Disseminated intravascular coagulation

Background

  1. Widespread and inappropriate activation of the coagulation and fibrinolytic systems
    1. Thrombosis
      1. Tissue factor activation -> thrombin -> fibrin clots in microcirculation
        1. Activation of the coagulation system leads to consumption of plts and coag factors
    2. Bleeding
      1. Thrombin/fibrin actives tPA and the fibrinolytic system
        1. Degree of fibrinolysis can be excessive -> bleeding

Causes

  1. Infection
    1. Most common cause of DIC
    2. 10%–20% of pts w/ Gram-neg sepsis have DIC
      1. Septic pts more likely to have bleeding than thrombosis
    3. More likely to develop in asplenic pts or cirrhosis
  2. Carcinoma
    1. DIC is often chronic and compensated
    2. Thrombosis is more common than bleeding
  3. Leukemia
    1. More likely to have bleeding than thrombosis
  4. Trauma
    1. Brain injury, crush injury, burns, rhabdo, fat embolism
  5. Liver disease
    1. May have chronic compensated DIC; acute DIC may occur in setting of acute liver failure
  6. Pregnancy
    1. Abruption, amniotic fluid embolus, septic abortion, HELLP syndrome
  7. Envenomation
    1. Rattlesnakes and other vipers
    2. Bleeding not as serious as expected from lab values
  8. ARDS
    1. 20% of pts with ARDS develop DIC; 20% of pts with DIC develop ARDS
  9. Transfusion reactions

Clinical Features

Diagnosis

  1. PT high
  2. PTT high
  3. Platlet low
  4. Fibrinogen low
  5. FDP high
  6. D-dimer high
  7. RBCs fragmented


Treatment

See Heme: Bleeding Treatment

Source

1/26/06 DONALDSON (addapted from Tintinalli)