The effect of critical illness on the gut

The mucosal cells of the gastrointestinal tract have one of the highest turnover rates of any body tissue. Endothelial renewal depends on the division and migration of stem cells within the mucosal crypts. Therefore an intact gut mucosa depends on a balance between cell renewal and exfoliation. The intact mucosal layer, tight junctions between cells, lymphocytes, macrophages, and neutrophils in the submucosa and Peyer's patches, and gut-generated IgA all contribute to barrier function of the gut (Thompson ...1995).

A fall in perfusion and tissue oxygenation, which occurs in many forms of critical illness, is a significant insult to the gut. Splanchnic hypoperfusion may persist after apparently adequate fluid resuscitation, and even short periods of circulatory compromise may result in prolonged gut ischemia/hypoxia. This may cause cell injury, necrosis, and loss of mucosal integrity, a state which may be exacerbated by coexisting malnutrition, bacterial overgrowth of the gut, and (possibly) reperfusion injury following periods of hypovolemia and hypotension.

Bacterial translocation (the migration of viable bacteria across the intestinal barrier to the liver, spleen, or mesenteric lymph nodes) and endotoxin translocation may occur following loss of barrier function. When such processes occur to a limited extent, which may be an everyday event, the Kupffer cells in the liver prevent spill-over into the systemic circulation. When there is a major deficiency in gut barrier function, systemic spill-over occurs because (i) the liver is overwhelmed by the amount of bacteria and/or endotoxin presented to it and (ii) often the cause of gut barrier failure (e.g. hypoperfusion) will also induce hepatic dysfunction, preventing efficient phagocytosis of bacteria and removal of endotoxin in portal blood.

Organisms which breech the mucosal element of the gut barrier may be phagocytosed by macrophages and transported to the mesenteric lymph nodes. Again, if the microbial load is excessive, these micro-organisms may reach the circulation via the lymph system. The presence of circulating endotoxin has itself been found to increase intestinal permeability in healthy humans.

Bacterial translocation has been implicated in the pathogenesis of multiple organ dysfunction in animal models of critical illness, but the clinical significance in humans is less clear. The overgrowth of pathogens in the upper gastrointestinal tract of critically ill patients may be followed by multiple organ failure in the majority. However, other work suggests no significant portal bacteremia after major trauma and no correlation between increased intestinal permeability and infective complications.

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