Collapse After the Marathon: Water, Sodium and the Brain
A 28-year-old club runner completes a marathon in 4 h 10 min on a warm, humid day (28 °C, 70% relative humidity). She weighs 58.0 kg before and 59.5 kg after, having drunk about 5 L of plain water and eaten little salty food. Twenty minutes after finishing she collapses with confusion, nausea and a severe headache. Paramedics record plasma sodium 121 mmol/L (reference 135–145), plasma osmolality 255 mOsm/kg (reference 275–295), urine osmolality 110 mOsm/kg and urine sodium 18 mmol/L. She is given 500 mL of 0.9% saline over 30 minutes and improves. A bystander suggests giving her more water because 'she is dehydrated after running'. The ambulance crew has 3% hypertonic saline available but no point-of-care sodium meter beyond the hospital.
1. Explain how drinking 5 L of plain water produced hyponatraemia. Use the weight change and the urine data in your answer.
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She gained 1.5 kg, about 1.5 L, while drinking 5 L, so she retained a substantial fraction of the water. Plasma sodium 121 mmol/L and osmolality 255 mOsm/kg confirm hypotonic hyponatraemia. Sweat contains sodium, so endurance exercise loses salt as well as water; replacing losses with plain water dilutes the extracellular fluid. The low urine osmolality of 110 mOsm/kg shows that ADH was suppressed at the time of sampling, so the kidneys were attempting to excrete dilute urine. However, maximal free-water clearance is roughly 0.8–1.0 L/h, and she probably drank faster than this, especially if exercise, nausea and stress raised ADH intermittently. When intake exceeds excretion, water is retained, extracellular osmolality falls and water moves by osmosis into cells, including brain cells. The weight gain, not dehydration, is the key evidence.
2. Explain why she developed confusion and headache, and why giving more plain water would be dangerous. Why was 0.9% saline appropriate here?
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Brain cells swell because water moves down its osmotic gradient from the hypotonic extracellular fluid into the intracellular compartment. The skull limits expansion, so even a small increase in brain volume raises intracranial pressure and causes headache, nausea and confusion; if untreated, seizures or herniation can follow. Giving more plain water would lower plasma osmolality further and worsen the swelling. The 0.9% saline is slightly hypertonic relative to her plasma, about 308 mOsm/kg versus 255, and expands the extracellular volume; with ADH suppressed, the kidneys can then excrete the excess water and the sodium concentration rises. If she had severe symptoms or seizures, 3% hypertonic saline in small boluses would be preferred to raise sodium rapidly but in a controlled way. The bystander's advice is dangerous because it treats a presumed dehydration that the weight record shows is not present.
3. Describe how her plasma sodium should be corrected and monitored, and explain the risk of correcting too quickly.
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Correction should be slow: aim for a rise of about 4–6 mmol/L in the first 24 hours and no more than 8–10 mmol/L, because over-rapid correction of hyponatraemia can cause osmotic demyelination. In acute symptomatic hyponatraemia, a 3% bolus may be used to control seizures, then stopped. Monitor plasma sodium every 2–4 hours initially, along with urine output, neurological status and fluid balance; stop active correction once symptoms resolve or the target rise is reached. The 500 mL of 0.9% saline is a reasonable first step here because her ADH is low and she needs gentle volume expansion, but sodium must be rechecked before any further fluid. The team should also look for other causes such as diuretics, SSRIs or adrenal insufficiency, and should document the rate of change, not just the single value.