Disseminated Intravascular Coagulation

SUMMARY Disseminated intravascular coagulation (DIC) is a syndrome characterized by systemic intravascular activation of coagulation, leading to widespread deposition of fibrin in the circulation. There is compelling evidence from clinical and experimental studies that DIC is involved in the pathogenesis of microvascular dysfunction and contributes to organ failure. In addition, the massive and ongoing activation of coagulation may result in depletion of platelets and coagulation factors, thereby causing bleeding. Recent insight into important pathogenetic mechanisms that may lead to DIC has resulted in novel preventive and therapeutic approaches to patients with sepsis and a derangement of coagulation. Thrombin generation proceeds via the (extrinsic) tissue factor/factor VIIa route and simultaneously occurring depression of inhibitory mechanisms, such as antithrombin III and the protein C system. Also, impaired fibrin degradation, due to high circulating levels of type 1 plasminogen activator inhibitor (PAI‐1), contributes to enhanced intravascular fibrin deposition. Supportive strategies aimed at the inhibition of coagulation activation may theoretically be justified and have been found to be beneficial in experimental and initial clinical studies. These strategies include inhibition of tissue factor‐mediated activation of coagulation or restoration of physiological anticoagulant pathways via the administration of antithrombin concentrate or recombinant human activated protein C.