文摘
Disseminated intravascular coagulation (DIC) is a syndrome characterized by systemic intravascular activation of coagulation, leading to widespread deposition of fibrin in the circulation. Recent knowledge on important pathogenetic mechanisms that may lead to DIC has resulted in novel preventive and therapeutic approaches to patients with this condition. Thrombin generation in DIC proceeds via the (extrinsic) tissue factor/factor VIIa route and simultaneously occurring depression of inhibitory mechanisms, such as antithrombin and the protein C system. Also, impaired fibrin degradation, due to high circulating levels of PAI-1, contributes to enhanced intravascular fibrin deposition. Coagulation may have a profound modulatory effect on inflammatory pathways as well. The diagnosis of DIC can be made by sensitive laboratory tests, however, most of these tests are not readily available in a routine setting. A reliable diagnosis can also be made on the basis of a small series of routine lab tests that can be combined in a scoring algorithm (ISTH-DIC score). The cornerstone of the management of DIC is the specific and vigorous treatment of the underlying disorder. Strategies aimed at the inhibition of coagulation activation or restoration of anticoagulant pathways have been found beneficial in experimental and initial clinical studies but their effect on clinically relevant outcomes is less clear.