Semin Thromb Hemost 2001; 27(6): 569-576
DOI: 10.1055/s-2001-18862
Copyright © 2001 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Advances in the Understanding of the Pathogenetic Pathways of Disseminated Intravascular Coagulation Result in More Insight in the Clinical Picture and Better Management Strategies

Marcel Levi1,2 , Evert de Jonge3 , Tom van der Poll2,4 , Hugo ten Cate1,5
  • 1Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam
  • 2Department of Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam
  • 3Department of Intensive Care, Academic Medical Center, University of Amsterdam, Amsterdam
  • 4The Laboratory of Experimental Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
  • 5Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
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Publication History

Publication Date:
06 December 2001 (online)

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ABSTRACT

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 ample experimental and pathological evidence that the fibrin deposition contributes to multiple organ failure. The massive and ongoing activation of coagulation may result in depletion of platelets and coagulation factors, which may cause bleeding (consumption coagulopathy). Recent knowledge on important pathogenetic mechanisms that may lead to DIC has resulted in novel preventive and therapeutic approaches to patients with DIC. DIC is not a disease in itself but is a complication of a variety of disorders. However, the pathogenesis of DIC follows similar pathways in almost all of these situations, with a pivotal role of proinflammatory cytokines. 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 may theoretically be justified and have been found to be beneficial in experimental and initial clinical studies. These strategies comprise inhibition of tissue factor-mediated activation of coagulation and restoration of physiological anticoagulant pathways by means of the administration of (activated) protein C concentrate or antithrombin concentrate.

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