Disseminated Intravascular Coagulation (DIC)

The first occurrence of Disseminated Intravascular Coagulation (DIC) in veterinary medicine has been documented as a result of incompatible blood transfusions given to dogs. The reaction that occurred, DIC was first described in the dog (Hardaway 1961; McKay, et al 1955).

DIC, a systemic process, results in and is characterized by thrombocytopenia secondary to thrombocyte consumption as a result of a massive activation of the coagulation cascade sytem³.

Severe systemic hemorrhage is a common presenting chief complaint, with blood oozing from seemingly every orifice, mucosal surface and wound (physical or iatrogenic)³. With DIC, Tissue Factor (TF) is released as a result of endothelial injury, monocytic responses to endotoxin exposure, or exposure to various cytokines. Other presenting symptomatology includes hypofibrinogenemia, fibrin degradation products, and prolonged PT. There will usually be an underlying serious illness and microangiopathic hemolytic anemia may be evident.

Epistaxis

Typically, coagulation is confined to local body areas by the combination of blood flow and circulating inhibitors of coagulation, especially antithrombin III⁹. The fact that these factors are able to circulate freely rather than remaining localized creates serious systemic consequences. Thrombin attaches fibrin to fibrinogen, causing thrombocyte aggregation. Thrombin further activates clotting Factors V and VIII while releasing plasminogen activator. Therefore, excessive thrombin activity produces hypofibrinogenemia, thrombocytopenia, depletion of coagulation factors, and fibrinolysis⁹.

DIC presenting as primary disease is rare but in those cases it is shown to be associated with infection, disorders of malparturition, leukemia and other malignancy. DIC precipitates in animals whose bodies cannot produce enough clotting factor to keep up with the consumption and is termed as Acute (decompensated). Acute DIC is caused by a variety of precipitating factors included but not limited to the venom of snakes (especially rattlesnakes), Heartworm Disease, sepsis, severe tissue injury (especially burns, head or crushing injuries), obstetric complications (amniotic fluid embolis, septic abortion, retained dead fetus), hepatic disease, acute or subacute Laminitis (cattle), Acute Renal Failure, IAHD, Acute Bronchointerstitial Pneumonia (foals), multiglandular mastitis, hepatitis, pancreatitis, selenium poisoning (grazing animals), E canis, Erysipelas (swine)²¹ major transfusion reactions⁹.

  Western Rattlesnake Dog with rattlesnake bite

When the clotting factors the animal produces are sufficient to be equal to the consumption, the disorder is termed Chronic DIC and is most commonly associated with malignancy (solid tumors) as a result of continuos slow

exposure of blood to small amounts of tissue factor (TF)^23-24. Chronic DIC typically presents with thrombosis rather than massive hemorrhage^23-24.

Regardless of acuity, DIC produces a complex coagulopathy as described herein. Of the fibrin degradation products, D-dimer is easiest detected and it is very sensitive as its cross-linking action implies direct origins from fibrin⁹. All fibrin products are cleared in the liver and thus liver enzymes may be reflective of this. The clinical hallmark of this disorder is declining fibrinogen levels. Few disorders (congenital hypofibrinogenemia, severe liver disease) cause a decrease in fibrinogen therefore it is considered to be diagnostic for DIC⁹.

Picture: D-dimer Assay Test Kit Fisher Diagnostics

Diagnosis of DIC relies upon history of the animal with important considerations being history of trauma, sepsis, malignancy, pregnancy and miscarriage. Moderate to severe thrombocytopenia and evidence of microangiopathic hemolytic anemia (schistocytes) in the peripheral blood smear. Clinically significant DIC is unlikely in the presence of normal Fibrinogen Degradation Products (FDP Latex Test) or normal D-dimer²³. Prolonged coagulation times (PT, PTT) may be noted as well as decreased fibrinogen levels being the diagnostic criteria. Thrombin time is prolonged, antithrombin III levels markedly depleted, and protein C & protein S levels are often depressed²³.