Heparin sodium

Context.-Recommendations for prevention and treatment of medical emergencies in participants in marathon races center on maintenance of adequate hydration status and administration of fluids. Recently, new recommendations for fluid replacement for marathon runners were promulgated by medical and athletic societies. These new guidelines encourage runners to drink ad libitum between 400 and 800 mL/h as opposed to the previous "as much as possible" advice.

Objective.-To assess the sodium and hydration (plasma osmolality) status of collapsed marathon runners after the promulgation of new hydration guidelines.

Design.-Plasma sodium and osmolality values of runners who presented to the medical tent at the finish line of the 2003 Boston Marathon were measured.

Results.-Using reference ranges derived from the general population, of 140 collapsed runners, 35 (25%) were hypernatremic (sodium, >146 mEq/L) and 6 (12%) were hyperosmolar (osmolality, >296 mOsm/kg H2O), whereas 9 (6%) were hyponatremic (sodium,

Conclusions.-Our findings indicate a significant incidence of hypernatremia with hyperosmolality and hyponatremia with hypo-osmolality among collapsed runners despite the new fluid intake recommendations, suggesting that either further educational measures are required or that the new guidelines are not entirely adequate to prevent abnormalities in fluid balance. Furthermore, the immediate medical management of hypernatremia and hyponatremia is different. Administration of fluids to severely hyponatremic patients may result in fatal cerebral edema. Our findings caution against institution of treatment until laboratory tests determine the patient's sodium status.

(Arch Pathol Lab Med. 2005;129:227-230)

Many modern-day marathon races are mass events with tens of thousands of participants. Most of these contestants are not professional athletes but recreational runners who are physically challenged by a 42.2-km (26.2-mile) race. In some marathons, hundreds of these amateurs collapse and require immediate medical attention, necessitating the establishment of medical support services at these events.1 Losses of water and electrolytes have historically been assumed to be the dominant cause of collapse in marathon runners. Consequently, the administration of intravenous fluids is frequently the first line of treatment for exercise-associated collapse.1

The best strategy to prevent the development of medical emergencies in marathon runners has been the subject of a longstanding debate centered on the ideal recommendations for fluid intake. From antiquity until the late 1960s, athletes were advised not to drink during exercise.2 This recommendation changed after a series of articles published after 1969 stressed the dangers of dehydration during marathon running. By 1996, various medical and athletic societies had issued forceful guidelines promoting vigorous fluid intake, usually encouraging runners to drink "as much as possible."1,3,4 Data obtained from healthy runners who did not experience any adverse medical events suggest that by 2001 these recommendations were achieving the desired effect and that the biochemical markers of dehydration could be largely mitigated by these recommendations.5 However, although these recommendations may have reduced the prevalence of dehydration among marathon runners, overhydration with hyponatremia has become an increasingly important problem.267 At least 250 cases of cerebral edema, 7 of them fatal, have been reported in the literature.2 Between 1989 and 1999, there were 190 hospitalized cases of water intoxication in the US Army alone, leading to a revision of the fluid replacement guidelines in the military in 1999.8 To protect runners from the effects of overhydration, the International Marathon Medical Directors Association (IMMDA), representing medical experts in the field, and USA Track and Field, the national governing body for long-distance running, also issued new fluid replacement guidelines in 2003. These recommendations advise runners to drink ad libitum between 400 and 800 mL/h, as opposed to the previous "as much as possible" recommendation.1

In view of the controversies and changes surrounding recommendations for fluid replacement for marathon runners, there is a clear need for up-to-date information on the fluid status of collapsed marathon runners. This need arises from the desire to know if the latest recommendations are effective and from the need for data to provide the best diagnostic tools and treatment to collapsed runners. We therefore investigated the incidence of hyponatremia and hypernatremia in a subset of participants in the Boston Marathon of 2003, which took place after the new fluid replacement guidelines were announced.

MATERIALS AND METHODS

Specimens

The study participants included 140 runners who took part in the 107th Boston Athletic Association Marathon in 2003 and who collapsed during or immediately after the race and for whom physicians at the medical station ordered a chemical blood analysis. To participate in the Boston Marathon, runners were required to have run a qualifying time at a certified marathon within the last 18 months. Qualifying times were age and sex specific and between 3 hours 10 minutes and 5 hours 30 minutes. The protocol for this study was approved by the institutional review board of McLean Hospital (Belmont, Mass).

Sample Analysis

Whole blood samples were obtained by trained phlebotomists using lithium heparin collection tubes. Samples were analyzed on Stat Profile M7 (Nova Biomedical, Waltham, Mass) instruments by trained personnel provided by the instruments' manufacturer. The Stat Profile M7 measures blood pH, PCO^sub 2^, PO^sub 2^, SO^sub 2^, hematocrit, Na+, K+, Cl-, Ca^sup 2+^, glucose, blood urea nitrogen (BUN), creatinine, and lactate directly and calculates the osmolality based on the following formula: osmolality = 1.86[Na] + [glucose]/18 + [BUN]/2.8 + 9. The osmolality of 50 randomly selected samples was also directly measured with a Vapro Vapor Pressure Osmometer (Wescor Inc, Logan, Utah).

RESULTS

The 2003 Boston Marathon was run at a temperature of 14.4°C to 21.6°C with a light northeasterly wind of 1 to 5 mph, near perfect conditions for a race. Of the 17548 runners who entered the marathon, 17030 (97.1%) made it to the finish line.

Physicians who provided emergency medical services in an aid station set up at the finish line ordered blood analysis for 140 collapsed runners. Direct measurement of the whole blood sodium levels of these patients indicated that one quarter (n = 35) were hypernatremic relative to the reference range for the general population in use at our hospital (sodium, 135-146 mEq/L) (Table I).9 Nine (6%) of the patients were hyponatremic relative to this standard reference range; one of these patients was severely hyponatremic, with a sodium level below 125 mEq/L. Hypernatremia appeared to be a larger concern for runners who finished within the first 4.5 hours of the race, during which time 10 of the 35 hypernatremic runners were sampled. The first of 9 hyponatremic runners was sampled at 4 hours 35 minutes. Seven of the 9 hyponatremic runners were sampled between 5 hours 50 minutes and 7 hours. The calculated osmolality derived by the instrument from the sodium, glucose, and BUN levels provided similar information as the sodium determination (Table 1 and Figure 1).

To obtain a direct measurement of the osmolality, 50 randomly selected samples were analyzed with an osmometer. Nonparametric (Spearman) correlation between the measured and the calculated osmolality was performed, and a positive association between the 2 variables was observed (p = 0.744, P

Our group has recently described modified reference ranges (or expected ranges) for a variety of hematologic and biochemical parameters in marathon runners derived from 37 athletes who had completed the Boston Marathon of 2001 without medical problems.5 At 134 to 149 mEq/L for sodium and 273 to 318 mOsm/kg H2O for osmolality, these ranges are considerably wider than for the general population. Comparison of the sodium and osmolality levels of the collapsed runners of the present study with these reference ranges still showed notable proportions of hyponatremic and hypo-osmolar collapsed runners (Table 2).

COMMENT

The new hydration guidelines of the IMMDA are intended to minimize the risk of overhydration and dehydration and represent a major change in the recommendations given to marathon runners regarding fluid intake before and during the race. We have determined the hydration status of collapsed marathon runners after the promulgation of these new guidelines and found that, when compared with the general population, approximately one third showed abnormalities in sodium levels and osmolality. Although hyperosmolar, hypernatremic runners represented most of these patients, a substantial fraction was hyponatremic and hypo-osmolar, findings consistent with overhydration. The proportion of hyponatremic and hypo-osmolar collapsed runners (relative to hypernatremic and hyperosmolar runners) was even larger when compared with reference ranges derived from runners who had uneventfully completed a similar race. The reference ranges for marathon runners have been derived from a relatively small sample size and are wider than the ranges for the general population. This explains the absence of hyperosmolar runners when reference ranges from marathon runners are used.

A number of earlier studies on the fluid status of collapsed athletes has focused on forms of exercise more physically challenging than a 42.2-km marathon race and were performed before the new fluid replacement guidelines went into effect. Speedy and colleagues10,11 studied athletes participating in the 1996 and 1997 New Zealand Ironman ultradistance triathlons (consisting of a 3.8-km swim, a 180-km cycle race, and a 42.2-km run) at temperatures of approximately 21°C. They found that between 9% and 23% of the athletes who required medical care after the competition were hyponatremic. In a study on participants in the Hawaii Ironman Triathlon, O'Toole et al12 found that hyponatremia occurred in 30% of athletes who required race-day medical care. Hyponatremic athletes had significantly lower postrace osmolality (276 vs 290 mOsm/kg H2O) than did normonatremic athletes. In this study, some of the participants had never before taken part in a triathlon; the temperature was between 22°C and 31°C. Holtzhausen and coworkers11 described the biochemical characteristics of collapsed participants in the 56-km Two Oceans Marathon held at 13°C to 19°C in 1990 and found an incidence of hyponatremia (sodium,

In a previous study on collapsed runners in the 2000 and 2001 Boston Marathons, which were run at temperatures between 20°C and 22°C, only 1 hyponatremic patient (1.2%) was present in a group of 86 collapsed runners.14 This relatively low incidence of hyponatremia may have resulted from selection bias introduced by testing predominantly faster runners (ie, those with finishing times between 3 and 5 hours), in whom the incidence of hyponatremia is lower. Three other groups have described the incidence of hyponatremia in participants in regular marathon races. In contrast to our study, these investigations were focused on hyponatremia and took place before the new fluid replacement guidelines were announced. Hsieh and colleagues15 found an incidence of 5.6% of hyponatremia in marathon runners who required medical treatment in a race run at temperatures between 65°F and 86°F and of 0.1% among all entrants in a race held in 2000. The authors noted that the weather on the race day was particularly hot and humid and may not have been representative of all marathons. Hew and colleagues16 found that among runners who sought medical care after the 2000 Houston Marathon, which was run at temperatures between 16.6°C and 25°C, 9% had hyponatremia; this represented 0.31% of the entrants. Similar to our findings, hyponatremic runners had longer finishing times. Reporting on the 1998 Suzuki Rock 'N' Roll Marathon in San Diego, Calif, Davis and coworkers17 found that of 19978 runners, 21 (0.1%) presented to area emergency departments with hyponatremia after a race that took place at a maximum air temperature of 22°C. Eleven of these patients were severely hyponatremic (sodium,

Although our findings are consistent with a decrease in the incidence of hyponatremia due to the new fluid replacement recommendations, they also indicate that despite these new guidelines, both dehydration and overhydration continue to occur among participants in marathon races that require medical attention. It is therefore possible that the latest recommendations are not optimal and will need to be adjusted further. Alternatively, it is conceivable that due to the short period between the promulgation of the new recommendations and the race, some runners were still following the old guidelines and drank "as much as possible," causing them to become fluid overloaded. Due to concerns for patient confidentiality, our study design did not allow us to investigate patient compliance with the new fluid replacement guidelines. Further studies, which will have to correlate fluid intake with hydration status, will be needed to address this question.

The clinical differentiation of dehydration from overhydration in a collapsed athlete can be difficult.16 This distinction is critical, since the treatment for the 2 conditions is fundamentally different. Dehydration is treated by the administration of fluids. In contrast, hyponatremia with fluid overload requires the opposite approach. In severe cases, the mistaken treatment of an overhydrated patient with intravenous fluids can be life threatening, resulting in cerebral edema and death. Our finding of a significant incidence of hyponatremia among collapsed marathon runners emphasizes the need for rapid measurement of sodium in the emergency workup of the collapsed runner. In most cases, laboratory testing must be immediately available at the point of care. If point-of-care testing had not been available for the workup of the collapsed runners in our study, some of the hyponatremic patients may have received unnecessary administration of intravenous fluids. However, as shown by Davis and colleagues,17 determination of sodium levels or osmolality is not always part of the medical workup of collapsed marathon runners; in their series, only 37 of 50 runners who presented to area emergency departments after a marathon had electrolyte panels performed (as mentioned, 21 of these individuals were hyponatremic).17

In conclusion, we have reevaluated the incidence of dehydration and fluid overload in collapsed marathon runners. Given our findings, it is obvious that either the new guidelines are inadequate or athletes are not always following the guidelines. The significant incidence of both hyponatremia and hypernatremia emphasizes the need for point-of-care testing devices for electrolytes or osmolality at the race site. Further studies on education of athletes are needed to address whether the new fluid replacement recommendations are optimal for all marathon runners.

References

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14. Adner MM, Gembarowicz R, casey J, et al. Point of care biochemical monitoring of Boston Marathon runners: a comparison of prerace and postrace controls to runners requiring on-site medical attention. Point Care J Near-Patient Testing Technol. 2002:1:237-240.

15. Hsieh M, Roth R, Davis DL, Larrabee H, Callaway CW. Hyponatremia in runners requiring on-site medical treatment at a single marathon. Med Sd Sports Exerc. 2002;34:185-189.

16. Hew TD, Chorley JN, Cianca JC, Divine JG. The incidence, risk factors, and clinical manifestations of hyponatremia in marathon runners. CHn I Sport Med. 2003:13:41-47.

17. Davis DP, Videen JS, Marino A, et al. Exercise-associated hyponatremia in marathon runners: a two-year experience. J Emerg Med. 2001:21:47-57.

Alexander Kratz, MD, PhD, MPH; Arthur J. Siegel, MD; Joseph C. Verbalis, MD; Marvin M. Adner, MD; Terry Shirey, PhD; Elizabeth Lee-Lewandrowski, PhD, MPH; Kent B. Lewandrowski, MD

Accepted for publication October 6, 2004.

From the Division of Laboratory Medicine, Department of Pathology, Massachusetts General Hospital, Boston (Drs Kratz, Lee-Lewandrowski, and Lewandrowski); Harvard Medical School, Boston, Mass (Drs Kratz, Siegel, Lee-Lewandrowski, and Lewandrowski); Department of Medicine, McLean Hospital, Belmont, Mass (Dr Siegel); Georgetown University Hospital, Washington, DC (Dr Verbalis); Department of Medicine, MetroWest Medical Center, Framingham, Mass (Dr Adner); and Nova Biomedical Corporation, Waltham, Mass (Dr Shirey).

The authors have no relevant financial interest in the products or companies described in this article.

Reprints: Alexander Kratz, MD, PhD, MPH, Department of Pathology, Massachusetts General Hospital, 55 Fruit St, GRJ 249D, Boston, MA 02114 (e-mail: akratz@partners.org).

Copyright College of American Pathologists Feb 2005
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