Semin Thromb Hemost 2014; 40(08): 874-880
DOI: 10.1055/s-0034-1395155
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

A Short Contemporary History of Disseminated Intravascular Coagulation

Marcel Levi
1   Department of Medicine, University of Amsterdam, Amsterdam, The Netherlands
,
Tom van der Poll
1   Department of Medicine, University of Amsterdam, Amsterdam, The Netherlands
2   Center for Experimental and Molecular Medicine, University of Amsterdam, Amsterdam, The Netherlands
3   Center for Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
› Author Affiliations
Further Information

Publication History

Publication Date:
06 November 2014 (online)

Abstract

Disseminated intravascular coagulation (DIC) is a syndrome characterized by systemic intravascular activation of coagulation, leading to a 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). The syndrome of DIC is well known in the medical literature for centuries, although a more precise description of the underlying mechanisms had to await the 20th century. Initial ideas on a role of the contact activation system as the primary trigger for the systemic activation of coagulation as well as a presumed hyperfibrinolytic response in DIC have been found to be misconceptions. Experimental and clinical evidence now indicate that the initiation of coagulation in DIC is caused by tissue factor expression, which in combination with downregulated physiological anticoagulant pathways and impaired fibrinolysis leads to widespread fibrin deposition. In addition, an extensive bidirectional interaction between coagulation and inflammation may further contribute to the pathogenesis of DIC.

 
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