Hyponatremia

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Hyponatremia

Nephrology
Learning Objectives:

By the end of this post you will be able to:

  1. Localize the cause of hyponatremia using serum osmolality, urine osmolality and urine sodium.
  2. Initiate first-line treatment for symptomatic and for asymptomatic hyponatremia.
  3. Apply the correction limit, and recognize and manage overcorrection.

TL;DR

What you need to know before seeing your first patient on your IM rotation with this condition

Estimated read time: 3 minutes

Hyponatremia infographic — MedicinePods

Written by Dr. Caitlyn Vlasschaert. Reviewed by Dr. Jeffrey Kott and Dr. Laiya Carayannopoulos. NephMadness x I@W — Hyponatremia.

Step 0: 3% saline is 100–150 mL over 10–20 minutes, up to three doses — not 50–100 mL every 2–3 minutes. Step 3: volume status is judged at the bedside; the urine sodium cut-off is 30 mmol/L, and a high value also fits renal salt loss. Rate: the goal is 4–8 mmol/L a day (4–6 if high risk), not 6–8; the limit is 10 in 24 hours, or 8 if high risk.

  • What it is: A serum sodium below 135 mmol/L, almost always from antidiuretic hormone holding onto free water.
  • How it presents: Symptoms track how fast the sodium fell, not how low it is. Moderately severe: nausea without vomiting, confusion, headache. Severe: persistent vomiting, seizures, reduced consciousness. Assess volume status: it decides the fluid.
  • Initial tests to order: Serum osmolality (below 275 mOsm/kg: hypotonic), urine osmolality (below 100: ADH off) and urine sodium (cut-off 30 mmol/L), with the first bloods; never delay treating symptoms for them. Add glucose, TSH and a morning cortisol. Look for thiazides, SSRIs, carbamazepine and desmopressin.
  • If symptomatic from the sodium — moderately severe or severe: Call your senior now; do not wait for a callback. In a monitored bed: 3% saline 150 mL IV over 20 minutes; check the sodium after each, repeat up to twice, stop once symptoms improve or it is up about 5 mmol/L.
  • If stable — treat the cause, cap the rise: Hypovolemic — 0.9% saline 0.5–1 mL/kg/h. Hypervolemic — restrict fluid; treat the cause with your senior. SIADH — restrict to under 1 L/day, then 500 mL/day below urine output. Limit: 10 mmol/L in the first 24 hours — 8 if high risk (sodium ≤105, low potassium, alcohol, malnutrition, liver disease).
  • Overcorrection: Past the limit, or a surge of dilute urine near it: stop what is raising it, call your senior; 5% dextrose 10 mL/kg over 1 hour ± desmopressin 2 µg IV.

Listen

Read Around the Case

Based on the US expert panel recommendations (Verbalis et al., 2013), the European clinical practice guideline on hyponatraemia (2014) and the Society for Endocrinology emergency guidance (2022). No Canadian guideline on hyponatremia exists — and these three disagree in places this post flags.

Estimated read time: 23 minutes

The Hyponatremia Sequence

FirstModerately severe or severe symptoms from the sodium? Call your senior now for 3% saline; never wait for the tests below. Seizing: check the glucose, give lorazepam. Hospital policy sets where 3% can run.
1
Is it real, and is it hypotonic?Serum osmolality
2
Is ADH on or off?Urine osmolality — the 100 mOsm/kg line
3
Which bucket?Volume status plus urine sodium
4
Treat the cause, and fix the ceiling10 mmol/L in the first 24 hours, 8 a day after that — 8 from the start if high risk
5
Recheck the sodiumAfter 3%: 6 and 12 hours, then daily. Otherwise, below 130: every 6 hours. Every 2 hours if the urine output surges

1. Is It Real, and Is It Hypotonic?

Estimated read time: 4 minutes

A low sodium is not always a water problem. Two situations produce a number below 135 mmol/L with no excess water at all, and serum osmolality separates them.

Calculate it while the measured value is pending: osmolality ≈ 2 × [Na] + glucose + urea (all in mmol/L). Urea and alcohol raise it without pulling water, so a high urea or blood alcohol can read 285 or more and still be hypotonic (the European guideline). Then use the two together:

  • Hypertonic (≥285 mOsm/kg) — another osmole is pulling water out of cells and diluting the sodium. Check the glucose; hyperglycemia is the usual one, and treating it treats the sodium. Hillier et al. measured the relationship: sodium falls about 2.4 mmol/L per 5.6 mmol/L (100 mg/dL) rise in glucose, more than the widely taught 1.6, and not linearly — 1.6 holds to a glucose near 22 mmol/L, above which 4.0 fits better.
  • Isotonic (275–285 mOsm/kg) — pseudohyponatremia. Severe hypertriglyceridemia or a paraprotein displaces enough plasma volume that the analyzer under-reads. The clue is a lipemic sample or known myeloma; the fix is to recheck the sodium on a blood gas, which uses a direct ion-selective electrode and is not fooled.
  • Hypotonic (<275 mOsm/kg) — real, and the rest of this post is about it. In practice, a normal glucose with no lipemia and no paraprotein means you are here, and the osmolality confirms rather than surprises.

A measured osmolality well above the calculated one means an unmeasured osmole — ethanol, mannitol, or a toxic alcohol. The last is a different problem, and an urgent one.

Send the osmolality and urine studies with the first bloods. Once saline is running, they no longer reflect the state you are diagnosing.

2. Is ADH On or Off?

Estimated read time: 3 minutes

Urine osmolality answers one question: is antidiuretic hormone working? Someone with excess free water and no ADH should be making maximally dilute urine. If they are not, ADH is on, and something is telling it to be.

  • Below 100 mOsm/kg — ADH is off and the kidney is doing its job, so the problem is upstream. Primary polydipsia: a normal kidney excretes at most about 800–1,000 mL an hour, so fast drinking outruns it. Low solute intake: beer potomania and the tea-and-toast diet — excreting water needs solute to carry it, so a diet with almost no protein or salt cannot clear a normal water load. Treatment there is food, not fluid restriction.
  • At or above 100 mOsm/kg — ADH is on. That is most ward hyponatremia, and section 3 sorts it.

100 mOsm/kg is a decision line, not a diagnosis — a part-treated patient can sit either side of it.

3. Which Bucket? Volume Status and Urine Sodium

Estimated read time: 5 minutes

With ADH on, the bedside volume assessment leads and the urine sodium supports it — not the other way round.

Volume status What to do Urine sodium — and what raises it
Hypovolemic
Dry mucous membranes, flat neck veins, tachycardia
Isotonic saline. Then watch closely — ADH switches off as volume is restored, and the sodium climbs on its own Usually 30 mmol/L or less. Above 30 when the kidney is the route of loss — diuretics (especially thiazides), adrenal insufficiency, cerebral salt wasting, salt-losing nephropathy, osmotic diuresis, or vomiting, where bicarbonaturia drags sodium out with it
Hypervolemic
Edema, ascites, raised JVP
Fluid restriction and diuresis. Total body sodium is already high; saline makes it worse Usually 30 mmol/L or less. Above 30 in acute or chronic kidney disease, where the kidney can no longer conserve sodium
Euvolemic
Neither dry nor overloaded
Fluid restriction, after thyroid and adrenal causes are excluded — see the box below Above 30 mmol/L. This is SIADH, and the high urine sodium is the expected finding rather than an exception

Thiazides deserve their own line

Thiazides act at the distal tubule and impair free water excretion while leaving urinary concentrating ability intact, so the picture looks euvolemic with a high urine sodium — indistinguishable from SIADH at the bedside, and a common cause on a general medicine ward.

A nationwide cohort of 1,943,345 adults found hospitalization for hyponatremia in 2.19% of thiazide users versus 1.45% (hazard ratio 1.44). Risk rose with age, diabetes and depression.

Stop the thiazide and watch — that is the diagnostic move, not another test. Loops do this less often, because they impair urinary concentration as well.

SIADH — and what has to be excluded first

SIADH is a diagnosis of exclusion: hypotonic hyponatremia, urine osmolality >100 mOsm/kg, urine sodium >30 mmol/L, clinically euvolemic, no recent diuretic use, and no adrenal, thyroid, pituitary or kidney insufficiency. Adrenal insufficiency and hypothyroidism look identical biochemically and are treated differently — check TSH and a morning cortisol before the label goes in the chart.

Five groups of causes, of which the medication list is the one to check first: CNS (stroke, hemorrhage, meningitis) · lung (pneumonia, tuberculosis, positive-pressure ventilation) · malignancy (classically small cell lung cancer) · medications (SSRIs, carbamazepine, antipsychotics, desmopressin, MDMA) · pain and nausea, including post-operatively.

Fluid restriction is first-line, and fails in a substantial minority. In a prospective study of 82 patients, 41% did not respond — sodium up 3 mmol/L or less in 24 hours — and a high urine sodium and high urine osmolality both predicted failure (odds ratio 15.0, 95% CI 2.4–95.8 for urine sodium).

So concentrated urine is a reason to plan the next step early — salt tablets or oral urea, nephrology involved — rather than tightening restriction and waiting. The evidence for urea is real but thin: in a prospective crossover study of 13 patients it matched vaptans over a year of treatment, and it has never been tested against placebo.

4. Treatment, and How Fast to Correct

Estimated read time: 8 minutes

Agent Dose Notes
Hypertonic (3%) saline 150 mL IV over 20 min (US panel: 100 mL over 10 min); repeat up to 2× until symptoms improve or the sodium rises about 5 mmol/L Moderately severe or severe symptoms; a senior decides and supervises, in a monitored bed. Recheck sodium at 20 minutes. A peripheral IV is acceptable — phlebitis and infiltration about 2% each in a 2025 meta-analysis
0.9% saline 0.5–1.0 mL/kg/h Hypovolemic hyponatremia only. In SIADH it can lower the sodium, because the kidney excretes the salt and keeps the water. If shocked, resuscitation overrides the limit
Fluid restriction Under 1 L/day to start; then 500 mL/day below the 24-hour urine output First-line for SIADH and for hypervolemic hyponatremia. Expect days, not hours
Salt tablets ± loop diuretic No guideline gives a dose — set it with nephrology Second-line for SIADH when restriction alone fails; the European guideline ranks it equal to oral urea
5% dextrose ± desmopressin D5W 10 mL/kg over 1 h; desmopressin 2 µg IV, no more often than every 8 h Rescue only — re-lowering an overcorrected sodium, with expert input; see below

Boluses, not a calculated infusion. SALSA randomized 178 patients (mean sodium 118.2 mmol/L) to bolus or continuous infusion of 3% saline. Overcorrection did not differ — 17.2% versus 24.2%, defined as a rise above 12 mmol/L in 24 hours — but the bolus group needed re-lowering less often, 41.4% versus 57.1%.

Do not set a rate from a deficit formula and walk away. The formulae assume a closed system, and cannot model the patient’s own kidney; the Society for Endocrinology guidance recommends against them. Give a bolus, measure, repeat.

How fast may you correct?

Set the ceiling as you write the first order. Almost every treatment above raises the sodium — hypertonic saline, isotonic saline in hypovolemia, even stopping the thiazide — and they all count toward one 24-hour total.

  • The limit. In the European guideline and the Society for Endocrinology guidance it is 10 mmol/L in the first 24 hours, then 8 per 24 hours. In the US panel it is 8 mmol/L in any 24 hours if high risk, otherwise 10–12 in 24 hours or 18 in 48.
  • The goal is lower than the limit — 4–8 mmol/L a day in the US panel, 4–6 if high risk, leaving room for overshoot.
  • The emergency is the exception, not a contradiction. A seizing patient needs a fast 4–6 mmol/L rise in the first hour — that is part of the daily allowance, not extra to it.
  • Write the ceiling down. Count from the lowest value, not from admission: a nadir of 112 means a maximum of 122 at the same hour tomorrow, or 120 if the patient is high risk.

Osmotic demyelination syndrome (ODS)

In chronic hyponatremia, brain cells extrude organic osmolytes to avoid swelling. Those take days to replace, so if the sodium rises quickly the adapted cell is left hypertonic to its surroundings, shrinks, and the myelin-maintaining oligodendrocytes are injured. It usually follows correction that was too fast, but not always: 7 of the 12 cases in a Toronto cohort had not been corrected rapidly.

  • Where. Classically the base of the pons — the old name central pontine myelinolysis — but also basal ganglia, thalamus and cerebellum. A normal pons does not rule it out.
  • When. Biphasic: the patient improves as the sodium normalizes, then deteriorates one to several days later.
  • How it presents. Dysarthria and dysphagia, then confusion, quadriparesis, pseudobulbar palsy, and at worst a locked-in state.
  • Who is at risk. Sodium 105 mmol/L or lower, hypokalemia, alcohol use disorder, malnutrition, advanced liver disease.
  • What happens to them. Across 541 reported patients, 51.9% recovered well and 24.8% died — so a severe presentation is not by itself a reason to withdraw care. No specific treatment exists; prevention is the whole point of the limit.
Sagittal T2 MRI of the brain, arrow marking a lesion in the pons

Osmotic demyelination in the pons (arrow), the classic site, on sagittal T2 MRI; on axial images the lesion takes the trident shape often described. Image by MBq, CC0 / public domain.
Clinical Pearl

Two things raise the sodium without anyone ordering it, and both count toward the daily ceiling. Replacing potassium raises the sodium, because potassium entering cells displaces sodium outward — a hidden contributor in exactly the malnourished, hypokalemic patients most at risk of demyelination. And correcting hypovolemia switches ADH off, after which the kidney dumps free water on its own.

If you overcorrect, it is reversible — act on it. Stopping whatever is raising the sodium is a clerk-level action, even at 03:00; then call your senior — the European guideline and the Society for Endocrinology guidance both advise expert input on the 5% dextrose and desmopressin in the table (the US panel allows 2–4 µg).

The limit is contested. On survival, the observational data point one way. Seethapathy (3,274 patients) and Kinoshita (1,024 ICU patients) found slower correction associated with higher mortality; a 2025 meta-analysis of 16 cohorts (11,811 patients) found the same, with no significant rise in ODS; and a 2026 cohort of 13,988 patients linked faster correction to less 90-day death or delayed neurologic injury. But sicker patients are corrected more slowly because they are sicker — confounding these designs cannot remove. In the one randomized trial, actively correcting a sodium below 130 did not change 30-day death or rehospitalization.

On ODS, the data point the other way. The Toronto cohort (22,858 admissions, mostly mild, mean sodium 125) had ODS in 0.05%; 64% were never imaged. In severe hyponatremia the rate is nearer 0.48%, and across 11 cohorts it was 0.73% after rapid correction against 0.10% without. The NephMadness 2024 hyponatremia region argues both sides at length.

What this changes for you: nothing yet. No guideline has moved, so the limit above is what you follow. What it should change is the reflex: both the rate and the patient matter; the risk list tells you whose ceiling to hold hardest.

5. On the Ward

Estimated read time: 3 minutes

Put the monitoring interval in the order, not just the fluid. After hypertonic saline, check the sodium at 6 and 12 hours, then daily until stable (the Society for Endocrinology guidance), and every 4 hours while a 3% infusion runs. Without 3% — 0.9% saline, a stopped thiazide, restriction — check a sodium below 130 every 6 hours until stable (the European guideline; the US panel: every 6–8 hours, particularly below 120). Every 2 hours if the urine output suddenly passes 100 mL/h.

Hand over the ceiling, not just the number. Correction crosses shift changes, so say all three parts out loud: “Sodium 118, up 6 from the nadir, ceiling 122 by 22:00 tonight.” A number on its own leaves the next person to reconstruct the arithmetic.

Count the diluent. Restriction prescribed but not enforced — the patient drinking from the tap, antibiotics arriving in 250 mL bags — is a common reason SIADH appears not to respond.

Hypernatremia, briefly — the mirror image

A sodium above 145 mmol/L is almost always a water deficit in someone who cannot get to water themselves: intubated, living with dementia, post-operative with no oral intake.

  • Estimate the deficit as a starting point: total body water × (serum sodium ÷ 140 − 1), taking total body water as 0.6 × weight in kg for younger men, 0.5 for younger women, and 0.5 and 0.45 for older men and women (the European guideline). Give it over 48–72 hours, then recheck the sodium and adjust
  • Replace it with water by mouth or nasogastric tube, or IV D5W if the gut cannot be used
  • Lower it gradually. A fall of no more than about 0.5 mmol/L an hour is often advised, but no guideline sets a limit, and an ICU cohort of 449 adults found no harm from faster correction
  • Think of diabetes insipidus if the urine stays dilute despite a rising serum sodium

Related Podcasts

Test Yourself

Click on your answer to reveal the explanation.

Medical Student Level

A 74-year-old woman is on day 3 of an admission for community-acquired pneumonia. She is comfortable, her blood pressure is 128/74 mmHg and has been stable, and she is not orthostatic. She has no edema and a normal jugular venous pressure. Morning bloodwork shows a sodium of 126 mmol/L, down from 138 on admission. Serum osmolality is 266 mOsm/kg, urine osmolality 505 mOsm/kg and urine sodium 62 mmol/L. Glucose, TSH and a morning cortisol are normal. She takes sertraline. She has no headache, nausea or confusion.

What is the most appropriate initial management?

  • A.Fluid restriction to under 1 L per day
  • B.Infuse 1 L of 0.9% saline over 4 hours
  • C.Give 150 mL of 3% saline over 20 minutes
  • D.Start furosemide 40 mg IV daily
Resident Level

A 52-year-old man with alcohol use disorder is admitted with a serum sodium of 104 mmol/L and a witnessed seizure. He receives two 150 mL boluses of 3% saline overnight, the seizures stop, and he is now alert and oriented. His blood pressure is 122/70 mmHg and stable. Twenty hours after presentation his sodium is 117 mmol/L. Urine output over the past four hours has been 900 mL of dilute urine. His potassium was 2.9 mmol/L on admission and has been replaced.

What is the most appropriate next step?

  • A.Continue current management and recheck in 6 hours
  • B.Restrict fluids to 800 mL per day
  • C.Give 5% dextrose and desmopressin
  • D.Give a further 150 mL bolus of 3% saline

Apply Your Learning

The observational studies in section 4 found slower correction associated with worse survival, not better. No guideline has changed, and you are still expected to cap correction at 10 mmol/L in 24 hours, or 8 in a high-risk patient. Describe how you would explain that tension to a patient’s family — that you are deliberately correcting slowly, using a limit that recent evidence has called into question.

Please do not include patient identifying details — no names, initials, dates, medical record numbers, or any detail that could identify a specific patient or encounter. Write about your reasoning, not about a real person.

Authors and Review

Dr. Zahra Merali, MB BCh BAO, FRCPC (IM & GIM), MHPE
General Internal Medicine Physician, Sunnybrook Health Sciences Centre. Assistant Professor, University of Toronto.

Dr. XX
Reviewer, Nephrology.

Content developed with the assistance of Claude (Anthropic). Reviewed annually and updated as needed. If you identify an inaccuracy, please contact medicinepods@gmail.com.

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Week 3

1 · Hyponatremia2 · Hyperkalemia3 · Upper GI bleed4 · Elevated LFTs5 · Pancreatitis