Methanol overdose vs Ethylene glycol overdose
How to tell Methanol overdose and Ethylene glycol overdose apart when a board question makes them look alike.
Methanol: visual loss from optic injury; ethylene glycol: acute kidney injury with calcium oxalate crystalluria.
Side by side
Visual blurring, photophobia, or blindness with osmolar gap followed by anion gap metabolic acidosis.
Renal injury, flank pain, hypocalcemia, and calcium oxalate crystals after toxic alcohol exposure.
Methanol is metabolized to formic acid, injuring the retina and optic nerve.
Ethylene glycol is metabolized to oxalic acid, causing renal tubular injury and oxalate crystal deposition.
Visual toxicity plus anion gap acidosis supports methanol poisoning.
Calcium oxalate crystals, hypocalcemia, and renal failure support ethylene glycol poisoning.
The trap
Both produce an osmolar gap early (the parent alcohol is in serum) and an anion gap metabolic acidosis later (after the toxic metabolite has accumulated). The deciding move is timing of treatment: when the patient arrives with an osmolar gap and clear sensorium, give fomepizole (or ethanol if fomepizole is unavailable) to block alcohol dehydrogenase BEFORE the metabolite accumulates. Once the anion gap acidosis has developed, the eyes (methanol) or kidneys plus calcium oxalate crystalluria (ethylene glycol) reveal the source. Hemodialysis is indicated for severe acidosis (pH below 7.25), end-organ damage, visual changes, or large ingestion.
Watch it explained
The repair move
For toxic alcohol acidosis, attach the signature organ: eyes for methanol, kidneys/crystals for ethylene glycol.
Try a free question
CoreA patient is brought in after ingesting windshield washer fluid. He has blurred vision, an osmolar gap, and later develops anion gap metabolic acidosis. Which toxic alcohol is most likely?
Show answer and explanation
Answer: A. Methanol. Methanol is metabolized to formic acid, which injures the retina and optic nerve.
Why the other choices are tempting
- B. Ethylene glycol causes renal injury and calcium oxalate crystals.
- C. Isopropyl alcohol causes ketosis without anion gap acidosis.
- D. Ethanol intoxication does not classically cause visual toxicity with formic acid acidosis.
- E. Propylene glycol is not the classic visual-toxicity alcohol.
Flashcards
Tap a card to flip it.
What is the fastest separator for Methanol overdose vs Ethylene glycol overdose?
Methanol: visual loss from optic injury; ethylene glycol: acute kidney injury with calcium oxalate crystalluria.
What clue should make you choose Methanol overdose?
Visual blurring, photophobia, or blindness with osmolar gap followed by anion gap metabolic acidosis.
Quick answers
What is the fastest way to tell Methanol overdose from Ethylene glycol overdose?
Methanol: visual loss from optic injury; ethylene glycol: acute kidney injury with calcium oxalate crystalluria.
What is the key clue for Methanol overdose?
Visual blurring, photophobia, or blindness with osmolar gap followed by anion gap metabolic acidosis.
What is the key clue for Ethylene glycol overdose?
Renal injury, flank pain, hypocalcemia, and calcium oxalate crystals after toxic alcohol exposure.
What is the common trap with Methanol overdose vs Ethylene glycol overdose?
Both produce an osmolar gap early (the parent alcohol is in serum) and an anion gap metabolic acidosis later (after the toxic metabolite has accumulated). The deciding move is timing of treatment: when the patient arrives with an osmolar gap and clear sensorium, give fomepizole (or ethanol if fomepizole is unavailable) to block alcohol dehydrogenase BEFORE the metabolite accumulates. Once the anion gap acidosis has developed, the eyes (methanol) or kidneys plus calcium oxalate crystalluria (ethylene glycol) reveal the source. Hemodialysis is indicated for severe acidosis (pH below 7.25), end-organ damage, visual changes, or large ingestion.