The Collapsed Runner with Dilutional Hyponatremia

Tonicity: This is hypotonic (true) hyponatremia. Serum sodium 118 mmol/L with measured serum osmolality 248 mOsm/kg confirms hypotonicity; a normal or high osmolality would instead suggest pseudohyponatremia or hyperglycemia-driven dilution, neither of which fits here (glucose 6.1 mmol/L).

Volume status: She is euvolemic to mildly hypervolemic, not hypovolemic. Supporting features:

• Moist mucous membranes, visible JVP at 30 degrees, no edema - no signs of depletion or overload.
• Bradycardia with a normal blood pressure argues against significant volume depletion (which typically produces tachycardia).
• Urine sodium 48 mmol/L with urine osmolality 420 mOsm/kg indicates the kidney is not conserving sodium and is concentrating urine - the expected renal response to hypovolemia would be a low urine sodium (<20–30 mmol/L).
• The high urine osmolality with dilute plasma points to ADH excess, which in this setting is inappropriate ADH secretion driven by nausea, vomiting, and possibly exercise-related non-osmotic stimuli, compounded by free-water intake exceeding excretory capacity.

Integration: The picture is exercise-associated dilutional hyponatremia - high free-water intake exceeding renal diluting capacity, with ADH activity maintained by nausea and stress. The history of large water intake is consistent but not sufficient on its own; the biochemistry and bedside signs establish euvolemia with impaired free-water excretion. This distinction matters because treating her as hypovolemic with isotonic saline would worsen the hyponatremia.

Immediate priorities:

1. Airway and neurological monitoring - she is drowsy with slurred speech; continuous observation, airway protection if consciousness declines, and serial neurological checks for seizures or deteriorating GCS.
2. Stop free-water intake - no oral fluids.
3. Hypertonic saline for symptomatic hyponatremia. Because she has symptoms beyond mild (vomiting, confusion), guidelines support a 100 mL bolus of 3% hypertonic saline over 10–20 minutes, repeated up to three times if symptoms persist, aiming for a rise of about 4–6 mmol/L to relieve cerebral edema. Vomiting itself is a red-flag symptom because it can rapidly escalate to seizures and herniation.
4. Treat the stimulus for ADH - antiemetic therapy; consider a small dose of intravenous furosemide only if she becomes volume-overloaded, not routinely.
5. Do not give isotonic saline as the default - in a euvolemic SIADH-like picture, saline can worsen hyponatremia by being excreted and leaving free water behind.

Correction limits and reasoning:

• Maximum 8–10 mmol/L in the first 24 hours, and ≤8 mmol/L in any 24-hour period in patients at high risk of osmotic demyelination.
• Her risk factors for osmotic demyelination are substantial: baseline sodium ≤120 mmol/L, and the presence of vomiting, malnutrition risk, and possibly low body mass. These lower the safe ceiling.
• Check serum sodium every 2–4 hours during active correction, then less frequently once stable.
• If correction overshoots, re-lower the sodium with desmopressin plus free water (or dextrose 5%) rather than simply stopping - the brain injury from over-rapid correction is often irreversible.

Disposition: Admit to a monitored bed; she is not a candidate for outpatient management given neurological symptoms and a sodium of 118 mmol/L.

Assessment: She has risen 8 mmol/L in roughly two hours, which is far too fast. The absolute change (8 mmol/L) is already at the upper limit for a 24-hour period, and it occurred in a fraction of that time. Her risk profile - baseline sodium 118 mmol/L, vomiting, possible low body mass - puts her at high risk of osmotic demyelination syndrome, which can present days later with dysarthria, dysphagia, quadriparesis, and locked-in syndrome.

Why the rise was unexpectedly large:

• A single 100 mL bolus of 3% saline raises sodium by a predictable amount (roughly 2–3 mmol/L in a 58 kg woman), so the remainder of the rise reflects renal free-water excretion once the ADH stimulus (nausea) was controlled by the antiemetic. This is the classic "aquaresis" overshoot seen when the cause of ADH secretion is removed.
• The lesson is that sodium must be rechecked frequently during active correction, and that the trajectory can accelerate once the underlying stimulus resolves.

Action:

1. Actively re-lower the sodium rather than merely observing. Give desmopressin 1–2 micrograms to stop further free-water loss, and administer intravenous 5% dextrose (or free water by other routes) to bring the sodium back down.
2. Target a re-lowering to below the 8–10 mmol/L cumulative ceiling, ideally aiming to keep the total 24-hour rise ≤8 mmol/L given her risk factors.
3. Recheck sodium hourly until the trajectory is controlled.
4. Monitor neurologically for the next several days; MRI is not immediately diagnostic and should not delay correction of the trajectory.
5. Document the event and review the protocol to ensure that boluses are followed by mandated early recheck, and that antiemetic use is anticipated as a trigger for aquaresis.