Hyponatremia at the marathon finish
A 42-year-old runner finished a marathon in 5 h 10 min. He weighed 70.0 kg before the race and 72.2 kg at the finish. During the race he drank 6 L of water and 2 L of a sports drink containing 20 mmol/L Na+. He produced about 1.5 L of urine and estimated 4 L of sweat loss. At the finish he was confused and had a seizure. Serum Na+ was 119 mmol/L, plasma osmolality 250 mOsm/kg, urine osmolality 480 mOsm/kg, and urine Na+ 40 mmol/L. He took no diuretics and had no known kidney disease. A volunteer physician suggests giving 2 L of 0.9% saline (154 mmol/L Na+) over 1 hour because his sodium is low. Another suggests 100 mL of 3% saline (513 mmol/L Na+) plus stopping fluid intake.
1. Explain why the runner's serum Na+ fell to 119 mmol/L even though he drank a sports drink containing sodium. Use water and sodium balance, and explain why the 2.2 kg weight gain is important.
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Serum Na+ concentration is total body Na+ divided by total body water, not sodium intake alone. He gained 2.2 kg, essentially 2.2 L of retained fluid, because intake of 8 L exceeded sweat loss (4 L), urine (1.5 L), and insensible losses (about 1 L). The sports drink supplied only 2 L × 20 mmol/L = 40 mmol Na+, while sweat at about 40 mmol/L over 4 L removed roughly 160 mmol Na+. Even without the sweat calculation, dilution is clear: adding water without proportional sodium lowers concentration. The weight gain is the key bedside finding because it shows positive water balance, not dehydration. A dehydrated runner with hyponatremia would have lost weight; this runner did not. The sodium in the sports drink was far too low to match the water load, and ADH acting to retain water worsened the dilution.
2. Interpret the urine osmolality of 480 mOsm/kg and urine Na+ of 40 mmol/L when plasma osmolality is 250 mOsm/kg. What hormone is active, and why is this response inappropriate?
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Plasma osmolality of 250 mOsm/kg is well below the normal threshold for ADH release, about 280 mOsm/kg. A urine osmolality of 480 mOsm/kg means the kidney is reabsorbing water under ADH, so ADH is high despite hypotonic plasma. That is inappropriate in the sense that the normal osmotic brake is absent. Non-osmotic stimuli such as nausea, pain, stress, exercise, and possibly falling plasma volume from sweat can override osmotic control. The urine Na+ of 40 mmol/L argues against true sodium depletion: if volume depletion were the main driver, ADH and aldosterone would tend to conserve sodium and urine Na+ would be lower. Instead, the picture fits exercise-associated hyponatremia with ADH-mediated water retention. The concentrated urine is not evidence of dehydration; it is evidence of ADH effect. Giving more hypotonic fluid would worsen the dilution.
3. Compare the two proposed treatments. Which is more appropriate acutely, and what are the dangers of correcting serum Na+ too quickly?
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The 3% saline is more appropriate for symptomatic hyponatremia with seizure because it delivers sodium in a small volume and raises plasma osmolality without adding 2 L of water. Two liters of 0.9% saline contains 308 mmol Na+ but also 2 L water; in a patient with ADH-driven water retention, much of that water may be retained, so the net effect on serum Na+ may be small or even diluting. The 3% solution (513 mmol/L) is hypertonic relative to plasma, so it draws water out of cells and raises serum Na+; 100 mL contains about 51 mmol Na+, which in roughly 43 L total body water raises Na+ by about 1.2 mmol/L before fluid shifts. The goal is not rapid normalization. Overly fast correction can cause osmotic demyelination, especially in chronic hyponatremia; current practice limits the rise to about 4-6 mmol/L in the first few hours and 8-10 mmol/L in 24 hours, with lower limits in high-risk patients. Stopping fluid intake and treating the seizure are essential. The first physician's plan mistakes low sodium for sodium deficiency and ignores the water excess.