743 Postgrad Med J: first published as 10.1136/pgmj.36.422.743 on 1 December 1960. Downloaded from

PYLORIC IN ADULTS C. T. HOWE, B.M., B.CH. Research Assistant, Department of Surgical Studies M. P. SPENCE, M.B., B.CHIR., M.R.C.P. Senior Medical Registrar Middlesex Hospital, London, W. i

Pyloric stenosis is defined as an obstruction to narrowing of the , but in almost all cases gastric emptying due to any cause situated above of pyloric stenosis distortion by inflammatory .he biliary ampulla. This article is concerned oedema is the precipitating cause of obstruction. with the clinical features, , This is why pre-operative preparation commonly assessment and treatment of patients with pyloric results in relief of both pain and gastric retention. stenosis; anatomical narrowing of the pyloric It is exceptional to find a healed ulcer in a patient canal without delay in gastric emptying is not with unrelieved pyloric stenosis. considered. In adults, symptoms due to the is the cardinal symptom and is rarely underlying lesion may precede by weeks, months absent. Usually it is preceded by a long history of Protected by copyright. or years those due to obstruction and contribute recurrent dyspepsia and is sometimes episodic, the to the clinical picture to a varying degree. Pyloric episodes coinciding with active phases of the ulcer. stenosis is unique among gastro-intestinal dis- In half the patients the vomit is copious, usually orders which produce electrolyte disturbances in free from and may contain undigested (and the constancy with which it causes extracellular recognizable) food taken many hours before. alkalosis and it is this aspect of the condition that Typically the vomiting occurs in the late hours of has received most attention in recent years. the evening or in the early hours of the morning. Anorexia and weight loss are the rule. Diarrhoea Clinical Features occurs more frequently (20% of cases) than might Benign peptic ulceration is the commonest be expected in an obstructive lesion of the upper cause of pyloric stenosis and was responsible for alimentary tract. Offensive eructation is a diag- 86% of 18 cases reviewed by Balint and Spence.' nostically helpful symptom when it occurs. In 80% the ulcer was situated at or near the In approximately half the patients in whom pylorus, but in 6% there was a remote gastric pyloric stenosis is diagnosed there are no abnormal http://pmj.bmj.com/ ulcer with surrounding inflammatory and fibrous physical signs. A gastric succussion splash, only tissue which shortened the lesser curve and significant if at least three hours have elapsed extended to envelop the pylorus. Carcinoma of since the last meal, is the commonest abnormal the pyloric region accounted for 11% of the cases finding. Visible waves of gastric cours- in this series. Uncommon causes are ing across the abdomen from left to right are of with involvement of the pylorus in adjacent in- great diagnostic value, and occasionally it is flammatory tissue and carcinoma of the pancreas possible to see the outline of a distended

grossly on September 29, 2021 by guest. or . Rarely patients present in adult . Signs of fluid depletion or latent tetany life with congenital conditions such as hyper- may be found. Gastric aspiration is the most trophic pyloric stenosis, duodenal diaphragmatic valuable single diagnostic procedure. The normal occlusion or compression of the pylorus by stomach is empty three to four hours after a meal, cholecysto-jejunal bands. but this time may be prolonged by such factors Earlier surgical treatment has reduced the as emotion, a fatty meal, or an attack of migraine. number of peptic ulcers that progress to pyloric Nevertheless, the repeated presence of a large stenosis. It has been estimated to arise in about gastric residue, i.e. more than 250 ml. in patients 3% of patients with duodenal ulcers (including on a normal hospital diet, four or more hours pyloric and pre-pyloric ulcers), and in I% of after the last meal, is an almost certain indication those with lesser curve ulcers. of pyloric stenosis. Benign duodenal ulceration causes cicatricial Barium-meal examination usually reveals pyloric G1 4 POSTGRADUATE MEDICAL JOURNAL December 1960 Postgrad Med J: first published as 10.1136/pgmj.36.422.743 on 1 December 1960. Downloaded from

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FIG. i.-Radiograph of the abdomen of a patient with FIG. 2.-Further radiograph of the same patient after pyloric stenosis one week after a barium meal. repeated gastric lavage. The stomach is smaller The whole lower abdomen is filled by a grossly but is still outlined by retained barium. distended stomach still containing a large barium residue. and vomiting in a patient with peptic ulceration may be attributed to food poisoning and this stenosis when it is present and is of additional may lead to omission of further investigation. value in determining the underlying lesion. Pre- The combination of body fluid depletion, vomiting liminary fluoroscopy may show a dilated stomach and a raised blood urea may suggest chronic and it is wise to empty this by aspiration before renal disease, but the high specific gravity of giving barium, otherwise it may be impossible to the urine and the increased plasma bicarbonate demonstrate the cause of the stenosis. Obstruc- level in pyloric stenosis make distinction easy. tion may be intermittent in the early stages and Rarely in the severely alkalotic patient the abdo- http://pmj.bmj.com/ cannot be excluded by the demonstration of minal symptoms may be concealed by mental normal emptying at one examination. A word of confusion or even coma.22 For this Hurst13 used caution is necessary about barium-meal examina- the term 'coma dyspepticum', attributing it to tion in suspected cases. In severe pyloric obstruc- Von Sakset. tion, barium, like food residues, may remain in The pre-operative diagnosis of the underlying the stomach for many days, presenting a major lesion in a patient with pyloric stenosis is not of obstacle to the and treatment but a short

proper preparation paramount importance, clinically on September 29, 2021 by guest. of the patient (Figs. i and 2). history of dyspeptic symptoms before the onset Usually the diagnosis of pyloric stenosis is of stenosis is suspicious of carcinoma. A mass is easy, but it may remain unsuspected if the rarely palpable in the abdomen nor is it certain vomiting is mistakenly ascribed to uncomplicated evidence of malignancy. Even radiology may be peptic ulceration. The vomitus may resemble inconclusive. that of exsanguinating haematemesis and diagnosis may be extremely difficult particularly as the Metabolic Changes conditions may co-exist. Significant blood loss Many patients with pyloric stenosis suffer from even in the presence of pyloric obstruction is the effects of loss of electrolytes and water pre- usually accompanied by melaena. If abdominal senting in its most severe form as gastric tetany. pain is severe its association with vomiting may This was first described in I886 by Kussmaul mimic an acute surgical emergency. Diarrheoa and in the early part of this century the disorder December I960 HOWE and SPENCE: Pyloric Stencsis in Adults 745 Postgrad Med J: first published as 10.1136/pgmj.36.422.743 on 1 December 1960. Downloaded from

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'.· .K, NE URINACIN ALKALINE ICI DECREASED E~.'' " HCO,INCREASED FIG. 3.-Typical changes in the extracellular electro- lytes in a patient with pyloric stenosis. (From Le Quesne.'5) FIG. 4.-The intracellular-extracellular ionic shifts and their effects in potassium depletion. (From was attributed to the secretion of toxins by the Le Quesne.15) pylorus or obstructed stomach. McCallum and and the plasma is more alkaline, i.e. a state of others in I92016 demonstrated that the blood was hypochloraemic alkalosis (Fig. 3). abnormally alkaline with an associated increase in Protected by copyright. neuromuscular excitability, and attributed these The kidney normally excretes an acid urine, changes to loss of acid and chlorides in the vomit. but as a result of the extracellular alkalosis in Gamble and Ross"' demonstrated, in dog experi- pyloric stenosis the urine formed is alkaline in ments, that an accompanying loss of sodium ions reaction. The sustained excretion of an alkaline caused the . They showed that water urine represents a considerable departure from or ammonium chloride solutions were ineffective normal, entailing the loss of large quantities of therapy but that saline was curative. Subsequent sodium or potassium in place of hydrogen ion, workers 4,6, 14, 17, 19 have demonstrated marked de- thus conserving the latter and limiting the degree pletion of potassium in gastric alkalosis. of extracellular alkalosis. By this increased urinary The metabolic disturbance of pyloric stenosis excretion of sodium and potassium the kidneys is caused by the loss of large amounts of acid convert a gastric loss of into a gastric contents, probably as much as four litres total body loss of sodium and potassium chloride. per day in the worst cases. The magnitude of In the early stages of pyloric stenosis the gastric the losses of the and urinary losses of sodium lead to considerable important electrolytes can be depletion. Gamble and Ross1 have described http://pmj.bmj.com/ seen from their mean concentrations in the gastric sodium as the skeleton of the extracellular fluid aspirate (Table I). The net effects of these losses and its depletion is accompanied by a propor- tionate loss of water thus reducing the extracellular TABLE I volume. This process is limited by marked ELECTROLYTE CONCENTRATIONS IN THE GASTRIC CONTENT reduction in the sodium content of the urine, OF PATIENTS WITH PYLORIC STENOSIS, AT THE TIME OF ADMISSION TO HOSPITAL but potassium excretion continues undiminished a level. It is the loss despite falling plasma by on September 29, 2021 by guest. Benign this route which is largely responsible for potas- Ulceration Carcinoma sium depletion.21 Sodium ..· ·· 50 55 It has long been known that the urine may Potassium ...... 11 II become acid in the late stages of extracellular Chloride ...... I I7.5 5I alkalosis.7, 13 This change in urinary reaction is 'Acid ' (by subtraction) .. 56.5 connected with internal rearrangements of the (All values as mEq./litre.) electrolytes between the intracellular and extra- cellular fluids due to potassium depletion.8s, 9, 20 are characteristic; the extracellular fluid and cir- Potassium is the principal cation of the intra- culating blood volumes are reduced, the plasma cellular fluid and, when it is lost from the body, chloride concentration is lowered with a corre- sodium and hydrogen ions from the extracellular sponding increase in the plasma bicarbonate level fluid enter the cells to replace it (Fig. 4). This 746 POSTGRADUATE MEDICAL JOURNAL December 1960Postgrad Med J: first published as 10.1136/pgmj.36.422.743 on 1 December 1960. Downloaded from aggravates the extracellular depletion of sodium. 15 Furthermore, the migration of hydrogen ion not Extracellula r only increases the extracellular alkalosis but also makes the intracellular fluid acid. The paradox Volume in 10 of an acid urine excreted in the face of increasing alkalinity of the plasma is in part explained by Litres these intracellular changes.2 5 The electrolyte and fluid deficiencies are re- flected in renal function. The blood urea rises, the urine is scanty, of high specific gravity and contains little or no chloride. Initially alkaline, it becomes acid in the later stages. Usually, adequate renal function returns as soon as the circulating blood volume and electrolyte deficiencies have been replenished, but slight impairment may Hoemotocriti persist.5 Nephrocalcinosis has been reported as a result of pyloric stenosis both in the experimental x X animal18 and in man.7 38r / Weight in Kg. t x Treatment 36 The aims of initial treatment of patients with 300 r pyloric stenosis are threefold: to promote healing of the causative ulcer and alleviate pain, to relieve CSodium & C the effects on the stomach of long-standing ob- struction, and by replenishing the fluid and Chloride N C Protected by copyright. electrolyte deficiencies to correct the metabolic 100 disturbance. The definitive treatment should be surgical. Bed rest and, possibly, antacids with BGlance in sedatives promote healing of the ulcer and regres- sion of the surrounding inflammatory reaction, thus helping to overcome the obstruction and mEq. easier. FIG. 5.-Changes resulting from infusion of normal making subsequent operation saline in a patient with pyloric stenosis due to or other anti-cholinergic drugs should not be carcinoma. In the first I2-hour period sodium given as any effects they may have in opening and chloride are retained equally. In the second the pylorus is offset their effect on period no further retention occurs, showing that by depressant approximate equilibrium has been achieved. The gastric motility. extracellular volume rises, as demonstrated by Local treatment of the stomach consists of direct measurement using 82Br., and indirectly emptying it and preventing the accumulation of by the fall in haematocrit level and the gain in stagnant contents. A large bore oesophageal tube weight. http://pmj.bmj.com/ may be necessary for the initial lavage. Subse- quently, a small bore tube of the Ryle's type may be used, but it is important to remember that without laboratory tests, although these make anything given by mouth may have to be with- management of a severe case much simpler. The drawn through the tube later. In the milder case severity of the vomiting and clinical signs of salt a traditional ulcer diet may be given, but the and water depletion or latent tetany will give an stomach should be each In index of the losses that have occurred. The

emptied evening. on September 29, 2021 by guest. more severe cases with persistently large residues simpler tests include the volume, specific gravity, the tube may be left in place and a fortified milk chloride content and reaction to litmus of the feed given through it during nine hours out of urine. If there is an appreciable electrolyte each twelve, the stomach being aspirated three deficiency an acid urine indicates severe potassium hours after each feed ends. Pain is rapidly re- depletion. The blood urea, bicarbonate (or alkali lieved, the pylorus opens up (as shown by a reserve) and haemoglobin are the most useful steadily decreasing aspirate), and the patient comes laboratory investigations. The plasma electrolyte to operation with a clean stomach that can be levels are helpful in the more complicated cases. handled and sutured with safety. Low plasma levels of sodium or potassium indi- In all but the mildest cases water and electro- cate a body deficit of these ions, but normal levels lytes should be given parenterally and an initial may be found despite significant degrees of assessment of the patient's needs can be made depletion. A raised blood urea is probably the December HOWE and SPENCE: 1960 Pyloric Stenosis in Adults 747 Postgrad Med J: first published as 10.1136/pgmj.36.422.743 on 1 December 1960. Downloaded from best indication for saline therapy and a raised plasma bicarbonate for potassium therapy. Pl·.nerp - In the simple case where there is little dis- turbance of acid-base equilibrium the adminis- tration of normal saline will increase the extra- cellular volume with clinical improvement, gain Urine pH' 7 - in weight, the establishment of an adequate .. urinary flow and a fall in the haematocrit reading 9-. (Fig. 5). Where considerable disturbance of acid-base balance has already occurred with signs umuti - of peripheral circulatory failure the overriding need is for fluid and salt. Although over-hydration is a danger, especially in cardiac disease, insuffi- cient infusion is a commoner error. Deficits of was administer ed and sodiumretained throughout 5oo-600 mEq. each of sodium and chloride repre- senting a need of 4 litres of normal saline for replenishment are commonly encountered and cases occur with total body deficits of sodium and chloride in excess of I,500 mEq. (io litres of normal saline). In estimating the deficit the following rules are helpful: if clinical signs of depletion are minimal mEq/L. but chloride is absent from the urine, 2 litres of saline will be needed; if obvious clinical signs are theperiodof study. The plasma electrolyte concen- present the loss equals 6% of the body weight Protected by copyright. (e.g. 4 litres in a 70-kg. man); if peripheral circu- latory failure is present it represents a loss of at FIG. 6.-Plasma and urinary changes during correction least 6 litres. In of the water and electrolyte deficit in a patient planning the intravenous treat- with pyloric stenosis due to carcinoma. Saline ment it is best to replace half the estimated deficit was administered and sodium retained throughout in the first I2 hours and then review the position, the period of study. The plasma electrolyte concen- aiming at complete replenishment in 48 hours. trations were restored almost to normal before the The losses by aspiration over each I2-hour period urine became alkaline. must be measured and an equivalent volume of normal saline should be added to the intake for the next period. These amounts are additional be administered conveniently by adding 40 ml. of to the basic requirements of a patient receiving io% potassium chloride to each litre of intra- little fi id by mouth. venous fluid, giving a concentration of approxi- In pyloric stenosis of any severity potassium mately 50 mEq. per litre. Not more than z litres is and of this should be given in 12 hours unless there depletion invariably present potassium http://pmj.bmj.com/ chloride should be given orally in all patients. is a dangerous degree of hypokalaemia. If tetany In the mnore severely depleted patient excreting an is present calcium gluconate can be given intra- acid urine despite severe extracellular alkalosis, venously. Ammonium chloride is contraindicated it may be advisable to break the general rule and as, apart from being inadequate replacement administer potassium parenterally before there is therapy for the multiple deficiencies, it has a an adequate urinary flow. The prolonged adminis- harmful diuretic effect. Re-expansion of the tration of saline alone in such a patient may extracellular space often unmasks anaemia in result in a dangerous lowering of the concen- patients with pyloric stenosis and this should be on September 29, 2021 by guest. tration of potassium in the extracellular space corrected by blood transfusion before operation. both by dilution and by increasing the renal Once the metabolic defects of a severe case excretion of potassium.10, 17 Furthermore, saline have been rectified and the stomach emptied administration, although it may occasionally make operation should not be delayed. The procedure the urine alkaline in reaction, only partly corrects of choice is partial gastrectomy, but gastro- the alkalosis.6, 8,14,23 Correction of potassium enterostomy has a limited place in irremovable depletion with potassium chloride results in dis- carcinoma of the stomach or in very ill patients. placement of sodium and hydrogen ions from the This operation has been advocated in the past for Intracellular fluid, thus helping to correct both long-standing cases where due to gastric the alkalosis and sodium depletion of the extra- retention has reduced acid section to a low level. cellular fluid (Fig. 6). Parenteral potassium may Such advanced cases are now rarely seen nor is 748 POSTGRADUATE MEDICAL JOURNAL December 1960 Postgrad Med J: first published as 10.1136/pgmj.36.422.743 on 1 December 1960. Downloaded from 5. BURNETT, C. H., BURROWS, B. A., and COMMONS, the associated hypochlorhydria necessarily per- R. R. (1950), J. din. Invest., 29, Part I, 169. manent. 6. BURNETT, C. H., BURROWS, B. A., COMMONS, R. R., stenosis used to be a dreaded and TOWERY, B. T. (I950), Ibid., 29, Part I, I75. Pyloric complica- 7. COOKE, A. M. (I933), Quart. J. Med., 2, 539. tion of peptic ulceration, carrying a mortality of 8. COOKE, R. E., SEGAR, W. E., CHEEK, D. B., COVILLE, some i6.5%3 in patients submitted to operation. F. E., and DARROW, D. C. (1952), J. din. Invest., 31, 798. In a recent the overall of cases 9. DARROW, D. C., SCHWARTZ, R., IANUCCI, J. F., and series' mortality COVILLE, F. (1948), Ibid., 27, 198. due to benign ulceration was 5%. This improved Io. ELKINTON, J. R., and WINKLER, A. W. (1944), Ibid;, prognosis is mainly due to the better under- 23, 93. of the metabolic involved and 1. GAMBLE, J. L., and ROSS, S. G. (1925), Ibid., 1, 403. standing problems I2. HOBSLEY, M., HOWE, C. T., and LE QUESNE, L. P. particularly to the use of saline in treatment. (1960). Unpublished observations. 13. HOUGHTON, L. W., VENABLES, J. F., and LLOYD, N. L. (1925), Guy's Hosp. Rep., 5, I47. Acknowledgments 14. LANS, H. S., STEIN, I. F., and MEYER, K. A. (1952), We thank Mr. D. H. Patey and Mr. L. P. Ann. Surg., 135, 441. Le for their advice and The radio- x5. LE QUESNE, L. P. (1960), Surg. Gynaec. Obstet., in press. Quesne help. i6. McCALLUM, W. G., LINTZ, J., VERMILYE, H. N., active bromine assay was carried out by Mr. LEGGETT, T. H., and BOAS, E. (1920), Bull. Johns Hopk. R. P. Ekins. and are Hosp., 31, I. Figs. 3 4 reproduced by 17. NELSON, R. M., FRIESEN, S. R., and KREMEN, A. J. kind permission of Mr. L. P. Le Quesne and the (1950), Surgery, 27, 26. Editor of' Surgery, Gynaecology and Obstetrics'. I8. PYRAH, L. N. (I949), Brit. J..uroi., 21, 27. I9. RITCHIE, J. B., and SMITH, A. N. (I959), Brit. J. Surg., REFERENCES 46, 625. 20. SAUNDERS, S. J., IRVINE, R. O. H., CRAWFORD, M. A., I. BALINT, J. A., and SPENCE, M. P. (1959), Brit. med. J. and MILNE, M. D. (1960), Lancer, i, 468. i, 890. 21. TARAIL, R., and ELKINTON, J. R. (1949), J. clin. Invest.; 2. BERLINER, R. W., KENNEDY, T. J., and ORLOFF, J. 28, (I95I), Amer. J. Med., II, 274. 99. 3. BERKMAN, D. M. (I92g), Med. Clin. N. Amer., 5, 41I. 22. UNGLEY, H. G. (1948), Lancet, ii, 2z8. 4. BLACK, D. A. K., and JEPSON, R. P. (I954), Quart. J. Med., 23. VAN SLYKE, K. K., and EVANS, E. I. (i947), Ann. Surg., 23, 367. 126, 545. Protected by copyright.

RENAL DISEASE (Postgraduate Medical Journal, November 1959) Price 6s. 6d. post free

RECENT DEVELOPMENTS IN THE STUDY HAEMODIALYSIS http://pmj.bmj.com/ OF THE KIDNEY M. Parsons, Ch.B. A. A. G. Lewis, B.Sc., M.D., M.R.C.P.F.F. M. Parsons, B.Sc., M.B., Ch.B. RENAL BIOPSY AND DIURETICS GLONMERULONEPHRITISGLOMEULONEPHITIS H. G. Lloyd-Thomas, M.A., M.B., M.R.C.P. J. H. Ross, M.D., M.R.C.P.

RECENT ADVANCES IN THE TREATMENT URINARY DIVERSION on September 29, 2021 by guest. OF RENAL DISEASE John Hopewell, F.R.C.S. A. G. Spencer, M.D., M.R.C.P. AORTOGRAPHY RENAL ARTERY STENOSIS I. H. Griffiths, F.R.C.S. Kenneth Owen, M.S., F.R.C.S. Published by THE FELLOWSHIP OF POSTGRADUATE MEDICINE 9, Gt. James Street, W.C.1