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

Treatment

Outcomes