Immunomodulation in the Critically Ill Surgical Patient
The critically ill surgical patient is at high risk for immune dysfunction. Severe stress states (such as multiple trauma and sepsis) produce a deleterious, potentially lethal, immunologic dichotomy. The uncontrolled disseminated activation of the normally protective immunoinflammatory cascades produces a “malignant systemic inflammation” that leads to diffuse multiple organ bystander injury, progressive organ dysfunction, and ultimate sequential organ failure referred to as multiple organ failure syndrome (MOFS) [1–3]. Concomitantly, this “malignant systemic inflammation” induces a simultaneous prolonged and excessive down-regulatory and ultimately immunosuppressive response. In addition, the diffuse activation of these inflammatory cascades leads to a consumptive depletion of the normal protective mechanisms of the immune system. Thus, the appropriate immunomodulation of the critically ill patient will not only prevent MOFS but also maintain normal host defense mechanisms and prevent nosocomial infections, which further induce the malignant systemic inflammatory response, and ultimate organ failure. A major challenge at present is the inability to identify the most critical abnormal components of the immunologic response present in the critically ill patient.
KeywordsToxicity Ischemia Glutathione Interferon Arginine
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