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Hyponatremia in Distance Athletes

Pulling the IV on the 'Dehydration Myth'

Timothy D. Noakes, MB ChB, MD


The strength of modern medicine is its relentless quest for an elusive perfection. That quest requires that we examine our errors even more closely than our successes. It is for this reason that the case report of Flinn and Sherer ("Seizure After Exercise in the Heat: Recognizing Life-Threatening Hyponatremia," page 61) is so important. For it records a potential tragedy that was prevented by expeditious and appropriate medical care (1)—care that conflicted with popular dogma. The timeworn understanding is that collapse during or after prolonged exercise is caused by heat exhaustion; heat exhaustion is caused by dehydration; both are prevented by inordinate fluid ingestion; and immediate treatment should be intravenous fluids. I have termed this traditional litany the "dehydration myth" (2,3). It has been relentlessly perpetuated, always in the guise of good science.

Drinking (Water) to Death

Flinn and Sherer conclude that their recruit developed the complications of hyponatremia as a result of drinking too much plain water during a series of exercises that included a 10-km hike with an 18-kg pack. He had been actively encouraged by his military leadership to drink water, presumably in copious amounts, to prevent exertional heat injury.

The debate of whether exercisers drink too little, too much, or the correct amount during endurance exercise—and whether such fluid ingestion actually influences the risk of heat injury—has been contested with vigor in the pages of this journal for more than a decade (3-9). In addition, the journal has previously reported a case of water intoxication in a marathon runner (10). Despite drinking copiously during and after the race, that runner (whose case was also described in the American Review of Respiratory Disease) received 1.5 L of intravenous fluids because "the emergency room physicians assumed that the patient was suffering from volume depletion, as they had observed repeatedly that day in other marathon runners" (11). The illogic in such assumptions has been repeatedly argued (1-3,9,12-15).

A characteristic of this debate has been the inability of some to comprehend the obvious. Whereas there are no case reports or clinical trials that unambiguously link exercise-induced dehydration with specific, life-threatening, exercise-related disorders (2,3,13), the evidence that iatrogenic fluid overload can have very serious consequences is absolute and irrefutable. Indeed, there are now at least 21 publications describing the life-threatening consequences of fluid overload in runners (10,11,16-24), triathletes (16,25-27), army personnel (28-30), and even recreational hikers (31-33). How is it possible that this evidence can be so long ignored and that athletes can continue to be encouraged to "consume the maximum amount that can be tolerated" during exercise (34), without any cautionary reference whatsoever to the dangers of drinking too much? It is a scientific paradox, for which any logical explanation continues to elude me.

Moderate Dehydration Not Hazardous

Compared with this irresistible proof, the evidence is nonexistent that the modest levels of dehydration in endurance athletes—body mass losses of 2% to 8% (12)—have any health consequences during exercise (2).

Consider first the definitive series of studies undertaken in the Nevada desert during World War II (35). There, in one study (36), groups of army conscripts exercised during the day in desert heat for as long as they could, usually up to 8 hours, without any fluid ingestion whatsoever. During this time they would cover up to 34 km. At the point of fatigue, caused by "dehydration exhaustion," subjects exhibited the following symptoms and signs: They "grew peevish and intractable; others walked in silence and were unresponsive." All developed marked physical fatigue and ultimately became "incapable of even mild physical effort." Yet "there were no obvious aftereffects of dehydration. . . . We do know that man can suffer a water deficit so incapacitating that he can neither walk nor stand; yet he recovers his walking ability within a few minutes of water ingestion, and his feelings of well-being within half an hour or less after he begins drinking. With a meal or two intervening, his recovery is practically complete in 6 to 12 hours."

If these army subjects, who developed levels of dehydration twice as great as those usually measured in modern endurance athletes, were able to recover within minutes of drinking fluids orally, where did the idea arise that much lesser degrees of dehydration are (1) life-threatening and (2) must be treated immediately with intravenous fluids? (8)

The second body of evidence—also conveniently ignored—is that up to 1969, endurance athletes were encouraged not to drink during exercise (2,12). Yet there are almost no documented case reports of complications experienced by these athletes. Thus, the impressively titled review article "Heat Stroke and Hyperthermia in Marathon Runners" (37) mentions only one case of heatstroke in a competitive marathon runner, that of Jim Peters in the 1954 Empire Games Marathon in Vancouver. The reasons other than dehydration that explained Peters' only collapse in a remarkable competitive career have been described (38). Generations of competitive distance runners were, like Peters, able to set world records at a wide range of running distances without ever consuming anything (let alone maximal quantities) and without apparently suffering life-threatening complications (as is now frequently reported in those who drink too much).

Perpetuated Error

The first error identified by the case reported in this issue may well be the perpetration and perpetuation of the dehydration myth within the United States Army (28,29) (and among other groups) despite an avalanche of contradictory evidence. So ingrained is this myth that attempts by a local Chicago columnist (39) to warn runners about the dangers of overhydration following the death of a runner in the 1998 Chicago Marathon were met with howls of indignant protests from runners, doctors, and exercise scientists (Eric Zorn, personal communication, October 1999).

I suggest that the resulting desire to administer intravenous fluids to collapsed exercisers, commendably avoided by Flinn and Sherer, has developed because the physiologic term dehydration has become established as a specific medical diagnosis encompassing almost any form of collapse in endurance athletes (2,3). But dehydration is not a diagnosis of a specific medical condition, and there is no proven relationship between dehydration and any condition associated with collapse in distance athletes (2,3). In my view, intravenous fluids are almost never required in the management of postexercise collapse, for the simple reason that they have no effect on the physiologic abnormality that is most usually present: postural hypotension secondary to peripheral blood pooling and inadequate peripheral vasoconstriction immediately on the cessation of exercise (3,14,15,40).

Diagnose, Then Treat

To return to the specifics of this case report, two points are of note regarding overall management. First, definitive treatment was not begun until diagnosis was complete. An intravenous line was placed at the field aid station only to provide intravenous access (not to treat a presumed dehydration with rapid infusion of a large volume of fluids), and the blood sodium concentration was measured as an immediate priority. Second, an appropriate treatment algorithm, presented in their figure 1, (not shown) was followed.

Diagnosis first. Diagnosis before treatment, in my view, identifies the kernel of solution. These authors avoided the usually uncontrollable urge to treat with intravenous fluids any exerciser admitted to a medical facility regardless of symptoms and clinical signs. Rather, they followed good medical practice, which is to establish a reasonable working diagnosis before initiating any therapy. This practice is especially important if that (unnecessary) therapy can also cause a fatal outcome in an otherwise healthy person (14).

My colleagues and I have shown that two factors predict the likely diagnosis in exercisers who are admitted to the medical facilities at endurance events (15,41). The first is whether collapse occurs before the finish of the race or after the athlete completes the event; the second is whether or not the athlete is fully conscious or has an altered level of consciousness, however subtle. Athletes who collapse after finishing the race are almost always fully conscious and are suffering from the sudden onset of postural hypotension, so-called exercise-associated collapse. Formerly, this condition was called heat exhaustion, but that term is inappropriate for reasons previously described (3,13). The patient described here did not finish the exercise bout; hence, the differential diagnosis excludes exercise-associated collapse, which should be diagnosed only in persons who collapse after finishing the race. As the patient had been exercising in the heat, the moment he lost consciousness, the initial differential diagnosis included hyponatremia, a cerebrovascular accident, and heatstroke, probably in that order. The initial distinction is made by measuring the rectal temperature (15), as was done in this case. As it was in the normal range of 37°C to 40°C, a diagnosis of heatstroke was excluded. The next most probable diagnosis then becomes the hyponatremia of exercise (1,15,19), confirmed by prompt measurement of the serum sodium concentration.

Although the authors report that the recruit was alert and oriented when first seen, the mental changes in hyponatremia are subtle. It is improbable that his very low serum sodium concentration (113 mmol/L) did not cause an altered level of consciousness, however elusive. Subtle mental changes without other clinical evidence of a defined medical condition, and with a normal body temperature, must always alert the clinician to a probable diagnosis of hyponatremia (1,15) in anyone who has exercised for a prolonged period with ready access to fluid—especially if the patient has been encouraged to "force fluids" to prevent heat injury.

Rational treatment. For the majority of collapsed athletes, then—ie, those with exercise-associated collapse—the sole treatment required is nursing in the head-down, Trendelenburg position (15). (See also "A Guide to Treating Ironman Triathletes at the Finish Line," August.) Since adopting this technique, we have essentially removed the need ever to give intravenous fluids to these athletes, regardless of the intensity or duration of the effort they had sustained. For example, in the recent 226-km Cape Town 2000 Ironman Triathlon, we intensively evaluated in the medical tent at the race finish all the athletes who completed the race. This included 290 triathletes and approximately 100 athletes who had either run the 42-km marathon or who had cycled the 180-km course as individual members of relay teams also participating in the race. It was not necessary to treat any athlete with intravenous fluids, despite the fact that the race was held in midsummer temperatures that approached 30°C at midday, the time the marathon race began. Treatment in the other exercise-related conditions, hyponatremia and heatstroke, is described ably by Flinn and Sherer and elsewhere (1,3,15,20,24,25,32).

Hyponatremia vs Heat Illness

Regarding the classification of exercise-related collapse, the only very minor quibble I have with Flinn and Sherer is their (albeit updated) definition of heat exhaustion. These authors suggest that heat exhaustion is a form of heatstroke in which there are only minor changes in mental status and function. As this distinction can only be made retrospectively, I would prefer that all patients with an elevated rectal temperature and mental changes at the time of collapse be diagnosed with heatstroke and the severity assigned only when the patient has recovered.

The danger in the novel definition proposed is that subjects with the subtle mental changes characteristic of hyponatremia—which, as this case report shows, can progress to convulsions and coma with frightening rapidity—may be diagnosed as cases of heat exhaustion and treated inappropriately, perhaps with intravenous fluids. Rather, I argue that, if the rectal temperature is not elevated to 40°C at the time of collapse, the patient does not have a heat illness, and another cause for collapse must be sought (3,13,15).

We have found that athletes who are fully conscious, and whose rectal temperatures are below 40°C, do not require active cooling because their body temperatures will normalize without intervention. Nor are their symptoms of collapse caused by their (normally) elevated body temperatures. Rather, they are likely to be suffering from postural hypotension and will recover rapidly when treated in the head-down position.

Introducing a new definition for heat exhaustion can only lead to more confusion and further hamper the general acceptance of a concise and logical approach to the assessment and management of the collapsed exerciser. Mental changes in an exerciser whose rectal temperature is less than 40°C should only be ascribed to a heat injury if hyponatremia and hypoglycemia have been excluded by appropriate blood testing.

Too Much Fluid Can Hurt

To summarize, once the recruit convulsed and lapsed into coma, the most likely diagnosis was the hyponatremia of exercise. Heatstroke was excluded by the expeditious measurement of the rectal temperature, and the correct diagnosis of this case was immediately established by the equally rapid measurement of the serum sodium concentration. The condition was caused by a fluid intake that was, at the very least, 6.5 L in excess of requirement during 9 hours of moderate military exercises. Such inappropriate fluid replacement was caused by the promotion of the twin dogmas that hold that heatstroke is caused by dehydration (2,34), and that it is prevented by copious fluid ingestion during exercise (42). There is no scientific evidence whatsoever for either belief (2,3,13). Rather, as this recruit and these authors discovered, "Too much fluid can hurt."

It is not a novel observation (1,16).


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Dr Noakes is the Discovery Health professor of exercise and sport science at the University of Cape Town and the Sports Science Institute of South Africa in Newlands, South Africa. Address correspondence to Timothy D. Noakes, MB ChB, MD, Sports Science Institute of South Africa, Boundary Rd, Newlands 7700, South Africa; e-mail to [email protected].