AIM:To explore the etiology,pathogenesis,diagnosis,andtreatment of postsurgical gastroparesis syndrome (PGS)after pancreatic cancer cryotherapy (PCC) or pancreatico-duodenectomy (PD),and to analyze the correlation betweenthe multiple factors and PGS caused by the operations.METHODS:Clinical data of 210 patients undergoing PDand 46 undergoing PCC were analyzed retrospectively.RESULTS:There were 31 (67%,31/46) patients sufferingPGS in PCC group,including 29 with pancreatic head anduncinate tumors and 2 with pancreatic body and tail tumors.Ten patients (4.8%,101210) developed PGS in PD group,which had a significantly lower incidence of PGS than PCCgroup (X=145,P<0.001).In PCC group,9 patients withPGS were managed with non-operative treatment (drugs,diet,nasogastric suction,etc.),and one receivedreoperation at the 16th day,but the symptoms were notrelieved.In PD group,all the patients with PGS weremanaged with non-operative treatment.The PGS inpatients undergoing PCC had close association with PCC,tumor location,but not with age,gender,obstructivejaundice,hypoproteinemia,preoperative gastric outletobstruction and the type and number of gastric biliary tractoperations.The mechanisms of PGS caused by PD weresimilar to those of PGS following gastrectomy.The damageto interstitial cells of Cajal might play a role in thepathogenesis of PGS after PCC,for which multiple factorswere possibly responsible,including ischemic and neuralinjury to the antropyloric muscle and the duodenum afterfreezing of the pancreatico-duodenal regions or reducedcirculating levels of motilin.CONCLUSION:PGS after PCC or PD is induced by multiplefactors and the exact mechanisms,which might differ betweenthese two operations,remain unknown.Radiography ofthe upper gastrointestinal tract and gastroscopy are maindiagnostic rnodalities for PGS.Non-operative treatmentsare effective for PGS,and reoperation should be avoidedin patients with PGS caused by PCC. To explore the etiology, pathogenesis, diagnosis, and treatment of postsurgical gastroparesis syndrome (PGS) after pancreatic cancer cryotherapy (PCC) or pancreatico-duodenectomy (PD), and to analyze the correlation betweent multiple factors and PGS caused by operations. METHODS There were 31 (67%, 31/46) patients suffering PGS in the PCC group, including 29 with pancreatic head and ending tumors and 2 with pancreatic body and tail tumors. PGC in PD group, which had a significantly lower incidence of PGS than PCCgroup (X = 145, P <0.001) .In PCC group, 9 patients with PGS were managed with non-operative treatment , diet, nasogastric suction, etc.), and one receivedreoperation at the 16th day, but the symptoms were notrelieved. In the PD group, all the patients with PGS weremanaged with non-operative treatment.The PGS inpatients undergoing PCC had close association with PCC, tumor location, but not with age, gender, obstructive jaundice, hypoproteinemia, preoperative gastric out of totruction and the type and number of gastric biliary tractoperations. these mechanisms of PGS caused by PD weresimilar to those of PGS following gastrectomy. The damage to interstitial cells of Cajal might play a role in the pathogenesis of PGS after PCC, for which multiple factorswere possibly responsible, including ischemic and neuralinjury to the antropyloric muscle and the duodenum afterfreezing of the pancreatico-duodenal regions or reduced circulating levels of motilin. CONCLUSION: PGS after PCC or PD is induced by multiple factors and the exact mechanisms, which make differ betweenthese two operations, remain unknown. Radiography of the upper gastrointestinal tract and gastroscopy are maindiagnostic rnodalities for PGS. Non-operative treatments for effective in PGS, and reoperation should be avoided in patients with PGS caused by PCC.