Pancreatitis and nutrition. The role of the gut and nutrition for septic complications

Septic complications are an important factor for the morbidity and mortalit y of acute pancreatitis. The gut has been identified as a source of infecti on early in the course of the disease allowing intestinal bacteria to trans locate into pancreatic necrosis and other organs. Bacterial translocation i s promoted by an impaired intestinal mucosal barrier which can be attribute d to the reduced oxygen and substrate supply of the intestine during the ea rly systemic response to the pancreatic injury. A rat model of severe acute pancreatitis has been used to confirm the hypothesis that an impaired muco sal barrier can be stabilized by supplying certain nutritients, vitamins an d trace elements. Following a discussion of the many aspects of bacterial t ranslocation and gut derived sepsis, the role of the gut and nutrition for the development of septic complications in acute pancreatitis is summarized as follows: Early in the course of acute pancreatitis the gut is a target organ of the primary systemic inflammatory response (SIRS) to pancreatic in jury. SIRS-induced gut barrier dysfunction promoting bacterial translocatio n makes the gut the motor for secondary (septic) complications. As a septic focus the gut becomes a target for therapeutic measures aimed at stabilizi ng the impaired gut barrier. Nutritive factors demonstrated to improve impa ired gut barrier function include early enteral feeding and specific factor s like glutamine which are essential for enterocytes and colonocytes in str ess. Experimental data are presented to underline the significance of these nutritive factors and subsequent randomized multicenter trials performed t o verify the positive experimental results are introduced. The effect of ot her nutritive factors (e.g. omega-3-fatty acids) has not yet been systemica lly investigated. Thus, experimental and clinical studies need to be perfor med for evaluating their effect on bacterial translocation and the disease course in acute pancreatitis.