Disseminated intravascular coagulation

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Background

  • Abbreviation = DIC
  • Widespread and inappropriate activation of the coagulation and fibrinolytic systems
    • Exposure of blood to procoagulants such as tissue factor and cancer procoagulant
    • Formation of fibrin within the circulation
    • Fibrinolysis
    • Depletion of clotting factors
    • End-organ damage
  • Chronic DIC occurs when hepatic/bone marrow production balances coag factor consumption

Causes

Clinical Features

In given patient either bleeding or thrombosis will predominate (bleeding is more common ~65%)

  • Shock (15%)
  • Acute renal failure (25-40%)
  • Hepatic dysfunction (19%)
  • Respiratory dysfunction (16%)
  • Thromboembolism (7%)
  • CNS involvement (2%)
  • Purpura fulminans (widespread arterial and venous thromboses)
    • Associated with significant bacteremia

Differential Diagnosis

Microangiopathic Hemolytic Anemia (MAHA)

Thrombocytopenia

Decreased production

  • Marrow infiltration (tumor or infection)
  • Viral infections (rubella, HIV)
  • Marrow Suppression (commonly chemotherapy or radiation)
  • Congentital thrombocytopenia
    • Fanconi anemia
    • Alport syndrome
    • Bernand Soulier
  • Vitamin B12 and/or folate deficiency

Increased platelet destruction or use

Drug Induced

  • sulfa antibiotics, ETOH, ASA, thiazides/furosemide

Comparision by Etiology

ITP TTP HUS HIT DIC
↓ PLT Yes Yes Yes Yes Yes
↑PT/INR No No No +/- Yes
MAHA No Yes Yes No No
↓ Fibrinogen No No No No Yes
Ok to give PLT Yes No No No Yes

Coagulopathy

Platelet Related

Factor Related

Vesiculobullous rashes

Febrile

Afebrile

Evaluation

Acute

  • Platelets[1]
    • Low (or dropping) in 98% of DIC patients
    • Sn, not Sp
    • Repeat platelets may be necessary if first level normal or if need to trend
  • PT and PTT
    • Prolonged
    • May be normal in as many as 50% of DIC patients[2]
    • Serial coagulation testing may be necessary
    • PT, not INR, is used for monitoring[3]
  • Fibrinogen
    • Low
    • <100 correlates with severe DIC
    • May be normal (acute phase reactant), up to 57% in DIC patients[4]
  • FDP
    • Elevated
  • D-dimer
    • Elevated
    • Sn but not Sp: may also see in patients with chronic liver or renal disease
    • Combination of elevated FDP and d-dimer may increase sensitivity and specificity
  • RBCs
    • Fragmented (not specific)

Chronic

  • FDP: Elevated
  • D-dimer: Elevated
  • Platelet: Variable
  • Fibrinogen: Normal-elevated
  • PT: Normal
  • PTT: Normal
  • RBCs
    • Fragmented

Management

  • Treat underlying illness
  • Replacement treatment
    • Only indicated in with documented DIC + bleeding or impending procedure
      • Fibrinogen
      • Platelets
        • Consider repletion if <50K with bleeding or <20K without bleeding
      • FFP
        • Consider repletion to goal of PT and PTT < 1.5 times the normal limit
      • Vitamin K
      • Folate
    • Heparin
      • Consider only if thromboembolic are predominant symptoms from chronic DIC

Disposition

  • Admit

See Also

References

  1. ↑ Spero JA, Lewis JH, Hasiba U. Disseminated intravascular coagulation. Findings in 346 patients. Thromb Haemost. 1980 Feb 29. 43(1):28-33.
  2. ↑ Olson JD, Kaufman HH, Moake J, O'Gorman TW, Hoots K, Wagner K, et al. The incidence and significance of hemostatic abnormalities in patients with head injuries. Neurosurgery. 1989 Jun. 24(6):825-32.
  3. ↑ Levi M, Toh CH, Thachil J, Watson HG. Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. Br J Haematol. 2009 Apr. 145(1):24-33.
  4. ↑ Spero JA, Lewis JH, Hasiba U. Disseminated intravascular coagulation. Findings in 346 patients. Thromb Haemost. 1980 Feb 29. 43(1):28-33.
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