Bacterial translocation: clinical implications and prevention

Abstract

The occurrence of BT has been well documented in experimental animal models of hemorrhagic shock, trauma, severe burns, cirrhosis, pancreatitis, and bacterial overgrowth. Translocation of viable bacteria and endotoxins into mesenteric lymph nodes and other gut-associated lymphatic tissue is thought to activate a complex interplay of mediators that initiates the SIRS. Multiple humoral and cellular systems cause synthesis, expression, and release of inflammatory mediators, such as toxic oxygen radicals, proteolytic enzymes, adherence molecules, and various cytokines. A massive sustained proinflammatory response can ultimately result in irreversible multiple organ dysfunction. Because BT is associated with splanchnic hypoperfusion, the cornerstone of therapy involves rapid resuscitation and restoration of tissue perfusion. If a septic focus can be identified, it should be removed. Gut protectants, promotility agents, antioxidants, and immune-enhancing diets have shown promise in improving length of survival in these critically ill patients.