Methanol Poisoning- Causes, Symptoms, Diagnosis, Treatment and Ongoing care
- Methanol (wood alcohol) is a clear, colorless solvent found in antifreeze, cleaning solutions, copy machine fluid, gasoline additives, paint, paint thinner, and liquid fuel (1).
- Methanol is less expensive than ethanol and may be used by chronic alcoholics as a substitute.
- Intoxication also can be secondary to methanol-contaminated grain alcohol (moonshine), accidental ingestion, or suicide attempt.
- Methanol produces inebriation, and its metabolic products may cause metabolic acidosis, blindness, and death.
Avoid ethanol therapy as treatment for methanol poisoning during 1st trimester of pregnancy; may substitute fomepizole, which is a pregnancy category C drug.
- Predominant age: Most >18 years of age, followed by <6 years of age
- Predominant sex: Male > Female
In the US, 683 methanol exposures were reported in 2007. Sixty-eight cases resulted in moderate–severe outcomes, and there were 9 fatalities.
- Epidemics may occur in institutionalized settings where ethyl alcohol is unavailable (e.g., prisons).
- Inappropriate storage leading to childhood exposure
- Substance education for those at risk
- Proper storage of methanol-containing products
- Methanol metabolism in brief (1,2):
- Methanol is readily absorbed and quickly distributed.
- The liver slowly metabolizes methanol into formaldehyde via alcohol dehydrogenase.
- Formaldehyde is rapidly converted into formic acid via aldehyde dehydrogenase.
- Formic acid is slowly converted to carbon dioxide and water through a folate-dependent process.
- A limited amount of methanol is also eliminated essentially unchanged through exhalation (12%) and the urine (3%).
- Methanol is minimally toxic, but formic acid causes anion-gap metabolic acidosis and ocular toxicity. Increased lactate owing to systemic toxicity contributes to the acidosis (1).
- Fatal dose is 15–240 mL depending on concentration.
- Peak blood levels occur 30–60 minutes after ingestion (1).
Commonly Associated Conditions
- Classic clinical picture includes nausea, vomiting, abdominal pain, visual disturbances, and metabolic acidosis. There is a latent period after ingestion of 6–24 hours before onset of symptoms; this may be delayed further with concomitant ethanol ingestion (2)[C].
- Overt clinical signs are expected with severe exposure, but at low doses (i.e., occupational exposure), elevated methanol levels may be the only sign.
- Initial CNS depression or inebriation (1)[C]
- Headache, vertigo, lethargy, confusion; severely intoxicated patients can present with coma and convulsions.
- Visual disturbance, ranging from mild blurring to complete blindness “like standing in a snowfield” (3)[B]
- GI symptoms may include nausea, vomiting, and marked abdominal pain.
Key physical findings (1,2)[C]:
- Initially, inebriation and gastritis
- Heart rate abnormalities including bradycardia in late stages
- Tachypnea with onset of metabolic acidosis
- Visual field defects, blurred or double vision; loss of visual acuity or pupillary reaction.
- Funduscopic exam may reveal retinal edema, hyperemia, or loss of disc cupping.
- Abdominal tenderness
- Stupor, confusion, seizure, or coma may be present.
- Parkinson-type symptoms have been reported in severe acute and low-level chronic methanol poisoning (4)[C].
Diagnostic Tests & Interpretation
- Serum methanol may be elevated acutely.
- After a latent period, serum formate is a better measure of toxicity.
- Elevated osmolar gap and anion gap; include lactate and ethanol levels to help identify acid contributing to elevated anion gap
- Urinalysis may show myoglobinuria.
- Other useful labs:
- Arterial blood gas
- Electrolytes, blood urea nitrogen (BUN), creatinine, calcium, liver function tests, amylase, lipase, creatinine phosphate
- Toxicologic screens if coingestants are suspected
CT scan or MRI of the brain if indicated by neurologic exam. Brain imaging may reveal optic pathway damage, hypodensities in the putamen or caudate nucleus, cerebral edema, cerebral hemorrhage, or cerebral infarct (1)[C].
- Ingestion of other alcohols, including ethyl alcohol, ethylene glycol, benzyl alcohol, and isopropyl alcohol
- Other toxic ingestions, including paraldehyde and formaldehyde.
- Increased anion-gap metabolic acidosis caused by renal failure, diabetic ketoacidosis, or lactic acidosis
- Ethanol and fomepizole saturated aldehyde dehydrogenase prevent formation of formic acid.
- Metabolism of formic acid is a folate-dependent pathway.
- Criteria for initiation of therapy in patients with known or suspected methanol poisoning (1)[C]:
- Plasma methanol >20 mg/dL or
- Recent history of ingestion of toxic amounts of methanol and an osmolar gap >10 mOsm/L or
- Suspected methanol ingestion with at least 2 of the following:
- Arterial pH <7.3
- Serum bicarbonate <20 mmol/L
- Osmolar gap >10 mOsm/L
- First 48 hours: IV load with 15 mg/kg, then dosed 10 mg/kg every 12 hours for 4 doses (1)[C]
- After 48 hours: Induces P-450 enzymes, so increase to 15 mg/kg until serum methanol <20 mg/dL (1)[C].
- Increase dosing to every 4 hours for hemodialysis. No adjustments in dosing are needed for renal or hepatic disease.
- Side effects: Mildly increased levels of alanine aminotransferase and aspartate aminotransferase that resolve without consequence (5)[B]
- Folinic acid (Leucovorin): May enhance formic acid metabolism (5)[C]
- 1 mg/kg (up to 50 mg) initially
- Folic acid can be given every 6 hours at the same dose until metabolic acidosis resolves.
- IV loading dose, then maintenance dosing based on hourly serum ethanol levels; target therapeutic ethanol level is 100–150 mg/dL. Treat until serum methanol is <20 mg/dL (1)[C].
- Side effects include inebriation, hypoglycemia, phlebitis, and volume overload.
- Avoid ethanol therapy with CNS depressants, and watch for disulfiram reactions.
- Prioritize management on timing and amount of exposure; if patient is intoxicated, history may be unreliable.
- A low or nondetectable methanol level does not rule out ingestion.
- Initial stabilization: IV access and isotonic fluids to maintain adequate urine output and prevent renal failure
- Initial management: Focused on preventing metabolic acidosis and ophthalmic complications
- Consider gastric decontamination with induced emesis, charcoal, or gastric lavage only if concomitant ingestion is known (1)[C].
- Sodium bicarbonate can be considered if serum pH <7.2.
- Hemodialysis (see “Inpatient Considerations”).
Issues for Referral
- For patients with substance abuse, referral to detox, rehabilitation, and/or AA/NA.
- Ophthalmology follow-up for patients with visual disturbances
Consider urgent hemodialysis if (1,6):
- Significant acidosis (pH <7.2) unresponsive to therapy
- Deteriorating vital signs despite intensive support
- Renal failure
- Severe electrolyte imbalance
- Visual or fundoscopic abnormalities
- Serum methanol concentration >50 mg/dL or >30 g ingested.
Isotonic IV fluid to maintain urine output
- Restricted activity if patient is inebriated, has altered level of consciousness, or has visual impairments
- Referral to psychiatry for suicidal patients
Thiamine supplementation in patients with long-term alcoholism
- Anticipatory guidance for parents regarding storage of hazardous chemicals
- Motivational interviewing for those with substance dependence and referral for additional treatment
- American Academy of Clinical Toxicology: http://www.clintox.org.
- Outcome varies depending on time to presentation and quantity of methanol ingested.
- Outcome is related to degree of acidosis, coma, or seizures at time of presentation.
- Diagnostic and treatment delays are correlated with poor outcome (3)[C].
- Blindness and other visual disturbances
- Myoglobinuric renal failure
- Parkinson syndrome
1. Barceloux DG. American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. Clin Toxicol. 2002;40:415–46.
2. Kraut JA, Kurtz I. Toxic Alcohol Ingestions: Clinical Features, Diagnosis, and Management. Clin J Am Soc Nephrol. 2007.
3. Hovda KE, et al. Methanol outbreak in Norway 2002–2004. J Int Med. 2005;258:181–90.
4. Airas L, Paavilainen T, Marttila RJ, et al. Methanol intoxication-induced nigrostriatal dysfunction detected using 6-[18F]fluoro-l-dopa PET. Neurotoxicology. 2008.
5. Brent J. Fomepizole for ethylene glycol and methanol poisoning. N Engl J Med. 2009;360:2216–23.
6. Mégarbane B, Borron SW, Baud FJ. Current recommendations for treatment of severe toxic alcohol poisonings. Intensive Care Med. 2005;31:189–95.
Comoğlu S, Ozen B, Ozbakir S. Methanol intoxication with bilateral basal ganglia infarct. Australas Radiol. 2001;45:357–8.
Litovitz TL, Klein-Schwartz W, White S, et al. 2000 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2001;19:337–95.
980.1 Toxic effect of methyl alcohol
212809004 methyl alcohol causing toxic effect (disorder)
- Formic acid, the toxic agent in methanol poisoning, causes anion-gap metabolic acidosis, optic disc edema, and myelin breakdown by direct toxic effects (1)[C].
- Ethanol has the longest history of use, is inexpensive, and is widely available. Fomepizole is preferred because dosing is simpler, it does not require hourly blood draws, and it is not a CNS depressant. No direct comparison of the 2 treatments is available.
- Common indications for hemodialysis in methanol overdose include severe acidosis, visual symptoms, unstable vital signs, refractory electrolyte disturbances, and methanol level >50 mg/dL (1)[C].
- Recent literature suggests that in the absence of neurologic impairment, ocular symptoms, and severe metabolic acidosis, fomepizole may obviate the need for hemodialysis (5,6)[B].