DIC

From Cow
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Disseminated intravascular coagulation (DIC), also known as consumptive coagulopathy, is a pathological activation of coagulation (blood clotting) mechanisms that happens in cats as a response to a variety of diseases.

As its name suggests, DIC leads to the formation of small blood clots inside the blood vessels throughout the body. As the small clots consume all the available coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin (e.g. from sites where blood samples were taken), the digestive tract, the respiratory tract and surgical wounds. The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result[1].

Cause

Concurrent intravascular activation of hemostasis and accelerated fibrinolysis lead to microvascular thrombosis and embolism. Thrombosis and embolism may lead to organ failure. Bleeding tendencies occur secondary to consumption of platelets and coagulation factors, increased plasmin activity, and circulating anti-coagulants, including fibrin degradation products (FDPs).

Numerous disease processes may trigger DIC in cattle, including:

DIC has wide clinical and pathological spectra and may be acute to chronic, localised to generalised, and subclinical to fulminant. A broad definition is used to include most cases of consumptive thrombocytopenia and microangiopathic disorders.

Acute DIC is not as common in cattle.

Diagnosis is controversial in all species and there is not a single test or combination of tests that rules in or rules out DIC.

Laboratory abnormalities consistent with DIC include: Low platelet count, prolonged ACT, prolonged aPTT, prolonged PT, prolonged TT, hypofibrinogenemia, decreased antithrombin II concentration, presence of FDPs, and red blood cell products. Presence of three of the above abnormalities as criteria for diagnosis of DIC.

Using low platelet count, prolonged PT, prolonged aPTT, and prolonged TT as diagnostic of DIC in liver disease.

Measuring antithrombin III which tends to be consumed in DIC, may add specificity but probably does not increased sensitivity to the diagnosis of DIC.

If a hemostatic defect is identified in the work-up of the primary disease, the possibility of a defect unrelated to the primary disease should be considered e.g. Hageman trait.

Treatment

Aggressive intravenous fluid therapy is critical to promote microvascular circulation. If obvious bleeding, transfuse to replace platelets and/or clotting factors and anti-thrombin II with fresh whole blood, platelet-rich plasma, or fresh/fresh-frozen plasma, 10-20 ml/kg.

Heparin therapy is controversial. It is recommended because, although bleeding is clinically more obvious, thrombosis causes most of the organ damage. The goal is to block microvascular thrombosis while not aggravate bleeding.

Blood transfusion may be indicated in some patients, to replace platelets or coagulation factors, especially if anaemia is severe enough to compromise oxygen-carrying capacity. However, survival rates are not necessarily greater with transfusions, and may be of palliative benefit only.

The prognosis is largely determined by the primary disease. Acute diffuse DIC has a very poor prognosis.