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EM TopicsToxicology and environmental emergencies

EM · Toxicology and environmental emergencies

Toxic alcohol poisoning (methanol and ethylene glycol)

Also known as Methanol poisoning · Ethylene glycol poisoning · Antifreeze poisoning · Windshield washer fluid ingestion · Toxic alcohol ingestion

Toxic alcohol poisoning — methanol (windshield washer, illicit spirits) and ethylene glycol (antifreeze) are small alcohols metabolised by alcohol dehydrogenase to the acids that do the harm: methanol to formaldehyde then formic acid (the blindness, the putaminal necrosis on CT, the high anion gap metabolic acidosis), ethylene glycol to glycolic acid and oxalic acid (the calcium oxalate crystals in the urine, the acute kidney injury). The bedside signature is a high anion gap metabolic acidosis paired with an elevated osmolar gap. Management is alcohol dehydrogenase blockade with fomepizole 15 mg/kg IV loading then 10 mg/kg every 12 hours (or 10 per cent ethanol at 10 mL/kg bolus then 1 to 2 mL/kg/h as the cheaper alternative), cofactors (folinic acid 1 mg/kg for methanol; thiamine and pyridoxine for ethylene glycol), and haemodialysis for the severe case. The differential is the high anion gap metabolic acidosis: lactic acidosis, DKA, salicylate, uraemia. ACEM-primary, globally tagged.

high9 referencesUpdated 13 Sept 202623 min readVerification in progress

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Red flags

  • A high anion gap metabolic acidosis with an elevated osmolar gap is a toxic alcohol until proven otherwise — measure the osmolar gap (measured minus calculated osmolarity) in any unexplained metabolic acidosis
  • The osmolar gap and the anion gap move in opposite directions over time: the gap is osmolar early (parent alcohol, before metabolism) and anionic late (metabolised to acids) — a normal osmolar gap does NOT exclude a toxic alcohol in a late presenter
  • Start fomepizole on clinical suspicion (the acidosis, the visual symptoms, the history) — do not wait for the serum methanol or ethylene glycol level, which takes hours and may not be available
  • Visual blurring, photophobia, a 'snowstorm' field, or optic disc oedema with a high anion gap acidosis is methanol poisoning until proven otherwise — the retina and optic nerve are the target of formate
  • Ethylene glycol produces calcium oxalate crystals in the urine sediment and an acute kidney injury — examine a fresh urine sample for envelope and needle-shaped crystals
  • Bilateral putaminal necrosis on CT in a comatose acidotic patient is characteristic of methanol poisoning and signals severe, established toxicity
On this page

Related topics

  • Salicylate poisoning
  • Paracetamol poisoning
  • DKA, HHS and hypoglycaemia
  • The toxidrome approach and the general management of the poisoned patient
  • Carbon monoxide poisoning
  • Electrolyte emergencies — potassium and sodium
  • Tricyclic antidepressant poisoning (emergency department diagnosis and management)
Study tools

Your progress

Saved on this device.

Target exams

ACEMFRCEMABEMFRCPCCCFPEMEBEEM

Red flags

  • A high anion gap metabolic acidosis with an elevated osmolar gap is a toxic alcohol until proven otherwise — measure the osmolar gap (measured minus calculated osmolarity) in any unexplained metabolic acidosis
  • The osmolar gap and the anion gap move in opposite directions over time: the gap is osmolar early (parent alcohol, before metabolism) and anionic late (metabolised to acids) — a normal osmolar gap does NOT exclude a toxic alcohol in a late presenter
  • Start fomepizole on clinical suspicion (the acidosis, the visual symptoms, the history) — do not wait for the serum methanol or ethylene glycol level, which takes hours and may not be available
  • Visual blurring, photophobia, a 'snowstorm' field, or optic disc oedema with a high anion gap acidosis is methanol poisoning until proven otherwise — the retina and optic nerve are the target of formate
  • Ethylene glycol produces calcium oxalate crystals in the urine sediment and an acute kidney injury — examine a fresh urine sample for envelope and needle-shaped crystals
  • Bilateral putaminal necrosis on CT in a comatose acidotic patient is characteristic of methanol poisoning and signals severe, established toxicity
The one-line answer

Toxic alcohol poisoning is two small alcohols — methanol and ethylene glycol — that are themselves almost harmless (mild inebriation, nothing more) but, once oxidised by alcohol dehydrogenase, become the acids that kill: methanol to formic acid (the blindness, the bilateral putaminal necrosis), ethylene glycol to glycolic and oxalic acid (the acute kidney injury, the hypocalcaemia). The bedside signature is a high anion gap metabolic acidosis paired with an elevated osmolar gap; the decisive move is to block the dehydrogenase with fomepizole 15 mg/kg IV loading then 10 mg/kg q12h on suspicion, add the cofactor (folinic acid for methanol, thiamine and pyridoxine for ethylene glycol), and dialyse the severe case (pH below 7.3, visual impairment, renal failure, or a level above 50 mg/dL).[1]

Meet the patient

A 48-year-old man is brought in 18 hours after a drinking session at a party. He looks drunk — ataxic, drowsy, slurring — but there is no smell of ethanol on his breath, and over the next hour his breathing deepens into a Kussmaul pattern while his GCS slides from 14 to 11. He keeps rubbing his eyes and says the fluorescent lights look like "a snowstorm". The venous gas returns pH 7.18, bicarbonate 9, anion gap 28; the measured osmolarity is 328 against a calculated 287.[6]

Hold three questions and the rest of the topic slots into place: is the acidosis a toxic alcohol? (calculate the osmolar gap — 328 minus 287 is 41, markedly raised), which alcohol? (the snowstorm vision points to methanol — the retina is formate's target), and what do I do in the next minute, before the serum level ever returns? (block the dehydrogenase).[1]

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References9ShowHide
  1. [1]Brent J, McMartin K, Phillips S, et al. Fomepizole for the treatment of ethylene glycol poisoning. Methylpyrazole for Toxic Alcohols Study Group. N Engl J Med, 1999.PMID 10080845
  2. [2]Brent J, McMartin K, Phillips S, et al. Fomepizole for the treatment of methanol poisoning. N Engl J Med, 2001.PMID 11172179
  3. [3]Roberts DM, Yates C, Megarbane B, et al. Recommendations for the role of extracorporeal treatments in the management of acute methanol poisoning: a systematic review and consensus statement. Crit Care Med, 2015.PMID 25493973
  4. [4]Ghannoum M, Gosselin S, Hoffman RS, et al. Extracorporeal treatment for ethylene glycol poisoning: systematic review and recommendations from the EXTRIP workgroup. Crit Care, 2023.PMID 36765419
  5. [5]McMartin K, Brent J Analysis of Fomepizole Elimination in Methanol- and Ethylene Glycol-Poisoned Patients. J Med Toxicol, 2022.PMID 34697779
  6. [6]Inman B, Maddry JK, Ng PC, et al. High risk and low prevalence diseases: Toxic alcohol ingestion. Am J Emerg Med, 2023.PMID 36796238
  7. [7]Barceloux DG, Krenzelok EP, Olson K, Watson W American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol Poisoning. Ad Hoc Committee. J Toxicol Clin Toxicol, 1999.PMID 10497633
  8. [8]Barceloux DG, Bond GR, Krenzelok EP, Cooper H, Vale JA American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. J Toxicol Clin Toxicol, 2002.PMID 12216995
  9. [9]Benitez JG, Swanson-Biearman B, Krenzelok EP Nystagmus secondary to fomepizole administration in a pediatric patient. J Toxicol Clin Toxicol, 2000.PMID 11192468
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Related topics

  • Salicylate poisoning
  • Paracetamol poisoning
  • DKA, HHS and hypoglycaemia
  • The toxidrome approach and the general management of the poisoned patient
  • Carbon monoxide poisoning
  • Electrolyte emergencies — potassium and sodium
  • Tricyclic antidepressant poisoning (emergency department diagnosis and management)