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Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is also known as consumption coagulopathy and defibrination syndrome. DIC complicates diseases and conditions that accelerate clotting, causing occlusion of small blood vessels, 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 can occur in the brain, lungs, pituitary and adrenal glands, and G1 mucosa. Other conditions, such as vitamin K deficiency, hepatic disease, and anticoagulant therapy, can cause similar hemorrhage.

DIC is usually acute but can be chronic in cancer patients. The prognosis depends on early detection and treatment, the severity of the hemorrhage, and treatment of the underlying disease or condition.


DIC may result from:

  • infection - gram-negative or gram-positive septicemia; viral, fungal, or rickettsial infection; protozoal infection
  • obstetric complications - abruptio placentae, amniotic fluid embolism, retained dead fetus, eclampsia, septic abortion, postpartum hemorrhage
  • neoplastic disease - acute leukemia, metastatic carcinoma, lymphomas
  • disorders that produce necrosis - extensive burns and trauma, brain tissue destruction, transplant rejection, hepatic necrosis, anorexia
  • 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, as is whether they lead to DlC through a common mechanism. In many patients, the triggering mechanisms may be the entrance of foreign protein into the circulation and vascular endothelial injury.

Regardless of how DlC begins, 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.

Signs and Symptoms

You may experience bleeding and haemorrhage from any or several body parts. The bleeding may be heavy.

Common signs of bleeding include:

  • Bloody vomit or red or black stools;
  • Vaginal bleeding;
  • Red or cloudy urine;
  • Unexplained bruising;
  • Severe abdominal or back pain caused by bleeding into body organs;
  • Rarely convulsions;
  • Rarely a coma.

Diagnostic tests

Although numerous blood tests are often performed on patients prone to DIC, the important measures are: full blood count (especially the platelet count), fibrin degradation products or D-dimer tests (markers of fibrinolysis ), bleeding time and fibrinogen levels. Decreased platelets, elevated FDPs or D-dimers, prolonged bleeding time and decreased fibrinogen are markers of DIC.


Successful management of DlC requires prompt recognition and adequate treatment of the underlying disorder. Treatment may be supportive (when the underlying disorder is self-limiting. for example) or highly specific. If the patient isn't actively bleeding, supportive care alone may reverse DIC. Active bleeding may require administration of blood, fresh frozen plasma, platelets, or packed RBCs to support hemostasis.

Heparin therapy is controversial. It may be used early in the disease to prevent microclotting but may be considered a last resort in the patient who is actively bleeding. If thrombosis does occur, heparin therapy is usually mandatory. In most cases, it's administered in combination with transfusion therapy.

Drugs such as antithrombin III and gabexate are being considered for use as antithrombins to inhibit the clotting cascade.


Get prompt treatment for conditions known to bring on this disorder.

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