Bacterial translocation

In addition to digestion and absorption of nutrients, a major function of the gastrointestinal tract is to serve as a barrier to microbial invasion of the host and to prevent systemic dissemination of bacterial toxins. During critical illness the gut barrier fails, allowing toxins and viable bacteria to escape the intestine and gain access to the circulation, primarily via mesenteric lymphatics and the portal circulation, leading to bacterial translocation. A number of components, including a normal enteric microflora and intestinal pH, enteral feeding, intraluminal secretion of immunoglobulin A, and clearance of escaping organisms by the reticuloendothelial system, contribute to the function of the gut as a barrier against intestinal microbial invasion of the host. A variety of direct and indirect insults to the gastrointestinal tract may lead to loss of effective barrier function. Increased intestinal permeability and the translocation of bacteria, endotoxin, or other toxins may then ensue.

Evidence for translocation in humans is largely circumstantial. Trauma patients in shock have bacteremia and endotoxemia in the absence of injury to a hollow viscus. Clinical reports suggest increased intestinal permeability after burns and sepsis, and increased permeability has been reported after endotoxemia in volunteers. Concern about nosocomial pneumonia in ICU patients has led to experiments to determine whether suppression of intestinal bacterial overgrowth will diminish this risk. Selective antibiotic decontamination of the digestive tract has been advocated to accomplish this goal; however, it lacks a defined role.

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