• Marcel Levi.
• Department of Vascular and Internal Medicine (F-4), Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. m.m.levi@amc.uva.nl
• Crit Care Clin. 2005 Jul 1;21(3):449-67.

AbstractDisseminated intravascular coagulation (DIC) is a syndrome characterized by a systemic activation of coagulation leading to the intravascular deposition of fibrin in the (micro) vasculature and the simultaneous consumption of coagulation factors and platelets. The occurrence of microvascular thrombosis as a consequence of DIC is underscored by pathological, experimental and clinical findings, demonstrating a link between DIC and organ dysfunction. Pathogenetic pathways that play a role in the development of DIC include tissue factor-dependent activation of coagulation, defective physiological anticoagulant pathways (such as the antithrombin system and the protein C system), and impaired fibrinolysis, caused by elevated levels of plasminogen activator inhibitor type 1. Novel therapeutic strategies are based on current insights into the pathogenesis of DIC, and include anticoagulant strategies (eg, directed at tissue factor) and strategies to restore physiological anticoagulant pathways (such as activated protein C concentrate).

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