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Hyponatraemia in an elderly patient after a fall

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Hyponatraemia in an elderly patient after a fall

An 81-year-old woman is brought in after a mechanical fall at home. She takes hydrochlorothiazide and sertraline. She is confused but has no focal neurology. Sodium 116 mmol/L, potassium 3.4 mmol/L, chloride 84 mmol/L, bicarbonate 26 mmol/L, glucose 6 mmol/L, urine osmolality 480 mOsm/kg, urine sodium 62 mmol/L. She is clinically euvolaemic with no oedema and normal jugular venous pressure. She is passing urine. CT head shows no acute bleed. Her confusion has been progressive over 5 days according to her daughter.

1. Classify the hyponatraemia, identify the likely cause, and state whether she needs urgent hypertonic saline.

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Classification. This is chronic hyponatraemia (present for at least 5 days by history, so adaptation has occurred) that is hypo-osmolar and euvolaemic. The biochemistry fits SIADH: urine osmolality 480 mOsm/kg is inappropriately concentrated relative to a low plasma osmolality, urine sodium 62 mmol/L is high with normal dietary salt intake, and she is clinically euvolaemic with no oedema. Thyroid and adrenal function should be checked to exclude other causes, and a careful drug history taken.

Cause. Two culprits are obvious: hydrochlorothiazide, which causes sodium wasting and volume depletion with ADH stimulation, and sertraline, a recognised cause of SIADH. The combination is a classic trap. The fall may itself be a consequence of the hyponatraemia rather than an independent event.

Does she need hypertonic saline? She has confusion, which is a moderate symptom. Current guidance distinguishes severe symptoms (seizures, coma, vomiting, cardiorespiratory distress) from moderate (confusion, headache, nausea). Severe symptoms warrant immediate 3% saline boluses. Moderate symptoms in chronic hyponatraemia generally do not - the risk of osmotic demyelination from over-rapid correction outweighs the benefit, and treatment should be cautious. However, if her conscious level deteriorates to coma or she seizes, give 100 to 150 mL of 3% saline over 20 minutes and repeat up to three times, targeting a small initial rise.

Immediate actions. Stop the thiazide and sertraline, allow free access to oral salt and fluid, and monitor sodium every 4 to 6 hours.

2. Describe your correction targets and what you would do if the sodium rose too fast.

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Targets. In chronic hyponatraemia the correction limit is 8 to 10 mmol/L in the first 24 hours and 18 mmol/L in the first 48 hours. In a patient with additional risk factors for osmotic demyelination - age over 65, alcohol use, malnutrition, hypokalaemia (she has a potassium of 3.4) - aim for the lower end, no more than 8 mmol/L in 24 hours. The goal is a modest, controlled rise, not a normal sodium.

Monitoring. Check sodium every 4 to 6 hours during active correction, and more often if the rise is brisk. Note that after stopping a thiazide, a brisk water diuresis can cause the sodium to rise rapidly and unpredictably; this is the commonest mechanism of over-correction.

If the sodium rises too fast.

  • Stop any active sodium administration and any fluid restriction that is driving the rise.
  • Give free water: oral water or 5% dextrose intravenously.
  • Consider desmopressin to blunt the water diuresis - this is now a recognised strategy to prevent and treat over-correction.
  • If the rise has already exceeded the limit, re-lower the sodium deliberately with desmopressin and 5% dextrose under close monitoring, aiming to bring it back within the safe range.
  • Seek specialist (nephrology or endocrine) advice early.

Counsel the team. Document the targets and the plan explicitly, because the greatest risk in this patient is not the low sodium itself but an over-enthusiastic correction by an on-call doctor who sees 116 mmol/L and reaches for saline.