Renal, Fluids, Electrolytes & Acid-Base · Topic 11 of 22
Hypernatremia
Renal & electrolytes · sodium and water
Hypernatremia
A free-water deficit. Restore perfusion first, calculate the deficit, then replace it — chronic cases no faster than 0.5 mEq/L per hour.
Key numbers
Serum sodium above 145 mEq/LNa⁺ > 145 mEq/L
Free-water deficit: TBW × (Na/140 − 1)TBW × (Na/140 − 1)
Chronic: ≤ 0.5 mEq/L per hour≤ 0.5 mEq/L/h
01 · Defined bySerum sodium above 145 mEq/L
Hypernatremia is a serum sodium above 145 mEq/L: a deficit of total body water relative to sodium, almost always from impaired thirst or no access to water.
02 · CalculateFree-water deficit: TBW × (Na/140 − 1)
Free-water deficit (L) = TBW × (serum Na/140 − 1), with TBW = 0.6 × weight in kg (men) or 0.5 × weight (women); it underestimates the deficit when the patient is also volume depleted.
03 · The ruleChronic: ≤ 0.5 mEq/L per hour
Correct chronic or unknown-duration hypernatremia no faster than 0.5 mEq/L per hour (at most 10–12 mEq/L per 24 h), spreading correction over about 48 hours, to avoid cerebral edema.
01
Causes & risk factors
Why it happensCauses sorted by volume statusHypovolemic: GI losses, loop diuretics, osmotic diuresis (hyperglycemia, mannitol, urea). Euvolemic: insensible losses, diabetes insipidus. Hypervolemic: hypertonic saline, sodium bicarbonate, or misformulated parenteral nutrition.
At risk: older, post-op, tube-fed, altered patientsHypernatremia is common in older adults, after surgery, in patients on tube feeds or parenteral nutrition, and in anyone intubated or confused who cannot express thirst or reach water.
02
Presentation
What you'll seeThirst, confusion, hyperreflexia, seizures, comaThe main symptom is thirst; brain-cell shrinkage causes confusion, neuromuscular excitability, hyperreflexia, seizures and coma. Rapid, severe rises can tear cerebral vessels and cause subcortical or subarachnoid hemorrhage, mostly reported in children.
03
Diagnosis & monitoring
Work-upRecheck sodium often; add ongoing lossesRecheck serum sodium repeatedly during correction and add ongoing renal or GI losses plus insensible losses to the calculated deficit; the formula alone underdoses free water.
04
Do right now
In this orderFirst moves
1
→Shock first: isotonic fluid regardless of sodium
2
→Free-water deficit: TBW × (Na/140 − 1)TBW × (Na/140 − 1)
3
→Replace free water with D5W or 0.45% saline
4
→Chronic: ≤ 0.5 mEq/L per hour≤ 0.5 mEq/L/h
5
Recheck sodium often; add ongoing losses
Why each step
Shock first: isotonic fluid regardless of sodiumWith hypotension or shock, resuscitate first with 0.9% saline or a balanced crystalloid regardless of the sodium; switch to hypotonic fluid for the free-water deficit once perfusion is restored.
Free-water deficit: TBW × (Na/140 − 1)Free-water deficit (L) = TBW × (serum Na/140 − 1), with TBW = 0.6 × weight in kg (men) or 0.5 × weight (women); it underestimates the deficit when the patient is also volume depleted.
Replace free water with D5W or 0.45% salineGive free water enterally when the patient can drink or has a tube; otherwise IV D5W or 0.45% saline (euvolemic), 0.45% saline after volume repletion (hypovolemic), or D5W plus a loop diuretic (hypervolemic).
Chronic: ≤ 0.5 mEq/L per hourCorrect chronic or unknown-duration hypernatremia no faster than 0.5 mEq/L per hour (at most 10–12 mEq/L per 24 h), spreading correction over about 48 hours, to avoid cerebral edema.
Recheck sodium often; add ongoing lossesRecheck serum sodium repeatedly during correction and add ongoing renal or GI losses plus insensible losses to the calculated deficit; the formula alone underdoses free water.
05
Management
OrdersAcute hypernatremia: correct quickly within 24 hoursHypernatremia that developed within hours (e.g. sodium loading) can be corrected fast — sodium falling 1–2 mEq/L per hour for 6–8 hours, normal within 24 hours — because the brain has not adapted.
06
Red flags & don'ts
Avoid harmToo-fast correction of chronic hypernatremia: cerebral edema complicationIn chronic hypernatremia brain cells generate idiogenic osmoles; correcting too fast lets water rush into them, causing cerebral edema and seizures.
07
The rules
Know theseUnder-correction also raises mortalityCorrecting too slowly is also harmful: adult studies link correction under about 6 mEq/L per day with higher mortality. If the target rate is overshot, do not deliberately re-raise sodium.
08
Acute or chronic hypernatremia?
Commonly confused| Brain adaptation | None yet — brain cells shrink abruptly |
|---|---|
| Correction speed | About 1–2 mEq/L per hour |
| Time to normal sodium | Within about 24 hours |
| Main danger | The hypernatremia itself (cerebral bleeding) |
09
Commonly confused
Tell apartUrine osmolality points to the causeUrine osmolality guides the cause: < 300 mOsm/kg with polyuria suggests diabetes insipidus; 300–800 suggests partial DI or osmotic diuresis; > 800 means the kidneys are concentrating — extrarenal water loss, hypodipsia or salt load.
Desmopressin response separates central from nephrogenic DIIn hypotonic polyuria, desmopressin raises urine osmolality by at least 50% in central DI but changes little in nephrogenic DI (see the diabetes insipidus sheet).
10
More detail
ReferenceShow 5 reference facts
Severity by sodium: mild 146–150, moderate 151–155, severe above 155 mEq/L; adult series report very high mortality (up to about 75%) above 160 mEq/L, reflecting both the underlying illness and the hypertonicity.
Infusing D5W too fast can cause glucosuria and an osmotic diuresis that worsens hypertonicity, especially in patients with diabetes; monitor glucose and potassium during free-water replacement.
In hyperglycemia, water shifts out of cells and lowers the measured sodium, masking the true hyperosmolality; osmotic diuresis then produces hypovolemic hypernatremia as glucose falls (see the HHS sheet).
A rough bedside rule: each 1 mEq/L fall in sodium needs about 3 mL/kg of electrolyte-free water; an empiric D5W start of about 1.35 mL/kg/h has also been suggested.
Hypokalemia and hypercalcemia impair renal concentrating ability (acquired nephrogenic DI) and can drive hypernatremia, so check potassium and calcium in unexplained cases.
Hypernatremia is a water problem, not a salt problem — almost always a patient who cannot get to water or cannot feel thirst.
Sources · Merck Manual Professional — Hypernatremia (reviewed Jun 2025) · Evaluation and management of hypernatremia in adults: clinical perspectives. Korean J Intern Med 2023 (open-access review) · Starter sheet built from the verified AGACNP fact map (facts reviewed 2026-10-15).