Symptomatic exercise-associated hyponatremia (EAH) is known to be a potential complication from overhydration during exercise, but there remains a general belief that sodium supplementation will prevent EAH. We present a case in which a runner with a prior history of EAH consulted a sports nutritionist who advised him to consume considerable supplemental sodium, which did not prevent him from developing symptomatic EAH during a subsequent long run. Emergency medical services were requested for this runner shortly after he finished a 17-hr, 72-km run and hike in Grand Canyon National Park during which he reported having consumed 9.2–10.6 L of water and >6,500 mg of sodium. First responders determined his serum sodium concentration with point-of-care testing was 122 mEq/L. His hyponatremia was documented to have improved from field treatment with an oral hypertonic solution of 800 mg of sodium in 200 ml of water, and it improved further after significant aquaresis despite in-hospital treatment with isotonic fluids (lactated Ringer’s). He was discharged about 5 hr after admission in good condition. This case demonstrates that while oral sodium supplementation does not necessarily prevent symptomatic EAH associated with overhydration, early recognition and field management with oral hypertonic saline in combination with fluid restriction can be effective treatment for mild EAH. There continues to be a lack of universal understanding of the underlying pathophysiology and appropriate hospital management of EAH.
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Martin D. Hoffman and Thomas M. Myers
Martin D. Hoffman, Kristin J. Stuempfle, Ian R. Rogers, Louise B. Weschler, and Tamara Hew-Butler
Purpose:
To determine the incidence of exercise-associated hyponatremia (EAH), the associated biochemical measurements and risk factors for EAH, and whether there is an association between postrace blood sodium concentration ([Na+]) and changes in body mass among participants in the 2009 Western States Endurance Run, a 161-km mountain trail run.
Methods:
Change in body mass, postrace [Na+], and blood creatine phosphokinase (CPK) concentration, and selected runner characteristics were evaluated among consenting competitors.
Results:
Of the 47 study participants, 14 (30%) had EAH as defined by a postrace [Na+] <135 mmol/L. Postrace [Na+] and percent change in body mass were directly related (r = .30, P = .044), and 50% of those with EAH had body mass losses of 3–6%. EAH was unrelated to age, sex, finish time, or use of nonsteroidal anti-inflammatory drugs during the run, but those with EAH had completed a smaller (P = .03) number of 161-km ultramarathons. The relationship of CPK levels to postrace [Na+] did not reach statistical significance (r = –.25, P = .097).
Conclusions:
EAH was common (30%) among finishers of this 161-km ultramarathon and it was not unusual for those with EAH to be dehydrated. As such, changes in body mass should not be relied upon in the assessment for EAH during 161-km ultramarathons.
Tessa Portlock, Natalie A. Hunt, Jason L. Zaremski, Asim Merchant, and Patricia M. Tripp
are more severe than expected Fatigue, inability to exercise, water-electrolyte imbalance, or body ache Dark or reddish urine (tea- or cola-colored) Decrease urine production Feeling weak or tired; unable to complete job tasks or finish a workout routine Nausea and/or emesis is uncommon Cramping or
