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Disseminated Intravascular Coagulation in Sepsis*

Sacha Zeerleder, MD; C. Erik Hack, MD, PhD; Walter A. Wuillemin, MD; PhD
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Affiliations: *From the Central Hematology Laboratory (Dr. Zeerleder), University Hospital, Berne, Switzerland; Department of Clinical Chemistry (Dr. Hack), VU University Medical Center, Amsterdam, the Netherlands; and Divison of Hematology and Central Hematology Laboratory (Dr. Wuillemin), Kantonsspital, Lucerne, Switzerland.,  Currently at Crucell N.V., Leiden, the Netherlands.

Correspondence to: Walter A. Wuillemin, MD, PhD, Division of Haematology and Central Hematology Laboratory, Kantonsspital, 6000 Luzern-16, Switzerland; e-mail: walter.wuillemin@KSL.ch



Chest. 2005;128(4):2864-2875. doi:10.1378/chest.128.4.2864
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Disseminated intravascular coagulation is a frequent complication of sepsis. Coagulation activation, inhibition of fibrinolysis, and consumption of coagulation inhibitors lead to a procoagulant state resulting in inadequate fibrin removal and fibrin deposition in the microvasculature. As a consequence, microvascular thrombosis contributes to promotion of organ dysfunction. Recently, three randomized, double-blind, placebo-controlled trials investigated the efficacy of antithrombin, activated protein C (APC), and tissue factor pathway inhibitor, respectively, in sepsis patients. A significant reduction in mortality was demonstrated in the APC trial. In this article, we first discuss the physiology of coagulation and fibrinolysis activation. Then, the pathophysiology of coagulation activation, consumption of coagulation inhibitors, and the inhibition of fibrinolysis leading to a procoagulant state are described in more detail. Moreover, therapeutic concepts as well as the three randomized, double-blind, placebo-controlled studies are discussed.

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