INTRODUCTION — Methanol and ethylene glycol poisonings cause scores of fatal intoxications annually, and even relatively small ingestions of these alcohols can produce significant toxicity. Rapid recognition and early treatment, including alcohol dehydrogenase (ADH) inhibition, are crucial. A summary table to facilitate emergency management is provided (table 1).

Methanol and ethylene glycol are frequently found in high concentrations in automotive coolant/antifreeze and de-icing solutions, windshield wiper fluid, solvents, cleaners, fuels, and other industrial products. Most serious poisonings occur following ingestion; inhalation and dermal exposures rarely cause toxicity [1]. Patients may ingest toxic alcohols as an ethanol substitute, to inflict self-harm, or by accident, sometimes following transfer from the original container. Multiple victim methanol poisonings can occur with illicit distillation ("moonshine") or occult substitution for ethanol.

The management of methanol and ethylene glycol intoxication are reviewed here. While there are differences between methanol and ethylene glycol poisoning, there is substantial overlap in management, and both the similarities and differences are described. The clinical manifestations, laboratory findings, and diagnosis of methanol and ethylene glycol are discussed separately. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

●Isopropyl alcohol intoxication is considerably different, and is discussed separately. (See "Isopropyl alcohol poisoning".)

●The approach to the poisoned adult or child is reviewed in detail separately. (See "General approach to drug poisoning in adults" and "Approach to the child with occult toxic exposure" and "Initial management of the critically ill adult with an unknown overdose".)

MANAGEMENT

Overview of emergency management — Rapid decision-making is critical in the management of the patient poisoned with methanol or ethylene glycol. The clinician must often make treatment decisions without definitive serum drug levels, based only upon clinical suspicion and readily available laboratory data. A summary table to facilitate emergency management is provided (table 1).

The management of methanol and ethylene glycol poisoning involves the following:

●Securing the patient's airway, breathing, and circulation; and providing appropriate supportive care

●Administering sodium bicarbonate to correct systemic acidosis, which limits the penetration of toxic acids (eg, formic acid) into end-organ tissues such as the retina by converting them to the anion (eg, formate), which cannot diffuse across cell membrane

●Inhibiting the enzyme alcohol dehydrogenase (ADH) with either fomepizole (preferred) or ethanol (if fomepizole is unavailable)

●Performing hemodialysis for elevated toxic alcohol levels, severe acid-base derangements, or evidence of end-organ toxicity

●Treating with cofactors (folic acid, thiamine, and pyridoxine) to optimize nontoxic metabolic pathways for the elimination of the parent alcohol or its metabolites

We also recommend immediate consultation with a medical toxicologist or poison control center if methanol or ethylene glycol intoxication is suspected. (See 'Additional resources' below.)

Airway, breathing, circulation — The clinician must first assess and secure the patient's airway, breathing, and circulation. Advanced cardiac life support measures are provided as required. A discussion of fundamental management of the poisoned patient is found elsewhere. (See "General approach to drug poisoning in adults".)

If endotracheal intubation is required, the patient should be hyperventilated if a significant metabolic acidosis exists or is suspected. Arterial and/or venous blood gas analysis should be performed frequently to evaluate pH and ensure adequate ventilation and oxygenation. Large minute ventilations may be required to prevent profound acidemia (pH <7.1) in patients with severe intoxication.

Gastrointestinal decontamination — There is little, if any, role for gastrointestinal decontamination in methanol or ethylene glycol poisoning, as these simple alcohols are rapidly absorbed. The rare patient known to have ingested a large amount of methanol or ethylene glycol may benefit from gastric aspiration via flexible nasogastric tubing if performed within 60 minutes of the ingestion. Activated charcoal, gastric lavage, and syrup of ipecac have no role in the management of toxic alcohol exposures.

Treatment with sodium bicarbonate — Methanol is metabolized to formate; and ethylene glycol to glycolate, glyoxylate, and oxalate. Acidemia leads to protonation of these species to uncharged molecules (eg, formic acid), making them more likely to penetrate end-organ tissues (such as the retina) and more likely to be reabsorbed across the renal epithelium from the urine. Thus, patients with methanol or ethylene glycol poisoning fare worse when systemic acidemia is present [2,3]. Treatment with sodium bicarbonate leads to deprotonation of these acid species, making them less likely to penetrate end-organ tissues and more likely to be excreted in the urine.

Despite this clear rationale, no clear evidence exists to determine how bicarbonate should be given. We suggest initial treatment with 1 to 2 meq/kg of sodium bicarbonate via intravenous (IV) bolus for any patient with a pH below 7.3 [4,5]. A maintenance infusion is then prepared by mixing approximately 133 meq of sodium bicarbonate in 1 liter of D5W. Infusion rates may range from 150 to 250 mL/hour in adults, or one to two times the maintenance fluid rate in children. The appropriate rate depends upon the initial pH and such parameters as fluid status and serum sodium concentration. The goal of treatment is maintenance of an arterial or venous pH above 7.35, at which point the infusion is discontinued.

Alcohol dehydrogenase inhibition

Approach and initiation — Inhibition of ADH blocks bioactivation of the parent alcohol to its toxic acid metabolites. Early treatment is crucial since ADH inhibition does not prevent toxicity if complete metabolism to acid species has already occurred.

Fomepizole or ethanol can be used to inhibit ADH (table 2). We recommend treatment with fomepizole. The American Academy of Clinical Toxicology practice guidelines provide some guidance for the initiation of ADH inhibitor therapy [4,5]. (See 'Fomepizole' below.)

The American Academy of Clinical Toxicology's minimum treatment threshold of 20 mg/dL of either methanol (SI equivalent 6.2 mmol/L) or ethylene glycol (SI equivalent 3.2 mmol/L) is not evidence based and is necessarily conservative [3,6-8]. Parent alcohol concentrations must be interpreted in clinical context. As an example, a patient with a methanol level of 25 mg/dL (or 7.8 mmol/L) and a normal acid-base status may only require one or two doses of fomepizole and observation, whereas a patient with the same level but a significant acidosis and vision deficits may require fomepizole, alkalinization, and hemodialysis. Making such determinations can be difficult, and we recommend consultation with a regional poison control center or medical toxicologist in such cases. (See 'Additional resources' below.)

In the absence of confirmatory drug levels, which are rarely (if ever) available as in-house laboratory tests, clinicians must rely upon their clinical judgment and readily available laboratory tests when deciding whether to initiate therapy with an ADH inhibitor. However, clinicians should be wary of initiating such therapy solely on the basis of an anion gap or small osmolal gap without at least circumstantial evidence of toxic alcohol ingestion, especially when ethanol therapy is contemplated. In addition, the clinician should not ascribe metabolic acidosis to a toxic alcohol ingestion if coingested ethanol is present: substantial oxidation of the toxic alcohol is highly unlikely in the presence of ethanol.

Fomepizole — Fomepizole has been used successfully for years to treat both methanol and ethylene glycol poisoning [9-11] and is a superior antidote to ethanol [3,12-15]. Fomepizole is easy to dose and administer, and clinically significant adverse effects are rare [16,17]. Its main disadvantage is its high cost. However, the cost compares favorably with the total cost of managing patients treated with ethanol, including ethanol titration and possibly hemodialysis and intensive care unit admission [14,18,19].

Fomepizole is loaded at 15 mg/kg IV, followed by 10 mg/kg every 12 hours, with adjustments for hemodialysis or after more than two days of therapy. (See 'Hemodialysis' below.)

Once begun, ADH inhibition with fomepizole should be continued until the diagnosis of toxic alcohol ingestion has been ruled out or until blood pH is normal and serum alcohol concentration is less than 20 mg/dL (SI units: methanol 6.2 mmol/L and ethylene glycol 3.2 mmol/L) in the presence of retinal or renal injury.

Ethanol — Historically, ethanol has been used as a competitive inhibitor of ADH, as ADH has greater affinity for ethanol than for methanol or ethylene glycol. Although effective [20,21], IV ethanol treatment creates several problems:

●Ethanol is difficult to dose, and appropriate levels are difficult to maintain; as a result, frequent testing and infusion adjustments are often required.

●Ethanol requires compounding by the hospital pharmacy, irritates veins when infused, and can complicate fluid balance in oliguric patients.

●Most limiting are the sedative and behavioral effects of ethanol, which can cause obtundation, thereby increasing the risk of aspiration, and other complications [16].

●Ethanol therapy may pose risks in certain patients (eg, upper gastrointestinal bleeding, first trimester pregnancy).

Thus, fomepizole is the preferred therapy. In the rare circumstance in which ethanol therapy must be used, many sources cite an absolute ethanol level of 100 mg/dL (or 22 mmol/L) as the therapeutic target. A table summarizing the dilution, dosing, and titration of IV ethanol is provided (table 3). In the next paragraph, we also offer a simplified approach to the loading and adjustment of IV ethanol, which aims to reduce confusion and the potential for dosing errors that can occur when making precise calculations for an antidote used infrequently and under time pressure. However, it should be noted that ADH inhibition is competitive, and therefore, the target ethanol concentration should be based on the estimated concentration of methanol or ethylene glycol. The appropriate target for antidotal therapy with ethanol is a concentration of at least one-quarter to one-third the serum methanol or ethylene glycol concentration expressed as mg/dL, rather than a single, arbitrary concentration of 100 mg/dL. In other words, a modest ethanol concentration of 20 mg/dL will effectively inhibit the metabolism of 60 to 80 mg/dL of methanol or ethylene glycol. Awareness of ethanol's antidotal potency often allows the dosing intensity of ethanol to be reduced when this is the only antidote available.

An IV loading dose of 10 mL/kg of a 10 percent ethanol (volume/volume) solution in D5W (ie, 800 mg/kg of ethanol) will raise serum ethanol concentrations by about 100 mg/dL. The loading dose should be given over 60 minutes to avoid excessive side effects (eg, hypotension, respiratory depression, somnolence). When treating patients who have coingested ethanol, this loading dose can be scaled back in proportion to their current serum ethanol concentration. A maintenance infusion of the 10 percent ethanol solution, starting at 1 mL/kg per hour, is appropriate to maintain any current ethanol concentration, as metabolism is zero order. This maintenance rate can be adjusted according to serial ethanol concentrations and increased by about 50 percent during hemodialysis. Ethanol concentrations should be measured every one to two hours initially, following any change in dose or infusion rate, during and after hemodialysis (see 'Hemodialysis' below), and every two to four hours otherwise.

Once begun, ADH inhibition with ethanol should be continued until the diagnosis of toxic alcohol ingestion has been ruled out, or until blood pH is normal and the serum alcohol concentration is less than 20 mg/dL (SI units: methanol 6.2 mmol/L and ethylene glycol 3.2 mmol/L) in the presence of retinal or renal injury.

Due to the risks associated with ethanol therapy, patients should be treated in a critical care setting where their mental status and respiratory function can be closely monitored. Whenever possible, ethanol should be administered by central venous catheter using an infusion pump to limit venous irritation.

Should both fomepizole and pharmaceutical-grade IV ethanol be unavailable, ethanol can also be administered orally, both to load and to maintain serum ethanol concentrations as described above. Distilled spirits (40 to 50 percent volume/volume) intended for human consumption can be diluted to a 20 percent solution and administered per os or via nasogastric tube at half the volumes recommended above (ie, 5 mL/kg of a 20 percent solution to raise serum concentrations by 100 mg/dL, and 0.5 mL/kg per hour for the initial maintenance dose). Gastritis and vomiting are occasionally encountered when using the enteral route for antidotal ethanol therapy, in addition to the other adverse effects of ethanol.

There is no benefit to adding ethanol therapy to fomepizole therapy in methanol- and ethylene glycol-poisoned patients.

Hemodialysis — Hemodialysis is the best method to rapidly remove both toxic acid metabolites and parent alcohols, and it plays a fundamental role in treating severely poisoned patients [4,5,22]. Emergency clinicians should initiate consultation with a nephrologist immediately if they suspect a toxic alcohol ingestion and the patient has evidence of end-organ dysfunction or acidemia, especially if transfer to a hemodialysis center may be necessary.

In such cases, consultation should not be delayed until confirmatory methanol or ethylene glycol levels are obtained. An arterial or venous blood gas is sufficient and serves as an essential triage tool in this setting. This is particularly true when caring simultaneously for multiple poisoned patients with limited hemodialysis capability [20,23].

We recommend immediate treatment with hemodialysis in the setting of a known methanol or ethylene glycol ingestion if either of the following conditions is present:

●High anion gap metabolic acidosis, regardless of drug level

●Evidence of end-organ damage (eg, visual changes, renal failure)

In addition, we suggest treatment with hemodialysis in any patient with a suspected toxic alcohol ingestion who has a severe, otherwise unexplained anion gap metabolic acidosis and significant plasma osmolal gap. It is difficult to provide precise thresholds for determining when hemodialysis should be performed when the ingestion is uncertain. If a toxic ingestion is strongly suspected, a threshold pH of 7.3 is reasonable; if suspicion is weaker, a pH of 7.1 may be more appropriate. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis", section on 'Laboratory evaluation'.)

Interpreting available clinical information (eg, nature and intent of exposure, pH, osmolarity) to decide whether to initiate hemodialysis can be challenging when confirmatory methanol and ethylene glycol concentrations are unavailable [24]. We encourage clinicians facing this difficulty to consult with a poison control center, medical toxicologist, or other physician experienced in the management of suspected toxic alcohol exposure.

For non-acidemic patients, hemodialysis can be used to remove the parent alcohol and abbreviate the course of antidotal therapy. There is less urgency to treat with hemodialysis if ADH inhibition is adequate. Hemodialysis is often unnecessary in patients with unmetabolized ethylene glycol provided that [4,25]:

●Fomepizole is given (prolonged ethanol therapy is impractical)

●The serum pH is normal or near normal (ie, little glycolate is present)

●The serum creatinine remains normal

Patients with ethylene glycol concentrations greater than 300 mg/dL (48 mmol/L) have been successfully treated with fomepizole alone when therapy was initiated before the appearance of acidosis. Treatment with hemodialysis is still recommended for large methanol ingestions because serum methanol elimination becomes extremely slow when ADH is inhibited [5,26,27].

The hemodialysis prescription should include a large surface area dialyzer (>1.5 m²), a blood flow rate in excess of 300 mL/min, and a bicarbonate bath. Hemodialysis should continue until the serum pH is normal and parent alcohol concentrations are less than approximately 25 mg/dL or 5 mmol/L. The duration of hemodialysis in hours can be estimated using the formula -V ln (5/A)/0.06 k, where V is total body water in liters, A is the initial alcohol concentration in mmol/L, and k is 80 percent of the dialyzer urea clearance in mL/min at the observed blood flow rate [28-30]. Such a calculation provides only an estimate, and the patient's clinical condition will also affect the dosing of hemodialysis. Serum alcohol concentrations and acid-base status should always be verified near the end of hemodialysis and again two hours post-hemodialysis to ascertain the adequacy of treatment [24]. (See "Acute hemodialysis prescription".)

More than one round of hemodialysis may be necessary in massive overdoses and for ethylene glycol-poisoned patients with renal failure. Renal function often recovers over a period of days to months in survivors of ethylene glycol poisoning.

Fomepizole is dialyzable, and the frequency of its dosing should be increased to every four hours during hemodialysis. An additional dose should be given at the beginning of hemodialysis if six or more hours have elapsed since the prior dose.

If ethanol is used for ADH inhibition, adjustments in the dose must be made during hemodialysis. A fall in ethanol levels can be avoided or ameliorated by increasing the rate of ethanol infusion and possibly by adding ethanol directly to the dialysate [31,32]. In one such case, a dialysate ethanol concentration of 100 mg/dL was prepared by administering a 95 percent ethanol solution into the dialysate inlet tubing at a rate of 40 mL/h via an infusion pump. The dialysate flow rate was maintained at 500 mL/min, and the dialyzer blood flow averaged 280 mL/min. An average plasma ethanol level of 90 mg/dL was obtained during the six-hour hemodialysis session.

Peritoneal dialysis and other forms of continuous renal replacement therapy are inefficient at clearing toxic alcohols and their metabolites and are not recommended [24].

Cofactor therapy — All methanol patients treated with ADH inhibition should also receive cofactor therapy: either leucovorin 50 mg IV or folic acid 50 mg IV every six hours [5,33,34]. It is not known whether supplemental thiamine (100 mg IV) or pyridoxine (50 mg IV) benefits patients poisoned with ethylene glycol, but we routinely administer both, particularly if the patient's nutritional status is suspect.

Preterminal care — Severely poisoned patients who present in coma and profound acidemia may not survive despite maximum intensive therapy [2,35,36]. Consideration should be given to organ harvesting prior to withdrawal of support for such patients, especially after severe methanol poisoning. Formate is a highly specific neurotoxin, and case series support the viability of organs harvested from such patients [37,38]. (See "Evaluation of the potential deceased organ donor (adult)".)

MULTIVICTIM OUTBREAKS — Methanol poisoning outbreaks with multiple victims are rare but continue to occur around the globe [2,36,39-42]. When the supply of "alcohol" (ie, ethanol) is contaminated, especially with methanol, a cluster of victims with a wide range of severities can easily overwhelm available critical care and hemodialysis resources. The timing of presentation and geographic range of victims will depend on the nature, distribution, and consumption of the contaminated product.

A 2019 consensus statement from an international panel of clinical toxicologists recommends that as few as three cases within 72 hours appearing in the same city or town should be considered a methanol poisoning outbreak, triggering active case-finding by public health and government authorities [36]. Triage elements should include level of consciousness, visual disturbances, and blood gas testing if possible, with antidotal and extracorporeal treatment allocated according to the severity of illness. The combination of coma at presentation with a pH <6.74 is strongly associated with death or severe neurologic sequelae in almost all cases [35,36]. On the other hand, a pH >7.2 at the time of initial treatment is rarely associated with subsequent visual deterioration [43].

Regarding antidotal therapy in such outbreaks, we concur with the consensus statement, which recommends a "use what you have" approach [36]. When both are available, we prefer fomepizole over ethanol. When there is insufficient fomepizole to treat all victims, we suggest using fomepizole preferentially for the more seriously ill, pregnant women, and children younger than 14 years. Prehospital distribution of ethanol to suspected victims has been used successfully in Estonia [41].

The oral bioavailability of fomepizole is excellent, allowing an alternative route of administration when obtaining intravenous (IV) access is delayed or impossible [44,45]. Moreover, the effective duration of alcohol dehydrogenase (ADH) inhibition after the initial 15 mg/kg loading dose likely lasts longer than 24 hours in the absence of hemodialysis [44]. While the expert panel did not reach consensus on the difficult issue of allocating scarce fomepizole during such disasters, and while individual circumstances will need to be considered with great care, a longer dosing interval, partitioning the loading dose, and avoiding doses during hemodialysis should allow more victims to be treated and additional time to prioritize hemodialysis and to confirm the diagnosis.

While many factors will determine the optimal approach, experience suggests that mobilizing and transferring resources to increase the critical care, antidotal, and hemodialysis capacity in a health care facility stretched thin with multiple sick patients is usually preferable to the interfacility transport of critically ill patients [36]. More stable patients (ie, alert, lack of visual symptoms, higher pH) are more suitable candidates for redistribution to other health care facilities during an outbreak. Consultation with toxicologists with specific expertise in methanol poisoning will be particularly important in guiding management decisions during these rare events. (See 'Additional resources' below.)

PEDIATRIC CONSIDERATIONS

Younger children — A common clinical presentation involves the child who may have swallowed one or two mouthfuls of a concentrated methanol or ethylene glycol solution. These children should not be managed at home [46].

Most victims of unintentional exposure present for evaluation shortly after ingestion and do not manifest significant metabolic acidosis or any evidence of end-organ dysfunction. The ideal approach is to measure the serum concentration of the specific alcohol in order to quantify the absorbed dose and predict the clinical course. Unfortunately, such concentrations are rarely available within a few hours of the ingestion, creating a diagnostic and therapeutic dilemma.

One approach to this problem (described below) can be used if all of the following criteria are met:

●The ingestion was unintentional and of small volume

●The product is accurately identified

●The patient is asymptomatic

●The patient has a normal pH and normal anion gap

●There is no coingestion or treatment with ethanol or fomepizole

If all conditions are met, the clinician can observe the patient and monitor venous blood gases and electrolytes every one to two hours to exclude the development of a metabolic acidosis or an increasing anion gap. If acidosis does not develop within eight hours of the ingestion, a toxic alcohol poisoning can be excluded. Alcohol dehydrogenase (ADH) inhibition with fomepizole or ethanol should not be initiated during this observation period as such treatment will prevent the development of acidosis even in patients with massive ingestions. In other words, the coingestion of ethanol or treatment with either fomepizole or ethanol invalidates the above protocol.

Parents should be counseled about safe storage of household products and pharmaceuticals prior to discharge.

For those pediatric patients who do demonstrate signs of methanol or ethylene glycol poisoning, the diagnostic and treatment considerations described above for adults largely hold. The limited published experience with fomepizole supports its safe and effective use in children using the same dosing protocol given above [47].

Occasionally, infants with inherited metabolic disorders such as methylmalonic acidemia present with features that resemble ethylene glycol poisoning, and vice versa [48,49]. The clinician should obtain organic acid testing in all infants presenting with unexplained metabolic acidosis. (See "Organic acidemias: An overview and specific defects".)

Adolescents — Groups of adolescents trying to become inebriated may consume toxic alcohols knowingly or accidentally in contaminated beverages. When treating an adolescent for a possible toxic alcohol ingestion, clinicians should always consider the possibility of other as-yet unidentified victims.

ADDITIONAL RESOURCES — Regional poison control centers in the United States are available at all times for consultation on patients who are critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have clinical and/or medical toxicologists available for bedside consultation and/or inpatient care. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is available at the website in the following reference [50].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Toxic alcohol poisoning".)

SUMMARY AND RECOMMENDATIONS

●Methanol and ethylene glycol poisonings are potentially fatal. Rapid recognition and early treatment are crucial. A summary table to facilitate emergency management is provided (table 1). (See 'Overview of emergency management' above.)

●First assess and secure the patient's airway, breathing, and circulation. If mechanical ventilation is required, large minute ventilations may be needed to prevent profound acidemia (pH <7.1) in patients with severe intoxication. (See 'Airway, breathing, circulation' above.)

●Patients with methanol or ethylene glycol poisoning fare worse when systemic acidemia is present. We recommend treatment with sodium bicarbonate for all patients who are acidemic (Grade 1C). We initiate sodium bicarbonate therapy for any patient with a serum pH below 7.3. Begin treatment with 1 to 2 meq/kg of sodium bicarbonate via intravenous (IV) bolus infusion. (See 'Treatment with sodium bicarbonate' above.)

●We recommend that alcohol dehydrogenase (ADH) inhibition therapy with fomepizole be initiated in any patient for whom the clinician has strong suspicion of poisoning with either methanol or ethylene glycol coupled with an elevated plasma osmolal gap, or acidemia, or a measured methanol or ethylene glycol concentration over 20 mg/dL (SI equivalent: methanol 6.2 mmol/L; ethylene glycol 3.2 mmol/L) (Grade 1B). Fomepizole is loaded at 15 mg/kg IV, followed by 10 mg/kg every 12 hours, with adjustments for hemodialysis or after more than two days of therapy. If fomepizole is unavailable, we recommend treatment with ethanol in these same circumstances (Grade 1B). We provide cofactor therapy to all patients receiving ADH inhibition. (See 'Alcohol dehydrogenase inhibition' above and 'Cofactor therapy' above.)

●We recommend immediate hemodialysis be performed in the setting of a known methanol or ethylene glycol ingestion when the following conditions are present (Grade 1B):

•Metabolic acidosis, regardless of drug level

•Elevated serum levels of methanol or ethylene glycol (more than 50 mg/dL [SI equivalent: methanol 15.6 mmol/L; ethylene glycol 8.1 mmol/L]) unless arterial pH is above 7.3

•Evidence of end-organ damage (eg, visual changes, renal failure)

We recommend treatment with hemodialysis if the clinician suspects a toxic alcohol ingestion in a patient with a severe, unexplained anion gap metabolic acidosis and significant osmolal gap (Grade 1B). We generally refrain from using hemodialysis to treat patients with elevated ethylene glycol concentrations, provided their serum pH is near normal, their renal function is normal, and fomepizole is given; this strategy is less helpful for methanol given its prolonged elimination with ADH inhibition. (See 'Hemodialysis' above.)

●Consultation with a medical toxicologist at a regional poison center is strongly recommended for all suspected exposures and for cases in which fomepizole, ethanol, or hemodialysis therapy may be used. Consultation with nephrology and emergency hemodialysis should be immediately obtained for severely acidotic patients in whom the diagnosis appears likely, especially if accompanied by visual or renal impairment. (See 'Additional resources' above.)

●A young child suspected of swallowing methanol or ethylene glycol should be brought immediately for medical evaluation; if the child appears well, antidotal treatment with fomepizole or ethanol should not be empirically given provided they meet explicit criteria provided in the text. (See 'Pediatric considerations' above.)

●Activated charcoal, gastric lavage, and syrup of ipecac have no role in the management of toxic alcohol exposures. (See 'Gastrointestinal decontamination' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges James Winchester, MD, who contributed to an earlier version of this topic review.