Disseminated Intravascular Coagulation (DIC) is a microangiopathic hemolytic anemia (MAHA) characterized by endothelial dysfunction, hemolysis, platelet aggregation, fibrin clot formation, and degradation. After clotting factors and platelets become depleted, bleeding may occur [1]. Because of this simultaneous thrombosis and bleeding, DIC is sometimes referred to as a “consumptive coagulopathy.” The underlying pathophysiology is generally initiated by endothelial or other cell injury, releasing thromboplastic factors which propagate the extrinsic coagulation pathway. This leads to overproduction of thrombin and systemic fibrin, and platelet activation, leading to systemic thrombosis. The simultaneous release of tissue plasminogen activator results in fibrin degradation, contributing to the bleeding diathesis [2]. Depending on the underlying etiology, the onset can be variable ranging from chronic to fulminant. Clinical manifestations of MAHAs include thrombocytopenia, altered mental status, bleeding, myocardial infarction, hemorrhagic/ischemic stroke, renal failure, bowel and limb ischemia, skin necrosis and purpura fulminans (discussed below). The differential diagnosis includes other MAHAs (hemolytic uremic syndrome and thrombotic thrombocytopenic purpura), as well as idiopathic thrombocytopenic purpura, end-stage liver disease, and heparin-induced thrombocytopenia (HIT). The most common underlying etiologies for DIC are sepsis, trauma, both hematologic and solid malignancies, ABO blood mismatch, obstetrical emergencies, and medications (particularly chemotherapeutic agents). Identification of a precipitating event is critical for diagnosis and treatment.