Collapse After a Marathon: Water, Sodium and ADH
A 68 kg runner finishes a charity marathon in 4 h 40 min in 28 °C heat and 70% humidity. During the race he drinks 6.5 L of plain water; over the next two hours he drinks another 2.0 L because he feels bloated and thirsty. His sweat rate in training is 1.1 L h⁻¹ at a sodium concentration of 35 mmol L⁻¹. He weighs 70.2 kg at the finish; he started at 68.0 kg. That evening he is confused and has a headache; he vomits once. Plasma sodium is 124 mmol L⁻¹ (reference 135–145), plasma osmolality is low, urine osmolality is 480 mOsm kg⁻¹, and urine sodium is 18 mmol L⁻¹. He takes no medication and has no history of kidney or endocrine disease. A teammate says, 'He sweated out salt, so he should take salt tablets and keep drinking water.' The race medical team considers giving 100 mL of 3% saline over 10 minutes.
1. Explain how plasma sodium fell to 124 mmol L⁻¹ despite heavy sweating. Include the meaning of the weight change and the urine osmolality.
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The runner finished 2.2 kg heavier than he started (70.2 − 68.0 kg), which is roughly 2.2 L of positive fluid balance. He drank 8.5 L and sweated about 1.1 × 4.67 ≈ 5.1 L, so the excess is plausible if urine output was low. Sweat is hypotonic to plasma: at 35 mmol L⁻¹ sodium, his sodium loss was about 5.1 × 35 ≈ 180 mmol, much less than the water lost. Replacing that sweat with plain water therefore dilutes the extracellular fluid and lowers plasma sodium. Normally a fall in osmolality suppresses ADH and the kidneys excrete dilute urine. Here urine osmolality is 480 mOsm kg⁻¹, inappropriately concentrated for a plasma osmolality that is low. That indicates ADH is still high, driven by nausea, vomiting, exercise and stress, so free water is retained. The low urine sodium (18 mmol L⁻¹) shows the kidney is conserving sodium. The result is dilutional hyponatraemia, not simple salt depletion.
2. Evaluate the teammate's advice. Why not simply give salt tablets and continue drinking water?
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The teammate's advice is unsafe. The problem is too much water relative to sodium, not a simple lack of salt. Salt tablets without fluid restriction add sodium but do not remove the excess water, and they often cause nausea and vomiting, which in turn stimulates ADH and worsens water retention. Continuing to drink water would lower sodium further. Mild cases are managed by restricting fluid and monitoring; hypertonic saline is reserved for severe symptoms such as confusion, vomiting, seizures or coma, because it can correct sodium too quickly. Rapid correction risks osmotic demyelination. The safe approach is to check the sodium, assess neurological status, and correct by no more than about 8–10 mmol L⁻¹ in 24 hours, with frequent measurements. The teammate is right only that sweat contains salt; that does not make salt tablets the treatment.
3. The team plans to give 100 mL of 3% saline. Calculate the amount of sodium (mmol) and comment on whether this is appropriate at this point.
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A 3% NaCl solution contains 30 g L⁻¹, which is about 513 mmol Na per litre; 100 mL therefore provides about 51 mmol Na. In a 68 kg person with total body water of roughly 0.6 × 68 ≈ 41 L, plus the retained excess, 51 mmol would raise plasma sodium by only about 1–1.5 mmol L⁻¹ before redistribution and excretion. That is a small, controlled increment, which is appropriate if the patient has severe symptoms and is being monitored. It is not a cure and should not be repeated blindly. The team should give it as a slow, monitored infusion, recheck sodium after each 100 mL or at short intervals, and aim for a rise of 4–6 mmol L⁻¹ if symptoms are severe, not rapid normalisation. If the patient is only confused and can be observed, fluid restriction may be enough. The decision depends on the neurological examination.