Winter 2021 Issue

Volume 13 | Number 1

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Exertional Heat Stroke in the Pediatric Athlete

Thomas Brown, DO, FAAFP, CAQ, SM
Department of Sports Medicine, Nova Southeastern University

Heat stroke, a life-threatening medical emergency, is directly resultant of temperature elevation and duration of exposure. It occurs when core temperature becomes greater than 104F (40C) and is associated with central nervous system dysfunction including seizure and coma.

Children possess intrinsic properties making them less effective at thermoregulation and thereby at increased risk for heat stroke. More children are involved in athletics today and are participating at a younger age. The incidence of heat related injuries is not uncommon. In fact, 9000 high school athletes are treated for exertional heat illness yearly. [7,8]

Heat stroke results in multi-organ dysfunction. It is estimated that 1/3 of victims will have permanent neurologic impairment with mortality reaching 3-5%. [1,2,3]

Prevention via acclimatization is of upmost importance. Once heat stroke is suspected immediate cooling is paramount as mortality increases with delay.            

Exertional Heat Stroke in the Pediatric Athlete

Children are involved in athletics at a younger age. As physicians and providers, we often chaperone athletic events. It is imperative to recognize signs of heat stroke as a condition resulting in serious sequele. In fact, 1/3 of patients surviving heat stroke will have permanent neurologic impairment [1,2,3]

Heat stroke is the third leading cause of death among young athletes in the United States, ranking behind head and spinal cord injuries [1,3,4]. Statistics relate incidence of heat related injuries is not uncommon, and the number is increasing [5,6]. The overall exertional heat related injury rate has more than doubled from 1.2 in 1997 to 2.5 in 2006. Patients less than 19 years of age account for the largest proportion of heat related injuries (47.6%) [6]. Each year 9,000 high school athletes are treated for exertional heat illness [7,8]. Football players are at highest risk especially during early season practices, resulting in 2 deaths per year [1,8].

Children naturally possess certain physiologic properties placing them at a disadvantage during physical exertion in the heat [1,9]. Morphologically, children have a greater body surface area to mass ratio [4,5,9,10]. This may prove beneficial in temperate climates but a serious limitation in extremes of temperature [4,5]. They have higher metabolic demands relative to body mass. Children also possess maturational patterns resulting in difficulties adjusting to environments. For instance, sweat rates between pre-pubertal boys and young men reveals sweat rate for pre-pubertal boys is one half the rate of young men [4,9]. Children also require higher temperatures before producing sweat and possess a blunted thirst response during exercise [5,6]. Lastly, children acclimatize to the environment at a slower rate [1,5,6].

Prevention through the process of acclimatization, is of utmost importance and should be present during the initial 14 consecutive days of preseason practice [5]. Athletes arriving after the first day or those missing any practice sessions should not count those days as part of the acclimation phase. Difficulties remain when placing all athletes into a “full go” status, as particular athletes may remain higher risk and require closer monitoring. For example, an overweight lineman recently recovering from gastrointestinal illness will have increased risk when compared to a fit running back training daily. Yet, both participated from day one.

It is imperative that physicians, parents, coaches, and athletic trainers meet prior to a season, ensuring all are knowledgeable and in agreement of current safety policies.  

Physiologically, acclimation includes increased sweat production, a decreased temperature to initiate sweating, reduced electrolyte losses in the sweat, increased skin blood flow, increased stroke volume, increased plasma volume and increased aldosterone production. [1].

Hydration is a key area often overlooked. It is imperative that fluid intake be encouraged during exertion. Athletes may lose 2-3% of body weight before becoming thirsty. Therefore, performance may already have begun to decline [5]. Weight loss of even 1-3% will limit aerobic performance. The process of hydration must be initiated prior to exercise and continued every 20 minutes during the activity. A suggested guideline for consumption is 5 oz (150 ml) for children weighing 88 pounds (40 kg), and 9 oz (250 ml) for children weighing 130 pounds (60 kg) [5].

During extended periods of exercise, pre-exercise body weight should be recorded, and one should replace each pound of weight loss with 8-9 ounces (235 ml) of fluid [5]. Offering flavored sports drinks is also recommended, thereby resulting in increased fluid intake [1,5,9] Although more expensive and possibly not readily available, consideration should be given to utilizing electrolyte supplemented beverages for extended practices [11].

Coaches, trainers, and parents possess a thorough understanding of correct clothing to be worn. Caution must be exercised during initial practice sessions and with addition of further equipment that may hinder heat loss.

The Secondary School Heat Acclimatization guideline by the Inter-Association Task Force for Preseason Secondary School Athletics in conjunction with the National Athletic Trainers’ Association’s Secondary School Athletics Trainers Committee is an excellent resource to review and follow. This resource documents limitations on hours of practice, walk-throughs, double practice sessions and mandatory rest periods [12].  

Temperature of the human body is regulated by the anterior hypothalamus which continuously attempts to keep the internal temperature between 97.7 and 99.5 degrees [4,9].  During exercise contracting muscles produce a heat load which may reach 10-20 times that of resting muscle state [5].

Four major mechanisms dissipate heat, including convection, conduction, radiation, and evaporation (Table 1). Failure of these mechanisms to operate effectively during heat exposure, especially the processes of convection and evaporation, results in a significant risk for development of heat related illness [4,5,7].

Table I.  Mechanisms of Heat Loss

  1. Evaporation: Occurs when sweat is vaporized at the skin surface. (This accounts for a primary mechanism of thermoregulation when ambient temperature rises above the body temperature).
  2. Convection: Occurs when body surface heat from the body surface is exposed to a cooler medium such as the surrounding air.
  3. Conduction: Occurs when body heat moves to a cooler surface by direct contact.
  4. Radiation: Occurs when body temperature is less than the ambient temperature.

Heat liberated by contracting muscles is transferred away by surrounding blood flow resulting in increased core body temperature. This elevation causes compensatory cutaneous vasodilatation providing convective heat loss from the skin surface. More importantly, change in skin temperature results in increased sweat production and heat loss by evaporation. As mentioned above, this method of heat dissipation is very important when exposed to increased ambient temperatures and humidity levels.

It is essential to monitor the ambient temperature for all activities. The Wet Bulb Globe Temperature (WBGT) has been the standard for heat assessment for many years and should be utilized if possible. The WBGT is composed of three thermometers and is based on air temperature (dry bulb), humidity (wet bulb) and solar radiation (black globe). If not available apps and internet sites can provide accurate local heat index information [5].

Heat Stroke
Heat stroke is a life-threatening medical emergency and is directly resultant of temperature elevation and duration. It occurs when homeostatic thermoregulatory mechanisms are overwhelmed by endogenous heat production [2]. Core temperatures greater than 107F (42C) and duration greater than 70 minutes carry a poor prognosis [3]. Mortality can be as high as 3-5% [3,7,13].

Classically, core temperature greater than 104F (40C) is associated with central nervous system dysfunction. This may include confusion, delirium, seizure, and coma [2]. Seizures occurring prior to or during the cooling phase carry little prognostic importance when compared with seizure activity occurring after cooling, which is often an ominous event.

Post-mortem autopsies suggest all body tissues are susceptible to heat related pathology. Histologically, this is manifested as cellular swelling, coagulation necrosis, microthrombosis and hemorrhage [2]. These pathologic changes commonly result in multi-organ dysfunction and onset of rhabdomyolysis from significant necrosis of muscle tissue [3,5,14,15].

Certain mediators may increase organ damage including endotoxin, cytokine levels, activated coagulation components and injured endothelium. Specifically, plasma concentrations of tumor necrosis factor-a, interleukin 1a and lipopolysaccharide as well as the anti-inflammatory cytokines, interleukin 6 and 10 are elevated in patients with heat stroke [2,3,16]

Blood pressure abnormalities are common and may change rapidly. Patients may present in a hyperdynamic state with tachycardia and low peripheral resistance. This occurs secondary to vasodilation as blood is shunted to the cutaneous tissues to cool, resulting in a wide pulse pressure [4].  This may rapidly change to a hypodynamic state with low cardiac output, hypotension, and volume depletion. These changes result in peripheral vasoconstriction as the body attempts to stabilize mean arterial blood pressure. Resulting increase in resistance concludes in the cessation of heat loss from cutaneous radiation and subsequently core temp rises.

Commonly, various cardiac arrhythmias develop, including non-sustained ventricular tachycardia, multiform PVC’s, atrial fibrillation, and flutter.  It is not uncommon for these rhythms to change spontaneously during treatment.

In addition to arrhythmias, marked ST and T wave abnormalities of the inferior and anterolateral leads associated with sub-endocardial injury are commonly observed. Troponin I may also be increased from direct heat induced heart injury and associated exercise induced increase in myocardial sarcolemma permeability. These findings may be confused with possible myocardial infarction, which is not common in young athletes. If infarction occurs, it is most likely associated with hypoxia caused by increased metabolic demands and not coronary obstruction [4].

Bleeding disorders may not come to mind when considering heat stroke, but coagulation abnormalities are routinely found [4,14,15,17]. Autopsy studies have shown hemorrhage and necrosis with widespread microthrombi in the lungs, brain, kidneys, heart, liver, and gut, which are invariably present in fatal heat stroke [17].  Patients with bleeding disorders present with higher rectal temperatures, more significant hypotension, higher incidence of shock and a higher mortality rate than patients without disordered bleeding [4].

Laboratory abnormalities that commonly present in heat stroke, especially in the early hours of onset. Table II suggests examples of lab results of a teenage cross-country runner with exertional heat stroke at admission and through the early post-discharge phases. Commonly laboratory abnormalities take weeks to normalize.

Creatine kinase (CK) may rapidly reach levels in the 30,000 rangeRhabdomyolysis is common and is often associated with the ensuing renal failure [14,15]. 

Renal function declines with elevations of creatinine and blood urea nitrogen which reflects both perfusion and volume deficits [4]. Urinalysis may show numerous abnormal components, including red and white blood cells along with hyaline, granular and white blood cell casts. Urine specific gravity may be low secondary to inability of a kidney to concentrate urine or may be super concentrated from passage of blood or myoglobin from muscle breakdown [4,14]

Hepatocellular necrosis is common as hepatocytes are very heat sensitive. The aspartate aminotransferase (AST) level is the first to elevate [2]. This commonly results in decreased synthesis of clotting factors [15].

Stress leukocytosis and thrombocytopenia are often seen.

Table II
Table ll. Lab results of teenage cross-country runner diagnosed with heatstroke from Westside Memorial Hospital and Nova Southeastern University Sports Medicine Clinic

Cooling must begin as soon as a diagnosis of heat stroke is suspected.  Mortality rate increases with delays [3,5]. Cooling processes should begin prior to transport of the patient. This may result in some degree of hesitation from the EMS transport team, but having some form of cooling mechanism immediately in place cannot be overstressed.

Ice bath immersion is the most effective method for cooling. Tubs may not be available and may even prove to be dangerous if a small child is placed in a standard sized tub. In addition to the risk of the child slipping below the surface, the occurrence of reflex bradycardia must be monitored [1].

More readily available options include placing the child in an Ice Taco, which is essentially wrapping the patient in an ice filled tarp. Application of ice in the axilla, neck and groin and evaporative methods such as spraying the patient with water while placing in front of fans may also be utilized [5].

Internal cooling devices on the market today may be available at hospitals based on treatment protocol [18]. These devices require special training and may be associated with increased risk. Limited evidence supports administering cold intravenous, peritoneal, gastric or bladder lavage but can certainly be employed if there is poor response to the external methods aforementioned [4]. A recent retrospective study concluded administration of intravenous fluids at 39.2F (4C) did reduce hospital days, decreased peak creatinine levels and normalized liver function more quickly than ambient temperature intravenous fluids in military personnel [7,18]

Once body temperature is lowered to 102.2F (39C) it is recommended to slow the cooling process to prevent over correction [5].  Approximately 75% of patients experience seizures during the cooling phase which likely occurs secondary to electrolyte abnormalities, cerebral hypoperfusion and hypoglycemia [3,5].  A decision to perform intubation should be considered early to protect the airway [5]. Benzodiazepines may be utilized to control shivering and agitation during cooling [5].

Immediately begin hydrating patients without allowing over correction to take place. Some patients may require large volumes of fluids while others are only minimally dehydrated and require much less. Since children have a higher body surface area per kilogram, they also have proportionally higher fluid requirements [10]. In the pediatric population a bolus of 20 ml/kg over 30 minutes of isotonic crystalloid (0.9% NaCl) or lactated ringers is recommended. This population may require greater than 60 ml/kg in boluses of 20 ml/kg over 30 minutes [5,10,19]. If there is no response a central line should be considered. Maintenance fluids are typically replaced with D5 0.45%NaCl with 20 mEq/L of KCl [10].

Many facilities will have a protocol in place for heat stroke events. This may commonly include in addition to methods discussed previously, arterial blood gas (ABG) testing especially if the patient requires intubation, a non-contrast CT of the head, cultures of the blood and urine and an echocardiogram.

Special thanks to Ms. Pamela Beegle, Medical Librarian, Martin Gail Press Library, Nova Southeastern University.

I have no disclosures to report, nor have I received any funding or financial support in the production of this article.


  1. Courtney W. Mangus, MD, Therese L. Canares MD. Heat related Illness in Children in an Era of Extreme temperatures. Pediatrics in Review. March 2019, Volume 40 / Issue 3
  2. Lisa R. Leon, Abderrezak Bouchama. Heat Stroke. Comprehensive Physiology. Volume 5, April 2015. 611-647.
  3. Lew, Henry MD, Lee, Eun-Ha MD, Date, Elaine S. MD, Melnik Irina MD. Rehabilitation of a Patient with Heat Stroke: A Case Report. American Journal of Physical Medicine and Rehabilitation. Volume 81 (8), August 2002 pp 629-632.
  4. Charles Stewart, MD FACEP. The Spectrum of Heat Illness in Children. Emergency Pediatrics May 1, 1999.
  5. Jeffery R. Bytomski DO, Deborah L. Squire MD. Current Sports Medicine Reports. 2003, 2:320-324.
  6. Nicholas Nelson MPH, Christy Collins MA, R. Dawn Comstock PhD, Laura B. McKenzie PhD. Exertional Heat Related Injuries Treated in Emergency Departments in the US 1997-2006. American Journal of Preventive Medicine Volume 40, Issue 1, Jan. 2011, Pages 54-60
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  8. Zachary Y. Kerr MPH, Douglas J. Casa PhD, Stephen W. Marshall PhD, R. Dawn Comstock PhD. American Journal of Preventive Medicine 2013;44(1):8-14
  9. Thomas Roland. Thermoregulation during exercise in the heat in children: old concepts revisited.  Journal of Applied Physiology 105: 718-724, 2008.
  10. Gary R. Strange MD, William R. Ahrens, MD, Robert W. Schafermeyer MD et al. Pediatric Emergency Medicine. Third edition. Mcgraw-Hill publishing. pages 658-659.
  11. Policy Statement-Climatic Heat Stress and Exercising Children and Adolescents. American Academy of Pediatrics. Pediatrics Volume 128 Number 3 Sept 2011
  12. Douglas J. Casa, PhD, ATC, David Csillan MS, ATC. Preseason Heat Acclimatization Guidelines for Secondary School Athletics. Journal of Athletic Training 2009;44(3):332-333.
  13.  Abderrezak Bouchama, Mohammed Dehbi and Enrique Chaves-Carballo. Cooling and hemodynamic management in heatstroke: practical recommendations. Critical Care 2007, 11:R54.
  14. GM Vargese, G John, K Thomas, OC Abraham, D Mathai. Predictors of multi-organ dysfunction in heat stroke. Emerg Med J 2005;22:185-187.
  15.  Tal Marom, David Itskoviz, Haim Lavon and Ishay Ostfeld. Acute Care for Exercise Induced Hyperthermia to Avoid Adverse Outcome from Exertional Heat Stroke. Journal of Sport Rehabilitation. 2011, 20, 219-227.
  16. Lior Zeller, Victor Novack, Leonid Barski, Alan Jotkowitz, Yaniv Almong. Exertional heat stroke: clinical characteristics, diagnostic and therapeutic considerations. European Journal of Internal Medicine. 22 (2011) 296-299.
  17. Abderrezak Bouchama, Francoise Bridey, Muhammad M Hammami, et al. Activation of Coagulation and Fibrinolysis in Heatstroke. Thromb Haemost 1996; 76:909.
  18. Gregor Broessner, Ronny Beer, Gerhard Franz, et al. Case report: Severe heat stroke with multiple organ dysfunction- a novel intravascular treatment approach. Critical care 2005; 9(5): R498-R501.
  19. Pediatric Emergency Medicine Resource. Fourth Edition Jones and Bartlett publishers Sadbury MA page 219.

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