Exercise Associated Hyponatremia - the effects of over-hydration

Exercise Associated Hyponatremia (EAH) is a decrease in sodium levels caused by over-hydrating;  this typically means consuming more fluid than the kidneys can excrete, typically during or up to 24 hours after prolonged physical activity.(1)   The outcome can be as serious as dehydration, the problem is that the signs and symptoms of both are very similar which means correct diagnosis and treatment for the condition is essential.

Sodium is required for several functions including blood pressure.  Under normal conditions, sodium and water levels are regulated by the renal and hormonal systems. 

When sodium levels outside the cells decrease  water moves into the cells causing swelling, commonly observed in the extremities.  Sodium is also important in regulating the amount of water which passes through the blood/brain barrier.  Extreme hyponatremia can cause swelling of the brain – hyponatremic encephalopathy - and eventually, death.

 

Incidence

As of 2012, 20 deaths have been attributed to EAH (2-4).   Most cases are seen in endurance events such as Iron Man and Ultra Marathons but an increasing number of cases are being reported in shorter distance events.   Military personnel are also at risk from prolonged training and operational roles in in hot environments.    Perhaps one of the most famous deaths associated with hyponatremia was Leah Betts, who in 1992, died shortly after he 18th birthday after consuming 7 litres of water within 90 minutes following advice to stay hydrated while taking Ecstasy.  

The symptoms of EAH are, unfortunately, very similar to heat related illness usually associated with dehydration:  nausea, vomiting, headache, swelling of hands and feet, reduced level of consciousness.  Because of the similar symptoms of dehydration and heatstroke, it is likely that many cases go unreported (5)

There are believed to be several contributory factors which increase the likelihood of EAH (1)

  • Females
  • Non Steroidal Anti Inflammatory Drugs (NSAIDs) such as ibuprofen
  • Low body weight
  • Event inexperience
  • Exercise exceeding 4 hours
  • Hot and extreme cold environments

 

Pathophysiology

There are two pathological pathways to EAH

Excessive fluid consumption
Individuals with normal renal function can excrete between 500 and 1000ml/h of water.(6)   With the additional non-renal losses of water (sweating, digestion, respiration etc.) athletes should be able to consume as much as 1000 to 1500ml/h before developing water retention and dilutional hyponatremia.  As such EAH is unlikely when fluid intake exceeds his limit.

Excessive Vasopressin secretion
Vasopressin, also known as antidiuretic hormone (ADH) and arginine vasopressin (AVP).  Its two primary functions are to retain water in the body and to constrict blood vessels.    Vasopressin regulates the body's retention of water by acting to increase water reabsorption.    Alcohol causes the pituitary gland in the brain to block the creation of vasopressin, the kidneys send water directly to the bladder instead of reabsorbing it into the body.   This is why drinking pints of beer, which is largely water, will still cause dehydration (one of the main mechanisms of a hangover) and once you have cracked the seal on a night out you will find yourself visiting the smallest room more frequently than normal!

Under normal circumstances, ingestion of excessive water should suppress vasopressin,  leading to production of dilute, high-volume urine.   If vasopressin is not appropriately suppressed, the ability to excrete excessive water is reduced causing fluid retention and dilutional hyponatremia.   Vasopressin secretion may be triggered by a range of stimuli including intense exercise, nausea,  vomiting, hypoglycaemia and non-specific stresses such as pain and emotion.(7-9)

Sodium loss through sweating
Normal sodium levels in the blood are 135mml/l.   Sodium levels in sweat varies between 15-65mmol/l meaning that sweat is hypotonic – lower levels of electrolytes than serum and cells.   While sweating does account for some sodium loss, it is not in proportion to fluid loss through sweat.  (10, 11)

 

Prevention

The key strategy in preventing EAH is to prevent over-hydration.   The best advice is to drink according to thirst.   This simple method is sufficient to prevent both dehydration and hyponatremia. (1, 12-15) 

This is in contrast to the traditional advice that athletes should consume as much fluids as tolerable.

There is little evidence to suggest that supplemental sodium prevents EAH during exercise lasting less than 18 hours or when athletes drink according to thirst.  (16-19).   EAH is a result of over-hydration not inadequate sodium intake.

 

Diagnosis

Given the similarities in signs and symptoms of EAH with dehydration, diagnosis in the field is exceptionally difficult.

 Signs & Symptoms

 EAH

 Dehydration

 Fatigue / Weakness

 Possible

 Possible

 Increased thirst

 Possible

 Likely

 Raised temperature

 Possible

 Yes

 Nausea / Vomiting

 Possible

 Possible

 Reduced Level of Response  / Neurological deficit (e.g.  blurred vision)

 Possible

 Possible

 Respiratory Distress

 Possible

 Not present

 Reduced urine output

 Possible

 Likely

After Bennet et al(20)

 

Laboratory testing

EAH is definitively categorised by having a blood serum sodium level of less than 135mmol/L.   This is only obtainable through laboratory testing.

Weight Gain
Given the pathophysiology of EAH is over-hydration combined with an inability to excrete excess water, weigh gain during exercise would be a logical indicator, however EAH is also seen with weight-loss (21-23) so is not, on it’s own, a reliable indicator.  Those who exhibit heat related illness without weight loss are, however, more likely to have developed EAH (24,25).

History
Understanding the casualty’s history is perhaps the greatest indicator.  Knowing their fluid intake  (>1500ml/h)  and over what time period is essential.

 

Treatment

Correct diagnosis is essential; the principle treatment is restriction of fluids – if the casualty is suffering from dehydration, fluid restriction will have as serious consequences as hydrating a casualty with EAH.

In the situation in which the diagnosis of EAH is uncertain, the potential benefits of fluid restriction if the individual has EAH must be weighed against the potential harm that could result when the individual might have dehydration.

When and where body weight can be monitored in organized events, and in the presence of weight gain during exercise, fluid and sodium intake should be reduced until weight returns to 2% to 4% of body weight loss from base line level. (20)  In all other contexts this is likely to be impractical if not impossible. 

Where the suspicion of EAH is high, fluids should be restricted and salt sodium supplementation started.  The definitive treatment is a 100ml bolus of 3% hypertonic saline, which can be repeated twice at 10 minute intervals (up to 3 doses in total) with the aim of acutely increasing serum sodium concentration by about 4 to 5mmol/l and reversing cerebral oedema. (20)

In the field or with a limited skill-set oral sodium supplementation with minimum fluids has seen positive results (26).   This may include:

  • concentrated chicken broth (four bouillon cubes in 125 ml/one-quarter cup of water).  (27)
  • 100 mL of 3% saline flavoured with low-calorie sweetener (28, 29)

Administration of hypotonic (low sodium) fluids are absolutely contraindicated where EAH is confirmed. (26)

Then evacuate the casualty to emergency care.

 

Related Article:  Heat Stroke & Heat Related Illness

 

References

  1. Hew-Butler T, Ayus JC, Kipps C, Maughan RJ, Mettler S; Meeuwisse WH, Page AJ, Reid SA, Rehrer NJ,  Roberts WO, Rogers IR, Rosner MH, Siegel AJ, Speedy DB, Stuempfle KJ, Verbalis JG, Weschler LB, Wharam P, (2008). "Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007". Clinical Journal of Sport Medicine. 18 (2): 111–21.
     
  2. Noakes T. (2012) “Waterlogged: The Serious Problem of Overhydration in Endurance Sports. Champaign”, IL: Human Kinetics
     
  3. Kipps C, Sharma S, Pedoe DT(2011)  “The incidence of exercise associated hyponatraemia in the London marathon”. British Journal of Sports Medicine. 45:14–19.
     
  4. Ayus JC, Varon J, Arieff AI(2000)  “Hyponatremia, cerebral edema and non-cardiogenic pulmonary edema in marathon runners”.  Annals of International Medicine. 132:711–714.
     
  5. Rogers IR, Hew-ButlerT.  (2009)  Exercise-associated hyponatremia: overzealous fluid consumption. Wilderness Environmental Medicine. ;20:139–143.
     
  6. Rose BD, Post TW. (2001)  Clinical Physiology of Acid-Base and Electrolyte Disorders. 5th ed.  NewYork.  McGraw Hill
     
  7. Rowe JW, Shelton RL, Helderman JH, Vestal RE, Robertson GL.  (1979)  “Influence of the emetic reflex on vasopressin release in man.”  Kidney International.  16:729–735.
     
  8. Baylis PH, Zerbe RL, Robertson GL.  (1981)  “Arginine vasopressin response to insulin-induced hypoglycaemia in man”.  Journal of Clinical Endocrinology and Metabolism.  53:935–940.
     
  9. Hew-Butler T, Jordaan E, Stuempfle KJ, (2008)  “Osmotic and non-osmotic regulation of arginine vasopressin during prolonged endurance exercise”.  Journal of Clinical Endocrinology and Metabolism.  93:2072–2078.
     
  10. Buono MJ, Ball KD, Kolkhorst FW.  (2007)  “Sodium ion concentration vs. sweat rate relationship in humans”.  Journal of Applied Physiology.  103:990–994.
     
  11. Buono MJ, Sjoholm NT. (1988)  “Effect of physical training on peripheral sweat production”.  Journal of Applied Physiology.  65:811–814
     
  12. Hew-Butler T, Verbalis JG, Noakes TD.  (2006)  “International Marathon Medical Directors Association.  Updated fluid recommendation: position statement from the International Marathon Medical Directors Association (IMMDA)”.  Clinical Journal of Sports Medicine.  16:283–292.
     
  13. Cheuvront SN, Haymes EM.  (2001)  “Ad libitum fluid intakes and thermoregulatory responses of female distance runners in three environments”.  Journal of Sports Science.  19:845–854.
     
  14. Armstrong LE, Maresh CM, Gabaree CV, Hoffman JR, Kavouras SA, Kenefick RW, Castellani JW, Ahlquist LE.  (1997)  “Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, and water intake”.  Journal of Applied Physiology.  82:2028–2035.
     
  15. Hoffman MD, Stuempfle KJ.  (2014)  “Hydration strategies, weight change and performance in a 161-km ultramarathons”.  Research in Sports Medicine. 22:213–225.
     
  16. Speedy DB, Thompson JM, Rodgers I, Collins M, Sharwood K, Noakes TD.  (2002)  “Oral salt supplementation during ultradistance exercise”. Clinical Journal of Sports Medicine.  12:279–284.
     
  17. Hew-Butler TD, Sharwood K, Collins M, Speedy D, Noakes T.  (2006) “Sodium supplementation is not required to maintain serum sodium concentrations during an Ironman triathlon”.  British Journal of Sports Medicine. 40:255–259.
     
  18. Twerenbold R, Knechtle B, Kakebeeke TH, Eser P, Müller G, von Arx P, Knecht H. (2003)  “Effects of different sodium concentrations in replacement fluids during prolonged exercise in women”.  British Journal of Sports Medicine.  37:300–303.
     
  19. Barr SI, Costill DL, Fink WJ.  (1991)  “Fluid replacement during prolonged exercise: effects of water, saline, or no fluid”.  Medicine and Science in Sports and Exercise.  23:811–817.
     
  20. Bennett BL, Hew-Butler T,  Hoffman MD, Rogers IR, Rosner MH, (2014)  “Wilderness Medical Society Practice Guidelines for Treatment of Exercise-Associated Hyponatremia: 2014 Update.”  Wilderness and Environmental Medicine.  25, S30–S42
     
  21. Lebus DK, Casazza GA, Hoffman MD, Van Loan MD.  (2010)  “Can changes in body mass and total body water accurately predict hyponatremia after a 161-kmrunning race?”  Clinical Journal of Sports Medicine.  2010;20:193–199.
     
  22. Hoffman MD, Stuempfle KJ, RogersIR, WeschlerLB, Hew-Butler T.  (2010)  “Hyponatremia in the 2009 161-kmWestern States Endurance Run.”  International Journal of Sports Physiology and Performance.  7:6–10.
     
  23. Hoffman MD, Hew-ButlerT, Stuempfle KJ.  (2013)  “Exercise-associated hyponatremia and hydration status in 161-km ultramarathoners.”  Medicine and Science in Sports and Exercise. 45:784–791.
     
  24. Noakes TD, Sharwood K, Speedy D,  (2005)  “Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proceedings of the National Academy of Science of the USA.  102:18550–18555.
     
  25. Hoffman MD, Stuempfle KJ, Sullivan K, Weiss RH.  (2014)  “Exercise-associated hyponatremia with exertional rhabdomyolysis: importance of proper treatment.”  Clinical Nephrology.  Apr; 83(4):235-42
     
  26. Hew-Butler T, Loi V, Pani A and Rosner MH.  (2017)  “Exercise-Associated Hyponatremia: 2017 Update.”  Frontiers in Medicine.  4.  21
     
  27. Siegel AJ, d’Hemecourt P, Adner MM, Shirey T, Brown JL, Lewandrowski KB.  (2009)  “Exertional dysnatremia in collapsed marathon runners: a critical role for point-of-care testing to guide appropriate therapy.”  American Journal of Clinical Pathology.  132(3):336–40.10.
     
  28. Owen BE, Rogers IR, Hoffman MD, Stuempfle KJ, Lewis D, Fogard K, et al.  (2014)  “Efficacy of oral versus intravenous hypertonic saline in runners with hyponatremia.”  Journal of Science and  Medicine in Sport.  17(5):457–62.
     
  29. Rogers IR, Hook G, Stuempfle KJ, Hoffman MD, Hew-Butler T.  (2011)  “An intervention study of oral versus intravenous hypertonic saline administration in runners with exercise-associated hyponatremia: a preliminary randomized trial.”  Clinical Journal of Sport Medicine.  21(3):200–3.