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AUGUST 11, 1928.

St. Cyres LectureON

HEART AND CIRCULATION IN A TROPICALAVITAMINOSIS (BERI-BERI).

Delivered at the National Hospital for Diseases of theHeart, London,

BY PROF. K. F. WENCKEBACH, M.D., F.R.C.P.

(From the First Medical Clinic, Vienna.)

FORTY years ago, as a young doctor in my owncountry, I was intimately acquainted with the twoDutch scientists, Pekelharing and Winkler, who, as agovernment committee, had studied beri-beri in theDutch Indies. In those days nothing was known ofits aetiology ; my authorities believed it to be aninfectious disease. Eykman and Grijns had not yetdiscovered its causation, but many of its clinicalfeatures had been described, and it was generallyknown that, to quote a British poet--

Beri-beri is very, veryHard on the nerves-,"

and, moreover, very " hard on the heart " also. Iwas greatly impressed by the astonishing facts thatpatients seem to die of complete failure of the rightheart only; that the opinion (accepted as a dogma)was that this heart failure must be due to a degenera-tion of the vagus nerve; that patients may die 24hours after having been in seemingly good health;that there was an " idiopathic " hypertrophy of thewhole heart with evident lack of contractile strengthas the chief characteristic ; and that vitamin B hada miraculous effect on a heart which refused to reactto any cardiac drugs-all these facts suggested tome the existence of some quite peculiar morbidprocess. Some seven years ago I explained thisimportant problem to a young friend, Dr. Aalsmeer,a lecturer on internal medicine at the medical schoolfor native doctors at Surabaya (Java). He devoteda good deal of time and interest to the question andlast autumn returned from the Dutch Indies withcomplete clinical records of the cardiac aspect ofthe disease. These data, illustrated by X rayphotographs and electrocardiograms, provide us

with a veritable " natural history " of the circulatoryapparatus in beri-beri cases.

CAUSE, SYMPTOMS, AND TREATJHENT OF BERI-BERIIN GENERAL.

The generally acknowledged astiology lies in theabsence of an accessory food factor (vitamin B),contained in the bran of rice and cereals. Thedisease makes its appearance where polished rice isthe exclusive diet. Proof of this pathogenesis isfurnished by the results of the sole treatment—viz.,addition to the diet of vitamin-containing foodstuff,such as rice-bran, bran extracts, or a certain bean,known in Japan for over ten centuries (Phaseolus1’adiatus. Malayan : katjang idjoe). Even in verysevere cases it relieves the serious symptoms. Theprincipal pathological changes are :-

(a) Degenerative processes in the peripheralnervous system, damaging and even destroying theperipheral motor and sensory, as well as the spnpa-thetic and parasympathetic elements. The symptomsare those of extensive polyneuritis.

(b) Anasarca and serous effusion in the largecavities. In chronic cases there may be a conditionof extreme general atrophy and dryness of skin andtissues, the so-called " dry form."

.

(e) Heart disease, characterised by general feeble-ness of the circulation, palpitations on the slightestexertion, swelling of the liver and oedema, withgeneral swelling of the limbs. This heart failureis very often the cause of death.

CLINICAL ASPECTS OF HEART AND CIRCULATION.I rely on the work of Aalsmeer, correlating it with

the earlier work of Vedder, Castellani, Chambers, andManson, in English; of Scheube, Nocht, and Mensein German; of the Dutch authors Pekelharing andWinkler, Kieviet de Jonge, de Langen; and the manyJapanese contributions, culminating in the importantwork of Shimazono, whose conceptions are in manyrespects identical with those of my collaborator.The following points may now be taken as well

established :-1. From the beginning of the disease the whole

heart, right and left, is enlarged ; X rays show not.only an enlargement to the right, but also bulgingof the left auricle in the so-called " taille " (left upperborder) of the heart shadow. The left ventricle, too,is clearly larger than normal. It is impossible todecide whether, in this first period, the enlargementis due to dilatation alone or to hypertrophy of themuscle wall also.

2. This enlargement and corresponding failureof the heart increases more or less rapidly, sometimes.in a few hours, but chiefly involves the right heart.The prevalence of right heart failure and right heartwidening and hypertrophy is mentioned by everyonewho has studied the disease at the bedside and postmortem. A remarkable clinical manifestation is thedisappearance of the apex-beat and the substitutionfor it of a curious wriggling, fluttering motion of theheart muscle, which the patient himself feels and whichis easily seen on inspection and felt by palpating withthe whole palm of the hand.

3. Increasing stasis takes place in the liver andvenee cavae, and in acute cases this causes an enormous,.painful swelling and bulging of the liver, ascites, andsometimes sudden death.

4. Even in the most serious cases there is neverany irregularity of the heart, no extrasystoles,flutter, or fibrillation. The electrocardiogram nevershows any disturbance of stimulus conduction. Theventricular complex is perfectly normal, and the sizeof the different waves rather exaggerated, the onlypeculiarity being a certain degree of preponderanceof the right ventricle.

5. The pulmonary circulation is completely freefrom any sign of stasis, oedema of the lungs onlyshowing itself in the last moments before death.There is no other disease of the lungs, no true emphy-sema, no arterio-sclerosis or spasm of the pulmonaryarteries, which might cause right heart failure.

6. Apart from variations in the course, dependent.on the relative intensity of neuritic manifestationson the one hand and of cardiac disease on the other,two forms of beri-beri are generally recognised-namely, a chronic and an acute, so-called perniciousand usually fatal form. The latter is now much lessoften seen than it used to be, since specific treatmenthas almost abolished it.

7. The whole series of heart remedies and diuretics(digitalis, strophanthin, caffeine. theobromine, thyroid,.novasurol, salyrgan, &c.) is of no real use for theberi-beri heart. Vitamin B alone is an immediateand usually complete success. At autopsy theheart shows enlargement of its cavities and apparenthypertrophy of its walls, both much more pronouncedin the right side of the heart. Microscopically thereare no striking changes in the heart muscle-fibres andno inflammation.

DILATATION AND FAILURE OF THE RIGHT HEART.The first unsolved problem of the beri-beri heart

is the extreme widening and failure of the right heartin contrast with the relative smallness of the leftventricle and the absence of pulmonary stasis. Thisseems the more enigmatic, as there is proof that bothsides of the heart suffer at the beginning of thedisease. The soft and frequent pulse, however,the curious wriggling motion of the enlarging heart,and the progressive e over-filling of the proximalparts of the venous system (v. cavse and liver),are undeniable signs of the heart’s incapacity toconvey the whole quantity of affluent blood from the

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venous into the arterial side of the vascular system.Clinical experience has taught me that in such casesof increasing insufficiency of the whole heart the rightheart is doomed beforehand to suffer much more

than the left, and even to suffer to the profit of thelatter. If the strength of systole is decreasingin both ventricles equally, the moment will comeat which both ventricles will fail to discharge theircontents completely. A larger amount of residualblood than normal is retained in the heart. Thislarger post-systolic ventricular blood volume, togetherwith a normal onflow of blood during the diastole,must necessarily result in a greater filling of the heartat the beginning of the next systole. This increasedload will soon become too much for a heart alreadyunable to discharge a normal quantity of blood. Theoutput will become smaller and smaller, the fillingof the arteries will be less, and the diastolic filling ofthe heart and the venous stasis before the entranceport of the heart must both increase. This being so,two factors will establish a marked difference betweenthe right and left heart.The first of these is the anatomical inequality of

the two ventricles, the right being of lighter build,and provided with a thinner wall. The tricuspidvalves are implanted on a much weaker ground thanthe mitral; there is no strong fibrous ring supportingthem, they are condemned to share the distensionof the right ventricle, and consequently are moreliable to incompetence. Once this incompetence isestablished, blood passes from the right heart back-wards into the veins and liver and the arterial outputof the right ventricle is greatly reduced.A still more important factor is at work. In the

blood stream, moving " quasi in circulo," the rightheart is located higher up the river than the left.As a consequence, the right heart has to deal underall circumstances with the whole volume of bloodreturning from the periphery to the heart, the leftheart not receiving more blood than the right heartis able to transmit. Consequently the right heartis all the time struggling for life against an ever-increasing overfilling and widening, but the leftheart is spared a similar burden. The more the rightheart suffers and fails, the safer the left heart becomes,working under easy conditions and decreasinglythreatened by such factors as might lead to over-filling and dilatation.

In such circulatory disturbances, despite a smaller outputof the left heart, this smaller minute volume will reachthe great veins and the right heart in due time. Thisholds good even in severe degrees of mitral stenosis, inwhich an extremely high arterial blood pressure may bemaintained. Even after the final standstill of the heartin the first moments of death this function of the arterialwall (perhaps the last of life) is maintained, so that postmortem the arteries are found empty and the venous systemfilled. Therefore a smaller supply of blood to the aorticsystem cannot be expected to relieve the difficulties of theright heart in the same way as a smaller supply to thepulmonary arteries relieves the left heart.

These explanations make it possible to understandthe cardiac and circulatory phenomena of beri-beri, theinitial widening of the whole heart, the ever-

increasing bulk of the right heart, the ever-decreasingcardiac systolic output, and the progressive engorge-ment of the proximal venous system, venae cavae,and liver. It is now easy to see how in acute attacksof beri-beri a sudden failure of the right ventriclewith tricuspid incompetence puts the great veinsand the liver under systolic ventricular pressure.These are distended to the highest degree and suddendeath ends a condition of extreme suffering, thehorror of which was so dramatically described byManson in his handbook of tropical diseases. Through-out this unsuccessful struggle of the right heart thelung fields on the X ray plate are quite clear; there isno lung stasis, no rales, and no pulmonary oedema,and the left heart is not greatly enlarged but, on thecontrary, is smaller and poorly filled. A small andrapid, but fairly palpable, pulse gives proof of therelative competence of the left ventricle, until at thelast moment before death the latter loses its systolic

, power, succumbs, and leaves the lungs with stagnating blood and signs of ante-mortem oedema.: This simple mechanism, which explains the wholei circulatory complex of beri-beri and the post-mortemi findings, has great importance for general cardi.: ology. The so-called safety-valve action of the: tricuspid valve, hepatic stasis relieving the lungfrom threatening high tide, is familiar to a goodnumber of ’ us, but well-defined conditions offunctional heart disease, involving both sides of theheart equally, are rather rare. They may be foundin the course of acute infectious diseases (pneumonia,diphtheria, and others), but here so many differenttoxic and reflex influences complicate the picturethat the separate influence of each is not easilydiscriminated. Another condition in which bothsides of the heart are hampered in their action toexactly the same extent is rapid paroxysmal tachv-cardia and auricular flutter and fibrillation. Inotherwise normal hearts it has been possible to showthat here also there is marked stasis in the largeveins and liver coincident with absence of lungstasis, rales, and dyspnoea. Since James Mackenziediscovered the change of circulation caused by theonset of what he called auricular paralysis, nowknown as fibrillation, in long-standing mitral stenosis,we have been acquainted with sudden, painfulswelling of the liver ; from personal experience thischange is often accompanied by a striking improve-ment in respiration, and relief of the suffocatingdyspncea.Once I recognised this mechanism, I was able to

find it in a great many cases of slowly progressive,general myocardial weakness. Careful treatment,with well-apportioned doses of digitalis and diuretics,may cause lung oedema and swelling of the liver todisappear, even in extreme conditions, but only fora time. These intervals, during which equilibriumbetween the right and left heart is maintained withdifficulty, become shorter and shorter, until at lasttreatment fails and the patient dies in a few hours.In many of these cases of recurrent heart failure thefirst and chief symptom is a rapid and very painfulswelling of the liver. Even in rapidly fatal cases

the same symptoms may be found, rales and lungcedema only showing themselves during the lasthours of life.

In all these conditions the curious relationshipbetween right and left heart failure may be recognised,but nowhere is it so uncomplicated, so regular, andso easily demonstrable as in the beri-beri heart. Thusthere is a law of circulatory correlation between thetwo sides of the heart which may be formulated asfollows : In equal and increasing feebleness of thewhole heart muscle the patient suffers most and diesfrom the failure of the right side of the heart only.

Shimazono and Aalsmeer do not accept the con-ventional view that degeneration of the vagus fibresis the cause of the heart failure. Considerabledilatation of the heart may be present long beforethe first manifestations of polyneuritis. There isno parallelism between the degree of degenerationof nerve-fibres and that of the heart affection ; indeed.it is the strong, apparently still healthy patientwho seems to be most liable to the serious suddenacute attacks, in contrast with the patient whose firstsymptoms are those of palsy from polyneuritis.Aalsmeer is probably right in thinking that therelatively good nerve-fibres of the strong man enablehim to undertake an amount of exercise which askstoo much of his already weakened heart and inducesthe sudden attack of heart failure.

This vagal factor being unacceptable, we haveto seek other clinical facts that would reveal the onepotent unknown factor of this disease. The firsthint is given by reasoning that, in our explanationof the development of myocardial failure in beri-beri,there seems to be no place for the hypertrophy of theheart muscle so often described. Why should themuscle that from the very beginning is showing allthe signs of reduced contractile force and lessenedoutput become hypertrophic ? Such conceptions as

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(. hypertrophie passive par faiblosse (lu myoc.&t’de,"or

’’ the individual fibres becoming weaker .. anattempt is therefore made to compensate by increasingthe number of fibres-i.e., hypertrophy," do notelucidate the problem. The only way out of thedifficulty seemed to be to look for another explanationof the post-mortem findings of increased weight ofthe whole heart and increased thickness of the musclewalls.Alsmeer found that, even in the worst conditions

of failure, the beri-beri heart gives a perfectly normalelectrocardiogram, without arrhythmia, extrasystoles,heterotopic rhythms or disturbance of conductivity inthe bundle or in the conducting fibres of the ventricle.This fact reminded me that the old observationsof MacWilliam record non-contracting heart musclewithout disturbance of conductivity. Thirty yearsago Engelmann found that the frog’s heart musclewhen immersed for a short time in water loses itscontractility but retains its excitability and its powerof stimulus conduction, showing that this phenomenon,discovered by Biedermann in voluntary muscle,holds good also for heart muscle. Later de Boerdemonstrated that the swelling of the heart muscle,caused by the water, reduces mechanically the con-tractile power of the muscle-fibre, but at the sametime the electrocardiogram may continue completelyunchanged. Skramlik, Lusanna, Zondek, and Krausdemonstrated the same phenomenon for other forms ofwater retention in muscle-fibres, and even found thatthe size of the waves of the electrocardiogram maybe enlarged and the rate of conduction increased.The presence in beri-beri also of this strange contrastbetween evident weakening of the heart muscle andthe undisturbed or accelerated automatic excitatoryprocesses suggests that here also the nature of theaffection might be water retention (" Quellung ") withconsequent swelling of the heart muscle-fibres, and thatthis swelling, rather than a true hypertrophy. may bethe cause of the increased weight and thickness ofthe heart muscle wall as found post mortem.

THE WATER RETENTION HYPOTHESIS.

Many arguments support this hypothesis. A fewmonths ago Tiemann showed that striated, in contrastwith smooth muscle-fibres, swell in water and in allhypertonic solutions. The gain in weight and theswelling, due to the quantity of water taken up, isless in heart muscle than in common voluntarymuscle. If the same process is at work in beri-beriwe should expect to find the skeletal muscles swollenat the same time as the heart. This swelling is,in fact, typical of the disease, especially at thebeginning, long before general tissue oedema or

signs of nerve degeneration appear. Swelling is mostconspicuous in the muscles of the calf, which are verypainful in walking and on being pinched. Pekelharing,Winkler, and Nocht compared the condition withthe " pseudo-hypertrophic stage " in progressivemuscular atrophy of childhood.On this hypothesis we should expect that no

treatment can succeed which does not free the heartmuscle from its surplus water and drain the muscle-fibre. When vitamin B is given, the heart rapidlydiminishes in size and recovers its power of con-traction, and the skeletal muscles share in thisprocess. The hard, thickened, and painful musclesof the calf melt away, as snow in the sun, tomuscles of normal size and function. De Langen,in his new monograph on beri-beri, mentions thisrapid disappearance of the swelling and equallyrapid cure of the motor paralysis, less than 24 hoursafter taking vitamin B-containing food. This remark-able improvement is accompanied by a markedincrease in the secretion of urine. Scheube states thatkatjang idjoe had the reputation in Japan a thousandyears ago of being a good diuretic. Of recent yearsthe diuretic action of rice-bran and katjang idjoehas been specially investigated by Japanese scientists.lFrom the extensive work on the regulation of waterexchange by Magnus and by the Vienna Pharmaco-

1 Japan Jour. of the Med. Sciences, 1927, viii.

logical Institute (B. P. Pick, Molitor Baer) we learnthat striated muscle may take up and, under certaincircumstances, can retain large quantities of waterinjected into the blood or taken by the mouth. Ourmuscular system may be regarded as one of thebiggest water reservoirs, and its contents do not

appear on the balance of intake and output.Recent research work by Tsunoda and Kura 2gives important information concerning the anatomyand treatment of beri-beri. In pigeons exclusivelyfed on polished rice the sensory nerves and theirendings in the skin show curious primary regressivemetamorphosis accompanied by swelling and otherchanges in their microscopical appearance. Afterthe injection of small doses of vitamin B all thesechanges and their clinical consequences disappearrapidly. The endings of the sensory and motornerves improve rapidly within five hours after theinjection. Twenty-four hours later the histologicalappearance is practically normal.The conception of water-retention in the heart

muscle-fibre explains all the symptoms and pecu-liarities of the beri-beri heart, which thus constitutesa hitherto unrecognised and unique form of heartmuscle disease. Before trying to bring this curiouspathogenesis into relation with other well-knownfacts of physiology and general pathology, I mustmention an equally unique phenomenon in thesymptomatology. Not only is the electrocardiogramnormal during the whole course of the disease, butthe rate of conduction is increased and the atrio-ventricular interval is shortened. Moreover, conductionquickens as the heart failure progresses. In the mostserious and acute cases the shortest atrio-ventricularintervals were found when the patient seemed tobe in imminent danger of death. With recoverythe conduction slowed down to normal, even withslowing of the rate of the heart beat. The factthat the same phenomenon was found experimentallyin water-swelling of the heart muscle is a strongargument in favour of the identity of this conditionwith beri-beri heart.

THEORETICAL CONSIDERATIONS.

It seems very probable that water-retention maybe the primary cause of other manifestations of beri-beri and, in the first place, of the important degenera-tive processes in the whole peripheral nervous

system. We have already seen that the swellingof nerve-endings in chicken beri-beri disappearscompletely a few hours after vitamin treatment. Themicroscopical anatomy of nerve-fibres and ganglioncells in beri-beri accords well with this conception,and it should not be forgotten that although motorand sensory paralysis may be found, as in poly-neuritis, the primary affection of the nerve elementin beri-beri is not inflammation. It is the generalopinion that the anasarca is not so much secondary toheart failure, as essentially an imbibition process of thetissues. Other organs may show temporary swellingat the same time. Some of the glands seem topossess a special predisposition for this kind of water-retention in beri-beri, just as striated muscle is thefirst tissue to swell while smooth muscle escapes.A familiar pathological finding in this disease isswelling of the mucous lining of the gall-bladder.Kieviet de Jonge mentions a curious broadness ofthe face, recalling parotitis, and he found that thereis enlargement of both parotid glands, the natureof which, he says, is " not oedema." Stepp thinksit probable that some of the glands, especially thosesecreting saliva, ceased to function.

It would be astonishing if beri-beri were the onlydisease in which water-retention directly damagedthe heart. When an ailing heart does not react toheart drugs we generally suspect a desperate ana-tomical and functional condition of the myocardium ;it seems possible that the cause found in beri-beriplays a part in the development of such events andmight be removed by analogous forms of treatment.The first disease to remember in this connexion

2 Virchow’s Archiv, 1928, p. 267.

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is myxcedema, where there is water-retention as

a consequence of insufficient thyroid secretion(" Quellung "), and where water is expelled (" Ent-quellung ") by thyroid treatment. A case of atypicalmyxcedema may be shortly related here :-Some 20 years ago a small Frisian community sent a

poor man to the medical clinic in Groningen because he

was more or less stupid and so easily tired that he wasincapable of any bodily work. His face showed a certaindegree of imbecility or apathy, and his muscular functionwas greatly diminished ; but his build was Herculean. Therewas no trace of oedema, the face was not swollen, and theheart seemed normal. The muscles were not only big,but very hard and of abnormal consistence ; I thought thismight be myxaedema of uncommon localisation. A fewthyroid tablets had a most astonishing effect; the firmvoluminous muscles that were very painful on pinchingbecame thinner, softer, and fit for use again. On palpationthe peculiar sensation of rolling muscle bundles returned,leaving only a few hard nodes, which disappeared in a dayor two. In a week’s time the normal intellect of the manhad returned and he was sent back to his village and advisedto take small doses of thyroid indefinitely. To the greatsatisfaction of his community he proved completely curedand able to do regular work, but with less Herculean muscles.The absence of heart and nerve lesions, on the one hand,

and the inactivity of thyroid in beri-beri on the other,prove that this case was not beri-beri, and the two conditionsof different nature.

Another important difference was noted byAalsmeer. In both diseases there is a greatlyincreased skin-resistance in the patient to the electro-cardiogram ; more in beri-beri than in myxoedema.But the deflections of the string are very small inanyxoedema and at the least normal, or sometimesmuch larger than normal, in beri-beri.

These clinical facts point to the quite peculiar andspecific nature of the swelling of the striated andheart muscle, which is certainly not a condition of- cedema.

HEART HORMONES AND AUTOMATINS.Our subject forms a bridge between scientific

research at the bedside and modern experimentalwork on heart " hormones " (Haberlandt) and" automatins " (Zwaardemaker). Rigler 3 found thatvitamin B, isolated as a pure chemical substance byJansen and Donath, belongs to this group of sub-stances. He believed it to be identical with histamin.The fact that the organism itself produces substances- which are able to bring an experimentally stoppedheart and its automatic functions back to life has- already induced experimental workers to recommendthese substances for the treatment of heart patients.’The beri-beri heart shows that at least in some rareconditions the revival of a seemingly lost heart ispossible. There are doubtless a ’great number ofdifferent conditions causing standstill of the heart,-and doubtless we shall hear, in the course of time, ofa great number of different substances which may,help. The beri-beri heart shows that not everyheart that stops its systolic action has lost its regularautomatic vital function. The automatism may goon undisturbed, but is prevented from manifestingitself by lack of conductivity or, as in beri-beri,by interference with contractility. In such cases

the active substance which restores the regularfunction should not be called an automatin ; whathappens in the heart is’ not revival from death, butrelease from bondage.

SUMMARY.

My subject shows eloquently that careful studyof the sick and their symptoms, and free experimentalresearch are equally indispensable to the advancementof medicine.

It teaches us the existence of a law of circulatory-correlation between the left and the right heart,working along simple mechanical lines of considerableclinical importance.

It leads us towards the better understanding of adisease, of which the successful treatment had alreadybeen found by experience at the bedside.

It brings us into close contact with the mostmnodern biological problems of water exchange, of

3 Med. Klinik, 1928.

hormones, of sudden death, and revival of vitalfunctions.

It seems permissible to formulate the hypothesisthat the fundamental process in beri-beri is water,retention and the consequent swelling of certainvital tissues, especially nerve and striated muscle.

THE LATER RESULTS OF PARTIALGASTRECTOMY.*

BY NORMAN C. LAKE, M.D., M.S., D.Sc. LOND.,F.R.C.S. ENG.,

SURGEON TO CHARING CROSS AND BOLINGBROKE HOSPITALS ;ASSOCIATE EXAMINER IN SURGERY, UNIVERSITY OF LONDON.

FEW subjects have received more attention or havebeen the cause of intenser controversy during recentyears than that of the nature and treatment of gastricand duodenal ulceration. From the surgical point ofview the discussions have, for the most part, rangedaround the relative merits of partial gastrectomy andgastro-enterostomy. It is not proposed in thisarticle to consider partial gastrectomy as a treatmentfor new growths-for here the obligations of thesurgeon are sufficiently clear-but to limit the reviewto cases of apparently non-malignant ulceration.

It will be well at the outset to summarise thestandpoints taken by the several schools of thought atthe present day. (1) The first school believe thatoperative treatment should never be adopted in theabsence of acute complications such as perforation;they maintain that the symptoms can be adequatelycontrolled by purely medical measures. For obviousreasons this group consists almost exclusively ofphysicians. (2) The second group comprises thosewho think that operation may be occasionally justifiedin very persistent cases, and especially in the presenceof such complications as pyloric stenosis. Into thisgroup fall many physicians and a few surgeons whohave been unfavourably impressed by the recurrenceof symptoms or the onset of jejunal ulceration aftergastro-enterostomy. (3) The majority of Englishsurgeons belong to the third group and favour gastro-enterostomy for chronic cases, after medical treatmenthas been given a trial, but would treat all acute casesmedically. (4) Others advocate gastro-enterostomy,with or without pyloric exclusion, for practically allcases. (5) Yet another school consider that for themajority of cases of gastric ulceration partial gastrec-tomy is indicated, but perform gastro-enterostomy forduodenal disease. (6) The last school believe partialgastrectomy to be the operation of choice in all cases,and would always perform it for both gastric andduodenal ulceration if the technical difficulties are notinsuperable.With such diversity of opinion the only safe guide

is a critical and, as far as possible, unbiased examina-tion of the results. Since this article will deal onlywith the surgical aspect it is essential, as a prologue,to give reasons why the claims of the first school, thatsurgical treatment is unnecessary, cannot be enter-tained. Unfortunately, perhaps, for the surgeon’sproper judgment, the great majority of the cases

upon which he operates have already received a

prolonged course of medical treatment, a circumstancelikely to prejudice his opinion of these claims. Thediscovery of signs of old healed ulcers is offset by thepresence of the fresh outbreak for which the operationis undertaken. The treatment therefore, even in suchcases, has done little more than allow the originalulcer to heal without removing the cause. Post-mortem evidence of completely healed ulcers is, in myexperience, much rarer than that found at operationfor a fresh outbreak ; it thus appears reasonable toconclude that medical treatment can rarely bringabout permanent cure. Moreover, relief of symptomsis not necessarily accompanied by cure of the ulcer.

* Being a paper delivered before the South-West LondonPost-Graduate Association.