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Exertional Heat Stroke in Competitive Athletes

Casa, Douglas J. PhD, ATC*; Armstrong, Lawrence E. PhD; Ganio, Matthew S. MS; Yeargin, Susan W. MS, ATC

Current Sports Medicine Reports: December 2005 - Volume 4 - Issue 6 - p 309–317
doi: 10.1097/01.CSMR.0000306292.64954.da
Article

Exertional heat stroke (EHS) is a serious medical condition that can have a tragic outcome if proper assessment and treatment are not initiated rapidly. This article focuses on critical misconceptions that pertain to the prevention, recognition, and treatment of EHS, including 1) the randomness of EHS cases, 2) the role of nutritional supplements in EHS, 3) temperature assessment, 4) onset of EHS and the possible lucid interval, 5) rapid cooling, and 6) return to play. Exploration of these topics will enhance the medical care regarding EHS.

Address *Human Performance Laboratory, Department of Kinesiology, Neag School of Education, University of Connecticut, 2095 Hillside Road, U-1110, Storrs, CT 06269-1110, USA. E-mail: douglas.casa@uconn.edu

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Introduction

Consider this premise regarding exertional heat stroke (EHS) within the confines of organized American sport: death from EHS is completely preventable. Any athlete who is suspected of suffering from EHS (with core temperature assessed via a rectal thermometer) and begins cold/ice water immersion within 10 minutes of the heat stroke will survive. We have strong evidence to suggest that prompt and accurate temperature assessment and prompt and rapid cooling guarantee survival, and no evidence to indicate otherwise.

So then, why do athletes continue to die from EHS at all levels of competitive sport in America? One clue can be found on the Internet. A search for “exertional heat stroke” or “heat stroke” results in over 2 million hits. Much of the preliminary hits do not contain current and accurate recommendations regarding the prevention, recognition, and treatment of EHS. The vast amount of misinformation available only serves to slow our progress in educating health care professionals and the public and often perpetuates long-held misconceptions.

The key diagnostic criteria for EHS are central nervous system (CNS) changes and a core body temperature of about 104°F or greater. Although these criteria are often clinically understood, many misconceptions hinder the recognition and treatment of EHS.

Our paper presents six key component areas of EHS and offer scientifically supported arguments for appropriate medical care, which can be incorporated into protocols at all levels of competitive sport. Along the way, we also rebuff many common misconceptions.

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Predisposing Factors of Exertional Heat Stroke

Misconception #1: randomness

Many sports medicine professionals have long considered the onset of EHS to be random and largely unpredictable. The truth is that studies of EHS and exercise heat tolerance find remarkable consistency. These patterns could help sports medicine professionals develop watch lists, modify protocols for certain individuals, and take proactive steps to prevent a case of EHS and enhance exercise heat tolerance [1•,2••,3,4,5••,6,7••]. Table 1, with concepts originally proposed and investigated by Minard [8••], serves as excellent starting point when considering the risk factors regarding the possibility of an athlete dying from EHS [5••]. Although the list is not exhaustive, it certainly addresses many of the key items that influence an athlete's exercise heat tolerance and factors related to treatment if an incident does occur. Table 1 provides an outstanding contribution to our understanding of EHS and should serve as a model for future research that can be done within this field. Rav-Acha et al. [5••] examined six EHS fatalities and compared them with 134 cases of EHS that did not lead to death. This provides two valuable pieces of information for the clinician. First, what factors tend to be present when an athlete suffers an EHS, and second, which of these seem to be most critical in turning the already unfortunate event into a tragedy. An examination of Table 1 reveals low physical fitness, overweight, and training at hottest hours were the greatest risk factors for nonfatal cases of EHS [5••]. For the fatal cases the following risk factors were present two thirds of the time or more: low physical fitness, sleep deprivation, improper acclimatization, heat load corresponding to wet bulb globe temperature green flag or above, high solar radiation, physical effort unmatched to physical fitness, improper work/rest cycles, absence of proper medical triage, training at hottest hours, and improper treatment [5••]. Many of the other items not mentioned were present in 50% of the fatal cases. Two items were present in 100% of the fatal EHS cases: physical effort unmatched to physical fitness and absence of proper medical triage [5••]. This is an important consideration, because intensity of exercise is a key component in the rate of rise in core temperature. A physical fitness regimen that is not matched for fitness status will require an unfit person to work at a higher relative intensity than his or her fit counterparts and thus drive the core temperature up at a much faster rate than his or her teammates. Absence of proper medical triage likely precipitates a delay in proper treatment and thus its role in the adverse outcome. The predisposing factors listed in Table 1, plus additional items that may be situation-specific or based on recent research [1], should be used to identify who may be at greatest risk prior to intense exercise in the heat. The team physician and athletic trainer can work together to lower the risk for these individuals by establishing an individualized program and encourage more rigid observation during activity.

Table 1

Table 1

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Misconception #2: nutritional supplements

It is common for the media to focus on the use of nutritional supplements following a high-profile case of EHS. This has occurred following the deaths of three Division I collegiate wrestlers in 1997, a National Football League football player in August 2001, and a Major League Baseball player during spring training in 2003. Creatine and ephedra have been two of the more common supplements cited as having caused or contributed to the onset of the EHS. Recent scientific articles by prestigious sports medicine professionals [9] and sports medicine organizations [10] help fuel the notion that these supplements played a role in the death from heat stroke. The media coverage following these tragic and emotional EHS stories often clouds our view of reality. The actual truth, based on controlled investigations, is that no evidence exists to indicate creatine use by athletes in any way inhibits exercise heat tolerance or contributes to the onset of EHS [11••,12,13,14•]. This information is not as glamorous as the alternative, but the truth, as we know it currently, should supercede a rush to judgment based on speculation. The truth is that the death could have easily been averted if prompt treatment via rapid cooling had been initiated. We use the term “easily” with a sense of sarcasm. It is quite difficult, if not impossible, to kill an otherwise healthy athlete suffering from EHS if rapid cooling via cold/ice water immersion is implemented within a few minutes after collapse.

When the story of a Major League Baseball pitcher who died from EHS during spring training in 2003 began to circulate in all the media outlets, the overwhelming thrust of the stories was centered around his purported use of ephedra. It was as if the ephedra was the only reason he died. Ephedra may have hindered his exercise heat tolerance (the scientific evidence in the years to come will tell us to what extent it had on altering his core temperature), but rest assured the outcome could have been completely different, and the story just a footnote instead of a headline, if EHS had been recognized promptly and treated properly. We do not advocate the use of ephedra or creatine for athletes. We realize that athletes will continue to use these substances and others to enhance performance. It is our responsibility to conduct, interpret, and disseminate the relevant research as it pertains to supplements and the role it may have on exercise heat tolerance and EHS.

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Recognition of Exertional Heat Stroke

Misconception #3: assessment of body temperature

We believe that no temperature assessment device currently available that utilizes a site on the outside of the body should be used for the assessment of EHS in an athlete who has been exercising in the heat. Table 2 shows that no device using a site on the outside of the body has ever been proven valid under the conditions of intense exercise in the heat and a significant degree of hyperthermia [15–18,19•,20•,21,22•,23••,24–26,27••–29••]. This includes, but is not limited to, the following measures and sites: axillary, oral, tympanic, aural (ear) canal, temporal artery swipe, temperature stickers on the temporal artery or chest, equations using multiple skin temperature sites, and nose bridge. Many of the companies that make the devices that use these sites to represent core temperature often provide some conversion equation to obtain true core temperature, but these also have not been validated during intense exercise in the heat. The body surface simply is not a good location to assess temperature for athletes who are copiously sweating and ingesting cool fluids. Additionally, these prediction equations have never been used in cases of EHS, where temperatures may reach 106°F or greater. Reliance on a temperature device that does not provide a valid indicator of core temperature can delay proper treatment of EHS, or miss the proper diagnosis all together.

Table 2

Table 2

What options exist for the sports medicine professional when an accurate assessment of core temperature is an absolute necessity in the management of EHS? Not many. Although esophageal temperature provides an accurate assessment of temperature, we do not advocate its use in the field for quick assessments of hyperthermia. At this point, we believe only two legitimate options exist for field testing. The first is rectal temperature. Rectal temperature assessment has guided successful EHS care for many years in the United States and Israeli armed services, as well as at many marathons and other sporting events. The most critical advantage of rectal temperature is the usefulness and accuracy of the measure [27••,29••,30••,31•]. The rectal temperature, whether via a flexible thermistor or glass thermometer, when placed 10 to 15 cm past the anal sphincter, will provide a temperature reading that is not affected by environmental or skin surface influences. Rectal temperature does not increase quite as fast as esophageal temperature during heat storage, and this lag has caused some to discredit the use of the rectum as a valid site for temperature assessment. But even with a lag of a few minutes, the course of action is unlikely to change. Rectal temperature assists the field management of exertional heat illnesses in two ways. First, it allows you to diagnose EHS (as compared with exertional hyponatremia or heat exhaustion). For example, an athlete who is measured at about 106°F or greater immediately after collapsing, while doing intense exercise in the heat, is likely suffering from EHS. Also, a prompt rectal temperature measure in an athlete who is quite lucid but who had difficulty in the heat can save valuable time in the treatment process and not force the sports medicine professional to wait until the CNS deteriorates to the point where EHS would be more obvious. Second, when EHS is present, it allows you to determine the rate of rectal temperature decrease during cooling and when to remove the cooling source and minimize risk of overcooling. An obvious drawback to rectal temperatures is the invasive nature of the technique. This is an important consideration.

The ingestible thermistor is a second viable field measure [28••,29••]. These temperature sensors, about the size of a multivitamin, are taken a couple of hours before activity. They transmit a signal that is obtained by a receiver that is held near the athlete by the sports medicine professional. The obvious advantages of this technique is the ability to assess temperature within about 2 seconds and the minimally invasive nature of the process [29••]. Additionally, these sensors can be used to track body temperature changes and assess potential hyperthermia before a problem arises. A few problems of this method include that 1) the thermistor has to be ingested before the problem arises; it can not be done when an athlete is already suffering from EHS; 2) it could be costly for some settings (∼ $30–$35 per pill; ∼ $2000 per receiver); 3) the sensor could malfunction; and 4) the pill could be passed in feces before the exercise bout in question. We believe these ingestible thermistors are an important advancement in the realm of temperature assessment. In high-risk athletes (eg, football lineman, athletes with history of EHS) on-field monitoring can provide an entirely new ability to monitor and prevent dangerous hyperthermia.

When it comes to the field recognition of EHS we believe that all sports medicine professionals need to have the training and equipment on site to assess rectal temperature in a suspected EHS case [32••–34••,35•,36•]. At this point, based on the available research, it would not be prudent to depend on another mode of temperature assessment for the on-field assessment of body temperature in a suspected EHS.

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Misconception #4: onset of condition/lucid interval

A few myths regarding EHS are pervasive in the medical community. One of these states that heat exhaustion will become EHS if left untreated. Heat exhaustion, by definition, is the inability to continue exercise in the heat due to exhaustion [32••]. Athletes who suffer EHS do not go through a continuum of heat ailments on the way to EHS. An athlete who collapses from EHS within 200 meters of the finish line of a 12-km road race does not have to have had a more mild heat illness at an earlier time point in the race. The first indication that EHS exists often is collapse. Prodromal symptoms may not present themselves, or may be mild enough to ignore during the heat of competition [37•]. Sometimes medical staff confuse EHS with heat exhaustion [35•,36•]. One factor that may obscure or delay diagnosis of EHS is the lucid interval that presents initially for many EHS patients [32••,38,39]. This lucid interval often coincides with only minimal CNS dysfunction and misleads the caregiver regarding the severity of the condition [32••]. At a recent marathon, one of the authors observed eight EHS cases within a 90-minute span; six of them were conscious and conversant upon immersion in the cold water baths. These patients eventually lapsed into unconsciousness and all eight recovered completely without incident and were discharged from medical care on the same day. However, caregivers were not mislead by the initial lucid interval, promptly measured rectal temperature (all initial rectal temperatures were greater than 106°F), and began cooling. If they had waited for the more severe CNS dysfunction, valuable time would have been lost. One interesting note, the medical professional often notices subtle changes from normal behavior during these lucid intervals. One athlete once retorted, “There is no ____ way you are putting a ____ rectal probe in my ____”. For some, this would have indicated that the person was coherent and belligerent. In this case, clinicians ignored the patient and measured a 109°F; the athlete was unconscious within 5 minutes. Despite this severe hyperthermia, the athlete was cooled in a cold water immersion bath and within 2 hours was normothermic, mobile, and able to converse. This example demonstrates that a brief lucid interval may occur before severe CNS signs and symptoms appear. Additionally, the argumentative nature of the patient described may serve as an indicator of CNS changes, even though the athlete was still cognizant of the surroundings. Common sense is the best approach. An athlete who is exhibiting difficulty during intense exercise in the heat should be suspected of having EHS regardless of the degree of CNS dysfunction initially.

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Treatment of Exertional Heat Stroke

Misconception #5: rapid cooling

Of all the misconceptions surrounding the topic of EHS none have had more staying power or more tragic consequences than the concept of cold/ice water immersion. Many medical professionals [40,41••,42] and companies [43] that manufacture rival cooling methods have repeatedly criticized the benefits of cold/ice water immersion for rapid cooling of EHS victims. The reasons cited include cardiovascular shock, hypothermia due to excessive cooling, inadequate access for other medical interventions, peripheral vasoconstriction, and shivering. Although all are important considerations none of them have been proven valid as reasons not to utilize rapid cooling via cold/ice water immersion to treat EHS. In fact, the first goal in treating an acute case of EHS is to rapidly cool the victim [2••,30••,31•,38,41••,44–47,48••]. This can be and should be done by the best available means [2••,34••,45,49•,50•]. For some military field settings, this may mean repeated soaking with cool water and fans [17], but for many athletic practice and competition venues where medical teams have ample time and resources to prepare for an incident, treatment should involve cold/ice water immersion in a sturdy rubber tub [2•,31•,32••,34••,35•,36•,38]. We propose that this course of action, if taken within 10 minutes of collapse from EHS, will guarantee survival. The cooling rates of cold/ice water immersion are the best ever reported in the literature [51••] and the survival rate is at or near 100% [52•,53••]. When cold/ice water immersion is not feasible, water, fans, shade, wet towels, and ice bags may be used to lower core temperature. Figure 1 shows the cooling rates that result from various cooling modalities, as published in the literature [51••,53••,54,55•,56,57,58•, 59–61,62•,63,64]. This figure clearly shows that cold/ice water immersion invokes deep body cooling that is superior to any other modality. Also, it clearly refutes the notion that cooling a hyperthermic athlete via cold/ice water immersion will somehow hinder cooling due to peripheral vasoconstriction, as suggested by experts and rival manufacturers. Some physiologic evidence indicates that core temperature may largely dictate these cooling responses and not be influenced as much by skin temperature [65]. Rapid cooling saves lives. Some limitations of cold/ice water immersion must be noted and should be considered. First, automatic external defibrillation can not be administered while the patient is in the immersion tub. Cardiovascular problems are not likely when rapid cooling takes place in young otherwise healthy athletes who are suffering from EHS. Second, temperature should be monitored during immersion to avoid excessive cooling. Third, multiple assistants may need to rehearse and actually conduct the placement of the athlete in the immersion bath, monitoring during the cooling, and removal from the bath due to the very large size of some athletes who suffer EHS.

Figure 1

Figure 1

The Inter-Association Task force on Exertional Heat Illnesses Consensus Statement proposes that an EHS victim should be cooled first and transported second when appropriate medical staff is present [34••]. This is a profound statement announcing that survival is linked to the speed of cooling.

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Misconception #6: return to play

Recovery and return to play are two of the most important areas for future research regarding EHS. Some sports medicine professionals have traditionally cleared athletes to return to participation following EHS without consideration of exercise heat tolerance deficits, neuropsychologic impairments, or the altered fitness status/acclimatization status from not being actively engaged in training during recovery [66••,67,68]. Return to play should, like any other injury, involve a carefully planned and incrementally increased physical challenge that is closely supervised by an athletic trainer and physician. The research indicates that most individuals will eventually recover fully from EHS; indeed, this occurs in the vast majority of cases if the athlete is treated promptly using aggressive cooling strategies (ie, ice water immersion) [31•,66••]. Unfortunately, concrete guidelines regarding return to play do not exist. Our baseline minimum recommendations, unless evidence contraindicates, involves the following procedures:

  1. Refrain from exercise for one week following the EHS
  2. Visit a physician following this week to assure no residual signs and symptoms, and for clearance to begin light exercise; the physician monitors the following steps, with assistance from an athletic trainer
  3. Perform light exercise indoors in an air-conditioned facility until well tolerated
  4. Perform intense exercise in the same facility until well tolerated
  5. Undergo an exercise heat tolerance test [69•] (to gain approval for exercising in the heat)
  6. Perform light exercise in the heat until well tolerated
  7. Perform intense exercise in the heat until well tolerated
  8. Perform light exercise in the heat with full equipment (if the sport requires equipment) until well tolerated
  9. Perform intense exercise in the heat with full equipment until well tolerated
  10. Return to normal practice/game conditions
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Future Directions

Recent research and concepts provide useful guidance regarding the prevention, recognition, and treatment of EHS. Within the realm of prevention, the concept of on-field body cooling (ie, any attempt to cool the body before, during, or between activities) has shown promise for enhancing performance and lowering body temperature [70•,71,72••]. Future research should clarify if this procedure could also reduce the risk of exertional heat illnesses, especially, EHS. Other promising areas of developing research include the development of regional WBGT practice guidelines, specific guidelines for youth participants [2••], gene expression associated with heat stress [73••], on-field/during activity monitoring of body temperature [74•], and physiologic cause and effects of EHS [75•,76•,77,78,79•,80]. Regarding recognition, the great challenge is to develop an easy to use, noninvasive device that is truly reflective of core body temperature. At this point it does not exist. Treatment of EHS will improve with education of medical staff regarding the critical need for rapid cooling of EHS victims. Additionally, enhancing the portability of cold/ice water immersion so that rapid cooling can occur conveniently in field settings will open many options for optimal EHS treatment.

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Conclusions

A case of EHS and death from EHS should be viewed separately. Prevention strategies can limit, but not eliminate, the number of cases of EHS; these strategies should be evaluated at an institutional/organizational level. Death from heat stroke, as we stated above, is a tragedy that can be averted within the confines of organized sport. Prevention strategies can limit but not eliminate the number of cases of EHS; these strategies should be evaluated at an institutional/organizational level. Every effort should be taken to ensure that proper medical staff is available on site to prevent, recognize, and treat EHS. Additionally, medical personnel should clearly understand that ice water immersion will ensure survival in virtually all cases of EHS. Although much can be learned regarding EHS, we currently have ample information to ensure that athletes do not die from EHS. The ultimate challenge will be to modify local EHS recognition, treatment, and return to play protocols so that athletes do not become victims of misinformation and lack of preparation.

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References and Recommended Reading

Papers of particular interest, published recently, have been highlighted as: • Of importance, •• Of major importance

1.• Armstrong LE, Casa DJ: Predisposing factors for exertional heat illnesses. Exertional Heat Illness. Edited by Armstrong LE. Champaign IL: Human Kinetics; 2003:151–167, 250–255.

A nice overview of the some of the causative factors of EHS.

2.•• Bergeron MF, McKeag DB, Casa DJ, et al.: Youth football: heat stress and injury risk. Med Sci Sports Exerc 2005, 37: in press.

A first of its kind report on the limited research relevant to heat stress issues in youth football players. Important due to the fact it highlights the many areas of research that still need to be conducted.

3. Cheung SS, McLellan TM: Heat acclimation, aerobic fitness, and hydration effects on tolerance during uncompensable heat stress. J Appl Physiol 1998, 84:1731–1739.
4. Kark JA, Burr PQ, Wenger CB, et al.: Exertional heat illness in marine corps recruit training. Aviat Space Environ Med 1996, 67:354–360.
5.•• Rav-Acha M, Hadad E, Epstein Y, et al.: Fatal exertional heat stroke: a case series. Am J Med Sci 2004, 328:84–87.

This research is an important contribution to the literature. Much can be learned from the fatal cases and these authors do a wonderful job of examining the cases in a manner so that we can learn from the unfortunate events.

6. Sawka MN, Latzka WA, Montain SJ, et al.: Physiologic tolerance to uncompensable heat: intermittent exercise, field vs laboratory. Med Sci Sports Exerc 2001, 33:422–430.
7.•• Wallace RF, Kriebel D, Punnett L, et al.: The effects of continuous hot weather training on risk of exertional heat illness. Med Sci Sports Exerc 2005, 37:84–90.

This research examines the effect of WBGT on the incidence of exertional heat illnesses and how this information can be used to predict and prevent casualties. This research is extremely well done and critical to advancing our understanding.

8.•• Minard C: Prevention of heat casualties in marine corps recruits. Mil Med 1961, 126:261–272.

A classic contribution to the exertional heat illness literature.

9. Bailes JE, Cantu RC, Day AL: The neurosurgeon in sport: awareness of the risks of heatstroke and dietary supplements. Neurosurgery 2002, 51:283–288.
10. Terjung RL, Clarkson P, Eichner ER, et al.: American College of Sports Medicine roundtable. The physiological and health effects of oral creatine supplementation. Med Sci Sports Exerc 2000, 32:706–717.
11.•• Kilduff LP, Georgiades E, James N, et al.: The effect of creatine supplementation on cardiovascular, metabolic, and thermoregulatory responses during exercise in the heat in endurance-trained humans. Int J Sports Nutr Exer Metab 2004, 14:443–460.

A comprehensive examination of the role creatine use has on exercise heat tolerance.

12. Pitsiladis YP, Georgiades E, Minnion RH, et al.: Effects of creatine supplementation on exercise performance in the heat in endurance-trained humans. Med Sci Sports Exerc 2003, 35:S32.
13. Volek JS, Mazzetti SA, Farquhar WB, et al.: Physiological responses to short-term exercise in the heat after creatine loading. Med Sci Sports Exerc 2001, 33:1101–1108.
14.• Watson G, Casa DJ, Fiala KA, et al.: Influence of creatine use on exercise heat tolerance in dehydrated men. J Athl Train 2006, 41: in press.

The study examines the influence of creatine use with regard to high-intensity excercise, dehydration, intermittent exercise, and heat exposure. These factors are often relevant for the population of athlete often at risk for EHS.

15. Chaturvedi D, Vilhekar KY, Chaturvedi P, Bharambe MS: Comparison of axillary temperature with rectal or oral temperature and determination of optimum placement time in children. Indian Pediatr 2004, 41:600–603.
16. Lee SM, Williams WJ, Fortney Schneider SM: Core temperature measurement during supine exercise: esophageal, rectal, and intestinal temperatures. Aviat Space Environ Med 2000, 71: 939–945.
17. Lefrant JY, Muller L, de La Coussaye JE, et al.: Temperature measurement in intensive care patients: comparison of urinary bladder, oesophageal, rectal, axillary, and inguinal methods versus pulmonary artery core method. Intens Care Med 2003, 29:414–418.
18. Jensen BN, Jensen FS, Madsen SN, Lossl K: Accuracy of digital tympanic, oral, axillary, and rectal thermometers compared with standard rectal mercury thermometers. Eur J Surg 2000, 166:848–851.
19.• Sparling PB, Snow TK, Millard-Stafford ML: Monitoring core temperature during exercise: ingestible sensor vs. rectal thermistor. Aviat Space Environ Med 1993, 64:760–763.

An important early study examining the ingestible thermistor.

20.• Newsham KR, Saunders JE, Nordin ES: Comparison of rectal and tympanic thermometry during exercise. South Med J 2002, 95:804–810.

An important study examining tympanic temperature.

21. Patel N, Smith CE, Pinchak AC, Hagen JF: Comparison of esophageal, tympanic, and forehead skin temperatures in adult patients. J Clin Anesth 1996, 8:462–468.
22.• Armstrong LE, Maresh CM, Crago AE, et al.: Interpretation of aural temperatures during exercise, hyperthermia, and cooling therapy. Med Exerc Nutr Health 1994, 3:9–16.

Another important study examining tympanic temperatures.

23.•• Deschamps A, Levy RD, Cosio MG, et al.: Tympanic temperature should not be used to assess exercise induced hyperthermia. Clin J Sport Med 1992, 2:27–32.

One of the original research studies to question validity of tympanic temperature assessment in athletes who have been exercising in the heat.

24. Allen GC, Horrow JC, Rosenberg H: Does forehead liquid crystal temperature accurately reflect “core” temperature? Can J Anaesth 1990, 37:659–662.
25. Greenes DS, Fleisher GR: When body temperature changes, does rectal temperature lag? J Pediatr 2004, 144:824–826.
26. Greenes DS, Fleisher GR: Accuracy of a noninvasive temporal artery thermometer for use in infants. Arch Pediatr Adolesc Med 2001, 155:376–381.
27.•• Moran DS, Mendal L: Core temperature measurement methods and current insights. Sports Med 2002, 32:879–885.

A well-done overview of the common modes of assessing body temperature in humans.

28.•• O'Brien C, Hoyt RW, Buller MJ, et al.: Telemetry pill measurement of core temperature in humans during active heating and cooling. Med Sci Sports Exerc 1998, 30:468–472.

One of the gold standards in this area of research.

29.•• Sawka MN, Pandolf KB: Physical exercise in hot climates: physiology, performance, and biomedical issues. Medical Aspects of Harsh Environments, vol 1. Textbooks of Military Medicine. Edited by Pandolf KB, Burr RE. Washington DC: TMM Publications; 2002:87–133.

An outstanding overview of exercise heat tolerance and the factors that mediate the response. The book that this chapter is in is one of the most important contributions to the field of exercise in the heat.

30.•• Gardner JW, Kark JA: Clinical diagnosis, management, and surveillance of exertional heat illness. Medical Aspects of Harsh Environments, vol 1. Textbooks of Military Medicine. Edited by Pandolf KB, Burr RE. Washington DC: TMM Publications; 2002:231–280.

Practical guidelines that the US military utilizes and that is currently warranted based on the available research.

31.• Roberts WO: Death in the heat: can football heat stroke be prevented. Curr Sports Med Rep 2004, 3:1–3.

An insightful perspective from one of the leading experts on EHS.

32.•• Armstrong LE, Casa DJ, Millard-Stafford M, et al.: Exertional heat illness during training and competition. Med Sci Sport Exerc 2006, in press.

This new position statement by the American College of Sports Medicine has a fresh look that is reflective of the most recent research available.

33.•• Binkley HM, Beckett J, Casa DJ, et al.: National Athletic Trainers' Association Position Statement: exertional heat illnesses. J Athl Train 2002, 37:329–343.

A comprehensive look at the common exertional heat illnesses.

34.•• Casa DJ, Almquist J, Anderson S, et al.: Inter-association task force on exertional heat illnesses consensus statement. NATA News June 2003,24–29.

These concise recommendations from a consensus of 18 health, governmental, and sports medicine organizations have provided important support for critical issues related to EHS.

35.• Casa DJ, Armstrong LE: Exertional heatstroke: a medical emergency. Exertional Heat Illness. Edited by Armstrong LE. Champaign, IL: Human Kinetics; 2003:29–56, 230–234.

A comprehensive look at EHS.

36.• Casa DJ, Roberts WO: Considerations for the medical staff: preventing identifying, and treating exertional heat illnesses. Exertional Heat Illness. Edited by Armstrong LE. Champaign, IL: Human Kinetics; 2003:169–196, 255–259.

Practical and applied information for clinicians.

37.• Epstein Y: Exertional heatstroke: lessons we tend to forget. Am J Med Sports 2000, 2:143–152.

A well-respected EHS researcher offers insight from years of examining this topic.

38. Casa DJ, Clarkson PM, Roberts WO: American College of Sports Medicine roundtable on hydration and physical activity: consensus statements. Curr Sports Med Rep 2005, 4: 115–127.
39. Schnirring L: Heatstroke fatalities fan discussion two deaths in high school football. Phys Sportsmed 2004, 32:8–10.
40. Chesney ML: Pediatric exertional heatstroke. Air Med J 2003, 22:6–8.
41.•• Heled Y, Rav-Acha M, Epstein Y, Moran DS: The “golden hour” for heatstroke treatment. Mil Med 2004, 169: 184–186.

Another recent contribution to the literature that places a big emphasis on the importance of rapid cooling.

42. Sriramachari S: Heat hyperpyrexia: time to act. Indian J Med Res 2004, 119:vii–x.
43. AVACORE Technologies, Inc: Through the wall: recovery. Rapid Thermal Exchange/Core Control Advertisements, 2003.
44. Chou YT, Lai ST, Lee CC, Lin MT: Hypothermia attenuates circulatory shock and cerebral ischemia in experimental heatstroke. Shock 2003, 19:388–393.
45. Hadad E, Moran DS, Epstein Y: Cooling heat stroke patients by available field measures. Intensive Care Med 2004, 30:338.
46. Lugo-Amador NM, Rothenhaus T, Moyer P: Heat related illness. Emerg Med Clin N Am 2004, 22:315–327.
47. Noakes TD: Body cooling as a method for reducing hyperthermia. S Afr Med J 1986, 70:373–374.
48.•• Varghese GM, John G, Thomas K, et al.: Predictors of multi-organ dysfunction in heatstroke. Emerg Med J 2005, 22: 185–187.

An important look at the consequences of delayed cooling.

49.• Hadad E, Rav-Acha M, Heled Y, et al.: Heat stroke a review of cooling methods. Sports Med 2004, 34:501–511.

A comprehensive look at the data regarding cooling methods that have been examined in previous research.

50.• Wyndham CH, Strydom NB, Cooke HM, et al.: Methods of cooling subjects with hyperpyrexia. J Appl Physiol 1959, 14:771–776.

One of the original studies examining cooling of hyperthermic athletes.

51.•• Proulx CI, Ducharme MB, Kenny GP: Effect of water temperature on cooling efficiency during hyperthermia in humans. J Appl Physiol 2003, 94:1317–1323.

The fastest cooling rates ever reported in the literature are in this research study.

52.• Brodeur VB, Dennett SR, Griffin LS: Hyperthermia, ice baths, and emergency care at the Falmouth road race. J Emerg Nurs 1989, 15:304–312.

An overview of the procedures utilized at the Falmouth Road Race. This is very relevant due to the relatively high incidence of EHS at this race and the excellent survival rates with ice baths.

53.•• Costrini A: Emergency treatment of exertional heatstroke and comparison of whole-body cooling techniques. Med Sci Sports Exerc 1990, 22:15–18.

Author provides evidence for 100% human survival rate associated with cold/ice water immersion.

54. Al-Aska AK, Abu-Aisha H, Yaqub B, et al.: Simplified cooling bed for heatstroke. Lancet 1987, 1:381.
55.• Armstrong LE: Performing in extreme environments. Champaign, IL: Human Kinetics; 2000.

A good overview of the physiological stresses faced in differing environmental conditions.

56. Armstrong LE, Crago AE, Adams R, et al.: Whole-body cooling of hyperthermic runners: comparison of two field therapies. Am J Emerg Med 1996, 14:355–358.
57. Clapp AJ, Bishop PA, Muir I, Walker JL: Rapid cooling techniques in joggers experiencing heat strain. J Sci Med Sport 2001, 4:160–167.
58.• 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, 37:146–150.

A comparison of optimal temperatures to determine which is best for cooling rates.

59. Grahn DA, Cao VH, Heller HC: Heat extraction through the palm of one hand improves aerobic exercise endurance in a hot environment. J Appl Physiol 2005, 99:972–978.
60. Khogali M, Weiner JS: Heatstroke: report on 19 cases. Lancet 1980, 2:276–278.
61. Kielblock AJ, Van Rensburg JP, Franz RM: Body cooling as a method for reducing hyperthermia. S Afr Med J 1986, 69: 378–380.
62.• Mitchell JB, Schiller ER, Miller JR, Dugas JP: The influence of different external cooling methods on thermoregulatory responses before and after intense intermittent exercise in the heat. J Strength Cond Res 2001, 15:247–254.

A relevant study from the body cooling literature.

63. Poulton TJ, Walker RA: Helicopter cooling of heatstroke victims. Aviat Space Environ Med 1987, 58:358–361.
64. Schiller ER: Effect of different cooling methods on thermoregulation following intermittent anaerobic exercise in the heat.
65. Frank SM, Raja SN, Bulcao CF, Goldstein DS: Relative contribution of core and cutaneous temperatures to thermal comfort and autonomic responses in humans. J Appl Physiol 1999, 86:1588–1593.
66.•• Armstrong LE, Maresh CM: Can humans avoid and recover from exertional heatstroke? Adaptation Biology and Medicine, vol 2. Edited by Pandolf KB, Takeda N, Singal PK. New Delhi, India: Narosa Publishing House; 1999:344–351.

Recovery and return-to-play following EHS is a topic that has not been adequately researched. This excellent review examines the existing literature and sets the stage for work that still needs to be done.

67. Mehta AC, Baker RN: Persistent neurological deficits in heat stroke. Neurology 1970, 20:336–340.
68. Royburt M, Epstein Y, Solomon Z, Shemer J: Long-term psychological and physiological effects of heat stroke. Physiol Behav 1993, 54:265–267.
69.• Moran DS, Heled Y, Still L, et al.: Assessment of heat tolerance for post exertional heat stroke individuals. Med Sci Monit 2004, 10:CR252–CR257.

In the limited body of knowledge regarding recovery and return to play following EHS this research shed some light on what would make a useful heat tolerance test.

70.• Arngrimsson SA, Petitt DS, Stueck MG, et al.: Cooling vest worn during active warm-up improves 5-km run performance in the heat. J Appl Physiol 2004, 96:1867–1874.

Another important resource from the body cooling literature.

71. Hasegawa H, Takatori T, Komura T, Yamasaki M: Wearing a cooling jacket during exercise reduces thermal strain and improves endurance exercise performance in a warm environment. J Strength Cond Res 2005, 19:122–128.
72.•• Yeargin SW, Casa DJ, McClung JM, et al.: Body cooling between two bouts of exercise in the heat enhances subsequent performance. J Strength Cond Res 2006, in press.

Body cooling between two bouts of exercise enhances performance and physiological function during subsequent exercise. Will future research examining body cooling during exercise in the heat also show that it reduces the incidence of exertional heat illnesses?

73.•• Sonna LA, Wenger CB, Flinn S, et al.: Exertional heat injury and gene expression changes: a DNA microarray analysis study. J Appl Physiol 2004, 96:1943–1953.

On the cutting-edge.

74.• Casa DJ, Armstrong LE, Watson G: Heat acclimatization of football players during initial summer practices. Med Sci Sports Exerc 2004, 36:S49.

Real-time core temperature data from collegiate football players during the first 8 days of football practices.

75.• Cheung SS, Sleivert GG: Multiple triggers for hyperthermic fatigue and exhaustion. Exerc Sport Sci Rev 2004, 32:100–106.

A physiological basis for some of the issues relevant to EHS.

76.• Goldstein LS, Dewhirst MW, Repacholi M, Kheifets L: Summary, conclusions and recommendation: adverse temperature levels in the human body. Int J Hyperthermia 2003, 19:373–384.

Unique and important perspectives on hyperthermia in humans.

77. Lambert GP: Role of gastrointestinal permeability in exertional heatstroke. Exerc Sport Sci Rev 2004, 32:185–190.
78. Mustafa S, Thulesius O, Ismael HN: Hyperthermia-induced vasoconstriction of the carotid artery, a possible causative factor of heatstroke. J Appl Physiol 2004, 96:1875–1878.
79.• Nielsen B, Nybo L: Cerebral changes during exercise in the heat. Sports Med 2003, 33:1–11.

An important area of future investigation.

80. Wen YS, Huang MS, Lin MT, Lee CH: Hypothermic retrograde jugular perfusion reduces brain damage in rats with heatstroke. Crit Care Med 2003, 31:2641–2645.
© 2005 American College of Sports Medicine