The serum osmolality is the concentration of all osmotically active particles dissolved in blood. Comparing a calculated estimate against a measured value yields the osmol gap — a fast screening tool that emergency physicians, toxicologists, and nephrologists use to detect dangerous unmeasured substances such as methanol and ethylene glycol.
How it works
The calculator estimates osmolality from the three solutes that dominate it. Using US conventional units:
Calculated osmolality = 2 × Na + glucose/18 + BUN/2.8
Sodium is in mmol/L; glucose and BUN are in mg/dL. The factor 2 accounts for
the anions (mostly chloride and bicarbonate) that accompany sodium. Dividing
glucose by 18 and BUN by 2.8 converts mg/dL to mmol/L for those solutes. In SI
units the formula simplifies to 2 × Na + glucose + urea with everything in
mmol/L. If an ethanol level is entered it is added (÷3.7 for mg/dL) so a second
unmeasured osmole can still be detected.
The osmol gap
Osmol gap = measured osmolality − calculated osmolality
A normal gap is roughly -10 to +10 mOsm/kg. A gap above about 10 flags
unmeasured osmoles — classically the toxic alcohols (methanol, ethylene
glycol, isopropanol), but also mannitol, propylene glycol, and severe
ketoacidosis.
The dual-gap approach to toxic alcohol diagnosis
Toxic alcohols evolve through two distinct phases, and the gap pattern shifts between them:
Early phase — the parent alcohol (methanol, ethylene glycol) is still largely unmetabolised. Its osmotic activity raises the measured osmolality, producing a high osmol gap. At this stage the anion gap is normal because the toxic organic acids have not yet accumulated.
Late phase — the liver has converted the parent alcohol into its toxic metabolites (formic acid from methanol; glycolic and oxalic acid from ethylene glycol). These acids consume bicarbonate and raise the anion gap. Paradoxically, the osmol gap falls as the osmotically active parent molecule disappears. A patient seen late can have a normal osmol gap with a high anion gap — and may be most critically ill at exactly this point.
This is why a normal osmol gap alone cannot rule out toxic alcohol poisoning. The timing of presentation relative to ingestion, the anion gap, the clinical picture, and direct serum alcohol levels (where available) must all be integrated.
Common causes of a raised osmol gap
| Substance | Clinical context |
|---|---|
| Methanol | Illicit alcohol, industrial solvent, antifreeze |
| Ethylene glycol | Antifreeze, industrial coolant |
| Isopropanol | Rubbing alcohol ingestion |
| Ethanol | Common; always enter an ethanol level when present |
| Propylene glycol | Medication diluent (IV lorazepam, vancomycin infusion) |
| Mannitol | Post-neurosurgical administration |
| Glycine | Post-TURP irrigation absorption |
| Ketones | Severe DKA or alcoholic ketoacidosis |
Notes and pitfalls
A normal osmol gap does not exclude toxic-alcohol poisoning. Early after ingestion the parent alcohol produces a large gap with a normal anion gap; later the alcohol is metabolised to organic acids, so the gap falls while the anion gap and acidosis worsen. The combination of both gaps over time is far more informative than either alone. All calculation runs locally in your browser.
This tool is for educational and reference purposes. Clinical decisions regarding toxic ingestion must involve direct physician assessment and appropriate laboratory testing.