Early cholecystectomy after ERCP, within 72 h, has better outcomes, probably due to the inflammatory processes.

Purpose. The most common complication of hydatid liver cysts is spontaneous rupture into the biliary tract. This study was conducted to evaluate the surgical management of spontaneous intrabiliary rupture of a hydatid liver cyst in 41 patients. Methods. The preoperative diagnosis was confirmed by ultrasound in all 41 patients, 37 of whom were jaundiced. Results. According to Gharbi's classification, 39% of the cysts were type III and they ranged from 3 to 18 cm in diameter, with a mean diameter of 9 cm. The mean total bilirubin and alkaline phosphatase values were 6.3 mg/dl and 450 IU, respectively. Partial cystectomy, cholecystectomy, and common bile duct exploration were performed in all patients. In seven patients, the visible biliary duct within the cyst cavity was sutured with 2/0 silk. Intraoperative cholangiography was performed in all patients, and choledochoscopy was performed in 11 patients. A T-tube was inserted after the biliary tract content was thought to have been totally cleaned out in 38 patients (93%), and a choledochoduodenostomy was performed in 3 patients (7%). An external biliary fistula developed in five patients, persisting for 11-25 days. The fistulae healed within a mean period of 5 days after endoscopic sphincterotomy (EST). For patients without a fistula the mean hospitalization time was 8 days and there was no mortality. Conclusion. These results suggest that when a hydatid liver cyst ruptures into the biliary tract, common bile duct exploration should be conducted using intraoperative cholangiography and choledochoscopy. If the biliary tract is cleaned of all cystic content, T-tube drainage should be sufficient, but EST is an effective technique for treating persistent extended external biliary fistulae.

Supplementation of parenteral Gln decreased the postoperative complications and hospital stay and in the patients undergoing the colorectal surgery for cancer.

Sepsis is one of the most important risk factors in acute respiratory distress syndrome (ARDS). beta-Glucan is a potent reticuloendothelial modulating agent, the immunobiological activity of which is mediated in part by an increase in the number and function of macrophages. In this study, we investigated the putative protective role of beta-glucan against sepsis-induced lung injury. Sepsis was induced by cecal ligation and puncture (CLP) in Wistar rats. The control group received saline, and the treatment groups received beta-glucan or beta-glucan + beta-1,3-D-glucanase. Five hours thereafter, plasma tumor necrosis factor (TNF) alpha, interleukin (IL) 1beta, and IL-6 levels were determined. Presence of lung injury was determined via lung tissue myeloperoxidase (MPO) activity, intercellular adhesion molecule (ICAM) 1 levels, and histopathological examination at 18 h after CLP. In a separate set of experiments, survival was monitored for 7 days after CLP. beta-Glucan treatment led to a significant increase in survival rate (63% in glucan-treated rats vs 38% in saline-treated rats). Administration of the beta-glucan inhibitor abrogated beta-glucan's survival benefit (50%). After CLP, plasma TNF-alpha, IL-1beta, and IL-6 concentrations were increased in control animals. When beta-glucan was administered, it completely blocked the elevation of TNF-alpha, IL-1beta, and IL-6. Administration of beta-1,3-D-glucanase suppressed glucan-induced decrease in cytokines. Animals treated with beta-glucan showed a significant reduction in lung injury score, a marked decrease in ICAM-1 expression, and a significant decrease in MPO levels. In contrast, beta-1,3-D-glucanase caused a significantly increased MPO and ICAM-1 levels in the lung. These data reveal that beta-glucan treatment improved the course of CLP-induced peritonitis and attenuated the lung injury. Administration of beta-glucanase inhibited the beta-glucan activity and resulted in enhanced lung injury.

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