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Intoxication with sodium monofluoroacetate (compound 1080)

Renee F Robinson1, Jill R Griffith, William R Wolowich

  • 1Pediatric Pharmacotherapy/NIH Clinical Research K30 Program, College of Pharmacy, The Ohio State University, Childrens Research Institute, The Central Ohio Poison Control Center, Columbus 43210, USA.

Veterinary and Human Toxicology
|April 5, 2002
PubMed

Insights

Intentional ingestion of sodium monofluoroacetate (SMFA), a banned rodenticide, caused severe toxicity, including seizures and anion gap metabolic acidosis. This case highlights the importance of recognizing SMFA poisoning despite its restricted use.

Area of Science:

  • Toxicology
  • Emergency Medicine
  • Clinical Case Reports

Background:

  • Sodium monofluoroacetate (SMFA) is a highly toxic compound previously used as a rodenticide in the U.S. and banned in 1972.
  • Intentional ingestion of SMFA is rare, with this case representing the first reported instance in the U.S. in over 15 years.

Observation:

  • A 47-year-old male presented with a tonic-clonic seizure following intentional SMFA ingestion.
  • The patient exhibited progressive neurological decline, requiring intubation and mechanical ventilation.
  • Clinical course included agitation, hypertension, and anion gap metabolic acidosis.

Findings:

  • The patient demonstrated severe central nervous system toxicity and metabolic derangement consistent with SMFA poisoning.
  • Despite the severity of initial symptoms, the patient experienced a remarkable recovery without apparent neurological sequelae.
  • Recovery occurred over several days with supportive care, including mechanical ventilation.

Implications:

  • This case underscores the persistent risk of SMFA toxicity, even after its ban, emphasizing the need for heightened awareness among healthcare professionals.
  • Early recognition and management of SMFA poisoning are crucial for patient survival and preventing long-term complications.
  • The case highlights SMFA's potential to induce severe anion gap metabolic acidosis and profound neurological impairment.

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