Felis ISSN 2398-2950

Acetaminophen (paracetamol) poisoning

Synonym(s): Paracetamol poisoning

Contributor(s): Rosalind Dalefield, Myra Forster-van Hijfte

Introduction

  • Rapidly absorbed, with peak levels occurring soon after ingestion.
  • Absorption from sustained release preparation can continue for many hours.
  • Signs: major manifestation hematological, can produce multi-organ failure.
  • Treatment: specific antidote N-acetylcysteine.
  • Prognosis: guarded.

Pathogenesis

Etiology

  • Access to owner's medication.
  • NB: Many cold remedies contain acetaminophen/paracetamol Paracetamol.
  • Clinical signs with dose of 50-100 mg/kg (0.5-1 tablet/cat) or 65 mg/kg/day for 3 days.
  • Owner attempting to medicate cat.
  • Feline toxic dosage 50-100 mg/kg, although clinical signs have been observed in some cats at doses as low as 10 mg/kg or 65 mg/kg/day for 3 days.

Pathophysiology

  • Multi-organ failure via the production of a toxic intermediate metabolite, N-acetyl-p-benzoquinonamine.
  • This requires glutathione for further metabolism to non-toxic metabolites (conjugation).
  • Once glutathione depleted, the toxic metabolite binds to cellular proteins causing damage.
  • Depletion of glutathione increases susceptibility of cells to oxidative injury.
  • Cat erythrocytes are particularly susceptible to oxidative injury due to their high level of sulfhydryl groups.
  • Rapidly absorbed from gastrointestinal tract.
  • At low doses acetaminophen/paracetamol is glucuronidated.
  • High doses result in N-hydroxylation by the cytochrome P-450 system, leading to formation of the reactive metabolite N-acetyl-p-benzoquinonamine   →   severe oxidative damage to red blood cells and hepatocytes.
  • Cats have limited capacity to conjugate glucoronides so very susceptible to poisoning.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Avizeh R, Najafzadeh H, Razijalali M et al (2010) Evaluation of prophylactic and therapeutic effects of silymarin and N-acetylcysteine in acetaminophen-induced hepatotoxicty in cats. J Vet Pharmacol Therap 33 (1), 95-99 PubMed.
  • Yang R, Miki K, He X et al (2009) Prolonged treatment with N-acetylcystine delays liver recovery from acetaminophen hepatotoxicity. Crit Care 13 (2), R55 PubMed.
  • Webb C B, Twedt D C, Fetttman M J et al (2003) S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. J Fel Med Surg (2), 69-75 PubMed.
  • Thomas A (2002) Paracetamol poisoning. UK Vet (5), 39-42.
  • Mayer S (1991) Poisons - paracetamol. In Practice 13 (1), 37 VetMedResource.

Other sources of information

  • Sellon R K (2001) Acetominophen. 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.
  • Lorgue G, Lechenet J and Reviere A (1966) Clinical Veterinary Toxicology.Oxford: Blackwell Scientific Publications, pp132-133.

Organisation(s)


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