Coagulopathies

67 Coagulopathies



Astrid Nielssen



ACQUIRED



Anticoagulant Rodenticide Intoxication



1. Which activated coagulation factors become deficient with warfarin and other vitamin K antagonists and why?

Factors II, VII, IX, and X all require posttranslational carboxylation for activation. The carboxylation of these proteins requires the presence of active vitamin K and results in the conversion of active, reduced vitamin K, by vitamin K epoxidase, to its inactive epoxide form. Vitamin K epoxide reductase then converts the inactive oxidized form back to the active form. Anticoagulant rodenticides competitively inhibit vitamin K epoxide reductase, preventing the regeneration of active vitamin K, and therefore inhibiting the production of functional vitamin K–dependent coagulation factors. Anticoagulant factors C and S also rely on vitamin K for posttranslational modification and activation.


2. How long after exposure to an anticoagulant rodenticide do clinical signs of a coagulopathy arise?

Typically, the onset of clinical symptoms occurs a few days after exposure, when all of the four affected coagulation factors have become profoundly deficient. The half-lives of the factors vary (41, 6.2, 13.9, and 16.5 hours for factors II, VII, IX, and X, respectively) and so it is possible for signs to arise earlier, in association with the depletion of factor VII. Clinical signs do not often arise this early, however, perhaps because the concurrent inhibition of anticoagulant protein C activity (half-life 8-10 hours) balances the loss of the procoagulant factor VII.


Clinical signs are those of disorders of secondary hemostasis: large volume hemorrhage, body cavity bleeds, and the absence of petechiae, ecchymoses, or mucosal bleeding.


3. What diagnostic findings may be noted in a case of anticoagulant rodenticide intoxication?

Typically with anticoagulant rodenticide intoxication, both the prothrombin time and activated partial thromboplastin time are prolonged at the time of clinical presentation, although because of the short half-life of factor VII, early in the course of the intoxication, only the prothrombin time may be prolonged. The animal’s complete blood cell count may reveal a nonregenerative anemia secondary to acute hemorrhage, but typically there is no significant aberrant red blood cell morphology. The platelet count is typically within normal limits but can be mildly to severely decreased in some cases. Antithrombin III and fibrinogen levels and the thrombin time are typically normal. A mild increase in the level of fibrin degradation products (FDPs) may be present. An alternative test to one-stage prothrombin time (OSPT) is PIVKA (proteins induced by vitamin K absence or antagonism). This test represents a diluted OSPT with greater sensitivity to decreased factor levels. The test is not specific to anticoagulant rodenticides; it will be elevated with many other coagulopathies that affect the vitamin K–dependent factors.


4. Are there any other conditions that can result in vitamin K–dependent factor deficiencies?

Diseases of the liver, pancreas, or alimentary tract that result in decreased vitamin K absorption, or severe dietary vitamin K deficiency can result in a coagulopathy.


5. How are cases of vitamin K antagonism or deficiency treated?

Initial stabilization therapy (fluids, blood products) is required for many of these animals. Care must be taken to minimize physical trauma. Thoracocentesis is not performed in those animals with hemothorax unless it is resulting in respiratory compromise. Vitamin K supplementation is implemented, often subcutaneously initially (never intravenously because it can cause anaphylaxis when administered via this route), and then as an oral maintenance therapy. Dogs with vitamin K deficiency as a result of diminished absorption require ongoing parenteral therapy. The recommended dose of vitamin K varies, but the newer generation of anticoagulant rodenticides requires higher doses and more prolonged treatment. Higher doses of vitamin K have been associated with a Heinz body anemia in some dogs. A prothrombin time can be used to assess the efficacy of therapy and should be determined 2 days after the discontinuation of therapy to ensure that the duration of treatment was adequate.



Disseminated Intravascular Coagulation



6. What is disseminated intravascular coagulation (DIC)?

DIC results from the generalized activation of the coagulation system, resulting in widespread microthrombosis. The resulting capillary injury further shifts the coagulation system into a procoagulant state and results in further consumption of procoagulant and anticoagulant factors. The older term used for DIC, consumptive coagulopathy, appropriately described a central feature of this disorder.


A mixed bleeding pattern (symptoms of abnormalities in both primary and secondary hemostasis) can be seen in dogs with DIC because of the decrease in both platelets and coagulation factors in combination with circulating inhibitors of hemostasis (e.g., FDPs). Dogs with DIC may occasionally present with the primary clinical signs of thrombosis.

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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Coagulopathies

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