Calculate serum osmolality, effective osmolality (tonicity), osmol gap, corrected sodium, and free water deficit with full differential diagnosis for hyponatremia and toxic alcohol ingestion.
Serum osmolality measures the total concentration of dissolved solutes per kilogram of body water, normally maintained within the tight range of 275–295 mOsm/kg through antidiuretic hormone (ADH) regulation and thirst mechanisms. Calculated osmolality, derived from sodium, glucose, and blood urea nitrogen, provides a reliable estimate that — when compared to measured osmolality — reveals the osmol gap, a critical diagnostic tool in toxicology.
This calculator computes the standard calculated osmolality (2×Na + Glu/18 + BUN/2.8), effective osmolality or tonicity (which excludes the freely permeable BUN and reflects the osmotic force driving water across cell membranes), the osmol gap (measured minus calculated, normal ≤10), and the corrected sodium for hyperglycemia. It also estimates free water deficit in hypernatremic patients.
The osmol gap is indispensable in the emergency evaluation of an altered patient with metabolic acidosis: an elevated osmol gap combined with an anion gap metabolic acidosis strongly suggests toxic alcohol ingestion (methanol, ethylene glycol), while an isolated osmol gap elevation without acidosis may indicate isopropanol or early toxic alcohol ingestion. Understanding the distinction between total osmolality and effective osmolality is essential for investigating hyponatremia — specifically differentiating hypotonic, isotonic, and hypertonic etiologies of low serum sodium.
This calculator integrates all osmolality-related calculations into a single tool: calculated osmolality, effective osmolality, osmol gap, corrected sodium, and free water deficit. The visual contribution breakdown and differential diagnosis tables guide the full workup for hyponatremia, hyperosmolar states, and toxic alcohol ingestions. Keep these notes focused on your operational context. Tie the context to the calculator’s intended domain.
Calculated Osmolality = 2 × Na + Glucose/18 + BUN/2.8 (mOsm/kg). Effective Osmolality (Tonicity) = 2 × Na + Glucose/18. Osmol Gap = Measured Osm − Calculated Osm | Normal ≤ 10. Corrected Na = Na + 1.6 × ((Glucose − 100) / 100). Free Water Deficit = TBW × (Na/140 − 1).
Result: Calculated Osmolality 281 mOsm/kg, Osmol Gap 39 → elevated, investigate toxic alcohol ingestion
The calculated osmolality of 281 is normal, but the measured osmolality of 320 creates an osmol gap of 39 — significantly elevated. This pattern with an unexplained gap should prompt testing for methanol or ethylene glycol levels.
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Osmolality is measured per kilogram of solvent (water), while osmolarity is per liter of solution. Osmolality is more accurate because it is unaffected by dissolved solutes or temperature. Clinically, the terms are often used interchangeably since values are very similar in dilute solutions like plasma.
BUN (urea) crosses cell membranes freely and distributes equally between intracellular and extracellular compartments. It does not create an osmotic gradient and therefore does not cause water movement. Effective osmolality (tonicity) reflects only the osmoles that drive water shifts, primarily sodium and glucose.
Suspect toxic alcohol (methanol, ethylene glycol) when you find an elevated osmol gap (>10) combined with an anion gap metabolic acidosis. Early after ingestion, the osmol gap is elevated before the parent alcohol is metabolized to acidic metabolites. As metabolism progresses, the osmol gap decreases while the anion gap increases.
No. A normal osmol gap does not exclude toxic alcohol ingestion. Late presentations (after metabolism is complete), small ingestions, or baseline variation in the osmol gap can all produce false-negative results. The osmol gap has limited sensitivity, and direct alcohol levels should be obtained when clinical suspicion exists.
The Katz correction adds 1.6 mEq/L to the measured sodium for each 100 mg/dL increase in glucose above 100. This reveals the "true" sodium that would be measured if glucose were normal, since hyperglycemia draws water into the vascular space doubling measured sodium. Some guidelines use 2.4 mEq/L per 100 mg/dL for glucose >400.
Replace free water deficit over 48–72 hours, aiming to lower sodium by no more than 10–12 mEq/L per 24 hours. Too-rapid correction of hypernatremia risks cerebral edema because brain cells have adapted by generating intracellular idiogenic osmoles. Frequent sodium monitoring (every 4–6 hours) is essential.