Introduction

• Rodenticide poison produced as grain-based bait or pellets.
• Signs: neurological signs with seizures.
• Diagnosis: signs and post-mortem demonstration of bromethalin or the metabolite desmethylbromethalin in tissues.
• Treatment: symptomatic with repeat dose activated charcoal and possibly lipid infusion.
• Prognosis: guarded and may need prolonged aftercare.

Pathogenesis

Etiology

• Direct ingestion of bait/pellets.
• Eating small vermin which have been poisoned.

Predisposing factors

• Young age.

Pathophysiology

• Both bromethalin and the active metabolite desmethylbromethalin uncouple oxidative phosphorylation.

• There is inadequate ATP production by mitochondria and then decreased sodium/potassium ion channel pump activity.
• Cells lose their osmotic control and retain sodium and swell with water resulting in cerebral edema and increased CSF pressure.
• The oral LD₅₀ in dogs has been reported as 3.65 mg/kg and 4.7 mg/kg.
• In toxicity studies, dogs remained asymptomatic after 0.5 to 1.5 mg/kg (5-15 mg/kg of 0.01% bait).
• In clinical cases signs have occurred with doses as low as 0.15 mg/kg with deaths from doses as low as 0.95-1.05 mg/kg.

Timecourse

• At low doses signs can occur within 1-7 days at higher doses (approximately 5 mg/kg) signs can occur within 2-36 hours. 
• At low doses signs can progress for 1-2 weeks.
• At high doses death can occur within 4-63 hours.

Epidemiology

• Cases are generally reported in North America and following changes in rodenticide regulations cases in companion animals are increasing.

Diagnosis

Treatment

Prevention

Outcomes