[Pathophysiology and management of disseminated intravascular coagulation: a disease-specific approach]

Disseminated intravascular coagulation (DIC) is an acquired systemic coagulation disorder that arises secondary to various underlying diseases. Its core pathophysiology is characterized by sustained thrombin generation leading to microvascular thrombosis, together with consumption of platelets and coagulation factors, resulting in consumptive coagulopathy and a paradoxical coexistence of thrombosis and bleeding. The 2001 definition emphasized intravascular coagulation activation and microvascular damage due to loss of localization. In contrast, the updated 2025 definition reconceptualizes DIC as a life-threatening intravascular disorder involving systemic coagulation activation, dysregulated fibrinolysis, and endothelial injury, highlighting its dynamic progression from a potentially asymptomatic early phase to advanced stages with hemorrhage and/or organ dysfunction. Although diagnostic scoring systems based on platelet counts and fibrin-related markers are widely used, comprehensive clinical assessment remains essential. Importantly, DIC exhibits marked heterogeneity depending on the underlying condition, for example, suppressed fibrinolysis in sepsis and enhanced fibrinolysis in hematologic malignancies. This review summarizes the evolving concept of DIC and discusses diagnostic and therapeutic strategies based on its pathophysiological diversity.