C H A P T E R 133 
Heat Illness
PRINCIPLES
Background
Humans have been plagued by heat illness throughout recorded
history, often as the result of military exercises, athletic events, or
recreational activities. When environmental heat stress is maximal,
strenuous exercise is not required to produce heat illness. Modern
military organizations continue to encounter heat illness because
of the requirement to train unacclimatized troops with heavy
physical exercise. Heat stroke is the third leading cause of death
among all US athletes. Of the major sports, football has the great-
est number of heat stroke fatalities and a 10 times higher rate for
heat illnesses.1 The health hazards associated with extreme envi-
ronmental working conditions in many industries have been
increasingly recognized worldwide.2-4
Older adults and the poor, who often lack adequate air condi-
tioning and nutrition, and those with preexisting disease are
prone to heat illness during environmental extremes. It is esti-
mated that at least 10 times as many heat-aggravated illnesses
occur in patients with comorbid conditions, such as coronary
artery disease, cerebrovascular disease, and diabetes. In heat wave
years in the United States, approximately 10 times as many deaths
are reported as during non–heat wave years. Climate models have
suggested an increase in frequency and intensity of heat waves in
temperate areas of the world.5 Before the advent of air condition-
ing, mortality increased three- to fivefold in nursing homes and
threefold in the general population during heat waves.6 Microcli-
mates conducive to heat illness are produced in the interiors of
automobiles, military tanks, and tents in the sun, as well as in
engine rooms, mines, hot tubs, and saunas.6 Children are more
susceptible to heat stressors because their higher surface area–to–
mass ratios allow increased absorption of heat. They also have
lower sweat rates per gland.
Anatomy and Physiology
Heat Production
Humans are essentially biochemical furnaces that burn food to
fuel with a complex array of metabolic functions. These chemical
reactions consume substrate, generate usable energy, and produce
byproducts that must be eliminated for continued operation of
the system. Water and carbon dioxide are produced and elimi-
nated in large quantities, as are urea, sulfates, phosphates, and
other chemical products. These reactions are exothermic and
combine to produce a basal metabolic rate that amounts to
approximately 100 kcal/hr for a 70-kg person. In the absence of
cooling mechanisms, this baseline metabolic activity would result
in a 1.1° C (2° F) hourly rise in body temperature.
Heat production can be increased 20-fold by strenuous exer-
tion. Rectal temperatures as high as 42° C (107.6° F) have been
recorded in trained marathon runners, without ill effects. Meta-
bolic factors, such as hyperthyroidism and sympathomimetic
drug ingestion, can dramatically increase heat production. Envi-
ronmental heat not only adds to the heat load but also interferes
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Melissa Platt | Timothy G. Price
with heat dissipation. The physics of heat transfer as it relates to
human physiology involves four mechanisms—conduction, con-
vection, radiation, and evaporation.6
Conduction.  This is the transfer of heat energy from warmer
to cooler objects by direct physical contact. Air is a good insulator;
therefore, only approximately 2% of the body heat loss is by
conduction. In contrast, the thermal conductivity of water is at
least 25 times that of air.
Convection.  This is heat loss to air and water vapor molecules
circulating around the body. As the ambient temperature rises, the
amount of heat dissipated by convection becomes minimal. Once
the air temperature exceeds the mean skin temperature, heat is
gained by the body. Convective heat loss varies directly with wind
velocity. Loose-fitting clothing maximizes convective, and also
evaporative, heat loss.
Radiation.  This is heat transfer by electromagnetic waves.
Although radiation accounts for approximately 65% of heat loss
in cool environments, it is a major source of heat gain in hot
climates. Up to 300 kcal/hr can be gained from radiation when
someone is directly exposed to the hot summer sun.
Evaporation.  This is the conversion of a liquid to the gaseous
phase. Evaporation of 1 mL of sweat from the skin cools the body
by 0.58 kcal. As the ambient temperature rises, evaporation
becomes the dominant mechanism of heat loss. Panting mammals
such as dogs have an oropharyngeal countercurrent flow mecha-
nism (carotid rete mirabile) that results in selective cooling of the
brain. In humans, respiratory and countercurrent mechanisms are
minimal sources of heat loss.
Heat Regulation
The regulation of body temperature involves three distinct
functions—thermosensors, a central integrative area, and ther-
moregulatory effectors.
Thermosensors.  Temperature-sensitive structures are
located peripherally in the skin and centrally in the body. Skin
temperature changes, however, correlate poorly with changes in
the rate of heat loss. Thermosensitive neurons, located in the
preoptic anterior hypothalamus, are activated when the tempera-
ture of the blood circulating through that area exceeds a set point
(Fig. 133.1).
The skin temperature affects heat loss when a person resting
in a warm environment initiates sweating, even though the core
temperature remains constant. In contrast, changes in core tem-
perature are more dominant than skin temperature changes in
producing heat-dissipating responses.
Central Integrative Area. The central nervous system
(CNS) interprets information received from the thermosensors to
instruct thermoregulatory effectors properly. The concept of a
central thermostat whereby an alteration shifts effector thresholds
1755
1756 PART IV  Environment and Toxicology  |  SECTION One  Environment
Nuclei of the hypothalamus
Anterior commisure
Paraventricular nucleus
(water balance/stress)
Anterior hypothalamic
area (body temperature)
Medial peroptic
(blood pressure)
Frontal cortex
Optic nerve
Optic chiasm
Anterior pituitary
Fig. 133.1.  Preoptic anterior hypothalamus. (Adapted from Nuclei of the hypothalamus. bhavanajagat
.files.wordpress.com/2012/07/nuclei-of-hypothalamus.jpg.)
in the same direction fits a variety of clinical situations. For
example, fever, the circadian rhythm of temperature variation,
and the difference in rectal temperature after ovulation can be
explained by variation of a thermal set point.
Thermoregulatory Effectors. Sweating and peripheral
vasodilation are the major mechanisms whereby heat loss can be
accelerated. In a warm environment, evaporation of sweat from
the skin is the most important mechanism of heat dissipation.
Heat loss from the skin by convection and radiation is maximized
by increased skin blood flow to facilitate sweating.
Humans possess apocrine and eccrine sweat glands. Apocrine
glands are concentrated in the axillae and produce milky sweat,
rich in carbohydrate and protein. They are adrenergically inner-
vated and respond to emotional stress as well as to heat. Most
glands producing so-called thermal sweat are eccrine glands.
These are cholinergically innervated and distributed over the
entire body, with the largest number on the palms and soles.
Eccrine sweat is colorless, odorless, and devoid of protein. Indi-
viduals exercising in hot environments commonly lose 1 or
2 L/hr of sweat. A loss of up to 4 L/hr is possible with strenuous
exercise.
Cooling is best achieved by evaporation from the body surface;
sweat that drips from the skin does not cool the body. Each liter
of completely evaporated sweat dissipates 580 kcal of heat. The
ability of the environment to evaporate sweat is termed atmo-
spheric cooling power and varies primarily with humidity, but also
with wind velocity. As humidity approaches 100%, evaporative
heat loss ceases.
The vascular response to heat stress is cutaneous vasodilation
and compensatory vasoconstriction of the splanchnic and renal
beds. These vascular changes are under neurogenic control and
allow heat to be dissipated quickly and efficiently, but they place
a tremendous burden on the heart.7 To maintain blood pressure,
cardiac output increases dramatically. For this reason, saunas and
hot tubs may be dangerous for patients with cardiac disease.
Cardiovascular and baroreceptor reflexes also affect skin blood
flow. Reduced forearm sweating and vasodilation have been
observed in severely dehydrated subjects exercising in a warm
environment.
Acclimatization
Acclimatization is the constellation of physiologic adaptations
that occur in a normal person as the result of repeated exposures
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Lateral
hypothalamic area
Dorsal
hypothalamic area
Posterior hypothalamic
area (shivering)
Dorsomedial nucleus
(GI tract)
Mammillary body
(feeding)
Ventromedial nucleus
(satiety)
Suprachiasmatic
(biologic clock)
Supra optic nucleus
(water balance)
Posterior pituitary
to heat stress. Daily exposure to work and heat for 100 min/day
results in near-maximal acclimatization within 7 to 14 days.8,9 This
is characterized by an earlier onset of sweating (at a lower core
temperature), increased sweat volume, and lowered sweat sodium
concentration.9 Acclimatization is hastened by modest salt depri-
vation and delayed by high dietary salt intake.
The cardiovascular system plays a major role in acclimatization
and endurance training, largely resulting from an expansion of
plasma volume. Heart rate is lower and associated with a higher
stroke volume. Other physiologic changes include earlier release
of aldosterone, although acclimatized individuals generate lower
plasma levels of aldosterone during exercise heat stress. Total body
potassium depletion of up to 20% (500 mEq) by the second week
of acclimatization can occur as a result of sweat and urine losses,
coupled with inadequate repletion.
Although many similarities exist among thermoregulatory
responses to heat and exercise, the well-conditioned athlete is
not necessarily heat-acclimatized. For heat- and exercise-induced
adaptive responses to be maintained, heat exposure needs to
continue intermittently, at least on 4-day intervals. Plasma volume
decreases considerably within 1 week in the absence of heat stress.
Pathophysiology
Predisposing Factors
Advanced age, psychiatric conditions, chronic disease, obesity, and
certain medications increase the risk for classic heatstroke during
periods of high heat and humidity.10 Adequate fluid intake is
essential. Older adults often overdress during hot weather condi-
tions. Heat loss is maximized by light, loose-fitting garments.
Exertional heatstroke is most likely to occur in young healthy
people involved in strenuous physical activity, especially if they
have not acclimatized to environmental factors that overwhelm
heat-dissipating mechanisms. Fluid intake is the most critical
variable. Dehydration can be minimized by education on work-
rest cycles and fluid consumption and through provision of cool
flavored fluids.
The goal is to maximize voluntary fluid intake and gastric
emptying so that fluid can rapidly enter the small intestine, where
it is absorbed. Gastric emptying is accelerated to 25 mL/min by
large fluid volumes (500–600 mL) and cool temperatures (10° C–
15.8° C [50° F–60.4° F]). High osmolality inhibits gastric empty-
ing; osmolality of less than 200 mOsm/L is optimal. Most
commercially available electrolyte solutions contain excessive
 C H APTER 133  Heat Illness 1757

sugar. Hydration can be monitored by measurement of body
weight before and after training or athletic competition. An
athlete with a loss of 2% to 3% body weight (1.5–2 L in a 70-kg
man) should drink extra fluid and be permitted to compete only
when his or her body weight is within 0.5 to 1 kg (1 or 2 pounds)
of the starting weight on the previous day. A weight loss of 5% or
6% represents a moderately severe deficit and usually is associated
with intense thirst, scanty urine, tachycardia, and increase in rectal
temperature of approximately 2° C (3.6° F). These athletes should
be restricted to light workouts after hydration until they return to
normal weight. A loss of 7% or more of body weight represents
severe water depletion; participation in sports should not be
permitted until the athlete is evaluated by a physician or sports
trainer. Wrestlers frequently fast, restrict food and fluid intake,
and exercise vigorously wearing vapor-impermeable clothing to
lose weight quickly so that they can compete in a lower weight
class.
The administration of salt tablets during strenuous exercise
can cause delayed gastric emptying, osmotic fluid shifts into the
gut, gastric mucosal damage, and hypernatremic dehydration. A
6-g sodium diet is sufficient for successful adaptation for work in
the heat, with sweat losses averaging 7 L/day. Excessively high salt
intake in relation to salt losses in sweat during initial heat exposure
can impair acclimatization because of the inhibition of aldoste-
rone secretion. Excessive salt ingestion can also exacerbate potas-
sium depletion.
Evaporative cooling can be lost when clothing inhibits air
convection and evaporation.11 Loose-fitting clothing or ventilated
fishnet jerseys allow efficient evaporation. Light-colored clothing
reflects rather than absorbs light. Water evaporated from clothing
is much less efficient for body cooling than water evaporated from
the skin.
The body’s heat dissipation mechanisms are analogous to the
cooling system of an automobile (Fig. 133.2). Coolant (blood) is
circulated by a pump (heart) from the hot inner core to a radiator
(skin surface cooled by the evaporation of sweat). Temperature is
sensed by a thermostat (CNS), which alters coolant flow by a
system of pipes, valves, and reservoirs (vasculature). Failure of any
of these components can result in overheating.
ENVIRONMENTAL
HEAT STRESS
THERMOSTAT PUMP MALFUNCTION
MALFUNCTION • Cardiac disease
• Hypothalamic • β-Adrenergic
hemorrhage blocking drugs
H C
DAMAGED
CONDUCTING
SYSTEM
• Atherosclerosis
• Diabetes
F INCREASED HEAT
Effective circulation requires an intact pump and adequate
coolant levels. Individuals with cardiac disease or those taking
β-adrenergic blocking agents or calcium channel blockers may be
unable to increase their cardiac output sufficiently to produce the
necessary peripheral vasodilation to dissipate heat. Dehydration
caused by gastroenteritis, diuretics, or inadequate fluid intake
predisposes to heat illness. Individuals working in the heat seldom
voluntarily drink as much fluid as they lose and replace only
approximately two-thirds of net water loss (so-called voluntary
dehydration). Dehydration alone increases body temperature at
rest by increasing the work of the sodium-potassium adenosine
triphosphatase pump, which accounts for 25% to 45% of the
basal metabolic rate. This is particularly true in cases of hyperna-
tremic dehydration. The pipes and valves of the coolant system
may be abnormal in diabetic or older patients with extensive
atherosclerosis.
Radiator function depends on the skin and sweat glands.
Occlusive, vapor-impermeable clothing hinders evaporative and
convective cooling. Anticholinergic medications and stimulant
drugs of abuse interfere with sweating and contribute to heat
illness.12 Various skin diseases, including miliaria (prickly heat
rash), extensive burns, scleroderma, ectodermal dysplasia, and
cystic fibrosis, are risk factors. Anhidrosis can also be secondary
to central or peripheral nervous system disorders.
Increased heat production causing heat illness most often
accompanies exercise in a hot humid environment. When heat
and humidity are extreme, exertion is not necessary to produce
heat-related problems. Several indices help objectify heat strain.
These indices can be divided into two categories, heat scales based
on meteorologic parameters and heat scales that combine envi-
ronmental and physiologic parameters.
The wet bulb globe temperature heat index is an excellent
meteorologic measure of environmental heat stress (Box 133.1).
It includes the effects of temperature, humidity, and radiant
thermal energy from the sun. When climatic conditions exceed
25° C (77° F) wet bulb, even healthy people are at high risk during
exercise. Above 28° C (82.4° F), exercise and strenuous work
should be avoided or limited to extremely short periods.
The heat strain index is widely accepted as an example of
an index that includes environmental and physiologic factors.
There are several variations and modified heat strain indices, with
varying ease of use and accuracy.13
Fever Versus Hyperthermia
It is diagnostically and therapeutically important to identify
patients suffering from a febrile response rather than heat illness.
Fever does not cause primary pathologic or physiologic damage
to humans and does not require primary emphasis in the thera-
peutic regimen, which is directed at the underlying disease state.
If temperature-related physiologic changes, such as febrile seizures
BOX 133.1 

RADIATOR
PRODUCTION
• Exercise
Wet Bulb Globe Temperature (WBGT)
LOW E
MALFUNCTION • Drugs
COOLANT WBGT = 0.7Tn + 0.2Tg + Ta
• Drugs (sympathomimetics)
LEVELS
(anticholinergics) • Fever
• Dehydration
(vomiting,
• Skin disease • Delirium Tn = “Natural” wet bulb temperature—the temperature achieved by a
• Occlusive • Thyroid storm thermometer covered with a moistened white wick and left
diarrhea,
clothing • Malignant exposed to the ambient environment
diuretics)
hyperthermia Tg = Globe temperature—the temperature inside a blackened hollow
• Neuroleptic
malignant
copper sphere exposed to the ambient environment
syndrome Ta = Ambient temperature
• Seizures These measurements can be done manually or calculated
automatically with the help of computer algorithms.
Fig. 133.2.  Predisposing factors for heat illness, an automotive analogy.

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1758 PART IV  Environment and Toxicology  |  SECTION One  Environment
and tachycardia, compromise a patient with marginal cardiac
reserve, her or his temperature should be artificially regulated
with antipyretics. These antipyretics are not effective against
heat illness and are not recommended to control environmental
hyperthermia.
MINOR HEAT ILLNESS
Prickly Heat
Principles
Prickly heat, also known as miliaria rubra, lichen tropicus, and
heat rash, is an acute inflammatory disorder of the skin that
occurs in tropical climates. It is the result of the blockage of sweat
gland pores by macerated stratum corneum and secondary
staphylococcal infection. The acute phase is characterized by
vesicles in the malpighian layer of the skin, caused by dilation and
rupture of the obstructed sweat gland ducts.
Clinical Features
Clinically, this initially produces intensely pruritic vesicles on an
erythematous base. The rash is confined to clothed areas, and the
affected area is often completely anhidrotic. During approximately
the next week, a keratin plug develops and fills these vesicles,
causing a deeper obstruction of the sweat gland duct. The
obstructed duct then ruptures a second time, producing a deeper
vesicle within the dermis. This is known as the profunda stage,
and it can persist for weeks. Profunda vesicles are not pruritic and
closely resemble the white papules of piloerection; chronic der-
matitis is a common complication (Fig. 133.3).
Differential Diagnosis
Alternatives diagnoses include, contact dermatitis, cellulitis, and
allergic reactions.
Fig. 133.3.  Prickly heat. (From Habif TP: Clinical dermatology: a color
guide to diagnosis and therapy, ed 3, St. Louis, 1996, Mosby.)
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Diagnostic Testing
Laboratory data is generally not indicated in cases of prickly heat.
Management and Disposition
Chlorhexidine in a light cream or lotion is the antibacterial treat-
ment of choice during the acute phase. Salicylic acid, 1% tid, can
be applied to localized affected areas to assist in desquamation,
but it should not be used in children or over large areas because
of possible salicylate intoxication. For diffuse or pustular rashes,
erythromycin can be helpful.
Patients can be discharged home, with a dermatologic
follow-up. Prickly heat can be prevented by wearing light, loose-
fitting, clean clothing and avoiding situations that produce con-
tinuous sweating. The routine use of talcum or baby powder
should be avoided.
Heat Cramps
Principles
Heat cramps are brief, intermittent, and often severe muscle
cramps occurring typically in muscles that are fatigued by heavy
work. Heat cramps appear to be related to a salt deficiency.
They usually occur during the first days of work in a hot environ-
ment and develop in persons who produce large amounts of
thermal sweat and subsequently drink copious amounts of hypo-
tonic fluid.
Clinical Features
Athletes, roofers, steelworkers, coal miners, field workers, and
boiler operators are among the most common victims of heat
cramps. Heat cramps tend to occur after exercise, when the victim
stops working and is relaxing (Box 133.2). In this respect, they
differ from the cramps experienced by athletes during exercise,
which tend to last for several minutes, are relieved by massage,
and resolve spontaneously.
Differential Diagnosis
Heat cramps are occasionally confused with hyperventilation
tetany, which can occur during heat exhaustion. Hyperventilation
tetany can be distinguished by the presence of carpopedal spasm
and paresthesias in the distal extremities and perioral area.
Diagnostic Testing
Heat cramps accompanied by systemic symptoms may be part of
salt depletion heat exhaustion. Heat cramp victims exhibit hypo-
natremia and hypochloremia, so serum electrolyte levels should
be measured. Rhabdomyolysis or resultant renal damage is not
present with isolated heat cramps.
BOX 133.2 
Heat Cramps: Essentials of Diagnosis
Cramps of most worked muscles
Usually occur after exertion
Copious sweating during exertion
Copious hypotonic fluid replacement during exertion
Hyperventilation not present in cool environment

Management and Disposition
Heat cramps are usually rapidly relieved by salt solutions. Com-
mercially available flavored electrolyte solutions are commonly
ingested. Mild cases without concurrent dehydration are treated
orally with a 0.1% or 0.2% salt solution (two to four 10-grain salt
tablets [56–112 mEq] or 1 4 to 1 2 teaspoon of table salt dissolved
in 1 quart of water), which is the general limit of palatability.
Severe cases respond rapidly to an intravenous (IV), isotonic salt
solution (0.9% NaCl). Salt tablets are gastric irritants, delay gastric
emptying, and are not recommended. Although most patients do
not seek medical treatment, most people with heat cramps may
be safely discharged after the administration of balanced salt
solutions and clinical improvement.
Heat Edema
Principles
It is presumed that hydrostatic pressure and vasodilation of
cutaneous vessels, combined with some degree of orthostatic
pooling, lead to vascular leak and accumulation of interstitial fluid
in the lower extremities. Simultaneously, the aldosterone level
increases in response to the heat stress and perceived central
volume deficit.
Clinical Features
Swollen feet and ankles are often reported by nonacclimatized
individuals, especially older adults, who encounter climatic
stresses of tropical and semitropical areas. Such individuals often
have no underlying cardiac, hepatic, venous, or lymphatic disease.
They commonly have schedules that involve long periods of
sitting or standing. The edema is usually minimal, is not accom-
panied by any significant impairment in function, and often
resolves after several days of acclimatization.
Differential Diagnosis
Heat edema should be differentiated from congestive heart failure,
liver disease states, lower extremity infections, and deep venous
thrombosis.
Diagnostic Testing
Awareness of this clinical presentation prevents overly vigorous
diagnostic and therapeutic intervention. A brief diagnostic evalu-
ation to rule out thrombophlebitis, lymphedema, or congestive
heart failure is appropriate, but invasive diagnostic techniques are
not indicated.
Management and Disposition
Pharmacologic therapy is not indicated, and diuretic therapy is
not effective. Simple leg elevation or thigh-high support hose
should be used. In most individuals, the problem resolves through
adequate acclimatization or with the individual’s return to a
temperate climate. Given its benign nature, patients with heat
edema can be safely discharged for outpatient management.
Heat Syncope
Principles
Individuals adapt to a hot humid environment by dilation of
cutaneous vessels to deliver heat to the body surface. Thus, an
increased portion of the intravascular pool is located in the
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C H APTER 133  Heat Illness 1759
periphery at any given time. Increasing blood flow to compliant
cutaneous veins raises skin vascular volume at the expense of
thoracic blood volume. Individuals who stand for protracted
periods tend to pool blood in the lower extremities. Combined
with volume loss and peripheral vasodilation, this pooling can
result in inadequate central venous return, a concomitant drop in
cardiac output, and cerebral perfusion inadequate to maintain
consciousness.
Clinical Features
Heat syncope is a multifactorial disorder that results in a tempo-
rary loss of consciousness in the presence of heat exposure. Older
adults have a special predilection for this disorder, with a host of
concomitant underlying mechanisms.
Differential Diagnosis
The diagnosis of heat syncope requires the appropriate clini-
cal setting and exclusion of other possible causes of syncope,
given a patient’s age and underlying medical disorders (see
Chapter 12).
Diagnostic Testing
Heat syncope can be precipitated by an underlying metabolic or
cardiac disorder, so cardiac monitoring, electrocardiography, and
hemoglobin determination are warranted. Other tests are indi-
vidualized based on clinical suspicion following a thorough
history and physical examination (see Chapter 12).
Management and Disposition
The disorder is self-limited, and placing the patient in a horizontal
position is generally curative. Older patients with comorbidities
may require admission to address cardiac or neurologic causative
factors. These individuals are at risk for recurrent heat syncope
and should be warned to move often, flex leg muscles repeatedly
when standing stationary, avoid protracted standing in hot envi-
ronments, and assume a sitting or horizontal position when
prodromal warning symptoms or signs occur.
MAJOR HEAT ILLNESS
Heat Exhaustion
Principles
Heat exhaustion (heat prostration) is a clinical syndrome charac-
terized by volume depletion that occurs under conditions of heat
stress. Two types of heat exhaustion are classically described, water
depletion and salt depletion.
Water depletion heat exhaustion results from inadequate
fluid replacement by individuals working in a hot environment
and incapacitated individuals without free access to water.
Those working in the heat seldom drink as much as they lose,
and this voluntary dehydration results in progressive hypovole-
mia. Left untreated, water depletion heat exhaustion will pro-
gress to heatstroke because they are a continuum of the same
disease.
Salt depletion heat exhaustion takes longer to develop than the
water depletion form. It occurs when large volumes of thermal
sweat are replaced by water with too little salt. It differs from heat
cramps in that systemic symptoms occur. Symptoms are similar
to those seen in water depletion heat exhaustion; the body tem-
perature usually remains nearly normal.
1760 PART IV  Environment and Toxicology  |  SECTION One  Environment
BOX 133.3  BOX 133.4
Heat Exhaustion: Diagnosis
• Vague malaise, fatigue, headache
• Core temperature often normal; if elevated, <40° C (104° F)
• Mental function essentially intact; no coma or seizures
• Tachycardia, orthostatic hypotension, clinical dehydration
(may occur)
• Other major illness ruled out
• If in doubt, treat as heatstroke.
Clinical Features
The symptoms and signs associated with both types of heat
exhaustion are variable and include weakness, fatigue, frontal
headache, impaired judgment, vertigo, nausea and vomiting and,
occasionally, muscle cramps (Box 133.3). Orthostatic dizziness
and syncope can occur. Sweating persists and may be profuse. The
core temperature is only moderately elevated, usually below 40° C
(104° F), and signs of severe CNS dysfunction (eg, altered mental
status) are not present.
Differential Diagnosis
Mild heat exhaustion and full-blown heatstroke represent extremes
of the spectrum of heat illness, and intermediate cases may prove
difficult to differentiate. Nevertheless, heat exhaustion should not
be diagnosed in the presence of major CNS dysfunction (eg, sei-
zures, coma) or severe hyperthermia (40.5° C [104.9° F]).
Diagnostic Testing
This syndrome is characterized by hyponatremia, hypochloremia,
and low urinary sodium and chloride concentrations. The creatine
phosphokinase (CPK) level and renal function should be deter-
mined. Measurement of hepatic transaminase levels may prove
helpful. Elevations to several thousand units can be seen in
patients with heat exhaustion or in healthy runners after a mara-
thon, whereas in patients with heatstroke, such levels are usually
in the tens of thousands after 24 hours.
Management
Pure forms of either type of heat exhaustion are rare, and most
cases of heat exhaustion involve mixed salt and water depletion.
Heat exhaustion is primarily a volume depletion problem, and
rapid recovery generally follows fluid administration. Decisions
regarding the type of fluid and electrolyte replacements should be
based on serum electrolyte level measurements and the estimation
of hydration status by clinical and laboratory parameters.
Patients with significant volume depletion or electrolyte
abnormalities require IV fluids. Normal saline should be admin-
istered until vital signs normalize. Free water deficits should be
replaced slowly during 48 hours to avoid a decrease of serum
osmolality of more than 2 mOsm/hr. Overly rapid correction of
hypernatremia is associated with cerebral edema and seizures.
Disposition
Young, otherwise healthy patients who do not have significant
laboratory abnormalities and who respond rapidly to hydration
do not require hospitalization. These patients should be instructed
to drink plenty of fluids and avoid heat stress for 24 to 48 hours.
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Heat Exhaustion: Management
Rest
Cool environment
Assessment of volume status—orthostatic vital signs blood urea
nitrogen level, hematocrit, serum sodium concentration
Fluid replacement—normal saline to replete volume if the patient is
orthostatic; replace free water deficits slowly to avoid cerebral
edema.
Healthy young patients are usually treated as outpatients; consider
admission if the patient is older, has significant electrolyte
abnormalities, or would be at risk for recurrence if discharged.
Older patients, particularly those with cardiovascular disease
or other chronic diseases, may benefit from more cautious inpa-
tient fluid and electrolyte replacement and frequent reassessment
(Box 133.4).
Heatstroke
Principles
In the previously discussed forms of heat illness, although the
body temperature rises, homeostatic thermoregulatory mecha-
nisms remain intact. Heatstroke is the catastrophic life-threatening
emergency that occurs when these mechanisms fail. This failure
results in the elevation of body temperature to extreme levels,
usually higher than 40.5° C (105° F), producing multisystem tissue
damage and organ dysfunction.
As heatstroke develops, energy will be insufficient to sustain
thermoregulatory mechanisms, resulting in dramatic increases in
core temperature and the clinical manifestations of heatstroke.
Tissue damage is a function of a complex interaction of body
temperature, exposure time, workload, tissue perfusion, and
individual factors. The exact temperature at which cellular damage
begins to occur in an individual patient varies. Full recovery is
possible, despite rectal temperatures up to 46.5° C (115.7° F).
Neurologic dysfunction is a hallmark of heatstroke, and cere-
bral edema is common. Other pathologic changes include pete-
chiae in the walls of the third and fourth ventricles and marked
cerebellar Purkinje cell damage.14 Interestingly, the hypothalamus,
the predominant site of central thermoregulatory control, is
usually not damaged.
Heat stress creates tremendous demands on the cardiovascular
system, and patients who succumb to heatstroke show signs
of circulatory failure. Although such pathologic changes are
common, cardiac damage alone is not lethal.
Prolonged heat stress produces impressive increases in skin
blood flow (peripheral vasodilation) and a reduction of the
thermal gradient between the core and the skin (Fig. 133.4).
Functional hypovolemia is avoided by compensatory vasocon-
striction of the splanchnic and renal vasculatures. The resulting
splanchnic and renal ischemia may explain the nausea, vomiting,
and diarrhea observed in runners after a marathon. Hepatic
damage is a consistent feature of heatstroke, and its absence
should cast doubt on the diagnosis.
If severe heat stress continues, compensatory splanchnic
vasoconstriction will eventually fail, resulting in reduced mean
arterial pressure and a continued cascade of exaggerated systemic
inflammatory responses. Failure to perfuse the skin with heated
blood from the core results in a dramatically increased rate of heat
storage. This produces elevated intracranial pressure, which, in

Fig. 133.4.  Human infrared image. Note that the palms and face are
substantially warmer than the rest of the body. (From Auerbach PS:
Wilderness medicine, ed 6, Philadelphia, 2012, Mosby/Elsevier.)
BOX 133.5 
Heatstroke: Diagnosis
• Exposure to heat stress, endogenous or exogenous
• Signs of severe central nervous system dysfunction (coma, seizures,
delirium)
• Core temperature usually > 40.5° C (105° F), but may be lower
• Hot skin common, and sweating may persist
• Marked elevation of hepatic transaminase levels
combination with the reduction in mean arterial pressure caused
by failure of compensatory splanchnic vasoconstriction, conspires
to produce a decrease in cerebral blood flow. This results in the
major CNS dysfunction characteristic of heatstroke.
Clinical Features
Heatstroke Versus Heat Exhaustion.  The onset of heat-
stroke is sudden, and the patient’s level of consciousness is altered.
Prodromal symptoms lasting minutes to hours occur in approxi-
mately 20% of cases. These are nonspecific and may include
weakness, dizziness, nausea, vomiting, anorexia, frontal headache,
confusion, drowsiness, disorientation, muscle twitching, ataxia
and signs of cerebellar dysfunction, and psychiatric symptoms,
ranging from anxiety and irritability to psychosis. These prodro-
mal symptoms are reminiscent of the description of heat exhaus-
tion. Heat exhaustion, particularly the water depletion variety, can
progress to heatstroke if untreated.
The usual manifestations of heatstroke include hyperpyrexia
above 40.5° C (105° F), profound CNS dysfunction, and hot skin
(Box 133.5). Persistent sweating can be observed in patients with
rectal temperatures of 41.5° C to 42.4° C (106.7° F–108.3° F). In
one large series of exertional heatstroke victims, sweating persisted
in 50% of cases. Therefore, the cessation of sweating is not the
cause of heatstroke, and continued sweating does not preclude the
diagnosis.
Although in heatstroke the core temperature is elevated above
40.5° C (105° F), significant cooling may occur in the out-of-
hospital phase, and the first temperature obtained in the emer-
gency department (ED) may not represent the original maximum
core temperature.
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C H APTER 133  Heat Illness 1761
TABLE 133.1 
Characteristics of Classic Versus
Exertional Heatstroke
EXERTIONAL CLASSIC
Healthy Predisposing factors or medications
Younger Older
Exercise Sedentary
Sporadic Heat wave occurrence
Diaphoresis Anhidrosis
Hypoglycemia Normoglycemia
DIC Mild coagulopathy
Rhabdomyolysis Mild CK level elevation
Acute renal failure Oliguria
Marked lactic acidosis Mild acidosis
Hypocalcemia Normocalcemia
CK, Creatine kinase; DIC, disseminated intravascular coagulation.
Classic Heatstroke Versus Exertional Heatstroke. The
two forms of heatstroke have significantly different presentations
and manifestations—classic (epidemic) heatstroke (CHS) and
exertional heatstroke (EHS; Table 133.1).
CHS occurs during periods of sustained high ambient tem-
peratures and humidity, such as during summer heat waves.
Victims are often older adults and poor and live in underventilated
dwellings without air conditioning. Debilitated patients who have
limited access to oral fluids may develop water depletion heat
exhaustion, which progresses to heatstroke if untreated. Victims
of CHS commonly suffer from chronic diseases, alcoholism, or
schizophrenia, which predisposes to heat illness. Such patients are
often prescribed medications (eg, diuretics, antihypertensives,
neuroleptics, anticholinergics) that impair the ability to tolerate
heat stress. Sweating ceases in most CHS patients. Factors such as
advanced age, hypotension, altered coagulation status, and the
necessity for endotracheal intubation on arrival at the ED predict
a poor outcome, despite successful cooling measures.
In contrast, patients with EHS are usually young and healthy
individuals whose heat-dispelling mechanisms are overwhelmed
by endogenous heat production. Athletes and military recruits are
typical victims. Rhabdomyolysis and acute renal failure, rarely
seen in patients with CHS, are common in patients with EHS.
Sweating is present in 50% of cases of EHS. Hypoglycemia may
occur as the result of increased glucose metabolism and hepatic
damage, resulting in impaired gluconeogenesis. Coagulopathy is
common; the mechanism is depicted in Fig. 133.5.
Hyponatremia with serum sodium levels of less than
130 mmol/L has been detected in summer hikers in the Grand
Canyon; many were found to have with neurologic symptoms or
seizures. Signs of profound CNS dysfunction dominate the early
course of heatstroke. Delirium or coma is characteristic, but virtu-
ally any neurologic abnormality, including bizarre behavior,
opisthotonos, hallucinations, decerebrate rigidity, oculogyric
crisis, and cerebellar dysfunction, can be seen. Convulsions occur
in up to 75% of patients and can be precipitated by therapeutic
cooling maneuvers. Profound muscle rigidity with tonic contrac-
tions, coarse tremor, and dystonic movements can mimic seizures.
Pupils may be fixed and dilated, and the electroencephalogram
may be isoelectric. All these changes are potentially reversible,
although permanent damage, including cerebellar deficits, hemi-
plegia, dementia, and personality changes, is common in severe
1762 PART IV  Environment and Toxicology  |  SECTION One  Environment
Hyperthermia
Activation Fibrinolysis Endothelial
of damage
clotting
Hepatic factors Megakaryocyte
damage damage
Intravascular Thrombolysis
clotting and
defibrination
Depletion Thrombocytopenia
of
clotting FSP
factors (anticoagulants)
Hemorrhage
Fig. 133.5.  Pathogenesis of hemorrhage. FSP, Fibrin split products.
cases. Patients with heatstroke usually have hyperdynamic cardio-
vascular systems with low peripheral vascular resistance, tachycar-
dia (up to 180 beats/min), and an elevated cardiac index.7 Elevation
of cardiac troponin I is not uncommon with CHS; however, it is
rarer in EHS. The central venous pressure (CVP) is usually ele-
vated. The combination of elevated CVP with right-sided cardiac
dilation suggests right-sided heart failure, which is also seen after
shock or sepsis.15 These changes are expected because skin blood
vessels dilate to dissipate heat; however, this low peripheral vas-
cular resistance has persisted in patients after reduction of body
temperature to nearly normal.
Respiratory alkalosis is a physiologic response to active or
passive heating and may be severe enough to produce tetany.
Although most patients with CHS have respiratory alkalosis, those
with EHS usually have a relatively pure lactic acidosis. Lactic
acidosis is associated with a poor prognosis in cases of CHS but
not necessarily in cases of EHS. Both CHS and EHS cause the
hemoglobin-oxygen dissociation curve to shift to the right. An
increase in the temperature denatures the bond between oxygen
and hemoglobin, decreasing the concentration of oxyhemoglobin.
Aberrations in coagulation are common in patients with severe
heatstroke, and their presence is a poor prognostic sign. Abnormal
hemostasis is manifested clinically by purpura, conjunctival
hemorrhage, melena, bloody diarrhea, hemoptysis, hematuria,
myocardial bleeding, or hemorrhage into the CNS. Diarrhea,
probably caused by intense splanchnic vasoconstriction, is com-
monly seen. Cooling aggravates the diarrhea, creating an unpleas-
ant treatment problem. Pancreatitis is described, with elevated
serum amylase and lipase levels.
Differential Diagnosis
Heatstroke occurs when the thermoregulatory responses are
overwhelmed and fail. If the patient is evaluated as this is occur-
ring, differentiation between heat exhaustion and heatstroke is
difficult. If heatstroke cannot be excluded, efforts to cool the
patient should begin immediately. Only after the initial assess-
ment and cooling have been initiated is the differential diagnosis
relevant. When a history of collapse under conditions of heat
stress is present, rapid improvement in mental status and blood
pressure with cooling essentially eliminates alternative diagnoses.
If, however, the temperature does not respond, and the patient
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BOX 133.6 
Differential Diagnosis of Heatstroke
• Central nervous system hemorrhage
• Toxins, drugs
• Seizures
• Malignant hyperthermia
• Neuroleptic malignant syndrome
• Serotonin syndrome
• Thyroid storm
• High fever, sepsis
• Encephalitis, meningitis
does not recover neurologically, other causes of fever and coma
should be considered (Box 133.6).
Meningitis and Encephalitis. These can masquerade as
heatstroke. In patients with heatstroke, the spinal fluid should be
clear, with occasional lymphocytic pleocytosis and elevated
protein levels. Cerebral falciparum malaria, which has a clinical
picture of high fever and encephalitis, is seen in tropical areas
where heat illness can also occur.
Thyroid Storm.  In patients with thyroid storm, the clinical
symptoms resemble those of heatstroke. It should be suspected if
the thyroid gland is enlarged or nodular, but a normal thyroid
gland does not exclude the diagnosis. Thyroid function test
results are elevated, but these are not available on an emergency
basis. Fortunately, thyroid storm is rare, and some critical aspects
of treatment, such as rapid cooling, coincide with those for
heatstroke.
Drug-Induced Heat Illness.  This is an important consider-
ation, particularly anticholinergic poisoning. Differentiation may
be difficult because heatstroke and anticholinergic poisoning
cause hyperpyrexia, hot and dry skin, tachycardia, and abnormal
mental status. Constricted pupils are present in many heatstroke
patients. Mydriasis should be present in patients with anticholin-
ergic poisoning, and its absence argues strongly against this
diagnosis. Typhoid fever, typhus, delirium tremens, and hypotha-
lamic hemorrhage all produce a symptom complex similar to that
of heatstroke.
Drug overdose of sympathomimetics or stimulants, such as
amphetamines, cocaine, and phencyclidine, can cause fatal hyper-
pyrexia. A high ambient temperature is associated with a signifi-
cant increase in mortality from cocaine overdose. Many younger
patients who die of hyperthermia test positive for cocaine. Heat-
stroke can occur with delirium resulting from ethanol withdrawal.
Aspirin and clopidogrel attenuates the skin vasodilatory response
and shifts the onset of peripheral thermoeffector mechanisms
toward a higher body temperature during exercise heat stress.14
Heatstroke has occurred in well-trained military soldiers and
athletes who ingested dietary supplements containing ephedrine
or the ergogenic aid creatine. Some antipsychotics also cause
suppression of thirst recognition. Individuals with a history of
heatstroke, with or without an inherent aberration that predis-
posed them to the initial episode, are at increased risk for a
recurrence.
Neuroleptic Malignant Syndrome. This is induced by
antipsychotic medications and is characterized by muscle rigidity,
severe dyskinesia or akinesia, hyperthermia, tachycardia, dyspnea,
dysphagia, and urinary incontinence. Although the so-called lead

pipe rigidity and hyperthermia are reminiscent of malignant
hyperthermia, the putative mechanism is different. Dopamine
receptor blockade in the corpus striatum caused by butyrophe-
nones (eg, haloperidol) and similar agents produces severe muscle
spasticity and dystonia, leading to the overproduction of heat (see
Chapter 155).
Serotonin Syndrome. This can also mimic heatstroke
because of the elevated body temperature tremors, clonus, and
CNS alterations that occur. Serotonin syndrome is classically a
triad of mental status changes, autonomic hyperactivity, and
neuromuscular abnormalities secondary to increased CNS sero-
tonergic activity. A history of recent exposure to an illicit or thera-
peutic medication is an important clue (see Chapter 146).
Diagnostic Testing
Most standard measurements of body temperature vary signifi-
cantly from the actual core temperature. Oral thermometry is
affected by mouth breathing and is a poor approximation of the
core. Rectal thermometry is less variable but responds to changes
in core temperature slowly. Thermistors that are inserted 15 cm
into the rectum offer continuous monitoring of temperature and
have less variability. Although rectal measurements are slower to
respond to changes in core temperature than tympanic tempera-
ture readings, rectal measurements are not biased by head skin
temperature. An esophageal thermistor positioned adjacent to the
heart is another option.
The hematologic evaluation should include arterial blood gas
determination, complete blood cell and platelet counts, electrolyte
values (including calcium), and glucose, blood urea nitrogen, and
serum creatinine levels. Hypoglycemia with a serum glucose level
less than 65 mg/dL is often found in cases of EHS. With the risk
of acute rhabdomyolysis, the creatine kinase and myoglobin levels
should be measured and urinalysis performed. Severe heatstroke
can induce disseminated intravascular coagulation (DIC); there-
fore, prothrombin and partial thromboplastin times, international
normalized ratio, and fibrin degradation products should be
measured. Serum cardiac troponin I levels should be obtained.12,16
Metabolic acidosis is common, especially in patients with EHS.
Lactate levels are usually elevated and may persist or even worsen
with improved extremity perfusion.
Renal damage is common. The initial urine specimen, usually
obtained by catheterization, is a scanty, brownish, turbid fluid
resembling machine oil. Microscopic examination reveals protein-
uria, with abundant granular casts and red blood cells. Acute
oliguric renal failure complicates 25% to 30% of EHS cases and
5% of CHS cases. The glomerular filtration rate, renal plasma
flow, urine flow, and sodium excretion diminish markedly during
exercise. Heavy physical exertion in hot climates produces acidic
and maximally concentrated urine, which can result in acute
oliguric renal failure in combination with hypotension and
myoglobinuria.
Because heatstroke patients are prone to liver failure, aspartate
transaminase, alanine transaminase, lactate dehydrogenase, and
other liver enzyme levels should be monitored. Hepatic transami-
nase level elevations may be diagnostically helpful. In most febrile
states that include altered mental status or coma, these enzyme
levels will be normal or minimally elevated, although they are
usually dramatically elevated early in the course of heatstroke.
Hepatic damage is consistently featured in heatstroke. Hepatic
injury is evidenced by markedly elevated levels of hepatic amino-
transferases (serum aspartate transaminase and alanine transami-
nase). Early experimental models have shown that high-mobility
group box 1(HMGB1) as a mediator of systemic inflammation is
elevated in heatstroke, and its inhibition may be liver-protective.15,17
Jaundice typically appears 24 to 72 hours after the onset of severe
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C H APTER 133  Heat Illness 1763
heatstroke and gradually recedes if the victim survives. Survivors
generally have no permanent impairment of liver function.
Management
Cooling.  Immediate cooling is the cornerstone of treatment.
Patients who present to the hospital with heatstroke have high
mortality rates ranging from 21% to 63%, and mortality increases
significantly when cooling is delayed. A thermistor probe should
be inserted as soon as possible, and the patient’s temperature
should be continuously monitored.
Evaporative cooling is recommended because it is effective,
easy to perform, noninvasive, and less likely to interfere with other
patient care activities than other cooling techniques. The patient
is stripped of all clothing, and tepid tap water is sprayed while fans
blow air continuously over the body, causing evaporative cooling.
One reported method of evaporative cooling uses a body cooling
unit on which the patient lies suspended on a net surface while
being sprayed with atomized 15° C (59° F) water from above and
below. Air warmed to 45° C to 48° C (113° F–118.4° F) is blown
over the skin surface at a rate of 3 m/min. This approach maxi-
mizes evaporative cooling by maintaining cutaneous vasodilation
and avoiding heat generation caused by shivering. When the
patient’s body temperature reaches 39° C (102.2°  F), cooling
measures should be discontinued to avoid hypothermic overshoot.
Continuous monitoring is necessary to maintain the core tem-
perature at 37° C to 38° C (98.6° F–100.4° F).
Immersion in ice water results in a rapid reduction of core
temperature to below 39° C within 10 to 40 minutes but can
complicate the resuscitation process. Vigorous skin massage to
maintain cutaneous circulation has been advocated, but there is
no evidence that this is efficacious. Military studies of EHS
patients treated with ice water immersion have reported no fatali-
ties or permanent sequelae. Immersion is technically difficult
in the ED. Vasoconstriction from ice water immersion may
be beneficial to hypotensive patients and may be better than
evaporative cooling for victims in shock who have poor peripheral
circulation.
Cooling modalities other than evaporation and immersion
should be considered adjunctive treatments (Box 133.7). Applica-
tion of ice packs to high heat transfer areas (eg, neck, groin,
axillae) is commonly used. Cooling blankets may be a useful
adjunct but will not produce rapid cooling if used exclusively.
Cold irrigant gastric or rectal lavage will not provide significant
heat exchange if used as the primary cooling modality. Antipyret-
ics have no role in the treatment of heat-related illness.18
BOX 133.7 
Cooling Modalities to Lower Body Temperature
in Heatstroke
PREFERRED
Evaporative cooling with large circulating fans and skin wetting
Ice water immersion
ADJUNCTS
Ice packs to axillae and groin
Cooling blanket
Peritoneal lavage (unproven efficacy in humans)
Rectal lavage
Gastric lavage
Cardiopulmonary bypass
1764 PART IV  Environment and Toxicology  |  SECTION One  Environment
Resuscitation.  Mortality correlates with the temperature
and number of dysfunctional organ systems, with an increased
risk of death if patients present with anuria, coma, or cardiovas-
cular failure. Aspiration and seizures are common in patients with
heatstroke, and airway control is indicated. Hypoxemia may occur
because of aspiration, pneumonitis and pulmonary infarction,
hemorrhage, or edema. Metabolic demands are high, and normal
pulmonary ventilation may be inadequate in this setting.
Crystalloid fluid resuscitation is essential. Circulatory fluid
requirements are modest in some cases, averaging 1200 mL of
isotonic crystalloid solution in the first 4 hours. Pulmonary edema
occurs in patients with heatstroke and can be exacerbated by
overzealous fluid administration. The use of a CVP catheter to
monitor fluid resuscitation may be deceptive. Most patients have
a hyperdynamic circulation with a high cardiac index, low periph-
eral vascular resistance, and elevated CVP as a result of right-sided
heart failure. These patients may require only modest IV fluids
because cooling produces vasoconstriction and increases blood
pressure. Hypotension is common in patients with heatstroke and
is usually caused by peripheral vasodilation resulting in high-
output cardiac failure in addition to dehydration. Blood pressure
usually rises with cooling. If this does not occur, or if the patient
being monitored invasively has a low CVP, a fluid challenge of 250
to 500 mL of 0.9% saline should be given rapidly while blood
pressure, pulse, and urine output are monitored. Fluid replace-
ment is continued until the blood pressure reaches 90/60 mm Hg
or the CVP exceeds 12 mL H2O. On occasion, patients exhibit
hypodynamic responses with a low cardiac index, elevated CVP,
and hypotension. These patients may be cyanotic, whereas patients
with hyperdynamic circulation are initially pink. This clinical
observation can be helpful in identifying patients who may
respond to catecholamines.
A variety of tachyarrhythmias commonly occur during heat-
stroke. These usually resolve with cooling, and electrical cardio-
version should be avoided until the myocardium is adequately
cooled. The use of α-adrenergic agents such as norepinephrine is
not recommended because they promote vasoconstriction without
improving cardiac output or perfusion, decrease cutaneous heat
exchange, and may exacerbate ischemic renal and hepatic damage.
Atropine and other anticholinergic drugs that inhibit sweating
should be avoided.
The pathophysiologic processes of heatstroke and fever differ,
so antipyretics are not indicated and may be harmful. Salicylates,
KEY CONCEPTS
• Classic heatstroke is generally diagnosed in older patients with
comorbidities during heat waves, whereas exertional heatstroke is
more common in young athletic patients or military personnel.
• Patients with exertional heatstroke are commonly diaphoretic.
• Rapid cooling of the potential heatstroke patient should be initiated
before the diagnosis is firmly established. The most effective
minimally invasive cooling measure is with evaporative techniques
using cool mist sprays and standing fans.
The references for this chapter can be found online by accessing the accompanying Expert Consult website.
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particularly in large doses, may worsen hyperthermia by uncou-
pling oxidative phosphorylation and aggravating coagulopathies.
Large doses of acetaminophen can result in further hepatic
damage. The efficacy of dantrolene has not been established.
If rhabdomyolysis is present, maintenance of urinary output
of at least 2 mL/kg/hr is recommended. Urinary alkalinization
higher than a pH of 6.5 should be considered early in these
patients with acidemia, dehydration, or underlying renal disease.
After volume repletion, administration of mannitol may be con-
sidered to increase intravascular volume and increase the glo-
merular filtration rate. Mannitol should not be used in an oliguric
patient. Persistent anuria, uremia, or hyperkalemia is an indica-
tion for consideration of hemodialysis.
Cooling modalities that drastically lower skin temperature may
induce violent shivering; this increases metabolic heat production
and may impede cooling. IV benzodiazepines are the treatment
of choice for shivering. The administration of neuroleptics, like
chlorpromazine, should be avoided. These agents have anticholin-
ergic properties that can interfere with sweating and cause
hypotension or precipitate seizures. Many patients are extremely
agitated during the initial cooling period. Short-acting benzodi-
azepines can be used for sedation and to control seizures. Barbi-
turates are less desirable because the metabolism is altered by
hepatic dysfunction.
Coagulopathies can occur during the first day of illness but are
more common on the second and third days. Initial treatment
after cooling should include replacement therapy with fresh-
frozen plasma and platelets. The emergency clinician should
monitor the laboratory signs of DIC—(hypofibrinogenemia,
elevated fibrin split products, prolonged prothrombin time,
and thrombocytopenia. The bleeding diathesis seen in patients
with heatstroke may be the result of fibrinolysis. Although
α-aminocaproic acid can impede fibrinolysis, administration of
this compound is associated with rhabdomyolysis, and its use is
not recommended in patients with heatstroke.
Disposition
Patients presenting with classic or exertional heat stroke should
be stabilized in the ED, with admission to an intensive care setting.
Patients with more complex end-organ damage (eg, renal failure
requiring dialysis) may require transfer to a center with more
comprehensive tertiary care capabilities.
• Antipyretics are ineffective and should not be used to control
environmental hyperthermia.
• Heatstroke can cause right-sided cardiac dilation and elevated CVP
and clinically resemble pulmonary edema, but still requires vigorous
crystalloid resuscitation.

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CHAPTER 133: QUESTIONS & ANSWERS
133.1. An 18-year-old female marathon runner presents to the
ED during a hot summer race. She is extremely irritable
and diaphoretic. She is complaining of generalized
weakness, dizziness, nausea, and headache. The physical
examination reveals an oral temperature of 40.5° C
(105° F), heart rate of 120 beats/min, muscle twitching,
and ataxia. What is the most appropriate management?
A. Assess her volume status and immediately start
normal saline to replete volume loss before transfer to
a hospital.
B. Encourage her to drink cold water to replace her free
water deficit rapidly.
C. Immediately remove her from the hot environment
and begin cooling before transfer to a hospital.
D. Prescribe immediate rest, after which she may be
allowed to finish the race.
Answer: C. The onset of heatstroke is sudden. Prodromal symp-
toms lasting minutes to hours can occur that are nonspecific and
similar to those of heat exhaustion. Signs and symptoms may
include weakness, dizziness, nausea, frontal headaches, confusion,
muscle twitching, ataxia and signs of cerebellar dysfunction, and
psychiatric symptoms, ranging from anxiety and irritability to
psychosis. Heat exhaustion can progress to heatstroke if it is
untreated. If the patient is evaluated as this is occurring, differen-
tiation between heat exhaustion and heatstroke is difficult. If
heatstroke cannot be excluded, efforts to cool the patient should
begin immediately.
Whereas rest is part of the treatment for heat exhaustion, it is
not the only treatment. She must be removed from the hot envi-
ronment, not be allowed to finish the race, and assessed for her
volume status. Normal saline is used to replete volume if the
patient is orthostatic; free water deficits are replaced slowly to
avoid cerebral edema.
133.2. Which of the following statements regarding heat
exhaustion is true?
A. It causes body temperatures that often exceed 40.5° C
(105° F).
B. It exists in two discrete forms, salt depletion and
water depletion.
C. It is associated with systemic symptoms.
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C H APTER 133  Heat Illness 1764.e1
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D. It is characterized by hyponatremia and
hyperchloremia.
E. It occurs when muscles are fatigued by heavy work.
Answer: C. Heat exhaustion is a clinical syndrome. Whereas there
are typically two types of heat exhaustion, water depletion and
salt depletion, pure forms of either type are rare. Most cases of
heat exhaustion involve mixed salt and water depletion. In salt
depletion heat exhaustion, the syndrome is characterized by
hyponatremia, hypochloremia, and low urinary sodium and
chloride concentrations. The symptoms and signs associated are
variable and nonspecific but usually systemic, such as weakness,
fatigue, frontal headache, vertigo, nausea, and vomiting. The body
temperature usually remains nearly normal.
133.3. Despite cooling measures, poor outcomes are seen in
heatstroke patients with which of the following?
A. Altered coagulation status
B. History of schizophrenia
C. Need for 100% oxygen
D. Presentation with acute renal failure
E. Presentation with acute rhabdomyolysis
Answer: A. Factors such as advanced age, hypotension, altered
coagulation status, and the necessity for endotracheal intubation
on arrival at the ED predict a poor outcome, despite successful
cooling measures.
133.4. The usual characteristics of classic heatstroke include
which of the following?
A. Diaphoresis
B. Disseminated intravascular coagulation
C. Hypoglycemia
D. Marked lactic acidosis
E. Usual occurrence during heat waves
Answer: E. Usual characteristics of classic heatstroke include
predisposing factors or medication, older population, sedentary
lifestyle, anhidrosis, normoglycemia, mild coagulopathy, mild
elevation in creatine kinase level, oliguria, mild acidosis, and
occurrence during heat waves. Diaphoresis, hypoglycemia, dis-
seminated intravascular coagulation, and marked lactic acidosis
are characteristics of exertional heatstroke.