Coagulation in Sepsis

Activation of inflammatory and coagulation pathways is an important event in the pathogenesis of sepsis. In sepsis, which can be defined as the disadvantageous systemic host response to infection, the blood coagulation system is triggered. Activation of coagulation and deposition of fibrin as a consequence of inflammation can be considered instrumental in containing inflammatory activity to the site of infection. However, inflammation-induced coagulation may be detrimental in those circumstances when the triggered blood coagulation system is insufficiently controlled, which can lead to the clinical syndrome of disseminated intravascular coagulation (DIC) and microvascular thrombosis. In recent years, the vital roles of several elements of the hemostatic mechanism have, in part, been unraveled, including those of tissue factor, thrombin, protease-activated cell receptors (PARs), and activated protein C (APC). Clinical trials of recombinant anticoagulants for sepsis have been conducted, of which only recombinant human APC reduced the 28-day mortality of sepsis patients.