Disseminated intravascular coagulation
Also known as consumption coagulopathy and defibrination syndrome, disseminated intravascular coagulation (DIC) complicates conditions that accelerate clotting, causing small-blood-vessel occlusion, organ necrosis, depletion of circulating clotting factors and platelets, and activation of the fibrinolytic system. This, in turn, can provoke severe hemorrhage.
Clotting in the microcirculation usually affects the kidneys and extremities but may occur in the brain, lungs, pituitary and adrenal glands, and GI mucosa. Other conditions, such as vitamin K deficiency, hepatic disease, and anticoagulant therapy, may cause a similar hemorrhage.
Although usually acute, DIC may be chronic in cancer patients. The prognosis depends on early detection and treatment, the severity of the hemorrhage, and treatment of the underlying condition.
Causes
DIC may result from:
infection—gram-negative or gram-positive septicemia; viral, fungal, or rickettsial infection; and protozoal infection
obstetric complications—abruptio placentae, amniotic fluid embolism, retained dead fetus, eclampsia, septic abortion, and postpartum hemorrhage
neoplastic disease—acute leukemia, metastatic carcinoma, and lymphomas
disorders that produce necrosis—extensive burns and trauma, brain tissue destruction, transplant rejection, hepatic necrosis, and anorexia nervosa
other disorders and conditions—heatstroke, shock, poisonous snakebite, cirrhosis, fat embolism, incompatible blood transfusion, drug reactions, cardiac arrest, surgery necessitating cardiopulmonary bypass, giant hemangioma, severe venous thrombosis, purpura fulminans, adrenal disease, adult respiratory distress syndrome, diabetic ketoacidosis, pulmonary embolism, and sickle cell anemia.
Why such conditions and disorders lead to DIC is unclear. Regardless of how DIC begins, however, the typical accelerated clotting results in generalized activation of prothrombin and a consequent excess of thrombin. Excess thrombin converts fibrinogen to fibrin, producing fibrin clots in the microcirculation. This process consumes exorbitant amounts of coagulation factors (especially platelets, factor V, prothrombin, fibrinogen, and factor VIII), causing thrombocytopenia, deficiencies in factors V and VIII, hypoprothrombinemia, and hypofibrinogenemia.
Circulating thrombin activates the fibrinolytic system, which lyses fibrin clots into fibrinogen degradation products (FDPs). The hemorrhage that occurs may be due largely to the anticoagulant activity of FDPs as well as to depletion of plasma coagulation factors.
Complications
DIC may be complicated by renal failure, hepatic damage, stroke, ischemic bowel, or respiratory distress. Hypoxia and anoxia can occur and can lead to severe striated muscle pain. Shock and coma can also
result. After fibrinolysis, severe to fatal hemorrhaging of vital organs can occur without warning.
result. After fibrinolysis, severe to fatal hemorrhaging of vital organs can occur without warning.
Assessment
The most significant clinical feature of DIC is abnormal bleeding without a history of a hemorrhagic disorder. Signs and symptoms are related to bleeding and thrombosis. Bleeding problems are usually more common than thrombotic problems unless coagulation occurs to a greater extent than fibrinolysis.
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