Atlas of pathophysiology, 2 Edition

Part II - Disorders

Hematologic Disorders

Disseminated intravascular coagulation

Disseminated intravascular coagulation (DIC) occurs as a complication of diseases and conditions that accelerate clotting. It causes small blood vessel occlusion, organ necrosis, depletion of circulating clotting factors and platelets, activation of the fibrinolytic system, and consequent 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. DIC, also called consumption coagulopathy or defibrination syndrome, is generally an acute condition but may be chronic in cancer patients (Trousseau's syndrome). Prognosis depends on early detection and treatment, the severity of the hemorrhage, and treatment of the underlying disease.


Etiology unclear (however, in many patients, the triggering mechanisms may be the entrance of foreign protein into the circulation and vascular endothelial injury)

DIC may result from:

·   Infections—gram-negative or gram-positive septicemia; viral, fungal, rickettsial, protozoal infection (malaria)

·   Obstetric complications—abruptio placentae, amniotic fluid embolism, retained dead fetus, septic abortion, eclampsia

·   Neoplasia—acute leukemia, metastatic carcinoma, especially adenocarcinoma

·   Necrosis—extensive burns or trauma, brain tissue destruction, transplant rejection, hepatic necrosis

·   Other causes—heatstroke, shock, poisonous snakebite, cirrhosis, fat embolism, incompatible blood transfusion, cardiac arrest, surgery necessitating cardiopulmonary bypass, giant hemangioma, severe venous thrombosis, purpura fulminans


Regardless of how DIC begins, the typical accelerated clotting results in generalized activation of prothrombin and a consequent excess of thrombin. The thrombin converts fibrinogen to fibrin, producing fibrin clots in the microcirculation. This process uses huge amounts of coagulation factors (especially fibrinogen, prothrombin, platelets, and factors V and VIII), causing hypofibrinogenemia, hypoprothrombinemia, thrombocytopenia, and deficiencies in factors V and VIII. Circulating thrombin also activates the fibrinolytic system, which dissolves fibrin clots into fibrin degradation products. Hemorrhage may be mostly the result of the anticoagulant activity of fibrin degradation products as well as depletion of plasma coagulation factors.

Signs and symptoms

·   Abnormal bleeding:

§  Cutaneous oozing of serum, bleeding from surgical or I.V. sites, bleeding from the GI tract

§  Petechiae or blood blisters (purpura), epistaxis, hemoptysis

·   Cyanosis; cold, mottled fingers and toes

·   Severe muscle, back, abdominal, and chest pain

·   Nausea and vomiting (may be a manifestation of GI bleeding)

·   Shock

·   Confusion

·   Dyspnea

·   Oliguria

·   Hematuria

Diagnostic test results

Laboratory analysis reveals:

·   decreased serum platelet count (less than 100,000/mm3)

·   decreased serum fibrinogen level (less than 150 mg/dl)

·   prolonged prothrombin time (more than 15 seconds)

·   prolonged partial thromboplastin time (more than 80 seconds)

·   increased fibrin degradation products (commonly greater than 45 mcg/ml, or positive at less than 1:100 dilution)

·   positive D-dimer test (specific fibrinogen test for DIC) at less than 1:8 dilution

·   diminished blood clotting factors V and VIII

·   complete blood count showing decreased hemoglobin levels (less than 10 g/dl)

·   elevated blood urea nitrogen (greater than 25 mg/dl) and elevated serum creatinine levels (greater than 1.3 mg/dl).


·   Prompt recognition and treatment of underlying disorder

·   Blood, fresh frozen plasma, platelet, packed red-blood-cell transfusions, or cryoprecipitate to support hemostasis in active bleeding

·   I.V. fluids

·   Vasopressors such as dopamine

·   Inhibitors of fibrinolysis such as epsilon-aminocaproic acid

·   Recombinant human activated protein C

·   Unfractionated or low-molecular weight heparin in early stages to prevent microclotting and as a last resort in hemorrhage (controversial in acute DIC after sepsis)






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