Disseminated Intravascular Coagulation

At the bedside, DIC is recognized as a trigger-driven shift in hemostasis rather than as an isolated laboratory abnormality. Systemic coagulation activation forms fibrin throughout the microcirculation, while the continuing process consumes platelets and clotting factors. The same patient may therefore ooze from an IV site, develop digital ischemia, and show worsening kidney or lung function. DIC can progress from a laboratory-first, compensated phase to overt hemorrhage and organ dysfunction. A falling platelet count, rising D-dimer, lengthening PT, or declining fibrinogen may precede visible bleeding. The practical model is concurrent: identify and treat the underlying trigger, obtain and trend the coagulation profile, support hemostasis when bleeding or an invasive procedure requires it, and assess continuously for impaired organ perfusion.