Acetone Unit Converter

Convert acetone between mg/dL, mg/L and mmol/L — the ketone that is not an acid, the metabolite of isopropanol, and the substance a nitroprusside ketone stick is actually detecting.

Last updated 13 Sep 2026

Acetone converter

Mass ⇄ molar

Serum acetone

Acetone is far more often reported as a nitroprusside reaction — negative, trace, small, moderate, large — than as a concentration. Enter a quantitative result if you have one.

8.61mmol/LExample

Serum acetone reported as 50 mg/dL

The conversion, and where acetone comes from

mmol/L = mg/dL × 0.172176
mg/dL = mmol/L ÷ 0.172176
because 0.172176 = 0.01 g/L ÷ 58.08 g/mol, the molecular weight of acetone

MW 58.08: acetone, C₃H₆O — propanone. The smallest ketone, volatile enough to be exhaled, which is why the breath smells of it
from isopropanol: alcohol dehydrogenase oxidises isopropanol to acetone. This is the one metabolic step in the toxic alcohol group that does not produce an acid, and it is why isopropanol causes ketosis without acidosis
from acetoacetate: acetone is also formed by the spontaneous, non-enzymatic decarboxylation of acetoacetate. So it appears in diabetic ketoacidosis, alcoholic ketoacidosis and starvation ketosis, entirely independently of any poisoning
not an acid: acetone is a ketone. It contributes no hydrogen ions and no anion, so it raises neither the anion gap nor the acid load — but it is osmotically active and does raise the osmolal gap
the long half-life: acetone is cleared far more slowly than isopropanol, so a positive ketone result and a raised osmolal gap can both persist for a day or more after the parent alcohol has gone

Worked example

Serum acetone reported as 50 mg/dL
50 mg/dL = 500 mg/L — the same concentration
50 × 0.172176 = 8.61 mmol/L
There is no treatment threshold to compare that with. Acetone is not itself toxic at the concentrations reached clinically — it is a marker of where the patient's metabolism, or their poisoning, has got to
The question the number cannot answer is which source it came from. Acetone from isopropanol comes with a normal bicarbonate and a normal anion gap; acetone from ketoacidosis comes with a low bicarbonate and a wide one
So read it beside the bicarbonate and the anion gap, not alone. That pairing distinguishes the two commonest reasons for a positive ketone result in an unwell patient
And in either case the treatment — supportive care, or insulin and fluids — is started on the clinical assessment and the acid-base picture, not on this concentration

Acetone has two entirely different origins

The bicarbonate is what separates them, which is why a ketone result should never be read without a gas or a bicarbonate beside it. Ketones with a normal bicarbonate point at isopropanol; ketones with a low bicarbonate and a wide anion gap point at a ketoacidosis. The <a href="/medical-laboratory-calculators/isopropanol-unit-converter/">isopropanol converter</a> covers the first and the <a href="/medical-laboratory-calculators/beta-hydroxybutyrate-unit-converter/">β-hydroxybutyrate converter</a> the second.
	From isopropanol	From ketoacidosis
Route	Alcohol dehydrogenase oxidises isopropanol	Spontaneous decarboxylation of acetoacetate
Bicarbonate	Normal	Low
Anion gap	Normal	Wide
Osmolal gap	Raised, by both isopropanol and acetone	Usually normal, unless ethanol is also present
Glucose	Normal or low	High in diabetic ketoacidosis; normal or low in alcoholic or starvation ketosis
Other ketones	None — acetone alone	β-hydroxybutyrate predominates, with acetoacetate
Treatment	Supportive; no antidote	Fluids, insulin and potassium, or carbohydrate and thiamine

What the nitroprusside ketone test can and cannot see

This is the most consequential limitation in routine ketone testing. The nitroprusside reaction sees acetoacetate and acetone but is blind to β-hydroxybutyrate, which is the ketone that predominates in severe or hypoxic ketoacidosis. So the test under-reads on arrival, when the patient is at their worst, and can paradoxically rise during treatment as β-hydroxybutyrate is reoxidised to acetoacetate — a rising ketone stick in an improving patient. The <a href="/medical-laboratory-calculators/ketone-body-ratio-calculator/">ketone body ratio calculator</a> quantifies the shift; where it is available, a direct β-hydroxybutyrate measurement avoids the problem entirely.
Ketone body	Detected by nitroprusside?	Share of ketones in severe ketoacidosis
Acetoacetate	Yes	Small — the ratio shifts against it
Acetone	Yes, weakly	Small
β-hydroxybutyrate	No	Dominant — up to about 10:1 over acetoacetate

Where acetone shows up, and why it lingers

Because acetone comes from two unrelated processes and clears slowly from both, a concentration on its own answers almost nothing. Its value is as one element of a pattern — with the bicarbonate, the anion gap, the osmolal gap and the glucose — and the treatment decision belongs to that pattern and the patient, never to the number.
Setting	Explanation
Isopropanol ingestion	The metabolite, present within hours and persisting longer than the isopropanol itself
Diabetic ketoacidosis	Decarboxylation of accumulated acetoacetate; the breath smells of it
Alcoholic ketoacidosis and starvation	Same route, with β-hydroxybutyrate strongly predominating over acetoacetate
Prolonged fasting, ketogenic diets, pregnancy	Physiological ketosis with a normal bicarbonate
A persistent raised osmolal gap after isopropanol	Acetone is osmotically active and slowly cleared, so the gap outlasts the parent alcohol
A positive ketone stick days into a ketogenic state	Acetone is exhaled and excreted slowly; the stick lags the metabolic state in both directions

One molecule, two origins, and the test that half-sees it

Acetone is reported in milligrams per decilitre, in milligrams per litre or in millimoles per litre. Its molecular weight is 58.08, so one milligram per decilitre is 0.172176 millimoles per litre. It is the smallest ketone, volatile enough that it is exhaled — the sweet, nail-varnish-remover smell on the breath of a patient in ketoacidosis or one who has drunk rubbing alcohol.

Its importance lies in two facts. The first is that acetone is a ketone and not an acid. It carries no ionisable proton, so it contributes nothing to the anion gap and nothing to the acid load — but it is a small, osmotically active molecule, so it does contribute to the osmolal gap. That combination is what makes isopropanol poisoning look the way it does: alcohol dehydrogenase converts isopropanol to acetone, ketones appear in blood and urine, the osmolal gap is raised, and the bicarbonate and anion gap stay resolutely normal. Ketosis without acidosis, in a patient who is far more sedated than their ethanol level explains, is close to diagnostic — and it also means the patient does not need fomepizole or dialysis, unlike methanol and ethylene glycol.

The second fact is that acetone has an entirely separate origin. Acetoacetate decarboxylates spontaneously to acetone, so acetone appears in diabetic ketoacidosis, alcoholic ketoacidosis, starvation and any other ketotic state, with no poisoning involved. The same molecule therefore turns up in two situations that require opposite responses, and the way to separate them is the bicarbonate: ketones with a normal bicarbonate and normal anion gap suggest isopropanol, while ketones with a low bicarbonate and a wide anion gap are a ketoacidosis.

That leads to the limitation every clinician should know about ketone testing. The common nitroprusside reaction — urine ketone sticks and most bedside serum ketone tablets — detects acetoacetate and, weakly, acetone, but it does not detect β-hydroxybutyrate at all. β-hydroxybutyrate is the dominant ketone in severe ketoacidosis, where the ratio can reach roughly ten to one against acetoacetate, and it dominates further when the patient is hypoxic or shocked. So the nitroprusside test reads falsely low precisely when the patient is sickest, and it can rise during successful treatment as β-hydroxybutyrate is reoxidised back to acetoacetate — a ketone result that worsens while the patient improves. A direct β-hydroxybutyrate measurement avoids this; where only nitroprusside is available, the ketone body ratio explains the size of the discrepancy. Either way, resolution of a ketoacidosis is judged on the bicarbonate, the anion gap and the patient — not on a ketone result, and not on an acetone concentration.

Frequently asked questions

How do you convert acetone from mg/dL to mmol/L?

Multiply by 0.172176, which is 0.01 g/L divided by acetone’s molecular weight of 58.08 g/mol. So 50 mg/dL is 8.61 mmol/L, and 1 mg/dL is 10 mg/L. Divide by the same factor to go back. Acetone is far more often reported semi-quantitatively as a nitroprusside reaction than as a concentration.

Why does acetone not cause acidosis?

Because it is a ketone, not a carboxylic acid. It has no ionisable proton to release, so it adds nothing to the hydrogen ion load and nothing to the anion gap. This is the reason isopropanol, whose metabolite is acetone, produces ketosis with a normal bicarbonate, while methanol and ethylene glycol — whose metabolites are formic and glycolic acid — produce severe metabolic acidosis. Acetone is still osmotically active, so it does keep the osmolal gap raised.

Do ketone sticks detect acetone?

Yes, weakly. The nitroprusside reaction used in urine ketone sticks and bedside ketone tablets reacts strongly with acetoacetate and weakly with acetone, which is why isopropanol poisoning gives positive ketones. What it does not detect at all is β-hydroxybutyrate, the ketone that predominates in severe ketoacidosis — so a nitroprusside result under-reads the true ketone load when the patient is most unwell.

Why can ketones rise while a patient with ketoacidosis is improving?

Because nitroprusside sees acetoacetate but not β-hydroxybutyrate. In severe ketoacidosis, and especially when the patient is hypoxic or shocked, the redox state pushes the ketone pool strongly towards β-hydroxybutyrate, which the test cannot see. As treatment restores the redox balance, β-hydroxybutyrate is reoxidised to acetoacetate, which the test can see — so the measured ketones rise as the patient recovers. Judge resolution on the bicarbonate, the anion gap and the patient.

Does a raised acetone level need treatment?

Not on its own. Acetone at the concentrations reached clinically is a marker rather than a toxin, and what needs treating is whatever produced it — supportive care for isopropanol ingestion, or fluids, insulin and potassium for diabetic ketoacidosis, or carbohydrate and thiamine for alcoholic ketoacidosis. Those decisions are made on the clinical assessment and the acid-base picture and are started before any acetone concentration is available.

Related calculators

References

Kraut JA, Mullins ME. Toxic alcohols. N Engl J Med. 2018;378(3):270–280.
Laffel L. Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes. Diabetes Metab Res Rev. 1999;15(6):412–426. The nitroprusside reaction detects acetoacetate and acetone but not β-hydroxybutyrate.
Slaughter RJ, Mason RW, Beasley DMG, Vale JA, Schep LJ. Isopropanol poisoning. Clin Toxicol (Phila). 2014;52(5):470–478.
Umpierrez GE, Davis GM, ElSayed NA, et al. Hyperglycaemic crises in adults with diabetes: a consensus report. Diabetologia. 2024;67(8):1455–1479. Resolution of ketoacidosis is judged on biochemical criteria, not on urine ketones.

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.