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.
Martin D. Hoffman and Thomas M. Myers
Rogerio Pessoto Hirata, Alexander W. Erbs, Erik Gadsbøll, Rannvá Winther, Sanne H. Christensen, and Morten Bilde Simonsen
the reduced maximum voluntary contraction force capacity from the adductor muscles to maintain their preferred walking speed, similar to baseline conditions. Comparable results were reported while experimental pain was induced via intramuscular injection of hypertonic saline solution in the tibialis