Table 2 Pathogenesis of disseminated intravascular coagulation in sepsis.
Mechanism | Pathophysiology |
|---|---|
1) Increased thrombin generation | Mediated predominantlyby tissue factor/factor VIIa pathway |
2) Impaired function of physiological anticoagulant pathway | Â |
   a) Reduction of antithrombin levels | The result of a combination of increased consumption, enzyme degradation, impaired liver synthesis and vascular leakage |
   b) Depression of protein C system | The result of a combination of increased consumption, impaired liver synthesis, vascular leakage and down- regulation of thrombomodulin |
   c) Insufficienttissue factor pathway inhibitor (TFPI) |  |
3) Impaired fibrinolysis | Mediated by release of plasminogen activators from endothelial cells immediately followed by an increase in the plasma levels of plasminogen activator inhibitor type 1 (PAI-1) |
4) Activation of inflammatory pathway | Mediated by activated coagulation proteins and by depression of the protein C system |