If the patient has normal platelet counts and clotting times, acute DIC is unlikely. If you suspect peracute or chronic DIC based on a decreasing platelet count or fibrinogen concentration, additional laboratory tests are justified. We recommend a D-dimer assay and antithrombin activity measurement.

D-dimers, FDPs, antithrombin, and fibrinogen
D-dimers are cross-linked fibrin-derived degradation products and result when fibrinolysis is activated with ongoing coagulation, thus D-dimers indicate activation of both the fibrinolytic and coagulation systems.^4,10,13,14 FDPs are produced with primary fibrinolysis or fibrinolysis secondary to coagulation. Their presence does not distinguish between fibrinogen or fibrin-derived products.^4,10,13 Thus FDPs only indicate activation of the fibrinolytic system. Since most forms of DIC activate both systems, D-dimer concentration measurement appears to be a sensitive ancillary test for DIC in dogs.⁹ D-dimers can be detected in association with degradation of any blood clot, so the results of a D-dimer assay must be interpreted with caution.

An increased D-dimer concentration is not diagnostic for DIC but supports the diagnosis in patients that have predisposing diseases and consumptive thrombocytopenia. In the face of elevated D-dimer concentrations or low antithrombin activities in patients with decreasing platelet and fibrinogen concentrations over time, DIC is probable. One study evaluating a point-of-care test showed that with normal D-dimer concentrations, DIC is highly unlikely.⁹ And in one study of dogs with DIC, FDP concentrations were elevated in 61% (correlated with low fibrinogen) and antithrombin activities were low in 85% of the patients.¹² D-dimer concentrations greater than 500 mg/ml were 100% sensitive for acute thromboembolism.¹¹ In a study in cats with DIC, FDP concentrations were elevated in 24% of the cats.¹

Diagnostic criteria

Analysis of the above tests may suggest the presence of DIC, but no test is pathognomonic. When presented with a patient with evidence of thrombosis or hemorrhage or with a condition that predisposes a patient to DIC, our clinic requires at least three of the following to establish a diagnosis:

• Decreasing serial platelet count in the face of megathrombocytosis
• Prolonged PT
• Prolonged APTT
• Increased FDP concentration
• Decreased fibrinogen concentration
• Increased D-dimer concentration
• Decreased antithrombin activity
• Schistocytosis

TREATMENT AND MONITORING

Treating DIC is difficult, especially without 24-hour intensive care and monitoring and point-of-care testing. Although unproven, early recognition of patients with DIC should facilitate the likelihood of a positive outcome. Once DIC has been confirmed or if the clinical suspicion is high, treatment should begin immediately. The goals of therapy are to

• Eliminate the underlying cause
• Control excessive intravascular coagulation
• Maintain organ perfusion
• Replace coagulation components, if necessary

Coagulation times and fibrinogen concentrations may normalize within hours of appropriate therapy. However, FDPs and thrombocyte counts take days to normalize. A favorable response to therapy is associated with clinical improvement and daily improvements in laboratory test results. The platelet count should increase in response to effective treatment.

Eliminate the underlying cause

DIC is always secondary to an underlying disease or disorder, so DIC will persist until the disease or disorder is eliminated. It is often impossible to eliminate the inciting cause quickly. Some exceptions include splenectomy to treat hemangiosarcoma, aggressive intravenous antibiotic treatment of bacteremia, surgical treatment of external or internal abscesses, and surgical excision of selected malignancies. Aggressive treatment is necessary and should never be overlooked. Once the procoagulant stimulus is controlled, spontaneous recovery is possible.⁷