Also referred to as consumptive coagulopathy, DIC involves the homeostatic imbalance between coagulation and bleeding. Tissue factor, which may be released into the circulation from vascular endothelial damage from trauma or certain cancer treatments, bacterial endotoxins, or cytokine exposure, activates coagulation factor VII to VIIa in the coagulation pathway. Via the extrinsic pathway, thrombin and fibrin are formed, forming clots in the circulation. As this process continues, thrombin and fibrin further impair the coagulation cascade through positive feedback loop stimulation and coagulation inhibitor consumption. Clotting factors, as a result, are consumed due to clotting, which can lead to excessive bleeding. Platelets may also become trapped and consumed during this process. Additionally, pathways, including the protein C system and antithrombin III, appear dysregulated in DIC. Furthermore, an increase in plasma activator inhibitor-1 can prevent the inhibition of fibrinolysis.[5][11]
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