Preoperative symptoms of irritable bowel syndrome predict poor outcome after laparoscopic cholecystectomy.

BACKGROUND: Laparoscopic cholecystectomy (LC) is the accepted treatment for symptomatic cholelithiasis. This study examines the effect LC has on quality of life (QOL) and gastrointestinal (GI) symptoms and determines whether patients with symptoms of irritable bowel syndrome (IBS) gain the same benefit as those without. METHODS: A total of 158 patients who underwent LC for symptomatic gallstones were recruited to this prospective observational study. IBS Manning scores were calculated and QOL was measured using the Gastrointestinal Quality of Life Index (GIQLI) preoperatively, at 6 weeks, 3 months, and 2 years postoperatively. Linear regression analysis was used to identify preoperative symptoms that predict outcome. RESULTS: One hundred twelve patients had sufficient data sets for inclusion. Patient's GIQLI scores were calculated for the four time points in the study. The mean preoperative score was 88.8 ± 1.3 (61.7% of 144, the highest score possible) and improved 6 weeks after surgery to 105.5 ± 1.3 (p < 0.001). This improvement was maintained at 3 months, but at 2 years analysis showed regression toward the baseline of 7.6 ± 2.3 (p = 0.003) points. There was a negative correlation of -5.2 ± 1.29 (p < 0.001) points between each Manning symptom and QOL scores. The largest effect was seen in patients describing loose bowel movement with the onset of pain. Patients with this symptom had a -17.3 ± 4.6 (p < 0.001) lower global QOL score. CONCLUSIONS: Patients with symptoms of IBS indicated by the Manning criteria show less improvement in quality of life after laparoscopic cholecystectomy for gallstones.

Differential preservation of lipopolysaccharide-induced chemokine/cytokine expression during experimental pancreatitis-associated organ failure in rats shows a regulatory expressed phenotype.

BACKGROUND: Altered lipopolysaccharide (LPS)-responsiveness is a key feature of acute pancreatitis (AP)-associated multiple organ failure (AP-MOF) in rats and humans. AIM: To determine the differential expression of 16 cytokines and chemokines in response to delayed LPS administration in established experimental AP-MOF in rats. METHODS: In a cubic factorial group design (12 groups, n = 6 rats/group), 0, 6 and 30 microg/kg Escherichia coli 0111:B4 LPS was administered intra-arterially, 18 h into experimental AP-MOF or sham laparotomy. AP was induced by intraductal glycodeoxycholic acid and intravenous caerulein. Central venous serum concentrations of 16 cytokines and chemokines were measured by Searchlight multiplex ELISA. RESULTS: Four patterns were observed: (1) TNF-alpha, IL-1alpha, IL-1beta, IL-6, IFN-gamma, MCP-1, MIP-2alpha, MIP-3alpha, fractalkine and RANTES showed a diminished LPS response in AP versus sham (p < 0.001, ANOVA); (2) IL-2, IL-4 and GM-CSF levels were undetectable; (3) CINC-2alpha and GRO/KC showed little or no difference between AP and controls, and (4) IL-10 concentrations after 0 and 6 microg/kg, but not 30 microg/kg LPS injection were significantly higher in AP than controls (p < 0.001, ANOVA). CONCLUSION: Experimental AP-MOF in rats results in differential preservation of the cytokine and chemokine response to LPS challenge, with a predominantly regulatory expressed phenotype.

Sinistral portal hypertension.

Sinistral, or left-sided, portal hypertension is a rare cause of upper gastrointestinal haemorrhage. There are many causes of sinistral portal hypertension. The primary pathology usually arises in the pancreas and results in compression of the pancreatic vein. This compression causes backpressure in the left portal venous system and subsequent gastric varices. Management is usually surgical to treat the underlying pathology and splenectomy to decompress the left portal venous system. This paper presents four cases of sinistral portal hypertension followed by a literature review of the reported causes and management issues.

Management of cystic tumours of the pancreas.

BACKGROUND: Cystic tumours of the pancreas account for 5% of pancreatic neoplasms and are frequently misdiagnosed as pancreatic pseudocysts. The authors' experience of managing these tumours is presented here, highlighting the clinical presentation, diagnostic difficulties and operative treatment. METHODS: This is a retrospective study of all patients diagnosed to have cystic tumours of the pancreas treated at The Mater Hospital, during a 5-year period from 1997 to 2002. Literature was reviewed and guidelines for the management of these tumours have been outlined. RESULTS: Seven patients with cystic pancreatic tumours were treated over this time-period. All patients were women with a median age of 40. Two of these patients were initially diagnosed as having pseudocysts and were treated elsewhere by cystgastrostomy. The tumour was resected in all patients. All but one was benign. At follow up, ranging from 13 to 66 months, all patients were alive and well. CONCLUSIONS: Cystic tumours of the pancreas are uncommon and generally slow growing. It is important not to assume that a cystic lesion in the pancreas, especially in middle-aged women, is a pseudocyst. Satisfactory surgical resection may be possible even after previous operative procedures on the pancreas. Prognosis after resection remains good.

The isolated perfused liver response to a 'second hit' of portal endotoxin during severe acute pancreatitis.

BACKGROUND/AIM: During severe acute pancreatitis (AP), the liver may show an exaggerated response to the inflammatory products of gut injury transported in the portal vein. Our aim was to explore liver proinflammatory mediator production after a 'second hit' of portal lipopolysaccharide (LPS) during AP. METHODS: Twenty-four rats underwent one of three 'first-hit' scenarios: (1) severe AP induced by intraductal glycodeoxycholic acid injection and intravenous caerulein infusion, (2) sham laparotomy, or (3) no first intervention. Eighteen hours later, all animals received a 'second hit' of portal LPS in an isolated liver perfusion system. Tumour necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6 concentrations were measured in portal and systemic serum, and in the perfusate 30 and 90 min after the 'second hit'. Neutrophil activation by the perfusate was assayed using dihydrorhodamine-123 fluorescence. RESULTS: We observed a six-fold increase in IL-6 concentration across the liver during AP. All livers produced TNF-alpha after the portal LPS challenge, but this was not exaggerated by AP. No differential neutrophil activation by the perfusate was seen. CONCLUSION: TNF-alpha, IL-1beta, IL-6 and neutrophil activator production by the isolated perfused liver, in response to a 'second hit' of portal LPS, does not appear to be enhanced during AP.

Early and long-term results of surgery for severe necrotising pancreatitis.

BACKGROUND: Necrotising pancreatitis is a challenging problem for the surgeon, as it is associated with considerable morbidity and mortality. The indications, timing of surgical intervention and type of procedure continue to be debated in an effort to improve the outcome of this devastating disease process. METHODS: A retrospective analysis of early and long-term results in a series of 44 consecutive patients (34 men, 10 women, median age 46.5, range 13-74 years) who underwent necrosectomy for severe necrotising pancreatitis. In 16 patients necrosectomy and primary abdominal closure with drains was performed, 14 patients had planned staged necrosectomy and delayed abdominal closure with drains, and in 14 patients necrosectomy with open laparostomy was undertaken. RESULTS: There were 8 deaths (18%) and 14 cases (32%) of significant hospital morbidity (fistula 10, pseudocyst 2, renal failure 2). Variables which correlated with mortality were: high APACHE II score, acute renal failure requiring dialysis, and requirement for surgical intervention at an early stage (within the first two weeks). A total of 28 late complications occurred in 21 of the surviving patients (endocrine pancreatic insufficiency 10, exocrine pancreatic insufficiency 2, pseudocyst 2, chronic renal failure 2, incisional hernia 10, recurrent pancreatitis 1, and chronic pain 1). CONCLUSIONS: Low mortality can be achieved in patients with severe necrotizing pancreatitis with aggressive surgical intervention and careful perioperative management. Long-term morbidity remains high, and emphasises the need for prolonged follow-up.