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Heatstroke

  • Author: Robert S Helman, MD; Chief Editor: Joe Alcock, MD, MS  more...
 
Updated: Jul 06, 2016
 

Background

Heat illness may be viewed as a continuum of illnesses relating to the body's inability to cope with heat. It includes minor illnesses, such as heat edema, heat rash (ie, prickly heat), heat cramps, and tetany, as well as heat syncope and heat exhaustion. Heatstroke is the most severe form of the heat-related illnesses and is defined as a body temperature higher than 41.1°C (106°F) associated with neurologic dysfunction.

Two forms of heatstroke exist. Exertional heatstroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment. Classic nonexertional heatstroke (NEHS) more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons. Classic NEHS occurs during environmental heat waves and is more common in areas that do not typically experience periods of prolonged hot weather. Both types of heatstroke are associated with high morbidity and mortality, especially when cooling therapy is delayed.

With the influence of global warming, it is predicted that the incidence of heatstroke cases and fatalities will also become more prevalent. Behavioral responses are important in the management of temperature elevations and may provide clues to preventing the development of heatstroke.

See Heat Illness: How To Cool Off Hyperthermic Patients, a Critical Images slideshow, for tips on treatment options for patients with heat-related illness.

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Pathophysiology

Despite wide variations in ambient temperatures, humans and other mammals can maintain a constant body temperature by balancing heat gain with heat loss. When heat gain overwhelms the body's mechanisms of heat loss, the body temperature rises, potentially leading to heatstroke. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death.

The exact temperature at which cardiovascular collapse occurs varies among individuals because coexisting disease, drugs, and other factors may contribute to or delay organ dysfunction. Full recovery has been observed in patients with temperatures as high as 46°C, and death has occurred in patients with much lower temperatures. Temperatures exceeding 106°F or 41.1°C generally are catastrophic and require immediate aggressive therapy.

Heat may be acquired by a number of different mechanisms. At rest, basal metabolic processes produce approximately 100 kcal of heat per hour or 1 kcal/kg/h. These reactions can raise the body temperature by 1.1°C/h if the heat-dissipating mechanisms are nonfunctional. Strenuous physical activity can increase heat production more than 10-fold, to levels exceeding 1000 kcal/h. Similarly, fever, shivering, tremors, convulsions, thyrotoxicosis, sepsis, sympathomimetic drugs, and many other conditions can increase heat production, thereby increasing body temperature.

The body also can acquire heat from the environment through some of the same mechanisms involved in heat dissipation, including conduction, convection, and radiation. These mechanisms occur at the level of the skin and require a properly functioning skin surface, sweat glands, and autonomic nervous system, but they also may be manipulated by behavioral responses.

Conduction refers to the transfer of heat between 2 surfaces with differing temperatures that are in direct contact. Convection refers to the transfer of heat between the body's surface and a gas or fluid with a differing temperature. Radiation refers to the transfer of heat in the form of electromagnetic waves between the body and its surroundings. The efficacy of radiation as a means of heat transfer depends on the position of the sun, the season, clouds, and other factors. For example, during summer, lying down in the sun can result in a heat gain of up to 150 kcal/h.

Under normal physiologic conditions, heat gain is counteracted by a commensurate heat loss. This is orchestrated by the hypothalamus, which functions as a thermostat, guiding the body through mechanisms of heat production or heat dissipation, thereby maintaining the body temperature at a constant physiologic range.

In a simplified model, thermosensors located in the skin, muscles, and spinal cord send information regarding the core body temperature to the anterior hypothalamus, where the information is processed and appropriate physiologic and behavioral responses are generated. Physiologic responses to heat include an increase in cardiac output and blood flow to the skin (as much as 8 L/min), which is the major heat-dissipating organ; dilatation of the peripheral venous system; and stimulation of the eccrine sweat glands to produce more sweat.

As the major heat-dissipating organ, the skin can transfer heat to the environment through conduction, convection, radiation, and evaporation. Radiation is the most important mechanism of heat transfer at rest in temperate climates, accounting for 65% of heat dissipation, and it can be modulated by clothing. At high ambient temperatures, conduction becomes the least important of the 4 mechanisms, while evaporation, which refers to the conversion of a liquid to a gaseous phase, becomes the most effective mechanism of heat loss.

The efficacy of evaporation as a mechanism of heat loss depends on the condition of the skin and sweat glands, the function of the lung, ambient temperature, humidity, air movement, and whether or not the person is acclimated to the high temperatures. For example, evaporation does not occur when the ambient humidity exceeds 75% and is less effective in individuals who are not acclimated. Nonacclimated individuals can only produce 1 L of sweat per hour, which only dispels 580 kcal of heat per hour, whereas acclimated individuals can produce 2-3 L of sweat per hour and can dissipate as much as 1740 kcal of heat per hour through evaporation. Acclimatization to hot environments usually occurs over 7-10 days and enables individuals to reduce the threshold at which sweating begins, increase sweat production, and increase the capacity of the sweat glands to reabsorb sweat sodium, thereby increasing the efficiency of heat dissipation.

When heat gain exceeds heat loss, the body temperature rises. Classic heatstroke occurs in individuals who lack the capacity to modulate the environment (eg, infants, elderly individuals, individuals who are chronically ill). Furthermore, elderly persons and patients with diminished cardiovascular reserves are unable to generate and cope with the physiologic responses to heat stress and, therefore, are at risk of heatstroke. Patients with skin diseases and those taking medications that interfere with sweating also are at increased risk for heatstroke because they are unable to dissipate heat adequately. Additionally, the redistribution of blood flow to the periphery, coupled with the loss of fluids and electrolytes in sweat, place a tremendous burden on the heart, which ultimately may fail to maintain an adequate cardiac output, leading to additional morbidity and mortality.

Factors that interfere with heat dissipation include an inadequate intravascular volume, cardiovascular dysfunction, and abnormal skin. Additionally, high ambient temperatures, high ambient humidity, and many drugs can interfere with heat dissipation, resulting in a major heat illness. Similarly, hypothalamic dysfunction may alter temperature regulation and may result in an unchecked rise in temperature and heat illness.

On a cellular level, heat directly influences the body by interfering with cellular processes along with denaturing proteins and cellular membranes. In turn, an array of inflammatory cytokines, interleukins and heat shock proteins (HSPs) are produced. In particular, HSP-70 allows the cell to endure the stress of its environment. If the stress continues, the cell will succumb to the stress (apoptosis) and die.

On a microvascular level, heat stroke resembles sepsis and involves inflammation, translocation of lipopolysaccharides from the gut, and activates the coagulation cascade. Certain preexisting factors, such as age, genetic makeup, and the nonacclimatized individual, may allow progression from heat stress to heatstroke, systemic inflammatory response syndrome (SIRS), multiorgan dysfunction syndrome (MODS), and ultimately death. Progression to heatstroke may occur through thermoregulatory failure, an amplified acute-phase response, and alterations in the expression of HSPs.

An index used by some, including the American College of Sports Medicine, is the Wet Bulb Globe Temperature (WBGT). It is an environmental heat stress index used to evaluate the risk of heat of heat-related illness on an individual. It is calculated using 3 parameters: temperature, humidity, and radiant heat. There is low risk if the WBGT is < 65ºF, moderate risk if it is between 65-73ºF, high risk if between 73-82ºF, and very high risk if >82ºF.

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Epidemiology

Frequency

United States

In the United States, heat waves claim more lives each year than all other weather-related exposures combined (hurricanes, tornadoes, floods, and earthquakes).[1] According to the Centers for Disease Control and Prevention, 8,015 deaths were attributed to excessive heat exposure from 1979-2003, or an average of approximately 334 deaths per year.[2]

Heatstroke and deaths from excessive heat exposure are more common during summers with prolonged heat waves. For example, during the heat wave of 1980 (a record year for heat), 1700 deaths were attributed to heat, compared to only 148 deaths attributed to heat the previous year. Persons older than 65 years accounted for at least 44% of cases. The numbers published by the NCHS are believed to grossly underestimate the true incidence of heat-related deaths because death rates from other causes (eg, cardiovascular disease, respiratory disease) also increase during the summer, and especially during heat waves.

International

Heatstroke is uncommon in subtropical climates. The condition is recognized increasingly in countries that experience heat waves rarely (eg, Japan), and it commonly affects people who undertake a pilgrimage to Mecca, especially pilgrims who come from a cold environment. In 1998, one of the worst heat waves to strike India in 50 years resulted in more than 2600 deaths in 10 weeks. Unofficial reports described the number of deaths as almost double that figure.

Racial and sexual disparities in incidence

With the same risk factors and under the same environmental conditions, heatstroke affects all races equally. However, because of differences in social advantages, the annual death rate due to environmental conditions is more than 3 times higher in blacks than in whites.

With the same risk factors and under the same environmental conditions, heatstroke affects both genders equally. However, because of gender differences in the workforce, the annual death rate due to environmental conditions is 2 times higher in men than in women.

Age-related disparities in incidence

Infants, children, and elderly persons have a higher incidence of heatstroke than young, healthy adults. Infants and children are at risk for heat illness due to inefficient sweating, a higher metabolic rate, and their inability to care for themselves and control their environment.

Elderly persons also are at increased risk for heat-related illnesses because of their limited cardiovascular reserves, preexisting illness, and use of many medications that may affect their volume status or sweating ability. In addition, elderly people who are unable to care for themselves are at increased risk for heatstroke, presumably because of their inability to control their environment.

Exertional heat stroke (EHS) is a leading cause of injury and death in high school athletes; approximately two-thirds of such cases occur in August and involve football players, often those who are obese or overweight.[3] Lack of acclimatization is a major risk factor for EHS in young adults.

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Prognosis

Indicators of poor prognosis during acute episodes include the following:

  • Initial temperature measurement higher than 41°C (106°F) or a temperature higher than 42°C (108°F) or a temperature persisting above 39°C (102°F) despite aggressive cooling measures
  • Coma duration longer than 2 hours
  • Severe pulmonary edema
  • Delayed or prolonged hypotension
  • Lactic acidosis in patients with classic heatstroke
  • Acute kidney injury and hyperkalemia
  • Aminotransferase levels greater than 1000 IU/L during the first 24 hours

Morbidity and mortality from heatstroke are related to the duration of the temperature elevation. When therapy is delayed, the mortality rate may be as high as 80%; however, with early diagnosis and immediate cooling, the mortality rate can be reduced to 10%. Mortality is highest among the elderly population, patients with preexisting disease, those confined to a bed, and those who are socially isolated. 

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Patient Education

Education is the single most important tool for the prevention of heatstroke. The media, public education, public health programs, and athlete safety programs can play a pivotal role in increasing the public's awareness of the dangers of heat during heat waves and advising the public on methods of remaining cool.

Similarly, drinking fluids on schedule (and not based only on thirst), frequent cooling breaks, and frequent visits to air-conditioned places are very important because even short stays in an air-conditioned environment may drastically reduce the incidence of heatstroke.

Recognition of host risk factors and modification of behavior (eg, limiting alcohol and drug intake and the use of medications and drugs that interfere with heat dissipation) and physical activity also will prevent heatstroke.

For patient education information, see the First Aid and Injuries Center and Healthy Living Center, as well as Heat Exhaustion and Heat Stroke and Heat Cramps.

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Contributor Information and Disclosures
Author

Robert S Helman, MD Director, Premier Care of Great Neck Urgent Care Center

Disclosure: Nothing to disclose.

Coauthor(s)

Rania Habal, MD Assistant Professor, Department of Emergency Medicine, New York Medical College

Rania Habal, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Laurie Robin Grier, MD Medical Director of MICU, Professor of Medicine, Emergency Medicine, Anesthesiology and Obstetrics/Gynecology, Fellowship Director for Critical Care Medicine, Section of Pulmonary and Critical Care Medicine, Louisiana State University Health Science Center at Shreveport

Laurie Robin Grier, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Society for Parenteral and Enteral Nutrition, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

References
  1. Centers for Disease Control and Prevention. Climate Effects on Health. Available at http://www.cdc.gov/climateandhealth/effects/default.htm. April 18, 2016; Accessed: July 6, 2016.

  2. Centers for Disease Control and Prevention. Extreme Heat: A Prevention Guide to Promote Your Personal Health and Safety. Available at http://emergency.cdc.gov/disasters/extremeheat/heat_guide.asp. September 22, 2015; Accessed: July 6, 2016.

  3. Heat illness among high school athletes --- United States, 2005-2009. MMWR Morb Mortal Wkly Rep. 2010 Aug 20. 59(32):1009-13. [Medline]. [Full Text].

  4. National Center for Catastrophic Injury Research. Catastrophic sport injury 32nd annual report. University of North Carolina. Available at https://nccsir.unc.edu/files/2013/10/NCCSIR-32nd-Annual-All-Sport-Report-1982_2014.pdf. November 13, 2015; Accessed: July 6, 2016.

  5. [Guideline] American College of Sports Medicine Joint Statement. National Athletic Trainers' Association. Inter-Association Task Force on Exertional Heat Illnesses Consensus Statement. 2003. Available at http://www.nata.org/sites/default/files/inter-association-task-force-exertional-heat-illness.pdf. Accessed: August 13, 2010.

  6. Mazerolle SM, Pinkus DE, Casa DJ, et al. Evidence-based medicine and the recognition and treatment of exertional heat stroke, part II: a perspective from the clinical athletic trainer. J Athl Train. 2011 Sep-Oct. 46(5):533-42. [Medline]. [Full Text].

  7. Mazerolle SM, Ganio MS, Casa DJ, Vingren J, Klau J. Is oral temperature an accurate measurement of deep body temperature? A systematic review. J Athl Train. 2011 Sep-Oct. 46(5):566-73. [Medline]. [Full Text].

  8. Heled Y, Rav-Acha M, Shani Y, Epstein Y, Moran DS. The "golden hour" for heatstroke treatment. Mil Med. 2004 Mar. 169(3):184-6. [Medline].

  9. Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Critical Care 2007. May 12, 2007. 11 (issue 3):1-17. [Full Text].

  10. [Guideline] Lipman GS, Eifling KP, Ellis MA, Gaudio FG, Otten EM, Grissom CK. Wilderness Medical Society practice guidelines for the prevention and treatment of heat-related illness. Wilderness Environ Med. 2013 Dec. 24(4):351-61. [Medline].

  11. Bongers CC, Thijssen DH, Veltmeijer MT, Hopman MT, Eijsvogels TM. Precooling and percooling (cooling during exercise) both improve performance in the heat: a meta-analytical review. Br J Sports Med. 2015 Mar. 49 (6):377-84. [Medline]. [Full Text].

  12. Tyler CJ, Sunderland C, Cheung SS. The effect of cooling prior to and during exercise on exercise performance and capacity in the heat: a meta-analysis. Br J Sports Med. 2015 Jan. 49 (1):7-13. [Medline].

  13. Sunderland C, Stevens R, Everson B, Tyler CJ. Neck-cooling improves repeated sprint performance in the heat. Front Physiol. 2015. 6:314. [Medline]. [Full Text].

 
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