A short contemporary history of disseminated intravascular coagulation

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 orga...

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Veröffentlicht in:Seminars in thrombosis and hemostasis Jg. 40; H. 8; S. 874
Hauptverfasser: Levi, Marcel, van der Poll, Tom
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.11.2014
Schlagworte:
Blood Coagulation
Disseminated Intravascular Coagulation - blood
Disseminated Intravascular Coagulation - etiology
Disseminated Intravascular Coagulation - history
History, 20th Century
History, 21st Century
Humans
Thromboplastin - metabolism
Thrombosis - etiology
ISSN:1098-9064, 1098-9064
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Zusammenfassung: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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ISSN:1098-9064
1098-9064
DOI:10.1055/s-0034-1395155