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Hepatic failure is one of serious complications after hepatectomy. The individual′s preoperative physical health status, laboratory indicators, liver diseases, surgical factors, portal hypertension, and drug factors are all risk factors for hepatic failure. The author summarizes the risk factors for post hepatectomy liver failure(PHLF), analyzes the existing liver function scoring models, proposes the perioperative management strategy for patients undergoing hepatectomy according to the score index, so as to reduce the incidence of PHLF, improve the prognosis and long-term survival of patients.
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Objective To investigate the clinical effect of laparoscopic splenectomy combined with pericardial devascularization for the treatment of portal hypertension.Methods The retrospective cross-sectional study was conducted.The clinical data of 310 patients with portal hypertension who underwent laparoscopic splenectomy combined with pericardial devascularization in the Tangdu Hospital of Fourth Military Medical University between January 2012 and June 2016 were collected.All the patients underwent laparoscopic splenectomy combined with pericardial devascularization.Observation indicators:(1) surgical and postoperative situations;(2) follow-up situations.Follow-up using outpatient examination and telephone interview was performed to detect the gastrointestinal rebleeding and postoperative survival of patients up to January 2017.Measurement data with normal distribution and skewed distribution were respectively represented as average number (range) and M (range).Results (1) Surgical and postoperative situations:all patients underwent successful operation.Twelve patients converted to open surgery due to intractable bleeding and 298 underwent totally laparoscopic splenectomy combined with pericardial devascularization.Average operation time,average volume of intraoperative blood loss,average time of gastrointestinal function recovery and average time of postoperative abdominal drainage-tube removal of 310 patients were 192.5 minutes (range,120.0-300.0 minutes),402.3 mL (range,150.0-1 200.0 mL),2.4 days (range,1.0-4.0 days) and 4.2 days (range,2.0-8.0 days),respectively.Among 11 of 310 patients with postoperative complications,1 died of acute severe hemorrhage of upper digestive tract,5 with intra-abdominal bleeding received successful hemostasis (3 undergoing reoperation and 2 undergoing conservative treatment),2 with pleural effusion were improved by thoracentesis and drainage,2 with pancreatic leakage and 1 with pulmonary infection were cured by conservative treatment.Other 299 patients didn't have postoperative complications.Duration of postoperative hospital stay of 310 patients was 6.4 days (range,5.0-9.0 days).(2) Follow-up situations:260 of 309 patients were followed up for 6-60 months,with a median time of 26 months.During the follow-up,1 patient died of acute portal vein thrombosis at 1 month postoperatively;15 with gastrointestinal rebleeding and melena were cured by conservative treatment;other patients had survival.Conclusion Laparoscopic splenectomy combined with pericardial devascularization for the treatment of portal hypertension is safe and effective.
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Objective To investigate the mechanism of anticancer activities of the extracts of prescription 921. Methods The inhibitory effects of the extracts of prescription 921 on DNA and RNA biosyntheses in cultured prostate PC-3M were investigated with 3H-TdR or 3H-UR incorporation. Flowcytometry was applied to analyze the regulating cell cycle of the extracts of prescription 921. The expression of cell cycle related factors CyclinA, CyclinB, p21 and p27 were detected by Western-blot. Results The extracts of prescription 921 showed inhibitory effect on DNA biosyntheses. The cells of PC-3M were arrested in S-phage when treated with the extracts for 72 h. The expression level of CyclinA was down-regulated while expression of CyclinB, p21 and p27 was not altered. Conclusion The extracts of prescription of 921 play its anticancer activities by inhibiting DNA biosyntheses and arresting the cells in S-phage by down-regulating the expression of Cyclin A.