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Disseminated intravascular coagulation (DIC) is characterized by systemic activation of the haemostasis. In many instances the release of inflammatory cytokines and tissue factor trigger the system in septic or traumatic conditions. Initially, the increased activation of haemostasis can be compensated by natural inhibitor systems. As release of the triggers persists, inhibitors (e.g. antithrombin and protein C) will be consumed leading to intravascular clotting. In this process many coagulation factors, most notably fibrinogen and platelets are consumed too, resulting in a failure of haemostasis system and in a diffuse bleeding (decompensated DIC). Fresh frozen plasma, blood transfusion, and fibrinogen concentrate correct the bleeding, if needed, in the case of traumatic (obstetric) DIC. Arrest of the activated haemostasis by heparin and natural anticoagulants (antithrombin or/and protein C) is recommended, mainly in septic conditions with systemic inflammatory reactions. A case of stercoral sepsis usefully treated by recombinant human activated protein C is reported.

Patients with severe sepsis are at increased risk for developing thrombembolic phenomena. This article aims to clarify the association between systemic inflammation activation and coagulation, pathogenesis of coagulation abnormalities during severe sepsis. The article reviews incidence and deep venous thrombosis risk factors among these patients and summarizes recent evidence-based guidelines for deep venous thrombosis prophylaxis.