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approximately 10% in patients with solid tumors, trauma, or obstetric calamities.1-3 The overall prevalence of DIC in hospitalized patients is unknown because the established clinical scoring systems for DIC are not systematically employed in clinical practice. Furthermore, the prevalence of DIC depends on the context of hospitalization and is higher in critically ill patients hospitalized in intensive care units (ICUs). In this subset of patients, the prevalence of DIC ranges from 8.5% to 34% depending on the underlying diagnoses and the diagnostic scoring system used.3-7 In critically ill patients with DIC, the 28-day mortality rate is 20% to 50%, significantly higher than that of critically ill patients who do not fulfill the DIC criteria.3 Early diagnosis and appropriate treatment of DIC is of critical importance to favorable patient outcomes. Definition of DIC Disseminated intravascular coagulation is an acquired syndrome characterized by dispersed and uncontrolled activation of blood coagulation leading to intravascular fibrin formation. The signature feature of DIC is the loss of localized activation of coagulation and the inefficiency of natural coagulation inhibitors to downregulate thrombin generation. According to the definition of the International Society of Thrombosis and Haemostasis scientific subcommittee, DIC is an acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes. It can originate from and cause damage to the microvasculature, which if sufficiently severe, can produce organ dysfunction.8 Pathogenesis of DIC Although the first clinical and pathological observations related to DIC were made in the 19th century,9 detailed knowledge on the pathogenesis of the syndrome has only been attained in past decades. In recent years, some of the mechanisms involved in pathological microvascular fibrin deposition in DIC have been clarified10,11: excessive thrombin generation triggered by tissue factor (TF) overexpression related to the underlying disease process platelet activation defective natural anticoagulant pathways, including tissue factor pathway inhibitor (TFPI), antithrombin (AT), and protein C (PC) insufficient fibrin degradation due to impaired fibrinolysis or exaggerated fibrin and fibrinogen degradation concomitant activation of the inflammatory process Fibrin formation is accompanied by activation of fibrinolysis, the extent of which depends on plasminogen activator inhibitor 1 (PAI-1), thrombin-activatable fibrinolysis inhibitor (TAFI), and other factors related to the underlying disease and the capacity of regulatory mechanisms. If not adequately counteracted by fibrinolysis, fibrin deposition may cause diffuse obstruction of the microvasculature. Microvascular thrombosis in conjunction with hemodynamic and metabolic derangements contributes to multiorgan dysfunction. Signs of organ dysfunction include renal Table 1. Clinical Conditions Associated With DIC. Clinical Conditions Triggering DIC Causes of DIC Sepsis or severe infection Potentially any microorganism but particularly gram-negative bacteria Viral infections (ie, viral hemorrhagic fever) Malaria Rickettsia infection Trauma Severe tissue injury Head injury Burns Fat embolism Surgery Heat stroke of shock Organ destruction Pancreatitis, severe inflammation, tissue necrosis Malignancy Solid tumors (pancreatic, stomach, colorectal cancer, mucin secreting adenocarcinoma) Hematological malignancies (acute promyelocytic leukemia) Obstetrical calamities Placental abruption Placenta previa Amniotic fluid embolism Intrauterine death Eclampsia HELLP syndrome Vascular abnormalities Aortic aneurysm Giant hemangiomas (Kasabach-Merritt syndrome) Vasculitis Liver disease Cirrhosis Acute hepatic necrosis Severe toxic or immunological reactions Graft-versus-host disease Transplant reaction Snake bites (such as from those belonging to the genus Echis) Severe transfusion reactions (incompatible blood transfusion reactions) Abbreviations: DIC, disseminated intravascular coagulation; HELLP, hemolysis, elevated liver enzyme levels, and low platelet levels. Papageorgiou et al 9S insufficiency, respiratory failure, hypotension, and circulatory failure or impaired cerebral function.