Disseminated intravascular coagulation (DIC) represents catastrophic dysregulation of the coagulation cascade, producing the paradox of simultaneous widespread microvascular thrombosis and hemorrhage due to consumption of clotting factors and platelets. DIC is ALWAYS secondary to an underlying trigger — it is never a primary diagnosis. Normal hemostasis maintains equilibrium between procoagulant forces (tissue factor pathway, contact activation pathway, thrombin generation, fibrin formation), anticoagulant forces (antithrombin III, protein C/protein S, tissue factor pathway inhibitor), and fibrinolysis (plasmin degradation of fibrin). In DIC, massive tissue factor release (from damaged endothelium, necrotic tissue, monocyte activation by endotoxin, or tumor procoagulants) overwhelms these regulatory mechanisms. The cascade unfolds: (1) Massive tissue factor exposure activates Factor VII → TF-VIIa complex → activates Factor X (common pathway) and Factor IX (intrinsic pathway amplification) → explosive thrombin generation. (2) Thrombin converts fibrinogen to fibrin monomers → widespread fibrin deposition in the microvasculature → organ ischemia (kidneys, lungs, liver, brain, skin). (3) Platelets are consumed at sites of microvascular thrombosis → thrombocytopenia → mucocutaneous bleeding. (4) Clotting factors (I, II, V, VIII, XIII) are consumed → coagulopathy → bleeding...