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METHANOL-INDUCED Outline of the Presentation

▪ Introduction about Methanol
BILATERAL OPTIC NEUROPATHY ▪ Case Presentation
Ranche, J.M., Cruz, R.D., Inocencio, F.P. (2004) ▪ Discussion of the Case
▪ Conclusion and Recommendations
▪ References

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Methanol
Methanol
▪ Also known as wood alcohol, methyl alcohol,
▪ Source wood spirits, and carbinol
▪ Mechanism of Toxic Action ▪ Common additive solvent in fuel, windshield
▪ Signs and symptoms of acute overdose washing fluids, photocopying fluids, and paint
▪ Laboratory analyses removers
▪ Management ▪ Also been used as an adulterant to bootleg liquor
▪ Treatment/Antidote

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Outbreaks of methanol poisoning How Does Methanol Come To Be in Alcoholic Drinks?

▪ 1904: 153 report cases of blindness (through the publication of Wood ▪ Higher concentrations are formed during
and Buller) incorrectly managed distillation processes
▪ 1951: 323 cases of methanol toxicity after intake of bootleg whiskey ▪ Deliberately added to fortify informally-
containing 35-40% methanol, later published as a comprehensive study produced spirits and illicit alcoholic drinks.
by Benton and Calhoun in 1953 ▪ LAMBANOG
▪ December, 2000: Finn developing visual deterioration resulting in ▪ Local liquor manufactured from coconut
monocular blindness (counting fingers in left eye) following ingestion of ▪ Gin bulag
locally produced coconut liquor in Indonesia

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Methanol: Mechanism of Toxic Action Mechanism of Toxic Action

▪ Slowly metabolized to formaldehyde by alcohol dehydrogenase and then
converted rapidly to formic acid (formate) which accounts for systemic
acidosis (with lactic acid) and ocular toxicity (blindness)

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Signs and Symptoms

▪ The major toxic effects do not manifest until methanol has been metabolized
to formic acid and this has accumulated to toxic levels
▪ There is a latent period between the consumption of methanol and the onset
of symptoms and signs
▪ Co-ingestion of ethanol will delay metabolism and further delay the onset of
toxicity for many hours

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Signs and Symptoms: Acute Overdose Methanol: Laboratory Analyses

▪ Inebriation and gastritis ▪ Serum Methanol Concentration
▪ Severe metabolic acidosis
▪ Visual disturbances (haziness or “like standing on a snowfield”)
▪ Blurred vision or diplopia progressing to blindness ▪ Metabolic acidosis
▪ Headache ▪ Elevated anion gap
▪ Dyspnea ▪ Elevated osmolal gap
▪ Seizures ▪ Positive serum methanol and/or serum formate assay
▪ Coma
▪ Death

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Methanol Toxicity: Management Methanol Toxicity: Treatment

▪ Prompt medical care ▪ Antidote therapy: ethanol, fomepizole
▪ Key to avoiding complications secondary to methanol intoxication ▪ Hemodialysis
▪ Supportive therapy
▪ Aimed at initiating airway management, correcting electrolyte disturbances, and providing
adequate hydration
▪ Administration of bicarbonate and assisted ventilation

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Methanol Toxicity: Antidote WHO Response

▪ Ethanol ▪ Developing good quality control
▪ Fomepizole ▪ Regulating sales of informally produced alcohol
▪ Folic Acid ▪ Creating an efficient control and enforcement system
▪ Sodium bicarbonate ▪ Developing or strengthening tracking and tracing systems for illicit alcohol
▪ Ensuring necessary cooperation and exchange of relevant information on
combating illicit alcohol
▪ Issuing relevant public warnings

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Patient History
▪ 72 year-old female
Case Presentation ▪ Regular alcohol drinker
▪ Medical and family history was unremarkable

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Case Timeline Case Timeline

17 days PTC: Consultation at the General Clinic of the Department of Ophthalmology, University
of the Philippines-Philippine General Hospital (UP-PGH)
▪ patient and six other female relatives drank lambanog
▪ Consumed about 1 liter of the liquor over a 9-hour drinking session ▪ Initial Examination
○ BP 120/80; HR 78; RR 20
16 days PTC: ○ No light perception on both eyes
○ Pupils were dilated at 5 mm and nonreactive to light
▪ experienced sudden clouding of vision with associated headache, nausea, and ○ Intraocular pressures were normal
○ 2+ nuclear sclerosis with posterior subcapsular cataract on both eyes
abdominal discomfort
○ Dilated fundoscopic examination showed distinct disc borders with generalize disc pallor, a
cup-disc ratio of 0.3 on both eyes, an artery-to-vein caliber ratio of 2:3
13 days PTC: ○ No hemorrhages or exudates were seen
○ neurologic examination was normal
▪ she became blind

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Case Timeline
Additional Examinations:

▪ Visual evoke response (VER) showed failure of optic-nerve conduction Discussion of the Case
▪ Electroretinogram (ERG) was normal
▪ Cranial computed tomography (CT) showed physiologic calcifications in the
basal ganglia, particularly in the area of the lentiform nucleus

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Discussion of the Case Discussion of the Case

▪ Signs and symptoms may be attributed to the direct toxic effects of methanol
▪ 18 hours after ingesting poison → blurring of vision
▪ Due to the lag time needed for the body to metabolize the poison to formic acid
▪ Fundus findings reveal optic-disc hyperemia or edema with associated blurring
of vision
▪ This results from mitochondrial disruption, leading to histotoxic anoxia
▪ Calcification in the brain
▪ Loss of mitochondrial function and the ensuing metabolic acidosis

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Pathophysiologic Mechanism of Methanol-induced Injury Poisoning Management

Primary Therapeutic Approach

▪ competitive inhibitors of alcohol dehydrogenase (ADH)

▪ Intravenous or oral ethanol
▪ 4-methylpyrazole or Fomepizole (Antizole)

Other Approaches to management of acute intoxication

▪ Hemodialysis
▪ Bicarbonate
▪ Folic acid or folinic acid

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Poisoning Management
Other approaches under animal study

● Photobiomodulation using red to near-infrared wavelengths to upregulate Conclusion and Recommendations

cytochrome oxidase
● Antioxidants as adjunct

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Conclusion Recommendations
▪ Incorrect distillation process or deliberate addition can lead to presence of ▪ Early detection is important for visual recovery
methanol in alcoholic beverages that may lead to toxicity. ▪ IV methylprednisolone to reverse blindness
▪ Thorough clinical history and physical examination, especially Some studies show significant visual improvement after therapy with IV
ophthalmological examination is important to assess methanol toxicity steroids
▪ Cornerstone of management is respiratory assessment and support. ▪ Increase monitoring and regulation of lambanog
Last Dec 2018, FDA warned the public to buy only FDA-registered
lambanog

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References
▪ Korabathina, K. (November, 2018). Methanol Toxicity. Medscape. Retrieved
Online: https://emedicine.medscape.com/article/1174890-overview
▪ Ranche, J.M., Cruz, R.D., and Inocencio, F.P. (2004). Methanol-induced
bilateral optic neuropathy. Philippine Journal of Opthalmology 29 (4): 189-192.
▪ World Health Organization (July 2014). Methanol Poisoning Outbreaks.
Retrieved Online:
https://www.who.int/environmental_health_emergencies/poisoning/methano
l_information.pdf?ua=1

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