Article
sports medicine
Heat Illness and Heat Stroke
David S. Jardine, MD*
Author Disclosure
Dr Jardine did not
disclose any financial
relationships relevant
to this article.
Objectives
1.
2.
3.
4.
5.
6.
7.
8.
After completing this article, readers should be able to:
Describe the laboratory abnormalities that accompany heat stroke.
Understand the relationship between core temperature and injury.
Discuss strategies to reduce the risk of heat stroke during athletic events.
Describe the physical findings of patients suffering from heat stroke.
List the most common sequelae of heat stroke.
Identify the body temperature above which heat injury begins to occur.
Explain the differences between malignant hyperthermia and heat stroke.
Discuss the differences between heat stress, heat exhaustion, and heat stroke.
Introduction
Heat illness is caused by an inability to maintain normal body temperature because of
excess heat production or decreased heat transfer to the environment. Heat stroke arises
when cellular injury is caused by excess body temperature. If the core temperature rises
above 105.8°F (41°C) for more than a short time, thermal injury results. Proteins are
denatured, and injured cells undergo apoptosis (programmed cell death) or necrosis. Even
before injury takes place, an individual may suffer transient mental and physical impairment, which is called heat exhaustion. Heat stroke is a medical emergency that is associated
with a mortality of approximately 12% in adult patients. Treatment requires aggressive
supportive care to minimize mortality.
It is important to recognize the difference between fever and heat stroke. Fever is a
normal response, during which the core temperature remains under the control of the
central thermoregulatory centers that reside in the hypothalamus and brainstem. When a
pyrogenic stimulus is received, core temperature is elevated rapidly to a new set point that
is regulated by normal mechanisms. Maximum febrile temperatures rarely exceed 105.8°F
(41°C). (1) In contrast, during heat illness, normal heat transfer mechanisms are overwhelmed and central thermoregulatory control is ineffective. Consequently, the core
temperature can rise quickly to injurious levels.
Forms of Heat Illness
Heat Stress
Before heat stroke occurs, lesser degrees of dysfunction result from the stress of responding
to a thermal load. A patient may be thermally challenged because of excess heat production, typically caused by exercise in a warm environment. Alternatively, patients who are
exposed to excessively warm environments even without exercise may develop heat stress.
This effect characteristically occurs during heat waves in the summertime. Heat stress is the
feeling of discomfort and physiologic strain that results from exposure to a hot environment. Although the individual is uncomfortable, core temperature remains within the
normal range. (2) Patients suffering from heat stress show decreased exercise performance
but usually no other symptoms.
Heat Exhaustion
Elevation of core body temperature is characteristic of heat exhaustion and heat stroke.
Heat exhaustion is defined as mild dehydration with or without sodium abnormalities,
which can include hypernatremia or hyponatremia. As with heat stress, heat exhaustion
*Children’s Hospital, Seattle, Wash.
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Table 1.
heat illness/heat stroke
Heat Exhaustion Versus Heat Stroke
Heat Exhaustion
Heat Stroke
●
●
●
●
●
●
●
●
●
●
●
Mild dehydration
Core temperature 100.4° to 104°F (38° to 40°C)*
Profuse sweating
Thirst, nausea, vomiting, confusion, headache
Feels faint or has collapsed
Usually severe dehydration
Core temperature may be >104°F (40°C)*
Flushed with hot, dry skin
Dizziness, vertigo, syncope, confusion, delirium
May be unconscious
Shock
*Core temperature may have fallen substantially by the time the patient reaches a medical facility.
usually follows periods of strenuous exercise or exposure
to high environmental temperatures. In heat exhaustion,
core temperatures are between 100.4°F (38°C) and
104°F (40°C). Symptoms include intense discomfort,
confusion, thirst, nausea, and vomiting. (2) The absence
of severe neurologic symptoms frequently is used to
differentiate heat exhaustion from heat stroke (Table 1).
although the relationship between this illness and heat
stroke was not recognized. Subsequently, a large number
of cases have been described, many of which clearly were
the result of heat stroke. (4) It is important to identify
hemorrhagic shock and encephalopathy syndrome correctly because the neurologic sequelae may be severe.
Malignant Hyperthermia is Not Heat Stroke
Heat Stroke
Heat stroke is defined as a core temperature greater than
104°F (40°C), an exposure to heat (exertional or nonexertional), and neurologic dysfunction. Frequently divided into nonexertional (classic) heat stroke and exertional heat stroke, the dangers to the patient and
therapeutic measures are similar.
Nonexertional heat stroke occurs in warm, often humid, environments. Affected patients become overheated without engaging in strenuous exercise. As the
patient becomes more ill, anhydrosis frequently develops, accelerating the rate of temperature rise and worsening the injury. Nonexertional heat stroke occurs during the summer, frequently during heat waves.
Exertional heat stroke affects actively exercising individuals. Highly motivated athletes, soldiers, and laborers
are at risk for this problem. Dehydration is a common
feature. Warm, humid weather increases the risk of this
illness, but cases frequently occur during cooler months.
The incidence of heat stroke is greater during periods
of unusually high temperatures, but the overall incidence
of heat stroke probably is underreported. This problem is
compounded for young children and infants because the
symptoms of heat stroke in pediatric patients are very
similar to those observed in bacterial sepsis. (3)
Hemorrhagic Shock and Encephalopathy
Syndrome
Infants are susceptible to a unique form of heat stroke
that is termed hemorrhagic shock and encephalopathy
syndrome. This illness was described initially in 1983,
Heat stroke sometimes is confused with malignant hyperthermia. Although both share the characteristic of
injurious elevation of body temperature, they are distinctly different illnesses that have different causes. In
heat stroke, the primary abnormality is the patient’s
inability to transfer normally produced heat (from normal metabolic activity or exercise) to the environment. In
contrast, malignant hyperthermia is caused by abnormalities in the ryanodine receptor, a calcium channel receptor in the smooth endoplasmic reticulum. Malignant
hyperthermia almost always follows treatment with a
known triggering agent (volatile halogenated anesthetics
and depolarizing muscle relaxants), causing skeletal muscle rigidity, hypercapnia, and rapid increase in core temperature to injurious levels. Dantrolene, a drug that
depresses excitation-contraction coupling in skeletal
muscle, has well-demonstrated efficacy in the treatment
of malignant hyperthermia, but appears to show little or
no benefit in treating heat stroke. Although malignant
hyperthermia has been reported in the absence of triggering agents, this occurrence appears to be rare. Thus,
malignant hyperthermia is not normally considered in
the differential diagnosis of heat stroke.
Risk Factors
Exertional heat stroke is caused by increased heat production over a period of sufficient duration to raise core
temperature to injurious levels. Vigorous exercise is not a
problem if the duration of the exercise is brief or if the
environment is cool. The combination of prolonged
exertion in a warm, humid environment, however, is
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dangerous. Among high school athletes, heat stroke is
the third leading cause of mortality. (5) Dehydration can
contribute significantly to the risk of heat stroke while
exercising.
Exertional heat stroke is reported more commonly
among adolescents and adults than among young children. The reasons for this discrepancy are unknown, but
it may be that the discomfort that precedes heat illness
usually causes younger children to decrease their activity
level before the onset of injury. Unfortunately, adolescents and adults may be sufficiently motivated to ignore
the discomfort until they collapse from heat stroke.
Nonexertional heat stroke occurs in the absence of
excessive physical activity among individuals who are
exposed to excessively warm, humid environments and
are unable to disperse heat produced by basal metabolic
processes. Sleeping infants may be at risk if they are
covered with excessive bedding. Because of their limited
motor skills, infants may be unable to remove the blankets in response to overheating; they depend on their
caretakers to provide a safe thermal environment. Both
infants and young children are at risk for nonexertional
heat during the summer if they are left unattended in an
automobile exposed directly to the sun or in hot environments. (6) Measurements of automobile temperatures in the summer show that the temperature can reach
145°F (62.8°C) in as few as 40 minutes, even in a
light-colored vehicle that has the windows partly open.
Heat stroke occurs rapidly in such an inhospitable environment.
Disabled children and adolescents as well as the elderly may have limited mobility and be unable to leave
their dwellings during hot weather. In France, during the
heat wave of 2003, an estimated 14,800 deaths were
attributed to the hot weather. Despite the obvious public
health risk of municipal heat waves, many cities at risk in
the United States have inadequate or no plans for managing this problem. (7)
Clinical and Laboratory Abnormalities in Heat
Stroke
Heat illness or heat stroke should be considered in any
patient whose core temperature is elevated significantly
(⬎104°F [40°C]) and who has mental status changes
such as confusion, irritability, or loss of consciousness.
Although heat illness may be differentiated from meningitis by the absence of nuchal rigidity, both of these
illnesses share the characteristics of depressed blood pressure and elevated body temperature.
Heat stroke is a multisystem illness (Table 2). The
signs observed in heat stroke are the result of one or more
heat illness/heat stroke
Clinical and Laboratory
Abnormalities in Heat Stroke
Table 2.
Clinical Findings
●
●
●
●
●
Hot, dry skin
Encephalopathy
Seizures
Shock
Diarrhea
Laboratory Abnormalities
●
●
●
●
●
●
Coagulopathy
Prerenal azotemia
Progressive anemia
Thrombocytopenia
Metabolic acidosis
Elevated alanine aminotransferase/aspartate
aminotransferase
systems failing. Individuals suffering from heat stroke
undergo a characteristic pattern of clinical and laboratory
changes.
Elevated Temperature
Patients who present with the signs of heat stroke have
been injured by core temperatures greater than 104°F to
105.8°F (40°C to 41°C). The severity of injury is cumulative, so exposure to a very high temperature (109.4°F
[43°C]) for a relatively brief time may produce an injury
that is similar to one produced by exposure to a lower
temperature (106.2°F [41.2°C]) for a longer period of
time. Removal of the patient from the offending circumstances often is enough to begin cooling. By the time the
patient reaches medical attention, his or her core temperature may be lower than 105.8°F (41°C), even though
he or she may have suffered a significant heat injury.
Because of this effect, it is important to recognize heat
stroke, even in the absence of an elevated core temperature on presentation. In fact, insistence on the temperature being greater than 105.8°F (41°C) leads to significant underdiagnosis of heat stroke and the potential for
misdiagnosis as intoxication or serious infection. For this
reason, a careful history of the patient’s recent exposure
to circumstances that can lead to overheating is invaluable. In the absence of elevated core temperature, heat
stroke may be diagnosed accurately by the presence of
appropriate risk factors, typical clinical signs, and laboratory abnormalities.
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heat illness/heat stroke
Central Nervous System (CNS) Failure
The onset of severe neurologic dysfunction (delirium,
coma, seizures) often is identified as one of the features
that distinguishes heat stroke from heat exhaustion. In
general, severe neurologic dysfunction is not observed
until the rectal temperature is greater than 105.8°F
(41°C). Confusion or delirium is the first sign of a
deteriorating neurologic status. Coma and seizures can
follow rapidly and often are associated with a poor outcome.
Shock
Hypotension is a common accompaniment of heat stroke
and is frequent when the temperature exceeds 107.6°F
(42°C). In the early stages of heat stroke, vasodilation
leads to a low blood pressure, even though the cardiac
index is increased and the central venous pressure is
normal. More severe heat stroke produces irreversible
myocardial impairment. Electrocardiographic findings
that are indistinguishable from coronary ischemia may be
observed. In the later stages of heat stroke, patients often
become hypovolemic from sweat losses. Hypotension in
heat stroke frequently is associated with diminished cerebral perfusion, which causes cerebral ischemia. These
effects compound the injurious effects of heat on the
CNS and may produce severe and potentially permanent
neurologic dysfunction.
Serum lactate concentrations frequently are elevated
in heat stroke. (8) Even after the blood pressure has
returned to normal and vasopressors no longer are necessary, blood lactate values may remain elevated and
only gradually return to normal. This delay is not unique
to heat stroke; it is seen following circulatory shock and
in patients who have hepatic dysfunction, which commonly accompanies heat stroke. In addition, vasomotor
tone may remain abnormally low, even after normal
temperature and intravascular volume have been restored. This outcome may be caused by the direct effects
of heat on the heart and vascular system, or it may be
mediated by the effects of endotoxin released from the
heat-injured gastrointestinal (GI) tract or other inflammatory mediators.
GI Abnormalities and Hepatic Injury
Heat stroke causes a number of GI abnormalities. Although mild heat stroke may cause little more than
diarrhea, more severe heat stroke produces significant
injury to the GI tract, including mucosal swelling, petechiae, and hemorrhages. Even after resuscitation and
return to normal temperature, GI tract injury can con-
tinue to evolve. As a consequence of these injuries,
circulating endotoxin rises and potentially toxic free radicals may be generated. Injury to the GI tract probably
contributes significantly to the hypotension and multisystem failure observed in heat stroke.
The liver may be injured severely in heat stroke. As a
metabolically active solid tissue, the liver normally is a
major site of heat production in the body. During periods of hyperthermia, the temperature of the liver is
among the highest of any site in the body, placing hepatic
tissue at high risk of injury. In addition, portal circulation
perfuses the liver with a variety of toxic substances generated by the GI tract during heat stroke, including
endotoxin and free radicals. Patients who survive heat
stroke demonstrate rapidly rising alanine aminotransferase and aspartate aminotransferase concentrations that
peak at 48 to 72 hours after injury and gradually return to
normal after 10 to 14 days. Bilirubin can be elevated, but
severe hyperbilirubinemia is unusual. Prolongation of
the prothrombin time is common.
Biopsy of the liver after heat stroke shows few changes
in mild heat stroke, although apoptosis can be an early
finding. After severe heat stroke, the liver shows widespread abnormalities, including areas of cholestasis and
necrosis.
Renal Failure
Renal insufficiency is a common finding in heat stroke,
affecting at least 50% of the patients who have nonexertional heat stroke and an even higher proportion of
patients who suffer from exertional heat stroke. The
usual clinical findings are those of prerenal azotemia,
with elevation of blood urea nitrogen to a greater extent
than creatinine. These abnormalities respond well to
rehydration and usually correct within the first few days.
Dialysis or other forms of renal support are required
infrequently in patients who have no pre-existing renal
disease.
Hematologic Abnormalities
Abnormalities in hematologic and coagulation values
commonly follow heat stroke. The hematocrit declines
rapidly in the first 24 hours following heat stroke. Although a portion of the decrease can be explained by
rehydration, the reduction in hematocrit often is much
greater than would be caused by rehydration. The cause
of this anemia may be multifactorial. Red blood cell
half-life is shortened after heat stroke. Further, red
blood cells that have been heated in vitro have greater
membrane rigidity and increased osmotic fragility, which
may contribute to red blood cell damage and ultimately
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heat illness/heat stroke
Postmortem Abnormalities
Death from heat stroke does not
produce any distinguishing postmortem abnormalities. Nonspecific
findings include hepatocellular necrosis, disseminated intravascular
coagulation, and in children, intrathoracic petechiae. Such histologic abnormalities are not immediately apparent at the onset of heat
stroke; the patient must survive for
at least 6 hours for the abnormalities to evolve. If the patient dies
rapidly from heat stroke, the histologic abnormalities associated with
Figure 1. Hypersegmented neutrophils showing “botryoid” nuclei (arrow). These cells heat stroke are not observed. In the
appear often during the first few hours after the onset of heat stroke.
absence of external evidence that
overheating may have been the
cause of death, the observed postlead to early removal from the circulation. Individuals
mortem abnormalities are sufficiently ambiguous that
suffering from heat stroke tend to have a much greater
heat stroke may not be considered in the differential
number of spherocytes, which may have a shortened life
diagnosis. For this reason, it is important to search for
span.
environmental clues that heat may have been the cause of
Thrombocytopenia is common, although the platelet
an otherwise unexplained death.
count may remain normal in mild heat stroke. The cause
Treatment
of thrombocytopenia has not been defined. The platelet
Heat Exhaustion
count often is normal at the time of presentation, but
To prevent injury from heat-related illnesses, it is impordeclines steadily for the first 24 hours. (3)
tant to maintain a high index of suspicion. Heat exhausIn a recent series, 45% of patients had evidence of
tion should be suspected if an individual is exercising in a
disseminated intravascular coagulation. Coagulation abwarm environment and feels faint or nauseated or is
normalities include prolongation of the prothrombin
confused or vomiting. Effective treatment requires imtime and partial thromboplastin time and elevation of the
mediate removal from the heat source, cessation of exerd-dimer. (9) Abnormalities of plasminogen activator incise, and hydration. If the patient has significant CNS
hibitor 1 also have been described. Although bleeding
symptoms (ataxia, confusion, seizures, coma) or sympdiatheses are reported most commonly, some patients
toms of heat illness do not resolve within 20 to 30 minmay experience a period of hypercoagulability shortly
utes, the diagnosis of heat stroke should be considered
after the onset of heat stroke. Within 24 hours, these
strongly and the patient treated accordingly.
findings are replaced by a picture of disseminated intravascular coagulation. Such abnormalities generally reHeat Stroke
solve within a few days. (3) In spite of the coagulation
Treatment of heat stroke consists of three phases. First,
abnormalities, clinically significant hemorrhage is unthe patient must be removed from the circumstances that
common.
led to heat stroke to prevent ongoing accumulation of
Hypersegmented neutrophils frequently are observed
heat and increasing core temperature. Once the patient
in the peripheral circulation for the first few hours after
has been removed from the offending circumstances, the
the onset of heat stroke and are cleared rapidly from the
core temperature will begin to fall, but it is important to
blood. These neutrophils, which have five or more nucool the patient to less than 104°F (40°C) as rapidly as
clear lobes (Fig. 1), are termed “botryoid” nuclei bepossible to prevent ongoing injury. After the patient’s
cause the morphology resembles a cluster of grapes.
temperature has been brought under control, therapy is
Although the cause of this abnormality is not known,
supportive, with the goal of ameliorating the derangeprobably these cells are undergoing the morphologic
ments produced by the heat injury and protecting the
changes of apoptosis.
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Table 3.
●
●
●
●
●
●
●
●
●
heat illness/heat stroke
Treatment of Heat Stroke
Cool the patient until core temperature is <102.2°F
(39°C)
Rehydrate with intravenous fluids
Administer vasopressor therapy if shock persists after
rehydration
Monitor for anemia and thrombocytopenia
Treat coagulopathy if clinical hemorrhage is present
Treat seizures
Monitor for cerebral edema
Institute mechanical ventilation for respiratory
failure
Liver transplantation not indicated for severe liver
failure
patient from additional injury caused by untreated hypotension and organ dysfunction (Table 3).
COOLING. Several techniques have been described for
cooling patients who have heat stroke. Immersion of the
patient in ice water may be the most effective means. (10)
In circumstances where this technique is not practical,
simple evaporative cooling may be as effective as some
active cooling methods (11) and is less uncomfortable
for the patient. Regardless of the method chosen, the
patient may not respond as rapidly as expected because
those who are in shock may have poor circulation to the
peripheral vasculature, thereby reducing heat transfer.
Dantrolene has no efficacy in treating hyperthermia from
heat stroke.
TREATMENT OF SHOCK. The mainstays of treating
shock are restoration of circulating volume and use of
vasopressors. If heat exhaustion is not treated rapidly
with cooling and rehydration, it may progress to heat
stroke. In most cases of heat exhaustion and in all cases of
heat stroke, intravenous rehydration should be undertaken. If the patient’s core temperature is greater than
104°F (40°C), chilled intravenous fluids may be used to
hasten cooling. In addition to dehydration, abnormalities of sodium and other electrolyte concentrations may
be present and should be addressed during resuscitation.
Because cardiac function may be diminished in heat
stroke, the patient should be monitored for signs of
congestive heart failure during rehydration.
Once the central vascular volume has been replenished, initiation of vasopressor therapy may be necessary
because of diminished cardiac function or persistently
low systemic vascular resistance. In pediatric patients,
vasopressor therapy usually is required for only 24 to
48 hours, after which cardiac function and vascular tone
return to normal.
TREATMENT OF HEMATOLOGIC AND COAGULATION
ABNORMALITIES. Because of the risk of anemia, thrombocytopenia, and prolongation of coagulation parameters, patients who have heat stroke should be monitored
daily with a complete blood count and coagulation studies. In cases of severe heat stroke, these parameters
should be monitored more frequently because clinically
significant abnormalities may develop within the first
24 hours. In mild cases of heat stroke, treatment of the
hematologic abnormalities usually is not necessary, but
in more severe cases of heat stroke, transfusion of packed
red blood cells may be needed to treat progressive anemia within the first 48 hours. Although it is unusual,
bleeding occasionally may become a problem and is
treated easily with fresh frozen plasma and platelets.
Consideration should be given to correcting these abnormalities before performing procedures such as a lumbar puncture that may be dangerous if accompanied by
bleeding.
TREATMENT OF NEUROLOGIC ABNORMALITIES. Acute
neurologic disability is one of the hallmarks of heat
stroke. This dysfunction can take the form of confusion,
obtundation, coma, or seizures. Seizures usually can be
controlled relatively easily, often with anticonvulsant
monotherapy. Although any of several anticonvulsants
can be effective, phenytoin has the advantage of not
producing additional CNS depression, which may be an
important consideration when attempting to assess the
progress of the patient’s condition.
Cerebral edema is believed to be common after heat
stroke, with local areas of cerebral infarction possibly
occurring in both pediatric and adult patients. Although
some have advocated close monitoring of serum sodium
concentrations as an approach to avoid cerebral edema, it
is probable that the cause of edema is thermal injury to
neuronal cells, making cerebral edema difficult to prevent.
TREATMENT OF RESPIRATORY FAILURE. In general,
the lungs are relatively unaffected by heat stroke, although respiratory failure is common in severe heat
stroke. The cause of respiratory failure is CNS dysfunction rather than parenchymal lung disease. Because of
this mechanism, patients usually require very modest
ventilator settings for a few days until they regain CNS
control of respiratory activities. During the period of
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respiratory failure, the chest radiographs often are clear.
The development of severe lung disease may indicate
aspiration of gastric contents prior to intubation or the
development of an intercurrent infection.
TREATMENT OF HEPATIC FAILURE. Marked elevation
of hepatic enzymes is so common in heat stroke that the
presence of such abnormalities may help confirm the
clinical diagnosis. In severe heat stroke, transient liver
failure with widespread hepatic necrosis may occur. Although liver transplantation occasionally has been employed in the treatment of severe hepatic failure caused
by heat stroke, spontaneous recovery of hepatic function
is likely, and transplantation is a last resort.
Outcome of Heat Stroke and Heat Illness
Patients suffering from heat exhaustion make a full,
prompt recovery once they are cooled and rehydrated.
The outcome is variable and depends on the extent of the
original injury. Typically, once the patient is removed
from the circumstances that led to hyperthermia, the
core temperature decreases to normal and injury ceases.
The severity of the injury appears related to the duration
of hyperthermia and to the height of the temperature.
Patients who have mild heat stroke generally recover
uneventfully. There usually are no sequelae, and neurologic functioning is intact when tested several months
later. Those who survive moderate-to-severe heat stroke
have a good chance of making an intact recovery, but the
risk of sequelae is higher. If the core temperatures have
been greater than 107.6°F (42°C), patients have a poorer
prognosis. Patients generally recover from the hepatic
and renal injuries, but neurologic injury often is permanent. Persistent neurologic abnormalities include behavioral changes, decreased visual acuity, dysarthria, impaired memory, ataxic gait, and poor coordination.
Among severe cases of heat stroke, one third have permanent moderate-to-severe impairment, including spasticity and pancerebellar syndrome. Computed tomography scan and MRI initially may show edema and ischemic
changes. Later, atrophy often is noted. The mortality rate
for severe cases appears to be at least 10%.
Preventing Heat Illness
Heat illness, especially heat stroke, is potentially devastating, and care is supportive. Consequently, prevention
is of utmost importance. Exertional heat stroke in children and adolescents is most likely to occur during
athletic activities, so planning should occur in advance of
these activities to reduce the likelihood of heat illness.
heat illness/heat stroke
Risk Assessment
Two methods are in widespread use to assess the risk of
heat illness. The Wet Bulb Globe Temperature Index
(http://www.usariem.army.mil/heatill/appendc.htm)
is used by the United States Armed Services to assess the
risk of heat illness. This measure takes into account
temperature and humidity but also measures the effect of
radiant thermal energy from the sun. Although this
measurement may be the most accurate predictor of heat
illness, it is complex to use and requires special equipment. A much more user-friendly measure of the risk of
heat illness is the Heat Index Chart (Fig. 2) produced by
the National Weather Service (http://www.crh.noaa.
gov/jkl/?n⫽heat_index_calculator). The Heat Index
Chart provides a ready means for assessing the risk of heat
illness based on the relative humidity and the temperature. Because the information needed to assess the risk of
overheating can be obtained quickly from the Weather
Service, it is far easier for coaches and other supervisory
personnel to employ this method. It should be noted
that the Heat Index Chart does not measure radiant
energy from the sun. On sunny days, therefore, the heat
index may be even higher than is indicated on the chart
(by as much as 15°F [9.5°C]).
Supervising Officials
Those who supervise young people during periods of
exercise should monitor them carefully for evidence of
heat illness. Because the signs and symptoms of heat
illness are nonspecific, this task may be difficult. The
presence of excessive fatigue, confusion, and muscle
cramps may indicate the onset of heat illness. If any of
these is present, the affected individual should be moved
to a cool environment for oral rehydration and observed
carefully for progression of signs and symptoms. Children who do not respond quickly to this intervention
should be evaluated by a physician.
When athletic events are planned during periods of
hot weather, designating an individual responsible for
determining whether the activities can be conducted
safely should be considered. Scheduling events late in
the day or in the evening when the risk is less also should
be considered. If this scheduling is not possible, the
temperature, humidity, and condition of the participants should be monitored. Frequent breaks, shade,
and fluids should be provided. During especially adverse
conditions, it may be impossible to ensure participant
safety, and cancellation of the event may be the only safe
option.
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heat illness/heat stroke
Figure 2. Heat Index Chart.
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Hydration
It is important to be attentive to adequacy of hydration
and maintenance of proper electrolyte balance. If sweat
losses are not replaced, patients may become hypovolemic, which can lead to decreased sweating and, in extreme cases, hypotension. Significant amounts of sodium
are lost in sweat, so electrolyte replacement is essential
to avoid hyponatremia. Individuals who will be exercising in a hot environment should be encouraged to consume liquids containing electrolyte solutions (ie, “sports
drinks”) to avoid the risk of hyponatremia. Consumption
of large quantities of hypotonic fluids should not be
encouraged because of the risk of electrolyte imbalance.
It is important for supervisory officials to encourage
appropriate intake of fluids during activities. Research
has shown that if fluid intake is left up to personal
preference, most individuals do not drink sufficient
quantities to maintain proper hydration. Although figures do not exist for pediatric patients, current recommendations for adults are to consume 500 mL of fluid
within 2 hours prior to exercise (assuming the patient is
euvolemic). During exercise, approximately 250 mL of
fluid every 20 minutes is recommended to offset sweat
losses. (5) Studies have shown that acclimated individuals are more likely to consume liquids to maintain hydration than are those who are not acclimated. Therefore,
special attention should be paid to individuals who are
not yet acclimated to hot weather.
Although it is important to emphasize adequate hydration, hydration alone does not prevent heat illness. It
is possible for well-hydrated individuals to suffer heat
illness or heat stroke if they continue to exercise at a rate
that generates heat more rapidly than it can be transferred to the environment.
Other Measures
Athletes should be encouraged to acclimate to warm
conditions for at least 3 to 4 days before competing.
Acclimatization reduces the likelihood of heat illness
through increased sweat rate and decreased electrolyte
loss. At least four exercise sessions of 1 to 4 hours each
are necessary for adolescents and adults to acclimate.
Children need a longer acclimatization program, requiring as many as 8 to 10 exercise sessions.
Clothing should be light colored to reduce radiant
heat absorption from the sun and loose to help sweat
evaporate. Athletes never should be allowed to exercise
in garments that restrict sweat loss, which is extremely
dangerous. Deaths have resulted when individuals trying
to reduce their weight through increased fluid loss exercised in waterproof garments.
heat illness/heat stroke
Consideration should be given to teaching youth and
adults about the risk of heat stroke. The involvement of
supervising adults in implementing this program can
help to disseminate up-to-date information among those
who are in the best position to assure the safety of
children and adolescents. Because the risk for exertional
heat stroke is the greatest during the summer, educational efforts can be timed for maximum impact.
Prevention of nonexertional heat stroke consists of
removing vulnerable populations (infants, small children, and disabled individuals) from environments that
place them at risk of overheating. Public health measures
should be directed at educating the public about the
dangers of excessively hot environments, especially for
individuals who have limited self-help skills (ie, the
young, disabled, and elderly). In general, it is relatively
simple to identify these environments (eg, excessively hot
rooms, closed cars in the summer sun). Parents should be
cautioned against overbundling their infants. They also
should be told that sweating during sleep is a dangerous
sign and clearly indicates that more of the infant’s body
surface should be exposed to allow adequate heat loss.
Conclusion
During periods of high temperature and humidity, encouraging hydration and the availability of sufficient
quantities of electrolyte-containing fluids is essential to
prevent heat injury. During periods of high risk, limiting
activity, enforcing periods of rest, and monitoring for
early signs of heat exhaustion are important. Using
readily available charts can facilitate identification of potentially dangerous environmental conditions and make
it easier to determine when physical activities should be
limited or rescheduled.
The care of patients who develop heat stroke is supportive and involves treating the symptoms of dehydration, shock, and neurologic impairment. Hematologic
abnormalities should be corrected and medical support
provided until the injury caused by excessive body temperature has abated. The outcome after heat stroke can
range from full recovery to death. Severe neurologic
sequelae are the permanent injuries seen most often.
Education of children and those who supervise them
during physical activities may help to prevent this potentially devastating illness.
References
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Pediatrics in Review Vol.28 No.7 July 2007 257
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sports medicine
heat illness/heat stroke
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8. al Harthi SS, Karrar O, al Mashhadani SA, Saddique AA. Metabolite and hormonal profiles in heat stroke patients at Mecca
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PIR Quiz
Quiz also available online at www.pedsinreview.org.
Match each clinical description with the most likely heat-related illness. Each answer may be used once,
more than once, or not at all.
6. Core temperature is within the normal range.
7. Core temperature is typically 100.4° to 104°F (38° to 40°C).
8. The affected patient is an infant.
9. Mucosal swelling, petechiae, and hemorrhages are present in the gastrointestinal tract.
A.
B.
C.
D.
E.
Heat exhaustion.
Heat stress.
Heat stroke.
Hemorrhagic shock and encephalopathy syndrome.
Malignant hyperthermia.
10. Treatment of increased body temperature with dantrolene is ineffective in treating heat stroke but is
efficacious in treating:
A.
B.
C.
D.
E.
Fever.
Heat exhaustion.
Heat stress.
Hemorrhagic shock and encephalopathy syndrome.
Malignant hyperthermia.
11. For any patient who has a heat-related illness, it is critical to lower body temperature to below:
A.
B.
C.
D.
E.
102.2°F (39°C).
103.1°F (39.5°C).
104°F (40°C).
104.9°F (40.5°C).
105.8°F (41°C).
258 Pediatrics in Review Vol.28 No.7 July 2007
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Heat Illness and Heat Stroke
David S. Jardine
Pediatrics in Review 2007;28;249
DOI: 10.1542/pir.28-7-249
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References
This article cites 11 articles, 2 of which you can access for free at:
http://pedsinreview.aappublications.org/content/28/7/249#BIBL
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Heat Illness and Heat Stroke
David S. Jardine
Pediatrics in Review 2007;28;249
DOI: 10.1542/pir.28-7-249
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