The horror autotoxicus and multiple-organ failure

Abstract

An injury or operation with tissue injury, ischemia, and sepsis provokes a neuroendocrine, immune, and inflammatory response to promote survival and heal the wound. If the injury is massive or complicated by infection, the inflammatory response may become generalized and excessive, producing organ and tissue damage and multiple-organ failure, a modern "horror autotoxicus." Many inflammatory mediators have been identified. In isolated organs, the use of blocking mediators to prevent combined ischemia-reperfusion injury is feasible. With regional ischemia, activator attenuation may be possible. It is unclear whether blockade or modulation of all or part of an excessive inflammatory response will be possible, helpful, and without hazard in patients with multisystem injuries or sepsis. Feedback loops and control mechanisms of these systems will better define such possibilities. Employment of growth factors and other protective agents to stimulate wound healing, infection control, and host resistance may be more helpful. Ultimately, prevention of multiple-organ failure requires sound surgical judgment, techniques, and organ support.