Canad. M. A. J.Oct. 1951, vol. 65 MURRAY: MITRAL STENOSIS

THE SURGICAL TREATMENT OFMITRAL STENOSIS*

Gordon Murray, M.D., F.R.C.S.[Eng.& C.]Toronto, Ont.

THE surgery of great vessels for congenitalheart disease lead naturally to a great deal

of enthusiasm for intracardiac surgery, butwhile the former is a development of very

recent years, it is interesting to note that at-temps at dealing with stenosed mitral valves,dates back to the beginning of the century.

Perhaps the earliest thoughts along these lines camewith the discovery of the circulation by Harvey. Thenin 1850 C. J. B. Williams described mitral valve diseaseand gave a very accurate description of the clinicalmurmurs and findings on. which the diagnosis could bemade clinically. A very acute observer, Samways in 1898,observed the rhythmic action in the heart of the horse.The organ was sufficiently large and had such a slow ratethat he was able to see the rhythmic contraction of theauricle followed by that of the ventricle. His observationwas probably the most important ever made in regardto the physiology of heart function. In 1902 Brunton'made a direct attack on the mitral valve, realizing itsimportance in obstruction in rheumatic heart disease andmade an incision in this structure. In the following years,1907 Cushing,2 1909 Bernheim,3 1912 Sheppelman,4 1922Graham and Allen,5 all had done a good deal of think-ing and made some attempts at doing something aboutmitral stenosis.

It was evident from the writings of these surgeonsthat they were aware of the significance of the mitralvalve and its importance in producing the symptoms ofmitral stenosis. The most determined attack in trying torelieve mltral obstruction was made in 1924 by Cutlerand Beck.6 They succeeded in punching out portions ofmitral valves with fairly good immediate results but theregurgitation seemed to be a greater handicap than wasthe pre-existing stenosis. For that reason they discon-tinued this work. In 1925 Souttar7 dilated the mitralvalve successfully. Then there appeared to be a lull inactivity in this regard until in 1947 Smithy,8 himselfa sufferer from this disease, made a surgical attack onthe mitral valve with considerable success. Since thattime the work of Bailey, Glover and 0 'Neill,9 Harken,ieBlalock,i" Potts,12 Murray'3 have added a good deal ofinformation to the surgical treatment of mitral stenosis.

My interest in the subject developed in theform of some experimental work in 1935, theresults of which were published in 1938.13 Lack-ing the support of my colleagues, or sufferingfrom a faint heart, I did not apply this until1945 when I operated upon my first patient. Iam glad to say that that patient is still aliveand working and does not seem to be failingin any sense, except from the inexorable marchof time.For the purposes of this paper, this subject

might be considered under the headings that

follow.

* The Mayo Foundation Lecture, delivered at TheMayo Clinic, Rochester, Minnesota, February 15, 1951.

WHAT IS THE DISEASE?I shall mention only the fact that rheumatic

infection, whatever may be its source, damages

both the musculature as well as the valvularsystems of the heart. It was thought in the timeof McKenzie and Ross, as well as by many phy-

sicians in recent years, that the damage to themuscle was more important than the damageto the valves. Medical treatment, by and large,was therefore designed to improve the func-tion of the muscle so that it might be more ableto overcome the obstruction or the leaking of

the valve systems. From my point of view, how-

ever, if there is increased work produced bystenosis or regurgitation at one or more valves,

this adds an extra load to a muscle which is

already damaged and, while the muscle can beimproved in many respects, and the conductionchanged to improve this function, if the heavyload imposed by obstructing valves could berelieved, then the muscle would be more able to

carry on adequate circulation.Added to these continuous difficulties, which

usually increase until the circulation ultimatelyfails, there are complications which are re-

sponsible for death in a fair number of suchpatients. There is impaired circulation of thegastrointestinal tract and liver, causing a great

deal of discomfort and contributing to a stateof poor health probably from poor metabolism,also changes in the pulmonary vascular treeand lungs causing disability and attacks ofasthma, pulmonary oedema and hemorrhage.The tendency to formation of thrombi in the

left auricle, especially its appendix, and oc-

casionally in massive form in the body of theauricle, may lead to embolism or, it is sug-

gested, ultimately the presence of the obstruct-ing thrombus in the auricle which embarrassesthe circulation may suddenly obstruct themitral valve. Post mortem evidence of deathresulting from such sudden valvular obstruc-tion from a thrombus, makes one wonder if

some of the clinical episodes of sudden tempo-rary failure of the circulation in such patientsmay not be the result of temporary blockingof such a nature, which fortuitously has re-

lieved itself -in time for survival. These pointsare mentioned because of their possible signifi-cance in relation to the criteria used for selec-tion of patients suitable for surgical operationi.

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HOW PREVALENT IS THE DISEASE?In the United States, and I suppose our

statistics in Canada, while not fully recorded,would follow closely those of that country, itis shown that rheumatic heart disease is theleading cause of death betweeii ten and sixteeniyears of age. It is seconid only to T.B. betweenthe ages of fifteemi and tweiity-four. Each yearthere are between six and seven hundredthouisanliid deaths from heart disease and ofthese about two hundred and sixty-fourthotusaind are rheumatic heart cases. A largenlmber of these patients are in poor health andare semi or complete invalids and this is a gianteconomic problem. While one would hope thatpreventive medical measures eventually wouldprevent this disease, still for the present itleaves a great mass of material asking for im-provement by surgery, medicine or any othermeans that can be provided. In Navour of thisdisease responding to preventive medicine isthe fact that it tends to occur mostly in poorerclasses where there is over-crowding, andfurther evidence of this is the fact that 35 to50%o of patients have others with the same dis-ease in the same famnily or in close relatives.Therefore, improvement of general conditionsand nutrition might have a great deal to do inpreventing this disease.

EFFECTS AND COURSE OF THE DISEASEStatistically it is shown that about 50% of

patients with mitral stenosis die in young lifeor middle age. The duration of life after de-veloping mitral stenosis which is recognizableis about twenty years. When regurgitation ispresent, this period is considerably shorter.When comsidering surgical treatment, it is wellto reimember that after the first evidence offailure in a chronic case, the patient may livefour to five years and after having an attackof hsemoptysis, which ordinarily is considereda late stage of the disease, the average dura-tion of life is two to four years. Therefore,surgery, if it is to have a place in the treatmentof this disease, must offer prospects better thanthose indicated.The result of injury to the vascular system is

of considerable interest to the surgeon. In about85% of patients having rheumatic fever, thereis evidence of valvular disease. In those inwhich the valves are involved, mitral stenosisalone occurs in about 50%. In another 19%,mitral stenosis is conmbined with aortic-valve

lesions. Mitral aortic and tricuspid are involvedin about 11%o and the tricuspid in 3%, whilethe pulmonary is involved only in about 1%with mitral valve disease.Symptoms will be considered only as they

have a bearing on the selection of patients foror against operations. For the present at least,most patients with an established diagnosis ofmitral stenosis are best treated medically. Sur-gery is indicated only if: (a) it is generallydecided that the duration of life is likely to beshortened by the disease and that surgery hasa prospect of prolonging this; (b) the patient'sdisability is sufficient to justify an operationand that surgery has a fair prospect of reduc-ing the disability; (c) the complications may

be prevented or diminished by operation.The decision on these problems falls to the

lot of the physician and every available formof investigation must be called into use to helpmake the decision. It has been my policy tooperate only on patients who have: (a) Un-equivocal signs of mitral stenosis. (b) No valvesother than the mitral involved, or, if so, onlyto a very slight degree. (e) There must be no

active heart infection present. (d) The rheu-matic fever must be in a quiescent stage. (e)Progressive failure and increasing disabilityin spite of medical treatment.

All the patients on whom I have operatedhave been under medical treatment and in spiteof this, they have shown signs of failure. Therehas beemi dyspnema, usually at rest, and alwayson exertion. In some orthopncea, occasionallypulmonary codema; some have had hmemoptysis;a varying amount of cyanosis with distensionof neck veins in some, with enlargement ofliver, aedema, ascites and an enlarged heart.All but 4 of 37 patients operated upon have hadauricular fibrillation. Various clinical, x-ray

and laboratory tests to establish the diagnosisand estimate the stage of the disease have beencarried out. In spite of all the evidence obtainedby investigation, I have found from my ex-

perience at operation that there are some otherhazards which are very perplexing. I feel theanswer to these must be found before a satis-factory decision can be made as to whether a

patient is suitable for operation or not.The first is the problem of massive thrombosis

in the left auricle. This has been a major factorin deciding whether something could be ac-

comnplished at operation or not. In 8 patients,other than the 37 named as patients operated

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upon, a massive thrombus was found in theleft auricle on exploration.'4 This thromnbus in-volved the left auricular appendage and formeda miiass within the auricle the size of one's fistor considerably larger and in one patient thethrombus extended right through and could befollowed well out in the upper pulmonary veinon the left side. In one such patient, the throm-bus was probably the size of one's fist, butthere seemed to be a fair amount of auricularwall which was flexible and it was thought one

might take a chance and divide the mitralvalve, taking as great care as possible not todisturb this thrombus. The instrument was

passed through the valve without difficulty andwas felt in the aur icle by depressing the flexibleportion of the wall, then a good incision was

made through the valve. The patient seemed tobe considerably benefited immediately by thisanid we were quite pleased with his conditionon returni to the ward. However, within twenty-four hours, it was evident that he had a massiveembolism at the bifurcation of the aorta.15 Withhis recent heart operation and his general poor

condition with this embolism, I was afraid to doanything further and he succumbed. ObviouslyI should not have done anything to the mitralvalve. In the other seven oii making this diag-nosis. I closedl the chest without doing anythingfurther.My great problem, therefore, is to determine

clinically beforehand whether there is a throm-bus in the left auricle or not. To my mind, thisis one of the heavy and difficult problems. Ongoinig over these patients very carefully, I havecomne to the conclusion that a massive thrombusof this sort is to be expected if: (a) there is a

doubtful looking shadow, added to the heartshadow, which might be interpreted as lying inthe region of the left auricle; (b) if a patienthas been doing fairly well but finally gets toa stage where there is relatively little responseto all forms of treatment and the general condi-tion seenis to be sagging with increasing failurein spite of treatment and rest. 'While this mightbe the result of other features, it has been a

factor which has been constant in this group;(3) calcium in the wall of the auricle.We have tried to do angiocardiograms, but

so far the results have not been very satis-factory. I saw one patient in Rio de Janeirorecently in whose x-ray there was a shadowwhich, I think, fairly certainly, might have

beell initerpreted as a thrombus in the left

auricle. However, as the patient was notoperated upon, one cannot prove that such was

the case. He was thin of stature and the heartshadow stood out in great contrast to thelighter surrounding somatic structures.The second problem which must be de-

termined beforehand, if possible, is the ques-

tion of permanent vascular changes in thepulmonary vascular tree and in the lung tissue.Unfortunately, two of my fatal results follow-ing operation were in patients in whom therewas no improvement following division of themitral valve, who at post mortem were shownto have basement membrane thickening of thepulmonary capillaries, and arterioscleroticchanges in smaller and larger pulmonary arteryvessels in the lung. Recent articles by Welsh,Johnston,'0 Larrabee, Parker and Edwards'7here, also Parker and Weiss,'8 describe theseconditions and there is an awareness about thislesion. It appears to be irreversible and I wouldconsider it an absolute contraindication tooperation. These studies have been on patho-logical material, as have been mine, and thisdoes not help in identifying it preoperatively.Not long ago I was congratulated by thepathologist on providing theni with such a case

following operatioil, but I must say that gave

me little satisfaction, because I wanIt to knowbefore making the decision to operate. The onlypositive information which may suggest sucha lesion, and it is not an unequivocal fiinding, ismarked pulmonary hypertension. All the pa-

tients on whom I have operated have had pul-monary hypertension, but it is alleged that ifthe pulmonary pressure goes above 100 milli-metres of mercury on catheterization, this is aIcontraindication. So far as I know to date, thisis the best warning of the presence of such vas-

cular changes in the lung and if established isa contraindication to operation.By and large, the patients who are likely to

benefit from operation are those in whom medi-cal treatment has failed, and who are unableto carry on, on this account. On the other hand,I have operated on a few patients who were inlate or final stages of heart failure with enor-

mously enlarged hearts who have benefitedtemporarily, but I think the results have notbeen worth while. There is a group, therefore, atthe farther end of the course of heart disease,who, for the present at least, are not suitable, or

do nIot stand to benefit by surgical treatment,and should not be operated upon.

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SURGICAL TREATMENTI shall mention only the question of relieving

pulmonary hypertension by producing inter-atrial septal defects, as suggested by Blalock,19Bailey,20 and the anastomosis of the pulmonaryto azygos vein, as suggested by Sweet,2' whichmethods have given improvement in groups ofpatients. There is also the possibility of reliev-ing some of the symptoms of heart disease byattacking the nerve supply, but that does notcome within the scope of this paper.The other possible surgical procedures are:

(1) Direct approach, when the valve is divided.(2) Resection of a portion of the stenosed valve.(3) Resection of a portion of the valve and re-placement by a new valve. (4) Short circuitingof the stenosed mitral area by various methods,where either vein grafts or the auricular ap-pendage has been used to produce a bypassfrom the auricle or pulmonary veins to theleft ventricle (Rapaport22).The possible approach for dealing with the

mitral valve directly may be either through theleft auricle or the left ventricle. You are allfamiliar with the successful work of the lateSmithy,8 of Bailey, Glover, O'Neill,9, Harken,10Brock23 in London, and many others. One mustdecide, therefore, on the approach to be used,and just what is to be attempted on the valveitself. In some of my earlier patients, the opera-tion was carried out through the left auricle,but my preference at the present time is for anapproach through the left ventricle. The incisionfor the anterior approach is rather a large dis-section. However, the patient tolerates this verywell and the time involved is not great. I havecompleted several of these operations within anhour and the average time is within an hourand a half. On all occasions, some of this timeis spent in watching the heart action and demon-strating the effect as well as in taking measure-ments, etc.

I make the large exposure, turning back aflap of the chest wall, and open the pericardiumwidely because it gives a picture of the conditionof the heart as a whole, which is not availablethrough a smaller approach to the left auricle.This approach exposes both right and leftauricles and right and left ventricles and it ismy custom, if things are going well, to get mano-metric pressure readings from the pulmonaryartery and both auricles on the operating tablebefore and after the valve has been attacked.

I am always greatly impressed with the greatrotation of the heart to the left, bringing theright ventricle entirely to the front and some-times the left ventricle does not appear at allon the anterior surface. The next feature is thetremendous enlargement of the right auricle. Ifan approach is made through the left auricle,this is not seen, and my medical colleagues havecriticized me for comments regarding the en-largement of the right auricle. However, thereis no question about the tremendous distensionof this chamber in the patients on whom I haveoperated.With intravenous novocaine running, with

positive ventilation anwsthesia and with somenovocaine in the pericardial sac, we have beenable on practically all occasions to carry outwhat we have designed to do. While I have ex-posed many others,24 I have operated upon 37mitral valves and what I am relating now is theresult of this experience. There have been nodeaths on the operating room table. Only oneof these patients has been transfused, before,during or after the operation.With novocaine injected at the site of entering

the left ventricle, there are some extra svstoles,but there has been very little concern regardingfailing heart action during this procedure. Intwo patients, ventricular fibrillation occurred.In one the manipulation within the left ven-tricle had been too vigorous and too prolonged.In both of these, we were able by cardiac mas-sage to restore normal rhythm. One of thesepatients, on whom I operated about a vear agowas in to see me a few weeks ago, and frombeing an in-and-out-of-bed invalid, she I10W isdoing her own work. She came to see me becauseone of the wires with which we had tied thesternum together was rubbing underneath theskin and was bothering her when she was bend-ing over the washing board doing the familywashing. One firm push with the thumb bent thewire down out of its prominent position and thepatient returned to her washing.The remainder of the work comes dowin to a

matter of gadgets. The instruments of severaloperators are beautiful specimens. Still, whatI use, with no special preference, is my ownhome made variety with which I am able toaccomplish this work fairly satisfactorily.

It consists of a cannula with a valve, muchas in a cytoscope, through which the instru-ment can be passed. Either a scissors or a punchcaii )e used to take out portions of the valve.

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A cardioscope25 has been devised with whichone can see something of what goes on inside.In most of the patients I have, with the scissors,divided the valves to produce the commissur-otomy effect. The results of this are excellentin some, as shown by the pressures in the leftauricle, right auricle and pulmonary arterybefore and after division of the valves.My best results have been in a small group

in whom I have removed a large portion of therough, scarred, stenosed valve and replacedthis with a new valve. Originally I thought thatthe more of this valve that could be removed,the better, but as Cutler6 showed, this producesregurgitation. It seemed that this rigid scarredvalve would be better removed and replacedby more flexible material, which would providethe ideal result, and such has been the case inthe small group in which it has been used. Ithas not been applied in all cases because of thegreatly enlarged hearts, and the more operat-ing required. Therefore, I thought it justifiableto do the lesser procedure in most, to observethe results and to have a fair proportion ofsurvivals.

If, however, a portion of the valve has beenresected or punched out, then I think it is a

necessity to put in a new valve. This has beenaccomplished by using material which isflexible, strong, will not produce clotting or

thrombosis, will not wear out and will live andget its nourishment from the blood stream. Forthese requirements, a sufficient length ofcephalic vein has been removed, turned insideout, and through the lumen has been passed a

tendon of palmaris longus. This has beensuspended between the front and back wallsof the heart in such a way that on systole itblows into the defect produced in the mitralvalve. It is placed sufficiently on the ventricularside that it floats freely out of the opening anddoes not prevent ventricular filling on dia-stole.24 One such valve, working in an animal'sheart for seven years, appears to be in goodcondition, and has worn well without signs ofdegeneration or deterioration. While I haveoperated on 37 valves, I have explored eightothers in whom there was massive thrombusin the left auricle on which nothing was done.Then there was another group of about twentyin whom an anaesthetic was given and under a

period of observation we were not satisfied withthe general condition of the patient. Thecyanosis did not improve with oxygen. The

blood pressure went down to sixty or seventyand did not return, or the neck veins became

more distended and tense, and the heart rate

accelerated, then we discontinued the ainees-thetic and nothing further was done.

RESULTS OF SURGICAL TREATMENT

Of 37 valves operated upon, the hospitalmortality rate has been about 20%. The firstpatient operated upon, now going in his sixthyear with a resected valve replaced by a niew

valve, is doing well and is fairly energetic.Fifty-five per cent of all operated upoIn havewhat might be termed fairly good results, withability to return to some sort of work. One maii,

for example, who was a semi-bed invalid, hasnow returned as a brakeman on a train and hasbeen at this job for about a year and a half. Hehas no failure, is losing no time and his condi-tion is excellent throughout. Several of thewomen are doing their own housework aiid are

very happy with their improved health.Another 25% are improved and go back towork and do fairly well for a time, but withina period of from four to six months, imally haverelapsed into failure and many of these havedied. The remaining 20%, have survived opera-

tion but within a matter of a few hours or a

few days, have increasing difficulty ancd havenot survived. In this group have been thosewith massive auricular thrombi and some havebeen shown to have irreversible changes in thepulmonary tree.While there is great enthusiasm at present

over the future of surgical treatment for thisdisease, I think this must be tempered with greatcaution. I am sure some patients are much im-proved, still the difficulty seems to be in theproper selection of the right cases. The situationis much the same as it was in respect to con-

genital heart disease26 when, with the advent ofsurgery, it became necessary for the physicianto separate and distinguish the various types ofthe disease so that those suitable for surgery

might be selected. The problem is similar inmitral disease and if the proper patients can

be selected, then surgical treatment offers themconsiderable improvement, for the present atleast. One does not know how long these resultswill last, nor whether the disease will reactivateand heal up the incisions made in valves, or

what the end result may be. My own efforts havebeen slowed down somewhat and the problemapproached more cautiously because of the pos-

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312 BINGHAM: PEPTIC ULCER Canadt. M. A.JOct191, ol.66

sibilitv of some day having a niethod of directapproach to these valves which would eliminatethese indirect methods. If such should be thecase, then these methods will become obsoleteover night.

REFERENCES1. BRUNTON, SIR L.: La4wet, 1: 352, 1902.2. CUSHING, H. AND BRANCH, J. R. B.: J. Med. Res., 12:

471, 1907-1908.3. BERNHEIM, B. M.: Bull. Johns Hopkims Hoa8p., 20: 107,

1909.4. SCHEPPELMANN, E.: Arch. f. Klin. Chir. Berl., 97: 739,

1912.5. ALLEN D. S. AND GRAHAM, E. S.: J. A. M. A., 79:1029, 1922.6. CUTLER, E., LEVINE, S. A,ND BECK, C.: Ai-ch. Surg., 9:

689, 1924.7. SOUTTAR, P. W.: Brit. M. J., 2: 603, 1925.8. SMITHY H. G.: Annual Assembly of the Southeastern

Surgfcal Congress, April 5 to 8, Hollywood, Fla.,1948.

9. BAILEY, C. P., GLOVER, R. P. AND O'NEILL, T. J. E.:J. Thoracsc Surg., 19: 16, 1950.

10. HARKEN, D. E.: J. Thoracic Surg., 11: 656, 1942.11. BLALOCK, A. AND TAUSSIG, H. B.: J. A. M. A., 128: 189,

1945.12. POTTS, W. J., SMITH, S. AND GIBSON, S.: J. A. M. A.,

132: 627, 1946.13. MURRAY, G., WILKINSON, F. R. AND MACKENZIE, R.:

Catnad. M. A. J., 38: 317, 1938.14. MURRAY, G.: Brit. J. Surg., 27: January, 1940.15. Idem: Surg. Gynec. & Obst., 77: 157, 1943.16. WELCH, K. J., JOHNSON, J. AND ZINSSER, H.: Annt.

Surg., 132: December, 1950.17. LARRABEE, W., PARKER, R. EDWARDS, J.: Proc. Staff

Meet. Mayo Clim, 24: 316, 1949.18. PARKER, F. AND WEISS, S.: Am. J. Path., 12: 573, 1936.19. BLALOCK, A. AND PARK, E. A.: Ann. Surg., 119: 445,

1944.20. BAILEY, C. P.: Dis. of Chest, 15: 377, 1949.

21. SWEET, R. H. AND BLAND, E. F.: Ann. Surg., 130: 384,1949.

22. RAPPAPORT, A. M. AND ScoTT, A. C.: Ann. Surg., 131:449, 1950.

23. BROCK, H. C.: Brit. M. J., 1: 1121, 1948.24. MURRAY, G.: Arch. Surg., 61: 903, 1950.25. Idem: Angiology, 1: August, 1950.26. Idem: Brit. M. J., 2: 905, 1947.

RMSUME1La plupart des malades souffrant de stenose mitrale

s 'accomodent mieux actuellement du traitement m6dicalde cette affection. La chirurgie n 'est indiquee que sil'on peut etre raisonnablement suar: a) de prolonger lavie du malade, b) de diminuer son degre d'impotence,c) de pr6venir les complications de la maladie.L 'auteur dit ne devoir operer que les malades ches

lesquels les signes de stenose mitrale sont nettementetablie et les autres valves en bon etat. En outre le coeurne doit pas etre le siege d 'une infection en activite ou derhumatisme articulaire. Tous ses malades, d 'ailleurs,avaient d6ja ete traites medicalement et montraient de1 'insuffisance cardiaque a certains degr6s.

Avant d 'op6rer, deux precautions sont indispensables,a savoir s 'assurer qu 'il n'existe pas de thrombose mas-sive dans 1 'oreillette gauche, ni de signes de change-ments vasculaires permanents dans la circulation pul-monaire, qui se traduisent ordinairement par une hyper-tension pulmonaire.

Apres s '8tre etendu sur la technique operatoire,1 'auteur discute sur les resultats obtenus: 20% demortalit6 op6ratoire, 55% d 'assez bons resultats avecreprise d'une activite a peu pres normale, et 25% dontles bons r6sultats ne se maintiennent que pour un certaintemps. En somme, il importe avant toute operation de cegenre de pratiquer une selection rigoureuse des cas quiconviennent.

THE TREATMENT OF PEPTIC ULCERIN GENERAL PRACTICE*

John Bingham, M.D., F.R.C.P.[C.]Toronto, Ont.

APPROXIMATELY 5 to 10% of the peopleof this country will develop a peptic ulcer

during a lifetime.' Thus the diagnosis and treat-ment of this disease is of major importance tothe practising physician.

This paper is devoted to the handling of theuncomplicated ulcer as it is met in the every-day practice of medicine. This includes bothtreatment of the acute attack and the preventionof recurrences. Reference will be made only tothose coimiplications which are treated medicallyor where the decision must be made betweenmedical and surgical treatment.The nmanagement of the uncomplicated gastric

and duodenal ulcer consists of: first, the treat-ment .of the acute attack, and second the pre-vention of a recurrence of the ulcer.

* From the Departments of Medicine of the Universityof Toronto and the Toronto Western Hospital, Toronto.

Read before the combined sections of Preventive Medi-cine and Hygiene, Industrial Medicine, and GeneralPractice of the Academy of Medicine of Toronto, Janu-ary 18, 1951.

TREATMENT OF THE ACUTE ATTACKIn managing the acute attack, rest, diet and

the reduction of gastric acidity form the fraine-work of treatment.

]BED REST

The length of bed rest will depend onthree factors: (1) the severity and durationof the symptoms, (2) the patient's economicstatus, and (3) his mental attitude. Normally,bed rest is enforced until the patient is com-pletely free of symptoms. Then follows a con-valescent period of a week or two. Sedativesshould be used freely to assist in the promo-tion of rest. Where economic or other factorsmake absolute confinement in bed impossible,one may be forced to follow an ambulatoryregimen. Only patients with the mildest symp-toms should be treated in this way.

.DIET

During the acute phase the diet shouldconsist of hourly feedings of a three ouncemixture of equal parts of milk and cream. Onthis regimen, most patients with uncomplicatedulcer will lose their symptoms within a fewdays. When the acute symptoms have subsided,three bland meals, chosen from the food listed