EUH Dressler Conference: What is the pathophysiology of disseminated intravascular coagulation (DIC)?

The Bottom Line: DIC is a systemic pathophysiologic process and not a single disease entity. The massive tissue factor stimulus results in excess intravascular thrombin, which overcomes the anticoagulant systems and leads to thrombosis. Because of consumption of coagulation factors and platelets, DIC also has a hemorrhagic phase. Treatment of the bleeding patient with DIC is supportive with the use of blood components. Some conditions associated with acute DIC include septic shock, exsanguinating trauma, burns, or acute promyelocytic leukemia.

Reference: Boral BM, Williams DJ, Boral LI. Disseminated intravascular coagulation. American Journal of Clinical Pathology. 2016 Dec; 146(6): 670-680. doi: 10.1093/ajcp/aqw195.

Summary:  DIC is relatively uncommon in the general hospitalized patient but accounts for 9% to 19% of ICU admissions and has a high mortality rate of 45% to 78%. The clinical course of DIC ranges from asymptomatic to life threatening. It is caused by excessive activation of coagulation so that the anticoagulation system is overwhelmed, secondary to a wide variety of clinical conditions. The pathogenesis involves the generation of high levels of thrombin, potentially leading to microvascular thrombosis, as well as the consumption of coagulation factors and the increased generation of plasmin, which could generate a hemorrhagic diathesis. Bleeding is related to several factors, including the consumption of factors, platelets, and fibrinogen, as well as the generation of D-dimers. Typical laboratory tests performed to evaluate DIC include PT, aPTT, platelet count, fibrinogen, and D-dimer.

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