Exercise-associated hyponatremic encephalopathy and exertional heatstroke in a soldier: high rates of fluid intake during exercise caused rather than prevented a fatal outcome

  • TITLE: Exercise-associated hyponatremic encephalopathy and exertional heatstroke in a soldier: high rates of fluid intake during exercise caused rather than prevented a fatal outcome
  • AUTHOR: Nolte HW1, Hew-Butler T, Noakes TD, Duvenage CS
  • REFERENCE: Phys Sportsmed. 2015 Jan 14:1-6. [Epub ahead of print]
  • YEAR: 2015

Athletes are often advised to drink in order to “fully replace bodyweight losses” in order to prevent exertional heatstroke (EHS) during exercise in the heat. There is little evidence that “dehydration” in the range experienced by athletes adversely affects thermoregulation or is the exclusive cause of EHS. In contrast it is established that excess fluid intake can cause exercise-associated hyponatremia (EAH) sometimes associated with encephalopathy (EAHE). As part of a series of experiments to determine optimal fluid replacement during exercise in the heat, we studied a group of exceptionally well-conditioned and heat-adapted members of the South African National Defence Force. A 20 year old male started a time restricted 50 km route-march in a dry bulb temperature that reached 37.5°C (WBGT of 33.6°C, relative humidity of 85%). Pre-march plasma osmolality, serum [Na+] and total body water measures indicated euhydration. Fluid was available ad libitum and isotonic sports drinks at 5 km intervals. Fluid intake and core body temperature (Tc) were recorded throughout while he was tracked by a global positioning system measuring distance travelled, position and speed. Comparing the total fluid intake of the soldier (12930 mL) to the rest of the participants (mean intake of 9 038 mL) up to 40 km, it is evident that his intake was 3892 mL (approximately 300 mL h-1) more than the mean for group. At approximately 17h14 the soldier was found lying by himself at the side of the route, 2.24 km from the finish point. He passed away the next day in a medical care facility. This tragic event provides the valuable opportunity to present data on the pacing, temperature regulation and fluid consumption of an exceptional athlete during the development of a fatal case of combined EAHE and EHS. Pacing, fluid intake, Tc and environmental condition data are presented for 5km intervals throughout the march. We propose a novel hypothesis on the possible contribution of EAHE to the development of EHS.

KEYWORDS: core temperature; exercise-associated hyponatremic encephalopathy; exertional heatstroke; fluid intake

http://www.ncbi.nlm.nih.gov/pubmed/25586818

>