Conclusions

Multiple organ failure is the consequence of many pathological processes, of which an acute reduction in oxygen supply is one of the most important. The splanchnic region is particularly susceptible to hypoxic injury, and the ischemic gut mucosa may act as a neutrophil activating site. This is followed by leukocyte adhesion to endothelium and migration into the tissues where cytotoxic chemicals are released, producing tissue injury. This process is aggravated by multiple and sequential physiological insults, some of which may not be identified using basic clinical monitoring. The factors which precipitate cell injury and organ failures may be amenable to relatively simple preventative interventions, but once damage has occurred the process becomes increasingly complex and self-sustaining. Natural defense systems may become pathologically hyperactive, or suppressed, at different stages in critical illness, making it difficult to target therapies directed at the immunoinflammatory casade with any degree of accuracy or safety. This may explain in part the failure of immunotherapy for sepsis.

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