Hyponatraemia in a woman starting a thiazide while on an SSRI
A 68-year-old woman is brought to the emergency department by her daughter with 2 days of confusion and one episode of vomiting. She started hydrochlorothiazide 25 mg daily three weeks earlier for newly diagnosed hypertension and has taken sertraline 50 mg daily for four years. She is afebrile, pulse 88, blood pressure 132/78 lying and 120/70 standing, mucous membranes moist, no oedema, and her weight is unchanged from a clinic visit two weeks ago. She is drowsy but rousable and oriented to person only. Investigations: sodium 116 mmol/L, potassium 3.4, chloride 88, bicarbonate 24, urea 3.1 mmol/L, creatinine 78 µmol/L, glucose 5.2 mmol/L, serum osmolality 248 mOsm/kg, urine osmolality 486 mOsm/kg, urine sodium 62 mmol/L. TSH and a 9 am cortisol are normal. She denies excessive water drinking and there is no history of heavy beer intake.
1. Which mechanism best explains the hyponatraemia, and which findings support and argue against your interpretation?
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The picture fits thiazide-induced hyponatraemia with a SIADH-like physiology, probably potentiated by sertraline.
Supporting features: true hypo-osmolar hyponatraemia (serum osmolality 248), urine osmolality that is inappropriately high (486, far above the ~100 expected with maximum dilution), urine sodium above 40 mmol/L despite low-normal volume, low urea and normal creatinine indicating dilution rather than dehydration, and clinical euvolemia with stable weight and no postural drop.
Against alternatives: volume depletion would usually give a postural drop, high urea, and urine sodium under 20–30; primary polydipsia would give a low urine osmolality; adrenal insufficiency and hypothyroidism are excluded by normal cortisol and TSH. Hyperglycaemia and pseudohyponatraemia are excluded by the glucose and the measured osmolality.
Mechanistically, thiazides block the distal convoluted tubule sodium-chloride cotransporter, producing mild natriuresis and volume contraction that stimulates antidiuretic hormone, while also reducing the kidney's capacity to dilute urine. The result is water retention. SSRIs are a recognised additional cause of SIADH, so the two drugs may act together. The vomiting may have contributed but is unlikely to be the primary driver given the high urine sodium and normal urea. Sodium should be rechecked after the thiazide is withdrawn to confirm the diagnosis.
2. Outline your immediate management, including the correction target, the role of hypertonic saline, and what monitoring you would arrange.
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This patient is symptomatic but not having seizures or coma, so she does not automatically need hypertonic saline. Management is: stop hydrochlorothiazide immediately; cardiac monitor and hourly neurological observations; fluid restriction of roughly 800–1000 mL per 24 hours; treat vomiting; check sodium 4–6 hourly initially.
Hypertonic 3% saline as a 100–150 mL bolus over 20 minutes is indicated if severe symptoms develop - seizure, reduced conscious level, vomiting with aspiration risk, or signs of cerebral oedema. The aim of a bolus is a rapid 4–6 mmol/L rise to relieve cerebral oedema, not normalisation.
The overall correction target is a rise of no more than 8 mmol/L in the first 24 hours for a patient at standard risk, since overcorrection risks osmotic demyelination, particularly with chronic hyponatraemia, low body weight, alcohol use, malnutrition or liver disease. If sodium overshoots the target, give free water orally or as 5% dextrose with desmopressin to re-lower it.
Isotonic saline is generally unhelpful in SIADH and may worsen the sodium by being excreted concentrated. In this patient, stopping the thiazide alone often produces a brisk water diuresis, so watch for overcorrection. Look for a precipitant (chest infection, pain, nausea) and review the sertraline with the prescriber - do not stop it abruptly without a plan.
3. What medication changes and discharge plan would you make, and what counselling does she need?
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Stop the hydrochlorothiazide permanently and record it as an adverse reaction. Replace it with an agent that does not cause hyponatraemia - for example amlodipine, already familiar to her, or an ACE inhibitor or angiotensin receptor blocker with renal function and potassium checks. Thiazides are a common and preventable cause of severe hyponatraemia, especially in older women and in the first weeks of therapy.
The sertraline should not simply be stopped: withdrawal can cause relapse of depression and discontinuation symptoms. Discuss with her and the prescriber whether it is still indicated, and if continued, document the interaction and check sodium again at about one and two weeks after any dose change. If the depression is in remission, a supervised taper may be reasonable.
Before discharge: confirm sodium is rising appropriately and not overshooting, check that she is eating and drinking, involve the daughter in monitoring for drowsiness or confusion, and provide written sick-day advice - during vomiting, diarrhoea or heat, hold the thiazide-type drugs and seek review. Arrange a repeat sodium and renal function at about one week. Reassess falls risk and driving. If she lives alone, ensure a follow-up appointment is booked rather than relying on her to present.