BOUGHT WITH THE INCOME 
 ~^ FROM THE 
 
 SAGE ENDOWMENT FUND 
 
 THE GIFT OF 
 
 Menrg M. Sage 
 
 1891 
 
 ..Mii.m.^ s. 
 
Cornell University Library 
 arV17123 
 
 The student's hand-book of medicine and 
 
 3 1924 031 262 698 
 
 olin,anx 
 
Cornell University 
 Library 
 
 The original of tliis book is in 
 tine Cornell University Library. 
 
 There are no known copyright restrictions in 
 the United States on the use of the text. 
 
 http://www.archive.org/details/cu31924031262698 
 
THE STUDENT'S HAND-BOOK 
 
 OF 
 
 MEDICINE & THERAPEUTICS 
 
 BY 
 
 ALEXANDER WHEELER, 
 
 Licentiate of the Royal College of Physicians, Edinburgh ; 
 
 Licentiate of the Royal College of Surgeons, Edvriburgh, etc. ; 
 
 Clinical Assistant, Out-Patient Department, Edinburgh Royal Infirmary. 
 
 Author of "Our Unseen Fobs, " etc. 
 
 EDlNBtTEGH : 
 E. & S. LIVINGSTONE, 15 TEVIOT PLACE. 
 
 189 4. 
 K 
 
PBINTED BY 
 
 E. & S. LIVINGSTONE 
 4 MELBOURNE PLACE 
 
 EDINBURGH. 
 
TO 
 
 JOHN WYLLIE, Esq., M.D., F.R.C.P.Ed., 
 
 M.R.C.S.Eng., etc., 
 Physician to Edinburgh Royal Infirmary ; 
 
 JOHN PLAYFAIR, ESQ., M.D., F.R.C.P.Ed., 
 
 Physician to the Royal Hospital for Sick Children ; 
 
 G. A. GIBSON, Esq., M.D., D.Sc, F.R.C.P., F.R.S.E., etc., 
 
 Assistant Physician, Edinburgh Royal Infirmary ; 
 
 ®Ha ^ook 12 reapEitfallj gj&iiateir 
 
 IN TOKEN OF MANY ACTS OF KINDNESS SHOWN BY THEM 
 TO THE AUTHOR. 
 
PREFACE. 
 
 IT may be thought that the number of Text-Books on 
 Medicine are already more than sufficient — Why 
 therefore add another? As a tutor of large experience I 
 venture the opinion that a work such as this aims to 
 be, is a distinct want in the Student worM. Practitioners 
 have long complained that recently qualiiied men are of 
 little use to them on account of their lack oi practical know- 
 ledge ; moreover, the General Medical Council have endorsed 
 this verdict, and given emphasis to it by adding a year 
 of practical clinical work to the ordinary curriculum. But 
 a question which should and must be answered is — Why 
 or how is it that in these days of splendid lectures and 
 excellent Text-Books the recently qualified man is so 
 impractical? The cause is not far to seek. We must 
 admit that the Student is lectured to far too much ; each 
 subject that he is taught is expounded to him as if it 
 were the essential one to the exclusion of others ; and the 
 fact is ignored that a practical knowledge of Medicine 
 can only be obtained by the application of the principles 
 of anatomy, physiology, and pathology to the deviations 
 from the normal standard of health as observed at the 
 bedside of disease. The Student's day in fact, is largely 
 taken up in listening to theories, brilliant and fascinating no 
 doubt, but not always correct or profitable, and by evening 
 
vi Preface. 
 
 time he too often is bewildered or disheartened. He has then 
 to read the excellent Text-Books that are at his command ; 
 and by the time the comprehensive descriptions given 
 therein are waded through, little time is left for ward 
 work. In other words, the exquisite and complete Text- 
 Books now published are sources of danger if not used at 
 the proper time — for to a sharp Student they afford such 
 graphic pictures, he fears not the absence of ward work for 
 his examination ; and, on the other hand, the less bright 
 Student fails to grasp the more essential points ; in 
 either case clinical or bedside experience goes to the 
 wall. The aims of the writer of this volume are therefore 
 two-fold : — 
 
 1. To enable the Student to digest the main features 
 of the various diseases in the most concise manner at the 
 time he is engaged in clinical work, thereby enabling him 
 to verify at the bedside the statements he has read. 
 
 2. To enable the busy practitioner to see at a glance the 
 principal points of each disease, which he can elaborate by 
 his experience. 
 
 I have further ventured to introduce an alteration on 
 the plan usually adopted in writing small Text-Books, 
 viz., I have placed before the reader a synopsis of the 
 anatomy, or physiology, or both, of the organ or system 
 dealt with, before describing the diseases of those various 
 organs. This I hope will direct the reader to anticipate 
 what should or ought to occur when the system in question 
 is diseased, — i.e, to think out the probable symptoms, not 
 learn them, oif like a parrot. No one is more sensible than 
 myself of the many short-comings of this work, and though 
 I have no right to expect leniency at the hands of my critics, 
 I hope they will not judge me by too high a standard, but that 
 
Preface. vii 
 
 they will appreciate an honest attempt to present the main 
 facts of medicine in such a way that the student need not 
 spend the time perusing voluminous works which would he 
 more profitably employed in acquiring a practical knowledge 
 of disease at the bedside. I have left out the Diseases of 
 the Skin, as no useful purpose would be served by giving 
 a condensed account of them. In writing this work, the 
 author has reaped his information from most of the leading 
 and latest Text-Books, the monographs of Gowers, Paton, 
 Erh, Douglas Powell, Ealfe, Horsley, the useful atlas of 
 Byrom Bramwell, &c. I must, however, specially thank 
 Dr John Wyllie for the liberal use of his notes, and my 
 friend, Dr Ryland Whitaker, for valuable help in the section 
 on parasitic diseases. I wish also to express my gratitude 
 to my friends, Miss Euphie Gumming, Dr Teacher, and 
 others, for reading the proof-sheets of the latter portion of 
 the book ; and to Miss Giflfen for the compilation of the 
 index. In conclusion, I return my sincere thanks to my 
 publishers and their manager for courtesy at all times. 
 
 THE AUTHOE. 
 
 31 MOKNINGSIDE DrIVE, 
 
 FebrvMry ISdJf. 
 
ERRATA. 
 
 
 ige 92 {8th line), fourth should be 
 
 'sixth.' 
 
 , 146, phination 
 
 ' phonatiou 
 
 , 202, opposition ,, 
 
 * apposii^ion 
 
 , 249, nitrate 
 
 ' nitrite. ' 
 
 , 74, loop 
 
 ' roof. ' 
 
 . 98, flying 
 
 'fly.' 
 
THE STUDENT'S 
 
 HAND-BOOK OF MEDICINE 
 
 AND THERAPEUTICS. 
 
 FEVERS. 
 
 FEVEES are characterised by a grave disturbance of the 
 system, attended with great increase of temperature and 
 diminished secretions ; or in other words, more fire and greater 
 accumulation of ashes. All the specific or " zymotic " diseases 
 are probably due to special germs setting up chemical or 
 fermentative changes in the blood. Some of these organisms 
 we know something about, of others we know nothing. 
 Pasteur was the first to elaborate the fermentation theory. 
 
 Suppose we put into a bottle — water, sugar, and barm ; then 
 cork it tightly, and let it stand in a warm place. At first 
 nothing seems to happen, but after a time a remarkable change 
 takes place — CO 2 and alcohol form; and a sediment sinks to 
 the bottom, that is, the sugar has been changed by the living 
 yeast cells into poisonous compounds, this process stops, as 
 so many waste and poisonous products are formed that the 
 yeast cells themselves are hilled! 
 
 Again, — put into a bottle some sugar and a solution of 
 nitrogenous material (say clear mutton broth), and instead 
 of corking, expose it to the air. Again fermentation takes 
 place, and a scum soon rises to the surface. If the scum 
 
2 Student's Hand-book of Medicine. 
 
 be examined under the microscope it will be found to consist 
 of millions of cells = bacteria. The fluid, instead of the harm- 
 less one it once was, has become highly poisonous; it rapidly 
 decomposes, and gives rise to a most disgusting odour. 
 
 Here then are two cases of fermentation : the tine 
 induced by cells introduced by human agency, the other by 
 bacteria which got in from the air. In both cases, poisons 
 were formed, and the bacteria, like the yeast cells, were 
 killed through their own products, or through exhaustion of 
 suitable food, and thus the fermentative process was stopped. 
 
 Now apply this to specific fevers. Take scarlet fever : — first, 
 the patient complains of general malaise, then severe symptoms 
 develop, and the sufierer may hang between life and death. 
 Next a rapid improvement takes place, and health becomes 
 more or less quickly restored. Is it not probable that certain 
 bacteria in the air or in the food taken gained an entrance 
 into the blood, and having there found suitable soil began to 
 multiply, to set up chemical changes, and to form poisons 
 which resulted in the production of scarlet fever — how 
 easy to understand the whole event ! 
 
 As in the yeast experiments, we have — 
 A quiescent period — i.e., period of incubation. 
 A period of brisk fermentation = development of the fever. 
 The arrest of fermentation = recovery of the patient, either 
 rapidly by crisis, or with slight exacerbation of fever by — lysis. 
 
 We have then the following facts to go upon — 
 
 1. Bacteria are in the air and food. 
 
 2. Bacteria can cause disease. 
 
 3. Bacteria in order to cause disease must have proper food 
 
 or . 
 
 Diseases which result from bacteria must have — 
 
 (1) An incubative period. 
 
 (2) A period of brisk multiplication, and therefore 
 
 severity of symptoms. 
 
 (3) A period of decline. 
 
Typhoid State. 3 
 
 We learn more, however, for we find that as regards treat- 
 ment we can — 
 
 First — help to prevent the formation of suitable soils by- 
 hygienic measures. 
 
 Secondly — help to make an already suitable soil unsuitable, 
 by antiseptics, stimulants, and tonics ; in other words, 
 fight the bacteria by making the resistance greater, 
 through increasing the vitality of the tissues. 
 
 To sum up : decrease if possible the number of bacteria 
 attacking, and make the soil more resistant ; also support the 
 patient's strength till the fight is finished. Let me impress 
 upon beginners, however, that "prevention'' promises a far 
 better prospect than cure : for bacteria, once they flourish 
 gaily in the body, are fearfully difficult to exterminate. 
 
 In describing any fever, begin with the marked features of 
 the invasion, then emphasise — 
 
 1. The special symptoms of the fever. 
 
 2. The manner in which it declines. 
 
 3. The complications. 
 
 4. The sequelae. 
 
 Remember that all fevers have more than one type ;- always 
 at least two — the simple and the severe ; some, indeed, have 
 many forms, such as small-pox and scarlet fever. 
 
 All may assume what is termed the " Typhoid State ''■ — a 
 condition of great gravity. In order to avoid constant repeti- 
 tion, we shall in the following pages, describe, only the peculiar 
 feature of each "malaise," and sum up the later and more 
 severe symptoms of each fever under the term "Typhoid State," 
 but note particularly that this condition is not synonymous with 
 Typhoid Fever. 
 
 TYPHOID STATE. 
 
 The Typhoid State is characterised by — 
 
 1. A decline of the previously more acute symptoms. 
 
4 Student's Hand-hook of Medicine. 
 
 2. Pulse becoming rapid and soft. 
 
 3. Tongue dry and brown, tremulous, and protruded with 
 difficulty. 
 
 4r. Collection of sordes (a mixture of dried mucus and 
 bacteria) around the teeth and lips. 
 
 5. /Increased muscular prostration — tremors and subsultus 
 tendinum. 
 
 6. Semi-comatose state, coma vigil = pupils dilated, but 
 patient does not see. 
 
 7. Picking at the bed-clothes and muttering delirium. 
 
 8. Slipping down to the foot of the bed. 
 
 This condition becomes well marked in all the malignant 
 forms of fevers — is very well seen in small-pox, 
 typhus, typhoid, pneumonia, etc. 
 
 Morbid Anatomy. — Each fever has its special foci, but 
 usually in addition to their peculiar lesions, all, when severe, 
 show more or less changes in the tissues generally, viz. — 
 
 1. Blood is dark and more fluid (thick in cholera). 
 
 2. Muscles dark-coloured, and show granular degeneration. 
 
 3. Heart is softened, perhaps dilated. 
 
 4. Congestion of the viscera, spleen, liver, and Iddneys 
 particularly. 
 
 5. Hypostatic congestion of lungs. 
 
 PHYSIOLOGY OF FEVER. 
 
 Before discussing the treatment of fever we must consider 
 a few physiological questions. In fever we have a dis- 
 turbance of the heat-regulating centre, so that in addition to 
 the pernicious products of the specific germ, we have also to 
 consider the excessive waste of tissue, and diminished excretion 
 (pro ratio), with, consequently, the accumulation within the 
 blood of tissue waste products, which are also poisonous in, 
 
General Treatment. 5 
 
 their nature. Thus a cycle of retrograde changes commences. 
 The liver heing engorged does its work less efficiently, proteid 
 waste is not broken down so completely, and the kidney has to 
 excrete not only a greater amount of waste nitrogenous material, 
 hut material of a more irritating nature, and this too, when 
 by reason of the deterioration of the blood, the organ itself 
 is but poorly nourished. 
 
 GENERAL TREATMENT OF ALL FEVERS. 
 
 I. Medicinal. — The indications of treatment are sufficiently 
 obvious — 
 
 1. Diminish heat production. 
 
 2. Increase heat loss. 
 
 3. Help the secretory organs. 
 
 4. Keep the heart going. 
 
 5. Treat complications as they arise. 
 
 Under the first heading we may employ antipyretics — 
 Drugs — (1) Antipyrin group. 
 
 (2) Salicylates. 
 
 (3) Quinine. 
 
 (4) Aconite. 
 
 Under the second heading we may choose — 
 Diaphoretics — Liq. Ammon. Acet. 
 
 Alkaline group generally. 
 Jaborandi. 
 
 To help the secreting organs — 
 
 (1) Diminish the amount of nitrogenous food, and 
 
 substitute milk and farinaceous material. 
 
 (2) Keep bowels moderately open. Malce the urates 
 
 more soluble by administration of citrates, 
 tartrates, etc. 
 
6 Student's Hand-hook of Medicine. 
 
 And lastly, to keep the heart going, we may employ — 
 
 (1) Digitalis. 
 
 (2) Strophanthus. 
 
 (3) Strychnine. 
 
 (4) Diffusible stimulants, brandy, ether. 
 
 No routine treatment can be prescribed, because of the many 
 complications and peculiarities of each case. In most cases we' 
 may start with a purge, if there be no contra-indication. 
 
 ]J Hyd. Snbolor. grs. iv. ; followed by 
 ^^i Haust Sennse Co., giss in i hours. 
 
 This may be combined with a mixture taken at intervals, say, 
 a tablespoonful every four hours — 
 
 ^ Liq. Animon. Aoet. Cono. 3iij- 
 
 Spt. .ffitheris Nitrosi . 3ij. 
 
 Potass. Citratis . . . 3ij. 
 
 Aqua Camph. ad. . . . 3viij. 
 
 This will keep skin and kidneys acting ; the citrate also rendering 
 the urates less irritating. 
 
 So much for routine treatment, the complications will be 
 considered under each fever. 
 
 II. Hygiene. — Frequently "drugs" will form the least im- 
 portant factor in successful treatment, and in all cases their 
 action will be assisted by careful diet and strict attention to 
 hygienic principles. 
 
 The essentials are — 
 
 1. A large well-ventilated room, with blinds which may be 
 so arranged as to let in plenty of light when wanted, or to 
 exclude light if necessary. 
 
 2. An absence of unnecessary furniture, which only serves 
 to form a nidus for retention of the germs. 
 
 3. A well-trained, non-oflS.cious nurse. 
 
 4. Absolute cleanliness. 
 
 6. Strict attention to physician's orders. 
 
DeliriuTn — Alcohol in Disease. 7 
 
 DELIRIUM 
 
 Is sucli a common complication, we may take it here. There 
 are two types commonly met with — 
 
 1. Eaving maniacal delirium, of early stages. 
 
 2. Low muttering delirium, which occurs later. ' 
 
 In the first case we may employ depressants — 
 ]^ Chloral Hydras. . gss. 
 Pot. Bromid. grs. xl. 
 Aqua ad. ... giij. 
 One half at once, the other half repeated in one hour if required. 
 
 The second type must he met with stimulants — ammonia, 
 alcohol in large doses is recommended by some in addition ; 
 indeed, we may sum up in similar words the treatment of the 
 typhoid state — i.e., diffusible stimulants with alcohol must be 
 the principal remedies. 
 
 ALCOHOL IN DISEASE. 
 
 Beunton sums up as follows : — If the alcohol tends to 
 bring the patient nearer his normal condition it is doing good ; 
 if it takes him away further from his healthy condition, it is 
 doing harm. For instance, if alcohol renders the tongue moist, 
 slows the guiclcened pulse or the hurried breathing, if it 
 renders the skin cooler when hot and dry, and if it lessens 
 delirium and brings on sleep, then use it. If the converse 
 happens, then withhold it — typhoid or any other condition. 
 
 Alcohol is chiefly indicated during the small hours of 
 the morning, when attendants are sleepy ; the fire perhaps 
 gets low and the external temperature is generally lowered. 
 (Whitla.) 
 
 INCUBATION AND RASHES. 
 
 The incubative period of most fevers is from two to twelve 
 days. Scarlet fever and chicken-pox seem to have the shortesti 
 
8 Student's Hand-book of Medicine. 
 
 The following table is fairly correct—Eash appears in— 
 
 Chicken-Pox . . 1st day. 
 
 Scarlet Fever . . 2nd day. 
 
 Small-Pox . . . 3rd day. 
 
 Measles 4th day. 
 
 Typhus ... 5th day. 
 
 Typhoid ... 7th to 12th day. 
 
 Most rashes disappear on pressure, if not Timmorrhagic. 
 If hfemorrhagic they do not disappear on pressure or after 
 death. 
 
 TYPHOID FEVER. 
 
 A specific infectious fever marked clinically by diarrhoea, 
 a rose-coloured rash (appearing in successive crops), running a 
 course of twenty-one days, and ending by lysis. 
 
 .ffitiology. — Prevails most in autumn months. Attacks 
 both sexes from fifteen to twenty-five years of age. Eare in 
 infancy or over sixty. 
 
 The poison is conveyed principally by — 
 
 1. Water, contaminated by stools. 
 
 2. Soiled linen of typhoid patients in public laundries. 
 
 3. Milk. 
 '4. Drains. 
 
 5. Direct contact with stools of patients. 
 
 6. Contamination of the soil. (Pettenkofer.) 
 
 The stools, when fresh are not poisonous, but become so 
 after fermentation has commenced. The most virulent period 
 being from twelve to thirty-sis hours after having been passed. 
 
 Sewer gas, filth, etc., do not of themselves cause typhoid 
 fever, but cause a suitable soil for the typhoid bacillus to 
 multiply in the intestines. 
 
Typhoid Fever. 9 
 
 Specific Germ — known as the bacillus of Eberth. It is 
 short, thick, and has rounded ends. Some authorities say 
 it is identical with the " bacterium coli commune " found in 
 all diarrhoeas, but it differs in chemical re-actions. The 
 bacilli act by forming (1) certain ptomaines = typho-toxin, and 
 (2) tox albumin. Cultures are easily destroyed by corrosive 
 sublimate 1-2500. The baciUi are found in the intestinal 
 glands, spleen, and stools. 
 
 Morbid Anatomy. — Principally inflammation of the lym- 
 phoid tissue of the lower portion of the ileum, with more or 
 less catarrh throughout the bowel. 
 
 Peyer's Patches — 
 1st Week. — Are swollen through infiltration of lymph cor- 
 puscles, the surfaces raised and fawn-coloured — the infiltration 
 involves the submucous coat. 
 
 2nd Week.^ — The surface becomes abraded ; sloughs form, 
 which are often bile-stained. 
 
 3rd Week. — Sloughs come away, leaving ulcerating surfaces. 
 Typical typhoid ulcers are thus formed. A few solitary glands 
 undergo the same process. 
 
 Mesenteric Glands may undergo the same changes, but 
 more often become swollen, red, and tender only, or break 
 down into cheesy masses. 
 
 Other Organs. — Spleen and liver are enlarged ; heart is soft 
 and flabby. The voluntary muscles undergo vitreous degenera- 
 tion ; in fact, similar changes to those found after death from 
 high temperature, etc. (See page 4.) 
 
 Symptoms. — Insidious onset — headache, epistaxis, increasing 
 weakness till patient is compelled to take to bed. 
 
 1st Week. — Temperature runs up in remarkable staircase 
 manner ^ — i.e., rising two in the evening and falling one in 
 
10 Student's Hand-hook of Medicine. 
 
 the morning. (Not always.) The malaise becomes more marked, 
 and exhaustion increases with the onset of — 
 
 (1) Diarrhoea — the stools quickly assuming their char- 
 
 acteristic appearance. 
 
 (2) Abdominal tenderness and enlarged spleen. 
 
 The specific rash appears on seventh to twelfth day. 
 
 2nd "Week is marked by the symptoms becoming more 
 aggravated; the morning temperature does not remit. A 
 tendency to typhoid state comes on, and death may take 
 place. 
 
 3rd Week is marked by even more profound symptoms. 
 Perforation is much more likely to occur at this than any 
 other period, or perhaps fatal epistaxis or the pneumonic 
 condition may end the scene. 
 
 ith Week.- — The temperature becomes normal, and usually 
 convalescence may be now said to commence. Frequently, 
 however, relapses occur. 
 
 Complications of typhoid fever are — - 
 
 1. Peritonitis, with or without perforation. 
 
 2. Hasmorrhage : from bowel, nose, or mucous surfaces. 
 
 3. Embolism of femoral vein. 
 
 4. ■ Meningitis. 
 
 5. Septic Pneumonia. 
 
 6. Early " typhoid state " or early cardiac failure. 
 
 7. Hyperpyrexia. 
 
 SPECIAL POINTS. 
 
 The Rash comes out in successive crops, on the seventh to 
 twelfth day, as small rose-coloured spots raised above the 
 surface, slightly convex ; they appear first on the abdomen and 
 chest ; and fade on pressure. Frequently no rash appears. 
 
 The Ulcer of Typhoid Fever — 
 
 Lies in the longitudinal axis. 
 Edges — thin, undermined. 
 
Typhoid Fev&r. 
 
 Base — may be formed of either — 
 
 1. Sub-mucous coat. 
 
 2. Muscular tissue, or 
 
 3. Peritoneum only. 
 
 They show a tendency to perforate, 
 constriction after they heal. 
 
 11 
 
 but do not cause 
 
 The Stools. — Very foetid and ammoniacal ; pea soup in 
 appearance, and contain — fsecal matter, sodium chloride, triple 
 phosphates, and frequently blood, shreds of mucous membranes, 
 and sloughs. 
 
 
 TYPHUS. 
 
 TYPHOID. 
 
 
 Males, 25 to 35. 
 
 Dirt ; filth ; overcrowding. 
 
 Both sexes, 15 to 25. 
 
 Contamination with typhoid 
 stools ; defective drain- 
 
 Cause 
 
 
 
 age. 
 
 Onset 
 
 Abrupt. 
 
 Insidious. 
 
 
 Ends by crisis on fourteenth 
 day. 
 
 By lysis after the twenty-first 
 day ; frequent relapses. 
 
 
 Chief Symptoms 
 
 Referable to the nervous 
 system ; more delirium, 
 and early appearance of 
 typhoid state. 
 
 Eeferable more to the ali- 
 mentary canal ; nervous 
 symptoms and typhoid 
 state later. 
 
 Pupils 
 
 Contracted. 
 
 Confined. 
 
 Dark dusky mulberry ; 
 comes out on fifth day ; 
 tends to becomehsemor- 
 rhagic. 
 
 Dilated. 
 
 Loose. 
 
 Rose-coloured, like flea-bites; 
 appear seventh to twelfth 
 day in successive crops. 
 
 Bowels 
 
 Eash . 
 
 
 Temperature .... 
 
 Goes up rapidly, and comes 
 down suddenly. ■ 
 
 Rises 2° in the evening ; 
 falls- 1° in the morning 
 for four days ; then oscil- 
 lates throughout the 
 disease. 
 
12 Student's Hand-book of Medicine. 
 
 Special Points of Treatment. — Here we have to do, with 
 a diseased alimentary canal: our treatment must be mainly 
 dietetic. 
 
 Give no solid food, or that which would not readily pass 
 through a fine sieve (Whitla). JNIilk, if it agrees, arrowroot, 
 beef-tea, and chicken-broth are the principal foods. 
 
 Medicinal. — Do not he too officious. 
 
 General principles hold good. If the diarrhoea becomes 
 excessive give bismuth and opium, or lead acetate and morphia, 
 or an enema of starch and opium. 
 
 If constipation be troublesome — enema of warm water, castor 
 oil. No irritating purge. 
 
 Hfemorrhage — opium, hypodermic injection of morphia, alum. 
 
 Perforation — paralyse gut with opium. 
 
 Bed Sores — cleanliness — wash with brandy, gentle galvanism, 
 water-bed. 
 
 TYPHUS FEVER. 
 
 An acute specific contagious fever, characterised by sudden 
 onset, marked nervous symptoms, a maculated rash, and ending 
 by crisis. 
 
 .ffitiology.— Known as Jail fever, Ship fever, etc., is much 
 more rare than formerly — occurs amongst the poor, overcrowded, 
 and in dirty districts, affects principally adults between twenty- 
 five and thirty-six years of age. Very infectious, especially to 
 doctors and nurses. 
 
 Morbid Anatomy. — Those of intense fever, and blood- 
 poisoning, plus the petechial rash. (See page 4.) 
 
 Symptoms. — After a period of incubation the fever rapidly 
 develops with a . malaise, characterised by intense headache, 
 nausea, and vomiting, with elevation of temperature. There 
 may be rigors, pains all over the body, constipation, contracted 
 pupils, thick-furred tongue, and rapid exhaustion. Mousy 
 
Typhus Fever. 13 
 
 odour, noisy delirium and a dull, heavy, apathetic appearance. 
 The rash appears in about the fifth day — first, on the abdomen, 
 and the extensor aspects of the hands and wrists. As the fever 
 progresses, the typhoid state comes on rapidly : the delirium 
 becomes of the low muttering type — pupils before contracted, 
 may now be dilated ; the grave complications tabulated may 
 appear : retention of urine and paralysis of the sphincters ; 
 gangrene of the extremities ; all these may appear and help to 
 terminate the disease. If the patient does not succumb, usually 
 about the thirteenth day, the temperature falls ; profuse sweat- 
 ing, a critical diarrhoea, and an abundance of lithates usually 
 usher in a crisis ; after which the patient gains strength rapidly, 
 and may be, in a short time, in better health than before the 
 attack. 
 
 Specific Poison. — The organism has not yet been isolated ; 
 it is probably a strepto-bacillus, which has been observed by 
 more than one pathologist. Whatever the poison is, there is 
 no doubt that it quickly succumbs to a free supply of oxygen. 
 
 The Rash — comes out rapidly about the fifth day. It 
 shows — 
 
 1. A sub-cuticular mottling, dushy-red in colour. 
 
 2. Distinct papular rose spots, which tend to become 
 
 petechial, and, therefore, neither disappear on 
 pressure or after death. 
 
 Complications. — 
 
 1. Early assumption of typhoid state. 
 
 2. Eetention of urine. 
 
 3. Hyperpyrexia. 
 
 4. Gangrene of extremities, or bed-sores. 
 
 5. Broncho-pneumonia, most common complication, may 
 
 become purulent. 
 
 6. Parotid bubo, and pysemic abscesses. 
 
 7. Embolism of femoral vein, more common than in 
 
 typhoid. 
 
14 Student's Hand-book of Medicine. 
 
 It should be noted that, notwithstanding the severity of 
 the cerebral symptoms, meningitis and nephritis are rare ; but 
 albuminuria may be present. 
 
 Treatment. — Special points to hear in mind. — Whatever be 
 the nature of the poison, oxygen has a remarkably destructive 
 power over it ; therefore, a plentiful supply of air is indicated 
 in this, perhaps more than any other fever. 
 
 The nurse should be one who has either had the fever, or who 
 has nursed "typhus" before. She should be specially instructed 
 to note the tendency to " retention of urine and bed-sores.'' 
 
 This fever seldom calls for lowering treatment, and frequently 
 stimulants are required from the beginning. Employ the general 
 principles detailed in opening chapter. A good mixture is the 
 following — • 
 
 J^ Acid Hydrobromic Dil. . gss. 
 
 QuiiiEE. Sulpli 3ss. 
 
 Aq^ua ad. 5viij. 
 
 5ss. i hor. 
 
 The contracted pupils and delirium suggest absence of ex- 
 cessive light, at least in the earlier stages. The food must be 
 nourishing, and as plentiful as the assimilative powers will 
 admit. 
 
 SMALL -POX. 
 
 A contagious, infectious disease, characterised by a rash, 
 which usually appears on the third day, and runs through 
 four stages, viz.: — (1) Papular; (2) Vesicular; (3) Pustular; 
 (4) Drying up or Scabbing. 
 
 JEtiology. — Common to all ages and both sexes. Pcetus may 
 be affected. Planted in a virgin soil it is very virulent. Its 
 virulence is much modified by successful vaccination. 
 
 The contagion spreads by air, infected clothes, contact with 
 people, and contact with contents of pustule. As the primary 
 fever declines on the third day, when the rash appears, the 
 
Sviall-Pox. 15 
 
 patients frequently walk about and apply at hospital for advice 
 respecting a "rash," and they may thus infect all in the waiting- 
 room. Of great importance to the State is the fact, that the 
 virus may be given off from the dead. 
 
 Symptoms. — After twelve days' incubation, the malaise of 
 onset comes on. Most notable features — frontal headache, pains 
 in bade, vomiting. Temperature runs up rapidly, with all the 
 phenomena of " fever.'' On third day fever usually declines, 
 and the rash appears as a papule. Soon, however, the symptoms 
 become worse and more pronounced than before, the fever in- 
 creases, and on the ninth day, when the rash becomes pustular, 
 the so-called secondary fever occurs, due to absorption of pus. 
 The fever then becomes septic in type. Temperature oscillates. 
 There may be severe rigors and a rapid assumption of the typhoid 
 state. There is great swelling of the face — the eyes may be even 
 closed up — and too frequently the patient dies ; or the fever may ' 
 subside, and the scabs commence to dry, falling off finally on 
 the eighteenth to twentieth day, leaving a more or less pitted 
 appearance. 
 
 The Specific Bash first appears on third day of fever, on the 
 face, forehead, and scalp, as slightly raised red papules ; feels 
 shotty beneath the skin. 
 
 Three days later (sixth day of fever) the " papules " become 
 vesicular, at first clear and transparent, then turbid, depressed 
 in the middle or umhilieated. Each vesicle is also loculated, 
 that is, divided into compartments by delicate connective tissue 
 partitions derived from proliferation of the cells of the rete 
 Malpighii. 
 
 Usually about three days later (ninth day of disease), the 
 vesicle becomes purulent, accompanied with an inflammatory 
 ring round each vesicle, which causes great swelling and 
 disfigurement of parts afiected, and attended with exacerba- 
 tion of symptoms due to absorption — i.e., secondary fever; then 
 the pustule begins to dry ; a black brown scab forms and drops 
 off, leaving a depressed scar as before mentioned. 
 
16 Student's Hand-hooh of Medicine. 
 
 Varieties.— 
 
 1. Modified, as seen occasionally after vaccination. 
 
 2. Simple or discrete = the pocks being few. 
 
 3. Confluent = where pocks run into one another. 
 
 4. HBemorrhagic or malignant. 
 
 5. Corymbose, where pocks cluster together like grapes. 
 
 Other varieties have been tabulated, but they only confuse 
 the student and serve no practical purpose. 
 
 How does the haemorrhagic form influence the clinical course? 
 
 1. The patient may be so overwhelmed with the poison 
 
 that he may die as early as the second day. 
 
 2. The haemorrhage may appear later, and prevent the 
 
 ordinary stages or course of the rash. 
 
 3. In any case the prognosis becomes more grave, and 
 
 the patient may be carried off by hsemorrhages from 
 mucous membrane, nose, lung, kidneys, etc. 
 
 Next to the hoemorrhagic, of course, the confluent is the most 
 severe form — fever does not fall on the third day. The fever 
 becomes more severe, the skin enormously swollen, and all the 
 symptoms tend to a low type. 
 
 Complications. — 
 
 1. Pysemic abscesses and albuminuria. 
 
 2. Suppurative keratitis, with ulceration of cornea. 
 
 3. Ulceration of pharynx, or larynx. 
 
 4. Septic pneumonia. 
 
 5. Haemorrhage of all kinds. 
 
 Sequelae. — 
 
 Otitis media. 
 Abscess of other bones. 
 Deep pitting. 
 Blindness. 
 Peripheral neuritis. 
 
Small- Pox. 17 
 
 Pathology. — Tissues generally — like those of fever. (See 
 page 4.) 
 
 1. Rash. — Papular stage. 
 
 (1) Proliferation of cells of rete Malpighii. 
 
 (2) Cell coagulation and central necrosis, due to 
 
 micro-cocci. 
 
 (3) Layer of leucocytes. 
 
 2. Formation of spaces containing — 
 
 Serum. \ 
 
 Fibrin. [-Vesicular stage. 
 
 Leucocytes. J 
 
 The umbUication corresponds to the area of 
 
 primary necrosis. Often determined by the 
 
 site of a hair follicle. 
 
 3. Degeneration into pus of vesicular contents — papillaa of 
 
 true skin are now very swollen and infiltrated ■with 
 leucocytes — pustular stage. 
 The blood shows no specific changes. 
 
 Initial Rashes — The specific rash may be preceded by other 
 rashes (which may appear on second day) — 
 
 1. Hemorrhagic — occupies lower half of abdomen. 
 
 (1) Extends in triangular form, apex at Scarpa's 
 
 triangle. Extensor aspects. 
 
 (2) Purpura variolosa — constitutes a severe type 
 
 of disease. 
 
 2. Erythematous form — similar to scarlet fever or measles. 
 
 If this happen, the true rash when it occurs seems 
 to spare the site of the initial rash. 
 
 Treatment. — General rules as laid down in introductory 
 remarks. 
 
 Special Points are — 
 1. Use a darkened room when eyes are affected. 
 
18 Student's Hand-book of Medicine. 
 
 2. Prevent itching by smearing witli carbolic ointment, or 
 sponging with some antiseptic, non-irritating fluid. 
 
 3. Eemember to thoroughly isolate, and 
 
 4. Bear in mind the good influence of successful vaccination 
 amongst the inhabitants of the afiected district. 
 
 VACCINATION IN MAN. 
 
 Jenner first inoculated cow-pox, with lymph obtained from 
 pustules on the udders of cows. The contents of the pustule 
 so set up may be used = arm-to-ann vaccination. 
 
 After inoculation (arm-to-arm) — 
 
 A papule forms second to third day. 
 Becomes vesicular on fifth to sixth day. 
 Becomes purulent on ninth day. 
 Dries up and scab falls end of third week leaving 
 a permanent scar. 
 
 The neighbouring lymphatics become enlarged. After 
 inoculation the arm usually swells, and more or less fever 
 is occasioned. 
 
 Where lymph is used "direct" from the cow, the process 
 is slightly slower. 
 
 British law requires all healthy children to be vaccinated 
 before three months old. 
 
 SCARLET FEVER. 
 
 A contagious infectious disease, characterised by fever, sore 
 throat, and a scarlet rash which freely desquamates. 
 
 .ffitiology. — Epidemics prevail at all seasons. One attack 
 usually prevents a future one. The poison is peculiarly per- 
 sistent, and may be carried to a great distance by letters, etc. 
 
Scarlet Fever. 19 
 
 Symptoms. — The principal features of the onset are — 
 rheumatic pains, soreness of throat, and headache. Soon, 
 however, the throat becomes very sore, the neck feels stiff, 
 and the glands at the angle of jaw are swollen. 
 
 On the second day the rash comes out, first on the chest, 
 then rapidly spreads over the face and body. 
 
 As the fever progresses, the throat symptoms become more 
 severe ; the tonsils approach the middle Une, yellowish points 
 appear. These may coalesce and form a "patch" resembling that 
 of diphtheria. Other severe complications (see tabulated list) 
 often arise and bring about a fatal issue; or the temperature 
 may fall gradually with the fading of the rash, and a slow 
 convalescence is gradually established. 
 
 The Tongue is at first covered with thick white fur, with 
 papUlsB projecting — i.e., the white strawberry tongue ; later, the 
 fur peels off, leaving the typical red strawberry appearance. 
 
 The Rash appears on the second day, fijst as a scarlet blush, 
 but if looked into carefuUy is seen to consist of small red 
 spots, with red areolae around them. 
 
 The severity of the rash varies, it may be absent or only 
 present in the " flexures " of limbs as bright red lines. 
 Diagnosis is then often difficult, but later on desquamation 
 settles the question. 
 
 Desquamation begins as early as the sixth day ; it may be 
 only to the extent of roughness, or the epidermis may peel off 
 in large flakes ; time occupied :^ 4 to 8 weeks. 
 
 Complications. — 
 
 1. Scarlatinal arthritis (may end in suppuration). 
 
 2. Endocarditis and pneumonia. 
 
 3. Ear troubles are exceedingly common. The suppurative 
 process going on in the middle ear may cause — 
 
 (1) Perforation of the drum. 
 
 (2) Permanent deafness, through suppuration extending 
 
 to middle ear. 
 
20 Student's Hand-hook of Medicine. 
 
 (3) Facial paralysis. 
 
 (4) Meningitis. 
 
 4. Extensive suppuration of glands. 
 
 5. Scarlatina nephritis is, however, more of a sequela, as it 
 most often begins about the third week of illness, when the 
 skin is freely desquamating. The symptoms are — 
 
 (1) High-coloured or smoky albuminous urine. 
 
 (2) Presence of tube casts. 
 
 (3) Dropsy of eyelids and ankles, but the dropsy may 
 
 extend all over the body. 
 
 Varieties. — 
 
 1. Simple. 
 
 2. The Anginoma form, where throat symptoms are severe 
 and a membranous exudation forms, or necrosis of the tissues 
 of the throat, with intense foetor. Extensive sloughing, causing 
 perforation of the ascending pharyngeal artery or even the 
 common carotid. 
 
 3. Hcemorrhagic form, in which extensive hjEmorrhages 
 occur, epistaxis and haematuria; and death takes place on the 
 second or third day. 
 
 Special Points in Scarlet Fever. — The skin is peculiarly 
 hot and pungent. Note the tendency to attack serous 
 membranes. 
 
 The nephritis is usually late, the explanation being that the 
 kidneys have been not only overworked, eliminating the products 
 of the fever, but in addition are deprived of the support of the 
 secretory function of the skin; and secondly, the new skin, 
 being more sensitive to draughts and chills, causes internal 
 congestion. Undoubtedly these are two powerful factors, but 
 it is probable that the scarlet fever poison has a peculiarly 
 irritating effect on the renal tubes. Scarlatina nephritis is said 
 to affect the glomeruli more than ordinary nephritis. 
 
Measles. 21 
 
 Treatment. — Same general principles detailed in opening 
 chapter. 
 
 Special Points are — 
 
 1. A minimum amount of nitrogenous food. 
 
 2. Danger of spreading the disease is greatest during the 
 desqiiamative period ; greater need, therefore, of prolonged 
 isolation. 
 
 Gomplieations. — The " Arthritis " demands warm applica- 
 tions. Wrap joints in cotton wool; salicylates internally. 
 (If the kidneys are also inflamed, trust to alkalies internally 
 and opium externally.) Elaterium, pulv. jalapse co. 
 
 Throat. — Antiseptic steam. Painting with tannic acid and 
 glycerine ; plenty of hot milk. 
 
 For the severe types. — Pure carbolic acid to patches, or 
 perchloride of iron, with free administration of ammonia ; 
 quinine, either alone or >vith perchloride of iron. 
 
 MEASLES. 
 
 An eruptive fever ushered ia with coryza. 
 
 .etiology. — Extremely infectious. Contagion is communi- 
 cated by the nasal secretions and breath ; also by fomites, or 
 a third person. Epidemics occur often, and seem peculiarly 
 associated with or related to whooping-cough, being often 
 followed by the latter. 
 
 Symptoms. — First, are those of catarrh — eyes water, con- 
 junctivae become suffused, discharge from nose, and bronchitic 
 symptoms. Often temperature falls on second day, but rapidly 
 rises with the eruption of the rash on the fourth day. As the 
 fever progresses the bronchial troubles increase, and the various 
 complications arise. 
 
 The Rash. — First appears on. fourth day at the roots of the 
 hair, and on forehead and face. The rash consists of raised, dark- 
 red spots, spreading in crescentic patches, and giving a velvety 
 feel to the touch. The eruption begins as a hypersemia around 
 
22 Student's Hand-book of Medicine. 
 
 the sebaceous follicles. There is usually much subcutaneous 
 oedema, and the child presents a peculiar, blotchy, swollen 
 appearance. , The rash fades in about three days, leaving a 
 slightly brown-stained appearance which soon passes away. 
 There may be slight, branny desquamation, hut it is alioays 
 slight. The rash differs from that of scarlet fever by — 
 
 1. Appearing on the fourth instead of the second day. 
 
 2. Being darker in colour. 
 
 3. The velvety feel. 
 
 4. Manner of spreading, but diagnosis is sometimes difficult. 
 
 5. The subcutaneous oedema. 
 
 The rash inay be slightly hwmorrhagie, even in non-severe 
 cases. 
 
 Complications. — 
 
 1. The extension of bronchial catarrh, causing capillary 
 bronchitis and collapse of the lung, or pneumonia either 
 catarrhal or croupous in nature. Dr John Playfair notes a 
 frequency of croupous pneumonia and bronchitis in the same 
 lung. In children, laryngitis is often formidable. 
 
 2. Purulent ophthalmia, etc. 
 
 3. Otitis media, and swollen cervical glands. 
 
 4. Gangrene of skin, vulva. 
 
 The various sequelse are very numerous. 
 
 Varieties. — 
 
 1. Simple. 
 
 2. Hsemorrhagic. Characterised like all other hsemorrhagic 
 forms of fever by bleeding from mucous surfaces, hsematuria, 
 and an early assumption of the typhoid state. 
 
 3. Measles, complicated with diphtheria of the fauces. 
 
 Pathology. — Braid wood and Vacher found, in the exhaled 
 breath, lungs, and liver, peculiar bright particles which did not 
 stain with carmine. Nothing definitely is known of the real 
 poison, as no organisms discovered meet the requirements of 
 Koch's law to identify them as being the cause of the disease. 
 
Itotheln. ^3 
 
 There is no special morbid anatomy except that of the various 
 complications. The respiratory organs, however, always show 
 marked catarrhal changes. Usually some subcutaneous oedema. 
 
 Treatment. — General principles hold good ; but note the 
 special claims of the respiratory organs, and the tardy con- 
 valescence. An expectorating saline mixture may be given early 
 (avoiding squills), antiseptic inhalation, and glyceriae applied 
 to the fauces are indicated. 
 
 ROTHELN— GERMAN MEASLES. 
 
 A highly infectious, contagious disease, ushered La with 
 catarrh (often Hi-marked) and an eruption. 
 
 .ffitiology. — Was formerly thought to be a mixture of scarlet 
 fever and measles, but is now held to be a separate disease. 
 
 Symptoms. — Those of bronchial catarrh, sore throat, and 
 swollen glands ; rarely are there severe complications. Many 
 patients do not feel ill at all, but Cheadle reports some severe 
 cases attended with albuminuria. 
 
 Rash. — Eound or oval, slightly raised, pinkish-red spots, 
 discrete usually, but sometimes confluent appear on the first, 
 second, or third day. 
 
 Diagnosis. — From Measles by — 
 
 1. Short prodromal stage. 
 
 2. Absence of the dark colour and crescentic 
 
 form of the measles rash. 
 
 From Scarlet Fever by — 
 
 1. Large size of spots. 
 
 2. Absence of severe symptoms and desquamation. 
 
 Treatment. — General principles. 
 
24 Student's Hand-book of Medicine. 
 
 DIPHTHERIA. 
 
 A specific contagious fever attended with grave throat 
 symptoms, and the formation of a false membrane or fibrinous 
 deposit on mucous and abraded surfaces. 
 
 etiology. — Is endemic in the larger towns, and becomes 
 often epidemic at various seasons. It is highly contagious, 
 and the poison is very concentrated in the pharyngeal 
 secretion; it is very fatal to doctors and nurses. (Possibly 
 the spluttering of secretion into the face whilst examining or 
 swabbing out the patient's throat may account for this great 
 tendency to attack the attendants.) 
 
 Eeoent evidence shows that most epidemics can be traced to 
 spreading through — 
 
 1. Contamination of milk supply. 
 
 2. Defective plumbing in water-closets 
 
 3. Transmission of the poison from distant parts by the 
 wind. 
 
 4. The prevalence of sore throat prior to epidemic — i.e., 
 formation of suitable soil for the germ. 
 
 Thome denies it has ever been distinctly traced to polluted 
 water. 
 
 Pathology. — Specific Germ — It is known as the Klebs- 
 Loeffler bacillus. It is non-mobile, slightly bent and knobbed ; 
 and multiplies readily in milk. It is found in the false 
 membrane associated with other germs, etc., strepto-cocci, and 
 staphylo-cocci. The false membrane shows — • 
 
 1. A heavy network of epithelium. 
 
 2- Fibrinous threads entangling masses of leucocytes, and 
 proliferated connective tissue corpuscles. 
 
 3, Colonies of micro-cocci with the Klebs bacilli. 
 
 4. Granular debris. 
 
Diphtheria. , 25 
 
 Dr Oeetel states : the poison first induces a necrosis of 
 the cells with which it comes in contact ; the superficial 
 epithelium thus first disappears. The deeper cells become 
 similarly affected, and a zone of inflammation forms around 
 the dead cells ; the membrane thus is really a mass of dea;d 
 cells undergoing hyaline degeneration, and presents the peculiar 
 laminated appearance considered characteristic. The neigh- 
 bouring lymphatic glands become much enlarged. 
 
 The other visceral changes are similar to those of any other 
 intense or malignant fever. 
 
 Symptoms. — After an incubation of two to seven days a 
 general malaise sets in ; there is slight fever, stiffness of neck, 
 swelling of angles of jaws. The soft palate is deeply congested, 
 and whitish patches soon appear ; these patches coalesce, become 
 "wash leather-like" in colour, and the false membrane is fully 
 formed. It may extend all over the fauces, or may begin on 
 the tonsils first and creeping forward surrounds the uvula like 
 a finger of a glove. The membrane is at first easily stripped, 
 but soon re-forms ; then it becomes firmly adherent, and if 
 torn away leaves a bleeding surface. If left alone it may 
 slough off. 
 
 The glands in the neighbourhood enlarge, but do not usually 
 suppurate. 
 
 The temperature varies, it may be 103° or higher, but is 
 usually from 100° to 102°, and indeed often subnormal. This 
 is peculiar, as most acute throat affections have high tempera- 
 tures. The exudation may now extend in any direction, 
 upwards into — 
 
 1. The pharynx, attended with regurgitation through the 
 nose, epistaxis, and a nasal twang of voice. 
 
 2. The larynx — '' diptheritic croup " — symptoms are 
 stridor, brassy cough, great dyspnoea, and sucking in of the 
 intercostal spaces. (Some hold this to be the true croup.) 
 
26 Student's Hand-book of Medicine. 
 
 3. The bronchi, with all the symptoms of severe capillary- 
 bronchitis. The membrane after extending to the first bifur- 
 cation of the bronchus speedily becomes purulent. 
 
 By this time the typhoid condition has been ushered in, 
 and the patient may die at any time from the second to the 
 sixth day from asthenia or from increasing asphyxia. 
 
 Albuminuria is frequently present from the earliest period. 
 There is usually no dropsy. 
 
 Complications, beside those described, are — 
 
 1. Ulcerative endocarditis. 
 
 2. Meningitis. 
 
 3. Otitis media, etc. 
 
 The most important sequela is post-dvpth&ritio paralysis. 
 This is a peripheral neuritis, and may vary much in its 
 distribution and severity — usually coming on vpithin three 
 weeks of apparent recovery. The more constant symptoms 
 are — 
 
 1. Ansesthesia and paralysis of soft palate. 
 
 2. Loss of accommodation, with squint or diplopia. 
 
 3. Loss of deep reflexes. 
 
 The paralysis may be much more extensive, and if the 
 intercostal muscles, or vagi become affected, then the prognosis 
 is very unfavourable. Usually, however, the paralysis passes 
 off in time under suitable treatment. 
 
 Special Points. — Note — 
 
 1. The tendency for serous membranes to be involved. 
 
 2. The marked depression. 
 
 3. The red areolae around the exudation. 
 
True Group. 27 
 
 Remember the membrane may be very localised, and not 
 visible without a post-nasal or laryngoscopic examination. 
 
 Treatment. — 
 
 1. General principles, as in Scarlet Fever. 
 
 2. Hot antiseptic inhalations and emetics. 
 
 3. Painting with chromic acid solution, or pure carbolic 
 
 acid. 
 
 4. Avoid all lowering measures. 
 
 The " P D " paralysis must be treated with careful hygiene, 
 strychnine, massage, and nourishing diet. 
 
 Tracheotomy must always be kept in mind when the 
 larynx is seriously involved. 
 
 TRUE CROUP. 
 
 An acute affection of the larynx, usually affecting children 
 under five years of age, and characterised by the formation of 
 a membrane, not contagious. Some authorities hold that all 
 cases of true croup are diphtheritic in nature. It is true that 
 the larynx when affected in diphtheria presents a most virulent 
 type of croup, but there is also no doubt that we have a 
 highly dangerous affection of the larynx caused by a " croupous 
 inflammation " which is not diphtheritic ; the membrane 
 formed showing nothing pathognomonic beyond a fibrinous 
 exudation, but the membrane may extend down to the most 
 minute bronchi. 
 
 Symptoms. — After a short period of febrile disturbance, 
 catarrh, and fretfulness, the cough becomes brassy, the cry 
 hoarse and metallic, and the breathing much embarrassed. 
 
28 Student's Hand-hook of Medicine. 
 
 The inspirations are peculiarly piping or hissing in character, 
 and fatal asphyxia may rapidly supervene. 
 
 The Complications may be bronchitis and pneumonia, 
 endocarditis, etc. 
 
 Treatment. — Hot bath, hot sponges to throat (some advise 
 ice) — a brisk emetic of ipecac, alum, or mustard and water, 
 followed by a saline mixture. Whitla advises small doses of 
 the following mixture for a child one year old ; — 
 
 9 Vin. Antim. Tart. . 3iv. 
 
 Vin. Ipecac. . . 3iv- 
 
 Synipi ScilliE . 5iv. 
 
 Aqua ad. . . . giij. misce. 
 
 A teaspoonful every fifteen minutes till vomiting occurs, 
 then half a teaspoonful every two or three hours whilst the 
 cough lasts. 
 
 Croup differs from diphtheria in — 
 
 1. Its onset — i.e., no special soreness of the throat. 
 
 2. Not being contagious. 
 
 3. There being no bleeding surface when membrane 
 
 is torn off. 
 
 4. Absence of the " diphtheria bacillus." 
 
 In some cases the diagnosis may be difficult, in that case 
 treat as if it were the graver disease. 
 
 Tracheotomy must be performed if dyspnoea becomes 
 extreme, and emetics fail to give relief Apparently hopeless 
 cases have been saved by the operation. 
 
Gerebro- Spinal Fever. 29 
 
 CEREBRO-SPINAL FEVER. 
 
 An acute specific fever characterised by sudden invasion, 
 and attended with, painful contractions of muscles, a purpuric 
 rash, and various grave nervous complications. 
 
 etiology. — According to Taylor, very little is known of 
 this fever. It has appeared in severe forms in Germany and 
 Ireland, but only in small epidemics in England. The disease 
 does not seem to be contagious from man to man, but it is 
 possible that the virus may be transmitted through the lower 
 animals. It affects young adults chiefly. 
 
 Symptoms. — The invasion is sudden ; there may be rigors, 
 and usually intense vertigo, vomiting, intolerable headache, 
 and noisy delirium. The face is pale, conjunctivse red, pupils 
 contracted ; painful contraction of the muscles of the neck, 
 causing retraction of the head. Herpes labiales and zoster are 
 most constant symptoms. The sensibility may be so acute 
 that the slightest movements are intolerable. This hyper- 
 sensitiveness is most marked along the spine. As the fever 
 progresses tetanic convulsions may bring about a fatal issue 
 from lock-jaw or asphyxia. Frequently the typhoid state super- 
 venes as soon as the fourth day, the pupils become dilated, 
 anaesthesia takes the place of hyperaesthesia, and the patient 
 quickly succumbs. 
 
 Rash. — Usually appears on second day ; consists of small 
 purpuric spots, not raised. They appear on the neck and 
 extensor aspects, rarely on the face. 
 
 Complications — 
 
 1. Purulent effusions into joints. 
 
 2. Painful urticaria. 
 
 3. Optic neuritis. 
 
 4. Hyperpyrexia. 
 
30 Student's Hand-book of Medicine. 
 
 Special Points to note in this meningitis are — 
 • The great tendency to opisthotonus. 
 
 The skin affections — herpes, purpura, erythema, etc. 
 
 The extremely rapid course. 
 
 Pathology. — Not to be regarded as a simple meningitis. 
 
 1. Oord. — Pia mater may be either intensely injected or 
 totally disorganised, and the subarachnoidal space may be filled 
 •with pus, causing the dura mater to bulge out. Usually the 
 pus collects most in the lumbar region. 
 
 2. Brain. — The meninges show intense inflammation, and 
 the ventricles are distended with pus ; the foramen of Majendie 
 may be plugged with pus, or the veins of Galen become 
 thrombosed, causing hydrocephalus.^ 
 
 Treatment. — General principles again hold good, but the 
 excessive pain and convulsions demand special attention — 
 absolute rest, antipyrin, chloral, and bromide ; chloroform to 
 subdue painful contractions. (In three cases I saw — chloroform 
 during the convulsions, iodoform to- shaved head, quinine, 
 and free purging with calomel, seemed to do good.) 
 
 MALARIAL FEVERS. 
 
 An infectious fever characterised by being associated with 
 certain soUs, and the organism known as hsematozoa of Laveran ; 
 also clinically, by paroxysms of (1) intermittent fever (true 
 ague) ; (2) continued fever with well-marked remissions (jungle 
 fever) ; (3) certain pernicious, rapidly fatal forms ; and (4) a 
 chronic cachexia with ansemia and enlarged spleen. 
 
 The Malarial Poison. 
 
 1. The Specific Germ.- — Klebs' discovery of a bacillus is not 
 yet confirmed (1893). If the blood of the patient be carefully 
 
Malarial Fevers. 31 
 
 examined, there are always found colonies of bodies termed 
 liSBmatozoa. These are regarded as parasites, but nothing is 
 known of their life history. They exist in six forms — all are 
 found in the red corpuscles : — 
 
 (1) Unpigmented, active, hyaline bodies. 
 
 (2) Pigmented amoeboid bodies. 
 
 (3) Segmented bodies. 
 
 (4) Creseentic masses, very distinctive. 
 
 (5) Flagellate organisms from the creseentic masses. 
 
 (6) Free flagella. 
 
 These parasites break up the haemoglobin, thus causing 
 excessive antemia on the one hand, and give rise to products 
 which probably are albumose in nature, and thus poison the 
 nerve centres. Quinine has been observed experimentally to 
 interfere greatly with the existence of these organisms. 
 
 2. The Soil. — The poison usually develops in low, marshy, 
 or badly drained districts, rich in vegetable matter. A tropical 
 climate is best for its production. The poison is contained in 
 the emanations of the soil. It does not rise high, is modified 
 by trees, especially the eucalyptus ; but the beneficial effect 
 produced by this tree is probably due more to its drying 
 influence than to its antiseptic qualities. 
 
 The Attack, — After some days of premonitory symptoms 
 of more or less general malaise, the typical attack comes on, 
 and usually consists of three stages — cold, hot, and sweating 
 
 Gold Stage. — Patient shivers violently, teeth chatter, skin 
 is pale and blue, and papillae are raised (goose-skin) ; there is 
 a great tendency to collapse. The temperature though much 
 lowered externally, is, however, raised in the rectum. As may 
 be expected with such an extreme contraction of the superficial 
 capillaries, the urine is pale, copious, and of low specific gravity. 
 
32 Student's Hand-book of Medicine. 
 
 TMs stage lasts from one-half to two hours. Towards the end 
 of the stage the temperature may be 103° to 106°. 
 
 Rot Stage. — It may he gradual or sudden in its onset. 
 The skin becomes hot and burning, and a patchy rash may 
 form. There is vomiting or complete anorexia; throbbing of 
 the carotids with intense headache, and there may be delirium. 
 Often crops of herpes form at the mouth. This stage lasts 
 from two to four hours. Urine is scanty, of high specific 
 gravity, and contains a large quantity of urates and urea. 
 
 Sweating Stage. — The sweating commences at the roots of 
 the hair, but soon becomes general and profuse. The pulse 
 gets softer, the temperature falls gradually to the normal, and 
 the patient is restored to the normal condition. During the 
 sweating stage the urine is of high density, and scant in 
 quantity ; urates are more abundant than urea. 
 
 The Spleen. — The spleen enlarges during hot and cold stages, 
 and repeated attacks finally induce the chronic, enlarged spleen 
 or ague-calce. The organ is enlarged, the capsule is thickened 
 and is often adherent to other organs. Internally it shows — 
 
 1. Fibrous stroma increased. 
 
 2. Infarcts. 
 
 3. Extravasations of blood. 
 
 4. Waxy degenerated patches. 
 
 The liver is often enlarged and blood-stained. 
 
 Malarial Cachexia is characterised by — 
 
 1. Anaemia, often intense, with a peculiar jaundiced or 
 parchment look. 
 
 2. Pains in the joints and great lassitude. 
 
 3. Foetid breath and anorexia. 
 
 4. Haemorrhages. Pathologically, the typical "ague-cake" 
 spleen, and pigment granules are to be found in the blood. 
 
ReTnittent Ague. 33 
 
 Varieties of Ague. 
 
 Quotidian = an attack every day. 
 Tertian = one day of health intervening. 
 Quartan z=z two days of health intervening between 
 the attacks. 
 
 There are also compounds of these. When a next attack 
 comes earlier than expected, it is said to be anticipated ; and 
 conversely, if the attack be delayed, it is said to be postponed. 
 
 The Pernicious Forms. — Sometimes an ague attack assumes 
 a very virulent type, and death takes place rapidly from 
 collapse, perforation of the gut, or a rupture of the enormously 
 swollen spleen. The best recognised forms are — 
 
 1. Comatose form. 
 
 2. Cholersec or Algide. 
 
 3. Dysenteric. 
 
 REMITTENT AGUE. 
 
 (Jungle Fever.) 
 
 DifiPers from true Ague by having — 
 
 1. A badly marked cold stage. 
 
 2. A well marked hot stage. 
 
 3. A short sweating stage, and no complete intermission 
 of fever. 
 
 The Symptoms are principally — 
 
 1. Chilliness (but not actually cold). 
 
 2. Intense headache and elevation of temperature. 
 
 3. Vomiting, first of stomach contents, then bile, and finally 
 blood (black vomit). 
 
 4. Delirium often marked. 
 
34 Student 's Hand- book of Medicine. 
 
 Symptoms usually abate somewhat in the morning, only to 
 be followed by an exacerbation in the evening. 
 
 There is a great tendency to intense jaundice and the 
 typhoid state. 
 
 Duration of attack — about twelve to fifteen days. 
 
 Treatment of Malarial Fevers. — During the attack, quinine 
 with hydrobromic acid, antipyrin, jaborandi, etc. If collapse 
 threatens, stimulants will be required. In the interval — 
 
 1. Eemoval from the malarial district. 
 
 2. Arsenic and quinine. 
 
 3. Careful diet and hygiene. 
 
 4. Hepatic purges. 
 
 Treat complications as they arise. Iron may be tried or 
 Easton's syrup. 
 
 RELAPSING FEVER. 
 
 A specific contagious disease, occuring in epidemics, and 
 characterised by terminating suddenly on the sixth or seventh 
 day, but followed by a relapse after an interval of a weeJc. The 
 fever is always associated with specific organisms in the blood. 
 
 .etiology. — Epidemics have a close connection with over- 
 crowding and destitution. Like typhus, it occurs amongst the 
 poor and filthy, but is more associated with poverty and famine 
 than filth. It attacks all ages, but males more than females. 
 
 The Organism. — The spirillum or spirochffita consists of 
 a coiled thread, varying from -g^ to y^Vfr o^ ^^ i^*'^ i^ length. 
 It is in constant movement of a lashing character. The spiriUa 
 tend to adhere around the red corpuscles. They are absent 
 during the non-febrile interval, but return again when the 
 relapse occurs. Just as they disappear before the crisis, small 
 glistening masses appear in the blood. It is not known yet 
 whether these are spores or not. 
 
Belapsing Fever. 35 
 
 Symptoms. — The fever is ushered in suddenly : rigors, frontal 
 headache, backache, and rapid elevation, of temperature which 
 may reach, even on the first day, 104°. The pulse is very rapid, 
 and respirations are also quickened. The tongue has a marked 
 white fur, and there is much thirst. Ahout the fifth night 
 the symptoms become greatly aggravated and the temperature 
 may reach 107° or 108° ; the delirium is increased, and a fatal 
 termination "seems imminent, when a profuse sweating takes 
 place, the bad symptoms rapidly abate, and the crisis has taken 
 place. In a few hours the patient feels comparatively well ; he 
 is ravenously hungry, and has apparently fully recovered. Then 
 in about a week, he is seized with similar symptoms as in the 
 first attack — usually the second attack, however, runs a less 
 severe course, and sJiorter duration than the first attack, but 
 sometimes the exhaustion is so profound, that the " typhoid " 
 condition rapidly supervenes, and a fatal issue results. Two, 
 or even more, relapses have occurred. Convalesence is usually 
 slow. It is much less fatal than typhus. 
 
 Oomplications. — 
 
 Pleurisy and Pneumonia. 
 Critical Diarrhoeas. 
 Severe Jaundice. 
 Ophthalmia. 
 Haemorrhages. 
 
 Special Points to note — 
 
 1. The Spirochssta. 
 
 2. Absence of Eash. (There may be petechial spots.) 
 
 3. The speedy, apparent recovery after the first attack. 
 
 4. The slow, real convalescence after a relapse. 
 
 5. Association of the fever with famine. 
 
 6. The Jaundice is not of the so-called obstructive kind. 
 
 Morbid Anatomy. — Beyond the presence of the organisms, 
 nothing special is seen in the tissues. The spleen is, however, 
 much distended, and presents numerous infarcts. 
 
36 Sti(,dent's Ho/nrl-book of Medicine. 
 
 Treatment. — General principles. — Avoid lowering treatment. 
 Quinine has no specific effect. During conyalescence — generous 
 diet, and fresh air. 
 
 DYSENTERY. 
 
 A contagious disease, characterised clinically by a peculiar 
 diarrhoea, tenesmus, tormina, and cachexia. Pathologically, by 
 an inflammation of the lower part of the small gut and large 
 intestines, resulting in extensive ulceration and sloughing. The 
 disease is always associated with amoebic organisms. 
 
 .etiology. — Endemic and epidemic in tropical climates, 
 where the epidemics are sometimes extremely fatal. In the tem- 
 perate regions the epidemics are less severe, and sporadic cases 
 are more common. Battlefields, dried up river beds, decayed 
 vegetation, and dung heaps, form suitable soil for the poison, 
 and a fitting nidus within the body is sometimes furnished by 
 the ingestion of unripe fruit. 
 
 The contagion probably spreads through the stools, as in 
 typhoid. 
 
 The Specific Germ. — Amoeba is a unicellular organism, 
 mobile, and shows — 
 
 1. Clear outer zone := ectosarc. 
 
 2. Granular inner zone = endosarc, containing vacuoles 
 
 and nuclei. 
 
 Kartulis found them in the stools, intestines, and in the 
 liver abscesses of dysenteric patients. 
 
 Symptoms of acute dysentery vary with the type, usually 
 there is first abdominal pain, with general malaise and anorexia. 
 Soon the characteristic diarrhoea sets in. 
 
 Each discharge is scanty, and may not be more than two 
 drachms ; the number of evacuations may be great ; there is 
 great straining (tenesmus), and severe griping pain around the 
 navel (tormina). 
 
Dysentery. 37 
 
 The stools show — 
 
 1. Yellowish transparent mucus. 
 
 2. Blood. 
 
 3. Pus and epithelial dehris. 
 
 4. Actual sloughed mucous memhrane. 
 
 5. Triple phosphates and chloride of sodium in excess. 
 
 The general appearance is described as "boiled sago" or 
 toad's "spawn." 
 
 The patient loses strength, and there is moderate fever, 
 great thirst, dirty tongue, dizziness, and dry skin. In the 
 graver forms the evacuations are not so numerous, but the 
 general condition rapidly assumes a low or typhoid state, 
 and a fatal result is only too often brought about. On 
 post-mortem examination the mucous membrane is seen as a 
 black, rotten, friable charred mass. (Eokitansky.) 
 
 Varieties — 
 
 1. Acute — 
 
 (1) Catarrhal. 
 
 (2) Amcebic. 
 
 (3) Diphtheritic, divided into primary and secondary. 
 
 2. Chronic. 
 
 The Morbid Anatomy, obviously, will vary with the type 
 of disease ; but after all, the essential lesions differ only in 
 degree. As a typical example, take — 
 
 1. Catarrhal Form. Site — lower part of ileum and large 
 intestine, here we have to do with a severe inflammation 
 of a particular mucous membrane ; therefore we get — 
 
 (1) Hypersemia. 
 
 (2) Exudation rapidly becoming purulent. 
 
 (3) Necrosis of exposed follicles. 
 
 (4) Separation uf sloughs and formation of dysenteric ulcer. 
 
38 Stv(hnt's Hand-book of Medicine. 
 
 Put into other words, the inflammatory process is very- 
 severe, and only differs from inflammation of any other mucous 
 membrane, because of the distinctive characters possessed by the 
 gut involved. 
 
 2. Amoebic Variety. — Ulceration is rfiore marked. The 
 whole of the large gut may be riddled with ulcers, and 
 abscess of the liver much more frequently results. 
 
 3. DijMheritic Type. — In the Primary form the "necrosis" 
 is extremely rapid, and the " typhoid " state replaces the usual 
 symptoms. 
 
 The Secondary type is peculiar as being associated with 
 pneumonia, chronic Bright's disease, or cardiac disease ; there 
 is more of a true diphtheritic membrane formed than in the 
 other forms ; or putting it simply, the croupous inflammation 
 is associated with disease elsewhere. 
 
 Dysenteric Ulcer — 
 
 1. Irregular undermined edges. 
 
 2. Base may be formed of any of the coats. 
 
 3. If they heal they cause much contraction. 
 
 4. Usually seen best marked on ridges of large intestine. 
 
 Complications. — As the blood from the intestines is returned 
 by way of the liver, we naturally may expect trouble from 
 products so carried, and usually we get — 
 
 1. Single or tropical abscess of liver, or (much less common) 
 
 2. Multiple pyaamic abscesses. Other complications are — 
 
 (1) Haemorrhages and perforation. 
 
 (2) Peritonitis or pneumonia, etc. 
 
 Chronic Dysentery may be subacute from the beginning, 
 or a result of an acute attack through persistent suppuration 
 of the submucous abscesses. 
 
Cholera. 39 
 
 Pathology. — 
 
 1. There are healing and healed, ulcers. 
 
 2. The deep coats of the gut are much thickened and 
 contracted, and sinuses are common. 
 
 3. The calibre of the bowel is much diminished. 
 
 Symptoms. — Slightly bloody, painful diarrhoea ; the appetite 
 is absent ; tongue glazed and red ; intense ansemia ; jaundice ; 
 and patient has the shrunken look of malignant cachexia. 
 The emaciation may be extreme, hut the spleen is not 
 usually enlarged. 
 
 Treatment. — 
 
 Acute. — Hygienic ; careful dieting, or as Gull puts it, rest, 
 warmth, and ipecac. Mag. sulph. largely diluted ; minute doses 
 of perchloride of mercury. Ipecac, gr. 20, followed by opium 
 and bismuth. Try salol and opium if ipecac, fails. 
 
 Chronic. — Careful diet ; plenty of fresh air ; salol, quinine, 
 bismuth, and Dover's powder; injections of silver nitrate, 
 20 grs. to 20 oz. of water; inject four pints. Arsenic and 
 hypophosphates. 
 
 CHOLERA. 
 
 A specific infectious disease, occurring in epidemic form, and 
 characterised by violent purging, pain, cramps in the legs, and 
 intense collapse. 
 
 The mouth of the Ganges is claimed as the home of cholera, 
 but epidemics have occurred in all parts of the world. 
 
 .etiology. — Contagion is conveyed by stools and contami- 
 nated water. It breaks out principally in summer and autumn, 
 and attacks all ages and both sexes alike. 
 
40 Student' i< Haiul-hooh of Medicine. 
 
 The Germ is probably a spirochseta, known as the comma 
 bacillus of Koch. It is about half the size of the tubercle 
 bacillus and is curved, but may be spiral or shaped like an S. 
 It is found in the dejecta and intestines of patients affected. 
 
 It grows in many media, but requires either a neutral or 
 a sKghtly alkaline soil to flourish. It lives in fresh water, but 
 does not multiply ; multiplies rapidly in water containing dead 
 vegetation. 
 
 Klein says the comma bacillus is found in abundance under 
 other conditions than cholera. 
 
 Pettenkofer holds that "germs" develop in the subsoil 
 during summer, and rise into the air as a "miasm." 
 
 Pathology. — That of a severe inflammation of the mucous 
 membrane of the smaU intestines, the process being specially 
 marked around Peyer's patches and solitary glands ; usually 
 there is no ulceration. 
 
 The blood is dark and thick, sometimes almost tarry through 
 the drain of water from the system. The other organs show 
 changes similar to those occurring in other virulent fevers. 
 Note, however, that there is rapid rigor mortis, and sometimes 
 post-mortem rise of temperature. 
 
 Symptoms. — After a' short incubative period, a preliminary 
 diarrhcBa sets in, with more or less headache, vertigo, ~ and 
 nausea ; then the characteristic diarrhoea commences. Most 
 clinicians divide the disease into three stages — 
 
 1. Evacuative. 
 
 2. Algide or coUapse. 
 
 3. Reaction. 
 
 Smcvative Stage. — Violent diarrhcea accompanied with 
 intense pain, and cramps in calves of legs. The stools are 
 
Cholera. 41 
 
 "rice water" in type, neutral or alkaline from ammonia. 
 Specific gravity 1006 to 1012 ; show on standing — 
 
 1. Epithelial debris. 
 
 2. Threads of algse. , 
 
 3. Bacteria. 
 
 4. NaCl and triple phosphates. 
 
 5. Blood pigment and albumen. 
 
 Sometimes the evacuations which are extremely copious are 
 quite painless. Then vomiting takes place, first of food, but 
 finally matter similar to the stools ; then the second, or 
 
 Algide Stage commences. The collapse becomes extreme ; 
 the features are shrunken, livid, or ashy grey ; eyeballs sunk 
 in ; the skin is shrivelled and wrinkled, and covered with a 
 cold, clammy sweat. Though the surface temperature is sub- 
 normal, the temperature rises in the rectum to 102° or more. 
 The voice is husky, and the pulse small and flickering. The 
 purging usually ceases, but the vomiting continues. There 
 may be complete suppression of urine, coma, and death 
 within a few hours ; or patient passes into the third, or 
 
 Reaction Stage.- — The temperature gradually rises, and a red 
 glow replaces the ashy appearance. Erythema and urticaria 
 are frequent. The patient gradually recovers, or the improve- 
 ment is checked by the onset of — 
 
 1. Pneumonia. 
 
 2. Eecurrence of severe diarrhoea. 
 
 3. Urfemia, coma, and death. 
 
 Treatment. — Do not disturb the stomach ; remember its 
 irritable condition and poor absorptive powers. Administer ice, 
 brandy in small quantities, hypodermic injections of morphia, 
 and apply hot bottles, etc., to feet and legs. Astringents are of 
 little use. Starch and opium, or salol and enemata are useful. 
 
42 Student's Hand-book of Medicine. 
 
 The older writers advised calomel and opium; as a last resort 
 try intra-venous injection of warm saline solution. 
 
 Prophylaxis. — The utmost sanitary vigilance, isolation, and 
 quarantine ; all soiled linen, etc., should be burnt ; drinking 
 water to be first boiled, and avoidance of all irritating food. 
 
 Protection by inoculation of cultivated virus, suggested and 
 practised by Ferran, reports are too conflicting to be of value. 
 
 VARICELLA or CHICKEN-POX. 
 
 An eruptive fever, occurring principally amongst children, 
 and characterised by a vesicular rash appearing on the first 
 day. 
 
 etiology. — Epidemics are very common, and the disease 
 once it starts usually spreads with great rapidity. Sporadic 
 cases, however, are common. Nothing is known of the cir- 
 cumstances under which the fever arises. 
 
 The Rash consists of small raised vesicles, containing either 
 transparent or turbid fluid — appearing first on the neck and 
 chest, but quickly spreads over the entire body. 
 
 It differs from Small-Pox in — 
 
 1. Not being umbilicated or loculated. 
 
 2. Having no inflammatory areola around the vesicles. 
 
 3. Appearing on the first instead of the third day. 
 i. Being vesicular from the beginning. 
 
 •5. The vesicles usually drying up as brownish scabs on 
 the fourth day, leaving no scarring or pitting. 
 
 Symptoms are not severe. There is usually slight fever and 
 fretfulness, with a very furred tongue and often vomiting. 
 
Mwmps. 43 
 
 Complications — 
 
 1. Severe itching, causing the child to scratch, producing 
 
 deep scars, or even ulceration. 
 
 2. Gangrene in debilitated children around vesicles. 
 
 (I have often seen this in children with con- 
 genital syphilis.) 
 
 3. Infantile paralysis (rare). 
 
 Treatment. — A gentle saline purge, careful dieting, and 
 where there is much itching, soothing lotions on lint — 
 morphine and lead. 
 
 MUMPS. 
 
 An infectious disease, characterised by inflammation of the 
 parotid gland, with a tendency to metastatic inflammation of 
 testes in males, or breasts in females. 
 
 ^Etiology. — Is frequently contagious, especially in schools, 
 and may be curiously localised in one district. Nothing is 
 known of the virus, though it is highly probable that it is 
 due to micro-organisms. Children from four to twelve years 
 of age are most often attacked — others say the adolescent period 
 is the favourite age. 
 
 Symptoms. — After a period of incubation, pain is felt 
 under one ear, with stiffness or soreness of neck and jaw. The 
 swelling first appears in the hollow between the angle of 
 the jaw and the mastoid process, gradually extends, and may 
 involve the sub-maxillary and sub-lingual glands. In about 
 two days the other side undergoes the same changes — both 
 swellings form a " collar," giving the child a ludicrous appear- 
 ance. Deglutition and mastication are often very painful, the 
 breath is foul, and tongue very furred. In about nine days 
 the swelling resolves, and rapid improvement takes place. The 
 glands seldom suppurate. 
 
44 Student's Hand -hook of Medicine. 
 
 Complications are — 
 
 1. Orchitis (as the gland aflfection subsides). 
 
 2. Vulvo vaginitis in girls. 
 
 3. Meningitis (not common). 
 
 Seq.uelse. — After severe cases the following have happened — 
 
 1. Permanent deafness. 
 
 2. Purulent Arthritis. 
 
 Treatment. — A simple saline purge, hot fomentations, and 
 antiseptic wash for the mouth is all that is usually required. 
 Treat complications as they arise. 
 
 WHOOPING-COUGH. 
 
 A specific contagious disease, affecting the respiratory organs, 
 and attended with a peculiar paroxysmal cough and whoop. 
 
 .^Etiology. — One attack procures future immunity. It is 
 highly contagious from person to person ; one single case 
 will frequently cause the infection of a whole village or town. 
 There can be little doubt about it being due to an organism, 
 but its true nature has not yet been determined. 
 
 The Eussian physicians claim to have discovered in the 
 sputum of infected patients a short bacillus, which if culti- 
 vated and inoculated .produces bronchial catarrh, but this, like 
 the discovery of many other bacilli, requires confirmation. 
 
 Symptoms. — The disease is usually divided into three 
 stages — 
 
 1. Invasion. 
 
 2. Paroxysmal. 
 
 3. Period of decline. 
 
 1. Stage of Invasion.^The symptoms are merely those of 
 bronchial catarrh with coryza, and last about seven days or so. 
 
Whooping -Cough. 45 
 
 2. Paroxysmal or Whooping Stage. — The paroxysm consists 
 of a series of short coughs or expiratory puffs, with no inter- 
 vening inspiration till about fifteen or more expulsive efforts 
 have been made in about seven seconds. Then occurs a deep, 
 prolonged inspiration, attended with the characteristic whoop; 
 a second bout of short coughs succeeds with another whoop, 
 and after three or four such sequences, a little plug of mucus 
 is expelled, or more frequently vomiting takes place, and the 
 child is all right until the next paroxysm. 
 
 During the severe cough the patient is perfectly helpless, 
 and when paroxysms are very violent we may get — 
 
 1. Haemorrhages from the nose, frsenum of the tongue, 
 
 sub-conjunctiv£e, or even in the brain. 
 
 2. Collapse of the lung. 
 
 3. Convulsions in infants. 
 
 4. Fatal asphyxia (rare). 
 
 The appearance of the child soon becomes puffy or bloated. 
 The whoop is due to partial closure of the glottis. The closure 
 is considered by some to be " reflex spasm " in nature. Others 
 say it is a mere passive approximation of the glottis. There 
 may be as many as forty attacks in the twenty-four hours, but 
 they range from four upwards ; this stage lasts three to six 
 weeks. Sometimes the " whoop " is delayed in its appearance ; 
 difficulty will be then experienced in diagnosis, and no general 
 law can be laid down. Niemeyer says, "If a child has a 
 violent prolonged cough attended with vomiting, suspect and 
 treat as if it were whooping-cough." I am certain this is 
 sound advice, borne out by experience of two epidemics I 
 saw in Monmouthshire. Taylor says, "vomiting is not fre- 
 quent." In the epidemics I witnessed, the bulk of the 
 cases were attended with vomiting after each paroxysm. 
 Osier states similarly. 
 
 3. Period of Decline. — This stage is marked by a gradual 
 decrease in the number of paroxysms and a slow convalescence, 
 usually lasting three months or longer. 
 
•16 Student's Hand-book of Medicine. 
 
 Complications. — Besides those mentioned which might 
 occur during paroxysm there might be — 
 
 1. Extensive capillary bronchitis, or 
 
 2. Broncho-pneumonia. 
 
 3. Cardiac strain ending in valvular disease. 
 
 Treatment. — Prompt isolation, a simple saline with pare- 
 goric. When the whoop develops we must try anti-spasmodics ; 
 bromides, belladonna, chloral, and hydrocyanic acid ; others 
 advise in addition — quinine, emetics, swabbing the throat with 
 a 2 per cent, solution of resorcin, etc. 
 
 If recovery be tedious, change of air, cod liver oil, and 
 Easton's syrup. 
 
 Special points to be noticed — 
 
 1. In infants, tendency to convulsions. 
 
 2. Older children, capillary bronchitis, causing — 
 
 (1) Collapse of Lung. 
 
 (2) Deformity of chest (pigeon shape). 
 
 YELLOW FEVER. 
 
 A contagious fever occurring in certain tropical districts, and 
 characterised by two well-defined stages. It is at first endemic, 
 then becomes contagious, and intensely malignant in its ravages. 
 
 .etiology. — It originates in crowded cities, on the shores of 
 large rivers, in ships, etc. Strangers landing in an infected dis- 
 trict are nearlj' always attacked. The nature of the poison is 
 supposed to be a miasm from decaying vegetable matter ; but from 
 its close resemblance to remittent ague it is more likely to be 
 due to a special organism, developed in such districts. 
 
Yellow Fever. 47 
 
 Sjnuptoms — 
 
 The First Stage. — After a "primary" depression or sense of 
 coldness, rigors occur, accompanied with elevation of temperature, 
 which ranges even on the first day from 101° to 110°- The pulse 
 is quick, full, and bounding, hut a fact of great value is — the 
 pulse tends to decrease when the temperature is high, and may 
 even heeome helow the normal standard. Intense headache and 
 vomiting of blood-stained mucus. The tongue is at first red at 
 the tip, and pointed, but thickly furred behind. 
 
 The Second Stage is marked by the advent of the typhoid 
 state (see page 3), but with the following prominent symptoms 
 in addition — 
 
 1. Black vomiting — i.e., bile and blood. 
 
 2. Intense jaundice. 
 
 3. Excessive albuminuria, 
 
 4. Suppression of urine, urasmia, and only too often 
 
 speedy death. 
 
 Pathology. — The blood shows marked changes. — 
 
 1. Marked diminution of fibrin. 
 
 2. Eed corpuscles, crenated, and diminished in number. 
 
 3. Increase of fatty matter, and antecedents of urea in 
 
 the blood. 
 
 After death the blood rapidly becomes acid. 
 
 The liver is extensively affected, deep golden yellow in 
 colour. It is at first firmer than ordinary fatty degenerated 
 tissue, but gradually approaches a condition similar to acute 
 yellow atrophy. There is no formed bile, but plenty of bile 
 pigment, also glycogen, but no grape sugar. Leucin and 
 tyrosin are sometimes present. 
 
 The other organs show the same changes as other acute, 
 malignant diseases. 
 
48 Student's Hand-book of Medicine. 
 
 Treatment — 
 
 1., Absolute rest in recumbent posture. 
 
 2. Free Ventilation, and light diet. 
 
 3. Antipyrin, quinine, ice, blood-letting, calomel. 
 
 Eemember opium, iron, and mineral acids are badly borne, 
 and are sometimes actually injurious. Later, champagne is the 
 best stimulant. 
 
 THE SEPTIC STATES. 
 
 Under this heading we mean the clinical phenomena attend- 
 ing the introduction of noxious material into the blood. There 
 are three types — 
 
 1. Saprcemia — i.e., the introduction of bacterial products 
 or substances which cannot multiply in the living tissues ; the 
 symptoms following being in proportion to the size of dose 
 introduced. 
 
 2. Septicmmia — The introduction of living organisms which 
 have the power of living and multiplying in the blood. The 
 symptoms following bear no relation to the amount of bacteria 
 introduced. 
 
 3. Pyaemia is now usually looked upon as a sub-acute septi- 
 caemia, attended with metastatic abscesses. Formerly it was held 
 to mean the symptoms consequent on the introduction of pus, 
 and pus only ; but obviously, as pus is held to contain micro- 
 cocci, and micro -cocci can set up thrombosis and metastatic 
 abscesses, it seems idle to quibble over terms. 
 
 Much confusion has arisen through the term " Septic Intoxi- 
 cation," being used at one time to express " Saprsemia," and at 
 another time " Septicaemia," but either ignore such an ambiguous 
 term or relegate it to its proper position, viz,, a convenient term 
 to express the peculiar symptoms attending the septic state. 
 
The Septic States. 49 
 
 Symptoms of Acute Sepsis — Rigors, rapid rise of the 
 temperature, flushed face, delirium, and rapid exhaustion ; the 
 typhoid condition may supervene. 
 
 Of the Sub-acute forms — frequent rigors ; oscillating tem- 
 perature; night sweats — i.e., hectic fever; rapid loss of flesh; 
 and general exhaustion are the cardinal symptoms. 
 
 Pyemia is characterised by running a much more chronic 
 course. Frequently periods of comparative convalescence seem 
 established, but are interrupted by exacerbations of hectic fever 
 and the formation of metastatic abscesses — often complicated 
 with pneumonia, purulent pleurisy, etc. 
 
 Mode of Abscess formation — 
 
 1. The bacteria cluster together and form by themselves 
 
 an embolus, which becomes arrested in the smaller 
 blood-vessels, causing local thrombosis, with intense 
 irritation, and formation of pus in a circumscribed 
 area — i.e., local abscess. 
 
 2. The bacteria may cause suppurative phlebitis. 
 
 3. The intense irritation leads to ordinary thrombosis, 
 
 but the bacteria enter the clot, causing central 
 necrosis and breaking down of the whole into a 
 greenish purulent mass. 
 
 Treatment. — Sapraemia is generally due to absorption of 
 products of putrefaction, such as decomposed placental remains, 
 blood clots, etc. ; or absorption of the microscopic layer of dead 
 tissues killed in' operations, even under antiseptic precautions. 
 Obviously the treatment will be to stop the local manufacture 
 of the poison by careful cleansing and rest; remember also 
 a septic condition may begin as a saprtemia, and end as a 
 true septicaemia, through the local condition of the first state 
 acting as a favourable nidus for the production of the second 
 condition. 
 
 E 
 
50 Stvdent'x Hand-hooJc of Medicine. 
 
 Septiecemia, due to the introduction of living organisms, 
 therefore, all we can do is to — 
 
 1. Stop the entrance of more organisms by using the 
 
 utmost antiseptic precautions. 
 
 2. Support our patient, till the fight between bacteria 
 
 and tissues is ended, by stimulants and quinine. 
 
 Antiseptics internally are advised by some, but it is very 
 doubtful if we can kill those organisms already in the blood ; 
 probably, some substance will be discovered which will render 
 the infected blood an unsuitable soil. 
 
 Pycemia, as regards treatment, requires the same as advised 
 under SepticEemia, but special care must be taken in opening 
 abscesses not to convert a sub-acute process into an acute one, 
 by causing putrefaction of the pus. 
 
 SYPHILIS. 
 
 By syphilis is now understood a constitutional affection, 
 resulting from (1) impure venereal intercourse ; (2) inoculation 
 with the virus obtained from syphilitic lesions ; (3) or trans- 
 mission through diseased parent or parents — i.e., congenital 
 syphilis. Syphilis is such an extensive subject, and so highly 
 important a factor in many diseases, that the reader is referred 
 to a monograph on the subject. 
 
 Briefly put, the following are the more important facts of 
 acquired syphilis — four periods are described — (1) Incubation j 
 (2) Primary Sore ; (3) Secondary Symptoms ; and (4) Tertiary 
 Stage. 
 
 1. Incubation Period = 6 weeks. 
 
 2. Primary Sore, or chancre, is a papule with an indurated 
 base. The surface may or may not ulcerate, but is usually 
 
Syphilis. 51 
 
 depressed in the centre. The hardness or induration extends 
 to the nearest lymphatic glands, and ultimately all the lym- 
 phatic glands may become involved. The chancre or "hard 
 sore'' finally disappears, leaving a cicatrix behind. 
 
 3. Secondary Symptoms — divided into two stages. 
 
 FIRST STAGE — 
 
 (1) Syphilitic fever, with transient hyperajmia of the 
 
 skin, roseola, etc. 
 
 (2) Sore throat. 
 
 SECOND STAGE — 
 
 The second stage is marked by skin eruption, clinically 
 distinguished by — 
 
 (1) Their symmetry. 
 
 (2) Copper colour, dull red at first, afterwards a 
 
 reddish brown. 
 
 (3) A tendency to circular form of patches. 
 
 (4) The scales when present are light and small. 
 
 (5) The crusts are greenish and thick, adhering firmly. 
 
 (6) Ulceration is common — sharp edges and ashy-grey 
 
 surfaces. 
 
 (7) The eruptions are often mixed, or poly-morphous. 
 
 (Tilbury Fox.) 
 
 The other changes are — 
 
 Mucous tubercles or condylomata on rectum, mouth, etc. 
 
 Ulceration of throat. 
 
 Syphilitic Iritis. 
 
 Syphilitic Periostitis. 
 
 Anaemia. 
 
 Loss of hair — not followed usually by permanent baldness. 
 
52 Student's Hand-book of Medicine. 
 
 4. Third or Tertiary Stage. — The anaemia has become more 
 marked, and the manifestations of the disease are those of seri- 
 ous mahiutrition, with deep-seated organic changes due to the 
 formation of peculiar growths termed " gummata.'' According 
 to some, any chronic disease may he caused directly or indirectly 
 by syphilis. Whilst no doubt syphilis is often a most powerful 
 or even the chief factor in many diseases, and its importance 
 cannot be over-estimated, still, probably, syphilis is often un- 
 justly held responsible for many serious lesions. 
 
 Structure of Gummata. — They are at first hard, firm, nodular 
 masses, fairly defined but adherent to surrounding tissue. Later, 
 they become somewhat softer, and show from within outwards — 
 
 1. A central mass of fatty degenerated cells, sometimes granu- 
 lar, but may be homogeneous and of gum-like consistence. 
 
 2. A fibrillated structure, with leucocytes in the meshwork. 
 
 3. A more fibrous layer, with young epithelial cells. 
 
 They are met with in the brain (Jacksonian epilepsy), bones, 
 testicle, and liver (syphilitic cirrhosis), etc., etc. The change 
 begins around the small arteries. 
 
 Syphilitic virus is peculiar in — 
 
 1. Producing changes in the lumen of vessels apart from 
 
 any external irritation, causing them to become 
 narrowed — i.e., arteries, larynx, intestine, etc. 
 
 2. In causing waxy disease without intervention of 
 
 suppuration. 
 
 Tertiary syphilis is neither inocuable or transmissible to 
 ofispring. 
 
 Congenital syphilis may take place — (1) from father; (2) 
 from mother ; (3) from both. If the father alone be syphilitic 
 then the sequence may be — • 
 
 1. Father. 
 ' 2. Child. 
 3. Mother through child. 
 
Syphilis. 53 
 
 Symptoms— 
 
 1. The child is bom with " snuffles." 
 
 2. Develops a peculiar " old man " appearance. 
 
 3. Mucous tubercles at the mouth or anus. 
 
 4. Eed patches on buttocks, ankles, or hands. 
 
 5. Sub-acute onychia, fissures at lips, and later, notched 
 
 "Hutchinson" teeth. 
 
 Specific Germ undoubtedly due to a special organism not 
 yet cultivated successfully. 
 
 Treatment. — We have a choice of two great schools — 
 
 1. The mercurialists. 
 
 2. The anti-mercurialists. 
 
 The former say mercury cures, while the latter say mercury 
 is not indicated, and even produces the worst features seen in 
 syphilitic cases. Probably the truth lies between them. Let 
 us review our data, and let each reader form his own opinion. 
 
 1. Syphilis is undoubtedly infectious, and, therefore, seems 
 due to — 
 
 (1) A living organism capable of multiplying within the 
 
 body ; therefore 
 
 (2) The severity of the disease must vary with the soU ; 
 
 and 
 
 (3) From analogy with other bacterial diseases, syphilis 
 
 must tend to cure itself. 
 
 2. It is extremely doubtful if we can kill the organism 
 directly, but we can make the soU more resistant by careful 
 hygiene, diet, fresh air, and tonics. 
 
 So much for the disease, now for the case of mercury. 
 
 The most sceptical must admit that in the skin eruptions 
 and congenital syphilis a marked improvement takes place 
 rapidly under the influence of any mercurial. Mercury then, 
 strongly influences demonstrable syphilitic affections. Take 
 the action of mercury in other diseases. We find it used in 
 
54 Student's Hand-book of Medicine. 
 
 general routine practice, in hepatic diseases, and it is a favourite 
 drug in the treatment of the most simple ailments of children. 
 It is also used to remove inflammatory products of inilamed 
 serous membranes. In all these cases it is used in small doses 
 with the best results. Then why deny the use of it in syphilis 1 
 However, men working amongst quicksilver become emaciated, 
 their teeth are loosened, deep ulcerations form, peripheral 
 neuritis or mercurial tremors supervene, and the man becomes 
 a decayed wreck. 
 
 Here then are the untoward effects of large doses of mercury. 
 Evidently the treatment of syphilis should consist of — 
 
 1. Small doses of mercury, alternating with 
 
 2. Tonics, fresh air, and careful diet, — these should be 
 
 kept up for two years or more. 
 
 A good plan of treatment is the following : — Small doses, 
 say two grains of pil. hydrarg. nightly for three months, then 
 Easton's syrup for three months; and this alternation of mer- 
 cury and tonic repeated for twelve months. Then an occasional 
 course of — 
 
 Vf Pot. lodid. . . . 5i. 
 Liq. Hydrarg. Perch. . gi. 
 Dec. Cinohon Co. ad. . Sviij. 
 Fiat mist. , gss ter in die. 
 
 No one is justified in pusMng mercury into a debilitated 
 constitution 
 
 TUBERCULOSIS. 
 
 A constitutional disease, produced by the pernicious action 
 of the bacillus tuberculosa. There may be special foci, and 
 when the disease is principally localised it receives definite 
 names according to the part affected, viz. — 
 
 Lungs = Consumption — pulmonary fihthisis. 
 Bones = Earefying Caries. 
 Joints = White Swelling. 
 
Tuberculosis. 55 
 
 The Bacillus is small (^ size of a red corpuscle), motion 
 less, and contains sijores. The spores are more resistant to 
 change than the mature bacillus, and requires temperature of 
 body (98'4°) to multiply; sterilized serum jelly is the best 
 medium for cultivation. 
 
 How to Stain — 
 
 1. Spread a portion of purulent sputum on a cover glass. 
 
 2. Press upon this another cover glass to get a clear film. 
 
 3. Heat gently tiU albumen is coagulated. 
 
 4. Place specimen (sputum downwards) in Neilson's fuchsin, 
 and heat; then 
 
 5. Wash in water. Next transfer it to 
 
 6. A solution of — 
 
 Methylblue . two grs. 
 
 Acid Sulph. . 20 cc. 
 
 Aqiia dest. . . 80 oo. 
 
 leave it for two minutes, then 
 
 7. Wash in water, and mount in balsam. 
 
 The " tubercles " formed by the bacilli are of two types — 
 
 1. The grey. 
 
 2. The yeUow. 
 
 The latter is but an advanced stage of the former. 
 
 The grey tubercles are small transparent, grey gelatinous 
 lumps, isolated or clustered in masses. 
 
 Microscopically, they show from within outwards — 
 
 1. The bacilli. 
 
 2. Giant ceUs, with branched processes forming a 
 
 scaffolding for the next layer. 
 
 3. A layer of small epithelioid cells. 
 i. A zone of leucocytes. 
 
 5. Often a dense fibrous capsule. 
 
56 Student's Hand-book of Medicine. 
 
 Later. — The central zone undergoes fatty degeneration and 
 bacillary liquefaction, or fatty degeneration witli caseation and 
 calcification, the nodule being converted into a fibrous calcified 
 
 The changes which tubercular nodules undergo are essentially 
 the same wherever the lesion is, though of course certain tissues 
 will modify the rapidity of such changes. Take the lung for 
 instance. 
 
 Always describe pathologically — 
 
 1. Preparation of the soil and invasion of the bacilli. 
 
 2. Inflammatory zone around bacilli, and formation of 
 
 tubercle. 
 
 3. Fibrous zone around tubercle. 
 
 4. Fatty degeneration of tubercle and formation of — 
 
 (1) Pus. 
 
 (2) Cavities. 
 
 5. BacUlary liquefaction ; or pus may dry up and calcify. 
 
 Tuberculosis spreads through lymphatics and blood-vessels, 
 from local foci. 
 
 Mode of Infection. 
 
 1. From phthisical patients' breath and sputum. 
 
 2. From tuberculous cattle, dogs, cats, etc. 
 
 Is tuberculosis hereditary ? This is stUl a vexed question. 
 It is usually taught, however, that it is not transmissible from 
 parent, but that the children of tubercular parents are born with 
 a highly favourable soil or predisposition. 
 
 Symptoms of tubercular disease vary according to — 
 
 1. Site. 
 
 2. Stage. 
 
Nervous Diseases. 57 
 
 After the breaking down process has commenced, however, 
 the symptoms are those of hectic fever. 
 
 1. Elevation of temperature, especially in the evening. 
 
 2. Night sweats. 
 
 3. Progressive emaciation. 
 
 4. Phthisical appearance is well known. 
 
 Treatment wUl be considered under the head of " Phthisis." 
 
 NERVOUS DISEASES. 
 
 The reader is strongly advised to digest the following brief 
 account of the anatomy and physiology of the nervous system, 
 before commencing the study of the various nervous diseases. 
 I shall not attempt anything approaching an anatomical de- 
 scription, but content myself with the the briefest description 
 of those facts whioh form the foundation of a clear under- 
 standing of clinical phenomena attendant upon pathological 
 changes. 
 
 The Spinal Cord consists of a tubular prolongation of the 
 brain enclosed in three membranes. — - 
 
 1. Dura mater, externally. 
 
 2. Arachnoid, in the middle. 
 
 3. Pia mater. 
 
 Between the arachnoid and pia mater is the sub-arachnoidal 
 space, filled with cerebro-spinal fluid. It should be noted that 
 this space is continuous with the ventricles of the brain. The 
 cord substance shows white matter externally, and grey matter 
 internally. Like all nervous tissue the white and the grey matter 
 have as a groundwork neuroglia, or nerve glue. 
 
58 Student's Hand-book of Medicine. 
 
 Neuroglia shows under the microscope — 
 
 1. Large and small cells. 
 
 2. Granules. 
 
 3. Fibres. 
 
 4. Interstitial cement substance. 
 
 Note that "sclerosis" means a great increase in neuroglia at 
 the expense of the special nerve elements. 
 
 The grey matter differs from the white in — 
 
 1. Colour, and being more vascular. 
 
 2. Having special groups of nerve cells arranged — 
 
 Anteriorly "j f Anterior vesicular column. 
 
 Laterally I termed-^ Lateral vesicular column. 
 Posteriorly J [ Posterior or aolmnn of Clarke. 
 
 The anterior cells are multipolar and give origin to motor 
 nerve roots ; they also act as trophic centres for motor fibres 
 in the nerve trunk. 
 
 The posterior cells (or column of Clarke) are very important 
 through being impHcated in the passage of sensory fibres, as 
 will be seen further on. 
 
 The white matter though apparently homogeneous, is really 
 mapped out into columns. Each column is specially concerned 
 in transference of certain impulses up to, or from, the brain. 
 Much that has been written about these columns has turned out 
 untrue, and indeed, even now (1893) very little is known of 
 the exact functions of any one column; but patient investigation 
 has shown that there are at least two motor or descending paths, 
 and four sensory or ascending paths. 
 
The Tracts. 59 
 
 THE TRACTS. 
 
 (See Diagram, p. 81.) 
 
 Motor Tracts — 
 
 1. Direct Pyramidal situated anteriorly. 
 
 2. Crossed Pyramidal situated laterally. 
 
 Sensory — 
 
 1. Comma Tract of Gowers. ■> -r 
 
 2. Direct Cerebellar. I * ^^^ ^' 
 
 3. Postero-Extemal, or column of Burdach. "> ^ . , 
 
 r Posteriori V. 
 
 4. Postero-Internal, or column of Goll. i 
 
 Cbrebeo-Spinal Nerves. 
 An ordinary mixed nerve is made up of — 
 
 1. Anterior or motor root fibres. 
 
 2. Posterior or sensory root fibres. 
 
 3. Sympathetic fibres 
 
 The branches of such a nerve may contain only (1) motor 
 fibres, or (2) sensory, or (3) principally sympathetic. 
 
 CouESB OF Motor Fibres. (See Diagram, page 81.) 
 
 As motor fibres proceed from the brain, we shall describe 
 them from above dmenwards. 
 
 Starting from the cortex, principally around the fissure of 
 Rolando, they proceed through — 
 
 1. Corona radiata. 
 
 2. Anterior two-thirds of posterior limb of internal capsule. 
 
 3. Crusta of Cms. 
 
 4. Pons Varolii. 
 
60 Student's Hand-book of Medicine. 
 
 5. Medulla, where the bulk of the fibres cross (decussation 
 of pyramids) to the opposite side, and pass down the cord as 
 the crossed pyramidal tract, thence to the multipolar cells of 
 the anterior horn of grey matter, and finally out by the anterior 
 motor roots. A few fibres pass down from the medulla without 
 decussation, and so form the direct pyramidal tract. 
 
 Note here the trophic centre for the motor tracts is situated 
 in the cortex, happily termed the first trophic realm by Wyllie. 
 The trophic, centres for the motor nerves are, as before stated, 
 the multipolar cells in the anterior horn of grey matter, named 
 by Wyllie the second trophic realm, or putting it briefly, a lesion 
 of the motor cortex, is followed by degeneration of motor tracts. 
 A lesion of the anterior grey horn is followed by degeneration 
 of motor nerves, plus other changes. 
 
 Sbnsobt Fibres. (See Diagram, page 81.) 
 Formerly they were supposed to enter the cord and immedi- 
 ately decussate over to opposite side. Eecent researches show 
 that little is reaUy known about sensory nerve fibres, and stUl 
 less about sensory tracts. The following will form a good 
 worhing basis, and is at least as correct as the unproved state- 
 ments of large text-books. 
 
 Sensory fibres enter the grey matter in two bundles — i.e.. 
 Bundle A and Bundle B. 
 
 Bundle A passes first into column of Burdach, descends and 
 ascends a little, then enters the column of Goll, passes straight 
 up to the medulla, and there decussates to the opposite side. 
 
 Bundle B passes into the grey matter. A few fibres go 
 to the anterior horn to form, with the motor cells, a complete 
 reflex loop. The bulk of the fibres, however, cross to the ' 
 column of Clarke, and thence to direct cerebellar and comma 
 tract of Gowers. 
 
 Thus in the cord we have four distinct sensory railroads — 
 viz., Burdach, Goll, Gowers, and direct cerebellar as high as the 
 
The Internal Capsule. 61 
 
 medulla oblongata. It is not known definitely how they ascend 
 from the medulla. For clinical purposes, however, we may say 
 that sensory fibres are scattered throughout the brain substance, 
 though possibly the larger number proceed as follows — 
 
 1. Direct cerebellar goes direct to cerebellum. 
 
 2. Gowers to the formatio reticularis. 
 
 3 & 4. Goll and Burdach — end as olavi in the medulla. 
 
 From each clavus fibres pass to the formatio reticularis. 
 Thus Goll, Burdach, and Gower are amalgamated at a common 
 junction. From this junction they pass upwards (behind the 
 motor fibres) as sensory fibres, strengthened by co-ordinating 
 fibres from the cerebellum, their course being through — 
 
 1. Medulla. 
 
 2. Pons. 
 
 3. Tegmentum of crus. 
 
 4. Posterior third, posterior limb of internal capsule. 
 
 5. Corona radiata. 
 
 6. Cortex, especially occipital lobe. 
 
 (A glance at the diagram will make this intelligible.) Some 
 of the fibres stop, en route, at the corpora quadrigemina and 
 optic thalamus. 
 
 WHAT IS THE INTERNAL CAPSULE? 
 
 It is the band of white matter between the basal ganglia, its 
 boundaries being — 
 
 Externally = Lenticular nucleus. 
 T + 11 — /Caudate nucleus (anteriorly). 
 I Optic thalamus (posteriorly). 
 
 In the middle of the internal capsule is a " bend " termed 
 the " genu " or knee ; the portion in front of the knee is 
 
62 Student's Hand-book of Medicine. 
 
 called the anterior limb ; the portion behind, the posterior limb. 
 The former contains various commissural fibres of various kinds, 
 whilst the "posterior " limb contains, as we have already seen, 
 the sensory and motor fibres from the spinal cord. 
 
 A lesion of the internal capsule involving the motor fibres 
 must give motor paralysis of side of face and limbs of the 
 opposite side of the body. 
 
 Sensation is not usually much affected as it will be readily 
 seen that a lesion, extensive enough to cause both sensory and 
 motor paralysis, would probably be fatal. 
 
 THE EXTERNAL CAPSULE. 
 
 The external capsule, as its name implies, is outside the 
 internal capsule, and is that portion of the cerebrum lying 
 between the — 
 
 Claustrum, externally ; 
 
 Lenticular nucleus, internally. 
 
 It is in close proximity to the Island of EeU. 
 
 REFLEXES. 
 
 The student is frequently puzzled as to when reflexes should 
 be lost, exaggerated, or impaired, but if he bears the following 
 facts in mind there should be no difl&culty. 
 
 A reflex act requires a continuity between an afferent nerve, 
 and an efferent nerve. The parts usually involved are — 
 
 1. A receiving surface (as skin). 
 
 2. A sensory nerve (afferent fibre). 
 
 3. A receiving station (cells in cord). 
 
 4. A motor nerve (efferent fibre). 
 
Degenerations. 63 
 
 These together constitute a reflex loop. A break in any 
 part of this loop must be attended with loss of reflex. What 
 is the effect of the brain on reflexes? The hram exercises an 
 inhibitive action; therefore, if the cord be out off from its 
 inhibitive influence, reflexes must be exaggerated. 
 
 Imagine the cord to be built up of segments, each segment 
 giving off a pair of spinal nerves ; then take a transverse lesion 
 of the cord, what state of reflexes would we get 1 
 
 1. At point of lesion — reflexes are lost (as the reflex loop is 
 destroyed). 
 
 2. Below lesion — reflexes are exaggerated (as inbibitive action 
 of brain is cut off). 
 
 3. Above the lesion — reflexes are normal. 
 
 Note, however, at the upper border of the lesion, the dead 
 part would act as an irritant to the healthy portion of the Cord, 
 and consequently cause irritation of any sensory nerves coming 
 off that area, causing a band of hyperaesthesia. 
 
 This painful zone, taken in conjunction until the condition 
 of reflexes, often enables an accurate localisation of the lesion 
 to he made. 
 
 The hypersBsthetic zone also explains the girdle pain present 
 in many lesions of the cord. 
 
 DEGENERATIONS. 
 
 When nerve fibres are cut off from their trophic centres, 
 they undergo disintegration, known as secondary degeneration 
 — viz., in the case of sensory fibres = ascending degeneration, 
 and in the case of motor fibres — descending degeneration. 
 
 R. D., or reaction of degeneration, is the common name in 
 clinical medicine for such degenerations. Tested by electricity, 
 the changes briefly are (on applying the electrodes to the 
 muscle) — 
 
64 Student's Hand-book of Medicine. 
 
 1. Increased excitability to galvanic and faradic currents ; 
 this quickly passes off, and we get 
 
 2. Decreased to faradic, but increased to galvanic; next, 
 
 3. Decreased to both galvanic and faradic. 
 
 4. Lost to both. 
 
 These peculiar changes are accompanied by "polar" 
 alterations. 
 
 In health we get in response to a minimum current — 
 
 1. K.C.C. = kathodal closing contraction is strongest; 
 
 next, 
 
 2. A.O.C. := anodal opening contraction | 
 
 3. A.C.C. := anodal closure contraction / 
 
 4. K.O.C. =^ kathodal opening contraction, the weakest. 
 
 But in disease — 
 
 A. 0. G or anodal opening contraction may be stronger than 
 the K.C.C. (kathodal closing contraction) — i.e., a reversed 
 condition to that seen in health. The main point, however, 
 to remember is, "that a muscle cut off from its nerve, or 
 supplied by a diseased nerve, undergoes — 
 
 1. Increased excitability. 
 
 2. Decreased excitability, and finally fails to respond 
 
 to any electrical stimulus.'' 
 
 Pathology of R. D. — The nerve structure shows — 
 
 1. Breaking up of white substance of Schwann. 
 
 2. Nuclei, swollen and granular. 
 
 3. Axes cylinders broken, and nerve substance 
 
 transformed into fibrous cords. 
 
 Tlie Muscles structure shows — 
 
 1. Muscular fibres atrophied. 
 
 2. Disappearance of transverse strias. 
 
 3. Granides. 
 
 4. Great increase of fibrous tissue. 
 
Nervous Diseases. 65 
 
 HOW TO LEARN NERVOUS DISEASES. 
 
 Having mastered the foregoing brief but fundamental 
 points, next consult diagrams (page 81), or better still, draw 
 them for yourself; then mark with a blue pencil the sites 
 of various lesions — you ■will then note what tracts, cells, or 
 fibres are interrupted ; and lastly, reason what must happen 
 in any given lesion. For instance, in diagram (page 81), I 
 have shown what happens in three typical lesions, affect- 
 ing the anterior horn, lateral columns, and posterior horn 
 and columns respectively. The advantages of such a method 
 are obvious, for having mastered three typical sites, all the 
 others mil he only mixtures or overflows of one or more of 
 these lesions, the symptoms of course varying according to 
 the portions of cord attacked. We have already learnt how 
 reilexes are altered, how atrophy begins, and why paralysis 
 occurs ; just one or two more points, then I think the reader 
 will find no difiiculty in mastering the essential features of 
 the more common nerve diseases. 
 
 SPASM AND RIGIDITY. 
 
 When a motor nerve is irritated, the muscles supplied 
 by that nerve contract. If the irritation be kept up, the 
 contractions are more or less constant, and cause " spasm." 
 Consequently, when the motor tracts are injured, let us say 
 by a severe hsemorrhage in the brain, there is not only 
 paralysis, but also " rigidity " of the limbs quickly supervening, 
 dm to irritation of the motor fibres; this is termed "early 
 rigidity," and soon passes off. 
 
 Suppose the patient recovers from the fit of apoplexy, with, 
 however, a resulting hemiplegia, it will be noted that later a 
 second rigidity takes place. This is also due to irritation, but 
 of a destroying nature — i.e., secondary degeneration. 
 
66 Student's Hand-book of Medicine. 
 
 "Spastic paralysis" is an excellent example of irritative 
 rigidity. 
 
 Irritation, then, gives rise to increased nerve action ; and 
 eompresmon, on the other hand, causes paralysis. 
 
 CONVULSIONS. 
 
 Convulsions are of two kinds — 
 
 Tonic, when the muscular contritions are continuous. 
 Clonic, when relaxations alternate with contractions. 
 
 Convulsions may be the result of either direct irritation, or 
 loss of inhibitive power, plus a hyper-excited condition of nerve 
 cells (epilepsy). 
 
 CO-ORDINATION AND INCO-ORDINATION. 
 
 By co-ordination is meant the harmonious action of muscles 
 involved in the carrying out of complicated movements. 
 
 Inco-ordination means failure of this harmony. 
 
 The cerebellum is said to be the chief centre for co-ordinated 
 movements. Whether this be true or not, the cerebellum is 
 an important centre, though there are subsidiary centres. The 
 centres seem to act through afferent impressions derived from — 
 
 1. The sense of touch (columns of Goll and Burdach). 
 
 2. Sight (optic nerves). 
 
 3. Auditory organs (semi-circular canals). 
 
 Lesions interfering with these afferent fibres are attended 
 with more or less inco-ordination. Inco-ordination may, 
 therefore, be due to — 
 
 1. Disease of the centres rendering them powerless to emit 
 
 the necessary influence. 
 
 2. Disease cutting off the means (afferent fibres) by which 
 
 the centres are stimulated. 
 
Nervous Diseases. 67 
 
 DEEP (SO-CALLED) REFLEXES. 
 
 Knee Jerk. — Present in health, and obtained by tapping 
 the patella tendon. 
 
 It is not a true reflex, but depends on tone of the extensor 
 muscles. As the muscles waste, however, if the nerves be 
 diseased, so will the knee jerk disappear, as the reflex loop is 
 then broken. But it is possible for the knee jerk to be lost 
 without any break of the reflex loop, or exaggerated when the 
 nerves are healthy if the muscles are fatigued. 
 
 Ankle Clonus.— Not present in health — means increased 
 excitability of muscles, prior to the advanced pathological 
 degeneration. 
 
 SCLEROSIS. 
 
 Sclerosis is a convenient term used to express the patho- 
 logical changes which take place in chronic nervous diseases. 
 We shall draw a picture of a typical " sclerosis," so as to avoid 
 a constant repetition of words. Then in describing eacli par- 
 ticular disease, merely point out the sites of such lesions. 
 
 Sclerosis. — Grey Matter shows — 
 
 1. Increased fibrous tissue (neuroglia). 
 
 2. Atrophy of proper nerve cells. 
 
 3. Blood-vessels thickened, some obliterated. 
 
 4. Extravasations of pigment. 
 
 5. Small patches of fatty degeneration. 
 
 White Matter shows — 
 
 1. Discolouration. 
 
 2, Absence of Myelin, 
 
! Student's Hand-booh of Medicine. 
 
 3. Great increase of fibrous tissue. 
 
 4. Granular debris. 
 
 Stains deeply with carmine. 
 Cbromic acid fails to stain. 
 
 Roots, when aifected, exhibit similar changes. 
 
 DISEASE OF THE SPINAL MEMBRANES. 
 
 Spinal meningitis or inflammation of the meninges may be 
 either acute or chronic. When the dura mater is principally 
 affected it is termed pachy -meningitis ; when the pia mater 
 is most involved — lepto- meningitis. This distinction is con- 
 venient when we have to deal with a slow process, as in 
 chronic meningitis. It should, however, be remembered in 
 acute inflammation, though one or other membrane may be 
 primarily affected, the disease quickly spreads, and involves the 
 whole three membranes equally. 
 
 ACUTE SPINAL MENINGITIS. 
 
 The process might begin in the cellular tissue outside the 
 dura mater — i.e., external meningitis; or within the sheath, 
 internal meningitis. The slight differences in the clinical 
 symptoms will be easily understood if we consider the respective 
 causes, and recall one or two physiological facts — 
 
 1. Irritation of nerve roots lead to severe radiating pains 
 and increased reflexes. 
 
 2. Oomp-ession of the cord substance causes paralysis, and 
 loss of reflexes in the area of the compression ; so, consequently, 
 we are prepared for a greater degree of local excitability when 
 the inflammation is external, and a more extensive area of the 
 lesion in the internal meningitis ; the cord substance will also 
 be involved more quickly. 
 
Acute Spinal Meningitis. 
 
 69 
 
 ExTEKNAL Meningitis. 
 Causes. — • 
 
 Extension of contiguous disease, 
 such as — 
 
 1. Caries of spine. 
 
 2. Fracture of spine. 
 
 3. Tumours. 
 
 Pathology. — 
 
 1. The dura mater is red and 
 injected, with loss of lustre. 
 
 2. Exudation of lymph. 
 
 3. Accumulation of pus be- 
 tween spine and membrane. The 
 pus frequently dries and forms a 
 caseous mass. 
 
 itoms vary greatly. — 
 
 1. Severe cutaneous pains, 
 followed by anesthesia. 
 
 2. Localised pain in the back, 
 worse on movement or pressure. 
 
 8. Exaggerated reflexes till pus 
 is formed, then "paralysis" sets in, 
 first in the legs, then ascends, 
 and reflexes become abolished. 
 Anaesthesia replaces hypersesthesia ; 
 sphincters are paralysed ; septic 
 fever and lividity of the skin 
 supervene ; large bed-sores form, 
 and the patient often succumbs 
 from exhaustion. 
 
 Treatment. — 
 
 1. Remove cause, if possible, by 
 trephining, or aspiration of abscess 
 cavity, etc. 
 
 2. Absolute rest. 
 
 3. Counter irritation, cupping, 
 actual cautery. 
 
 4. Drugs — bromides, chloral, 
 antipyrin, etc. 
 
 Intbknal Meningitis. 
 
 1. Extension of external men- 
 ingitis on the one hand, or of 
 myelitis on the other. 
 
 2. Extension of cerebral men- 
 ingitis. 
 
 3. Septic state of blood, as in 
 fevers, etc. 
 
 Pathology. — 
 
 The membranes are involved 
 to a much wider extent. The 
 internal membranes suffer early. 
 The arachnoid is frequently wholly 
 disorganised, the pia mater deeply 
 injected, and the dura mater bulged 
 outwards from accumulation of pus ; 
 in severe cases, the cord substance 
 is semi-fluid. 
 
 Symptoms. — 
 
 Are much the same, but of 
 greater severity. There is more 
 general excitement; opisthotonus, 
 and retraction of the head are more 
 marked; vaso motor centres are more- 
 deranged ; and cerebral symptoms 
 are much more common. Cheyne- 
 Stokes' breathing is often typically 
 seen. It may be impossible to 
 distinguish this form from cerebro- 
 spinal fever, or even acute myelitis. 
 
 Treatment. — 
 
 The same treatment, but Gowers 
 advises in addition, the free appli- 
 cation of oleate of mercury, and 
 internal administration of 'calomel. 
 
70 Student's Hand-book of Medicine. 
 
 CHRONIC SPINAL MENINGITIS. 
 
 This is frequently the sequel to the acute afifection, therefore, 
 dependent on the same causes ; but it is sometimes chronic 
 from the beginning. In these cases, syphilis, alcoholism, certain 
 poisons, or extension of any chronic disease of the cord are held 
 as probable causes. 
 
 Pathology. — It varies much in different cases, from a mere 
 thickening and cloudiness of the membrane with increase of 
 cerebro-spinal fluid, to obliteration of the subarachnoidal space, 
 by complete organisation of the inflammatory lymph, which 
 matted the pia mater and dura mater together. 
 
 Nerve Roots. — At first are swollen and injected, but become 
 fibrous and atrophied. 
 
 Spinal Cord suffers in proportion to — 
 
 1. The amount of compression from without. 
 
 2. The amount of thickening of the processes of the 
 
 pia mater which run into the cord. 
 
 It should be noted when there is much fibrous formation 
 between the dura mater and the cord substance it is termed 
 Hypertrophic Internal Meningitis. 
 
 Symptoms are those of local irritation of the nerve roots, 
 followed by paralysis ; thus, from irritation of sensory fibres 
 we ,get — 
 
 1. Pain in back with stiffness. 
 
 2. Sharp, darting, burning pains ; occurring in various parts 
 of the body, paroxysmal in character. 
 
 3. Spasm and rigidity. 
 
 4. After the cord has become invaded the symptoms wUl 
 be those of local myelitis (which see). 
 
 Treatment. — Eemove any cause if possible, then treat the 
 myelitis. 
 
Myelitis. 71 
 
 MYELITIS. 
 
 Inflammation of the cord substance may be acute or chronic. 
 Under the latter will be considered the various chronic spinal 
 diseases ; and under acute we shall consider — 
 
 1. A total transverse myelitis. 
 
 2. An unilateral myelitis (affecting one side only). 
 
 (1) Extension of acute spinal or cerebral meningitis. 
 
 (2) Exposure to cold, etc. 
 
 (3) Occurring in the course of fevers. 
 
 (4) Concussion. 
 
 Symptoms again are due (1) to irritation of nerve roots, 
 and (2) to paralysis from implication of cord substance. The 
 following is a good table of the results of a total transverse 
 lesion after paralysis has become established : — 
 
 Above the lesion — 
 
 1. Eeilexes, etc., normal. 
 
 2. HyperaBsthesia at upper margin of lesion. 
 
 At the point of lesion — 
 
 1. Loss of reflexes. 
 
 2. Atrophy of muscles supplied by the implicated nerves. 
 
 3. Altered electrical conditions {B.D.). 
 
 4. Cutaneous insensibility. 
 
 Below the lesion — 
 
 1. Total loss of sensation. 
 
 2. Complete paralysis. 
 
 3. Muscular rigidity or spasm. 
 
 4. No alteration in trophic relations except from non-use, 
 
 5. Vaso-motor dilatation. 
 
72 Student's Hand-hook of Medicine. 
 
 6. Reded Centre. — Unconsciousness of need, and inability 
 to prevent evacuation; therefore, we get constipation; and, 
 incontinence of fceces after an aperient. 
 
 7. Vesical Centre. — Again unconsciousness of need, and 
 inability to prevent micturition; so we get reflex evacuation 
 in gushes at intervals. 
 
 8. Sexual Centre. — Absence of desire, but frequent reflex 
 erections and emissions. (Charlton Bastian.) 
 
 9. Ordinary reflexes are exaggerated ; the slightest touch 
 of the bedclothes, catheter, etc. causing severe spasm. 
 
 It should be noted, however, that as time goes on the 
 muscles from non-use may become flaccid and soft, with con- 
 siderable wasting, and the reflexes also become exhausted. 
 
 Treatment. — As in acute meningitis. 
 
 Unilateral Lesion. 
 At the point of lesion. — 
 
 1. On the side of paralysis, same as transverse lesion. 
 
 (vide supra). 
 
 2. On the opposite side — anaesthesia without paralysis (f) 
 
 Beloio the Lesion. 
 
 SAME SIDE. OPPOSITE SIDE. 
 
 Paralysis. 
 
 HyiiercRslhesia of skin. (?) Ansestliesia (total ?) 
 
 Diminished muscular sense. 
 Kefiexes at first excited. 
 
 Vaso-motor dilatation. Other conditions normal. (?) 
 
 No atrophy. 
 
 It will be seen, that as regards unilateral lesions, the queries 
 placed show there is by no means an unanimous opinion. This 
 is because, not only are clinical records conflicting, but physio- 
 logical experiments are equally disappointing ; indeed, in spite 
 of much honest and hard work by experimenters, we are still 
 far off from certainty regarding the spinal cord function. 
 
Infantile Paralysis. 73 
 
 INFANTILE PARALYSIS OR ANTERIOR 
 POLIOMYELITIS ACUTA. 
 
 This, as the name implies, is an acute iniiammation of the 
 anterior horn of grey matter. 
 
 " Infantile " is not a good, term, for though infants and young 
 children under eight are most often affected, adults sometimes 
 develop the affection. Women during the puerperal state some- 
 times become afflicted with this paralysis. 
 
 Causes. — Not known. " Chills" from exposure to wet and 
 cold are usually blamed. Haemorrhage into the cord, etc. 
 
 Pathology. — At first — 
 
 1. Anterior grey horn is red and swollen. 
 
 2. Minute extravasations of blood occur. 
 
 3. Cloudy swelling of anterior multipolar cells. 
 
 Later — 
 
 4. The motor nerve trunks show marked changes, being 
 smaller and fewer in number. 
 
 5. The "neuroglia" becomes increased, and the grey horn 
 as a whole is shrunken. (See Sclerosis, page 67.) 
 
 Muscles are pale and flabby ; atrophy begins early, and is 
 well marked. 
 
 Microscopically, the same changes take place (as before de- 
 scribed) when muscles are cut off from trophic nerves. 
 
 1. Disappearance of strias. 
 
 2. Atrophy of muscle cells, and 
 
 3. An increase of fibrous elements (see page 64). 
 
74 Student's Hand-book of Medicine. 
 
 Symptoms. — First, reason what we might expect. We 
 have an interference of the reflex roof, destruction of motor cells 
 and motor trophic influence. The symptoms must be paralysis, 
 absence of reflexes, and atrophy; the extent and severity of these 
 symptoms will vary with the extent of the lesion. The onset 
 is sudden, and after two or three days of rheumatic feverishness 
 the paralysis becomes established. Usually the loioer limbs are 
 first affected, but all four limbs or only one, or only a group 
 of muscles may be implicated. However, once the paralytic 
 condition is established, atrophy, loss of reflexes, and reaction 
 of degeneration, quickly supervene (see page 63). Note that 
 "muscle wasting" may be concealed by fat. 
 
 Bladder and rectum usually escape. Sensation is but slightly 
 affected, if at aU. 
 
 Results — 
 
 1. Nutrition of bones, etc., is seriously affected, and the child 
 may recover motor power, with a wasted limb. 
 
 2. Permanent deformities produced by — 
 
 (1) Want of antagonism or unresisted contraction. 
 
 (2) Weight of foot, etc., causing extension, and the 
 
 occurrence of ankylosis in that position. 
 (Talipes equinus.) 
 
 3. Even in most favourable cases there is some slight 
 permanent deviation from a perfectly normal muscular 
 apparatus. 
 
 Treatment. — Eest, salicylates, and warmth. 
 
 Later. — Strychnine, cod-liver oil, lacto-phosphate of iron 
 and lime, electricity, and massage. 
 
 Gowers emphasises that complete recovery is impossible after 
 a year, though a gradual improvement may to a certain extent 
 take place from increased movements on the part of the patient. 
 
Progressive Muscular Atrophy. 75 
 
 CHRONIC DISEASES OF SPINAL CORD. 
 
 Having described the more common acute affections, we will 
 now take up the more common chronic affections of the cord. 
 
 PROGRESSIVE MUSCULAR ATROPHY. 
 
 Progressive muscular atrophy, or chronic anterior polio- 
 myelitis, is the example of a chronic affection of the anterior 
 grey horn and motor roots; and again, from the pathological 
 site, we are (as in the acute form) prepared for disturbances 
 of reflexes, atrophy, and deficient muscular power; but the 
 sclerotic changes being more localised and of slow growth, the 
 clinical symptoms will vary. 
 
 Pathology. — Sclerosis of anterior horn, anterior roots and 
 nerve trunks, with changes in groups of muscles. 
 
 1. Anterior grey horns are pale, but not altered much 
 
 in shape. 
 
 2. Great increase of neuroglia, and 
 
 3. Obliteration of nerve cells. 
 
 Anterior nerve roots are markedly atrophied. 
 
 Nerve Trunks. — Changes are not so marked as in the roots, 
 for the sensory fibres in the mixed nerve trunk are unaffected, 
 and frequently some of the motor fibres escape. 
 
 Muscles. — Pale, flabby, etc., like in the acute affection ; but 
 sometimes fatty, vitreous, or waxy changes are also present. 
 They exhibit the reaction of degeneration in proportion to the 
 amount of wasting. 
 
 Symptoms. — Disease usually begins in the " iipper " extrem- 
 ities with atrophy of — 
 
 1. Thenar and hypothenar eminences. 
 
 2. Interossei. 
 
76 Student's Hand-book of Medicine. 
 
 3. Shortening of extensors of the wrist, producing the claw- 
 like hand — i.e., the first phalanges are hyper-extended, the middle 
 and distal phalanges are flexed on the first phalanges ; next, the 
 deltoid or hiceps, and then the forearm become attacked. After 
 this, the extension is extremely gradual, and years pass before 
 both arms, both legs, intercostals, or diaphragm are attacked. 
 The affected muscles exhibit the peculiar fibuUar twitchings of 
 dying or exhausted muscle. These twitches can be readily pro- 
 duced by a gentle tapping ; they are often visible to the patient, 
 lasting two or three minutes, and starting without any apparent 
 stimulus. Probably no fatal case of pure anterior poliomyelitis 
 chronica has occured. Gowers remarks he has always seen in 
 fatal cases evidence of a wider distribution of sclerosis. 
 
 Treatment will be summed up under chronic nerve diseases. 
 
 Differential Diagnosis. (See Table.) 
 
 PRIMARY SPASTIC PARAPLEGIA. 
 
 (Peimaby Lateral Sclerosis.) 
 
 Primary spastic paraplegia is a paralysis attended with spasm 
 and rigidity, resulting from sclerosis of the anterior pyramidal 
 and crossed pyramidal tracts. 
 
 Let us just consider what we must expect from interruption 
 of these two tracts. 
 
 1. The brain being cut off from the motor nerves, two con- 
 ditions are brought about : — 
 
 (1) Voluntary motion must be imperfect, according to 
 
 the extent of lesion. 
 
 (2) Reflexes must also be exaggerated, as they are cut 
 
 off from the inhibitive influence of the brain, 
 but the reflex loops are not interfered with. 
 (See Diagram, page 81.) 
 
Primary Spastic Paraplegia. 77 
 
 2. The motor tracts, being cut off from the first trophic realm 
 in the coHex, will undergo secondary degeneration, which causes 
 at first increased irritability, which will excite motor roots and 
 cause spasm and rigidity. 
 
 3. The anterior horn not being affected, there will be no 
 interference with the second trophic realm, and consequently 
 no atrophy of muscles. 
 
 Etiology. — Most common in males about twenty. Children 
 sometimes get the disease, through imperfect development of the 
 tracts. 
 
 Symptoms — 
 
 1. Weakness and stiffness of the lower limbs. 
 
 2. Exaggerated knee jerk, and presence of ankle clonus. 
 
 3. Spasm and rigidity causing forcible adduction and extension 
 of the limbs, rendering the gait characteristic. (See " Gaits.") 
 
 The rigidity is nearly continuous, and when relaxations take 
 place the slightest stimulus causes spasm. 
 
 Though the legs are the limbs usually attacked, still the 
 muscles of the trunk, and the arms occasionally, are first 
 involved; but it is better to consider the latter as "amyo- 
 trophic paralysis " — i.e., one of the " overflows " presently 
 to be described. 
 
 The disease runs an extremely chronic course, as, until the 
 disease becomes widely spread, the muscles remain plump, 
 sensation unaffected, and sphincters unimpaired. 
 
 Differential Diagnosis. — (See Table.) 
 
 Treatment is considered under " Chronic Nervous Diseases." 
 
 Pathology. — Sclerosis of anterior and crossed pyramidal 
 tracts (see page 67). 
 
78 Student's Hand-book of Medicine. 
 
 LOCOMOTOR ATAXIA. 
 
 Definition. — A nervous disease characterised by an. indefinite 
 onset ; chronic, but progressive course ; and attended with marked 
 symptoms of Lnco-ordination, trophical changes, and disturbances 
 of special sense. 
 
 This disease is the best example of disease affecting the 
 posterior columns — though it is, as will be seen, associated with 
 sclerotic changes in the cerebrum, etc. 
 
 .etiology. — Most common ia middle-aged men. Syphilis, 
 exposure to severe weather, etc., sexual excesses are the usual 
 causes. The last two are doubtful, but syphilis is most certainly 
 a factor in producing this disease. 
 
 Pathology. — Sclerotic changes in (see page 67) — 
 
 1. Posterior nerve roots. 
 
 2. Posterior columns — Burdach first, then by 
 
 secondary degeneration into GoU's column. 
 
 3. Eestiform body (medulla). 
 
 4. Optic thalamus. 
 
 5. Certain nuclei of cranial nerves. 
 
 6. When the disease has advanced, it may attack 
 
 any area. 
 
 Symptoms. — A careful digest of the foregoing pathological 
 sites, will at once show that the symptonis will vary much in 
 each case, but we are at once prepared for sensory changes, 
 inco-ordination, and changes in the sight apparatus. 
 
 The disease is usually divided into three stages — 
 
 1. Pre-ataxic. 
 
 2. Ataxic, or stage of inco-ordination. 
 
 3. Stage of Paralysis. 
 
Locomotor Ataxia. 79 
 
 PRE-ATAXIC STAGE. 
 
 Symptoms are most insidious. Taking a typical case we 
 shall get — 
 
 1. Changes due to irritation of sensory roots — 
 
 (1) Lightning pains over the body : hot, burning, and 
 
 tingling in character ; lasting a few seconds. 
 
 (2) Girdle pains (from the upper margin of sclerosis), 
 
 the patient complaining of constriction, as if an 
 iron band was around him. 
 
 2. Early loss of knee jerk. 
 
 3. Symptoms in connection with the optical apparatus — 
 
 (1) Argyll-Eobertson's pupil (pupil fails to react to 
 
 light, but accommodation remains unaffected). 
 
 (2) Diplopia or double vision. 1 May occur early 
 
 (3) Optic neuritis. f or late. 
 
 4. Increased sexual desire, this is important in reference to 
 charges of rape ; later, sexual desire is abolished. 
 
 ATAXIC STAGE. 
 
 Often the first sign of inco-ordination is tumbling forward 
 into the basin on closing the eyes during the morning wash, 
 but once begun the inco-ordination often rapidly develops into 
 the characteristic " Ataxic-gait." - (See "Gaits.") 
 
 Soon anassthesia of the soles of the feet comes on, the patient 
 feels as if he were walking on wool, he feels unsteady on 
 turning around or standing with his eyes shut, and fails to 
 walk on a straight line, etc. 
 
 Both the tactile and muscular senses become markedly 
 affected, and the patient fails to distinguish with his feet 
 the difference between a hot and cold body, or between heavy 
 and light weights, provided they are similar in appearance. 
 
80 Student's Hand-book of Medicine. 
 
 It should be noted particularly that the muscular power is 
 not diminished, for the patient can resist movement or push 
 away a heavy weight. 
 
 Often at this period, occur peculiar visceral disturbances, 
 termed crises. The best known are — 
 
 1. Gastric crisis — intense epigastric pain, hyper-acidity, and 
 vomiting. 
 
 2. Larnygeal crisis — noisy stridulous breathing, with great 
 dyspnoea. 
 
 3. Vesical crisis — paroxysmal retention of urine. 
 i. Rectal crisis — tenesmus, etc. 
 
 The other most marked changes are the so-called " trophic " 
 alterations : — 
 
 1. Skin becomes dry, or shiny and glossy with absence of 
 hair ; nails crack, etc. 
 
 2. Joints. — Charcot's disease — identical in its pathological 
 changes with rheumatoid arthritis (which see). 
 
 3. Perforating ulcer of foot. 
 
 4. Ulceration of bones, cartilage, etc. 
 
 PARALYTIC STAGK. 
 
 The patient becomes bed-ridden, and liable to grave inter- 
 current diseases; and hemiplegia, pneumonia, or gangrene, etc.. 
 usher in a fatal ending. 
 
 It must be particularly noted that some cases run an 
 extremely lengthened course, others very rapid, and though it 
 is convenient to divide the disease into three stages, there is no 
 hard-and-fast line or distinct margin between them. 
 
 Treatment will be considered under " Chronic Nervous 
 Diseases.'' 
 
A Diagram, designed by the author, to show the course of the motor fibres (green) 
 and the sensory fibres (red) in the cord and nerve roots. 
 
 Note the motor fibres pass from the direct and crossed pyramidal tracts to the 
 anterior horn of grey matter, and thence to the anterior or motor nerve root. 
 
 The sensory fibres pass in, in two bundles, A & B. Observe bundle A crosses to 
 the opposite side, a few fibres however going; to the anterior horn to form the reflex 
 loop; bundle B passes into Burdach first, then at a higher level into Goll's tract 
 (bo that some sensory fibres cross to the other side at once, others do not). 
 
 Diagrammatic Drawing to show the fibres involved by lesions at A, B, C, D, & E. 
 
 A, Progressive Muscular Atrophy. C, Locomotor Ataxia. 
 
 B, Spastic Paralysis, D, Amytrophic Lateral Sclerosis. 
 
 E, Spastic Ataxia. 
 
SENSORY 
 
 FORMATIO 
 RETICULARIS 
 
 CEREBELLUM 
 
 GOLL. BURDACH. COMMA 
 
 TRACT OF GQWERS. 
 
 Diagrammatic Scheme, by the writer, to show a possible re-arrangement 
 of the Sensory Tracts in the Medulla before passing up to the Cortex 
 as sensory fibres. (See pages 60, 61.) 
 
FDRMATID RETICULARIS 
 MEDULLA 
 
 CROSSED PYRAMIDAL 
 TRACT. 
 
 OiRECT 
 
 PVRAMtDAL 
 
 TRACT 
 
 Diagrammatic Drawing, designed by the writer, to show the course of the 
 principal motor (green) and sensory fibres (red) between the medulla and 
 cortex. (See pages 59-61,) 
 
Amyotrophic Lateral Sclerosis. 81 
 
 CHRONIC SPINAL DISEASES, 
 With mixed Lesions or "Overflows." 
 
 We have, in the foregoing, studied total and partial lesions ; 
 and, found that in the 
 
 Anterior affection — atrophy and loss of reflexes were the 
 prominent symptoms. 
 
 Lateral aifection — spasm and rigidity -with increased reflexes. 
 
 Posterior affection — inco-ordination and anaesthesia were the 
 marked features. 
 
 It is easy to see that we might get compounds of these ; 
 for instance, we might have an — 
 
 Antero-lateral lesion = incomplete atrophy with spasm ; or 
 Posterolateral = inco-ordination and spasm. 
 
 Indeed, it would seem more probable at first sight to get 
 these " mixed " conditions rather than isolated or limited 
 lesions. 
 
 We shall next describe the three best known mixed lesions, 
 viz. : — 
 
 1. Antero-lateral or Amyotrophic paralysis. 
 
 2. Postero-lateral or Ataxic paraplegia. 
 
 3. Hereditary Ataxia. 
 
 The .etiology of these three affections will be considered 
 under "Diagnostic Tables.'' 
 
 AMYOTROPHIC LATERAL SCLEROSIS. 
 
 Pathology. — Sclerosis of — 
 
 1. Crossed pyramidal tracts. 
 
 2. Anterior horns of grey matter. 
 
82 Student's Hand -hook of Medicine, 
 
 Symptoms. — 
 
 1. Weakness and wasting of the upper extremities coming 
 on very slowly. 
 
 2. Increase of reflexes with spasm (until the wasting is 
 profound; then, the anterior multipolar cells being extensively 
 diseased, the reflexes may lie actually abolished). The spasm 
 and rigidity cause a peculiar deformity which is characteristic, 
 viz. : — 
 
 Arm extended close to the body. 
 Forearm semi-flexed and pronated. 
 Wrist strongly flexed. 
 Fingers bent into the palms. (Charcot.) 
 
 3. In about twelve months, wasting and rigidity commences 
 in the lower extremities. 
 
 4. Symptoms dependent on extension of the disease to the 
 medidla, tongue, face, etc. Any of these may be involved and 
 undergo atrophic changes, then the vital centres soon become 
 involved, and the patient dies. 
 
 The disease runs a quicker course than the three chronic 
 spinal diseases' already described, and death usually occurs in 
 from one to three years. 
 
 The beginner is frequently puzzled to understand why, in 
 this disease where the anterior horn is involved, reflexes are 
 increased instead of lost. The explanation is, that this afiection 
 begins in the "lateral" regibn but extends into the anterior 
 horn, paralysing only a certain number of motor cells, and 
 irritating others. Sensation is not impaired, and the sphinc- 
 ters are normal. 
 
 ATAXIC PARAPLEGIA. 
 Pathology. — Sclerosis of — 
 
 1. Lateral columns, (direct cerebellar and crossed 
 
 pyramidal). 
 
 2. Posterior columns (but not the roots). 
 
Hereditary Ataxia. 83 
 
 Symptoms. — Obscure in the early stages. 
 
 1. Patient complains of tiredness and weakness of the limhs 
 {no lightning pains). 
 
 2. Inco-ordifiation, patient reels or sways if the eyes be 
 closed, and he fails to walk on a straight chalked line. 
 
 3. Increase of knee jerk (ankle clonus is often present). 
 
 4. As the disease progresses the tendency is to become more 
 spastic, and less ataxic in character — i.e., inco-ordination does 
 not increase, but spasm and rigidity become markedly increased. 
 
 It should be noted that there is no anaesthesia, lightning 
 pains, or alterations of the optical apparatus ; points which dis- 
 tinguish it from locomotor ataxia ; and this is what we should 
 expect, seeing there is no involvement of the posterior nerve 
 roots, or cranial nerves. We might consider here an interesting 
 form of ataxia, called — 
 
 FRIKDRKIGH'S DISEASE (Hereditary Ataxia). 
 
 Pathology. — Sclerosis involving principally the "neuroglia" 
 element in — 
 
 1. Lateral columns — Gower's, direct cerebellar, and part 
 
 of crossed pyramidal. 
 
 2. Posterior columns. 
 
 3. Clarke's columns in grey matter (to a slight degree). 
 
 4. Certain cranial nuclei. 
 
 Symptoms — 
 
 1. Inco-ordination of a jerky kind of the lower extremities. 
 
 2. Inco-ordination of the arms (somewhat later). 
 
 3. Hesitation in speaking, or a jerky manner in delivery 
 of speech. 
 
 4. Irregular movements of the head and eyeballs (nystagmus). 
 
84 Student's Hand-hook of Medicine. 
 
 5. Impairment of sensation — the anaesthesia is not marked 
 in most cases. 
 
 6. Absence of knee jerk. 
 
 7. Talipes equinus and other deformities, especially curvatures 
 of the spine. 
 
 Note absence of lightning pains, trophic changes, and the 
 Argyll Rohertson pupil to distinguish this disease from locomotor 
 ataxia. The marked inco-ordination and nystagmus renders the 
 diagnosis easy from that of spastic paralysis. 
 
 The most marked feature in the setiology of this disease is, 
 its congenital tendency, and its appearance in more than one 
 member of a family. It is transmitted through the father, and 
 is usually first noticed in the child about the age of eight years. 
 
 PSEUDO- HYPERTROPHIC PARALYSIS. 
 
 A nervous disease which manifests itself during the later 
 developmental period of childhood, and characterised by a 
 progressive change in size and diminution in the power of 
 many muscles (Gowers). 
 
 .ffitiology — occurs principally amongst boys ; and, in the 
 few cases of which we have any authentic account, there seems 
 a strange tendency to aifect more than one male member in the 
 same family. It is hereditary in a peculiar manner, as whilst it 
 affects males, it is transmitted through the females — i.e., in a 
 certain family a son was affected ; his sister married, and had 
 two daughters and one son ; the daughters escaped, but the boy 
 was affected. The writer has a great friend, whom he had under 
 his observation for four years ; he is now twenty-six, and has 
 been seen by Drs Byrom Bramwell and Gowers. In this case 
 I can detect nothing which would suggest even a possible 
 cause ; indeed, after four years' steady and minute search of the 
 literature of this disease, I fear there is absolutely nothing 
 
Pseudo-Hypertrophic Pa/ralysis. 85 
 
 known of the origin of tMs paralysis. All tlie suggestions 
 thrown out are weak, and as devoid of any real explanation 
 as Dr Gowers statement — "It is a perverted tendency of 
 development inherent in the germinal tissue of the muscular 
 system." 
 
 Symptoms are very characteristic when the disease is fully 
 developed, but in the earlier periods they are somewhat obscure. 
 
 1. Impaired locomotion from> muscular weakness, the little 
 fellow lags behind his playfellows. 
 
 2. Hypertrophy of muscles with atrophy of others. 
 
 3. Certain deformities, through contraction of muscles un- 
 antagonised by the paralysed ones. 
 
 4. The characteristic gait and movements. 
 
 During walking the abdomen is thrown out, with a corres- 
 ponding hoUoioing of the back ; the legs are widely spread out, 
 the whole effect being a waddling gait. 
 
 The getting up from a recumbent position is most character- 
 istic, especially if there be no objects near, by which he can aid 
 himself He first gets on his hands and knees ; then, extends 
 his knees to the utmost ; and lastly, by a climbing movement — 
 i.e., grasping the knees with his hands alternately, moves 
 higher and higher up the thigh till the trunk is raised. 
 
 It is remarkable how easily some patients can manage these 
 movements; later, the muscular weakness is such that they 
 require the aid of near objects to grasp at, but finally failure 
 is complete, the patient being helpless. 
 
 Pathology. — The essential changes seems to be in the muscu- 
 lar tissues alone. Changes in the cord are rare, and probably 
 are only accidental complications. Microscopically there are 
 seen in the affected muscles — 
 
 1. Increase of fibrous tissue. 
 
 2. Atrophy of muscle fibres. 
 
 3. Large deposit of fat. 
 
86 Student's Hand -hook of Medicine. 
 
 The enlarged appearance of the muscles is due more to fat 
 than the increase of fibrous tissue. The muscles mostly involved 
 are as follows — 
 
 ENLAEGED. WASTED. 
 
 1. Calves. 
 
 2. Glutei. 
 
 3. Infra spinatus. 
 
 1. Latissimus dorsi. 
 
 2. Teres major. 
 
 3. Pectoral muscles. 
 
 The above table of course is only approximate, there seems 
 to be no hard and fast line as to what muscles will show most 
 changes. 
 
 The reaction of degeneration is in proportion to the atrophy ; 
 as long as any true muscular tissue is left there wiU be response 
 to stimulation. The knee jerk is lost when the tonicity of the 
 extensors fails. 
 
 Treatment. — Expect most benefit from a thorough system 
 of continued massage, well planned gymnastic exercises, and 
 careful hygiene. 
 
 Tonics such as strychnine and phosphorus may be given. 
 The writer thinks there was decided improvement in two cases 
 he attended, after hypodermic injections of arsenic, ij minims 
 three times a week ; but, untoward circumstances prevented an 
 extended trial. The thinness of the chest walls renders the 
 patient very prone to chest affections, which, should they occur, 
 often carry off the patient, and are to be particularly guarded 
 against. 
 
 DISEASES OF CRANIAL NERVES. 
 
 All have at least two origins — viz., deep and superficial ; all 
 behind the 4th nerve may be said to have their deep origin m 
 the 4th ventricle. The nerves of the special senses — i.e., 1st 
 (smell), 2nd (sight), 8th (hearing), have in addition a special 
 
Cranial Nerves. 87 
 
 connection with the so-called " centres," situated in the cortex of 
 the brain. We have left out the sense of " taste " here, for no two 
 authorities agree upon which is the special nerve, though there 
 is increasing evidence in favour of the 5th being the nerve most 
 implicated. For a special "sense" to be carried out properly, 
 we can at once see that there must be a healthy continuity 
 between centre, nerve trunk, and special ending; destruction 
 of any of these will interfere with the carrying out of the 
 function. We shall see when we proceed to study the brain, 
 that there are in all probability, connections between all five 
 senses (possibly through commissural fibres connecting the 
 centres); thus, "taste is impaired when the smell is interfered 
 with ; hearing is sometimes more acute when blindness ensues, 
 and so on." 
 
 OLFACTORY OR FIRST PAIR. 
 
 Anatomy. — They arise from the olfactory bulbs, pass through 
 the ethmoidal plate, and are distributed to the mucous mem- 
 brane in the upper part of the nose. 
 
 Physiology. — The nerves of smell. Pungency should be 
 carefully distinguished from the sense of smell, or the detection 
 of odours ; pungency is indeed due to painful stimulation of the 
 5th nerve in the lower part of the nose. 
 
 Clinical. — Highly nervous or insane people often complain 
 of— 
 
 1. Hallucinations of Smell. — They may complain of un- 
 pleasant odours, or that totally different odours are all alike — 
 such as a rose and a herring having the same odour, which 
 may be to them either pleasant or otherwise. 
 
 2. Increased Sensitiveness. — Perfumes become intolerable, 
 or patients may tell by odour alone the difi'erent members of 
 their own family. 
 
88 Student's Hand-book of Medicine. 
 
 3. Total loss of Smell. — This may be due to — 
 
 (1) Affections of the terminations of the uerve (most 
 
 often associated with uasal catarrh or polypi). 
 
 (2) Lesions of the nerve t)imJc. 
 
 (3) Lesions of the centre, in the uncinate gyrus. 
 
 Treatment. — Ferrier's snuff, douching with carbolic acid 
 solution, after removal of any apparent cause, such as polypi, 
 etc., are the remedies indicated. 
 
 OPTIC NERVES. 
 
 (See Diagram.) 
 
 Anatomy. — Given off from the sides of the chiasma, they 
 pass through the optic forainen, pierce the sclerotic, then be- 
 come distributed as delicate filaments over the retina. Thus 
 we get, on tracing backwards — 
 
 1. Optic Nerves. 
 
 2. Optic chiasma or partial decussation. 
 
 3. Optic tracts, 
 
 [■ Optic thalamus. 
 
 4. Ganglionic Centres. -] Corpora geniculata. 
 
 [Corpora quadrigemina. 
 
 5. Cortical centres — i.e., radiation in the occipital lobes. 
 
 There are no less than three sets of fibres, as shown in the 
 diagram — 
 
 1. Outer set to eyeball of same side. 
 
 2. Middle fibres which decussate with the fibres of the 
 
 opposite tract, forming the commissure. 
 
 3. Fibres having no real connection with vision (Ferrier). 
 
 Physiology. — Xerves of sight. 
 
^^^^^i;::*'*. 
 
 The Optic and Visual Tracts (Starr). 
 
 N, Lesion causing nasal hemianopia. T, Lesions causing temporal hemianopia^ 
 H, Lesion causing bilateral heteronymous hemianopia. B, Lesion of tract 
 causing homonymous hemianopia. 
 
Optic Nerves. 89 
 
 Clinical — 
 
 1. Affections of the terminations in the retina include — 
 
 (a) Functional disturbances due to toxic effects, viz. — 
 
 (1) Ursemia. 
 
 (2) Jaundice. 
 
 (3) Drugs — quinine, santonine, etc. 
 (6) Hysterical amaurosis. 
 
 (c) Tobacco amblyopia. The loss of sight is gradual, 
 
 but, if the disorder persists, there may be perma- 
 nent changes in the optic disc. 
 
 (d) Mght blindness — (nyctalopia). Objects are clearly 
 
 seen by day, but not in the dusk; or (hemeralopia); 
 objects are easily seen in the shade, but, in the 
 sunshine, with difficulty. 
 
 2. Lesions of the Nerve. 
 
 (a) Optic Neuritis. — The disc becomes blurred, swollen 
 and red from coipgestion ; there may be slight ex- 
 travasations of blood ; finally, there is an increase 
 in the fibrous tissue, and atrophy of the nerve 
 elements, causing often total blindness. It is 
 common in Bright's disease, tumours of the brain 
 and cerebellum, and other interoranial affections. 
 The blindness is preceded by changes in three directions— 
 
 (1) Diminished acuity of vision. 
 
 (2) Alteration in the field of vision. 
 
 (3) Altered perception of colour (Gowers). 
 
 3. Lesions of the Ghiasma. — If the lesion is confined to 
 the central portion — i.e., the decussation, the fibres passing 
 to the inner or nasal portion of each retinse will be involved, 
 causing blindness of the outer half of each field — temporal 
 hemianopia. If the lesion is more extensive there may be total 
 blindness of the eye on same side, with temporal hemianopia 
 of the opposite; or, a more extensive lesion still, may cause total 
 blindness. 
 
90 Student's Hand -hook of Medicine. 
 
 4. A Lesion behind the Chiasma, whether in optic tracts, 
 optic thalamus, 'corpora quadrigemina or geniculate bodies, 
 causes lateral hemianopia, that is, blindness of the temporal 
 half on the same side, and the nasal on the opposite side. 
 A lesion in the occipital — 
 
 5. Cortex also causes lateral hemianopia ; but there is in 
 addition, word blindness, i.e., the patient can see but fails to 
 read letters. (See Aphasia.) 
 
 THIRD NERVE. 
 
 Anatomy. — Arises from the floor of aqueduct of Sylvius, 
 passes through tegmentum of crus on the inner side, and 
 forwards to be distributed to — 
 
 1. The sphincter pupillse. 
 
 2. Ciliary muscle. 
 
 3. All the muscles of the eyebaU except superior 
 
 oblique, and external rectus. It also supplies 
 levator palpebrce superioris. 
 
 Physiology. — The nerve concerned in accommodation of 
 vision and certain movements of the eyeballs. 
 
 PARALYSIS. 
 
 1. Ptosis or drooping of upper lid. 
 
 2. Divergent squint, with inability 
 
 to move the eye inwards, 
 downwards, or upwards. 
 
 3. Loss of accommodation. 
 
 i. Paralysis of sphincter of iris = 
 
 dilatation of pupil. 
 5. Double vision. 
 
 IKMTATION. 
 
 1. Convulsions or spasm of the 
 
 the muscles. 
 
 2. Convergent squint. 
 
 3. Contraction of pupil. 
 
 4. Great interference with field of 
 
 vision. 
 
 Clmical. — Sympjioms due to paralysis, or irritation of the 
 third nerve, are common in many intercranial affections ; for 
 instance, the former condition is usually well marked in 
 
Third Nerve. 91 
 
 fractures of the base of the skull, the "compression" stage of 
 meningitis, etc. ; whilst irritation of the nerve is often brought 
 about by tumours, the first stage of meningitis, reflexly by 
 stimulation of the sensory fibres through intestinal irritation, 
 (worms, etc.) 
 
 It should be noted that only a few of the great number of 
 fibres running in the third nerve may be afiected, and the 
 clinical phenomena will obviously vary with the number of 
 fibres involved. We will consider the fibres to the iris first — 
 
 Paralysis of the Iris. — May be of three types — 
 
 1. Accommodative iridoplegia^ failure to accommodate for 
 near vision. 
 
 2. Eeflex iridoplegia=: failure of reaction to "light" stimu- 
 lus, constituting the Argyll-Eobertson pupU, a most important 
 symptom in loco-motor ataxia. In this case, the lesion pro- 
 bably interrupts the fibres between the corpora quadrigemina 
 and the aqueduct of Sylvius. ' 
 
 3. Loss of skin reflex — failure of the pupil to dilate when 
 the skin of the forehead is pinched. 
 
 Affections due to Alterations in the Muscular Apparatus 
 of the Eye — 
 
 1. Nystagmus, or clonic convulsions of both eye-balls. 
 
 2. Strabismus or squinting. 
 
 Nystagmus may he due to — 
 
 1. Irritation of fibres in connection with the third nerve 
 nuclei, as seen in — 
 
 (1) Lesions of the restiform body in the mediiUa. 
 
 (2) Lesions interrupting the afferent fibres administrating 
 
 to the functions of the cerebellum — i.e., eighth 
 nerve which conveys impulses from the semi- 
 circular canals. 
 
 2. Tiredness or exhaustion of the ocular muscles after severe 
 strain, common in miners after working with small Davy lamps; 
 or after excessive glare, as seen in electric light employes. 
 
92 Student's Hand -hook of Medicine. 
 
 Squinting or Strabismus. — In order to have perfect sight, 
 there must be perfect harmony between all the ocular muscles ; 
 for instance, when we look at an object to the right, we turn 
 both eyes in that direction, and thus we call into action the 
 external rectus (sixth nerve) of the right eye, and the internal 
 rectus (third nerve) of the left eye. In other words, on looking 
 to the right side, we employ the services of two nerves, the 
 third and fourth. Other movements will involve other com- 
 binations, such as the third and sixth nerves, third, fourth, and 
 sixth, etc. Obviously then, there must be a centre for the 
 harmonious or co-ordinated actions of the third, fourth, and 
 sixth nerves. This centre is placed by physiologists under 
 the corpora quadrigemina, or in the " iter.'' A failure of this 
 harmonious action produces, on certain movements of the eyes, 
 an alteration in vision termed strabismus, characterised by — 
 
 1. Diminished field of vision in certain directions. 
 
 2. Diplopia or double vision — i.e., the appearance of a true 
 and false image of the same object. 
 
 3. Erroneous projection — i.e., errors in the judgment of the 
 distance of objects (due to greater effort being required to 
 focus for distant objects). 
 
 4. Secondary deviation— i.e., if the affected eye be fixed on 
 an object, it requires a greater effort than usual: but the muscle 
 of the opposite eye, which acts in combination, will then be 
 unduly strained and make a greater excursion than usual = 
 secondary deviation. 
 
 Eesults of Paralysis of Special Ooulae Muscles 
 when the othbbs are sound. 
 
 Paiulysis of Rectus Superior: inability to raise eyeball properly above 
 horizontal level; pupil may diverge somewhat downwards, and a little 
 outwards (from action of the rectus inferior and the obliqiii). 
 
 Paralysis of Rectus Inferior : inability to lower eyeball properly below 
 horizontal level ; pupil may diverge somewhat upwards, and a little out- 
 wards (from action of the rectus superior and the obliqui). 
 
 Paralysis of Rectus Externus : inability to turn eyeball properly out- 
 wards ; pupil diverges inwards (from action of rectus internus). 
 
Results of Ocular Paralysis. 93 
 
 Paralysis of Rectus Internus ; inability to turn eyeball properly in- 
 wards ; pupil diverges outwards (from action of rectus extenius). 
 
 Paralysis of Obliquus Superior : but little alteration in movements 
 of eyeball ; slight deviation of cornea upwards and inwards, or simply 
 upwards. 
 
 Paralysis of Obliquus Inferior : but little alteration in movements of 
 the eyeball ; slight deviation of the cornea downwards and inwards. 
 (Paralysis of the sphincter of the iris, giving rise to a moderate dilatation 
 of the pupil, and paralysis of the accommodation, often accompany this 
 form of paralysis ; this depends on the branch to the lenticular ganglion 
 being given off from that branch of the third nerve which goes to the 
 inferior oblique muscle. Occasionally, however, the lenticular branch 
 arises from the sixth nerve. ) — Finlayson's Manual. 
 
 Left. Eight. 
 
 Inferior Oblitiue (3). Sttpertor JicctuB (3). Superior Rectus (3). Inferior Ohliquc (3). 
 
 Superior Oblique {i). Rectus Inferior {^). Rectus Inferior [S). Superior Oblique 14). 
 
 Diagram to illustrate the directions towards which the pupil is moved 
 by the separate action of the six muscles of the eyeball. The eyes are 
 turned inwards and outwards by the external and internal recti ; the 
 internal rectus of one side is the yoke-fellow of the external rectus of the 
 opposite side in these conjugate movements. The eyes are turned upwards 
 by the superior rectus and inferior oblique, downwards by the inferior 
 rectus and superior oblique. 
 
 The eyes are represented facing the observer ; if it be imagined that the 
 eyes are looked at from the hack, so that the diagram right-left becomes 
 left-right, it wiU serve to illustrate the displacements in the field of 
 vision caused by paralysis of individual muscles and nerves. — "Wallee's 
 Physiology. 
 
 Strabismus is a most frequent cause of headache, etc., and. 
 probably many of the failures to treat hemi-crania successfully, 
 etc., are due to the neglect of testing the visual apparatus, and 
 thereby failing to rectify " eye-strain." 
 
94 Student's Hand-book of Medicine. 
 
 FIFTH CRANIAL NERVE. 
 
 Anatomy. ^- The fifth cranial nerve has a most extensive 
 origin. The middle or motor root arises from the floor of the 
 fourth ventricle ; the two sensory (ascending and descending) 
 arise from cells in the lower part of the medulla, and also from 
 the outer wall of the aqueduct of Sylvius. The nerve in front 
 of the Gasserian-ganglion divides into three branches — 
 
 1. Ophthalmic. 
 
 2. Superior Maxillary. 
 
 3. Inferior Maxillary. 
 
 By means of these branches, the fifth nerve has connections 
 with four important ganglia — viz., ophthalmic, Meckel's otic 
 and sub-maxillary, so that there is a tendency to assume, 
 reasoning from its wide origin and distribution, that all nerves 
 after the fifth contain fibres derived from that nerve. Much 
 accurate knowledge, indeed, is wanted regarding this nerve, 
 anatomically, physiologically, and more so, clinically. 
 
 Physiology. — It contains — 
 
 1. Sensory fibres to whole of head, except pharynx. Eusta- 
 chian tube, tympanic cavity, and palate. 
 
 2. Motor fibres to temporal, masseter, both pterygoids, 
 anterior beUy of digastric, mylohyoid (muscles of mastication), 
 and tensor tympani. 
 
 3. Trophic Hires, widely distributed (though disputed by 
 some). 
 
 4. Fibres derived from — 
 
 (1) Sympathetic = dilator pupillBS, sweat fibres, vasa 
 
 dilators and constrictors. 
 
 (2) Chorda Tympani from seventh = vasa dilator, and 
 
 .secretory to sub-maxiUary gland, and taste (?) 
 
 (3) Jacobson's nerve to parotid, from the ninth. 
 
Fifth Cranial Nerve. 95 
 
 Paralysis of the whole nerve causes — 
 
 1. Loss of sensation to parts supplied. 
 
 2. Inflammatory changes in the cornea, due to — 
 
 (1) Ansesthesia (irritating particles are not felt, 
 
 therefore not removed). 
 
 (2) Atrophic changes ? 
 
 3. Impaired taste in anterior two-thirds of tongue. Gowers 
 suggests that the fifth is the nerve of taste, and that the other 
 nerves — viz., seventh and ninth — administer to taste only in as 
 much as they contain fibres from the fifth. 
 
 4. Inability to detect pungent odours. 
 
 Clinically, we get various disturbances of this nerve. 
 
 Paralysis may he due to — 
 
 1. Disease of the pons. 
 
 2. Injury or disease at hase of brain, meduUa, etc. 
 
 3. Pressure from tumours, etc., on the branches as they pass 
 through their foramina. 
 
 4. Peripheral neuritis. 
 
 A reference to the distribution of the nerve wiU give 
 the symptoms attendant on paralysis of the whole 
 or different branches. 
 
 Neuralgia may occur in aU the branches of the fifth nerve. 
 It is most often unilateral, or confined even to one twig. Caries 
 of the teeth, or disease of the various bony canals, are most 
 common causes. 
 
 Redness of the part affected is very characteristic ; due to 
 reflex disturbance of the sympathetic. 
 
 Trismus or spasm of the muscle of mastication may occur 
 from irritation of the third division. This condition may be 
 produced reflexly by stimulation of various nerves of the head. 
 
96 Student's Hand-book of Medicine. 
 
 Trophic changes may be confined to — 
 
 1. The cornea. 
 
 2. Hair roots (hair becoming grey). 
 
 3. Circumscribed areas of skin, affected with eruption of 
 herpes. The pain is often intense, and may persist for years 
 after the herpes have disappeared. 
 
 4. Progressive unilateral atrophy of the face. (Very rare.) 
 
 Treatment. — Paralysis. — (See general treatment on Nervous 
 Disease.) 
 
 Tor Neuralgia. — Extract carious teeth; give quinine, gelsem- 
 inum, tonga, croton-choral hydras, salycilates if there be a 
 rheumatic history, or iodide of potassium and strychnine in 
 syphilitic or broken down constitution. Morphia, hypoder- 
 mically, may be required for continued suffering. Excision 
 of the Gasserian ganglion is of doubtful value. 
 
 SEVENTH NERVE. 
 
 Anatomy. — This nerve consists of two parts, the facial part 
 (portio dura), and the auditory part (portio mollis) ; but, in 
 mediciae, the facial portion only is meant when speaking of 
 the seventh nerve. 
 
 The facial part arises from a groove between the pons and 
 restif orm body ; its deep origin from the dorsal aspect of the 
 pons and 4th ventricle. It is also connected by motor fibres 
 with the cortex in the fissure of Kolando. Briefly, its dis- 
 tribution is as follows : — 
 
 1. Motor to — 
 
 (1) Muscles of expression. 
 
 (2) Stylo-hyoid. 
 
 (3) Posterior belly of digastric. 
 
 (4) Stapedius. 
 
 (5) Platysma Myoides. 
 
Seventh Nerve. 97 
 
 2. Secretory to — 
 
 (1) Sub-maxillary gland. 
 
 (2) Sub-lingual gland. 
 
 (3) Glands of moufcli and tongue. 
 
 3. Sensory. — Nerve of taste, for anterior two-thirds of 
 
 the tongue. 
 
 Paralysis Causes — 
 
 1. Motor changes — 
 
 Face drawn to opposite side. 
 Eye wide open, unwinking. 
 Cheek puffs out with expiration. 
 Food collects between cheek and teeth. 
 Absence of wrinkles. 
 
 2. Sensory changes — 
 
 Loss of taste in anterior two-thirds of the tongue. 
 
 Clinical. — Paralysis naay be due to lesions affecting — 
 
 1. The cortical iibres — supra-nuclear paralysis. 
 
 2. The nucleus itself. 
 
 3. Nerve trunk in its tortuous course through the pons 
 
 and bony canals. 
 
 The former (cortical) is associated with hemiplegia; and it 
 should be at once noted that the paralysis will vary with the 
 site of the lesion. 
 
 When it is a part of hemiplegia, the paralysis is on the 
 opposite side of the lesion, that is, on the same side as the 
 paralysed limbs; but the upper branches of the nerve escape, 
 the orbicularis palpebrarum is not involved, thus movements of 
 the eyelids are not affected — i.e., winking is possible. 
 
 If the lesion be in the lower section of the pons, it wiU 
 involve the facial fibres between the nucleus and their emer- 
 gence in the pons. Thus we get " crossed paralysis"- — i.e., the 
 face is paralysed on the same side as the lesion, the arms and 
 legs (as before) on the opposite side. 
 
98 Student's Hand-book of Medicine. 
 
 Symptoms. — When the whole nerve is paralysed, the 
 affected side is immobile, smooth, and expressionless. The 
 eye cannot be shut, and usually waters freely. Smiling or 
 whistling, etc., bring out the contrasts markedly. The food 
 collects between the teeth, because of the buccinator paralysis. 
 The paralysis of the stapedius C!) causes increased hearing to 
 low sounds. The soft palate is not affected (being supplied 
 by the spinal accessory nerve). The anterior part of the 
 tongue is insensible to taste. 
 
 The electrical reactions are highly important. When there 
 are no polar changes, the ease recovers rapidly. If the reaction 
 of degeneration be present, the prognosis is much more un- 
 favourable. To sum up — 
 
 In the nuclear form of paralysis the whole of the one side of 
 the face is involved, and typical " Bell's paralysis '' results, 
 
 When of cortical origin it is — 
 
 1. Associated with hemiplegia. 
 
 2. Upper part of face escapes. 
 
 3. Voluntary movements are more affected than 
 
 emotional movements. 
 
 4. The affected muscles seldom atrophy. 
 
 When in the lower portion of the pons, we get crossed 
 paralysis, but of the nuclear type, as regards the muscles 
 affected. 
 
 Causes — 
 
 Cortical Form. — Those of hemiplegia. 
 Periplieral. — Exposure to draughts, rheumatic neuritis, 
 disease of the middle ear, etc. 
 
 Nuclear. — Extension of chronic spinal diseases, etc. 
 
 Treatment. — Remove if possible any pressure on the nerve 
 by causing absorption of inflammatory products. Massage, 
 electricity, and flying blisters are all useful. The peripheral 
 type is usually very amenable to treatment. 
 
Eighth Nerve. 99 
 
 EIGHTH OR AUDITORY NERVE. 
 
 Anatomy. — It arises from two nuclei in the floor of the 
 fourth, ventricle. Some of its fibres are connected with the 
 cerebellum, and also with the cortical centre situated in the 
 superior temporo-sphenoidal lobe. 
 
 Physiology. — The nerve fulfils two functions — 
 
 Firstly, it is the nerve of hearing, or that by which sound 
 undulations are conducted from the labyrinth to the cortex, and 
 there analysed. 
 
 Secondly, by means of its fibres in connection with the 
 ampulla and semi-circular canals it transmits impulses from the 
 oscillations of the endolymph in those regions, to the cerebellum, 
 and thus assists the co-ordinating function in the maintenance 
 of the equipoise of the body. 
 
 Paralysis causes total deafness, often attended by certain 
 unpleasant subjective and objective symptoms. 
 
 Excitation of the auditory fibres cause unpleasant noises 
 often accompanied with intense giddiness, nausea, and oscUla- 
 tions of the eyeballs. 
 
 It is highly important to remember the close sympathy and 
 relation that exist between the optic, third, and auditory 
 nerves; and again, between these nerves and the cerebellum. 
 
 Clinically we get — 
 
 1. Functional disturbances of the auditory nerve, including 
 noises, buzzing, or "bell in the ear," and is often due to the 
 accumulation of wax, altered tympanic pressure, etc. 
 
 2. Lesions afiecting the cortical centre, causing word deaf- 
 ness — i.e., spoken words are heard as noises, and not understood. 
 (This condition may be associated with " word blindness," and 
 " word aphasia,'' which see.) 
 
100 Student's Hand-book of Medicine. 
 
 3. Lesions of the nerve at the base of the brain, causing 
 permanent deafness. 
 
 4. Disease of the labyrinth of the ear. The symptoms will 
 depend on the extent of the lesion, there may be — 
 
 (1) Hyper-sensitiveness. 
 
 (2) Diminished hearing. 
 
 (3) Total deafness. 
 
 The subjective symptoms are typically brought out 
 in — 
 
 5. Meniere's Disease. — An affection characterised by sudden 
 and intense nausea, vomiting, vertigo, noises in the ear, and 
 deafness of one ear. As we have already mentioned, nystagmus 
 is frequently present. The attacks occur paroxysmally. The 
 pathology is nnknown, but it seems to be due to either — 
 
 1. Some affection of the semi-circular canals. 
 
 2. Disease affecting the cortical centre, or 
 
 3. Vaso-motor neurosis of the vessels of the labyrinth. 
 
 Treatment. — In any affection of this nerve first try to 
 remove any discoverable cause. If associated with gout or 
 syphilis treat these diseases primarily. Keep the external 
 meatus clean, as deafness, giddiness, etc, are often caused by 
 dried wax pressing on the drum. During an attack of 
 Meniere's disease, the patient should be kept quiet in a 
 darkened room ; a brisk purge may be administered ; and 
 antipyrin, with an effervescing mixture containing caffeine, may 
 be prescribed. When the nerve is affected through disease of 
 the bony canal, the treatment is highly unsatisfactory. 
 
 DISEASES OF THE MEDULLA. 
 
 Much that has been said about the spinal cord may be also 
 said about the meduUa, or bulb. It is a conductor of impulses 
 
Diseases of the Medulla. 101 
 
 to and from the brain, and it also contains the principal reflex 
 centres. The more important points may be summed up as 
 follows — 
 
 1. It contains the deep origin of all the cranial nerves after 
 the fourth. 
 
 2. The motor fibres decussate to form the crossed and 
 direct pyramidal tracts in the cord. 
 
 3. The sensory tracts become re-arranged as sensory fibres, 
 prior to their course to the cortex. 
 
 4. It contains the following centres — 
 
 (a) Centres essential to life. 
 
 1. Eespiratory centres. 
 
 2. Cardiac centres — motor and inhibitory. 
 
 3. Vaso-Motor centres. 
 
 (b) Centres connected with the alimentary canal. 
 
 1. Centre for sucking. 
 
 2. Centre for mastication. 
 
 3. Centre for vomiting. 
 
 4. Centre for deglutition. 
 
 (c) Centres cpnnected with the eye. 
 
 1. Centre for winking. 
 
 2. Centre for dUator pupillse. 
 
 (d) Centres for secretion. 
 
 1. Salivary centre. 
 
 2. Lachrymal centre. 
 
 3. Sweat centre. 
 
 It will be seen from the above table that even a small 
 lesion may be attended by grave and diverse symptoms. 
 An extensive lesion would be incompatible with life. Some 
 authorities doubt if the medulla is ever diseased primarily 
 without a speedily fatal issue ; it is often, however, affected in 
 the later stages of spinal basal disease, disseminated sclerosis, 
 etc. Probably the best example of disease of the medulla is 
 the so-called chronic progressive bulbar paralysis, often termed 
 glosso-labial paralysis. 
 
102 Student's Hand-hook of Medicine. 
 
 GLOSSO-LABIAL PARALYSIS. 
 
 An affection characterised by progressive paralysis and 
 atrophy of the tongue, lips, etc., accompanied by difficult 
 articulation and deglutition, ending in suffocation or inanition. 
 
 .etiology. — It occurs most frequently in old people, but 
 is sometimes seen in persons as early as thirty years of age. 
 Men are more frequently attacked than women. Exposure to 
 cold, blows and injuries to the neck, are usually put down as 
 the principal causes. Often this disease is associated with 
 chronic diseases of the spinal cord. 
 
 Pathology. — 
 
 1. Sclerotic changes are found in the — 
 
 (1) Motor nerve nuclei of the medulla. 
 
 (2) Motor nerve roots directly connected with the bulb. 
 
 2. Degenerative changes are found in the — 
 
 (1) Trunks and motor endings of the glosso-pharyngeal, 
 
 spinal accessory, and hypo-glossal nerves. 
 
 (2) Atrophy of the tongue, lips, and muscles, supplied 
 
 by the above nerves. 
 
 Authorities dififer as to how the disease commences. Some 
 say that the lesion first starts in the nerve cells; others say 
 that the primary lesion is a subacute or chronic inflammation 
 of the neuroglia, which ultimately causes atrophy by pressure. 
 Bramwell believes both views are correct — i.e., that cases be- 
 ginning in either way are met with. 
 
 Symptoms. — Obviously, with so widespread a lesion, the 
 symptoms must vary with the nuclei involved; also, whether 
 associated or not with spinal or basal disease. Yet, in spite of 
 
Glosso-Labial Paralysis. 103 
 
 these facts, a fairly typical picture of glosso-labial paralysis may 
 be presented. Tabulated, the principal symptoms are- — ■ 
 
 1. Impairment of articulation due at first to defective move- 
 ments of the tongue, but later, to the atrophy of the lips ; 
 consequently, defective pronunciation of the letters involving 
 the tip of the tongue is first most marked — i.e., the letters 
 T, B, D, or the exclamation sh!; later, oo, w, etc., or articu- 
 lations which involve the lips become defective. Finally, 
 speech may be entirely abolished. 
 
 2. Difficulty in swallowing. 
 
 3. Symptoms indicative of paralysis of the palate — i.e., 
 nasal twang of voice, regurgitation of fluids through the nose. 
 
 4. Dribbling of saliva from the mouth. This is a most 
 marked symptom, and the patient is continually wiping the 
 secretion away. Possibly more saliva is secreted than normally, 
 but this symptom may be due to deficient deglutition, so that 
 saliva is not swallowed. 
 
 5. Symptoms indicative of paralysis of the larynx are 
 lowering of the pitch of voice, aphonia, etc. "When the 
 superior-laryngeal nerve is paralysed, particles of food get into 
 the lung and excite a fatal pneumonia. 
 
 6. Symptoms indicative of paralysis of the cardiac centre 
 are paroxysmal attacks of dyspnoea, a sensation of tightness 
 across the chest, irregular action of heart, etc. 
 
 The patient has usually a most sad expression, which is a 
 contrast to his often buoyant spirits. The condition of the 
 tongue is very charactferistic when the disease is well marked. 
 Its muscular tissue is much atrophied, and the mucous mem- 
 brane hangs in sack-like folds, wrinkled and covered with a 
 dirty yellowish fur. It is tremulous, lies helpless in the 
 mouth, and is only moved with great difiiculty, hence the 
 collecting of food between teeth and cheeks. The muscles of 
 mastication may be also involved (showing implication of the 
 fifth nerve). 
 
104 Student's Hand-book of Medicine. 
 
 Prognosis. — Invariably fatal. Death may occur from 
 emaciation, but is more often due to tbe various complications 
 that arise, especially pneumonia. 
 
 Treatment. — A mild course of galvanism, combined with 
 careful hygiene are the only remedies likely to influence the 
 duration of this disease. 
 
 Dr Byrom Bramwell's clinical atlas may be consulted with 
 advantage for all that is known of this disease. 
 
 DISEASES OF THE BRAIN. 
 
 Before beginning the study of cerebral disease, we will first 
 consider a few of the elementary anatomical and physiological 
 facts; without a knowledge of such facts brain diseases are 
 quite incomprehensible. 
 
 The brain proper, consists of two large hemispheres, partly 
 separated from each other by the great longitudinal fissure ; but, 
 bound together below by various commissures. 
 
 Externally, each hemisphere is covered with grey matter, 
 named the cortex ; which is mapped out by furrows into a 
 series of folds, termed convolutions. These convolutions are of 
 the highest importance ; absent in the lower type of animals, 
 they become gradually more marked in the higher animal, well 
 marked in monkeys, but only seen in perfection in the Mghly- 
 edueated adult human brain. 
 
 Of the Fissures of the hemispheres the largest and most 
 evident subdivide the surface of the cerebrum into lobes, and 
 
 may be called interlobular ; the smaller fissures — intralobular 
 
 divide the lobes into convolutions, which, in most cases, have 
 received definite designations. 
 
Diseases of the Brain. 105 
 
 The Interlobular Fissures are — 
 
 1. The fissure of Sylvius. 
 
 2. The fissure of Rolando. 
 
 3. The parieto-oeeipital fissure. 
 
 The Lobes of the cerebrum are five in number; four are 
 bounded by the interlobular fissures, and take their names from 
 the bones of the skull in relation to which they lie. 
 
 They are — 
 
 1. The frontal. 
 
 2. The parietal. 
 
 3. The occipital. 
 
 4. The terwporo-sphenoidal. 
 
 The fifth lobe — the central lobe — {insula or isle of Reil) is 
 not in contact with the bones of the skull, but is hidden loithin 
 the fissure of Sylvius, the margins of which must be separated 
 in order to see it. 
 
 The external convolutions of these lobes are — 
 
 1. Of the Frontal lobe- 
 
 Ascending -v 
 
 nSr [ Convolutions. 
 
 Inferior (or Brocas) ) 
 
 2. Of the Parietal lobe— 
 
 Ascending parietal 1 ^ , ^. 
 
 ° '^. , , !- Convolutions. 
 Superior parietal I 
 
 3. Of the Occipital lobe — 
 
 Superior "| 
 
 Middle J- Convolutions. 
 
 Inferior J 
 
 4. Of the Temporo-sphenoidal — 
 
 Superior "j 
 
 Middle j- Convolutions. 
 
 Inferior j 
 
106 Student's Hand-book of Medicine. 
 
 The convolutions seen on the mesial surface of the hrain 
 are — 
 
 Gyrus fornicatus. 
 
 Marginal. 
 
 Hippocampal (uncinate). 
 
 Dentate. 
 
 Quadrate (Prsecuneus). 
 
 Cuneus. 
 
 Paracentral lobule. 
 
 INTERIOR OF CEREBRUM. 
 
 Internally the cerebrum consists of white matter, and 
 ganglionic masses of grey matter. The solid mass of white 
 matter above the corpus callosum is termed the centre ovale. 
 
 Below the corpus callosum is an irregular and somewhat 
 T shaped cavity, divided by septa into smaller spaces, termed 
 ventricles. The ventricles communicate with each other by 
 variously named canals — thus, the lateral ventricles com- 
 municate with each other and the third ventricle, by the 
 foramen of Munro ; the third and the fourth ventricles by 
 the " iter " or aqueduct of Sylvius ; the fourth ventricle and 
 the sub-arachnoidal space by the foramen of Majendie. 
 
 Basal Ganglia are masses of gr6y matter situated at the 
 base of the brain, viz. — 
 
 1. The Corpora Striata, consists of two portions — 
 
 (1) Caudate nucleus := intra-ventricular portion. 
 
 (2) Lenticular nucleus = extra-ventricular portion. 
 
 2. Optic Thalami contain sensory and optic fibres. The 
 upper part of each thalamus appears in the lateral ventricles. 
 The under surface rests upon the crura cerebri. (Between the 
 lenticular nucleus externally, and the caudate nucleus and optic 
 thalamus internally, lie the mass of white matter termed the 
 internal capsule. See page 61.) 
 
Blood Supply of the Brain. 107 
 
 3. Glaustrum is a narrow band of grey matter outside the 
 lenticular nucleus. Function unknown. (See page 62.) 
 
 4. Corpora Oeniculata are masses of grey matter in con- 
 nection with, the optic tracts. 
 
 5. Corpora Quudrigemiiia contain sensory fibres, and are 
 also implicated in the movements of the eye. 
 
 6. Pineal Gland. Function unknown. 
 
 BLOOD SUPPLY OF THE BRAIN. 
 
 The arteries of the brain are derived from the two internal 
 carotids, and the two vertebral arteries.- 
 
 The branches are practically arranged in two sets, viz. : — 
 The Cortical group — (anterior, middle, and posterior cerebral 
 arteries). 
 
 The Basal group — (comprising the circle of Willis, and the 
 central arteries passing from it. 
 
 The circle of "Willis may be represented in tabular form. 
 
 In front 
 Antbbiob Communicating. 
 
 On each side. 
 Antekiok Cbrebkal. Antemok Ceeebeal. 
 
 Internal Carotij). Internal Carotid. 
 
 PosTEEioK Communicating. Posterioe Communicating. 
 
 Behind the 
 
 Two Posterior Cerebrals, 
 
 Branches of the 
 
 Basilar. 
 
 So many pathological conditions result from Cerebral hiemor- 
 rhage, that special attention should be directed to the course of 
 the middle cerebral artery, branches of which so often rupture, 
 that it is really the artery of hsemorrhage, 
 
108 Student's Hand-book of Medicine. 
 
 Middle Cerebral or Sylvian Arteries are the largest branches 
 of the internal carotid, and pass upwards and outwards in the 
 fissure of Sylvius till they reach the surface of the island of Reil, 
 where they ramify in the pia mater, forming part of the cortical 
 system of arteries ; they anastomose freely with the anterior 
 and posterior cerebral arteries. Other branches, furnished 
 through the anterior perforated spot to the corpus striatum, 
 are all terminal arteries and belong to the " ganglionic system " 
 of branches. They are (1) the lenticular; (2) the lenticulo- 
 striate ; (3) the lenticulo-optic. 
 
 Cerebral Veins. — The veins do not accompany the arteries, 
 but open into the various sinuses in the dura mater. They are 
 arranged in two sets. 
 
 1. The Superficial set, which open into the superior longi- 
 
 tudinal, the lateral, and cavernous sinuses. 
 
 2. The Deep set, which gather the blood from the interior 
 
 of the brain, and empty into the straight siuus. 
 
 The special characters of the cerebral circulation are — 
 
 1. The free anastomosis at the circle of Willis, which pro- 
 vides a ready supply of blood from other vessels in case of the 
 sudden blocking of any of the more direct channels. 
 
 2. The tortuous course through bony canals of the arteries as 
 they enter the skull, thus mitigating the force of the heart's beat. 
 
 3. Their ramifications in the pia mater before entering the 
 substance of the brain. 
 
 4. The thinness of the arterial walls, and the smallness of 
 the capillaries. 
 
 5. The existence of venous sinuses which are without valves, 
 and which do not run with the arteries ; the larger arteries, in 
 fact, having no companion veins. (" "Whitaker's Anatomy of 
 the Brain and Spinal Cord.") 
 
Functions of the Brain. 109 
 
 SUMMARY OF THE FUNCTIONS OF 
 THE BRAIN. 
 
 It has long been known that the cerebrum contains the 
 highest nerve centres — viz., those centres v^hose activity is 
 associated with volition, intelligence, thinking, consciousness, 
 and analysis of sensation, etc.; but, it was not proved untO. 
 recently (1882), that the cortex is sensible to direct excitation. 
 Hitzig and Fritsch in Germany; Ferrier, Horsley, and others 
 in England, have not only proved that the cortex itself is 
 sensible to irritation, but, in addition they have shown that 
 the brain does not act as a whole in all its various functions ; 
 indeed, on the contrary, certain parts have special duties 
 allotted to them ; in other words, " Stimulation of certain areas 
 cause definite and particular movements, sensations, etc." 
 
 The Localisation of such areas are briefly — 
 
 1. The Frontal lobes which are concerned in the higher 
 psychical functions. 
 
 2. The Rolandie area — associated with motor functions. 
 
 3. The Occipital lobes which have to do principally with 
 sensation. 
 
 Tabulated, we have the following centres — 
 
 1. The motor centres for the legs, arms, face, lips, and 
 tongue (in order from above downwards), in the region of 
 the ascending frontal and ascending parietal convolutions. 
 
 2. The centre for speech is in the left inferior frontal con- 
 volution. (If the person be left handed, the speech centre is 
 in the right convolution.) 
 
 Sensory Centres. 
 
 3. The centres for sigJit are in the occipital lobe and angular 
 gyrus (see "Optic Nerve.") 
 
110 Student's Hand-book of Medicine. 
 
 4. The centres for smell and taste are in the hippocampal 
 region in the temporal lobes. 
 
 5. The centres for hearing are in the superior temporo- 
 sphenoidal lobes. 
 
 The results of stimulation of these centres are seen on 
 the opposite side of the body, though sometimes they are bi- 
 lateral (especially as regards movements of the eyes, trunk, 
 and mouth). 
 
 In the case of speech, not only does the cortical centre of 
 one side govern the intricate movements of the mouth and 
 throat, but the right centre may actually loose its power or 
 function. Cases have been frequently recorded where, through 
 disease of the left frontal lobe, speech for a time has been 
 entirely abolished, but, regained in time through the right 
 centre re-acquiring its function — in these cases the patients 
 have had to learn language as a child does. 
 
 It only remains now for us to consider a few more simple 
 facts, then, I think, brain diseases will be rendered fairly iu- 
 teUigible, even to a beginner. 
 
 Note that irritation causes increased action ; paralysis abolish 
 the functions of the centres. It must also be remembered that 
 though the cerebral cortex alone has to do with sensation and 
 voluntary movement, these functions may be abolished by 
 interrupting the afferent and efferent fibres to and from the 
 cortex. The cortex, in fact, is the commander-in-chief; it 
 receives its information by means of inferior officers — basal 
 ganglia, afferent nerves, etc. ; and then issues its orders through 
 a similar efferent mechanism. The functions of the basal ganglia 
 will now be readily understood. They are subordinate centres 
 conveying and receiving orders from the cerebrum, but they are 
 also able to act as it were, on their own responsibility as regards 
 certain complex reflexes and co-ordination of movements ; thus, 
 the optic thalami contain a large number of sensory fibres 
 passing to the brain, and also a number of filaments in con- 
 nection with vision. Lesions of the optic thalamus, or of the 
 
J?T TROPHIC REOLM 
 ARM 
 
 EXTERNA-t 
 .^-■J-'' CAPSULE 
 
 CLAUSTRUM 
 
 Diagrammatic Drawing intended to show the effect of lesions interrupting 
 the motor fibres at various levels. Observe a lesion at 1 involves but few fibres ; 
 at 2, a much larger number. Note the relations of the facial nerve at 3 and 4. 
 (See Hemiplegia and Bell's Paralysis.) 
 
Functions of the Brain. Ill 
 
 corpora striata do not produce entire loss of sensation, but only 
 in proportion to the number of sensory fibres interrupted en route 
 to the brain. Indeed, when a lesion in this neighbourhood is 
 followed by loss of sensation, it is probably due to implication 
 of the posterior limb of the internal capsule. 
 
 Summary of the effect of lesions (destructive and irritative) 
 from the cortex to the spinal cord. 
 
 2%e Cerebral Cortex. — Destructive lesions produce paralysis 
 of the opposite muscles of the body ; as the motor fibres are cut 
 off from the first trophic realms secondary degeneration occurs, 
 causing the paralysis to be of a spastic nature. Note that the 
 fibres are spread out in a fan-like manner, so, consequently, the 
 lesion may only affect a few fibres going to one or more groups 
 of muscles. 
 
 Irritative lesions are described under " Jacksonian epilepsy." 
 
 Centrum Ovale. — A lesion will involve a larger number of 
 fibres than in the cortex. 
 
 Internal Capsule. — The motor and sensory fibres here con- 
 verge to the posterior limb. A lesion usually produces typical 
 hemiplegia (which see). 
 
 Crura Cerebri. — A lesion produces a similar hemiplegia, but 
 owing to its relations with the third nerve, the ocular muscles 
 may be paralysed on the same side, i.e., on the same side as 
 the lesion. 
 
 Pons. — Note that here the sixth and seventh nerves may 
 be paralysed in the resulting hemiplegia (see seventh nerve). 
 Eemember the crossed nature of the paralysis before-mentioned. 
 
 Clinical considerations — 
 Lesions of the cranial contents cause either irritation or 
 paralysis of the nervous apparatus, motor, sensory, or reflex. 
 Irritation of motor structures is shown by muscular twitchings 
 or spasms ; irritation of sensory parts causes pain and hyper- 
 CBsthesia ,■ irritation of reflex nerve centres leads to increased 
 reflex action. 
 
112 
 
 Student's Hand-book of Medicine. 
 
 Motor paralysis is estimated by noticing the posifion of 
 the limbs, the absence of all resistance to passive movements, 
 and stertorous breathing, or flapping of the lips and cheeks 
 with respiration. 
 
 Sensory paralysis is recognised by the insensibility of the 
 patient to all external impressions, such as sound, light, 
 pinching, pricking. 
 
 Reflex palsy is specially, indicated by a fixed condition of 
 the pupils, and the failure of contraction of the orbicularis 
 palpebrarum when the conjunctiva is stimulated. 
 
 DIFFUSE IRRITATION. 
 
 1. Increased insenai - 
 bility ; patient shows great 
 irritability of temper. 
 
 2. Beapiration may be 
 quick. 
 
 3. Falae quick. 
 
 4. Fupila contracted. 
 
 5. Reflexes exaggerated. 
 
 6. Increased irritability 
 of organic reflexes. 
 
 7. Cornea on acme time 
 after injury, or insidiously 
 from diaease. 
 
 8. Vomiting eommon. 
 
 COMPRESSION, 
 
 1. Total inaensibility. 
 
 2. Respiration stertor- 
 ous, slow, and puffing. 
 
 3. Pulse full, alow, 
 laboured. 
 
 4. Pupils widely dilated, 
 or sometimes one dilated 
 and the other normal or 
 contracted. 
 
 5. Sphincters may be 
 paralysed, but bowela are 
 torpid. 
 
 6. Bladder paralysed. 
 Consequent retention of 
 urine. 
 
 7. Does not usually 
 appear at moment of injury, 
 but often preceded by signs 
 of irritation, 
 
 8. Vomiting may occur 
 — not usually. 
 
 CONCUSSION. 
 
 1. Insensibility, from 
 which patient oan uauaJly 
 be partly aroused. 
 
 2. Respiration feeble, 
 like that of a person in a 
 faint condition. 
 
 3. Pulse weak, irregular, 
 and often frequent. 
 
 4. Pupila variable, but 
 usually sensitive to light. 
 
 6. Bowela relaxed, but 
 sphincters not paralysed. 
 
 6. Bladder can 
 water. 
 
 expel 
 
 7. Comes on inatantane- 
 oualy and jjasaes off 
 gradually after injury. 
 
 8. Vomiting as recovery 
 is taking place. 
 
 We have thus seen that the brain is the initiator or starter 
 of impulses on the one hand, and exercises a controlling or 
 inhibitive power on the other hand. In other words — on the 
 normal exercise of brain function depends the healthy activity 
 of every organ and structure in the body ; but the carrying out 
 of this function is dependent on a perfect maintenance of the 
 anatomical and physiological relations of the component parts. 
 Lastly, remember that just as the commander-in-chief of an army 
 may be temporarily absent without any great disadvantage, so 
 
Cerebral Ilcemorrhage. 113 
 
 is it possible for life to be maintained, and, indeed, a fair 
 standard of bealtb to persist for a time, after tbe higher centres 
 have been destroyed or abolished by disease. Such a condition, 
 however, can only last for a limited period, for the inhibitive 
 power being removed, the reflexes run riot, harmony is replaced 
 by anarchy, premature decay supervenes, and often speedy 
 death terminates a miserable existence. Paralysis of the insane 
 furnishes an example of this. 
 
 CEREBRAL HAEMORRHAGE. 
 
 .etiology. — It occurs most frequently in men in advanced 
 life. Amongst the more important pre-disposing causes are — 
 
 1. A certain type of build — viz., stout, plethoric men, with 
 short, thick necks. 
 
 2. Certain diathesis, — hsemophilia, gouty, etc. 
 
 3. Certain occuptions — viz. (1) butchers, publicans, by pro- 
 ducing arterial changes through excessive consumption of nitro- 
 genous food and alcohol; (2) carters, hammermen, etc., by 
 producing vascular strain. 
 
 4. Certain blood diseases — leucocythsemia, pernicious 
 ansemia, scurvy, Bright's disease, syphilis, etc. 
 
 5. Removal of the natural vascular support, as in the 
 cerebral softening. 
 
 6. Injuries from without the cranium, etc. 
 
 The most important immediate factors, however, are — 
 
 1. Disease of the vascular walls. — 
 
 (1) Miliary and other aneurismal dilatations. 
 
 (2) Atheroma. 
 
 (3) Fatty degeneration. 
 
 (4) Waxy degeneration. 
 
 2. Vascular strain. 
 
114 Student's Hand-book of Medicine. 
 
 Site of the Haemorrhage. — The most common form of cere- 
 bral haemorrhage is into the substance of the brain, and is usually 
 due to rupture of the lenticulo-striate branch of the middle 
 cerebral artery which supplies (as we have seen) the basal 
 ganglia. The explanation why this artery is so frequently 
 ruptured, is probably due to the fact that it is the most direct 
 branch of the middle cerebral, which is in turn the most direct 
 branch of the internal carotid. 
 
 Anatomical Changes. — If the haemorrhage be severe it tears 
 up the brain tissue, or it may destroy the basal ganglia, and 
 bursting into the lateral ventricles distend them, and flow 
 through the aqueduct of Sylvius into the fourth ventricle. 
 The hsemorrbage, however, may be small. The subsequent 
 changes in the effused blood are of the utmost importance, 
 viz. ; — 
 
 1. Changes in the clot — 
 
 (1) Retraction and exudation of serum (which is partially 
 
 absorbed). 
 
 (2) Discolouration of the clot through infiltration of 
 
 leucocytes, and partial breaking-down of red 
 corpuscles. 
 
 (3) Formation of hsematoidin crystals. Hamatoidin is 
 
 a form of reduced hsematin which contains no 
 iron. (It cannot be formed artificially.) 
 
 (4) Formation of a fibrous scar. 
 
 2. Changes in the tissues around — 
 
 (1) Irritation causing hypersemia. 
 
 (2) Diapedesis of leucocytes, and proliferation of the 
 
 tissue cells. 
 
 (3) Increased fibrous formation, forming a capsule around 
 
 the clot. 
 
 The above are favourable terminations; but, too fre- 
 quently the inflammatory reaction is intense, the vessels become 
 
Cerebral Haemorrhage. 115 
 
 thrombosed, and the brain substance thus cut oflf from nutri- 
 ment, rapidly breaks down (red softening) ; or the process may 
 be less acute, but also attended with purulent degeneration 
 (white softening), in such a case a " central abscess " is often 
 thus produced. 
 
 3. Changes in the fibres interrupted by the haemorrhage, and 
 thus cut off from the first trophic realm (cortex). Secondary 
 descending degeneration occurs of the motor tracts on the 
 affected side. 
 
 Summary. — After cerebral haemorrhage, if the patient sur- 
 vives the primary shock (the apoplectic fit), he has to run the 
 gauntlet of — 
 
 1. Eeaction. (Inflammation of brain substance, softening, 
 
 and abscess formation may occur.) 
 
 2. Eesulting motor-paralysis (hemiplegia). 
 
 3. Secondary degeneration of motor fibres, and possible 
 
 involvement of important nerve nuclei. 
 
 Symptoms. — There may be premonitory warnings of the 
 attack, such as giddiness, headache, etc. The attack may 
 occur when the patient is resting or asleep, but much more 
 frequently is it directly attributable to an over-loaded stomach, 
 a severe strain, coughing, or the exertion in running to catch 
 a train. Apoplexy is not synonymous with cerebral hasmor- 
 rhage; stUl, the condition which supervenes on such a lesion 
 is generally summed up in the description of an — 
 
 Apoplectic Fit. — The patient is suddenly seized with severe 
 pain in the head, feels faint, giddy, and quickly falls into a state 
 of collapse, which in a short time passes into a comatose con- 
 dition. The face is flushed, the pulse full and tense, breathing 
 stertorous, and cheeks puffed out. The snoring noise is due 
 to the paralysed tongue and palate falling back, and impeding 
 the entrance of air. The pupils are dilated or irregular. The 
 limbs at first are flaccid, but soon become somewhat rigid (so- 
 called early rigidity). The skin reflexes are lost, but the deep 
 
116 Student's Hand-book of Medicine. 
 
 reflexes are increased. The head and eyes are usually turned 
 to one side — i.e., patient looks towards the lesion away from 
 the paralysed side (conjugate deviation). When the case is 
 going to end fatally, the coma increases, temperature falls, and 
 Cheyne-Stokes' respirations usher in the fatal end. In favour- 
 able cases the primary disturbance is not so grave, and the 
 patient may regain consciousness in a few hours, or even after 
 two or three days. Eecovery, however, is rarely complete, but 
 usually with more or less paralysis or typical hemiplegia. 
 
 HEMIPLEGIA. 
 
 By hemiplegia is meant paralysis of the face, arm, and leg 
 of the opposite side. The reason why the trunk and eyes are not 
 usually affected, according to Broadbent, is briefly as follows : — 
 " That when groups of muscles are usually associated together, 
 there must be commissural fibres running between the centres 
 in either hemisphere. These fibres are so well drilled by 
 constant stimulation, that if one centre be destroyed, the 
 opposite centre is equal to the task of commanding the well 
 disciplined fibres on both sides, and consequently both sets of 
 muscles act harmoniously." 
 
 Causes. — Though most commonly the result of a free 
 haemorrhage, embolism, or thrombosis, hemiplegia may be 
 caused by depressed fractures, tumours, etc., involving the 
 motor fibres anywhere between the cortex and the medulla; 
 the symptoms will also vary with the sites of such lesions. 
 
 Symptoms. — "When the hemiplegia is not preceded by an 
 apoplectic fit, the patient often first becomes aware of anything 
 wrong by finding on awakening from sleep — 
 
 1. Loss of power on one side, or 
 
 2. Difficulty in speaking, or even loss of speech. 
 
Embolism and Thrombosis. 117 
 
 Unconsciousness may develop and pass into complete coma^ 
 or, instead of unconsciousness there may be only a feeling of 
 cloudiness or bewilderment, wHcli may or may not develop 
 into coma. 
 
 The arm is usually paralysed to a greater degree than the 
 leg. The tongue is not put out readily, and deviates towards 
 the paralysed side. Sensation is rarely affected to a marked 
 extent. The facial paralysis has already been described (page 
 98), but we may again note it implicates the loioer part of the 
 side affected, thus differing from true Bell's paralysis. As time 
 wears on, certain important symptoms appear, as a result of the 
 secondary degeneration of the motor fibres cut off from their 
 trophic centres. The limbs before flaccid, now become rigid. 
 The arm is flexed at the elbow, and resists extension ; fre- 
 quently the wrist and fingers are also flexed. Atrophy does 
 not usually occur, but there may be wasting consequent on 
 non-use. The reflexes are exaggerated, and ankle clonus is 
 often obtained. 
 
 The later changes are — peculiar tremors of the affected limbs, 
 enlargement of the joints, and inability to maintain one position 
 of the flngers and toes (athetosis), post hemiplegic chorea, etc. 
 Eemember the peculiarities before mentioned, when the lesion 
 is in the crus (third nerve), or pons (sixth and seventh nerves). 
 
 Diagnosis must be made from hysterical paralysis, which 
 often simulates very closely the organic lesion. 
 
 EMBOLISM AND THROMBOSIS. 
 
 Instead of a free extravasation of blood we may get blocking 
 of blood-vessels through detached clots (embolism), or a local 
 clotting of blood (thrombosis). The following table shows the 
 more important points. 
 
118 
 
 Student's Hand-hook of Medicine. 
 
 Diagnostic Table. 
 
 CEKBBKAL EMBOLISM. 
 
 Causes. — 
 
 Most commonly associated with 
 valvular lesions of the heart, aneur- 
 isms, or a suppurating thrombus. 
 
 Sex. — 
 
 Most frequent in females. 
 Onset. — 
 
 Sudden — no prodromal symp- 
 toms. 
 Convulsions. — 
 
 Rare. 
 
 Paralysis. — 
 
 A sudden hemiplegia of the 
 right side, with aphasia. 
 
 Consciousness. — 
 
 Not Visually entirely abolished. 
 
 CEREBRAL THROMBOSIS. 
 
 Causes. — 
 
 1. Atheroma and morbid states 
 of the arteries, as seen in chronic 
 Blight's disease, syphilis, pyeemia, 
 etc. 
 
 2. Pressure upon the veins or 
 arteries. 
 
 Sex. — 
 
 Equally frequent in both sexes. 
 Onset, — 
 
 Gradual — with prodromal symp- 
 toms. 
 Convulsions. — 
 
 Convulsive attacks are common, 
 and may exist for some time in 
 venous thrombosis. 
 
 Paralysis may occur suddenly 
 in arterial thrombosis, but aphasia 
 is not so common. 
 
 Profound coma supervenes. 
 
 Lastly, we must remember that hsemorrliage, embolism, or 
 thrombosis, may be confined to the small vessels of the cortex 
 alone. 
 
 In cortical hcemorrhage — 
 
 1. Consciousness is seldom completely lost at the onset of 
 paralysis. 
 
 2. The resulting paralysis is of a " monoplegic " type. 
 
 3. The paralysis is often transitory. 
 
 4. Eigidity of affected muscles comes on earlier. 
 
 5. Prognosis is much more favourable. 
 
Embolisin and ThroTnibosis. 119 
 
 Anatomical Changes following thrombosis ,and embolism 
 will vary accordiag to the site and size of blood-vessels affected. 
 Briefly, the ultimate results are degeneration and softening of 
 the parts supplied by the affected artery. Blocking of a ter- 
 minal artery causes the affected area to look slightly paler at 
 first ; then extravasation from the engorged veins or collateral 
 circulation may take place and cause an infiltration of blood. 
 The resulting softening may be of the red, yellow, or white 
 types, and the clot undergoes the changes before described. 
 Two things the student must remember — 
 
 1. If the clot be of a septic nature, an abscess is likely 
 to form. 
 
 2. If not septic, it is surprising how slow the symptoms 
 dependent on softening develop. 
 
 Blocking of particular arteries. 
 
 1. Vertebral. — Eare, left more common than right. The 
 symptoms are those of acute bulbar paralysis. 
 
 2. Basilar. — Bilateral paralysis with rise of temperature. 
 
 3. Posterior Cerebral. — Affections of vision and hemi- 
 ansesthesia (posterior portion of internal capsule). 
 
 4. Middle Gerebral. — Hemiplegia with aphasia. 
 
 5. Anterior Gerebral. — Grave interference with the higher 
 intellectual faculties. 
 
 Treatment of Cerebral Hfemorrhage. — Place the head high, 
 and put ice to head, and warmth to feet ; administer an enema, 
 calomel grains v. on the tongue, or a minim of croton oil. Vene- 
 section should be performed if the pulse is full and of high 
 tension ; if, on the other hand, the pulse be weak, or we are 
 fairly certain the symptoms are due to thrombosis or embolism, 
 it is best not to resort to bleeding. The resulting paralysis must 
 be treated on the general principles detailed in the chapter on 
 Chronic Nerve Lesions. 
 
120 Student's Hand-book of Medicine. 
 
 APHASIA. 
 
 Aphasia is a morbid condition consequent on a cortical lesion 
 ■whereby speech, writing, or reading may become impaired either 
 from (1) an inability to co-ordinate the necessary movements 
 involved in speech; or (2) from a defective interpretation of 
 sounds or visual impressions. 
 
 To understand the various forms of aphasia it is necessary 
 iirst to consider the factors employed in expressing our thoughts. 
 Language is gradually learned. For instance, a child has first to 
 learn the movements necessary to articulate the word. Having 
 learned the word, he then associates it with a particular some- 
 thing he has seen or heard. Later, he learns the alphabet — that 
 is, he invests certain letters with definite sounds and meanings, 
 and as his vocabulary increases he can express ideas in speech, 
 and finally spell and write. Thus, intelligent and rational 
 speech, though apparently simple, involves many complex pro- 
 cesses. It requires — 
 
 1. The aid of memory to co-ordinate the necessary ideas 
 formed by incoming impressions derived through hearing, see- 
 ing, and in the case of the blind, through the sense of touch. 
 
 2. A mechanism by which these ideas can be spoken and 
 written. 
 
 In short, speech involves a healthy continuity between — 
 
 The chief motor centre in the left inferior frontal lobe, 
 and the visual and acoustic centres on the one 
 hand, and — 
 
 The chief motor centre and the muscles employed in 
 speech, writing, or reading aloud. 
 
 Lesions of the occipital lobe cause word blindness — i.e., 
 the patient can see print, but cannot read it. 
 
 Lesions of temporo-sphenoidal lobe cause word deafness 
 
 the patient hears, but does not understand words. 
 
Twnwu/rs in the Brain. 
 
 121 
 
 A large number of forms of aphasia are described, but they 
 cannot be gone into here. Two forms will only be described — 
 i.e., sensory. and motor aphasia : — 
 
 MOTOE APHASIA. 
 
 Patient is almost speechless, but 
 may manage words like oaths, yes, 
 or no. 
 
 Understands what is said to him. 
 
 Cannot repeat words. 
 Cannot write words hut can copy. 
 Is aware of his errors — he can 
 recall words but cannot utter them. 
 
 SENSORY APHASIA. 
 
 Has a slightly greater command 
 over words in a purely automatic 
 manner, and may make the same 
 stilled remark to all questions. 
 
 Cannot understand what is said 
 to Mm (word deafness). 
 
 Cannot repeat words. 
 
 Is unaware of his mistakes — he 
 cannot recall to his mind the mean- 
 ing of words. 
 
 TUMOURS IN THE BRAIN. 
 
 The most important are — 
 
 1. Tubercle. — They may vary in size from a millet seed to 
 a hazel nut. Usually they are multiple, and most common in 
 the cerebellum and about the base of the brain. Histological 
 characters are the same as already described under tuberculosis. 
 
 2. Glioma, or neuro-glioma.—Thej are usually dense, firm 
 tumours, but may be soft and vascular. Histological characters 
 consist of round or oval nucleated cells, with branched pro- 
 cesses, forming a network. Often enormous, single-nucleated, 
 spindle-shaped cells are present. They are usually innocent 
 tumours, and may remain for years without creating very 
 marked symptoms. 
 
 3. Sarcoma — attacks the membranes and pons — may attain 
 a large size. 
 
 4. Sarco-glioma — found chieily in the retina. They differ 
 from simple glioma in a tendency to assume a malignant 
 character. 
 
122 Stvdent's Hand-book of Medicine. 
 
 5. Carcinoma — rare — secondary to cancer elsewhere. 
 
 6. Cysts — may be tlie result of — 
 
 (1) Hsemorrhage. 
 
 (2) Congenital defects. 
 
 (3) Hydatids. 
 
 Symptoms. — They vary according to the site, size, and 
 nature of the tumour. The more constant symptoms are — 
 
 1. Headache. — May be diffuse, and dull aching' in char- 
 acter, but is much more often of aii acute stabbing nature, 
 persistent, and localised. 
 
 2. Vertigo. — A most marked symptom, especially when the 
 tumour affects the cerebellar region. 
 
 3. Vomiting. — Very persistent, and occurs whether food be 
 taken or not. 
 
 4. Double Optic Neuritis. — Choked disc (is almost partho- 
 gnomonic). 
 
 5. More or Less Mental Disturbance. — Sometimes absent, 
 but the patient is nearly always either highly emotional or dull 
 and apathetic. 
 
 6. Motor Disturbance. — There may be slight paralysis of a 
 monoplegic type, but much more frequently convulsions of a 
 Jacksonian type occur. 
 
 Whilst the above are the cardinal symptoms, it is easy 
 to see that the symptoms may be very numerous, and on the 
 other hand, very obscure. Inco- ordination, spastic rigidity, 
 nystagmus, and hydrocephalus are frequently present. 
 
 Diagnosis. — Having well considered the various symptoms, 
 if they are pronounced, little difficulty will be experienced on 
 approximating the site of the tumour ; but, when obscure, the 
 diagnosis will have to be made from cerebral softening, cerebral 
 abscess, uraemia, and hysterical paralysis, etc. 
 
Meningitis. 123 
 
 Treatment — 
 
 Medical. — If sypMlitic, iodide of potassium in heroic 
 doses; other forms are practically unamenable, at least to any 
 known medicinal treatment. 
 
 Surgical. — Trephine and remove if possible, but few cases 
 are available for this treatment. Consult a surgical work 
 for details. 
 
 Though so many cases cannot be permanently benefited by 
 treatment, everything should be done to make the patient's life 
 bearable, by relieving pain, etc., with opiates. 
 
 MENINGITIS. 
 
 Inflammation of the meninges of the brain is of two 
 types, i.e. — 
 
 1. The simple or traumatic form, attacking most frequently 
 the convexity of the brain. 
 
 2. The tubercular form, which principally affects the base of 
 the brain, and is usually part of a general tuberculosis. 
 
 THE SIMPLE FORM. 
 
 Causes. — Injuries of all kinds to the skull, extension of 
 infla,mmation from other parts — i.e., disease of the middle 
 ear, irritation from tumours, minute haemorrhages, etc., or as 
 a complication in fevers, syphilis, etc. The inilammation may 
 be most marked in one membrane, and thus, when the dura 
 mater is principally involved, it is called pachymeningitis; when 
 the arachnoid and pia mater are most affected, it is termed lepto- 
 meningitis. Such distinction is of doubtful value in the acute 
 form, though it is well to remember such forms in the chronic 
 variety. Bear in mind also that the dura mater acts as the 
 periosteum to the inner table, so therefore it is easy to see lepto- 
 meningitis is most common when the cause is from within the 
 cranium ; pachymeningitis when the causes are from without. 
 
124 Student's Hand-book of Medicine. 
 
 Symptoms. — They are divided into three stages. — 
 
 1. Premonitory. — Headache, more or less constant ; vomiting 
 and restlessness. 
 
 2. Stage of Irritation is marked by febrile symptoms, great 
 intolerance of light, contracted pupils, exaggerated reflexes, and 
 convulsions. The patient lies curled up in a characteristic 
 manner. 
 
 3. Stage of Compression. — Temperature tends to fall, irri- 
 tability is replaced by stupor, and convulsions by paralysis. 
 Pupils now become uneven or dilated. Optic neuritis may 
 rapidly develop. The peculiar cephalic cry is a constant 
 sjTnptom. Cheyne-Stokes' breathing, involuntary escape of 
 fseces and urine, and stertorous breathing, usher in death, 
 ■which often takes place very soon after the onset of grave 
 symptoms. 
 
 Pathology. — 
 
 1. Hyperaemia of the meninges which become swollen and 
 injected. 
 
 2. Exudation of lymph. 
 
 3. Efiusion, which rapidly becomes purulent. 
 
 THE TUBBECULAR POEM. 
 
 The symptoms of the tubercular form of meningitis are also 
 divided into three stages — 
 
 1. Prodromal. — The child usually shows more or less definite 
 symptoms of the tubercular diathesis, such as, emaciation, want 
 of appetite, constipation, alternating with diarrhoea ; irrita- 
 bility of temper, and headache, perhaps form the more common 
 features, untU definite symptoms of the meningeal affection 
 arises. 
 
 2. Irritative Stage. — The symptoms are similar to those 
 described under the simple variety, but the head is usually 
 
Meningitis. 125 
 
 more retracted and neck more rigid ; abdomen is hollowed out 
 or boat-shaped, temperature oscillates, internal strabismus, and 
 often marked vaso-motor paralysis (taehe eerehrale). 
 
 3. Compression Stage. — The symptoms that accompany 
 coma develop, and death may take place in from ten days 
 to six weeks from the onset of acute symptoms. 
 
 Pathology. — The inflammatory conditions associated with 
 the presence of tubercle, viz. — 
 
 1. Invasion of the bacilli into the meninges (pia mater 
 principally), and formation of tubercles. 
 
 2. Irritation set up by the tubercles. The tubercles may 
 then go through the stages of (1) softening, (2) bacillary 
 liquefaction — (formation of a greenish pus,) or (1) fatty de- 
 generation, (2) caseation, with very little lymph, (3) calcification 
 (rare). 
 
 The down-grade process seems to commence in the peri- 
 vascular tissue of the Sylvian and other arteries at the base 
 of the brain, hence the ventricles are often distended, and the 
 brain substance flattened up against the skuU. Hydrocephalus 
 has been produced by thus obstructing the veins of Galen. 
 
 Treatment — 
 
 Simple Meningitis. — Eemove any obvious cause ; darken 
 the room ; shave the head and apply ice ; administer a calomel 
 purge, bromides, hyoscyamus, and potass, iodid. Support the 
 patient with fluid nourishment, and prevent bed-sores and over 
 distension of bladder during the later stages. 
 
 Tubercular Meningitis. — This form needs no different treat- 
 ment after symptoms are developed, but during the prodromal 
 stage, everything should be done to combat the tubercular 
 condition by careful hygiene, diet, etc., with the administration 
 of cod-liver oil, fresh air, etc. 
 
126 
 
 Shident's Hand -hook of Medicine. 
 
 Diagnostic Table. 
 
 SIMPLE. 
 
 Age. — Any age. 
 
 Cause. — 
 
 Injury or local causes, fevers, etc. 
 
 Ccnirse. — 
 Short. 
 
 Convulsions. — 
 
 They may be present. 
 
 Abdomen. — Nothing marked. 
 
 Pathology. — 
 
 1. That of simple or suppurative 
 inflammation. 
 
 2. Attacks convexity of brain. 
 
 3. Ventricles not distended. 
 
 Prognosis. — 
 
 Almost hopeless. 
 
 TUBEKCULAR. 
 
 Age. — Young children. 
 
 Cause. — 
 
 No local cause, but symptoms 
 of tubercle elsewhere. 
 
 Course. — 
 
 Longer than simple, especially 
 the prodromal stage. 
 
 Conmilsions. — 
 
 Common,, even during the com- 
 pression stage, often precedes death. 
 
 Abdomen. — Markedly retracted. 
 
 1. That which is associated with 
 the presence of tubercle, and forma- 
 tion of peculiar greenish pus. 
 
 2. Attacks the base of brain. 
 
 3. Ventricles are distended, and 
 may cause hydrocephalus. 
 
 Prognosis. — 
 
 Depends on cause and extent. 
 
 DISSEMINATED SCLEROSIS. 
 
 Disseminated sclerosis, or the so-called " insular " paralysis 
 (want of insulation of the axis-cylinders being referred to as 
 a cause of this peculiar affection,) is a disease characterised 
 pathologically by scattered patches of sclerosis throughout the 
 central nervous system. The condition may be most marked in 
 the brain, or in the spinal cord ; but the cerebrospinal variety 
 is much more common. 
 
 .etiology occurs in youth or middle age ; both sexes are 
 liable to the affection. Exposure to cold, injuries, and mental 
 worry are possible exciting causes. 
 
Disseminated Sclerosis. 127 
 
 Pathology. — Patolies of sclerosis, sharply defined, and 
 varying in colour from pink to ashy greyj some hard and 
 leathery, others soft, are found scattered throughout the white 
 matter of the cord and surfaces of the medulla and cerebrum. 
 
 Symptoms. — With such wide spread pathological changes, 
 it is practically impossible to say what symptoms may, or may 
 not be present, as the symptoms will of course depend on the 
 site and extent of the sclerosed areas. Taking a typical case 
 however, we usually find the following symptoms more or 
 less marked : — 
 
 1. Impaired Speech. — The person has a slow, monotonous 
 way of pronouncing every syllable distinct, Uke the staccato 
 delivery of music. 
 
 2. A peculiar tremor of muscles, which become very marked 
 when voluntary movements are attempted; the movements of 
 the hands are specially embarrassed by the tremor, and directed 
 with difficulty. 
 
 3. Ifystagmus, worse on trying to fix the eyes. 
 
 4. Impaired sensibility. 
 
 5. Impaired intellectual functions, as loss of memory, etc. 
 
 6. More or less paresis with spasm. 
 
 7. Peculiar Gait. — There is marked inco-ordination of not 
 only the legs, but arms, trnnJc, and head. When walking, the 
 patient shoots suddenly forward or to one side, and may fall, 
 or bruise himself by bumping against various obstacles. 
 
 8. Occurence of peculiar apoplectic attacks, from which the 
 patient recovers in one or two days. 
 
 Diagnosis. — The peculiar gait and speech usually renders 
 the diagnosis easy, but remember that the dissemination of the 
 lesion might be due to an extension of a hitherto local lesion. 
 
128 Student's Hand-book of Medicine. 
 
 PARALYSIS OF THE INSANE. 
 
 (G.P.) 
 
 A condition marked by progressive derangement of the 
 mind accompanied by paralysis. 
 
 .etiology. — The disease seldom occurs before twenty years 
 of age — most frequently about forty. It affects the rich more 
 than the poor. The most important causes are excessive study, 
 drinking, and syphilis. 
 
 Pathology. — The post-mortem appearances vary greatly. 
 In some cases little anatomical change has been discovered ; 
 but, usually the following conditions exist : — 
 
 1. Thickening of the inner table of the skull, which is 
 
 marked by Pacchionian bodies. 
 
 2. Thickening of the membranes. 
 
 3. Degeneration of cerebral blood-vessels. 
 
 4. Patches of sclerosis throughout the white matter of 
 
 the cord and brain. 
 •5. Atrophy of the frontal lobes. 
 6. Distension of the ventricles by fluid. 
 
 Symptoms. — It is impossible to give a typical clinical 
 description, as individual cases vary so much. Perhaps it is 
 best to describe three stages : — 
 
 First Period marked by changed mental conditions such as — 
 
 1. Irritability of temper, jealousy, hallucinations. 
 
 2. Loss of memory. 
 
 3. Defective speech — patient is unable to repeat similar 
 
 or many syllabled words. 
 
 4. Exaltation of ideas, and loss of judgment. Patient 
 
 may fancy he is rich, or may buy a stud of 
 horses, order a banquet, etc. 
 
Hydrocephalus. 129 
 
 Second or Epileptiform Period. — 
 
 1. Patient has a series of convulsions which render his 
 
 mental condition worse than before. 
 
 2. Symptoms of paralysis appear ; first, in the execution 
 
 of fine movements, such as writing, etc.; later, the 
 paralysis involves the face and tongue, or paresis 
 of the limbs and common sensibility develops. 
 
 Third or Paralytic Stage. — 
 
 The mind finally totters, even to complete dementia. 
 The rectum and bladder act involuntary. Bed 
 sores form, and grave interference with the vital 
 centres, or pulmonary affections soon put an end 
 to a pitiful existence. 
 
 Whilst we have described three stages and sketched a clinical 
 course, cases occur where the symptoms are chiefly ataxic, plus 
 mental impairment ; or mental, pliis symptoms of disseminated 
 sclerosis ; but differential diagnosis or enumeration of the 
 various types cannot be entered into here. Eemember, however, 
 that the optic discs are not often affected, and wasting is rare ; 
 the patient often being fat, even to -the end. 
 
 Treatment. — Put patient under asylum treatment — i.e., use 
 common-sense principles, and by careful supervision, hygiene, 
 and diet, try to prevent the disease progressing. Rest, and 
 firm, hut gentle, control, do more good than drugs. 
 
 HYDROCEPHALUS. 
 
 Acute hydrocephalus has already been described under 
 tubercular meningitis. Under the term chronic hydrocephalus 
 is meant that form arising from — 
 
 1. Congenital malformations. 
 
 2. A low type of inflammation attacking the lining of 
 
 the ventricles during foetal life or early infancy. 
 
 K 
 
130 Student's Hand-hook of Medicine. 
 
 Morbid Anatomy. — 
 
 Skull. — Sutures fail to unite, and the skull as a whole does 
 not ossify as in health. A characteristic deformitj' thus develops 
 — viz., overhanging hrow, great increase of the circumference 
 of the cranium and its disproportion to the size of the face, 
 open fontanelles. 
 
 Ventricles. — They are distended — one, two, or more ventricles 
 may be affected. The lining is granular, and the ependyma 
 thickened. Fluid contains albumen, chloride of sodium, traces 
 of urea, cholesterine, flakes of lymph, etc. The quantity varies 
 — may reach fifteen pints or more. 
 
 Brain Substance — Is much compressed, convolutions flat- 
 tened out, and cortex much thinner. 
 
 Cranial Nerves. — Certain nerves may at first be inflamed, 
 and subsequently atrophy, especially the optic nerves. 
 
 Symptoms. — The size and shape of the head sufiiciently 
 indicate the nature of the disease, even at an early period ; 
 later, the symptoms that develop are — 
 
 1. Arrest of development generally. 
 
 2. Impaired digestive functions — distended abdomen, etc. 
 
 3. Walking power is slowly gained, or not at all. 
 
 4. Mental deficiency, sometimes complete idiocy. 
 
 5. Convulsions. 
 
 6. Condition of apathy, coma, and death, usually in 
 
 from five to seven years. Cases have been known 
 to attaia the age of thirty years. 
 
 Treatment. — Very unsatisfactory, if not hopeless : — 
 
 1. Pressure by strips of plaster or elastic bands. 
 
 2. Application of iodoform to scalp. 
 
 3. Puncturing at various intervals, and drawing off the 
 
 fluid. 
 
Paralysis Agitans. ' 131 
 
 FUNCTIONAL DISEASES OF NERVOUS 
 SYSTEM. 
 
 PARALYSIS AGITANS. 
 
 Shaking palsy or Parkinson's disease is an affection character- 
 ised by rhythmical contractions of certain muscles, progressive 
 weakness and deformity. 
 
 etiology. — It affects men more than women, and is rarely 
 found in patients under forty years of age. Hereditary ; 
 excesses in alcohol and tobacco; gout, etc., are put down as 
 the predisposing causes. 
 
 Symptoms. — They are very insidious; insomnia, unnatural 
 irritability and weakness of the limbs generally precede the 
 more characteristic symptoms, which are, — 
 
 1. Rhythmical contr action of certain muscles of the fingers 
 and arms ; the fingers are flexed with the thumb resting against 
 the forefinger, the alternating flexion and extension causes 
 movements like rolling pills. The tremors usually spread to 
 the leg of the same side, and finally trunk and face become 
 affected. The movements at first are . checked by voluntary 
 effort or support, but later (like chorea) the movements 
 are actually increased on attempting any voluntary restraint. 
 They cease during sleep. 
 
 2. Wealaness of the affected musdes. 
 
 3. Rigidity and contraction, causing deformity and peculiar 
 gait. The body is bent forwards, head held stiffly, the 
 " vertebra prominens " stands out in bold relief, and the 
 elbows are flexed at right angles and stand out from the 
 sides. The gait is very characteristic, the first steps are 
 hesitating and slow, but become quick, and the patient appears 
 to trot rather than walk. If the patient be gently pushed 
 
132 Student'-'i Hand-hook of Medicine. 
 
 forwards or backwards he is unable to stop himself. The 
 movements forward are called "festination," and backwards, 
 retropulsion. 
 
 4. Defect of Speech. — When the tongue is affected the 
 speech is at first quick, but becomes slow. 
 
 5. Certain subjective symptoms, hot flushes, rheumatic pains, 
 etc. 
 
 The disease runs a very chronic course, and is fatal only- 
 through some intercurrent diseases. 
 
 Pathology. — Unknown ; probably it is an advanced and 
 premature senile change in the cerebral cortex, rendering 
 certain motor points highly irritable, and diminishing at the 
 same time the inhibitive power of the brain. 
 
 Treatment. — Unsatisfactory. Arsenic, chloride of barium, 
 sedatives and attendance to hygiene and diet, avoidance of 
 alcohol, etc., are the chief lines to go upon. 
 
 CHOREA OR ST VITUS'S DANCE, 
 
 .ffitiology. — It is most frequently seen amongst female 
 children of the lower classes, between five and ten years of 
 age, and also during the adolescent period. Emotional or 
 hysterical children are prone to this affection, a point which 
 is of great importance when discussing the pathology of the 
 disease. Clinical records show a more or less constant relation- 
 ship between chorea, endocarditis, and rheumatism. However, 
 there are cases in which neither a history of rheumatism nor 
 endocarditis can be traced. 
 
 The Causes briefly are — 
 1. Disturbed mental conditions, brought about by hereditary 
 weakness, excessive study, school strain, and astigmatism, etc. 
 
Chorea or St Vitus'a Dance. 133 
 
 2. Imitating ch.oreic movements (very doubtful). 
 
 3. Endocarditis. 
 
 4. Eheumatism. 
 
 5. Traumatisms. 
 
 Pathology, — No constant lesion is found in chorea. Many 
 observers have noticed punctiform hasmorrhages in the cortex, 
 and also embolic plugging of the small capillaries; but such 
 conditions are not invariably found. The embolic condition 
 fits in well v^ith the theory, " That chorea is caused by detached 
 bits of endocardial vegetations which become arrested in the 
 cortical vessels, and there set up irritative changes." At present, 
 however, the pathology may be summed up as follows : — " An 
 altered condition of the cerebral cortex, in virtue of which, ex- 
 plosions of energy are discharged from the motor area, either 
 through want of inhihitive or controlling power, or as a result 
 of undue irritation and an/xmia of the motor cells caused by 
 minute emboli." 
 
 Symptoms. — 
 
 1. Are irregular and purposeless convulsive movements of 
 hands, facial muscles, etc., rendered worse on attempting to 
 execute voluntary acts, or fine movements — such as picking 
 up pins, conveying a cup to the lips, writing, or touching a 
 particular point, etc. Dr Sturges sums up the symptoms " as 
 an extremely exaggerated fidgetiness." The movements cease 
 as a rule during sleep. 
 
 2. Altered mental conditions are sometimes most marked ; 
 the patient laughing or crying in turns on being spoken to. 
 When these symptoms are present they point strongly towards 
 the "functional character of the disorder." 
 
 3. Characteristic attitude when in bed — child lies extended 
 in bed, twisted to one side (pleurosthotonos), and then changes 
 suddenly to an exactly opposite condition. 
 
 4. Irregular and rapid action of the heart. 
 
 5. Soft systolic murmurs at the apex of the heart. 
 
134 Student's Hand -hook of Medicine. 
 
 Treatment. — 
 
 1. Dr Goodhart insists upon rest in bed as the first and 
 essential point of treatment. 
 
 2. Careful attention to the bowels, in order to obviate any 
 reflex irritation from that quarter. 
 
 3. Arsenic and cod-liver oil. 
 
 As soon as convalescence seems established, allow the patient 
 plenty of fresh air and gymnastic exercises. 
 
 EPILEPSY. 
 
 A paroxysmal affection characterised by sudden attacks of 
 unconsciousness, with or without convulsions. Two forms will 
 be described under this heading — 
 
 1. Petit mal. 
 
 2. Grand mal. 
 
 Jacksonian epilepsy differs so much in tetiology, treatment, 
 and pathology, that it will be dealt with by itself. 
 
 .ffitiology. — The disease most frequently begins in early 
 childhood; probably one-fourth of the cases begin before the 
 child is ten years of age, and three-fourths between ten and 
 twenty years of age. When it begins in adults look for a local 
 cause; probably all such cases are either of a Jacksonian or 
 hysteroid type. 
 
 Heredity is a most important factor, in so far as children of 
 families in which insanity, hysteria, alcoholism, neuralgic affec- 
 tions, etc., are prone to this affection. 
 
 Exciting Causes. — Those put down are — 
 
 1. Excessive worry. 
 
 2. Puberty. 
 
 3. Masturbation. 
 
 4. Fright. 
 
 It will be seen that these "causes" are similar to those of 
 chorea, and such a list is probably the result of anything but 
 
Epilepsy. 135 
 
 careful analysis. Given, however, a person horn with a marked 
 and distinctly neurotic temperament, it needs little skiU to come 
 to the conclusion, that any undue cause of nervous irritation, 
 ranging from a tight foreskin to absolute debauchery, must be 
 potent factors in producing epilepsy. 
 
 Pathology. — At present it is entirely speculative. Reason- 
 ing from what we know through direct experiments on the 
 cortex, the great symptoms of epilepsy — i.e., loss of conscious- 
 ness, convulsions, and coma, point to a disturbance of the higher 
 centres of the cortex ; but the explanations given of such 
 disturbances are diverse and many. Thoy are — 
 
 1. Diminished resistance on the part of the grey matter 
 
 (GOWEKS). 
 
 2. A paroxysmal nerve storm, consequent on an unstable 
 
 condition of the motor cells (Hughlings Jackson). 
 
 3. Yasa motor changes in the medulla (Van der Kolk). 
 
 4. Disturbances of the basal ganglia (Faggb). 
 
 Symptoms. — 
 
 Grand mal — divided into three stages. — 
 
 1. Aura or warning, peculiar sensations felt in the 
 
 stomach, toes ; palpitation, or vertigo, etc. 
 
 2. Fit.— 
 
 (a) The patient drops down suddenly after uttering a 
 piercing shriek (epileptic cry). 
 
 (6) Tonic stage. — The head is turned to one side, the hands 
 clenched, and the muscles of the chest by their contraction 
 interfere with the respirations, so that the preliminary pallor 
 is succeeded by lividity. The pupils are dilated, eyes fixed, and 
 sensibility is abolished. This stage lasts from thirty to forty 
 seconds, and then passes into the — 
 
 (c) Clonic (Stogre.— Convulsions of the face quickly extend 
 to all the muscles of the body ; tongue may be pushed between 
 
136 Student's Hand-book of Medicine. 
 
 the teeth and bitten severely ; and the foam at the mouth is 
 then coloured with hlood. The face assumes a purplish hue, 
 and the eyes seem to protrude from their sockets. Urine, 
 semen, or faeces may escape involuntarily, and the pulse is often 
 much embarrassed by the muscular contractions. This stage 
 lasts about four minutes or so, and then the convulsions cease. 
 The breathing gradually becomes easier, features regain their 
 natural colour, and consciousness may be quickly recovered ; or, 
 what is more common, pass into the fourth stage — namely — 
 
 3. Post-epileptic condition. — Patient falls into a comatose 
 stage, succeeded by a natural sleep. Rarely in this form are 
 there post-epileptic maniacal manifestations. 
 
 Petit mal, or minor epilepsy. — 
 In this form the patient is suddenly seized with unconscious- 
 ness, the eyes become fixed, speech incoherent, but there are no 
 convulsions. The attacks vary much in severity. Sometimes 
 they are so sUght as not to be noticed by others than the 
 patient. This form of epilepsy must be remembered, for though 
 the fits are often trifling, yet, the "post- epileptic" condition 
 is sometimes of a very serious nature : two such forms are 
 described — 
 
 Post-epileptic conditions — 
 
 1. A condition in which the patient performs automatic 
 actions, of which he is then and afterwards entirely unconscious. 
 A father may kiU his child ; weU-to-do patients may steal ; etc. 
 
 2. A condition characterised by maniacal manifestations, 
 intense passion, etc. 
 
 Prognosis. — Frequency of epileptic attacks vary considerably. 
 Females are more frequently attacked during a menstrual period. 
 Epileptics may be fairly strong between the attacks, and finally 
 recover completely ; but too often some mental weakness shows 
 itself in. a permanent form. Imbecility has developed after a 
 few fits in children. The dangers during the fit must not be 
 forgotten — fatal falls, burns, or other injuries are common. 
 
Epilepsy. 
 
 137 
 
 Diagnosis. — Must be distinguish.ed from hysteroid convul- 
 sionsj ursemia, malingering, etc. 
 
 Consciousness. — 
 
 Pupils. — 
 
 Tongue.— 
 
 Restraint. — 
 Onset. — 
 
 Becovery. — 
 
 liOSt. 
 
 Dilated durine 
 fit. 
 
 Often bitten. 
 
 Necessary to 
 prevent accident. 
 
 Eapid and sud- 
 den, patient falls 
 unconscious. 
 
 Moderately 
 rapid. 
 
 May be par- 
 tially lost. 
 
 WormaL 
 
 Wormal, 
 
 Necessary to 
 control violence. 
 
 Usually after 
 some mental ex- 
 citement, patient 
 may fall into a 
 " dazed " con- 
 dition. 
 
 Very variable. 
 
 MALINGEREBS. 
 
 Normal, 
 
 Normal, 
 
 May be bitten 
 to simulate real 
 fit. 
 
 Not neceesary. 
 
 Always under 
 conditions where 
 the &aud may 
 hope to gain 
 sympathy. He 
 falls m abusinesB- 
 like manner, 
 taking care not 
 to sustain painful 
 injuries. 
 
 Very rapid 
 after object has 
 been gained. 
 
 TTEJEMIC 
 CONVULSIONS. 
 
 Lost in later 
 stages; coma is 
 
 Srolonged and 
 eep. 
 
 J?irst con- 
 
 traction,followed 
 by (Hlatation. 
 
 Normal. 
 
 Not necessary. 
 
 Preceded by 
 alterations in 
 health, urine, 
 etc. Patient is 
 usually in bed 
 before convul- 
 sions come on. 
 
 Slow, if not 
 fatal. 
 
 Treatment. — Try to discover any cause of reflex irritation 
 and remove it if possible. Try to keep the general health as 
 perfect as possible. Of drugs, bromides stand first; no per- 
 manent ill effects have been definitely traced to a very prolonged 
 use of this drug. Some authorities advise an occasional course 
 of bromides and arsenic. Careful attention must be paid to the 
 state of the bowels, menses, etc. 
 
 During the Fit. — Loosen the collar, corset, etc., and put 
 something between the teeth to prevent the tongue being 
 bitten ; inhalation of nitrate of amyl ; dash cold water on 
 face, etc.; and prevent patient from injury through his 
 convulsive movements. 
 
138 Student's Havd-book of Medicine. 
 
 JACKSONIAN EPILEPSY. 
 
 Jacksonian epilepsy is an affection characterised by epilepti- 
 form convulsions, not attended ■with loss of consciousness and 
 dependent on a coarse lesion of the cerebral cortex. 
 
 .ffitiology. — It is usually associated with syphilis, and 
 therefore most frequently seen amongst adult men; but other 
 tumours besides gummata are held responsible, also trauma- 
 tisms, blood clot, etc. 
 
 Symptoms. — First twitchings of a muscle or group of muscles 
 in the arm, leg, or face. The spasms may be distinctly localised, 
 and the patient being conscious, often watches the progress of 
 the march, and thus affords most important information, which 
 often enables the physician to localise the lesion. The con- 
 vulsions very rarely become general. They may be followed by 
 a transitory paralysis of the affected muscles. 
 
 Diagnosis. — 
 
 1. The slow onset. 
 
 2. Absence of unconsciousness. 
 
 3. Localised type of the convulsions. 
 
 Sufficiently distinguish it from ordinary epilepsy. The part 
 which first shows rigidity during the convulsion points toward 
 the motor centre for that part as the seat of the greatest 
 irritation. 
 
 Treatment. — 
 
 1. If syphilis be the cause, give heroic doses of iodide of 
 potassium. 
 
 2. If not syphilitic, then trephine, explore, and remove if 
 possible any discoverable source of irritation. 
 
Infantile Convulsions. 139 
 
 INFANTILE CONVULSIONS. 
 
 Causes. — 
 
 1. Eeflex irritation, especially from gastro-intestinal irrita- 
 tion, and teething; worms, otitis media, and phimosis are also 
 occasional reflex causes. 
 
 2. Infectious fevers. 
 
 3. Cerebral congestion, well seen in severe cases of whoop- 
 ing cough, and after exposure to the sun in a perambulator, etc. 
 
 4. Eickets. 
 
 5. Cranio-tabes induced by syphilis. 
 
 6. Hydrocephalus. 
 
 Treatment. — During the fit. Seek cause, and if associated 
 with a full stomach give an emetic, if with dentition lance gums, 
 and so on. A few whifis of chloroform, warm bath, ice to head, 
 small doses of chloral, etc. The treatment after the fit must 
 be conducted on general principles. 
 
 HYSTERIA. 
 
 Hysteria is a form of functional disturbance of the nervous 
 system, characterised by an abnormal susceptibility to external 
 impressions, and a deficient power of the will to restrain its 
 manifestations. 
 
 .etiology. — It is seen principally amongst women, and has 
 long been considered symptomatic of disorders of the ovaries or 
 uterine fulictions. It may be the result of nerve exhaustion 
 from any cause. 
 
 Symptoms. — They are too varied to tabulate. Indeed, it is 
 difficult to say what some authorities consider to he hysterical 
 symptoms. The more common phenomena are — 
 
140 Student's Hand-book of Medicine. 
 
 1. Disturbances of the sensory apparatus. — 
 
 (1) Hypersesthesia of localised areas. 
 
 (2) Ansesthesia, generally of left side. 
 
 (3) Loss of muscular sense. 
 
 (4) Neuralgias. 
 
 2. Disturbances of the motor apparatus. — 
 
 (1) Hystero-epUepsy. 
 
 (2) Tonic spasms. Example — -vaginismus. 
 
 (3) Clonic spasms. Examples — globus hystericus, un- 
 
 controllable laughter, hiccough, etc. 
 
 (4) Motor paralysis — aphonia, simulated hemiplegia, etc. 
 
 3. Visceral Disturbances. — 
 
 (1) Palpitation. 
 
 (2) Vicarious menstruation. 
 
 (3) Vomiting, belching, etc. 
 
 4. Physical disturbances. — 
 
 Morbid desire for sympathy. 
 
 Apathy and obstinacy. 
 
 Sudden transition from the joyous to the sad. 
 
 Melancholia. 
 
 Somnambulism. 
 
 Nympho-mania. 
 
 Catalepsy — may simulate death. 
 
 5. Vaso-motor disturbances. 
 
 It will be seen from the above table, that it -ivould not be 
 easy to mention what symptoms may not crop up in various 
 forms of hysteria. So closely does hysteria, simulate real 
 disease that the best diagnosticians have been deceived. When 
 grave symptoms appear, even after a careful consideration of the 
 history, etc., of the patient, a provisional diagnosis should be 
 made until the patient has been for some time under treatment. 
 (Dr Eanny's Lectures). 
 
 Treatment of hysteria depends on the type. All forms, 
 however, require firm, kind, and judicious treatment. The 
 
Neurasthenia. 
 
 141 
 
 physician must first gain tlie patient's full confidence, and 
 having done this he may use bromides, tonics, massage, and 
 "Weir-Mitchell's" treatment. The various special symptoms 
 must be treated on general principles. It is doubtful if such 
 drastic measures as excision of the clitoris, removal of the 
 ovaries, or applications of the actual cautery are admissible, 
 though they have been practised by eminent authorities. 
 
 NEURASTHENIA. 
 
 By neurasthenia is meant the manifestations of nerve ex- 
 haustion. Hysteria may therefore be considered a symptom 
 per se of neurasthenia, but there are some important differences. 
 
 NEUKASTHENIA. 
 
 Occurs most often in men. 
 
 Usually directly attributable to 
 over work. 
 
 No desire for sympathy. 
 
 Usually wasting is present. 
 
 Very amenable to proper treat- 
 ment. 
 
 HYSTEMA. 
 
 1. "Women most frequently. 
 
 2. Often seen amongst the indolent 
 
 and the rich. 
 
 3. Great desire for sympathy. 
 
 4. Often plump or fat. 
 
 5. Anything but amenable to treat- 
 
 ment. 
 
 The chief reasons v^hy so much prominence has been given 
 to neurasthenia as an independent condition are as follows : — 
 
 1. The tendency of the age is towards brain work. 
 
 2. Brain workers have enormous competition in life's fight. 
 
 3. The neurotic element is largely increased thereby. 
 
 4. This neurotic element renders its possessor more suscep- 
 tible to external impressions. 
 
 5. Abuse of stimulants, alcohol and tobacco especially being 
 taken at too frequent intervals, in order to lash up the flagging 
 energy. 
 
 6. Modern cooking. 
 
 Treatment. — The causes and definition of the disorder 
 makes it sufficiently obvious what line of treatment should be 
 employed ; indeed, it may be summed up in four words — 
 complete change, rest, tonics. 
 
142 Student's Hand -book of Medicine. 
 
 THOMSEN'S DISEASE. 
 
 It is a condition too rare to require a lengthened description 
 in such a work as this. 
 
 The main features are a tendency of the muscles to tonic 
 spasm during attempts at voluntary movements. 
 
 Etiology. — Probahly it is always associated with some con- 
 genital defect. Heredity is a strong and important factor, and 
 more than one member of a family may be affected. 
 
 Pathology unknown. Possibly it is a muscular disease, 
 and not a nervous lesion at all. The muscles are usually well 
 developed as far as appearance goes ; indeed, they often appear 
 hypertrophied. 
 
 Electrical Reactions. — There is an entire upset in that 
 relationship, which exists in normal muscles between C. C. C. 
 and A.C.C. This tempts one to think the disease may be due 
 to local metabolic changes, setting up an irritability of the 
 muscular tissue, such irritability being specially brought out 
 on attempts at movements ; but vihy such a condition occurs 
 is wrapped up in that obscurity, associated with congenital 
 defects. 
 
 Symptoms. — 
 
 1. After rest the patient experiences tension and stiffness of 
 the muscles on attempting to rise, etc. 
 
 2. Difficulty in relaxing the muscles. 
 
 3. The muscles of the tongue, face, and eyes, may also be 
 similarly affected. ■ 
 
 Note that continued movements and warmth decrease the 
 spasm ; mental worry and cold usually aggravate it. 
 
 Treatment. — -Massage, gymnastic exercises, electricity, and 
 warm baths. 
 
Tetany. 
 
 143 
 
 TETANY. 
 
 Tetany is anotlier rare disease which I only mention as it is 
 so often confounded with tetanus. 
 
 Symptoms. — Paroxysmal tonic muscular spasms. When 
 the upper limbs are attacked, the forearms are flexed and 
 drawn across the chest, and the wrist and fingers are also 
 usually flexed. If the trunk be afPected, there may be 
 oposthotonos or pleurosthotonos. When the lower limbs are 
 implicated, the thighs are adducted ; big toe brought under 
 the other, and leg extended. 
 
 Trousseau lays stress upon the fact that the attacks can be 
 induced at will by pressing upon either the arteries or nerve 
 trunks. The great point is to diagnose this disease from 
 tetanus, which may be done by remembering that in tetanus 
 the muscles of the jaw are mostly implicated, and there is more 
 pain and general rigidity ^ also a traumatic history and a more 
 acute onset and rapid course. 
 
 Diagnostic Table No. 1. 
 
 Causes- 
 
 ArgyU-Mohertson 
 pv/pil — 
 
 Lightning Fains — 
 
 Xnee Jferk — 
 Nystagmus — 
 
 Tnco'ordinaiion — 
 
 LOCOMOTOB ATAXIA. 
 
 Middle-aged men. 
 
 Syphilis, intem- 
 perance. 
 
 Present. 
 
 A prominent 
 symptom. 
 
 Lost. 
 Absent. 
 N^ot involved. 
 
 Marked aa regards 
 "gait" and lower 
 limbs. 
 
 SPASTIC ATAXIA. 
 
 Middle life. 
 
 Exposure to cold, 
 traumatisms, etc. 
 
 Absent. 
 Absent. 
 
 Increased. 
 Absent. 
 Earely involved. 
 
 Marked, but 
 
 attended by spasm. 
 Spasm tends to 
 increase, but vnco- 
 ordvnaUon does not. 
 
 PEEIDEICH 8 ATAXIA. 
 
 Early life. 
 
 Hereditary. Often 
 more than one in 
 same family. 
 
 Absent. 
 
 May be present, 
 but more often 
 absent. 
 
 Lost. 
 
 Present. 
 
 Often markedly 
 involved. 
 
 Marked, but ir- 
 regular and jerky ; 
 aftects upper limbs 
 as well. 
 
144 
 
 Student's Hand-hook of Medicine. 
 
 Diagnostic Table No. 2. 
 
 
 PEOGEBSBITE 
 MUSCULAB ATKOPHT. 
 
 AJVTTO-TEOPHIC 
 PARALYSIS. 
 
 PBIMAKT SPASTIC 
 PABAPLEGIA. 
 
 lAmhs most 
 
 affected — 
 
 Upper — atrophy 
 begins in thenar ana 
 hypo-themw emi- 
 nenciea. TJnilateral 
 at firat. 
 
 Upper — atrophy 
 may begin in musolea 
 of iore-arm or deltoid. 
 Unilateral. 
 
 Lower— no atrophy; 
 but rigidity and 
 spasm are present. 
 BUateral. 
 
 Deformity— 
 
 The "claw -like" 
 hand. 
 
 Fleadon of elbow, 
 pronation of band, 
 flexion of wrists, and 
 
 Adduction of logs. 
 They may cross each 
 other. 
 
 Tendon reflexes 
 (kneej— 
 
 Unaffected. 
 
 Unaffected. 
 
 Exaggerated on 
 both sidea. 
 
 Electrical 
 
 changes — 
 
 Keaction of degen- 
 eration. 
 
 Partial. 
 
 Normal as a rule. 
 
 GAITS. 
 
 Locomotor Ataxia. — Feet are brought down with extended 
 heels, creating a stamping gait. Greatest difficulty is experi- 
 enced ia turning around, or standing with feet close together. 
 Patient's eyes are usually steadily fixed on the floor to guide 
 movements. 
 
 Cerebellar Disease. — Here the inco-ordination is of the type 
 of a drunken man. The greatest difficulty is experienced on 
 trying to walk along, a straight line. On standing, note the 
 movements of the toes as if they were digging into the carpet. 
 The patient may sway to the front, backwards, or laterally. 
 
 Disseminated Sclerosis. — Ataxia gait is accompanied with 
 marked inco-ordination of the trunk. The patient shoots 
 suddenly forward to one side. Note jerky movements of 
 the head. 
 
 Spastic. — Feet are turned inwards, and are scraped along the 
 ground; later, the patient may "hop" (when the muscles of 
 the calves are implicated). The back is arched and the chest 
 pushed forward. The feet, by forcible adduction, often cross 
 each other. 
 
Diseases of the Nerves. 145 
 
 DISEASES OF THE NERVES. 
 
 In the opening remarks on nervous diseases in general, we 
 considered the functions and structure of peripheral nerves. 
 We also considered briefly, the more important changes in 
 their structure and function when they became diseased or 
 cut off from their trophic centres. In order to save time 
 and space, we shall not repeat the details of those minute 
 pathological changes ; but, just add that the morbid con- 
 ditions may be most marked in — 
 
 1. The nerve sheath. 
 
 2. Nerve fibres. 
 
 3. Interstitial substance. 
 
 And it will be readily understood that sclerosis, whether 
 in sheath or interstitial matter, must powerfully influence the 
 function of that nerve. By "multiple sclerosis" is meant 
 more or less scattered sclerosis of many peripheral nerves. 
 The symptoms of such a condition are very many; when 
 tabulated they are : — 
 
 1. Sensory Symptoms. — Patches of hypersesthesia and anses- 
 thesia, especially below the elbows and knees. Tenderness 
 over the affected nerves and muscles. Delayed transmission 
 of pain sensations and temperature sensations. 
 
 2. Motor Symptoms. — 
 
 (1) Progressive muscular weakness and a sense of fatigue, 
 which in a few weeks develops into paralysis. The extensors 
 of hands and feet are most frequently attacked. 
 
 (2) Atrophy of the muscles. 
 
 (3) Deformities due partly to the weight of the hands and 
 feet not being supported by the paralysed muscles. 
 
 (4) Tendon reflexes are abolished. 
 
146 Student's Hand-book of Medicine. 
 
 3. Trophic Symptoms. — 
 
 (1) Glossy skin is usually very persistent. 
 
 (2) (Edema of the feet and hands, often present in the 
 early stage. 
 
 (3) Excessive perspiration or marked dryness of the hands 
 and feet. 
 
 ALCOHOLIC PARALYSIS. 
 
 Alcoholic paralysis is one of the best examples of multiple 
 neuritis. 
 
 .etiology. — It usually occurs amongst secret drinkers, and 
 for that reason women are more often attacked. Most- cases 
 occur after thirty-five years of age. Glub-men and brewers 
 furnish a number of cases. 
 
 Symptoms. — We must remember that the manifestations of 
 chronic alcoholism differ much in individuals ; there are at least 
 four weU marked types. 
 
 1. That in which tremor predominates. 
 
 2. The anaesthetic type. 
 
 3. The paralytic type. 
 
 4. The ataxic form. 
 
 First there is tingling like pins and needles in the muscles 
 generally, then numbness of the fingers and toes ; vasa-motor 
 spasm causing dead fingers, and muscular cramps. Progressive 
 paralysis compels the patient to take to his bed ; the extensors 
 are more implicated than the flexors, and consequently the 
 patient lies with dropped feet and dropped wrists (the feet 
 generally first). Other muscles are gradually involved, and 
 phiSnation may be lost or much weakened. Atrophy of the 
 
Special N&rves. 147 
 
 affected muscles rapidly supervenes, being especially well 
 marked in. the extensors below the knee and elbow. The 
 atrophied muscles are often exquisitely tender. 
 
 The mental state often suffers : the memory is almost lost, 
 and often delusions are marked features. The reaction of 
 degeneration is present to a partial extent. Earely, if ever, 
 is there complete failure of response to faradic stimulation. 
 The ataxic form resembles tabetic ataxy in the numbness of 
 the feet, absence of knee jerk, locomotion, and non-wasting 
 of the anterior tibial muscles ; but, in such cases the gait is 
 different from the true ataxic walk, as the patient not only 
 throws out Ms feet brusquely, hut steps high in order to clear 
 his toes of the ground. (Dr Ferrier.) 
 
 Treatment. — Cut off the supply of alcohol entirely. Perfect 
 rest. To ease the pain — iodide of sodium, antipyrin, and 
 croton-chloral may be given. Afterwards — good feeding, mass- 
 age, and electrical stimulation as a rule, will, if persevered 
 
 SPECIAL NERVES. 
 
 After what has been said about the cranial nerves and 
 multiple neuritis, there is no need to devote time to special 
 descriptions of affections of special peripheral nerves. A 
 knowledge of their anatomical distribution and function should 
 enable us to reason what to expect when such nerves are injured. 
 
148 Student's Hand-book of Medicine. 
 
 DISEASES of the RESPIRATORY SYSTEM. 
 
 Dr John Wyllie's Notes on Examination of tlie Respiratory System. 
 
 AUSCULTATION. 
 
 Listen for — (1) Type of Breathing, (2) Accompaniments, (3) Vocal Resonance. 
 
 1. Types of Breathing. 
 
 (1) Vesioulak or Rtjshing — 
 
 A A A o A A 
 
 Puerile. Normal in Feeble. None. Interrupted. Harsh, with 
 
 Adult. expir. prolougod. 
 
 Transition Type — 
 
 /\\ /A 
 
 (Broncho-vesicular or " indeterminate" breathing.) 
 
 (2) Bronchial or Blowing — 
 
 /A //W //W 
 
 High-pitched or Tubular. Medium-pitched. Low-pitched or Cavernous. 
 
 (3) Amphoric — 
 
 00 00 00 
 
 High-pitched. Medium-pitched. Low-pitched. 
 
 Notes. — (1) Vesicular Breath-sounds. — In the auscultation of normal Vesi- 
 cular Breathing, the Inspiratory sound, represented in the diagrams by a single 
 line, is a fine, continuous, rushing sound, soft in the adult and loud in the child, 
 and audible from beginning to end of the act. The Expiratory sound, on the 
 other hand, is thin in quality and of short duration, being audible only during 
 the earlier part of the Expiratory act. It is generally believed that in normal 
 Vesicular Breathing the Inspiratory sound passes, as represented in the diagram, 
 directly into the Expiratory without a break. Having, however, paid special 
 attention to this point, Dr W. believes that there is often, in perfectly normal 
 Vesicular Breatliing, a clistinct break between the two sounds. When the 
 breathing is quiet and easy, the Expiratory sound is often totally inaudible, 
 
Diseases of the Respiratory Sy stein. 149 
 
 even in children ; but in such cases it can usually be brought out by causing 
 the patient to breathe deeply. The term "prolonged expiration" is used to 
 signify not a prolongation of the act of Expiration, but only a prolongation of 
 the expiratory aoimd, resulting from the encroachment of the audible upon the 
 inaudible part of the act. There is indeed one form of breathing, common to 
 advanced Emphysema and Asthma, in which the act itself is really prolonged, 
 being often much longer than the Inspiration. In such "Asthmatic " breathing, 
 the type of respiration, primarily Vesicular, is as a rule totally masked by the 
 loud wheezing accompaniments of both Inspiration and Expiration. 
 
 (2) Bronchial Breathing. — The auscultatory soimd of Bronchial Breathing, 
 indicated in the diagrams by a double line, can be imitated, as pointed out by 
 Skoda, by holding the tongue in the position for the pronunciation of the 
 guttural ch sound ( as in the German word Ach, or the Scotch word Loch), and 
 causing the air to pass inwards and outwards over it. The blowing sound thus 
 produced can be made to represent the various pitches indicated in the diagram. 
 There is always in Bronchial Breathing a distinct break between the sounds of 
 Inspiration and Expiration, and the two sounds closely resemble each other. 
 The higher-pitched varieties of Bronchial Breathing should be associated in the 
 mind with conditions of consolidation of Lung Substance, such as that of 
 Pneumonia, and the Low-pitched or Cavernous variety with Excavation, as in 
 Phthisical cavity. Bronchial Breathing is never produced by Bronchitis. 
 
 (3) The Amphoric type of breath-sound can be well imitated by whistling 
 with the mouth. Inspiratory and Expiratory sounds can thus be produced by 
 causing the air to pass inwards and outwards, and the pitch can be varied 
 according to the variety of Amphoric Breathing that is being imitated. 
 Amphoric Breathing is best developed in Pneumothorax, but is also sometimes 
 met with in very large Phthisical cavities. 
 
 (4) In the Healthy Chest the respiratory sounds are purely Vesicular 
 (without harshness of quality or prolongation of expiration) over the whole 
 surface of the lungs, except (a) opposite the Roots of the Lungs, at level of 
 third dorsal vertebra behind, and lower part of manubrium sterni in front, 
 where the proximity of the large Bronchi generally renders the breathing 
 Broncho-vesicular, by the addition of a Blowing or Bronchial element, most 
 distinct during expiration ; (6) over the Apex of the Right Lung, especially 
 above the Clavicle and Spine of Scapula, where, in health, from causes as yet 
 imperfectly ascertained, the Vesicular Breath-sound hasvery generally a more 
 or less prolonged, and often harsh or even somewhat blowing, expiration. 
 
 The only example of purely Bronchial Breathing that can be heard on 
 auscultating the healthy subject, is the " Tracheal" Breathing, to be obtained 
 by placing the stethoscope over the Larynx or Trachea. This is low in pitch, 
 and if heard over the apex of the Lung would be termed " Cavernous." 
 
 [Unfortunately some of the great original authorities on Auscultation applied 
 the term "Bronchial" to the type of breathing heard over the roots of the 
 Lungs, but, as this is partly of Bronchial and partly of Vesicular origin, the 
 term "Broncho-vesicular" is much more appropriate.] 
 
150 Stvdent's Hand-booh of Medicine 
 
 '/ 'I 
 
 jdinm. Coarsf 
 
 onchitis) — 
 
 /// /// /// 
 
 2. Accompaniments. 
 
 (1) Friction (in Pleurisy)- 
 
 Fine. Medium. Coarse. 
 
 (2) Dey Sounds, or Rhonchi (in Bronchitis) — 
 
 High-pitched. Medium-pitched. Low-pitched. 
 
 (Cooing, Wheezing, etc., (Sonorous.) 
 
 called *' Sibilant") 
 
 (3) Moist RAles or Cbepitations (1 and 2 in Pneumonia ; 
 2 in Bronchitis ; 2 and 3 in Phthisis) — 
 
 oo _ o 
 
 ooo 
 
 oo 
 
 1. Fine. 2. Medium. S. Coarse (Bubbling). 
 
 *■ ' Y ^ 
 
 May I)e Coruanating In three degrees — tough, 
 metallic, tinkling. (Tinkling lules nre Bpeeinlly 
 important in connection with Fueumothorax.) 
 
 3. Vocal Resonance. 
 
 (1) Simple Increase — 
 
 (a) Slight, comparative. 
 
 (S) Marked (Bronchophony), 
 
 (c) Very marked (Pectoriloquy), 
 
 (The chief conditions which cause Increase of Vocal Resonance are 
 Consolidation and Excavation of the Lung substance.) 
 
 (2) Simple Decrease — 
 
 {a) Slight, comparative. 
 
 (i) Marked decrease. 
 
 (c) Total absence, 
 
 (Decrease of Vocal Resonance is most frequently due to Thickening 
 of the Pleura or to Pleuritic Effusion.) 
 
 (3) Qualitative Altbeations— 
 
 (a) Aegophony (Nasal timbre). 
 (J) With metallic echo (Amphoric Resonance or 
 Nach-klang), 
 
 (Aegophony occurs in Pleurisy with Effusion when the layer of fluid 
 is thin. Metallic echo is one of the signs of Pneumothorax.) 
 
 PKRCUSSION, 
 1. Htpek-Resonance — 
 
 (1) Slight. 
 
 (2) Marked. 
 
Diseases of the Respiratory System. 151 
 
 (3) Very marked (Tympanites), 
 (a) High-pitched. 
 (6) Medium-pitched, 
 (c) Low-pitched. 
 (Emphysema causes slight Hyper-Resonance. Relaxation of Lung 
 substance, as in the Superior lobe when the Inferior is solid 
 from Pneumonia or compressed by Pleuritic Effusion, is a cause 
 of marked Hyper-resonance. Pneumothorax is the commonest 
 cause of true Tyrap-inites.) 
 
 2. Deficient Resonance — 
 
 (1) Slight, comparative dulness. 
 
 (2) Marked dulness. 
 
 (3) Absolute dulness. 
 
 (Consolidation of Lung substance, thickening of the Pleura, and 
 Pleuritic Effusions are the chief causes of Deficient Resonance.) 
 
 3. Mixture of Dulness and Resonance— i.e., a Wooden or Boxy Note. 
 
 (This is one of the most important signs of a Phthisical Cavity.) 
 
 4. Special Quality — 
 
 (1) Cracked-pot sound. 
 
 (Another very important sign of a Phthisical Cavity.) 
 
 (2) Bell sound, got with two coins and stethoscope. 
 
 (One of the signs of Pneumothorax.) 
 
 SUCCUSSION. 
 
 Called " Hippocratic ;" used in Myd/ro- and Pyo- pnm.irw(horax. 
 
 INSPECTION, PALPATION, AND MENSURATION. 
 
 1. Form and Size of Chest — 
 
 (1) Circumference of Chest at line of nipples. 
 
 (2) General Form (flat, barrel-shaped, etc. ) 
 
 (3) Local alterations in Form (local flattening, bulging, etc.) 
 
 2. Movements of Chest — 
 
 (1) Number of respirations per minute. 
 
 (2) General type of movement (thoracico-abdominal, abdominal, 
 
 thoracic). 
 
 (3) Rhythm and Volume of respirations ; and their Special 
 
 Character, as in the ' ' Cheyne-Stokes' " type, etc. 
 
 (4) Local Movements (sucking in of intercostal spaces, etc.) 
 
 (5) Deficient Expansion (over one apex, over one side, etc. ) 
 
 3. Parts outside Chest — 
 
 (1) Box of Larynx (its upward and downward movement). 
 
 (2) Alae Nasi (their action in difficult breathing). 
 
 (3) Bulging of Apices in neck on coughing. 
 
 (4) Action of the Scaleni and other Extraordinary Muscles of 
 
 Respiration. 
 
 4. Palpate foe THE Vocal Fremitus. (Note increase or diminution.) 
 
152 Student's Hand-book of Medicine. 
 
 EXTRA AUSCULTATION. 
 
 1. Of the Sounds of Obstruction in Eespiratokt Passages. 
 
 (1) Obstecction to Breathing ( (a) From hardened ov fluid Mucus. \ Nasal Bubbling 
 
 IN Nose \ (6) From Paralysis of Alae. / and Sniffling. 
 
 (2) Obstroction is Back of /(o) Nasal Snore. \ Stertorous 
 
 Throat \ ( 6) Oral Snore; / Breathing. 
 
 ,„. „ . f (a) Swelling of Cords. \Stridulous 
 
 (3) Obstruction in Larynx ■ • • | ( jj Paralysis or Spasm of Glottis. / Breathing. 
 
 ... _ ~ ((a) From Aneurism (Leopard-growl). 
 
 (4) Obstruction IN Trachea .. .j^ J j^, jj^^jjj U^tyj, 
 
 „. „ __ „ f (a) Musical Sounds (Wheezing, etc.) 
 
 (5) Oestrdction in Bronchi . . | Jjj crepitant Sounds. 
 
 2. Of the Cough. 
 
 The following are some of the more common varieties of Cough : — 
 
 (1) Cough, of the ordinary type, suoli as is met with in — (a) Common 
 
 Colds ; (i) Some conditions of mere nervousness ; (c) Irritation of 
 certain peripheral nerves, as those of stomach, ear, etc. ; (d) Early 
 Phthisis, when, however, it is apt to be specially hacking and 
 irritating ; («) Later Phthisis, when it may vary much in severity, 
 from moderate, though frequent, to severely paroxysmal. Phthisical 
 cough is often succeeded by vomiting. 
 
 (2) The frequent, prolonged, paroxysmal, and often wheezing Cough 
 
 that is characteristic of severe Bronchitis. 
 
 (3) The frequent, short, "suppressed" Cough of Pneumonia with 
 
 associated Pleurisy, and of^ simple acute Pleurisy. It is "sup- 
 pressed" because it excites pain in the side. 
 
 (4) The husky and sometimes stridulous or "croupy" Cough that is 
 characteristic of Laryngitis. 
 
 (5) The peculiarly " brassy " or ringing Cough (like the cry of a gander) 
 that is met with in many cases of Aortic Aneurism or Mediastinal 
 Tumour with pressure on the Trachea. 
 
 (6) The prolonged paroxysm of fully developed Whooping-Cough, with 
 its rapid and long-continued succession of short, sharp coughs, and 
 its final long-drawn stridulous inspiration. A succession of these 
 paroxysms is very often succeeded by vomiting. 
 
 (7) The loud Barking Cough met with in some cases of Hysteria. 
 
 Note. — The Sputum should he carefully examined and described. Its 
 more common types are — 
 
 {a) Viscid, mucous, and often pigmented, in Common Catarrh ; (J) Bloody 
 in Hemoptysis; (c) "Nummular," in advanced Phthisis; {d) Copi- 
 ous, frothy, mucous or muco-purulent, in Bronchitis ; (e) Sticky 
 gelatinous, and rusty, in Pneumonia ; and (/) extremely foetid in 
 Gangrene of the Lung and some cases of Bronchiectasis. 
 
 In special cases a report should be made of the Microscopic characters 
 of the Sputum. 
 
 When, with cough, there is no expectoration, its absence should be noted. 
 
Bronchitis. 153 
 
 BRONCHITIS. 
 
 INFLAMMATION OF THE BRONCltl. 
 
 etiology. — Occurs most frequently in winter amongst 
 elderly people, but tlie capillary variety is more often seen 
 amongst young children, especially in connection witli whooping- 
 cougli and measles ; insufficient food, scanty clothing, or on the 
 other hand, excessive confinement in warm rooms, and too 
 warm wrapping up, are the great predisposing causes. ' 
 
 Exciting Causes — 
 
 1. Spreading of nasal catarrh. 
 
 2. Foreign bodies in larynx, etc. 
 
 3. Certain infectious diseases, e.g., influenza, measles, 
 
 diphtheria, etc. 
 i. Extension of inflammation from other parts. 
 
 Pathology.— That of a typical inflammation of a mucous 
 membrane, i.e. — 
 
 1. Hypersemia. — The membrane is injected, dry, and secre- 
 tion scanty. 
 
 2. Exudation of lymph with increase of mucus — secretion 
 more profuse. 
 
 3. Purulent degeneration of the exudation — muco-purulent 
 phlegm. 
 
 4. Changes in the tissues beneath, slight at first, but repeated 
 attacks cause grave changes, viz. : — 
 
 (1) Epithelium becomes to a large extent destroyed. 
 
 (2) Muscular coats are fi.brosed and rigid. 
 
 (3) Tubes themselves become dilated or varicose, causing 
 
 (as we shall see further on) bronchiectasis. 
 
 (a) Acute Bronchitis. — Ushered in with coryza and jisdns 
 about the chest, and cough. The pain is burning in character, 
 and situated behind the sternum. The expectoration at first 
 
154 Student's Hand-book of Medicine. 
 
 is frothy and scant, but soon becomes abundant and purulent, 
 and often is expectorated in greenish jelly-like masses ; later, 
 it is more muco-purulent. The breathing is much embarrassed, 
 and noisy or whistling in character ; the temperature is not high 
 as a rule, and the skin is moist. The urine is of a febrile type, 
 scanty and high coloured. After a few days the more acute 
 symptoms subside, and convalescence becomes rather slowly 
 established. Death is rare in uncomplicated casete, but is often 
 fatal through extension to the capillaries or air cells. 
 
 (6) Capillary Bronchitis. — This variety more frequently 
 affects children, and is characterised by great dyspnoea, sucking 
 in of the intercostal spaces, high temperature, quick feeble pulse, 
 a tendency to drowsiness or coma, and coUapse of the lung. 
 
 Physical Examination. — Ehonchi and rales are heard all 
 over the chest. Percussion yields a slight hyper-resonant note, 
 except where there are collapsed portions of lung ; then there 
 is, of course, impaired resonance and absence of breath sounds. 
 
 Treatment. — In the first stage employ the bronchitic kettle, 
 containing a solution of eucalyptus or pinol ; administer a brisk 
 saline purge, and a diaphoretic mixture such as — 
 
 ^ Pot. Citras . . 
 Vin. Antim Tart. 
 Spt. iEther Nit. 
 Spt. Chloroformi 
 Aq. ad ... . 
 
 5"J' 
 Sviij. 
 
 Fiat mist. A tablespoouful every three hours for an adult. 
 
 Later — ammonia, with senega and ipecac. ; or ammonia and 
 pot. iodid., with the compound tincture of camphor. 
 
 In the capillary form lowering measures are seldom called for. 
 The two great dangers are — 
 
 1. Collapse of the lung. 
 
 2. Early heart failure. 
 
Chronic Bronchitis. 
 
 155 
 
 If the former threatens, as evidenced by increasing lividity 
 and dyspnoea, a brisk emetic should be given, followed at once 
 by a stimulant, such as the compound spirit of aether with 
 ammon. carb. Sedatives are nearly always contraAndicated. 
 
 CHRONIC BRONCHITIS. 
 
 (Winter Cough.) 
 
 Chronic bronchitis may be the result of the acute form ; but 
 it more often results from a series of sub-acute attacks in old 
 people, whereby the bronchial tubes are "devitalised " and prone 
 to inflame on slight provocation, especially in winter time. 
 
 Symptoms are dyspnoea, harsh paroxysmal cough, and 
 copious expectoration of phlegm, which varies much in 
 character, from being mucoid and serated, to non-aerated 
 muco-purulent, or even pus alone. Chronic bronchitis is too 
 frequently looked upon as a mere bronchial affection, for- 
 getting the wide spread and grave changes induced, as the 
 following table shows : — 
 
 PatJiological Changes. 
 
 1. In the tubes them- 
 selves— rigidity of walls 
 and subsequent dilata- 
 tion. 
 
 2. Dilatation of the 
 air vesicles = emphy- 
 sema. 
 
 3. Hypertrophy of 
 right side of the heart, 
 (quickly masked by 
 great dilatation). 
 
 Physical Examination. 
 
 1. Abundance 
 rales. Signs of 
 distinct cavities. 
 
 of 
 
 2. Altered shape of 
 chest, hyper-resonance, 
 decreased breath sounds 
 
 3. Increase of cardiac 
 dulness. Epigastric 
 pulsation. Later, signs 
 of tricuspid leakage- 
 i.e., 
 congestion 
 
 Clinical Symptoms. 
 
 1. Copious expecto- 
 ration at intervals of 
 foetid, pus-like secre- 
 tion. 
 
 2. Dyspno3a through 
 imperfect feration, in- 
 creased on exertion. 
 
 3. Feeble 
 oedema — 
 
 pulse — 
 perhaps 
 anasarca ; in fact all 
 the troubles consequent 
 on general venous con- 
 gestion of the viscera. 
 
156 Student's Hand-book of Medicins. 
 
 Treatment. — Hygienic measures rank first in the treatment ; 
 proper clothing, careful dieting and change of air do more good 
 than drugs. Of drugs, the iodides with ammonia are useful, 
 terebine is praised ; digitalis and strychnine are extremely 
 beneficial when the pulmonary circulation is more sluggish 
 than usual. 
 
 BRONCHIECTASIS. 
 
 Dilatation of the bronchi has already been referred to, as a 
 complication or result of bronchial disease. We must now 
 consider more fully how the condition is produced. 
 
 1. It may be a congenital defect, or produced by — 
 
 2. Primary disease of the bronchial walls. 
 
 3. Contraction of lung tissue in phthisis, etc. 
 
 Two forms occur : — 
 
 (1) Cylindrical or fusiform. 
 
 (2) Saccular. 
 
 The former is more often produced by strain from within, 
 such as violent coughing, the rigid walls yielding to the expira- 
 tory inter-pulmonary pressure. 
 
 The saccular form is most often produced by — 
 
 1. Contraction of new fibrous tissue outside the tubes. 
 
 2. Breaking down of the lung substance, causing dimin- 
 
 ished support, and yielding of the walls at that 
 point. 
 
 The dilated portion is usually smooth, until ulceration from 
 retained secretion occurs. The walls are very thin, the muscular 
 and elastic tissue being much atrophied. 
 
 Symptoms. — Physical examination may reveal all the signs 
 of a cavity. The expectoration is copious and foetid, and if 
 
Pneumonia. 157 
 
 allowed to stand it separates into three layers, the lower layer 
 being almost pure pus ; next, a more granular zone ; and a clear 
 frothy layer on top of this. 
 
 Microscopically it shows — 
 
 1. Pus cells and epithelial debris. 
 
 2. Crystals of fatty acids. 
 
 3. Elastic fibres (may be absent). 
 
 The horrible odour is due to valerianic and butyric acids, 
 H2S, etc. The mode of expectoration is characteristic, patient 
 usually brings up a huge quantity in the morning, or on moving 
 after resting in an horizontal position for some time. 
 
 Treatment. — Antiseptic inhalations, capsules of creosote, 
 etc. Terebine is warmly praised by some. 
 
 PNEUMONIA. 
 
 By pneumonia is meant inflammation of the lung substance. 
 Three types are usually described, viz. : — (1) Croupous, lobar 
 or acute pneumonia ; (2) Catarrhal or lobular pneumonia ; 
 (3) Chronic or interstitial pneumonia. We shall first describe 
 
 CROUPOUS OR ACUTE PNEUMONIA. 
 This form is characterised — pathologically : by an inflamma- 
 tion giving rise to an exudation, rich in fibrin, and showing 
 colonies of special organisms — i.e., pneumo-cocci ; — clinically: 
 by its abrupt onset, by running a definite course, and ending 
 by crisis. It usually begins at the base, and may involve one 
 or more lobes. 
 
 .etiology. — Croupous pneumonia is a most common affection, 
 occurs most frequently in winter and spring, and attacks all ages, 
 though adults, perhaps, are more often affected than children. 
 Amongst the more common exciting causes are draughts, intem- 
 perance, exposure to inclement weather, or irritating gases. 
 
158 Student's Hand-book of Medicine. 
 
 Frequently this kind of pneumonia occurs in epidemic form ; 
 indeed, there is an increasing tendency to look upon this form 
 as a " specific fever with marked lung symptoms." 
 
 Pathology. — It is convenient to describe four stages, viz. : — 
 
 1. Hypersemia or engorgement. 
 
 2. Eed hepatization. 
 
 3. Grey hepatization. 
 
 4. Eesolution. 
 
 It is more than doubtful whether grey hepatization occurs, 
 except in fated cases ; indeed, the condition is looked upon by 
 many as a post-mortem change, and not a pneumonic process. 
 
 1st Stage. — The lung is injected, heavy, and more friable; 
 on pressure, there exudes a frothy serum tinged with blood and 
 slightly aerated. 
 
 2nd Stage or Eed Hepatization. — The part involved is solid, 
 and presents a granular or red granite appearance. (Dr Alex. 
 Bruce denies the appearance being "liver like'' or uniformly 
 red.) The alveoli are fiUed with a coagulated exudation, which 
 shows under the microscope — 
 
 1. Fibrin. 
 
 2. Proliferated cells. 
 
 3. Leucocytes. 
 
 4. Eed corpuscles.. 
 
 5. Granules and cell debris. 
 
 6. Pneumo-cocci. 
 
 3rd Stage or Grey Hepatization. — The lobe has now the 
 appearance of grey granite, the lung substance is softer and 
 more friable ; on pressure, a dirty purulent fluid exudes. The 
 grey appearance is due to four factors — 
 
 1. Decolourization of the red blood corpuscles. 
 
 2. Obliteration of the alveoli blood vessels from pressure. 
 
 3. Fatty degeneration of the coagulated material. 
 
 4. Great infiltration of leucocytes. 
 
 It wiU be seen at a glance that such an advanced change is 
 hardly compatible with life. 
 
Pneumonia. 159 
 
 4th Stage or Eesolution. — Means resolution of the inflam- 
 matory exudation, principally by absorption, but partly by 
 liquefaction and expectoration. 
 
 The Germ or diplo- coccus pneumonise of Frank el, consists (in 
 cultures) of cells arranged in pairs, and sometimes in chains. 
 In the tissues the microbes become lancet-shaped. They retain 
 the aniline stain when treated by Gram's method. Further 
 evidence is wanted to prove that these are the organisms which 
 cause acute pneumonia. 
 
 Physical Examination. 
 
 1st Stage. — Percussion yields a slight dullness, but sometimes 
 even a slight hyper-resonance may be present. Auscultation 
 reveals the characteristic fine crepitations, compared to the sound 
 produced by the rubbing together of hair between the fingers. 
 Many explanations of these sounds are offered, but the writer 
 thinks the fine crepitations are due to the crackling of the 
 elastic tissue of the alveoli in the inflamed condition. 
 
 2nd Stage. — Gives the signs of consolidation, viz. — 
 Inspection shows diminished movement. 
 
 Palpation confirms this, and also demonstrates increased 
 vocal fremitus. 
 
 Auscultation reveals the absence of vesicular breathing, but, 
 presence of typical tubular breathing. Vocal resonance is 
 increased to the pitch of broncophony, or even whispering 
 .pectriloquy. 
 
 Percussion yields a dull note (not absolutely so flat as in 
 pleuritic effusion). 
 
 3rd Stage. — This stage of grey hepatization can scarcely be 
 detected by physical examination. 
 
 4th Stage or Resolution. — Here we have a speedy clearing up 
 of the exudation, and a return to the normal condition. Small 
 rales or redux coarse crepitations are heard, the dulness is less 
 marked, and the movement increased. 
 
160 Student's Hand-hook of Medicine. 
 
 Symptoms. — Croupous pneumonia may be ushered in with 
 one or more rigors, rapid rise of temperature, and localised pain, 
 plus the ordinary accompaniments of the febrile state. As the 
 disease progresses, several characteristic features develop. The 
 pain becomes less marked, but there is greater dyspnoaa, and 
 a marked disproportion between respiration and pulse. The 
 former may be from thirty to seventy, and the pulse perhaps 
 only 110. The cough becomes either hacking or paroxysmal in 
 character, and there is expectoration of the rustt/, viscid phlegm, 
 parthognomonie of this condition. The pneumonic countenance 
 develops — i.e., flushed face, malar lividity, dilated pupils, and 
 crops of herpes round the mouth. The urine is highly febrile, 
 chlorides are markedly diminished and urates increased. Between 
 the fifth and eighth day the symptoms most frequently abate quite 
 suddenly, and rapid recovery takes place ; but often, instead of 
 this happy termination, the temperature increases, or perhaps 
 falls to sub-normal, the pulse becomes more rapid, tongue dry and 
 brown, the sputum less viscid and prune coloured, the patient 
 quickly falls into the typhoid state, and death takes place most 
 frequently from heart failure. Sometimes, prolonged exhaustion, 
 or oedema of the sound lung brings about a fatal issue. 
 
 Special Points to Note — 
 
 1. The viscid, rusty phlegm (if it becomes prune-coloured, is 
 an extremely bad sign). 
 
 2. Marked disproportion between pulse and respiration. 
 
 3. Diminished chlorides in the urine. 
 
 As failure of the right side of the heart is the more common 
 mode of death, special attention should be paid to the state of 
 the pulse, and condition of the second sound of the heart. 
 
 Treatment depends entirely on the type of case, and con- 
 dition of the patient. In no disease has there been more serious 
 blundering ; and, routine treatment is the worst of all treatments. 
 Answer the following questions before prescribing. Is the 
 patient full blooded, and is there a fuU bounding pulse ? Is 
 the pulse feeble, irregular, or intermittent ] 
 
Catarrhal- Pneumonia. 161 
 
 In the first case we may proceed cautiously with, depressants, 
 such as ^ grain of tartar emetic, in comhination with nitric Esther 
 and citrate of potash. 
 
 In the latter case we can hope for nothing from a depressing 
 treatment, so stimulants must he resorted to, such as alcohol, 
 ammon. carb., egg and brandy mixture, quinine, aether, etc. 
 When the sputum is very bloody, I have seen nothing act as 
 well as twenty minims of tinct. ferri perchlor., with five grains 
 of quinine every four hours or even oftener. Chloral should 
 be avoided. 
 
 Eemember also that narcotics are not well borne in respiratory 
 embarrassment as a rule, but if pain be excessive a hypodermic 
 injection of morphia does more good than harm, notwithstanding 
 that theoretically morphia is contra-indicated. Poultices may 
 be applied to the chest, but they are of doubtful use where 
 they are carelessly made. Some authorities advocate the local 
 application of ice. 
 
 CATARRHAL- PNEUMONIA. 
 
 ( Beoncho-Pnbumonia. ) 
 
 Catarrhal Pneumonia as the name implies, is an extension 
 of inflammation of the bronchioles into the air vesicles. Fre- 
 quently the process is set up in collapsed lobules. 
 
 .etiology. — It is most frequently seen amongst children, old 
 people, and those who have to assume the recumbent position. 
 Perhaps this, more than any other affection brings about a fatal 
 issue in specific fevers. It is an almost constant accompaniment 
 of whooping cough and measles. 
 
 Causes. — The more common are — 
 
 1. Chills, and exposure to inclement weather. 
 
 2. Extension of bronchial affections. 
 
 3. Inhalation of irritating vapours, gases, etc. 
 ■4. As a part of the tuberculous process. 
 
 5. As a sequence of infectious fevers. 
 
 M 
 
162 Student's Hand-book of Medicine. 
 
 Symptoms. — At first merely those of broncliial catarrh, the 
 temperature rapidly hecomes high, and markedly oscillating, 
 or irregularly remittent in character. The dyspnoea hecomes 
 marked; the pulse feehle and irregular; and the cough harsh, 
 short, and painful ; the sputam is scanty, never rusty, hut 
 may he streaked with hlood. The disease ends hy lysis, and 
 frequently the exacerbations of fever after the temperature has 
 hecome normal, are most numerous. Loss of flesh is marked and 
 difficulty might he experienced in diagnosing this affection from 
 acute tuberculosis. Indeed, some authorities look upon this 
 affection as an acute phthisis. Undoubtedly catarrhal pneumonia 
 is often followed by phthisis. Erunton's explanation is : " That 
 the delayed resolution of the inflammatory products form a 
 suitable nidus for the tubercle bacillus," and he further suggests 
 the use of arsenic to hasten fatty degeneration and absorption. 
 Death often takes place from asthenia ; or recovery is followed 
 by a rather tardy convalescence. 
 
 Pathology. — We find consolidated patches, indefinite or 
 sometimes sharply defined. The air vesicles in the consolidated 
 area are — • 
 
 1. Usually collapsed, with congested walls and swollen 
 epithelial lining. There are — 
 
 2. Proliferated epithelial cells in abundance. 
 
 3. Leucocytes. 
 
 4. Mucus, and a slight amount of fibrin. 
 
 The bronchioles are inflamed, frequently plugged, and their 
 walls infiltrated with small cells. 
 
 The surrounding lobules are somewhat congested, and emphy- 
 sematous (compensatory emphysema). 
 
 Physical Signs are very uncertain. The chief signs over the 
 consolidated areas are, increased vocal resonance and fremitus 
 slight tubular breathing with small rales. The intercostal 
 spaces are often sucked in over the collapsed areas. 
 
Pleurisy. 163 
 
 Treatment. — Avoid lowering treatment. Give ammonia, 
 senega, and ipecac. Quinine, whisky, egg mixture, and anti- 
 pyrin, are all useful ; also the use of antiseptic inhalations. 
 Great care should he taken during convalescence. "Woollen 
 clothing, cod-liver oil, hypophosphites, and malt extract, etc., 
 must not be forgotten. 
 
 PLEURISY. 
 
 An acute inflammation of the lining membrane of the lungs 
 and thorax. 
 
 Causes — 
 
 1. Exposure to cold. 
 
 2. Extension of inflammation from other parts, as 
 
 pneumonia, hepatitis, tuberculosis. 
 
 3. Irritation from tumours — i.e., aneurism of aorta, 
 
 tumours of lung, mediastinal glands, etc. 
 
 4. Injuries from without. 
 
 5. In the course of other fevers. 
 
 Pathology. — That of a typical serous membrane, viz. — 
 
 1. Hypermmia — loss of lustre, membrane is dry and red. 
 
 2. Exudation of lymph, which coagulates, and gives a shaggy 
 appearance to the membranes. 
 
 3. Effusion of Fluid which is sero-fibrinous, yellowish-green 
 in colour, with floating flakes of lymph. Specific gravity 1010 
 to 1020; coagulates on boiling (from amount of albumen); it 
 also contains a large amount of fibrin. 
 
 4. Resolution, with more or less permanent adhesions. 
 (See Inflammation of Serous Membranes.) 
 
 The process, however, may stop at the second stage, and the 
 exudation speedily resolve — i.e., dry pleurisy ; or the effusion 
 may become purulent, and constitute an empyema. 
 
164 Student's Hand-hook of Medicine. 
 
 Effects of the Effusion.— li large, it produces grave symptoms 
 by the pressure on the lung tissue and viscera near. 
 
 1. It causes collapse of a portion, or sometimes the whole 
 of the lung. (The lung naturally tends to collapse, hy virtue 
 of its own elasticity.) 
 
 2. The lung may be actually pushed across the middle line. 
 
 3. In extreme cases the heart, great vessels, and mediastinum 
 are pushed to the opposite side. 
 
 The thorax bulges forward, and the liver or spleen get dis- 
 placed downwards. The intercostal spaces may be slightly 
 distended, and the diaphragm much embarrassed. 
 
 Absorption should occur in from 9 to 21 days. If it is 
 unusually slow in absorbing, suspect empyema. 
 
 Are there any absolute signs of the fluid being purulent? 
 No ; but there are usually some signs, such as — 
 
 1. Period of absolute dulness persisting. 
 
 2. Temperature becoming septic in character. 
 
 3. Night sweats. (Patient often complains that his 
 
 night clothes are wet through.) 
 
 4. Intercostal spaces are said to " bulge" more. (?) 
 
 The only cei-tain way of ascertaining the presence of pus, 
 however, is to use a hypodermic needle as an aspirator. 
 
 S3nnptoms. — Pleurisy is ushered in by — 
 
 1 . Chills or rigors. 
 
 2. Eapid ascent of temperature (which is not so high as 
 
 in pneumonia.) 
 
 3. Lancinating, tearing pain in the side, rendered worse 
 
 by any respiratory act. 
 
 As the disease advances, and effusion takes place, the severe 
 pain becomes replaced by dyspnoea. The patient lies on the 
 
Pleurisy. 165 
 
 affected side to give tlie sound lung more freedom. The 
 respirations are hurried, pulse quickened, and cough is hacking 
 in character ; the sputum is, however, slight in amount. Death 
 may occur from collapse of the lung, or through the advent of 
 some — 
 
 Complications such as — 
 Empyema. 
 Pneumonia. 
 Meningitis. 
 Heart failure. 
 
 Physical Signs. — Vary with the stage. 
 
 1. Stage of Exudation. 
 
 (1) Auscultation reveals the characteristic friction rub. 
 
 This sound, synchronous with the chest move- 
 ments, is usually leathery-creaking in character, 
 but is sometimes quite musical, like rubbing a 
 pane of glass with a moist finger. 
 
 (2) Palpation yields friction fremitus. 
 
 2. State of Effusion. — The physical signs over the affected 
 
 area are — 
 
 (1) Absence of breath sounds. 
 
 (2) Absence of vocal resonance and fremitus. 
 
 (3) Marked dulness on percussion. 
 
 (4) Diminished movement. 
 
 3. Above the line of Effusion. 
 
 Just above is a small area where the voice is transmitted 
 through — • 
 
 (1) Slightly condensed lung ; 
 
 (2) A thin layer of effusion ; consequently giving rise to a 
 
 peculiar modification of the voice, termed oegophony 
 — compared by some writers to the bleating of a goat 
 
166 Student's Hand-book of Medicine. 
 
 I have never found the resemblance. Perhaps the 
 older writers' goats were different to those of the 
 present generation. 
 4. Over the lung above the effusion. 
 
 The signs wiU depend on the amount of pressure. 
 Usually, we get on — 
 Inspection — Diminished movement. 
 
 Palpation — Vocal fremitus increased. Vocal resonance in- 
 creased to the extent of broncophony. 
 
 Percussion — " Skodic resonance." If heavily percussed, we 
 get almost a " cracked-pot " sound. 
 
 Sometimes in the effusion stage, over the fluid, the breath 
 sounds are replaced by slight tubular breathing (Oslee). This, 
 however, must be due to collapse of lung tissue around patent 
 tubes, or a patch of pneumonia; and cannot, therefore, be looked 
 upon as a sign of effusion, but of a complication. I earnestly 
 ask the student to get a thorough understanding of (1) how 
 breath sounds are produced, and (2) what the necessary 
 conditions are to modify those sounds — then, reason for himseK 
 what " ought to occur under certain conditions.'' If we speak 
 of possibilities of what might be heard in effusion, it would 
 fill a book, and surely " typical " signs are enough for a junior 
 student to get up intelligently. 
 
 Signs of displaced organs — 
 
 1. Altered position of "apex beat." 
 
 2. Ensiform cartilage pushed aside. 
 
 3. Liver pushed downwards. 
 
 Empyema — special points — 
 
 1. Whilst an empyema is frequently due to the pleuritic 
 effusion becoming purulent, it may be pi-imary — i.e., purulent 
 from the beginning. 
 
 2. Note that when " pleurisy " is a sequela or complication 
 of the zymotic fevers or pycemic state, it nearly always becomes 
 purulent. 
 
Pleurisy. 167 
 
 3. If pleurisy is a result of pneumonia, cancer, or tubercle, 
 it is usually purulent from the start. 
 
 4. Dr Cathcart has called attention to the peculiar state of 
 the ribs in old empysemas, Tiz. — 
 
 (1) A crowding together of the lower ribs. 
 
 (2) Absorption of a portion of rib (atrophy). 
 
 (3) With a deposit of new bone (hypertrophy). 
 
 (4) Giving the rib on section a a appearance — i.e., 
 
 atrophy at apex, and hypertrophy at base. 
 
 5. The prognosis is much more unfavourable, and demands 
 surgical interference, as pus may burrow anywhere. 
 
 Treatment of pleurisy 
 O'rtse^.^General principles of " fever." Relieve the intense 
 pain by — 
 
 1. Poultices or blisters. 
 
 2. Hypodermic injection of morphia, or 
 
 3. Fifteen grains of pulv. ipecac, co. 
 
 4. Strapping the affected side (to diminish movement). 
 
 5. Leeches. 
 
 During Effusion. — Salines, quinine or antipyrin, digitalis 
 and ammonia. 
 
 To Promote Absorption. — Pot. iodid., ammonia carb., 
 ammonia chloride, arsenic and iron. 
 
 During Convalescence. — If slow, nourishing diet, cod liver 
 oil, arsenic and quinine, or phosphorus. 
 
 Empyema. — 
 
 1. Evacuate pus — by — 
 
 (1) Aspiration. 
 
 (2) Eesection and free drainage. 
 
 2. Tonics ; remember the tendency of this complication to 
 be associated with tuberculosis. 
 
168 
 
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170 Student's Hand-book of Medicine. 
 
 PHTHISIS. 
 
 By phthisis we mean a morbid condition of the lung tissue 
 due to the invasion of a specific bacillus ; and characterised 
 pathologically by formation of tubercles, which subsequently 
 undergo retrograde changes, involving destruction of lung 
 substance. 
 
 etiology. — It is still much debated whether- phthisis is 
 hereditary or not. It is certainly true that consumption does 
 affect some families generation after generation, but still it is 
 doubtful whether it is transmitted from parent to child. It is 
 probable that whilst the disease is not strictly hereditary, a 
 predisposition to it is. Or putting it plainer, whilst the off- 
 spring of consumptive parents are not horn with the disease, 
 they are bom with a highly suitable soil for the development 
 of such. The more common causes tabulated are — 
 
 Causes. — 
 
 1. Hereditary tendency. 
 
 2. Bad sanitary surroundings. 
 
 3. Deficient food. 
 
 4. Living on damp soils. 
 
 5. Undue exposure. 
 
 6. Certain occupations — stone-masons, knife-grinders, etc. 
 
 7. Excessive lactation. 
 
 8. Result of exhausting diseases, especially catarrhal 
 pneumonia. 
 
 "We have at page 55 considered the main facts relative to 
 the baciUus, and the peculiar manner in which it exerts its 
 pernicious influence. We have only to apply to the lung that 
 which we have already seen occurs in tissues generally, to get a 
 fair picture of a typical case of pulmonary consumption. 
 
Phthisis. 
 
 171 
 
 PATHOLOGY. 
 
 1. Damage to the lung 
 tissue and invasion of the 
 bacilli. 
 
 2, Inflammatory changes 
 around bacilli, resulting 
 in the formation of grey 
 tubercles. 
 
 3. Inflammatory zone 
 around the tuherclea. 
 
 4. Commencement of 
 breaking down. 
 
 5. Formation of cavities. 
 
 PHYSICAL SIGNS, 
 
 Weakened breathing ; pro- 
 longed expiratioUj cog-wheel 
 inspiration, etc., phis adven- 
 titious signs of the particular 
 exciting cause. 
 
 g Diminished movement. 
 
 .^ Slight flattening. 
 
 Q Dull note. 
 
 ■^ Vocal fremitus, and 
 
 g Tocal resonance increased. 
 
 I BroncMal breathing fmay 
 
 ^ be 'tubular' m quality J. 
 
 Consolidation, but attended 
 with moist sounds. 
 
 Flattening is marked ; move- 
 ment much diminished; boxy 
 note or cracked - pot sound ; 
 whispering pectriloquy ; am- 
 phoric or eavernouB breathing, 
 plus adventitious sounds. 
 
 CLINICAL SYMPTOMS. 
 
 Possibly no symptoms 
 beyond a slight persistent 
 cough, weakness, anorexia, 
 etc. 
 
 Increased weakness and 
 cough; elevation of tem- 
 perature, especially in the 
 evening ; dmuse pain in 
 cheat. 
 
 Increase in the severity 
 of abovesymptoms: there 
 is now great emaciation, 
 night sweats, oscillating 
 temperature, hsemopty- 
 .sis, distressing bouts of 
 coughing, characteristic 
 sputum, diarrhosa. Evi- 
 dence of lardaceous 
 disease in other organs, 
 especially Imer. 
 
 Whilst the above tahle gives a short summary of the various 
 aspects of this disease, it must in addition be remembered that 
 cases widely differ. For instancSj the disease may commence 
 with very marked symptoms of bronchial catarrh ; others 
 again are so insidious in their onset that the greater part of a 
 lung may be consolidated before any severe symptoms develop. 
 And so with the physical signs, they vary enormously. We have, 
 it is true, sketched the typical signs of typical damage to the 
 elasticity of the lung, of consolidation, and of a cavity ; but 
 such typical signs are often absent or masked by the bronchial 
 affection ; indeed, the student, who has a clear idea how the 
 various sounds are produced, will learn more by carefully ex- 
 amining six cases of phthisis than he will by digesting the 
 most admirably written treatise on the subject. We shaU 
 now consider the Various symptoms in detail. 
 
 Onset, — The disease usually commences at the apex of the 
 lung by the formation of tubercles in the peri-bronchial tissue ; 
 but gradually deposits of tubercles form at lower levels, especially 
 along the anterior margins. When the lower lobes are affected, 
 
172 Student's Hand-book of Medicine. 
 
 the seat of invasion is about that part of the lung corresponding 
 to the vertebral border of the scapula, when the hand of that 
 side is hooked over the opposite shoulder. Owing to the peculiar 
 manner in which the disease begins and progresses, it is possible 
 in one case to get the signs of invasion of tubercle at the base, 
 consolidation in the middle, and excavations at the apex. 
 
 Course. — The disease may be rapid or extremely chronic. 
 It may be hastened by severe complications, bad treatment, 
 unusually suitable soil, or putrefaction of cavity contents. It 
 may on the other hand be arrested or hindered by — 
 
 1. Formation of fibrous tissue encapsulating the tubercles. 
 
 2. Caseation and calcification of the tubercles or tubercular 
 debris, thus causing cavities to dry up (natural cure). Eemem- 
 ber, however, the disease having become chronic, may take on 
 a rapid form through some inflammatory condition elsewhere. 
 
 (1) Hcemoptysis. — The blood is bright and frothy in the 
 early stage, but later it may be dark from stagnation or venous 
 congestion. During the excavation stage, small aneurismal 
 swellings on unsupported blood-vessels may burst and cause 
 speedy death. Often slight haemoptysis is the first symptom 
 of phthisis. 
 
 (2) Cough is a constant symptom ; at first slight, then gradu- 
 ally becomes hacking, paroxysmal, and painful. 
 
 (3) Expectoration at first is muco-purulent, but later becomes 
 more purulent and copious. It is non-serated, often blood- 
 stained, and shows the peculiar coin like arrangement when 
 expectorated into water. Often little grey hard pellets are 
 present, with abundance of elastic tissue and bacilli. 
 
 (4) Pyrexia. — At first the temperature is elevated only in 
 the evening, but towards the end the temperature may oscillate 
 continually between 100° and 104° F. Such a temperature 
 is highly suspicious of sepsis due to absorption of broken down 
 tissue. It is usually accompanied by the "hectic" flush, dilated 
 pupils, and severe night sweats. When the so called night sweats 
 
Phthisis. 173 
 
 occur in the earlier stages, it is probably due to reflex vaso- 
 motor disturbances and not sepsis. 
 
 (5) Loss of Flesh. — This is nearly always most marked, but 
 extensive fatty degeneration or waxy degeneration, may some- 
 what mask the real wasting of muscle. 
 
 (6) Diarrhoea.- — This is most often due to tubercular infil- 
 tration of the intestines, but may be excited by indigestible 
 food, high pyrexia, or quinine, etc. 
 
 Complications. — 
 
 1. Pleurisy ia most commonly present, but it is doubtful 
 whether it should be looked up as a complication. Professor 
 Gairdner in his excellent monograph says : " It is not to be 
 regarded as a fatal complication, but as a healing power, in as 
 much as it prevents perforation of the pleura, or even obliterates 
 the cavity between the two layers, thus preventing empyema, 
 pneumo-thorax, etc. It is a curious and beautifully conservative 
 arrangement that in most cases the pleuritic adhesions are often 
 in advance of the actual deposit of tubercle near the surface, 
 and still more in advance of its softening." 
 
 2. Pyo-thorax. 
 
 3. Pneumo-thorax. 
 
 4. Spreading of the tubercular disease to the larynx 
 meninges, peritoneum, etc. 
 
 Physical Signs. — We have already pointed out that the 
 typical signs given in the table are often absent or masked 
 by various conditions. It is often difBcult to say whether a 
 cavity exists or not, owing to — 
 
 1. Its small size. 
 
 2. It being deep down and more or less healthy lung 
 intervening between it and the surface. 
 
 3. Thickened pleura. 
 
 4. Compensatory emphysema. 
 
 5. Breath sounds being drowned by extensive bronchitis. 
 
 6. Blocking of the tubes. 
 
174 Student' f: Hand-book of Medicine. 
 
 Again bronchial breathing is often heard in very thia 
 healthy people ; the " crack-pot sound " may be elicited in 
 healthy children, and so on. "We thus see there are many 
 pros and cons to be considered before diagnosing a cavity, 
 and unless the general condition and history of the patient 
 are well considered, physical signs will often lead to an 
 erroneous diagnosis. Post-mortem examinations prove this 
 to be so. 
 
 Treatment wUl be considered under three heads — hygienic, 
 dietetic, and medicinal. 
 
 Hygiene. — Patient must wear wool or flannel next to skin, 
 take gentle out-door exercise, and sleep alone ia an airy bed- 
 room. He should be weU rubbed after tepid baths, and absolute 
 cleanliness observed as regards the teeth and mouth. The 
 expectoration should be received into an antiseptic solution, and 
 never allowed to dry on the carpet, etc. Whilst the patient 
 should be kept warm, do not overload him with heavy clothes — 
 do not, in fact, coddle him. 
 
 Dietetic. — We should aim at giving our patient as much 
 food as he can possibly assimilate. Rum and milk is deser- 
 vedly a favourite (though old-fashioned) remedy, given early 
 in the morning. The p.itient's great dislike to fats of all kinds, 
 hampers dietetic treatment a great deal. Koumiss and pep- 
 tonised meats must always be remembered when the assimilative 
 powers are weak. 
 
 Medicinal. — 
 
 1. General. — Tonics, such as hypophosphites, maltine and 
 cod-liver oil are the principal remedies prescribed. 
 
 2. Symptomatic. — Any grave complication must be treated 
 energetically. 
 
 (1) The cough. — As this is a persistent and constant 
 feature of the disease, avoid rushing to the usual 
 cough mixtures at once. A most common excit- 
 ing cause of the nightly cough is the changing 
 
Phthisis. 175 
 
 from a warm room to a cold bedroom ; or again, 
 tickling of the fances by the uvula. A very good 
 cough mixture is — 
 
 I^ Tinct. Chloroformi et Morphinae . . 3ij. 
 
 Acid, Nitric Dil 3ij- 
 
 Glycerine ad giss. 
 
 Mat mist. 3i when the cough is very troublesome. 
 Inhalations " moist or dry " are of the utmost 
 value. 
 
 (2) The night sweats. — Picrotoxin, quinine, atropine, 
 
 and oxide of zinc are the favourite remedies. 
 
 (3) The diarrhosa. — It is usually best controlled by 
 
 mineral astringents, in combination with opium. 
 
 (4) Hssmoptysis. — Absolute rest and cold applications. 
 
 Tincture ferri, hamamelis, gallic acid, erogotine, 
 or best of all a full dose of opium. 
 
 Other complications must be treated on general principles. 
 
 Change of Air. — Under this heading we shall include — 
 
 1. Sea voyages. 
 
 2. Change of residence. 
 
 Sea voyages undoubtedly do good in many cases of early 
 phthisis. Whether the benefit is due to a general bracing up 
 of the nervous and muscular systems, or whether the sea air 
 (containing as it does, iodine bromine, etc.), exerts a beneficial 
 local influence is not yet determined, but probably both factors 
 contribute to the cure. Before deciding to send a patient on a 
 long voyage several points must be considered. Is the patient a 
 good sailor 1 If not, is the severe sea sickness likely to produce 
 haemoptysis, or prevent proper feeding 1 Is the patient well off 
 and likely to receive every comfort on board? Eemember a 
 woman cannot " rough things " as easily as a man ; and further, 
 many things which are not mconvenient to a man, must be so 
 to a woman. No patient should go without a relative or friend 
 accompanying him. Lastly, sea voyages are contra-indicated in 
 the later stages of phthisis. , 
 
176 Student's Hand -hook of Medicine. 
 
 Cfhange of Air. — A phthisical patient requires either dry 
 cold or warm air. In the earlier stage cold dry air is the 
 best. New Mexico, Davos, and Canada, are the best ex- 
 amples of such residences. For warm climates we might 
 select New Zealand, Madeira, Algiers, Torquay, Hastings, 
 etc. Eemember it is absolutely cruel quackery to send a 
 patient far advanced in phthisis, away from home and friends, 
 only too frequently to die amongst strangers. 
 
 Special Treatments.— Many special forms of treatment have 
 been advocated — 
 
 1. By Koch's Tuberculin — 
 
 A treatment which is the outcome of much patient 
 research, and based upon very scientific grounds. 
 Eesults are very conflicting, and this treatment 
 at present is in evil repute. Possibly its failure 
 is the outcome of imperfect trial. 
 
 2. Intra-laryngeal injections of guaicol, iodopyrin. Much 
 
 success has been obtained by different physicians 
 by this method. 
 
 3. Surgical Treatment. — Aspirating the cavities, followed 
 
 by injections of antiseptics. 
 
 Amongst other treatments may be mentioned those which 
 imitate natural cure by causing fibrosis or calcification. Alcohol 
 in large doses. Eectal injections of carbonic acid gas. Other 
 special treatments have been advised by many physicians resid- 
 ing at popular health resorts ; many are either the result of 
 fanaticism or something worse. 
 
 Laryngeal Phthisis wUl be considered under diseases of the 
 larynx. 
 
 PNEUMO-THORAX. 
 
 Pneumo-thorax means the presence of air in the pleural 
 cavity. 
 
Hyd/ro- Pneumothorax. 177 
 
 Causes. — 
 
 1. Traumatisms, such as punctured wounds, laceration from 
 the end of a hroken rib. 
 
 2. Causes from the lung side^- 
 
 (1) Bursting of a pulmonary abscess into the pleura. 
 
 (2) Gangrene of the lung. 
 
 (3) Excessive intra-pulmonary pressure. 
 
 (4) Tubercules breaking down, causing undermining and 
 
 perforation of the pleura when adhesions have 
 not been set up. 
 
 Physical Signs. — 
 
 Inspection. — Bulging may be local or general on the affected 
 side. 
 
 Percussion. — Usually yields a hyper-resonant note. K the 
 valvular-like opening be patent, a typical crack-pot sound can 
 be elicited. 
 
 Palpation. — Absence of vocal fremitus. 
 
 Auscultation. — Absence of breath sounds. On coughing the 
 sounds produced are peculiarly amphoric and have a metallic 
 ring. If the chest be struck with two coins whilst listening 
 with the stethoscope the characteristic bell or anvil sound 
 is heard. 
 
 HYDRO-PNEUMOTHORAX. 
 
 A condition where air is present above and fluid ielow in the 
 pleural cavity. 
 
 Physical Signs, ^/n the upper part — those signs already 
 described as diagnostic of pneumo-thorax, plus hippocratic suc- 
 cvssion (the term applied to the splashing sound heard on 
 shaking the patient.) 
 
178 Student's Hand-hook of Medicine. 
 
 Beloio — the signs diagnostic of fluid already discussed under 
 pleurisy. 
 
 Symptoms. — The symptoms of pneumo-thorax will depend 
 largely upon the manner in which it was produced, and the 
 quantity of air present. They may be summed up as follows — 
 
 1. Sudden pain at time of rupture with or 
 
 without coUapse. 
 
 2. Great dyspnoea. 
 
 3. Quick and small pulse. 
 
 4. Shallow and rapid breathing. 
 
 Treatment. — Subdue the pain by a hypodermic injection of 
 morphine, hot poultices, diffusible stimulants, etc. Aspiration 
 is of doubtful value. 
 
 HYDRO-THORAX. 
 
 Hydro-thorax — i.e., dropsy of the pleurae, is a term used to 
 denote fluid jn the pleural cavity, the result of a passive process, 
 as seen in Bright's disease, etc. 
 
 The main points of difference between it and real pleuritic 
 effusion are — 
 
 1. Not being preceded by acute symptoms of inflammation, 
 therefore, absence of friction. 
 
 2. Usually bi-lateral. 
 
 3. The fluid gravitates with movements of the patient to a 
 far greater extent (like ascites). 
 
 4. Aspiration is not likely to do more than temporarily 
 relieve pressure. 
 
 5. Associated with signs of dropsy elsewhere. 
 
 6. Absence of pain, but dyspncea is greater than in acute 
 pleurisy. 
 
Asthma. 179 
 
 ASTHMA. 
 
 Asthma is a disease characterised by sudden attacks of 
 dyspnoea, which suhside after a time, but tend to recur 
 at intervals. 
 
 etiology. — Heredity is a most important factor. When it 
 develops in children there is usually a history of post pharyn- 
 geal trouble, measles, whooping cough, or imperfect recovery 
 after capillary bronchitis ; gout, malaria, and subsidence of skin 
 eruptions, are also held responsible for many cases. Probably, 
 however, most cases have a neurotic origin. It is much more 
 frequent in males than in females, possibly because of their 
 greater liability to bronchial affections generally. 
 
 Pathology. — AU authorities agree that the affection is due 
 to diminished calibre of the smaller bronchioles, but the nature 
 of such contraction is still disputed. The most probable 
 theory is the first, viz. : — 
 
 1. Reflex spasm of the bronchial muscles, associated with 
 hypersemia and turgescence of the mucous membrane lining 
 the smaller bronchioles, and the exudation of a characteristic 
 mucus. 
 
 2. Hypercemic swelling of the mucous membrane, like 
 "nettle rash" (Sir A. Clark). 
 
 3. Vasa-motor paralysis. 
 
 Possibly all three theories are necessary to explain all cases. 
 
 Symptoms. — 
 
 1. Premonitory Symptoms. — There is usually some visceral 
 disturbance as flatulence, etc. 
 
 2. The Attach — It occurs most frequently during the night, 
 the patient waking up with a feeling of great dyspnoea ; he 
 
180 Student's Hand-book of Medicine. 
 
 feels as if there is not sufficient air in the room, and asks for 
 the -windows and doors to be opened. ' The characteristic 
 attitude of asthma is assumed — i.e., the patient grasps some 
 support to fix the shoulder girdle, in order to bring his ex- 
 traordinary muscles of respiration into play. Expiration is 
 prolonged. Sibilant rhonchi cause a peculiar, noisy, pipe-like 
 ■wheezing; but in spite of the extraordinary efforts little air 
 enters the lung. A paroxysm of coughing and expectoration 
 gives slight relief or even terminates the intense dyspnoea, and 
 sleep may supervene, or a slight lull may be succeeded by 
 another paroxysm. 
 
 The Sputum is usually expelled with the greatest difficulty, 
 and is distinctly peculiar in its composition. The baU-like 
 gelatinous masses can be unfolded, and is then found to repre- 
 sent casts of the small bronchioles. 
 
 Curschman describes the expectoration under the microscope 
 as foUows : — 
 
 At First. — The pellets show two forms of spiral threads. 
 The one form entangles within its mesh work cells in various 
 stages of fatty degeneration. The other form contains a central 
 clear filament, surrounded by a network of other filaments. 
 
 Later. — The filaments disappear, and octahedral crystals of 
 phosphates appear in the now muco-purulent expectoration. 
 The course of the attack depend? on the immediate cause, and 
 the amount of bronchitis associated with it. As a rule, the 
 asthmatic attacks tend to become less severe, but the bronchial 
 affection more pronounced. Death seldom or never takes place 
 from pure asthma. 
 
 Physical Signs. 
 
 During the Attack. — The thorax is expanded and fixed. 
 Diaphragm moves but slightly, inspiration is short, and expir- 
 ation prolonged. Auscultation : vesicular breathing is drowned 
 by sibilant rhonchi, or later, with bubbling rales. Percussion 
 reveals little, beyond slight hyper-resonance. 
 
EmphyseTna. 181 
 
 Treatment. — 
 
 During the Attack. — Eemove any obvious cause of reflex 
 irritation, such as an overloaded stomach. A brisk emetic often 
 cuts an attack short ; nitrites, especially nitrite of amyl or 
 chloroform may be inhaled. Belladonna, stramonium, and 
 lobelia in combination with ammonia are useful remedies ; the 
 fumes of burnt nitre paper, etc., are also recommended. 
 
 During Convalescence. — Change of air, careful diet, cod-liver 
 oil, tonics, etc. 
 
 EMPHYSEMA. 
 
 By emphysema of the lungs is meant — (1) A condition 
 where the air cells are over distended -■ vesicular emphysema ; 
 (2) A condition where the air has accumulated in the inter- 
 stitial tissue = interstitial emphysema. 
 
 Emphysema is again divided into — 
 
 1. Compensatory Envphysema.—A condition where a portion 
 of lung expands to take the place of a collapsed portion; seen 
 in catarrhal pneumonia, pleuritic adhesions, in areas of old 
 cicatrices, etc. 
 
 2. Atrophic Emphysema, or small lung emphysema, due to 
 senile atrophy. The chest is of course small. 
 
 3. Hypertrophic or ordinary Emphysema. — A condition 
 characterised by — 
 
 (1) Over distension of the vesicles. 
 
 (2) Atrophy of their walls. 
 
 (3) Obliteration of blood-vessels, and a consequent dim- 
 
 inished " oxygenating" area. 
 
 (4) Changes in the shape of the chest. 
 
 (5) Changes in the'heart (right). 
 
 (6) Changes generally, due to imperfect exchange of 
 
 gases between the blood and the air. 
 
182 Student's Hand-book of Medicine. 
 
 Causes. — They include all those factors which keep up a 
 more or less persistent high intra-alveolar tension. 
 
 1. Playing on wind instrument. 
 
 2. Certain occupations, such as glass blowing, colliers, etc. 
 
 3. Dr Jackson of Boston, lays great stress upon the heredi- 
 tary character of emphysema. 
 
 Pathology. — The pleurae are pale. The lungs pit readily on 
 pressure, and have a peculiar soft downy feel. The dilated 
 vesicles are well seen on the surfaces, and also projecting 
 from the free margins of the lungs. The vesicles first 
 become dilated, coalesce, atrophy, and the septa between 
 the neighbouring cells get absorbed. The capillaries dis- 
 appear. Though the changes are principally in the lung 
 vesicles, there are always more or less marked changes in 
 the bronchial tubes. Bronchiectasis is often a marked 
 feature. 
 
 Symptoms. — They are too well known to require details ; 
 the important points to remember are — deficient aeration 
 means dyspnoea and cyanosis ; 'the retention of waste products 
 within the blood means impure blood and defective nutrition j 
 the venous congestion is increased by the dilatation of the right 
 heart, and thus a cycle of down grade changes is brought about, 
 ending in, perhaps, dropsy, uraemia, or collapse of lung, etc. 
 
 Physical Signs. — Barrel shaped chest, prominent sternum, 
 deep sternal fossa, prolonged expiration, and hyper-resonance are 
 the more common features. A zone of dilated venules along 
 the attachment of the diaphragm is spoken of by some writers. 
 The epigastric pulsation and altered position of apex beat are 
 important signs. 
 
 Treatment. — That of chronic bronchitis. Sudden and 
 grave attacks of dyspnoea may be treated by inhalation 
 of nitrite of amy], venesection, etc. Sometimes a brisk 
 emetic is the best treatment. 
 
Collapse and (Edeina of the Lung. 183 
 
 COLLAPSE OF THE LUNG. 
 
 Collapse of the lung may be of four types — 
 
 1. Atelectasis. — A condition found in weakly new -bom 
 children, when there is not sufficient inspiratory power to 
 inflate the alveoli. The coUapsed patches are of a slate colour 
 and sink in water. 
 
 2. The form due to pressure from pleuritic effusion. The 
 whole lung may coUapse. 
 
 3. Collapse due to wounds of the chest wall, and perforation 
 of the pleura. In this form the lung at first is congested, but 
 finally becomes anaemic. 
 
 4. Ordinary or lobular collapse, as seen in broncho- 
 pneumonia. Two theories are advanced to explain this 
 condition-^ 
 
 (1) That a bronchus is plugged by a pellet of mucus 
 
 which acts as a ball valve — i.e., allowing air to 
 pass out, but none to enter. 
 
 (2) That the plug does not move at all, but merely 
 
 prevents access of air during inspiration. The 
 alveolar air is exhausted by absorption, and none 
 being taken in to replace it, the lobule collapses. 
 
 Symptoms. — Great dyspnoea, rapid pulse, cyanosis, all 
 depending on the extent of the coUapsed area. It occurs 
 often in measles, whooping-cough, croup, and other conditions 
 which give cause to catarrhal pneumonia. 
 
 Treatment. — Depends on the cause. Emetics and diffusible 
 stimulants. 
 
 CEDEMA OF THE LUNG. 
 
 Definition. — An accumulation of fluid in the interstices of 
 the lungs, air vesicles, and bronchioles. 
 
184 Student's Nand-book of Medicine. 
 
 Causes. — Nearly always associated with general blood 
 diseases, such as Bright's, the anaemic diseases, etc. It is 
 common in the later stages of — 
 
 1. Valvular disease of the heart. 
 
 2. Malignant fevers. \ 
 
 3. Paralysis. [Hypostatic congestion. 
 
 4. Long continued rest on the back. ) 
 
 5. After the use of pilocarpine. 
 
 Pathology. — The lung is heavy and bulky. On pressure a 
 quantity of blood-stained serum exudes. 
 
 Physical Signs. — The breath sounds are deficient, and 
 masked by fine rales. Contrary to what one might expect, 
 the percussion note is more frequently resonant than duU. 
 The explanation given is that a lung, when partially 
 collapsed outside the body, gives forth a resonant sound, 
 due to diminished tension of the lung tissue. 
 
 Symptoms. — Those of serious pulmonary embarrassment 
 (already described under collapse of the lung), plus the 
 abundant expectoration of a frothy serum. 
 
 CHRONIC OR INTERSTITIAL PNEUMONIA. 
 
 It is a most difiicult task to explain what is exactly meant 
 by chronic pneumonia. We have already seen how interstitial 
 changes are present in all chronic afiections of the lung. We 
 have discussed such changes in Emphysema, Phthisis, Bronchi- 
 ectasis, etc. Further, we have clearly demonstrated the fact, 
 " that when the pulmonary tissue is damaged it forms a highly 
 suitable soU for the development of tuberculosis." This state- 
 ment makes it extremely difficult to say where chronic pneumonia 
 ends and fibroid phthisis begins. I shall here describe as chronic 
 pneumonia, that condition of the lung tissue characterised by 
 
Chronic or Interstitial Pnev/monia. 185 
 
 overgrowth of the fibrous elements, due to the action of slowly 
 acting irritants, and attended clinically with symptoms of pul- 
 monary embarrassment; later on, the symptoms are dependant 
 on grave structural change and breaking down of lung substance. 
 
 Causes. — 
 
 1. Inhalation of dust particles (pneumonokoniosis). Ex- 
 amples, anthracosis (coal miner's lung) ; silicosis. (mason's lung). 
 
 2. Irritants in the form of animal poisons. — Glanders, 
 syphilis (white hepatization). 
 
 3. Excessive use of alcohol. 
 
 4. Eesult of acute pneumonia, pleurisy, etc. 
 
 Pathology. — The morbid anatomical changes depend on the 
 cause, and so the reader is referred to a text book on pathology. 
 We shall merely state here the conditions common to aU. 
 
 1. Great overgrowth of interstitial connective tissue, en- 
 croaching upon and destroying the air vesicles. 
 
 2. Changes in the bronchial tubes; their muscular coats 
 are replaced by fibrous tissue, which subsequently yield to 
 intra pulmonary pressure, and form bronchiectic cavities 
 (see bronchiectasis). Sometimes their lumen are occupied 
 by caseous masses, and very frequently obliterative changes 
 take place, and the lumen becomes totally obliterated. 
 
 3. Obliterative changes in the pulmonary and bronchial 
 blood-vessels, leading to severe systematic and local changes. 
 
 Symptoms. — A careful digest of the outstanding features of 
 the morbid structural changes ought to enable us to anticipate 
 the more constant symptoms. The disease runs a very chronic 
 course, and is usually unilateral. Cough may be the only sym- 
 ptom complained of for a long time. Later, the symptoms are 
 those of bronchiectasis. 
 
 Physical Signs. — ■ The affected side is retracted, much 
 flattened, and the intercostal spaces more or less obliterated. 
 
186 Stvdent's Hand-book of Medicine. 
 
 The percussion note -will depend on the state of the bronchi, 
 ranging from absolute dulness to a boxy note; indeed, in the 
 later stages, the physical signs may be those of small cavities 
 with extensive bronchitis. 
 
 Treatment. — Eemove if possible the exciting cause, and 
 then treat on general principles already laid down, in speaking 
 of the various pulmonary affections. 
 
 TUMOURS OF THE LUNGS. 
 CANCKR. 
 
 Primary cancer of the lung is very rare. The secondary 
 variety occurs in the form of either dense, hard, irregular 
 nodules, or soft (medullary) masses, scattered throughout 
 the lung tissue. The original sources are mostly — 
 
 1. Cancer of the bronchial glands, which spreads inwards 
 at the root of the lung, or 
 
 2. Cancer of the liver, which invades the diaphragm, and 
 finally the pleura and lung. 
 
 Symptoms are insidious and varied. The amount of con- 
 solidation often causes pneumonic symptoms. The ulcerative 
 process gives similar signs to phthisis ; and haemoptysis 
 is generally present. 
 
 Diagnosis. — When there are symptoms of malignant mis- 
 chief elsewhere, marJced pulmonary symptoms point to the 
 invasion of the lung. Pleuritic effusion may be so well 
 simulated that puncture is sometimes required to clear up 
 the diagnosis. The disease is usually fatal in about six 
 months from the onset of symptoms. 
 
 Other tumours are too rare to need a detailed account in a 
 work like this. 
 
Acute Laryngitis. 187 
 
 DISEASES OF THE LARYNX. 
 
 Inflammatiou of the larynx may be acute or chronio. 
 
 ACUTB LARYNGITIS. 
 
 Causes. — Contact with irritating vapours, drinking scalding 
 water, impaction of foreign bodies, exposure to damp and cold 
 air, extension of inflammation from other parts, and malignant 
 blood conditions. 
 
 We have already referred to diphtheria as a cause, and we 
 also discussed the differential diagnosis of croup and laryngeal 
 diphtheria. 
 
 Pathology. — It is similar to that of bronchitis. 
 
 1. Hypersemia, causing dryness. 
 
 2. Exudation of lymph = increased muco-purulent secretion. 
 
 3. Changes in the tissues beneath, etc., especially — 
 
 (1) CEdema of the submucous coat and the glottis. 
 
 (2) Changes in the nervo-muscular apparatus of the 
 
 larynx. 
 
 Symptoms — Soreness and dryness accompanied by hoarse- 
 ness, or complete loss of voice. Respiration may be stridulous 
 and noisy. Ehonchi and rMes are often abundant. 
 
 The loss of the voice is due to failure of the vocal cords to 
 meet in the middle line, and to thyro-arytenoid paralysis. 
 
 When the glottis becomes oedematous the symptoms are 
 most alarming. Intense dyspnoea, dysphagia, and stridor are 
 the marked features. Death may occur in a few hours. 
 Laryngoscopically : the epiglottis is seen to be much swollen 
 and bright red in colour; the vocal cords may or may not 
 be infl.amed. 
 
188 Student's Hand -hook of Medicine. 
 
 Treatment. — 
 
 Catarrhal Form. — Eest in bed, steam antiseptic inhalations 
 of eucalyptol, and benzoin. A full dose of Dover's powder 
 often cuts the attack short. Demulcent drinks and absolute 
 rest to the voice. 
 
 (Edematous Variety. — Scarification of the glottis, sucking 
 ice, aether spray, and tracheotomy. 
 
 It should particularly be remembered that very little irri- 
 tation may provoke oedema of the glottis in gouty individuals. 
 
 •B.O^fi TO USK THK LARYNGOSCOPE. 
 
 1. Position of Patient: sitting, body and head erect, knees 
 together, head slightly thrown back. 
 
 2. Lamp : in line with patient's ear, nine inches to the left 
 of his head. 
 
 3. Position of physician : opposite patient with niirror pro- 
 perly adjusted to head and eye. 
 
 4. Mouth : wide open. 
 
 5. Reflect light upon fauces at correct focal distance of 
 reflector. 
 
 6. Warm laryngeal mirror over lamp. Test it against cheek 
 or hand. 
 
 7. Direct patient to protrude his tongue. 
 
 8. Hold it between thumb and index-finger, in napkin 
 (thumb uppermost). 
 
 9. Hold laryngeal mirror like a pen. 
 
 10. Place its back gently against uvula. 
 
 11. Move your hand slightly towards patient's left, so as to 
 keep it out of line of view. 
 
 12. Patient to drawn a deep breath, and say ' ah,' 'ur,' 'eh,' 
 or ' ee.' Be always quiet and gentle ; encourage the patient ; 
 let each examination be short, even if unsuccessful. Be careful 
 not to hurt patient's tongue, or to burn his mouth, or to push 
 either his uvula or the mirror against the back of the pharynx. 
 Use cocaine to lessen sensitiveness of fauces (Keetley). 
 
Chronic Laryngitis. 
 
 189 
 
 CHRONIC LARYNGITIS. 
 
 Chronic laryngitis may be the sequel of acute laryngitis, hut 
 it is much more commonly due to — 
 
 1. Excessive use of the voice — i.e., " dysphonia clericorum," 
 a condition characterised by an cedematous unhealthy condition 
 of the mucous follicles, which present a raw or even ulcerated 
 condition. Aphonia is very common after prolonged speaking. 
 
 2. Tumours, fibroid polypi, epitheliomata, etc. 
 
 3. Gout. 
 
 4. Various nervous affections — functional and organic. 
 
 5. Specific ulcerations — i.e., syphilitic and tubercular. 
 
 PHTHISICAL ULCBEATION. 
 
 1. Attacks first near artenoid 
 cartilages. 
 
 2. Does not advance rapidly. 
 
 3. Great thickening. 
 
 4. Granular appearance of pos- 
 terior surface of epiglottis. 
 
 5. Expectoration, frothy, thin, 
 muco-purulent. 
 
 TEKTIABY ULCER. 
 
 1. Attacks epiglottis first. 
 
 2. Progresses rapidly, 
 
 3. Little thickening. 
 
 4. Inflamed appearance of the 
 hase. 
 
 5. Expectoration thick, ten- 
 acious, yellowish. 
 
 Symptoms. — The severity of the symptoms depend on the 
 cause. The more common are — 
 
 1. Constant hawking and desire to swallow. 
 
 2. Expectoration of muco-purulent phlegm. 
 
 3. Attacks of aphonia. 
 
 4. Spasmodic breathing (most often associated with 
 
 irritation by tumours). 
 
 Treatment. — Depends on cause. Nervine tonics, such as 
 strychniae and iron are nearly always indicated along with 
 
190 Student's Hand-book of Medicine. 
 
 plenty of fresli air; rest to the voice, and douching the throat 
 with cold water. Locally, we may use astringents, such, as tannic 
 acid, nitrate of silver (10 grains to gj), chloride of ammonium 
 vapour, and various antiseptic sprays. 
 
 If Syphilitic. — Pot. iodide internally, with the local 
 application of bichromate of potash. Tracheotomy may he 
 necessary. 
 
 If Tubercular. — Insuifiations of morphia, scrape tumours 
 with curette and apply lactic acid. Intra-laiyngeal medica- 
 tion already described. 
 
 LARYNGISMUS STRIDULUS. 
 
 FALSE CROUP. 
 
 False croup or chUd crowing is a spasmodic disease of the 
 larynx, occurring in infants and young children, consisting of a 
 temporary closure of the rima-glottidis, causing great dyspnoea 
 and other symptoms dependant on temporary suffocation. 
 
 .ffitiology. — Predisposing causes are malnutrition brought 
 about by imperfect feeding; syphilis, rickets, enlarged tonsUs, 
 and the tubercular diathesis. The exciting 
 
 Causes are reflex nervous disturbances, brought about by — 
 
 1. Intestinal irritation. 1 „ 
 
 „ ..^ Y oensory nerves. 
 
 2. Worms. / ■' 
 
 3. Teething (via trifacial nerve). 
 
 4. Exposure to cold (vasa motor). 
 
 5. Overloading the stomach (pneumogastric). 
 
 6. Frights and "starts'' (cortical). 
 
 It will thus be seen that the disease is essentially associated 
 with a neurotic temperament, and disturbances of the various 
 
Laryngismus Stridulus. 191 
 
 nerve centres. There are three or four varieties of laryngismus. 
 Goodhart describes three forms-7- 
 
 1. Direct Spasm, a crowing of a convulsive nature often 
 
 rachitic. 
 
 2. Infantile Spasm. — crowing is due to a congenital 
 
 valvular formation of the upper orifice of the 
 larynx. 
 
 3. Reflex Spasm. 
 
 Symptoms. — Sometimes a slight cold precedes the attack 
 (catarrhal form), but often the child is apparently well on going 
 to bed, and wakes up suddenly at night with a brassy croupy 
 cough and dyspnoea. The spasm is usually worse on first 
 awaking. After a time the spasm passes off and the child, 
 beyond having a slight croupy cough for a day or two, seems 
 none the worse for the attack. Often a series of paroxysms, 
 however, takes place, or recur at night only. The mother is 
 usually much alarmed, and is very anxious for the arrival 
 of the doctor. 
 
 Pathology. — It is to be regarded as a neurosis at present, 
 but the palate and mucous membrane around the laryngeal 
 orifice are often cedematous 
 
 Diagnosis from Croup, viz. — 
 
 1. Absence of false membrane. 
 
 2. Absence of marked local inflammation. 
 
 3. History. 
 
 Treatment. — When in doubt, treat as if it were the more 
 severe disease. 
 
 1. Steam kettle and medicated vapour. 
 
 2. Emetic of ipecacuanha. 
 
 3. Clear out the bowels of any offending matter. 
 
 4. Bromides in the interval. 
 
192 
 
 Student's Hand-book of Medicine. 
 
 LARYNGEAL PARALYSIS. 
 
 During ordinary respiration, tb.e glottis remains partially 
 open, being widened with every inspiration. For the pro- 
 duction of voice, the free borders of the vocal cords must be 
 brought almost close to each other in the middle line, only a 
 very narrow chink being between their parallel sides. At the 
 same time the cords must be rendered tense. The narrowing 
 of the chink is brought about by the adductors, viz., the lateral 
 crico-arytaenoid, assisted by the posterior aryt£enoid and external 
 thyro-arytsenoid muscles. The tightening is due to contraction 
 of the crico-thyroid. The nerves involved are the superior 
 laryngeal and recurrent laryngeal branches of the vagus. It 
 will be easily understood that aphonia or loss of voice may be 
 brought about by local muscular causes or central nervous 
 lesions, and we have already referred to aphonia complicating 
 bulbar paralysis, etc. Again the paralysis may be partial, or 
 complete, of a functional nature, or due to organic lesions. 
 
 Dr Gower's gives the following table : — 
 
 Total bilateral 
 
 paralysis — 
 
 Total unilateral 
 
 paralysis — 
 
 Total abductor 
 
 paralysis — 
 
 Unilateral abductor 
 paralysis — 
 
 Adductor 
 
 paralysis — 
 
 SYMPTOMS. 
 
 5fo voice ; no cough ; 
 stridor only on deep inspira- 
 tion. 
 
 Absence of stridor except 
 ondeepbreatMng; nocougli; 
 voice low and hoarse. 
 
 The voice is little changed ; 
 cough normal ; in^iration 
 difficult and long, witli loud 
 stridor. 
 
 Little affection of either 
 voice or cough. 
 
 No voice ; perfect cough ; 
 no stridor or dyspnoea. 
 
 POSITIOW OF OOBDS. 
 
 Both cords slightly ab- 
 ducted and motionless. 
 
 One cord motionless ; the 
 other moving freely, and 
 even beyond middle Une in 
 phonation. 
 
 Both cords lie together, 
 and not separated during 
 inspiration. 
 
 One cord not moving dur- 
 ing inspiration. 
 
 Cords are not brought 
 together, but move during 
 respiration. 
 
Laryngeal Paralysis. 193 
 
 Causes of Laryngeal Paralysis. 
 
 1. From the nerve side. 
 
 (1) Central lesions. — Bulbar paralysis, disseminated 
 
 paralysis, etc. 
 
 (2) Peripheral. — Aortic aneurisms, mediastinal tumours, 
 
 enlarged thyroid gland, diphtheritic paralysis, all 
 through affecting the recurrent laryngeal nerve. 
 
 2. Local lesions. — Ulceration, due to syphilis, tubercle, or 
 malignant laryngeal tumours affecting the cords. 
 
 3. Functional or hysterical paralysis (nearly always affect 
 the adductors.) 
 
 To sum up. If there be an inability to cough or speak, 
 suspect a serious paralysis. If the voice is preserved and the 
 cough lost — means unilateral paralysis. If there is normal 
 cough, but no voice — unimportant. Loud inspiratory stridor, 
 means — double abductor paralysis. 
 
 Treatment. — Hysterical aphonia must be treated with 
 galvanism. The other forms must be treated on general 
 principles. For detailed treatment consult a good treatise or 
 manual on the Throat. 
 
 DISEASES of the CIRCULATORY SYSTEM. 
 
 [The matter printed in small print is taken by permission 
 from Dr Wyllie's original notes and diagrams. — Though printed 
 in smaller type the reader must not think it less important on 
 that account ; on the contrary I think it a most essential 
 part of the book. — A. Wheeler.] 
 
 PHYSICAL EXAMINATION. 
 
 PERCUSSION. 
 
 1. In health the area of Superficial Cardiac DuTmess is of triangular shape ; 
 the apex or upper angle (truncated) reaches as high as the fourth left costal 
 cartilage ; the right border descends vertically along the middle of the sternum ; 
 
 
 
194 Student's Hand-book of Medicine. 
 
 the left border passes obliquely downwards aud to the left until it readies the 
 outer limit of the apex beat ; the base cannot be percussed out owing to the 
 proximity of the Liver, but corresponds to a line drawn from the outer and 
 inferior limit of the apex beat inwards until it meets the perpendicular limit 
 of cardiac dulness, about mid-sternum. The measurement of the basic line is 
 important ; normally it measures about three or four inches. 
 
 2. The area of Deep Dulness, obtained by heavy percussion, corresponds in 
 shape to the area of superficial dulness, but is more extensive. It overlaps it 
 about an inch on every side. 
 
 Note. — In Disease the areas of Superficial and Deep Dulness may be 
 specially extended to the right or left, according as the right or left 
 chambers of the heart are specially enlarged. 
 
 3. The percussion of the region of the Aortic Arch (above the level of the 
 third costal cartilages) is especially important in cases of aneurism and of 
 mediastinal tumour. 
 
 PALPATION. 
 
 1. Of the Precordia. 
 
 (a) Determine the position of the apex beat. The normal position is 
 between the fifth and sixth ribs, about half an inch within the vertical 
 line of the nipple. Wlien the left ventricle is enlarged there is displace- 
 ment of the apex beat downwards and to the left. When the right 
 ventricle is enlarged there is apparent displacement of the apex beat 
 to the right, and there is often pulsation in the epigastrium. 
 
 (6) Note the limitation or diffimon of the apex beat. 
 
 (c) Note the force and character of the beat : whether moderate and 
 deliberate, as in health ; or strong and sudden, as in nervous excite- 
 ment ; or strong and slow (heaving) as in hypertrophy ; or weak or 
 imperceptible, as in debility. 
 The range of variation is considerable even in health, owing to the shape 
 of the chest, etc. 
 
 2. Of the Aortic Region. In cases of suspected aneurism note presence or 
 absence of pulsation. 
 
 3. Of the gre<ft vessels at the root of the neck. Venous pulsation is scarcely 
 palpable, though strikingly visible ; arterial pulsation is as strikingly palpable 
 as visible. 
 
 INSPKCTION. 
 
 1. Of t\i& Precordia &ai Aortic Region. 
 
 (a) Form. Is there bulging over the precordia or over the aortic region ? 
 
 (b) Movements. (1) Movement of the apex beat : its situation, amount, 
 
 and difi'usion ; (2) Pulsation in the Epigastrium ; (3) Pulsation in the 
 region of the Pulmonary Artery, common in anaemic debility ; (4) 
 Pulsation in the Aortic Region, often present in cases of aortic 
 aneurism. 
 
Diseases of the Circulatory System. 
 
 195 
 
 2. Of the great vessels of the neck, (a) Fulness of the great veins ; (6) 
 Pulsation in these veins ; (c) Excessive pulsation in the arteries. 
 
 3. Of the General Oirculation : as exhibited in the patient's complexion, 
 the condition of his peripheral arteries and veins, the presence or absence of 
 dropsy, etc. 
 
 4. Of the Pupils, in oases of Aneurism of the Aortic Arch. 
 
 KXAMINATION OF THE RADIAL PULSE. 
 
 1. Give the Pulse Rate per minute. 
 
 2. Give the Rhythm: regular or irregular; if intermittent, note the average 
 proportion of the intermissions to the pulse-beats. 
 
 3. Note the size, force, and character of the Blood-wave : large, moderate, 
 or small ; deliberate or sudden ; strong or weak ; a double wave (dicrotism). 
 
 Note. — In weak heart the radial pulse may be almost or wholly impercep- 
 tible ; or only a proportion of the heart's contractions may produce 
 blood-waves sufficiently strong to be propagated perceptibly to the 
 radial artery, and thus the radial pulse may appear to be much slower 
 than the rate of the heart's contractions ; or the weak pulse may be 
 affected by the patient's respiration, its beat being weakened by 
 Inspiration and strengthened by Expiration. 
 
 4. Between the beats of the pulse, test particularly the Resistance of the 
 artery to pressure. Marked resistance may be due either to rigidity of the 
 artery's coats or to high blood-pressure. Press the artery firmly against the 
 hone, and examine the coats by roUing them beneath the finger. 
 
 5. Compare the two radial pulses, and note any difference in strength, or 
 want of synchronism, in their beats. 
 
 6. In special, cases take a sphygmographic tracing. 
 
 AUSCULTATION. 
 UNDOCABSIAIi BBXJITS. 
 
 1st Sound marks beginning of Systole. Systole continues through nearly 
 whole of short pause. 
 
 2nd Sound marks beginning of Diastole. Diastole continues through nearly 
 whole of long pause. 
 
 1. Aortic— 
 
 LL n I k, n 
 
 Systolic. 
 (Obstructive.) 
 
 Diastolic. 
 
 (Regurgitant.) 
 
 2. Mitral- 
 
 JUL n n jn 
 
 Systolic. 
 
 (Regurgitant.) 
 
 Prosystolic. 
 
 (Obstructive.) 
 
 Systolic and Diastolic. 
 (Double.) 
 
 Presystolic and Systolic, 
 
 (Double.) 
 
196 Student's Hand -hook of Medicine. 
 
 1. Aortic Bruits. As shoivn in the above diagram, there may be at the 
 Aortic Orifice, a Systolic bruit, indicative of obstruction, or a Diastolic, 
 indicative of regurgitation ; and these bruits are frequently combined so as to 
 constitute a Double Aortic bruit. A Systolic bruit is not always due to organic 
 disease, being sometimes of Aua;mio origin, as will be explained below, under 
 "6. The Bruits of Debility." This Hsemic bruit is usually softer than a 
 bruit of Organic origin. Aortic bruits, organic and hsemic, are produced at 
 the Aortic Orifice, which is situated at the Sternal Articulation of the third 
 left costal cartilage. They are thus Basic bruits. 
 
 2. MiTKAL Bruits. Tliese are heard best at the apex of the heart. A 
 Systolic bruit indicates Regurgitation. This may be due either to Organic ' 
 disease of the Valve, or to dilatation of the Ventricle and its Aurioulo- 
 ventricular Orifice, the latter causing a "bruit of debility," owing to "Disparity 
 of size " between the dilated orifice and its valve. The Obstructive bruits are 
 always Organic, being due to stenosis of the Mitral valve. Two forces cause 
 the blood to flow through the Mitral Orifice during the diastole of the 
 Ventricle, viz., the suction of the Ventricle (a vis afronte), and the propelling 
 force of the Auricle (a vis a tergo). The suction is strongest near the beginning 
 of the diastole, and the propelling force at the end of it, immediately before 
 the Ventricular Systole. When there is obstructive disease, the bruit is 
 developed at the time when the flow of blood through the contracted oriflce is 
 rapid enough to produce a bruit. Generally it is limited to the period of 
 Auricular contraction, and is therefore Presystolic. - Sometimes, when the 
 Auricle is weak, its occurs only at the period of greatest Ventricular suction, 
 and is therefore Diastolic. Occasionally, again, it may be both Diastolic and 
 Presystolic. Obstructive bruits are rough and purring. They are often 
 succeeded by the blowing bruit of Regurgitation, since the disease which 
 produces obstruction often renders the valve incompetent at the same time. 
 A common double Mitral bruit is thus a rough, obstructive Presystolic, running 
 up to, and immediately succeeded by, a blowing. Systolic, regurgitant bruit. 
 The relations of these bruits to each other are shown in the diagrams. In 
 sound the rough Presystolic bruit might be represented by the letters mp, 
 the terminal p representing the first sound of the heart, which, in such cases, 
 is often loudly accentuated. A double Mitral bruit may be represented by the 
 letters rrrfff. 
 
 3. Bruits at the Pulmonary Orifice correspond in time to Aortic Bruits. 
 A Sj/stolic bruit in this situation is pretty common. It may be "functional," 
 and due to H»mic causes, as Ansemia ; or it may be due to organic disease that 
 has produced Pulmonary stenosis— a form of congenital heart disease. A 
 Diastolic bruit at this orifice is extremely rare. 
 
 4. Tricuspid Bruits correspond in time to Mitral. Practically the only 
 Tricuspid bruit that is not extremely rare is a Systolic Regurgitant. It is a 
 "bruit of disparity of size," and is due to enlargement of the orifice without 
 corresponding enlargement of the cusps, a condition that is always present 
 when there is much dilatation of the ventricular chamber. With this bruit 
 venous pulsation in the neck is generally associated. 
 
\ Diseases of the Circulatory System. 197 
 
 5. In oases of Aseubism a Systolic bruit over the sac is pretty common. 
 In very rare cases a double bruit (Systolic and Diastolic) is produced by the 
 flow of blood into and then out of the sac. In many cases there is no bruit 
 at all. 
 
 6. The Bruits op Dbbilitt, so common in Ansemia, are both Vascular 
 and Cardiac. 
 
 The Vascular bruits are {a) The Arterial bruit, systolic in time, heard over 
 the great arteries of the neck. This is generally supposed to be common, but 
 it is very often produced artificially by the pressure of the stethoscope, (b) 
 The venous hum (the humming-top bruit, or "Bruit de Diable"), heard over 
 the great veins of the neck, and sometimes over other large veins, such as the 
 ophthalmic veins and the cerebral sinuses. This , is very common and 
 important. 
 
 The Cardiac bruits of Debility are variously classified and explained. A 
 view largely supported is that they are four in number, one for each orifice of 
 the ventricles : that two are therefore basic and are heard over the Aortic and 
 Pulmonary regions respectively, being probably due to the onward rushing of 
 the thin anemic blood through the Aortic and Pulmonary orifices ; and that 
 the other two, Mitral and Tricuspid, are heard over the left and right apices, 
 and are due to dilatation of the ventricular chambers, which has produced the 
 "disparity of size" between the auriculo-ventrioular orifices and their cusps, 
 already alluded to. Both of the latter are thus regurgitant. 
 
 Of these six bruits (Vascular and Cardiac) three are common in Anasmia, 
 namely, (1) the Bruit de Diable in the neck, (2) the Basic bruit in the 
 Pulmonary region, (3) the Mitral bruit at the Apex ; and that is the order of 
 their development. 
 
 Observe that all the Cardiac bruits of debility are Systolic in time. 
 Systolic bruits may thus be either of functional or of organic origin, while 
 Presystolic and Diastolic bruits are always of organic origin. 
 
 7. ExoOAEDlAL BBniTS. (a) Pericardial friction, due to Pericarditis, is 
 generally a "to-and-fro" or double bruit (Systolic and Diastolic). It is most 
 apt to be confounded with a double Aortic bruit, but its superficial rubbing 
 and shuffling character generally renders the distinction easy. In most cases 
 it appears first at the base of the heart, and spreads thence, if not arrested, 
 over the whole organ, (b) A to-aud-fro friction sound, of precisely the same 
 character as the above, is sometimes produced by a Pleurisy in the Precordial 
 region, the subjacent heart causing the inflamed surfaces of the pleura to rub 
 against each other synchronously with its own movements. 
 
 PROPAGATION OF ENDOCARDIAL BRUITS. 
 
 1. Aortic Bruits are clearly heard about the third left costal cartilage at 
 its junction with the sternum, that being the position of the Aortic valve. 
 They are propagated to a distance by three agents, namely, (a) the iCeart 
 itself, which often carries them to the Apex ; (6) the Aorta and its great 
 branches, a spot of special importance in this respect being the junction of the 
 second right costal cartilage with the sternum (here the Aorta makes it first 
 
198 Student's Hand-book of Medicine. 
 
 bend, and Aortic bruits are often heard even more distinctly than over the 
 valve itself) ; and (c) the Sternum, which often conducts the sonorous 
 vibrations of such bruits throughout its whole length. Obstructive Aortic 
 bruits (Systolic) are carried best upwards, in the direction of the blood current, 
 and are specially loud over the first bend of the aorta. Regurgitant Aortic 
 bruits, produced by a descending current, are carried best downwards ; and 
 are very often heard better at the left edge of the sternum, close above its 
 junction with the xiphisternum, than even over the Aortic valve. 
 
 2. PuLMONAKY BRUITS, starting like the Aortic from opposite the third 
 left costal cartilage at the Sternum, are carried obliquely upwards and to the 
 left, in the second left costal interspace, for a distance of about two inches, 
 the agent of propagation being the trunk of the Pulmonary artery. 
 
 3. MiTEAL Bruits are loudest at the left apex. The Regurgitant (Systolic) 
 is propagated upwards and outwards towards the axilla and the angle of the 
 scapula. The Obstructive (Presystolic and Diastolic) are not propagated in 
 any special direction. 
 
 4. TEionspiD Bruits are heard best over the right ventricle, being audible 
 over an area of some inches in diameter, whose centre is situated at the left 
 edge of the sternum, close to its junction with the xiphisternum. 
 
 PERICARDITIS. 
 
 Inflammation of tlie pericardium may be primary, but is far 
 more frequently secondary to some infective process. 
 
 Causes. — 
 
 1. Primary. — It is usually the result of direct injury, but 
 sometimes it occurs idiopatbically in children. 
 
 2. Secondary. — 
 
 (1) Eheumatic fever. 
 
 (2) Eruptive fevers, especially scarlet fever. 
 
 (3) Septicsemia. 
 
 (4) Tuberculosis. 
 
 (5) Gouty state of blood. 
 
 (6) Bright's disease. 
 
 (7) Extension of inflammation from neighbouring parts. 
 
 Pathology. — That of inflammation of a serous sac already 
 described under pleurisy — i.e., 
 
Pericarditis. 199 
 
 1. Hypersemia, with loss of lustre. 
 
 2. Exudation of lymph, which coagulates and gives a peculiar 
 shaggy, or "bread and butter sandwich" appearance. The 
 process might stop at this stage causing the dry or plastic type 
 of pericarditis. Much oftener the process goes on to the next 
 stage. 
 
 3. Effusion of fluid. 
 
 4. Absorption with more or less adhesions, which may 
 or may not (as we shall see) subsequently hamper the 
 heart permanently. 
 
 The fluid is similar to that described under pleurisy ; it 
 may, however, be purulent or hsemorrhagic when associated 
 with tubercle or malignant disease. 
 
 Symptoms. — The symptoms are somewhat obscure, and 
 may be masked by the previous existing disease. Taking a 
 typical case as it occurs in the course of rheumatic fever, we 
 usually get — 
 
 1. Precordial distress — sharp pain is rare, when present it is 
 most marked at the lower end of sternum. 
 
 2. Dyspnoea, and dusky appearance of the face. 
 
 3. Kapid action of the heart with feeble pulse. 
 
 4. Symptoms due to pressure by the fluid on the neighbour- 
 ing organs (trachea, and oesophagus, etc.) 
 
 5. Great restlessness. 
 
 It will be easily understood from the above table that we 
 must rely more upon phj'sical signs than subjective symptoms 
 for diagnostic information. 
 
 Physical Signs. — 
 
 1. Before Effusion of Fluid. — On auscultation, is heard the 
 
 • characteristic " to and fro " friction rub. It usually begins at 
 
 the base of the heart and then extends more or less over the 
 
 whole surface. The friction may be felt by the hand. 4^s the 
 
200 Student's Hand-book of Medicine. 
 
 effusion takes place the friction becomes less pronounced, but is 
 rarely entirely absent at the base until complete resolution or 
 organisation takes place. 
 
 2. Effusion Stage. — The physical signs are — 
 
 (1) Marked increase of the cardiac dulness. 
 
 (2) Displacement of the apex beat. 
 
 (3) Muffling of the heart sounds. 
 
 (4) Displacement of other organs (if effusion be great). 
 The shape of the dulness is characteristic. It is conical, the 
 
 apex of the cone being at the first rib, owing to the close attach- 
 ment of the pericardium to the great vessels. The apex beat 
 is generally pushed upwards and to the left. The amount of 
 bulging and displacement of organs will, of course, vary with 
 the amount of fluid present. As resolution takes place the 
 friction returns, and may be very coarse in character. 
 
 Diagnosis. — Often difficult in fat people suffering from acute 
 rheumatism, and also, when great dilitation of the heart is 
 present. Eemember, however, the "conical" dulness of the 
 pericardial effusion. The friction rub may be simulated by 
 friction of the pectoral muscle. It is by no means uncommon 
 to detect friction sounds over " rheumatic " muscles. The 
 " pleuritic '' rub can be readily distinguished by the difference 
 in time. Do not forget that both pleurisy and pericarditis 
 may however co-exist. See " exocardial bruits.'' 
 
 Prognosis. — Depends on cause, that of simple serofibrinous 
 pericarditis is good, the fluid may absorb in from two to four 
 days. Frequently in children though, permanent adhesions 
 may cause some important alterations. 
 
 Signs due to permanent and extensive adhesions — 
 
 1. The heart remains hypertrophied. 
 
 2. A peculiar retraction in the '-apex" region during 
 
 systole. 
 
 3. Collapse of the cervical veins during diastole 
 
 (Friedrich's sign). 
 
Endocarditis. 201 
 
 Treatment. — 
 
 1. Absolute rest in bed. 
 
 2. A fly blister over the precordia. 
 
 3. An hypodermic injection of morphia if pain be severe. 
 
 4. Treat cause — if due to "rheumatic" poison, push 
 
 salycilates (Brackenridge). 
 
 5. If heart failure threatens, give digitalis, strychnine, 
 
 and diffusible stimulants. Paracentesis (?) 
 To promote absorption after the acute symptoms have 
 subsided, — 
 
 1. Blister. 
 
 2. Purge with hydrogogue cathartics — i.e., pulv. jalapse 
 
 CO. 
 
 3. Administer iodides or chloride of ammonia. 
 
 4. "When these fail, paracentesis should be performed. 
 
 The puncture should be made one inch from the 
 left sternal margin in the fourth or fifth inter- 
 space. If the fluid be purulent, incise and drain. 
 
 ENDOCARDITIS. 
 
 By endocarditis is meant inflammation of the lining mem- 
 brane of the valves of the heart. It may be acute or chronic. 
 The acute form is divided into the simple and mahgnant or 
 ulcerative forms. 
 
 iGtiology. — Endocarditis is rarely a primary disease, but 
 secondary to other affections, like pericarditis, which we have 
 already discussed; and again we must emphasise the close 
 relationship (before referred to) that exists between endocar- 
 ditis, acute rheumatism, and chorea. 
 
 Malignant endocarditis may be primary, but is much more 
 frequently the result of some septic or profound morbid change 
 in the blood, such as diphtheria, scarlet fever, pneumonia, etc. 
 The malignant form is not nearly as often associated with 
 rheumatism and chorea as the simple endocarditis. 
 
202 Student's Hand-book of Medicine. 
 
 Pathology. — Simple Form — 
 
 1. Hypersemia of the membrane of the valves. 
 
 2. Exudation of lymph and proliferation of cells. 
 
 3. Formation of small granulations. 
 
 4. Deposit of layers of fibrin from the blood, the whole 
 
 process resulting in the formation of small vegeta- 
 tions. These vegetations are most marked at a 
 slight distance from the free borders of the 
 valves — i.e., those parts which come into apposi- 
 tion during closure. 
 
 Malignant Form. — The initial changes are similar, but there 
 are some important differences, inasmuch as ulcerations may 
 completely replace the vegetations. When tabulated, the patho- 
 logical differences are — 
 
 1. The vegetations when present are larger. 
 
 2. They have suppurating bases. 
 
 3. They contain colonies of micrococci. 
 
 4. When they become detached they form septic emboli, 
 
 giving rise to metastatic abscesses. 
 
 5. The ulcerative process causes great destruction of the 
 
 valves. 
 
 6. The subsequent or permanent changes in the valves 
 
 are much more marked. 
 
 7. If the vegetation touches the endocardium as it flaps 
 
 to and fro, the part touched is inflamed from 
 contact. 
 As regards the side of the heart most afiected, it seems that — 
 
 1. Congenital endocarditis attacks the right side of 
 
 the heart. 
 
 2. The simple endocarditis attacks the left only. 
 
 3. The malignant attacks both sides, though the left 
 
 is much more implicated than the right side. 
 The vegetations are upon that side of the valve opposed to 
 the blood stream — viz., at the aortic valve the vegetations pro- 
 ject into the ventricle, at the mitral valve into the auricle. 
 
Endocarditis. 203 
 
 Symptoms. — 
 
 Simple Endocarditis. — The signs are extremely ill marked ; 
 possibly increased rapidity of pulse, dyspncsa, precordial distress, 
 etc., may attract attention to the heart. On examination a 
 recently developed murmur of a soft blowing or bellows-like 
 character may be heard in the mitral or aortic areas. 
 
 It should be remembered, however, that in most fevers the 
 heart is somewhat dilated, and a murmur, not due to endocarditis, 
 may be present. "We must, therefore, be cautious in coming to 
 a too rapid conclusion that a suddenly developed murmur is 
 indicative of endocarditis. 
 
 Malignant Form. — Two types are described. 
 
 1. The Septic Type. — Is characterised by the symptoms 
 
 of septic infection — viz., rigors, sweats, oscillating 
 temperature, emaciation and metastatic abscesses. 
 Often this form occurs in patients afflicted with 
 chronic valvular disease. The symptoms may 
 continue for months. 
 
 2. The Typhoid Type. — Is characterised by irregular 
 
 or intermittent temperature, looseness of bowels, 
 petechial rashes, and a rapid assumption of the 
 typhoid state. Great difficulty may be ex- 
 perienced in diagnosing this form from typhoid 
 fever or meningitis. 
 It should not be forgotten that patients with chronic 
 valvular disease may get frequent attacks of 
 sub-acute endocarditis. 
 
 Treatment. — AU forms of endocarditis require absolute rest. 
 The primary disease should be treated, and special treatment 
 directed to prevent heart failure. It is impossible to lay down 
 any hard and fast treatment beyond repeating, that the utmost 
 vigilance should he kept up for signs of syncope or embolisms, 
 and such conditions treated on rational grounds. Much that 
 has been said in the treatment of pericarditis may be said of 
 endocarditis. 
 
204 Student's Hand-hook of Medicine. 
 
 CHRONIC ENDOCARDITIS. 
 
 Chronic Endocarditis is usually the result of an acute 
 endocarditis, but may be sub-acute in its onset, as a result of 
 alcoholism, syphilis, gout, and Bright's disease. Amongst other 
 factors is vascular strain, however brought about. One or more 
 valves may be affected. 
 
 Pathology. — In those cases not directly attributable to acute 
 endocarditis, the changes briefly are — 
 
 1. Formation of small nodular prominences, with thickening 
 of the valve. 
 
 2. Formation of yellowish, opaque, fatty patches. 
 
 3. Great increase of fibrous tissue, which subsequently con- 
 tracts, producing much deformity. The cusps become rigid, 
 curled, and may cause great obstruction to the onward flow of 
 blood, and at the same time fail to accurately close together 
 when required. 
 
 4. Great narrowing of the valvular orifice. 
 
 5. Shortening of the chordae tendineee and papillary muscles. 
 
 6. Calcification of the fibrosed portion. 
 
 EFFECTS OF CHRONIC VALVULAR 
 DISEASE. 
 
 We have seen that as a result of inflammatory afiections 
 very serious structural changes occur in the valves of the heart. 
 We must, however, consider in detail the effects of such morbid 
 changes. The points which must ever be borne in mind are 
 that normally — • 
 
 1. By means of the pumping force of the heart, the tissues 
 generally are supplied with oxygenated blood necessary for their 
 perfect nutrition, and to enable the various organs to carry out 
 their functions. 
 
Chronic Valvular Disease. 205 
 
 2. The perfection witli which organs carry out their functions 
 depends upon the amount of oxygenated blood passing through 
 them in a given time. 
 
 3. In ordet, therefore, for the heart to do that which is 
 required of it, it must he perfect in its structure and properly 
 nourished. 
 
 We can then have untoward and down-grade changes brought 
 about by — 
 
 (1) Interfering with the heart's nutrition. 
 
 (2) Valvular defects. 
 
 (3) Changes in the innervation. 
 
 We shall study these changes in detail, but meanwhile let 
 us bear in mind three other important points. — ■ 
 
 1. The normal cardiac mechanism is adapted to meet a 
 certain amount of sudden strain. 
 
 2. This reserve power is developed, and actually increased 
 under increased strain, provided the heart is adequately supplied 
 with blood, and the strain gi-adually applied. 
 
 3. Notwithstanding this grand reserve, a time comes when 
 reserve force must fail, and symptoms of heart failure develop 
 — in other words, hypertrophy keeps up the balance for a time ; 
 but ultimately dilatation becomes excessive, the downgrade 
 process commences, to finally end in complete failure. Let 
 us take for an example "aortic stenosis." The first effect 
 will be an extra strain upon the valve and chamber behind. 
 Under the extra strain the chamber dilates slightly, the walls 
 hypertrophy greatly, and compensation is so thoroughly esta- 
 blished that no bad symptom for a time may develop. Finally, 
 however, nutrition of the cardiac muscle fails, dilatation 
 becomes excessive, the valve behind (mitral) proves incom- 
 petent, and the aortic symptoms first developed become 
 masked by mitral symptoms. 
 
206 Student's Hand -book of Medicine. 
 
 HYPERTROPHY OF THE HEART. 
 
 We have already seen that hypertrophy of the heart is a 
 natural sequence of increased vascular strain, however brought 
 about, provided the heart muscle itself receives a sufficient blood 
 supply to Jceep up its nutrition. 
 
 Causes. — 
 
 1. Secondary to valvular lesions. 
 
 2. Adherent pericardium. 
 
 3. Secondary to diseases of the lungs. 
 
 4. As a result of increased peripheral arterial resistance — 
 
 (1) Obstruction of arteries by pressure of morbid growths. 
 
 (2) Atheromatous degenerations, as seen in Bright's 
 
 disease, gout, etc. 
 
 5. Aneurism of the aorta, etc. 
 
 6. Over-exertion of a healthy heart, as seen in soldiers, 
 hammer-men, professional runners, etc. 
 
 7. Long continued functional excitement. 
 
 It will be readily understood that hypertrophy is a com- 
 pensatory change — i.e., increased growth to meet increased work. 
 But, whilst hypertrophy per se is a beneficial condition, it must 
 also be regarded as a distinct weakness ; for the patient has 
 already called upon his normal reserve force ; and a time comes 
 when the nutrition becomes inadequate, dilatation replaces hyper- 
 trophy, and then compensation fails. The man with a hyper- 
 trophied heart may be compared to a country menaced and 
 irritated by an enemy ; and in order to prevent actual war the 
 reserve forces are called out to supplement the standing army, 
 which causes an additional drain upon the country's exchequer. 
 
Dilatation of the Heart. 207 
 
 Signs of Hypertrophy— 
 
 1. Bulging of the precordia. 
 
 2. Alterations in tlie apex beat. 
 
 (1) Its visible area is largely increased. 
 
 (2) It is slow and heaving. 
 
 (3) The apex heat may be felt in the sixth, seventh, or 
 
 even eighth interspace outside the nipple. 
 
 The above, of course, are the signs of hypertrophy of the 
 left ventricle. 
 
 Hypertrophy of the right ventricle is usually due to lung 
 disease and mitral obstruction. When it is due to mitral 
 regurgitation, dilatation usually accompanies the hypertrophy. 
 For years the effects of mitral stenosis may be counter- 
 balanced by perfect hypertrophy. 
 
 Symptoms of right ventricular hypertrophy. 
 
 1. Bulging of the lower part of the sternum. 
 
 2. Diffuse " apex" beat. 
 
 3. Great increase in the cardiac dulness towards the right. 
 
 4. Accentuation of the second sound in the pulmonary 
 
 area. 
 
 DILATATION OF THE HEART. 
 
 Under "Failure of Compensation" we have already considered 
 the main points in dilatation of the heart. It only remains for 
 us now to consider the more minute changes that occur in this 
 condition. Whilst undoubtedly the main factor in the pro- 
 duction of dilatation is obstruction, either through valvular 
 disease or increased peripheral resistance, still, we must re- 
 member that dilatation is hastened and even brought about 
 by degenerative changes in the ventricular walls, such as — 
 
 1. Fatty degeneration. 
 
 2. Fibrosis. 
 
 3. Anagmia. 
 
208 Student's Hand-book of Medicine. 
 
 High temperature has already been referred to as a frequent 
 cause of dilatation. 
 
 Anatomical Changes. — The heart is more globular in shape. 
 The walls are much thinned, especially at the apex. The 
 auricular-ventricular valves are usually markedly incompetent. 
 
 Physical Signs. — As described under hypertrophy, the pre- 
 cordial dulness is much increased, and the apex beat displaced, 
 etc.; but in contra-distinction to hypertrophy the impulse and 
 heart sounds are very feeble in pure dilatation. 
 
 Symptoms will be summed up under "Incompetence of 
 Valves." 
 
 VALVULAR LESIONS. 
 
 "We shall have to reiterate much that has already been said 
 under endo-carditis. We have already seen that each valve 
 may be affected in one, two, or three ways — viz., — 
 
 1. They may be rendered obstructive — stenosis. 
 
 2. They may be incompetent — regurgitation. 
 
 3. Incompetent and obstructive. 
 
 These conditions are diagnosed by — 
 
 (1) The position of the murmurs accompanying such 
 
 conditions, 
 
 (2) The general symptoms produced by such lesions. 
 
 Murmurs are propagated in the direction of the blood 
 stream, and are best heard a little way from the valvular 
 orifice where they are produced. 
 
 Always in describing a murmur, state — 
 
 1. Position. 
 
 2. Time. 
 
 3. Propagation. 
 
 4. What sound (if any) is modified thereby. 
 
 5. Accompaniments (if any). 
 
Valvular Lesions. 209 
 
 Examples — 
 
 Aortic Stenosis. — A murmur heard in tlie aortic area,' systolic 
 in time ; propagated up the sternum into the carotids, and 
 usually accompanied by a loud first sound. 
 
 Aortic Regurgitation. — A murmur heard in the aortic area, 
 diastolic in time ; propagated down the sternum, and modifying 
 or replacing the second sound. 
 
 Mitral Stenosis. — A murmur heard in the mitral area, 
 ^re-systolic in time ; runs up to the first sound — not propagated, 
 but often accompanied by a marked thrill. 
 
 Mitral Regurgitation. — A murmur heard in the mitral area, 
 systolic in time ; propagated to the aiilla, and modifying or 
 replacing the first sound. 
 
 Tricuspid Regurgitation. — A murmur heard over the fourth 
 right costal cartilage ; propagated to the left and towards the 
 apex beat ; systolic in time. 
 
 Other murmurs are too rare to require a description in such 
 a book as this. One cannot help thinking two much importance 
 is paid nowadays to the localisation of murmurs, and too little 
 notice taken of the state of the heart nutrition. Post-diastolic 
 and mid-diastolic murmurs are often diagnosed with lightning 
 rapidity by the student, who, at the same time, fails to note 
 whether compensation is established or beginning to fail. 
 Perhaps this fault after all is due to faulty teaching. Ee-dupli- 
 cation of sounds indicates a want of synchronism between both 
 sides of the heart. Remember, the second soij^nd is produced 
 by the closure and stretching of the aortic and pulmonary 
 valves ; the first sound, by closure and stretching of the auriculo- 
 ventricular valves, plus the contraction of the ventricular muscle. 
 Lastly, do not forget that the loudness of a murmur is but a 
 poor index of the gravity of the lesion. A careful consideration 
 of the general state of the heart and general symptoms is of far 
 greater importance than mere attention to any murmurs that 
 exist. , The diagnosis of cardiac lesions is sometimes extremely 
 
 P 
 
210 
 
 Student's Hand-hook of Medicine. 
 
 easy, and at other times very diflicult. Aortic disease may be 
 masked by mitral disease; mitral disease, by extensive pul- 
 monary disease, and so on. Remember tbat the tendency of all 
 organic cardiac lesions is to finally produce arterial emptiness 
 and venous congestion. The following table will show the more 
 important differences. 
 
 AOKTIC DISEASE. 
 
 Symptoms are mainly due to 
 ana;mia — viz. , — 
 
 1. Pallor. 
 
 2. Throbbing of the carotids. 
 
 3. Attacks, of an "angina 
 pectoris" type of pain. 
 
 4. Breathlessness on slight exer- 
 tion. 
 
 5. Menses usually absent. 
 
 6. Nervous symptoms are pro- 
 minent. 
 
 7. The left ventricle is usually 
 much hypertrophied. 
 
 MITKAL DISEASE. 
 
 Symptoms are mainly due to 
 venous congestion — viz., — 
 
 1. Cyanosis. 
 
 2. May get pulsation in the 
 veins of the neck. 
 
 3. Sudden attacks of severe 
 dyspnoja — actual acute pain is 
 rare. 
 
 4. Breathlessness, but often 
 present without exertion. 
 
 5. Often there is menorrhagia. 
 
 6. Pulmonar}' symptoms are 
 most prominent — i.e., — 
 
 (1) Cough in the morning. 
 
 (2) Chronic Bronchitis. 
 
 (3) Hajmoptysis. 
 
 (4) Dilated right side of 
 
 heart, and later — 
 
 (5) Symptoms due to tri- 
 
 cuspid leakage. 
 
 7. The left cmricU is much 
 hypertrophied. 
 
 Tricuspid Disease. — The symptoms of failure of the right 
 side of the heart may be summed up as — those symptoms which 
 always arise from imperfect asration of blood, and venous 
 congestion of the organs, generally. Those in connection 
 with the congested organs are — 
 
 1. Lungs = dyspnoea, bronchitis, pulmonary oedema. 
 
 2. Liver (nutmeg) = dyspepsia, hsematemesis, ascites. 
 
 3. Kidney = albuminuria, general dropsy, uraemia. 
 
BRAIN 
 
 CAPrLLARIES 
 
 D1AORA.M for studying the results of backward pressure. Note the areas in blue 
 will become the seat of changes consequent on venous congestion. 
 
Valvular Lesions. 211 
 
 The symptoms are, in fact, merely an exaggeration of those 
 arising from mitral disease. The patient finally becomes 
 water-logged. Locally there is epigastric pulsation. The 
 jugular vein, if obstructed by the finger, fills up from below 
 during systole. 
 
 THE PULSE IN CARDIAC LESIONS. 
 
 Aortic stenosis. — Here the blood is obstructed in its flow 
 into the aorta. The pulse is thus rendered somewhat slow 
 in its ascent. The tension wUl depend on the amount of 
 obstruction and degree of hypertrophy. The force with which 
 the blood is sent through the narrow orifice often causes an 
 aneurism of the first part of the aorta. 
 
 Aortic Regurgitation. — The ventricle in this condition is 
 filled during diastole by two streams — one the regurgitant aortic 
 stream, and the other in the usual way from the auricle. The 
 chamber is thus filled more quickly, and the pulse made to 
 beat faster. The sudden rise and the sudden fall of the 
 pulse gives it a peculiar kicking or water-hammer character. 
 The throbbing of the carotids often prevent sleep. Capillary 
 pulsation is often well marlced. 
 
 Prognosis — 
 
 Aortic Stenosis is the least dangerous, as hypertrophy is 
 usually well marked and maintained. Often there are no 
 symptoms suggestive of such a grave condition. 
 
 Aortic regurgitation on the other hand is by far the most 
 dangerous lesion ; sudden syncope through anaemia of the brain 
 is often fatal. Angina pectoris is common in this lesion and 
 may cause speedy death. 
 
 Mitral disease is characterised by frequent breakdowns, but 
 patients often quickly recover their usual condition and may 
 be long lived. 
 
212 Student's Hand -hook of Medicine. 
 
 Tricuspid disease is always grave and it is impossible to 
 give any general prognosis. Each case must be carefully 
 considered on its own merits. 
 
 Treatment. — The beginner has my full sympathy in trying 
 to understand the rational treatment of cardiac lesions. He is 
 taught by some that " rest " is the best thing — ^by others, " mics- 
 cular exercise" is the proper treatment, — again "Digitalis" is the 
 only drug, or " Strophanthus " must be the sheet anchor ; and lastly 
 use the whole lot if he wishes to be successful. Possibly the 
 last is correct; but at any rate, no routine treatment can 
 possibly be prescribed. Eemember, however, a few points and 
 the indications for any particular treatment will soon be 
 apparent. 
 
 1. Hypertrophy is nature's cure ; and, in order 
 
 2. To get hypertrophy there must be a wholesome supply of 
 blood to the heart tissue. 
 
 3. Eemember the golden rule " avoid putting excessive 
 strain on a diseased tissue." 
 
 4. " Don't " look upon the heart as an isolated structure, but 
 as a component and essential part of a complex machine ; 
 and consequently sharing in the anabolic and cataholic changes 
 of the body generally. In other words, if the system generally 
 be lowered, then the heart must also suffer ; but this does not 
 prevent us from using those drugs which have a distinctly and 
 particular action upon the heart. Our treatment must be then — 
 
 GENERAL AND MEDICINAL. 
 
 (1) Diet. — Avoid excesses, especially of nitrogenous food 
 which tends to increase peripheral resistance. 
 
 Note — A full or distended stomach is a constant' source 
 of cardiac embarrassment. 
 
 (2) Exercise. — Provided the assimilative powers are good, 
 and plenty of food can he taken to provide for the increased 
 
Valvular Lesions. 213 
 
 expenditure of energy, then exercise must be good, as it 
 imitates or helps the natural way of producing hypertrophy 
 of the chamhers behind the lesion ; on the other hand 
 
 (3) Absolute rest is the treatment when the assimilative 
 powers are weak, or compensation once established is failing. 
 
 (4) Drugs include (1) general tonics, and (2) those having 
 a special action on the heart. Of the former, iron and arsenic 
 with strychnine is always a valuable mixture. 
 
 Of the latter digitalis stands first. It acts beneficially 
 by- 
 
 (a) Decreasing the rapid action of the heart, so increasing its 
 
 natural rest, and diminishing its work in a given time. 
 
 (b) It aids the nutrition of the heart, which is supposed to 
 
 be nourished during diastole. (1) 
 
 Its disadvantage is, that it increases peripheral resistance, 
 and so produces greater strain. Digitalis can be given in all 
 cases where the arteries are empty, and the pulse quick and 
 irregular. Especial care, however, is required in aortic regurgi- 
 tation for fear of prolonging diastole too long. " Don't " give 
 digitalis, though there be cardiac disease, if compensation is well 
 established; and secondly "don't" continue giving digitalis if 
 the urine decreases in quantity after its administration. 
 
 Strychnine is always a powerful adjuvant to digitalis, and is 
 possibly the best " cardiac tonic." 
 
 Strophanthus is held in high repute in Edinburgh, in cases 
 where digitalis fails ; it is supposed to have similar tonic effects 
 to digitalis without the drawback of increasing peripheral 
 resistance ; opinions as to this are conflicting. Sudden break- 
 downs of compensation call for stimulants such as aether, 
 ammonia, brandy mixture, complete rest, cupping over the 
 lungs, etc. 
 
 Cardiac pain is best relieved by morphia and iodide of 
 potassium. If there be arterial constriction, nitrite of amyl is 
 
214 Student's Hand-book of Medicine. 
 
 the best remedy. Do not forget the judicious use of an 
 emetic in " mitral " disease when sudden dyspnoea occurs 
 after a meal. 
 
 A Caution. — If your are called to see a patient who has 
 been picked up insensible, and smells strongly of alcohol, do 
 not hastily conclude he is drunk, but malce sure of the state 
 of the heart. Many patients finding themselves getting faint, 
 take a dram of brandy, which, however, may fail to prevent 
 syncope. Eough usage or a cold cell would probably kill a 
 patient under such circumstances. 
 
 ANEURISM. 
 
 Before discussing the essential features of thoracic aneurism 
 we must recall a few facts relative to aneurisms in general. An 
 aneurism may be defined as "a localised and persistent dilatation 
 of a blood vessel." Surgeons employ the term in a wider sense. 
 Classified according to shape we have the following varieties — 
 
 1. Fusiform or spindle shaped, involving the whole cir- 
 cumference. 
 
 2. Sacculated — where one side of the vessel only is 
 dilated. 
 
 3. Diffuse — where a large portion of the vessel is irregu- 
 larly dilated. 
 
 Causes. — The two main factors are — 
 
 1. Damage to the vessels walls. 
 
 2. Increased vascular strain. 
 
 Consequently we shall have to consider predisposing, and 
 exciting causes when dealing with any particular aneurism. 
 
 Pathology. — 
 
 The inner coat may be much thickened by atheromatous 
 changes, but much more frequently it disappears altogether, 
 a delicate layer of hyaline tissue taking its place. 
 
Thoracic Aortic Aneurism. 215 
 
 The muscular coat — The muscular fibres become stretched 
 and dissociated, and ultimately disappear. 
 
 The outer coat becomes much fibrosed, and adherent to the 
 surrounding tissues by an inflammatory process; thus the "sac" 
 of an aneurism is most frequently composed of dense fibrous 
 tissue. 
 
 Course. — An aneurism once started tends to increase, and, 
 if not arrested, finally ruptures. But an aneurism may cure 
 itself by becoming so large that the sac, by pressing on the 
 artery, checks or even obliterates the blood supply. Again, 
 ■when the orifice is small in a sacculated aneurism the circula- 
 tion in the sac may be so impeded that thrombi form, ending 
 in a large pale laminated clot, which may ultimately organise 
 and transform the aneurism into a fibrous nodule. This 
 occurs, however, only in the smaller aneurisms ; but this 
 natural cure gives the physician the cue as to what he should 
 attempt. 
 
 Symptoms. — The cardinal symptoms of an aneurism are — 
 (1) Tumour. (2) Pulsation. (3) Systolic murmurs. (4) Pain. 
 (5) Other pressure effects. 
 
 The extent of these symptoms depend upon the site of the 
 tumour and the nature of the adjacent structures. A word 
 of caution is needed to guard the beginner against diagnosing 
 an aneurism of the aorta too quickly ; frequently there are 
 no symptoms indicative of such a serious condition, and on the 
 other hand, there are often grave and suggestive .symptoms 
 present, but no aneurism. We shall now consider the special 
 points of 
 
 THORACIC AORTIC ANEURISM. 
 
 The aorta is the most frequent seat of aneurism in the 
 body, and all varieties have been found here. There are 
 
216 Student's Hand -hook of Medicine. 
 
 many reasons given wliy aneurisms should be so common m 
 the arch of the aorta — 
 
 1. It is much curved. 
 
 2. The first part of the arch has very little support. 
 
 3. The blood stream ejected during systole of the heart, 
 
 tends to bulge the aorta locally (especially in 
 aortic stenosis). 
 
 4. This part is much more affected by the variation of 
 
 the cardiac pressure than the distal arteries. 
 
 5. It gives off large branches in a very small area. 
 
 6. The vessels tend to dilate during inspiration. 
 
 Occurs most frequently amongst men who are either pre- 
 maturely old through intemperance, syphilis, etc. ; or in those 
 engaged in occupations which tend to increase the normal 
 aortic strain, such as hammermen, brewers, young soldiers, 
 etc. Septic emboli lodging in the inner coat account for 
 some cases. Traumatisms may also cause aortic aneurism. 
 
 Symptoms. — They depend on the portion of the arch 
 affected, and size and shape of the aneurism. 
 Briefly they are — 
 
 1. Symptoms in connection with the Circulation. — Palpitation, 
 angina pains, the arteries are filled less perfectly, and there 
 may be a difference in the two radial pulses. 
 
 2. Symptoms due to Pressure — 
 
 (1) CEsophagits. — There is difficulty in swallowing, 
 
 especially solids. 
 
 (2) Respiratory System. — Less air enters the lung 
 
 pressed upon, and the breath sounds are con- 
 sequently weak. There is much dyspnoea, or 
 attacks of the so-called aneurismal asthma, a 
 peculiar alteration of the voice and cough 
 (leopard growl and gander cough). Haemo- 
 ptysis may occur later due to " weeping " of the 
 aneurism. 
 
Thoracic Aortic Aneurism. 
 
 217 
 
 (3) Implication of Nerves. — The symptoms will depend 
 on the amount of pressure exerted on the nerves. 
 Thus, if slight, we get symptoms due to irrita- 
 tion ; if severe, symptoms due to paralysis. The 
 nerves most likely to be involved are — 
 
 Left Uecurrent Laryngeal . 
 
 Fhrenic . 
 
 Vagus . 
 
 IKEITATION. 
 
 Alteration of voice ; and 
 stridor, due to spasm. 
 
 Painful and persistent 
 hiccough. 
 
 DUatation of the pupils. 
 Palor from constriction 
 of the vessels on the 
 one side. Eapid action 
 of the heart. 
 
 Depressed action of the 
 heart. Vomiting and 
 nausea. 
 
 PARALYSIS. 
 
 Aphonia. 
 
 Intercostal breathing. 
 Death. 
 
 Contraction of the pupil 
 and flushine; of that 
 side of the race. 
 
 Irregular action of the 
 
 heart. 
 Pneumonia. Death. 
 
 Veins. — CEdema of superior extremities, one side of the 
 head, etc. 
 
 Thoracic Duct — produces rapid emaciation, and fatty stools. 
 
 Bones — are eroded and absorbed ; the process being accom- 
 panied usually with intense boring pain. When the spine is 
 involved the pain is intense, due to irritation of the intercostal 
 nerves and meninges — there may be much deformity, and even 
 paraplegia through implication of the spinal marrow — a murmur 
 may be heard over the spine. 
 
 Such then are the clinical symptoms ; on 
 
 Physical Examination. 
 
 Inspection may reveal a swelling ; or there may be a diffuse 
 heaving impulse above the third costal cartilage, and displace- 
 ment of the apex beat. 
 
 Palyation often detects the expansile character of the 
 tumour, with its systolic thrill and diastolic shock. 
 
 Percussion. — Note is dull or flat and gives a feeling of 
 resistance. 
 
 Auscultation may reveal, over the dull area, a ringing accentu- 
 ated second sound and a systolic bruit. 
 
218 
 
 Student's Hand-book of Medicine. 
 
 Dr Osier calls attention to the absence of pulsation in the 
 abdominal aorta or the femorals in cases of large thoracic 
 aneurisms. 
 
 Surgeon-Major Porter lays stress upon the fact that if the 
 chin be brought forward to relax the neck, and the cricoid 
 jerked upwards, there is felt a peculiar tugging if the 
 aneurism be attached to the bronchus or trachea. He 
 says the same feeling is not produced by any other tumour. 
 
 The following table shows the structures most likely to be 
 implicated according to the site of the aneurism : — 
 
 ASCENDING. 
 Right pleura. 
 
 Second and tliird in- 
 terspaces. 
 
 Sternum. 
 
 Superior Vena Cava. 
 
 Right recurrent 
 Laryngeal Nerve. 
 
 Left pulmonary 
 artery. 
 
 Rupture into peri- 
 cardium. 
 
 TRANSVERSE. 
 
 external 
 
 Rarely 
 tumour. 
 
 Both Plurffi. 
 
 Sympathetic. 
 
 Trachea. 
 
 Left Bronchus. 
 
 Left recurrent 
 Laryngeal Nerve. 
 
 Aneurismal Phthisis. 
 
 Ruptures outside the 
 pericardium. 
 
 DESCENDING. 
 
 (Esophagus. 
 Thoracic Duct. 
 
 Erosion of spine. 
 
 Often ruptures into 
 pleurae. 
 
 Treatment. — 
 
 General. — Everything must be done to quiet the circulation, 
 by the observance of rest and abstinence from all alcoholic 
 drinks, etc. The diet should be nourishing, but limited, and 
 the quantity of liquid taken reduced to a minimum. 
 
 Medicinal. — Anodynes and sedatives are called for, but 
 iodide of potassium in large doses daily, seems the most 
 efficacious of drugs. It is difficult to say how the iodide 
 acts, it certainly does not lower the blood pressure to the 
 same extent as many other drugs which are less efficacious 
 in benefitting the aneurismal condition. Possibly the bene- 
 ficial effects are due to the iodides causing absorption of 
 inflammatory material, which would otherwise induce sclerosis. 
 
Abdominal Aneurism. 219 
 
 Local treatment is highly unsatisfactory. All methods aim 
 at starting coagulation. Briefly, they are — 
 
 1. Introducing needles, and scratching the walls of the 
 
 sac to form a rough surface, and so hring about 
 coagulation. 
 
 2. Introduction of fine steel wire or horse hair. 
 
 3. Electrolysis. 
 
 Considering the hopeless character of this affection, it is 
 more than cruel where pain is severe to withhold morphia, 
 as some anti-opium fanatics would have us do. 
 
 ABDOMINAL ANEURISM. 
 
 Site. — Most common near the cceliac axis. It may grow 
 upwards and push the diaphragm before it, or forwards 
 and project anteriorly, or backwards and erode the spine. 
 
 Diagnosis. — Palpation reveals a definite tumour with the 
 characteristics of aneurism already described. The tumour 
 may be better felt in the knee and elbow position. 
 
 Especial care must be taken in diagnosing this condition 
 in pregnant or hysterical females ; also in cases of tumours 
 lying beneath the aorta. 
 
 Treatment. — As in thoracic aneurism. Compression under 
 chloroform may be tried, though it is decidedly risky. 
 
 Prognosis. — Bad. Death may take place from — 
 
 1. Compression paraplegia. 
 
 2. Embolism of superior mesenteric artery. 
 
 3. Complete obliteration of the lumen by clots, 
 
 4. Eupture (oftenest into duodenum). 
 
 CONGENITAL ANEURISM. 
 
 A peculiar condition of the arteries, characterised by con- 
 genital deficiency of the muscular coat, thickening of the 
 intima and a small cell infiltration of the outer coat, causing 
 a nodular condition. The coronary arteries are most affected. 
 
220 Student's Hand-book of Medicine. 
 
 FUNCTIONAL DISORDERS OF THE HEART. 
 
 The functional disorders include — 
 
 1. Palpitation — i.e., forcible and often irregular action 
 
 of the heart, perceptible to the individual. 
 
 2. Arrhythmia, or intermittent condition of the cardiac 
 
 beats. 
 
 3. Tachycardia or rapid heart. 
 
 4. Bradycardia or slow heart. 
 
 [For the details of these various conditions, the reader is 
 referred to a standard work on physiology.] 
 
 Eapidity of the heart is usually associated with a neurotic 
 temperament, menstrual epochs, excessive use of stimulants, 
 mental excitement, use of certain drugs, such as belladonna, etc. 
 
 Slowness of the heart is most commonly associated with 
 hunger, the puerperal state and melancholia, use of digitalis, 
 excessive use of tobacco, poisoning by bile, lead, etc. Often, 
 however, the same conditions will produce rapidity in one 
 individual, and slowness in another. 
 
 ANGINA PECTORIS. 
 
 A condition characterised by a sudden severe pain in the 
 chest, with a sense of impending death. 
 
 .etiology. — It occurs most frequently amongst men above 
 the middle age. Predisposing causes are "all conditions which 
 interfere with the nutrition of the walls of the heart : " such as 
 extensive fatty disease, valvular diseases, atheroma, however 
 brought about, etc. ; the exciting causes are : — 
 
 Stidden strain, an over distended stomach, powerful emotional 
 disturbances, etc. 
 
 Symptoms. — The patient is suddenly seized with an acute 
 and sudden pain across the chest. The pain is most marked at 
 the lower end of the sternum and radiates down the left arm 
 
Angina Pectoris. 221 
 
 most frequently, though the right arm is often implicated. The 
 patient feels as if an iron band was fixed around the chest. 
 The feeling of suffocation is intense, but the usual cyanosis of 
 dyspnoea is absent, the face often being extremely pale. A 
 sphygmographic tracing of the pulse taken during an attack, 
 shows increased arterial tension. An attack may last from a 
 few seconds' to many minutes ; may kill the first time, or recur 
 at various intervals. 
 
 Pathology. — Post-mortem ■ — the heart is distended with 
 blood, and the walls and valves show extensive morbid 
 changes. The coronary arteries are extensively diseased. 
 
 Causation of the Attack. — Many people have extensive 
 heart disease without getting angina. Again, a patient may 
 have only one attack, or have an interval of years between 
 them, so, per se, heart disease is not of itself sufficient to pro- 
 duce angina. "We must confess that at present the explanations 
 of the condition given are not altogether satisfactory. The 
 following statements possibly show the extent of our knowledge 
 at present. Atheromatous coronary arteries cause — 
 
 1. More or less anaemia of the heart's substance. 
 
 2. Irritability of the intra-cardiac ganglia. 
 
 3. Diminished contractile power of the ventricles. 
 
 Let us suppose a heart with all these disadvantages is 
 subjected to a severe strain. What will result? 
 
 1. Over distension of the ventricle. 
 
 2. A reflex message will be transmitted from the irritable 
 
 ganglia to the medulla, resulting in sudden gen- 
 eral vasa motor constriction. Therefore, the heart 
 already emhaxiass&d,has to pump against increased 
 peripheral resistance, hence the feeling of suffoca- 
 tion, etc. 
 If this be true, then the use of nitrites is at once ap- 
 parent, for, as they cause dilatation of the arterioles, the 
 peripheral resistance is at once diminished, and the over 
 distended ventricle allowed or enabled to empty itself. 
 
222 
 
 Student's Hand-book of Medicine. 
 
 Indeed, the only flaw in the foregoing explanation is, "That 
 in some instances of angina no increase of arterial tension 
 has been observed." This is but a poor argument though, 
 for we can easily understand that the propelling force of the 
 heart may be insufficient to cause any appreciable tension, 
 notwithstanding the increase of peripheral resistance. 
 
 Treatment. — During the attack administer nitrites, prefer- 
 ably by inhalation ; chloroform may be used as a substitute. 
 During the interval, careful attention to the bowels, diet, and 
 avoidance of severe mental or muscular exercise, with the 
 administration of iodides, considerably lessens the ch^ince of 
 another attack. Lastly it must be remembered that many 
 patients complain of something like angina, which, however, 
 is not the true disease. 
 
 TEUE ANGINA. 
 
 Moat common past middle life. 
 
 Most common in men. 
 
 Attacks — rarely nocturnal or peri- 
 odical. 
 
 Not associated with other .symptoms. 
 
 Agonising pain and sense of con- 
 striction. 
 
 Pain of short duration. 
 
 Lesions — arterial sclerosis. 
 
 Prognosis grave ; often fatal. 
 
 PSEUDO ANGINA. 
 
 At every age from six years. 
 Most common in females. 
 Often periodical and nocturnal. 
 
 Associated with nervous symptoms. 
 Pain less severe — distension more 
 
 than constriction. 
 Pain lasts one or two hours. ~ 
 Neuralgic affection. ' 
 
 Never fatal. 
 
 (Huchard's table.) 
 
 by- 
 
 EXOPHTHALMIC GOITRE. 
 
 Exophthalmic Goitre is a remarkable condition characterised 
 
 1. Rapid beating of the heart and palpitation. 
 
 2. Enlargement of the thyroid gland. 
 
 3. Exophthalmos or projection of the eyeballs. 
 
 4. Imperfectly co-ordinated movements of the upper 
 eyelid. 
 
 5. Certain visceral disturbances. 
 
 6. Atrophic changes in the epidermal structures. 
 
Exophthalmic Goitre. 223 
 
 Pathology. — Quite unknown, and until we know more of 
 the physiology of the sympathetic system, very little beyond 
 speculation can result. Post-mortem — no constant or definite 
 changes are found. Professor Grainger Stewart and Dr Gibson 
 point out " no advantage can accrue from a discussion in favour 
 of the disease being due to either — 
 
 1 . A paralysis of the vagus. 
 
 2. Stimulation or paralysis of the sympathetic. 
 
 3. Changes in the medulla." 
 
 Any one who knows anything of physiology will endorse 
 this honestly expressed opinion, and I cannot help expressing 
 here, how much better it would be, if the heads of our 
 profession would abstain from dogmatically expressing any 
 definite opinion on a subject ",sm6 judice " ; and still more, 
 how unjust it is for an examiner to ask a candidate for ex- 
 planations of such difficult pathological problems. 
 
 FUehne says : — Injury to the upper part of both restiform 
 bodies in rabbits, will produce all the characteristic symptoms. 
 It may be so in rabbits, but I was once present at the post- 
 mortem of a patient where extensive disease of the restiform 
 bodies was found, and no such symptoms were evident during 
 life. For examination purposes it should be remembered that 
 exophthalmos may be produced by — 
 
 1. Stimulation of the sympathetic. 
 
 2. Over growth of the fat in the orbit. 
 
 3. Contraction of the muscular fibres of Miiller in the 
 
 lining membrane of the orbit. 
 
 Symptoms. — The patient is usually nervous, and complains 
 of headache, vertigo, and great weakness. The prominence 
 of both eyeballs gives a terrified aspect to the patient; the 
 eyelids fail to meet and the upper eyelid is not depressed when 
 the patient looks down. The temperature is periodically raised, 
 and marked dyspepsia is often present. Diarrhoea is also a 
 prominent symptom in many cases. Professor Grainger 
 Stewart and Dr Gibson emphasise the marked changes in 
 
224 Student's Hand-book of Medicine. 
 
 the nails, whicli are brittle, corrugated, etc., and also other 
 changes in the skin or its appendages, dependant on vasa-motor 
 disturbance. The thjToid gland is enlarged as a whole, due to 
 a general hyperplasia ; the minute changes are by no means 
 identical in all cases. The menses are usually absent. 
 
 Frognosis. — Bad. Excessive dilatation of the heart often 
 brings about a fatal result after exertion. Htemorrhages, diar- 
 rhoea, or other complications, usually terminate the disease in a 
 few years after the marked symptoms appear. 
 
 Treatment. — Must of course be symptomatic. Iron is 
 badly borne, and the amount of anaemia does not particidarly 
 suggest its use. Large doses of digitalis may be tried. 
 
 DISEASES OF THE LIVER AND KIDNEY. 
 
 Before attempting the study of diseases of the liver and 
 kidney, the reader is earnestly advised to recall to mind, the 
 chief physiological facts regarding their functions and relations 
 to each other. It wiU be remembered that the kidney is to a 
 large extent the hand servant of the liver ; it excretes the 
 waste material formed by the former, and thus enables the 
 liver to perform its duties efficiently, and, at the same time 
 keep the blood free from morbid products. But it must also 
 be understood that an alteration in their perfect physiological 
 relation may be disturbed by — 
 
 1. The liver putting excessive strain on the kidney; or, 
 
 2. The kidney, through disease, being unable to perform its 
 normal functions, and thus clog the liver. 
 
 FUNCTIONS OF THK LIVKR. 
 Will be considered briefly under four heads — 
 
 1. The metabolism of proteid material. 
 
 2. The metabolism of carbo-hydrates. 
 
 3. The manufacture of bile. 
 
 4. As a source of heat and energy to the body generally. 
 
Diseases of the Liver and Kidney. 225 
 
 If we study these carefully, though, briefly, it wUl be easy 
 for even a beginner to understand those facts which are neces- 
 sary, in Older to get a grasp of " how " such conditions as gout, 
 diabetes, Bright's disease, jaundice, and so on, are brought about. 
 I must however warn the student, that though the following 
 statements represent our present knowledge of such metabolic 
 changes, they must be regarded as distinctly hypothetical, 
 though sanctioned by the latest research. 
 
 1. PROTKID METABOLISM. 
 
 Proteids, after being subjected to the various digestive 
 agents, saliva (mastication), gastric juice, pancreatic juice, and 
 succus entericus, are finally absorbed into the portal circu- 
 lation ; carried to the liver, and there broken up or divided 
 into (1) That which is to be used for building up the tissues. 
 (2) That which is to be excreted. That which is excreted 
 goes through many changes before it can be eliminated via 
 the bile and urine. Graphically we might represent such 
 changes as follows. 
 
 Proteids = substances of an albuminous nature, rich in 
 nitrogen. Under the action of — 
 
 1. Saliva, — they are finely divided or masticated ; 
 
 2. Under the action of gastric juice they are converted into — 
 
 (1) Albuminates (acid). ^ 
 
 (2) Albumoses (many kinds), j- = Acid chyme. 
 
 (3) Peptones. J 
 
 3. Under the action of pancreatic juice and succus entericus 
 they are converted into — 
 
 (1) Alkali albuminates. 
 
 (2) Albumoses. 
 
 (3) Peptones. 
 
 (4) Leucin, tyrosin — to a slight extent. 
 
 Skatol, indol, and phenol — bodies which residt from putre- 
 faction (of course under bacterial influence) are also formed, 
 especially if absorption be delayed. 
 
 R 
 
226 
 
 Student's Hand-book of Medicine. 
 
 Proteids are thus (if fully digested) converted from non- 
 diffusible into diffusible bodies termed "peptones," with the 
 addition of some putrefactive bodies (which ordinarily should 
 be excreted via the faeces). We thus see even at this stage 
 how powerfully constipation can affect the system, by increas- 
 ing the formation of these poisonous products, and by the 
 same delay, increase the chance of their absorption, and thus 
 break down corpuscles and cause profound anaemia. The 
 further fate of peptones is wrapped up in much obscurity. 
 Possibly the following table is correct as far as our present 
 knowledge goes. 
 
 FATE OF PEPTONES. 
 
 Passing through the intestinal walls they are converted 
 into albiiminous bodies, and carried by the portal circulation 
 to the liver. 
 
 In the liver they are broken up into that which is used 
 for nourishment, and that which is to be excreted. That 
 which is to be excreted undergoes the following changes : — 
 
 Proteid Waste. Result of Retention. 
 
 1st Group of 
 Compounds. 
 
 2. Intermediate 
 
 /Leucin. 
 \Tyrosin. 
 
 I Atrophy of the 
 
 Acute Yellow 
 
 Liver. 
 
 ) 
 
 atermediate Creatinine or \ au having NH 3 ( 
 Products. Zanthin Group. / for a base \ 
 
 3. End Products. 
 
 like the vegetable 
 AikaloidB. 
 
 See \ 
 
 Urxmia. / 
 
 Uric Acid.. 
 Urea. 
 
 ./ See Gout. \ 
 VChronic Bright's. / 
 
 In other words, within the liver, the waste products 
 are converted into a very fine ash termed urea, which 
 escapes into the blood, and is then excreted by the kidney. 
 Nearly aU the nitrogen is thus excreted from the body. 
 
Fate of Peptones. 227 
 
 Apply this to disease. — A failure on the part of the liver 
 to do its work must result in imperfect oxidation of waste 
 products. The nature of the products so formed will depend 
 on the extent or degree of oxidation. Thus a slight failure 
 would mean excessive uric acid formation, and probably cause 
 gout. A more serious failure would cause retention of 
 the intermediate ammoniacal products, and cause uraemia. 
 Whilst a still more serious handicapping of the liver would 
 cause leucin and tyrosin to appear in the urine, as seen 
 in acute yellow atrophy of the liver. We have seen that 
 the perfection with which any organ performs its function 
 depends on — 
 
 1. The quantity of oxygenated blood that passes 
 
 through the organ in a given time. 
 
 2. The rapidity with which the waste products 
 
 formed are excreted. (Every living act builds 
 up and breaks down — i.e., anabolic and kata- 
 bolic changes.) 
 We can easily reason then, how much, vasa motor changes 
 can affect an organ's nutrition, and consequently its work. 
 Further, imperfect oxidation means the formation of a coarser 
 "ash" as it were — i.e., uric acid instead of urea, and as 
 the kidney has in such cases to excrete highly irritating 
 particles, "is it any wonder that it becomes fibrosed, and 
 the red granular kidney form of chronic Bright's disease 
 results ? " Can we not easily understand that such irritating 
 products floating in the blood must cause vasa motor peri- 
 pheral constriction, and so heighten blood tension? — finally 
 causing sclerotic changes in the vessels, and hypertrophy of the 
 heart to overcome the obstruction ? Further, will not such a 
 state begin a cycle of down grade changes 1 Just a few more 
 words in reference to the intermediate products or Zanthin 
 group. We find there are many of these compounds, but all 
 seem to have (like the vegetable alkaloids) NH3 for a base. 
 Now we know that different alkaloids have different poison- 
 ous and medicinal qualities, thus strychnine and morphia have 
 
228 Student's Hand-book of Medicine. 
 
 very dififerent properties, and though hoth may cause death, 
 they do so in totally different ways. Can we not grant the 
 same thing in reference to the antecedents of urea? Surely 
 one of these products may be more abundant than another ! 
 Tf so, we can easily understand why in uraemia some cases are 
 attended with convulsions, whilst other cases are not. So 
 much for proteid metabolism, as far as it is possible to reason 
 at present. Do not forget, however, that the down grade 
 changes just pictured, though described as beginning ia the 
 Uver, we must allow that deficient excretion on the part of 
 the kidney may be the starting point. 
 
 MKTABOLISM OF CARBOHYDRATES. 
 
 Under the action of — 
 
 Starch is converted into 
 
 1. Saliva. | 
 
 1 I 
 
 Aohroo-dextrine and Erythro-dextrine 
 
 l_ ^1 
 
 2. Lactic Acid. (?) Maltose. 
 
 3. Pancreatic Juice. Dextrose. 
 
 4. Succus Entericus. Lsevulose — Dextrose. 
 
 I I 
 
 Absorbed into portal circulation. 
 
 5. In the Liver. Glycogen, and pass out when required into 
 
 the Blood as Dextrose again : then in the 
 
 Tissues. 00 A Energy. 
 
 6. (Muscles, etc.) HjOJHeat. 
 
 (Final Products.) 
 
 We see by the above table that carbohydrates, after 
 passing through various changes, get to the liver as grape 
 sugar. In the liver a portion is, however, stored up for a time, 
 not as sugar, but as a peculiar starch, termed glycogen. This 
 glycogen is again broken up by the liver cells into 
 grape sugar or glucose; and, then by means of the blood 
 
Fate of Peptones. 229 
 
 stream is conveyed to the various tissues, v^liere it is finally 
 oxidised to CO 2 and HjO. Supposing the liver is too richly 
 supplied ■with sugar, vfhat might happen ? It might store up 
 a large amount as glycogen, but allow a large quantity to pass 
 on unchanged. The blood would then be surcharged with sugar; 
 the muscles say, "we do not want so much : " there is an in- 
 crease of the supply over the demand — " a glut in the market " 
 as it were, and the sugar thus rejected by liver and muscles 
 is excreted by the kidneys, and glycosuria results. But sup- 
 posing the liver did not allow the sugar to pass too quickly or 
 unchanged, but the tissues through some wide spread neurosis 
 or other condition, were unable to use the normal amount of 
 sugar : then we should get glycosuria plus wasting of muscles ; 
 or in other words, diabetes. We thus see that glycosuria is a tem- 
 porary excessive supply ; diabetes on the other hand is a serious 
 organic disease. But we must remember that a mere excess 
 oi sugar persistently floating in the blood must act as foreign 
 matter and induce changes in the tissues by its irritating action; 
 so a continued glycosuria may induce real diabetes. Other 
 theories of diabetes will be discussed under that disease. 
 
 3. Bile Formation. — Bile consists principally of water, 
 cholesterine, salts, bile pigments and mucin. It is to be 
 regarded as — 
 
 (1) A secretion — concerned in the proper assimilation 
 
 of fats, etc. 
 
 (2) An excretion — a means by which broken down blood 
 
 pigments are excreted, with also a certain amount 
 of proteid waste (glycin etc.) 
 
 FATE OF BLOOD PIGMENTS. 
 
 Hsemoglobin is converted into — 
 
 
 In the Liver. \ Hsematoidin into — 
 
 . I 
 
 ' Bile Pigments which are — 
 
 I I 
 
 Excreted as — Stercobilin. Urobilin. 
 
 (Fffioes) (Urine.) 
 
230 Student's Hand-book of Medicine. 
 
 The pigment of bile being derived from hsemaglobin, 
 per se, we must have a larger amount of bile pigment in those 
 diseases attended with the destruction of red corpuscles. Now 
 bile pigment increases the thickness of bile, and Quincke has 
 shown " "When there is great destruction of red corpuscles in 
 the liver, mucin is also increased, which in turn materially 
 increases the viscosity of bile." Thus in pernicious ansemia 
 the bile is rendered thicker by — 
 
 1. Increased pigment. 
 
 2. Increased mucin. 
 
 K we increase the thickness of a fluid running through 
 a tube, we do two things — 
 
 1. Retard the flow. 
 
 2. Cause a greater tension of the tubal walls. 
 
 Now remembering all this takes place in the liver in all 
 exhausting diseases, it is no wonder we get a sallow complexion, 
 for the bUe tension being higher than normal, there is every 
 facility for transudation of bile into the blood. This is well 
 seen in pernicious ansemia. Probably all cases of jaundice are 
 obstructive, not indeed actual stoppage or suppression of bile, but 
 through the iacreased tension' within the bile ducts. Brunton has 
 done much to throw light on this subject. Lastly, in summing 
 up the functions of the liver, we must remember exercise and 
 moderate eating and drinking must increase its functional activ- 
 ity; then the bile moves on more quickly, glycogen is properly 
 stored up, and though more is formed than usual, it does not 
 accumulate, as the muscles use it up more rapidly to furnish 
 fuel for their increased work. Urates decrease and urea 
 increases. The reverse must happen by sluggish habits and 
 intemperance. Local vasa dilatation as a result of disease may 
 also increase for a time tlie functional activity, but soon, venous 
 congestion would occur under stfch circumstances, and torpidity 
 succeed the activity. 
 
Jaundice. 231 
 
 JAUNDICE. 
 
 Jaundice is the name applied to a group of symptoms, 
 arising from tlie circulation of bile in the blood. We have 
 already pointed out that bUe is to be looked upon as a 
 secretion and also as an excretion. Its retention within the 
 liver and its absorption into the blood must therefore give 
 rise to symptoms due to — 
 
 1. Its absence from the intestines, — This interferes largely 
 with the perfect assimilation of fat, and the imperfect absorption 
 causes serious decomposition or putrefactive changes to take 
 place in the intestines, skatol and indol are formed in excessive 
 quantities, complete proteid digestion cannot go on, and thus 
 we get absorption of albumoses and other poisonous compounds, 
 which contribute largely to the serious blood changes to be next 
 described. 
 
 2. The circulation of bile within the blood causes destruction 
 of red corpuscles, and therefore ansemia ; bile is also a neuro- 
 muscular poison, paralysing both nerve centres and muscular 
 fibres ; consequently we get imperfect action of the heart, slow 
 pulse, depression of the spirits, mental torpidity, and possibly 
 profound coma. Two types of jaundice are described— viz., 
 obstructive and non-obstructive. 
 
 In the former case no bile enters the intestine, and the 
 seats of obstruction are probably in the large ducts. By non- 
 obstructive jaundice is meant a condition of icterus in which a 
 certain amount of bUe escapes into the intestine. We have 
 already shown how the increased viscosity of bile resulting 
 from excessive breaking down of red corpuscles, might raise 
 the bile pressure sufficiently to cause absorption of bile into 
 the blood, and it is highly probable that all the so-called cases 
 of non-obstructive jaundice are due to this condition, and a 
 much better name would be Hsematogenous Jaundice. It ipust 
 be remembered however, that after jaundice due to obstruction 
 
232 Student's Hand-book of Medicine. 
 
 has existed for a time, the distended bile ducts may obliterate 
 or obstruct the vascular supply to the hepatic lobules, and 
 thus cause true suppression of bile formation. Obviously the 
 sjrmptoms of jaundice are not due to actual suppressiop, but to 
 the causes which lead to such abolition of the biliary function. 
 I append Dr Murchison's tabulated causes of jaundice. 
 
 A. — Jawndicefrom Mechanical Obstruction of the Bile Duct. 
 I. Obstruction by Foebibn Bodies within the Duct. 
 
 1. Gall-stones and inspissated bile. 
 
 2. Hydatids and distoraata. 
 
 3. Foreign bodies from the intestines, 
 
 II. Obsteuotion by Inflammatoey Tumefaction of the Duodenum, 
 OE OF THE Lining Mbmbeane of the Duct, with Exudation 
 into its Intebioe. 
 
 III. Obsteuotion by Steiotuee oe Obliteeation of the duct. 
 
 1. Congenital deficiency of the duct. 
 
 2. Stricture from perihepatitis. 
 
 3. Closure of orifice of duct in consequence of an ulcer in the 
 
 duodenum. 
 
 4. Stricture from cicatrisation of ulcers in the bile ducts. 
 
 5. Spasmodic stricture. 
 
 IV. Obsteuotion by Tumoues closing the Oeifioe op the Duct, or 
 
 QEOWING in its InTEEIOE. 
 
 V. Obsteuotion by Pressueb on the Duct feom without, by — 
 
 1. Tumours projecting from the liver itself. 
 
 2. Enlarged glands in the fissure of the liver. 
 
 3. Tumour of the stomach. 
 
 4. Tumour of the pancreas. 
 
 5. Tumour of the kidney. 
 
 6. Postperitoneal or omental tumour. 
 
 7. An abdominal aneurism. 
 
 8. Accumulation of faeces in the bowels. 
 
 9. A pregnant uterus. 
 
 10. Ovarian and uterine tumours. 
 
Jaundice. 233 
 
 B. — Jaundice independent of Mechanical Obstruction of the Bile Duct. 
 
 I. Poisons in the Blood interfering with the Normal Meta- 
 morphosis OF Bile. 
 
 1. The poisons of the various specific fevers. 
 
 (a) Yellow fever. (6) Remittent and intermittent fevers. 
 (c) Relapsing fever, (d) Typhus, (e). Enteric or 
 pythogenie fever. (/) Scarlatina, [g) "Epidemic 
 jaundice." 
 
 2. Animal Poisons. 
 
 {a) Pyaemia. (I) Snake-poison. 
 
 3. Mineral Poisons. 
 
 {a) Phosphorus. (6) Mercury. (c) Copper. 
 (d) Antimony, etc. 
 
 4. Chloroform or ether. 
 
 5. Acute atrophy of the liver. 
 
 II. Impaired or Deranoed Innervation interfering with the 
 Normal Metamorphosis of Bile. 
 
 1. Severe mental emotions, fright, anxiety, etc. 
 
 2. Concussion of the brain. 
 
 III. Deficient Oxygenation of the Blood interfering with the 
 
 Normal Metamorphosis of Bile. 
 
 IV. Excessive Secretion of Bile, more of which is absorbed than 
 
 can undergo the Normal Metamorphosis. 
 
 1. Congestion of the liver. 
 
 (a) Mechanical. (6) Active, (c) Passive. 
 
 V. Undue Absorption of Bile into the Blood from habitual ok 
 protracted Constipation. 
 
 It will be seen from the above table that Dr Murchison 
 looked upon the liver as the sole organ in the production of 
 bile. Physiologists, however, are not quite agreed on that 
 point, but it would be out of place to discuss the various 
 pros and eons, and unfortunately physiological facts are of 
 a fleeting character. 
 
234 Student's Hand-book of Medicine. 
 
 Symptoms of Jaundice — 
 
 1. Icterus or tinting of the skin, conjunctivas secretions, 
 etc. The colour ranges considerably, from a lemon-yellow to 
 a deep greenish-black (black jaundice). 
 
 2. Gastric disturbances, flatulence, nausea, and often com- 
 plete anorexia. 
 
 3. Constipation often alternating with diarrhoea ; the faeces 
 are pale, intensely foetid and pasty in character. 
 
 4. Slow pulse (has been observed in some cases to number 
 only 20 per minute). 
 
 5. Extravasations of blood. 
 
 6. Cerebral ' symptoms. Marked depression of spirits, 
 " patient sees things with a jaundiced eye,'' melancholia, 
 and in the graver forms, an assumption of the typhoid state 
 ending in death. 
 
 7. Itchiness of the skin. 
 
 The tests for bile acids and bile pigments wiU be found 
 under "Examination of Urine." 
 
 Treatment. — As jaundice is merely symptomatic, the cause 
 must be treated. In the milder forms a catarrh of the alimentary 
 canal, or the presence of small biliary calculi will require atten- 
 tion. For detailed treatment see "Hepatic Diseases and Gail- 
 Stones." Eemember, however, the indications always are to — 
 
 1. Kemove obstruction if possible. 
 
 2. Promote functional activitij by hepatic stimulants, 
 
 after clearing old bile away with saline purges 
 and calomel. 
 
 It is nonsense to talk of the liver being too active, the liver 
 cannot be too active. If there be an abnormal activity, 
 untoward symptoms will not crop up until incompetence of 
 the liver takes place. 
 
Jaundice. 235 
 
 ICTERUS NEONATORUM. 
 
 The form of jaundice -whicli occurs amongst new bom infants, 
 may be of either a mild or a malignant type. The mild form 
 appears on the second to the third day, and lasts from seven to 
 fourteen days; beyond the pigmentation few symptoms are 
 present. 
 
 Causes. — 
 
 1. The jaundice is probably due to the large destruction 
 of red corpuscles, which takes place the first few 
 days after birth (haematogenous jaundice). 
 
 ■2. Patency of the ductus venosus allowing the portal 
 blood (which contains at this time bile pigment) 
 to mix with the systemic circulation. 
 
 3. Diminished pressure in the portal circulation after 
 severence of the placenta, the bile pressure may 
 then exceed the blood pressure. 
 
 Malignant Form. — Causes. — 
 
 1. Congenital absence of the hepatic duct. 
 
 2. Congenital syphilitic hepatitis. 
 
 3. Phlebitis of the umbilical vein. 
 This form is almost invariably fatal. 
 
 ACUTE YELLOW ATROPHY OF THE LIVER. 
 
 (fatal jaundice). 
 
 A peculiar and rare disease probably due to septic organisms, 
 and characterised by a rapid and often complete destruction of 
 the hepatic cells throughout the gland. 
 
 jffitiology. — Women are more often attacked, and pregnancy is 
 sometimes associated with the condition. Other causes put down 
 
236 Student's Hand-book of Medicine. 
 
 are abuse of mercury, fright, the poisons of malaria, and typhus. 
 (Though there are many points of resemblance between acute 
 atrophy, yellow fever, and pathological phosphorous poisoning, 
 the conditions of each are not identical.) 
 
 Pathology. — The liver is much diminished in size, soft and 
 flaccid. The capsule is wrinkled. On section, extensive fatty 
 degeneration, destruction of hepatic cells, and empty bile ducts, 
 are the marked features. Masses of golden pigment, red 
 patches, and course granules are often present, leucin and tyrosin 
 can always be detected, and may crystallise spontaneously after 
 death. 
 
 Symptoms. — Usually there are precursory symptoms such 
 as mental and bodily depression, constipation, and tenderness 
 in the hepatic region. In the confirmed stage, intense jaundice 
 sets in, with vomiting, etc., severe hsemorrhages, evacuations of 
 pale fseces (or the fseces may be black from mixture of blood) ; 
 pregnant women abort, and the typical typhoid state ushers in 
 the end. Death usually takes place within seven days of the 
 confirmed stage. 
 
 Diagnosis, — 27*6 severity of the symptoms, with the jaun- 
 diced aspect, diminished hepatic dulness, and the presence 
 of leucin and tyrosin in the urine makes the diagnosis 
 fairly easy. 
 
 We have already seen that leucin and tyrosin are probably 
 the earliest antecedents of urea. Their appearance in the urine, 
 and disappearance of urea in a condition where the liver is so 
 largely affected, forms a strong link in the chain of evidence in 
 favour of the liver being the chief seat of proteid metabolism, 
 and urea the final product of such metabolism. 
 
 Treatment. — Probably useless. Large doses of quinine with 
 the mineral acids, and diffusible stimulants may be tried. 
 
Tropical Abscess. 237 
 
 ABSCESSES IN THE LIVER. 
 
 An abscess in the liver may be due to many causes, 
 such, as — 
 
 1. Traumatisms. 
 
 2. Suppuration of the bile ducts set up by gall-stones, 
 parasites, etc. 
 
 3. Suppurating cysts, tubercular nodules, or syphilitic 
 gummata. 
 
 But there are two forms which requires special mention — 
 ■vit, the tropical or single abscess, and pyaemic or multiple 
 
 TROPICAL ABSCESS. 
 
 Is probably due to the amoeba coli flourishing in a suitable 
 soil furnished by dysentery, excessive use of alcohol in hot 
 climates, etc. 
 
 Pathology. — The abscess is usually single, but there may 
 be two or more. 
 
 Situation. — Eight lobe. 
 
 Walls. — Firm and thick, and have often three distinct 
 layers — 
 
 1. Inner. — Gray in colour, and composed of necrosed 
 
 tissue, amcebse, and pus cells — no membrane 
 internally. 
 
 2. Middle. — Brownish-red friable liver tissue. 
 
 3. Outer. — Hypersemic liver tissue. 
 
 Contents. — Pus, often like anchovy sauce, and of a peculiar 
 disgusting sourish odour. The abscess if left alone most often 
 bursts into the right lung. 
 
238 Student's Hand-book of Medicine. 
 
 Symptoms. — The earlier symptoms are — 
 
 1. Pain, sense of weiglit and fulness, and tenderness 
 
 in the right hypochondrium. 
 
 2. More or less jaundice. 
 
 Later. — We get rigors, elevation of temperature, "septic" 
 in character ; symptoms dependant on more or less peritonitis ; 
 the tongue becomes furred and dry, a sickly odour emanates 
 from the breath ; jaundice may become marked, and ascites 
 develop. It must be remembered that the symptoms may be 
 latent untU those of rupture appear. When it hursts into 
 the lungs, the expectoration of anchovy paste-like sputum is 
 characteristic. If there be doubt about the diagnosis, puncture 
 ■with a fine trocar. 
 
 Treatment. — Avoidance of alcohol ; removal from tropical 
 climate; treat on general principles. Eest, ipecac, warmth, 
 and tonics. When pus has formed and can be fairly localised, 
 aspirate. 
 
 PY.<EMIC ABSCESSES. 
 
 Pyasmic abscesses of the liver are usually small and scattered 
 throughout the liver substance. 
 
 Pathology. — The condition is essentially dependant on the 
 presence of micrococci, and is most frequently a part of a 
 general pysemia. The micrococci may gain an entrance into 
 the liver substance either — 
 
 1. Through the hepatic artery in cases of general pysemia, 
 especially after head injuries, (in which case the organisms 
 must have first passed through the capillaries of the lung). 
 
 2. Through the portal vein in lesions of the portal area. 
 
 3. Through the hile ducts in ulceration from gall stones, etc. 
 In these cases the suppuration is in the course of the distribu- 
 tion of the portal vein (Dr F. Taylor). 
 
Cirrhosis of the Liver. 239 
 
 The formation of pyaamic abscesses has already heen described 
 under "Pysemia." 
 
 Symptoms. — Hectic fever, jaundice, with a tender, painful, 
 enlarged liver, are the main symptoms. Often the symptoms 
 are very obscure, and pain may be conspicuous by its absence, 
 "Febrile jaundice" is a valuable diagnostic when present. 
 
 Treatment. — Almost hopeless. Can only hope to support 
 patient until the septic processes have ceased. 
 
 CIRRHOSIS OF THE LIVER. 
 
 This is a condition characterised by a great increase of 
 connective tissue at the expense of the proper glandular 
 tissue. 
 
 .etiology. — By far the most important factor in producing 
 this disease is the excessive use of alcohol, especially spirits. 
 Though essentially a disease of adult life, children who are 
 addicted to intemperance frequently afford typical examples 
 of hepatic cirrhosis. Other factors are supposed to be gout 
 and syphilis, but as these two conditions are often associated 
 with intemperance, possibly the alcohol, even in these con- 
 ditions, is the most potent agent. Congenital syphilis may 
 produce cirrhosis, but, I certainly have seen many hundreds of 
 cases of congenital syphilis without serious hepatic troubles. 
 The other factors enumerated as causes of cirrhosis are malaria, 
 tuberculosis, and excessive use of hot condiments. 
 
 Morbid Anatomy. — During the hypertrophic stage, the liver 
 is often enormous in size, extending even below the umbUicus ; 
 towards the latter end of the atrophic stage the liver may only 
 
240 
 
 Student's Hand-book of Medicine. 
 
 weigh two pounds, and be quite inaccessible to the touch. The 
 more atrophied the liver, the more rough, nodular, or hobnailed 
 is it likely to be. Conversely, the larger the liver the greater 
 probability of it being smooth or but slightly roughened. There 
 is a great tendency at present to regard all cases of cirrhosis 
 as the result of a simple chronic inflammation, and therefore 
 all have — (1) a stage of hypertrophy, and (2) a stage of atrophy. 
 This seems to me to be by far the most probably theory, and 
 we have no less an authority than Dr Frederick Taylor of Guy's 
 Hospital, for this statement. If we grant this, then we can 
 easily understand why few symptoms are present in the earlier 
 stages, and why they become so pronounced (almost malignant) 
 in character during the atrophic stage. Clinicians and path- 
 ologists, however, do not agree. 
 
 I append Dr Woodhead's table of the " biliary '' and the 
 ordinary cirrhosis : — 
 
 Common Cirrhosis. 
 
 1. The bile ducts are not involved 
 in the growth of connective tissue 
 at first ; consequently, jaundice is 
 a late symptom. 
 
 2. The new growth involving the 
 portal circulation is likely to cause 
 ascites, haemorrhoids, haematemeses, 
 etc. 
 
 3. In the earlier stages the in- 
 creased growth of young connective 
 tissue in the portal spaces cause 
 considerable increase in the size of 
 the organ ; but, in the later stages, 
 this tissue contracts, and in con- 
 tracting cause, a considerable de- 
 crease in the size of the liver. 
 
 4. The liver rough and hobnailed 
 on its surface ; and the capsule 
 much thickened. 
 
 Biliary Cieehosis. 
 
 1. The bile ducts are involved 
 early, and jaundice is a severe 
 symptom. Apparently there is a 
 new formation of bile ducts. 
 
 2. The portal veins are not in- 
 volved, and symptoms dependant 
 on portal obstruction are rare. 
 
 3. The large amount of new 
 tissue diffused throughout the 
 organ, causes a great enlargement 
 of the liver. 
 
 4. Surface is smooth (like Morocco 
 leather) ; the capsule is not thick- 
 ened. 
 
Cirrhosis of the Liver. 
 
 241 
 
 5. The masses of liver cells vary 
 in size, some consisting of several 
 lobules, whilst others are smaller 
 than a lobule. Each of these 
 masses form a distinct area having 
 a rounded outline surrounded by 
 a fibrous zone, and from the fibrous 
 mass the mass of liver cells can 
 be easily turned out. 
 
 6. On microscopic examination 
 it Ls seen that the process is going 
 on chiefly at the periphery of the 
 lobules, but, that gi'oups of lobules 
 are affected. 
 
 5. The masses of liver cells con- 
 sist of atrophied lobules, and the 
 cut surface has a more or less 
 uniform, and finely granulated 
 appearance. 
 
 6. The single lobules above men- 
 tioned are surrounded by bands 
 of fibrous tissue, which bands, 
 however, are not confined to the 
 periphery, but invade the substance 
 of the lobules. 
 
 However th.e main thing to remember is not the varieties, 
 but to look upon cirrhosis pathologically as a condition charac- 
 terised by — 
 
 1. Increased growth of fibrous tissue in Glisson's capsule, 
 
 and in the prolongations of it running into the 
 liver substance. 
 
 2. Obstruction to the portal circulation. 
 
 3. Increased blood pressure in the hepatic arteries. 
 
 4. Obliteration of hepatic cells. \ 
 
 5. Obstruction of biliary ducts. / 
 
 later. 
 
 Symptoms. — At first there may be little disturbance be- 
 yond chronic gastric catarrh symptoms — viz., morning vomiting, 
 anorexia, and acid eructations, but soon a severe hsematemeses 
 coupled with a distinct sense of weight in the hepatic region 
 reveals the true nature of the disease, and on examination, the 
 Kver is found to be much enlarged. As time wears on the more 
 characteristic features are — 
 
 1. Ascites. 
 
 2. Emaciation. 
 
 3. Jaundice (often very late). 
 
 And now on examination the liver is found atrophied. 
 
 s 
 
242 Student's Hand-hook of Medicine. 
 
 The ascites as a rule is particularly well marked. The 
 surface of the abdomen is covered by large distended veins, 
 showing an attempt at collateral circulation to carry on the 
 now obstructed portal circulation. This condition is highly 
 important from a prognostical point of view. The more com- 
 mon anastamoses are between — 
 
 1. The gastric and oesophageal veins. 
 
 2. Middle hsemorrhoidal of the inferior mesenteric and 
 
 inferior hsemorrhoidal of the internal iliac vein. 
 
 3. Coronary veins of stomach and phrenic veins. 
 
 4. Accessory portal vein of Sappey — i.e., a vein running 
 
 alongside the round ligament of the liver, com- 
 municating the portal vein with branches of the 
 epigastric veins near the navel. This often 
 produces a large bunch of varicose veins, the 
 so-called caput medusse. 
 
 It will be thus seen that the later symptoms are dependant 
 on a grave interference with the hepatic metabolism plus 
 general venous congestion. The toxaemia and exhaustion, con- 
 sequent on serious obstruction, may bring about a fatal issue. 
 
 The clinical symptoms of the i so called " biliary " cirrhosis 
 already referred to are (as described by the French School) — 
 
 Acute intense jaundice, but no ascites. 
 
 Elevation of temperature. 
 
 Delirium and the rapid assumption of the typhoid state. 
 
 Death often occurs within ten days or three weeks. 
 
 Prognosis. — Bad as regards cure; but if the collateral 
 circulation be well established, the atrophy not marked, and 
 the patient made to live temperately, bad symptoms may not 
 arise for a considerable period. There is very grave doubt as 
 to the possibility of far advanced cirrhosis being cured. 
 
Waxy Liver. 243 
 
 Treatment. — It must be (1) general, and (2) symptomatic. 
 
 General. — Absolute temperance in eating and drinking must 
 be observed with abstinence from hot condiments, etc. ; the 
 portal circulation should be depleted by the administration of 
 a saturated solution of Epsom salts. Exercise, massage to the 
 liver, and careful avoidance of chills, are the main points to 
 remember. Ammon. chlor., arsenic, strychnine, etc., may be 
 given. 
 
 Symptomatic. — Ascites, the fluid should be evacuated 
 quickly by tapping, or by the slow method by means of 
 Southey's tubes. Hydrogogue cathartics are sometimes of 
 use. The hEematemeses should not be treated too energetic- 
 ally as it often acts as a safety valve, i.e., preventing internal 
 hsemorrhage. If it be excessive, ice, recumbent position, 
 ergot, acid sulph. dil., full dose of morphia, hydrastis, hazeline, 
 etc., should be resorted to. 
 
 The Emaciation, calls for tonics, and the most nutritious 
 diet compatible with the imperfect assimilative powers. Some 
 authorities advise skim-milk diet. 
 
 WAXY LIVER. 
 
 The liver is often affected with lardaceous disease, and as 
 elsewhere, the degeneration begins in the middle coats of the 
 blood-vessels. The lobules are invaded from without in- 
 wards, the hepatic cells become destroyed, and the glandular 
 structure converted into a firm, dense material. The liver 
 is enormously enlarged, and smooth. On section, the sub- 
 stance is glistening, firm, and resembles yellow wax, the 
 cut surfaces showing only faint traces of lobules. It must 
 be remembered that waxy disease may co-exist with fatty 
 liver, syphilitic disease, etc. 
 
 Causes, — Prolonged suppuration, as in strumous ulcerations, 
 caries, and necrosis ; as a result of malignant fevers, etc. 
 
244 Student's Hand-hook of Medicine. 
 
 Symptoms. — Sense of weight in the hepatic region, anorexia 
 and other dyspeptic symptoms ; diarrhoea, the stools being pale 
 and often fatty. Later, there may be jaundice, ascites, and 
 albuminuria. Pain is rare. The disease is usually fatal. 
 
 Treatment. — Remove cause as far as possible. Iodide of 
 potassium is often of great service, especially vi^hen the disease 
 is due to syphilis. The general treatment is the same as that 
 of tuberculosis. 
 
 FATTY LIVER. 
 
 By fatty liver is meant, a great increase in the quantity of 
 fattj"^ globules, naturally contained in the hepatic cells ; so that 
 on examination the cells are found loaded with oil globules, 
 often obscuring the nuclei. The change takes place first at the 
 periphery, but later the whole of the lobule is invaded. The 
 liver is usually much enlarged with a smoothish surface. 
 
 Causes. — General obesity ; emaciating diseases, such as 
 cancer and phthisis ; venous congestion may cause both 
 nutmeg and fatty liver. Care should be taken not to con- 
 found fatty infiltration with fatty degeneration. In the latter 
 condition the hepatic cells undergo a complete metamorphosis. 
 Physiological chemistry leads us to anticipate fatty infiltration, 
 in those cases where the oxidising power is insufficient to 
 dispose of the ordinary fat forming elements of the daOy food. 
 Fatty degeneration is also due to deficient oxidation, but the 
 tissues themselves form the fat, and experience has shown 
 it is always associated with either mineral poisons or bacterial 
 action. I do not think it can be proved to be ever due to 
 imperfect oxidation simply. 
 
 Symptoms. — Often are very obscure, but the symptoms of 
 chronic gastric catarrh, constipation alternating with diarrhoea, 
 pasty complexion, together with the physical signs of an 
 enlarged liver, not accompanied by either pain or jaundice, 
 renders the diagnosis fairly easy. 
 
Oancer of the Liver. 245 
 
 Treatment. — Eegulate the diet, avoid excess of proteids 
 or carbohydrates particularly. Prescribe alkaline aperients, 
 chloride of ammonia, calomel and podophyllin, massage arid 
 exercise. 
 
 CANCER OF THE LIVER. 
 
 Cancer of the liver may be primary, but is more often 
 secondary to cancer elsewhere. 
 
 .3Itiology. — Men are more frequently attacked than women: 
 from forty to sixty years seems the most favourable period. The 
 predisposing causes are similar to those of cancer elsewhere, 
 viz., — heredity, injuries, etc. 
 
 Pathology. — All types of cancer have been found in the 
 liver, but the primary forms are nearly always epitheliomatous. 
 
 Primary Oancer. — Two distinct types are distinguished^ 
 
 1. The massive liver, greyish white in colour, occupies 
 
 a large portion of the liver and is abruptly 
 defined from the liver tissue. 
 
 2. ITodular cancer, in which the nodules vary much in 
 
 size, and are irregularly scattered throughout 
 the organ. 
 
 Secondary Cancer. — The organ becomes enormously enlarged, 
 and the nodules can easily be felt through the emaciated ab- 
 dominal walls ; indeed, they may be near enough to the surface 
 to be visible (the so-called "Farre's tubercles"). On section 
 we find — 
 
 1. Extensive areas of fibrosis. 
 
 2. Extensive areas of fatty degeneration. 
 
 3. Extravasations of blood. 
 
 4. Dense greyish hyaline masses. 
 
246 
 
 Student's Hand-book of Medicine. 
 
 Symptoms of Cancer of the Liver. — Daily increasing 
 emaciation, hepatic pain, malignant cachexia, jaundice, some- 
 times ascites, attacks of local peritonitis, together with the 
 characteristic physical signs of the rough, uneven, enlarged 
 liver, are the principal features. It should, however, be 
 remembered that cancer may be added to a cirrhosis of the 
 liver. When the growth is of a melanotic sarcoma type, the 
 pigmentation plus other symptoms, points to the true nature 
 of the disease. 
 
 Diagnosis between cancer and cirrhosis is often difficult 
 when there is a strong history of alcoholism. The following 
 table may help — 
 
 
 CIBBH0SI5. 
 
 CAirCEB. 
 
 JProgrens . . .^ . . 
 
 1. Often slow. 
 
 1. Always rapid. 
 
 Liver 
 
 2. Enlarged atfirBt.tliensmaller, 
 and more nodular aa atrophy 
 becomes more marked. 
 
 2. Is large, and the nodular 
 character developed from 
 the first. 
 
 Fain 
 
 S. Not marked. 
 
 3. Well marked. 
 
 Ascites 
 
 Jaundice .... 
 
 4. XTsually present. 
 
 5. Not till late. 
 
 4. Often absent. 
 
 5. Often a marked feature. 
 
 HEPATIC TUMOURS. 
 
 The more common tumours and growths, otherwise than 
 malignant, are — 
 
 1. Hydatid tumours. 
 
 2. Cystic tumours. 
 
 3. Cavernous tumours (angioma). 
 
 4. Tuberculosis. 
 
 Hydatid Tumours occur more frequently in the liver than 
 in any other organ (see " Tsenia.") 
 
 Symptoms. — A hydatid tumour of the liver grows slowly, 
 and usually in one particular direction. It is painless (until it 
 
Hepatic Tv/mours. 247 
 
 suppurates), and may cause no symptoms until it becomes 
 extremely large or bursts. 
 
 Physical Examination. — Tumour is globular, tense, elastic, 
 and -with care fluctuation is detected. On palpation a peculiar 
 vibratory thrill may be felt. 
 
 Prognosis. — The cyst may undergo spontaneous cure without 
 rupture. Death of the parasite causes the cyst to contract. 
 Eupture may take place into the lung or through the abdominal 
 wall, into the intestines, or into the hepatic duct. 
 
 Treatment. — As soon as the cyst is discovered employ 
 surgical means, such as — 
 
 1. Aspiration, and subsequent injection of iodine. 
 
 2. Electrolysis. 
 
 3. Careful incision, and free evacuation of cyst contents. 
 
 Cystic Tumours are due to inflammation of the hepatic 
 ducts, and consist of a cheese-like substance showing under 
 the microscope, granular debris, cholesterine crystals, oil 
 globules, etc. 
 
 Cavernous Tumours, oeeasionally in children attain a great 
 size, but are more common in aged people. They are found on 
 the upper surface of the liver ; on cutting into them they present 
 a similar appearance to that of the corpora cavernosa of the 
 penis, hence the name " ereotUe tumour." 
 
 Tuberculosis. — Typical tubercular deposits occur in the liver, 
 secondarily to tubercle elsewhere, especially the abdominal 
 viscera. Patient usually dies before the disease is far 
 advanced. 
 
 As regards the treatment of these tumours, it must be 
 entirely symptomatic, combined with careful hygienic measures 
 in all cases. 
 
248 Student's Hand-book of Medicine. 
 
 DISEASES OF THE GALL BLADDER. 
 
 Inflammation of the gall bladder is most frequently due to 
 extension of inflammation from neighbouring parts, but it may 
 be caused by direct irritation of the cystic mucous membrane 
 through the passage or impaction of gall-stones, parasites, etc. 
 
 Dropsy. — "When the cystic duct is blocked, the mucous 
 membrane of the gall bladder undergoes a peculiar degener- 
 ation, I'esulting in a secretion of watery fluid, which may 
 distend the gall bladder enormously. Often the tumour is so 
 freely movable as to cause it to he mistaken for a movable 
 kidney. 
 
 Gallstones. — Biliary calculi are most common in females 
 between the age of thirty and forty-five. 
 
 Composition — 
 
 Single gall-stones are almost entirely composed of choles- 
 terine (a monatomic alcohol). The nucleus is usually a bit 
 of dried mucus. The stone is semi-translucent, glistening, 
 with a somewhat granular surface, and is very light. 
 
 Multiple gall-stones are much more common ; a few or a 
 hundred stones may be present. They difi'er from the single 
 stone by — 
 
 1. Being stratified : the strata are of difierent shades 
 
 of colour, some being very deeply coloured. 
 
 2. Presenting facets on their surface from pressure. 
 
 Effects of Gall'Stones are — ■ 
 
 1. To cause more or less inflammation of the mucous mem- 
 brane. 
 
 2. Impaction of the ducts, consequently giving rise to 
 jaundice etc. 
 
Diseases of the Gall Bladder. 249 
 
 3. They may cause serious ulceration. 
 
 4. During their passage along the ducts they cause the 
 intensely painful " biliary colic," and often 
 
 5. Subsequent appendicitis, obstruction of bowels, etc. 
 
 Symptoms of Biliary Colic. — 
 
 1. Excruciating pain in the hepatic region, and radiating all 
 over the thorax to the shoulders, and with a sense of general 
 thoracic constriction. 
 
 2. Vomiting, which often gives relief (probably by the con- 
 tractions of the diaphragm so induced, aiding peristalsis). 
 
 3. Subsequently to the attack, jaundice is more or less 
 pronounced. 
 
 4. A local rise of temperature (?). 
 
 It must be remembered that (as in renal calculus) the stone 
 after obstructing for a time, may slip back again into the cystic 
 duct or gall bladder, giving a sequence of events which may 
 be several times repeated. Moreover, gall-stones may be the 
 cause of hypertrophic cirrhosis, or the exciting cause of 
 cancer. (Dr Sadnby.) 
 
 Many observers have shown conclusively that the presence 
 of gall-stones may give rise to a " bastard ague.'' 
 
 Treatment of Biliary Colic. — 
 
 1. Hypodermic injection of morphia. 
 
 2. Chloroform inhalations until morphia acts. 
 
 3. Hot fomentations over liver. 
 
 4. Mtrite of amyl. 
 
 Subsequently : purgatives, careful dieting, regular exercise, 
 and avoidance of any constriction of the hepatic circulation 
 by tight corsets, etc. 
 
 •■Persistent Biliary Obstruction. — Demands surgical inter- 
 ference, but care must be t^ken to diagnose the cause of 
 
250 Student's Hand-hooh of Medicine. 
 
 obstruction first. Harley advises a trial of massage and olive 
 oil internally. I removed eighty gall-stones by this method 
 in one case. 
 
 Diagnosis of Gall Bladder Affections. — A distended gall 
 bladder forms a smooth ovoidal tumour below the ninth right 
 costal cartUage. Take into consideration the history, jaundice, 
 character of pain, etc. 
 
 DISEASES OF THE KIDNEY. 
 ALBUMINURIA. 
 
 By albuminuria is meant, "the presence of albumin in the 
 urine." As albumin is one of the essential constituents of the 
 blood, an escape of it in the urine must necessarily be looked 
 upon with suspicion, if not with anxiety. Formerly, all cases 
 of albuminuria were regarded as varieties of Bright's disease, 
 but it has been conclusively shown, that albuminuria is often 
 present in (as far as we can make out) healthy individuals. 
 However, " a persistent albuminuria, especially if the albumin 
 tends to increase, must always be looked upon as a grave and 
 significant condition." In other words, just as palpitation of 
 the heart may exist without cardiac disease, it may on the 
 other hand be a prominent symptom of a grave organic lesion ; 
 so with albuminuria, it may or may not be a serious omen. 
 
 Theories of albuminuria are at present speculative, possibly 
 the best is number 1. — • 
 
 1. That the cells lining the glomeruli exert a selective in- 
 fluence in excretion, inasmuch as they allow the water and 
 certain soluble salts to pass, but prevent albumin from so doing. 
 
 2. That albumin normally escapes through the glomeruli 
 into the tubules, but is rapidly taken up again by the cells 
 
Diseases of the Kidney. 251 
 
 of th.6 tubules, and re-absorbed into the blood. This is doubt- 
 ful, but on tbe other hand, the cells of the convoluted tubules 
 certainly have a decided selective function, as shown in the 
 excretion of urea, etc. 
 
 The first theory would demand for the production of 
 albuminuria) a diseased condition of, or at least some alter- 
 ation in the epithelium of the glomeruli. 
 
 The second theory demands " increased blood pressure," in 
 order to explain the escape. A great increase of the renal 
 blood pressure injures the cells, and causes the urine to rush 
 past the cells so quickly that re-absorption is prevented. Most 
 probably both conditions play their parts, but neither one nor 
 both are sufficient to explain all cases. 
 
 Experimentally, we may produce albuminuria by — 
 
 1. Pressure upon (not closure of) the renal veins; the 
 pressure in the glomeruli is increased thereby. 
 
 2. Closure of the renal artery, and subsequent re-establish- 
 ment of the circulation ; this interferes with the nutrition 
 of the renal cells. 
 
 3. Ligature of the aorta below one kidney, and extirpation 
 of the other. 
 
 4. Ligature of the aorta above the renal arteries. 
 
 5. Compression of the trachea ; this leads to asphyxia, 
 and consequent rise of blood pressure. (Ha-LLIBUrton.) 
 
 Glinically, we get albuminuria — 
 
 1. Due to — 
 
 Morbid conditions of the kidney, such as acute and 
 
 chronic inflammation, waxy degeneration, renal 
 
 calculi, tumours, etc. 
 Diseases of the urinary apparatus below the kidney. 
 Hsomic changes — ansemia, leucooythemia, etc. 
 Certain fevers, especially scarlet fever and diphtheria. 
 
252 Student's Hand-book of Medicine. 
 
 Pregnancy. 
 
 Certain poisons — arsenic, phosphorus, excessive use of 
 
 morphia, etc. 
 Venous congestion, consequent on hepatic, pulmonary, 
 
 or cardiac disease, etc. 
 
 2. After certain diets, especially in those who pass much 
 oxalates in their urine (oxaluria). 
 
 3. In a remittent or cyclic form, occurs in apparently 
 healthy people; alhumin is in such cases only present in 
 the urine at certain periods of the day. 
 
 4. In the so-called "paroxysmal" form, associated with a 
 more or less jaundiced apppearance, and anaemia. Possibly 
 is due to functional disturbance of the liver, whereby the 
 breaking down of corpuscles is much increased. 
 
 5. After severe exercise. 
 
 Treatment of Albuminuria. — No condition requires more 
 careful treatment. The first thing to do is to settle if possible 
 whether it is functional, or the result of structural disease of the 
 kidney or winary passages. This can only be done by careful 
 consideration, and frequent examinations of the urine. Do not 
 forget that albumin is temporarily absent in many grave cases 
 of renal disease. The following are the chief indications of 
 treatment. — 
 
 1. Eemove if possible any obvious cause. 
 
 2. Prescribe a non-nitrogenous diet as far as possible. 
 
 3. Avoidance of all substances (food or drugs) likely 
 
 to increase unduly the blood pressure, or cause 
 irritation of the renal tubules. 
 
 4. Give ergot, jaboiandi, gallic acid, nitrite of amyl. 
 
 Fvirther treatment will be discussed under 
 "Nephritis." For tests for albumin see exami- 
 nation of the urine. 
 
Blood in the Urine. 253 
 
 BLOOD IN THE URINE. 
 
 Blood in the Urine is another very grave symptom. Two 
 forms are described — 
 
 1. Hsematuria, or bloody urine proper. 
 
 2. Haemoglobinuria, a condition marked by the presence of 
 blood-pigment in the urine, but few or no blood corpuscles. 
 The blood pigment is generally meihoemoglohin (chocolate 
 colour). 
 
 Causes of Heematuria. — 
 
 Diseases of the kidneys and urinary apparatus below them. 
 
 Extensive bruises (absorption of blood pigment). 
 
 Scurvy (especially in children). 
 
 Malignant forms of fevers, especially the malarial type. 
 
 Traumatisms. 
 
 No discoverable cause (Gull's "epistaxis of the kidney"). 
 
 Drugs which directly irritate the kidney, turpentine, can- 
 
 tharides, carbolic acid, etc. 
 Parasites, especially the bilharzia hsematobia. 
 
 Diagnosis. — 
 
 1. By the colour of the urine, which ranges from a slight 
 smoky tint to deep red or even porter colour. 
 
 2. Microscope. — Detection of blood discs (ia fresh urines). 
 
 3. Spectroscope. — The characteristic bands of haemoglobin 
 (generally the reduced Hb). 
 
 4. Ozonic sether and guaicum gives a blue tint. (This is a 
 very fallacious test.) 
 
 If the blood comes from above the ureters, it is usually freely 
 mixed with the urine. 
 
 If from the ureters, blood may be clotted in the form of 
 moulds. 
 
254 Student's Hand-book of Medicine. 
 
 If from the bladder, is either mixed, or appears after urine 
 has been passed. 
 
 If from the urethra. — Before or during the first part of 
 micturition. 
 
 There are no definite means of ascertaining the site of the 
 haemorrhage by mere examination of the urine alone. 
 
 Treatment. — Eest in the recumbent posture. Full doses 
 of opium. Ergot. — Lead Acetate. — Hazeline. — ^Hydrastis Canad. 
 
 Parasitic Variety, — Injections into the bladder, of iodide of 
 potassium (5 grains to 3i.) Santonine, or male fern, internally. 
 
 Causes of Hsemoglobinuria. — 
 
 1. Toxic Form. — Due to the action of certain poisons, such 
 as nitrites, arsenuretted hydrogen, carbon monoxide, bUe, etc. 
 
 2. Paroxysmal Form. — This condition is characterised by the 
 occasional passage of bloody urine, the pigments only being 
 present. The causes are not known, hut there seems to be a 
 great causal relation between this condition and disturbances of 
 the vasa-motor system ; so much so, that it has been termed 
 " Eaynaud's " disease of the kidneys. The most commonly 
 associated conditions are — 
 
 (1) Vasa-motor disturbances. 
 
 (2) Increased hseraolytic action of the liver and spleen. 
 
 (3) Extensive superficial burns. 
 
 (I saw three such cases in a colliery practice). 
 In newly bom infants haemoglohinuria may accompany the 
 usual destruction of red corpuscles. 
 
 Symptoms. — The attack may come on after the morning 
 bath, mental exhaustion, or exposure to cold. There is usually 
 pain in the lumbar region during the attack. Vomiting, 
 anorexia and jaundice are often present. 
 
 Treatment. — Fresh air and tonics. During the attack keep 
 the patient warm and give hot drinks. 
 
UrcBmia. 255 
 
 UREMIA. 
 
 Is the name given to the symptoms that arise from retention 
 of urea (or what is much more prohable the antecedents of urea). 
 It is usually associated with disease of the kidneys and supres- 
 sion of, or diminished quantity of urine. The two theories 
 before the profession at present are— 
 
 1. Inability of the kidney to eliminate the urea, which being 
 retained in the blood, splits up into carbonate of ammonia 
 which is considered the toxic element. 
 
 2. The liver being extensively handicapped by the deficient 
 assistance of the kidneys, breaks down proteid waste imper- 
 fectly, and, consequently, the intermediate products similar to 
 alkaloids accumulate and exert their poisonous action in different 
 ways. Bouchard has shown conclusively that these poisons 
 have markedly different qualities. This is probably the correct 
 theory. 
 
 Against the first theory are four facts, viz. — 
 
 (1) Urea, if injected into the blood will not cause ursemic 
 
 symptoms. 
 
 (2) Ursemic symptoms are not the same as those of 
 
 poisoning by carbonate of ammonia. 
 
 (3) No two cases of uraemia are exactly ahke. 
 
 (4) Urea which is present only in minute quantities in 
 
 normal bile and faeces is much increased in these 
 secretions during ursemia. 
 
 Symptoms of Urtemia are diverse and many. Taking a 
 typical case we may expect — 
 
 Vomiting. 
 
 Headache of a dull character, especially in the occipital 
 region. 
 
256 Student's Hand-hook of Medicine. 
 
 Peculiar and characteristic dyspnoea, " Cheyne - Stokes' 
 breathing" persisting for weeks ■without coma. 
 
 Muscular twitchings, deepening into 
 
 Convulsions. 
 
 Contraction of pupils (often uneven). 
 
 Suppression of urine. 
 
 Coma and death. 
 
 The odour of the breath is said to be ammoniacal, or 
 sweetish like new mown hay ; much oftener the breath is 
 offensive from severe stomatitis. 
 
 Diagnosis. — The utmost care should be taken not to mistake 
 the disease for alcoholism, apoplexy, opium poisoning, etc., but 
 such diagnosis is often extremely difficult. Examination of the 
 urine, of the eyes for albuminuric retinitis, of the pulse for 
 evidence of arterio-sclerosis, are the chief points to be remembered. 
 Lastly, remember that haemorrhage into the brain during cirrhotic 
 Bright's disease is common. 
 
 ACUTE BRIGHT'S DISEASE. 
 
 Acute inflammation of the kidneys is a disease characterised 
 by febrile disturbances, grave changes in the urine, and dropsy. 
 
 Causes. — 
 
 1. Exposure to cold, especially when the body is over- 
 heated. 
 
 2. Acute specific fevers and septic states, especially scarlet 
 fever and ulcerative endocarditis. (Albuminuria without the 
 other symptoms of acute nephritis is common in diphtheria.) 
 
 3. Certain irritating drugs, e.g. — cantharides, copaiba, tur- 
 pentine, etc. 
 
 4. Extensive burns involving the abdomen. 
 
 5. Parasites, etc. 
 
Acute Bright' s Disease. 257 
 
 Pathology. — Two types are usually distinguished, — i.e., tlie 
 ordinary or catarrhal form, and the so-called infective or 
 glomerulo-nephritis. 
 
 1. Catarrlial Nephritis. — The kidneys are large, much in- 
 jected, and the cortex is seen to be disproportionately enlarged. 
 On section, the cut surfaces show up the Malpighian bodies as deep 
 red points ; here and there are patches of extravasated blood. 
 The tubules show marked changes, especially the convoluted 
 portions, the epithelium undergoes cloudy swelling, followed by 
 proliferation and detachment of the cells, which form casts or 
 masses of granular fatty debris, often to the extent of blocking 
 up the tubules. It must not be forgotten, however, that though 
 the tubules are the parts principally involved, the interstitial 
 portion also takes part in the inflammatory process. 
 
 2. Glomerulo- Nephritis. — In this form the glomeruli prin- 
 cipally suffer, and is usually the result of infective fevers. 
 After a preliminary engorgement of the blood-vessels, extensive 
 leucocyte emigration takes place, fiUing the glomerular capsule, 
 the capillary vessels often burst, and the blood flows into the 
 tubules. The epithelium of Bowman's capsules often proliferate 
 to such an extent that the tufts become obliterated by the 
 pressure, aad in time the latter may be actually changed into 
 fibrous nodules. Of course the tubules and interstitial tissue 
 are also involved, though not to the same extent. 
 
 Symptoms are at first, chilliness, pain in the back, vomiting 
 and pain over the brows ; the temperature is raised (but may 
 never be high), the characteristic oedema rapidly appears, at 
 first in the conjunctivae, eyelids, and cheeks, but later it becomes 
 general. The pulse is usually quick and of high tension from the 
 beginning. The urine is voided frequently, but scant in quantity, 
 and indeed may be suppressed for a time. It is dark from the 
 presence of blood, exhibits the weU-known smoky hue, and 
 generally gives a copious deposit of urates, blood discs, granular 
 debris, fatty and hyaline casts, and a large amount of albumin. 
 Though of such high specific gravity, the total amount of urea 
 
 T 
 
258 Student's Hand-book of Medicine. 
 
 passed daily is much decreased. As the disease advances, the 
 anasarca becomes more marked ; there may be dangerous 
 dropsy of the serous sacs, oedema of the base of the lung or 
 of the glottis. The bowels become constipated, the tongue dry, 
 and there is great thirst. Hypertrophy of the heart is often 
 marked. ' If improvement does not quickly take place, grave 
 dangers arise from the accumulation of excrementitious material 
 in the blood ; anaemia becomes pronounced, and intense head- 
 ache, convulsions, and coma often usher in a fatal urasmia. 
 Most cases however, with care, recover ; others pass into the 
 subacute stage or " large white kidney." 
 
 The more important complications to remember are — 
 
 1 . Excessive delatation of the heart in debilitatedpatients. 
 
 2. Dropsy of the lungs, pericardium, and glottis. 
 
 3. Albuminuric retinitis and optic neuritis. 
 
 4. Uraemia. 
 
 Treatment. — Absolute rest in bed; patient to be laid 
 between blankets ; hot poultices (not blisters), or dry cupping 
 over the loins, a free saline purge, diluents in an effervescing 
 form, and a non-nitrogenous diet, forms the routine treatment. 
 Eemember that urates are highly irritating to an inflamed 
 kidney, hence the necessity of diminishing the quantity of proteida 
 taken, and the indication for the use of these drugs which 
 render the urates more soluble. Acetate of potash and nitrous 
 aether with hyoscyamus, form a splendid mixture, as we have at 
 once a solvent of urates, a dilator of the peripheral arterioles, 
 and a sedative to the urinary tract. Complications must be 
 treated as they appear. 
 
 Excessive Dropsy.— Kot air baths, pilocarpine, compound 
 jalap powder, elaterium, Southey's tubes, tapping, etc. 
 
 Urmmia. — Same as for excessive dropsy plus chloroform 
 during the convulsions, and wet cupping, or even venesection. 
 
 Severe Dyspnoea. — Nitrite of Amyl is of great service. 
 
Chronic Bright's Disease. 259 
 
 CHRONIC BRIGHT'S DISEASE. 
 
 " By Bright's disease we mean a non-suppurative inflammation 
 of the kidneys. To understand the classifications that have 
 been made, it is necessary to recognise the following structures 
 in the kidney, which are liable to diseases, more or less in- 
 dependent of one another. They are — 
 
 1. The Tubules with their epithelium, forming the paren- 
 chyma of the kidney. 
 
 2. The Interstitial tissue, very small in quantity in the 
 healthy organ, but liable to considerable increase by inflammatory 
 processes. 
 
 3. The Blood-vessels and the glomeruli ; consisting of the 
 vascular tufts, the capsule, and the epithelial cells covering 
 the former and lining the latter." (Dr Taylor's "Practice of 
 Medicine.") 
 
 Obviously in a nephritis the inflammatory changes may be 
 most marked in the tubules, or in the interstitial tissue, or 
 in the blood-vessels ; but it must be equally clear that neither 
 one of these special tissues can be affected to any great extent 
 without implicating the other components of the kidney structure. 
 In other words, though the various types of Bright's disease are 
 based upon the variety of tissue principally involved, still, it 
 must be distinctly understood that the kidney structure as a 
 wliole shares in the degenerative changes. This applies with 
 particular emphasis in acute cases. 
 
 The best known forms of chronic Bright's disease are— 
 
 1. The chronic tubal nephritis (large white kidney). 
 
 2. Chronic interstitial nephritis (small red or gouty 
 
 kidney). 
 
 3. Lardaceous or waxy disease of the kidney (pale waxy 
 
 kidney). 
 
260 Student's Hand-hook of Medicine. 
 
 Beginners in medicine frequently complain that they get 
 hopelessly muddled on trying to distinguish or to remember 
 these varieties ; we must therefore, before describing them 
 in detail, consider some general facts in reference to renal 
 disease. Now suppose we get defective renal secretion, 
 what must happen 1 
 
 1. Eetention of waste and poisonous products in the blood, 
 
 2. Damage to the vascular walls by those poisonous products. 
 
 3. Anaemia; and consequently all the troubles produced 
 through imperfect nutrition of all the tissues and organs in the 
 body. 
 
 We must expect and therefore describe changes under six 
 headings — 
 
 1. Changes in the kidney structure — 
 
 Interstitial tissue. 
 
 Tubules and their epithelium. 
 
 Blood-vessels. 
 
 2. Changes in the urine — as regards quantity and quality — 
 i.e., the presence of pathological constituents — 
 
 Albumin. 
 
 Blood. 
 
 Casts, which may be granular, fatty, or hyaline. 
 
 3. Changes in the circulatory system — 
 
 The heart is often enormously hypertrophied and 
 
 dUated. 
 The arteries are sclerosed and thickened. 
 The pulse is characteristic — it is peculiarly hard, 
 
 and of high tension, the dichrotic wave 
 
 being almost obliterated. 
 
 [The cause of the hypertrophy, and the nature of the artero- 
 sclerosis are stiU unsettled. As the high tension occurs quite 
 early in even acute Bright's disease, increased peripheral tension 
 
Chronic Bright' 8 Disease. 261 
 
 set up by irritation of the vascular walls is the probable cause, 
 and this would account for subsequent hypertrophy of the heart. 
 Cohnheim considered that the fact of more force being required 
 to drive the blood through a diseased kidney, would explain the 
 cardiac hypertrophy. The question, however, is still sub judice.] 
 
 i. Ocular changes consisting of — 
 
 CEdema of the retina, causing opacity and swelling. 
 White glistening patches due to fatty degeneration 
 
 of Miiller's fibres, etc. 
 Flame-shaped extravasations of blood. 
 More or less atrophy of the optic disc. 
 
 5. Dropsy first appears as oedema of the conjunctivae or lower 
 eyelids : later, general anasarca, and dropsy of the serous 
 cavities — i.e., ascites, hydro-thorax, or immense dropsy of the 
 scrotum, may all occur. 
 
 The dropsy is at first most apparent in the morning. Many 
 factors contribute to the causation of renal dropsy — 
 
 (1) The anaemic and hydraemic state of the blood. 
 
 (2) Degeneration of the vascular walls. 
 
 (3) Deficient secretion of urine. 
 
 (4) Imperfect cardiac action and pulmonary engorge- 
 
 ment (late). 
 
 6. Tendency to Urcemia. — Ursemia has already been dis- 
 cussed fully. 
 
 There is no doubt that Professor Grainger Stewart struck 
 the keynote to the proper understanding of the various clinical 
 phenomena, when he pointed out "that chronic inflammation 
 of the kidney differed in no way from that of other organs; that, 
 given a slowly progressing inflammatory action, we should expect 
 at first a stage of enlargement, and finally a state of atrophy.'' 
 
 Chronic inflammation may or may not be preceded by an 
 acute attack ; and lastly, when the condition begins as an 
 acute nephritis, before it can become chronic, there must he 
 an intermediate or subacute stage. 
 
262 Student's Hand-hook of Medicine. 
 
 ^ I would strongly urge the junior student to digest the fore- 
 going remarks, and especially rememher the relations between the 
 liver and kidneys. If he does this, there can be no difficulty 
 in understanding a most important section of practical medicine. 
 
 The " large white kidney " is more frequently a sequel of an 
 acute attack ; the " red gouty," on the other hand, is more often 
 due to overwork, eliminating coarse products, or poisons. I 
 would advise the reader to get up thoroughly the symptoms of 
 a typical acute nephritis — and then a typical case of chronic 
 interstitial nephritis. He will easily understand then that the 
 "subacute" form will at first approximate to the acute form 
 (scanty and albuminous urine), and later, to the chronic form 
 (urine more copious and less albuminous). 
 
 The onset of chronic Bright's disease when not preceded by 
 acute nephritis, is most insidious. Often there is nothing to 
 attract the patient's attention to such a serious condition, beyond 
 langour, a desire to micturate more frequently, diffuse headache, 
 and slight stiffness of the eyes in the morning. When the disease 
 is well marked, and failure of cardiac hypertrophy begins, the 
 symptoms become very pronounce^l, such as marked pallor, 
 breathlessness, attacks of ursemic asthma, dimness of vision, and 
 dropsy of serous cavities. It is very essential that the condition 
 should be early diagnosed, and careful examination of the pulse, 
 retina, and urine, ought to go far to make an accurate as well 
 as an early diagnosis. A diagnostic table, and the foregoing 
 remarks, should enable the beginner to have a clear idea of 
 the elementary facts of Bright's disease. A more exhaustive 
 account cannot be given here, but after the final examination 
 is passed, no practitioner should lose time before perusing 
 one of the many valuable monographs on the subject. 
 
 Treatment of chronic Bright's disease must be considered 
 under two heads. — 
 
 1. General treatment. 
 
 2. Symptomatic treatment. 
 
Chronic Bright' s Disease. 263 
 
 General Treatment. — 
 
 Our indications under the first heading are to put the 
 patient under the most favourable hygienic conditions. Exer- 
 cise in. the open air, and woollen or flannel underclothing are 
 imperative. Diet is no less important; therefore food which 
 contains the most nutritive properties with the least nitrogenous 
 compounds must be prescribed. No rigid diet can be laid 
 down for aU cases, each must be treated on its own merits, but 
 in all cases, beer, heavy wines, and excessive consumption 
 of sugar should be condemned. 
 
 Medicinal Treatment. — Keep the bowels open by the use of 
 saline purges. Improve the vascular tone by the administration 
 of strychnine and iron. 
 
 Though it is generally held that mercurials are badly borne 
 in renal affections, there can be no doubt as to the efficacy 
 of small doses of pil. hydrarg., or calomel, given at night- 
 time, and followed by a tumblerful of Friedrichshall water 
 in the morning. Hepatic depletion by brisk cathartics is often 
 more efficacious than any other treatment in allaying urgent 
 symptoms. 
 
 Symptomatic Treatment. — 
 
 Headache may be relieved by a mixture containing pot. 
 iodid., digitalis, and caffeine. When the tension is very high, 
 a good purge and a few whiffs of nitrite of amyl often act like 
 a charm. 
 
 Dropsy. — When excessive, may demand removal of the fluid 
 by Southey's tubes. A saturated solution of mag. sulph., ad- 
 ministered in the morning often removes enormous quantities 
 of water. 
 
 Albuminuria. — If the escape of albumin be excessive, ergot 
 or gallic acid may be tried. 
 
264 
 
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Pyelitis. 265 
 
 PYELITIS. 
 
 By pyelitis is meant an inflammation limited to the pelvis of 
 the kidney. If the kidney substance be also inflamed then it 
 is termed pyelonephritis ; and if the inflammation terminates 
 in pus formation, the resulting collection of pus is called a 
 "pyonephrosis." Kow, it is most improbable, that the pelvis 
 of the kidney ever becomes inflamed without involving the 
 kidney substance ; still more improbable, that such a condition 
 could be diagnosed during life, so that cHncally at all events, 
 by pyelitis is meant a suppurative inflammation of the pelvis 
 of the kidney, such a condition being usually associated with 
 a certain amount of nephritis and pyonephrosis. 
 
 Causes. — Anything which causes severe irritation of the 
 lining of the pelvis of the kidney, such as — 
 
 1. Calculi, blood-clots, parasites, tumours. 
 
 2. Morbid states of the blood, such as malignant fevers, 
 diabetes, Bright's disease, etc. 
 
 .3. Certain drugs — cantharides, etc. 
 
 4. Extension of inflammation from below (surgical kidney). 
 
 5. Pressure upon the ureter, by causing the urine to be 
 dammed back, and this urine subsequently undergoing putre- 
 faction may cause intense pyelitis; 
 
 6. Injuries to the spinal cord. 
 
 Symptoms. — Depend upon the cause, the stage, and the 
 complications. A simple pyelitis gives rise to but few definite 
 symptoms, a localised pain in the lumbar region may be the 
 chief or only complaint on the part of the patient, or perhaps 
 he seeks advice on account of passing too little urine, which, 
 on examination, may be found to contain epithelia, blood, etc. 
 When suppuration commences the symptoms are much more 
 definite : the urine now contains blood, pus cells, and albumin. 
 
266 Student's Hand-book of Medicine. 
 
 but may he still faintly acid in reaction. As the kidney sub- 
 stance becomes involved, the symptoms of more or less acute 
 nephritis appear. If the suppurative process becomes marked, 
 there are usually rigors, sweating, and fluctuating temperature, 
 and the urine becomes ammoniacal, viscid, and "ropy," from 
 the excessive amount of mucus and pus. 
 
 Sometimes the debris chokes up the ureter and the urine 
 which escapes by the free ureter will be clear for a short time, 
 only to become purulent again when the plug moves away. If 
 the pus be pent up, it then causes a cystic swelling of the renal 
 pelvis, that is " pyo-nephrosis. It will of course be easily 
 understood, that if such a condition occurred in both kidneys, 
 death would speedily result from ursemia. 
 The physical signs of pyonephrosis are — 
 A tumour which (when large) causes distinct bulging in 
 front and behind. Such a tumour 
 
 Can be separated from the liver and spleen ; 
 
 Is always crossed by the colon ; 
 
 Yields a dull note on percussion ; and 
 
 Tenderness on pressure. 
 
 Prognosis. — Is of course always grave, but recent advances 
 in surgery have rendered the outlook much brighter. If left 
 alone the condition is frequently fatal, but sometimes even 
 after pyo-nephrosis has occured, the pus dries up, the walls 
 of the cyst become coated with patchy layers of phosphatic 
 deposits, and the cavity in time contracts. In other cases the 
 abscess bursts externally into the perinephritic tissue, or into 
 the kidney substances, or through the peritoneum. Death may 
 be brought about by extensive lardaceous disease. 
 
 Treatment. — Our treatment should aim to — 
 
 1. Kemove the cause if possible. 
 
 2. EeUeve the inflamed kidney by rest, cupping, and the 
 administration of sedative salines, such as pot. citras. with 
 hyoscyamus, and the free drinking of warm liquids. 
 
 3. Treat complications as they arise. 
 
Diabetes Insipidus. 267 
 
 The removal of a caloiUus, the emptying of a pyonephrotic 
 cyst or hydronephrosis demand surgical treatment, for details 
 of which consult a surgical work. 
 
 DIABETES INSIPIDUS. 
 
 Is a rare condition in which an excessive quantity of pale 
 limpid urine is secreted, free from sugar, albumin, and other 
 abnormal constituents ; and accompanied by insatiable thirst. 
 
 Causes. — Unknown. Bernard produced polyuria by punc- 
 turing the fourth ventricle higher than the centre for producing 
 saccharine urine; and it has been suggested that diabetes 
 insipidus is due to some disturbance of this centre, but it 
 is far more probable that the condition is due to a local vaso- 
 motor paralysis of the renal blood-vessels. It has sometimes 
 been produced by severe mental shock. The temporary 
 polyuria after a hysterical fit is well known. 
 
 Symptoms. — Polyuria, the watery constituents alone being 
 increased; as much as 15 to 20 pints of this pale urine may 
 be voided in the tweiity-four hours. Dyspepsia, great thirst, 
 mental irritability, and muscular weakness are also frequently 
 prominent symptoms. Though the disease is rarely fatal, 
 the persistent thirst and frequent micturition prevents sound 
 sleep, and undermines the general h,ealth. 
 
 Treatment. — Valerianates, iron, strychnine, gallic acid, 
 galvanism, and iodide of potassium. 
 
 Diagnosis. — Care must be taken not to mistake this con- 
 dition for the polyuria of Bright's disease, etc. Note the 
 absence of casts, and the low sp. gr. 
 
268 Stvdent's Hand-book of Medicine. 
 
 EXAMINATION OF THE URINE. 
 
 The examination of the urine in disease is of the utmost 
 importance. Where quantitative analysis is required a speci- 
 men of the wine passed in the twenty-four hours should be used, 
 as ohviously the urine is richer in certain constituents at certain 
 parts of the day. Observe — 
 
 1. Quantity. — Normal, 45 to 52 ounces (1300 cc. to 
 1500 cc). 
 
 2. Specific Gravity. — formal, 1015 to 1025. If above 
 1025, test for sugar. If necessary, estimate the total amount 
 of solids from the sp. gr. and quantity. 
 
 3. Odour. — The normal odour is pecuUai and characteristic 
 It becomes ammoniacal and putrid when the urine decomposes. 
 It smells like honey when sugar is present, and like sweet 
 violets after the administration of turpentine. 
 
 4. Reaction is normally acid, except after a meal containing 
 much vegetable food. Decomposed urine is alkaline. 
 
 5. Colour. — Normal, pale-straw to dark-amber. 
 
 (1) If red, or reddish-brown, or smoky, suspect presence 
 
 of blood, and search for blood corpuscles; test 
 with guaiacum and ozonic ether, and if necessary, 
 examine with the spectroscope. 
 
 (2) If greenish or yellowish-brown, suspect presence of 
 
 bUe pigment ; olDserve colour of froth ; test for 
 bile pigment and bile acids. 
 
 (3) If pale, quantity large and sp. gr. over 1025, test 
 
 for sugar. 
 
 6. Deposit. — Allow the urine to settle in a cylindrical or 
 conical glass and a cloud of mucus invariably forms. It is 
 always light and moves easily with the fluid. 
 
Exwmination of the Urine. 269 
 
 A deposit of urates is the next most common. It is usually 
 of a brick-dust colour, and moves easily when the vessel is 
 inclined. 
 
 . A deposit of earthy phosphates has usually a white or dirty- 
 white appearance and is somewhat heavy. 
 
 If the deposit be slimy, it probably contains much mucin 
 or pus. 
 
 If the urine is milky on passing, it is usually due to deposit 
 of the earthy phosphates. It is common after a full meal, 
 especially when vegetables have been freely partaken of; the 
 uriue in such a case is usually neutral or alkaline. Do not 
 mistake this deposit for pus, nor confound earthy phosphates 
 with triple phosphates. 
 
 
 URATES. 
 
 Usually brick red. 
 
 EABTHT PHOSPHATES. 
 
 Colour 
 
 White or milky. 
 
 Umi 
 
 Usually clears iip. 
 
 Unaffected. 
 
 Alkalies 
 
 Dissolve. 
 
 Do not dissolve. 
 
 Aoida 
 
 Insoluble. 
 
 Soluble. 
 
 Albumin. — The tests for albumins depend on their coagu- 
 lability by heat and precipitation by nitric acid, picric acid, etc. 
 The most delicate test is — 
 
 1. Heller's Test. — Put a little nitric acid in a test tube, 
 pour the albuminous urine cautiously upon it, and an opales- 
 cent ring of coagulated albumin appears above the acid. If 
 the albumin is abundant it appears quickly; if there is only 
 a trace of albumin, its appearance may be delayed for two or 
 three minutes. 
 
 But nitric acid in the cold also precipitates albumose ; this 
 is distinguished from albumin by the precipitate dissolving 
 when heated and returning when cooled. 
 
 In using Heller's test, remember that the addition of nitric 
 acid to undiluted urine may cause a precipitate of uric acid ; 
 this, however, is always very scanty, and the microscope shows 
 crystals. Further, if the urine be very concentrated the addition 
 
270 Student's Hand-book of Medicine. 
 
 of nitric acid may cause a precipitate of nitrate of urea, but 
 its appearance is very different from that of the flooculent 
 precipitate of coagulated albumin. Nitrate of urea is not thrown 
 down when the urine is diluted before adding the acid. 
 
 2. Tlie quantitative ted may be roughly performed by 
 Esbach's Albuminimeter — but since picric acid is the reagent 
 used, it should be remembered that " all the proteids '' in the 
 urine, other than albumin, are thereby precipitated. 
 
 Method. — Esbach's Albuminimeter is a graduated tube for 
 roughly estimating the percentage of albumin in urine. It 
 cannot be successfully used if the percentage is large. It 
 succeeds best when the urine is diluted until its sp. gr. is not 
 above 1010. K necessary therefore, an equal volume or two 
 volumes of water may require to be added to the urine, and 
 this must be taken into account in making the calculation. 
 
 1. FLU tube with urine up to mark U. 
 
 2. Add picric and citric acid s6lution to mark R. 
 
 3. Mix thoroughly and set aside for twenty-four hours. 
 
 4. Eead height of coagulum on scale. The numbers on the 
 scale indicate grammes of albumin per litre of urine. Eesult 
 only approximative, because the bulk of the coagulum depends 
 much upon its density. 
 
 The most accurate method of determining the exact quantity 
 of albumin is Brandberg's modification of Sir W. Eobert's 
 method — the process is a tedious one and requires much 
 practice to be accurate. (For details of this test see von 
 Jaksch's Handbook.) 
 
 Globulins in the urine are precipitated by a saturated solu- 
 tion of magnesium sulphate. 
 
 Peptones are tested by the Buiret test — i.e., giving a pink 
 or violet reaction with KOH and a trace of sulphate of copper. 
 Peptones are not coagulated by heat. 
 
Examination of the Urine. 271 
 
 SUGAR OR DEXTROSE IN THE URINE. 
 
 The various tests used are those of Moore, Fehling, Trommer, 
 the phenyl-hydrazin test, the fermentation test, and by means 
 of the polarising saccharometer. 
 
 Fehling's solution is an alkaline solution of potassio-tartrate 
 of copper, and is made of such a standard strength, that 1 cc. 
 of recently prepared Fehling's solution is reduced by 5 milli- 
 grammes of grape sugar. It may be used to demonstrate the 
 presence of a reducing sugar, or for the quantitative estimation, 
 but in the latter case it is better to use the Pavy-Fehling 
 solution, -which contains ammonia in addition to the other 
 salts. The ammonia prevents the precipitation of cuprous- 
 oxide, and thus the complete reduction is indicated at once by 
 the disappearance of the blue colour of the re-agent. 
 
 Method. — Having removed albumin (if present) from a 
 sample of the urine passed in twenty-four hours.— 
 
 1. Dilute the urine to 1 in 20 (5 cc. urine — 95 ec. water). 
 
 2. Place the urine in a burette. 
 
 3. Measure '50 cc. Pavy-Fehling solution, and place in 
 porcelain basin. 
 
 4. Heat to boiling, and while boUing drop in urine until 
 blue colour just disappears. 
 
 5. Calculate the total amount of sugar in the urine passed in 
 twenty-foui hours. 
 
 For details of the other tests consult a work on Examination 
 of the Urine. 
 
 It must not be forgotten that traces of sugar may exist in 
 healthy urine. 
 
 Acetone. — A very dilute alkaline solution of sodium nitro- 
 prusside is added to the urine. If acetone be present a red 
 
272 Student's Hand-book of Medicine. 
 
 colour is developed which, changes to yellow ; on boiling after 
 the addition of an acid, the yellow colour gives way to a violet 
 hue. Acetone does not strike a Bordeaux red with ferric 
 chloride, thus differing from sethyl-diacetio acid. (See Diabetes.) 
 
 Bile in the Urine. — 
 
 Bile pigments give from a deep yellow to almost a porter- 
 like hue to the urine ; it froths easily, the froth, being tinged 
 with the pigment. 
 
 Method. — Add impure nitric acid (nitric-nitrous) cautiously 
 to the urine in a test tube, at the junction of urine and acid a 
 display of colours occurs, due to oxidation of the pigments. 
 
 Bile Acids. — Cannot be delected in bilious urine without 
 evaporating, or unless the amount of bile is excessive. 
 
 Method. — ^Add a solution of cane sugar to the urine in a 
 test tube, shake let a drop of H2SO4 trickle down he tube, 
 at the junction of the acid and froth a cherry rose-red colour 
 will develop. 
 
 Blood in the Urine. — (See page 253.) 
 
 Urea. — The quantitative test is of the utmost importance ; 
 for by comparing the amount of nitrogenous material taken in, 
 with the amount of urea passed, we are enabled to gauge the 
 state of metabolism in the body. Urea is increased during 
 active metabolism as in fevers, etc., and is of course de- 
 creased when the metabolic functions are in abeyance. It 
 must not be forgotten, however, that the formation of urea may 
 be for a time excessive, and yet not appear in the urine through 
 inability of the kidneys to excrete it. 
 
 Volumetric Estimation of Urea by the Hypobromite process 
 depends on the fact that the solution of sodium hypobromite 
 decomposes urea into CO2, N, and HjO. The CO2 combines 
 
Exaonination of the Urine. 273 
 
 with the free soda, and nitrogen therefore alone passes into the 
 burette. One gramme of urea by this method yields 371 cc. 
 of nitrogen, therefore 37'1 nitrogen equals 1 decigramme of 
 urea. If we measure therefore, the amount of N given off 
 from a known quantity of urine, we can calculate the total 
 amount of urea passed daily. ' 
 
 Apparatus. — Burette inverted in tall jar of water. Burette 
 connected by elastic tube with a small glass flask in which 
 urine is to be decomposed. A jar with water to cool uritie and 
 gas during decomposition. A glass tube to contain a measured 
 quantity of urine. 
 
 Process — 
 
 1. Place about 15 cc. hypobromite solution in flask. 
 
 2. Place 5 cc. mixed urine of twenty-four hours in small 
 tube, and introduce it into flask without tilting. 
 
 3. Elevate burette in jar till water inside it is at the 50 cc. 
 line. Cork the flask, and read position of water in burette 
 again. 
 
 4. Tilt flask slowly and mix the urine with the hypobromite. 
 Jar should be left to cool for ten minutes. 
 
 5. Elevate burette till water inside is on the same level with 
 that outside, and read oif gas, then calculate amount of urea 
 present in 5 cc. urine, and then the amount in the total urine 
 in twenty-four hours. 
 
 For perfect accuracy, the volume of the gas should be corrected 
 for temperature and barometric pressure. 
 
 It would be useless to calculate the amount of urea passed 
 per day if we did not know how much should be passed. 
 All things being equal^i.e., an average diet, average labour, 
 and average health — the excretion should at least reach three 
 grains for every pound weight. In other words, a man weighing 
 
 u 
 
274 Student's Hand-book of Medicine. 
 
 150 lbs. should excrete at the lowest 450 grains of urea; he 
 might with advantage excrete up to 500 grains, but it should 
 not fall less than 450 grains per diem. 
 
 Uric Acid appears in the urine to the extent of 7 to 12 
 grains ia combination with soda, etc., as urates. It is much 
 increased in fevers, deficient action of the liver, gout, etc. In 
 order to test for its presence we first displace it from its base .by 
 adding an acid, HCL or acetic acid, and letting the urine 
 stand awhile. When uric acid is deposited it forms a cayenne 
 pepper or red sand-like deposit. 
 
 Tests for Uric Acid. — 1. Garrod's Thread test. Concentrate 
 fluid. Place 5 cc. in a watch glass. Add ten drops glacial 
 acetic acid. Place thread in fluid, and leave in cool place for 
 twenty-four hours to allow crystals to form. 
 
 2. Murexide test. Place five drops urine in porcelain capsule. 
 Add one drop nitric acid. Evaporate gently nearly to dryness. 
 Add small drop of ammonia = purple colour, due to murexide or 
 purpurate of ammonia. 
 
 3. The Volumetric test is estimated by Haycraft's method. 
 Uric acid is made to combine with silver, forming a gelatinous 
 precipitate; this is separated by filtration and made into a 
 solution with nitric acid. The amount of silver is then tested 
 by a colour test and the amount of uric acid calculated by the 
 amount of silver found. 
 
 Chlorides. — The amount of chlorine excreted daily amounts 
 to about 100 grains, chiefly in combination with soda. 
 
 Test. — Silver nitrate preceded by acidulation with nitric 
 acid. 
 
 The chlorides are markedly diminished in all cases of 
 croupous or fibrinous inflammations; this is particularly the 
 case in croupous pneumonia. 
 
Examination of the Urime. 275 
 
 Quantitative Estimation. — 
 Silver Method. — The solutions required are — 
 
 1. Solution of silver nitrate, containing 29'075 grms. of 
 
 the fused salt in 1000 cc. of distilled water; 
 of this solution 1 cc. = 0-01 grms. of sodium 
 chloride. 
 
 2. Saturated solution ot j)otassium chromate (neutral). 
 
 Method. — Take 10 cc. of the urine, and dilute with 100 cc. 
 of distilled water. Add to it a few drops of solution (2). To 
 this mixture in a beaker allow the standard solution (1) to drop 
 in from a burette. A precipitate of silver chloride wUl occur as 
 long as any chloride is uncombined. When the whole of the 
 chloride is satisfied, a reddish or pink (since there is much white 
 precipitate present) precipitate of silver chromate appears. This 
 indicates the time to stop the addition of the silver nitrate, and 
 the amount of the solution which has been used is read off. 
 This win indicate the amount of silver nitrate necessary to 
 convert all the chlorine present in 10 cc. into silver chloride. 
 It is known that 1 cc. of the solution = 0'005837 grm. of 
 salt, and from this the total amount of chloride present can be 
 estimated. A correction should be made by subtracting 1 cc. of 
 the silver solution used, as the white contains certain other 
 substances more easily precipitated than the chromate. — 
 ("Power and Harris' Handbook.") 
 
 Phosphates. — The test for phosphates generally, have already 
 been considered. The test for orthophosphoric acid is precipita- 
 tion by uranium acetate, the precipitate being insoluble in 
 acetic acid. 
 
 Pus.— 
 
 1. Examine under microscope for pus cells. 
 
 2. KOH added to the urine causes it to become stringy. 
 
 For the various casts and calculi found in the urine, see a 
 work on examination of the urine. (Beale's plates are excellent.) 
 
276 Student's Hand-book of Medicine. 
 
 UNCLASSED SPECIAL DISEASES. 
 
 DIABETES MELLITUS. 
 
 A disease characterised by an increased discharge of pale 
 urine of high specific gravity, containing a quantity of sugar 
 and attended with great debility and progressive emaciation. 
 
 .ffitiology. — Many cases are distinctly hereditary. Men are 
 more often affected than women. Jews especially seem prone 
 to this affection. It is rarely seen amongst children. The 
 principal exciting causes are — 
 
 1. Tumours (especially gummata) affecting the fourth ventricle. 
 
 2. Mental disturbances, such as worry, grief, fright, etc. 
 
 3. The gouty state. 
 
 Lately much attention has been drawn to the fact that obese 
 persons frequently suffer from diabetes ; but it is quite unsettled 
 to what extent the "fatty habit" may play the part of an 
 setiological factor. 
 
 Morbid Anatomy. — 
 
 1. The Nervous System shows no constant changes. In 
 many cases, tumours in the medulla, and sclerosis of various 
 sympathetic fibres have been found. 
 
 2. The Pancreas. — Is nearly always atrophied, fibrosed, and 
 on section shows extensive areas of fatty degeneration, and fat 
 necrosis. 
 
 3. The Liver. — Is often cirrhosed and peculiarly pigmented, 
 the changes however are by no means constant. 
 
 4. The Kidneys are usually cirrhosed, though not extensively 
 so ; hyaline degeneration of the tubules is usually most marked. 
 
Diabetes Mellitus. 277 
 
 5. The Blood shows four remarkable changes. — 
 
 (1) The presence of polynuelear leucocytes containing, 
 
 much glycogen. 
 
 (2) An excessive amount of sugar in the plasma. 
 
 (3) The presence of much fat; which may form a 
 
 creamy layer on the clotted blood. 
 
 (4) A reduction in the dlJcalinity of the blood. 
 
 The Urine. — Both, quantity and specific gravity are increased, 
 the former to the extent of ten or even twenty pints per diem — 
 the latter from 1025 to 1045. It is brilliant in colour, and 
 notwithstanding the presence of ammonia, is acid in reaction. 
 The quantity of sugar ranges from two to forty grains per ounce, 
 or twenty ounces and upwards daily. Uric acid is not increased, 
 but both urea and phosphates are. Amongst other constituents 
 which must be remembered are /3-oxybutyric acid, and lethyl- 
 diacetic acid. The relations of these products to diabetes are 
 still undetermined. Outside the body, glucose can, by taking up 
 oxygen, be transformed into /3-oxybutyric acid, with an inter- 
 mediate stage of aldehyde. A very tempting theory is to assume 
 that such a change takes place in diabetes. 
 
 .^ithyl-diacetic acid is also important, for it has often been 
 confused with and mistaken for acetone. This is of the .utmost 
 importance, for "Acetonuria" has been held responsible for 
 causing the well known coma ,of diabetes. It has however been 
 conclusively shown by von Jaksch and others, that acetone 
 cannot be the cause of the coma ; yet even von Jaksch admits 
 that when the appearance of the acetone reaction appears in 
 the urine, it usually heralds the onset of the coma and death. 
 Possibly the explanation is that aethyl-diacetic acid undergoes 
 the following changes in the alkaline plasma. It iirst combines 
 with the soda in the blood ; then splits up into acetone, alcohol; 
 and the bi-carbonate of soda — CgHgNaOa + 2H2O = CgllgO + 
 CaHgO -t-NaHCOg. This change would account for the 
 
278 Student's Hand-book of Medicine. 
 
 diminished alialiiiity of the blood, and possibly the alcohol so 
 formed may account for the coma. But the coma is usually 
 held to be due to fat embolism, or the circulation of fatty acids, 
 or to the same causes as ureemic coma. 
 
 Pathology. — When we come to discuss the real causation of 
 diabetes, we are beset with great difficulties ; in fact we are not 
 even out of the realm of speculation, in spite of much hard 
 honest labour expended on the subject ; nor, do I see how we 
 are to get nearer the truth until it is decided first by physio- 
 logists, how sugar is formed in the body, where it is formed, and 
 what its functions or uses are. It would certainly be out of 
 place here to add more speculation or guess-work on the subject. 
 "We briefly sketched the fate of carbohydrates in the opening 
 chapters on Liver and Kidney ; and we then discussed what 
 would happen from excessive intake 6f carbohydrates on the 
 one hand, and inability on the other hand, of the tissues to 
 utilise the normal amount, and we then suggested possible 
 explanations of the occurrence of glycosuria and diabetes. But 
 it must be remembered that sugar may be formed by destruction 
 of proteids. Seegen goes so far as to assume that the diabetic 
 sugar is entirely derived from this source ; he concludes that in 
 diabetes the liver takes on an increased destructive power as 
 regards proteids, and the sugar so formed, is excreted by the 
 kidney. He, however, does not explain how or why such a 
 peculiar and perverted state of hepatic function is brought about. 
 
 The Pancreatic Theory is also a tempting one, for we 
 know — 
 
 1. That normally the pancreas is much concerned in splitting 
 up proteids, fats, and sugar. 
 
 2. Excision of the pancreas in animals, is followed by 
 diabetes. 
 
 3. The presence of an excessive amount of fat and sugar 
 in the blood points not to excessive consumption of such, but 
 
Diabetes Mellitus. 279 
 
 to the conclusion that they have not been sufficiently acted 
 upon by a certain " something " which must be placed amongst 
 either the pancreatic or hepatic functions. 
 
 Seegen's views are the outcome of much hard work and 
 skilful reasoning, yet it is difficult to imagine a too active 
 liver linked on to excess of fat in the blood. Is it not 
 possible, however, that through a perverted state of the 
 pancreatic functions, the food-stuffs are given up in such ' an 
 incompletely digested state, that the liver is unable to perform 
 its full metabolic functions, resulting in the formation of 
 albumoses and fatty acids, and hence a toxic condition of the 
 blood 1 The products so formed would account for many of the 
 manifold symptoms of diabetes. It is impossible to conjecture 
 what poisonous compounds these albumoses may not form, 
 acting as they do like vegetable alkaloids, and ever ready to 
 form new combinations. The relation of fatty acids to acetonuria, 
 and also to the synthetical building up of fats cannot be over- 
 estimated. The pathology of diabetes, then, is quite spectilative, 
 and no good can arise from a dogmatic statement that the chief 
 blame lies with either the pancreas, liver, or nervous system ; 
 such statements only tend to keep up the ignorance and 
 mystery surrounding this important disease. 
 
 Symptoms. — There can be no doubt that tieo forms of diabetes 
 exist — viz., the acute and the chronic forms. In the acute form, 
 the symptoms assume a grave type very rapidly, and post-mortem 
 in such cases, the pancreas has been found to be extensively 
 diseased. In the chronic form, on the other hand, the symptoms 
 are often obscure, and beyond the peculiar characters of the 
 urine and attacks of dyspepsia, the patient may for a long 
 time maintain a fair standard of health. 
 
 Taking a typical case of diabetes, the characteristic symptoms 
 are, the passage of large quantities of pale urine, great thirst, 
 voracious appetite, progressive muscular weakness, a dry parch- 
 ment-like sallow skin, emaciation, and the development of some 
 
280 Student's Hand-book of Medicine. 
 
 of the complications tabulated below. In the later stages the 
 pulse becomes very feeble, severe attacks of diabetic dyspnoea, 
 or "air hunger " add to the general misery, the breath gives out 
 a peculiar sweetish apple-like odour, and only too frequently 
 coma ends the scene suddenly. Often, however, the patient is 
 carried off by a critical diarrhoea, pneumonia, etc. 
 
 In chronic diabetes some of the more common complications 
 require special mention. They are — 
 
 1. Cutaneom Lesions. — Boils, carbuncle, eczema, especially 
 of the vulva in women, and accompanied by intolerable itching. 
 
 2. Visual Changes. — Eetinitis, soft cataract, and more or 
 less optic neuritis. These are most common complications. 
 
 3. Atrophic Changes. — Gangrene, especially perforating ulcer 
 of the foot, brittleness of the naUs, etc. 
 
 4. Renal Glianges. — Albuminuria; with more or less cirr- 
 hosis of the kidney and symptoms arising from such a condition. 
 
 In addition to the above common complications, there are 
 often grave mental changes. A peculiar form of high stepping 
 ataxia has been described by some authors. It should not be 
 forgotten that in diabetes diarrhoea may be easily provoked, 
 and I have seen two - deaths from this cause, following the 
 administration of simple purges. The dyspnoea is 'distinctly 
 peculiar, for it is rarely accompanied by cyanosis and has 
 received the name of "air hunger." 
 
 Diagnosis. — The urine properly tested at frequent intervals 
 forms the best means of diagnosis, see "Examination of Urine.'' 
 Eemember the wasting of muscle may be concealed by obesity. 
 
 Prognosis. — In confirmed cases the outlook is bad. In the 
 more chronic varieties the disease may be arrested for a consider- 
 able time. Some patients have had diabetes for twenty years. 
 
Diabetes Mellitus. 281 
 
 Treatment. — Diabetic patients often eat enormously, and it 
 must be at once apparent liow difficult it is to balance the 
 economy under such conditions, for if we limit the carbohydrates 
 we must increase the proteids, and thus throw an enormous 
 amount of work upon the already handicapped liver and kidneys. 
 If physiology be correct, to give an excessive amount of proteids 
 is certain to prove in time disastrous to the liver, and hence 
 such practice is to try to cure diabetes by doubtful means. 
 But all authoiities agree that the use of carhohydrates must 
 he restricted to a minimum. Fatty diet has been suggested 
 as a compromise ; but there is already an excessive amount 
 of fat in the blood in most cases, and further it must be 
 remembered that the tissues have the power of building up 
 fat'from the fatty acids which must be formed during excessive 
 decomposition of proteids; still some eminent authorities advise 
 a more or less fatty diet. Sir William Eobert's dietary is 
 appended as a guide. 
 
 ALLO"W. 
 
 Butcher's meat, poultry, game and fish. Cheese, eggs, butter, 
 fat and oil. Broths, soups, and jellies made without meal or 
 sugar. Cabbage, endive, spinach, broccoli, lettuce, spring-onions, 
 water-cress, celery. Dry sherry, claret, brandy and whisky. 
 Tea, coffee (without sugar), soda-water, bitartrate of potash 
 water. 
 
 FORBID. 
 
 All saccharine and farinaceous food, bread, potatoes, rice, 
 tapioca, sago, arrow-root, maccaroni ; turnips, carrots, parsnips, 
 beans and peas. 
 
 Liver contains much sugar-forming substances, therefore, 
 oysters, cockles, and mussels, which contain enormous livers, 
 are forbidden. 
 
 All sweet fruits. All sweet wines. 
 
 It will be seen from the above table that there is a pretty 
 extensive range or choice of food, but unfortunately the two 
 great drawbacks are the non-allowance of bread and potatoes. 
 
282 Student's Hand-book of Medicine. 
 
 The substitutes for bread are either nauseous or too expensive 
 for general use. The principal substitutes are almond biscuits, 
 gluten bread, charred bread, soya bread, etc. 
 
 Donkin's treatment, by an exclusive diet of skimmed milk, 
 does not usually act well, except in obese people. 
 
 MEDICINAL TRKATMENT. 
 
 Codeine or morphine seem to be the most beneficial drugs. 
 Antipyrin is credited with the power of reducing the amount 
 of sugar, if given in doses of ten grains thrice daily. Saccharine 
 and glycerine are no good as curative agents, but they may be 
 used for sweetening purposes; Arsenic with strychnine are 
 useful tonics. Massage, electricity, cod-liver oil, etc., are aU 
 useful in various cases. The great thirst may be relieved by 
 the administration of large doses of citrate of potassium freely 
 diluted. The complications must be treated on those principles 
 laid down under their respective headings. 
 
 MYXCEDEMA. 
 
 A disease associated with atrophy of the thyroid gland, a 
 peculiar condition of the skin, over-growth of the subcutaneous 
 tissue, and serious mental conditions. 
 
 .etiology.— Most common in women between thirty and 
 fifty-five years of age ; hereditary factors have not yet been 
 proved; the poorer classes are said to furnish the larger 
 number of cases. 
 
 Pathology. — That the disease is dependant on atrophic 
 changes in the thyroid gland seems now certain, reasoning 
 from the results of the removal of the gland on the one hand, 
 and from the beneficial effects following the internal administra- 
 tion of the healthy thyroid. 
 
Myxcedema. 
 
 283 
 
 Professor Horsley distinguislies three stages after removal of 
 the thyroid gland in monkeys. 
 
 STAGES, 
 
 1. Neurotic . . 
 
 2. Mucinoid . 
 
 3. Atrophic . 
 
 DUBATlOlf, 
 
 1 to 3 weeks. 
 3 to 7 weeks. 
 
 5 to 8 weeks. 
 
 SYMPTOMS. 
 
 Tremors, rigidity, 
 dyspnoea. 
 
 Commencing hebi- 
 tude, and mncinoid 
 degeneration of the 
 connective tissue. 
 
 Complete imbecil- 
 ity, atrophy of all 
 the tissues. 
 
 Young monkeys 
 often die in this stage. 
 
 Older monkeys die 
 at this stage u not 
 treated. 
 
 Monkeys survive if 
 kept in warm air 
 bath. 
 
 The untoward symptoms were associated with enormous fall 
 of hlood pressure and temperature. 
 
 It will therefore be seen that the presence of the thyroid is 
 necessary to avert myxoedema. Possibly its normal functions 
 are to Iceep the Mood pure and free from some pernicious 
 products, the nature of which has not yet been discovered, but 
 which if retained causes myxcedema. 
 
 The morbid anatomical changes are most marked in the 
 subcutaneous tissues — 
 
 1. Nuclear proliferation or formation of connective tissue 
 all around the hair follicles and sweat glands. 
 
 2. Increased deposit of subcutaneous fat. 
 
 3. Presence of mucin (not always present.) 
 
 4. Formation of elastic oedematous swellings above the 
 clavicles. 
 
 The Thyroid Gland is atrophied, often indurated, and shows 
 scattered groups of cells, the remains of the^normal vesicles. 
 
 Interstitial nephritis has been observed in some cases, but 
 this is probably an accidental coincidence. 
 
 Symptoms. — Patient presents a heavy stolid countenance, 
 with injected or diffuse red cheeks. The hair is scant, coarse, 
 and brittle. She speaks in a heavy, slow, and thick manner 
 (leathery voice). Exhibits great intolerance of cold — skin is 
 
284 Student's Hand-book of Medicine. 
 
 enormously tluckened, dry, and often scaly, but does not pit 
 on. pressure. The hands are said to be spade-like. Teeth 
 become carious. The gait is peculiarly clumsy. Bowels are 
 constipated. Later, the mental condition becomes very grave ; 
 haUucLnations, convulsions, and coma may occur. It must not 
 be forgotten that often towards the end albuminuria may occur, 
 and the skin may pit on pressure. 
 
 Treatment. — Guard patient against cold — give- nourishing 
 food. Pilocarpine and arsenic are useful sometimes. 
 Specific Treatment — Injections of — 
 
 1. Emulsionised thyroid gland, 
 
 2. Extract of thyroid gland hypodermically. 
 
 Lately, it has been shown that eating the cooked thyroid 
 is equally efi&cacious. 
 
 SPORADIC CRETINISM. 
 
 Is to be regarded as the infantile form of myxoedema, and, 
 like that disease, is due either to the congenital absence of the 
 thyroid body, or an absence of its functions. Formerly it was 
 assumed to be a form of goitre, and endemic in certain districts ; 
 but an enlarged thyroid has rarely been associated with cretinism, 
 and the cases cited have not been fully investigated, as the 
 thyroids were not examined post-mortem. 
 
 Symptoms and Signs.^ — The condition as regards the sub- 
 cutaneous oedema, supra-clavicular swellings, and mental defects 
 are much the same as in myxoedema, only more marked. No 
 disease presents more strikingly characteristic features. The child 
 is dwarfed or stunted in growth ; the face is very ugly, moon- 
 shaped, and the cheeks hang in pendulous folds ; tongue is too 
 large for the mouth; and the voice is peculiarly harsh or 
 squeaky, like Punch in the show. The hair is abundant but 
 coarse, except over the swellings between the scapulae, which 
 are covered by a soft down-like hair. The swellings are due 
 
Sporadic Cretinism. 285 
 
 to fatty deposits. The belly is very prominent and pendulous ; 
 umbilical and inguinal bernia are very common. Tbe gait is 
 clumsy, and of a waddling type. The sexual organs are rarely 
 developed, though in female children the menses may appear 
 once or twice ; but sexual desire is never excited, even in those 
 cases that live to adult age. Cretins are usually incapable 
 of being taught reading or writing, and their vocabulary is 
 always limited. They are often peevish and cross, but the bulk 
 are placcid and aifectionate. Death most often occurs during 
 childhood, though a few cases have reached adult life, without 
 however advancing at all in intelligence. 
 
 Treatment. — At present hopeless. A trial may be made of 
 the same treatment as in myxoedema. Granting even the 
 possibility of arresting the disease, it seems doubtful if the 
 brain would under such circumstances greatly improve and 
 develop, unless the treatment be commenced early. 
 
 .etiology. — Nothing definite is known. For examination 
 purposes it may as well be remembered that the following 
 theories have been advanced as aetiological factors : — 
 
 1. That the ancestors of cretinic children have suffered from 
 goitre, and thereby transmitted a weakness in the development 
 of the thyroid body in successive generations. 
 
 2. That such children were conceived during intoxication on 
 the part of one or both parents. If this had any claim for 
 serious attention, we should expect sporadic cretinism to be very 
 common, considering the large families many drunken parents 
 rear. It must be admitted, however, that drunken parents are 
 often sterile, showing some change in the condition necessary 
 for procreation. 
 
 ■ 3. Traumatisms during foetal life. This is too vague for 
 serious thought. 
 
 Lastly, it would be better not to bias or retard future 
 research by assuming any aetiological factor at present. 
 
286 Student's Hand -book of Medicine. 
 
 ADDISON'S DISEASE. 
 
 Is a peculiar constitutional affection, first described in 1855, 
 by Dr Addison of Guy's Hospital, as a " disease of tlie supra- 
 renal capsules, attended with a bronze discolouration of the 
 skin, and incurable progressive anaemia. His description, 
 however, requires modification ; as ancemia is by no means 
 always a prominent feature. Dr Byrom Bramwell sums up the 
 condition in his beautiful atlas (page 51), as a condition 
 marked by — 
 
 1. Asthenia, feebleness of the action of the heart, and the 
 symptoms and signs which result therefrom. 
 
 2. Nausea, vomiting, and other symptoms which result from 
 gastro-intestinal irritation. 
 
 3. Pain in the neighbourhood of the supra-renal bodies. 
 
 4. Pigmentation of the skin and mucous membranes. 
 
 5. Ansemia. — Often absent until the later stages. 
 
 6. Symptoms due to derangements of the cerebro-spinal nerve 
 apparatus, such as headache, delirium, convulsions, etc. 
 
 7. The absence of — 
 
 (1) Elevation of temperature. 
 
 (2) Marked emaciation. 
 
 (3) Signs or symptoms of local organic disease (other 
 
 than the supra-renal capsules) to account for the 
 asthenia and other symptoms enumerated. 
 
 Pathology. — At present is obscure. All observers agree that 
 it is essentially a disease of the adrenal bodies, plus implication 
 of the abdominal symp?ithetic system. Some lay most stress 
 upon the adrenal disease ; others upon the involvement of the 
 sympathetic system. Bramwell, after a most exhaustive 
 
Addison's Disease. 287 
 
 analysis of this disease, considers it "to be, in the majority of 
 cases, a tubercular degeneration of the capsules primarily, and 
 that the alterations in the nervous structures are secondary." 
 
 So far so good, but when we attempt to explain the 
 symptoms, we are at once floored by the fact that we know 
 little about the functions of the abdominal sympathetic, and 
 still less about the adrenal bodies. 
 
 It is held, judging from the enormous vascular supply of the 
 adrenal bodies, that they are blood glands, and that their function 
 is to prevent the retention within the system of certain poisonous 
 products, which, if retained, produce the peculiar symptoms of 
 Addison's disease ; and if we bear in mind the case of thyroid 
 myxcedema, this sounds feasible. 
 
 If it be due to the involvement of the sympathetic, the 
 symptoms must be the outcome of atrophic changes, and 
 the consequent disturbed and imperfect metabolism through 
 imperfect innervation. 
 
 Anatomical Changes are — 
 
 1. Atrophy of one or both glands ; presenting 
 
 2. The various stages of tubercular degeneration — 
 
 (1) Interstitial growth. 
 
 (2) Fatty degenerated patches. 
 
 (3) Caseous masses. 
 
 The semilunar ganglia are degenerated and much pigmented, 
 and they may through cicatricial contraction become entangled 
 as it were in the diseased tissue of the adrenals. The nerve 
 fibres show extensive sclerotic changes. 
 
 Dr Alezais and Arnaud assert that " Addison's disease wUl 
 not result if the perieapsular ganglia be not affected, though 
 the other portions of the adrenal bodies are at the same time 
 extensively diseased." We have already summed up the main 
 symptoms. It is peculiar that even when the exhaustion and 
 anaemia are profound, that the temperature tends to keep down; 
 this is in marked contrast to pernicious anaemia. 
 
288 Student's Hand-book of Medicine. 
 
 The pigmentation is most marked where pigment is normally 
 found.. — i.e., areolae, scrotum, axilla, etc. The mucous membranes 
 are often deeply pigmented, presenting blackish patches. The 
 marked exhaustion is altogether out of proportion to the general 
 condition, and it must not be forgotten that the slightest un- 
 toward circumstance, such as a simple purge or chill, may cause 
 death. Provided, however, the patient be treated as a hothouse 
 plant, the disease may run a protracted course. In some cases, 
 after very slight symptoms (and a still slighter amount of 
 bronzing) have been noticed for a few months, the patient, 
 without any obvious cause, sinks into a semi-comatose state 
 which rapidly proves fatal. 
 
 Diagnosis. — It must be remembered that bronzing may occur 
 in pregnancy, through exposure to the sun, through dirt and 
 vermin, in diabetes, etc. 
 
 Treatment can be summed up as foUows — Treat the patient 
 as a rare and valuable exotic plant. It has been suggested to 
 introduce the extract, etc., of healthy adrenal bodies, after the 
 manner of the thyroid in myxoedema. Arsenic, phosphorus, 
 iron, strychnine, etc., have their advocates. 
 
 RHEUMATIC FEVER. 
 
 An acute febrile disease characterised by poly-arthritis, a 
 tendency to hyper-pyrexia, a special tendency to involve the 
 pericardium and endocardium, and marked anaemia. 
 
 .etiology.- — The larger number of cases can be traced to 
 exposure to cold, inclement weather, etc. It is most common 
 during spring, in humid climates, and aifects young adults most 
 frequently. Males are more often attacked than females. 
 
 Pathology. — The true cause or causes of rheumatic fever are 
 still unknown; and never has there been a clearer case of 
 
Rheumatic Fever. 289 
 
 arrested research through the dogmatic statement " that acute 
 rheumatism is due to the presence of lactic acid." Lactic acid 
 has never been found in excessive quantity in the blood, or in 
 the effusion of the inflamed joints in this affection; moreover, 
 the only evidence yet advanced in favour of such a theory, is 
 that certain physicians have produced acute arthritis by inject- 
 ing lactic acid. AU I can say is that we can produce a similar 
 arthritis by injecting many other substances. 
 
 The Germ Theory assumes that the arthritis is due to a 
 specific but as yet undiscovered microbe ; and certainly reason- 
 ing from analogy of many other acute affections, this seems a 
 feasible theory. 
 
 The Nervous Theory assumes that the nerve centres are 
 primarily affected by cold and exposure; this interferes with 
 metabolism ; the products of imperfect metabolism accumulate 
 and irritate certain tissues, which are also rendered more 
 vulnerable by the diminished trophic influence, through the 
 depression of the said nerve centres. 
 
 The nature of the materies morbi is therefore still undecided 
 and offers a grand field for original research. One thing, how- 
 ever, is certain, that the poison causes a very rapid destruction 
 of red corpuscles. 
 
 Morbid Anatomy. — The synovial membrane undergoes the 
 changes common to inflammation of serous membranes — viz., 
 hyperaemia, exudation of lymph, and effusion of fluid. The 
 fluid is usually turbid, but seldom becomes purulent. The 
 ligamentous structures are swollen, and often the cartilages 
 are eroded by central necrosis. The blood, though it contains 
 an excess of fibrin, clots more slowly than normal ; this, how- 
 ever, occurs in many other conditions. 
 
 The fluid of the secondary affections such as pericarditis, 
 pleurisy, and the vegetations of the endocarditis contain pus 
 organisms. 
 
290 Student's Hand-book of Medicine. 
 
 Symptoms. — After a feeling of more or less soreness, and 
 general stiffness, the pain becomes localised in one or more 
 joints : usually the knee, wrists, or ankles. 
 
 The arthritis extends very rapidly to any of the medium- 
 sized joints. At first the affected joints are red, hot, swollen, 
 and intensely painful ; later, the redness becomes less marked, 
 and the joint may assume a dead white appearance. Frequently 
 the inflammation rapidly subsides in one joint only to appear 
 in another. 
 
 The temperature may be very high, even to 107°; indeed, 
 hyper-pyrexia is common in this fever. In the bulk of cases, 
 however, it remains between 101° and 103°. 
 
 Marked sweating of a peculiar sourish smell is a constant 
 feature, and the various hair follicles, and other cutaneous 
 glands may become inflamed and painful thereby. 
 
 As the disease advances anomnia hecomes very pronounced. 
 This anaemia may be increased by the salycUates, but is mainly 
 due to the rheumatic poison. 
 
 The tongue is usually very large, flat, and covered with such 
 an extremely thick fur that it has been named the " blanket " 
 tongue. 
 
 The urine is scanty, highly coloured, and often loaded with 
 urates. 
 
 The more common complications are— 
 
 1. Pericarditis. 
 
 2. Endocarditis. 
 
 3. Pleurisy. 
 
 4. Hyper-pyrexia. 
 
 5. Certain skin eruptions, such as sudamina, milaria, 
 
 and "pelioses" or small red petechial spots around 
 the ankles. 
 
 6. Pharyngitis and tonsillitis, 
 
 7. Meningitis, 
 
Gout. 291 
 
 Frequently suljcutaneous fibrous nodules develop over bony 
 ridges. Though, rarely fatal, and though the severe symptoms 
 usually subside in about fourteen days, no disease is more often 
 attended mth relapses and grave results. Chorea, valvular 
 diseases of the heart, etc., constantly follow in its wake. 
 
 Treatment as regards the general management. See there 
 is absolute rest, perfect protection of the limbs by wrapping 
 them up in cotton-wool, and support the bed-clothes by cradles. 
 The diet should consist principally of milk and soda water; 
 beef-tea and chicken may be allowed later on. 
 
 As regards treatment, undoubtedly the salycilates rank first 
 now-a-days. There can be no two opinions as to their efficacy 
 in easing pain, but from the experience of fourteen well-marked 
 and well-watched cases, I share the belief of that school which 
 attaches more value to the old alkaline treatment — i.e., letting 
 the patient drink ad libitum of citrate or bicarbonate of potash, 
 with an occasional dose of quinine, and the administration of 
 pulv. ipecac, co. to ease the pain. Dr. Brackeniidge asserts 
 that salycilates if pushed, even whfen heart failure threatens, 
 is the only treatment for rheumatic fever. A solution of the 
 salycilates locally as a lotion or fomentation is of the utmost 
 value. Pot. iodid. may be combined with salycilates in obstinate 
 cases. Treat complications on rational principles already laid 
 down. 
 
 GOUT. 
 
 Is a disorder possibly nutritional in its character, associated 
 with an excessive amount of uric acid in the blood, and deposits 
 of biurate of sodium in the joints. Clinically, it is manifested 
 by periodical attacks of acute arthritis, certain visceral disturb- 
 ances, and later, deformity of the joints attacked. 
 
 JGtiology. — 1. Heredity is certainly a most important factor, 
 and is curiously developed in the grand-children. 
 
292 Student's Hand-book of Medicine. 
 
 2. Alcoholism, especially indulgence in sweet wines, and 
 heavy malt liquors. Strange to say, Italians who drink large 
 quantities of light wines, and Scotsmen who certainly freely 
 indulge in good whisky, are singularly free from gout. 
 
 3. Gluttony. This is as important a factor as excessive 
 drinking. 
 
 4. Certain poisons ; such as lead, etc., which tend to decrease 
 the metabolic activity of the body. 
 
 5. Insufficient food (the poor man's gout). This condition 
 however, is associated with defective hygiene, and only too 
 frequently, with excessive consumption of poor or raw spirits, 
 etc. 
 
 Pathology. — In no disease can we point to a more constant 
 feature than excess of uric acid in cases of gout. This salt is 
 found in excess in. the gouty blood in the gouty joints, and in 
 the exuded serum of the gouty arthritis ; therefore there cannot 
 be the least possible doubt that the disease is due either to the 
 accumulation of uric acid in excess, or, to those conditions which 
 give rise to the excessive formation of uric acid. Now, if we 
 were to inject uric acid into the blood of a fairly healthy 
 individual we would not produce gout; and, moreover, von 
 Jaksch and others show that uric acid may be always produced 
 by deficient oxidation, and that excess of uric acid is common in 
 many diseases, such as leucocythaemia, pernicious anaemia, etc.; 
 yet gouty arthritis is by no means a common complication in 
 these diseases, therefore there must be a "something more" 
 than mere uric acid in excess to cause such a condition as gout. 
 
 Sir Dyce Duckworth assumes, "There is a basic arthritic 
 stock — a diathetic habit of which gout and rheumatism are two 
 distinct branches. The gouty diathesis is expressed in (1) a 
 neurosis of the nerve centres, which may be inherited or 
 acquired ; and (2) a peculiar incapacity for normal elaboration 
 within the whole body, not merely in the liver, or in one or 
 two organs of food, whereby uric acid is formed at times, or is 
 
Qouut. 293 
 
 incapable of being duly transformed into more soluble and less 
 noxious products'." (Sir Dyce Duckworth's Handbook on Gout.) 
 According to such an eminent authority, gout means some- 
 thing more than uric acid in excess. 
 
 Sir WiUiam Eoberts has shown that normal uric acid is a 
 quadurate which requires an alkaline medium, in order to be 
 kept in a perfectly soluble condition. In other words, the 
 quadurate is deposited in a wealc alkaline medium as a biurate 
 compound, a salt which is found in the joints affected by gout. 
 I would suggest the following statement as representing our 
 present knowledge of the pathology of gout : — Mere excessive 
 formation of uric acid within the body is either the outcome of 
 excessive nitrogenous (or proteid) consumption, or of deficient 
 oxidation on the part of the tissues (liver, etc.) This condition 
 constitutes the "lithaemia" of the older writers, and is one 
 highly predisposing to gout. Now, if we assume that through 
 certain changes, nervous or otherwise, the blood, or certain 
 tissues, become less alkaline than is sufiicient to hold the 
 quadurate in solution, a precipitation of a more insoluble salt, 
 viz., the biurate, must occur ; and, if such a precipitation takes 
 place in the joints, no wonder that acute arthritis is excited 
 thereby. Excess of the quadurate may be physiological and 
 compatible for a time with health ; deposit of the biurate, on the 
 other hand, is pathological, and results in gout. This seems 
 rational when we remember that the circulation in the smaller 
 joints is very sluggish, and consequently such parts are prone to 
 low inflammatory processes, resulting in a local diminished 
 alkalinity of the blood, thus favouring the local precipitation 
 of the circulating quadurate. The consequent arthritis and 
 febrile disturbance set up further explains why gouty patients 
 feel so much better after an attack of gout, for the increase of 
 metabolism of the febrile state, and the alkaline treatment, aU 
 tend to burn up as it were, or promote the excretion of the 
 excessive uric acid in the blood. The restricted diet also gives 
 the liver a holiday, and enables it to perform its functions with 
 renewed vigour. 
 
294 Student's Hand-hook of Medicine. 
 
 Further, our theory harmonises with the suggestion that 
 gout is more or less of a neurotic origin, for we pre-suppose 
 some devitalisation of the tissues and joints, and joints are 
 notoriously influenced hy atrophic nervous changes, as witness 
 Charcot's joint, etc. 
 
 Let us remember one thing more, that once a joint is 
 affected with gout, if the deposit is not all cleared away, like a 
 calculus in the bladder, it simply forms a nidus for the formation 
 of a large concretion. 
 
 Morbid Anatomy. — The metatarso-phalangeal joint of the 
 great toe is most often affected. If we examine the joint at 
 various stages, we find the following conditions — 
 
 A deposit of fine crystalline needles in the superflcial parts 
 of the cartilages ; next, the synovial membranes, cartilages, and 
 ligaments become covered with a chalk-like deposit of biurate 
 of soda. Underneath the deposit, the tissues are in a more or 
 less necrosed condition. The synovial fluid contains crystals of 
 uric acid. 
 
 Later, collections of biurate of soda plvs calcium phosphate 
 form the so-called chalk stones or tophi of chronic gout. These 
 deposits may occur elsewhere than in the joints, such as the 
 lobes of the ear, tendinous aponeurosis of muscles, sclerotic of 
 the eye, etc. Garrod believes these concretions are merely 
 calcification of gouty inflammatory products, and no doubt he 
 is right. ■ 
 
 Symptoms of Acute Gout. — Usually there are some pre- 
 monitory symptoms, such as giddiness, mental depression, 
 flatulence, irritability of temper, scanty and high-coloured urine, 
 etc. The attack most commonly commences in the early hours 
 of the morning, with severe pain in the big toe. The pain 
 increases to acute agony in some eases, rendering sleep or rest 
 out of the question. The patient becomes very feverish, or 
 he may feel chilly, and shiver violently without any rise of 
 temperature. The joint at first is bright red, and exquisitely 
 
Gowt. 295 
 
 tender ; later, it is more swollen, and of a livid or dull dusky 
 red, with distended venules standing out The swelling 
 extends some distance from the joints. The skin desquamates 
 in thick flakes when the attack is over. An attack lasts from 
 five to twelve days, but the severe pain is not constant, or 
 rather there are lulls, with exacerbations of severe pain at 
 intervals of the day, especially at night-time. The urine at 
 first is scanty and high-coloured, hut the uric acid is diminished 
 in amount; later, the excretion of uric acid is very much 
 increased. During the attack the patient usually is most 
 irritable, the tongue is furred, the breath may be offensive, he 
 has no appetite, and the bowels are constipated. Subsequent 
 attacks may affect the same joitit first implicated, or a number 
 of joints become involved. If the attacks are fairly frequent, 
 they cause the so-called chronic gout ; that is, a condition 
 characterised by a characteristic deformity of the joints, impor- 
 tant changes in various organs, especially the red granular 
 cirrhotic, or "gouty kidney." 
 
 No disease is quoted more frequently than chronic gout 
 as an important setiological factor in the causation of other 
 diseases. Such a statement, however, is largely the outcome 
 of habit and fashion. Many eminent men employ the terms, 
 " gouty habit," " specific taint," in a ridiculously loose fashion. 
 It is sometimes actually refreshing to hear a nervous disease 
 described as not dependant on one of these causes. 
 
 Chronic Gout. — Must not be confounded with rheumatoid 
 arthritis, though the sufferer may be crippled in much the 
 same manner. 
 
 The small joints of the toes and fingers are most often 
 affected. They are often distended by " tophi," which at first 
 lie under the skin, but may ulcerate through. 
 
 The kidney undergoes a marked cirrhotic change (see Chronic 
 Bright's Disease). In such cases, the pyramidal area of the 
 kidney often show yellowish-white streaks of urate crystals. 
 
296 Student's Hand-book of Medicine. 
 
 Other complications than those of " gouty kidney," are — 
 
 1. (Edema of the glottis, which is most easily excited, and 
 is singularly fatal in the gouty state. 
 
 2. " Gouty " urethritis, which may resemble a gleet. 
 
 3. Benal calculi. 
 
 4. Extensive sclerosis of the arteries, and the dangers arising 
 therefrom. 
 
 5. Eetention of urine. 
 
 6. Cirrhosis of the liver, with its train of symptoms. 
 
 Treatment. — During the acute stage — 
 
 1. Absolute rest, elevation of the limb, and hot fomentations 
 to the joints affected. 
 
 2. Diet to consist of milk and potash water, or at least non- 
 nitrogenovs food. 
 
 3. Medicinal treatment. — Clear out the bowels with five 
 grains of calomel, followed by a full dose of Carlsbad salts. 
 Give a mixture containing colchicum, iodide of potassium, 
 bicarbonate of potassium, and hyoscyamus. Iodide of potas- 
 sium, with laudanum and salycUate of soda added to the 
 hot fomentations, speedily relieves the painful joint. 
 
 When the acute attack subsides, massage must be employed, 
 for it is absurd to think " medicines " will remove the biurate 
 deposit from the joints. 
 
 Treatment of Chronic Gout. — Careful regulation of diet, 
 avoidance of alcoholic excesses, and proper exercise, are the 
 principal points to remember. Arsenic and strychnine as 
 medicines, lithia water as an habitual beverage, frequent 
 Turkish baths (when they agree), and massage to the 
 affected limbs, go far to complete a cure. 
 
Rickets. 297 
 
 RICKETS. 
 
 Eickets is a general disorder, wMch attacks infants and 
 young children who are subjected to improper feeding, want of 
 sunlight, and other unhealthy hygienic conditions. 
 
 Clinically, it is manifested by wasting, stunted growth, 
 characteristic physiognomy and deformities. 
 
 .Etiology. — Occurs mostly among the poor of overcrowded 
 cities. It is occasionally seen among the offspring of the 
 wealthy in whom there is a taint of syphilis or tuberculosis. 
 There cannot be any doubt that many cases of congenital 
 syphilis subsequently develop rickets. The absence of lime 
 salts in the food must be looked upon as an important setio- 
 logical factor, if such absence is prolonged. Often, however, 
 calcium salts are abundantly supplied in very marked cases of 
 rickets. 
 
 Pathology. — Again we have to do with a disease, the causa- 
 tion of which is shrouded in mystery. We must iirst briefly 
 consider the more constant morbid anatomical characters. 
 
 1. Change in bones — 
 
 (1) Their specific gravity falls, the water and organic 
 
 matter are increased, whilst the earthy matter is 
 decreased. 
 
 (2) The amount of fat is increased. 
 
 (3) They occasionally do not yield normal gelatine. 
 
 (4) The epiphyseal ends show under the microscope — 
 
 increased vascularity, irregtilar calcification, small 
 islets of uncalcified matrix, and large spaces due 
 to absorption by osteoclasts ; at the junction of 
 the epiphysis with the shaft, the bluish cartila- 
 genous zone is thickened, and very irregular ; 
 the bone formed is more vascular and spongy 
 than ordinary bone. 
 
298 Student's Hand-hook of Medicine. 
 
 2. The blood changes are a deficiency of red corpuscles, 
 and of hsemoglobia in the corpuscles present ; associated with 
 the presence of much granular detritus (Goodhart). 
 
 3. Changes in the lymphoid tissues. — The spleen, and lymph- 
 atic glands nearly always show extensive fibrous changes. 
 
 As rickets is often associated with a too excessive admini- 
 stration of starches, it has been assumed that lactic acid is 
 thereby formed in abundance, and that this excess of acid is 
 the real cause of rickets, by causing solution of the calcium salts. 
 This has not been proved, and, according to Gamgee, cannot 
 be the cause. But I must add, that whilst Gamgee has held 
 this theory up to ridicule, his chemical criticism is by no 
 means faultless. 
 
 From a careful consideration of the morbid anatomy, we 
 must assume at present that rickets is due to either — 
 
 1. Non-absorption into the blood of lime salts, through some 
 
 morbid condition of the alimentary canal ; or — 
 
 2. An inability on the part of the bone-forming tissues to 
 
 appropriate the lime which is conveyed to them. 
 
 The first theory may be usefully contrasted with the explan- 
 ation of chlorosis — i.e., disordered condition of the alimentary 
 canal, interfering with the assimilation of iron. 
 
 Symptoms. — The symptoms of a typical case of rickets are 
 very characteristic. 
 
 General configuration. — The head is elongated from back to 
 front, the forehead is square and overhanging, the fontanelles 
 are slow in closing, and the veins ia the skin are distended. 
 The flat bones are usually much thickened, and indeed, are 
 frequently "bossed" by irregular masses of calcified material. 
 It is important, however, to remember that very often the 
 occipital bone, and certaiu parts of the parietal bones are 
 thinned out. Though the skull as a whole is enlarged, the 
 
Rickets. 299 
 
 puny face makes the enlargement more noticeable by comparison; 
 measurements show the enlargement to be more apparent than 
 real. The brain development may be seriously handicapped by 
 this peculiar deformity, inasmuch as it allows the hind part to 
 develop, but not the intellectual portion — i.e., the frontal lobes. 
 Hydrocephalus is a somewhat common complication. 
 
 The ribs often show characteristic " beading " at the junction 
 of the costal cartilages. The thorax tends to become cottage- 
 loaf in shape. 
 
 The lower limbs are bowed, or sickle-shaped, and show the 
 well marked epiphyseal enlargements, especially at the lower 
 end of the tibia. 
 
 The upper limbs also show the most marked changes at the 
 lower ends of the ulna and radius, but the humerus, scapula, 
 etc., are also affected. 
 
 The pelvis is often much deformed, and may add serious 
 complications to parturition. 
 
 The spine is frequently distorted. 
 
 It will be seen from the above, that the deformities depend 
 partly on excessive deposits of calcareous material, and to a 
 certain extent to the yielding of the softened bone to mechanical 
 causes ; hence the necessity of rickety subjects avoiding any 
 undue or avoidable strain, such as too early walking, sitting in 
 cramped positions, carrying weights, etc. 
 
 The abdomen is usually prominent from distension by gas, 
 and the presence of the enlarged liver and spleen. 
 
 The other clinical symptoms are — general and marked 
 tenderness of the body, throwing off the bed clothes at 
 night, profuse sweating, and constipation alternating with 
 diarrhoea. The stools are usually pasty, or green, like boiled 
 spinach, and are intensely foetid at times. These symptoms, 
 taken with the general emaciation and deformities already 
 
300 Student's Hand-hook of Medicine. 
 
 described, make a diagnosis very easy. Of the complications 
 there are no end, but we must specially mention, convulsions, 
 tetany, strabismus, and laryngismus stridulus. Green- stick 
 fractures are not uncommon. 
 
 Treatment. — No cases deserve and require more thoughtful 
 and careful treatment. If the mother be unhealthy, a wet 
 nurse, or the " sterilised mUk " plan of artificial feeding must 
 be prescribed. Plenty of fresh air, sunny rooms, and gentle 
 massage, must be the routine treatment in all cases. The diet 
 for older children must be varied, and an excess of carbo- 
 hydrates avoided. Carefully planned gymnastic exercises may 
 help to prevent deformities, or cure those already formed. Of 
 drugs, phosphorus, lacto-phosphate of iron, arsenic, iodide of 
 iron, cod-liver oU, etc., all have their advocates. But careful 
 hygiene is of far more value than medicinal treatment. Dr 
 Palm, of Wigton, points out "that sunlight in the dwelling 
 not only reveals unsuspected dirt, but is nature's disinfectant 
 as well as a stimulant and tonic." There can be no possible 
 doubt as to the all important influence of sunlight to con- 
 sumers of large quantities of carbohydrates. 
 
 CHRONIC RHEUMATISM. 
 
 Chronic rheumatism is sometimes a sequel of rheumatic 
 fever, but is generally a separate constitutional afiection. 
 
 .etiology. — Is most common amongst the middle-aged poor. 
 Senility seems to be a predisposing cause, both amongst poor 
 and rich. 
 
 Pathology. — Is at present ill - understood ; the fibrous 
 textures around joints, enveloping nerves, or the aponeurotic 
 sheaths of the muscles, periosteum of bones and tendons 
 all suffer more or less. Though these structures become 
 
Chronic Rheumatism. 301 
 
 inflamed, very little alteration results — i.e., the joints are 
 rarely deformed, though the ligaments and synovial mem- 
 branes may become much thickened, and the movements 
 of the joint limited. 
 
 Symptoms. — Pain and stiffness of the parts involved are 
 the main features. The pain is usually worse on movement, 
 but it should be noted that continued exercise mitigates the 
 pain : for example, a man goes to bed with muscular rheuma- 
 tism, as long as he keeps quiet the pain is not severe, but the 
 slightest movement causes acute suffering. In the morning, 
 on attempting to rise the pain may be very severe, but after 
 working for a time the pain becomes tolerable though it does 
 not disappear. 
 
 Varieties — 
 
 1. Lumbago. — The aponeurosis of the erector spinal and 
 latissimus dorsi are most frequently involved. The pain is 
 often intense, and may affect the locomotion markedly. Often 
 the onset of the pain is traced to some physical exertion, such 
 as getting up into the saddle, or lifting heavy weights. The 
 latter point must be borne in mind in colliery practices, for 
 the colliers frequently demand pay on account of injury — i.e., 
 "strained back." 
 
 2. Pleurodynia. — The sheaths of the pectoral muscles, 
 intercostals, or serratus magnus, are most commonly affected. 
 The respiratory movements of the affected side are much 
 embarrassed. This affection may be mistaken for pleurisy, 
 as the movements of the affected muscles often cause a distinct 
 fremitus. The absence of other physical signs should prevent 
 such an error. 
 
 3. Muscular Torticollis, or Stiff Neck. — ^Here the cervical 
 muscles, especially the sterno-mastoid, are affected. This con- 
 dition must not be confounded with spasmodic torticollis, 
 Many other varieties are described. 
 
802 Student's Hand-book of Medicine. 
 
 Treatment. — Keep the bowels well open by' saline aperients. 
 Turkish baths and massage, combined with the administration 
 of iodides, form the routine treatment. The A. B. C. liniment 
 is most useful for local application. If the condition does not 
 speedily improve, a visit to Buxton or Bath, etc., should be 
 insisted upon, where the patient may undergo a thorough 
 system of massage, and course of saline waters. 
 
 RHEUMATOID ARTHRITIS. 
 
 Rheumatoid arthritis is a chronic inflammatory affection of 
 the joints, resembling gout and chronic rheumatism in many 
 of its characters, but differing essentially from both. Although 
 a chronic disease, the patient may have acute or subacute 
 attacks superadded. 
 
 .ffitiology. — Most common amongst females, between the 
 age of twenty and thirty. The disease may, however, attack 
 any age. Heredity, phthisical history, ovaritis, grief, worry, 
 etc., are looked upon as important setiological factors. 
 
 Pathology. — At present speculative. Probably it is due to 
 neuro-trophic changes ; and reasoning from the number of joints 
 attacked, the symmetrical distribution of the trophic changes 
 which lead to such grave alterations in the skin, naUs, etc., 
 this view seems to be the correct one. 
 
 The morbid changes found in the joints affected, are identical 
 with those of Charcot's joint disease, so frequently a complica- 
 tion in cases of locomotor ataxia. According to Adams, the 
 disease begins in the cartilages and synovial membranes — as 
 splitting of the cartilage and liberation of the cells ; next, 
 absorption of the cartilage and approximation of the two articu- 
 lar surfaces of the joint, which by rubbing together, become 
 very dense, hard, and highly polished ; the surfaces at the same 
 time, through pressure, become broadened out — i.e., lateral 
 
Rheumatoid Arthritis. 308 
 
 expansion, Underneatli the new and dense ivory-like bone, 
 rarefaction and atrophy occur, leading to much shortening and 
 deformity. 
 
 Meanwhile the synovial membranes become indamed and 
 thickened ; often portions become detached, and form loose 
 bodies in the joint. The ligaments become much thickened, 
 and often contracted ; sometimes they calcify and cause more 
 or less ankylosis. At the margins of the joints where the 
 pressure is less, ossification goes on, resulting in the formation 
 of irregular bony outgrowths, termed osteophytes. The anky- 
 losis of rheumatoid arthritis is never complete, and there is 
 no tendency to suppuration. 
 
 Synlptoms — 
 
 The Ordinary Chronic Form. — The joints are involved 
 symmetrically. At first the joints may be swollen, red, and 
 tender, but the more constant features are stiffness and gradual 
 deformity, without any marked signs of inflammation. In 
 confirmed cases the joint changes, and the accompanying 
 muscular atrophy cause the deformities to assume a very 
 characteristic appearance. The lower ends of the ulna and 
 radius project at the wrist, the metacarpo -phalangeal are flexed, 
 the first phalangeal joints are over-extended, the second are 
 flexed, and the fingers deviate to the ulnar side. The joints 
 give forth a creaking sound when moved. 
 
 When the disease is confined to the hands, the osteophytes 
 receives the name of " Hebeden's Nodosities." After the 
 hands and wrist, the knees and ankles are most commonly 
 attacked, but cases have been known where all the articulations 
 of the body have become implicated. The muscular atrophy, 
 though no doubt due largely to atrophic influences, is largely 
 contributed to by non-use. 
 
 Besides Heberden's nodosities, a mono-articular form of 
 rheumatoid arthritis has been described. This type differs 
 from the poly-articular form, by affecting the spine or hip-Joint, 
 in elderly men. 
 
304 Student's Hand-book of Medicine. 
 
 Diagnosis. — From Charcot's joint, by the history and 
 absence of ataxic symptoms. From gout, by the absence of 
 tophi, no excess of uric acid, etc. 
 
 Treatment. — No treatment can cure this disease, but it is 
 often arrested by careful attention to the general health. 
 Arsenic and iodide of potassium with strychnine are often of 
 great service. Massage, however, is probably the best treat- 
 ment that has yet been adopted. 
 
 GONORRHCEAL SYNOVITIS. 
 
 Gonorrhoeal synovitis is a more or less acute arthritis, 
 following in the waJie of gonorrhoea, and probably due to 
 the introduction of some specific virus. It must not, how- 
 ever, be concluded that it is the gonorrhoeal poison which sets 
 up the condition, for it has followed balanitis and ordinary 
 profuse leucorrho3a. Probably the gonorrhoeal poison creates 
 a suitable nidus for another specific organism to flourish. Some 
 authorities still hold that it is ordinary acute rheumatism added 
 to a gonorrhoea. 
 
 Symptoms. — They are much the same as regards the joint 
 condition described under Kheumatic Fever, but the redness 
 may be more intense. The fever is not usually high. The 
 peculiarities of the sub-acute cases are — iritis, extreme pain in 
 the plantar fascia, the occurrence of conjunctivitis, and the 
 tendency to involve the sterno-clavicular and temporo-maxillary 
 joints — i.e., those joints not usually involved in ordinary acute 
 rheumatism. The disease is extremely likely to recur, and 
 may render life miserable. 
 
 Treatment. — The alkaline treatment may be pursued for 
 a short time, but quinine and liquor ferri are the best drugs 
 in this aifection. If the joints remain obstinately swollen, 
 nothing is more efficacious than the hypodermic injection of 
 two or three minims of carbolic acid into them. The actual 
 cautery may be of use in chronic cases ; galvanism, etc. 
 
Ancemia. 305 
 
 DISEASES OF THE BLOOD. 
 
 Healthy blood means perfect health, therefore in all diseases 
 the blood must be altered in its quality; so it is difficult 
 to explain what is really meant by the above heading; but, 
 under this title we mean those diseases which show the most 
 marked changes in the blood, either in quantity or quality. 
 
 ANEMIA. 
 
 Ansemia really means want of blood, but, we employ the 
 term in a much wider sense, and we shall under anaemia, 
 include — 
 
 1. Oligsemia — deficiency of blood. 
 
 2. Hydraemia — thin or watery blood. 
 
 3. Oligocythsemia — a diminution of the number of corpuscles. 
 
 4. Poikilocythssmia — irregularity in the shape of the cor- 
 puscles. 
 
 Special Anaemias. — 
 
 (1) Simple. 
 
 (2) Chlorosis. 
 
 (3) Pernicious Anaemia. 
 
 It wUl save much recapitulation and help to avoid much 
 haziness regarding these affections, if we start with a clear idea 
 what anaemia really means, as regards its effects upon the body 
 generally. 
 
 Pathology. — We must expect imperfect oxygenation, 
 deficient nutrition, and, therefore — impaired function, fatty 
 degeneration, atrophy of certain tissues, and, softening of the 
 blood-vessels ; a vicious cycle of retrograde changes thus begins, 
 each new failure on the part of an organ increasing the original 
 
 T 
 
306 Student's Hand-book of Medicine. 
 
 condition. The nerve centres are only too frequently hyper- 
 excited at first, as shown by powerful emotional manifestations ; 
 or diminished sensibility, as seen in the dilated pupils, 
 which shows the depressed condition of the retina. (Edema 
 in unsupported tissues is most common. 
 
 SIMPLE AN/EMIA. 
 
 Causes. — 
 
 Deficiency of food, either through actual want, or inability 
 to take food — as in cancer of the oesophagus, etc. 
 
 Excessive discharges — i.e., pysemic abscesses, diarrhoea, etc. 
 
 Smmorrhages. — The blood in these cases, if the bleeding is 
 profuse, becomes rapidly diluted with lymph. 
 
 Certain occupations — lead workers, coUiers, etc. 
 
 In these cases, removal of the cause, and placing the patient 
 under favourable hygienic conditions, bring about a cure. 
 
 CHLOROSIS. 
 
 The usual definition in text-books is, — a peculiar anaemia 
 attended with a greenish, transparent, wax-like condition of the 
 skin, common in females at the age of puberty. 
 
 .SItiology. — From a careful observation of the cases deserving 
 the name " green sickness," seen in the out-patient department 
 of Edinburgh Eoyal Infirmary, I am convinced that the con- 
 dition is more common at a slightly older age than puberty, 
 'i.e., between eighteen and twenty-one years. 
 
 Symptoms. — Languor, palpitation on exertion, headache, 
 noises in the ears, and dyspeptic symptoms, as in simple 
 anaemia. The more characteristic symptoms in addition are 
 
Chlorosis. 307 
 
 plumpness, systolic murmuTS at the base of the heart, " bruit 
 de diable" at the lower end of the jugular vein, constipation, 
 irregular, profuse, or scanty menstruation, and the waxy appear- 
 ance of the skin already referred to. 
 
 Pathology. — The red corpuscles are diminished in number, 
 and of various shapes ; some swollen, others crenated, but all 
 show a remarkable diminution of hcemoglobin, which must be 
 considered the chief peculiarity of chlorosis. There cannot be 
 the least possible doubt that chlorosis is due to defective blood 
 formation — something wrong in the building up, not an ex- 
 cessive breaking down. The theories advanced to explain such 
 a condition are numerous, and the following may be borne in 
 mind for examination purposes — 
 
 1. Due to constipation. (Sir Andrew Clark.) 
 
 2. That the period of puberty causes an increased demand 
 on the blood-forming glands, which are unable to meet the call. 
 
 3. The demands of puberty reveals a congenital narrowness 
 of the aorta, which prevents a proper supply of blood to the 
 various tissues. 
 
 4. That the organic iron-compounds of the food are broken 
 up by excessive decomposition in the alimentary canal, and the 
 iron thus liberated, is rendered incapable of being absorbed into 
 the blood. (Bunge.) 
 
 5. The development in the female, of a peculiar gum-like 
 substance intended for the nourishment of the future embryo, 
 {i.e., in preparation of the demands of pregnancy), which acts 
 injuriously on the hsemoglobin molecule. (Landwehr). 
 
 It is painfully interesting to note that neither of the above 
 explain the disease, for constipated subjects are not always 
 chlorotic, chlorosis is not confined entirely to women, and 
 chlorosis may be present with a sound aorta. At present we 
 may assume that chlorosis is due to many factors, — the chief 
 being the adolescent period, which causes an increased demand 
 on the blood-forming glands, and develops latent weaknesses; 
 
308 Student's Hand-book of Medicine. 
 
 further, such period conduces towards an unstable state of the 
 nervous system, manifested by dyspepsia, constipation, etc. 
 
 As to the immediate cause, it is highly probable that Bunge's 
 theory is correct. 
 
 Treatment. — Is highly satisfactory. Fresh air, exercise, nitro- 
 genous food, purgatives, and iron will cure the worst cases. 
 
 An excellent combination is iron, aloes, and carbonate of 
 potash. The iron acts in two ways — 
 
 1. It combines with many of the products of decomposition 
 in the duodenum, and thereby forms insoluble and inert salts, 
 which are excreted, thus preventing the pernicious gases, etc., 
 entering the portal system. 
 
 2. No doubt a small amount of the iron itself is absorbed 
 and assimilated. 
 
 Carbohydrates as a rule are harmful. Chlorotic girls should 
 be released from all studies, and exciting literature should be 
 kept from them. 
 
 PERNICIOUS ANAEMIA. 
 
 This is a progressive and profound anaemia, developing 
 without any evident cause, and ending most frequently in 
 death. 
 
 .etiology. — Most frequent in the Swiss Cantons. Affects 
 males more than females. Is rare under 25 years of age. 
 Many cases have started during pregnancy. 
 
 Pathology. — The Blood, shows a remarkable diminution of 
 red corpuscles; they may sink to less than half a million 
 per cubic millimeter. The amount of haemoglobin in each 
 corpuscle, so far from being diminished is often relatively 
 increased. The corpuscles exhibit a number of various shapes, 
 some are tailed, others crenated ; often the haemoglobin can be 
 
Pernicious Ancemia 309 
 
 seen protruding prior to its escape from the stroma, some discs 
 are extremely minute, and may be nucleated. A large number 
 of yellowish bodies termed miorocytes' are usually found. The 
 blood when shed coagulates with difficulty. 
 
 The Liver shows marked changes — 
 
 1. Is exceedingly rich in iron. 
 
 2. There is an excess of pigment within the liver cells. 
 
 3. There is fatty degeneration in the central third of each 
 lobule. 
 
 Neither the marrow nor the spleen show any constant or 
 definite changes, beyond those that result from deficient oxy- 
 genation. 
 
 There can be no doubt that pernicious ansemia is due to 
 excessive destruction of the cellular elements of the hlood. 
 Dr Hunter, of Cambridge, after a most exhaustive and critical 
 analysis of this disease, believes that pernicious ansemia is 
 due to the circulation of poisonous cadaveric alkaloids within 
 the portal circulation, which hasten the disintegration of the 
 red corpuscles. Possibly the disease is due to a special 
 organism rather than cadaveric products. 
 
 Prognosis. — Highly unfavourable, most cases die in from 
 six to fifteen months. 
 
 Symptoms. — Are those of profound ansemia already de- 
 scribed, but in addition we have in pernicious ansemia — 
 
 1. Fever. — The pyrexia is usually paroxysmal. 
 
 2. Indican in the urine. 
 
 3. Hsemoglobinuria. 
 
 4. Eetinal hsemorrhages. 
 
 5. Primrose colour of the complexion. 
 
 Though of course the muscular wasting is considerable, the 
 subcutaneous fat is often increased; hence the wasting is not 
 apparent, and the patient may present a fairly well nourished 
 appearance as regards the general contour of the body. 
 
310 Student's Hand -hook of Medicine. 
 
 Treatment. — Is far from satisfactory. Arsenic, transfusion 
 of blood, iS-napthol, etc., have in certain cases proved successful, 
 but the bulk of the cases are quite unamenable to any treat- 
 ment yet discovered. 
 
 There cannot be the slightest possible doubt that an aseptic 
 state of the intestines as far as possible is highly desirable, 
 and salol and )3-napthol are certainly our best drugs for 
 obtaining such a state. 
 
 Iron seemingly is of no use. 
 
 LEUCOCYTH.ffiMIA. 
 
 Leucocythsemia is an affection characterised by persistent 
 increase of white corpuscles, hsemorrhages, and changes in the 
 blood, marrow, spleen, lymphatic glands, etc. 
 
 iEtiology. — The disease may develop at any age, but by 
 far the bulk of cases occur in the middle aged. Men are more 
 often attacked than women. The more important setiological 
 factors that have been' observed are — 
 
 Heredity, 
 Syphilis, 
 Malaria, 
 
 Traumatisms, and 
 Pregnancy. 
 
 Pathology. — The Mood is markedly altered, and shows — 
 
 1. The white corpuscles to be enormously increased, so 
 that the proportion of white to red corpuscles may be as high 
 as 1 to 6, or even 1 to 3, instead of 1 to .350 as in normal 
 blood. The white corpuscles are of different shapes and sizes, 
 and hence an attempt has been made to distinguish various 
 types of the disease : — i.e., The small ko?! -nucleated cells are 
 
LeucocythcB'mia. 311 
 
 held, to be derived from the marrow, the small nucleated 
 cells from the lymphatic glands, large coarsely-granular cor- 
 puscles of various shapes from the spleen. Thus the 
 preponderance of any particular shape points to the structure 
 mostly involved. 
 
 2. An excess of fat, so that a drop of the leuksemic blood 
 dropped on to white paper leaves a greasy stain. 
 
 3. The presence of elongated, octahedral, colourless, 
 phosphatic crystals (similar to those found in asthma). 
 
 4. The abundance of hypo-zanthin and other antecedents 
 of urea. 
 
 5. A substance which is soluble in hot water, and which 
 hke gelatine sets into a jelly when its solution is cooled. 
 
 The Spleen. — It is usually firm, much enlarged and may 
 be bound by adhesions to the abdominal wall, the diaphragm, 
 or the stomach. The capsule is much thickened. On section, 
 the organ presents a pinkish appesCitoce, appears fatty, and 
 feels greasy to the touch. The pulp is dark, and the Malpighian 
 tufts stand out as pale spots. The sinuses are often distended 
 with leucocytes. Hsemorrhagic infarctions, old and recent, 
 are very common. Later, the changes are more fibrous in 
 character, and the splenic pulp may be much atrophied from 
 the pressure. 
 
 The Lymphatic Glands. — Nearly all the lymphatic glands 
 are enlarged and softened ; later, they may assume the same 
 characters as observed in Hodgkin's disease. 
 
 The Marrow. — The marrow may be dark brown in colour, 
 or present a peculiar yellowish-red appearance. Large numbers 
 of nucleated red corpuscles and non-nucleated leucocytes are 
 found. 
 
 The other tissues and organs, such as the liver, heart, etc., 
 show those grave changes consequent upon deficient oxy- 
 genation, plus extravasations of blood. 
 
312 Student's Hand-book of Medicine. 
 
 Symptoms. — The onset is most insidious, and the patient 
 usually applies for medical advice on account of breathlessness, 
 dyspeptic symptoms, palpitation, and other symptoms of 
 anaemia. Haemorrhages of various kinds may be the first 
 symptoms. When the disease has advanced, the condition of 
 the patient is most characteristic. The abdomen is prominent ; 
 the countenance of a deadly white, or with a slightly saUow 
 tint ; the sclerotic of a pearly lustre ; pupils dilated, mucous 
 membranes blanched. The pulse is soft and compressible, 
 contrasting well with the high tension pulse of chronic 
 Bright's disease. Haemorrhages are common under the stin 
 in mucous membranes, and into the retina. The retinal 
 changes are often most marked, the vessels being tortuous 
 and pften distended with the white corpuscles. Towards the 
 end, grave waxy changes set in and intermittent diarrhoea, 
 attacks of fever and oedema, or general dropsy ushers in a 
 fatal issue. It must not be forgotten that the urine usually 
 is of high specific gravity, containing excess of uric acid and 
 urea. The pallor, usually so well marked, is sometimes wanting. 
 The special points to note are the condition of the blood, 
 marked exhaustion, pyrexia, and the tendency to dropsy 
 associated with highly coloured urine. 
 
 Diagnosis of the enlarged Spleen. — It enlarges in the axis 
 of the tenth rib, and, therefore, tends to go forward to the 
 light iliac fossa. If much enlarged, it is found to present 
 as a firm, hard tumour, having a distinct notch in its anterior 
 border ; it may reach from the flank to or below the umbilicus, 
 and weigh from six to eighteen pounds. Note in contrast to 
 floating kidney — the colon never lies in front of an enlarged 
 spleen. 
 
 Treatment.- — Everything must be done to protect the 
 patient from cold, and the general hygiene must be as perfect 
 as possible. Massage and galvanism may be applied with 
 advantage to the spleen. The medicinal treatment is as 
 described under the treatment of the Pernicious Anaemia. 
 
HodgJcin's Disease. 313 
 
 HODGKIN'S DISEASE. 
 
 It is an afifection characterised by progressive enlargement 
 of the lymphatic glands, destruction of red corpuscles, and 
 secondary lymphoid growths in the various organs. 
 
 .Etiology. — It may attack any age, but is by far more 
 common in children and young adults. No special Eetiological 
 factor is known. Possibly syphilis, tlibercle, and traumatisms 
 are important factors, in as much as they weaken the glandular 
 system. 
 
 Pathology. — The exact cause of Hodgkin's disease is quite 
 unknown, though there can be no doubt that it is due to some 
 chemical irritant formed either in the blood, or introduced from 
 without, but which, when in the blood, causes an overgrowth 
 of lymphoid tissue. 
 
 The aifected glands are usually much enlarged, single, 
 painless, and non-adherent to the skin. Though they may 
 feel to the touch hard and solid, they are far more frequently 
 somewhat soft and elastic. Their tieo gfeat characteristics 
 are — they neither tend to suppurate or caseate. Of coiirse, 
 like all other growths, they may under certain circumstances 
 suppurate and mass together ; but, as Dr Bramwell emphasizes, 
 "such results are to be regarded as accidental.'' The disease 
 may cause large deposits of lymphoid tissue in the sub- 
 cutaneous tissue and marrow of long bones. 
 
 Histologically. — 
 
 The Glands. — The chief change is a general hyperplasia 
 of the whole gland, accompanied by the formation of a large 
 number of small cells resembling leucocytes. The amount 
 of new fibrous tissue formed governs the degree of hardness : 
 if the lymphoid cells are abundant, the gland is soft; but when 
 the fibrous tissue element is in excess the glands are hard. 
 
314 StvAent's Hand-hook of Medicine. 
 
 The Spleen. — Is always enlarged in Hodgkin's disease, but 
 not nearly to the same extent as in leucocythsemia. In con- 
 sistence it is firm, and purple patclies from venous congestion 
 often appear on the surface. On section can be seen golden- 
 yellowish masses, consisting of lymph corpuscles and pigment 
 enclosed in a fibrous reticulum. The Malpighian bodies appear 
 as translucent yellowish suet-like masses. The general fibrous 
 stroma is much increased like in the lymphatic glands. 
 
 Symptoms. — Briefly are — 
 
 1. Enlargement of the lymphatic glands. 
 
 2. Ansemia — Often marked decrease of red corpuscles, and 
 slight increase of the white. 
 
 3. Symptoms pointing to the malignant nature of the 
 disease — i.e. marked emaciation, cachexia, secondary deposits of 
 lymphoid tissue. 
 
 4. Attacks of pyrexia. 
 
 5. Symptoms due to pressure from the lymphoid growth. 
 The glandular enlargement most frequently begins in the 
 
 anterior chain of glands at the posterior border of the stemo- 
 mastoid, then the axillary, inguinal, and finally all the glands 
 of the body may show extensive changes. Often both sides 
 of the neck become involved, and the growths meeting 
 anteriorly in the middle line may compress the trachea to a 
 dangerous extent. Osier points out that when the abdominal 
 glands are affected the sympathetic system is often profoundly 
 disturbed and pigmentation of the skin may occur. The 
 enlarged mediastinal growth may cause severe dyspnoea, in- 
 equality of the pupil, pleurisy, etc. 
 
 The periodical elevations of temperature may be so marked 
 as to simulate ague. It will be at once seen, that almost any 
 symptom may crop up in Hodgkin's disease, and no wonder 
 if we remember the extensive nature of the disease, and the 
 important structures that may be involved thereby. Lastly 
 note, that in some cases the red corpuscles are not diminished 
 untU marked cachexia has set in. 
 
Ulcer of the StoTnach. 315 
 
 Treatment.— It has been suggested that when the disease 
 has affected only one set of glands, that the diseased portion 
 should be excised : such procedure is certainly as rational as 
 operative measures in other malignant conditions. We may 
 hope for benefit from subcutaneous injections of arsenic, or 
 thyroid extract, combined with massage and careful hygiene. 
 The disease is, however, only too frequently fatal in from two 
 to four years. 
 
 DISEASES OF THE STOMACH. 
 
 ULCER OF THE STOMACH. 
 
 l>y this lesion is meant a form of ulcer, which is peculiar 
 to the stomach, the first part of the duodenum, and (accord- 
 ing to some authorities) the lower end of the cesophagus. 
 Though usually single, there may be more than one ulcer 
 present. 
 
 Site. — Solitary ulcers are nearly always situated on the 
 posterior wall, near to, or involving the lesser curvature. 
 Sometimes they are observed near the pylorus, but rarely 
 do they attack the greater curvature. 
 
 Characters. — In size the ulcer varies much, but is usually 
 about an inch or slightly less in diameter, and of a circular 
 or oval shape. Its appearance suggests that it might have 
 been produced by punching out a piece of mucous membrane. 
 The edges are ??.oi5 undermined, and there is an absence of 
 vascularity in the margins and base. The floor is formed 
 by either the submucosa, by the muscular coat, or the serous 
 coat; the latter is not unfrequently thickened, and adherent 
 to the neighbouring organs. These adhesions are of the 
 utmost importance, and go far to explain why perforation is 
 
316 Student's Hand-book of Medicine. 
 
 not more common in cases of gastric ulcer. As the ulcer 
 deepens, its floor or base becomes narrower, so that the walls 
 come to have a terraced appearance, and an oblique direction. 
 If perforation occurs, the aperture in the serous coat is of 
 small size, but presents the same clean cut punched - out 
 appearance, that distinguishes the margins. In the healing 
 of the ulcer, if the mucosa be alone involved, the granulation 
 tissue develops from the edges and the floor, and the newly 
 formed tissue gradually contracts and unites the margins, 
 leaving a smooth scar. 
 
 In larger ulcers which have become deep, and involved 
 the muscular coat, the cicatricial contraction may cause 
 serious changes, the most important of which is, narrowing 
 of the pyloric orifice, and dilatation of the stomach 
 (Dr Osler). a common result of the ulcerative process 
 is perforation of the gastric walls, and consequent fatal 
 peritonitis. On the other hand, it is not uncommon for 
 adhesions to form between the walls of the stomach and 
 neighbouring organs, and the ulcer after perforating the 
 gastric walls, burrows into the pancreas, spleen, or liver. 
 Large vessels may be eaten into in a similar manner, and 
 bring about a fatal issue from haemorrhage. Other compli- 
 cations through the ulcerating process are — 
 
 1. Perforation into the pleura. 
 
 2. Gastro-duodenal fistula. 
 
 3. Perforation into the lesser peritoneum, constituting the 
 so-called subphrenic-pyopneumothorax. 
 
 Pathology. — Nearly all observers agree that the ulcer is due 
 to two immediate factors — 
 
 1. A devitalisation of certain areas of the gastric mucous 
 membrane. 
 
 2. Erosion of these areas through either the digestive 
 action of the gastric juice, or the mechanical irritation of 
 indigestible food. 
 
Ulcer of the Stomach. 317 
 
 Probably in all cases many factors are present, and I think 
 the best way of summing up is as follows : deficient or in- 
 different quality of blood supply to the walls of the stomach 
 tend to cause — 
 
 1. Alterations in its secretions. 
 
 2. Local thrombosis of the nutrient arteries. 
 
 3. Deficient movement or peristalsis of the viscus. 
 
 Thus we may get hyperacidity of the gastric juice ; certain 
 areas of the stomach are rendered very vulnerable through the 
 local thrombosis, and lastly the defective peristalsis favours the 
 concentration of the irritating gastric contents at certain points. 
 Consequently there can be no difficulty in understanding how 
 ulceration of the mucous membrane comes about in the throm- 
 bosed areas. If we grant this, then we must allow that such 
 a downgrade process must be powerfully assisted by irritating 
 food, and anything which tends to diminish the alkalinity of 
 the blood, for it must be remembered that physiologists hold 
 that the alkalinity of the blood normally plays a part in pre- 
 venting the stomach from digesting itself. 
 
 Bucquoy emphasizes the following symptoms as diagnostic 
 of the duodenal ulcer — 
 
 1. Sudden intestinal hsemorrhage in an apparently healthy 
 person, which tends to recur. 
 
 2. Severe pain in the right hypochondrium, two or three 
 hours after a meal. 
 
 3. Local tenderness. 
 
 4. Severe gastralgia. 
 
 Treatment.— What are our indications in such a case ? 
 Obviously (1) Improve the general hygienic surroundings ; 
 (2) Give the inflamed stomach rest ; (3) Promote the healing 
 of the ulcer; (4) Improve the blood condition; (5) After the 
 acute symptoms are over, improve the local supply of blood 
 by gentle massage to the stomach. 
 
318 Stvdent's Hand-book of Medicine. 
 
 Diet. — A wine-glassful of milk, -with a little lime water 
 added, every two hours, must be the only food allowed by 
 mouth. It may, however, be supplemented in some cases by 
 nutrient enemata of pancreatised beef extract. 
 
 Medicinal. — The favourite remedies are bismuth (powder) 
 with morphia, and the administration of Carlsbad salts. The 
 former act mechanically by coating the ulcer, the latter, by 
 depleting the portal circulation, removing the constipation, and 
 adding to the alkalinity of the blood. 
 
 iEtiology. — Gastric ulcer is most commonly met with in 
 young women, especially those who Idad a sedentary life, who 
 live in areas shut out from the sunlight, etc. Tight-fitting 
 corsets are undoubtedly important factors. In men — shoemakers 
 are prone to this affection, due probably to pressure of the "last" 
 on the stomach, thereby impeding or hampering the gastric 
 circulation. Extensive burns may be followed by gastric ulcer, 
 especially of the duodenal type. 
 
 Symptoms. — No disease or condition may have on the one 
 hand more characteristic symptoms, and on the other hand 
 more ill-defined ones than gastric ulcer. Taking a typical 
 case, we may expect — 
 
 1. Pain and tenderness over the epigastric region. The 
 pain is severe and shoots through to the back (xiphi-vertebral), 
 is rendered worse by eating, or by firm pressure. 
 
 2. Vomiting ; the food usually returns quickly, and often 
 gives much temporary relief. 
 
 3. Hsematemesis may be very copious, but is not 'frequent. 
 
 These symptoms in combination with the history, anaemia, 
 and the absence of a tumour, point strongly to the presence 
 of an ulcer. I must, however, warn beginners not to always 
 expect such typical signs. Often, indeed, the symptoms are 
 
Cancer of the Stomach 319 
 
 very slight, and a copious or even fatal hsemorrliage may be 
 the first indication of such a condition. 
 
 Note. — When the healing process has fairly advanced, the 
 patient may have bland broths, raw meat sandwiches, whipped 
 cream and eggs, etc. Pepsin is often of great use. The great 
 drawback to successful treatment is the lack of co-operation on 
 the part of the patient as regards diet. 
 
 CANCER OF THE STOMACH. 
 
 Cancer of the stomach is by no means a rare condition, 
 and most varieties have been found at one time or other; 
 the principal primary forms however are — 
 
 1. Malignant adenoma at the pyloric and the cardiac end. 
 
 2. Sohirrus cancer; this form constitutes the bulk of 
 
 the pyloric growths. 
 
 3. Encephaloid. 
 
 4. Colloid. 
 
 3 and 4 are in all probability degenerations of the other two. 
 Epithelioma at the cardiac orifice is probably an oesophageal 
 cancer which has extended. 
 
 .etiology. — The majority of cases occur between the ages 
 of forty and sixty years. Eich and poor, male and female, 
 seem to furnish an equal number of cases. 
 
 Pathology. — As the pylorus is the most common site, and 
 hard schirrus the most common variety of cancer in that region, 
 we, shall discuss its growth briefly. 
 
 The cancer usually begins as an overgrowth of the epithelial 
 cells lining the gastric glands ; the new growths infiltrate the 
 
320 Student's Hand-book of Medicine. 
 
 submucous tissue, proliferate rapidly, and finally all coats are 
 invaded resulting in the formation of hard nodular masses. 
 The pyloric opening becomes much narrowed, and the resulting 
 stenosis gives rise to the marked dilatation of the stomach, so 
 characteristic of pyloric cancer. The subsequent pathological 
 course of the cancer does not differ from that of cancer else- 
 where. It may remain more or less stationary for a time, then 
 undergo one of the various degenerations that morbid growths 
 are liable to — i.e., colloid degeneration, ulceration, etc. If 
 we get a clear idea of these changes, remember the anatomical 
 site, and the physiological importance of the neighbouring 
 viscera, there cannot be any doubt as to what symptom may 
 or should crop up. The ulcerative process may invade im- 
 portant blood-vessels, cause hsematemesis, or form adhesions 
 with other organs, and seriously handicap their functions by 
 actual invasion, and lastly aggravate or hasten the malignant 
 cachexia. 
 
 Symptoms. — They are for a time most insidious, but 
 sooner or later the persistent vomiting, hsematemesis, constant 
 pain, emaciation, and cachexia, with the presence of a local 
 tumour, declares the true condition. The symptoms are 
 considered in detail in the diagnostic table appended. 
 
 Just a few words about hydrochloric acid being absent in 
 this condition. I have examined the vomited matter of many 
 cases of gastric cancer, and have found hydrochloric acid ia 
 some cases, and none in others. As HCl may be absent in 
 other conditions than gastric cancer, I cannot help thinking 
 that its absence as a diagnostic agent in cancer had better be 
 dismissed. Have we a reliable test for hydrochlorid acid? 
 Moreover, as the absence of HCl is not noted until the disease 
 is advanced, one faUs to see its great importance. 
 
 Prognosis.- — The disease is usually fatal in from six months 
 to two years, but severe complications may bring about a fatal 
 issue very speedily. 
 
Cancer of the Stomach. 321 
 
 Physical Examination. — A tumour may be discovered, three 
 or four months after the onset of symptoms. It is found 
 anywhere within an area formed by joining the ensiform carti- 
 lage with the umbilicus, and the umbilicus with the ninth 
 costal cartilage. The tumour is painful on handling, may 
 receive an impulse from the abdominal aorta, and though at 
 first is somewhat mobile, it afterwards becomes fixed. 
 
 Physical examination also reveals the dilated condition of 
 the stomach. It should however be remembered, when the 
 body of the stomach is involved, that the stomach is atrophied 
 and hour-glass shaped instead of being dilated. 
 
 Diagnosis. — See Table appended. 
 
 Treatment. — Must be mainly palliative. Digestible food 
 and hypodermic injections of morphia help to make the 
 patient's life tolerable. Surgical proceedures seem to offer 
 some chance of prolonging life. Dr Mayo Eobson says : — 
 when the disease involves the pylorus there are three 
 courses open — 
 
 1. Complete removal by pylorectomy with suture of the 
 ends of the stomach and duodenum. 
 
 2. Pylorectomy with closure of the open ends of the 
 duodenum and stomach by invagination and suture, the 
 communication between the stomach and bowel being that 
 efi'ected by gastro-enterostomy. 
 
 3. In extensive disease, or where the patient is unable 
 or unfit to bear the major operation, gastro-enterostomy may 
 be performed, the stomach and jejunum being fixed in 
 apposition by means of Senn's plates. 
 
 [Table 
 
322 
 
 Stvdent's Hand-book of Medicine.- 
 
 1. Is rare under forty years of 
 age. 
 
 2. Epigastric pain is more or 
 less continnons, and not much re- 
 lieved by vomiting. 
 
 3. Vomiting is not frequent, but 
 is copious ; and in the vomited mat- 
 ter may be found — Saroinse ventri- 
 culi, torula, etc. Cancerous frag- 
 ments (rare). HCl is absent (?) 
 
 4. Heemorrhage is seldom co- 
 pious, but may be frequent ; most 
 common in the later stages. 
 
 5. Loss of ilesh ; the development 
 of cache^iia is rapid. 
 
 6. Epigastric tumour is usually 
 easily detected. 
 
 ULOBE OF STOMACH. 
 
 1. Usually in young adults 
 especially women. 
 
 2. The pain is rendered worse 
 by food, and vomiting gives much 
 relief. The pain is also more 
 localised and xiphi - vertebral in 
 character. 
 
 3. Vomiting is frequent, and the 
 vomited matter contains HCl. 
 
 4. Hsemorrhage is not ^o fre- 
 quent, but is copious at times. 
 May be the fii-st symptom. 
 
 5. When the gastric symptoms 
 are severe and prolonged, a cachectic 
 appearance may develop, but never 
 to the same extent as cancer. 
 
 6. No epigastric tumour, though 
 there may be some thickening of 
 the walls. 
 
 EXAMINATION OF THE STOMACH. 
 
 In order to have a clear idea of the various disorders this 
 viscus is suhjected to, it will be necessary to recall the main 
 facts relative to the digestive processes that go on in the 
 stomach. We know that starchy foods become converted into 
 maltose, with an intermediate stage of dextrines ; proteids into 
 peptones, with an intermediate stage of albumoses; and that 
 fats are also acted upon to a slight extent, inasmuch as the 
 proteid envelopes of the fat cells are dissolved. We can easily 
 understand then, that such digestive processes can be retarded 
 by- 
 
 1. Putting into the stomach a larger amount of food 
 than it is capable of digesting. 
 
Eooamination of the Stomach. 323 
 
 2. Deficiency either in quantity or quality of gastric 
 
 secretion. 
 
 3. Deficient movements of the stomach, through 
 
 muscular atony. 
 
 It is highly necessary then, to know the exact state of 
 secretion, and the amount of motor or peristaltic power. 
 
 During the process of digestion, the stomach contents at 
 various intervals give three distinct reactions — 
 
 1. Immediately after food is taken it is faintly alkaline 
 
 from the saliva swallowed. 
 
 2. The next half-hour it reaches the neutral stage. 
 
 3. After this time it gradually becomes acid from the 
 
 presence of HCl. 
 
 The first acid to appear as a rule is lactic acid, and it must 
 be remembered that this acid is a perfectly normal constituent 
 during the first half-hour or so of digestion ; after an hour 
 there should only be the faintest traces. It must not be forgotten 
 also, that HCl is hostile to the action of bacteria ; consequently, 
 if lactic acid is found in excess two hours after a standard 
 meal, we can at once conclude that HCl is deficient. 
 
 When it is desired to ascertain whether gastric digestion is 
 normal, a test meal is first given ; then a portion of the gastric 
 contents are pumped out at various intervals through an elastic 
 oesophageal tube, and chemically examined. 
 
 Unfortunately we have no reliable test for free HCl, but if 
 we assume that HCl is the only mineral acid in the stomach, 
 then the anilLae dye, Congo-red, forms a splendid test. 
 
 Method. — Take the filtered gastric contents, add to it a 
 solution of Congo-red, the reagent immediately turns blue. 
 Wash in sether, and if the red colour be restored, the acid is 
 organic, if not, the acid is mineral, and therefore HCl is 
 present, as we assume it to be the only mineral acid present 
 in the stomach. 
 
324 Student's Hand-book of Medicine. 
 
 Uffleman's Reagent is a most convenient one for general 
 practice. The reagent is made by colouring (violet) a one per 
 cent, solution of carbolic acid, by the addition of tinct. ferri 
 perchlor. 
 
 Method. — Take filtered gastric contents, add an equal 
 quantity of the reagent. 
 
 If HCl. is normal — colour is discharged. 
 If lactic acid be present — canary yellow. 
 If butyric acid be present — dirty grey. 
 An alcoholic solution of vanillin and phloro-glucin is also 
 a good test for mineral acids, for if it be added to a sample of 
 the gastric contents, and then evaporated, a brown-pink residue 
 is left, if a mineral acid he present. 
 
 Tests for Peptone — 
 
 Characters. — 
 
 1. Like aU proteids it is — 
 
 (1) Insoluble in strong alcohol. 
 
 (2) Gives xanthoproteic reaction. 
 
 (3) Gives a pink colour reaction with copper 
 
 sulphate. 
 
 2. Unlike aU other proteids peptone is diffusible. 
 
 3. Heat does not coagulate peptone (unliJce albumin). 
 
 4. Nitric acid does not precipitate peptone {unlike albumin). 
 
 5. Pure neutral ammonium sulphate does not precipitate 
 peptone, while it precipitates albumin, globulin, and albumose. 
 
 Albumose or Fropeptone is intermediate between albumin 
 and peptone. Gives the typical reactions of proteids. Like 
 albumin it is non-diffusible. Like albumin it is precipitated 
 by nitric acid in the cold, but the precipitate dissolves on 
 heating and returns on cooling. Neutral ammon. sulphate 
 precipitates it as it does albumin. 
 
 Rennin is the milk-curdling ferment of the gastric juice. 
 Pancreatic juice contains a similar ferment. 
 
Examination of the Stomach. 325 
 
 The curdling of milk is due to the coagulation of the 
 alkali-albumin casein. Any acid will curdle milk, but rennin 
 does something more than mere curdling — it renders the curd 
 more digestible. It is a remarkable fact that rennin fails to 
 " curdle " milk if lime salts are not present. 
 
 Presence of Pepsin. — The presence of pepsin can be inferred 
 by the following process : — Take a filtered solution of the 
 gastric contents, add to it 0'2 per cent, of HClj place in 
 this solution boiled fibrin — the fibrin will be dissolved as in 
 normal gastric juice. 
 
 Vomited Matter may be tested, instead of drawing off the 
 contents of the stomach by the oesophageal bougie, but the 
 results are likely in such cases to lead to erroneous opinions. 
 
 Power of Absorption can be tested (so it is said) by 
 observing the rapidity with which KI (which has been 
 swallowed in a gelatine capsule) appears in the saliva. 
 
 Motor Power of the Stomach is estimated by testing with 
 ferric chloride for salicyluric acid in the urine at various 
 intervals after a certain quantity of salol has been taken 
 by the mouth. Salol should not be decomposed by the 
 stomach contents which are acid, but only when it meets 
 with an alkaline fluid — i.e., in the small intestines. If the 
 urinary reaction (a violet colour) is delayed beyond half-an- 
 hour, the motor power of the stomach is held to be deficient. 
 
 I have placed the foregoing tests, etc., before the reader, 
 because the student is expected to know such statements, and 
 the practitioner will find them useful in case of a consultation ; 
 but the writer has the courage to assert, that we must admit 
 these tests are of more theoretical than practical importance if 
 we duly consider their many fallacies, and the difficulty of 
 carrying them out in routine practice. 
 
 Alkalies are said to increase the secretion of HCl if given 
 before food, but the use of alkalies should not be continued 
 for an indefinite time as is only too often done. 
 
326 
 
 Student's Hand -book of Medicine. 
 
 DYSPEPSIA. 
 
 It is difficult to draw a satisfactory distinction between 
 gastritis and dyspepsia, for dyspepsia is often symptomatic of 
 gastritis. If we were obliged to draw a hard and fast line 
 of distinction, we might say — Gastritis means a diseased 
 stomach — ^,e., one in which pathological changes have taken 
 place ; dyspepsia, on the other hand, means a stomach " on 
 strike,'' a functional disturbance in fact, which may or may 
 not be highly amenable to treatment. 
 
 The following Table may assist the reader in diagnosing the 
 two conditions : — 
 
 Fain 
 
 Fever 
 
 TkwBi 
 
 Vomiting 
 
 Causes 
 
 Tongue, etc 
 
 l^orbid Anatomy. 
 
 CHRONIC GASTRITIS. 
 
 Often severe with local ten- 
 derness. 
 
 Temperature is often raised. 
 
 Often a marked symptom. 
 
 Frequent, especially in the 
 morning. . Lactic, butyric, and 
 acetic acids often present. Fain 
 is not usually relieved by vomit- 
 ing. 
 
 TTsmdly the constant intro- 
 duction of irritants, such as 
 alcohol in exeeas, abuse of tea, 
 morphia, etc. 
 
 Is furred, red at the lip and 
 edges. The lips are cracked, and 
 the gums spongy and red. 
 
 Stomach is much thickened, 
 the mucous membrane is often 
 much atrophied, and fibrous in 
 structure. It presents a rough 
 mammillated appearance with 
 suppurating points, localised vas- 
 cular areas, and hiemorrhagic 
 
 Note. — Though the membrane 
 is thickened, the essential glan- 
 dular character is atrophied. 
 
 DYSPEPSIA. 
 
 Less severe ; tendei'ness is 
 usually absent, or if present not 
 localised. 
 
 Not raised. 
 
 Absent. 
 
 Vomiting is not frequent except 
 after certam foods, then relief is 
 obtained. 
 
 See list of causes tabulated. 
 Often there is no obvious cause 
 and the best dietetic treatment 
 often fails to cure. 
 
 Tongue broad, flabby, and 
 indented by the teeth. Gums 
 are soft and anaemic. Lips are 
 not usually fissured. 
 
 In pure dyspepsia these 
 changes are not present. The 
 mucous membrane may be 
 thickened and injected. The 
 muscular fibres are pale, flabby, 
 and relaxed. 
 
Dyspepsia. 327 
 
 Causes of Dyspepsia. — 
 
 Faults on tlie part of the organs — 
 
 1. Bad teeth. 
 
 2. General dehility of the digestive organs after fevers, 
 
 etc. 
 
 3. Deficiency in the quantity or quality of the gastric 
 
 juice, pancreatic secretion, and bUe. 
 
 Faults on the part of the patient — 
 
 1. Habitual use of the same land of food. 
 
 2. Intemperance in eating and drinking. 
 
 3. Excessive use of tobacco, especially if attended with 
 
 excessive expectoration of saliva. 
 
 4. Bolting food. 
 
 5. Cold drinks during meals. 
 
 6. Mental work immediately after eating. 
 
 7. "Dirty "teeth. 
 
 8. Deficiency of food. 
 
 9. Excessive use of tea, coffee, alcohol, etc. 
 10. Sound sleep after dinner. 
 
 By the above table it will at once be seen that it is most 
 difiicult to enumerate all the causes of indigestion, but it should 
 be remembered that many persons may eat with impunity what 
 would cause much distress in others. 
 
 The more common symptoms are pyrosis, flatulence, eructa- 
 tions of acrid matters, disagreeable breath, vertigo, etc. 
 
 Many forms of dyspepsia are described, and I append a 
 table showing the principal points of the three more distinct 
 forms ; at the same time it must be remembered the table 
 is only a guide, for the types usually overlap each other. 
 
 [Table 
 
328 
 
 Student's Hand-book of Medicine. 
 
 Immediate Cause . . . 
 Fain, etc 
 
 JBructations 
 
 Urine 
 
 Testing Gastric 
 Contents shows. 
 
 Tongue 
 
 Special points . 
 
 ATONIC DTSPEPSIA. 
 
 Want of functional 
 power, both as re- 
 gards gastrio secre- 
 tion and moTements. 
 
 Some hoxirs after 
 food ; vomiting not 
 common. 
 
 CO 2 principally, 
 but may be acid. 
 
 ^formal or high- 
 coloured from urates. 
 
 Deficiency of HCl. 
 Excess of laotio aoid. 
 
 Broad, flabby, 
 
 papiUse raised, furred 
 at the back, and 
 tremulous. 
 
 Most common 
 amongst young 
 women. Apt to 
 pereifit. 
 
 BILIOUS DYSPEPSIA. 
 
 Constitutional 
 "hthsemia," vitiated 
 bile, hepatic conges- 
 tion. 
 
 Fain not marked, 
 but nausea and 
 vomiting often in- 
 tense. 
 
 HaS, Butyric aoid, 
 CO2, etc. 
 
 Hi^h - coloured 
 deposits, " gravel," 
 and oxalates. 
 
 KEttVOUB DYSPEPSIA. 
 
 Mental strain from 
 worry, over - study, 
 always being in a 
 hurry, etc. 
 
 Fain ia severe, 
 often relieved tem- 
 porarily by eating, 
 but pain recurs in 
 two hours or so. 
 
 CO 2 — generally 
 
 odourless. 
 
 Pale deposits, 
 
 amorphous phos- 
 phates. 
 
 Lactio or butyric HCl is sometimes 
 acids in excess. Bile in excess, but &&• 
 salts and pigment quently the secretion 
 may be present. is normal. 
 
 Broad also, but 
 uBuaUv covered with 
 a thick yellowish fur. 
 
 Most common 
 amongst middle-aged 
 people of generous 
 build. Faroxysmal 
 in character ,inigraine 
 and mental depres- 
 sion marked during 
 the attack. 
 
 Is usuallT clean, 
 raw beef-like in 
 character, pointed 
 tip, firm not flabby. 
 
 Most common 
 amongst literary 
 workers, speculative, 
 thin, wiry people. 
 Mental irritabihty ; 
 desire for air; art- 
 eries are tense; local- 
 ised hyperBBsthetic 
 points; sleeplessnesB. 
 
 Treatment. — Stock prescriptions and rigid diet charts 
 account for the failures in treating dyspepsia. Dyspepsia is 
 not a disease, it is symptomatic of an altered digestive tract, 
 and it is our first duty to find out the most probable cause, 
 then, having fully considered the constitution of the patient, 
 advise careful dieting, fresh air, exercise, etc. It is at all 
 times our duty to suggest the avoidance of those things we 
 know are indigestible, but he is a conceited man who thinks 
 he knows better than the patient what best agrees with him. 
 What ought to agree is often the thing that does not. If the 
 cause be obscure, and the treatment slow in producing benefit, 
 a careful examination of the gastric secretion after a standard 
 meal should be made. The main points to remember are — 
 
_ Acute Gastritis. 329 
 
 1. First allay any undue irritability of the stomach by 
 a restricted amount of food, and the administration of hydro- 
 cyanic acid, bismuth and morphine in an effervescing form. 
 
 2. Promote gastric secretion by giving alkalies before meals ; 
 or imitate the secretion by giving pepsin and hydrochloric acid 
 after meals. 
 
 3. Promote healthy peristalsis by giving muscular tonics 
 such as acid nitro-hydrochloric with liquor strychnine. 
 
 4. Keep the bowels open. 
 
 5. Avoid turning the patient's stomach into a chemist's shop. 
 
 6. If there be much fermentation and evidence of the 
 collection of ropy mucus in the stomach, wash it out and 
 give a pill containing a minim or two of carbolic acid twice 
 a day for a short period. 
 
 Eemember that a healthy co-operation on the part of the 
 patient is necessary, and this can only be obtained by showing 
 him that we thoroughly understand what is wrong. When 
 the patient is highly neurotic, a blister over the epigastrium 
 is of great value. 
 
 ACUTE GASTRITIS. 
 
 Acute inflammation of the stomach is due to the severe 
 irritation set up by the ingestion of unripe fruits, decomposed 
 tinned meats, shell-fish, etc. It is frequently a complication 
 of the malignant fevers, low inflammation, etc. 
 
 Pathology. — The mucous membranes show the usual hy- 
 persemia, exudation, and increased mucus secretion observed 
 when mucous membranes are inflamed. The various epithelial 
 cells of the numerous glands may become highly granular, 
 undergo mucoid degeneration or desquamate. There may be 
 minute extravasations of blood, haemorrhagic erosions, pustules 
 or aphthous patches. 
 
 The submucous coat is infiltrated and the whole stomach 
 wall may be congested. 
 
330 Student's Hand-book of Medicine. 
 
 Treatment — 
 
 If the irritating food is still in the stomach give a brisk 
 emetic, followed by gastric sedatives. 
 
 Ice, an effervescing mixture containing morphia, etc., wiU 
 be found very grateful to the patient. 
 
 The stomach should have perfect rest for at least twenty- 
 four hours. If it is desired to increase that rest nutrient 
 enemata may be given. 
 
 DILATATION OF THE STOMACH. 
 
 The stomach may be dilated through atony of its walls, 
 consequent on constant distension by excess of food, but it is 
 much more frequently an accompaniment of pyloric obstruction 
 as in cancer, etc., or of chronic gastritis. 
 
 Diagnosis. — 1. By the combined method of percussion and 
 auscultation, as suggested by Dr E. A. Fleming. He writes 
 " In the cases tested I used both the finger and also an ivory 
 pleximeter, and percussed with one finger. The stomach note 
 could be at once detected by the auscultating ear, whenever 
 the stroke was made over it, even though the colon overlapped." 
 
 The dilation is apt to assume a more or less U-shape, since 
 the oesophagus and pylorus are more or less fixed points. 
 
 Other methods recommended are distending the stomach 
 with carbonic acid gas, water, etc. 
 
 The vomited matter, when vomiting occurs, is said to be 
 characteristic : it is large in quantity and contains sarcinse 
 ventriculi, yeast, and other ferments. 
 
 H^MATEMESIS. 
 
 Vomiting of blood may be an important symptom in 
 many diseases. 
 
 The source of the haemorrhage may be either congested 
 and distended venules or capillaries in the gastric mucous 
 
HcemateTYiesis. 331 
 
 membrane, or through the bursting of a large vessel ; for 
 example, the splenic artery in gastric" ulcer. 
 
 Causes. — The more common are — 
 
 1. Erosion of vessels by gastric ulcer, cancer, chronic 
 gastritis. 
 
 2. Congestion of the portal circulation from any cause, but 
 especially cirrhosis of the liver, extreme backward pressure 
 from cardiac disease, cancer and other growths in the liver. 
 
 3. The action of irritant poisons. 
 
 4. Alterations in the blood, and blood-vessels by which 
 blood oozes through, as seen in malignant fevers, purpura, 
 severe jaundice, etc. 
 
 Symptoms. — Of course depend on the extent of the 
 haemorrhage ; when it is severe the symptoms of collapse 
 are marked. The attack is usually sudden, and accompanied 
 by a feeling of intense nausea and a feeling of weight in 
 the stomach. 
 
 Diagnosis. — When the hsemorrhage is not profuse it is 
 sometimes difficult to distinguish this condition from bleeding 
 from the lungs. 
 
 I append a table showing the chief differences : — 
 
 HAEMOPTYSIS. HiEMATEMESIS. 
 
 1. Previous history of pulmonary 1. Previous history of gastric 
 troubles. disturbance. 
 
 2. Blood is coughed up. 2. Blood vomited. 
 
 3. Blood is frothy and bright 3. Blood is dark-coloured and 
 red. not frothy. 
 
 4. Blood may be mixed with 4. Blood may be mixed with 
 sputa. food. 
 
 5. Dyspnoea and pains in the 5. Nausea, and weight in epi- 
 chest. gastrium. 
 
 6. Is not usually succeeded by 6. Often followed by malsena. 
 malsena. 
 
 Whilst the above differences are of the utmost value, 
 they are not always conclusive. For instance, in cases of 
 
332 Student's Hand-book of Medicine. 
 
 haemoptysis the blood is frequently not frothy, or an amount 
 of the pulmonary blood may be swallowed and vomited 
 afterwards. Again, the hEemorrhage may be so severe, so 
 sudden, and so inexplicable as regards its real cause, that 
 a hasty judgment may be quite erroneous. 
 
 Treatment. — The first thing to be decided if possible is 
 the source of the bleeding ; and secondly, whether it is 
 advisable to check the haBmorrhage, knowing that hsema- 
 temesis is so often a safety valve in portal congestion. 
 Having decided to check the haemorrhage, absolute quiet, 
 mentally and bodily, must be obtained, and no treatment 
 is more efficacious than a full hypodermic injection of mor- 
 phia, combined with the administration of ice and dilute 
 sulphuric acid. 
 
 ATROPHY OF THE STOMACH 
 
 May occur in long continued exhausting diseases, cancer of 
 the cardiac end of the stomach, bulbar paralysis, or malignant 
 stricture in any part of the CBSophagus. 
 
 DISEASES OF THE INTESTINES. 
 
 TYPHLITIS, PERITYPHLITIS, AND 
 APPENDICITIS. 
 
 By typhlitis is meant, inflammation of the csecum proper ; 
 by perityphilitis is meant a phlegmonous inflammation in the 
 cellular tissue uniting the caecum with the psoas and iliac 
 muscles ; and by appendicitis is meant inflammation of the 
 appendix cseci. 
 
Appendicitis. 333 
 
 It appears, however, that the two former conditions are 
 merely an extension of appendicitis, and it is becoming more 
 and more recognised that the terms, typhlitis and perityphlitis 
 ought to be abolished and the term appendicitis substituted 
 to include all three conditions. This may be scientific and 
 even convenient, but I think such a course open to grave 
 criticism. "We shall first consider the anatomical peculiarities 
 of this region. 
 
 1. The caecum marks the junction of the small with the 
 large intestine, the junction being guarded by the ileo-csecal 
 valve, which allows faeces, etc., to pass from the small to the 
 larger gut, but at the same time prevents regurgitation. The 
 ileum joins it on its inner aspect about two-and-a-half inches 
 above its blind end. 
 
 2. The caecum is not invested posteriorly by peritoneum, 
 but by loose cellular tissue. 
 
 3. The close proximity of the appendix cseci. 
 
 The vermiform appendix is situated at the inner lower 
 and back part of the caecum, and usually looks towards the 
 spleen. Unfortunately for clinical purposes, the exact position 
 can scarcely be diagnosed during life, and post mortem it has 
 been found in almost every region of the abdomen. 
 
 Solid bodies of all kinds may find their way into the 
 appendix. Osier asserts that " foreign bodies rarely lodge in it, 
 but that concretions of inspissated mucus and faeces in which 
 lime salts are deposited forming enteroliths are common." 
 
 APPENDICITIS. 
 
 Usually occurs in young people. 
 
 Causes. — Foreign bodies, concretions, tubercular ulceration, 
 malignant growths, constipation, habitual use of indigestible 
 food, etc. 
 
334 Student's Hand-hook of Medicine. 
 
 Pathology.— 
 
 Varieties. — 1. The catarrhal form. 
 
 2. The ulcerative variety (apt to end in 
 perforation). 
 
 In the catarrhal appendicitis the tuhe is thickened as a 
 whole, the muscular walls are somewhat thickened or fibrosed, 
 and the mucous coat is covered with a thick viscid mucus. 
 Its serous coat may become adherent to the neighbouring 
 peritoneum forming adhesive bands, which may cause a loop 
 of gut to be strangulated or to kink over it. 
 
 The ulcerative variety shows in addition to the above 
 changes, one or more ulcers ; moreover, the ulcerative process 
 is followed by most important results. 
 
 1. Perforation may occur after adhesions have formed, and 
 be followed by a circumscribed intra-peritoneal abscess. This 
 localised abscess may after a time excite a most intense 
 general peritonitis, and instead of bursting externally, open 
 into the peritoneal cavity. 
 
 2. When the appendix is not within the general peritoneum, 
 perforation produces a retro-peritoneal abscess ; in such cases, 
 the pus may burrow in the cellular tissue, between the gut and 
 the iliac fascia, and may then extend in three directions — 
 
 (1) Upwards, forming a peri-nephritic abscess. 
 
 (2) Downwards to Poupart's ligament, where it is 
 
 prevented from extending down the thigh, by 
 the union of the ligament and fascia, and so 
 bursts externally. 
 
 (3) Into the true pelvis, and then burst into the rectum, 
 
 bladder, or through the obturator foramen. 
 
 3. Perforation may occur bbfoee adhesions are formed, the 
 appendix hanging free in the peritoneal cavity. ' In such cases, 
 a speedy death results from the violent septic peritonitis. 
 
Intestinal Obstruction. 335 
 
 Symptoms. — In the catarrhal variety, the chief symptoms 
 at first are localised pain in the right iliac fossa, local tenderness, 
 elevation of temperature, furred tongue, and vomiting ; later, 
 if suppuration occurs, a tumour may be detected above Pou- 
 part's ligament, possibly occupying the whole of the right iliac 
 fossa ; it may be absolutely duU on percussion, or give a 
 modified resonant note. The pain is often paroxysmal, and 
 shoots down the right leg, which is flexed ; the tempera- 
 ture becomes septic in character ; constipation, is usually 
 a marked feature, but there may be diarrhoea, painful micturi- 
 tion, etc. In the ulcerative form, when perforation occurs 
 into the peritoneum, the symptoms are those of shock, or 
 those described under general peritonitis. 
 
 Diagnosis. — The diagnosis is often very difficult, and the 
 symptoms may simulate obstruction of the bowels very 
 closely; but in appendicitis, the tumour is diffuse, and 
 faecal vomiting is rare, or according to some authorities 
 never present. In children, the history, tenesmus, bloody 
 discharge, and rectal examination under chloroform, makes 
 a diagnosis of intussusception fairly easy, though it sometimes 
 simulates appendicitis. Psoas abscess, and pelvic cellulitis 
 in women are also conditions which must be eliminated before 
 arriving at a diagnosis. 
 
 An attack of appendicitis after passing off^ is extremely 
 likely to recur under slight provocation. 
 
 Treatment. — Palliative, as detailed under general peritonitis. 
 If the symptoms become alarming, surgical measures must 
 be adopted. 
 
 INTESTINAL OBSTRUCTION 
 
 May be due to many causes, as the following Table taken 
 from Dr Tanner's work shows. 
 
336 Student's Hand-hook of Medicine. 
 
 1. Inter-mural, or those originating in, and implicating, the 
 mucous and muscular coats of the intestinal walls. — 
 
 (1) Cancerous stricture, 
 
 (2) Non-cancerous stricture, comprising — (a) Contraction 
 
 of cicatrices, following ulcerations. (6) Contrac- 
 tion of walls of intestine from inflammation, 
 non-cancerous deposit and injury. 
 
 (3) Intussusception. 
 
 (4) Intussusception, associated with polypi. 
 
 2. Extra-mural, or those causes acting from without, or 
 affecting the serous covering — 
 
 (1) Bands and adhesions from effusion or lymph. 
 
 (2) Twists or displacements. 
 
 (3) Diverticula. 
 
 (4) External tumours or ahscesses. 
 
 (5) Mesocolic and mesenteric hernia. 
 
 (6) Diaphragmatic hernia. 
 
 (7) Omental hernia. 
 
 (8) Obturator hernia. 
 
 3. Intro-mural, or obstructions produced by the lodgment 
 of foreign substances — 
 
 Foreign bodies, hardened fseces, concretions having for 
 their nuclei, gall-stones, etc. 
 
 As the subject of intestinal obstruction really belongs to the 
 domain of surgery, only the main clinical points wUl be con- 
 densed here. 
 
 The obstruction may be of an acute or chronic nature. 
 
 General Symptoms of any Complete Obstruction. — The 
 
 more common are pain, distension of the abdomen, and 
 stercoraceous or fsecal vomiting, with complete constipation. 
 
 The pain is variable, but is usually intense, at first par- 
 oxysmal, but later, continuous. It is not always referred to 
 the part obstructed. 
 
Intestiiial Obstruction. 337 
 
 The constipation is absolute, but the bowel below the 
 stricture may pass faeces, or the masses may be removed by an 
 enema. 
 
 The vomited matter consists at first of the stomach contents, 
 then bilious matter, and finally faecal matter, which may in 
 addition be tinged with blood. 
 
 The patient, if unrelieved, falls into a typhoid state from 
 intense peritonitis, etc., and usually succumbs in from four to 
 six days after the onset of the severe acute symptoms. 
 
 Special Forms of Obstruction. — 
 
 I. INTUSSUSCEPTION. 
 
 Occurs most frequently at the ilio-csecal valve. Usually the 
 ileum and caecum preceded by the valve, pass into the larger 
 colon. The valve forms the apex of the intussuscepted gut, 
 and is an important aid to diagnosis on rectal examination. 
 
 Causes. — Severe and sudden peristalsis, especially in young 
 children. 
 
 Special Symptoms. — A sausage-like tumour felt through the 
 abdomen, glairy mucoid and bloody discharge, and tenesmus. 
 Spontaneous reduction may take place, or the gangrenous 
 invaginated portion may slough and pass per anum. 
 
 Treatment. — Inversion of the patient, gentle manipulation 
 under chloroform, and copious injection of hot water into the 
 rectum may be tried prior to laparotomy being performed. 
 
 II. VOLVULUS. 
 
 Is a twisting or bending of a coil of intestine in such a 
 manner that its calibre is obliterated at that spot. Is most 
 common in the sigmoid flexure, and towards the back of the 
 abdominal cavity. 
 
338 Student's Hand-hook of Medicine. 
 
 Special Symptoms. — Volvulus furnishes the most typical 
 symptoms of acute obstruction. 
 
 Treatment. — If it can be diagnosed with a fair amount 
 of precision, palliative measures may be tried for a longer 
 period than in strangulated hernia, as the twist is very likely 
 to recur after being replaced. 
 
 III. IMPACTION OF F^CKS, AND OTHER 
 FOREIGN BODIES. 
 
 Treatment. — Try clearing out the lower bowel with copious 
 enemata, breaking up hardened faeces, massage under chloroform, 
 etc., prior to laparotomy. 
 
 It will be seen from the foregoing statements, that as the 
 relief of intestinal obstruction usually resolves into surgical 
 measures, the reader should look for details of these important 
 conditions in a work on surgery. As, however, these cases 
 frequently first come under the notice of the physician, and 
 also as the patient and his or her friends frequently object to 
 operative measures, the physician must take a determined stand 
 or attitude ; for he must remember every hour of delay in 
 obtaining relief is fraught with extreme danger, and he should 
 therefore lose no time in advising laparotomy the moment he 
 is convinced that the obstruction is complete. We may, how- 
 ever, temporise in cases of faecal accumulation, and in the more 
 chronic forms of intestinal obstruction met with in old people, 
 in malignant disease, etc., where surgical measures are little less 
 than hopeless. 
 
 When we decide to temporise, we must put the patient 
 under the most favourable circumstances we can — alleviate the 
 pain by opium, the distressing vomiting by ice, and apply hot 
 fomentations to the tender abdomen. No cases require graver 
 thought than intestinal obstruction, and if there be the slightest 
 chance of only temporary relief by surgical procedure, the 
 patient should have his choice. 
 
Enteritis. 339 
 
 ENTERITIS. 
 
 It is somewhat difficult to define what is meant by enteritis, 
 for the mucous membrane of the intestines is inflamed in very 
 many diseases, especially in cholera, typhoid fever, dysentery, 
 etc. But we may assume at present, that by enteritis is meant 
 an inflammation of the alimentary tract, due to irritation 
 by indigestible food, or a general catarrhal condition following 
 exposure to cold, etc. 
 
 Like all other inflammations of mucous membranes, we may 
 get the following varieties — 
 
 1. The ordinary, or catarrhal inflammation. 
 
 2. The croupous or fibrinous form, when the inflammatory 
 exudation is unusually rich in fibrin, and tends to coagulate. 
 
 3. The phlegmonous type ; when the sub-mucous coat is 
 deeply involved, and presents a number of suppurative points 
 which burst and form ulcers. 
 
 INTESTINAL CATARRH. 
 
 Acute Catarrh is most frequent in the hot summer months, 
 possibly because of the ingestion of large quantities of unripe or 
 decomposed fruit, sour milk, etc. We must, however, admit, 
 that excessive decomposition in the intestines forms a favour- 
 able nidus for the multiplication of bacteria, which otherwise 
 would lie dormant. 
 
 Pathology. — The more marked changes are observable in 
 the ileum as hyperBsmia of the valvules conniventes, a swollen 
 condition of the solitary glands which project like small shots, 
 and frequently present ulcerated surfaces. The mucous secretion 
 is much increased, and a slight amount of pus may be formed. 
 
 Chronic Catarrh most frequently is due to alcoholism, 
 portal congestion, atony of the gut from constitutional diseases, 
 habitual constipation, etc. 
 
340 Student's Hand-book of Medicine. 
 
 Pathology. — The more marked changes are observable in 
 the large gut. The mucous membrane is much thickened, often 
 pigmented, and shows extensive small follicular ulcers, which 
 after healing give a peculiar worm-eaten character to the gut 
 on holding it up to the light. The superficial veins are dis- 
 tended, piles are often prominent in the rectum, and polypoid 
 outgrowths may spring from the mucous surface. 
 
 Symptoms of Acute Enteritis. The chief symptoms are — 
 
 1. Diarrhoea. 
 
 2. Abdominal pain, especially around umbilicus. 
 
 3. Nausea, anorexia, and vomiting. 
 
 4. Pyrexia. 
 
 The above are the so-called cardinal symptoms, but it does 
 not need a genius to at once grasp that the inflammatory 
 condition, if severe, is likely to be complicated with peritonitis. 
 Taking a typical case of enteritis, the diarrhoea is the chief 
 symptom, and as in such cases excessive decomposition takes 
 place in the intestines, we naturally expect the stools to be 
 offensive, and to consist principally of undigested food, 
 epithelial debris, triple phosphates, biliary pigments, and 
 mucus. A word of caution is necessary, however, as regards 
 bile pigments. The faeces may appear to contain an excessive 
 amount of bile through the haste with which the duodenal 
 contents are hurried on ; or on the other hand, the same catarrh 
 that caused the enteritis may block up the common bile duct 
 and prevent the bUe from entering the bowels, in which case 
 the feces will be pale and clay-like, and a subsequent jaundice 
 may develop. Without a careful examination of the stools, it 
 is impossible to diagnose whether the morbid process is confined 
 to the duodenum, jejunum, or ileum. 
 
 Treatment. — First clear out any offending matter with 
 castor oil. Believe pain with an hypodermic injection of 
 morphia, and the application of hot poultices or turpentine 
 
Biarrhoea. 341 
 
 stupes to the abdomen. An effervescing mixture containing 
 hydrocyanic acid and bismuth is useful in allaying undue 
 irritability of the stomach. Salol or ^s-napthol are our best 
 intestinal disinfectants. 
 
 Symptoms of Chronic Enteritis. — 
 
 1. Haemorrhoids. 
 
 2. Constipation, alternating with diarrhoea. 
 
 3. Discharges of blood and mucus from the anus. 
 
 The faeces do not present the same "undigested food" 
 character as in acute enteritis, but there is more tenesmus 
 or violent straining at stool. The fseoes often resemble the 
 chronic dysenteric stools — viz., boiled sago streaked with blood; 
 but, unlike dysentery, the diarrhoea is easily provoked by hot 
 liquids, and only too often by any meal ; this shows that the 
 irritable state of the gut is by no means localised to the large 
 gat, though the more marked pathological changes occur in that 
 part of the alimentary canal. 
 
 Treatment. — Remove any obvious cause. Salol in 15 grain 
 doses nightly, with the addition of 3 minims of liq. arsenicalis 
 and 10 minims of tinct. opii before each meal, occasionally act 
 like a charm. If these measures do not succeed, treat according 
 to the principles laid down under "Chronic Dysentery." 
 
 DIARRHCEA. 
 
 We have already seen that the frequent passage of 
 loose motions from the bowels occur in many diseases, but 
 whilst diarrhcEa is often associated with grave lesions of the 
 intestines, such as cancer, typhoid, tubercular ulcers, enteritis, 
 etc., it may come on without any apparent cause, or after 
 slight nervous disturbance, fright, etc.; in other words, diarrhoea 
 may be merely a functional disorder, or symptomatic of a grave 
 disease. 
 
342 Student's Hand-hook of Medicine. 
 
 Causes. — Increased discharge of feces can be induced by — 
 
 1. Increasing the intestinal secretions. 
 
 2. Exciting peristalsis, directly through irritants, or indirectly 
 through the nervous system. 
 
 The more common causes independent of actual disease of 
 the intestines are — eating indigestible food, unripe fruit, etc.; 
 drinking cold liquids ; certain nervous states, especially at the 
 climacteric period. I once had a patient who had an attack of 
 diarrhoea every Friday night after making his weekly visit to 
 his bakehouses; the change from cold to heat was evidently 
 the cause in this case. 
 
 Diagnosis. — It is not always easy to say whether the 
 diarrhoea is a mere temporary disturbance, or the evidence of a 
 disease, acute or otherwise. In all cases note — 
 
 1. How the looseness commenced. 
 
 2. The consistency, colour, and odour of the faeces. Look 
 for blood, fat, calculi, etc. 
 
 3. Pain and abdominal tenderness. 
 
 4. The amount of pain at the time and immediately after 
 defaecation. 
 
 Treatment. — Having satisfied ourselves that the diarrhoea is 
 due to an irritant or irritating products still in the gut, clear 
 out the bowels with a full dose of castor oil, then we may give 
 opium in various forms, a full dose of the tincture, Dover's 
 powder and bismuth, chalk mixture, etc. 
 
 Broadly speaking, acute diarrhoea is best treated with alkalies 
 and opium ; chronic diarrhoea with astringent minerals, or acids, 
 with opium. Hot fomentations to the abdomen, diffusible 
 stimulants if the patient feels chilly, and a restricted diet, are 
 the main points to be remembered. 
 
 In that form of diarrhoea which comes on immediately after 
 food in nervous people, nothing succeeds better than two 
 
Ascites. 343 
 
 minims of liq. arsenicalis with five minims of laudanum, given 
 just before meals. 
 
 Diarrhoea in young children or infants, if not associated 
 with other diseases, such as rickets, tubercular conditions, 
 etc., is nearly always due to improper feeding, or irritation 
 from worms. 
 
 DISEASES OF THE PERITONEUM. 
 
 ASCITES. 
 
 Ascites or dropsy of the peritoneum is not a disease of itself, 
 but merely symptomatic of some condition which causes an in- 
 creased transudation of fluid into the peritoneum. Dropsy means 
 some abnormal changes in the blood-vessel walls, either the result 
 of inflammation, vaso-motor paralysis, or obstruction ; and since 
 we know that the venous blood of the intestines is returned 
 via the portal circulation, we naturally look for the more 
 common causes of ascites in morbid states of the portal vein ; 
 but it must be remembered that inflammatory changes of local 
 blood-vessels in connection with morbid processes set up in the 
 peritoneum and various abdominal organs, tend to bring about 
 dropsy of the peritoneum. It is highly important to remember 
 that the causes of ascites are not confined to obstruction of the 
 portal vein, sometimes the dropsy is of local inflammatory 
 origin, and the fluid is then frequently collected into localised 
 pools — i.e., within the mesh-work of inflammatory adhesions. 
 The typical signs of ascites are often masked by the large 
 deposits of inflammatory lymph between the intestines, etc. 
 
 Causes. — The more common causes of ascites tabulated are — 
 1. Portal obstruction, either within or outside the liver, 
 
344 Student's Hand-book of Medicine. 
 
 2. Phlebitis of the portal vein. 
 
 3. Disease (usually malignant or tubercular) of the peri- 
 toneum itself. 
 
 4. Morbid states of the blood associated with renal disease, 
 leucocythsemia, etc. 
 
 It must be remembered that obstruction of a vein does not 
 of itself produce dropsy until some retrograde change is set up 
 in the walls of the vessels. Obstruction must of course produce 
 such changes in time. 
 
 Under portal obstruction, we may mention cirrhosis of the 
 liver, neoplasms of the liver, pancreas, spleen, etc.; malignant 
 disease of, or growths in connection with the intestines, and 
 other abdominal organs. 
 
 When ascites is caused by cardiac or pulmonary disease, 
 probably it is due to two factors, viz., portal congestion, and 
 a deteriorated character of the blood. 
 
 Diagnosis. — The cardinal symptoms are — 
 
 1. Enlargement of the abdomen : the skin is tense and 
 shiny with dilated superficial veins on the surface. 
 
 2. Fluctuation, and vibration on palpation. 
 
 3. Percussion yields a dull note, which alters on the patient 
 assuming a new position of the body. 
 
 4. The above conditions are associated with anasarca, and 
 other symptoms of dropsy elsewhere. 
 
 When the patient lies on the back, the dulness on percussion 
 is most marked in the flanJcs / whilst the note is resonant at the 
 umbilicus. Turn the patient on the side, the fluid moves to 
 the most dependent part, and consequently a resonant note may 
 be obtained in the opposite flank. 
 
 Caution, however, is necessary as regards this resonance; 
 it may be absent through adhesions binding the intestines 
 
Ascites. 
 
 345 
 
 down to the posterior wall ; or the fluid may not gravitate, 
 because of being hemmed in by inflammatory lymph. On the 
 other hand, if the fluid be small in amount and the distension 
 of the intestines marked, the dvlness may be diflScult to 
 demonstrate. 
 
 Treatment. — Seek the primary disease, and direct the 
 treatment to improving the general health of the patient 
 on the principles already laid down under hepatic disease. 
 
 If the fluid causes much dyspnoea, or other symptoms, the 
 fluid should be evacuated by Southey's tubes, or by tapping. 
 It must not be forgotten that in old cases, the vessels of the 
 abdomen may be so far devitalised, that a sudden removal of 
 the support afforded them by the dropsical fluid causes them 
 to become engorged with blood, and set up fatal syncope. 
 
 OVARIAN TITMOTJE. 
 
 1. Growth begins on 
 one side. 
 
 2. Slow growth. 
 
 3. Fiuctnation general 
 over the tumour. 
 
 4. No eigna of preg- 
 nancy and health de- 
 teriorated. 
 
 DIAGNOSTIC TABLE. 
 
 PKEGNANCT. 
 
 1. Begins in median 
 line. 
 
 2. Uniform and de- 
 finite rate. 
 
 3. Fluctuation absent 
 except in hydramnios. 
 
 4. Signs of pregnancy 
 and health normal. 
 
 1. Fluid moves on alter- 
 ing position. Swelling is 
 uniform. 
 
 2. May be rapid or 
 not. 
 
 3. Fluctuation general 
 over the whole abdomen. 
 
 4. No signs of preg- 
 nancy, and health much 
 impaired. 
 
 In all cases an examination should be made of the ascitic 
 fluid, both microscopically and macroscopically. 
 
 Ordinary Ascitic Fluid. — Is light yellow or straw coloured, 
 of generally 1010 sp. gr. ; contains albumin. In chylous 
 ascites associated with disease of the pancreas and lacteals, 
 the fluid is turbid and milky, exhibiting oil globules. In 
 malignant ascites, the fluid is often dark from the presence of 
 blood. "Cancer" cells may be discovered under the micro- 
 scope. 
 
34:6 Student's Hand-book of Medicine. 
 
 PERITONITIS. 
 
 Inflammation of the peritoneum may be either of an acute 
 or of a chronic nature. Eecent and extensive observations 
 in the mortuary go to show that primary or idiopathic 
 peritonitis is seldom or never seen. In order to understand 
 this, I cannot do better than borrow Dr Fagge's words : " The 
 peritoneum is a huge areolar space or lymph sac, and its most 
 intimate pathological relations are not with skin or mucous 
 membrane, not even with joints, or the so -called arachnoid 
 space, but with pleura, pericardium, and tunica vaginalis ; all 
 of which parts are embryologicaUy parts of the great body 
 cavity, formed by the splitting of the mesoblast into somato- 
 pleurse and splanchno-pleurae. The diseases of these three 
 divisions of the same original cavity are the same : acute 
 inflammation, serous or purulent, traumatic or septic, chronic 
 irritative effusion and passive dropsical effusion, hydjothorax, 
 hydropericardium, and ascites ; chronic adhesive inflammation 
 with hypertrophy. All three are liable to be invaded by 
 tubercle and also by cancer. AU three are prone to follow 
 the pathological fate of the viscera which they cover ; they 
 are all apt to suffer in the course of Bright's disease, and, 
 lastly, they are often all affected together by inflammation, by 
 tubercle, or more rarely by cancer. (Second edition of Fagge's 
 Medicine.) 
 
 A peritonitic effusion differs, however, from pleuritic effusion 
 in showing a strong tendency to become purulent. Possibly 
 this purulent state is to be explained by the close proximity 
 of the septic intestinal contents. 
 
 Varieties. — 1. Acute — divided into 
 
 (a) Local ) •, ., . 
 (6) General }P^"*°^^t^« 
 
Peritonitis. 347 
 
 3. Subacute — in which form, attacks are nearly always due 
 to the action of local irritation. 
 
 3. Chronic. — This form is usually due to irritation from 
 specific, infective, or malignant growths — e.g., chronic dysentery, 
 tuberculosis, syphilis, cancer, etc. 
 
 Symptoms. — The symptoms of a general acute peritonitis 
 present a most characteristic clinical picture, the main features 
 of which are — 
 
 1. Great pain and tenderness over the abdomen, which is 
 usually tense from tympanites. 
 
 2. Quick, wiry and incompressible pulse. 
 
 3. Facies Hippocratica — i.e., "a sharp nose, hollow eyes, 
 collapsed temples ; the ears cold, contracted, and their lobes 
 turned out; the skin about the fore-head being rough, distended 
 and parched ; the colour of the whole face being brown, black, 
 livid, or lead colour." Face is also anxious. 
 
 4. Constipation. 
 
 5. Vomiting. 
 
 6. Dry, small red tongue. 
 
 7. High fever. (1) 
 
 The abdominal tenderness is sometimes so marked, that the 
 slightest touch or even the respiratory movements — sneezing, 
 passing ilatus, and coughing — causes exquisite agony. Possibly 
 the constipation, and the small wiry pulse, may be due to 
 paralysis of the splanchnic nerves. Whilst the above are the 
 cardinal symptoms of a general acute peritonitis, it must not 
 be forgotten that the temperature may be sub-normal, diarrhcea 
 be present instead of constipation, and the patient's face may 
 be actually apathetic instead of anxious. This latter state is 
 probably more frequent when the -peritonitic fluid speedily 
 becomes purulent, as seen in some oases of puerperal fever, 
 typhoid fever, and strangulated hernia. 
 
348 Student's Hand-book of Medicine. 
 
 Causation. — Nearly always secondary to perforations of 
 some viscus, gastric ulcer, typhoid ulcer, obstructed bowel, 
 etc. ; or to extension of inflammation of neighbouring parts, 
 such as ovaritis, salpingitis, parametritis, etc. ; or to blood 
 poisons, such as malignant fevers, especially puerperal fever; 
 
 or to morbid state of the blood, as seen in Bright's disease, etc. 
 
 t 
 
 Pathology — 
 
 1. Hypersemia with loss of lustre : the hypersemia is most 
 marked where the intestinal coils are not in close contact 
 with one another. 
 
 2. Exudation of lymph, giving a more or less shaggy 
 appearance. 
 
 3. Effusion of fluid, which may be highly fibrinous and 
 coagulates easily, forming extensive adhesions ; or which may 
 become 
 
 4. Eapidly purulent. 
 
 Prognosis. — Depends largely on the cause. When the 
 result of perforation and extravasation of blood into the 
 peritoneal cavity, the condition may be fatal in a few hours. 
 It is of course much more favourable when the peritonitis is 
 localised. 
 
 Treatment. — Give full doses of morphia or opium, one 
 to two grains of the latter may be given every four hours 
 until pain and peristalsis are quite subdued. Hot fomentations, 
 if they can be borne, to the abdomen ; ice or leeches are 
 advised by some. As the knees are usually drawn up to 
 relax the abdominal walls, we may add to the patient's comfort 
 by placing a soft pillow under the hams. Ice to swallow is 
 often most grateful. "Avoid purgatives" — this is a golden 
 rule ; but the lower gut may be often emptied with advantage 
 by an enema of hot water. When the acute symptoms sub- 
 side, and the danger of collapse is diminished, if there be 
 reason to suspect pus formation, laparotomy should be per- 
 formed, and the whole cavity treated as a huge abscess. 
 
Peritonitis. 349 
 
 Chronic Peritonitis includes at least four well marked, 
 types — i.e., — 
 
 1. Peritonitis, as a result of the invasion and subsequent 
 breaking down of tubercles. 
 
 2. A form associated with, and due to irritation of 
 malignant growths. 
 
 3. A localised form associated with chronic inflammation, 
 diseases of certain organs — i.e., the uterus and appendages — 
 chronic constipation, and other affections of the lumen of the 
 intestines. 
 
 4. A form which tends to occur at more or less definite and 
 regular periods without any obvious cause. 
 
 Symptoms vary with the cause, the extent of the effusion, 
 and adhesions. 
 
 Constipation alternating with diarrhoea, colicky pains, loss 
 of flesh, exacerbations of fever, and localised tenderness, are 
 the chief symptoms complained of. 
 
 Though ascites is often prominent, much more frequently 
 the fluid is collected into small pools in the meshes of the 
 bands Of lymph. 
 
 The mesentery is usually much shortened, and the calibre of 
 the gut diminished. 
 
 Physical Examination. — May reveal hard masses of tuber- 
 cular or malignant growths, etc. The abdomen may be either 
 flat and dull, or distended and resonant. 
 
 Treatment. — First seek the cause, and if possible remove it, 
 but obviously, when dependent on tubercle, etc., all that can be 
 done is to allay painful symptoms. Massage, with the ad- 
 ministration of the iodides and tonics, may be of use. It must 
 not be forgotten that chronic peritonitis is often fatal through 
 an acute exacerbation of inflammation. 
 
350 Student's Hand-book of Medicine. 
 
 TABES MESENTERICA. 
 
 Is a disease due to tubercular degeneration of the mesenteric 
 glands. Though associated with tubercular peritonitis, it may 
 be a primary disease, especially in infants and young children. 
 
 Pathology. — The glands are much increased in size, and all 
 stages of tuberculosis may be seen ; in some cases, the glands 
 are soft from fatty or caseous degeneration ; others, again, 
 show a great increase of the fibrous tissue elements, and 
 may consequently be harder than normal. 
 
 Symptoms. — A condition which so seriously interferes with 
 the lacteal absorption, must of necessity cause grave symptoms 
 of mal-nutrition ; and indeed, the cardinal symptoms of tabes 
 mesenterica may be summed up — as great wasting of the limbs, 
 thorax, and face, with a large abdomen, unhealthy action of the 
 bowels, and general exhaustion. The abdomen may be (as 
 pointed out in Chronic Peritonitis) either resonant or dull. 
 The enlarged glands can be distinctly felt, and ascitic fluid is 
 often present. Diarrhoea usually alternates with constipation. 
 The stools are slimy and pasty in character; they often 
 contain undigested milk, fat globules, and sometimes much 
 brown pigment. 
 
 Diagnosis. — Care must be taken not to diagnose as tabes 
 mesenterica, those cases of mal-nutrition with large abdomen, 
 the result of improper feeding, congenital syphilis, and rickets. 
 A careful examination of the abdomen should prevent such 
 mistakes. 
 
 Treatment. — Everything must be done to put the child 
 under the most favourable hygienic conditions, as detailed 
 under Rickets. Iodide of iron is often most useful. Iodoform 
 applied at night to the abdomen, in the form of an ointment 
 spread on strips of calico, followed by gentle massage in the 
 morning, sometimes does a great deal of good. 
 
Animal Parasites. 351 
 
 PAEASITES AND PARASITIC DISEASES.* 
 
 Definition. — Parasites are low forms of organisms — animals 
 or vegetables — which infect other animals or plants, lodging 
 upon them or within them, and deriving their nourishment 
 from the tissues and juices of their host. 
 
 Division. — Parasites are divided into two great classes — 
 
 1. Animal Parasites. 
 
 2. Vegetable Parasites. 
 
 ANIMAL PARASITES. 
 
 General Characters. — Animal parasites belong to the lowest 
 types of the animal kingdom and are characterised by the 
 greater simplicity of their structure as compared with that 
 of the allied nonparasitic forms. 
 
 Life History. — 
 
 1. Metamorphosis. — Most animal parasites exist in two or 
 more forms ; the immature, larval, or embryonic form, and 
 the mature form. Many of them undergo a series of 
 changes — alternation of generation — before reaching maturity ; 
 first, by sexual union producing ova which give rise to 
 embryoes or larva, which ultimately develop into adult forms, 
 or by a process of budding, produce colonies of the mature 
 organisms. 
 
 2. Host. — The animal infected by the parasite is called 
 the host. 
 
 * I am miioh indebted to my friend Dr Eyland Whitaker for valuable 
 help in this portion on Parasites and Parasitic Diseases. 
 
352 Student's Hand-book of Medicine. 
 
 3. Intermediate Host is the organism in which the im- 
 mature forms are lodged. 
 
 4. Habitat. — Is the part of the body of the host in which 
 the parasite, or its immature form, takes up its abode. 
 
 CESTODA. 
 
 ( Keo-tos — a gii'dle. ) 
 
 The Cestoda are all endoparasitic worms and infect the 
 intestinal canal of vertebrata. 
 
 General Characters. — The Cestodes differ from the 
 Trematodes in being multiple in character. The tape-worm 
 is not a single individual, but a multitude of organisms 
 arranged in a chain, thus forming a compound jointed colony. 
 
 1. Shape. — The Cestoda are compound, flat, parasitic 
 worms. 
 
 2. Size. — ^Varies much : some forms measure ^ of an 
 inch, others 24 feet in length. 
 
 3. Structure. — The adult worm or Strobilus consists 
 of a number of complete sexual individuals arranged in a 
 chain. We have— 
 
 (1) The Head or Nurse, which is usually small in size, 
 pyriform in shape and has one or two suckers surrounded 
 by a riag of chitinous booklets, to enable the worm to cling 
 to the intestines of its host. It has neither an alimentary 
 system nor sexual organs. 
 
 (2) The Proglottides. — These are a series of segments 
 produced one behind the other by a process of budding from 
 the head or nurse. Each segment or proglottis resembles 
 its neighbours except in size and degree of maturity. The 
 segments furthest from the head are the oldest, the largest, 
 and most mature; the segments next the head being im- 
 mature and having no sexual organs. In an ordinary 
 tapeworm there may be as many as 1200 of these segments. 
 
Cestoda. 353 
 
 Each proglottis has a complete water-vascular system, 
 composed of parallel canals running on each side of the 
 body, and united at the hinder end of each segment by 
 cross branches. The proglottides have no digestive organs 
 of any kind, being nourished by imbibition. They are 
 hermaphrodite, and produce ova by sexual union with the 
 proglottides of other cestodes. A single proglottis may 
 contain as many as 35,000 eggs. 
 
 Life History. — As above stated, the ova of the cestoda 
 are produced in the proglottides, which when ripe break off 
 from the rest of the chaia and are cast out by the body of 
 their host. Within these ripe proglottides the ova are already 
 partially developed, and when ejected are fuU of active embryoes. 
 These embryoes are enclosed in a membrane to protect them from 
 injury, and consist of a head furnished with three pairs of 
 sUicious spines or booklets. By the decomposition of the 
 proglottides the embryo-bearing ova are set free, reach water, 
 and thence find their way into the stomach and intestines of 
 their host. 
 
 The membrane enclosing the embryo is now ruptured 
 mechanically, or digested by the gastric juice, and the em- 
 bryoes are liberated. They are called prosoolexes (scolex, 
 a worm), and consist of a small vesicle with three pairs of 
 silicious spines. By means of these booklets the proscolex 
 fastens itself to the intestinal wall, bores through it, and 
 makes its way to the liver or other organ of its host. Here 
 it becomes encysted, loses its hooks, and from its hinder end 
 develops a small vesicle fuU of fluid. 
 
 It is now called a scolex which in some tseniada are 
 known as hydatids, in others as cysticercus. When thus 
 encysted, the scolex is composed of a vesicle united by a 
 narrow neck to a head similar to that of the adult tape worm, 
 being armed with a circlet of booklets, and having four 
 oscula or suckers. It has no reproductive system, nor, 
 in fact, organs of any kind, and can undergo no further 
 
 2 B 
 
354 Student's Hand -hook of Medicine. 
 
 development unless it gains entrance into the intestinal canal 
 of man or other host. This is effected by an animal eating 
 flesh, etc., containing the scolices, when the cysts are digested 
 and the scolices set free. They at once lose their caudal 
 vesicle, attach themselves to the intestinal ■wall of their 
 host hut do not perforate it, and in this situation soon 
 become the head of the future tape-worm and begin to 
 produce proglottides which again pass through the cycle 
 of development above described. Thus we have — 
 
 1. The Ova discharged from the ripe proglottis. 
 
 2. The Proscolex. — The minute embryo liberated from the 
 ova when taken up from water, etc., by some animal. 
 
 3. The Seolex. — The more advanced, but still sexually im- 
 mature, embryo into which the proscolex develops when it has 
 become encysted in the tissues. 
 
 4. The Strobilus or adult tape-worm, infecting the ali- 
 mentary canal of its host, and composed of a head, neck, 
 and proglottides. 
 
 Division — The Cestodes which infest man are — 
 
 1. Toeniada — 
 
 (1) Taenia solium. 
 
 (2) Tsenia mediocanellata. 
 
 (3) Tsenia echinococcus. 
 
 2. Bothrioeephalida — Bothriocephalus latus. 
 
 I.— T^NIA SOLIUM. 
 
 Synonyms — Tsenia oucurbitina, Ttenia humana arniata, 
 
 Tsenia lata, Tsenia vulgaris. 
 ■Larva — Simple seolex, Measle, Cysticercus cellnlosse. 
 
 General Characters. — 1. Size — The adult worm or stro- 
 bilus measures about 2 to 10 feet long. 
 
 2. Shape — It has a small head, long narrow neck, and 
 transversely segmented body. 
 
Cestoda. 355 
 
 3. Structure — 
 
 The Head is small, rounded, about the size of a pin-head, 
 and consists of rostellum or beak with twenty-six booklets, 
 and of a wider part on which are four suckers. 
 
 Body. — Next the head comes a long, narrow, thread-like 
 neck, followed by a series of larger segments — the proglot- 
 tides. At first the segments are broader than they are long, 
 and are immature — the remaining segments are the reverse, 
 longer than broad, and are' sexually mature proglottides. 
 These proglottides are hermaphrodite, the genital orifices 
 being placed alternately on each side of the body, and the 
 male and female organs open by this common genital pore. 
 They have a complete water-vascular system. 
 
 The Ovary consists of a central stem, with a number of 
 lateral branches, each of which again branches. The testes 
 appear as clear, white, convoluted tubes, with vesicles. 
 
 Ova are nearly spherical in shape, about ^-i^ inch in 
 diameter, and are surrounded by a dense capsule which 
 encloses the partly-developed, six-hooked embryoes. These 
 embryoes give rise to the scolices in the flesh of the pig, 
 the scolex in this case being called a " measle," or cysti- 
 cercus cellulosse, or bladder-worm. 
 
 Life History — As above described. 
 
 Intermediate Host. — The pig, which gets the embryoes 
 from water — the scoKces forming the " measles " of pork. 
 Within these measles or cysts, the booklets, which do not 
 decompose, are often found after the scolex has perished. 
 They are short, broad, hook-shaped bodies, with a small knob 
 at their base. 
 
 Host. — Man; owing to eating imperfectly cooked, measly 
 pork. It infects man, not only as the mature worm, but as 
 cysticerci. The adult worm is found in man only. 
 
 Habitat. — The immature worm is found in subcutaneous 
 tissues, muscle, brain, eye, liver of the pig ; the mature form, 
 in the small intestine of man. 
 
356 Student's Hand-hook of Medicine. 
 
 II.— TAENIA MEDIOCANKLLATA. 
 
 Synonyms— Txaia, saginata, Tsenia dentata, Tsenia inermis, 
 
 Beef tape-worm. 
 
 Larva — Cysticercus bovis. 
 
 General Characters — 
 
 1. Size. — Larger than tsenia solium, Both in length and 
 breadth, often measuring from 14 to 24 feet. 
 
 2. Strdcture — 
 
 The Head has four suckers, but no rostellum nor hook- 
 lets. Following the head is a narrow neck, and then the 
 several segments or proglottides. 
 
 The Ovaries consist of many lateral processes, but these 
 do not, as in the case of tsenia solium, again branch, a char- 
 acter by which the proglottis of the one can be distinguished 
 from that of the other. 
 
 Ova — Similar to those of tsenia solium. 
 
 Life History — Similar to that of tsenia solium. 
 Intermediate Host. — Cattle. 
 Host. — Man. 
 
 Habitat. — Immature form, in the muscles of cattle : as many 
 as 300 having been found in a pound of flesh taken from psoas 
 muscles. 
 
 The mature form occurs in the intestine of man. 
 
 III.— BOTHRIOCEPHALUS LATUS. 
 
 Synonyms — Broad tape-worm, Tfenia lata, Taenia grisea, 
 Dibothrium latum. 
 
 General Characters — 
 
 1. Size. — The largest known human tape-worm. It measures 
 from 16 to 25 feet long, and about 1 inch broad, and consists 
 of three or four thousand segments. 
 
Cestoda. 357 
 
 2. Structure. — The Head is small, oval or club-shaped, 
 with a longitudinal groove or slit on each side. It has neither 
 proboscis, nor suckers, nor booklets. 
 
 The Proglottides are about 4000 in number, the ^largest 
 being in the middle of the chain. They are each bi- sexual. 
 The uterus consists of a simple, coiled-up tube, and the genital 
 orifices are placed along the middle line of the ventral aspect — 
 not on the sides, as in the last group. 
 
 The Ova are oval in shape, and about ^^ of an inch long. 
 They have an operculum and a brown coloured shell. 
 
 Life History — ^The ova are set free in the body of the host, 
 and on reaching water are there hatched. The proglottides 
 themselves are not discharged from the intestine as is the case 
 with taenia solium. The embryo, which has a ciliated envelope, 
 swims about in the water till the envelope bursts and liberates 
 six-hooked embryoes. These make their way into the muscles 
 of some fresh water fish, and there develop into the asexual 
 larval worm. 
 
 If the fish be eaten by man, the larva develops into the 
 sexual form above described. 
 
 Intermediate Host. — Probably certain fish, as pike, turbot,etc. 
 
 Host. — Man, dog. 
 
 Habitat. — Intestinal canal. 
 
 Effects — Intestinal catarrh in children, but no serious effects 
 in the adult. ■ 
 
 Distribution — Germany, Eussia, Poland, Sweden, Holland, 
 Belgium, Ireland, England, France. 
 
 Symptoms due to either of these three worms. 
 
 Frequently they give rise to no symptoms : there are in fact 
 no pathognomonic symptoms ; but certain reflex disturbances 
 are common, such as itching of the nose or anus, colicky pains, 
 constipation alternating with diarrhoea, mental trouble, such as 
 
358 Stvdent's Hand-book of Medicine. 
 
 melancholia, epilepsy, etc., voracious appetite, and painless vomit- 
 ing which may simulate brain disease. I have known all the 
 symptoms of stone in the bladder to arise in a case dependent 
 on reflex irritation from tapeworm. If the above symptoms are 
 present without any ohvious cause or reason, always examine the 
 faeces for segments of these worms. A discharge of the segments 
 is of course conclusive. 
 
 Treatment. — Having diagnosed the presence of the worm, 
 then administer something which will kill the worm and expel 
 its carcase. The following treatment may be tried. — Give at 
 night-time for six nights running, four grains of ipecac, with 
 one grain of pil. hydrarg.j the seventh morning on an empty 
 stomach give 3j of the liquid extract of male fern suspended in 
 mucilage, and four hours afterwards give half-an-ounce of 
 Epsom salts and a drachm of ammon. chloride in a tumbler of 
 effervescing water. I tried this course in eighteen consecutive 
 cases of tapeworm, and in only two cases was the treatment 
 unsuccessful in expelling the whole worm. Turpentine, 
 pumpkin seeds, etc., have their advocates. 
 
 Caution. — Be sure the head is expelled. 
 
 TiENIA ECHINOCOCCUS. 
 
 General Characters — 
 
 1. SiZE.^ — Taenia echinococcus is a small worm, about 
 ^ to ^ inch long. 
 
 2. Steuctore. — This worm consists of only four segments, 
 including the head. The Head is pointed, has four suckers 
 and a double circlet of hooks. These hooks are about 30 
 to 40 in number, and are shaped like those of taenia solium, 
 but are much smaller. 
 
 The last proglottis, when mature, is equal in size to the 
 rest of the body, and contains the reproductive organs. The 
 genital pores are placed on the lateral aspect of the body. The 
 
Tcenia Echinococcus. 359 
 
 ovaries are complicated, and th.e ova are small but exceed- 
 ingly numerous, and in them are developed the six-hooked 
 embryoes. 
 
 Life History. — When ripe the proglottides drop off, pass 
 out of the body of the host — the dog or wolf. The embryoes 
 are now liberated on the ground, on plants, or in water, and 
 thus gain access to the stomach of man. They then perforate 
 the intestinal walls, and getting into the circulation, are by 
 this or other means carried to the liver or other organ, where 
 they become encysted and develop a spherical vesicle which 
 may reach a great size. They are now called HyDATiDS. 
 
 Hydatid Cysts — 
 
 1. Struotuhe. — These cysts when fully formed are com- 
 posed of three parts — 
 
 (1) The false cyst formed by the tissues of the part. 
 
 (2) The ectocyst — an opaque, gelatinous membrane of great 
 thickness, white in colour, smooth, glistening, and laminated. 
 
 (3) The endocyst — a more opaque, granular layer, coniposed 
 of nucleated cells, and covered by small white spots— brood 
 capsules. 
 
 (4) Inside the cyst there is a colourless watery fluid which 
 contains salts, but no albumin, a point of value in diagnosis. 
 
 Hydatid cysts are, moreover, much larger than those of 
 cysticercus cellulosa. 
 
 2. Development. — Within these cysts the scolices — • 
 echinococcus heads — are developed in the following 
 manner : — 
 
 The inner wall of the cyst forms small vesicles — called 
 brood capsules — which project into the cavity of the cyst. 
 From the walls of these brood capsules small cup-Hke buds 
 or hollows are formed, each of which gradually elongates 
 and becomes a csecum with its cavity opening outwards — 
 
360 Student's Hand-book of Medicine. 
 
 i.e., it communicates with the cavity of the brood capsule. 
 Within these depressions or hollow buds the echinococcus 
 head is developed, and, when mature, turns itself inside out 
 — i.e., everts itself, so that the head now projects iato the 
 brood capsule. These heads are similar to those of the adult 
 worm, having a double circlet of booklets and four suckers. 
 
 Development cannot proceed further than this in the human 
 body, but if the cysts gain access to the dog, etc., then the adult 
 tape-worm is formed in the intestine. 
 
 Secondary Ctsts are often found in connection with the 
 primary cyst. This may occur in one of three modes — 
 
 1. By a process of budding out of the wall of the ectocyst, 
 thus giving rise to a number of daughter-cysts^ side by side — 
 exogen<ms cysts. 
 
 2. Again, the daughter-cysts may be formed inside the 
 primary cyst — these are called endogenous cysts. 
 
 3. Or, the cysts may be multi-locular — i.e., composed of 
 many separate alveoli divided from each other by dense fibrous 
 tissue. They occur as hard, firm tumours in the liver. 
 
 Intermediate Host. — The cystic form is alone found in man. 
 
 Host. — The adult worm in the dog and wolf. 
 
 Habitat. — The cystic form is found in the liver, lungs, 
 brain, heart, muscle ; the mature form, in the intestine. 
 
 Diagnosis and Treatment — See Tumours of the Liver. 
 
 NEMATODA, 
 
 Synonym — Thread worms. 
 
 General Characters. -^ The thread worms are a very 
 large and well-known group of helminths; They are simple. 
 
Nematoda. 361 
 
 not compound, and do not form colonies. They closely 
 resemble the common earth-worm, being round and thread- 
 like without segmentation or appendages. They undergo no 
 metamorphosis, the sexes are distinct, and there is a marked 
 difference between the male and female - — the male being 
 smaller than the female. 
 
 Stbucturb. — The Nematoda have a distinct alimentary 
 canal with a mouth furnished with soft horny lips, an 
 oesophagus, stomach, intestine, and anus. There is a thick 
 elastic ectoderm or cuticle and a well-developed muscular 
 system. The genital pore placed on the ventral aspect is, 
 in the female, situated about the middle of its length ; in 
 the male, near the anus, where there is a ohitinous prehensile 
 investment. 
 
 The most common Nematoda are — 
 
 1. Trichina spiralis. 
 
 2. Filaria sanguinis hominis. 
 
 3. Filaria medinensis. 
 
 4. Dochmius duodenalis. 
 
 5. Ascaris lumbricoides. 
 
 6. Ascaris mystax. 
 
 7. Eustrongylus gigas. 
 
 8. Trichocephalus dispar. 
 
 9. Oxyuris vermicularis. 
 
 I.— TRICHINA SPIRALIS. 
 
 Synonyms — Flesh worm, Pseudalius trichina. 
 Larva — Muscle trichinee, Encysted trichinae, Flesh worms. 
 
 General Characters. — Trichina spiralis is a very minute 
 worm, the male and female being distinct. 
 
 1 . Size. — Male, -jV inch ; female ^ inch long. 
 
362 Student's Hand-book of Medicine. 
 
 2. Structure — 
 
 The Head is narrow, pointed, unarmed, with a simple 
 central oval aperture. 
 
 The Body is thread-like, bent upon itself, thicker behind 
 than in front, and in both male and female the hinder part of 
 the body is straight. In the male, however, it has a short, 
 bilobed caudle appendage, between the lobes of which is the 
 anus. The testes are convoluted tubes. The female is about 
 ^ of an inch long, rounder and shorter behind than the male. 
 There is an ovary, vagina, uterus, and the genital orifice is 
 near the head. 
 
 The Ova are y^ inch long, and are hatched within the 
 parent (ovoviviparous). 
 
 Larval Form — the trichina of muscle — is a very small 
 worm, about -^-^ inch long, coiled up in a spiral manner 
 within a fibrous capsule or cyst, the long axis of which lies 
 in the long axis of the muscular bundles. A single capsule 
 may contain two or more larvae and there may be as many 
 as 325,000 of these capsules in an ounce of meat. They 
 are especially common in the abdominal and thoracic 
 muscles and appear as whitish spots from the cyst being 
 often calcified towards the poles. This small worm has a 
 digestive system and an imperfect sexual apparatus. 
 
 Life History. — When a piece of meat affected with 
 trichinae is eaten by an animal, the capsules are dissolved, 
 and the embryo parasites which they contain are liberated. 
 These mature in a day or two in the intestinal canal of the 
 host. The sexes unite and give birth to ova and embryoes; 
 a single ova producing over 1000 embryoes, and a single female 
 discharging over 16,000 ova. 
 
 The embryoes migrate from the intestine to the striped 
 muscles, passing through the intestinal walls, but it is not clear 
 how they reach the muscles — possibly through the peritoneal 
 cavity or through the blood and lymph. 
 
Nematoda. 363 
 
 Once in the muscles the embryoes penetrate the primitive 
 bundles, reduce their contents to debris and soon become 
 mature muscular trichinae, forming cysts, part of which is 
 made up of a chitinous secretion of the parasite, part by a 
 wall of fibrous tissue formed of the perimysium of the muscle 
 bundles. These cysts, as above stated, may become partly 
 calcareous, giving rise to white shining spots in the muscle. 
 They may remain quiescent for years. 
 
 Irderm.ediate Host.- — The trichinae are found in pigs, rabbits, 
 sheep, dogs, rats, mice. The pig gets them from the rat, which 
 acquires them from human faeces. 
 
 Host. — Man, finding their way into his body through 
 eating uncooked pork. 
 
 Habitat. — The adult worm only inhabits the intestine and 
 only lives for a few weeks. 
 
 Symptoms of Trichinosis. — • Unless there be a large 
 number of embryoes eaten definite symptoms may not arise, 
 but in well-marked cases of trichinosis the symptoms are very 
 characteristic. A few days after eating the infected flesh, 
 symptoms of gastro-intestinal irritation appear, there may be 
 vomiting, diarrhoea, and abdominal pain. 
 
 Towards the second week, great soreness and stiffness of 
 muscles develop, the temperature runs up, and may be 
 remarkably remittent in character, a characteristic oedema 
 sets in at first in the face, but becomes specially marked in 
 the affected muscles. In protracted cases the patient becomes 
 emaciated, exhausted, and a typhoid condition may supervene 
 and carry off the sufferer. 
 
 It wUl be easily understood that the more important 
 muscles such as the diaphragm may be early implicated, and 
 a fatal issue is then speedily brought about. 
 
 The disease occurs in epidemic form in some countries. 
 
364 Student's Hand -hook of Medicine. 
 
 Diagnosis. — Examine stools, or pieces of muscle that have 
 been harpooned. The more important diagnostic features are — 
 
 1. Severe pains in the joints without marked swelling. 
 
 2. CEdema. 
 
 3. Dyspnoea. 
 
 4. Marked muscular pain. 
 
 Prophylaxis. — All meat to be thoroughly well done. 
 Avoidance of pork in an infected district. 
 
 Treatment. — Purgatives at first, combined with twenty 
 grains of salol every night. Later, give five grains of quinine 
 suspended in two drachms of glycerine thrice daily. Treat 
 symptoms as they arise. No specific remedy. Morphia may 
 be required in large doses to relieve the intolerable pain. 
 
 II. FILARIA SANGUINIS HOMINIS. 
 Synonyms — Filaria Bancroft!, Filaria cystica, Trichina cystica. 
 
 General Characters — The mature forms are rarely seen. 
 The sexes are distinct. The male is said to be smaller than 
 the female and lives in the same vessels. __ 
 
 "The female is described as a smaU slender hair-like worm 
 with a club-shaped head, a narrow alimentary canal, a two- 
 horned uterus usually full of embryoes. These are discharged 
 through the vagina, which opens near the mouth." 
 
 The embryoes measure about -^ inch long, have a rounded 
 head, a tapering tail, and are enclosed in a fine membrane 
 which does not burst, but which elongates as the embryo 
 uncoils itself, thus forming a delicate sheath to the embryo. 
 
 Life History. — The adult worms inhabit the lymphatics. 
 The embryoes gain access to the stomach of their host through 
 drinking water ; they thence make their way to the vessels. 
 
Nematoda. 365 
 
 Here the sexes unite, and the embryoes are discharged into 
 the lymphatics. In the daytime the embryoes are found in 
 the lymphatics, but at night they crowd the blood stream. 
 They cannot, however, undergo further development in man, 
 and hence are taken up by a species of mosquito, in the body 
 of which the embryoes are matured. When the insect dies, 
 they find their way to water, thence to the stomach of their 
 host, and, on reaching the blood and lymphatic system, form 
 the mature filaria. 
 
 Intermediate Host. — Mosquito. 
 
 Host. — Man. 
 
 Habitat. — The embryo, called filaria sanguinis hominis 
 — in the blood and urine ; the mature form, called filaria 
 Bancrofti — in the lymphatics. 
 
 Symptoms. — The passage of an opaque milky urine tinged 
 with blood, is the most prominent symptom in the bulk of 
 cases; but the enormous lymph scrotum and certain forms of 
 elephantiasis are also supposed to be due to the presence of 
 this parasite. Sometimes a blood-clot may form either in the 
 bladder or pelvis of the kidney giving rise to troublesome 
 symptoms. 
 
 Treatment. — At present very unsatisfactory. Iodide of 
 potassium, turpentine, carbolic acid, etc., have their advocates. 
 
 III.— ASCARIS LUMBRICOIDES. 
 
 Synonyms — Round worm, Lumbricus teres hominis. 
 
 General Characters — These parasites closely resemble the 
 common earth worm. 
 
 Size. — The male measures about 4 to 6 inches ; the female, 
 10 to 12 inches long. 
 
 Structure. — This parasite is a broad, smooth, fusiform, 
 translucent, brown or red coloured worm, with fine circular 
 
366 Student's Hand-hook of Medicine. 
 
 striae. Its anterior extremity has a three-lobed mouth. The 
 tail is bluntly curved in the male, and has a double spicula 
 near its end. 
 
 Ova, oval shaped, -^^ to ^\^ inch in diameter, and have a 
 hard shell and an albuminous envelope. 
 
 Life History — Not fully known. 
 
 Host. — Man, pig. 
 
 Intermediate Host. — Not required. 
 
 Habitat. — The ileum, colon, also mouth and nose. They 
 are passed by the fseces, or are vomited. 
 
 Symptoms. — Very indefinite, in fact there are no charac- 
 teristic symptoms. Picking of the nose, grinding the teeth, 
 foul breath, etc., are the popular symptoms of the presence of 
 this worm, but obviously any irritation of the intestinal canal 
 may cause such symptoms. Perhaps we regard the presence 
 of worms as a source of peripheral and intestinal irritation 
 too lightly at present. Our forefathers distinguished a "worm 
 fever " and prescribed successfully for that ailment. 
 
 Treatment. — Santonin four grains followed by three grains 
 of calomel. 
 
 TREMATODA. 
 
 Synonyms — Fliiies, Flat-worms, Suctorial-worms. 
 The only parasite under this class that we shall consider is 
 
 DISTOMA H./EMATOBIUM. 
 
 Synonyms — Bilharzia Hseraat'obia, Thecosoma, Schistosoma, 
 Gynsecophorua. 
 
 General Characters. — They are dioecious, the sexes being 
 distinct. 
 
Trematoda. 367 
 
 1. Male — 
 
 (1) Size. — About ^ inch long. 
 
 (2) Shape. — Cylindrical, with a canal or groove — 
 
 gynophoric canal — at the posterior end of 
 the body in which the female is lodged. 
 ,2. Female — 
 
 (1) Size. — i inch long. 
 
 (2) Shape.— Thread-like. 
 
 Both male and female have two ventral suckers, and the 
 reproductive orifice is below the ventral sucker. 
 
 Ova. — Oval in form, -^^-^ to j-^ ^^'^^ in diameter, with a 
 spine at the ends or at the sides of each egg. 
 
 Life History. — Not known. 
 
 Intermediate Host. — Not known. 
 
 Host. — Man and monkey ; got by drinking water. 
 
 Habitat, — The blood. Is especially found in the inferior 
 vena cava and portal veins, and in the vesical and hsemor- 
 rhoidal veins. 
 
 Effects — The sexes unite in the blood — the ova are dis- 
 charged, and pass through the walls of the bladder and ureter 
 by means of the ulcerated surfaces caused by the parents. If 
 in large numbers, they give rise to inflammation and haemor- 
 rhage from the- affected mucous membrane, causing endemic 
 hsematuria — or if the large intestine be affected, a special form 
 of diarrhoea is the result. The ova pass out of the body by 
 these channels, and can be found in the urine of the patient. 
 If placed in warm water, the ova give rise to the free ciliated 
 jembryoes. 
 
 Distribution.^ — This parasite is rarely met with in England, 
 but is common in Egypt, Cape, Natal, also in Brazil. 
 
368 Student's Hand-book of Medicine. 
 
 DISEASES OF THE MOUTH. 
 
 THRUSH OR PARASITIC STOMATITIS. 
 
 Is a specific disease dependent on the development and 
 multiplication of a special fungus termed the odium albicarts; 
 is frequently met with ia weakly children and infants. 
 
 By some the fungus is regarded as belonging to the yeast 
 tribe, by others it is looked upon as a mould ; whatever its 
 nature is, it causes the formation of milk-white or greyish 
 adherent patches on the mucous membranes of the mouth and 
 pharynx of the child attacked. 
 
 Microscopically these patches consists of epithelium united 
 into a membrane by twisted filaments (the fungus) which are 
 often branched and composed of long cells joined end to end, 
 and constricted at the joints. 
 
 The patches may extend to the oesophagus, stomach, and 
 caecum. 
 
 Symptoms. — The mouth is dry, and tender or painful; 
 there is usually much debility and gastric disturbance. (This 
 affection must not be confounded with aphthous stomatitis, 
 presently to be described.) 
 
 Treatment. — Absolute cleanliness of the feeding bottles, the 
 avoidance of stale milk, and the frequent swabbing out of the 
 mouth with a solution of boracic acid or permanganate of 
 potash, are the principle indications for successful treatment. 
 Everything must be done to improve the debilitated condition 
 generally. 
 
Stomatitis. 369 
 
 STOMATITIS. 
 
 An inflamed condition of the mouth is common during 
 dentition, certain fevers, and morbid states of the blood. 
 
 Such a condition, however caused, is likely to be attended 
 with the following symptoms — 
 
 1. Pain and difficulty in mastication, articulation, and 
 deglutition, in proportion to the severity of the disease. 
 
 2. Increased salivation. 
 
 3. Fcetor of breath. 
 
 4. Constitutional disturbances. 
 
 Like all inflammations of mucous membranes, the condition 
 varies much in severity, and accordingly the following types 
 are described : — 
 
 The simple or erythematous stomatitis, a mild form which 
 readily yields to the local application of glycerine and borax. 
 
 Aphthous stomatitis, characterised by the formation of small 
 vesicles or yellowish patches of a diphtheroid nature. The 
 vesicles after rupturing leave small greyish ulcers. They 
 appear on the gums, tongue, lips, etc., but seldom upon 
 the pharynx ; they spread by contact. 
 
 This type has assumed an epidemic form in localities where 
 cattle afiected with foot-and-mouth disease were presenlj, The 
 relation between the two conditions have, however, not yet 
 been determined. Some authorities term this epidemic form 
 ulcerative stomatitis, or putrid sore throat. 
 
 Treatment. — Touch the ulcers with solid nitrate of silver. 
 Improve the general health of the patient with tonics. A 
 mixture of hydrochloric acid, chlorate of potash and glycerine, 
 freely swabbed over the mouth, often acts like magic. 
 
 Note. — True aphthous stomatitis is more common after 
 the period of dentition. 
 
 2 c 
 
370 Student's Hand-book of Medicine. 
 
 CANCRUM ORIS. 
 
 This is a form of gangrenous stomatitis, happily now rare, 
 but sometimes seen in debilitated children between the ages of 
 two and five years. 
 
 Pathology. — At first there appears a small diphtheroid patch 
 of necrosed tissue with a general inflammation around it. This 
 inflammatory zone extends and becomes brawny in character, 
 the slough separates, and the ulceration goes on until the 
 cheek is perforated. The disease frequently kills the patient 
 before necrosis is well marked, but sometimes the gangrene 
 extends to the jaw, malar bones, tongue, etc., before a fatal 
 termination is brought about. 
 
 Symptoms. — The constitutional disturbance is very great, 
 and usually the typical typhoid state rapidly ushers in a 
 fatal ending. 
 
 Treatment. — Highly unsatisfactory, for it has been fairly 
 well demonstrated that the virulence of the affection is not 
 so dependent on the poison as much as the peculiar debilitated 
 state of the patient, and the unhealthy surroundings in which 
 he exists. 
 
 The application of the Paquelin cautery, with the admini- 
 stration of quinine and stimulants are the best measures, 
 
 SUPPURATIVE TONSILLITIS OR QUINSY. 
 
 Inflammation of the tonsils is not only a common complica- 
 tion or symptom of many fevers, but is also a common primary 
 affection; but when the inflammatory process goes on to sup- 
 puration (as it frequently does) it is termed quinsy. 
 
 .Etiology. — Quinsy occurs most frequently in young people, 
 but may occur at any age. There seems to be some relation 
 
Sv/ppurative Tonsillitis or Quinsy. 371 
 
 between the poison of quinsy and acute rheumatism, as the 
 latter frequently begins as the former, and moreover, the tem- 
 perature is remarkably high at times in cases of suppurative 
 tonsillitis, and the joints are often very painful. Is quinsy a 
 local affection, or is it a constitutional fever with marked local 
 symptoms ? These questions are not easily answered, but there 
 can be no doubt that — 
 
 1. Suppurative tonsillitis is often epidemic in character, 
 
 2. It tends to recur at certain seasons in the same individual. 
 
 3. Once begun, the inflammation is not easily aborted until 
 suppuration commences. 
 
 4. The fever and other constitutional symptoms are often 
 out of all proportion to the local affection. 
 
 Pathology. — The crypts or follicles become much inflamed. 
 Their epithelium proliferates and their lumen becomes fiUed 
 with yellowish pus-like debris. These points may coalesce 
 and form a dirty patch. The whole tonsil becomes swollen, 
 intensely injected and oedematous, and in three or four days 
 the interior of the tonsil becomes converted into an abscess. 
 Usually one tonsil only is attacked, but the other frequently 
 becomes similarly affected as the first gets better. 
 
 Symptoms. — First there is a slight soreness at one side of 
 the throat, and a desire to swallow more frequently; this 
 soreness increases as the tonsils become more inflamed. The 
 angle of the jaw is also swollen, and any movement of the jaw 
 or deglutition is attended with great pain. The temperature 
 tends to run up rapidly, and I have notes of nine cases where 
 the temperature exceeded 106° F. There is often intolerable 
 headache rendered worse by movement, especially on rising 
 from the horizontal position. The tongue is foul and the 
 breath foetid. 
 
 Diagnostic Points. — The rapid onset — the one tonsil affected 
 — great tendency to suppurate — high temperature, 
 
372 Student's Hand-book of Medicine. 
 
 Treatment. — Open the bowels freely by saline purges. 
 Subdue fever and relieve headache by antipyrin or salicylates. 
 Gargle the throat with hot milk, or brush it with a hot solution 
 of soda and morphia. Don't use astringents in the acute stage, 
 they only irritate the inflamed part. In the low subacute forms, 
 frequently seen ia over-worked patients, nothing succeeds better 
 than a good swabbing once for all of the liq. ferri perch, 
 fort. It is not a pleasant application, but is very efficacious. 
 Nourishing diet and tonics are absolutely required during 
 convalescence. 
 
 MISCELLANEOUS DISEASES. 
 
 RAYNAUD'S DISEASE. 
 
 For a description of this peculiar disease we are indebted 
 to the researches and writings of Dr Eaynaud, and also, to a 
 large extent, to Dr T. Barlow's able translation of Eaynaud's 
 work (1888). Raynaud's disease may be more or less cor- 
 rectly defined as a vascular disorder, dependent on vaso-motor 
 disturbances which cause constriction of the peripheral arteri- 
 oles, and so induce changes of various degrees conveniently 
 termed — (1) Local syncope ; (2) Local asphyxia ; (3) "Local 
 and symmetrical gangrene. 
 
 1. Local Syncope. — This condition resembles the dead 
 fingers or toes produced by intense cold — one or more fingers, 
 or the whole hand, may be affected. Often a severe reaction 
 sets in, and the parts numbed before now become intensely 
 red, hot, and painfuL 
 
 2. Local Asphxia. — This condition is characterised by the 
 fingers, ears, and certain patches of skin on the arms and 
 legs, becoming intensely congested, livid, and the capillary 
 circulation arrested. The congestion gives rise to swelling, 
 
Scurvy. 37S 
 
 stiffness, and pain ; tlie latter is often succeeded by marked 
 ansesthesia. 
 
 These attacks may occur at winter time for many years 
 as "chilblains." 
 3. Local or Symmetrical Gangrene. — The parts asphyxiated 
 become cold, insensible, and black in colour — i.e., changes 
 identical with necrosis elsewhere. Usually a line of demarca- 
 tion forms and limits the necrotic condition. 
 
 Complications — 
 
 1. Hsemoglobinuria is so frequently present, that it is more 
 like a symptom than a complication of Eaynaud's disease. 
 
 2. TJrsemia. 
 
 3. CEdema of the glottis and lungs. 
 
 4. Heart failure. 
 
 5. Inflammation of serous sacs. 
 
 6. Cerebral symptoms, independent (apparently) of uraemia. 
 
 Pathology. — Unknown. Vaso-motor constriction, vaso- 
 motor dilatation with subsequent venous engorgement, altered 
 conditions of the blood, etc., have been advanced as the causes. 
 Better be frank and say we don't know anything about the 
 pathology of this disease at present. 
 
 Treatment. — Improve any obvious condition of iU-health. 
 Locally, make the circulation more brisk by gentle friction, 
 warmth, and gentle galvanism. Soothe pain by sedatives 
 such as belladonna, morphia, conium, etc. 
 
 SCURVY. 
 
 Is a constitutional afiection characterised by great debihty, 
 a spongy condition of the gums, a tendency to haemorrhages, 
 and cachexia. 
 
 .etiology. — Is much less common now compared with 
 former times. The disease is usually associated with improper 
 
374 Student's Hand-hoolc of Medicine. 
 
 and insufficient food, unhealthy hygienic surroundings, etc. 
 Sailors afford the best examples, as a rule, of this disease. 
 
 Pathology. — There are three theories as to the causation 
 of scurvy — viz., that it 
 
 1. Depends on the presence of a specific organism. 
 
 2. Deficiency of potassium salts in the blood. 
 
 3. Eeduction of the alkalinity of the blood, not necessarily 
 through the absence of potash, but a reduction in quantity 
 of all the salts that tend to keep the blood alkaline. 
 
 Moreover, as citrates, malates tartrates, etc., become changed 
 into carbonates in the blood, we may assume at present that 
 scurvy is really due to an inadequate supply of organic acids, 
 salts, etc., which are to be found in fresh vegetables, fruits, etc. 
 
 Symptoms. — Are insidious at first; the patient becomes 
 weak, breathless, drowsy or languid, with more or less aching 
 of the bones and joints generally. The gums become soft and 
 swollen, bleeding easily on the slightest pressure. 
 
 As the disease becomes marked, the teeth may come out, 
 the mouth becomes ulcerated and emits a frightful foetid odour. 
 Petechial haemorrhages around the hair follicles, may be fol- 
 lowed by large subcutaneous extravasations of blood on the 
 extensor aspects, into the conjunctivae, popliteal spaces, etc. 
 The patient assumes a cachectic appearance, and is rendered 
 quite unfit for mental or physical exertion. In some oases 
 a peculiar form of night blindness develops ; this condition is 
 not dependent on permanent ocular changes, though optic 
 atrophy has been observed in more than one case. 
 
 Treatment — 
 
 1. General hygiene must be attended to. 
 
 2. Diet should consist of good soup, fresh milk, cream, etc. 
 Effervescing drinks made with fresh lemon juice are of special 
 importance. 
 
 3. Medicinal. — Quinine dissolved in citric acid. 
 
Hcemophilia. 875 
 
 HEMOPHILIA. 
 
 Is a peculiar diatliesis characterised by a tendency to 
 excessive and uncontrollable bleeding. It differs from purpura 
 in being always present throughout the patient's life. 
 
 Many varieties have been described such as — 
 
 1. Those in which a slight traumatism is followed by 
 excessive haemorrhage. 
 
 2. Those which exhibit the condition after injuries of 
 certain regions only. 
 
 3. Those in which the haemorrhages take the form of attacks 
 of spontaneous bleeding from the nose, uterus, mucous mem- 
 branes, etc. 
 
 Pathology. — Unknown, as no constant condition or changes 
 have been found post mortem either in the blood-vessels or 
 blood; probably the fault lies in some structural changes in 
 the walls of the capillaries. The diathesis is marked by being 
 hereditary and is transmitted through the female line. 
 
 Symptoms. — Are sufficiently obvious, and need no detailed 
 description. It must be remembered that in these cases death 
 has followed the extraction of a tooth, cutting a com too 
 deeply, snipping a wart off, and other usually trifling opera- 
 tions. Often the first severe attack of bleeding ocdurs in 
 infancy, or, on the other hand, it may first appear after 
 adult age. 
 
 Treatment. — When we suspect the presence of this diathesis, 
 a careful watch should be made over the patient, and on the 
 slightest appearance of haemorrhage, energetic treatment with 
 styptics must be at once employed. Obviously, the bleeder 
 tnust live on a non-stimulating diet, lead as even and placid 
 a life as possible, avoid excesses of all kinds, especially the 
 
376 Student's Hand-book of Medicine. 
 
 ingestion of liquids and other compounds which tend to 
 raise the hlood pressure. No female of the hs8mophilic 
 stock should marry. 
 
 PURPURA. 
 
 Purpura is not a disease, but symptomatic of some grave 
 change in either the blood or blood-vessels,, whereby extra- 
 vasations of blood into various tissues occur, producing red 
 or blue patches which do not disappear on pressure or after 
 death. Being symptomatic in character, we may expect several 
 varieties, such as — 
 
 1. A form associated with the malignant fevers — i.e., those 
 fevers in which the "rashes" become hcemorrhagic, as already 
 described under typhus, black measles, etc. 
 
 2. A form associated with grave conetitutional changes — i.e., 
 syphilis, chronic Bright's disease, cardiac diseases, scurvy, etc. 
 
 3. A form associated with the circulation of certain poisons, 
 to wit, snake poison, quinine, ergot, mercury, etc. 
 
 4. A form associated with arthritis — i.e., ( 1 ) PeUosis 
 rheumatica, already referred to under rheumatic fever ; and 
 (2) Febrile purpuric oedema — a condition in which many joints 
 become inflamed from other causes than rheumatic poison. 
 
 5. A form probably neurotic in character, as seen in cases 
 of myelitis, locomotor ataxia, severe neuralgia, purpura 
 urticans, etc. 
 
 6. Purpura haemorrhagica, a form which occurs without 
 any apparent reason, and not associated, with any particular 
 condition. It differs from haemophilia in not being a constant 
 possession or factor, but a temporary condition which may or 
 may not be highly amenable to treatment. 
 
 Symptoms. — The presence of petechiae in the skin, etc., are 
 sufficiently obvious to demonstrate the condition. When not 
 
Acromegalia. 377 
 
 associated with, any apparent cause, the more common symptoms 
 are — marked anaemia, sallow complexion, local oedema or general 
 anasarca, and more or less severe muscular pains. Death may 
 occur from progressive exhaustion, or from internal haemor- 
 rhages. Unlike scurvy, the gums are not swollen, no history 
 of want of fresh air, vegetables, etc. 
 
 Treatment. — As we know nothing about the pathology of 
 this disease, the treatment must be entirely emperical, or 
 experimental. Aim at removing any apparent cause of iU- 
 health, restoring tone of blood-vessels, etc. Ergot, iron, 
 turpentine, strychnine, gallic acid, opium, etc., may be tried. 
 
 ACROMEGALIA. 
 
 Is a peculiar disease characterised clinically by an excessive 
 growth chiefly of the face and extremities, and associated 
 pathologically with enormous hypertrophy of the. pituitary 
 body. In some cases the thyroid gland has been found 
 enlarged, and a persistence of the thymus glands noted, but 
 these two changes are looked upon as accidental occurrences. 
 
 Symptoms. — Earely is a more characteristic clinical picture 
 presented than a confirmed case of acromegalia. The face 
 is egg-shaped, with its broad end downwards; the lower jaw- 
 bone particularly is much increased in size, and may cause 
 the lower teeth which are wide apart to project, giving any- 
 thing but a pleasing appearance; the tongue is somewhat 
 enlarged and may cause a similar leathery speech to that of 
 myxoedema. The extremities are markedly altered, the hands 
 being huge, spade-shaped, and the nails broad and large- 
 The lower extremities show similar abnormal overgrowth, and 
 may render the gait peculiarly clumsy. The spine is often 
 of the kyphotic type, and the abdomen being thrown outwards 
 at the same time causes a characteristic " double hump." 
 
378 Stud-ent's Hand-book of Medicine. 
 
 There is much general lassitude and weakness, and usually 
 marked headache and anaemia. 
 
 The menses in women may be arrested. Defects of ■vision 
 are often present, the more common being either single or 
 double hemianopsia; such conditions, however, are not always 
 permanent. Polyuria and glycosuria may be present in some 
 cases. The skin often presents pedunculated tumours and in 
 marked contrast to myxoedema often is bathed in sweat. 
 
 Pathology. — At present is very obscure, though, from tjie 
 constant presence in these cases of a much hypertrophied 
 pituitary body, the condition seems to be dependent on changes 
 in that gland. This, however, must be regarded at present as 
 purely speculative, for cases of atrophy of the pituitary body 
 have apparently been attended with no particular changes. 
 The persistence of the thymus gland rests upon the slender 
 evidence of increased dulness in its normal area. 
 
 Treatment. — Arsenic, strychnine, massage, galvanism, and 
 the injection of extract of thyroid gland, or extract of pituitary 
 body may be tried. 
 
 ACTINOMYCOSIS. 
 
 Is a chronic inflammatory affection set up through the 
 irritation caused by the presence and multiplication of the ray 
 fungus. 
 
 General Characters (Macroscopic) — 
 
 1. In Cattle. — The disease usually begins in the lower jaw, 
 and causes sarcomatous-like growths — bulky tumour-like masses 
 ^connected with the bone. The bone is softened, eroded, 
 leading to the formation of an abscess. The tongue is also 
 affected, hard indurated nodules being produced which give 
 a gritty, woody feel ; hence the name, Woody Tongue. The 
 virus is carried by grain. It does not affect carnivora. 
 
A ctinomycosis. 379 
 
 Sites of the lesion — 
 
 1. Jaws — tongue — neck — glands beneath the jaw. 
 
 2. Larynx — lung — alimentary tract. 
 
 2. In Man. — The disease also affects the jaw, and leads, 
 as in cattle, to the formation of nodular masses, of deep-seated 
 abscesses (retro-pharyngeal) in the region of the spine, etc. 
 
 Nodules also occur in the lungs — patches of chronic indura- 
 tion, abscesses, and cavities. 
 
 The liver, intestines, the kidneys, and ovaries are also affected. 
 
 The masses tend to suppurate, not to caseate. 
 
 Structure (Microscopic) — 
 
 The nodules are seen to consist of masses of granulation 
 tissue. They have a sponge-like arrangement, and contain 
 small yellowish granules. They have a structure very similar 
 to that found in tubercle, being composed of — 
 
 1. The fungus — ray fungus in the centre. 
 
 2. Eound this there are the giant cells. 
 
 3. Epithelioid cells. 
 
 4. Masses of granulation tissue. 
 
 Mode of Inoculation — 
 
 1. Through the mouth by carious teeth, etc. 
 
 2. By the respiratory tract. 
 
 3. Through the intestinal tract. 
 
 4. Through the intestinal vaginal orifice. 
 
 5. In many cases the mode of inoculation is unknown. 
 
 Ray Fungus — 
 
 1. Characters. — The exact botanical position of the ray fun- 
 gus is not known. By some it is regarded as a mycelium, 
 by others as a leptothrix or cladothrix. 
 
 2. Structure. — The fungus consists of short threads or 
 rods, often club-shaped, dotted, branched, sometimes calcified, 
 
380 Student's Hand-hook of Medicine. 
 
 arranged in a radiating manner round a common centre, 
 composed of fine filamentous fibres. They form the globular 
 masses already spoken of. The central part of the mass is 
 the living oladothrix, the rays are degenerated filaments. 
 
 3. Oultivation. — Actinomycosis has been cultivated but not 
 with uniform success. It has also been inoculated, but here, 
 also, the results have not been altogether very satisfactory. 
 
 Symptoms. — The symptoms of this remarkable disease 
 depend entirely upon its mode of entrance, and the site of 
 its most rapid multiplication; thus its pernicious influence 
 may be most marked in — 
 
 1. The alimentary canal. 
 
 2. The pulmonary organs. 
 
 3. The brain. 
 
 4. The skin, etc. 
 
 Professor Grainger Stewart, in conjunction with Dr Robert 
 Muir, gives, in "Edinburgh Hospital Eeports," vol. 1., a most 
 exhaustive account of a case which began in the ovaries. 
 
 Treatment. — It is at present unsatisfactory, because the 
 condition, in the first place, is not easily diagnosed; and 
 secondly, when it is diagnosed in man, the extensive inflam- 
 matory changes, the numberless adhesions set up, etc., give 
 little chance of even successful surgical treatment. Medicinal 
 measures are certaialy less efiective. The cases, indeed, require 
 similar treatment to that of chronic pyaemia. 
 
 ANTHRAX. 
 
 Anthrax — also called charbon, malignant pustule, wool- 
 sorters' disease, splenic fever, splenic apoplexy — is a disease 
 which especially attacks cattle, ' horses, sheep, deer ; less 
 
Anthrax. 381 
 
 commonly swine, dogs, etc. ; but it also occurs in man, 
 and is due to the agency of a specific bacillus — bacillus 
 anthracis. 
 
 Division. — Anthrax, as it occurs in man and animals, may 
 be — (1) Local ; (2) General. 
 
 In man the disease manifests itself chiefly in the local 
 form; in cattle, etc., the general form is more common. 
 
 Characters. — (1) In animals ; (2) In man. 
 
 1. Anthrax in Animals — 
 
 1. There is but little local lesion. The chief changes are 
 in the spleen, which becomes like a mass of blood-clot — hence 
 the name, splenic apoplexy. 
 
 2. Hsemorrhages occur in such organs as the lungs, wall 
 of heart, cortex of kidney, brain and its membranes. 
 
 3. There are areas of inflammatory exudation — cellulitis, , 
 effusions into serous cavities. 
 
 4. The blood has a dark colour, and is crowded with bacilli. 
 
 5. Lymphatic glands are also affected — more especially in 
 animals, not so much in man. 
 
 2. Anthrax in Man — 
 
 Anthrax occurs in persons working amongst hides, hair of 
 cattle, etc.; hence in tanners, wool-sorters. The poison, how- 
 ever, can be carried by flies. 
 
 1. Mode op Inoculation — 
 
 (1) By wounds. 
 
 (2) By the respiratory tract. 
 
 (3) By the alimentary tract. 
 
 2. Division. — There are two forms in man — 
 
 (1) Local Form. — Malignant Pustule — due to inoculation; 
 hence it occurs on exposed parts — on the face, neck, lips. 
 
382 Student's Hand-book of Medicine. 
 
 hands, arms. It commences as a small pimple surrounded 
 by a bluish inflammatory zone. The pimple may or may not 
 burst, but in two or three days it enlarges and fresh vesicles 
 form — bullae follow, and wo get local gangrene and necrosis. 
 General blood-poisoning usually ensues. The bacillus is found 
 in the superficial and subcutaneous lymphatics of the afiected 
 area, and afterwards in the blood, etc. 
 
 (2) General Form. — Eare in man, but may affect — 
 
 (a) The Respiratory Tract. — Wool-sorters' disease. The 
 primary lesion is usually in the lower part of the 
 trachea ahd larger bronchi, where there are patches 
 of intense swelling of the mucous membrane, with 
 hasmorrhages and ulcerations. Great swelling of 
 mediastinal glands, which, from haemorrhages, look 
 like blood-clots. 
 
 (6) The Gastro-intestinal form gives rise to diffuse in- 
 flammation, with partial detachment of mucous 
 membranes. Haemorrhages also occur in this situ- 
 ation. In these cases there are few bacilli in the 
 blood, but they are found in great numbers in the 
 bronchi and in lymphatic glands. 
 
 BACILLUS ANTHRACIS. 
 
 1. Characters — 
 
 (1) Shape. — As it occurs in the blood of affected animals, 
 bacillus anthracis consists of straight rods joined end to end, 
 with blunt, slightly curved extremities. Motionless — thus 
 differing from bacillus subtilis. There are no spores in the 
 blood ; these have been seen in the kidneys only. 
 
 (2) Size. — They vary considerably — from 5 to 10 or 20 m. 
 in length — 1 -2 m. broad. 
 
Hydrophobia. 383 
 
 2. Cultivation. — Bacillus anthracis ■wiU grow on gelatine, 
 agar-agar, potatoes, in hay infusions, in aqueous humour. It 
 liquefies jelly, and sinks to the bottom of the vessel in whitish 
 masses. It requires oxygen for its growth. When cultivated 
 in potatoes, it gives rise to dry, creamy, yellow-coloured masses. 
 "When grown at a temperature of 15° to 42° C, it forms long 
 filaments fuU of spores. 
 
 Treatment. — The site of inoculation should he at once 
 incised or touched by the actual cautery. 
 
 If seen after marked symptoms have developed, support 
 the patient with stimulants and quinine. Locally, carbolic 
 acid may be injected into the brawny induration around the 
 seat of inoculation. 
 
 HYDROPHOBIA. 
 
 Is a disease due to the inoculation of a specific poison 
 generated in animals suffering from rabies. 
 
 Symptoms. — The wound by which the poison was intro- 
 duced, as a rule, rapidly heals, and for a time nothing happens 
 to attract the patient's attention to the scar. In about nine 
 weeks or so, the scar may become painful and nervous dis- 
 turbances manifest themselves. The patient becomes sleepless, 
 peevish, irritable, and experiences a choking sensation about 
 the throat. "When the disease is fully developed the spasms 
 become intense, the respiratory muscles and those of deglu- 
 tition are specially involved-; but a more or less tetanoid 
 condition may be observed of nearly all the muscles. The 
 features may be horribly contorted or wear an aspect of 
 extreme terror ; the saliva is not swallowed, and the collection 
 of this in the mouth, causes the so-caUed foaming of the mouth. 
 
384 Student's Hand -hook of Medicine. 
 
 The peculiar hissing character of the inspirations has been 
 magnified hy attendants to barking like a dog. The face is 
 usually flushed or livid during the attacks, and there may be 
 raving delirium, delusions, and hallucinations. It should be 
 noted that, though the patient is very thirsty, he is afraid 
 to drink, as any attempt at swallowing brings on the spasms 
 at once; even the sound of running water wiU excite the 
 attacks. The disease is usually fatal, if left alone, in from 
 two to ten days after the development of the characteristic 
 symptoms. 
 
 Treatment. — The wound when inflicted should be at once 
 sucked, if the mucous membrane of the mouth be unbroken ; 
 ligature when possible above the bite, cauterise the wound or 
 excise the injured part entirely. Watch for symptoms. When 
 practicable send patient to Pasteur's Institute. 
 
 Pasteur's Method. — He obtains a strong virus by successive 
 cultivations of specially inoculated rabbits. When he has 
 succeeded in getting a virus which will cause madness in the 
 shortest possible period, he next exposes certain portions of 
 the prepared or inoculated spinal cord to the air. The air 
 has the power of destroying the virus if it be long enough 
 exposed, consequently the virulence or strength can be gradu- 
 ated by the length of time exposed. Pasteur has found that 
 by inoculating with an extremely weak virus at first, he can 
 by successive inoculations of stronger but graduated virus, 
 render the patient incapable of being afiected with this disease. 
 In other words — he uses up the necessary soil for the develop- 
 ment of rabies, by injections of graduated strengths of the 
 virus. As this can be done during the ordinary incubation 
 period after a bite from a rabid animal, by the time the 
 symptoms of rabies are due as it were, the soil is no longer 
 suitable for the poison to develop, hence no bad results follow 
 the wound first inflicted. 
 
Tetanus or Lock-jaw. 385 
 
 TETANUS or LOCK-JAW. 
 
 It is an infectious disease dependent on the presence and 
 multiplication of a special bacillus, and characterised clinically 
 by severe tonic spasms of the muscles, especially those of the 
 jaw. 
 
 iEtiology. — It most often occurs after trivial injuries to 
 the hands or feet. It has been known to occur in epidemic 
 form amongst newly-born children. When idiopathic in its 
 origin, there is generally a history of sleeping on damp and 
 infected soil. The organism is known as the " bacillus of 
 Nicolaier," who has cultivated it from cprtain putrefying fluids 
 and surface soil. The bacillus has one end knobbed like a 
 drumstick, grows into long threads, is mobile and anaerobic. 
 A ptomaine "tetanine" obtained from a body after death from 
 tetanus will, if inoculated into a healthy animal, produce 
 lock-jaw (Bribgor). 
 
 Symptoms. — Usually within ten days of the injury, the 
 patient complains of stiffness in the neck and muscles of 
 the jaw. Gradually lock-jaw is produced by the tetanic 
 spasm of the muscles ; the eyebrows at the same time become 
 elevated, and the angles of the mouth drawn out, causing the 
 so-called risus sardonicus. Soon all the muscles may be affected 
 with paroxysms of tetanic spasms. The body may be arched, 
 the patient resting on his head and heels (opisthotonus) ; 
 pleurosthotonus or emprosthotonus are also common condi- 
 tions. The pain amounts to agony during the paroxysms. 
 The patient may be bathed in sweat, and the temperature 
 reaches sometimes as high as 110° or 112° before death. 
 
 Diagnosis. — A diagnosis must be made from poisoning by 
 strychnine. It is difficult to confound tetanus with strychnine 
 poisoning, for the latter never causes the jaws to remain 
 tetanically closed between the spasms. 
 
 2 D 
 
386 Student's Hand-book of Medicine. 
 
 Treatment. — Darkened room — absence of any source of 
 irritation. During the severe paroxysms, give chloroform ; be- 
 tween, administer hypodermic injections of morphia, hyoscine, 
 curara, or atropine. The patient may be fed, per rectum, with 
 pancreatised meat extract, etc. 
 
 RUSSIAN INFLUENZA, 
 
 It is extremely difficult to define what condition is exactly 
 meant by the above heading, but possibly the following de- 
 scription will convey the main or essential points. Eussian 
 influenza is a convenient name given to an epidemic disease 
 which has of late swept over Europe, and characterised 
 clinically by — 
 
 1. Sudden onset. 
 
 2. Severe prostration or nervous exhaustion. 
 
 3. Tardy convalescence. 
 
 4. Serious sequelae. 
 
 The disease has but few of the characteristic features of 
 ordinary influenza cold. It is impossible to present a clinical 
 picture that will embrace even the majority of cases. Three 
 distinct types are met with — 
 
 1. Nephritic Type. — When the lumbar pain is intense, 
 general aching of the joints, etc. The urine is scant, high 
 coloured, but contains no albumin. 
 
 2. Respiratory Type. — In which form the thoracic organs 
 tend to become most involved, pneumonia being very common. 
 
 3. Cerebrospinal Type. — A form which simulates cerebro- 
 spinal fever, even unto the petechial rash on the wrists. 
 
 Kitasato claims to have discovered the organism that causes 
 this disease : he describes it as consisting of " small rodlets 
 strung together in threads. These baciUi are found in great 
 numbers in the saliva and sputa of influenza patients." 
 
Russian Influenza., 387 
 
 "The history of the recorded epidemics of La Grippe is 
 marvellously complete for centuries. Every country and every 
 climate in the world is subject to it, yet it appears to find a 
 permanent home nowhere as a constant or endemic resident, 
 but to disappear from the face of the earth for a series of 
 years. This ubiquitous disease has attacked humanity in its 
 own violent fashion at short intervals from probably the 
 earliest ages." (A. B. Griffith's "Bacteriology.") 
 
 Whatever the poison may be, several things are certain : — 
 It carries off the aged and the feeble, and renders ordinary 
 pulmonary diseases much more fatal; for instance, a patient 
 may be recovering from some pulmonary attack, but influenza 
 asserts its presence, and in such cases the patient only too 
 frequently dies in spite of all attention and skill. Blindness, 
 insanity, deafness, and a host of other severe conditions have 
 been reported as results of this peculiar disease. In spite 
 of the many monographs written on this subject, we may 
 as well confess we know little about it ; indeed, it is 
 difficult to get accurate details. The mild form attacks those 
 who can be laid up conveniently — i.e., those whose salaries 
 continue during illness. One is tempted to ask, "Is there 
 a mild form of this disease?" To account for the extreme 
 nervous depression in the real disease, the following theories 
 are suggested — i.e., that 
 
 1. The poison paralyses the cardiac ganglia. 
 
 2. The poison paralyses the cardiac muscle. 
 
 3. The poison paralyses the chief centres of the medulla. 
 
 Treatment. — Stimulants seem absolutely necessary in the 
 bulk of cases. Of drugs, hydrobromic acid, quinine, antipyrin, 
 salicylates, etc., have their advocates, but each case must be 
 considered in detail and treated accordingly. 
 
INDEX. 
 
 Abdomen, tubercular disease of, see 
 
 Tabes Mesenterica, 
 Abdominal aneurism, 219 
 Abscess of brain, 115 
 
 liver, 237 
 
 peri-nephritic, see Pyelitis 
 
 Abscesses, metastatic, 48 
 
 Acromegalia, 377 
 
 Actinomycosis, 378 
 
 Addison's disease, 286 
 
 Addnie, see Hodgkin's Disease ' 
 
 Adherent pericardium, 199, 200 
 
 Ague, 33 
 
 cake, 32 
 
 Albuminuria, 250 
 
 physiological, 251 
 
 in levers, 251 
 
 Alcohol, in disease, 7 
 
 neuritis, 146 
 
 Amaurosis, 89 
 
 Amblyopia, 89 
 
 Amyotrophic lateral sclerosis, 81 
 
 AuEBmia, 305 
 
 idiopathic, 305 
 
 lymphatica, see HodgMn's 
 
 Disease 
 
 pernicious, 305, 308 
 
 Anaesthesia, 69, 72 
 Aneurism, abdominal, 219 
 
 bronchial, 172 
 
 congenital, 219 
 
 miliary, 113 
 
 thoracic, 216 
 
 Angina pectoris, 220 
 Ankle clonus, 67 
 Anthrax, 380 
 
 Aortic aneurism, 215, 218, 
 
 regui'gitation, 209 
 
 stenosis, 209 
 
 Aphasia, 120 
 
 Aphonia, hysterical, 193 
 
 Apoplexy, cerebral, 115 
 Appendicitis, 332 
 Argyll-Kobertson pupil, 79 
 Arrhythmia, 220 
 Arterial atheroma and thrombosis, 118 
 
 degeneration, 62 
 
 Arteries of brain, 107 
 Arthritis, gonorrhoeal, 302 
 
 rheumatic, 302 
 
 Ascaris lumbricoides, 365 
 Ascites, 241, 843 
 
 treatment of, 243, 345 
 
 Asiatic cholera, 39 
 Asthma, 179 
 
 — — treatment of, 181 
 
 varieties of, 179 
 
 Ataxy, locomotor, 78 
 Ataxic paraplegia, 82 
 Atelectasis, 183 
 Athetosis, 117 
 Atrophy, 73 
 acute yellow, 235 
 
 of liver, 239 
 
 Aura, epileptic, 136 
 
 BaciBi, method of staining, 55 
 
 Bacillus anthracis, 382 
 
 Bile acids and pigment, tests for, 234 
 
 ducts, catarrh of, 232 
 
 Biliary colic, 249 
 
 Bleeders, 375 
 
 Blood, diseases of, 305 
 
 in leucocythsemia, 310 
 
 Bones in rickets, 297 
 Bothriocephalus latus, 366 
 Bowels, cancer of, 336 
 - — - catarrh of, 339 
 
 inflammation of, 339 
 
 intussusception of, 337 
 
 obstruction of, 335 
 
 Bradycardia, 220 
 
390 
 
 Index. 
 
 Brain, abscese of, 115 
 
 ai'teries, lesions of, 113 
 
 blood clot in, 114 
 
 • circulation of the, 107 
 
 ■ cortical centres of, 109 
 
 embolism of, 117 
 
 functions of, 109 
 
 glioma of, 121 
 
 hsemorrhage into, 113 
 
 internal capsule of, 61 
 
 softening of, 113 
 
 thrombosis of, 117 
 
 tumours of, 121 
 
 water in the, 129 
 
 Breast pang, angina pectoris, 220 
 Bright's disease, acute, 256 
 
 chronic, 259 
 
 Bronchial aneurisms, 172 
 
 tubes, ulceration of, 156 
 
 Bronchiectasis, 156 
 Bronchitis, acute, 1S3 
 
 capillary, 154 
 
 chronic, 155 
 
 Broncho-pneumonia, 161 
 Bubo, parotid, 13 
 Bulbar paralysis, 102 
 
 Calculi, biliary, 248 
 
 renal, 265 
 
 Calculous pyelitis, 265 
 Cancer of bowel, 386 
 Kver, 246 
 
 lung, 186 
 
 cesophagus, 319 
 
 peritoneum, 347 
 
 stomach, 319 
 
 Oancrum oris, 370 
 Capillary pulse, 125 
 Carbuncle in diabetes, 280 
 Cardiac diseases, 193 
 Cardio-vascular changes in Bright's 
 
 disease, 257, 260 
 Casts, renal, 257, 260 
 Catarrh, 
 acute gastric, 329 
 
 bronchial, 163 
 
 chronic enteric, 339 
 
 of bile ducts, 232 
 
 of bowels, 339 
 
 Catarrhal pneumonia, 161 
 Centres, cerebral motor, 109 
 
 for eyeball movements, 90 
 
 for hearing, 110 
 
 for smell, 110 
 
 for taste, 110 
 
 for vision, 109 
 
 Cerebral abscess, 115 
 Cerebral apoplexy, 115 
 
 arteries, lesions of, 113 
 
 blood-Bxipply, 107 
 
 cysts from blood clots, 122 
 
 embolism, 117 
 
 hajmorrhage, seats of, 114 
 
 meningitis, 123 
 
 miliary aneurisms, 113 
 
 softening, 113 
 
 thrombosis, 117 
 
 tumours, 121 
 
 veins and sinuses, 108 
 
 Cerebro-spinal meningitis, 28 
 
 sclerosis, 126 
 
 cestoda, 352 
 
 Charbon, 380 
 
 Charcot's joint disease, 80 
 
 Cheyne-Stokes' respiration, 151 
 
 Chicken-pox, 42 
 
 Chlorosis, 305 
 
 Cholera, Asiatic, 89 
 
 Chorea, 132 
 
 its relation to rheumatism and 
 
 heart disease, 132 
 Chyluria, 367 
 Cirrhosis of kidneys, 259 
 liver, 289 
 
 lung, 184 
 
 Clonus, ankle, 67 
 Colic, hepatic, 249 
 Collapse, pulmonary, 183 
 Coma, diabetic, 278 
 in apoplexy, 116 
 
 ursemio, 256 
 
 vigil, 4 
 
 Conjugate deviation of head and 
 
 eyes, 116 
 Constitutional syphilis, 60 
 Consumption, pulmonary, 170 
 Convulsions, epileptic, 66 
 clonic, 66 
 
 infantile, 139 
 
 tetanic, 29 
 
 tonic, 66 
 
 ursemic, 256 
 
 Co-ordination, 66 
 Cortical motor centres, 109 
 Cranial nerves, affections of, 86 
 Cranio-tabes, 139 
 Cretinism, 284 
 
 Crisis, 11 
 
 Croup, true, 27 
 
 — ^ tracheotomy in, 28 
 
 treatment of, 28 
 
 Cms cerebri, lesion of, 20 
 
Index. 
 
 391 
 
 Cursohman's spirals, 180 
 
 Cystic disease of kidneys, see Pyelitis 
 
 Cysticercus cellulosie, see Trichinss 
 
 Degeneration, arterial, see Fatty 
 Heart, etc. 
 
 " reaction of," 63 
 
 of nerve's and cord, 63 
 
 of muscles, 63, 66 
 
 Delirium in fevers, 7 
 Diabetes insipidus, 267 
 
 mellituB, 276 
 
 diet in, 281 
 
 treatment of, 281 
 
 Diarrhoea, 341 
 
 in enteric fever, 11 
 
 in tubercular ulceration, 341 
 
 lienteric, see Chronic Diarrhasa 
 
 Dilatation of bronchi, 153, 155, 156 
 
 heart, 207 
 
 stomach, 330 
 
 Diphtheria, 24 
 Diphtheritic paralysis, 26 
 Disease, Addison's, 286 
 
 causation of, 286 
 
 Graves', 222 
 
 the complexion in, 
 
 Disseminated sclerosis, 126 
 Distoma hsematobium, 366 
 Dropsy, 343 
 
 fluid in, see Ascites 
 
 Duodenal ulceration, see Ulcer of 
 
 Stomach, 
 Dura mater, inflammation of, 123 
 Dysentery, 36 
 Dyspepsia, 
 
 varieties, 328 
 
 treatment of chronic, 328 
 
 Electrical reactions in health, 64 
 Embolism, 117 
 
 cerebral, 118 
 
 in chorea, 133 
 
 infective, 119 
 
 Emphysema, 187 
 
 atrophous. 181 
 
 compensatory, 181 
 
 ^— hypertrophous, 181 
 
 - treatment of, 182 
 
 vesicular, 181 
 
 Empyema, 168 
 Endocarditis, acute, 201 
 -^ — chronic, 204 
 
 ulcerative, 202 
 
 treatment of, 203 
 
 Enteric fever, 8 
 
 Enteritis, 399 
 Epilepsia gravior, 134 
 
 minor, 134 
 
 Epilepsy, 134 
 Epilepsy, feigned, 137 
 — : — Jacksonian, 138 
 Epileptic aura, 135 
 
 convulsions, 136 
 
 Exophthalmic goitre, 222 
 
 Facial paralysis, 97 
 
 Fatty degeneration of heart, 220 
 
 of liver, 244 
 
 infiltration, 244 
 
 Fever, cerebro-spinal, 29 i 
 
 course and terminations of, 29 
 
 enteric, 8 
 
 gastric, 8 
 
 intermittent, 30 
 
 malarial, 30 
 
 pa.thology, 36 
 
 pbysiology, 4 
 
 relapsing, 34 
 
 remittent, 33 
 
 rheum'atic, 288 
 
 scarlet, 18 
 
 anginose, 18 
 
 malignant, 16 
 
 simple continued, 3 
 
 symptoms of, 3 
 
 treatment of, 5 
 
 typhoid, 8 
 
 typhus, 12 
 
 yellow, 46 
 
 Fibroid phthisis, 176 
 Filaria sanguinis hominis, 364 
 Foot and mouth disease, 369 
 Friedreich's disease, 83 
 Friction sounds, pericardial, 199 
 
 pleural, 166 
 
 Functional disorders of heart, 196 
 
 Gaits, table of, 144 
 
 in paralysis agitans, 131 
 
 in spastic paraplegia, 144 
 
 in tabes dorsalis, 144 
 
 Gall stones, 244 
 
 Gangrene of lung, 169 
 
 Gastric carcinoma, see Cancer of 
 
 Stomach 
 ^— catarrh, acute, 329 
 chronic, 326 
 
 crisis, 80 
 
 ulcer, 316 
 
 • treatment, 317 
 
 ■ vomiting, 318 
 
392 
 
 Index. 
 
 Gastritis, 326, 329 
 Gastrodynia, 318 
 German measles, 23 
 Gliomata of brain, 121 
 Glosso-labio-pliaryngeal palsy, 102 
 Glottis, oedema of, 187 
 
 spasm of, 191 
 
 Glycosuria, 229 
 Goitre, exophthalmic, 222 
 Gonorrhoea! synovitis, 304 
 Gout, acute, 294 
 
 causes of, 281 
 
 chronic, 295 
 
 pathology of, 292 
 
 retrocedent, see Gout 
 
 rheumatic, see Gout 
 
 treatment of, 296 
 
 Granular kidney, 264 
 Graves' disease, 222 
 
 Hfflmatemesis, 330 
 
 treatment of, 332 
 
 Haematinuria, paros^ysmal, 254 
 Ha^maturia, 253 
 
 causes of, 253 
 
 parasitic, 253, 254 
 
 Hemoglobinuria, 253 
 Haemophily, 375 
 Hemoptysis, 171, 172, 175, 331 
 HiBmorrhage, 
 
 cerebral, 115 
 
 pons, 97, 117 
 
 meningeal, 123 
 
 Hsemorrhagic diathesis, 375 
 Haut mal, 134 
 
 Heart disorders, 188 
 
 chronic valvular lesions of, 204 
 
 dilatation of, 207 
 
 Heart, fatty degeneration of, 207 
 
 functional disorders of, 220 
 
 hypertrophy of, 206 
 
 in acute fevers, 4 
 
 organic disease of, 198 
 
 prognosis in, 211 
 
 ■ palpitation of, 220 
 
 treatment in disease of, 212 
 
 Hemianesthesia, 117 
 Hemiopia, 89 
 
 Hemiplegia, 116 
 
 causes and diagnosis of, 116, 117 
 
 rigidity in, 117 
 
 Hepatic abscess, 237 
 
 colic 
 
 Hepatitis, 235 
 
 Hippocratic succession, 177 
 Hobnail liver, 240 
 
 Hodgkin's disease, 313 
 Hydatid cyst, 359 
 Hydatids of liver, 246 
 Hydremia, 305 
 HydrooephaJuB, 129 
 Hydroneplirosis, 267 
 Hydropericardium, 198 
 Hydrophobia, 383 
 Hydrothorax, 178 
 Hydro-pneumothorax, 177 
 Hyperesthesia, 71 
 Hyperpyrexia, 10 
 Hypoglossal nerve, 102 
 Hypostatic congestion, see CEdema 
 
 of Lung 
 Hysteria, 138 
 Hysterical fit, 140 
 Hystero-epilepsy, 140 
 
 Icterus neonatorum, 235 
 Idiopathic anemia, see Anemia 
 Indigestion, see Dyspepsia 
 Infantile convulsions, 139 
 
 paralysis, 73 
 
 Inflammation of bowels, 299 
 Influenza, 386 
 Intermittent fever, 30 
 Intestinal iroi'ms, 351 
 Intestines, cancer of, 336 
 
 catarrh of, 339 
 
 diseases of, 332 
 
 obstruction of, 336 
 
 tubercular, see Phthisis 
 
 Intussusception, 336 
 
 Jacksonian epilepsy, 138 
 
 Jaundice, 231 
 
 in duodenal infiammation, 232 
 
 treatment of, 234 
 
 Joints, inflamed in nervous diseases, 
 
 see Locomotor Ataxia 
 Kidney, 
 ■ congestion of, 254 
 
 granular, 264 
 
 large red, 264 
 
 • white, 264 
 
 waxy, 259 
 
 Knee jerk, causes of loss of, 63, 67 
 - — in spastic paraplegia, see Spastic 
 Paraplegia 
 
 in tabes dorsalis, 79 
 
 Labio-glossal paralysis, 102 
 Lardaceous disease, 243 
 
 from phthisis, suppuration, 
 
 and syphilis, 62, 171, 243 
 
Index. 
 
 393 
 
 Laryngeal, 
 
 palsy, 19:i 
 
 phthisis, 189 
 
 Laryngismus stridulus, 190 
 Laryngitis, acute, 187 
 
 chronic, 189 
 
 Larynx, acute diseases of, 187 
 ■ acute cedema of, 187 
 
 obronio diseases of, 189 
 
 new growths of, 189 
 
 symptoms common to organic 
 
 lesions of, 189 
 
 ulcerations of, 189 
 
 Lepto-meningitis, 123 
 Leucin, 226 
 Leucocythsemia, 310 
 Lightning pains, 79 
 
 Liver, remarks on diseases of the, 224 
 
 abscess of the, 237 
 
 acute yellow atrophy of, 235 
 
 atrophy of the, 47 
 
 cancer of the, 245 
 
 common cirrhosis of the, 239 
 
 fatty, 244 
 
 hydatid of the, 246 
 
 ' inflammation of the, 235 
 
 lardaceous or waxy, 243 
 
 nutmeg, 210 
 
 syphilitic, 236 
 
 Lobar pneumonia, 157 
 Lobular pneumonia, 161 
 Locomotor ataxia, 78 
 Lumbago, see Rheumatism 
 Lung, 148 
 
 atelectasis, 183 
 
 cancer of, 186 
 
 cirrhosis of, 184 
 
 collapse of, 183 
 
 emphysema of, 181 
 
 • gangrene of, see Croupous Pneu- 
 monia 
 
 haemorrhage from, 171, 172, 175 
 
 oedema of , 183 
 
 tuberculosis of, 170 
 
 tumours of, 186 
 
 Lymphadenoma, see Hodgkin's 
 
 Disease 
 Lysis, 8 
 
 Malai'ial fever, 30 
 
 dysentery in, 33 
 
 Malignant, pustule, see Anthrax 
 Measles, 21 
 
 -i Grerman, 23 
 
 tumours, see Hodgkin's Disease 
 
 Meningeal htemorrhage, 123 
 Meningitis, 123 
 
 cerebro-spinal, 27 
 
 chronic, 70 
 
 simple, 123 
 
 spinal, 68 
 
 tubercular, 123, 124 
 
 varieties of, 123 
 
 Metastatic abscesses, 48, 203 
 Miliary aneurisms, 11 3 
 Mitral regurgitation, 209 
 
 stenosis, 209 
 
 Motor centres, 109 
 Mouth, diseases of, 368 
 Mumps, 43 
 Murmurs, hsemic, 197 
 Muscles, degeneration of, 63,. 65 
 Muscular, atrophy, 74 
 
 progressive, 75 
 
 Muscular rheumatism, 301 
 Mydi'iasie, causes of, 90 
 Myelitis, acute, 71 
 
 differential diagnosis, 72 
 
 Myocarditis, 220 
 Myxoedema, 282 
 
 Nematoid worms, 360 
 Nephritis, acute, 256 
 
 interstitial, 259 
 
 lardaceous, 259 
 
 parenchymatous, 259 
 
 Nerve storms, 135 
 
 facial, 96 
 
 fifth, 94 
 
 hypoglossal, 102 
 
 sixth, 92 
 
 spinal accessory, 102 
 
 third, 90 
 
 Nerves, cranial, 86 
 degeneration of, 63 
 
 diseases of the, 145 
 
 Nervous system, diseases of, 57 
 
 functional diseases of, 131 
 
 tracts, 59 
 
 reflexes, 62, 67 
 
 spasm and rigidity, 65 
 
 Neuralgia, 147 
 Neurasthenia, 141 
 Nem'itis, alcoholic, 146 
 
 multiplex, see Alcoholic Neuritis 
 
 peripheral, 146 
 
 Nutmeg liver, 210 
 
 Nutrition, diseases of, see Infautile 
 
 Nystagmus, 91 
 
394 
 
 Index. 
 
 Obstruction of the bowels, 335 
 
 pyloric, see CaDcer of Stomach 
 
 oegophony, 165 
 
 Oidium albicans, see Stomatitis 
 Olfactory nerves, 87 
 Oligsemia, 305 
 
 Opisthotonos, cervical, 30, 69 
 Ophthalmoplegia externa, see sixth 
 Nerve 
 
 interna, see sixth Nerve 
 
 Optic nerve atrophy, 89 
 neuritis, 89 
 
 tracts, disease of, 88 
 
 Organic heart disease, 198 
 Oxyuris vermicularis, 361 
 
 Pachymeningitis, 123 
 
 Palpitation, 220 
 
 Pancreas, diseases of, see Diabetes 
 
 Mellitus 
 Paralysis, acute atrophic, 72 
 
 agitans, 131 
 
 bulbar, 102 
 
 diphtheritic, 26 
 
 ■ facial, 96 
 
 general, 128 
 
 glosso-labial, 102 
 
 Paralysis, hysterical, 140 
 
 infantile, see Poliomyelitis 
 
 Anterior Acuta 
 
 in progressive muscular 
 
 atrophy, 76 
 
 laryngeal, 192 
 
 of fifth nerve, 94 
 
 hypoglossal nerve, 102 
 
 peripheral nerves, 146 
 
 sixth nerve, 92 
 
 spinal accessory nerve, 102 
 
 third nerve, 90 
 
 1. ulnar nerve, 147 
 
 pseudo-hypertropic, 84 
 
 Paraplegia, 71 
 
 hysterical, see Hysteria 
 
 spastic, 76 
 
 parasitic, 351 
 
 Parkinson's disease, see Paralysis 
 
 Agitans 
 Parotid bubo, 13 
 Parotitis, 43 
 
 Paroxysmal hEematinnria, 254 
 Pectoris, angina, 220 
 Pericarditis, 198 
 
 treatment, 201 ' 
 
 Pericardium, adherent, 199, 200 
 
 pyo-, 199 
 
 Perihepatitis, see Liver 
 Perinephric abscess, see Pyelitis 
 Peripheral neuritis, 146 
 Peritoneum, diseases of, 343 
 Peritonitis, 346 
 
 varieties of, 346 
 
 treatment, 348 
 
 Perityphlitis, 332 
 Pernicious auEemia, 308 
 Pertussis, 44 
 PetechiiB, 203 
 
 Petit mal, 134 
 Phthisis, 170 
 
 acute, 168 
 
 common, 170 
 
 complications of, 175 
 
 fibroid, 176 
 
 hsemorrhagic, 171, 172, 176 
 
 treatment, 174 
 
 Pleura, air in the, 176 
 
 dropsy of the, 178 
 
 Pleurisy, acute, 163 
 
 treatment, 167 
 
 Pueumonia, acute, croupous, or 
 
 lobar, 157 
 — - broncho - lobular or catarrhal, 
 
 161 
 indurated, 184 
 
 interstitial, 181 
 
 pulse-respiration, ratio in, 160 
 
 treatment, 160 
 
 Pneumothorax, 176 
 Podagra, see Gout 
 Poikilocythsemia, 306 
 Poliomyelitis, 73 
 Polyneuritis, 146 
 
 Polyuria, see Diabetes Insipidus 
 Post-hemiplegic chorea, 117 
 Pressure signs, thoracic, 216 
 Progressive muscular atrophy, 75 
 Pseudo-hypertrophic paralysis, 84 
 Ptosis, spasmodic, 90 
 Pulmonary system, 148 
 
 collapse, 154 
 
 consumption, 170 
 
 stenosis, 196 
 
 Pulse in aortic disease, 211 
 Pupils, Argyll-Eobertson, 79 
 
 contracted, dilated and 
 
 irregular, 90 
 Purpura, 376 
 
 varieties of, 376 
 
 Pus in urine, 275 
 Pustule, malignant, 380 
 Pysemia, arterial, 48 
 
 in dysentery, 38 
 
Index. 
 
 395 
 
 Pyelitis, 265 
 
 Pyloric stenosis, 319, 320 
 Pyo-nephrosis, 265 
 Pyrexia, symptoms of, 3 
 Pyuria, 276 
 
 Quinsy, 370 
 
 Babies, 383 
 Bachitis, 297 
 Baynaud's disease, 372 
 Eegurgitation, aortic, 209 
 mitral, 209 
 
 tricuspid, 209 
 
 of food, 25 
 
 Belapsing fever, 34 
 Bemittent fever, 33 
 Bespiration, Oheyne Stokes', 151 
 Betinal hEemorrhages, 309 
 Bheumatic arthritis, 290, 302 
 Bheumatic fever, 288 
 
 ■ complications of, 290 
 
 treatment of, 291 
 
 gout, see Gout 
 
 Eheumatism, chronic, 300 
 
 gonorrhoea!, 304 
 
 muscular, 301 
 
 Rickets, 297 
 Bigidity of limbs, 65 
 Romberg's symptom, 79 
 Rotheln, 23 
 
 Bound worms, 365 
 Bubeola, 23 
 
 Sago spleen, 32 
 Sapreemia, 48 
 SepticEemia, 48 
 Sarcinse ventriouli, 330 
 Scarlatina, 18 
 Sclerois, 67 
 
 cerebro-spinal, 126 
 
 disseminated, 126 
 
 lateral, 76 
 
 posterior spinal, 78 
 
 Scybala, 336 
 Scurvy, 373 
 Sensory crossway, 60 
 
 path, 59 
 
 Skodaic resonance, 166 
 Small-pox, 14 
 Softening of brain, 113 
 Sore throat, 370 
 Spasm, 66 
 
 Spastic paraplegia, 76 
 
 Spinal accessory nerve, 102 
 
 degenerations of, 63 
 
 diseases of, 71 
 
 irritation of, 68 
 
 meningitis, 68 
 
 myelitis, 72 
 
 sclerosis, posterior, 78 
 
 Spleen, diseases of, 313 
 Status epilepticus, 136 
 Stomach, atrophy of, 332 
 
 cancer of, 319 
 
 catarrh of, 329 
 
 dilatation of, 330 
 
 diseases of, 315 
 
 ulcer of, 315 
 
 washing out, 330 
 
 Stomatitis, varieties of, 369 
 Stools, lient6ric,342 
 
 of cholera, 40 
 
 of dysentery, 37 
 
 of enteric fever, 11 
 
 of enteritis, 340 
 
 of intussusception, 337 
 
 of jaundice, 234 
 
 of rickets, 299 
 
 Subsultue tendinum, 4 
 Sugar in the urine, 276 
 Suppression of urine, 255 
 Symmetrical gangrene, 372 
 Syncope, 211 
 
 Syphilis, 50 
 
 Syphilitic arterial disease, 52 
 
 eruptions, 51 
 
 Tabes dorsalis, 78 
 
 mesenterica, 350 
 
 Tachycardia, 220 
 TEenia solium, 354 
 
 echinococcus, 368 
 
 mediocanellata, 356 
 
 Tapeworms, 352 
 Tenesmus, 36 
 Tetanus, 385 
 Tetany, 143 
 Thomsen's disease, 142 
 Thread worms, 360 
 Thrombosis, 117 
 
 cerebral, 118 
 
 Thrush, 368 
 Thyroid, enlarged, 222 
 Tongue, inflamed, 369 
 Tonsils, inflammation of, 370 
 Tormina, 36 
 
 Torticollis, 301 
 
 Tremors in disseminated sclerosis, 127 
 
 in paralysis agitaus, 131 
 
396 
 
 Index. 
 
 Trichinosis, 363 
 TricuBjad regurgitatiou, 209 
 
 stenosis, 209 
 
 Trophic changes in skin, 80 
 Tubercular meningitis, 123, 124 
 
 disease of abdomen, 348 
 
 Tuberculosis. 54 
 Typhlitis, 332 
 
 Typhoid fever, 8 
 
 state, 3 
 
 Typhus fever, 12 
 Tyrosin, 226 
 
 Ulcer, gastric, 315 
 Ulceration of intestines, 341 
 Ulcerative endocarditis, 201 
 Urcemia, 256 
 
 Urinary system, diseases of, 250 
 Urine, albumin in, 250 
 
 alkaline tide of, 268 
 
 ammoniacal, 268 
 
 blood in, 253 
 
 • decomposition of, 268 
 
 effects of medicines on, 253 
 
 in acute yellow atrophy, 236 
 
 in Bright's disease, 267, 260 
 
 in diabetes, 277 
 
 in hsematuria, 263 
 
 in hasmoglobinuria, 253 
 
 in health, 268 
 
 in hydronephrosis, 265 
 
 in paroxysmal heematinuria, 264 
 
 in pneumonia, 160 
 
 Urine, milky, see Filaria Sanguinis 
 Homiuis 
 
 pigments of the, 272 
 
 — - pus in, 275 
 
 solids of, 268 
 
 suppression of, 256 
 
 tests for albumin in, 269 
 
 for sugar in, 271 
 
 Vaooitiia, 18 
 
 Valvular disease of heart, 208 
 
 diagnosis of, 209 
 
 Varicella, 42 
 Variola, 14 
 
 Vaso-renal change, 260 
 Voice affections, 187 
 Volvulus, 337 
 Vomiting, 318, 320 
 
 symptomatic, 122 
 
 Von Graefe's symptom, 222, 223 
 
 Wallerian degeneration , fee Secondary 
 Degeneration of Nerves 
 
 Wasting diseases, nerves and muscles 
 in, 63 
 
 Whooping-cough, 44 
 
 Willis, circle of, 107 
 
 Worms, intestinal, 361 
 
 Wrist drop, 146 
 
 Wry neck, see Rheumatism 
 
 Yellow fever, 46 
 
 atrophy of liver, acute, 236 
 
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 A MAGNIFICENT WORK. 
 
 Makes a Handsome Present to a Senior Medical 
 Student or Practitioner. 
 
 THE 
 
 Topographical Anatomy 
 of the Child 
 
 JOHNSON SYMINGTON, M.D., 
 
 F.R.S.E., F.R.C.S.E., 
 
 Frqfeesor of Anatomy, Queen's College, Belfast; formerly Lecturer on Anatomy, 
 School of Medicine, and Examiner in Anatomy, University of Edinburgh. 
 
 ILLUSTRATED LY 
 
 FOUKTEEN BEAUTIFUL AND COBREOTLY COLOURED PLATES (NEAHLY ALT, 
 OF WHICH ABE LIFE SIZE) AND THIRTY-THBEE WOODCUTS. 
 
 This magnificent work forms one of the most important and most valuahleof 
 the recent contributions to human anatomy. Topographical Anatomy is usually 
 considered independently of the age and sex of the subject, and there can he no 
 question that many of its data require reconsideration. 
 
 The present work is founded upon the examination of a series of frozen^sectioiis 
 of the bodies of children. It is illustrated by fourteen life-sized coloured Plates, 
 and by a number of Woodcuts. Of the excellence and fidelity of the Plates it is 
 impossible to speak too highly. They reflect the greatest credit upon the 
 Publishers. 
 
E. & a LIVINGSTONES' PUBUCATIONS. 
 
 THE TOPOGEAPHICAL ANATOMY OF THE CHILD. 
 
 The Tertical medial sections and some coronal sections of the thorax are the 
 most valuable. Sections are ^iven (»f all parts of the trunk; of the skull, to show 
 the orbits and nasal fossse; of the neck, to show the position of the larynx; of 
 iha thorax, abdomen, and pelvis. 
 
 The First Part of the work is devoted to a critical explanation of the Plates. 
 The Second Part deals systematically with the more conspicuous results of the 
 author's inrestigations. The topographical anatomy of the auditory meatus and 
 tympanum, tlie condition of the spinal curve in children, the topography of the 
 brain, and the relational anatomy of the male and female genital organs, are all 
 dealt with in an able aud original manner. 
 
 Dr Symington's book abounds in original material. It is a work that no 
 anatomist can afford to overlook. It adds materially to ovir knowledge of the 
 mnst practical branch of anatomy, and is a credit to modern sclentlflc research. 
 — The Inter-national Journal of the Medical Sdmces, October 1887. 
 
 " While the anatomy of the human subject, during the earlier months of intra- 
 uterine life, has been investigated with great care and minuteness, and while 
 our knowledge of the topographical anatomy of the adult has been enriched by 
 the labours of numerous Investigators, comparatively little attention has been 
 paid to the peculiarities in the anatomy of the infant, and the changes that occur 
 from the time of birth up to that of adult life."— In these words Dr Symington 
 gives the reasons that have moved him to undertake and carry through the 
 investigation of which this volume forms the very tangible result. Not only is 
 it true that very litUe has been published on the subject, but it is also true that 
 no inconsiderable part of that little was erroneous; and there is scarcely a page 
 of this book but corrects some common error, or throws new light on anatomical 
 relations as they occur in the child. 
 
 The mode of investigation pursued lias been mainly that by sagittal, horizontal, 
 and coronal frozen sections of the body made at different levels, but supplemented 
 by other methods where fuller information was required. The work is divided 
 into two Sections, the First foimlng a running commentary on the Plates, and the 
 Second a formal discussion of the points wherein differences are observable 
 between the anatomy of the adult and that of the child. 
 
 Hitherto, anatomists have had no very clear ideas as to the date of formation 
 ni the air cavities in the mastoid, frontal, and superior maxillary bones, in all of 
 which, but more especially the first, accurate knowledge as to their presence or 
 absence at a given age might be of essential importance in a surgical aspect. Dr 
 Symington has brought much evidence to bear on the subject, and if he has not 
 settled the question, has done much to elucidate it. He found that the antrum 
 mastoideum (a cavity, as he remarks, generally overlooked by anatomists) waa 
 present at the time of birth in all the specimens examined by him; but he Is oi 
 opinion that the pneumatic cavities generally are not formed in the lower part 
 of the mastoid till about the time of puberty. This it will be seen is an important 
 observation in connection with the question of trephining the mastoid for suppura^ 
 tion of the middle ear. The frontal sinuses he found in his specimens to be absent 
 at six years of age and present at nine, so that we have thus pretty clearly indicated 
 the date at which they commence to form. In regard to the antrum oi Highmore, 
 he notes that, as a rule, it opens into the infimdibulum, and not. as is commonly 
 stated, into the middle meatus, although sometimes a second opening is found 
 leading directly into the latter. 
 
 On the much disputed point as to the position of the heart in children, he 
 dissents from the view that in them the base of the heart is higher than in adults. 
 He calls attention, however, to the greater relative size of the heart, and the 
 nai rown^s of the front of the chest in children , and remarks that as a consequence 
 tlie apex of the heart reaches to, or even beyond, the nipple line, and may be 
 felt in the fourth intercostal space as well aa the fifth* 
 
 We would note as especially worthy of careful perusal, the section on the 
 position and growth of the larynx, that on the production of the lumber curve 
 of the vertebral column, and the elaborate account of Dr Symington's researches 
 into the development of the jaws and teeth. 
 
E. & S LIVINGSTONES' PUBLICATIONS. 
 
 THE TOPOGRAPHICAL ANATOMY OF THE CHILD. 
 
 The numerous references at the bottom of each page testify to the painstftking 
 care with which the author has studied the subject, as well as displaying a 
 praiseworthy anxiety to give full credit to all fellow-workers in the same field. 
 
 We must not omit to express our high appreciation of the clearness, accuracy. 
 and artistic finish of the coloured Plates. The numerous reference lines crossing 
 their surface do to some extent mar their beauty, but these lines greatly simplify 
 the understanding of the plates, and render unnecessary the usual reference tables, 
 and to obtain so desirable a result even greater sacrifices miglit have been excused. 
 We congratulate I)r Symington on the successful termination of his important 
 investigation.— 7%e Glasgow MedicalJoumal, November 1887. 
 
 To the study of sections of the frozen human body we owe most of the recent 
 great advances in our knowledge of Topographical Anatomy. The older method 
 of dissection catises a certain amount of displacement, and often destroys the 
 lelations of important deep parts to tlieir supei-ficial landmarks; and, therefore, 
 until this new method enabled us to check the results of dissection, many false 
 views were current concerning the actual situation of organs. Dr Symington's 
 work is one of the most valuable contributions to the literature of Sectional 
 Anatomy; aud is one of the most creditable pieces of original research in this 
 department that have been produced in Britain within the last few years. He has 
 illustrated the topography of a number of parts which are of the deepest interest 
 to tlie practical surgeon and physician as well as to the anatomist, such as the 
 relative positions of the heart, lungs, and liver at different levels, the relations of 
 the larynx and trachea, and the pelvic viscera in children of the two sexes. All of 
 these are points concerning which the practitioner requires to have the most precise 
 knowledce, on account of their bearing on tracheotomy, lithotomy, i&c 
 
 'I'he letterpress has been written with much care, and shows an extensive 
 acquaintance with the literature of the subject. We note with special interest the 
 sections on the Topography of the Eui-, the Jaws and Teeth, the Heart, and the 
 Bladder, us worthy of particular attention. Altogether we can commend the work 
 as an excellent and trustworthy guide, and one which the practical physician and 
 the operating surgeon will do well to consult.— f/ie Practitioner, August 1887. 
 
 I'he book before us is probably one of the must important contributions to our 
 knowledge of human Anatomy that the ILdinburgh School has furnished for many 
 years, and Dr Symington itiay be congratulated on the completion of a work of such 
 sterling worth. The task which the authoi- set before him was the Investigation of 
 those peculiarities of structure which are to be seen between the time of birth and 
 the attainment of maturity. These two extremes of the period have been often 
 fully discussed, but not so the intermediate stages; hence the importance of trying 
 to trace the steps of change from one to the other. Although it might have been 
 possible to infer the association of peculiarities of structure from some that are 
 well known, the method would have been a dangerous one, and unscientific ; and 
 Dr Symington has carefully and methodically followed the safer plan of original 
 investigation. Since the differences to be expected are chiefiy questions of the 
 relative size and position of various parts and organs, no method of research was 
 likely to yield such good results as that of frozen sections— the one adopted in the 
 present instance. 
 
 The work is divided into two Parts. The First Part consists of a series of Plates, 
 illustrating sections of the bodies of children cut in various directions, with 
 sufflcient explanatory text to make clear all peculiarities of structure, and with 
 the addition of Woodcuts where considered advisable. The general plan of the 
 sections is much the same as that carried out by Braune and other investigators 
 of adult structure. The first Plate represents a mesial section of a girl, set. 13 ; 
 the next, a similar one of a boy, skt 6. The third and fourth Plates represent 
 various sections of the head; while from Plates V. to X. inclusive, serial cross 
 sections of the trunk are represented. Plate XI. has one cross section, and one 
 in the mesial plane illustrating the lower part of the abdomen and pelvis Plate 
 XII consists of two most valuable figures, illustrating the relation of Internal 
 viscera to the abdominal and thoracic walls constructed synthetically from cross 
 
E. & a LIVINGSTONES' PUBLICATIONS. 
 
 THE TOPOGRAPHICAL ANATOMY OF THE CHILD. 
 
 sections. One is from the body of the (firl, set. 6, from which the series of cross 
 sections has been figured ; and the other is ftom the body of a boy, set. fi, which 
 was used to illustrate several doubtful points, and from which several woodcuts 
 were drawn. Both views are from the front, and, of course, represent the thorax 
 in extreme expiration. An extra view from behind might have been an advantage. 
 On the figure of the female child's body are marked delicate lines, indicating the 
 sections and a reference to the Plate where the view of the section itself may be 
 found. Tliis will prove of great service in the study of tbe Plates. Corresponding 
 references to the woodcuts in the other built-up figure sei-ve a similar purpose. 
 Plates XIII. and XIV. are from vertical transverse sections of the thorax and 
 abdomen. The execution of the Plates is excellent, and gives evidence of care no 
 less than of artistic skill. 
 
 In the explanatory text Dr Symington has entered as much into detail as each 
 Part seems to require. It wonld have been better had he mentioned the thickness 
 of each section, so as to enable the reader to follow the series more easily, but the 
 need for this is less since tbe synthetical figure has been given on Plate XII. 
 
 The Second Fart is perhaps the more valuable portion of the work. Here, under 
 separate sections, the peculiarities of structure of the child are systematically 
 discussed. After an inti'oductory sketchof the literature of the subject, the author 
 takes up the Brain, and points out the important differences in its topographical 
 relations to the skull in children and adults. The Ear is next discussed, and many 
 facts eitiier hitherto unknown or almost forgotten are brought under our notice. 
 'I'he Frontal Sinuses having been briefly referred to, a most interesting l!:ssay 
 follows on the Mode of Eruption of the Permanent Teeth, which will repay carefiU 
 study. In like manner are treated the Vertebral Column and its Curves, the 
 Spinal Cord, the Neck, Thorax, Abdomen, Male Pelvic Viscera, and Female Genita.ls. 
 In all of these there is evidence of the same honest and careful Investigation ; while 
 references to the work of others show that this department of inquiry has not beun 
 neglected. Some of the Sections have already appeared as original papers, but 
 they are not less welcome when combined with much that seems quite new in a 
 connected form. 
 
 "Thb Tofoqrapbical Anatomy of the Child" will undoubtedly remain a 
 standard work on the subject ; and, while adding very distinctly to Dr Symington's 
 reputation as an anatomist, will reflect credit on the School to which he belongs.— 
 The Edinburgh Medical Journal^ August 1887. 
 
 In der Bearbeitung der theoretiuchen Grundlagen llegt die Zuknnft der 
 Kinderheilkunde. Nur wenn durch immer neue Forschungen die Beaonderheiten 
 des wachsenden Menschen erforscht werden, muss die Berechtigung der Padiatrie 
 als Fachwissenschaft allseitig anerkannt werden. Nattirllch darf solches Studium 
 nicht allein dem Tlieoretiker iiberlassen bleiben. Auf dem Gebiete der Physiologic 
 des Kindesalters haben auch thatsachlich die Kinderarzte wacker mitgeholfen, wcit 
 weniger auf dem der Anatomic (z, B. Fleischmann). Aber auch die Anatomen 
 haben dieses Feld selten betreten, und als Henke far die erste Auflage des Ger- 
 hardf schen Handbuches die Anatomie schreiben soUte, konnte er si(£ nicht auf 
 eine Zusammanfa^ung des bisher Bekannten bescbranken, sondem musste an 
 alien Punkten neue Untersuchungen anstellen, diefUr die zweite Auflage bedeutend 
 erweitert wurden, aber noch immer kein vollstandiges Bild liefern. Seither hat 
 DwiGBT (Frozen Sections of a Child, New York, 1881) fiinfzehn aufeinanderfolgende 
 Horizoutalachnitte durch ein 3 jahriges Madchen abgebildet und erl3.utert, die uns 
 iiber einige Verhaitnisse aufklSren. Dieses Buch wird durch das vorliegende, 
 dessen Erseheinen wir mit besonderer Freude begriissen, bei weitem iibertroffen. 
 S., Lecturer der Anatomie in Edinburgh, hat bereits durch einige anatomische 
 Arbeiten (The External Auditory Meatus in the Cliild, Journal of Anatomy and 
 Physiology, 1885 ; Position of the Empty and Distended Bladder in the Male Child, 
 Das. 1885; On the Relations of the Larynx and Trachea to the Vertebi'al Column 
 in the Foetus and Child, Das. Vol. IX. u. a. ra.) den Dank der Einder&rzte verdient, 
 im vorhegenden, W. Braune in Leipzig gewldmeten, prachtvollen Werke vereinigt 
 er eigene und ^mbe Studien auf diesem Gebiete zu einem Ganzen 
 
E. & S. LIVINGSTONES' PUBLICATIONS. 
 
 THE TOPOGEAPHICAL ANATOMY OF THE CHILD. 
 
 Auf die wichtigen Ergebnlsae kSnnen wir leider uicht im Einzelnen eingehen, 
 empfehlen dagegeu alien Fachleuten das Buch auft wannste und hoffen, dasa ea 
 auch auBserhall) des Gebietes der engUschen Zunge zahlrelche Kaufer flnden werde. 
 Der erste Theil enthait in grossen farbigen Tafeln : Sagittal schnltt durch ein 13 
 jahrigea Madchen, den gleichen durch einen 6 jahrigen Knaben, drei Frontalsclinitte 
 durch den Kopf eines 5 jahrigen Madchen, einen Horizon talschnitte durch den Kopf 
 eines 4J jahrigen Knaben, 13 Horizontalschiiitte durch den Kumpf eines 6 jahrigen 
 Madchens, Sagittalschnitt durch den Unterleib desselben Kindes, zwei schematlsche 
 Bilder iiber die Lage der Bruste— und Baucheingeweide bei einem 6 jahrigen 
 Madchen und einem 6 jahrigen Knaben, zwei Frontalschnitte durch einem 4^ 
 jahrigen Knaben. Einzelheiten aind in besonderen Holzschnitten erkiart. Jede 
 Tafel wird von einer Eriauterung begleitet, welche auf die Unterschiede gegeutiber 
 dem Erwachsenen eingeht. 
 
 Der zweitt Theil linthait die Literatur der anatomischen Abbildungen des 
 Kindes und geht dann systematisch auf die Anatomie desselben ein. Es werden 
 nacheinander besprochen : Gehim, Ohr, StinibeinhOhlen, Kiefer und Zahne. 
 WirbelBau".e, Hals. Bnistkorb, Unterleib, mannliche und weibliche Beckenorgane. 
 Auch hier helfen sehr deutliche schematlsche Zeichnungen zum VerstS-ndniss der 
 Worte. Auch auf praktische Frageu (Tracheotoinie, Steinschnitt) wird Huckslcht 
 genommen. Der einzige Fehler dieses Werkes scheint uns die geringe Beriick- 
 sichtigung des ersten Lebensjahres zu sein. Im Uebrigen kftnnen wir nur den 
 Wunsch wiederholen, das Buch moere unter den Kinderarzten die verdiente 
 Verbreitung finden.— Fiir die Ausstattung verdient die Veriagsbuchliandlung ein 
 besonderes Lob, und es lage vielleicht in ihrem Interesae, wenn sie die Tafeln 
 auch mit deutscher Erklarung erscheinen lassen wurde, umsomehr als die englische 
 Auflage, wie wir erfahren, eine sehr niedrige ist.— IJadunitz {PT&g),—Centralblatt 
 fur Kinderheilkunde, 3rd September 1887. 
 
 T)r Johnson Symington has well filled a gap in our Topographical Anatomy. 
 This department of anatomical Bcience lias been worked at most extensively and 
 ably by Pirogoff, Braune, Luschka, and others, in the adult ; but the method of frozen 
 sections has hitherto been systematically applied to the child, in one case only, by 
 Professor Dwight. Dr Symington has added to our knowledge by presenting 
 us in this work with fourteen coloured lithographic illustrations, all life-size, 
 and thirty-three woodcuts taken from sections of male and female children, aged 
 four years and a halt five years, six years, and thirteen years, and has given ua 
 a large number of very accurate observations on the position of the various organs 
 and viscera, and the changes which they undergo in the earlier periods of life. The 
 horizontal sections have been taken from a girl six years of age, whilst the vertical 
 sections (both coronal and sagittal) are from children of both sexes and various 
 ages. In addition to the illustrations, the work is most valuable for excellent 
 letterpress, treating very fully and minutely of the position of structures at all 
 periods of early life, and it is evident that many of the views generally held in 
 regard thereto will have to undergo considerable alteration. For example, Dr 
 Symington shows that the external auditory meatus is relatively as long in the 
 child as in the adult, when examined in the fresh state in subjects with the entire 
 head frozen; that the spinal cord in the newly-bom child ceases at much the 
 same point as in the adult ; that the child's neck is not relatively short, but that 
 it is higher in relation to the vertebral column than in the adult. The common 
 assumption that the position of the stomach in the child is vertical is also shown 
 to be erroneous, and is proved by figui'es taken from an infant four days old, and 
 from a girl six years of age. The portion of the book devoted to the position of 
 the pelvic viscera in male children is of great importance to surgeons, and will be 
 carefully studied in view of operations on the urinary organs in early life. Too 
 much praise cannot be bestowed upon the author for the obvious care and industry 
 with which he has pursued his investigation, and the accuracy and fidelity with 
 which he has reproduced its results. Its dedication to Professor Braune is a most 
 graceful compliment to an anatomist who has done more to advance the knowledge 
 of Topographical Anatomy tlian any other worker in this special branch.— TAe 
 Lancet, 22nd October 1887. 
 
10 E. & S. LIVINGSTONES' PUBLICATIONS. 
 
 Third Edition, in 2 vols., price 18s. 
 ILLUSTRATED WITH 238 USEFUL ENGRAVINGS. 
 
 APPLIED ANATOMY 
 
 BY 
 
 JOHN M'LACHLAN, M.D., B.Sc, F.E.C.S.E., etc. 
 
 The Book includes what is usually known as — 
 1. SURGICAL ANATOMY. 2. MEDICAL ANATOMY. 
 3. OPERATIVE SURGERY. 
 
 USED AS A TEXT-BOOK IN THE PRINCIPAL UNIVERSITIES £ MEDICAL COLLEGES. 
 
 The modus operandi of all the more important Surgical 
 Operations — Instruments required, Duties of Assistants, 
 etc., etc. — are carefully described, as well as Fractures and 
 Dislocations, together with their necessary Treatment. 
 
 GENERAL CONTENTS OF VOL. 1. 
 
 Aneurism and its Treatment — Medical Anatomy of Thoracic 
 Aorta and its Branches — Ligature of Arteries — AmputationB — 
 Excision of Bones and Joints — DislooationB and Fractures, with 
 their Treatment — ^The Eye and Bar. 
 
 GENERAL CONTENTS OF VOL. IL 
 
 Operations on, and Anatomy of — The Air Passages, The Larynz, 
 CEsophagus, Cut Throat, The Pharynx. Operations on— Nerves, 
 Tonsils. Lower Jaw, Branchial Clefts and Fistula, Ranula, Hare 
 Lip and Cleit Palate, The Teeth, Scalp. Operations, Fractures, 
 and Medical Anatomy of — Cranium and Brain, Thyroid and 
 Parotid G-lands, Tongue, Nose, The Antrum, Cranial Nerves, 
 Upper Extremity, Lower Extremity, The Chest Medical and 
 Surgical Anatomy of— The Mamma, The Spine, The Spinal Cord. 
 Medical Anatomy of — Spina Bifida, The Abdomen. Operations 
 on, and Anatomy of — Liver, Spleen, Pancreas, Kidney, Hernia, 
 The Perineum. Operations for Stone in the Bladder, The Urethra, 
 Operations on — ^The Testicle and Hydrocele, Rectum, Penis, Fascia 
 of Ahdomen. G-ynaecological Operations. Origin and Insertion 
 of Muscles. Explanation of Terma used in Eye Surgery. 
 
E. & S. LIVINGSTONES' PUBLICATIONS. 
 
 OPINIONS OF THE PRKSS. 
 
 ' It deserves every success. ' — Sir George Macleod, Professor 
 of Surgery, University of Glasgow. 
 
 ' If the medical student of to-day comes to an examination 
 unprepared, and retires without his diploma, he certainly cannot 
 lay the blame of his failure on want of instruction. With systematic 
 courses of lectures constantly increasing in number and severity, 
 with tutorial classes, with extra fees and extra hours, to assist him 
 I n assimilating the indigesta moles that is spooned into his unlucky 
 brain, by the constant yearly deciphering of ancient manuscripts, 
 with text-books to be mastered which contain not only all that is 
 really known on any subject, but also all the facts which the 
 respective authors have evolved from their own conceit, and there- 
 fore believed to be valuable, — no wonder the poor victim appears 
 at the examination stuffed, not taught, with material, crammed, not 
 digested. To help the student in his difiiculties, to guide him in the 
 waste wilderness of his poor lecture-room notes, and to give him a 
 chance of learning something, the student has to find for himself men 
 that can really teach him, and books that convey useful information, 
 information that will bear not only on the work of the examination, 
 but also on his future professional life. Dr M 'Lachlan is such a 
 teacher, and his book is of the kind we mean. It is a successful 
 attempt to show how the facts of Anatomy are necessary as a 
 groundwork both of Surgery and Medicine. If mastered it will do 
 the student more good than acres of MSS. dealing with theory and 
 fad, for it makes his anatomy interesting, and the bedside or the 
 operating theatre intelligible, and, except, where vested interests in 
 fees come in, it is pretty generally acknowledged now that the 
 dissecting-room, the laboratory, and the hospital are the real claces 
 of study. * — Rdinbur^h Medical JournaL 
 
 ' The text is copiously illustrated with well executed engravings, 
 numbering altogether 238 as against 74 in the former edition. The 
 author has produced a work which is more fitted to meet the wants 
 of the student and the practising surgeon in the application of anatomy 
 to practice, than any other which has come under our notice.' — 
 Hospital Gazelle. 
 
 ' The book is written specially with a view to the requirements 
 of students preparing for the higher examinations ; and its successive 
 editions have, in this regard, been each one more perfect than the 
 last. In this issue much new matter and many new illustrations 
 have been added. The work may be cordially recommended to 
 students as a complete and practically useful text-book.' — Scotsman. 
 
B. & S. LIVINGSTONES' PUBLICATIONS. 
 
 Sixth Edition, Eevised and considerably Enlarged. 
 Illustrated by Coloured Plates, price 10s. 6d. net. 
 
 THE STUDENT'S HANDBOOK 
 
 OP 
 
 FORENSIC MEDICINE, TOXICOLOGY, 
 
 PUBLIC HEALTH 
 
 By H. AUBEEY HUSBAND, M.B., CM., 
 
 B.Bo., M.E.C.S., L.S.A., F.R.C.S.B., 
 Author of 'Student's Handbook of (he Practice of Medicine,' etc. 
 
 Used as a Text-book in the principal Universities and Medical Schools in 
 Great Britain, India, and the Colonies. 
 
 ' It is intended for students, and is for them very convenient. 
 This edition fully sustains the acceptableness of the work.' — 
 Lancet. 
 
 'The work is an excellent epitome of the subjects on which it 
 treats, and contains all that the student need know to pass his 
 examinations, or that the ordinary practilioner will require in the 
 course of his practice. ... As ii ti-ustworthy and readable guide 
 to the study of forensic medicine, we can strongly recommend it to 
 both students and practitioners.' — Student's Journal. 
 
 'The book is one which can be commended, and will in the 
 future, as in the past, doubtless smooth the passage of many medical 
 students througli the difficulties of the examination room.' — Pvhlic 
 Health. 
 
 ' The work has long enjoyed a pre-eminent reputation as a book 
 useful to students about to proceed to examination in the subjects 
 of which it treats ; and men have been known to boast of having 
 secured academic degrees by no more than a cursory perusal of its 
 pages. They toiled not; but, being possessed of thin handhook, 
 neither were they spun. The new edition gives the book in an im- 
 proved shape. The text has been revised, new matter lias been 
 added; and some professionally beautiful illustrations now appear 
 in the work. For the rest, this edition keeps the handbook well 
 abreast of its reputation.' — Scotsman. 
 
B. ft S. LIVINGSTONES' PUBLICATIONS. 
 
 Fif til Edition. Eevised and Enlarged, with. Illustrations 
 and Tables, price 7s. 6d. net. 
 
 THE STUDENT'S HAND-BOOK 
 
 OP 
 
 The Practice of Medicine 
 
 DESIGNED FOR THE USE OF STUDENTS PREPARING 
 FOR EXAMINATION, 
 
 By H. AUBEEY HUSBAND, M.B., CM., 
 
 B.Sc., M.B.O.S., L.S.A., F.B.O.S.E.. 
 
 Autkor of tke * Student's Hand-book of Forensic Medicine and 
 Public Healthy ^Sanitary Lam' etc. 
 
 ' The book before us is an excellent example of its class ; the whole 
 of medicine is digested and tabulated^ and, in fact, served up ready 
 prepared at infinite pains to render it easily assimilated.' — Lancet. 
 
 * The distinguishing features of Br Husband's hand-book are con- 
 densation and clearness of diction — qualities which are certain to ensure 
 for the book a favourable reception by those for whom it is intended. 
 We have pleasure in recommending it to our readers as a most useful 
 work to peruse immediately before presenting one's self for a Medical 
 Examination.* — Students* Journal. 
 
 ' The book is not put forth as a systematic treatise upon diseases and 
 their treatment, but under each section will be found a brief statement 
 of the main points connected with all the diseases enumerated in the 
 nomenclature of the Royal College of Physicians, London. From the 
 point of view of the uses to which this Manual is designed, we know 
 of no work that can be put in comparison with it.' — Provincial Medical 
 Journal. 
 
 ' Whether as a hand-book for use as an introduction to the systematic 
 study of disease, or for the purpose of refreshing the memory on the 
 eve of an examination, the work is equally to be conmiended, and one 
 may safely assert that it will retain its well earned popularity.'— 
 Hoifpital Gazette. 
 
 * A Fourth Edition of this hand-book needs but little notice. From 
 the time when it was first offered as a help to students working for 
 examination, it has with each edition increased in size and fulness. A 
 special feature of this edition, and one which will commend it to 
 students, is the addition of a set of Tables for diagnostic and other 
 purposes. The increased size of the book is due to these tables, and 
 to additions made to the chapters on the nervous and circulatory 
 systems. It would be altogether undesirable if the excellence of this 
 book were to keep any man in his student days from reading the 
 classical text-books; on the other hand, while the present examination 
 system is in force, such a book as Dr Husband's is a necessity, and 
 his we can recommend.' — Edinburgh Medical Journal. 
 
E. & S. LIVINGSTONES' PUBLICATION& 
 
 Second Edition, price 6s. 
 THE 
 
 Student's Hand-'book of Chemistry 
 
 By H. LEICESTEE GEEVILLE, 
 
 F.I.O., F.O.S., etc. 
 
 This book contains a large amount of information, 
 condensed into Tables; also, the most important 
 Chemical Calculations and Illustrations. 
 
 ' The tabulation of facts, containiDg groups of elements and com- 
 pounds, is a good feature in this book, and likely to prove very useful 
 to the student. The chapters dealing with Organic Chemistry are 
 clear and succinct.' — Nature. 
 
 • This book has many merits. It is clearly and pleasantly written, 
 is well arranged, and contains a great deal of useful and important fact, 
 much of it embodied in Tables.' — Lancet. 
 
 • A concise and useful Manual. The work has been revised and 
 made more valuable by the addition of several Tables and much new 
 matter in the text. The calculations are very useful.' — Scotsman. 
 
 ' A series of Tables forms a useful feature of the work.' — Pluirma- 
 ceutical Journal. 
 
 ' This compact and handy little Manual will be found a useful 
 guide by ordinary and especially medical students.' — Medical Pren 
 and Circular. 
 
 ' The work before us, however, may claim some very decided merits. 
 We may venture to say that the author's primary object is to enable the 
 student not so much to " pass " as to " know." He lias appended to tlie 
 treatise a very useful glossary or collection of definitions of the principd 
 terms used in Chemistry.' — Chemical News. 
 
 ' This is an excellent Manual, and is likely to maintain its place 
 among the many manuals of Chemistry. It is likely to be popular 
 with students-' — Edinburgh Medical Journal. 
 
 ' This is an elementary treatise embodying several valuable original 
 features, among them Tables and examples for general Chemical 
 calculations, also Tables in which a great deal of information has 
 been compressed into a small space, making it more accessible to 
 the student.' — American Chemical Seview. 
 
 ' The work deals with both Organic and luorganic Chemistry, and 
 much information has been compressed into small compass. It is well 
 adapted as a hand-book for medical students, being furnished with a 
 copious index, and the text is given in such a form as will render it 
 readily accessible to the student. We commend the 'irork to the 
 attention of Canadian students.* — CoTiadian lancet 
 
E. & S. LIVINGSTONES' PUBLICATIOKS. 
 
 Fifth Edition, Eevised and Enlarged, price 6s. 
 
 lateria ledica and Therapeutics 
 
 FOR THE USE OF STUDENTS AND PRACTITIONERS. 
 
 By ^SATILLIAM CRAIG, M.D., 
 
 CM.. F.R.S.E., F.R.O.S.E., etc., 
 
 Lfctwer on Materia Medica in the JBdmburgh School of Medicine, 
 
 Examiner at the Royal College of Surgeam, Bdiiihurgh, 
 
 Examiner at Edinbv/rah University. 
 
 Used as a Text-book in the principal Universities and Colleges in 
 Great Britain. India, and the Colonies, 
 
 ' As the work stands it forms a very clear and complete guide to the 
 study of the properties and uses of the pharmacopoeial preparations, and 
 we can endorse thoroughly the good opinion we were enabled to pass 
 upon the previous edition. The excellent Posologioal Table is very 
 valuable, as are the hints on Prescription Writing, and the very succinct 
 Index of Diseases with their Remedies. As a compendium of Materia 
 Medica and Therapeutics, of moderate size, but full of information, we 
 know few to surpass, even if to equal, the Manual before us. We have 
 ourselves made a constant companion of the former edition, which has 
 never failed us.' — Students' Jowrnal. 
 
 - * This book contains sound sense and original information, and will 
 prove a good pocket companion for the student.' — Medical Times and 
 Gazette. 
 
 * Your " Manual " will be useful to me ia various ways, teaching 
 included, and I should think it will be regarded as a boon by students 
 preparing for their examination.' — Professor Haevey, Aberdeen. 
 
 ' This concise little Manual, though intended primai*ily to assist 
 students attending the author's own classes, possesses several charac- 
 teristics which have rendered it more generally popular. Special 
 emphasis is laid upon alterations in nomenclature which might other- 
 wise escape attention. The volume concludes with a Posological 
 Table, a Schedule of Poisons and their Antidotes, together with an 
 Appendix of Contracted Terms in Common Use. It is beautifully 
 printed, and is altogether a very handy and convenient volume for 
 the use of students preparing themselves for examination.' — British 
 Medical Jowmal. 
 
 * This being a fifth edition, calls for very little remark. The amount 
 of condensation of material is truly surprising; useful facts are stated 
 so briefly that, a priori^ it would give the impression of a peculiarly 
 dry and uninteresting introduction to a very difficult subject. The 
 author's hope that the book would be of service to students preparing 
 for their professional examinations can surely only be realised when a 
 concise epitome is required in the few weeks immediately preceding 
 examination, and wh*'n the student is already familiar with the subject.* 
 — Lancet. - 
 
E. k a. LIVINGSTONES' PUBLICATIONS. 
 
 Demy 4to., price 7s. 6d. 
 
 Illustrated with lO Coloured Plates. 
 
 NERVES OF THE HUMAN BODY 
 
 BY 
 
 ALFEED W. HUGHES, M.B. & CM. Edin.; 
 
 F.R.C.S.Bdin.; M.E.C.S. Eng.; 
 Professor of Anatomy, South Wales Medical College, Cardiff. 
 
 'An excellent work of reference for students, quite in place in a 
 Medical School library. The drawings are large and bold, demon- 
 strating the distributions and connections of ttie cranial and spinal 
 nerves with clearness and accuracy. The cranial nerves in particular 
 
 are well represented The preparation of " Nerves of the Human 
 
 Body " must have cost its author much trouble, and Dr Hughes may 
 be congratulated on the result of his labours.' — British Medical Joumai. 
 
 'As regards the work little is left to be desired. As far as the 
 diagrammatic and literal description of the nerves goes, this work is 
 undoubtedly good ; and there is no doubt that the anatomical details 
 are an improvement on those usually given. It will be found a help 
 to students in their practical work, and of equal help to the prac- 
 titioner in his pathological and therapeutic investigations.' — Provincial 
 Medical Jrmrmil. 
 
 ' The diagrams are very clear. The text contains a well arranged 
 summary of the main facts of the origin, course, and distribution of the 
 cranial, spinal, and sympathetic nerves. It is a work that maybe con- 
 sulted with confidence by the student, and which he will find a useful 
 aid in gaining a knowledge of the nervous system.' — Edinburgh Medical 
 JowTwl. 
 
 ' A thoroughly excellent contribution to anatomical literature, will 
 be valuable to those struggling hard with the most difficult subject in 
 human anatomy. The diagrams cannot be praised too much.^ — The 
 Student. 
 
 ' Dr Hughes' book, " The Nerves of the Human Body," simplifies 
 the task in a way unknown to the student of Gray and Quain. The 
 diagrams are beautifully executed.' — Scotsman. 
 
 ' Mr Hughes has shown more daylight into that dark subject than 
 any of bis predecessors. The book can be safely recommended to all 
 students.' — College Column. 
 
 ' The special feature of the book, is a series of ten beautifully 
 executed Plates of Diagrams, in which the different nerves are very 
 distinctly figured. The work is intended as a special adjunct to the 
 standard text-books of Practical Anatomy, and as such it can scarcely 
 fail to be of great assistance to students who will use it intelligently.' 
 — Scottish Leader. 
 
K. & S. LIVINGSTONES' PUBLICATIONS. 
 
 Second Edition, Price 6s. 
 BeTised and Enlarged, witb 12 Tinted Plates and 40 WoodcatB. 
 
 OF THE 
 
 linor Grynecological Operations and 
 
 Appliances 
 
 By J. HALLIDAY CEOOM, M.D., 
 
 F.R.C.P.E., P.R.C.S.E., 
 
 Lecturer on Midwifefy and Diseases of Women, School of Medicine ; 
 
 President of the Obstetrical Society ^ Edinburgh ; and 
 
 Examiner in Midwifery in the University of Edinburgh and Royal College 
 
 of Physicians, Edinburgh. 
 
 ' The descriptions and recommendations of Dr Croom seem entirely 
 familiar, intelligible, and wholesome. A number of well-executed 
 lithographic plates, giving various relations of the pelvic organs, add 
 to the value of the book.' — Am^Hcan Journal of Obstetrics. 
 
 * The work is admirably adapted as a practical guide to obstetric 
 clinical clerks, house surgeons, and physicians, as well as medical 
 practitioners. It is well arranged throughout, and will, no doubt, 
 retain the hold it has already taken.' — London Medical Record. 
 
 ' The Second Edition is considerably modiiled, and forms almost a 
 completely new book. The clearness and conciseness of the author 
 make his Hanual most useful both for practitioners and students.* — 
 Bulletin General de TherapeuUque. 
 
 ' All that is of doubtful value is purposely omitted, and only the 
 methods of examination and treatment recognised as the best are 
 described concisely and with capital illustrations. The book, which 
 embraces all the gynecological operations with the exception of the 
 abdominal, is in a high degree likely to fulfil its aim for students.'— 
 C&itralblatt fwr Gyncekologie. 
 
 'We are glad to see that this valuable Manual has run into a 
 Second Edition. Its arrangement is such as will commend itself both 
 to the student and busy practitioner. We finish the perusal of this 
 work impressed with its simplicity of arrangement and lucidity of 
 expression.' — Liverpool Medico- Chirurgical Journal. 
 
 ' This is an admirable book, for which we are sure the student in 
 midwifery and the diseases of women will be very grateful. We 
 commend it heartily to students, for whose use it is chiefly written, 
 and even practitioners will find it very handy and suggestive in many 
 of the emergencies of practice.' — Lancet. 
 
 * Both students and practitioners will find in it descriptions, hints, 
 and directions — clu»r, practical, and useful.* — PracHHonvr. 
 
 B 2,99- 
 
B. & S. LIVINGSTONES' PUBLICATIONS. 
 
 THIRD EDITION. 
 
 Fifth Thousand, price 5s. net. 
 
 IlluEtrated by about 40 Plates (many Coloured) or 109 Figoras. 
 
 Anatomy of the Brain and 
 Spinal Cord 
 
 J. RYLAND WHITAKER, B.A., M.B. (Lond.), 
 F.R.C.P., L.E.C.S.(Edin.); 
 
 Lecturer on Anatomy ^ Surgeons' Sail, Edinburgh; 
 Examiner /or the Triple Qtialification, 
 
 Used as a Text-Book in the principal UniverBities and Medical Colleges 
 in Great Britain, India, the Colonies, U.S.A., and Italy. 
 
 ©pinions of t^e ^r^ss. 
 
 ' The book is an excellent Manual for the use of Students and 
 makes a good introduction to the heavier text-books. This Edition 
 is made more valuable by the inclusion of some new matter in the 
 text, and by the addition of many new figures and tables.' — 
 Scotsman. 
 
 ' The book consists of an exceedingly clear account of the central 
 nervous system.' — British Medical Journal. 
 
 ' For a clear and concise description of the nervous centres it 
 has not been surpassed.' — Journal of Mental Science. 
 
 'We are pleased to see that Messrs E. & S. Livingstone have 
 issued a Second Edition of Dr Whitaker'a admirable Anatomy of 
 the Brain and Spinal Cord.' — Edinburgh Medical Journal. 
 
E. & S. LIVINGSTONES' PUBLICATIONS. 
 
 Price 4s. 6d. net. 
 
 Notes on Pathology 
 
 By J. EYLAND WHITAKEE, 
 
 B.A., M.B.(Loiia.), F.E.O.P., L.B.C.S.(Eam.) i 
 
 Lecturer on Anatomy, Surgeons' ffall, Edinburgh; 
 Examiner for tfie Triple Qualification. 
 
 AUTHOR OF ' ANATOMY OF THE BEAIN AND SPINAL CORD.' 
 
 Vol. I.— GENERAL. Vol. \\.—SPEG\M {in /rej^arafwn). 
 
 Used as a, Handbook in the principal UuiversitieB and Colleges. 
 
 ' These " Notes," which traverse the whole range of General Pathol- 
 ogy, have evidently been compiled with great care. Together, they 
 form an outline of the subject of which it will not be difficult for the 
 s-tudent to fill in such details as he gathers from his lecturer or his text- 
 book. The author himself recognises this as the main object of his 
 publication, and we may say at once that he has done his work well, 
 and that it should prove of much utility. In these days of "compendia" 
 of knowledge, where the aim often seems to be to condense into as 
 small a space as possible the facts of science, so that the student may 
 be saved the trouble of learning them step by step, it is gratifying to 
 find a writer who takes a higher view of the kind of assistance that the 
 student needs. The information he conveys in his little work is con- 
 siderable, and also accurate ; in parts even — e.g., in the sections deal- 
 ing with Inflammation and the Parasites — it is almost, if not quite, as 
 full as is to be found in many a text-book. But it would be diflicult 
 for the student to use the work simply for the purpose of " cram." 
 We believe, moreover, that teachers also may be glad of so concise a 
 summary of the subject as Mr Whitaker has given.' — Lancet, 
 
 ' This is evidently the first part of what may be described as a useful 
 synopsis for students, and it deals purely with General Pathology. The 
 author has attempted to outline the causation and pathological characters 
 of disease ; and in a neat, concise way every subject is dealt with so as 
 to give a concentrated idea of the varieties of disease and the nature 
 of their pathological processes. The arrangement of the book is in 
 Sections — the first of which is devoted to Altered Conditions of the 
 Circulation ; another treats of Inflammation and its Results ; a third 
 of Eetrogressive and Progressive Changes ; and the last of Parasites and 
 Parasitic Diseases. As a digest it is a remarkably good book, without 
 padding or unnecessary verbiage, and with a oomprehensive survey of 
 causation and the varieties of allied or similar pathological processes. 
 For the student it will prove an admirable memory help, and for the 
 practitioner it will frequently be sufficient when he does not require 
 to dip exhaustively into a subject.' — Glasgow Herald. 
 
E. 4 a LIVINGSTONES' PUBLICATIONS, 
 
 Price 10s. 6d. 
 
 THE STUDENTS' 
 
 Handbook of Medicine 
 
 AND 
 
 Therapeutics. 
 
 By ALEXANDEE WHEELER, 
 
 Clinical Aiaiatant, Out-patient Department, Edinburgh Royal Xnfrmary. 
 Author of "Cub Unseen Foes," &c. 
 
 Used as a Text-Book in the principal Universities and Colieges. 
 
 ' It is distinctly designed to refresh the memory on salient points, 
 as well as to enunciate the leading principles of treatment. These 
 aims haye been faithfully carried out, and that too with an originality 
 for which it might be thought there could be little scope. Clear, 
 concise, and accurate.' — Lancet. 
 
 'This excellent little volume . . . Many good coloured and 
 uncoloured diagrams illustrate the book, and we think the young 
 practitioner can hardly make a better investment than the purchase 
 of Mr Wheeler's work. It is up to date in ^pathology and treatment, 
 and is a model of clear, terse ■wa.tmg.' —Medwal Press amd Circula/r. 
 
 ' This is an exceedingly good little work, unpretentious, it is true, 
 but fulfilling far more than it pretends. We have nothing but praise 
 for the work. As a whole, it shows a remarkable power of imparting 
 information in a clear and easily remembered style ; and the author's 
 practice of giving explanations and reasons for every step in the treat- 
 ment of disease strikes us as being particularly suitable for the needs 
 of the men to whom he appeals. We heartily recommend it to the 
 overworked final man.' — The Student. 
 
 'The volume is carefully compiled and well written, and is, in our 
 opinion, destined to take high rank amongst its competitors. It can 
 be profitably read either by the student on the eve of an examination 
 to refresh his memory, or by the busy practitioner for the same pur- 
 pose. We venture to predict that a Second Edition will shortly be 
 called for.' — The Quarterly Medical Jov/nial. 
 
is. & a LIVINGSTONES' PUBLICATIONS. 
 
 Price 4s. 6d. net. 
 ILLTJSTEATED WITH 8 COLOTJEED PLATES. 
 
 MANUAL of SURGICAL ANATOMY 
 
 ALFKED W. HUGHES, 
 
 M.B., CM., r.E.C.S. Edin. ; M.R.O.S. Eng. ; 
 
 Profeitsor of Anatomy^ jLing'e College, London. Author of 
 
 * Serves of the Huntan Body,' ^c. 
 
 Used as a Handbook in all the Universities and Medical Colleges. 
 
 * This little book contains very terse descriptions of tlie anatomical 
 facts most important to students about to present tliemselves for their 
 Pinal Examination in Surgery. Clearness sometimes, and elegance 
 of diction often, have been sacrificed to brevity. It -will commend 
 itself to those for whom it is specially prepared.' — Lancet. 
 
 ' Dr Hughes evidently possesses the faculty of condensing a large 
 amount of information into a small space in a clear and methodical 
 manner. The student will find it a very reliable guide. The work 
 contains a number of excellent illustrations, which will greatly assist 
 the student in learning the relative positions of various structures 
 which he would encounter in the ligature of the principal arteries.' — 
 Edmbv/rgh Medical Jowmal. 
 
 ' No book could be better adapted for Examination purposes. The 
 book may be safely recommended.' — Hospital. 
 
 ' Here is a simple book plainly written with the main facts of the 
 subject clearly exposed; it is easily understood, easily remembered; 
 it can be read through in half-a-dozen hours. We recommend it to 
 you, its perusal will supply you with many excellent and useful 
 anatomical facts which you ought to know.' — Dublin Jowmal of 
 Medical Sciem:e. 
 
 ' Dr Hughes' book will supply the gap existing betwixt the more 
 elaborate Manuals of Surgical Anatomy on the one hand, and the 
 mere outlines, used for "cramming" purposes, on the other. The 
 work is a useful one, and we have perused it with the result of finding 
 that most of the important points involved in the common work of the 
 Surgeon have been duly noted. The section on Hernia in particular 
 strikes us as being excellently done. The Plates illustrating the book 
 have the relations of Arteries, Veins, and Nerves printed in colours, 
 this plan facilitating easy reference to the details they expound.' — 
 Glasgow Herald. 
 
 ' A brief concisely-written handbook, covering that department of 
 Anatomy which concerns students who seek only the usual Surgical 
 qualifications.' — Scotsman. 
 
E. k S. LIVINGSTONES' PUBLICATIONS. 
 
 Demy 8vo, price 4s. 6d. net. 
 
 Vaccination Eruptions: 
 
 ©riginal §l*s«arf^. 
 
 Bt THOMAS DOBSON POOLE, M.D., 
 
 Magter in Surgery^ University of Edinburgh; Fellow of the Obstetrical Society. 
 
 'The author classifies eruptions as follows: — (1) Those due to pure 
 vaccine Inoculatiou, (2) those due to mixed inoculation. He enters at 
 length, and very properly, into the question of the qualities of the 
 lymph itself, of its origin and cultivation, and here is the crux of the 
 whole question. The question of the artificial cultivation of the lymph 
 is a very important one, and the author suggests a method which we 
 trust may either solve the problem or mature its consideration. The 
 work is one well worthy of consideration.' — Glasgow Herald. 
 
 ' The title of this very interesting work concisely indicates its con- 
 tents. A good acquaintance with the literature of the subject is shown 
 on every page, and the cited oases are of great interest, especially those 
 in connection with the subject of generalised vaccine eruption {vaccine 
 }ln4ralisSe). The differential diagnosis between vaccination ulcers and 
 primary chancres, also between vaccination eruptions and secondary 
 syphilitic majiifestations, is given in extenso from Portalier's summary 
 of Fournier's lectures. The author concludes from a study of tuber- 
 culosis, including his own experiments, that its transmission by means 
 of official vaccination is "beyond the limits of possibility." In con- 
 clusion, this work deserves perusal by all who are interested in the 
 subject of vaccination, therefore by all medical practitioners.'— .Bri^isA 
 Medical Jowrnai. 
 
 ' The author of this little work has made himself well acquainted 
 with most of the reliable literature of recent date bearing on his 
 theme, and has put into a convenient and useful form a great deal of 
 iuformation that could otherwise be obtained only by hunting through 
 a variety of medical periodicals and other publications. The work 
 ought therefore to be welcomed by all who have much to do with 
 vaccination, and especially by public vaccinators, who are the only 
 persons likely to have the opportunity of meeting with some of the 
 very rare vaccinal sequelae of which he principally treats. A chapter 
 is veiy profitably devoted to vaccine syphilis. The chapter on tuber- 
 culosis is one of the best in the book. Other subjects shortly dis- 
 cussed are leprosy, erysipelas, vaccinia gangrenosa, etc. The work 
 forms a really useful addition to the literature of vaccination, and 
 ought especially to be read by every public vaccinator in the kingdom.' 
 — Glasgow Medical Jowmal. 
 
E, & 8. LIVINGSTONES' PUBLICATIONS. !i 
 
 Price Five Shillings. 
 
 THE STUDENT'S HAIfDBOOK 
 
 OP 
 
 GYNECOLOGY. 
 
 THE MOST PRACTICAL HANDBOOK 
 EVER PUBLISHED. 
 
 Used as an Introductory Text-Book in all the 
 Universities and Medical Schools. 
 
 ' Everything 1b stated in a most clear and concise way, and as the 
 volume is nicely illustrated, it should be of great assistance to final 
 men especially.' — Dispatch. 
 
 ' There are many who have serious doubts as to any real value 
 being obtainable fr 'm such condensed forms of imparting infor- 
 mation, but they are clearly very popular among medical students. 
 The present volume makes no pretensions to compete with more 
 exhaustive works, but it is hoped it will prove useful to beginners 
 and to those who wish to synopsise and focus the knowledge 
 obtained from larger works. It is clearly and concisely written, and 
 it is surprising to find that it has succeeded so well, in the small 
 space at its disposal, in covering the ground necessary for an ele- 
 mentary knowledge of this progressive and important branch of 
 medical learning.' — Scotsman. 
 
E. & S. LTVINGSTONES' PUBLICATIONS. 
 
 4to, price Sixpence net. 
 
 SCHEDULES FOR 
 
 PLANT DESCRIPTION 
 
 (aUnstratEit) 
 By JOHN WISHART, 
 
 Lecturer on Zoology and Q-eneral Siology in Robert Gordon's College, Aberdeen ; 
 Merbarium 3£edallUt of the Fharmacetttical Society of Great Britain. 
 
 USED IN ALL UNIVERSITIES AND COLLEGES. 
 
 ' The use of these Schedules by pupils will train their powers of obserratioii 
 &nd reasoning, and prevent them from being contented with book knowledge.' 
 — DiAHn Journal of Medical Scieiice. 
 
 * These tables are admirably adapted and arranged on a scientific principle 
 for building up an instructive record of plant examination.' — Abej'deen Daily 
 Free Press. 
 
 B-H" THE S-A-IvIE -A-TromOH. 
 
 Price Two Shillings net. 
 THE 
 
 Botanist's Vade Mecum. 
 
 ' A very handy little pocket guide to the classification of plants, intended for 
 use during botanical excursions. The matter is very concise aud well arranged, 
 and the value of the book is very materially enhanced by an ingenious and 
 novel form of index.' — Guy's Hospital Gaselte. 
 
 * This little manual, of a size suitable for the pocket, will form a useful com- 
 panion to students of botany in their field-days. Its arrangement is concise, 
 and its information conveniently scheduled. A useful ledger-index adds to the 
 convenience of the manual.'— G/cwffow Herald. 
 
 'We commend this Vade Mecum as a very useful guide to all botanical 
 excursion students, who will find it an invaluable aid to recognising the char- 
 acters of the various divisions and natural orders.' — British and Colonial Druggist. 
 
E. & S. LIVINGSTONES' PUBLICATIONS. 
 
 Price 2s. 6d. net. 
 
 The Rotatory Movements 
 
 OF 
 
 The Human Vertebral Column 
 
 AND THE 
 
 So-called Musculi Rotatores. 
 
 ey alfeed w. hughes, 
 
 M.B. & CM. Edin.; F.B.C.3. Eng. ; P.R.C.B. Edin. ; 
 
 Professor of Anatomy, Kmg's College, London; Author of 
 ' Nerves of the Hvman Body^ mid '■Manual of Surgical Anatomy .^ 
 
 'The entire work bears evidence of careiul observation, and forms a useful con- 
 tribution to the mechanism of the human skeleton.'— £din6ur^A Medical JournaL 
 
 ISTE^V^ JEJDITIO:^r. 
 
 Revised in accordance with the British Pharmacopoeia, 1898. 
 Price One Shilling net. 
 
 POSOLOGICAL TABLES; 
 
 Appendix on Poisons ; Index of Diseases ; 
 and Medicines arranged according to their Actions. 
 
 By WILLIAM CEAIG, M.D., 
 
 CM., F.R.S.E., 
 
 Lecturer on Materia Medica, Edinburgh School of Medicine ; Examiner in Materia 
 
 Medica, Edinburgh University; Examiner, Royal College of Surgeons. 
 
 Being a Tabular Arrangement of all the Medicines contained in the 
 British Pharmacopoeia, with Dose, &c. 
 
 ' This is a useful little book, containing a tabular arrangement of all the Phar- 
 macopceial preparations, with their doses and methods of administration, A table 
 on Poisons and an Index of Diseases with Appropriate Remedies are included/ — 
 Lancet. 
 
E. & 8. LIVINGSTONES' PUBUCATIOSS. 
 
 Price Is. 6d. net. 
 
 Materia Medica Tables. 
 
 Designed for the Use of Students. 
 
 BY 
 
 A. HEEBERT BUTCHER, 
 
 L.R.C.P., L.R.C.S. «k L.M., 
 Honorary Surgeon to Birkenhead Borough Hospital. 
 
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 will be found to contain much information arranged in an admirably simple 
 manner.' — Publisher's Circular. 
 
 Price 2s. 6d. net. 
 
 THE STUDENT'S 
 
 HandlDook of Diseases of tlie Skin. 
 
 lUnstrateir bg Colonreb ^IhIbs snir ^oob (KngrHfaings. 
 
 ' It is clearly and syBtematically arranged, and the student who masters its 
 contents will have acquired a useful general knowledge of the pathological 
 classification, course, and methods of treatment of all but the rarest diseases of 
 the skin.'— i/amcAesicr Guardian. 
 
 ' It will prove of service to the young practitioner, and also to older men in 
 country practices, whose work leaves them but little time for the study of 
 books of greater pretensions. A number of well-executed illustrations increase 
 the working value of the book.' — The Pvhlishers Circular. 
 
 Second Edition. Price 6d. net. 
 ReviBed in accordance with the British Fharmacopceia, 1898. 
 
 Dose TaWes of Materia ledica 
 
 Containing all the Doses required for Examinations and 
 Prescribing. 
 
 By T. HOMER, L.RC.S., L.R.C.P.Edin. 
 
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 Being Tabular Views of the Motor Nerves to Muscles, 
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 DETTTEEOmiY SMITH 
 
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 OK, 
 
 The Life History of a Medical Student. 
 
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 for a long time.^— Evening Express. 
 

46 E. & S. UVINGST0NE8' PUBLICATIONS. 
 
 Crowu 8vo., 411 pp., price 3s. 6d. 
 
 CLAUDE GARTON 
 
 BY 
 
 THOMAS J. HENRY, F.RC.S.E., 
 
 AUTHOR OF DEUTERONOMY SMITH." 
 
 'This highly interesting story by the author of ' ' Deuteronomy Smith," 
 itself an excellent testimonial, deals with the life and adventures of an 
 Edinburgh medical student. It is written obviously by a man who 
 knows all the ins and outs of our University. Our Professors and 
 customs are faithfully depicted in a skilful and interesting manner. 
 Claude Garton comes up to Edinburgh, or Dunburgh, as it is called 
 in the book, and goes tlu-ough the usual life of a man up here. We 
 have been unable to find any instance of his being the worse for drink, 
 thereby upholding the well-known sobriety of medical students. He 
 experiences a Symposium, a Bectorial, and Professional Examinations, 
 and finally graduates. One of the best and most faithful descriptions 
 in the book is that of a Police Court the day after a torchlight pro- 
 cession. Garton falls in love with a damsel called Gipsy, who resides 
 in an establishment known as the Eoyal Britannia, and shortly termed 
 " K.B." It will be seen that the book is well up to date, and deals with 
 incidents of much interest to Edinburgh men. We are introduced to 
 many whose names are curiously familiar. The story is interestingly 
 written, and will be read with avidity by Edinburgh men in particidar 
 and medical students in general.' — The Student. 
 
 ' Mr Henry has given us a very striking book, even more powerful, 
 in its way, than George Moore's masterpiece, " Esther Waters." It 
 describes the experiences of a medical student in Edinburgh, from his 
 entry to the day when he is " capped " for his diploma, and each scene 
 stands out distinct and clear, a triiunph of detailed and effective realism. 
 " The dissecting room," " The liectorial election," " The setting of a 
 star," " The mysteries of quackery," " A chloroform case," " Professor 
 Frean performs an operation," — to read these chapters, and they are a 
 sample of the rest, is never to forget them ; it is as though we had 
 been present at the scenes described. Conan Doyle has done nothing 
 
E. & S. LIVINGSTONES' PUBLICATIONS. 
 
 better, aud they stand comparieon ■with, Mr Henley's poems. The 
 "weak points in the book are the story and the hero, but these are 
 throughout subordinate, and their weakness merely goes to show that 
 the author's sense of humour is defective. The defect is not one to be 
 regretted, for, probably, it is the necessary accompaniment of the rare 
 gift which goes along with it. Mr Henry has done for the Medical 
 School of Edinburgh what Tom Hughes did for Rugby; in the work 
 of either there is something to condone, but the something is as nothing 
 when we regard the whole. The book should be in the hands of all 
 medical students, and of all who are interested in the science of 
 medicine. It does not address itself to others, and the "general 
 reader" had, perhaps, better keep away from it.' — Sheffield Daily 
 TehgrapK 
 
 * In " Claude Garton " the career of a medical student during his five 
 years' course at Duubiu'gh University — the indentity of which with the 
 chief of Scottish Universities is thus thinly veiled — is related with 
 unusual ability. So perfect an acquaintance with the customs and routine 
 of the University is revealed as to warrant the belief that the author 
 is^ describing none other than his own alma mater. Some of the 
 descriptions — especially those of the operating rooms and a couple of 
 operations therein — are, perhaps, rather too realistic to be pleasant; 
 and we can imagine that not a few sensitive readers will turn from the 
 further perusal of the book with disgust. But they will do well to 
 persevere, for the story is one of extraordinary fascination and dramatic 
 power, and it is, moreover, written in excellent, if somewhat grandilo- 
 quent English. It is not, however, a book for boys ; it will be better 
 appreciated by grown-up readers. ' — St Jcum&i Gazette. 
 
 ' The career of a medical student is a subject that does not suggest 
 material for an attractive story, yet here we have not only a readable 
 but really an admirable book. The ways and methods of the budding 
 doctor the author has hit off to a nicety, and Claude Garten's connec- 
 tion with Dunburgh University is a refreshing episode of life that is 
 strong in its realism. Many types of character are to be found in its 
 pages that have their counterparts in real life. One dwells with 
 appreciation in the society of Maclvor, Mostyn, and Murchiston ; though 
 sadness describes the feeling at the fate of poor White. The love 
 entanglements of Claude lend interest, at times pathetic, to the work, 
 while the light that is thrown on the ordinary life of the medical 
 practitioner with his diflS.culties and disappointments, is lucid and 
 entertaining. Jack Lasting, the champion boozer of the University, 
 serves to illustrate the quackery of to-day in all its hideousness. 
 Mr Henry is to be congratulated on this excellent contribution to the 
 season's literature.' — Manchester Cowrier. 
 
 ' As a story this can be recommended to all who like their literature 
 clean and wholesome, and yet with a thorough spice of life and sensa- 
 tionalism. It is the career of a medical student as lived at the great 
 university, interwoven with a thrilling and romantic love story. The 
 action never lags, and the glimpses of science we are allowed to get 
 now and again in the operating theatre and dissecting-room, are 
 up-to-date, and redolent of the newest discoveries. It is not only 
 a book to amuse, but one from which something of profit may be 
 gained.' — Lloyd^s Weekly News. 
 
E. ft S. LIVINGSTONES' PUBLICATIONS. 
 
 PUBLISHED ANNUALLY. 
 
 Crown 8vo, price 2s.; by post, 2s. 3d. 
 
 FOR SCOTLAND, 
 
 7s the only hook that contains all the i/nformation required for 
 Oradrtation in Medicine, Surgery, and Public Health at Edin- 
 burgh, A berdeen, Glasgow, and St Andrews Universities; Fellowship, 
 Membership, and Licence of Royal CoHege of Physicians ; Fellowship), 
 Licence, and Licence in Dental Surgery; Diploma in Public Health 
 of Royal College of Surgeons; Triple Qualification of Scottish Conjoint 
 Board; Classes in the Universities and Schools of Medicine, with 
 short Syllabus of each Class; Classes and Schools for Women; Asylums, 
 Dispensaries, Students' Societies, Jkc; also the 
 
 FS07ESSI0NAL EXAMINATION aUESTIONS 
 
 set by the Universities, Royal College of Physicians, Royal College of 
 Swgeons, amd the Triple Board, for several years past; the R.O.P. 
 Lond., and R.G.S. Eng., set last yeair; the Universities Prelimmary 
 Examination Questions set in October amd March, amd the Pre- 
 liminary Examination Questions set by the Educational Institute of 
 Scotland in July last. 
 
 * It is fall of the tnoBt useful Information. It ouf^bt to be a most valnable 
 work of reference for the medical BtnAenV— Edinburgh MedicalJmimal. 
 
 ' Much time and money may be saved by a careful perusal of this book.' — 
 Medical Press and Oirculsr. 
 
 ''I'he Medical School Calendar maintains its reputation for comprehensiveness 
 and accuracy of information.'— ^cotemaw. 
 
 The book is crammed Tvith information on all subjects which a student 
 requires to Isnow in piloting his way through a course of medical study. A page 
 of well- compiled advice to tlie student as to the most advantageous method of 
 study ia given. A glance through the pages of the Calendar shows the extensive 
 provision for medical education in Ediuborgh, and is itself the most convincing 
 argument for the necessity of the publication.'— ^tftn&ur^A Evening News.