Localised and following systemic inflammatory reaction accompanying progression of infection causes generation of anti-inflammatory cytokines. They activate leucocytes, endothelium, coagulation and fibrinolysis. Sepsis is usually accompanied by already decompensated disseminated intravascular coagulation which significantly affects mortality of patients with this disease. The main cause of hypercoagulation state during sepsis seems to be inhibition of fibrinolysis as a result of overproduction of plasminogen activator inhibitor-1 in later stages of the disease. Some microorganisms have specific properties which affect individual components of hemostasis and thus increase their virulence. Because natural inhibitors of coagulation have not only anticoagulation but also strong anti-inflammatory effect, they seem to be an optimum remedy for fluorid coagulopathy during sepsis. Moreover, their use usually does not increase risk of bleeding.

Keywords: Blood Coagulation; Blood Coagulation Disorders /complications/; Cytokines /physiology/; Disseminated Intravascular Coagulation /blood/; Endothelium, Vascular /physiopathology/; Fibrinolysis; Hemostasis; Humans; Prothrombin /physiology/; Sepsis /blood/