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Sepsis and disseminated intravascular coagulation
Marcel Levi1, Evert de Jonge, Tom van der Poll
1Department of Internal Medicine/Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. m.m.levi@amc.uva.nl
Journal of Thrombosis and Thrombolysis
|February 5, 2004
Summary
Sepsis frequently causes coagulation disorders like disseminated intravascular coagulation (DIC), leading to organ failure. Novel therapies targeting coagulation activation show promise in managing sepsis-induced hemostatic abnormalities.
Area of Science:
- Critical Care Medicine
- Hematology
- Pathophysiology
Background:
- Sepsis commonly induces hemostatic abnormalities, ranging from mild changes to severe disseminated intravascular coagulation (DIC).
- DIC plays a crucial role in sepsis-induced microvascular dysfunction and organ failure.
- Coagulation activation in sepsis can lead to depletion of platelets and clotting factors, resulting in bleeding complications.
Purpose of the Study:
- To review recent insights into the pathogenetic mechanisms of sepsis-induced DIC.
- To discuss novel preventive and therapeutic strategies for managing coagulation derangements in sepsis.
Main Methods:
- Review of clinical and experimental studies on sepsis and hemostasis.
- Analysis of pathogenetic mechanisms including the tissue factor/factor VIIa route, impaired anticoagulant pathways (antithrombin III, protein C), and fibrin degradation.
- Evaluation of supportive strategies targeting coagulation activation.
Main Results:
- Thrombin generation involves the extrinsic pathway and is exacerbated by suppressed inhibitory mechanisms.
- High levels of plasminogen activator inhibitor-1 (PAI-1) impair fibrinolysis, promoting intravascular fibrin deposition.
- Experimental and initial clinical studies suggest benefits from inhibiting coagulation activation or restoring anticoagulant pathways.
Conclusions:
- Understanding sepsis-induced DIC pathogenesis has led to new therapeutic approaches.
- Strategies inhibiting coagulation activation or restoring physiological anticoagulation show potential.
- Inhibition of tissue factor or administration of antithrombin/activated protein C are promising supportive therapies.