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Sideline and Event Management: Case Report

Case Series of Exertional Heat Stroke in Runners During Early Spring: 2014 to 2016 Cincinnati Flying Pig Marathon

Divine, Jon G. MD, MS1; Daggy, Matthew W. MD2; Dixon, Emily E. DO2; LeBlanc, Dustin P. MD3; Okragly, Richard A. MD2; Hasselfeld, Kimberly A. MS1

Author Information
Current Sports Medicine Reports: May 2018 - Volume 17 - Issue 5 - p 151-158
doi: 10.1249/JSR.0000000000000485
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In Brief

Introduction

Participation in mass endurance events continues to increase annually in the United States. Running USA’s 2014 Annual “State of The Sport” reports a record breaking 19+ million finishers in U.S. endurance events last year, with double-digit growth led by nontraditional running events, such as mud runs and obstacle courses, which accounted for 49% and 40% of all participants, respectively (1). The half marathon continues to have the greatest composition of female participants. Sixty-one percent of 1.98 million U.S. finishers were women; a demographic that has continued to rise over the five preceding years. Of the 509,000 marathon participants, the majority are men (56%) (2).

Marathon running is a reasonably safe endeavor (3): the overall death rates for the 10-yr period from 2000 to 2009 were 0.75 deaths per 100,000 finishers, with the vast majority being due to cardiac causes (4). In a similar review, Yankelson et al. (5) reported that from 2007 to 2013, 137,580 runners participated in “popular endurance running events” in Tel Aviv and that there were 21 cases of serious exertional heat stroke (EHS) and two heat-related fatalities, or an incidence of 2.74 fatalities per 100,000 runners and 2.8 cases of EHS per 10,000 runners.

Running performance has been shown to directly diminish in relation to increase in ambient temperature (6–10). When the athlete continues exercising without regard for increasing heat stress other nonspecific symptoms present in clusters. Headache, muscle cramping, dizziness, nausea/vomiting, and confusion are all nonspecific findings found early in those with EHS. As these symptoms are common after an endurance race, to diagnose (and treat) EHS the rectal temperature (CBT) must be measured as >40°C and must be accompanied by clinical signs of altered mental status (AMS), central nervous system (CNS) dysfunction, seizures, and ultimately end-organ failure (11).

The relationship between environmental conditions and running performance has been extensively studied (3–9). Most notably, in a review of race finishers over 18 yr at the Falmouth Road Race held annually in Cape Cod, Massachusetts, in August when the average heat index was 24.6°C ± 3.5°C, the incidence of EHS was 10 to 20 cases per 10,000 entrants (12). Also, as Roberts (13) has reported, the number of marathon participants who “successfully complete” a marathon decreases as the heat stress increases and that the risk of requiring medical attention and not finishing a marathon event rises considerably when the wet bulb globe temperature (WBGT) is >15.5°C (60°F) (14).

On the other hand, the incidence of marathon-associated, serious heat illness or EHS in other endurance runs in more temperate climates is much lower. In a study of the Indianapolis Half Marathon, which is held annually on the first weekend in May, Sloan et al. (15) reported a total of 32 runners out of over 235,000 (1.36 per 10000) with EHS over a period of 8 yr (2005–2012). Of these, 78% occurred on the three race days with the highest ambient temperature of 18.3°C (64.9°F). Roberts (16) has reported a similar incidence of one to two cases of EHS per 10,000 entrants, over 12 Twin Cities Marathon races held annually in early October where the temperature ranged from −4°C to −16°C at the start and 5°C to 20°C at the finish.

With such a high incidence, EHS can be anticipated with prolonged, intense exercise in a hot, humid, and/or sunny environment. The greatest risk for EHS exists when (17–19):

  • 1) the WBGT exceeds 28°C (82°F);
  • 2) during high-intensity exercise (75% V˙O2max) and;
  • 3) when strenuous exercise lasts longer than 1 h.

All three risks can be associated with participation in either a full or half marathon, with the WBGT being the most likely variation.

Although extreme environmental conditions decrease performance and increase the risk of acquiring EHS, it is important to consider other factors that can exaggerate the risk of EHS (20). It is important to keep in mind that EHS also has been reported to occur in marathon race participants during what is often felt to be an “ideal” temperature (8°C–18°C [45°F–65°F]) weather conditions (21). It is important to keep the clustering of EHS symptoms in mind: under all-weather circumstances, during or after an endurance race (22). Because of this, all athletes with acute, atraumatic AMS, especially those participating in endurance events, should be considered as having EHS until proven otherwise.

Once EHS is diagnosed the current use of rapid cooling, in the form of ice-water immersion (IWI) at the earliest recognition of EHS, has been associated with lower morbidity and mortality and is recognized as the “best practice” for mass participant and competitive events and training (23–25). Several studies have reported that once elevated CBT (>40 °C) is identified, immediate “dunking” or immersion into an ice-water tub is the most effective method for rapidly decreasing elevated CBT and reducing the risk of potentially fatal end-organ damage (20,23,25,26). Any delay in rapidly cooling the elevated core temperature increases the risk of morbidity/mortality.

Several potential risk factors for EHS have been previously described. In a 2004 report by Rav-Acha et al. (27) on six fatal EHS military cases predisposing factors included low level of physical fitness, sleep deprivation, high ambient temperature, intense solar radiation, exercise intensity not matched with physical fitness, ineffective or absent medical triage, and disregard for organizational safety regulations. Other general risk factors include body mass index (BMI), sex, body leanness or obesity (28,29), fluid intake before competitive endurance activity (17,18,30), inadequate physical fitness (31–34), incomplete heat acclimatization (11,17,27,35–39), episodes of previous heat illness (40–42), or other temporary factors, such as illness or medication use (21,43). Elevated CBT during warm-up also has been shown to have a strong relationship to developing post-run EHS (44). There have been no reports looking specifically at the sex differences in risk of EHS; especially within the growing number of woman who are participating in half marathon events.

The purpose of this case series is two-fold: to review and compare differences in EHS incidence in male and female participants occurring over 3 yr in Cincinnati Flying Pig full and half marathons and to describe our findings using IWI to treat EHS.

The Flying Pig Cincinnati Marathon (42.2 km) and Half Marathon (21.1 km) are held annually on the first Sunday in May in Cincinnati, Ohio, located roughly at 39.1° N latitude and 84.5° W longitude. The course, certified by USA Track & Field, is paved and made up of rolling hills with a start line elevation of 500 ft above sea level and a maximum elevation of 827 ft at about eight miles after the race start. The half marathon is run concurrently. Half marathon participants follow the same course as the full marathoners until the 8-mile mark where they return downhill over the final five miles to the same finish area where the marathoners will finish (see course elevation map and average heat and humidity for 2014, 2015, and 2016 marathons, Fig. 1). Weather data were obtained using WBGT (Kestrel 5400; Heat stress tracker, Minneapolis, MN) and compared with historical data housed on the National Weather Service website.

Subjects studied retrospectively were male and female runners who completed either the half or full Flying Pig marathons during the years 2014 to 2016. There was an experienced medical staff member at the finish line area providing medical care which followed pre-established treatment protocols comparable to other major road races in the United States. Runners presenting to the medical tent with AMS immediately received an assessment of vital signs including a rectal temperature. Ice-water immersion was done by placing the runner with EHS into a 150-gal rubber (RubberMaid) tank with a mix of cold water and ice and the runner immersed totally so the water/ice line met the chin. Water/ice was stirred regularly while the runner was immersed to improve heat conduction from the runner and optimize convective cooling.

F1
Figure 1:
Course elevation map.

Statistical Analysis

EHS incidence frequency of occurrence was expressed as EHS cases per 10,000 finishers per year for uniformity of the denominator with previous literature reports. The EHS incidence frequency was calculated for each of four groups: females finishing full marathon, females finishing half marathon, males finishing full marathon, and males finishing half marathon. A Chi square test was utilized for statistical testing to decide whether there was a difference between the observed incidence of EHS (per 10,000 runners finishing either event) for male or female runners completing either a full or half marathon and the expected value.

Over the 3-yr period, 2014 to 2016, 46,063 finished either the full (11,593) or half (34,470) Flying Pig Marathon events (Table 1). A higher number of women (26,890) than men (19,173) finished: the higher relative number of women completing the half (21,793 vs 12,677 men) and a slightly higher number of men finishing the full marathon (6,496 vs 5,097). There was not much deviation in the annual number of runners: the mean annual number of overall race finishers from 2014 to 2016 was 3,863 and 11,490 for the full and the half marathons, respectively. Finish times average 4:44 for the full and 2:31 for the half marathon.

T1
Table 1:
Statistics for 3 yr of marathons.

During the 3-yr series, weather conditions could be described as temperate with an annual, elevated humidity. The mean temperature for all 3 yr was 18.1°C +/− 1.3°C (64.6°F) with 80% to 9.4% humidity. The WBGT temperature during the 3-yr series ranged from 7.2°C (45°F) +/- 26.7°C (80°F) with the low WBGT at the start of the 2015 race and the peak WBGT at 6 h during the 2016 race.

Annually, the start of the race is at 6:30 a.m., roughly sunrise, with cool starting temperatures and high humidity. On race days, the average low temperatures were at the start of the race (12.2°C [54°F]/84% humidity) with relatively calm winds all 3 yr. As the run progressed, mean ambient temperatures gradually increased to 17.2°C (63°F)/83% humidity, on average, 3 h into the race. Mean temperatures at 6 h from the start, were 22.2°C (72°F)/73% humidity. Wind speeds were annually reported as calm within a range of 0 to 16 kph (0–10 mph). Cloud cover all 3 yr was reported as moderate to minimal, with periods of maximum sun exposure all 3 yr.

A total of 28 finishers (Table 1) of varying distances (6 to 26 miles) presented for medical care over the 3-yr series with AMS and were assumed to be hyperthermic. Each had CBT (rectal) temperature measured within 2 min of presentation: mean CBT was 41.3°C (106.3°F, +/−1.3°F) (range, 40.2°C [104.3°F] to 42.8°C [109.0°F]). Data were normalized to calculate the incidence of runners with EHS per 10,000 finishers and provided in Table 1. There were no differences in the annual absolute numbers of total finishers treated for EHS; however, the mean absolute number of men treated for EHS annually was 6.3, over twice the mean absolute number of 3.0 for females. Normalized, the incidence of males treated for EHS was 2.6× that for female finishers with 8.9 male finishers per 10,000 person years treated and the incidence for females was 3.3 finishers/10,000 person years.

Per prerace treatment protocol, all runners identified with a CBT >40°C (104°F) were immediately treated with IWI (immersed completely — with only head exposed), with the fluid being stirred around the immersed runner. The thermistor remained in place for CBT monitoring while being cooled. Intravenous (IV) access also was established (if possible) before immersion. It is important to note that none of the runners with EHS were delayed immersion because of lack of IV access after immersion. Target CBT for removal from immersion was <39.0°C (102.5°F). The IWI data are summarized in Table 2. The mean duration for time in IWI was 12.9 min (95% confidence interval [CI], 11.3–14.5 min). The rate of CBT decrease was 0.22°C·min−1 (95% CI, 0.17–0.27°C·min−1) and is shown in Figure 2. There were no sex or half-participation versus full-participation differences in rate of cooling indices.

F2
Figure 2:
The rate of CBT decrease was 0.22°C·min−1 (95% CI, 0.17–0.27°C·min−1).
T2
Table 2:
IWI data for runners of both half and full marathon.

Once CBT reached <39.0°C (102.5°F) runners were removed from the IWI treatment and based on their postcooling mental and physical status were either observed closely at the finish area (n = 7) or transported to a local level 1 emergency center (n = 21) where further monitoring could be done. After the initial treatment, none of the runners experienced a repeat rise in core temperature. All continued to receive an additional 1 L to 2 L of 0.9 NS IV fluids. Each of the 28 runners improved rapidly and had no further problems during observation. Within 4 h of finish, all runners observed at the finish line or in the ED were back to their normal mental status. All 21 observed in the ED were discharged to home the following day.

During the 2014 race, there was one healthy, 26-yr-old male runner (not included in this data series of 28 finishers treated at the finish line) who collapsed on the racecourse and was reported by police observers to have AMS. Soon after initial observation, he lost consciousness at the 16-mile mark. He was intubated to maintain his airway and transported off the course by the local EMS to the “closest local hospital” with a CBT measured at 41.0°C (106°F). Despite efforts to cool the runner using ice packs, fans, and IV fluid (without IWI), the runner did not respond to cooling treatments, continuing to have a CBT of 40.6°C (105°F) and was transported roughly 1 h from when he was found down on the course to the same level 1 emergency center as the other (17) runners. He was admitted to the intensive care unit (ICU) where he regained consciousness, and with the use of cooling blankets, fans, and room-temperature IV fluids, he had a gradual decrease in CBT, approximately 2 h after his acute episode. He remained sedated because of the intubation for the next 24 h. Although he did develop an elevated INR, no other end-organ damage was observed during the three additional days of ICU monitoring. By the time of discharge, 4 d after his CBT elevated event, his INR returned to 1.0, and he returned back to his normal mental state. This is the only known runner during this 3-yr series diagnosed with EHS who did not receive IWI therapy and who also required the most intensive medical care.

When broken down by event, the incidence of EHS for half marathon finishers over the 3-yr period was 3.19/10,000 and 12.94/10,000 for full marathon finishers. When broken down further by event and sex, male full marathon finishers had a 20.01/10,000 incidence of EHS which was significantly (P < 0.05) higher than the remaining three categories: female full marathon finishers (3.92/10,000), female half marathon finishers (3.21/10,000), and male half marathon finishers (3.16/10,000). There was no difference in presenting CBT or rate of cooling for sex or events.

Of the 28 with EHS, we were surprised that two runners completed only a six-mile leg of a corporate relay not having run in either the half or full race: of note, one of the 6-mile runners presented with a CBT of 42.2°C (107.9°F) and reported having had a prior history of EHS; however, no other specific details about the previous EHS episode could be obtained. The total number of relay finishers could not be accurately secured, thus these two runners were not included in the calculation of EHS incidence in this case series. Therefore, the total incidence of EHS in our series was calculated at 5.64/10,000 half or full marathon finishers.

Discussion

Although the weather for the 2014 to 2016 Flying Pig Marathon can be described as “temperate” (mean temperature, 18.1°C; mean humidity, 80%), 28 (6.1/10,000) runners presented with AMS during these three race years and were diagnosed with EHS >40°C (104°F). Of those 28 runners, a total of 26 runners finished either the half or full marathon and two male runners who finished only a 6-mile leg of a marathon relay were all treated for EHS with IWI. After a mean cooling time of 12.9 min, all runners returned to baseline mental status and did not have any further complications. It is also important to note that during this case series period, there was one runner (not included in data analysis) who collapsed on the course with AMS, had a measured CPT of 41°C (106°F) and who did not receive immediate IWI. He survived, but was treated by more conventional methods of cooling (ice bags and fanning) within an emergency room setting and required four additional days of intensive care monitoring and management. After the 2014 race, local EMS changed protocol for transport of runners with AMS suspected of having hyperthermia during the Flying Pig. Runners are now transported to the closest facility capable of immediate IWI treatment: either the local level 1 trauma center or the finish line medical tent. Rav-Acha et al. (27) alluded to this in a report of risk factors associated with six military fatalities, due to EHS, during military training. They concluded that in addition to individual and environmental risks commonly associated with EHS were “ineffective or absent medical triage and disregard for organizational safety regulations” specifically related to treatment protocol for rapid cooling of EHS victims.

When an elevated CBT is present it can be fatal if it is not recognized and treated promptly (12,21,45,46). The successful outcomes in this clinical series of 28 runners with EHS strongly supports the use of IWI, primarily advocated by Casa (23,26) and others (20,24,25,47), to rapidly reduce dangerously high core temperature. All of the runners in this case series, who presented with AMS, were initially presumed to have EHS. Once CBT was determined, all were treated successfully with IWI. The mean time to reduce CBT in our series of runners to <39°C (102.5°F) was 12.9 min (range, 4–20 min) at a rate of 0.22°C·min−1 and most importantly, returned back to normal mental status within 2 h of the EHS event. This rate of cooling is consistent with previous studies reporting a generalized decrease of 0.18 to 0.34°C·min−1 or roughly 15 min of IWI (23,24,47).

Previous studies comparing alternative cooling methods consistently demonstrate that the rate of decrease in CBT is greatest with IWI. CBT decreased most rapidly (0.18°C·min−1) when persons with EHS were “dunked”: with exposure of ice water between the shoulders and hips (24). Our study supports the concept that when cooling is rapidly initiated, both the body temperature and cognitive function of the athlete with EHS return to the normal range within an hour of onset of symptoms and most EHS patients recover fully (46,48). Outcomes of cases of EHS during military training (38) showed that in cases when hyperthermia lasts less than 1 h, brief coma and temporary organ failure can occur (49,50). We were fortunate that the one runner who was not treated with IWI survived without known permanent health problems. In cases when hyperthermia (CBT >40.5°C) has been either unrecognized or ineffectively treated for longer than an hour, permanent organ failure, brain damage, and death occur at a much higher rate. Event medical staff must remember that EHS is a “potentially fatal cause of runner collapse during or immediately after competitions and must be ruled out early in the decision process to avoid the complications of delayed diagnosis and prolonged elevation of rectal temperature.” Medical providers must think, “Heat attack” (21,46) with a quick response time, perhaps “quicker” than a “heart attack” to reduce morbidity and mortality in athletes stricken with EHS. As was observed in our series, all athletes with an elevated CBT treated with onsite IWI to obtain a CBT <102°C in <20 min will more than likely have a better outcome then those who do not receive immediate IWI after transfer to an emergency facility. The exception to this rule would be for those who are in acute cardiac arrest who require immediate defibrillation. If this were to occur in the field it would perhaps be best to stabilize the heart rhythm on site and then transport the runner immediately to an emergency center with ready access to hypothermic treatment and other aggressive methods often utilized after cardiac arrest (51).

The incidence of EHS deaths in American high school and collegiate sports remains high when compared with the previous 35 to 40 yr, with the incidence from 2010 to 2014 being the highest ever recorded (52). In a review of all causes of mortality associated with marathon running, Kim et al. (53) reported that only 3% of all running-related deaths were due to EHS (incidence rate, 0.54 per 100,000 participants; 95% confidence interval [CI], 0.41 to 0.70). Fortunately, there were no EHS-related mortalities in our case series; however, the incidence of EHS in our study within a population of men completing a full marathon is one of the highest reported. Despite similar diagnostic protocol, men who were full marathon finishers had a much higher incidence of EHS (20.01/10,000), roughly six times the risk of all others (3.4/100000) evaluated. This is a surprisingly higher incidence when compared with previous reports of incidence of EHS in marathon finishers, especially when the average ambient temperature (18.1°C) is much lower than similar distance races with a higher mean temperature.

To place this finding within perspective, Roberts (16) has reported an average incidence of EHS to be approximately 1–2/10, 000 in runners over a 12-yr observation of the Twin Cities Marathon. When WBGT was <13 °C, EHS cases averaged 0 to 1 per race; but rose to 11 to 12 cases per race when the WBGT was >22°C (13,16). Twin Cities is held in October when ambient temperature is cooler, which explains their lower incidence of EHS. By comparison, the incidence rates of EHS reported for the shorter, but arguably more intense pace during the Falmouth Road Race, held in August when ambient temperatures are >23°C (20), is 11/10,000. DeMartini et al. (20) reported that in 8 of the 11 yr when the temperature was >22 °C, the number of EHS cases was at or above the 18-yr average for EHS cases. In this case series, we are reporting that the overall incidence of EHS was 5.64/10,000 finishers of either the half or full marathon. Similar to previous reports (17–19,21), we have demonstrated EHS also can occur at a relatively cool mean annual ambient temperature of 18.1°C with a range of 7°C to 22°C which is between the mean temperatures reported for the Minneapolis (12.1°C) and Falmouth (22°C) series.

High humidity and low wind speed also were a factor limiting evaporative cooling of runners in all three series. Lack of wind in the presence of high humidity and high ambient temperature increases the relative heat stress when sweat is not effectively evaporating from the skin, exacerbating EHS (54). In addition to the peak heat stress, the rate of increase in heat stress also may play a role in the development of EHS. In military studies, heat illness rates similar to those in our race were observed at temperatures as low as 18°C (55). Additionally, rates are at the highest from 7:00 a.m. to 9:00 a.m. when the WBGT increases most rapidly, which is also similar to the timing of occurrences in our race. It is most likely that the risk of EHS occurrence is not only related to the actual levels of ambient heat and humidity but also related to the rate of increase of heat stress (44) which may inhibit the body's usual cooling mechanisms.

Other exogenous factors that contribute to heat load include solar radiation (direct and indirect), ground thermal radiation, and clothing (34,56,57). Local neighborhood temperature variations due to buildings or other structures can provide valued shade from the sun but also will block wind which reduces sweat evaporation. Within an urban race location such as ours, it is possible for local “thermal heat islands” to form resulting in pockets of higher heat load (58). Direct overhead sun exposure (surrounded by concrete structures) is highest during the final five miles of the Flying Pig full marathon and hypothetically contributed to our findings.

A surprise finding in our series was that the EHS incidence in male full marathon finishers was one of the highest ever reported. Male runners who completed our full marathon had a nearly six times higher incidence of EHS (20.01/10,000) then female full marathon and male and female half marathon finishers (3.4/10,000). The majority of EHS runners had completed the full marathon (n = 15) with an incidence of 12.94/10,000. Finishers in the half marathon (n = 11) had a much lower incidence rate of 3.19/10,000. Several factors could explain this phenomenon; however, we cannot clearly identify one overriding factor as a cause. The relative ambient heat stress load played a role; however, absolute heat and humidity had an equal effect on all runners, suggesting individual differences in sensitivity to heat stress were present. This supports the widely held concept that there is a great deal of individual variability in susceptibility to EHS (17,18,28–30,59,60). Individual heat acclimatization, relative fitness/exercise (31–34), intensity during the event, the rate of increased exposure to heat (44), and other individual factors such as sex, hydration status (61–65), recent viral illness or medication use (21,43), sleep patterns (27), individual BMI (66), and an individual’s history of previous heat illness (40–42) are all potential variables that can play a role in the development of EHS.

Increases in relative exercise intensity have been known to have the greatest influence on the rate of rise of CBT (27,67) for many years and are well known to increase the risk of EHS despite the environmental conditions. To support this point, Roberts (21) described a case of EHS suffered by an individual male marathon finisher in mild environmental conditions (WBGT = 7.9°C at the time of collapse) where the primary factor leading to EHS was the runner's pace for the last 16 km of the race. As a result, the runner likely ignored his internal cues of a dangerous level of hyperthermia and ran at a higher intensity. Similar to the runner described by Roberts, male runners in our series may also have ignored symptoms and early warning signs of impending EHS, while running at a high relative pace and exercise intensity. On the other hand, in a recent study, Deaner et al. (68) reported during marathon events that men adjusted their pace during the second half of a marathon and slowed their pace more than women. They showed that, after controlling for age and ability and making a 12% adjustment for sex differences in V˙O2max, women had approximately one third the odds as men to experience marked slowing (running the second half of the race more than 30% slower than the first half). Therefore, it is unclear if sex differences in relative running pace played a role in men having a higher incidence of EHS.

Previous studies indicate that, in general, women exercising have between 1.18 and 3.7× greater risk of exertional heat illness (EHI) or EHS then men (69,70).

In general, healthy (71) and unhealthy (72) men have a higher hospitalization incidence rate for heat-related illnesses. However, both military recruit and civilian studies indicate that when work is added, exertional heat illness (EHI) is more common in women. When baseline rates are corrected for sex participation, women have a slightly higher incidence of EHI (1.30 per 10,000) (not EHS) than men, (1.19/10,000) both in the military (69,73,74) and in the general population (75,76).

Our results did not support the concept that women are at higher risk of either EHI or EHS as we saw relatively equal incidence of EHS in both male and female half marathon finishers and female full marathon finishers and a much higher incidence of EHS in male full marathon finishers. Previous military reports by Sawka et al. (77) and Kazman et al. (70) conclude that if men and women are matched for physical fitness, V˙O2max, % body fat, and heat acclimatization status, that little differences exist for their ability to thermoregulate during exercise-heat stress (18).

In fact, in male military recruits with an elevated BMI, there was a 9% increase in risk for EHI, while BMI was not associated with EHI risk among female recruits (66). Perhaps our male full marathon finishers who experienced EHS had higher BMI values than men who did not experience EHS problems? Future studies as to why recreational male marathon finishers had a higher incidence of EHI or EHS should focus on body composition and or elevated BMI as an individual risk factor for EHS.

Individuals with a previous history of EHS are generally felt to be at risk for future EHS episodes. There was only one individual in this series who reported a previous history of exercise-related heat illness (without supporting evidence). This runner participated in the shortest event, completing a six-mile relay leg of the full marathon relay event, developed post run AMS and was found to have an elevated CBT of 42.2°C. There were no runners in the 3-yr series who had a reoccurrence of EHS during this marathon. Despite the commonly held belief that an individual with a history of EHS is at risk for future episodes of EHS, there is very little evidence in our study to support this belief. There are limited reasons for reoccurrence risk reported in the medical literature. Advancements in genetic technology have identified approximately 700 genes that are activated or suppressed by exercise heat stress in patients who had prior EHS (40,42), suggesting an inherent genetic risk of EHS may be present. Additional studies are needed to determine if athletes have a higher risk of recurrent EHS; and, if so, which factors contribute to this increased risk.

Conclusions

Ice-water immersion is an effective means of rapidly reducing CBT and improving potentially fatal outcomes associated with EHS. One male runner participating in the full marathon, who did not finish developed AMS and EHS; however, he was not treated with IWI and required four additional hospital days to recover compared to those who finished and received IWI. This study supports the encouragement of IWI utilization and that IWI be available for endurance sporting events regardless of ambient temperature during the event.

Male marathon finishers have a higher incidence of EHS then female full-marathon finishers or half-marathon finishers of either sex. Reasons for a significantly elevated incidence of EHS in male marathon runners in our series are unknown. Several individual risk factors could be at play; however, based on previous literature, causes include males having a higher BMI. Further investigation is needed to determine why male marathon finishers have a higher incidence of EHS.

Although only one runner had a previous history of EHS, his CBT reached a dangerously high level over a relatively short 10 k mile leg of a “marathon relay,” indicating that providers should be able to provide IWI even for shorter races.

The authors wish to thank the many members of our Flying Pig Marathon Medical group for their commitment and friendship during the many years volunteering to help the thousands who have participated in this annual event, especially during the 20th anniversary year. We wish to specifically acknowledge: Jessica Mann, Ron Gerdes, Yvette Gerdes, Robert Good, Jen Jackson, Jessie Moore, Corey Jacobs, and Helene Apke (get well soon!). We have been fortunate to partner with a tremendous Board of Directors and executive leaders, John Cappella, Shaun Verhoff, and our most wonderful executive director, Iris Simpson-Bush.

The authors declare no conflict of interest and do not have any financial disclosures.

References

1. Running USA. 2014 State of the Sport - Part I: Non-Traditional Running Events. Running USA website. April 27, 2014. [ cited 2018 March 18]. Available from: http://www.runningusa.org/index.cfm?fuseaction=news.details&ArticleId=2945.
2. Running USA. 2016 State of the Sport - U.S. Road Race Trends. Running USA website. May 6, 2016. [cited 2018 March 18]. Available from: http://www.runningusa.org/state-of-sport-us-trends-2015.
3. Levine BD, Thompson PD. Marathon maladies. N. Engl. J. Med. 2005; 352:1516–8.
4. Mathews SC, Narotsky DL, Bernholt DL, et al. Mortality among marathon runners in the United States, 2000–2009. Am. J. Sports Med. 2012; 40:1495–500.
5. Yankelson L, Sadeh B, Gershovitz L, et al. Life-threatening events during endurance sports: is heat stroke more prevalent than arrhythmic death? J. Am. Coll. Cardiol. 2015; 65:408–9.
6. Ely MR, Cheuvront SN, Roberts WO, Montain SJ. Impact of weather on marathon-running performance. Med. Sci. Sports Exerc. 2007; 39:487–93.
7. Ely MR, Martin DE, Cheuvront SN, Montain SJ. Effect of ambient temperature on marathon pacing is dependent on runner ability. Med. Sci. Sports Exerc. 2008; 40:1675–80.
8. Martin DE, Gynn RWH. The Olympic Marathon. Champaign (IL): Human Kinetics, 2000.
9. Trapasso LM, Cooper JD. Record performances at the Boston Marathon: biometeorological factors. Int. J. Biometeorol. 1989; 33:233–7.
10. Vihma T. Effects of weather on the performance of marathon runners. Int. J. Biometeorol. 2010; 54:297–306.
11. Armstrong LE, Casa DJ, Millard-Stafford M, et al. American College of Sports Medicine position stand; Exertional heat illness during training and competition. Med. Sci. Sports Exerc. 2007; 39:556–72.
12. Brodeur VB, Dennett SR, Griffin LS. Exertional hyperthermia, ice baths, and emergency care at the Falmouth Road Race. J. Emerg. Nurs. 1989; 15:304–12.
13. Roberts WO. Determining a “do not start” temperature for a marathon on the basis of adverse outcomes. Med. Sci. Sports Exerc. 2010; 42:226–32.
14. Zhang S, Meng G, Wang Y, Li J. Study of the relationships between weather conditions and the marathon race, and of meteorotropic effects on distance runners. Int. J. Biometeorol. 1992; 36:63–8.
15. Sloan BK, Kraft EM, Clark D, et al. On-site treatment of exertional heat stroke. Am. J. Sports Med. 2015; 43:823–9.
16. Roberts WO. A 12-yr profile of medical injury and illness for the Twin Cities Marathon. Med. Sci. Sports Exerc. 2000; 32:1549–55.
17. Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior exertional heatstroke patients. Med. Sci. Sports Exerc. 1990; 22:36–48.
18. Epstein Y, Sohar E, Shapiro Y. Exertional heatstroke: a preventable condition. Isr. J. Med. Sci. 1995; 31:454–62.
19. Roberts WO. Exercise-associated collapse in endurance events: a classification system. Phys. Sportsmed. 1989; 17:49–59.
20. DeMartini JK, Casa DJ, Belval LN, et al. Environmental conditions and the occurrence of exertional heat illnesses and exertional heat stroke at the Falmouth Road Race. J. Athl. Train. 2014; 49:478–85.
21. Roberts WO. Exertional heat stroke during a cool weather marathon: a case study. Med. Sci. Sports Exerc. 2006; 38:1197–203.
22. Cianca JC. Distance running: organization of a medical team. J. Back Musculoskelet. Rehabil. 1996; 6:59–69.
23. Casa DJ, McDermott BP, Lee EC, et al. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc. Sport Sci. Rev. 2007; 35:141–9.
24. Clements JM, Casa DJ, Knight JC, et al. Ice-water immersion and cold-water immersion provide similar cooling rates in runners with exercise-induced hyperthermia. J. Athl. Train. 2002; 37:146–50.
25. McDermott BP, Casa DJ, Ganio MS, et al. Acute whole-body cooling for exercise-induced hyperthermia: a systematic review. J. Athl. Train. 2009; 44:84–93.
26. Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainers' Association Position Statement: exertional heat illnesses. J. Athl. Train. 2015; 50:986–1000.
27. Rav-Acha M, Hadad E, Epstein Y, et al. Fatal exertional heat stroke: a case series. Am. J. Med. Sci. 2004; 328:84–7.
28. Bar-Or O, Lundegren HM, Buskirk ER. Heat tolerance of exercising obese and lean women. J. Appl. Physiol. 1969; 26:403–9.
29. Haymes EM, McCormick RJ, Buskirk ER. Heat tolerance of exercising lean and obese prepubertal boys. J. Appl. Physiol. 1975; 39:457–61.
30. Epstein Y. Heat intolerance: predisposing factor or residual injury? Med. Sci. Sports Exerc. 1990; 22:29–35.
31. Buskirk ER, Puhl SM. Effects of acute body weight loss in weight controlling athletes. In: Buskirk ER, Puhl SM, editors. Body Fluid Balance: Exercise and Sport. New York (NY): CRC Press, 1996, pp. 283–96.
32. Irion GL. Responses of distance runners and sprinters to exercise in a hot environment. Aviat. Space Environ. Med. 1987; 58:948–53.
33. Sawka MN, Montain SJ, Latzka WA. Body fluid balance during exercise-heat exposure. In: Buskirk EW, Puhl SM, editors. Body Fluid Balance: Exercise and Sport. New York (NY): CRC Press; 1996. p. 139–57.
34. Werner J. Temperature regulation during exercise: an overview. In: Gisolfi CV, Lamb DR, Nadel ER, editors. Exercise, Heat, and Thermoregulation. Dubuque (IA): Brown and Benchmark; 1993. p. 49–77.
35. Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med. (New Zealand). 1991; 12:302–12.
36. Buskirk ER, Iampietro PF, Bass DE. Work performance after dehydration: effects of physical conditioning and heat acclimatization. J. Appl. Physiol. 1958; 12:189–94.
37. Knochel JP. Environmental heat illness. An eclectic review. Arch. Intern. Med. 1974; 133:841–64.
38. Shibolet S, Lancaster MC, Danon Y. Heat stroke: a review. Aviat. Space Environ. Med. 1976; 47:280–301.
39. Yarbrough BE, Hubbard RW. Heat-related illnesses. In: Management of Wilderness and Environmental Emergencies. 2nd edition. Army Research Institute of Environmental Medicine. Natick, MA. Accession Number: ADA197730.
40. Casa DJ, Armstrong LE, Kenny GP, et al. Exertional heat stroke: new concepts regarding cause and care. Curr. Sports Med. Rep. 2012; 11:115–23.
41. Shapiro Y, Magazanik A, Udassin R, et al. Heat intolerance in former heatstroke patients. Ann. Intern. Med. 1979; 90:913–6.
42. Sonna LA, Wenger CB, Flinn S, et al. Exertional heat injury and gene expression changes: a DNA microarray analysis study. J. Appl. Physiol. (1985). 2004; 96:1943–53.
43. Keren G, Epstein Y, Magazanik A. Temporary heat intolerance in a heatstroke patient. Aviat. Space Environ. Med. 1981; 52:116–7.
44. Veltmeijer MT, Eijsvogels TM, Thijssen DH, Hopman MT. Incidence and predictors of exertional hyperthermia after a 15-km road race in cool environmental conditions. J. Sci. Med. Sport. 2015; 18:333–7.
45. Costrini A. Emergency treatment of exertional heatstroke and comparison of whole body cooling techniques. Med. Sci. Sports Exerc. 1990; 22:15–8.
46. Roberts WO. Managing heatstroke: on-site cooling. Phys. Sportsmed. 1992; 20:17–28.
47. Zhang Y, Davis JK, Casa DJ, Bishop PA. Optimizing cold water immersion for exercise-induced hyperthermia: a meta-analysis. Med. Sci. Sports Exerc. 2015; 47:2464–72.
48. Costrini AM, Pitt HA, Gustafson AB, Uddin DE. Cardiovascular and metabolic manifestations of heat stroke and severe heat exhaustion. Am. J. Med. 1979; 66:296–302.
49. Hubbard RW, Matthew CB, Durkot MJ, Francesconi RP. Novel approaches to the pathophysiology of heatstroke: the energy depletion model. Ann. Emerg. Med. 1987; 16:1066–75.
50. Wyndham CH, Kew MC, Kok R, et al. Serum enzyme changes in unacclimatized and acclimatized men under severe heat stress. J. Appl. Physiol. 1974; 37:695–8.
51. Nolan JP, Morley PT, Vanden Hoek TL, et al. Therapeutic hypothermia after cardiac arrest: an advisory statement by the advanced life support task force of the International Liaison Committee on Resuscitation. Circulation. 2003; 108:118–21.
52. Stearns RL, Casa DJ, O’Connor FG, Kenny GP. Exertional heat stroke. In: Casa DJ, editor. Preventing Sudden Death in Sport and Physical Activity. Sudbury (MA): Jones and Bartlett; 2012. p. 53–73.
53. Kim JH, Malhotra R, Chiampas G, et al. Cardiac arrest during long-distance running races. N. Engl. J. Med. 2012; 366:130–40.
54. Nadel ER. Limits imposed on exercise in a hot environment. Sports Sci Exchange. 1990; 3:27.
55. Kark JA, Burr PQ, Wenger CB, et al. Exertional heat illness in Marine Corps recruit training. Aviat. Space Environ. Med. 1996; 67:354–60.
56. Armstrong LE, Maresh CM. The exertional heat illnesses: a risk of athletic participation. Med. Exerc. Nutr. Health. 1993; 2:125–34.
57. Stitt JT. Central regulation of body temperature. In: Gisolfi CV, Lamb DR, Nadel ER, editors. Exercise, Heat, and Thermoregulation. Dubuque (IA): Brown and Benchmark; 1993. p. 1–39.
58. Harlan SL, Brazel AJ, Prashad L, et al. Neighborhood microclimates and vulnerability to heat stress. Soc. Sci. Med. 2006; 63:2847–63.
59. Armstrong LE. Classification, nomenclature, and incidence of the exertional heat illnesses. In: Exertional Heat Illnesses. Champaign (IL): Human Kinetics; 2003. p. 17–28.
60. Kenefick RW, Cheuvront SN, Sawka MN. Thermoregulatory function during the marathon. Sports Med. 2007; 37:312–5.
61. Buono MJ, Wall AJ. Effect of hypohydration on core temperature during exercise in temperate and hot environments. Pflugers Arch. 2000; 440:476–80.
62. Montain SJ, Coyle EF. Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise. J. Appl. Physiol. (1985). 1992; 73:1340–50.
63. Pinchan G, Gauttam RK, Tomar OS, Bajaj AC. Effect of primary hypohydration on physical work capacity. Int. J. Biometeorol. 1988; 32:176–80.
64. Sawka MN, Young AJ, Francesconi RP, et al. Thermoregulatory and blood responses during exercise at graded hypohydration levels. J. Appl. Physiol. (1985). 1985; 59:1394–401.
65. Walsh RM, Noakes TD, Hawley JA, Dennis SC. Impaired high-intensity cycling performance time at low levels of dehydration. Int. J. Sports Med. 1994; 15:392–8.
66. Wallace RF, Kriebel D, Punnett L, et al. Risk factors for recruit exertional heat illness by gender and training period. Aviat. Space Environ. Med. 2006; 77:415–21.
67. Saltin B, Hermansen L. Esophageal, rectal, and muscle temperature during exercise. J. Appl. Physiol. 1966; 21:1757–62.
68. Deaner RO, Carter RE, Joyner MJ, Hunter SK. Men are more likely than women to slow in the marathon. Med. Sci. Sports Exerc. 2015; 47:607–16.
69. Carter R 3rd, Cheuvront SN, Williams JO, et al. Epidemiology of hospitalizations and deaths from heat illness in soldiers. Med. Sci. Sports Exerc. 2005; 37:1338–44.
70. Kazman JB, Purvis DL, Heled Y, et al. Women and exertional heat illness: identification of gender specific risk factors. US Army Med. Dep. J. 2015:58–66.
71. Yang M, Li Z, Zhao Y, et al. Outcome and risk factors associated with extent of central nervous system injury due to exertional heat stroke. Medicine (Baltimore). 2017; 96:e8417.
72. Schmeltz MT, Marcotullio PJ, Himmelstein DU, et al. Outcomes of hospitalizations for common illnesses associated with a comorbid heat-related illness in the United States, 2001-2010. Clim. Change. 2016; 138:567. https://doi.org/10.1007/s10584-016-1747-5.
73. Armed Forces Health Surveillance Center. Heat injuries, active component, U.S. Armed Forces, 2013. MSMR. 2014; 21:10–3.
74. Dellinger AM, Kachur SP, Sternberg E, Russell J. Risk of heat-related injury to disaster relief workers in a slow-onset flood disaster. J. Occup. Environ. Med. 1996; 38:689–92.
75. Kerr ZY, Casa DJ, Marshall SW, Comstock RD. Epidemiology of exertional heat illness among U.S. high school athletes. Am. J. Prev. Med. 2013; 44:8–14.
76. Nelson NG, Collins CL, Comstock RD, McKenzie LB. Exertional heat-related injuries treated in emergency departments in the U.S., 1997-2006. Am. J. Prev. Med. 2011; 40:54–60.
77. Sawka MN, Wenger CB, Pandolf KB. Thermoregulatory responses to acute exercise-heat stress and heat acclimation. In: Fregly MJ, Blatteis CM, editors. Handbook of Physiology, Section 4, Environmental Physiology. New York (NY): Oxford University Press; 1996. p. 157–85.
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