Dong Ke, Yu Xiao Jiong, Li Bo, Wen Er Gang, Xiong Wei, Guan Quan Lin
Department of General Surgery, Sichuan Province People's Hospital, Chengdu, China.
Chin J Dig Dis. 2006;7(2):76-82. doi: 10.1111/j.1443-9573.2006.00255.x.
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.
术后胃轻瘫综合征（PGS）是一种复杂的疾病，其特征为餐后恶心和呕吐，以及在无机械性胃出口梗阻的情况下出现胃无力，常由上腹部手术引起，尤其是胃或胰腺切除术，有时也由下腹部手术引起，如妇产科手术。PGS在术后经口摄入食物或食物形式改变时容易发生。这些症状可能使人丧失活动能力，并且药物治疗往往无法缓解，胃再次手术通常也不成功。PGS的病因尚未明确，其机制也尚未完全阐明。既往许多研究报道了胃切除术后的PGS，发生率约为0.4%-5.0%。PGS也是保留幽门胰十二指肠切除术（PPPD）的常见并发症，20%-50%的患者在术后早期出现该并发症。胰腺癌冷冻消融术（PCC）引起的PGS在约50%-70%的患者中被报道。因此，PGS病因复杂，可能由多种因素和机制引起。该并发症的发生率与所施行的胃部手术的类型和数量直接相关。迷走神经切断术导致的胃副交感神经控制丧失通过多种机制促成PGS。据报道， Cajal间质细胞（ICC）可能在PGS的发病机制中起作用。最近在糖尿病动物模型中的研究表明，肠神经系统的特定分子变化可能导致胃排空延迟。十二指肠缺失，进而胃的第三期缺失，可能是胃潴留的一个原因。人们认为，PPPD术后的PGS至少部分归因于胃第三期恢复延迟，这是由于十二指肠切除术后血浆胃动素浓度降低所致。ICC的损伤可能在PCC术后PGS的发病机制中起作用，对此可能有多种因素负责，包括胰十二指肠区域冷冻后胃幽门肌和十二指肠的缺血及神经损伤，或胃动素循环水平降低。由于胃轻瘫的治疗远非理想，非传统方法和非标准药物可能会有用。多种治疗优于单一治疗。本文综述了近年来发表在中英文各类期刊上的几乎所有与PGS相关的论文，以便更好地了解PGS。
