Gastric colonisation, intestinal permeability and septic morbidity in acute pancreatitis

Bacterial translocation (BT) may represent an important cause of septic morbidity in patients with acute pancreatitis. We have previously demonstrated an association between BT, septic morbidity and colonisation of the proximal GI tract. Alterations in intestinal permeability (IP) may also predispose to BT. The aim of this study was to assess the extent of gastric colonisation, measure IP in patients with acute pancreatitis and relate these to both disease severity and septic complications.

Gastric colonisation was determined by culturing a sample of nasogastric aspirate, and IP was measured using a dual sugar probe technique (lactulose/rhamnose test). Disease severity was assessed according to the modified Glasgow (Imrie) criteria. All septic complications were recorded prospectively.

A total of 59 patients were studied (M:F ratio 32:27, median age 66 years, range 18-89), 24 (31%) of whom had severe disease. A nasogastric aspirate was obtained in 56 patients. There was a significantly higher incidence of colonisation with potentially pathogenic enteric bacteria in patients with severe disease compared to those with mild disease (57 vs. 6%, p < 0.001). Septic morbidity occurred in 29% of severe patients and 11% mild patients (p = 0.17). 33% of patients colonised with enteric organisms developed sepsis, compared to 16% with no enteric bacteria in the NG aspirate (p = 0.34). Enteric bacteria caused 77% of the septic complications. Intestinal permeability was neither associated with disease severity nor was it predictive of septic morbidity.

There is significantly higher incidence of gastric colonisation with enteric bacteria in patients with severe acute pancreatitis, but no difference in IP. Enteric bacteria were implicated in the majority of septic complications. These findings support the gut origin of sepsis hypothesis in acute pancreatitis.