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.
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 cats, including:
- viral - FeLV, FPV, FIP
- fungal - Toxoplasmosis, yeast septicaemia
- Inflammatory disease - pancreatitis
- Infectious disease - sepsis due to tuberculosis, histoplasmosis, cytauxzoonosis, toxoplasmosis
- Coagulopathy - aortic thromboembolism due to cardiomyopathy, blood transfusion, neonatal isoerythrolysis
- Neoplasia - e.g. haemangiosarcoma, hepatic, biliary and pulmonary carcinomas, mesothelioma, lymphoma, myeloid leukaemia, malignant histiocytosis)
- Immune disorders - Immune-mediated haemolytic anaemia, immune-mediated articular disease
- Trauma - heat stroke, physical trauma, shock
- Toxins and snake bite envenomation
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 cats as dogs. The most common causes are panleukopenia virus infection, other overwhelming infections (e.g. cytauxzoonosis), and neoplasia. The most common causes of subacute to chronic DIC are liver diseases, neoplasia and FIP (due to vasculitis).
Thrombocytopenia also has been noted with several other diseases where the thrombocytopenia is likely consumptive in origin (e.g. diabetes mellitus, HCM, Mycoplasma haemofelis infection, hyperthyroidism, hypertension, kidney disease, urethral obstruction and urinary tract infections.
Depression and lethargy are usually the first signs of DIC in cats. This is usually followed by hypothermia, weak femoral pulses, tachycardia, hyperthermia, a palpable abdominal mass, cardiac murmur and presence of a gallop rhythm.
Most DIC in cats is subclinical, unless in severe cases, such as is seen in neonatal isoerythrolysis and blood transfusion, where collapse occurs, associated with cyanosis, rapid breathing, pale mucous membranes and sometimes death.
Superficial and deep spontaneous bleeding may occur, such as epistaxis, rectal bleeding, haemothorax and haematuria, but it is uncommon. Venipuncture and biopsy sites, suture lines, and internal and external injuries may bleed excessively. Signs due to anaemia and local effects of haemorrhage vary with severity of blood loss.
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.
The probability of DIC increases with the number of consistent laboratory abnormalities e.g. it is possible that a cat with only thrombocytopenia has DIC, but it is more likely that a cat with thrombocytopenia and prolonged ACT has DIC, while it is highly probable that a cat with thrombocytopenia, prolonged PT and aPTT, hypofibrinogenemia and increased FDPs has DIC. Scoring systems based on this approach have been used in humans.
Measuring antithrombin III which tends to be consumed in DIC, may add specificity but probably does not increased sensitivity to the diagnosis of DIC.
Measurements of D-Dimer are being used with increasing frequency to support the diagnosis of DIC in dogs. Little is currently known of the utility of D-Dimer assay in the diagnosis of DIC in cats. D-Dimer is a more specific marker of thrombosis than are FDPs, but D-Dimer is not specific for DIC. D-Dimer levels will be increased in thromboembolic disorders including arterial and pulmonary thromboembolism. There is poor correlation between degrees of coagulation abnormalities, severity of underlying clinical disease and risk for haemorrhage.
If a hemostatic defect is identified in the work-up of the primary disease, the possibility of a defect unrelated to the primary disease shold be considered e.g. Hageman trait.
In cats with neutropenia due to myelosuppression and secondary sepsis, thrombocytopenia may be die to concurrent megakaryocytic hypoplasia rather than DIC.
Adequate fluid therapy to promote microvascular circulation, but not excessive fluid therapy, which will promote oedema and bleeding is vital. If clinical 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. In cats with fulminant DIC, doses of 50-200 units/kg SQ q 6 - 8 hrs have been recommended; 75 - 100 units/kg SQ a 8 hrs is used most often. The dose may be incubated for 30 mins in the blood product prior to transfusion to activate antithrombin III, although the value of this practise is unproven. An initial goal is prolongation of the ACT or aPTT to 1.5 - 2 times the mean value of normal range or aPTT control value. It should not be used in cats with subclinical, subacute or chronic DIC, unless thromboembolism is present. If thromboembolism is present, an initial dose of 200 units/kg SQ q 6 - 8 hrs is recommended. Low molecular weight heparin is contraindicated for the treatment of feline DIC.
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 in cats, and may be of palliative benefit only (Estrin et al, 2006).
The prognosis is largely determined by the primary disease. Acute diffuse DIC has a very poor prognosis.
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