Disseminated Intravascular Coagulation



DIC represents the consumption of coagulation factors resulting from intravascular activation of the coagulation process with secondary activation of fibrinolysis. Depending upon the rates of these two processes, the compensatory synthesis of pro-coagulants, and the nature of the underlying dis­ease, DIC may cause either thrombosis or hem­orrhage. DIC is always secondary to another disease process and often resolves when the pri­mary disease is controlled. Intravascular coagu­lation is initiated by release of procoagulant sub­stances into the blood (amniotic fluid embolism, snakebite, abruptio placenta, malignancy, crush injury), by contact of blood with an abnormal sur­face (infections, burns, extracorporeal circulation, grafts), or by generation of procoagulants in the blood (promyelocytic leukemia, hemolytic trans;, fusion reactions). The formation of mierothrombyj within the circulation secondarily activates fibri-jj nolysis, as does the presence of injured endothej? Hum. Circulating plasmm may’further deplete’ Factors V and VIII and cleave fibrinogen. The deg* radation products of both’fibrinogen and fibrin’ (formed by thrombin or plasmin action) act as cir’^’ culating anticoagulants, delay fibrin polymeriza^ tion, and impair platelet function.




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coagulation factors