Level 1 of 6Core

Disorders of sodium and water: hyponatraemia and hypernatraemia

The core to-do list — diagnose and manage, at a glance

Diagnose— recognise it

The plasma sodium measures water, not salt: it is a ratio of exchangeable sodium plus potassium to total body water, so a sodium disorder is almost always a water disorder — and the organ that suffers is the brain. Hyponatraemia is below 135 mmol/L (mild 130–134, moderate 125–129, severe below 125); hypernatraemia is above 145 mmol/L, nearly always a water deficit, with mortality up to 40–60%.
Ask the brain question first — the only thing that justifies emergency treatment: seizure; coma, obtundation or a falling GCS; vomiting with headache and drowsiness; or cardiorespiratory distress or respiratory arrest. Their absence is what permits slow, calculated correction. The number alone never places a patient in the emergency category, and never keeps them out of it.
Duration matters more than depth: acute means present for less than 48 hours, chronic means longer — the single most useful piece of history is the date of the last normal plasma sodium. When duration is unknown, treat as chronic.
Exclude the two false hyponatraemias before treating: pseudohyponatraemia (artefact of severe hyperlipidaemia or hyperproteinaemia — no treatment) and hypertonic hyponatraemia (glucose or mannitol drawing water out of cells — treat the glucose, not the sodium; sodium falls about 1.6–2.4 mmol/L per 5.6 mmol/L rise in glucose). True hypotonic hyponatraemia has an effective osmolality below 275 mOsm/kg.
Score the risk of osmotic demyelination (ODS) before you correct anything: sodium below 120 mmol/L, alcohol use disorder, chronic liver disease, malnutrition, hypokalaemia especially below 3.0 mmol/L, hypoxaemia. Assess volume status clinically, read the drug and fluid charts (thiazides are the most important single drug cause), and send a paired urine sodium and osmolality before any fluid or diuretic — the single most informative test and the one most often omitted.Not available at your setup — Serum electrolytes.
In hypernatraemia the first aetiological question is always: why could this person not drink? (the frail elderly, the sedated, dysphagia after stroke, the infant, nil by mouth — thirst is blunted in old age). Above 160 mmol/L expect lethargy, irritability and weakness progressing to hyperthermia, delirium, seizures and coma — and the circulation is defended, so the patient may look less unwell than the biochemistry suggests.

Manage now— do this, in order

Severe symptoms mean hypertonic saline regardless of aetiology, volume status or presumed duration, without waiting for osmolality or urine results: 3% sodium chloride 100 mL IV over 10 minutes, repeatable twice (or 150 mL over 20 minutes, repeatable once or twice). Each 100 mL raises the sodium 1–2 mmol/L; recheck after every bolus. Stop when symptoms resolve or the sodium has risen 4–6 mmol/L — the goal is deliberately modest. Child with seizure or coma: 3% sodium chloride 2 mL/kg over 10–20 minutes, max 100 mL per bolus, repeatable twice.Doctor / Nurse
Give benzodiazepines for a hyponatraemic seizure but do not rely on them — they will not reliably terminate it; the hypertonic saline is the definitive anticonvulsant. Hypertonic saline is irritant: use a large, well-sited cannula, though central access must never delay the first bolus. Never infuse sterile or distilled water intravenously — it causes haemolysis.Doctor / Nurse
Respect the correction limits: 4–6 mmol/L total in the emergency phase, then no more than 8 mmol/L in the first 24 hours in a chronic patient, under 6 mmol/L in each subsequent 24 hours, no more than 15 mmol/L over 48 hours, and only 4–6 mmol/L per 24 hours where ODS risk is high. Eight is a limit, not a target — and count administered potassium within the sodium budget: replacing a large potassium deficit itself raises the sodium.
Hypovolaemic hyponatraemia: rehydrate with 0.9% sodium chloride — 1 litre over 12 hours in mild depletion, conventional resuscitation in shock — and correct the cause (stop the thiazide, treat the vomiting or diarrhoea, hydrocortisone if adrenal insufficiency is possible). Watch for the water diuresis after volume repletion: sodium 2-hourly, urine output hourly — an output rising above 100–200 mL/hour demands an immediate sodium measurement; this abrupt unheralded rise is the classic mechanism of iatrogenic ODS.
Where hypovolaemia cannot be distinguished from euvolaemia, use a diagnostic fluid challenge: 0.9% sodium chloride 500 mL over 1–2 hours (250 mL over 1 hour in the elderly or cardiac disease), sodium re-measured at 2 hours — a rising sodium indicates hypovolaemia, a falling sodium indicates SIADH.
Euvolaemic hyponatraemia / SIADH: fluid restriction to 500–1000 mL/day counting ALL liquids (tea, soup, milk, the water with tablets, IV flushes), withdrawal of the precipitant, and active treatment of pain and nausea — both potent vasopressin secretagogues. Never give isotonic saline for SIADH: it often lowers the sodium further. Hypervolaemic: restrict both fluid and salt, treat the underlying disease, loop diuretics cautiously.
If you overcorrect, act rather than observe: stop all saline, give free water as IV 5% dextrose, and give desmopressin to re-induce or stabilise the hyponatraemia, re-measuring hourly until back inside the intended corridor.Doctor / Nurse
Hypernatraemia — circulation before tonicity: in shock restore euvolaemia with 0.9% sodium chloride first, then correct the free-water deficit: water deficit (L) = TBW (0.5 x weight in kg) x [(plasma Na / 140) − 1], plus insensible losses of 500–1000 mL/day plus measured output, replaced over 48 hours. Lower the sodium no faster than 10–12 mmol/L per 24 hours (about 0.5 mmol/L/hour). Give water orally or by NG tube wherever safe; use 5% dextrose or 0.45% sodium chloride at 146–170 mmol/L, but begin with 0.9% sodium chloride above 170 mmol/L or in shock. Recalculate at every sodium measurement; check glucose at least 4-hourly on high-volume dextrose.Doctor / Nurse
Children: never give hypotonic maintenance fluid to a sick child — a classic avoidable cause of fatal hyponatraemic encephalopathy; maintenance should be isotonic (0.9% sodium chloride with glucose) with daily sodium checks. In hypernatraemic dehydration restore the circulation with 0.9% sodium chloride 10–20 mL/kg, then rehydrate over at least 48 hours; convulsions during rehydration signify cerebral oedema — stop the hypotonic fluid at once, and if the sodium falls too fast, increase the sodium content of the fluid rather than simply slowing it.Doctor / Nurse

Correction limits for hyponatraemia — memorise these

Situation	Maximum permitted rise
Emergency phase, symptomatic	4–6 mmol/L total, at 1–2 mmol/L/hour, then stop
First 24 h, chronic patient	No more than 8 mmol/L (a limit, not a target)
Each subsequent 24 h	Under 6 mmol/L
Total over 48 h	No more than 15 mmol/L
High ODS risk	4–6 mmol/L per 24 h
Hypernatraemia (rate of fall)	No more than 10–12 mmol/L per 24 h (~0.5 mmol/L/hour)

Refer / escalate

Escalate or transfer urgently any patient with seizure, coma, obtundation or a falling GCS from hyponatraemia (after giving hypertonic saline), any sodium above 160 mmol/L or below 120 mmol/L, any patient with shock, anuria or a high ODS risk profile, any deterioration in conscious level during correction, and any patient in whom sodium cannot be measured at least 1–2 hourly during active correction.

Disorders of potassium: hyperkalaemia and hypokalaemia — Level 6: DepthPrevious Disorders of sodium and water: hyponatraemia and hypernatraemia — Level 2: Must-rememberNext

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