eMedicine Specialties > Neurology > Neurotoxicology

Methanol: Treatment & Medication

Author: Kalyani Korabathina, MD, Consulting Physician, North County Neurology Associates, Inc., Oceanside, California
Coauthor(s): Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital; David Likosky, MD, Clinical Instructor, Department of Neurology, University of Washington
Contributor Information and Disclosures

Updated: Nov 9, 2009

Treatment

Medical Care

Prompt medical care is key to avoiding complications secondary to methanol intoxication.

  • Supportive therapy is aimed at initiating airway management, correcting electrolyte disturbances, and providing adequate hydration.
  • The metabolic acidosis may necessitate administration of bicarbonate and assisted ventilation. Bicarbonate potentially may reverse visual deficits. In addition, bicarbonate may help to decrease the amount of active formic acid.
    • Antidote therapy is directed towards delaying methanol metabolism until the methanol is eliminated from the system either naturally or via dialysis. This is often accomplished in 2 ways: ethanol or fomepizole. Ethanol is also metabolized by ADH, and the enzyme has 10-20 times higher affinity for ethanol compared with methanol. Fomepizole is also metabolized by ADH; however, its use is limited because of high costs and lack of availability.1
    • Hemodialysis can easily remove methanol and formic acid. Indications include (1) greater than 30 mL of methanol ingested, (2) serum methanol level greater than 20 mg/dL, (3) observation of visual complications, and (4) no improvement in acidosis despite repeated sodium bicarbonate infusions.

Consultations

  • Consultation with a nephrologist is advisable to aid in the correction of the metabolic disturbance. The nephrologist can also help to arrange dialysis, respiratory care, or both.
  • Consultation with an ophthalmologist is recommended to assess ocular damage.
  • Consultation with a neurologist is arranged to assist with the management of seizures in the acute setting or the treatment of any subsequent movement disorders that may develop.

Medication

For a number of years, only one treatment was available for methanol toxicity. Recently, advances have been made with potential for more effective therapy.

Antidotal treatment

Inhibit the toxic effects of methanol via competitive inhibition.


Ethanol

Believed to compete with methanol for ADH, thus preventing metabolism of methanol to its toxic by-products. ADH has 10- to 20-fold increased affinity for ethanol compared with methanol. By slowing degradation, assumed to prevent accumulation of high levels of formic acid.
Goal of therapy is to achieve ethanol blood concentration of 100 mg/dL (Brown, 2001). At this level, ethanol is thought to become a competitive substrate for ADH and be sufficient to block methanol metabolism.

Adult

10% ethanol solution typically administered as 600-mg/kg bolus followed by continuous infusion

Pediatric

Administer as in adults

May increase toxicity of benzodiazepines or barbiturates and result in death; additive toxicity may occur with other CNS depressants; cimetidine may increase toxicity; disulfiram and other drugs (eg, ketoconazole, metronidazole) cause alcohol intolerance (eg, facial flushing, nausea, vomiting); may increase serum levels of drugs metabolized by ADH (eg, abacavir)

Ingestion of other CNS depressants

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

IV administration may cause thrombophlebitis; oral administration may cause severe gastritis


Fomepizole/4-methylpyrazole (Antizol)

Acts similarly to ethanol. Stronger competitive inhibitor of ADH. In addition, does not cause hypoglycemia or sedation. Relatively easier to administer than ethanol. Does not require monitoring of serum concentrations.

Adult

Clinical dose not established; however, 20 mg/kg/d used in small series (Jacobsen, 1997)

Pediatric

Not established

Inhibitory effects on ADH increased in presence of ethanol

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not give as bolus; caution in breastfeeding because no information available on excretion in breast milk; caution in renal impairment

More on Methanol

Overview: Methanol
Differential Diagnoses & Workup: Methanol
Treatment & Medication: Methanol
Follow-up: Methanol
References

References

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  2. Casarett LJ, Doull J, Klaassen CD, eds. Casarett and Doull's Toxicology: The Basic Science of Poisons. 5th ed. New York, NY: McGraw-Hill; 1996:604-5, 756-7.

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Further Reading

Keywords

organic solvent, formaldehyde, alcohol dehydrogenase, methanol ingestion, methanol toxicity, methanol intoxication, antifreeze ingestion, perfume ingestion, paint solvent ingestion, inhalation of methanol, methanol fumes, methanol poisoning

Contributor Information and Disclosures

Author

Kalyani Korabathina, MD, Consulting Physician, North County Neurology Associates, Inc., Oceanside, California
Kalyani Korabathina is a member of the following medical societies: American Academy of Neurology and American Epilepsy Society
Disclosure: Nothing to disclose.

Coauthor(s)

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

David Likosky, MD, Clinical Instructor, Department of Neurology, University of Washington
David Likosky, MD is a member of the following medical societies: American Academy of Neurology, American College of Physicians-American Society of Internal Medicine, and American Heart Association
Disclosure: Nothing to disclose.

Medical Editor

Jonathan S Rutchik, MD, MPH, Assistant Professor, Department of Occupational and Environmental Medicine, University of California at San Francisco
Jonathan S Rutchik, MD, MPH is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Occupational and Environmental Medicine, and Society of Toxicology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Nestor Galvez-Jimenez, MD, MSc, MHA, Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida
Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society
Disclosure: Nothing to disclose.

Chief Editor

Tarakad S Ramachandran, MBBS, FRCP(C), FACP, Professor of Neurology, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Chair, Department of Neurology, Crouse Irving Memorial Hospital
Tarakad S Ramachandran, MBBS, FRCP(C), FACP is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners, American College of International Physicians, American College of Managed Care Medicine, American College of Physicians, American Heart Association, American Stroke Association, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, and Royal Society of Medicine
Disclosure: Abbott Labs  Honoraria Consulting; Teva Marion Honoraria Consulting; Boeringer-Ingelheim Honoraria Speaking and teaching

 
 
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