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Sphincter of Oddi dysfunction (SOD) is associated with abdominal pain and is treated by sphincterotomy. Of 215 patients who underwent biliary sphincterotomy for SOD in our institution, 26 reported no improvement and 25 of those were found to have pancreatic sphincter dysfunction and subsequently underwent pancreatic septotomy. Nine patients remained symptomatic after the second intervention. Six of those nine patients, and seven of the 16 patients who improved after the septotomy, agreed to undergo an ambulatory duodenojejunal (DJ) manometry. DJ manometry was abnormal in four of the six symptomatic patients but only in one of seven patients who became asymptomatic after endoscopic treatment. We conclude that the persistence of symptoms after endoscopic ablation of the biliary and pancreatic sphincters is associated with abnormal intestinal motility, which may explain in part the lack of response to the endoscopic treatment.

Although sphincter of Oddi dysfunction (SOD) has been extensively studied in the nontransplant setting, the diagnostic criteria after liver transplantation are not well defined and have been based on clinical features without manometric documentation. The purpose of this study was twofold: (1) to determine the manometric patterns associated with SOD following orthotopic liver transplantation (OLT) and (2) to define the usefulness of bedside T-tube manometry as a screening tool for SOD. ERCP with simultaneous manometry of the sphincter of Oddi (SO) was performed in five patients following OLT with choledochocholedochostomy (CDCD) between 1990 and 1992. The diagnosis of SOD was suspected based on persistently elevated liver function tests, distal common bile duct dilatation in the absence of strictures, and an elevated resting bile duct pressure as measured by bedside T-tube manometry. Two different manometric patterns of SOD were observed. The first pattern (N = 4) consisted of elevated SO basal pressures, infrequent simultaneous phasic activity, and an abnormal response to cholecystokinin-octapeptide (CCK-OP). The second pattern (N = 1) consisted of low basal pressures and absent phasic activity. Four patients were successfully treated with papillotomy and stenting, while the fifth patient required conversion to a choledochojejunostomy because of a concomitant anastomotic stricture. The abnormal SO manometric profiles in patients suspected of having SOD after OLT were different from those observed in the nontransplant setting. Bedside T-tube manometry allowed measurement of the resting bile duct pressure and may be a useful screening tool for SOD.

Endoscopic injection sclerotherapy (EIS) is a standard and definitive therapy for bleeding esophageal varices. While the overall complication rate of the procedure is low, a substantial minority of patients treated by EIS develop refractory mucosal ulceration and/or esophageal strictures. However, despite the prophylactic use of H2 blockers and sucralfate in our EIS protocol, we observed a number of patients who developed nonhealing esophageal and/or gastroduodenal ulceration. We conducted an open trial in which we enrolled nine patients who had refractory ulcer disease. Patients that enrolled in the trial exhibited complete healing of their mucosal ulcers. These results suggest that acid is an important contributory factor in the pathogenesis and perpetuation of EIS-associated mucosal ulceration. Patients with alcohol-associated liver disease may be at increased risk for the development of EIS-associated complications.