March 1954 PARSONS and WATKINSON: The Treatment of Pyloric Stenosis

proximal to the pylorus, he should later carry outa further operation for the removal of the pylorusand the residual portion of the antrum. The Bill-roth I method of anastomosis between the stumpof the stomach and duodenum also appears to beinadvisable. This technique is excellent forgastric lesions, but appears to carry an increasedrisk of stomal ulcer if it is used for duodenal cases,even though the ulcer has been completely re-moved. The addition of an enteroanastomosisbetween the jejunal loops at the stoma is as unwisein partial gastrectomy as it is with gastro-entero-stomy. It should never be necessary. Althoughthe bulk of the acid-secreting mucosa may havebeen removed, it is asking too much of the resis-tance of the jejunum to divert the alkaline juicesbeyond the stoma altogether.The basic problem remains with us. We

understand very little of the essential defencemechanism of the mucosa against erosion. Weknow that acid peptic activity is the essentialfactor in the eroding force and that the operationof partial gastrectomy properly performed will,by reducing the scale of the attack, prevent theformation of new ulceration in most cases. Thisoperation, with or without modifications, entailsdisabilities which in the present state of ourknowledge we must accept as a necessary andworthwhile sacrifice to secure freedom from furtherulceration. The disquieting reflection, however,is that this sacrifice is really necessary in only athird of the patients, but that all are called uponto make it, because there is yet no practicable pre-operative means of selection of cases into thoseprone to anastomotic ulcer and those not soprone.

THE TREATMENT OF PYLORIC STENOSISIN PEPTIC ULCERATIONS

By F. M. PARSONS, B.Sc., M.B., Ch.B (Leeds)*Research Fellow iu Urology in the University of Leeds

and G. WATKINSON, M.D., M.R.C.P.Lecturer in Medicine in the University of Leeds

A combination of spasm, oedema and cicatricaldeformity in relation to an ulcer near the pyloricring produces a temporary or permanent re-tention of gastric contents accompanied by theclinical syndrome of loss of weight, vomiting anddehydration known as pyloric stenosis. The fre-quent failure of antispasmodic drugs to relieve thecondition is in part due to inadequate therapy butis also due to the presence of oedema and scarring.Physiological Effects

Obstruction at the pyloric ring leads to in-creasing retention of gastric contents, gastritis anddilatation of the stomach which eventually leads tovomiting. The reduction in absorption of foodcauses starvation but it is the extrarenal loss ofwater, chloride, sodium and potassium, secretedby the gastric mucosa and then vomited, which is

*Aided by grants from the University of Leeds; theYorkshire Council of the British Empire Cancer Cam-paign; the Board of Governors, United Leeds Hospitals;and the Leeds Regional Hospital Board.

more serious and lethal. As a result of thegastritis there is an increased excretion of gastricmucus which has a high concentration of sodium.This loss of sodium, which leads to a total bodydeficit, largely determines the extent of the de-hydration present. The chloride loss, from thegastric juice, is still, however, in excess of that ofthe sodium (at least 50 per cent., Gamble, 1950) sothat an alkalosis results which may be severeenough to cause latent or manifest tetany (Fig. i).Whether this tetany is due to a decrease in ioniz-able calcium in the extracellular fluid or to othercauses has not been clarified. Of equal, if notmore, importance is the development of severerenal impairment which occurs in alkalosis.Nazzari (1904) observed calcareous infiltration inthe renal tubules in two patients who died as aresult of pyloric obstruction. Brown, Eusterman,Hartman and Rowntree (1923) observed at autopsycalcification in the proximal tubules in fourpatients who died with pyloric stenosis. Theytied the pylorus of cats and within 48 hours of

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i

:. " ::'::'..iii;;::i:i···iP···iii;:::L·:··

FIG. i.-Latent tetany in a patient with pyloric stenosis.(Upper) before and (lower) after occlusion of theblood supply.

operation observed degeneration and calcificationof the tubules. These findings were confirmed byPyrah (I949) and similar results have been obtainedin the dog (Pyrah and Bonser), calcification oc-curring in the cells of the renal cortex and in thelumina of the proximal tubules. Cooke (I933)reported six cases of pyloric stenosis and atautopsy renal calcification, restricted mainly to thecortical area, was found in each case. Pyrah(1949) reported three similar cases and in additionobserved calcareous debris in the lumina-of thetubules. Fig. 2 is an example of this type of renalcalcification. This renal calcification and tubulardegeneration results in severe renal impairmentwhich is frequently intensified by the pre-renalfactors of dehydration and hypochloraemia. Theurine in early cases is alkaline but when sodiumand potassium deficiencies develop it becomes acid(Kennedy, Winkley and Dunning, I949).Clinical Assessment of the PatientThe history associated with benign pyloric ob-

struction is usually long; a preceding ulcerdyspepsia has often been present for many yearsbut the commencement of vomiting is usuallyfairly recent. The volume and frequency of vomit-ing, in conjunction with the quantity of fluid

Jj':?,."'~......i;'~·.. ..i"~'~,~''~..._-i.~ ~,."~,:'~:"iji:i::~i" ','~"i'-~i"~~?

~:j*i .1

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ii:i ~':;xe!-,i'i· "i·

.......e.-:--,;!:';'lii:i'~:':' ~'~:'~d' :·i.:·'Fi

n:;;i::::··:'I';~;Jt.J?c · :.. . . .........81:ii)iC,'ii:''·''"......

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'~-~ ?'.:i,.

~ir'~i"-"i'"Z"~'"'~~d" " ""~:::¥''ii],~,%".""

FIG. 2.-Microphotograph of kidney showing calcareousdeposits, from a patient who died with pyloricstenosis.

drunk, is often a useful guide to the severity of thecondition as is the degree of weight lost, if known.Symptoms of weakness, drowsiness, musclecramps and tetany are suggestive of severe bio-chemical abnormalities. In eight of our recentcases one half have had mental confusion as aprominent feature-indeed one was referredinitially to a neurologist and a second to a psy-chiatrist.

Clinical examination usually reveals localevidence of gastric dilatation in the form of asuccussion splash but visible peristalsis is morerarely observed. The remainder of the clinicalsigns are secondary to the obstruction. Besidesevidence of loss of weight, dehydration is almostinvariably present in the severe case, the skin beingdry and inelastic and the tongue dry, wrinkled andcoated. Difficulty in articulation may be duemore to the severe dehydration than to nervousdysfunction developing as a result of biochemicalimbalance. In severe cases we have observed deeppitting ' oedema' (Fig. 3) even in the presence ofmanifest clinical evidence of severe dehydration.

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March 1954 PARSONS and WATKINSON: The Treatment-of Pyloric Stenosis49

··:·:·

:::::·:C$·..C..t.B%E.-.i.:: ·i ii::'':::

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I::.'?? ·'$.·.I-r .3..(. .ki....··S.Eb.j.BI.%.t...j.SXaa: ..,

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FIG. 3.-' Finger-printing' of the abdominal wall ina severe case of pyloric stenosis (obtained bypressing the tips of left fingers and thumb into theabdominal wall for 15 secs.).

Whether this is due to intracellular or hydrostaticchanges, avitaminosis or other causes has not beenascertained but it has been observed in many othercases exhibiting dehydration and low osmoticpressures of the extracellular fluid. Many of thesymptoms of biochemical imbalance, for exampleanorexia and vomiting, are masked by the primarypathology of pyloric obstruction.

Serious cases of pyloric stenosis can only satis-factorily be treated where full laboratory facilitiesare available. It is advisable to estimate the plasmalevels of chloride, sodium, potassium, carbon di-oxide combining power, urea and proteins to makean accurate assessment of the state of the internalenvironment. Additional information of the bodypotassium may be obtained by electrocardiographyfor normal serum levels have been reported inthe presence of frank deficiency (Hawkins, Hardyand Sampson, I95I). The severity of the de-hydration is best estimated clinically for no reliablechemical test suitable for routine investigation isavailable; certainly the plasma protein and haema-tocrit levels are unreliable as these values are so

often subnormal in pyloric stenosis reflecting onlythe malnutrition of the patient. A high bloodurea level may be indicative of dehydration butmay also be partly due to irreversible renal damage(Fig. 2).

Examination of the urine is essential. The 24hour volume, its specific gravity, chloride contentand pH are valuable estimations as a guide totherapy. In the more severe forms of pyloricstenosis a small volume of acid urine with a lowchloride content is found frequently. A progresschart of the patient's intake of water, electrolytesand food should be kept together with one of theurine volume and fluid loss from vomiting andgastric aspiration, making full allowance for theinsensible loss of approximately i 1./24,hours oc-curring from the lungs and skin.

Principles of TreatmentTreatment should be planned along the follow-

ing lines:I. To correct the fluid depletion and the electro-

lyte abnormalities which have developed.2. To empty the stomach daily thereby pre-

venting overdistension and also to reduce thedegree of gastritis present. This will allow themuscle tone of the stomach to improve and mayreduce spasm and oedema at the pyloric ring. Itmust be realized, however, that gastric aspirationremoves vital inorganic chemicals from the body(particularly chloride) and these must be replacedby routes other than oral.

3. Whilst the electrolyte correction is proceed-ing, antispasmodic drugs and medical treatmentmay be given in the hope that spasm in relation tothe ulcer will be overcome and a temporary ob-struction relieved.

4. If medical treatment is not successful,surgical relief of the obstruction must be under-taken after the patient has been suitably prepared.If, on the other hand, the obstruction is relievedduring medical therapy, the nutritional stateshould be improved and then the advisability ofelective surgery can carefully be considered.

Management of the Early CaseOn admission, the diagnosis should be confirmed

by the demonstration of an excess of gastric con-tents by passing an oesophageal tube and emptyingthe stomach with a Senoran's evacuator. Thisprocedure is more effective and less laborious thanthe use of a Ryle's tube and syringe and isfacilitated by local anaesthesia of the throat with2 per cent. anethaine. Fluid must be given, byroutes other than oral, to correct the dehydrationresulting from vomiting or gastric aspiration andloss from the skin, lungs and kidneys. Care mustbe exercised to avoid administering fluid in excess

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150 POSTGRADUATE MEDICAL JOURNAL March I954

of requirements as temporary renal impairmentmay cause water retention and oedema, a con-dition induced in one of our cases but, fortunately,renal function recovered rapidly and no harmresulted.

Correction of the electrolyte abnormalitiesshould be done as quickly as possible using theintravenous route. A chloride deficit may be cor-rected by administering normal physiologicalsaline; the clinical rule suggested by Bartlett,Bingham and Pederson (1938) is helpful in thisrespect. For each ioo mg. per cent. (I7 mEq./l.)that the plasma chlorides need to be raised to reachthe normal (585 mg. per cent. as NaCI or ioomEq./l.) the patient should be given 0.5 g. (8.5mEq.) of NaCl per kg. of body weight. (In pyloricstenosis unlike most other types of biochemicalimbalance, the plasma chloride level is of morevalue than that of the sodium in assessing thequantity of salt required to correct the abnor-malities.)

Sodium deficiency is usually more rapidly cor-rected than chloride deficiency, following theadministration of saline. Hypokalaemia is bestcorrected by intravenous administration of potas-sium chloride and in addition the daily basalrequirement of potassium (6 g. of potassiumchloride) should be given provided that theurinary output is adequate to deal with any excessthat might be administered.

Milk feeds (5 oz. two-hourly) may be startedafter two days but often a milk drip is of morevalue in controlling pain and improving thenutrition of the patient. The routine addition ofsodium citrate to milk is to be deprecated as theadditional base supplied tends to increase thedegree of alkalosis present. Soluble antacidsshould not be used as they might increase thealkalosis but full doses of tincture of belladonna,if necessary up to the limit of tolerance, should begiven if any degree of spasm is suspected. Dailyvitamin supplementation is administered parenter-ally as ascorbic acid 500 mg., nicotinamide 50 mg.and riboflavine 25 mg. Blood transfusion is fre-quently required to raise the haemoglobin level tonormal values.

Satisfactory progress is indicated by a pro-gressive reduction of the volume of fasting juiceaspirated from the stomach and a small propor-tion of patients are able to take a convalescentulcer diet after one to two weeks. Fortified milkfeeds containing milk, lactose, dried milk and'Trufood' provide a high protein diet to improvethe nutrition prior to operation. In the remaindersome degree of gastric retention persists and opera-tive relief of the condition is required either bygastrectomy or gastro-enterostomy.The importance of replacing the chloride and

water aspirated from the stomach by routes otherthan oral is illustrated by the following case:

Case x

A female, aged 49, was admitted with pyloric stenosis.The blood chemistry was: Plasma protein, 7.4 g. percent.; chloride, 65 mEq./l.; Co2 combining power,39.2 mEq./l.; sodium, 130 mEq./l.; potassium, 3.3mEq./l.; and blood urea nitrogen, 25 mg. per cent.

She was given an intragastric milk drip and in theevening her stomach was washed out. The chemistryof the stomach washout was as follows:

Blood .. .. .. NilBile .. .. .. .. Nil

NAcidity .. .. .. 15 ml. free acid

10N

80 ml.- total acidIo

Starch .. .. .. NilN

Total chloride .. 73 ml. - percent.I0,

The chloride figure shows that -each litre of stomachwashout contains as much chloride, as approximately730 ml. of normal plasma. However,, as. this patient'sblood chloride was only 65 mEq./l.,, one litre of stomachwashout would have contained as much chloride as1,120 ml. of plasma.

Management of the Severe CaseIn this group severe dehydration, alkalosis and

hypochloraemia are present, the chloride depletionbeing grossly in excess of that, of the sodium.. Toa certain extent this excessive loss of chlorideover and above sodium can be made good bygiving normal saline which has a sodium: chlorideratio of i: I, whilst that of normal plasma is 1.4: I.However, it has long been recognized that salinealone will not always correct a hypochloraemicalkalosis in severe pyloric stenosis (Deeds, 1938Jones, I939) and some form of chloride therapy,without fixed base, is often indicated. This isof paramount importance in severe cases, for anybase given in excess of requirements will have tobe eliminated by the kidney, already under strainand frequently showing evidence of permanentdamage.

Previous experience by one of us in the manage-ment of ureteric transplants led us to believe thata solution whose ionic concentration was similarto urine might be suitable for this purpose

Calcium chloride .. ...... o.4 g.Citric Acid .. . . . 1.15 g.Disodium hydrogen phosphate .. . 4 g.Potassium chloride .. .2 g.Magnesium sulphate (7H20) .. . I.5 g.Sodium chloride .. .. ...0.0 g.Water .. ... . I 1.

TABLE i.-The composition of Solution ' P.'

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March 1954 PARSONS and WATKINSON:- The Treatment of Pyloric Stenosis 1

Volume Chloride Sodium Potassium Urea N2Day ml. mEq./l. g. NaC1/24 hours mEq./l. g./21 hours mEq./l. g./24 hours g./24 hours--,4 --- -

4-5 1135 o.68 0.04 87 2.27 65.5 2.9 2.75-6 1335 6.5 o.5I 95.6 2.94 I7.o 0.89 6.256-7 I485 34.2 2.97 o109 3.71 6.5 o.96 8.6

TABLE 2.-The urine chemistry of Case 2 during treatment.

(Solution 'P,' Table i). It has been shown byGoldschmidt and Dayton (I919) that sulphateand phosphate enhance absorption of chloride fromthe intestine, and Parsons, Powell and Pyrah(1952) were able to show that differential absorp-tion of chloride ions occurred in the large intestine.A patient treated by rectal administration of thisfluid is described below:

Case 2A male patient, aged 56 years, had had a duodenal

ulcer for 12 years and for the greater part of this timesymptoms had been relieved by diet and medicines.Six months before his admission he developed in-frequent attacks of vomiting but later it became a dailyoccurrence, usually starting in the evening and lastinguntil 2.30 a.m. the following morning. Progressive lossof weight occurred. Examination revealed a succussionsplash with slight epigastric tenderness over the duo-denal area. He was treated initially with stomach wash-outs and milk was given by intragastric drip. Despitethis treatment he continued to vomit copiously and onthe fourth day he became, quite suddenly, very con-fused and physically violent; a few minutes later hebecame unconscious for half an hour but then becamequite normal mentally. This cycle of events recurredfour hours later.He was seen, by one of us, for the first time between

these attacks. There was clinical evidence of severe de-hydration-indeed he had become anuric during theprevious 24 hours. The blood chemistry (Fig. 4, Day 3)revealed a severe hypochloraemia, alkalosis, low valuesfor plasma sodium and potassium and a relatively highplasma protein.

In view of the persistent vomiting, the stomach waskept empty by gastric suction and oral administration offood and fluid withheld. Intravenous therapy was givenas shown in Fig. 4, and 2 1. of Solution ' P ' were givenby proctolysis. The next day he was mentally quitealert and the dehydration was less marked, 1.4 1. of fluidbeing aspirated from his stomach. The blood chemistry(Fig. 4, Day 5) showed a rise in the plasma chloride,sodium and CO2 combining power, satisfactory urinaryexcretion returning that day. The plasma potassiumlevel had fallen but this was not altogether surprising asthe amount of potassium excreted in the urine (Table 2)was nearly as high as that administered intravenously,and dilution of the extracellular fluid was occurring.During the next 24 hours the intravenous and rectaltherapy was continued (Fig. 4). The next day noclinical evidence of dehydration could be detected. Theblood chemistry (Fig. 4, Day 6) was normal except foran elevated blood urea nitrogen. Investigation of theurine (Table 2) revealed a rapid rise in the chloridelevel during therapy but the sodium excretion remainedrelatively constant. The excretion of potassium fell onthe fifth-sixth day and this coincided with a rise in theplasma level (Fig. 4). On the sixth day milk was givenby intragastric drip but again profuse vomiting occurred.

i:ii:i.:ii~ri%i:i._. ..... .... ... ....... ... ...........':::':" '"

·i...........·-;··

- v a

SQ.f

UftE

· iI

FIG. 4.-The blood chemistry and treatment of Case 2.

(The horizontal dotted lines repre3ent averagenormal values.)

Intravenous and rectal therapy was recommenced andon the seventh day after admission a laparotomy was per-formed. The duodenum and distal third of the stomachwere grossly oedematous and obstructed by an activeduodenal ulcer. A posterior gastro-enterostomy wasperformed and the patient made an uninterrupted re-covery. He was reviewed one year later and wassymptomless. His diet was unrestricted, he had gainedin weight and he was doing a full day's work. The bloodchemistry was satisfactory (Fig. 4) and the urea clearancetest was 30 per cent. of average normal.

Solution ' P' cannot be regarded as an idealfluid to correct the biochemical abnormalitiesoccurring in severe cases of pyloric stenosis, fora certain amount of sodium is absorbed by thelarge bowel. We believe that sodium should be

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administered -y the intravenous route alone(normal physiological saline (9 g. NaCl/l. or 154mEq./l.) being the solution of choice) until thereis no clinical evidence of dehydration and theplasma sodium level has returned to normal.The chloride depletion in excess of sodium canthen be corrected rectally by sodium-free solutions,the chloride level in the plasma being used toascertain when correction has occurred. Hydro-chloric acid in concentrations sufficient materiallyto affect the hypochloraemia is too irritant forproctolysis; calcium chloride (22.I g./l. or 200mEq./l.) has been used in a case of hypochloraemiafrom excessive vomiting following a nephrectomy(Parsons, 1953), but, although the chloride de-ficiency was corrected, it appeared that someabsorption of calcium occurred which would seemhighly undesirable in cases of pyloric stenosiswhen renal calcification is likely to occur. Wethen turned our attention to the use of ammoniumchloride (15 g./l. or 280 mEq./l.). Absorptionof these ions, even in hypertonic solutions, hasbeen shown to occur in the colon of the dog(Boyce and Vest. 1952). Admittedly ammoniumchloride can be given intravenously (McCann,1922; Deeds, 1938). However, in an emergency,sterile ammonium chloride may not be availableand, further, using the rectal route, hypertonicsolutions can be used without difficulty, thuskeeping the fluid administered within reasonableproportions.The following case illustrates the use of am-

monium chloride solution given by proctolysis:Case 3A male, aged 4I, proved, on admission, to be confused

and unable to give an accurate account of past events.His relatives were also unable to contribute any usefulinformation. He had a marked delay in cerebration,taking half to one minute to answer questions. Thisconfused mental state led the patient's doctor to enlistthe aid of a consultant neurologist. On examinationthere was moderate dehydration; this was in contrast toour other cases who had severe dehydration. He wasvomiting (the vomitus contained blood) and an ab-dominal succussion splash was present. There wasgeneralized muscular twitching and a positive Chvostek'sand Trousseau's sign (Fig. i). The blood pressure wasI30/70, the pulse rate 48 per min. and an E.C.G. re-vealed a 2:I heart block. The haemoglobin was 9.I g.per cent. and the R.B.C. 3.2 million/cmm.

After treatment he was able to give a 20 years' historyof duodenal ulcer with typical periods of remission ofsymptoms. He had had numerous attacks of haema-temesis and melaena and once required blood trans-fusion. Six months before admission he started to vomiteach evening. Twice during this period he had becomeunconscious for a ' short period of time ' and after thesecond attack his legs were paralyzed for a few hours.On admission the blood chemistry (Fig. 5, Day o-I)

revealed a severe hypochloraemic alkalosis, hypokalaemiaand azotaemia. For the first 36 hours of treatment 3 1.of 5 per cent. glucose were given intravenously along

%ii:idE ii:i2iiiPOT%:%~B25iiiiiii~isi!~ieiii$ODBUM ' i;i~hQt-i:l--~~i - ...~mEi~i/L*w.iQ~! -.;~iyiiil-·

ac:I. :i:·::;·:·ii i.ii:i:iiiiisi:.;i:ii.::.::,;,i: ,; ii: :iii-i.ii i.riliii"ii:i~::·i:;I i::ii i:,:i.ii

;i·i.:::ii.i;;:ii~ .-.- .::'':::i'li;'iiii:ij'4~i

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UREA:'·?f:iiif;iiisiiiii' iieiii!W8 i:ini"l!iifi~ii ri

o *iiiiiiiPjiii~,i~ ::'':i::i::iii:iri;i ...4ii~~i:(iii:·::;..:.:::;; liii;__iliiii~ :'"iiiiiir!'!iiiriiii~~iiiiii:r:i:ii :iilciiiii~ei:iitii

FIG. 5.-The blood chemistry and treatment of Case 3.

with inorganic chemical supplementation (Fig. 5). Inorder to correct the gross chloride deficit (estimated tobe about ,000o mEq.), 75 g. of ammonium chloride(1,400 mEq.) in 5 1. of water were given by rectal drip.Not all the ammonium chloride was retained owing torectal incontinence, but sufficient was absorbed almostto correct the chloride deficit. As the patient had in-continence of urine, no urinary investigations were pos-sible and it was deemed unwise to pass a self-retainingcatheter.On the second day there was no sign of latent tetany

but there was little change in the mental state. Furthertreatment was given (Fig. 5) and on the fourth day aslight hyperchloraemic acidosis was produced whilst thepotassium level had returned to normal. On this dayhe was mentally alert and was able to give an accurateaccount of past events. By this time it was consideredthat his condition had improved sufficiently to undergo agastro-enterostomy as an emergency procedure butideally a partial gastrectomy seemed more desirable,particularly in view of the history of haemorrhage. Forthis reason a period of medical treatment was given inthe hope that spasm or oedema at the pylorus would sub-side. This resulted in further vomiting with dehydra-tion, hypochloraemia and hypokalaemia and clinical de-terioration. After these abnormalities and the lowhaemoglobin level had been corrected by intravenoustherapy, a gastro-enterostomy was performed as anemergency procedure. At laparotomy there was a severecicatrical deformity of the pyloric ring but there was nooedema or evidence of spasm.Three months later the patient was well and had no

symptoms. The blood chemistry was normal except fora blood urea nitrogen of 44 mgm. per cent. The urea

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March 1954 PARSONS and WATKINSON: The Treatment of Pyloric Stenosis53

clearance test was 35 per cent. of average normal, butno abnormalities were found on routine urinalysis. Asthere was no hypertension or history of renal disease andthe retinae were normal it was presumed that the renalimpairment was a direct result of the pyloric stenosisand the accompanying alkalosis.

Five months after operation he developed melaenafrom an anastomotic ulcer and a partial gastrectomy wasperformed from which he made a satisfactory recovery.ConclusionsThe treatment of pyloric stenosis must of

necessity bring physician, surgeon and biochemisttogether. It is imperative that the biochemicalabnormalities should be treated first and as quicklyas possible. This will prevent further deteriora-tion in renal function by correcting the conditionslikely to cause renal calcification and tubulardegeneration. There are theoretical objections totreating, with saline alone, the sodium andchloride deficiencies which occur in the severecase. Firstly, the excess sodium that will beadministered to correct the chloride depletionmay result in the formation of an alkaline urine,which in turn may increase the chances of furtherdeposition of calcium salts in the kidney. Secondly,if severe renal impairment is already present, theexcretion of any sodium given in excess of require-ments may be impaired, with subsequent hyper-natraemia and delay in the correction of the alka-lotic state. We believe that in all severe casesadministration of chloride should always exceedthat of sodium, a mixture of ammonium andsodium chlorides being eminently satisfactory.

In pyloric stenosis, potassium deficiency iscommon and is not confined to the extracellularfluid alone, for Mudge and Vislocky (I949)demonstrated an intracellular deficiency. Inaddition, excessive excretion of potassium mayoccur (see Case 2 above) during therapy. Potas-sium therapy must therefore be adequate to coverthe daily excretion and the total body deficit.

Correction of the specific abnormalities presentin the internal environment leads to a rapidimprovement in the clinical state. It is at thispoint that the definitive treatment of the obstruc-tion begins. Many of these patients are unsuitablefor major surgical procedures because of the severestate of malnutrition. Ideally, a period of medicaltreatment should always be tried. If this is

successful the question of surgery can be delayeduntil the nutritional state has been improved. Ifthere is no apparent relief of the obstruction,surgery should not be withheld too long in thehope that spasm or oedema of the pyloric ringwill subside, for the return of the biochemicalabnormalities may be accompanied by a markedclinical deterioration. In our own small series ofeight cases, seven required surgery after correctionof the biochemical abnormalities, whilst the eighthresponded to medical treatment, but he refusedoperation later.

AcknowledgementsOur thanks are due to Mr. D. B. Feather,

Dr. H. G. Garland, Mr. A. J. C. Latchmore,Dr. A. Leese, Mr. H. S. Shucksmith and Prof.R. E. Tunbridge for permission to publish thesecases; to Mr. F. J. N. Powell for the biochemicaldata on Case I and to Mr. J. Hainsworth andMiss C. E. Campbell, of the Department ofMedical Photography, St. James' Hospital, Leeds,for the figures.

Fig. 5 is reproduced by kind permission of theeditor, Recenti Progressi in Medicina.

Fig. 2 was kindly lent by Mr. L. N. Pyrah andDr. G. M. Bonser.

BIBLIOGRAPHYBARTLETT, R. M., BINGHAM, D. L. C., and PEDERSON, S.

(1938), Surgery, 4, 614.BOYCE, W. H., and VEST, S. A. (1952), J. Urol., 67, 169.BROWN, G. E., EUSTERMAN, G. B., HARTMAN, H. R., and

ROWNTREE, L. G. (I923), Arch. Int. Med., 32, 425.COOKE, A. M. (x933), Quart. J. Med. N.S., 2, 539.DEEDS, C. D. (I938), Proc. Mayo Clin., 13, 456.GAMBLE, J. L. (I950), 'Extracellular Fluid,' Harvard Univ.

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