Disseminated intravascular coagulation (DIC) is an acquired, systemic disorder of hemostasis in which widespread, dysregulated activation of the clotting cascade produces fibrin thrombi throughout the microvasculature while simultaneously consuming platelets and coagulation factors. This dual process can cause micro…
Disseminated intravascular coagulation (DIC) is an acquired, systemic disorder of hemostasis in which widespread, dysregulated activation of the clotting cascade produces fibrin thrombi throughout the microvasculature while simultaneously consuming platelets and coagulation factors. This dual process can cause microvascular thrombosis with tissue ischemia and organ dysfunction and, through depletion of clotting components and secondary fibrinolysis, a concurrent bleeding tendency. DIC is not a primary disease but a complication of an underlying condition, most often sepsis and severe infection, major trauma, obstetric emergencies, and malignancy—particularly acute leukemias and metastatic solid tumors—where tissue factor expression and inflammatory cytokines trigger excessive thrombin generation. Pathophysiologically, it reflects an imbalance between procoagulant drive, impaired natural anticoagulant pathways, and altered fibrinolysis. Laboratory features evolve over the course of the syndrome and characteristically include thrombocytopenia, prolonged prothrombin and activated partial thromboplastin times, reduced fibrinogen, and elevated fibrin-related markers such as D-dimer, sometimes with schistocytes on the blood film. Diagnosis is established by combining these findings, often through scoring systems, with the clinical context. Management centers on treating the precipitating illness, supplemented by supportive transfusion of platelets, fresh frozen plasma, or cryoprecipitate and, in selected presentations, anticoagulation, making prompt recognition essential to outcome.
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