Simple, requires minimal equipment (mist-sprayer and fan), can be applied in remote locations
Simple, effective, does not require lifting/immersion of patient, can be applied in remote locations
Most rapid means of cooling patient with suspected EHS
Slower cooling than immersion, most effective when relative humidity is low
Requires proper equipment on-hand (towels, ice water)
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.
Pearls and Pitfalls
In athletes with changes in mental status or neurologic dysfunction, treat as EHS and cool rapidly.
Failure to recognize heat exhaustion or to fully recover from heat exhaustion prior to resumption of activity may lead to cumulative heat stress and the possibility of development of EHS.
Proper acclimatization and modification of activity in extreme heat may reduce risk of heat exhaustion.
Rehydrate with a sports drink or another electrolyte containing fluid, or use NS for IV resuscitation if needed in the ED.
Heat cramps
General Description
One of the earliest indicators of heat stress in the individual athlete.
Painful muscle cramps/spasm occurring in active muscle groups following exercise challenge.
Cramps most likely to occur after prolonged exercise (more than two hours) but may occur anytime.
High incidence among football players, tennis players, and military.1,3
Mechanism
Poorly understood, multifactorial etiology.
Most likely results from some combination of dehydration, salt loss, and neuromuscular fatigue.3,9,31
Sodium (as opposed to potassium) appears to be the predominant electrolyte deficiency linked to heat cramp development.
Individuals with more concentrated (saltier) sweat develop heat cramps more commonly.
Presentation
Painful contractions usually inhibit athlete’s ability to continue participation/play.
Occurs most often in gastrocnemius, hamstrings, quadriceps, or abdominal muscles.
May occur alone or in conjunction with heat exhaustion.
Heat cramps alone do not indicate increased risk of development of heat stroke.
Physical Exam
If the athlete has collapsed to the ground, quickly assess circulatory status, airway/breathing, and neurologic function.
Assess for any acute injury that may have caused the athlete to collapse or may have occurred if the athlete collapsed to the ground due to cramping.
Physical exam may reveal tight, actively contracting muscle.
Essential Diagnostics
Beyond a focused history and physical exam, further diagnostic testing is not indicated.
Should cramps occur in conjunction with other symptoms (altered sensorium, nausea and vomiting, etc.), obtain a core temperature and consider assessing serum electrolytes to look for significant hyponatremia.
ED Treatment
Disposition
Athletes may be safely discharged home following resolution of symptoms.
Advise against vigorous physical activity until fully rested, rehydrated, and asymptomatic. Athlete should not return to vigorous activity on the same day.
Further acclimatization and conditioning may be beneficial prior to resumption of vigorous activity.
Encourage the athlete to consume adequate hydration to restore body weight and to consume sodium-containing meal.
Peals and Pitfalls
Acclimatized, hydrated, and conditioned athletes are less likely to develop heat cramps.
Treat cramps with massage, stretching, ice, and consumption of sodium-containing fluids.
Sodium is the key electrolyte deficiency in heat cramps, not potassium. Emphasis on potassium supplementation (such as bananas, potassium salt, etc.) in severe cramps is misguided.
Do not miss an acute musculotendinous injury such as a gastrocnemius or hamstring tear.
Do not miss concurrent heat exhaustion or stroke.
Heat Syncope
General Description/Mechanism
Syncope or near syncope occurring secondary to orthostatic hypotension. This may also be referred to as exercise- associated collapse (EAC).
Orthostasis results from peripheral vasodilation, venous pooling, and relative hypovolemia.
Prolonged standing in the heat, prolonged standing after significant exertion, and rapid changes of body position following exertion all may precipitate heat syncope.1,9
Prolonged standing or a change in position tend to create venous pooling in the lower extremities. This pooling is exaggerated when peripheral vasodilation occurs in response to heat production.
Cessation of intense activity such as running also results in venous pooling, along with the loss of muscle action contributing to venous return.
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