Lab result explainedMetabolic panelLast updated November 10, 2026

Serum osmolality: what high and low osmolality mean, how it is calculated and the osmolar gap

Serum osmolality · Serum osmolality (stand-alone test, often paired with urine osmolality) · reported in mOsm/kg of water (some labs write mOsm/kg H2O or mmol/kg)

Serum osmolality is a measure of how concentrated your blood is: the number of dissolved particles (sodium and its accompanying ions, glucose, urea and anything else in solution) per kilogram of water. It is reported in milliosmoles per kilogram (mOsm/kg), and the normal range is about 275 to 295 mOsm/kg. Because sodium salts account for more than 90 percent of the particles, osmolality mostly tracks the sodium level, and the body defends it tightly: a rise of just 1 to 2 percent triggers thirst and the release of antidiuretic hormone (ADH, vasopressin), which makes the kidneys hold on to water.

The test is used in three situations. The first is unexplained high or low sodium, where measured osmolality confirms whether the blood really is concentrated or dilute and, paired with a urine osmolality, shows whether the kidneys are responding correctly (the key test for SIADH and diabetes insipidus). The second is dehydration and hyperglycemic emergencies, where an osmolality above 320 mOsm/kg signals danger. The third is suspected poisoning: by comparing the measured osmolality with one calculated from sodium, glucose and BUN, the lab produces an osmolar gap, and a gap above about 10 means something unmeasured is in the blood, most often ethanol and, in emergencies, methanol, ethylene glycol (antifreeze) or isopropanol.

The calculation people search for is simple: osmolality is approximately 2 × sodium + glucose ÷ 18 + BUN ÷ 2.8, with sodium in mmol/L and glucose and BUN in mg/dL. A sodium of 140, glucose of 90 and BUN of 14 gives 280 + 5 + 5 = 290 mOsm/kg. Clinicians also use effective osmolality (tonicity), which drops the urea term because urea crosses cell membranes freely and does not pull water out of cells; it is the number that matters for brain symptoms and is the one used to define the hyperosmolar hyperglycemic state.

Serum osmolality at a glance

What it is: the concentration of dissolved particles in the blood, in mOsm/kg of water; it mostly reflects sodium, with contributions from glucose and urea.
Normal (adults): 275–295 mOsm/kg; some labs use 280–300. Measured by freezing-point depression on a serum or plasma sample.
Calculated osmolality: 2 × Na (mmol/L) + glucose (mg/dL) ÷ 18 + BUN (mg/dL) ÷ 2.8. Effective osmolality leaves out the BUN term.
Osmolar gap: measured minus calculated. Under 10 mOsm/kg is normal; above 10 to 15 means unmeasured particles, usually ethanol or a toxic alcohol (methanol, ethylene glycol, isopropanol), mannitol or propylene glycol.
High osmolality (above 295): water loss or dehydration, high sodium, high glucose (above 320 mOsm/kg with glucose over 600 mg/dL defines the hyperosmolar hyperglycemic state), kidney failure, diabetes insipidus or alcohol. Low osmolality (below 275): nearly always low sodium from SIADH, diuretics, heart or liver failure, or excess water intake.
Next step: it is read with sodium, glucose, BUN, urine osmolality and urine sodium and an assessment of fluid status; confusion, seizures or a suspected poisoning with an abnormal result need emergency care.

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What Serum osmolality measures

Osmolality counts particles regardless of their size or charge. In the blood these are mainly sodium and the chloride and bicarbonate that balance it (which is why sodium is doubled in the formula), plus glucose, urea, potassium, calcium and small amounts of other solutes. Proteins and lipids contribute almost nothing because, although they weigh a lot, there are relatively few molecules. The laboratory measures osmolality directly by freezing-point depression: the more particles in solution, the lower the temperature at which the sample freezes.

The calculated osmolality uses the three solutes the chemistry panel already measures. Dividing glucose by 18 and BUN by 2.8 converts their mg/dL values to mmol/L, so each 100 mg/dL of glucose adds about 5.6 mOsm/kg and each 28 mg/dL of BUN adds 10. Ethanol adds roughly its mg/dL value divided by 3.7 to 4.6, so a blood alcohol of 100 mg/dL (0.1 percent) raises osmolality by about 22 to 27 mOsm/kg. If ethanol is measured and included, the remaining gap points to other alcohols or glycols. The normal gap is slightly positive and varies with the formula used, which is why most labs treat under 10 as normal and above 10 to 15 as abnormal.

What the body regulates is effective osmolality, or tonicity, the force that moves water across cell membranes. Sodium and glucose are effective osmoles that pull water out of cells when high; urea and ethanol cross membranes freely and raise the measured number without shrinking cells. This is why a dialysis patient with a BUN of 100 mg/dL can have a measured osmolality of 320 and a normal brain, while someone with a glucose of 800 mg/dL and the same osmolality is drowsy. No fasting is needed for the test, but a recent large fluid intake, alcohol or intravenous fluids will change the result.

Normal range for Serum osmolality

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (mOsm/kg of water (some labs write mOsm/kg H2O or mmol/kg))	Notes
Adults, measured serum osmolality	275–295 mOsm/kg	Some labs use 280–300 mOsm/kg. Older adults sit slightly higher on average. Use the printed range.
Calculated osmolality	2 × Na + glucose/18 + BUN/2.8 (mg/dL units)	Example: Na 140, glucose 90, BUN 14 gives 290 mOsm/kg. With SI units: 2 × Na + glucose (mmol/L) + urea (mmol/L).
Effective osmolality (tonicity)	About 275–290 mOsm/kg	2 × Na + glucose/18, omitting BUN. Used for the hyperosmolar hyperglycemic state (above 320) and for judging brain risk.
Osmolar gap, normal	Below 10 mOsm/kg	Measured minus calculated. Small positive values are usual; a negative gap suggests a lab or arithmetic error.
Osmolar gap, raised	10–25 mOsm/kg	Ethanol, ketoacidosis, lactic acidosis, kidney failure, mannitol, propylene glycol, or pseudohyponatremia from very high lipids or protein. Above 25 strongly suggests ethanol or a toxic alcohol.
Mildly high	295–320 mOsm/kg	Dehydration, early hypernatremia, moderate hyperglycemia, uremia. Above 300 mOsm/kg is the laboratory definition of water-loss dehydration in older adults.
Markedly high	Above 320 mOsm/kg	Hyperosmolar hyperglycemic state (with glucose above 600 mg/dL), severe hypernatremia (sodium above about 160 mmol/L), severe dehydration. Lethargy and confusion are common; coma and seizures occur above about 340.
Low	Below 275 mOsm/kg	Hypotonic hyponatremia (sodium below about 135 mmol/L). Below 260 (sodium below about 125) carries a risk of brain swelling, especially if the fall was fast.
Urine osmolality, for comparison	50–1,200 mOsm/kg	Above 100 with a low serum osmolality defines SIADH; below 300 with a high serum osmolality suggests diabetes insipidus.

High serum osmolality (hyperosmolality)

A high osmolality means there is too little water in the blood for the amount of solute. The commonest reason is loss of water without replacing it: fever, sweating, diarrhea, vomiting, diuretics, or simply not drinking enough, which is why frail older adults and infants, who cannot always respond to thirst, are the groups most often affected. In these cases sodium is high (hypernatremia, above 145 mmol/L) and the urine is concentrated as the kidneys try to conserve water. If instead the urine is dilute despite a high osmolality, the kidneys are failing to conserve water, which is the hallmark of diabetes insipidus, either central (not enough ADH, after head injury, pituitary surgery or tumors) or nephrogenic (kidneys do not respond, classically from lithium).

The second group of causes adds solute rather than removing water. Glucose is the important one: the hyperosmolar hyperglycemic state of poorly controlled type 2 diabetes is defined by a glucose above 600 mg/dL, an effective osmolality above 320 mOsm/kg and altered consciousness, and it develops over days as the osmotic diuresis drains water. Urea raises the measured osmolality in kidney failure without the same effect on the brain. Ethanol and the toxic alcohols raise it and produce an osmolar gap; methanol and ethylene glycol are the emergencies, because they are metabolized over hours into acids that cause blindness, kidney failure and death, and the osmolar gap is the early clue before the anion gap acidosis appears.

Symptoms come from brain cells shrinking as water is pulled out of them: thirst, then irritability, confusion and lethargy, and above about 320 to 340 mOsm/kg, seizures and coma. The brain adapts to a slow rise by generating its own osmoles, so chronic hypernatremia can be surprisingly well tolerated, and that adaptation is why correction has to be gradual: lowering sodium faster than about 10 to 12 mmol/L in 24 hours can cause brain swelling. Treatment is replacing water and dealing with the cause, which is a clinical decision rather than something to attempt at home.

Common causes

Water loss and inadequate intake (dehydration)
Diarrhea, vomiting, fever, heavy sweating, heat exposure and an inability to drink enough (frail older adults, infants, people with dementia or reduced consciousness) all concentrate the blood. Sodium, BUN and hematocrit rise together and urine is dark and concentrated.
Hyperglycemia and the hyperosmolar hyperglycemic state
Every 100 mg/dL of glucose adds about 5.6 mOsm/kg, and high glucose drags water out through the kidneys. A glucose above 600 mg/dL with an effective osmolality above 320 mOsm/kg and drowsiness defines HHS, which carries a mortality of 10 to 20 percent and needs intensive treatment.
Diabetes insipidus
Lack of ADH (central: pituitary surgery, head injury, tumors, infiltrative disease) or kidney resistance to it (nephrogenic: lithium, high calcium, low potassium, inherited) produces liters of dilute urine; osmolality rises as soon as water intake cannot keep up. Urine osmolality stays below 300 mOsm/kg despite a serum osmolality above 295.
Kidney failure
Urea accumulates and raises the measured osmolality by 10 mOsm/kg for every 28 mg/dL of BUN. Because urea crosses cell membranes, this is not an effective osmole and the brain is not dehydrated, but the number on the report is high.
Ethanol
The commonest cause of an osmolar gap. Blood alcohol of 100 mg/dL adds roughly 22 to 27 mOsm/kg; a gap that is fully explained by the measured ethanol level is reassuring, while a gap larger than ethanol accounts for raises the possibility of another alcohol.
Methanol, ethylene glycol and isopropanol poisoning
Windshield fluid, antifreeze and rubbing alcohol each add to osmolality within an hour of ingestion. Methanol and ethylene glycol are then converted into formic and glycolic acid, so the osmolar gap falls as the anion gap acidosis rises; a gap above 25 with an unexplained acidosis is treated as toxic alcohol poisoning until levels are back.
Mannitol, propylene glycol, glycerol and contrast agents
Mannitol given to reduce brain swelling, propylene glycol in intravenous lorazepam, diazepam and phenytoin, glycerol and radiographic contrast all raise osmolality and the osmolar gap in hospital patients.
Excess sodium intake
Salt tablets, hypertonic saline, sodium bicarbonate, seawater ingestion and improperly made infant formula raise sodium and osmolality directly; this is rarer than water loss but can be severe.
Diuretics and osmotic diuresis
Loop diuretics remove water as well as salt, and the osmotic diuresis of uncontrolled diabetes or high-protein tube feeding draws water out through the kidneys, raising osmolality if intake does not match.
Ketoacidosis and lactic acidosis
Ketones, lactate and the glycerol and amino acids released in these states produce a modest osmolar gap of 10 to 20 mOsm/kg, which can confuse the picture when toxic alcohols are also being considered.

Symptoms that can go with it

Thirst and a dry mouth, the earliest and most reliable signs in people who can report them
Dark, concentrated urine and reduced urine output; or, in diabetes insipidus, large volumes of pale urine with relentless thirst
Dizziness on standing, a fast heart rate, low blood pressure and sunken eyes with dehydration
Irritability, restlessness and confusion, especially in older adults and infants
Lethargy, muscle twitching and weakness
Seizures, stupor or coma when osmolality passes about 320–340 mOsm/kg
Frequent urination, extreme thirst, weight loss and drowsiness developing over days in the hyperosmolar hyperglycemic state
Visual disturbance, abdominal pain or rapid breathing after a suspected toxic alcohol ingestion

Low serum osmolality (hypo-osmolality)

A low osmolality means there is too much water relative to solute, and in practice it is the same thing as hypotonic hyponatremia: a sodium below about 135 mmol/L with an osmolality below 275 mOsm/kg. The measured osmolality is what proves the low sodium is real. Two kinds of low sodium are not hypotonic: pseudohyponatremia, where very high lipids or protein (as in myeloma) make older sodium assays read low while osmolality is normal, and the translocational hyponatremia of severe hyperglycemia, where glucose pulls water into the blood and dilutes sodium while osmolality is actually high (sodium falls about 1.6 to 2.4 mmol/L for every 100 mg/dL of glucose above normal).

Once it is clear the blood really is dilute, the question is why the kidneys are not excreting the excess water, and a paired urine osmolality and urine sodium answer most of it. A urine osmolality below 100 mOsm/kg means the kidneys are dumping water appropriately and the problem is intake: primary polydipsia, or the low-solute diets of beer drinkers and frail older adults who eat little (beer potomania, tea-and-toast syndrome), where there is simply not enough salt and protein to excrete the water with. A urine osmolality above 100 means ADH is active when it should not be. With a normal fluid volume and a urine sodium above 30 mmol/L, that is SIADH: lung disease, small cell lung cancer, brain disorders, pain, nausea, and drugs including SSRIs, carbamazepine, antipsychotics and cyclophosphamide. With fluid overload it is heart failure, cirrhosis or nephrotic syndrome; with fluid depletion it is vomiting, diarrhea or diuretics with water replacement. Thiazide diuretics are the commonest drug cause, typically within the first two weeks of starting, and adrenal insufficiency and severe hypothyroidism are the two hormonal causes that must be checked.

Symptoms come from brain cells swelling as water moves in. A sodium above about 125 mmol/L that developed slowly often causes nothing more than mild unsteadiness, poor concentration and, in older adults, falls and fractures. Below 120, or with a fast fall over hours (as in exercise-associated hyponatremia or after MDMA with heavy water drinking), there is headache, nausea, vomiting, confusion, seizures and coma, which is a medical emergency. As with high osmolality, slow adaptation means slow correction: raising sodium faster than 8 to 10 mmol/L in 24 hours in chronic hyponatremia risks osmotic demyelination, a form of permanent brain injury.

Common causes

Syndrome of inappropriate antidiuresis (SIADH)
ADH is released without an osmotic reason, so the kidneys keep water. Causes include pneumonia and other lung disease, small cell lung cancer, stroke, head injury, meningitis, pain and nausea after surgery, and drugs such as SSRIs, carbamazepine, oxcarbazepine, antipsychotics, cyclophosphamide and desmopressin. Serum osmolality is below 275, urine osmolality above 100 and urine sodium above 30 mmol/L.
Thiazide diuretics
Hydrochlorothiazide, chlorthalidone and indapamide impair the kidney's ability to dilute urine; hyponatremia usually appears within 2 weeks of starting and is commonest in older women. Loop diuretics cause it far less often.
Heart failure, cirrhosis and nephrotic syndrome
Low effective circulating volume despite fluid overload stimulates ADH; the resulting hyponatremia is a marker of disease severity in all three and carries a worse prognosis.
Vomiting, diarrhea and sweating replaced with plain water
Losing salt and water and replacing only the water dilutes the blood; the kidneys, sensing volume loss, retain water through ADH. Urine sodium is low (below 20 mmol/L) when the loss is through the gut or skin.
Primary polydipsia
Drinking more than about 10 to 15 liters a day, usually in the setting of psychiatric illness or compulsive water drinking, overwhelms the kidneys' maximum water excretion. Urine osmolality is very low (below 100 mOsm/kg).
Low solute intake (beer potomania, tea-and-toast syndrome)
The kidneys need solute to excrete water; a diet of beer, or of tea and toast in a frail older person, provides so little salt and protein that water excretion is capped at 2 to 4 liters a day and anything beyond that dilutes the blood.
Adrenal insufficiency and severe hypothyroidism
Cortisol deficiency removes a brake on ADH release, and severe hypothyroidism reduces water excretion; both are checked with a morning cortisol and TSH in any unexplained hyponatremia.
Exercise-associated hyponatremia
Drinking more than is lost in sweat during marathons, ultramarathons, triathlons and long hikes, while exercise suppresses water excretion, lowers sodium within hours. In some events 5 to 15 percent of finishers have a sodium below 135, mostly without symptoms, but deaths have occurred from brain swelling in those who overdrink.
MDMA (ecstasy) and some other drugs
MDMA stimulates ADH release and thirst; combined with heavy water drinking in a hot venue it has caused fatal hyponatremia, particularly in young women. Oxytocin, desmopressin and nicotine also promote water retention.
Advanced kidney failure and post-operative hypotonic fluids
Kidneys that can no longer dilute urine, and hypotonic intravenous fluids given after surgery when ADH is high from pain and stress, both dilute the blood; hospital-acquired hyponatremia is common.

Symptoms that can go with it

Often none when sodium is above about 130 mmol/L and the fall was gradual
Nausea, loss of appetite, headache and a general feeling of being unwell
Poor concentration, mild confusion and unsteadiness; in older adults, falls and fractures
Muscle cramps and weakness
Drowsiness, vomiting and marked confusion as sodium falls below about 125 mmol/L
Seizures, coma and breathing difficulty from brain swelling with a sodium below 120 or a rapid fall
Swelling of the legs or abdomen when heart failure, cirrhosis or kidney disease is the cause

Read it alongside

Sodium — accounts for most of the osmolality; measured osmolality confirms whether a high or low sodium is real and hypertonic or hypotonic.
Glucose — adds 5.6 mOsm/kg per 100 mg/dL; defines the hyperosmolar hyperglycemic state and explains a low sodium with a high osmolality.
BUN — raises measured but not effective osmolality; needed for the calculated value and the osmolar gap.
Urine osmolality — above 100 mOsm/kg with a low serum osmolality means ADH is active (SIADH, volume depletion, heart or liver failure); below 300 with a high serum osmolality suggests diabetes insipidus.
Urine sodium — above 30 mmol/L with euvolemia supports SIADH; below 20 suggests gut or skin losses or heart failure.
Anion gap and blood pH — a rising anion gap acidosis after an osmolar gap is the signature of methanol or ethylene glycol poisoning.
Ethanol level — subtracted from the gap; what remains points to other alcohols or glycols.
Potassium, creatinine, TSH and morning cortisol — low potassium worsens nephrogenic diabetes insipidus and thiazide hyponatremia; thyroid and adrenal failure are hormonal causes of low osmolality that must be excluded.

What usually happens next

The result is read with sodium, glucose, BUN and a clinical assessment of fluid status (blood pressure, pulse, weight, swelling), which together usually identify the mechanism.
The osmolar gap is calculated; a gap above 10 to 15 with an unexplained acidosis, a history of ingestion or visual symptoms triggers urgent methanol and ethylene glycol levels and treatment without waiting for them.
A paired urine osmolality and urine sodium are sent before any treatment changes, because fluids or diuretics quickly alter the picture.
Medications are reviewed, especially thiazides, SSRIs, carbamazepine, antipsychotics, lithium and desmopressin, and TSH and cortisol are checked in unexplained low osmolality.
Suspected diabetes insipidus is confirmed with a supervised water deprivation test or a copeptin measurement, never by restricting fluids at home.
Correction of either extreme is paced: sodium is changed by no more than about 8 to 10 mmol/L in the first 24 hours in chronic hyponatremia and about 10 to 12 mmol/L in 24 hours in hypernatremia, so expect repeat sodium checks every few hours in hospital.

Diet, lifestyle and natural levers with evidence

What can move Serum osmolality once the cause is known. Nothing here replaces finding the cause.

Regular fluid intake in older adults, by schedule rather than thirst

Moderate evidence

Thirst weakens with age, and a measured serum osmolality above 300 mOsm/kg (295 to 300 is impending) is the reference standard for water-loss dehydration in older people, found in 20 to 30 percent of residents in care homes in European surveys. The European Food Safety Authority's adequate intakes are 2.0 liters of total water a day for women and 2.5 for men, of which about 70 to 80 percent comes from drinks; cohort studies in older adults link osmolality in the upper part of the normal range with higher rates of kidney injury, delirium and hospital admission. Drinking at set times, with meals and medications, is the practical approach when thirst cannot be relied on.

People with heart failure, advanced kidney disease or SIADH may have a prescribed fluid limit; do not increase intake against that advice.

Drink to thirst, not to a schedule, during endurance exercise

Strong evidence

Exercise-associated hyponatremia is caused by drinking more than you sweat, and the 2015 international consensus statement concluded that drinking according to thirst prevents it in essentially all settings while still protecting against meaningful dehydration. Weight gain during an event is the clearest sign of overdrinking. Sports drinks are nearly as hypotonic as water (about 10 to 20 mmol/L of sodium) and do not prevent it, and salt tablets do not reliably prevent it either; the only proven measure is not drinking beyond thirst.

Headache, nausea, vomiting or confusion after a long event should be treated as possible hyponatremia, not dehydration; giving more fluid can be fatal.

Blood glucose control and sick-day fluid planning in diabetes

Strong evidence

Each 100 mg/dL of glucose above normal adds about 5.6 mOsm/kg, and the hyperosmolar hyperglycemic state develops over days when high glucose drives an osmotic diuresis in someone who cannot drink enough, typically an older adult with type 2 diabetes during an infection. Keeping A1C in target, checking glucose more often during illness, continuing diabetes medication as advised and drinking sugar-free fluids regularly during infections are the standard sick-day measures that prevent it; HHS carries a mortality of 10 to 20 percent once established.

Adequate salt and protein when intake is poor

Moderate evidence

The kidneys can only excrete water alongside solute, and a typical diet supplies 600 to 900 mOsm of solute a day, allowing up to 10 to 15 liters of urine. On a diet of beer alone, or tea and toast in a frail older person, solute intake can fall below 250 mOsm a day, capping water excretion at 2 to 4 liters and producing hyponatremia. Restoring protein and a normal salt intake corrects it, and the same principle (sometimes as prescribed urea or salt tablets) is used in SIADH.

Increase salt only if your clinician has confirmed low solute intake is the cause; in heart failure, cirrhosis and kidney disease extra salt worsens fluid retention.

Limiting alcohol

Moderate evidence

Ethanol is the commonest cause of an osmolar gap, adding about 22 to 27 mOsm/kg per 100 mg/dL of blood alcohol, and heavy drinking also suppresses ADH acutely (causing water loss) while the beer-only diet of some heavy drinkers causes hyponatremia through low solute intake. Chronic heavy drinking raises the risk of both dehydration and hyponatremia, and in people with cirrhosis, hyponatremia below 130 mmol/L is one of the strongest predictors of death on the transplant waiting list.

When to see a clinician promptly

Confusion, seizures, severe drowsiness or difficulty waking with any abnormal osmolality or sodium: emergency care, because brain swelling or shrinkage can be fatal within hours.
Any suspected swallowing of antifreeze, windshield washer fluid, methanol, rubbing alcohol or brake fluid, in a child or adult, even without symptoms: call Poison Control (1-800-222-1222 in the US) or go to an emergency department immediately; treatment works best before the acids form.
Blood glucose above 600 mg/dL, or above 300 with vomiting, drowsiness or inability to keep fluids down: possible hyperosmolar hyperglycemic state or ketoacidosis.
A sodium above 155 mmol/L or below 125 mmol/L on any test, or any sodium that has changed by more than 10 mmol/L since the last result.
Vomiting, diarrhea or fever in an infant or a frail older adult who is not drinking, passing little urine or becoming drowsy.
Passing very large volumes of pale urine (more than about 3 liters a day) with unquenchable thirst, which needs assessment for diabetes insipidus or uncontrolled diabetes.
Headache, nausea, vomiting or confusion after a marathon, triathlon, long hike or a night of heavy water drinking: possible exercise-associated or drug-related hyponatremia; do not drink more water while waiting for help.

Frequently asked questions

What is a normal serum osmolality?

About 275 to 295 mOsm/kg of water in adults; some laboratories use 280 to 300. Values are kept within a few percent of each person's set point by thirst and antidiuretic hormone, so a result outside the range is a genuine signal rather than normal variation. Older adults tend to run a few mOsm/kg higher.

How do you calculate osmolality?

Calculated osmolality = 2 × sodium (mmol/L) + glucose (mg/dL) ÷ 18 + BUN (mg/dL) ÷ 2.8. For example, sodium 140, glucose 90 and BUN 14 give 280 + 5 + 5 = 290 mOsm/kg. If your lab reports in SI units, use 2 × sodium + glucose (mmol/L) + urea (mmol/L). To include alcohol, add ethanol (mg/dL) ÷ 3.7. Effective osmolality, the number that matters for the brain, leaves out the BUN term.

What is the osmolar gap and what does a high gap mean?

It is the measured osmolality minus the calculated one. Normally it is under 10 mOsm/kg. A gap above 10 to 15 means the blood contains particles the formula does not account for: most commonly ethanol, and in emergencies methanol, ethylene glycol or isopropanol, as well as mannitol, propylene glycol, glycerol, ketones or lactate. A gap above 25 with an unexplained metabolic acidosis is treated as toxic alcohol poisoning until proven otherwise.

What does high osmolality mean?

That your blood is more concentrated than it should be. The usual causes are water loss without replacement (dehydration, high sodium), very high blood glucose, kidney failure raising urea, diabetes insipidus, or alcohol and other unmeasured substances. Above about 320 mOsm/kg confusion and drowsiness are common, and above 340 seizures and coma can occur, so a high result with any change in alertness is an emergency.

What does low osmolality mean?

That there is too much water relative to salt, which is the same as hypotonic hyponatremia. Common causes are SIADH from lung, brain or cancer-related causes or medications, thiazide diuretics, heart failure, cirrhosis, vomiting or diarrhea replaced with plain water, excessive water drinking, and very low salt and protein intake. A urine osmolality and urine sodium sort these out. Symptoms range from mild unsteadiness and nausea to seizures when sodium falls below about 120 mmol/L or falls quickly.

What is the difference between osmolality and osmolarity?

Osmolality is particles per kilogram of water (mOsm/kg) and is what the laboratory measures; osmolarity is particles per liter of solution (mOsm/L). In blood the two differ by less than 1 to 2 percent, because a liter of plasma is about 93 percent water, so the terms are used interchangeably in practice. The calculated value from sodium, glucose and BUN is strictly an osmolarity, which is one small reason for the normal osmolar gap.

What osmolality means you are dehydrated?

In studies of older adults, a directly measured serum osmolality above 300 mOsm/kg is the agreed laboratory definition of water-loss dehydration, with 295 to 300 counted as impending dehydration. Urine color, specific gravity and skin turgor are unreliable in this age group. In younger people, thirst, a high sodium and a rising BUN and hematocrit usually make the diagnosis before osmolality is measured.

Does alcohol affect osmolality?

Yes. Ethanol is a small molecule that adds about 22 to 27 mOsm/kg for every 100 mg/dL of blood alcohol, raising measured osmolality and producing an osmolar gap. Because it crosses cell membranes it does not dehydrate brain cells the way sodium or glucose do, but it does suppress antidiuretic hormone, causing water loss, and a diet of beer with little food can cause the opposite problem, hyponatremia, through lack of solute.

References

Osmolality tests. MedlinePlus, US National Library of Medicine (2023)View source
Verbalis JG, Goldsmith SR, Greenberg A, et al.. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. American Journal of Medicine (2013)
Spasovski G, Vanholder R, Allolio B, et al.. Clinical practice guideline on diagnosis and treatment of hyponatraemia. European Journal of Endocrinology (2014)
Adrogué HJ, Madias NE. Hypernatremia. New England Journal of Medicine (2000)
Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care (2009)
Kraut JA, Kurtz I. Toxic alcohol ingestions: clinical features, diagnosis, and management. Clinical Journal of the American Society of Nephrology (2008)
Purssell RA, Pudek M, Brubacher J, Abu-Laban RB. Derivation and validation of a formula to calculate the contribution of ethanol to the osmolal gap. Annals of Emergency Medicine (2001)
Fazekas AS, Funk GC, Klobassa DS, et al.. Evaluation of 36 formulas for calculating plasma osmolality. Intensive Care Medicine (2013)
Hew-Butler T, Rosner MH, Fowkes-Godek S, et al.. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015. Clinical Journal of Sport Medicine (2015)
Hooper L, Abdelhamid A, Attreed NJ, et al.. Clinical symptoms, signs and tests for identification of impending and current water-loss dehydration in older people. Cochrane Database of Systematic Reviews (2015)
Rasouli M. Basic concepts and practical equations on osmolality: biochemical approach. Clinical Biochemistry (2016)
Hyponatremia. Merck Manual Professional Version (2024)

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