Hyponatraemia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Hyponatraemia means serum sodium below 135 mmol/L, but sodium is primarily a marker of water balance relative to exchangeable sodium and potassium. Hypotonic hyponatraemia develops when water intake exceeds renal excretory capacity under antidiuretic influence or low solute delivery. Volume depletion, heart failure, cirrhosis, kidney disease, medicines, adrenal insufficiency, primary polydipsia and SIAD are common mechanisms.

Brain cells adapt to chronic hypotonicity by losing osmolytes. This protects against swelling but creates vulnerability if sodium is then raised too quickly, particularly with very low starting sodium, malnutrition, alcohol dependence, advanced liver disease or hypokalaemia. Conversely, acute water gain can cause cerebral oedema before adaptation, producing headache, vomiting, confusion, seizure and herniation risk.

Safe care has two simultaneous tracks: rescue threatening cerebral symptoms and define the water-balance mechanism. This adult framework does not replace the live hypertonic-saline chart, specialist overcorrection plan or obstetric, paediatric and neurosurgical protocols. Use one analytical platform during active correction and involve an experienced clinician for every hypertonic prescription.

Key points

Base emergency treatment on neurological symptoms and their likely relation to hyponatraemia, not on the sodium concentration alone; profound chronic hyponatraemia may be asymptomatic while a rapid moderate fall can cause cerebral oedema.
Confirm tonicity: hyperglycaemia causes translocational hyponatraemia, and very high lipid or protein can create measurement artefact with some laboratory methods.
For severe or moderately severe symptoms, the Society for Endocrinology recommends 150 mL of 3% sodium chloride over 20 minutes, repeated according to the measured response in a suitable monitored environment.
Target a 5 mmol/L rise during the first hour, then limit total increase to no more than 10 mmol/L in the first 24 hours and 8 mmol/L per 24 hours thereafter.
Obtain paired serum osmolality, urine osmolality and urine sodium early, but do not delay emergency hypertonic treatment to complete aetiological classification.
Exclude adrenal insufficiency and clinically important hypothyroidism before calling euvolaemic hypotonic hyponatraemia syndrome of inappropriate antidiuresis.
A sudden water diuresis after volume or cortisol restoration can make sodium rise much faster than predicted; urine output is an early warning signal for overcorrection.
Vaptans are not recommended for severe or moderately severely symptomatic presentations; cause-specific longer-term treatment requires endocrine, renal and local formulary governance.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Hypovolaemic antidiuresis

Gastrointestinal, renal or skin sodium and water loss triggers vasopressin, so replacement of water without enough solute lowers serum sodium.

Inappropriate vasopressin effect

Pain, nausea, medicines, pulmonary or neurological disease and malignancy can sustain water retention despite low plasma tonicity.

Low effective circulating volume

Heart failure, cirrhosis and advanced kidney disease promote neurohormonal water retention even when total-body fluid is increased.

Excess water or low solute

Primary polydipsia and very low dietary solute can exceed renal water-excretion capacity, particularly when another antidiuretic stimulus coexists.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Water exceeds exchangeable solute
Retained or excessive water dilutes sodium relative to total exchangeable sodium and potassium, usually lowering plasma tonicity.
2
Water enters brain cells
Hypotonic extracellular fluid drives water intracellularly, causing cerebral swelling and neurological symptoms when the fall is rapid or severe.
3
Brain cells adapt
During slower onset, brain tissue sheds osmolytes to limit swelling, reducing acute symptoms but increasing vulnerability to rapid correction.
4
Overcorrection causes osmotic injury
An abrupt sodium rise draws water out of adapted brain cells and can produce delayed, severe neurological damage.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Severe cerebral symptomsRed flag

Seizure, cardiorespiratory arrest, persistent vomiting, coma or Glasgow Coma Scale at or below eight defines the highest emergency category in Society guidance.

Moderately severe syndromeRed flag

Confusion, headache or nausea without vomiting may still reflect cerebral oedema and warrants immediate experienced assessment and the symptomatic pathway.

Hypovolaemic clues

Postural symptoms, tachycardia, dry mucosa, gastrointestinal loss, bleeding or diuretic exposure suggests sodium and water loss with non-osmotic antidiuretic secretion.

Oedematous dilution

Peripheral oedema, ascites, raised jugular venous pressure or pulmonary congestion supports reduced effective arterial volume from heart, liver or renal disease.

Overcorrection warningRed flag

A brisk new dilute urine output, rapidly improving cause or unexpectedly large sodium increment predicts aquaresis and demands immediate intensified monitoring and senior action.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Repeat serum sodium on a consistent platformFirst step
Why
Confirm the value and measure correction without inter-method variation obscuring small but important changes.
Interpretation and limitations
Compare time-stamped results and sampling method; a dramatic unexpected difference requires urgent verification while management follows the patient’s neurological state.
02
Serum osmolality and glucose
Why
Distinguish hypotonic disease from hypertonic translocation or isotonic analytical artefact.
Interpretation and limitations
Low measured osmolality confirms true hypotonicity; high glucose explains water shift, while normal osmolality prompts review of lipids, proteins and the measurement method.
03
Paired urine osmolality
Why
Determine whether the kidney is appropriately excreting dilute water.
Interpretation and limitations
Urine below about 100 mOsm/kg suggests suppressed antidiuresis, primary polydipsia or low solute; a more concentrated urine indicates persistent antidiuretic effect.
04
Paired urine sodium
Why
Refine effective circulating volume and renal sodium handling after urine concentration is known.
Interpretation and limitations
A low value supports reduced effective arterial volume, whereas a higher value occurs with SIAD, adrenal deficiency, renal salt loss or diuretics; recent treatment can invalidate simple thresholds.
05
Renal profile, potassium and bicarbonate
Why
Identify kidney failure, hypokalaemia and acid–base clues that alter mechanism and correction risk.
Interpretation and limitations
Potassium replacement itself can raise sodium-related tonicity, and hypokalaemia increases osmotic demyelination risk; interpret all electrolyte treatment together.
06
Cortisol and thyroid assessment
Why
Exclude adrenal insufficiency and material hypothyroidism before diagnosing SIAD.
Interpretation and limitations
Obtain cortisol before steroids if this causes no delay, but suspected adrenal crisis requires immediate treatment; interpret cortisol timing and illness with endocrine support.
07
Medicine, fluid and intake timeline
Why
Find thiazides, antidepressants, antiepileptics, desmopressin, hypotonic fluid, excess water or low solute.
Interpretation and limitations
Relate the last doses and intake to sodium and urine trends; drug withdrawal can trigger sudden water diuresis and overcorrection.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Hyperglycaemic translocation

High extracellular glucose draws water from cells and lowers measured sodium without the same pure water-retention mechanism.

Pseudohyponatraemia

Marked lipid or protein disturbance can lower sodium on some analytical methods while measured plasma tonicity remains normal.

Adrenal insufficiency

Hypotension, weight loss, steroid exposure, hyperkalaemia or hypoglycaemia suggests cortisol deficiency, which can closely mimic SIAD physiology.

Hypovolaemia

Postural symptoms, dry mucosa, sodium losses and concentrated urine support volume depletion rather than clinically euvolaemic inappropriate antidiuresis.

Additional chapter-specific clues

Endocrine mimicRed flag

Hypotension, weight loss, hyperkalaemia, hypoglycaemia or steroid exposure raises adrenal insufficiency; pituitary disease can lack hyperkalaemia and still cause dangerous cortisol deficiency.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01RescueTreat symptomatic cerebral oedemaFirst stepHyponatraemia accompanies severe or moderately severe neurological symptoms without a more convincing immediate explanation.

1Use ABCDE, bedside glucose and seizure care, call an experienced senior clinician and transfer to an environment able to deliver hypertonic saline with rapid sodium measurement.
2Give 150 mL 3% sodium chloride or locally equivalent hypertonic solution over 20 minutes, remeasure sodium using the same platform and repeat as the Society algorithm directs towards a 5 mmol/L first-hour rise.
3Once symptoms improve or the initial target is reached, stop hypertonic treatment, begin cause-specific care and enforce the subsequent 24-hour correction limits.

02ClassifyBuild a physiological diagnosisImmediate danger is controlled or the patient has mild or absent symptoms.

1Confirm hypotonicity with serum osmolality and glucose, then interpret paired urine osmolality to establish whether renal water excretion is suppressed.
2Combine urine sodium with examination, renal function, medicines and recent fluids, recognising that diuretics, CKD and prior saline weaken volume-based thresholds.
3Check cortisol and thyroid status and investigate pulmonary, neurological, malignant or medicine triggers before documenting SIAD as a diagnosis of exclusion.

03TargetTreat the water-balance causeTonicity and volume mechanism have been established after emergency stabilisation.

1Replace true volume depletion with the appropriate isotonic fluid and stop causal losses, while anticipating that antidiuresis may switch off and accelerate sodium rise.
2For SIAD, remove reversible medicines and treat the underlying disorder, then use specialist-guided fluid and solute measures rather than reflex isotonic saline that may worsen concentrated urine losses.
3Manage heart, liver, renal, adrenal or thyroid disease through its dedicated pathway, with renal or endocrine advice for persistent profound hyponatraemia.

04BrakeStop and manage overcorrectionSodium rises beyond the planned trajectory, urine output surges or the limit exceeds 10 mmol/L initially or 8 mmol/L per day thereafter.

1Stop hypertonic and other sodium-raising inputs, measure sodium and urine output more frequently and call a clinician experienced in controlled relowering immediately.
2Review all potassium, nutrition, steroid and fluid treatment that contributes to tonicity, and calculate the complete timed rise from the original baseline.
3Use hypotonic fluid with or without parenteral desmopressin only under an explicit specialist protocol, continuing close neurological and biochemical surveillance.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Raises extracellular tonicity promptly enough to reduce threatening cerebral oedema while setting a deliberately small initial biochemical objective.

Hypertonic sodium chloride 3%

For severe or moderately severely symptomatic adult hyponatraemia, Society for Endocrinology guidance uses 150 mL intravenously over 20 minutes, rechecking sodium and repeating up to the algorithm limit to achieve about a 5 mmol/L first-hour rise.

This is a senior-supervised high-risk prescription requiring a close-monitoring area, consistent sodium assay and documented stop limits. Avoid continuous unstructured infusion, vaptans in this presentation and formula-led dosing that ignores dynamic urine water loss.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cerebral oedema

Acute hypotonicity drives brain-cell swelling, causing headache, vomiting, confusion, seizure, reduced consciousness and, in extreme cases, herniation.

Falls and functional decline

Even less dramatic chronic hyponatraemia can impair gait, attention and bone health, increasing falls and fracture risk.

Osmotic demyelination

Excessively rapid correction, particularly in malnutrition, alcohol dependence, liver disease or hypokalaemia, can cause delayed severe neurological deficits.

Treatment overshoot

Resolution of nausea, cortisol deficiency or another vasopressin stimulus can trigger brisk water diuresis and an unexpectedly rapid sodium rise.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Check sodium after each hypertonic bolus and frequently through the first day, using the local Society-aligned schedule and shortening intervals when the rise or urine output accelerates.
Record cumulative sodium change from the true pretreatment value: aim for about 5 mmol/L initially and do not exceed 10 mmol/L in the first 24 hours or 8 mmol/L in each day thereafter.
Measure hourly urine output during active rescue and whenever the cause is reversed, because abrupt aquaresis can precede a dangerous sodium jump.
Repeat neurological observations, respiratory status and seizure assessment; persistent symptoms after the planned initial rise should trigger alternative neurological investigation rather than uncontrolled extra saline.
Track potassium, glucose and administered solute because their correction changes effective tonicity and the risk calculation even if sodium-containing fluid is unchanged.
After stabilisation, monitor the disease-specific plan and recurrence risk, including medicine changes, fluid advice and access to timely repeat testing after discharge.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Symptoms outrank categories

The Society biochemical labels are useful, but treatment urgency follows cerebral manifestations, rate of fall and alternative diagnoses rather than a number alone.

Urine pair beats volume guessing

Simultaneous urine osmolality and sodium expose renal water and sodium handling more reliably than an isolated label of clinically euvolaemic.

Normal PTH logic has a sodium parallel

A urine that remains concentrated during hypotonicity is physiologically inappropriate even if its osmolality lies within the laboratory reference interval.

Potassium contributes to correction

Replacing a large potassium deficit increases effective body cation, so it must be counted conceptually when controlling the sodium trajectory.

Self-correction is still dangerous

Osmotic demyelination can follow spontaneous water diuresis after cortisol or volume restoration even when no excessive hypertonic saline was prescribed.

SIAD is a conclusion

Appropriate urine findings are necessary but insufficient; adrenal, thyroid, renal, diuretic and effective-volume causes must be addressed first.

11Common pitfallsFrequent interpretation and management errors.

01
Withholding emergency hypertonic saline from a fitting patient because the sodium is not below an arbitrary profound threshold.
02
Treating an asymptomatic chronic value rapidly to normal rather than setting conservative limits that respect cerebral adaptation.
03
Diagnosing SIAD from low sodium alone without serum osmolality, paired urine studies, cortisol, thyroid and medicine review.
04
Using a predicted formula as though urine composition will remain fixed after volume, steroid or drug treatment changes physiology.
05
Missing a brisk water diuresis and discovering overcorrection only on the next routine morning blood test.
06
Continuing hypertonic saline for persistent confusion after the planned first-hour rise without investigating seizure, infection, stroke or another cause.