Anticoagulant rodenticide poisoning
Introduction
- Anticoagulant rodenticides available commercially in cereal-based baits at a concentration of 0.02% to 1.0%.
- Cats are rarely poisoned.
- Cause:ingestion of rodenticide → blocks action of Vitamin K1.
- Signs: delayed from 1-5 days post exposure: internal and external hemorrhage and bruising.
- Treatment: vitamin K1 (phytomenadione) Vitamin K , whole blood transfusion if required.
Do not use vitamin K3 as it is less effective. - Prognosis: good with appropriate therapy.
Presenting signs
- Weakness.
- Lethargy.
- Dyspnea.
- Pallor.
- Epistaxis and/or melena and/or hemoptysis and/or hematomas and/or lameness.
- Seizures, paresis or paralysis may occur if bleeding occurs within the CNS.
- Hemorrhage into a major body cavity may cause acute collapse.
- Single doses of short acting anticoagulants may produce minimal symptoms.
Petechiae on mucous membranes indicate defect primary hemostasis, eg thrombocytopenia, NOT a feature of anticoagulant rodenticide toxicity.
Acute presentation
- Hypovolemic shock following massive internal bleeding.
- May be accompanied by dyspnea in hemo-thorax or abdominal distension in hemo-peritoneum.
Geographic incidence
- Outdoor cats with access to poison or poisoned prey.
Pathogenesis
Etiology
- Cats are less often poisoned by dogs, but poisoning may follow ingestion of poisoned rodents.
- Reported acute oral LD 50s for the cat:
- Warfarin 5-30 mg/kg
- Diphacinone 15 mg/kg
- Brodifacoum >25 mg/kg.
- Bromadiolone > 25 mg/kg.
Pathophysiology
- Anticoagulant rodenticides inhibit Vitamin K epoxide reductase, the enzyme involved in production of active vitamin K.
- Clotting factors II (prothrombin), VII, IX and X all require active vitamin K to function effectively.
- Factor VII has shortest half-life and is therefore first to be affected by anti-coagulant poisoning.
- Depletion of clotting factors results in coagulopathy and profuse bleeding following trauma.
- Short acting rodenticides (eg warfarin, coumafuryl and pindone) generally require multiple exposures before coagulopathy occurs and toxic effects may resolve after 7 to 10 days.
- Second generation (longer acting) rodenticides (eg diphacinone, brodifacoum and bromadiolone) may produce a coagulopathy after a single dose and toxic effects may persist for more than 3 weeks.
- Signs do not develop until body reserves of vitamin K have been depleted, ie >24 hours after ingestion of rodenticide.
- Toxicity may be potentiated by phenylbutazone, diphenylhydantoin, adrenocorticosteroids, and sulfonamides.
Timecourse
- Clinical signs of poisoning usually appear 3-5 days following ingestion.
- Morbidity/recovery related to site of hemorrhage.
- Death, if it occurs, is usually within 1-6 days.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Kohn B, Weingart C & Giger U (2003) Haemorrhage in seven cats with suspected anticoagulant rodenticide intoxication. J Feline Med Surg 5 (5), 295-304 PubMed.
Other sources of information
- Murphy M J & Talcott P A (2001) Anticoagulant Rodenticides. In: Small Animal Toxicology.Eds: M E Peterson and P A Talcott. Philadelphia: W B Saunders. ISBN: 0 7216 7826 2.
- Osweiler G D (1995) Toxicology. Philadelphia: Williams and Wilkins. ISBN: 0 6830 6664 1.
Organisation(s)
- ASPCA Animal Poison Control Center: www.aspca.org/pet-care/animal-poison-control, telephone (888) 426-4435.
- Veterinary Poisons Information Service (VPIS); www.vpisglobal.com, telephone + 44 (0) 2073 055 055.