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Exercise-Associated Hyponatremia: Water, Water Everywhere and Waaaaaay too Much to Drink

Exercise-Associated Hyponatremia: Water, Water Everywhere and Waaaaaay too Much to Drink

Nothing is scarier for ER personnel than to have a young patient going downhill fast in front of your eyes, and to be faced with two completely opposite explanations. With two completely opposite approaches to therapy. Pick the wrong direction, and it could mean the difference between life and death. And you have very little to guide you in either direction at the moment.

And this patient was in the shape of his/her life less than 3 hours ago.

Yet that is the scenario one can face when presented with the collapsed and unresponsive marathon runner. Is the sodium too high (hyPERnatremia) or is it too low (hyPOnatremia)?

Along with the rising popularity of marathons and other endurance sports has come an increased occurrence (or at least recognition) of what is called exercise-associated hyponatremia (EAH). EAH can be defined as hyponatremia (sodium levels less than 135 mEq/liter) occurring within 24 hours of physical activity (3, 4, 6). Like all forms of hyponatremia, it ultimately represents either an excess of water in the blood stream or a deficiency in sodium, or both. However, in most cases this appears to be due to an excess of fluid consumption (6, 8, 10, 11, 13).

It is difficult to pin down how common it truly is. Mild, asympomatic hyponatremia is likely fairly common in endurance sports, up to 51% by some estimates (6). Symptomatic hyponatremia, on the other hand, is seen much less often, by some estimates closer to 1% (6). Although it is likely underestimated since many do not seek medical help and simply attribute their symptoms (dizziness, lethargy, nausea) to the normal post-race or post-game exhaustion.

What causes EAH? Three theories predominate at present. Excess water consumed in relation to sodium consumed, excessive loss of sodium in sweat, and insufficient activation of non-osmotic sodium stores within the body.

The most likely scenario, in my view and in the view of many others (6, 7, 10), is that excessive fluid is being consumed during these events. Most commonly, this is water. However, even most commercially available sports drinks do not prevent this problem as they are usually hypotonic with respect to plasma. In either case, too much water intake with respect to sodium will lower the sodium level in your blood.

In normal situations, this is a very transient and harmless thing. Whenever your blood sodium levels go low after drinking a tall glass of water, a hormone called “anti-diuretic hormone” (ADH) becomes suppressed and you produce a very dilute urine bringing your sodium levels back to normal.

However, for reasons that are as yet not entirely clear, in many endurance athletes ADH is not appropriately suppressed, and the normal correction by the kidneys does not take place (7, 9). This could be due to the many other potential stimuli for ADH release (nausea, elevated body temperature, etc.) that take place during endurance exercise. But likely the cause is multi-factorial and we still do not have a complete picture of what causes the inappropriately high ADH levels.

Clearly, though, the data supports that excessive fluid consumption is the primary driving factor of EAH. Noakes et al analyzed data on 2,135 athletes competing in endurance events and found an inverse relationship between post-race sodium levels and weight gain (2). In other words, with weight loss the tendency was towards higher sodium levels, and with weight gain the tendency was towards lower sodium levels.

This finding is fairly consistent across studies (6, 8, 11, 13), with increasing weight gain and excessive fluid consumption during long-distance races comes higher risk for EAH.

Which is why the current recommendations (4, 6, 10, 11) are to simply drink according to thirst. The old adage of “don’t wait until you’re thirsty”, commonly taught by coaches in the past, not only won’t help your performance but may actually end up leading to catastrophic results.

This brings us back to what can be done as a healthcare professional when this patient ends up in your ER? You are presented with a collapsed runner, unable to give you any information as he or she is lethargic, or even comatose. You most likely will not be able to know if the patient has gained or lost weight during the race.

Is the patient hypOnatremic or hypERnatremic?

Most ideally, you would quickly determine the sodium level by sending a blood sample to the lab. However, if you are in the medical tent, or in the ambulance, or even in an ER where the lab turn-around time isn’t fast enough, you may have to make a decision prior to truly knowing whether the sodium is high or low.

Do you give them normal saline (i.e. 0.9%)? That has a sodium level (154 mEq/liter) relatively close to plasma (135-145 mEq/liter). Intuitively, that may seem to be a good idea because it would restore blood volume and bring the sodium levels closer to normal regardless of whether the patient is either hyper- or hypo- natremic.

Unfortunately, this could actually be a very bad idea if the above theory of inappropriately elevated ADH is true. In the Syndrome of Inappropriate ADH (SIADH), the kidneys will secrete a fixed osmolality of urine that is almost double what normal saline contains. That is, they will secrete out most of the sodium and retain more of the water, worsening the hyponatremia. So giving normal saline may potentially be catastrophic.

Do you give hypertonic (i.e. 3%) saline? One concern with that is that more than likely the patient is actually hyPER-natremic, a much more common scenario (2).

However, giving hypertonic saline (or hypertonic broth if the patient is capable of drinking) is actually your best bet, since the risk of harm is small if the patient is hypERnatremic (a 100 milliter bolus of 3% saline contains only 51 milliequivalents of sodium), and, if the patient is severely hypOnatremic, this small amount may be enough to get you out of trouble until a definitive diagnosis can be made.

As a result, these are the current recommendations for treatment of an acutely collapsed runner whose presentation is consistent with EAH (6, 11): immediately give a 100 milliliter bolus of 3% saline over 10 minutes, followed by an infusion of approximately 1 milliliter per kilogram per minute (up to 70 milliliters) until the sensorium clears or the sodium has returned to greater than 135 milliequivalents per liter.

As with all medicine, though, the best treatment comes in prevention. The traditional teaching of giving large amounts of fluid during endurance competition, beyond what thirst requires, needs to be abandoned. One should NEVER gain weight during endurance sports or competition. During your training sessions, tailor your fluid replacement strategies so that you are not gaining weight. Up to 2% weight loss is acceptable in endurance competition (12).

EAH represents a potential tragedy that can for the most part be avoided. Take considerable caution in the amount of fluid you consume during a race. Put simply: in endurance sports, if you are not thirsty, do not drink.

References:

  1. Danz M, Pöttgen K, Tönjes PM, Hinkelbein J, Braunecker S. Hyponatremia among Triathletes in the Ironman European Championship. N Engl J Med. 2016 Mar 10;374(10):997-998.
  2. Noakes TD, Sharwood K, Speedy D, Hew T, Reid S, Dugas J, Almond C, Wharam P, Weschler L. Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18550-5.
  3. Casa DJ, Clarkson PM, Roberts WO. American College of Sports Medicine roundtable on hydration and physical activity: consensus statements. Curr Sports Med Rep. 2005 Jun;4(3):115-27.
  4. Sawka MN, Burke LM, Eichner ER, et al. American College of Sports Medicine: Exercise and fluid replacement. Med Sci Sports Exerc. 2007 Feb;39(2):377-90.
  5. Hoffman MD, Stuempfle KJ. Is Sodium Supplementation Necessary to Avoid Dehydration During Prolonged Exercise in the Heat? J Strength Cond Res. 2016 Mar;30(3):615-20
  6. Hew-Butler T, Rosner MH, Fowkes-Godek S, et al. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015. Clin J Sport Med 2015; 25:303-320.
  7. Verbalis JG. Renal function and vasopressin during marathon running. Sports Med 2007; 37:455.
  8. Hew TD, Chorley JN, Cianca JC, et al. The incidence, risk factors, and clinical manifestations of hyponatremia in marathon runners. Clin J Sport Med 2003; 13 (1): 41-7
  9. Siegel AJ, Verbalis JG, Clement S, et al. Hyponatremia in marathon runners due to inappropriate arginine vasopressin secretion. Am J Med2007 May;120(5):461.e11-7.
  10. Rosner M. Preventing Deaths Due to Exercise-Associated Hyponatremia: The 2015 Consensus Guidelines. Clin J Sport Med 2015; 25:301-302.
  11. Chorley, JN. Hyponatraemia: Identification and Evaluation in the Marathon Medical Area. Sports Med 2007; 37 (4-5): 451-454
  12. Cheuvront SN, Montain SJ, and Sawka MN. Fluid Replacement and Performance During the Marathon. Sports Med 2007; 37 (4-5): 353-357.
  13. Almond CS, Shin AY, Fortescue EB, et al. Hyponatremia among runners in the Boston Marathon. N Engl J Med 2005; 352:1550-1556.