Pyloric Sphincter Incompetence in Man

Pyloric Sphincter Incompetence in Man

Vol. 59. No.1 GASTHOENTEHOLOGY Copyright © 1970 by The Williams & Wilkins Co. Printed in U.S.A. PYLORIC SPHINCTER INCOMPETENCE IN MAN A physiologi...

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Vol. 59. No.1

GASTHOENTEHOLOGY

Copyright © 1970 by The Williams & Wilkins Co.

Printed in U.S.A.

PYLORIC SPHINCTER INCOMPETENCE IN MAN A physiological variant THOMA S C. BENEVENTANO,

M.D.,

AND CLARENCE

J.

SCHE IN,

M.D.

Division of Diagnostic Radiology and the Surgical Division , Monte(iore Hospital and Medical Center. and the Albert Einstein Colle~te of Medicine. N ew York. New York

Thirty-six consecutive cholecystectomized patients with indwelling T-tubes were examined for pyloric sphincter competence by a cineradiographic technique. Fifty per cent sodium diatrozoate was passed through a T-tube to fill the duodenum. Twelve patients (33 '13 %) demonstrated pyloric insufficiency with regurgitation of the of the contrast material through the sphincter into the stomach. None of the patients with regurgitation were symptomatic or had roentgen or direct observation disease of the stomach or duodenum. Pyloric sphincter incompetence appears to be a physiological variant in some individuals. This report deals with a study of pyloric cecal sphincter. There is no disease or dissphincter competence in man. The sphinc- tress from this reflux and it is not clinically ters of the gastrointestinal tract are con- significant. The role of the gastric outlet sphincter sidered to function in a normal fashion when they permit food and digestive prod- was studied to determine whether reflux ucts to pass sequentially from the mouth is normally present, and whether such retoward the rectum. This ab oral progres- flux is of clinical importance. sion of nutritive materials is regulated, in Materials and Methods part, by the muscular areas at the juncIn order to evaluate pyloric sphincter comtion of various anatomic segments of the gastrointestinal tract. When these sphinc- petence, one may utilize direct duodenal opacters are incompetent the normal ab oral ification via an enterostomy, direct endoscopic current is reversed. If the wall of the visualization, or analyze the gastric aspirate bowel is unfavorably affected by the re- for the presence of duodenal contents and bile. Indirect duodenal opacification via a T-tube in gurgitated contents then a disease results the common bile duct with subsequent demonfrom the loss of this sphincter guard ac- stration of contrast in the duodenum and stomtion. ach is another route of study of the sphincter This is seen with the incompetent competence. esophagogastric sphincter, where regurgiAny method utilizing intubation across the tation of acid contents produces esopha- pyloric sphincter may in itself produce insufgitis. On the other hand, a sphincter may ficiency and compromise the interpretation. be incompetent and have no clinically Furthermore, incompetency is not readily derelated disease. Thus, ileal reflux can be tected in a barium-opacified stomach where demonstrated during barium enema exam- small degrees of reflux may be obscured. Therefore, the oral barium meal method is not inations due to incompetence of the ilea- entirely satisfactory. Direct enterostomy manipulates the area being studied, and introduces an undesirable traumatic interference element. Opacification of the duodenum via the Ttube route does not interfere with the normal

Received November 26, 1969. Accepted March 12, 1970. Address requests for reprints to: Dr. Thomas C. Beneventano, Montefiore Hospital and Medical Center, 111 East 210th Street, Bronx, New York 10467. filS

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physiology of the duodenum and offers a challenge to retrograde sphincter competence that simulates the clinical problem. The method permits roentgen documentation of this aspect of pyloric function and is a satisfactory way to investigate the problem in man under basal conditions. Therefore, postoperative cholecystectomized patients who have indwelling Ttubes and require radiological examination prior to the removal of these tubes provide an excellent preparation for these studies. Thirty-six consecutive female patients, from 24 to 65 years of age, were evaluated. Each of them had undergone a cholecystectomy and common bile duct exploration for cholecystolithiasis. No vagotomy, duodenostomy, or gastrostomy had been performed. A T-tube was placed in the common bile duct at the time of operation. No patient in this series had duodenal or gastric ulcer disease by radiographic, surgical or clinical criteria. The common bile duct, except for dilation, was normal in all cases. There were no retained stones, strictures, or radiographic evidence of obstruction or inflammation. Ten to 14 days postoperatively, these patients were radiographed in a fasting state, without premedication or maintenance on any drug known to affect smooth muscle tone. With the patient in a supine position, the long arm of the T-tube was connected to a manometer filled with (50 %) sodium diatrozoate at room temperature. In every case enough contrast material was delivered through the Ttube to fill the duodenum and the duodenal bulb completely. This complete retrograde opacification of the duodenal bulb was considered necessary for the demonstration of pyloric zone competence and its evaluation from the duodenal side of the sphincter. While the common bile duct was perfused, cineradiography was performed, using 16 mm cine at 15 frames per sec under television monitoring. No hand injection was employed and palpation was not utilized during the roentgenographic examination. Increasing increments of manometric pressure permitted the contrast to flow through the T-tube, the common bile duct, and out into the duodenum. The range was 15 to 65 em of water with a maximum choledochal perfusion pressure of 65 em of water. In each patient the perfusion pressure within the common bile duct was recorded and sufficient pressure was achieved to produce pain. The pain was the result of the distention of the common bile duct and was used as the end point for each study. This pain-producing pressure referred only to the perfusion pressure in the common

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bile duct and did not reflect the intraluminal pressure of the duodenum. The intraluminal duodenal pressure was not monitored. The total volume of contrast material used in each case was less than 100 ml" of 50 '/i, sodium diatrozoate . The major portion proceeded through the duodenum and into the small bowel in the usual ab oral peristaltic movement, and only a small, unknown volume was identified as reflux. The exact volume of refluxed contrast material in the stomach was not determined in the study, but we have been able to visualize volumes as small as 2 ml in the common bile duct as well as in the stomach. When the water-soluble contrast material appeared in the gastric cavity, it was possible to observe and record this reflux at the moment that it happened because the gastric antral mucosa became radiographically visible at that time. The status of gastric contraction or relaxation of the pyloroantral portion of the stomach, prior to reflux, and visualization were not determined , but the gastric antrum was not contracted at the time of reflux visualization. The films were used to confirm and record the direct fluorographic observations.

Results Twelve of the 36 patients (33 1/:11/ (,) demonstrated reflux of contrast material into the stomach. There was no pain, nausea, or any symptom associated with this reflux. The patient was totally unaware of the phenomenon. The intraluminal pressure of the duodenum could not be measured by our technique. In the patients with this transpyloric regurgitation, the reflux was evident before maximum choledochal distention was attained and before pain was produced. The motor activity of the biliary induced duodenal peristalsis varied from occasional retrograde contraction to the usual propulsive contraction of the duodenum as it is normally observed with the oral barium meal stimulus. Every patient had a radiographically normal duodenal bulb. The pylorus, the antrum, and the body of the stomach were also demonstrated to be radiologically free of ulceration, inflammation, and tumor. Each patient had the advantage of direct confirmatory inspection at the time of the cholecystectomy. The only disease demonstrated at the time of laparotomy was cal-

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culus gallbladder disease which was the indication for the original surgery.

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ance in this area related to physiological pressure gradients. Otherwise, pyloric sphincter incompetence should be demon. strable in all challenged subjects. The normal intraluminal pressures of the duodenum have been reported by Friedman et al. 6 to reach levels as high as 45 mm of mercury (61 em of water). Our studies utilizing pressures between 15 and 65 em of water perfusion levels in the common bile duct should have resulted in even lower respective pressures in the duodenal lumen. Therefore, these choledochal pressures, when dissipated into the duodenum, should not exceed the norw'll introduodenal pressure. The reflux across the sphincter zone should, therefore, not be attributed to an excessive test perfusion pressure. Incompetence of the pyloric sphincter is reported by Wangensteen 1 as a constant concomitant of small bowel obstruction. Connell8 reported the presence of bile in the gastric aspirate of 46% of 413 fasting patients. These figures were collected during the course of routine gastric aspirations and analysis. Pyloric incompetence as a disease entity has been presented by Rhodes et al. 9 as a factor in the genesis of gastric ulcer when the gastric mucosa is affected by excessive concentration of bile acids presumably regurgitated after eating. Our observations in cholecystectomized patients indicate that pyloric incompetence may occur without symptomatic or roentgen evidence of gastric disease in appropriately challenged patients. Pyloric sphincter incompetence with reflux is not a disease or necessarily associated with disease in the undefended proximal stomach. It appears to be a physiological variant in the interdigestive phase.

Discussion Capper has stated that reflux does not occur across the normal pyloric sphincter, but was able to demonstrate reflux in 56% of cases with duodenal ulcer disease. This observation was substantiated by Nelson 2 who demonstrated reflux in 2 patients with duodenal ulcer disease, whereas 6 normal patients failed to reveal such reflux despite attempts to accomplish it by compression in various positions. Capper et al. 3 examined their patients with a fine nasoenteric tube across the sphincter. This may compromise the technique. Nelson's patients were examined postoperatively via a T-tube or a duodenal catheter placed in the cystic duct. Perfusion pressures were not described. Jorgens et al. 4 in a cineradiographic study of the duodenum, described retrograde reflux through the pyloric sphincter with barium passing during a midbulbar contraction of the duodenal bulb. The number of cases in which this occurred was not reported. Atkinson et al. 5 employing balloon manometry, demonstrated that there is no complete physiological sphincter mechanism at the level Q[ the pylorus. Indeed, their observations demonstrated that the pyloric sphincter zone remained patent most of the time; the circular muscle sphincter guard is active only at the conclusion of the gastric peristaltic contraction. However, even during this relaxed phase there appears to be an individual variation in competence as far as reflux is concerned. An apparent discrepancy between a theoretical continual anterograde emptying of the stomach and the fluoroscopic and clinical observation of intermittent emptying of the stomach was considered to be related to the viscosity of the REFERENCES ingested meal and the state of contraction 1. Capper WM : Factors in the pathogenesis of gas· of the gastric muscle wall. The stomach is tric ulcer. Ann Royal Col! Surg (England) 40:21considered to empty via a filtration pump35, 1967 ing mechanism. 2. Nelson PG: Gastric ulcer a nd alkaline regurgita· The absence of universal · reflux through tion. Med J Austr 1:216- 219, 1969 the normally patent pyloric sphincter 3. Capper WM, Airth GR, Kolby JO: A test for PY· must be attributed to variations in resistloric regurgitation. Lancet 2:621- 623, 1966 1

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4..)orl(ens J, Kiesel 10, Leonard JP: A cinef1uorographic study of the duodenum. Radiology 79: 760-762, 1962 li. Atkinson M, Edwards DAW, Honour AJ, et al: Comparison of cardiac and pyloric sphi ncters: a manometric study. Lancet 273:918-922, 1957 6. Friedman G, Wolf BS, Waye JD, et al: Correlation of cineradiographic and intraluminal pressure changes in the human duod e num: an analysis of the functional significance of monophasic waves. Gastroenterology:49:37-49, 1965

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7. Connel AM: The role of pylorus in the aetiolO!,'Y of gastric ulcer. Rendic RR Gastrocnt 1:25-34, 1969 8. Wangensteen OW: The therapeutic problem in bowel obstruction. Springfield, Charles C Thomas, 1937, pp. 47 9. Rhodes J, Bernardo DE, Phillips SF, et al: Increased reflux of bile into the stomach in patients with gastric ulcer. GastroenterolOf.,'Y 57:241-252, 1969