Overview
Toxic Alcohol Poisoning (Methanol & Ethylene Glycol)
Topic Overview
Summary
Toxic alcohol poisoning refers to ingestion of methanol or ethylene glycol, both of which are metabolised to toxic metabolites causing severe morbidity and mortality. Methanol metabolises to formic acid (causes blindness). Ethylene glycol metabolises to oxalic acid (causes renal failure). Both cause high anion gap metabolic acidosis. Treatment is fomepizole (or ethanol) to block alcohol dehydrogenase, plus haemodialysis for severe cases.
Key Facts
- Methanol: Metabolised to formic acid → optic nerve damage → blindness ("blind drunk")
- Ethylene glycol: Metabolised to oxalic acid, glycolic acid → renal failure
- Presentation: Inebriation followed by high anion gap metabolic acidosis (HAGMA)
- Investigations: Osmolar gap (early), anion gap (later), specific levels if available
- Treatment: Fomepizole (or ethanol) + haemodialysis + supportive care
Clinical Pearls
Early presentation = osmolar gap (parent compound); Late = anion gap (toxic metabolites)
"Blind drunk" = methanol poisoning (visual disturbance is a red flag)
Calcium oxalate crystals in urine = ethylene glycol
Why This Matters Clinically
Toxic alcohols cause irreversible end-organ damage (blindness, renal failure) and death. Early treatment with fomepizole prevents metabolism to toxic metabolites and is life-saving.
Visual Summary
Visual assets to be added:
- Toxic alcohol metabolism pathway
- Osmolar gap vs anion gap timeline
- Calcium oxalate crystals in urine
- Toxic alcohol management algorithm
Epidemiology
Incidence
- Uncommon but often fatal if untreated
- Outbreaks in developing countries (contaminated alcohol)
- Accidental ingestion (children, dementia)
Demographics
- Adults: Intentional self-harm, alcohol substitutes
- Children: Accidental (antifreeze is sweet-tasting)
- Alcoholics: Drinking methanol-containing products
Sources
| Toxic Alcohol | Sources |
|---|---|
| Methanol | Industrial solvents, windscreen washer fluid, model fuel, illicit spirits |
| Ethylene glycol | Antifreeze, brake fluid, de-icing products |
Pathophysiology
Methanol Metabolism
- Methanol absorbed rapidly (small molecule)
- Metabolised by alcohol dehydrogenase (ADH) → formaldehyde
- Formaldehyde → formic acid (via aldehyde dehydrogenase)
- Formic acid inhibits cytochrome oxidase → cellular hypoxia
- Ocular toxicity (retinal damage) → blindness
Ethylene Glycol Metabolism
- Ethylene glycol absorbed rapidly
- Metabolised by ADH → glycoaldehyde → glycolic acid → oxalic acid
- Glycolic acid causes acidosis
- Oxalic acid precipitates as calcium oxalate crystite in kidneys → AKI
- Hypocalcaemia (calcium bound by oxalate)
Why Osmolar Gap Then Anion Gap
- Early: Parent compound (methanol/EG) present → osmolar gap
- Late: Metabolites (formic/glycolic acid) accumulate → anion gap
- If treated early, anion gap may never develop
Clinical Presentation
Early (0-12 Hours)
Late (12-24+ Hours)
Methanol:
Ethylene Glycol:
Red Flags
| Finding | Significance |
|---|---|
| Visual symptoms | Methanol toxicity |
| AKI | Ethylene glycol |
| Severe metabolic acidosis | Urgent treatment needed |
| Osmolar gap over 10 | Suggests toxic alcohol (early) |
Inebriation (similar to ethanol)
Common presentation.
Nausea, vomiting
Common presentation.
Abdominal pain
Common presentation.
No acidosis yet (or minimal)
Common presentation.
Clinical Examination
General
- Drowsiness, confusion, coma
- Tachypnoea (Kussmaul breathing — acidosis)
Eyes (Methanol)
- Dilated pupils
- Reduced visual acuity
- Optic disc hyperaemia or pallor
Cardiovascular
- Tachycardia
- Hypotension (severe)
Investigations
Blood Tests
| Test | Finding |
|---|---|
| ABG/VBG | High anion gap metabolic acidosis |
| U&E | AKI (ethylene glycol) |
| Glucose | May be low |
| Calcium | Low (ethylene glycol) |
| Lactate | May be elevated |
| Serum osmolality | Elevated (osmolar gap) |
Anion Gap
- Anion gap = Na − (Cl + HCO3)
- Normal: 8-12
- Elevated: indicates accumulation of unmeasured anions (formic/glycolic acid)
Osmolar Gap
- Osmolar gap = Measured osmolality − Calculated osmolality
- Calculated = 2(Na) + urea + glucose
- Gap over 10 suggests unmeasured osmoles (methanol, ethylene glycol, ethanol)
Specific Levels
- Methanol level
- Ethylene glycol level
- (Often not immediately available — treat empirically)
Urine
- Calcium oxalate crystals (envelope or needle-shaped) — ethylene glycol
- Fluorescence under Wood's lamp (some antifreeze contains fluorescein)
Classification & Staging
By Severity
| Severity | Features |
|---|---|
| Mild | Ingestion suspected; no acidosis; osmolar gap |
| Moderate | Mild acidosis; no end-organ damage |
| Severe | pH under 7.25; visual symptoms (methanol); AKI (EG) |
Management
Immediate
| Action | Details |
|---|---|
| Airway | Protect if reduced GCS |
| IV access | Bloods |
| Correct acidosis | Sodium bicarbonate if pH under 7.1 |
| Correct hypocalcaemia | Calcium gluconate (ethylene glycol) |
| Supportive care | ICU admission |
Antidote — Block Alcohol Dehydrogenase
Fomepizole (First-Line):
- Loading: 15 mg/kg IV
- Maintenance: 10 mg/kg every 12 hours
- Blocks ADH → prevents metabolism to toxic metabolites
Ethanol (Alternative if Fomepizole Unavailable):
- Loading: 0.6-0.8 g/kg IV or PO
- Maintenance: 0.1-0.15 g/kg/hr (target ethanol 100-150 mg/dL)
- Competes for ADH
Haemodialysis
| Indication | Notes |
|---|---|
| Severe metabolic acidosis | pH under 7.25 |
| Renal failure | Ethylene glycol |
| Visual symptoms | Methanol |
| Serum level over 50 mg/dL | Either toxic alcohol |
| End-organ damage | Any |
Adjunctive
| Treatment | Indication |
|---|---|
| Folinic acid/folic acid | Methanol (enhances formate metabolism) |
| Thiamine, pyridoxine | Ethylene glycol (enhances metabolism) |
Monitoring
- Serial ABGs
- Osmolar and anion gap
- Methanol/EG levels if available
- Renal function
Complications
Methanol
- Permanent blindness
- Parkinsonism (basal ganglia damage)
- Death
Ethylene Glycol
- Acute renal failure (may be permanent)
- Hypocalcaemia → seizures, arrhythmias
- Pulmonary oedema
- Death
Prognosis & Outcomes
Prognosis
- Good if treated early (before metabolite accumulation)
- Poor if delayed — permanent end-organ damage
Factors Affecting Outcome
- Time to treatment
- pH at presentation (pH under 7.0 = poor)
- Presence of end-organ damage at presentation
Evidence & Guidelines
Key Guidelines
- EXTRIP Workgroup Recommendations on Methanol and Ethylene Glycol
- TOXBASE (UK National Poisons Information Service)
Key Evidence
- Fomepizole is as effective as ethanol with fewer side effects
- Early haemodialysis improves survival in severe cases
Patient & Family Information
What is Toxic Alcohol Poisoning?
Toxic alcohol poisoning happens when someone drinks substances like antifreeze or industrial solvents. These are broken down into harmful chemicals that can damage the eyes, kidneys, and brain.
Symptoms
- Feeling drunk
- Nausea and vomiting
- Blurred vision or blindness (methanol)
- Reduced urine output (ethylene glycol)
Treatment
- Medication to stop the poison being broken down
- Dialysis to remove the poison from the blood
- Hospital care
Prevention
- Keep antifreeze and solvents locked away from children
- Never drink unknown or home-made alcohol
Resources
References
Primary Guidelines
- Roberts DM, et al. Recommendations for the role of extracorporeal treatments in the management of acute methanol poisoning: a systematic review and consensus statement (EXTRIP). Crit Care Med. 2015;43(2):461-472. PMID: 25493973
- Kraut JA, Kurtz I. Toxic alcohol ingestions. N Engl J Med. 2018;378(3):270-280. PMID: 29342391
Key Reviews
- Barceloux DG, et al. American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. J Toxicol Clin Toxicol. 2002;40(4):415-446. PMID: 12216995