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Exercise-Induced Hyponatremia
Erik Adams MD, PhD Of all the conditions encountered in an endurance race, especially in an ultra-endurance race, exercise-induced hyponatremia should be considered the most dangerous. Certainly, a triathlete may be hit by a car on the course, but such events are exceedingly rare, compared to the incidence of hyponatremia. Hyponatremia means low blood sodium concentration. Normal levels are 135-145 mEq/L (milliequivalents per liter), and anything below this range is considered to be hyponatremia. However, symptoms typically do not occur until sodium levels are on the 120's. The rate of decrease of the sodium concentration is also an important factor. Rapid changes in sodium levels result in changes in the cerebrospinal fluid (CSF). Rapid lowering of sodium in the blood results in an influx of free water into the CSF, across the blood-brain barrier. This would be an osmotic effect and results in increased intra-cerebral pressure. With slower changes in blood sodium levels, sodium levels within the CSF are allowed to equilibrate with those in blood, and these fluid shifts do not occur. I have seen patients having sodium levels of 120 meq/L who were asymptomatic, but whose change in the sodium concentration occurred over days. Slow correction of the sodium level over a two-day period resulted in no adverse symptoms. Exercise-induced hyponatremia was the subject of an interesting presentation at the American College of Sports Medicine 2005 annual meeting, which I attended in Nashville. The presenter was Dr. Joseph Verbalis, an endocrinologist from Georgetown University Medical Center. His talk seemed to me to be the most often discussed by attendees in the days following. Dr. Verbalis presented evidence that exertional hyponatremia may in fact be due to the syndrome of inappropriate ADH secretion (SIADH). ADH, also known as arginine vasopressin, is a peptide hormone that is secreted by the pituitary gland in response to a variety of stimuli, and its effect is to promote resorption of free water from the urine, prior to its delivery to the bladder. ADH is an incredibly efficient hormone. Serum levels can vary between 0 and 8 pg/mL (picograms per milliliter), but increasing ADH from zero to one pg/mL results in halving of the urine output. When ADH secretion is regulated appropriately, the kidneys are capable of maintaining appropriate water and solute levels within the body. A person taking in an excess of water will produce dilute urine, and a person who is dehydrated produces a concentrated urine. One would expect, then, that triathletes who have gained weight throughout the race would produce a large volume of urine, and if their sodium level is low, their urine would be dilute. However, this has been found not to be the case. Studies at Ironman competitions and also of military personnel on long marches have shown low urine output and an inappropriately high sodium concentration within the urine. In SIADH, the urine sodium concentration usually exceeds 30 mEq/L (in fact, 95% of the time it does), whereas when urine output is low due to dehydration (which us medical people like to call volume contraction), sodium concentration in the urine is low. This is because in plain volume contraction, the kidneys are functioning appropriately and are conserving sodium, in an effort to boost the intra-vascular volume. Stimuli for ADH secretion are shown in the table below. It should be noted that some of these are appropriate and some inappropriate. For example, it is entirely appropriate for the pituitary to release ADH in response to hyperosmolarity (high solute concentration within the blood). When metabolic conditions do not call for dilution of the blood, ADH secretion should be considered inappropriate.
Table. Stimuli
for ADH release from the pituitary gland For a list of causative drugs, see www.endocrinology.med.ucla.edu/siadh/htm. Nausea is a potent stimulus for ADH secretion, and the combination of nausea, stress and pain in a triathlete should really get our attention, when we are considering whether exercise-induced hyponatremia is due to SIADH. It has been well known that triathletes who most often develop hyponatremia are those with slower finishing times. It has been hypothesized that they are at risk because they have more opportunity to consume fluids while out on the course. Certainly, limiting the amount of fluid available on the course has substantially decreased the incidence of hyponatremia. However, this explanation may either be incomplete or inaccurate, as SIADH does appear to play a substantial role. If these triathletes do have inappropriately high ADH levels, consuming the same amount of fluid as the faster and normonatremic (normal sodium level) triathletes will get them into trouble. Symptoms of exercise-induced hyponatremia Neurologic symptoms can occur at any sodium level below about 130 mEq/L, but there is great variability. Some endurance athletes with levels of 125 are asymptomatic. Symptoms can range from restlessness, headache, nausea and irritability to seizures, declining mental status, coma and death. It should not be assumed that a patient with exercise-induced hyponatremia will maintain the same severity of symptoms, once they present for medical care. That is, they can get worse. To complicate the situation, an athlete with milder symptoms may merely be irritable and uncooperative, but because of the possibility that symptoms may worsen, their cooperation with medical evaluation is essential. Prevention Consumption of sodium during the race does not seem to fix the problem. Dr. Verbalis showed an interesting slide during his talk, in which athletes consuming a sodium-containing drink were compared to those who drank only water, and their sodium levels were compared as throughout an ultra-endurance event. At the end of approximately 8 hours, their sodium levels differed by only about 1.5 mEq/L. Certainly I think the advice to avoid drinking any more water than you know you need is sound. This involves weighing yourself (nude weight) before and after exercise, taking into account any fluid intake and not urinating during the exercise bout, to determine your sweat losses during exercise. The amount of these losses vary widely between athletes. Keep also in mind, however, that you should expect to lose some weight during exercise by the burning of fuel (glycogen and fat). Therefore, consuming enough fluid to keep your weight constant may in fact be excessive. In the 1999 New Zealand Ironman, an 8% weight loss was associated with a sodium level of 140 mEq/L, so you should aim for a rate of weight loss similar to this. Considering that SIADH appears to play a prominent role in exercise-induced hyponatremia, it would be prudent to avoid all the factors that stimulate inappropriate ADH secretion. Nausea is a prime target, since it is such a potent stimulator of ADH secretion. Any endurance athlete knows that nausea is a frequent accompaniment to exercise, but it is often made worse by food intake or by drinking a sweet or salty beverage. My fellowship director remembers well what I ended up doing to our canoe leg of the multi-stage Casco Bay Challenge by deciding at the last moment to drink Gatorade instead of water, despite the fact that I have always used water during training and competition. Considering how little effect the consumption of a sodium-containing rehydration solution has on serum sodium levels, it is simply not worth it to force down a salty drink, if this makes you nauseated. Stick with what you are used to and with what does not give you nausea. The same advice would apply to the consumption of solid food during the face. Stress is a difficult component to control during an ultra-endurance race. These events are, by their nature, stressful. It is interesting to note, though, that the top finishers at these events do not appear stressed at the finish line. One woman in the Wisconsin Ironman in 2004 did cartwheels as she approached the finish line. These are the same athletes that do not develop exercise-induced hyponatremia. The much later finishers, despite the fact that they ran the race slower, are the ones that are stressed. Whether there is a direct correlation between their obvious stress and SIADH is unknown, but for now, running the race at a comfortable pace may be good advice. Dr. Verbalis also showed a slide demonstrating the influence that anti-inflammatory medication has on the effect of ADH on the kidney. These medications, such as ibuprofen, naproxen, Celebrex, potentiate the effects of ADH, resulting in increased resorption of free water and a more concentrated urine. I would therefore advise that no athlete run an ultra-endurance race while taking anti-inflammatory medication. Treatment Medical personnel need to rapidly determine the cause of any neurologic symptoms in an endurance athlete. Exercise-induced hyponatremia is not the only possibility but should always be kept in mind. An iStat machine at the finish line is helpful, as these provide rapid determination of blood sodium. Unfortunately, the manufacturer is no longer renting or lending these devices, as of summer 2005. Evaluation should include a full set of vital signs, including rectal temperature, fingerstick glucose level, and consideration of cardiac disease in the older or at-risk athlete. An athlete who developed altered mental status at a race I was covering had bradycardia (slow heart rate), due to coronary artery disease. A urine sample by straight cath, with determination of urine sodium level, can also be helpful in some cases. The athlete should be immediately given oxygen by mask, and IV access should be obtained. An infusion of 150cc of 3% saline (physiologic saline is 0.9%) often reverses or decreases symptoms and is also useful as a therapeutic trial is ambiguous cases. Above all, when exercise-induced hyponatremia is suspected or confirmed, the athlete should be given nothing to drink and normal saline or lactated Ringer's IV is inappropriate and dangerous. Finally, anybody with mental status changes or seizures due to hyponatremia requires hospitalization.
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