Introduction

• Rodenticide, rat poison.
• Signs: extensor rigidity, seizures, tremors, sensitivity to light and/or sound.
• Diagnosis: history, clinical signs, analysis of vomit or stomach contents.
• Treatment: symptomatic - no specific antidote.
• Prognosis: good if seizures controlled and decontamination procedures followed.

Pathogenesis

Etiology

• Strychnine is a plant alkaloid derived from seeds ofStrychnos nux-vomicaandStrychnos ignatii. These are trees native to southern Asia and northern Australia.
• Accidental ingestion of bait containing strychnine.
• Professional strength rodenticides typically contain more than 0.5% strychnine. Baits available to the public typically contain <0.5% strychnine.
• Malicious use of bait to poison dogs.

Pathophysiology

• Strychnine is rapidly absorbed following ingestion and the severity of signs is dependent on the amount of toxin ingested.
• Strychnine reversibly blocks the binding of glycine, an inhibitory neurotransmitter, at postsynaptic spinal neurons.
• This results in uncontrolled excitation of the spinal cord reflexes.
• The extensor muscles are predominantly stimulated resulting in extensor rigidity and the classic sawhorse stance.
• Death can occur when the muscles of respiration are affected, leading to apnea and hypoxia.
• Strychnine is metabolized by the liver to strychnine N-oxide and eliminated as hepatic metabolites. The parent compound is also eliminated in the urine.
• The half life of strychnine is about 10 hours.
• Dogs are more susceptible than cats. LD50 in dogs is >0.2 mg/kg. In cats, the LD50 is >0.5 mg/kg.
• Ingestion of recently poisoned rodents and birds can result in relay toxicosis.

Timecourse

• Signs typically develop within 15 minutes to 2 hours after ingestion.
• If low levels are ingested, delayed and mild symptoms may occur.

Diagnosis

Treatment

Prevention

Outcomes