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Exertional Heat Stroke

Navarro, Chelsea S. MS, ATC, LAT, CES1; Casa, Douglas J. PhD, ATC, FNAK, FACSM, FNATA2; Belval, Luke N. MS, ATC2; Nye, Nathaniel S. MD, CAQSM1

doi: 10.1249/JSR.0000000000000403
CAQ Review

1559th Trainee Health Squadron, JBSA-Lackland, TX; and 2Korey Stringer Institute, University of Connecticut, Storrs, CT

Address for correspondence: Chelsea Navarro, MS, ATC, LAT, CES, Trainee Health Squadron, Lackland, TX; E-mail: chelsea.s.navarro@gmail.com. Column Editor: Nailah Coleman, MD, FACSM, ncoleman@childrensnational.org

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Background

Exertional heat stroke (EHS) is a medical emergency defined as life-threatening hyperthermia (core body temperature ≥ 40.5°C [105°F]) and central nervous system [CNS] dysfunction (1,4). EHS is one of the top three causes of sudden death in athletes (4). Early recognition and rapid cooling can reduce (or possibly even eliminate) both the morbidity and mortality associated with the organ damage that results from an extended time period of dangerous hyperthermia (1).

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Pathophysiology

Thermoregulation is controlled by the hypothalamus, with responses mediated principally in the skin (sweating, vasodilation) and cardiovascular system (increased cardiac output, gut vasoconstriction) (1). During strenuous exercise, especially in hot and humid climates, heat is stored faster than the body can dissipate it. This is why it is typical to have body temperatures between 38.9°C and 40.3°C (102.0°F to 104.5°F) during intense exercise in the heat. When the cell is heated beyond its thermal threshold, cell damage occurs, which may lead to organ dysfunction and failure/death (1). Some individuals may have underlying risk factors that can lead to EHS (see below) (4).

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Risk Factors

Several intrinsic factors that increase risk for EHS include the following (1–4):

  • Lack of heat acclimatization
  • Current febrile illness
  • Skin disorders: anhidrosis, sunburn, psoriasis, etc.
  • Dehydration
  • Medications/supplements (e.g., diuretics, antihistamines, CNS stimulants, antidepressants)
  • Sleep deprivation
  • Recent alcohol use
  • Low physical fitness
  • Overweight/obesity
  • Cardiovascular disorders (e.g., hypertension, peripheral vascular disease)
  • Malignant hyperthermia susceptibility

Extrinsic risk factors also play a large role in the risk for EHS and include the following (1–4):

  • Hot, humid environment (especially wet bulb globe temperature exceeding 28°C [82 °F])
  • Exercise intensity
  • Inappropriate work-to-rest ratios
  • Heavy equipment/clothing
  • Lack of education and awareness among athletes, coaches, medical staff
  • Lack of emergency plans to identify and treat EHS
  • Lack of proper infrastructure (heat acclimatization period, access to fluids, preventative cooling strategies, etc.)
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Recognition

Early signs and symptoms of EHS include the following (1,3,4):

  • CNS dysfunction (disorientation, irrational behavior, combativeness, convulsions, collapse, loss of consciousness)
  • Rectal temperature ≥ 40.5°C (105°F), taken at point of collapse
  • Dizziness, lightheadedness
  • Extreme fatigue not typical for that activity
  • Headache
  • Nausea, vomiting, diarrhea
  • Tachycardia
  • Hyperventilation
  • Ataxia

Skin color, temperature, and wetness are unreliable indicators of EHS.

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Treatment

EHS-related death is preventable through immediate recognition of symptoms, core (rectal) temperature assessment, and rapid treatment via cold-water immersion (CWI) (1–5). EHS victims should be aggressively cooled, onsite if possible, within the “golden half hour” after collapse/cessation of activity (2). Morbidity and mortality are more strongly linked to duration, rather than degree, of hyperthermia; hence, the “cool first, transport second” principle (2). CWI provides the fastest whole-body cooling rate and the lowest morbidity and mortality for EHS (1,3,5). When body temperature is reduced to < 40 °C (104 °F) within 30 min of symptom onset, mortality approaches or is actually zero, and most recover without sequelae (1,5).

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Return to Play Guidelines

As recommended by the American College of Sports Medicine (1):

  1. Refrain from exercise for ≥ 7 d after release from medical care.
  2. Follow-up in about 1 wk for physical examination and repeat lab testing or diagnostic imaging of affected organs that may be indicated, based on physician evaluation.
  3. When cleared, begin exercise in cool environment; gradually increase duration, intensity, and heat exposure for 2 wk to acclimatize and demonstrate heat tolerance.
  4. If return to activity is difficult, consider laboratory exercise-heat tolerance test about 1 month postincident.
  5. Clear the athlete for full competition if heat tolerance exists after 2 to 4 wk of training.

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

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References

1. Armstrong LE, Casa DJ, Millard-Stafford M, et al. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med. Sci. Sports Exerc . 2007;39:556–72.
2. Casa DJ, Armstrong LE, Kenny GP, et al. Exertional heat stroke: new concepts regarding cause and care. Curr. Sports Med. Rep. 2012; 11:115–23.
3. Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainers' Association position statement: exertional heat illnesses. J. Athl. Train . 2015;50:986–1000.
4. Casa DJ, Stearns RL. Preventing Sudden Death in Sports & Physical Activity . Burlington, MA: Jones & Bartlett Publishers; 2017.
5. Demartini JK, Casa DJ, Stearns R, et al. Effectiveness of cold water immersion in the treatment of exertional heat stroke at the Falmouth Road Race. Med. Sci. Sports Exerc . 2015;47:240–5.
Copyright © 2017 by the American College of Sports Medicine.