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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Na⁺ <135 mmol/L = hyponatraemia. Commonest electrolyte abnormality in hospital. Mild (130–134), moderate (125–129), severe (<125)
- Classify by VOLUME STATUS: hypovolaemic (dehydration, diuretics), euvolaemic (SIADH — commonest cause of euvolaemic hyponatraemia), hypervolaemic (heart failure, cirrhosis, nephrotic syndrome)
- SIADH: euvolaemic hyponatraemia + low serum osmolality + inappropriately concentrated urine (osmolality >100). Causes: lung disease, CNS disease, drugs (SSRIs, carbamazepine), post-operative pain
- Treatment: hypovolaemic → IV 0.9% saline. Euvolaemic (SIADH) → fluid restriction (750–1000 mL/day). Hypervolaemic → fluid restriction + treat underlying cause
- CRITICAL: correct Na⁺ SLOWLY — max 10 mmol/L per 24 hours. Rapid correction → osmotic demyelination syndrome (central pontine myelinolysis)
Overview
Hyponatraemia is defined as serum sodium <135 mmol/L and is the commonest electrolyte disturbance in hospitalised patients, affecting approximately 15–30% of admissions. It is almost always caused by an excess of water relative to sodium (dilutional), rather than absolute sodium depletion. Assessment requires determination of volume status (clinical examination), serum osmolality, and urine osmolality/sodium. The most important diagnostic distinction is between depletional (hypovolaemic) hyponatraemia requiring saline and dilutional (euvolaemic — SIADH or hypervolaemic) hyponatraemia requiring fluid restriction. Correction must be gradual to avoid osmotic demyelination syndrome (ODS), a devastating neurological complication of overly rapid correction.
Epidemiology
Hyponatraemia is present in 15–30% of hospitalised patients and is an independent predictor of mortality. SIADH is the commonest cause of euvolaemic hyponatraemia. Thiazide diuretics are the commonest drug cause. Elderly patients, particularly women, are most susceptible (reduced renal concentrating ability, polypharmacy). Severe hyponatraemia (<120 mmol/L) carries significant mortality and morbidity from cerebral oedema and seizures.
Clinical Features
Symptoms
Mild (130–134): often asymptomatic or subtle (fatigue, reduced concentration)
Moderate (125–129): nausea, headache, confusion, unsteadiness
Severe (<125): drowsiness, seizures, reduced GCS, coma
Symptoms depend more on RATE of onset than absolute level (acute drop is more dangerous than chronic)
Signs
Assess VOLUME STATUS: skin turgor, mucous membranes, JVP, oedema, postural BP
Hypovolaemic: dry mucous membranes, reduced skin turgor, tachycardia, postural hypotension
Euvolaemic: clinically normal volume status (SIADH — neither overloaded nor dehydrated)
Hypervolaemic: peripheral oedema, raised JVP, ascites, pulmonary crackles (heart failure, cirrhosis)
Altered consciousness, seizures (severe — cerebral oedema)
Investigations
First-line
Serum sodium and osmolalityLow osmolality (<275 mOsm/kg) confirms true hypotonic hyponatraemia. Normal/high osmolality → pseudohyponatraemia (hyperlipidaemia, hyperproteinaemia) or translocational (hyperglycaemia)
Urine osmolality and urine sodiumUrine osmolality >100 mOsm/kg with low serum osmolality = inappropriately concentrated urine (the kidney SHOULD be diluting). Urine Na >30 mmol/L in SIADH, renal salt wasting, diuretics
Volume status assessmentClinical: JVP, skin turgor, mucous membranes, oedema, postural BP. This is the MOST important step in determining cause
Second-line
Thyroid function testsHypothyroidism can cause hyponatraemia (impaired free water excretion)
Cortisol (9 am) and short Synacthen testAdrenal insufficiency causes hyponatraemia (cortisol deficiency impairs free water excretion + sodium loss). MUST exclude before diagnosing SIADH
CXRSIADH causes: lung pathology (pneumonia, TB, small cell lung cancer), post-operative
CT headIf CNS cause suspected (SAH, meningitis, tumour) or if seizures/reduced consciousness
Specialist
Drug reviewThiazides (commonest drug cause), SSRIs, carbamazepine, PPIs, desmopressin — common culprits
1
Acute severe/symptomatic (seizures, reduced GCS)
- Hypertonic saline: 150 mL 2.7% NaCl IV over 20 minutes (urgent). Can repeat ×3 (check Na after each bolus)
- Target: raise Na by 5 mmol/L in first 1–2 hours to stop seizures/herniation
- Then slow correction: max 10 mmol/L per 24 hours total (and max 8 mmol/L per 24 hours in chronic hyponatraemia)
- Senior/specialist input mandatory
2
Hypovolaemic hyponatraemia
- IV 0.9% normal saline: replaces both sodium and volume
- Stop diuretics (especially thiazides)
- Monitor Na every 4–6 hours — risk of overcorrection once hypovolaemia corrected (kidneys produce dilute urine → rapid Na rise)
- If Na rising too fast: consider desmopressin 1–2 µg IV to slow correction (specialist advice)
3
Euvolaemic (SIADH)
- Fluid restriction: 750–1000 mL/day (first-line)
- Treat/remove underlying cause: stop offending drugs, treat infection/tumour
- If resistant to fluid restriction: demeclocycline 300–600 mg BD (induces nephrogenic DI) or tolvaptan (vasopressin antagonist — specialist only, monitor Na closely)
- Salt tablets (slow sodium) may help in chronic mild hyponatraemia
4
Hypervolaemic hyponatraemia
- Fluid restriction (1000–1500 mL/day)
- Treat underlying cause: optimise heart failure therapy (ACEi, diuretics), treat cirrhosis
- Diuretics with caution (loop diuretics — avoid thiazides)
- SGLT2 inhibitors in heart failure also help correct hyponatraemia
5
SIADH diagnostic criteria
- Serum osmolality <275 mOsm/kg
- Urine osmolality >100 mOsm/kg (inappropriately concentrated)
- Urine sodium >30 mmol/L
- Clinically euvolaemic
- Normal thyroid and adrenal function (MUST exclude hypothyroidism and cortisol deficiency first)
- No diuretic use in preceding 24–48 hours
Complications
- Cerebral oedema and brain herniation: Acute severe hyponatraemia (<120 mmol/L) — water moves into brain cells by osmosis → swelling → herniation → death
- Seizures: From acute hyponatraemia — often the presenting feature
- Osmotic demyelination syndrome (ODS): Central pontine myelinolysis — from overly rapid correction. Presents 2–6 days after correction with dysarthria, dysphagia, quadriparesis, "locked-in" syndrome. Irreversible. PREVENT by correcting Na slowly (≤10 mmol/L per 24h)
- Falls and fractures: Even mild chronic hyponatraemia increases fall risk and osteoporosis
UKMLA Exam Tips
- 1Step 1: check serum osmolality (is it true hyponatraemia?). Step 2: assess volume status. Step 3: check urine osmolality and Na. This algorithm is commonly examined
- 2SIADH = euvolaemic + low serum osmolality + inappropriately concentrated urine (>100 mOsm/kg) + urine Na >30 + normal thyroid/adrenal function
- 3MUST exclude hypothyroidism and adrenal insufficiency BEFORE diagnosing SIADH — they mimic it exactly
- 4Max Na correction rate: 10 mmol/L per 24 hours (8 mmol/L if chronic/high risk). Faster → osmotic demyelination syndrome (ODS)
- 5Thiazides cause hyponatraemia (impair diluting ability). Loop diuretics LESS commonly cause hyponatraemia (impair concentrating ability)
- 6Commonest SIADH causes: small cell lung cancer, CNS disease (SAH, meningitis, tumour), drugs (SSRIs, carbamazepine), post-operative pain/nausea
- 7Hyperglycaemia causes "pseudo" dilutional hyponatraemia — corrected Na rises by ~2.4 mmol/L for every 5.5 mmol/L glucose above normal
practicetest your knowledge on hyponatraemiaApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — renal and beyond.
open q-bank