Disseminated Intravascular Coagulation
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- Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by diffuse activation of intravascular coagulation. It can originate from and cause damage to the microvasculature, which, if sufficiently severe, can produce organ dysfunction.
- Excessive activation of coagulation cascade can cause microvascular thrombi from the deposition of fibrin. However, ongoing consumption of coagulation proteins and platelets may also cause severe bleeding.
- Acute DIC occurs when rapid consumption of coagulation factors and platelets cannot be adequately compensated. It is caused by sudden exposure of blood to one or more procoagulants, such as tissue factor (TF) or lipopolysaccharides. It has a high tendency to cause bleeding, often requiring urgent or emergent treatment.
- Chronic DIC is typically seen in patients with smaller amounts of thrombin for prolonged periods such as in advanced malignancy, vasculitis, aneurysms, or with large healing hematomas. It presents more frequently with thrombosis.
- Synonym(s): consumptive coagulopathy or defibrination syndrome
- It could be as common as 1% in hospitalized patients.
- Incidence of DIC increases with age.
- Predominant sex: male > female (1)
Systemic formation of fibrin is the result of the simultaneous coexistence of the following (2):
- TF expressed by cancer cells, endothelial cells, and mononuclear cells complexes with factor VIIa and activates thrombin formation. Thrombin then cleaves fibrinogen to form fibrin, activates factors for further thrombin formation, and enhances platelet aggregation.
- Suppression of the physiologic anticoagulant pathways
- Antithrombin is depleted by consumption, degradation, and impaired synthesis.
- Low proteins C and S due to decreased synthesis and decreased levels of thrombomodulin (TM)
- Impaired fibrinolysis
- Thrombin causes release of plasminogen activator inhibitor, type 1 (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI), both of which impair plasminogen activation.
- Activation of inflammatory pathways increasing platelet adhesion
Etiology and Pathophysiology
- Causes can be classified as acute or chronic, systemic or localized.
- Sepsis/severe infection (any microorganism)
- Trauma (polytrauma, neurotrauma, fat embolism)
- Obstetric calamities (amniotic fluid embolism, abruptio placentae, hemorrhage, acute fatty liver of pregnancy, fetal demise, hemolysis, elevated liver function, and low platelets [HELLP] syndrome, preeclampsia)
- Solid tumors (pancreatic, gastric, ovarian) and leukemias (especially acute promyelocytic leukemia)
- Vascular disorders, such as Kasabach-Merritt syndrome, large vascular aneurysms, and thrombosis
- Organ destruction (severe pancreatitis, severe liver failure)
- Severe toxic or immunologic reactions
- Snake bite
- Recreational drugs
- Transfusion reactions
- Transplant rejection
- Thermal injury
- Infant and adult respiratory distress syndrome
- Neonatal purpura fulminans
See “Etiology and Pathophsiology.”
Aggressive interventions aimed at early treatment of the underlying clinical conditions
Commonly Associated Conditions
Thromboembolic phenomena are associated with venous thrombosis, thrombotic vegetations on the aortic heart valve, arterial emboli, and neonatal purpura fulminans (homozygous protein C or protein S deficiency).
Neonatal purpura fulminans is associated with DIC and protein C or protein S deficiency (homozygous).