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Hyponatraemia

SNOMED: 206490007985 words•Updated 03/03/2026
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Exam Tips

  • Classify every case in this order: tonicity (serum osmolality) -> volume status -> urine osmolality/urine sodium; this prevents common diagnostic errors.
  • Do not treat the sodium number alone: severe symptoms can occur at moderate sodium and vice versa, so symptom severity and onset speed drive urgency.
  • In OSCE/viva, always state safe correction limits and the danger of osmotic demyelination with over-rapid correction.
  • Thiazides are a classic exam trigger; explicitly ask about recent diuretic/SSRI/antiepileptic changes.
  • SIAD is a diagnosis of exclusion: document normal adrenal and thyroid function before confirming it.
  • Image cue: revise the standard ADH-collecting duct (aquaporin-2) physiology diagram and the hyponatraemia diagnostic flowchart from your renal/endocrine textbook figures.

Definition

Hyponatraemia is a disorder of water balance in which serum sodium is below 135 mmol/L, usually because total body water is disproportionately high relative to total body sodium rather than true sodium depletion alone. It is classified by severity (mild 130–135, moderate 125–129, severe <125 mmol/L), by duration (acute <48 hours vs chronic/unknown), and by tonicity/volume status, which directs diagnosis and treatment.

Pathophysiology

Serum sodium reflects plasma tonicity and water handling. In most patients, hyponatraemia develops when antidiuretic hormone (ADH, vasopressin) is not appropriately suppressed, so the collecting ducts reabsorb free water and dilute serum sodium. ADH release may be physiological (hypovolaemia), pathological (heart failure, cirrhosis, SIAD), endocrine-related (adrenal insufficiency, hypothyroidism), or drug-induced (especially thiazides, SSRIs, antipsychotics, carbamazepine, NSAIDs). Hypotonic hyponatraemia is then subdivided into hypovolaemic (net sodium loss > water loss), euvolaemic (water gain with near-normal sodium stores, classically SIAD), and hypervolaemic (both sodium and water excess, but water excess predominates). Acute falls in sodium risk cerebral oedema; chronic hyponatraemia allows cerebral adaptation but becomes vulnerable to osmotic demyelination if corrected too rapidly.

Risk Factors

  • Thiazide or thiazide-like diuretic use (major iatrogenic risk)
  • Older age, especially with reduced renal diluting capacity
  • Polypharmacy (for example SSRIs, antipsychotics, anticonvulsants, ACE inhibitors/ARBs, PPIs, opioids, NSAIDs)
  • Female sex
  • Low body mass index and/or low solute intake
  • Heart failure, cirrhosis, chronic kidney disease, nephrotic states
  • Malignancy (especially small-cell lung cancer), CNS disease, pneumonia (SIAD triggers)
  • Post-operative stress, nausea, pain, endurance exercise, MDMA use
  • Hospital admission (hyponatraemia often present on admission or acquired during stay)

Clinical Features

Symptoms

  • Often asymptomatic when mild/chronic
  • Nausea, malaise, lethargy, fatigue
  • Headache, dizziness, reduced concentration, irritability
  • Confusion, disorientation, altered mood/cognition
  • Vomiting, drowsiness, seizures, coma in severe or rapid-onset cases
  • Gait disturbance and falls in chronic mild hyponatraemia

Signs

  • Volume depletion signs (dry mucosa, postural hypotension, tachycardia) in hypovolaemic states
  • Peripheral oedema, raised JVP, ascites in hypervolaemic states
  • Usually no overt oedema/dehydration in euvolaemic hyponatraemia (e. g. SIAD)
  • Reduced GCS or focal/brainstem features in severe cerebral oedema or osmotic demyelination
  • Underlying-cause clues (pigmentation/hypotension in Addison disease, stigmata of liver disease, heart failure signs)

Investigations

Repeat U&E with paired serum osmolality:Confirms true hypotonic hyponatraemia (low sodium with low serum osmolality); excludes pseudohyponatraemia/isotonic and hypertonic causes
Blood glucose:Raised glucose suggests translocational (hypertonic) hyponatraemia rather than true hypotonic excess-water state
Urine osmolality:Low (<100 mOsm/kg) suggests excess water intake/low solute intake; inappropriately high (>100 mOsm/kg) implies ADH effect
Urine sodium:Typically <30 mmol/L in extra-renal sodium loss or effective arterial underfilling; often >30 mmol/L in SIAD, renal salt loss, or diuretic effect
Clinical volume assessment:Classifies as hypo/eu/hypervolaemic, which is central to cause-directed management
Morning cortisol (and short Synacthen test if needed):Low cortisol supports adrenal insufficiency as reversible cause
TSH and free T4:Identifies hypothyroidism contributing to impaired free-water clearance
Renal, liver, cardiac assessment (creatinine/eGFR, LFTs, BNP/echo as indicated):Supports CKD, cirrhosis, or heart failure in hypervolaemic hyponatraemia
Medication and fluid intake review:Detects common iatrogenic and behavioural precipitants (thiazides, SSRIs, polydipsia, low-solute diet)
Chest imaging/CNS imaging when clinically indicated:Looks for SIAD drivers such as lung malignancy, pneumonia, intracranial pathology

Management

Lifestyle Modifications

  • Stop precipitating excess hypotonic fluid intake; in chronic euvolaemic/hypervolaemic states use fluid restriction (commonly 500–1000 mL/day, tailored to urine output/osmolality)
  • Increase dietary solute intake (salt/protein) where low-solute intake contributes
  • Falls prevention and bone-health review in chronic hyponatraemia
  • Avoid offending recreational triggers (for example MDMA) and educate on recurrence risk

Pharmacological Treatment

Emergency hypertonic therapy for severe or symptomatic hyponatraemia

  • Sodium chloride 3% IV 150 mL over 20 minutes, then reassess sodium and symptoms; may repeat up to two further times if severe symptoms persist

Use close monitoring (usually HDU/ICU-level). Target initial rise of about 4–6 mmol/L to control cerebral oedema, then slow correction. Do not exceed correction limits (generally <=10 mmol/L in first 24 h and <=8 mmol/L per 24 h thereafter; use stricter <=8 mmol/L/24 h in high-risk patients: alcoholism, malnutrition, liver disease, hypokalaemia, very low starting sodium). Over-rapid correction risks osmotic demyelination syndrome.

Cause-directed endocrine replacement

  • Hydrocortisone 100 mg IV stat in suspected adrenal crisis, then 200 mg over 24 h (continuous infusion or 50 mg IV/IM every 6 h)

Treat suspected adrenal insufficiency promptly; do not delay for test results if clinically unstable. Add isotonic saline resuscitation where hypovolaemic.

Diuretic and medication optimisation

  • Stop thiazide/thiazide-like diuretics (for example bendroflumethiazide, indapamide) when drug-induced hyponatraemia suspected
  • Review/withhold contributory drugs where possible (for example SSRIs, carbamazepine, antipsychotics, NSAIDs)

Medication withdrawal is often definitive in iatrogenic cases. Recheck sodium frequently after changes.

Vasopressin V2 receptor antagonist (specialist use, selected cases)

  • Tolvaptan initially 15 mg once daily; may increase to 30 mg then 60 mg once daily depending on response and sodium trajectory

Typically reserved for euvolaemic/hypervolaemic hyponatraemia (e. g. SIAD) under specialist supervision. Contraindicated in hypovolaemic hyponatraemia. Avoid with inability to sense/respond to thirst, anuria, pregnancy/breastfeeding, and significant liver-risk scenarios; monitor sodium closely to avoid rapid correction.

Adjuncts in chronic SIAD when fluid restriction fails (specialist)

  • Demeclocycline 600–1200 mg daily in divided doses (off-label in many settings)

Risk of nephrotoxicity and photosensitivity; avoid in significant renal impairment, pregnancy, and children. Consider only after specialist review.

Complications

  • Cerebral oedema with raised intracranial pressure, seizures, coma, and possible cardiorespiratory arrest in acute/severe cases
  • Osmotic demyelination syndrome (typically 2–6 days after over-rapid correction), causing dysarthria, dysphagia, quadriparesis, parkinsonism, or death
  • Gait disturbance, falls, fragility fractures, and osteoporosis in chronic hyponatraemia
  • Non-cardiogenic pulmonary oedema in acute water intoxication (e. g. endurance events, MDMA use)
  • Increased hospital morbidity, length of stay, readmission, and mortality

Prognosis

Outcome depends on acuity, severity, speed of correction, and underlying cause. Mild chronic hyponatraemia may appear stable but is linked to falls and frailty; acute severe hyponatraemia carries high neurological risk. Prognosis improves with prompt cause identification, careful volume/osmolality-guided treatment, and strict avoidance of over-rapid sodium correction.

Sources & References

💊BNF Drug References(18)

✅NICE Guidelines(1)

📖Textbook References(2)

  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 255)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 255)[context]

Sources

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