SN4 SHORT NOTE 5M

Write a short note on methanol and ethylene glycol (toxic alcohol) poisoning.

General Medicine · Final Professional

Introduction

Methanol is found in adulterated country liquor (hooch tragedies are a recurring cause of mass poisoning and death in India), industrial solvents, antifreeze, varnish and windshield washer fluid. Ethylene glycol is found in antifreeze, brake fluid and coolants, and is sometimes ingested deliberately or accidentally because of its sweet taste.

Both are relatively non-toxic themselves — the damage is done by their metabolites, which is the central principle governing treatment.

Metabolism and Mechanism

Both are metabolised by alcohol dehydrogenase (ADH), then by aldehyde dehydrogenase:

Methanol → formaldehyde → formic acid. Formic acid inhibits cytochrome oxidase, causing severe metabolic acidosis and selective injury to the optic nerve and retina and to the basal ganglia.
Ethylene glycol → glycoaldehyde → glycolic acid → oxalic acid. Glycolic acid causes the acidosis; oxalic acid precipitates as calcium oxalate crystals in the renal tubules, causing acute kidney injury and hypocalcaemia.

Because metabolism takes time, there is a characteristic latent period of several hours between ingestion and the onset of severe features — longer if ethanol has been co-ingested, since ethanol competes for ADH.

Clinical Features

Feature	Methanol	Ethylene Glycol
Early (0–12 h)	Inebriation, nausea, vomiting, abdominal pain	Inebriation without the smell of alcohol, vomiting
Characteristic organ	Eye — blurred vision, "snowstorm" vision, photophobia, dilated unreactive pupils, papilloedema, permanent BLINDNESS	Kidney — flank pain, oliguria, acute kidney injury
Later	Severe metabolic acidosis, Kussmaul breathing, seizures, coma; basal ganglia (putaminal) haemorrhage or necrosis with parkinsonism in survivors	Stage 2: tachycardia, hypertension, pulmonary oedema, heart failure. Stage 3: acute tubular necrosis
Biochemistry	High anion gap acidosis, raised osmolar gap; normal calcium	High anion gap acidosis, raised osmolar gap, hypocalcaemia, calcium oxalate crystals in urine

Investigations

Arterial blood gas — severe high anion gap metabolic acidosis.
Osmolar gap — measured minus calculated osmolality. Raised early (when unmetabolised parent alcohol is present) and falls as the anion gap rises with metabolite formation. A normal osmolar gap late in the course does not exclude poisoning.
Serum methanol or ethylene glycol levels where available — rarely available in time in Indian practice, so treatment is started on clinical and biochemical grounds.
Serum calcium (low in ethylene glycol), renal function, electrolytes, lactate.
Urine microscopy — calcium oxalate crystals (needle-shaped monohydrate or envelope-shaped dihydrate); urine fluorescence under Wood's lamp if fluorescein-containing antifreeze was ingested (unreliable).
Ophthalmological examination in suspected methanol poisoning; CT brain for putaminal lesions.

Management

1. Block the enzyme — the specific treatment

Fomepizole — a direct competitive inhibitor of alcohol dehydrogenase; the agent of choice where available, requiring no monitoring of levels and causing no sedation. Cost and availability limit its use in India.
Ethanol — an effective alternative, since ADH has far higher affinity for ethanol than for methanol or ethylene glycol. Given orally or intravenously with the aim of maintaining a steady blood ethanol concentration. It requires frequent monitoring of ethanol levels and blood glucose, and causes sedation, so the airway must be watched.
Indications to start an ADH blocker: strong suspicion of ingestion, an osmolar gap, or an unexplained high anion gap metabolic acidosis — do not wait for confirmatory levels.

2. Enhance elimination

Haemodialysis — removes both the parent alcohol and its toxic metabolites, and corrects acidosis. Indicated for severe metabolic acidosis, visual symptoms in methanol poisoning, renal failure, high measured levels, or clinical deterioration. It is the definitive treatment in significant poisoning.

3. Cofactor and supportive therapy

Methanol: folinic acid (or folic acid) accelerates the conversion of formic acid to carbon dioxide and water.
Ethylene glycol: thiamine and pyridoxine divert metabolism away from oxalate production.
Sodium bicarbonate for severe acidaemia — it also reduces tissue penetration of formic acid.
Correct hypocalcaemia in ethylene glycol poisoning, but cautiously — replacing calcium generates more calcium oxalate.
Airway protection, ventilation, seizure control, and intensive care support.
Gastric lavage and charcoal are of little value: absorption is rapid and charcoal binds alcohols poorly.

DANGER / REMEMBER

The blindness of methanol poisoning is preventable but irreversible once established. Any patient from a suspected hooch tragedy with visual complaints, unexplained severe metabolic acidosis or an osmolar gap must be treated immediately with an ADH blocker and considered for urgent dialysis — before levels return and before vision is lost. In a mass poisoning, treat on clinical suspicion and triage for dialysis early.

NEEDS VERIFICATION

Fomepizole and ethanol dosing regimens, target ethanol concentration, and dialysis thresholds — confirm against current toxicology protocol before publication.

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