Methanol Half-Life During Ethanol Administration: Implications for Management of Methanol Poisoning

Palatnick, Wesley; Redman, Lyle W; Sitar, Daniel S.; Tenenbein, Milton

doi:10.1016/s0196-0644(95)70152-4

Cited by 50 publications

(29 citation statements)

References 24 publications

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“…This combination should reduce morbidity and mortality and decrease the duration of hospitalization. Other investigators, based on their clinical experience, have come to a similar conclusion (28,72). These treatment measures should be continued until methanol concentration is Ͻ16 mg/dl or undetectable, if possible, and blood pH is Ͼ7.3 (12,54,74).…”

Section: Treatmentmentioning

confidence: 86%

“…Hemodialysis has been used to remove methanol and formate and to correct the metabolic acidosis (12,15,28,58,67,72,73). A recent study (74) established a formula to determine the duration of dialysis necessary to achieve a serum methanol concentration (or that of other alcohols) of Ͻ5 mmol/L (approximately 16 mg/dl with methanol), based on the predialysis serum alcohol concentration, blood flow, gender, age, height, weight, and urea clearance of the dialyzer:…”

Section: Treatmentmentioning

confidence: 99%

See 1 more Smart Citation

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

355

326

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Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Table 1. Methanol, ethylene glycol, diethylene glycol, and propylene glycol intoxication and alcoholic ketoacidosis can produce hyperosmolality and metabolic acidosis (3-9). Isopropanol intoxication is usually associated with hyperosmolality alone (4,5). Importantly, several of these disorders can be fatal or produce irreversible tissue damage if they are not quickly recognized and treated appropriately (4 -15). Effect of Alcohols on Serum Osmolality and the Osmolal GapThe normal serum osmolality of 285 to 290 mOsm/L is due to sodium and its counterbalancing ions, bicarbonate and chloride, and glucose and urea. It can be calculated using the following equation:Serum osmolality (mOsm/L) ϭ 2 ϫ Na ϩ ϩ blood urea nitrogen (mg/dl)/2.8 ϩ glucose (mg/dl)/18. The serum osmolality measured by freezing point depression is usually within 10 mOsm/L of the calculated serum osmolality (16). Accumulation of low molecular weight substances in the serum (such as each of the alcohols) will raise the measured serum osmolality above that of the calculated serum osmolality, producing an osmolal gap (4,5,16 -18). The effect of each of the alcohols on serum osmolality is shown in Table 2. Methanol gives rise to the greatest increment in serum osmolality, followed by ethanol, isopropanol, ethylene glycol, propylene glycol, and diethylene glycol in that...

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Section: Treatmentmentioning

confidence: 86%

Section: Treatmentmentioning

confidence: 99%

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

355

326

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“…It could be possible that EtOH, the affinity of which to alcohol dehydrogenase is much higher than that of MeOH, was metabolized first 10. Indeed, toxicological analysis revealed that EtOH was almost completely metabolized, but a lethal amount of MeOH remained in the patient's body.…”

Section: Discussionmentioning

confidence: 99%

Mild manifestation of methanol poisoning half a day after massive ingestion of a fuel alcohol product containing 70% ethanol and 30% methanol: a case report

Yoshizawa

Kamijo

Fujita

et al. 2018

Acute Medicine & Surgery

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CaseIs fomepizole necessary after massive ingestion of a mixture of methanol and ethanol? We report the case of a 37‐year‐old man who was transported to our Poison Center 12 h after ingesting 500 mL of fuel alcohol containing 70% methanol and 30% ethanol in a suicide attempt. On admission, he presented only with somnolence and mild metabolic acidosis. We hypothesized that most of the ethanol had been metabolized.OutcomeAs the estimated serum concentration of methanol was lethal (242.6 mg/dL), fomepizole was given i.v. and hemodialysis was carried out twice, resulting in complete recovery. Later, the serum concentrations of both methanol and ethanol on admission were found to be 224.1 and 0.51 mg/dL, respectively.ConclusionTherapeutic intervention was delayed by half a day after ingestion of a product containing methanol and ethanol in the present case. If the patient had arrived earlier, he may have only been treated with hemodialysis, but not fomepizole.

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“…When methanol level is low or ethanol is absent, the half-life time of methanol is within 3 hours. But if ethanol is ingested with methanol, the half-life time is prolonged up to 52 hours (6). Early toxicity of methanol intoxication is due to methanol itself and appears as symptoms such as nausea, vomiting, headache and abdominal pain.…”

Section: Discussionmentioning

confidence: 99%

Methanol Intoxication: Differential Diagnosis from Anion Gap-increased Acidosis

et al. 2004

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We report a case of methanol intoxication, which was not distinguished from ethylene glycol intoxication during treatment. A 65-year-old man was transferred to our emergency department because of drowsiness and remarkable metabolic acidosis. He was intubated because his consciousness disturbance worsened. The diagnosis was suspected as methanol or ethylene glycol intoxication in addition to ethanol intoxication. Administration of ethanol and hemodialysis were chosen for his essential treatments. When he was extubated, he complained about visual loss. His brain computed tomography scans revealed putaminal lesions, which are rarely reported in methanol intoxication. Diagnosis of methanol intoxication was confirmed by the serum high methanol levels.

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Methanol Half-Life During Ethanol Administration: Implications for Management of Methanol Poisoning

Cited by 50 publications

References 24 publications

Toxic Alcohol Ingestions

Toxic Alcohol Ingestions

Mild manifestation of methanol poisoning half a day after massive ingestion of a fuel alcohol product containing 70% ethanol and 30% methanol: a case report

Methanol Intoxication: Differential Diagnosis from Anion Gap-increased Acidosis

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