® THE ORGANS OF GENERATION. 699. There are then two cervical portions of the uterus projecting into a single vagina, or each into a separate vagina. Or there is only a single cervix. The septum in the uterus may be complete or only partial. We also find abnormal size of the uterus, abnormal flexions ; the cervix may be solid or may be closed by the vaginal mucous mem- brane. Or the cervix may have an abnormal form with a small opening or canal.’ CHANGES IN SIZE. In the new-born infant the uterus is small, the body flattened, the cervix disproportionately large. During childhood the organ increases in size, but the body remains small in proportion to the cervix. At puberty the shape changes and the body becomes larger. At every menstruation the uterus is somewhat swollen and con- gested. After pregnancy it does not return to its virgin size, but re- mains somewhat larger. In old age it gradually becomes smaller ; its walls are harder and more fibrous. Abnormal Smaliness of the uterus is sometimes found as an ar- rest of development. The uterus in adult life retains the size and shape of that of the infant. It may result, however, from chronic endometritis, from repeated pregnancies, from old age, or from chronic exhausting diseases. Its cavity may be smaller than nor- mal, or distended with mucus. Large myomata sometimes cause marked atrophy of the uterine wall. Atrophy of the vaginal portion of the uterus is sometimes observed after repeated pregnancies, some- times without known cause. Narrowing and obliteration of the cavity of the uterus and of the cervix are usually produced by chronic inflammation. Enlargement of the Uterus may be due to too early develop- ment. It is accompanied by abnormally early development of all the sexual organs and functions. The uterus may be enlarged in con- nection with heart disease, prolapse and abnormal flexions and ver- sions, chronic inflammations, repeated pregnancies, myomata, and accumulations of blood or mucus in the uterine cavity. Enlarge- ment of the vaginal portion may be produced by the above causes, and is also found without known cause. One or both lips of the cervix may be uniformly increased in size, or they may be lobulated. Dilatation of the uterus is produced by accumulations of blood, mucus, or pus in consequence of narrowing or obliteration of the cer- vix or vagina. The uterine walls may retain their normal thickness, be thickened or thinned. The most frequent position of the stenosis 1 Illustrations of various forms of malformation of the cervix may be found in the translation by McLaren of Courty’s ‘‘ Diseases of the Uterus, Ovaries, etc.,” 1883. Digitized by Microsoft® 700 THE ORGANS OF GENERATION. is the os internum. The retained contents after a time change in character, forming a thin, serous fluid—hydrometra—or they may be mixed with blood. The dilated uterus is not usually larger than an apple, but it sometimes reaches enormous dimensions, If both os internum and os externum are closed the cervical cavity may be also dilated and the uterus have an hour-glass shape. If the obstruction is in the vagina, the uterus and vagina may form a large, flask- shaped body, and the line of demarcation between cervix and vagina be lost. In some cases the dilatation is confined to the cervix. If the obstruction is not complete the retained fluid may escape into the vagina and afterward accumulate again. Accumulation of menstrual blood in the cavity of the uterus— hematometra—is usually produced by congenital stenosis of the cervix or vagina. The dilated uterus may reach an enormous size. If the fluid is not evacuated by surgical interference there may be either rupture or ulcerative perforation of the uterus. The blood may escape into the abdominal cavity, or be shut in by adhesions, or perforate into the bladder or intestines. Sometimes the blood passes into the Fallopian tubes, dilates them, and escapes through their ab- dominal ends. CHANGES IN POSITION. The body of the uterus may become fixed in an abnormal position, while the situation of the cervix is unchanged. The body may be bent forward—anteflexion ; backward—retroflexion ; or sideways —lateral flecion. The flexion may be slight, or so great that the neck and body form an acute angle. Anteflexion is the most com- mon variety, and that in which the flexion is greatest. Peritoneal adhesions, flaccidity of the uterine walls, particularly after delivery, atrophy of the walls, ovarian and other tumors, etc., are the usual causes of flexions. The Versions of the uterus consist in an abnormal inclination of the long axis of the organ to that of the vagina. The uterus may be inclined backward, forward, or to one side. Retroversion is very much the most common. The fundus uteri is directed backward and downward, the cervix forward and up- ward. This condition is found in various degrees ; in the highest the fundus lies in Douglas’ cul-de-sac with the cervix upward, so that the axis of the uterus is parallel to that of the vagina, but in a direction nearly opposite to the normal one. Abnormal looseness of the ute- rine ligaments, abnormally large capacity of the pelvis, hypertrophy or tumors of the uterus, and pregnancy during the first four months, are some of the more common conditions under which this lesion occurs. Anteversion.—Inclination of the fundus forward and downward, Digitized by Microsoft® THE ORGANS OF GENERATION. 701 and of the cervix backward and upward, is not common and sel- dom reaches a high degree. It occurs under the same general ex- ternal conditions as anteflexion. Lateroversion is not very common as a simple lesion, but is not infrequently combined with other displacements. It may be pro- duced by congenital shortening of one of the broad ligaments, by ad- hesions, or by the pressure of tumors. The greater degrees of version may produce very grave lesions. The urethra and rectum may be compressed. Cystitis, perforation of the bladder, dilatation of the ureters and hydronephrosis, and fatal obstruction of the bowels may follow. If pregnancy exists abortion may take place, or the inverted uterus may be forced through the peritoneum and posterior wall of the vagina and project through the vulva. In the non-pregnant uterus pressure on the veins and consequent chronic inflammation of the organ may follow. Prolapsus Utert consists of a descent of the uterus into the vagina. The uterus may be only slightly lowered or it may project at the vulva. In complete prolapse we find a tumor projecting through the vulva, partly covered by the distended vagina, and pre- senting the opening of the os externum near its centre. The blad- der and rectum may be drawn down with the vagina or may remain in place. The exposed cervix and vagina usually become inflamed and sometimes ulcerated, or the mucous membrane may become thickened. The lesion is frequently complicated by hypertrophy of the cervix. Gradual prolapse, which is most frequent, may be due to an in- creased weight of the uterus, as in pregnancy, inflammatory enlarge- ment, the presence of tumors, etc.; or to some abnormal condition of the uterine supports. Itis frequently caused by a vaginal cystocele or rectocele. Sudden prolapse is most apt to occur in an enlarged uterus or one unduly heavy by reason of tumors connected with it. It is most common in subinvolution after parturition. Elevation of the uterus is produced by mechanical causes crowd- ing or dragging it upward, as adhesions, tumors, etc. The vagina ig drawn up and lengthened, and the vaginal portion of the cervix may be obliterated. Inversion of the uterus consists of an invagination of the fun- dus. The fundus may be invaginated in the body, the fundus and body in the cervix, or the entire organ in the vagina. It usually oc- curs when the uterine walls are relaxed, and is very frequently due to traction on the placenta during parturition. It may take place spontaneously after parturition. It may be produced by intra-ute- rine tumors. The mucous membrane of the inverted organ is fre- quently inflamed, particularly when the inversion is complete. Digitized by Microsoft® 702 THE ORGANS OF GENERATION. Hernice of the uterus are rare. Ventral hernice may occur dur- ing the latter months of pregnancy, the peritoneum, aponeuroses, and skin being forced outward to form a sac in which the uterus lies. Orural herni@ are produced by the drawing-down of the ute- rus and ovaries into the sac of an intestinal hernia. Inguinal her- nia may be produced in the same way or be congenital. IJschiatic hernia has been seen. Pregnancy may occur in the uterus while situated in a crural or inguinal hernia. RUPTURE AND PERFORATION. Rupture of the unimpregnated uterusis rare. It may, however, occur when the uterine cavity is distended with blood or serum, or in connection with large myomata of the uterine walls. In the gravid uterus ruptures have been seen in nearly every month of pregnancy, but most frequently toward the end. The rup- ture may be produced by thinning of the uterine wall by tumors, or by violent contusions, or as the result of cicatricial contraction of the os. : The act of parturition is the most frequent cause. Malpositions of the foetus, narrowing of the pelvis, protracted labor, thinning of the uterine wall from tumors, forcible use of the forceps and other instruments, are the ordinary causes. The rupture may be in the body of the uterus or the cervix, or both ; it may be large or small ; it may extend completely or only partly through the uterine wall. The consequences of partial rupture are hemorrhage, gangrenous inflammation of the edges of the rupture, peritonitis, and usually death. In rare cases the rupture cicatrizes and the patient recov- ers. Complete rupture usually causes death in a short time. The foetus escapes partly or completely into the abdominal cavity. If the patient survives the immediate shock, fatal peritonitis soon en- sues. In rare cases the foetus is shut in by adhesions and the pa- tient survives. Perforations of the uterus may be produced by carcinoma, by abscesses in its neighborhood, and by ovarian cysts. HYPERAMIA—UTERINE AND PERI-UTERINE HEMORRHAGE. Hypercemia.—Aside from the active menstrual hyperemia, the uterus may be hypereemic in acute and chronic inflammation, as a re- sult of displacement of the organ, and in certain forms of heart dis- ease. The organ is usually enlarged, the mucous membrane swol- len, and the veins more or less evidently dilated. Hemorrhage.—Effusion of blood into the cavity of the uterus occurs normally at the menstrual periods. For the abnormalities to which this function is subject we refer to works on gynecology. Digitized by Microsoft® THE ORGANS OF GENERATION. 403 Effusions of blood at other than the menstrual periods may be caused by mechanical hyperemia, by heemorrhoids, by acute hyperemia, by intra-uterine polypi and other tumors, by acute and chronic in- flammation, by typhus fever, scurvy, etc., by ulcerating carcinoma, by abortions and miscarriages. A peculiar form of hemorrhage is the polypoid heematoma, or fibrinous polypus of the uterus. It occursafter parturition and after abortions. The portion of the uterine wall where the placenta was attached, with or without a portion of retained placenta, forms the point of attachment of the pedicle of the polypus. We find a large, polypoid, bloody mass firmly attached by a pedicle to the uterine wall. The uterus enlarges with the growth of the polypus, the cer- vix is dilated, and the thrombus projects into and may even fill up the vagina. The formation of such a thrombus is accompanied by repeated hemorrhages. Hemorrhage in the substance of the uterus occurs in old age. The mucous membrane and uterine wall are infiltrated with blood, and there is some blood in the uterine cavity. Several cases of he- morrhagic infarction in the cervical portion of the uterus have been described.’ Pert-uterine or Retro-uterine Hoematocele consists in an accu- mulation of blood around the uterus or in Douglas’ cul-de-sac. It may consist of blood extravasated into the abdominal cavity, which settles into the pelvis; or, in consequence of local hyperemia, there may be repeated extravasations of blood. Inthe latter case the local peritonitis may produce false membranes, between the layers of which hemorrhages take place. A similar condition rarely occurs in the male. The hemorrhagic mass may become encapsulated, or may soften or suppurate and perforate into the rectum or vagina, or may be absorbed. A form of extraperitoneal hematocele is de- scribed in which the blood lies between the folds of the broad liga- ment. The extravasation may proceed from hemorrhage of any of the abdominal viscera or rupture of aneurisms ; from vascular new- formed false membranes ; from rupture of the varicose veins of the broad ligaments ; from rupture of hemorrhagic cysts of the ovaries ; from the Fallopian tubes in tubal pregnancy or in hematometra ; or from general causes, such as scurvy, purpura, etc. In some cases the extravasation begins at a menstrual period, and increases at the succeeding periods. Ante-uterine Heematocele is of occasional occurrence, either in connection with the retro-uterine form or when the posterior cul-de- sac is obliterated. 1See Chiart, Prager med. Wochenschr., Bd. xxi., No. 12, 1896. Digitized by Microsoft® 704 THE ORGANS OF GENERATION. INFLAMMATION. I. Inflammation of the Unimpregnated Uterus. Acute Catarrhal Endometritis.—In this disease, which in its lighter grades may leave but little alteration after death, the mucous membrane is swollen, hyperemic, and sometimes the seat of punc- tate hemorrhages. The epithelium may desquamate, and the mu- Fig, 332.—CHROoNIC ENDOMETRITIS WITH THE FORMATION OF A POLYPOID OUTGROWTH FROM THE Mucous MEMBRANE. cosa contain an undue quantity of small spheroidal cells. The sur- face is more or less thickly covered with muco-purulent exudation. In severe cases shreds of mucous membrane may be exfoliated. The lesion is usually most marked in the mucous membrane of the body, but may involve the cervix at the same time, or the cervix alone. The body of the uterus may be swollen and hyperemic. In dys- menorrhea membranacea there may be an expulsion, with more or less blood, of membranous masses consisting of fibrin mingled with blood and pus cells, oT QMPASstin gy ef exfehated superficial layers of THE ORGANS OF GENERATION. 705 epithelium. This exfoliated epithelium is frequently much flattened so as to considerably resemble the vaginal epithelium. When the shreds are large the openings of the uterine glands may be seen as perforations. Acute catarrhal inflammation of the uterus may be due to injury, exposure during menstruation, the gonorrhceal infec- tion, local infection with other bacteria, or it may accompany the general acute infectious diseases. Chronic Endometritis.—This may be a continuation of an acute inflammation or begin as a chronic disease. In some of the lesser degrees of inflammation we find but slight changes after death. The mucous membrane, on the other hand, may be swollen, hyperee- 2 150 LE ARO tray et NEE ge oie Sh Bae" a! ff eee ea it ez Te as Ong € his ab am REUSE Neb We Lore f gee 4 . 1? DP =e rs CsI, Lose “ng Aerie Lene, GES Zsa iia ILD Cove gat ES EEE § LER EL Fer ih Gp rca 2 Ara a VEE CALE BE (AOS: LBL CEA, 5 FTES é OL EEL 9 Be, SP He fi, CNG 2 By PL, : Lote So ee Oise Fei Se CO ; Shy are oo, le “isos Fic. 333._ADENOMATOUS HYPERPLASIA OF THE UTERINE Mucous MEMBRANE. This section is from a large polypoid outgrowth which protruded from the cervix uteri. mic, and covered with muco-purulent exudation. In oither cases there is more or less well-marked thickening of the mucous mem- brane, which may present a smooth or a rough papillary surface or polypoid outgrowths (Fig. 332). Owing to the hypertrophy of the uterine glands in this condition, these papillary outgrowths, which are not infrequently scraped off by the surgeon, often present the appearance of adenomata. This condition is called “adenomatous hyperplasia of the uterine mucous membrane” (see Fig. 333). Some- times a thick layer of new-formed, very vascular tissue develops over the surface of the mucous membrane, largely covering in the uterine glands (Fig. 334). From the decomposition of extravasated blood in the mucous membrane the latter may be mottled with brown or 55 Digitized by Microsoft® 706 THE ORGANS OF GENERATION. black. The glandular elements of the mucosa may be partially or almost entirely destroyed. The papillz of the cervix may be hyper- trophied, the mucous follicles swollen and their outlets obstructed, leading to the formation of the so-called ovula Nabothi. The uter- ine wall becomes flaccid and atrophied, or it may be hypertrophied, especially in the cervical portion. Ulceration of the mucous mem- brane, especially of the cervix, may occur. Contraction or oblitera- tion of the cervical canal may occur. The inflammation may extend to the Fallopian tubes or to the vagina. Chronic endometritis may exist at any age, but is most common Fie. 334.-CHRronic ENDOMETRITIS WITH THE FORMATION OF A THICK LAYER OF NEW-FORMED, VERY VASCULAR TISSUE OVER THE SURFACE OF THE Mucous MEMBRANE. a, uterine muscle tissue; b, mucous membrane of uterus; c, new-formed vascular tissue. after puberty, and is produced by a great variety of causes. It may occur in ill-nourished persons or in those suffering from exhausting diseases. It may be due to displacements and tumors of the uterus, subinvolution, injuries, etc. Croupous Endometritis.—This form of inflaramation is not very common. It occasicnally occurs in the puerperal uterus, in acute infectious diseases, cholera, typhoid fever, the exanthemata, etc. The disease sometimes involves the vulva, vagina, and Fallopian tubes. It may co-exist with croupous inflammation of the colon. Tuberculous Endometritis.—This usually occurs as part of tuber- Digitized by Microsoft® THE ORGANS OF GENERATION. OV culous inflammation of the genito-urinary tract. We find a part or the whole of the cavity of the uterus lined with a rough, yellowish or gray, cheesy mass, which may deeply involve the muscular walls of the organ. At the edges of the ulcerating cheesy areas we may find well-defined miliary tubercles, or we may find tubercles scattered through the otherwise intact mucosa. The lesions resemble those of tuberculous nephritis. Syphilitic Hndometritis.—The results of this infection are usually confined to the cervical portion, and consist of shallow or deep ulcerations and condylomata of the mucous membrane ; or there may be a diffuse thickening of the mucosa. Acute Metritis is usually the result of acute catarrhal endome- tritis. The organ is swollen, succulent, congested; the mucous membrane covered with muco-pus; the peritoneal coat congested. There may be small extravasations of blood in the wall or cavity of the uterus. The inflammation, in rare cases, becomes suppurative, and abscesses are formed in the uterine wall; these may perforate into the peritoneal cavity or into the rectum. Chronic Metritis is the result of an acute metritis or accompanies acute or chronic endometritis, andis dependent upon the same con- ditions: subinvolution, displacements, tumors, active irritants, etc. The uterus is enlarged, the wall congested, thickened, and soft, or, owing to the new formation of connective tissue, hard and dense. The lesion may be most marked in the body or in the cervical portion. Pertmetritis.—The peritoneal coat of the uterus may be inflamed, with the production of membranous adhesions or of pus. The adhesions may be small or very extensive, and, owing to their con- tractions, may cause various distortions and displacements of the pelvic organs. The inflammation is usually an accompaniment of chronic metritis and endometritis. In prostitutes such adhesions are of very common occurrence. Parametritis.—The connective tissue about the uterus, between that organ and the reflexions of the peritoneum, may be the seat of suppurative inflammation. It most frequently causes the death of the patient, but may result in the formation of dense connective tissue about the uterus. IT, Inflammation of the Pregnant Uterus. The forms of inflammation which have just been described may attack the pregnant uterus. Catarrhal endometritis may produce effusion of serum, extravasations of blood, and abortions. Metritis may lead to softening of the uterine wall, so that rupture takes place during labor. Perimetritis and parametritis produce adhesions and abscesses about the OATH Re d by Microsoft® 708 THE ORGANS OF GENERATION. Puerperal Inflammation. For a week or more after delivery we find the inner surface of the still dilated uterus rough, especially at the insertion of the pla- centa, and covered with blackened, gangrenous-looking shreds of blood, mucous membrane, and placenta. This condition is not to be mistaken for inflammation. As a result of some injury to the uterus or vagina during or after delivery, and the action of some infectious material which may gain access to the tissues, the puerperal uterus is liable to become Fic. 335.—UTrERINE PHLEBITIS FOLLOWING DELIVERY WITH RETAINED PLACENTA. Death nine days after delivery. Micrococci in the walls of the inflamed veins stained violet. the seat of a series of severe and often destructive inflammatory and necrotic changes. These may be confined to the uterus; they may induce serious alterations in surrounding parts; they may lead to an involvement of the peritoneum, or to pyeemia and its accompanying lesions in the most distant parts of the body. In one series of cases a more or less extensive gangrenous inflammation of the mucous membrane and the underlying parts may lead to the casting-off of larger and smaller shreds of necrotic tissueand the formation of deep and spreading ulcers, which may be accompanied by severe para- metritis and fatal peritonitis. This condition may be due to in- jury or to the presence of decomposing portions of retained placenta. In other cases the inflammation has a croupous character, which may Digitized by Microsoft® THE ORGANS OF GENERATION. 709 affect the vagina and lead to necrosis and gangrene, ulceration, and. peritonitis. In connection with either of the above forms of inflam- mation, or without them, there may be thrombosis of the uterine sinuses, purulent inflammation of the veins, suppuration and ab- scess in the uterine wall, suppurative inflammation of the ovaries and tubes, and, owing to the generalization of the infectious mate- rial, metastatic abscesses in the lungs, spleen, kidneys, etc. Or acute pleurisy, ulcerative endocarditis, purulent inflammation of the joints, hyperplastic swelling of the spleen and lymph nodes, may fur- nish characteristic features of the presence of an acute infectious dis- ease. In some cases which rapidly pass to a fatal termination the local lesions may be but slightly marked, and general alterations characteristic of pyzemia, such as metastatic abscesses, etc., be en- tirely wanting. Life seems to be overcome by an acute septic in- toxication. Micrococci are very constantly present in the exudation, in the lymph vessels, veins, and inflamed tissue of the uterus (see Fig. 335) ; often in enormous quantities in the peritoneal exudation and in the metastatic inflammatory foci. There is good reason for be- lieving that the destructive local processes are due, in the majority of cases, to the presence of the Streptococcus pyogenes, and that the general infection in this, asin other forms of septicemia and pyx- mia, is dependent upon the same cause (see Septiczemia). ULCERATION AND DEGENERATION. Catarrhal, tubercular, and syphilitic ulceration have been mentioned above. ; Phagedenic or Corroding Ulcer.—This rare form of ulceration usually occurs in old age, without assignable cause. It begins in the cervix and gradually extends until it may destroy the greater part of the uterus or even invade the bladder and rectum. The ulcer is. of irregular form; its base is rough and blackish, its walls indu- rated. It should not be confounded with carcinomatous ulcer, which it considerably resembles. Fatty Degeneration.—This may occur in connection with in- flammatory changes, in acute infectious diseases, and in phosphorus poisoning. Amyloid Degeneration inthe uterus is of rare occurrence. It may affect the muscle fibres or the walls of the blood vessels. TUMORS. Fibromata.—Dense nodular fibromata of the uterus are exceed- ingly rare, the so-called fibromata being in most cases myomata or fibro-myomata. Fibroma papillare, on the other hand, is a com- 56 Digitized by Microsoft® 710 THE ORGANS OF GENERATION. mon form of growth from the mucous membrane. It consists of a more or less vascular connective-tissue stroma covered with epithe- lium. The surface may be smooth or villous. It may contain very numerous gland follicles, and then approaches the type of adenoma, or even carcinoma. The stroma may be loose and succu- lent, and resemble mucous tissue, forming the so-called mucous polypi ; and these again may contain glandular structures. In any of these forms the blood vessels may be abundant and dilated, form- ing telangiectatic or cavernous polypi. The adenomatous polypi may become cystic from the dilatation of the gland follicles. Polypi of the uterus may be multiple or single, small or large. Numerous smaller and larger papillary outgrowths from the mucous membrane may occur in chronic endometritis. Single polypi may grow from the mucosa of the body of the uterus or from the cervix, and hang by a long pedicle down into the vagina. The large number of glandular structures in many of these chro- nic inflammatory, papillary, and polypoid outgrowths (Figs. 332 and 333) often justifies the name of adenomatous hyperplasia of the mucous membrane or of adenomatous papillomata or polyps. Syphilitic papillary growths in the form of pointed condylomata may form finely papillary, wart-like excrescences of variable size, particularly on the cervix. Myomata.—These tumors, whose characteristic structural ele- ments are smooth muscle cells (see Fig. 137), are the most common of uterine tumors and are frequently of no special practical importance, but are sometimes of very serious import. They are especially com- mon in negroes. They are most frequently composed of both mus- cular and fibrous tissue—fibro-myomata—but the relative amount of the two kinds of tissue is subject to great variation. They are most apt to occur after puberty, and usually in advanced life. They may be single or multiple, small or of enormous size; are usually sharply circumscribed, whitish or pink, dense and hard, or some- times soft, and present on section interlacing bands or irregular masses of glistening tissue. Their favorite situation is in connection with the body of the uterus, but they may occur in the cervix or in the folds of the broad ligaments. According to their position we may distinguish subserous, submucous, and intraparietal forms. The subserous myomata grow from the outer muscular layers of the uterus in the form of little nodules. As they increase in size they may become separated from the uterine wall and remain at- tached only by a narrow pedicle or by a little connective tissue. They may work their way between the folds of the broad ligament until they are at some distance from their point of origin. Some authors mention cases in which the tumors became entirely detacl Digitized by Microsoft® y detached THE ORGANS OF GENERATION. 711 from the uterus and were free in the abdominal cavity. In some cases the tumors excite inflammation of the adjacent peritoneum, leading to the formation of adhesions or of collections of pus. Cases are recorded in which, owing to the atrophy of the pedicle, subserous myomata have become completely detached from the uterus and were held in place and nourished by peritoneal adhesions. In other cases the tumor reaches a large size, but remains firmly attached to the uterus. This organ may then be drawn upward, the cervix and vagina being elongated and narrowed. The traction may be so great that the body of the uterus is entirely separated from the cervix. The bladder may also be drawn upward, producing incontinence of urine and cystitis. Subserous myomata are very often multiple and frequently attain great size. The submucous myomata grow from the inner muscular layers of the uterine wall. They commence as rounded nodules which lift up the mucous membrane. The usual position is the fundus uteri. They rarely occur in the cervix. As the tumors increase in size they project into the uterine cavity. They then remain continuous with the uterine wall over a large area, or are attached by a large or small pedicle. They are usually well supplied with vessels. The uterus dilates with the growth of the tumor, and its walls may be also thickened. The tumor may reach such a size as to entirely fill the cavity of the dilated uterus and project through the cervix into the vagina. The submucous myomata are usually single, although there may be at the same time subserous and intraparietal tumors. They are frequently soft. If they are of large size and polypoid in form, they may project through the cervix and drag down the fundus of the uterus, producing inversion. The mucous membrane covering them may be atrophied or hyperzemic, with dilated blood vessels, and may thus give rise to severe and repeated hemorrhages. Hemorrhage may occur in the substance of these tumors. Inflammation, suppu- ration, and gangrene may also occur. The surface may be ulcerated. In some cases the pedicle of the tumor is destroyed and it is sponta- neously expelled. The intraparietal myomata grow in the substance of the uterine wall, but, if they attain a large size, project beneath the serous or the mucous coat. They are found in every part of the uterus, but are most frequent in the posterior wall. The shape of the uterus is altered in a great variety of ways by the presence of these tumors ; its cavity is narrowed, dilated, or misshapen ; it undergoes flexion and version in every direction. The tumors may sink downward and become attached to the posterior wall of the vagina, lpoking dy) they grew from it. They may, Y12 THE ORGANS OF GENERATION. without the formation of a pedicle, project into the cavity of the uterus, fill it up, and project through the cervix. The uterus is dilated, its wall hypertrophied or atrophied. The tumors themselves may undergo a variety of secondary altera- tions. The muscle fibres may undergo fatty degeneration, and the tumor diminish in size, or may even undergo, it is said, entire destruc- tion and atrophy. Calcification may occur, converting a part or the whole of the tumor into a stony mass. The intraparietal and sub- mucous myomata may give rise to profuse hemorrhages ; thay may suppurate and become gangrenous. Sometimes the tumors or circumscribed portions of them are very vascular, constituting the telangiectatic or cavernous variety. These tumors, which possess some of the characters of erectile tissue, may suddenly change in size from a variation in the amount of blood which they contain. A very important change which is sometimes found in these tumors is the development of cysts in their interior (fibro-cystic tu- mors). This sometimes takes place in those tumors which grow out- ward beneath the peritoneal coat. We find one or more cavities communicating with each other, with rough, trabeculated walls. The appearance is more that of cavities than of cysts. There may be a number of smaller cavities, or they may fuse to form one large ‘one. The fluid contained in the cavities is like synovia, or is mixed with blood. These cystic myomata may reach an immense size and fill the abdominal cavity. The diagnosis, during life, between them and ovarian cysts is often very difficult, and they have frequently been the subjects of fatal operations. The cystic may be lined with ciliated epithelium.’ In the cervix uteri myomata are rare. They may grow as polypi beneath the mucous coat, or produce enlargement of the anterior or posterior lips, or may grow outward into the abdominal cavity. Combinations of myoma and sarcoma sometimes occur—myo- sarcoma. Sarcomata may occur as primary tumors in the mucous mem- brane of the uterus, either in the form of a diffuse infiltration or as a circumscribed nodular or polypoid mass. They frequently involve the muscular wall, are liable to hemorrhage and gangrene, and, particularly in the diffuse form, are liable to recur after removal. They may consist largely of spindle or spheroidal cells, or both. It is said that sarcomaof the uterus is more liable to occur at an advanced age than at an early period, as is the rule with sarcomata of other organs. Giant-celled sarcomata have been described. ‘ ee ee ee Brens, “Ueber wahre Epithel. fihrende Cystenbil- ung d. Uterus-Myomen, ” Leipzig, 1894, : Digitized b ry ‘Microsoft® THE ORGANS OF GENERATION. 713 Angioma.—Cavernous angiomata of the wall of the uterus have been described. Adenoma.—Between a simple adenomatous hyperplasia of the mucous membrane of the uterus, on the one hand (see Figs. 332 and 333), and carcinoma on the other, there is no absolutely sharp mor- phological distinction. But there is a considerable group of growths, to which the name adenoma is properly applied, which lie on the border zone between the distinctly benign and the definitely malig- nant new epithelial tissue growths. Many epithelial cell growths of the uterus, while adenomatous in structure, are so distinctly malignant, and are so liable to develop that structural lawlessness characteristic of carcinoma, that it has seemed Fig. 336.—ADENOMA OF THE UTERUS. Showing papillary outgrowths and commencing infiltration of the submucous tissue. wise to many observers to avoid the name adenoma altogether and class all the epithelial tumors of the uterus among the carcinomata. Others, recognizing the benign character of many of the epithelial tumors of the uterus, have adopted a sharp distinction between benign and malignant adenoma. It seems to the writer wise to preserve here, as elsewhere in the body, the morphological distinction between adenoma and carcinoma. But in doing this it should always be borne in mind that the adeno- mata of the uterus, as those of the gastro-intestinal canal, may not only be extremely malignant as adenomata, but that the more benign forms are extremely prone to develop, both in structure and malig- into carcinomata. ...In fact, in ma ases we can only expr eens aie By Microsone oe eee 714 THE ORGANS OF GENERATION. the peculiarities of structure in these tumors by calling them adeno- carcinoma. The adenomata of the uterus may begin in a simple hyperplasia of the mucous membrane, in which glandular development is pre- ponderant. This new glandular growth is most common in the form of irregular, often dilated follicular structure with a well- marked lumen lined with cylindrical or cuboidal cells. The new growth may project from the inner surface of the uterus in the form of papillary masses, or it may infitrate the submucous tissues. Or growth in both directions may occur at once. (See Figs. 336 and 337.) The topographical features and clinical stories of many adeno- Fig. 337._ADENOMA OF THE UTERUvs, Small portion of specimen shown in Fig. 272, more highly magnified. mata of the uterus are identical with those of the infiltrating and ulcerating carcinomata. Carcinoma.—The carcinomata of the uterus commence most fre- quently in the cervix and portio vaginalis, and the most common form is the epithelioma. The growth of epitheliomata of the cervix uteri proceeds under three tolerably distinct forms, which, however, frequently merge into one another. 1. The Flat, Ulcerating Epithelioma.—This form of cancer commences as a somewhat elevated, flat induration of the s hea Digitized by Microsoft® uperficial THE ORGANS OF GENERATION. 715 layers of the cervix, sometimes circumscribed, sometimes diffuse. This induration is due to the growth of plugs and irregular masses of epithelial cells into the underlying tissue. Ulceration usually commences early and may proceed slowly or rapidly. The edges of the ulcer are irregular, indurated, and somewhat elevated. The ulceration of the new-formed cancerous tissue at the edges is usually progressive, so that the vaginal portion of the cervix, the cervical canal, the vagina, and even the bladder and rectum may be in- volved. More or less extensive hemorrhages and necrosis of the base of the ulcer are liable to occur. The entire cervix may be de- stroyed. Fig. 338.—CaRcinoMa of THE Cervix Uteri (U Icerating). 2. In another class of cases the carcinomatous growth develops under the form of papillary or fungous excrescences, which may form larger or smaller masses composed of epitheliomatous tissue. Hand-in-hand with this projecting growth there may occur an epi- thelial infiltration of the underlying tissue of the cervix. These growths are often quite vascular and may give rise to severe haemor- rhages. They may ulcerate and thus produce great destruction of tissue. Digitized by Microsoft® 716 THE ORGANS OF GENERATION. 3. In still another class of cases there is a more or less deep infil- tration of the submucous tissue, either diffuse or in circumscribed nodules, with epithelial cell masses. We find at first, in the vaginal portion of the cervix, in the submucous connective tissue, either nodules or a general infiltration of a whitish new growth. The cer- vix then appears large and hard. Very soon the mucous membrane over the new growth degenerates and falls off; the superficial lay- ers of the new growth undergo the same changes. After this the Fig. 339.—CaRctInoMA CEPITHELIOMA) OF THE Urerrus. Showing ramifying epithelial cell masses. formation of the new growth and its ulceration go on simultane- ously, producing first an infiltration and then destruction of the cer- vix, and often of a part of the body of the uterus. The growth fre- quently extends to the vagina, the bladder, and the rectum with the same destructive character, so that we often find the cervix and upper part of the vagina destroyed, and in their place a large cavity Digitized by Microsoft® THE ORGANS OF GENERATION. 1% with ragged, gangrenous, cancerous walls (Fig. 338). Less fre- quently the pelvic bones are invaded in the same way. Not infre- quently the ureters are surrounded and compressed by the new growth, so that they become dilated. The dilatation may extend to the pelves and calyces of the kidneys. The new growth may begin in the cervix and extend uniformly over the internal surface of the cervix and of the body of theuterus. The entire uterus is converted into alarge sac, of which the walls are infiltrated with the new growth, while the internal surface is ulcerating and gangrenous. In some cases there is a considerable formation of new, dense connec- tive tissue, so that the growth has a scirrhous form. In rare cases the growth begins in the upper part of the cervix or in the body of the uterus, while the lower part of the cervix is not involved. In all of these cases the epithelial cells of the new growth follow more or less closely the type of the epithelial cells of the part from which they spring (Fig. 339). In still another class of cases, in which the new growth may be in the form of nodules, or diffuse infiltrations, or polypoid masses, or may present more or less extensive alterations, the cells are irregu- lar, polyhedral in shape, the tumor belonging to the class of glan- dular or medullary carcinomata. These also usually commence in the cervix, and, according to the views of many writers, probably in the mucous glands. In rare cases the entire wall of the uterus is infiltrated with the new growth and the organ is much enlarged. Colloid carcinoma sometimes occurs, but is rare. While we may for convenience recognize the above types of car- cinoma of the uterus, it should be borne in mind, as above stated, that they are not apt to be perfectly distinct, and some of them may merge into one another or exist simultaneously. Hxudative inflam- mation is of frequent occurrence in these as in other tumors of the uterus. As a result of the ulceration of these various forms of carcinoma recto-vaginal fistulae may be formed ; the lumbar lymph nodes may be involved, and metastases in distant organs are occasionally though not frequently formed. Frequent and profuse hemorrhages, gangrenous destruction of tissue, the absorption of deleterious mate- rials, etc., are apt to lead to the development of a more or less pro- found anzmia and cachexia. Deciduoma Malignum.—Under various names several curious tumors of the uterus have been described which resemble each other, but which differ in structures from any of those in the! usual lists. They are, however, most closely allied to the sarcomata. They all occur in the uterus afterpregmancys and @ikappear to be derived from remains of the decidua or its associated structures (Fig. 340). They 5Y 718 THE ORGANS OF GENERATION. frequently give rise to hemorrhages and are apt to form metastases, especially in the vagina and lungs. The structure of these tumors varies considerably. The most typical forms consist of irregular clusters of trabecula of large irreg- ular-shaped cells with prominent nuclei or of masses of protoplasm. These cells and cell masses often enclose blood spaces. There is little or no stroma, On the other hand, some of the tumors in which the connective tissue elements more largely share are appropriately called Sarcoma deciduo-cellulare. Whether these tumors are derived from the foetal or from the Fic. 340, FRAGMENT OF DECIDUA IN CURETTINGS FROM THE UTERUS. maternal tissues is not in all cases clear; perhaps only one or both may in the different cases be concerned in the growth." PARASITES AND CYSTS. Various forms of bacteria are of frequent occurrence in the cavity of the uterus when the organ is diseased. The presence of some is significant, and of others not. Echinococcus has been found in the body and neck of the uterus, and may rupture into the peritoneal cavity or into the vagina. Cysts.—Aside from the cysts which develop in tumors of the uterus, in the cervix uteri the mucous follicles are frequently so dilated as to form cysts filled with a gelatinous material and more or less epithelium. These cysts may be large or small, and are fre- quently called ovula Nabothi. Sometimes there is an inflammatory growth of new connective tissue about these cysts. In other cases 1 For a careful description and consideration of these tumors consult the article by Willams in the Johns Hopkins Hospital Reports, vol. iv., No. 9, 1895. Digitized by Microsoft® THE ORGANS OF GENERATION. 719 the cysts may project from the mucous membrane in the form of polypi. Similar changes are infrequently found in the body of the uterus from the dilatation of occluded uterine glands. Dermoid cysts are rarely found in the walls of the uterus. THE OVARIES. MALFORMATIONS. One or both ovaries may be absent, the other organs of generation being also absent or undeveloped. Or the ovaries may be only par- tially developed. Absence or arrest of development of one ovary is sometimes met with in otherwise well-formed individuals. It is sometimes accompanied by a low position of the kidney on the same side. The ovaries may pass into the inguinal canal or into the labia majora, and remain fixed there through life. Less frequently they are found in the crural canal or the foramen ovale. CHANGES IN SIZE. The ovaries may become larger than normal by chronic inflam- mation, by the formation of cysts and tumors. They may become atrophied in old age, the Graafian follicles disappearing and the organ shrivelling into a small, irregular, fibrous body. Atrophy may be produced by ascites, by chronic inflammation, or from un- known causes. As the result of the maturing and rupture of the Graafian follicles, with and without pregnancy, the surface of the ovary, which before puberty is smooth, may become roughened by irregular cicatricial depressions. CHANGES IN POSITION. In adult life the ovaries may pass as lierniz into the inguinal or crural canal, the foramen ovale, or the umbilicus. The position of the ovaries in the abdomen may be changed by the pressure of tumors, the traction of false membranes, etc. It may occur in enlarged ovaries or in those of normal size, and by the com- pression of the veins may lead to congestion and chronic inflammation of the organ. HYPERAMIA AND HEMORRHAGE. Aside from the normal hyperemia of the ovaries during menstru- ation, the vessels may be congested in inflammation, in displace- ments with interference with the venous circulation, in certain diseases of the heart, etc., and may then be followed by chronic inflammation. trual periods are accompanied by the effusion of blood The MenbHnue’ Per iaiieed by Micioson® * 720 THE ORGANS OF GENERATION. into a Graafian follicle. Normally the amount of blood is small, becomes solid, is decolorized and then gradually absorbed. Some- times the effusion of blood is much greater ; the follicle filled with blood is as large as a pigeon’s egg. The blood may remain in the follicle and be absorbed, and replaced by a serous fluid, or it may rupture it and escape into the peritoneal cavity. Death may ensue from the hemorrhage, or the blood may collect in Douglas’ cul-de-sac and be enclosed in false membranes. Hzemorrhages also occur in follicles which have become cystic. Interstitial hemorrhage in the ovary sometimes occurs without known cause. INFLAMMATION (OOPHORITIS). Acute Inflammation of the ovaries occurs most frequently in the puerperal condition, either as part of a general peritonitis or as a primary affection. With puerperal peritonitis both ovaries are usually inflamed ; they are swollen, congested, soft, infiltrated with serum or pus, or gangrenous. The inflammation may attack principally the capsule, the stroma, or the follicles. Inflammation of the capsule results in adhesions and collections of pus, shut in by false membranes ; of the stroma, in abscesses and fibrous induration ; of the follicles, in their dilatation with purulent serum. If the inflammation of the ovary is the primary lesion itis usually confined to one organ. The stroma of the ovary is infiltrated with serum and pus, and may contain ab- scesses of large size. In other cases the ovary itself is but little changed, but is surrounded by a mass of fibrinous and purulent exu- dation. Such idiopathic forms of inflammation may terminate in recovery ; or the abscesses may perforate into the rectum and va- gina ; or the ovary is left indurated and bound down by adhesions ;. or the patient dies from the violence of the disease. Acute inflammation of the ovaries unconnected with the puerperal condition is not common, but it may occur in connection with acute or chronic peritonitis or perimetritis. It is usually confined to one ovary. Either the follicles, stroma, or capsule, or all together, may be involved. The inflamed follicles are enlarged, their walls thick- ened ; they may contain bloody or purulent fluid. The stroma be- comes infiltrated with serum or pus, and later we may find abscesses or fibrous induration of the organ. The inflammation of the capsule may lead to the formation of membranous adhesions between the ovary, Fallopian tube, and surrounding parts. Chronic Interstitial Odphorvtis is not infrequently preceded by an acute inflammation, or it may gradually develop as an indepen- dent condition, often determined by some mechanical interference with the blood current. The organ may be increased in size, owing Digitized by Microsoft® THE ORGANS OF GENERATION. 721 to the formation of loose cellular or of dense, firm, new connective tissue. Under these conditions the blood vessels, especially the veins, may be widely dilated, and cysts in varying number and size may be present (Fig. 341). Sometimes the new-formed dense con- nective tissue may be largely limited to the surface of the organ, so that the albuginea may become so dense and thick that the functions of the organ must, as it would seem, be permanently interfered with. Under these conditions the surface of the ovary may be smooth or rough. On the other hand, the organ may be smaller than normal as the result of the formation of dense new interstitial connective tissue, and its surface greatly roughened and distorted. Sometimes the forma- Fig. 341._Curonic OdpHORITIS WITH DILATED BLoop VESSELS AND Cysts. a, dense connective-tissue stroma; b, dilated veins; c, cysts; d, cyst with granular contents; e, cortical zone of immature Graafian follicles. tion of new dense tissue may be largely confined to the walls of the arteries, which become prominent and tortuous. Obliterating en- darteritis is not infrequently present. The atrophied ovary may be largely made up of thick-walled arteries and fibrous masses which are the result of incomplete resolution of the corpora lutea (Fig. 342). Sealine a more or less extensive hyperplasia of cells in the corpus luteum leads to the development of larger or smaller new- formed, convoluted, nodular masses in the ovary, which are sometimes regarded as tumors. These structures may, according to Freeborn, soften at the centre and thus give rise to a special form of small Digitized by Microsoft® 722 THE ORGANS OF GENERATION. ovarian cyst. Certain sarcomata of the ovary appear to originate in such an hyperplasia (see Fig. 343). Tuberculous Inflammation of the ovaries is rare, and may ac- company tubercular inflammation of other organs, particularly the peritoneum and Fallopian tubes. It usually results in the production of cheesy nodules of considerable size. Syphilitic Inflammation in the form of gummatais uncommon. TUMORS. Fibromata.—These tumors are not very common nor usually of great importance. They may be very small or of great size. They are usually dense in texture, and in a considerable number of cases seem to originate in the tissue formed in the closure of the ruptured. Fig. 342.—CHronic OOPHORITIS WITH ATROPHY. From a case of valvular disease of the heart with chronic metritis and endometritis. a, thick- ened and dense interstitial tissue; b, old corpora lutea; c, arteries with greatly thickened walls; d, dilated veins. Graafian follicle. They may contain cysts or be accompanied by cysts of the surrounding stroma. Papillary fibromata of the surface of the ovary are sometimes seen, and the growth may be transplanted from this situation to the general peritoneal surfaces (Fig. 344). Letomyomata containing more or less fibrous tissue are of occa- sional occurrence. Sarcoma of the ovaries is not common. It is usually primary, but may be metastatic. It is usually of the spindle-celled variety, but may contain areas of spheroidal-celled tissue or more or less fibrous tissue. The tumors may be hard or soft, and are apt to in- volve both ovaries. Endotheliomata may be found in the ovaries. Chondroma of the ovaries is described, but is rare; cartilage not infrequently occurs, however, in dermoid cysts. Digitized by Microsoft® THE ORGANS OF GENERATION. 723 Carcinoma, usually of the glandular variety, may occur as a primary tumor of the ovary. It may be due to a continuous infec- tion from neighboring organs, or more rarely it is of metastatic ori- gin. Although the glandular medullary carcinomata are the most common, scirrhous, melanotic, and colloid cancer sometimes occur. Some forms of carcinoma stand in very close relation with certain of the cystic adenomata (see below). Adenomata (Cystic Adenomata ; Compound Ovarian’ Cysts).— These growths, which may occur in one or both ovaries, form one of the most common and important classes of ovarian tumors. Some of their most noteworthy and important features depend upon their Fig. 343.—CoMMENCEMENT OF SARCOMATOUS GROWTH IN THE OvaRY. From hyperplastic cells of corpus luteum. Specimen prepared by Dr. G. C. Freeborn. tendency to the formation of cysts. It should be remembered, how- ever, that the primary lesion is a true new formation of glandular tissue, and not, as in the case of most cysts, a transformation, by re- tention or otherwise, of pre-existing structures. The growth primarily consists of a fibrous stroma, in which are tubular follicles lined with cylindrical epithelium. Or, in some cases, it consists of papillary outgrowths from a fibrous stroma, which are covered with cylindrical epithelium. Glandular Cyst-Adenoma.—There is, as above stated, a marked tendency, particularly jp the glandples fore of adenoma, to a dilate- 724 THE ORGANS OF GENERATION, tion of the follicles by a semi-fluid material, and the formation of cysts. There may bea number of follicles equally dilated, so as to form a number of cysts of moderate size ; or only a few follicles are enormously dilated to form a large multilocular cyst with but few compartments. The walls of the cysts may fuse together and be ab- sorbed, so as to form one large cyst divided by incomplete septa—unv- locular cysts. The stroma in which the follicles and cysts are em- bedded may be largely developed or very scanty. Fig. 344.—PaPILLOMA OF PERITONEUM. Transplanted from a similar growth on the surface of the ovary. The walls of the larger cysts are composed of fibrous tissue which is dense in the outer layers, more cellular in the inner, upon which the epithelium is placed. They may be thin and membranous, or we find developed on their internal surfaces an intracystic growth com- posed of a fibrous stroma and tubular follicles. These secondary follicles may also be filled with fluid and form larger and smaller cysts. The intracystic growths may be so large as to fill up the original cysts. Sometimes the intracystic growth presents very little dilatation of its follicles, so that the entire tumor has more the cha- racter of a solid growth thane a pystosot® THE ORGANS OF GENERATION. 495 The cylindrical epithelium lining the cysts usually forms a single layer (Fig. 345), but, owing to the accumulation of fluid, the cells may become flattened and atrophied, or they may be fatty or desqua- mated. The contents of the cysts differ considerably in different cases, and even in different cysts in the same case. They may be tough and ropy, or gelatinous or serous; transparent and colorless, or yellow or reddish, or reddish-brown ; or they may be turbid and colorless, or variously colored—red, brown, or chocolate. Chemically the cyst contents, when thick and ropy, contain mucin or paralbumin, and perhaps other less well-known compounds belong- ing to the same class. It is believed that the peculiar ropy character which the fluid often possesses is due to the paralbumin, but the chemical nature and relations of this substance are still matters of Hrs Q tee peau [ee Re 13 Fig. 345.—Cystic ADENOMA OF Ovary. Glandular form. dispute. It is probable that the contents of these cysts are, so far as the mucin and paralbumin are concerned, produced by a meta- morphosis of the protoplasm of the lining cells, similar to that by which the mucin is produced in the mucous glands and in mucous membranes. We frequently find the cylindrical cells presenting the form of the so-called ‘‘ beaker cells,” and in some cases the mucous contents of the cysts are seen to be continuous with the similar con- tents of the beaker cells. Itis probable that much of the fluid con- tents of the cysts comes from simple transudation. Microscopically the contents of these cysts present also considerable variation. We may find almost no structural elements ; or there may be red blood cells in variable quantity, and pus cells in various ‘ tty d ti f disi i stages arena ote ity Shy Minhsep Fo isintegration, so that 726 THE ORGANS OF GENERATION. variously shaped fragments of the cells appear. Then we may find cylindrical, or flattened, or polyhedral cells, either well preserved, swollen, or in a state of fatty degeneration (Fig. 346), or we may find fragments of these cells. It is these various forms of cells, often more or less swollen and in a condition of more or less well-marked Fria. 346.—CELLS FROM CONTENTS OF AN OVARIAN CysT IN A CONDITION oF Fatty DEGENERATION. granular and fatty degeneration, which have been considered cha- racteristic of the ovarian cysts and are sometimes called Drysdale’s ‘corpuscles. While, however, they are of frequent occurrence under these conditions, they are by no means pathognomonic, since we find them in the contents of various kinds of cysts and cavities where the ‘cells are undergoing degeneration. In addition to the above struc- Fia. 347,—Cystic ADENOMA OF Ovary (Papillary form). tural elements we may find free fat droplets, cholesterin crystals, pigment granules, and more or less granular detritus. The material filling these cysts is sometimes called colloid, and the cysts are fre- quently called colloid cysts; but we believe that the above view of their nature is the correct one. Numerous secondanyigheai ges \azeoleie to occur in these cysts. THE ORGANS OF GENERATION. G27 The cells may become fatty and peel off, so that we may find in some parts only a connective-tissue wall. The walls may atrophy, may become infiltrated with salts of lime, or contain concentrically lamel- lated lime concretions. Inflammatory changes may occur in them. There may be a suppurative inflammation of the walls leading to the formation of abscesses, or pus may be mingled with the cyst contents ; the epithelium may be exfoliated and granulation tissue may form in the walls. Chronic inflammation may lead to consider- able thickening of the walls and to adhesions with neighboring parts. Hemorrhages, sometimes very extensive, may occur in inflammation, or as the result of other disturbances of the circulation, so that some of the cysts may be filled with blood. Inflammatory softening, gan- grene, etc., of the walls may lead to perforation, so that the contents Ovary. The papillary outgrowths are themselves becoming softened at their centres, forming acces- sory cysts. Drawn from specimen loaned by Dr. G. C Freeborn. of the cysts may be discharged into the peritoneal cavity, or, in virtue of adhesions, into the bladder, vagina, or rectum. Carcinoma may be developed from the epithelium of the cysts. Since these cysts sometimes reach a very large size, they may produce the greatest variety of disturbances in the abdominal cavity, which need not be enumerated here. They probably originate in the glandular epithelium of the ovary either before or after the formation of the Graafian follicles.’ 1For more extended descriptions of the cyst-adenomata of the ovaries see Wal- deyer, ‘Die epithelialen Eierstécksgeschwiiste,” Archiv ftir Gynikologie, Bd. i., Heft 2, pp. 252-316, 1870. Also Kiebs, ‘‘ Handbuch der pathologischen Anatomie,” vierte Lieferung, p. 796, 1873. Pozed, “‘ Treatise on Gynecology,” edited by Brooks H. Wells, M.D., 1892. Digitized by Microsoft® 728 THE ORGANS OF GENERATION, Papillary Cyst-Adenoma.—This form of cyst-adenoma was formerly regarded as but a variety of the form above described—a variety characterized by papillary outgrowths in cauliflower-like tufts from the walls of the cysts, which often in large degree fill the cyst spaces (Fig. 347). There appears, however, to be sufficient evi- dence, both anatomical and clinical, to justify the separation of the papillary from the glandular form of cyst-adenoma. The papillary cyst-adenomata are not, as a rule, as large as the glandularform. The cysts are fewer and they do not contain colloid material. The papillary outgrowths often break through the cyst Fia, 349,—ApDENO-SARCOMA OF THE OVARY (ENDOTHELIOMA?), Specimen loaned by Dr. G. C. Freeborn, walls, and may be transplanted to the peritoneal or other surfaces in the form of multiple cystic or papillary tumors (Fig. 348). The papillae and cyst walls may be lined by cylindrical and often by cil- iated epithelium. They may develop from the follicular or germinal epithelium, and probably, according to Williams, sometimes from the tubular epithelium. ' Cyst-adenomata of the ovary may, through an unusual prolifera- 1 Williams, Johns Hopkins Hospital Reports, vol. ii 1898 ; Amer. Jour. of Obstetrics, June, 1895, p. 84é, = arer Digitized by Microsoft® THE ORGANS OF GENERATION. 729 tion of the epithelial cells, form such dense, closely packed cellular masses that the type of structure seems changed. Such a change is shown in Fig. 349, in which, in addition to the excessive production of epithelium, the stroma is sarcomatous. Follicular Cysts of the Ovary.—The Graafian follicles may be dilated so as to form cysts. This may occur in one or both ovaries, and the cysts may be small or large, single or multiple. They are usually found after middle life, but may occur during youth, child- hood, or even in the foetus. The follicles dilate from the accumula- tion of fluid within them; the ovum is destroyed, the epithelium flattened. The contents are usually serous and colorless, but may be viscid, turbid, purulent, or variously colored, red, yellow, or brown. The ovary may be crowded with numerous cysts of moderate size, whose adjacent walls may coalesce and atrophy, forming communi- cations between them. A variety of this form of cyst is formed by the dilatation, either with or without the hyperplasia above described, of a corpus luteum. Such cysts may communicate with a Fallopian tube. Dermoid Cysts.—These cysts may be uni- or multilocular, are usually of moderate size, but sometimes become as large as a man’s head or larger. Their fibrous walls may be thick or thin, and por- tions of the internal surface may present more or less completely de- veloped cuticular structures, such as corium, papille, epidermis, hairs and hair follicles, sebaceous glands, ete. The cavity may contain a thick, whitish, greasy material composed of flattened epithelium, fat, or cholesterin crystals. Or the cavity or walls may contain massef of irregularly formed hair, teeth, bone, cartilage, striated muscle, and nerve fibres and cells. Such growths, which are doubtless of embryonal origin, may exist for many years without causing incon- venience ; but inflammatory changes may occur in them, leading to adhesions and perforations into adjacent organs. They may form the nidus for the development of carcinoma, or they may calcify. In addition to the above-described adenoid, dermoid, and simple follicular cysts, there are a number of composite forms of not infre- quent occurrence. Thus, in connection with dermoid cysts or sepa- rately, we find larger and smaller cysts lined with ciliated epithe- lium. Then there are several cases described of cysts which partake of the characters of both adenoid and dermoid cysts. Such cysts may be multilocular and be lined with flattened, cylindrical, or ciliated epithelium, and may contain epidermal cells, cholesterin or mucin, etc. Small cysts, sometimes pediculated, sometimes not, of doubtful origin and usually of no special significance, are frequently found growing from the bropd, LESTE Rees dhe ovary. The walls are ’ 730 ORGANS OF GENERATION. usually very thin, lined with flattened epithelial cells, and the con- tents serous. Solid teratomata are of occasional occurrence in the ovary.’ Cysts of the Parovarium, lying between the peritoneal layers of the broad ligament, are usually small, but may be as large as a man’s head. They are usually lined with ciliated epithelium, but some- times with flattened non-ciliated cells. The contents may be serous, or may be thick and contain mucin and paralbumin. THE FALLOPIAN TUBES. MALFORMATIONS. Absence of both tubes occurs with absence of the uterus. One tube may be absent, with arrested development of the corresponding Fig. 850.—HypRo SALPINX. side of the uterus. Both tubes may beimperfectly developed ; either of their ends may be closed ; they may be inserted into the uterus at an abnormal place; they may terminate in two or three abdominal ostia. CHANGES IN POSITION AND SIZE. The Fallopian tubes may participate in the various malpositions of the uterus and ovaries ; but they are most frequently displaced by the contraction of adhesions formed in perimetritic and periovarial inflammations. The lumen of the tube may be partially or completely closed as the result of inflammation of the mucous membrane ; of peritonitis about the fimbriated extremity ; of tumors or inflammation of the ‘Consult Wilms, Zie@éegis/Pedhid y. Yicnosow#® Ba. xix., p. 867, 1896. THE ORGANS OF GENERATION. V31 uterus ; or by pressure from without, or by adhesions, tumors, ete. It may become stopped by plugs of mucus or pus. Dilatation of the tubes may be produced by an accumulation of catarrhal or other exudation, when there is partial or complete ste- nosis at some portion of the tube. The dilatation may be moderate, converting the tube into a tortuous, sacculated canal containing mucous or serous fluid; or, more rarely, large cysts may form con- taining several pounds of serous fluid—hydro-salpinz (Fig. 350). As the fluid collects the epithelium may become flattened or fatty or may desquamate. Asa result of an inflammation in the walls of the dilated tube, the contents may be mixed with pus or blood. Rup- ture of a dilated tube sometimes occurs; or severe and even fatal hemorrhage may take place into its cavity. Papillary growths are sometimes found springing from the inner wall of the cysts. HAMORRHAGE. Hemorrhage into the tube may occur in puerperal women with retroversion of the uterus, with abortions ; hematometra and tubal pregnancy ; in acute infectious diseases. The blood may undergo degenerative changes and be largely absorbed, or it may escape into the peritoneal cavity and cause peritonitis, INFLAMMATION (SALPINGITIS). Catarrhal Inflammation of the mucous membrane of the Fallo- pian tubes commonly occurs in connection with endometritis, fre- quently in the puerperal condition. In the acute stage the mucous membrane is hyperemic and swollen, and covered with a muco- purulent exudation. The inflammation may subside, leaving no lesions, but it more frequently becomes chronic, and may then result in peritoneal adhesions, thickening of the walls, obliteration of the tubes, dilatation, etc. Suppurative Salpingitis.—This inflammation of the mucous membrane may assume a suppurative character, particularly in con- nection with puerperal metritis and peritonitis, but sometimes as a result of gonorrhceal inflammation. Under these conditions the wall of the tube may be involved and pus may exude from the abdominal ends. It is difficult, in many cases of suppurative salpingitis associated with peritonitis, to say which is the primary lesion. Jn some cases there is a considerable collection of pus in the tubes, causing dilatation—pyo-salpinx. These collections may rupture into the peritoneal cavity, or the pus may escape into a cavity shut in by adhesions, or may perforate into the intestine or bladder, Or i d finally bec calcified. Sema cy ee nanigitized by Microsoft® 732 THE ORGANS OF GENERATION. Suppurative salpingitis is believed to be most commonly caused by the gonococcus or the pyogenic bacteria. Tuberculous Inflammation.—This form of inflammation in the tubes is most frequently seen in its later stages, when the mucous membrane is partially or entirely converted into a thick, cheesy, often ulcerating layer. The lumen of the tubes may be dilated, the walls thickened from chronic inflammation. This lesion may occur by itself, or may be associated with tubercular inflammation of the lungs, or of the other genito-urinary organs, or of the peritoneum. The lesion usually commences at the abdominal ends of the tubes, and both tubes are apt to be involved. Syphilittc Inflammation, in the form of a diffuse thickening of the wall by gummatous tissue, has been described. TUMORS. Small fibromata and fibro-myomata sometimes occur in the wall of the tubes or in the fimbria#. Small /ipomata have been seen between the folds of the broad ligament in close connection with the tubes. Carcinoma of the tubes is usually, if not always, secondary to carcinoma of the uterus or the ovaries. Cysts, usually of small size, sometimes pediculated and with thin walls, are frequently seen in the peritoneal covering of the tubes or in the fimbriz. They are believed to be of embryonal origin. Dilatation of the tubes, as above described, may convert them into cyst-like structures. EXTRA-UTERINE PREGNANCY. Tubal Pregnancy.—The impregnated ovum is in some way hin- dered from passing into the uterus, becomes fixed in the tube, and is there developed. The villi of the chorion grow into the mucous membrane of the tube, forming an incomplete placenta. Rare cases are recorded in which the placenta was situated in the uterus while the foetus was developed in the tube. The embryo and its mem- branes are developed until they reach such a size that the tube sur- rounding them ruptures. This may occur in the first month or not until much later. In rare cases, when the wall of the tube was ex- tensively involved in the formation of the placenta, the development has gone on until term. The ovum may remainin the tube after the rupture ; or may escape into the peritoneal cavity, still enveloped in its membranes ; or the membranes may be ruptured and left in the tube. The rupture is generally attended with fatal hemorrhage. In some cases death is ca it Re qypture ha dilated vein while the THE ORGANS OF GENERATION. 733 tube is still intact. Hzemorrhage into the sac may occur before its rupture. In rare cases death does not take place and the foetus is shut in by adhesions and false membranes. Theembryo soon dies. In fa- vorable cases there is a slow absorption of the soft parts of the fo- tus, the bones are separated and left embedded in a mass of fibrous tissue, fat, cholesterin, and pigment ; or the foetus retains its shape and becomes mummified, and may then be encrusted with the salts of lime (lithopedion). In unfavorable cases degeneration and gangrene of the foetus take place rapidly, with inflammation and suppuration of the surround- ing tissues. There may be perforation and escape of the broken- down foetus through the rectum, vagina, bladder, or abdominal wall. The patient may die from peritonitis or exhaustion, or may recover after the escape of the foetus. In some cases the foetus may escape through a rupture of the tube into the space between the folds of the broad ligament. Tubo-abdominal Pregnancy is produced by the development of the ovum in the fimbriated extremity of the Fallopian tube. Adhe- sions are formed, so that the foetusis partly in the end of the tube and partly in the abdomen. Interstitial Pregnancy.—The ovum in these cases is arrested and developed in the portion of the tube which passes through the wall of the uterus. Abdominal Pregnancy.—The ovum, after escaping from the ovary, does not enter the Fallopian tube, but becomes fixed to the peritoneum, usually at some part near the ovary. It is surrounded by thickened peritoneum and develops in that position. Ovarian Pregnancy.—The existence of this form of pregnancy is doubtful and difficult to prove, but there are some cases in which it seems probable that the ovum develops in its Graafian follicle. The placenta may be attached to the tube or to the abdominal wall. In all forms of extra-uterine pregnancy the uterus becomes en- larged and a sort of decidua is formed on its internal surface. LESIONS OF THE PLACENTA.’ Aside from the variations from the normal in size, shape, and po- sition, for a description of which we refer to the works on obstet- rics, we may briefly mention here some of the more important struc- tural changes which the placenta may undergo. Heemorrhage.—This may occur either on the maternal surface in the decidua ; or between the foetal surface and the membranes ; or in the substance of the placenta. | The latter form of hemorrhage con- 1 For structure of plarente Consul tien ourna of Pathology and Bacteriology, vol. iii., p. 449 (bibliography). 34 THE ORGANS OF GENERATION. stitutes the true placental apoplexy. This may occur as the result of rupture of a placental sinus. The placental tissue is crowded apart, and a blood clot, often infiltrating the parenchyma, is formed. This may lead to abortion, or the blood may undergo disintegration and absorption and its place be occupied by a cicatrix. The placen- tal tissue in its vicinity may undergo fatty degeneration. Under other conditions, without evidence of rupture of the vessels, the pla- cental tissue may become infiltrated with blood in the form of an in- farction. In this, degenerative changes similar to the above may oc- cur, leading to fibrous induration of the placenta. The so-called ‘‘ white infarctions” of the placenta appear to be al- tered thrombi in the maternal blood spaces. They consist of lamel- lated or homogeneous or fibrillar fibrin, and form important larger and smaller yellowish-white or reddish, irregular masses, and appear to be of pathological significance only when they occur early or are of great extent. INFLAMMATION (PLACENTITIS). Suppurative Inflammation of the placenta, with the formation of abscesses, is of rare occurrence as the result of injury. Chronic Indurative Inflammation of the placenta may result in the formation of circumscribed masses of cellular and loose, or dense and cicatricial, connective tissue, or in a diffuse formation of connective tissue, which may interfere with the nutrition of the fcetus and cause abortion. The new-formed connective tissue may undergo fatty degeneration or calcification. In another class of cases the new connective tissue is formed mainly in the walls of the vessels, particularly the arteries. This may occur in circumscribed portions of the vessels, leading to nodular growths around the arteries, or it may occur extensively along the various ramifications of the vessels, converting them into thick fibrous cords. The change is primarily in the adventitia, but all the coats of the vessel may become involved, leading to more or less complete obliteration of the lumen. Various proliferative and indurative changes in the placenta may occur as the result of syphilitic infection. DEGENERATIONS. Fatty and amyloid degeneration and calcification of the placental tissue are of not infrequent occurrence. Cysts of the placenta are of occasional occurrence ; their origin is in most cases obscure.’ ‘See Ahifeldt, Arch. fiir Gynikologie, Bd. ii., p. 397. Fenomenodes, ibid., Bd. xv., p. 343. Hofmeier, ‘‘ Die menschliche Placenta,” 1890. Digitized by Microsoft® THE ORGANS OF GENERATION. 735 Fragments of placenta remaining in the uterus after delivery may serve as a nidus for a blood thrombus, or they may undergo proliferation, thus forming tumors, deciduwomata (see page 718). An hypertrophy of the villi of the chorion may give rise to the fibrous structures known as fibrous moles. When to the fibrous change mucous degeneration is added the so-called hydatid moles are formed.! THE MAMMA. MALFORMATIONS. Absence of both mamme is only found in connection with other marked malformations. Absence of one mamma has been observed in a few cases, with and without defective development of the corresponding half of the thorax. Absence of one or of both nipples is more common. Arrest of development of the mamme is found in connection with arrest of development of the organs of generation, and, to a less degree, alone. Supernumerary mamme and nipples have been observed in a number of cases. The glands may all secrete milk during lactation. Too early development of the mamme is sometimes found in young children in connection with abnormal development of the organs of generation. HEMORRHAGE. In young women who suffer from amenorrhcea or dysmenorrhea, small hemorrhages sometimes occur in the mamme at the time of menstruation. The blood may find its way into the milk ducts and exude in small quantities at the nipple. Contusions of the breast may produce extravasations of blood in the mammary gland or the surrounding connective tissue. This may become absorbed, or may remain and be surrounded by fibrous tissue or be converted into cysts. INFLAMMATION. During lactation the nipple is liable to become inflamed in three ways, which may occur separately or be combined together. 1. The epidermis is rubbed off by nursing, the cutis becomes in- flamed and converted into granulation tissue ; in this way small or large ulcers may be formed. 2, Fissures are formed at the base of the nipple, which extend completely through the skin, and are lined at the bottom with granu- lation tissue. 1Consult Marchand, Bes iZboGspupyoso FEnak., Bd. xxxii., p. 405; also Fraenkel, Arch. f. Gyniik., Bd. xlix.. 736 THE ORGANS OF GENERATION. 3. There is a diffuse inflammation of the whole nipple, which does not, however, go on to suppuration. The nipple is conical, red, swollen, and very painful. There isa form of eczema-like inflammation of the nipple and areola which tends to ulcerate and develop into carcinoma. This is known as Paget’s disease, and is believed by some observers to be associated with coccidia (see page 129). Acute Inflammation of the Mamma (Mastitis) occurs most fre- quently during lactation; it also occurs during pregnancy, and occasionally in women who are neither pregnant nor nursing. Fig. 351.—SUPPURATIVE MASTITIS OCCURRING IN THE NON-FUNCTIONATING GLAND. a, milk duct; b, interstitial tissue; c, dense collections of pus; d, diffuse infiltration of lobule with pus, The inflammation may involve the subcutaneous connective tissue, the gland itself, or the connective tissue between the gland and the wall of the thorax. The inflamed tissues are at first congested, swollen, hard, and painful. The inflammation may stop at this point and resolution take place, but more frequently it is succeeded by suppuration. If the inflammation involves the subcutaneous con- nective tissue the abscess may be superficial and soon open through the skin. If the Bland AS PBS Roane after another may THE ORGANS OF GENERATION, 134 become inflamed (Fig. 351), so that successive abscesses are formed in different parts of the gland. If the connective tissue beneath the gland is inflamed a deep abscess of large size may be formed, which usually perforates through the skin, but sometimes into the pleural cavity. In both these latter forms of abscess there is apt to be ne- crosis of large portions of tissue. These abscesses may cicatrize, or they may pass into a chronic condition and remain as suppurating, fistulous tracts for a long time. Suppurative mastitis is usually due to the presence of Streptococcus and Staphylococcus pyogenes. In new-born children there is often a painful swelling of the breasts, which usually subsides in a few days, but may go on to suppuration, Epidemic parotitis is sometimes complicated by mastitis. Chronic Inflammation of the interstitial connective tissue of the Fig. 852.—CHRoNIo INFLAMMATION OF MamMMARY GLAND. mammary gland may result in the formation of dense connective tissue (Fig. 352), with or without cystic dilatation of the milk ducts and atrophy of the glandular elements. Acute exudative inflamma- tion may occur in a gland which is the seat of chronic inflammation, and abscesses may be formed. Eczema sometimes affects the skin of the nipple. Attention has lately been drawn to the relationship between this inflammation and carcinoma of the nipple, for the two are frequently associated. It is possible that the eczema may lead to the subsequent development of the carcinoma. Tuberculous Inflammation of the mammary gland and its excre- tory ducts is of occasional occurrence. It may manifest itself in the form of miliary tubercles, larger and smaller cheesy masses of new- formed tissue, or coldieiizessseys. Microsoft® 738 THE ORGANS OF GENERATION. Syphilitic ulcers may occur in the nipple either as primary chan- cres or as mucous patches. Gummy tumors have been observed in the mamma. TUMORS. There may be a general hypertrophy of one or both breasts. This is usually found in young, unmarried women, but sometimes 1n SS Fic. 353,—INTRACANALICULAR FIBROMA OF TH& Mamma, X 170 and reduced. Cross-section cf a milk duct with polypoid ingrowths. advanced life. There is an increase in all the elements of the gland, both the glandular and the connective-tissue. Cysts of the mamma, seem to be for the most part retention cysts, formed by the dilatation of the glandular ducts or acini. During lactation such retention cysts are sometimes formed, and then con- tain milk. They may reach an enormous size. At other times re- tention cysts are aS ieothe pero ee viscid, brownish fluid, THE ORGANS OF GENERATION. 39 which often exudes through the nipple. These cysts may be large or small, single or multiple. There is usually at the same time some growth and induration of the connective tissue of the gland. In some cases there are polypoid outgrowths of connective tissue from the wall of the cyst. These cysts are not to be confounded with the cysts which are developed with the intracanalicular tumors, of which we shall speak below. Fibroma.—Circumscribed tumors composed of connective tissue are sometimes found in the breast. They are dense and hard, and may enclose in them some of the gland ducts and acini. Intracanalicular Fibroma.—These tumors are formed by a dif- Fic. 354.—PERICANALICULAR FIBROMA OF THE Mamma. fuse growth of connective tissue, a dilatation of the milk ducts, and a growth of polypoid fibrous tumors from the walls of the ducts into their cavities. The glandular acini may be atrophied, or enlarged, or cystic. A section of such a tumor looks like a solid mass of fibrous tissue, divided by clefts and fissures lined with cylindrical or cuboidal epithelium (Fig. 353), or containing cysts into which project poly- poid fibrous outgrowths. These tumors grow slowly, but if left to themselves may reach an enormous size. The skin over them may ulcerate and the tumor project through the opening in fungous masses. Pericanalicular Fibroma.—Sometimes the new connective tissue forms a more or less thigkizylinduidardavéstment of the duct with- 740 THE ORGANS OF GENERATION. out growing into its lumen. This formation, which is shown in Fig. 354, is sometimes called pertcanalicular fibroma. Myxoma.—This form of tumor may occur as a circumscribed growth replacing part of the mamma, or it may be developed in the same way as the intracanalicular fibromata., It is not uncommon in these intracanalicular tumors to find a combination of fibrous, mu- cous, and sarcomatous tissue in the same tumor. Chondromais a very rare forra of tumor in themamma. A few cases have been described in which it was combined with carcinoma. Adenoma.—Tumors composed of glandular acini, and ducts sur- rounded by connective tissue, are of frequent occurrence in the mamma (Fig. 145). They are either single or multiple, or sev- eral may be developed successively in the same breast. They grow at first slowly, afterward more rapidly. Their structure may be further complicated by the dilatation of one or more of the ducts which compose the tumor into cysts, and the ingrowth of connective tissue from the walls of these cysts. Sarcoma.—This form of growth may be developed as a circum- scribed tumor of small or large size. Its basement substance is that of connective or of mucous tissue, and may be scanty or abundant. The cells are spheroidal, fusiform, branched, or polygonal. These tumors may simply replace the gland ; or glandular acini and ducts may be enclosed within them ; or these ducts and acini may be di- lated so as to form cysts ; or there may be a new growth of the gland tissue so as to form an adeno-sarcoma. In other cases the sarcoma takes the intracanalicular form. There is a diffuse growth of sarcomatous tissue, a dilatation of milk ducts, and an outgrowth of sarcomatous tissue from the walls of the dilated ducts into their cavities. These tumors often reach an enor- mous size, and there is apt to be ulceration of the skin over them. Carcinoma of the mamma is most common in women between the ages of thirty-five and fifty-five, but it sometimes occurs in women not over twenty years old, and sometimes in old persons. It occurs in either breast, in the right rather more frequently than in the left, but sometimes in both. The growth begins more frequently at the periphery of the gland than at its centre, and more frequently in the upper edge of the gland than in any other place. The growth most frequently begins as a small, circumscribed nodule, which enlarges and involves more and more of the breast rf sometimes, however, it is diffuse from the first, and sometimes it be- gins in the nipple. It may infiltrate the adjacent tissues and the axillary and cervical glands, and form metastatic tumors in different parts of the body. There are several ESHA ia Sab Arms of the growth : THE ORGANS OF GENERATION. 741 1. Those in which the epithelial elements preponderate, the soft or so-called medullary carcinomata. 2. Those in which both the connective-tissue stroma and the epithelial cells are prominently developed, the cells lying in well- defined larger and smaller irregular-shaped spaces, so that the simu- lation of gland tissue is tolerably close. These are called carcinoma simplex. 3. The tumors in which the connective-tissue stroma preponder- ates, giving the tumor its hard, dense character. This is the carct- nome fibrosum, or scirrhous. Colloid carcinoma of the mamma is rare. Various secondary changes may occur in these tumors, such as have been described in the section on Tumors. In any of these forms of cancer there may be cystic dilatations of the ducts and acini. Besides the primary carcinomata of the mamma, secondary car- cinomata are met with in rare cases. MALE GENERATIVE ORGANS. THE PENIS. MALFORMATIONS. Entire absence of the penis is met with in connection with great defects of development of the rest of the body. Absence of the penis, with proper development of the other organs of generation, is rare. The urethra then usually opens into the rectum. An abnormally small penis is found, with absence or arrested de- velopment of the testicles. Absence or a rudimentary form of the prepuce has been observed in a number of cases. Congenital phimosis is also not infrequent. Hypospadia consists in an arrest of development of the penis and scrotum. In its highest degree the penis is one-half to one inch long, the glans penis small and resembling a clitoris. On the lower side of the penis is a deep cleft lined with mucous membrane. Into this cleft the urethra opens at the root of the penis. The scrotum remains separated into two halves, resembling labia majora. The testes descend into their proper position on each side or remain in the abdomen. If the testicles continue to develop normally the in- dividual has the appearance and capacities of a man ; if their de- velopment is arrested the individual is small and has a womanish ap- pean Digitized by Microsoft® W422 THE ORGANS OF GENERATION. In lesser grades of the same malformation the two halves of the scrotum are joined and the penis is larger, but a part of the urethra remains open as a cleft at any point of the penis. Epispadias is an opening of the urethra on the upper side of the penis. It presents various grades and forms. Hermaphroditism.—This is a union of two sexes in the same person, the test of which is the presence of the secreting organs, the ovaries and testicles. True hermaphroditism is rare, but it does occur, while most of the conditions called hermaphroditism are in reality due to varying malformations of the external generative organs. Pseudo-hermaphroditism.—This malformation consists in an abnormal change in the transition from the foetal condition of the parts to their fully developed form. In the male, normally, the greater part of Miiller’s canal disappears and its lower end forms the vesicula prostatica. In this malformation Miiller’s canal is changed, as it is in the female, into Fallopian tubes, uterus, and vagina, while at the same time the testes, epididymes, vesicule seminales, and spermatic’cord are formed as usual. In the lesser degrees of this malformation we find, in the place of the vesicula prostatica, a pear- shaped sac as large as a pigeon’s egg, with muscular walls and an epithelial lining. This sac may be incompletely divided into a ute- rus and vagina, and it opens into the urethra. In the higher grades we find a well-formed vagina and uterus. The uterus may or may not have Fallopian tubes. The testicles are usually retained in the abdomen or inguinal canals, and are small. The spermatic ducts run on the sides of the uterus and open into the urethra or are closed. The penis and scrotum appear as in hypospadia, or are well formed. The appearance of the individual varies with the develop- ment of the testicles. True Hermaphroditism may be lateral. In this condition there is hypospadia ; a vagina and uterus and a Fallopian tube and ovary on one side, and a testicle and spermatic cord on the other. In certain cases, which may be called bilateral hermaphrodtt- zsm, there is a testicle on one side and an ovary on the other.’ Enlargement of the penis is sometimes caused by venous conges- tion from heart disease ; by long-continued masturbation, asa result of which the corpus cavernosum may lose its contractility ; and in rare cases by hypertrophy of the stroma of the corpus cavernosum. 1 For a detailed consideration of the malformations of the male and female gene- rative organs consult Avebs, ‘‘ Handbuch der pathologischen Anatomie,” and more re- cent cases of hermaphroditism by Heppner, Arch. f. Anat. u. Physiol., 1870, and by Hofmann, Wien. med, Jahrb., 1877. Digitized by Microsoft® THE ORGANS OF GENERATION. 743 Injury and Hemorrhage.—Injuries to the penis are liable to give rise to severe hemorrhage on account of its peculiar vascu- lar character ; suppurative inflammation, gangrene, infiltration with urine and its consequences, are alsoliable to occur. The contractions of the cicatricial tissue by which wounds are healed frequently give rise to various distortions of the organ and not infrequently prevent subsequent erections. INFLAMMATION. Balanitis, inflammation of the prepuce, is usually produced by gonorrhcea or by accumulations of smegma. The skin is red and swollen and may ulcerate. Condylomata may be formed, and adhe- sions between the prepuce and glans. The glans may ulcerate and the prepuce may be much thickened. If the prepuce is long there is an inflammatory phimosis, and the products of inflammation accu- mulate within the swollen prepuce. In some cases the prepuce be- comes gangrenous. Paraphimosts is produced by the retraction of a narrow prepuce behind the glans, with consequent stricture, inflammation, and some- times gangrene. Inflammation of the Corpora Cavernosa may be the result of injury, may follow fistulae, may occur in connection with inflamma- tion of the connective tissue of the pelvis, and may accompany the acute infectious diseases, such as pyzemia, small-pox, measles, ty- phus, etc. It may result in fibrous induration of portions of the cor- pora cavernosa ; in rare cases in abscesses or diffuse purulent infil- tration ; sometimes in gangrene. Tubercular inflammation of the penis has repeatedly followed circumcision performed by uncleanly tubercular persons, Syphilitic Ulcers frequently occur on the glans penis and pre- puce. The indurated chancre is formed either from an excoriation in which a pustule is formed or from a little nodule. The pustule breaks and its walls are infiltrated with small round cells. The nodule softens, breaks down, and forms an ulcer, of which the walls are infiltrated with cells in the same way. Syphilitic condylomata are of frequent occurrence on the glans. Phagedenic ulcers occur and may destroy a considerable part of the penis. Herpes of the prepuce occursin the form of small vesicles, which may later become ulcers. Erysipelatous and furuncular in- flammation sometimes involves the skin of the penis. TUMORS. Paptlioma is found on the prepuce and glans penis. It occurs in the form of little a See o of eee, cauliflower masses, igitized by Microso G44 THE ORGANS OF GENERATION. even as large asa fist. In either case the structure is the same— hypertrophied papillze covered with epithelium. Sometimes the epi- thelial layers become thick and horny, forming large, dense projec- tions. Fibroma diffusum, or elephantiasis of the prepuce, may occur, leading to immense thickening of the structure. It consists in a dif- fuse growth of the deep fibrous tissue of the cutis. Lipomata, angiomata, circumscribed fibromata, and sebaceous cysts may occur in the penis. Carcinoma of the penis usually occurs in the form of epitheliomata. These are most frequent in the prepuce and glans penis. They may have the form of flat ulcers, or of infiltrat- ing, ulcerating ‘nodules, or very frequently assume the form of papillary outgrowths, which may attain great size, ulcerate, or un- dergo a variety of inflammatory changes. These growths may in- volve the entire skin of the penis ; they may invade deeper parts. The inguinal glands may be invaded. Distant metastases may occur, but are not frequent. Glandular carcinoma of the penis is not common. It may be sec- ondary to carcinoma in some other part of the body. Calcification and Ossification of the connective tissue of the corpora cavernosa sometimes occur. Large and small preputial cal- culi are occasionally found between the prepuce and the glans. These may be formed in sztu, may come from the bladder or from without, and may later increase in size. THE SCROTUM. The skin of the scrotum is subject to the various forms of lesions which may occur in any part of the integument. Elephantiasts of the scrotum consists in the main of a develop- ment of new connective tissue from the cutis, which is sometimes ac- companied by dilatation of the lymph vessels. The thickened scrotum sometimes forms very large tumors, often rough upon the surface, which may entirely cover in the penis. Lipomata, fibromata, atheromatous or sebaceous cysts, and dermoid cysts containing hair, bone, cartilage, etc., are sometimes found. Occasionally the skin of the scrotum is beset with numerous larger and smaller seba- ceous cysts, which raise the surface into little globular or wart-like projections. Hpitheliomata, in the form of flat or papillary ulcerat- ing tumors, are of frequent occurrence among chimney sweepers, and may lead to extensive ulcerations of the adjacent parts and in- volvement of neighboring lymph nodes. Dermoids and Teratomata of the scrotum are not uncommon. In very rare cases tumors containing a considerable portion of a foetal skeleton have been found in the scrotum. Digitized by Microsoft® THE ORGANS OF GENERATION. 745 THE TESTICLES. MALFORMATIONS. Absence of both testicles, either with or without absence of the epididymes, spermatic cords, and vesicules seminales, occurs in rare cases. The scrotum is only indicated or may contain the epididymes. The penis is small, and the individuals are small and poorly de- veloped. Instead of being entirely wanting, the testes may be imperfectly developed. The individuals are weakly and effeminate. Absence of one testicle, with healthy development of the other, is more fre- quent. The corresponding epididymis and cord may be absent or present. The spermatic cords and vesiculze seminales may be absent or im- perfectly developed on one or both sides, while the testes are normal. Either one or both testicles may remain permanently in their foetal position, or may not descend into the scrotum for several years after birth (cryptorchismus). Their descent may even be delayed until the thirtieth year of life. This condition may depend on an arrest of development in the testes or the gubernaculum testis ; on adhesions produced by intra-uterine peritonitis ; on narrowing of the inguinal canal; on narrowing or shortening of the vaginal process ‘of the peritoneum ; or on abnormal size or position of the testicle. Usually the malformation is confined to one testicle, and then is more frequent on the left side. The testicle is usually found in the abdo- men close to the mouth of the inguinal canal, or in the inguinal canal just below the external ring; but it may be beneath the skin in the perineum, or in the crural canal with the femoral vessels, or elsewhere. The retained testis is usually not fully developed, or undergoes fatty or fibrous degeneration. The retention of one or even of both testicles does not preclude the possibility of procreation. Retained testicles are prone to inflammatory changes and liable to become the seat of malignant tumors. Sometimes, while the testis is retained, the epididymis and sper- matic cord descend into the scrotum. In rare cases the position of the testis may be changed so that the epididymis and cord are in front. The existence of a supernumerary testis has been asserted in some cases, but is rather loubtful. Atrophy of the testicle may occur in old age or in persons who are in a condition of premature senility ; or as the result of pressure from herniz, hydrocele, or inflammatory products. HYDROCELE, Hydrocele of the Rie ee BAS Soa REE in an accumulation of 746 THE ORGANS OF GENERATION, serum in the cavity of this membrane. It is usually confined to one side, It is caused by acute or chronic inflammation of the tunica vaginalis, by varicocele, or by general dropsy. The serum is found in small or in large quantities ; it is usually transparent, may contain cholesterin, or be purulent and contain the pyogenic bacteria, or be mixed with blood. The tunica vaginalis remains unchanged, or is thickened, or contains plates of bone, or is covered with polypoid fibrous bodies which fall off and are found free in the cavity of the sac. There may be adhesions between the layers of the tunica vagi- nalis, and in this way the fluid becomes sacculated. The testis is pushed downward and backward ; it remains unchanged or is atro- phied. Hydrocele of the processus vaginalis consists in an accumulation of serum in the cavity of the vaginal process of the peritoneum, which remains open after the descent of the testicle. There are sev- eral different varieties. (a) The vaginal process is entirely open and there is a free com- munication with the peritoneal cavity. The serum may originate in the cavity of the peritoneum or of the vaginal process, and passes freely from one to the other. (6) The processus vaginalis is closed in the inguinal canal, while its lower portion is filled with serum. (c) The processus vaginalis is closed about the testis and the vis- ceral layer of the tunica vaginalis is formed. The serum accumu- lates in the upper part of the vaginal process which communicates with the peritoneal cavity. , (d) The vaginal process is closed in the inguinal canal and over the testis; the serum accumulates so as to form one or more sacs between these two points. Inguinal hernia may complicate this form of hydrocele. Hydrocele of the spermatic cord consists in a general cedema of the connective tissue of the cord, or in the development of circum- scribed cysts in this connective tissue. A peculiar form of hydrocele is produced by the accumulation of serum in the sac of an inguinal hernia, from which the intestine has become retracted. HEMATOCELE. Hematocele of the tunica vaginalis consists in an effusion of blood into the cavity of this sac. It may be produced by injury ; in scurvy, or the heemorrhagic diathesis ; or it may complicate a pre- existing hydrocele. The effused blood usually soon degenerates, and we find the sac filled with a brownish fluid or a thick, grumous mass. The tunica vaginalis may be thickened. ° The testis remains normal or is atrophied. Digitized by Microsoft® THE ORGANS OF GENERATION. V4 Effusion of blood into the loose connective tissue of the scrotum is often called extravaginal hematocele. Heematocele of the spermatic cord occurs in rare cases as a dif- fused infiltration of blood in the connective tissue of the cord. Or blood may be effused into a hydrocele of the cord. SPERMATOCELE. Cysts containing spermatic fluid not infrequently arise from the epididymis or from the rete testis. These sometimes acquire a large size and crowd the tunica vaginalis before them, so that they simulate a collection of fluid in the cavity of the latter. The wall of the cyst may be lined with ciliated or with flattened epithelium. The contents are sometimes simply serous, but more frequently opal- escent and contain great numbers of spermatozoa. INFLAMMATION. Inflammation of the testicles may be caused by injuries, exposure to cold, inflammation of the urethra, syphilis ; or it may occur in parotitis and in connection with various infectious diseases. The testes, epididymis, or tunica albuginea may be principally involved. Usually only one testicle is inflamed, sometimes both. The inflam- mation may extend to the vas deferens. The inflammation may be acute or chronic. Acute Orchitis is most frequent in the epididymis and tunica albuginea. When the testis is involved the organ is congested and infiltrated with serum or pus. From this condition it may return to the normal state; or small abscesses may form which may be ab- sorbed, or they may increase in size so as to involve nearly the entire organ. They may perforate externally, and then healing may occur by means of granulation tissue ; or extensive gangrenous destruc- tion of the scrotum may occur. They may become enclosed in a fibrous capsule, and the contents dry and become cheesy or calcified, and so persist for a long time. The acute inflammation may pass over into the chronic form. Acute epididymitis is frequently the result of gonorrhceal infection, and may or may not be associated with inflammation of the testis. The products of inflammation may collect in varying quantity in the lumina of the seminiferous tubules and in the ducts of the epidi- dymis, and the epithelium of these structures may degenerate. _ Chronic Orchitis occurs as a sequel of acute inflammation or as an original condition. It may affect the testis, the epididymis, or the spermatic cord. The seminiferous tubules may be filled with des- quamated and degenerated epithelium ; they may be atrophied, or their walls may be greatly thickened so that they are converted into Digitized by Microsoft® 748 THE ORGANS OF GENERATION. dense fibrous cords, with almost or quite complete obliteration of their lumina. There is usually a marked increase in the interstitial tissue, which causes atrophy of the tubules (Fig. 355). The albuginea may be greatly thickened. In some cases the testis is converted into a mass of dense connective tissue, in which but little trace of the original structure can be made out. The new-formed connective tissue may become calcified. A periorchitis may lead to thickening and union of the layers of the tunica vaginalis testis, Abscesses are not infre- quent in connection with chronic orchitis. Tubercular Orchitis may occur in connection with tuberculosis Fic. 355,—CHRonIc INTERSTITIAL ORCHITIS WITH ATROPHY OF THE SEMINIFEROUS TUBULES. a, thickened interstitial tissue; c, thickened membrana propria of the tubules; d, separated epithelial cell mass in the lumen of the tubules. of the other genito-urinary organs or the lungs, in acute general miliary tuberculosis, or by itself. It usually begins in the epididy- mis and may extend from there to the testis, or it may commence in the testis itself. The appearances which the testicles present, when the seat of this form of inflammation, are exceedingly varied and difficult of interpretation. This is partly due to the complex struc- ture of the organ, partly to the varied complicating simple inflam- matory changes which the different parts of the organ undergo in connection with the special tubercular inflammation, and the impos- Digitized by Microsoft® THE ORGANS OF GENERATION, 749 sibility of making any definite morphological distinction between them. Further researches are urgently needed in this direction, and it seems probable that in the presence or absence of the tubercle bacillus we shall find the needed differentiating factor between va- rious inflammatory processes which are at present grouped under the general heading of tuberculosis testis. We may find in the testicle small circumscribed masses of cells, visible to the naked eye as whitish spots, which are sometimes com- posed of small spheroidal cells or of larger polyhedral or fusiform or round cells. These occur in the walls of seminiferous tubules and blood vessels, and in the interstitial tissue. Sometimes associated with these smaller nodules, and sometimes not, we find larger, ir- regular yellowish or gray cheesy masses, which are believed by many to be formed by the confluence and degeneration of the smaller Fic. 356 —CHRoNIC ORCHITIS WITH THE FORMATION oF STRUCTURES RESEMBLING MILIARY TUBERCLES. u, thickened interstitial tissue; b, mass of granular cells in the interstitial tissue; c, thickened membrana propria of seminiferous tubule; d, mass of separated epithelium in tubule; e, accumula- tion of small spheroidal cells around tubules; f, thickened membrana propria enclosing g, a multi- nuclear mass resembling a giant cell. nodules. The cheesy masses may break down and open externally, giving rise to fistula, gangrenous inflammation, etc. Hand-in-hand with this nodular formation of tissue, which is disposed to degenera- tive changes, there are various more or less diffuse alterations of the parenchyma, and. interstitial tissue of the organ which must not be overlooked, and which often constitute a most prominent and im- portant factor in the lesion. The interstitial tissue may be more or less densely and diffusely infiltrated with small spheroidal cells. The arteries are often the seat of obliterating endarteritis. The walls of the seminiferous tubules may be very much thickened, so that the lumen may be entirely obliterated. The epithelium lining the tubules may be fatty, disintegrates pind apesled, of, or it may have largely BO THE ORGANS OF GENERATION. disappeared. The lumen of the tubules may be filled with a granular, nucleated mass which in transverse sections looks like a giant cell. The thickened walls of the tubules may be infiltrated with small spheroidal cells, so that the underlying stroma is scarcely visible. When this occurs in connection with a similar infiltration of the in- terstitial tissue and the formation of giant cells in the lumina, we have structures which present the greatest resemblance to some forms of tubercle granula (Fig. 356). Tubercular inflammation may extend from the testis to the vas deferens, vesiculze seminales, and prostate. Syphilitic Orchitis.—This may occur in the form of a diffuse new formation of connective tissue, which may occur in some par- ticular part of the organ or be widely distributed through it, and by reason of which the organ becomes dense and firm. Morphologically there is no difference between this form of orchitis and chronic in- durative orchitis from other causes. It may occur in children affected with congenital syphilis. Gummata may form in connection with the interstitial induration. These may disappear, leaving irregular cicatrices. Inflammatory foci in the testicle are common in leprosy. TUMORS. Fibroma occurs in the form of small dendritic or polypoid growths of the visceral layer of the tunica vaginalis. These sometimes be- come free and are found in the sac, usually in connection with hydro- cele. Small nodular fibromata occasionally occur in the albuginea and in the spermatic cord. Lipomata, either pure or in combination with myxoma and sar- coma, may arise from the connective tissue of the spermatic cord or from the tunica albuginea. Chondroma, sometimes in a pure form, but more frequently com- bined with myxoma and sarcoma, occurs in the testicles and may attain a large size. Osteoma has been described. Sarcomata occur in the testes and epididymis, most frequently in the former. They present the greatest variety in structure. They may be composed of spheroidal or spindle-shaped cells ; they may be soft or contain much fibrous tissue; they are very frequently com- bined with myxoma, chondroma, lipoma, etc. Owing to the occlu- sion of the seminiferous tubules, cysts may be formed in these sarco- mata. In these cysts polypoid growths of sarcomatous tissue may occur in the form of intracanalicular growths. Thus the so-called cysto-sarcomata of the testicle are formed. The walls of these cysts may coalesce, so that large, irregular cavities may be formed. When the cysts are not filled by polypoid outgrowths from their walls they Digitized by Microsoft® THE ORGANS OF GENERATION. VbL may contain a mucous, serous, or bloody fluid, cr masses of flattened cells, fat, and cholesterin. The cysts may be lined with cylindrical, ciliated, or flattened cells. Rhabdomyomata have been several times observed, frequently in combination with cysts. Adenoma is occasionally found, usually in combination with sar- coma or carcinoma, or with cyst formation. Carcinoma of the testicle is commonly of the soft medullary form, of rapid growth, and usually primary. It may commence in the testis or epididymis. Usually only. one testicle is involved. Fre- quently the entire glandular portion of the organs is replaced by the new growth. The albuginea expands with the growth of the tumor, and may continue to enclose it even when of large size. The tissues are often very vascular, and hemorrhages, areas of softening, fatty and mucous degeneration are frequent. The inguinal and lumbar lymph nodes are apt to become involved, and distant metastasis may occur. Rarely the growth assumes a scirrhous form. Cysts.—Aside from the above-mentioned cysts which occur in connection with tumors and spermatocele, cysts may be formed from -persistent remnants of Miiller’s canal in the epididymis, or from ob- struction of the seminiferous tubules or ducts by inflammatory pro- ducts or tissue. Teratoid tumors of various kinds, with or without cysts, are of infrequent occurrence, and are sometimes quite complex in char. acter. They may be embedded in the substance of the gland.’ Probably some of the above-mentioned cystic rhabdomyomata be- long here. PARASITES. Echinococcus may occur in the testis or epididymis. THE SEMINAL VESICLES. The seminai vesicles may be the seat of acute or chronic inflam- mation, which is most frequently connected with inflammatory changes in adjacent parts, prostate, urethra, etc. As a result of chronic inflammation the vesicles may be atrophied, or they may be greatly dilated as a result of constriction of the ducts. Tubercular inflammation is usually secondary. Carcinoma of the rectum or other genito-urinary organs may secondarily involve the seminal vesicles. Small concretions, sometimes containing masses of permatozoa, are occasionally found in the seminal vesicles. THE PROSTATE. Hypertrophy of the prostate is a frequent senile change ; it is general or partial.Digitized by Microsoft® ‘areas aa UTD: be eetde Tedd: 2) cee Hescd oA . te 752 THE ORGANS OF GENERATION. In general hypertrophy the entire organ is enlarged and may reach the size of a man’s fist. The enlargement is symmetrical, or is most marked in one half or in the so-called middle lobe. The organ is hard and dense, or soft or alveolar, containing numerous small openings from which a turbid fluid exudes. These different appear- ances depend upon the character of the hypertrophy. The muscular and fibrous tissue alone may be increased, which is most common, or at the same time the glandular tissue, or the glandular tissue alone. In the latter case the lesion is more properly an adenoma. The in- crease of muscular tissue properly constitutes a myoma. In partial hypertrophy we find circumscribed nodules of muscular tissue or of muscular and glandular tissue. They are usually situ- ated at the periphery of the organ and project into the bladder. They may become detached from the prostate, and are found as small, movable tumors beneath the mucous membrane of the blad- der. Both forms of hypertrophy frequently produce, by pressure, reten- tion of urine and changes in the bladder. Atrophy of the prostate is sometimes seen in connection with atrophy of the testicles, with castration, and as a result of inflamma- tion. Sometimes the ducts of the glandular portion are enlarged, or there may be fibrous degeneration of the organ. INFLAMMATION. Inflammation of the prostate is caused by gonorrhcea, by injuries, or, more rarely, isidiopathic. It may run an acute or chronic course. The gland may after a time return to its normal condition, or is grad- ually converted into a mass of fibrous tissue filled with abscesses. The abscesses may perforate into the bladder, urethra, vesicule seminales, rectum, or peritoneum. Or the inflammation may extend to the connective tissue of the scrotum or beneath the pelvic perito- neum. The pus may become thickened and cheesy, or even calcified. Tubercular Inflammation of the prostate usually accompanies a similar lesion of some of the other genito-urinary organs, and is rarely of primary occurrence. Large cheesy masses are often formed, which may break down and open into the bladder or rec- tum. TUMORS. Adenoma of the prostate occurs in one of the forms of hypertro- phy of the gland, either with or without an increase in the fibro- muscular interstitial tissue. Carcinoma is of occasional occurrence, and may be primary or secondary. Digitized by Microsoft® THE ORGANS OF GENERATION. 753 Cysts of the prostate are sometimes found either as a result of occlusion of the ducts by hypertrophy of the interstitial tissue, tu- mors, etc., or as a result of faulty development. PARASITES. Echinococcus of the prostate has been described, but is rare. CONCRETIONS. Small ovoidal or spheroidal, often brown or black bodies, having the characters of corpora amylacea, are of very frequent occurrence in the alveoli of the prostate, particularly in old persons. We find a certain number of them in the prostate of nearly all old men, but they are sometimes present in great numbers. Larger, irregular concretions, apparently formed by the coalescence or growth of the smaller ones, are less frequently found, and may be encrusted with lime salts. These concretions may give rise to ulceration of the ducts of the gland or to interference with the passage of urine, but in a majority of cases they seem to be of little or no practical impor- tance. COWPER’S GLANDS. These glands may be enlarged and encroach upon the lumen of the urethra, either in acute or chronic inflammation. Cysts formed by the closure of the excretory ducts may also project into the ure- thral canal. THE MALE MAMMA. There may be an abnormal number of mamme. In boys, at about the time of puberty, the mamme may be swollen and inflamed or they may secrete milk. Cases are recorded in which adult males possessed large mammz which secreted milk. The breasts may be enlarged from an increase of fat or of connective tissue. Cysts of the male breast are not very infrequent. Fzbromata, sarcomata, cysto-sarcomata, myxomata, and various forms of car- cinomata are recorded.’ 1 For literature of tumor of male mamma see Gross, ‘‘Tumors of the Mammary Gland,” p. 237. Digitized by Microsoft® THE BONES. DISTURBANCES OF CIRCULATION. Hyperceemia.—The evidences of this condition are most marked to the naked eye in the periosteum and marrow, particularly the lat- ter. It should be remembered that the color of the marrow varies considerably under normal conditions, depending upon age and situ- ation. In the bones of the fcetus and new-born, and near the areas of ossification in the young, the marrow is normally red in color. In adults the marrow of the sternum, vertebre, and to a certain de- gree that of the ribs, pelvic and cranial bones, and the cancellous tissue of the ends of the long bones, is red or reddish in color. But most of the marrow, particularly in long bones of the extremities, is of a yellowish color from the presence of fat cells. In old age the marrow of all the bones is apt to become pale, and to assume a more or less translucent or gelatinous appearance. Hyperemia usually occurs as an accompaniment of inflammatory processes in the bone, and, when marked, the periosteum is swollen and red; the compact bone tissue may appear of a pink color, while the marrow, either by an increase in the amount of blood or absorp- tion of its fat, or both, may be of a uniform dark-red color or mot- tled with red and reddish-yellow. Hemorrhage.—This may be due to wounds and injuries, to in- flammatory and necrotic processes; and small haemorrhages often accompany scurvy, purpura, hemorrhagic diathesis, and leukemia. Heemorrhages of considerable size between the periosteum and bone may lead to serious consequences, by cutting off the blood supply to the superficial layers of bone and thus inducing necrosis ; but when not in contact with the air they are not usually of serious import, since they are readily absorbed. The smaller heemorrhages of the medulla are not usually of much importance. The decomposition of the ex- travasated blood may lead to extensive pigmentation of the marrow. WOUNDS, FRACTURES, AND DISLOCATIONS. For details of the varied alterations produced under these con- ditions, and the secondary changes involved in the healing process, Digitized by Microsoft® THE BONES. 755 we refer to the section on repair, page 98, and to works on surgery. It may be stated here, however, that the healing of fractures occurs by the formation of granulation tissue in greater or less amount about the seat of fracture, and the direct formation of bone under the influence of osteoblasts, or by a preliminary formation of carti- lage or fibrous tissue and the gradual conversion of this into bone by metaplasia. INFLAMMATION. The periosteum, bone tissue, and marrow are so intimately con- nected that in most cases they all share to a greater or less degree in the pathological alterations of the bones. But as sometimes one, sometimes another is most markedly involved, it is convenient to consider separately here the inflammatory changes by which they are respectively affected. Periostitts. We may distinguish several varieties : 1. Stmple Acute Periostitis.—This form is apt to occur in chil- dren and ill-nourished persons from comparatively slight injuries or from unknown causes. The periosteum is thickened, succulent, congested, and more or less abundantly infiltrated with leucocytes, while the connective-tissue fibres are swollen. The periosteum be- comes less firmly adherent to the bone, and the cells of the inner layers are increased in number. This variety of inflammation may terminate in the disappearance of the new elements and complete resolution, or it may represent a preliminary stage of one of the . other varieties of inflammation. 2. Suppurative Periostitis may begin as a simple or as a puru- Jent inflammation. The pus is formed in the inner layers of the periosteum, and between it and the bone. The outer layers of the periosteum may resist for a long time the suppurative process. The accumulation of pus may dissect up the membrane from the bone and leave the latter bare. The pus thus formed may remain in this position for a long time, may be absorbed, may become dry and cheesy, or may burst through the periosteum and form abscesses in the soft parts. The bone, if separated from its nutrient membrane, may remain unchanged, but more frequently necrosis or inflamma- tion of the bone itself is set up. Such a periostitis may run an acute or a chronic course. Sometimes suppurative peritostitis takes on a very malignant character. Pus is developed not only beneath but in the periosteum, forming abscesses filled with foul pus. The periosteum breaks down into a gangrenous, foul-smelling mass, and the same change may af- fect the neighboring soft parts. The medulla may take part in the Digitized by Microsoft® 756 THE BONES. process and break down into a purulent, gangrenous mass. Hzemor- rhages may complicate the process. The lymphatic nodes are en- larged and swollen; abscesses may form in different parts of the body, and the patient may die with the symptoms of pyemia. The pyogenic cocci may be found, under these conditions, in the exuda- tions of the periosteum as well as in the metastatic abscesses. 3. Fibrous Periostitis.—This is a slow, chronic form of inflam- mation, resulting in the formation of new connective tissue in the periosteum, which becomes thickened and dense and unusually adhe- rent to the bone. It may be the result of necrosis, chronic arthritis, chronic ulcers of adjacent soft parts, etc. It may follow a simple acute periostitis. 4. Ossifying Periostitis results in the formation of new bone from the inner layers of the periosteum. The masses of new-formed bone, called osteophytes, are of variable shape. They may form a thin, velvet-like, villous layer; or they are little spicule ; or they form larger, rounded masses, or a thick, uniform layer extending over a large part of a bone. They may be at first very loosely con- nected with the bone. The new bone has at first a loose, spongy character. Itis formed of thin plates of bone enclosing large cavities filled with marrow. Layers of compact bone tissue are formed from the medulla on the sides of the original plates, and thus the medul- lary cavities are gradually filled up with bone. The new bone may thus become as compact or even denser than normalbone. The hyper- ostoses and exostoses thus formed may remain indefinitely, or they may gradually become smaller and finally disappear by absorption. The formation of new bone in the form of osteophytes, or in dense . masses beneath and in the periosteum, occurs as a result of the same process by which bone tissue is normally formed. Certain rather large cells, called osteoblasts, which are formed along the blood vessels, possess the power of depositing osseous basement substance -about themselves and so forming bone. Pathological new forma- tion of bone differs from the normal mainly in the conditions under which it occurs. The blood vessels around which the pathological bone develops, which grow out of the old vessels, as in the formation of granulation tissue, are irregularly arranged and subjectto a variety of abnormal nutritive and mechanical conditions, so that the new bone is not usually formed in a series of definite systems of lamella, but, as above described, in a series of irregular spicule or masses. Moreover, as will be seen further on, the conditions under which it is formed being liable to change, and itself serving no definite purpose in the economy, as does normal bone, pathological new bone is often an evanescent structure. The details of its disappearance will be considered below. Digitized by Microsoft® THE BONES. Ti? 5. Syphilitic Periostitis.—Syphilitic poisoning may give rise to simple, purulent, fibrous, and ossifying periostitis. Or, in addition to these, gummy tumors may be developed in the periosteum. The bone tissue is usually more or less involved. The gummata may be absorbed or undergo cheesy degeneration, or be converted into fibrous tissue, or they may suppurate. 6. Tuberculous Periostitis.—In badly nourished persons, particu- larly in children suffering from so-called scrofula (see page 528), a chronic purulent periostitis is frequently associated with the forma- tion of miliary tubercles. Abscesses are apt to form in and about the periosteum, and when these are evacuated granulation tissue may develop, in which miliary tubercles are formed. In these tubercles the Bacillus tuberculosis may be found. The bone is apt to be in- volved to a greater or less extent in the form of inflammatory changes or caries. Ostertis. Inflammation in bone tissue is dependent upon the same general conditions and presents essentially the same series of phenomena as inflammation in other kinds of connective tissue. But it is variously modified in detail by the peculiar dense and unyielding character of the basement substance, and by certain peculiarities of the blood supply and the nutritive conditions under which the cells are placed. In simple exudative inflammation the same series of phenomena occur in connection with the blood vessels, resulting in the production of serum, fibrin, and pus, as in other tissues ; but the extent to which these changes can occur is limited and constantly associated with striking alterations in the basement substance. It is these secondary alterations in the basement substance which lend to inflammations of the bone their most peculiar characters, and in the prominence which these assume the fundamental alterations are often overlooked. The most common of these secondary alterations are the absorption of the hard basement substance of the bone and its replacement by, or conversion into, young cellular forms of fibrillar connective tissue or marrow tissue, and the new formation, in more or less atypical manner, of new bone. Asaresult of these changes the bones in simple inflammation undergo alterations either in the direction of greater vascularity and increase of the spaces filled with granulation or marrow tissue, and so become more porous and less compact at the expense of the dense basement substance ; or they undergo alterations in the direction of an increase in density at the expense of new- formed or pre-existing marrow spaces. Or, as is frequently the case, both series of changes occur either simultaneously in different regions, or follow one another, or are variously associated together. Very th h i i . ay one or Bioiee ner Pine Le opposing forms of alteration pre 758 THE BONES. dominates, or one may occur to the exclusion of the other, and we thus have two prominent forms of inflammation, which are called rarefying osteitis or osteo-porosis, and condensing osteitis or osteo-sclerosis. The exact nature of the conditions under which in one case the bones become more, in another less dense, we do not understand. In addition to these phases of inflammation in bone, and in fre- quent and varied association with them, there are alterations leading to death and destruction of bone tissue in greater or less amount, which we call caries and necrosis ; and also inflammatory changes, more or less characteristic, due to the influence of peculiar specific agencies, such as the syphilitic and tuberculous infection, and we Fic, 357,—-RAREFYING OsTEITIS IN ULNA OF CHILD. a, isolated bone fragment with rough edges; b. marrow tissue; c, Howship’s lacune with ~osteoclasts. ‘thus recognize tubercular and syphilitic osteitis. Again, the pro- ‘duction of pus is so prominent a feature in some cases as to represent a purulent phase of the inflammatory process. Finally, any of these forms, and commonly several of them at once, are variously asso- ciated with more or less marked inflammatory or degenerative alter- ations of the periosteum on the one hand, or the marrow tissue on the other, or of both combined. Rarefying Osteitis consists essentially in the formation in the marrow spaces, Haversian canals, or beneath the periosteum, of new, very cellular and vascular tissue, resembling granulation or young marrow tissue, in connection with which, or under whose influence, the basementysuhstanagiorh sthie® bone is absorbed. The THE BONES. 759 absorption of the bone occurs chiefly in the same way in which the bone is absorbed in normal growth, namely, under the influ- ence of certain large cells, called osteoclasts, which are grouped around the blood vessels. If we examine a thin section of bone which is undergoing absorption (Fig. 357), we find the edges of the bone which border on the vascular surfaces irregularly indented by deep or shallow depressions, sometimes simple, sometimes quite com- plex. These are called Howship’s lacune and are usually filled or lined by larger and smaller granular, frequently multinuclear cells-— the so-called osteoclasts. Inthe larger lacunz there may be granu- lation tissue with loops of blood vessels, with or without cells which have the morphological characters of osteoclasts. Under the influ- ence of these peculiar cells, or of the new vascular tissue, the bone is gradually absorbed. In other cases we find irregular branching channels through the bone across the lamellx, which appear to be due to the enlargement and coalescence of the lacune and canaliculi, without the direct influence of blood vessels or other cells than the fixed cells of the bone. The tissue which replaces the absorbed bone may be very rich in small spheroidal cells, or it may be more or less fibrillar. As a result of this process irregular islets of bone tissue may be entirely separated from adjacent bone and surrounded by a more or less fibrillar vascular tissue ; this is most apt to occur in the cancellous tissue. Or the originally compact bone may become traversed by a series of larger and smaller irregular branching, com- municating channels with ragged walls. These progressive altera- tions may cease and be succeeded by a new formation of bone along the edges of the channels or cavities; it may result in necrotic changes ; the vascular changes may become prominent and suppura- tion ensue. Rarefying osteitis may occur as an idiopathic disease from un- known causes ; it is often associated with the scrofulous diathesis, with diseases of the joints, with fractures or other injuries to the bone ; it often forms a predominant feature in tubercular inflamma- tion of the bones, etc. Itis chiefly by a rarefying osteitis that bone tissue is eroded and destroyed in the vicinity of tumors, aneurisms, etc., which exert pressure on the bones. By the same process the sharp ends of fractured bones may be rounded off as healing pro- ceeds. When this form of inflammation occurs in cancellous bone tissue the marrow is red or gelatinous, and the bony septa may disappear altogether, so that in extreme cases we may have, instead of can- cellous bone, a mass of granulation tissue. When the disease occurs in the articular extremity of a bone the granulating medulla may send little offshoots through the articular cartilage. These may Digitized by Microsoft® 760 THE BONES. become fused together and inflammation of the joint follow. The walls of the shafts of the long bones may be converted into spongy tissue. If, as is sometimes the case, an ossifying periostitis occurs at the same time, the bone is thickened but spongy ; or sometimes there are concentric layers of compact bone tissue, separated by rare- fied bone. Condensing Osteitis (Osteo-sclerosis).—This lesion 1s character- ized by the new formation of bone in the walls of the marrow cavi- ties or Haversian canals. The bone is formed under the influence of the blood vessels and osteoblasts, as in normal bone formation, but with less regularity. It may result in the conversion of cancellous tissue into compact bone, in the filling-up of the medullary cavity of Fic. 858.—CoNDENSING OSTEITIS, OR OSTEO-SCLEROS1S, OF ULNA oF CHILD. u, fragment of old bone with roughened, sinuous edges; b, old Howship’s lacune covered with more recently formed bone lamelle. long bones with more or less dense bone tissue. The compact bone, owing to the filling of its Haversian canals, may become very dense and ivory-like. When the medullary cavities of long bones are in- volved the yellow marrow is converted into red marrow by the ab- sorption of fat and increased vascularity. It is frequently associated with ossifying periostitis. It very frequently follows rarefying osteitis, and under the micro- scope we can then often see the Howship’s lacune resulting from the original absorption process filled and covered in with new bone lamellee (Fig. 358). It is apt to occur in connection with necrosis or some chronic inflammation of adjacent soft parts, but it is sometimes, idiopathic or occurs under unknown conditions. Digitized by Microsoft® THE BONES. 761 Suppurative Osteitis (Abscess of Bone).—This process occurs usually in the ends of the long bones. It begins with a rarefying osteitis. The medulla undergoes actual suppuration, the bone tissue is destroyed, and a circumscribed cavity is formed in the bone, filled with pus and lined with granulation tissue. Less frequently abscesses are formed in the shaft of a long bone by a circumscribed suppuration of the medulla. These abscesses usu- ally occur in old people. They last for many years, have little ten- dency to perforation, may gradually enlarge and be accompanied by an ossifying periostitis, so that the bone is expanded. Very rarely acute suppurative osteitis, with rapid formation of an abscess, and perforation, has been observed. Fic. 359.—TuBERCULOUS OSTEITIS. A miliary tubercle formed in the cancellous tissue near the joint in tubercular arthritis. In some cases, instead of abscess, there may be a diffuse infiltra- tion with pus of the Haversian canals or the spaces formed by rare- fying osteitis (see Osteomyelitis, page 763). Tuberculous Osteitis is essentially a rarefying osteitis associated with the formation of tubercle tissue and cheesy degeneration. The tubercles are sometimes small, scattered, and miliary in form (see Fig. 359); sometimes they unite to form larger and smaller masses. There may be extensive involvement of the medulla. There may be much simple granulation tissue or the formation of abscess associated with the process. Condensing osteitis and necrosis are not infre- quently present. Tuberculous osteitis is often associated with tuber- cularinflammation of thejpintsy » This mostapt to occur in cancellous 762 THE BONES. bone tissue, and is most common in the bodies of the vertebrze and in the carpal and tarsal bone. Tubercle bacilli may be found in the tuberculous masses, sometimes in considerable numbers. Syphilitic Osteitis.—The syphilitic poison may induce one of the above-mentioned varieties of osteitis, or it may produce gummy tumors. The gummatous osteitis usually commences in the peri- osteum, which becomes thickened and infiltrated with cells, so that there may be a circumscribed thickening of the periosteum, with or without distinct gummata. The vessels which extend from the periosteum into the bone become surrounded by new cellular tissue, which causes an enlargement of the canals. At this stage, if we strip off the periosteum, we drag with it the vessels surrounded by the new cell growth, leaving the bones beneath with numerous small perforations extending inward. As the disease progresses the gum- matous tissue around the vessels continues to increase, and the chan- nels in the bone enlarge by a rarefying osteitis and coalesce, form- ing large, irregular defects filled with gummatous tissue. In these masses of new tissue cheesy degeneration and the formation of fibrous tissue occur, giving them the characteristic appearance. In the vicinity of these gumma-filled spaces a condensing osteitis may occur, both in the substance of the bone and on the surface, in the form of osteophytes, so that the opening in the bone may be sur- rounded by an elevated, irregular ring of bone tissue. All this may occur beneath the uninvolved skin, or the skin may participate by a suppurative inflammation, resulting in ulceration. These processes may be circumscribed or involve a large part of a bone. It is not infrequently associated with necrosis of larger and smaller portions of bone. The gummatous tissue may be absorbed and its place be more or less filled with fibrous tissue. Syphilitic osteitis is most fre- quent in the cranial bones, but may occur elsewhere, as in the sternum, clavicle, tibia and fibula, the ribs, ete. Congenital Syphilis.—The bones of young children in this con- dition may occasionally show increased density or evidences of peri- ostitis, or irregular thickenings, particularly of the skull. The re- searches of Wegner,’ which have been frequently confirmed by -other observers, have shown that exceedingly characteristic changes very uniformly occur in the long bones in still-born or young: chil- dren who are the victims of hereditary syphilis. These changes are found for the most part along the border zone between the epiphysis and diaphysis. It will be remembered that, in normal ossification of the long bones, the border line between the calcification and ossi- fication zones is narrow, sharply defined, and straight, or gently and 1 Virchow’'s Arch., Bd. 1., 1870, p. 305. Digitized by Microsoft®” ¢ THE BONES. 763: evenly curved. In the syphilitic bones, on the contrary, this line is broader, uneven, and presents various modifications, depending upon the stage of the disease. Wegner distinguishes three promi- nent stages, which, however, merge into one another, so that all in- termediate forms may be seen. In the first stage there may be seen, between the cartilage and the new-formed spongy bone, a white or reddish-white zone, about two mm. in breadth, with very irregular borders, consisting of calcified cartilage, in which the linear groups of cartilage cells are more abundant than normal. In the second stage the calcified zone, still containing an unusual number of carti- lage cells, is broader and still more irregular and less sharply out- lined against the ossification zone. The cartilage just beyond it is softer and almost gelatinous, and may contain numerous blood ves- sels, islets of connective tissue or of calcification, or irregular ossifi- cation. In the third stage the bone may be pouched out at the sides around the ossification and calcification zones, and the perichondrium and periosteum thickened. The whitish, irregular calcified zone is hard and friable. Between this and the new-formed bone there is an irregular, soft, gray or grayish-yellow zone, from two to four mm. in thickness, which forms aloose, readily separated connection between the cartilage and the diaphysis. The white, friable zone consists mainly of irregular rows of degenerated and distorted cartilage cells lying in a calcified basement substance, of irregular masses of atypi- cal bone tissue, and of blood vessels surrounded by variously shaped cells. The soft zone consists of more or less vascular tissue with homogeneous basement substance, and round and spindle-shaped cells. This soft zone is not sharply outlined against the adjoining new-formed spongy bone, which, instead of consisting of the nor- mal marrow spaces with bony lamelle between them, is largely com- posed of granulation tissue. Different stages of this faulty development may be seen in differ- ent bones in the same individual. According to Wegner the lesion is usually most advanced in the lower end of the femur, then in the lower ends of the leg bones and of the forearm, then in the upper ends of the tibia, femur, and fibula. Not infrequently there is fatty degeneration of the marrow cells and blood vessels, giving the marrow a reddish-yellow color. These alterations of the bones may occur, not only in children who have gummata in other parts of the body, but also in those in which other evidences of syphilitic poisoning are absent. So uniform is their oc- currence that their presence alone suffices for the establishment of a. diagnosis. OSTEOMYELITIS. In most of the inflammatory processes which affect the bones the Digitized by Microsoft® 764 THE BONES. medulla has an important share, so that many conditions described as osteitis are really osteomyelitis. It is customary, however, to reserve the latter name for these cases in which the medulla is pri- marily or chiefly involved. Acute Infectious Osteomyelitis. This may occur as the result of a local injury which permits the access or favors the development of pyogenic micro-organisms; it may be metastatic, resulting from the transportation of infectious material from other part of the body in septicemia and pyemia, in typhoid fever, in the exanthematous fevers, and under other con- ditions; or it may occur without evidence of local predisposition or of infectious processes in other parts of the body. The lesions of acute infectious osteomyelitis are, in the large majority of cases at least, due to the presence and action of the pyo- genic cocci, the Staphylococcus pyogenes and the Streptococcus pyogenes, and in many of its forms it may be regarded as one of the phases of septicemia or septico-pyeemia. : While the lesions vary widely, the following general description is applicable to a considerable proportion of the cases: At the commencement of the disease, which usually begins in the shaft of one of the long bones, there is hyperemia and cedema of the medulla, so that if the bone be opened the marrow is soft and of a dark-red color. A diffuse suppuration now rapidly ensues, and the marrow becomes streaked or mottled with gray. Occasionally, though not often, larger and smaller abscesses may form in the mar- row. The inflammatory areas may be circumscribed; or, in the more malignant cases, the entire marrow may become rapidly in- volved. The cancellous tissue of one or both of the epiphyses usually becomes involved. The disease, however, is not commonly confined to the medullary spaces. The periosteum becomes cedematous and infiltrated with pus, and the surrounding soft parts may become the seat of intense inflammatory changes. Abscesses of the periosteum or surorunding tissues are apt to form. Asa result of these changes necrosis of greater or less portions of the bone may ensue. The medullary cavity may become enlarged as pus accumulates, and the wall of the bone may be broken through, permitting the discharge of pus outward. Sometimes several bones are involved at once. Secondary involvement of the joints is very frequent. There may be only a serous or purulent exudation; or the acute and destructive inflammatory process may extend to the joint and produce extensive alterations. In young persons the epiphyses very frequently become separated from the shaft by the destruction of the cartilage which binds them together. Digitized by Microsoft® THE BONES. 765 In the severer cases, which are often denominated, par excel- lence, malignant osteomyelitis, the changes may be very rapid and destructive. The medulla becomes broken duwn and gangrenous; the joints are soon involved; large portions of the boue, sometimes the whole shaft, necrose; the periosteum and surrounding parts be- come gangrenous; the veins contain thrombi, and pysemic infarc- tions and abscesses may form in various parts of the body.’ Chronic Osteomyelitis.—In the more chronic forms of osteomye- litis there is apt to be more or less ossifying periostitis and osteo- sclerosis, and fistula may form in the bone, through which the exu- dations are discharged.’ NECROSIS. By necrosis we understand the death of a larger or smaller por- tion of bone. This condition is induced by causes which deprive the bone of its proper vascular supply from the periosteum and medulla, Suppurative periostitis, osteomyelitis, and osteitis, traumatic sepa- ration of the periosteum, ulcers of neighboring soft parts, emboli, the action of phosphorus vapor, and diseases, like typhus, which diminish the vitality, may cause necrosis. Necrosis is a pure form of gangrene, differing from gangrene of soft parts in that the dead bone has at first, and may retain for a long time, the general outward characters of the normal bone; while in dead soft parts the phenom- ena of decomposition, under the influence of bacteria, rapidly ensue, inducing marked complicating appearances in the dead tissue. When a portion of bone has died an inflammation is set up at the dividing line between the dead and living bone. This inflammation has the characters of a rarefying osteitis (see above), and finally sep- arates the dead from the living bone. The dead bone, or seques- trum, may remain smooth and unaltered, or it may be eroded by the influence of surrounding pus or granulation tissue or osteoclasts. In this way it is possible for the sequestrum, if it be small, to be entirely absorbed. More frequently there is a production of new bone around the sequestrum, either beneath the periosteum or in the substance of the bone, and this becomes lined with granulation tissue, from which pus may continue to be formed, bathing the sequestrum. Necrosis may involve the superficial layers, or the entire thick- 1 Consult for an elaborate treatment of acute osteomyelitis in its relationship to other forms of inflammation, with bibliography, Jordan, Beitr. z. klin. Chir., Bd. x., p. 587. For a study of this condition in childhood see Koplik and Van Arsdale, Am. Jour. Med. Sciences, April and May, 1892. 2 For a résumé of the deformities resulting from osteomyelitis consult Park, Medical Record, November 2d, 1895. Digitized by Microsoft® 166 THE BONES. ness of the wall of a long bone, or only the spongy tissue and inner layers of the wall, or an entire bone, or a number of different por- tions of the sarne bone, but it is most apt to occur in compact bone. The death and separation of the bone are very soon followed by the growth of new bone to repair the loss. The periosteum, the medulla, and the surrounding soft tissues may all take part in this new growth. The new bone is usually irregular, rough, perforated with openings through which pus formed around the sequestrum may be discharged. If the sequestrum be removed healing may oc- cur by the formation of new bone ; but the bone is usually more or less distorted by the irregular new ossification. Phosphorus Necrosis.—Under the influence of phosphorus vapor, periostitis and osteitis, particularly of the jaw, are apt to occur, which usually lead to more or less extensive necrosis, usually associ- ated with prolonged and often extensive suppuration. CARIES, Caries of bone is essentially an ulcerative osteitis resulting in pro- gressive molecular destruction of the bone tissue. It differs from necrosis in that, in the latter, larger and smaller masses of bone die, while in caries the destruction is molecular and gradual. It may occur in connection with any form of osteitis, with periostitis and osteomyelitis, or it may be secondary to inflammatory or destructive processes in the joints or adjacent soft parts. The depressed surfaces of bones in which caries is progressing are rough and more or less finely jagged, and may be covered with granulations. The minute changes by which ulceration and destruction of the bone are produced in caries are somewhat analogous with those in rarefying osteitis, but there are marked degenerative changes in the bone cells, which may become fatty or converted into a granular material. Moreover, the basement substance of the bone, instead of being absorbed, may disintegrate, with the formation of larger aud smaller masses of detritus. Sometimes the lime salts are removed from the basement substance, which is converted into atypical fibrillar tissue and fatty and granular detritus. Very extensive suppurations and necrosis may be associated with caries. Long-continued caries, especially in badly nourished individuals, is apt to become complicated with tubercular inflammation. There is very little tendency to spontaneous healing in caries, but it may occur, and the defects produced may be more or less supplied by means of new-formed bone. RACHITIS (RICKETS). Rickets is a disease affecting the development of bone, prevent- Digitized by Microsoft® THE BONES. V6? ing its proper ossification. The disease usually occurs during the first two years of life, but may be congenital,’ or may occur as late as the twelfth year. The physiological growth of bones depends upon three conditions. They grow in length by the production of bone in the cartilage be- tween the epiphysis and diaphysis ; in thickness, by the growth of bone from the inner layers of the periosteum. At the same time the medullary canal is enlarged, in proportion to the growth of the bone, by the disappearance of the inner layers of bone. In rickets these three conditions are abnormally affected. The cartilaginous and subperiosteal cell growth, which precedes ossifi- cation, goes on with increased rapidity and exuberance and in an ae Y Sh09 58 ay Pe COP MS Ss yw Rs GM: woe ad Vy Se ze eee Fie. 360.—RacHiTic Bong. Showing ossification zone in a longitudinal section of a rib. irregular manner, both between the epiphyses and diaphyses and beneath the periosteum, while the actual ossification is imperfect, irregular, or wanting. At the same time the dilatation of the me- dullary cavity goes on irregularly and often to an excessive degree. If we examine microscopically the region between the epiphysis and diaphysis (Fig. 360), we find that the cartilage cells are not reg- ularly arranged in rows along a definite zone in advance of the line of ossification, as in normal development, but that there is an irreg- ular heaping-up of cartilage cells, sometimes in rows, sometimes not, over an ill-defined and irregular area. The zone of calcification also, instead of being narrow, regular, and sharply defined, is quite lack- ing in uniformity. Areas of calcification may be isolated in the re, 1 Consult Salvetti, Liege Bia. MC RGa” Bd. xvi, p. 29 (bibliography), 168 THE BONES. gion of proliferating cartilage cells, or calcification may be altogether absent over considerable areas. Corresponding to these irregularities the ossification zone is also irregular. New-formed bone and marrow cavities containing blood vessels may lie in the midst of the cartilage, or masses of cartilage may lie deep in the region which should be completely ossified. In other places it seems as if the cartilage tissue were directly con- verted into an ill-formed bone tissue by metaplasia or direct trans- formation. It will readily be seen from this that the medullary spa- ces of the new-formed bone are irregular, and this abnormality is enhanced by the premature intramedullary absorption of the bone. The same sort of irregularity in the bone formation may be seen beneath the periosteum. An excessive proliferation of cells in the inner layers of the periosteum, the irregular calcification which oc- curs about them, and the absence of uniformity in the elaboration of ill-structured bone, conspire to produce an irregular, spongy bone tissue instead of the compact, lamellated tissue which is so necessary here for the solidity of the structure. The increased cell growth be- tween the epiphyses and diaphyses produces the peculiar knobby swellings which are characteristic of rickets. At the same time the medullary cavity increases rapidly in size and the inner layers of the bone become spongy. The medulla may be congested, and fat, if it has formed, may be absorbed, and a modified form of osteitis may ensue. The result of these processes is that the bones do not possess so- lidity and cannot resist the traction of the muscles or outside pres- sure. The epiphyses may be displaced or bent, especially in the ribs, less frequently in the long bones. The long bones and the pelvic bones may be bent into a variety of forms. Incomplete fractures are not infrequent. Complete fractures do not usually occur until the later stages of the disease, when the bones have become more solid. In the head, the cranium may be unnaturally large for the size of the face ; the fontanelles and sutures may remain open; the bones may be soft, porous, and hypereemic, while at their edges there may be rough, bony projections beneath the pericranium. Sometimes, especially in the occipital bone, there are rounded de- fects in the bone, filled only with a fibrous membrane ; this consti- tutes one of the forms of so-called craniotabes, It does not fail within the scope of this work to describe the vari- ous deformities which may occur as a result of this disease. The familiar pigeon breast ; the rows of knobs along the sides of the chest from bending and dilatation of the ribs at the point of junction of cartilage and bone ; the knock-knee, bow-legs, spinal curvatures, . etc., may all be the result of rachitic weakening of the bones. Digitized by Microsoft® THE BONES. 769 After a time the rachitic process may stop and the bones take on a more normal character. The porous bone tissue becomes compact and even unnaturally dense ; the swellings at the epiphyses disap- pear ; many of the deformed bones may become of a normal shape. In severe cases, however, the deformities continue through life ; es- pecially is there a cessation of the growth of the bones in their long axis, so that the persons affected are dwarfed. The disease may have an acute or a chronic character. The acute form begins usually during the first six months of life. The children are apt to suffer from vomiting, diarrhcea, profuse sweat- ing, chronic bronchitis and pneumonia, general anzemia, and wast- ing. They either die or the rachitic process is gradually developed. The chronic form is seen in older children, and often in those appa- rently healthy. The changes in the bones may take place without any constitutional symptoms, though there is often catarrhal bron- chitis, pneumonia, and anzemia. OSTEOMALACIA. This lesion consists in the softening of fully formed hard bone tissue by the removal of its inorganic salts. It is to be clearly distin- guished from rickets, whose lesions are due to a faulty development of bone, although in certain external characters the two diseases sometimes present considerable similarity. Osteomalacia usually occurs in adults, most frequently in females during pregnancy and after parturition ; more rarely it occurs in males, and in females un- associated with the above conditions. Its cause is not known. Microscopical examination shows that the decalcification occurs first in the periphery of the Haversian canals and in the inner layers of the walls of the marrow spaces. As the salts of lime are removed the basement substance at first remains as a finely fibrillated mate- rial, still preserving the original lamellation. The bone cells may be changed in shape ordegenerated. After atime the decalcified tissue may disintegrate and be absorbed, and its place occupied by new- formed marrow or granulation tissue. As the disease goes on the marrow tissue is congested and red, the fat absorbed, and there is a great accumulation of small spheroidal cells ; or the marrow may assume a gelatinous appearance. The decalcification and absorption of the bone from within may proceed so far that the bony substance in the cancellous tissue almost entirely disappears, and the compact bone is reduced to a thin, soft, decalcified tissue. The disease is not always continuously progressive, but may be subject to temporary cessation. As a result of this softened condition of the bones, the weight : nl : of the body and the waite I Foe may induce a series of “mH THE BONES. deformities which are sometimes excessive: curvatures of the spine, complete and incomplete fractures of the bone, distortions of the pel- vis, sternum, etc. There is a tendency in this disease to a general involvement of the bones, but the changes are sometimes confined to single bones or groups of bones. The cranium is rarely much affected. ALTERATIONS OF THE BONE MARROW IN LEUKAEMIA AND ANAMIA., In certain forms of leukemia the marrow of the bones is very markedly altered. The change consists mainly in an accumulation in the marrow tissue of spheroidal cells, often in a condition of fatty degeneration, which lie in the meshes of reticular connective tissue and in and along the walls of the blood vessels. There may also be absorption of the fat, and sometimes enlargement of the marrow cavity from absorption of the bone. These alterations seem to be primarily due to an hyperplasia of the marrow cells. The new cells which accumulate in the marrow under these conditions are of vari- ous forms. Most characteristic are colorless, spheroidal cells which considerably resemble the large lymphocytes of normal blood (see page 82). But they are usually larger, though varying much in size, have one large, often vesicular nucleus staining less strongly than the lymphocyte nuclei, while the protoplasm usually contains neutro- phile granules (page 85). These cells are called myelocytes. In addition to these the marrow may contain, mingled with its usual elements, nucleated red blood cells, spheroidal cells containing red blood cells, and not infrequently considerable numbers of small octa- hedral crystals (called Charcot’s crystals). The degree to which this accumulation of cells varies much in different cases, and the gross appearances of the marrow are conse- quently very variable. In some cases the marrow is soft and has a uniform red appearance, or it is variously mottled with gray and red. Occasionally circumscribed hemorrhages are seen. In an- other class of cases, in which the cell accumulation is more excessive, the marrow may be gray, grayish-yellow, or puriform in appearance. These changes may occur in the central marrow cavity, as well as in the marrow spaces of the spongy bone. They may be present in several or many of the bones. They are usually accompanied by analogous changes in the spleen and lymph nodes. In certain cases of acute and chronic ancemia, particularly in the pernicious and progressive varieties, the marrow, especially of the larger long bones, may lose its yellow color from absorption of the fat, and become red. Microscopical examination of the marrow under these conditions may show myelocytes and sometimes an abun- dance of developing nucleated red blood cells and Charcot’s crystals. Digitized by Microsoft® THE BONES. GL In many of the acute infectious diseases, typhus and typhoid fever, ulcerative endocarditis, recurrent fever, etc., the bone marrow bas been found hyperemic and may, it is asserted by Ehrlich, con- tain myelocytes in increased numbers. All of these lesions of the marrow, although our knowledge of them is still very incomplete, together with what is known of the physiological functions of the marrow, point to a close relationship between the marrow and the spleen and lymph nodes as _ blood- producing organs.’ ATROPHY. In old age or in senile conditions the bones may become atrophied by the absorption of the hard tissue; the medullary spaces are en- larged, the marrow tissue contains less fat and is often gelatinous in appearance. As the result of the lack of use, or from any cause which interferes with the nutrition of the bone, such as paralysis of the muscles or diseases of the joints, the bones may atrophy. In connection with atrophy there may be an ossifying periostitis, which results in making the bone look even larger than normal. Many of the conditions commonly called atrophy, such as the erosions of bones from tumors, etc., pressing upon them, are really due toa rarefying osteitis. The bones, sometimes as the result of atrophy and sometimes from causes which we do not understand, are unusually brittle and liable to fracture. This disposition is sometimes hereditary. TUMORS. Tumors of the bone may involve either the periosteum, the com- pact bone, or the medulla, or, as is more frequently the case, two or more of these structures are involved at once. Tumors of the bone are usually accompanied by various secondary and sometimes very marked alterations of the bone tissue, osteoporosis, osteosclerosis, ossifying periostitis, etc. The new growths are very apt to undergo calcification and ossification. Fibromata may grow either from the periosteum or medulla. Their most common seat is in the periosteum of the bones of the head and face. They are apt to form polypoid tumors projecting into the posterior nares, pharynx, mouth, and antrum of Highmore. Cen- tral fibromata, ¢.e., those growing from the medulla, are rare. They usually occur in the lower jaw, but have been found in the ends of the long bones, the phalanges of the fingers, and the vertebre. The 1 The literature of the researches on the diseases of the spleen, which are impor- tant in this connection, may be found in part in Orth's “Lehrbuch der speciellen pathologischen Anatomie, ” Berlin, 1883, erste Lieferung, p. 119 et seq. Digitized by Microsoft® 972 : THE BONES. fibromata may calcify or ossify, contain cysts, and not infrequently occur in combination with sarcoma. Myxomata are of occasional occurrence in bone. Osteomata.—New formations of bone as a result of inflammatory processes are, as we have already seen, of frequent occurrence in bone, and although not, strictly speaking, tumors, some of their forms are very closely allied to them, and they may therefore be con- veniently mentioned here. New growths of bone which arise from the surfaces are called exostoses or enostoses, according to their origin from the external surface or interior of the bone. They may contain all the constituents of normal bone: bone, medulla, vessels, periosteum, and cartilage. The new bone may be compact and like ivory, or spongy, or contain large cavities filled with marrow. The shape of exostoses varies greatly ; they may be in the form of sharp, narrow spicule and processes, and, occurring in connection with periostitis, are called osteophytes. They may be polypoid in shape or form rounded tumors with a broad base. They may forma general enlargement of the bone, with much roughening of the sur- face ; this condition is often called hyperostosts. The bone beneath these new growths may ‘be normal, or sclerosed, or rarefied, or.the medullary cavity of the bone may communicate with that of the exostosis. Hxostoses are usually developed from the periosteum, sometimes in the insertion of tendons and ligaments. They are very frequently multiple and may occur at all ages, even during uterine life. Enostoses are developed in the interior of bones from the medulla. They may increase in size, with absorption of the surrounding bone, until they project from the surface like exostoses. Their most fre- quent situation is in the bones of the cranium and face. Chondromata.—These tumors may be single or multiple, and most frequently grow from the interior of the bone, but sometimes from the periosteum. They are prone to form various combinations with other forms of tumors, as fibroma, myxoma, sarcoma, ete. They are frequently congenital, and are most common in young people. They occur most frequently in the bones of the hand and foot, There is a form of chondroma, called osteoid chondroma, which develops beneath the periosteum, most frequently in the femur and tibia near the knee joint, forming a club-shaped enlargement of the bone. The characteristics of the tissue composing these tumors are that it resembles somewhat the immature bone tissue which is seen beneath the periosteum in developing bone. It differs from cartj- lage in the irregular shape of its cells, in the fibrillation and density of the basement substance, and in its general vascularity. On the other hand, it has not the ARTS iro REERES or appearance of true THE BONES. 773 bone. It resembles considerably the callous tissue forming about fractures of the bones. It may, however, and most frequently does, become converted, in some parts of the tumor, into true bone. On the other hand, combinations with sarcomatous tissue are of frequent occurrence (see below). Sarcoma.—This form of tumor is especially common in the bones. It grows from the inner layers of the periosteum or from the medulla, so that we may distinguish a periosteal and a mye- logenic sarcoma. Sometimes the tumor attacks the bone itself so early that it is impossible to say whether the tumor began in the periosteum or in the medulla. There is also a variety which grows close to the outside of the periosteum and becomes connected with it —parosteal sarcoma. The periosteal sarcomata usually belong to the varieties fibro-, myxo-, chondro-, and osteo-sarcoma, more rarely to the medullary variety. They commence from the inner layers of the periosteum, pushing this membrane outward. After a time the periosteum is attacked and the tumor invades the surrounding soft parts. The bone beneath may remain normal, or may be eroded and gradually disappear until the tumor is continuous with the medulla. Portions of the tumor may be calcified, or a growth of new bone may accom- pany its growth. The new bone usually takes the form of plates, or spicule, radiating outward. The minute anatomy of these tumors is very variable. The simplest—the fibro-sarcomata—are composed of fusiform, round, stellate, and sometimes giant cells (myeloplaxes), in varying proportions, packed closely in a fibrous stroma. In the medullary form the stroma is diminished to a minimum and the round cells are most numerous. In the chondro- and myxo-sar- coma the basement substance may be hyalin or mucous, and the cells follow the type of cartilage and mucous tissue more or less closely. There is a mixed form of tumor, called osteoid sarcoma, which is very apt to spread and to form metastases. The growth consists in part of tissue corresponding to fibro-sarcoma and round- celled sarcoma. In addition to this there occurs, in greater or less quantity, immature bone tissue, called osteoid tissue, which may in part become calcified, the calcification usually occurring in the cen- tral portions, leaving a softer peripheral zone. This form of tumor is most apt to occur at the ends of thelong bones, and may form tumors of large size. It is often called, on account of its tendency to spread and to form metastases, malignant osteoma or osteoid cancer. Myelogenic sarcomata commence in the medulla and may grow rapidly. The bone surrounding them is destroyed and they project as rounded tumors. Most frequently new bone is formed beneath the periosteum, so that the tumor is enclosed in a thin, bony shell ; fl Digitized by Microsoft® 74 THE BONES. sometimes there are also plates of bone in the tumor ; sometimes the periosteum is unaltered ; sometimes it is perforated and the tumor invades the surrounding soft parts. The tumors are frequently very soft, vascular, and hemorrhagic in parts, or may enclose cysts filled with tumor detritus and blood. They are usually of the spindle or round-celled variety, and not infrequently contain giant cells, The parosteal sarcomata resemble the periosteal, but they ap- pear to grow from the outer layers of the periosteum. They may be as firmly connected with the bone as the periosteal form. The periosteum may remain intact between the tumor and the bone, or it may disappear and leave them in apposition. Angiomata and Aneurism of Bone.—A very large number of the tumors which have been described under these names are really sarcomata, or other tumors which happened to be very vascular. Some authors, indeed, are disposed to deny altogether the existence of real vascular tumors in bones. There are, however, reliable cases of cavernous angiomata growing between the periosteum and bone and intimately connected with the latter. Whether myelogenic an- giomata occur is doubtful. There are several cases described of cavities filled with blood in the interior of bones, which it is difficult to interpret. They have mostly been found in the head of the tibia. They are said to have consisted of single sacs composed of thickened periosteum, lined with plates of bone, and filled with fluid and clot- ted blood. No large vessels communicated with the sacs, but their walls were covered with a rich vascular plexus, branches of which opened into the cavity of the sac. Carcinomata.—Primary carcinomata are of very doubtful oc- currence in the bones. Most of the structures thus named have doubtless been sarcomata. Secondary carcinomata, on the other hand, as a result of metastases or local extension, are of not infre- quent occurrence and present various structural forms. Metastatic carcinomata may occur in the bones of various parts of the body at the same time, and are most apt to be secondary to carcinoma of the mamma. . Cysts.—These most frequently occur in the maxillary bones, doubtless in connection with the teeth. They may be unilocular or multilocular, and contain clear serum or a mucous or brown fluid, and sometimes cholesterin. They may be lined with epithelium. They begin in the interior of the bone, and, as they increase in size, expand it until they may be covered with only a thin shell of bone, They may reach a large size, even as large as a child’s head. Dermoid Cysts are occasionally found in connection with the bones, particularly of the skull. Digitized by Microsoft® DISEASES OF THE JOINTS. For a description of the dislocations, misplacements, and injuries of the joints we refer to works on surgery. INFLAMMATION. _fcute Arthritts.—The earlier stages of acute inflammation of the synovial membranes are better known from experiments on ani- mals than from post-mortem examinations. The first changes are swelling and congestion of the membrane, with increased growth and desquamation of epithelium, and infiltration of the membrane with lymphoid cells. These conditions are soon followed by an exu- dation. The exudation may be a clear serum, in which epithelial cells, lymphoid cells, and sometimes blood will be found. Or floc- culi of fibrin may float in the serum, or the fibrin may be in excess and the serum nearly absent. Or there is an excessive production of lymphoid cells, and the synovial sac is filled with pus. In Serous Arthritis the accumulation of serum within the syno- vial sac is the most prominent lesion. The disease may terminate in recovery, or become chronic, or pass into the suppurative form. It may be caused by contusions, penetrating wounds, gonorrhea, rheu- matism, or it may occur without evident cause. Sero-fibrinous Arthritis may occur under the same conditions as those which lead to simple serous inflammation. The fibrin may be present largely as flocculi in the serum, or it may form false mem- branes over the surfaces of the joint. Purulent Arthritvs may follow or be associated with the above forms of inflammation. The synovial membrane is thickened and cloudy, and there may be but a moderate amount of pus in the joint, and aslight degree of infiltration of the synovial membrane with pus cells. Under these conditions resolution may readily occur. In other cases the accumulation of pus in the cavity may be great, the synovial membrane and its surrounding tissue densely in- filtrated with pus cells. Under these conditions granulation tissue is apt to be found and the cartilages of the joints are apt to become Digitized by Microsoft® 776 DISEASES OF THE JOINTS. involved. There are swelling and proliferation or degeneration of the cartilage cells ; the basement substance becomes disintegrated, ulce- rates, and exposes the bone, in which osteitis, caries, rarefaction, etc., may occur. The new-formed granulation tissue may penetrate the cartilage, absorbing the basement substance, and by metaplasia the cartilage tissue may be converted into embryonal or granulation tissue. The pus may break through the capsule of the joint and form large abscesses in the adjacent soft parts. Sometimes the in- flammation is not only suppurative but gangrenous and runs a rapidly fatal course. The synovial membrane, articular cartilages, and ends of the bone all undergo a rapid suppuration and gangrene. Pyzemia and septicemia, small-pox, measles, scarlet fever, pneu- monia, gonorrheea,’ diphtheria, mumps, typhus fever, glanders, the puerperal condition, exposure to cold, penetrating wounds, and in- juries, may all give rise to or favor the development of purulent synovitis. Chronic Arthritis may begin as such or it may be the result of previous acute inflammation. There is an increase of fluid in the joint. This fluid is thin and serous, or is thickened with flocculi of fibrin and epithelial and lymphoid cells, or is thick, syrupy, or even gelatinous. The synovial membrane is at first congested, its tufts prominent. Later it becomes thickened, sclerosed, and anzemic ; the epithelium is destroyed and the tufts become large and projecting. From the distention of the capsule there may be subluxations or lux- ations of the joint, or the capsule may be ruptured. Chronic Rheumatic Arthritis is most common in elderly per- sons, usually affecting several joints and advancing slowly and steadily. There isa chronic thickening of the synovial membrane and the fibrous tissue adjacent toit. Fluid accumulations are not common. The articular cartilages are apt to degenerate or ossify, or become softened and fibrillated, and they may disappear. The contracting synovial membranes and fibrous tissue render the joints stiff and may cause considerable deformity. Not infrequently fibrous and bony anchyloses are formed between the ends of the bones. Arthritis deformans.—This name has been applied to a variety of chronic inflammation of the joints which, combined with degene- ration of parts of the joint and the new formation of bone, may re- sult in marked deformities of the part. It usually occurs in elderly persons and is apt to involve several joints, most frequently the hip, knee, fingers, and feet. I¢ may be idiopathic, or due to rheumatism or to injuries, or follow an acute arthritis. The capsules of the affected joints are thickened and scle- 1 For discussion of gonorrheal arthritis consult Northrup, Trans. Assn. Am. Phys., vol. x., p. 141, 1895 es ; Digitized by Microsoft® DISEASES OF THE JOINTS. G77 rosed. The synovial fluid is at first increased in quantity ; later, diminished and thickened. The tufts of the synovial membrane be- come much enlarged and vascular; they may be converted into cartilage. Sometimes the capsule becomes ossified. The new bone grows from the edge of the cartilage within the capsule and its articular surface is covered with cartilage. The articular cartilages are much changed. The basement substance splits into tufts, while the cartilage cells are increased innumber. Or the basement sub- stance becomes fibrous ; or it is split into lamell and the cartilage cells are multiplied ; or there is fatty degeneration and atrophy. Asa result of these changes larger or smaller portions of the cartilage are destroyed and the bone beneath is laid bare. The ex- posed bone may become compact and of an ivory smoothness. The ends of the bones are much deformed. They are flattened and made broader by irregular new growths of bone, while at the same time they atrophy. The new growth of bone starts from the articular cartilages. The cartilage cells increase in number and the basement substance in quantity. This growth is most excessive at the edge of the cartilage, so that a projecting rim is formed there. This pro- jecting rim may ossify next the bone, and at the same time new carti- lage may form on its surface, so that we may find large masses of bone covered with cartilage. All these changes occur in various combinations and sequences, so that joints in this condition present the greatest variety of appearances. Arthritis uritica (Gouty Arthritis)—This disease is character- ized by the deposit of salts of uric acid in the cartilages, bones, and ligaments, and also in the cavities of joints. The deposits may be in the form of stellate masses of acicular crystals in and about the cartilage cells or in the basement substance ; or they may be deposited in the fibrillar connective-tissue structures of the joint in single crys- tals, or in the subcutaneous tissue about the joint as white concre- tions. The deposits may occur in repeated attacks of the disease, and are accompanied by acute inflammatory changes. They may lead to various forms of chronic inflammation of the joints. Tuberculous Arthritis (Chronic Fungous Arthritis; Strumous Arthritis).—This disease may commence in the joint itself, or be transmitted to it from a tubercular inflammation of the bone. It is characterized by the formation of granulation tissue containing tubercles, sometimes in great quantity, and usually associated with secondary inflammatory and degenerative changes of surrounding parts. According to the prominence of one or other of these second- ary alterations, several forms of tubercular arthritis may be dis- tinguished. If there is an excessive growth of granulation tissue without much suppuratipn, this epnstitutes 9 £uugous form. Some- W78 DISEASES OF THE JOINTS. times there is extensive suppuration, so that the cavity of the joint may be filled with pus, which may be discharged through openings in the skin ; or there may be more or less extensive formation of abscesses, or infiltration of the soft parts about the joint with pus. In other cases there is a predominant tendency to breaking-down of the new-formed tubercular tissue and of the tissues of the joint— ulcerative form. The cartilage basement substance may become split into fragments and the cells degenerate, and thus deep and de- structive ulcers of the cartilage be formed. Or the granulation tissue may work its way through the cartilage into the bone beneath, by absorption of the basement substance of the cartilage, with or with- out proliferation of its cells. Caries and necrosis of the underlying bone may lead to extensive destruction. Hand-in-hand with these alterations subperiosteal new formation of bone may occur, or sclero- sis of the adjacent bone tissue. There may also be a great increase of fibrous tissue about the joint. Tubercle bacilli may be found in the tubercular tissue and in the exudations. This disease is most common in children and young persons. The so-called scrofulous diathesis is said to predispose to it, but local injuries are frequently the predisposing factors. It is most common in the large joints. It may occur in connection with tubercular in- flammation in other parts of the body, but it is frequently quite local, and may remain so for a very long time or permanently, since general infection from tubercular arthritis is comparatively infre- quent. The disease always runs a very chronic course and may destroy the patient’s life. If recovery takes place before the cartilages and bones are involved the joint is preserved ; but it may be stiffened, or even immovable, from the contraction of the new fibrous tissue around it. If the cartilages and bones are diseased the joint is de- stroyed, and either bony or fibrous anchylosis results. Sometimes from the change in the articulating surfaces, and the contraction of the muscles and the new fibrous tissue, partial or complete disloca- tions are produced. Occasionally miliary tubercles occur in the synovial membranes in cases of general miliary tuberculosis, with but little accompanying simple inflammatory change. TUMORS. Secondary tumors of the joints as a result of local extension from the adjacent parts are not uncommon, and the tumors may be of various kinds. Primary tumors of the joints, on the contrary, are not very common. Lipoma.—A n th of fatty tissue may begin in the oth - Digitized by Microsoft® ea esc ay DISEASES OF THE JOINTS. 779 portions of the synovial membrane, push this inward, and project into the joint in a mass of tufts—lipoma arborescens. Fibroma occurs as an hypertrophy of the little tufts and fringes of the synovial membrane. In this way large polypoid and dendritic bodies are formed. The pedicles of these growths may atrophy and even disappear, so that the growths are left free in the cavities of the joints. Corpora aliena Articulorum (Loose Cartilages in the Joints).— This name is given to bodies, of various structure and origin, which are found free or attached by slender pedicles in the cavities of the joints. They are most frequently found in the knee ; next in order of frequency in the elbow, hips, ankle, shoulder, and maxillary joints. They may be single or in hundreds. Their size varies from that of a pin’s head to that of the patella. They are polypoid, rounded, egg- shaped, or almond-shaped ; their surface is smooth or faceted, or rough and mulberry-like. They are composed of fibrous tissue, car- tilage, and bone in various proportions. These bodies are formed in different ways. 1. By hypertrophy of the synovial tufts and production of car- tilage and bone in them. 2. More frequently by a change into cartilage of portions of the synovial membrane. Small, flat plates of cartilage form on the inner surface of the synovial membrane, and these increase in size and their outer layers ossify. They may remain fixed in the synovial membrane ; or they project and become detached from it, and they then appear as flattened, concave bodies composed of bone covered with cartilage on one side. 3. The growth of cartilage and bone begins in the outer layers of the synovial membrane or in the periosteum near the joint. The new growth pushes the synovial membrane inward, and projects into the joint as a polypoid body covered with the inner layers of the synovial membrane. Later the membrane atrophies and the growth becomes free in the joint. 4, There may be cartilaginous outgrowths from the edges of the articular cartilage. 5. Rarely portions of the articular cartilages may be detached by violence or disease; or fibrinous and other concretions may result from arthritis, or under conditions which we do not understand. Digitized by Microsoft® MUSCLE. LESIONS OF VOLUNTARY STRIATED MUSCLE. Hemorrhage.—This may occur as a result of mechanical injury ; from rupture of the fibres by convulsive contraction, as in tetanus ; or it may occur when the muscle fibres are degenerated, as in typhoid fever ; or in connection with certain general diseases, as scurvy, purpura, hemorrhagic diathesis, septicemia, etc. The blood is usu- ally readily absorbed. Embolic Infarction of Muscles in connection with heart dis- ease has been described in a few cases, but it is rare. Wounds and Rupture.—When the muscle fibres are severed by wounds or rupture there is more or less degeneration of the divided fibres, and the wound may heal by the production of granulation tis- sue, which gradually becomes converted into cicatricial tissue, thus binding the severed parts together. In some cases there is a new formation of muscle fibres, which penetrate the cicatrix and establish muscular connection between the parts. When the wound does not gape, so that the severed ends are not much separated, there may be, it would seem, a direct re-establishment of muscular continuity by new development of muscle, without the formation of much new con- nective tissue. The exact way in which muscle fibres are regenerated is yet somewhat uncertain. In many cases there seems to be a prolifera- tion of the so-called muscle corpuscles, leading to the formation of elongated cells or strings of cells, which are gradually converted into striated muscle. In some cases the appearances would seem to in- dicate that connective-tissue cells may participate in the formation of new muscle fibres, but this is not certain.’ INFLAMMATION. Suppurative Myositis.—In the early stages of this lesion we 1For literature on muscle regeneration consult Zaborowski, Arch. fiir exp. Patho- logie u. Pharm., Bd. xxv., Heft. 5 und 6, p. 415, 1889. Digitized by Microsoft® MUSCLE. Y81 find the muscle hyperemic and cedematous, and the interstitial tis- sue more or less infiltrated with small spheroidal cells, doubtless the result of emigration. If the inflammation becomes intense there may be an excessive accumulation of pus cells, either diffusely in the interstitial tissue or in larger and smaller masses. Hand-in-hand with this cell accumulation occur degenerative changes in the mus- cle fibres. By pressure their nutrition is interfered with and they undergo granular, fatty, or hyalin degeneration. They may com- pletely disintegrate and gangrene may occur, so that larger and smaller masses of the infiltrated muscle tissue become soft, foul- smelling, and converted into a mass of detritus in which but little muscle structure can be detected, and which is intermingled with bacteria. In other cases there may be larger and smaller abscesses formed in the muscle, the muscle tissue itself either degenerating and disintegrating and mixing with the contents of the abscess, or being pressed aside and undergoing atrophy and degeneration. In some cases, when the formation of pus is moderate in amount, there may be restoration by formation of granulation tissue between the muscle fibres. This becomes gradually dense and firm, and leads to more or less atrophy of the muscle fibres by pressure. Acute suppurative myositis may accompany wounds; it is very common in acute phlegmonous inflammations of the skin and subcu- taneous tissue, and often accompanies acute infectious diseases, such as pyeemia, erysipelas, etc. In most cases the pyogenic bacteria are present in the inflammatory foci. Itis not infrequently seen in the muscles adjacent to the inflamed mucous membranes in diphtheria. Chronic Interstitial Myositis.—In this lesion there is a new formation of connective tissue between the muscle fibres or bundles of fibres. This new tissue is sometimes very cellular, resembling gran- ulation tissue, and this probably represents an early stage of the disease. In other cases (Fig. 361) we find dense cicatricial tissue crowding the muscle fibres apart, inducing atrophy in them, and sometimes causing their complete destruction. This lesion, which is the analogue of chronic interstitial inflammation of the internal organs, may occur in muscles which are adjacent to other parts which are the seat of chronic inflammatory processes. It may occur in muscles which are not used. The new formation of connective tissue would in some cases seem to be secondary to atrophy of the muscle fibres. In this case it would more appropriately be called replace- ment fibrous hyperplasia. Myositis ossificans.—Under conditions and for reasons which we do not understand, there occasionally occurs, usually in young persons, a new formation of bone tissue in the interstitial tissue of muscles, in the tendons, ligaments, fasciee, and aponeuroses. This Digitized by Microsoft® 782 MUSCLE. sometimes apparently starts as outgrowths from the periosteum, sometimes not. The bone formations are apt to commence about the neck and back, and may become very widespread over the body. So far as the muscles are concerned, there is usually an increase of con- nective tissue between the fibres and bundles, in which new bone is formed, usually in elongated and sometimes in spicula-like masses. The muscle fibres undergo secondarily a greater or less degree of atrophy or degeneration. There may be fatty infiltration between the Fie. 361.—CHRonic INTERSTITIAL Myosiris. The connective tissue is dense in texture, and the muscle fibres are atrophied and partially destroyed. fibres, and various deformities are produced by the shortening and progressive immobility of the affected parts.’ While the above disease is a progressive and frequently a general one, there may be new formation of bone in muscle as a result of pro- longed or repeated mechanical irritation. Thusin the adductors of the thigh in persons who are constantly in the saddle, or in the del- toid muscle of soldiers who strike this part with their weapons in drill, there may be a formation of bone. Gummata and occasionally tubercles occur in the connective tis- sue of muscle. 1 The literature of Myositis ossificans may be found, together with a description of some interesting cases, in an article by Mays in Virch. Archiv, Bd. lxxiv., p. 145. Digitized by Microsoft® MUSCLE. 783 DEGENERATIVE CHANGES IN THE MUSCLES. Simple Atrophy.—This may occur in old age, in prolonged ex- hausting diseases, or as a result of pressure from a foreign body, tumors, etc. The muscle fibres grow narrower, the degree of narrow- ing frequently varying considerably in different parts. They usually retain the striations, but these may be obscured by degenerative changes. The sarcolemma may become thickened, and there may be a considerable increase in connective tissue between the muscle fibres and bundles. : Progressive Muscular Atrophy.—This lesion consists essentially in a combination of simple or degenerative atrophy of the muscle fibres with chronic interstitial inflammation, and is sometimes associ- ated with proliferative changes in the muscle nuclei. In the earlier Fia. 362.—ProGressive Muscutar ATRopHy (Soleus muscle, longitudinal section). a, atrophied muscle fibre; b, degenerated muscle fibre; c, interstitial tissue; d, clusters of pro- liferated muscle nuclei. stages of the disease the muscles may be pale and soft, but exhibit otherwise to the naked eye butlittle alteration. Gradually, however, the muscle substance becomes replaced by connective tissue, so that in marked and advanced cases the muscles are converted into fibrous bands or cords, whose cicatricial contraction may induce great de- formities. Microscopical examination shows in the early stages of the disease a proliferation of cells in the interstitial tissue, so that this may have the appearance of granulation or embryonal tissue ; also in some cases marked proliferative changes in the muscle nuclei (Fig. 362), Digitized by Microsoft® 784 MUSCLE. leading to the formation of new cells which may more or less replace the contractile substance within the sarcolemma. The new inter- stitial tissue increases in quantity and grows denser, and may crowd the muscle fibres apart (Fig. 363). The walls of the blood vessels may also become thickened. Hand-in-hand with these interstitial alterations the atrophy of the muscle fibres proceeds. These may simply grow narrower, retaining their striations; or they may split up into longitudinal fibrille, or transversely into discoid masses, and in this condition disappear. In other cases a certain amount of fatty or hyalin degeneration may be present. These degenerative and Fia. 363.—ProGREssIve Muscutar ATRopHY (Soleus muscle, transverse section). a, increased interstitial tissue; b, nearly normal muscle fibres; c, degenerated muscle fibres; d, atrophied muscle fibres; e, clusters of proliferated muscle nuclei. proliferative changes do not, as a rule, occur uniformly in the affected muscles, but some parts are affected earlier and more markedly than others. The atrophied muscle may be replaced by fat. Progressive muscular atrophy is apt to commence in the small muscles of the extremities, in many cases in the muscles of the ball of the thumb. It may commence in the muscles of the shoulder, the arms, or the back. It may have a continuous extension, or it may jump single muscles or groups of muscles. Death may be in- duced by the affection of the muscles of respiration or deglutition. The causes of this lesion are in many cases unknown, and there Digitized by Microsoft® MUSCLE. 785 is considerable lack of unanimity of opinion as to whether it is pri- marily a disease of the muscles or of the nervous system. Ina considerable proportion of cases the muscle lesion is associated with atrophy of the ganglion cells in the anterior cornua of the spinal cord and the development of connective tissue about them In other cases these changes in the cord may apparently be absent. It is sometimes accompanied by atrophy of the nerves which are distributed to the muscles, and atrophy of the anterior roots has been described. It is probable that there are several varieties of progressive mus- cular atrophy, which our present knowledge does not enable us to jee (ee Ee 5 KAP IOe tee ap : BOs (1 Ata 4 cs ES TEC Sper Cx Frere UB) Wi YLT) Sr ae ee = a C0 MMM Tie Teh AEE ea ao nce hh paeee a Fic. 364.—PssUD0-HYPERTROPHY OF GASTROCNEMIUS MuscLE (Fatty INFILTRATION). The specimen is from the case mentioned below, accompanying multiple neuroma. clearly distinguish. Muscular atrophy in some cases follows over- straining of groups of muscles, or injuries, and may occur as one of the sequel of typhoid fever and diphtheria. Atrophia Musculorum lipomatosa (Pseudo-hypertrophy of the Muscles).—In some eases, hand-in-hand with the production of new connective tissue in the muscles and the atrophy of the muscle fibres, or after these changes have made considerable progress, there occurs a development of fat tissue between the fibres (Fig. 364) which may prevent any apparent diminution in the size of the muscles, or in some cases may even give them a great increase in size. This condi- Digitized by Microsoft® 736 MUSCLE. tion is of most frequent occurrence in children, and is most apt to appear in the gastrocnemii muscles. In the upper extremities the deltoid and triceps are most frequently involved. The lesion may be symmetrical, affecting similar muscles on both sides of the body, or it may be unilateral. Parts of muscle bellies may be affected. The cause of this form of atrophy is not definitely known. Vari- ous lesions of the spinal cord have been described as occurring with it; but, in many cases at least, alterations of the nervous system cannot be detected. The writer has described a case * in which this lesion was marked in the gastrocnemii in connection with multiple false neuromata.” Fatty Degeneration, with greater or less destruction of the mus- cles, may commence with a simple swelling and fine granulation of the fibres. As the process goes on, smaller and larger fat droplets appear in the contractile substance, which loses its striations and becomes friable, and may be entirely destroyed, leaving within the sarcolemma a mass of fatty detritus which may finally be absorbed and disappear. This alteration may occur in acute parenchymatous myositis in connection with various forms of atrophy, in prolonged exhausting diseases, and in phosphorus poisoning. Hyalin Degeneration.—Under a variety of conditions the mus- cle fibres undergo a peculiar series of changes, leading to their con- version into a translucent, highly refractile material, somewhat re- sembling amyloid but not giving its micro-chemical reactions, and apparently more nearly allied to the material produced in the so- called hyalin degeneration. The lesion in the muscle which we are considering is commonly called waxy degeneration, from the peculiar appearance which the muscles present. When the lesion is far advanced and extensive the muscles are brittle and have a gray- ish-yellow, translucent appearance. Microscopical examination of various stages of hyalin degeneration of muscle shows that the con- tractile substance of the fibres becomes at first swollen and granular, and gradually converted into hyalin material which may present the outlines of the swollen fibres, but is more frequently broken into larger and smaller shapeless clumps (Fig. 365), which may disin- tegrate and finally be absorbed. Hand-in-hand with these changes there usually occurs an increase in the interfibrillar connective tissue, and in certain cases there may be a proliferation of the muscle nuclei and a new formation of variously shaped cells within the sarco- 1 Prudden, American Journal of Medical Sciences, July, 1880, p. 184. 2 For bibliography of muscular atrophy consult Friedreich, ‘‘Ueber progressive Muskelatrophie,” etc., Berlin, 1873 ; also ‘‘ Dictionnaire encyclopédique des Sciences médicales,” 2 ser., i., x.; or Eulenberg's ‘‘ Real-Encyclopiidie der gesammten Heil- kunde,” article by Pick on AS BP inicroso A) MUSCLE. 187 lemma which leads to the regeneration of the fibres. As a result of the brittleness of the degenerated muscles they are apt to rupture, and in this way hemorrhage may occur. This form of degeneration may occur in progressive muscular atrophy, in variola, cerebro-spinal meningitis, trichinosis, in connec- tion with inflammation, injuries, freezing, etc. Itis, however, most marked and frequent in typhoid fever. In this disease the rectus abdominis and the adductors of the thigh are most frequently affected. Experimental investigations have shown that, under certain con- ditions, very similar appearances may be produced in the muscles by post-mortem changes. It is not unlikely that a variety of changes are at present included under the name waxy or hyalin degeneration of the muscles.’ Hypertrophy of Muscle.—True hypertrophy of muscle as a pathological condition is rare, but it has been described in a few qu Ri all Lace ccc TG Fie. 365.—HyaLin DEGENERATION (SO-CALLED Waxy DEGENERATION) OF ABDOMINAL MUSCLE IN TYPHOID FEVER. eases. It is usually confined to circumscribed groups of muscles. On microscopical examination the diameter of the fibres is increased, sometimes considerably, though not uniformly. The transverse stri- ation is unaltered and the muscle nuclei are in some cases enlarged. The cause of the change is unknown. TUMORS. The tumors of the muscles usually develop in the connective tissue. Fubroma, chondroma, lipoma, myxoma, sarcoma may occur as primary tumors. Carcinomata and sarcomata may occur secondarily in the muscles as a result of local extension from adjacent parts. The muscle fibres are, as a rule, only secondarily affected by pressure, etc., in tumors of the muscles, but there exist observations 1Consult Zenker, ‘‘ Ueber die Verinderung der willktrlichen Muskeln in Typhus abdominalis,” Leipzig, 1864; also Wechl, ‘‘Exp. Unters. ti. d. wachsartige Degene- yation der quergestr. Muskeln,” Virch. Arch., Bd. lxi., p. 258, 1874. Digitized by Microsoft® 788 MUSCLE. which point to the possibility of a proliferation of the muscle nuclei and the new formation from them of cells which may take part in the growth of the tumor. PARASITES. The Trichina spiralis is the most common parasite in the mus- cles. Cysticercus cellulose and Echinococcus occasionally occur. ‘ Digitized by Microsoft® PART IV. THE LESIONS FOUND IN THE GENERAL DISEASES, IN POISONING, AND IN VIOLENT DEATHS, ae Digitized by Microsoft® Digitized by Microsoft® DISEASES CHARACTERIZED BY ALTERA- TIONS IN THE COMPOSITION OF THE BLOOD. There is a group of diseases in which the essential lesion seems to be an alteration in the composition of the blood, although in some members of the group other lesions are also present. This group embraces Chlorosis, Pernicious Anzmia, Addison’s Disease, Leu- keemia, and Pseudo-leukzemia. CHLOROSIS. Chlorosis is a disease of the blood attended with a diminution in the hemoglobin, and usually in the number of the red blood cells. Of the essential element in the causation of this disease and of the exact method of its origin we are ignorant. The condition has been attributed to congenital hypoplasia of the heart and blood vessels, to prolonged innutrition, to intestinal intoxication, and to functional disturbance of an unknown nature in the blood-producing organs. In the mildest grade of chlorosis the only change to be observed is a uniform diminution of hemoglobin. In severer forms may be added a diminution in number and moderate vuriations in size and shape of the red cells. In very severe and relapsing cases the he- moglobin may be excessively decreased; the red cells may number less than two million per centimetre; considerable alterations in size and shape of the red cells may occur; megalocytes, microcytes, and poikilocytes may appear, and the morphology of the blood as well as the clinical aspect of the disease may closely resemble or even become identical with progressive pernicious anzemia (see PLATE, Fig. 2, page 80). The albuminous constituents of the plasma and the specific gravity of the blood are uniformly diminished, but the alkalinity and power of coagulation are slightly or not at all affected. Even in cases of considerable severity the degenerative changes in the viscera characterizing other forms of aneemia have been found wanting, al- though degenerative changes in the red cells may occur in accordance Digitized by Microsoft® 792 DISEASES CHARACTERIZED BY ALTERATIONS with the severity of the disease. Hemoglobin is not set free in the plasma, the liver does not contain an excess of iron, and the urine is free from pathological urinary pigments. ‘ Tho regeneration of the blood in chlorosis under rest and treat- ment with iron may usually be rather promptly effected by increased activity probably accompanied by hyperplasia of the red marrow. This regenerative process may be indicated in the blood by the peri- odical appearance of considerable numbers of normoblasts. The appearance of these nucleated red cells may be accompanied by a moderate increase of leucocytes, both mononuclear and polynuclear, constituting the mixed leucocytosis characteristic of primary chlo- rosis. Myelocytes also may rarely be seen. PERNICIOUS ANAEMIA. Pernicious anzemia is a disease of the blood and blood-forming organs, characterized by excessive destruction associated with defec- tive production of red cells. The exact relation of the factors concerned in the causation of the disease has not been determined. It may be said, however, that while very rapid cases of pernicious anzmia have been observed unaccom- panied by the usual lesions in the bone marrow causing defective hzematogenesis, the disease seems not to exist without excessive hz- matolysis. Pernicious anzemia may probably originate as a primary disease of the blood or bone marrow, but many cases apparently idiopathic have been shown at autopsy to be secondary to such conditions as cancer, nephritis, tuberculosis, atrophy of the gastric mucosa, or the presence of parasites in the blood or intestine. The studies of Hunter indicate that the destruction of the blood may in some cases result principally in the portal circulation and particularly in the spleen from the action of toxic principles absorbed from the intestines. Whatever its origin, the distinguishing feature of pernicious anzemia is the fact that the anzemia is entirely disproportionate to any appar- ent cause, and when once established tends to progress to a fatal issue. The essential lesion is an extreme and progressive diminution in number and very great variation in size and form of the red blood cells (see PLATE, Figs. 3 and 4, page 80). Nearly constant is a general lesion of the bone marrow in which the normal nucleated red cells are replaced by an excessive number of larger nucleated corpuscles with hyperemia and atrophy of fat cells. There is thus established an ab- normal type of development of red cells which closely resembles the embryonal type. The destruction of hemoglobin is followed by a considerable deposit of iron in the liver, spleen, marrow, and other Digitized by Microsoft® IN THE COMPOSITION OF THE BLOOD. 793 organs, by the appearance of abnormal pigments in the urine, and by a yellowish discolorization of the skin. The prolonged anemia may cause fatty degeneration of the viscera, especially of the liver, kidneys, and heart muscle. As a combined result of fatty changes in the arterial walls and of the diminution in albuminous principles and coagulability of the blood, hemorrhages in various parts of the body are of frequent occurrence. Disseminated areas of sclerosis in the spinal cord have been described and regarded as the result of minute hzemorrhages in this region. In the blood the red cells are usually reduced to less than two million and often to half a million per cubic millimetre. Of the remaining cells a considerable percentage or nearly all may be ab- normally large (megalocytes). On the other hand, in a certain type of the disease many of the red cells are very small (microcytes). Cells of very irregular shape are often present in abundance (poiki- locytes). The quantity of hemoglobin in the majority of the cells is either increased as in one distinct type of the disease, or diminished as in other cases in which the individual cells may resemble those of chlorosis. The “haemoglobin index”—that is, the relation of the total percentage of hemoglobin to the total number of cells—may be normal when a deficiency of hemoglobin in one cell is counter- balanced by a proportionate excess in another. A variety of degenerative changes in the red cells are commonly present, including especially the change from hzemoglobin to methe- moglobin, as indicated in those cells which stain reddish-brown with eosin. Nucleated red cells of normal size (normoblasts) are of rather in- frequent occurrence in the blood of well-established pernicious ane- mia. Abnormally large nucleated red cells (megaloblasts) are a nearly constant element and of great diagnostic importance, as they indicate the presence of a grave lesion in the bone marrow. Megalocytes and megaloblasts usually show an excess of haemo- globin, may exhibit amceboid movement, and have no tendency toward the formation of rouleaux. Extremely large nucleated red cells (gigantoblasts) are frequently found in advanced cases, and in these cells as well as in the megaloblasts the nuclei may be seen in various stages of normal or pathological mitosis, while in their protoplasm may occasionally be demonstrated small basophile granules. In very rapid cases of pernicious anzmia both normoblasts and megaloblasts may be absent from the blood, in which event the yellow marrow of the long bones is not replaced by normal or pathological red marrow. During the rapid destruction of red cells hemoglobin may be dis- solved in the plasma, which in dry preparations stained with eosin takes on a reddish tinge. Digitized by Microsoft® 794 DISEASES CHARACTERIZED BY ALTERATIONS In the absence of complications producing leucocytosis, in perni- cious anemia the leucocytes are usually diminished in number. Of the remaining white cells the mononuclear cells may be most abun- dant and a few myelocytes may be found. LEUKAMIA (LEUCOCYTHAMIA). Leukzemia is characterized by a progressive increase of the white cells and decrease of the red cells of the blood, and by alterations of varying extent in the spleen, lymph nodes, and bone marrow. Leu- keemia is probably to be regarded as a primary disease of the blood- forming organs. Many authorities, however, consider a change in the blood plasma to be the primary cause, and others, influenced by the discovery of bacteria in the blood of a few cases, believe in the infectious nature of the malady. The increase of uric acid in the blood and urine of leukemia is thought by many to be of etiological importance. A close relation between leukeemia and some other diseases of the blood is indicated by the occasional undoubted devel- opment of leukemia during the course of pernicious anemia or pseudo-leukeemia. According to the predominance of the changes in one or other of the organs, various types of the affection may be distinguished. Myelogenous leukcemia indicates a special involvement of the bone marrow, but a pure form of this variety is extremely rare. Spleno- myelogenous leukemia with changes in the spleen and marrow is morecommonly seen. Lymphatic leukemia, with alterations promi- nent in the lymph nodes, absent or inconsiderable in the spleen or marrow, is acommon variety. Usually all three organs are simul- taneously involved. As a rule, other internal organs, liver, kid- neys, lungs, etc., show an infiltration of their capillaries with leu- cocytes, or the presence of numerous small collections of spheroidal cells. The lymphatic tissue in the gastro-intestinal tract and of other regions may be in a condition of hyperplasia. The changes referable to diminution of red cells and prolonged anzemia are similar to, but less pronounced than, those of pernicious anzemia. Ecchy moses in the serous and mucous membranes, or severe he- morrhages on slight provocation, and fatty degeneration of the heart and kidneys, are frequent complications. Aside from various other foreign chemical substances which may exist in the blood in leuke- mia, there are very frequently found in the blood, marrow, spleen, liver, etc., after death elongated octahedral crystals, called Charcot’s crystals, which are believed to be formed by a combination of phos- phoric acid with some organic base. Digitized by Microsoft® IN THE COMPOSITION OF THE BLOOD. 795 For a detailed description of the lesions of the different parts of the body in leuksemia, see chapters on Blood, Spleen, Lymph Nodes, Bones, ete. The specific gravity, alkalinity, and coagulability of the blood are uniformly diminished in leukemia, as in other forms of progres- sive anemia, but the morphology of the blood varies with the type of the disease and the predominance of the lesion in different organs. Aside from the rare conditions when, under proper treatment, the number of colorless cells may approach the normal, or when the toxemia of an infectious disease replaces the mixed leucocytosis by the ordinary polynuclear leucocytosis, leukemic blood always con- tains an excessive number of leucocytes (see PLATE, Figs. 5 and 6, page 80). The colorless cells may even outnumber the red, but often more characteristic than the increase in numbers is the abnormal proportion of mononuclear cells and the abundance of myelocytes. In splenic and lymphatic leukemia the increase is in the small and large mononuclear leucocytes. The presence of myelocytes in con- siderable numbers is a very constant feature of leukeemic blood and is believed to indicate the hyperemia or further involvement of the bone marrow. Although found in moderate numbers in many other conditions, a considerable percentage of myelocytes is important diagnostic evidence of leukemia. In nearly pure lymphatic leu- keemia, large mononuclear and polynuclear leucocytes, myelocytes, and nucleated red cells may be comparatively infrequent, while the lymphocytes are greatly increased. The chronic process in the blood-producing organs, and the gen- eral disturbance of nutrition, may be indicated by an increase of eosinophile cells which is frequently observed, least often in the lym- phatic type of the disease. Mast cells are very constantly found in leukzemic blood, and the great rarity of their occurrence in other conditions renders their identification in the blood a valuable diagnostic sign. The leucocytes of leukemia commonly show a diminution or absence of amceboid motion. In the nuclei of myelocytes mitotic figures may be seen; more frequently the nuclei show a deficiency of chromatin. In dry preparations from the blood of advanced cases, large, basket-shaped, faintly staining nuclei, apparently devoid of protoplasm, are frequently encountered (PLATE, Fig. 5, page 80). Fatty degeneration of the protoplasm of leucocytes has been demon- strated, both in the circulation and in the bone marrow, and an increase cohesiveness may frequently be noted. The red blood cells in leukzemia exhibit, in a lesser degree, many of the changes characteristic of pernicious anemia. In the lym- phatic type, normoblasts and megaloblasts may be very infrequent, Digitized by Microsoft® 796 DISEASES CHARACTERIZED BY ALTERATIONS but with the involvement of the marrow, especially in children, they may appear in considerable numbers. ' PSEUEO-LEUK4MIA (“HODGKIN’S DISEASE,” “ADENIE”). Under this term it has been customary to describe a rather hetero- geneous group of cases characterized by progressive anzemia, by hyperplasia of the lymph nodes and nodules, with an occasional but by no means constant involvement of the spleen, liver, and bone marrow, and by new growths of lymphatic tissues in many parts of the body. While anzemia of moderate or severe grade is very con- stantly present in this disease, the increase of leucocytes characteris- tic of leukeemia is wanting. Of the exact nature of the disease (if it be a single disease) very little is definitely known. The enlargement of the lymph nodes is in typical cases due to simple hyperplasia. The blood changes may present the type of pernicious anwmia, and in well-authenticated cases the condition has developed into true leukemia. Recent evi- dence favors the belief that some cases classed under this heading may be of an infectious character.’ Cases of primary sarcoma of the lymph nodes have been described as cases of pseudo-leukemia. The condition found at autopsy varies greatly according to the distribution and character of the new growths of lymphatic tissue. The lymphatic nodules involved may be principally limited to the subcutaneous connective tissue (dermal type). Or the lymph nodes of the pharynx and neck may be chiefly involved (tonsillar type). Or the axillary or inguinal or mediastinal or retroperitoneal groups may be involved. A somewhat characteristic condition is produced by hyperplasia, often followed by ulceration, of the lymph nodules of the gastro-intestinal tract (intestinal type). The hyperplastic lymph nodes may be isolated or they may be joined to form large lobulated masses. The enlarged lymph nodules may in the intestine project far into the lumen in spheroidal or polypoid form, and are sometimes dark in color as the result of the decomposition of hemoglobin of extravasated blood in the congested mucous membrane covering the nodules. Hyperplasia of the thymus has been described in associa- tion with the lesions of the lymph nodes.*® A distinct sub-variety is that which terminates in leukemia. In general any of the lymph- nodes or collections of lymphoid tissue may be involved, and nearly ‘For further data with bibliography consult Miller, Central. f. allg. Pathol., v., 1894. ® Fleaner, “Multiple Lympho-sarcomata, ” Johns Hopkins Hospital Reports, vol. iii, p. 158. 5 Brigidio and Piccoli, Ziegler’s Beitr. z. path. Anat., Bd. xvi., p. 388. Digitized by Microsoft® IN THE COMPOSITION OF THE BLOOD. 197 every region has been a site of origin for the new growths of lym- phoid tissue, so that a great variety of combinations may be seen. The leucocytes in the blood may be slightly increased or dimin- ished, and in either case the mononuclear forms are usually in excess. Myelocytes have been observed in moderate percentage, but never in such proportions as in leukemia.’ Anemia infantum pseudo-leukeemica (von Jaksch) is a some- what peculiar form of anemia occurring in children, and character- ized by progressive anzemia, by a considerable increase of leucocytes, by enlargement of the spleen and liver, and often by hyperplasia of the lymph nodes. By some authorities it is regarded as an early stage of leukeemia, by others asa form of secondary anzemia following rachitis, tuber- culosis, or syphilis. The histological changes in the blood-forming organs are, so far as is known, very similar to, but less pronounced than those of leukeemia. The enlargement of the spleen is usually greater than that of the liver, thus differing from infantile leukeemia, in which the liver and spleen are equally affected—while the involvement of the lymph nodes is less frequent than in leukeemia. The red cells present most of the changes of pernicious anemia, but nucleated red cells are often found in greatabundance. The leu- cocytes may number one hundred thousand per cubic millimetre, the increase affecting the mononuclear cells chiefly, the eosinophile cells slightly, and of both a considerable percentage may be myelocytes. 1 Consult Monte and Berggrun, “Die chronische Anemie d. Kindesalter, ” Leipsic, 1892. Digitized by Microsoft® SCORBUTUS—PURPURA—HAMATOPHILIA. SCORBUTUS (SCURVY). This disease appears to result from imperfect nutrition under conditions which cannot be considered here, and whose immediate cause we do not understand. The lesions are variable, the most prominent being anzemia; extravasation of blood in the skin, subcu- taneous tissue, and muscles; swelling and ulceration of the gums. Small and sometimes extensive hemorrhages are apt to occur in the mucous membranes and on serous surfaces. Small ulcers may form in the mucous membranes. Fatty degeneration of the heart, liver, and kidneys is not uncommon. The spleen may be large and soft. No constant characteristic changes have been discovered, either in the blood vessels or the blood, which would satisfactorily account for the extravasations and other lesions. The body is apt to decompose early. The skin may be mottled with small and large purple, blue, brown, or blackish spots produced by degenerative changes in the extravasated blood in the cutis. Sometimes ulcers are produced by the perforation of effused blood on to the surface. The joints may be inflamed, may contain serum or blood. Rarely the hemorrhages are followed by destruction of the cartilages and ends of the bones. Very rarely there is hemorrhage between the periosteum and bone, and in the bone itself, producing softening and destruction of the bone, and separation of the epiphyses. The sternal ends of the ribs are the most frequent seat of this change. That some forms or phases of scorbutus are of infectious nature is not improbable, but definite data in this direction are wanting.’ PURPURA HAIMORRHAGICA (MORBUS MACULOSUS). This disease is characterized by the occurrence of ecchymoses in the skin, mucous and serous membranes. Hemorrhages, particu- ‘ For a study of scorbutus in infants consult Northrup and Crandail, New York Med. Jour., May 26th, 1894. Digitized by Microsoft® SCORBUTUS—PURPURA—HAMATOPHILIA. 799 larly from the mucous membranes, may be very severe and even fatal. The cause of the disease is unknown. A few cases have been described under this name in which the characteristic ecchymoses were associated with the pyogenic bacteria, representing, it would seem, a phase of pyeemia. Whether any considerable number of cases of this disease are associated with bacteria we do not yet know.’ HAMATOPHILIA (HAMORRHAGIC DIATHESIS). This abnormal condition consists in a liability to persistent he- morrhage on the slightest provocation, and is dependent upon some constitutional peculiarity which is unknown to us. It is frequently hereditary. An unusual thinness of the intima of the arteries has been noticed in some cases, and other changes have been described ; but there are no constant lesions associated with hzemorrhages, as yet discovered, which would satisfactorily explain their occurrence. The hemorrhages may be traumatic in origin, or they may occur sponta- neously from the mucous membranes. 1 For a more detailed consideration in the light of recent studies of cases often grouped under the name “ Hemorrhagic Infections,” consult Honl, Ergebnisse der allg. Aetiologie, 1896, p. 798 (bibliography). Digitized by Microsoft® ADDISON’S DISEASE. This name is applied to a disease especially characterized by a peculiar pigmentation of the skin and by certain changes in the ad- renals. The patients become very anemic, but are not emaciated. They suffer from cerebral symptoms, great prostration, syncope, and derangements of the functions of the stomach and intestines. The pigmentation of the skin is the symptom which has especially attacted attention. The change in color usually begins and becomes most marked in those parts of the skin which are not covered by the clothing or are naturally darker colored. The rest of the skin after- ward changes color, but not uniformly, white patches being left. The color is at first a light yellow or brown; this becomes darker un- til it is of a dark greenish, grayish, or blackish brown. The mucous membrane of the tongue, lips, and gums may be pigmented in the same way. Under the name of Addison’s disease different observers have de- scribed cases in which the symptoms and bronzed skin existed with- out disease of the adrenals; cases in which the bronzed skin was the only lesion; and cases in which the adrenals were diseased without symptoms or bronzed skin. We hardly know as yet what are really the characteristic lesions of the disease. The Skin.—The discoloration of the skin is due to deposit of yel- lowish-brown pigment in the deeper layers of the epidermis, espe- cially in the layer covering the papille, and less constantly in the connective tissue of the cutis. The Brain.—Pigmentation of the gray matter, acute meningitis, chronic meningitis, and distention of the ventricles with serum have been observed. The Heart.—The muscular fibres may be the seat of fatty degen- eration. The Sympathetic Nerves may show a variety of changes ap- parently due to chronic inflammation, especially the nerves which are in contact with the adrenals. Various changes in the semilunar ganglia have been described. Digitized by Microsoft® ADDISON’S DISEASE. 801 The Adrenals.—The most common lesion of these bodies is a tuberculous inflammation, and this or some other lesion of the ad- renals has been found in nearly one-half of the cases. On the other hand, it should be remembered that similar lesions of the adrenals often occur without other indications of Addison’s disease. Tuberculous adrenals may be large, hard, and nodular; less fre- quently of normal size or smaller than normal. On section they may contain cheesy masses surrounded by zones of gray, semi-translucent tissue. Later the cheesy masses may become calcified or they may soften and break down. The grayish zones are composed of tubercle tissue, or denser connective tissue. Other cases have been described in which the adrenals were the seat of carcinoma or of fatty or waxy degeneration. The adrenals in some cases appear normal or they may be atrophied. On the whole the clinical, morphological, and experimental data now available seem to point to both the sympathetic system and to the adrenals as of greatest significance in determining this disease. But exact knowledge in the matter depends upon a much more defi- nite understanding than is now possible of the functions and rela- tionship of the adrenals and the nervous system.' ' For a summary of the available observations on Addison’s disease up to 1893 consult Thompson, Trans. Assn. Am. Phys., vol. viii., p. 384. Consult also 2. Kahlden, Ziegler’s Beitr. z. path. Anat., Bd. x., p. 494. On the relationship of the suprarenal bodies to the nervous system, consult Alezander, ibid., Bd. xi., p. 145. For observations on the effects of removal of suprarenal body see Tizzont, ibid., Bd. vi. For recent and general bibliography consult Lubarsch, Ergebnisse d. spec. path. Morphologie u. Physiologie, 1896, p. 488. Digitized by Microsoft® ACUTE RHEUMATISM, There are no characteristic lesions in this disease, which in many respects resembles the infectious maladies. It is apt to be associated with inflammation, with little exudate in various joints, and with inflammation of the heart or pericardium. In cases in which sup- purative inflammation has occurred, pyogenic bacteria have been occasionally found. But the cause of the disease itself is unknown. Digitized by Microsoft® GOUT. The characteristic lesion of gout is the presence of an abnormal amount of uric acid in the blood and the deposit of urate of soda in the articular cartilages, the ligaments of the joints, the ears, and the eyelids. The most frequent situation is the metatarso-phalangeal joint of the great toe. The cartilage may be infiltrated or encrusted with the deposit. A very important feature of gout is that patients with the gouty diathesis are especially liable to derangements of digestion and to certain chronic inflammations, such as chronic inflammation of the arteries, chronic bronchitis, and chronic nephritis. Digitized by Microsoft® DIABETES MELLITUS. There are no constant or characteristic morphological lesions of this disease, which involves such defects in nutrition as lead to an abnormal accumulation of sugar in the blood and its discharge by the urine. A great variety of lesions have been found in the body after death from diabetes, but none of them and no combination of them appear to be of well-defined significance in this special relationship. The Brain may appear to be entirely normal; it may be con- gested; there may be an increase of serum; the convolutions may be shrunken; there may be meningitis; there may be dilatation of the blood vessels, small extravasations of blood around the vessels, en- largement of the perivascular spaces, and alterations in thé perivas- cular sheaths and nerve tissue bounding the cavities; there may be tumors at the base of the brain. The Spinal Cord may present dilatation of the blood vessels; dilatation of the central canal; changes in the gray matter of the an- terior cornua. The Lungs.—There may be pleurisy, bronchitis, broncho-pneu- monia, lobar pneumonia, gangrene of the lung, chronic pulmonary phthisis. The Heart is often small; there may be chronic endocarditis. The Stomach and Intestines.—The stomach may be dilated, its walls may be thickened, there may be hemorrhagic erosions of the mucous membrane. Jn the intestines there may be tuberculous ulcers or enteritis. The Liver may be cirrhotic or fatty. The Kidneys may be enlarged; they may be the seat of paren- chymatous degeneration or diffuse nephritis; there may be glycogenic degeneration of the epithelium of Henle’s loops. The Blood.—In a few cases fat has been found in the blood, and fat emboli in the vessels of the lungs. Attention has, however, been called to the pancreas, which in a considerable proportion of cases may show atrophy of the parenchyma Digitized by Microsoft® DIABETES MELLITUS. 805 with increase of the interstitial tissue or other lesions. Similar le- sions of the pancreas may, however, occur without the existence of diabetes. The results of partial or total extirpation of the pancreas lend weight to the importance of this organ in the etiology of dia- betes.’ ' Reference to the more important work on this subject may be found in an article by Kasahara, Virch. Arch., Bd. exliii., p. 111, 1896 63 Digitized by Microsoft® SUNSTROKE (INSOLATION). During the hot summer months cases of sunstroke are of frequent occurrence in New York. The persons affected are, for the most part, adult male laborers, usually of intemperate habits. It is necessary to separate from the cases of sunstroke proper, when the patient is attacked while exposed to the heat of the sun, the cases of exhaustion from heat and fatigue, which may occur as well in the house. The patients who are seriously affected by sunstroke exhibit, dur- ing life, an intense heat of the skin, convulsions, and coma. Death in many cases soon ensues. In other cases the symptoms are more protracted. After death, decomposition sets in very early, owing to the state of the weather. Inautopsies which we have made within two hours after death the increased heat of the skin was still maintained. The Brain and its membranes were in some cases congested, in others not. Sometimes there was an increased amount of serum be- neath the pia mater ; sometimes there were small and thin extrava- sations of blood beneath the pia mater and between the pia and dura mater. Tn the other viscera there were no lesions except those due to the condition of coma existing before death. The lungs and kidneys were frequently congested. In the cases in which cerebral symptoms are protracted for anum- ber of days the lesions of meningitis have been found after death. Attention has been called by Dr. H. C. Wood, Jr., to the rigid condition of the wall of the heart after death, but this rigidity is cer- tainly not present in all cases. According to Cramer,’ persons surviving for some time the first severe effects of the heat may suffer important alterations in certain nerve fibres of the brain. ! Cramer, Centralblatt fur allg. Path., etc., March 15th, 1890. Digitized by Microsoft® DEATH FROM BURNING. Death may be caused by the inspiration of smoke and flame; by drinking of hot fluids ; by the direct contact of flame or hot sub- stances with the external surface of body. It may be due to the di- rect effect of the agents, to secondary affections of the viscera, or to the exhaustion produced by long-continued inflammation and sup- puration. Sudden death may occur after extensive burnings of the skin.’ The entire body may be burned to a coal or completely roasted, or only a larger or smaller area of the skin be burned. We find the burned skin divested of epidermis and presenting a peculiar red, hard, parchment-like appearance. If the patient has lived some time, this is replaced by a suppurating surface. Or there are small, bladder-like elevations of the epidermis. The base of these blisters is red and they are surrounded by a red zone, or sup- puration may have commenced. These appearances cannot be produced by heat applied to the skin after death. The Brain may be congested, cedematous, or softened. More frequently it is normal. The Larynx and Trachea may be congested and the seat of croupous inflammation. There may be oedema of the glottis. The Lungs may be congested and cedematous, or hepatized, or the seat of pyeemic infarctions. There may be pleurisy. Inflammation of the peritoneum is not very infrequent. There may be swelling of the solitary and agminated nodules of the small intestine. The duodenum may be the seat of perforating ulcers, and the mu- cous membrane of the entire gastro-intestinal canal may be con- gested. The Liver, Spleen, and Kidneys may be the seat of pa- renchymatous degeneration or of pyzemic infarctions. 1For literature on sudden death following severe burns consult Silbermann, Virch. Arch., Bd. cxix., p. 488, 1890. Digitized by Microsoft® DEATH FROM ELECTRICITY. Lightning.—Persons who are struck by lightning may die in- stantly ; or may continue for several hours comatose or delirious, and then either die or recover ; or they may die after some time from the effects of the burns and injuries received. The post-mortem appearances are very variable. Sometimes there are no marks of ‘external violence or internal lesions. Some- times the clothes are burnt and torn, while the skin beneath them is unchanged. Usually there are marks of contusion and laceration, or ecchymoses, or lacerated, punctured wounds, or fractures of the bones, or superficial or deep burns. The track of the electric fluid may sometimes be marked by dark-red arborescent streaks on the skin. Fractures are rare. The internal viscera may be lacerated and disorganized from lightning. Artificial Electrical Currents.—In death from powerful artifi- cial electrical currents, either by accident, as in linemen and others, or in electrical executions, there may be local burnings of varying degree where the wires or electrodes come in contact with the skin. The clothes may be pierced with holes at the point of exit of the current. Internally there appear to be no marked or characteristic lesions, either gross or microscopical, in this form of death. Van Gieson’* and others have observed the occasional, but not constant, occurrence of small hemorrhages in the floor of the fourth ventricle, the significance of which is doubtful. Other petechial spots have been observed beneath the serous surfaces of the endo- cardium, pericardium, and pleura, and on the spleen. 1 Van Gieson, ‘‘ A Report of the Gross and Microscopical Examination of Six Cases of Death by Strong Electrical Currents,” Reprint from the New York Medi- cal Journal, May 7th and 14th, 1892. Digitized by Microsoft® DEATH FROM SUFFOCATION—ASPHYXIA. By suffocation we understand that condition in which air is pre- vented from penetrating into the lungs without direct pressure on the larynx or trachea. The interruption of the function of respira- tion which is thus brought about induces the condition known as asphyxia. Many deaths from drowning and strangulation take place in this way. The methods in which the supply of air may be cut off from the lungs are very various. The mouth and nose may be closed by the hand, by plasters and cloths, by wrapping up the head in cloths, by covering the face with earth, hay, grain, etc. Foreign bodies may be introduced into the mouth, pharynx, and larynx. Blood may pass into the trachea from an aneurism or from a wound. The glot- tis may be closed by inflammatory swelling. Matters which are vomited may lodge in the larynx. On the other hand, injury or disease of the medulla oblongata, or paralysis or spasm of the muscles of respiration from drugs, tumors pressing upon the air passages, or diseases of the lungs themselves, may induce asphyxia. EXTERNAL INSPECTION. The body should be examined for marks of violence, the cavities of the mouth and nose for foreign substances. The face may be livid and swollen or present a natural appear- ance. The conjunctiva may be congested and ecchymotic. There may be small ecchymoses on the face, neck, and chest. The mouth often contains frothy blood and mucus. The tongue may be pro- truded. INTERNAL EXAMINATION. The Brain and its membranes may be congested, or anzemic and cedematous, or unchanged. The Blood throughout the body is unusually dark-colored and fluid. Digitized by Microsoft® 810 DEATH FROM SUFFOCATION—ASPHYXIA. The Larynx may contain foreign bodies which have produced the suffocation. The mucous membrane of the larynx, trachea, and bronchi is congested and sometimes ecchymotic. These passages contain frothy blood and mucus. The Lungs are usually congested and cedematous, but sometimes do not differ from their ordinary appearance. There may be small patches of emphysema near the surface of the lungs. Sometimes, especially in infants, small ecchymoses are found in the costal and pulmonary pleura. The Heart usually presents its right cavities full of blood, its left cavities empty ; but to this there are frequent exceptions. The Abdominal Viscera are usually congested. DEATH FROM STRANGULATION—HANGING. Strangulation is effected by the weight of the body in hanging, by pressure on the neck with the hands or by some other object, or by constriction of the neck with a cord or ligature of some kind. Death is usually produced by asphyxia, or by asphyxia combined with the effect of the cutting-off of the blood supply to the brain by pressure on the large vessels of the neck. In some cases of hanging, death ensues as a result of fracture or dislocation of the cervical ver- tebree. EXTERNAL INSPECTION. The face may be livid and swollen, the eyes prominent, the lips swollen, and the tongue protruded. These appearances are, how- ever, often absent. rection of the penis, 2jaculation of semen, and evacuation of faeces and urine are frequently observed. In most cases marks are left upon the neck by the objects which have directly produced the strangulation. In cases of hanging, the mark about the neck varies considerably in position, direction, and general characters, depending upon the kind of ligature employed, the time of suspension, period after death at which the observation is made, etc. The most common mark left by a cord about the neck is a dry, dense, brownish furrow, whose breadth corresponds but in a very general way with the diameter of the cord. In some cases, according to Tidy and others, there may be no mark at all if the hanging is quickly accomplished with a soft ligature and the body cut down immediately after death. There may be abrasions and ecchymoses of the skin at the seat of ligature. In cases of strangulation by the fingers the marks on the neck may correspond in a general way to the shape of the fingers. Digitized by Microsoft® DEATH FROM SUFFOCATION—ASPHYXIA. 81t The application of the same forces immediately after death may produce the same marks as when death is induced by them. INTERNAL EXAMINATION. The Brain and its membranes may be congested, or there may be extravasation of blood, or there may be no abnormal appearances. The Neck.—In some cases there is effusion of blood beneath the ligature, rupture of the cervical muscles, fracture of the os hyoides and cartilages of the larynx, fracture and dislocation of the cervical vertebra, rupture of the internal vertebral ligaments and of the inner and middle coats of the carotid arteries. Similar changes may be produced in the dead body by the use of great violence. In death from asphyxia the lesions are similar to those described above. In some cases—for example, where death has occurred from fright or shock—the results of post-mortem examination are entirely negative. DEATH FROM DROWNING. In exa.nining the bodies of persons who have been drowned it is necessary to bear in mind a number of questions which may arise : Whether the person came into the water alive or dead? How long a time has elapsed since death ? Whether the person committed sui- cide, or was drowned by accident, or was murdered ? These ques- tions are to be solved sometimes certainly, sometimes with proba- bility, sometimes not at all, by the post-mortem examination. Persons dying in the water, to which condition the term drowning is commonly applied, may die from asphyxia, from exhaustion, from fright or syncope, from diseases of the heart, apoplexy, injuries, etc. While in the majority of cases asphyxia is a predominant or impor- tant factor in death by drowning, the conditions under which death occurs are so apt to be complex that in the minority of cases only are the lesions of pure asphyxia found after death, while in most cases the bodies present the more or less well-marked lesions of asphyxia together with those indicative of complicating conditions. There are no post-mortem conditions which alone are absolutely characteristic of drowning, and it is only by considering all the facts elicited by the autopsy together that any just conclusion can be arrived at. It should always be borne in mind, moreover, that even the most char- acteristic of the evidences of drowning are apt to be modified or to disappear as decomposition goes on. EXTERNAL INSPECTION. Post-mortem rigidity usually sets in early, sometimes immediately after death. Decomposition goes on, especially in summer, with. Digitized by Microsoft® $12 DEATH FROM SUFFOCATION—ASPHYXIA. unusual rapidity in bodies which have been removed from the water. Frequently, but by no means constantly, the peculiar roughening of the skin, known as goose skin (cutis anserina), is found, but this may occur after death from other causes. A light, lathery froth, either white or blood-stained, is frequently seen about the mouth and nos- trils within twelve to twenty-four hours after removal of the body from the water, but it may be absent, and may be seen after death from other causes. After the body has lain for several hours in the water (twelve to twenty-four) the thick skin of the palms of the hands and soles of the feet may become macerated and thrown into coarse wrinkles, just as it may after prolonged soaking during life, or in a dead body thrown into the water. The penis and nipples may be retracted and the scrotum shrunken, but this is not constant nor characteristic. . If the person has struggled in the water and clutched at objects within his reach, there may be evidences of this in excoriations of the fingers or in the presence of sand, weeds, etc., under the nails or grasped in the hands. External marks of injury, bruises, etc., should be sought for, since persons in diving, or on being thrown into the water with homi- cidal intent, may have died from the violence, and not, strictly speak- ing, from drowning. It should also be borne in mind in such com- plex cases that injuries, not in themselves fatal, may, when the body is in the water, prove so on account of the inability of the person to rescue himself or gain time for recovery from the injury, and that then the struggle for breath may be but slight, and the more promi- nent signs of drowning but little marked. INTERNAL EXAMINATION. The Brain.—Congestion of the brain and its membranesis found only in a small proportion of cases. The Blood, when death occurs from asphyxia, is usually fluid throughout the body and of a dark color, as in asphyxia from other causes. The Avr Passages.—In persons who die from asphyxia the mu- cous membrane of the larynx, trachea, and bronchi is usually con- gested, and the air passages contain a variable quantity of bloody or mucous froth. In persons dying in the water from other causes than asphyxia these appearances are absent. Foreign substances from the water, such as sand, weeds, etc., or matters regurgitated from the stomach, may find their way into the air passages during the act of drowning or as a post-mortem occurrence. Thus, in bodies washed about on the bottom, sand or mud may get into the air passages for a certain distance, from the mechanical action of the water. Digitized by Microsoft® DEATH FROM SUFFOCATION—ASPHXIA,. 813 The Lungs in typical cases are distended so that they fill the thorax and cover the heart. The increased size is due partly to con- gestion, partly to the presence of the fluid in which the person was drowned, which is often inspired during the act of drowning, and partly to the distention of the air vesicles with air. While, in cases of drowning in which there is a struggle and water is breathed in, the lungs contain more or less fluid, this may, as a result of decom- position, find its way in greater or less quantity into the pleural cavi- ties by transudation, leaving the lungs comparatively empty. It should be remembered, however, that a considerable quantity of reddish fluid may collect in the pleural cavities under other condi- tions than drowning, as a post-mortem change, by transudation from the blood vessels and other adjacent tissue. The Heart.—In those who die from asphyxia the right cavities are usually filled with fluid blood, while the left cavities are empty. But where death is due to complex causes this may not be the case. The Stomach.—The fluid in which the person was drowned, sometimes mixed with sand, weeds, etc., may be swallowed during the act of drowning. Sand may wash for a short distance into the cesophagus after death, in bodies washing about the bottom. The Abdominal Viscera may be congested in persons who die from asphyxia. In persons dying from syncope, shock, etc., we may find no lesions. When the death is partly due to asphyxia and partly to other causes, the conditions will vary in various ways, which need not be described in detail here. In important cases of doubtful drowning it is desirable to care- fully collect and save some of the fluid from the lungs and stomach for micro-chemical examination, since the identification of these fluids with those in which the person was presumably drowned will often give certainty to an otherwise doubtful case. For the detailed consideration of the anatomical diagnosis of drowning, the changes which bodies dead from drowning undergo from decomposition, and the factors bearing on the question of sui- cide, homicide, etc., we refer to works on medical jurisprudence.’ 1 Tidy, ‘‘Legal Medicine,” vol. ii, pp. 342-3873. Guy and Ferrier, ‘‘ Forensic Medicine,” pp. 274-285. Digitized by Microsoft® DEATH FROM POISONING. In cases of suspected poisoning which may possibly have a medi- co-legal bearing the examination should be made with extreme care and thoroughness. The inspection of the body and the examination of all the viscera should be thorough and detailed. Every appear- ance should be noted at the time and nothing left to the memory. It is well to have an assistant record the observations as they are made. The disposition of the parts and organs in jars should also be noted at the same time. It is important to remember that many poisons destroy life with- out producing appreciable lesions, and also that many cases of sud- den death occur, not due to poisons, and without any discoverable cause. In bodies which are exhumed for examination the tissues may be so changed by decomposition that it is impossible to say whether lesions have or have not existed. In such cases the careful and separate preservation of the viscera and other parts for chemical ex- amination is often all thatcan bedone. For directions for preserving tissues and organs for the chemist in medico-legal cases, see Part I. (page 41). SULPHURIC ACID. The effects of this poison vary with the amount taken and with its strength. Death usually takes place in from two to twenty-four hours after the taking of the concentrated acid. A case of death within an hour is recorded. When the poison is less concentrated or its effects less intense, the patient may survive for months. The skin of the face about the mouth may be blackened and charred by the acid. The mouth and pharynx are of a grayish or blackish color, or are covered with a whitish layer, while the deeper tissues are reddened. Sometimes these regions escape the action of the poison. The larynx, trachea, and lungs are sometimes acted on, softened and blackened by the accidental passage of the acid into them. Digitized by Microsoft® DEATH FROM POISONING. 813 This may even take place when the acid does not pass into the ceso- phagus. The wsophagus seldom escapes. It is grayish or blackish col- ored, softened, and the mucous membrane comes off in shreds. If life is prolonged, cicatrices and strictures are formed. The stomach may contain a blackish, pulpy fluid, due to the action of the acid on mucus, blood, etc. Itis coated on its internal surface with a black, sticky layer, beneath which the mucous membrane is reddened. The mucous membrane may be blackened in patches or stripes. The organ may be contracted and the mucous membrane corrugated. Sometimes perforation takes place and the acid blackens and softens the adjoining viscera. In protracted cases cicatrices are formed and the organ is contracted. If the poison is dilute there may be only the lesions of chronic gastritis. The blood is sometimes thickened, syrupy, acid, and may form thrombi in the vessels. The body may be partially preserved from decomposition, owing tothe action of the acid upon the tissues. Fatty degeneration of the renal epithelium is mentioned by some authors, The solution of indigo in sulphuric acid, commonly known as sulphate of indigo, produces the same lesions as sulphuric acid, and also stains the tissues with which it comes in contact of a dark-blue color. It is stated that an indigo-blue tint is often found in the mucous membranes after poisoning by pure sulphuric acid.’ NITRIC ACID. Death may occur very soon after the taking of the poison, but does not usually occur for several hours, and may not take place for several days or weeks. The surface of the mucous membrane of the mouth, pharynx, and esophagus is covered with yellow eschars wherever the acid has touched it. Beneath and around the eschars the tissues are con- gested and red. The poison may be introduced into the cesophagus without acting on the mouth. The stomach contains a viscous, sanguinolent, yellow-or greenish fluid. The mucous membrane is congested, red, swollen and softened, ecchymotic. It is rarely per- forated. The dwodenum may be inflamed, and the inflammation extend to its peritoneal coat. The rest of the intestines usually - escapes the action of the acid. The larynx is very frequently acted on by the acid. There are 1 Woodman and Tidy, ‘‘ Forensic Medicine and Toxicology,” ed. 1877, p. 237, Digitized by Microsoft® 816 DEATH FROM POISONING. yellow eschars, congestion and swelling of the mucous membrane, sometimes cedema of the glottis. The trachea may be inflamed and the lungs congested. If the patient survives the first effects of the poison the lesions of chronic inflammation, cicatrization, and contraction may be found at a later period. The acid nitrate of mercury, if taken in a concentrated form into the stomach, may produce the same lesions as nitric acid. HYDROCHLORIC ACID. In fatal cases death occurs on the average in about twenty-four hours. The lesions are in general similar to those produced by sul- phuric and nitric acids, except that the eschars are usually of a whit- ish color at first, becoming, after a time, discolored and disinte- grated. It is also more common to find false membranes on the in- flamed surfaces. OXALIC ACID. In fatal cases death may occur within ten minutes (in one casein three minutes) or may be delayed for two or three weeks. The pe- riod of death does not depend, as do in general the symptoms, upon the amount and concentration of the poison. The mucous membrane of the mouth, pharynx, and esophagus is usually white and shrivelled, and easily peeled off, and may be covered with brownish vomit from the stomach. The cesophagus may be much contracted. The stomach is usually contracted and contains a dark-brown, acid, mucous fluid. The mucous membrane of the stomach may be pale, soft, and easily detached, sometimes looking as if it had been boiled in water. Sometimes it is red and congested ; sometimes blackened and gangrenous ; sometimes peeled off in patches. Perforation is of rare occurrence. If life be pro- longed the whitened condition of the mucous membrane is succeeded by congestion and inflammation. The smallintestines may be in- flamed. Inflammation of the pleura and peritoneum, and conges- tion of the lungs, are of occasional occurrence. In some cases of death from oxalic acid there are no well-marked lesions. Potassium oxalate produces the same lesions as oxalic acid. TARTARIC ACID. This acid is seldom used as a poison, but in large doses may prove fatal. The lesions in the cases observed were redness and inflam- mation of the mucous membrane of the gastro-intestinal canal. Digitized by Microsoft® DEATH FROM POISONING. 817 POTASH, SODA, AND THEIR CARBONATES. These substances are not commonly used as poisons with suicidal or homicidal intent, but may be taken by mistake. They may cause death in a few hours, or life may be prolonged for several weeks. The mucous membrane of the mouth, pharynx, esophagus, and stomach is softened, swollen, congested, and inflamed, or may be peeled off. It may be blackened from local changes in the blood. The mucous membrane of the larynx and trachea may also be swol- len and inflamed. If life is prolonged for some time, cicatrices and strictures of the a@sophagus and stomach are apt to be produced as a result of the reparative inflammation. AMMONIA. The vapor of strong ammonia may cause death from inflamma- tion of the larynx and air passages. The strong solution of am- monia produces lesions similar to those of potash and soda. The larynx, trachea, and bronchi are frequently inflamed, and may be covered with false membranes. Fatal inflammation of the rectum and colon has been produced by an enema of strong solution of am- monia. POTASSIUM NITRATE. Accidental poisoning sometimes occurs from large doses of this salt. In the observed cases there were intense congestion and in- flammation of the stomach and intestines, and in one case a small perforation of the stomach. For the effects of several infrequently employed salts of the alka- lies and alkaline earths, which for the most part produce simple in- flammation of the gastro-intestinal canal, we refer to special works on toxicology. PHOSPHORUS. Poisoning by phosphorus is much more common in France and Germany than in this country. Some of the forms of rat poison, of which this is a frequent ingredient, and the ends of matches, are common media for its administration. It is more often used with suicidal than homicidal intent. The post-mortem appearances vary according to the length of time which elapses before death, which may be from a few hours to several months. If death takes place in a few hours the only lesions may be those produced by the direct local action of the poison. The mouth, pha- Digitized by Microsoft 818 DEATH FROM POISONING. rynx, and csophagus usually escape. The stomach may be only slightly reddened, or there may be patches of inflammation and erosion. The contents of the stomach are often mixed with blood and may have the peculiar smell of phosphorus. There may be little bits of wood present when the poison has been taken from the heads of lucifer matches. It is said that the mucous membrane of the stomach may emit a phosphorescent light in the dark. If death does not ensue until after several days the lesions are more marked. The body is usually jaundiced. There may be ecchy- mosis beneath the pericardium, pleura, and peritoneum, in the lungs, the kidneys, the bladder, the uterus, the muscles, and the subcuta- neous connective tissue, and bloody fluid in the visceral cavities. The heart and voluntary muscles, the walls of the blood vessels, and the endothelium of the air vesicles of the lungs may be in the condition of fatty degeneration. The blood is usually dark and fluid. The stomach sometimes presents no very striking changes. There may be small circumscribed spots of inflammation, erosion, or gan- grene, and occasionally perforation. The most constant change is a granular degeneration of the cells which fill the gastric follicles. In consequence of this the mucous membrane appears thickened, opaque, of white, gray, or yellow color. The small intestine appears normal or is congested. The izver is found in different degrees of parenchymatous and fatty degeneration, and is often stained yellow from the jaundice. It is usually increased in size and of a grayish, grayish-yellow, or light-yellow color, unless stained by the bile. Less frequently the centres of the acini are congested, or the entire liver is congested, or there are small hemorrhages in the liver tissue. The liver may be soft, flabby, and smaller than normal. In the interstitial tissue of the liver and along the branches of the portal vein there may be marked infiltration with small spheroidal cells. The kidneys often present parenchymatous and fatty degenera- tion of the epithelium. The mesenteric lymph nodes may be soft and swollen. ARSENIC, This poison is very frequently employed with suicidal intent. Death may occur in a longer or shorter time from the direct irrita- tive effects of the poison upon the gastro-intestinal canal, with the symptoms which usually accompany the ingestion of irritant poisons ; or it may occur with symptoms of collapse, or coma, or shock ; or the symptoms may resemble those of cholera. The average time of death in acute fatal cases is about twenty hours, but death has occurred in twenty minutes and has been prolonged for two or three weeks. =, of : Digitized by Microsoft® DEATH FROM POISONING. 819 The mouth, pharynx, and esophagus may be inflamed, but are ‘more frequently unaltered. The stomach may be empty or contain mucus mixed with blood. The arsenic, in substance, may be found adherent to the mucous membrane or mixed with the contents of the organ. It has, in rare cases, been found encysted in the stomach in considerable quantity. When invisible to the naked eye a micro- scopical examination of the stomach contents will not infrequently reveal characteristic crystals of arsenious acid or some of its com- pounds. The stomach may be contracted and its mucous membrane corrugated. The entire inner surface may be red and inflamed, or there may be patches or streaks of inflammation or deep congestion. The inflamed and congested patches may be thickened and covered with false membrane mixed with larger and smaller particles or masses of the poison. Ulceration, perforation, and gangrene are rare. Blood may be extravasated into the mucosa and submucosa, and with the congestion give the mucous membrane a very dark-red or brown appearance. Frequently the mucous membrane is studded with small petechiz. Sometimes the arsenic is converted in the stomach into the yellow sulphide. There may be acute gastritis, even when the poison is absorbed by the skin or otherwise and not introduced into the stomach. Taylor mentions a case in which the coats of the stomach were thickened and gelatinous, but not con- gested. The epithelium of the gastric glands may undergo granular and fatty degeneration. The entire length of the entestine may be congested and inflamed, but the action of the poison does not usually extend beyond the duo- denum. In some cases the solitary lymph nodules, Peyer’s patches, and the mesenteric nodes are swollen. Inflammation of the bladder and peritoneum, and congestion and cedema of the brain, have been observed, but are neither frequent nor in any way characteristic. Fatty degeneration of the muscles, liver, kidneys, blood vessels, and vesicular epithelium of the lungs may be produced in arsenical poisoning. Alterations in the spinal cord indicative of acute myelitis have been described by Popon’ as occurring in dogs poisoned with arse- nious acid. The walls of the stomach and intestines and other parts of the body may be preserved from renee for a long time after death by arsenical poisoning. Tt should always be borne in mind, in examining cases of sus- * Popon, ‘‘ Ueber die Verinderungen im Riickenmarke nach Vergiftung mit Arsen,” ., Virch. Arch., Bd. xciti Bol, 3 Senn Digitized by Microsoft® 820 DEATH FROM POISONING. pected arsenical poisoning, that death may be produced by arsenic and its compounds without any appreciable lesions. While in gene- ral it may be said that in the cases in which no lesions are discovered death has been rapid, the death may be delayed in such cases until long after a period at which, in other cases, marked inflammatory changes have occurred. Compounds of arsenic, such as the chloride and sulphide, and the arsenite (Scheele’s green, Paris green), are sometimes used for sui- cidal purposes, and produce lesions similar to those of arsenious acid. Paris green is a favorite article in New York, particularly among Germans, for suicidal purposes. It is usually taken in con- siderable quantities, and is often found in the stomach after death. * CORROSIVE SUBLIMATE. The mucous membrane of the mouth and throat may be swollen, inflamed, or have a grayish-white appearance. The @sophagus may be swollen and white, or congested, or unaltered. The mucous mem- brane of the stomach is usually congested or inflamed, or there may be patches of softening, ulceration, or gangrene. Perforation is of rare occurrence. Small ecchymoses in the mucosa are not uncom- mon. Sometimes there is little or no change in the stomach. Some- times the mucous membrane of the stomach is slate-colored from the deposition of metallic mercury from the decomposed salt. The ¢n- testines may appear normal, or there may be patches of congestion and ecchymosis. The larynx and trachea may be congested. The kidneys may show parenchymatous and fatty degeneration of the epithelium. LEAD. The ‘different preparations of lead may prove fatal either from the immediate effect of large doses or from the gradual effects of re- 1It is advisable, in cases of suspected arsenic poisoning, particularly if the body have lain for some time, as in exhumations, to preserve not only all of the internal organs entire for the chemist, but also portions of the muscles (back, thigh, arm, and abdomen), and also one of the long bones, preferably the femur, since arsenious acid and its compounds are quite diffusible, and may be present in proportionately larger quantity in other parts than in the gastro-intestinal canal. It is desirable to save the whole of the internal organs, and to weigh the muscle and bones as well as the whole body at the autopsy, in order that the calculations of the chemist, in case arsenic be found, may rest upon a definite basis, and be as little as possible dependent upon esti- mates, whose value may be questioned by lawyers should the case come into the courts. An interesting artic.e on arsenic as a poison, with various collateral data by Peilew, will be found in Hamilton’s “System of Legal Medicine, ” vol. i., p 349. Digitized by Microsoft® DEATH FROM POISONING. 821 peated small doses. Although there may be marked symptoms dur- ing life, the post-mortem lesions are few and variable. Large doses may produce acute gastritis, and sometimes a whiten- ing of the mucous membrane. The intestines are generally con- tracted, and there may be fatty degeneration of the renal epithelium ; very frequently there are no appreciable lesions. In chronic lead poisoning the intestines may be contracted, the voluntary muscles flabby and light-colored, or partially replaced by connective tissue, and there may be chronic meningitis. COPPER. Acute poisoning by salts of copper is not very common, but it is of occasional accidental occurrence, and the salts are infrequently used with suicidal intent. The sulphate and acetate are the most important salts in this respect. Soluble salts of copper may be formed in the use of copper cooking utensils, and accidents most fre- quently occur in this way. The post-mortem appearances are somewhat variable. The pharynx and @sophagus may be somewhat inflamed or unchanged. The mucous membrane of the stomach and intestines may be in- flamed, ulcerated, or gangrenous, and perforation and peritonitis may occur. The mucous membrane may have a diffuse greenish color, or particles of the salt may be found adhering to it. TARTAR EMETIC. This preparation of antimony may prove fatal when administered in a single large dose or in repeated small doses. The post-mortem lesions are not constant. In cases of chronic poisoning there are usually no appreciable lesions. In cases of acute poisoning there may be evidence of acute in- flammation of the w@sophagus, stomach, intestines, and perito- neum. Sometimes the stomach exhibits no lesions, while the intes- tine is involved. The larynx and lungs may be deeply congested. VEGETABLE IRRITANTS. Aloes, colocynth, gamboge, jalap, scammony, savin, croton oil, colchicum, veratria, hellebore, elatertum, and turpentine. All these drugs may produce poisonous effects. The post-mortem lesions are congestion, inflammation, and sometimes ulceration of the gastro-intestinal mucous membrane ; but these lesions are some- times present and sometimes absent. 4 Digitized by Microsoft® 822 DEATH FROM POISONING. CANTHARIDES. This substance may be given in powder or tincture. The entire length or only a portion of the alimentary canal may be congested or inflamed. There may be patches of gangrene of the mucous membrane of the stomach. When the poison-was taken in sub- stance a microscopical examination of the contents of the alimentary canal or of the mucous membrane may reveal the glistening green and gold particles of the fly. The kidneys, ureters, and bladder may be congested and in- flamed. There is sometimes congestion of the brain and its mem- branes. OPIUM. The post-mortem appearances in persons who have died from ‘opium poisoning are inconstant and not characteristic. Congestion of the brain and its membranes, with serous effusion in the mem- branes and ventricles, and congestion of the lungs, are changes oc- easionally seen, but they are frequently entirely absent, and when present are not characteristic of death from this poison. POISONOUS FUNGI. The action of these substances varies greatly, and the post-mor. tem appearances are inconstant and not characteristic. In general, when any lesions are present, they are those of gastro-intestinal irri- tation or of venous congestion, or both. Microscopical examination may reveal characteristic fragments of fungi in the contents of the alimentary canal. HYDROCYANIC ACID. This poison in fatal doses may destroy life in a very short time. ‘The post-mortem appearances are inconstant and not characteristic. The skin may be livid and the muscles contracted. The stomach may be congested or normal. The most frequent internal appear- ances are those of general venous congestion. Under favorable con- ditions the odor of prussic acid may be detected in the stomach or blood or brain, or other parts of the body. It may be absent in the stomach and present in other parts of the body. If the patient have lived for some time the odor may be absent altogether. Cyanide of potassium may produce the same lesions as prussic acid, and there is the same inconstancy in their occurrence. Nitrobenzole.—This substance soo nce general venous conges- Digitized by Microsoft® DEATH FROM POISONING. 823 tion, and the odor of the oil of bitter almonds may be more or less well marked in the body after death. CARBOLIC ACID. When this poison is taken into the stomach the mucous mem- brane of the mouth, esophagus, and stomach may be white, cor- rugated, and partially detached in patches, and the edges of the affected parts may be hypereemic or there may be patches of extra- vasation. Brownish, shrunken patches may be present about the mouth. The brain and meninges may be congested. There may be congestion and oedema of the Jungs, and congestion of the liver and spleen. The blood is usually dark and fluid. The urine is usually of a dark or greenish color. The odor of the poison may be evident in the body and in the urine. ALCOHOL. The different preparations of alcohol, when taken in concentrated form or in large quantities, sometimes produce sudden coma and death in from half an hour to several hours. In acute poisoning, if death have followed soon after the ingestion of the poison, the body may resist decomposition for an unusual length of time. The stomach and tissues may even have a more or less well-marked alcoholic odor. The stomach, and even the esophagus and duodenum, may be of a deep-red color. There may be punctiform ecchymoses in the gastric mucous membrane. In many cases the stomach is apparently quite normal. There is apt to be venous congestionin some of the internal organs, but this is not constant. There is frequently congestion and sometimes extravasation of blood in the brain and its membranes, and cedema of the membranes or of the brain substance, or both. There may be a serous effusion in the ventricles of the brain. The bladder is frequently distended with urine, as in other cases in which death is preceded by a period of unconsciousness. Chronic alcohol poisoning is of a different nature. The subjects of it may die from some other disease, or they die after a debauch without anything else to account for their death. In the latter case there may be delirium tremens, or the patient dies exhausted and comatose. Chronicalcoholism is not infrequently mistaken clinically for meningitis. The post-mortem lesions are sometimes marked, sometimes absent. Theremay be chronic pachymeningitis, resulting in thickening of the dura mater and its close adherence to the skull, The pra mater may be thickened and cedematous. The brain may be normal or cedematous or atrophied. The lungs are frequently Digitized by Microsoft® 824 DEATH FROM POISONING. congested. The heart may be thickly covered with fat, and its walls may be flabby and fatty. The stomach frequently presents the lesions of chronic gastritis. The liver may be cirrhotic, with or with- out fatty infiltration. The kidneys may present the lesions of paren- chymatous or fatty degeneration or of chronic diffuse nephritis. It should always be remembered, however, that all or a part of the above lesions may be absent in the bodies of drunkards, and, furthermore, that the same lesions may be due to other causes. CHLOROFORM. Chloroform may cause death when it is taken in fluid form into the stomach or when inhaled. Death from swallowing liquid chlo- roform is rare, and its immediate cause is usually uncertain. The post-mortem changes are variable ; sometimes there are no lesions. In some cases there is simple reddening of the gastric mucous mem- brane ; occasionally there is acute gastritis or ulceration of the mu- cous membrane. The odor of chloroform may or may not be evi- dent. Discoloration and softening of the mucous membrane of the pharynx, cesophagus, and duodenum have been observed. There may be general venous congestion ; the heart may be flabby. Bub- bles of gas have been frequently seen in the blood, but this is not characteristic. Death from inhalation of chloroform is a not infre- quent accident in surgical practice. After death from inhalation the results of the examination are usually quite negative. ETHER. The inhalation of ether occasionally causes death. The post- mortem examination is negative. The ingestion of fluid ether may induce inflammation of the stomach. The odor of ether may be per- ceptible if the autopsy is made soon after death. CHLORAL HYDRATE. There are no characteristic post-mortem appearances after death by chloral. Hyperzemia of the brain, and the odor of the drug, have been noticed. STRYCHNIA—NUX VOMICA. The post-mortem appearances after poisoning by these drugs are not characteristic and are inconstant. The body is usually relaxed at the time of death, but the rigor mortis usually comes on early and remains long. There may be congestion of the brain and spinal cord, and sometimes of thekurgs apsdstamach. DEATH FROM POISONING. 825 CONIUM, ACONITE, LOBELIA INFLATA, DIGITALIS, STRAMONIUM. These vegetable poisons are administered in their natural form of leaves, berries, and roots, or in tinctures, infusions, and extracts, or in the form of their active alkaloid principles. If the leaves, berries, or seeds are given they may be detected in the contents of the stomach by microscopical examination. Other- wise the results of autopsies are not characteristic. The brain and its membranes, and the lungs, may be congested. The stomach may present patches of congestion, inflammation, and extravasation, or its entire mucous coat may be inflamed, or it may appear normal. Microscopical examination of the contents of the alimentary canal may reveal characteristic seeds or fragments of leaves.’ PTOMAINES AND OTHER PUTREFACTIVE PRODUCTS. The effects upon the tissues of various forms of bacterial poisons have been considered in the section on Infectious Diseases and else- where. Too little is as yet known of the chemistry of these toxic products to render their systematic consideration at all satisfactory. But it seems likely that these products may have medico-legal bear- ings which will in the future make their consideration of importance in certain cases of death from obscure causes.’ CARBONIC OXIDE. This is one of the gases formed in the burning of charcoal, and forms one of the ingredients of illuminating gas. The most charac- teristic post-mortem appearance is the cherry-red color of the blood, and of the tissues and viscera which contain blood. The presence of carbonic acid in the gas may obscure the bright red of the carbonic oxide by the dark color which it induces in the blood. CARBONIC ACID. The lesions are essentially those of asphyxia, but the brain is said 1 Consult Guy and Ferrier, “ Principles of Forensic Medicine, ” 7th ed., 1895. ° For certain chemical aspects of this newly opened field in toxicology consult Vaughan in Hamilton’s “System of Legal Medicine, ” vol. i., p. 475, and Vaughaz and Novy, “ Ptomaines and Leucomaines, ” 3d ed., 1896. Digitized by Microsoft® 826 DEATH FROM POISONING. to be more frequently congested than in asphyxia by simple obstruc- tion of respiration. For a more detailed consideration of poisons, their effects, modes of detection, etc., consult Taylor on Poisons ; Muschka’s “ Handbuch der gerichtlichen Medicin, ” Bd. ii. ; Woedman and Tidy, “Foreusic Medicine.” Wormley’s “ Micro-chemistry of Poisons” contains a series of good plates of the microscopical appearance of vari- ous forms of crystals of poisonous substances. Lesser’s “ Atlas der gerichtlichen Medicin” contains a series of fine colored plates showing the appearance of the stomach after the action of various poisons. The work of Guy and Ferrier on “Forensic Medicine, ” 7th ed. revised by Smith, con- tains in very compact and reliable form much information on the general subjects treated in the foregoing section. Digitized by Microsoft® INDEX. Abbot, bacteriology, ref., 182 and Ghiriskey, diphtheria in animals, ref., 253 rhinitis, membranous, ref., 538 Abel, capsulated bacillus, ref., 260 ozeena, ref., 538 Abdomen, examination of portion of, 22, 30 Achard and Phulpin, bacteria in body after death, 167 Achorion Schénleinii, 169 Acid, carbolic, poisoning, lesions of, 823 carbonic, poisoning, lesions of, 825 hydrochloric, poisoning, lesions of, 816 hydrocyanic, poisoning, lesions of, 822 nitric, poisoning, lesions of, 815 osmic, use of, in preserving tissues, 54 oxalic, poisoning, lesions of, 816 picric, use of, in decalcifying, 52 sulphuric, poisoning, lesions of, 814 tartaric, poisoning, lesions of, 816 Aconite poisoning, lesions of, 825 Acrania, 387 Acromegalia, 410 Abscess, 124 of the brain, 381 Actinomyces, 262 Actinomycosis, 262 Addison’s disease, 800 Adénie, 796 Adenoid polyp of pharynx, 544 Adenoma, 328, 330 Adrenals, examination and preservation, 32 lesions of, 644, 801 Aérobic bacteria, 148 Agar, nutrient, 160 Aguillula, 141 Ahlfeldt, placental cysts, ref., 734 Akerlund, membranous enteritis, ref., 564 Albumen fixative, 59 Alcohol, as preservative and hardening agent, 19, 52 poisoning, 823 Alexander, lymph nodules in bladder, ref., 684 Alexander, adrenals and nervous system, ref., 644 Alexins, 178 Alimentary canal, 533 Aloes poisoning, 821 Ammonia poisoning, 817 Ameeba coli, 127, 569 colitis, 569 dysenterica, 127 Amyelia, 405 Amyloid degeneration, 100 degeneration, tests for, 32, 35, 101 Amyotrophic lateral sclerosis, 396 Anemia, 69, 77 changes of blood in, 79 infantum pseudo-leukeemica, 797 of children, 797 pernicious, 792 pernicious, changes of blood in, 79, 793 Anaérobic bacteria, 148 Anencephalia, 387 Aneurism, aortic, 512 cirsoid, 509 dissecting, 515, 516 false, 515 heart, 500 miliary, of brain, 375 minute, of brain, 15 multiple, 507 Angina, membranous, 204 Angiocholitis, 617 Angioma, 324, 326 Anhydremia, 76 Anilin-gentian-violet solution, 156 Animals, infectious diseases of, 285 Anthrax, 209 bacillus of, 210 immunity, artificial, in cattle, 212 intestinalis, 577 Antitoxin, 181 ; diphtheria, 253 ‘ pneumonia, 202 streptococcus, 193 tetanus, 256 Aorta, aneurism of, 512 Digitized by Microsoft® 828 Aorta, inflammation of, 508 Aphthe, 170 Apoplexy, brain, 374 serous, 373 Appendicitis, 573 bacteria in, 575 Appendix vermiformis, tumors of, 575 Archiblast and parablast, relation of tu- mors to, 294 Arndt, peritonitis, ref., 583 Arnold, acromegalie, ref., 410 hairy polyps of pharynx, ref., 543 lymphatic tissues in liver, ref., 614 Arsenic poisoning, lesions of, 818 Arteries, atheroma of, 509 dilatation of, 509 inflammation of, 503, 509 rupture of, 514 sclerosis of, 507 stenosis of, 513 terminal character of, 74 tumors of, 516 wounds of, 514 Arteritis, 503 aneurisms of, 509 chronic, 504 obliterating, 505 tuberculous, 509 Arthritis, acute, 775 chronic, 776 deformans, 776 gouty, 777 tuberculous, 777 Arthropods, 141 Arthrogenous spores in heart, 147 Ascaris, 136, 141 Aschoff, parenchyma-cell emboli, ref., 73 Asiatic cholera, 265 Askanazy, endothelioma of kidney, ref., 680 Asphyxia, 809, 813 Atelectasis of lungs, 436 Atelomyelia, 405 Atheroma of arteries, 509 Autopsies, medico-legal, 41 method of making, 3 Babes, hydrophobia, ref., 276 Bacillus, 144 aérogenes capsulatus, 193, 261 anthracis, 210 coli communis, 198, 260 diphtheriz, 250 lepree, 230 mallei, 235 edematis maligni, 259 of bubonic plague, 239 INDEX. Bacillus of influenza, 257 of measles, 274 pneumonie (Friedlinder), 259 proteus, 193, 261 pyocyaneus, 193, 261 pyogenes, 193 pyogenes foetidus, 193 pyogenes soli, 193 rhinoscleromatis, 238 tetani, 255 tuberculosis, 213, 215 typhi abdominalis, 240, 246 Bacteria, 143 action of cold on, 148 action of heat on, 148 action of, in the body, 172, 173, 174 aérobic, 148 anaérobic, 148 blood serum as culture medium for, 162 capsules of, 146 changes in the body induced by, 172 chromogenic, 150 classification of, 153 collection of, by sterilized swab, 166, 167 colonies of, 159 cultivation of, 158 culture medium for, 159 disinfectants, action on, 149 distribution in nature, 151 Esmarch’s soil culture of, 166 examination for, at post mortems, 167 fermentations by, 150 forms of, 144 growth, forms of, 145 importance, relative, of, in disease, 175 in fluids, to stain, 154 in tissues, to stain, 156 in water, 151 light, action of, on, 11, 19 method of staining, Gram’s, 156 method of study of, 154 morphological examination of, 154 nitrifying, 150 nutrition and functions of, 148 parasites, 152 Petri plate culture of, 163 photogenic, 150 plate culture of, 163 proof of relation of, to disease, 175 protective mechanism of the body against, 171 putrefaction by, 150 relations of, to diseases, 171 role of, in nature, 149 Digitized by Microsoft® INDEX. Bacteria, safeguards of the body against, 171 saprophytic, 152 solid media for cultivation of, 159 spore staining in, 155 spores of, 147 staining of, 154 thermophyliic, 148 various forms of, 152 varieties in, 147 zymogenic, 150 Bacterial emboli, 172 inoculations of animals, 166 Bacterio-protein, 173 Bailey and Ewing, Landry’s paralysis, 400 Bailey’s knife fer division of spinal cord, 12 Balanitis, 743 Balantidium coli, 129 Barker, malaria, ref., 283 Flexner and, meningitis, ref., 200 Baumgarten, ‘‘ Jabresbericht,”’ ref., 182, 226 Basedow’s disease, 643 Beck, influenza bacillus, ref., 258 Beebe, Park and, diphtheria, ref., 252 Benecke, 73 Bergeron, stomatite ulcerosa, ref., 534 Berkley, nerve lesions, ref., 377 Berry, appendicitis, ref., 575 Berthenson, heart tumors, ref., 502 Biedl and Kraus, bacteria eliminated from the body, 178 . Biggs, Park, and Beebe, diphtheria, bacteri- ological diagnosis in, ref., 254 Biliary calculi, 619 passages, inflammations of, 617 Birch-Hirschfeld, epithelioma of pleura, ref., 426 Bladder, urinary, bacteria in, 685 calculi, 687 ‘ dilatation of, 681 displacements of, 681 diverticula of, 682 hemorrbage of, 683 hernie of, 682 hyperemia of, 683 inflammation of, 683, 685 lesions of, 680 malformations, 680 parasites of, 687 perforation of, 682 rupture of, 687 Blood, air in, 90 alkaline changes in, 76 anemia, pernicious, 792 chlorosis, 791 829 Blood composition, alterations of, 791 changes in, after extravasation, 71 changes in circulation of, 69 changes in structure of, 77 circulation of, changes of, in inflamma- tion, 111 clots in heart, 27 coagulability, changes in, 76 coagulation of, in body after death, 10 composition of, changes in, 76 distribution of, in body after death, 10 examination, morphological, 86, 87 extravasation of, 69, 70 fat in, method of staining, 89 foreign bodies in, 89 leukemia, 794 plethora, 77 Blood cells, diapedesis of, in inflamma- tion, 112 red, changes in, 77 red, nucleated, 81 red, regeneration of, 95 white, changes in, 82 white, forms of, 82 white, regeneration of, 95 Blood serum, as culture medium, 162 immunization, 181 Blood, staining methods, 88 Blood vessels, atrophy of, 502 brain, preservation of, 19 calcification of, 503 degeneration of, 503 formation of new, 121 hypertrophy, 502 inflammation of, 503 volume of, increase of, 77 Bone, abscess, 761 atrophy, 771 caries, 766 dislocations, 754 fractures, 754 hemorrhage, 754 healing of fractures of, 125 hyperemia, 754 inflammation, 755 necrosis, 765 parasites, 774 tumors, 771 wounds, 754 Bone marrow, alterations of, in anseemia,770 alterations of in leukemia, 770 Bolton, Bacillus pyogenes soli, ref., 193 Bordont-Uffreduzzi, cultivation of lepra bacillus, 230 Bothriocephalus, 135 Brain, abscess, 381 Digitized by Microsoft® 830 Brain, anemia of, 373 atrophy of, 378 axis, method of separation of, 17 changes in toxemia, 376 cystsin, 380, 387 degeneration of, 371 dura mater, 347 embolism, 370 hemorrhage in, 379 hernia of, 388 holes in, 380 hyperemia of, 373 hypertrophy of, 378 inflammation of, 380, 382 inflammation in new-born, 383 inflammation, syphilitic, 384 inflammation, tuberculous, 384 malformations of, 387 Meynert’s method of dissection, 15 oedema of, 373 parasites in, 387 paresis, lesions of, in, 385 pia mater, 352 pigmentation, 86 post-mortem examination and preser- vation of, 11, 18, 15, 17, 18 sand, 368 sclerosis of, 382 secondary degeneration of, 377 softening, 381 thrombosis, 370 tumors of, 386 ventricles, 365 weight of, 12 wounds of, 379 Bramann, cysts of mesentery, ref., 589 Brannan and Cheesman, typhus fever, ref., 275 Brens, cysts of myomata, ref., 712 Bright's disease, acute, 650, 655 chronic, 659, 660, 668 Brigidi and Piccoli, persistent thymus, ref., 643, 796 Brockway, specimen of trichocephalis dis- par, 138 Bronchi, examination and preservation of, 28, 29 inflammation of, 426 tumors of, 431 Bronchiectasia, 429 Bronchiolitis exudativa, 429 Bronchitis, croupous, 429 acute catarrhal, 426 chronic catarrhal, 428 Broncho-pneumonia, 443 Broth, nutrient, 161 INDEX. Brown induration, 449 Bruises, post-mortem, appearance of, 8 Buboes, 524 Bubonic plague, 239 Bulbar paralysis, 396 Burning, death from, 807 Butler, membranous enteritis, ref., 564 Byron, cultivation of lepra bacillus, 230 Cadaveric lividity, 5 Ceecum, 573 Calcareous degeneration, 105 Calcification, 105 Calculi, biliary, 619 renal, 677 urinary, 687 Calvarium, method of opening of, 10 Campbell, pharyngo-mycosis, ref., 284 Cancer of brain, 351 Canon, bacteria in sepsis, ref., 197 Pfeifer, Kitasato and, influenza bacillus, ref., 257 and FPielicke, bacillus of measles, ref., 274 Cantharides poisoning, 822 Capillaries, blood, 520 Capillary bronchitis, 443 Capsules, suprarenal, 32 Carbonic oxide poisoning , 825 Carbuncle, 209 Carcinoma, 331 alveolar, 342 cells, 334 colloid, 341 epithelial pearls in, 340 forms of, 336 genesis of, 328, 333 metastasis in, 334 myomatous, 343 relation of sporozoa to, 129 Caries, 766 Carnoy’s fluid, 50 Caspar, description of foetus, 42 Catarrhal fever, 257 inflammation, 114 Cell division, 92 nucleus, changesin, during division, 92 Cells, epithelioid, in granulation tissue, 122 new, in inflammation, 109 pus, 117 Celloidin as embedding agent, 56 Cephalocele, 388 Cercomonas intestinalis, 129 Cerebro-spinal meningitis, bacteria in, 200 Cestoda, 131 Chancre, 233 Digitized by Microsoft® INDEX. Charbon, 209 Charcot’s crystals, 85 Chemotaxis, 149, 175 Cheesman and Brannan, typhus fever, ret. 275 Cheesy degeneration, 97 Chest serum as cultivating medium for bacteria, 162 Chiari, infarction of uterus, ref., 708 Chloral hydrate poisoning, 824 Chloroform poisoning, 824 Chloroma, 312 Chlorosis, 791 Cholecystitis, 617 Cholera, Asiatic, 265 Cholesteatoma, 315 Chondroma, 317 Choroid plexus, lesions of, 14, 365 Chromic and acetic acid mixture of Flem- ming, 64 Chromosomes, 93 Cicatrices, post-mortem appearance of, 9 Cicatrix, formation of, 123 Circulation, changes in, 69 Cirrhosis, hypertrophic, of liver, 605 of kidney, 668 of liver, 604 Clostridium forms of bacteria, 144 Clots of heart, pre-examination of, 27 Cloudy swelling, 98 Coagulation necrosis, 96 of blood in heart, 27 Cobbold, entozoa of man, 142 Cocci, 144 Coccidium oviforme, 128 Colchicum poisoning, 821 Colitis, amcebic, 569 bacteria in, 572 catarrhal, acute, 563 chronic, 573 croupous, 567 follicular, 568 membranous, 564 necrotic, 572 Colloid degeneration, 103 carcinoma, 341 Colocynth poisoning, 821 Colon bacillus, 260 Comma bacillus, 266 Commensals, bacterial, 152 Concurrent infection in tuberculosis, 224 Condyloma, syphilitic, 233 Congestion in inflammation, 108 Cohnheim, theory of origin of tumors, 290, 332 on infarction, 74 831 Conium poisoning, 825 Contagious diseases, 187 Contusions, post-mortem appearance of, 7 Cooling, post-mortem rate of, 6 Copper, poisoning by, 821 Cornil, myelocytes, 85 Corpora aliena articulorum, 779 amylacea, 101 Corrosive sublimate fixative agent, 55 sublimate poisoning, 821 Councilman, sudden death from heart, ref., 487 and Lafleur, on amcebic dysentery, 182 Courty, hymen, lesions of, 692 Cowper’s glands, 753 Cramer, sunstroke, ref., 806 Craniotabes, 768 Croton oil poisoning, 821 Cryptogenetic pyzemia, 197 Cryptorchismus, 745 Cultivation of bacteria, 158 Cullen, rapid method of hardening, 51 Cyclopia, 387 Cylindroma, 316 Cystitis, 683 Cysts, 295 ciliated, 297 method of preserving, 64 Darling, Bacillus coli communis, ref., 260 David, bacteria of mouth, ref., 538 Death, causes of, 3. ; Decalcification of bone, 51 Decidua, remains of, in uterus, 718 Deciduoma malignum, 717 Deck plugs, for mounting specimens in celloidin, 57 Decomposition, post-mortem, 495 Defensive proteids, 178 Degeneration, acute, 98 amyloid, 100 calcareous, 105 cheesy, 97, 219 coagulation necrosis, 96 colloid, 103 fatty, 98 forms of, 96 glycogen, 102 granular, 98 gray, of nervous system, 396 hyalin, 104 inflammatory, 107 mucous, 102 parenchymatous, 98 secondary, of spinal cord, 393 Degeneration, waxy, 100 Digitized by Microsoft® 832 Delafield’s heematoxylin, 60 Demonstration specimens, and preserva- tion of, 63 Dentrites, 393 Diabetes mellitus, 804 Diapedesis, 70, 112 Diastematomyelia, 405 Digitalis poisoning, 825 Dinwiddie, veterinary microbiology, ref., 285 Diphtheria, 250 antitoxin of, 181, 250, 253 heart lesions in, ref., 250 pseudo, 204 toxin, 253 Diphtheroid-angina, 204 Diplobacillus, 146 pheumonie, 193 Diplococcus, 145 intracellularis meningitidis, 200 lanceolatus, 200, 201, 438 pneumonie, 438 Diplomyelia, 405 Discoloration, post-mortem, 5 Distoma, 130 Dittel, urethral strictures, ref., 689 Dmochowski and Janowski, adenoma of liver, ref., 612 pyogenic powers of typhoid bacillus, ref., 247 Dobrowolski, lymph nodules, ref., 540 Dochmius duodenalis, 137 Dock, chloroma, ref., 312 trichomonas, 130 Dowd, pyogenic bacteria in New York, ref,, 192 Dropsy, 71 Drowning, 811 Dunbar, Asiatic cholera, ref., 268 typhoid fever, ref., 249 Dunin, fragmentation of heart muscle, ref., 493 Duodenum, removal, examination, and preservation of, 35 ulcers of, 562 Dura mater, 347 examination and preservation of, 11,18 heemorrhage, 347 inflammation, 348 thrombosis, 348 tumors, 351 Dust, anthrax bacilli in, 309 bacilli in, inducing tuberculosis, 223 pyogenic bacteria in, 190 Ear, internal, pre-examination of, 18 INDEX. Echinococcus, 132, 134 multilocularis of liver, 615 of liver, 614 Ecchondroses, 318 Ecchymoses, 8, 70 Edebohls, hepatic abscess, ref., 602 Edel, diverticula, false, intestines, ref., 577 Eden, placental structure, ref., 733 Edmunds, Basedow’s disease, ref., 643 Ehrlich, change in red blood cells, ref., 81 and Birch-Hirschfeld, ansemia, ref., 77 Ebrlich’s method of fixing blood, 88 Elaterium poisoning, 824 Electricity, death from, 808 Ely, diverticula of bladder, ref., 681 Embedding in celloidin, 56 in paraffin, 58 Emboli, 73 fat, 89 parenchyma cell, 73 Embolism, 73 Embryo, human, size of, at various pe- riods, 42 Emigration in inflammation, 109, 111 Empyema, 421 Encephalitis, 380 chronic, 382 in new-born, 383 Encephalocele, 388 Encephaloid cancer, 341 Endogenous spores in bacteria, 147 Endocarditis, acute, 494 chronic, 496 malignant, 494 mycotic, 494 tuberculous, 498 ulcerative, 494, 498 Endocardium, fatty degeneration of, 491 post-mortem appearance of, 27 staining process of, 27 Endometritis, acute, 704 chronic, 705 croupous, 706 syphilitic. 707 tuberculous, 706 Endothelioma, 312 Enteroliths, 577 Enzymes, bacterial, 150 Eosin, use of, in tissue staining, 61 Eosinophile cells, 82 Ependyma, 365 inflammation of, 365 preservation of, 18 tumors of, 368 Ependymitis, 365 Epispadias, 742 Digitized by Microsoft® INDEX. Epithelioma, 336 Epulis, 309 Erysipelas, 194 Esmarch roll culture, 166 Ether poisoning, 824 Eulenberg, Basedow’s disease, ref., 643 Ewing, Bailey and, Landry’s paralysis, ref., 400 Exophthalnic goitre, 643 Exostoses, 319 Exudates, 72 in inflammation, 110 inflammatory disposal of, 115 Eyes, post-mortem examination of, 18 Fallopian tubes, displacement and disten- tion of, 730 tubes, heemorrhage of, 731 tubes, inflammation of, 731 tubes, length of, 40 tubes, malformation of, 730 tubes, tumors of, 732 Famine fever, 269 Farcy, 235 Farner, Basedow’s disease, ref., 643 Fatty degeneration, 98 infiltration, 98 Fenomenodes, placental cysts, ref., 734 Ferguson, specimen of filaria, 140 Fibrin, formation of, in inflammation, 114 Fibroblasts, 122 Fibroma, 299 Fibrosis, 125 Filaria, 140 Finkler, pneumonia, vef., 257 Fission fungi, 143 Fistula, vesico-vaginal, 696 Fistulee, recto-vaginal, 696 Fitz, pancreas lesions, ref., 634 Fixative, albumen, 59 Flemming’s chromic and acetic acid mix- ture, 64 osmic acid mixture, 54 Flexner, action of toxalbumins, ref., 173 Bacillus pyogenes filiformis, ref., 193 bacteriological examination at autop- sies, ref., 148 . lympho-sarcoma, ref., 796 neuro-epithelioma, ref., 340 terminal infections, ref., 185 typhoid bacilli, ref., 247 and Barker, meningitis, ref., 200 Welch and, Bacillus aérogenes capsu- latus, ref., 261 Welch and, effects of diphtheria ba- cilli in animals, ref., 253 53 833 Feetal tissues, preservation of, 49 Feetus, size of human, at various periods, 42 Foote, oysters and typhoid, ref., 249 Formad, colon, large, ref., 558 Formalin as preservative and hardening agent, 19, 54 Fractures, healing of, 125 post-mortem marks of, 9 Fraenkel, endothelioma of pleura, ref., 426 hydatid moles, ref., 735 pneumococcus of, 201 Freeborn, formula for picric acid fuchsin, 62 ovarian papillomata, ref., 728 Freeman, milk and typhoid fever, ref., 249 Freudweiler, phlebitis, ref., 519 Friedlander’s pneumococcus, 259 Friedreich, muscle atrophy, ref., 786 Frog, exudative inflammation in, 110 Frozen sections, 51 Fuchsin, picro-acid, 61 Fungi, poisonous, 822 Gage’s hematoxylin, 61 Gall bladder, lesions of, 617 tumors of, 620 Gall ducts, inflammation of, 617 tumors of, 620 Gamboge poisoning, 821 Ganglion cells, changes of, in toxeemia, 376 Gangrene, hospital, of vulva, 693 Gastritis, catarrhal, acute, 547 catarrhal, chronic, 547 croupous, 549 phlegmonous, 549 suppurative, 549 toxic, 550 Gelatin, nutrient, 159 Generative organs, female, 39, 692 organs, male, 38, 741 Genito-urinary organs, post-mortem ex- amination of, 38 Germs, 143 Ghriskey, Abbott and, diphtheria in animals, ref., 253 Giant cells, 92, 218 Gigantoblasts, 82 Gill clefts, persistent, 538 Glanders, 235 Glands, agminated, of intestine, 561 Glazier, trichina, ref., 142 Glioma, 320 Gliomyxoma, 321 Glio-sarcoma, 321 Digitized by Microsoft® 834 Glomerulo-nephritis, 650, 655, 669 Glossitis, 537 Gluge’s corpuscles, 372 Glycogen degeneration, 102 Goitre, 639 exophthalmic, 643 Golden coccus, 189 Goldscheider, puerperal fever, bacteria in, ref., 197 Golgi, silver stain, 62 hydrophobia, ref., 276 Gonococcus, 206, 207 bacterial associates of, 208 Gonorrheea, 206 Gout, 802 Graham, displacements of liver, ref., 591 Gram’s method of staining bacteria, 156 method of staining bacteria, Weigert’s modification of, 157 Granulation tissue, 121, 124 Granulomata, 397 Graves’ disease, 643 Grawitz, lung infarctions, ref., 434 Gregaring, 128 Gross, tumors of male mamma, ref., 753 Guarnieri, agar for pneumococcus, 201 Guinea-worm, 140 Gumma, 233 Hemangioma, 326 Heematocele, 746 uterine, 703 Heematogenesis, defective, 78 Heematoidin, 78 Hematolysis, excessive, 78 Hematoma, 70 Hematomyelia, 391 Heematomyelopore, 391 Hematophilia, 799 Heematoxylin, Delafield’s, 60 Gage’s, 61 Heidenhain’s iron of, 61 Heematozoon of malaria, 280 Hemoglobineemia, 77 Hemorrhage by diapedesis, 70 by rhexis, 69 Hemorrhagic diathesis, 799 infarction, 70 infections, 799 Hemosiderin, 78 Hahn, cysts of mesentery, ref., 589 Halliburton, chemical physiology, ref., 174 Hanging, 8, 810 Hansemann, diverticula, false, of intestine, ref., 577 Hardening of tissues, 52 INDEX. Hayem’s method of fixing blood, 88 solution in blood examination, 87 Head, method of post-mortem examina- tion of, 10 Healing, first and second intention, 128 of wounds, 120 regeneration of tissue in, 94 Heart, abnormal size of, 485 aneurism of, 500 atrophy of, 487 changes in position of, 485 clots in, 27 degeneration of, 490 dilatation of, 489 examination of, 25, 26, 28 fat tissue of, atrophy of, 492 fatty, 490, 492 fragmentation of muscle of, 493 hyperplasia of, fibrous, 500 hypertrophy of, 487 inflammation of, 494 lipomatosis of, 492 malformations of, 483 malpositions of, 485 ‘parasites in, 502 rupture of, 486 softening of, 493 thrombosis of, 501 tumors of, 502 valves, lesions of, 500 valves, test for sufficiency of, 26 vegetations, 494, 497 weight of, 27 wounds of, 486 Heidenhain’s iron hematoxylin, 61 Heiman, chest serum, 162 study of gonococcus, ref., 207 Hellebore poisoning, 821 Hepatic artery, lesions of, 593 veins, 598 Hepatitis, acute, 601 chronic, 604 syphilitic, 608 tuberculous, 609 Heppner, hermaphroditism, ref., 742 Hermaphroditism, 742 Hernia intestino-vaginalis, 696 uterine, 702 vesico-vaginalis, 695 Hess, cysts, ciliated, ref., 297 Heterotopia, 406 false, 407 Hewetson, Thayer and, malaria, ref, 283 Hintze and Lubarsch, elimination of bac- teria from body, 178 Hodenpyl, actinomycosis of lung, ref., 263 Digitized by Microsoft® INDEX. Hodenpyl, on appendicitis, ref., 575 rapid method of hardening, 51 tonsils, faucial, ref., 540 Prudden and, action of dead tubercle bacilli, 222 Hodgkin’s disease, 796 Hoffman, hermaphroditism, ref., 742 Hofmeier, placenta, ref., 734 Horseshoe kidney, 646 Hospital fever, 275 Foul, heemorrhagic infections, 799 Hueppe on bacteriology, ref., 182 Huetes, intestinal tumors, ref., 577 Hun and Prudden, myxcedema, ref., 642 Hyalin degeneration, 104 thrombi, 72 Hydatid moles, 304, 735 Hydreemia, 77 Hydrencephalocele, 388 Hydrocele, 745 Hydrocephalus, 362, 367, 388 Hydromeningocele, 388 Hydromyelia, 405 Hydronephrosis, 674 Hydrophobia, 276 Hydrothorax, 417 Hydrorrhachis interna, 405, 406 Hymen, 692 Hypereemia, 69 Hyperplasia, 91 ‘replacement, fibrous, 125 Hypertrophy, 91 Hyphomycetes, 143 Hypoleucocytosis, 83, 84 Hypophysis cerebri, 369 Hypospadia, 741 Hypostasis, post-mortem, 5 Identification, post-mortem features to be noticed in, 4 Il/, echinococcus of liver, ref., 615 Immunity, 177 | artificial, 178, 179, 180 forms of, 178 Infarction, hemorrhagic, 70, 74 Infarctions of lungs, 433 Infection, 183 and immunity, 177 concurrent, 184 congenital, 185 mixed, 184 terminal, 185 Infectious disease, 183 disease, communicability of, 185 disease, conditions influencing occur- rence of, 176 835 Infectious disease, definition of, 177 disease, nature of, 183 disease, non-communicable, 186 disease, predisposition to, 176 disease, hypoleucocytosis in, 83 disease of animals, 285 disease produced by the pyogenic bac- teria, 188 inflammation, pseudo-membranous, 204 Infiltration, fatty, 98 ‘ Inflammation, 107 catarrhal, 114 congestion in, 108 croupous, 119 degeneration in, 107 diphtheritic, 120 emigration in, 109, 111 exudative, 110 exudative fibrinous, 114 exudative, hemorrhagic, 114 exudative, mucous, 114 exudative, purulent, 114 exudative, serous, 114 forms of, 110 interstitial, 118 necrotic, 107, 119 productive, 117 productive, reparative, 120 pseudo-membranous, of mucous mem- branes, 204 reparative, 120 suppurative, 188 syphilitic, 232 transudation in, 109 tuberculous, 215, 216, 220 Influenza, 257 Infusoria, 129 Inoculation, protective, 181 Insolation, 806 Intestinal mycosis, 210 Intestine, large, inflammation, 563 small, emboli, 562 small, inflammation, 561 small, lesions of lymph nodules, 561 Intestines, appearance of, at autopsies, 34 atresia of, 558 concretions in, 577 diverticula of, 557, 577 examination and preservation of, 36 examination, post-mortem, of, 23, 30, 34 incarcerations of, 558 intussusception, 559 malformations of, 557 parasites in, 578 post-mortem changes in, 34 Digitized by Microsoft® 836 Intestines, preservation of, 35 rupture of, 560 transposition, 560 tumors of, 575 waxy degeneration of, test for, 35 wounds of, 560 Intoxication by bacterial products, 174 involution forms of bacteria, 144 Iodin as test for amyloid in fresh tissue, 32 solution in Gram’s stain, 157 use of, in removal of sublimate from tissues, 55 Itch insect, 141 Jiger, acute yellow atrophy of liver, ref., 601 meningitis, ref., 200 Jail fever, 275 Jakowski, pyocyaneus, ref., 261 Jalap poisoning, 821 Janeway, E. G., foreign body in portal vein, 594 Janeway, T. C., reaction of culture media for pneumococcus, 202 Janowski, inflammatory suppuration, bac- teria in, ref., 192 Joints, inflammatory, 775 loose bodies in, 779 tumors of, 778 Jordan, osteomyelitis, ref., 765 Jores, formula for gross specimen preser- vation, 63 Jiirgenson, air in the blood, ref., 90 Justi, tumors of heart, ref., 502 Karyokinesis, 93 asymmetrical, ref., 93 Karyomitosis, 93 Kelynack, appendicitis, ref., 575 Kidney, abscess, 671 arterio-sclerotic, 668 bacteria in, 671, 672 Bright's disease of, 647 calculi of, 677 cirrhosis of, 668 congestion, acute, 647 congestion, chronic, 658 cysts of, 675 degeneration, acute, 648 degeneration, chronic, 659 degeneration, granular, 668 degeneration, parenchymatous, 648 degeneration, waxy, tests for, 32 displacements of, 646 embolism of, 673 INDEX. Kidney, examination of, 31, 32 fatty, 659 hydronephrosis, 674 inflammation of, 650 malformations, 646 parasites of, 680 perinephritis, 676 surgical, 672 thrombosis, 673 tumors of, 677 waxy, 660 Kinnicutt, Graves’ disease, ref., 643 Kitasato, Pfeiffer, Canon and, influenza ba- cillus, ref., 257 Klebs, cysts of ovaries, ref., 727 malformations of genital organs, ref., 742 Klemperer, pneumonia antitoxin, ref., 202 Koch’s culture media, solid, 159 discovery of tubercle bacillus, ref., 226 report on Asiatic cholera, ref., 268 Koplik and Van Arsdale, osteomyelitis, ref., 765 Kossel, Bacillus pyocyaneus, ref., 261 Kotlar, heart thrombus, ref., 502 Kraus, Biedl and, bacteria, elimination of, from body, 178 Kruse and Pasquale, intestinal microbes, ref., 573 liver, micro-organisms in abscess of, ref., 603 Kiichenmeister and Ziirn, parasites, 142 La grippe, 257 Landry’s paralysis, Bailey and Ewing, ref., 400 Lang, chloroma, ref., 312 Lang’s solution, 55 Langerhans, fat necrosis, ref., 634 Laryngitis, 413 : Larynx, examination and preservation of, 29 inflammation, 413 malformations, 413 tumors of, 416 Lead poisoning, 820 Legry, lung stones, ref., 423 Leiomyoma, 321 Lepra, 229 bacillus, 230 Leprosy, 229 Leptothrix, 145, 146, 284 Leptomeningitis, 354 Leuckart, parasites, 142 Leucocytes, changes in, 82 degeneration of, in blood, 86 Digitized by Microsoft® INDEX. Leucocytes, emigration of, in inflamma- tion, 112 fate of, in inflammatory exudates, 116 formation, of, 95 forms of, 82 Leucocythemia, 794 Leucocytosis, form of, 83 in infectious disease, 83 Leukemia, 794 changes in blood cells in, 85 pseudo-, 796 Lewin and Heller, scleroderma, ref., 410 Lipzmia, 89 Lipoma, 317 Lividities, post-mortem, 5 Liver, abscess of, 601 abscess, micro-organism in, 602 amyloid, 597 amyloid, tests for, 37 anemia, 591 atrophy of, 595 atrophy, acute yellow, 600 - bronze, 599 cirrhosis of, 604 congestion of, 591 cysts of, 612-614 degenerations of, 598 discoloration, post-mortem of, 37 examination and preservation of, 36 examination, post-mortem, 23 fatty, 596 hemorrhage of, 593 holes in, 614 hyperemia, 591 inflammation of, 601 lymphatic tissue, hyperplasia of, 611 malformations of, 590 nutmeg, 605 parasites of, 614 pigmentation of, 599 portal vein, lesions of, 593 position of, 36 / position of, changes in, 24, 590 preservation of, 37 regenerative powers of, 95 rupture of, 593 size and weight of, 36 tumors of, 612 veins, lesions of, 595 waxy, 597 wounds of, 593 Lobelia poisoning, 825 Lockjaw, 255 Locomotor ataxia, 402 Loffler’s alkalin-methyl-blue stain, 158 65 837: Léffler’s blood serum mixture as culture medium, 162 Loomis, gumnia of heart, ref., 502 Léwit, edema of lungs, ref., 433 Lubarsch, Addison’s disease, ref., 801 endothelioma of kidney, 680 and Hintze, elimination of bacteria from body, ref., 178 and Ostertag’s ‘‘ Ergebnisse,” etc., ref., 182 Lungs, atelectasis of, 436 congestion of, 432 emphysema of, 434 d examination and preservation of, 28, 29 gangrene of, 437 heemorrhage of, 433 hepatization of, 439 hypostatic congestion of, 433 infarctions of, 433 inflammation of, 438 inflammation, syphilitic, of, 475 inflammation, tuberculous, of, 452 injuries of, 432 malformations of, 432 cedema of, 432 organized tissues in air vesicles of, 441 parasites in, 477 perforations of, 432 phthisis, acute, 459 phthisis, chronic, 469 tuberculous, 452 tuberculous, miliary acute, 453 tuberculous, miliary chronic, 457 tuberculous, miliary subacute, 456 tumors of, 476 Lung stones, 423 Lupus, 227 Lustgarten’s bacillus, 234 Lymphangiectasis, 522 Lymphangioma, 327, 522 Lymphangitis, 521 Lymph glands, see Lymph nodes, 522 nodes, 522 nodes, degeneration in, 527, 536 nodes, hyperplasia of, 531 nodes, inflammation of, 523 nodes, inflammation of syphilitic, 529 nodes, parasites of, 532 nodes, pigmentation of, 526 nodes, scrofulous inflammation of, 528 nodes, tuberculous inflammation of, 528 nodes, tumors of, 532 nodules, intestinal, 561 nodules of larynx, cesophagus, etc., ref., 540 Digitized by Microsoft® 838 Lymph vessels, 520 vessels, inflammation of, 521 vessels, tumors of, 522 Lymphocytes, forms of, 82 Lymphocytosis, 85 Lymphoma, 531 Malarial fevers, 280 Malignant pustule, 309 Mamma, inflammation of, 735 hemorrhage of, 735 male, lesions of, 753 malformations of, 735 tumors of, 738 Manneberg, résumé of parasitic protozoa, ref., 127 Marchand, giant cells, ref., 218 hydatid moles, ref., 735 Mast cells, 85 Mastitis, 736 Mays, myositis ossificans, ref., 782 Measles, 274 Mediastinum, 477 inflammation of, 478 tumors of, 478 Megaloblasts, 79, 81 Megalocytes, 81 Melanzemia, 86 Mégnin, parasites, ref., 142 Melchior, cystitis, ref., 685 Meltzer, empyema and subphrenic abscess, ref,, 423 -Meningitis, 354 acute cellular, 355 acute exudative, 355 cerebro-spinal, 199 chronic, 358 ‘spinal, 390 ‘syphilitic, 362 tuberculous, 359 “Merismopedia, 146 Mesentery, cysts of, 588 tumors of, 589 Messmates, bacteria as, 152 Metaplasia, 95 Methyl-blue, Léffler’s alkalin formula for, 158 Metritis, 707 Meynert’s method of opening brain, 15 Microbes, safeguards of the body against, 171 Microcephalia, 388 Micrococci, 144° Microccoccus gonorrhcese, 206 tetragenus, 193, 261 Microcytes, 79 INDEX. Micron, 144 Micro-organisms, 143 safeguards of the body against, 171 Microscope, form of, for bacterial study, 158 Microsporon furfur, 170 Microtome, forms of, 60 Miliary tubercles, 216 Milk as culture medium, 161 Miller, bacteria of mouth, ref., 538 Mitosis, 93 Moeller’s method of spore staining, 155 Moles, 735 hydatid, 304 Monte and Berggrun, anemia of childhood, ref., 797 Morbus maculosus, 798 Mosselman and Liénaux, veterinary micro- biology, ref., 285 Moulds, 143, 168, 170 Mouth, bacteria in (footnote), 538 gangrene, 535 hypertrophy, 534 inflammation, 534 malformations, 533 tumors, 535 Mucous degeneration, 102 membranes, pseudo-membranous in- flammation of, 204 polyp, 303 Miller, leukeemia, ref., 796 thyroid gland, structure of, ref., 639 Miiller’s fluid as hardening and _ preser- vative agent, 19, 53 Muscle atrophy, 396, 783 degeneration of, 783 emboli, 780 hemorrhage, 780 hypertrophy, 787 hypertrophy, pseudo-, 785 inflammation, 780 parasitic, 788 regeneration, 780 rupture, 780 tumors, 787 wounds, 780 Museum specimens, preservation of, 63 Mycelium in moulds, 168 Mycosis, intestinal, 210, 577 of pharynx, 284 Myelitis, 397, 400 Myelocytes, 85 Myocarditis, 498 Myocardium, fragmentation of, 493 inflammation of, 498 Myoma, 321 Myomalacia, 493 Digitized by Microsoft® INDEX. Myositis, chronic, 781 ossificans, 781 suppurative, 780 Myxcedema, 641 Myxoma, 300 Neevi, vascular, 326 Neck, cysts of, 538 Necrosis, 96, 107 coagulation, 96, 219 fat, of pancreas, 634 foci of, caused by bacteria, 172 foci of, caused by toxins, 173 Neisser and Schiffer, gonococcus, ref., 208 Nematoda, 135 eggs of, 187 Nephritis, acute diffuse, 655 catarrhal, 650 croupous, 650, 655 desquamative, 650, 660 diffuse, 655, 660 exudative, acute, 650 glomerulo-, 650, 655 indurative, chronic, 668 interstitial, 668 parenchymatous, 648, 650, 655, 659, 660 productive, 655, 660 productive chronic, without exuda- tion, 668 suppurative, 671 tubal, 650 tuberculous, 673 Nerves, peripheral, inflammation of, 408 peripheral, degeneration and regenera- tion, 408 peripheral, tumors of, 409 Nerve fibres, method of preservation of, 22 tissue, hardening and study of, 410 Nervous system, 347 Neuritis, 408 Neuro-epithelioma, 340 Neuroglia, character of, 294, 320 Neuroma, 322 false, 323 multiple, 325 Neuron, 393 Nicolaier, capsulated bacillus, ref., 260 Nikiforoff’s method of fixing blood, 88 Nissl’s staining method, 412 Nocard and Leclainche, animal infections, ref., 285 Noma, 693, 697 Normoblasts, 79, 81 Northrup, tuberculosis in children, ref., 215 839 Northrup, Crandall and, scorbutus in chil- dren, ref., 798 Prudden and, etiology of pneumonia, ref,, 449 Novy, bacillus of malignant oedema, ref., 259 Vaughan and, ptomaines, ref., 174 Noyes, sporadic cretinism, ref., 642 Nucleus, changes in, during cell division, 92 Nuttall, Welch and, capsule bacillus, ref., 261 Nux vomica poisoning, 824 Obermeier, spirochete of, 270 Odontoma, 319 (Edema, 71 malignant bacillus of, 259 of glottis, 416 of lungs, 432 Csophagitis, 540 Csvophagus, cysts of, 542 dilatation, 541 examination of, 29 inflammation of, 540 malformations, 538 perforation, 541 rupture of, 541 stenosis of, 548 tumors, 543 Oestreich, fragmentation of heart muscle, ref., 493 Oidium albicans, 170 Oligocythemia, 77, 78 Ollivier, lesions of typhoid, ref., 246 Omentum, displacement of, 23 lesions of, 578 Oodphoritis, 720 Opium poisoning, 822 Oppenheim, brain sclerosis, ref., 383 Orchitis, 747 Orth, spleen in leukemia, ref., 771 Osler, sporadic cretinism, ref., 642 Osmic acid as hardening agent, 54, 56 Osteitis, 757 syphilitic, 762 tuberculous, 761 Osteoid tissue, 126 Osteoma, 319 Osteomalacia, 769 Osteomyelitis, 763 Osteophytes, 319 Osteosclerosis, 760 Ovaries, cysts of, 723 displacements of, 719 examination of, 40 Digitized by Microsoft® 840 Ovaries, hemorrhage, 719 hyperemia, 719 inflammation of, 720 malformations of, 719 size of, 719 tumors of, 722 Oxyuris, 186 Ozcena, bacteria in, ref., 538 Pacchionian bodies, 11, 352 Pachydermia laryngis, 414 Pachymeningitis, 348 Paget's disease, coccidia in, 129 Paltauf, endothelioma of nerves, ref., 410 Pancreas, concretions of, 635 cysts of, 635 degenerations of, 633 displacements of, 636 fat necrosis of, 634 foreign bodies in, 635 hemorrhage of, 632 inflammation of, 632 malformations of, 636 situation, removal, examination, and preservation of, 37 size and weight of, 37 tumors of, 635 Pancreatitis, 632 Paoli, endothelioma of kidney, ref., 680 Papilloma, 300 Paraftin embedding, 58 Parametritis, 707 Paraphiimosis, 743 Parasites, 127 animal, 127 animal, methods of study, 142 animal, bibliography, 142 bacterial, 152 vegetable, 143 Parenchymatous degeneration, 98 Paresis, general, of tissue, brain lesions, 385 Park, diphtheria, etc., ref., 205 chronic osteomyelitis, ref., 7 fat embolism, 90 and Beebe, diphtheria, ref., 252 Biggs and Beebe, diphtheria, bacterio- logical diagnosis in, ref., 254 Parotid gland lesions of, 637 Parovarium, cysts of, 730 Parsons, bone lesions of typhoid, ref., 246 Pearls, epithelial, in carcinoma, 336 Pediculus capitis, 141 Penis, calcification, 744 hemorrhage, 743 inflammation, 743 injury, 743 INDEX. Penis, malformation, 741 tumors, 743 Periarteritis nodosa, 507 Pericarditis, 481 tuberculous, 483 Pericardium, air in, 480 dropsy, 480 hemorrhage, 480 * inflammation of, 481 injuries, 480 obliteration of, 482 post-mortem examination of, 25 tumors of, 483 Perihepatitis, 611 Perimetritis, 707 Perinephritis, 676 Periostitis, 755 Perisplenitis, 628 Peritoneum, 578 inflammation, 579 malformations of, 578 parasites of, 589 tumors, 587 Peritonitis, acute, 579 bacteria in, 582 chronic, 583 heemorrhagic, 585 tuberculous, 586 Petechiee, 70 Petri’s plates for bacteria cultures, 163 Petruschky, bacteria in septiczemia, ref., 197 Pfeiffer, Kitasato, and Canon, influenza ba- cillus, ref., 257 Phagocytes, 178 in disposal of extravasated blood, 71 nature and action of, 126 Pharyngitis, 540 Pharyngo-mycosis, 284 Pharynx, diverticula, 540 inflammation of, 540 malformations, 538 removal from body, examination and preservation of, 29 ulceration of, 541 Phlebitis, 518 tuberculous, 519 Phleboliths, 73 Phloroglucin for decalcification, 52 Phosphorus poisoning, 817 Phthisis, pulmonary, 459 pulmonary, acute, 459 pulmonary, chronic, 469 pulmonary, experimental, 460 Pia mater, 352 hemorrhage, 354 hyperemia, 353 Digitized by Microsoft® INDEX. Pia mater, inflammation, 354 method of preservation of, 18 cedema, 353 parasites in, 364 post-mortem examination of, 11 spinalis, hemorrhage, 390 spinalis, inflammation, 390 spinalis, tumors and parasites, 391 tumors, 362 Picric acid for decalcification, 52 Picro-acid fuchsin as staining agent, 61 Pielicke, Canon and, bacillus of measles, ref., 274 Pigmentation, 106 Pineal gland, 369 Pin worm, 136 Pituitary body, 369 degeneration, 734 inflammation, 734 Placenta, lesions of, 733 Placentitis, 734 Plague, bubonic, 239 Plasmodium malarie, 129, 280 Plate cultures of bacteria, 163 Pleura, cysts of, 426 hemorrhage of, 417 hydrothorax, 417 inflammation of, 417 lymphangitis of, 423 tumors of, 425 Pleural cavities, method of post-mortein determination of presence of air in, 24 cavities, post-mortem examination of, 28 Pleurisy, 417 chronic, 423 Pleuritis, 417 acute, 418 chronic, 423 tuberculous, 424 Pneumococcus, 201, 438 capsule, to stain, 203 Pneumonatosis, 480 Pneumonia, 438 acute lobar, 201, 438 broncho-, 442 catarrhal, 443 complicating, 448 interstitial, 451 interstitial, in phthisis, 472 lobular, 443 of heart disease, 449 “ organizing,”’ 441 secondary, 448 syphilitic, 475 841 Pneumonia, tuberculous, 452 Pneumonitis, 438 Pneumotoxin, 202 Poikilocytes, 79 Poisoning, autopsies in cases of, 41 suspected, care of stomach and duode- num in, 35 Poisons, action of, in body, 814 Polaillon, lung stones, ref., 423 Poliomyelitis anterior, 399 Polyp, mucous, 303 Popon, arsenic poisoning, 819 Porencephalus, 380 Portal vein, lesions of, 593 Post-mortem bacterial examination, 167 changes, 4 changes in abdominal organs, 23 cooling of the body, 6 decomposition, 4 discolorations, 4, 5, 23, 34 examination in suspected poisoning, 35, 41 examination, internal, 9 examination, medico-legal, 41 examination, objects in, 3 examination, observations on identity in, 4 examination of abdomen, 30 examination of brain, 11 examination of new-born children, general inspection, 42 examination of new-born children, in- ternal inspection, 46 examination of spinal cord, 19 examination of thorax, 22 examination of wounds, 8 examinations, external inspection, 4 examinations, methods of making, 3 examinations, weight of the body in, 5 fractures, 9 hypostasis, 5 injuries, 8 putrefaction, 5 rigidity, or rigor mortis, 7 Potash poisoning, 817 Potassium nitrate poisoning, 817 Potatoes, as culture media for bacteria, 162 Pozzi, ovarian tumors, ref., 727 Predisposition to infectious diseases, 176 Pregnancy, extra-uterine, 732 Preservation of tissues, importance of careful, 64 of tissues, methods of, 52 Productive inflammation, 117 Progressive spinal muscle atrophy, 896 Prostate, atrophy of, 752 Digitized by Microsoft® 842 Prostate, concretion of, 753 hypertrophy of, 751 inflammation of, 752 tumors of, 753 Proteids, defensive, 178 Protozoa, 127 . Prudden, cold on bacteria, 148 endocarditis, malignant, ref., 495 rhabdomyoma, ref., 638 Psammoma, 312, 351, 363 Pseudo-diphtheria, 204 Pseudo-leukeemia, 796 Pseudo-tubercles, 222 Psorospermie, 128 Ptomaine poisoning, 825 Ptomaines, 150 Puerperal fever, 197 Pulmonary phthisis, 459 Purpura hemorrhagica, 798 Pus cells, 117 nature of, 116 Putnam, nervous system in infectious dis- eases, ref., 377 Putrefaction, post-mortem, 5 Putrefactive changes in abdominal vis- cera, 23 Pyzmia, 196 Pyelitis, suppurative, 672 Pyelo-nephritis, chronic, 672 suppurative, 672 Pye-Smith, cysts of liver, ref., 614 Pyogenic bacteria, 188 Pyo-pneumothorax, 422 Pyo-salpinx, 731 Rabies, 276 Rabinowitsch, pathogenic yeasts, ref., 168 thermophyllic bacteria, ref., 148 Rachitis, 766 Ray fungus, 263 Rectocele vaginalis, 696 Rectum, 573 Reed, lymph nodules in typhoid, ref., 245 Regeneration of tissues, 91, 94 Reinbach, colloid, ref., 640 Relapsing fever, 269 Respiratory system, 413 Rhabdomyoma, 322 Rhabdonema, 140 Rheumatism, 803 Rhexis, hemorrhage by, 69 Rhinitis, membranous, ref., 538 Rhinoscleroma, 238 Rhizopods, 127 Ribbert, appendicitis, ref., 575 carcinoma, histogenesis, ref., 291 INDEX. Ribbert, lymph glands, ref., 526 myoma, ref., 322 Ricker, yeasts and moulds, ref., 171 Rickets, 766 Rigor mortis, 7 Robinson, cysts of mesentery, ref., 589 Saccharomyces, 168 Saccharomycetes, 143 Salivary glands, 637 Salpingitis, 731 Salvetti, rachitis, ref., 767 Saphrophytes, 152 Sarcina, 146 Sarcoma, 304 adeno-, 312 alveolar, 311 angio-, 310 chondro-, 312 cysto-, 312 endothelial, 312 fibro-, 305 giant-celled, 308 glio-, 308 lipo-, 312 lympho-, 308 melano-, 308 mixed forms of, 311 myeloid, 308 myo-, 312 myxo-, 311 osteo-, 309 round-celled, 307 spindle-celled, 305 Sarcoptes, 141 Savin poisoning, 821 Scammony poisoning, 821 Scarlatina, 273 Scarlet fever, 273 Scars, post-mortem, appearance of, 9 Schamschin, heart lesions in diphtheria, ref., 250 Schmidt and Aschoff, pyelonephritis, ref., 685 Schulz, endothelioma of pleura, 426 Scirrhus, 341 Scleroderma, 410 Sclerosis, amyotrophic lateral, 396 of spinal cord, 394, 400, 402 Scolices of tapeworms, 131 Scorbutus, 798 Scrofula, 528 Scrotum, lesions of, 744 Section cutting, 56, 60 Seminal vesicles, 751 Septiceemia, 183, 196 Digitized by Microsoft® INDEX. Sestic intoxication, 174 Serum, inflammatory, 112 therapy in diphtheria, 253 Seven-day fever, 269 Shakespere, report on cholera, ref., 268 Sherrington, bacteria in secretions, ref., 178 Ship fever, 275 Silbermann, death from burning, ref., 807 Silberschmidt, peritonitis, ref., 582 Silver stain, Golgi’s, 62 Sittmann, bacterial study of blood,ref., 90 Skull-cap, method of removal of, 10 Small-pox, 271 Soda poisoning, 817 Spermatocele, 747 Spider cells, 320 Spina bifida, 407 Spinal cord, bruising of, in removal, 20 cysts of, 403 degenerations of, 393 dura mater of, lesions of, 387 examination and preservation of, 19-21 heematomyelia, 391 hematomyelopore, 391 heemorrhage, 391 inflammation, 397 injuries, 393 malformations of, 405 membranes of, 387 parasites, 390 pia mater, lesions of, 390 progressive muscle atrophy of, 396 sclerosis of, 326 syringomyelia, 404 tubercles of, 403 tumors of, 39° Spirillum, 144 cholerez Asiatica, 266 fever, 269 Spirochete Obermeieri, 270 Spleen, accessory, 34 anzemia of, 622 atrophy of, 629 bile duct, post-mortem examination of, 736 congestion of, 623 degenerations of, 629 displacements of, 631 examination and preservation of, 33 hemorrhage of, 622 hypereemia of, 622 infarctions of, 623 inflammations of, 624 malformations of, 631 parasites of, 630 843 Spleen, pigmentation of, 630 rupture of, 621 sago, 629 tumors of, 630 wounds of, 621 Splenic fever, 309 Splenitis, 624 Sporangium in moulds, 168 Sporozoa, 128 Spotted fever, 275 Sprouting fungi, 143 Sputum, tuberculous, number of bacilli in, 223 Staining, methods of, 60 Staphylococcus epidermidis albus, 190 cereus albus, 193 cereus flavus, 193 gilvus, 193 pyogenes albus, 190 pyogenes aureus, 188 pyogenes citreus, 193 salivarius pyogenes, 193 Starr, roultiple neuritis, ref., 409 Stein, bladder tumors, ref., 686 plates of cestoda, 142 Stern, tumors in childhood, ref., 343 Sternberg, discovery of pneumococcus by, 201 “Manual of Bacteria,”’ ref., 182 yellow fever studies, ref., 279 Stoeltzner, cartilage in tonsils, ref., 543 Stokes, Wright and, bacteriological exam- ination at autopsies, 168 Stomach, appearance, post-mortem, of, 24 care of, in cases of suspected poisoning, 35 degenerations of, 557 dilatation of, 553 erosions of, 553 examination and preservation of, 35 foreign bodies in, 557 hemorrhage, 546 inflammation, 547 injuries, 546 malformations, 546 post-mortem changes, 546 tumors of, 554 ulcers of, 550-553 wounds of, 546 Stomacace, 534 Stomatite ulcero-membraneuse, 534 Stomatitis, 534 Stoos, bacteria in angina, ref., 538 Stramonium poisoning, 825 Strangulation, 8, 810 “Strawberry marks,” 326 Digitized by Microsoft® 844 Streptobacillus, 146 Streptococcus, 195 antitoxin, 193 brevis, 191 conglomeratus, 191 erysipelatis, 194 in meningitis, 200 longus, 191 pyogenes, 191, 204 Stroebe, parasites in tumors, ref., 293 regeneration in nerve tissue, ref., 377 Strongylus, 136, 137 Struma, 639 lipomatosa suprarenalis, 645 Strumitis, 640 Strychnia poisoning, 824 Sublimate, corrosive, as fixative agent, 55 Sublingual gland, lesions of, 637 Submaxillary gland, lesions of, 637 Sudeck, endothelioma of kidney, ref., 680 Suffocation, 809 Suggillations, 70 Sunstroke, 806 Suprarenal bodies, 32, 644 Sutton, tumors, ref., 343 Swab, sterilized, for bacteria collection, 166, 167 Symbiosis, 152 Syphilis, 231 Syringomyelia, 404 Tabes, 402 Teenia, 131-135 echinococcus of liver, 614 Tape-worms, 131 Tartar emetic, poisoning by, 821 Tattoo marks, post-mortem appearance of, 9 Tavel, intestinal bacteria, ref., 573 and Lanz, peritonitis, ref., 582 Temperature, post-mortem, 6, 7 Teratomata, 295 Testicle, atrophy of, 745 cysts of, 751 inflammation of, 747 malformations of, 745 parasites of, 751 tumors of, 750 weight of, 38 Tetano-toxin, 256 Tetanus, 255 Thacher, melanuria, ref., 308 Thayer and Blume, bacteriain malignant endocarditis, ref., 495 and Hewetson, malaria, ref., 283 INDEX. Thierfelder, endothelioma of pleura, ref., 426 Thiersch, carcinoma, ref., 291 Thoma, nervous system malformations, ref,, 388 Thoma’s text-book, ref., 126 microtome, 60 Thompson, Addison’s disease, ref., 801 Thorax, examination of, 22, 25 Thread worm, 136 Thrombi, forms and occurrence of, 72 Thrombosis, 72 - Thrombus, organization of, 124 Thymus, 643 Thyroid gland, examination of, 29 exophthalmic goitre, 643 lesions of, 639 malformations of, 641 myxcedema of, 641 parasites of, 641 regenerative power of, 95 Tilger, cysts-of pancreas, ref., 635 Tissues, fresh, methods of study of, 50 methods of preservation, 52 Tongue, cysts of, 537 hypertrophy of, 536 inflammation of, 537 malformations of, 536 tumors of, 537 Tonsillitis, 540 Tonsils, faucial, 540 Toxemia, 174, 183 ganglion cell changes in, 376 Toxalbumins, bacterial, 151, 173 Toxins, bacterial, 150, 173 Trachea, malformations of, 413 tumors of, 416 Transudation, 71, 109, 112 Trematoda, 130 Triacid mixture of Ehrlich for blood stain- ing, 88 - Trichina spiralis, 138, 139 Trichocephalus, 137 Trichomonas vaginalis, 129 Trichophyton tonsurans, 169 Tubercle, 216 bacilli, 213 bacilli, action of, in lungs, 452 bacilli, cultivation of, 214 bacilli, dead, lesions caused by, 222 bacilli, numbers of, in tuberculous sputum, 223 bacilli, staining of, 224 granulum, 217 tissue, 217 Tubercles, coagulation necrosis in, 219 Digitized by Microsoft® INDEX. . Tubercles, conglomerate, 217 epithelioid-celled, 220 forms of, 220 lymphoid, 220 Tuberculin, 224 Tuberculosis, concurrent infection in, 224 in the lower animals, 215 localized, 215 Tuberculous inflammation, 213. 216 Tumors, archiblastic, 294 cause of, 290 classification of, 294 congenital ,295 cystic, 295 epithelial, 358 histioid, 294 hypoblastic, 294 inclusions of, 292 malignancy, nature of, 289 mesoblastic, 294 metaplasia in, 317 mixed, 295 * nature and growth of, 286, 287 nomenclature of, 294, 297 parablastic, 294 parasitic origin of, 292 preservation of, 298 special forms of, 299 spread of, 288 Turpentine poisoning, 821 Typhoid fever, 240 Typhus fever, 275 recurrens, 269 Ulrich, adrenals and adenoma of kidney, ref., 645 Ureter, examination of, 30 Ureteritis, 672 Urethra, bacteria in, 690 displacement of, 688 inflammation of, 690 malformations of, 688 perforation, 689 prolapse, 689 rupture of, 689 strictures of, 689 tumors of, 691 wounds of, 689 Urethral hemorrhoids, 691 Urethritis, 690 Urinary apparatus, 676 bladder, lesions of, 680 Uterine hematocele, 703 Uterus, cysts of, 718 degeneration of, 709 displacements of, 700 845 Uterus, examination of, 39 hyperemia of, 707 hyperplasia of mucous membrane of, 705 inflammation, 704, 707, 708 malformations of, 698 parasites of, 718 perforation of, 702 rupture of, 702 size, changes in, 699 tumors of, 709 ulceration of, 709 Vagina, displacements of, 695 gangrene of, 697 hernia of, 695 inflammation of, 697 malformations of, 695 parasites of, 698 perforations of, 697 prolapse of, 695 tumors of, 697 wounds of, 696 Variola, 271 Vascular system, 480 Vaughan and Novy, ptomaines, ref., 174 Veins, dilatation of, 517 inflammation of, 518 parasites of, 520 rupture of, 518 tumors of, 520 wounds of, 518 Vein stones, 73 Ventricles of brain, 365 Veratria poisoning, 821 Vermiform appendix, 573 Vibrio of cholera, 266 Virchow, tumors, ref., 343 Van Gieson, false heterotopia, ref., 407 hematomyelopore, 392 malformation of spinal cord, ref., 405 picro-acid fuchsin, 61 stain for amyloid hyalin, etc., 101 Volkmann, endothelioma, ref., 316 Von Hibler, gonococeus, ref., 208 Von Kahlden, Addison’s disease, 801 endothelioma of kidney, ref., 680 porencephalie, ref., 380 Von Limbeck, blood examination, 89 Vulva, hemorrhage, 692 hyperemia, 692 inflammation, 693 malformations, 692 tumors, 694 Wagner, endothelioma of pleura, ref., 426 Digitized by Microsoft® 846 Waldeyer, cysts of ovaries, ref., 727 Water, bacteria in, 151 contamination of, with bacteria, 152 Waxy degeneration, 100 Weichselbawm, cysts of mesentery, ref., 589 malignant endocarditis, ref., 495 Weigert, adenoma of esophagus, ref., 543 modification of Gram’s stain, 157 stain for nerve tissue, 411 Weihl, waxy degeneration of muscle, ex- perimental, ref., 787 Weil’s disease, 601 Welch, Bacillus coli communis, ref., 260 bacterial flora of body, ref., 171 bacteriological examination at autop- sies, ref., 168 infection and immunity, ref., 182 modification of Guarnieri’s agar for pneumococcus, 201 cedema of lungs, ref., 433 staining method for capsules of bac- teria, 203 wound infection, ref., 190 Welch and Flexner, Bacillus aérogenes cap- sulatus, ref., 261 effects of diphtheria bacilli in animals, ref, 233 INDEX. Whip worm, 137 Wilks, kidney fibroma, ref., 677 Williams, deciduoma, ref., 718 ovarian papillomata, ref., 728 Wilms, tumors of testicle, ref., 751 ‘“Wool-sorters’ ’’ disease, 309 Wounds, 130 healing of, 120 post-mortem, 8 Wright and Stokes, bacteriological examina- tion at autopsies, ref., 168 Xylol, use of, in paraffin embedding, 58 Yeasts, 143, 168, 170 Yellow fever, 279 Yersin, Calmette, plague, ref., 239 and Borrel, bubonic Zaborowski, muscle regeneration, ref., 780 Zahn, ciliated cysts, ref., 297, 543 ciliated cysts of pleura, ref., 426 Zenker, muscle degeneration, ref., 787 Ziegler, views on catarrhal inflammation 114 Zobglea 146 Digitized by Microsoft® Digitized by Microsoft® Digitized by Microsoft® Digitized by Microsoft® Digitized by Microsoft® Digitized by Microsoft® : an CSCI ee mee CC aS < * i n & see f CELE 3 = = oe a CSG AK a ae es 2 oe a ) PEPPER) iS Bpetbehee Bret e beter ee Ht HE oe tata PePEEre! e Pha) if aa Cpe r rere Soa Pease j tea certs rt ity He Byte eee aE - PTE M EEE ) Peerat srt et tet Peet) By ers aa aH ert) rH ri eet ‘ eth 2 5 by) 3 ee O ae rj net Yor Pee ae re ep PEERED e Eeror ee Serre) bos ‘ vOrER bree Prieapet oy pee RSS Ses ee Ses actor er ex y net tasatad pre ey bepb ptt ESDP Prorat rrr rEy ey) Seon) Sees) rh BEE ey y bey) SURETY ae SECS prota, rover Ree ee ee > PLeses! 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