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[Updated 1 Jul 2026]
To guide the management of patients suspected of toxic alcohol (excluding ethanol) exposure in the deployed environment.
This guideline describes the management of patients with suspected toxic alcohol (methanol, ethylene glycol, diethylene glycol and isopropyl alcohol) exposure in a forward medical context or deployed Emergency Department.
It should not be used in the Firm Base or when access is available to TOXBASE® and UK equivalent laboratory testing.
This guideline is intended for the use of registered healthcare professionals fulfilling a general role in forward medical locations or in an Emergency Department on deployed operations.
Poisoning by toxic alcohol is relatively common globally. Most poisoning occur following ingestion and may occur in clusters or epidemics due to exposure to contaminated beverages. Inhalation and cutaneous exposures may result in symptoms but are rarer due to the chemical properties of the agents. All alcohols cause inebriation (ataxia, slurred speech, nystagmus, reduced consciousness) but this may not be apparent at the time of presentation and does not correlate to the severity of the exposure.
For methanol, ethylene glycol and diethylene glycol early treatment with an antidote minimises toxicity and may be lifesaving.
What was the substance the patient drank or was exposed to. Do they have the original container? Does the ingredients list include toxic alcohols?
Ask about intake of ‘bootleg’ alcohol, antifreeze, screen washes, perfumes, industrial chemicals. Are there other people similarly effected?
Was ethanol (commercial alcohol) also consumed?
Common sources of toxic alcohols, their mechanism of toxicity and their clinical features are listed below:
Toxic alcohols cause initial inebriation (ataxia, slurred speech, nystagmus, reduced consciousness) but this may resolve faster than would be expected with ethanol and may not be apparent at the time of presentation. Inebriation does not correlate to the severity of the exposure.
Clinical features of poisoning with toxic alcohols may take hours to days to develop depending on the type of toxic alcohol and the dose ingested. Toxicity results from metabolite formation (see specific agents below).
The patient may appear well at first presentation. A lack of clinical features does not rule out a toxic exposure. Co-ingestion of ethanol alongside any of the toxic alcohols will delay toxic metabolite formation and the onset of symptoms.
Key features suggestive of toxic alcohol exposure, progressive over 0-48 hours:
All patients exposed to toxic alcohols should be evacuated for blood gas analysis if possible.
Check blood glucose and correct as required.
Maintain hydration and good urine output (0.5ml/kg/hour) with oral or intravenous fluids.
If symptomatic, monitor for arrhythmias with continuous cardiac monitoring if available.
If the patient is thought to have ingested:
10 g or more (12.7 mL of 100% ) methanol OR
10 g or more (9.12 mL of 100%) ethylene glycol OR
5 g or more (4.5 mL of 100%) diethylene glycol
start antidote treatment without delay, regardless of symptoms:
Give fomepizole / ethanol
+ bicarbonate if tachypnoeic or acidotic
Otherwise, continue assessment including checking blood gas
If the patient is symptomatic and/or there is any derangement in blood gases or raised anion gap, start antidote treatment as above.
If the patient is asymptomatic including no hyperventilation, no visual disturbance and no flank plain
and blood gases are normal including anion gap <16
then observe for at least 24 hours.
during this time repeat blood gases every 4 hours
if any symptoms develop, any derangement in blood gases develops or anion gap exceeds 16 then start antidotes immediately
Patients may be discharged following completion of observation if they:
remain asymptomatic
have a normal blood gas with an anion gap of less than or equal to 16 mmol/L
have normal renal function and electrolytes
Due to the potential toxicity of these agents, as a general principle treat suspected ingestion if there are any symptoms and/or blood gas derangement.
However, if exposure to toxic alcohols is genuinely uncertain and the patient has no symptoms apart from hyperventilation (respiratory rate 20-25) with bicarbonate >15, base deficit <10 and pH >7.2 then trial stabilising treatment:
Review following the above; if hyperventilation resolved and blood gas improving then consider alcoholic ketoacidosis or diabetic ketoacidosis, and check ketones if possible, but continue to observe for 48hrs with 4 hourly blood gases until at least 24 hours after suspected ingestion and fully normalised. If hyperventilation persists or recurs, or blood gases are not improving (or worsen at any point) then start antidotes as above.
This approach is only appropriate if ingestion is uncertain - if toxic alcohol ingestion is confirmed then start antidotes if any symptoms and/or any derangement in blood gases.
If the patient is confirmed to have ingested isopropyl alcohol:
Fomepizole / ethanol are not indicated. Treatment is supportive only.
If asymptomatic observe for minimum 24 hours after exposure with 4 hourly blood gases.
If symptomatic or any blood gas abnormality, evacuate for haemodialysis/haemofiltration.
Be aware that toxic alcohol ingestion often occurs in patients with a history of ethanol dependence. Monitor for ethanol withdrawal and treat as required in accordance with separate guidance (link to follow).
If evacuation to a higher level of care is delayed the following should be considered:
Antidote treatment with ethanol. If unable to evacuate consider administration of oral or nasogastric tube ethanol. Commercially produced alcoholic beverages may be used in extremis and may be lifesaving (see dosing above). Treatment should be continued for 5-7 days then stopped and the patient monitored for 24 hours, restarting if hyperventilation reoccurs. Treat for 2 more consecutive days and reassess. Maintaining ethanol treatment for this long will require considerable resources to safely monitor the patient for ethanol overdose or under dosing with worsening acidosis.
Fluid balance. Measure urine output (via urinary catheter or otherwise) and maintain >0.5ml/kg/hour with oral or IV fluids. Beware of oliguria / anuria secondary to renal failure and monitor for fluid overload.
Nutrition. Oral feeding can be trialled provided the patient is conscious and the airway protected. If unable to eat maintain normoglycaemia with IV glucose.
The principles of management of toxic alcohols in children are the same as in adults. Note paediatric doses for antidotes are provided alongside the adult doses below.
A rising high anion gap acidosis (HAGMA) is highly suggestive of the presence of toxic metabolites.
Patients can present early after exposure with a normal pH or anion gap which do not exclude toxic alcohol exposure.
A high anion gap suggests a later presentation and that significant amounts of toxic alcohols have been metabolised.
The anion gap is calculated in mmol/l as (Sodium + Potassium) – (Bicarbonate + Chloride).
Normal result is <16.
Bloods. Check FBC, U&E, LFTs, calcium, magnesium, VBG. Plasma lactate may be falsely elevated in cases of ethylene glycol and methanol poison due to cross reactivity in some blood gas analysers. The anion gap should be calculated (see below) and the blood gases repeated every 1-2 hours to monitor for a rising anion gap.
Ketones. The presence of urinary or blood ketones without metabolic acidosis is highly suggestive of isopropyl alcohol exposure. If metabolic acidosis is present alcohol ketoacidosis or diabetic ketoacidosis (if high blood glucose) should be considered. Alcoholic ketoacidosis (see below) can be difficult to distinguish from toxic alcohol exposure when the history is not clear.
Alcoholic ketoacidosis differentiation. Alcoholic ketoacidosis may follow an alcoholic binge in a chronic ethanol users who are nutritionally deplete. Urinary or blood ketones are raised with pH <7.3 and HCO3 <15 mEq/L, without significant hyperglycaemia (blood glucose may be low, normal or slightly high). Treating with the following over 1 hour will aid differentiation:
If hyperventilation resolves or acidosis improves toxic alcohols are unlikely and treatment should be continued for alcoholic ketoacidosis or diabetic ketoacidosis considered. If toxic alcohols are present the acidosis will continue to worsen.
ECG. A 12-lead ECGs should be taken (if available) and serial ECGs may be required.
Both fomepizole and ethanol competitively inhibit ADH and prevent the formation of toxic metabolites. They DO NOT enhance elimination and significantly increase the elimination half-life of the parent compound up to 80+ hours for methanol. In serious overdoses treatment is likely to be required for many days to unless renal replacement therapy is available.
Fomepizole is the preferred antidote for toxic alcohols as it does not cause inebriation, sedation, hypoglycaemia or require as close monitoring as ethanol. However, it may not be readily available and antidote treatment should not be delayed attempting to transfer or source fomepizole. Ethanol should be used as the alternative (see below).
Fomepizole loading dose:
15 mg/kg IV dilute to 500ml in normal saline and give over 30 minutes (max weight for calculation 110kg)
In children dilute to at least 100 mL with a maximum concentration of 16.5 mg/mL
Fomepizole maintenance dose:
10 mg/kg over 30 min every 12 hours for 4 doses
After 4 doses increase to 15 mg/kg every 12 hours
Ethanol is the second line antidote due to its causing inebriation and risk of reduced consciousness, reduced consciousness and erratic patient specific metabolism. Ideally a pharmaceutical intravenous preparation is administered, however, any beverage containing ethanol e.g whisky, gin, vodka, beer can be used either oral or by nasogastric tube. Concentrations of greater than 40% ethanol should be diluted to avoid gastric irritation. Intravenous preparations should be diluted to maximum 10% ethanol in 5% or 10% glucose.
Ethanol loading dose:
10 mL/kg of 10% ethanol IV (if available) over 30 minutes via a large proximal cannular OR 2 mL/kg of 40% ethanol orally. Followed by a continuous infusion. See table below.
|
5% ethanol oral (e.g. beer) |
10% ethanol IV preparation |
40% ethanol oral (e.g. spirits) |
|
|
Loading dose |
20 ml/kg | 10 ml/kg | 2.5 ml/kg |
|
Maintenance dose in patient with no regular alcohol consumption |
2 ml/kg/hr | 1 ml/kg/hr | 0.5 ml/kg/hr |
|
Maintenance dose in patient with regular alcohol consumption |
4 ml/kg/hr | 2 ml/kg/hr | 1 ml/kg/hr |
All patients on ethanol treatment require continuous monitoring in the highest level of care available due to the risk of respiratory and CNS depression. Treatment effect can be monitored with serial blood gases and calculation of the anion gap as effective ethanol treatment should reduced toxic metabolite formation and improve the pH and anion gap. Care should be taken if using beer due to its high water and low sodium content resulting in hyponatraemia (beer potomania).
Sodium bicarbonate. If metabolic acidosis persists despite fluid resuscitation and correction of hypoxia consider administration of sodium bicarbonate to correct acidosis. Ensure serum potassium is within normal range prior to administration of sodium bicarbonate and monitor pH and electrolytes closely. Repeated doses may be required aiming for a normal pH guided by blood gas monitoring.
Adult dose: 50 mL 8.4% or 100 mL 4.2% sodium bicarbonate
Paediatric patients: 1 mL/kg 8.4% or 2 mL/kg 4.2% over 20 minutes
Folic acid 1 mg/kg (50 mg usual adult dose) IV or PO every 6 hours, if available, is an adjunctive therapy which may enhance folate elimination and should be administered for methanol poisoning.
Magnesium. Correct low magnesium concentrations with 8-10 mmol IV magnesium sulphate.
Potassium. Monitor levels closely, especially if sodium bicarbonate is required and maintain normal concentration.
Thiamine. Patients requiring treatment for potential toxic alcohol poisoning and with a history of chronic ethanol excess should be given pabrinex 2 pairs TDS IV or thiamine 400 mg TDS IV for the first three days of admission. Reduced to 200 mg OD for the next 3 days. See the Alcohol Withdrawal CGO for further detail.
Renal replacement therapy (RRT). Evacuation for RRT should be considered due to the very prolonged elimination half-life of toxic alcohol when fomepizole or ethanol is administered. Methanol’s half-life may extend up to 87 hours when metabolism is blocked.
Synonyms: Methyl alcohol, carbinol, wood alcohol, wood spirit
Sources: Windscreen washer fluid, engine coolant / antifreeze, brake fluid, model aircraft fuel, colognes / perfumes, hydraulic fracking fluid.
Mechanism of toxicity: Metabolised by alcohol dehydrogenase (ADH) to formaldehyde and formic acid by alcohol dehydrogenase. Rapidly absorbed following ingestion but the onset of toxic features may be delayed several hours, particularly if co-ingested with ethanol.
Clinical features: Severe high anion gap metabolic acidosis (HAGMA) and visual change leading to blindness are key features. Initial features of inebriation followed by a latent period of 12 -24 hours before metabolic features develop. Subsequently central nervous system features of headache, confusion, vertigo, seizures, progressing to coma. Visual features of blurred vision (‘snow storm’), photophobia, reduced pupillary response to light. Nausea, vomiting and abdominal pain are common. Acute pancreatitis may occur. pH and anion gap will be normal early following exposure but will rise as metabolites form.
Synonyms: 1,2-dihydroxyethane, ethylene alcohol, monoethylene glycol (MEG), and 1,2-ethanediol):
Sources: Windscreen washer fluid, engine coolant / antifreeze, brake fluid.
Mechanism of toxicity: Metabolised through ADH to glycolic acid and oxalic acid resulting in calcium oxalate crystal formation which deposit in the renal tubules and brain causing acute kidney injury and cerebral oedema. Hypocalcaemia may cause cardiac arrythmias.
Clinical features: Inebriation lasting between 30 minutes and 12 hours after exposure. 12 -24 hours after ingestion: worsening metabolic acidosis, increased respiratory rate, tachycardia, pulmonary oedema and congestive cardiac failure. 24-72 hours after ingestion: flank pain and tenderness, acute renal failure, hypocalcaemia, hypomagnesaemia and hyperkalaemia. Cerebral oedema, seizures and coma may occur.
Synonyms: Ethylene diglycol; DEG; diglycol; glycol ethyl ether; dihydroxy diethyl ether; 2,2'-oxybisethanol; 3-oxa-1,5-pentanediol):
Sources: Antifreeze, lubricants, inks, adhesives, polyurethane and resins.
Mechanism of toxicity: Metabolised by ADH to toxic metabolites HEAA and DGA resulting in nephrotoxicity and neurotoxicity.
Clinical features: Initial features of inebriation may be present along with nausea, vomiting and abdominal pain. Confusion, disorientation and drowsiness with metabolic acidosis develop subsequently. Over the next 1-3 days metabolic acidosis worsens with associated abnormal clinical observations, renal damage develops with acute kidney injury, oliguria and eventually anuria. Hepatotoxicity may also be present. Five to ten days post exposure neuropathies occur including isolated palsies and upper and lower limb weakness. Respiratory muscle weakness can result in respiratory depression.
Synonyms: isopropanol, 2-propanol, propan-2-ol, propanol-2, rubbing alcohol, IPA, dimethyl carbinol):
Sources: Used as solvent in oils, gums, creosote, resins, cosmetics, fuels, inks, pesticides, cleaning products and hand sanitisers.
Mechanism of toxicity: CND depression and gastrointestinal (GI) upset result directly from the isopropyl alcohol. It is metabolised to acetone which is much less toxic than the metabolites of methanol or ethylene glycol.
Clinical features: Fruity odour on breath. Initial inebriation with ataxia, CNS depression, coma and GI upset including haemorrhagic gastritis. Ketosis without acidosis results from the acetone although a metabolic acidosis may be seen in very large ingestions. Corneal injury may result from eye exposure and prolonged skin exposure causes irritation, dermatitis or burns. Prolonged inhalation may cause haemoptysis and respiratory failure.
