Hypernatremia
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
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
- Hypotensive: start isotonic fluid. It restores circulation better and is still hypotonic relative to the patient.1
- Acute or severe symptoms: start hypotonic fluid now, whatever the cause and before the workup is done.1
- Everyone else: replace water by mouth, by tube, or IV as D5W or 0.45% saline with 2.5% glucose.1
- Find the cause and ask why thirst didn't protect the patient.1
- Recheck sodium and make sure it is falling.2
- Hypotensive?YesIsotonic fluid first. It restores circulation better and is still hypotonic relative to the patient.1
- Once stableAcute onset or severe symptoms?YesHypotonic fluid now, before the workup. Early correction can run 1–2 mmol/L per hour; a 5 mmol/L change usually eases symptoms.1
- NoReplace 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
- Either way
- 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
Treatment
| Situation | What to give | Notes |
|---|---|---|
| Hypotensive | Isotonic crystalloid first | Switch to water replacement once circulation is restored.1 |
| Acute or severe symptoms | Hypotonic fluid immediately | Initial correction may be faster, 1–2 mmol/L per hour.1 |
| Stable, can drink or has a tube | Water by mouth or tube | Oral or nasogastric water is an option.1 |
| Stable, needs IV | D5W, or 0.45% saline with 2.5% glucose | Glucose is metabolized, leaving free water.1 |
| Central diabetes insipidus | Desmopressin 2–4 mcg/day IV or SC, in 1–2 doses | Check sodium, urine volume and osmolality before and during treatment.9 |
| Nephrogenic diabetes insipidus | Thiazide or amiloride; treat the cause | Desmopressin 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
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
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?
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?
Q2Why does D5W lower sodium when it contains none?
Q3What correction limit does the Dutch guideline set, and what does newer evidence say?
Q4What are the most common reasons ED patients become hypernatremic?
Q5Desmopressin for a patient with lithium-induced nephrogenic diabetes insipidus?
Q6Sodium is rising while you treat hyperglycemia. Should you chase it?
References
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.
Checked by the writer, not a physician. The dots show how each source was read, not that anyone has confirmed the claims.
- 1Hoorn EJ, Tuut MK, Hoorntje SJ, van Saase JL, Zietse R, Geers AB. Dutch guideline for the management of electrolyte disorders: 2012 revision. Neth J Med. 2013;71(3):153–165.
- 2Ravioli S, Rohn V, Lindner G. Hypernatremia at presentation to the emergency department: a case series. Intern Emerg Med. 2022;17(8):2323–2328.
- 3Otterness K, Singer AJ, Thode HC Jr, Peacock WF. Hyponatremia and hypernatremia in the emergency department: severity and outcomes. Clin Exp Emerg Med. 2023;10(2):172–180.
- 4Feigin E, Feigin L, Ingbir M, Ben-Bassat OK, Shepshelovich D. Rate of correction and all-cause mortality in patients with severe hypernatremia. JAMA Netw Open. 2023;6(9):e2335415.
- 5Chauhan K, Pattharanitima P, Patel N, et al. Rate of correction of hypernatremia and health outcomes in critically ill patients. Clin J Am Soc Nephrol. 2019;14(5):656–663.
- 6Kitisin N, Raykateeraroj N, Hikasa Y, et al. Systematic review and meta-analysis of the treatment of hypernatremia in adult hospitalized patients: impact on mortality, morbidity, and treatment-related side effects. J Crit Care. 2025;87:155012.
- 7Chacon-Palma G, Teixeira JP, Litvinovich I, et al. Relationship between rate of hypernatremia correction and outcomes in hospitalized patients. Kidney360. 2025;6(8):1305–1316.
- 8Koyama T, Machida S, Shibagaki Y, Imai N. Severe hypernatremia in the emergency department: a retrospective, single-center study. Clin Exp Nephrol. 2026;30(8):1179–1184.
- 9Desmopressin acetate injection (Sun Pharmaceutical). US prescribing information. DailyMed.
- 10Nickson C. Hypernatraemia. Life in the Fast Lane, Critical Care Compendium; November 2020.
- 11Pattamin N, Chuasuwan A. Clinical outcomes of early fast compared to slow sodium correction rate in adults with severe hypernatremia: a comparative effectiveness study. J Crit Care. 2026;92:155354.
- 12Farkas J. Hypernatremia. Internet Book of Critical Care, EMCrit. Further reading; not used for any claim above.
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