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reached a high degree of precision through the observations ofthe surgeon, the pathologist, and the bacteriologist. It was, Ibelieve, Sir Samuel Wilks who, in the first edition of his workon Morbid Anatomy and Pathology, emphasised the factthat in inflammation and abscess in the right iliac region-perityphlitis-it was usually the vermiform appendix thatwas at fault and not the csecum as was then generallytaught. To the surgeons in this country and in America weowe the great extension of our knowledge that in inflamma-tory affections of the abdomen the appendix was at fault witha frequency not previously imagined and they have pointed outthe anatomical conditions in the appendix that favour andpredispose the appendix to disease. The bacteriologists havedetermined the micro-organisms that play such an importantr6le as the excitors of the inflammation and its con-

sequences in the appendix. Thus, on the one hand, wehave learned that micro-organisms are always concerned inthe inflammation, ulceration, sloughing, and necrosis thatoccur in appendicitis. The bacillus coli communis appearsto be the most common-a bacterium in ordinary circum-stances saprophytic and harmless but which may becomevirulent and deadly when growing in diseased tissues. Morerarely the pus cocci, the streptococcus pyogenes, the staphy-lococcus, the proteus, and bacillus pyocyaneus are concerned,and the bacillus typhosus has been found to be the organismat fault. On the other hand, we have learnt that peculiaritiesof position and anatomical formation of the appendix andits mesentery tend to produce contortions and contrac-tions and interference with the circulation in the appendixwhich prevent the discharge of its secretions, favourthe formation of fsecal concretions, and prevent the expul-sion of foreign bodies accidentally entering its canal. Inone of these ways the vitality of this portion of the intestinaltract, probably owing to its being a vestigial remnant neverso high as other parts of the intestine with active functionsto perform, becomes impaired. The organisms in the

appendix find a medium which enables them to grow and tomultiply, often with intense virulence, by which they inflameor destroy the appendix and pass through its walls to theperitoneum and other contiguous parts. Sir Frederick Trevestells us that "it is impossible not to be struck with the factthat perityphlitis runs often in families," not so much asan inherited disease as a family disease. It is much more fre-quent in the second and third decennia and in the male sex.So we find the seed and the soil in appendicitis the excitors

of active disease and the predisposing conditions-the per-sonal factor in this disease-each essential for its occurrence.But whereas in tuberculosis and rheumatism we are oftenable to detect the mischief by the history, the patient’sappearance, the evidence of individual predisposition, thereis nothing in appendicitis that reveals a tendency to thiscondition until the occurrence of an attack of appendicitis.Moreover, whilst the tendency to most of the infectivediseases is a general one more or less distributed throughoutthe system, though in each there is a favourite mode ofentrance of the virus, here it is an entirely local one

extending over an area of only a few inches.Reviewing the group of diseases which I have selected to I

illustrate my thesis we have seen that in each there are twofactors-the soil and the seed, each necessary to constitutethe disease, but that the relative share which they appear totake varies in importance in different diseases. We as

practical physicians have to obtain our knowledge as to themicro-organisms concerned in these diseases and their

chemio-physiological action from those who devote them-selves to these studies, whilst we have to observe the effectsof the micro-organisms on the human body and how the bodyreacts to the germs of the disease. The infective diseasesexisted long before the discovery of the germs and we haveaccumulated a large store of knowledge of the clinical course,the treatment, and the issue of these diseases. This accumu-lated experience is of great value though apt to be over-

looked by the keen interest excited by fresh discoveries. Itis against this tendency that I wish to enter a protest andto point out that what is true is not necessarily new. Wemust never forget that the soil is of as great importance tostudy as is the seed in the proper understanding andtreatment of diseases of microbic origin.

HEALTH OF ST. IVES.-Mr. J. M. Nicholls, themedical officer of health of St. Ives, Cornwall, in his annualreport for 1901 states that 197 births were registered duringthe year, corresponding to a rate of 29-41 per 1000. Thedeaths numbered 129, equal to a rate of 19-26 per 1000.

A Clinical LectureON A CASE OF

SUPPOSED INTESTINAL OBSTRUCTION, DUETO A VASCULAR LESION,

RAPIDLY FATAL FROM INCIPIENT GANGRENE OFTHE STOMACH AND THE DUODENUM.

Delivered at St. Mary’s Hospital on Feb. 25th, 1902,

BY HERBERT W. PAGE, M.C. CANTAB.,SURGEON TO THE HOSPITAL.

GENTLEMEN,-I promised you a fortnight ago that I

would tell you something about a remarkable case of intes-tinal obstruction which had been under my care recently.The case was one of singular interest and as far as myresearches have carried me I believe it to have been unique.You will hear that there was no true intestinal obstructionat all, but nevertheless the case must be so described, forintestinal obstruction was a prominent feature of it and itwas intestinal obstruction that I was called upon to relieve.Were I to ask you for the causes of intestinal obstruction youwould doubtless be readily able to give me a list, as, forexample, obstruction by band, by volvulus or kink, by growthswhich narrow the lumen of the bowel, by impaction of aforeign body, by accumulation of fasces, by any form of

strangulation whether external and visible or internal andout of sight, and these various conditions you might speakof as true causes of obstruction in that they severally inter-fered with the lumen of the bowel and prevented the onwardpassage of its contents. And if I pressed you further youmight remember other causes which rather may be regardedas those of false obstruction in that there is no mechanicalinterference with the lumen of the gut-the paralysisof bowel, for example, such as you may meet withfrom sundry nervous conditions, or the distension which

may arise in the course of peritonitis when all peri-stalsis has been lost. Your list would be fairlycomplete, but I doubt whether you would think ofvascular lesion alone as being a possible cause of intestinalobstruction. And yet there have been cases recorded fromtime to time where a vascular lesion-thrombosis of thesuperior mesenteric vein, for example-has given rise to

symptoms of intestinal obstruction for which operation hasbeen undertaken. I shall presently refer to a case of thissort which was brought before the Clinical Society ofLondon by Dr. J. Rose Bradford and there have been othercases like it.’ We ought, therefore, to have this cause ofintestinal obstruction in mind, although from its exceedingrarity we may hardly expect to meet with a case ourselves.Now let me tell you of my own case.On Monday, Feb. 10th, I was sent for by my friend and

former house surgeon, Dr. J. A. Wright, to see a patientwith intestinal obstruction and to come prepared to operate.I went and this was the story which I was told. The

patient, a man aged 50 years, thin and spare, had enjoyedthe best of health until three and a half years previously,when he had a very bad attack of typhoid fever which kepthim in bed for some 10 weeks and which was complicatedby thrombosis in the right leg. His health had neverbeen the same since ; he had lost his former strengthand his capacity for continuous work. In the summer of .’

1899 he had thrombosis in the left leg following a bicycleaccident and again in the spring of 1901 he was laid up fora month with thrombosis of the left femoral vein. I ask

your special attention to these several attacks of throm-bosis for they go far to explain his present illness.A week previously he had had rather a bad cold and hadstayed indoors, but on the afternoon of Feb. 9th (Sunday)he was able to go out for a country walk. During the walkhe was suddenly seized with pain above the umbilicus andthis was soon followed by diarrhoea. As a matter of fact hehad to relieve himself behind a hedge more than once, and

1 Notably since this lecture was given the case of " IntestinalObstruction due to Embolism of a Branch of the Superior MesenterieArtery " brought before the Clinical Society of London by my friendsDr. W. J. Tyson and Mr. W. W. Linington of Folkestone, on April 11th(see THE LANCET, April 19th, 1902, p. 1109). Coffee-ground vomit was,there also a prominent symptom.

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the pain continuing he was obliged to rest in a cottage.Here the pain continued and the diarrhoea was more profuse.In about an hour he was able to get home and Dr. Wrightfirst saw him at half-past five o’clock. The diarrhoea hadthen ceased and the pain was less, but there was muchuneasiness or discomfort in the epigastrium and he felt as ifhe must be sick. He was cold but was not collapsed. At9 P.M. when Dr. Wright next saw him he was restless andhad considerable epigastric pain. He had vomited a little.Flatus had been passed from the bowel. Abdominalexamination was negative. A subcutaneous injection ofmorphine and atropine was administered. The night wasbroken and he had occasional vomiting of a small quantityof odourless coffee-coloured fluid. There was some hiccough.Before daylight there was a return of the epigastric pain andat 6 A.M. the injection was repeated. At 10 A.M. he wasfairly easy, but he still had epigastric pain and there wasslight tenderness. The pulse ranged from 90 to 100. The

temperature in the axilla was normal. Abdominal examina-tion was again negative ; there was no distension whatever.A rectal examination discovered nothing and a soap-and-water enema was entirely without result. At 1 P.M. Dr.

Wright detected some resistance and tenderness midwaybetween the umbilicus and the left costal margin and thesebecame more marked in the course of the afternoon. Theother symptoms continued and no flatus was passed. The

pulse rose to 120.I saw the patient soon after 7 P. m. It was obvious at once

that the man was extremely ill, and from his aspect alone Iformed a grave prognosis His pulse was then 108 and it wasoccasionally intermittent ; he was vomiting copious quan-tities of the coffee-coloured liquid. The abdomen, which wasabsolutely flaccid, moved on respiration and was free from allsuspicion of tenderness save only between the umbilicus andthe left costal margin where were the resistance, the slightfulness, and the tenderness which Dr. Wright had described.It was clear that operation, if to be undertaken at all, couldbe delayed no longer. And I must tell you frankly that Inever undertook an operation with less idea as to what couldbe the matter. Every conceivable lesion had been turnedover in our minds : Dr. Wright himself even went so far asto suggest embolism of an intestinal vessel. A kink fromformer typhoid ulceration was one of the more unusual

things which occurred to us, but from the symptoms andhistory the seat of probable obstruction was presum-ably high up in the intestinal tube, while kink theresult of typhoid fever would rather be low down. It wasunder these unsatisfactory conditions that I opened theabdomen in the middle line above the umbilicus. A re-markable state of things was immediately disclosed. Thestomach was seen to be enormously tense and distended,dark purple in colour, with here and there small flakesof lymph upon its surface, and conveying the impression thatit would not bear much handling. Had it been a piece of

gut exposed in operation for strangulated hernia I unques-tionably should have hesitated to return it to the peritonealcavity, for it had all the appearances which indicateapproaching gangrene. It was suggested to me that Ishould puncture the stomach and let out the contents, but Ifelt that this would be a dangerous procedure as there mightbe difficulty in closing the opening. My search was nextdirected to the discovery of some cause for the supposedobstruction, and the bowel, large and small, was thereforesystematically examined from end to end. Both large andsmall were found to be empty ; I may say, in fact, that Ihave never seen small bowel so completely collapsed.Tracing it upwards no cause of obstruction was anywhere tobe found, but as we approached the stomach so did collapsedbowel of natural colour gradually merge into distended anddiscoloured bowel until at its union with the pylorus theduodenum was seen to be enormously dilated like thestomach, and here, also, it had the purple colour andstructural change which have already been described in thestomach itself. Satisfied that there was no mechanicalcause for obstruction and that none could possibly have beenoverlooked, there was nothing left to us but to close thewound The condition of the patient was now extremelygrave ; there was profuse vomiting, and at one time wethought that he must die on the operating table. Happilythat was obviated and he rallied sufficiently to talk to hisfriends. He died three hours afterwards.We had now little doubt in our minds that a vascular

lesion was at the root of the patient’s symptoms and of thesingular state of things which we had seen in the stomach

and the duodenum. And here I am sorry to tell you that our

story is incomplete. A partial necropsy was made byDr. Wright through the operation wound and if you thinkof the difficulties of a necropsy unassisted in a countryhouse it will hardly surprise you that the post-mortemrecord is not as complete as we could wish. Nevertheless,very valuable information was obtained and I will read to youDr. Wright’s notes. "The parts," he says, "looked verymuch the same as at the operation. I took out the whole

gut, beginning at the sigmoid flexure. It was practicallyempty and collapsed until the beginning of the duodenumwas reached. There was no obstruction whatever to be foundat this or at any other place, but from it to the cardiac end ofthe stomach the whole length was hugely distended, even thepylorus being dilated. On opening the stomach there wereabout two pints of the dark, fluid, altered blood. Thestomach and duodenum were stained with it, but none ofthe fluid had passed any further downwards in the intestine.There was certainly some difference in the mucous membraneof the stomach and duodenum as compared with the rest ofthe gut. The stomach-wall was greatly stretched, theveins were engorged, and on its anterior surface therewas very slight superficial ulceration. Running here andthere were some peculiar raised patches which looked mostlike thickened tortuous blood-vessels. I searched very care-

fully for arterial clot but could find nothing to swear to." Inanswer to further inquiry Dr. Wright told me that there wascertainly no plugging of the portal vein itself.

This, then, is all the post-mortem evidence which I can

give you, but yet I think there is hardly room for doubt thata vascular lesion was after all the real cause of the symptomsand of the state of the stomach and duodenum. Nothingelse could well have accounted for them. I will give you thereasons for this conclusion.

! First, there is the evidence of other cases of a like kind,and here I cannot do better than tell you of Dr. RoseBradford’s case,2 entitled, "A Case of Thrombosis of the

Superior Mesenteric Vein causing Intestinal Obstruction."A man, 20 years of age, was seized in the night with pain inthe upper abdomen and he felt sick, but he was able to go towork in the morning. He was worse on the second day andon the third day he had diarrhoea. Then he took to bed.On the sixth day he went to University College Hospitaland the summary of his history from that day to the eleventhday is in these words : "Since admission patient had remainedin much the same condition, complaining of a good deal ofabdominal pain, especially at the umbilicus and between thisand the costal margin. The abdomen is not distended ; if

anything it is slightly retracted. There is no markedtenderness on palpation. Patient has had slight occasionalvomiting of the contents of the stomach and the bowels havenot been opened without enemata, but with these normalmotions have been obtained." The scene then changed. Theman began to vomit frequently and on the thirteenth day thepain was still more severe and the vomit, which had becomeincessant, was distinctly stercoraceous. He was worse onthe day following and it was decided to open the abdomenas it was thought that there ’was some form of intestinalobstruction." A piece of the small intestine about a footlong was found to be greatly swollen and thickened andpurple in colour. There was no volvulus and no constrict-

ing band was found. There was a little reddish fluid inthe peritoneal cavity and a little lymph on the intestine.The patient did not survive the operation long and at thenecropsy a coil of small intestine at the upper part of thejejunum was seen to be dark-purple in colour and consider-ably swollen and thickened for a distance of about 18 inches.There was no band or other cause of strangulation. Themesentery was thickened and the veins were obviously throm-

: bosed. The trunk of the superior mesenteric vein was greatly: thickened, the wall of the vessel being as thick as the wall ofL the superior mesenteric artery. The vein contained flakes of

coagulum adherent to the inner surface and forming analmost continuous layer of decolourised blood-clot. The

l lumen of the main vessel was filled with reddish puriformmaterial. The upper part of the vein was occupied by firm,

, partly decolourised, clot. The disease of the superior mesen-teric vein extends into the main tributaries of this vessel-

r to a varying extent, however, in different ones. As the; intestine is approached the thickening of the walls of the

veins becomes less and less marked, until in most of the ter-r minal branches the walls of the veins have their normal

2 Transactions of the Clinical Society of London, vol. xxxi., p. 203.

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thickness and appearance." Those are the chief facts andI need not quote more, for they are sufficient for my purpose,which is to show you that plugging of a superior mesentericvein may lead to symptoms suggestive of intestinal obstruc-tion and that operation may be undertaken to discover andrelieve the condition in the absence of any certain diagnosis.Were there no other cases of the kind, this case recorded byDr. Rose Bradford would of itself be sufficient to suggest thata similar vascular lesion must have been present in our case.The patient’s own history is, however, not less suggestive.You remember that on three previous occasions he had hadattacks of thrombosis, and whatever may be the causes ofblood-clotting in veins I think we may say that in some wayor other this man was predisposed to the same thing again.The suddenness of onset, moreover, of the attack on this lastoccasion was very suggestive of a sudder vascular lesionand I venture to think that nothing else could possibly haveproduced in so short a time as 24 hours the striking changeswhich were found in the stomach and duodenum. I believe,moreover, that venous rather than arterial thrombosis musthave been the cause of the impending gangrene. Dr. Wrighthas told us that he searched carefully for arterial clot butfound none. Furthermore, the valves of the heart werehealthy and free from vegetations from which an embolusmight have been detached and lodged in some vessel. Ihold, therefore, that we are justified in the conclusion thatvenous thrombosis was the actual disease and that we mayregard the coronary vein and its tributaries, and in all prob-ability the pyloric vein also, as having been the vesselsaffected.

It will interest you to know that an excellent account ofall the conditions pertaining to thrombosis is to be foundin Allbutt’s " system " from the pen of Professor Welch.This is accessible to you in the library, but I will readone short passage which bears upon our present case:-"The symptoms "-he is writing of thrombosis of the mesen-teric veins-" are the same as with occlusion of the mesen-teric arteries, but as a rule are even more violent and rapidin course. They are as follows : sudden onset of very intense,colicky, not definitely localised, abdominal pain ; distended,tender, tympanitic abdomen ; vomiting which may be bloody;obstipation, or bloody diarrhoea ; and rapid collapse, withcold sweat and subnormal temperature. The diagnosis is

likely to be acute ileus and laparotomy to be performed.Death generally occurs within two or three days. The sym-ptoms may, however, be less violent and the course less

rapid than those mentioned. At the autopsy are foundhasmorrhagic infarction and gangrene of the intestine,hsemorrhages in the mesentery, bloody fluid in the peritonealcavity, and sometimes, although not regularly, peritonitisThe cases without symptoms have been usually thromboses ofslower formation, but this does not appear to have been

always the case." "

Such, gentlemen, is the story which I bring before you.A consideration of it is not likely, I fear, to lessen the diffi-culties which beset the diagnosis and treatment of intestinalobstruction. Of all the conditions which may present them-selves at operation this surely of which I have spoken is theleast amenable to relief. Nevertheless I commend it to yournotice preparatory to the wider publication which I think itdeserves.

I am indebted to Mr. Arthur E. Fidian for shorthand notesof this lecture.

THE CONGENITAL FACTOR IN HERNIA.1

BY R. HAMILTON RUSSELL, F.R.C.S. ENG.,SURGEON TO THE ALFRED HOSPITAL, MELBOURNE ; LATE SURGEON TO

THE MELBOURNE HOSPITAL FOR SICK CHILDREN.

IT may perhaps be within your memory that at the lastmeeting of our congress at Brisbane I contributed a paper tothe transactions of this section entitled, ’’ The Etiology and ’,Treatment of Inguinal Hernia in the Young," and I placed ’,before you certain important conclusions at which I had ’,arrived in respect of the etiology of inguinal hernia in young Ichildren. My operative experience of 60 cases was very i

1 A paper read before the Surgical Section of the IntercolonialMedical Congress of Australasia. Hobart. Tasmania. February. 1902.

2 THE LANCET, Nov. 18th, 1899, p. 1353, and Intercolonial MedicalJournal of Australasia, Sept. 20th, 1899.

small, it is true, when compared with the enormous seriesthat are frequently placed before us by surgeons at the

present day ; but I would point out that my series was anindiscriminate one, comprising an unbroken record of everycase of inguinal hernia that had come into my hands duringa certain period, and that the evidence afforded by an indis-criminate series of 60 cases when that evidence is unanimousis more weighty than any evidence that could be deducedfrom 600 cases that have been selected by reason of certainclinical characters that were deemed to call for operation.The conclusions at which I arrived and which I believe to

be of fundamental importance for a clear understanding,not merelv of inguinal but of all other forms of abdominalhernia, I will set forth in the following propositions :-1. Oblique inguinal hernia is invariably caused by the

presence of a congenital sac which in the vast majority ofcases is provided by patency of the whole or a portion of theprocessus vaginalis. 2. There is no evidence in favour of theview that congenital weakness of the abdominal wall in theinguinal region is a factor in the causation of inguinalhernia. 3. While actual weakness of the abdominal wall inthe inguinal region is frequently met with and is an

occasional cause of recurrence after operation, such weaknessis not congenital but is an acquired weakness due to theexistence of the hernia and the use of a truss during alengthened period. 4. Complete removal of the sac, whenperformed before the abdominal wall has sustained suchdamage, will not be followed by recurrence. 5. The causesof recurrence after operation are three in number-viz., (1)the above-mentioned acquired weakness ; (2) incompleteremoval of the sac ; and (3) traumatism, the result of mis-guided methods of operating.

These, then, are my articles of faith ; the arguments onwhich they are based have been already published very fully 3and I do not intend to trouble you with them again. The

only new argument that I will bring forward to-day, if youwill be so courteous as to regard it as an argument, is this..My former series of 60 cases has in the last two yearsbeen extended to well-nigh double that number, with theresult that so far from having observed anything to shake mybelief my confidence in the truth of the foregoing state-ments has been redoubled. To-day I will ask you, whetheryou agree with me or not, to assume for a few minutes thatmy views are correct, for I wish to suggest to you that theyapply equally to inguinal hernia in the adult-that there isno difference etiologically between the inguinal hernia ofchildren and that of older people and that the managementof the affection in either case will be the same in principle,differing somewhat in detail but differing only by reason ofcertain factors that are often imported into the case of the-adult but from which the young child is free.When hernia has existed for some years the inguinal canal

becomes converted into a large hole in the abdominal wall,because the curved fibres have been stretched, atrophied,and displaced during a period of years and are quiteincapacitated from performing their natural function as theinguinal sphincter. This leads me at once to draw yourattention to one of the singular and fundamental errors thathave pervaded the whole theory of inguinal hernia. The-belief is almost universally held that inguinal hernia is oftenthe result of some congenital weakness of the inguinalabdominal wall which permits the descent of a rupture.This generally accepted view is the exact converse of thatwhich I believe to be the truth, for instead of the weaknessbeing congenital and the hernia consequently acquired itis the hernial sac that is congenital and the weakness thatultimately becomes acquired. It is of the utmost importancethat this fact should be appreciated, for its teaching, whenreduced to practice, means that if on the first occurrence ofhernia the sac be removed the abdominal wall will thence-forward be unimpaired and the patient will be no more-

predisposed to recurrence than he would have been if he hadnever had a congenital sac and had never had a hernia.

Let me illustrate this point by citing the case of a man,aged 24 years, who became suddenly ruptured while playingfootball in August, 1899. At the operation four months later-the bowel was found to have entered one portion of abilocular congenital sac ; the entire sac was ligatured at theneck and removed after incision of the external obliqueaponeurosis but no attempt was made to close the canal bysutures. The patient was kept in bed for a fortnight andwas told to exercise caution for a month afterwards ; after

3 THE LANCET, Nov. 18th, 1899, p. 1353, and Oct. 20th, 1900, p. 1128.