Symptomatic Hyponatraemia with Seizure and the Risk of Overcorrection
A 58-year-old woman with treatment-resistant depression is brought in after a witnessed generalised tonic–clonic seizure lasting 90 seconds. She started hydrochlorothiazide 3 weeks ago for hypertension and reports 2 weeks of nausea, poor appetite and drinking large volumes of water. She is confused but protecting her airway. Blood pressure 138/82 mmHg, heart rate 88/min, SpO₂ 97% on room air. Serum sodium 108 mmol/L, potassium 3.1 mmol/L, chloride 74 mmol/L, bicarbonate 24 mmol/L, glucose 96 mg/dL, serum osmolality 232 mOsm/kg, urine osmolality 410 mOsm/kg, urine sodium 68 mmol/L. Thyroid function and cortisol are normal, and she has no oedema or ascites. CT head shows no acute haemorrhage or mass. Her weight is 60 kg.
1. Confirm the diagnosis and explain the immediate management of her seizure, including a calculation of how much 3% saline is needed to raise the sodium by 4–6 mmol/L.
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Diagnosis. She has severe hypotonic hyponatraemia: serum osmolality 232 mOsm/kg, urine osmolality 410 mOsm/kg (inappropriately concentrated), urine sodium 68 mmol/L, clinically euvolaemic, with normal thyroid and adrenal function. The combination of a thiazide, high water intake and an SIADH-like picture is classic thiazide-induced hyponatraemia. The seizure makes this a neurological emergency requiring hypertonic saline, not fluid restriction.
Immediate treatment. Give 3% saline 100–150 mL as a bolus over 10–20 minutes, aiming to raise serum sodium by 4–6 mmol/L to abort the seizure; the bolus may be repeated up to three times until symptoms improve or the sodium has risen by 4–6 mmol/L. Protect the airway, give oxygen and monitor continuously. Treat the seizure with a benzodiazepine if it recurs; hypoxic or prolonged seizures worsen cerebral oedema.
Calculation. Total body water is roughly 0.5 × 60 kg = 30 L. Sodium needed to raise the sodium by 6 mmol/L = 30 × 6 = 180 mmol. 3% saline contains 513 mmol/L, so about 350 mL would deliver 180 mmol. This figure is used to plan the rate, not to justify a rapid infusion: the symptomatic bolus is given first, and the remainder of the 24-hour correction is paced to stay within the limit.
Electrolytes. Correct the potassium, which contributes to the sodium rise and, like the chronic hyponatraemia itself, increases the risk of osmotic demyelination.
2. Write the correction plan for the next 24 hours, including the safe rate of correction, monitoring intervals and how you would prevent overcorrection.
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Target rate. Because this is chronic hyponatraemia of at least 2 weeks' duration, limit correction to about 6–8 mmol/L in the first 24 hours (and no more than 8 mmol/L in any 24-hour period), with a lower limit of 4–6 mmol/L if she is high risk. The initial 4–6 mmol/L used to stop the seizure counts towards that total. Her serum sodium should therefore not exceed roughly 114–116 mmol/L on day one.
Plan. After the bolus, stop the 3% saline once the seizure has resolved. Stop hydrochlorothiazide permanently. Restrict free water (for example 800–1000 mL/day) and, if the sodium continues to rise faster than desired, use the desmopressin clamp: desmopressin 1–2 µg intravenously or subcutaneously plus 5% dextrose to match urine output, which stabilises the sodium and allows controlled correction. Do not use vasopressin receptor antagonists acutely in a seizing patient.
Monitoring. Check serum sodium every 2 hours during active correction, then every 4 hours once the rate is stable. Measure urine output and urine osmolality to understand the trajectory, and monitor for symptoms of osmotic demyelination (dysarthria, dysphagia, paraparesis, behavioural change).
Avoid traps. Overly rapid correction is the main iatrogenic danger; hypokalaemia, malnutrition, alcohol use, liver disease and low body weight all lower the safe ceiling. Correct potassium cautiously, because each 1 mmol/L rise in potassium can contribute to the sodium rise. Involve a nephrologist or endocrinologist early, and document the target range and stop rules in the chart.
3. At 12 hours the repeat sodium is 122 mmol/L. What has happened, why is it dangerous, and what would you do now?
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What has happened. The sodium has risen 14 mmol/L in 12 hours, far beyond the 8 mmol/L per 24-hour ceiling. The likely drivers are the 3% saline already given, cessation of the thiazide, delayed water diuresis and correction of hypokalaemia, all of which can combine to produce an unanticipated rapid rise.
Why it is dangerous. Rapid correction of chronic hyponatraemia causes osmotic demyelination, typically 2–6 days later, with dysarthria, dysphagia, quadriparesis, pseudobulbar palsy and the locked-in syndrome. The risk is highest in patients with chronic hyponatraemia, hypokalaemia, malnutrition or alcohol use.
What to do now. Actively re-lower the sodium to within the safe window, aiming for no more than 8–10 mmol/L above baseline in 24 hours, that is, roughly 116–118 mmol/L. Give desmopressin 1–2 µg intravenously or subcutaneously to stop the water diuresis, then give 5% dextrose (for example 3–5 mL/kg/h) with electrolyte-free water to bring the sodium down. Recheck the sodium every 1–2 hours during re-lowering, since relowering is itself easy to overshoot.
Further steps. Relowering is most effective if started within 24–48 hours of the overcorrection. Monitor neurologically and image the brain with MRI if symptoms of demyelination appear; there is no specific antidote, so prevention by protocol is the real treatment. Document the event, review what allowed the overshoot, and debrief the team so that the next patient gets a desmopressin clamp before the sodium starts to run.