Medical Musing of The Week: DIC


  • Disseminated Intravascular Coagulation
  • Can be acute or chronic subclinical presentation


  • Mechanisms and feedback loops of clotting and fibrinolysis function inappropriately.
  • Clotting can occur for too long or without presence of vessel injury.
  • Presence of lipopolysaccharides
  • Tissue Factor (a procoagulant)can be present Meningococcal sepsis
  • Trauma can damage the endothelium triggering the release of procoagulants
  • Protein C deficiency
  • Fibrin Degradation Products can interfere with fibrin clot formation and platelet aggregation
  • Delay of procoagulant factors being removed from the site of damage (endothelial) may result in prolonging the process of coagulation
  • Acute:
    • Sepsis
    • Trauma
    • Acute Promyelocytic Leukemia
    • Prolonged clotting times and thrombocytopenia
    • OB complications (pre-eclampsia, retained products and fatty liver of pregnancy)
  • Chronic
    •  Advanced Malignancy (pancreatic, gastric, ovarian and brain)
    • Normal clotting times and platelet counts may be normal (the body has learned how to compensate
  • Less common but possible:
    • Heat stroke
    • Crush injuries
    • Amphetamine OD
    • Fat Embolism
    • Snake bite
    • Organ transplant rejection

Clinical Manifestations and Diagnosis

  • Acute:
    • Prolonged PT, aPTT
    • Elevated Fibrin Degradation products & D-Dimer
    • Reduced Platelets, Factor V & Factor VIII
    • Bleeding
    • Renal Dysfunction
    • Shock
    • Thromboembolism
    • Liver Dysfunction, jaundice
    • Pulmonary hemorrhage w hemoptysis, dyspnea, may progress to ARDS
    • Coma, delirium, transient neurological changes
    • Purpura Fulminans (purpuric lesions caused from hemorrhagic skin necrosis—very rare and can also occur in some variants of protein C deficiency)
  • Chronic
    • Platelet count is variable
    • Fibrin and Dimer also elevated as in acute
    • Other lab findings WNL (PT, aPTT, platelets )
    • History of malignancy
    • Thromboembolism without other clear etiology
  • Evidence of end organ damage including but not limited to low urine output, hypotension, bradycardia, elevated LFT’s etc.


  • Generally until patients show signs of bleeding or clotting they are not treated prophylactically–management is usually focused on reversing the underlying cause
  • Based on evidence platelets are not administered until <10,000
  • Prolonged PT or aPTT with significantly low fibrinogen level w/ serious bleeding should receive factor replacement or FFP
  • Fibrinogen <100 give cryoprecipitate (goal of Fibrinogen >100; if >100 and PT or aPTT significantly prolonged)
  • Antithrombin is NEVER used for treatment

Complications & Prognosis

  • Ensure patient is able to support their airway depending on their respiratory status
  • Prognosis depends on how severe their clotting/bleeding abnormalities are and the ability to reverse the underlying condition pushing the pt into DIC
  • Mortality rate ranges 40-80%


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