Abstract

Critically ill patients, especially those suffering from sepsis, frequently present with disturbances in the coagulation system, varying from mild prolongation of coagulation tests and low platelet counts, to more severe conditions like disseminated intravascular coagulation. Indeed, sepsis is characterized by a systemic inflammatory response, resulting in a shift of the haemostatic balance towards a procoagulant and antifibrinolytic state. Both activation of coagulation and relative insufficiency of the natural anticoagulant systems, cause enhanced fibrin formation, while on the other hand fibrin degradation is impaired due to inhibition of fibrinolysis. Thus, in the course of sepsis, systemic fibrin depositions are greatly promoted. These clotting disturbances are largely influenced by proinflammatory cytokines, such as tumor necrosis factor alpha (TNF) and various interleukins (ILs). IL-6 exerts its procoagulant effects by stimulating the expression of tissue factor, the main initiator of the coagulati...

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