Secondary organ dysfunction. From clinical perspectives to molecular mediators.

The systemic inflammatory response and progression to secondary organ dysfunction are manifestations of the host's responses to injury. This article outlines the clinical manifestations of this injury-response cascade. The potential roles of cytokines, eicosanoids, platelet-activating factor, nitric oxide, oxygen-free radicals, and the leukocyte-endothelial interaction are explored in some detail. A goal-directed therapy of source control, resuscitation, and metabolic support is reviewed, and new therapies with monoclonal antibodies and immunomodulated nutrition are described. These new therapies hold great potential for finally improving the outcome of this fatal syndrome.