Bacterial translocation: clinical implications and prevention

摘要

The occurrence of bacterial translocation has been well documented in experimental animal models. 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 systemic inflammatory response syndrome. Multiple humoral and cellular systems cause synthesis, expression, and release of inflammatory mediators. A massive sustained proinflammatory response can ultimately result in irreversible multiple organ dysfunction. Because bacterial translocation 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.