Heat Related Illness: How to Cool ‘Em and What to Do After

Author: Linda Sanders, MD (EM Resident Physician, Temple University Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Stephen Alerhand, MD (@SAlerhand)

Heat related illnesses comprise a spectrum of diseases ranging from heat cramps, heat edema, and heat syncope to heat exhaustion and the potentially lethal heat stroke.


Data averaged over recent years suggests that there are approximately 650 deaths from heat stroke annually.1 However, extreme temperatures such as during the heat wave of 2003 in Europe have claimed the lives of 70,000 individuals, of which over 50% were found deceased in their own homes.2 The mortality of heat stroke is 10% but may reach 30% if hypotension is present.3,4

Mechanisms of Thermoregulation

Body heat is both gained by the environment and produced by metabolic activity. Thermoregulation is managed by heat receptors on the skin and central receptors in the hypothalamus.5,6 When hyperthermia occurs, the hypothalamus can stimulate the diversion of cardiac output to the periphery via vasodilation for heat dissipation. Flow to the skin can increase from 0.5 L per minute to as much as 8 L per minute.7

Heat dissipation requires a gradient between the core body temperature and the skin. When there is high environmental heat and humidity, this mechanism of heat loss is reduced. Additionally, in conditions of increased heat production due to exertion, heat generation may outpace heat transfer.5,6

woman in heat


Heat transfer can occur by conduction, radiation, convection, and evaporation. Conduction is the transfer of heat by direct contact from the skin to the surrounding environment. Radiation is the transfer of heat by electromagnetic waves given off by an object. Convection works by moving gas or liquid over an object, absorbing its heat. The human body’s most effective method of heat loss is by evaporation which occurs via sweating.5,6,8 Each 1.7 mL of water that is vaporized to a gas consumes 1 kcal of heat.8 The heat index is a measure of the contribution of high temperature and high humidity in reducing the body’s ability to cool itself.5 Again, evaporation is most effective in a dry environment.

Heat Edema, Heat Cramps, and Heat Syncope

The more mild heat illnesses include heat edema, heat cramps and heat syncope.

Heat edema is lower extremity swelling that occurs secondary to compensatory vasodilation resulting in elevated hydrostatic pressures and vascular leak. It is managed with lower extremity elevation, compression devices, and removal of heat exposure. Diuretics are ineffective and may cause worsening dehydration and heat stress.5

Heat cramps are involuntary skeletal muscle contractions usually occurring in the calves. These are associated with electrolyte-poor hydration and are treated with oral salt replacement with a 0.1-0.2% saline solution made by adding ½ teaspoon of table salt to a quart of water.5
When syncope occurs in an individual with significant heat exposure, a broad differential diagnosis for syncope should be considered. This typically occurs in an individual that has had prolonged standing and has had a significant heat exposure. Peripheral vasodilation, orthostatic blood pooling, and low blood volume secondary to dehydration are typically the contributing factors to this process, especially with comorbidities such as cardiovascular disease and advanced age.5 Management includes simple measures including laying the patient flat and providing oral hydration. 5 Any patient with repeat syncopal episodes or prolonged loss of consciousness should be evacuated and evaluated for other causes of syncope.9

Heat Exhaustion versus Heat Stroke

Heat exhaustion is defined as a constellation of symptoms associated with a core body temperature of 37 to 40°C. Symptoms may include intense thirst, anxiety, dizziness, weakness, and syncope.5,9 As opposed to heat exhaustion, the defining feature of Heat Stroke is encephalopathy. Heat Stroke is defined as a temperature of greater than 40°C with associated encephalopathy that may present as ataxia, delirium, seizures or coma.5,6,10 It is recommended to treat empirically rather than confirming a temperature in a case of suspected heat stroke.5

There are two types of heat stroke, classic and exertional heat stroke. Classic heat stroke results from exposure to high environmental temperatures, usually in an elderly individual. These individuals typically have hot dry skin. Exertional heat stroke is a result from elevated core body temperatures as a result of strenuous activity and is more likely to present as a young person with profuse sweating.5,6


Cells respond to heat by producing protective heat-shock proteins. These heat-shock proteins likely function as molecular chaperones, preventing denaturation and may also act as central regulators of the baroreceptor response. There may be a critical temperature at which heat shock proteins are altered, resulting increased sensitivity of the cells to heat injury and denaturation of enzymes.5,6

Heat stress also causes an acute phase reaction resulting in the release of interleukins, cytokines, inflammatory markers, and coagulation responses. This cascade causes a type of distributive shock similar to that seen in sepsis.

Diversion of blood flow from the splanchnic circulation also leads to gastrointestinal ischemia. Gastrointestinal hypoperfusion leads to mucosal permeability and the release of endotoxins into the circulation, further promoting this shock state.6 Further, hyperthermia itself promotes a thrombotic state with activation of procoagulants and causes direct injury to the microvasculature, thus enhancing vascular permeability. This process, along with the shock response, can also lead to DIC.6

Risk Factors

Conditions that limit heat loss pose a particular risk for heat stroke. These include burns and skin diseases such as scleroderma.6,9 Cardiovascular and endocrine conditions reduce cardiac output needed to dissipate heat.5,6,11 Psychiatric illness in particular have been associated with heat stroke—this may be secondary to medication side effects and behavioral characteristics in this population.11

Medications which pose an increased risk for heat stroke include alcohol, amphetamines, alpha adrenergics, antipsychotics, anticholinergics, antihistamines, benzodiazepines, calcium channel blockers, beta blockers, clopidogrel, diuretics, thyroid agonists, and tricyclic antidepressants.6 In one study, almost 20% of nonfatal heat stroke cases involved patients on cardiovascular medications.12

The elderly and very young are likely the most vulnerable populations, as risk factors associated with heat related deaths including being confined to bed, not leaving home daily, and being unable to care for oneself.10


With regards to prevention, access to working home air conditioning and increased social contact are protective factors.10 Other helpful behavioral modifications include exercising during cool times of the day, wearing loose fitting clothing, and maintaining adequate hydration.5 Ineffective methods of prevention include hyper-hydration and pre-cooling.5 Instead, it is recommended to “drink to thirst” with a goal of clear urine and to consume salt-containing foods or water if heat exposure exceeds 3 hours.9

Acclimatization via continuous exposure for one to two hours a day over the course of two weeks is recommended and associated with decreased core temperature and heart rates during heat exposure.13,14 This process involves activation of the renin-angiotensin-aldosterone axis, increased sweat and cardiovascular activity via catecholamine release, and salt conservation by the kidneys and sweat glands resulting in expansion of intravascular volume.

Presentation and Diagnostics

As discussed previously, the clinical presentation of Exertional and Classic Heat stroke are similar. A rectal temperature is the gold standard for monitoring core temperature, though environmental conditions and hygienic concerns may limit its use in certain circumstances. All patients have tachycardia and tachypnea.

Because heat stroke is associated with multisystem organ dysfunction, shock, and potentially death, labs should be obtained to assess for renal dysfunction, rhabdomyolysis, myocardial injury, hepatocellular injury, ARDS, and coagulation abnormalities such as thrombocytopenia and DIC. Exertional heat stroke is associated with a lactic acidosis and will likely have a compensatory respiratory alkalosis. 5,6,8,12

Pre-hospital Management

The initial management of heat stroke involves removal from the heat source and removing any tight fitting clothing that may reduce evaporative cooling. This can be accomplished by placing the individual on a sleeping mat to decrease conductive heat transfer between them and the ground. Unfortunately, this is less effective if the ambient temperature is over 20°C (68°F).5

Active cooling via Cold Water Immersion (CWI) is now the standard of care and should be done immediately. This is a Grade IA recommendation.5 The patient should be immersed in ice water 1 to 3°C. There is no data to support a specific endpoint but general recommendations are to stop cooling at a rectal temperature of 38.5-39°C as there has been no morbidity reported.5,6 Cold water immersion has been compared to evaporative cooling in one RCT and has been found to cut cooling times in half compared to evaporative cooling although there is questionable mortality benefit.10,15,16 Of note, CWI was less effective in classic heat stroke than exertional heat stroke, perhaps secondary to this population’s comorbidities. Some have argued that CWI causes a shivering response that increases core body temperature, but this argument has been refuted.17 Natural bodies of water may be effective for CWI.5



If CWI is not available, evaporative cooling is another option. It can be accomplished by wetting the individual with tepid water and then fanning. Evaporative cooling is also an effective method and can be accomplished by removing clothing then spraying or dousing the patient with water and fanning the individual.5,6,10 Ice packs application to groin, neck, and axillae where large vessels are present is less effective than immersion or evaporative cooling.20 Chemical cold packs applied to glabrous areas such as the palms, soles, and face which contain retia venosa may be effective pre-hospital methods as well.18


evaporative cooling

Regardless of method, the time to cooling is particularly important and thus should begin emergently in the field.19 Shorter cooling times have an association with lower mortality.10 These patients must be evacuated.9

Fluid management

Fluid management and electrolyte balance in heat stroke is a complex system. In an effort to increase circulating plasma volume, vasopressin can cause free water retention out of proportion to sodium, resulting in hyponatremia. Similarly, aldosterone stimulation for water retention may also lead to potassium wasting.6 Regardless, hypo-hydration reduces sweat rates and thus oral or IV hydration should be initiated.5,6,9 There is little data to support the type or amount of fluid but 1-2 L of NS is generally recommended.5 In cases of altered mental status in a heat exposed individual without hyperthermia, hyponatremia is an important differential diagnosis and the patient may require 3% saline.

Hospital Management

In-hospital management should include continued cooling and IV hydration. Cooling may occur via CWI, or evaporative cooling if invasive monitoring is required and logistically difficult with CWI. Cold intravenous fluids at 4°C decrease temperature 2-fold compared to room temperature. There is no data to support invasive body cavity lavage as a cooling method.5,21,22

Those with significant encephalopathy may require intubation and mechanical ventilation. Patients with hypotension may require central access, vasopressors, and foley catheters to monitor urine output. However, there is no support for a specific pressor or fluid type.5,6,23,24 An ICU admission is warranted for these patients.

Pharmacologic interventions such as antipyretics and dantrolene are ineffective. Dantrolene acts by inhibiting calcium release from the sarcoplasmic reticulum in skeletal muscle and thereby reducing muscle rigidity, but has not been shown to reduce cooling time.23

Heat Stroke in Children

Children are at increased risk for heat stroke. They have a greater surface area to mass ratio and thus absorb more heat from radiation; have a higher metabolic rate; with a lower circulating blood volume and inadequate sweat production due to less sensitive, smaller sweat glands.6

They present with dehydration, poor peripheral circulation, and impaired consciousness. The major risk factor in these cases is severe chronic disease such as MR due to difficulty feeding and the failure to realize extra fluid needs.25 Fluid losses in children with heat stroke have been found to be double those of adults. It is suggested to dilute all milk feedings and keep the child in a cool place. Treatment otherwise remains similar – cold water immersion is still the recommended treatment but evaporative cooling may be more comfortable in small children.25


References / Further Reading
  1. Minino AM, Murphy SL, Xu J, Kochanek KD. Deaths: final data for 2008; Natl Vital Stat Rep. 2011; 59:1-126.
  2. Robine JM. The excess mortality in summer 2003: results of the Canicule Project. Paper presented at: the World Health Organization Meeting, Regional Office for Europe: Public Health Responses to Extreme Weather Events—euroHEAT; March 22-23, 2007; Bonn, Germany.
  3. Overgaard J, Suit HD. Time-temperature relationship in hypothermic treatment of malignant and normal tissue in vivo. Cancer Res. 1970; 39: 3248-3253.
  4. Austin MG, Berry JW. Observations on one hundred cases of heatstroke. J Am Med Assoc 1956, 161: 1525-1529.
  5. Lipman GS, Eifling KP, Ellis MA, Gaudio FG, Otten EM, and Grissom CK. Wilderness Medical Society practice guidelines for the prevention and treatment of heat-related illness: 2014 update. Wild Environ Med 2014;25:S55-S65.
  6. Bouchama A, Knochel JP. Heat Stroke. N Engl J Med 2002; 346(25): 1978-1988.
  7. Rowell LB. Human cardiovascular adjustments to exercise and thermal stress. Phsyiol Rev 1974; 54(1): 75-159.
  8. Hadad E, Rav-Acha M, Heled Y, Epstein Y and Moran DS. Heat Stroke: A review of cooling methods. Sports Med 2004; 34(8): 501-511.
  9. Della-Giustina D, Ingebretson R. Advanced Wilderness Life Support. Edition 8.0 AdventureMed 2013: University of Utah.
  10. Bouchama, A et al. Prognostic factors in heat wave-related illness: a meta-analysis. Arch Intern Med 2007; 167(20): 2170-2176
  11. Obrien KK, Leon LR, Kenefick RW. Clinical management of heat-related illnesses. In: Auerbach P, ed. Wilderness Medicine. 6th ed. St. Louis, MO: Mosby, Inc; 2012 232-238
  12. Noe R.S et al. Exertional heat-related illnesses at the grand canyon national park, 2004-2009. Wilderness & Environmental Medicine 2013; 24: 422-428
  13. Gill N, Phed B, and Sleivert G. Effect of daily versus intermittent exposure on heat acclimation. Aviat Space Environ Med 2000; 71:385-390.
  14. Cheung SS, McLellan TM. Heat acclimation, aerobic fitness, and hydration effects on tolerance during uncompensable heat stress. J Appl Physiol. 1998;84:1731-1739.
  15. Armstrong LE, Cargo AE, Adams R, Roberts WO, Maresh CM. Whole-body cooling of hyperthermic runners: comparison of two field therapies. Am J Emerg Med 1996; 14: 355-358.
  16. Bouchama A, Dehbi M, and Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Critical Care 2007; 11: R54.
  17. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev 2007;35:141-149.
  18. Lissoway JB, Lipman GS, Grahn DA, Cao VH, Shaheen M, Phan S, Weiss EA, and Heller HC. Novel application of chemical cold packs for treatment of exercise induced hyperthermia: a randomized controlled trial. Wild Environ Med 2015; 26:173-179.
  19. Heled Y, Rav-Acha M, Shani Y, Epstein Y, Moran DS. The golden hour for heatstroke treatment. Mil Med 2004;169(3). 184-6.
  20. Keilblock AJ, Van Rensburg JP, Franz RM. Body cooling as a method for reducing hyperthermia: an evaluation of techniques. S Afr Med J 1986 Mar 15; 69(6):378-380.
  21. White JD, Kamath R, Nucci R, et al. Evaporation versus iced peritoneal lavage treatment of heatstroke: comparative efficacy in a canine model. Am J Emerg Med 1993; 11(1):1-3.
  22. White JD, Riccobene E, Nucci R, et al. Evaporation versus iced gastric lavage treatment of heatstroke: comparative efficacy in a canine model. Crit Care Med 1987; 15(8):748-750.
  23. Bouchama A, Cafege A, Devol EB et al. Ineffectiveness of dantrolene sodium in the treatment of heatstroke. Crit Care Med 1991’ 19(2): 176-180.
  24. Dahmash NS, Al-Harthi SS, Akhtar J. Invasive evaluation of patients with heat stroke. Chest 1993; 103:1210-1214.
  25. Odonell TF Jr, Clowes GH Jr. The circulatory abnormalities of heat stroke. N Engl J Med 1972; 287:734-737
  26. Danks DM, Webb DW, and Allen J. Excerpts from: Heat Illness in Infants and Young Children: a study of 47 cases. Wilderness and Environmental Medicine 2004; 15: 293-300.
  27. Grubenhoff JA, du Ford K, Roosevelt GE. Heat-related illness. Clin Ped Emerg Med 2007;8:59-64.
  28. http://www.ncbi.nlm.nih.gov/pubmed/24176481

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