What Is the Clinical Problem?
Athletes, elite, recreational and tactical, and occupational laborers, regularly perform stressful physical activities in warm to hot environments, sometimes wearing heavy equipment (e.g., football player), protective clothing (e.g., firefighter), or both (e.g., warfighters). Heat stress impairs exercise performance and causes physiological strain that may evolve into exertional heat illness in a wide range of temperature conditions starting as low as 15°C (1). Based on data from the National Center for Catastrophic Sport Injury Research at the University of North Carolina at Chapel Hill, deaths in athletes from exertional heat stroke (EHS) have averaged three per year since 1995, mainly in high school football players (2). Despite educational and preventive efforts to lessen EHS morbidity and mortality, recent literature reveals little to no change in the annual number of EHS deaths among athletes (3). The prevalence of exertional heat illness across all sports is not known (4). The difficulty assessing the data and trends surrounding the epidemiology of exertional heat illness is partly explained by the number of cases that are not treated and documented in medical care facilities, and the inconsistent terminology and case definitions (5).
The incidence rate of exertional heat illness increases as ambient temperature and relative humidity rise during the warmer months of the year (6–10); this rate is predicted to increase as average world temperature and relative humidity continue to escalate with climate change (11). The increased prevalence of obesity, physical inactivity, low physical fitness, and lack of heat acclimatization may contribute to the increase incidence rate. However, other factors such as more frequent heat waves and suboptimal prevention strategies may be responsible (7,12–14). Many medical management issues related to the recognition, treatment, and recovery of exertional heat illnesses remain controversial (15,16).
A systematic review of 62 epidemiological studies reported the highest incidence of exertional heat illness in American football, running, cycling, and adventure races (5). Marathon running and triathlons report the highest number of hospitalizations due to the extended duration of vigorous exercise (5). Few sports are immune from exertional heat illness and examples of rates (per 100,000 athlete exposures) during training and competition in National Collegiate Athletic Association sports are: men's American rules football (15.5), wrestling (2.9), cross-country (4.8), basketball (4.1), soccer (3.1), and women's cross country (3.5), outdoor track & field (5.9), tennis (4.3), field hockey (0.20), and soccer (3.0) (9). High school rates also vary by sport (17), some examples include girl's field hockey (3.9), lacrosse (0.6), volleyball (0.3), soccer (1.1), cross-county (2.8); and boy’s baseball (0.57) and soccer (0.51) (7,18). Boy's American rules football consistently has the highest rate of exertional heat illness, with Kerr et al. (7,18) reporting 11 times the rate (4.42 to 5.2) of all other high school sports combined. In military and occupational settings, Army and Marine Corps personnel and laborers in occupations with heat-exposed physical activity consistently have the highest rates of exertional heat illness (19–21).
This American College of Sports Medicine (ACSM) consensus statement replaces the position statement published in 2007 (22) with emerging practices for recognition, prevention, and management of exertional heat illness (15,16) and focuses on exertional heat exhaustion (EHE), exertional heat injury (EHI), and EHS. Additional conditions, such as exercise-associated muscle cramps, exertional rhabdomyolysis, exercise collapse associated with sickle cell trait, and exercise-associated hyponatremia, are not included in this statement, although they are important to consider in the initial evaluation of a collapsed athlete. The consensus statement will identify evidence-based strategies to reduce morbidity and mortality of exertional heat illness, including introducing a staged return to activity (RTA) for athletes recovering from an EHS event.
What Is Serious Exertional Heat Illness?
Serious exertional heat illness includes EHS, EHI, and EHE; whether these entities occur independently or on a spectrum has not been determined. Exertional heat illness related to strenuous exercise and elevated body temperatures often presents with athlete collapse and can range from self-limited EHE to potentially life-threatening EHS (23–27). Any athlete or laborer presenting with a clinical picture, suggesting a potentially life-threating exertional heat illness, should be cooled until a more thorough evaluation can be completed.
EHE is defined as the inability to sustain the required cardiac output and blood pressure to continue physical activity because of high skin blood flow requirements and/or dehydration related to heat stress. Body temperature is elevated by the metabolic heat produced during exercise but is usually <40°C (27–29). Common signs and symptoms consistent with the etiology are listed in Table 1. EHE generally has no chronic health effects and after body cooling and restoring fluid-electrolyte balance most athletes and laborers can RTA in 1 d to 2 d. However, repeated episodes of EHE within a 24-month span should have a thorough medical evaluation (30).
Table 1 -
Signs and symptoms of exertional heat illness that often resolve with rapid cooling.
|Common Signs and Symptoms of Exertional
||Signs and Symptoms Suggesting EHS
||Persistent mental status changes
||Personality changes (frontal lobe)
||Inappropriate behavior or aggressiveness
||High rectal temperature, >40°C (104°F)
||Loss of ambulatory function (ataxia)
||Flaccid muscles or persistent rigidity
|Missing assigned tasks (cognitive function)
|Sweaty skin (not dry), warm or cool to touch
|Skin color varies from pale to flushed
|Weak or rapid pulse
EHS is defined as a life-threatening condition characterized by central nervous system (CNS) disturbances and hyperthermia, usually >40°C rectal temperature. The term “heat stroke” reflects the presence of focal “stroke-like” symptoms associated with warm environments and hyperthermia, although the symptoms in most victims are more global (encephalopathy) than focal (stroke syndrome). CNS changes associated with EHS vary from mild personality deviations to the continuum of confusion, delirium, stupor, or unconsciousness. Altered mental status with loss of orientation to person, place, or time is common. Severe agitation with florid psychosis can occur, and some victims are verbally and physically aggressive with potential to injure caregivers. In addition to CNS dysfunction, EHS is usually associated with body temperature >40°C, along with signs and symptoms of cardiovascular and other organ system distress (see Table 1). Organ and tissue damage occur with prolonged hyperthermia, sometimes due to delayed recognition and cooling, but the damage may not be clinically evident until later in the disease process. Clinical management following EHS may require critical care interventions for organ and tissue damage induced by hyperthermia and sequelae, including systemic inflammatory response syndrome (SIRS) and disseminated intravascular coagulopathy (DIC) (24–26).
A presenting core temperature ≥40°C alone is not sufficient to establish the diagnosis of EHS (15,24,25,27). Core temperature values ≥40°C (exertional hyperthermia) have been documented during high-intensity physical activity in both warm and hot weather with no apparent adverse effects on performance or health (31–33).
EHI is characterized by evidence of organ (e.g., gastrointestinal, kidney, liver, muscle) damage and dysfunction in the presence of hyperthermia without CNS changes seen in EHS and requires laboratory testing to establish the diagnosis (24–26). In an exercise setting, EHI also can be a consequence of delayed recognition and/or inadequate cooling of EHS. The exact clinical pathway to tissue or organ injury is unknown but may be a result of dehydration and reduced blood flow during a more severe EHE episode or a direct thermal injury during an EHS episode in which CNS dysfunction was minor or missed. EHI may or may not be on a continuum as an intermediate condition between EHE and EHS. EHI typically causes tissue and organ dysfunction that may persist for several weeks (30), including acute kidney injury, transient diarrhea (gut injury), and/or transaminitis associated with liver injury. More severe EHI-associated EHS can result in liver or kidney failure requiring organ transplantation for patient survival.
What Is the Pathophysiology of Exertional Heat Illness?
During exercise in the heat, the primary physiological challenge is an increase in cardiac output to support both high skin blood flow for heat dissipation and high muscle blood flow for metabolism at the expense of compensatory reductions in renal and splanchnic blood flow (27,34). When these compensatory responses are insufficient, skin, muscle, and even brain blood flow are compromised affecting tissue metabolism and heat exchange (25,27,34). In addition, as ambient temperature increases, sweating increases, and sweat evaporation become the primary heat transfer mechanism (35). If the high rates of sweating fluid loss are not replaced, the reduced plasma volume (from dehydration) further elevates physiological strain, impairing work capabilities and increasing the risk of exertional heat illness (25,27,34).
Figure 1 diagrams progression from exercise heat stress to exertional heat illness. The greater the heat stress the greater the physiological strain as evidenced by hyperthermia, blood pressure regulation challenges, reduced tissue perfusion, ischemia, and both elevated oxidative and nitrosative stress (27,34).
If the physiological strain is not excessive, multiple heat exposures will stimulate adaptations, such as heat acclimation (35) and acquired thermal (heat) tolerance (36), which help to improve performance in the heat and protect from exertional heat illness (27). The adaptive changes will induce molecular adaptions, including heat shock protein (HSP) expression, which improve tissue/organ protection or thermal tolerance. If the physiological strain is excessive, it will induce pathological events, including increased gut permeability, endotoxemia, exaggerated acute phase response and SIRS, coagulopathy, and cell death (25,27,37). In addition, reduced cerebral blood flow, combined with abnormal local metabolism and coagulopathy, can lead to dysfunction of the CNS. These perturbations induce changes are associated with EHS and EHI. There is no evidence that EHI or EHS will induce abnormalities to hypothalamic regions, but thermoregulatory feedback loops may be damaged (15). Of particular concern is intestinal barrier damage accentuating endotoxin leakage and potentiating liver damage, endotoxemia, SIRS, and sepsis (25,37). The composition of an athlete's gut microbiome may predispose an EHS or EHI victim to endotoxemia and SIRS (38).
Preliminary research indicates there may be an association with EHS/EHI and long-term health issues. For example, EHS/EHI victims were reported to have a 3.9 times higher incidence of major cardiovascular events, a 5.5 times greater incidence of ischemic stroke, and a 15 times greater incidence of atrial fibrillation during a 14-year follow-up period (39,40). Similarly, a cohort mortality study of male and female U.S. Army personnel hospitalized for exertional heat illness with an unknown duration of hyperthermia prior to cooling demonstrated a 40% increased long-term mortality risk when compared with hospital admissions for appendicitis as reference cases (39). Recent evidence from an animal model suggests that 30-d post-EHS epigenetic memory changes can suppress the immune system and alter HSP responses (41). In heat-tolerant athletes believed to be fully recovered from a prior EHS/EHI episode (ranging from 6 wk to 10 years), after a bout of exercise-heat stress, the lymphocyte HSP72 level was lower and in vitro lymphocyte HSP70 induction tended to be lower in post-EHI patients suggesting potential for reduced acquired cellular tolerance (42). There were no differences between control and post-EHS groups for core temperature or heart rate (HR), emphasizing the ability to have similar physiological strain responses during a modest heat exposure and the need for more detailed molecular biomarkers (42). These findings suggest that future research is needed to examine the relationship between residual tissue damage from EHS/EHI and long-term morbidity and mortality.
How Is Exertional Heat Illness Optimally Managed?
Evaluating and managing an athlete or laborer with exertional heat illness requires an effective “chain of survival” comparable to the American Heart Association's paradigm for out of hospital cardiac arrest. The “chain of survival” for exertional heat illness includes four linked steps: prehospital management; emergency medical service (EMS); advanced clinical management in a medical treatment facility; and finally, guiding the RTA (See Fig. 2). The first three links in clinical care are detailed in this section on optimal management; the final step of facilitating a RTA with attention to precipitating risk factors is discussed in sections V and VI.
Exertional heat illness clinical management depends on early recognition, immediate cooling, and transport to a medical facility for advanced care (see Fig. 3). The observation that the best outcomes are achieved with rapid reversal of body hyperthermia through early aggressive cooling is supported by robust literature (43–45); accordingly, prehospital management is the most critical element of limiting the morbidity and mortality of an exertional heat illness event. A recent consensus statement proposed several key steps in the paradigm of prehospital EHS victim care, including rapid recognition, rapid assessment, and rapid cooling (43).
An evaluation for EHS is usually triggered by the collapse or near collapse of an athlete or laborer during or immediately following physical activity with heat stress. The differential diagnosis in a collapsed athlete is extensive, but most often due to sudden cardiac arrest, exertional heat illness, sports-related concussion, exercise-associated hyponatremia, hypoglycemia, hypothermia, or exercise-associated postural hypotension (exercise-associated collapse). Many of these diagnoses have overlapping clinical presentations and a systematic approach incorporating vital signs and a brief cognitive assessment will expedite recognition and initial management, especially for providers in a field setting (Table 1). In all weather conditions, self-limiting postexercise collapse is usually due to sudden discontinuation of skeletal muscle pump activity causing venous pooling and postural hypotension rather than heat illness or dehydration, and the associated orthostatic instability usually resolves in less than 30 min with leg elevation and rest (46,47). A missed EHS diagnosis or delayed whole-body cooling may lead to single or multiple organ failure or death (14). The entire clinical picture, including the history of events leading up to the collapse, mental status changes, vital signs, including rectal temperature, available point of care on site laboratory results, and regular reassessment, should be considered to optimally establish a diagnosis and manage the athlete with exertional collapse (24).
An unconscious athlete with spontaneous respirations or a conscious athlete with CNS changes should be assessed for EHS with an onsite core (rectal) temperature measurement. However, whole-body cooling should not be delayed for a core temperature measurement when EHS is suspected based on clinical circumstances and working diagnosis. Rectal temperature measurement is the best estimate of core body temperature in the field (48–50). Shell temperature measured in the aural canal or tympanic measures, oral sublingual, temporal artery or forehead, and axilla sites correlate poorly with rectal temperature and should not be used for clinical decision making for heat-related problems (48–52).
The best outcomes for EHS and EHI require rapid on-site whole-body cooling. On-site cooling prevents treatment delays and cooling interruptions associated with transportation to medical facilities and emergency department (ED) evaluation protocols for encephalopathy. Body cooling serves two purposes: 1) reducing organ and tissue temperatures and 2) supporting tissue perfusion by vasoconstricting skin and superficial tissue vessels moving blood volume from the peripheral to the central circulation. Cooling rates >0.15°C·min−1 are best for survival without medical complications. Insufficient or delayed cooling can result in the medical complications of EHI or death (45).
Reducing body temperature by any means possible is essential to decrease the morbidity and mortality associated with EHS, and conductive heat exchange methods are the most effective in the field. The thermal conductivity of water is 32 times that of air and using circulating cold water to facilitate convective heat exchange at the skin level is the best means of rapidly reducing core body temperature (51,53,54). Ice water tub immersion is very effective for whole body cooling in hot, humid conditions (55,56). At the Falmouth Road Race (11.4 km), there have been no fatalities and limited hospitalizations in 274 consecutive runners, aged 11 to 70 years, rapidly cooled on-site with ice water tub immersion (56).
Other whole-body cooling methods like rotating ice water-soaked towels on the trunk, extremities, and head augmented with ice packs in the neck, axilla, and groin; repeatedly dousing the body with ice water; or spraying with tap water can effectively cool hyperthermic patients (see Table 2). Evaporative cooling methods are more effective in airconditioned spaces or low relative humidity environments and often not effective in the field as high relative humidity limits evaporative heat transfer. Placing ice packs over major blood vessels in the groin, axilla, and neck can be combined with other cooling strategies, but is not recommended as a lone treatment modality. However, in a “first aid” situation ice packs over the major vessels may be a lifesaving start to therapy.
Table 2 -
Onsite whole-body cooling strategies for EHS casualties that are effective in the field.
|Body Cooling Strategies
|Ice water (~2°C) or cold water (~20°C) immersion with stirring: whole body
||Immerse body to neck, circulate or stir the water to increase heat transfer, add ice during cooling, support head above water level. Continuous supervision.
|Ice water immersion: half body
||Immerse the torso and pelvic region
|Rotating ice water-soaked towels applied to the limbs, trunk, and head with ice packs in the groin, axilla, and neck; whole body
||2 people, 6–8 towels, change rapidly, wring towels after soaking in bucket of ice water
|Tarp-assisted water immersion: partial body
||6–8 people to hold the sides of the tarp. Ensure as much of the torso and groin are immersed as possible
|Cold water dousing: whole body
||Free flowing hose or bucket with cool tap water
|Ice water-soaked sheets only or with fanning: whole body
||Frequently re-wet sheets with cold water
|High powered spray misters: whole body
||1–2 people to supervise
|Water spray and fans: whole body
||1 person to spray
|Cold water immersion in portable water-impermeable bag: whole body with head out.
||1–2 people, add ice and water as needed
|Cooling blanket — cold air (Bair Hugger)
||Available in EMS vehicles
The approximate cooling rates will vary with body mass, body fat, surface area, blood flow, and other factors. The strategy must be practical and achievable at the site. Starting whole body cooling immediately is critical to achieve the best outcomes and should not be delayed by starting IV fluids or transfer to an emergency medical facility.
Initiating whole-body cooling as soon as possible is essential, and Table 2 lists potential methods for use in the field. The method used will be site-dependent and a blend of several elements, including clinical experience of the providers, site assets and limitations, water and ice access, patient size and body type, and the incidence rate of EHS at the site (57). Victims with low body mass and with high surface area to mass ratio (such as children or thin endurance athletes) may cool more rapidly than victims with large body mass and relatively low surface area (football linemen) who can store more heat in the tissues (58). While cold water immersion is very effective, in some situations the use of 40-gallon tubs and 20 lbs to 30 lbs of ice may be impractical, and more portable methods may be an alternative to rapidly initiate whole-body cooling (59).
The primary goal of prehospital cooling is to lower the body temperature, prioritizing core temperature reduction to below 39°C within 30 min to 60 min of collapse to protect the critical organs. Athletes with indwelling rectal thermistors can be monitored continuously without interrupting body cooling. Repeatedly measuring rectal temperature every 10 min, when an indwelling thermistor is not available, interrupts body cooling and reduces the overall cooling rate. The recommendation to stop active cooling at ~38°C (101°F) to prevent hypothermic overshoot is empirical and not based on data showing adverse outcomes. There are no known disadvantages or adverse outcomes from cooling below 38°C and most “overcooled” athletes will be in the 35°C to 37°C (95°F to 97°F) range, which has no adverse physiological effect (24). Simply continuing uninterrupted cooling until the victim “wakes up” (eyes open, normal behavior, and conversational) is the more effective cooling strategy in this clinical scenario. Checking a rectal temperature at the point of waking up will confirm cooling to the goal level and cooling can be discontinued. If a victim does not wake up in 30 min to 40 min, clinical reassessment is indicated.
Intravenous fluid replacement requirements vary based on the duration of physical activity and individual sweating rates. The need for intravenous (IV) fluid replacement is often clinically apparent following cooling and the return of peripheral blood volume to the central circulation. Peripheral IV sites complicate cooling procedures, and initiating IV fluids can be delayed if the patient is responding well to cooling measures (60–63). Oral fluids are preferred to IV fluid replacement and should be started when the patient can tolerate oral intake.
Emergency Medical Transport
An EHS victim cooled on-site should be transported, as soon as possible, to a hospital ED that is equipped to evaluate and manage the complications of EHS and EHI. In road race settings that manage many exertional heat illness-related problems, casualties with EHS who are promptly recognized, treated, wake up easily, and clinically stable are often discharged to home with family. In other settings not accustomed to exertional heat illness and EHS field management, ED evaluation is strongly recommended following on-site cooling.
If on-site cooling was not started or completed, a suspected EHS casualty is best managed at the nearest medical facility with the capability for cooling and medical management of exertional heat illness complications. EMS vehicles in areas with high exertional heat illness incidence rate should be equipped to begin or continue cooling therapy treatment en route (chilled IV fluids, ice packs, cooling blankets [Bair Hugger™], fans) and use the vehicle air conditioning at high settings when EHS is suspected. Many EMS vehicles now carry refrigerated IV fluid chilled to 4°C (39°F) to augment induction of therapeutic hypothermia in cardiovascular emergencies.
Advanced Medical Treatment Facility Management
The third phase of clinical management involves advanced care using an ED and hospital with inpatient critical care capability. When an individual with suspected exertional heat illness is transported to the hospital, the EMS dispatcher should ideally direct the patient to a facility with known experience and familiarity with heat casualties and notify the ED medical team in advance to allow preparation for immediate treatment upon arrival. The diagnosis of EHI and/or EHS can be challenging, as the patient may present with a temperature <40°C due to either active or passive cooling that occurred prior to or during transport. In addition, many medical care facilities are not equipped with various modalities for total body cooling, making rapid cooling difficult to achieve once the patient arrives. Sports event administrators and medical directors who expect the potential for exertional heat illness casualties should work with local hospital systems to facilitate appropriate treatment protocols and treatment areas.
In addition to being equipped with whole-body cooling options, the ED and hospital should be prepared for a patient that may be combative and require sedation with advanced airway management. The medical team must be aware of common EHS sequelae, including acute kidney injury, rhabdomyolysis, liver failure, DIC, and SIRS. Organ and tissue damage may not be detected initially, and serial clinical testing is required to measure the extent of tissue damage (see Table 3)(11,64,65). Intensive care and organ system support protocols will be necessary in some EHS victims. This document is not intended to outline either ED or inpatient intensive care clinical management because there are multiple resources with detailed care protocols.
Table 3 -
Some of the following laboratory tests may be needed to assess clinical status and guide management.
|• Complete blood count with platelet count
|• Serum electrolytes (sodium, potassium, chloride, bicarb)
|• Serum calcium and phosphorus
|• Serum glucose
|• Serum creatinine and blood urea nitrogen
|• Serum uric acid
|• Serum AST, ALT, LDH, alkaline phosphatase, and total bilirubin
|• Creatine kinase
|• Myoglobin blood and urine
|• Fibrinogen, fibrinogen degradation products
|• PT and activated partial thromboplastin
|• Serum lactate
|• Arterial blood gases
All these laboratories should be normal before beginning a return protocol (16,61,62
AST, aspartate aminotransferase; ALT, aspartate transaminase; LDH, lactate dehydrogenase; PT, prothrombin time.
How Can an Athlete with a Serious Exertional Heat Illness Safely RTA?
RTA and play decisions are challenging for medical providers managing athletes and laborers because our understanding of the pathophysiological processes involved in the evolution and recovery from EHS/EHI is incomplete (15,44,66–68). Returning an athlete safely and effectively to the full preheat illness level of performance is the primary task for the medical decision-making team. The final plan sometimes requires involving an athlete's coaches, supervisors, athletic trainers, and/or family members. Key clinical considerations include assessing organ system recovery and physical function abilities in warm or hot conditions (19).
Current research suggests that most individuals recover completely within a few weeks, especially if the heat illness incident was recognized promptly and cooled aggressively (15,68,69). However, some people with more serious cases experience long-term complications that may include multisystem organ (liver, kidney, muscle) dysfunction, neurologic damage, reduced exercise capacity, and/or heat intolerance (70–72).
A progressive increase in exercise intensity and duration in warm and hot conditions can be used to assess recovery. If an athlete can gradually regain preheat injury exercise tolerance and expected performance for their activities in heat stress conditions, return to play is usually safe and advancing to full training and competition is acceptable. Medical eligibility for sports or occupational activity requires the individual to have no medical ill effects (exercise-related symptoms or abnormal clinical test outcomes) during the return process.
What Is Heat Tolerance?
Heat tolerance is the ability to sustain physical activity in warm to hot conditions and is partly dependent on an individual's physical conditioning and heat acclimation status (73,74). Integrated cardiovascular, neurobiological, and systemic cellular responses determine an individual's heat tolerance (27,34). Heat intolerance may be linked to maladaptation in the acclimatization process, prior illness or injury, and certain inherent or genetic characteristics (75). Some heat intolerant individuals have lost prior heat acclimatization or have inefficient heat loss responses (skin blood flow or sweating) related to a prior heat illness. Post-EHS heat intolerance may be either temporary or permanent and has been observed to last from a few weeks to 5 years (76,77).
In the Severe Exertional Heat Illness Victim, What Clinical Criteria or Biomarkers Can Assist with Return to Exercise Activity Decisions?
Current RTA strategies are largely based on anecdotal observations and rely on provider experience for decision making to safely advance activity (22,67,77). Most guidelines require full symptom resolution at rest and normal laboratory findings for organs most often affected by EHI or EHS (e.g., liver and kidney) before starting a cautious reintroduction of physical activity and a gradual heat acclimatization program. Assessing the basic hematologic parameters and blood chemistries for normal renal, hepatic, and coagulation normal function will give a baseline at the onset of activity; however, validated instruments to accurately predict continuing tissue or organ damage are not available and changes may only become evident with subsequent exercise-related heat stress.
An evaluation about 1-wk postincident for a physical examination and laboratory testing or diagnostic imaging (biomarkers) of the affected organs is usually suggested for EHS follow-up (22). While there is wide variability in the recovery of affected organs, recent research does outline biomarker recovery (16,78,79). A retrospective review of 2529 EHS episodes showed indicators of acute kidney injury (creatinine, blood urea nitrogen, and blood and protein in urine) peak on the day of the injury and normalize within 24 h to 48 h; muscle damage and liver function-associated markers peak within 4 d after injury and can persist outside the reference ranges for 2 d to 16 d; and biochemical recovery from EHS is complete within 16 d for most casualties (80).
Can a Graduated Increase in Activity Be Used to Facilitate Acclimatization and a RTA?
Evidence-based data to facilitate RTA following EHI or EHS is limited and individual recovery following severe exertional heat illness is highly variable. Research is needed to evaluate the role of a graduated increase in structured physical exercise to assist in RTA decisions (69). The U.S. Military Services have the most extensive guidelines for RTA (loss of productivity) following serious heat illness (20,30) and athletes suffering EHI or EHS can be managed following similar guidelines.
Following EHI or EHS, a medical evaluation of the patient is completed every week until all symptoms, signs, and abnormal laboratory values have resolved. Activities of daily living are the only “exercise” allowed for 2 wk. When all the symptoms and signs have resolved, physical training can be gradually increased to 60 min·d−1 at low to moderate intensity. When this level of exercise is well tolerated, a heat acclimatization plan (gradually increasing the duration and intensity of exercise and heat stress each day) can be started. If no symptoms of heat intolerance or abnormal blood work values are observed, the patient is released to unsupervised sport specific physical activity.
The authors of this position stand recommend the following staged process to guide RTA following a serious exertional heat illness (see Table 4). The return protocol relies on subjective measures, and the athlete is advanced to the next stage if there is no evidence of exercise intolerance or fatigue. Each stage is individualized but may require up to 2 wk to complete in EHS victims. It is important that incremental elevations in both exercise intensity and heat stress be incorporated as these have additive effects on reducing gut blood flow and challenging gut permeability (81,82). If an athlete is unable to appropriately advance (stages 3 through 6), additional evaluation may be needed to determine the capacity for strenuous exercise in the heat, which may include heat tolerance testing (HTT) to assess current heat tolerance.
Table 4 -
Staged RTA/play after EHS.
||Example: HS Cross Country Runner
||Early Medical Recovery
Physician-guided Organ system recovery
|Activities of daily living for 1 to 2 wk
||Gradual increase in home activities without fatigue
||Home rest and return to school
||Mid Medical Recovery
Sustain minimal aerobic fitness and develop confidence
|Self-paced comfortable walk in low heat stress conditions (e.g., an air-conditioned gymnasium)
||20–60 min at maximal intensity of HR < 100 or <50% Age Adjusted maximal HR
||Return to practice and walk through the warm-up and practice, if the environmental conditions are not stressful. If not, use an air conditioned area of the school
||Early Exercise Adaptation
Athletic trainer guided with physician; Gradually improve aerobic exercise capability
|Walk at 3.5 mph in low heat stress conditions
||60 min at HR < 140 bpm or <70% of age adjusted maximal HR
||Warm-up and cool-down with team, 1 of 4 reps at half speed
||Mid Exercise Adaptation
Athletic Trainer Guided with Physician Gradually improve aerobic exercise capability and fitness
|Walk and run in low heat stress conditions
||60 min of progressively increasing run to walk ratio until constant run for 60 min
||1 of 3 reps, half speed
1 of 2 reps, ¾ speed
Athletic Trainer Guided
Gradually improve heat acclimation status
|Run in ambient warm or hot conditions
||60 min of progressively increasing run until constant run for 60 min
||All reps, ¾ speed
Athletic trainer and/or coach guided. Improve sport specific heat acclimation and fitness
|Participate in practice in ambient conditions
||Initially participate in sports specific drills with sports specific equipment then progress to training and scrimmage
||All reps, full speed
||Full Return to Sport
Athletic trainer monitors during warm-up and game
|Normal game or competition participation in ambient conditions
||Meet 1 run to finish the race
Meet 2 race to place
A suggested plan for staged RTA or competition after EHS. The return protocol relies on subjective measures and the athlete is advanced to the next stage if there is no evidence of exercise intolerance or fatigue. Each stage may require 1 wk to 2 wk and athletes who do not progress easily through the stages may require additional evaluation.
What Is the Role for HTT in RTA and Medical Eligibility?
HTT is a potential clinical decision-making tool for athletes who are unable to advance activities in a reasonable time frame (see Table 4) or who have repeat episodes of exertional heat illness. The Israel Defense Force (IDF) Medical Corps uses an exercise HTT about 6 wk postexertional heat illness as part of the “return to duty” criteria based on changes in rectal temperature (Trec) and HR during the test (73,83). A recent study of IDF military personnel calculated the sensitivity, specificity, and diagnostic accuracy of the HTT at 66.7%, 77.7%, and 77.2%, respectively (84). The authors concluded that the risk of EHI recurrence is measurable and that a negative HTT result is associated with a substantial reduction of EHI risk. The IDF has introduced mathematical modeling that calculates the probability of heat tolerance to improve test interpretation (84).
While case studies have demonstrated the efficacy of the IDF HTT in determining RTA for military warfighters and athletes afflicted by EHS (22,72,78,85,86), there are some concerns about the test's internal and external validity (87). In a recent review article, Mitchell et al. (87) question the test's external validity for tasks with high metabolic load, and the ability of the test to accurately determine true recovery and predict people who are not likely to experience another EHS episode. The outcomes of an HTT are significantly influenced by heat acclimatization of the individual, which confounds the test interpretation (88). The HTT has potential value as a tool to facilitate RTA; however, limitations in test validity and access to the facilities required to perform the test limit the use to challenging cases that can be individually evaluated at special centers and high-risk populations involved in research protocols. Further research will help establish the role of the HTT in the RTA decision-making process.
Consensus strategies for RTA following severe exertional heat illness are summarized in Table 5.
Table 5 -
ACSM RTA considerations following EHS or EHI.
|• A detailed history and physical examination including unique intrinsic and extrinsic risk factors, the timing of treatment, and the rate of cooling must be considered it the RTA decision.
|• The athlete should refrain from exercise for at least 7 d after release from initial medical care, at which time the clinician will address the clinical course of the heat stroke incident and carefully assess the status of end-organ function (neurocognitive, renal, hepatic, muscle, hematologic as clinically indicated).
|• The clinician should carefully address any intrinsic and extrinsic risk factors associated with the EHS event.
|• When medically eligible for RTA/RTP based upon the return of normal end organ function, an individual can begin exercise in a cool environment and gradually increase the duration, intensity, and heat exposure over 2 wk to 4 wk to initiate environmental acclimatization, improve fitness, and demonstrate heat tolerance.
|• If return to vigorous activity and evidence of the patient's ability to adapt to exercise-heat stress over several days is not accomplished within 4 to 6 wk, consider referral to a physician with experience in heat-related disorders for further evaluation that may include HTT in a controlled setting.
|• The timing for full RTP is highly variable based upon the inter-individual severity and recovery of each EHS event. In general, an athlete may be allowed to resume full competition after demonstrating sports specific exercise acclimatization and heat tolerance with no abnormal symptoms during the re-acclimatization period; this process normally requires a minimum of 2 wk to 4 wk (see Table 4).
What Increases Individual Risk and How Can Risk for Serious Exertional Heat Illness Be Reduced?
Exertional heat illness can occur in both healthy and “high-risk” individuals when performing vigorous activity in warm or hot conditions. Risk factors for exertional heat illness listed in Table 6 can be unique to a particular exertional event or a given individual, and often, more than one risk factor is present in an individual victim. While EHS is not completely understood and is challenging to predict, numerous risk factors associated with EHS have been identified by epidemiologic data that include environmental, physiological, drug use, and compromised health factors (25,26). For athletes, the most common risk factors are low physical fitness, lack of heat acclimatization, obesity, and heat waves or unexpectedly hot weather (14,25,89). Risk factors outlined in Table 6 can help identify individuals who should be more closely monitored by the sports medicine team and staff stakeholders during participation or have a “buddy” assigned to report any signs or symptoms (24,26). The most physically fit, heat acclimated, and motivated individuals tend to sustain high rates of metabolic heat production during intense physical activity and are highly motivated to continue activity even when experiencing excessive fatigue or symptoms of exertional heat illness (see Fig. 4).
Table 6 -
Predisposing factors to exertional heat illness [modified from (24,26
| • Warm-hot weather conditions
| • Unusually hot for region and season
| • Heat wave defined as >3 d of >32°C (90°F)
| • Wearing heavy clothes, equipment, or uniforms
| • Age (infants, older adults)
| • Overweight, high body mass index
| • Poor physical fitness
| • Inappropriate work to rest ratios
| • Inadequate heat acclimatization for current conditions
| • Heat stress in the previous 1 d to 3 d
| • Hypohydration
|Medications and drugs
| • Diuretics
| • Anticholinergics
| • B-adrenergic blockers
| • Antihistamines
| • Antidepressants
| • Stimulants (amphetamines, cocaine, ecstasy, ephedra)
| • Viral or bacterial infections
| • Fever
| • Diarrhea or vomiting
| • Skin disorders (rash, large area of burned skin)
| • Diabetes mellitus
| • Cystic fibrosis/trait
| • Cardiovascular disease
| • Self-imposed motivation to excel
| • Leadership or organizational structure
| • Peer or coach pressure to excel
In addition, the presence of a predisposing factor (e.g., recent viral illness or fever) on a particular day increases the risk of heat stroke in subsequent days and sets up the “multiple-hit hypothesis” (25,27), which may account for athletes who have completed the same exercise-heat stress task many times in the past without any pathological events but on a subsequent day suffer an EHS event (15,25,27). The multiple hit hypothesis suggests that events leading up to the day may prime the system for failure by allowing an unopposed immune response.
Athletes with an EHS episode are at higher risk for a subsequent event (13). In an 11.4-km warm-hot weather road race, the relative risk of a second EHS was 3.3 in the 2 years following the initial episode and the relative risk dropped to 1.3 in years 3 to 5 following the episode based on a total of 333 EHS patients from 174,853 finishers (91). Studies of French and U.S. military personnel show an association between hospitalization for EHS following a previous episode (92,93). Among active-duty soldiers, those with a prior serious EHI event had fourfold greater odds of experiencing a mild EHI event and those with a prior mild EHI had a 1.8-fold greater risk of having a serious EHI event at a future date (94). Malignant hyperthermia trait has recently been suggested to be a predisposing factor for exertional hyperthermia, but this is controversial, and more research is needed (95).
An important risk factor for EHS is extrinsic pressure to perform beyond the level of acclimatization or fitness. EHI and EHS sometimes occur in sport, work, or military activities when a healthy individual is pushed by a coach or a supervisor to the point of collapse during exercise in cool to hot environmental conditions. Leadership plays an important role of in the evolution and prevention of EHI and EHS (43,72).
Heat acclimatization is an adaptive physiological and perceived exertion change that occurs with repeated exposure to exercise heat stress. These adaptations improve physical function in the heat to reduce physiological strain (96) and induce molecular adaptations that protect organs and tissues (36) by favorably influencing fluid-electrolyte balance (e.g., decreased sweat and urine sodium concentration), cardiovascular function (e.g., regulated HR, circulating blood volume, and exercising blood pressure), and body temperature (e.g., increased sweat rate and skin blood flow during exercise) (96,97). A period of 1 wk to 2 wk of heat acclimatization is recommended to induce most physiological adaptations which optimize performance and reduce the risk of exertional heat illness (96–99). When training for a specific event or task, this process is accomplished by gradually increasing the intensity and duration of exercise during daily heat exposure. Adaptations can be customized to the athlete and sport (97,100).
Dehydration directly contributes to heat exhaustion (101) but a direct link to EHI and EHS has not been established; although it is reasonable to believe that dehydration indirectly augments physiological strain (27). Regardless, athletes often dehydrate during training and competition, and rehydration strategies are important for athletes to safely perform physical activity in warm to hot conditions (35). Hydration supports vascular volume and sweating, both essential to temperature regulation. Athletes experience wide-ranging sweat losses during vigorous exercise, especially in hot environments (102) and may incur substantial body water deficits if fluid is not replaced during exercise (103). Replacing mild-to-moderate fluid losses during recovery is best done by combining eating with fluid intake. For athletes with signs and symptoms of dehydration (i.e., dizziness, rapid heat rate, fatigue, headache), the use of commercial oral rehydration fluids is more effective than sports drinks with lower sodium content) (103,104). A variety of methods can be used to self-assess dehydration, but for athletes and active laborers the most common approaches involve monitoring body weight changes, thirst, and urine volume or concentration (22,35,103).
Given the chance to compete, most athletes override innate behavioral thermoregulation that reduces the risk of exertional heat illness. Decreasing the work-to-rest ratio or reducing exercise intensity as the environmental heat stress increases can minimize the risk of exertional heat illness and optimize work completed. In higher-risk conditions, site leaders should change training sessions by adding longer and more frequent rest breaks to allow heat dissipation and shorter bouts of high intensity exercise duration to decrease heat production. Longer rest breaks permit better fluid replacement when athletes have unlimited fluid access. Other factors to consider when modifying training or competition include heat acclimatization status of participants, fitness and age of participants, intensity and duration of exercise, time of day, clothing or uniform requirements, and playing surface for radiant and conductive heat exchange (i.e., grass vs synthetic fields).
Acclimatization and heat tolerance are regional, and different geographical areas require different environmental algorithms for modifying and canceling activity (105). The recommendations for curtailing activity may change through a season as athletes become fit and acclimatized to the conditions. Modifying, postponing, or canceling an event can be based on data specific to event outcomes (106,107). A region-specific exercise modification table (Table 7) is an essential primary risk reduction strategy that works for all sports and laborers (105,108,109). Heat safety tables used by institutions should include modifications in activity duration and intensity, increased rest breaks, and removal of extra clothing or equipment.
Stakeholders should understand predisposing factors of EHS (Table 6) and recognize early signs. More importantly, mandated heat safety policies and an emergency action plan should be in place at each institution to increase exertional heat illness preparedness and reduce EHS deaths (110,111). Stakeholders also should strive to have on-site health care by trained and licensed providers at their institutions to ensure early triage and reduce morbidity and mortality associated with improper diagnosis and treatment (14,18).
EHS is a true medical emergency with potential for organ injury and death. This consensus statement emphasizes that optimal exertional heat illness management is promoted by a synchronized chain of survival that promotes rapid recognition and management, as well as communication between care teams (Table 8). Health care providers should be confident in the definitions, etiologies, and nuances of EHE, EHI, and EHS. Early identification of the athlete with suspected EHS and the rapid provision of total body cooling is essential for survival, and like any ischemic situation, time is tissue. Recovery from EHS is variable, and outcomes are likely related to the duration of severe hyperthermia. Those treated before cell injury and the exaggerated acute phase response usually return to full activity within a few weeks, while those with a more complicated and prolonged course require a graduated and supervised return to prior activity levels. Finally, exertional heat illnesses are preventable, with the recognition and mitigation of well-described risk factors ideally addressed through leadership, policy, and on-site health care.
Table 8 -
Consensus summary statements and evidence grades assessed using the strength of recommendation taxonomy (107
||Level of Evidence
|Sports, military, and labor site administrators should be prepared for exertional heat illness evaluation and management
|CNS changes and rectal temperature are the primary identifying signs of EHS
|The prehospital chain of survival sequence improves exertional heat illness outcomes and communication between care teams
|Cooling rates >0.15°C·min−1 are best for survival without medical complications
|Insufficient or delayed cooling can result in the medical complications of EHI or death
|Regional environmental conditions influence the risk for exertional heat illness
|Heat acclimatization reduces physiological strain and improves physical performance in the heat
|Heat acclimatization is a primary reduction strategy for exertional heat illness rates
|Administrative strategies and focused leadership can reduce exertional heat illness rates and deaths
|Motivated, healthy athletes are at high risk for EHS.
Consensus summary statements and evidence grades assessed using the Strength of Recommendation Taxonomy (112
Research Needs and Knowledge Gaps
- Examine impact of cooling method and duration on clinical outcomes of EHI/EHS victims.
- How does body morphology impact cooling rates in EHS?
- Identify novel clinical-molecular biomarkers that predict heat intolerance, morbidity or mortality, and return-to play for EHI/EHS victims.
- Evaluate pharmacological interventions that reduce risk of morbidity and mortality in EHI/EHS patients.
- Are there different HTT strategies that will accurately predict heat safety?
- Evaluate effectiveness of different functional protocols for safe return to play after EHI/EHS.
- Can the proposed return protocol be safely accelerated?
Click here (http://links.lww.com/CSMR/A121) to download a slide deck that summarizes this consensus statement on Exertional Heat Illness: Recognition, Management, and Return to Activity.
The authors declare no conflict of interest and do not have any financial disclosures.
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