Hyponatremia

Hyponatraemia is serum sodium below 135 mmol/L, the commonest electrolyte disorder (up to 30% of hospitalised patients), reflecting excess water relative to sodium and usually hypo-osmolar.

• Severity: mild 130–134, moderate 125–129, profound under 125 mmol/L; acute if under 48 hours, chronic if longer.
• Causes by volume status and tonicity:
  • Hypovolaemic: renal (diuretics, salt-wasting nephropathy, cerebral salt wasting, mineralocorticoid deficiency) or extrarenal (vomiting, diarrhoea, burns, third spacing).
  • Euvolaemic: SIADH, glucocorticoid deficiency, hypothyroidism, primary polydipsia, low solute intake (tea and toast, beer potomania), exercise-associated.
  • Hypervolaemic: heart failure, cirrhosis, nephrotic syndrome, renal failure.
  • Non-hypotonic: pseudohyponatraemia (hyperlipidaemia, hyperproteinaemia), hyperglycaemia (lowers by 2.4 mmol/L per 100 mg/dL above normal), mannitol.
• Complications: cerebral oedema with seizures, coma, herniation (acute); osmotic demyelination syndrome with overcorrection of chronic hyponatraemia; falls, gait disturbance, fractures.

• Mild/chronic: nausea, headache, forgetfulness, unsteadiness, falls, fatigue.
• Moderately severe: confusion, vomiting, disorientation.
• Severe: seizures, coma, respiratory arrest, brain herniation.
• Clinical volume status: hypovolaemia (orthostasis, dry mucosa), hypervolaemia (oedema, ascites, raised JVP), euvolaemia.
• Drugs: thiazides, SSRIs, carbamazepine, oxytocin, vincristine, MDMA, desmopressin.

• Serum sodium, serum osmolality (confirm hypotonic: under 275 mOsm/kg), glucose, urea, creatinine, lipids, protein.
• Urine osmolality (under 100 mOsm/kg implies primary polydipsia or low solute), urine sodium (over 30 mmol/L in SIADH, renal salt loss; under 30 in extrarenal loss, heart failure, cirrhosis).
• Uric acid (low in SIADH), TSH, morning cortisol, potassium.
• Algorithm: low urine osmolality → polydipsia/low solute; high urine osmolality with urine sodium over 30 → SIADH, diuretics, adrenal insufficiency, salt-wasting; low urine sodium → hypovolaemic extrarenal loss or hypervolaemic states.
• Evaluate SIADH causes: pulmonary (pneumonia, small cell cancer), CNS (stroke, haemorrhage, meningitis), malignancy, drugs, pain, nausea.
• Response to isotonic saline (rise in sodium indicates hypovolaemia; fall indicates SIADH).

Severely symptomatic hyponatraemia (seizures, coma, vomiting, somnolence)

• 3% hypertonic saline 150 mL IV over 20 minutes (or 2 mL/kg), repeat up to two further times until sodium rises 5 mmol/L or symptoms improve; target rise 4–6 mmol/L in first 6 hours; do not exceed 10 mmol/L in first 24 hours and 8 mmol/L each following 24 hours (6 mmol/L in high-risk patients: alcoholism, malnutrition, hypokalaemia, liver disease).
• If overcorrection occurs: 5% dextrose 3 mL/kg/h and desmopressin 2 micrograms IV every 6–8 hours to re-lower sodium.

Moderately symptomatic or chronic

• Treat cause; fluid restriction.
• Hypovolaemic: isotonic saline 0.5–1 L (monitor for brisk water diuresis and overcorrection once volume restored).
• SIADH: fluid restriction 800–1000 mL/day; salt tablets 3 g/day with loop diuretic furosemide 20–40 mg; urea 15–30 g daily; tolvaptan 15 mg daily titrated to 60 mg (start in hospital, avoid in liver disease, monitor sodium every 6 hours, never with fluid restriction in first day); empagliflozin 10–25 mg; demeclocycline 600–1200 mg/day (nephrotoxic).
• Hypervolaemic: fluid and sodium restriction, loop diuretic, treat heart failure; tolvaptan in selected; avoid in cirrhosis (hepatotoxicity).
• Adrenal insufficiency: hydrocortisone 100 mg IV then 50 mg every 6 hours; hypothyroidism: levothyroxine.
• Stop offending drugs.
• Exercise-associated: 3% saline 100 mL bolus; oral fluid restriction.
• Monitor sodium every 2–4 hours during correction; avoid hypotonic fluids; correct hypokalaemia (raises sodium), and recognise potassium contribution.
• Prevent ODS: monitor neurological status; if ODS develops (dysarthria, quadriparesis, locked-in), consider re-lowering sodium.