Perioperative morbidity affects long-term survival in patients following liver resection for colorectal metastases.

BACKGROUND: Hepatic resection is the treatment of choice in patients with colorectal liver metastases. Perioperative morbidity is associated with decreased long-term survival in several cancers. The aim of this study was to assess the impact of perioperative morbidity and other prognostic factors on the outcome of patients undergoing liver resection for colorectal metastases. METHODS: One hundred ninety seven patients undergoing liver resection with curative intent were investigated. The influence of prognostic factors, such as complications, tumor stage, margins, age, sex, number of lesions, transfusion, portal inflow obstruction, and era and type of resection, was assessed using univariate and multivariate analysis. Complications were graded using an objective surgical complication classification. RESULTS: The 5-year survival rate was 38%, with a median follow up of 4.5 years. The disease-free survival rate at 5 years was 23%. The perioperative morbidity and mortality rates were 30 and 2.5%, respectively. The median survival of patients with perioperative complications was 3.2 years, compared to 4.4 years in those patients without complications (p < 0.01). For patients with positive resection margins, the median survival was 2.1 years, compared 4.4 years in patients with a margin (p = 0.019). CONCLUSION: Perioperative morbidity and a positive resection margin had a negative impact on long-term survival in patients following liver resection for colorectal metastases.

Scorpion venom stimulates biliary/duodenal motility and pancreatic exocrine secretion.

Scorpion envenomation causes severe upper abdominal pain associated with nausea and vomiting. Although scorpion venom (SV) stimulates pancreatic and gastric secretion in animal models, its effects on duodenal and biliary motility have not been reported. The aim of this study was to determine the effects of SV on sphincter of Oddi (SO), duodenal and gall bladder motility and pancreatic amylase output. Anaesthetized Australian possums (n = 21) were infused with SV via intravenous or closed intra-arterial routes. Blood pressure, SO, duodenal and gall bladder motility were continuously monitored for 4 h. Trans-sphincteric flow (TSF), an indicator of bile duct resistance, was measured concurrently. The amylase output in pancreatic juice was also measured. SV infusion resulted in profound transient increase in blood pressure, SO motility and a significant decrease in TSF. No significant differences were noted in SO basal pressure changes. A transient increase in gall bladder tone, duodenal contraction amplitude and frequency, and amylase output were noted. Following the peak in blood pressure, amylase output, SO, gall bladder and duodenal motility were depressed. SV induces a rapid but transient increase in biliary and duodenal motility that is associated with stimulation of pancreatic amylase output. These changes may contribute to gastrointestinal symptoms associated with early phases of envenomation.

Endothelin-1 stimulates sphincter of Oddi motility and decreases trans-sphincteric flow: a possible mechanism contributes to cholestasis in disease states.

Endothelin-1 (ET-1) is a potent stimulator of gallbladder contractility. Its role in modulation of sphincter of Oddi (SO) motility and trans-sphincteric flow (TSF) has not been evaluated. To characterize the effects of ET-1 on SO motility and TSF, 10 anaesthetized Australian possums (in vivo, n = 6) were given graded doses of ET-1 (5-200 pmol kg-1) via closed intra-arterial injection. Blood pressure, TSF and SO motility (basal pressure, phasic amplitude, contraction frequency) were analysed. For in vitro studies, eight SO rings were subjected to 10-12-10-7 mol L-1 cumulative concentrations of ET-1 in organ bath and SO motility was measured. Data are expressed as mean +/- SEM. Statistical analysis used anova. ET-1 induced a dose-related increase in blood pressure with a maximal increase of 37.5 +/- 2.5 mmHg at 200 pmol kg-1, (P < 0.001). ET-1 also increases SO basal pressure (P < 0.001) and contraction frequency (P < 0.0001). However, the contraction amplitude was not significantly affected. ET-1 decreased TSF in a dose-related manner (P < 0.001) with cessation of TSF at the highest dose (P < 0.001). In vitro studies showed a significant increase in mean SO motility index, and frequency of contractions at higher ET-1 concentrations (10-9-10-7 mol L-1). ET-1 is a potent stimulator of SO motility resulting in a reduction in TSF.

Effects of acute pancreatic duct obstruction on pancreatic perfusion: implication of acute pancreatic duct decompression.

BACKGROUND: Acute pancreatitis can result in pancreatic ischaemia and necrosis. Pancreatic duct (PD) obstruction may be the first step causing ischaemia in acute pancreatitis. Nitric oxide donors can attenuate acute pancreatitis through improvement in compromised pancreatic perfusion (PP). In this study, we determined if (1) PD obstruction altered PP and (2) PD decompression or L-arginine administration reversed this change. METHODS: Fifteen Australian possums were randomly assigned to two groups: Animals in group A (n = 6) were subjected to 30 min of PD obstruction and 60 min of PD decompression. Animals in group B (n = 9) were subjected to 120 min PD ligation and 60 min PD decompression. A subset group B (n = 6) were subjected to intravenous L-arginine (100 microg/kg) at the end of 120 min of ligation and at the end of PD decompression. The PP (Laser Doppler fluxmetry), PD pressure and blood pressure were continuously monitored. RESULTS: PD pressure increased from 2.9 +/- 2.5 to 18.1 +/- 4.9 mmHg following PD ligation. PP was reduced to 67.1% +/- 4.5% (P<0.01) and 46.2% +/- 7.5% (P<0.001) of baseline following 30 and 120 min of PD ligation, respectively. Following 60 min of PD decompression, PP was restored to 89.1% +/- 13.4% (P<0.02) of the baseline in the 30-min group. However, following 120 min PD ligation, PP remained depressed. L-arginine administration after 120 min of PD ligation transiently increased PP from 46.2% +/- 7.5% to 81.1% +/- 8.6% (P<0.03) of baseline. This effect was reproduced if L-arginine was administered at the end of decompression (P<0.05). CONCLUSION: In patients with acute pancreatitis due to obstructive causes, early decompression of the PD may prevent early pancreatic ischaemia.