Current Drug Treatment Strategies for Disseminated Intravascular Coagulation
- Evert de JongeAffiliated withDepartment of Intensive Care, Academic Medical Center, University of Amsterdam Email author
- , Marcel LeviAffiliated withCenter for Haemostasis, Thrombosis, Atherosclerosis and Inflammation Research, Academic Medical Center, University of Amsterdam
- , Christiaan P. StoutenbeekAffiliated withDepartment of Intensive Care, Academic Medical Center, University of Amsterdam
- , Sander J. H. van DeventerAffiliated withDepartment of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam
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Disseminated intravascular coagulation (DIC) can be caused by a variety of diseases. Experimental models of DIC have provided substantial insight into the pathogenesis of this disorder, which may ultimately result in improved treatment. Disseminated coagulation is the result of a complex imbalance of coagulation and fibrinolysis. Simultaneously occurring tissue factor-dependent activation of coagulation, depression of natural anticoagulant pathways and shutdown of endogenous fibrinolysis all contribute to the clinical picture of widespread thrombotic deposition in the microvasculature and subsequent multiple organ failure.
Cornerstone for the treatment of DIC is the optimal management of the underlying disorder. At present, specific treatment of the coagulation disorders themselves is not based on firm evidence from controlled clinical trials. Plasma and platelet transfusion are used in patients with bleeding or at risk for bleeding and low levels of coagulation factors or thrombocytopenia. The role of heparin and low molecular weight heparin is controversial, but their use may be justified in patients with active DIC and clinical signs of extensive fibrin deposition such as those with meningococcal sepsis. There is some evidence to indicate that low molecular weight heparin is as effective as unfractionated heparin but may be associated with a decreased bleeding risk.
Antithrombin III (AT III) replacement appears to be effective in decreasing the signs of DIC if high doses are administered, but effects on survival or other clinically significant parameters are at best uncertain. If AT III supplementation is used, the dosage should be selected to achieve normal or supranormal plasma levels of 100% or higher. Results of studies on protein C concentrate, thrombomodulin or inhibitors of tissue factor are promising, but the efficacy and safety of these novel strategies remains to be established in appropriate clinical trials.
- Current Drug Treatment Strategies for Disseminated Intravascular Coagulation
Volume 55, Issue 6 , pp 767-777
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- 1. Department of Intensive Care, Academic Medical Center, University of Amsterdam, P.O. Box 22660, 1100 DD, Amsterdam, The Netherlands
- 2. Center for Haemostasis, Thrombosis, Atherosclerosis and Inflammation Research, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
- 3. Department of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands