Anticoagulant rodenticide poisoning in Cats (Felis) | Vetlexicon
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Anticoagulant rodenticide poisoning

ISSN 2398-2950

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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 intoxicationJ Feline Med Surg (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.

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