NUR 6400 Module 4 Fluid and Electrolyte Case: Hyponatremia After a Marathon Example

Drinking at Every Table: Water, Vasopressin and Brain Swelling in a 38-Year-Old First-Time Marathoner With a Sodium of 121

Student Name

Master of Science in Nursing, Thomas Edison State University

NUR-6400: Advanced Pathophysiology

Mentor Name

Month Day, Year

Drinking at Every Table: Water, Vasopressin and Brain Swelling in a 38-Year-Old First-Time Marathoner With a Sodium of 121

Introduction

Ms. R. is a composite patient, a 38-year-old high school teacher who trained for six months for her first marathon after reading that dehydration was the main danger in long races. On a cool October morning she drank a cup of water or sports drink at each of the 24 aid stations and carried a bottle besides. She crossed the finish line in five hours and forty minutes, about a kilogram heavier than at the start. Twenty minutes later she vomited twice, complained of a pounding headache and could not remember where she had parked. Her serum sodium in the medical tent was 121 millimoles per liter. This paper explains how a healthy woman can dilute her own blood during exercise and why the brain is the organ that suffers.

Normal Water Balance

Serum sodium concentration depends on the ratio between total body sodium and total body water. Adrogué and Madias (2000) explain that nearly every case of hyponatremia reflects too much water relative to sodium rather than an absolute loss of sodium. In health, the kidney protects that ratio. When plasma becomes dilute, the hypothalamus stops releasing arginine vasopressin, also called antidiuretic hormone. Without vasopressin, the collecting ducts remove their aquaporin water channels from the cell membrane and the kidney can excrete large volumes of dilute urine, up to about 800 to 1,000 milliliters an hour in a healthy adult at rest.

What Went Wrong During the Race

Two failures combined in Ms. R. The first was intake. Almond et al. (2005) studied 488 runners in the 2002 Boston Marathon and found that 13 percent finished with a sodium of 135 or less and 0.6 percent with 120 or less. The strongest predictor was weight gain during the race, which can only come from drinking more than is lost in sweat and urine. Racing time over four hours was another, because slower runners have more time and more aid stations at which to drink, while losing less fluid each hour. Ms. R. fit both.

The second failure was in the kidney's ability to get rid of the extra water. The Third International Exercise-Associated Hyponatremia Consensus statement (Hew-Butler et al., 2015) describes nonosmotic release of vasopressin during prolonged exercise. Nausea, pain, low blood sugar, the stress of exertion and inflammatory signals such as interleukin 6 can all trigger vasopressin release even when plasma is already dilute. With vasopressin present, the kidney holds on to water it should be shedding. Exercise also reduces blood flow to the kidneys, lowering how much urine can be formed at all. Ms. R. was taking in water faster than her kidneys were allowed to excrete it.

Sodium Losses Play a Smaller Part

Sweat contains sodium, and a runner who sweats heavily for hours loses some. Students often assume that this explains marathon hyponatremia and that the answer is salt tablets. The consensus statement does not support that view: sodium lost in sweat contributes little in most cases, and runners who gain weight cannot be explained by losses at all (Hew-Butler et al., 2015). Sports drinks contain far less sodium than plasma, so drinking them in excess still dilutes the blood. Ms. R. switching between water and sports drink did not protect her.

Why the Brain Swells

The symptoms that matter come from the brain. As plasma sodium falls, plasma becomes hypotonic compared with the inside of cells, and water moves into cells to equalize concentration. Most tissues can swell a little without harm, but the brain sits inside a rigid skull, so every increase in volume raises pressure. Adrogué and Madias (2000) describe how brain cells defend themselves by exporting potassium and organic solutes such as amino acids and myo-inositol, which lowers their internal concentration and limits swelling. That adaptation takes hours to days. In a marathon the sodium falls over a few hours, faster than the brain can adapt, which is why acute exercise-associated hyponatremia can cause headache, vomiting and confusion at a level of sodium that would be tolerated in someone whose sodium fell slowly over weeks.

Severe cases progress to seizures, coma and noncardiogenic pulmonary edema, which may follow from raised intracranial pressure. Several runners have died this way in large races, which is why the consensus guidance treats confusion in a runner as a medical emergency.

Treatment Follows the Mechanism

Because the brain is swelling, the immediate aim is to raise sodium a little and quickly. The consensus statement recommends a 100 milliliter bolus of 3 percent hypertonic saline for a runner with symptoms, repeated up to two more times if symptoms persist (Hew-Butler et al., 2015). The concentrated saline pulls water out of brain cells. Giving normal saline or more fluid by mouth would make things worse, since it adds water the kidney cannot yet excrete. The rapid correction that is dangerous in chronic hyponatremia, where adapted brain cells can be injured by osmotic demyelination, is much less of a risk in acute cases where cells have not yet adapted, although monitoring is still needed once vasopressin falls and the kidney begins excreting the extra water.

Lifespan and Predisposing Factors

Older adults and people taking thiazide diuretics or selective serotonin reuptake inhibitors are at greater risk of hyponatremia in daily life because both drug groups impair water excretion. In endurance events, low body weight, slower pace and inexperience are the common threads. The cultural message that runners must drink as much as possible, which Ms. R. absorbed in training, is itself a risk factor. Current advice is to drink according to thirst.

Conclusion

Ms. R.'s hyponatremia came from water, not from salt loss. She drank far more than she lost while nonosmotic vasopressin release prevented her kidneys from excreting the excess, and her slow finish gave both processes more time. Water entered her brain cells faster than they could adapt, producing headache, vomiting and confusion. Hypertonic saline works because it reverses that water movement, and the most useful prevention is the simplest: drink to thirst.

References

Adrogué, H. J., & Madias, N. E. (2000). Hyponatremia. New England Journal of Medicine, 342(21), 1581-1589. https://doi.org/10.1056/NEJM200005253422107

Almond, C. S. D., Shin, A. Y., Fortescue, E. B., Mannix, R. C., Wypij, D., Binstadt, B. A., Duncan, C. N., Olson, D. P., Salerno, A. E., Newburger, J. W., & Greenes, D. S. (2005). Hyponatremia among runners in the Boston Marathon. New England Journal of Medicine, 352(15), 1550-1556. https://doi.org/10.1056/NEJMoa043901

Hew-Butler, T., Rosner, M. H., Fowkes-Godek, S., Dugas, J. P., Hoffman, M. D., Lewis, D. P., Maughan, R. J., Miller, K. C., Montain, S. J., Rehrer, N. J., Roberts, W. O., Rogers, I. R., Siegel, A. J., Stuempfle, K. J., Winger, J. M., & Verbalis, J. G. (2015). Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015. Clinical Journal of Sport Medicine, 25(4), 303-320. https://doi.org/10.1097/JSM.0000000000000221