Jan 29, 2015
More Awareness Needed for EAH

Headlines were made this past summer when two high school football athletes died from exercise associated hyponatremia (EAH) after drinking too much fluid following preseason workouts. EAH is also suspected in the death of a 14-year-old football player in Florida. Caused by the overconsumption of fluids, hyponatremia, or low blood sodium concentration, can lead to swelling in the brain and eventually death.

In response to the recent tragedies, an international group of experts on hydration and EAH have been assembled to present at a conference and participate in a consensus meeting Feb. 20 in San Diego. The following is an editorial from that group written in hopes of increasing awareness of this deadly condition.

When we hear about catastrophic injury and death amongst athletes, we typically think about concussion (1), cardiac arrest (2) and exertional heatstroke (3). Exercise-associated hyponatremia (EAH) is rarely mentioned alongside the “big three,” despite its insidious extension into more diverse sporting events beyond the ultramarathon, where it was first described three decades ago (4). The recent and tragic deaths of two otherwise healthy 17-year old high school football players from hyponatremic encephalopathy (5,6), underscores the need for more education towards translating evidenced-based science into clinical practice. All EAH deaths are tragic because they are unnecessary and preventable. The single greatest risk factor for EAH and its associated complications is over-hydration (4). Although severely symptomatic hyponatremia is relatively rare, the evidence supports that death from EAH is avoidable if athletes adhere to rational hydration strategies and avoid excessive and unneeded fluid intake (7).

Nearly a decade ago, the perils of over-hydration during exercise were confirmed in two seminal studies performed on 488 Boston Marathon runners (8) and 2135 endurance athletes (7). These reports followed the back-to-back deaths of two female marathon runners in 2002 from EAH (9). Subsequently, an international group of experts consolidated the existing evidence that strongly suggested that hyponatremia resulted from sustained or exuberant fluid intake beyond the body’s maximal fluid excretion rates (i.e., fluids consumed above the dictates of thirst or delivered intravenously) (10). But despite strong evidence to the contrary, sporting culture continues to embrace hyper-hydration, with yet another pair of fatal outcomes as a result of this misinformation.

American football players are noted for their high sweat rates (often >2 liters/hour) due to large body surface area, protective equipment and intensity of play (11). American college football players’ fluid consumption can exceed 12 liters per day. Given this, high fluid intake has become indoctrinated within football culture. For example, 75 percent of athletic trainers reported administering pre-game intravenous fluids to professional football players (12). A college football player recently developed hyponatremia after receiving five liters of intravenous fluids while ingesting 3 additional liters of hypotonic fluid (a sports beverage) within five hours (13). One of the high school athletes who died this year reportedly drank 16 liters of fluid during practice to alleviate muscle cramps (5), despite recent experimental evidence suggesting severe dehydration does not impact cramp susceptibility (14). Thus, while solid evidence published in a breadth of scientific journals clearly warn against the perils of hyper-hydration during exercise, responsible drinking during exercise has yet to be effectively translated onto the playing field. While concerns regarding dehydration and exertional heatstroke are valid, this occurrence is also rare. Current recommended safe drinking guidelines, advising athletes to drink to the dictates of thirst take all of these risks into account, such that extreme hydration is never warranted and the adverse effects can be avoided (10).

In 2014, it is clear that EAH is preventable. We can control the amount of fluid that enters our body and must reconsider, re-educate and reinforce appropriate fluid intake and intravenous fluid guidelines (10). The recent preventable deaths of two young football players (as well as several others in the recent past) should serve as a tragic reminder that medical personnel, professional societies and industry must strive harder to translate evolving scientific recommendations and guidelines to practical use by athletes and those who train them.

Mitchell H. Rosner; University of Virginia Health System, Charlottesville VA
Tamara Hew-Butler; Oakland University, Oakland MI
Sandra Fowkes-Godek: West Chester University, West Chester PA
Martin D. Hoffman; University of California Davis Medical Center and VA Northern California Health Care System, Sacramento, CA
Douglas Lewis; University of Kansas School of Medicine-Wichita; Wichita, KS
Ronald J. Maughan: Loughborough University, UK
Kevin C. Miller: Central Michigan University, Mt. Pleasant MI
Scott Montain: US Army Research Institute of Environmental Medicine, Natick MA
Nancy J. Rehrer: University of Otago, NZ
William O. Roberts: University of Minnesota School of Medicine, Minneapolis MN
Ian R Rogers: St John of God Murdoch Hospital & University of Notre Dame, Australia
Arthur J. Siegel: Harvard Medical School, Boston MA
Dale Benjamin Speedy: Sportscare Auckland, New Zealand
Kristin J. Stuempfle: Gettysburg College, Gettysburg PA
Joseph G. Verbalis: Georgetown University Medical Center, Washington DC
James Winger: Loyola University Chicago Stritch School of Medicine, Chicago IL


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(2) Kim JH, Malhotra R, Chiampas G, d’Hemecourt P, Troyanos C, Cianca J et al. Cardiac arrest during long-distance running races. N Engl J Med 2012; 366(2):130-140.
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(5) Stevens A. Update: Douglas County football player has died. The Atlanta Journal-Constitution 14 A.D. Aug 11.
(6) Blevins R, Apel T. Preps Sports Report. The Clarion-Ledger 2014 Aug 27.
(7) Noakes TD, Sharwood K, Speedy D, Hew T, Reid S, Dugas J et al. Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci U S A 2005; 102(51):18550-18555.
(8) Almond CS, Shin AY, Fortescue EB, Mannix R, Wypij D, BinstadtBA et al. Hyponatremia among Runners in the Boston Marathon. N Engl J Med 2005; 352(15):1550-1556.
(9) Siegel AJ, Verbalis JG, Clement S, Mendelson JH, Mello NK, Adner M et al. Hyponatremia in marathon runners due to inappropriate arginine vasopressin secretion. Am J Med 2007; 120(5):461.e11-467.e17.
(10) Hew-Butler TD, Ayus JC, Kipps C, Maughan RJ, Mettler S, Meeuwisse WH et al. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007. Clin J Sport Med 2008; 18(2):111-121.
(11) Godek SF, Bartolozzi AR, Godek JJ. Sweat rate and fluid turnover in American football players compared with runners in a hot and humid environment. Br J Sports Med 2005; 39(4):205-211.
(12) Fitzsimmons S, Tucker A, Martins D. Seventy-five percent of National Football League teams use pregame hyperhydration with intravenous fluid. Clin J Sport Med2011; 21(3):192-199.
(13) Herfel R, Stone CK, Koury SI, Blake JJ. Iatrogenic acute hyponatraemia in a college athlete. Br J Sports Med 1998; 32(3):257-258
(14) Braulick K, Miller K, Albrecht J, Tucker J, Deal J. Significant and serious dehydration does not affect skeletal muscle cramp threshold frequency. Br J Sports Med. 2012;47:710-4.

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