Impact intestinal du choc septique

Severe and prolonged states of catabolic stress like septic shock have been shown to have profound effects on the intestinal function. Gut-derived sepsis is a term to describe a state of systemic inflammation with organ dysfunction after catabolic stress hypothesized to be initiated and perpetuated by the intestinal tract. The intestinal epithelium has various immunological and non-immunological components. This epithelium maintains a physical barrier to prevent microbial invasion while modulating an immune component, which activates host defenses to eliminate invading pathogens. The gastrointestinal tract and its associated mesenteric lymphatics present the body's largest absorptive surface that is exposed to foreign antigens, microbes and other injurious elements. The failure of the intestinal barrier is primarily characterized by impaired nutriments absorption, compromised intestinal immunologic response and increased intestinal permeability. The increase in intestinal mucosa permeability is triggered by a set of changes such as oxidative stress, inflammatory response, reduction of intramucosal pH and hypoxia. Alteration in all of the components of the intestinal barrier has been reported to be responsible for bacterial and toxin translocation. Despite the attractive hypotheses, no clinical studies have shown that bacterial translocation correlates with the incidence of septic complications or mortality. Gut ischemia reperfusion is an important initiating factor in the alteration in mucosal permeability. The gut then becomes a significant source of inflammatory mediators upon reperfusion. The dual functions of selective absorption and constant protection make the gastrointestinal tract both critical to the body's functioning and vulnerable to infection and multi-organ dysfunction in situations of septic shock. The gastrointestinal tract should be considered in physiopathologic hypothesis and therapeutic management in septic patient.