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 M.A., B.Sc., M.D., F.R.C.P.E. 
 
 PRACTICAL PATHOLOGY 
 
 INCLUDING MORBID ANATOMY AND 
 POST-MORTEM TECHNIQUE 
 
IN THE SAME SERIES 
 
 TEXT-BOOK OF MIDWIFERY. For 
 Students and Practitioners. By R. W. 
 JOHNSTONE, M.A., M.D., F.R.C.S., 
 M R.C.P.E. Crown 8vo, cloth, with 
 264 Illustrations (3 coloured). Price 
 $3.25 net. 
 
 DISEASES AND INJURIES OF THE 
 EVE. A Text-Book for Students and 
 Practitioners. By WM. GEORGE SYM. 
 M.D., F.R.C.S.E. Containing 25 Full- 
 page Illustrations, 16 of them in colour, 
 and 88 Figures in the Text; also a Type 
 Test-Card at end of Volume. Small 
 crown 8vo, cloth. Price $2.50 ret. 
 
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PRACTICAL PATHOLOGY 
 
 INCLUDING 
 
 MORBID ANATOMY 
 
 AND 
 
 POST-MORTEM TECHNIQUE 
 
 BY 
 
 JAMES MILLER 
 
 M.D., D.Sc./F.R.C. P.E. 
 
 LECTURER ON PATHOLOGY AND BACTERIOLOGY, SCHOOL OF MEDICINE 
 OF THE ROYAL COLLEGES, EDINBURGH, AND EDINBURGH SCHOOL OF 
 MEDICINE FOR WOMEN; EXAMINER IN PATHOLOGY, UNIVERSITY OF 
 ABERDEEN AND ROYAL COLLEGE OF PHYSICIANS, EDINBURGH; 
 PATHOLOGIST, ROYAL VICTORIA HOSPITAL, ROYAL HOSPITAL FOR 
 
 INCURABLES, AND DEACONESS HOSPITAL, EDINBURGH; ASSISTANT 
 PATHOLOGIST, ROYAL INFIRMARY, AND ROYAL MATERNITY HOSPITAL, 
 EDINBURGH; LATB VISITING PATHOLOGIST, GENERAL HOSPITAL, 
 BIRMINGHAM; LECTURER, BIRMINGHAM UNIVERSITY, EXAMINER IN 
 
 PATHOLOGY, UNIVERSITY OF ST. ANDREWS 
 
 JJeto 
 
 THE MACMILLAN COMPANY 
 1914 
 
 All rights reserved 
 
' \ 
 
PREFACE 
 
 THE object of this volume is to give the student of medicine 
 and the practitioner, in a handy form, the information 
 required for practical work in relation to Pathology. There 
 will be found short descriptions of the appearances in the 
 more common morbid processes to be met with in the 
 organs and tissues ; at the same time these are co-related 
 with the changes in the other organs and tissues of the body 
 in the various diseases. The main points in the microscopic 
 appearances are also given very shortly, merely in order to 
 remind the student what he should look for when going over 
 his slides. In dealing with post-mortem technique, fixing 
 and mounting of preparations, cutting and staining of 
 sections, the endeavour has been to give one reliable method 
 in every case, rather than numerous alternative methods. 
 Hence the book is not one for the specialist. The chapter 
 on Tumours is added to supplement the necessarily short 
 descriptions of neoplasms under the heading of the various 
 organs. For the benefit of the practitioner, a short chapter 
 dealing with the medico-legal aspects of post-mortem work 
 has been included. Owing to the frequent occurrence of 
 cross references, it was decided to bind the illustrations 
 together in the form of an atlas at the end of the book. 
 Illustrations of microscopic preparations have been omitted, 
 as the student has his slides to which he can refer. 
 
 The author has made extensive use of volumes such as Sims 
 Woodhead's Practical Pathology ; Shennan's Post-Mortems 
 and Morbid Anatomy, Orth's Pathologisch - anatomische 
 Diagnostik and Erlduterungen zu den Vorschriften fur das 
 Verfahren der Gerichtsdrzte bei den gerichtlichen Untersuchungen 
 menschlicher Leichen ; Herxheimer's Grundriss der patho- 
 
VI 
 
 PREFACE 
 
 logischen Anatomic and Technik der pathologisch-histologischen 
 Untersuchung ; Mann's Physiological Histology ; Mallory 
 and Wright's Pathological Technique ; Letulle's La Pratique 
 des autopsies ; Adami's various works ; Beattie and Dickson's 
 Pathology ; Pembrey and Ritchie's General Pathology ; also 
 Lorrain Smith and Mair's classical work on staining methods 
 for fats in the Journal of Pathology and Bacteriology. 
 
 To the personal teaching of Professors Greenfield, Muir, 
 and Leith, and of the late Professors Ziegler and Weigert, 
 a deep debt of gratitude is also due. 
 
 The author has great pleasure in expressing his indebted- 
 ness to Professor Harvey Little John for invaluable help in 
 preparing the chapter on medico-legal post-mortems and for 
 his permission to use two typical post-mortem reports. His 
 thanks are also due to Dr. John Fraser for revising the 
 chapter on diseases of bones ; to Dr. James Young for many 
 suggestions in Chapter XII. ; to Dr. W. G. Porter for assistance 
 in preparing Figure 12 ; to Dr. Sidney Smith for the use of 
 his fine preparations illustrating centres of ossification in the 
 infant in connection with the table on p. 309 ; also to .Mr. W. 
 Waldie of the Royal College of Surgeons' Museum, Edinburgh, 
 for his advice as to the fixing and mounting of specimens. 
 
 The illustrations have, with one or two exceptions, been 
 made by Mr. Glass from preparations in the author's collection. 
 For the care and trouble taken, the author wishes to express 
 his hearty thanks. If acknowledgment has not in every 
 instance been made to the physician or surgeon who had 
 charge of the case, the author begs to offer his apologies. 
 His thanks are due to Professor Sutherland for the specimen 
 from which Fig. 33 was drawn. 
 
 For much useful advice and criticism, I have to thank 
 the Editor of the Edinburgh Medical Series Dr. J. D. 
 Comrie. For reading the proofs and for drawing up the 
 index, I have to express my hearty thanks to my assistant, 
 Dr. Fergus Hewat. 
 
 J. M. 
 
 SURGEONS' HALL, EDINBURGH, 
 October 27, 1913. 
 
CONTENTS 
 
 CHAPTER I 
 
 PAGE 
 
 INTRODUCTORY ... i 
 
 CHAPTER II 
 
 EQUIPMENT OF THE PATHOLOGIST . . , 5 
 
 CHAPTER III 
 
 METHOD OF PROCEDURE . . . . .13 
 
 Removal of Thoracic Contents . . . .22 
 
 Removal of Abdominal Contents . . .28 
 Removal of the Brain ..... 35 
 
 Removal of the Spinal Cord . . . -39 
 
 CHAPTER IV 
 
 DISEASES OF THE HEART AND PERICARDIUM . ' f 46 
 
 Malformation of the Heart and Great Vessels . . 46 
 
 Diseases of the Pericardium . . . . 48 
 
 Diseases of the Myocardium . . ,. 53 
 
 Diseases of the Endocardium . . V " 60 
 
 Effect on the Heart and Circulation of the Different 
 
 Types of Chronic Valvular Disease . .. 69 
 vii 
 
viii CONTENTS 
 
 CHAPTER V 
 
 PAGE 
 
 DISEASES OF THE VESSELS ... 77 
 
 Diseases of the Arteries . . . . . 77 
 
 Diseases of Veins . . . %7 
 
 CHAPTER VI 
 
 DISEASES OF THE BLOOD, BONE MARROW, LYMPH GLANDS, 
 
 SPLEEN, AND DUCTLESS GLANDS . . . . 91 
 
 Diseases of the Blood . . . . . 91 
 
 Haemorrhagic Diseases . . . . 99 
 
 Diseases of the Bone Marrow . . . 100 
 
 Diseases of Lymph Glands . , ,. . . 102 
 
 Diseases of the Spleen . . . IO 5 
 
 Diseases of the Thyroid Gland . J . . 1 1 1 
 
 Diseases of the Thymus Gland . . ... 113 
 
 Diseases of the Suprarenal Glands . . . 113 
 
 CHAPTER VII 
 
 DISEASES OF THE RESPIRATORY SYSTEM . . .116 
 
 Diseases of the Larynx . . . . .116 
 
 Diseases of the Bronchi . . . . .117 
 
 Diseases of the Lungs . . . . .119 
 
 Diseases of the Pleura . . . . .149 
 
 CHAPTER VIII 
 
 DISEASES OF THE INTESTINAL TRACT AND PERITONEUM . 153 
 
 Diseases of the Stomach . . . .154 
 
 Diseases of the Intestine . . . 159 
 
 Diseases of the Peritoneum . . . .172 
 
CONTENTS ix 
 
 CHAPTER IX 
 
 PAGE 
 
 DISEASES OF THE LIVER, BILE PASSAGES, AND PANCREAS 175 
 Diseases of the Liver . . . . .175 
 
 Diseases of the Gall Bladder and Bile Ducts . .194 
 
 Diseases of the Pancreas . . . .197 
 
 CHAPTER X 
 
 DISEASES OF THE KIDNEY AND BLADDER . . . 200 
 
 Diseases of the Kidney ..... 200 
 Diseases of the Pelvis of the Kidney . . .225 
 
 Diseases of the Urinary Bladder . . .227 
 
 CHAPTER XI 
 
 DISEASES OF THE BRAIN AND SPINAL CORD AND THEIR 
 
 MEMBRANES ...... 229 
 
 Diseases of the Brain ..... 233 
 
 Diseases of the Spinal Cord .... 244 
 
 Diseases of the Cord to which Special Names are given . 248 
 
 Diseases of the Peripheral Nerves . . . 252 
 
 CHAPTER XII 
 
 DISEASES OF BONES AND JOINTS .... 254 
 Diseases of Bones . . . . .254 
 
 Diseases of Joints . . . . .261 
 
 CHAPTER XIII 
 
 DISEASES OF THE REPRODUCTIVE ORGANS AND MAMMARY 
 
 GLAND DISEASES OF PREGNANCY . . . 264 
 
 Diseases of the Ovaries . . . . .264 
 
 Diseases of the Fallopian Tubes . . . 265 
 
 Diseases of the Uterus ..... 266 
 
x CONTENTS 
 
 PAGE 
 
 Diseases of the Placenta , 268 
 
 Diseases of Pregnancy and the Puerperium . , 269 
 
 Diseases of the Mammary Gland . . .272 
 
 Diseases of the Testicle . . ... . 273 
 
 Diseases of the Prostate . . . , . .274 
 
 CHAPTER XIV 
 
 TUMOURS . . . . . . 275 
 
 Simple Tumours . . . . . 277 
 
 Malignant Tumours * . . . . 286 
 
 Teratomata . . . . . ". 303 
 
 CHAPTER XV. 
 
 POINTS TO BE REMEMBERED IN PERFORMING AUTOPSIES 
 
 ON CASES WITH A MEDICO-LEGAL ASPECT. . 306 
 
 General Method of Procedure in Medico-Legal Cases . 306 
 
 Post- Mortems on Newly- Born Infants . . . 308 
 
 Post- Mortem Changes produced by Poisons . . 311 
 
 Specimen Post-Mortem Reports . . . 315 
 
 APPENDIX 
 
 TREATMENT OF SPECIMENS FOR MOUNTING . . 319 
 
 TREATMENT OF TISSUES FOR MICROSCOPIC PURPOSES . 324 
 
 STAINING METHODS . . ; . . 337 
 
 MAKING OF BLOOD FILMS . . . . . 357 
 
 BACTERIOLOGICAL METHODS OF INVESTIGATION . 358 
 EXAMINATION OF SPUTUM, Pus, ETC., FOR THE TUBERCLE 
 
 BACILLUS . . . . . . 370 
 
 THE BACTERIOLOGICAL DIAGNOSIS OF DIPHTHERIA . 372 
 
 AGGLUTINATION TEST FOR ORGANISMS . . . 374 
 
 METHOD OF MAKING PIPETTES .... 375 
 
 EMBALMING . . . . . . 376 
 
 INDEX . ' . . . . . 377 
 
LIST OF ILLUSTRATIONS 
 
 FIG. PAGE 
 
 Sections of liver and kidney (in colour} . . Frontispiece 
 
 Plan of the circulation to show the origin and destination 
 
 of the more common emboli ... 62 
 
 Plan of the circulation in the kidney . . . 206 
 
 1 . Method of opening the abdominal cavity . . ^ 
 
 2. Reflecting the skin and muscles from the sternum and ribs/ 
 
 3. Method of cutting through sterno-clavicular joint . 
 
 4. Method of cutting through floor of mouth 
 
 '} 398 
 
 5. Lines of incisions for opening up the cavities of the heart 
 
 6. Method of incising the lung 
 
 7. Method of opening the coronary arteries . 
 
 8. Method of testing the competence of the sernilunar valves . J 
 
 9. Method of removing the small intestine . 
 
 } 399 
 
 401 
 
 10. Method of opening the bowel after it has been removed 
 
 11. Cutting through tentorium cerebelli in removing the brain \ 
 
 12. Position of the accessory cavities in relation to the base r 4 2 
 
 of the skull . . . . . J 
 
 13. Method of incising the kidney . . . . ^ 
 
 14. Method of stitching up . . . . ./ 
 
 15. Heart, acute pericarditis . . . . \ 
 
 1 6. Acute aneurysm following abscess of left ventricle in r 44 
 
 case of osteomyelitis . . i .J 
 
 17. Heart, chronic interstitial myocarditis . . . ^ 
 
 1 8. Section through wall of right ventricle, showing increase I 
 
 of sub-pericardial fat and fatty infiltration of the muscle j 
 
 19. Thrombus in right auricular appendix . .- . J 
 
 xi 
 
xii LIST OF ILLUSTRATIONS 
 
 FIG. PAGE 
 
 20. Simple (vegetative) endocarditis in a case of chorea, heart 
 
 of child ...... 406 
 
 21. Simple endocarditis, aortic valve . . . ^ 
 
 22. Heart, ulcerative endocarditis of mitral valve . . J 
 
 23. Ulcerative endocarditis, aortic valve . . . ^ 
 
 24. Transverse section of heart, showing hypertrophy of the r 48 
 
 left ventricle in case of chronic interstitial nephritis . J 
 
 25. Anterior aspect of heart from case of mitral stenosis,^ 
 
 showing dilatation of right auricle and well-marked 
 
 hypertrophy as well as dilatation of right ventricle 
 
 , 409 
 
 26. Same heart from above, showing dilatation of both I 
 
 auricles. The narrowed mitral valve (button -hole) 
 can be seen . . . . . . J 
 
 27. Chronic endocarditis of aortic valve, with stenosis .~\ 
 
 28. Portion of descending thoracic aorta, showing atheroma . I 410 
 
 29. Arteries at base of brain, showing atheroma , .J 
 
 30. Saccular aneurysm of descending aorta adherent to and 
 
 eroding the bodies of the vertebrae ". . . 411 
 
 31. Spleen considerably enlarged from chronic venous con-^i 
 
 gestion, showing infarcts 
 
 32. Spleen, myelogenous leukaemia and infarction . . j 
 
 33. Spleen, tuberculous masses ". . . . J 
 
 34. Spleen and spleniculus, sago waxy . . .->, 
 
 35. Spleen, Hodgkin's disease, showing numerous scattered 
 
 white masses varying in size . . . . I 413 
 
 36. Spleen, Hodgkin's disease, showing white masses arranged I 
 
 in groups . . . . . . J 
 
 37. Mass of tuberculous lymphatic glands in section, showing 
 
 numerous caseous foci . . . ' 
 
 38. Lymphatic glands, lymphadenoma (Hodgkin's disease) . 
 
 39. Thyroid gland, exophthalmic goitre . . 
 
 40. Lung, emphysema . . . . ./ 
 
 41. Lung, collapse due to empyema . . . .416 
 
 42. Lung, lobar pneumonia . . . . .417 
 
 43. Lung and bronchi, showing acute bronchitis and septic 
 
 broncho-pneumonia . . . , . 418 
 
LIST OF ILLUSTRATIONS xiii 
 
 PAGE 
 
 44. False membrane in trachea in diphtheria . . ^ 
 
 45. Portion of lung, showing two recent infarcts . . v 419 
 
 46. Lung, gangrene . . . . . . J 
 
 47. Lung, silicosis . . . . . . 420 
 
 48. Lung, anthracosis .... 
 
 40. Lung, acute miliary tuberculosis . 
 
 h 4 21 
 
 50. Mediastinal glands and lung of infant, showing caseous 
 
 tuberculosis ..... 
 
 51. Lung, caseous (tuberculous) pneumonia with cavitation . 422 
 
 52. Lung, chronic tuberculosis, with cavity in which an'' 
 
 aneurysm has formed .... 
 
 53. Lung, fibro-caseous tuberculosis, with marked tendency V 423 
 
 to healing ..... 
 
 54. Surface of lung, acute pleurisy 
 
 55. Section of lung, showing large number of nodules of\ 
 
 secondary carcinoma . . . . .1 
 
 56. Lympho-sarcoma of the mediastinal glands invading the | 
 
 root of the lung . . . . . / 
 
 57. Squamous epithelioma of oesophagus, with marked narrow- 
 
 ing of lumen ...... 
 
 58. Peptic ulcer of stomach, with opening into vessel in floor 425 
 
 of ulcer . . 
 
 59. Large duodenal ulcer .... 
 
 60. Stomach opened up anteriorly to display encephaloid 
 
 cancer close to cardiac opening . . . 426 
 
 61. Intussusception of small intestine and mesentery into 
 
 large intestine ..... 
 
 62. Typhoid lesion of small intestine (early stage) 
 
 63. Typhoid lesion of small intestine (later stage) 
 
 64. Tuberculous ulcer of small intestine 
 
 65. Tuberculous ulcer, peritoneal aspect, showing raised 
 
 tubercles under peritoneum . .' . 
 
 66. Large intestine, ulcerative colitis (dysentery) . 
 
 67. Portion of large bowel from case of amoebic dysentery, 
 
 showing characteristic early lesion 
 
 427 
 
xiv LIST OF ILLUSTRATIONS 
 
 FIG. 
 
 68. Acute appendicitis and peritonitis 
 
 69. Pelvic colon, with adeno-carcinoma projecting into j* 4 2 9 
 
 interior ..... 
 
 70. Peritoneal aspect of loop of intestine, showing tuberculous \ 
 
 peritonitis . . j. 430 
 
 71. Abscesses of liver, portal pysemia type 
 
 72. Liver, large tropical abscess, with much necrotic liver' 
 
 tissue ...... 
 
 73. Liver of child, showing multiple nodular hyperplasia 
 
 (regeneration of liver substance) following an acute 
 
 431 
 
 degenerative process 
 
 74. Liver, common cirrhosis 
 
 75. Liver, showing group of gummata . . .^ 
 
 76. Liver, cavernous angioma . . . . V 432 
 
 77. Section of liver with secondary deposits of sarcoma . J 
 
 78. Liver, greatly enlarged, with numerous secondary nodules> 
 
 of carcinoma . . ... 
 
 v 433 
 
 79. Section of liver, with hydatid cyst from which numerous 
 
 smaller cysts are protruding . . . . J 
 
 So. Biliary calculi or gall-stones . . . . ^ 
 
 81. Congenital cystic kidney . . . .1 434 
 
 82. Infarcts of the kidney . . . . . J 
 
 83-86. Kidneys illustrating the various types of Bright's 
 
 Disease ...... 435 
 
 87, 88. Kidney, pyaemic abscesses . . . . ^ 
 
 89, 90. Kidney, tuberculosis . . . ,f 
 
 91. Kidney, hydronephrosis . . . . .\ 
 
 92. Kidney, hypernephroma . . . . . I 437 
 
 93. Coralline calculus in kidney . . . . J 
 
 94. Brain, showing acute meningitis . . . . ^ 
 
 95. Brain, tuberculous meningitis . . . . / 
 
 96. Section of brain, showing acquired hydrocephalus . -j 
 
 97. Section of brain, showing haemorrhages into the basal f 439 
 
 ganglia on right side . . . . . J 
 
440 
 
 LIST OF ILLUSTRATIONS xv 
 
 98. Cerebellum, with depressed areas from softening of" 
 
 brain substance due to thrombosis in arteries . 
 
 99. Vertical section of brain, showing solitary abscess in 
 
 temporo-sphenoidal lobe .... 
 
 100. Transverse section of pons, showing haemorrhages into 
 
 its substance . 
 
 101. Cholesteatoma in frontal lobe . A 
 
 102. Teratoma (dermoid) of ovary containing sebaceous [ 
 
 material and hairs. Solitary cyst above it .1 
 
 103. Scirrhous cancer of the breast, with indrawing of nipple J 
 
 104. Myomata in wall of uterus . . . . ^ 
 
 105. Enlargement of costo-chondral junctions (rickety rosary) r 44 2 
 
 in rickets . . . . . . J 
 
 1 06. Osteomyelitis of lower end of femur . . .\ 
 
 107. Lower lumbar vertebrae and sacrum in section, showing r 443 
 
 tuberculous disease of bodies and psoas abscess . J 
 
 1 08. Osteo-sarcoma of shaft of femur . . .^\ 
 
 f 444 
 
 109. Myeloid sarcoma of jaw . . . . J 
 
PRACTICAL PATHOLOGY 
 
 CHAPTER I 
 
 INTRODUCTORY 
 
 THE post-mortem examination, sectio cadaveris, or autopsy 
 is an essential part of the scientific investigation of all fatal 
 cases of disease. It is obvious that only by its means can 
 the medical man acquire an accurate knowledge of the nature, 
 extent, distribution, and complications of a morbid condition. 
 It is not too much to say that however plain and simple the 
 diagnosis of a disease may be, some additional light will be 
 thrown upon the case at the post-mortem examination. In 
 a very considerable number of instances, conditions quite 
 unexpected during life will be found, and, in a few, the 
 diagnosis of the clinician will be entirely upset by the patholo- 
 gist 's investigations. 
 
 A post-mortem examination should therefore be performed 
 whenever feasible. Further, the examination should be as 
 thorough as possible : should, in other words, include as 
 many parts of the body as possible, and should be followed 
 by microscopic, and, if necessary, bacteriological examination 
 of the diseased organs and tissues. In not a few instances 
 the pathologist's view of a case obtained by naked-eye 
 
 i i 
 
2 INTRODUCTORY 
 
 examination alone is greatly altered by subsequent micro- 
 scopic or bacteriological investigation. 
 
 For example, in a case which came under the author's 
 notice there was a stricture of the small intestines which, 
 from the clinical history as well as from the naked-eye appear- 
 ances, was believed to be malignant. Microscopic examina- 
 tion showed the condition to be tuberculous. 
 
 In another case, where haemorrhagic infiltration of the 
 mediastinal tissues was the main post-mortem finding, the 
 true nature of the disease was only found on making cultures, 
 when a pure growth of the anthrax bacillus was obtained, the 
 case proving to be one of " woolsorter's disease." 
 
 From another point of view a post-mortem examination 
 may be required; that is the medico-legal. Cases of suspected 
 poisoning may prove to be ordinary diseased conditions, 
 and, vice versa, cases where foul play is unsuspected may turn 
 out to be due to poisoning. 
 
 To give another example from the author's experience. 
 A well-to-do contractor died suddenly with symptoms of 
 severe jaundice. His will was known to be drawn out in 
 favour of the foreman of his works, with whom he lived. The 
 medical attendant considered phosphorous poisoning a possi- 
 bility, but post-mortem examination revealed the presence of a 
 large impacted calculus in the common bile duct. 
 
 In all cases of sudden death where the cause is unknown, 
 or of violent or suspected violent deaths, notice must be sent 
 at once to the Procurator-Fiscal or Coroner. Such bodies 
 become the property of the Fiscal or Coroner, and cannot be 
 touched without his consent. (For further information on 
 this point see Chapter XV.) 
 
 Precautions to be taken. Before proceeding in any 
 way to carry out a post-mortem examination, it is absolutely 
 necessary that the permission of the nearest relative of the 
 deceased be obtained. In certain hospitals, more happily 
 situated than their fellows, the regulation is, that unless 
 
INTRODUCTORY 3 
 
 notice to the contrary be received from the relatives within 
 twenty-four hours of the death of the patient, an autopsy 
 will be performed. This is a far better system than the one 
 under which permission has to be asked for in each case. 
 When not confronted with the choice, the relatives, as a rule, 
 except in the case of certain religious creeds, think little of 
 the matter. When permission is asked for, they at once 
 begin to conjure up visions of mutilation, and it requires in 
 most instances no little tact on the part of the medical man 
 to obtain permission. In every case, however, where leave 
 has to be asked, it should be obtained in writing from the 
 nearest relative. The absolute necessity for this precaution, 
 if the doctor is to protect himself, has been emphasised on 
 several occasions recently in the law courts. In a case tried 
 before the Court of Session in Edinburgh, the judge, in 
 charging the jury, said that the holding of an unauthorised 
 post-mortem " gave a legal remedy/' and that when per- 
 formed without consent " the case would be treated very 
 smartly " ; further, the defender, a medical man who had 
 performed the sectio, " would have been well advised had he 
 obtained permission from the father in writing" 
 
 Medico-legal Cases. When the case is a medico-legal 
 one, it is necessary to receive permission from the Procurator- 
 Fiscal (Scotland) or the Coroner (England) before a post- 
 mortem examination is performed. This permission having 
 been obtained, none other is required. Although in all cases 
 it is advisable to take full notes at the time, these should be 
 taken with special care in cases which have, or are likely to 
 have, a medico-legal aspect (e.g. workmen's compensation 
 cases). 
 
 In certain cases with a medico-legal aspect the Coroner 
 or Fiscal will order an autopsy to be performed. When 
 reporting such a case the pathologist should avoid as far as 
 possible the use of technical terms. In Scotland such a 
 
4 INTRODUCTORY 
 
 report requires to be drawn up in what is known as the 
 " soul and conscience form " (see Chapter XV.). 
 
 Importance of Post-mortem Change. It is quite obvious 
 that the sooner the post-mortem examination is carried 
 out after the death of the patient the better, but unless 
 there is any special reason to the contrary it is usual to wait 
 for twenty-four hours. 
 
 The changes which begin to take place in a body after death 
 tend to mask, and eventually to obliterate entirely, the 
 characteristic appearances of most pathological conditions. 
 Diseased conditions have been found in Egyptian mummies, 
 and caries of teeth and evidence of rickets in the skeletons of 
 prehistoric men, but as a rule the softer parts, and more parti- 
 cularly the hollow viscera and abdominal organs, rapidly lose 
 the characteristic signs of disease through decomposition. 
 The extent and rapidity of this change will, of course, depend 
 upon circumstances. The processes take place much more 
 rapidly in warm weather. Conversely in cold weather, or if, 
 as is possible in some hospitals, the bodies are placed in an 
 apparatus artificially cooled, they will retain their freshness 
 for a much longer period. Another factor bearing upon this 
 is the disease from which the patient has died. In septic 
 conditions, more particularly in the abdominal cavity, 
 decomposition occurs more quickly, and tends to alter the 
 appearance of organs in the neighbourhood. 
 
CHAPTER II 
 
 THE EQUIPMENT OF THE PATHOLOGIST 
 
 Rubber Gloves. One of the most important parts of the 
 pathologist's equipment is a good, sound pair of rubber 
 gloves. Fifteen or twenty years ago gloves were seldom 
 worn. In consequence, those carrying out post-mortem 
 work suffered periodically from septic wounds, if not from 
 the more serious infections, such as tuberculosis. Nowadays 
 there is no excuse for such accidents, as gloves are cheap, 
 and with care they last a considerable time. The best type 
 of glove is the thin rubber glove used by the surgeon. The 
 thicker ones naturally last longer, but they are more expensive, 
 more difficult to work with, and are more troublesome to 
 mend. 
 
 It is very necessary that the pathologist should care for 
 his gloves, seeing so much depends upon them. During a 
 post-mortem the gloves should be frequently washed under 
 running water to prevent the drying of blood or pus upon 
 their surface. After the operation is finished, they should 
 be washed while on the hands, first with soap and water, and 
 then with water alone, afterwards dried, and while still on 
 the hands moistened all over with biniodide of mercury 
 spirit (biniodide of mercury i part, methylated spirit 
 500) and dried again with a towel. If punctured, the 
 
 5 
 
6 THE EQUIPMENT OF THE PATHOLOGIST 
 
 interior of the glove should, of course, be similarly treated. 
 The exact position of a puncture can be found by distending 
 the glove with water. A patch can then be applied, just as 
 one mends a punctured tyre. The gloves should subsequently 
 be folded up and placed in the cardboard box supplied with 
 them. 
 
 If long intervals elapse between post-mortems, the gloves 
 may become hard and brittle. A few minutes' immersion in 
 hot water will make them soft again. 
 
 Where gloves are not obtainable, the hands may be smeared 
 with carbolic oil. 
 
 Post-mortem Wounds. In the case of a punctured 
 wound obtained at a post-mortem it is well to wash the part 
 thoroughly in warm water, suck it, and then dress it with 
 some weak antiseptic, such as i : 40 carbolic. Some recom- 
 mend the use of pure carbolic or other strong acid in the 
 first instance. If slight, the wound can be covered with a 
 layer of celloidin dissolved in equal parts of alcohol and 
 ether, or with " new skin." 
 
 In his movements with knife or needle, the pathologist 
 should always be slow and cautious. When dealing with 
 purulent or other infective fluid, or with faecal material, 
 great care should be taken not to splash it about. Severe 
 eye infections sometimes result in this way, and the author 
 knows of cases in which typhoid infection resulted from the 
 splashing of infected faeces. For this reason it is well to 
 avoid using a strong stream of water when washing intestines, 
 or, indeed, at any time. 
 
 Eye Infections. When some foreign material has 
 entered the eye, the conjunctival sac should be washed out 
 with a little warm saline. The method of washing out is to 
 place the individual on a chair with head well thrown back, 
 and to squeeze the saline fluid into the eye with a piece of 
 cotton wool. There is no need to use an antiseptic, as the 
 
THE EQUIPMENT OF THE PATHOLOGIST 7 
 
 conjunctival sac can of itself destroy a considerable amount 
 of infective material. The object of the washing is merely 
 to remove as much of the irritant as possible. In any case 
 the eye should not be rubbed or irritated in any way. 
 
 Another source of danger for the pathologist is flies. 
 These are excessively troublesome in warm climates, and are, 
 undoubtedly, a means of conveying infection. Fly-papers 
 will be found useful in reducing the number. 
 
 Turning to the question of instruments, these need not be 
 numerous or elaborate. The following are essential : 
 
 Instruments. i. A sharp large-bladed knife for making 
 incisions in the skin and for removing organs. Several of 
 these should be kept. 
 
 2. A long, flat knife for cutting into the solid organs. 
 
 3. A straight probe-pointed bistoury for opening the heart, 
 the smaller vessels, such as the coronary arteries, for opening 
 the bronchi, and for incising the dura and cutting nerves in 
 removing the brain. 
 
 4. A pair of dissecting forceps for finer work. 
 
 5. A pair of fairly large round-ended scissors for opening 
 the bowel. These may be of the special type commonly 
 used, but an ordinary pair, provided the edges are sharp and 
 the ends blunt, will do almost equally well. 
 
 6. A good saw, with removable back. 
 
 7. A chisel. 
 
 8. A wooden or soft metal mallet. 
 
 9. Several flexible probes. 
 
 10. A packing needle. 
 
 11. Strong twine. 
 
 12. Wooden cones for measuring the diameter or circum- 
 ference of the heart valves (e.g. those advocated by 
 Shennan) will be found useful. 
 
 In addition it is well to have one or more sharp-pointed 
 scalpels for any finer dissection that may be required ; also a 
 
8 THE EQUIPMENT OF THE PATHOLOGIST 
 
 pair of small sharp-pointed scissors for fine work, a catheter, 
 sponges, and a wooden block for supporting the head. A 
 screw-driver for coffin lids may also on occasions be found 
 useful. 
 
 Knives should, of course, be sharp, and it is advisable to 
 have the means of sharpening them at hand, in the shape of 
 a hone and oil. With a little practice it is possible to put a 
 keen edge on a knife in a very few minutes. Instead of the 
 finer large knives sold by the instrument-makers, butcher's 
 knives will do admirably, and will cost a fourth or fifth of 
 the price. 
 
 Another necessary item in the pathologist's equipment 
 is a pair of scales with weights from one gramme to five kilos. 
 
 Post-mortem Table and Accessories. The post-mortem 
 table should be at least 6 feet long and 2 feet broad. It 
 should be either a solid slate slab or wood covered with zinc. 
 The edge should be raised, and runnels arranged so that 
 fluids will pass to a central waste-pipe enclosed in an iron 
 pillar supporting the table, and on which it revolves. There 
 should be a plentiful supply of water ; a tap overhead with 
 hose attached ; a basin with hot and cold supply close by 
 for washing the hands ; a large sink with an ordinary tap, 
 and a tap with rose attached, used for washing organs, the 
 stream from which can be easily controlled by the operator 
 either by the foot or elbow. The operator should frequently 
 cleanse his gloves under running water to prevent blood, 
 pus, or other discharge from drying on them. 
 
 It is useful to have accessible a number of bottles containing 
 reagents likely to be required, such as Gram's iodine for 
 testing for waxy disease (see p. 363), dilute hydrochloric acid 
 and ferrocyanide of potassium for testing for hsemosiderin 
 in the organs (see p. 353), 10 per cent formalin, and other 
 fixatives for tissues, and a supply of empty bottles with 
 corks. 
 
THE EQUIPMENT OF THE PATHOLOGIST 9 
 
 A Bunsen burner, a platinum needle, a piece of metal for 
 searing the surface of organs, slides, and culture media should 
 be close at hand. A number of large sponges will be found 
 very useful for mopping out cavities, also a glass measure and 
 a syringe and trocars for injecting specimens with preserva- 
 tives. A large jar of Pick's or other fixative should be at 
 hand for this purpose, and pots of various sizes for containing 
 specimens. 
 
 The post-mortem room of a hospital should be in a detached 
 building. The room itself should be airy and well lighted. 
 It should communicate with a preparation room, and a 
 laboratory for microscopic and bacteriological work. 
 
 The operator should, of course, wear a clean overall to 
 protect his clothing. A waterproof apron over or under 
 this is advisable. A pair of spectacles for the protection of 
 the eyes is a good thing. 
 
 Note-taking. Previous to the performance of the sectio, 
 <a short resume of the main clinical features of the case should 
 be sent to the pathologist. Notes dictated by the operator 
 during the sectio should be taken by a competent person. 
 This is absolutely necessary, as the more minute points in 
 the case cannot be put down unless the organs are actually 
 before the operator. Organs change considerably in colour 
 even during the course of the sectio, so that it is not safe to 
 trust to the description of a case written up afterwards, 
 even when the more important organs are preserved. 
 
 Post-mortems in Private. In carrying out a post- 
 mortem in private, the body should be placed on a kitchen 
 table, with an old sheet and newspapers, or, if possible, 
 a waterproof sheet, underneath. Sometimes the bed is the 
 only place available, in which case the waterproof is very 
 necessary. The head should be supported with a brick, a 
 block of wood, or a suitable box wrapped in newspaper. A 
 slop-pail and basins, with a plentiful supply of water, should 
 
io THE EQUIPMENT OF THE PATHOLOGIST 
 
 be procured. To mask unpleasant odours, a piece of twisted 
 brown paper lit at one end, the other end being thrust into 
 a jug and left to smoulder, or a handful of ground coffee 
 thrown on a shovelful of burning coals will be found useful. 
 In private, if the spinal cord has to be examined, it is well 
 to begin with that. A number of newspapers, bottles for 
 specimens, sponges, soap and towels should not be forgotten. 
 
 Rules to be observed in examining Organs. A few 
 simple rules should be borne in mind when examining an 
 organ. It is well to have some definite method in order that 
 nothing be passed over. The student should remember, in 
 the first place, to look before touching, the former being much 
 the more important process. Note in the first instance the 
 size of the organ, and mentally compare it with what, in 
 your experience, is the normal size, remembering always 
 that the age of the subject from which the specimen was 
 taken is an important item in drawing a conclusion as to 
 size. The general form of the organ should next be examined, 
 and any deviation from the normal noted, such as swellings 
 or shrinking. Examine next the surface of the organ, 
 looking for exudate, which, if recent, is friable and readily 
 scraped away; if organised, it is stringy and difficult to 
 remove. Opaque, white, pearly areas indicate chronic 
 inflammation. Cicatrices with indrawing or puckering of 
 the surface indicate old infarcts or healed tuberculous or 
 syphilitic lesions. A finer roughening, giving the appearance 
 of morocco leather, is always indicative of fibrosis in the 
 organ. 
 
 Next, the organ should be incised, and in doing so some 
 idea of its consistence may be arrived at. An organ which is 
 the seat of fibrosis will be tougher and more difficult to cut. 
 In incising an organ it is usual to do so from the rounded 
 outer and broader surface towards the root or hilum where 
 the vessels enter and the ducts leave. 
 
THE EQUIPMENT OF THE PATHOLOGIST n 
 
 The cut edge is another point to which attention should be 
 directed, and which bears upon the question of consistence. 
 A rounded edge after a cut indicates soft consistence, and 
 is associated with cloudy swelling and fatty change ; a sharp 
 edge is found when the organ is firm. That is the reason for 
 the existence of a sharp edge in organs the seat of amyloid 
 disease the waxy material gives consistency and firmness 
 to the tissue, unless complicated by other degenerative 
 conditions, such as fatty change. 
 
 The student is apt to consider that in diseased conditions 
 associated with fatty change, a greasy feel is imparted to the 
 organ. As a matter of fact, adipose tissue and fat generally 
 is greasy to the touch, but it is only comparatively rarely 
 that fatty change (when the change is actually a degenerative 
 one in the parenchymatous cells) gives to the organs which 
 are the seat of the change a greasy sensation when touched. 
 
 The next step is to examine the cut surface. The colour 
 and any irregularity in the distribution of the colouring 
 should be noticed. The presence of bands of fibrous tissue, 
 pigmentations of various kinds, opaque spots. Grey, trans- 
 lucent areas indicate waxy disease or accumulations of cells, 
 such as tubercle foci and leukaemia. Opaque white spots 
 are indicative of degenerative and necrotic foci, such as areas 
 of focal necrosis in the liver in typhoid, eclampsia, etc. Note 
 also the condition of the vessels of the organ. If they stand 
 out prominently, it is an indication that their walls are 
 thickened. Their contents should also be noted, whether 
 that is fluid or solid, and the character of the clot if present. 
 The presence of gas in the blood should be looked for. 
 
 Use of Knife in making Incisions. In incising an organ, 
 the way in which the knife is used is a matter of no little 
 importance. The knife should, in the first place, be a large 
 one, considerably larger than the organ itself ; the larger the 
 better. It must, further, be a sharp knife. As regards the 
 
12 THE EQUIPMENT OF THE PATHOLOGIST 
 
 character of the cut, the knife should be drawn along and not 
 pressed into the substance of the organ. The cut made by 
 drawing the knife leaves a smooth surface, that made by 
 pressing the knife leaves a rough surface. Further, the cuts 
 must be large and sweeping, not a to-and-fro movement 
 which will leave a series of ridges. If possible, the whole 
 cut should be carried out in a single sweep. As Virchow was 
 accustomed to say to his students, " Smooth, though wrong, 
 incisions are better than correct and uneven ones." 
 
CHAPTER III 
 
 METHOD OF PROCEDURE 
 
 Object of Post-mortem Examination. The object of a 
 post-mortem examination is twofold first, the discovery 
 of the disease condition which has led to a fatal termination 
 in the particular case in point ; second, the investigation, as 
 minutely as possible, of that disease condition with a view 
 to advancing medical science in general. 
 
 The first object may in some cases be attained by the 
 most cursory examination limited to a single organ or 
 part; in other cases only the closest attention to detail 
 and the investigation of the apparently insignificant will 
 be followed by success ; the second object can only be 
 attained after every system has been examined with the 
 greatest care and after minute investigation, assisted by the 
 microscope, and, it may be, by the chemical laboratory. It 
 follows from this that wherever possible a detailed examina- 
 tion should be carried out. There are cases where the 
 cursory investigation will give all the information required, 
 but in a large proportion of cases the pathologist is not doing 
 his duty unless the more detailed examination be resorted to, 
 that is, provided always permission for the extended sectio 
 be obtained and the time and apparatus be available. 
 
 Necessity for definite Plan of Operation. In order 
 13 
 
14 METHOD OF PROCEDURE 
 
 to carry out this detailed examination some definite plan of 
 operation is necessary. In other words, before starting to 
 carry out the autopsy it is quite essential that the operator 
 should have some idea of how he is going to proceed : of the 
 order in which he is going to examine the -various body 
 cavities and their contents. It is by no means necessary 
 to adhere to the same plan invariably. In fact, the experi- 
 enced pathologist will alter his routine frequently, accord- 
 ing to the indications given him by the clinical history 
 as to the parts actually diseased. At the same time it is 
 advisable to have some definite plan, some order in which 
 the various parts are to be examined, so that no detail may 
 be omitted. 
 
 It is generally stated that it is better . to begin when 
 possible with the head, as otherwise blood may escape from 
 the vessels of the head while the thorax is being examined, 
 and so appearances be altered. This is not a very strong 
 argument. Virchow long ago emphasised the necessity of 
 opening the abdominal cavity, before the thoracic, in order 
 that the true position of the diaphragm might be ascertained. 
 As a matter of fact this is usually done, but not for that 
 reason. As a rule, after making an examination of the 
 organs in situ and of the large serous sacs pleura, peri- 
 cardium, peritoneum one begins with the more detailed 
 examination first of the thoracic organs. 
 
 Different Methods of Procedure. As Letulle points 
 out, there are really two parts in a complete autopsy, (i) The 
 examination of the cerebro-spinal system. (2) The examina- 
 tion of the viscera. One might add as a third part the 
 examination of bones, muscles, vessels, and nerves. But 
 having admitted that this division exists, it should be realised 
 that the further examination of these parts, more particularly 
 in the case of the viscera, must be carried out in continuity. 
 That is to say, taking, for example, the vascular system, 
 
METHOD OF PROCEDURE 15 
 
 heart, arteries, and veins should be examined before cutting 
 through any large vessel. * The alimentary system should be 
 exposed and inspected from pharynx to rectum before it is 
 divided into sections ; more than that, the various canals, 
 such as bile and pancreatic ducts, must be examined while 
 they are in continuity with the alimentary tract. This is 
 the ideal method, and it is the method advocated and carried 
 out by Le tulle and others. The whole of the thoracic and 
 abdominal viscera are removed and examined first in con- 
 tinuity, arid then the various organs removed and examined 
 by themselves. In practice, however, this method is some- 
 what tedious, and cannot in many instances be carried -out, 
 owing to leave being obtained for the examination only of 
 certain parts of the body. 
 
 Two great rules emphasised by Orth should always be 
 kept in view. The first is that a part should never be removed 
 from its position before its relationship to its surroundings 
 has been established. Thus the heart should never be 
 removed for examination before the contents of the pulmonary 
 artery and its larger branches have been investigated. 
 Secondly, no part should be taken away if the removal of it 
 will interfere with the investigation later on of other parts. 
 
 To sum up, it is well for the pathologist to have some 
 routine to which he is accustomed, thus avoiding the danger 
 of omissions, but this plan may be modified according to 
 
 the exigencies of the case. 
 
 
 
 Surface Examination. First there comes the examina- 
 tion of the body, before any incision is made. The following 
 points should be attended to : 
 
 Development of the Body. Height, breadth, etc., presence 
 or absence of deformities. Any alterations in the shape of 
 the chest should be particularly noted ; the barrel-shaped 
 chest of bronchitis and emphysema, the pigeon breast indica- 
 tive of rickets in early life are two- common malformations. 
 
16 METHOD OF PROCEDURE 
 
 Nutrition. Whether the body is well nourished, poorly 
 nourished, or emaciated. 
 
 Age and Sex. 
 
 Presence and degree of rigor mortis. This is observed 
 first in the muscles of the face, and spreads from above 
 downwards, passing off in the same order. The time of onset 
 of rigor mortis varies according to the time which has elapsed 
 since death and according to the cause of death. In cases of 
 sudden death due to injury of the spinal cord, in tetanus, in 
 strychnine poisoning, and in wasting diseases, such as tuber- 
 culosis and cancer, the condition may come on very early. 
 As a rule it appears in from three to six hours after death. 
 Usually the condition begins to pass off in twenty-four 
 to forty-eight hours, the time depending upon the cause of 
 death and the conditions under which the body is kept. In 
 septic conditions and in warm weather rigor mortis passes 
 off rapidly. 
 
 Alteration in Colour. Pallor. Any deepening of the normal 
 colour of the skin or the presence of jaundice. 
 
 Lividity. This naturally occurs after death, owing to the 
 accumulation of blood in the dependent parts. Post-mortem 
 lividity is thus most marked in dependent parts. Where lips 
 or face are livid, some abnormality in the circulation or 
 death from suffocation may be suspected. Lividity may 
 also be due to bruising. Such livid patches, when pressed 
 upon, remain of the same colour, unlike post-mortem lividity, 
 which can be pressed away. When bruised parts are cut 
 into, the blood is found diffused through the tissues. A 
 livid colour along the lines of the superficial vessels may be 
 due to the advance of decomposition, owing to the diffusion 
 of the blood-colouring matter into the surrounding tissues. 
 Green coloration, an indication of the onset of decomposition, 
 should also be noted. It appears first over the abdomen 
 and in the spaces between the lower ribs. 
 
 Skin eruptions, superficial tumours, scars, or recent 
 
METHOD OF PROCEDURE 17 
 
 wounds should be carefully noted, and their extent esti- 
 mated. 
 
 Note the presence of oedema and its distribution. 
 
 Examine the various orifices of the body mouth, nose, 
 ears for discharges, foreign bodies, etc. Note the condition 
 of the teeth. Examine for the presence of 'inguinal or femoral 
 hernia. Note the condition of the external genitals. 
 
 Primary Incision. Standing on the right side of the 
 body, the pathologist grasps his knife firmly with the right 
 hand (Fig. i). The incision is commenced either immedi- 
 ately under the chin, at the thyroid cartilage, or just above 
 the manubrium sterni in the middle line. It is carried 
 downwards through skin and subcutaneous tissue to left of 
 the umbilicus, as far as the symphysis pubis. Any cicatrices 
 or recent incisions should be avoided. Care must be taken 
 not to go too deeply when incising the abdomen, in order to 
 avoid cutting the liver or bowel. At one point, usually in the 
 epigastric region, the incision is carried through muscle and 
 peritoneum into the cavity. The index and middle finger 
 of the left hand are then inserted into the opening, and 
 separated so as to put the tissue on stretch (Fig. i). With 
 the knife the incision is prolonged, the two fingers following 
 down, to the pubes. To obtain more room, the rectus muscle 
 on either side should be cut transversely through immediately 
 above the pubic bone without injuring the skin. 
 
 In cases where permission is obtained only for the 
 examination of a part of the body e.g. thorax or abdomen 
 the incision should be correspondingly limited. 
 
 Reflection of Skin and Muscles. The next step in the 
 process is the dissection of the skin and muscles of the chest 
 from sternum, cartilages, and ribs, and, at the same time, of the 
 skin of the neck from the subjacent tissue. This should be 
 done by grasping the skin, etc., with the left hand and steadily 
 pulling away from the sternum or ribs. The areolar tissue 
 
i8 METHOD OF PROCEDURE 
 
 and muscles are then touched here and there with the edge 
 of the knife as they are put upon the stretch (Fig. 2). At 
 this stage the operator will be in a position to determine the 
 amount of subcutaneous fat, also the appearance of the muscles, 
 which in wasting diseases are often abnormally dark and dry, 
 and in toxic conditions such as typhoid fever may show (more 
 especially the recti abdominales) translucent, glassy-looking 
 areas the so-called vitreus degeneration of Zenker. Also 
 at this stage the mammcz may be incised through the pectoral 
 muscles and examined for growths, etc. The ribs should also 
 be examined for fractures and enlargement of the costo- 
 chondral junctions (rickety rosary). 
 
 Removal of Sternum. Before opening the thoracic 
 cavity the level of the diaphragm may be noted. Note also 
 the level of the lower border of the liver, and the position 
 of the stomach and other viscera, as regards the lower costal 
 margin. Then, commencing at the second costal cartilage 
 close to its attachment to the rib, and cutting obliquely 
 outwards, so as to avoid injuring the underlying lung, one 
 divides the cartilages on either side. 
 
 In many cases of muscular, and more particularly of old 
 men, it will be found impossible to do this with a knife. The 
 saw should then be used, and the cartilages severed, holding 
 the saw perpendicularly to the ribs. Great care should be 
 taken not to splinter the ribs in any way, so to avoid puncture 
 wounds of the hands in subsequent manipulations. An 
 excellent way of avoiding such wounds is to fold the skin 
 which has been dissected from sternum and ribs in over the 
 severed ends of the ribs. 
 
 The sterno-clavicular joint on either side should then be 
 disarticulated by inserting the point of the knife perpendicu- 
 larly (Fig. 3), the knife being afterwards turned edge out- 
 wards, the incision prolonged between clavicle and first rib 
 for half an inch, and the rib cartilage divided external to the 
 
METHOD OF PROCEDURE 19 
 
 point of disarticulation. If the cartilage of the first rib is 
 ossified it will be necessary to use a pair of bone forceps or 
 a saw to divide it. 
 
 The sternum and cartilages should then be removed from 
 below upwards, the diaphragmatic attachment being, in the 
 first instance, cut through. If the sternum be firmly adherent 
 to the mediastinal tissues, great care should be taken not 
 to damage aneurysm or tumour, to which this adherence may 
 be due. 
 
 Serous Sacs. The removal of the sternum opens both 
 pleural cavities, and at this stage of the proceedings the 
 serous sacs peritoneum, pleurse, and pericardium should 
 be examined. The pericardium is opened by two incisions, 
 commencing at the lower corner on the right side and ex- 
 tending, the one upwards to the aorta, the other outwards to 
 the apex of the heart. In cases where air embolism is sus- 
 pected the pericardial sac should be filled with water, and the 
 right ventricle punctured and pressed, when, if air be present 
 in the right side of the heart, bubbles will appear. 
 
 The general aspect of the thoracic contents should at this 
 point be noted. The size of the heart and the extent to 
 which it is overlapped by the lungs are points of importance. 
 
 In examining the serous sacs look for the presence of fluid 
 in excess note its colour, whether it is clear or turbid or 
 blood-stained. Examine the surfaces of the viscera. These 
 ought to be shiny and perfectly smooth. Any dimming of 
 the surfaces indicates inflammatory exudate. Where there 
 are indications of such exudate, films and cultures should be 
 made from the fluid with all necessary precautions. Where 
 pus or fcecal matter is present in the abdomen) careful search 
 should be made for perforation of the viscera, more particularly 
 the vermiform appendix, the lower end of the ileum, the 
 stomach, and the duodenum. A careful examination should 
 also be made of the surface of the viscera for any thickening 
 
20 METHOD OF PROCEDURE 
 
 or adhesions, indicative of ulcerations or tumour formations 
 within. 
 
 When blood or blood clot is present in the abdomen, search 
 should be made for a ruptured organ, viscus, or vessel. An 
 area with adherent blood clot is often an indication of the 
 source of the haemorrhage. 
 
 Examine for adhesions between visceral and parietal layers 
 of pleura, and note the degree of force required to break down 
 these adhesions. 
 
 At this stage, both lungs should be freed from any abnormal 
 attachment. If there are extensive adhesions which cannot 
 readily be broken down, an incision should be made through 
 the parietal pleura, and the latter by means of the fingers 
 torn from the ribs. 
 
 Procedure for removing Contents of Thoracic and 
 Abdominal Cavities. Having examined the serous sacs, 
 the next step is to remove and examine the contents of the 
 thoracic and abdominal cavities. The way in which this is 
 done will be determined not infrequently by the nature of 
 the case, the pathologist being guided by the summary of 
 the clinical history, or whatever information is available. 
 To put the matter shortly, there are two main methods of 
 procedure : (i) to remove the organs one by one and examine 
 them separate from their surroundings ; (2) to remove the 
 contents of the cavities entire or in groups, afterwards to 
 examine canals, vessels, ducts, etc., in continuity with the 
 viscera, and then, and only then, to sever attachments and 
 remove and examine the organs themselves. Unquestionably 
 the latter is the proper method. If the former be adopted, 
 although in many cases no harm will be done, in some in- 
 stances points will be missed and valuable specimens be 
 ruined. The experienced pathologist can, as a rule, decide 
 whether he may risk adopting the first method, but the 
 tyro ought, if it is at all possible, to make use of the 
 
METHOD OF PROCEDURE 21 
 
 second. But even if one decide for the second method, 
 certain options present themselves. One may remove the 
 whole contents of both cavities together as Letulle does, 
 but, as already indicated, this has its disadvantages. One 
 may compromise matters somewhat and adopt the method 
 advocated by Shennan, which is excellent, but which necessi- 
 tates postponing the removal of the thoracic contents (the 
 most important organs in the majority of cases) until all the 
 abdominal organs have been removed. 
 
 The method recommended by the author is the removal, in 
 the first instance, of the thoracic contents entire, the examination 
 of the vessels, etc., in continuity, then the separation of the 
 organs and their investigation separately. Subsequently one 
 deals with the abdomen, from which the organs are removed, 
 not en masse, but in groups. This should be the routine 
 method. It has certain disadvantages : oesophagus, aorta, 
 vena cava, and thoracic duct will be cut through. But, 
 as regards the first, the cases in which it is advisable to 
 preserve the continuity of oesophagus with stomach tumours 
 of oesophagus, cases of poisoning, cases of severe hsematemesis 
 from varicose veins are comparatively rare, easily recognised, 
 and special methods can be adopted for the preservation of 
 the continuity. As regards aorta, there is no great dis- 
 advantage in examining it in two sections. And as regards 
 the thoracic duct, it is only very rarely (as in cases of acute 
 miliary tuberculosis) that it is advisable to dissect it out and 
 investigate it in its entire length. 
 
 (1) Removal of the Organs one by one. Nothing special 
 need be said about the method of procedure in this case. 
 It is usual to begin with the heart, then the lungs, spleen, 
 liver, kidneys, etc. In many cases the pathologist will 
 begin with the organ believed to be mainly affected. As 
 far as possible Orth's rules (p. 15) should be carried out. 
 
 (2) Method of examining the Thoracic and Abdominal Con- 
 tents by removing them in Groups : 
 
22 METHOD OF PROCEDURE 
 
 EXAMINATION OF THE THORACIC CONTENTS 
 
 If not originally begun below the chin, the primary skin 
 incision should be carried upwards to that point. In many 
 cases this may not be necessary, the trachea being cut through 
 at some point above the level of the clavicles. But in some 
 cases it is necessary to have tongue and pharynx attached to 
 trachea. The skin and sterno-mastoid muscles are dissected 
 away from the structures in the neck and beneath the chin. 
 The knife is then passed upwards through the floor of the 
 mouth below the symphysis menti, and by sweeping it round 
 on either side, keeping close to the rami of the lower jaw, the 
 attachments of the muscles are cut through (Fig. 4). The 
 tongue can then be pulled through the opening, and by drawing 
 upon it a view of the pharynx can be obtained. The attach- 
 ment of soft to hard palate can then be cut through ; the 
 posterior wall of the pharynx is incised and dissected down. 
 Care should be taken to include both tonsils in the structures 
 removed. Further traction upon the tongue will then enable 
 the operator to tear through the loose cellular tissue attaching 
 the oesophagus to the prevertebral fascia. At some point 
 the carotids are cut through, also the subclavian vessels. 
 While all this is being done, attention should be paid to 
 any enlarged glands, ihrombosed veins, etc., which may be met 
 with. 
 
 The lungs having been at an earlier stage freed from 
 adhesions, a few touches of the knife will enable the 
 operator, by traction on the trachea in a downward direction, 
 to detach the thoracic contents from the prevertebral 
 fascia as far down as the diaphragm. The oesophagus is 
 then ligatured to prevent the escape of stomach contents. 
 The oesophagus, aorta, and attachment of pericardium 
 to diaphragm are next cut through and the thoracic 
 
METHOD OF PROCEDURE 23 
 
 viscera are removed and placed upon a table or in the 
 sink. 
 
 When it is desired to preserve the continuity of the 
 oesophagus with stomach, and of the thoracic duct and aorta, 
 then the whole of the body contents (thoracic and abdominal) 
 should be removed together, as in Letulle's method. 
 
 (Esophagus and Trachea. The thoracic contents are 
 now placed, anterior aspect downwards, on the table or sink. 
 The oesophagus is slit open with a pair of bowel scissors. 
 The trachea and bronchi are opened in a similar manner. If 
 it is desired to preserve the oesophagus, it can be first removed 
 or turned to the left side. After opening the air passages, 
 the nature of the contents of bronchi and trachea are noted. 
 
 Aorta. In the same way the aorta is slit up and examined 
 as far round as the ascending portion. If it be extensively 
 diseased, its continuity with the heart should be preserved. 
 The organs should then be placed anterior aspect upwards, 
 and attention should in the first place be directed to the 
 heart. 
 
 Pulmonary Artery. Incise the pulmonary artery 
 longitudinally, and examine carefully for the presence of 
 thrombi, following the branches going to the two lungs as 
 far as possible. Very commonly post-mortem or agonal 
 clots are present, but these are readily distinguished from 
 thrombi (see p. 63). 
 
 Superior Vena Cava. The superior vena cava should 
 then be opened as far as the right auricle. The incision is 
 afterwards carried down to the inferior vena cava. 
 
 Heart. The heart is now separated from the two lungs. 
 For this purpose it is advisable to get an assistant to steady 
 the other viscera. The organ is pulled upwards and over 
 towards the right lung, and the pulmonary veins are cut 
 through as they enter the left auricle. After this the pul- 
 
24 METHOD OF PROCEDURE 
 
 monary artery and aorta are severed. In cases where the 
 latter is diseased it may be advisable, as already stated, to 
 preserve its continuity with the heart. To do this, a little 
 further dissection is necessary, the aorta being separated 
 from the surrounding structures. 
 
 Surface of Heart. The heart is now taken in the hand 
 and a more careful examination of the surface made. Note 
 should be taken of its shape and size, of any areas of thickened 
 pericardium (milk spots), small haemorrhages , fibrinous 
 exudate. The amount of subpericar dial fat should also be 
 noted. 
 
 Right Auricle. Then, attention being turned in the first 
 place to the right auricle, an incision is made from the centre 
 of the previous one joining the two venae cavse into the 
 auricular appendix, search being made for thrombi. 
 
 Eight Ventricle. Passing the forefinger of the left 
 hand through the tricuspid valve into the right ventricle 
 and grasping the wall between the ringer and thumb, incise 
 the wall of the right ventricle by means of a probe-pointed 
 bistoury, commencing just below the pulmonary artery and 
 carrying the incision down parallel to the interventricular 
 septum and half an inch to the left of it (Fig. 5). 
 
 Tricuspid Valve. Now test the size of the tricuspid valve 
 either by means of a suitable cone or with the fingers, the 
 normal orifice admitting three digits. The segments of the 
 valve should then be examined. This can be done quite 
 easily from the auricular aspect. One of the segments, 
 the largest as a rule, is situated anteriorly and slightly to 
 the left. It separates the orifice of the valve from the 
 infundibulum or conus arteriosus } and is therefore known as 
 infundibular segment. The second is situated to the right, 
 corresponding to the free margin of the ventricle ; the third 
 lies internally and posteriorly against the ventricular septum, 
 and is known as the septal segment. 
 
METHOD OF PROCEDURE 25 
 
 Pulmonary Valve. The competence of the pulmonary 
 valve is now tested by allowing a stream of water to fall from 
 a height into the cut end, the sides of the vessel being sup- 
 ported (Fig. 8). The primary incision into the ventricle is 
 then prolonged upwards into the artery, care being taken 
 to cut between the right and left anterior segments. Examine 
 the segments for thickening or vegetations. Before leaving 
 the right side of the heart examine the thickness of the muscle 
 of the right ventricle. Note the amount of fat lying over it, 
 and particularly if there is any infiltration of the fat into the 
 muscle. 
 
 Left Auricle. Open the left auricle by an incision 
 joining the two upper pulmonary veins. Continue the incision 
 so as to open the auricular appendix in its entire length 
 (Fig. 5). Examine the interior of the auricle for thrombi, 
 vegetations, and thickening of the endocardium. 
 
 Mitral Valve. A longitudinal incision is now made 
 into the wall of the left ventricle, somewhat anterior to the 
 left border (Fig. 5). The mitral valve is inspected from above 
 and its diameter measured. This may be done roughly by 
 the fingers, the valve admitting two digits. Run the knife 
 through the valve and out at the opening in the wall of the 
 ventricle and cut outwards. The segments of the valve are 
 arranged, the larger in front and to the right, between the 
 auricular and aortic openings, the smaller to the left and 
 behind, so that, if done properly, the cut will lie between 
 the segments. 
 
 Left Ventricle. Examine the valve for thickening, 
 calcareous deposits, vegetations, etc., also the chordce tendinece 
 for thickening, shortening, vegetations, or rupture. Note the 
 appearance of the papillary muscles, incising them and 
 examining for fibrous change. Note the colour and appearance 
 of the muscle generally, looking tor fatty and fibrous changes. 
 Examine more particularly the state of the muscle towards 
 
26 METHOD OF PROCEDURE 
 
 the apex of the ventricle where interstitial myocarditis is 
 usually found. Incise the interventricular septum, looking 
 for interstitial change. Measure the breadth of the wall of 
 the ventricle and test the consistence of the muscle. 
 
 Aortic Valve. Turn next to the aortic valve. A good 
 way of exposing this valve is to run the probe-pointed bistoury 
 successively into the two coronary arteries, and then to cut 
 upwards and outwards (Fig. 7), thus slitting up the aorta 
 on either side, and at the same time the commencement of 
 the two coronary arteries. Test the competence of the aortic 
 valve by a stream of water poured in from above (Fig. 8) ; 
 examine the condition of the segments (there are three an 
 anterior and a right and left posterior) and measure the 
 circumference. 
 
 Coronary Arteries. Next examine carefully the condi- 
 tion of the two coronary arteries, opening up their various 
 branches by slitting with knife or scissors, or, in the case of 
 the finer ones, by cutting them across. This should be done 
 most carefully in cases of sudden death, search being made 
 for impacted emboli or thrombi on atheromatous patches. If 
 required, the aortic valve may be exposed more fully by 
 cutting between the anterior and the left posterior segment 
 downwards through the anterior wall of the left ventricle 
 until the lateral cut in the ventricular wall is reached. 
 
 Certain anatomical points regarding the coronary arteries 
 and their distribution should be remembered. The right 
 vessel, which arises from the anterior sinus of Valsalva, is 
 usually smaller than the left ; it supplies the greater part of 
 the wall of the right ventricle, the right auricle, and the 
 greater portion of the left auricle. The left coronary artery, 
 which arises from the left posterior sinus of Valsalva, soon 
 after its commencement divides into two branches. It 
 supplies the outer wall of the left ventricle and the anterior 
 two-thirds of the septum ventriculorum, a small part of the 
 
METHOD OF PROCEDURE 27 
 
 right ventricle near the septum anteriorly, and the inferior 
 portion of the left auricle. The more important of the two 
 divisions of the left coronary is the descending branch which 
 passes down the anterior inter ventricular groove. This 
 branch is the one most frequently the seat of atheromatous 
 change. It supplies the apex of the left ventricle and the 
 septum as well as the anterior wall and papillary muscles. 
 Hence it is in these positions that chronic interstitial myo- 
 carditis is most frequently met with. 
 
 Lungs. The lungs should now be separated from the 
 mediastinal tissues by cutting through their roots. 
 
 Pleural Surface. Examine, in the first instance, the 
 pleural surfaces, looking for petechial hemorrhages, fibrinous 
 exudate, fibrous thickening, puckering, and cicatrisation, more 
 particularly at the apices. Note the colour of the organs, 
 especially at the posterior and the lower parts. Note also 
 the consistence ; feel for any solid areas or points at apex 
 and along borders. Next cut into the organs by a perpendicu- 
 lar incision directed from above downwards, and from its 
 outer, rounded, thick border towards its inner, anterior sharp 
 border (Fig. 6). Other cuts should be made from the original 
 incision forwards to the anterior border in the case of each 
 lobe. 
 
 Cut Surface of Lungs. On the cut surface, note in the 
 first place alterations in colour, the presence of cavities, areas 
 of caseation, etc. Next feel the lung substance and squeeze it, 
 looking for the presence or absence of air bubbles or for the 
 presence of fluid ; note the colour and appearance of the fluid 
 expressed. Examine carefully all solid areas, and determine 
 whether the solidity is due to some exudate filling the air 
 cells or to interstitial fibrous change. Suspected solid areas 
 should be placed in a glass beaker of water. Consolidated 
 areas sink in water. 
 
28 METHOD OF PROCEDURE 
 
 Bronchi. Next open up the bronchi with the probe- 
 pointed bistoury and note the appearance of any fluid they 
 contain ; also the appearance of their walls. Open up the 
 branches of the pulmonary artery similarly, looking for thrombi 
 or emboli. Incise the bronchial glands, noting the degree of 
 pigmentation) the presence of caseous areas or of calcification. 
 
 Lastly, the thyroid, parathyroid, and thymus glands 
 should be, examined, also the remaining mediastinal tissue. 
 
 Thyroid Gland. The thyroid gland should be examined 
 as regards its size. Longitudinal incisions are made into its 
 substance and the cut surface examined for colloid material, 
 the presence of cysts, etc. 
 
 Parathyroid Glands. The average number of para- 
 thyroids is four. They are found in close proximity with 
 the thyroid gland, usually posteriorly. They are minute, 
 oval, pink bodies, averaging from 6 to 8 mm. in length. 
 
 Thymus Gland. The thymus gland is situated partly 
 in the neck, partly in the mediastinum immediately behind 
 the manubrium sterni. It is largest during the second year 
 of life (} oz. or 20-25 gm.). Until puberty it remains large, 
 thereafter undergoing atrophy, until about the twenty-fifth 
 year it has practically disappeared. Occasionally it may 
 persist throughout life. An abnormally large thymus gland 
 has been found in certain cases of sudden death, particularly 
 in young children. 
 
 EXAMINATION OF THE ABDOMINAL CONTENTS 
 
 Removal of Intestines. The first step in this procedure 
 is to remove the intestines, small and large. The actual 
 examination of these should be deferred to the last moment, 
 in order to avoid the odour of faecal matter. Before cutting 
 through the mesentery search should be made for any enlarged 
 
METHOD OF PROCEDURE 29 
 
 glands, more particularly caseous or calcareous glands, and 
 the relationship of these glands to the bowel established. 
 Next look for the duodeno-jejunal junction, and having cut 
 through the mesentery at that point, place two ligatures round 
 the bowel and divide it between them. Place a ligature also 
 round the lower end of the rectum and cut it through as low down 
 as possible. Next cut through the mesentery, close to the bowel, 
 from the jejunum to ileo-csecal valve. This is easily done by 
 pulling upon the bowel with the left hand and merely touching 
 the mesentery with the knife, which, however, cannot be 
 too sharp for the purpose. The knife should be held with its 
 blade perpendicular to the bowel (see Fig. 9). 
 
 Having freed the bowel as far as the cczcum, the latter 
 should be removed from its attachments, along with the ascending 
 colon and appendix. The transverse colon should next be 
 detached from the stomach and removed with the splenic 
 flexure, descending and pelvic colon. In this way the whole 
 of the bowel from jejunum to rectum can be examined in 
 continuity. As previously stated, it is well to defer opening 
 it to a late stage in the post-mortem examination. 
 
 Method of opening Bowel. The bowel is opened by 
 means of a pair of bowel or other probe-pointed, sharp-edged 
 scissors, along its mesenteric attachment in the case of the 
 small, along one of the longitudinal muscular bands in the case 
 of the large intestine (Fig. 10). The colour and general 
 appearance of the contents should, at the same time, be 
 noted. 
 
 Examination of Intestine. Having opened the gut, 
 take it up, piece by piece, commencing with its upper end, 
 and wash it carefully under a gentle stream of water. More 
 particular attention should be paid to the lower end of the 
 ileum, where typhoid and tuberculous ulcerations are specially 
 found, and to the large bowel generally. Look for increase 
 of vascularity, ulcerations, tumours, animal parasites. 
 
3 o METHOD OF PROCEDURE 
 
 Vermiform Appendix. The appendix has been looked 
 at during the preliminary investigation of the abdominal 
 cavity. It should now be more carefully examined. 
 
 It should always be remembered in connection with the 
 intestinal canal that post-mortem changes are most marked 
 in the hollow viscera, and that these changes tend to mask the 
 appearances in pathological conditions. Black and greenish- 
 black coloration of the bowel and neighbouring organs is 
 common, and is due to the action of the sulphuretted hydrogen 
 gas from the gut upon the iron pigment of the blood. 
 
 Removal of Liver, etc. In the next place, the liver , with 
 the stomachy duodenum, pancreas, and spleen, should be removed 
 without disturbing the vascular and duct connections of these 
 organs. This can best be done by standing, in the first 
 instance, on the left side of the body, pulling upon the liver 
 with the left hand and cutting through its connections with 
 diaphragm and posterior abdominal wall. Care should be 
 taken at the start to leave intact the right suprarenal gland, 
 which is in close contact with the liver. The duodenum is 
 then detached by cutting through its peritoneal covering. 
 The liver is then pulled still further over to the left side of 
 the body, and its connection with the large vessels and 
 retroperitoneal tissue cut through. Standing on the right 
 side of the body, the cardiac end of the stomach is cut through, 
 the spleen detached all but its vascular connections, the tail 
 of the pancreas dissected away from left suprarenal, the left 
 lobe of the liver freed from the diaphragm, and the whole 
 group of viscera lifted out. It is more particularly in remov- 
 ing the intestines and other abdominal viscera that an 
 assistant is desirable. 
 
 Stomach and Duodenum. Having placed this group 
 of viscera in the sink or on the table near it, the first procedure 
 is to open the stomach and duodenum. This is usually 
 
METHOD OF PROCEDURE 31 
 
 done by cutting with the scissors along the greater curvature of 
 the stomach and along the anterior wall of the duodenum. 
 Of all organs, the stomach is the one which suffers most from 
 post-mortem changes, so that a great deal of what appears to 
 be abnormal in the stomach must be discounted. Look 
 more especially for ulcers and tumours towards the pyloric 
 end of the stomach, and in the first part of the duodenum. 
 Press upon the gall bladder to see if bile can readily be made 
 to flow along the common duct into the duodenum. 
 
 Bile and Pancreatic Ducts. Incise the common bile 
 duct and pancreatic duct, pass a probe along them, and if 
 necessary open them up. 
 
 Gall Bladder. Open the gall bladder and note its 
 contents, the colour and consistence of the bile, and any gall 
 stones which may be present. Ascertain whether the cystic 
 duct is patent by passing a probe along it. 
 
 Liver. Attention should next be turned upon the liver. 
 In removing that organ, any adhesions between it and the 
 pariet,es will have been noted. Any exudate on the surface 
 of the organ, thickenings of the capsule, cicatrices, etc., should 
 be searched for. The size of the organ should be noted, also 
 any alteration in shape, the presence of perpendicular or 
 horizontal sulci, such as are caused by tight lacing and the 
 wearing of tight belts. 
 
 OUTER SURFACE. Note whether the surface is smooth or 
 rough, also the colour of the organ and any irregularity in 
 colouring. Incise the organ by means of a number of cuts in 
 a perpendicular direction. Note the character of the cut edge, 
 whether rounded or sharp. 
 
 CUT SURFACE. Examine carefully the cut surfaces, 
 noting colour, the outline of the lobules, irregularities in colour, 
 etc. Next test the consistence of the liver substance by 
 pushing the finger into it. 
 
32 METHOD OF PROCEDURE 
 
 Pancreas. The pancreas is best examined further by 
 a series of transverse cuts. The fat in the neighbourhood 
 of the organ should be examined for areas of fat necrosis. 
 
 The portal and splenic veins should then be opened up and 
 search made for thrombi. The lymph glands in the neighbour- 
 hood of the head of the pancreas should also be examined. 
 
 Spleen. The spleen, which may be removed by itself 
 or along with stomach and liver, should be weighed, its size 
 noted, also any roughening of its surface or thickening of its 
 capsule, also irregularities in colour indicating infarcts. Its 
 consistence should be noted, and the organ opened by a longi- 
 tudinal incision from its outer surface to its hilum. On the 
 cut surface the general colour, the appearance of the Malpighian 
 bodies, should they be visible, and the existence of any tubercle 
 nodules or other opaque areas should be noted. 
 
 All the organs have now been removed from the abdomen 
 with the exception of the kidneys, the pelvic organs, and the 
 large vessels. 
 
 Removal of Kidneys with Bladder. Note the position 
 of the kidneys and the courses of the ureters. The kidneys 
 and suprarenals should be removed together. Where the 
 existence of renal and bladder conditions is suspected, it is well 
 to remove kidneys, ureters, and bladder together. This can be 
 done by cutting through the blood-vessels of the kidneys 
 and dissecting down the ureters to the brim of the pelvis. 
 A cut is now made through peritoneum round the brim of 
 the pelvis, down to the bone, and by means of the fingers 
 the bladder, pelvic colon, and, in the female, the genital 
 organs are all separated from their attachments to the 
 parietes, the vessels, etc. being cut through close to the bone. 
 Grasp these organs with the left hand, pull them upwards 
 and backwards, and cut through the urethra. The point 
 of the knife is then pushed down through the skin of the 
 perineum close to the anus. A circular cut is made round 
 
METHOD OF PROCEDURE 33 
 
 the anal orifice and the group of organs is removed and placed 
 in the sink. 
 
 In the case of the male, when it is desired to retain the 
 continuity between bladder and urethra, as in prostatic disease, 
 cases of rupture of the urethra from fracture of the pelvis, 
 etc., a special method of procedure should be adopted. The 
 pelvic contents are freed from the bony wall as before. The 
 original abdominal incision is then carried downwards for an 
 inch or so along the penis. The penis is then cut through. 
 After freeing the pubic bones from skin and muscular attach- 
 ments the two rami are sawn through on either side. A little 
 further dissection will enable the operator to remove the 
 whole pelvic contents with the symphysis pubis and root of 
 penis. 
 
 If it be desired to remove the female genital organs with 
 bladder and rectum, a cut is made all round the brim of the 
 pelvis through the peritoneum ; this is separated as above by 
 means of the fingers from the walls of the pelvis, the knife 
 being used occasionally to divide vessels and nerves. The 
 point of the knife is next pushed down through the skin at 
 one side of the perineum and, by an elliptical cut, the whole 
 floor of the pelvis, including vulva and anus, is cut out. The 
 pelvic organs can now be lifted out from above. 
 
 Suprarenals. Examine the two suprarenals by detaching 
 them from the kidneys and making a series of transverse 
 incisions. 
 
 Bladder. The bladder may now be opened by inserting 
 the probe-pointed bistoury into the urethra and cutting 
 upwards to the fundus. Note any enlargements of the prostate) 
 ulcer ations of the mucous membrane } stone in the bladder, etc. 
 Examine the ureters, and if necessary slit them up. 
 
 If there is no obvious reason for keeping the kidneys 
 attached, the ureters are severed at their commencement 
 and the kidneys weighed. 
 
 The kidneys may be removed by themselves either after the 
 removal of the intestines, or, in cases where it is not considered 
 
 3 
 
34 METHOD OF PROCEDURE 
 
 necessary to examine these, before the other viscera are 
 touched. This is done by making a cut through the peri- 
 toneum and fascia, inserting the fingers, stripping the organ 
 from its surroundings and pulling it forward. The vessels 
 and ureter are then cut through. 
 
 Kidneys. Note in the first place the size of the organs. 
 Examine the surface for irregularities and cysts, the more 
 obvious irregularities of persistent fcetal lobulation or old 
 infarction, or the finer markings due to chronic interstitial 
 nephritis. Next incise the organ by cutting with the large knife 
 from the outer border to the hilum (Fig. 13) ; in doing so, note 
 the consistence of the organ. Examine the cortex, noting its 
 colour, its width, comparing it with that of the medulla. 
 Look for the glomeruli, which may be seen as dark red 
 spots. Note any opaque lines or patches indicating fatty 
 degeneration in the tubules. Look at the large vessels 
 between cortex and medulla, and note any tortuosity of 
 the interlobular vessels which run upwards from them into 
 the cortex. Lastly, note the amount of fat which is present 
 between the kidney substance and the pelvis (peripelvic fat) 
 and examine the pelvis itself. 
 
 Then, taking the kidney in the right hand, grasp the capsule 
 of the organ with a pair of dissecting forceps and strip it 
 backwards. In a normal kidney this can be done quite 
 easily, and the surface displayed is perfectly smooth. If the 
 capsule is thickened and adherent, or if the surface is rough, 
 the presence of chronic interstitial nephritis is certain. The 
 appearance of the small cysts, so frequently found under the 
 capsule under similar conditions, should also be noted. Note 
 also whether small veins (venae stellatse) under the capsule 
 are unduly prominent. 
 
 Uterus and Appendages. The uterus is examined by 
 making an incision into it from fundus to cervix, and trans- 
 verse incisions along the upper border, so as to display the 
 
METHOD OF PROCEDURE 35 
 
 openings of the Fallopian tubes. The ovaries are incised 
 in their longest diameter. 
 
 Testicles. The testicles may be examined without 
 injuring the scrotum by incising the tissues at the external 
 abdominal ring and pressing the testicle upwards. The 
 gland is opened by an incision in its longest diameter. 
 
 Thoracic Duct, etc. There only remain now for examina- 
 tion the large vessels, the thoracic duct, the retroperitoneal 
 glands, and the cosliac ganglia. The inferior vena cava, 
 aorta, and their branches are slit with scissors along their 
 anterior walls and search made for thrombi and emboli. 
 
 The thoracic duct will be found behind and to the right 
 of the aorta. In the thorax it lies to the right between the 
 aorta and the azygos vein. It should be examined more 
 especially in cases of miliary tuberculosis, and its relation to 
 any caseous lymph gland investigated. 
 
 The semilunar ganglia will be found on the aorta around 
 the cceliac axis. 
 
 EXAMINATION OF THE BEAIN 
 
 Scalp Incision. Place a block under the nape of the 
 neck to support the head. Insert a small knife with its 
 back to the skull under the skin immediately behind the 
 right ear, cut upwards and outwards to the vertex, and from 
 the vertex in the same manner down to a corresponding 
 point behind the left ear. It is advisable to cut outwards 
 in this way in order that the hair may not be cut off. It is 
 well also, in the case of women, to separate the hair along 
 the line of the incision, throwing part forwards and the other 
 part backwards. Raise a portion of the scalp by means of 
 the hair and cut below it with the knife. Then grasp the 
 portion of scalp freed with the left hand, and, pulling forwards 
 
36 METHOD OF PROCEDURE 
 
 or backwards as the case may be, put the tissues joining 
 scalp to skull and temporal muscle on the stretch, rendering 
 the cutting of them more easy. This should be done forward, 
 nearly to the supraciliary ridges, and backwards to below 
 the occipital protuberance. In carrying this out, note the 
 presence of any extravasation of blood below the scalp and 
 examine the surface of the skull for fracture. 
 
 Saw-Cuts. Next, by means of an old knife, mark out 
 the line along which the bone is to be sawn through. In 
 front, this line should run below the frontal eminences, and 
 be carried back on either side, cutting through the temporal 
 muscles to a point just above and behind the ears. Another 
 cut starts from one of these points, and, making an angle 
 of about 1 60 with the former cut, runs across the back of 
 the skull a little in front of the occipital protuberance to 
 the corresponding point on the other side. 
 
 Next, standing on the right side of the body, take a dry 
 towel and throw it over the skull, place the left hand on the 
 towel and through it grasp the calvarium, throwing the 
 anterior portion of the towel over the back of the hand. 
 Take the saw in the right hand and commence to saw through 
 the outer table of the frontal bone, following the previously 
 mentioned lines as closely as possible. The saw-cut should 
 be carried nearly, but not quite, through the inner table, in 
 order to avoid injuring the membranes and brain. When 
 a fracture is suspected, however, it is well to carry the saw- 
 cut through both tables. Then, taking the hammer and 
 chisel, insert the edge of the latter into the saw-cut, and, by 
 a series of sharp taps, crack through the remainder of the 
 inner table. It is well to tilt the chisel slightly, so that the 
 angle of the instrument enters first. 
 
 Eemoval of Calvarium. The next step is to pull back 
 the calvarium by means of the hook on the cross-piece of 
 the chisel, at the same time separating the dura from the 
 
METHOD OF PROCEDURE 37 
 
 bone with such an instrument as a periosteum separator. 
 In the case of old people, alcoholics, and also young children 
 the dura may be found too firmly adherent to the bone for 
 this. In such a case the dura should be divided all along 
 the saw cut and removed at the same time as the calvarium. 
 Incise the superior longitudinal sinus and examine for clots 
 or thrombi. 
 
 m Dura Mater. With a pair of dissecting forceps pick 
 up a portion of the dura mater anteriorly and incise it. 
 Insert a probe-pointed bistoury into the opening and cut 
 round the dura on both sides, at the level at which the skull 
 was sawn through. Insert the knife between the left frontal 
 lobe and the falx cerebri, with the edge towards the falx. 
 Cut through the latter and pull back the dura mater. The 
 dura will usually be found adherent over the vertex by 
 means of vessels and Pacchionian bodies. 
 
 Brain Surface. Examine the exposed surface of the 
 brain, noting its vascularity, any flattening of the convolutions, 
 or filling up of the sulci with exudate or blood. 
 
 Removal of Brain. Insert two fingers of the left hand 
 under each frontal lobe and gently pull the brain back. 
 Detach the olfactory bulbs from the cribriform plate with the 
 handle of the knife. Cut through the optic nerves and the 
 internal carotid vessels as near the bone as possible. Cut 
 through the 3rd, 4th, 5th, 6th, and yth nerves. Cut the 
 tentorium cerebelli along its attachment to the petrous 
 portion of the temporal on either side (Fig. n). Divide the 
 8th and Qth nerves. Pass the bistoury down the cord and 
 divide it obliquely as low down as possible. Sever the two 
 vertebral arteries and a few nerve roots and the brain will 
 tilt back into the left hand. 
 
 Cerebro-spinal Fluid. During ail this process, cerebro- 
 spinal fluid will escape. Note the amount and character of 
 
38 METHOD OF PROCEDURE 
 
 this fluid, whether clear or opaque, and, if necessary, secure 
 a specimen for further examination. 
 
 Base of Skull. Either before or after the examination 
 of the brain, the base of the skull should be further investi- 
 gated. The lateral and other venous sinuses should be slit 
 open and their contents examined. Where fracture is sus- 
 pected, strip off the dura mater from the bones by means 
 of dissecting forceps. 
 
 Examination of Brain. The brain should now be 
 weighed and its surf ace further examined. Note the condition 
 of the vessels, more particularly those at the base, looking 
 for opaque areas of atheroma, thrombi, or small aneurysms. 
 Note thickening or opacity of the pia-arachnoid. Examine 
 for exudate in the subarachnoid space, more particularly 
 at the base of the brain. Examine the Sylvian fissures 
 on either side for small tubercles along the lines of the 
 vessels. Pass the fingers carefully over the whole surface 
 of the organ, noting the presence of any area of exceptional 
 softness. 
 
 The method of proceeding further with the examination 
 of the brain depends to a great extent upon the patho- 
 logical condition present. In a large proportion of cases 
 it is advisable to fix the organ before cutting it up. This 
 is done by injecting 10 per cent formalin, or Pick's or some 
 other preservative, into the larger vessels at the base, placing 
 the whole organ in similar fluid, padding the jar, in which 
 it is suspended by means of a piece of string run through the 
 basilar artery and attached to the lid of the jar, with cotton 
 wool, and leaving it there for some days at least. 
 
 Section of Brain. When it is necessary at once to 
 examine the whole organ, it should be placed vertex down- 
 wards and the pons and medulla removed by cutting through 
 the crura cerebri. The cerebrum is then placed upon its 
 
METHOD OF PROCEDURE 39 
 
 base, and with a large and sharp knife a series of horizontal 
 sections are made at intervals of half an inch, commencing 
 at the vertex, the organ being steadied by means of the 
 left hand placed flat upon it. The pons and medulla are 
 then opened up by means of a series of transverse cuts and 
 the cerebellum examined by an incision from its posterior 
 border to the peduncles. Search is then made on the cut 
 surfaces for hcemorrhages , areas of softening, tumours, etc. 
 
 EXAMINATION OF THE SPINAL CORD 
 
 Removal of Spinal Cord. Turn the body over on the 
 face, with the head hanging well down over the end of the 
 table. Make an incision through the skin over the spinous 
 processes from the occiput to the sacrum. Cut the muscles 
 through on either side down to the laminae, pulling aside the 
 muscles from the spinous processes. Then saw through the 
 laminae on either side about one half-inch from the middle 
 line, directing the edge of the saw slightly inwards. It is 
 unnecessary to saw below the third or fourth lumbar vertebra, 
 as the cord does not reach farther than the second lumbar. 
 A rough guide for the lower end is the crest of the ilium. 
 
 Having partially sawn through the laminae, complete the 
 process with the hammer and chisel, taking care not to 
 damage the cord. Lift up the spinous processes thus set 
 free at some point, and then, with the bone forceps, proceed 
 to bite through the remainder of the laminae on either side, 
 lifting up the spinous processes as you proceed. This should 
 be done above as high as the atlas and below as far as the 
 3rd or 4th lumbar. Free the cord at the lower end by 
 cutting through the nerve-roots and the dura ; then, holding 
 dura and cord, cut through the nerve-roots upwards, if 
 necessary removing the ganglia with the roots. 
 
 At the upper end of the cord cut through the dura from 
 above, i.e. through the foramen magnum, and remove the 
 
40 METHOD OF PROCEDURE 
 
 whole cord. Next lay the cord on a flat surface, incise the 
 dura anteriorly, and preserve the cord in the first instance in 
 10 per cent formalin. After two or three days make a series 
 of transverse cuts, dividing the cord into a number of segments 
 which remain attached posteriorly to the dura. Subse- 
 quently, thinner portions may be placed in Miiller's, Marchi's, 
 or other fixative. 
 
 In cases where it is desirable to retain the continuity 
 between brain and cord, as in cases of lesions of the cervical 
 region, the cord should be exposed first and all the nerve- 
 roots severed. The dura mater of the upper portion of the 
 cord is cut through from above, also the upper nerve-roots, 
 and if desired the cord at the level of the foramen magnum 
 may be exposed by taking a wedge-shaped piece of bone from 
 the back of the skull. The cord will now come away with the 
 brain. 
 
 Eye and Orbit. The eye and contents of the orbit may 
 be examined by chipping through the orbital plate of the 
 frontal and removing the pieces of bone with a pair of bone 
 forceps beginning at the optic foramen. The posterior half 
 of the eye can then be removed by making an equatorial cut 
 with a pair of sharp-pointed scissors without damaging the 
 appearance of the face. 
 
 Middle Ear. The middle ear and mastoid antrum can 
 be readily examined after stripping the dura from the base 
 of the skull, by chipping off the upper surface of the petrous 
 portion of the temporal bone with a chisel, or by merely 
 opening through the thin tegmen tympani. For more careful 
 examination it will be necessary to remove the petrous portion 
 of the temporal entire and decalcify it in bulk, afterwards 
 cutting it up (Fig. 12). 
 
 Other Accessory Cavities. The frontal, ethmoidal and 
 sphenoidal sinuses can be opened up by chipping away 
 portions of their bony walls (Fig. 12). 
 
METHOD OF PROCEDURE 41 
 
 Another method is, after stripping the dura, to make a 
 saw-cut (Harke's) through the base of the skull in its 
 sagittal diameter a little to the right of the middle 
 line (Fig. 12), care having been taken in the first instance 
 to dissect the anterior flap of skin down to the root of the 
 nose, the posterior well down behind the occiput. In 
 making the saw -cut the hard palate and two upper 
 cervical vertebrae must be severed, and great care must 
 be taken not to injure the external surface of the face. 
 The two halves of the skull can then be separated and 
 the right frontal sinus, the ethmoidal labyrinth, and the 
 sphenoidal sinus examined. The nasal cavities can be 
 examined at the same time. 
 
 In all cases of meningitis careful examination should be 
 made of the cavities in the skull. 
 
 The maxillary antrum is best opened by lifting the upper 
 lip, dissecting upwards and subsequently chiselling through 
 the bony wall of the cavity. 
 
 Summary of Steps in Method of Procedure. 
 
 1. External appearances. 
 
 2. Primary incision, reflection of skin and muscles, removal 
 of sternum. 
 
 3. Examination of serous sacs pleurse, pericardium, 
 peritoneum. 
 
 4. Removal of contents of thoracic cavity, examination of 
 
 (a) (Esophagus. 
 
 (b) Larynx and trachea. 
 
 (c) Aorta. 
 
 (d) Pulmonary artery. 
 
 (e) Heart. 
 
 CO Lun g s - 
 
 (g) Mediastinal contents. 
 
 5. Ligature of intestine at junction of duodenum and 
 jejunum, and removal of whole intestinal tract. 
 
42 METHOD OF PROCEDURE 
 
 6. Removal of stomach and duodenum, liver, spleen and 
 pancreas, and examination of these in detail. 
 
 7. Removal of kidneys, suprarenals, ureters, and, if 
 necessary, of the bladder in continuity with these. 
 
 8. Removal and examination of pelvic contents and 
 testicles. 
 
 9. Examination of abdominal aorta, etc. 
 
 10. Opening up skull, removal and examination of brain. 
 
 11. Examination of base of skull and accessory cavities. 
 
 12. Removal of spinal cord. 
 
 13. Examination of peripheral nerves, bones, joints, 
 vessels, etc. 
 
 14. Opening and examination of intestine. 
 
 LETULLE'S METHOD 
 
 After the preliminary incision and the removal of the 
 sternum, the floor of the mouth is cut through close to the 
 jaw, and the tongue, pharynx, tonsils, larynx, oesophagus are 
 dissected down along with the carotid arteries, jugular veins, 
 thyroid and lymphatic glands. The pleurae are then examined. 
 Should there be no adhesions present, the left lung is drawn 
 over, the operator standing on the right side. The pleura is 
 then cut through longitudinally where it is reflected from the 
 vertebrae on to the lungs and mediastinal contents. The 
 intercostal arteries are then cut through and the oesophagus 
 and other contents of the posterior mediastinum detached from 
 the prevertebral fascia by pulling gently. The same thing is 
 then done for the right pleura, the operator standing on the 
 left side, care being taken in this case not to injure the 
 thoracic duct and the vena azygos major. The brachial plexus 
 and the subclavian arteries and veins are then cut through at 
 the inner margin of the first rib, and the whole contents of 
 neck and thorax are free. In cases where there are extensive 
 firm adhesions between parietal and visceral pleura it is 
 necessary to tear away the parietal pleura from the ribs and 
 intercostal muscles by means of the fingers. The attachments 
 
METHOD OF PROCEDURE 43 
 
 of the diaphragm are then cut through, taking care not to 
 injure stomach or liver. The whole of the parietal peritoneum 
 is then stripped, along with the abdominal contents, including 
 kidneys, vessels, etc., leaving only the psoas muscles. The 
 iliac vessels are cut through as low down as possible. The 
 peritoneum is stripped from the sides of the pelvis, the skin 
 is cut through round the anal orifice, and the whole of the 
 viscera removed and placed upon a dissecting table. 
 
 The examination of the parts in detail commences by 
 placing the viscera with their posterior aspect upwards and 
 opening the venae azygos major and minor and the thoracic 
 duct. The suprarenal glands are then removed and examined. 
 The ureters are isolated and opened, the kidneys removed and 
 examined. The aorta and the inferior vena cava are then 
 opened throughout their length. The trunk and rootlets of 
 the portal vein are isolated and opened up and the common 
 bile duct examined. The aorta is then dissected away from 
 other structures and the oesophagus and cardiac end of the 
 stomach isolated. The tongue, pharynx, and tonsils are then 
 examined and the oesophagus, trachea, and bronchi opened 
 up. The vagus and other nerves and the lymph glands 
 of the neck are investigated. The viscera being turned over, 
 the thymus and thyroid glands are examined. The superior 
 vena cava and its tributaries are then opened. Next, the 
 pericardium is opened, and the first part of the aorta, the 
 pulmonary artery and veins and their branches outside the 
 lungs are opened up. The heart is next examined externally 
 and removed from its attachments. The lungs are also 
 detached and examined. After examination of the diaphragm, 
 the liver and its bile passages are investigated and detached, 
 also the spleen. Next, the stomach, pancreas, and duodenum 
 are isolated and, along with the oesophagus, removed, opened 
 up, and examined. The intestinal canal is then examined 
 from the outside, detached, opened, and investigated in its 
 various sections. The examination finishes with the genital 
 organs and urinary bladder. 
 
 SHENNAN'S METHOD 
 The organs are removed in the following order : 
 
44 METHOD OF PROCEDURE 
 
 (1) Small intestine, with or without 
 
 (2) Large intestine. 
 
 (3) Stomach and duodenum, with liver, bile ducts through- 
 out their whole length, pancreas, spleen, and mesentery. 
 
 (4) Kidneys with suprarenals and ureters. 
 
 (5) Thoracic contents along with the cervical soft 
 structures, the aorta in its whole length, inferior -vena cava, 
 crura of the diaphragm with solar plexus and receptaculum 
 chyli. 
 
 (6) Pelvic organs, which in certain cases may be removed 
 in continuity with large intestine, and kidneys. 
 
 Stitching up Incisions. Toilet of the Body. After the 
 completion of the examination it is absolutely essential that 
 the body be restored as nearly as possible to its original 
 condition. 
 
 In the first place all fluid should be got rid of by tilting 
 the body or by swabbing out the cavities with sponges. 
 The organs are then replaced and sawdust, wool, tow, 
 or newspapers used to compensate for the loss of fluids, 
 etc. Firm plugs of wool are then placed in the mouth, 
 anus, vagina, etc., in order to prevent the escape of any 
 fluids. 
 
 The skin incisions are closed by means of the glover's or 
 blanket stitch, a packing needle and strong twine being used. 
 In carrying out this procedure the needle is always passed 
 from within outwards, the slack of the twine being held 
 firmly between the fingers of the left hand (Fig. 14). The 
 stitches should be about half an inch apart. 
 
 Finally, all trace of blood is removed from the surface of 
 the body by sponging. 
 
 Cleansing of Gloves and Hands. After completing all 
 operations in which the hands come in contact with the 
 body or its contents, the gloves, while still on the hand, 
 should be washed in cold running water, at first without, 
 then with soap. Subsequently they are washed in biniodide 
 
METHOD OF PROCEDURE 45 
 
 of mercury spirit. They are then removed from the hands, 
 and if any leakage of blood or other fluid has occurred the 
 interior should be treated in a similar fashion. 
 
 The hands are then thoroughly washed with soap in cold 
 running water. 
 
CHAPTER IV 
 
 DISEASES OF THE HEART AND PERICARDIUM 
 
 MALFORMATION OF THE HEART AND GREAT 
 VESSELS 
 
 THE heart is developed in the first instance as a single tube, 
 with primitive auricle, ventricle, and aortic bulb. The 
 structure later becomes bent upon itself and septa appear 
 in all three divisions, so that eventually there are two auricles, 
 two ventricles, and two vessels the aorta and pulmonary 
 artery. The commonest congenital malformations of the 
 heart are associated with defects in the formation of these 
 septa. 
 
 1. Defective Inter-auricular Septum. A degree of this, 
 i.e. slight patency of the foramen ovale, is a very common 
 occurrence (30-50 per cent of cases). In the vast majority 
 of the cases, owing to the smallness of the aperture and to 
 its oblique direction, there is no interference with the function 
 of the organ. In cases of stenosis of the pulmonary artery 
 or aorta, however, the defect in the septum may be marked. 
 
 2. Defective Interventricular Septum. The separa- 
 tion of the ventricle into two begins near the apex. The 
 septum rises towards the base. The last portion to form 
 is the portion represented by the " undefended spot " in the 
 
 46 
 
DISEASES OF THE HEART AND PERICARDIUM 47 
 
 fully developed heart. It is at this point that defects in the 
 septum most commonly occur. As in the case of defective 
 interauricular septum, patency is usually associated with 
 defects in the vessels, most commonly with stenosis of the 
 pulmonary artery. Complete absence of the septum results 
 in the so-called three-chambered heart. 
 
 3. Congenital Stenosis of the Pulmonary Artery. 
 
 This is one of the commonest congenital defects, and its 
 existence leads to a number of others defective inter- 
 auricular and interventricular septa and patency of the 
 ductus arteriosus. The narrowing may occur at the valves 
 or in the artery beyond the valve. The cause may be (i) 
 malformation of the septum dividing pulmonary artery from 
 aorta, the septum being found too far to the right. (2) Fcetal 
 endocarditis. All degrees of the condition to complete 
 obliteration or atresia may be found. 
 
 4. Congenital Stenosis of the Aorta. This is much 
 more rare than the preceding condition. Again, it may 
 occur at the valve or in the vessel beyond. When it occurs 
 at the valve there is usually defect of the septa superadded. 
 Stenosis of the vessel beyond, owing to the persistence of the 
 ductus arteriosus, is not of so much importance, the circulation 
 being carried on through the latter vessel. Stenosis is some- 
 times caused by a circular fibrous band at the point where 
 the ductus arteriosus joins the aorta. 
 
 5. Persistence of the Ductus Arteriosus, or, in other 
 words, patency in extrauterine life of the communication 
 between the pulmonary artery and the thoracic aorta accom- 
 panies other defects, such as narrowing of the pulmonary or 
 aortic orifices. 
 
 6. Abnormalities in the Valves. These mostly occur 
 in the semilunar valves, (a) There may in the first place be 
 complete fusion of the segments leading to stenosis, (b) There 
 
48 DISEASES OF THE HEART AND PERICARDIUM 
 
 may be only two cusps, a large and a small one, the larger in 
 some cases showing evidence of partial division into two. 
 (c) The segments may be abnormally numerous. There may 
 be four instead of three, and all differing in size, (d) The 
 segments may showfenestrations. This is a common occurrence, 
 but as the openings are usually close to the free margin, and 
 as the area of contact of the segments extends some distance 
 from the free margin, there is no incompetence of the valve 
 as a result. 
 
 Of congenital anomalies of the auriculo-ventricular valves 
 the commonest is coalescence oj the segments oj the tricuspid 
 valve. This may be due to fcetal endocarditis. It leads to 
 patency of the foramen ovale. 
 
 7. Abnormalities in the Great Vessels. There may 
 be transposition of the aorta and pulmonary artery, so that 
 the latter takes origin from the left ventricle, the former 
 from the right. Occasionally a double aorta is met with a 
 condition found normally in reptiles. Or the aorta may pass 
 to the right, the condition found in birds. 
 
 The heart may be situated to the right side of the body. This 
 may or may not be associated with transposition of the other 
 viscera. Occasionally the pericardial sac is absent and the 
 heart may be situated in the abdomen (ectopia cordis). 
 
 DISEASES OF THE PERICARDIUM 
 
 Under the term pericardium are included (i) the sac 
 formed of fibrous tissue, triangular in shape, whose base rests 
 upon the diaphragm, and whose sides are attached to the 
 pleurae laterally, the lower portion of the sternum anteriorly, 
 and the mediastinum posteriorly ; (2) the serous endothelial 
 lining of this (parietal pericardium) which is reflected on to 
 the surface of the heart (visceral pericardium or epicardium), 
 and (3) the subserous connective tissue and fat. No hard- 
 and-fast line can, of course, be drawn between diseased 
 conditions of the epicardium and those of the myocardium. 
 
DISEASES OF THE HEART AND PERICARDIUM 49 
 
 If one is affected, the other of necessity must be. For purposes 
 of classification it is necessary, however, to draw a distinction 
 between them. 
 
 After the removal of the sternum and costal cartilages the 
 position of the pericardial sac and its contents as regards the 
 other structures in the thoracic cavity should be noted, also 
 any abnormal distention of the sac. The pericardial sac is, 
 of course, one of the serous sacs or large lymphatic spaces of 
 the body, and as such it is liable to conditions which tend to 
 affect these sacs. Such are oedema or over-filling of these 
 spaces with lymph, inflammatory conditions, more particularly 
 in acute rheumatism. 
 
 Hydropericardium, or dropsy of the sac. There is 
 always a small quantity of clear, straw-coloured fluid in the 
 sac (about oz.). When this is increased to any extent the 
 term dropsy is applied. The condition is usually a late 
 manifestation of general dropsy, the cause being commonly 
 kidney or heart disease. (Edema of the tissues of the 
 pericardium themselves may not infrequently be observed, 
 either accompanied by dropsy of the sac or without it. 
 
 Hsemopericardium, or blood in the sac. This is a very 
 rare condition. It may be due to (i.) a penetrating wound 
 bullet wound or stab ; (ii.) rupture of the heart from (a) 
 degenerative changes in the muscle associated with obstruc- 
 tion to the coronary arteries (common position, the anterior 
 aspect of the left ventricle close to the septum and not far 
 from the apex), (b) abscess of the heart wall communicating 
 with one of the cavities (Fig. 16), (c) injury & crush (common 
 position, base of heart) ; (iii.) rupture of an aneurysm of the 
 heart itself, of one of the coronary arteries or of the commence- 
 ment of the aorta ; (iv.) very acute inflammation of the 
 pericardial sac. 
 
 Small extravasations of blood into the substance of the 
 subpericardial tissue (ecchymoses or petechial haemorrhages) 
 are fairly common. They are found in toxic conditions and 
 
 4 
 
50 DISEASES OF THE HEART AND PERICARDIUM 
 
 in severe anaemias. They are chiefly situated at the base 
 of the heart, and often on the posterior aspect. 
 
 Pneumopericardium, or air in the sac. A very rare 
 condition, usually associated with purulent pericarditis due 
 to rupture of the oesophagus or stomach into the sac. The 
 gas may be due to the presence of germs, e.g. B. aerogenes 
 capsulatus . 
 
 INFLAMMATION OF THE PERICARDIUM 
 (PERICARDITIS) 
 
 Types. 
 
 1. Acute pericarditis. 
 
 (a) Fibrinous, (b) serous, sero-fibrinous, (c) puru- 
 lent, (d) hsemorrhagic. 
 
 2. Chronic pericarditis, (a) following acute, (b) " milk 
 
 spot." 
 
 3. Adherent pericardium. 
 
 4. Tuberculous pericarditis. 
 
 i. Acute Pericarditis. This is due invariably to the 
 presence of some germ. Those more commonly found are 
 micrococcus rheumaticus, staphylo cocci, streptococci, pneumo- 
 cocci, etc. The condition occurs in the course of acute 
 rheumatism, pyaemia, pneumonia, kidney disease, the 
 organisms reaching the per;cardial sac by the blood or by 
 continuity of tissue from lung, pleura, mediastinum, or 
 heart wall. 
 
 The essential point in pericarditis is the presence of an 
 exudate on the surface of the pericardium which coagulates, 
 thus roughening it and causing it to lose its gloss. The 
 amount of this exudate may be very small, forming a mere 
 roughness on the surface, or it may occur as an irregular, 
 thick, opaque, white layer producing a shaggy appearance 
 (cor villoswn) (Fig. 15). If the pericardial surface is visible 
 the vessels are seen to be injected. The exudate may be 
 
DISEASES OF THE HEART AND PERICARDIUM 51 
 
 red in colour from haemorrhage. The amount of fluid in 
 the sac in this condition is variable. Sometimes it is small, 
 forming the so-called " dry/' plastic, or fibrinous variety, 
 found more especially in kidney disease and in pneumonia. 
 More commonly there is some free fluid with flakes of lymph 
 floating in it. In such a case the term " serous " or " sero- 
 fibrinous " may be applied. In some cases the fluid is 
 purulent, more especially in pyaemia or septicaemia. Occa- 
 sionally, in intense inflammations, blood in considerable 
 amount is mixed with the exudate (hcemorrhagic pericarditis). 
 In the early stages the fibrinous exudate can easily be re- 
 moved. Later on, when organisation has commenced, it 
 will be found bound down by fine threads which represent 
 penetrating young blood-vessels. 
 
 Microscopic Appearances. The vessels of the subpericardial 
 tissue are dilated. There is a meshwork of fibrin on the 
 surface of the pericardium, and some in the spaces of the 
 tissue itself. Numerous leucocytes (chiefly polymorphonuclear) 
 are found infiltrating the pericardial tissue and caught in the 
 meshes of the fibrin on the surface. In the early stages the 
 endothelial cells are swollen and vacuolated ; later they 
 become detached and occur in the fibrin. 
 
 Later on, evidence of organisation of the exudate is found. 
 The endothelial cells of the vessels of the subepicardial tissue 
 are swollen and show evidence of proliferation. Small buds 
 can be seen protruding from these vessels and making their 
 way into the fibrinous exudate. At the same time there is 
 swelling and proliferation of the connective-tissue cells generally. 
 The newly formed cells (fibroblasts), which are at first small 
 and rounded, with a fair amount of pale-staining protoplasm 
 and a rounded, relatively small nucleus, accompany the newly 
 formed vessels into the exudate. Where organisation is 
 advanced, the fibroblasts farthest from the pericardium will 
 still be rounded, the deeper ones will be spindle-shaped and 
 arranged parallel with the vessels ; still nearer the pericardial 
 surface they tend to lie parallel with that surface and perpen- 
 dicular to the direction of the new blood-vessels. From the 
 
52 DISEASES OF THE HEART AND PERICARDIUM 
 
 protoplasm of these older fibroblasts the collagenous fibres of 
 the new tissue are developed. 
 
 In suitably stained specimens micro-organisms may be 
 found. 
 
 Results : (i) the exudate may be absorbed, and matters 
 return to the normal. 
 
 (2) Organisation with union between heart and pericardial 
 sac may take place (Adherent Pericardium). This union 
 may be partial or complete. If complete, more especially if 
 the surrounding tissues of the mediastinum participate in the 
 inflammatory process, great interference takes place with the 
 action of the heart, with the result that it tends to dilate. 
 
 (3) If the exudate be not absorbed it may be the seat 
 of deposit of lime salts, the result being the formation of 
 calcareous plates. This is a rare occurrence. 
 
 2. Chronic Pericarditis. This may follow acute, or it 
 may develop slowly, the result of friction, (a) Following 
 acute, the condition is usually associated with adhesion be- 
 tween visceral and parietal pericardium, (b) A more common 
 variety of it consists in the fibrous thickenings of the peri- 
 cardium, of ten called "milk spots" or "soldier's spots." These 
 are white, opaque, well-defined areas, often with a tendinous 
 appearance. They are most frequently found on the anterior 
 surface of the right ventricle. Another common site is the 
 anterior surface of the left ventricle close to the apex. Similar 
 areas are often found thickly covering the surface of the 
 auricles. They are also not infrequently found along the 
 course of the coronary arteries. They are more particularly 
 found in hypertrophied and dilated hearts, and are due to 
 constant friction. 
 
 Microscopically all that is to be seen is a thickening of 
 the fibrous tissue under the endothelium. 
 
 3. Adherent Pericardium. This condition not infre- 
 quently follows acute fibrinous pericarditis. The layers of 
 
DISEASES OF THE HEART AND PERICARDIUM 53 
 
 fibrin on visceral and parietal pericardium become organised. 
 Young connective tissue forms between these layers, and the 
 heart is permanently attached to the pericardial sac. This 
 may occur over a limited area, frequently at the apex of the 
 left ventricle. Very often, however, it occurs all over. The 
 inflammatory change may also spread to surrounding struc- 
 tures, such as pleura, mediastinum. The mediastinal glands 
 are enlarged and firm. In this condition the heart is usually 
 enlarged, the cavities being dilated and their walls thickened. 
 There is backward pressure from relative incompetence of 
 the valves, and chronic venous congestion of the organs, 
 such as lung, liver, and spleen. The condition not in- 
 frequently causes death from constant excessive strain on 
 the heart. 
 
 4. Tuberculous Pericarditis. This may occur as a sub- 
 acute condition associated with the presence of small grey 
 and yellow nodules of tubercle. It is often combined with 
 general miliary tuberculosis. Sometimes the tubercle nodules 
 are found along the course of the coronary vessels without 
 any other evidence of inflammation being present, and some- 
 times there is excessive distention of the pericardial sac by 
 fluid. Tuberculous pericarditis is, however, a rare condition 
 in the human subject. It is relatively much more frequent 
 in the bovine species. 
 
 DISEASES OF THE MYOCARDIUM 
 
 DEGENERATIVE CHANGES 
 
 Atrophy. In old age and in wasting diseases, such as 
 tuberculosis and cancer, the heart tends to get smaller, 
 sometimes being reduced to one-third of its usual size. As 
 the process goes on, the epicardium, which does not participate 
 in the shrinkage, becomes wrinkled, the vessels more tortuous, 
 
54 DISEASES OF THE HEART AND PERICARDIUM 
 
 and the fat under the epicardium reduced in amount. At 
 the same time the muscle substance becomes a darker brown 
 colour. This condition is known as brown atrophy. The 
 brown colour is due to the increase of the pigment found 
 normally in the muscle cells, and is probably a coloured fat 
 or lipochrome. 
 
 Microscopically the individual fibres of the myocardium 
 are sometimes smaller than normal, but the main change is 
 an increase of the golden yellow granules of pigment which 
 are found in small amount normally at the two poles of the 
 nuclei. 
 
 Cloudy Swelling. This condition is found accompanying 
 infective diseases, more especially those associated with high 
 temperature. The muscle substance is pale, soft, and friable. 
 The friability can be tested by pushing a ringer into the 
 muscle. 
 
 Microscopically there is often very little alteration to be 
 seen. The individual fibres are somewhat swollen and 
 granular, and there may be some loss of longitudinal and 
 occasionally of transverse striation. 
 
 Fatty Changes. Types. 
 
 1. Due to increase in the subpericardial fat. 
 
 (a) Fatty loading. 
 
 (b) Fatty infiltration. 
 
 2. Due to degenerative changes in the muscle fibres 
 
 (fatty degeneration). 
 
 (a) Diffuse form. 
 
 (b) Patchy form. 
 
 i. Fatty Loading and Fatty Infiltration. This condition 
 comes, strictly speaking, under diseases of the pericardium, 
 but for the sake of contrast with fatty degeneration it may 
 be taken here. 
 
 There is in all healthy hearts a certain amount of fat in 
 the subpericardial tissue, more especially in that covering 
 
DISEASES OF THE HEART AND PERICARDIUM 55 
 
 the right ventricle. It occurs particularly along the lines of 
 the vessels and at the base between the auricles and ventricles. 
 In very fat people this adipose tissue is increased in amount, 
 so that not infrequently the whole of the anterior surface of 
 the right ventricle may be covered by it. This is what is 
 known as fatty loading of the heart. The increase of fat may 
 also occur in anaemia and in association with atrophy of the 
 heart muscle. 
 
 As the fat increases in amount it tends to make its way 
 along the lines of the vessels which penetrate into the muscle 
 substance, leading to indistinctness in the line which separates 
 fat from muscle. When this has occurred, the term fatty 
 infiltration is applicable (Fig. 18). The fat in this way tends 
 to separate the bundles of muscle substance from one another, 
 and to cause an atrophy of these by pressure. This fatty 
 infiltration of the heart often accompanies fatty loading, but 
 it may occur where there is relatively little increase in the 
 amount of subpericardial fat. 
 
 Microscopically, the rounded fat globules can be seen 
 passing down from the subpericardial fat along the lines of 
 the vessels into the muscle substance. The muscle fibres 
 themselves are compressed and atrophied. 
 
 2. Fatty Degeneration. This is a totally different condition 
 from the preceding. It is a degenerative change in the 
 muscle fibres themselves. It is found more especially in toxic 
 conditions, such as alcoholic or phosphorus poisoning, 
 bacterial diseases, and in severe anaemias. Two forms of 
 it are distinguished : (i) a diffuse form, where the whole 
 muscle substance is uniformly pale, soft, and friable ; (2) a 
 patchy form, which is usually best seen towards the inner 
 portion of the wall of the left ventricle, more especially in 
 the papillary muscles. In this position the muscle has a 
 mottled appearance, with small transverse parallel patches 
 the so-called " thrush breast " mottling or " tabby cat " 
 striation. 
 
56 DISEASES OF THE HEART AND PERICARDIUM 
 
 Microscopically groups of muscle fibres are found contain- 
 ing numerous small droplets of fat in their protoplasm. 
 
 ALTERATIONS OF THE CIRCULATION 
 
 Chronic Venous Congestion. This occurs in conditions 
 where there is backward pressure on the right auricle and 
 therefore on the blood in the coronary sinus. It is accom- 
 panied by chronic venous congestion in other organs. The 
 muscle substance is firmer and thicker than usual and is dark 
 in colour. 
 
 Microscopically there is distention of the veins and 
 capillaries with blood. 
 
 Effects of Obstruction of the Coronary Arteries on the 
 Myocardium. The branches of the coronary arteries within 
 the heart belong to the group of what were originally called 
 " end " arteries. They are not as a matter of fact entirely 
 devoid of collateral communications, as the name would 
 indicate, but such communications as they have are small, so 
 that when a branch is blocked the circulation cannot be fully 
 restored, and infarction occurs. The effect of the obstruction 
 of these branches upon the heart depends to a large extent 
 upon whether it is sudden and complete, or whether it occurs 
 slowly y and is therefore, for some time at any rate, partial. 
 
 i. The effect of sudden obstruction of a large branch of one 
 of the coronary arteries is, as a rule, to produce instant death. 
 When the branch is a small one and the patient survives, 
 infarction occurs. The cause of the obstruction is either 
 thrombosis upon an atheromatous patch in the artery or 
 impaction of an embolus. More usually it is the former. 
 In all cases of unexplained sudden death careful search should 
 be made for such thrombi by slitting up the branches of the 
 coronary vessels. 
 
 The infarcted area is commonly in the anterior wall of the 
 left ventricle, in the part of the myocardium, that is to say, 
 
DISEASES OF THE HEART AND PERICARDIUM 57 
 
 supplied by the left coronary artery. The area is roughly 
 triangular in shape, with the broad base towards the interior 
 of the ventricle. It may be red or pale. In the early stages 
 it is usually red, becoming pale later on, as necrosis supervenes. 
 Ultimately connective tissue develops, and all that is left 
 is a fibrous scar. 
 
 Owing to the weakening of the muscle at the point of 
 infarction, aneurysmal dilatation of the wall may occur, or 
 even sudden, complete rupture. 
 
 Microscopic Appearances. In the early stages the muscle 
 is found infiltrated with red blood corpuscles. The muscle 
 fibres are swollen, have lost their transverse striation, and 
 stain deeply. The nuclei lose their staining reaction. Later, 
 the area becomes infiltrated with leucocytes and young con- 
 nective-tissue cells. The degenerated fibres are absorbed 
 and connective tissue takes their place. 
 
 2 . Slow Progressive Narrowing of the Coronary Arteries. This 
 is due as a rule to thickening of the intimafrom atheromatous 
 change. It leads to degenerative changes of a fatty nature 
 in the muscle fibres of the area supplied, and a gradual replace- 
 ment of these by well-developed fibrous tissue. As it is the 
 anterior or descending branch of the left coronary artery which 
 is usually the seat of the most marked change, the fibrosis 
 occurs in the wall of the left ventricle near its apex, in the 
 papillary muscles (Fig. 17), and in the interventricular septum. 
 Owing to the weakening of the heart wall, rupture or 
 aneurysmal dilatation may occur. The change produced 
 is precisely the same as that described under chronic interstitial 
 myocarditis. Indeed, slow progressive narrowing of the 
 branches of the coronary artery is the commonest cause of 
 that condition. 
 
 Aneurysm of the Heart. This is most frequently met 
 with towards the apex of the left ventricle. The causation 
 in such cases is usually progressive narrowing of the descending 
 branch of the left coronary artery. The connective tissue 
 
58 DISEASES OF THE HEART AND PERICARDIUM 
 
 which takes the place of the degenerating muscle is unable 
 to withstand the pressure within the ventricle. The condition 
 may also develop acutely from infarction of the heart muscle 
 or acute myocarditis (Fig. 16). On the inner aspect of such 
 dilatations, thrombosis tends to occur. An aneurysm of 
 one of the sinuses of Valsalva may also penetrate the heart 
 muscle. 
 
 INFLAMMATION OF THE MYOCARDIUM 
 
 (MYOCARDITIS) 
 Types. 
 
 1. Acute myocarditis. 
 
 (a) Non-suppurative, (b) suppurative. 
 
 2. Chronic interstitial myocarditis. 
 
 (a) Following acute, (b) associated with narrowing 
 of the coronary arteries, (c) due to chronic 
 inflammatory conditions (tubercle, syphilis). 
 
 1. Acute Myocarditis. This maybe due to (i) spread of 
 inflammation from the pericardium or endocardium, or to 
 (2) blood infection, as in acute rheumatism, ulcerative endo- 
 carditis, pyaemia, etc. The muscle substance may show little 
 alteration from the normal. It is somewhat soft, friable, 
 pale, and mottled. In the special type suppurative 
 myocarditis small abscesses are seen as minute white points 
 surrounded by zones of congestion and haemorrhage. Very 
 occasionally large abscesses may form which lead to rupture 
 of the heart (Fig. 16). 
 
 Microscopically the muscle substance is found infiltrated with 
 leucocytes, more especially in the neighbourhood of vessels. 
 The leucocytes may be aggregated into large masses, with 
 haemorrhage around and plugs of cocci in the centre of the 
 abscesses. The muscle fibres themselves show cloudy swelling, 
 or, in the neighbourhood of abscesses, actual necrotic change. 
 
 2. Chronic Interstitial Myocarditis. In this condition 
 there is a replacement of the muscle substance by fibrous tissue. 
 
DISEASES OF THE HEART AND PERICARDIUM 59 
 
 It may (i) follow acute myocarditis, (2) be associated with 
 narrowing or obstruction of the coronary artery or its branches, 
 (3) occur in connection with chronic inflammatory diseases, 
 such as tubercle and syphilis. The commonest cause is 
 undoubtedly narrowing of branches of the coronary artery. A 
 slight degree of the condition is often seen in old age due to 
 the same cause. 
 
 The condition is usually most marked in the wall of the 
 left ventricle near the apex. It should also be sought in 
 the papillary muscles. The muscle substance in these areas 
 is partially replaced by white or grey fibrous strands 
 (Fig. 17). The endocardium is often thickened over a 
 corresponding area and thrombosis is frequently associated. 
 The condition may give rise to aneurysmal dilatation of the 
 heart wall. 
 
 Microscopically the groups of muscle fibres are found 
 separated from one another by bands of well-developed fibrous 
 tissue. The isolated muscle fibres are often unusually large, 
 with large, dark-staining nuclei. 
 
 Syphilis of the myocardium is occasionally met with 
 either as gumma formation or as a diffuse interstitial myo- 
 carditis associated with arterial disease. 
 
 Tuberculosis of the myocardium is also a very rare 
 condition. It may be met with as small miliary tubercles 
 or as large caseous masses. 
 
 HYPERTROPHY OF THE HEART 
 
 A general hypertrophy of the heart occurs in those, such 
 as athletes, who constantly over-exert themselves. It also 
 occurs in pregnancy. Hypertrophy of one or more chambers 
 of the heart is usually associated with chronic valvular 
 lesions. Conditions, other than cardiac lesions, associated 
 with hypertrophy of certain cavities are emphysema and 
 
60 DISEASES OF THE HEART AND PERICARDIUM 
 
 chronic interstitial disease of the lungs with hypertrophy of 
 the right ventricle, chronic kidney disease, and arteriosclerosis 
 with hypertrophy of the left ventricle (Fig. 24). 
 
 DILATATION OF THE HEART 
 
 General dilatation of the heart is found in association 
 with degenerative changes, such as cloudy swelling and fatty 
 degeneration. The dilatation is usually most marked on 
 the right side. In adherent pericardium of any marked 
 degree the heart as a whole tends to dilate. 
 
 Dilatation of the right side is found as a rule in cases of 
 death from heart failure. It also occurs in chronic valvular 
 disease involving the mitral or aortic valve. Dilatation of 
 the left ventricle associated with hypertrophy occurs in a 
 marked degree in cases of aortic incompetence. 
 
 Tumours of the heart are excessively rare. Primary 
 tumours such as fibromata or myomata are described. 
 Secondary tumours sarcomata and carcinomata occa- 
 sionally occur, but may involve the heart very extensively 
 before they result in death. 
 
 DISEASES OF THE ENDOCARDIUM 
 
 DEGENERATIVE CHANGES 
 
 Bed staining of the endocardium is found as a result of 
 putrefactive processes, also in septic conditions. It is due to 
 the setting free of haemoglobin from the red blood cells. 
 
 Small haemorrhages may occur under the endocardium in 
 infective conditions and anaemia. 
 
 Areas of fatty degeneration occur as white specks or 
 patches, more especially in infective conditions, in anaemias, 
 and in cases of phosphorus and chloroform poisoning. These 
 areas occur chiefly on the valves. Under the microscope the 
 
DISEASES OF THE HEART AND PERICARDIUM 61 
 
 protoplasm of the endothelial and of the subjacent connective- 
 tissue cells is found filled with fat globules. 
 
 Calcareous and uratic deposits are found more especially 
 in the valves, and chiefly in association with chronic inflam- 
 mation. They appear as opaque white or yellow areas of 
 thickening, sometimes with a roughened surface, on which 
 thrombi may be deposited. 
 
 Atheromatous change, both the early stage with thicken- 
 ing of the endocardium and fatty degeneration and the later 
 stage of calcification, may be found, more especially as an 
 extension from the aorta. There is no hard-and-fast line 
 between this condition and the fatty change already men- 
 tioned. 
 
 CLOTS IN THE HEART 
 
 Thrombi are clots formed within the heart or the vessels 
 during life. In the heart they form chiefly where the blood 
 current is slow or where there are eddies. These conditions 
 are present more especially in the auricular appendices. 
 The commonest site for thrombi is the right auricular appendix 
 (Fig. 19). Thrombi also occur in the ventricles towards the 
 apex, when they are usually associated with degenerative 
 changes in the myocardium. They also occur behind the 
 curtains of the auriculo- ventricular valves. They are 
 frequent on the surfaces of the valves, being known in this 
 situation as vegetations. 
 
 Thrombi are usually of the mixed red and white type. 
 The colourless portions are opaque white, and more or less 
 stringy. Thrombi are usually adherent to the heart wall. 
 
 When thrombi are present in the chambers of the heart 
 infarcts should be looked for in the various organs. If the 
 thrombus is on the right side the infarcts will be found in 
 the lung (except in the rare case of a patent foramen ovale), 
 if on the left side the infarcts may be in brain, spleen, kidney 
 or intestine (see Diagram, p. 62). 
 
Plan of the Circulation to show the Origin and Destination of the more 
 
 common Emboli. 
 
 i, i, i are thrombi in iliac vein (I.V.), or its branches, e.g. superficial veins of leg 
 uterine veins, Superior Vena Cava (S.V.C.)> or its branches, e.g. cerebral sinuses, 
 right auricular appendix (R.A.A.) and right ventricle (R.V.), which may give 
 rise, by washing away of portions, to infarcts (li) in the lung (Lu). 2, 2, 2 are thrombi 
 in left auricular appendix (L.A.A.), on mitral valve (M.V.)> in left ventricle (L.V.), on 
 aortic valve (A.V.) and on wall of aorta (A), which may give rise, by washing away 
 of particles, to infarcts 2i, 2i, 2i in brain (B), intestine (i), spleen (S), kidney (K). 
 3 is a thrombus in rootlet of portal vein (PV) which might give rise to infarction or, 
 if septic, to abscess-formation in the liver (L). 
 
DISEASES OF THE HEART AND PERICARDIUM 63 
 
 Post-mortem clots, on the other hand, are red or yellow, 
 translucent or transparent, jelly-like masses which are not 
 adherent. Clots often cling to the columnae carneae, but they 
 are not really adherent to the heart wall. 
 
 " Agonal " clots occupy a position between the true 
 thrombi and the post-mortem clots. They are more opaque 
 than the clots, they may be stringy, but are not adherent. 
 They are found more particularly on the right side of the 
 heart, extending up into the pulmonary artery. They may 
 completely fill the right auricle and ventricle. They are 
 found especially in pneumonia and other infective conditions. 
 
 Rounded thrombi lying free in the auricles, so-called 
 " ball " thrombi, are sometimes found in cases of stenosis of 
 the mitral valve. They, as well as other thrombi in the 
 auricles, often show softening, sometimes liquefaction of their 
 interior (red or simple softening). 
 
 (For microscopic appearances of thrombi, see p. 88.) 
 
 
 Thrombi. 
 
 Agonal Clots. 
 
 Post-mortem 
 Clots. 
 
 Position. 
 
 Auricular appendices, 
 valves (vegetations). 
 Apices of ventricles. 
 
 Mainly right auricle, 
 ventricle and pul- 
 monary artery. 
 
 Anywhere, but 
 chiefly on 
 right side. 
 
 Appearances. 
 
 Opaque, white, buff- 
 coloured or red. 
 
 Semi-opaque. Often 
 fill cavity. 
 
 Transparent. 
 
 Consistence. 
 
 Stringy, friable, some- 
 times softened in 
 
 Soft and gelatinous. 
 
 
 centre. 
 
 
 Relations 
 to heart 
 walls. 
 
 Adherent. When 
 broken off, leaving 
 portions behind. 
 
 Non-adherent. May cling to columnse 
 carneae, hordae tendinaceae, etc. 
 
 Associated 
 
 Chronic valvular dis- 
 
 Infective conditions such as acute 
 
 diseased 
 conditions 
 
 ease of heart. 
 Chronic interstitial 
 
 lobar pneumonia, pyaemia, septi- 
 caemia. 
 
 
 myocarditis. Aneu- 
 rysm of heart wall. 
 
 
64 DISEASES OF THE HEART AND PERICARDIUM 
 
 INFLAMMATION OF THE ENDOCARDIUM 
 (ENDOCARDITIS) 
 
 The endocardium possesses no direct blood-supply, nor 
 do the semilunar or auriculo-ventricular valves. This fact 
 in all probability accounts for the rarity of inflammatory 
 phenomena in the ordinary sense of the term in connection 
 with these structures. On the other hand, the intimate 
 connection between endocardium and valves and the circulating 
 blood renders these structures peculiarly susceptible to the 
 action of germs or poisons which may be present in the blood- 
 stream. Once the endocardium is damaged, thrombosis tends 
 to occur upon the injured surface, with the formation of what 
 are called vegetations. Another fact in the production of 
 the more chronic types of endocarditis is strain. Thus the 
 valves of a dilated and powerfully acting heart tend to become 
 thickened. 
 
 Types. 
 
 1. Acute endocarditis. 
 
 (a) Simple or vegetative. 
 
 (b) Ulcerative or malignant. 
 
 2. Chronic endocarditis. 
 
 (a) Following acute. 
 
 (b) Associated with atheroma. 
 
 (c) Associated with strain. 
 
 i. Acute Endocarditis. This condition is probably in- 
 variably due to the presence of germs upon the endocardium. 
 Two sub- varieties are distinguished : (a) simple or vegetative, 
 and (b) ulcerative or malignant. There is no hard-and-fast 
 line between these two. They are both due to the presence 
 of germs, and may be due to the same germs. The simple 
 type, however, has a very constant relationship to acute 
 rheumatism, and is thus caused probably by the micrococcus 
 rheumaticus. The malignant type may be caused by a 
 variety of germs, such as pneumococcus , streptococci, staphy- 
 lococci, gonococcus. 
 
DISEASES OF THE HEART AND PERICARDIUM 65 
 
 In both varieties the essential change is the presence on 
 the damaged valve of vegetations or thrombi, and, as stated 
 above, no hard-and-fast line can be drawn between the two 
 conditions. In deciding in any case as to which condition 
 is present the following points should be attended to. (i) 
 Character of vegetations. These in the ulcerative type tend 
 to be larger and more friable. (2) Extent. In simple 
 endocarditis the vegetations are limited to a line close to the 
 free margin of the valve ; in ulcerative endocarditis they 
 extend not merely all over the valve but on to the surface 
 of auricle in the case of mitral disease, on to aorta or heart 
 wall in the case of aortic disease ; also in the case of 
 the mitral valve they extend on to the chordae tendinese. 
 (3) Effect on valves. In the case of simple endocarditis 
 beyond swelling of the valve no special change is observed. 
 In the ulcerative type destruction of the valve, aneurysm or 
 rupture of the valve or of the chordae tendinese is often 
 met with. As regards the site, both varieties are found 
 much more commonly on the left side of the heart. When 
 endocarditis occurs during foetal life it is found more fre- 
 quently on the right side. 
 
 (a) Simple Acute Endocarditis. This is usually met in 
 connection with the mitral and aortic valves, more rarely 
 on tricuspid or pulmonary valves. It is most commonly 
 associated with acute rheumatism, but may be found in cases 
 of tonsillitis, chorea, scarlet fever, and septicaemia . The 
 valves themselves are somewhat swollen, and on the 
 segments is a fringe consisting of larger or smaller numbers 
 of warty projections (vegetations) (Figs. 20 and 21). These 
 vegetations are found not at the free margin but on a line 
 a short distance from that margin. In the case of the 
 mitral valve they are to be found on the upper or auricular 
 surface, in the case of the aortic valve on the lower or 
 ventricular. The line on which they occur is that of 
 
 5 
 
66 DISEASES OF THE HEART AND PERICARDIUM 
 
 maximum pressure of the valves during closure. The 
 vegetations may be soft, friable, and easily removed, or firm 
 and adherent. Infarcts are frequently found in such organs 
 as spleen and kidney. 
 
 Microscopic Appearances. The various cellular and fibrous 
 elements in the valve are separated from one another owing 
 to oedema. There may be fibrin present in the connective- 
 tissue spaces, and usually polymorphonuclear leucocytes and 
 young connective-tissue cells and other wandering cells are 
 found, in addition to the fixed tissue elements. On the surface 
 of the valve there is a mass of granular material staining 
 with acid dyes, and consisting of blood platelets and fibrin. 
 In addition there may be fibrin threads. There are usually 
 numerous white blood corpuscles which are found in groups. 
 Red cells may be present at the free margin, and masses of 
 germs can be demonstrated by suitable methods in some cases. 
 In the later stages evidence of organisation may be found at 
 the junction of valve and thrombus. Spindle-shaped and 
 rounded cells may be seen making their way in from the valve 
 to the vegetation. These are fibroblasts resulting from the 
 division of the connective-tissue cells of the valve. 
 
 (b) Ulcerative Endocarditis. In this type the valve may 
 present the same appearance of slight swelling. It is often 
 thickened from previous endocarditis. The vegetations tend 
 to be larger and more friable. They are not limited to the 
 margin of the valve but extend on to auricle or chordce tendinece 
 (Fig. 22), ventricle, or aorta. There may be destruction of 
 the valve substance with ulceration, aneurysmal dilation of a 
 segment, or complete rupture (Fig. 23). Rupture of such 
 structures as chordce tendinece also occurs. Owing to the 
 greater friability there is an increased tendency to embolism 
 and infarction. Also the infarcts may be septic. 
 
 Microscopically, the infiltration of the valve with inflam- 
 matory cells is more marked. The other appearances are 
 the same, except that masses of micro-organisms tend to be 
 larger and more numerous. Actual destruction of the valve 
 substance may be found. 
 
DISEASES OF THE HEART AND PERICARDIUM 67 
 
 Simple or Vegetative. Malignant or Ulcerative. 
 
 Character of 
 vegetations. 
 
 Extent. 
 
 Appearance of 
 valves. 
 
 Associated 
 conditions. 
 
 Causal organ- 
 ism. 
 
 Small, firm. 
 
 Limited to line close to 
 free margin of valve. 
 
 Very little alteration, 
 slight swelling. 
 
 Chorea, acute rheu- 
 matism, scarlet fever, 
 infarcts in spleen, 
 etc. 
 
 Micrococcus rheumati- 
 cus, found in many 
 cases. 
 
 Large, friable. 
 
 Tendency to extend to wall of 
 auricle, and ventricle, to 
 chordae tendineae, aorta, etc. 
 
 Destruction of valve, aneur- 
 ysm- formation, rupture of 
 valve or chordae tendineae. 
 Valve often already thick- 
 ened from previous acute 
 endocarditis. 
 
 Pyaemia, greater tendency to 
 formation of infarcts and 
 embolic abscesses. 
 
 Pneumococcus, Gonococcus, 
 Staphylococci, Streptococci. 
 
 Results of Acute Endocarditis. 
 
 (a) The conditions may return to the normal, the inflam- 
 matory exudate and vegetations being absorbed. 
 
 (b) The proliferated connective -tissue cells may settle 
 down and form new connective tissue, vessels at the same 
 time penetrating the valve from the nearest vascular area. 
 The new connective tissue shrinks and the valve remains 
 permanently thickened and altered. In other words, what is 
 called chronic endocarditis supervenes. This very frequently 
 happens with resulting stenosis or incompetence of the valve. 
 
 (c) A second attack is not infrequent when a valve has once 
 been the seat of inflammatory change. As already stated, 
 the ulcerative type tends specially to occur in the case of 
 valves already damaged. 
 
68 DISEASES OF THE HEART AND PERICARDIUM 
 
 (d) Embolism and infarction due to blocking of branches 
 of the systemic arteries are very commonly met with, more 
 especially in the case of the ulcerative type of the disease. 
 
 2. Chronic Endocarditis. This condition may (i) follow 
 an acute endocarditis owing to organisation and subsequent 
 laying down of new connective tissue, (2) arise slowly owing 
 to the action of chronically acting poisons, such as lead, 
 alcohol, syphilis, retained products of metabolism (gout), or 
 (3) it may be due to strain. Chronic thickening of the 
 endocardium lining the cavities of the heart occurs sometimes 
 when the cavities are the seat of chronic dilatation. 
 
 The valve which is the seat of this change is thickened. 
 The thickening may be chiefly at the line of attachment, 
 may be near the margin, or may occur throughout. The 
 valve is thus opaque and white or yellow in colour. The 
 segments are usually shrunken, misshapen, and may be united 
 together so that the orifice is narrowed (Figs. 26 and 27). 
 Such thickened valves are often the seat of calcareous 
 deposits which appear as more opaque, yellow masses in the 
 substance of the valve. Sometimes the endocardium over 
 the calcareous deposit necroses from want of nourishment, 
 and so thrombus formation may take place upon the cal- 
 careous surface laid bare. 
 
 Microscopically such valves may show little beyond an 
 amount of well-developed fibrous tissue greater than usual. 
 Hyaline degeneration may take place in this connective tissue, 
 also calcareous deposit. 
 
 Results of Chronic Endocarditis. The chief results are : 
 (i) Narrowing of the valve from adhesion between its 
 segments, contraction of its fibrous elements, or from both 
 causes (stenosis). (2) Failure of the valve to perform its 
 function of closure of the orifice, due to shrinkage and contrac- 
 tion of its segments (incompetence). In consequence of 
 these two results of the changes in the valves themselves an 
 
DISEASES OF THE HEART AND PERICARDIUM 69 
 
 extensive series of alterations may take place in the various 
 chambers of the heart and in the circulation generally. The 
 diseased condition of the valves, with the accompanying 
 changes in the circulation, is generally known as chronic 
 valvular disease of the heart. According to the valve affected 
 and the type of the lesion, different varieties are distinguished. 
 
 EFFECT ON THE HEART AND CIRCULATION OF 
 THE DIFFERENT TYPES OF CHRONIC VAL- 
 VULAR DISEASE 
 
 i. Mitral Stenosis. This is perhaps the best defined 
 type of chronic valvular disease. It is found chiefly in 
 women, and is due invariably to the adhesion, shrinking, 
 and contraction of the two segments of the mitral valve 
 following acute endocarditis of the valve, very often of 
 rheumatic origin. The valve is thickened, opaque, the 
 segments are united together, and the opening may be a slit 
 and nearly flush with the attachment of the valve (buttonhole 
 mitral) (Fig. 26), or more or less circular and some distance 
 below the level of the attachment of the segments (funnel- 
 shaped mitral). The amount of narrowing varies in different 
 cases. Occasionally the contraction is so marked that the 
 valve will not admit the tip of the finger, scarcely a crow 
 quill. 
 
 The process of narrowing occurs slowly, so that the effect 
 is only gradually felt by the heart. This being the case, the 
 left auricle, upon which the strain falls, gradually dilates and 
 its wall thickens in order to overcome the obstruction. For 
 a time the hypertrophied left auricle may be equal to the 
 task of driving the blood through the narrowed orifice. 
 Eventually, however, the tendency is for the backward 
 pressure to tell upon the pulmonary circulation, so that the 
 lungs show chronic venous congestion. Not infrequently 
 the pulmonary artery exhibits in this condition well-marked 
 
70 DISEASES OF THE HEART AND PERICARDIUM 
 
 patches of fatty change (atheroma). Through the lungs 
 the pressure tells back upon the right side of the heart, the 
 cavities of which become dilated and their walls thickened 
 (Fig. 25). At the same time the backward pressure tells upon 
 the whole venous system, with the result that chronic venous 
 congestion develops in all the organs and viscera, including 
 the heart, as well as in the tissues and limbs. The degree of 
 this congestion depends upon the capacity of the heart to 
 respond to the demands made upon it. When the heart 
 fails to respond, or, as it is usually expressed, when com- 
 pensation fails, the congestion becomes extreme, and oedema 
 or dropsy tends to appear, more especially in the tissues of 
 the lower limbs. 
 
 The left ventricle in mitral stenosis tends to receive less 
 blood than usual. Its work is not necessarily interfered 
 with. In consequence, it either does not enlarge or it may 
 even become smaller. A degree of incompetence of the 
 valve is usually present in mitral stenosis, especially in 
 advanced cases owing to stiffness of the segments. In cases 
 where the incompetence is marked the left ventricle will tend 
 to dilate. 
 
 2. Mitral Incompetence. This lesion may occur alone, 
 or it may be combined with a degree of narrowing. It may 
 be associated with thickening and contraction of the valves 
 from a previous acute attack of endocarditis, or, on the other 
 hand, the incompetence of the valve may be merely relative, 
 due to a lax or stretched condition of the band of circular 
 muscle fibres which surround the base of the valve and 
 assist in its closure, or due to dilatation of the ventricle 
 carrying outward the attached papillary muscles. In appear- 
 ance the valves are usually thickened, shrunken, and con- 
 tracted towards their attachment. Not infrequently the 
 chordae tendineae are also thickened and shortened. The 
 lesion is associated with dilatation and hypertrophy of the 
 
DISEASES OF THE HEART AND PERICARDIUM 71 
 
 left ventricle, then of the left auricle. The lungs become 
 congested, and through the lungs the pressure tells back 
 upon the right side of the heart. Thus the heart in this con- 
 dition tends to undergo more or less uniform enlargement. 
 
 3. Aortic Incompetence. This condition is due to 
 thickening and shrinking of the segments of the aortic valve. 
 It is often associated with a degree of stenosis. The cause 
 may be : (a) a previous acute endocarditis of the aortic 
 valve which is not infrequently associated with endocarditis 
 of the mitral valve ; (b) the spread of disease (atheromatous 
 or syphilitic) from the aorta ; (c) occasionally it may be 
 due to traumatic rupture of a segment which, however, is 
 usually already the seat of chronic changes ; (d) very rarely it 
 is caused by congenital malformation or fcetal disease. The 
 condition occurs most commonly in men and in later life. 
 
 In consequence of the failure of the segments to close 
 the orifice during diastole, blood flows backwards again into 
 the left ventricle from the aorta. The cavity has thus to 
 accommodate this blood in addition to what comes normally 
 through the mitral orifice. The left ventricle therefore 
 dilates. At the same time the wall of the cavity hyper- 
 trophies in order to drive on the large quantity of blood. 
 This dilatation and hypertrophy of the left ventricle is often 
 very great. The largest hearts on record are from cases of 
 aortic incompetence. The term cor bovinum has been 
 applied to them. Subsequently, owing to the great dilatation 
 of the left ventricle, a relative incompetence of the mitral 
 valve may be brought about. Thus there is backward 
 pressure on the left auricle, then on the lungs and the right 
 heart. Owing to the injection of the blood into the aorta 
 by the powerfully acting left ventricle, aneurysmal dilatation 
 of the aorta may occur, more especially as the vessel is 
 frequently the seat of disease. Owing to the rapid empty- 
 ing of the arteries, those going to the head are badly supplied 
 
72 DISEASES OF THE HEART AND PERICARDIUM 
 
 with blood. Hence the marked pallor of individuals suffer- 
 ing from this condition, and hence the tendency to fatal 
 syncope. 
 
 4. Aortic Stenosis. This is usually accompanied by 
 more or less incompetence. The cause may be a previous 
 attack of acute endocarditis, or it may be associated with 
 atheroma of the aorta. The segments of the valve are 
 thickened and often the seat of calcareous change. They 
 are usually united together, sometimes leaving only a minute 
 aperture for the passage of the blood (Fig. 27). The effect 
 upon the heart is to cause hypertrophy of the left ventricle, 
 which is usually at the same time dilated, owing to the exist- 
 ence of a certain amount of incompetence. 
 
 5. Tricuspid incompetence is the commonest valvular 
 lesion on the right side of the heart, and is most commonly 
 merely relative, due to a dilated condition of the right 
 ventricle. It is more rarely due to endocarditis, either 
 during extrauterine or foetal life. It leads to dilatation and 
 some hypertrophy of the right auricle, and is associated with 
 marked venous engorgement, and often with pulsation in the 
 veins of the neck and in the liver. 
 
 6. Tricuspid stenosis is a rare condition by itself. It 
 is usually associated with stenosis of the mitral valve. It is due 
 to endocarditis occurring either during foetal or extrauterine 
 life. 
 
 7. Lesions of the pulmonary valve are very rare, and 
 are usually congenital, being due either to malformation or 
 foetal endocarditis. 
 
 (EDEMA OR DROPSY IN CARDIAC DISEASE 
 
 When the heart is failing from degenerative changes in 
 its musculature or from dilatation associated with chronic 
 valvular disease, oedema tends to appear. Cardiac oedema 
 is usually distributed about the body in accordance with the 
 
DISEASES OF THE HEART AND PERICARDIUM 73 
 
 effect of gravity, appearing first and being most marked in 
 the more dependent parts, such as the tissue round the ankles. 
 Later on it spreads to other parts and to the serous sacs 
 peritoneum, pleura, pericardium. As regards the causation 
 ofjthis type of cedema, increased pressure within the capillaries 
 from venous congestion is certainly an important factor. 
 Experimentally produced venous obstruction is, however, 
 not necessarily followed by dropsy. Another factor must be 
 presupposed. This factor is the damage to the endothelium 
 due to defective nutrition of the cells from mal-oxygenation 
 of the blood and retention of waste products. At the same 
 time there is also obstruction to the lymphatic return owing 
 to the fact that the larger lymph channels open into veins 
 over-distended with blood. 
 
 PRIMITIVE MUSCULAR TISSUE OF THE HEART AND 
 ITS RELATION TO " HEART BLOCK " 
 
 There are two main portions of primitive muscular tissue 
 which should be examined : 
 
 (1) The sino-auricular node^ the site of origin of the 
 normal stimuli for the heart's contraction which is situated 
 between the opening of the superior vena cava and the right 
 auricular appendix. It is composed of slender muscle fibres, 
 nerve-cells and fibres. It has been found to show subacute 
 and chronic inflammatory change in cases of arrhythmia. 
 
 (2) The auricula-ventricular bundle -, which starts from the 
 auriculo-ventricular node, situated on the right side of the 
 inter-auricular septum in front of the opening of the coronary 
 sinus, and above the attachment of the septal cusp of the 
 tricuspid valve. The auriculo-ventricular node consists of 
 tissue similar to the sino-auricular node. From the node the 
 bundle runs forward almost horizontally, but somewhat down- 
 wards, and usually to the left in the pars membranacea septi. 
 At the anterior part of the membrane, a little in front of the 
 anterior end of the attachment of the median and septate 
 segments of the tricuspid valve, the bundle divides into two 
 parts. The left division passes downwards and perforates the 
 
74 DISEASES OF THE HEART AND PERICARDIUM 
 
 membrane, entering the subendocardial tissue of the left 
 ventricle at a point immediately beneath the union of the 
 anterior and right posterior cusps of the aortic valve. It 
 then spreads out in a fan-shaped fashion under the endocardium 
 of the left side of the septum, going to the papillary muscles 
 of the mitral valve and the ventricular muscle. The right 
 branch runs downwards and enters the moderator band, and 
 subsequently passes to the papillary muscles and wall of right 
 ventricle. 
 
 In cases of "heart block" the bundle has been found 
 implicated or destroyed in some part of its course. The 
 lesions found have been : (i) Acute inflammation from spread 
 ofulcerative endocarditis of mitral or aortic valve; (2) chronic 
 interstitial myocarditis and sometimes calcification associated 
 with arteriosclerosis of the coronary artery ; (3) fibrosis 
 following acute rheumatic inflammation of myocardium ; 
 (4) fatty infiltration; (5) tumour formation, e.g. sarcoma; 
 (6) gumma of heart wall ; (7) aneurysm of one of the 
 sinuses of Valsalva involving the septum. 
 
 GENERAL METHOD OF SETTING ABOUT THE EXAMINA- 
 TION OF A HEART WHICH HAS BEEN EXCISED AND 
 OPENED UP 
 
 Note in the first instance the size of the organ. A rough 
 approximation to the normal size of a heart is obtained by 
 comparing it with the closed fist of the individual. Next 
 note the shape. The normal heart is conical. This shape 
 is retained when the heart is enlarged, if that enlargement be 
 due to uniform increase in size of all the cavities. If, however, 
 the left ventricle be hypertrophied (as in kidney and arterial 
 disease) out of proportion to the rest, although still conical the 
 organ is elongated. In cases where the right side of the 
 heart is enlarged out of proportion to the left, as in mitral 
 stenosis and in chronic pulmonary disease, the organ, instead 
 of being conical, is ovoid (Fig. 15). 
 
 Next examine the visceral pericardium for milk spots, 
 petechial haemorrhages, fibrinous exudate, adhesions to the 
 pericardial sac. Then turn to the right side and examine the 
 right auricle as to its size, the thickness of its walls, its 
 contents (looking more especially for thrombi in the appendix). 
 
DISEASES OF THE HEART AND PERICARDIUM 75 
 
 Next examine the right ventricle as to its size, the thickness 
 of the walls, the amount of fat in the subpericardial tissue, 
 and whether this fat is actually invading the muscle substance. 
 Estimate the diameter of the tricuspid valve and examine its 
 segments for thickening and vegetations. The diameter may 
 be measured roughly with the fingers. The opening normally 
 admits three digits. Glance at the pulmonary valve for the 
 presence of thickening and vegetations. 
 
 Now turn the heart round and examine the left auricle as 
 to size, thickness 6f walls, thickening of the endocardium, the 
 presence of vegetations or thrombi (more especially in the 
 auricle). Examine the left ventricle as to its size, the thick- 
 ness of its walls, the appearance of the cut surface of the 
 muscle. Note the colour of the muscle. Look for fatty 
 change, more especially in the papillary muscles, for fibrous 
 tissue (indicating the existence of chronic interstitial myo- 
 carditis), more particularly towards the apex of the ventricle, 
 in the interventricular septum, and in the incised papillary 
 muscles. Estimate the consistence of the muscle by testing 
 its friability. 
 
 Now examine the mitral valve as to its diameter. The 
 opening normally admits two digits. Look for thickening of 
 the segments and of the chordae tendineae, for vegetations on 
 its surface or fatty change in the endothelium. 
 
 Then turn to the aortic valve, estimate its circumference. 
 Look for thickening, calcification, vegetations. Examine the 
 portion of the aorta still attached for atheroma. Lastly, look 
 at both coronary arteries, more especially the left, for the 
 presence of dilatation or narrowing, for fatty or calcareous 
 atheroma, and for thrombosis. 
 
 HEART WEIGHTS AND MEASUREMENTS 
 
 Weight, 9-13 oz. (250-370 grammes). 
 Length of left ventricle, 3-3 J in. (7-6-8-4 cm.). 
 Thickness of wall of left ventricle, \ in. (at thinnest) to J in. 
 (-6-1-2 cm.). 
 
 Length of right ventricle, 3^ to 3 in. (7-8-8-6 cm.). 
 Thickness of wall of right ventricle, ^ in. (0-32 cm.). 
 
76 DISEASES OF THE HEART AND PERICARDIUM 
 
 DIAMETERS AND CIRCUMFERENCES OF THE HEART VALVES 
 (Shennan) 
 
 
 Diameters. 
 
 Circumferences. 
 
 Tricuspid 
 
 : . . ins. 
 cm. 
 
 1-5 to 1-8 
 3-8 to 4-7 
 
 4-5 to 5-5 
 11-4 to 14-0 
 
 Pulmonary . 
 
 ins. 
 cm. 
 
 I-I tO 1-2 
 
 2-8 to 3-0 
 
 3-4 to 3-7 
 8-6 to 9-5 
 
 Mitral . 
 
 ins. 
 
 1-2 to i -4 
 
 3-7 to 4-4 
 
 
 cm. 
 
 3-o to 3-5 
 
 9'5 to ii-o 
 
 Aortic . 
 
 ins. 
 cm. 
 
 0-9 to i-o 
 2-3 to 2-5 
 
 2-8 to 3-2 
 7-2 to 8-0 
 
CHAPTER V 
 
 DISEASES OF THE VESSELS 
 
 THESE may be divided into (A) Diseases of the Arteries, 
 (B) Diseases of the Veins. 
 
 A. DISEASES OF THE ARTERIES 
 
 In all cases of sudden death the arteries of the internal 
 organs should be slit up and carefully examined for the 
 presence of impacted emboli. More particularly is this the 
 case with the pulmonary and coronary arteries. 
 
 In cases of senile gangrene the vessels of the affected limb 
 should be opened up and thrombi or impacted emboli sought 
 for. 
 
 Amyloid or Waxy Degeneration. This is a condition 
 which usually starts in the arterioles, particularly those of 
 the internal organs spleen, kidney, liver, intestine and 
 spreads forwards to the capillaries and backwards to the 
 larger vessels. In the case of the medium-sized vessels the 
 change occurs in the middle coat, affecting the bands of 
 connective tissue which lie between the circular muscle 
 fibres. The condition is only found on microscopic examina- 
 tion, although by means of iodine, when advanced, it may 
 be made visible to the naked eye. With iodine the affected 
 area gives a mahogany brown colour. Amyloid degeneration 
 
 77 
 
78 DISEASES OF THE VESSELS 
 
 should be looked for especially in (i) advanced tuberculosis, 
 (2) visceral syphilis, (3) chronic suppuration, e.g. long- 
 existent empyema, bone disease, etc. 
 
 Fatty Degeneration of the Intima. This may be 
 seen, more particularly in the aorta, in the form of pale 
 yellow streaks or patches often arranged in the long axis of 
 the vessel. It is associated with anaemia and toxaemias. 
 
 Microscopically, the fatty change is found in the endothelial 
 cells and in the subendothelial connective tissue. 
 
 Calcareous Degeneration of the Media. This is a 
 change found chiefly in old age. It may be preceded by 
 fatty or hyaline change, and it affects the medium-sized 
 arteries, such as the femoral, brachial, and radial. The 
 arteries which are the seat of the change are hard and brittle 
 and show a transverse striping very noticeable to the naked 
 eye. 
 
 Acute Inflammation. This may occur in the first part 
 of the aorta due to extension of inflammation from aortic 
 endocarditis of the ulcerative form. It may occur in arteries 
 passing through areas which are the seat of acute inflam- 
 matory change. More frequently it is caused by the 
 impaction of an embolus containing germs, which sets up 
 inflammation in the wall of the vessel and may lead to the 
 formation of an acute aneurysm, e.g. in a branch of the 
 pulmonary artery. 
 
 ARTERIOSCLEROSIS 
 
 Arteriosclerosis, or hardening of the arteries, is an 
 exceedingly common condition, and as defined includes a 
 number of diseases of somewhat different nature and origin. 
 The calcareous degeneration of the media already mentioned 
 is one type. Another type is endarteritis deformans, 
 atheroma, or, as it has more recently been called, athero- 
 sclerosis. Another type is syphilitic disease of arteries. 
 
DISEASES OF THE VESSELS 79 
 
 Lastly, there is hypertrophy of the middle coat of the 
 medium-sized and smaller vessels. 
 Types of arteriosclerosis. 
 
 1. Atheroma, atherosclerosis, endarteritis deformans. 
 
 2. Hypertrophy of the media. 
 
 3. Endarteritis obliterans. 
 
 4. Calcareous degeneration of the media (see above). 
 
 Atheroma (Gr. d^/or/, porridge), Atherosclerosis, 
 Endarteritis Deformans 
 
 A nodular and a diffuse form of the condition are 
 sometimes distinguished, the former affecting the aorta, 
 the coronary, pulmonary, and cerebral arteries, the latter 
 more associated with the medium-sized and smaller vessels, 
 such as the renal and its branches, the radial, and some- 
 times the coronary and cerebral. The nodular form is, 
 however, not infrequently found in the smaller vessels 
 mentioned. 
 
 In the aorta the condition appears first as streaks or 
 patches of a grey or pearly white appearance, slightly raised 
 above the surface, and due to thickening of the intima. These 
 patches occur especially round the openings where smaller 
 branches, such as the intercostals, leave the main trunk, 
 also in the arch of the aorta. Very early in their formation 
 they become opaque and yellow in colour owing to fatty 
 change. The patches gradually increase in size, and eventually 
 become the seat of a calcareous deposit, thus forming hard 
 brittle plates in the intima of the vessel (Fig. 28). The intima 
 then tends to degenerate and disappear, leaving a cavity, the 
 floor of which is formed of pulpy necrotic material the 
 atheromatous ulcer. Thrombosis may occur on the diseased 
 area even before the formation of the ulcer. There is an 
 increased tendency to it after the ulcer has developed. When 
 well marked, the change is often found throughout the entire 
 
8o DISEASES OF THE VESSELS 
 
 length of the aorta thoracic and abdominal. It tends to 
 be more advanced in the arch and in the lower part of the 
 abdominal aorta just before it bifurcates. Similar changes 
 are to be seen in the larger branches and in the medium- 
 sized vessels, such as coronaries, cerebrals, etc. The patchy 
 character of the disease is often particularly well seen in the 
 vessels of the brain (Fig. 29), where, owing to their transpar- 
 ency, the yellow areas can be seen even in the smaller branches. 
 In these medium-sized and smaller vessels, such as cerebral 
 and coronary, the thickening of the intima often leads to 
 very marked narrowing of the lumen. 
 
 A special type of atheroma, termed syphilitic, may be 
 distinguished. It is frequently combined with true atheroma. 
 In position, however, it is found especially in the first 
 part of the aorta, often spreading to and involving the 
 segments of the aortic valve, thus leading to aortic 
 incompetence. Whereas atheroma is a disease of more 
 advanced age, this type is often found in comparatively 
 young people. It may not always be syphilitic in origin, but 
 in many cases it undoubtedly is so, spirochsetes having been 
 found in the lesions in the vessel wall. This type is char- 
 acterised by the formation of large, white, raised, semi-trans- 
 lucent or opaque white patches. There is not the same tendency 
 to fatty and calcareous change, so that the patches remain 
 white and there is no formation of atheromatous ulcers. 
 Puckering not infrequently occurs in the centres of these 
 areas. 
 
 Effects of Atheroma. 
 
 (1) Loss of power of the vessel to dilate and contract. 
 
 (2) Narrowing of lumen of vessel, with tendency to de- 
 generative changes in organ or tissue supplied, with replace- 
 ment of functioning cells by fibrous tissue. In kidney 
 chronic interstitial nephritis ; in heart chronic interstitial 
 myocarditis. 
 
 (3) As a result of narrowing of the lumen there is increased 
 
DISEASES OF THE VESSELS 81 
 
 difficulty in driving the blood along, hence hypertrophy of 
 the left ventricle occurs, 
 
 (4) Weakening of the vessel wall, with tendency to dilate 
 at some point and form an aneurysm with tendency also to 
 rupture. 
 
 (5) Tendency to thrombosis on the diseased areas, with 
 consequent tendency to embolism. 
 
 Microscopically^ the earliest change is found to be a pro- 
 liferation of the subendothelial connective-tissue cells. This 
 leads to a thickening of the intima formed of layers of rounded 
 and spindle-shaped connective -tissue cells with intercellular 
 fibrils. Owing to the fact that the nourishment of the intima 
 and of the inner portion of the media is obtained from the 
 blood circulating within the vessel itself, the deeper portions 
 of the thickened intima undergo fatty, and eventually calcareous, 
 change. Fatty globules and crystals of fatty acids are found in 
 the degenerated area, also granules of calcium salts. Changes 
 are also to be observed in the internal elastic lamina. It 
 splits into fine fibrils and becomes fragmented. This damage 
 to the internal elastic lamina is regarded generally as the 
 primary change. The media may also show fatty degeneration, 
 owing to interference with its nourishment. It not infrequently 
 gives way, and the vessel becomes dilated. 
 
 In the case of the aorta the changes in the media may be 
 more marked. There may be invasion of vessels from the 
 vasa vasorum into the media, and around these vessels there 
 are numerous round cells. 
 
 In the syphilitic type, in addition to the greatly thickened 
 intima composed of layers of well-formed fibrous tissue without 
 fatty or calcareous change, there is marked change in the 
 media. This takes the form of an invasion of the media by 
 vessels accompanied by connective tissue. This results in a 
 replacement of the media by fibrous scar tissue, the contraction 
 of which causes the puckerings. 
 
 Causation. During the first twenty years of life there is 
 a progressive thickening of the coats of the vessels with a 
 progressive development of elastic tissue. For the next 
 twenty years of life approximately things remain stationary. 
 
 6 
 
82 DISEASES OF THE VESSELS 
 
 After that there is a progressive deterioration in the elastic 
 tissue, with consequent weakening of the vessel wall. In 
 certain individuals the elastic tissue of the vessels is congenially 
 deficient. Atheroma is a disease which develops at the time 
 of life when the vessels are beginning to deteriorate, but the 
 individual is at the height of his physical activities. High 
 blood pressure from bodily exertion, combined with degenerat- 
 ing elastic tissue, are the two main factors in the disease. 
 Sometimes the one, sometimes the other is the more prominent. 
 That high pressure of itself can produce the condition is 
 proved by the experimental work on animals. By the 
 administration of doses of adrenalin over periods of weeks 
 and months, thus causing contraction of the vessels and 
 raising the blood pressure, it has been found possible to 
 produce changes in the vessels of rabbits analogous to 
 atheroma in the human subject. The same thing has been 
 effected by holding the animal up by the hind legs for a few 
 minutes every day for some weeks. In this way well- 
 marked degenerative changes very similar to human atheroma 
 have been produced in the vessels above the diaphragm. 
 
 Infective conditions such as syphilis act by causing pro- 
 liferative changes of an inflammatory nature in the intima. 
 As a result there is malnutrition of the vessel wall subjacent to 
 the thickened area with consequent degenerative changes. 
 
 In the human subject toxic conditions associated with high 
 blood pressure, such as renal disease, lead poisoning, gout, 
 alcoholic poisoning, are also factors in the production of the 
 disease. At the same time, infective conditions such as 
 syphilis cannot be ignored. 
 
 As to the nature of the primary change, this is generally 
 regarded as being a fragmentation and fibrillation of the 
 internal elastic lamina. Subsequent to this, and with a view 
 to repairing the damage, there is a proliferation of the cells 
 of the intima, with resultant thickening. Owing to the fact 
 that the intima and outer portion of the media obtain their 
 nourishment from the blood flowing in the vessel itself, the 
 deeper portion of this new tissue and the adjacent media 
 undergo degeneration of a fatty nature. The fatty acids 
 which are formed are believed to combine with alkalies to 
 form soaps. Among these soaps are calcium combinations. 
 The fatty acid is rejected by the calcium in favour of carbonic 
 
DISEASES OF THE VESSELS 83 
 
 and phosphoric acid, with resulting deposition of calcium 
 carbonate and phosphate in a granular form. 
 
 Summary of Causes of Atheroma. 
 
 (1) Old age. 
 
 (2) Congenital deficiency in elastic tissue of vessels. 
 
 (3) Strain. 
 
 (4) Chronic toxaemias alcohol, gout. 
 
 (5) Infective conditions syphilis. 
 
 Hypertrophy of the Media. 
 
 This is another form of arteriosclerosis due to contrac- 
 tion under prolonged stimulation by the influence of toxic 
 substances circulating within the vessel. It is very character- 
 istically associated with the subacute and chronic forms of 
 Bright's disease. The condition affects the medium-sized 
 and smaller vessels. The hypertrophy of the muscular coat 
 is followed by a fibrous transformation. 
 
 Endarteritis Obliterans or Proliferans 
 
 This is a type of arterial disease associated with thickening 
 of the intima in which there is no tendency to degenerative 
 change, as in atheroma. The reason is that the new tissue laid 
 down within the internal elastic lamina carries with it its 
 own blood-vessels. This tissue is, in other words, granulation 
 tissue. The condition is found associated with all types of 
 chronic inflammation, e.g. tuberculosis, syphilis, leprosy. 
 It is usually regarded as being specially significant of the 
 presence of syphilitic disease, but it is just as frequent in 
 tuberculosis. It is found in the vessels in the neighbourhood 
 of syphilitic gummata and in vessels in the lung, bones and 
 joints in tuberculosis. Sometimes it occurs in the vessels 
 of the brain in syphilis, thrombosis in these vessels in early 
 life being a not infrequent cause of cerebral paralysis. In 
 the lung in tuberculosis the change is a most beneficial one, 
 as the tendency to rupture of vessels in the neighbourhood 
 of cavities is thereby greatly diminished. It is probable 
 
84 DISEASES OF THE VESSELS 
 
 that the atrophy of limbs in tuberculous joint and bone 
 affections may in part be explained by malnutrition following 
 diminution in size of lumen of the nourishing vessels. As 
 might be anticipated, the change is often accompanied by 
 inflammation of the other coats of the vessel, more especially 
 the adventitia. 
 
 Microscopically^ the condition is characterised by the laying 
 down of layers of new tissue within the internal elastic lamina. 
 At first the tissue is cellular, later on it becomes well-developed 
 connective tissue. Very often new layers of elastic tissue are 
 formed, and sometimes there are several small vessels within 
 the compass of the original vessel wall. In addition, there 
 are inflammatory changes in media and adventitia, more 
 especially the latter. 
 
 Arterial Disease in Syphilis. Syphilis affects the 
 arteries in several ways. It is one of the infective conditions 
 leading to atheroma, more especially to that type called 
 syphilitic, where the aorta is the seat of formation of raised, 
 white, semi-translucent areas with a tendency to puckering. 
 
 Another type of lesion found more especially in the smaller 
 arteries is the above-mentioned endarteritis obliterans, with 
 accompanying periarteritis. 
 
 Syphilitic disease of vessels is a frequent cause of aneurysm 
 formation and of thrombosis. 
 
 Arterial Disease in Tuberculosis. Tuberculous disease 
 has a marked tendency to spread by the perivascular lymph- 
 atics, and thus has from the commencement an intimate 
 association with vessels. This condition of periarteritis 
 leads to a thickening of the vessel. The process may spread 
 inwards and produce an endarteritis. Sometimes a tuber- 
 culous focus may burst its way through a vessel wall, thus 
 giving rise to a general blood infection. 
 
 This endarteritis is found in a marked degree in all cases 
 of chronic pulmonary tuberculosis. It is also found in 
 the smaller vessels in the neighbourhood of tuberculous 
 
DISEASES OF THE VESSELS 85 
 
 lesions of bones and joints. As in syphilis the thickened 
 intima shows no tendency to degeneration in its deeper 
 parts. 
 
 The inflammatory change in the vessel walls in the neigh- 
 bourhood of cavities may lead to weakening, aneurysm 
 formation, or rupture. As previously stated, it more fre- 
 quently causes more or less complete obliteration. 
 
 Aneurysm 
 
 An aneurysm is a localised enlargement of the lumen of 
 an artery. The enlargement may involve the whole lumen 
 for a short distance (fusiform aneurysm) , or it may be a 
 diverticulum from one side of the vessel (saccular aneurysm) 
 
 (Fig. 31)' 
 
 The term acute aneurysm is applied to any rapid dilatation 
 of an artery through an inflammatory process in its wall, 
 usually due to the presence of a septic thrombus within 
 its lumen. A false aneurysm is an accumulation of blood 
 communicating with a vessel and surrounded, not by the 
 vessel wall, but by a condensation of tissue in the neighbour- 
 hood. A dissecting aneurysm is a condition, found usually 
 in the aorta, where the blood finds its way, commonly by a 
 split in a calcareous atheromatous patch, between the intima 
 and media, or between media and adventitia, or again between 
 two layers of media. Sometimes the blood finds its way back 
 again at a different level into the lumen. The term miliary 
 aneurysm is applied to minute dilatations, usually of a 
 saccular type, occurring on the course of the smaller cerebral 
 arteries. 
 
 The most common site for aneurysm is the thoracic aorta 
 the ascending portion, the arch or descending portion. The 
 next most common site is the abdominal aorta, then come 
 the popliteal and carotid arteries. The special type, miliary 
 aneurysm, is found in the cerebral vessels. Aneurysms also 
 occur in the branches of the pulmonary artery in the neigh- 
 
86 DISEASES OF THE VESSELS 
 
 bourhood of tuberculous cavities (Fig. 52), and as the result 
 of septic embolism. 
 
 Aneurysms vary greatly in size and shape. The cavity 
 may be largely filled with white and red thrombus, often 
 with a laminated appearance. This thrombus is seldom 
 the seat of organisation. The wall may be formed of all 
 the coats of the vessel. Usually, however, the intima, if 
 present at all, is in patches. This, no doubt, is the explana- 
 tion of the non-occurrence of organisation in the thrombus 
 contents. The media may also disappear and the wall be 
 formed only of adventitia and condensed connective tissue 
 surrounding. Occasionally the wall is partly formed of bony 
 structures such as the vertebrae (Fig. 31). The wall of the 
 vessel in the neighbourhood is usually the seat of athero- 
 matous change, frequently of the syphilitic type. 
 
 Changes produced in Surrounding Parts. These depend 
 upon the position of the aneurysm. The dilating vessel 
 presses upon viscera, such as trachea, bronchi, oesophagus, 
 upon nerves and vessels. Thus irritation or paralysis of 
 nerves recurrent laryngeal, trunks of the brachial plexus 
 results. Pressure on trachea and bronchi leads to accumula- 
 tion of secretion, and sometimes to gangrene of the lung, also 
 to erosion and rupture. Pressure on oesophagus similarly 
 causes obstruction, and may result in rupture. Bones such 
 as sternum and vertebrae are eroded, also cartilage, but the 
 softer the tissue the better it resists, so that intervertebral 
 discs may project beyond the harder bone. Pressure upon 
 lung leads to collapse and atrophy. 
 
 Smaller vessels arising from the aneurysmal portion of the 
 vessel tend to be contorted, and sometimes their lumen 
 obstructed by thrombus. The heart may be displaced 
 downwards, and may be hypertrophied. 
 
 Rupture may occur through the skin in thoracic aneurysm, 
 projecting forwards, into the trachea, bronchi, oesophagus, 
 per icar dial sac, pulmonary artery. In the case of cerebral 
 
DISEASES OF THE VESSELS 87 
 
 aneurysms, into the brain substance or under the membranes ; 
 in phthisical aneurysms, into the lung cavity, with con- 
 sequent haemoptysis. 
 
 Causation. Two factors are concerned in the causation. 
 
 (1) Conditions which lead to weakening of the vessel wall, 
 (a) injury as from a gunshot wound, (b) disease, such as (i.) 
 acute arteritis from inflammation around the vessel or from 
 impaction of a septic embolus in the vessel, (ii.) chronic 
 arteritis from atheroma, more especially the syphilitic 
 type. 
 
 (2) Conditions leading to sudden rise of blood pressure, 
 e.g. lifting of heavy weights. 
 
 The condition is far more frequent in males than in females 
 (out of 189 cases, 171 males). It occurs as a rule above forty 
 years of age, i.e. at the period when the vessels are beginning 
 to degenerate while the individual is still in active work. In 
 something over 50 per cent of cases a history of syphilis may 
 be obtained. 
 
 B. DISEASES OF VEINS 
 
 Thrombosis occurs in veins where the blood current is 
 slowed from dilatation and varicosity. In all probability in 
 addition there must be some inflammatory condition of the 
 vessel wall leading to damage of the endothelium. The 
 condition may be found in any vein where walls are inflamed. 
 Thus the small venous radicles in the neighbourhood of any 
 inflammatory focus tend to undergo thrombosis. When 
 organisms invade such thrombi and soften and break them 
 down, portions of the thrombus containing germs are apt to 
 be carried away by the blood current and deposited in distant 
 organs. The liver is affected when the rootlets of the portal 
 vein are thrombous ; the lung, in the case of other venous 
 radicles, becomes the seat of septic embolism and abscess 
 formation (see diagram, p. 62). 
 
88 DISEASES OF THE VESSELS 
 
 Thrombosis once started tends to spread. Not infre- 
 quently the change begins in the pouch of a valve. The 
 thrombus grows until it blocks the lumen of the vessel. Then 
 the blood current being stopped, thrombosis occurs in the 
 vessel up to the next large branch. Subsequently another 
 slow thrombotic process starts, until again the vessel is 
 blocked. In this way the process initiated in a small rootlet 
 of the femoral vein may pass up as far as the inferior vena 
 cava. 
 
 Thrombi in veins may become organised and may lead to 
 obliteration of the vessel. Or they may be the seat of 
 deposit of calcareous material forming so-called phleboliths. 
 Again, sometimes the thrombus in course of organisation may 
 be tunnelled and the circulation re-established. 
 
 Two types of thrombi are distinguished according to 
 their colour, (a) red, (b) white. Red thrombi form when 
 the blood is suddenly brought to a standstill, white thrombi 
 are formed when the blood is in motion. 
 
 Thrombi in veins not infrequently undergo softening. 
 Two types of softening are distinguished : (a) simple soften- 
 ing ; (b) septic, due to the action of germs. 
 
 Microscopically ', thrombi consist of the blood elements (red 
 corpuscles, white cells, and blood platelets) in varying pro- 
 portion, bound together by filaments of fibrin. 
 
 (a) In the case of red thrombi the predominant element is 
 the red blood corpuscle. There are a few white cells, and 
 between the cell elements filamentous and granular fibrin. 
 Sometimes the red cells stain well, at other times they have 
 lost their characteristic staining reaction and only their outlines 
 are visible. 
 
 (b) In white thrombi leucocytes, platelets, and fibrin pre- 
 dominate. Organisation is frequently seen. The first stage 
 in the process is a covering over of the thrombus with a layer 
 of spindle-shaped endothelial cells from a proliferation of those 
 lining the vessel. Then from the subendothelial and other 
 connective-tissue layers, young connective-tissue cells emigrate 
 
DISEASES OF THE VESSELS 89 
 
 into the thrombus. They appear as rounded mononuclear 
 cells to begin with ; later on they become spindle-shaped. At 
 the same time the endothelial cells of the vasa vasorum pro- 
 liferate, forming buds of vessels which penetrate the thrombus. 
 Both these processes occur at points where the thrombus is in 
 contact with the vessel wall. Elsewhere the endothelium 
 covering the thrombus develops buds which penetrate the 
 substance of the coagulum and become rilled with blood from 
 the original lumen. Subsequently these various blood channels 
 unite with one another, become enlarged, and thus the 
 thrombus becomes tunnelled. During the process of organisa- 
 tion, pigment (haematoidin) granules are deposited in large 
 numbers in the cells. 
 
 Dilatation and Varicosity. This is a condition which 
 is found more especially in the superficial veins of the lower 
 limbs, in the veins of the scrotum (varicocele), rectum 
 (haemorrhoids), and oesophagus. 
 
 As regards causation there is undoubtedly a tendency to 
 the condition in certain individuals owing to a congenital 
 weakness in the elastic tissue of the vessel wall. The condi- 
 tion is aggravated by gravity. It may also be caused by 
 obstruction to the return of the blood by the wearing of tight 
 garters, by the presence of a tumour or hard faecal masses 
 pressing on the iliac veins, or by a cirrhotic liver interfer- 
 ing with the flow of blood through the portal veins, and 
 affecting more especially the rootlets from the rectum and 
 oesophagus. 
 
 The veins which are the seat of the change are dilated 
 and tortuous. Their walls are thickened and there 
 may be thrombosis within them. Ulceration from skin, 
 oesophagus, or rectum may lead to erosion and consequent 
 haemorrhage. 
 
 Phlebitis, or inflammation of the wall of a vein, may be 
 due to injury, or to an inflammatory focus in the neighbour- 
 hood of a vein, as in appendicitis, osteomyelitis, erysipelas. 
 It may also occur in syphilis and in gout. The condition is 
 
go DISEASES OF THE VESSELS 
 
 always associated with more or less thrombosis or clotting of 
 the blood within the vessel. 
 
 Results. Obliteration of the vein, washing away of portions 
 of thrombi, and so formation of emboli, reabsorption, or 
 tunnelling. 
 
CHAPTER. VI 
 
 DISEASES OF THE BLOOD, BONE MARROW, LYMPH GLANDS, 
 SPLEEN, AND DUCTLESS GLANDS 
 
 DISEASES OF THE BLOOD 
 
 ALTHOUGH it is unquestionably better to examine the blood 
 during the life of the patient, it is still possible to do so after 
 death. The ease with which this can be done depends to a 
 great extent upon how far the blood has coagulated within 
 vessels and heart. There is, however, in blood diseases, such 
 as anaemias and leukaemias, a tendency for the blood to 
 remain fluid so that films may often be readily obtained 
 either from heart blood or vessels. 
 
 (For the bacteriological examination of the blood, see p. 359). 
 
 Septicaemia and Pyaemia. Micro-organisms enter the 
 blood in many infective conditions. In fact, in most acute 
 infective diseases the causal organism can be cultivated 
 from the blood at some period. Even in the more chronic 
 forms, such as tuberculosis, germs can be detected in the 
 blood in a considerable proportion of cases. Such con- 
 ditions, in which living organisms are circulating in the 
 blood-stream, are usually known as septiccemias. Formerly 
 the term was somewhat restricted in its use ; now it may 
 be applied to a large number of acute infective processes 
 
 91 
 
92 DISEASES OF THE BLOOD 
 
 including typhoid fever and pneumonia. In the human 
 subject the germs are almost never present in numbers 
 sufficient for their demonstration readily in stained blood 
 films. Concentration or cultural methods have to be adopted 
 before their presence can be detected. On the other hand, 
 the same germs may, when introduced into one of the lower 
 animals, give rise to a condition in which immense numbers 
 of film organisms can be demonstrated microscopically in the 
 blood. This is notably the case with the pneumococcus and 
 the anthrax bacillus. 
 
 The organisms may enter the blood, in the case of the 
 smaller blood-vessels, through an intact vessels' wall. In 
 other instances an abscess or similar infective focus (in 
 tuberculosis a caseous focus) may rupture directly into the 
 blood-stream, it. may be into a vessel of considerable size, 
 usually a vein. In a majority of instances, in the more acute 
 infective diseases, the actual invasion of the vessel is pre- 
 ceded by a thrombosis within the lumen ; the thrombus 
 then becomes infected with germs, and portions of the infected 
 clot are carried to other parts of the body, there to set up 
 metastatic inflammatory foci, or abscesses. This condition 
 of invasion of the blood-stream by organisms plus the forma- 
 tion of metastatic abscesses is usually known as pycemia. 
 
 The primary focus from which the infection of the blood 
 originates varies very much. It may be the intestine as in 
 typhoid fever, the organism probably reaching the blood by 
 way of the lymphatics. It may be the lung as in acute lobar 
 pneumonia, the organisms passing directly from the alveoli 
 into the pulmonary capillaries. In the conditions more 
 usually characterised by the term septicaemia, it is commonly 
 a suppurative focus in the throat, appendix, bone (in osteo- 
 myelitis), or an endocarditis of the malignant or ulcerative 
 type. 
 
 When secondary suppurative foci develop these may be 
 found in kidneys, liver, brain, or indeed in any part of the 
 
DISEASES OF THE BLOOD 93 
 
 body in the case of an ulcerative endocarditis, in the lungs 
 most commonly in the case of an osteomyelitis, in the liver 
 in the case of the appendix (portal pyaemic type of liver 
 abscess). 
 
 Sometimes a condition may start by being merely a 
 septicaemia. Subsequently it develops into an ulcerative 
 endocarditis and pyaemia. Apparently organisms in the 
 blood-stream have a special tendency to become deposited 
 on the heart valves, especially such as have already been 
 damaged. 
 
 Both in miliary tuberculosis and in septicaemia the 
 secondary infective foci invade blood-vessels in their neigh- 
 bourhood and so further infect the blood-stream with germs. 
 
 Pernicious Anaemia. In performing a post-mortem 
 examination in a case of this disease the following changes 
 will be found with a remarkable degree of constancy. 
 
 The skin is pale, often with a lemon-yellow tint due to a 
 slight degree of jaundice. The subcutaneous fat may be 
 considerable in amount and shows a bright yellow colour. In 
 examining the serous sacs minute haemorrhages will be found, 
 more especially under the visceral pleura and pericardium. 
 The lungs are pale and show atrophic emphysema. Not 
 infrequently small haemorrhages are found in the substance 
 of the lungs as well as under the pleura, and on microscopic 
 examination fatty change may be found in the endothelial 
 cells of the vessels. The heart may be dilated, and is very 
 constantly the seat of a fatty degeneration of the muscular 
 substance, which is best seen on the inner aspect of the left 
 ventricle, more especially on the papillary muscle. The 
 change is of the patchy type described as " thrush breast 
 heart." The blood within the heart cavities is often fluid and 
 always pale. 
 
 The liver is pale and of a yellow-brown colour. It shows 
 fatty degeneration and a marked increase of iron-containing 
 
94 DISEASES OF THE BLOOD 
 
 pigment (haemosiderin). This can be demonstrated by 
 pouring over the organ ferrocyanide of potassium (2 per cent) 
 and hydrochloric acid (i per cent), repeating the process 
 several times if the characteristic " Prussian blue " colour 
 does not at once appear. The pigment is present mainly 
 round the outer part of each lobule (frontispiece, Fig. i). 
 
 Microscopic Appearances. The granules are found within 
 the liver cells mainly in the outer two-thirds of the lobule, and 
 also in the endothelial cells of the vessels. Necrotic areas 
 are sometimes present in the lobules. In the vessels nucleated 
 red cells and endothelial cells containing red corpuscles as well 
 as pigment granules are to be found. Fatty degeneration is 
 present in the central part of the lobule. 
 
 The spleen is of a dark brownish-red colour. Haemosiderin 
 may be present in sufficient amount to be demonstrated 
 macroscopically. In any case it will be found microscopically 
 within the endothelial cells of the pulp sinuses, which also 
 show marked phagocytosis for red blood corpuscles. 
 
 The kidney may show nephritis of a catarrhal or interstitial 
 type. It is very pale in colour and often exhibits the 
 same Prussian blue reaction as is found in liver and spleen. 
 
 The mucous membrane of the stomach and intestine is 
 pale, petechial haemorrhages are often present, and there is 
 atrophy of the mucous membrane. 
 
 The bone marrow in the shafts of the long bones, which is 
 normally of a yellow colour and is composed of fat, is trans- 
 formed into a bright red marrow with a gelatinous appearance 
 and consistence. 
 
 Microscopically, there is a marked erythroblastic reaction, 
 the red cells showing evidence of active proliferation. Many 
 of them are of the large nucleated type known as megaloblasts. 
 There is also evidence of phagocytic activity on the part of 
 large endothelial cells, many of which contain red blood 
 corpuscles. 
 
DISEASES OF THE BLOOD 95 
 
 Occasionally in the spinal cord degenerative changes, with 
 consequent sclerosis, are found in the posterior and postero- 
 lateral columns. 
 
 The chief blood changes of pernicious anaemia may be 
 briefly recapitulated. There is marked diminution in the 
 number of red blood corpuscles (average count i-| millions), 
 with a less marked diminution in haemoglobin (average 40 
 per cent), so that the colour index (the ratio of the percentage 
 of haemoglobin to the percentage number of corpuscles, 
 e.g. as above, |~) is greater than unity. On the examination 
 of a film of blood the main change is found to be variation in 
 size of the blood corpuscles (macrocytes and microcytes being 
 present), with marked variation in shape (poikilocytosis). 
 Nucleated red corpuscles are usually to be found, and of these 
 the large variety (megaloblast) predominates over the normo- 
 blast. In addition, basophil granules are often found scattered 
 through the corpuscles (punctate basophilia or granular 
 degeneration), and not infrequently the red cell takes on both 
 acid and basic dye, assuming thus a bluish colour (poly- 
 chromatophilia). The leucocytes are commonly reduced in 
 number, with a slight relative increase of the lymphocytes. 
 The blood plates are also fewer in number. 
 
 Splenic Anaemia. This term is commonly used to 
 characterise cases of severe, unexplained anaemia, in which 
 splenic enlargement is a prominent feature. Undoubtedly 
 a number of different conditions have been included. An 
 adult and an infantile type are described. 
 
 Under the adult form the condition known as Band's 
 disease may be classified. This is characterised by an en- 
 largement of the spleen with cirrhosis of the liver and 
 atheroma of the splenic and portal vessels. Microscopically, 
 the spleen shows a diffuse fibrosis both of the Malpighian 
 bodies and of the reticulum. The Gaucher type of splenic 
 enlargement also comes under this heading. In it the spleen 
 is enormously enlarged and the parenchyma is transformed 
 
96 DISEASES OF THE BLOOD 
 
 into spaces resembling the alveoli of a gland. These spaces 
 are lined by peculiar, large mononuclear cells. The liver 
 is also enlarged and contains groups of these cells. Similar 
 cells are also present in the bone marrow. 
 
 The infantile type of splenic anaemia has no constant 
 features. The enlarged spleen shows microscopically a 
 general fibrosis. 
 
 The blood pictures in splenic anaemia are not constant or 
 characteristic. The general type is that of a secondary 
 anaemia with a relatively excessive diminution in the per- 
 centage of haemoglobin, hence a low colour index. As a rule 
 the leucocytes are diminished. 
 
 Leukaemia (Leucocythemia) 
 Two main types of this condition are recognised : 
 
 (1) Myelocythemia, myel&mia, spleno-medullary leuk&mia. 
 
 (2) Lymphocytkemia, lymphcemia, lymphatic leukcemia. 
 
 (i) Myelocythemia. This is a condition in which there 
 is an enormous proliferation of leucocytes and leucocyte- 
 forming cells, mainly of the granular variety, chiefly in the 
 bone marrow. The result is that fully developed leucocytes 
 and immature forms (myelocytes) overflow into the circula- 
 tion in large numbers. The disease is probably a tumour 
 formation related to the sarcomata. 
 
 The blood is often paler than normal. Large greenish- 
 yellow or white clots may be found in the heart and vessels. 
 Films show an enormous preponderance of white blood 
 corpuscles. Instead of the normal proportion of i white 
 to 500 reds, there may be i to 10, or even i to i. The 
 prevailing types of leucocyte present are the polymorpho- 
 nuclear and the neutrophil myelocyte. These latter are 
 very large cells, not infrequently 20 ^ in diameter, with 
 large, pale nuclei and neutrophil granules in their protoplasm. 
 In addition, there is a marked increase in the number of 
 eosinophils, and eosinophil myelocytes are also present in 
 
DISEASES OF THE BLOOD 97 
 
 large numbers. Mast cells (cells with basophil granules) are 
 present, often in great numbers. There are considerable 
 numbers of lymphocytes and other hyaline cells, but these 
 are relatively greatly diminished. The red cells are reduced 
 in number and nucleated red cells of the normoblast type 
 are usually present. 
 
 The organs generally tend to be enlarged and have a pale 
 appearance. 
 
 The spleen is usually greatly enlarged (Fig. 33). It may 
 weigh as much as 18 Ibs. The enlargement is uniform, and 
 the shape with the notches is preserved. The organ may reach 
 as far down as the pubis. In consistence the organ is firm. 
 The surface often shows chronic perisplenitis. Infarcts are 
 very commonly present. On section, the cut surface has a 
 uniformly pale pink, flesh-like appearance. The Malpighian 
 bodies are invisible. 
 
 Microscopic Appearances. The sinuses of the pulp are 
 filled with leucocytes of the different types. In addition, there 
 are numerous swollen endothelial cells, in some of which red 
 blood corpuscles can be seen. There is increase of fibrous 
 tissue and pigment, the fibrous tissue spreading from around 
 trabeculae and vessels. Malpighian bodies are inconspicuous. 
 
 The bone marrow throughout the body has a pale pink 
 colour. The marrow of the shafts of the long bones, instead 
 of being fatty, has a similar pale pink appearance. 
 
 Microscopically, granular cells of all kinds are found present 
 in greatly increased numbers. There is evidence of great 
 rapidity of division (mitotic figures) among all types of myelo- 
 cytes. Red cells are relatively few in number. 
 
 The liver (p. 191) and kidneys (p. 223) are enlarged and 
 pale, and show microscopically more or less infiltration with 
 leucocytic cells. The lymphatic glands may or may not be 
 enlarged. 
 
 (2) Lymphocythemia. In this type of the disease there 
 
 7 
 
9 8 DISEASES OF THE BLOOD 
 
 is a proliferation of the leucocytes of the non-granular or 
 hyaline type. These overflow into the blood and infiltrate 
 the organs. The condition, like the previous, is probably 
 neoplastic in nature. 
 
 The blood is pale, and films show usually a marked increase 
 of white corpuscles. This is seldom so marked as in the 
 previous type of the disease. Occasionally there is no 
 increase. The prevailing type of leucocyte is the lymphocyte, 
 large or small. These form from 90 per cent to 99 per cent 
 of the white corpuscles. Granular cells are few and far 
 between. The red blood cells are reduced in numbers, and 
 nucleated corpuscles are usually present. 
 
 The appearance of the bone marrow is similar to that 
 found in myelocythemia. But on microscopic examination 
 lymphocytes instead of the granular cells predominate. 
 
 The lymphatic glands are very commonly enlarged, some- 
 times attaining the size of a hen's egg. 
 
 Microscopically, they are found infiltrated with immense 
 numbers of lymphocytes. 
 
 The spleen is usually enlarged, although it does not attain 
 the size of the organ in well-marked cases of myelocythemia. 
 
 Liver and kidneys tend also to be enlarged ; the latter 
 are usually very pale and show numerous haemorrhages 
 scattered through them. 
 
 Chloroma. This is a rare condition, found chiefly in 
 male infants. It is characterised by the presence of greenish- 
 coloured tumours, mainly in connection with the periosteum 
 of bones, e.g. in the orbit, causing marked protrusion of the 
 eyeballs and on the vertebrae. These, on microscopic examina- 
 tion, show the character of round-cell sarcomata. Deposits 
 with similar characters may be found in the lymphatic glands 
 and bone marrow, and in the liver and kidneys. The colora- 
 tion of the masses is due to a pigment which occurs in a 
 granular form, and is probably of a fatty nature. 
 
ILEMORRHAGIC DISEASES 99 
 
 Blood films show appearances similar to those seen in 
 lymphocythemia. 
 
 BJEMORRHAQIC DISEASES 
 
 Haemorrhages into the skin, serous and mucous membranes, 
 are characteristic of a number of conditions. 
 
 (1) Infective diseases, such as pyaemia and ulcerative 
 endocarditis. 
 
 (2) Toxic conditions, such as jaundice, snake bite, quinine 
 poisoning. 
 
 (3) Cachectic conditions, as scurvy and severe anaemias. . 
 The term " pur pur a " is often applied when haemorrhages 
 
 form a marked feature of a case. The term, however, un- 
 doubtedly includes a great many diseases of very different 
 nature. 
 
 Scurvy is a disease caused by improper diet an excess 
 of meat (especially salted meat), and an absence of fresh 
 vegetables. It is characterised by a swollen, spongy con- 
 dition of the gums which readily bleed, and by haemorrhages 
 under the skin and into the muscles. The disease is believed 
 to be an acid intoxication with diminished alkalinity of the 
 blood. The coagulation of the blood is slow and incomplete, 
 the other characters being those of a secondary anaemia. 
 Post-mortem, beyond the appearances of cachexia and the 
 haemorrhages into the skin and muscles, there is little to note. 
 
 Infantile Scurvy (Barlow's disease) is a condition 
 which is occasionally seen in infants, not infrequently those 
 of the well-to-do. It is due to improper dieting, especially 
 to an absence of fresh milk and to an excess of proprietary 
 foods. Marked cases are characterised by fusiform swellings 
 of the shafts of the long bones, particularly the tibia and 
 femur. These swellings are due to haemorrhage beneath 
 the periosteum. The periosteum is always highly vascular. 
 Occasionally the condition is seen also in the upper ex- 
 
ioo DISEASES OF THE BONE MARROW 
 
 tremities. Fracture of the shafts of the long bones is 
 occasionally met with. Microscopically, the bones are 
 abnormally vascular and there is absorption of the bony 
 trabeculse. 
 
 Haemophilia is a hereditary disease occurring almost 
 exclusively in the males but transmitted exclusively by the 
 females of a family. It is characterised by a tendency to 
 persistent bleeding either spontaneous, or from slight wounds, 
 such as the socket of a tooth. Although sometimes fatal, 
 nothing abnormal is to be found post-mortem. It is stated 
 that there is an unusual thinness of the blood-vessels with 
 fatty change in the intima. This, however, is not always 
 , present, and may be merely the result of secondary anaemia. 
 Without doubt the uncontrolled bleedings are to be ascribed 
 to defective coagulability in the blood, in all probability to 
 a deficiency in the amount of prothrombin. Sometimes 
 the large joints, especially the knee, show in this condition 
 appearances not unlike those found in rheumatoid arthritis. 
 There is thickening and fibrillation of the synovial membrane 
 with the formation of fringes which are coloured yellow-red 
 from old haemorrhages. At the same time there is also 
 destruction of the articular cartilages. 
 
 DISEASES OF THE BONE MARROW 
 
 The bone marrow should be examined in such a readily 
 accessible position as the ribs by compressing the marrow out 
 by means of bone forceps ; also in the shaft of one of the 
 long bones, such as the femur. In the latter position the 
 marrow consists normally almost entirely of fatty tissue, the 
 red marrow of the long bones being confined in the adult to 
 the cancellous tissue at the ends. The bone (by preference 
 the femur) should be sawn across near the upper end of 
 the shaft. Films should be made on slides or cover-glasses 
 by smearing the marrow over the surface. These can be 
 
DISEASES OF THE BONE MARROW 101 
 
 stained directly by Irishman's or Jenner's stain. Portions 
 of marrow may also be fixed (best in corrosive sublimate) 
 cut in paraffin and stained by other means. 
 
 The marrow should be examined more especially in all 
 cases of anaemia, and in cases where there is enlargement of 
 spleen or lymph glands, also in infective conditions such as 
 pneumonia. 
 
 The two main functions of the marrow being the formation 
 of red and white blood corpuscles, two chief alterations are 
 found : (i.) associated with increased activity in the white 
 cell-forming function (Leucoblastic marrow) ; (ii.) associated with 
 increased activity in the red cell-forming function (erythroblastic 
 marrow). Where either of those functions is markedly 
 stimulated, the fatty marrow of the long bones becomes 
 replaced by leucoblastic or erythroblastic marrow, as the 
 case may be. 
 
 Leucoblastic Marrow is found in most infective condi- 
 tions associated with the presence of excess of leucocytes in 
 the circulating blood. It is also found in the two types of 
 leukaemia. Leucoblastic marrow has a pink appearance 
 and soft consistence. 
 
 Microscopically, it shows increased proliferative activity 
 as evidenced by presence of mitotic figures in the nuclei of 
 the myelocytes (infective conditions and myelocythemia) or 
 lymphocytes (lymphocythemia), as the case may be. Red 
 blood corpuscles both nucleated and fully formed are relatively 
 diminished in number. 
 
 Erythroblastic Marrow is found in cases where there 
 has been a call upon the red cell-forming function, such as 
 anaemias of all kinds. The marrow is redder than normal, 
 and the yellow fatty marrow of the shafts of the long bones 
 is more or less altered into red marrow. In cases of pernicious 
 anaemia this alteration is usually complete, and, in addition, 
 the bony trabeculae may be absorbed to a certain extent, 
 leaving the interior of the shaft fairly smooth. 
 
102 DISEASES OF LYMPH GLANDS 
 
 Microscopically^ this type of marrow is characterised by 
 marked increase in the numbers of the red blood corpuscles, 
 many of which show nuclei in process of division. More 
 especially in pernicious anaemia this is associated with the 
 presence of large numbers of large nucleated red cells or 
 megaloblasts. 
 
 Degenerations. Fibrous and myxomatous transforma- 
 tion of the marrow tend to occur in old age, syphilis, and 
 other debilitating diseases. In old-standing cases of leukaemia 
 and pernicious anaemia degenerative changes may occur. 
 
 Pigmentary Changes. Another function of the marrow, 
 which it shares along with liver and spleen, is destruction of 
 effete red blood corpuscles. In severe anaemias this function 
 may be increased, giving rise in certain cases to a brownish- 
 red coloration, which appears on microscopic examination 
 to be due to the presence of blood pigment. 
 
 DISEASES OF LYMPH GLANDS 
 
 For pathological purposes the chief groups of lymph 
 glands are : cervical, axillary, mediastinal, bronchial, 
 mesenteric, retroperitoneal, pelvic, and inguinal. 
 
 These groups should be examined carefully as the regions 
 in which they lie are dealt with. Particular attention should 
 always be paid to the condition of the glands in suspected or 
 obvious tuberculosis or malignant disease. 
 
 Pigmentary Changes. These are to be observed, con- 
 stantly but in varying degree, in the bronchial glands, also 
 in the axillary glands in cases of tattooing of the skin of the 
 arm. 
 
 Acute Lymphadenitis. This is to be seen in the glands 
 through which drain the lymphatics of any area that happens 
 to be th3 seat of acute inflammatory changes ; the axillary or 
 inguinal % glands in cases of poisoned wounds and bubonic 
 
DISEASES OF LYMPH GLANDS 103 
 
 plague ; the mesenteric glands in typhoid fever. The gland 
 is enlarged, often congested, fairly firm in consistence, some- 
 times with areas of haemorrhage or necrosis, or even softening 
 and suppuration. 
 
 Microscopically ', there is infiltration with inflammatory 
 exudate, which is sometimes fibrinous ; proliferation and 
 throwing-off of the endothelial cells lining the sinuses ; areas 
 of haemorrhage and necrosis, with possibly accumulations of 
 polymorphonuclear leucocytes, and in some cases (plague, 
 typhoid), the causal organism in considerable numbers. 
 
 Chronic Lymphadenitis. This is to be observed in 
 connection with areas where there is chronic inflammation of 
 any kind. The gland is enlarged and firm, the capsule 
 thickened and often adherent to neighbouring glands. On 
 section, the structure is pale. 
 
 Microscopically, there is fibrous overgrowth in the capsule 
 and trabeculae. There is also catarrh and proliferation of the 
 endothelial cells of the sinuses and proliferation of the 
 lymphoid cells. 
 
 Tuberculous Lymphadenitis. This is a very common 
 condition, and should be carefully looked for in all cases. 
 The glands which are the seat of the change are enlarged. 
 In the early stage they are discrete, and, on section, grey and 
 translucent, with, as. a rule, areas of opaque white or yellow 
 caseation. In the later stages they tend to be adherent to 
 one another and to surrounding structures, their capsules are 
 thickened, and, on section, the gland substance shows caseous 
 (Fig. 37) and sometimes also calcareous change. Evidence 
 of tuberculosis should be looked for more especially in the 
 cervical, mediastinal, bronchial, mesenteric, and retro- 
 peritoneal groups of glands. 
 
 Microscopically, in addition to the changes found in a non- 
 specific chronic inflammation (see above), there are typical 
 tubercle follicles and areas of caseation. Tubercle bacilli are 
 commonly few and scattered. When they occur they are usually 
 
104 DISEASES OF LYMPH GLANDS 
 
 to be found in a zone at the margin of the caseous area. Occa- 
 sionally they may be found in considerable numbers, and 
 sometimes in the giant and epithelioid cells. 
 
 Lymphadenoma or Hodgkin's Disease (also known as 
 Pseudoleuksemia). This is a condition which, on the one 
 hand, resembles malignant growths, and, on the other hand, 
 the chronic inflammatory conditions, such as tuberculosis. 
 Certain cases, with all the characteristic appearances of 
 lymphadenoma, have been proved to be tuberculous by 
 inoculating animals with portions of glands. Other cases 
 resemble very closely the appearance in lymphosarcoma. 
 
 The changes in the glands consist of an enlargement, 
 usually greater than that found in tuberculosis, of a group or 
 of several groups, such as the cervical, axillary, mediastinal, 
 abdominal, inguinal. The cervical group is the one most 
 frequently first affected (Fig. 38). The glands while enlarging 
 tend to remain discrete (cf. tuberculosis). They vary in 
 size from a pea up to a hen's egg. They are usually firm. 
 On section, they are grey and somewhat translucent with 
 obvious bands of shining connective tissue, and possibly with 
 yellow areas of necrosis. These areas of necrosis differ from 
 the caseous areas found in tuberculosis in being small and 
 less opaque. 
 
 Microscopically^ in the earliest stage there is a hyperplasia 
 of the lymphocyte cell elements ; later there is a multiplication 
 of the endothelial elements at the expense of the lymphoid 
 cells, which may be relatively few and far between. Many of 
 these endothelial cells have more than one nucleus, but when 
 there are several nuclei these are in a group, not peripherally 
 arranged as in the typical giant cell of tuberculosis. The 
 tissue not infrequently shows infiltration with eosinophil leuco- 
 cytes. There is always a greater or less amount of con- 
 nective-tissue fibres, both in connection with the capsule and 
 in the substance of the gland. The fibrous transformation is 
 found most marked in the more advanced cases. Areas of 
 necrosis may be present. 
 
DISEASES OF THE SPLEEN 105 
 
 Similar changes are to be found in certain of the internal 
 organs, more particularly the spleen (see p. no), less frequently 
 the liver (p. 191) and lungs. 
 
 Tumours of the Lymph Glands. Lymphomata or 
 tumours of lymphatic tissue, in which the various elements 
 retain their normal proportions, may be found in the medi- 
 astinum, tonsils, etc. 
 
 Lymphosarcomata or malignant growths arising in connec- 
 tion with, and having the structure of lymphatic tissue, are 
 found not infrequently in the mediastinum invading the 
 roots of the lungs, or in the abdomen. They tend to produce 
 metastases in the other organs. They form a very malignant 
 type of tumour, and usually show microscopically the appear- 
 ance of a round-cell sarcoma. 
 
 Secondary growths in glands are to be looked for in all 
 cases of malignant disease, more especially in carcinoma. 
 
 DISEASES OF THE SPLEEN 
 
 Atrophy. This is practically a normal process in extreme 
 old age. The organ becomes smaller, its capsule thickened 
 and shrivelled. On section, there is found an increase 
 of fibrous tissue, the pulp is of a dull, reddish-brown 
 colour and bloodless. The organ is somewhat tough in 
 consistence. 
 
 Waxy or Amyloid Degeneration. This change is to be 
 looked for in all cases of prolonged suppuration, advanced 
 tuberculosis, and visceral syphilis. There are two types of 
 the condition. 
 
 (i) Sago. The organ is usually somewhat increased in 
 size, but the increase may not be marked. In consistence 
 it is usually firm, and, when cut into, the edges remain sharp. 
 The cut surface shows numbers of round, translucent areas, 
 uniform in size, but varying in size in different cases, and 
 
io6 DISEASES OF THE SPLEEN 
 
 regular in distribution (Fig. 34). These give the typical 
 mahogany brown reaction with iodine solution. 
 
 Microscopically ', the waxy change is found to be chiefly in 
 the Malpighian bodies. The central artery may or may not 
 be affected. Round the artery there is often an area com- 
 paratively free from the change. The elements affected are 
 (i) the connective tissue of the capillaries, which run from 
 the central artery to open into the pulp ; and (2) the reticulum 
 of the lymphoid tissue. The lymphocytes themselves are 
 pressed upon and disappear. In addition (3) the inter- 
 muscular connective tissue of the middle coat of the arterioles 
 running through the pulp will probably show the change. 
 
 (2) Diffuse. In this variety the organ is always distinctly 
 enlarged. It is firm, shows a sharp margin on cutting, and 
 its cut surface has a translucent appearance and is of a pinkish- 
 red colour. With iodine a diffuse mahogany brown reaction 
 is given. This type is the one most usually found in syphilitic 
 cases. 
 
 Microscopically ', the change may be found, as in the previous 
 variety, in the Malpighian bodies, but often it is restricted to 
 the walls (periendothelial connective tissue) of the venous 
 sinuses. Frequently the sinuses are particularly well seen, 
 owing to the organ being the seat of chronic venous congestion. 
 The arterioles of the pulp, and sometimes those of the 
 Malpighian bodies, may show the change. 
 
 Hyaline Degeneration of the arterioles of the spleen is 
 found in certain infective fevers, such as diphtheria and 
 scarlatina. The condition gives rise of itself to no obvious 
 alteration. 
 
 Microscopically ', the change is found chiefly in the intima 
 of the arterioles, which show a homogeneous swelling, partially 
 obliterating the lumen of the vessels. 
 
 Pigmentation. The spleen is specially liable to post- 
 mortem pigmentation owing to its position close to the 
 stomach and large bowel. The organ shows a greenish.- 
 
DISEASES OF THE SPLEEN 107 
 
 black colour, which penetrates for a variable distance into its 
 substance. It is due to the action of the sulphuretted 
 hydrogen escaping from the hollow viscera and acting upon 
 the free iron in the organ, producing black sulphide of iron. 
 
 In severe anaemias, in malaria, and in toxic conditions 
 there is increase of iron-containing pigment in the organ. 
 This, more particularly in the case of anaemias, may be in 
 such quantity as to be demonstrable to the naked eye. The 
 Prussian blue reaction with dilute hydrochloric acid and 
 potassium ferrocyanide is usually not well seen in the case 
 of the spleen, owing to the large quantity of blood in the 
 pulp. 
 
 CIRCULATORY DISTURBANCES 
 
 Acute Congestion or Active Hyperaemia. This is 
 constantly seen in acute toxic conditions, such as pneumonia, 
 septicaemia, acute fevers, etc. The spleen is enlarged, soft 
 as a rule (although in typhoid fever it is often fairly firm), 
 and pale in colour. On section, the pulp is found to be very 
 soft, often capable of being washed away in a stream of 
 water. The colour is a creamy pink. The Malpighian 
 bodies are sometimes prominent, more especially in children. 
 There are not infrequently haemorrhages. 
 
 Microscopical 'fy, the sinuses are found to be distended with 
 blood, which shows a larger proportion of white cells than 
 usual. There is swelling of the endothelial cells lining the 
 sinuses, and these can often be seen to contain red blood 
 corpuscles. In typhoid fever, areas of focal necrosis are 
 always found, and often distinct masses of bacilli. In other 
 conditions, organisms may be demonstrable, and even the 
 commencement of abscess formation may be found. True 
 abscess formation in the spleen is rare. 
 
 Chronic Venous Congestion or Passive Hypersemia. 
 
 This condition is found in (i) chronic valvular disease of the 
 heart, (2) chronic pulmonary disease, (3) cirrhosis of the liver. 
 
io8 DISEASES OF THE SPLEEN 
 
 The spleen is uniformly enlarged, retaining its normal 
 shape and notches. There may be opaque areas of chronic 
 perisplenitis. Not infrequently depressed yellow areas (pale 
 infarcts) or dimples or puckerings indicating absorbed infarcts 
 are visible on the surface (Fig. 32). The remainder of the 
 organ is of a dark purple colour. In consistence it is firm. 
 The cut surface is dark purple, with white specks and lines 
 indicating trabeculse, which may be more prominent than 
 usual. Malpighian bodies are not easily seen. 
 
 Microscopically, there may be some increase of the periendo- 
 thelial connective tissue in the walls of the sinuses. The 
 sinuses themselves are distended with blood. Their endo- 
 thelial cells are swollen and show increased phagocytosis of 
 red blood corpuscles. Pigment derived from these latter may 
 be seen in the cells. Under the microscope it is exceedingly 
 difficult to distinguish chronic from acute congestion. 
 
 Infarction. This may be due to (i) embolism, (2) 
 thrombosis occurring in a diseased artery or vein. 
 
 The infarcted areas may be red or pale, and in the early 
 stages are raised above the surface (Fig. 31). Later on they 
 become depressed, and eventually form a pucker on the 
 surface and cicatrix in the substance. The larger infarcts 
 may extend right across the surface of the organ. On 
 section, the smaller ones are, as a rule, wedge-shape, and 
 situated superficially. The blocked vessel may be visible 
 at the apex of the wedge, the base being formed by the 
 surface of the organ. In the case of the older infarcts a 
 zone of fibrous tissue forms round the margin. Within this 
 there is frequently a zone of yellow (hsematoidin) pigment. 
 Rarely the infarcted areas may undergo softening. This 
 softening may be simple or septic. 
 
 Microscopic Appearances. In the earliest stage (red 
 infarct) all that is to be noted is overfilling of the sinuses with 
 blood and the presence of fibrin filaments between the blood 
 cells. Later (pale infarct) the nuclei of the splenic cells are 
 
DISEASES OF THE SPLEEN 109 
 
 found to have lost their characteristic staining reaction. The 
 outline of the sinuses and individual cells may still be seen. 
 Still later, all evidence of structure disappears. Round the 
 infarcted area there develops a zone of granulation tissue, con- 
 sisting of young blood-vessels, leucocytes, and fibroblasts in 
 various stages of development. Within this zone, bunches of 
 yellow acicular crystals of hasmatoidin are frequently to be 
 observed. 
 
 INFLAMMATIONS 
 
 Acute Perisplenitis is seen in all cases of acute general 
 peritonitis. 
 
 Chronic Perisplenitis is very frequently seen as pearly 
 white areas of thickening in the capsule of the organ. The 
 thickening may be considerable and very hard, even like 
 cartilages. It is frequent in cases where the organ is enlarged, 
 as in leukaemia. Adhesions to the parietes are not in- 
 frequently associated. In cases of tuberculous peritonitis 
 the capsule of the organ often shows characteristic tubercle 
 granulations. 
 
 Acute Inflammation of the Spleen Substance is rare. 
 In cases of septic infarction the commencement of abscess 
 formation may be seen. 
 
 Chronic Interstitial Splenitis, or overgrowth of the 
 fibrous tissue of the organ, is to be found in many conditions, 
 lymphadenoma, leukaemia, malaria. 
 
 Tuberculosis of the spleen is invariably associated with 
 tubercle elsewhere. Two types of the condition occur. 
 (i) The commonest form is miliary tuberculosis associated 
 with generalised infection. The organ is usually not much 
 altered in size. Scattered through it are numerous minute 
 grey, white, or yellow points, which are often difficult to 
 distinguish from Malpighian bodies. 
 
 Microscopically ) there are found tubercle follicles with giant 
 cells and surrounding epithelioid cells, or centres of commenc- 
 ing caseation. 
 
no DISEASES OF THE SPLEEN 
 
 (2) The other form of tuberculosis in the spleen shows 
 large, rounded, opaque white or yellow caseous masses 
 scattered through the organ, the so-called "hard -bake" 
 spleen, from the resemblance to almond toffee (Fig. 33). 
 This variety is found chiefly in children. 
 
 Lymphadenoma or Hodgkin's Disease (also known as 
 Pseudoleuksemia). This is a disease primarily of the 
 lymphatic glands (p. 104). The spleen is, however, very 
 constantly affected, especially in advanced cases. When 
 affected the organ is almost invariably enlarged. The 
 enlargement is uniform, although there may be projections 
 on the surface. On section, numerous opaque, pale bodies, 
 angular in shape and more or less uniformly distributed 
 (Fig. 35), are to be seen. Sometimes they are grouped into 
 masses (Fig. 36). At first grey and somewhat translucent, 
 they become more opaque white in the later stages, and 
 stand out in marked contrast to the general colour of the 
 spleen which is pink to dark red. The whole appearance 
 of the cut surface is compared to masses of suet in a 
 pudding. 
 
 Microscopically ', the appearances are essentially those seen 
 in the lymphatic glands. The change is primarily in the 
 Malpighian bodies, which in the early stage show merely 
 hyperplasia of the lymphocyte cell elements. Soon the large 
 spindle-shaped endothelial cells appear, many of which are 
 multi-nucleated, while the lymphocytes diminish in numbers. 
 The large endothelial cells tend to pass into the pulp, and as 
 they are actively phagocytic they take up red cells, and later 
 show hasmatoidin pigment. Fibrosis commences at a com- 
 paratively early stage, and later the Malpighian body may 
 become entirely transformed into a knot of well -developed 
 fibrous tissue. Not infrequently areas of necrosis occur, as in 
 the lymphatic glands. 
 
 Tumours of the spleen are rare. 
 
 Angiomata and angiosarcomata, the latter with secondary 
 deposits in the liver, are described. 
 
DISEASES OF THE THYROID GLAND in 
 
 Secondary tumours are also rare, sarcomata being occasion- 
 ally found. 
 
 EXAMINATION OF THE SPLEEN REMOVED FROM THE BODY 
 
 Note in the first instance the size of the spleen. The 
 normal organ measures about 5 inches by 3 (12.5 x 7-5 cm.), 
 and the weight is 5-8 oz. (150-250 gm.). If the spleen is 
 enlarged, note whether this enlargement is uniform, the organ 
 retaining its normal shape, or localised. The spleen is uni- 
 formly enlarged in acute congestion, chronic venous congestion, 
 amyloid disease, lymphadenoma, leukaemia, malaria, etc. It 
 is irregularly enlarged in some cases of lymphadenoma, in 
 tumour and cyst formations. It is diminished in size in the 
 atrophy of old age and in wasting diseases. 
 
 Examine the surface for thickenings of the capsule, peri- 
 toneal tubercles, evidence of infarction, etc. Determine the 
 consistence. The normal organ is moderately firm. In 
 acute congestion it is soft, in chronic venous congestion, 
 waxy disease, lymphadenoma, and leukaemia the consistence 
 is increased. After making a longitudinal incision into the 
 organ, note whether the edge of the cut becomes rounded, 
 as is the case when the consistence is soft, or remains sharp, 
 as is the case when the consistence is increased. Examine 
 the cut surface for the relative prominence of the Malpighian 
 bodies (these are usually much more obvious in children than 
 in adults), for haemorrhages, infarcts, opacities, etc. Note 
 the general colour of the organ, which normally is brownish 
 purple. 
 
 DISEASES OF THE THYROID GLAND 
 
 Congenital absence of the thyroid is found in cases of 
 cretinism. Atrophy of the gland in early life is another 
 cause of the same condition. Atrophy in adult life gives rise 
 to the disease myxcedema. In this disease the gland is 
 reduced to a mass of fibrous tissue, in which a few gland acini 
 may still be found. Associated with the change in the 
 thyroid is a myxornatous degeneration of the subcutaneous 
 
H2 DISEASES OF THE THYROID GLAND 
 
 tissue, with atrophy of the sebaceous glands, hair follicles, 
 and other cutaneous structures. 
 
 Waxy Degeneration is sometimes found well marked 
 in the thyroid, the gland being considerably enlarged. 
 
 Enlargement of the Thyroid, Goitre, Struma, or 
 Bronchocele. 
 
 1. Simple Goitre. A degree of enlargement of the organ 
 is not infrequently found, more especially and markedly in 
 individuals from certain districts, such as Derbyshire. 
 Whether this is a tumour formation, or merely a dilatation 
 of the existing acini, is doubtful. In some cases there is 
 evidence of proliferation of the gland elements, in others 
 none. In certain cases there is marked overgrowth of 
 fibrous tissue. 
 
 Microscopic Appearances. Gland acini are seen, varying 
 in size, some being greatly dilated, lined with cubical cells, 
 and filled with colloid material. There is a variable amount 
 of supporting connective tissue. 
 
 2. Exophthalmic Goitre. In the condition often known 
 as Graves 's disease there is a uniform enlargement of the 
 thyroid gland (Fig. 39). The gland is pale pink or white, 
 and on section shows no evidence of colloid material. Cysts 
 may be present, but their contents are usually liquid. The 
 cut surface is more like that of the pancreas or of a salivary 
 gland than of the normal thyroid. 
 
 Microscopic Appearances. The most striking thing is the 
 absence, or almost complete absence, of colloid material. The 
 acini are relatively small and vary in shape and size. The 
 cells lining them are columnar instead of being cubical. 
 Papillary ingrowths into the acini may be seen. Shedding of 
 the cells may be found. There is marked vascularity of the 
 interacinous tissue. 
 
 Tumours. Adenomata and cystic adenomata are some- 
 times found. Carcinomata, and, more rarely, sarcomata 
 
DISEASES OF SUPRARENAL GLANDS 113 
 
 occur. The normal thyroid weighs rather more than an 
 ounce (30-40 gm.). 
 
 DISEASES OF THE THYMUS GLAND 
 
 This gland is largest about the second year, after which 
 it becomes progressively smaller, and is usually atrophied 
 after the twenty-fifth year of life. It may, however, persist, 
 and may be found enlarged in conditions such as exophthalmic 
 goitre. It is also enlarged, along with the lymph glands of 
 the body generally, in a condition sometimes found in children, 
 where death may occur suddenly under the administration 
 of chloroform, or without any obvious reason. This condition 
 has been called status lymphaticus or " lymphatism." 
 
 Inflammation of the thymus is found in cases of severe 
 inflammation of the neck, spreading downwards. 
 
 Tumours of the gland are rare, although mediastinal 
 sarcomata sometimes take their origin in it. 
 
 DISEASES OF THE SUPRARENAL GLANDS 
 
 It should be remembered that the suprarenal gland 
 represents a combination of two types of tissue, probably 
 with totally different functions. The cortical portion is 
 formed of columns of gland cells with intervening capillary 
 vessels. The cells are polygonal, and, in the fresh condition, 
 contain large quantities of myelin and other fatty bodies ; 
 hence the yellow colour of the cortex. The function of the 
 cortical portion has not yet been satisfactorily decided. 
 
 The medullary portion of the gland is grey to the naked 
 eye, with red spots scattered through it, indicating vessels. 
 Microscopically, it is found to consist of blood spaces lined 
 with endothelium, and between these ganglion cells with a 
 peculiar affinity for neutral salts of chromic acid. These 
 chromaffin or chromophil cells, which are also found in the 
 
 8 
 
ii4 DISEASES OF SUPRARENAL GLANDS 
 
 pituitary gland, the carotid body, and the coccygeal glands, 
 are believed to be the cells which secrete adrenin. In all 
 cases where the suprarenal is suspected to be at fault the 
 gland, as well as other parts containing chromaffin cells, should 
 be fixed in a chrome salt fixative, such as Miiller's fluid, and 
 cut in gum (see p. 354). 
 
 Accessory Suprarenals. These may be found not only in 
 the kidney, liver, and tissue in the immediate neighbourhood 
 of the suprarenal, but also in the broad ligament and ovary. 
 They are known as suprarenal or adrenal rests, and it is 
 believed that they form the starting-point of certain tumours 
 known as hypernephromata. These " rests " are formed 
 usually only of the cortical portion of the gland. 
 
 Haemorrhages into the suprarenal are not very infrequent. 
 They occur, more especially in children, in fevers and in 
 wasting conditions. Such haemorrhages may be the cause 
 of sudden death. 
 
 Tuberculosis. This shows itself in two forms. 
 
 1. As a part of a general tuberculosis with small caseous 
 nodules in the gland, as in other organs and tissues. 
 
 2. As a fibro-caseous process involving both glands, often 
 the only tuberculous manifestation in the body, causing 
 complete destruction of the organ. This is the type of 
 change commonly associated with Addison's disease. 
 
 Addison's Disease. Besides the above-mentioned chronic 
 tuberculosis of the suprarenals, there have been found in 
 cases of Addison's disease fibroid atrophy of the suprarenal 
 and tumour formation. In a few cases the glands have 
 been found normal, but the semilunar ganglia and chrom- 
 affin tissue generally have been affected. 
 
 Tumours. Hypernephromata or tumours, the cells of 
 which resemble those of the cortex of the normal gland 
 may grow from the suprarenal. They may be simple or 
 malignant (p. 224). 
 
DISEASES OF SUPRARENAL GLANDS 115 
 
 Carcinomata and sarcomata may also be found. They 
 are usually secondary, and commonly there are deposits in 
 both organs. The weight of the suprarenals varies consider- 
 ably. It has been given as 4-7 grammes. The left is slightly 
 the heavier. 
 
CHAPTER VII 
 
 DISEASES OF THE RESPIRATORY SYSTEM 
 
 DISEASES OF THE LARYNX 
 
 (Edema, also called oedema glottidis. This may be due 
 to the swallowing of boiling water, to acute inflammation 
 in the neighbourhood, e.g. acute tonsillitis. It may also occur 
 in association with kidney and heart disease. The parts 
 most affected are the posterior surface of the epiglottis, the 
 aryteno-epiglottic folds, and the false cords. The condition 
 is serious, from its interference with respiration. It shows 
 itself by swelling of the parts affected, which are pale and 
 have a translucent appearance. 
 
 Laryngitis. Acute and chronic catarrhal conditions of 
 the larynx show little that is obvious after death. There may 
 be hypersemia and collection of mucus. 
 
 Membranous Laryngitis. This is most commonly 
 diphtheritic in origin, although it may be due to streptococcal 
 infection. It may occur in the course of other specific 
 fevers, such as typhoid and smallpox. It occasionally is 
 caused by the presence of foreign bodies, such as fish bones. 
 The membrane usually occurs also over the tonsils and 
 pharynx, and may spread downwards into trachea and 
 bronchi. The membrane is commonly firmly adherent in 
 
 116 
 
DISEASES OF THE BRONCHI 117 
 
 the pharyngeal region. In trachea and bronchi it is easily 
 removable (Fig. 44). The membrane has a white or grey 
 appearance, and the subjacent tissue and surrounding parts 
 are acutely congested. 
 
 Tuberculosis of the Larynx. This condition is usually 
 secondary to pulmonary tuberculosis. It is characterised 
 by the deposit of tuberculous granulations, with subsequent 
 ulceration. The ulcers are found over the epiglottis, aryteno- 
 epiglottic and inter-arytenoid folds. At first superficial, 
 they tend to extend deeply, eroding the vocal cords, and 
 even the cartilage in the neighbourhood. The margins of 
 the ulcers are raised and nodular. 
 
 Syphilis of the Larynx. This may occur both in 
 hereditary and in acquired syphilis, and both as a secondary 
 and tertiary manifestation. In the secondary stage catarrhal 
 inflammation and mucous patches occur, in the tertiary 
 stage gummata, ulceration, and subsequent cicatrisation and 
 stenosis. Ulceration, when it occurs, tends to destroy cartilage 
 as well as soft parts, such as the base of the tongue and 
 pharynx. 
 
 Tumours of the Larynx. Among simple tumours, 
 papillomata and fibromata occur. Of malignant growths, 
 carcinomata are more common than sarcomata. 
 
 DISEASES OF THE BRONCHI 
 
 Acute Bronchitis. Inflammation of the bronchi may 
 be caused by many different organisms, e.g. staphylo cocci, 
 streptococci) pneumococcus , micrococcus catarrhalis. In 
 addition, irritating fumes, such as those of ammonia, may 
 produce it. Inflammatory conditions of the smaller bronchi 
 are often accompanied by inflammation in the contiguous 
 portions of lung (broncho-pneumonia). 
 
 The appearances in acute bronchitis are swelling and 
 
n8 DISEASES OF THE RESPIRATORY SYSTEM 
 
 congestion of the mucous membrane, with the presence of 
 a fibrinous or purulent exudate. When the bronchi within 
 the lung substance are affected, squeezing of the lung 
 expresses beads of purulent material. 
 
 Microscopic Appearances. The most striking change is 
 desquamation of the ciliated epithelial cells, which are found 
 lying free in the exudate along with polymorphonuclear 
 leucocytes. The basement membrane upon which the epithelial 
 cells rest is swollen. The underlying vessels are congested, 
 and the surrounding tissue infiltrated with inflammatory cells. 
 The cells of the mucous glands are swollen and granular. 
 
 Chronic Bronchitis. This condition may be organismal, 
 following the acute form, or it may be associated with the 
 occupation, the individual working in an atmosphere in 
 which there are many foreign particles, e.g. carbon, stone, 
 steel, etc. In appearance there may be little alteration 
 from the normal. Sometimes the lumen of the tubes is 
 dilated. The mucous membrane may be pale or congested. 
 Occasionally there may be superficial ulceration. There is 
 always a considerable amount of frothy muco-purulent 
 secretion in the tubes, which may show more or less pigmenta- 
 tion from the presence of foreign particles. The condition 
 is usually accompanied by emphysema of the lungs, and 
 often by dilatation of the right side of the heart. 
 
 Microscopically, the epithelium, when present, is of a 
 cubical rather than of a columnar type. In places the 
 epithelium may be entirely absent. The basement membrane 
 is often thickened and the subjacent tissue infiltrated with 
 inflammatory cells of a small, round, lymphocyte-like type. 
 There is usually overgrowth of fibrous tissue, and structures 
 such as bronchial muscle and mucous glands may be atrophied. 
 The lumen of the tubes contains desquamated epithelial cells 
 and polymorphonuclear leucocytes, mixed with strings of 
 fibrinous material. 
 
 Tuberculous Bronchitis. Tuberculous lesions of the 
 larger bronchi are not commonly met with, although tubercles 
 
DISEASES OF THE LUNGS 119 
 
 may develop in the mucous membrane and subsequently 
 ulcerate. Lesions of the smaller bronchi within the lung are 
 common in pulmonary tuberculosis. Peribronchial tubercles 
 may break through into the lumen of the tubes and lead to 
 ulceration. The smaller bronchi not infrequently dilate 
 through weakening of their walls by inflammatory change. 
 Such dilatations may form the starting-point of cavities. 
 
 Syphilitic Bronchitis. Gumma formation, with sub- 
 sequent ulceration, although uncommon, is met in the 
 larger bronchi, usually at their commencement, and in the 
 trachea at its bifurcation. 
 
 A number of cases of sudden death from haemorrhage 
 through erosion of a large vessel (pulmonary artery, left 
 bronchial artery, superior vena cava) by such an ulcer have 
 been recorded. 
 
 Bronchiectasis, or dilatation of the bronchi, is usually 
 met with in connection with an interstitial pneumonia 
 (tuberculosis, syphilis). The dilatation may be fusiform or 
 saccular. It is produced by traction on the part of the 
 contracting fibrous tissue in the neighbourhood together with 
 adherence of the lung to the chest wall. A generalised 
 dilatation of the bronchi may follow collapse of a lung. 
 
 Bronchiolectasis, or dilatation of the bronchioles, is a 
 common occurrence in broncho-pneumonia, more especially 
 in children. The walls of the tubes, weakened by the in- 
 flammatory process and under pressure from within through 
 coughing, distend. As a rule the amount of distention is 
 small, but in certain cases it may go on to such a degree that 
 large cavities are produced in which secretion accumulates. 
 Such a condition has been called " honeycomb lung." 
 
 DISEASES OF THE LUNGS 
 
 Collapse. A lung which is not consolidated, and which 
 is not held in position by adhesions between the two layers 
 
120 DISEASES OF THE RESPIRATORY SYSTEM 
 
 of the pleura, the moment that the pleural cavity is opened 
 collapses to about one-third of its bulk. Such lungs are 
 therefore always observed in this semi-collapsed condition. 
 A similar condition, or one which is more complete, may be 
 produced during life by the presence of air in the pleural 
 cavity, or from dropsical or purulent fluid in the sac. In 
 such a case the lung is of a slate-grey colour (Fig. 41), 
 anaemic, tough, and sinks in water. On squeezing, few or no 
 air-bubbles can be expressed from the cut surface. If the 
 collapsed condition have persisted for long, there will be 
 overgrowth of fibrous tissue, and sometimes dilatation of 
 the bronchi. If adhesions bind portions of the lung to the 
 parietal pleura, the collapse will be partial. 
 
 Collapse of small portions of lung is often observed post- 
 mortem, more particularly in the lower and posterior parts 
 of the organ. These appear as dark purple areas slightly 
 depressed below the general surface. They can be reinflated 
 by pressing air into them from neighbouring parts. 
 
 Similar small areas of collapse are found in cases of broncho- 
 pneumonia. They are due to blocking of the smaller bronchi 
 with exudate, and the subsequent absorption of the air by 
 the blood. 
 
 Localised collapse may also be found in the lung in the 
 neighbourhood of aneurysms or tumours pressing directly 
 upon the lung. 
 
 Microscopic Appearances. The alveolar walls are relaxed 
 and approximated. The vessels are usually dilated. There 
 may be evidence of catarrh in the alveoli. Increase of fibrous 
 tissue may be observed. The elastic tissue appears to be 
 increased, but that is merely because of the relaxation of the 
 lung substance and the condensation of the fibres. 
 
 Atelectasis. This is a condition similar to the above, 
 which may be found in the new-born child, but as it is due 
 to want of expansion, the term " collapse," although some- 
 times used, is scarcely applicable. The condition may be 
 
DISEASES OF THE LUNGS 121 
 
 complete or partial. When partial, it is commonest in the 
 lower lobe, especially in its posterior part. The organ which 
 is the seat of the change, instead of being pale pink and 
 crepitant, is dark red, tough, and airless. If the condition 
 is partial, the area affected is depressed below the air-contain- 
 ing portion. The affected portion sinks in water (see p. 310). 
 
 Emphysema. Two varieties of this condition are found 
 in the lung : (i) vesicular emphysema, or over-distention 
 of the air vesicles of the lung ; (2) interstitial emphysema, 
 or the escape of air into the fibrous supporting tissue of 
 the lung. 
 
 (i) Vesicular Emphysema. This is a condition of over- 
 distention of the lung alveoli caused by (a) forcible distention 
 of the air vesicles from constant coughing, as in chronic 
 bronchitis, or from the blowing of wind instruments; (b) 
 the giving way of the elastic network of alveolar walls 
 before a normal pressure ; this may be due to wasting disease, 
 to old age, or to an inherent imperfect development of the 
 tissue. The portions of the lung most affected are the apex, 
 the anterior and lower borders, that is to say, those portions 
 where over-distention can occur most readily. The lung is 
 pale (Fig. 40), light, and has a spongy feel, like the sensation 
 given on pressing a bag of feathers. On section, it is dry 
 and bloodless. There may be areas of very marked dis- 
 tention forming small bladders or bullae. The condition 
 is usually associated with chronic bronchitis and enlargement 
 of the right side of the heart. Hypertrophic and atrophic 
 forms of emphysema are distinguished; in the former the 
 organ is more voluminous, in the latter it is smaller than 
 usual. The hyper trophic type is found in cases where 
 forcible distention from coughing is the cause, the atrophic 
 type in cases of wasting disease in old age, or where the 
 elastic tissue of the organ is naturally imperfectly developed. 
 
 Complementary or compensatory emphysema is found in 
 
122 DISEASES OF THE RESPIRATORY SYSTEM 
 
 small areas of lung in close approximation to areas of collapse 
 or to areas of shrinkage from fibrosis. This latter type, 
 found in the neighbourhood of healed tubercle foci, may be 
 called traction emphysema (p. 146). 
 
 Microscopic Appearances. There is marked over-distention 
 of the air vesicles and smaller air passages. The smaller 
 vessels have, to a great extent, disappeared. The elastic fibres 
 of the alveolar walls are stretched and widely separated. 
 The bronchi may show evidence of chronic catarrh. 
 
 (2) Interstitial emphysema is a rare condition when, owing 
 to rupture of the lung from injury (e.g. fractured rib, stab, 
 or bullet wound) or disease (e.g. gangrene, emphysema), the 
 air escapes into the fibrous supporting tissue. In this 
 position it works its way to the root of the lung, and eventually 
 into the mediastinum and areolar tissue of the neck, 
 
 CIRCULATORY CHANGES 
 
 Acute Congestion or Hyperaemia. This condition is 
 usually found preceding or associated with inflammation 
 of the lung. It will be described in connection with 
 pneumonia. 
 
 Passive Congestion or Hypersemia. Two varieties of 
 this condition may be distinguished. 
 
 1. Hypostatic congestion, a condition frequently found 
 post-mortem, more especially in cases where the circulation 
 has been slowly failing. As the name indicates, it is in the 
 posterior parts of the lung (the parts where gravity has most 
 influence on the blood) that the condition is most marked. 
 The area involved is dark purple in colour, and is often the 
 seat of oedema and inflammatory consolidation. 
 
 2. Chronic Venous Congestion of the Lung. This occurs 
 where there is long-standing obstruction to the passage of 
 the blood through the lungs, as in cases of chronic valvular 
 disease of the left side of the heart. The organ is of a dark 
 
DISEASES OF THE LUNGS 123 
 
 red, sometimes brick -red colour, and in the later stages 
 it is of firmer consistence, hence the term " brown 
 induration.' 7 Not infrequently infarcts are present in such 
 lungs. 
 
 Microscopic Appearances. The vessels generally are dilated, 
 and, in the case of the alveolar capillaries, they project into the 
 interior of the air vesicles and are obviously thickened. Red 
 blood cells may be found free in the spaces, also shed endothelial 
 (catarrhal cells) containing pigment derived from broken-down 
 red corpuscles. Catarrhal changes will also probably be found 
 in the bronchi, and there may be some increase of fibrous 
 tissue, but this is seldom in sufficient amount as to be obvious 
 under the microscope. In the hypostatic variety oedema and 
 more acute inflammatory changes may be present. 
 
 Haemorrhage into the lung substance may occur in the 
 form of minute petechial hemorrhages, usually under the 
 pleura. Such are found in severe anaemias, in cases of death 
 from suffocation, and in infective conditions. Larger haemor- 
 rhages are found in infarction, in severe inflammations, 
 and in gangrene ; also sometimes in tuberculosis. 
 
 Infarction (Pulmonary Apoplexy). This is a common 
 condition to find in lungs the seat of chronic venous 
 congestion. When the area of lung involved is large, the 
 condition may be the cause of sudden death. The causation 
 of the condition is not quite clear, as it is difficult to produce 
 infarction experimentally by the injection of artificial emboli. 
 In a majority of cases, however, the artery leading to the 
 area will be found plugged with an embolus, and on careful 
 examination a source will be found for the embolus, e.g. a 
 thrombus in the right auricular appendix or in a vein (see 
 diagram, p. 62). Another view of the causation is that it is 
 due to thrombosis in the vessel, not to embolism. Another 
 that it is merely due to escape of blood from a burst 
 capillary into the spongy tissue of the lung. 
 
 The condition is more frequently found in the lower lobes 
 
124 DISEASES OF THE RESPIRATORY SYSTEM 
 
 than in the upper. It occurs specially at the margins of the 
 lung (anterior and lower) and towards the surface, not in 
 the substance. 
 
 The area involved is more or less angular (Fig. 45). It is 
 raised above the general surface of the organ ; that is to say^ 
 it remains distended when the neighbouring lung undergoes 
 partial collapse. It is usually dark purple in colour and 
 hard in consistence. Occasionally it may be pale from sub- 
 sequent decolorisation. Sometimes a zone of fibrous tissue 
 develops around the infarct, and the area may undergo 
 softening or it may cicatrise. Infarcts of the lung, however, 
 seldom show the later changes found in infarcts elsewhere. 
 This is no doubt partly due to the fact of the double blood 
 supply of the lung. It is also due to the fact that many of 
 the infarcts occur shortly before death, and in some instances 
 are the actual cause of death. 
 
 Microscopic Appearances. In the area involved, the alveoli 
 are filled with red blood cells and fibrin, or, in other words, 
 with blood clot. There are also leucocytes present, more 
 especially at the margin. The cells of the alveolar walls show 
 some loss of staining reaction, but necrotic changes are not 
 frequently found in infarcts of the lung. There may also be a 
 development of fibrous tissue round the area. 
 
 (Edema. This is an exceedingly common condition. It 
 is found in cases in which dropsy tends to occur elsewhere, 
 as in heart disease and in Bright's disease. It is also very 
 commonly present in cases where death has occurred slowly, as 
 in wasting diseases, e.g. cancer, anaemia. It is frequently com- 
 bined with hypostatic congestion, and tends to occur in 
 the more dependent portions of the lung. Thus it is more 
 frequent in the posterior portions of the lower lobe. Occasion- 
 ally, however, it is most marked in the upper lobe. (Edema 
 frequently occurs in the neighbourhood of pneumonic areas. 
 The organ is pale unless congestion is superadded. It is 
 bulky and feels fairly solid, but, unlike a pneumonic 
 
DISEASES OF THE LUNGS 125 
 
 lung, it pits on pressure. When one cuts into it and presses 
 the lung substance, frothy fluid escapes. 
 
 Microscopically, the alveoli are found distended, their 
 contents being finely granular material, which is all that is left 
 of the albuminous exudate after the tissue has been fixed, 
 hardened, and cut. Catarrhal cells and leucocytes are also 
 usually present within the alveoli. 
 
 INFLAMMATIONS OF THE LUNG PNEUMONIA 
 
 Types of Pneumonia. 
 
 1. Acute lobar pneumonia (croupous pneumonia). 
 
 2. Lobular pneumonia (catarrhal pneumonia). 
 
 3. Purulent (septic) broncho-pneumonia. 
 
 4. Hypostatic pneumonia. 
 
 5. Interstitial pneumonia. 
 
 1. Acute Lobar Pneumonia 
 
 This condition, also called Croupous Pneumonia, is so well 
 defined that it may be called a specific disease. It is due in 
 the vast majority of cases to the diplo coccus pneumonia. This 
 organism is accompanied not infrequently by B. pneumonia, 
 streptococci) staphylococci, B. influenza, B. typhosus. Occasion- 
 ally these organisms are present by themselves. 
 
 The condition, as its name indicates, is one which usually 
 involves the whole or the greater part of the lobe of a lung. The 
 right lung is more frequently the seat of the disease than the 
 left, and the lower lobe than the upper lobe. Not infre- 
 quently the whole of one lobe and a portion of another lobe 
 may be affected, and less frequently both lungs may show 
 the change. Orth gives the percentage of involvement of 
 the two lungs as follows : right, 52 ; left, 33 ; both lungs, 15. 
 
 The term croupous is applied because of the type of exudate 
 present in the lung alveoli, which is essentially fibrinous. 
 
126 DISEASES OF THE RESPIRATORY SYSTEM 
 
 For reasons of convenience it is customary to divide the 
 process into four stages : (i) stage of active hypercemia or 
 acute congestion, (2) stage of red hepatisation, (3) stage of 
 grey hepatisation, (4) stage of resolution. The distinction 
 between these stages is an entirely artificial one. Frequently 
 more than one of them are to be observed in one and the same 
 lung. By themselves the first two are rarely seen/ owing 
 to the fact that death does not often occur during the early 
 stages of the disease. They are, however, not infrequently 
 seen in areas of the lung in which the later stages are present 
 in neighbouring parts. 
 
 (1) Stage of Acute Congestion. As regards the naked-eye 
 appearances at this stage there is little more to be observed 
 than a bright red colour in the lung substance on section. 
 The lung substance is still crepitant and spongy. 
 
 Microscopic Appearances. The vessels of the lung gener- 
 ally, and the capillaries in the wall of the alveoli in particular, 
 are distended with blood. This condition of the capillaries 
 gives a beaded appearance to the walls of the air vesicles. 
 Within the lumen of the vesicles may be found a few red blood 
 corpuscles, a few catarrhal cells thrown off from the wall, and 
 a minute quantity of exudate. Suitably stained specimens 
 may show germs. 
 
 (2) Stage of Red Hepatisation. Naked-eye Appearances. 
 The lung is distended and contrasts markedly with the semi- 
 collapsed condition of the ordinary lung. Not infrequently 
 the markings of the ribs may be seen. There is usually some 
 slight amount of fibrinous exudate over the area of lung 
 involved. In consistence the organ isfirm^ like a solid organ 
 such as the liver. It cuts readily, quite unlike the soft, 
 yielding, unconsolidated lung. The organ is immensely 
 increased in weight. A small portion removed and placed 
 in water at once sinks. 
 
 The cut surface of that portion of the lung which shows 
 the change has a reddish colour, which, on account of its 
 
DISEASES OF THE LUNGS 127 
 
 being mottled with paler areas and accumulations of black 
 pigment, has been compared with red granite. Usually 
 the cut surface, more especially the paler areas, has a granular 
 appearance, owing to the projection of plugs from the alveoli. 
 On squeezing the lung substance, only a little blood and 
 serous fluid, but no air, can be expressed. Those portions 
 of lung not 'actually consolidated may show congestion, and 
 sometimes cedema. 
 
 On opening up the bronchi their mucous membrane is 
 found swollen and injected and their lumen filled with sticky 
 rust-tinged exudate. The bronchial glands are swollen and 
 pink in colour. 
 
 Microscopic Appearances. Instead of the fenestrated 
 appearance of the normal lung section, the lung which is the 
 seat of this change appears like a solid organ. The alveoli 
 are filled with plugs consisting of a network of fibrin threads, 
 sometimes communicating with the coagulum in a neighbour- 
 ing vesicle through one of the stomata. In the meshes of the 
 fibrin are catarrhal cells, a few red blood corpuscles, and con- 
 siderable numbers of leucocytes, chiefly of the polymorpho- 
 nuclear type. In suitably stained specimens organisms can 
 usually be found. 
 
 In the walls of the alveoli the vessels are still distended 
 with blood. The bronchi show evidence of acute inflamma- 
 tion. The interlobular septa and the supporting fibrous tissue 
 of the lung generally are swollen and infiltrated with fibrin and 
 leucocytes. The pleura shows the changes of acute inflamma- 
 tion. Films made from the bronchial exudate will show 
 leucocytes, fibrin, desquamated epithelium, both flattened and 
 columnar, and characteristic germs. This last is the best 
 source from which to demonstrate the pneumococcus. 
 
 (3) Stage of Grey Hepatisation. Naked-eye Appearance. 
 The organ is distended as before, shows rib markings and 
 fibrinous exudate on the pleura over the affected lobe. As 
 before, it is firm, heavy, and a portion removed sinks in water. 
 The cut surface, however, is pale, and, with the black mottling 
 of the carbon, is not unlike grey granite in appearance (Fig. 42). 
 
128 DISEASES OF THE RESPIRATORY SYSTEM 
 
 The granularity of the cut surface is more marked, and, on 
 scraping the surface with a knife, turbid fluid and plugs from 
 the alveoli can be removed. On squeezing, similar fluid can 
 be expressed, but no air-bubbles. On opening up the bronchi 
 the mucous membrane, as before, is found to be swollen and 
 injected ; the contents have a more opaque white appearance. 
 
 Microscopic Appearances. The alveoli and smaller air 
 passages are filled, as before, with plugs, which are, however, 
 at this stage retracted from the walls, this space having been 
 filled during life with fluid. The fibrin threads are not so 
 obvious ; they are broken down and granular. In the meshes 
 of the coagulum are vastly more numerous cells, the increase 
 being entirely due to the accumulation of polymorphonuclear 
 leucocytes. Many of these stain badly owing to degenerative 
 changes. Germs are often difficult to find at this stage. The 
 capillaries in the walls of the alveoli are, to a large extent, 
 obliterated by the pressure of the contents of the air vesicles. 
 Bronchi, interlobular septa, and pleura show, as in the earlier 
 stage, evidence of inflammation. 
 
 (4) Stage of Resolution. Naked-eye Appearances. The 
 lung is still somewhat distended, but is now much softer. 
 From the cut surface considerable quantities of grey, milky 
 fluid can be expressed. 
 
 Microscopic Appearances. The alveolar plug is contracted 
 still more, and may be absent altogether. The contents of 
 the alveoli are granular material and degenerated leucocytes. 
 Multiplication in the endothelial cells of the alveoli is often 
 seen, as evidenced by their greatly increased number. These 
 may be found surrounding the remains of the plug. The 
 capillaries of the alveolar walls are again distended with 
 blood. 
 
 Other terminations than resolution in the case of lobar 
 pneumonia are : (i) septic softening, which may go on to 
 gangrene ; (2) fibrosis, or overgrowth of the fibrous support- 
 ing tissue of the lung, producing chronic interstitial pneumonia. 
 
 In carrying out a post-mortem in a case of acute lobar 
 
DISEASES OF THE LUNGS 129 
 
 pneumonia, the following conditions, more especially, should 
 be looked for in organs other than the lung : 
 
 (1) A leucoblastic condition of the bone marrow associated 
 with the marked polymorphonuclear leucocytosis of the 
 blood in the disease. 
 
 (2) Acute congestion of the spleen. 
 
 (3) Cloudy swelling of liver, kidneys, and heart muscle. 
 Other conditions which may complicate the disease are 
 
 ulcerative endocarditis, pericarditis, meningitis, peritonitis. 
 
 2. Lobular Pneumonia 
 
 Synonymous terms for this condition are : (i) broncho- 
 pneumonia, from the fact that areas of lung in connection 
 with, and around bronchi are involved; (2) catanhal 
 pneumonia, from the character of the exudate most 
 characteristically found in the alveoli. 
 
 The etiology of the condition may be said to be the same 
 as in the lobar form of pneumonia. It is more frequent 
 in children, and is the form of inflammation of the lung found 
 in the specific fevers. The matter might be put in this way ; 
 that pneumocpccic infection of the lung in children usually 
 shows the lobular type. When the lobular type occurs in 
 adults, the causal germ is usually some other organism than 
 the pneumococcus , e.g. streptococci, staphylo cocci. 
 
 Naked-eye Appearances. The lung may be slightly more 
 distended than normal. It has a mottled, red surface, 
 with (i) dark purple depressed areas of collapse, (2) red, firm 
 areas of consolidation, and (3) pale areas of compensatory 
 emphysema. On handling it, irregularly scattered areas of 
 a firmer consistence than the rest can be felt. On section, 
 the same mottled appearance is visible, with dark purple 
 areas of collapse where a bronchus has become plugged, pink 
 areas of consolidation, more or less rounded (Fig. 43), in the 
 centre of which can often be seen a small bronchus, from 
 
 9 
 
130 DISEASES OF THE RESPIRATORY SYSTEM 
 
 which, on squeezing the lung, a small bead of thick white 
 secretion can be pressed, also paler emphysematous areas. 
 The lung tissue generally is congested. On opening up the 
 bronchi, their mucous membrane is found swollen and con- 
 gested, with more or less purulent-looking secretion. The 
 bronchial glands are congested and swollen. The smaller 
 bronchi and bronchioles within the lung substance are not 
 infrequently dilated, sometimes to such an extent that a 
 " honeycomb " appearance is produced (see Bronchiolectasis). 
 
 Microscopic Appearances. To realise the true nature of the 
 change, large sections of lung should be cut. The consolida- 
 tion will then be seen to be patchy in its distribution, the 
 plugged alveoli being usually situated round a small bronchus 
 or bronchiole as their centre. This bronchus shows the 
 appearance of acute bronchitis, and its wall is infiltrated 
 with inflammatory cells. The elastic coat may be ruptured, 
 and not infrequently the lumen is dilated. The alveoli around 
 contain plugs which may be more fibrinous or more leucocytic, 
 the appearances varying considerably in different types of the 
 disease and in different positions. Towards the margin of the 
 area more of the cells filling the alveoli are of the catarrhal 
 type, i.e. they are cast off, swollen endothelial cells. Hence 
 the term "catarrhal pneumonia." The walls of the alveoli 
 generally show congestion of their vessels. 
 
 Broncho-pneumonia may resolve or may pass into septic 
 pneumonia or gangrene. 
 
 The associated changes in spleen, bone marrow, etc., are 
 the same as in lobar pneumonia. 
 
 3. Purulent or Septic Broncho-Pneumonia 
 
 This condition may occur : 
 
 (1) As a sequel to broncho-pneumonia, especially when of 
 the so-called aspiration type, e.g. associated with the inhala- 
 tion of septic material, as after operations on the mouth. 
 
 (2) Associated with obstruction to the bronchi, as by tumour 
 
DISEASES OF THE LUNGS 131 
 
 or aneurysm leading to retention of secretion (so-called 
 " retention " pneumonia). 
 
 (3) Associated with the presence of a foreign body in the 
 bronchi. 
 
 (4) As a blood infection due to the deposition of organisms 
 or infective thrombi in the pulmonary vessels (embolic or 
 metastatic pneumonia)) found specially in such conditions 
 as osteomyelitis and pyaemia. Septic infarcts are not in- 
 frequently associated. Such infarcts have the same distribu- 
 tion and often very much the same appearance as the 
 non-septic type (see p. 123), but they tend to be paler and 
 often show softening in their centre. Under the microscope 
 such infarcts are characterised by immense numbers of 
 polymorphonuclear leucocytes in addition to red blood cells, 
 also by masses of organisms. 
 
 The appearances are the same as in broncho-pneumonia, 
 but the inflammatory changes are more acute, and there is 
 a greater tendency to destruction of pulmonary tissue. The 
 bronchi are filled with purulent material. 
 
 Abscess. This condition is usually associated with 
 embolic pneumonia or septic infarction. The abscesses are 
 commonly small, but they may extend and pass on to gangrene. 
 They are surrounded with a zone of consolidated lung. 
 
 Gangrene. This is usually a secondary condition, the 
 result of putrefactive organisms reaching a consolidated or 
 necrosed portion of lung. Thus it may follow lobar or septic 
 pneumonia, infarction or abscess. It may also be due to 
 direct extension, as from a ruptured ulcer of the oesophagus, 
 or from a subphrenic abscess. It may be due to the presence 
 of foreign bodies in the bronchi, such as coins or false teeth. 
 
 The area involved is at first intensely congested, later it 
 becomes black, and the lung substance breaks down and 
 comes away, leaving a cavity (Fig. 46) lined with black or 
 greenish-black walls, the colour being due to changes in the 
 
132 DISEASES OF THE RESPIRATORY SYSTEM 
 
 effused blood. The contents of these cavities and of the 
 bronchi are usually brown, like prune juice, but may be paler, 
 like pus or putty. The neighbouring portions of lung show 
 pneumonic consolidation. The odour is always most offensive. 
 
 4. Hypostatic Pneumonia 
 
 This is a type of pneumonia associated with hypostatic 
 congestion and O3dema of the lungs, and therefore found in the 
 posterior and lower portions. It is the type of inflammation 
 which supervenes in old age, and in wasting diseases generally. 
 
 The distribution of the change allows of immediate 
 recognition. The consolidation is usually partial and 
 associated with oedema. 
 
 Microscopically ', the appearances differ in different parts 
 congestion, oedema, with catarrhal, fibrinous, and leucocytic 
 consolidation, all being found in close contact. 
 
 5. Interstitial Pneumonias 
 
 These are conditions in which there is increase in the 
 fibrous tissue of the lung. They may be divided into three 
 groups : 
 
 (1) Those following previous acute pneumonia. 
 
 (2) Those due to the inhalation of dust of various kinds. 
 
 (3) Those due to chronically acting bacterial poisons, tuber- 
 culosis, syphilis, actinomycosis. 
 
 Interstitial Pneumonia following acute lobar or lobular 
 pneumonia is a comparatively rare condition. It usually 
 shows itself as localised areas of thickening of pleura and 
 interlobular septa also of the fibrous tissue at the root of the 
 organ. Sometimes it is more diffuse, involving considerable 
 areas of lung tissue. In this condition, as in other types 
 where there is marked thickening of the alveolar walls, 
 the endothelial cells of the alveoli may become cubical. 
 
 Interstitial Pneumonia due to the Inhalation of Dust 
 
DISEASES OF THE LUNGS 133 
 
 (Pneumokoniosis). There are three common varieties of 
 this, according to the type of dust inhaled : 
 
 (1) Anthracosis or coalminer's lung. 
 
 (2) Silicosis or stonemason's lung, also known as Chalicosis. 
 
 (3) Siderosis or needle-grinder's lung. 
 
 In all these conditions the foreign particles which are 
 inhaled are absorbed into the lymphatics, partly by the 
 action of phagocytes. They tend to be deposited along the 
 course of the lymphatics, and there to set up irritation and 
 consequent fibrosis. Thus nodules of fibrous tissue develop 
 beneath the pleura, along the interlobular septa, bronchi, 
 and vessels. The lymph glands at the root of the lung are 
 enlarged and indurated. Owing to the irritant action of the 
 foreign particles preparing the way for germs, tuberculosis 
 is a very common accompaniment of all these conditions. 
 They are also frequently complicated by chronic bronchitis 
 and emphysema, and by a degree of catarrhal pneumonia, 
 and occasionally by bronchiectasis. The siliceous particles 
 are more irritating than the carbon, hence the nodules of 
 fibrous tissue tend to be larger in silicosis than in anthracosis ; 
 there are also more catarrhal changes in the alveoli. The 
 steel particles are more irritating than the siliceous, hence 
 the changes are most marked of all in siderosis. 
 
 Anthracosis. There is always a certain amount of 
 pigmentation in the lung of town dwellers, and also in most 
 country dwellers. This is enormously accentuated in those 
 who work in coal mines. When well marked the condition 
 is known as anthracosis. The lung is usually black, or almost 
 black, with small, hard, black nodules scattered under the 
 pleura and in the lung substance (Fig. 48). On squeezing, 
 there exudes an inky-black fluid. The bronchial glands are 
 enlarged, deeply pigmented, and indurated. 
 
 Microscopic Appearances. The nodules are found to 
 consist of well -formed fibrous tissue mixed with carbon 
 
134 DISEASES OF THE RESPIRATORY SYSTEM 
 
 pigment. They occur under the pleura, along the interlobular 
 septa, bronchi, and vessels. The superficial layer of the pleura 
 is, however, free from pigment. There is some degree of 
 catarrhal change in bronchi and alveoli, and some thickening 
 of the vessels. 
 
 Silicosis. The lungs in this condition are grey in appear- 
 ance, and, scattered through them, are numerous grey nodules, 
 which are hard and gritty to the touch. Similar nodules are 
 present in large numbers under the visceral pleura. They 
 tend to be larger than those in anthracosis (Fig. 47). 
 
 The disease is not unlike the more chronic forms of tuber- 
 culosis, and, as already pointed out, it is not infrequently 
 complicated by it. The pure condition may be distinguished 
 from tuberculosis by the hard and gritty character of the 
 nodules and by the absence of cavitation. 
 
 Microscopic Appearances. These are the same as in 
 anthracosis but the pigment is not so obvious (although carbon 
 pigment is also present), and there is more catarrhal change in 
 the surrounding lung. There may be endarteritis obliterans 
 of the vessels. Tuberculosis is often superadded. 
 
 Siderosis. The nodules in this type are larger, owing 
 to the greater irritation of the metal particles. The lungs 
 have a grey appearance and may be almost solid. Evidence 
 of tuberculous disease is very frequently present in addition. 
 
 Microscopically, in addition to the larger areas of fibrosis, 
 there is more catarrhal change in the alveoli, between the 
 nodules of fibrous tissue. 
 
 Syphilitic Disease : (a) White Pneumonia. This is a 
 condition occasionally found in children suffering from 
 congenital syphilis. The lungs are pale and firmer than 
 normal. 
 
 Microscopically, there is found an overgrowth of fibrous 
 tissue involving the walls of the individual alveoli. The 
 endothelium lining the alveoli is cubical instead of being- 
 flattened. 
 
DISEASES OF THE LUNGS 135 
 
 (b) Gummata. These occur as small caseous foci surrounded 
 by fibrous tissue. They are not infrequently absorbed, 
 leaving puckered cicatrices behind. They are indistinguish- 
 able from tuberculous caseous masses. 
 
 (c) Interstitial Pneumonia in acquired syphilis occurs as 
 areas under the pleura or towards the root of the lung. There 
 is thickening of the pleura, of the interlobular septa, and 
 increase of fibrous tissue around the bronchi and vessels. 
 The last usually show endarteritis obliterans. 
 
 Microscopically, there is overgrowth of fibrous tissue, 
 usually catarrh of the alveoli, and often accumulations of small 
 round, cells (miliary gummata). 
 
 TUBERCULOSIS 
 
 Tuberculosis. The lungs are by far the commonest 
 site for tuberculous disease. In a large proportion of cases 
 the disease does not progress far and soon heals, leaving 
 merely some cicatricial tissue behind. The apex of the lung 
 is the seat of election for the disease. Very often the 
 apices of both the upper and lower lobes are affected. 
 The disease may reach the lung by any of four paths : (i) 
 the air passages, (2) the blood-vessels, (3) the lymphatic 
 vessels, or (4) by direct extension. In most cases it is im- 
 possible to say by what avenue the disease originally came. 
 Nevertheless, certain statements can be made regarding 
 this question of the path of entrance, (i) Where the tubercle 
 lesions are uniformly scattered through the organ, the disease 
 has been brought by the blood-stream, and search should be 
 made for some older focus of infection in some other part of 
 the body or in the lung itself. This focus is commonly a 
 lymph gland which has become adherent to, and eventually 
 has ruptured into, a vein or a large lymphatic trunk, such as 
 the thoracic duct. Not infrequently the source is a focus 
 in the lung itself which has invaded a branch of the pulmonary 
 
136 DISEASES OF THE RESPIRATORY SYSTEM 
 
 vein. The condition is always associated with disseminated 
 metastatic tuberculosis in other organs, although the areas 
 may not be visible to the naked eye. 
 
 (2) Where the lesions are arranged in groups, in a cluster 
 like a bunch of grapes (staphyloid arrangement), the condition 
 has probably been spread by the lymphatics, and a vessel or 
 bronchus will be found in the centre of the group. This 
 arrangement is sometimes found distributed throughout the 
 lung. More often, however, this appearance is seen in 
 areas of the lung where there is an older lesion at some point, 
 and it is always seen at the margin of a spreading lesion of 
 the more chronic type. 
 
 (3) Where there is a localised lesion (and commonly, as 
 we have seen, it is at the apex of the upper lobe or at the 
 apex of both upper and lower lobe) the general view is 
 that the infective agent has been inhaled. The reason for 
 the apical position is probably because that portion of the lung 
 receives relatively less blood. Moreover, it is the portion 
 of lung which moves least during respiration. There is great 
 diversity of opinion upon this question. Another view is 
 that the infection has spread from the lymphatics of the 
 neck to the apex of the pleural cavity. There it sets up a 
 localised pleurisy with the formation of adhesions, along which 
 the bacillus passes to the apex of the lung. Again, the spread 
 may be less direct, the infection passing from the cervical 
 glands to the mediastinal and bronchial, and so outward into 
 the lymphatics of the lung itself. In these cases of infection 
 by way of the cervical lymph channels the tonsil is, in all 
 probability, the portal through which the germs enter. A 
 third view is that the infection is by way of the blood-stream, 
 and that, owing to the greater susceptibility of the apex, 
 the disease has progressed at that point and not at others. 
 
 (4) Very occasionally the disease may spread directly 
 from a diseased rib or vertebra, or through the diaphragm 
 from the abdominal cavity. 
 
DISEASES OF THE LUNGS 137 
 
 Mode of Spread. Once started, the tuberculous lesion 
 tends to spread in four ways : 
 
 (1) By direct continuity, passing from alveolus to alveolus, 
 and from one part of the lung to another. 
 
 (2) By the Air Passages. A focus invades a bronchus, and 
 sets up a tuberculous inflammation. The secretion is inhaled 
 into the areas of lung to which that bronchus passes. Or 
 infected secretion is coughed up for some distance and, in 
 the deep inspiration following a fit of coughing, it is inhaled 
 into the bronchi in other portions of the lung, even into the 
 bronchi of the opposite lung. 
 
 (3) By the Lymphatics. Tuberculosis is essentially a disease 
 which spreads by lymphatics. This lymphatic spread shows 
 itself in the occurrence of areas of fibro-caseous change in 
 the lymph channels around a focus of the disease, having 
 the staphyloid arrangement already mentioned. It is also 
 shown by implication of the nearest lymphatic glands. 
 
 (4) By the Blood Chronic tuberculosis leads to thickening 
 of the vessels. Acute tuberculosis tends to invasion of the 
 vessel wall and the infection of the blood. The vessels of the 
 lung are relatively thin walled. Invasion of a branch of the 
 pulmonary artery will lead to further infection of the area 
 of lung supplied by that artery. Invasion of a branch of a 
 pulmonary vein will lead to systemic infection in which the 
 lungs will participate. This is, however, not such a common 
 occurrence as might be expected, owing to the fact that the 
 tuberculous process is accompanied by non-specific in- 
 flammatory changes, which tend to obliterate a vessel before 
 invasion with tuberculous material can occur. 
 
 According to one authority this is the way in which the 
 lung is infected in most cases. Infection of the bronchial 
 glands occurs first, one of the affected glands becomes 
 adherent to a large branch of the pulmonary artery, and 
 infective material in this way enters the pulmonary circula- 
 tion. 
 
138 DISEASES OF THE RESPIRATORY SYSTEM 
 
 Characters of the Lesions. The tuberculous lesions tend 
 to occur in the form of isolated foci. These may be widely 
 separated from one another, or so closely packed that they 
 are practically continuous. They are either grey and more 
 or less translucent when they are formed of cellular elements 
 and fibrous tissue, or opaque white or yellow when these 
 elements have undergone caseation. There is always a 
 certain amount of interstitial change or fibrous tissue forma- 
 tion, both in the lesions and in the lung around. 
 
 In the more acute cases this fibrous tissue formation is 
 minimal. In such cases the condition tends to spread 
 diffusely, involving more or less of lung substance and 
 producing a catarrhal consolidation of the alveoli which sub- 
 sequently undergoes a caseous change (caseous pneumonia). 
 
 Microscopically, the tuberculous lesion is characterised by 
 a cell aggregation, the individual cell elements showing three 
 types : ( i ) large multinucleated or giant cells, the nuclei of 
 which are arranged commonly in a circle, or part of a circle, 
 round a central clear, necrotic area ; (2) spindle-shaped and 
 branched cells, with nuclei resembling those of the giant cell, 
 and, arranged round that cell (epithelioid or endothelioid cells) ; 
 (3) lymphocyte-like cells, with small dark-staining nuclei and 
 little protoplasm. 
 
 Polymorphonuclear leucocytes are, except in very acute cases, 
 relatively few in number. The giant cell is not infrequently 
 absent, and its place occupied by an area where the cells are 
 breaking down. This area, as it enlarges, loses all appearance 
 of structure. It is the commencement of the caseous process. 
 In addition, there is always more or less overgrowth of fibrous 
 tissue. In the more acute cases caseation predominates, 
 in the more chronic, fibrous tissue formation. Where this 
 inflammatory process invades the alveoli there is consolidation 
 of the lung, a consolidation characterised by the presence of 
 some exudate, not as a rule fibrinous, with numerous catarrhal 
 cells and leucocytes. This consolidated area of lung also tends 
 to undergo the caseous alteration whereby it becomes ap- 
 parently structureless, but in this caseous focus the fibrous 
 
DISEASES OF THE LUNGS 139 
 
 tissues, and more especially the elastic fibres, persist for long 
 almost unchanged. 
 
 The elastic fibres of the lung undergo some destruction both 
 by fragmentation and solution, in the area where cells and 
 nuclei are breaking down. The fibres which escape this 
 primary destruction may persist in the caseous area for an 
 almost indefinite period. It is largely for this reason that 
 necrotic caseous areas of lung remain firm. When secondary 
 infection with pyogenic and other forms of microbes occurs, 
 complete destruction of the elastic fibres and softening of the 
 caseous area takes place, the softened material is coughed up, 
 and a cavity results. Another way in which cavity formation 
 not infrequently starts is by inflammation of the walls of a 
 bronchus or bronchiole. The wall, weakened by the inflam- 
 matory process, next gives way under the increased pressure 
 associated with coughing. Destructive changes then occur, 
 and a cavity results which subsequently extends. 
 
 Classification of Tuberculous Affections of the Lungs. 
 The most satisfactory classification would probably be 
 upon the basis of the path of infection, but, owing to the 
 fact that in most instances it is practically impossible to be 
 certain of the path of entrance of the disease, owing, further, 
 to the fact that even in a case of probable air-passage infec- 
 tion the disease may spread by the lymphatics, and even by 
 the blood-vessels, this method is not entirely satisfactory. 
 Another method of classification is on the basis of the main 
 underlying histological change. As we have seen, there are 
 essentially two such changes in pulmonary tuberculosis : 
 (i) a filling up of the alveoli with exudate and cells (mainly 
 catarrhal) ; in other words, pneumonia or inflammatory 
 consolidation. The consolidated area subsequently under- 
 goes a necrotic (caseous) change. This type of lesion is 
 characteristic of the more acute conditions, i.e. where the 
 virulence of the organism is high or the resistance of the in- 
 dividual low. (2) A laying down of new fibrous tissue usually 
 in relation to pre-existing fibrous tissue (interalveolar, inter- 
 lobular, etc.), i.e. fibrosis, or interstitial pneumonia. This 
 
140 DISEASES OF THE RESPIRATORY SYSTEM 
 
 occurs in cases where the organism possesses a relatively low 
 degree of virulence or where the soil (i.e. the individual) is 
 unusually resistant. The two changes are commonly found 
 side by side, but sometimes the one predominates, sometimes 
 the other. 
 
 Probably no method of classification is completely satis- 
 factory, but the following has for long been found useful by 
 the author. It has the advantage of describing in general 
 terms the appearance of the lung condition as a whole. It 
 may be regarded as a compromise between the two methods 
 mentioned above. 
 
 1. Miliary or Disseminated Metastatic Tuberculosis (as 
 suggested by Orth). 
 
 2. Caseous or Tuberculous Broncho-Pneumonia, or, if 
 diffuse, Caseous or Tuberculous Pneumonia. This condition 
 may or may not be accompanied by cavity formation. This 
 includes the conditions which are usually described as acute 
 phthisis. 
 
 3. Fibro-caseous Tuberculosis, again either with or without 
 cavitation. This includes the condition known as chronic 
 phthisis. 
 
 There are objections to the above method of classification, 
 but on the whole it will be found that most types of pulmonary 
 tuberculosis can in this way be satisfactorily described. 
 
 The method avoids the use of the term " phthisis," which 
 is really a clinical one, and not infrequently incorrect at that, 
 meaning, as it does, a wasting disease. The terms used 
 merely form a starting-ground from which to detail the more 
 minute changes. 
 
 1. Miliary Tuberculosis or Disseminated Metastatic 
 Tuberculosis 
 
 This condition is usually blood-spread, but may be spread 
 by the lymphatics. It is associated with an older tuberculous 
 
DISEASES OF THE LUNGS 141 
 
 focus in the lung, bronchial glands, or a lesion in some 
 other part of the body. This primary focus should be sought 
 for. Where the condition is blood-spread, tubercles will be 
 found scattered through other organs and tissues ; if not 
 large enough to be seen by the naked eye, they will be 
 found on microscopic examination. 
 
 Naked-eye Appearance. The lung is uniformly congested. 
 Scattered through its substance are immense numbers of 
 grey, white, or yellow foci (Fig. 49), which may vary in size 
 from something just visible to an area one or two millimetres 
 in diameter. Frequently the areas vary in size in different 
 parts of the lung. Sometimes they are found to be larger 
 in the upper portions of the lung. Sometimes the areas are 
 arranged in groups (staphyloid arrangement) round blood- 
 vessels or bronchi, indicating that the spread has been by 
 way of the lymphatics. Where the distribution is uniform 
 throughout, spread by the blood-stream is most probable. 
 
 Microscopic Appearances. Scattered through the lung 
 substance between individual alveoli, around bronchi and 
 blood-vessels and interlobular septa, are rounded areas of cell 
 accumulation. The cells composing these are chiefly mono- 
 nuclear, of the epithelioid and lymphocyte type with catarrhal 
 cells and a few polymorphs. Sometimes in the centre there are 
 giant cells ; at other times the centre is occupied by an area 
 where the cells and their nuclei are breaking down. Not in- 
 frequently there is a distinct structureless caseous centre. In 
 specimens stained for elastic fibres there will be found some 
 destruction of these in the central area if they have been included. 
 In other cases (the more chronic type) the fibres are merely 
 pushed aside by the aggregating cells. 
 
 There is always a certain amount of involvement of the 
 surrounding lung alveoli. Those alveoli in the immediate 
 neighbourhood are consolidated with exudate, catarrhal cells, 
 and leucocytes. As this area of alveolar involvement enlarges, 
 the condition tends to pass into the second type caseous 
 broncho - pneumonia. There is usually more or less new 
 formation of fibrous tissue in and around the nodules. In the 
 
142 DISEASES OF THE RESPIRATORY SYSTEM 
 
 more acute type with necrotic centre this is minimal. In 
 suitably stained specimens tubercle bacilli, although few in 
 number, will be found, more particularly in the acute type. 
 Not infrequently bronchi and vessels will be seen in course 
 of invasion by the nodules. It is this secondary invasion of 
 vessels which largely accounts for the great number of the 
 tubercles, and for their variation in size, due to the fact that 
 they are of different ages. 
 
 2. Gaseous or Tuberculous Broncho-Pneumonia 
 or Caseous Pneumonia 
 
 Two types of this condition can be distinguished : 
 
 (1) A type in which there are areas of consolidation 
 scattered through the lung, spread by the blood or by the 
 lymphatics. This type is merely an example of the previous 
 condition where there has been fairly extensive spread into 
 the surrounding lung, so that a considerable group of alveoli 
 have become consolidated and have then undergone the 
 caseous change (Fig. 50). This type is found practically ex- 
 clusively in children. The individual areas may fuse with one 
 another, so that the consolidation may be complete, involving 
 a whole lobe. Occasionally cavity formation may be found. 
 
 (2) A type which commences in one particular portion of 
 the lung, usually near the apex of the upper lobe, and spreads 
 from that point. In such a case the infection is generally 
 
 believed to have been by way of the air passages. This type 
 is the common one found in progressive acute tuberculosis 
 in the adult. It is only occasionally seen in the early stages, 
 owing to the fact that it does not prove fatal until well 
 advanced. Sometimes, however, the initial stages are met 
 with in cases dying of diabetes or other wasting disease. 
 Usually, as the condition is met with in the post-mortem 
 room, the area of consolidation is extensive and cavitation 
 present (Fig. 51). Sometimes a less advanced type of the 
 disease is found in one lung when in the other a more 
 advanced stage exists. 
 
DISEASES OF THE LUNGS 143 
 
 Naked-eye Appearances. The lung shows chronic, occasion- 
 ally acute, pleurisy on the surface. It is partially consolidated, 
 usually the area of consolidation being towards the apex. 
 The cut surface shows areas of a white or slightly yellow, opaque 
 appearance, not unlike grey hepatisation. These may be 
 isolated and scattered, but there is usually one considerable 
 area which may involve the greater part of a lobe. In these 
 areas are cavities, usually small and often numerous, with 
 ragged walls. In advance of these areas, and often widely 
 scattered through the lung, are grey or yellow tubercles in 
 groups, indicating lymphatic spread (Fig. 51). Besides spread 
 by the lymphatics, spread by the bronchi (aspiration) and by 
 direct continuity of tissue is observed in this condition. The 
 bronchi show evidence of acute bronchitis and the lymph 
 glands at the root of the lung are enlarged and show grey 
 tubercles and caseous foci. There is usually more or less 
 fibrosis in connection with this type. As the fibrosis pre- 
 dominates, it passes into the next type. 
 
 This type of the disease has to be differentiated from acute 
 lobar and lobular pneumonia and gangrene of the lung, also 
 from growths of the lung. The main points to remember 
 in making this distinction are : i. Position tuberculous 
 lesions commonly apical. 2. Extent tuberculous lesions 
 as a rule involving only a portion of a lobe. 3. Surrounding 
 parts the presence in the case of tuberculosis of foci of 
 lymph-spread disease in the neighbouring portions of lung. 
 4. Cavities characteristic of tuberculosis, present also in 
 gangrene, but in the latter the cavities possessing soft friable 
 black-coloured margins and the other appearances character- 
 istic of tuberculosis (e.g. lymphatic-spread nodules) being 
 absent. 
 
 Microscopic Appearances. The two essential processes 
 going on are : (i) a catarrhal consolidation of the lung alveoli 
 which undergoes a caseous change ; (2) lymphatic spread of 
 the disease, with formation of caseating tubercles along the lines 
 
144 DISEASES OF THE RESPIRATORY SYSTEM 
 
 of the lymphatics. These tend to spread into surrounding 
 alveoli and bronchi, and so to initiate fresh areas of caseous 
 pneumonia. The elastic tissue of the lung undergoes a certain 
 amount of destruction, but in the caseous areas the network is 
 preserved and tends to persist until cavitation occurs. There 
 is usually a certain amount of increase of fibrous tissue as 
 evidenced by thickening of interalveolar walls, interlobular 
 septa, etc. 
 
 Cavities may arise (i) in dilated bronchi or bronchioles ; 
 (2) as the result of infection of a caseous area with pyogenic 
 organisms, and so the softening of the area ; (3) as the result 
 of the bursting of a caseous area into a bronchus. 
 
 The cavities are lined with breaking-down, caseous lung 
 tissue. Suitably stained preparations will demonstrate tubercle 
 bacilli often in very large numbers, both in catarrhal pneumonic 
 areas and in caseous foci or walls of cavities. 
 
 The vessels are often involved in the process, and blood 
 infection by invasion of a caseous focus into a vessel is not 
 infrequent. 
 
 3. Fibro-caseous Tuberculosis 
 
 This is the common condition found in cases of chronic 
 pulmonary tuberculosis. It passes, on the one hand, by 
 insensible gradations into the previous more acute type of the 
 disease. On the other hand, with increase in the fibrous 
 tissue element, it passes into so-called " fibroid phthisis." 
 The term is one which is perhaps not the best possible, but 
 it is descriptive, and is preferable to the purely clinical one 
 of chronic " phthisis." 
 
 The condition is usually complicated by cavitation. Hence 
 in speaking of this type one would refer to it as fibro- 
 caseous tuberculosis with cavitation. 
 
 Naked-eye Appearances. The lung shows on its surface 
 evidence of chronic pleurisy. It is usually firmly adherent 
 to the chest wall. For its removal it is advisable to strip 
 the parietal pleura from the ribs in the way described on p. 20. 
 The organ is distended, and on palpation it will be found 
 
DISEASES OF THE LUNGS 145 
 
 partially consolidated. Usually this consolidation is more 
 marked towards the upper part. 
 
 On cutting into the lung the increase in consistence will 
 be noted. The section will show the following appearances 
 (Fig. 53). Towards the apex of the upper lobe will usually be 
 found one or more cavities, one of which commonly is distinctly 
 larger than the other, varying in size from a walnut to a 
 tangerine orange. Indeed, in some cases the cavity may 
 be found to occupy the whole of the upper lobe. The walls 
 of the cavity are formed of fibrous tissue and are often com- 
 paratively smooth. Frequently bronchi and vessels of con- 
 siderable size can be seen crossing the cavity, the lung tissue 
 having largely disappeared from around these more resistant 
 structures. Occasionally aneurysms may be found on the 
 course of such vessels (Fig. 52). 
 
 Throughout the remainder of the lung there is a general 
 increase in the amount of fibrous tissue. From the thickened 
 pleura, thickened interlobular septa can be seen passing in. 
 The vessels and bronchi are thickened. This thickening is 
 usually more marked towards the root of the lung. The 
 bronchi are not infrequently dilated, their walls being pulled 
 upon by the contracting tissue around. They show evidence 
 of acute bronchitis and contain more or less muco-purulent 
 secretion. 
 
 The bronchial glands at the root of the lung are enlarged 
 and show caseous or calcareous change. 
 
 Around the cavity, or cavities, the lung substance is largely 
 consolidated by a fibro-caseous process. On analysis it will 
 be found to consist of firm nodules, larger and smaller, which 
 are pigmented and show caseous change. 
 
 In advance of this more completely consolidated area, i.e. 
 in the lower part of the upper lobe and in the lower lobes, 
 will be found isolated areas of consolidation of a similar type, 
 having a staphyloid arrangement indicating lymphatic spread. 
 In addition, there are often areas of caseous pneumonia, 
 
146 DISEASES OF THE RESPIRATORY SYSTEM 
 
 indicating recent acute spread of the disease. The presence 
 of the latter areas suggests " aspiration " spread. 
 
 As a rule, in such chronic cases both lungs are affected , 
 one, usually the right, showing the more advanced lesions. 
 
 Contraction of the fibrous tissue in the various parts of 
 the lung tends to occur, pulling upon bronchi and air vesicles. 
 Dilation is thus caused, producing bronchiectasis or 
 emphysema (traction emphysema), as the case may be. 
 
 The above appearances are found mainly in tuberculosis 
 of adults, but similar changes are occasionally met with in 
 children. 
 
 This type of the disease requires to be distinguished from 
 the other interstitial pneumonias, more especially from 
 syphilitic disease and from silicosis. Again, the distribution 
 of the disease apical in the case of tuberculosis, at the root 
 of the lung or under the pleura in the case of syphilis is the 
 chief means of differentiation. The presence of cavities is 
 characteristic only of tuberculosis, although it should be 
 remembered that silicosis maybe accompanied by tuberculosis. 
 Lastly, the nodules in silicosis are much harder and have a 
 characteristic gritty feel. 
 
 Microscopic Appearances. One of the most striking changes 
 is the increase of fibrous tissue thickening of pleura, of inter- 
 lobular septa, thickening round vessels and bronchi. The 
 fibrous tissue in these structures often shows a marked new 
 development of elastic-tissue fibres. The lung substance itself 
 shows irregular consolidation due to the presence of numerous 
 fibro-caseous areas, some of which are nodules of tuberculous 
 granulation tissue displacing the lung tissue. Others represent 
 areas of caseous pneumonia, in which the elastic tissue network 
 in suitably stained specimens is still visible, and which are 
 surrounded by zones of fibrous tissue. The blood - vessels 
 generally, more particularly those in the neighbourhood of 
 cavities, show thickening of their intima as well as adventitia. 
 Some have, in this way, their lumen completely obliterated. 
 In others the closure is only partial, and new vessels possessing 
 their own elastic laminae develop within the compass of the 
 
DISEASES OF THE LUNGS 147 
 
 old. The bronchi show evidence of catarrhal inflammation, 
 as also the remaining lung alveoli. The lining cells of the 
 alveoli are often cubical instead of being flat. The cavities 
 are lined with a zone of granulation tissue or of well-formed 
 fibrous tissue. The vessels in the neighbourhood become 
 partially or completely occluded by the occurrence of endarteritis 
 obliterans. In suitably stained specimens, tubercle bacilli may 
 be found, but they are commonly very few and scattered. 
 They occur chiefly in the walls of the cavities and in areas 
 of caseous pneumonia. 
 
 Changes in other Organs in Cases of Pulmonary Tuber- 
 culosis. In cases of miliary tuberculosis, metastatic foci 
 are found in liver, spleen, and kidneys as in the lung. 
 Acute degenerative changes, such as cloudy swelling and 
 early fatty change , will be seen in the parenchymatous organs, 
 also acute congestion of the spleen. In carrying out post- 
 mortem examinations upon cases of miliary tuberculosis 
 careful search should be made for the site of invasion of the 
 vessel. Attention should be specially directed to the con- 
 dition of the thoracic duct and the retroperitonal lymph 
 glands. The various branches of the pulmonary artery 
 within the lung should also be slit up. 
 
 In the more usual form of caseous pneumonia or fibro- 
 caseous tuberculosis, cloudy swelling and fatty change in such 
 organs as heart, liver, and kidneys is constantly present. 
 Not infrequently the liver is greatly enlarged from an extreme 
 degree of fatty infiltration. Waxy disease also should be 
 sought in spleen, liver, kidneys, etc. Very often acute 
 metastatic spread of the disease occurs terminally in these 
 cases also, with the presence of miliary foci in all the internal 
 organs. Intestinal tuberculosis ulceration of bowel and 
 caseous mesenteric glands is not uncommon as a secondary 
 manifestation due to the swallowing of infected sputum. In 
 the more chronic forms of pulmonary tuberculosis the right 
 side of the heart will be found hypertrophied and dilated, 
 
148 DISEASES OF THE RESPIRATORY SYSTEM 
 
 and, as a sequel, chronic venous congestion of liver, spleen, etc. 
 Tuberculous meningitis due to spread of the disease to brain 
 or cord is a common termination of the more rapidly pro- 
 gressive cases. 
 
 Careful investigation should always be made of the various 
 groups of lymphatic glands cervical, bronchial, mesenteric 
 with a view to deciding the point of origin of the disease. 
 The condition of the bones and joints should also be looked 
 into. Finally, in investigating cases of tuberculosis where 
 there are many lesions present, with a view to determining 
 the site of origin of the disease (in other words, the oldest 
 lesion), the following points should be attended to: (i) 
 Nature of lesion caseous foci are always older than grey, 
 cellular foci ; calcareous foci are older than caseous. 
 Fibrosis is also indicative of long-standing disease. (2) 
 Extent of lesion other things being equal, an extensive 
 lesion is older than a small one. 
 
 Tumours of the Lung. Simple growths of the lung are very 
 rare. Malignant growths are comparatively common, more 
 especially sarcomata, but primary growths of a malignant 
 nature are rare. Straining as they do the whole of the venous 
 blood of the body which has not been strained in the capillaries 
 of the liver, the lungs are apt to be the seat of deposit of 
 metastatic growths which invade the veins. Thus secondary 
 growths are common. Sarcomata are much more frequent in 
 the lungs than carcinomata. The latter occur, but in appear- 
 ance they are almost indistinguishable from the sarcomata. 
 Another common type of growth in the lung is a sarcoma 
 arising in the glands of the mediastinum and spreading into 
 the lung substance by direct extension (Fig. 56). Occasionally 
 the growth starts in the pleural surface, and either remains 
 limited to it or penetrates the lung. 
 
 Naked-eye Appearances. The growth may occur in the 
 form of white or grey isolated nodules (Fig. 55), or there may 
 
DISEASES OF THE PLEURA 149 
 
 be large areas of lung infiltrated with growth. In both 
 instances the condition is not very easily distinguished from 
 grey hepatisation or tuberculosis, especially as necrosis is 
 common and spread along the lymphatics of vessels and 
 bronchi can be seen. In the case of growth, however, the 
 infiltrated areas have a more translucent appearance, due to 
 the fact that they are formed of cellular tissue. Another 
 point of distinction is that cavitation is not observed in 
 growths. Also it should be remembered that the seat of 
 election in tuberculosis is the apex. There is no particular 
 portion of the lung specially liable to be affected by growth 
 unless it be the root. 
 
 DISEASES OF THE PLEURA 
 
 Hydrothorax or Dropsy of the Pleural Cavity. A 
 slight amount of free fluid is a common finding at a post- 
 mortem. Where there is any large quantity, a careful note 
 should be made of the appearance, distribution, and approxi- 
 mate amount of the fluid. It is usually pale, clear, and straw- 
 coloured, and has a specific gravity of 1009-1012. On 
 microscopic examination of the centrifugalised deposit, a 
 few endothelial cells and lymphocytes will be found. As a 
 rule the fluid is situated at the most dependent portion of 
 the pleural cavity, but accumulations may occur, limited by 
 adhesions, at other parts. The condition of hydrothorax 
 is found in cases of chronic heart and kidney disease, where, 
 as a rule, there is dropsy of other parts. 
 
 Haematothorax, or blood in the pleural cavity, is a rare 
 occurrence. Free blood is only found in connection with 
 injuries to the lung or chest wall and in malignant disease. 
 Small extravasations of blood may be found under the visceral 
 pleura in acute infections, in anaemias, and in asphyxia. 
 
 Pneumothorax, i.e. gas or air in the pleural cavity. This 
 may be due to a wound of the chest wall or lung, rupture of an 
 
150 DISEASES OF THE RESPIRATORY SYSTEM 
 
 acute tuberculous cavity, of healthy lung or emphysematous 
 lung in a paroxysm of coughing. It may also be due to the 
 presence of gas-producing organisms in the pleura, these 
 organisms coming usually from a ruptured cesophageal or 
 gastric ulcer, or spreading through the diaphragm from a 
 liver abscess or peritonitis. In the last case a purulent in- 
 flammation of the cavity is present as well, the condition 
 being known as pyopneumothorax. 
 
 In all the above conditions, in the absence of adhesions 
 which would bind the lung to the chest wall, complete collapse 
 of the lung occurs. 
 
 Acute Pleurisy. This condition may be primary, due 
 to spread by blood or lymph, or secondary, due to extension 
 from lung, pericardium, mediastinum, peritoneum, etc. 
 Three types of the condition may be distinguished : 
 
 (1) Dry vrfibrinous, where there is little or no free fluid. 
 
 (2) Serous or sero-fibrinous , where there is more or less 
 free fluid, in which there are commonly flakes of fibrin floating. 
 
 (3) Purulent, where there is purulent fluid. 
 The last is usually known as empyema. 
 
 Naked-eye Appearances. The surface of the lung shows, 
 over a larger or smaller area, a rough granular or thick opaque 
 white or yellow deposit (Fig. 54). This may be adherent or 
 easily removed according to the duration of the inflammatory 
 process. The pleura underneath shows injection of its 
 vessels, and the subjacent lung may show pneumonic con- 
 solidation, or sometimes abscess formation. If the fluid 
 be large in amount, and if there are no adhesions binding the 
 lung, the organ shows collapse. 
 
 In the case of empyemas which have been in existence 
 for some time, there is usually considerable thickening of 
 both parietal and visceral pleura (Fig. 41). 
 
 Microscopic Appearances. The vessels of the pleura are 
 distended with blood. There is a fibrinous coagulum on the 
 
DISEASES OF THE PLEURA 151 
 
 surface, and also in the interstices of the pleura, in the meshes 
 of which are entangled leucocytes, chiefly of the polymorpho- 
 nuclear variety in the earlier stages. The endothelial cells of 
 the pleural surface may be swollen but still attached, or they 
 may be thrown off and occur free amongst the fibrin. If the 
 condition has lasted for some time, there is evidence of organisa- 
 tion young blood-vessels budding out from the pre-existing 
 ones of the pleura, and young connective-tissue cells ac- 
 companying these into the exudate. These latter (fibroblasts) 
 are at first rounded, and possess a relatively large amount of 
 protoplasm. Later they tend to become spindle-shaped, and 
 eventually to arrange themselves parallel to the pleural surface. 
 From their protoplasm, fibres are split off which form the 
 intercellular fibres of the new tissue. 
 
 In empyemas which have lasted for some time these later 
 changes are more in evidence. 
 
 Chronic Pleurisy. This is a very common condition, 
 either in the form of adhesions between lung and chest wall, 
 or as areas of thickened pleura without adhesions. It is a 
 constant occurrence in subacute or chronic disease of the 
 lung, such as tuberculosis. In this disease the pleura may 
 be very greatly thickened, as much as one inch in certain cases. 
 
 Microscopic Appearances. The thickened pleura consists 
 of spindle-shaped connective tissue cells arranged parallel to 
 the surface with intervening sinuous collagenous fibres. Some- 
 times these latter are separated more or less widely from one 
 another owing to oedema. Through this tissue are scattered 
 a few wandering (lymphocyte-like) cells. Running at right 
 angles to the surface of the original pleura are vessels which 
 vary in size and thickness. 
 
 METHOD OF EXAMINING A LUNG REMOVED FROM THE BODY 
 
 Look in the first place at the shape of the organ. The normal 
 lung will become flattened on being placed upon a table, 
 whereas the consolidated lung (whether the consolidation be 
 due to fluid or solid exudate in the alveoli) retains its rounded 
 shape. Note the size of the organ. An organ the seat of 
 
152 DISEASES OF THE RESPIRATORY SYSTEM 
 
 emphysema is usually more voluminous than usual. Weigh 
 the lung. The weight of the normal lung is about i Ib. 3 oz. 
 to i Ib. 12 oz. (538-764 grammes), the right being a little 
 heavier than the left, and the lung of the male somewhat 
 heavier than that of the female. Examine the surface of the 
 organ for exudate, fibrous thickening, small haemorrhages. 
 Note the amount of pigment present at the points where the 
 interlobular septa join the pleura. Examine the margin for 
 evidence of emphysema and look for any puckering of the 
 surface, especially at the apex. Next feel the organ carefully 
 all over, searching specially for any hard areas which would 
 indicate consolidation. Note the distribution of the firm areas, 
 whether discrete or diffuse. Incise the organ longitudinally 
 (see p. 27) and examine the cut surface as to colour. Note 
 the distribution of any congested areas. Feel the surface 
 carefully and squeeze the tissue between the fingers, noting if 
 any fluid escapes and the character of such fluid. Any areas 
 of consolidation should now receive more careful attention as 
 regards colour, distribution, etc. It may be necessary further 
 to incise firm nodules or areas and to remove portions in order 
 to ascertain whether they sink or float in water. Where cavities 
 are present their position, shape, character of contents, wall, 
 and surroundings are all points to note. The large bronchi 
 should then be opened and the character of their contents and 
 appearances of their walls noted. The bronchial and medi- 
 astinal glands should be examined as to size, consistence, 
 presence of grey or yellow tubercles, etc. The branches of 
 the pulmonary artery should be slit up and examined for 
 impacted thrombi. 
 
CHAPTER VIII 
 
 DISEASES OF THE INTESTINAL TRACT AND PERITONEUM 
 
 Diseases of Mouth, Pharynx, etc. The condition of 
 the teeth should always be investigated. The presence of 
 caries should be noted. More particularly in cases of severe 
 anaemia, suppuration should be looked for in the mouth 
 cavity. Pyorrhoea alveolaris is commonly associated with 
 chronic toxaemia and anaemia. In any case where enlarge- 
 ment of the cervical glands is present, the mouth and pharynx 
 should be carefully investigated for tumour formation, 
 suppurative foci, actinomycosis, etc. 
 
 In diphtheria the tonsils and pharynx should be examined 
 for false membrane. It appears as grey opaque areas sur- 
 rounded with congestion. The membrane in this position 
 is not easily removed, as it is formed of the covering epithelium 
 infiltrated with fibrinous exudate. In any suspicious case 
 not diagnosed during life, cultures on blood serum as well as 
 films should be made. 
 
 Diseases of the (Esophagus. When any condition 
 affecting the oesophagus is suspected, as in poisoning, dys- 
 phagia, hsematemesis, care should be taken to remove the 
 viscus entire along with the pharynx and stomach. This 
 can best be done by removing tongue, pharynx, contents 
 of chest and abdomen in one piece as described on p. 23 
 and then removing the individual organs as required, opening 
 
 i53 
 
154 DISEASES OF THE STOMACH 
 
 the oesophagus from behind and examining it in continuity 
 with the stomach. 
 
 The oesophagus is not infrequently the seat of varicose 
 veins in cirrhosis of the liver. This is due to the fact that the 
 veins from the lower part of the oesophagus drain indirectly 
 into the portal vein, which in cirrhosis of the liver is obstructed. 
 The cesophageal veins dilate and become varicose. Such 
 veins may rupture, and severe, even fatal, haemorrhage result. 
 
 The oesophagus suffers along with the stomach in corrosive 
 poisoning, and presents much the same appearance as that 
 organ (see p. 312). Rarely it may be the seat of peptic ulcer in 
 its lower part. Such an ulcer may rupture into one or other 
 pleural cavity and cause a pyopneumothorax. 
 
 Tumours of the oesophagus are occasionally found, by far 
 the most common being squamous epitheliomata. Very infre- 
 quently leio-myomata are found. The squamous epithelioma 
 of the oesophagus is found in the form of an ulcer with 
 raised infiltrating margin. It tends to form a ring-shaped 
 area of constriction, and is situated either high up about the 
 level of the cricoid cartilage, low down near the cardiac 
 orifice of the stomach, or at the level of the bifurcation of 
 the trachea (Fig. 57). The ulcer may extend deeply, perforat- 
 ing the trachea, bronchi, one or other pleural cavity, or peri- 
 cardial sac. 
 
 DISEASES OF THE STOMACH 
 
 Owing to the action of the digestive juices of the organ 
 itself, and owing to decomposition in its contents and in the 
 contents of the neighbouring viscera, the stomach undergoes 
 considerable changes after death, and the longer the sectio 
 is delayed the greater will be those changes. Blood tends 
 to accumulate in the vessels of the organ at its more 
 dependent parts, giving the appearance of congestion, and 
 even of haemorrhage. As the result of decomposition in this 
 
DISEASES OF THE STOMACH 155 
 
 blood, green discoloration takes place. Frequently there is 
 softening of the wall owing to digestion by the gastric juice. 
 This may occur to the extent of causing actual perforation. 
 Obviously, therefore, care must be taken in interpreting 
 changes found in the stomach post-mortem. Changes such 
 as softening when they occur before death tend to be diffuse 
 in their distribution, whereas post-mortem softening is found 
 mainly in the more dependent, and therefore posterior, part 
 of the viscus. 
 
 Dilatation of the Stomach. Gastrectasis. Acute 
 dilatation may be due to the ingestion of excessively large 
 quantities of food, or it may be nervous in origin, sometimes 
 following surgical operations. 
 
 Chronic dilatation may be due to (i) narrowing of the 
 pylorus from tumour, (2) the presence of abnormal contents 
 from fermentation and atony of the muscular wall associated 
 with chronic catarrh. 
 
 Contractions of the Stomach. Narrowing of the 
 pyloric orifice (congenital pyloric stenosis) through thickening 
 of the muscular coat is a somewhat rare condition. 
 Localised contraction of the organ may occur as a sequel to 
 ulceration. It tends to produce the condition of " hour- 
 glass" stomach. 
 
 Chronic Venous Congestion. In- chronic valvular 
 disease of the heart, chronic lung and liver disease, passive 
 hypersemia tends to occur in the stomach as in other organs. 
 It is usually associated with the appearances of chronic 
 catarrh, accompanied by congestion of the vessels of the 
 mucous membrane. Minute haemorrhages may occur, and 
 these may be followed by small superficial ulcerations 
 (hcemorrhagic erosions). 
 
 Acute Catarrh of the Stomach may occur as the result 
 of (i) dietetic errors ; (2) the ingestion of irritant or corrosive 
 poisons ; (3) in the course of infective fevers. 
 
156 DISPOSES OF THE STOMACH 
 
 Naked-eye Appearances. In slight cases there may be 
 little or no alteration. In severe cases the walls of the viscus 
 are swollen, the mucous membrane congested, and covered 
 with strings of sticky mucus. Small haemorrhages may 
 occur. Where the cause has been one of the corrosive 
 poisons there may be necrosis and sloughing of the mucous 
 membrane, sometimes with perforation. In the case of 
 certain poisons characteristic colouring may be present. For 
 further information on the appearances of the stomach in 
 cases of poisoning see pp. 311-13. 
 
 Microscopically, the vessels of the wall are dilated. There 
 is shedding of the superficial epithelium, and, in the more 
 severe varieties, necrosis. The wall is infiltrated with inflam- 
 matory cells and exudate from the vessels. 
 
 Acute Suppurative Gastritis sometimes occurs in the 
 course of specific fevers and pyaemia or as the result of spread 
 of inflammation from neighbouring parts. The portion of 
 the wall affected is thickened, pale yellow in colour, and 
 found, on microscopic examination, to be infiltrated with 
 fibrin and leucocytes. The mucous membrane superficial 
 to the area shows acute catarrh, and sometimes exudate. 
 
 Chronic Catarrh. This may follow acute catarrh or 
 develop independently. It is frequent in chronic alcoholics, 
 and occurs in association with chronic venous congestion, 
 peptic ulcer, and carcinoma. 
 
 The stomach is usually dilated. The mucous membrane 
 is pale and atrophied. There may be scattered small haemor- 
 rhages or pigmented black areas following such. The surface 
 of the mucous membrane is covered with thick sticky mucous 
 secretion. Small follicular ulcers may be present. These 
 ulcers are shallow with undermined edges. They may heal, 
 leaving a small puckered scar. 
 
 Microscopically, beyond some overgrowth of fibrous tissue, 
 catarrh of the gland cells, and infiltration of the coats with 
 round cells, there is little to be seen. 
 
DISEASES OF THE STOMACH 157 
 
 Peptic, Perforating, or Chronic Ulcer. This condition 
 is found more frequently in females than in males. It is chiefly 
 found in young, anaemic girls between the ages of twenty and 
 thirty. It may be associated with chronic gastric catarrh. 
 
 The ulcer is commonly single, but occasionally there is 
 more than one. It is situated usually on the posterior 
 wall near the lesser curvature, and nearer the pylorus than 
 the cardia. About i per cent occur on the anterior wall. 
 The ulcer varies in size. Usually it is about the size of a 
 sixpence, but it may be much larger. The margins of the 
 ulcer are rounded, smooth, and devoid of evidence of inflam- 
 mation, presenting a punched-out appearance (Fig. 58). The 
 floor may be formed by one of the coats of the stomach, but not 
 infrequently it is formed of fibrous tissue, or of one or more 
 of the organs behind the stomach, such as pancreas or liver. 
 
 Owing to the fact that the opening in the mucous membrane 
 is larger, the opening in the muscular coat smaller, the ulcer 
 may show a terraced appearance. The associated chronic 
 inflammation in the wall of the viscus causes the formation 
 of adhesions to structures lying posterior ; hence with increase 
 of depth these organs become exposed in the floor of the 
 ulcer. Not infrequently, however, before such adhesions 
 can form perforation occurs. In the case of the ulcer on the 
 posterior wall this will take place into the lesser sac of the 
 peritoneum. The acute peritonitis resulting is thus, at first, 
 limited. In the case of the anterior ulcer, perforation occurs 
 more rapidly, and takes place directly into the peritoneal 
 cavity, causing a general peritonitis. Healing may take 
 place, associated with cicatrisation and sometimes the forma- 
 tion of an " hour-glass " stomach. Besides perforation, 
 another accident which may occur is hcemorrhage due to 
 erosion of a vessel in the wall of the stomach, or possibly one 
 of the larger vessels lying behind the organ. 
 
 A similar type of ulcer is sometimes found in the duodenum 
 immediately beyond the pylorus. It resembles the peptic 
 
158 DISEASES OF THE STOMACH 
 
 ulcer of the stomach in every respect except that it is more 
 frequent in the male sex. As a rule the ulcer is small, but it 
 may attain a large size (Fig. 59). As in the case of the stomach 
 ulcer, the floor may be formed by fibrous tissue or by an organ 
 such as the pancreas. Perforation and haemorrhage are 
 accidents not infrequently met with in this case also. 
 
 The causation of both types of ulcer is obscure. Throm- 
 bosis occurring in a vessel supplying the mucous membrane, 
 with consequent malnutrition and then digestion by the 
 juices within, has been suggested as an explanation of their 
 occurrence. 
 
 Fibromatosis. Occasionally the stomach is the seat of 
 a diffuse fibrous overgrowth implicating chiefly the sub- 
 mucous and muscular coats, and commonly associated with 
 a chronic ulcer. This condition, which is usually most marked 
 at the pyloric end of the organ, has been called fibromatosis. 
 It is sometimes mistaken for malignant new growth. 
 
 Tumours. Simple tumours of the stomach are rare. 
 Fibromata, myomata, adenomata are described. Mucous 
 papillomata also occur. 
 
 Of malignant tumours, sarcomata are uncommon. 
 
 Carcinoma.-^- This is the common stomach tumour. It 
 is most frequently situated at the pyloric end (60 per cent). 
 The next most frequent site is the lesser curvature (20 per 
 cent). Abo.ut 10 per cent occur at the cardiac orifice (Fig. 60). 
 As regards the type of cancer found, the most common is 
 the encephaloid variety of the adeno-carcinoma. The next 
 most common is the scirrhous, then the colloid, and least 
 frequent is the squamous epithelioma, which is occasionally 
 found at the cardiac end. 
 
 The tumour may lead to a localised or diffuse thickening 
 of the stomach wall. More frequently there is an ulcerated 
 surface with a raised, hard, infiltrated margin. Sometimes 
 the growth projects into the interior of the viscus as a cauli- 
 
DISEASES OF THE INTESTINE 159 
 
 flower-like mass (Fig. 60). The floor is formed of necrosed 
 tumour substance. Perforation rarely occurs. Secondary 
 deposits are very commonly found in the neighbouring glands 
 and in the liver. 
 
 DISEASES OF THE INTESTINE 
 
 Malformations. MeckePs diverticulum is a finger-like 
 cul-de-sac, the remains of the omphalo - mesenteric duct, 
 usually 2-3 inches in length, occurring some 2 or 3 feet 
 above the ileo-csecal valve. It is sometimes attached to the 
 umbilicus. It may become closed and give rise to cyst or 
 abscess formation, or it may become adherent to the parietes, 
 thus forming a band under which a loop of bowel may 
 become strangulated. 
 
 Smaller diverticula may be found in connection with 
 other parts of the small intestine, such as the duodenum, 
 and pouches between the layers of the mesentery may be 
 found. 
 
 Dilatation of the bowel is found as the result of peri- 
 tonitis (paralytic distention), constipation, obstruction from 
 strangulation, infarction or tumour formation. When the 
 obstruction is long-continued the wall of the bowel above 
 shows hypertrophy (Fig. 69). 
 
 A condition of dilatation of the large intestine, more 
 especially the ascending colon, associated with hypertrophy 
 of the muscular coat, known as Hirschspmng's disease, 
 occasionally occurs. It is believed to be congenital. 
 
 Stenosis, or narrowing of the bowel, may be due to con- 
 traction associated with ulceration (especially tuberculous), 
 tumour formation, or chronic peritonitis. 
 
 Volvulus is a condition in which the bowel is obstructed 
 by a loop of intestine becoming twisted upon itself. Half the 
 cases occur in the pelvic colon. An abnormally long mesentery 
 
160 DISEASES OF THE INTESTINE 
 
 predisposes to its occurrence. The blood-supply of the 
 portion of gut is interfered with and gangrene tends to occur. 
 
 Intussusception is a condition in which a portion of the 
 bowel is invaginated into the section immediately below. 
 It occurs chiefly in infants, and is believed to be caused by 
 violent peristalsis due to active purgation or diarrhoea. The 
 condition may occur in the ileum or the colon, or at the 
 ileo-csecal valve. The portion of bowel involved forms a 
 sausage-shaped tumour (Fig. 61). Pressure on the mesentery 
 of the intussuscepted portion causes interference with its 
 circulation and a tendency to gangrene. 
 
 A similar condition, easily reduced and often multiple, is 
 not infrequently found post-mortem. It is believed to 
 develop very shortly before death. In this type there is, of 
 course, no congestion of the intussuscepted portion, and there 
 are no adhesions between the various layers of gut. 
 
 Hernia. A hernia is usually defined as a condition in 
 which there is a protrusion of any of the abdominal contents 
 from the cavity of the abdomen. The term is also used in 
 connection with the rare occurrence of a protrusion of gut 
 through an opening, such as the foramen of Winslow, within 
 the abdomen. 
 
 As a rule it is either a portion of bowel or a portion of 
 amentum, or both, which protrudes. Occasionally it may be 
 a Meckel' s diverticulum or an organ such as liver, spleen, or 
 stomach. The sac of the hernia is usually lined by peritoneum, 
 although this may disappear. 
 
 The condition may be congenital, the sac being formed by a 
 diverticulum of the peritoneum such as the processus vaginalis. 
 More usually it is acquired through increased abdominal 
 pressure from coughing, crying, straining, or through weak- 
 ness of the abdominal wall, or from these two factors combined. 
 It may also be due to violence, such as a crush driving some 
 of the abdominal contents through the diaphragm. 
 
DISEASES OF THE INTESTINE 161 
 
 The protrusions are found at points of weakness in the 
 abdominal wall, usually where vessels enter and leave. The 
 commonest type is the inguinal hernia which occurs in the 
 inguinal canal and may be congenital or acquired. The 
 second commonest type is the femoral hernia, a projection 
 through the femoral ring. In addition, there is an umbilical 
 type found at the umbilicus which may be congenital or 
 acquired. The latter type is found chiefly in very fat women. 
 Certain rarer forms are occasionally met with, such as 
 obturator hernia, also hernise through the abdominal wall at 
 points which have been weakened by scars following opera- 
 tions. 
 
 The condition is not of much importance to the morbid 
 anatomist. Hernise are not infrequently met with by 
 accident at a post-mortem. Strangulation of the hernia, i.e. 
 interference with the circulation of blood through the gut 
 with consequent acute congestion and sometimes gangrene, 
 is a cause of acute peritonitis, but it is rarely seen post-mortem. 
 Internal hernise, e.g. hernise through the diaphragm, are 
 sometimes met with as the result of severe crushing of the 
 abdomen. 
 
 Chronic Venous Congestion of the bowel is found in 
 cirrhosis of the liver and in chronic heart and lung disease. 
 There is swelling and congestion of the wall of the gut, 
 especially of the mucous membrane. A degree of catarrhal 
 inflammation is very constantly associated. 
 
 Infarction of a portion of bowel, most frequently of that 
 part supplied by the superior mesenteric artery, is sometimes 
 found. It should be looked for in cases which die with 
 symptoms of intestinal obstruction. The portion of gut 
 involved is deep purple in colour, and usually shows peri- 
 tonitis on its surface. The aorta and its branches should be 
 slit up to find the point where the block occurred. Careful 
 search should be made for a possible source of the embolus, 
 
 ii 
 
162 DISEASES OF THE INTESTINE 
 
 e.g. a thrombus on an atheromatous patch of the aorta, 
 or in the left side of the heart (see diag. p. 62). 
 
 Haemorrhage occurs into the mucous membrane of the 
 bowel in the form of small extravasations in cases of infective 
 diseases, anaemias, etc. 
 
 Large haemorrhages may occur from ulcerated surfaces, 
 such as duodenal or typhoid ulcers. The blood, mixed with 
 faecal matter, tends to undergo alteration into a black mass 
 of putty-like consistence which can be seen through the wall 
 of the gut before it is opened. 
 
 INFLAMMATION OF THE SMALL INTESTINE- 
 ENTERITIS 
 
 Acute Catarrhal Enteritis may be caused by irritating 
 foods, poisons, dust, by normal bacterial inhabitants of the 
 bowel, such as B. coli or streptococci, or by specific bacteria 
 such as B. typhosus and Vib. cholera. 
 
 Naked-eye Appearances. These are often unsatisfactory. 
 The clinical symptoms are frequently out of all proportion 
 to the pathological findings. Usually there is some conges- 
 tion of the vessels of the mucous membrane, which is more 
 or less swollen. This congestion may be diffuse or patchy. 
 Often it is most marked at the apices of the folds in the 
 mucous membrane. When due to the action of a micro- 
 organism the changes are commonly more marked in the lower 
 part of the ileum. In cases of poisoning, on the other hand, 
 the duodenum and upper part of the jejunum in addition 
 to the stomach are the parts most affected, although it 
 must be noted that irritant poisoning often causes little 
 change (see p. 313). Not infrequently the lymph follicles 
 of the bowel are swollen (follicular enteritis) and may ulcerate 
 (follicular ulcers). The mucous membrane may be covered 
 with viscid mucus. Sometimes there is a distinct membrane 
 formed of exudate (membranous enteritis). Occasionally, 
 
DISEASES OF THE INTESTINE 163 
 
 in the more intense forms, the mucous membrane may 
 undergo necrosis, forming a greenish slough. Small embolic 
 abscesses may be found in pyaemia, or there may be a general 
 infiltration of the wall of the gut with pus (suppurative 
 enteritis). 
 
 Microscopic Appearances. There is dilatation of the vessels 
 of the bowel, infiltration of the wall with inflammatory cells 
 and exudate ; increase of the lymphoid elements and swelling 
 of the endothelial cells in the solitary glands ; catarrh of the 
 superficial epithelium. In suppurative enteritis small abscesses 
 and more intense inflammatory infiltration are found. 
 
 SPECIAL FORMS OF ENTERITIS 
 
 1. Cholera. The changes are most marked in the lower 
 portion of the ileum. There is intense swelling and conges- 
 tion of the mucous membrane. The lymphoid follicles may 
 be swollen and pale. Small haemorrhages may be present. 
 Membranous enteritis may occur, due to the exudation of 
 fibrin on the surface of the mucous membrane. The contents 
 of the bowel are pale and watery (rice water). 
 
 Microscopically, there is marked catarrh of the epithelium, 
 possibly exudate on the mucous membrane, and infiltration of 
 the wall of the bowel with inflammatory cells. The specific 
 organisms do not penetrate the wall for any distance, but 
 they are found in immense numbers along with desquamated 
 epithelial cells in the rice-water contents of the bowel. 
 
 2. Typhoid. In this condition also the change is most 
 marked in the lowest portion of the ileum. It consists, in the 
 early stage, in a swelling, of the lymphoid tissue generally, 
 both Peyer's patches and solitary follicles (Fig. 62). These 
 areas are pale, but the bowel between may show congestion. 
 At about the beginning of the second week of the disease, 
 necrosis commences in these swollen accumulations of lymph- 
 oid tissue (Fig. 63). In this way sloughs form which take 
 
164 DISEASES OF THE INTESTINE 
 
 on a yellow or green colour from bile staining. These sloughs 
 separate towards the end of the third week of the disease and 
 ulcers are left which have the following characters : The 
 larger ones, representing as they do an ulcerated Peyer's 
 patch, are usually in the longitudinal direction of the bowel ; 
 during the separation of the sloughs hczmorrhage tends to 
 occur. The smaller ones, representing the solitary follicles, 
 are rounded. The edges of the ulcers are ragged and over- 
 hanging. The floor is formed of one of the coats of the bowel 
 the submucous, muscular, or peritoneal. Perforation is not 
 infrequent. The peritoneal aspect of the portion of bowel 
 may show evidence of acute inflammation by injection of 
 vessels and even fibrinous exudate. 
 
 Occasionally, in cases dying from complications late in 
 the disease, the ulcers may be found in process of cicatrisa- 
 tion. 
 
 In a case of typhoid fever, in addition to the condition 
 of the intestine, attention should be paid to (i) the mesenteric 
 glands, which are constantly enlarged, congested, and may 
 show haemorrhages and necrotic foci ; (2) the spleen, which 
 shows acute congestion, and, microscopically, areas of focal 
 necrosis ; (3) the liver, with cloudy swelling and areas of focal 
 necrosis ; (4) the kidneys and heart, which show cloudy 
 swelling ; (5) in contrast to most cases of infective disease, 
 the bone marrow, in uncomplicated cases, shows little or no 
 evidence of leucoblastic reaction. 
 
 Cultures should be made from the common bile duct, the 
 spleen, or the contents of the small intestine (see p. 360). 
 
 Microscopic Appearances. In the stage of swelling, separa- 
 tion of the cell elements of the Payer's patch due to oedema is 
 found. There is also swelling and proliferation of the endo- 
 thelial cells of the lymphoid tissue and catarrh of the mucous 
 membrane generally. Bacilli may be found in groups in the 
 swollen patch. Necrosis begins in areas at the centre of the 
 Peyer's patch and spreads. The typhoid ulcer merely shows 
 
DISEASES OF THE INTESTINE 165 
 
 the appearance of an acute ulcer with overhanging edges, 
 floor formed of muscular coat as a rule. Inflammatory changes 
 are present in muscular coat and tissue around. In suitably 
 stained specimens bacilli are found in masses, both superficially 
 and deep in the wall. 
 
 The mesenteric glands, in addition to the appearance of an 
 acute lymphadenitis swelling and loosening of endothelial 
 cells of sinuses, etc. show areas of necrosis and haemorrhage, 
 with occasional masses of bacilli. 
 
 3. Tuberculosis. This is usually secondary to tuber- 
 culosis of the lungs, the intestine becoming infected by the 
 swallowing of sputum containing tubercle bacilli. As a 
 primary condition of the bowel, the disease is comparatively 
 rare, although it has been found in as large a proportion as 
 12 per cent of all cases of tuberculosis. 
 
 Tuberculosis of the mucous membrane of the bowel is, 
 however, by no means necessarily found in cases where the 
 intestine is the path of entrance of the tubercle bacillus. 
 The disease may show itself first in the mesenteric glands or 
 in the peritoneum, no demonstrable lesion of the bowel 
 itself being present. 
 
 Naked-eye Appearances. The part commonly affected is, 
 as in typhoid, the lower portion of the ileum. The earliest 
 lesion consists in a tubercle nodule underneath the mucous 
 membrane. Ulceration occurs over this, and tends, owing 
 to the distribution of the lymphatics of the bowel, to spread 
 laterally, often encircling the bowel, with the exception of that 
 portion over the attachment of the mesentery. The appear- 
 ances in the fully developed ulcer are as follows (Fig. 64) : the 
 direction is transverse to that of the bowel, although this 
 character is by no means constant ; the edge is irregular, 
 nodular, but rounded ; the floor is formed of tuberculous 
 granulation tissue ; the peritoneal aspect shows opaque white 
 thickening of the wall, the presence of tubercle nodules (Fig. 
 65) under the peritoneum, and sometimes white lines of 
 
i66 
 
 DISEASES OF THE INTESTINE 
 
 injected lymphatics radiating from the area. Constriction 
 of the bowel is common, as also is adhesion to surroundings. 
 
 Perforation is a comparatively rare occurrence in tuber- 
 culous ulceration, as also is haemorrhage. 
 
 The mesenteric glands are constantly enlarged and show 
 caseous areas or grey granulations, occasionally calcification. 
 
 Microscopic Appearances. At the margins of the ulcer, in 
 the floor, often replacing the muscle substance, and under the 
 peritoneal coat, there are tubercle granulations with giant-cell 
 or caseous centres. Tubercle bacilli are not, as a rule, 
 numerous. 
 
 TUBERCULOSIS AND TYPHOID ULCERS CONTRASTED AS 
 REGARDS THEIR NAKED-EYE APPEARANCES 
 
 
 Tuberculous Ulcer. 
 
 Typhoid Ulcer. 
 
 Direction . 
 
 Typically transverse. 
 
 Typically longitudinal. 
 
 Margin 
 
 Raised, rounded, nodular. 
 
 Overhanging, ragged. 
 
 Floor . . 
 
 Irregular, formed of tuber- 
 culous granulation tissue. 
 
 Smooth, formed of one of 
 the coats of the bowel. 
 
 Peritoneal 
 aspect 
 
 Raised, grey or yellow 
 tubercles. Thickening 
 and sometimes constric- 
 tion. Perforation rare. 
 Adhesions frequent. 
 
 Evidence of acute inflam- 
 mation, congestion, exu- 
 date. Perforation fre- 
 quent. No adhesions 
 or constriction. 
 
 Associated 
 mesenteric 
 glands 
 
 Enlarged and firm, caseous. 
 Sometimes calcareous. 
 
 Enlarged, congested with 
 necrotic foci, soft. 
 
 4. Syphilis. This is a rare condition. It may occur in 
 the form of gummata, ulceration, or cicatrisation with stenosis. 
 
 5. Actinomycosis. This is also rare. It may affect the 
 
 intestine or appendix, 
 in the liver. 
 
 Secondary abscesses usually occur 
 
DISEASES OF THE INTESTINE 167 
 
 INFLAMMATION OF THE LARGE INTESTINE 
 
 In its slighter forms this condition is known as colitis, 
 in its more severe forms as ulcerative colitis or dysentery. 
 
 As regards causation, (i) the slighter forms of the disease 
 may be due to indiscretions of diet, chill, germs of various 
 kinds. Of the more severe types, two varieties are dis- 
 tinguished : (2) Bacterial Dysentery, with which organisms 
 closely related to B. coli, e.g. Shiga's bacillus and Flexner's 
 bacillus, are more especially associated; (3) Tropical Dysen- 
 tery, generally believed to be caused by a protozoon, the 
 Entamceba histolytica. 
 
 (1) The milder types of inflammation show congestion 
 of the mucous membrane, some cedema, swelling of the 
 lymphoid follicles, and, sometimes, slight superficial ulceration. 
 
 Microscopically, beyond catarrh of the mucous membrane, 
 congestion of vessels, and infiltration of the coats with inflam- 
 matory cells, there is little to be seen. 
 
 (2) Ulcerative Colitis or Bacterial Dysentery. The wall 
 of the bowel is usually thickened. On opening the gut there 
 is irregular ulceration with tags of thickened mucous membrane 
 between the ulcers (Fig. 66). These tags often occur in longi- 
 tudinal ridges. The edges of the ulcers are overhanging, and 
 the floor is usually formed by the submucous or muscular coat. 
 Occasionally, destruction of the muscular coat is found, and 
 sometimes perforation. 
 
 Microscopic Appearances. There is catarrh of the mucous 
 membrane and thickening of the submucous and muscular 
 coats. These are infiltrated with inflammatory cells and 
 exudate, and there is marked swelling of the endothelial cells 
 of the lymphatics and vessels. 
 
 The above description holds good more especially for the 
 type of the disease found in Great Britain. In the type 
 
168 DISEASES OF THE INTESTINE 
 
 found in Japan, haemorrhages into the mucous membrane, 
 purulent and fibrinous exudates on to the surface of the 
 mucous membrane are described in addition to ulceration. 
 
 (3) Tropical or Amoebic Dysentery- The wall of the bowel 
 is thickened, due largely to a thickening of the submucous 
 coat, partly from fibrous change, partly from inflammatory 
 infiltration. Scattered through the mucous membrane are 
 numerous small raised nodules the size of pin heads or small 
 peas, most of which show a small opening in the mucous 
 membrane through which a whitish slough can be seen (Fig. 
 67). The bowel between is congested. These minute ulcers 
 tend to run together, forming areas of more extensive 
 ulceration. In the case of the larger ulcers the edges are 
 overhanging and the floor is formed of submucous or muscular 
 coat. Rarely perforation of the bowel may occur. 
 
 The seat of the more intense changes varies in different 
 cases. Sometimes it is the caecum and ascending colon, 
 sometimes the transverse, sometimes the descending or 
 pelvic colon. 
 
 The condition is very commonly associated with the 
 tropical form of liver abscess. 
 
 Microscopic Appearances. The wall of the bowel is 
 thickened, more especially the submucous coat. It is also 
 infiltrated with inflammatory exudate and cells. The nodules 
 above mentioned are found to be flask-shaped ulcers in the 
 submucous coat, with overhanging margins and a small opening 
 into the lumen of the bowel. The centre is occupied with a 
 slough consisting of necrotic tissue and leucocytes. Amoebae 
 are found in the slough and in the submucous coat around. 
 They appear as large rounded cells with vacuolated protoplasm 
 and a relatively small round nucleus. They can be seen in 
 specimens stained with haematin and eosin, but are better 
 demonstrated by eosin, methylene blue (p. 243). In the areas 
 of more extensive ulceration the ulcers lose their characteristic 
 appearance, and the changes are more like those found in the 
 other type of dysentery. 
 
DISEASES OF THE INTESTINE ' 169 
 
 Mucous Colitis. This is a condition in which tubular 
 casts of the bowel or strings and masses of clear mucus are 
 evacuated from time to time. The casts consist of inspissated 
 mucus due to hypersecretion. The condition is frequently 
 of nervous origin aggravated by growth of bacteria and is 
 accompanied by dilatation of the large intestine. 
 
 Appendicitis. The appendix is a cul de sac in continuity 
 with the caecum having the structure of the large intestine, 
 and being subject to inflammatory changes spreading from 
 the large bowel, as well as to such changes originating in 
 itself. Foreign bodies, animal parasites, such as thread 
 worms, and faecal matter may lodge in its lumen, the last, 
 along with inspissated secretion from its own glands, forming 
 the so-called concretions. The actual cause of the inflam- 
 mation is a micro-organism, usually one derived from the 
 bowel, e.g. B. coli, streptococci) B. lactis cerogenes, B. proteus, 
 occasionally B. tuberculosis and streptothrix actinomyces. 
 Three degrees of intensity of inflammatory change may be 
 recognised, viz. (i) Catarrhal, (2) Ulcerative, (3) Gangrenous. 
 
 1. Catarrhal Appendicitis. Sometimes there is little 
 alteration from the normal to be observed in this type. As 
 a rule the organ is somewhat swollen and congested. 
 
 2. Ulcerative Appendicitis. In this type the inflammatory 
 change is more intense. In addition to swelling and conges- 
 tion there is destruction of the mucous membrane, sometimes 
 with perforation. 
 
 3. Gangrenous Appendicitis. The organ, or parts of it, is 
 of a deep purple colour. There is exudate on the peritoneal 
 surface and ulceration of the mucous membrane, sometimes 
 with abscess formation or perforation (Fig. 68). 
 
 Peritonitis, either localised or general, is very commonly 
 associated with appendicitis. When limited by adhesions 
 an abscess may develop, having the appendix as its centre 
 and starting-point. Occasionally such abscesses burrow 
 
170 DISEASES OF THE INTESTINE 
 
 behind the caecum. As the result of inflammation the 
 organ may become obliterated and reduced in whole or part 
 to a fibrous cord. Not infrequently adhesions form between 
 the appendix and neighbouring parts, such as uterus, bowel, 
 or abdominal wall ; under the band thus formed, portions 
 of bowel sometimes become strangulated. Phlebitis, with 
 resulting thrombosis, tends to occur in the veins of the 
 appendix as in any acute inflammatory condition of the 
 bowel. Organisms may cause softening of the thrombi, and 
 portions of these may be carried to the liver, where they give 
 rise to the portal pyaemia type of liver abscess. 
 
 Microscopically r , in the catarrh al type there is distension of 
 the vessels with blood, infiltration of the coats with exudate, 
 which may be fibrinous, also with leucocytes. There is, in 
 addition, catarrh of the mucous membrane, as evidenced by 
 shedding of the gland cells. 
 
 In the more severe types of the disease the inflammatory 
 changes are more intense ; there is necrosis of the mucous 
 membrane with ulceration. In the floor of the ulcers germs 
 are present in large numbers. There is also more or less 
 marked peritonitis. 
 
 Animal Parasites. The important animal parasites 
 which may be met with in the intestines are : Protozoa : 
 Entamceba histolytica causing the tropical form of dysentery, 
 and amoeba coli of little or no importance. Worms : (i) 
 Trematodes Bilharzia hcematobia which may give rise to 
 polypoid outgrowths of the mucous membrane of the rectum. 
 (2) Cestodes Tcenia solium, the cystic stage of which is found 
 in the pig. Tcenia mediocanellata or saginata, the cystic stage 
 of which occurs in the ox. Bothriocephalus latus, the cystic 
 stage of which is found in the pike, (3) Nematodes Ascaris 
 lumbricoides , found chiefly in the upper part of the small 
 intestine, occasionally in the bile duct. Oxynris vermicularis , 
 the " thread " or " seat " worm, found in the large bowel in 
 children. Ankylostoma duodenale, the " hook," " tunnel/' 
 
DISEASES OF THE INTESTINE 171 
 
 or "miner's" worm, found attached to the mucous membrane 
 of the jejunum. This worm is of more importance than the 
 other round worms, as it may cause a severe type of anaemia. 
 Trichocephalus dispar, or " whip " worm, a common in- 
 habitant of the caecum. 
 
 Tumours. Simple tumours, such as fibromata, lipo- 
 mata, myomata, and cysts of various kinds, are occasionally 
 met with. Of malignant tumours, sarcomata are rare. 
 
 By far the commonest type of growth in the bowel is the 
 carcinoma. Of these, all types may be met with : squamous 
 epitheliomata in the rectum, the various types of adeno- 
 carcinomata, as columnar -cell carcinoma, colloid cancer, 
 scirrhous cancer. The growth is usually small. It may be 
 a mere ring of infiltration round the wall of the gut, produc- 
 ing a constriction when looked at from the outside, with 
 narrowing of the lumen. In other cases it forms a fungating 
 growth projecting into the interior (Fig. 69). Ulceration of 
 the bowels is very commonly associated, and perforation 
 may occur. There are often adhesions with neighbouring 
 structures, and the nearest lymphatic glands are usually 
 enlarged and infiltrated. Secondary growths in the liver are 
 very commonly present. Diffusion of the growth throughout 
 the peritoneal cavity is sometimes seen. 
 
 As regards site, carcinomata may occur at any part of the 
 small or large intestine. They are, however, much more 
 common in the latter, occurring more especially at points of 
 narrowing of the gut, such as the ileo-caecal valve and the 
 ascending colon immediately above the caecum; at points 
 where the intestine changes its direction, as, for example, at 
 the hepatic, splenic, and sigmoid flexures. A large proportion 
 of cases show the growth in the lower bowel, usually 2 to 
 3 inches from the anal orifice. 
 
 The appendix is occasionally the seat of a malignant 
 growth of the adeno-carcinoma type. This growth seems 
 
172 DISEASES OF THE PERITONEUM 
 
 to arise in appendices which have been previously inflamed 
 and are partially obliterated. Such tumours show little 
 tendency to spread, being apparently of low malignancy. 
 
 DISEASES OF THE PERITONEUM 
 
 Haemorrhage. Small petechial haemorrhages occur into 
 the subperitoneal tissue in infective conditions and in severe 
 anaemias. Free blood and blood -clots in the peritoneal 
 cavity may be due to rupture of an organ (liver or spleen) 
 from injury, acute peritonitis, rupture of a vascular tumour, 
 as, for example, in the spleen, or rupture of an aneurysm. 
 
 Dropsy of the Peritoneal Cavity or Ascites. This 
 condition may be found in diseases which tend to produce 
 dropsy elsewhere, such as chronic heart and renal disease, 
 or it may be due to cirrhosis of the liver. In long-standing 
 cases the peritoneum is frequently opaque and thickened. 
 The fluid is usually clear ; when it is milky the turbidity is 
 usually caused by the presence of protein bodies of the nature 
 of globulins. Very rarely milkiness is due to the presence of 
 fat globules (chylous ascites) escaped from an injured lacteal 
 vessel (e.g. in filariasis). 
 
 Acute Peritonitis. This may be due to (i) spread of 
 inflammation from structures within the abdomen, such as 
 the appendix and Fallopian tubes or from the pleura ; (2) 
 rupture of the gut from injury or perforation associated with 
 ulceration ; (3) blood or lymph infection. It may be general- 
 ised throughout the peritoneal cavity or localised by adhesions. 
 
 Naked-eye Appearances. There is more or less free fluid 
 in the cavity, more especially in the pelvis and in dependent 
 parts. The fluid may be yellow or brownish and contains 
 flakes of lymph. It is often mixed with faecal matter or 
 stomach contents, and usually has a foul smell. The omentum 
 is swollen and its vessels injected. There is fibrinous exudate 
 
DISEASES OF THE PERITONEUM 173 
 
 on the surface of the bowel, more especially between the coils 
 of the intestine (Fig. 68). The coils are thus glued together. 
 Not infrequently on separating the coils small abscesses are 
 opened into. 
 
 Microscopic Appearances of the Omentum in Cases of 
 Peritonitis. There is distension of the vessels, exudation 
 of fibrin on the surface and in the substance, swelling and 
 throwing-off of the endothelial cells. These are found amongst 
 the fibrin threads as large, swollen, and vacuolated cells, often 
 containing germs and polymorphonuclear leucocytes. Numer- 
 ous polymorphs are found in the fibrin on the surface and 
 infiltrating the tissue generally. There is swelling of the 
 collections of lymphoid tissue along the vessels, and many 
 free lymphocytes are found in the exudate. 
 
 Film preparations of the exudate show numerous poly- 
 morphonuclear leucocytes in various stages of degeneration, 
 large mononuclear cells often vacuolated and frequently con- 
 taining leucocytes which they have ingested, lymphocytes, and 
 micro-organisms. 
 
 Chronic Peritonitis. Large or smaller areas of thicken- 
 ing of the peritoneum, or rather of the subendothelial fibrous 
 tissue of the peritoneum, are found frequently, more especially 
 over liver and spleen. They may be associated with adhesions, 
 and are specially frequent in syphilis. A more general 
 thickening of the peritoneum is found in cases of long-standing 
 ascites. 
 
 Tuberculous Peritonitis. This may be associated with 
 tuberculous ulceration of the bowel, but not infrequently 
 no such lesion of the bowel can be found. Usually, however, 
 the mesenteric glands are the seat of tuberculosis. The 
 condition may also occur as a part of a generalised blood 
 infection. 
 
 Naked-eye Appearances. The coils of the intestine are 
 commonly adherent more or less firmly to one another. On 
 separating the coils, if this be possible, there will be found 
 covering the surface of the bowel and mesentery, also the 
 
174 DISEASES OF THE PERITONEUM 
 
 surface of liver and spleen, as well as the parietal peritoneum, 
 numerous small opaque white or yellow areas, the size of a 
 pin head or larger (Fig. 70). Often the coils of bowel are too 
 firmly adherent to one another to be separated without 
 tearing. The great omentum is thickened, drawn up and 
 infiltrated with grey tubercles. Occasionally free fluid may 
 be present. The matting of the intestines leads to interfer- 
 ence with peristalsis. Adhesions may lead to the formation 
 of bands under which loops of bowel may subsequently 
 become strangulated. Occasionally rupture of the bowel 
 may occur as the result of erosion of the wall from the 
 peritoneal aspect. 
 
 Microscopically, the appearances are those characteristic of 
 tubercle. Giant cells are often specially numerous and well 
 developed. 
 
 Tumours. Growths primary in the peritoneum are rare. 
 Endotheliomata are met with occasionally growing in the form 
 of multiple polypoid masses. Dissemination of carcinoma 
 sometimes occurs secondary to rupture of a cystic growth 
 of the ovary or the invasion of a bowel tumour into the 
 peritoneal cavity. 
 
CHAPTER IX 
 
 DISEASES OF THE LIVER, BILE PASSAGES, AND PANCREAS 
 
 DISEASES OF THE LIVER 
 
 Deformities. A transverse sulcus across the lower por- 
 tion of the right lobe of the organ is frequently seen, due 
 to the wearing of tight corsets. Perpendicular sulci are also 
 met with, due to folding of the liver from a similar cause. 
 
 ALTERATIONS IN THE CIRCULATION 
 
 1. Anaemia. Yellow or white patches are frequently 
 seen on the surface of the organ. They are due to localised 
 ansemia from pressure. 
 
 2. Chronic Venous Congestion. This condition is found 
 in cases of chronic valvular disease of the heart and in chronic 
 pulmonary lesions. The organ is enlarged in the early 
 stages. In the later stages it may be smaller than normal. 
 It has a dark purple colour with paler areas (Frontispiece, 
 Fig. 5), and is firmer than usual. On section, the cut surface 
 shows a mottled appearance, likened to nutmeg. There are 
 areas of congestion, dark purple in colour, and areas of fatty 
 change, pale yellow. The branches of the hepatic vein are 
 dilated. 
 
 Microscopic Appearances. In the very earliest stage there 
 may be little more than the deposit of yellow pigment in a 
 
 175 
 
176 DISEASES OF THE LIVER 
 
 zone of liver cells round the central vein. In the later stages 
 there is dilatation of the central veins and the capillaries 
 draining into them, with compression and atrophy of the 
 columns of liver cells between. The liver cells, more par- 
 ticularly those at the margin, may show fatty infiltration. There 
 is some increase of the fibrous tissue of the organ in the more 
 advanced cases. 
 
 3. Embolism and Thrombosis in the Portal Vein. 
 
 Thrombosis of the portal vein is sometimes found in connection 
 with cirrhosis of the liver and malignant disease. It may 
 also occur as the result of inflammation round a perforating 
 ulcer of the stomach. 
 
 Portions of thrombi from rootlets of the portal vein in 
 the neighbourhood of inflammatory foci, e.g. the appendix, 
 are caught in the branches of that vein within the liver. 
 Secondary thrombosis occurs in connection with such emboli, 
 the condition sometimes spreading to large branches of the 
 vein. As the emboli contain organisms, abscess formation 
 is set up. 
 
 As regards the effect upon the liver of blocking of a branch 
 of the portal vein, this may be very slight, owing to the fact 
 that the liver lobule is also supplied with blood from the 
 hepatic artery. Sometimes the area supplied assumes a 
 darker brown, even a red colour, but on microscopic examina- 
 tion little is seen in such an area beyond dilatation of the 
 capillaries. The liver cells commonly show no evidence of 
 necrosis. Occasionally, however, in such an area a partial 
 necrosis of the inner two-thirds of the lobule may be seen. 
 
 DEGENERATIVE CHANGES 
 
 i. Cloudy Swelling. This is found in varying degrees in 
 all infective conditions, and occasionally apart from infections, 
 as in haemorrhage of the pons where there was a markedly 
 raised temperature during life. 
 
DISEASES OF THE LIVER 177 
 
 The organ is slightly enlarged and has a pale appearance. 
 It is soft and friable. The last point is tested by the ease 
 with which the finger may be pushed into the substance of 
 the organ. On section, the cut surface has a hazy, misty 
 appearance, described as like the effect of plunging a portion 
 of normal liver into boiling water. The outline of the liver 
 lobules is no longer visible. The condition may be associated 
 with congestion of some of the vessels of the organ. It is 
 also commonly combined with a degree of fatty change. 
 
 Microscopic Appearances. The liver cells are swollen and 
 granular. In the fresh condition the nuclei are obscured by 
 the granules, but these are readily dissolved with dilute acetic 
 acid, when the nucleus is rendered visible again. The cells 
 often show a tendency to separate from one another owing to 
 solution of their cement substance. There may be some 
 infiltration of the portal spaces with inflammatory cells. 
 
 The condition is usually complicated with some fatty change 
 in the liver cells. The nucleus in the earlier stages stains 
 more intensely ; in the later stages it tends to lose its 
 characteristic staining reaction with basic dyes. 
 
 2. Fatty Change. Two types of this condition are 
 commonly distinguished : 
 
 (a) Fatty degeneration, by which is usually meant the 
 breaking down of the chemical constituents, more especially 
 the combinations of proteins with fatty compounds, under 
 the action of some poison, chemical or bacterial. 
 
 The organ may not be much altered in size or it may 
 be smaller than normal. It is paler than usual, of a bright 
 yellow colour, soft, and friable. On section, the parts 
 showing more advanced fatty change are seen as opaque 
 yellow areas. These may be in the centre of the lobules, 
 or they may form a zone at the periphery, or the change 
 may be present throughout. 
 
 Microscopic Appearances. Sections should be stained 
 with Sudan III., Scharlach R, or Nile blue sulphate. As 
 
178 DISEASES OF THE LIVER 
 
 already stated, the change may be at the periphery of the 
 lobule, in the centre or throughout. It is usually described 
 as occurring most characteristically at the centre. The 
 globules of fat in the cells tend to be numerous and small. 
 The nucleus may show degenerative changes : either increased 
 intensity of staining in the early stages, or loss of staining 
 reaction in the more advanced condition. 
 
 (b) Fatty infiltration may be defined as the absorption in 
 excess of fatty material and the deposition of it in a demon- 
 strable form in the protoplasm of the liver cell. A rigid 
 distinction between this and the preceding type cannot, 
 however, be made. The two conditions pass into one 
 another and are frequently combined. Thus there is reason 
 to believe that in the fatty degeneration of phosphorus 
 poisoning the fat in the liver cell is largely derived from out- 
 side. Hence in very many cases it is safer to use the term 
 fatty change. It is convenient, however, in certain cases to 
 make a distinction into two types, the extremes of which are 
 readily separated from one another. 
 
 The organ tends to be larger than normal, in some 
 cases very markedly so. It is pale yellow in colour 
 (Frontispiece, Fig. 2). Its consistence varies in different 
 cases. It may be softer and more friable, or it may be (in 
 cases where there is cirrhosis combined) firmer. On section, 
 the change may appear most marked in the periphery of 
 the lobule, or it may be diffuse. 
 
 Microscopic Appearances. The globules of fat within the 
 liver cells tend to be large, pressing aside the protoplasm and 
 nucleus of the liver cell. The change may be at the periphery 
 of the lobule, i.e. merely an exaggeration of a change found 
 normally in the liver during digestion, or it may be diffuse. 
 It is frequently combined with increase of fibrous tissue in the 
 organ. 
 
 3. Focal Necrosis. Areas of focal necrosis are found 
 in the liver in typhoid j 'ever and in eclampsia. They appear 
 
DISEASES OF THE LIVER 179 
 
 as opaque white or yellow points scattered through the liver 
 substance, but often they are too minute to be seen with 
 the unaided eye. Cloudy swelling is always associated. 
 
 In eclampsia the liver shows three characteristic changes, 
 which may not, however, all be present in a given case 
 (see p. 271). 
 
 (1) Hemorrhage under the capsule, which may be very 
 extensive ; also haemorrhage into the substance of the organ. 
 
 (2) Fatty change, usually most marked at the margin of 
 the necrotic areas. 
 
 (3) Areas of focal necrosis, usually situated at the periphery 
 of the lobules, and often too small to be seen with the naked 
 eye. 
 
 4. Amyloid (Waxy) Degeneration. For causation of 
 waxy change see p. 105. 
 
 The organ is commonly enlarged, often very much so. 
 It is anaemic and has a translucent appearance if the condition 
 be advanced. It is firm and elastic in consistence like india- 
 rubber. On section, the cut edge remains sharp. The cut 
 surface has the same translucent appearance. The condition 
 is often combined with some degree of fatty change. When 
 the cut surface is treated with a solution of iodine, the 
 waxy areas take on a mahogany brown colour (Frontispiece, 
 Fig. 4). 
 
 Microscopic Appearances. The waxy material has a clear 
 translucent appearance in unstained specimens. In prepara- 
 tions treated with methyl violet it shows a rose-pink to purple 
 colour. 
 
 In the early stages the change is limited to the middle 
 coats of the branches of the hepatic arteries and portal veins 
 in the portal tracts. It is the bands of connective tissue 
 between the muscle fibres which show the change. Later on, 
 the peri-endothelial connective tissue of the capillaries in the 
 middle zone of the lobules is affected. Still later, the change 
 becomes diffuse. The capillaries and also the liver cells 
 become compressed by the swollen amyloid material, and 
 
i8o DISEASES OF THE LIVER 
 
 occasionally little or nothing is seen in certain areas but masses 
 of waxy tissue. 
 
 5. Pigmentary Changes. A black coloration of those 
 portions of the organ nearest the intestines is often seen, 
 due to the action of the H 2 S from the gut upon the iron pig- 
 ment of the organ. This is, of course, a post-mortem change. 
 Increase in the amount of iron-containing pigment in the liver 
 is found in cases where there is an increase in the destruction 
 of the red blood corpuscles within the liver, as in septicaemias 
 and severe anaemias, notably in pernicious anaemia. This 
 increase of hsemosiderin pigment gives a yellow-brown colour 
 to the organ. The pigment may be brought out in a striking 
 fashion by pouring some ferrocyanide of potassium (2 per cent) 
 over the cut surface of the organ, and then some dilute HC1 
 (i per cent), repeating the process once or twice until the 
 Prussian blue colour appears (Frontispiece, Fig. i). Micro- 
 scopic sections of the organ should be treated in a similar 
 way. In chronic venous congestion, also in malaria, there is 
 a deposition of pigment in the liver cells. In cases where 
 there is obstruction to the outflow of the bile there is a yellow 
 coloration of the organ, which becomes green on exposure to 
 the oxygen of the air (Frontispiece, Fig. 3). 
 
 ACUTE INFLAMMATIONS OF THE LIVER 
 
 1. Acute Perihepatitis is found as a part of a general 
 peritonitis. The surface of the liver is covered with more 
 or less fibrinous exudate. 
 
 2. Acute Hepatitis. Acute inflammation of the liver 
 substance is found in slight degree in all infective fevers. It 
 is always combined with cloudy swelling, and may be associated 
 with focal necrosis, as in typhoid fever. The evidences of 
 inflammation are usually slight, being confined to infiltration 
 of the portal tracts with inflammatory cells. 
 
DISEASES OF THE LIVER 181 
 
 3. Suppurative Hepatitis. In discussing the types of 
 liver abscess the paths by which organisms may reach the 
 liver should be called to mind. There are three, (a) the 
 hepatic artery, (b) the portal vein draining the whole of the 
 abdominal contents, (c) the excretory duct of the organ 
 the bile duct. Thus at once we may distinguish three types 
 of abscess or suppurative hepatitis. 
 
 There are, in addition, three other types to v/hich special 
 names are given. 
 
 Types of Liver Abscess. 
 
 1. Pyaemic. 
 
 2. Portal pyaemic. 
 
 3. Biliary. 
 
 4. Actinomycotic. 
 
 5. Tropical. 
 
 6. Suppurating hydatid cyst. 
 
 (1) Suppurative Hepatitis of Arterial Origin Pycemic 
 Abscess. This type is found in cases of pyaemia, septicaemia, 
 and ulcerative endocarditis, where there are organisms 
 circulating in the blood of the body generally. The abscesses 
 in this case are minute and usually numerous. They are 
 scarcely visible to the naked eye, and there are similar 
 abscesses in other organs. 
 
 (2) Suppurative Hepatitis of Portal Origin Portal Pycemic 
 Abscess. In this type the infective agent comes to the liver 
 by way of the portal vein. It is usually a germ-laden thrombus 
 from a thrombosed vein in the neighbourhood of an inflam- 
 matory focus, such as an appendicitis. The abscesses in 
 this case are usually about the size of a pea. They occur in 
 groups or clusters like bunches of grapes (Fig. 71). They 
 form cavities containing yellow or greenish pus, their walls 
 being formed of necrosed liver tissue. Septic thrombi can 
 usually be found in branches of the portal vein (Fig. 7 1). The 
 condition is sometimes known as portal pyaemia. 
 
 (3) Sitppurative Hepatitis of Bile -Duct Origin Biliary 
 
i82 DISEASES OF THE LIVER 
 
 Abscess. This is associated with suppurative cholangitis 
 (suppurative inflammation of the bile ducts), which is commonly 
 caused by obstruction to the bile passages from the presence 
 of gall stones or a tumour. The abscesses are numerous, 
 usually minute and scattered uniformly throughout the 
 organ. The liver is bile stained. Cirrhosis of the liver is 
 not infrequently present in addition. 
 
 (4) Actinomycotic Abscess. This type is usually a special 
 variety of the portal pysemic abscess. It is associated with 
 a focus of infection with the Streptothrix actinomyces in some 
 part of the intestinal tract, e.g. the vermiform appendix. 
 The affected portion of liver has a worm-eaten appearance 
 owing to the presence of numerous small cavities containing 
 pus, with areas of necrotic liver around, in which there is 
 some fibrosis. 
 
 (5) Tropical Abscess. This is usually single and fairly 
 large (Fig. 72). The process is more a necrosis of the liver 
 substance than a true suppurative inflammation. The 
 contents of the abscess have a pink colour and creamy 
 consistence. The condition is commonly associated with 
 tropical dysentery. The Entamceba histolytica is found in 
 large numbers in the tissue in the margin of the abscesses, 
 and usually in the pus also. 
 
 (6) Suppuration in a Hydatid Cyst. In this case also the 
 abscess cavity is large and may be solitary. Mixed with the 
 pus there will be the ectocyst of the parasite. The cavity 
 is usually limited by fibrous tissue. 
 
 ACUTE AND SUBACUTE LIVER ATROPHY 
 
 This is a condition which is associated clinically with 
 jaundice, vomiting, a diminishing liver dulness, and eventu- 
 ally coma. It is often connected more or less closely with 
 such diseases as syphilis, tuberculosis, and influenza, and a 
 number of cases have developed in women during the later 
 
DISEASES OF THE LIVER 183 
 
 months of pregnancy. There is a general consensus of opinion 
 that the condition is a toxic one, but what the nature of the 
 toxin is and where it originates has not yet been determined. 
 It has been suggested that it has its seat in the intestine, 
 and very commonly one finds in these cases evidence of acute 
 inflammation of the duodenum and upper bowel, but this 
 condition has also been ascribed to the action of toxic bile 
 from the necrosed liver. 
 
 Two stages in the disease may be recognised, and, as a 
 result, two types of cases are met with post mortem. 
 
 (1) Acute cases in which death occurs within one or two 
 weeks of the onset of the symptoms, and in which degenerative 
 changes predominate in the liver. There is usually little 
 evidence of overgrowth of fibrous tissue. To this type the 
 name " acute yellow atrophy " or " acute liver atrophy " is 
 more particularly applicable. 
 
 (2) Subacute cases, lasting some weeks, or even months, 
 in which there is more or less evidence of the reformation of 
 functioning liver tissue with overgrowth of fibrous tissue. 
 For such cases the terms " subacute yellow atrophy," " sub- 
 acute liver atrophy," and for the cases with marked regenera- 
 tion " multiple nodular hyperplasia," have been suggested. 
 
 (i) Acute Atrophy Naked-eye Appearances. The liver 
 is reduced in size, often markedly so. Its capsule tends to 
 be shrivelled. The organ shows, as a rule, areas of different 
 colours, yellow and red. In the more acute types the yellow 
 areas predominate. 
 
 Microscopic Appearances. In the yellow areas the liver 
 cells are usually visible, but they show marked evidence of 
 degenerative changes. They are swollen, granular, frequently 
 contain fatty globules, and their nuclei have to a great extent 
 lost their staining reaction. In addition, there is usually more 
 or less overgrowth of fibrous tissue extending from the portal 
 tracts. This fibrous tissue is vascular and cellular. In the 
 neighbourhood of the portal tracts are small vermiform strings 
 of cells whose nuclei stain deeply. Sometimes these have an 
 
184 DISEASES OF THE LIVER 
 
 obvious lumen. They represent the remains of pre-existing 
 and of proliferating small bile ducts. In process of degener- 
 ating the liver cell undergoes coagulation of its substance, 
 followed by disappearance first of the carbohydrate and fatty 
 elements, second of the albuminous constituents. 
 
 In the red areas little that is characteristic of liver structure 
 remains. The tissue is a vascular connective tissue with 
 dilated capillaries, and shows large numbers of endothelial 
 cells which may contain pigment, a loose connective-tissue 
 stroma, occasional degenerated liver cells scarcely recognisable 
 as such, and a few leucocytes. In the neighbourhood of the 
 portal tracts the small bile ducts are numerous, and may show 
 evidence of proliferation of their cells (mitotic figures). 
 
 (2) Subacute Atrophy Naked-eye Appearances. The 
 organ is of a brownish-red colour, with yellow or greenish 
 nodules varying much in size, sometimes projecting beyond the 
 general surface (Fig. 73). On section, these yellow nodules 
 may be isolated, or may be found scattered through the sub- 
 stance of the liver. Where the nodules are numerous the 
 organ presents the appearance of a coarse cirrhosis, from 
 which condition it is often very difficult to distinguish it. 
 
 Microscopic Appearances. The red-bfown portion of the 
 organ consists of a fairly vascular connective tissue with groups 
 of small bile ducts, scattered endothelial cells, and, as a rule, 
 with no liver tissue to be found. The yellow nodules present 
 the appearance of liver tissue. They are composed of masses 
 of liver cells, sometimes arranged in columns, at other times 
 closely packed together. Lobular arrangement is imperfect. 
 Many of the cells are large and multinucleated ; some may be 
 found showing mitotic division of their nuclei. The appear- 
 ances at the margin of these nodules suggest that they are 
 enlarging and pressing aside the surrounding tissue. The 
 fibrous tissue, being newly formed, contains few elastic fibres. 
 
 It will thus be seen that the disease is essentially a 
 degeneration of the liver parenchyma under the action of 
 some poison. Complementary to this, there is an overgrowth 
 of fibrous tissue starting from the portal tracts. 
 
DISEASES OF THE LIVER 185 
 
 The condition may thus be regarded as an acute cirrhosis. 
 It forms a connecting link between the purely degenerative 
 changes, such as occur in phosphorus poisoning, and the 
 chronic interstitial inflammations or cirrhoses. 
 
 Following the degenerative changes, attempts, more or 
 less successful, are made to regenerate liver tissue in two 
 ways : (i) By proliferation of the bile ducts. This, although 
 it is an imitation of the way in which the liver lobules are 
 produced in embryonic life, seldom results in the formation 
 of liver parenchyma. (2) By proliferation of liver cells which 
 survive the destructive influence of the poison, with resulting 
 formation of nodules of glandular cells more or less resembling 
 in structure liver lobules, and probably functioning as such* 
 
 CHRONIC INFLAMMATION OF THE LIVER 
 
 Types. 
 
 1. Cirrhosis. 
 
 (a) Common. 
 
 (b) Biliary. 
 
 (c) Syphilitic. 
 
 2. Syphilis. 
 
 3. Tuberculosis. 
 
 Cirrhosis 
 
 The term " cirrhosis," introduced by Laennec, simply 
 means " yellow." It has, however, come to be synonymous 
 with fibrosis, and is applied to all conditions of the liver 
 in which there is abnormal development of connective 
 tissue. 
 
 The condition is caused by any slowly acting poison or 
 irritant. Thus chronic intoxications, such as alcohol or lead, 
 produce it. Infective conditions, such as syphilis, may also 
 cause it. Retention of the bile from obstruction to the bile 
 ducts will produce it ; also inflammatory conditions of the 
 small bile ducts, which so commonly accompany obstruction. 
 
186 DISEASES OF THE LIVER 
 
 Lastly, abnormal accumulation of pigment, as in malaria and 
 chronic venous congestion, is a factor. 
 
 The liver consists of two types of cellular elements : (i) 
 highly differentiated and functioning gland cells very sus- 
 ceptible to the action of poisons, and capable of little in the way 
 of reaction ; (2) cells less highly differentiated connective - 
 tissue cells not so readily damaged by the action of poisons, 
 and capable of reaction and proliferation in circumstances 
 where the liver cells degenerate. The mere disappearance 
 of the glandular cells is followed by a complementary pro- 
 liferation of connective tissue. This is well seen in the less 
 acute types of liver atrophy. But where there is an irritant 
 constantly present, as in syphilis, alcoholism, retention of 
 bile, and inflammation of the small bile ducts, another factor 
 comes into play, namely, the proliferative reaction of the 
 connective-tissue cell under irritation. These two factors 
 are, no doubt, both operative in the production of cirrhosis 
 of the liver. 
 
 Where there is any great amount of destruction of hepatic 
 gland cells the stimulus to regenerate is felt by the organ, 
 and is answered by the formation of new areas of liver tissue. 
 This is a prominent feature in subacute liver atrophy, and 
 evidence of it is usually present in cirrhosis also. 
 
 Classification. The terms monolobular (where the areas 
 of liver cut off by bands of fibrous tissue represent single 
 lobules) and polylobular (where such areas represent groups 
 of lobules) are often used to characterise types of cirrhosis. 
 They are practically the same as fine and coarse cirrhosis 
 respectively. They are not very useful as a basis of classifica- 
 tion, owing to the fact that the two conditions are usually 
 to be seen alongside one another in the same liver. Another 
 couple of terms used sometimes are " hypertrophic " (meaning 
 an abnormally large liver) and"atrophic" (abnormally small). 
 Owing to the fact that in many instances it is impossible to 
 decide whether a liver is enlarged or not, these terms are 
 
DISEASES OF THE LIVER 187 
 
 rather to be avoided. The method of classification adopted 
 is as follows : 
 
 A, Common Cirrhosis. The ordinary type found in asso- 
 ciation with chronic intoxications, distinguishing (a) an early 
 stage where the liver is large, and (b) a late stage where it is 
 small. This variety is usually polylobular. 
 
 1. Early Stage. The liver is enlarged and has a somewhat 
 rough surface. In some cases it is red, from congestion ; in 
 other cases it is yellow, from fatty change. 
 
 The organ is firmer and tougher than normal, and on 
 section shows bands of vascular fibrous tissue running through 
 it. These, as a rule, are not very obvious. 
 
 Microscopic Appearances. Bands of vascular and cellular 
 connective tissue divide up the liver into areas, at one time 
 representing a single lobule, at another time a group of lobules. 
 The liver cells may show little change, or there may be more 
 or less fatty infiltration. 
 
 2. Advanced, Stage. This is the more common type of 
 the disease, known as " hobnail," " drunkard's," or " gin- 
 drinker's " liver. 
 
 The liver is distinctly reduced in size. It has a roughened 
 surface t owing to the presence of nodules varying much in 
 size. It usually has a pale yellow colour. The capsule 
 may be thickened. It is distinctly tougher and firmer than 
 normal. On section, it shows bands of grey fibrous tissue 
 passing through the organ in all directions, dividing it up 
 into rounded areas varying much in size (Fig. 74). A number 
 of cases are recorded in which primary carcinoma of the 
 organ was associated with this type of cirrhosis. 
 
 Microscopic Appearances. The most striking change is 
 the overgrowth of fibrous tissue which spreads from the portal 
 tracts, forming bands, thicker or thinner, cutting off individual 
 lobules or groups of lobules. This fibrous tissue is well formed, 
 but it often shows here and there accumulations of small 
 
i88 DISEASES OF THE LIVER 
 
 round cells, indicating that the fibrous proliferation is still 
 progressing. There is considerable development of new elastic 
 fibres in the bands of fibrous tissue. There is a varying 
 number of small bile ducts. These in some cases appear to 
 arise from retrograde changes in columns of liver cells, the 
 latter reverting to their embryonic condition under the pressure 
 of the surrounding fibrous tissue. In other cases the ducts 
 represent an attempt to reform liver tissue, just as in subacute 
 liver atrophy. There is a tendency for the fibrous tissue to 
 invade the liver lobule at its margin to a certain small extent, 
 individual liver cells or groups of them being cut off. The 
 liver cells themselves commonly show more or less fatty 
 infiltration. Not infrequently small nodules of regenerated 
 liver tissue are met with. These are recognised by the 
 evidence of multiplication in the liver cells, some of them 
 having two nuclei, others showing evidence of division. Such 
 nodules also show imperfect lobule formation. 
 
 B. Biliary Cirrhosis. This condition is commonly associ- 
 ated with obstruction to the bile ducts. This may be due to con- 
 genital obliteration, to gall stones, or to tumour. It is also 
 very commonly associated, as, indeed, obstruction is, with 
 inflammatory conditions of the bile ducts. 
 
 The organ is sometimes enlarged, sometimes reduced in 
 size. Its surface is not so rough as in common cirrhosis. It 
 is a much finer cirrhosis, corresponding more to the mono- 
 lobular type. The organ usually has a deep yellow colour , 
 turning green on exposure to the air, due to the bile staining 
 which so constantly accompanies it. The organ is firmer 
 and tougher than normal. On section, bands of fibrous 
 tissue can be seen radiating through the liver tissue and 
 dividing it up into small lobules which have a yellow or 
 green colour. Sometimes abscess formation of biliary origin 
 is present. 
 
 Microscopic Appearances. As in the common type, the 
 most striking change is an overgrowth of the fibrous tissue of 
 the organ, extending from the portal tract and tending to 
 
DISEASES OF THE LIVER 189 
 
 separate individual liver lobules from one another. The fibrous 
 tissue is, on the whole, more cellular than in the common type 
 of cirrhosis, and small bile ducts are a more conspicuous 
 feature. The liver cells show marked degenerative changes, 
 areas of necrosis being frequently met with. Bile pigment 
 may be seen in and between the liver cells. Catarrhal changes 
 in the bile ducts, sometimes with the development of abscesses, 
 is common. In suitably stained specimens germs may be 
 found, especially where abscess formation is present. 
 
 C. Syphilitic Cirrhosis (see Syphilis). 
 
 Results of Cirrhosis. Owing to the pressure of the con- 
 tracting fibrous tissue upon the branches of the portal vein 
 within the liver, there is obstruction to the blood passing 
 through the organ and coming from spleen and bowel, with 
 the following results : 
 
 i. Ascites or dropsy of the abdominal cavity. 
 ^2. Chronic venous congestion of oesophagus, stomach, 
 intestine, and spleen, with a tendency to chronic catarrh, 
 varicose veins, haemorrhage, and, in the case of the spleen, 
 enlargement. 
 
 These two changes occur especially in common cirrhosis. 
 
 3. Jaundice, which is more characteristic of biliary cirrhosis. 
 
 Syphilis of the Liver 
 
 (a) Congenital. In this type of the disease a diffuse 
 cirrhotic condition is sometimes met with (congenital 
 syphilitic cirrhosis). The organ is enlarged, commonly bile- 
 stained, firmer than normal, but otherwise little altered. 
 
 Microscopic Appearances. The organ is the seat of a 
 diffuse overgrowth of fibrous tissue. This is more marked in 
 some places than in others. It is not specially restricted to 
 the portal tracts ; on the contrary, it is found within the lobule 
 separating groups of cells and individual cells from one 
 another. In the fibrous tissue are to be found numerous small 
 round cells aggregated in places into small masses, sometimes 
 
DISEASES OF THE LIVER 
 
 with caseous centres (miliary gummata). In suitably treated 
 material, spirochaetes may be demonstrated in large numbers. 
 
 (b) Acquired. In acquired syphilis the lesions found 
 in the liver are : 
 
 1. Areas of chronic perihepatitis } sometimes with adhesions 
 to the abdominal wall and diaphragm. 
 
 2. Gummata. These are caseous foci surrounded by a 
 zone of fibrous tissue (Fig. 75), sometimes with cirrhotic 
 change radiating from it into the liver substance. They 
 may occur singly or in groups. They are frequently absorbed , 
 leaving behind scars which show themselves as puckerings 
 on the surface. When these are numerous, sometimes a 
 coarse cirrhotic condition is produced, with marked deformity 
 of the organ. Waxy degeneration is sometimes combined 
 with the above. 
 
 Tuberculosis of the Liver 
 
 Tuberculosis seldom develops to any extent in the liver, 
 that organ apparently not forming a suitable nidus for the 
 growth of the tubercle bacillus. Two types of the disease 
 are found : 
 
 (a) Miliary Tuberculosis. Small scattered foci which 
 may or may not be visible to the naked eye. When visible, 
 they appear as minute white or yellow spots ; sometimes 
 they are bile-stained. Similar areas are found in other 
 organs. 
 
 Microscopic Appearance. Numerous cellular areas are 
 scattered through the organ. They are made up chiefly of 
 large and small mononuclear cells. They may have caseous 
 necrotic centres or may show giant cells. 
 
 (b) Larger caseous nodules, which may be single or numer- 
 ous, and are usually bile-stained. This is a rare type, more 
 commonly met with in children than in adults. 
 
DISEASES OF THE LIVER 
 
 191 
 
 Leukaemia of the Liver 
 
 The organ is usually enlarged, paler than normal, some- 
 times with distinct, small, whitish areas scattered through it. 
 
 Microscopic Appearances. There is infiltration of the liver 
 substance with rounded cells, which vary in type according to 
 whether the condition is myelaemia or lymphsemia. These 
 cells are found in the portal tracts and between the columns 
 of liver cells. In the more advanced cases the individual 
 liver cells may be separated from one another. Here and 
 there are cell accumulations without any liver structure. These 
 are the above-mentioned pale areas. The endothelial cells of 
 the capillaries are swollen. 
 
 Lymphadenoma (Hodgkin's Disease) 
 
 The liver may or may not be affected in this condition. 
 When it is, numerous irregularly shaped pale areas similar 
 to those seen in the spleen are scattered through it. The 
 condition is sometimes indistinguishable from true tumour 
 formation. In most cases, however, the pale areas are more 
 diffusely distributed, smaller, and less well defined. 
 
 Microscopically, the appearance of the areas is similar to 
 those found in the spleen in the same disease (see p. 1 10). 
 
 Tumours 
 
 A. Simple growths of the liver are not common. The 
 cavernous angioma is the one most frequently found. It 
 appears as a dark red area under the capsule of the organ. 
 On section, it is found to be more or less irregularly wedge- 
 shaped. On close inspection, bands of white fibrous tissue 
 may be seen dividing the area up into spaces filled with 
 blood (Fig. 76). Its appearance is suggestive of an infarct, 
 but it should be remembered that true infarction of the 
 liver does not occur. 
 
 Adenomata of the liver are occasionally met with. They 
 
192 DISEASES OF THE LIVER 
 
 appear as circular, well-defined nodules in the substance of 
 the organ, yellow or reddish-brown in colour. They are 
 single or multiple, and microscopically show an approxima- 
 tion to the normal structure of the liver, but without the 
 regular lobular arrangement. Areas of regenerated liver 
 tissue have a somewhat similar appearance. 
 
 B. Malignant growths are very common in the liver. 
 
 Primary growths are not very frequent, but secondary 
 growths, more particularly carcinomata, are very common. 
 The venous blood from the various portions of the bowel 
 passes through the organ, and is naturally strained of any 
 emboli, tumour or otherwise, in it. Inasmuch as the malig- 
 nant growth of the bowel is almost invariably a carcinoma, 
 the secondary malignant neoplasms of the liver are commonly 
 of this type. 
 
 It is seldom possible, with any great amount of certainty, 
 to decide from its appearance whether a tumour is sarcoma 
 or carcinoma, primary or secondary. The growth, or growths, 
 appear as white or yellow areas scattered through the sub- 
 stance of the organ, varying in size, rounded or irregular 
 in shape. The liver is often greatly enlarged (Fig. 78). In 
 the tumour masses, necrotic areas, and haemorrhages are 
 commonly seen. Owing to sinking in of the necrotic centres 
 the masses on the surface often show crater-like hollows. 
 The intervening liver substance frequently shows bile-staining, 
 and occasionally cirrhosis. The connection between primary 
 cancer and cirrhosis is well recognised. 
 
 1. Primary cancers of the liver are of two types : 
 
 (1) A type resembling more or less "closely the structure 
 of the liver, the tumour cells occurring in columns. 
 
 (2) A type arising from the bile ducts and resembling 
 other adeno-carcinomata. 
 
 The association between primary cancer and cirrhosis of 
 the liver has already been noted. 
 
 2. Secondary cancers vary very much in appearance 
 
DISEASES OF THE LIVER 193 
 
 and in character. All types of adeno-carcinoma of the 
 bowel columnar cell, scirrhous, encephaloid, colloid occur, 
 also chorionepithelioma. 
 
 Of sarcomata (Fig. 77) only the melanotic shows appear- 
 ances which are distinctive. 
 
 Cysts of the Liver 
 
 Congenital cystic disease is sometimes met with in the 
 liver, although not so frequently as in the kidney. The 
 cysts are numerous, vary in size, and contain clear fluid. 
 
 Hydatid cysts are relatively frequent in the liver. They 
 often attain a very large size, are surrounded with a fibrous 
 capsule, and contain ecto- and endo-cyst, with the character- 
 istic " white of egg " appearance (Fig. 79). 
 
 Gas Cysts of small size, caused by the development of 
 bubbles of gas in the liver substance through the action of 
 an organism (B. cerogenes capsulatus, also called B. Welchit), 
 are occasionally met. They are found in association with sup- 
 puration in the abdominal cavity. Pressure upon the liver 
 produces a sensation of crackling, such as is normally present 
 in the lungs. Microscopically, spaces representing dilated 
 vessels are found lined with a layer of bacteria. A similar 
 change may be present in other organs, e.g. pancreas. 
 
 The organism causing this condition is a normal inhabitant 
 of the intestinal tract and is often found in the blood in cases 
 where the sectio is deferred for some time after death. The 
 blood in such cases has a frothy appearance. Occasionally 
 this invasion of the blood occurs during life when the above 
 appearances are produced in the liver and other organs. 
 
 METHOD OF EXAMINING A LIVER REMOVED FROM THE BODY 
 
 The general size, colour, and shape of the organ should be 
 noted, also the appearance of the lobules as they shine through 
 the capsule. The capsule is then examined for evidence of 
 
 13 
 
I 9 4 GALL BLADDER AND BILE DUCTS 
 
 adhesions with the abdominal parietes, for depressions such 
 as are produced by gummata, for the fine or coarse generalised 
 roughening of cirrhosis, also for the fibrinous exudate of 
 acute peritonitis and the caseous foci of tuberculous peritonitis. 
 The organ is weighed , the normal weight of the liver being 
 45 to 58 oz. (1420-1649 grm.). It is opened up by a series of 
 perpendicular cuts. In so doing the consistence of the organ 
 is noted. Pressure is made upon the cut surface in order 
 further to investigate this point. The cut edge should be 
 looked at in order to see whether it is rounded (indicating 
 soft consistence) or sharp. The cut surface is then in- 
 vestigated as to colour, the presence of abscesses, tumours, 
 etc. Lastly, the gall bladder is opened up, and the amount of 
 bile, also its colour noted. Gall stones should be searched for. 
 
 DISEASES OF GALL BLADDER AND BILE DUCTS 
 
 Congenital obliteration of the common bile duct is a 
 condition occasionally met with. The exact cause is unknown, 
 but it is believed to be, in some cases, syphilitic in origin. 
 It is associated with a fine cirrhosis of the liver and bile 
 pigmentation of that organ as well as jaundice. 
 
 Inflammation of Gall Bladder (Cholecystitis), of Bile 
 Ducts (Cholangitis). 
 
 Catarrhal Inflammation. A mild degree of inflamma- 
 tion of the bile passages is sometimes associated with a 
 catarrhal condition of the stomach, and, owing to the low 
 pressure at which the bile is excreted, blocking of the bile 
 passages from swelling of the walls, with resulting jaundice, 
 may occur. A similar condition is sometimes brought about 
 by the invasion of organisms, such as the B. typhosus'm 
 typhoid fever. The bacilli, in all probability, reach the bile 
 ducts from the blood by way of the liver, but it is possible 
 that they pass upwards from the duodenum. In the gall 
 
GALL BLADDER AND BILE DUCTS 195 
 
 bladder and larger bile ducts a catarrhal inflammation is 
 set up which may persist for months or years after the attack 
 of fever. In many instances this inflammatory change leads 
 to gall-stone formation. When the typhoid bacillus is the 
 cause of this condition the patient suffering from it is con- 
 stantly voiding with his stools living, virulent organisms, 
 which may contaminate food or drink and lead to the dis- 
 semination of the disease. Such individuals are known as 
 " typhoid carriers" 
 
 Suppurative inflammation of the bile ducts (suppurative 
 cholangitis) is a very common accompaniment of obstruction 
 to the outlet of the bile from gall stones or tumour formation. 
 The organisms found are usually staphylococci or B. coli. 
 The condition results, not infrequently, in abscesses (biliary) 
 within the liver substance. 
 
 Suppurative Inflammation (empyema) of the gall bladder 
 is sometimes met with apart from cholangitis. The acute 
 inflammation may pass through the wall of the bladder and 
 give rise to acute peritonitis. 
 
 Biliary Concretions or Gall Stones (Cholelithiasis) 
 
 Gall stones are much more common in women than 
 in men, something like three-quarters of the cases occurr- 
 ing in the female sex. They usually make themselves 
 felt about the age of forty, although, not infrequently, the 
 stones are found post-mortem without there being in the 
 history of the case anything to indicate their presence. As 
 regards causation, tight lacing, good living, and sedentary 
 habits are predisposing factors, but the actual cause of the 
 condition is commonly a catarrhal inflammation of the bile 
 passages associated with the presence of organisms. Aschoff 
 distinguishes two types of gall stones : (i) Those produced 
 by congestion of bile and disturbances of metabolism ; the 
 stones belonging to this category consist almost entirely 
 
196 GALL BLADDER AND BILE DUCTS 
 
 of cholesterin. (2) Those caused by inflammatory change 
 due to the presence of organisms. The germs which have 
 been separated, in some cases actually from the interior 
 of the stones themselves, are staphylococci, B. coli, and B. 
 typhosus. The mode of formation of the concretions is as 
 follows : a nucleus of mucus and epithelial debris is formed, 
 and round this are deposited cholesterin (largely derived from 
 disintegrated epithelium), lime and magnesium salts, and bile 
 pigment. Cholesterin is the main constituent, being present 
 usually to the amount of 70-80 per cent ; hence the lightness 
 of the stones. Some stones are formed almost entirely of 
 cholesterin. The colour, which varies from pale yellow to 
 black, depends upon the amount of bile pigment present. 
 The concretions vary much in size, from minute particles 
 (gall sand) to masses measuring, it may be, two inches across. 
 Those formed in the bile ducts are usually small ; the larger 
 ones develop in the gall bladder. Gall stones are usually 
 multiple, hence commonly facetted (Fig. 80). Sometimes 
 they have a mulberry-like surface and occasionally they are 
 smooth. The smooth stones are, of course, solitary. On 
 section, the concretions often show concentric lamination; 
 sometimes they exhibit radiating lines. 
 
 As regards the effects of the presence of gall stones, they 
 tend to keep up the chronic irritation which caused their 
 formation. Thus they lead to thickening of the gall bladder 
 and bile ducts and to adhesions to surrounding parts. More 
 acute, suppurative inflammation may be set up. They may 
 ulcerate through into the intestine, and, when very large, 
 have been known to cause intestinal obstruction. They 
 may obstruct the cystic duct, thus leading to atrophy, or, in 
 some cases, to dilatation of the gall bladder. They not 
 infrequently obstruct the common bile duct and give rise 
 to jaundice. Lastly, there is a very definite relationship 
 between cancer of the gall bladder and the presence of gall 
 stones. 
 
DISEASES OF THE PANCREAS 197 
 
 Tumours. The carcinoma is the most important tumour of 
 the gall bladder. It is usually a columnar cell adeno-car- 
 cinoma, but may be a scirrhus or colloid cancer, or even a 
 squamous epithelioma. 
 
 DISEASES OF THE PANCREAS 
 
 The pancreas is an organ which tends to show marked post- 
 mortem changes, partly because of the action of the digestive 
 juices which it secretes, partly because of its proximity to 
 stomach and intestine, and so to infection with putrefactive 
 germs. Thus, just as in the case of the stomach, so with the 
 pancreas, the pathologist must be careful not to regard as 
 evidence of disease, changes which are merely due to altera- 
 tions taking place after death. 
 
 Where a lesion of the pancreas is suspected, careful search 
 should be made for areas of fat necrosis. Conversely, the 
 presence of these areas of fat necrosis s is evidence of a 
 lesion of the pancreatic gland. Such areas are found in the 
 fat of the pancreas itself, of the mesentery and omentum, 
 occasionally even of the mediastinum. They appear as 
 opaque white spots the size of pin heads, or even as large as 
 peas. The change in the fat is brought about by a setting 
 free in the peritoneal cavity of the fat-splitting ferment of 
 the pancreas. The neutral fat is at first split into fatty acid 
 and glycerine, the fatty acid probably combining subsequently 
 with a calcium base. 
 
 Atrophy of the pancreas is sometimes met in old age 
 and wasting diseases. In diabetes not infrequently the only 
 alteration found is a diminution in the size of this organ. 
 
 Fatty infiltration, or penetration of fat into the sub- 
 stance of the gland, with atrophy of the gland tissue, is 
 occasionally seen. 
 
igS DISEASES OF THE PANCREAS 
 
 Inflammation 
 
 1. Acute H&morrhagic Pancreatitis. This is a somewhat 
 rare condition, the etiology of which is not quite clear. The 
 symptoms are those of acute intestinal obstruction. In 
 many instances it is an acute infective process due to the 
 presence of germs, and it is not infrequently found in associa- 
 tion with cholangitis and gall stones which may be found 
 blocking the ampulla of Vater. Some regard the haemorrhage 
 as the primary change, others consider that it is, like the fat 
 necrosis, due to the setting free of the digestive juices of the 
 organ, and the action of these upon the blood-vessels. 
 
 As regards appearances, the organ is swollen and dark red 
 in colour, due to infiltration with blood. More or less extensive 
 fat necrosis is always found in the fat in the neighbourhood. 
 
 Microscopically, areas of necrosed pancreatic tissue are 
 found, also infiltration of the interacinous tissue with red blood 
 corpuscles, fibrin, and leucocytes. The areas of fat necrosis 
 are well brought out with Nile Blue which stains the necrosed 
 fat blue, the normal fat red. 
 
 2. Suppurative Pancreatitis. Organisms may reach the 
 pancreas by way of the blood-stream or by the duct of Wirsung, 
 or again by extension from neighbouring parts. The abscesses 
 may be minute and numerous or large and solitary. Some- 
 times the change is associated with suppurative cholangitis 
 and gall stones. The abscesses may rupture into the peri- 
 toneal cavity and cause peritonitis. 
 
 3. Chronic interstitial pancreatitis or cirrhosis of the 
 pancreas may be met with in association with alcoholism, 
 syphilis, and obstruction to the duct of Wirsung by calculi 
 or tumour formation. In some cases of diabetes a fine 
 fibrosis, involving more especially the islands of Langerhans, 
 has been described. 
 
 Tumours. Primary carcinomata are occasionally met 
 with. By pressure upon the common bile duct such tumours 
 
DISEASES OF THE PANCREAS 199 
 
 cause an extreme degree of jaundice. Many of the cases of 
 so-called malignant jaundice are due, not to a neoplasm in 
 the pancreas, but to some secondary deposit in a retroperi- 
 toneal gland in the neighbourhood. As a rule carcinomata 
 show microscopically the characters of a columnar cell 
 glandular cancer. 
 
 Cysts. The pancreas, like the liver and kidneys, is 
 sometimes the seat of congenital cystic disease. Such cysts 
 are multiple and small. Large solitary cysts are also met with, 
 due in all probability to obstruction of a duct of the gland. 
 
 Relationship between Lesions of the Pancreas arid Diabetes. 
 Since the middle of last century a relationship between changes 
 in the pancreas and the disease diabetes has been recognised. 
 In 1889 it was shown by Minkowski that total extirpation of 
 the organ produced a fatal diabetes. Ligature of the duct 
 was, however, found not to have this effect. It was concluded 
 that the pancreas gave origin to an internal secretion which, 
 in cases of diabetes, was absent. Search was made for some 
 element in the gland which might be the source of such an 
 internal secretion, and the islands of Langerhans, first observed 
 in 1869, were selected as the probable source. Somewhat 
 conflicting statements are at present made regarding the 
 presence of lesions of these structures in diabetes. Some have 
 found fibrosis or hyaline degeneration in a large proportion of 
 cases. There can be no doubt that in many cases no obvious 
 lesion of any structure in the pancreas can be found. The 
 lesions which have been described are simple atrophy, fatty 
 infiltration associated with atrophy, a fine fibrosis, hyaline 
 change in the connective tissue of the islands of Langerhans. 
 
CHAPTER X 
 
 DISEASES OF THE KIDNEY AND BLADDER 
 
 DISEASES OF THE KIDNEY 
 
 CONGENITAL ANOMALIES 
 
 Persistence of Foetal Lobulation is a fairly common finding. 
 It is best seen after stripping the capsule from the organ, 
 and shows itself by a series of intersecting lines dividing the 
 organ into irregularly shaped areas. 
 
 Horse-shoe Kidney, a condition in which the two organs 
 are united, usually at their lower end across the vertebral 
 column, is not infrequently found. 
 
 Congenital Cystic Kidney. In this condition, which is 
 always bilateral, the organ is enlarged, often greatly so. The 
 outer surface is studded with projecting cysts, with trans- 
 parent contents varying in size from something just visible 
 to a walnut. In some cases there is very little kidney tissue 
 left between the cysts. On section, a similar appearance 
 is seen (Fig. 81). The condition is believed to be due to a 
 failure of union between the glomerular and the tubular 
 portions of the kidney tissue, which are developed separ- 
 ately. 
 
 Solitary congenital cysts, sometimes of large size, may 
 be met with. 
 
 200 
 
DISEASES OF THE KIDNEY 201 
 
 Congenital Hydronephrosis may occur in one kidney 
 owing to defective formation of the ureter. 
 
 CIRCULATORY CHANGES 
 
 1. Chronic Venous Congestion. This condition is found 
 in cases where there is obstruction to the passage of blood 
 through the heart or lungs. 
 
 Naked-eye Appearances. The organ is somewhat enlarged. 
 It is firm. On section, the medulla has a dark purple appear- 
 ance, the cortex is paler than the medulla,, but shows dark lines 
 and dots indicating vessels and glomeruli. On stripping the 
 capsule, the venae stellatae are often very prominent. 
 
 Microscopic Appearances. The vessels generally are dilated, 
 more especially those of the medulla. The glomerular capil- 
 laries are distended. Sometimes haemorrhages into the 
 tubules are seen. Catarrhal and interstitial changes may be 
 superadded. 
 
 2. Infarction. Infarcts of the kidney are common. They 
 are almost invariably due to embolism of one of the branches 
 of the renal artery. Occasionally the whole vessel may be 
 blocked. The embolism may be caused by the impaction 
 of portions of thrombi from vegetations on the aortic or 
 mitral valve, thrombi in the left auricle or its appendix, or 
 on atheromatous patches in the aorta. The infarcts are 
 wedge-shaped areas in the cortex, usually white or yellow 
 in appearance, surrounded by a haemorrhagic zone, more 
 especially where they come in contact with the medulla 
 (Fig. 82). At first the area is level with the rest of the surface. 
 Later on it becomes depressed, and eventually absorbed, 
 leaving a cicatrix. 
 
 Very similar irregularly scattered depressed areas are found 
 on the surface of the organ which, on section, prove to 
 be areas where the cortex is narrow and fibrosed. They are 
 due to interstitial change following blocking of vessels owing 
 
202 DISEASES OF THE KIDNEY AND BLADDER 
 
 to disease. This condition when well marked is usually 
 referred to as arterio-sclerotic kidney (see p. 214). 
 
 Microscopic Appearance. The infarcted portion shows 
 swelling, granularity, and more intense staining of the columnar 
 cells of its tubules. The nuclei usually are broken into 
 masses of chromatin or fail to stain altogether. At the margin 
 the tubules and intertubular tissue are infiltrated with red 
 blood cells, and frequently with leucocytes. The thrombosed 
 vessel can often be seen towards the apex of the wedge. 
 When the embolus contains organisms these may be seen in 
 masses. In such a case polymorphonuclear leucocytes are 
 very numerous. 
 
 DEGENERATIONS 
 
 1. Cloudy Swelling. This is found in all infective diseases. 
 It is particularly well marked in cases of pneumonia. 
 
 The organ is somewhat enlarged, softer, and more friable 
 than normal. On section, the cortex is pale, opaque, and 
 swollen. The cut surface of the cortex protrudes above the 
 level of the medulla. 
 
 Microscopic Appearances. The condition affects most 
 markedly the cells of the convoluted tubules, i.e. the largest 
 columnar cells. Such cells are swollen and project into the 
 lumen of the tubule giving a characteristic star-like appear- 
 ance. Their protoplasm is granular. The nucleus in some 
 cases stains more intensely, in others it is paler than usual. 
 Sections stained for fat will often show a few globules 
 within the cells. There is a tendency to separation of 
 the cells lining the tubules owing to loosening of cement 
 substance, and occasionally cells may be thrown off into the 
 lumen of the tubule. Where this last change is a prominent 
 feature the term catarrhal nephritis is applicable. In fact 
 there is no hard-and-fast line between cloudy swelling and 
 parenchymatous or catarrhal nephritis (see p. 209). 
 
 2. Fatty. Two forms of this condition may be distin- 
 guished, although no very hard-and-fast line can be drawn 
 between them. 
 
DISEASES OF THE KIDNEY 203 
 
 (1) Primary fatty degeneration caused by organisms and 
 their products, and therefore found in infective conditions 
 often as a sequel to cloudy swelling ; caused also by chemical 
 poisons such as phosphorus and chloroform. 
 
 (2) Fatty change secondary to catarrh of the tubules, and 
 found in association with Bright's disease and waxy degenera- 
 tion. 
 
 Naked-eye Appearances. In the first condition there is 
 usually no great alteration in size in the organ. On section, 
 the cortex is pale opaque-white in appearance, and contrasts 
 with the more vascular medulla. 
 
 In the second variety the appearances depend upon the 
 stage of the disease, and will be described in connection with 
 the various types of nephritis and waxy change. 
 
 Microscopic Appearances. In sections stained by ordinary 
 methods, such as haematein and eosin, the cells of the convoluted 
 tubules appear swollen and granular, and their nuclei may show 
 degenerative changes. In sections stained with Sudan III. or 
 Scharlach R. the same cells will be found to show numerous 
 fat granules and globules, more especially in the deeper part 
 of their protoplasm. In the collecting and other forms of 
 tubules the same change will be found, but less marked. 
 
 3. Waxy (Amyloid). This may be found in association 
 with advanced tuberculosis, visceral syphilis, or chronic 
 suppuration, e.g. empyema, bone or joint disease. 
 
 The kidney is usually enlarged, in the more advanced stages 
 very markedly so, although, when combined with interstitial 
 change, it may be reduced in size. It is pale from anaemia 
 and associated fatty change (frontispiece, Fig. 6). As a rule 
 it is firm, and shows a sharp edge on section ; occasionally it 
 may be soft. The appearances are very similar to those 
 seen in the subacute form of Bright's disease (large white 
 kidney). In some instances it is possible to distinguish 
 between the two conditions only on testing with iodine. 
 Sometimes the glomeruli can be seen as minute translucent 
 
204 DISEASES OF THE KIDNEY AND BLADDER 
 
 specks. In the more advanced stages the whole cut surface 
 has a translucent appearance. On treatment with iodine the 
 glomeruli and vessels are brought out as mahogany brown 
 specks and lines. The capsule commonly strips well and 
 leaves a smooth, pale, mottled surface. 
 
 Microscopically, the change is observed first in the afferent 
 arterioles (see plan, p. 206) ; it then spreads to the glomeruli 
 and efferent vessels, and also to the middle coat of the larger 
 arteries. The arteriolae rectae in the medulla are early affected. 
 In the advanced stages of the disease the basement membrane 
 of the tubules, the periendothelial connective tissue of the 
 intertubular capillaries, and other strands of supporting fibrous 
 tissue are implicated. The waxy material is homogeneous 
 and translucent when unstained. It appears yellow with 
 transmitted, dark brown, with reflected light after treatment 
 with iodine, and gives a rose pink to purple colour, with methyl 
 violet and subsequent differentiation in dilute acid. There is 
 usually a considerable amount of fatty change, catarrh of the 
 tubules, and, in the later stages, overgrowth of fibrous tissue. 
 
 4. Pigmentary Changes. In pernicious anaemia the 
 kidney, like the liver and spleen, may be the seat of the 
 deposit of hsemosiderin. In jaundice the kidney is the first 
 organ to be affected and shows a yellow tinge which becomes 
 green on exposure to the air. 
 
 INFLAMMATION OF THE KIDNEY OR NEPHRITIS 
 
 General Facts. The kidney is an organ essentially con- 
 cerned with the elimination of waste products of metabolism 
 and poisonous substances. In any condition in which poisons 
 are circulating in the blood, whether these be of chemical 
 nature or bacterial origin, the organ is apt to be damaged. 
 Once this damage has occurred and the eliminating function 
 of the organ interfered with, matters are made worse, for the 
 irritating poison accumulates, as do also waste products of 
 metabolism which further injure the delicate secreting tissue. 
 Thus a vicious circle tends to be set up, which intensifies the 
 action of the poisonous substance. 
 
DISEASES OF THE KIDNEY 205 
 
 There are two other eliminating channels for waste products 
 in the body the lungs and the skin. These to a certain 
 small extent are capable of taking on vicariously the function 
 of the kidney, but only to a very minor extent. Thus in cases 
 of kidney insufficiency the breath and the sweat may contain 
 urea. The converse also holds good, in that when elimination 
 by the skin is interfered with more work is thrown upon the 
 kidney. Thus, on passing from a warm atmosphere where the 
 skin is acting freely into a cold one, there is a sudden change 
 of the excretory responsibility from the one organ to the other. 
 In addition, the internal organs, among them the kidney, tend 
 suddenly to be flooded with more blood, owing to the contrac- 
 tion of the cutaneous vessels. In this way it is possible to 
 understand the causation of nephritis through chill. 
 
 The kidney is a very vascular organ, and one which is 
 specially dependent upon its blood-supply for the integrity of 
 its secreting tissue. Thus any localised disease of the vessels 
 of the organ or any general vascular change implicating the 
 renal vessels will tell detrimentally upon its function, and will 
 produce structural changes of the nature of degeneration in 
 the secreting epithelium with subsequent replacement of 
 this by fibrous tissue. Thus, extensive vascular disease 
 is accompanied inevitably by alterations in the kidney. The 
 converse also holds good. When the kidney is damaged, 
 products of metabolism are retained within the circulation 
 which irritate and damage the vessels, leading to thickening 
 and degenerative changes. Thus vascular and renal conditions 
 very frequently coexist, and, inasmuch as the condition of the 
 vessels affects the heart, cardiac disease is eventually super- 
 added. 
 
 The vascular supply of the organ is peculiar, and it is well 
 to remember this, as it affords a means of understanding how 
 structural changes may follow alterations in blood-supply. The 
 renal arches which pass between cortex and medulla give off from 
 their cortical aspect branches known as interlobular ; from the 
 medullary aspect come the arteriolae rectse, which pass down- 
 wards into the medulla. The interlobular arteries give off the 
 afferent arterioles which supply the glomeruli. The blood 
 leaves the glomerulus at the same point as it enters it by the 
 efferent vessels. The glomerulus is a bag of coiled capillary 
 
206 DISEASES OF THE KIDNEY AND BLADDER 
 
 vessels with a narrow neck, through which the blood enters and 
 leaves the structure. But the blood does not at once return 
 to the veins by the efferent channel. The vessel again breaks 
 up into a series of capillaries (see plan), supplying the 
 kidney tubules with blood. Thus any interference with the 
 flow of blood through the glomerulus will inevitably tell upon 
 the tubules leading to degenerative changes in these. Such 
 
 AA. 
 
 RV. 
 
 Plan of the Circulation in the Kidney. 
 
 R.A., branch of renal artery; I. A., interlobular artery; A.A. afferent arteriole ; 
 G., glomerulus; E.A., efferent arteriole ; I.C., interlobular capillaries; T., tubule ; 
 V., venous rootlets; R.V., branch of renal vein; A., arteriae rectae ; V.R., venae 
 rectae. 
 
 interference may be rapid in its onset from sudden circulatory 
 disturbances as in " chill," or slowly progressing from a gradual 
 narrowing of the vessel lumen. 
 
 Causation. The causes of nephritis thus are : 
 i. Chemical poisons, such as alcohol, lead, cantharides, 
 taken into the body ; also poisons formed by the body itself, 
 such as abnormal products of metabolism or normal products 
 present in excess, as in the disease commonly called gout. 
 
DISEASES OF THE KIDNEY 207 
 
 2. Bacteria and their poisons in process of excretion, as 
 in the specific fevers, scarlet fever, typhoid, small-pox, etc. 
 
 3. Bacteria multiplying locally, as in suppurative nephritis 
 and tuberculosis. 
 
 4. Circulatory alterations, acute congestion associated 
 with " chill," and, to a certain extent, chronic venous con- 
 gestion. 
 
 Classification. It is customary and convenient to dis- 
 tinguish two primary groups : (i) Organismal nephritis, 
 where the germs are actually present and multiplying in the 
 organ. Of this there are two main types : (a) septic nephritis, 
 and (b) tuberculosis of the kidney. (2) Non-organismal 
 nephritis, that is to say, where the germs, although they may 
 be present, are not multiplying in the organ. In the commonest 
 type of this disease there may be no germs or bacterial poisons 
 at all, the condition being due to sudden alterations in the 
 circulation of the blood or to toxins. This non-organismal 
 type of nephritis corresponds to what is usually called " Bright 's 
 disease." 
 
 Bright's disease may be divided, according to the stage 
 of the disease, or rather the degree of acuteness, into three 
 subgroups : (a) acute nephritis, (b) subacute nephritis, and 
 (c) chronic nephritis. Of these subgroups (a) may pass into 
 (b), and (a) and (b) into (c). There is no hard-and-fast line 
 between them, and as a result transitional types are not 
 infrequently met with. The method is, however, useful for 
 purposes of classification and description. As Bright's disease 
 is the most important type of nephritis it will be considered 
 first. 
 
 Types. 
 
 I. Non-organismal nephritis (Bright's Disease). 
 i. Acute. 
 
 (a) Glomerular. 
 
 (b) Tubular or catarrhal. 
 
 (c) Interstitial. 
 
208 DISEASES OF THE KIDNEY AND BLADDER 
 
 2. Subacute (large white kidney). 
 
 3. Chronic interstitial (granular contracted). 
 
 Sub-group Arteriosclerotic. 
 Amyloid degeneration may occur in combina- 
 tion with Nos. 2 and 3. 
 II. Organismal Nephritis. 
 
 1. Acute (septic nephritis). 
 
 (a) Embolic or pysemic. 
 
 (b) Pyelonephritis (surgical kidney). 
 
 2. Tuberculosis. 
 
 (a) Embolic or miliary. 
 
 (b) Tuberculous pyelonephritis or chronic 
 tuberculosis. 
 
 3. Syphilis. 
 
 Acute Nephritis 
 
 In studying the microscopic changes in the kidney 
 in nephritis, and in describing these changes, it is well 
 to remember that there are three more or less distinct 
 structures or types of tissue in the organ, (a) the tubules, 
 (b) the glomeruli, (c) the supporting, interstitial fibrous 
 tissue carrying the vessels. The poisons which cause nephritis 
 tend to exercise a selective faculty to a certain extent, and 
 one finds that in one case the tubules are more affected, in 
 another the glomeruli, and in a third the interstitial tissue. 
 For example, the poison of scarlet fever has a special tendency 
 to affect the glomeruli. Of course this is true only up to a 
 certain point. These structures are closely related to one 
 another, and it is almost inconceivable that a poison could 
 affect one and not another, and as a matter of fact they are 
 all affected to a certain degree in all cases. But in given 
 instances one structure may show such marked changes 
 that one is warranted in taking these changes as a basis for 
 classification. Thus three subgroups of acute nephritis 
 may be distinguished : (a) glomerular, (b) tubular, (c) inter- 
 
DISEASES OF THE KIDNEY 209 
 
 stitial. As a matter of fact, the naked-eye appearances, 
 never very characteristic in acute nephritis, do not differ 
 to any extent in the three types. 
 
 Naked-eye Appearances. These, as already mentioned, 
 are not very characteristic. In some cases the organ presents 
 very little by way of variation from the normal. In other 
 cases the appearances are merely those of a well-marked 
 cloudy swelling. 
 
 As regards size the organ is usually somewhat swollen, 
 and in certain cases swelling may be a very marked feature. 
 It is softer than usual and may be paler or congested. On 
 section, in many cases (probably in most) the cortex is 
 swollen, opaque white, or pale yellow, contrasting markedly 
 with the congested medulla (Fig. 83). There may be small 
 haemorrhages scattered through the cortex. In other cases 
 the whole organ is deeply congested and filled with blood, 
 which drips from the cut surface. The capsule shows no 
 alteration and strips readily from the organ, leaving a smooth 
 surface. Occasionally the Malpighian bodies are prominent. 
 
 Microscopic Appearances (a) Tubular Changes. The 
 cells lining the tubules are swollen and granular. Many of 
 them have become thrown off, and are found lying free within 
 the lumen of the tube. Some of the collecting tubules may 
 be filled up with these desquamated cells. In suitably 
 stained specimens, fat globules in varying amounts will be 
 found within the cells, both those still attached and those lying 
 free. In the more acute types of the condition the nuclei 
 show degenerative changes, as evidenced by pale staining or 
 complete loss of staining reaction. In the less acute types 
 there may be evidence of nuclear division. In many cases 
 there is a granular exudate present within the lumen of the 
 tubules. In all cases the degenerative changes tend to be 
 more marked in the convoluted tubules. 
 
 (b) Glomerular Changes. In many instances these are 
 slight. There is swelling, and possibly desquamation of the cells 
 covering the tuft and of those lining Bowman's capsule. There 
 is congestion of the capillaries of the tuft, and increase of the 
 
 14 
 
210 DISEASES OF THE KIDNEY AND BLADDER 
 
 number of cells in the tuft owing to the presence of leucocytes. 
 In other cases more extensive glomerular changes are present 
 desquamation and proliferation of the cells covering tuft and 
 lining the capsule. Haemorrhage into the space between tuft 
 and capsule may be found. 
 
 (c) Interstitial Changes. The vessels are distended with 
 blood. There tends to be more or less infiltration of the 
 intertubular supporting tissue with cells, chiefly small, round, 
 lymphocyte-like cells. Where this latter change is a marked 
 feature, the term " acute interstitial nephritis " has been 
 applied. 
 
 All the above changes have a tendency to be irregular in 
 their distribution, being often more intense in one part of the 
 cortex than in another. 
 
 Changes in the Urine in Acute Nephritis. The amount 
 secreted is diminished. In colour it is " smoky " to dark 
 red, owing to admixture with blood. On standing it deposits 
 a sediment which contains hyaline, epithelial, and blood tube 
 casts, red blood corpuscles and free epithelial cells. Albumin 
 is usually abundant. The total amount of urea excreted 
 is considerably diminished. 
 
 Subacute Nephritis Large White Kidney 
 
 Acute nephritis passes by almost insensible gradations 
 into the subacute type. The latter may follow the acute 
 condition or it may develop insidiously. The causes are 
 the same in the two types. Once degenerative changes 
 have begun in the kidney, products of metabolism are 
 retained. These, accumulating, act themselves as poisons 
 upon the renal cells. Thus a vicious circle is established. 
 It is much more difficult for matters to return to the normal 
 in the case of the kidney once degenerative processes have 
 commenced than it is in the case of any other glandular 
 organ. 
 
 Naked-eye Appearances. The organ is enlarged and pale. 
 Hence the terms " large pale/' " large white " kidney. This 
 
DISEASES OF THE KIDNEY 211 
 
 increase in size may be slight, but in many cases it is very 
 marked. It is firm in consistence and the surface is smooth. 
 Through the capsule, which is not thickened, the pallor of 
 the cortex can be made out, also the superficial veins, which 
 are sometimes prominent. On section, the most striking 
 change is the swelling of the cortex, both superficial and inter- 
 pyramidal (Fig. 84). The cortex may be twice the usual 
 breadth. In other cases there is no great alteration in 
 diameter. It has an opaque white appearance, and presents 
 a marked contrast to the medulla, which has the usual dark 
 red colour. Portions of the cortex, representing groups of 
 tubules with more marked fatty change, have a more opaque 
 appearance. Thus there is often a mottling of the cortex. 
 The line between cortex and medulla is well defined. The 
 capsule is not usually thickened, and on stripping, which is 
 easily carried out, it leaves a smooth surface behind. 
 
 Microscopic Appearances (a) Tubules. The epithelium 
 lining the tubules tends to be of a lower type. That is to say, 
 instead of being columnar, it is cubical, or even flattened. It 
 may show evidence of multiplication. Many of the cells are 
 cast off and lying free in the lumen. In suitably stained 
 specimens fat will be found present in many cells, particularly 
 in those which have been thrown off, and especially in the 
 cells of the convoluted tubules. Globules of fat are also to be 
 found in the stroma. Evidence of nuclear degeneration is not 
 so prominently present as in the acute stage. Some of the 
 tubules contain transparent, hyaline, homogeneous casts. 
 
 (b) Glomeruli. The changes in the glomeruli are usually 
 well marked, although less marked in some cases than in 
 others. There is multiplication of the cells lining Bowman's 
 capsule, and of those covering the tuft, so that frequently a 
 number of layers of cells are present between the capsule and 
 the capillary tuft. These cells may contain fat. In other 
 cases there is a fibrous change in the glomerulus. Connective 
 tissue is laid down within the structure, with the result that it 
 becomes transformed into a fibrous knot. Both these changes 
 are not infrequently present in the same case. 
 
212 DISEASES OF THE KIDNEY AND BLADDER 
 
 (c) Interstitial. The intertubular and interglomerular tissue 
 is uniformly increased. This new tissue is fairly cellular, con- 
 taining considerable numbers of small round cells, scattered 
 and in groups. This is occasionally the predominant change 
 when the term " subacute interstitial nephritis " may be em- 
 ployed to characterise the condition. 
 
 The vessels may show a beginning of the thickening 
 which is so prominent a feature of chronic nephritis. This 
 thickening involves both the inner and middle coats. 
 
 Waxy disease is not infrequently associated with subacute 
 nephritis. 
 
 Changes in the Urine in Subacute Nephritis. The amount 
 is diminished. The total amount of urea excreted is re- 
 duced. Albumin is present, usually in large amount. 
 Blood is sometimes present. The deposit shows large 
 numbers of tube casts (fatty, granular, colloid and 
 hyaline), leucocytes, epithelial cells, and sometimes red 
 blood corpuscles. As the condition becomes more chronic 
 the urine tends to show the characters found in chronic 
 interstitial nephritis. 
 
 Chronic Interstitial Nephritis 
 
 This condition may follow one or other of the previous 
 types, or it may arise slowly and insidiously as the 
 result of the action of some irritant circulating in the 
 blood-stream. Such irritants are alcohol, lead, and pro- 
 ducts of metabolism which are not being got rid of, as in 
 gout. There is a very intimate relationship between this type 
 of nephritis and arterial disease. It is not always possible 
 to decide which condition is the primary one. Certainly 
 arterial disease may lead to renal changes such as are found 
 in chronic nephritis, but just as certainly arterial changes 
 may be the result of renal inadequacy, products of meta- 
 bolism not being excreted by the kidney, and leading to 
 arterial degeneration. Or again, the two sets of changes 
 
DISEASES OF THE KIDNEY 213 
 
 may advance pari passu, being due to one and the same 
 cause. 
 
 The causes of chronic nephritis may thus be summed up : 
 
 1. The condition may follow acute or subacute nephritis, 
 and the cause may thus be the same. 
 
 2. Chronic toxaemias : alcohol, lead, gout. 
 
 3. Arterial disease. 
 
 Inasmuch as the main change in this condition is a fibrosis 
 or replacement of the kidney tissue by connective tissue, the 
 term " chronic interstitial nephritis " is generally applicable, 
 and on account of the appearance of the organ the term 
 " granular contracted kidney " is sometimes used. 
 
 The essential nature of the process in chronic nephritis, 
 just as in cirrhosis of the liver, is the degeneration and dis- 
 appearance of the secreting elements, and the replacement 
 of them by fibrous tissue. This may be brought about by 
 chronically acting poison, but is not infrequently secondary 
 to interference with the blood-supply. Thus sclerotic 
 changes in a glomerulus will inevitably lead to interference 
 with the nutrition of the tubules around which its efferent 
 vessel breaks up. Similarly endarteritis in the interlobular 
 arteries will act by causing malnutrition of the area supplied. 
 
 Naked-eye Appearances. The kidney is always reduced 
 in size, sometimes very markedly so. It may be adherent 
 to the peri-renal tissue, and thus present some difficulty in 
 removal. It is, of course, lighter in weight than normal. 
 Instead of the normal 5 ounces it may weigh 3 or even 2 ounces. 
 The surface is more or less rough, and usually shows a varying 
 number of small cysts under the capsule. On cutting into it 
 the organ is found to be tougher than usual. The cut surface 
 presents great variation in colour in different cases, and the 
 changes are not always uniform, but there are certain funda- 
 mental alterations which are commonly present. In the first 
 place the cortex is narrowed, more especially the superficial 
 cortex (Fig. 85). In colour, as already stated, the kidney varies. 
 
214 DISEASES OF THE KIDNEY AND BLADDER 
 
 In some cases there is no great alteration,, in others, where 
 congestion of vessels is present, the organ is more intensely 
 red than normal ; in other cases, again, where tubular changes 
 of an acute or subacute type are superadded to the chronic 
 process the cortex may be pale. Sometimes the colour of the 
 organ in general, and of the cortex in particular, is employed 
 as a basis of classification ; thus the terms small red and small 
 white kidney are used. Such terms are unnecessary. A 
 striking point is that there is not the usual difference in colour 
 between cortex and medulla, nor is there the usual line of 
 demarcation. The two seem to pass into one another. The 
 larger vessels at the line of junction between cortex and 
 medulla are thickened and project, and the lines of the inter- 
 lobular arteries passing upwards into the cortex are tortuous. 
 This irregularity in the vessel markings is very character- 
 istic. There is in many cases an increase in the fat around 
 the pelvis of the kidney. This is due to a shrinkage of the 
 organ away from the pelvis, the place of the kidney tissue 
 being taken by the fat. As a result the organ is, if one may 
 use the expression, smaller than it looks from the outside. 
 The capsule of the organ is usually more or less thickened and 
 shows abnormal attachment to the surface of the kidney, so 
 that in stripping the capsule, portions of the kidney tissue 
 may be removed with it. In other cases this adherence of 
 the capsule is not marked, but in all cases the surface of the 
 organ when stripped of the capsule shows more or less irregu- 
 larity (Fig. 86). This roughening may be slight (morocco- 
 leather appearance) or it may be very marked. The sub- 
 capsular cysts, already mentioned, will be obvious on removing 
 the capsule. They contain a clear colourless fluid. 
 
 Arterio-sclerotic kidney is the name applied to a 
 special type of chronic nephritis associated with, and be- 
 lieved to be subsequent to, advanced chronic arterial disease. 
 The kidney in this condition is often red and the roughening 
 of the surface and the narrowing of the cortex is irregular in 
 
DISEASES OF THE KIDNEY 215 
 
 its distribution. Thus there are areas of extreme narrowing 
 of the cortex, with marked depression of the surface corre- 
 sponding to the distribution of those vessels which show 
 most marked narrowing of their lumen. Other areas of 
 the organ are comparatively normal. 
 
 Microscopic Appearances. A striking fact on examining 
 large sections of such kidneys under the microscope is the 
 variation in the appearances seen in one part from those seen 
 in another. Areas will be found in which the alterations are 
 slight, alternating with areas in which they are marked. In 
 the early stage of the condition wedge-shaped areas of inter- 
 stitial change will be found extending inwards from the cortex. 
 In the more advanced stages this is exaggerated, areas of 
 marked fibrosis alternating with areas more or less normal in 
 appearance. In other cases the interstitial change is diffuse. 
 
 (a) Changes in the Tubules. The epithelium lining the 
 tubules is cubical rather than columnar, and shows more or 
 less evidence of catarrhal change. In some cases where an 
 acute or subacute attack has been superimposed upon the 
 chronic process the catarrhal changes are marked. Many of 
 the tubules contain hyaline or colloid casts. In the more 
 condensed areas the tubules are compressed and narrowed. 
 In the intervening portions of the cortex the tubules are more 
 normal in size or, in many instances, dilated, and the cells 
 lining them are often enlarged. Sometimes dilated tubules 
 show papillomatous projections into their lumen. 
 
 (b) Changes in the Glomeruli. These consist in a fibroid 
 change, all stages of which may be seen. In the earlier stage 
 the capillaries of the structure are still visible although their 
 walls are thickened. In the later stage the glomerulus is 
 reduced to a knot of fibrous tissue, which may show hyaline 
 alteration, and often contains no cells. Again this change 
 shows irregularity in its distribution. It is more marked in 
 the condensed areas, less marked in the intervening portions. 
 
 (c) Interstitial Changes. These consist in an overgrowth 
 of fibrous tissue. In the earliest stage this, as a rule, occurs 
 in wedge-shaped areas extending inwards from the capsule. 
 The fibrous tissue is well formed, although accumulations of 
 small round cells may occur. The vessels show more or less 
 
216 DISEASES OF THE KIDNEY AND BLADDER 
 
 obvious alteration. As a rule this is most marked in the 
 intima, and consists in a thickening, with narrowing of the 
 lumen. At the same time the middle and outer coats tend to 
 be thickened. These alterations are seen in vessels of all sizes. 
 Sometimes in cases where the organ has a red appearance 
 the intertubular capillaries are dilated. 
 
 In the arteriosclerotic type the vascular changes are more 
 marked, otherwise the appearances are very similar. 
 
 The overgrowth of fibrous tissue occurs round tubules and 
 glomeruli as well as in the neighbourhood of vessels. Oc- 
 casionally the fibrous change occurs diffusely throughout the 
 organ. 
 
 Changes in the Urine in Chronic Interstitial Nephritis. 
 The amount tends to be increased. The urine is pale and 
 has a low specific gravity. The amount of urea is 
 diminished. As a rule no blood is present and albumin 
 is scanty; sometimes there is merely a trace. The centri- 
 fugalised deposit shows only occasional tube casts. These 
 are chiefly hyaline or granular. 
 
 Pathological Conditions associated with Nephritis 
 
 Cardiac Changes. In acute nephritis degenerative changes 
 may be met with in the heart muscle due to the action of the 
 toxic agent which also causes the nephritis. At any stage 
 of the disease pericarditis and endocarditis may occur as 
 complications. The most common alteration in the heart , 
 and one that is specially characteristic of the chronic form of 
 nephritis, is hypertrophy of the left ventricle. This is due 
 largely to the associated arterial sclerosis. 
 
 Arterial Changes. These consist in a thickening of the 
 medium-sized and smaller vessels which in the earlier stages 
 is probably due largely to a contraction and thickening of 
 the media, in the later stages to a fibrous transformation of 
 the media and to a thickening of the intima of an athero- 
 matous type. The frequent association of chronic interstitial 
 nephritis with atheroma is well illustrated by a series of 144 
 
DISEASES OF THE KIDNEY 217 
 
 cases recorded by Lorrain-Smith of which 67-6 per cent 
 showed atheroma of one or more groups of vessels. The 
 hypertrophy of the left ventricle and the arterial thickening 
 are both associated with the rise in blood pressure which is so 
 characteristic of the more chronic types of renal disease. 
 In connection with this it may be noted that in cases of 
 cerebral haemorrhage of the variety found in older people some 
 degree of chronic nephritis as well as arterial disease and hyper- 
 trophy of the left ventricle may be confidently looked for. 
 
 Blood Changes. An anaemia of the secondary type occurs 
 in all cases of subacute and in many cases of chronic nephritis. 
 
 Lung Changes. Pneumonia and pleurisy are not un- 
 common complications of kidney disease. (Edema is also 
 common, and is a not infrequent cause of death. 
 
 Dropsy. Abnormal accumulation of fluid in the lymphatic 
 spaces and in the serous cavities is very constantly met with 
 in nephritis, both in its acute and in its subacute manifesta- 
 tions. In chronic interstitial nephritis, so long as the heart 
 does not fail, oedema is not a prominent feature. The 
 oedema of nephritis is probably due to a combination of a 
 number of factors : 
 
 (1) Damage to the endothelial lining of the vessel from 
 the circulation in it of poisonous waste products. 
 
 (2) A watery condition of the blood, due to the anaemia. 
 
 (3) Feeble action of the heart. 
 
 (4) Retention of salt in the tissues. 
 
 The cedema often shows itself in situations, such as round 
 the eye, where the tissue is loose, but it may spread and 
 involve the whole subcutaneous tissue (anasarca), the serous 
 cavities, and lungs. The oedema of nephritis is relatively 
 soft to the touch. In the later stages of chronic nephritis a 
 dropsy having the distribution and character of cardiac 
 dropsy may appear. It is more connected with the failing 
 heart than with the kidney condition. 
 
 Changes in Connection with the Nervous System. In cases 
 
218 DISEASES OF THE KIDNEY AND BLADDER 
 
 which die with symptoms of uraemia, oedema of the brain 
 is commonly present. In all cases albuminuric retinitis 
 should be looked for. This shows itself in the form of minute 
 haemorrhages in the retina. As already stated, cerebral 
 haemorrhage is a frequent cause of death in cases of chronic 
 interstitial nephritis. Of the above-mentioned series of 
 144 cases 55 died of cerebral haemorrhage. 
 
 Tube Casts 
 
 These structures, so characteristic of nephritis in all 
 its stages, are casts of the kidney tubules occurring in 
 these or in the urine. In order to examine for their 
 presence the urine should be centrifugalised or allowed 
 to deposit for some hours. A little of the sediment is 
 then removed with a pipette and placed on a slide under 
 the microscope. In order to see the tube casts properly 
 an ordinary high power lens should be used, and the iris 
 diaphragm of the sub-stage should be shut to a consider- 
 able extent. The following varieties of tube casts may be 
 distinguished : 
 
 (1) Hyaline Casts are difficult to see owing to their 
 transparency. They may occur in the acute type of nephritis, 
 being formed of an exudation from the blood. They form 
 the basis for other types of casts, such as the cellular variety. 
 In the later subacute or chronic stages, transparent casts with 
 a sharper outline are also met with. They are often spoken 
 of as colloid or waxy casts. They are due to changes occurring 
 in shed and long retained epithelium. 
 
 (2) Cellular Casts. These may consist of (a) red blood 
 corpuscles, (b) leucocytes, (c) desquamated epithelium, or 
 of a mixture of these. They are characteristically present 
 in the acute and subacute stages of the disease. 
 
 (3) Fatty Casts are produced by fatty change occurring 
 in cellular casts of the epithelial type. They are most 
 characteristic of subacute nephritis. 
 
DISEASES OF THE KIDNEY 
 
 219 
 
 (4) Granular Casts. These are found mainly in subacute 
 and chronic nephritis. They are due to changes occurring in 
 cellular casts. They may also be produced by the deposit 
 of granules of urates upon hyaline casts. 
 
 (5) Crystalline and Pigmentary Casts are occasionally met. 
 
 TABLE OF COMPARISON BETWEEN THE VARIOUS TYPES OF 
 BRIGHT'S DISEASE. 
 
 
 Acute Nephritis. 
 
 Subacute Nephritis 
 or Large White 
 Kidney. 
 
 Chronic Interstitial 
 Nephritis or Granular 
 Contracted Kidney. 
 
 Size of organ. 
 
 Slight swelling. 
 
 Considerable en- 
 largement. 
 
 Reduction in size, 
 often very small. 
 
 Consistence. 
 
 Softer than nor- 
 mal. 
 
 Firm. 
 
 Tough. 
 
 Appearance of 
 cortex. 
 
 Varies consider- 
 ably. Often 
 pale as in 
 cloudy swell- 
 ing. May be 
 congested. 
 
 Greatly increased 
 in breadth, 
 pale and 
 mottled. 
 
 Always narrowed, 
 colour varies, 
 pale or red. 
 
 Capsule. 
 
 Non-adherent. 
 
 Thickened and 
 often adherent. 
 
 Surface after 
 stripping. 
 
 Smooth. 
 
 Always rough, usu- 
 ally with small 
 
 Vessels. 
 
 Not as a rule altered. 
 
 cysts. 
 Thickened, cut ends 
 
 
 
 prominent. 
 
 Peripelvic fat. 
 
 Not altered. 
 
 Increased. 
 
 Associated 
 Conditions. 
 
 (Edema of brain, other forms of 
 dropsy ; inflammatory condi- 
 tions, e.g. pneumonia, pericar- 
 ditis, etc. 
 
 Arteriosclerosis ; 
 hypertrophy of 
 left ventricle ; 
 cerebral haemor- 
 rhage. 
 
220 DISEASES OF THE KIDNEY AND BLADDER 
 
 Suppurative Nephritis 
 
 This is a form of nephritis in which germs themselves 
 are present and are multiplying in the kidney tissue. It is 
 associated with more or less obvious suppurative foci or 
 abscesses. 
 
 There are clearly two paths by which bacteria may reach 
 the kidney tissue the blood-stream and the ureter. Thus 
 there are two types of suppurative nephritis. 
 
 i. Hcematogenous Suppurative Nephritis Pycemic or 
 Embolic Abscesses of the Kidney. This condition is associated 
 with the presence of organisms in the circulating blood with 
 pyaemia, ulcerative endocarditis, etc. The suppurative foci 
 are usually numerous and irregularly scattered through both 
 kidneys. Occasionally the abscesses may occur in groups, 
 or even one group, and the condition may be limited to one 
 organ. The germs found are those associated with pyaemia 
 and ulcerative endocarditis (see p. 64). 
 
 Naked-eye Appearances. The organ may be slightly 
 enlarged, and is somewhat softer than normal. On section, 
 opaque yellow foci are found scattered through cortex and 
 medulla quite irregularly or in groups (Fig. 87). These foci 
 vary in size, but are usually minute, and are surrounded by 
 a zone of congestion and haemorrhage. The intervening 
 portions of cortical substance are pale. The capsule strips 
 well and the abscesses are often particularly well seen (Fig. 88) 
 from the outer aspect. Infarcts are not infrequently 
 associated. 
 
 Microscopic Appearances. All the appearances of an acute 
 nephritis are present. There is marked cloudy swelling and 
 catarrhal change in the tubules, and, in the neighbourhood of 
 suppurative foci, actual necrosis. The most striking change, 
 however, is an acute interstitial change, the fibrous structures 
 being infiltrated with numbers of cells, chiefly polymorpho- 
 nuclear leucocytes. This change is intensified in parts so 
 
DISEASES OF THE KIDNEY 221 
 
 that the kidney tissue disappears, and its place is taken by a 
 mass of leucocytes in other words, there is an abscess. In 
 the centre of this area masses of germs are not infrequently 
 found, and around the mass of leucocytes a zone of haemorrhage 
 occurs. The vessels generally are congested. Leucocytes 
 may also be found within the lumen of tubules. 
 
 2. Suppurative Pyelonephritis or Surgical Kidney. In 
 this type the infective agent arrives by way of the ureter. 
 It is thus associated with inflammation of the bladder, 
 ureter, and pelvis of the kidney. It is usually bilateral, but 
 is often more marked on one side than on the other. It 
 may occur in cases of cystitis due to infection by the passing 
 of a catheter. It is thus found in connection with obstruc- 
 tion to the urinary passages from stricture or enlarged 
 prostate. It not infrequently follows lesions of the spinal 
 cord where there is loss of control of the bladder and the urine 
 dribbles away. Organisms readily pass up the tract under 
 these conditions and infect first the bladder, then the ureter, 
 the pelvis of the kidney, and kidney itself. The organisms 
 found are very frequently inhabitants of the lower bowel ; 
 thus B. coli is very commonly present, also streptococci) 
 siaphylococcij etc. 
 
 Naked-eye Appearances. The organ is often enlarged, 
 soft, and pale. It may, however, be abnormally small from 
 pre-existing chronic nephritis. On section, pus is found in 
 the pelvis, which may show thickening, injection of vessels, 
 fibrinoiis exudation, or haemorrhage, but which frequently 
 shows no very obvious alteration. Running up into the 
 medulla are yellow lines representing spread of the sup- 
 purative process into the pyramids. In the cortex are 
 similar but more rounded areas (abscesses) with a zone of 
 haemorrhage surrounding them. The intervening portions 
 of cortex are pale. The capsule may or may not strip easily 
 according as chronic interstitial changes are present or not. 
 The abscesses are often well seen from the outer surface. 
 
222 DISEASES OF THE KIDNEY AND BLADDER 
 
 Microscopically^ the changes are precisely similar to those 
 found in the previous type. 
 
 Tuberculosis of the Kidney 
 
 Two types of tuberculosis of the kidney may be dis- 
 tinguished. 
 
 1. A type associated with blood infection, and therefore 
 with miliary tuberculosis of other organs. In this type 
 there are small, scattered white or yellow foci, usually minute, 
 and mainly in the cortex. 
 
 Microscopically, these are found to be typical tubercle 
 follicles with giant cells or caseous centres (see p. 138). 
 
 2. Tuberculous Pyelonephritis or Chronic Tuberculosis. 
 This type may be associated with tuberculosis of the lung 
 or other organs. Not infrequently, however, the lesions, in 
 the renal tract, are the most striking manifestation of the 
 disease. The condition of the kidney is very frequently 
 associated with tuberculosis in other parts of the uro-genital 
 tract, with tuberculosis of testicle, vesiculae seminales, vas 
 deferens, bladder, and ureter. Undoubtedly in some cases 
 the infection is an ascending one, but in many cases the 
 bladder may be infected from the kidney. 
 
 Naked-eye Appearances. The appearances vary much 
 according to the stage of the disease. The condition may 
 be limited to one kidney ; in most cases it is more advanced 
 in one organ than in the other. The organ may be enlarged 
 and is usually pale. The change begins in the pelvis in most 
 cases, and spreads backwards into the substance of the organ. 
 The pelvis is thus lined with caseous necrotic material, and 
 scattered through the kidney substance are fibro-caseous 
 foci (Fig. 89). Destruction of the kidney substance proceeds 
 with the formation of cavities or excavations (Fig. 90). In 
 advanced cases the organ may be transformed into a bag 
 containing structureless caseous material. 
 
DISEASES OF THE KIDNEY 223 
 
 The condition is sometimes, in its more acute manifestations, 
 difficult to distinguish from suppurative nephritis. The foci 
 in tuberculosis tend, however, to be firmer, more yellow, and 
 to stand out more from the surrounding kidney tissue. 
 
 Microscopically, the changes are those usually associated 
 with the more chronic types of tuberculosis fibrosis, tubercle 
 follicles, and caseous foci. 
 
 Syphilis of the Kidney. In some cases of syphilis a 
 diffuse interstitial nephritis may be met with. This may or 
 may not be combined with amyloid disease. Gummata of 
 the kidney occasionally occur. 
 
 Leukaemia of the Kidney. In some cases of leukaemia 
 the kidney undergoes little or no alteration. In other cases, 
 more especially in the lymphatic type, the changes may be 
 extreme. 
 
 In a well-marked case of leukaemia kidney the organ is 
 enlarged and pale (one type of large white kidney) and through 
 it and under its capsule are scattered numerous hemorrhages. 
 The characteristic appearance of the cut surface of the organ 
 is to a great extent lost. 
 
 Microscopically, there is a marked infiltration of the organ 
 with round cells, lymphocytes, or myelocytes, as the case may 
 be, with a separation of the kidney structures glomeruli and 
 tubules from one another. Areas of infiltration with red 
 blood corpuscles are also met with. 
 
 Tumours. 
 
 Simple tumours are infrequent, with the exception of 
 small fibromata of the medulla of the kidney, which are very 
 common and appear as small white rounded areas. Adeno- 
 mata occasionally occur. 
 
 Of malignant growths sarcomata are more common than 
 cancers. They are specially frequent in children. 
 
224 DISEASES OF THE KIDNEY AND BLADDER 
 
 Rhabdomyomata or striped muscle tumours of sarcomatous 
 nature are occasionally met with. 
 
 Hypernephromata are among the commonest type of kidney 
 growth. They occupy a position by themselves. They are 
 believed to arise from suprarenal rests. Such rests are 
 not infrequently found under the capsule of the kidney as 
 small yellow spots. The hypernephroma varies very much 
 in size and appearance. It usually has opaque yellow areas 
 resembling the cortex of the suprarenal in appearance, 
 mixed often with hsemorrhagic areas and brownish areas of 
 necrosis (Fig. 92). The tumour is undoubtedly simple in 
 many cases, but in others, where it attains a very large size, 
 it shows malignant characters. 
 
 Microscopically, the appearances of the hypernephroma 
 vary a good deal, but, as a rule, the cells contain a large 
 amount of fat, myelin, etc., are vacuolated, and generally show 
 some approximation to the appearance of the cells in the cortex 
 of the suprarenal. 
 
 METHOD OF EXAMINING A KIDNEY REMOVED FROM 
 THE BODY 
 
 Having removed all adherent fat which, except in cases of 
 chronic interstitial nephritis, is easily done, note, in the first 
 instance, the size of the organ and its weight. The normal 
 kidney measures about 4^ inches (11-12 cm.) in length, 
 2 inches (5-6 cm.) in breadth, and ij inches (3-4 cm.) in 
 thickness. The average weight is 5^ ounces (150 gm.). 
 Next examine the surface for any gross irregularities, yellow 
 areas under capsule indicating suprarenal rests and cysts or 
 cicatrices. Holding the organ in the left hand, with the hilum 
 towards the palm, cut it longitudinally with a large knife from 
 its convexity to the pelvis, taking care not to injure the glove 
 or the hand which is holding the organ (see Fig. 13). While 
 cutting, note the consistence of the kidney tissue. Examine 
 the cut surface, attending to the following points : 
 
 (i) The cortex, its breadth relative to that of the medulla. 
 This should be as one to three, the cortex measuring about 
 
DISEASES OF THE PELVIS OF THE KIDNEY 225 
 
 one-fifth of an inch (5-6 mm.) in width. Its colour, which 
 should be reddish-brown, somewhat paler than the medulla. The 
 lines of the vessels running through it for any tortuosity or un- 
 usual distinctness from congestion. The glomeruli for unusual 
 prominence and alteration of colour on treatment with iodine. 
 
 (2) The line between cortex and medulla, which should be 
 fairly distinct, forming a series of arches. In cases of inter- 
 stitial nephritis this line is indistinct and irregular. Note also 
 the appearance of the larger vessels (renal arches) running 
 between cortex and medulla. 
 
 (3) The medulla for its colour, any opaque lines indicating de- 
 posits of urates, the presence of small grey nodules fibromata. 
 
 (4) The pelvis for thickening, haemorrhage, calculus or 
 exudate indicating inflammation. 
 
 (5) The peripelvic fat for its relative amount. In the 
 normal organ there is only a very small amount of this. In 
 chronic interstitial nephritis, on the other hand, where there 
 has been a more or less marked shrinkage of the organ, it is 
 often greatly increased. 
 
 (6) With a pair of dissecting forceps take hold of the 
 capsule of the organ, ensuring that the whole capsule is grasped 
 by crushing through a small portion of the most superficial 
 cortex with the instrument. Strip the capsule from the cortex, 
 noting the relative ease with which this is done, i.e. whether 
 portions of cortex are removed along with the capsule. Then 
 note the appearance of the outer surface of the organ, whether 
 it is smooth or rough. If rough, whether the roughness is 
 uniform or irregular. Look for subcapsular cysts, cicatrices 
 indicating old infarcts or the more regular markings of foetal 
 lobulation. Note lastly the thickness of the capsule. 
 
 DISEASES OF THE PELVIS OF THE KIDNEY 
 
 Hydronephrosis, or dilatation of the pelvis of the kidney, 
 is due to obstruction to the outflow of the urine. The 
 condition may be bilateral or unilateral. 
 
 (i) Bilateral hydronephrosis is due, as a rule, to some 
 obstruction to the passage of urine through the urethra, 
 e.g. stricture, enlarged prostate, calculus in the bladder. 
 
 15 
 
226 DISEASES OF THE KIDNEY AND BLADDER 
 
 Occasionally it is produced by a large tumour in the pelvis 
 pressing upon both ureters. The ureters in this type are 
 dilated throughout as well as the pelves. 
 
 (2) Unilateral hydronephrosis is due to some obstruction 
 to the flow of urine through one of the ureters. This may be 
 (a) something blocking the lumen of the ureter, usually a 
 calculus ; (b) kinking of the ureter from cicatricial changes 
 following injury, with the formation often of one or more 
 S-shaped bends (Fig. 91) ; (c) a tumour pressing upon the 
 ureter from the outside. 
 
 As the result of the increased pressure within the pelvis, 
 the calyces become distended and the pyramids flattened. 
 Gradually the pressure causes atrophy of the kidney sub- 
 stance, until eventually it may disappear altogether, leaving 
 a fibrous bag containing a fluid which shows only traces 
 of urea and urinary salts. This distention occurs only if 
 the obstruction is incomplete. Complete obstruction to the 
 outflow of urine leads, not to hydronephrosis, but to atrophy 
 of the kidney. 
 
 Pyonephrosis is a precisely similar condition to the pre- 
 ceding, in which the fluid in the dilated pelvis is pus. In- 
 fection may occur from the bladder or by way of the blood. 
 
 Pyelitis, or inflammation of the pelvis of the kidney, may 
 be associated with the irritation due to the presence of a 
 calculus. More often it is caused by an organism such as 
 B. coli or one of the pyogenic cocci. Occasionally it may be 
 due to the presence of animal parasites such as filarise. In 
 the organismal type, infection may come from the bladder 
 or from the kidney. 
 
 In many cases there is very little alteration. In well- 
 marked cases there is congestion of the vessels, minute 
 haemorrhages and exudate. 
 
 The inflammatory process tends to spread to the kidney it- 
 self, giving rise to suppurative pyelonephritis (surgical kidney). 
 
DISEASES OF THE URINARY BLADDER 227 
 
 Turbid fluid in the pelvis of the kidney should be examined 
 microscopically in doubtful cases, as phosphates in the urine 
 give an appearance very similar to that of pus. 
 
 DISEASES OF THE URINARY BLADDER 
 
 Inflammation (Cystitis). Organisms may reach the 
 bladder (i) from the blood, often by way of the kidney, or 
 (2) from without by the urethra. The latter is the commoner 
 path of infection, the organisms being introduced by means 
 of a catheter or finding their own way up in cases where there 
 is incontinence of urine. The commonest germ found in 
 cases of cystitis is B. coli, but B. proteus and cocci of various 
 types are met with. Cystitis may also be associated with 
 inflammation in neighbouring organs, such as the rectum. 
 A degree of inflammation is usually present along with 
 calculi^ but the calculus may be a sequel of cystitis. 
 
 In slight degrees of the disease there may be merely an 
 increased vascularity of the mucous membrane of the organ. 
 In more severe types there is ulceration and in some cases 
 necrosis of the mucous membrane with slough formation. 
 
 The urine in cystitis may be acid when voided, but it tends 
 rapidly to become alkaline. In some cases this change occurs 
 within the bladder. There is usually a copious deposit con- 
 sisting, in addition to phosphates, of transitional epithelial 
 cells from the bladder wall, pus cells and" micro-organisms. 
 
 Tuberculosis of the bladder is usually associated with 
 tuberculosis of the kidney. It appears first as small tubercles 
 under the mucous membrane. These are found either 
 grouped thickly round the orifices of the ureters (descending 
 infection) or at the trigone and neck of the bladder (ascending 
 infection). Later, ulceration occurs, due to coalescence of 
 the small tubercles and destruction of the mucous membrane. 
 As in other types of bladder ulceration urinary salts are 
 frequently deposited upon the floor of the ulcer. 
 
228 DISEASES OF THE KIDNEY AND BLADDER 
 
 Tumours. The common tumours of the bladder are the 
 villous papilloma and the carcinoma. 
 
 The former occurs as a soft, friable, " sea-anemone "-like 
 outgrowth, usually from the base of the bladder. Filaments 
 from the growth not infrequently break away and are found 
 along with isolated epithelial cells in the urine. Haemorrhage 
 is very common in such cases. Very frequently these 
 papillomata are multiple. 
 
 Carcinoma of the bladder is usually of the squamous 
 epithelioma type. It appears as an ulcerated area with 
 raised hard margins. 
 
 Calculi in the Urinary Tract. These are found in 
 the pelvis of the kidney or in the bladder, also occasionally 
 in process of passing down the ureter or urethra. Stones 
 which originate in the pelvis of the kidney may in this way 
 be found in the bladder. Urinary calculi are rarely found 
 in the post-mortem room. They are usually solitary, but may 
 attain a very large size and may show branching as in the so- 
 called " coralline " calculus of the kidney (Fig. 93). 
 
 Those which form hi the pelvis of the kidney are usually 
 composed of uric acid, urates or oxalate of lime, or a combina- 
 tion of these with phosphates. Those which arise in the 
 bladder are usually composed of phosphates. 
 
 By blocking the pelvis of the kidney, calculi not infre- 
 quently cause hydronephrosis. The presence of a stone in 
 the bladder leads to hypertrophy of the wall of the viscus 
 and to a degree of cystitis. 
 
 Parasites. Bilharzia hcematobia is sometimes found in 
 the bladder. The adult worms occur in the vesical veins. 
 The ova, which show a characteristic terminal spine, are 
 found in the submucosa, where they cause thickenings and 
 papular elevations. They also occur in the urine along 
 with red blood corpuscles. 
 
CHAPTER XI 
 
 DISEASES OF THE BRAIN AND SPINAL CORD AND 
 THEIR MEMBRANES 
 
 INFLAMMATION OF THE MEMBRANES OF THE 
 BRAIN (MENINGITIS) 
 
 TYPES. 
 
 1. Pachy meningitis. 
 
 (1) Acute. 
 
 (2) Chronic. 
 
 (3) Pachymeningitis haemorrhagica. 
 
 2. Leptomeningitis. 
 
 (1) Acute, due to various pyogenic organisms. 
 
 (2) Tuberculous. 
 
 (3) Syphilitic. 
 
 (4) Serous. 
 
 Two main types of this may be distinguished, although 
 the two very frequently occur together, (i) Pachymeningitis, 
 or inflammation of the dura mater. (2) Leptomeningitis, or 
 inflammation of the pia-arachnoid. 
 
 i, Pachymeningitis, or inflammation of the dura mater, 
 is usually secondary to suppurative inflammation in one of 
 the cavities in the bone, such as middle ear and mastoid disease, 
 or to a penetrating wound of the skull. It may be accompanied 
 by septic thrombosis in the venous sinuses in the neighbour- 
 hood of the inflammatory focus, or by abscess of the brain 
 
 229 
 
230 DISEASES OF THE BRAIN 
 
 or leptomeningitis. The membrane is somewhat swollen, 
 the vessels are injected, and there is exudate on the sur- 
 face. The pia-arachnoid may adhere to the affected area. 
 
 Chronic pachymeningitis may occur in connection with 
 fractures or with chronic bone disease. 
 
 A rare condition known as pachymeningitis hcemorrhagica 
 is sometimes found in cases of insanity, such as general 
 paralysis and senile dementia, and in alcoholism and scurvy. 
 On the inner aspect of the dura mater which covers the 
 vertex, as a rule close to the j 'ah cerebri, laminated blood 
 clot is found. Some regard the condition as being merely a 
 haemorrhage due to rupture of a degenerated vessel, others 
 consider it to be inflammatory. Under the latter supposition 
 the primary change is believed to be a fibrinous exudate on 
 the surface of the membrane. This becomes organised. 
 Some of the young blood-vessels in this granulation tissue 
 give way from time to time and so layer upon layer of blood 
 clot is formed. Those who hold the view that the condition 
 is purely hsemorrhagic see in the granulation tissue merely 
 an attempt to organise the blood clot. 
 
 2. Leptomeningitis, or inflammation of the pia-arachnoid. 
 This may be due to : 
 
 (1) Infection passing from a fracture or a penetrating 
 wound of the skull or from a fracture of the base by way of 
 the ear or nose. 
 
 (2) Spread of inflammation through the bone from a sup- 
 purative focus in middle ear, mastoid antrum, or other space. 
 
 (3) Infection from the Blood. In cases where organisms 
 are circulating in the blood the germs may settle down in the 
 membranes of the brain, because for some reason these form 
 a favourable site for their growth. 
 
 As regards the organisms found : inasmuch as pneumo- 
 cocci in children and streptococci in adults are common 
 causes of middle-ear disease, such germs are very frequently 
 
DISEASES OF THE BRAIN 231 
 
 found either by themselves or in combination with others. 
 Staphylococci and B. pyocyaneus occasionally occur. B. in- 
 fluenza may be met with sometimes as a bacillus or in the form 
 of filaments. The Diplococcus intracellularis meningitidis is 
 found in cases of epidemic cerebro-spinal meningitis (spotted 
 fever). B. tuberculosis is responsible for a large number of 
 cases. Rarer organisms are B. anthracis and Streptothrix 
 actinomyces. In tuberculous meningitis, and, more rarely, 
 in other forms, infection may be due to spread from diseased 
 vertebrae. 
 
 Naked-eye Appearances. There is congestion of the menin- 
 geal vessels, and vessels normally invisible can be seen. In 
 some cases of rapidly fatal cerebro-spinal meningitis this is 
 all that can be noted. After one or two days there is usually 
 more or less exudate. This exudate may be fibrinous or puru- 
 lent. It may be very obvious, yellow and creamy, or thin 
 and inconspicuous. It tends to accumulate in the spaces 
 between arachnoid and pia (Fig. 94), more especially in the 
 interpeduncular space and in the sulci along the lines of the 
 vessels. The distribution of the change varies in different 
 types. In most types, notably in cerebro-spinal meningitis 
 and in the tuberculous type, the condition is most marked 
 at the base, the exudate occurring in the interpeduncular 
 space and spreading up on either side along the Sylvian 
 fissure, also on to the surface of pons, cerebellum and occipital 
 lobes. In other cases the change is most marked on the 
 vertex or over the frontal lobes (pneumococcal cases). The 
 convolutions tend to be flattened. There is usually an excess 
 of cerebro-spinal fluid, which is turbid and may be purulent. 
 The inflammatory change may extend to the ventricles, 
 and in many cases these spaces show more or less distention 
 with fluid (hydrocephalus). 
 
 The membranes of the spinal cord are very constantly 
 affected to a greater or less extent. When this is the case 
 the term cerebro-spinal meningitis may be applied. 
 
232 DISEASES OF THE BRAIN 
 
 Microscopic Appearances. These are similar to those found 
 in inflammations of other serous surfaces. There is dilatation 
 of blood-vessels, exudation of fibrinous material on the surface 
 and in the substance of the membranes, and emigration of 
 leucocytes, chiefly of the polymorphonuclear type. Organisms 
 may be found in suitably stained specimens. There is usually 
 more or less inflammation of the underlying cerebral substance 
 (encephalitis), as indicated by cellular infiltration around 
 vessels dipping into the brain substance. 
 
 Microscopic examination of the cerebro-spinal fluid obtained 
 during life by lumbar puncture shows polymorphonuclear 
 leucocytes in greater or less abundance, and sometimes germs. 
 
 Tuberculous meningitis requires special mention. 
 
 It is essentially a basal inflammation and is usually 
 associated with a similar inflammation of the spinal meninges. 
 A more or less marked increase of cerebro-spinal fluid is 
 found, which is often fairly clear. In the sub -arachnoid 
 space at the base of the brain and spreading up the sylvian 
 fissures there may be an opalescent exudate. Sometimes 
 it is conspicuous and creamy, at other times it is difficult to 
 make out at all. The smaller vessels appear thickened, owing 
 to perivascular infiltration, and at the spreading margin, 
 along the vessels of the Sylvian fissure, or upper surface of 
 cerebellum, etc., minute grey or yellow tubercles are found 
 (Fig. 95). Sometimes these are only discovered on stripping 
 the membranes and examining them most carefully by 
 floating them out in water. The ventricles are more or less 
 distended with fluid which may be clear or slightly turbid. 
 
 Microscopic Appearances. The cells in the exudate tend 
 to be of the mononuclear type, but in the more acute cases 
 polymorphs are often abundant. Here and there, especially 
 round vessels, are follicular aggregations of cells with giant 
 cells or necrotic centres. Tubercle bacilli may be numerous, 
 but are often difficult to find. 
 
 Microscopic examination of the fluid obtained by lumbar 
 puncture shows cells which tend to be of a mononuclear type, 
 
DISEASES OF THE BRAIN 233 
 
 but polymorphs are not infrequently present in considerable 
 numbers. On careful search tubercle bacilli are generally to 
 be found, but it is necessary, in most cases, to centrifugalise 
 the fluid, and to make several films from the deposit. 
 
 Syphilitic Meningitis. This may be acute associated 
 with an infiltration of the pia-arachnoid with small round 
 cells. It may be accompanied by gummata in the shape of 
 small foci with yellow caseous centres which show a tendency 
 to infiltrate the brain substance. Or it may be chronic, 
 associated with fibrous thickening at the base of the brain 
 and leading to compression of the cranial nerves. 
 
 Serous meningitis is a condition comparatively recently 
 recognised which is characterised by congestion and oedema 
 of the meninges with production . of a serous and cellular 
 exudate. It is most frequently found in children and is 
 associated with infective diseases, e.g. measles and scarlet 
 fever ; in adults it is sometimes found in relation to alcoholism 
 and kidney disease. The appearances are sometimes more 
 marked at the base of the brain, sometimes at the convexity. 
 The causal factor is not always clear. 
 
 DISEASES OF THE BRAIN 
 
 CIRCULATORY CHANGES 
 
 1. Congestion of the cerebral vessels may be due to 
 active hypersemia in inflammations such as lepto-meningitis 
 or to chronic venous congestion, the result of valvular disease 
 of the heart. 
 
 2. Aneemia may be part of a general want of blood, as 
 in pernicious or other type of anaemia or severe haemorrhage, 
 or it may be local, due to accumulation of blood elsewhere or 
 to the pressure of a tumour. 
 
 3. (Edema is a common condition which may occur as 
 part of a more general dropsy or may be localised to the 
 
234 DISEASES OF THE BRAIN 
 
 cerebral substance. The causes are those of oedema in general, 
 such as renal and heart disease. Alcoholism is a not un- 
 common cause. Chronic alcoholics not infrequently die, 
 apparently from this cause alone. Clinically such cases may 
 simulate, as regards their symptoms, many different types 
 of cerebral lesion, haemorrhage, thrombosis, etc. and at 
 the post-mortem the only brain condition found is oedema. 
 
 On section the brain in cedema has a moist shiny appearance. 
 The grey matter is often rather more obvious than usual from 
 congestion of minute vessels. A small amount of fluid may 
 be squeezed from the cerebral substance, and the ventricles 
 are usually distended with fluid. 
 
 4. Hydrocephalus, or excess of fluid in the lateral 
 ventricles, may be congenital or acquired. 
 
 In the congenital form the head may attain an enormous 
 size. The cranial bones are thinned and separated from one 
 another. There is great distention of the lateral ventricles 
 and narrowing of the cerebral substance. The large size of 
 the head leads to difficulty at parturition. The cause of the 
 condition is obscure, but it is probably mainly due to obstruc- 
 tion to the outflow of fluid from the ventricles into the 
 meningeal spaces. 
 
 Acquired hydrocephalus follows sometimes from basal 
 meningitis or tumour formation at the base of the brain. 
 It is due to the matting of the meninges and consequent 
 obstruction to lymph -flow, following on the inflammatory 
 condition (Fig. 96), or to direct pressure of the neoplasm on 
 the vessels. 
 
 Excess of cerebro-spinal fluid in subdural and subarachnoid 
 spaces is met with in a large variety of diseases. It may occur 
 as part of a general cedema ; it may be due to inflammation 
 of the meninges ; or may accompany atrophy of the cerebral 
 substance in chronic alcoholism and in various forms of 
 mental disease. 
 
DISEASES OF THE BRAIN 235 
 
 5. Arterial Obstruction. This may be due either to 
 thrombosis or embolism. Thrombosis is usually secondary to 
 disease of the arterial wall, either atheroma or syphilitic 
 disease (endarteritis obliterans). It also occurs secondary to 
 embolism. It is met with more commonly in the branches 
 of the posterior cerebral and basilar arteries and in the 
 small superficial cortical branches. Embolism is brought 
 about by the impaction of an embolus, usually a portion of 
 a thrombus, in a vessel the lumen of which is too small for 
 its passage. The portion of thrombus may come from (i) 
 a vegetation on the mitral or aortic valve ; (2) a thrombus 
 in the auricle or ventricle ; (3) a thrombus on a patch of 
 atheroma in the ascending aorta; or (4) from a thrombus 
 in an aneurysm of the ascending aorta or aortic arch (see 
 diagram, p. 62). The arteries at the base of the brain are 
 specially apt to be involved. The commonest vessel to be 
 blocked, because it offers the most direct route for the embolus, 
 is the middle cerebral (usually the left) or its branches. Then, 
 in order of frequency, come the posterior cerebral, the verte- 
 bral, the anterior cerebral, the cerebellar and basilar. As 
 a result of the presence of the embolus blocking the vessel, 
 thrombosis occurs to a varying extent. 
 
 Results of Arterial Obstruction. The cerebral arteries, 
 more especially those branches going to the ganglia at the 
 base of the brain, belong to the group of " end arteries," i.e. 
 arteries whose collateral anastomosis is not equal to the 
 re-establishment of the circulation after blocking of the vessel. 
 Infarction therefore occurs, and the type of infarct which 
 develops is the pale infarct. The reason for this is that, 
 owing to swelling of the nerve elements in the primary 
 stages of degeneration, the return of blood by way of minute 
 collaterals cannot occur or occurs only to a very small extent. 
 In contrast to other organs such as kidney and spleen, where 
 pale infarcts also occur, the necrotic change which takes 
 place results in progressive softening (colliquative necrosis), 
 
236 DISEASES OF THE BRAIN 
 
 instead of, as in kidney and spleen, coagulation necrosis. 
 Such a pale, softened area is often called an area of white 
 softening. Sometimes there is a certain amount of return of 
 blood which escapes from the degenerating vessels with 
 resulting numerous small haemorrhages (red softening). Later 
 on, as liquefaction proceeds and changes occur in the blood- 
 pigment, the area tends to become yellow (yellow softening). 
 Ultimately, removal of the degenerated material occurs with 
 the formation of a cyst, the walls and sometimes the contents 
 of which show yellow pigmentation (Fig. 98). 
 
 In the later stages such areas are, of course, easily recognised. 
 Sometimes, when death occurs rapidly owing to the area 
 involved being large or including some vital centre, the recogni- 
 tion is somewhat difficult. There may be nothing more than 
 a very slight softening of the cerebral substance. Thus in 
 all cases where arterial obstruction is suspected the consistence 
 of the brain substance should be estimated by careful palpation ; 
 suspected areas being compared as regards their consistence 
 with the corresponding areas on the other side as well as with 
 surrounding parts of the brain. 
 
 Microscopic Appearances. These are the changes usually 
 found in degenerations of the central nervous system : 
 
 Ganglion cells show loss of staining of their Nissl bodies 
 and nuclei. The nucleus loses its central position and is eventu- 
 ally extruded. The cell processes become fragmented. 
 
 Myelin substance absorbs water, swells and breaks up into 
 fatty material, which may be demonstrated by fat stains, 
 cholesterin, lecithin, etc. The fat globules are taken up to a 
 certain extent by phagocytes, thus forming granular-looking 
 cells sometimes called compound granular corpuscles. 
 
 In the later stages the neuroglia and other connective 
 tissue elements proliferate, the young mononuclear cells which 
 are thus produced acting as phagocytes for fat, blood corpuscles 
 and blood pigment. The area is invaded by leucocytes, mainly 
 mononuclear, which also act as phagocytes. Haematoidin 
 crystals are often found at the margin of the area, also in the 
 fluid contents of the cysts. 
 
DISEASES OF THE BRAIN 237 
 
 6. Cerebral Haemorrhage. Although capable of con- 
 siderable resistance to strain, the arteries of the brain are 
 much thinner- walled than those of any other organ or part. 
 More especially are they deficient as regards muscular sub- 
 stance. Moreover, they are less well supported owing to 
 the relative softness of the brain substance. For these 
 reasons, rupture of vessels and consequent haemorrhage is 
 more common in the brain than in any other organ. 
 
 There are two main factors operative in cerebral haemor- 
 rhage : (i) degenerative changes in the vessel wall ; (2) increased 
 blood pressure. As regards the degenerative changes, these 
 may be relatively acute as in the vessels of an infarcted area 
 or in the inflammation following septic embolism (e.g. in 
 ulcerative endocarditis), or slowly progressive as in atheroma 
 or syphilitic disease. Not infrequently the vessel, previous 
 to rupture, undergoes localised dilatation with the formation 
 of an aneurysm. Increased blood pressure is either sudden 
 from strain, or chronic, as met with in cases of generalised 
 thickening of the vessels and in kidney disease, which is so 
 frequently accompanied by chronic vascular disease. Thus 
 the two factors often occur together, and in all cases of 
 cerebral hemorrhage careful examination of the vascular 
 system and of the kidneys should be made. 
 
 Types. 
 
 1. Small capillary (petechial) haemorrhages. 
 
 2. Large haemorrhages which may be into 
 
 (a) Basal ganglia sometimes extending into the 
 
 lateral ventricle. 
 
 (b) Pons Varolii. 
 
 (c) Pia-arachnoid on cerebral cortex. 
 
 (d) Cerebellum. 
 
 (e) Other parts of the brain. 
 
 3. Haemorrhage due to laceration of brain. 
 
 As regards haemorrhage caused by disease, one may dis- 
 tinguish, (i) small capillary hemorrhages , which are found in 
 
238 DISEASES OF THE BRAIN 
 
 acute inflammation of the cerebral substance, infective 
 diseases, cerebral softenings, blood diseases such as purpura 
 and pernicious anaemia, or in tumours ; (2) large, extensive 
 hcemorrhages , which are usually due to chronic disease of 
 the vessels, much less frequently due to septic embolism 
 in cases of acute (usually ulcerative) endocarditis, and may 
 occasionally be due to rupture of a vessel in a tumour such 
 as a glioma. The first type of cause is met with most commonly 
 in individuals past the prime of life, the second and third 
 types may be met with at any age. It is stated that in 
 something like one-third to a half of the cases of the first type 
 the point of actual rupture is a small aneurysm. Some of 
 these aneurysms, more especially those in the vessels at the 
 base of the brain, are easily visible with the naked-eye. 
 Others, which are usually in connection with the more minute 
 vessels inside the cerebral substance, are only visible under a 
 low power of the microscope. Such aneurysms have been 
 called miliary. Some of these miliary aneurysms are in 
 reality false aneurysms. 
 
 The most common site for cerebral haemorrhage is the 
 region of the basal ganglia (Fig. 97). Something like 75 per 
 cent of cases occur in this position. The vessel which ruptures 
 is usually the lenticulo-striate branch of the middle cerebral 
 artery, which supplies the outer segment of the lenticular 
 nucleus and the external capsule. It then perforates the 
 internal capsule and ends in the caudate nucleus. So fre- 
 quently is this vessel the site of origin of the haemorrhage 
 that it has been called the artery of cerebral haemorrhage. 
 
 The next most frequent site for haemorrhage is the pons 
 Varolii (12 per cent) (Fig. 100). In something like 12 per 
 cent the haemorrhage commences in one of the superficial 
 vessels, i.e. one of the cerebral arteries which has not 
 yet penetrated the brain substance. A rare situation for 
 haemorrhage is the cerebellum and other parts of the cerebrum, 
 such as the frontal lobe. When the cause of the haemorrhage 
 
DISEASES OF THE BRAIN 239 
 
 is a septic embolus or one of the haemorrhagic diseases such 
 as purpura, the site may be almost anywhere, e.g. the frontal 
 lobe. In the case of a haemorrhage into the basal ganglia 
 or internal capsule, if there is much tearing up of the brain 
 substance the blood may escape into the lateral ventricles and 
 from there extend under the pia-arachnoid. Haemorrhage 
 under the pia mater is also observed when the ruptured 
 vessel is outside the brain substance. 
 
 Naked-eye Appearances. On removing the skull cap and 
 reflecting the dura mater, a general flattening of the convolu- 
 tions is usually observed. Sometimes the flattening is more 
 marked on one side (the side of the haemorrhage) than the 
 other. In the case of haemorrhage into the lateral ventricles, 
 or haemorrhage from one of the larger vessels before it enters 
 the brain substance, or from an aneurysm of a large vessel, 
 extravasated blood may be seen in the subarachnoid space 
 sometimes extending on to the vertex, but usually more 
 marked at the base of the brain. 
 
 On section of the brain, a larger or smaller area of cerebral 
 substance is found torn up and the space occupied by blood 
 clot. In older haemorrhages the clot becomes brownish in 
 colour, and the surrounding tissue is stained yellow. 
 
 In all cases of cerebral haemorrhage, as already stated, 
 careful examination should be made of the vascular system 
 vessels and heart and of the kidneys. The vessels as a 
 rule show more or less marked arterio-sclerosis, the heart 
 shows hypertrophy of the left ventricle and in some rare 
 cases acute endocarditis. The kidneys very constantly show 
 more or less marked chronic interstitial nephritis, which may 
 be of the arterio-sclerotic type. 
 
 Following on a haemorrhage there is always, if the patient 
 survive, more or less secondary degenerative change in the 
 nerve tracts which have been interrupted. Thus when the 
 haemorrhage occurs into one internal capsule there will be 
 descending degeneration in the direct pyramidal tract of the 
 
240 DISEASES OF THE BRAIN 
 
 same side and in the crossed pyramidal tract of the opposite 
 side in the spinal cord. 
 
 Superficial haemorrhage may also be caused by laceration 
 of the brain substance due to injury. If the patient survive 
 some time, red or yellow softening occurs (see p. 236). 
 
 Microscopically, there is little to be seen beyond the 
 extravasation of red blood-cells. In older haemorrhages there 
 is more or less pigmentation from deposit of hasmatoidin in 
 the parts around. There tends also to be an increase of 
 connective tissue (neuroglia and fibrous tissue) around the clot. 
 
 INFLAMMATION OF THE BRAIN (ENCEPHALITIS) 
 
 In the brain substance subjacent to inflamed meninges, 
 in the neighbourhood of injuries, blood clots, areas of softening 
 and tumours there is always more or less marked inflammatory 
 change, showing itself in degenerative changes in the ganglion 
 cells and nerve processes, proliferation of neuroglia, infiltra- 
 tion with mononuclear cells, particularly around vessels. 
 
 Types. 
 
 1. Simple encephalitis following injuries, etc. (see above). 
 
 2. Suppurative encephalitis (abscess). 
 
 (d) Pyaemic type. 
 (b) Solitary abscess. 
 
 3. Tuberculosis. 
 
 4. Syphilis. 
 
 Suppurative Encephalitis (Cerebral Abscess). Two 
 types may be distinguished : (i) Pycemic, (2) Solitary. 
 
 The pycemic type is usually minute, and consists of 
 numerous abscesses scattered irregularly through the brain 
 substance. There is usually haemorrhage around the 
 abscesses owing to the vessels damaged by the inflammatory 
 process giving way. 
 
 The solitary abscess is commonly due to extension of 
 inflammation from neighbouring parts, as a rule to middle 
 
DISEASES OF THE BRAIN 241 
 
 ear disease (suppurative otitis media) or suppuration in the 
 mastoid antrum. Thus the common sites of abscess of the 
 brain are the temporo-sphenoidal lobe (Fig. 99) and the cere- 
 bellum, the two portions of the brain nearest to this sup- 
 purative focus. Occasionally such abscesses are due to 
 injuries. The size of the abscess varies much. It may be 
 the size of a walnut or even a tangerine orange. The wall 
 may be formed of softened, ragged cerebral tissue, or of a 
 layer of granulation tissue, depending upon the age of the 
 abscess. The contents consist of pus, which may be white, 
 yellow or greenish, and is often very foul -smelling. The 
 organisms found are many and various streptococci) staphy- 
 lococci, B. pyocyaneus, etc. 
 
 There is a rare and unexplained association between 
 solitary abscess of the brain and pulmonary diseases such as 
 bronchiectasis and empyema, 
 
 Microscopically, the appearances are those usually seen 
 in abscess formations accumulations of polymorphonuclear 
 leucocytes with necrotic debris and germs of various kinds. 
 In the brain substance around are seen haemorrhages, infiltra- 
 tion of the cerebral substance with 'inflammatory cells of 
 various types, particularly round the vessels, and degenerative 
 changes in the ganglion cells and other nerve elements. 
 
 Tuberculosis. Miliary tuberculosis , when it occurs in the 
 brain, shows a more marked tendency to affect the meninges 
 than the cerebral substance. In tuberculous meningitis, 
 however, there is always a tendency for the inflammatory 
 change to pass downwards into the brain substance. Occasion- 
 ally one meets with multiple caseous foci in the brain substance, 
 but a more common manifestation is the solitary nodule which 
 is found specially in relation to the cerebellum and more 
 commonly in children. Such nodules often act like tumours, 
 producing pressure symptoms. 
 
 Syphilis, like tuberculosis, when it occurs in the brain, 
 shows a tendency to affect the meninges and vessels. In the 
 
 16 
 
242 DISEASES OF THE BRAIN 
 
 latter case, periarteritis and endarteritis are not uncommon. 
 Occasionally, gummata are met with, which, like the solitary 
 tubercle nodules, act as tumour formations. Such gummata 
 consist of a caseous centre with surrounding granulation 
 tissue. 
 
 General Paralysis. This is a disease which is found 
 chiefly in males, between the ages of thirty and fifty. Like 
 locomotor ataxia, it has a very close relationship to syphilis ; 
 in fact, quite recently, spirochsetes have been found in the 
 brain in cases of general paralysis. 
 
 If death occur during the early stages, little more than 
 swelling and congestion of the brain substance is found. In 
 the later, paralytic stages there is found thickening of the 
 membranes of the brain, which are very adherent to the 
 cerebral substance. Sometimes pachymeningitis hsemor- 
 rhagica (see p. 230) is present. There is a general atrophy of 
 the brain substance. On section, oedema of the cerebral 
 tissue is often found, the lateral ventricles are dilated and 
 their ependyma shows minute granulations. In advanced 
 cases the calvarium is usually more or less thickened and 
 condensed. 
 
 Microscopically, there are found degenerative changes in 
 the ganglion cells and wasting of their dendritic processes, 
 proliferation of neuroglia, thickening of the blood-vessels, and 
 infiltration of the perivascular lymph sheath with lymphocyte- 
 like cells. 
 
 TUMOURS 
 
 The brain substance is formed of (i) nerve cells and 
 their processes, which are epiblastic in origin and prac- 
 tically never give rise to tumour formations ; (2) neuroglia 
 or binding connective tissue of the brain, also epiblastic in 
 origin, which is the source of a majority of the primary growths 
 of the brain; (3) vessels, endothelium of meninges and 
 ordinary connective tissue, mesoblastic in origin, which may 
 
DISEASES OF THE BRAIN 243 
 
 be the origin of sarcomata and angiosarcomata ; (4) the 
 ependyma lining the ventricles from which carcinomatous 
 tumours may arise. 
 Types. 
 
 A. Primary Tumours. 
 
 1. Gliomata. 
 
 2. Sarcomata, endotheliomata, angiosarcomata, 
 
 psammomata, etc. 
 
 3. Carcinomata. 
 
 4. Cholesteatomata. 
 
 B. Secondary Tumours. 
 
 1. Granulomata. 
 
 (a) Tuberculous nodules. 
 
 (b) Gummata. 
 
 2. Sarcomata. 
 
 3. Carcinomata. 
 
 Primary Tumours of the Brain. The commonest of these 
 is the glioma. This may occur in any part of the brain. 
 The tumour varies in size, and has a grey, pink or white 
 appearance, and is not well defined. Sometimes it is 
 translucent, at other times opaque. Haemorrhages fre- 
 quently occur in it. The tumour may be simple, but 
 often is malignant, and is then called glw-sarcoma. 
 
 Microscopically, the simple type shows branching cells 
 with small round nuclei and long " spider-leg" processes which 
 interlace with one another, forming a felted network between 
 the cells. In the malignant types the cells are more numerous, 
 larger and more irregular, and the intercellular material is 
 correspondingly reduced in amount. 
 
 Other forms of sarcomata found in the brain are angio- 
 sarcomata, characterised by marked vascularity and tendency 
 to haemorrhage ; endotheliomata , with the sub - variety 
 psammoma, which occur mainly in connection with the 
 meninges (see pp. 292-93). 
 
244 DISEASES OF THE SPINAL CORD 
 
 As already mentioned, primary carcinomata are occasion- 
 ally met in the brain, arising from the ependyma of the 
 ventricles. 
 
 A curious and rare but interesting tumour is the chole- 
 steatoma (Fig. 101), also known as the " pearl " tumour from 
 the mother-of-pearl appearance of the surface. It is a solitary 
 tumour, well defined from the brain substance, occurring in 
 connection with the meninges chiefly towards the middle 
 line. On section it is soft and has a white, laminated appear- 
 ance. On microscopic examination it shows layers of what 
 appear to be epithelial cells, with a small amount of subjacent 
 connective tissue and a large amount of laminated dead 
 epithelium. Some regard the tumour as arising from the 
 pia mater, and therefore as being an endothelioma ; others 
 consider it to be formed of skin epithelium and therefore a 
 teratoma. 
 
 Secondary tumours are relatively common in the brain. 
 Both sarcomata and carcinomata are met with. The growths 
 may be single and large or numerous and small. 
 
 Under this heading may be included the so-called 
 " granulomata " or nodules composed of chronic inflam- 
 matory tissue usually with caseous centres, and either 
 tuberculous or syphilitic in origin. In no other part of the 
 body are such nodules regarded as tumours. In the brain, 
 however, not only because of their appearance but also on 
 account of the effects which they produce, the term tumour 
 may be applied to them. 
 
 DISEASES OF THE SPINAL COED 
 
 CONGENITAL ABNORMALITIES 
 
 Spina Bifida. This is a congenital malformation due to 
 incomplete closure of the coverings of the spinal cord, as a 
 rule, in its lower part. Various degrees of the condition are 
 met with, from one where the only superficial indication of 
 
DISEASES OF THE SPINAL CORD 245 
 
 the presence of an abnormality is a tuft of hair over the lower 
 lumbar region (spina bifida occulta) to one where skin in 
 addition to the posterior bony wall of the spinal canal is absent. 
 The common type is one where there is incomplete closure of 
 the bony canal posteriorly associated with a tumour in the 
 lumbar region which may contain meninges only (meningocele), 
 or nerve elements in addition to meninges (meningo-myelocele). 
 Cases of spina bifida, if at all marked, do not live long. Infec- 
 tion occurs sooner or later through the skin and spinal 
 meningitis results. 
 
 Syringomyelia is a rare condition of the spinal cord in 
 which there is a tumour -like overgrowth of the neuroglia 
 (gliosis) in or near the centre of the cord. The overgrowth 
 is in a longitudinal direction and is found in the cervical, 
 sometimes in the cervical and dorsal regions of the cord. 
 Usually, either throughout the affected part or in some portions 
 of it, there is a cavity in the centre of the area of gliosis. 
 This condition of gliosis associated with cavitation is known 
 as syringomyelia. The cavity is larger than and distinct 
 from the central canal. The proper nerve structures of the 
 cord are atrophied in consequence of the pressure of this 
 mass of connective tissue. In outward appearance the cord 
 may be unaltered or may be enlarged. 
 
 Microscopically, in the affected area tissue consisting 
 entirely of neuroglia is found. In this tissue there is a space 
 or cavity which may or may not be lined with epithelium. 
 
 Hydromyelia. This is a condition corresponding to hydro- 
 cephalus, in which there is an over-distention of the central 
 canal with fluid. 
 
 INFLAMMATION OF THE MEMBRANES OF THE 
 
 CORD (SPINAL MENINGITIS) 
 
 As in the case of the brain, two primary types may be 
 distinguished: (i) pachymeningitis or inflammation of the 
 
246 DISEASES OF THE SPINAL CORD 
 
 dura mater; (2) leptomeningitis or inflammation of the 
 pia-arachnoid. It is unnecessary to discuss the causation 
 and the various forms of the condition, as these have already 
 been considered under cerebral meningitis. The two con- 
 ditions are commonly combined, the term cerebro-spinal 
 meningitis being employed. Sometimes the inflammatory 
 change commences in the brain and spreads secondarily to 
 the cord ; at other times the reverse is the case. In addition 
 to spread from the brain, infection may reach the spinal 
 meninges from an inflammatory focus in one of the vertebrae, 
 from the blood or from the skin surface in cases of spina 
 bifida and bed sores. 
 
 INFLAMMATION OF THE CORD (MYELITIS) 
 
 Under this heading are included a number of conditions of 
 very various origin. Myelitis may be due to the action of 
 irritants and organisms, or it may be due merely to pressure 
 or alterations of circulation. The causes may be classified as 
 follows : (i) Extension of inflammation from vertebrae or 
 meninges. (2) Organisms and toxins brought by the blood stream, 
 such as the viruses of tetanus, hydrophobia, influenza, acute 
 poliomyelitis, etc. (3) Pressure of dislocated vertebra or tumour. 
 (4) Circulatory disturbances thrombosis in sunstroke, embolism 
 in " Caisson " disease. Probably under this heading may 
 also be included the cases due to " chill." 
 
 As regards the distribution of the change, the part involved 
 may be mainly the grey matter, when the name poliomyelitis 
 has been applied. Or it may be that the white matter is 
 chiefly affected. As a rule, both are implicated. When the 
 whole diameter of a section of cord is affected, the term 
 transverse myelitis is used. If the change is irregularly 
 scattered up and down the cord, the term disseminated is 
 employed. 
 
 The morbid anatomy of the condition varies according to 
 
DISEASES OF THE SPINAL CORD 247 
 
 the rapidity of the change and the stage at which it is observed. 
 In the early stages all types are characterised by a softening 
 of the cord substance. In testing for the presence of the 
 condition, the finger should be gently passed down the cord 
 and any alteration in consistence noted. 
 
 On section of the cord, in addition to the softening, there 
 may be increased vascularity, which gives a pink appearance 
 to the grey matter more especially. Sometimes small 
 hcemorrhages are present, and occasionally the cord is so 
 softened that the line of demarcation between grey and white 
 matter is rendered indistinct. 
 
 The later stages are accompanied by an overgrowth of 
 neuroglia replacing the degenerated nerve elements. This 
 may manifest itself by atrophy and contraction and by the 
 appearance of grey translucent areas with variable distribu- 
 tion, a condition often characterised by the term sclerosis. 
 Degenerative changes occur in the tracts running upwards 
 and downwards from the area or areas involved. 
 
 Microscopic changes. These are similar to those found in 
 encephalitis. 
 
 (i.) Changes in the nerve cells. These consist in a 
 disappearance of the Nissl spindles, loss of staining capacity 
 in the nuclei with margination and eventual extrusion. 
 
 (ii.) Changes in the processes of the cells. Swelling, bead- 
 ing and fragmentation of axis cylinders and other processes. 
 Degenerative changes in the myelin sheath associated with 
 setting free of fat in a demonstrable form. 
 
 (iii.) Changes in the neuroglia. Swelling and proliferation 
 of the cells, many of which become free and act as phagocytes 
 taking up fat globules and appearing as large vacuolated cells 
 (compound granular corpuscles). In the later stages the 
 proliferated glia cells settle down to form more or less extensive 
 areas of gliosis, replacing the nerve elements. 
 
 (iv.) Vascular changes. Haemorrhage or thrombosis may 
 be met with. Exudation of fluid and of leucocytes occurs to 
 a greater or less marked extent, depending upon the acuteness 
 of the inflammatory change. A very constant appearance is 
 
248 DISEASES OF THE SPINAL CORD 
 
 a filling of the lymph space which surrounds the vessels of 
 the cord (perivascular lymph space) with cells which may 
 be polymorphonuclear leucocytes, lymphocytes or vacuolated 
 phagocytic cells of uncertain origin, according to the type and 
 the acuteness of the change. 
 
 In the areas of secondary degeneration above and below the 
 level of the lesion there is disappearance of the nerve elements 
 axis cylinders and myelin sheaths and a replacement of 
 these by an overgrowth of neuroglia. 
 
 DISEASES OF THE SPINAL CORD TO WHICH 
 SPECIAL NAMES ARE GIVEN 
 
 There is a number of diseases which affect mainly the 
 spinal cord to which special names are given. Some of these 
 are inflammatory in orgin, due to the action of poisons upon 
 cells and their processes, others are degenerative. No hard 
 and fast line can be drawn between these two sets of causes, 
 however. No system of classification is attempted, because 
 in many cases the site of the primary change, whether in nerve 
 cell, nerve process or nerve ending, is uncertain. Only the 
 more important conditions are included. 
 
 Acute Poliomyelitis. This condition was originally 
 known as acute anterior poliomyelitis and, in its later stages, 
 as infantile paralysis. At first thought to be circulatory in 
 origin, due to blocking of the anterior spinal artery by embolus 
 or thrombus, it is now regarded as organismal in nature, 
 due to a specific virus the exact nature of which has not yet 
 been shown. The virus passes through a porcelain filter and 
 is infectious for monkeys. The disease may be epidemic or 
 sporadic. It occurs mainly in young children, usually in the 
 late summer and autumn months. It is associated with more 
 or less marked fever, and later on with the development of 
 paralysis in muscles. 
 
 The condition may be met by the pathologist in the 
 
DISEASES OF THE SPINAL CORD 249 
 
 early, acute stage, or in the later stage, when there is atrophy 
 arid contracture of limbs. 
 
 In the early stage the condition has the appearance of 
 a myelitis affecting the whole of the substance of the cord, 
 not merely the grey matter, although the change may be 
 most intense in the latter. As regards distribution the 
 change may be met with in the cervical or lumbar portions of 
 the cord. Usually there are alterations to be found throughout 
 the cord, sometimes also in the medulla and cerebrum. The 
 site of the most intense change may or may not show softening. 
 Sometimes there is a slight degree of inflammation of the 
 rneninges. On section of the cord there is usually congestion 
 of the grey matter, and sometimes there are scattered haemor- 
 rhages. 
 
 Microscopically, all the changes described in connection 
 with myelitis may be met with. There are degenerative 
 changes in the anterior horn cells, infiltration of the grey 
 matter with cells, partly leucocytes, more especially lympho- 
 cytes, partly multiplied neuroglia and connective tissue cells. 
 Small haemorrhages may be present. Degenerative changes 
 may also be found in the white matter, but the most obvious 
 change is an infiltration of the perivascular lymph sheath of 
 the vessels with cells, chiefly lymphocytes. There is usually 
 a varying amount of inflammatory change in the rneninges. 
 
 The later stage of the disease is connected pathologically 
 with atrophy of the grey matter, more especially of the 
 anterior horn, sometimes unilateral, at other times bilateral. 
 This shrinkage is associated microscopically with a disappear- 
 ance of the nerve elements and overgrowth of neuroglia. 
 There is also present a descending degeneration in the motor 
 tracts and nerves. 
 
 Progressive Muscular Atrophy (chronic anterior polio- 
 myelitis). This is a condition which develops in middle life, 
 usually in males. Overstrain, injury, exposure to severe cold 
 and infective disease have been put down as causes. It is 
 
250 DISEASES OF THE SPINAL CORD 
 
 characterised by a progressive atrophy of the muscles, 
 usually beginning in hand and arm, especially the right hand. 
 
 The primary pathological change is a degeneration with 
 atrophy in the anterior horn cells of the grey matter in the 
 lower cervical region. 
 
 In the disease known as amyotrophic lateral sclerosis, which 
 is believed by many to be the same condition, in addition to 
 the degenerative change in the motor cells, there is sclerosis 
 in the crossed pyramidal tracts. 
 
 Disseminated or Insular Sclerosis. This is a disease 
 which usually commences in early adult life. Nothing 
 definite is known as regards its etiology, although in some 
 cases an association with acute infective disease has been 
 established. It is characterised clinically by (i) a spastic 
 condition of the limbs associated with weakness ; (2) tremors ; 
 (3) alterations of speech ; (4) nystagmus. 
 
 As regards the pathological anatomy, the lesions are 
 usually found in the spinal cord, less frequently in brain, 
 pons and medulla, and consist in scattered, grey, transparent 
 areas of sclerosis, varying much in size and shape, and having 
 no relation to any structures or tracts of nerves. 
 
 The patches occur in grey and white matter alike and are 
 sharply defined from the surrounding healthy tissue. As a 
 rule, ascending and descending degenerations are absent. 
 
 Microscopically, in the sclerosed areas the medullary sheath 
 is found to have disappeared entirely, although sometimes the 
 axis cylinder is still present. The place of the degenerated 
 nerve elements has been taken by proliferated neuroglia. 
 Ganglion cells persist for long in diseased patches. In the 
 earlier stages and at the margin of older areas numerous 
 granular cells containing fat globules are found. The vessels in 
 relation to the patches often show alteration, such as peri- and 
 endarteritis. 
 
 Locomotor Ataxia (Tabes Dorsalis). This disease has 
 a very definite relationship to syphilis. It is characterised 
 
DISEASES OF THE SPINAL CORD 251 
 
 clinically by a peculiar stamping gait, absence of knee-jerks, 
 loss of sense of position, Argyll -Robertson pupil, optic 
 atrophy, various paralyses, etc. 
 
 The changes found in fatal cases of the disease are most 
 marked in the spinal cord, which shows a sclerosis of the 
 posterior columns. To the naked eye these columns are 
 translucent and shrunken. There is often thickening of the 
 membranes over the posterior portion of the cord. On more 
 careful examination the distribution of the sclerosis is found 
 to vary according to the level examined. In the common 
 variety, where the change commences in the lumbar region, 
 examination of the cord at that level shows degeneration 
 in the postero- external column. Sometimes, in the more 
 advanced cases, both postero-external and postero-internal 
 are sclerosed. In such cases the upper dorsal and the cervical 
 segments show the degeneration mainly in the postero- 
 internal tract. This is due to the fact that the sensory fibres 
 which run in the posterior columns do so first in the postero- 
 external tract and then gradually pass into the postero- 
 internal on their way to the ganglia in the medulla. In 
 cases of cervical tabes, on the other hand, the change is found 
 in the postero-external tract in the cervical region. In 
 combined cervical and lumbar cases, the whole of the posterior 
 columns is affected. Occasionally other ascending tracts, 
 such as the direct cerebellar and antero-lateral-ascending, are 
 implicated. 
 
 Microscopically ', in the sclerosed areas there is found a 
 disappearance more or less complete of the axis cylinders and 
 medullary sheaths, and a replacement of these by neuroglia. 
 
 In addition, degenerative changes are found in the cells 
 of the spinal ganglia in some cases (see changes in nerve cells, 
 p. 247), also in the peripheral portions of the sensory nerves. 
 
 Thus there is in tabes a progressive degenerative change 
 in the sensory neurons of the cord, most marked in the intra- 
 medullary fibres of the posterior sensory neuron, followed by 
 
252 DISEASES OF THE NERVES 
 
 a proliferation of the neuroglia. As regards the primary 
 change there is great uncertainty and considerable difference 
 of opinion. Some regard it as being the sclerosis of the 
 posterior columns, others a local meningitis implicating the 
 posterior roots as they pass through the meninges and so 
 cutting them off from their trophic centres. Others again 
 say that the degeneration of the cells in the posterior root 
 ganglion is the first lesion. 
 
 Hereditary Spinal Ataxia (Friedreich's Ataxia). This 
 is a disease which usually affects several members of the 
 same family. The lesion in the spinal cord is similar to 
 that found in locomotor ataxia, but in addition to the 
 sclerosis of the posterior columns there is a similar change 
 in the lateral parts of the cord affecting the crossed pyramidal 
 tracts, sometimes also the direct cerebellar and antero- 
 lateral-ascending tracts. 
 
 Tumours 
 
 Tumours of the cord or its membranes are rare. Apart 
 from tubercle nodules and gummata, the commonest growth 
 is the glioma ; next comes the sarcoma. Secondary growths, 
 both sarcomata and carcinomata, are occasionally met with. 
 
 More common are tumours in the vertebrae sarcomata 
 and carcinomata pressing upon the cord and leading to 
 myelitis. 
 
 DISEASES OF THE PERIPHERAL NERVES 
 
 Neuritis^ or inflammation of the nerves, may be due to ( i ) 
 bacterial poisons such as in diphtheria, (2) chemical poisons 
 such as alcohol, arsenic, lead and gout, (3) trauma, (4) extension 
 of inflammation from adjacent parts. 
 
 It is customary to distinguish two types : (a) parenchymatous 
 neuritis, in which the degenerative change in the axis cylinders 
 and medullary sheath is the main thing. (b) Interstitial 
 
DISEASES OF THE NERVES 253 
 
 neuritis, in which the overgrowth of the fibrous tissue elements 
 of the nerve is the chief process. There is in reality no hard 
 and fast line between the two types. When the poison is, 
 as in diphtheria, rapid in its action, the degenerative change 
 predominates ; when the poison is, like tuberculosis or leprosy, 
 slow in its effect, the interstitial process is in the ascendant. 
 
 In the more acute cases, beyond some swelling and 
 increased vascularity of the nerve, there is little to be seen 
 with the naked eye. In the more chronic types, nodules of 
 granulation tissue and fibrous thickening are met with. 
 
 Microscopically ', specimens treated with osmic-acid will 
 show black colouration of the myelin sheath. There is 
 infiltration of the connective tissue with inflammatory cells, 
 more marked in the chronic cases. 
 
 Tumours. The commonest growth is the fibroma (so-called 
 neuro-fibroma). Such tumours are often multiple. Occasionally 
 they undergo a sarcomatous change. 
 
 Microscopically, the swellings are found to consist entirely 
 of fibrous tissue, the nerve fibres running through them. 
 
CHAPTER XII 
 
 DISEASES OF BONES AND JOINTS 
 
 DISEASES OF BONES 
 
 RICKETS 
 
 THIS is essentially a disease of infancy, although the results 
 of it tend to persist throughout life. The underlying factor 
 in its production is a deficiency of calcareous material in 
 the newly-formed bone. 
 
 The causation of the disease is still obscure,, but deficient 
 amount of lime salts in the food or failure to make use of the 
 lime salts already present is, in all probability, the explanation 
 of the relative absence of these salts in the bones. Some 
 ascribe the condition to defective action of ductless glands, 
 which produce an internal secretion, such as the pituitary 
 and suprarenal. 
 
 The changes found in the body in cases of rickets are as 
 follows : 
 
 1. Enlargement of the head with prominence of the pro- 
 tuberances of the skull and thinning of the remainder of 
 the bony walls (cranio tabes). The fontanelles remain open 
 for an unusually long period. 
 
 2. Enlargement of the epiphyses of the long bones and of 
 the co sto-chondral junctions. The latter condition results 
 in the formation of a double row of nodules, the so-called 
 
 254 
 
DISEASES OF BONES 255 
 
 "rickety-rosary" (Fig. 105). On section of one of these 
 nodules the line of junction between bone and cartilage, which 
 should be more or less straight, is very irregular and vascular. 
 3. Deformation of the bony skeleton as a result of the 
 softening associated with the absence of lime salts. 
 
 (a) Prominence of the sternum. 
 
 (b) Curvature of the spine (kyphosis and scoliosis). 
 
 (c) Curvature (occasionally fracture) of the long bones 
 such as the femur. Sometimes, consequent on the bending, 
 a new formation of bone takes place along the concavity of 
 the tibia or femur (buttressing). 
 
 (d) Narrowing of the pelvis antero-posteriorly, resulting 
 in difficulty during parturition. Also throwing out of the 
 iliac bones. 
 
 In addition, there is often abnormal prominence of the 
 abdomen, and dentition is usually delayed. 
 
 Microscopically \ there is found at the epiphyses of the bones 
 and at the costo-chondral junctions (a) a broadening of the 
 zone where the cartilage cells are undergoing multiplication ; at 
 the same time there is irregularity in the arrangement of the 
 cartilage cells. 
 
 (b} Irregular calcification of the cartilage. 
 
 (c) Penetration of blood-vessels into the cartilage. 
 
 (tf) Formation of a spongy osteoid tissue with deposition of 
 lime salts which can be demonstrated as granular material, 
 rather than a combination of the lime salts with connective 
 tissue to form true bone. 
 
 At the same time there is a laying down of a layer of 
 vascular tissue under the periosteum, which later undergoes 
 ossification. 
 
 OSTEOMALACIA 
 
 This is a rare disease, found especially in certain localities, 
 e.g. the Rhine Valley and Flanders. It is more frequent in 
 females and has a definite relationship to pregnancy. 
 
 It is stated to have been cured by the removal of the 
 ovaries. 
 
256 DISEASES OF BONES AND JOINTS 
 
 The condition is essentially a decalcification of the bony 
 trabeculse, beginning at the surface of the bones, with, at 
 the same time, a tendency to the formation of new bone 
 which remains imperfectly calcified. As the result of the 
 process of softening and under the influence of pressure, the 
 bones become deformed and sometimes fractured. 
 
 The pelvic bones, owing to the great pressure to which 
 they are subjected, are usually the most deformed, with the 
 result that there is a crumpling of the bony wall of the pelvis, 
 so that the cavity is greatly narrowed. Other bones, such as 
 the vertebrae, clavicles, and femur, undergo a similar process 
 of bending. 
 
 INFLAMMATION OF BONE 
 
 The inflammatory process as it occurs in relation to 
 bone shows certain peculiarities due in great measure to 
 the physical characters of the tissue and to the anatomical 
 arrangement of its constituents. 
 
 From the point of view of inflammation, three different 
 parts of a bone may be distinguished (i) the periosteum, a 
 vascular connective tissue structure which covers the exterior 
 of the bone and from which the nourishing vessels enter the 
 bone. When the periosteum is stripped from the underlying 
 bone, as it may be artificially or by the accumulation of 
 exudate, the more superficial parts of that bone tend to 
 undergo necrosis. Further, the periosteum has the capacity 
 of forming new bone, and under the influence of chronically 
 acting poisons this function is stimulated. (2) The bone 
 itself is a rigid non-expansible tissue, dependent for its nourish- 
 ment upon the vessels which pass into it from periosteum 
 and medulla. When it is the seat of the more acute types of 
 inflammation, the exudate from the vessels, unable to infil- 
 trate the rigid tissue around, accumulates and presses upon 
 the vessels, thus leading to necrosis of the bone. In the less 
 acute types of inflammation, probably in order that there 
 
DISEASES OF BONES 257 
 
 may be space for the inflammatory reaction, the hard re- 
 sisting bone is excavated by means of large cells (osteo- 
 clasts). This rarefaction of the bone is known variously as 
 osteo-porosis or caries. (3) The medulla or bone marrow, also 
 a vascular tissue, having as its function the nourishment of 
 the bone and also the formation and destruction of blood. 
 
 When inflammation attacks bones the process usually 
 commences in one or other of the vascular structures 
 periosteum or medulla ; by far most commonly in the latter. 
 As the process extends, it tends to involve the other structures, 
 so that periostitis usually accompanies osteomyelitis and 
 vice versa. 
 
 The causation of the inflammatory process may be (i) 
 injury ; (2) organisms such as the pyogenic cocci, B. typhosus, 
 B. tuberculosis, the organism of syphilis, etc. 
 
 Three processes are found going on, often side by side, in 
 inflammation of bone : (i) Necrosis or death of bone ; (2) 
 New formation of bone which is often hard (sclerosis) but may 
 be porous ; (3) Rarefaction of the pre-existing or newly-formed 
 bone (osteo-porosis or caries). In the case of the more acutely 
 acting irritants the necrotic process tends to predominate, 
 owing to the tendency for exudate to accumulate and to 
 obliterate vessels and separate periosteum. In the case of the 
 more chronically acting poisons prolonged coccal infection, 
 tuberculosis and syphilis the rarefying process is met with 
 along with new formation of bone. This laying down of new 
 bone is merely a modification of fibrosis or interstitial inflam- 
 mation due to the fact that the new connective tissue contains 
 bone-forming elements. 
 
 Acute Osteomyelitis. This condition sometimes occurs 
 during the course of specific fevers, but often occurs spontane- 
 ously. Young children are particularly susceptible. Some- 
 times there is a history of an injury to the bone, at other 
 times the disease arises without any such predisposing cause. 
 
 17 
 
258 DISEASES OF BONES AND JOINTS 
 
 The condition is an organismal one, staphylococcus pyogenes 
 aureus being very commonly present, but other staphylococci, 
 streptococci and B. typhosus are occasionally found. The 
 organism reaches the bone marrow by way of the blood- 
 stream, having been absorbed from the throat or intestinal 
 tract or other focus of infection. The area of marrow in- 
 volved shows congestion of its vessels, purulent infiltration 
 and haemorrhages. Sometimes localised areas of suppuration 
 (abscesses) develop in the bone. The periosteum is very 
 commonly involved and pus may accumulate under that 
 membrane. In this way necrosis, more or less extensive, 
 may occur in the shaft of the bone with formation of 
 sequestra. Sometimes the epiphyses and joints are involved. 
 
 Owing to the occurrence of thrombosis in the veins in the 
 neighbourhood and subsequent infective softening of the 
 thrombi, metastatic abscesses and septic infarcts may form 
 in other parts and organs, especially in the lungs. Peri- 
 carditis is not an uncommon accompaniment of acute osteo- 
 myelitis, the infection being carried by the blood. 
 
 The bones which are most frequently affected are the 
 femur and tibia, although other bones may be the seat of the 
 change by extension of inflammation from neighbouring parts, 
 e.g. the bones of the skull or finger in cases of septic wounds. 
 Rarely the vertebrae may be affected. 
 
 Chronic Osteomyelitis. Healing of the inflamed focus 
 may occur spontaneously, or, as is most usually the case, the 
 diseased area may be removed by the surgeon, and healing 
 result. At other times the inflammatory change persists. 
 Organisms remain in portions of dead bone (sequestra), and 
 the irritation is kept up. From such foci a purulent dis- 
 charge is constantly flowing, which finds its way to the surface 
 by openings in the bone (cloacae) and sinuses in the soft parts. 
 At the same time the periosteum, kept in a constant state 
 of proliferation, forms new bone which may enclose the 
 
DISEASES OF BONES 259 
 
 sequestra or dead areas, forming what is called a " new case." 
 This new bone usually has a spongy character but may be 
 dense (Fig. 106). 
 
 Waxy disease is not infrequently found in relation to 
 chronic suppurative conditions of bone. 
 
 Tuberculosis of Bone. Tuberculous disease of bones is 
 met with more especially in young children, i.e. in growing 
 bones, although the results of such disease are often seen in 
 the adult. A large percentage of cases are due to infection 
 with the bovine type of the tubercle bacillus. The organism 
 may reach the bone by the blood-stream or by the lymphatics. 
 In the latter instance the primary focus is usually the synovial 
 membrane of a neighbouring joint. The bones most frequently 
 involved are the vertebrae (Fig. 107), femora, the tarsal and 
 carpal bones, and the ribs. 
 
 The condition may begin in the interior of the bone, 
 usually in the cancellous tissue at the ends (in the case of the 
 long bones) or, much less frequently, in the periosteum. 
 It appears first as a grey translucent area surrounded by a 
 vascular zone. This area spreads, gradually absorbing the 
 bone, and so producing rarefaction or caries. At the same 
 time, owing to the irritation of the focus, new bone may be 
 laid down in the neighbourhood, particularly under the 
 periosteum. In rapidly progressive cases, largely owing to 
 obliterative changes in the vessels, but also due to the action 
 of the tubercle poison, necrosis of larger or smaller areas of 
 bone occurs, with formation of sequestra. 
 
 The change may spread to the surrounding parts and a 
 tuberculous (so-called " cold ") abscess develop in the tissues. 
 This is particularly the case in tuberculosis of the vertebrae ; 
 retropharyngeal abscess occurring in connection with cervical 
 disease, psoas abscess in relation to lumbar disease (Fig. 107). 
 Sometimes the focus infects the spinal cord, setting up a 
 meningitis. 
 
260 DISEASES OF BONES AND JOINTS 
 
 Deformity of bone frequently follows tuberculous disease. 
 This is more especially seen in tuberculosis of the spine. 
 
 Syphilis of Bone. Bone may be the seat of disease both 
 in congenital and acquired syphilis. 
 
 In congenital syphilis the disease shows itself chiefly at the 
 ends of the long bones in the part where ossification is taking 
 place (syphilitic epiphysitis). The line of calcification is 
 broader and more irregular than normal. The result of this 
 is an interference with growth leading to a form of dwarfing. 
 
 In the acquired form of the disease the lesion is essentially 
 gummatous. Such gummata may occur in the periosteum 
 or in the medulla of the bone. The process may be found in 
 any part of the skeleton, but it is commonest in the tibia, 
 ulna, sternum and calvarium. Underneath the gumma there 
 is erosion of the bone which has, in the case of the calvarium, 
 a characteristic circular appearance (corona veneris). 
 
 Sometimes thickenings occur in the bones (long and flat) 
 leading to the formation of raised areas (syphilitic nodes). 
 The newly-formed bone is in these cases very dense. 
 
 Osteitis Deformans (Paget's disease of bone). This is a 
 rare disease of advanced life. 
 
 There is a general thickening of such bones as the tibiae 
 clavicles, skull, and vertebrae. The bones are at the same 
 time spongy and relatively light, although the medullary 
 cavity is narrowed from the formation of new bone. Owing 
 to the softness of the bones deformity occurs, particularly 
 in bones, such as the lower extremities, spine and clavicles, 
 which are subjected to pressure. 
 
 Acromegaly, a condition caused by disease of the pituitary 
 gland, is associated with an enlargement of certain bones, 
 e.g. the lower jaw, bones of the face, hands and feet. The 
 enlargement is due to a laying down of new bone as well as 
 to a thickening of the periosteum. 
 
DISEASES OF JOINTS 261 
 
 Tumours of Bone. Of simple tumours, osteomata, 
 chondromata and fibromata are met with. 
 
 Of malignant growths, sarcomata of various kinds 
 occur primarily Osteo-sarcomata (Fig. 108), chrondro sar- 
 comata, myeloid sarcomata (Fig. 109), and myelomata. 
 
 Secondary deposits of carcinoma are occasionally met, 
 particularly in carcinoma of the breast and prostate. 
 
 DISEASES OF JOINTS 
 
 INFLAMMATION (ARTHRITIS) 
 
 Acute Arthritis. 
 
 1. Non-suppurative. This is found following injury and 
 in connection with acute rheumatism. In the latter instance, 
 the synovial membrane is swollen and shows irregularly 
 scattered areas of congestion. There is excess of a thin 
 yellowish fluid in the joint. From the inflamed synovial 
 membrane (not from the fluid as a rule) micrococcus rheumaticus 
 can in some cases be cultivated. 
 
 2. Suppurative Arthritis. This may occur in the course 
 of a pyaemia, the organisms being conveyed by the blood, 
 or infection may take place directly, due to a penetrating 
 wound or inflammation in bone or neighbouring tissues. 
 The germs found are the pyogenic cocci, more especially 
 streptococci and gonococci. 
 
 The synovial membrane is swollen and its vessels injected. 
 The joint contains more or less purulent fluid, often mixed 
 with blood. In the more severe forms, particularly the 
 gonococcal, there is destruction of the cartilages of the bones. 
 
 Tuberculous Disease. Tuberculosis may commence in 
 the synovial membrane of the joint or it may spread from the 
 adjacent bone. 
 
 In a well-marked case of joint disease there is a general 
 pallor of the tissues in the neighbourhood. There is some 
 
262 DISEASES OF BONES AND JOINTS 
 
 increase of synovial fluid which is serofibrinous and occasion- 
 ally purulent. The synovial membrane is thickened, some- 
 times with the formation of fringes. The cartilage is eroded 
 through the invasion of granulation tissue from the margins 
 of the bones. There may be caries or sequestrum formation 
 in the exposed bone. In advanced cases the tendons and 
 ligaments in connection with the joint are infiltrated with 
 tubercle. The joints most commonly affected are hip, knee, 
 elbow and ankle. The condition may heal, with the result 
 that ankylosis frequently occurs. 
 
 Rheumatoid Arthritis. This is a disease which is 
 found most frequently in females. The small joints of the 
 hands and feet are usually first affected. Later on those of 
 the elbow and knee are involved. The joints show a fusiform 
 swelling and contain excess of clear synovial fluid. The 
 synovial membrane is swollen and congested, and, even in 
 the early stage, there may be some fibrillation and destruc- 
 tion of cartilage. The condition is not often found in the 
 post-mortem room in the early stage. 
 
 In the later stages of the disease, erosion of cartilage with 
 eburnation or polishing of the bone laid bare, also new forma- 
 tion of bone at the margins of the joint (lipping), are character- 
 istically present. At the same time there is marked deformity 
 as well as restriction of movement, due both to the lipping 
 of the bones and to the formation of fibrous tissue between 
 them. 
 
 Gout. This condition should be looked for specially in the 
 metatarsophalangeal joint of the great toe. It shows itself 
 by deposits of opaque white material (salts of uric acid) 
 in the cartilage and in advanced cases in ligaments and 
 soft tissues. There is chronic inflammation in the tissues 
 around. 
 
 Charcot's Disease of Joints. This is a rare condition, 
 found sometimes in individuals suffering from locomotor 
 
, DISEASES OF JOINTS 263 
 
 ataxia and syringomyelia. There is a great enlargement of 
 the joint due to the accumulation of fluid in it, also increased 
 mobility. There is later destruction of the cartilage, bones 
 and ligaments, the condition being, however, painless. The 
 synovial membrane is thickened, and may show villous 
 outgrowths. 
 
CHAPTER XIII 
 
 DISEASES OF THE REPRODUCTIVE ORGANS AND MAMMARY 
 GLAND DISEASES OF PREGNANCY 
 
 DISEASES OF THE OVARIES 
 
 THE appearances of the ovary in menstruating women should 
 be carefully differentiated from those seen in disease. 
 
 The organ is swollen and vascular, and haemorrhagic areas 
 occur in it. Occasionally severe haemorrhage may occur 
 into the peritoneal cavity. Similarly corpora lutea, with their 
 yellow colour and characteristic wavy outline, should be 
 distinguished from tumours. 
 
 In acute inflammations of the peritoneum the ovaries and 
 tubes participate in the inflammatory condition, and often 
 show marked vascularity. This should not be mistaken for 
 evidence of primary inflammation in these organs. In old age 
 the organs undergo atrophy. The capsule becomes thickened 
 and shrivelled. 
 
 Tumours. The ovary is one of the organs in which 
 tumours are exceedingly common. As a rule such tumours 
 are cystic. 
 
 Single cysts occasionally occur from dilatation of a Graafian 
 follicle. Solitary cysts also develop sometimes from the 
 parovarium. 
 
 Compound Cystic Adenoma. This is a common tumour 
 which may attain an enormous size. It consists of a number 
 
 264 
 
DISEASES OF THE FALLOPIAN TUBES 265 
 
 of rounded or irregularly shaped spaces enclosing a translucent 
 or transparent gelatinous or semi-solid material containing 
 various mucinous constituents. Not infrequently small 
 papillomatous ingrowths are found within the cysts which 
 divide and subdivide. When such are present the term 
 papilliferous cystadenoma is applied. Such a tumour, like the 
 similar one found in the breast, may undergo a malignant 
 transformation. When these cystic tumours of the ovary 
 rupture they sometimes give rise to the formation of immense 
 numbers of secondary growths scattered through the peri- 
 toneum. 
 
 For microscopic appearances see pp. 285, 286. 
 
 Dermoid Cysts (Teratomatd). The ovary is the commonest 
 site for this type of tumour. They vary much in size. 
 They are recognised by the soapy-looking contents mixed 
 with hair and containing often teeth, cartilage, bone, etc. 
 (Fig. 102). 
 
 Fibromata occasionally occur in the ovary, also fibro- 
 sarcomata which may attain a large size. 
 
 DISEASES OF THE FALLOPIAN TUBES 
 
 Salpingitis. Two types of this condition are met with, 
 viz. gonococcal and tuberculous. In the former the tubes 
 are thickened and dilated, and contain creamy or cheesy- 
 looking pus, which in many cases is found to be sterile. 
 
 In the tuberculous type there is a similar dilatation, thicken- 
 ing and tortuosity. Minute grey tubercles may be visible 
 in the walls ; the contents are often caseous. These two 
 conditions are sometimes to be differentiated only on micro- 
 scopic examination. 
 
 Both give rise to localised peritonitis with adhesions, and 
 both may be the starting-point of a generalised inflammation 
 of the peritoneum. 
 
 The Fallopian tube is the commonest site for the occur- 
 
266 DISEASES OF THE REPRODUCTIVE ORGANS 
 
 rence of ectopic gestation. Death occurs from rupture and 
 haemorrhage into the peritoneal cavity. 
 
 DISEASES OF THE UTEEUS 
 
 The size of the uterus should in all cases be measured and 
 its cavity investigated for developing ovum or foetus. 
 
 Thrombosis in the uterine veins is a constant occurrence 
 after parturition. Occasionally portions of such thrombi are 
 carried away, and produce fatal pulmonary embolism. 
 
 Sometimes, after operations on the uterus or ovaries, a 
 similar accident may occur. In such cases the emboli may 
 originate from vessels in the neighbourhood of the removed 
 growth or organ or from the abdominal wound. 
 
 Acute Endometritis. This condition is a not uncommon 
 cause of death in puerperal cases. The disease is an infective 
 one, due as a rule to a streptococcus. A gram-negative coccus 
 not unlike the gonococcus has been recently described as 
 occurring in the uterus in such cases. 
 
 The organ is of course enlarged. The interior has a grey 
 appearance, owing to the presence of septic sloughs in the wall. 
 There is usually a foul odour. Films from the soft necrotic 
 interior show immense numbers of organisms, among them 
 streptococci. The uterine veins are filled with thrombi, which 
 may be undergoing septic softening. Septic infarcts are not 
 uncommonly present in the lungs. 
 
 Organs such as liver, kidneys, and heart show extreme 
 cloudy swelling. Acute peritonitis localised to the neighbour- 
 hood of the uterus or generalised throughout the peritoneum 
 may be present. 
 
 Microscopically, the innermost portion of the uterine wall 
 shows necrosis. Numerous germs of various kinds are present. 
 Further from the lumen the uterine muscle is infiltrated with 
 inflammatory cells, and thrombi are found in the vessels ; in 
 
DISEASES OF THE UTERUS 267 
 
 this position in suitably stained specimens streptococci are 
 usually the only organisms seen. 
 
 Chronic Endometritis. Two types of this condition 
 are commonly distinguished : (i) glandular endometritis, (2) 
 interstitial endometritis. 
 
 1. Glandular endometritis is also called glandular hyper- 
 plasia. It is questionable whether this condition is in reality 
 an inflammatory one. There is little or no evidence of 
 inflammation from the microscopic point of view. The 
 main change is a hyperplasia of the gland elements of the 
 endometrium. Many regard it as neoplastic in nature, i.e. 
 an adenoma. 
 
 The uterus is enlarged and its mucous membrane thick- 
 ened, vascular and spongy. Polypoid outgrowths may be 
 associated. 
 
 Microscopic Appearances. Sections of the uterine wall show 
 gland acini more or less regularly arranged, but often tortuous 
 and sometimes dilated, between which is a delicate stroma of 
 connective tissue. The gland acini may often be seen pene- 
 trating the muscular wall for some distance, so that the con- 
 dition may be confused with an adeno-carcinoma of the uterine 
 wall. The gland cells are, however, only a single layer in 
 thickness, and are arranged regularly upon a basement mem- 
 brane, although there is sometimes shedding of the cells. 
 
 Sections of curettings from a case of this kind present a 
 similar appearance. 
 
 2. Interstitial endometritis is often combined with chronic 
 metritis. It has been called fibrosis uteri. The uterus is 
 larger, firmer, and heavier than normal. 
 
 Microscopically ', curettings show a dense fibrous stroma, 
 in which the vessels are thickened. The gland acini are 
 usually few in number and widely separated from one another. 
 
 Tuberculosis of the uterus is a rare condition. It may 
 occur as an endometritis with the development of ragged 
 
268 DISEASES OF THE REPRODUCTIVE ORGANS 
 
 caseous walls, or fibro-caseous nodules may occur in the wall 
 of the uterus which is usually considerably thickened. 
 
 Tumours. Of simple growths the fibro-myoma (leio- 
 myoma), or tumour composed of non-striped muscle and 
 fibrous tissue, is the commonest (Fig. 104). A full description 
 is found under Tumours, p. 280. 
 
 Of malignant growths the carcinoma is very common. 
 Two main types are found : 
 
 1. Squamous epithelioma occurring in the cervix. 
 
 2. Columnar cell carcinoma occurring in the body or cervix. 
 
 DISEASES OF THE PLACENTA 
 
 Infarcts, i.e. areas of necrosis in the placenta, are not 
 uncommon. They are best developed in cases of eclampsia. 
 They appear as opaque white or pale yellow areas, 
 more or less wedge shaped, and towards the maternal surface. 
 They are caused by thrombosis in the intervillous blood 
 spaces. 
 
 Fibrosis. Under the influence of the syphilitic virus the 
 placenta becomes larger, firmer, and paler, and may present 
 a dull, greasy appearance. 
 
 Microscopically, the chorionic villi are found to be thicker 
 and show a marked decrease in the number of vessels. In the 
 thickened stroma are numerous round and spindle-shaped cells. 
 
 Tumours. Hydatid mole or myxoma of the chorion is a 
 condition in which chorionic villi become greatly enlarged and 
 cedematous. The tumour shows immense numbers of 
 translucent globular masses like white currants, varying much 
 in size, strung upon thin filaments. The condition occurs 
 after an abortion. It may become malignant, passing into 
 the condition known as chorion-epithelioma (p. 304). 
 
 Microscopically, the globular masses show the structure of 
 myxomatous tissue, hence the term myxoma of the chorion. 
 
DISEASES OF PREGNANCY 269 
 
 There is at the same time proliferation of the covering epithelial 
 layers syncytium and Langhan's layer. 
 
 Chorion epiihelioma or Deciduoma malignum is a tumour 
 formation which, like the preceding, has a distinct relation- 
 ship to pregnancy and abortion. Its appearance and nature 
 are discussed under Tumours (p. 304). It is associated with the 
 development of secondary growths, particularly in the lung. 
 
 DISEASES OF PREGNANCY AND THE PUEBPERIUM 
 WHICH MAY BE FATAL 
 
 It is convenient to discuss here some of the diseases of 
 pregnancy and the puerperium which may be seen in the post- 
 mortem room. Pregnant and puerperal women may, of course, 
 die of intercurrent diseases of various kinds. Thus, heart 
 disease and kidney disease are not uncommonly a cause of 
 death under such circumstances. There are, however, certain 
 conditions more directly associated with the pregnant state 
 which may prove fatal. 
 
 In the first place there is ectopic gestation. When an 
 ovum develops in a situation other than the uterus, such 
 as the Fallopian tubes or ovary, death not infrequently 
 occurs from haemorrhage into the peritoneal cavity. 
 
 Rupture of the uterus may occur during pregnancy or 
 during labour, with resulting fatal haemorrhage. 
 
 Pulmonary embolism has already been alluded to as a 
 cause of sudden death after labour. 
 
 Chorea gravidarum may prove fatal. In a case which came 
 under the author's notice recently there was present what 
 is usually found in any fatal case of chorea acute simple 
 endocarditis of the mitral valve. 
 
 Puerperal fever, one of the commonest causes of death 
 after labour, has already been dealt with under Diseases of 
 the Uterus (acute endometritis) (p. 266). 
 
270 DISEASES OF THE REPRODUCTIVE ORGANS 
 
 Hyperemesis Gravidarum or Pernicious Vomiting of 
 Pregnancy. This condition of severe and sometimes fatal 
 vomiting developing during pregnancy is believed by authori- 
 ties to be toxsemic in origin, and probably allied to such 
 diseases as eclampsia and acute liver atrophy. In many 
 cases lesions of the liver, similar to those occurring in the 
 latter disease, are found. In some cases the liver shows a 
 fatty degeneration of an extreme degree ; in others there are 
 areas of necrosis similar to those found in eclampsia, but 
 instead of being situated at the periphery of the lobule, as 
 in that disease, they occur in the centre. Degenerative 
 changes of a type similar to those in eclampsia are found in 
 the kidney. The condition is associated with a high ammonia 
 co-efficient in the urine, and there is a corresponding marked 
 reduction in the output of urea. 
 
 Acute Liver Atrophy. As already stated, there is a 
 distinct relationship between this condition and the pregnant 
 state. For a description of the lesions found in the liver see 
 p. 183. 
 
 Eclampsia. This is perhaps the commonest cause of 
 death in such cases. The disease may prove fatal either 
 during pregnancy or after the birth of the child. It is 
 associated clinically with more or less marked albuminuria 
 (sometimes also blood and casts) and with the occurrence 
 of fits. 
 
 The cause of the condition is at present uncertain. 
 
 As regards the post-mortem findings in fatal cases of the 
 disease, these vary considerably in different cases. There 
 are, however, certain appearances found with considerable 
 constancy. Post-mortem changes are often specially well 
 marked. There is often a general icteric tint of the skin. 
 (Edema of the subcutaneous tissues may be present. 
 Excess of fluid in the peritoneal, pleural, and pericardial sacs 
 is also a fairly constant finding. The heart muscle is pale 
 
DISEASES OF PREGNANCY, ETC. 271 
 
 and soft. The organs which show the most constant changes 
 are the liver and kidneys. 
 
 The appearances in the liver when well marked are exceed- 
 ingly characteristic. The organ is usually somewhat enlarged. 
 The surface has a dark red appearance, either in whole or in 
 part from the occurrence of more or less extensive subcapsular 
 haemorrhage. In consistence it is usually soft. The cut 
 surface shows a yellow appearance, with haemorrhages 
 scattered through the substance, chiefly in the portal spaces. 
 The necrotic areas, so characteristically present when sections 
 are examined under the microscope, are, as a rule, too small 
 to be seen by the naked eye. Occasionally the liver may 
 show the appearances of cloudy swelling and early fatty 
 change without the occurrence of haemorrhages. 
 
 Microscopically, there are found (i) changes in the liver 
 cells characteristic of cloudy swelling ; (2) more or less marked 
 fatty change intensified round the necrotic foci ; (3) areas of 
 focal necrosis somewhat similar to those found in typhoid fever 
 in which the liver cells have undergone extreme degenerative 
 changes. They are swollen and vacuolated, or have broken 
 down and disappeared. Fatty change is not as a rule present 
 in the cells within such foci. Endothelial cells and leucocytes 
 are present along with red blood corpuscles. These necrotic 
 foci are found chiefly at the margin of the lobules ; (4) areas 
 of haemorrhage in which the tissue is infiltrated with red blood 
 corpuscles. 
 
 Changes in the Kidney. As previously stated, there is in 
 the urine distinct evidence that the kidney is damaged, that, 
 in other words, a degree of acute nephritis is present. But 
 even in cases where the urine shows most indications of 
 disease comparatively little change may be found in the 
 kidney itself, more especially microscopically. The organ is 
 somewhat enlarged and pale. On section, the cortex is 
 swollen and tends to stand up above the level of the medulla 
 (Fig. 83). The colour of the cortex is a pale yellow, 
 
272 DISEASES OF THE REPRODUCTIVE ORGANS 
 
 occasionally with haemorrhages scattered through it. In 
 consistence the organ is softer than usual. Unless the case 
 is complicated with chronic renal disease, the capsule strips 
 perfectly, leaving a smooth, pale surface. 
 
 Microscopically, as already indicated, the changes are less 
 marked than one would have expected from the examination 
 of the urine. There is ( i ) always more or less evidence of 
 cloudy swelling of the renal epithelial cells, especially of the 
 cells lining the convoluted tubules. (2) There is more or 
 less fatty change in these cells, but this is never very marked. 
 
 (3) There is a certain amount of shedding (catarrh) of these 
 cells with a massing of the shed cells in the collecting tubules. 
 
 (4) There may be escape of red cells into the tubules. 
 
 The appearances are, in short, those of marked cloudy 
 swelling or of an acute catarrhal nephritis, and, as already 
 stated, between these two conditions there is no very hard and 
 fast line. 
 
 It should be remembered in connection with the micro- 
 scopic appearances of the kidneys that a degree of cloudy 
 swelling (toxic change) is practically constantly found in 
 pregnancy. 
 
 As already mentioned, infarcts in the placenta are specially 
 frequent in cases of eclampsia. 
 
 DISEASES OF THE MAMMAEY GLAND 
 
 Little need be said in such a treatise about diseases of the 
 mammary gland. Owing to their being readily removable, 
 growths of the gland are seldom seen post mortem. 
 
 Acute inflammatory conditions (acute mastitis) with 
 abscess formation are not uncommon. 
 
 Chronic inflammation (chronic interstitial mastitis) is 
 difficult to distinguish clinically and by the naked eye from 
 carcinoma. It occurs as a hard mass, ill defined, in the 
 substance of the gland. On section it appears as white- 
 looking tissue radiating through the fatty tissue of the breast. 
 
DISEASES OF THE TESTICLE 273 
 
 Microscopically -, the condition is characterised by the develop- 
 ment of a large amount of well-formed fibrous tissue with 
 isolated islands of gland tissue scattered through it. Cysts 
 formed by dilated gland acini are often present. 
 
 Tuberculosis is occasionally met with in the form of 
 multiple caseous foci surrounded with fibrous tissue scattered 
 through the gland substance. 
 
 Tumours. The mammary gland is one of the organs in 
 which tumour formation is most common. No doubt this 
 is due to the fact that the breast is periodically undergoing 
 hypertrophy and involution and also to the irritation to which 
 it is subjected from trauma and acute inflammatory processes. 
 
 Simple tumours, such as adenoma and cystic adenoma, 
 are dealt with among tumours under these headings (p. 285). 
 
 Carcinomata are dealt with under adeno-carcinomata. 
 
 Although primary carcinomata of the breast are seldom 
 met with in the post-mortem room, the secondary deposits 
 are frequently seen. They may occur in the lungs (Fig. 
 55), or disseminated through the body, often showing a 
 marked preference for bone. 
 
 DISEASES OF THE TESTICLE 
 
 Such diseases do not often come under the notice of the 
 pathologist. 
 
 Tuberculosis of the testicle is not infrequently 
 associated with generalised tubercle and with tubercle of the 
 genito-urinary tract. The condition tends to develop first 
 in the epididymis and may remain localised there. 
 
 Syphilis. Two chief types of syphilis are found in the 
 testicle. 
 
 1. Gummata. These are firm white or yellow caseous- 
 looking masses which ha veto be distinguished from sarcomata. 
 
 2. Interstitial Inflammation or Fibrosis. A slight degree 
 
 18 
 
274 DISEASES OF THE REPRODUCTIVE ORGANS 
 
 of this is not uncommonly met with even in cases which 
 show few other manifestations of the disease. Bands of white 
 fibrous tissue are seen running through the characteristic 
 slightly brownish tinged, soft testicular substance. 
 
 Tumours. Sarcoma is the commonest tumour of the 
 testicle. It is often of the large round cell type, and in appear- 
 ance (owing to accompanying necrosis) sometimes resembles 
 a gumma. Such tumours are rarely seen in the post-mortem 
 room, but the recurrences in the retroperitoneal glands may 
 be met. Such recurrent sarcomata may attain a large size. 
 
 DISEASES OF THE PEOSTATE 
 
 Hypertrophy. Simple enlargement of the prostate is a 
 common condition in men of sixty years of age and upwards. 
 It leads to obstruction of the urethra and to dilatation and 
 hypertrophy of the bladder. A fibrous and a glandular 
 variety are distinguished, the former being hard and the latter 
 soft. 
 
 Microscopically, sections show the structure of the normal 
 prostate-gland spaces and intervening fibre-muscular tissues. 
 In some cases the former, in others the latter, predominate. 
 
 Corpora amylacea are commonly present in the gland spaces 
 in this condition. They are produced by a transformation 
 occurring in desquamated epithelial cells and appear as rounded 
 or oval bodies showing concentric lamination not unlike starch 
 grains. 
 
 Acute Prostatitis, with abscess formation, is occasionally 
 met with following the formation of a false passage in cathe- 
 terisation of the urinary bladder. 
 
 Tumours. Carcinoma of the prostate is the commonest 
 tumour. It has a special tendency to show secondary 
 deposits in bone. The types met with are : columnar-celled, 
 scirrhous, and encephaloid. 
 
CHAPTER XIV 
 
 TUMOURS 
 
 TUMOURS may be primarily divided into (i) Simple and (2) 
 Malignant. There is actually no very hard and fast line 
 between the two varieties, certain tumours being less malig- 
 nant than others. Moreover, a simple tumour may become 
 malignant. On the whole, however, the distinction is suffi- 
 ciently well marked to serve as a basis for classification. 
 
 The main morphological difference between the two types 
 is that the simple tumour is encapsuled, i.e. is more or less 
 sharply defined from the tissues in its immediate neighbour- 
 hood, while the malignant tumour infiltrates surrounding 
 tissues and erodes structures such as blood-vessels. The 
 tendency to recur when removed, and to produce metastases 
 or secondary growths, both characters belonging to malignant 
 tumours, are explained by this character of infiltration. 
 
 In deciding in a given instance whether a tumour is simple 
 or malignant, certain points should be attended to. 
 
 1. Position. Tumours of the intestine are usually 
 malignant, while in the case of the uterus the commonest 
 tumour is the simple myoma. 
 
 2. Size. On the whole a large tumour is more likely to 
 be malignant than a small one, although there are notable 
 exceptions to this. 
 
 3. Ulcer ation. An ulcerating tumour is much more likely 
 to be malignant than simple. 
 
 275 
 
276 TUMOURS 
 
 4. Necrosis. Necrotic changes are more frequently met 
 with in malignant growths, owing to their tendency to over- 
 grow their blood-supply and from other causes. 
 
 5. Hcemorrhage is much more frequently met with around 
 and in malignant growths, owing to their capacity to erode 
 blood-vessels, and owing to the fact that their own blood- 
 vessels are thin walled and badly supported. 
 
 6. Infiltration of the surrounding parts, as already in- 
 dicated, is characteristic of malignant growths, while the 
 simple tumour is, as a rule, well defined. 
 
 7. Occurrence of Metastases. If such are present the 
 tumour is malignant. It should be borne in mind, however, 
 that simple tumours, such as the myoma of the uterus, may 
 be multiple. 
 
 Microscopic points of distinction between the two groups 
 are as follows : 
 
 1. Resemblance to Homologous Normal Tissue. This is 
 much more characteristic of simple growths. Malignant 
 growths deviate more or less markedly from the normal 
 tissues which they represent. They tend to resemble more 
 closely the embryonic equivalent of the tissue. 
 
 2. Character of Cells. The cells of malignant growths 
 tend to be larger and to vary in size and shape. Their nuclei 
 also are larger and often multiple. Mitotic figures are fre- 
 quently numerous in malignant growths and may show 
 aberrant types, such as multipolar division. 
 
 3. Infiltration of surrounding tissues is again a micro- 
 scopic character of malignant growths, while simple tumours 
 are encapsuled . Associated with this character is the tendency 
 to erode blood-vessels and other normal structures. 
 
 4. Inflammatory changes in the tissues around are found in 
 connection with malignant growths, while simple tumours 
 excite little reaction. 
 
 5. Necrosis is again more characteristic of the malignant 
 type than of the simple. 
 
SIMPLE TUMOURS 277 
 
 6. Hemorrhage more or less extensive is very characteristic 
 of malignant growths and is due as a rule to escape of red 
 blood cells from thin-walled, imperfectly-developed blood- 
 vessels, but may also be due to erosion of vessels by cancer 
 cells. 
 
 7. Relation of epithelial cells to stroma. In glandular 
 tumours of the simple type a basement membrane is usually 
 present. In malignant growths this is absent. 
 
 In the following description of the common tumour 
 formations no elaborate system of classification is adopted. 
 Any such system of classification must of necessity be tentative, 
 pending the discovery of the cause of tumour growth. 
 Further, exceptions to rules are so frequently met with in 
 relation to neoplasms that the most elaborate system breaks 
 down at many points unless each tumour be placed in a 
 category by itself. 
 
 A. SIMPLE TUMOURS 
 
 Tumours composed of Fibrous Tissue 
 
 Fibroma. This is a tumour composed of connective 
 tissue cells and fibres. Two types, soft and hard, are 
 distinguished, according as the cells or the fibres pre- 
 dominate. 
 
 Sites. They may arise anywhere where there is connective 
 tissue, cutis, fascia, periosteum, dura mater, submucous 
 tissue, pharynx and nose (polypi). They are also common 
 as minute growths in the medulla of the kidney. Sometimes 
 they occur in connection with scars (cheloids). A special 
 type, the neurofibroma, occurs in relation to nerves. 
 
 Appearance. Usually a well-defined rounded or lobulated 
 and encapsuled nodule, soft or hard, firm in consistence, pink 
 or white, the softer type tending to be pink from its greater 
 vascularity. The cut surface sometimes has a watered silk 
 
278 TUMOURS 
 
 appearance. Degenerative changes, such as myxomatous, 
 cedematous, calcareous, are sometimes met with. 
 
 Microscopically^ the appearances are those of ordinary 
 connective tissue. Sometimes the cells predominate, at other 
 times the intercellular material, according as the tumour is of 
 the hard or soft variety. The cells are usually spindle-shaped, 
 but in the more cellular types may be rounded. The inter- 
 cellular material consists of wavy collagenous fibres, staining 
 deep red with eosin and with acid fuchsin. 
 
 Tumours composed of Myxomatous Tissue 
 
 Myxoma. This is a somewhat rare tumour composed of 
 mucoid or myxomatous tissue, an embryonic form of con- 
 nective tissue. The umbilical cord is largely composed of 
 such tissue. Certain connective tissue tumours fibromata, 
 fibro-myomata, chondromata are not infrequently in part 
 composed of myxomatous tissue. When occurring in relation 
 to tumours composed of more adult tissue, the change is 
 regarded as a degenerative one. 
 
 Sites. Such tumours may be found in any of the sites in 
 which fibromata occur ; most commonly in subcutaneous 
 and submucous tissue. Not infrequently such growths 
 show a tendency to diffuse themselves and invade surrounding 
 structures ; such are to be regarded as sarcomata. The 
 placental or hydatid mole is often classified as a myxoma 
 (myxoma of the chorion, p. 268). 
 
 Appearance. Very soft and gelatinous, not infrequently 
 the material when manipulated forming long strings. Trans- 
 lucent, sometimes with minute haemorrhages. 
 
 Microscopically, the growth is found to be made up of 
 rounded, spindle-shaped and branching cells, widely separated 
 from one another. The material between the cells is homo- 
 geneous or slightly fibrillated, and usually stains very faintly. 
 Vessels are of course present and haemorrhages may be found. 
 
SIMPLE TUMOURS 279 
 
 Tumours composed of Fatty Tissue 
 
 Lipoma. Sites. Subcutaneous tissue, especially parts 
 liable to pressure, e.g. shoulders, buttocks, wall of large 
 bowel, kidney, rarely brain. 
 
 Appearance. Such tumours vary much in size, may be 
 very minute, occasionally very large, are usually lobulated, 
 and resemble fatty tissue. 
 
 Microscopical fy, they consist of adipose tissue with bands of 
 supporting fibrous tissue carrying blood-vessels. All stages in 
 development of fat cell are found from fibrous tissue cell, with 
 minute globule of fat, up to cell with merely thin rim of proto- 
 plasm and nucleus pressed aside by large fat globule. Crystals 
 of fatty acids are often present in the cells. 
 
 Tumours composed of Cartilage 
 
 Chondroma. A tumour composed of cartilage either 
 hyaline or fibre-cartilage. 
 
 Sites. It is occasionally found growing from cartilage of 
 rib or larynx (ecchondroma) more usually in relation to 
 bone or in the interior of glands such as parotid, testicle 
 (enchondroma). One of the commonest sites is the perios- 
 teum of long bones, especially at the ends of the metacarpals 
 and phalanges. 
 
 Appearance. It is a rounded or lobulated tumour, firm 
 and elastic, surrounded with a fibrous capsule which sends 
 in trabeculae between the lobules. Not infrequently it shows 
 calcification or soft areas of myxomatous degeneration. 
 
 Microscopically, the tumour is found to consist of lobules of 
 cartilaginous material composed of rounded or branched 
 cartilage cells lying in spaces between which is a matrix, 
 sometimes homogeneous, at other times fibrillated, occasionally 
 myxometous. Calcified areas which take on the haematoxylin 
 stain deeply are not infrequently met with. The tumour is 
 surrounded with a connective tissue capsule carrying blood- 
 vessels, prolongations of which dip down between the lobules. 
 
280 TUMOURS 
 
 Tumours composed of Bone 
 
 Osteoma. Two varieties are distinguished : (i) the com- 
 pact or eburnated ivory exostosis found in connection with 
 the bones of the skull ; (2) the spongy osteoma, in which the 
 bony trabeculae are thinner and more widely separated. 
 The exostoses found in connection with the attachment of 
 muscles are probably not true tumours. They are more of 
 the nature of hypertrophies of bony tissue, i.e. ossification 
 following trauma or irritation. 
 
 Tumours composed of Muscle 
 
 Myoma. Two varieties are distinguished : (i) the rhabdo- 
 myoma or tumour composed of striped muscle fibres, which 
 is very rare, usually congenital and commonly malignant 
 (sarcomatous). It is found in the kidney and testicle, and is 
 due to inclusion of portions of the lumbar muscles. (2) 
 Leiomyoma, a very common tumour composed of non-striped 
 muscle fibres. 
 
 Sites. Leiomyomata are found by far most frequently 
 growing in the wall of the uterus. They may also occur 
 in other positions where non-striped muscle is found, such as 
 the alimentary tract, more especially the oesophagus, also 
 bladder and prostate. 
 
 Appearance. In the uterus the tumours are frequently 
 multiple. They vary greatly in size, from something just 
 visible by the unaided eye to a tumour the size of a foetal 
 head. They are most frequent in the body of the uterus 
 but also occur in the cervix. 
 
 Three varieties are distinguished according to the position 
 in the uterine wall, viz. (i) intramural ; (2) subserous, when 
 projecting into the peritoneal cavity and covered with peri- 
 toneum over the greater part of its surface ; (3) submucous, 
 when projecting into the cavity of the uterus (Fig. 104). 
 
SIMPLE TUMOURS 281 
 
 The tumours are rounded and well defined from the 
 neighbouring muscle. On the cut surface they are usually 
 pink in colour and show an appearance like watered silk 
 or balls of cotton. Degenerative changes are common in 
 myomata, e.g. myxomatous change, calcification and a 
 necrotic change known as " red softening." 
 
 Microscopic Appearance. The tumour does not differ in 
 any essential respect from the normal uterine-wall tissue. It is 
 composed of bundles of (i) non- striped muscle fibres running 
 in all directions and therefore in sections cut sometimes longi- 
 tudinally, sometimes obliquely, sometimes transversely ; (2) 
 fibrous tissue running between the bundles and between the 
 individual fibres. So markedly does this fibrous element 
 enter into the composition of the tumour that the term " fibro- 
 myoma " is often employed. In the myomata found in the 
 oesophagus the amount of fibrous tissue is much less. The 
 individual muscle fibres when cut longitudinally are elongated, 
 often sinuous structures with similarly elongated nuclei. The 
 fibrous tissue often shows degenerative changes : (i)myxomatous, 
 (2) hyaline, (3) calcareous. Blood-vessels with well-developed 
 walls are always present. Sometimes gland acini are scattered 
 through the fibro-muscular tumour (adeno-myoma). 
 
 Tumours composed of Vascular Tissue 
 
 Angioma. Two primary varieties may be distinguished, 
 viz. (i) hsemangioma, (2) lymphangioma ; a further sub- 
 division of each variety into (a) plexiform or capillary, and 
 (b) cavernous may be made. 
 
 Sites and Appearance. Hcemangiomata are most usually 
 found in relation to skin or mucous membrane. They may 
 be merely areas of purple colour, the so-called " port wine 
 stains," or they may project and may even be pendulous. 
 They are always dark red in colour and are often pulsatile. 
 These cutaneous angiomata most usually belong to the plexi- 
 form variety, but may be cavernous. The cavernous type is 
 most common in the liver, but may occur in relation to the 
 
282 TUMOURS 
 
 membranes of the brain and in the skin. It appears as a 
 dark purple area, more or less wedge shaped, immediately 
 under the capsule of the organ (Fig. 76). The condition is 
 much more common in the ox than in man. Lymphangiomata 
 are found in relation to skin and tongue. They are probably 
 always congenital and mostly belong to the cavernous type. 
 
 Microscopic Appearances. ( i ) Capillary Angioma. Instead 
 of the dense fibrous tissue of the cutis, great numbers of 
 minute spaces lined with fairly large endothelial cells are 
 found. Some of these spaces contain blood, others are empty. 
 Between the capillaries there is more or less loose connective 
 tissue. 
 
 (2) Cavernous Angioma. In this type, large spaces are 
 found lined with spindle-shaped endothelial cells and filled with 
 blood, sometimes with thrombi. The walls of the spaces are 
 formed of well-developed fibrous tissue. 
 
 Tumours composed of Lymphoid Tissue 
 
 Lymphoma. A simple lymphoma is a rare tumour, usually 
 small and solitary. Microscopically, it has the appearance 
 of normal lymphoid tissue, having a capsule, a reticulum in 
 which are large numbers of lymphocytes also endothelial 
 cells. The condition is very difficult to distinguish from 
 mere hypertrophy of lymphoid tissue. The malignant type, 
 lymphosarcoma, is more common and much more important. 
 
 Tumours composed of Neuroglia 
 
 G-lioma. Such tumours, arising as they do from the 
 neuroblast, are epiblastic in origin. 
 
 Sites. They are found in the brain, retina and spinal 
 cord. 
 
 Appearance. As a rule they are not well defined, but 
 merge into the surrounding brain substance. They vary 
 much in size, may be opaque or translucent, white or pink. 
 
SIMPLE TUMOURS 283 
 
 A slow-growing, simple type is recognised, but many of them 
 have the characters of malignant growths and may be called 
 glio-sarcomata (see p. 243). Haemorrhages frequently occur 
 into their substance. 
 
 Microscopically ', such tumours are formed of small round cells 
 with branching prolongations (spider cells), the latter forming a 
 felted mesh work between the cells. In the case of the retinal 
 glioma, the branching processes may be absent. Vessels are 
 present which are often thin walled and may rupture, leading 
 to haemorrhages. 
 
 Epithelial Tumours 
 
 Such tumours, in addition to their epithelial elements, 
 always possess a greater or smaller amount of supporting 
 fibrous tissue stroma. 
 
 i. Papilloma. This is a tumour projecting from an epi- 
 thelium-covered surface, composed of connective tissue and 
 epithelial cells. Two types, (a) squamous papilloma and (b) 
 mucous papilloma, may be distinguished according to the 
 type of epithelial surface from which the tumour grows. 
 
 (a) Squamous papillomata. Sites. These are found in 
 relation to skin, mouth, larynx, pharynx, oesophagus or 
 vagina. 
 
 Appearance. They consist of a series of projections com- 
 posed of a connective tissue core carrying blood-vessels and 
 a covering of squamous epithelium. The epithelium is 
 frequently much thickened and the dead material tends 
 to accumulate between the prolongations. The skin 
 papilloma or ordinary wart is sometimes congenital. It is 
 commonest in childhood and is often infective, being prob- 
 ably due to some micro-organism. One of the infective 
 papillomata, the venereal wart, is found in relation to the 
 genitals. Some are due to the irritation of chemicals, such 
 as paraffin. Molluscum contagiosum is a condition appearing 
 as small red elevations, affecting more especially the skin 
 
284 TUMOURS 
 
 of the head, face and hands. The elevations break down 
 in the centre and discharge a cheesy material. The disease is 
 regarded as being due to some germ not yet discovered. 
 
 Microscopic Appearances. The connective tissue core con- 
 taining vessels is seen in places in connection with the cutis. 
 In other places there are isolated rounded areas of fibrous 
 tissue produced by the cutting transversely of one of the finger- 
 like processes. Upon this connective tissue is placed the 
 epithelium which corresponds to the stratified epithelium of 
 the skin and like it shows differentiation into layers. The 
 epithelium shows a sharp line of demarkation from the 
 subjacent connective tissue. Occasionally whorl-like masses 
 of cornified epithelium are seen simulating the " cell-nests " of 
 cancers, but these are buried in the thick layer of epithelium 
 and do not penetrate the fibrous stroma. 
 
 (b) Mucous papillomata. Sites. These may grow from 
 any mucous membrane alimentary canal, bile ducts, bladder, 
 pelvis of kidney. Some of these are undoubtedly due to 
 organisms, viz. the condition known as coccidiosis, which 
 is a papillomatous condition of the bile ducts, found specially 
 in the rabbit, due to a protozoon the coccidium oviforme. 
 A somewhat similar condition in the stomach of the rat is 
 due to the presence of a small nematode. 
 
 Appearance. In structure the mucous papilloma consists 
 of a slender connective tissue core carrying blood-vessels, 
 and covered by a layer of epithelium which may be columnar, 
 cubical or transitional, according to the site. One of the 
 commonest sites for this type is the bladder, where the growth 
 consists of numerous delicate processes forming a sea-anemone- 
 like mass. 
 
 Microscopic Appearances. A connective tissue core of 
 great delicacy, carrying blood-vessels, dividing and again 
 dividing, is seen in connection with the submucous coat of the 
 viscus if the section be accurately through the root of the 
 tumour. Many of the branches are, however, cut transversely. 
 Upon this connective tissue core is placed the epithelium 
 
SIMPLE TUMOURS 285 
 
 which may be transitional (in the case of the bladder) show- 
 ing numerous layers of elongated epithelial cells tending to 
 become loosened and to separate in the more superficial 
 layers. In the case of the intestinal and bile duct papilloma 
 the epithelial cells are columnar. Mitotic figures are often 
 numerous in the cells of the villous papilloma of the bladder. 
 
 2. Adenoma is the term applied to a simple tumour com- 
 posed of gland elements. Such tumours contain, in addition 
 to the epithelial gland cells, a larger or smaller amount of 
 supporting fibrous tissue. In this connective tissue the 
 nutrient vessels run. When the fibrous tissue is large in 
 amount, the term fibro-adenoma is used. Often the gland 
 acini in the tumour become dilated (cystic adenoma). 
 Occasionally (breast and ovarian adenomata) within the 
 cysts there is a papillomatous development of the epithelial 
 elements supported by fibrous tissue (papilliferous cystic 
 adenoma). Such tumours are generally regarded as being of 
 doubtful simplicity. 
 
 Sites. Any gland may be the site of origin of an adenoma. 
 The commonest site for such tumours is undoubtedly the 
 mammary gland. The prostate, thyroid, liver and other 
 glands may be the seats of similar tumours. 
 
 Appearance. Such tumours are round or lobulated, 
 vary much in size, and are surrounded by a fibrous capsule 
 so that they are readily shelled out. The colour is white or 
 pink, and on section minute clear foci representing groups 
 of gland acini may be seen. Cysts are often present. 
 Another common site for adenomata is the ovary, forming 
 the so-called compound cystic adenoma. The cysts are 
 often very large and contain mucinous material. 
 
 Microscopically, the essential parts of the tumour are (i) 
 gland acini lined with epithelium, resembling that of the gland 
 from which the tumour arises, set upon a basement membrane. 
 Secretion may be present, colloid material in the case of 
 tumours of the thyroid gland, mucinous material in the 
 
286 TUMOURS 
 
 compound cystic ovarian tumour. The acini are not in- 
 frequently dilated, forming cysts of various size. Intracystic 
 papillomatous projections also covered with epithelium may be 
 found, and in the case of the breast tumours small rounded 
 masses of fibrous tissue, the so-called intracanalicular fibromata. 
 The epithelium in the case of the ovarian tumours is markedly 
 columnar in type. 
 
 (2) Fibrous supporting tissue, which varies much in amount, 
 sometimes, in the case of the fibro-adenomata, occurring in 
 large bands which separate the groups of gland acini widely 
 from one another. Running in this connective tissue stroma 
 are the blood-vessels of the tumour, as a rule, well developed. 
 
 B. MALIGNANT TUMOURS 
 
 The general characters of malignant growths and the 
 points wherein they differ from the simple tumour have 
 already been discussed. The chief characteristic of such 
 growths is the tendency to invade normal structures, so that 
 they infiltrate the tissues in which they arise and tend to 
 erode blood- and lymph-vessels, and to pass by these in the 
 form of tumour emboli to other parts of the body. 
 
 The term cancer is sometimes used generically for such 
 growths, but the pathologist usually reserves that term for 
 the epithelial type of malignant growth. 
 
 Microscopically, the malignant tumour is characterised by 
 an imperfect repetition of the normal tissues. Whereas the 
 simple growth resembles, in many cases very closely, the 
 normal adult tissue from which it arises, the malignant tumour 
 shows considerable deviation from the homologous normal 
 tissue. It tends to resemble in many instances the embryonic 
 type of the tissue. Hence the use of the term " atypical " in 
 relation to them. 
 
 Just as simple tumours may be divided primarily into (i) 
 those arising from and composed of connective tissue and (2) 
 those arising from and partly composed of epithelial tissue, 
 so in the case of the malignant growths we may distinguish 
 
MALIGNANT TUMOURS 287 
 
 a connective tissue and an epithelial group. The former 
 are sarcomata, the latter carcinomata or true cancers. 
 
 SARCOMATA 
 
 These are tumours which are essentially cellular, i.e. 
 contain a minimal amount of intercellular material. The cells 
 are of the connective tissue type and are embryonic, i.e. 
 imperfectly differentiated. So that what appears to be the 
 most advanced stage of development of which the tumour 
 cells are capable corresponds with an early stage in the 
 development of a fibrous tissue cell from the primitive round 
 connective tissue corpuscle. 
 
 Under normal circumstances, either during development 
 or in the course of the laying down of new tissue in the 
 process of healing, the connective tissue corpuscle passes 
 from a 'small round cell with small round, relatively large, 
 nucleus and small amount of protoplasm to the large round 
 cell with abundant protoplasm. The cell then becomes oval 
 and eventually spindle shaped. Subsequently from the 
 protoplasm there are split off collagenous fibrils which form 
 the intercellular material. 
 
 In this type of growth the cell which has taken on tumour 
 characters may stop at any one of these stages and subse- 
 quently reproduce cells of a similar stage of development 
 and no other type. Seldom does it occur that the fully- 
 developed type of connective tissue cell is found in the 
 sarcomata. It is usually the more primitive types which are 
 found. Occasionally a tumour which shows a high degree 
 of differentiation may on recurring exhibit a differentiation 
 of a less high degree. Thus a tumour with the characters of 
 a fibroma may on recurring (recurrent fibroid) assume the 
 characters of a sarcoma. 
 
 As the name sarcoma indicates, such tumours are flesh- 
 like. As a rule they form large masses of opaque white or 
 
288 TUMOURS 
 
 faintly pink material. Necrotic areas are not infrequently 
 present, and haemorrhages are very common. Certain types 
 are very vascular (angiosarcomata) and some develop pig- 
 ment (melanotic sarcomata). 
 
 In consistence sarcomata are commonly soft, sometimes 
 diffluent, and often show areas of more marked softening. 
 They are, however, sometimes firm and may even be hard. 
 Like other forms of malignant growth, they show a marked 
 tendency to infiltrate and thus are seldom encapsuled. 
 
 Although, as already stated, they tend to stop short of the 
 fully-developed form of the connective tissue from which 
 they arise, such tumours not infrequently reach a fair degree 
 of differentiation of tissue. Thus those arising from cartilage 
 tend to produce cartilage, those arising from bone produce 
 bone-like tissue, those arising from muscle may produce 
 muscle cells, and so on. This differentiation forms a basis 
 for classification. Hence we speak of chondro-sarcomata, 
 osteo-sarcomata, etc. A majority of these tumours, however, 
 merely exhibit the various stages of development of the 
 connective tissue cell. In order to classify them we use such 
 terms as small round cell sarcoma, large round cell sarcoma, 
 small spindle cell sarcoma, large spindle cell, fibre-sarcoma, 
 mixed cell sarcoma. 
 
 As a rule, the less differentiated the type of cell composing 
 the tumour the more malignant it is. Thus the small round 
 cell sarcoma is one of the most malignant types. Sometimes 
 a tumour starts by being simple but becomes malignant, 
 either a portion of the growth assuming the malignant type, 
 or the whole tumour, as in the so-called recurrent fibroid, 
 becoming more and more malignant at each recurrence. This 
 prepares one for the fact that there are degrees of malignancy. 
 
 Sarcomata very commonly produce metastases. Such 
 metastatic growths are found not so frequently in lymph 
 glands as in the internal organs. Hence the statement that 
 these tumours spread more by the blood than by the lymph 
 
MALIGNANT TUMOURS 289 
 
 channels. This is true up to a certain point ; but there are 
 exceptions, particularly in the case of the melanotic tumour 
 which often spreads by the lymphatics. 
 
 As regards sites of origin, such growths may arise in any 
 part of the body in which connective tissue is found, and this 
 means anywhere at all. There are, however, certain parts 
 and tissues more commonly affected than others. Thus, 
 subcutaneous tissue, intermuscular septa, fasciae, perios- 
 teum, bone, lymph glands are common sites of origin. As 
 regards the secondary deposits, these occur more commonly 
 in the lung than in any other organ (see p. 148). 
 
 Types of Sarcomata 
 
 Small Round -Cell Sarcoma. This is a white, grey or 
 pink, soft, sometimes diffluent tumour, found primarily in 
 connection with subcutaneous tissue, bone, muscles, brain 
 testicle, and secondarily anywhere, but most commonly in the 
 lungs. Haemorrhages and areas of necrosis are frequent. 
 The tumour is one of the most malignant types known. 
 
 Microscopically, such tumours are composed of small round 
 cells closely packed, with scanty protoplasm and small dark- 
 staining nuclei. The cells resemble very closely the lympho- 
 cyte of the blood and lymph glands. The intercellular 
 material is scanty, granular or slightly fibrillated. The vessels 
 are thin walled, often consisting of a single layer of cells. 
 Haemorrhages and areas of necrosis are frequent. 
 
 The so-called Lymphosarcoma may be regarded as a sub- 
 variety of the above. It originates in lymphoid tissue, 
 very commonly the lymphatic glands of the mediastinum, 
 and is very malignant. In appearance it resembles other 
 types of sarcoma (Fig. 56). 
 
 Microscopically, such tumours are composed in large part of 
 small round lymphocyte-like cells with rather more intercellular 
 material than in the case of the ordinary type of small round- 
 
 19 
 
290 TUMOURS 
 
 cell sarcoma. There is often a fair number of larger flattened 
 or polygonal cells, representing the endothelial elements of 
 lymphoid tissue. Occasionally this larger type of cell is the 
 predominant one (endothelioma). 
 
 Large Round-Cell Sarcoma. These tumours have much 
 the same appearance as the above, but tend to be on the 
 whole firmer in consistence. The sites of origin are also 
 much the same, but the testicle, pharynx and posterior nares 
 and muscle are perhaps more commonly affected. 
 
 Microscopically, as in the previous type, the tumour is 
 composed essentially of cells, but there is more intercellular 
 material, and the fibrils of which it is composed are thicker. 
 The cells are of course larger, rounded or polygonal, with 
 more abundant protoplasm and a nucleus with a wider-meshed 
 network, hence staining less deeply. Areas of necrosis and 
 haemorrhages are common. The vessels are better developed. 
 Sometimes the cells have an alveolar arrangement. 
 
 Small Spindle -Cell Sarcoma. Such tumours resemble 
 the preceding but are more benign. 
 
 Microscopically, the tumour is composed of small oat-shaped 
 cells arranged irregularly in bundles. The cells represent a 
 further stage in the development of the connective tissue 
 corpuscle. The vessels are, however, still very imperfectly 
 formed. 
 
 Large Spindle -Cell Sarcoma. In this type the fas- 
 ciculation may be visible to the naked eye. The tumour 
 bears considerable resemblance to .a fibroma. It is, more- 
 over, firmer than most other types. Such tumours occur in 
 relation to periosteum, muscles, mamma, or ovary. 
 
 Microscopically, the cells are arranged in bundles. There 
 is a considerable amount of intercellular fibrillated material, 
 and the vessels are fairly well supported. It is difficult in 
 many instances to differentiate such growths from cellular 
 fibromata. The cells tend, however, to be larger and to vary 
 more in size, and mitotic figures are often present. 
 
MALIGNANT TUMOURS 291 
 
 From the microscopic point of view it is a matter of great 
 difficulty in many instances, especially when only a minute 
 portion of tissue is available, to differentiate such tumours 
 from granulation tissue. Nothing less than long experience 
 will enable the pathologist to do this in many cases. The 
 point to attend to is : the uniformity of type in the cells. 
 In the case of granulation tissue all stages of development of 
 the fibrous tissue cell will be met with, whereas in the case 
 of the sarcoma the cells tend to be all of one type, round or 
 spindle, as the case may be. 
 
 Mixed Cell Sarcomata are met with occasionally. In 
 such, in addition to round and spindle cells, giant cells 
 (multinucleated masses of protoplasm) are often found. 
 
 To this type belongs the myeloid or giant cell sarcoma 
 found in relation to bone. 
 
 Sites. Such tumours occur in young subjects, chiefly in 
 the upper end of the tibia and fibula, the lower end of the 
 femur and in the lower jaw (malignant epulis, Fig. 109). 
 
 Appearance. These tumours are slow growing and show 
 generally a low degree of malignancy. They do not tend to 
 produce metastasis and rarely recur when removed. They 
 grow from the interior of the bone, distending and thinning 
 the overlying bony tissue. They show the appearances of 
 sarcomata generally, but haemorrhages are specially frequent. 
 
 Microscopically, myeloid sarcomata are usually composed 
 of spindle-shaped cells with large multinucleated masses of 
 protoplasm scattered more or less regularly through them. 
 These giant cells are sometimes absent over considerable areas. 
 They may be differentiated from the giant cells of tuberculosis 
 by their nuclei occurring all through the cell, especially in the 
 centre, whereas the tubercle giant cell has its nuclei arranged 
 in a zone at the margin. Haemorrhages are frequent. 
 
 Glio-sarcoma is a type found in the central nervous 
 system and retina. It is the malignant analogue of the 
 glioma and resembles it in appearance (see p. 243). 
 
292 TUMOURS 
 
 Sarcomata sometimes show a greater amount of differentia- 
 tion of tissue. Those arising in connection with bone may show 
 a tendency to form cartilage (chondro - sarcoma) or bone 
 (osteo-sarcoma) or a mixture of the two. Such tissue only 
 imperfectly reproduces the structure of its normal homologue. 
 The cartilage is very irregular and has a marked tendency 
 to undergo myxomatous change. The bony tissue is only 
 imperfectly formed, the calcareous material being deposited in 
 rather than combined with the intercellular tissue. Necrosis 
 and haemorrhage are prominent features of such tumours. 
 
 Endothelioma. Sites. This is a term of somewhat 
 indefinite significance applied to tumours occurring in 
 connection with serous membranes such as the pleura, 
 peritoneum and dura mater, but also in other parts of the 
 body in relation to lymph and blood channels and lymph 
 glands. Apparently they may originate in any position 
 where connective tissue tends to assume a flattened 
 character in consequence of forming a lining to a channel, 
 space or cavity. 
 
 Appearance. Such tumours have the characters and 
 appearances of sarcomata in general. 
 
 Microscopically, the chief characteristic is a tendency for the 
 cells to group themselves so as to form rounded or irregularly 
 shaped spaces into which the flattened or polygonal cells pro- 
 ject. Owing to the above-mentioned microscopic appearances 
 the term alveolar sarcoma is often applied to these tumours. 
 
 Perithelioma is a term applied to a neoplasm in which 
 there is whorl -like arrangement of the constituent cells 
 round a central blood or lymph space, the cells being of a 
 flattened or polygonal shape. Such tumours are found, 
 specially in the central nervous system, growing from the 
 membranes of the brain or cord. Sometimes in the centres 
 of these whorls of cells instead of a space there may be a 
 mass of calcareous material. Such tumours have been 
 
MALIGNANT TUMOURS 293 
 
 called Psammomata or " brain sand tumours." They occur 
 in relation to the cerebral meninges and ventricles. 
 
 Angiosarcoma. Closely related to the above are malig- 
 nant growths in which spaces containing blood are the 
 principal feature. The spaces are lined with endothelial- 
 like cells. Such tumours have of course a very vascular 
 appearance. They are not uncommon in the brain, and are 
 found occasionally in the spleen. 
 
 Myelomata are tumours which arise from one or other 
 of the blood-forming elements in the bone marrow. The 
 cells composing them are rounded or polygonal and may 
 resemble the myelocyte, lymphocyte, nucleated red cell or 
 plasma cell. They occur as multiple white masses in the 
 interior of bones such as sternum, ribs, spinal column, skull, 
 femur, humerus. They destroy and distend the bone, 
 leading sometimes to spontaneous fracture. In the urine a 
 peculiar form of albumose (Bence- Jones albumose) is some- 
 times found in such cases. 
 
 Malignant Melanotic Tumours 
 
 Melanin pigment occurs normally in the deeper cells of 
 the stratum Malpighii. Subjacent to these, in the cutis vera, 
 are certain spindle-shaped cells which may contain pigment 
 and which are known as chromatophore cells. Whether these 
 cells elaborate the pigment from the blood or bear it to other 
 destinations from the epithelial cells is uncertain. Similar 
 pigment is also found in the choroid and in the iris. The 
 chemical characters of the pigment vary somewhat according 
 to the site, but as a rule it contains a considerable quantity 
 of sulphur and little or no iron. In colour, under the micro- 
 scope, the pigment varies from yellow to dark brown. To 
 the naked eye it usually appears black. 
 
 The exact position from the point of view of classification 
 
294 TUMOURS 
 
 of many of these melanotic tumours is uncertain. Some 
 have the microscopic characters of sarcomata of the spindle- 
 cell type. In others the cells are polygonal and others again 
 have the appearance of epitheliomata. Pigment ed meso- 
 blastic cells are found in the choroid and iris, and, as we have 
 seen, cells resembling connective tissue corpuscles (chroma- 
 tophore cells) are found in the cutis, but whether these latter 
 form the origin of melanotic tumours is uncertain. The 
 pigment-containing cells in the pigment ed moles are also of 
 uncertain nature. Many of these melanotic tumours probably 
 arise from the cells in the deeper layers of the stratum 
 Malpighii, and are therefore of epithelial origin and should 
 be classified with the carcinomata. 
 
 Sites. Tumours which contain melanin are met with 
 primarily in connection with the skin (particularly in 
 relation to pigmented moles) and with the eye. Secondary 
 deposits occur specially in lymphatic glands and in the liver. 
 Such tumours, as a rule, are exceedingly malignant in the 
 sense that secondary growths may occur early when the 
 primary tumour is minute. 
 
 Appearance. The appearance of such tumours is very 
 characteristic owing to the presence of the melanin, which 
 imparts a dark-brown to black colour to the growth. The 
 pigment may, however, be present only in parts, the pigment- 
 free areas having the appearance of an ordinary sarcoma. 
 The student should be careful not to fall into the error of 
 calling a neoplasm in the lung, where carbon pigment is 
 normally present, melanotic. 
 
 Microscopically, such tumours, as already stated, vary 
 considerably. The cells may be spindle shaped, polygonal or 
 epithelioid. The pigment is present within the cells and in 
 masses outside. Considerable areas of the tumour may have 
 no pigment present at all. The pigment is yellow to dark 
 brown in colour and is exceedingly resistant to reagents of all 
 kinds. For its demonstration sections of the tumour should 
 
MALIGNANT TUMOURS 295 
 
 be stained in the nuclear dye (e.g. hasmatein) only. The cells 
 often have an alveolar arrangement. 
 
 CARCINOMATA OR CANCERS 
 
 These are malignant tumours, the essential constituent of 
 which is epithelium. In addition to the epithelium there is 
 always a greater or smaller amount of connective tissue stroma, 
 which supports the epithelial elements and in which run the 
 nutrient vessels. This stroma is derived in part from the 
 pre-existing tissue of the area in which the tumour occurs ; 
 to a much greater extent it is a new development from the 
 fibrous tissue of the host. It is this occurrence of two 
 distinct types of tissue epithelial elements and supporting 
 connective tissue scaffolding which distinguishes this type 
 of malignant growth from the sarcomata. In the case of the 
 latter the cells tend to be all of one type and are diffusely 
 arranged. 
 
 Inasmuch as there are two main types of epithelium 
 (i) the stratified squamous type, covering skin and lining 
 mouth and oesophagus ; (2) the glandular type, covering the 
 intestine and forming the secreting elements of glands so 
 there are two main types of carcinomata : (i) Squamous 
 epitheliomata ; (2) Adeno-carcinomata. 
 
 The characters of these tumours are those of malignant 
 growths in general. The main underlying property is that 
 of invasion of the normal tissues. Sometimes, in the case 
 of a tumour of a surface such as the skin or of a lining 
 membrane of a viscus such as the bowel, enlargement may 
 take place mainly by projection of the growth. Such an 
 appearance often receives the name " fungating " tumour 
 (Fig. 69). As a rule, however, the tumour grows chiefly by 
 penetrating the healthy tissues around. 
 
 When growing on one of the surfaces skin or bowel 
 ulceration of the growth very soon occurs. This leads to 
 
296 TUMOURS 
 
 invasion of organisms and absorption of toxins, an important 
 factor in the production of the cachexia of cancer. 
 
 The erosion of the tissues by the cancer cell elements 
 leads to invasion of lymph- and blood-vessels. It is chiefly by 
 the former that carcinomata spread, so that the secondary 
 deposits are to be sought for first of all in the nearest 
 lymphatic glands. Spread may also occur by way of the 
 blood-stream, secondary foci occurring in the internal organs 
 such as liver and lungs. 
 
 This invasion by the cancer cells is resented by the normal 
 tissues, with the result that an inflammatory reaction of a 
 subacute type occurs in the tissues at the growing margins of 
 such growths. This inflammatory reaction manifests itself 
 by an infiltration of the tissues with small round cells, similar 
 in appearance to the lymphocytes of the blood but in reality 
 of diverse origin. 
 
 The metastases resemble as a rule the primary growth fairly 
 closely. They show the same division into epithelial elements 
 and supporting fibrous tissue. The tendency is, however, 
 for the epithelial elements to show less marked differentiation. 
 Thus in squamous epitheliomata the secondary deposits 
 may show little or no tendency to cornification and formation 
 of cell nests. 
 
 The cancer cells themselves vary greatly in shape and 
 appearance. As a rule they tend to be larger than their 
 normal homologues. They may show evidence of secretory 
 activity when they arise from glandular epithelium. This is 
 indicated by vacuolation of the cells and by the accumulation 
 of mucinous or colloid material in the gland spaces. They 
 do not preserve the normal relationship with their surroundings. 
 Thus the groups of gland cells have no basement membrane. 
 Instead of the normal single layer of cells forming an acinus 
 there are often several layers. 
 
 Mitotic figures are often numerous, their number being 
 taken as a measure of the rapidity of the growth of the tumour. 
 
MALIGNANT TUMOURS 297 
 
 The figures are frequently abnormal , showing multipolar 
 division. The chromosomes are more often he tero typical 
 (i.e. rounded instead of V-shaped a condition characteristic 
 of the stage of maturation of the sexual cells) than is the 
 case in the cell dividing normally. 
 
 Various forms of inclusions are commonly met with in 
 the cancer cells. These are known as " cancer bodies," and 
 have from time to time been taken as representing parasites 
 of various types. They are produced by the phagocytic 
 activity of the cells taking up leucocytes, other cancer cells , 
 red blood corpuscles, etc. They appear as rounded bodies, 
 usually with a distinct space surrounding them. Other 
 bodies occurring mainly between the cells, usually in groups, 
 are found. They are known as Russell's fuchsin bodies, and 
 probably represent hyaline degenerations of cells or segrega- 
 tions of albuminous material. 
 
 Carcinomata occur (i) at or near the orifices of the body 
 lip, tongue, rectum, vagina; (2) at points where normally 
 there is narrowing of a canal pylorus, ileo-caecal valve ; 
 (3) at points where a canal changes its direction hepatic, 
 splenic, simoid flexures of large intestine ; (4) in glands such 
 as the mammary, and in organs such as the uterus, which 
 are periodically undergoing hypertrophy and involution. In 
 other words, there is a marked association of cancer with 
 chronic irritation of various kinds. 
 
 The tumours commonly grow from a single centre. The 
 various prolongations of the growth will be found all to 
 radiate from a single point. 
 
 As previously indicated, carcinomata may be divided 
 into two main groups (i) Squamous epitheliomata ; (2) 
 Adeno-carcinomata or glandular cancers. 
 
 I. Squamous Epitheliomata 
 
 Sites. These grow from (a) the skin ; (b) mucous membranes 
 covered with stratified squamous epithelium , such as mouth) 
 
298 TUMOURS 
 
 (esophagus, vagina, cervix uteri ; (c) embryonic epithelial canals, 
 such as the thyro-glossal duct. Occasionally they occur where 
 no squamous epithelium is found normally, e.g. in stomach 
 and gall-bladder. 
 
 Appearances. Such tumours occasionally project beyond 
 the general surface, forming a fungating mass. More com- 
 monly they appear as ulcerated areas, the margins of the ulcer 
 being raised and hard (Fig. 57). On cutting down through the 
 floor of the ulcer so that the relationship with the subjacent 
 tissues is displayed, the opaque white epithelium will be found 
 penetrating the tissue for a variable distance. 
 
 Microscopically, such tumours are found to be formed of 
 tongue-like prolongations of epithelium. Sometimes these can 
 be traced in continuity with the original mass, at other times 
 they are cut transversely and appear as isolated rounded 
 masses. At the spreading margin and in the early stage of 
 the condition these columns of epithelial cells, being only a 
 few cells thick, show no differentiation into layers. In the 
 larger masses the central cells become flattened and undergo 
 a change similar to the keratinisation of the stratum corneum. 
 When the columns are cut transversely the appearance is that 
 of a central whorl of flattened cells concentrically arranged, 
 representing the stratum corneum and surrounded by the poly- 
 gonal epithelial cells representing the cells of the stratum 
 Malpighii, and like them showing intercellular bridges. This 
 appearance is known as a "cell nest." These cell nests must 
 be distinguished from hair follicles and other normal structures. 
 
 The cells forming these epithelial down-growths resemble 
 the normal cells found in the deeper layers of the stratum 
 Malpighii. They tend, however, to be somewhat larger than 
 their normal homologue. Mitotic figures are usually to be 
 found amongst their nuclei, sometimes in large numbers. 
 
 Between these columns of epithelial cells are the tissues 
 muscle, connective tissue, glandular structures which have 
 been invaded by the growth. These are infiltrated by small 
 round cells. These cells are specially well seen at the growing 
 margin of the tumour, the appearance being known as small 
 round -cell infiltration. Such small round cells may be 
 
MALIGNANT TUMOURS 299 
 
 lymphocytes from the blood or young connective tissue cells. 
 Haemorrhages are not uncommonly met with in the marginal 
 portions of the growth. In addition to the pre-existing tissues 
 of the part there are strands of newly-formed connective tissue 
 between the masses of epithelium. These constitute the 
 scaffolding of the new growth, and are composed of granula- 
 tion tissue, with a large proportion of small round cells. 
 
 Rodent Ulcer. This is a variety of squamous epithelioma 
 with a low degree of malignancy. 
 
 Site. The condition occurs in old people on any part of 
 the skin, but most frequently on the upper part of the face, 
 about the root of the nose, the external angle of orbit, the 
 side of the cheek and the forehead. 
 
 Appearance. It appears as an ulcerated area with raised 
 margins, which erodes down to the bone and may destroy 
 the nose or ear, but which does not produce metastases and 
 is very amenable to treatment. The tumour is believed to 
 originate from the hair follicles or sweat glands, rather than 
 from the epithelium proper. 
 
 Microscopically, the condition is characterised by the 
 presence of masses of epithelial cells penetrating the subjacent 
 tissues. There are certain points of distinction between this 
 and the ordinary squamous epithelioma. (i) The cells are 
 cylindrical or spindle shaped, and are as a rule smaller than 
 those found in the epithelioma. (2) There are no cell nests or 
 only imperfect attempts at keratinisation in the centres of the 
 epithelial masses. (3) There is little or no evidence of cell 
 reaction (round-cell infiltration) in the tissues which are being 
 invaded. (4) The line between epithelial masses and fibrous 
 stroma is sharply marked. 
 
 II. Adeno-Carcinomata, Malignant Adenomata, or 
 Glandular Cancers 
 
 These tumours are composed of gland cells arranged in 
 alveoli or in solid masses and of intervening supporting fibrous 
 
300 TUMOURS 
 
 tissue. This stroma is often absent at the spreading margin 
 of the growth, the gland cells occurring in and between the 
 tissue elements of the part. 
 
 As stated above, the epithelial elements show two fairly 
 well-marked types of arrangement. They may occur in 
 acini, i.e. with an arrangement of the cells similar to what is 
 found in most normal glands, the epithelial elements lining 
 a space; or, on the other hand, they may occur in solid 
 masses. In the first type the cells tend to be columnar ; in 
 the second type from mutual pressure they assume a rounded 
 or spheroidal form. This difference in the shape of the 
 cancer cells is usually taken as a basis for further division 
 into two types, viz. : (i) Columnar cell carcinoma, and 
 (2) Spheroidal cell carcinoma. By some authorities the 
 term adeno- carcinoma is reserved exclusively for the first 
 type. 
 
 There are other types of carcinomata occurring in certain 
 glandular organs, the cells of which are arranged not in acini 
 but in columns. This arrangement obtains in the liver, and 
 in glandular cancer of the liver the columnar structure may 
 be reproduced. 
 
 Occasionally a tumour may show an acinous arrangement 
 in one part and in another the cells may be massed together. 
 At the same time the tumours of the two types preserve their 
 characters with a fair degree of constancy. 
 
 1. Columnar Cell Carcinoma. Sites. These tumours 
 are found most frequently in the stomach and the intestinal 
 tract. They are also found in the liver, pancreas, uterus, 
 mammary gland, etc. 
 
 Appearance. They may occur as projecting fungating 
 masses (Fig. 69), or merely as ulcerated surfaces with 
 infiltration and thickening of the walls of the gut. There is 
 commonly annular contraction of the gut at the affected 
 point. Secondary deposits are common in the nearest 
 
MALIGNANT TUMOURS 301 
 
 lymph glands and in the liver. Such secondary growths 
 have a very variable appearance. 
 
 Microscopically, these tumours are mainly characterised by 
 a downward growth of the gland elements into the wall of the 
 viscus, so that gland acini are present in the submucous and 
 muscular layers. At the same time the cancerous epithelium 
 differs from the normal. The cells tend to be larger ; they 
 vary somewhat in size and shape. They possess no basement 
 membrane. Mitotic figures may be found in considerable 
 numbers. There is a tendency to form several layers of 
 epithelium instead of one, and sometimes there is no lumen 
 present owing to the multiplication of the gland cells. There 
 is an inflammatory infiltration of the normal tissues at the 
 spreading margin of the growth. Where the tumour is pro- 
 jecting into the lumen of the gut, also when it occurs as large 
 solid masses in organs such as the liver, also in the secondary 
 deposits in glands, a stroma of connective tissue forms which 
 carries the nutrient blood-vessels. 
 
 2. Spheroidal Cell Carcinomata. These tumours are 
 commoner in certain situations, e.g. breast, but they may 
 occur anywhere. It has been customary for long to distin- 
 guish them according to their physical characters into 
 Scirrhous or hard cancers, and Encephaloid or soft cancers. 
 Such names are still in use, and although the distinction 
 depends merely upon the relative preponderance of fibrous 
 tissue and cancer cells, it is convenient to describe them 
 under these headings. 
 
 (a) Scirrhous Cancer. Sites. This is found most typically 
 in the breast, although it also occurs in stomach, intestine, 
 pleura, ovary. 
 
 Appearance. Such tumours are opaque white, tendinous- 
 looking masses radiating into the surrounding parts (Fig. 103). 
 They are very hard, and creak on being cut. Opaque yellow 
 areas of necrotic change are sometimes visible, although 
 these are not nearly so numerous as in the encephaloid type. 
 In the case of the breast there is very commonly indrawing 
 
302 TUMOURS 
 
 of the nipple. The cut surface often becomes depressed and 
 cup shaped. 
 
 Microscopically ', the tumour shows a large preponderance 
 of the fibrous stroma element. This connective tissue in the 
 more central parts is well developed and shows few cells. At 
 the growing margin it is more cellular. In this fibrous stroma 
 are elliptical spaces filled with cancer cells. The cancer cells 
 themselves are spheroidal from mutual pressure, and there is 
 often a space (artificially produced by shrinkage) between them 
 and the fibrous stroma. Mitotic figures may be found. No 
 basement membrane is present. In the centre of the growth 
 the groups of cancer cells may be few and far between. At 
 the growing margin they are more numerous. Occasionally 
 there may be attempts at the formation of a lumen. 
 
 (b) Encephaloid, Medullary or Soft Cancer. Sites. They 
 occur in sites such as the breast, stomach and pancreas. 
 
 Appearance. The tumours in this type tend to be larger, 
 softer, more vascular, and there are more often areas of 
 necrosis. 
 
 Microscopically, they are characterised by a smaller pro- 
 portion of fibrous stroma and a larger proportion of glandular 
 epithelium. The cancer cells vary in size, but they occur 
 in much larger masses than in the scirrhous type. Further, 
 necrotic changes are very commonly present amongst them. 
 
 3. Colloid Cancer is a special type of Adeno-carcinoma, 
 characterised by the accumulation of mucinous material in 
 the spaces, which becomes inspissated and hence gum-like in 
 consistence. 
 
 Sites. The stomach, large intestine and mammary gland 
 are the common sites for such growths. 
 
 Appearance. It appears as gelatinous translucent material, 
 in greater or less amount, in the tumour and its secondary 
 deposits. Otherwise the growth has the appearance of a 
 columnar cell carcinoma. 
 
TERATOMATA 303 
 
 Microscopically, these tumours often show in parts the 
 characters of the ordinary columnar cell carcinoma. In other 
 parts, the gland acini are dilated and the lumen filled with 
 homogeneous or slightly fibrillated material. The cells are 
 often vacuolated from the presence of secretion. They 
 become detached from the fibrous stroma and eventually 
 disappear altogether, fusing with the mucinous contents of the 
 spaces. 
 
 0. TERATOMATA 
 
 There remains for consideration a number of tumour 
 formations traceable to some defect in the development of 
 the individual, also others due to the grafting of the embryo's 
 tissues upon the maternal organism. 
 
 To the first group belongs the Teratoma properly so 
 called or Dermoid Cyst. 
 
 Such tumours are, as their name indicates, usually found 
 in the form of cysts. The cyst wall is developed from the 
 tissues of the host. The wall is lined by skin epithelium and 
 encloses chiefly soapy-looking material and hairs, frequently 
 also teeth, skin, bone, cartilage, muscle, nerve elements it 
 may be, and rudimentary viscera. The causation of the 
 condition is, in most cases, the inclusion of the elements of 
 one individual within the body of another. The growth is 
 simple in nature. 
 
 Site. The site of such tumours is commonly in or near the 
 ovary (Fig. 102), but they may also occur in the testicle, the 
 neighbourhood of the sacrum, the side of the neck and face ; 
 also very occasionally in the brain. 
 
 Appearance. The tumour varies much in size. Occasionally 
 it may be as large as a foetal head. As a rule there is a point, 
 the so-called " protuberance/' which represents the head and 
 from which arises a tuft of long hairs. 
 
 Microscopically, dermoid cysts show a great variety of types 
 of tissue stratified squamous epithelium, sweat glands, hair 
 
304 TUMOURS 
 
 follicles, cartilage, bone, gland acini lined by epithelium of 
 various kinds, etc. 
 
 To the second group (those due to the grafting of embryo 
 tissues upon the maternal organism) belong (a) the placental 
 mole, or myxoma of the chorion, already described on p. 268 ; 
 and (b) the chorion-epitlielioma or deciduoma malignum. 
 
 Chorion-Epithelioma 
 
 This is an exceedingly malignant condition which may 
 follow an abortion or full-time pregnancy, also its simple 
 analogue the placental mole. 
 
 The outer surface of the chorionic villi consists of the layers 
 of foetal epiderm. The most external (syncytium) is formed of 
 multinucleated masses of protoplasm (giant cells). These 
 possess normally intense phagocytic properties, whereby the 
 villi are enabled to penetrate the maternal tissue and come to 
 lie within the blood sinuses of the uterus. Underneath this layer 
 is a second, in which the cells are separate and do not stain so 
 deeply. This is what is known as the Langhans layer. 
 
 After an abortion or full-time pregnancy the layers of cells 
 covering the chorionic villi may take on abnormal growth ; 
 developing into a tumour which is essentially cellular (having 
 no intercellular material), which shows no arrangement of its 
 elements and possesses no blood-vessels. 
 
 Sites. The usual site for such tumours is the uterus, 
 following abortion or full-time pregnancy. Occasionally 
 they occur independently of pregnancy, as for example 
 in the testicle. Such are probably due to germ cells taking 
 on active development and producing a trophoblast (the two 
 layers of cells covering the villi are known as trophoblast) 
 from which the tumour arises. 
 
 Appearance. Such a tumour appears as a soft spongy 
 vascular mass in the wall of the uterus. Necrosis and haemor- 
 rhage are characteristic features of it, Metastatic growths 
 
TERATOMATA 305 
 
 develop very early and are found especially in the lungs, but 
 also in the liver and kidneys. 
 
 Microscopically, two types of cells are found in the parts of 
 the tumour which are not necrosed : (i) large plasmodial 
 masses, mostly multinucleated, derived from the synctium, the 
 nuclei of which are in rapid division and show all varieties of 
 abnormal mitoses ; (2) groups of smaller, polyhedral cells 
 derived from the Langhans layer. Both types of cell are 
 found in the uterine wall penetrating the tissues and eroding 
 blood-vessels. 
 
 TABLE OF TUMOURS 
 
 A. SIMPLE TUMOURS 
 
 Fibroma, Myxoma, Lipoma, Chondroma, Osteoma, Myoma, 
 Angioma, Lymphoma, Glioma, Papilloma, Adenoma. 
 
 B. MALIGNANT TUMOURS 
 
 (a) Sarcomata 
 
 Small round-celled, Lymphosarcoma, Large round-celled, Small 
 spindle-celled, Large spindle-celled, Mixed celled, Myeloid, 
 Chondro-sarcoma, Osteo-sarcoma, Endothelioma, Alveolar, 
 Peritheiioma, Angiosarcoma, Myeloma, Melanotic. 
 
 (b) Carcinomata 
 
 I. Squamous Epitheliomata. 
 
 Rodent ulcer. 
 II. Adeno-Carcinomata. 
 
 1. Columnar Cell Carcinoma. 
 
 2. Spheroidal Cell Carcinomata. 
 Scirrhous, Encephaloid. 
 
 3. Colloid Cancer. 
 
 C. TERATOMATA 
 
 I. Dermoid Cyst. 
 II. Embryomata. 
 
 Myxoma of Chorion (simple). 
 Chorion-Epithelioma (malignant). 
 
CHAPTER XV 
 
 POINTS TO BE REMEMBERED IN PERFORMING AUTOPSIES 
 ON CASES WITH A MEDICO-LEGAL ASPECT 
 
 GENERAL METHOD OF PROCEDURE IN 
 MEDICO-LEGAL CASES 
 
 IT must be remembered that all cases of death which have occurred 
 suddenly or unexpectedly, and cases of death where no medical 
 man has been in attendance, as well as all cases of death from 
 violence whether the result of accident, suicide or homicide, are 
 the subject of inquiry by the authorities in Scotland the Pro- 
 curator-fiscal and in England the Coroner and that in all 
 cases of the above nature a post-mortem should not be made 
 without instruction from the authorities. 
 
 It must also be noted that in cases of accidental injury to 
 work-people, in which death ensues either at the time, or, it 
 may be, months afterwards, a public inquiry may be held by 
 the authorities, and that therefore a post-mortem should not 
 be made until the authorities have been communicated with. 
 
 In performing a medico-legal post-mortem, the following 
 precautions should be exercised. 
 
 1. The body should, if possible, be identified by relations 
 or the police in the presence of the doctor before the post-mortem 
 is commenced. 
 
 2. Under all circumstances, such a post-mortem must be 
 complete, i.e. every cavity and organ must be examined. 
 
 306 
 
MEDICO-LEGAL POST-MORTEMS 307 
 
 Note. Unless there are special circumstances indicating 
 its necessity, it is not usual to examine the spinal cord. 
 
 3. If there is any suspicion of poisoning, the following 
 tissues should be preserved : 
 
 (1) Stomach and its contents. 
 
 (2) Intestines and their contents. 
 
 (3) Liver (at least half). 
 
 (4) Kidney and spleen. 
 
 (5) Some blood. 
 
 (6) Urine. 
 
 In special cases it may be advisable to remove other organs, 
 such as the brain, lungs, etc. 
 
 4. All tissues, etc., removed must be placed in glass vessels 
 which are chemically clean, which should then be made air- 
 tight, sealed and labelled. The label should bear on it the 
 nature of its contents, and the date of the post-mortem, and 
 should be signed by the doctor. 
 
 Each tissue or organ should be preserved in a sepa- 
 rate vessel, and no preservative of any sort should be 
 used. 
 
 In Scotland the medical examiner must write a report of 
 the examination in " soul and conscience" form. 
 
 This medical report must contain the following : 
 
 (1) Date and place. 
 
 (2) State by whom body has been identified. 
 
 (3) Where the examination was performed. 
 
 (4) An account of the external appearances. 
 
 (5) An account of the internal appearances. 
 
 (6) Conclusion from above as to the cause of death. 
 
 It is essential that any alterations should be initialled, 
 but it is better to rewrite the report if additions or alterations 
 have to be made. 
 
 No opinions other than the conclusion as to the cause of 
 death should be given in the report. 
 
 No technical terms should be employed in writing the 
 
308 MEDICO-LEGAL POST-MORTEMS 
 
 report. The language used should be, as far as possible, 
 popular. 
 
 The report should be signed by the medical man or men, 
 their medical qualifications being appended. 
 
 The report is sent to the Procurator - Fiscal of the 
 district. 
 
 In England a written report is not as a rule sent to the 
 Coroner. The doctor gives his evidence usually at the 
 Coroner's inquest, and should have his notes of the post- 
 mortem examination with him. His evidence at the inquest 
 is given on oath, and it should be remembered that all state- 
 ments made there are written down, forming his " deposition/' 
 and that this deposition is produced in any subsequent 
 proceedings. 
 
 POST-MORTEMS ON NEWLY-BORN INFANTS 
 
 In performing sectios upon newly -born children the 
 questions which require answering are : 
 
 1. Was the child viable ? i.e. was development sufficiently 
 far advanced for the child to be able to live apart from the 
 mother ? 
 
 2. Did the child actually live (i.e. breathe) either during 
 or after birth ? 
 
 3. If the child lived, what was the cause of its death ? 
 In order to be able to answer these questions the points of 
 
 chief importance to note are : 
 
 External Examination. Note the length of body, weight, 
 the condition of the finger-nails, the presence of the testicles 
 in the scrotum ; the presence or absence of a caput succeda- 
 neum (the presence of such indicating that the blood was 
 circulating during birth) and head moulding. 
 
 The condition of the umbilical cord, whether cut or torn, 
 and whether any evidence of a line of separation having 
 formed. 
 
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3io MEDICO-LEGAL POST-MORTEMS 
 
 The presence of vernix caseosa, blood and injuries to the 
 skin. 
 
 The neck should especially be observed for abrasions. 
 
 The mouth and nostrils should be inspected for the presence 
 of froth or any obstructing body. 
 
 Internal Examination. Attention should be first con- 
 centrated upon the air-passages and lungs in order to deter- 
 mine the question, Has the child breathed ? 
 
 The trachea should be opened and carefully examined for 
 the presence of froth. Some authorities recommend the 
 tying of the trachea before opening the thorax. This is not 
 necessary. 
 
 After opening the thorax, the contents of the thoracic 
 cavity lungs, heart and thymus gland are removed and 
 placed entire in a pail of water. If the whole mass floats, 
 there can be no further doubt about the question of the child 
 having breathed. Should the organs sink, then the individual 
 lungs should be carefully examined as to the presence of any 
 mottled areas that would indicate partial aeration. The 
 organs should then be cut up and the separate portions tested 
 as to their capacity to float. It may be advisable in some 
 cases to examine portions of the organs microscopically. 
 (For the appearance of the non-aerated lung, see Atelectasis, 
 p. 120.) 
 
 Thereafter the examination proceeds in the usual manner, 
 attention being, however, specially directed to the presence of 
 air in the stomach and small intestine as conclusive evidence 
 of breathing ; also to the presence of food in the stomach as 
 evidence of the child having survived its birth for some 
 time. 
 
 In all cases the presence or absence of an ossific node at the 
 lower end of the femur must be determined in connection with 
 the conclusion as to the stage of maturity attained (see table, 
 p. 309). For this purpose the cartilage of the epiphysis 
 should be cut away in thin layers. This should be done until 
 
MEDICO-LEGAL POST-MORTEMS 311 
 
 the diaphysis is reached in order to be quite certain as to the 
 presence or absence of such a node. Another important 
 centre of ossification for purposes of determining the stage 
 of maturity reached by the child is that of the cuboid (see 
 table, p. 309). 
 
 The common causes of death in the new-born child are 
 as follows : 
 
 1. Compression of the umbilical cord. 
 
 2. Protracted delivery. 
 
 3. Malnutrition and immaturity. 
 
 4. Haemorrhage from the cord. 
 
 5. Fracture, usually of bones of skull. 
 
 6. Accidental asphyxia. 
 
 7. Congenital malformation or disease. 
 
 Among the modes by which death may be caused in cases 
 of infanticide are the following : 
 
 1. Suffocation. 
 
 2. Strangulation. 
 
 3. Drowning. 
 
 4. Fracture of skull. 
 
 5. Exposure and neglect. 
 
 6. Haemorrhage from the cord. 
 
 POST-MORTEM CHANGES PRODUCED 
 BY POISONS 
 
 As stated elsewhere (p. 21), in cases of poisoning or sus- 
 pected poisoning, after examination of the lips and mouth, 
 the tongue, together with the fauces, oesophagus, stomach, 
 and duodenum, should be removed and examined in con- 
 tinuity. 
 
 It should be carefully borne in mind that with certain ex- 
 ceptions the appearances in cases of poisoning are by no means 
 characteristic. There may be nothing at all in the alimentary 
 tract to suggest poisoning. Hence the necessity in all suspicious 
 
312 MEDICO-LEGAL POST-MORTEMS 
 
 cases for the preservation of the organs and stomach contents for 
 subsequent chemical analysis. 
 
 Appearances in Poisoning with Corrosives. In all such 
 cases there is softening of the tissues of the upper alimentary 
 tract lips, mouth, oesophagus and stomach. Sometimes 
 there is necrosis of the superficial layers of viscera. The stomach 
 shows swelling and contraction of its walls, extravasation of 
 blood, which under the influence of the acid becomes black) 
 ulceration, and sometimes perforation. The lining shows in 
 some cases a characteristic colouring, e.g. in the case of nitric 
 acid a yellow colour. The appearances in sulphuric and hydro- 
 chloric acid poisoning are very similar and cannot in many 
 cases be differentiated. The only point of distinction is that 
 sulphuric is a stronger acid than hydrochloric, hence the 
 corrosion is more intense and there is a greater tendency to 
 perforation ; the appearances varying, however, according to 
 the dilution of the poison. The mucous membrane may be 
 charred to a dark brown or black colour, or the appearances 
 may be merely those of an intense gastritis. In poisoning 
 with carbolic, if the acid has been taken in a concentrated 
 form, there is necrosis of the mucous membrane particularly of 
 the stomach with the formation of a putty-like layer. If the 
 acid has been dilute, the interior of the stomach is dusky 
 red from hyperaemia. 
 
 In the case of oxalic acid there are as a rule no external 
 appearances. When the acid has been taken in the concen- 
 trated form there is a whitish appearance of the mucous membrane 
 inside the mouth. When dilute, the appearances are those 
 of irritation, viz. congestion. 
 
 In poisoning with caustic alkalies the appearances are 
 somewhat similar to those found in the case of acids, but the 
 tissues have a characteristic soapy feel. In ammonia poisoning, 
 in addition to the appearances of corrosion in the alimentary 
 tract, there is generally acute inflammation in the air-passages. 
 
MEDICO-LEGAL POST-MORTEMS 313 
 
 Appearances in Irritant Poisoning. The common irritant 
 poisons, such as arsenic, antimony, mercury, produce changes 
 which do not differ to any extent from one another. By the 
 mere naked-eye examination of the parts, beyond the fact that 
 the appearances may be those of acute gastritis and enteritis, 
 there is little that is characteristic. In some instances, even when 
 the poison has been taken in a concentrated form, there 
 may be little to suggest that the case is one of poisoning. 
 As a rule, however, the mucous membrane of the alimentary 
 canal in its upper part is swollen and in parts hyper&mic. In 
 other words, the appearances are those of gastro-enteritis. 
 Occasionally there is ulceration. 
 
 In the case of phosphorus poisoning, in addition to the 
 evidence of irritation in the alimentary tract, there is extreme 
 fatty change in the liver (which is of a bright yellow colour), 
 also in the kidney and heart. Such cases have to be distin- 
 guished from acute yellow atrophy of the liver (see p. 183), 
 severe anaemias, and toxaemias. The distinction can, of 
 course, be readily made on carrying out a chemical analysis 
 of the organs. 
 
 Appearances in Poisoning with Gases. In poisoning with 
 carbon dioxide the appearances are merely those of suffocation. 
 The face, lips, and ears have a dark purple colour. 
 
 The appearances in carbon monoxide (carbonic oxide) 
 poisoning are as a rule typical. Externally, the post-mortem 
 lividity is of a pink or light red colour, and the same colour 
 can often be seen in the lips, conjunctive, and nails. 
 Internally, while the blood in bulk may show no change yet 
 wherever it is in a thin layer, e.g. the mesentery, etc., the 
 pink or light red colour is most striking. The liver, spleen, 
 kidneys and other organs frequently show the same change 
 of colour. 
 
 A simple but effective test can be carried out as follows : 
 Take two test-tubes partly filled with tap water ; add to one 
 
314 MEDICO-LEGAL POST-MORTEMS 
 
 a few drops of normal blood and to the other a few drops of 
 blood from the body which is being examined. Normal blood 
 when diluted in this way will always give a yellow colour. 
 Blood containing carbonic oxide, on the other hand, however 
 much it is diluted, will always be pink. 
 
 A conclusive diagnosis can be made chemically as follows : 
 A small quantity of normal blood is placed in a test-tube and 
 diluted with three or four times the amount of tap water. A 
 small quantity of blood from the case under investigation is 
 similarly treated. A small amount of tannic acid is dissolved 
 in three times its bulk of water. Add some of this solution to 
 both test-tubes and shake. In the case of the normal blood a 
 chocolate brown precipitate will form. Should the blood from 
 the case contain carbon monoxide the precipitate will be a 
 rose red. 
 
 In poisoning with ammonia gas there is intense inflamma- 
 tion in the respiratory passages. 
 
 In poisoning with alkaloids, such as morphine, strychnine, 
 etc., there is usually absolutely no abnormality visible. 
 Occasionally tablets of the poison are found in the stomach. 
 
 In cyanide poisoning the characteristic odour may be 
 observed by those with a trained sense of smell. Similarly 
 in poisoning with chloral, sulphonal and chloroform. 
 
 The appearances in cases of vegetable poisoning are in 
 no case very characteristic. Search should be made in the 
 intestinal tract for the presence of seeds, leaves, or other 
 evidence of vegetable tissue. 
 
 In cases of meat poisoning, cultures should be made from 
 the intestinal contents and from the spleen. Blood should 
 be removed in order to test the serum against various micro- 
 organisms for the presence of specific agglutinins (see p. 374). 
 
MEDICO-LEGAL POST-MORTEMS 315 
 
 SPECIMEN POST-MORTEM REPORTS 
 
 The following are typical post-mortem reports in the form 
 in which they should be sent to the Procurator-Fiscal : 
 
 EDINBURGH, ^th June 1909. 
 
 WE hereby certify on soul and conscience, that by instructions 
 of the Procurator-Fiscal of the County of Midlothian, on 
 
 SATURDAY, $rdjune 1909, 
 
 in the Mortuary of Edinburgh Castle, we examined the body 
 of a man which was identified in our presence by 
 
 Sergeant JOHN SMITH, 
 and by one of us, 
 
 Captain JONES, R.A.M.C., 
 
 as that of 
 
 Private JAMES SCOTT. 
 
 The body was that of a well-built muscular man, 7o| inches 
 in height, and apparently about thirty-five years of age. The 
 body showed no signs of putrefaction, and the usual post- 
 mortem rigidity and lividity were present. 
 
 Situated on the right side of the chest, and in a line drawn 
 between the junction of the collar bone and breast bone above 
 and the right nipple below, there was a linear wound one and 
 a half inches in length, the edges of which had been brought 
 together by means of three stitches. The upper extremity of 
 this wound was distant one and a half inches and the lower 
 end two and a quarter inches from the middle line of the body. 
 This wound was found, in the first instance, by means of a 
 blunt probe, and subsequently, during the course of the dissec- 
 tion, to proceed obliquely through the second intercostal space 
 downwards, backwards, and towards the left side, and to pass 
 through the upper lobe of the right lung near its anterior 
 
3i6 MEDICO-LEGAL POST-MORTEMS 
 
 margin, into the pericardium, and finally to enter the right 
 auricle of the heart above the auricular appendage and close to 
 the junction of the superior vena cava with the auricle. The 
 length of the wounds in the lung and pericardium was one 
 inch, and that in the auricle half an inch. 
 
 With the exception of the injury above described, the body 
 presented no marks of external violence. 
 
 The right pleural cavity was full of coagulated blood. The 
 right lung was collapsed and bloodless. The left lung was 
 healthy. The heart contained some coagulated blood, and 
 with the exception of the wound in the right auricle, was 
 normal. 
 
 The liver, spleen, kidneys, and other abdominal organs 
 presented normal appearances. 
 
 The stomach contained a quantity of green bilious fluid. 
 Its mucous membrane was in the condition of chronic catarrh. 
 
 The mouth, upper air-passages and trachea were healthy. 
 
 The brain and its membranes were congested, but other- 
 wise they were normal. 
 
 From the foregoing examination we are of opinion that 
 death was due to loss of blood from a wound of the heart 
 produced by a sharp, pointed instrument. 
 
 Signed by the two medical men 
 present at the post-mortem. 
 
 B 
 
 EDINBURGH, 2otk May 1897. 
 
 WE hereby certify upon soul and conscience, that we 
 yesterday, 
 
 THURSDAY, zoth May 1897, 
 
 examined, in the Royal Infirmary, the body of a man, which 
 was identified in our presence by 
 
MEDICO-LEGAL POST-MORTEMS 317 
 
 the Wife of the deceased, 
 by a Police Constable, and by the 
 House Surgeon attending the case, 
 as that of 
 
 THOMAS ROBINSON. 
 
 Deceased was an able-bodied person, apparently about 
 sixty years of age. The only mark of violence observable was 
 a lacerated wound of the nose, situated on the prominence, 
 and about a quarter of an inch in length. Its edges were 
 somewhat swollen and gaping. It was partially covered with 
 a soft scab. The root of the nose was also somewhat swollen. 
 
 The various cavities and their contents were carefully 
 examined ; but with the exception of marked congestion of the 
 spinal cord, and the effects of the wear and tear of life, nothing 
 unusual was detected. 
 
 Portions of the heart, liver, and kidneys were subjected to 
 examination by the microscope. They were all more or less 
 fatty, but not to a great extent. 
 
 We are of opinion that the cause of death in this case was 
 acute congestion of the spinal cord, such as we are conversant 
 with in fatal cases of Tetanus. 
 
 Signed by the two medical men 
 present at the post-mortem. 
 
APPENDIX A 
 
 TREATMENT OF SPECIMENS FOR MOUNTING 
 
 Fixatives. In many cases the pathologist will meet with 
 specimens which he wishes to preserve for purposes of 
 further examination, reference, or teaching. It is his object 
 to keep, as far as possible, the form of the organ or part 
 and its natural colour. For this purpose the tissue must be 
 fixed. The best all-round fixative is certainly formalin, but 
 by itself it does not penetrate well, and the colour is not well 
 preserved. Salts of various kinds should be mixed with it. 
 The resulting fluids are variously known as Pick's, Jores's, and 
 Kaiserling's solutions. The formulae for making up these are 
 given on pp. 322-3. Of the three, probably Pick's solution 
 costs least to prepare. There is, however, little to choose 
 between them as regards results. The explanation underlying 
 the preservation of the colour of the organ in the case of all 
 three is as follows : the oxyhaemoglobin is transformed by the 
 formalin into acid haematin which has a brown colour ; this, 
 under the influence of the alcohol, becomes alkaline haematin, 
 which has a bright red colour so like the original oxyhaemo- 
 globin that the natural colour appears to have returned. 
 
 Method of preparing Specimens. The specimen is placed 
 in this fluid after having been cut open, or after having the 
 fluid injected into it, the object being to secure the penetration 
 of the organ or part by the fluid so as to prevent subsequent 
 shrinkage or deformity. Specimens are treated differently 
 according to their nature and consistence. It should always 
 be remembered that a large excess of fluid is necessary for 
 proper fixation. 
 
 319 
 
320 APPENDIX A 
 
 Solid Organs. There are two ways of dealing with solid 
 organs, such as liver and spleen, if it is desired to preserve 
 the organ whole. Fixative must either be injected into the 
 main vessel in the case of the liver, the portal vein or the 
 fluid is injected here and there into the substance of the 
 organ with a syringe. 
 
 In most cases it is not necessary to preserve the whole 
 organ, in which case the best way is to cut it into a series of 
 parallel slices about an inch thick. In the case of the kidney 
 it is sufficient to open up the organ in the usual way. The 
 brain is best injected through the large arteries at the base. 
 In the case of superficial exudates in the meninges or else- 
 where some stronger formalin may be smeared over the 
 surface so as at once to fix the material. When dealing with 
 large tumours, it is well to inject fluid with a syringe here and 
 there, more especially in the softer parts. 
 
 Groups of Organs. When dealing with a group of organs, 
 it may be necessary to fix them prior to removal. This can 
 be done by injecting fixative into the circulation through one 
 of the carotids or into a main vessel going to the part. 
 
 Lungs. In the case of the lungs, it is best to inject the 
 fluid into the bronchi, and, in addition, into any cavity or area 
 of softening, before opening up the organs. If they have 
 already been opened, it is usually sufficient to immerse each 
 half in fixative. 
 
 Cysts. When dealing with cysts, such as hydronephrosis, 
 pyonephrosis, hydatid cysts, etc., the greater part of the fluid 
 in the cyst should be removed with a syringe and replaced by 
 fixative. 
 
 Intestine. Portions of the intestine should either be opened 
 up, washed, laid flat or pinned out flat, and immersed in 
 fixative ; or they may be washed out by running water through 
 them, then, having tied one end, fixative is poured in at the 
 upper end, the upper end tied, and the whole immersed in 
 fluid. This latter method is more especially adapted to the 
 preservation of tumours, the bowel being subsequently slit up 
 into two halves, as has been done in the case of Fig. 69. 
 
 Time necessary for Fixation. As regards the time during 
 which specimens should remain in the fixative, this depends 
 upon their size and consistence. Thin tissues, such as 
 
APPENDIX A 321 
 
 intestines treated as above, are fixed in twenty-four hours. 
 Lungs injected through the bronchi, and brains injected 
 through their vessels, will be fixed sufficiently for cutting in 
 forty-eight hours. It is necessary, however, to leave the 
 slices some time longer in the fixative. For more solid organs, 
 such as liver, kidney, spleen, or heart, ten days to three weeks 
 will usually suffice, but the specimens take no harm from 
 remaining considerably longer. A good test as to whether 
 or no an organ is fixed is to squeeze it. If red blood exude, 
 it is well to leave the specimen some time longer. Another 
 test is, of course, the consistence of the organ. As a rule, so 
 long as it is soft, further fixation is required. 
 
 Mounting Fluid. When properly fixed, the organ is 
 washed in clean water for some minutes and placed over- 
 night in methylated spirit, which may have been previously 
 used. It is then placed in fresh, clean spirit, until the colour 
 has returned ; a few hours is usually sufficient. The specimen 
 is then washed again in running water for a few minutes, and 
 placed in the following fluid : 
 
 Glycerine (pure) . . I part. 
 
 Water . . . . .2 parts. 
 
 To each Winchester quart of the above, I fluid oz. of formalin 
 (40 per cent) is added, also I oz. of a saturated solution of pure 
 potassium acetate. The object of the formalin is to prevent 
 the growth of mould. This fluid should be changed once or 
 twice, and when the specimen is finally mounted in a glass 
 jar, the same fluid should be filtered in. In such a fluid a 
 specimen will remain soft and retain its natural colour for 
 many years. Care should, however, be taken not to expose 
 the specimen to direct sunlight, otherwise fading of the colour 
 will occur. 
 
 Mounting. When selecting a jar for permanent mounting, 
 the nature and size of the specimen will, of course, be taken 
 into consideration. As a rule, the rectangular glass jars are 
 the best, the specimen being fixed to one side of the jar by 
 means of a little gelatine, or secured to a plate of glass 
 with strong thread. Whole hearts and spleens are best sus- 
 pended in round jars. Portions of intestine laid open can 
 
322 APPENDIX A 
 
 be stretched upon sheets of glass or mica, or within a frame 
 formed of a bent glass rod. The interior of cavities and the 
 "surfaces of organs are best coated with gelatine fluid, which is 
 prepared as follows, in order to prevent portions coming away 
 and producing turbidity : 
 
 100 grains pure gelatine 
 
 800 c.c. thymol water (saturated in the cold) 
 
 200 c.c. glycerine. 
 
 This is gently heated until the gelatine melts. A few drops 
 of acetic acid are added, and the whole is clarified with white 
 of egg. The gelatine is poured upon the specimen while 
 warm and fluid and allowed to solidify before the specimen is 
 mounted. For fixing on the cover of the jar the best medium 
 is a mixture of litharge and Archangel tar in quantities 
 sufficient to make a thick paste. A band of Berlin black 
 should then be painted round the margin of the cover. 
 
 Summary of Steps in Treatment of Specimens 
 for Mounting 
 
 1. Place in Pick's, Jores's, or Kaiserling's fixative (for 
 composition see below) for a variable period depending upon 
 size, consistence, etc., of specimen. 
 
 2. Wash in clean water for some minutes. 
 
 3. Place overnight in methylated spirit which has been 
 previously used. 
 
 4. Transfer to fresh spirit for a few hours until colour 
 returns. 
 
 5. Wash in running water for a few minutes. 
 
 6. Place in glycerine and water (one part of the former to 
 two of the latter), to which potassium acetate ('i ounce sat. 
 sol. to Winchester quart) is added, also formalin to prevent 
 the growth of moulds. 
 
 7. Mount in fresh fluid of similar composition. 
 
 Pictts Fixative 
 
 Formalin (pure, i.e. 40 per cent) . . 50 c.c. 
 Artificial Carlsbad salt . . . .50 grm. 
 Distilled water . . j litre. 
 
APPENDIX A 323 
 
 The Carlsbad salt is prepared by mixing Sod. sulphate 22 
 parts, Sod. bicarb. 18 parts, Sod. chloride 9 parts, Pot. 
 sulphate i part. The last ingredient is not essential. 
 
 Kaiserling's Fixative 
 Formalin ...... 100-200 c.c. 
 
 Pot. nitrate . . . . . 15 grm. 
 
 Pot. acetate . . . . -3 g rm - 
 
 Water ...... I litre. 
 
 Jores*s Fixative 
 Formalin . . . . . .50-100 c.c. 
 
 Mag. sulph. . . . . .20 grm. 
 
 Sod. sulph. ...... 20 grm. 
 
 Sod. chloride . . . . .10 grm. 
 
 Water . . . . . . i litre. 
 
 In each case to obtain the best results the formalin used should 
 be Schering's. It costs about twice the price of the ordinary 
 commercial formalin, but it is greatly superior in quality. 
 
 The salts for the various fixatives may be made up in 
 packets and mixed with the water and formalin as required. 
 
 In the case of each of the methods, after fixation is 
 complete the specimen is transferred to methylated spirit in 
 which the acid haematin becomes alkaline and the colour thus 
 returns to the blood in the tissue. 
 
 After twenty-four hours in spirit the specimen is placed in 
 a preservative which in each instance contains glycerine as 
 its principal ingredient. As a rule the glycerine is diluted 
 with double the quantity of water to which potassium acetate 
 (in the case. of Pick's and Kaiserling's method) is added. 
 
 Recently Mr. R. Frost of Sheffield (Proc. Path. Soc. Great 
 Britain and Ireland, Jan. 1912) has proposed the following as 
 a preserving medium : 
 
 Sod. fluoride . . . . .80 grm. 
 Chloral hydrate . . . . .80 grm. 
 
 Pot. acetate 160 grm. 
 
 Cane sugar (Tate's cube) . . .3500 grm. 
 Thymol water (saturated) . . .8 litres. 
 
 The chief advantage of this medium is its cheapness. 
 
324 APPENDIX A 
 
 TREATMENT OF TISSUES FOR MICROSCOPIC 
 PURPOSES 
 
 Necessity for Routine Microscopic Examinations 
 
 For a complete investigation of a fatal case of disease, it is 
 necessary not only to examine as many parts of the body as 
 possible with the unaided eye, but to investigate them further 
 by means of the microscope. This routine examination of the 
 organs microscopically cannot be too strongly insisted upon. 
 Where only specimens of exceptional interest are put through and 
 cut, the pathologist will never be able to acquire skill in differ- 
 entiating the finer shades of pathological change. Further, 
 diseased tissues do not always bear their secrets stamped 
 upon them plainly, and unless a microscopic examination is 
 carried out as a matter of routine, much that is of exceptional 
 interest will be lost. 
 
 Selection of Portions of Organs or Tissues 
 
 As regards selection of a portion of a diseased organ, no 
 definite rules can be laid down. It is well not to be satisfied with 
 a single portion, but to take several pieces from different parts. 
 Where one is dealing with a tumour, one section should include 
 the capsule or a portion of any invaded tissue. If the tumour 
 be in the bowel, along with the portion should be taken a piece 
 of the normal gut wall. In the case of such organs as kidney, 
 liver, and spleen, one section at any rate should include the 
 capsule. Sections of the kidney should of course include both 
 cortex and medulla. 
 
 It is not at all a bad plan to cut the different organs in 
 different ways, or at any rate to pare them down to different 
 shapes after they have been passed into spirit. Thus, kidney 
 may be cut as a triangle, the base being the capsule, liver cut 
 in squares, and spleen in the form of a rectangle. The 
 advantage of this method is that afterwards, when the tissues 
 are being passed through the various reagents and also when 
 in paraffin, they may be recognised at a glance. 
 
 In any case, the section of the organ should be thin. It 
 
APPENDIX A 325 
 
 cannot well be too thin. A good average thickness, except 
 for certain purposes, is -| inch. In the case of tissue which is 
 to be fixed in such mixtures as Flemming's or Marchi's still 
 thinner sections are required. This does not mean that the 
 pieces of tissue must not be large. Asa matter of fact, it is 
 most advantageous to have large sections, although they are 
 much more difficult to cut with the microtome. In the case 
 of lung preparations, it may be safely said that the sections 
 cannot be too large. It is exceedingly difficult, if not im- 
 possible, to judge of the nature and distribution of pulmonary 
 diseases from a minute portion of lung taken out at random. 
 
 These statements do not apply to sections for all purposes. 
 When examining minute changes by serial sections, it is 
 well to have small pieces for cutting, because it is obviously 
 much more easy to find corresponding areas in the sections 
 above and below any given point if the portion of tissue is 
 minute. 
 
 When dealing with portions of the bowel, it is well to pin 
 out a fairly large area of intestine upon a small block of wood 
 and immerse both in the fixative. Subsequently, smaller 
 portions may be cut or snipped out. For any of the above 
 purposes a sharp scalpel or razor is required. In certain cases 
 it may be advisable to fix the specimen entire before cutting 
 away any portion for microscopic examination. This par- 
 ticularly applies to tumours of the stomach and bowel. In 
 any case, it never spoils a specimen neatly to cut out a small 
 piece for microscopic purposes. 
 
 It is well at the same time as one takes the sections to 
 make a note of any matter of importance upon the label of the 
 bottle in which the tissues are to be placed, such as the part of 
 the organ from which the specimen was taken. Instead of 
 pasting it on the bottle, the label written in pencil may be 
 placed inside the bottle along with the specimens. 
 
 Fixation of Tissue 
 
 It is impossible to cut in the fresh condition sections of 
 organs thin enough for microscopic purposes. Parenchy- 
 matous cells and softer parts* fall out, leaving a mere 
 skeleton of fibrous tissue. It is necessary therefore, in the 
 
326 APPENDIX A 
 
 first place, to fix the tissue. There are many fixatives for 
 tissues, but for ordinary purposes 10 per cent formalin (i.e. 
 10 per cent of the commercial 40 per cent formaldehyde) 
 is probably the best. It is readily procured and made up, 
 penetrates well, and gives excellent results. For this purpose 
 undoubtedly Schering's formalin is the best. With other brands, 
 costing less, precipitates are very apt to form, especially 
 in tissues containing much blood. For certain purposes other 
 fixatives may be employed, and as a matter of fact, when 
 dealing with cases of special interest, it is well to use more 
 than one fixative. One of the advantages of formalin is that 
 other methods of fixation can be employed subsequently, such 
 as bichromate of potash and osmic acid ; another is that sections 
 can be placed in gum, frozen, and cut directly from the formalin 
 solution. As in all methods of fixation, it is essential to have 
 plenty of fluid at least twenty volumes of fluid to one of 
 tissue. 
 
 Treatment of Tissue for cutting in Gum 
 
 Suitable portions of tissue are placed in the 10 per cent 
 formalin, and are left for twenty-four hours. In the case of thick 
 pieces, it is well to leave them longer. At the end of that time, 
 if a rapid diagnosis is required or if it is necessary to stain for 
 the presence of fat, pieces of the organs can be transferred 
 directly from the formalin to a gum solution made up as 
 follows : 
 
 Gum Arabic . . i part, 
 Water . . .3 parts, 
 Thymol, a few crystals, 
 
 and subsequently frozen and cut. 
 
 Although good results are obtained by cutting directly after 
 fixation in formalin it is better to harden in spirit for 24 hours 
 or longer, to wash out the spirit in running water overnight, 
 and subsequently to place in gum solution for some hours. 
 
 Other Methods of Fixation 
 
 i. For the brain, cord, or other portion of the nervous 
 system, where it is desired to preserve the myelin sheath of 
 
APPENDIX A 327 
 
 the nerve elements, it is necessary to fix the myelin substance 
 by bichromate of potassium or other similar salt. For this 
 purpose, Miille^s fluid is as good as many others of more 
 recent introduction. It is made up as follows : 
 
 Bichromate of potassium . . 2-5 grm. 
 
 Sulphate of sodium . . I grm. 
 
 Water . . . . . .100 c.c. 
 
 The sodium sulphate of the Miiller's fluid may, according to 
 Mann, be omitted without the solution suffering as a fixative. 
 
 Portions of brain or cord may be placed in this direct or, 
 better, transferred to it from formalin. They should be left in 
 the fluid for six to eight weeks, washed thoroughly in running 
 water for some hours, and transferred first to 50 per cent 
 spirit, then 75 per cent, lastly pure spirit. The bichromate 
 fluid should be changed freqitently during the process of 
 fixation. The process can be hastened considerably by 
 placing the fixative containing the pieces of cord in the 
 incubator at 37 C. 
 
 Although tedious, the above method gives very good 
 results, even with specimens which have to be stained with 
 ordinary methods. Miiller's fluid also forms the basis of a 
 number of other fixation methods, so that it is advisable to 
 keep it in considerable quantity in stock. 
 
 2. Zenker's Fluid. This can be made from Miiller's fluid by 
 adding corrosive sublimate, 5 grams, and glacial acetic acid, 
 5 c.c. to every 100 c.c. It is advisable to add the acetic acid 
 as required to the quantity of stock solution used, as it readily 
 evaporates if kept. The tissues should be fixed in the above 
 for twelve to twenty-four hours. At the end of that time wash 
 in running water for some hours and place in methylated spirit 
 till required. 
 
 This is an exceedingly good method of fixation for most 
 purposes. The solution penetrates well and preserves nuclear 
 structure admirably. One objection which it has in common 
 with all mercury fixatives is that the mercury becomes pre- 
 cipitated in the tissues. This can be removed by means 
 of iodine, which forms with it a colourless soluble compound. 
 The iodine may be added to the spirit in which the tissues are 
 
328 APPENDIX A 
 
 preserved, or, what is a better way, the sections may be treated 
 with Lugol's fluid (see p. 350) or a I per cent alcoholic 
 solution of iodine for ten to twenty minutes before staining, 
 followed by treatment with spirit to remove the iodine. 
 
 3. OrtWs Fluid. This is simply Miiller's fluid in which 
 10 c.c. pure commercial formalin is added to the 100 c.c. 
 The formaldehyde should be added immediately before the fixa- 
 tive is used. Fixation is complete in three to four days. The 
 specimens are afterwards washed in running water, and placed 
 in methylated spirit. Mallory states that the addition of 5 per 
 cent acetic acid improves the fluid. The fluid is an excellent 
 fixative for most purposes. 
 
 4. March? s Fluid. This is Miiller's fluid two parts, to osmic 
 acid ( i per cent aqueous solution) one part. ' As in the case of 
 all osmic acid fixatives the sections should be very thin. 
 They should remain in the fluid three days protected from light. 
 They are afterwards washed in running water and hardened in 
 spirit. The method is specially applicable to the demonstra- 
 tion of recent areas and tracts of degeneration in the spinal 
 cord and brain (see p. 356). 
 
 5. Flemmings solution is made up as follows : 
 
 Osmic acid 2 per cent aqueous solution . 4 parts. 
 Chromic acid I percent ,, ,, . 15 ,, 
 
 Glacial acetic acid ..... i part. 
 
 The portions of tissue should be exceedingly thin, as the 
 osmic acid penetrates badly. They are left in the fluid for one 
 to three days in the dark, subsequently washed in water, and 
 hardened in spirit. The method is specially applicable to the 
 study of nuclear changes, and to the demonstration of olein fats. 
 
 6. Corrosive sublimate, a saturated solution in normal 
 saline with, if desired, the addition of 5 per cent glacial acetic 
 acid. The tissues are fixed for twelve to twenty-four hours, 
 washed thoroughly in water and hardened in spirit. This is an 
 exceedingly good all-round fixative. More especially is it 
 applicable to the fixation of tissues when it is desired to 
 demonstrate granules in the leucocytes and other cells. The 
 same objection as in the case of Zenker's fluid holds good with 
 corrosive sublimate. The sections must be treated with iodine 
 before staining in order to dissolve the mercury. 
 
APPENDIX A 329 
 
 7. Absolute alcohol and methylated spirit are both fixa- 
 tives as well as hardening agents. Under their influence, 
 however, the tissues and cell elements tend to shrink consider- 
 ably. They are said to be specially good for tissues in which 
 it is desired to demonstrate bacteria. But as a matter of fact 
 formalin and corrosive sublimate are equally as good. 
 
 It is always desirable to place a little cotton-wool in the 
 bottle in which the fixation is carried out, in order to prevent 
 sections adhering to the bottom. It is also desirable, parti- 
 cularly when dealing with unconsolidated lung, to place some 
 at the top, in order to prevent the pieces of tissue from float- 
 ing. Remember always to have a large excess of fluid 
 present. 
 
 Sending Material to a Distance 
 
 The practitioner not infrequently desires to send pathological 
 material to some institute or hospital where expert opinion can 
 be obtained. For this purpose the best fluid in which to place 
 the tissue is 10 per cent formalin. The pieces of tissue should 
 be small, and at least ten times as much fluid as tissue should 
 be present in the bottle, otherwise penetration of the fixative 
 will be incomplete and putrefactive processes will progress. 
 In the absence of formalin, methylated spirit or absolute 
 alcohol may be used. 
 
 Treatment after Fixation 
 
 After fixation is complete, as a rule it is advisable to wash 
 the tissue in running water. This is absolutely necessary when 
 fixatives, such as Zenker's, Orth's fluid, corrosive sublimate, 
 Flemming's, have been used. It is not necessary in the case 
 of formalin-fixed tissue. The latter may be placed directly in 
 methylated spirit. 
 
 Hardening. After fixation, or if necessary after fixation and 
 washing, the tissue is placed in methylated spirit. This can 
 be done by placing directly in commercial methylated spirit or 
 by passing through dilutions (50 per cent and 70 per cent) 
 first. For ordinary purposes the dilutions may be omitted, 
 especially when one is dealing with material removed from 
 the body twenty-four or forty-eight hours after death. When 
 
330 APPENDIX A 
 
 it is desired to preserve the finer details, more especially when 
 one is dealing with the central nervous system, then passage 
 through the dilutions is advisable, as there will probably be 
 somewhat less shrinkage in the cell elements. In addition to 
 hardening the specimen, the passage through spirit also to a 
 certain extent dehydrates. 
 
 Dehydration. The next process is dehydration, or the 
 removal of all water from the tissue. Some tissues are more 
 difficult to dehydrate than others. As a rule the denser the 
 tissue the more difficult it is to dehydrate. For this reason 
 any specimen containing well-formed connective tissue requires 
 longer than a specimen such as, for example, normal liver. 
 For purposes of dehydration it is well to use two changes of 
 absolute alcohol. As a rule, a few hours in the first alcohol 
 and twenty-four hours in the second is sufficient. The alcohol 
 must be replaced by fresh after being used for a succession of 
 specimens during a few days. 
 
 Embedding 
 
 The further treatment of the specimen depends upon 
 whether one wishes to cut the sections in paraffin or celloidin. 
 In the case of most organs and tissues, it is necessary to 
 impregnate with some substance which will hold together the 
 cellular elements during the process of cutting and staining. 
 For this purpose, paraffin or celloidin is commonly employed. 
 Each has its own special advantages, each therefore has its 
 supporters. Probably paraffin is more generally used, so we 
 shall consider it first. 
 
 Embedding in Paraffin. From the absolute alcohol, the 
 sections are placed in a clearing fluid, which may be chloro- 
 form, benzol, xylol or some such chemical substance, benzol 
 being the cheapest of those mentioned. All these have this in 
 common that they readily mix with alcohol on the one hand, 
 and with paraffin on the other. At least twenty-four hours 
 should be allowed for this clearing process, and it is well to use 
 two changes of the clearing medium. 
 
 The sections should then be transferred to benzol, or what- 
 ever clearing agent is employed, to which some pieces of 
 paraffin have been previously added, and the bottle placed on 
 
APPENDIX A 331 
 
 the top of the paraffin oven, or inside the incubator. At this 
 temperature, which will be about 37-4o C., benzol will, of 
 course, take up much more paraffin. From this mixture, at the 
 end of twenty-four hours, the pieces of tissue are placed in a 
 shallow uncovered dish containing pure paraffin, in the interior 
 of the paraffin oven. Here they remain until all the benzol 
 has been driven off. If the sections are not too thick or if 
 they are turned over at intervals, a few hours will suffice. It 
 is important on the one hand not to leave the specimens too 
 long, because the heat of the oven shrivels them. On the 
 other hand, it is necessary to drive off all the benzol, else the 
 tissue will shrivel afterwards and will not cut well. As a rule, 
 if they are placed in the pure paraffin (melting-point 50- 5 3 C.) 
 the first thing in the morning, they may be cast the same day, 
 some time during the afternoon. The criterion for the whole 
 of the benzol having been driven off is the absence of the char- 
 acteristic odour on shaking the dish containing the pieces of 
 tissue. 
 
 To cast the specimens, two L-shaped moulds are placed 
 upon a porcelain slab, so as to shut in a space the size of 
 which will vary with the number and size of the specimens. 
 Melted paraffin from a large dish is then poured in, to the 
 depth of about i centimetre, the specimens are transferred by 
 means of a warm pair of forceps, and placed, according to the 
 direction in which it is desired to cut them, in the fluid paraffin 
 upon the porcelain slab. When the surface of the paraffin has 
 solidified, slab, paraffin and moulds may be placed in cold 
 water and the blocks removed when solidification is complete. 
 
 The above periods for dehydration, clearing, etc., may be 
 considerably shortened if the specimens be small and thin. 
 Various abridged methods are in use, of which the following is 
 a reliable one. At the same time, it must be remembered that 
 leisurely methods give the best results. 
 
 Quick Method for embedding in Paraffin (Mallory and 
 Wright). Small pieces of tissue or organ are placed in two 
 changes of acetone for half to two hours. The acetone must 
 be in large excess. From this they are transferred to xylol 
 or chloroform for fifteen to thirty minutes. They are then 
 placed in pure melted paraffin for half an hour to an hour and 
 a half at 57 C. Embed in paraffin. 
 
332 APPENDIX A 
 
 Summary of Method of embedding in Paraffin 
 
 Fixation in formalin for . . .24 hours. 
 
 Hardening in spirit for at least. . 24 ,, 
 
 Absolute alcohol, two changes . . 24-48 
 Benzol, xylol, or chloroform, two 
 
 changes ..... 24 ,, 
 Benzol, etc., saturated with paraffin 
 
 at 37 C. . . . .24 
 
 Pure paraffin, melting-point 5o-53 C. 6-12 ,, 
 
 Cutting Preparations embedded in Paraffin. For cutting 
 sections embedded in paraffin, one of the improved rocking 
 microtomes made by the Cambridge Scientific Instrument 
 Company is probably the best. No special knife is required. 
 Suitable razors are supplied by Milliard, Edinburgh, for 35. 
 They must be kept in good order by frequent stropping and 
 occasional setting on a Canadian hone. The block of paraffin, 
 in which the specimen has been cast, is pared down to a con- 
 venient size with a penknife. It is fixed to one of the dies, 
 which screws on to the arm of the microtome, by means of 
 a heated piece of metal the end of a copper section-lifter will 
 do admirably. The screw regulating the thickness of the 
 section is adjusted to the desired position (about 10 microns), 
 and a number of sections are cut. These can be lifted by 
 means of a fine-pointed pair of forceps and a small brush, and 
 placed in warm water about 44 C. When the sections have 
 flattened out they are mounted singly, or, if desired, in a 
 series, on a clean slide. Slides previously smeared with 
 albumin (egg albumin in water) have this advantage, that 
 the sections adhere to them more firmly. The slide, or series 
 of slides, is then placed in a slanting position till dry. They 
 are then placed on the top of, or in, the paraffin bath, or in an 
 incubator at 37 C. 
 
 Embedding in Celloidin. The sections are taken from 
 absolute alcohol and placed for twenty-four hours in a mixture 
 of equal parts of absolute alcohol and ether. From this they 
 are transferred to a dilute solution (2 per cent) of celloidin 
 (Schering's granular) in equal parts of alcohol and ether. 
 
APPENDIX A 333 
 
 They may be left in this for twenty-four hours or longer, and 
 at the end of that time are transferred to a 6 per cent solution 
 of the same material. Here they remain for twenty-four hours 
 more. 
 
 To cast the specimens, take a cube of wood of a suitable 
 size. Pour a little celloidin over the cross-grained surface, 
 then place the specimen on it and pour a little more over. 
 Allow the whole to dry till it is of a firm consistence, then 
 place in 85 per cent methylated spirit. 
 
 The celloidin method of embedding is more especially used 
 for sections of the brain, spinal cord, bone, and skin, but it is ap- 
 plicable to all types of tissue. Its chief advantage is, that during 
 the process of impregnating the specimen with the celloidin 
 no heat is applied. Another advantage which it has over the 
 paraffin method is that the sections are floated in the staining 
 fluids and not fixed to slide or cover-glass. This allows of the 
 stain acting from two surfaces, and undoubtedly has the result 
 of giving a more natural appearance to the tissue elements. 
 
 Cutting Preparations embedded in Celloidin. For 
 cutting such preparations a number of microtomes are avail- 
 able. Among them the Schanze, Minot, and, for large sections, 
 the Bruce microtome are the best known. Special knives are 
 always supplied with these, which require great care in order 
 to keep sharp. 
 
 While cutting, the specimen and the knife are always kept 
 moist with 80 per cent spirit, applied one or two drops at a 
 time by means of a large brush. Serial sections may be 
 obtained by placing the sections as they are cut upon tissue 
 paper moistened with spirit. The sections are lifted with a 
 brush, and placed in 80 per cent spirit until they must be 
 stained. From this they are taken and either washed first or 
 placed directly in the staining fluid. 
 
 Cutting Sections in Gum. As previously stated, it is 
 advisable to fix specimens before cutting them. It is possible, 
 however, to obtain sections good enough for making a 
 diagnosis, as, for instance, at an operation while the surgeon 
 is waiting, by placing a small piece of tissue in gum and 
 immediately cutting it. When such rapidity is not demanded, 
 twenty-four hours' fixation in 10 per cent formalin is sufficient, 
 but where time permits, and when it is not desired subsequently 
 
334 APPENDIX A 
 
 to stain for fat, it is well in addition to harden the tissue in 
 spirit for a day or two. This should not, of course, be done 
 with sections which are subsequently to be stained for fat. At 
 the end of that time the spirit should be washed out in running 
 water over night, and the specimen placed in gum for some 
 hours. It is absolutely necessary to wash out the spirit 
 thoroughly, and to allow sufficient time for the gum to pene- 
 trate. Sections cut in this way give as good results as any. 
 when suitably stained. For many tissues, notably lung, the 
 results are as good as those obtained with the best celloidin 
 sections, and the tissues are less subjected to the influence of 
 chemicals, and in consequence are less shrunken. Further, 
 very large sections can be obtained by freezing, the size only 
 being limited by the size of the freezing stage, and this, as 
 has been already emphasised, is a matter of supreme import- 
 ance in studying lung disease. Formerly, when ice and salt 
 had to be used for freezing, the method was clumsy. Later, 
 the introduction of ether simplified the process ; but in these 
 days of liquid CO 2 no method of cutting sections is more 
 simple or effective. 
 
 With regard to the type of microtome, the Cathcart, with 
 ether freezing, is a useful little instrument, particularly for 
 travelling purposes, when the pathologist accompanies the 
 surgeon to an operation. 
 
 For laboratory purposes undoubtedly one of the numerous 
 CO 2 freezers is preferable, owing to its more rapid and more 
 powerful action. Of the more elaborate CO 2 microtomes, the 
 Aschoff-Becker is very good. A simple one is that introduced 
 by Dr. Mixter, and used largely in America. 
 
 The piece of tissue is placed upon the stage of the 
 microtome, and some gum poured on the top and round it. 
 The carbonic acid gas is then turned on and off a number of 
 times till the specimen is opaque, white, and hard. In this 
 condition the knife will not cut it, but when it is just com- 
 mencing to thaw the best sections will be obtained. To 
 prevent the deeper portions from thawing, the gas should be 
 turned on every now and then. A razor, the blade of a 
 carpenter's smoothing-plane, or one of the special knives 
 supplied with the microtomes is used for cutting. The 
 sections are removed with a brush and placed in a basin of 
 
APPENDIX A 335 
 
 cold water, where they will gradually flatten out. The sections 
 may be stained at once, or preserved in formalin water, or 
 better, in spirit, for future use. When it is desired to stain 
 fat, spirit cannot of course be used. 
 
 Decalcification 
 
 Tissues which contain bone or calcium salts, such as 
 atheromatous patches in the aorta, calcareous tuberculous 
 glands, etc., require to be decalcified before being cut, 
 otherwise the razor or knife employed will be ruined. 
 Before decalcifying, the portion of bone or tissue is fixed, 
 having been previously sawn or cut to the desired size. As 
 fixative, formalin 10 per cent, Zenker's or Orth's fluid may 
 be used. After washing, the specimen is placed in methylated 
 spirit for at least twenty-four hours. 
 
 There are many decalcifying fluids, the chief constituent 
 being, in all cases, some acid. In order to ensure the penetra- 
 tion of the acid, the fluid should be frequently changed, and 
 should be used in large quantity. Unfortunately, nuclei are 
 always damaged by such acids, so that the sections require 
 to be stained for longer periods and never give quite such 
 good results as tissues which are not so treated. 
 
 Nitric acid is one of the most effective decalcifying agents. 
 It is used in a 5 per cent aqueous solution. For rapidity of 
 action Perenny's solution can be strongly recommended. It 
 is made up as follows : 
 
 Nitric acid, 10 per cent . . . . 400 c.c. 
 
 Absolute alcohol 300 c.c. 
 
 Chromic acid, ^ per cent . . . 300 c.c. 
 
 In the above solution decalcification is usually complete, if 
 moderately thin pieces of tissue are used, in from ten to 
 fourteen days. 
 
 Apparatus required in Staining 
 
 As regards apparatus required, this depends upon the way in 
 which the sections have been cut. Slides 3 in. x I in. for ordinary 
 sections, and 3 in. x i^ in. for larger sections, as well as cover- 
 
336 APPENDIX A 
 
 glasses (No. i and No. 2) will always be required. For sections 
 cut frozen or in celloidin, a series of watch-glasses to hold the 
 staining fluids and reagents, a bowl of water for washing 
 between the processes, needles for lifting the sections, drop- 
 bottles containing absolute alcohol and xylol, and a bottle of 
 Canada balsam, also glycerine jelly or Farrant's medium, are 
 all that is required. In the case of sections cut in paraffin, 
 these may have been mounted either upon cover-glasses or 
 on slides. In the former case, a series of drop-bottles con- 
 taining the reagents and a pair of Cornet's forceps to hold 
 the specimen are all that is necessary. In the latter case it 
 is well to have a series of stoppered jars, of a size suitable 
 for holding at least two slides, back to back, for stains and 
 reagents. A tap for cold water and a sink should be at hand, 
 also a jar containing distilled water. A pair of scales for 
 weighing out stains is also necessary. 
 
 For sections cut in celloidin, watch-glasses or other small 
 glass dishes for the stains and reagents, and needles for lifting 
 the sections, are required. 
 
 Slides and cover-glasses should always be clean ; more 
 especially they should be free from grease. The best way of 
 securing this is to place them in strong hydrochloric acid for 
 a short time, then wash in running water, and finally put them 
 into a jar with a properly fitting top containing methylated 
 spirit. From this spirit they are taken and dried with a clean 
 cloth as they are required. 
 
 Mounting Media 
 
 Canada Balsam. This is prepared by dissolving the balsam 
 either in benzol or xylol. The solvent is added in sufficient 
 quantity to give a yellow fluid with a syrupy consistence. The 
 balsam should be kept in one of the specially prepared stoppered 
 bottles. It is necessary to add a little of the solvent from time 
 to time to replace that which evaporates. 
 
 In the case of tissues treated with osmic acid, chloroform 
 should take the place of the benzol or xylol. 
 
 Sections which have been stained in anilin dyes such as 
 thionin tend to become discolourised when mounted in ordinary 
 balsam. This is due to the fact that ordinary balsam is acid 
 
APPENDIX A 337 
 
 as a result of oxidation. In neutral balsam, which may be 
 obtained from Griibler, Leipzig, the colour is preserved for 
 a much longer period. Another way of getting over the 
 difficulty is to mount the section in Colophonium dissolved in 
 terpentine oil. 
 
 Glycerine Jelly. This is specially useful in mounting 
 sections which have been stained for fat or waxy material. 
 It contains 
 
 Gelatine (Coignet's) . . 30 parts. 
 Distilled water . . . 70 ,, 
 Glycerine . . 4 .100 ,, 
 Alcoholic solution of camphor 5 ,, 
 
 After standing overnight in the distilled water the gelatine 
 and water are boiled and subsequently strained through a 
 warm filter. The glycerine and camphor are added and mixed 
 thoroughly. Before use the medium should be liquefied by 
 being placed in warm water. 
 
 Farr ant's Medium. Equal parts of water, glycerine and 
 a saturated watery solution of arsenious acid (saturated by 
 boiling) are mixed together thoroughly. To this is added 
 about half its bulk of gum-arabic. The mixture is stirred 
 from time to time until solution is complete. It is then filtered 
 and a little carbolic (i : 20) added. 
 
 STAINING METHODS 
 
 Treatment of Sections cut in Paraffin before Staining. Before 
 staining, sections which have been cut in paraffin require to 
 be treated with some solvent for paraffin, such as benzol or 
 xylol. The reagent is dropped on to the section and the slide 
 or cover-glass gently tilted backwards and forwards for some 
 seconds. The benzol is then poured off and replaced by fresh. 
 The process of solution of the paraffin may be hastened by 
 warming the slide or cover-glass very gently well above the 
 flame of a bunsen until the paraffin is seen to melt. The 
 benzol is then poured on and allowed to remain for a few 
 seconds. 
 
 The benzol must now be washed off by means of a few 
 drops of methylated spirit, the slide being inclined so as to 
 
338 APPENDIX A 
 
 allow the fluid to run away. The section is now gently 
 immersed in water and left for a few minutes before staining. 
 The stain is then dropped or filtered on to the section, or the 
 section and slide are placed in a suitable jar containing the 
 stain. 
 
 Treatment of Sections cut in Celloidin and Gum. Sections 
 cut in gum or in celloidin are taken direct from water by 
 means of a needle and placed in the staining fluid, usually in 
 a watch-glass or similar hollow dish. Such sections stain 
 much more rapidly than those cut in paraffin, by reason of the 
 fact that the stain acting upon the tissue from both sides 
 penetrates more readily. 
 
 Picro-Carmine 
 
 This is a combined nuclear and protoplasmic stain. It 
 also has the advantage of differentiating between various 
 types of tissues and cells. The nuclei of cells and fibrous 
 tissue are stained brilliant crimson. Epithelial cells, necrotic 
 material, fibrin and elastic tissue are stained yellow. The 
 stain is prepared as follows : 
 
 Pure carmine I part. 
 
 Liq. ammoniae fort. . . 3 parts. 
 
 Dist. water . . . 3 
 
 Dissolve the stain in a test tube in the ammonia and water 
 and add 200 parts of a cold, saturated, and filtered solution 
 of picric acid, and mix thoroughly. Place the fluid in a basin 
 covered with glass and allow to ripen in direct sunlight, 
 testing its powers of staining from time to time. To prevent 
 the picric acid crystallising out, add 10 to 20 per cent of 
 distilled water to the fluid that remains. Add also 2 to 6 drops 
 of i to 20 carbolic to prevent the growth of fungi. 
 
 Method. 
 
 Spread the section out on a cover-glass, drain off super- 
 fluous water. Run several drops of staining fluid over and 
 allow to stand for fifteen to twenty minutes. Drain off excess 
 of stain. Do not wash. Mount in Farrant's medium. 
 
 The method is specially useful for sections cut in gum. 
 
APPENDIX A 339 
 
 Haematoxylin (Hsematein), Eosin 
 
 Haematoxylin is obtained from the wood of Hamatoxylon 
 catnpechianum by extraction with ether. It is not in itself a dye 
 but becomes one on oxidation. In its oxidised form it is known 
 as haematein. Neither the original substance nor the oxidation 
 product is capable of staining directly. Each requires a 
 mordant added to it or used separately. As mordants, alum 
 and iron are very commonly used. 
 
 There are many useful methods for staining with haema- 
 toxylin and haematein. They all give very similar results, the 
 nuclei staining a dark blue or purple colour. 
 
 Of the haematoxylin methods probably the best, both as 
 regards ease of preparation of the stain and rapidity of action, 
 is Weigert's iron-haematoxylin. 
 
 Weigerfs Iron-Hcematoxylin. Two solutions are prepared, 
 No. i containing the haematoxylin, No. 2 the mordant (iron). 
 These solutions keep well separately. For use, equal parts of 
 the two are mixed together. The mixture will stain at once, 
 but is better after twenty-four hours. It will keep good for 
 eight to fourteen days. 
 
 The solutions are made up as follows : 
 
 Solution i 
 
 Haematoxylin . . . . i grm. 
 Alcohol 96 per cent j - 100 c.c. 
 
 Solution 2 
 
 Liq. ferri perchlor. (S.G. 1-124) 4 c.c. 
 
 Dist. water . . . .100 c.c. 
 Hydrochloric acid (cone.) . . i c.c. 
 
 The mixture, which has a brownish-black colour, is dropped 
 on to the section and allowed to remain from one to five minutes. 
 Better results are obtained by differentiation for one or two 
 seconds in acid alcohol (i per cent hydrochloric acid in 
 methylated spirit). The section is then thoroughly well washed 
 in tap water and counterstained with eosin or picro-fuchsin 
 (van Gieson's stain). 
 
340 APPENDIX A 
 
 An excellent hasmatein is that recommended by Mayer. 
 It is prepared as follows : 
 
 Hsematein i grm. 
 
 90 per cent alcohol . .50 c.c. 
 Alum . . . . -So grm. 
 Water i litre. 
 
 A crystal of thymol is added to prevent the growth of 
 moulds. The haematein should be dissolved first in the 
 alcohol by the aid of warmth, and then added to the water in 
 which the alum has been already dissolved. 
 
 The stain improves on keeping. The ripening process is 
 more rapid if the stain be exposed to sunlight. At first it may 
 require half an hour or even longer to stain ; later, ten to fifteen 
 minutes is sufficient. If the stain is too deep or too diffuse a 
 few seconds in acid alcohol (hydrochloric acid I per cent in 
 methylated spirit) will differentiate. The section is then washed 
 thoroughly in tap water until the blue colour returns. 
 
 Method. 
 
 i. Stain in haematoxylin for two to five minutes or haematein 
 ten to thirty minutes. 
 
 (2. Differentiate in acid alcohol if necessary.) 
 
 3. Wash thoroughly in water. 
 
 4. Counterstain in \ per cent 'watery eosin for one to four 
 minutes. 
 
 5. Wash in water. 
 
 6. Dehydrate, and at the same time take out some of the 
 eosin in absolute alcohol. 
 
 7. Clear in benzol. 
 
 8. Mount in balsam. 
 
 In the case of sections cut in gum or in celloidin a much 
 shorter period is required for staining in the haematein and 
 eosin solutions. 
 
 Hsematoxylin combined with Picro-fuchsin (van Gieson's 
 stain) 
 
 For this combination the haematoxylin or haematein may 
 be any of those in common use, such as the above mentioned, 
 but it is necessary when using these with picro-fuchsin to stain 
 
APPENDIX A 341 
 
 for a longer period than when eosin is used, as the picric acid 
 tends to decolourise the haematein. Another alternative is to 
 use a stronger nuclear stain, and for this purpose Weigert's 
 iron-haematoxylin has no rival. 
 
 Van Giesorts Solution. It is best to prepare a stock 
 solution as follows : 
 
 Acid fuchsin . , . -1*5 grm. 
 Saturated watery solution of picric 
 
 acid (about 0-6 per cent) . 150 c.c. 
 
 This solution keeps well. For use, mix i c.c. of the stock 
 solution with 10 c.c. saturated watery solution of picric acid. 
 This solution will also keep for some weeks. 
 
 Method. 
 
 1. Stain in iron-haematoxylin for two to five minutes or in 
 haematein for fifteen to thirty minutes. 
 
 2. Wash in water. 
 
 3. Stain in picro-fuchsin ten to thirty seconds. 
 
 4. Wash rapidly in water. 
 
 5. Dehydrate rapidly in absolute alcohol. 
 
 6. Clear in carbol-xylol (or carbol-benzol). 
 
 The advantages of the carbol-xylol is that dehydration need 
 not be very complete if it is used. This is of importance 
 because prolonged treatment in alcohol extracts the stain. 
 The mixture consists of three parts xylol (or benzol) to one 
 of melted crystalline carbolic acid. 
 
 7. Clear again in xylol (in order to get rid of the carbolic). 
 
 8. Mount in Canada balsam. 
 
 The special advantage of the van Gieson method is that 
 a differentiation is effected between certain types of cells and 
 tissues. Red blood corpuscles are stained a bright yellow 
 colour, connective tissue fibres red, and muscle fibres yellow 
 or brownish-yellow. 
 
 In staining sections cut in gum or in celloidin with picro- 
 fuchsin a longer period of washing in water is required. 
 
 Eosin, Methylene Blue Staining Method 
 
 This is a method of very general applicability. In some 
 schools in America it is used as the routine staining method. 
 
342 APPENDIX A 
 
 It has many advantages. It is a fairly sharp nuclear stain, 
 but its chief advantage is as a stain for protoplasm. The 
 structure of the protoplasm, more particularly any granules 
 which it may contain, are brought out with the characteristic 
 reaction to the acid (eosin) and basic (methylene blue) dyes. 
 The outline of the individual cells will be brought out very 
 clearly and their relative size thus more easily estimated. 
 Moreover, any bacteria present will be stained with the 
 methylene blue. 
 
 In order to get the best results the tissue should be fixed in 
 Zenker's fluid or in saturated corrosive sublimate. Fairly good 
 results will, however, be obtained with formalin-fixed tissue. 
 
 Method. A simple method of using the stains is as 
 follows : 
 
 1. Stain in eosin (i per cent aq. solution) five to ten 
 minutes. 
 
 2. Wash in water. 
 
 3. Stain in methylene blue (i per cent aq. solution) half 
 minute. 
 
 4. Wash in water. 
 
 5. Differentiate and dehydrate in absolute alcohol. 
 
 6. Clear in xylol or benzol and mount in balsam. 
 
 After staining with the eosin, Potas. Alum (sat. sol.) may 
 be used for fixing the stain. 
 
 The differentiation should be carefully carried out and 
 controlled by putting the section under a low power of the 
 microscope, and noting the point at which the nuclei of the 
 cells become sufficiently clear. The method requires some 
 'practice before the best results are obtained. 
 
 Mallory and Wright recommend the following : 
 
 1. Stain in eosin (5 percent aq. sol.) for twenty minutes or 
 longer. 
 
 2. Wash in water. 
 
 3. Stain in Unna's alkaline methylene blue (one part in 
 five of water) for ten to fifteen minutes. 
 
 Unna's Alkaline Methylene Blue 
 
 Methylene blue . . . . . i grm. 
 Carbonate of potassium . . i grm. 
 
 Water 100 c.c. 
 
APPENDIX A 343 
 
 4. Wash in water. 
 
 5. Differentiate in alcohol, clear and mount. 
 
 According to Mallory and Wright the success of the 
 method depends upon the presence of colophonium in the 
 alcohol used for differentiation. This is usually present in 
 alcohol, but it may be necessary to add it in such quantity 
 as to make a I o per cent solution. 
 
 A stain which gives very similar results is prepared by 
 diluting Leishman's stain with nine parts of water. The 
 sections are allowed to remain in this stain for twenty-four 
 hours. They are then differentiated in a very dilute solution 
 of acetic acid (i :iooo), washed in water, dehydrated, cleared 
 and mounted in balsam. This makes an excellent counterstain 
 instead of methylene blue after using Ziehl-Neelsen's carbol- 
 fuchsin for staining tubercle bacilli. 
 
 Pyronin-Methylgreen Method (Unna-Pappenheim) 
 
 This is a useful method for differentiating the various 
 types of cells in inflammatory tissue, more especially for 
 demonstrating " plasma cells." The staining mixture 
 (pyronin-methylgreen) is best obtained ready made from 
 Grubler. 
 
 1. Fix in alcohol, formalin, or Orth's fixative. 
 
 2. Stain in pyronin-methylgreen mixture for 10-15 minutes, 
 warming the slide slightly. 
 
 3. Wash in water for several minutes. 
 
 4. Differentiate in 70 per cent alcohol. 
 
 5. Dehydrate rapidly, clear, mount. 
 
 By the above method the protoplasm of the " plasma 
 cells" is deep red, the nucleus green. 
 
 Elastic Tissue Stain 
 
 Elastic fibres enter into the formation of many tissues and 
 organs in the body. More especially is this the case with 
 the lungs and testicle and with vessels (other than capillaries) 
 and skin. In studying pathological changes in these tissues 
 it is therefore absolutely necessary to employ some method 
 for the demonstration of the elastic fibres. A number of 
 
344 APPENDIX A 
 
 staining methods will show elastic fibres, but for the study of 
 changes in these fibres special selective methods must be 
 employed. Of these selective methods, undoubtedly the best 
 is Weigert's resorcin-fuchsin method. 
 
 The stain may be obtained in the form of powder or fluid, 
 but it is easily prepared as follows : 
 
 Resorcin . . .4 grin. 
 Fuchsin (Griibler) . . 2 grm. 
 Water . . . 200 c.c. 
 
 Bring the mixture to the boil in a porcelain dish, and add 
 25 c.c. of the liquor ferri sesquichloridi (Pharm. Germ. S.G. ii). 
 Boil for five minutes, stirring at the same time. A pre- 
 cipitate forms which after cooling is filtered. . This precipitate 
 is dissolved in 200 c.c. of 94 per cent alcohol, heat being 
 applied till the alcohol boils. The solution is then allowed 
 to cool, made up to 200 c.c. with alcohol, and 4 c.c. of hydro- 
 chloric acid added. 
 
 Method. 
 
 1. Tissues are fixed in formalin or corrosive, hardened 
 in alcohol and cut in paraffin, celloidin, or better, in gum with 
 the freezing microtome. It is well to cut the sections fairly 
 thick (20-40 /x) in order that the sinuosities of the fibres may 
 be followed. Tissue hardened in alcohol must of course be 
 washed thoroughly in water (twenty-four hours) before being 
 placed in gum. 
 
 2. Stain sections in lithium carmine one to five minutes 
 (paraffin sections twenty-four hours). 
 
 Orttts Lithiitm Carmine 
 
 Carmine ...... 5 grm. 
 
 Sat. aq. sol. of lithium carbonate . . 100 c.c. 
 Thymol, a few crystals. 
 
 3. Differentiate in acid alcohol (p. 339) for one to twenty-four 
 hours. The longer the sections are left in this the better the 
 result. 
 
 4. Place direct in resorcin-fuchsin mixture for ten minutes 
 (gum sections) to one hour (paraffin sections). The stain 
 
APPENDIX A 345 
 
 tends to become less active on keeping, but the differentiation 
 is better. 
 
 5. Differentiate and dehydrate in absolute alcohol. In the 
 case of gum sections, this is. best done in a " Petri dish " so 
 that the section can be spread out on the slide while in the 
 alcohol. 
 
 6. Clear in carbol-xylol or carbol-benzol. 
 
 7. Afterwards in xylol or benzol and mount in balsam. 
 
 By this method the elastic fibres are stained dark blue, the 
 cell nuclei red. The elastic tissue stain can be used along with 
 other staining methods. A very good combination is the 
 following : 
 
 Stain in iron-haematoxylin, then in Weigert's resorcin-fuchsin, 
 and finish up with picro-fuchsin. 
 
 Fibrin Staining Method 
 
 Weigert's fibrin method is merely a modification of the 
 Weigert - Gram method for staining bacteria, and sections 
 stained with it will also show gram positive organisms. The 
 method is particularly adapted for demonstrating the exudate 
 in acute inflammations of pleura, pericardium and lung, also 
 for the fibrin network in thrombi. 
 
 Method. 
 
 1. Fix in formalin or corrosive sublimate, but not in M tiller's 
 or Orth's fluid. 
 
 2. Cut in gum, paraffin or celloidin. 
 
 3. Stain in lithium carmine (see p. 344), in the case of 
 paraffin sections for some hours, in the case of gum or celloidin 
 sections for one to five minutes. 
 
 4. Differentiate in acid alcohol for some time, best twenty- 
 four hours. 
 
 5. Wash well in water. 
 
 6. Stain in anilin gentian violet (p. 363) five to ten minutes. 
 
 7. Pour off excess and blot carefully. 
 
 8. Mordant in iodine solution for two minutes. 
 
 Potassium iodide . . . . 5 grm. 
 
 Water 100 c.c. 
 
 Iodine in excess. 
 
34^ APPENDIX A 
 
 9. Pour off excess and blot firmly. 
 
 10. Differentiate in anilin-xylol (equal parts of anilin oil 
 and xylol). 
 
 11. Clear in xylol, mount. 
 
 By this method the fibrin is stained blue while the nuclei 
 of cells are stained red. 
 
 Staining of Fat in the Tissues 1 
 
 Fat occurs in the tissues as (i) neutral fats (combinations 
 of fatty acid and glycerine) ; (2) fatty acids (palmitic, stearic, 
 or oleic) ; (3) soaps (combinations of fatty acids and alkalies 
 potassium, sodium, or calcium) ; (4) combinations of fat with 
 protein (albumin soaps). All the first three varieties are 
 demonstrable by microchemical means, the last only by 
 chemical analysis. 
 
 In order to demonstrate fat by staining methods it is neces- 
 sary to cut sections of the tissues fresh or, better, after fixation 
 with formalin. The portion of tissue is taken direct from the 
 formalin and frozen, or it is placed for some hours in gum 
 (p. 326) and then cut. Tissues passed through the usual re- 
 agents and cut in paraffin or celloidin have all their fat removed, 
 unless they have been fixed previously in osmic acid, which 
 stains certain fats black, or in a chrome salt such as bichrom- 
 ate of potash. 
 
 Basic anilin dyes will stain fats in the form of free fatty 
 acid by combining with them to form coloured soaps. As a 
 rule fatty acids occur in small amount in the fat of tissues, 
 although in some morbid conditions (e.g. fat necrosis) they are 
 present in large amount. The neutral fats, which are the pre- 
 dominant form, are, however, readily hydrolysed by the action 
 of acids and so split into fatty acid and glycerine. The car- 
 bonic acid of the atmosphere will act in this way. This 
 hydrolysed fat will take on the basic anilin dye. In this way 
 the fat in sections stained with such a dye and exposed to the 
 air or to the action of an acid such as sulphurous acid gradu- 
 ally combines with the dye and so becomes coloured. In 
 
 1 Lorrain-Smith and Mair, Journal of Pathology and Bacteriology, 
 1906, vol. xi. p. 415 ; ibid., 1908, vol. xii. pp. i, 126, 134 ; ibid. t 1908, 
 vol. xiii. pp. 14, 345; ibid tt 1911, vol. xv. pp. 53, 180. 
 
APPENDIX A 347 
 
 other words, globules of acid fat are stained immediately with 
 basic anilin dyes, while globules of neutral fat remain un- 
 stained until they have been hydrolysed and the fat has 
 become acid. 
 
 Demonstration of Fat by Haematoxylin. Fat in the 
 tissues will stain with hcBmatoxylin^ in a similar way to myelin 
 in Weigert's method, after partial oxidation by fixation in bi- 
 chromate of potash or in chromic acid. The fat, however, 
 takes considerably longer than the myelin to reach the stage 
 of oxidation at which it will " lake " hasmatoxylin. 
 
 In order to stain sections of fatty liver in this way the 
 piece of tissue, after rapid fixation in formalin, should be cut 
 in gum and the sections placed in a saturated solution of 
 potassium bichromate at 37 C. for a fortnight. At the end 
 of this time they are stained in Kultschitzky's haematoxylin, 
 and differentiated as on p. 355, or by means of Weigert's 
 borax-ferricyanide mixture prepared as follows : 
 
 Borax . . . . .2 grm. 
 Pot. ferricyanide , : . . 2-5 grm. 
 Water . . . .100 c.c. 
 
 Demonstration of Fat by Osmic Acid. For this purpose 
 osmic acid i per cent solution in water or any of the fixatives 
 containing osmic acid, such as Flemming's (p. 328) or 
 Marchi's (p. 328) solutions, may be used. The action de- 
 pends upon the reduction of the osmium peroxide to osmium 
 oxide. Only certain fats are blackened in this way, more 
 especially olein and oleic acid. The pieces of tissue treated 
 should be very thin as the osmic acid does not penetrate well. 
 
 One advantage of the method is that the tissue can after- 
 wards be embedded in paraffin or celloidin, although in the 
 case of paraffin embedding xylol should not be used. Subse- 
 quent staining with safranin (i per cent) gives very good 
 results. 
 
 The staining with osmic acid can also be carried out with 
 sections cut in gum. The sections are placed in per cent 
 solution of perosmic acid for 12 hours in the dark, washed 
 well in water, and mounted in Farrant's solution. 
 
 Lorrain-Smith's Nile Blue Sulphate Method. Nile blue 
 sulphate (A) is a dye of the oxazine series, and, like other basic 
 
348 APPENDIX A 
 
 anilin dyes, it combines with fatty acid forming a coloured 
 soap. When sections of tissue containing fat are stained with 
 it, the larger proportion of the fat globules are found stained a 
 brilliant red, others are stained a deep blue, while others are 
 purple. The explanation of this is that the dye in watery 
 solution contains a red substance (oxazone base), which is 
 derived from the blue dye (oxazine base) by a process of oxida- 
 tion. This transformation can be carried out more rapidly 
 by heating the blue stain for some hours in the presence of 
 acid. This red oxazone base is readily soluble in both fatty 
 acids and neutral fats, and in virtue of this leaves the stain 
 and concentrates in the fat. This solution of the dye in the 
 fat is a rapid process. Hence the great proportion of the fat 
 in the tissue will be coloured red. The blue stained globules 
 represent the fatty acid portion of the fat which has combined 
 with the basic dye (oxazine base) to form a soap. This pro- 
 cess is a relatively slow one. 
 
 When both neutral fat and fatty acid are present in a 
 globule, both stains act, thus giving a purple colour. 
 
 Method. 
 
 1. Fix in formalin. 
 
 2. Cut in gum with freezing microtome. 
 
 3. Place the sections in a concentrated watery solution of 
 Nile blue sulphate for ten minutes. 
 
 4. Wash in water. 
 
 5. Differentiate in i per cent acetic acid. 
 
 6. Wash thoroughly. 
 
 7. Mount in Farrant or in glycerine jelly. 
 
 Method of staining Fats with Sudan III. and Scharlach 
 R. Sudan III. and Scharlach R. are two anilin dyes belonging 
 to the azo group, closely allied to one another, the latter being 
 richer by two methyl groups than the former, and in conse- 
 quence being the stronger stain. Both dyes are readily 
 soluble in alcohol and in fat, but not in water. It is in virtue 
 of their solubility in fat that the colouration takes place. Both 
 stains are capable of colouring all types of fat fatty acid, 
 neutral fat, and soaps. This fact, in conjunction with the ease 
 of staining, renders them the best all-round dyes for fatty 
 changes. Because of its more intense staining, Scharlach R. 
 is to be preferred to Sudan III. 
 
APPENDIX A 349 
 
 Method. 
 
 1. Formalin fixed tissue. 
 
 2. Cut in gum with freezing microtome. 
 
 3. Place sections in 70 per cent spirit for a few seconds. 
 
 4. Then in a saturated solution of Scharlach R. in 70 per 
 cent alcohol, previously filtered, for ten minutes to twenty-four 
 hours in covered dish. (The longer the sections remain in the 
 solution, the more intense is the staining.) 
 
 5. Transfer to 70 per cent spirit. 
 
 6. Wash in water. 
 
 7. Counterstain for five minutes in alum hasmatein. 
 
 8. Mount in Farrant or in glycerine jelly. 
 
 Owing to the fact that the stains are not very soluble in 
 70 per cent alcohol, a relatively long period is necessary for 
 perfect staining. The time can be shortened considerably by 
 using one of Herxheimer's methods, of which the following is 
 the best : 
 
 70 per cent alcohol . . -5 c - c 
 Pure acetone . .; . . 50 c.c. 
 Scharlach R. . . . excess. 
 
 In the mixture of alcohol and acetone the Scharlach R. is 
 much more soluble than in the alcohol alone. Hence two to 
 five minutes suffices for staining. Care should be taken to 
 filter the stain before use and to keep the dish covered in 
 which the staining is carried out as otherwise precipitates 
 may occur. 
 
 Demonstration of G-lycogen in the Tissues 
 
 Glycogen is a carbohydrate which occurs in cells, e.g. 
 liver, muscle, kidney, and, more rarely, in intercellular sub- 
 stance. It is readily soluble in water but insoluble in alcohol, 
 therefore the tissue under examination must not be treated 
 with water or watery stains. It gives a dark brown colour 
 with iodine. For ordinary purposes Ehrlich's method is 
 quite good. 
 
 Method. 
 
 1. Place tissue at once in absolute alcohol. 
 
 2. Embed in paraffin. 
 
 3. Stretch the cut sections in 50 per cent alcohol. 
 
350 APPENDIX A 
 
 4. Place a drop of the following mixture on the slide : 
 
 Gum-arabic . . . . .100 parts. 
 Lugol's iodine solution (see below) . I part. 
 
 LugoFs Solution 
 
 Iodine . i grm. 
 
 Pot. iodide . 2 grm. 
 
 Water .... 300 c.c. 
 
 Place a cover-glass on the specimen and investigate. 
 In order to obtain permanent preparations, more elaborate 
 methods, such as Lubarsch's and Best's, must be adopted. 
 
 Lubarsch's Method 
 
 1. Fix tissue in absolute alcohol, embed in paraffin, cut, 
 stretching sections in 50 per cent alcohol. 
 
 2. Stain in Mayer's alcoholic carmine for several minutes. 
 
 Carmine . . 4 grm. 
 
 Water . . . . .15 c.c. 
 Hydrochloric acid . . .30 drops. 
 
 Dissolve by boiling, add 95 c.c. of 85 per cent alcohol ; filter 
 in warm condition and neutralise with ammonia until a perma- 
 nent precipitate forms, then filter in the cold., 
 
 3. Differentiate in acid alcohol (see p. 339). 
 
 4. Wash in absolute alcohol. 
 
 5. Stain in methylanilin violet solution as for Weigert's 
 fibrin method (p. 345), warming slightly for two minutes. 
 
 6. Wash very rapidly in water. 
 
 7. Pour on Lugol's solution (see above), and leave for 
 10 seconds. 
 
 8. Dry with filter paper. 
 
 9. Differentiate in 
 
 Anilin oil .... 2 parts. 
 Xylol i part. 
 
 10. Clear in xylol and mount in balsam. 
 
APPENDIX A 351 
 
 By this method the glycogen is coloured blue-violet and the 
 nuclei of the cells red. 
 
 Best's Method 
 
 1. Fix in absolute alcohol, embed in celloidin and cut. 
 
 2. Stain in Weigert's iron-haematoxylin (p. 339). 
 
 3. Differentiate in acid alcohol. 
 
 4. Wash rapidly in water. 
 
 5. Stain in ammonia carmine prepared as follows : 
 
 Carmine . . . . .2 grm. 
 
 Pot. carbonate . . . . i 
 
 Pot. chloride . . . . 5 
 
 Dist. water , . . . 60 c.c. 
 
 Boil for a few minutes, and after cooling add ammonia 
 20 c.c. For use take 
 
 Carmine solution . . .20 parts. 
 Ammonia . . 30 ,, 
 
 Methyl alcohol , . . 30 
 
 Stain in this for 5 minutes to 24 hours. 
 
 6. Place in differentiating fluid for several minutes until 
 the section is again blue. Differentiating fluid 
 
 Abs. alcohol . . . . 40 parts. 
 Methyl alcohol . . . 20 
 Dist. water . . . 50 ,, 
 
 7. Wash in 80 per cent alcohol. 
 
 8. Dehydrate in alcohol, clear in xylol, mount in balsam. 
 In the above method the hasmatoxylin may of course be 
 
 omitted. Paraffin sections may be treated similarly if, after 
 dissolving out the paraffin with xylol and washing off the 
 xylol with alcohol, the sections are placed in thin celloidin for 
 3 to 4 hours. At the end of that time they are placed upon a 
 slide and stained in Best's carmine. The glycogen by this 
 method is stained red. 
 
352 APPENDIX A 
 
 Demonstration of Calcareous Material in the Tissues 
 
 Haematoxylin and hsematein stain calcareous material 
 dark blue. 
 
 Von Kossa's Silver Method. 
 
 1. Fix in formalin for a short period, and cut with freezing 
 microtome. 
 
 2. Lay the sections in 5 per cent silver nitrate in the light 
 for 10 minutes to I hour. 
 
 3. Wash in distilled water. 
 
 4. Transfer to a 5 per cent solution of sodium hypo- 
 sulphite in order to remove excess of silver nitrate. 
 
 5. Wash thoroughly in water. 
 
 6. As a counterstain safranin (i per cent watery solution) 
 may be used. 
 
 7. Dehydrate, clear, mount. 
 
 In carrying out the above method phosphate of silver is 
 formed by interaction between the silver nitrate and the 
 phosphates of calcium and magnesium. Under the influence 
 of light the silver salt is reduced to metallic silver which 
 appears in the section black. 
 
 Stains for Amyloid or Waxy Substance 
 
 Amyloid or waxy degeneration is a change which affects 
 connective tissue, chiefly that in relation to blood-vessels. 
 
 The tissue becomes swollen, transparent, and homogeneous. 
 The material of which this degenerated tissue is composed is 
 an albuminous body combined with chondroitin sulphuric acid. 
 
 Tissues containing waxy substance should be fixed in 
 formalin and hardened in spirit, but should not be kept too 
 long in either fluid, as the amyloid material tends to lose its 
 characteristic staining properties in these fluids. It is possible, 
 however, to stain sections successfully which have been kept 
 for years in spirit. 
 
 Sections are best cut in gum after the spirit has been 
 thoroughly washed out with water. The waxy material is well 
 demonstrated by such ordinary methods as haematoxylin and 
 picro-fuchsin, by which means it is stained a yellow-brown 
 
APPENDIX A 353 
 
 colour. There are two selective methods for waxy material 
 (a) iodine, (b] anilin stains. 
 
 (a) Iodine Method. The sections cut in gum are placed 
 in an iodine solution Gram's or Weigert's (p. 363) solutions 
 are both suitable and left there for two to five minutes. 
 They are then mounted in glycerine jelly without washing. 
 
 By this means the waxy material appears, by trans- 
 mitted light, a golden yellow, by reflected light a mahogany 
 brown. 
 
 (b) Anilin Stains. A number of anilin dyes, which are 
 mixtures of several different chemical compounds, such as methyl 
 violet (a mixture of tretra, penta, and hexamethyl-rosanilin), 
 gentian violet (a mixture of the chloride of penta and hexa- 
 methyl-pararosanilin), polychrome methylene blue (formed by 
 boiling methylene blue with an alkali and containing methylene 
 violet), show characteristic staining with tissues containing 
 waxy material. In other words, such tissues when stained by 
 one of these dyes show the waxy material a pink or purple 
 colour while the rest of the tissue is stained blue. Methyl 
 violet is probably the best-known stain. 
 
 Method 
 
 1. Stain sections in a i per cent solution of methyl violet 
 in water for several minutes. 
 
 2. Differentiate in acetic acid, i per cent in water. 
 
 3. Wash thoroughly in water. Best for twenty-four hours 
 in several changes. 
 
 4. Mount in glycerine jelly or a watery solution of levulose. 
 
 Demonstration of Iron-containing Pigment in the Tissues 
 
 The sections may be fixed in formalin and cut in paraffin 
 or in gum. The latter is best for the purpose. 
 Method 
 
 1. Lay the sections in a 2 per cent watery solution of 
 ferrocyanide of potassium for a few minutes. 
 
 2. Transfer to hydrochloric acid i per cent in water 
 (acid alcohol may be used), and leave*for one to two hours. 
 
 3. Wash in water. 
 
 The sections may be counterstained in eosin or, better, in 
 alum carmine prepared as follows : 
 
 23 
 
354 APPENDIX A 
 
 Carmine . . .2 grm. 
 Alum .... 5 grrn. 
 Water . . . .100 c.c. 
 
 Boil for one hour, allow to cool, and filter. 
 Sections should be stained for ten minutes (gum or celloidin 
 sections) to twenty-four hours (paraffin sections). 
 
 Demonstration of Chromaffin Cells 
 
 In cases which had symptoms suggestive of Addison's 
 disease during life it is necessary (p. 114) to investigate the 
 chromafrln tissue of the body. Chromafrin cells (cells, i.e., 
 which have an affinity for chrome salts) are found in the 
 medullary portion of the suprarenals, in the carotid body, etc. 
 For the demonstration of such cells the tissues should be 
 fixed in Miiller's or Orth's fluids, cut in gum, and stained in 
 some nuclear stain, e.g. polychrome methylene blue, to bring 
 out the nuclei of the cells. After such treatment the chromaffin 
 cells assume a grass-green colour. 
 
 Weigert's Method for staining the Medullary Sheath 
 of Nerves 
 
 Methods for staining the medullary sheath of nerves are 
 all founded upon Weigert's method, which consists in fixing 
 the tissue in potassium bichromate, fluor chrome, or some such 
 mordant, subsequently staining in hasmatoxylin and differen- 
 tiating. Under the action of the bichromate, the myelin 
 substance of the medullary sheath becomes partially oxidised. 
 Lorrain Smith and Mair l bring forward evidence to show that 
 it is probably cholesterin in the form of a loose combination 
 with a fatty acid which becomes oxidised during bichromating. 
 The oxidation, if not too prolonged, is only partial. There 
 is still an unsaturated grouping. On treatment with 
 haematoxylin further oxidation occurs. The oxide of chromium 
 present in the myelin combines with the haematoxylin, so that 
 "laking" of the haemajpxylin, and therefore staining of the 
 myelin sheath takes place. It is possible to prolong the treat- 
 ment with the bichromate to such an extent that there is 
 
 1 Journal of Pathology and Bacteriology, 1909, vol. xiii. p. 14. 
 
APPENDIX A 355 
 
 complete oxidation of the myelin substance, when no staining 
 occurs on placing the tissue in haematoxylin. 
 
 By this method the myelin sheath is stained a dark blue- 
 black. Any area of brain, cord, or nerve, where the myelin 
 substance has disappeared, will remain unstained. The 
 method is adapted for demonstrating such degenerated areas. 
 They may be brought into greater prominence by counter- 
 staining in picro-fuchsin (van Gieson's stain) when the 
 degenerated area appears bright red. 
 
 The tissue having been mordanted in potassium bichromate, 
 e.g. in Miiller's fluid (see p. 327), for some six weeks, hardened 
 in alcohol, embedded in celloidin, and cut, sections are placed 
 in some preparation of haematoxylin, of which one of the best 
 is Kultschitzky and Welter's, prepared as follows : 
 
 Hasmatoxylin i grm. 
 
 Absolute alcohol . . .10 c.c. 
 Acetic acid (2 per cent) . . 90 c.c. 
 
 This solution should be prepared at least a week previous to 
 using. It keeps well, and indeed improves on keeping. 
 Method 
 
 1. Stain in haematoxylin twelve hours at 37 C. 
 
 2. Wash in water. 
 
 3. Place in ^ per cent watery solution of potassium 
 permanganate for twenty to thirty seconds. 
 
 4. Wash in water. 
 
 5. Differentiate in equal parts of sulphurous acid and 
 water for a few minutes, i.e. until the grey matter is colourless. 
 
 6. Wash thoroughly in water. 
 
 7. If desired, counterstain in picro-fuchsin (p. 341). 
 
 8. Wash in methylated spirit. 
 
 9. Dehydrate in absolute alcohol. 
 
 10. Clear in benzol. 
 
 1 1. Mount in balsam. 
 
 After washing with water (2) and (6), it is advisable to 
 leave the sections for some time (one to two hours) in water to 
 which a small quantity of a solution of lithium carbonate has 
 been added. 
 
356 APPENDIX A 
 
 Marchi's Method for demonstrating Degenerated Myelin 
 
 In areas of degeneration in brain, cord, or nerve, as the 
 result of disintegration of the myelin sheath, globules of fatty 
 substance are set free. These fatty globules will blacken on 
 treatment with perosmic acid, because the fatty substances, 
 having an unsaturated grouping, are oxidised at the expense of 
 the perosmic acid, which is reduced to black oxide of osmium. 
 The normal myelin substance of nerve tissue will act in the 
 same way if sections are placed in perosmic acid, directly or 
 after fixation in formalin. On the other hand, if the nerve 
 tissue containing the degenerated focus be exposed for a short 
 time to the action of bichromate, the normal myelin sheath 
 will not blacken, because oxidation of the myelin substance 
 occurs. The globules of fat in the degenerated area are only 
 slowly oxidised by the bichromate, thus reduction of perosmic 
 acid and blackening of the globules results. As stated else- 
 where (p. 347), only the olein compounds react in this way. 
 
 In order to demonstrate degenerating myelin in this way 
 a portion of spinal cord, brain, or nerve is placed in formalin 
 for twenty-four hours. At the end of that time very thin 
 portions are removed from the larger piece and placed in 
 Marchi's fluid (see p. 328) for three days. They are then 
 washed thoroughly in running water and cut in celloidin. In 
 order to show the nuclei of the cells safranin (i per cent) may 
 be used. 
 
 Method of demonstrating Ganglion Cells and their 
 Nissl Bodies 
 
 For fixation, any of the fixatives may be used. Nissl 
 recommends absolute alcohol. Small portions only of the 
 tissue (brain or cord) should be taken. Fixation and hardening 
 is complete in the alcohol in two to three days. Nissl cuts 
 the tissue embedded in gum arabic hardened by alcohol, but 
 embedding in celloidin or paraffin gives quite good results. 
 
 Method 
 
 1. Stain sections in Unna's polychrome methylene blue 
 (Grubler) for ten minutes. 
 
 2. Wash in distilled water for some minutes. 
 
APPENDIX A 357 
 
 3. Rinse in methylated spirit, and then in 
 
 4. Absolute alcohol to which one or two drops of acetic 
 acid have been added, and afterwards in pure abs. ale. 
 
 Differentiation may also be carried out in Unna's glycerin- 
 ether mixture (Griibler's) diluted with water. 
 
 5. Clear. 
 
 6. Mount. (Colophonium dissolved in xylol is recommended 
 for this purpose.) 
 
 Instead of the polychrome methylene blue, thionin or toluidin 
 blue may be used. 
 
 MAKING OF BLOOD FILMS 
 
 (a) Take some perfectly clean slides. Knock off the corner 
 of one of them (so that the end measures a little less than one 
 inch) by making a small scratch with a glass cutter. Place 
 a small drop of blood at the end of another slide and with the 
 broken end of the first guide the drop along the surface. In 
 this way a thin film of blood will be obtained which reaches 
 not quite to the margins of the slide on either side. 
 
 (b} Take a number of perfectly clean square No. 2 cover- 
 glasses. Place them on filter paper. Lift one of them with 
 a pair of small forceps and remove from the pricked finger 
 or ear a very small drop of blood. (The size of the drop 
 required depends upon the size of the cover-glass ; only ex- 
 perience will teach the operator.) Allow this cover-glass to 
 rest upon another, the drop of blood being between and the 
 angles of the slips not coinciding. The weight of the upper 
 cover-glass will spread the blood, and if both slips be clean an 
 eveTi film will be obtained. The lower cover-glass is then lifted 
 by means of the forceps by one of the projecting angles and 
 grasped between finger and thumb by two opposite angles. 
 The upper cover-glass is then grasped at a projecting angle by 
 the forceps and gently slid off the lower. 
 
 Each film is then allowed to dry in the air. The forceps 
 used should be preferably non-serrated at the points. 
 
 Staining of Blood Films. For ordinary purposes this is 
 best done by Jenner's, Leishman's, or Wright's stains. In 
 each case the stain is an eosinated methylene blue dissolved in 
 pure methylic alcohol. The stains may be bought ready made 
 
358 APPENDIX A 
 
 up, or tabloids prepared by Burroughs, Wellcome, & Co. may 
 be used. These should be dissolved in 10 c.c. of methylic 
 alcohol. No preliminary fixation is required as the methylic 
 alcohol acts as a fixative. The action of the stain can be limited 
 by drawing two lines across the slide with a grease pencil. 
 
 Leishmarfs and Wright's Stains 
 
 i. The stain is poured on to the film and allowed to remain 
 for one to two minutes. 
 
 2. Add an equal quantity (circa] of distilled water by means 
 of a glass pipette. Mix by gently rocking, and leave for three 
 to five minutes. 
 
 3. Pour off the stain and add from time to time distilled 
 water, rocking the specimen to and fro until the thinner portions 
 become pink. 
 
 4. Pour off the water and allow the film to dry in the air. 
 These stains are also excellent for demonstrating parasites, 
 
 such as malaria, trypanosomes, etc. 
 Jennets Stain 
 
 1. Pour on stain and leave for two to four minutes. 
 
 2. Wash off with distilled water, controlling the differentia- 
 tion by examining under the microscope. 
 
 3. Dry in the air, placing in a sloping position. 
 
 BACTERIOLOGICAL METHODS OF INVESTIGATION 
 
 Requisites 
 
 A bunsen burner or, in the absence of gas, a spirit lamp 
 should be close at hand. A number of sterile pipettes made 
 by drawing out suitable glass tubing in a blow pipe, and rubber 
 teats ; a looped platinum needle ; a flat piece of metal for 
 searing organs ; a rack with culture tubes (broth and agar and 
 blood-agar slopes), and a number of clean slides should be 
 within reach. When culture tubes are not available, several 
 sterile test-tubes, or, better, sterile swabs in test-tubes for 
 removing samples of exudate, will serve the purpose. In his 
 laboratory the pathologist should, of course, have an incubator, 
 dyes for staining, etc., etc. A pencil for writing on glass will 
 be found useful. 
 
APPENDIX A 359 
 
 Method of inoculating Culture Tubes 
 
 Sterilise the platinum needle by holding it obliquely in the 
 flame. Turn round the cotton wool plug of the culture tube 
 to be inoculated so as to ensure its easy removal. Holding 
 the platinum needle in the right hand like a pen and the 
 culture tube in the left, remove some of the exudate or pus, an 
 assistant holding open with forceps the incision previously 
 made into the serous sac, abscess, or organ. Grasp the cotton 
 wool plug between the right ring and little fingers and remove 
 it. Smear the surface of the agar tube with the exudate. In 
 the case of the broth tube, rub the loop of the needle against 
 the side of the tube at the upper level of the fluid. 
 
 Owing to the fact that bacteria of all kinds rapidly invade 
 the body after death, chiefly from the alimentary canal, bac- 
 teriological investigations carried out upon the cadaver are 
 not nearly so reliable as those performed during the life of the 
 patient. Pathogenic microbes tend to die out and their place 
 to be taken by the unimportant saprophytic forms which have 
 invaded the tissues. At the same time, where cultural investi- 
 gations have not been made during life, or where the affected 
 focus is in a part of the body which ordinary clinical methods 
 could not reach, it becomes necessary for the pathologist to 
 elucidate as far as he can the bacteriological aspect of the 
 diseased condition. Although, as we have seen, it is advisable 
 to carry out the examination as soon as possible after the death 
 of the patient for ordinary purposes, it is doubly so when the 
 pathologist has in view any bacteriological investigation. The 
 bacteria which invade the tissues multiply and spread at such 
 a rapid rate that ultimately any exact bacteriological observa- 
 tions become impossible. 
 
 
 Examination of the Blood 
 
 This is, of course, best done during the life of the patient 
 by drawing off 1-5 c.c. of blood from one of the arm veins. 
 In cases of bacteriaemia, when this has been omitted during 
 life, it is still possible to carry out the observation after death. 
 Unfortunately the blood is the tissue of the body most rapidly 
 
360 APPENDIX A 
 
 invaded by the saprophytic germs. Nevertheless, when care- 
 fully done, the investigation is undoubtedly useful. 
 
 It has been shown by Canon 1 that it is the blood in the 
 peripheral veins which gives the most reliable results, much 
 more reliable than in the case of the heart. 
 
 A large vein in the arm should be exposed by cutting 
 through the skin, incised with a sterile knife, and by pressing 
 down from above, a fair amount of blood or blood serum can 
 be collected in a syringe or pipette. The fluid is then added 
 to one or more broth tubes, or smeared over an agar slope, 
 and incubated. 
 
 The blood may also be obtained from the heart or from 
 the interior of one of the solid organs, such as the spleen, as 
 will be detailed later. 
 
 Examination of the Solid Organs 
 
 The spleen in typhoid fever, the lung in pneumonia, the 
 liver in cases of abscess formation, the brain in meningitis may 
 be examined in this way. 
 
 The surface of the organ is seared by means of a red-hot 
 flat piece of metal. A useful instrument for this purpose is a 
 copper section lifter. A knife is sterilised either in the flame 
 or by boiling, and a cut is made into the substance of the 
 organ through the seared portion of the surface. A platinum 
 loop is then inserted through the opening, pushed further in if 
 that is possible, withdrawn, and then smeared over the surface 
 of an agar slope or shaken in a broth tube. 
 
 Smears on slides may also be made from the solid organs, 
 more especially spleen or lung, and stained to demonstrate 
 bacteria. 
 
 Examination of Contents of Hollow Viscera 
 
 Bacteriological examination of the intestinal canal is seldom 
 of much use, owing to the multiplication of the organisms of 
 putrefaction. In certain cases, however, useful information may 
 be obtained. In typhoid fever, for example, pure cultures of 
 the bacillus typhosus may be obtained from the upper part of the 
 
 1 Die Bakteriologie des Blutes bei Infektionskrankheiten, Jena, 1905. 
 
APPENDIX A 361 
 
 jejunum as well as from the urinary bladder and gall bladder. 
 In opening these viscera for such a purpose, it is well to sear 
 the surface, incise with a sterile knife, and remove a sample of 
 the contents with platinum loop or pipette. 
 
 Examination of the Contents of Serous Sacs 
 
 This is usually the first and the commonest bacteriological 
 problem which the pathologist encounters. Where the presence 
 of pus is suspected in one of the serous sacs, it is necessary to 
 open the sac with certain precautions. 
 
 Having dissected down to the lining membrane pleura, 
 pericardium, peritoneum, as the case may be a clean knife 
 (bistoury) and pair of dissecting forceps are taken, the 
 membrane is raised with the forceps and a small incision 
 made. Through this a sterile platinum loop or a pipette is 
 inserted, a small quantity of the fluid removed and inoculated 
 into a series of culture tubes. 
 
 As a rule, the media employed will be broth or agar slope, 
 and where the presence of one of the more delicate germs is 
 suspected, such as the streptococcus, pneumococcus, or influenza 
 bacillus, blood agar or blood serum. Subsequently, a number 
 of films from the fluid should be made and stained. 
 
 Where the cavity has been already opened into, that is, 
 before its infected nature was realised, pressure should be exerted 
 upon the deeper parts so that some fresh fluid appears, and as 
 this flows over the edge of the opening a sample for inocula- 
 tion may be obtained by means of a platinum loop or pipette. 
 
 Blood agar culture media may be readily obtained from 
 ordinary agar slopes by smearing with a platinum loop a little 
 blood from the finger over the surface. The finger should be 
 first rubbed at the root of the nail with a little methylated spirit 
 which is allowed to dry. A sharp stab is then made by means 
 of a sharp -pointed knife similarly sterilised, a cloth being 
 wrapped round the finger to congest it. 
 
 Method of making Films from Pus and Sputum 
 
 When the pus or sputum is thick, an excellent method is 
 to place a drop of the fluid on a clean slide, place another 
 
362 APPENDIX A 
 
 on the top until the pus has spread between the two, then slide 
 them rapidly apart. In this way two good films are obtained. 
 Another method is to spread the fluid with the platinum needle 
 laid flat on the glass. 
 
 The film is then dried by moving it to and fro well above 
 the bunsen flame, and ultimately fixed by passing it thrice 
 through the flame. Another method of fixation is by means of 
 absolute alcohol. The alcohol is dropped on and left for some 
 minutes, after which it is washed off in water. Still another 
 fixative for films is the following mixture : 
 
 Methylated spirit . . .9 parts. 
 Formaldehyde . . i part. 
 
 This is dropped on and left for thirty seconds to a minute, and 
 then washed off with water. 
 
 Staining Methods for Bacteria 
 
 Bacteria are composed to a large extent of nuclear material. 
 Thus when it is desired to demonstrate them microscopically, 
 they are stained with nuclear dyes. Hasmatoxylin and similar 
 dyes, however, only stain organisms faintly. It is the basic 
 anilin dyes which are most commonly used for this purpose, 
 such as methylene blue, gentian violet, basic fuchsin. 
 
 As a rule, bacteria do not take up these dyes nearly so 
 readily as the nuclei of cells. In consequence, it is necessary 
 to enforce their action by (a) allowing the stain to act for a 
 prolonged period, (b) by heating, or (c) by the addition of 
 some mordant to the stain, such as carbolic acid, caustic 
 potash, anilin oil. Once stained, however, the bacteria retain 
 the dye with much more persistence than the nuclei of cells 
 amongst which they may lie. Hence it is possible by the use 
 of a decolourising or differentiating agent, such as alcohol or 
 some dilute acid, to bring the bacteria into greater prominence 
 and differentiate them from the surrounding cells. This 
 resistance to decolourising agents is more marked in a group 
 of bacteria which includes the tubercle bacillus. In con- 
 sequence, the term "acid-fast" is applied to them. The 
 tubercle bacillus, after having been stained, resists also the 
 decolourising action of alcohol as well as of acid. 
 
APPENDIX A 363 
 
 Gram's Method and Weigert's Modification 
 
 1. Fix film. 
 
 2. Filter on to film or section anilin or carbol- gentian 
 violet made up as follows : 
 
 Saturated solution of anilin oil in water or 
 
 carbolic acid i to 40 . . . .9 parts. 
 
 Saturated alcoholic solution of methyl or gentian 
 
 violet ....... i part. 
 
 For films of bacteria or pus this should be left on for two 
 minutes. 
 
 For sections of tissue it should remain five minutes. 
 
 3. Wash in water. 
 
 4. Pour on Gram's or Weigert's iodine solution. The 
 latter is three times the strength of the former and is better for 
 this reason. It is prepared as follows : 
 
 Iodine ..... excess. 
 Potassium iodide . . .5 grm. 
 Water . . . . . 100 c.c. 
 
 The iodine is left on for one minute in the case of films, 
 for two minutes in the case of sections. 
 
 5. Differentiate in methylated spirit. 
 
 Some experience is required before this can be done suc- 
 cessfully. A few seconds is usually all that is required for 
 films. In the case of sections, not quite all the blue should be 
 removed. 
 
 A better method with sections is to blot the section firmly 
 but carefully with filter paper after the iodine. Then drop on 
 anilin xylol (equal parts of anilin oil and xylol). This may 
 be allowed to act until all the blue has been removed. Rapidly 
 treat with spirit to remove the anilin xylol. 
 
 6. Wash in water. 
 
 7. Counterstain for half a minute in some red or brown 
 stain, such as fuchsin, safranin, Bismarck brown, or lithium 
 carmine considerably diluted. 
 
 8. Wash in water. 
 
 9. In the case of films, dry them well above the flame. In 
 
364 APPENDIX A 
 
 the case of sections, dehydrate, clear, and mount in Canada 
 balsam. 
 
 Carbol- Thionin Blue 
 
 1. Filter on staining solution consisting of i gramme 
 thionin blue dissolved in 100 c.c. carbolic (i to 40). The 
 author has found this stronger solution preferable to the dilu- 
 tion of the above, in the proportion of i of the stain to 3 of 
 water, recommended by Muir and Ritchie. 
 
 Films should be stained for three to five minutes, sections 
 from five to ten minutes. 
 
 2. Wash in water. 
 
 In the case of films, blot, dry, and, if necessary, mount. 
 In the case of sections and thick films of pus 
 
 3. Decolourise very rapidly in i per cent acetic acid in 
 water. 
 
 4. Wash in water. 
 
 5. Dehydrate, clear, and mount. 
 
 The above is an excellent method for demonstrating the 
 ordinary bacteria in films from cultures, in pus and in tissues. 
 It is specially suitable for showing up masses of typhoid 
 bacilli in spleen and mesenteric glands, bacillus coli in liver, 
 bacillus pestis in spleen or bubo, entamoeba hystolytica in 
 dysentery, etc. The organisms stain a deeper purple than the 
 nuclei of the cells. Red blood corpuscles in properly stained 
 specimens are yellow. 
 
 Where the organisms are too readily decolourised, as in the 
 case of bacillus pestis sometimes, after staining, instead of 
 washing in water and decolourising, blot the specimen and pour 
 on some anilin oil and rock the slide to and fro until the 
 greater portion of the stain has come out, then use xylol and 
 mount in balsam. 
 
 This staining method may also be used for demonstrating 
 mucus which takes on a red or purple colour with Thionin 
 blue. 
 
 Eosin Methylene Blue 
 
 This method is given above (p. 342). It is well adapted 
 for demonstrating masses of cocci in vegetations, diphtheria 
 
APPENDIX A 365 
 
 bacilli in false membrane, abscesses, etc., also entamcebae in the 
 large bowel or liver. 
 
 Both this method and the previous one have this advantage 
 over Gram's method that the cells and intercellular fibres of 
 the tissues and bacteria are stained more naturally. In Gram's 
 method the organisms appear often abnormally large, and the 
 tissues tend to be altered by the iodine. 
 
 Staining Methods for the Tubercle Bacillus 
 
 A. Ziehl-Neelsen Method 
 
 1. Filter on the following stain usually known as Ziehl- 
 Neelsen's carbol-fuchsin stain : 
 
 Basic fuchsin ..... I part. 
 Absolute alcohol . . . .10 parts. 
 Carbolic acid in water (i : 20) . .100 parts. 
 
 Instead of the carbolic (i : 20) a saturated solution of anilin 
 oil in water may be used. This should of course be filtered 
 previous to making up. 
 
 The best way is to keep in a stock bottle absolute alcohol 
 saturated with basic fuchsin. This is added to the carbolic 
 water as required. 
 
 In the case of films, hold over flame or place upon hot 
 metal slab or coin while steam rises. Remove the specimen 
 and repeat the process twice, the staining occupying three to 
 five minutes. 
 
 In the case of sections, the above method may be used, the 
 staining process occupying at least five minutes. 
 
 The author has, however, found that placing the sections 
 in the carbol- or anilin -fuchsin in ajar in the paraffin bath at 
 50-55 C. gives much better results, the tissues being less 
 damaged by the heating. 
 
 2. Wash in water. 
 
 3. Differentiate in i per cent hydrochloric acid in methy- 
 lated spirit. This the author has found very much better 
 than the usual 25 per cent H 2 SO 4 in water. The advantages 
 
366 APPENDIX A 
 
 are that there is no danger of decolourising ; the alcohol test 
 is applied to the organism at the same time as the acid, 
 and, in the case of sections, the tissues are not damaged 
 as they certainly are by the stronger acid. Differentiation 
 should be carried out until there is just a slight pink tinge 
 in the film or section. Thick portions of the film will 
 probably be still red, but in any case, in searching for tubercle 
 bacilli, such thick areas should be avoided. 
 
 4. Wash in water. 
 
 5. Counterstain in a i per cent watery solution of methylene 
 blue for half a minute. 
 
 With sections, diluted Leishman's stain gives excellent 
 results. One part of Leishman's stain is added to 10 of ordinary 
 tap water ; the section is left in this in a jar over night. It is 
 then differentiated rapidly in acetic acid (i : 1000), dehydrated, 
 cleared, and mounted. 
 
 6. In the case of films, wash in water, blot, dry, and 
 mount. 
 
 In the case of sections, dehydrate thoroughly, thus removing 
 excess of methylene blue, clear in xylol or benzol, and mount 
 in balsam. 
 
 B. Much-Gram Method 
 
 1. Stain film in the following mixture, either heating above 
 the flame for a few minutes till steam rises or leaving in the 
 incubator at 37 C. for twenty-four to forty-eight hours : 
 
 Saturated alcoholic solution of methyl 
 
 violet B.N. . . . . .10 c.c. 
 
 2 per cent water solution of carbolic acid. 100 c.c. 
 
 2. Apply Gram's iodine for one to five minutes. 
 
 3. Drop on 5 per cent nitric acid and leave for one minute. 
 
 4. Drop on 3 per cent hydrochloric acid and leave for ten 
 seconds. 
 
 5. Differentiate in acetone and alcohol equal parts. 
 
 6. Wash in water. 
 
 7. Counterstain in dilute fuchsin if required. 
 
 8. Wash, dry. 
 
APPENDIX A 367 
 
 More recently Much has used instead of 2, 3, and 4 the 
 following mixture : 
 
 Potassium iodide . . .5 grm. 
 2 per cent hydrogen peroxide . 100 c.c. 
 
 The film is then differentiated in absolute alcohol. 
 
 By either of the above methods, in addition to the ordinary 
 form of the tubercle bacillus which is demonstrated by methods 
 such as Ziehl-Neelsen's, a granular form of the organism which 
 appears as minute blue-black granules is shown. This form 
 is believed by many to be a resting stage or spore form of the 
 bacillus. The granules may occur in a bacillary form or may 
 be found free. 
 
 C. Method combining Ziehl-Neelsen with Much-Gram 
 (Much-Weiss) 
 
 i. Stain in the following mixture for twenty-four to forty- 
 eight hours. 
 
 Much's carbol methyl violet solution . i part. 
 Carbol-fuchsin 3 parts. 
 
 Subsequently treat with iodine, nitric acid, etc., as in the 
 Much-Gram method. 
 
 Method of demonstrating the Club Form of Streptothrix 
 Actinomyces 
 
 These bodies are exceedingly variable in their staining 
 reactions. They are sometimes demonstrable by means of 
 Gram's method, but they are more often decolourised. The 
 author has introduced the following method, which has the 
 advantage of bringing the bodies out in striking contrast 
 to their surroundings. 
 
 The tissues may be fixed in either 10 per cent formalin or 
 in saturated corrosive sublimate. The section is placed in the 
 following mixture, which is known as Mann's methyl-blue and 
 eosin stain : 
 
368 APPENDIX A 
 
 i. i per cent methyl-blue in distilled water . 35 c.c. 
 i per cent eosin in distilled water . . 45 c.c. 
 Distilled water . . . . .100 c.c. 
 
 The section should be left in this for twenty-four hours. A 
 few hours would suffice, but in order to obtain the best results, 
 the longer period is necessary. 
 
 2. Wash in water. 
 
 3. Dehydrate in absolute alcohol to which a few drops of a 
 i per cent solution of caustic potash in absolute alcohol has 
 been added. 
 
 Treat the specimen with the above reagent until it becomes 
 a bright pink colour. 
 
 4. Wash in i per cent acetic acid in water. The section 
 will now become bright blue. 
 
 5. Wash in water. 
 
 Examine under microscope, and if necessary repeat 3 and 4. 
 
 6. Dehydrate, clear, and mount. 
 
 The above method is a slight modification of Mann's 
 methyl-blue and eosin stain. By means of it the clubs will be 
 stained a bright red colour, while the cells surrounding them, 
 as well as the mycelium on the fungus, stain blue. The stain 
 is not absolutely specific, as red blood corpuscles and inflam- 
 matory exudate as well as the granules of eosinophil leucocytes 
 and pancreatic cells react in a similar fashion. 
 
 Method for staining the Capsules of Bacteria 
 
 The following is a slight modification of Muir's capsule 
 method, suggested by Dr. F. E. Reynolds. It is useful 
 for staining the capsule of the pneumococcus or pneumobacillus 
 in blood, sputum, or pus films : 
 
 1. Stain in Carbol-fuchsin, steaming, for one minute. 
 
 2. Wash well in water. 
 
 3. Apply Muir's mordant for one to two minutes. 
 Muir's mordant is prepared as follows : 
 
 Saturated solution of corrosive sublimate . 2 parts. 
 Tannic acid (20 per cent solution) . . 2 parts. 
 Saturated solution of potash alum . . 5 parts. 
 
APPENDIX A 369 
 
 4. Wash well in water. 
 
 5. Differentiate in methylated spirit for one minute. 
 
 6. Wash well in water. 
 
 7. Stain in methylene blue for one to two minutes, 
 
 8. Wash in water. 
 
 9. Dehydrate quickly in absolute alcohol. 
 
 i o. Clear in xylol or benzol for five minutes. 
 ii. Mount in Canada balsam. 
 
 By this method the organisms are stained red, while the 
 capsules of the bacteria, the pus cells, etc., are stained blue. 
 
 Hiss's Method 
 
 1. Stain in the following mixture, heating for a few seconds 
 over the flame until steam rises. 
 
 Saturated alcoholic solution of acid fuchsin . i part. 
 Distilled water 19 parts. 
 
 2. Wash off the staining fluid with a 20 per cent solution 
 of copper sulphate. 
 
 3. Without washing in water dry with filter paper. 
 
 By this method the capsules of organisms growing in both 
 as well as these in blood and pus films can be demonstrated. 
 
 Methods for demonstrating Spirochsetes 
 
 In Films 
 
 1 i ) Giemstfs Method. 
 
 1. Make a thin film of the fluid to be examined. 
 
 2. Fix it in absolute alcohol for fifteen minutes. 
 
 3. Dilute Giemsa's stain by adding 10 drops to 10 c.c. 
 distilled water and pour over film, leaving for ten to thirty 
 minutes. 
 
 4. Wash well in a stream of water and dry. 
 
 (2) Burros Ink Method. 
 
 For this purpose a little " Chin-chin, Pelican " ink is 
 mixed with an equal quantity of distilled water. This mixture 
 should be sterilised in the autoclave and allowed to sediment 
 for some time (two weeks). It is then decanted off the 
 
370 APPENDIX A 
 
 sediment. With a platinum needle a small quantity of the 
 fluid to be investigated is mixed with a little of the ink on a 
 clean slide and a film made. This is allowed to dry and is 
 then examined with the oil immersion lens. 
 
 In Tissues 
 
 For this purpose Levaditi's method gives excellent results. 
 
 1. Thin pieces of the tissues are placed in 10 per cent 
 formalin for twenty-four hours. 
 
 2. Transfer to 96 per cent alcohol for twenty-four hours. 
 
 3. Place in distilled water until they sink. 
 
 4. Transfer to 1^-3 per cent solution of silver nitrate in 
 distilled water and leave there for three days in the incubator 
 at 37 C. 
 
 5. Wash rapidly in distilled water. 
 
 6. Reduce by placing for twenty-four to forty-eight hours 
 at room temperature in the dark in 
 
 Pyrogallic acid . ... 4 grm. 
 Formalin (40 per cent) . . 5 c.c. 
 
 Distilled water . . . . 100 c.c. 
 
 7. Wash in water. 
 
 8. Embed in paraffin or celloidin. 
 
 After cutting, the paraffin sections merely require solution of 
 the paraffin and mounting in balsam. 
 
 By this method the spirochaetes appear black, from the 
 silver which is precipitated in their substance. 
 
 EXAMINATION OF SPUTUM, PUS, ETC., 
 FOR THE TUBERCLE BACILLUS 
 
 The sputum should be poured into a Petri dish, and by 
 means of sharp-pointed forceps and scissors a suitable portion 
 is removed and placed upon a clean slide. A second slide is 
 placed upon the top of the first and the sputum spread out by 
 pressing the slides together. The two slides are then slid 
 apart and the two films dried and fixed in the flame. Suitable 
 portions for examination are any rounded yellow or white 
 
APPENDIX A 371 
 
 masses, or, in the absence of these, opaque white streaky 
 material. Both slides are then stained with carbol-fuchsin for 
 three to five minutes, the stain being heated until the steam 
 rises. A convenient way of doing this is to heat a penny in the 
 flame and then place the slide covered with carbol-fuchsin upon 
 the coin. Where a number of slides have to be stained at once 
 a useful method is to place two pieces of glass tubing across a 
 sink ; the slides are then placed across these, the stain is filtered 
 on, and the slides heated by playing a bunsen flame on them 
 from below. Having been stained, the films are washed in 
 water and differentiated in a i per cent mixture of hydrochloric 
 acid and methylated spirit. This medium for differentiating 
 has the advantage that the alcohol and acid test are applied at 
 one and the same time. The slide is then washed in water, 
 counter-stained in methylene blue (i per cent watery), washed 
 again in water, dried, and examined under the oil immersion. 
 It is well to examine both slides systematically from one end to 
 the other. 
 
 Pus or caseous material may be examined in a similar way. 
 
 The reason for differentiating with acid is because a majority 
 of organisms, after staining in carbol-fuchsin and heating, are 
 readily decolourised with dilute acid. The tubercle bacillus 
 and other germs, such as the bacillus of leprosy, the smegma 
 bacillus, the Timothy-grass bacillus, the butter bacillus, etc., are 
 not decolourised with dilute acid. They thus form a group of 
 acid-fast bacilli. Spirit or alcohol forms another differentiating 
 medium, because the tubercle bacillus resists it, whereas the 
 smegma bacillus is decolourised. 
 
 Concentration Method for Sputum, Pus, etc. 
 
 Add to the sputum, pus, etc. an equal quantity of 50 per 
 cent antiformin. 
 
 Antiformin may be made up as follows : 
 
 Solution i 
 
 Sod. carb 10 grm. 
 
 Calx chlorinata (bleaching powder) . 50 grm. 
 
 Dist. water 100 c.c. 
 
372 APPENDIX A 
 
 Solution 2 
 
 Sod. hydrate . . 1 5 grm. 
 
 Dist. water. . . . icoc.c. 
 
 For use mix equal parts of i and 2, and dilute with 
 equal quantity of water. 
 
 The mixture is then shaken thoroughly and allowed to 
 remain for two to twenty-four hours. At the end of that time 
 it will form a more or less homogeneous fluid. This may be 
 centrifugalised at once and the deposit examined by staining, 
 or Eurich's method may be employed as follows : Acetone 
 and ether (equal parts) are shaken up with the antiformin 
 mixture in a narrow glass vessel. The fluids will then separate 
 into two layers, the acetone and ether being above, and at the 
 point of junction a white precipitate, which contains the larger 
 proportion of any cellular debris in the sputum, also the 
 micro-organisms and- among these the tubercle bacilli. The 
 precipitate is easily removed (after pipetting of! the ether) 
 by means of a glass pipette and rubber teat. Films are 
 made from this, stained, and examined. In cases where no 
 precipitate forms at the junction of the fluids, the acetone 
 and ether should be decanted off, and some of the antiformin 
 mixture centrifugalised. Films are made" from the deposit. 
 Should such deposit be found difficult to spread on a slide, 
 a little of the original sputum mixed with it will assist matters. 
 
 Caseous tissue should be cut up into thin shreds by 
 sectioning with the freezing microtome and the resulting pulp 
 treated with antiformin and centrifugalised. The deposit is then 
 smeared on slides and stained by the Ziehl-Neelsen or Much- 
 Gram method. 
 
 Care should always be taken to see that any distilled or 
 tap water used in carrying out these processes is itself free 
 from acid-fast organisms. 
 
 THE BACTERIOLOGICAL DIAGNOSIS OF 
 DIPHTHERIA 
 
 It may be necessary in some fatal cases of disease to 
 ascertain whether or not diphtheria bacilli are present in the 
 
APPENDIX A 373 
 
 fauces, tonsils, or mucous membrane of the air passages. The 
 method of diagnosis is the same as in the case of the living 
 subject, and should be carried out as follows : 
 
 (a) Films should be made from suspicious exudate in any 
 of the above situations and stained by (i.) Gram's method ; (ii.) 
 carbol-thionin blue ; (iii.) Neisser's method (see below). Char- 
 acteristic organisms may or may not be found. If none are 
 seen, cultures should be made. 
 
 (b) A sterile swab or platinum needle is rubbed over the 
 surface of any exudate which may be present. If no exudate 
 is present, the secretion covering the tonsil is removed and 
 smeared over the surface of a tube of blood serum or blood 
 agar. This is incubated at blood heat for 12 to 24 hours. 
 Films are then made from the growth which develops, and 
 stained by the above methods. 
 
 Neisser's Staining Method for the Diphtheria Bacillus 
 
 Solutions 
 
 A. Methylene blue (Griibler), i grm., dis- 
 
 solved in 20 c.c. of 96 per cent alcohol. 
 Add to this 950 c.c. of distilled water 
 and 50 c.c. glacial acetic acid. 
 
 B. Bismarck-brown (Vesuvin) . 2 grm. 
 Distilled water . . i litre. 
 
 Method. 
 
 Stain films for one to three seconds in A, pour off the 
 excess of stain and blot. Drop on B and leave for three to 
 nine minutes. Wash, dry, and examine. 
 
 By this method the body of the diphtheria organism is 
 stained brown while the granules are dark blue. 
 
 A modification of the method is as follows : 
 
 Prepare two staining fluids : 
 
 A. Methylene blue . . i grm. 
 
 96 per cent Ale. . . .20 c.c. 
 
 Glacial acetic acid . . 50 c.c. 
 
 Distilled water . . . i litre. 
 
374 APPENDIX A 
 
 B. Crystal violet (Hochst). . i grm. 
 
 Abs. ale 10 c.c. 
 
 Distilled water . . . 300 c.c. 
 Mix two parts of A with one of B. 
 Method. 
 
 1. Stain in mixture for about ten seconds. 
 
 2. Wash in water. 
 
 3. Stain in cresoidin (2 grm. in 300 c.c. water) for about ten 
 seconds (the stain should be dissolved in hot water and filtered). 
 
 4. Wash, dry, and mount. 
 
 The appearance of the organism is the same as with the 
 first method. 
 
 AGGLUTINATION TEST FOR ORGANISMS 
 
 It is sometimes necessary to carry out an agglutination test 
 in the case of an organismal condition such as typhoid fever 
 (Widal reaction), or in cases of suspected meat poisoning (see 
 p. 314) ; the serum of the individual being tested as regards 
 its agglutinating power against the germ or germs cultivated 
 from the lesion or from intestinal contents or against stock 
 cultures of known organisms. 
 
 The method of carrying out the test is as follows : 
 
 1. The serum of the case is secured by centrifugalising a 
 quantity of blood or blood-clot obtained from the heart and 
 pipetting off the supernatant fluid. This is mixed with normal 
 saline solution by means of a graduated pipette so as to make 
 dilutions of i in 5, i in 20, and i in 40, etc. 
 
 Another method is to prepare a capillary pipette (see below), 
 make a mark upon it with a grease pencil, and draw up, by 
 means of a rubber teat, to the mark one portion of the serum 
 and subsequently four portions of the normal saline solution, 
 allowing a bubble of air to intervene between the various 
 portions. These are then blown out and mixed in a watch 
 glass, thus forming a dilution of one in five. From this the 
 other dilutions can be made in a similar fashion. 
 
 2. kpure culture on solid medium, e.g. agar slope, of the 
 organism against which it is desired to test the serum is 
 obtained. An emulsion is made by mixing some of the growth, 
 
APPENDIX A 375 
 
 removed by a platinum needle, in normal saline, thus making a 
 solution with a distinctly opalescent, but not too turbid, appear- 
 ance. This is allowed to settle for an hour, or centrifugalised 
 for a few minutes, in order to get rid of any clumps of bacteria. 
 A slide with a hollow in the centre is then taken and 
 smeared round the margin of the hollow with vaseline. A 
 cover slip is cleaned, and by means of a platinum loop a 
 minute spot of the serum ( I in five) and one of the emulsion are 
 placed side by side on the cover glass, and, after heating the 
 loop in order to dry it and allowing it to cool, the two are mixed 
 together. The cover slip is then lifted with a pair of forceps, 
 turned over, and placed upon the slide so that the drop hangs in 
 the hollow. The slide is examined under a J objective, care 
 being taken to cut off the greater part of the light coming from 
 the mirror of the microscope, by means of the iris diaphragm. 
 The organisms will usually be seen as minute highly refractile 
 bodies, darting hither and thither. Similar hanging- drop 
 preparations should be made with the other dilutions of the 
 serum. Dilutions of I in 10, i in 40, and I in 80 are thus 
 obtained. Control preparations may also be made with a 
 normal serum. 
 
 After examining the slides under the microscope to see that 
 the bacteria are visible and motile they should be placed in 
 the incubator and again examined after one-half to one hour. 
 The presence of clumps of motionless bacteria is indicative of 
 a positive reaction. At the same time a positive result with a 
 dilution of I in 10 should be neglected unless there is agglutina- 
 tion in the higher dilutions as well. 
 
 In the absence of the hollow slides, ordinary slides may 
 be used. 
 
 METHOD OF MAKING PIPETTES FOR REMOVING 
 FLUIDS, ETC. 
 
 Mark off a section, 6-8 inches long, of soft glass tubing 
 (J inch bore) with a file and break it across. This is held in 
 the hands so that the centre lies in the flame of a blow-pipe 
 or an ordinary Bunsen burner, the tubing being constantly 
 turned between the fingers so that the flame plays upon all sides 
 of it. No attempt should be made to draw the two ends 
 
376 APPENDIX B 
 
 apart until the central portion is quite soft. When this has 
 been effected, the tube is withdrawn from the flame, and very 
 slowly the two ends are separated, until a capillary tube of at 
 least 12 inches long has been made. The tubing should be 
 held in the same position until it has cooled sufficiently to 
 prevent it bending. It is then broken across in the centre, 
 thus forming two pipettes. The end of the pipette should be 
 passed through the flame before using for the removal of 
 exudate, blood, etc. A rubber teat attached at the broad end 
 will enable the operator to withdraw a considerable quantity 
 of fluid. 
 
 APPENDIX B 
 EMBALMING 
 
 In cases where bodies have to be sent long distances, it 
 may be necessary to inject a preservative into the circulation 
 in order to stay the progress of putrefaction. The simplest 
 fluid for the purpose is made up as follows : 
 
 Formalin . . . . -4 pints. 
 Acid-carbolic (cryst.) . . I Ib. 
 
 Water . . . . .2 gallons. 
 
 This fluid, to the amount of two gallons (in the case of an 
 adult male), should be introduced by means of a cannula into 
 the femoral artery or abdominal aorta. The time selected for 
 the operation should be at least twenty-four hours after death, 
 i.e. at a time when rigor mortis has just passed off. If the 
 femoral artery is selected, the injection should be made in 
 Scarpa's triangle, and the nozzle of the injector directed 
 upwards towards the heart. 
 
 If a post-mortem examination has to be performed in 
 addition, this should be carried out at least twenty-four hours 
 after the injection. 
 
 Preservative fluid should also be introduced into the 
 stomach, intestines, bladder, pleura, and other spaces. 
 
 The surface of the body may, in addition, be washed with 
 a saturated solution of corrosive sublimate in methylated spirit 
 mixed with five times the amount of glycerine. (C. R. Box, 
 Post-Mortem Manual.) 
 
INDEX 
 
 Abdominal contents, examination 
 
 of, 28 
 Abscess, cerebral, 240 
 
 actinomycotic, 182 
 
 association with pulmonary 
 disease, 241 
 
 of liver, 181 
 
 of lung, 131 
 
 tropical, 182 
 
 Absolute alcohol, as fixative, 329 
 Acid alcohol, 339 
 Acromegaly, 260 
 Actinomycosis of liver, 182 
 
 of intestine, 1 66 
 
 of mouth, 153 
 Acute yellow atrophy of liver, 
 
 182, 183, 270 
 Addison's disease, 114 
 Adeno- carcinoma, 299 
 
 of breast, 273 
 
 of intestine, 171 
 
 of liver, 192 
 
 of stomach, 158 
 Adenoma, 285 
 
 malignant, 300 
 
 of breast, 273 
 
 of thyroid, 112 
 Agglutination test for organisms, 
 
 374 
 
 Agonal thrombi, 63 
 Albumose, Ben ce- Jones, 293 
 Alimentary tract, parasites of, 170 
 Alveolar sarcoma, 292 
 Ammonia carmine, 351 
 Ammonia gas, poisoning from, 314 
 Amoebic dysentery, 168 
 
 Amyloid, stains for, 352 
 Amyo trophic lateral sclerosis, 250 
 Anaemia, pernicious, 93 
 Anasarca, 217 
 Aneurysm, causes of, 87 
 
 dissecting, 85 
 
 effects on surrounding parts, 86 
 
 false, 85 
 
 fusiform, 85 
 
 miliary, 85 
 
 rupture of, 86 
 
 saccular, 85 
 
 sites of, 85 
 
 types of, 85 
 Angio-sarcoma, 293 
 Angioma, cavernous, 281 
 
 lymph, 282 
 
 plexiform, 281 
 Anilin stains for waxy material, 
 
 353 
 
 Anthracosis of lung, 133 
 Anthrax, 2 
 Antiformin, 371 
 Antrum, maxillary, examination 
 
 of, 41 
 Aorta, abnormalities of, 48 
 
 atheroma of, 79 
 
 congenital stenosis of, 47 
 
 examination of, 23 
 Aortic valve, diseases of, 71, 72 
 
 effects of disease of, 71 
 Apoplexy, cerebral, 237 
 
 pulmonary, 123 
 Appendicitis, 169 
 Arteries, calcareous degeneration 
 of, 78 
 
 377 
 
378 
 
 INDEX 
 
 Arteries, diseases of, 77 
 
 fatty degeneration of intima of, 
 78 
 
 hypertrophy of media of, 80 
 
 inflammation of, 78 
 
 waxy degeneration of, 78 
 Arteries in nephritis, 216 
 
 in syphilis, 84 
 
 in tuberculosis, 84 
 Arteriosclerosis, 78 
 Arteriosclerotic kidney, 214 
 Artery, pulmonary, congenital 
 stenosis of, 47 
 
 pulmonary, examination of, 
 
 23 
 Arthritis, acute, 261 
 
 rheumatoid, 262 
 
 suppurative, 261 
 
 tuberculous, 261 
 Aschoff-Becker microtome, 334 
 Aschofif on gall stones, 195 
 Ascites, 172 
 
 chylous, 172 
 Atelectasis of lung, 120 
 Atheroma, 79 
 
 aneurysm from, 81 
 
 calcareous deposit in, 79 
 
 causes of, 82 
 
 diffuse, 79 
 
 effects of, 8 1 
 
 interstitial nephritis in, 81 
 
 nodular, 79 
 
 syphilitic, 80 
 
 thrombosis in, 81 
 Atherosclerosis, 79 
 Atrophy, brown, of heart, 54 
 
 yellow, of liver, 182, 183 
 
 progressive muscular, 249 
 Auriculo-ventricular bundle, 73 
 Autopsy, i 
 
 B. diphtheria, stain for, 373 
 B. pestis, staining of, 364 
 Bacteria, acid-fast, 362 
 stain for (acid- fast), 365 
 carbol-thionin blue stain for, 
 
 364 
 eosin methylene blue stain for, 
 
 364 
 Gram's stain for, 363' 
 
 Bacteria, Gram-Weigert's stain, 
 363 
 
 methods of staining, 362 
 
 staining of capsules, 368 
 Bacteriological investigation, 
 methods of, 358 
 
 capillary pipettes, 375 
 
 for diphtheria, 372 
 
 of blood, 359 
 
 of hollow viscera, 360 
 
 of serous sacs, 361 
 
 of solid organs, 360 
 
 requisites for, 358 
 Ball thrombus, 63 
 Banti's disease, 95 
 Barlow's disease, 99 
 Base of skull, Harke's saw-cut for, 
 
 4i 
 
 Bence- Jones albumose, 293 
 Best's method of demonstrating 
 
 glycogen, 351 
 
 Bile ducts, diseases of, 194 
 inflammation of, 194 
 obliteration of, 194 
 obliteration of in fine cirrhosis, 
 
 194 
 
 suppuration of, 195 
 Bile and pancreatic ducts, ex- 
 amination of, 31 
 Biliary concretions, 195 
 Bladder, urinary, diseases of, 227 
 tumours of, 228 
 calculi of, 228 
 Bladder and urethra, examination 
 
 of, 33 
 
 removal of, 33 
 
 Blood, bacteriological examina- 
 tion of, 359 
 diseases of, 91 
 in carbon monoxide poisoning, 
 
 3i3 
 
 in nephritis, 217 
 
 post-mortem examination of, 91, 
 358 
 
 test for carbon monoxide in, 314 
 Blood-film, making of, 357 
 Blood-vessels, diseases of, 77 
 Body, external examination of, 13 
 
 indentification of, 307 
 
 toilet of, 44 
 
INDEX 
 
 379 
 
 Bone, osteitis deformans, 260 
 
 syphilis of, 260 
 
 tuberculosis of, 259 
 
 tumours of, 260 
 
 Bone marrow, degeneration of, 
 1 02 
 
 diseases of, 100 
 
 erythroblastic, 101 
 
 examination of, 100 
 
 functions of, 101 
 
 in pneumonia, 129 
 
 leucoblastic, 101 
 
 pigmentary changes in, 102 
 Bowels, examination of, 28 
 
 diseases of, 159 
 Brain, circulatory disturbances, 
 
 233 
 
 diseases of, 229, 233 
 
 embolism of, 235 
 
 examination of, 38 
 
 gumma of, 242 
 
 hydrocephalus of, 234 
 
 inflammation of, 240 
 
 osdema of, 233 
 
 removal of, 35, 37 
 
 syphilis of, 241 
 
 thrombosis of, 235 
 
 tuberculosis of, 241 
 
 tumours of, 242 
 Breast, diseases of, 272 
 Bright' s disease, 207 
 Bronchi, dilatation of, 119 
 
 diseases of, 117 
 
 examination of, 28 
 Bronchiectasis, 119 
 Bronchiolectasis, 119 
 Bronchitis, acute, 117 
 
 chronic, 118 
 
 syphilitic, 119 
 
 tuberculous, 118 
 Bronchocele, 112 
 Broncho- pneumonia, 129, 130 
 Broncho-pneumonia, purulent, 
 
 130 
 
 " Brown atrophy " of heart, 54 
 " Brown induration " of lung, 123 
 Bruce microtome, 333 
 Bum's ink stain for spirochaetes, 
 
 369 
 " Button-hole," mitral, 69 
 
 Caisson disease, 246 
 
 Calcareous degeneration of media, 
 
 78 
 
 Calcareous material, staining of, 
 352 
 
 Von Kossa silver stain for, 352 
 Calculus, biliary, 195 
 
 urinary, 228 
 
 Calvarium, removal of, 36 
 Canada balsam, 336 
 Cancer, general use of term, 286 
 " Cancer bodies," 297 
 Cancers, 295 
 Canon on bacteria in peripheral 
 
 veins, 360 
 
 Capsule stains for bacteria, 368 
 Carbol-fuchsin stain, 365 
 Carbol-thionin blue stain for bac- 
 teria, 364 
 Carbolic oil in place of rubber 
 
 gloves, 6 
 
 Carbon monoxide poisoning, 313 
 Carcinoma, adeno-, 299 
 
 colloid, 302 
 
 columnar cell, 300 
 
 differences from sarcomata, 295 
 
 encephaloid, 302 
 
 general characteristics of, 295 
 
 glandular, general character- 
 istics of, 300 
 
 inclusions, 297 
 
 medullary, 302 
 
 metastases, 296 
 
 of bladder, 228 
 
 of bone, 261 
 
 of brain, 224 
 
 of breast, 273 
 
 of gall bladder, 197 
 
 of heart, 60 
 
 of intestine, 171 
 
 of kidney, 223 
 
 of larynx, 117 
 
 of liver, 192 
 
 of lung, 148 
 
 of lymph glands, 105 
 
 of pancreas, 198 
 
 of prostate, 274 
 
 of spinal cord, 252 
 
 of stomach, 158 
 
 of suprarenal, 115 
 
38o 
 
 INDEX 
 
 Carcinoma of thyroid, 112 
 
 of uterus, 268 
 
 scirrhous, 301 
 
 sites of, 295, 297 
 
 soft, 302 
 
 spheroidal cell, 301 
 
 spread to glands, 296 
 
 types, 295 
 
 ulceration of, 295 
 Capsules, staining of, 368 
 Cathcart, freezing microtome, 334 
 Cavernous angioma, 281 
 " Cell nest," 298 
 Celloidin, embedding in, 332 
 
 sections, cutting, 333 
 
 staining of, 338 
 Cerebral haBmorrhage, 237 
 
 artery of, 238 
 
 causes of, 237 
 
 site of, 238 
 
 types of, 237 
 
 Cerebro-spinal fluid, excess of, 234 
 Cerebro-spinal meningitis, 231 
 Chalicosis of lung, 133 
 Charcot's joint, 262 
 Cheloids, 277 
 Chest, barrel-shaped, 15 
 
 pigeon, 15 
 
 Chloroform poisoning, 314 
 Chloroma, 98 
 
 blood in, 99 
 Cholangitis, 194 
 
 suppurative, 181 
 Cholecystitis, 194 
 Cholelithiasis, 195 
 Cholera, 163 
 Cholesteatoma, 244 
 Chondroma, 279 
 Chondro-sarcoma, 292 
 Chorea gravidarurn, 269 
 Chorionepithelioma, 268, 304 
 Chromaffin cells, staining of, 354 
 Chromatophore cells in melanotic 
 
 tumours, 294 
 
 Chronic venous congestion, of 
 intestine, 161 
 
 of kidney, 201 
 
 of liver, 175 
 
 of lung, 122 
 
 of myocardium, 56 
 
 Chronic venous congestion, of 
 spleen, 107 
 
 of stomach, 155 
 
 in valvular disease, 70 
 Cirrhosis, acute, 183, 185 
 
 atrophic, 186 
 
 biliary, 188 
 
 common, 187 
 
 hyper trophic, 186 
 
 monolobular, 186 
 
 of liver, 185 
 results of, 189 
 
 polylobular, 186 
 
 syphilitic, 189 
 
 Clots, agonal,in pulmonary artery, 
 23 
 
 post-mortem, 61, 62 
 Cloudy swelling of heart, 54 
 
 of kidney, 202 
 
 of liver, 176 
 CO 2 for freezing, 334 
 Coal-gas poisoning, 313 
 " Coal miner's lung," 133 
 Colitis, 167 
 
 mucous, 169 
 Collapse of lung, 119, 120 
 
 medico-legal, 310 
 Colliquative necrosis, 235 
 Colloid cancer, 302 
 Colophonium as mountant, 337 
 Colour, preservation of in mount- 
 ing specimens, 319 
 Columnar cell carcinoma, 300 
 Compound cystic adenoma, 264 
 Concentration method of examin- 
 ing pus and sputum, 371 > 
 Congenital cystic kidney, 200 
 Cornet's forceps, 336 
 Coronary arteries, anatomy of, 26 
 
 effects of obstruction, 56 
 
 narrowing of, 57 
 " Corona veneris," 260 
 Coroner, 2, 3, 307 
 Corpora amylacea in prostate, 274 
 Corpus luteum, 264 
 Corrosive sublimate, as fixative, 
 
 328. 
 
 Cover glasses, cleaning of, 336 
 Cretinism, in 
 Cuboid, ossific node in," 310 
 
INDEX 
 
 Culture tubes, innoculation of, 
 
 359 
 
 Cutting paraffin sections, 332 
 Cutting sections in celloidin, 333 
 Cutting sections in gum, 333 
 Cyanide poisoning, 314 
 Cystic adenoma, 285 
 Cysts of pancreas, 199 
 
 Death, causes of in infanticide, 
 
 3ii 
 
 causes of in new-born, 311 
 
 sudden, 26, 28, 77, 114 
 Decalcification of tissues, 335 
 Decalcifying fluid, 335 
 Deciduoma malignum, 268 
 Degeneration, fatty, of endo- 
 cardium, 60 
 
 fatty, of heart, 55, 60 
 
 fatty, of kidney, 202 
 
 fatty, of liver, 177 
 
 fatty, of myocardium, 55 
 
 Zenker's, 18 
 
 waxy, of liver, 179 
 
 waxy, of kidney, 203 
 
 waxy, of spleen, 105 
 Dehydration of tissue for micro- 
 scopic sections, 330 
 " Deposition," medico-legal, 308 
 Dermoid cyst, 265, 303 
 Developmental changes in foetus, 
 
 309 
 
 Dextrocardia, 48 
 Diabetes, pancreas in, 199 
 Diffuse-waxy spleen, 106 
 Digestion, post-mortem, 155 
 Dilatation of heart, 60 
 Diphtheria of mouth, 153 
 
 method of examination, 372 
 Disseminated sclerosis, 250 
 Dropsy, 217 
 
 in cardiac disease, 72 
 
 of peritoneum, 172 
 
 of pleura, 149 
 
 renal, 217 
 Ductus arteriosus, persistence of, 
 
 47 
 Duodenum, examination of, 30 
 
 ulcer of, 157 
 " Dust diseases," 133 
 
 Dysentery, amoebic, 167, 168 
 bacterial, 167 
 
 Eclampsia, 270 
 
 kidney in, 271 
 
 liver in, 179, 271 
 Ectopic gestation, 265, 269 
 Egyptian mummies, 4 
 Ehrlich's stain for glycogen, 349 
 Elastic tissue stain, 343 
 Embalming, 376 
 Embedding in celloidin, 332 
 
 in gum, 326 
 
 in paraffin, 330 
 quick method, 331 
 summary of, 332 
 Emboli, septic, of lung, 131 
 Embolism from acute endocar- 
 ditis, 68 
 
 of brain, 235 
 
 of intestine, 161 
 
 of kidney, 201 
 
 of liver, 176 
 
 of lung, 123 
 
 of portal vein, 176 
 
 of spleen, 108 
 
 of uterine veins, 266 
 
 pulmonary, 123, 269 
 Emphysema of lung, 121 
 Empyema, 150 
 
 of gall bladder, 195 
 Encephalitis, suppurative, 240 
 Encephaloid cancer, 302 
 Endarteritis, in brain syphilis, 242 
 
 deformans, 79 
 
 obliterans, 83 
 
 proliferans, 83 
 Endocarditis, acute, 64 
 
 acute results of, 67 
 
 chronic, 68 
 
 difference between simple and 
 ulcerative, table of, 67 
 
 results of chronic, 68 
 
 simple acute, 65 
 
 ulcerative, 66 
 
 in pneumonia, 129 
 results of, 66 
 Endocardium, atheromatous, 61 
 
 calcareous deposits in, 61 
 
 diseases of, 60 
 
382 
 
 INDEX 
 
 Endocardium, fatty degeneration 
 of, 60 
 
 red staining of, 60 
 Endometritis, acute, 266 
 
 chronic, 267 
 
 tuberculosis, 267 
 Endotheliomata, 292 
 Entamoeba hystolytica, stain for, 
 
 364 
 
 dysentery due to, 167 
 Enteritis, 162 
 
 acute, 162 
 
 tuberculous, 165 
 
 typhoid, 165 
 Eosin, 339 
 
 methylene blue, Mallory and 
 Wright's method, 342 
 stain for bacteria, 364 
 staining method, 341 
 Epithelioma, squamous, 297 
 
 of gall bladder, 197 
 
 of intestine, 171 
 
 of oesophagus, 154 
 
 of stomach, 158 
 
 of uterus, 268 
 Epulis, malignant, 291 
 Equipment of pathologist, 5 
 Ether for freezing, 334 
 Examination of abdominal con- 
 tents, 28 
 
 of aorta, 23 
 
 of bile and pancreatic ducts, 31 
 
 of bladder and urethra, 33 
 
 of brain, 35, 38 
 
 of bronchi, 28 
 
 of duodenum, 30 
 
 of eye and orbit, 40 
 
 of gall bladder, 31 
 
 of heart, 23 
 
 of intestines, 29 
 
 of kidneys, 34 
 
 of liver, 31 
 
 of lungs, 27 
 
 of maxillary antrum, 41 
 
 of middle ear, 40 
 
 of pancreas, 32 
 
 of plural cavities, 19 
 
 of sinuses of head, 40 
 
 of spinal cord, 39 
 
 of spleen, 32 
 
 Examination of stomach, 30 
 
 of suprarenals, 33 
 
 of surface of heart, 24 
 
 of testicles, 35 
 
 of thoracic contents, 23 
 
 of thoracic duct, 35 
 
 of thyroid gland, 28 
 
 of uterus, 34 
 
 of valves of heart, 24, 25, 26 
 
 of venaa cavae, 23 
 
 of vermiform appendix, 30 
 Exostosis, 280 
 Eye and orbit, examination of, 40 
 
 Fallopian tubes, diseases of, 265 
 Farrant's medium for mounting, 
 
 337 
 Fat necrosis, 197 
 
 Nile blue sulphate stain for, 347 
 osmic acid stain for, 347 
 Scharlach R., stain for, 348 
 staining by haematoxylin, 347 
 Sudan III. stain for, 348 
 Fat in tissues, staining of, 346 
 Fatty change in phosphorous 
 
 poisoning, 313 
 degeneration of endocardium, 
 
 60 
 
 of heart, 54 
 of intima, 78 
 of kidney, 202 
 of liver, 177 
 of myocardium, 55 
 infiltration of heart, 54 
 
 of liver, 178 
 loading of heart, 54 
 Femur, ossific node in, 310 
 Fever, puerperal, 269 
 Fibrin staining method, 345 
 Fibro- adenoma, 285 
 Fibro-myoma, 280 
 
 of uterus, 268 
 Fibroid phthisis, 144 
 Fibroid, recurrent, 287 
 Fibroma, 277 
 
 in ovary, 265 
 
 Fibromatosis of stomach, 158 
 Fibrosis of lung, 146 
 Fixation of nervous tissue for 
 microscopic sections, 325, 327 
 
INDEX 
 
 383 
 
 Fixative, absolute alcohol, 329 
 
 corrosive sublimate, 328 
 
 Flemming's, 325, 328 
 
 Jores's, 323 
 
 Kaiserling's, 323 
 
 Marchi's, 325, 328 
 
 methylated spirit, 329 
 
 Miiller's, 327 
 
 Orth's, 328 
 
 Pick's, 322 
 
 Zenker, 327 
 Fixing paraffin sections on slides, 
 
 332 
 Flemming's fixative, 325 
 
 solution, 328 
 Flies at post-mortem, 7 
 Focal necrosis, 178 
 Foetus, table of, developmental 
 
 changes in, 309 
 Formalin, Schering's, 323 
 Fracture of skull, examination 
 
 for, 35 
 
 Freezing gum sections, 334 
 Friedreich's ataxia, 252 
 Frost's preservative, 323 
 " Fuchsin bodies," 297 
 
 Gall bladder, diseases of, 194 
 
 empyema of, 195 
 
 examination of, 31 
 
 inflammation of, 194 
 
 suppuration of, 195 
 
 tumours of, 197 
 Gall stones, types of, 195 
 Ganglion cells, staining of, 356 
 Gangrene of lung, 131 
 Gastrectasis, 155 
 Gastritis, suppurative, 156 
 Gelatine fluid for mounting speci- 
 mens, 322 
 
 General paralysis of insane, 242 
 Gentian violet stain, 353 
 Giant cell sarcoma, 291 
 Giemsa's stain for spirochaetes, 369 
 " Gin-drinker's " liver, 187 
 Glioma, 282 
 
 Glio-sarcoma, 243, 283, 292 
 Gliosis of spinal cord, 245 
 Gloves, rubber, cleansing of, 44 
 care of, 15 
 
 Glycerine jelly, 337 
 Glycogen, Best's method of stain- 
 ing, 351 
 
 Lubarsch's method of demon- 
 strating, 350 
 in tissues, demonstration of, 
 
 349 
 Ehrlich method of staining, 
 
 349 
 Goitre, 112 
 
 exophthalmic, 112 
 
 simple, 112 
 Gout, 262 
 Gram's method of staining, 
 
 363 
 
 Grave's disease, 112 
 Grey hepatization of lung, 127 
 Gum, cutting sections in, 333 
 
 sections, staining of, 338 
 Gumma, of bone, 260 
 
 of brain, 242 
 
 of heart, 59 
 
 of liver, 190 
 
 of lung, 135 
 
 of spinal cord, 252 
 
 of testicle, 273 
 
 Haemangioma, 281 
 Haematein, eosin stain, 339 
 Haematothorax, 149 
 Haematoxylin, Kultschitzky and 
 Welter's, 355 
 
 stain for fat, 347 
 
 eosin, method of staining, 
 
 340 
 
 stain, 339 
 Weigert's iron, 339 
 Haemophilia, 100 
 clotting in, 100 
 Haemorrhage, cerebral, 239 
 
 into pericardium, 49 
 Haemorrhagic diseases, 99 
 Haemosiderin in liver, 180' 
 
 method of demonstrating in 
 
 tissues, 353 
 
 Hands, cleansing of, 44 
 Hardening tissue for microscopic 
 
 sections, 329 
 Harke's saw-cut for base of skull, 
 
INDEX 
 
 Heart and great vessels, malfor- 
 mations of, 46 
 
 and pericardium, disease of, 46 
 aneurysm of, 57 
 auriculo-ventricular bundle of, 
 
 73 
 
 brown atrophy of, 54 
 
 cloudy swelling of, 54 
 
 congenital abnormalities of, 46 
 
 development of, 46 
 
 dilatation of, 60 - 
 
 " ectopia cordis," 48 
 
 examination of, 23 
 
 examination of excised, 74 
 
 fatty infiltration of, 54 
 
 fatty loading, 54 
 
 gumma of, 59 
 
 hypertrophy of, 59 
 
 in nephritis, 216 
 
 in pneumonia, 129 
 
 primitive muscular tissue of, 73 
 
 surface of examination of, 24 
 
 syphilis of, 59 
 
 tumours of, 60 
 
 valves, table of diameter and 
 circumference of, 76 
 
 weight and measurement of, 75 
 Heart-block, causes of, 74 
 Hepatitis, acute, 180 
 
 chronic interstitial, 185 
 
 suppurative, 181 
 Hereditary spinal ataxia, 252 
 Hernia, 160 
 
 strangulated, 161 
 Herxheimer's method of Scharlach 
 
 R. staining, 349 
 Hirschsprung's disease, 159 
 Hiss's capsule stain, 369 
 " Hobnailed " liver, 187 
 Hodgkin's disease, 104 
 " Honey- comb " lung, 119 
 Hydatid cyst of liver, 193 
 
 suppuration in, 182 
 Hydatid mole, 268, 278 
 Hydrocephalus, 234 
 Hydromyelia, 245 
 Hydronephrosis, 275 
 
 congenital, 201 
 Hydropericardium, 49 
 Hydrothorax, 149 
 
 Hyperemesis gravidarum, 269 
 Hypernephrorna, 114, 224 
 Hypertrophy of heart, 60 
 
 Incising organ, use of knife in, 1 1 
 Indian ink method, Burri's, 369 
 Infant, signs of maturity in, 309 
 Infanticide, causes of death in, 
 
 3ii 
 
 Infarction from acute endo- 
 carditis, 68 
 
 of brain, 235 
 
 of intestine, 161 
 
 of kidney, 201 
 
 of liver, 176 
 
 of lung, 123 
 
 of placenta, 268 
 
 septic, of lung, 131 
 
 of spleen, 108 
 Infections of eye, 6 
 Infiltration, fatty, of liver, 178 
 
 of heart, 54 
 Ink method of demonstrating 
 
 spirochaetes, 369 
 Instruments for post-mortem, 7 
 Insular sclerosis, 250 
 Intestine, actinomycosis of, 166 
 
 chronic venous congestion, 161 
 
 dilation of, 159 
 
 diseases of, 159 
 
 examination of, 29 
 
 haemorrhage of, 162 
 
 hernia of, 160 
 
 infarction of, 161 
 
 inflammation of large, 167 
 
 inflammation of small, 162 
 
 intussusception of, 160 
 
 malformations of, 159 
 
 parasites of, 170 
 
 removal of, 28 
 
 stenosis of, 159 
 
 syphilis of, 166 
 
 tuberculosis of, 165 
 
 tuberculous ulceration of, 165 
 table of differences from 
 typhoid ulceration, 166 
 
 tumours of, 171 
 
 typhoid of, 163 
 
 typhoid ulceration of, 164 
 
 volvulus of, 159 
 
INDEX 
 
 385 
 
 Interauricular septum, defective, 
 
 46 
 Interventricular septum, defec- 
 
 tive, 46 
 
 Intussusception, 160 
 Iodine stain for waxy material, 
 
 352 
 test in waxy disease of arteries, 
 
 77 
 Iron-containing pigment, demon- 
 
 stration of, 353 
 Iron-haematoxylin, 339 
 Irritant poisoning, appearances, 
 
 Jaundice, obstructive, JJpm pan- 
 
 creatic tumours, 199 
 Jenner's stain, 358 
 Joint, CharCot's, 262 
 
 gouty, 262* 
 Joints, diseases of, 261 
 
 rheumatoid arthritis of, 262 
 
 tuberculosis of, 261 
 Jores's fixative, 323 
 
 Kaiserling's fixative, 323 
 Kidney, arterio-sclerotic, 214 
 
 Bright's disease, 207 
 
 chronic venous congestion, 201 
 
 cloudy swelling of, 202 
 
 congenital anomalies of, 200 
 
 congenital cystic, 200 
 
 congenital cysts of, 200 
 
 degenerations of, 202 
 
 diseases of, 200 
 
 examination of, 35, 224 
 
 fatty degeneration associated 
 with Bright's, 203 
 
 fatty degeneration of, 202 
 
 hydronephrosis, 225 
 
 in eclampsia, 271 
 
 infarction of, 201 
 
 inflammation of, 204 
 
 large white, 210 
 
 leukaemia of, 223 
 
 pigmentary changes of, 204 
 
 pyelitis of, 226 
 
 removal of, with bladder, 32 
 
 suppuration of, 221 
 
 syphilis of, 223 
 
 Kidney, tube casts of, 218 
 
 tuberculosis of, 222 
 
 tumours of, 223 
 
 waxy disease of, 203 
 
 waxy, in tuberculosis, 147 
 Kultschitzky's ha3matoxylin, 347 
 
 Laryngitis, 116 
 
 diphtheritic, 116 
 Larynx, diseases of, 116 
 
 syphilis of, 117 
 
 tuberculosis of, 117 
 
 tumours of, 117 
 Leiomyoma, 280 
 Leishman's stain, 358 
 Leptomeningitis, 230, 231 
 
 cerebral, 230 
 
 spinal, 246 
 
 Letulle's method of making post- 
 mortem, 14, 42 
 Leucocythaemia, 96 
 Leukaemia, 96 
 
 liver in, 191, 97 
 
 kidney in, 223 
 
 pseudo-, 104 
 Levaditi's stain for spirochaetes, 
 
 370 
 
 Lipoma, 279 
 Lithium carmine, 344 
 Liver, abscess of, 181 
 
 actinomycosis, 182 
 
 acute yellow atrophy of, 182, 
 183, 270 
 
 amyloid degeneration, 179 
 
 chronic venous congestion of, 
 175 
 
 circulatory disturbances of, 175 
 
 cirrhosis of, 185 
 
 cloudy swelling of, 176 
 
 congenital syphilis, 189 
 
 deformities of, 175 
 
 degenerations of, 176 
 
 diseases of, 175 
 
 examination of, 31, 193 
 
 fatty degeneration of, 177 
 
 fatty infiltration of, 178 
 
 focal necrosis in, 178 
 
 gumma of, 190 
 
 in eclampsia, 179, 271 
 
 inflammation of, 180 
 
 25 
 
386 
 
 INDEX 
 
 Liver, leukaemia of, 191 
 
 lymphadenoma of, 191 
 
 nutmeg, 175 
 
 pigmentary changes in, 180 
 
 pigment in chronic venous con- 
 gestion, 1 80 
 
 regeneration of, 185 
 
 results of cirrhosis of, 189 
 
 subacute yellow atrophy, 184 
 
 syphilis of, 190 
 
 tropical abscess of, 182 
 
 tuberculosis of, 190 
 
 tumours of, 192 
 
 waxy degeneration of, 179 
 
 waxy, in tuberculosis* 147 
 Lobar pneumonia, 125 
 Lobular pneumonia, 129 
 Locomotor ataxia, 251 
 Lorrain-Smith's Nile blue sul- 
 phate stain for fat, 347 
 Lubarsch's method of demon- 
 strating glycogen, 350 
 Lugol's iodine, 350 
 Lung, abscess of, 131 
 
 acute congestion of, 122 
 
 anthracosis, 133 
 
 atelectasis of, 120 
 
 brown induration of, 123 
 
 caseous tuberculosis, differences 
 from lobular pneumonia, etc., 
 143 
 
 caseous tuberculosis of, 142 
 
 coal-miner's, 133 
 
 collapse in new born, medico- 
 legal, 310 
 
 collapse of, 119 
 
 chronic venous congestion of, 
 122 
 
 chronic venous congestion with 
 tuberculosis, 148 
 
 diseases of, 119 
 
 emphysema of, 121 
 
 examination of, 27, 151 
 
 nbro-caseous tuberculosis with 
 cavitation, 146 
 
 fibrosis, 146 
 
 gangrene of, 131 
 
 gumma of, 135 
 
 haemorrhage of, 123 
 
 hypostatic congestion of, 122 
 
 Lung, hypostatic pneumonia, 
 
 132 
 
 infarction of, 123 
 inflammation of, 125 
 in nephritis, 217 
 interstitial pneumonia of, 132, 
 
 133 
 
 miliary tuberculosis of, 140 
 
 oedema of, 124 
 
 passive congestion of, 122 
 
 pneumokoniosis of, 133 
 
 pneumonia of, 125 
 
 septic pneumonia, 131 
 
 siderosis of, 134 
 
 silicosis of, 134 
 
 stone mason's, 134 
 
 syphilis of, 134 
 
 tuberculosis of, 135 
 classification, 139 
 metastasis, 147 
 mode of spread, 137 
 paths of entry of infection, 
 
 135 
 " seat of election," 135 
 
 tumours of, 148 
 
 water test, medico-legal in 
 infant, 310 
 
 water test, in pneumonia, 120 
 Lymphadenitis, 102 
 
 tuberculous, 103 
 Lymphadenoma, 104 
 
 glands in, 104 
 
 liver in, 105, 191 
 
 lungs in, 105 
 
 spleen in, 105, 110 
 Lymphangioma, 281 
 Lymphatic leukaemia, 97 
 Lymph glands, diseases of, 102 
 
 examination of, 102 
 
 pigmentary changes in, 102 
 
 tumours of, 105 
 Lymphocythaemia, 97 
 
 blood in, 98 
 
 bone marrow in, 98 
 
 kidney in, 98 
 
 liver in, 98 
 
 lymph gland in, 98 
 
 spleen in, 98 
 Lymphoma, 282 
 Lympho-sarcoma, 282, 289 
 
INDEX 
 
 Mallory and Wright's eosin, 
 
 methylene blue stain, 342 
 Mammary gland, tuberculosis of, 
 273 
 
 inflammation of, 272 
 
 tumours of, 273 
 Mann's methylene blue stain, 367 
 
 modification of Miiller's fluid, 
 
 327 
 Marchi's fixative, 328 
 
 staining method, 356 
 Mastitis, 272 
 Maturity, table of signs in new 
 
 born of, 309 
 Mayer's hasmatein, 340 
 Meckel's diverticulum, 159 
 Medico-legal post-mortem, 2, 306 
 
 preservation of organs in, 311 
 
 procedure in, 306 
 
 report in England, 308 
 
 report in Scotland, 307 
 
 typical reports, 215, 216 
 Medullary cancer, 302 
 
 sheaths, staining of, 354 
 Melanotic tumours, 294 
 Meninges of brain, diseases of, 229 
 Meningitis, cerebral, 229 
 
 cerebro-spinal, 231 
 
 serous, 233 
 
 spinal, 245 
 
 syphilitic, 233 
 
 tuberculous, 232 
 Meningocele, 245 
 Meningo-myelocele, 245 
 Methylated spirit as fixative, 329 
 Methylene blue, eosin stain, 341 
 Methyl- violet stain, 353 
 
 in Much's method, 366 
 Microscopic examination, routine 
 of, 324 
 
 selection of urine for, 324 
 Microscopic sections, cutting in 
 gum, 333 
 
 cutting in celloidin, 333 
 
 cutting in paraffin, 332 
 
 decalcification, 335 
 
 dehydration, 330 
 
 embedding in celloidin, 332 
 
 embedding in gum, 326 
 
 embedding in paraffin, 330 
 
 387 
 
 quick 
 
 Microscopic sections, 
 method, 331 
 
 fixation of tissue, 325 
 
 freezing of, 334 
 
 hardening of tissues, 329 
 
 mounting media, 336 
 
 preparation of, 324 
 
 staining methods, 337 
 Microtome, Aschoff- Becker, 334 
 
 Bruce, 333 
 
 Cathcart, 334 
 
 Minot, 333 
 
 Mixter, 334 
 
 making use of, 332 
 
 Schanze, 333 
 Middle ear, examination of, 40 
 
 association with meningitis, 
 
 227 
 
 " Milk spots," 52 
 Miller's method of staining clubs 
 
 of actinomyces, 368 
 Minot, microtome, 333 
 Mitral valve, disease of, 69, 70 
 
 effects of disease of, 70 
 Mixed cell, sarcoma, 291 
 Mixter, microtome, 334 
 Mole, placental, 304 
 Molluscum contagiosum, 283 
 Mordant, alum, 339 
 
 iron, 339 
 
 Morphia poisoning, 314 
 Mounting, fluid for specimens, 
 321 
 
 media for sections, 336 
 
 of specimens, 319 
 Mouth, diseases of, 153 
 
 tumours of, 153 
 
 Much-Gram stain combined with 
 Ziehl Neelsen stain, 366, 
 
 367 
 Much's peroxide of hydrogen 
 
 method, 367 
 Mucous colitis, 169 
 Muir's capsule stain, 368 
 Miiller's fixative, 327 
 Muscles, vitreous degeneration of 
 
 Zenker of, 18 
 Muscular atrophy, progressive, 
 
 249 
 Myelaamia, 96 
 
388 
 
 INDEX 
 
 Myelin, degenerated staining of, 356 
 Myelitis, 246, 247 
 Myelocythaemia, 96 
 
 blood in, 96 
 
 bone marrow in, 97 
 
 kidney in, 97 
 
 liver in, 97 
 
 spleen in, 97 
 
 Myeloid sarcoma, 261, 291 
 Myeloma, 261, 293 
 Myocarditis, 58 
 
 chronic interstitial, 58 
 Myocardium, chronic venous con- 
 gestion of, 53 
 
 degeneration of, 53 
 
 diseases of, 53, 55 
 
 fatty degeneration of, 55 
 
 syphilis of, 59 
 
 tuberculosis of, 59 
 Myoma, 280 
 Myx oedema, in 
 Myxoma, 278 
 Myxoma of chorion, 268, 278, 304 
 
 Neisser's stain for diphtheria, 373 
 Nephritis, 204 
 
 acute, 208 
 
 table of comparison, 219 
 
 blood in, 217 
 
 cardio- vascular changes in, 216 
 
 causes, 208 
 
 chronic interstitial, 212 
 
 chronic interstitial urine in, 216 
 
 classification, 207 
 
 dropsy in, 217 
 
 haematogenous, 220 
 
 heart in, 216 
 
 lungs in, 217 
 
 changes in nervous system in, 218 
 
 subacute, 210 
 
 suppurative, 220 
 Nerve sheaths, staining of, 354 
 Nerves, diseases of, 252 
 
 tumours of, 253 
 Nervous system in nephritis, 218 
 
 tissue embedding in celloidin, 
 
 333 
 Neuritis, 252 
 
 interstitial, 253 
 
 parenchymatous, 252 
 
 Neuro-fibroma, 253 
 
 New-born, causes of death of, 311 
 infants, post-mortem in, 308 
 table of signs of maturity in, 309 
 
 Nile blue sulphate stain for fat, 
 347 
 
 Nissl bodies, staining of, 356 
 
 Nitric acid as decalcifying fluid, 
 335 
 
 " Nutmeg " liver, 175 
 
 Oedema in cardiac disease, 72 
 
 of brain, 233 
 
 of glottis, 116 
 
 of lung, 124 
 
 renal, 217 
 
 subcutaneous, 217 
 (Esophagus, corrosive poisoning 
 of, 154 
 
 examination of, 23 
 
 peptic ulcer of, 154 
 
 removal of, in suspected poison- 
 ing, 153 
 
 tumours of, 154 
 
 varicose veins of, 153 
 Omphalo-mesenteric duct, 159 
 Orbit, examination of, 40 
 Organs, bacteriological investiga- 
 tion of, 360 
 Orth's fixative, 328 
 
 lithium carmine, 344 
 
 rules for making post-mortem, 
 
 15 
 
 Osmic acid, stain for fat, 347 
 Ossific node in cuboid, 309, 311 
 
 in femur, 309, 310 
 Osteitis deform ans, 260 
 Osteoma, 280 
 Osteo-sarcoma, 292 
 Ovaritis, 264 
 Ovary, tumours of, 264 
 
 Pachymeningitis, cerebral, 229 
 
 acute, 229 
 
 chronic, 230 
 
 hsemorrhagica, 230 
 
 spinal, 245 
 
 Paget's disease of bone, 260 
 Pancreas, cysts of, 199 
 
 diseases of, 197 
 
INDEX 
 
 389 
 
 Pancreas, examination of, 32 
 
 fatty infiltration of, 197 
 
 relation to diabetes, 199 
 
 tumours of, 198 
 Pancreatic duct, examination of, 
 
 3i 
 
 Pancreatitis, acute haemorrhagic, 
 198 
 
 chronic interstitial, 198 
 
 fat necrosis in, 197 
 
 suppurative, 198 
 Papilliferous, cystic adenoma, 
 
 265, 285 
 Papilloma, 284 
 
 of larynx, 117 
 Papilloma, mucous, 283 
 
 of bladder, 228 
 
 squamous, 283 
 Pappenheim's stain, 343 
 Paraffin, embedding in, 330 
 
 quick method, 331 
 Paraffin sections, cutting of, 332 
 
 fixing on slides, 332 
 
 staining for bacteria, 363 
 
 treatment before staining, 337 
 Paralysis, general, of insane, 
 242 
 
 infantile, 248 
 Parasites of alimentary tract, 170 
 
 of bladder, 228 
 Parathyroids, 28 
 Pathologist, equipment of, 5 
 
 infection of eye, 6 
 
 wound of finger of, 6 
 Perenny's decalcifying fluid, 335 
 Pericarditis, acute, 50 
 
 chronic, 52 
 
 classification of, 51 
 
 results of, 52 
 
 tuberculous, 53 
 Pericardium, adherent, 52 
 
 air in, 50 
 
 anatomy of, 48 
 
 blood in, 49 
 
 diseases of, 46, 48 
 
 dropsy of, 49 
 
 incision of, 19 
 
 tuberculosis of, 53 
 Perihepatitis, 180 
 Perithelioma, 292 
 
 Peritoneum, ascites of, 172 
 
 diseases of, 172 
 
 haemorrhage of, 172 
 
 tuberculosis of, 173 
 
 tumours of, 174 
 Peritonitis, acute, 172 
 
 chronic, 173 
 
 tuberculous, 173 
 Pernicious anaemia, 93 
 
 bone marrow in, 94 
 
 colour index, 95 
 
 heart in, 93 
 
 intestines in, 94 
 
 kidney in, 94 
 
 liver in, 93 
 
 lungs in, 93 
 
 red blood corpuscles in, 95 
 
 skin in, 93 
 
 spinal cord in, 95 
 
 spleen in, 94 
 
 stomach in, 94 
 
 subcutaneous fat in, 93 
 
 white blood corpuscles in, 95 
 Phlebitis, 89 
 results of, 90 
 Phosphorus poisoning, 313 
 Phthisis, 140 
 
 fibroid, 144 
 Pick's fixative, 322 
 Picro- car mine, 340 
 
 methods of staining with, 338 
 Picro- fuchsin, 340, 341 
 Pipettes, method of making, 375 
 Placenta, diseases of, 268 
 Plasma cells, staining of, 343 
 Pleura, diseases of, 149 
 Pleural cavities, examination of, 
 
 19 
 Pleural cavity, dropsy of, 149 
 
 gas in, 150 
 Pleurisy, 150 
 
 chronic, 151 
 
 classification, 150 
 
 in tuberculosis, 151 
 Plexiform angioma, 281 
 Pneumokoniosis, 133 
 Pneumonia, 125 
 
 broncho, 129 
 
 catarrhal, 129 
 
 congestion of spleen in, 129 
 
39 
 
 INDEX 
 
 Pneumonia, croupous, 125 
 
 grey hepatisation, 127 
 
 heart in, 129 
 
 hypostatic, 132 
 
 interstitial, 132, 133 
 
 leucoblastic marrow in, 129 
 
 lobar, acute congestion in, 126 
 
 lobar, causes of, 125 
 
 lobular, 129 
 
 other organs in, 129 
 
 red hepatization, 126 
 
 resolution in, 128 
 
 septic, 131 
 
 syphilitic, 135 
 
 tuberculous, 142 
 
 types of, 125 
 
 white, 134 
 
 Pneumopericardium, 50 
 Pneumothorax, 150 
 Poisoning, ammonia gas, 314 
 
 carbon monoxide, 313 
 
 chloroform, 314 
 
 cyanide, 314 
 
 irritant, 313 
 
 morphia, 314 
 
 phosphorus, 313 
 
 ptomaine, 314 
 
 strychnine, 314 
 
 vegetable, 314 
 Poisons, post-mortem changes in 
 
 organs. from, 311 
 Poliomyelitis, 248 
 Polychrome methylene blue, 353 
 Polypi, 277 
 Portal pyaemia, 181 
 Portal vein, embolus of, 176 
 
 thrombosis of, 176 
 Post-mortem, i 
 
 hospital regulations for, 2 
 
 importance of changes, 4 
 
 in private, 9 
 
 instruments for, 7 
 
 Letulle's method, 14, 42 
 
 medico-legal, 2, 3 
 procedure in, 306 
 
 notes of, 9 
 
 object of, 13 
 
 permission for, 2 
 
 primary incision, 17 
 
 procedure in making, 13 
 
 Post - mortem, reflection of 
 
 muscles, etc., 17 
 rules for examining organ at, 10 
 Shennan's method of, 43, 21 
 surface examination, 15 
 table and accessories, 8 
 wounds, treatment of, 6 
 Post-mortem report, medico-legal, 
 in England, 308 
 in Scotland, 307 
 
 Post-mortem medico-legal, speci- 
 men reports, 215, 216 
 Post-mortem room, equipment of, 
 
 9 
 
 solutions, etc., for, 8 
 Pregnancy, diseases of, 269 
 Preparation of tissue for dispatch, 
 
 329 
 
 Preservative, Frost's, 323 
 Primary incision at post-mortem, 
 
 17 
 
 Procurator-fiscal, 2, 3, 307 
 Progressive muscular atrophy, 250 
 Prostate, diseases of, 274- 
 
 hypertrophy of, 274 
 
 tumours of, 274 
 Prostatitis, acute, 274 
 Prussian blue reaction, 94 
 Psammoma, 293 
 Ptomaine poisoning, 314 
 Puerperium, diseases of, 269 
 " Pulmonary apoplexy," 123 
 
 artery, congenital stenosis of, 
 
 47 
 
 examination of, 23 
 tuberculosis, 135 
 valve, lesions of, 72 
 Purpura, 99 
 Pus, examination for tubercle 
 
 bacillus, 371 
 
 making of films from, 362 
 Pyelonephritis, 221 
 Pyloric stenosis, congenital, 155 
 Pyopneumothorax, 150 
 Pyorrhoea alveolaris, 153 
 Pyronin-methylgreen stain, 343 
 
 Red hepatization of lung, 126 
 Redressing of body, 44 
 " Red softening," 281 
 
INDEX 
 
 39 1 
 
 " Red staining of intima," 60 
 Removal of organs from thorax 
 and abdomen, 20 
 
 Shennan's method, 21 
 Resolution of lung, 128 
 Resorcin-fuchsin stain, 344 
 Respiratory system, diseases of, 
 
 116 
 
 Reynold's capsule stain, 368 
 Rhabdomyoma, 280 
 " Rice water stools," 163 
 Rickety rosary, 18, 255 
 Rigor mortis, 16 
 Rodent ulcer, 299 
 Round cell sarcoma, large, 290 
 
 small, 289 
 Rules for examination of an organ 
 
 at a post-mortem, 10 
 Russell's " fuchsin bodies," 297 
 
 Sago-waxy spleen, 105 
 Salpingitis, 265 
 Sarcoma, 287 
 
 alveolar, 292 
 
 angio-, 293 
 
 characteristics of, 287 
 
 chondro-, 292 
 
 classification of, 288 
 
 difference from granulation 
 tissue, 291 
 
 large round cell, 290 
 
 large spindle cell, 290 
 
 lympho-, 289 
 
 melanotic, 294 
 
 mixed cell, 291 
 
 myeloid, 291 
 
 of bone, 260 
 
 of brain 243 
 
 of heart, 60 
 
 of intestine, 171 
 
 of kidney, 223 
 
 of larynx, 117 
 
 of liver, 193 
 
 of lymphatic glands, 105 
 
 of nerve, 253 
 
 of ovary, 265 
 
 of spleen, no 
 
 of stomach, 158 
 
 of testicle, 274 
 
 of vertebrae, 252 
 
 Sarcoma, osteo-, 292 
 
 small round cell, 289 
 
 small spindle cell, 290 
 
 sites of origin of, 289 
 Schanze microtome, 333 
 Scharlach R. stain for fat, 348 
 Schering's celloidin, 332 
 
 formalin, 323 
 Scirrhous cancer, 301 
 Sclerosis of spinal cord, 247 
 
 disseminated, 250 
 Scurvy, 99 
 
 infantile, 99 
 Sectio cadaveris, i 
 Serous sacs, bacteriological in- 
 vestigation of, 361 
 examination of, 19 
 Shennan's method of post- 
 mortems, 21, 43 
 Siderosis of lung, 134 
 Silicosis of lung, 134 
 Sino- auricular node, 73 
 Sinuses, accessory, of head, ex- 
 amination of, 40 
 Skull, fracture of, examination 
 
 for, 35 
 
 Slides, cleaning of, 336 
 Soft cancer, 302 
 " Soldier's spots," 52 
 " Soul and Conscience," form of 
 
 report, 4, 307 
 
 Specimens, method of mounting, 
 321 
 
 mounting of, 319, 321 
 
 preparation for transmission, 
 
 329 
 
 preservation of, 319 
 
 preservation of, in medico-legal 
 
 work, 307 
 Spina bifida, 244 
 
 occulta, 245 
 
 Spinal cord, congenital abnor- 
 malities of, 244 
 
 diseases of, 244 
 
 examination of, 39 
 
 gumma of, 252 
 
 inflammation of, 246 
 
 named diseases of, 248 
 
 tuberculosis of, 252 
 
 tumours of, 252 
 
39 2 
 
 INDEX 
 
 Spindle cell sarcoma, large, 290 
 
 small, 290 
 
 Spirochaetes in atheroma lesion, 
 80 
 
 in tissues, staining of, 370 
 
 methods of staining, 369 
 
 in brain, 242 
 Spleen, acute congestion, 107 
 
 atrophy of, 105 
 
 chronic venous congestion of, 
 107 
 
 circulatory disturbances, 107 
 
 diseases of, 105 
 
 examination of, 30, 32, 111 
 
 iron pigment in, 107 
 
 hyaline degeneration of, 106 
 
 in Banti's disease, 95 
 
 infarction of, 108 
 
 inflammation of, 109 
 
 in pneumonia, 129 
 
 lymphadenoma of, 105, 110 
 
 miliary tuberculosis of, 109 
 
 pigmentation of, 106, 107 
 
 tuberculosis of, 109 
 
 tumours of, no 
 
 waxy degeneration of, 105, 147 
 Splenic anaemia, 95 
 Splenomedullary leukaemia, 96 
 Sputum, examination for tubercle 
 bacillus, 370 
 
 making of films from, 361 
 Squamous epithelioma (see Epi- 
 thelioma), 297 
 
 papilloma, 283 
 Staining methods, 337 
 
 sections, apparatus required, 
 
 335 
 Sterno-clavicular joint, disarticu- 
 
 lation of, 18 
 
 Sternum, removal of, 18, 19 
 Stomach, acute catarrh of, 155 
 chronic catarrh of, 156 
 chronic venous congestion of, 
 
 155 
 
 congenital pyloric stenosis, 155 
 dilatation of, 155 
 diseases of, 154 
 effect of acids on, 156 
 examination of, 30 
 fibromatosis of, 158 
 
 Stomach, haemorrhagic erosions 
 of, 155 
 
 hour-glass contraction of, 155 
 
 post-mortem digestion in, 155 
 
 suppurative catarrh of, 156 
 
 tumours of, 158 
 
 ulcer of, 157 
 Stone in bladder, 228 
 " Stone-mason's lung," 134 
 Streptothrix actinomyces, stain- 
 ing of club forms, 268 
 Strychnine poisoning, 314 
 Struma, 112 
 Subacute nephritis, 210 
 
 urine in, 212 
 Subacute atrophy of liver, 
 
 184 
 
 Sudan III. stain for fat, 348 
 Sudden death, arteries in, 77 
 
 examination o'f coronary 
 
 arteries in, 26 
 in relation to haemorrhage 
 
 into supra-renals, 114 
 thymus gland in, 28 
 Supra-renals, accessory, 114 
 
 diseases of, 113 
 
 examination of, 33 
 
 haemorrhage into, 114 
 
 hypernephroma, 114 
 
 removal of, 33 
 
 structure of, 113 
 
 tuberculosis of, 114 
 
 tumours of, 114 
 Surgical kidney, 221 
 Syphilis, congenital, of liver, 
 189 
 
 of arteries, 80, 84 
 
 of bone, 260 
 
 of brain, 241 
 
 of bronchi, 119 
 
 of heart, 59 
 
 of intestine, 106 
 
 of kidney, 223 
 
 of larynx, 117 
 
 of liver, 189, 190 
 
 waxy degeneration in, 190 
 
 of lung, 134 
 
 of meninges, 233 
 
 of testicle, 273 
 Syringomyelia, 245 
 
INDEX 
 
 393 
 
 " Tabby cat " heart, 55 
 Tabes dorsal is, 251 
 Tabloids for making stains, 358 
 Teratoma, 303 
 
 of ovary, 265 
 Test for carbon monoxide in 
 
 blood, 314 
 
 Testicle, chorionepithelioma of, 
 304 
 
 diseases of, 273 
 
 examination of, 35 
 
 fibrosis, 273 
 
 gumma of, 273 
 
 removal of, 35 
 
 syphilis of, 273 
 
 tuberculosis of, 273 
 
 tumours of, 274 
 Thoracic contents, examination 
 
 of, 22, 23 
 Thoracic duct, examination of, 
 
 35 
 
 Thrombi, 61, 88 
 
 Thrombosis, in vessels of brain, 
 235 
 
 of portal vein, 176 
 
 of uterine veins, 266 
 
 of veins, 87 
 Thrombus, red, 88 
 
 septic, softening of, 88 
 
 simple, 88 
 
 white, 88 
 
 " Thrush breast " heart, 55 
 Thymus gland, 28 
 Thyroid gland, diseases of, in 
 
 examination of, 28, 113 
 
 tumours of, 112 
 
 waxy degeneration of, 112 
 Tissues, preparation of, for micro- 
 scopic examination, 324 
 Tricuspid valve, diseases of, 72 
 Tropical abscess of liver, 182 
 
 associated with dysentery, 182 
 " Tube casts," 218 
 Tubercle bacillus, concentration 
 method of examining for, 
 
 371 
 extraction with acetone and 
 
 ether, 372 
 
 in sections, staining of, 366 
 in sputum, examination for, 370 
 
 Tubercle bacillus, Much - Gram 
 
 stain, 366 
 
 Ziehl-Neelsen method, 365 
 staining for, 365 
 Tuberculosis, arteries in, 84 
 miliary, of lung, 140 
 of bladder, 227 
 of bone, 259 
 of brain, 241 
 of breast, 273 
 of epididymis, 273 
 of Fallopian tubes, 265 
 of heart, 59 
 of intestine, 165 
 of joints, 261 
 of kidney, 222 
 of larynx, 117 
 of liver, 190 
 of lung, 135 
 
 broncho- pneumonic, 142 
 
 caseous, 142 
 
 changes in other organs, 
 147 
 
 classification of, 139 
 
 nbro-caseous, 144, 147 
 
 hypertrophy of heart in, 
 'i47 
 
 interstitial, 147 
 
 mode of spread, 137 
 
 paths of entry of infection, 
 135 
 
 " seat of election," 135 
 
 waxy disease in, 147 
 of myocardium, 59 
 of pericardium, 53 
 of peritoneum, 173 
 of spinal cord, 252 
 of spleen, 109 
 of suprarenal, 114 
 of testicle, 273 
 pleurisy in, 151 
 Tuberculous enteritis, 165 
 lymphadenitis, 103 
 meningitis, 232 
 pneumonia, 142 
 ulceration of intestine, 164 
 Tumours, difference between 
 " simple and malignant, 275 
 epithelial, 283 
 malignant, 286 
 
394 
 
 INDEX 
 
 Tumours, myxoma of chorion, 
 
 304 
 
 neuroglial, 282 
 
 of bladder, 228 
 
 of bone, 260, 280 
 
 of brain, 242 
 
 of cartilage, 279 
 
 of fatty tissue, 279 
 
 of gall bladder, 197 
 
 of heart, 60 
 
 of intestine, 171 
 
 of kidney, 223 
 
 of larynx, 117 
 
 of liver, 192 
 
 of lung, 148 
 
 of lymph gland, 105 
 
 of lymphoid tissue, 282 
 
 of mammary gland, 273 
 
 of mouth, 153 
 
 of muscle, 280 
 
 of myxomatous tissue, 278 
 
 of myocardium, 60 
 
 of nerves, 253 
 
 of O3sophagus, 154 
 
 of ovaries, 264 
 
 of pancreas, 198 
 
 of peritoneum, 174 
 
 of placenta, 268 
 
 of prostate, 274 
 
 of spinal cord, 252 
 
 of stomach, 158 
 
 of suprarenal, 114 
 
 of testicle, 274 
 
 of uterus, 268 
 
 of vascular tissue, 281 
 
 of vertebrae, 252 
 
 simple, 277 
 
 types, 275 
 Typhoid carriers, 195 
 
 fever, 163 
 kidney in, 164 
 liver in, 164 
 spleen in, 164 
 
 ulcers compared with tuber- 
 culous ulcers of intestine, 
 166 
 
 Ulcer, rodent, 299 
 Unna's alkaline methylene blue, 
 343 
 
 Unna-Pappenheim stain, 343 
 Urine in acute nephritis, 210 
 
 in chronic interstitial nephritis, 
 216 
 
 in subacute nephritis, 212 
 Uterus, diseases of, 266 
 
 examination of, 34 
 
 rupture of, 269 
 
 tuberculosis of, 267 
 
 tumours of, 268 
 
 Valves of heart, abnormalities of, 
 
 47 
 diameter and circumference of, 
 
 76 
 
 examination of, 24, 25, 26 
 Van Gieson stain, method of use, 
 
 34i 
 
 Varicose veins, 89 
 
 Veins, diseases of, 87 
 thrombosis of, 87 
 varicose, 89 
 
 Venae Cavae, examination of, 23, 
 35 
 
 Vermiform appendix, examina- 
 tion of, 30 
 
 Vertebrae, tumours of, 252 
 
 Virchow, opening of abdominal 
 cavity, 14 
 
 Viscera (hollow) bacteriological 
 investigation of, 360 
 
 Volvulus, 159 
 
 Von Kossa silver stain, 352 
 
 Water test for lungs, 310 
 Waxy degeneration in tuber- 
 culosis, 147 
 
 of arteries, 78 
 
 of liver, 179 
 
 disease of kidney, 203 
 
 of spleen, 105 
 
 material, anilin stains for, 353 
 iodine stain for, 353 
 methyl-violet stain for, 353 
 stains for, 352 
 
 Weigert's borax - ferricyanide 
 differentiating mixture, 347 
 
 elastic stain, 344 
 
 fibrin stain, 345 
 
 iron-hsematoxylin stain, 339 
 
INDEX 
 
 395 
 
 Weigert's medullary sheath stain, 
 
 354 
 
 modification of Gram's stain, 363 
 White softening, 236 
 Widal reaction, 374 
 Woolsorter's disease, 2 
 Wright's stain, 358 
 
 Zenker's degeneration of muscle, 
 
 18 
 
 fixative, 327 
 Ziehl-Neelsen stain for tubercle 
 
 bacillus, 365 
 Ziehl-Neelsen with Much-Gram 
 
 stain, 369 
 
 THE END 
 
 Printed by R. & R. CLARK, LIMITED, Edinburgh. 
 
397 
 
 FIG. i. Method of opening the abdominal cavity. 
 
 FIG. 2. Reflecting the skin and muscles from the sternum and ribs. 
 
 26 
 
FIG. 3. Method of cutting through sterno-clavicular joint. 
 
 FIG. 4. Method of cutting through floor of mouth. 
 
399 
 
 ^(bfc : 
 
 x 
 
 O X Xrt 
 
 'TO 
 
 = a rt fa 
 
400 
 
401 
 
 FIG. 9. Method of removing the small intestine. 
 
 FIG. 10. Method of opening the bowel after it has been removed. 
 
402 
 
4^3 
 
 FIG. 13. Method of incising the kidney. 
 
 FIG. 14. Method of stitching [up. 
 
404 
 
405 
 
 FIG. 17. Heart, chronic interstitial 
 myocarditis. ^. 
 
 Apical portion of left ventricle showing white 
 patches of fibrous tissue replacing the muscle sub- 
 stance. The change is most marked at the apex and 
 in the right papillary muscle, which has been cut 
 open. 
 
 FlG. 1 8. Section through wall 
 of right ventricle, showing in- 
 crease of sub-pericardial fat and 
 fatty infiltration of the muscle. \. 
 
 FIG. 19. Thrombus in right auricular appendix. 
 
406 
 
 FIG. 20. Heart of child, simple (vegetative) endocarditis 
 in a case of chorea, y. 
 
 Minute rounded vegetations covering mitral valve close to free margin. 
 
407 
 
 FIG. 21. Aortic valve, simple endocarditis. ^. 
 
 Vegetations along margin of two segments, with red thrombus 
 attached to one of the vegetations. 
 
 FIG. 22. Heart, ulcerative endocarditis of mitral valve. ^. 
 
 The valve has been the seat of a previous endocarditis as evidenced by the 
 thickening of the segments and of the chordae tendineae. Both sets of structures 
 are covered with vegetations, which also extend on to the wall of the left auricle 
 and chordae tendineae. The wall of the left ventricle is thickened, and the cavity 
 dilated, due to the incompetence of the mitral valve which existed previous to the 
 ulcerative endocarditis. One or two of the chordae tendineae have ruptured. 
 
408 
 
 FIG. 23. Ulcerative endocarditis, aortic valve. 
 The segments had been thickened previously. They are covered with vegetations. One 
 of the segments has ruptured. There are also vegetations visible on the mitral valve to the 
 right. There is marked dilatation of the left ventricle, largely due to the incompetence of the 
 previously thickened valve. 
 
 FIG. 24. Transverse section of heart. ^. 
 Marked hypertrophy of left ventricle in case of chronic nephritis. Right ventricle dilated. 
 
409 
 
410 
 
 FIG. 27. Chronic endocarditis of aortic valve, y. 
 
 Calcareous deposits in the thickened cusps, also union ot the segments 
 with consequent s.enosis. 
 
 FIG. 28. Portion of descending thoracic FIG. 29. Arteries at base of brain. |. 
 
 aorta. 2 . Showing white patches of atheromatous change. 
 Showing advanced atheroma. Thrombi have 
 formed in one or two places. 
 

 
 
 FIG. 30. Saccular aneurysm of descending aorta adherent to and eroding 
 the bodies of the vertebrae. . 
 
412 
 
 
 S s 
 
 " U 
 
 33 
 
 3..S "2<S & 
 
 C/2 G v 3 8 
 
 [I *i 
 
 ^i ill 
 
413 
 
 1 
 
 FIG. 34. Spleen and spleniculus, 
 sago waxy. ^. 
 
 FIG. 35. Spleen, Hodgkin's disease, showing numerous 
 scattered white masses varying in size. |. 
 The organ is considerably enlarged. 
 
 FIG. 36. Spleen, Hodgkin's disease. (Dr. Byrom Bram well's case.) 
 Suet-like areas forming large tumour-like masses. 
 
 2 7 
 
CO w 
 
 ^ rt 
 
 Q 1 
 
 0) 
 
 -5T ^ 
 
 U3 
 
 ss -a 
 
 I 
 
 G W> 
 
 OJ _ 
 
 T3 rt 
 
 | 8 
 "S, * 
 
 Si 
 
4^5 
 
 P .2 
 
 II 
 
416 
 
 FIG. 41. Lung, collapse due to empyema. 
 Thickening of parietal and visceral pleura. 
 
417 
 
 FIG. 42. Lung, lobar pneumonia. |. 
 
 The whole of the upper lobe and the upper portion of the lower lobe are consolidated 
 and in the stage of grey hepatisation. The lower portion of the lower lobe is congested. 
 
4i8 
 
 FIG. 43. Lung and bronchi, showing acute bronchitis and septic 
 broncho-pneumonia. ^. 
 
 The bronchitis is indicated by the congested mucous membrane of the bronchi, the 
 broncho-pneumonia by the ill-defined pale areas of consolidation scattered through the 
 lung. 
 
419 
 
420 
 
 
 
 M^H 
 
 a*sS&SKfe'. 
 
 >' -*>-v-- / *> 
 
 4 - 
 
 -:i-# V 
 
 FIG. 47. Lung, silicosis. (Dr. J. D. Comrie's collection. ) ^. 
 
 Raised, hard, grey areas, surrounded with black pigment, scattered in groups 
 under pleura, around vessels and bronchi, and along interlobular septa. 
 
421 
 
422 
 
 m 
 
 A \ 
 
 FIG. 51. Lung, caseous (tuberculous) pneumonia vv 
 cavitation. ^. 
 
 ith 
 
 There is caseous consolidation of the upper portion, with numerous 
 acute cavities. In the lower portion there are groups of tubercles 
 arranged in a staphyloid manner indicating lymphatic spread. The 
 pleura is thickened. 
 
423 
 
424 
 
 te-r 
 
425 
 
 FIG. 58. Peptic ulcer of stomach, with 
 opening into vessel in floor of ulcer. ^. 
 
 
 FIG. 59. Large duodenal ulcer. 
 (Dr. Cattenach's case. ) . 
 
 :G. 57. Squamous epithelioma of oesophagus, Pancreas forming floor. Opening into large 
 with marked narrowing of lumen. ^. vessel at one point", from which fatal haemor- 
 
 rhage occurred. 
 
426 
 
 FIG. 60. Stomach opened up anteriorly to display encephaloid cancer 
 close to cardiac opening. ^. 
 
427 
 
 FIG. 61. Intussusception of small intestine and 
 mesentery into large. \. 
 
 Wall of large intestine has been removed at one point, 
 showing congested bowel within. 
 
 
 FIG. 62. Typhoid lesion of small 
 intestine. ^. 
 
 Early stage, showing swelling of Peyer's 
 patch and solitary follicles. 
 
 FIG. 63.. Typhoid lesion of small 
 intestine. |. 
 
 Later stage, with necrosis of swollen 
 patch and formation of slough. 
 
 F IG> 64. Tuberculous ulcer, lower 
 portion of ileum. \. 
 
 Note transverse direction, raised margin, 
 and irregular floor. 
 
 FIG. 65. Tuberculous ulcer, peri- 
 toneal aspect, showing raised tubercles 
 under peritoneum. ^. 
 
428 
 
 FIG. 66. Large intestine, ulcerative colitis (dysentery). ^. 
 
 Lines of hypertrophied mucous membrane with ulcerated surfaces between, 
 in which the muscular coat is laid bare. 
 
 FIG. 67. Portion of large bowel from case of amoebic dysentery, 
 showing characteristic early lesion. ^. 
 
 Minute crater-like ulcers with central slough. 
 
429 
 
 FIG. 68. Acute appendicitis and peritonitis. \. 
 
 The appendix is swollen and congested, and has ruptured at two points. 
 The portion of small intestine seen is covered in part with a thick layer of 
 
 fibrinous exudate. 
 
 FIG. 69. Pelvic colon with adeno-carcinoma projecting into interior. 
 The wall of the gut is hypertrophied above. 
 
430 
 
 FIG. 70. Peritoneal aspect of loop of intestine showing tuberculous peritonitis. \. 
 There are also swellings in the mesentery from enlarged mesenteric glands. 
 
 FIG. 71. Abscesses of liver, portal pyaemia type. \. 
 A thrombus is seen projecting from one of the branches of the portal vein (A) 
 
FIG. 72. Liver, large tropical abscess with much necrotic liver tiss 
 
 FIG. 73. Liver of child showing 
 nultiple nodular hyperplasia (re- 
 generation of liver substance) follow- 
 ng an acute degenerative process. 
 Dr. Byrom Bramwell's case. A. 
 
 FIG. 74. Liver, common cirrhosis. . 
 ^ Surface of organ shows " hob-nail " projections. Sec- 
 tion shows areas of liver tissue varying in size seoar- 
 
 nl-^rl fr^rr, ^,-,0 -.-.^k^,. U,, 1 J., -r_-__ _ . ^ 
 
432 
 
 
 
433 
 
 1 
 
 o 
 
 
 
434 
 
 FIG. 80. Biliary calculi or gall-stones. ^ 
 
 , common facetted type. 
 /', mulberry type. 
 
 c, rounded, solitary stone composed of pure 
 cholesterin. 
 
 FIG. 81. Congenital cystic kidney, i. 
 
 Rounded spaces, varying greatly in size, some empty, 
 others containing translucent gelatinous material. 
 
 FIG. 82. Infarcts of the kidney. ^. 
 
 Three infarcts varying in size are seen 
 in the upper part of the organ. 
 
435 
 
436 
 
 FlG. 87. Kidney, pysemic abscesses. 
 Cut surface. 
 
 FIG. 88. Kidney, pysemic abscesses. \. 
 Surface with capsule stripped. 
 
 FIG. 90. Kidn 
 
 berculosis. 
 
 FIG. 89. Kidney, tuberculosis. |. 
 
 Partial destruction of renal tissue form- 
 ing cavities with ragged walls, and with 
 a zone of caseous tissue around. 
 
 Acute type of the disease. Large masses of tuberculous 
 foci scattered, mainly in groups, through organ. Pelvis 
 lined with zone of caseous tissue. 
 
437 
 
 o 
 
 6 
 
 o 
 
 
FIG. 94. Brain, showing acute meningitis. ^. 
 
 There is general prominence of the vessels and exudate in the sulci and fissures, 
 especially the Sylvian fissure. 
 
 FIG. 95. Brain, tuberculous meningitis. -|. 
 
 Exudate extending up the Sylvian fissure and breaking up into discrete foci (tubercles) along 
 the distribution of the smaller arteries in the sulci and over, the convolutions. 
 
439 
 
 2, s 
 
 * 
 
 1 1 
 
 i 
 
440 
 
 FIG. 98. Cerebellum with depressed 
 areas from softening of brain substance 
 due to thrombosis in arteries. ^. 
 
 FIG. 99. Vertical section of brain, showing large solitary abscess 
 in temporo-sphenoidal lobe. ^. 
 
 FIG. loo. Transverse section of pons, showing haemorrhages 
 into its substance. ^. 
 
441 
 
 I -a '5 
 S>|o 
 
 M fa/) 
 
 o .S 
 
442 
 
 FIG. 104. Myomata in wall of uterus. \. 
 a., subserous type. 6, intramural type. c. submucous type. d indicates position of os uteri. 
 
 FlG. 105. Enlargement of costo-chondral junctions (rickety rosary) in rickets. \. 
 
443 
 
 FIG. 107. Lower lumbar vertebrce and sacrum 
 in section. ^. 
 
 Showing destruction of the body of one vertebra (A), 
 with abscess containing caseous material extending from 
 it anteriorly, the cauda equina being pressed upon behind. 
 The body of the vertebra above shows infiltration with 
 tuberculous foci. 
 
 FIG. 106. Chronic osteomyelitis 
 of lower end of femur. |. 
 
 A new casing of bone is seen above, 
 below is necrosed bone with openings 
 (cloacae). 
 
444 
 
 FIG. 109. Myeloid sarcoma 
 of jaw. f . 
 
 T indicates three teeth. 
 
 FIG. 108. Osteo-sarcoma of shaft 
 of femur. ^. 
 
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