摘要
Disseminated intravascular coagulation (DIC) is an acquired and dynamic syndrome associated with high morbidity and mortality in intensive care units, most commonly related to sepsis, but also observed in trauma, malignancy, obstetric emergencies, and severe inflammatory conditions. Contemporary concepts no longer define DIC solely as a consumptive coagulopathy; instead, it is recognised as a systemic immunothrombotic syndrome resulting from the interaction between endothelial injury, dysregulated thrombin generation, impaired fibrinolysis, and innate immune ac-tivation. With the 2025 update to the International Society on Thrombosis and Haemostasis (ISTH) guidelines, DIC has been redefined as a condition that can be identified early and targeted therapeu-tically. In sepsis-associated DIC, endotoxins, pro-inflammatory cytokines, and circulating histones induce endothelial injury, while tissue factor expression and neutrophil extracellular traps (NETs) promote widespread coagulation activation. Suppressed fibrinolysis accompanying microvascular fibrin deposition and consumption of coagulation factors prevents adequate thrombus clearance. Consequently, DIC presents as a paradoxical clinical spectrum characterised by both bleeding di-athesis and life-threatening macro- and microvascular thrombosis. For the diagnosis of DIC, the ISTH, Japanese Association for Acute Medicine (JAAM), and Sepsis-Induced Coagulopathy (SIC) scoring systems should be considered complementary tools. While SIC and JAAM scores are more sensitive for detecting the early immunothrombotic phase, the ISTH score provides greater speci-ficity for diagnosing overt, advanced-stage DIC. Platelet count, PT/INR, fibrinogen, and D-dimer constitute the core laboratory parameters; however, these tests often reflect late-stage disease. In this context, viscoelastic assays such as thromboelastography (TEG) and rotational thromboelas-tometry (ROTEM) offer real-time functional assessment of coagulation phenotypes and support diagnostic and therapeutic decision-making. The cornerstone of DIC management is prompt and effective treatment of the underlying cause. Supportive and specific interventions should be indi-vidualised according to the dominant clinical phenotype: haemorrhagic, thrombotic, or mixed. A phenotype-guided, dynamic, and patient-centred approach is essential to reduce organ dysfunction and mortality in critically ill patients with DIC.