Bacterial Translocation, Gut Barrier Function and Nutritional Support

Abstract

Most reviewers of nutritional support therapy advocate the use of enteral (as opposed to parenteral) nutrition. After all, it is said, enteral nutrition (EN) maintains gut function, is safer and cheaper. Parenteral nutrition, in contrast, results in mucosal atrophy and increased intestinal permeability, which reflect damage to the intestinal barrier. This predisposes to bacterial translocation and septic morbidity. So common have these comments about parenteral nutrition become that they are almost accepted as a universal truth. They are often stated without qualification in reviews of nutritional support therapy, in standard texts and even in training manuals for postgraduate study. This ‘gut origin of sepsis’ hypothesis as an explanation for increased septic morbidity in patients receiving total parenteral nutrition (TPN) presupposes that bacterial translocation does occur in man and is associated with increased incidences of sepsis. Furthermore, the hypothesis assumes that an absence of luminal nutrients (as may occur during starvation, malnutrition or parenteral nutrition) is associated with deleterious consequences to the gut barrier which predispose to translocation, and finally that septic morbidity is proven to be significantly higher in patients receiving TPN.