ISSN 2398-2969      

Anticoagulant rodenticide poisoning

icanis

Synonym(s): Brodifacoum Bromadiolone Chlorofacinone Coumafen Coumatetralyl Difethialone Diphacinone Warfarin


Introduction

  • Anticoagulant rodenticides available commercially in cereal-based baits at a concentration of 0.005%.
  • Some professional-use products may be at concentrations as high as 0.1%.
  • Second generation anticoagulants are more toxic in repeated small doses than a single dose.
  • Cause: ingestion of contaminated bait → blocks action of Vitamin K1.
  • Signs: delayed from 2-10 days post-exposure: internal and external hemorrhage and bruising.
  • Treatment: SQ vitamin K1, whole blood transfusion.
    Do not use vitamin K3 as it is less effective.
  • Prognosis: good with appropriate therapy.
Follow the diagnostic tree for Anticoagulant rodenticide ingestion Anticoagulant rodenticide ingestion.

Pathogenesis

Etiology

  • Ingestion of rodenticides, eg:
    • Difenacoum LD50 50 mg/kg.
    • Warfarin LD50 20-300 mg/kg.
    • Brodifacoum LD50 0.2-4 mg/kg.
    • Bromodialone LD50 6-15 mg/kg.
  • Poisoning rarely follows ingestion of poisoned rodents. Must be major portion of diet.

Pathophysiology

  • Anticoagulant rodenticides inhibit 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.
  • Coagulopathy when clotting factors reduced to 25% of normal levels → profuse bleeding following trauma.
  • Short-acting rodenticides, eg warfarin, coumafuryl and pindone, generally require multiple exposures before coagulopathy occurs and toxic effects usually last <1 week.
  • Second generation (longer acting) rodenticides, eg diphacinone, brodifacoum and bromadiolone, may produce a coagulopathy after a single dose and toxic effects may persist for >3 weeks.
  • Signs do not develop until body reserves of vitamin K have been depleted, ie 24-48 h after ingestion of rodenticide.
  • Similar coagulation defects may be iatrogenic, eg induced by anticoagulant therapy with warfarin.

Timecourse

  • Clinical signs of poisoning appear 2-10 days following ingestion.
  • Synthesis of clotting factors takes 8 h hence cannot show improvement in less than this time after treatment.
  • Morbidity/recovery related to site and extent 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.
  • Blocker T L et al (1999) Acute tracheal obstruction associated with anticoagulant rodenticide intoxication in a dog. JSAP 40 (12), 577-80 PubMed.
  • Sheafer S E , Couto C G (1999) Anticoagulant rodenticide toxicity in 21 dogs. JAVMA 35, 38-46 PubMed.
  • Lewis D C et al (1997) Thrombocytopenia in dogs with anticoagulent rodenticide induced haemorrhage- eight cases (1990-1995). JAAHA 33, 417-422 PubMed.
  • Berry C R et al (1993) Thoracic radiographic features of anticoagulant rodenticide toxicity in 14 dogs. Vet Rad 34 (6), 391-396 VetMedResource.
  • Mayer S (1990) Poisons - Coumarin derivatives. In Practice 12 (4), 174-174 VetMedResource.

Other sources of information

  • Campbell A (VPIS) (2002) The management of anticoagulant rodenticide poisoning in companion animals. UK VET 7(3), 23-25.

Organisation(s)

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