Isopropanol Unit Converter
Isopropanol Unit Converter
Convert isopropanol between mg/dL, mg/L and mmol/L — and note the exception that makes this alcohol different: it is metabolised to acetone, which is a ketone and not an acid, so isopropanol causes ketosis without acidosis.
Isopropanol converter
Mass ⇄ molarSerum isopropanol reported as 100 mg/dL
The conversion, and the metabolite that is not an acid
mg/dL = mmol/L ÷ 0.166389
because 0.166389 = 0.01 g/L ÷ 60.10 g/mol, the molecular weight of isopropanol
- MW 60.10
- isopropyl alcohol, C₃H₈O — propan-2-ol. Numerically almost identical to ethylene glycol's 62.07, so the two have nearly the same mass-to-molar factor despite behaving completely differently
- acetone
- the metabolite, made by alcohol dehydrogenase. It is a <b>ketone</b>, not a carboxylic acid, so it generates no hydrogen ions. This single chemical fact is why isopropanol does not cause a metabolic acidosis and why it needs neither fomepizole nor, usually, dialysis
- roughly twice as intoxicating as ethanol
- isopropanol is a more potent central nervous system depressant than ethanol at the same concentration, and acetone adds its own sedation, so deep coma occurs at concentrations that would be merely drunk for ethanol
- the osmolal gap
- raised, and it stays raised — acetone is itself osmotically active, so unlike methanol and ethylene glycol the gap does not close as metabolism proceeds
Worked example
Serum isopropanol reported as 100 mg/dL
100 mg/dL = 1000 mg/L — the same concentration
100 × 0.166389 = 16.64 mmol/L
There is no antidote threshold to compare that with, because there is no antidote: isopropanol poisoning is managed supportively
What decides management is the pattern beside it. If this patient has ketones in blood or urine, a normal bicarbonate and a normal anion gap, and a raised osmolal gap, that triad is close to diagnostic of isopropanol
If instead the bicarbonate is low and the anion gap is wide, stop and reconsider: that is not isopropanol alone, and a co-ingested methanol or ethylene glycol needs an antidote started now rather than after the levels return
Blocking alcohol dehydrogenase with fomepizole here would prolong the coma by preventing isopropanol being cleared as acetone, which is the opposite of what is wanted
Why isopropanol is the exception
| Methanol | Ethylene glycol | <b>Isopropanol</b> | |
|---|---|---|---|
| Toxic metabolite | Formic acid | Glycolic and oxalic acid | Acetone — a ketone, not an acid |
| Metabolic acidosis | Yes, severe and late | Yes, severe and late | No (unless from shock, starvation or a co-ingestion) |
| Anion gap | Widens as the alcohol is metabolised | Widens as the alcohol is metabolised | Normal |
| Ketones | No | No | Yes — in blood and urine, with a normal or high glucose that is not diabetic |
| Osmolal gap | Raised early, closes late | Raised early, closes late | Raised, and stays raised — acetone is osmotically active too |
| Fomepizole | Yes, urgently | Yes, urgently | No — blocking the enzyme prolongs the coma |
| Haemodialysis | For acidosis, visual loss, high levels | For acidosis, kidney injury, high levels | Rarely — considered for refractory hypotension or very high concentrations |
| What kills | Blindness, acidosis, basal ganglia injury | Acidosis and acute kidney injury | Respiratory depression and hypotension — a sedative death, not a metabolic one |
Ketosis without acidosis: how to read it
| Test | Isopropanol | Diabetic ketoacidosis | Alcoholic ketoacidosis |
|---|---|---|---|
| Glucose | Normal, or low from the alcohol | High | Normal or low |
| Bicarbonate | Normal | Low | Low |
| Anion gap | Normal | Wide | Wide |
| Ketones | Present (acetone predominates) | Present (β-hydroxybutyrate predominates) | Present (β-hydroxybutyrate strongly predominates) |
| Osmolal gap | Raised | Normal unless another alcohol is present | Often raised, from ethanol |
What treatment actually consists of
| Measure | Role |
|---|---|
| Airway, breathing and circulation | The whole of it, in most cases. Deaths are from respiratory depression and hypotension, so these are the interventions that matter |
| Intravenous fluids and vasopressors if needed | Hypotension is a marker of severity and responds to supportive care |
| Glucose monitoring | Hypoglycaemia occurs, particularly in children and in the malnourished |
| Fomepizole | Not indicated. Blocking alcohol dehydrogenase prevents isopropanol becoming acetone, prolonging the sedation without preventing any toxic metabolite |
| Haemodialysis | Rarely needed; reserved for refractory hypotension or very high concentrations, and a decision for critical care and renal together |
| Reassess the diagnosis if there is acidosis | A wide anion gap acidosis means either a co-ingestion or a different diagnosis, and it changes management immediately |
A ketone, not an acid — and why that changes everything
Isopropanol is reported in milligrams per decilitre, in milligrams per litre or in millimoles per litre. Its molecular weight is 60.10, so one milligram per decilitre is 0.166389 millimoles per litre. It is found in rubbing alcohol, hand sanitisers, window cleaners, disinfectant wipes and many antifreezes, usually at 70% or more, and it is swallowed both deliberately and — increasingly — by people who cannot obtain ethanol.
Isopropanol belongs in a group with methanol and ethylene glycol because it raises the osmolal gap and because it is metabolised by the same enzyme, alcohol dehydrogenase. It does not belong with them clinically, and the reason is a single chemical fact: its metabolite is acetone. Acetone is a ketone, not a carboxylic acid. It releases no hydrogen ions, so no matter how completely isopropanol is metabolised, it cannot generate a metabolic acidosis. Methanol becomes formic acid and ethylene glycol becomes glycolic and oxalic acid; isopropanol becomes a solvent that makes people sleepy and smells of nail varnish remover on the breath.
That gives a pattern which is close to diagnostic at the bedside: ketones present, bicarbonate normal, anion gap normal, osmolal gap raised. A patient who is deeply intoxicated with positive ketones and no acidosis, in whom the glucose is not high enough for diabetic ketoacidosis, has taken isopropanol until proved otherwise. The osmolal gap behaves differently here too. With methanol and ethylene glycol the gap closes as the parent alcohol is converted into acids; with isopropanol the metabolite is itself a small osmotically active molecule, so the gap stays raised for as long as the acetone does — which can be considerably longer than the isopropanol itself, because acetone’s half-life is much the longer of the two.
The practical consequence is that isopropanol needs neither fomepizole nor, in most cases, dialysis. Giving fomepizole blocks the conversion of isopropanol to acetone, and since acetone is not the problem, all that achieves is a longer coma. Treatment is supportive: airway, ventilation, fluids and vasopressors for the hypotension that marks severe poisoning, and glucose monitoring. Deaths are respiratory and circulatory rather than metabolic. Haemodialysis removes both isopropanol and acetone efficiently and is occasionally used for refractory hypotension or very high concentrations, but that is a decision made with critical care and nephrology on the patient in front of them, not on a number. The one thing that should never be waved away is a metabolic acidosis: if the bicarbonate is low and the anion gap wide, this is not isopropanol alone. Assume a co-ingested methanol or ethylene glycol, start an alcohol-dehydrogenase blocker on that suspicion, and do not wait for the levels.
Frequently asked questions
How do you convert isopropanol from mg/dL to mmol/L?
Multiply by 0.166389, which is 0.01 g/L divided by isopropanol’s molecular weight of 60.10 g/mol. So 100 mg/dL is 16.64 mmol/L, and 1 mg/dL is 10 mg/L. The factor is very close to ethylene glycol’s 0.161108 because the two molecular weights are similar — which is a coincidence of mass and tells you nothing about how differently the two behave.
Why does isopropanol cause ketosis but not acidosis?
Because its metabolite is acetone, which is a ketone rather than a carboxylic acid and therefore contributes no hydrogen ions. Methanol is oxidised to formic acid and ethylene glycol to glycolic and oxalic acid, and those acids are what produce the severe high anion gap acidosis in those poisonings. Isopropanol stops at acetone. The result is the distinctive combination of positive ketones with a normal bicarbonate and a normal anion gap.
Does isopropanol poisoning need fomepizole?
No. Fomepizole blocks alcohol dehydrogenase, which in methanol and ethylene glycol poisoning prevents the formation of the acids that cause the harm. In isopropanol poisoning the metabolite is harmless by comparison with the parent alcohol, so blocking the enzyme simply keeps the more sedating compound in circulation for longer and prolongs the coma. Management is supportive, and the presence of a metabolic acidosis is the signal to reconsider the diagnosis or suspect a co-ingestion.
What does a raised osmolal gap with normal bicarbonate suggest?
Isopropanol, most characteristically, particularly with positive ketones and a glucose that does not fit diabetic ketoacidosis. Unlike methanol and ethylene glycol, where the osmolal gap closes as the alcohol is metabolised into acids, isopropanol’s metabolite acetone is itself osmotically active, so the gap persists. Ethanol also raises the gap and must be accounted for in the calculation. A raised gap with a wide anion gap acidosis points instead at methanol or ethylene glycol and warrants an antidote on suspicion.
Is a high isopropanol level the reason to intubate or dialyse?
No. The decisions are clinical: airway protection is based on conscious level and the ability to maintain and protect the airway, and the small number of patients considered for haemodialysis are those with hypotension refractory to fluids and vasopressors, assessed by critical care and nephrology together. A concentration confirms what was taken and helps explain the clinical picture, but treatment starts and escalates on the patient, not on the number.
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References
- Slaughter RJ, Mason RW, Beasley DMG, Vale JA, Schep LJ. Isopropanol poisoning. Clin Toxicol (Phila). 2014;52(5):470–478.
- Kraut JA, Mullins ME. Toxic alcohols. N Engl J Med. 2018;378(3):270–280. Isopropanol is metabolised to acetone and characteristically causes ketosis without a metabolic acidosis.
- Zaman F, Pervez A, Abreo K. Isopropyl alcohol intoxication: a diagnostic challenge. Am J Kidney Dis. 2002;40(3):E12.
- Kraut JA, Kurtz I. Toxic alcohol ingestions: clinical features, diagnosis, and management. Clin J Am Soc Nephrol. 2008;3(1):208–225.
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.