Professor and Associate Chair, University of Florida, College of Veterinary Medicine
Gainesville, FL, USA
Disseminated intravascular coagulation (DIC) is a pathologic process that is caused by a coexisting serious medical or surgical disorder. It results from the activation of both the coagulation and fibrinolytic systems and is triggered by the activation of tissue factor. The most common causes and mechanisms of DIC in the dog and cat are shown below. Most begin with the production of excess tissue factor which feeds into and activates the coagulation process.
|
Clinical Setting |
Mechanism |
|
Infection: bacterial, viral, fungal |
Especially common in gram-negative sepsis where endotoxin stimulates monocytes and endothelial cells to express tissue factor. |
|
Neoplasia |
Malignant cells cause endothelial damage and allow the expression of tissue factor as well as other procoagulant materials. |
|
Trauma |
Burns, hypo- and hyperthermia, rhabdomyolysis, and hypoxia damage endothelial cells and allow for the exposure of tissue factor. |
|
Liver disease |
Both acute and chronic. In acute form, tissue factor is expressed, but in the chronic form, the liver cannot clear the system of fibrin split products which have their own fibrinolytic effect.
Also in chronic disease the liver can cease producing coagulation factors. |
|
Vascular disease |
Commonly seen in hemangiosarcomas because of damaged endothelial cells, release of tissue factor. |
|
Envenomation |
Varies with species and toxin. Endothelial cells can be damaged and tissue factor released. |
|
Transfusion reaction and acute hemolytic reaction |
Release of tissue factor. DIC can be severe. |
Clinical Findings
The complications are related to the primary disease process in addition to the bleeding and/or thrombosis that predominates. The skin and mucous membranes can have petechia and ecchymotic hemorrhages, and bleeding can occur just about anywhere in the body including the GI, urinary and central nervous system. Bleeding can also occur from any orifice, venipuncture sites and surgical wounds.
Signs resulting from organ ischemia can occur wherever pathologic thromboses occur, and this might become evident as intestinal infarction, stroke, and myocardial dysfunction. Other signs reflecting other sites of involvement will also occur.
Diagnosis
The clinical suspicion occurs whenever sudden thrombosis or hemorrhage occurs in any patient that has a condition known to predispose to this disorder. The typical laboratory findings include a prolonged prothrombin and partial thromboplastin times, low platelet and serum fibrinogen levels, increased fibrin split products, and increased D-dimer blood levels. Other findings include the presence of fragmented red cells and low specific clotting factor assays for Factors II, V, VII, VIII, and IX.
Treatment
The treatment priorities should be toward treating the primary disease process concomitant to providing hemodynamic stabilization with intravenous fluids. Coagulation factor replacement is necessary if overt bleeding is present. The factor needs can be met with fresh frozen plasma (FFP) while fibrinogen needs are replenished with cryoprecipitate. If severe thrombocytopenia is present (platelet count <10,000), platelet transfusions are indicated. Vitamin K should also be administered subcutaneously.
If thrombosis is apparent, heparin can be given at a dosage ranging 50-200 units/kg. Iatrogenic hemorrhage due to heparin is lessened if it is given slowly by constant rate infusion (cri) after the initial bolus injection. It can also be given SQ every 6 hours. It is common in veterinary medicine to administer the FFP and the heparin simultaneously. Heparin might not be beneficial where chronic liver disease decreases the production of antithrombin 3 globulin.