Disseminated intravascular coagulation (DIC) is a complex disorder in which the clotting cascade is activated within blood vessels throughout the body. There is excessive and unregulated generation of thrombin, usually due to mechanical tissue or endothelial injury. Despite the systemic thrombosis taking place in the macro- and microvasculature, bleeding is also seen as fibrinolysis is activated and coagulation factors and platelets are depleted by the process. The combination of hemorrhage and thrombosis leads to inadequate tissue perfusion and infarction, often resulting in end-organ damage in severe and acute cases. DIC has no apparent age, race, or sex predilection.

DIC may be triggered by a variety of conditions, including trauma or burns, severe infections or sepsis, obstetrical complications, malignancies, severe snakebite reactions, and giant hemangiomas. Systemic signs and symptoms may include mental status changes, fever, dyspnea, hypotension, tachycardia, hematuria, and oliguria. Dermatologic signs include mucosal bleeding, retiform purpura, petechiae, and acral gangrene. In severe cases, fatality may occur rapidly. Complications from DIC include acute renal failure, severe hemorrhage in various locations (eg, cardiac tamponade, intracerebral hemorrhage, hemothorax), and gangrene.

DIC may be acute, chronic, or localized. Severe acute DIC is a medical emergency generally caused by trauma, malignancy, infection, or an obstetric emergency. It often presents with generalized bleeding and a shock-like picture (hypotension and tachycardia). Chronic DIC demonstrates subacute bleeding and diffuse thrombosis; its causes are often malignancies, other obstetrical complications, and autoimmune / inflammatory disorders. Many patients with low-grade chronic DIC can be managed on an outpatient basis. Localized DIC, as the name suggests, is confined to a specific body location. It is associated with giant hemangiomas (Kasabach-Merritt syndrome), aortic aneurysms, and hyperacute kidney transplant rejection.