Mean serum sodium, chloride, BUN, glucose, and Hct values for the treatment groups are shown in Table 2. Many samples hemolyzed before measurement with resultant unusable potassium values; therefore, serum potassium was excluded from analysis. The groups did not differ significantly with respect to the remaining parameters (sodium, P [t52 = 1.68] = 0.10, missing = 8; chloride, P [t52 = 1.37] = 0.18, missing = 8; BUN, P [t52 = −1.16] = 0.25, missing = 8; glucose, P [t55 = 1.23] = 0.22, missing = 5; Hct, P [t52 = 0.01] = 1.00, missing = 8). The frequency distribution of serum sodium values is shown in Figure 1.
The incidence of hyponatremia, defined as serum sodium value less than 130 mEq/L, is 5.6% in this study (N = 3; missing = 8; 95% CI, 0–11.9). All three hyponatremic subjects received intravenous hydration and drank at least some sports drink at every aid station. Detailed oral intake can only be estimated. If each runner finished one 100-mL cup of drink at each station, about 2.5 L of fluid would be consumed over the entire course. The amount of intravenous fluid administered was recorded for one of the three hyponatremic runners. Table 3 lists the descriptive data as well as clinical course for those three individuals. No unique sign or symptom identified the hyponatremia runners. In addition to the three hyponatremic runners, 16 normonatremic subjects presented with vomiting, 19 with dizziness, four with headache, and eight with initial systolic blood pressure below 90 mm Hg. None of the three patients suffered any neurologic complication. Interestingly, one subject who did present to the medical tent with new-onset seizure had a normal serum sodium value of 142 mEq/L. His initial temperature at the medical tent was 106°F. The small number of subjects with hyponatremia prohibited the performance of logistic regression analysis to determine the possible contribution of the type of fluid intake or NSAID use on the development of hyponatremia. The subject with sodium of 122 mEq/L did not use any NSAID before the race. This information was not available for the other two subjects.
As the most comprehensive evaluation to date of the incidence of hyponatremia in marathon runners requiring on-site medical treatment, this study demonstrated a clinically significant proportion (5.6%; 95% CI, 0–11.9) of hyponatremic runners. However, this marathon was conducted during a particularly hot and humid day. It may not have been representative of all marathons. Interestingly, Nelson et al. (12) examined electrolyte changes in 47 runners in the 1987 marathon in the same city and did not report any occurrence of hyponatremia. The more severe heat stress in the 2000 race may have predisposed runners to health complications such as hyponatremia. The actual incidence of hyponatremia for all runners requiring medical treatment in this marathon may have been underestimated because some runners were transported from aid stations on the course before completion of the race. This group who do not reach the finish line may be at higher risk because they could represent the less prepared runners. Others sought medical attention on their own at local emergency departments after the race. There are no data estimating the incidence of hyponatremia in that population. Although the incidence of hyponatremia in the runners who required medical treatment is clinically significant, this entity is still a rare event in all the runners of this race (∼0.1% of all finishers). We chose to focus on the subset of runners who required medical treatment because that was the population of concern to the medical providers. The incidence of hyponatremia is understandably higher in this subgroup of runners than in the general population of marathon runners.
Although none of the hyponatremic runners suffered neurologic or pulmonary complications, the fact that the runner with the lowest sodium value sought further medical attention after discharge from the medical tent suggests that clinical appearance and vital signs of the runners alone may be inadequate for determining readiness for discharge. Symptoms of exertional hyponatremia include nausea, vomiting, headache, and altered mental status. Unfortunately, these symptoms also overlap those of other exercise- and heat-related illnesses. During a follow-up telephone interview, that runner reported that she continued to have nausea and a headache after her discharge from the medical tent, and that her serum sodium was found to be low during an emergency department evaluation that evening. This protracted course of hyponatremia may reflect inadequate medical treatment initially or continuation of the physiologic forces causing this condition.
The design of this study could not determine the relative contribution of salt loss or excessive intake of water to the hyponatremia observed in some runners. Although sodium loss through sweat (6) and replacement with hypotonic solutions (10,25) may contribute to hyponatremia, the problem is fundamentally caused by an inability to secrete free water appropriately (28). Renal damage from exercise (13), medication (2,11) or myoglobin (3), and inappropriate secretion of vasopressin and antidiuretic hormone (1,20,30) have been postulated to play a role. Since these mechanisms take some time to reverse, runners may be at prolonged risk. Furthermore, delayed hyponatremia may develop in initially normonatremic finishers with the relief of splanchnic vasoconstriction and increased gastric absorption of fluid ingested during the race (4). The present data may support the idea that exertional hyponatremia may result from diverse causes. For example, the woman with sodium of 122 mEq/L had a Hct somewhat lower (37%) than observed in other subjects (Tables 1 and 3). At the same time, one other hyponatremic subject had an unusually high Hct (54%). It is possible that the former subject exhibited hemodilution secondary to excessive water intake, whereas the latter subject was hemoconcentrated after excessive fluid loss. The relative contribution of these factors to hyponatremia could be distinguished by a prospective measurement of prerace and postrace sodium levels as well as fluid intake and output and weights of individual runners during a race.
Although clinically significant, the small number of hyponatremic runners in this study precluded the analysis of fluid type ingested or NSAID use as possible contributing factors. For the same reason, one could not build a model of clinical variables to predict hyponatremia on the basis of these data. Further studies could increase the number of hyponatremic cases by obtaining hospital data of the runners transported from the course or combining data from several marathons. These larger data sets may give improved estimates of actual incidence of hyponatremia. Since we did not measure prerace sodium, we do not know whether the hyponatremic runners may have had low sodium to start with; however, other studies that did measure preevent sodium reported no occurrence of preevent hyponatremia (12,15,21,27). Furthermore, this study makes no attempt to evaluate the incidence of hyponatremia in marathon runners not seeking treatment or the incidence of prolonged or delayed hyponatremia. This assessment would require canvassing of local emergency departments for runners presenting for medical evaluation as well as measurement of pretreatment and posttreatment sodium values of runners receiving treatment at the medical tents.
Results of this study challenge the belief that hyponatremia is uncommon in athletes participating in nonultraendurance events. The prevalent medical practice of treatment on-site and disposition on the basis of clinical status may need to be reevaluated in light of the clinically significant incidence of hyponatremia, the current inability to predict hyponatremia on the basis of unique presenting signs or symptoms, and the protracted and delayed nature of the postulated mechanisms for the development of hyponatremia. The fact that all three hyponatremic runners had a finishing time over 4 h may be a helpful triaging criterion. On-site electrolyte testing may be helpful, especially for race conditions that place runners at increased risk of heat-related illnesses according to ACSM guidelines. On the basis of these guidelines, hyponatremia or other metabolic disturbances might have been anticipated in runners becoming ill during the hot and humid conditions of the present marathon. Because of the findings of this study, the upcoming race will be started a 30 min earlier to help alleviate the heat stress, and runners will receive more frequent updates on the weather and race condition. The medical staff of this marathon will be testing on-site the sodium levels of all runners requiring intravenous hydration before and after infusion. A finding of hyponatremia will be added as a criterion for hospital transfer. The cost of this practice will be approximately $10 per test in addition to the purchase of portable analyzers at approximately $6000 each. More extensive testing of runners requiring treatment and increased follow-up data would be helpful in assessing the cost-effectiveness of those measures.
This study was supported by a grant from the Pittsburgh Emergency Medicine Foundation.
We thank Shawn Hicks, Christopher Lightfoot, David Newman, M.D., and Lori Wylie, M.D., for their assistance during the marathon.
Address for correspondence: Margaret Hsieh, M.D., 230 McKee Place, Suite 400, Pittsburgh, PA 15213; E-mail: firstname.lastname@example.org.
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