The Effect of Heparin and Its Preparations on Disseminated Intravascular Coagulation Mortality and Hospitalization: A Systematic Review

Figure 1

Pathogenetic pathways in DIC. Activation of coagulation is driven by TF overexpression leading to explosive and disseminated thrombin generation, which results in the consumption of natural coagulation inhibitors (mainly AT and PC) and in a hypercoagulable state. Thrombin, among other inducers, enhances platelet activation. Activated platelets amplify hypercoagulable state. Inhibition of fibrinolysis, through TAFI activation, increases fibrin formation and deposition in the microvasculature. This mechanism—among others—is implicated in the pathogenesis of organ dysfunction and multiorgan failure. Sustained thrombin generation has, as a consequence, the consumption of clotting factors, platelets, and fibrinogen. Severe clotting factor and fibrinogen deficiency together with severe thrombocytopenia are in the origin of the hemorrhagic syndrome in DIC. AT: antithrombin; DIC: disseminated intravascular coagulation; PC: protein C; and TF: tissue factor.