Sodium 114 in a drowsy elderly woman on a thiazide

Tonicity Measured osmolality 240 mOsm/kg against a calculated value of roughly 2 × 114 + glucose/18 ≈ 233 establishes hypotonic hyponatraemia. Pseudo-hyponatraemia (normal osmolality) and hypertonic hyponatraemia (hyperglycaemia, mannitol) are excluded.

Volume and the urine data Vomiting and dry mucosae suggest hypovolaemia, but in true hypovolaemia with ongoing losses, urine sodium should fall below 20–30 mmol/L to conserve salt. A urine sodium of 62 mmol/L with a urine osmolality of 470 mOsm/kg means the kidney is both natriuretic and unable to dilute - concentrated urine that is inappropriately concentrated for a serum osmolality of 240. That pattern points to non-osmotic ADH release with thiazide-related salt wasting. The low urea (20 mg/dL) and low uric acid (2.0 mg/dL) with a normal creatinine argue against true volume depletion and are typical of the vasopressin-excess state.

Synthesis A mixed picture: thiazide-induced hyponatraemia (impaired diluting capacity, sodium loss, plus ADH release from vomiting) compounded by sertraline-associated SIADH and severe hypokalaemia. Adrenal insufficiency should still be excluded with a morning cortisol; hypothyroidism is already excluded.

The order is unsafe The hyponatraemia is of unknown but probably chronic duration, and she has two ODS risk factors (age and hypokalaemia) plus a low body weight. Saline in a patient with concentrated urine and continued ADH effect can worsen the sodium by desalination; conversely, if ADH falls once the vomiting stops and the thiazide is withdrawn, a brisk water diuresis can raise the sodium 10–15 mmol/L in hours. Either direction is wrong.

Safe plan

• Stop hydrochlorothiazide and sertraline immediately, and check a morning cortisol.
• Correct potassium: every 1 mmol/L rise in potassium raises the sodium by about 1 mmol/L, so potassium replacement must be counted in the sodium budget.
• If she is genuinely hypovolaemic, use cautious isotonic saline (about 25–30 mL/kg/day) with sodium checks every 2–4 hours; if euvolemic SIADH dominates, fluid restriction (about 800–1,000 mL/day) or a single 100 mL bolus of 3% saline.
• Limit correction to 8–10 mmol/L in 24 hours and 18 mmol/L in 48 hours.

If she seizes Give 3% saline 100–150 mL over 10–20 minutes, aiming for a 4–6 mmol/L rise to abort the seizure, then stop, recheck and escalate to intensive care. Use 100 mL aliquots, not a free-running infusion, and document the aim: symptomatic relief, not normalisation.

Recognition A 7 mmol/L rise in six hours projects to about 28 mmol/L in 24 hours - a clear overcorrection, probably from a spontaneous water diuresis after withdrawal of the thiazide and cessation of vomiting, possibly aggravated by saline. Overcorrection is the engine of osmotic demyelination syndrome, which is a retrospective diagnosis: it appears 2–6 days later with dysarthria, dysphagia, behavioural change, flaccid quadriparesis, and can progress to 'locked-in' state. MRI changes in the central pons may lag by days.

Immediate actions

1. Stop the saline and withhold any free water restriction.
2. Give desmopressin 2 micrograms IV or subcutaneously to switch off the free water clearance, and replace with 5% dextrose at a rate calculated to reduce the sodium back to a cumulative rise of 8–10 mmol/L in 24 hours - the DDAVP clamp.
3. Measure urine output, urine osmolality and electrolytes hourly; recheck serum sodium every 2 hours until it is stable and clearly within the safe envelope.
4. Involve the intensive care team and document the plan and the reasoning.

Teaching point If overcorrection exceeds about 12 mmol/L, deliberate re-lowering is indicated even in an asymptomatic patient, because the risk window has not yet closed.