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.
Department of Surgery, University of Minnesota Hospital and Clinic, Minneapolis.
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MD
Cipolle
M D
MD
Pasquale
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FB
Cerra
D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D003422:Critical Care; D016207:Cytokines / Q000502:physiology; D015777:Eicosanoids / Q000502:physiology; D004734:Energy Metabolism; D006801:Humans; D007249:Inflammation; D009102:Multiple Organ Failure / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy; D009569:Nitric Oxide; D010972:Platelet Activating Factor / Q000502:physiology; D017382:Reactive Oxygen Species; D012151:Resuscitation; D012307:Risk Factors; D012720:Severity of Illness Index; D015996:Survival Rate
D000911:Antibodies, Monoclonal; D016207:Cytokines; D015777:Eicosanoids; D010972:Platelet Activating Factor; D017382:Reactive Oxygen Species; D009569:Nitric Oxide