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# Hypernatraemia

Blood sodium is high because water is lacking; it happens in people who cannot drink or lose a lot of water, and neurons shrink.

Updated 2026-11-01

## Structures involved

Tap one to see what it is and open it in 3D.

- [Hypothalamus](https://durgical.com/en/anatomy/hypothalamus/)
- [Kidneys](https://durgical.com/en/anatomy/kidney/)
- [Pituitary gland](https://durgical.com/en/anatomy/pituitary-gland/)
- [White matter](https://durgical.com/en/anatomy/white-matter-of-telencephalon/)

## In biochemistry

- [Serum osmolality and osmolar gap](https://durgical.com/en/biochemistry/topics/serum-osmolality-and-osmolar-gap/)

## In physiology

- [Body fluid compartments](https://durgical.com/en/physiology/body-fluid-compartments/)
- [Osmosis, osmolarity and tonicity](https://durgical.com/en/physiology/osmosis-osmolarity-and-tonicity/)
- [Cell volume regulation](https://durgical.com/en/physiology/cell-volume-regulation/)
- [The posterior pituitary: ADH and oxytocin](https://durgical.com/en/physiology/the-posterior-pituitary-adh-and-oxytocin/)
- [Heat exhaustion and heat stroke](https://durgical.com/en/physiology/heat-exhaustion-and-heat-stroke/)
- [The countercurrent mechanism, urea recycling and urine concentration](https://durgical.com/en/physiology/the-countercurrent-mechanism-urea-recycling-and-urine-concentration/)
- [ADH, thirst and water balance](https://durgical.com/en/physiology/adh-thirst-and-water-balance/)
- [Reasoning through fluid and electrolyte imbalances](https://durgical.com/en/physiology/reasoning-through-fluid-and-electrolyte-imbalances/)
- [Fluid shifts between compartments](https://durgical.com/en/physiology/fluid-shifts-between-compartments/)
- [Urine dilution, free water and osmotic diuresis](https://durgical.com/en/physiology/urine-dilution-free-water-and-osmotic-diuresis/)

## What it is

A high serum sodium that nearly always reflects a deficit of free water relative to sodium, with hyperosmolality.

## Who gets it

It mainly affects dependent older adults, infants with diarrhoea and intensive care patients; thirst protects anyone with free access to water.

## Causes

- Water loss without replacement: fever, sweating, burns, osmotic diarrhoea, vomiting
- Central diabetes insipidus (no ADH: head trauma, pituitary surgery, tumours) or nephrogenic (lithium, hypercalcaemia, hypokalaemia)
- Osmotic diuresis: hyperglycaemia, mannitol, urea from high-protein feeds
- No access to water or impaired thirst: dementia, infants, intubated patients
- Sodium gain: hypertonic solutions or bicarbonate, errors in mixing infant formula

## Risk factors

- Older age or dementia
- Infants with diarrhoea
- Critically ill or tube-fed patients
- Lithium treatment
- Surgery or trauma near the pituitary

## Pathophysiology

When free water is lacking, plasma osmolality rises; water leaves cells by osmosis and neurons shrink, stretching and tearing bridging veins (haemorrhage) and disturbing their function: irritability, lethargy, seizures and coma. Normally hyperosmolality triggers thirst and ADH release from the posterior pituitary; if thirst, water access or ADH action fails, sodium rises. Over days neurons generate osmolytes to regain volume, so overly fast correction produces brain oedema.

## Classification

- Hypovolaemic: loss of water and some sodium (diarrhoea, sweat)
- Euvolaemic: pure water loss (diabetes insipidus, fever)
- Hypervolaemic: sodium gain (hypertonic solutions)
- Acute (
- Intense thirst (if preserved)
- Irritability and high-pitched cry in infants
- Lethargy, confusion
- Weakness and muscle twitching
- Seizures and coma when severe
- Polyuria with dilute urine in diabetes insipidus

## Red flags

- Falling consciousness or seizures
- Dehydrated infant with extreme irritability
- Fast correction of chronic hypernatraemia (risk of brain oedema)

## Diagnosis

**Clinical**
Assess hydration, access to water, urine output and drugs.

**Tests**
Serum sodium and osmolality, urine osmolality and sodium, glucose, calcium, potassium, creatinine; water deprivation test and response to desmopressin to tell central from nephrogenic diabetes insipidus.

**Imaging**
MRI of the sella and [hypothalamus](https://durgical.com/en/anatomy/hypothalamus/) if central diabetes insipidus is confirmed; head CT if neurological status worsens.

## Treatment

**Medical**
Replace the free water deficit (oral, by tube or with intravenous hypotonic fluids) gradually

**Medical**
Central diabetes insipidus: desmopressin; nephrogenic: treat the cause (stop lithium, correct calcium and potassium) and thiazides or a low-solute diet

**Medical**
Hypovolaemia or shock: isotonic fluid first to restore perfusion

**Follow-up**
Frequent sodium checks so it is not lowered faster than is safe in chronic forms

## Complications

- Brain haemorrhage from shrinkage
- Venous sinus thrombosis
- Brain oedema from fast correction
- Rhabdomyolysis

## Prognosis

Hypernatraemia in older adults and critically ill patients is linked to high mortality, partly from the underlying illness.

## Prevention

- Offering water to dependent people
- Mixing infant formula correctly
- Monitoring sodium and urine output on lithium or after pituitary surgery

## Test yourself

Think of the answer, then tap the question to see it.

## What does hypernatraemia nearly always reflect?

A deficit of free water relative to sodium, not an excess of body sodium.

## Which mechanism protects a healthy person from hypernatraemia?

Thirst, triggered by hyperosmolality, together with ADH release.

## How is central diabetes insipidus told from nephrogenic?

After water deprivation, urine concentrates with desmopressin in the central form and not in the nephrogenic form.

## Why is chronic hypernatraemia corrected slowly?

Neurons have generated osmolytes; lowering sodium fast draws water in and causes brain oedema.

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## Related conditions

- [Hyponatraemia](https://durgical.com/en/conditions/hyponatraemia/)
- [Hypercalcaemia](https://durgical.com/en/conditions/hypercalcaemia/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)
- [Acute (viral) gastroenteritis](https://durgical.com/en/conditions/acute-gastroenteritis/)
- [Traumatic brain injury](https://durgical.com/en/conditions/traumatic-brain-injury/)

Educational information, not medical advice. For any symptom, see a health professional.

Sources: [Sodium Blood Test: MedlinePlus Medical Test](https://medlineplus.gov/lab-tests/sodium-blood-test/) (MedlinePlus, US National Library of Medicine, 2026); [Sodium blood test: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/003481.htm) (MedlinePlus, US National Library of Medicine, 2026); [Dehydration: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000982.htm) (MedlinePlus, US National Library of Medicine, 2026); [Diabetes insipidus: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000377.htm) (MedlinePlus, US National Library of Medicine, 2026); [Nephrogenic diabetes insipidus: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000511.htm) (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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Source: https://durgical.com/en/conditions/hypernatraemia/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/conditions/hypernatraemia/
