A 74-Year-Old Woman with Hyponatraemia, Falls and a Normal Volume Status
A 74-year-old woman is admitted after two falls at home. She is confused and lethargic. She takes bendroflumethiazide 2.5 mg daily for hypertension and has done so for 12 years; her GP recently added indapamide 1.5 mg SR. She is clinically euvolaemic: JVP not raised, no oedema, mucous membranes moist, BP 118/70 mmHg (lying) and 100/62 mmHg (standing). Serum sodium is 116 mmol/L, potassium 3.1 mmol/L, chloride 84 mmol/L, bicarbonate 26 mmol/L, urea 3.0 mmol/L, creatinine 72 micromol/L. Serum osmolality is 248 mOsm/kg. Urine osmolality is 420 mOsm/kg and urine sodium is 62 mmol/L. TSH, cortisol and glucose are normal.
1. Classify the hyponatraemia and explain the significance of the urine studies.
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This is chronic (likely >48 h) hypotonic hyponatraemia with serum osmolality 248 mOsm/kg - true hypo-osmolar hyponatraemia, not pseudohyponatraemia or hyperosmolar hyponatraemia.
Volume status: clinically euvolaemic, but with postural hypotension (BP drop of 18 mmHg systolic) suggesting subtle volume depletion. The history of a thiazide plus indapamide is the key clue.
Urine studies - the discriminator:
- Urine osmolality 420 mOsm/kg (>100) indicates ADH is active and the kidney is concentrating - this excludes primary polydipsia (where urine would be dilute, <100).
- Urine sodium 62 mmol/L (>30) in a euvolaemic patient is consistent with SIADH or with thiazide-induced hyponatraemia (thiazides cause natriuresis plus ADH-driven water retention).
- The low urea (3.0) supports dilutional hyponatraemia.
Most likely diagnosis: thiazide-induced hyponatraemia, possibly compounded by SIADH-like physiology. Thiazides impair free water clearance and cause sodium loss; they are the commonest cause of drug-induced hyponatraemia in older women. The recent addition of indapamide is the precipitant. Other causes to exclude: adrenal insufficiency (cortisol normal), hypothyroidism (TSH normal), SIADH from other drugs, and occult malignancy.
Severity: Na 116 with confusion and falls = severe symptomatic hyponatraemia requiring urgent but controlled correction.
2. Outline your correction strategy, including the rate of correction and the risks you are trying to avoid.
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Principles: treat the cause, correct sodium slowly, and avoid osmotic demyelination.
Immediate steps:
- Stop the thiazide and indapamide - this is the single most important intervention. Also review other culprit drugs (PPIs, SSRIs, carbamazepine).
- Assess for severe symptoms - confusion and falls constitute severe symptoms. If there were seizures, coma or respiratory compromise, give a 100 mL bolus of 3% hypertonic saline over 10 minutes, repeated up to 3 times, aiming for a 4-6 mmol/L rise to reverse the acute crisis.
- In this patient (confusion, not seizing): cautious hypertonic saline or slow IV saline with frequent monitoring is appropriate. A reasonable target is a rise of 4-6 mmol/L in the first 6 hours, then ≤8 mmol/L in 24 hours and ≤18 mmol/L in 48 hours.
- Monitor sodium every 2-4 hours initially - thiazide-induced hyponatraemia can correct rapidly once the drug is stopped, especially with volume repletion.
Risks:
- Over-correction → osmotic demyelination syndrome (central pontine myelinolysis), especially in chronic hyponatraemia, malnutrition, alcoholism, liver disease. If over-correction occurs, re-lower sodium with desmopressin plus free water (5% dextrose).
- Under-correction → cerebral oedema, seizures, death.
Other measures: correct potassium (K 3.1 - potassium repletion raises sodium), treat the cause, and avoid rapid fluid shifts. If SIADH is confirmed after drug withdrawal, fluid restriction is the mainstay; demeclocycline or tolvaptan are second-line.
3. Two days later her sodium is 134 mmol/L and she is clinically improved. What is the long-term plan and what counselling does she need?
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Long-term plan:
- Medication review: thiazides are permanently contraindicated. Use an alternative antihypertensive (e.g. ACE inhibitor/ARB, calcium channel blocker, or beta-blocker). Document the adverse drug reaction clearly.
- Identify and avoid other precipitants: SSRIs, PPIs, carbamazepine, NSAIDs, and excessive fluid intake.
- Monitor: check sodium at follow-up (e.g. 1-2 weeks, then as needed), especially if any new drug is started.
- Investigate any residual cause: if sodium does not normalise off the drug, reinvestigate for SIADH (malignancy, pulmonary disease, CNS disease) with chest imaging and appropriate screening.
Counselling:
- Explain that the diuretic caused a dangerous drop in salt levels, causing confusion and falls.
- Advise that she must tell any doctor or pharmacist about this reaction before starting new medicines.
- Warn about symptoms of hyponatraemia: confusion, headache, nausea, unsteadiness, falls - and to seek urgent review.
- Discuss fall prevention: home safety assessment, review of other sedating medications, and consideration of bone health (DEXA, vitamin D, calcium) given the falls.
- Emphasise the importance of not over-restricting or over-drinking fluids without advice.