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Chin J Dig Dis. 2006;7(2):76-82.

Advances in mechanisms of postsurgical gastroparesis syndrome and its diagnosis and treatment.

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1
Department of General Surgery, Sichuan Province People's Hospital, Chengdu, China. dongke1134@hotmail.com

Abstract

Postsurgical gastroparesis syndrome (PGS) is a complex disorder characterized by post-prandial nausea and vomiting, and gastric atony in the absence of mechanical gastric outlet obstruction, and is often caused by operation at the upper abdomen, especially by gastric or pancreatic resection, and sometimes also by operation at the lower abdomen, such as gynecological or obstetrical procedures. PGS occurs easily with oral intake of food or change in the form of food after operation. These symptoms can be disabling and often fail to be alleviated by drug therapy, and gastric reoperations usually prove unsuccessful. The cause of PGS has not been identified, nor has its mechanism quite been clarified. PGS after gastrectomy has been reported in many previous studies, with an incidence of approximately 0.4-5.0%. PGS is also a frequent complication of pylorus-preserving pancreatoduodenectomy (PPPD), and the complication occurs in the early postoperative period in 20-50% of patients. PGS caused by pancreatic cancer cryoablation (PCC) has been reported about in 50-70% of patients. Therefore, PGS has a complex etiology and might be caused by multiple factors and mechanisms. The frequency of this complication varies directly with the type and number of gastric operations performed. The loss of gastric parasympathetic control resulting from vagotomy contributes to PGS via several mechanisms. It has been reported that the interstitial cells of Cajal (ICC) may play a role in the pathogenesis of PGS. Recent studies in animal models of diabetes suggest specific molecular changes in the enteric nervous system may result in delayed gastric emptying. The absence of the duodenum, and hence gastric phase III, may be a cause of gastric stasis. It was thought that PGS after PPPD might be attributable, at least in part, to delayed recovery of gastric phase III, due to lowered concentrations of plasma motilin after resection of the duodenum. The damage to ICC might play a role in the pathogenesis of PGS after PCC, for which multiple factors are possibly responsible, including ischemic and neural injury to the antropyloric muscle and the duodenum after freezing of the pancreatoduodenal regions or reduction of circulating levels of motilin. As the treatment of gastroparesis is far from ideal, non-conventional approaches and non-standard medications might be of use. Multiple treatments are better than single treatment. This article reviews almost all the papers related to PGS from various journals published in English and Chinese in recent years in order to facilitate a better understanding of PGS.

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