Although any alcohol can be toxic if ingested in large enough quantities, the term toxic alcohol has traditionally referred to isopropanol, methanol, and ethylene glycol.[1, 2] Prompt recognition and treatment of patients intoxicated with these substances can reduce the morbidity and mortality associated with these alcohols.
This article discusses not only the three toxic alcohols but also ethanol. For discussion of the individual agents, see Methanol Toxicity and Ethylene Glycol Toxicity; for discussion of pediatric ethanol ingestion, see Ethanol Toxicity. Ethanol withdrawal is a serious and potentially life-threatening problem, which is discussed in Withdrawal Syndromes.
Ethyl alcohol (ethanol; CH3 -CH2 -OH) is a low molecular weight hydrocarbon that is derived from the fermentation of sugars and cereals. It is widely available both as a beverage and as an ingredient in food extracts, cough and cold medications, and mouthwashes.
Ethanol is rapidly absorbed across both the gastric mucosa and the small intestines, reaching a peak concentration 20-60 minutes after ingestion. Once absorbed, it is converted to acetaldehyde. This conversion involves three discrete enzymes: the microsomal cytochrome P450 isoenzyme CYP2E1, the cytosol-based enzyme alcohol dehydrogenase (ADH), and the peroxisome catalase system. Acetaldehyde is then converted to acetate, which is converted to acetyl Co A, and ultimately carbon dioxide and water.[3]
Genetic polymorphisms coding for alcohol dehydrogenase, the amount of alcohol consumed, and the rate at which ethanol is consumed all affect the speed of metabolism. As a general rule, ethanol is metabolized at a rate of 20-25 mg/dL in the nonalcoholic but at an increased rate in chronic alcoholics.
Isopropyl alcohol (isopropanol; CH3 -CHOH-CH3) is a low molecular weight hydrocarbon. It is commonly found as both a solvent as well as a disinfectant.[4] It can be found in many mouthwashes, skin lotions, rubbing alcohol, and hand sanitizers. Because of its widespread availability, lack of purchasing restrictions, and profound intoxicating properties, it is commonly used as an ethanol substitute.
Isopropanol is rapidly absorbed across the gastric mucosa and reaches a peak concentration approximately 30-120 minutes after ingestion. Isopropanol is primarily metabolized via alcohol dehydrogenase to acetone. A small portion of isopropanol is excreted unchanged in the urine. The peak concentration of acetone is not present until approximately 4 hours after ingestion. The acetone produces CNS depressant effects and a fruity odor on the breath.[5]
Methyl alcohol (methanol; CH3 OH) is widely used as an industrial and marine solvent and paint remover. It is also used in photocopying fluid, shellacs, and windshield-washing fluids. Although toxicity primarily occurs from ingestion, it can also occur from prolonged inhalation or skin absorption.[6, 7, 8, 9] Methanol is rapidly absorbed from the gastric mucosa, and achieves a maximal concentration 30-90 minutes after ingestion.[10]
Methanol is primarily metabolized in the liver via alcohol dehydrogenase into formaldehyde. Formaldehyde is subsequently metabolized via aldehyde dehydrogenase into formic acid, which ultimately is metabolized to folic acid, folinic acid, carbon dioxide, and water. A small portion is excreted unchanged by the lungs.
Formic acid is responsible for the majority of the toxicity associated with methanol. Without competition for alcohol dehydrogenase, methanol undergoes zero-order metabolism, and is thus is excreted at a rate of 8.5 mg/dL/h to 20 mg/dL/h. Once methanol experiences competitive inhibition, from either ethanol or fomepizole, the metabolism changes to first order. In this later scenario, the excretion half-life ranges from 22-87 hours.
Ethylene glycol (CH2 OH-CH2 OH) is an odorless, colorless, sweet-tasting liquid, which is used in many manufacturing processes. Domestically, it is probably most commonly encountered in antifreeze. It is absorbed somewhat rapidly from the gastrointestinal tract, and peak concentrations are observed 1-4 hours after ingestion.[8]
Ethylene glycol itself is nontoxic, but it is metabolized into toxic compounds. Ethylene glycol is oxidized via alcohol dehydrogenase into glycoaldehyde, which then undergoes metabolism via aldehyde dehydrogenase into glycolic acid.[11] The conversion to glycolic acid is somewhat rapid. In contrast, the conversion of glycolic acid to glyoxylic acid is slower and is the rate-limiting step in the metabolism of ethylene glycol.
Glyoxylic acid is subsequently metabolized into several different products, including oxalic acid (oxalate), glycine, and alpha-hydroxy-beta-ketoadipate. The conversion to glycine requires pyridoxine as a cofactor, while the conversion to alpha-hydroxy-beta-ketoadipate requires thiamine as a cofactor. The oxalic acid combines with calcium to form calcium oxalate crystals.
In the presence of normal renal function and no competitive inhibition for alcohol dehydrogenase, the excretion half-life of ethylene glycol is approximately 3 hours. However, in the presence of fomepizole or ethanol, alcohol dehydrogenase undergoes competitive inhibition, and the resulting excretion half-life increases to approximately 17-20 hours.
Alcohol intoxication is common in modern society, largely because of its widespread availability. More than 8 million Americans are believed to be dependent on alcohol, and up to 15% of the population is considered at risk. In some studies, more than half of all trauma patients are intoxicated with ethanol at the time of arrival to the trauma center. In addition, ethanol is a common coingestant in suicide attempts.
Acute intoxication with any of the alcohols can result in respiratory depression, aspiration, hypotension, and cardiovascular collapse.
Ethanol
In 2016, 7802 single exposures to ethanol in beverages, with 229 major outcomes and 9 deaths, were reported to US Poison Control Centers. There were 2324 non-beverage exposures, with 9 major outcomes and 1 death. Ethanol-based hand sanitizers accounted for 19,949 single exposures, with 20 major outcomes and 1 death, and ethanol-containing mouthwashes accounted for 5700 single exposures, with 15 major outcomes and 2 deaths.[12]
Ethanol poisoning is typically caused by high-intensity binge drinking (ie, consumption of a very large amount of alcohol during an episode of binge drinking). Approximately 38 million US adults report binge drinking an average of four times per month and consuming an average of eight drinks per episode. In 2010–2012, an annual average of 2,221 ethanol poisoning deaths (8.8 deaths per 1 million population) occurred in persons aged ≥15 years in the United States. Of those deaths, 1,681 (75.7%) involved adults aged 35–64 years, and 1,696 (76.4%) involved men.[13]
Although many patients present with ethanol intoxication as their sole issue, many other patients have ethanol intoxication as part of a larger picture. Thus, the morbidity is often from coingestants or coexisting injuries and illnesses.
Long-term use results in hepatic and gastrointestinal injuries. Coma, stupor, respiratory depression, hypothermia, and death can result from high concentrations of acute ethanol intoxication. Chronic alcoholics, as well as children, are at risk for hypoglycemia.
The World Health Organization estimates that in 2016, ethanol use resulted in about 3 million deaths (mostly in men), or 5.3% of all deaths around the world—more than tuberculosis, HIV/AIDS, or diabetes. Of alcohol-related deaths, 28% were due to injuries (eg, from traffic accidents, self-harm, and violence), 21% inivolved digestive disorders, and 19% involved cardiovascular diseases.[14, 15]
Isopropanol, methanol, and ethylene glycol
In 2016, 14,537 single exposures to isopropanol (from sources including rubbing alcohol, cleaning agents, and hand sanitizers) were reported to US Poison Control Centers. Of these, 60 patients were classified as experiencing "major" morbidity, with 3 patients dying.[12]
In the same year, 1,150 single exposures to methanol, including automotive products, and 6,325 exposures to ethylene glycol were reported. Of those intoxicated with methanol, 7 patients were classified as experiencing "major" disability, and 4 additional patients died. For those patients who were intoxicated with ethylene glycol, 196 patients were classified as having "major" disability, with an additional 17 patients dying.[12] It is important to recognize that these numbers likely underestimate the true incidence of exposure, however, because of both a failure to recognize the ingestion as well as a failure to report the suspected or known ingestion to a poison control center.
Most cases of methanol toxicity involve single patients. Rarely, outbreaks may occur in settings where access to ethanol is limited and methanol is consumed as a substitute. Collister et al reported a methanol outbreak resulting from recreational ingestion of fracking fluid.[16]
The primary toxicity with isopropanol is CNS depression. These CNS manifestations can include lethargy, ataxia, and coma. In addition, isopropanol is irritating to the GI tract. Therefore, abdominal pain, hemorrhagic gastritis, and vomiting can be observed. Unlike methanol and ethylene glycol, isopropanol does not cause a metabolic acidosis.
The toxicity with methanol occurs from both the ensuing metabolic acidosis, as well as the formate anion (formic acid) itself.[17] Although the eye is the primary site of organ toxicity, in the later stages of severe methanol toxicity, specific changes can occur in the basal ganglia as well. Pancreatitis has been reported following methanol ingestion. Hyperventilation will occur as a compensatory mechanism to counteract the acidosis.
As previously stated, ethylene glycol itself is nontoxic. The majority of the metabolic acidosis occurs from glycolic acid. One form of morbidity occurs when oxalate combines with calcium to form calcium oxalate crystals, which accumulate in the proximal renal tubules, thereby inducing renal failure. Hypocalcemia can ensue, and cause coma, seizures, and dysrhythmias. Autopsy studies have confirmed that the calcium oxalate crystals are deposited not only in the kidneys but in many other organs, including the brain, heart, and lungs.
Ethanol intoxication is common in older teenagers through adulthood. The toxic dose for an adult is 5 mg/dL, whereas the toxic dose in a child is 3 mg/dL. Children are at higher risks of developing hypoglycemia following a single ingestion than are adults.
Most isopropanol ingestions occur in children younger than 6 years. Most methanol and ethylene glycol ingestions occur in adults older than 19 years.
A history of inebriation with associated slurred speech, ataxia, and impaired judgment is common in the initial stages of intoxication of each of these alcohols. Depending on the dose ingested, this may be followed by progressive levels of CNS depression, coma, and premorbid multiorgan failure. The history that can be obtained varies with the timing of presentation. The onset of the later stages of toxic alcohol intoxication can also be delayed if ethanol is coingested, prolonging the time it takes to develop metabolic acidosis and other symptoms. The following focuses on symptoms that may be unique to each alcohol.
The history itself can often point to a diagnosis of ethanol intoxication. An associated history of chronic alcoholism alters metabolism, associated comorbidities, and the expected course of recovery. A detailed discussion of this topic is beyond the scope of this article (see Ethanol Toxicity).
Attempting to elicit what has changed recently may reveal the immediate reason for presentation. A history of coingestants may also alter the patient's course.
Following an isopropanol ingestion, the patient may not complain of anything specific. Rather, the patient may simply appear intoxicated, as with ethanol intoxication.
A history of abdominal pain, nausea, and sometimes hematemesis may be obtained.
Following methanol ingestion, a patient is initially inebriated as with the other alcohols. Other symptoms can be delayed for up to 12-24 hours.
The patient may complain of headache, nausea, or anorexia. Occasionally, the patient may complain of shortness of breath related to hyperventilation.
Because one of the primary end-organs involved in methanol is the eye, the patient may complain of difficulty seeing. Specifically, vision is often described as a "snow field," though a variety of visual complaints may be verbalized.
Ethylene glycol toxicity occurs in three stages, as follows:
The symptoms of ethanol intoxication depend on both the serum concentration as well as the frequency at which an individual ingests ethanol. Thus, a person who consumes large amounts of ethanol on a daily basis may appear sober at the same serum ethanol level at which a novice drinker exhibits cerebellar dysfunction.
As a general rule, levels less than 25 mg/dL are associated with a sense of warmth and well-being. Euphoria and decreased judgment occur at levels between 25-50 mg/dL. Incoordination, decreased reaction time/reflexes, and ataxia occur at levels of 50-100 mg/dL. Cerebellar dysfunction (ie, ataxia, slurred speech, nystagmus) are common at levels of 100-250 mg/dL. Coma can occur at levels of greater than 250 mg/dL, whereas respiratory depression, loss of protective reflexes, and death occur at levels greater than 400 mg/dL.
As previously stated, the patient who consumes isopropanol may appear inebriated, as with ethanol. Isopropanol concentrations of 50-100 mg/dL typically result in intoxication, which can progress to include symptoms such as dysarthria and ataxia, while lethargy or coma can be seen with levels exceeding 150 mg/dL. Cardiovascular depression can occur with levels exceeding 450 mg/dL.
The presence of acetone may induce a fruity odor on the patient's breath.
Unlike ethanol or isopropanol, methanol does not cause nearly as much of an inebriated state. If a patient has coingested ethanol, signs or symptoms specific to methanol intoxication are delayed.
The patient may be hyperventilating.
If vision is impaired, ocular examination may reveal dilated pupils that are minimally or unreactive to light with hyperemia of the optic disc. Over several days, the red disc becomes pale, and the patient may become blind. Typically, subjective complaints precede physical findings in the eye.
The physical findings depend on the stage of the presentation. Thus, the patient may present simply inebriated or progressively more acidotic as renal failure, cardiovascular dysfunction, and coma develop.
Examination findings correlate with the symptoms, as previously described.
In patients who survive severe intoxication, calcium oxalate crystal deposition may occur in the brain parenchyma and can induce cranial neuropathies. These findings typically occur as the patient is recovering from the initial intoxication. Cranial nerves II, V, VII, VIII, IX, X, and XII are most commonly involved.
Following consumption of any type of alcohol, the extent of the workup depends partly on the history. However, because the patient's sensorium is likely to be altered and a history unobtainable or inaccurate, a thorough physical examination is important to evaluate for occult injuries; laboratory clues can also become invaluable.
If the possibility of a suicide attempt is raised, an electrocardiogram and basic toxicology screen, including measurement of salicylate and acetaminophen concentrations, become important.
In addition, if ingestion of a toxic alcohol is suspected, a serum ethanol level and basic electrolytes, including a serum bicarbonate level are vital, as the latter are needed to calculate an anion gap. In such a situation, specific serum toxic alcohol levels immensely help guide management. If these are unavailable, calculation of an osmolar gap can sometimes be helpful, though its exclusive use is fraught with pitfalls.[18] These issues are best discussed with the local poison control center. Arterial blood gases and other tests that measure associated organ dysfunction also become important in cases of poisoning with toxic alcohols.
An important point is that laboratory abnormalities vary dramatically over the course of the patient's presentation and any laboratory abnormalities must be interpreted with the time frame of the patient's presentation in mind. Failing to do so is a common and important pitfall. Thus, early in the course of intoxication with a toxic alcohol, a patient will have neither an anion gap nor an osmolar gap though their serum toxic alcohol level will be highest shortly after ingestion. However, as metabolism of the toxic alcohol occurs, the anion and osmolar gaps develop as metabolites are formed and the toxic alcohol level drops.[19]
Other laboratory abnormalities also develop as end-organ damage occurs. Coingestion of alcohol delays all the laboratory value changes as well as the signs and symptoms of toxic alcohol-induced injury.
The single most important laboratory test in a patient who appears intoxicated with ethanol is a serum glucose level. Hypoxia, head injury, seizures, and other metabolic disturbances must be excluded by either history or physical examination or sought with the appropriate tests. The routine use of a serum blood alcohol level is controversial, largely because it is unlikely to affect management in a patient who is awake and alert. Many clinicians consider the patient safe for discharge once they are clinically (not numerically) no longer intoxicated.
In patients who are chronic alcoholics, anemia, thrombocytopenia, elevation of hepatic transaminase levels, and a prolongation of the prothrombin time can be observed. These need not be routinely checked in a patient who presents simply for alcohol intoxication but may be useful if changes from baseline are suspected.
Serum levels of isopropanol can be obtained but are somewhat of limited value, as the treatment is largely supportive. However, they can be useful in confirming the diagnosis.
After correcting for all other variables, including ethanol, the serum isopropanol level can be estimated by multiplying the remaining osmolar gap by 6.0. Serum ketones will often be positive, although the patient should not be acidotic. Because ketones will be present in the serum as early as 30 minutes after ingestion, if there is no coexisting ethanol ingestion, the absence of ketones effectively rules out isopropanol ingestion.
Depending on the assay used in the laboratory, significant ketosis can cause interference with the creatinine assay. As such, the serum creatinine level can be falsely elevated.
Serum methanol levels should be obtained when this diagnosis is suspected. As previously stated, both the osmolar and anion gap should be obtained. After correcting for all other variables, including ethanol, the serum methanol level can be estimated by multiplying the remaining osmolar gap by 3.2.
A serum ethylene glycol level should be obtained when this diagnosis is suspected. The osmolar gap and anion gap should also be obtained. After correcting for other variables, including ethanol, the serum ethylene glycol level can be estimated by multiplying the remaining osmolar gap by 6.2.
A baseline creatinine and BUN level should be obtained in all cases of ethylene glycol intoxication. These values can then be followed to check for the development of renal failure.
In addition, the urine can be examined for evidence of fluorescence. In antifreeze, fluorescein is added to the liquid to permit mechanics to identify the source of a fluid leaking from a car. However, fluorescein is excreted in the urine faster than ethylene glycol. Thus, fluorescence can be eliminated before the patient even arrives in the emergency department. As such, the presence of fluorescence of urine under a Wood's lamp is not a sensitive test. In addition, because certain containers themselves fluoresce, the presence of fluorescence is neither sensitive nor specific. Despite this, a positive test that differentiates urine fluorescence from that of its container may be a quick bedside clue pointing toward ethylene glycol intoxication.
Both a serum calcium level and an electrocardiogram should be obtained, since hypocalcemia may occur as calcium combines with oxalate in the form of calcium oxalate crystals.[20]
Measuring the osmolar gap is important when toxic alcohols ingestion is suspected. The osmolar gap is determined by subtracting the calculated osmolality from the measured osmolality. The serum osmolality should be determined by freezing point depression rather than by heat of vaporization.
The serum osmolality can be calculated by the following formula:
Osm = (2) (Na+) + BUN/2.8 + Glucose/18 + EtOH/4.6 + Isopropanol/6.0 + MeOH/3.2 + Ethylene glycol/6.2
In the above formula, if, for example, an ingestion of methanol is suspected, the osmolality should be calculated using the sodium, BUN, and glucose. The ethanol level is also measured and then factored into the equation. If isopropanol and ethylene glycol are not suspected, they can be eliminated from the equation. Then, once the osmolar gap is determined, multiply the osmolar gap by 3.2 to determine the estimated methanol level.
It is important to recognize that neither the presence nor absence of an osmolar gap can be used to confirm or exclude a toxic alcohol ingestion. With both methanol and ethylene glycol, the alcohols are metabolized from an alcohol to an aldehyde, and ultimately to an acid. As such, shortly after an ingestion, the patient may have an osmolar gap without an anion gap. Similarly, in the later stages of an ingestion, a patient may have an anion gap without an osmolar gap.
The prehospital care provider has several important tasks. First, the prehospital provider should search for any empty containers near the patient. In addition, a blood sugar level should be obtained on anyone who appears intoxicated. Local protocols and the skill level of the provider dictate additional prehospital care for patients with altered mental status.
As with all emergency patients, initial treatment should focus on the airway, breathing, and circulation. Gastric decontamination is rarely necessary for any of the alcohols. An exception to this may be a patient who presents immediately after ingestion of a toxic alcohol in whom one might reasonably expect to be able to recover a significant amount of the toxin via aspiration through a nasogastric tube.
Treatment of ethanol and isopropanol intoxication is largely supportive.[21] Because of the hemorrhagic gastritis that can follow isopropanol ingestion, H2 blockade or proton-pump inhibitors may be helpful. Hemodialysis, while effective, is rarely indicated, and should only be used in the setting of profound hemodynamic compromise.[5]
Once either methanol or ethylene glycol intoxication are suspected, treatment should be initiated without delay. Fortunately, since both alcohols are metabolized by alcohol dehydrogenase, the treatment is the same, and differentiating which of the two toxic alcohols is responsible is not necessary before implementing treatment.[21]
The primary antidotal treatment of methanol or ethylene glycol involves blocking alcohol dehydrogenase. This enzyme can be inhibited by either ethanol or fomepizole.[22, 23, 24] Toxic alcohol levels are frequently not immediately available. Thus, ideally, if methanol or ethylene glycol poisoning is suspected, the patient should receive a loading dose of fomepizole while the levels are being obtained. Because the next dose of fomepizole is not due for an additional 12 hours, this strategy allows 12 hours for the blood to be processed at a reference laboratory before additional treatment is needed.
Inhibition of alcohol dehydrogenase with ethanol may be substituted for treatment with fomepizole (see below), though studies have highlighted the greater safety of fomepizole as a treatment, when available.[11] In some patients, treatment with fomepizole alone may represent definitive treatment and can prevent the need for hemodialysis.[25]
In addition to blocking alcohol dehydrogenase, significant metabolic acidosis should be treated with sodium bicarbonate infusions. If methanol is suspected, folinic acid should be administered at a dose of 1 mg/kg, with a maximal dose of 50 mg. It should be repeated every 4 hours. If folinic acid is not immediately available, folic acid can be substituted at the same dose.
If ethylene glycol overdose is suspected, the patient should also receive 100 mg of intravenous thiamine every 6 hours and 50 mg of pyridoxine every 6 hours. The purpose of the thiamine and pyridoxine is to shunt metabolism of glyoxylic acid away from oxalate and favor the formation of less toxic metabolites.
In methanol overdose, sodium bicarbonate should be administered liberally, with the goal being to completely reverse the acidosis. Experimental studies suggest that formate is excreted in the kidneys at a much higher rate when the patient is not acidotic. In addition, when the patient is not acidotic, formic acid dissociates to formate at lower rates so that less formate crosses the blood-brain barrier. Thus, in methanol intoxication, correcting the acidosis actually speeds up elimination of the toxic compound and decreases toxicity.
If ethanol is used as an antidote, the recommended target serum concentration is 100-150 mg/dL. Because ethanol inhibits gluconeogenesis, hypoglycemia is common in patients on an ethanol infusion.[26] Hypoglycemia is particularly prevalent in pediatric patients on such drips. Thus, serum glucose levels must be checked frequently, at least every 2 hours. In addition, because it is difficult to attain a steady serum concentration of ethanol, the ethanol level also must be checked frequently, and titrations made.
A 5% or 10% ethanol solution can be made in the pharmacy. If giving ethanol, administer a loading dose of 600 mg/kg, followed by a drip of 66-154 mg/kg/h, with chronic alcoholics requiring doses at the higher end of the scale. Ethanol can be given either intravenously or orally.
In addition to hypoglycemia, additional adverse effects from ethanol infusion include inebriation, CNS depression, pancreatitis, and local phlebitis. Because of the phlebitis that occurs with ethanol infusions, some advocate that ethanol should only be administered via a central venous line.
Ethanol infusions are not only labor intensive, but once the costs of the frequent blood glucose and serum ethanol level assays are accounted for, ethanol antidotal therapy is frequently more expensive than fomepizole. Ethanol has also been associated with more frequent adverse reactions than fomepizole.[27] Thus, because of the lower overall cost and the ease of administration and safety considerations, fomepizole has become the preferred antidote for methanol or ethylene glycol poisoning.[28]
Fomepizole should be administered as a loading dose of 15 mg/kg. Subsequent doses should be at 10 mg/kg every 12 hours for 4 doses. Because fomepizole actually induces its own metabolism after 48 hours of treatment, if additional doses are needed, the dose should be increased to 15 mg/kg. Fomepizole needs to be re-dosed during hemodialysis. The package insert or local poison center can help with the re-dosing strategy. Fomepizole should be continued until the serum ethylene glycol or methanol concentrations are less than 20 mg/dL.
Hemodialysis is frequently required in patients with significant methanol or ethylene glycol ingestions.[21, 25] Indications for hemodialysis include the following:
For patients with ethanol intoxication who appear to have issues with dependence or abuse, consider referral to an alcohol detoxification facility. Consult a toxicologist for all known or suspected cases of isopropanol, methanol, or ethylene glycol ingestion. If a toxicologist is not immediately available at the medical center where the patient is located, the regional poison control center can be contacted at (800) 222-1222.
Consult a nephrologist for any known or suspected cases of methanol or ethylene glycol intoxication to assist in the decision making for hemodialysis.
Fomepizole (eg, 4-methylpyrizole, 4-MP, Antizol) has greater affinity for alcohol dehydrogenase than ethanol or methanol and has a considerably better safety profile than ethanol. Fomepizole has been approved by the US Food and Drug Administration (FDA) for ethylene glycol poisoning, but it is also useful for managing methanol poisoning.
B vitamins (ie, folic acid, pyridoxine, thiamine) may be useful in selected cases to reduce the toxicity of alcohol metabolites.
Clinical Context: DOC for ethylene glycol and methanol poisoning because of ease of administration and better safety profile than ethanol. Inhibitor of alcohol dehydrogenase. In contrast to ethanol, 4-MP levels do not require monitoring during therapy.
Begin fomepizole treatment immediately upon suspicion of methanol/ethylene glycol ingestion based on the patient's history or anion gap metabolic acidosis, increased osmolar gap, oxalate crystals in the urine, or a documented serum methanol/ethylene glycol level. Adjust dosing during hemodialysis; see package insert.
Clinical Context: Has 10-20 times greater affinity for enzyme alcohol dehydrogenase than methanol does, blocking production of toxic metabolites.
Believed to inhibit ADH when serum levels exceed 0.05 g/dL (50 mg/dL). Titration to serum levels between 0.10 g/dL (100 mg/dL) and 0.15 g/dL (150 mg/dL) typically used.
Measure patient's initial blood level. May be administered PO/IV.
Clinical Context: Adjunctive agent in methanol ingestion. Member of vitamin B-complex that may enhance elimination of toxic metabolite formic acid produced when methanol is metabolized. Useful in methanol and possibly ethylene glycol toxicity. Leucovorin (folinic acid) is active form of folate and may be substituted for folic acid.
Folic acid should be administered for several days to enhance folate-dependent metabolism of formic acid to carbon dioxide and water.
These agents prevent formation of toxic metabolites in methanol ingestions (not useful with isopropanol or ethanol ingestions). Therapy generally is maintained until methanol levels are less than 20 mg/dL.
In ethylene glycol poisoning, thiamine and pyridoxine shunt metabolism of glyoxylic acid away from oxalate and favor the formation of less toxic metabolites. In patients with ethanol-related hypoglycemia, especially those who are malnourished or alcoholics, pretreatment with thiamine may be necessary.
Patients with significant ingestions of toxic alcohols require hospital admission in a closely monitored setting such as the intensive care unit. Patients who are alcoholics may be at risk of alcohol withdrawal if admitted to the hospital.
See the list below:
Ethanol ingestion complications include the following:
Complications of other alcohols include the following: