Exercise-associated hyponatremia (EAH) is an important, amazingly common, and potentially life-threatening condition that affects athletes who participate in sustained activity. It is also preventable. The following is a true vignette.
An experienced, very fit, non-anorexic, middle-aged female, accompanied by family members, hiked up to a 14,000+ foot summit on a mountain in the United States. She had spent three days acclimatizing before this hike. Her nutrition on the morning she began the hike may have been an energy bar (at around 6 AM). During the hike, she had an apple and a handful of nuts, but not much else. She was mainly thirsty, not hungry. To sate her thirst she drank water that had been collected and filtered from streams along the way. She did not carry much hydration from the start to minimize weight and she did not add electrolytes to her filtered water.
She summited the mountain and began to descend back down the trail. At around 1 PM, at about 10,000 feet of elevation, she began to complain that she felt “weird” and had a headache. She developed increasing disorientation and fatigue and then began to develop very unusual behaviors, which she does not remember. Her confusion continued to progress to the point at which she was unable to speak. She then began to stumble and could not stand. She was carried, using a makeshift litter, by Good Samaritan hikers to a location further down the mountain. While being carried, the woman experienced a “full body seizure.” A rescue team had been contacted. When they arrived on the scene, according to their report, the woman was responsive to painful stimuli only. She was unable to speak or to follow commands. She then vomited. The rescue team, which, along the way, grew in size to 13 individuals, carried the patient down the mountain to a waiting ambulance.
She arrived at the hospital at approximately 3:45 AM and had a very low sodium of 118 and a reportedly normal head CT. The woman was intubated (a breathing tube was put into her throat so that her airway could be protected and physicians could control her breathing) and she was airlifted to another medical center. She received IV fluids and a repeat head CT reportedly showed brain swelling. By noon on that same day, her sodium was normal and she was extubated. However, her creatinine kinase (which is released when muscle is damaged) was very high at 27,000 and she was kept in the hospital for 3 more days until this level dropped to 3,000.
This very fortunate woman is alive, well, and, apparently, has no lasting damage from this event. This is fantastic news. Unfortunately, other people have not done as well with exercise-associated hyponatremia. There have been a number of known fatalities from this condition (at least 14 in athletes since 1981). As recently as the summer of 2014, two otherwise healthy 17-year-old high-school football players died from hyponatremic encephalopathy, which is the usual cause of death from EAH. Deaths from EAH have occured during participation in the following activities/sports: marathon, canoe race, hiking, military exercises, police training, American football, and fraternity hazing.
Definition of exercise-associated hyponatremia
The lower limit of normal for sodium is 135 mmol/L. EAH is defined as a sodium value below 135 occurring up to 24 hours after exercise. This condition is often asymptomatic. But a much lower level of sodium (below 125) and a more rapid, but smaller fall to higher levels of sodium (as high as 130) can be associated with symptoms. The individual described, above, with a sodium level of 118 had a critically low level.
Epidemiology and Presentation of EAH
Prior to 1981, athletes were advised to avoid drinking during exercise (doesn’t this sound nuts today?). This led to a number of cases of hypernatremia (high blood sodium). Therefore, authorities, around 1981, began to suggest drinking as much water as possible during exercise. This led to a number of cases of EAH and ongoing misunderstanding about the dangers of overhydration.
EAH can be asymptomatic or symptomatic. Symptomatic individuals can have mild symptoms such as lightheadedness and nausea or more severe symptoms such as headache, vomiting, confusion, seizures, and respiratory distress. The confusion and seizures arise from swelling of the brain (exercise-associated hyponatremic encephalopathy) and the respiratory distress arises from non-cardiogenic pulmonary edema.
Asymptomatic EAH has most prominently been noted in 161-km ultramarathons, in which the incidence has ranged from 5% to 51%. In Ironman triathlons, the range of incidence has been negligible to 25%. For cyclists participating in a 109-km race, the rate was reported as 12%. In a 26.4-km swim, the incidence was 17%. For marathoners, the incidence has ranged from 0% to 13% of finishers. After an 80-minute rugby competition, premier league UK players had a rate of 33%. Finally during a 28-day training camp, 70% of elite rowers had asymptomatic EAH.
Symptomatic EAH is much less common than asymptomatic EAH. In one study of 2135 endurance athletes drawn from 8 events of varying distances, the incidence of symptomatic EAH was 1% (versus a 6% incidence of asymptomatic EAH in this study). In another study of 669 161-km ultramarathon runners, there was only one case of symptomatic EAH, an incidence of under 0.1% (versus a 13% incidence of asymptomatic EAH in this study).
The most important risk factor for the development of EAH is the over-consumption of water, sports drink, or other fluids with electrolyte content lower than human plasma. That’s right: guzzling sports drink DOES NOT, repeat DOES NOT prevent dangerous EAH from occurring, due to dilution of the plasma.
Additional risk factors include being smaller in size and being slower (e.g. marathon times over 4 hours). The use of NSAIDs (please see my extensive series of articles about NSAIDs and athletes to learn a lot more about this subject), also, at least theoretically, can be a risk factor for EAH by leading the kidneys to retain more water (by strengthening the effects of arginine vasopressin (AVP), which leads to more production of anti-diuretic hormone). Interestingly, there is not much evidence about the “salty sweater” and relative risk of developing EAH.
Mechanism of EAH
EAH is a result of dilution. In this condition, the rate of increase in total body water exceeds the rate of removal of body water (through sweat, respiration, and urine) and the rate of replacement of sodium is inadequate to keep up with needs. This mostly occurs through drinking too much water or other drinks, including sports drinks, that do not have as much electrolytes as human plasma. Another mechanism at play is decreased clearance of water from the kidneys due to heightened activity of the hormone, AVP. This hormone is released by the pituitary gland in the brain and is usually responsive to the osmolality of the blood (changes in levels of sodium in the blood change the osmolality). However, during sustained exercise, AVP production is responsive to other stimuli and (probably from teleological reasons) typically increases, which leads to heightened retention of water by the kidneys. Interestingly, another source of extra water is the release of water, which had been bound to glucagon, when glucagon is consumed for energy.
Most of the damage to the body, from EAH, is a result of water entering comparatively salty cells throughout the body (biological forces lead water to go to more salty areas). The most important area affected by this phenomenon, by far, is the brain. This leads to swelling of the brain. In fatalities from EAH, typically the brain swelling becomes so severe that the brain stem is forced into a narrow opening at the base of the skull. This severely damages the brain stem and leads to death.
Treatment of EAH
Most of the treatment of EAH is beyond the scope of this article. However, there are a few important concepts that medical personnel keep in mind when treating this condition. The most important of these concepts is that giving routine fluids used for ill people, such as normal saline, can dilute the plasma more and make EAH, with associated brain swelling, worse. Therefore, hypertonic saline (saline with very high salt content) is the mainstay of treatment. The challenge, however, for medical personnel is that athletes can collapse for a number of reasons and, for most of them, normal saline is appropriate. For example, in a study of over 1300 people who collapsed during Boston Marathon events between 2001 and 2008, only 5% had hyponatremia whereas 28% had hypernatremia. Therefore, medical personnel need to rely on key aspects of the history to correctly make the diagnosis, such as sustained exercise and consumption of a lot of fluids, along with confusion and other evidence of brain swelling. Some organized events attempt to aid medical personnel by obtaining pre-race weights of athletes. An athlete with signs and symptoms of EAH who has gained weight or has lost less weight than can be expected for the circumstances of the race, is much more likely to, indeed, have EAH. There has also been a call to have plasma sodium measuring devices available to medical personnel to truly establish the diagnosis.
Prevention of EAH
If you, the reader, remember nothing else from this article, please remember this:
DRINK TO THIRST!
The thirst mechanism of the human body is finely tuned to respond to small changes in osmolality. Furthermore, it is difficult to accurately predict sweat rates and other aspects of fluid balance in all conditions, especially for slower athletes, so drinking to thirst is the most appropriate gauge of fluid needs for most athletes. In fact, a small study of 8 female marathon participants demonstrated that drinking to thirst did not lead to overhydration. The Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference (2015) states:
“Earlier published recommendations to begin drinking before thirst was largely meant for situations where sweating rates were high, above maximal rates of gastric emptying, and dehydration would rapidly accrue over time. Unfortunately, this advice has fostered the misconception that thirst is a poor guide to fluid replacement and has facilitated inadvertent overdrinking and pathological dilutional EAH.”
As mentioned previously, sports drinks have much less sodium than the serum. Therefore, overdrinking sports drinks can lead to dangerous dilution of sodium and, therefore, EAH. The take home message is that a sports drink will not protect you from developing EAH if you drink too much.
Another approach to preventing EAH is to provide fewer hydration stations at races. For example, studies have shown that spacing fluid stations 20 km apart on the bike in an Ironman triathlon or 5 km apart in a stand-alone marathon has reduced or prevented EAH.
Exercise-associated hyponatremia is common, dangerous, and preventable. The most important concept to keep in mind to prevent EAH is to drink to thirst. Sports drinks are great for a lot of reasons, but they do not prevent EAH.
Please be careful out there!
Hew-Butler T. Arginine vasopressin, fluid balance and exercise: is exercise-associated hyponatremia a disorder of arginine vasopressin secretion? Sports Med. 2010 Jun;40(6):459-47
Hew-Butler T, Rosner M, Fowkes-Godek S, et al. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015. Clin J Sport Med. 2015 Jul;25(4):303-320.
Rosner M. Preventing Deaths Due to Exercise-Associated Hyponatremia: The 2015 Consensus Guidelines. Clin J Sport Med. 2015 Jul;25(4):301-302.