Background/Epidemiology
Much like sudden cardiac death, exertional heat illness receives a great deal of public attention. High profile cases of heat-associated death have occurred at the high school, collegiate, and professional level. It also remains a major concern of U.S. military forces in basic training and during training and operations, domestically and overseas.1, 2
Exertional heat stroke (EHS) is currently the third leading cause of death in athletes, behind sudden cardiac death and head/cervical spine trauma.2, 3
For reasons not yet understood, under identical environmental conditions some athletes go on to develop exertional heat illness while others do not.
Many cases of exertional heat illness occur without the presence of a medical professional.
Lack of knowledge on heat illness prevention, recognition, and treatment by athletes and coaches puts athletes at unnecessary risk.
Efforts should focus on prevention in order to reduce the morbidity and mortality associated with exertional heat illness. Athletes and coaches should be educated on proper acclimatization, equipment, and fluid replacement strategies. When practicing/playing in challenging environmental conditions, athletes, coaches, and medical staff must monitor closely for early signs of heat illness.
True incidence of exertional heat illness remains unknown.
There is no large, systematic database that tracks prevalence of exertional heat illness during athletic activities. Smaller studies tend to focus on specific groups and settings (high school athletes, military recruits, popular road races, etc.). While deaths are often reported to the press, nonfatal exertional heat illness is usually not reported to the press unless it is a high profile athlete.
Cases are often misdiagnosed, and terminology such as EHS and exertional heat exhaustion are often used without a uniform case definition.
Exertional heat exhaustion is the most common heat-related disorder in active populations.3
Prevalence of EHS in sport, military, and industrial populations seems to be on the increase, with a greater number of reported deaths being reported in the past several years.4
While reports vary, between 400 and 800 deaths may be attributed to all types of heat-related illness in the U.S. annually. 1, 5
Highest rates of death are among elderly adults and those with comorbid disease. Among teenage athletes, heat illness is the third leading cause of death, behind trauma and cardiac causes of death.6
Over 9,000 high school athletes are treated for exertional heat illness annually, occurring at a rate of 1.2 per 100,000 athlete exposures:7
Among American high school students, exertional heat illness rates in football (4.42 per 100,000 athlete exposures) is over ten times greater than all other sports combined.
Over one-half (60.3 percent) of high school cases occur in August. Of those cases reported during practice, one-third occur over two hours into practice.
Heat illness occurs worldwide with prolonged activity in almost any intensely physical sport.
EHS and exertional heat exhaustion occur most frequently in hot and humid conditions, but may occur in cool conditions with prolonged activity:3, 7
Fatal EHS occurs in American football most frequently during the first days of preseason conditioning (1 in 350,000), when high temperatures and high humidity are present.
High overall incidence of EHS is seen during road races and other activities involving continuous exercise.
Studies of exertional heat exhaustion among religious pilgrims in desert conditions and soldiers in summer maneuvers show individuals affected at a rate of 4–13 per 10,000 individuals per day.
Fit competitors in a 14-K road race in mild temperatures, that is 52–68°F (11–20°C), are affected at 14 per 100,000 individuals per day, presumably demonstrating the effect of high-intensity exercise in lower heat.
Competitors in a multi-day youth soccer tournament in hot weather are affected by heat exhaustion at 85 per 10,000 individuals per day, with a sharp increase on the second day, presumably due to cumulative effects of heat exposure.
Pathophysiology
The human body eliminates excess heat through four basic mechanisms: convection, conduction, radiation, and evaporation.
Environmental, physiologic, and equipment factors all may play a role in impairing those mechanisms.
Convection is minimized in still air and when overlying clothing and equipment prevent moving air from contacting the skin.
Air is an insulator and conduction provides only minimal heat loss. An exception is when the individual is submerged in cold water. Conduction then becomes the most effective means of heat loss, an important concept in the treatment of heat illness.
Radiation is ineffective when the environmental temperature exceeds skin temperature, and may also be impeded by overlying equipment and clothing.
Evaporation of sweat from the skin surface becomes less efficient as humidity increases. In addition, medications and dehydration may impair the body’s sweating mechanism, rendering evaporation ineffective as a heat-loss method.
The common element to exertional heat illness is the effect of heat stress on the exercising individual.
Heat stress is cumulative. Presence of any heat illness indicates presence of heat stress and should be taken seriously, with the individual closely monitored.
Heat illness is often looked at as a continuum from mild (heat edema, heat rash, heat cramps, heat syncope) to severe (heat exhaustion, heat stroke). There is no evidence that mild illness will progress to severe disease if untreated. However, heat exhaustion left untreated may lead to development of heat stroke.1
Heat stroke may occur in athletes exercising in hot conditions without any prodromal signs of dehydration or heat exhaustion.
In general, inability to continue exercise (exhaustion) occurs due to a combination of hyperthermia-induced central and peripheral reduction of muscle activation, diminished hydration, electrolyte imbalance, and energy depletion.3, 4
In hot conditions this is more pronounced due to rapid depletion of energy stores.
Variables affecting the individual athlete include duration/intensity of exercise, environmental conditions, acclimatization, VO2 max, conditioning, hydration status, medications, sleep, and recent illness.
Combined effects of heat stress and dehydration reduce exercise performance greater than either alone.
The removal of body heat is controlled by the central nervous system (CNS) centers in the hypothalamus and spinal cord and by peripheral centers in skin and organs.
Exertional hyperthermia with a core temperature above 104°F (40°C) occurs during physical exertion when muscle-generated heat accumulates faster than heat dissipation via sweating and skin blood flow.
Heat tolerance and risk for exertional heat illness is affected by exercise intensity, environmental conditions, clothing, equipment, and individual host factors.8 (See Table 13.1)
Wide variations of heat tolerance exist among individuals. Some athletes tolerate prolonged hyperthermia well above 104°F (40°C) and show no signs of heat illness.
Dehydration occurs more rapidly in hot environments where sweat loss occurs faster than fluid intake. Fluid deficits as little as 3–5 percent of body weight result in diminished sweat production and declining skin blood flow with resultant impaired heat dissipation.
Excessive sweating results in salt loss which may result in muscle cramps. Prolonged endurance events in the heat may also lead to hypovolemic hyponatremia.
Elevated core temperatures and dehydration both diminish compensatory splanchnic and skin vasoconstriction. This results in reduced total vascular resistance, decreased removal of heat from exercising muscle, and increased cardiac insufficiency.
Acclimatization:9
Defined by a marked improvement in physiologic response of healthy humans to exercise in heat.
Effects of acclimatization demonstrated by reduction in occurrence and severity of heat illness, and increased work output concurrent with reduced cardiovascular, thermal, and metabolic strain.
Both passive exposure to hot conditions and intensive exercise in cool conditions aid with acclimatization, but the most effective means of acclimatization is exercise in a hot environment.
Physiologic adaptations include:
Sweating begins at lower core temperature.
Increased skin blood flow facilitates heat dissipation to environment.
Increased plasma volume facilitates heat removal from core.
Diminished excretion of NaCl in sweat and urine produces expanded extracellular fluid volume.
Improved exercise economy and diminished heart rate decrease overall cardiovascular strain.
Complete acclimatization takes up to fourteen days. Increased fluid and electrolyte intake do not enhance speed of acclimatization, but dehydration may result in delay.
Host factors may influence acclimatization capacity:
When matched for pertinent physical and morphological characteristics, males and females show little difference in acclimatization capacity.
Heat intolerance in older individuals is most likely due to diminished training intensity and reduced aerobic output as opposed to the aging process itself.
Adaptations to exercise in the heat disappear after eighteen to twenty-eight days of inactivity. Cardiovascular adaptations are the first to diminish.
Pediatric considerations
Anatomic and physiologic differences between children and adults affect response to heat.
These differences alone do not appear to put children at higher risk for heat illness.
Children produce greater metabolic heat per kilogram than adults due to higher basal metabolic rate.
Young children have a greater surface area to mass ratio, allowing greater environmental heat absorption.
In older children and adolescents, increased body fat and diminished fitness levels increase risk of heat illness.
Children have lower cardiac output and absolute blood volume than adults, impeding transfer of heat from core to body surface during physical activity.
Children begin sweating at higher body temperature than adults.
Children have lower sweat rates per gland than adults.
Children tend to acclimatize to a hot environment more slowly than adults.
Children are less likely to replenish fluid losses following exercise.
Classic heat stroke (as opposed to EHS) is more common in younger children unable to escape from a hot environment (for example, a locked automobile) or having chronic underlying medical conditions that impair thermoregulation.11
| Weather conditions | High ambient temperatures, relative humidity, and solar load all decrease time to development of heat stress and increase risk of illness |
| Lack of acclimatization | Individual acclimatization up to 14 days reduces heat illness risk; benefit is lost following 18–28 days inactivity |
| Exercise duration/Intensity | Prolonged or intense activity without adequate recovery creates immediate and cumulative heat stress |
| Dehydration | Reduced volume creates reduced removal of heat from the core and reduced heat loss via evaporation from the skin |
| Overweight/Obese/Sedentary | Diminished VO2 max and excess body fat have both been linked to risk of exertional heat stroke. Excess body fat may also exacerbate the heat-retaining effects of athletic clothing/protective equipment |
| Sleep loss | Linked to risk of exertional heat stroke and death, exact etiology currently unknown |
| Recent illness | Fever, gastroenteritis, diarrhea, and vomiting all impair heat dissipation and increase heat stress |
| Medications | Prescription medications, over-the-counter medications, and supplements may increase risk of heat illness by reducing sweating, diminishing blood flow to skin, and increasing heat production |
Focused History and Physical Exam
Priority in any individual experiencing exertional heat illness is assessment of circulatory status, airway/breathing, and evidence of neurologic disability.
Neurologic disability in early EHS may be subtle. Confusion, disorientation, and personality changes may precede more pronounced findings such as delirium, seizure or coma.3, 4
Core temperature in suspected exertional heat illness must be accurately measured. This generally means a rectal temperature in the field, and a rectal or esophageal temperature in the emergency department.
Tympanic and temporal thermometers are not sufficiently accurate at temperature extremes to be used in suspected exertional heat illness. 12
Elevation in core temperature in the digestive tract measured by swallowed monitors have correlated with core temperature elevations and risk of exertional heat illness.13
In cases of suspected associated trauma (such as a fall from a height or significant collision with another athlete) initiate cervical spine precautions.
Differential Diagnosis – Emergent and Common Diagnoses
Table 13.2 Emergent and Common Diagnoses in the Emergency Department
| Emergent Diagnoses | Common Diagnoses |
|---|---|
| Heat stroke | Heat Cramps |
| Heat exhaustion | Heat Syncope |
| Exertional hyponatremia |
Exertional Heat Stroke
General Description
Characterized by hyperthermia (core temperature of more than 104°F (40°C), CNS disturbances and (if untreated) multiple organ failure.
When heat production outpaces heat loss, core temperature rises to levels that ultimately cause end organ damage.
Most EHS patients present initially with profuse sweating, as opposed to the hot dry skin seen in classic heat stroke.
In cases of suspected heat illness where the core temperature is less than 104°F (40°C) but mental status is abnormal, consider EHS as some cooling may have occurred prior to assessment.14
Classic vs. exertional heat stroke:1, 15
In classic heat stroke, the environment plays a major role in an individual’s ability to dissipate heat. In EHS, intrinsic heat production is the major source.
Most cases of classic heat stroke are linked to heat waves. Elderly and other vulnerable individuals, often on medications that may impair thermoregulation, develop thermoregulatory dysfunction over time with resultant hyperthermia and end organ damage. EHS occurs in all types of weather.
Anhidrotic skin is a hallmark of classic heat stroke, whereas those with EHS demonstrate profuse sweating. Therefore, presence or absence of sweating has no role in the diagnosis of EHS.
Treatment for both conditions is identical: rapidly cool the individual as quickly as possible to minimize organ dysfunction.
Mechanism
When internal organ tissue temperature reaches critical threshold levels of 104°F (40°C) cell dysfunction occurs.
Temperatures above threshold levels impair cell volume, metabolism, and membrane permeability. Initial dysfunction may lead to cell death and organ failure.
Organ systems typically affected include brain, heart, kidneys, GI, muscle, and hematologic.
Degree of multisystem injury and death correlate directly to time spent subjected to elevated body temperature.16, 17, 18
Rapid cooling and return to normal range of body temperature within one hour allows full recovery in most cases of EHS.
Athletes with unrecognized EHS or delay in cooling have increased morbidity and mortality.
Athletes who present comatose and with evidence of multiorgan injury but are cooled in less than one hour do well.
The primary difference between mild and severe EHS appears to be the duration of time from collapse to cooling.18
Once organ dysfunction begins, without rapid cooling a life-threatening spiral begins.3
Cardiac hyperthermia reduces cardiac output, impairing oxygen delivery to tissues as well as vascular transport of heat from core to periphery. This accelerates hyperthermia and worsens tissue hypoxia.
CNS hyperthermia results in hypothalamic dysfunction, further impairing thermoregulation and circulatory maintenance.
Hyperthermia increases muscle membrane permeability, promoting rhabdomyolysis.
Both renal tissue hypothermia as well as impaired renal flow due to the earlier mentioned mechanisms may lead to renal failure and increased susceptibility to rhabdomyolysis.
Predisposing factors to development of EHS include:4, 19
Exercise in hot and humid environment. Greatest risk exists with wet bulb globe temperature (WBGT) exceeding 82°F (28°C), high-intensity exercise, especially when longer than one hour.
Lack of acclimatization.
Poor physical fitness.
EHS may occur in cool to moderate environments, suggesting significant individual variation in susceptibility.20, 21
Why people die from EHS:4
No treatment or delayed treatment: most often this is due to failure to recognize EHS. Having qualified medical personnel (physicians, athletic trainers) on site can mitigate this risk.
Ineffective cooling: cold water immersion is the gold standard of rapid cooling; however, access to this modality may be limited. Also, now-debunked concerns over creation of shivering or monitoring difficulties may result in use of less effective methods of cooling.
Immediate or delayed transport: if means exist to rapidly cool on-site, they should be utilized. Rapid transport either prior to cooling or interrupting cooling begun in the field may delay time to reduction of core temperature to safe levels. Delayed transport may lengthen time to treatment if no means of effective cooling are available/begun in the field.
Rapid return to activity: sufficient time must pass for an individual to fully recover from heat illness; otherwise, the patient may be at risk for recurrence of EHS.
Presentation
Rapid recognition of EHS is critical so that cooling may be initiated as soon as possible.
Appearance of signs and symptoms of EHS depends on the degree and duration of hyperthermia. Signs and symptoms may be nonspecific. They include:16, 22
Confusion, disorientation, unusual behaviors or inappropriate comments, changes in personality and increased irritability, headache, fatigue, nausea and vomiting, diarrhea, seizure, or frank coma. The patient may be stumbling, clumsy, or completely collapse.
Abnormal vital signs may include tachycardia, tachypnea, and hypotension.
Skin is often cool and sweaty.
Any change in personality or performance, especially in hot conditions, should prompt consideration of EHS.
Body core temperature estimate is critical in establishing the diagnosis.
Measure a rectal temperature in any athlete with suspected EHS.
Tympanic, oral, temporal, and axillary temperature measurements are susceptible to inaccuracy, especially at extremes of temperature, and should not be used.12
Ingested devices to measure gastrointestinal core temperature are useful, but only if they have been ingested prior to onset of heat illness.13
Physical Exam
Rapid initial assessment of circulatory status, airway and breathing, and neurological status.
Obtain vital signs, to include heart rate, respiratory rate, and blood pressure.
Obtain a rectal temperature.
Lay the individual on the side and pull down shorts to easily access the rectum.
Shielding for privacy is optimal but should not delay measurement.
Auscultate heart and check peripheral pulses to assess adequate perfusion.
Check mucous membranes and skin turgor for signs of dehydration.
Examine extremities for signs of edema, which may be present in overhydration.
Auscultate lungs for wheezes to ensure athlete has not collapsed secondary to asthma, allergy, or anaphylaxis.
Perform a focused neurological exam, being especially alert for subtle changes in CNS function. Some individuals may present with a deceptive “lucid interval.” In retrospect, subtle CNS changes (such as irritability or personality changes) are usually present.22
Essential Diagnostics
Initial recognition of EHS via careful assessment for subtle CNS dysfunction.
Rapidly obtaining a rectal or core temperature.
ED Treatment
Remember that the most critical element of treating EHS is rapid lowering of core temperature.
If not begun in the field or during transport, it should commence immediately upon ED arrival.
Cooling that has begun in the field should be continued in the ED in conjunction with assessment.
Goal is to bring the temperature down to 104°F (40°C) or less in under 30 minutes.
If cooling is started in the field via an effective modality such as cold water immersion, consideration should be given to delaying transport until the core temperature is between 102°F–104°F (38.9–40°C).
Assess circulatory status, airway, and breathing.
Recheck core temperature to guide therapy.
The patient should have vital signs monitored. However, repeat vital signs, cardiac monitoring, IV access, and so forth, should NOT interfere with cooling. The most important initial monitoring should be placement of a rectal temperature probe.
The gold standard for treatment is cold water/ice water immersion.4, 23, 24, 25 If a tub is available in the field or in the ED, it should be utilized. (See Table 13.3)
Immerse individual in cold 35–57°F (1.7–13.9°C) or ice water over as much of the body as possible.
Apply a wet towel around the head.
Water should be continually stirred to maintain contact of cold water on the skin surface.
This modality of cooling may bring the patient’s core temperature to under 104°F (40°C) in under 20 minutes.
If cold/ice water is not available, temperate water may be used, although it is a less effective modality.4
Peripheral vasoconstriction and shivering may be less with temperate water immersion.
Cold water immersion, however, cools more rapidly, and minimizes time of exposure to the cooling modality. Thus, heat production via shivering is limited.
If cold water immersion is not available in the field or ED, an alternative cooling modality is use of towels soaked in ice water.18
Maintain twice the number of towels needed to cover the patient.
Rotate towels used every several minutes to ensure cold towels are on the patient while the others are recooled.
Maintain this modality until a tub for immersion is available or core temperature goal has been achieved.
Combined with application of icepacks to the neck, axillae, and groin, this method provides a rapid method of cooling.
The use of warm air mist and fanning has been shown to be effective for rapid cooling of large numbers of individuals. This method relies heavily on evaporative cooling and is effective only when relative humidity is low.
Cooling should cease when rectal temperature reaches 102°F–104°F (38.9–40°C). Continued cooling may result in hypothermia.26
Even if the patient regains lucidity, continue cooling until rectal temperature is below 104°F (40°C). Observe to ensure maintenance of normal temperatures and mental status once recovered.
Replace intravascular volume losses with normal saline.
Fluid resuscitation improves renal blood flow and protects from rhabdomyolysis.
Optimized volume status improves tissue perfusion, enhancing heat exchange, oxygenation, and removal of waste products.
Patients who fail to respond to cooling should be checked for other potential life-threatening causes of collapse.
Check bedside glucose and treat for hypo- or hyperglycemia as indicated.
Obtain a 12-lead EKG.
Check serum electrolytes for hyper- or hyponatremia or hypokalemia. Check renal function for evidence of prerenal azotemia or kidney injury due to rhabdomyolysis.
Check serum creatine kinase (CK) levels. Urinalysis positive for blood on dipstick but negative for blood on microscopic may indicate myoglobinuria and subsequent risk of rhabdomyolysis.
Check coagulation studies including PT/INR and PTT, as EHS may cause a coagulopathy.
EHS patients with prolonged core temperature elevations and development of multiple organ failure require more extensive interventions.
Clinical markers of disseminated intravascular coagulopathy, multiple organ failure, and prolonged elevations of CK carry a poor prognosis.27
Do not allow testing to interfere with ongoing cooling efforts.
Table 13.3: Rapid Cooling of Patients with Exertional Heat Stroke: Good, Better, Best 1, 3, 4, 23, 24, 25
| GOOD | BETTER | BEST |
|---|---|---|
| Water Mist/Fan | Ice Water-Soaked Towels | Cold/Ice Water Immersion |
| Pros: Simple, requires minimal equipment (mist-sprayer and fan), can be applied in remote locations | Pros: Simple, effective, does not require lifting/immersion of patient, can be applied in remote locations | Pros: Most rapid means of cooling patient with suspected EHS |
| Cons: Slower cooling than immersion, most effective when relative humidity is low | Cons: Requires proper equipment on-hand (towels, ice water) | Cons: Requires access to tub and very cold/ice water, requires personnel to lift/place patient in water |
Disposition
In patients who have a rapid return of normal mental status and normalized core temperature, consideration may be given for discharge.
There are multiple reports of road race competitors with rectal temperatures above 107.6°F (42°C) and profound CNS dysfunction who, following rapid diagnosis and treatment with ice water cooling, are discharged home from the medical tent without hospitalization.22
Return-to-play decision making is a complex and sometimes controversial subject that is based on limited evidence.
Current guidelines vary widely; suggested return to play varies from seven days to fifteen months.3
Athletes who receive prompt cooling have an excellent prognosis for full recovery and return to play.
In some individuals, thermoregulation, exercise heat tolerance, and acclimatization ability may take months to return to normal following EHS.
In those who experience severe hepatic injury, full recovery may take over one year.
Decision making on RTP (return to play) requires input from physicians, athletic trainers, coaches, as well as the athlete.
American College of Sports Medicine has five recommendations for RTP following EHS:
Refrain from exercise at least seven days following release from medical care.
Follow-up in one week for physical exam and repeat testing of affected organs (based on the clinical course of illness).
Once cleared for RTP, begin exercise in a cool environment. Gradually increase duration, intensity, and heat exposure for two weeks to allow for acclimatization and demonstrated heat tolerance.
If return to activity has not been achieved in one month, consider a laboratory-based exercise heat tolerance test.28, 29, 30
No standard of care exists in the performance of HTT (heat tolerance test).
Classic walking HTT may not be appropriate for the elite athlete.
Tailor HTT protocol to duplicate the demands of the elite athlete.
If heat tolerance exists after two to four weeks of full training, the athlete may be cleared for full activity.
Pearls and Pitfalls
Duration of hyperthermia is linked to outcome: the sooner cooling is commenced, the lower the risk of morbidity and mortality.
Recognition of EHS is critical. Early signs may be subtle and include behavioral disturbances.
Core temperature should be measured with a rectal thermometer, or correlated to GI temperature via a swallowed monitor.
Cold water or ice water immersion is the gold standard of cooling in EHS and should not be delayed nor ceased for transportation until core temperature is below 104°F (40°C).
Proper acclimatization and education for athletes and coaches are essential.
Heat Exhaustion
General Description
May be the initial presentation of heat illness.
Inability to continue exercise; may occur with heavy exertion in all temperatures and may or may not be associated with physical collapse.
Often presents with complaints of malaise, dizziness, headache, and nausea.
Core temperature may be normal or elevated, but is below 104°F (40°C).
Unlike heat stroke, the athlete with heat exhaustion will have normal mentation and neurological exam.
Mechanism
Evidence suggests heat exhaustion results from central fatigue inducing peripheral vasodilation and subsequent collapse.
This central failure may be a mechanism of protecting the body against overexertion in hot/stressful environments.3, 9
Heat exhaustion related to dehydration is more common in hot and humid conditions.
Combination of tachycardia, high cardiac output, and lowered peripheral vascular resistance result in hypotension and cardiovascular insufficiency.
Blood volume pooling in skin impairs heat transport from core to surface. This is compounded by high humidity, where evaporative cooling is impaired, signaling the body to increase cutaneous blood flow to increase non-evaporative heat loss.
Predisposing factors for development of heat exhaustion include:1, 3, 19
Increased body mass index (>27 kg/m2).
Exertion during the hottest months of the year.
Inadequate fluid intake.
Increased air temperature (>91.4°F, 33°C) and diminished air velocity (<2.0 m/s).
Presentation
Signs and symptoms of heat exhaustion are nonspecific.1
Athletes may present with generalized weakness, headache, nausea and vomiting, diarrhea, dizziness, and irritability.
Acutely, athletes are tachycardic, tachypneic, and have low blood pressure.
Athletes may appear sweaty and pale and have cool and clammy skin.
Piloerection may be present.
Muscle cramping may accompany heat exhaustion.
Rectal temperature may be normal or elevated, but should be less than 40°C.
Physical Exam
Rapid initial assessment of circulatory status, airway and breathing, and neurological status.
Obtain vital signs, to include heart rate, respiratory rate, and blood pressure.
Obtain a rectal temperature.
Auscultate heart and check peripheral pulses to assess adequate perfusion.
Check mucous membranes and skin turgor for signs of dehydration.
Examine extremities for signs of edema, which may be present in overhydration.
Perform a focused neurological exam, being especially alert for changes in sensorium that may indicate more severe EHS.
Orthostatic vital signs add little to assessment, especially early in evaluation.
Essential Diagnostics
Obtaining a rectal temperature in the field may help discriminate between heat exhaustion and heat stroke. (See Table 13.4)
In heat exhaustion, rectal temperature is <104°F (40°C) whereas in EHS temperature is >104°F (40°C).
If a rectal temperature cannot be rapidly obtained, consider instituting rapid cooling for empiric treatment of EHS, particularly if there are signs of CNS dysfunction.
Altered sensorium should prompt pursuit of hyperthermia, hypoglycemia, hyponatremia, or other medical problem.
| Heat Exhaustion | Heat Stroke |
|---|---|
| Core temperature < 104°F (40°C) | Core temperature ≥ 104°F (40°C) |
| Significant dehydration | May not be significantly dehydrated |
| Unaltered sensorium and neurologic exam | CNS disturbances (confusion, disorientation, personality changes, irritability, seizure, coma) |
| Profuse sweating | Profuse sweating early; anhidrosis is a late finding in EHS |
ED Treatment
Treatment should begin in the field by moving the athlete out of the heat and into a shaded or air-conditioned area.
Remove athletic equipment and constrictive clothing.
Place athlete in supine position with legs elevated to improve central and cerebral blood flow.
The majority of athletes improve symptomatically with removal from hot environment, rest, and oral rehydration.
Continually monitor vital signs and neurologic status.
Recheck a rectal temperature following field treatment.
Should the athlete not improve with these measures, transport to an emergency facility.
Once in the emergency department, the same basic measures should be instituted as in the field:
Remove any equipment or constrictive clothes.
Keep athlete in a cool environment.
Monitor heart rate and blood pressure and check rectal temperature.
Do frequent neurological checks looking for CNS dysfunction.
Routine labs are unnecessary unless the physician suspects another cause of collapse or the athlete fails to respond to initial treatment.
A bedside blood glucose check may be useful to determine if hypoglycemia is present.
In athletes who are awake, alert, able to swallow well, and not severely nauseated or losing fluids rapidly through diarrhea or emesis, oral rehydration is preferred.1, 3, 9
As electrolyte losses may contribute to the patient’s symptoms, hypotonic fluids should be avoided for oral resuscitation.
Sport drinks, oral rehydration fluids, or Pedialyte are all reasonable options to facilitate rehydration.
If blood pressure, pulse, and temperature improve with treatment and there are no ongoing fluid losses (such as diarrhea) then IV fluids are not required.
If the athlete has ongoing abnormal vital signs, cannot tolerate oral rehydration, or has ongoing fluid losses, institute resuscitation with IV fluids.
IV fluids have been shown to enhance rapid recovery from heat exhaustion in those who cannot ingest oral fluids or have severe dehydration.
Normal saline is the most recommended resuscitation fluid for the dehydrated athlete.
Administer 1–4 liters. The end goal is improvement of vital signs and symptoms.
If the athlete is hypoglycemic, 5% dextrose in NS may be used.
Cooled fluids may be used initially for the moderately hyperthermic athlete, but be careful not to create hypothermia.
Routine IV rehydration on the sidelines of games is neither evidence based nor recommended.
If the collapsed athlete is not clearly clinically dehydrated or showing signs of overhydration, consider exertional hyponatremia.1
Worsening of mental status or failure to clinically improve should prompt a more detailed medical assessment.
Recheck rectal temperature, looking for hyper- or hypothermia.
Obtain serum electrolytes, looking for hyper- or hyponatremia and hypoglycemia.
Obtain 12-lead EKG in cases of suspected electrolyte abnormalities, dysrhythmias, ACS, or in the collapsed athlete with ongoing hemodynamic instability.
Disposition
As noted, most athletes with heat exhaustion quickly recover with treatment on site or in the emergency department.
Once clinically stable, they may be discharged home with instructions for continued rest and rehydration.
Urine color can be a useful gauge for hydration status.
Advise maintenance of pale yellow to clear urine for the next forty-eight hours, prior to resumption of activity.
If asymptomatic and hydrated after twenty-four to forty-eight hours, the athlete may resume activity with caution.30
Immediate return to activity is not advised.
Even with rest and cooling, athletes should not return to full exercise capacity the same day.
More severe cases of heat exhaustion (delayed recovery, severe symptoms) should follow-up with a physician or athletic trainer prior to resumption of activity.
Athletes who remain severely symptomatic in the ED (ongoing nausea, vomiting, diarrhea, or abnormal vital signs) should be brought into the hospital for continued IV therapy and monitoring.
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