Symptomatic hyponatraemia in an older adult on a thiazide
A 78-year-old woman is brought in by her daughter with 2 days of confusion and one generalised tonic-clonic seizure lasting about 1 minute. She has hypertension treated with hydrochlorothiazide 25 mg daily and depression treated with fluoxetine 20 mg daily. She is drowsy but rousable, with no focal neurology and no signs of dehydration or oedema. Serum sodium is 112 mmol/L, serum osmolality 248 mOsm/kg, urine osmolality 480 mOsm/kg, and urine sodium 60 mmol/L. Non-contrast head CT is normal. The hospital has 3% hypertonic saline, but no intensive care unit; the ward nurse-to-patient ratio is 1:6 and hourly neurological observations cannot be guaranteed overnight. The daughter asks whether the sodium can be corrected quickly because the seizure frightened her.
1. What is the immediate treatment for this patient, and what correction rate would you prescribe? Explain the risk you are trying to avoid.
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This is severe symptomatic hyponatraemia, probably due to thiazide use and possibly SIADH from fluoxetine. The seizure makes it an emergency, so hypertonic saline is indicated despite the ward staffing limitations.
Immediate treatment:
- Give 3% sodium chloride 100 mL IV over 10 minutes. If the seizure persists or neurological symptoms remain severe, repeat up to two more times, checking sodium between boluses if possible.
- Aim for a 5 mmol/L rise in the first hour or until symptoms improve, not a full correction to normal.
- After symptoms improve, stop the hypertonic bolus and aim for a total rise of no more than 8–10 mmol/L in 24 hours.
Risk being avoided: overcorrection causes osmotic demyelination syndrome, which can produce irreversible neurological damage. The daughter needs a clear explanation that the first bolus is to stop the seizure, not to make the sodium normal quickly. The sodium should be checked every 2–4 hours initially, and the patient needs a setting where seizures and neurological deterioration can be recognised. If the ward cannot provide that, transfer to a monitored bed after the first bolus is the safer plan.
2. Which medications and other factors should be reviewed, and how would you counsel the daughter?
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The likely contributors are hydrochlorothiazide and fluoxetine. Thiazides cause hyponatraemia through sodium loss and impaired dilution of urine; fluoxetine can cause SIADH. Both should be reviewed with the prescriber. The thiazide should be stopped during the acute illness and not simply restarted without rechecking sodium. Fluoxetine should be reviewed for an alternative antidepressant, but it should not be stopped abruptly without a plan because of discontinuation effects.
Other factors to check include recent vomiting or diarrhoea, fluid intake, alcohol use, thyroid function, and adrenal function if the cause remains unclear. After the acute phase, fluid restriction of about 800–1000 mL/day may be appropriate if SIADH is confirmed.
The daughter should be told that the seizure was caused by a low sodium level, that the first treatment is a concentrated salt solution to raise the sodium safely, and that rapid full correction can harm the brain. She should also be warned that confusion may take days to settle and that the sodium will be rechecked frequently. The explanation should acknowledge her fear without promising a quick normalisation.