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Hypernatremia

Updated Nov 1, 2026Adults · ED management12 sources · 9 checked in PubMed1 figureDutch guideline 2012

Bottom line

  • Hypernatremia is a water problem. Sodium is above 145 mEq/L, usually because water was lost and not replaced.1 In one ED series, impaired thirst and no free access to water were the main causes.2
  • It marks very sick patients. In a US ED, in-hospital death was 5%, 14% and 57% for mild, moderate and severe hypernatremia.3
  • Hypotensive? Isotonic fluid first. Otherwise give water: by mouth, by tube, or IV as D5W or half-normal saline with glucose.1
  • The speed limit is disputed. The Dutch guideline caps correction at 8 mmol/L in 24 hours.1 Observational studies found no cerebral edema with faster correction, and some found lower mortality.4,5,6 The largest cohort found higher mortality with fast correction.7
  • Under-correction is the common error. In one ED series, 35% of patients had sodium fall less than 2 mmol/L, or rise, over the first 24 hours.2

Severity

Mild146–149mEq/L
Moderate150–169mEq/L
Severe> 170mEq/L

Bands from a US ED study of 57,427 adults.3 Correction studies call 155 or more "severe".4,5 The Dutch guideline classifies hypernatremia instead as acute (usually under 48 hours) or chronic, and symptomatic or not.1 For sodium, 1 mmol/L equals 1 mEq/L.

Recognize

  • Symptoms: thirst, fever, altered sensorium, seizures, focal neurological deficits and hyperventilation.1 In ED patients, somnolence (42%), disorientation (30%) and recent falls (17%) were most common.2
  • Dangers: brain cell shrinkage can cause intracranial hemorrhage and dural sinus thrombosis. Cerebral edema is a risk during treatment of chronic hypernatremia.1
  • Onset is usually unknown when patients arrive, so judge acute versus chronic by the symptoms.1
  • Who gets it: older adults (less thirst, weaker urine concentration), people who can't reach water or say they are thirsty, and ICU patients.1
  • Outcomes: hypernatremia carried a higher risk of death than hyponatremia in a US ED (adjusted OR 55.75 for severe hypernatremia).3 In a Japanese ED, hospitalized patients with hypernatremia had 44% in-hospital mortality versus 14% with normal sodium.8

Tests

Send creatinine, urea, glucose, calcium and potassium, plus urine sodium and urine osmolality. Urine osmolality, urine sodium and urine output usually separate the causes. A desmopressin response test tells central from nephrogenic diabetes insipidus.1

First steps

  1. Hypotensive: start isotonic fluid. It restores circulation better and is still hypotonic relative to the patient.1
  2. Acute or severe symptoms: start hypotonic fluid now, whatever the cause and before the workup is done.1
  3. Everyone else: replace water by mouth, by tube, or IV as D5W or 0.45% saline with 2.5% glucose.1
  4. Find the cause and ask why thirst didn't protect the patient.1
  5. Recheck sodium and make sure it is falling.2
FIG 1 · Decision flowCited
  1. Sodium above 145. Send glucose, calcium, potassium, creatinine, urea, urine sodium and urine osmolality.1 Look for somnolence, confusion and falls.2
  2. Hypotensive?
    Yes
    Isotonic fluid first. It restores circulation better and is still hypotonic relative to the patient.1
  3. Acute onset or severe symptoms?
    Yes
    Hypotonic fluid now, before the workup. Early correction can run 1–2 mmol/L per hour; a 5 mmol/L change usually eases symptoms.1
  4. Replace water: by mouth or tube, or IV D5W or 0.45% saline with glucose. Estimate the deficit and the change per liter before you start.1
  5. Correction speed is disputed. The Dutch guideline caps it at 8 mmol/L in 24 h and 18 in 48 h.1 Observational studies found no cerebral edema with faster correction.4,5,6
  6. Large volumes of dilute urine (diabetes insipidus)?
    Yes
    Central: desmopressin 2–4 mcg a day IV or SC, in one or two doses. Check sodium during treatment.9
    Nephrogenic: desmopressin doesn't work. Thiazides or amiloride are options.1,9
  7. Ask why the patient couldn't drink: impaired thirst, no access to water, immobility.1,2
  8. Recheck sodium and keep it falling. In one ED series, 35% fell less than 2 mmol/L, or rose, in the first 24 hours.2
FIG 1High sodium in the ED. Drawn for this page from the Dutch electrolyte guideline, ED cohort studies and the desmopressin label. Each box carries its own citations.1,2,9

Treatment

SituationWhat to giveNotes
HypotensiveIsotonic crystalloid firstSwitch to water replacement once circulation is restored.1
Acute or severe symptomsHypotonic fluid immediatelyInitial correction may be faster, 1–2 mmol/L per hour.1
Stable, can drink or has a tubeWater by mouth or tubeOral or nasogastric water is an option.1
Stable, needs IVD5W, or 0.45% saline with 2.5% glucoseGlucose is metabolized, leaving free water.1
Central diabetes insipidusDesmopressin 2–4 mcg/day IV or SC, in 1–2 dosesCheck sodium, urine volume and osmolality before and during treatment.9
Nephrogenic diabetes insipidusThiazide or amiloride; treat the causeDesmopressin is ineffective.1,9

How much water

  • Water deficit (Dutch guideline): 0.6 × lean body weight × (sodium ÷ 140 − 1).1
  • Expected change per liter (Adrogué-Madias): (infusate sodium + infusate potassium − serum sodium) ÷ (total body water + 1). Total body water is usually 0.6 × body weight. Divide the change you want by the change per liter to get the volume.1
  • Both are estimates. The deficit formula doesn't count ongoing losses.10 Recheck sodium rather than trust the arithmetic.2
Sources disagree

The water-deficit formula comes in two forms. The Dutch guideline uses 0.6 × lean body weight × (sodium ÷ 140 − 1).1 LITFL uses 0.6 × premorbid weight × (1 − 140 ÷ sodium), which gives a smaller number.10

How fast

The Dutch guideline limits correction to 8 mmol/L in the first 24 hours and 18 mmol/L in 48 hours for all causes, because fast correction of chronic hypernatremia risks cerebral edema. Acute hypernatremia may be corrected faster at first.1

  • Tel Aviv, 4,265 inpatients with sodium ≥ 155: slow correction (≤ 0.5 mmol/L/h) was linked to higher 30-day mortality than fast correction (50.7% vs 31.8%; adjusted OR 2.02). No neurological complications were attributed to fast correction.4
  • MIMIC-III ICU patients with sodium > 155: mortality did not differ by correction rate, and chart review found no cerebral edema from rapid correction.5
  • Meta-analysis of 12 studies: overall, faster correction did not clearly change mortality (OR 0.68, 95% CI 0.38–1.24). For hypernatremia present on admission, faster correction was linked to lower mortality (OR 0.48). No major neurological complications were reported at rates under 1 mmol/L/h.6
  • MIMIC-IV target trial emulation, sodium ≥ 155: early fast correction was linked to lower 30-day mortality (adjusted HR 0.49).11
  • 37,913 inpatients with hypernatremia on admission: slow correction was linked to lower in-hospital mortality (adjusted OR 0.63), but to more discharges to hospice or nursing facilities.7
Sources disagree

The Dutch guideline's limit rests on the risk of cerebral edema.1 Most recent observational data found no such harm with faster correction and some found lower mortality,4,5,6,11 but the largest cohort found the opposite for mortality.7 None of these studies was randomized. All of them studied inpatients, not ED care.

Special situations

  • Hyperglycemia: sodium often rises as glucose falls during treatment. This helps prevent a rapid fall in effective osmolality and cerebral edema.1
  • Hospital-acquired: often involves a sodium load from isotonic fluids in patients who can't concentrate urine. Treat by giving more water; diuretics may help.1

Disposition

  • Admission rises with severity. In a US ED, every patient with severe hypernatremia was admitted.3
  • Severe hypernatremia is often an ICU problem. In a Japanese ED series, most severe cases had altered mental status and needed ICU care, and 42% died. Sodium fell only modestly over the first 24 hours in most.8
  • Poor correction tracks with death. In one ED series, patients who died had lower correction rates in the first 24 hours than survivors.2

Pitfalls

  • Leaving a stable patient on isotonic saline. In a patient who can't concentrate urine, it adds sodium.1
  • Ordering fluids without rechecking sodium. Under-correction is common.2,8
  • Trusting the water-deficit formula. It ignores ongoing losses.10
  • Giving desmopressin for nephrogenic diabetes insipidus. It doesn't work.9
  • Forgetting that desmopressin can cause hyponatremia. Check sodium during treatment.9
  • Fixing the number without asking why the patient couldn't drink.1,2

How strong is the evidence?

Weak. The Dutch guideline is the only society guideline we found that covers hypernatremia, and its correction limit predates the newer cohort data.1 Every study of correction speed is retrospective, and they disagree on mortality.4,6,7 No trial has compared correction rates.

On-shift teaching

Questions to ask a learner at the bedside. Tap a question to see the answer. Every answer uses facts cited above.

Q1A hypernatremic patient is hypotensive. Why is normal saline the right first fluid?
It restores circulation more efficiently and is still hypotonic relative to the patient. Switch to water replacement once they are stable.1
Q2Why does D5W lower sodium when it contains none?
The glucose is metabolized, leaving free water.1
Q3What correction limit does the Dutch guideline set, and what does newer evidence say?
8 mmol/L in 24 hours and 18 in 48 hours.1 Retrospective studies found no cerebral edema with correction faster than 0.5 mmol/L/h, and some linked it to lower mortality.4,5,6 The largest cohort found lower mortality with slow correction.7
Q4What are the most common reasons ED patients become hypernatremic?
Impaired thirst (70%) and no free access to water (46%) in one ED series.2
Q5Desmopressin for a patient with lithium-induced nephrogenic diabetes insipidus?
No. Desmopressin is ineffective in nephrogenic diabetes insipidus.9 Thiazides or amiloride are options.1
Q6Sodium is rising while you treat hyperglycemia. Should you chase it?
Not reflexively. As glucose falls, less water is pulled out of cells. The rise helps prevent a rapid fall in effective osmolality and cerebral edema.1

References

Evidence base

What this page is built on

12 sources, cited 87 times. Dots are sources, filled by how far each was read; stronger color means a larger share of the citations. Tap a tier to see its sources.

Read in full · 4Abstract read · 7Record only · 0Link checked · 1

Checked by the writer, not a physician. The dots show how each source was read, not that anyone has confirmed the claims.

How this page was made
  • Written from scratch. No source text was copied; facts are restated and cited.
  • No US or European society guideline on hypernatremia was found. The anchor is the Dutch Society of Internal Medicine's 2012 electrolyte guideline, read in full. Its correction limit predates the newer cohort studies, which are summarized separately.
  • The desmopressin dose comes from the FDA label on DailyMed. No other drug doses are given. Study results were checked against PubMed abstracts; the US ED study's severity bands were read in its full text on Europe PMC.
  • Adults only. Hypernatremia in infants and children, including breastfeeding-related cases, is managed differently and is not covered.
  • Figure 1 was drawn for this page from cited data. No openly licensed image that would help at the bedside was found.
  • Not for clinical use.
Not for clinical use

AI-generated draft. Not reviewed by a physician. This page is for education only and may contain errors, including in doses. Do not use it to diagnose, treat or make decisions about any patient. Rely on your own clinical judgment, your institution's protocols and current drug labeling. Reading this page does not create a physician-patient relationship. Full terms