Strychnine toxicity

Strychnine has had a colorful history from Wes Anderson’s “The Grand Budapest Hotel” to Tovery swallowing some down with a charcoal chaser to prove how effective charcoal can be at the French Academy of Medicine in 1831. Strychnine is not exactly a subtle toxicity, generalised muscle spasms can be seen within 30 seconds and death from respiratory failure follows. It is an ergot-type alkaloid used as a rodenticide.

Toxic Mechanism:

Strychnine is a competitive glycine antagonist at the brainstem and spinal postsynaptic receptors. Glycine is normally an inhibitory neurotransmitter, once antagonised there is loss of normal descending inhibitory motor tone resulting in muscle spasm. Ventilatory failure occurs secondary to severe muscular spasm.

Toxicokinetics: 

  • Rapid absorption following ingestion or inhalation (not dermal)
  • Large volume of distribution 13 L/kg
  • 30% excreted uncharge in the urine whereas the rest undergoes microsomal hepatic metabolism before renal excretion.
  • Elimination half life 10 – 16 hours

Resuscitation:

  • Potential life threats: Generalised muscle rigidity and respiratory failure.
  • Prompt neuromuscular paralysis, intubation and ventilation are life saving.

Risk Assessment

  • Adults: As little as 30 – 100 mg can be lethal (equal to 1 g of 0.03% powder).
  • In children: an accidental taste is potentially lethal.
  • Death can occur within 30 minutes.
  • Sublethal doses can cause painful generalised muscle spasms and stiffness precipitated by external stimuli.
  • Clinical features range from the following:
    • Nausea, agitation, twitching and muscle spasm occurs within minutes progressing to painful muscles spasms in all voluntary muscles (risus sardonicus and opisthotonos can be seen).
    • In severe cases hyperthermia, rhabdomyolysis, lactic acidosis and respiratory paralysis.
    • Loss of consciousness does not occur until secondary hypoxia occurs.
    • Muscle spasms and rigidity resolve within 24 hours if ventilation and oxygenation is maintained. The recovery phase is then complicated by myoglobinuria and renal failure. Depending on how soon supportive care is initiated, hypoxic brain injury can be a complication.

Supportive Care

  • Muscle spasm in less severe cases: titrated doses of benzodiazepines are effective e.g. diazepam 2.5 – 5 mg every 5 minutes IV until a reduction in spasms are achieved
  • If intubated consider FASTHUGSINBED Please

Investigations

  • Screening: 12 lead ECG, BSL, Paracetamol level
  • Specific:
    • Serum or urine strychnine levels are only good for confirming the diagnosis retrospectively i.e. forensics.
    • EUC, CK, blood gas, lactate and troponin

Decontamination:

  • Activated Charcoal 50 gram PO (1 g/kg in children) only once the airway is secured.

Enhanced Elimination

  • Not clinically useful

Antidotes

  • None available

Disposition

  • Patients who are clinically well 4 hours post exposure without muscle twitching or spasms are not poisoned and medically cleared. Discharge should not occur overnight.
  • Patient who are symptomatic require ICU level of care and can be cleared once muscle spasms and rigidity have subsided. Secondary complications of spasm or hypoxia will need to be sought and treated.

References and Additional Resources:

Additional Resources:

References:


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Dr Neil Long BMBS FACEM FRCEM FRCPC. Emergency Physician at Burnaby Hospital in Vancouver. Loves the misery of alpine climbing and working in austere environments. Supporter of FOAMed, toxicology, tropical medicine, sim and ultrasound

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