Hypernatraemia

Last updated 19 August 2026.

Key points

Hypernatraemia: serum sodium above 145 mmol/L. Far less common than hyponatraemia, but carries higher mortality because of the frail populations it affects.
It is a water deficit: hypernatraemia is almost always a deficit of water relative to sodium, not an excess of salt. Total body sodium is usually normal or low.
It requires two failures: an intact thirst mechanism with access to water will correct almost any water loss. So hypernatraemia implies water loss PLUS an inability to drink - the very young, the elderly, the confused, the sedated and the dependent.
Commonest causes: inadequate intake in dependent patients, GI losses, osmotic diuresis (hyperglycaemia, HHS), diabetes insipidus, and excessive insensible loss from fever and burns.
The urine tells you the cause: concentrated urine (osmolality >700) means the kidney is responding appropriately to extrarenal loss. Inappropriately dilute urine (<300) with hypernatraemia means diabetes insipidus.
Symptoms: thirst (if the mechanism is intact), lethargy, irritability, weakness, confusion, and in severe cases seizures and coma from cerebral cell shrinkage.
The correction limit: do not lower sodium faster than 10-12 mmol/L in 24 hours (8-10 in chronic cases). Over-rapid correction causes cerebral oedema and seizures.
Route matters: oral or enteral water is preferred where possible. If IV is needed, use 5% dextrose or 0.45% saline, with 0.9% saline first if the patient is shocked.

Introduction

Hypernatraemia is a serum sodium above 145 mmol/L. It is considerably less common than hyponatraemia but is clinically important because it is associated with mortality of 40-60% in hospitalised patients - a figure that reflects the frailty and severity of illness of the people who develop it far more than the direct toxicity of the sodium itself.¹

The concept that makes hypernatraemia make sense

A conscious person with an intact thirst mechanism and a glass of water will almost never become hypernatraemic, however much water they lose. Thirst is an extraordinarily powerful and sensitive defence.

Therefore hypernatraemia nearly always requires two things to go wrong: water loss (or, rarely, a sodium load), and an inability to access or drink water
This explains the classic at-risk groups: infants, frail and dependent older people, those with dementia or delirium, intubated or sedated patients, those with impaired consciousness, and patients with hypothalamic disease affecting the thirst centre (adipsia)
In practice, hypernatraemia in a hospital inpatient is frequently a marker of inadequate care - a dependent patient not offered enough fluid - and is regarded as a nursing and clinical quality indicator
The corollary for management: as well as replacing water, always ask why could this patient not drink?

Because sodium is the principal extracellular osmole, a rise in serum sodium raises plasma osmolality and draws water out of cells by osmosis. In the brain this causes cell shrinkage, which produces the neurological symptoms and, in severe or rapid cases, can tear bridging veins to cause intracranial haemorrhage. As with hyponatraemia, the brain adapts over 48 hours by generating intracellular osmolytes - and that adaptation is what makes rapid correction dangerous.

Schematic diagram showing the relative volumes of body fluid compartments in an adult, with total body water divided into the larger intracellular compartment and the smaller extracellular compartment, which is further split into interstitial fluid and plasma. — **Body fluid compartments.** Total body water is roughly **60% of body weight in adult men and 50% in women**, of which about **two-thirds is intracellular**. Because water moves freely between compartments, a **water deficit is shared across all of them** - which is why the water deficit in hypernatraemia is calculated from **total body water**, and why replacing it corrects intracellular as well as circulating volume.Alan Sved and David Walsh, CC BY-SA 4.0, via Wikimedia Commons

Causes

Causes are best grouped by volume status, exactly as for hyponatraemia, because this determines the fluid used for replacement.

Causes of hypernatraemia by volume status.
Volume status	Mechanism	Causes
Hypovolaemic (water loss exceeding sodium loss) - the commonest pattern	Loss of hypotonic fluid	Renal: osmotic diuresis (hyperglycaemia, HHS, mannitol, high-protein feeds), loop diuretics, post-obstructive diuresis, recovery phase of AKI. Extrarenal: diarrhoea (especially in infants), vomiting, sweating and fever, burns, and losses from fistulae or stomas
Euvolaemic (pure water loss)	Loss of water without sodium	Diabetes insipidus - cranial (pituitary surgery, trauma, tumours, infiltration) or nephrogenic (lithium, hypercalcaemia, hypokalaemia, CKD, demeclocycline). Also increased insensible losses through skin and lungs (fever, tachypnoea, hot environments, mechanical ventilation), and inadequate intake in dependent patients
Hypervolaemic (sodium gain) - uncommon	Excess sodium administration or retention	Hypertonic saline, sodium bicarbonate in resuscitation, hypertonic feeds or incorrectly made-up infant formula, salt poisoning (accidental or non-accidental), primary hyperaldosteronism and Cushing syndrome (usually only mild hypernatraemia), and near-drowning in sea water

Diabetes insipidus - the pure water loss

DI is the classic cause of euvolaemic hypernatraemia, and is characterised by large volumes of inappropriately dilute urine despite a rising serum sodium.

Cranial (central) DI - deficient ADH production; caused by pituitary surgery, head injury, tumours, infiltrative disease (sarcoid, Langerhans cell histiocytosis), infection or Sheehan syndrome. Responds to desmopressin
Nephrogenic DI - renal resistance to ADH; caused by lithium (the commonest drug cause), hypercalcaemia, hypokalaemia, chronic kidney disease, and inherited channel defects. Does not respond to desmopressin
Patients with intact thirst and access to water often maintain a normal sodium despite passing many litres of urine - so DI frequently presents as polyuria and polydipsia rather than hypernatraemia. Hypernatraemia develops when water is withheld, for example when the patient is nil by mouth, unconscious or postoperative
This is why postoperative pituitary patients need close sodium and fluid balance monitoring

Clinical features

Symptoms are predominantly neurological, and reflect cellular dehydration of the brain. As with hyponatraemia, the rate of change matters more than the absolute value.

Thirst - the earliest and most prominent symptom, but only if the thirst mechanism is intact and the patient can communicate. Its absence in a dependent or obtunded patient is precisely why the diagnosis is missed
Lethargy, weakness and irritability
Confusion and delirium
Nausea and vomiting
Muscle twitching, hyperreflexia and tremor; in severe cases rigidity
Seizures and coma in severe hypernatraemia (typically above 158-160 mmol/L, or with rapid onset)
Intracranial haemorrhage - subarachnoid or subdural, from tearing of bridging veins as the brain shrinks; a particular risk in infants
Polyuria and polydipsia - pointing towards diabetes insipidus or osmotic diuresis
Signs of volume depletion - dry mucous membranes, reduced skin turgor, tachycardia, postural hypotension, oliguria, sunken eyes and, in infants, a depressed fontanelle
In infants: a high-pitched cry, irritability alternating with lethargy, poor feeding and fever - hypernatraemic dehydration in a breastfed neonate with inadequate feeding is a recognised and serious presentation

A practical point on examination: hypernatraemic dehydration preserves circulating volume relatively well, because water is drawn out of cells into the extracellular space. Signs of shock therefore appear later than in isotonic dehydration - which means a child or adult may be considerably more depleted than they look.

Investigations

U&Es, creatinine and eGFR - confirm hypernatraemia and assess renal function
Serum osmolality - raised, confirming true hypertonicity
Urine osmolality - the single most discriminating test (see below)
Urinary sodium - helps establish whether losses are renal or extrarenal
Glucose - hyperglycaemia causing osmotic diuresis is a very common contributor; exclude HHS, which combines profound hyperglycaemia, hyperosmolality and hypernatraemia
Fluid balance chart and daily weights - essential, and often more informative than any blood test; weight loss quantifies the water deficit
Calcium and potassium - hypercalcaemia and hypokalaemia both cause nephrogenic DI
Lithium level - if the patient takes lithium
Paired serum and urine osmolality with a water deprivation test - to diagnose and classify DI, followed by desmopressin to separate cranial from nephrogenic
MRI pituitary - if cranial DI is suspected; the normal posterior pituitary bright spot is characteristically absent
Review the drug chart and feed prescription - hypertonic feeds, sodium-containing drugs and diuretics are frequently implicated

Management

The principles are: restore circulating volume first if the patient is shocked, then replace the water deficit slowly, replace ongoing losses, and treat the underlying cause - including the reason the patient could not drink.²

Step 1 - resuscitate if shocked

If there is haemodynamic compromise, give 0.9% sodium chloride to restore circulating volume, even though it is relatively hypotonic compared with the patient's plasma and will not lower the sodium quickly. Perfusion takes priority over the sodium concentration. Once the patient is haemodynamically stable, switch to correcting the water deficit.

Step 2 - estimate the water deficit

Step 3 - replace the water at a safe rate

The correction limits

Lowering the sodium too quickly causes cerebral oedema, seizures and death - the mirror image of the osmotic demyelination risk in hyponatraemia. The brain has adapted to hypertonicity by accumulating intracellular osmolytes, and a rapid fall in extracellular osmolality drives water into brain cells.

Do not lower serum sodium by more than 10-12 mmol/L in 24 hours; many guidelines advise 8-10 mmol/L per 24 hours in chronic hypernatraemia (present more than 48 hours, or of unknown duration - which should be the default assumption)
In children, be more cautious still - typically no more than 0.5 mmol/L per hour, correcting over 48 hours or longer. Children are at particular risk of cerebral oedema
Acute hypernatraemia (clearly under 48 hours, for example after salt ingestion or rapid hypertonic saline) can be corrected more quickly, as the brain has not yet adapted
Check the sodium every 4-6 hours during active correction, and more frequently if it is changing quickly
Slow down or pause if the sodium is falling faster than intended

Choosing the replacement fluid.
Situation	Fluid	Notes
Patient can drink or has enteral access	Oral or nasogastric water	Preferred route wherever possible - safest, most physiological, and self-limiting. Often the whole treatment in a dependent patient
Haemodynamically compromised	0.9% sodium chloride	Restore perfusion first. Switch once stable
Euvolaemic / pure water deficit	5% dextrose	Provides free water once the glucose is metabolised. Monitor blood glucose - infusing large volumes can cause hyperglycaemia and a further osmotic diuresis
Hypovolaemic with ongoing losses	0.45% sodium chloride	Provides both water and some sodium; a common practical choice
Sodium overload (hypervolaemic)	Stop the sodium source; loop diuretic plus water replacement	Dialysis if there is renal failure or severe overload
Cranial diabetes insipidus	Desmopressin plus water replacement	Monitor closely - sodium can then fall rapidly
Nephrogenic diabetes insipidus	Remove the cause (stop lithium, correct calcium and potassium); thiazide diuretic and low-salt diet, sometimes with NSAIDs	Paradoxically, thiazides reduce urine output in nephrogenic DI

Step 4 - treat the cause and prevent recurrence

Identify and address why the patient could not drink - this is the step most often omitted. Ensure fluids are within reach, that assistance with drinking is provided and documented, and consider a fluid balance chart and daily weights
Treat hyperglycaemia, particularly HHS, which requires careful simultaneous management of glucose, sodium and osmolality
Review medications - lithium, diuretics, hypertonic feeds and sodium-containing preparations
Dietitian review of enteral feed composition and free water flushes; inadequate water flushes with concentrated feeds is a classic hospital cause
Speech and language therapy assessment where swallowing is impaired
In infants, review feeding technique and adequacy, and check formula is being made up correctly; consider safeguarding if salt poisoning is a possibility
Refer to endocrinology for diabetes insipidus

Complications

Seizures, coma and death - from severe cellular dehydration of the brain
Intracranial and subarachnoid haemorrhage - from tearing of bridging veins as the brain shrinks away from the skull; particularly in infants and with rapid onset
Cerebral venous sinus thrombosis - promoted by haemoconcentration and dehydration
Cerebral oedema and seizures from over-rapid correction - the principal iatrogenic hazard, and the mirror image of osmotic demyelination in hyponatraemia
Central pontine myelinolysis - rarely reported with rapid osmotic shifts in hypernatraemia too, although far more characteristic of hyponatraemia correction
Acute kidney injury - from volume depletion
Rhabdomyolysis - a recognised complication of severe hypernatraemia
Hyperglycaemia - from large-volume 5% dextrose infusion, potentially worsening the osmotic diuresis
Venous thromboembolism - from haemoconcentration and immobility
Pressure ulcers, falls and functional decline in the frail dependent patients who typically develop it
Long-term neurological deficit - particularly in infants who have had severe hypernatraemic dehydration or intracranial haemorrhage

Red flags

Act on these

Seizures, reduced GCS or coma with hypernatraemia - a medical emergency; protect the airway, involve critical care, and correct carefully rather than rapidly
Sodium falling faster than 10-12 mmol/L in 24 hours - slow or pause correction; over-rapid correction causes cerebral oedema
Hypernatraemia with shock - give 0.9% saline first to restore perfusion; do not withhold resuscitation fluid because of the sodium level
Large volumes of dilute urine with a rising sodium - diabetes insipidus; check paired osmolalities and involve endocrinology, especially postoperatively after pituitary surgery
A nil-by-mouth or postoperative pituitary patient - monitor sodium and fluid balance closely; DI is easily unmasked when water is withheld
Hypernatraemia in a hospital inpatient - treat as a care quality issue as well as a clinical one; establish why the patient did not receive adequate water
Profound hyperglycaemia with hypernatraemia and altered consciousness - consider hyperosmolar hyperglycaemic state, and correct osmolality slowly
A patient on lithium with polyuria and hypernatraemia - nephrogenic DI; check lithium level and involve psychiatry before altering treatment
Hypernatraemia in a neonate or infant - urgent paediatric assessment; risk of intracranial haemorrhage and long-term neurological injury, and correction must be slower
Unexplained hypernatraemia in a child with an inconsistent history - consider salt poisoning and follow safeguarding procedures
Enteral feeding with inadequate water flushes - a common and entirely preventable hospital cause

Prognosis

Mortality in hospitalised patients with hypernatraemia is high - commonly quoted at 40-60% in adults, and higher still in those who develop it after admission rather than presenting with it. This figure should be interpreted carefully: hypernatraemia is only rarely the direct cause of death. It is far more often a marker of severe underlying illness, frailty and dependency - the patients who cannot drink are the patients who are already sickest.

Hospital-acquired hypernatraemia carries particular significance. Unlike community-acquired cases, which usually reflect an acute illness with fluid loss, hypernatraemia developing during an admission generally means a dependent patient did not receive the water they needed. It is therefore treated in many trusts as a marker of care quality, and it is largely preventable through attention to fluid balance charts, assisted drinking, adequate free water with enteral feeds, and daily weights.

Outcome depends principally on the underlying cause and on the rate of correction. Hypernatraemia from a reversible cause in an otherwise well patient corrects completely with water and carries no lasting consequence. The two situations that cause avoidable harm are failure to recognise it - allowing sodium to climb to levels causing seizures and intracranial haemorrhage - and over-enthusiastic correction, which causes cerebral oedema. Infants and children are the most vulnerable at both ends, having the highest risk of intracranial haemorrhage from severe hypernatraemia and of cerebral oedema from rapid correction, which is why paediatric correction is deliberately slower and why severe paediatric hypernatraemic dehydration can leave permanent neurological deficit.

References

Adrogué HJ, Madias NE. Hypernatremia. New England Journal of Medicine. 2000. Available here
NICE CG174. Intravenous fluid therapy in adults in hospital. 2013, updated 2017. Available here
NICE NG29. Intravenous fluid therapy in children and young people in hospital. 2015, updated 2020. Available here
Society for Endocrinology. Emergency Endocrine Guidance: diabetes insipidus (arginine vasopressin deficiency) in hospital. Available here
Joint British Diabetes Societies. The Management of the Hyperosmolar Hyperglycaemic State (HHS) in Adults. Available here
NHS England / NPSA. Risks of hypernatraemia and inadequate hydration in hospital inpatients. Available here
Alan Sved and David Walsh, CC BY-SA 4.0, via Wikimedia Commons. Available here

This article is written for revision and education. It is not clinical guidance and must not be used to make decisions about the care of a patient. Always check current NICE guidance and local protocols.