Abstract
AbstractGastric ulceration is a cause of significant morbidity in approximately 3% of patients undergoing fundoplication. The etiology of this complication remains unsettled. A patient who presented with gastric ulceration following fundoplication is described. Gastric emptying of solids was markedly delayed (28% retention at 120 minutes; normal range, 3–17%). The integrated gastrin response to 180 g of lean meat (368%) demonstrated marked derangement of the antrat gastrin mechanism (normal, 44±8%). Metoclopramide therapy resulted in normalization of gastric emptying (13% retention at 120 minutes), while the integrated gastrin response showed a decided decrease (257%). This patient clearly implicates gastric stasis and hypergastrinemia secondary to vagal dysfunction as a contributing factor in the etiology of gastric ulceration following fundoplication. The question as to whether this vagal dysfunction is a preexisting condition or the result of operative manipulations remains unresolved.
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