Methanol exposure in a toddler with 3-Methylcrotonyl CoA Carboxylase Deficiency [abstract] Abstract uri icon
  • Introduction: Methanol exposure is a common toxicologic problem in children, however methanol exposure in a child with a pre-existing metabolic disorder that causes metabolic acidosis represents a unique challenge. A review of the literature reveals no cases of methanol exposure in children with pre-existing metabolic disorders. We report such a case.
    Case Report: A 16 month-old girl with a history of 3-Methylcrotonyl CoA Carboxylase Deficiency (3-MCCD) was brought to the emergency department by her parents 2 hours after she accidentally drank a mouthful of windshield wiper fluid that contained 50% methanol. Her parents witnessed the incident and were certain this was an acute isolated exposure. On arrival the patient had no complaints and was noted to be acting normally by her parents. Her physical exam, including vital signs, was normal. Laboratory values were as follows: methanol 6 mg/dL, sodium 145 mEq/L, chloride 110 mEq/L, bicarbonate 16 mEq/L, (anion gap 19), BUN 16 mg/dL, glucose 110 mg/dL, serum osmolality 298 mOsm (mOsm gap 4) and urine drug screen, including high performance liquid chromatography and mass spectrometry, was negative. Because of the wide anion gap metabolic acidosis she was treated with fomepizole and admitted for observation. The following morning her methanol level was zero, her acidosis had resolved (bicarbonate 22 mEq/L, anion gap 9), and she was discharged home.
    Discussion: 3-MCCD is an inherited autosomal recessive metabolic disorder resulting in an inability to correctly metabolize the amino acid Leucine. Patients with 3-MCCD have clinical presentations that range from severe to benign but are susceptible to the development of significant catabolic stress resulting in lethargy, apnea, hypotonia, and seizures. Metabolic disturbances of the disease include hypoglycemia, metabolic acidosis, and ketonuria. Methanol ingestion can also result in a signifi cant metabolic acidosis. It is uncertain if this child's acidosis was the result of her 3-MCCD, her methanol exposure, or both. It is also possible the time of ingestion was not correct, however there was no reason to suspect this clinically. Given the accepted "non-toxic" level of 20 mg/dL has dubious supporting evidence, it is uncertain if any detectable level of methanol in these children can truly be considered non-toxic.
    Conclusion: Children with pre-existing metabolic disorders prone to acidosis who ingest methanol present a clinical dilemma. Clinicians who care for these patients should consider treatment with fomepizole, even when measured methanol concentrations fall in the traditionally non-toxic range.

  • publication date
  • 2011
  • Research
  • Drugs and Drug Therapy
  • Emergency Medicine
  • Pediatrics
  • Poisoning
  • Additional Document Info
  • 49
  • issue
  • 6