Home Improvement’s Toxic and Never Bored, Review

Ethylene Glycol toxicity – found in antifreeze. Ethylene glycol is sweet and odorless, making it irresistible for unsupervised kids (and pets!). Toxic effects are from the downstream metabolites from ethylene glycol–glycolic acid and oxalic acid–which forms crystals with calcium and deposits in tissues throughout the body, leading to widespread damage.  The hallmark lab findings of ethylene glycol tox is the ‘double gap’ — anion gap metabolic acidosis with an osmolar gap, as well as crystaluria. But beware, as an anion or osmolar gap doesn’t appear until at least 4-12 hours after ingestion when the metabolites cause their damage.   Although the best test for ethylene glycol is a direct serum level, this takes too long to return and you should treat based on the other labs (osmolar gap) immediately.  

Anion gap = [Na] – [Cl + HCO3]. Our patient’s gap is 27. Normal is 8-16.

Osmol gap = Measured Osm – calculated Osm ; where calculated serum Osm = (2 * (Na) + (BUN / 2.8) + (glucose / 18) + (ethanol/3.7-4.6)   (Or, thank you Mdcalc.com)

Normal Osmol gap is -14 to +10. Our patient has an osmol gap of -17. Osmolar gaps of > 50 are especially indicative of toxic alcohol poisoning.  

There are 4 stages of toxicity:

1) Acute neurologic stage, similar to ethanol toxicity: with CNS depression, slurred speech, ataxia, nausea and vomiting.

2) Cardiopulmunary stage, 12-24 hours after ingestion: tachypnea (compensation for metabolic acidosis), ARDS and pulmunary edema from deposition in lungs, myositis and cardiac depression from deposition in skeletal and cardiac muscle. Hypocalcemia from calcium oxalate formation can also cause QT prolongation and dysrhythmias.

3) Renal stage, 24-72 hours post-ingestion: causing severe acute renal failure.  Calcium oxalate crystal deposition reeks havoc on the kidneys, causing hematuria, proteinuria, and oligouria. This will be compounded by rhabdo from muscle breakdown.

4) Delayed neurologic sequelae stage, 6-12 days after ingestion. This is only in severe cases with significant renal failure.  Cranial neuropathy is the hallmark of this stage, with damage to cranial nerves from crystal deposition as well as cognitive and motor deficits reported. 

3 major treatment goals: prevent formation of the toxic metabolites (ethanol or fomepizol), fix the acidosis, and clear the metabolites and alcohol from the blood (hemodialysis). Admit to the ICU.

Ethanol and fomepizole have a higher affinity for ADH enzyme than ethylene glycol and will saturate the enzymes, leaving more unmetabolized ethylene glycol and therefore fewer free toxic metabolites. Fomepizol works in the same way, and is both safer with fewer side effects (i.e. your 6 year-old patient won’t be getting more drunk and somnolent) however is much more expensive and not well tested in children. Pyridoxine and thiamine also aid as cofactors in alcohol metabolism into less toxic metabolites, so definitely give your patient some B6 and thiamine boosts.