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Health condition · Clinically reviewed

Hyponatraemia, the electrolyte disorder that hides in plain sight.

Low sodium is common, often silent, and occasionally life threatening. The right treatment starts with volume status - not the number on the blood test.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against the European hyponatraemia guideline, BMJ Best Practice and NICE clinical topics.

  • 03

    Current for 2026

    Reflects modern UK practice on volume assessment, hypertonic saline, tolvaptan and osmotic demyelination risk.

Key facts

Hyponatraemia at a glance.

The essentials in plain English - what it is, how it is graded, and why volume status matters more than the number.

  • What it is

    Hyponatraemia is a serum sodium below 135 mmol/L, the most common electrolyte disturbance in hospital medicine.

  • Severity

    Mild 130-134, moderate 125-129, severe below 125 mmol/L. Symptoms track more closely with speed of fall than with number.

  • Acute vs chronic

    Under 48 hours is acute and higher risk from cerebral oedema. Over 48 hours is chronic and higher risk from over-rapid correction.

  • Volume status

    Classified as hypovolaemic, euvolaemic (usually SIADH) or hypervolaemic. Volume assessment shapes every treatment decision.

  • Investigations

    Paired plasma and urinary osmolality, urinary sodium, thyroid function and cortisol - a small panel that answers most cases.

  • Correction limits

    Chronic hyponatraemia should not be corrected by more than 10 mmol/L in 24 hours to avoid osmotic demyelination syndrome.

Why this guide matters

A common finding with an uncommon amount of nuance.

Hyponatraemia is easy to spot and easy to mishandle. Three principles shape everything else on this page.

  • Volume status guides treatment

    Hypovolaemic, euvolaemic and hypervolaemic patients need different fluid strategies. The bedside examination sets the plan.

  • Correct at the right speed

    Chronic hyponatraemia must not rise faster than 10 mmol/L in 24 hours - overshoot causes osmotic demyelination.

  • SIADH deserves specialist care

    When fluid restriction fails, tolvaptan and other options exist in specialist commissioned endocrine clinics.

How the diagnosis is made

From a low sodium result to a clear plan.

The steps a UK physician or endocrinologist typically follows, in order - built around the European hyponatraemia guideline.

  1. 01

    Assessing

    Confirm and grade the sodium

    Repeat serum sodium to confirm, and grade severity as mild, moderate or severe. Check glucose to exclude a translational drop.

  2. 02

    Assessing

    History and drug review

    Time course, symptoms, thirst, fluid intake, endurance sport, and a careful medicines review - thiazides, SSRIs, PPIs, carbamazepine and chemotherapy stand out.

  3. 03

    Assessing

    Assess volume status

    Postural pulse and blood pressure, mucous membranes, JVP and oedema. This single step directs the rest of the workup.

  4. 04

    Confirming

    Osmolality and urinary sodium

    Plasma osmolality, urinary osmolality and urinary sodium separate true hypotonic hyponatraemia from pseudo and hypertonic causes.

  5. 05

    Confirming

    Endocrine bloods

    Thyroid function and a 9am cortisol - hypothyroidism and adrenal insufficiency (see /conditions/addisons-disease/) are easily missed and highly treatable.

  6. 06

    Escalating

    Specialist endocrinology review

    For confirmed SIADH, refractory or recurrent cases, specialist commissioned endocrinology input guides fluid restriction and vaptan use.

  7. 07

    Escalating

    Imaging when indicated

    CNS or thoracic imaging (see /tests/private-ct-scan/ and /tests/private-mri-scan/) may be needed to look for a driver of SIADH or a hypervolaemic cause.

Typical timeline: from an abnormal blood test to a working diagnosis in a single day.

Symptoms

What low sodium can look like.

Symptoms depend on how quickly the sodium has fallen. Mild chronic cases are often silent, whereas acute severe hyponatraemia is a medical emergency.

  • Often silent

    Mild chronic hyponatraemia is usually asymptomatic and picked up on routine bloods.

  • Nausea and headache

    Common early symptoms as brain cells begin to swell, particularly in moderate hyponatraemia.

  • Confusion and lethargy

    Slowed thinking, poor concentration and drowsiness signal cerebral oedema and warrant urgent review.

  • Falls and unsteadiness

    Even mild chronic hyponatraemia impairs balance and gait - a well-recognised cause of falls in older adults.

  • Seizures

    A red flag for severe or rapidly falling sodium - needs immediate hospital assessment.

  • Coma and brainstem signs

    Reduced consciousness or brainstem compromise indicate life-threatening cerebral oedema.

  • Postural symptoms

    Dizziness on standing and reduced skin turgor point towards a hypovolaemic pattern.

  • Red flag - osmotic demyelination

    Delayed neurological deterioration after correction suggests osmotic demyelination syndrome - a preventable iatrogenic injury.

Treatment

How hyponatraemia is treated in the UK.

The right treatment depends on severity, chronicity and volume status - from cautious fluid restriction to emergency hypertonic saline.

  • Hypertonic saline (severe symptomatic)

    150 mL of 3% sodium chloride as a specialist-commissioned emergency bolus, with strict monitoring. The aim is to lift symptoms, not the number.

  • Stop the driver

    Discontinue the culprit drug, treat sepsis, correct hypothyroidism and replace cortisol. Many cases resolve once the trigger is removed.

  • Fluid restriction (SIADH)

    First-line for confirmed SIADH - typically 800 to 1000 mL per day, tailored to urinary electrolytes and response.

  • Tolvaptan

    A vasopressin V2 receptor antagonist for refractory SIADH, initiated under specialist commissioned supervision - see /treatments/tolvaptan-clinic/.

  • Demeclocycline

    A second-line option in SIADH when fluid restriction fails and a vaptan is unsuitable. Slower onset and needs renal monitoring.

  • Isotonic saline (hypovolaemic)

    Restore circulating volume with 0.9% sodium chloride. Sodium usually rises as ADH switches off - watch for over-rapid correction.

  • Treat the underlying disease

    Optimise heart failure (see /conditions/heart-failure/), cirrhosis (see /conditions/cirrhosis/) or CKD (see /conditions/chronic-kidney-disease/) alongside cautious fluid restriction.

  • Sports and endurance guidance

    Avoid excess hypotonic fluid intake during endurance events - drink to thirst rather than to a schedule.

What this guide is based on

The sources behind every claim on this page.

European and UK guidance and specialist society standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP, physician or endocrinologist knows your history and can tell you which parts apply to you. If in doubt, get seen.

  • Spasovski G et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. European Journal of Endocrinology.

  • BMJ Best Practice. Assessment of hyponatraemia.

  • NICE Clinical Knowledge Summaries. Hyponatraemia.

  • Society for Endocrinology. UK guidance on SIADH and tolvaptan use.

Red flags

When hyponatraemia needs urgent attention.

Many patients can be safely managed in the community. These are the situations that cannot - and where a specialist opinion is needed.

  • Seizures or reduced consciousness

    Signs of severe cerebral oedema - call 999 or the on-call medical team for urgent hypertonic saline.

  • Sodium below 125 mmol/L

    Severe hyponatraemia carries a high risk of neurological injury and needs same-day hospital assessment.

  • Acute drop under 48 hours

    A rapid fall - typical after endurance events or post-operative fluids - is dangerous even at higher numerical values.

  • Suspected adrenal crisis

    Hyponatraemia with hyperkalaemia, hypotension or pigmentation - treat as adrenal crisis and refer immediately (see /conditions/addisons-disease/).

  • Osmotic demyelination risk

    Sodium correction exceeding 10 mmol/L in 24 hours - stop, review, and consider re-lowering with dextrose or desmopressin under specialist advice.

  • New neurology after correction

    Delayed dysarthria, dysphagia, quadriparesis or altered behaviour days after correction - urgent neurology and MRI review.

  • Refractory or recurrent SIADH

    When fluid restriction fails, or hyponatraemia keeps returning, specialist commissioned endocrinology input is needed.

  • Malignancy suspicion

    SIADH can be the first sign of small-cell lung cancer or other tumours - a low threshold for imaging is appropriate.

  • Pregnancy or endurance athlete

    Exercise-associated hyponatraemia in marathon runners and peripartum women needs careful, cautious correction.

Living with it

A manageable condition, with a few clear rules.

Four practical points that make the biggest difference day to day - especially for those on high-risk medicines or with chronic SIADH.

A quiet reminder

More water is not always better.

For a lot of people with hyponatraemia the safest thing is to drink to thirst, not to a target - and to check bloods on schedule.

  1. 01 Fluids

    Drink to thirst, not to a target

    For many people prone to hyponatraemia, forcing extra water does more harm than good. Let thirst be the guide.

  2. 02 Medicines

    Know your risky drugs

    Thiazides, SSRIs, carbamazepine and PPIs are common culprits. Never stop them on your own - review with your GP or specialist.

  3. 03 Monitoring

    Regular bloods matter

    If you have chronic hyponatraemia or take a high-risk medicine, periodic sodium checks catch a drop before symptoms.

  4. 04 Escalate

    Sudden confusion is an emergency

    New confusion, seizure or collapse in someone with known hyponatraemia is a 999 call - do not wait.

Frequently asked

Everything we get asked about hyponatraemia.

Quick answers on SIADH, hypertonic saline, tolvaptan and osmotic demyelination.

  • What is hyponatraemia?

    Hyponatraemia is a serum sodium concentration below 135 mmol/L. It is the most common electrolyte disorder and is graded as mild (130-134), moderate (125-129) or severe (below 125 mmol/L). Symptoms depend more on how quickly the sodium has fallen than on the absolute number.

  • What causes it?

    Causes are grouped by volume status. Hypovolaemic causes include vomiting, diarrhoea, diuretics and Addison disease. Euvolaemic causes are led by SIADH, driven by CNS disease, malignancy, drugs, surgery or pain, plus hypothyroidism and cortisol deficiency. Hypervolaemic causes include heart failure, cirrhosis, chronic kidney disease and nephrotic syndrome.

  • What is SIADH?

    SIADH is the syndrome of inappropriate antidiuretic hormone secretion. The body retains water despite a low serum sodium, producing a concentrated urine and a dilute plasma. It is the commonest cause of euvolaemic hyponatraemia and is often triggered by drugs, malignancy, chest or brain disease.

  • How is severe hyponatraemia treated?

    Severely symptomatic hyponatraemia - seizures, coma or profound confusion - is treated as an emergency with 150 mL of 3% hypertonic saline under specialist commissioned supervision. Correction is capped at 10 mmol/L in the first 24 hours to prevent osmotic demyelination syndrome.

  • What is tolvaptan and when is it used?

    Tolvaptan is a vasopressin V2 receptor antagonist that promotes water excretion without losing sodium. It is used in specialist commissioned SIADH clinics when fluid restriction fails, and needs careful in-patient initiation with regular sodium checks. See our tolvaptan clinic guide for detail.

  • What is osmotic demyelination syndrome?

    Osmotic demyelination syndrome is a rare but serious neurological injury caused by correcting chronic hyponatraemia too quickly. It typically appears days after treatment as dysarthria, dysphagia, quadriparesis or behavioural change. Prevention - slow, capped correction - is far better than any available treatment.

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