DIC and Thrombosis

Disseminated intravascular coagulation is a devastating clinical syndrome triggered by systemic activation of the coagulation cascade. DIC is always an acquired syndrome; occurring because of a primary disease. Many common diseases are capable of initiating DIC, including neoplasia, shock, sepsis, pancreatitis, and hemolytic anemia. The disease process is dynamic, with early thrombosis progressing to diffuse bleeding. The clinical signs of DIC are highly variable and depend on the underlying disease and the balance between thrombosis and hemorrhage.

  • Thrombosis and thromboembolism develop in association with many conditions causing blood stasis, vascular endothelial injury, or hypercoagulability of blood. Pulmonary thromboembolism is common in dogs and has been reported in association with hyperadrenocorticism, nephrotic syndrome, neoplasia, and immune-mediated hemolysis.
  • The early diagnosis of DIC or thromboembolism is difficult, yet intervention early in the disease process is most likely to benefit the patient. Careful physical examination and laboratory testing are the most effective means for their identification.

Identification of DIC and Thrombotic Disorders

To identify DIC and thrombosis, use the following tests:

  • DIC panel: (aPTT, PT, fibrinogen, antithrombin, and quantitative D-dimer)
    • Fulminant or hemorrhagic DIC is characterized by prolongation of aPTT, PT, low fibrinogen, and high D-dimer. In chronic or thrombotic DIC, coagulation screening tests may be within normal limits, but D-dimer concentration is high.

Antithrombin is a natural anticoagulant, and is often depleted during thrombus formation in active DIC. Antithrombin loss also accompanies protein-losing nephropathies and enteropathies, leading to a hypercoagulable state and risk for thrombosis in these conditions.

D-dimer is a breakdown product of cross-linked fibrin.

  • A rise in plasma D-dimer concentration is an indication of fibrin clot (thrombus) formation and secondary clot lysis.

Plasminogen is the inactive precursor of the fibrinolytic enzyme plasmin.

  • Plasminogen levels may fall below normal range as systemic clots and thromboemboli are degraded.