toxic alcohols (methanol & ethylene glycol)

sources

• Methanol: Windshield washer fluid, fuels, solvents, moonshine, hand sanitiser.
• Ethylene Glycol: Antifreeze, de-icers, some cleaners.

pathophysiology: the “gaps”

• Key Concept: The parent alcohol causes the Osmolar Gap. The metabolite (acid) causes the Anion Gap.
• Course:
  • Early (<12h): High Osmolar Gap, Normal Anion Gap (parent alcohol present).
  • Late (>12h): Normal Osmolar Gap, High Anion Gap (parent metabolised to acid).
  • Important: A normal Osmolar Gap does not rule out toxic alcohol ingestion if enough time has passed for metabolism to occur.

clinical presentation & signs

methanol

• CNS: Decreased LOC, headache.
• Ocular: Retinal injury, “snowfield vision”, blindness, afferent pupillary defect, retinal sheen, optic disc hyperaemia.
• GI: Abdominal pain, nausea, vomiting.

ethylene glycol

• CNS: Decreased LOC, cranial nerve palsies, tetany (due to hypocalcaemia).
• Renal: Flank pain, oliguria, frank haematuria.
• Cardiac: Prolonged QTc (due to hypocalcaemia).

diagnosis & interpretation

laboratory findings

• Classically: High Anion Gap and high Osmolar Gap (early presentation).
• Routine Labs: Lytes, Creatinine, Urine R&M (for oxalate crystals), ECG (watch QTc).
• Toxicology: Serum Methanol & Ethylene Glycol levels.

toxicology differential of anion gap and osm gaps

anion gap	osmolar gap	differential diagnosis
High	Normal	Ketones (DKA), Salicylate, Lactate (shock), Late Toxic Alcohol Ingestion
High	High	Ethylene Glycol, Methanol, Propylene Glycol, Chronic Kidney Disease (with no haemodialysis)
Normal	High	Isopropyl Alcohol, Ethanol

| Note: Severe hyperproteinaemia/hyperlipidaemia can cause pseudohyponatraemia, leading to a perceived osmolar gap.

management

1. stabilisation & supportive care

• ABCs, IV access, O2, Cardiac monitors, Foley.
• Supportive care for hypotension, seizures.

2. decontamination & enhanced elimination

• Decontamination: No role for activated charcoal. Consider NG aspirate if within 60 minutes of ingestion.
• Acidemia Correction: Administer Sodium Bicarbonate (1–2 mEq/kg bolus, then infusion 150-250 cc/hr, target pH 7.35). Acidemia drives toxic metabolites into end-organ tissues.

3. alcohol dehydrogenase (adh) inhibition

Blocks degradation of parent alcohol, preventing toxic metabolite formation.

• Fomepizole: First line.
• Ethanol: Second line (hard to titrate, causes sedation).
• Indications (if high index of suspicion, do not delay treatment):
  • Confirmed Methanol > 6.2 mmol/L OR Ethylene Glycol > 3.2 mmol/L.
  • OR Confirmed toxic ingestion + Osmolar Gap > 10.
  • OR Suspected ingestion + $\ge 2$ of: pH < 7.3, Bicarbonate < 20 mmol/L, Osmolar Gap > 10, Urine oxalate crystals.

4. cofactors

• Methanol: Folic acid 50 mg IV q6h.
• Ethylene Glycol: Thiamine 100 mg IV + Pyridoxine 50 mg IV.

5. haemodialysis

The definitive therapy, clearing both parent alcohol and toxic metabolites.

• Indications (any one of):
  • End-organ dysfunction (e.g., coma, seizures, visual defects, renal failure).
  • pH $\le 7.15$.
  • Persistent metabolic acidosis despite bicarbonate.
  • High Anion Gap metabolic acidosis not explained by other causes.
  • Very high level of parent alcohol (e.g., Methanol > 15 mmol/L, Ethylene Glycol > 8 mmol/L).
  • No antidote available (e.g., if fomepizole/ethanol unavailable).

exam pearl

Isopropyl Alcohol and Ethanol overdose treatment is primarily supportive, as their metabolites are not highly toxic.