Correspondence

Altered Mental Status after a Marathon

N Engl J Med 2005; 352:1613-1614April 14, 2005

Article

To the Editor:

Hyperthermia has long been recognized as a cause of altered mental status after a marathon, but in recent years exercise-associated hyponatremia has become increasingly common.1 In 2003, there was an unexpected increase in the number of London Marathon runners who presented to St. Thomas' Hospital, situated near the finish line of the race, among them 17 runners with altered mental status (Glasgow Coma Scale scores, 11 to 13). Six of these 17 runners received a diagnosis of hyperthermia (temperature, >37.7°C), and 11 a diagnosis of exercise-associated hyponatremia (serum sodium level, <135 mmol per liter). There were distinct differences between these two groups in their characteristics at presentation (Table 1Table 1Diagnoses and Symptoms among Runners Presenting to St. Thomas' Hospital after the 2003 London Marathon.).

All six of the runners with hyperthermia presented with collapse and confusion 185 to 385 minutes after the race had begun; five of them had not completed the marathon. Fourteen runners received a diagnosis of exercise-associated hyponatremia. Eleven of these runners were confused, and one had seizures. All of them had completed the marathon. Their serum sodium levels ranged from 116 to 133 mmol per liter. The first runner in this group presented 398 minutes after the race had begun, after the last runner with hyperthermia had arrived. There was a substantial delay between completion of the marathon and presentation at the hospital among the runners with hyponatremia (mean, 243 minutes; range, 132 to 391). None of these runners could recall having completed the event, but a collateral history, available for some, described them as having been lucid when they finished the race and then becoming confused later.

The exact pathophysiology of exercise-associated hyponatremia is still debated, but it is thought to be due to excessive ingestion of hypotonic fluids in the setting of neurohumoral changes that reduce free water excretion.1-3 It is usually assumed that the fluid ingestion occurs during the exertion, and most previous reports have described the development of symptoms during or at the end of an event, although late presentations (including presentation after a marathon) have been reported.3 We postulate that delayed presentation is due to absorption of hypotonic fluid after the completion of an event, often leading to delayed symptoms and presentation to a hospital not primarily designated to receive event participants. After an educational campaign warning runners of the dangers of excessive drinking, there was only one reported case of exercise-associated hyponatremia after the 2004 London Marathon.

Adrian M. Goudie, F.A.C.E.M.
Swan District Hospital, Perth 6056, Australia
adrian.goudie@health.wa.gov.au

Dan S. Tunstall-Pedoe, D.Phil, F.R.C.P.
Homerton Hospital, London E9 6SR, United Kingdom

Mary Kerins, F.F.A.E.M.
King's College Hospital, London SE5 9RS, United Kingdom

3 References

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   Speedy DB, Noakes TD, Schneider C. Exercise-associated hyponatremia: a review. Emerg Med (Fremantle) 2001;13:17-27
   CrossRef | Medline

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   Hew TD, Chorley JN, Cianca JC, Divine JG. The incidence, risk factors, and clinical manifestations of hyponatremia in marathon runners. Clin J Sport Med 2003;13:41-47
   CrossRef | Web of Science | Medline

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   Davis DP, Videen JS, Marino A, et al. Exercise-associated hyponatremia in marathon runners: a two-year experience. J Emerg Med 2001;21:47-57
   CrossRef | Web of Science | Medline

Citing Articles (3)

Citing Articles

1. 1

   Richard H. Sterns, Sagar U. Nigwekar, John Kevin Hix. (2009) The Treatment of Hyponatremia. Seminars in Nephrology 29:3, 282-299
   CrossRef

2. 2

   Erika Richtig, Christina M. Ambros-Rudolph, Michael Trapp, Helmut K. Lackner, Rainer Hofmann-Wellenhof, Helmut Kerl, Guenther Schwaberger. (2008) Melanoma Markers in Marathon Runners: Increase with Sun Exposure and Physical Strain. Dermatology 217:1, 38-44
   CrossRef

3. 3

   J.A. Stockman. (2006) Mechanism of Cerebral Edema in Children With Diabetic Ketoacidosis. Yearbook of Pediatrics 2006, 345-346
   CrossRef