Methanol toxicity: Difference between revisions
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== Clinical |
== Clinical Manifestations == |
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* Decreased LOC |
* Decreased LOC |
Latest revision as of 14:00, 16 July 2020
Summary
- AGMA with osmolar gap
- Formic acid is the toxic metabolite
Pathophysiology
graph TD methanol["Methanol"] --> |Alcohol dehydrogenase|formaldehyde formaldehyde["Formaldehyde"] --> |Aldehyde dehydrogenase|formicacid["Formic acid"] formicacid --> |Folate|co2h2o["CO2 and H2O"]
Sources
- Wood alcohol
- Moonshine
- Fuels
- Cleaners
- Antifreeze
- Windshield fluid
Clinical Manifestations
- Decreased LOC
- Retinal injury
- Blindness
- Afferent pupillary defect
- Mydriasis
- Retinal sheen
- Optic disc hyperemia
- Coma, seizures, hyperpnea, and hypotension are late findings
Investigations
- Elevated anion gap metabolic acidosis with an osmolar gap
- As metabolism progresses the initial osmolar gap is replaced by an anion gap
- Also get acetaminophen and salicylate levels
- Follow renal function, including electrolytes and creatinine
Management
- ABCs
- NG aspiration if within 60 minutes
- Sodium bicarb if pH <7.3, with infusion to target pH ≥ 7.35
- Folinic acid (or folic acid), to help metabolise formic acid
- Fomepizole or ethanol, which competitively inhibit alcohol dehydrogenase
- Serum methanol >6.2 mmol/L, or
- Documented toxic ingestion and an osmolar gap > 10, or
- Suspected toxic ingestion and 2 of:
- pH < 7.3
- Bicarb < 20
- Gap (which one?) > 10
- Hemodialysis if ongoing acidosis and evidence of end-organ damage
- Visual loss is an indication, as well