Rodenticide Toxicoses

Chapter 31


Rodenticide Toxicoses



Pesticides account for about 25% of toxin exposures in pets. Insecticides (see Chapter 32) and rodenticides represent the majority of these pesticide exposures. The rodenticides most frequently encountered by dogs and cats are anticoagulant rodenticides, cholecalciferol, strychnine, zinc phosphide, and bromethalin. Cholecalciferol is discussed in Web Chapter 5. The prevalence of rodenticide exposure in pets may change in upcoming years because the U.S. Environmental Protection Agency issued a direct final rule in 2008, with a final implementation date of June 2011 regarding residential rodenticide use. Briefly, rodenticides for residential use should be distributed in bait stations, and the second-generation anticoagulant rodenticides may no longer be directly available to residential users. The key aspects of toxicosis associated with anticoagulant rodenticides, bromethalin, strychnine, and zinc phosphide follow.



Anticoagulant Rodenticides


The anticoagulant rodenticides continue to be the pesticide most commonly inquired about by animal owners. These compounds (including warfarin, brodifacoum, bromadiolone, diphacenone, and chlorophacinone) represent a substantial proportion of actual toxicoses treated in veterinary and emergency clinics. All anticoagulant rodenticides act by inhibiting the recycling of vitamin K1 from vitamin K1 epoxide reductase. This inhibition leads to a reduction in the active forms of clotting factors II, VII, IX, and X in circulation, with factor VII and the extrinsic pathway affected initially. The reduction in the active forms of these factors leads to prolonged clotting times. Prolonged clotting time is most commonly measured by activated clotting time (ACT), one-stage prothrombin time (PT), activated partial thromboplastin time (APTT), or a combination of these tests in the clinic. Prolongation of these times to 15% to 25% above the upper end of the normal range is commonly interpreted as a coagulopathy. Toxic doses of anticoagulant rodenticides induce a coagulopathy. The coagulopathy is not always apparent on clinical presentation and typically is delayed for a number of days following ingestion. The so-called second-generation anticoagulant rodenticides have a much longer duration of action when compared to warfarin. The toxic dose and median lethal dose (LD50) for various anticoagulant rodenticides in dogs and cats is quite variable. Data for specific compounds can be found in consultation with veterinary toxicologists (see www.abvt.org).


Anticoagulant rodenticide toxicosis should be considered in dogs or cats with dyspnea, exercise intolerance, coughing, or hemoptysis related to intrathoracic or intrapulmonary hemorrhage. Intrapulmonary hemorrhage occurs commonly in anticoagulant rodenticide toxicosis. Large pleural effusions and marked intrapulmonary bleeding (seen as a coarse, alveolar lung pattern) may be evident on thoracic radiography. Prolonged bleeding from venipuncture sites may be observed. Hematomas, hematemesis, melena, hemoptysis, hematuria, and pallor of mucous membranes are other relatively common clinical signs observed in animals with anticoagulant rodenticide toxicosis. Bleeding may occur in unusual locations such as the pericardial space or into the spinal cord. Of course, anticoagulant rodenticides represent just one cause of coagulopathies in dogs and cats, and other bleeding disorders must be considered.


Detection of the specific anticoagulant rodenticide in serum is the most definitive means of confirming exposure to an anticoagulant rodenticide in a live animal. Liver is the specimen of choice for a dead animal. This testing is now available in many veterinary diagnostic laboratories throughout the United States (see www.aavld.org).


Anticoagulant rodenticide–induced coagulopathies are commonly distinguished from other causes of coagulopathy in the clinic by a relatively rapid response to vitamin K1 treatment. ACT, PT, and APTT are each dramatically shortened within 24 hours of initiating daily therapy with 2.5 to 5 mg/kg of vitamin K1 administered orally or subcutaneously (but not intravenously or intramuscularly) with a small-gauge needle. Anaphylaxis can occur with parenteral administration of K1 by any route. Failure to see an initial response may suggest that the coagulopathy is not caused by anticoagulant rodenticide exposure. Oral therapy is very effective; some clinicians divide the daily dose into two or three treatments and aim to enhance absorption of the vitamin by administration with a fatty meal, such as some canned dog foods.


In certain cases of recent ingestion (within 2 to 4 hours of presentation), general measures for treatment of toxicosis should be considered, including induction of emesis and administration of activated charcoal (see Chapter 23). Clotting tests are often normal in these cases, so they should be monitored for at least 3 days. Vitamin K1 treatment should be administered if the clotting time is prolonged.


A severe coagulopathy may call for more than simple vitamin K1 treatment, and the clinician must appreciate that effects of vitamin K1 are not immediate. Animals with a packed cell volume less than 15 or those demonstrating complications of anemia may need fresh whole blood immediately. Furthermore, vitamin K1 alone may be insufficient when results of coagulation tests show rapidly progressing prolongation in clotting times. In these cases, administration of fresh or frozen plasma may be needed to provide clotting factors. Blood product therapy may be required for 12 to 36 hours after initiating vitamin K1 therapy to allow time for the synthesis of new functional clotting factors. Thoracocentesis may be needed if there is significant dyspnea related to bleeding within the pleural space. Rest, mild sedation, and oxygen are appropriate for intrapulmonary hemorrhage unless respiratory failure has developed, in which case short-term ventilation may be needed.


The dose and duration indicated for vitamin K1 vary with the specific anticoagulant rodenticide responsible for the coagulopathy. Dosages of 1 to 2.5 mg/kg daily for 3 to 5 days were often effective in treating toxicoses caused by warfarin. Treatment of brodifacoum, diphacenone, and chlorophacinone often requires vitamin K1 at 2.5 to 5 mg/kg daily for 2 to 4 weeks. Tests of clotting function can be useful guides for the duration of therapy. The bioavailability of vitamin K1 is greatest when given orally; thus this route is preferred unless contraindicated because of vomiting. Vitamin K1 may be given subcutaneously but should not be given intramuscularly or intravenously because of the increased risk of massive hemorrhage or anaphylaxis, respectively. Vitamin K3 therapy is contraindicated because it is not effective and may induce oxidative damage to red cells.


Clients should be educated to remove all anticoagulant rodenticide bait from the pet’s environment. Unfortunately, pets occasionally are reexposed to rodenticide bait following discharge from the clinic. The long-acting anticoagulant rodenticides may be present in the serum and liver of the pet for weeks following successful treatment and recovery. Accordingly some anticoagulant rodenticides may be detected by analytic chemistry techniques in animals with no demonstrable coagulopathy and consequently no toxicosis.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Rodenticide Toxicoses

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