Ethylene Glycol Unit Converter
Ethylene Glycol Unit Converter
Convert ethylene glycol between mg/dL, mg/L and mmol/L — and read the result knowing that glycolic and oxalic acid, not the glycol, cause the acidosis and the renal failure, so a falling level can mean the damage is being done rather than averted.
Ethylene Glycol converter
Mass ⇄ molarSerum ethylene glycol reported as 25 mg/dL, read against the antidote threshold
The conversion, and the acids that do the damage
mg/dL = mmol/L ÷ 0.161108
because 0.161108 = 0.01 g/L ÷ 62.07 g/mol, the molecular weight of ethylene glycol
- MW 62.07
- ethylene glycol, C₂H₆O₂ — heavier than methanol, so a given mass raises the osmolal gap by roughly half as much per milligram, which is one reason the osmolal gap is even less reliable here
- mg/dL and mg/L
- 1 mg/dL = 10 mg/L. EXTRIP publishes its ethylene glycol thresholds in mmol/L, so 10 mmol/L is 62 mg/dL and 50 mmol/L is 310 mg/dL
- glycolic acid
- the metabolite that causes the high anion gap acidosis, and the one that correlates best with severity. It is not measured in most hospitals, which is part of why the anion gap is used as its proxy
- oxalic acid
- the end metabolite. It binds calcium, causing hypocalcaemia with a prolonged QT interval and tetany, and precipitates as calcium oxalate monohydrate in the renal tubules — the mechanism of the acute kidney injury, and the source of the envelope-shaped or needle-shaped crystals in the urine
- the latent period
- 6 to 12 hours of apparent drunkenness before the acidosis appears, and 24 to 72 hours before renal failure. Concurrent ethanol lengthens it, because ethanol competes for the same enzyme
Worked example
Serum ethylene glycol reported as 25 mg/dL, read against the antidote threshold
25 mg/dL = 250 mg/L — the same concentration
25 × 0.161108 = 4.03 mmol/L
The AACT antidote threshold of 20 mg/dL is 3.22 mmol/L, so 4.03 mmol/L is above it
EXTRIP's no-antidote haemodialysis threshold of 10 mmol/L is 62 mg/dL, and its on-fomepizole figure of 50 mmol/L is 310 mg/dL — so this concentration alone would not mandate dialysis, though coma, seizures, an anion gap above 27 mmol/L or kidney impairment would, whatever the level
The comparison with methanol is worth keeping in mind: because ethylene glycol is nearly twice as heavy, 25 mg/dL of it is 4.03 mmol/L while 25 mg/dL of methanol is 7.80 mmol/L. The same mass is far fewer particles, so it raises the osmolal gap far less
And in a patient with a bicarbonate of 6 mmol/L, hypocalcaemia and oxalate crystals in the urine, a level of 25 mg/dL is the remains of a much larger ingestion. Treat what the metabolites are doing
Thresholds as published, in both units
| Threshold | mmol/L | mg/dL |
|---|---|---|
| AACT — start an alcohol-dehydrogenase blocker (or on suspicion plus two of acidosis, low bicarbonate, osmolal gap, oxalate crystals) | 3.22 | 20 |
| EXTRIP — haemodialysis recommended, no antidote given | above 10 | above 62 |
| EXTRIP — haemodialysis suggested, on ethanol | 20 – 50 | 124 – 310 |
| EXTRIP — haemodialysis suggested, on fomepizole | above 50 | above 310 |
| Fomepizole may be stopped (label) | under 3.22 | under 20, asymptomatic with a normal pH |
The osmolal gap and the anion gap cross over
| Time since ingestion | Glycol level | Osmolal gap | Anion gap | Clinical picture |
|---|---|---|---|---|
| Early (0–6 h) | High | Raised | Normal | Apparent drunkenness without the smell of ethanol; normal bicarbonate |
| Intermediate (6–12 h) | Falling | Falling | Rising | Tachypnoea, tachycardia, the acidosis declaring itself |
| Late (12–72 h) | Low | Normal | Wide | Severe acidosis, hypocalcaemia, oxalate crystalluria, then acute kidney injury |
Findings that point at ethylene glycol before any level returns
| Finding | Why it happens | Caveat |
|---|---|---|
| Wide anion gap metabolic acidosis with no lactate explanation | Glycolic acid accumulation | Some blood gas analysers read glycolate as lactate, producing a spurious lactate and a ‘lactate gap’ between analysers — a useful clue in itself |
| Hypocalcaemia, long QT, tetany | Oxalate binds ionised calcium | Not universal, and a normal calcium excludes nothing |
| Calcium oxalate crystals in the urine | Precipitation in the tubules | Absent in up to half of poisoned patients, and present in other conditions — their absence is not reassurance |
| Urine fluorescence under a Wood’s lamp | Fluorescein added to some antifreeze products | Unreliable and should not be used — many normal urines fluoresce and many antifreezes contain no fluorescein |
| Acute kidney injury at 24–72 hours | Tubular deposition of calcium oxalate monohydrate | By the time this appears, the therapeutic window for blocking the enzyme has closed |
Two acids, a closing osmolal gap and a widening anion gap
Ethylene glycol is reported in milligrams per decilitre, in milligrams per litre or in millimoles per litre. Its molecular weight is 62.07, so one milligram per decilitre is 0.161108 millimoles per litre, and the 20 mg/dL of the guidelines is 3.22 mmol/L. Because ethylene glycol is nearly twice as heavy as methanol, the same mass concentration is roughly half the molar concentration — which matters more than it sounds, because osmotic effects depend on particles rather than grams, so ethylene glycol raises the osmolal gap considerably less per milligram than methanol does.
As with methanol, the parent compound is not the poison. Ethylene glycol is a sweet-tasting, intoxicating but relatively harmless alcohol until alcohol dehydrogenase begins converting it, through glycolaldehyde, to glycolic acid and then to oxalic acid. Glycolic acid produces the severe high anion gap metabolic acidosis and is the metabolite that tracks severity. Oxalic acid binds calcium — hence the hypocalcaemia, the prolonged QT interval and occasionally tetany — and precipitates as calcium oxalate monohydrate in the renal tubules, which is the mechanism of the acute kidney injury that appears at one to three days. Everything that kills or maims in ethylene glycol poisoning is downstream of the enzyme.
So the same trap applies. A low or falling ethylene glycol concentration in an acidotic patient is not reassurance; it is more likely to mean the conversion has already happened. Early, while the glycol is still glycol, it contributes osmotically active particles and the osmolal gap is raised with a normal anion gap. Late, once it has become glycolate and oxalate, the osmolal gap has closed and the anion gap is wide. The two tests are each normal at the moment the other is abnormal, and a normal osmolal gap therefore never excludes poisoning — particularly here, where the higher molecular weight makes the gap an insensitive test even during the window in which it should work.
Treatment does not wait for a number. The American Academy of Clinical Toxicology guideline gives a documented concentration above 20 mg/dL as one indication for blocking alcohol dehydrogenase, and then gives two more that need no assay at all: a history or suspicion of ingestion with an osmolal gap above 10, or a history or strong suspicion plus any two of an arterial pH below 7.3, a bicarbonate below 20 mmol/L, an osmolal gap above 10 and calcium oxalate crystals in the urine. Very few hospitals can measure ethylene glycol at all, fewer can do it overnight, and the window in which blocking the enzyme prevents renal failure is measured in hours. Fomepizole, or ethanol where fomepizole is not held, is started on clinical suspicion in any patient with an unexplained wide anion gap acidosis and a plausible history — and because it only prevents further metabolite formation, haemodialysis is what removes the glycolate and corrects the acidosis in a patient who is already acidotic or in established renal failure. The fomepizole dose calculator sets out the schedule and why the dose frequency increases during dialysis.
Frequently asked questions
How do you convert ethylene glycol from mg/dL to mmol/L?
Multiply by 0.161108, which is 0.01 g/L divided by ethylene glycol’s molecular weight of 62.07 g/mol. So 20 mg/dL is 3.22 mmol/L, 62 mg/dL is 10.0 mmol/L and 310 mg/dL is 50 mmol/L. Divide by the same factor to go back, and remember that 1 mg/dL is 10 mg/L. The EXTRIP dialysis thresholds are published in mmol/L, which is why those two round figures appear.
What ethylene glycol level needs treatment?
The American Academy of Clinical Toxicology guideline gives 20 mg/dL (3.22 mmol/L) as one indication for an alcohol-dehydrogenase blocker, but its other limbs deliberately need no level: suspicion of ingestion with an osmolal gap above 10, or suspicion plus any two of arterial pH below 7.3, bicarbonate below 20 mmol/L, osmolal gap above 10, and calcium oxalate crystalluria. In practice the antidote is started on clinical suspicion, because the assay is rarely available inside the window in which it would change anything.
Why can a falling ethylene glycol level be a bad sign?
Because the glycol is not what harms the patient. It is metabolised to glycolic acid, which causes the acidosis, and to oxalic acid, which binds calcium and precipitates in the renal tubules. A falling level with a widening anion gap means the conversion is proceeding, not that the patient is recovering. The reassuring interpretation of a falling level only holds once an alcohol-dehydrogenase blocker is running, because then the fall reflects renal and pulmonary clearance of unchanged glycol.
Do calcium oxalate crystals in the urine confirm or exclude the diagnosis?
Neither. They support it when present, but they are absent in a substantial proportion of poisoned patients — including many who present early, before oxalate has been formed — and they occur in other conditions. Their absence is not a reason to withhold an antidote. The same applies, more strongly, to urine fluorescence under a Wood’s lamp, which is unreliable in both directions and should not be used to make or exclude the diagnosis.
Why might the lactate be high in ethylene glycol poisoning?
Sometimes genuinely, from shock or seizures, but often spuriously: glycolate is structurally similar to lactate and is misread as lactate by some point-of-care and blood gas analysers, while the laboratory’s enzymatic method reads it correctly. The difference between the two results — the so-called lactate gap — is itself a useful pointer to ethylene glycol in a patient with an unexplained acidosis. Do not treat a falsely raised lactate as the explanation for the anion gap.
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References
- Barceloux DG, Krenzelok EP, Olson K, Watson W; American Academy of Clinical Toxicology Ad Hoc Committee on the Treatment Guidelines for Ethylene Glycol Poisoning. American Academy of Clinical Toxicology practice guidelines on the treatment of ethylene glycol poisoning. J Toxicol Clin Toxicol. 1999;37(5):537–560.
- EXTRIP Work Group. Extracorporeal treatment for ethylene glycol poisoning: systematic review and recommendations. Extracorporeal treatment recommended above 10 mmol/L (62 mg/dL) with no antidote and suggested above 50 mmol/L (310 mg/dL) on fomepizole, and for coma, seizures, an anion gap above 27 mmol/L or kidney impairment.
- Brent J, McMartin K, Phillips S, et al; Methylpyrazole for Toxic Alcohols Study Group. Fomepizole for the treatment of ethylene glycol poisoning. N Engl J Med. 1999;340(11):832–838.
- Kraut JA, Mullins ME. Toxic alcohols. N Engl J Med. 2018;378(3):270–280.
- Fomepizole injection, USP — prescribing information. DailyMed, US National Library of Medicine. Loading dose 15 mg/kg, then 10 mg/kg every 12 hours for four doses, then 15 mg/kg every 12 hours; every 4 hours during haemodialysis.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.