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Acute pancreatitis can be a mild, transitory illness or a severe, rapidly fatal disease. About 80% of cases of the disease are acute interstitial oedematous pancreatitis which has a low morbidity and mortality rate (<1%) and roughly 20% of patients with acute pancreatitis develop necrosis of pancreatic and peripancreatic tissues. The course of severe acute pancreatitis may include an early vasoactive and toxic phase, and a late period dominated by septic complications. Improved intensive care treatment can reduce the early cardiorespiratory and renal complications related to systemic inflammatory response syndrome (SIRS).1 ,2 Pancreatic infection is reported to develop in 40–70% of patients with necrotising pancreatitis and is the main life threatening complication of the disease; furthermore, consecutive sepsis and sepsis related multiple organ failure are responsible for a mortality rate of up to 50%.3-5 In the early phase of acute pancreatitis, a broad range of specific treatment modalities have been evaluated, but all have proved ineffective.6-8 Therefore, interest has focussed on the prophylactic administration of antibiotics. The use of antibiotic treatment is based on the rationale that reduction of pancreatic infection will decrease late morbidity and mortality. However, the beneficial effects of antibiotic prophylaxis are still controversial.
Possible pathways for pancreatic infection
There are several hypothetical mechanisms by which bacteria may enter pancreatic and peripancreatic necrosis (fig 1): the haematogenous route via the circulation9 ,10; transmural migration through the colonic bowel wall either to the pancreas (translocation),11 via ascites to the pancreas,9 ,12 ,13 or via the lymphatics to the circulation12 ,14; via the biliary duct system15 ,16; from the duodenum via the main pancreatic duct.11 ,17
Animal studies have shown spontaneous bacterial infection of the pancreas.19 …