Clinical meaning
Disseminated intravascular coagulation (DIC) is a life-threatening acquired coagulopathy characterized by simultaneous, widespread activation of coagulation and fibrinolysis. DIC is always secondary to an underlying condition — it is never a primary disease. The pathophysiology begins with massive release of tissue factor (TF) or other procoagulant substances into the bloodstream from damaged tissues, endotoxins, or inflammatory mediators. This triggers widespread thrombin generation, leading to diffuse microvascular fibrin deposition (microthrombi) throughout the vasculature. These microthrombi cause ischemic organ damage (kidneys, lungs, brain, liver, skin). Simultaneously, the massive consumption of clotting factors (I, II, V, VIII, XIII) and platelets depletes hemostatic reserves, causing a consumptive coagulopathy. The body activates the fibrinolytic system (plasmin) to break down the fibrin clots, generating fibrin degradation products (FDPs) and D-dimers. FDPs themselves are anticoagulant, further impairing hemostasis. The result is the paradox of DIC: simultaneous thrombosis (organ ischemia from microthrombi) and hemorrhage (from factor and platelet consumption). The balance between thrombosis and hemorrhage determines clinical presentation: acute DIC presents predominantly with bleeding, while chronic (compensated) DIC may present with thrombotic manifestations. The pathologic sequence is: trigger → tissue factor release → widespread thrombin generation → microvascular fibrin deposition → consumption of factors and platelets → secondary fibrinolysis → FDP generation → hemorrhage and organ damage.