medical disorders comprise a spectrum of illness that
can result from excessive exposure to hot environments:
heat syncope, hear cramps, heat exhaustion, and heat
stroke. A stable internal temperature requires a balance
between heat production and heat loss, which the hypothalamus
regulates in initiating changes in muscle tone, vascular
tone, and sweat gland function.
production and evaporation is a major mechanism of
heat removal. Conduction - the direct transfer of
heat from the skin to the surrounding air - also occurs,
but with diminished efficiency as the ambient temperature
rises. The passive transfer of heat from a warmer
to a cooler object by radiation accounts for 65% of
body heat loss decreases as the temperature of the
surrounding environment increases up to 37.2, the
point at which heat transfer reverses direction. At
normal temperatures, evaporation accounts for approximately
20% of the body's heat loss, but at high temperature
is becomes the major mechanism for dissipation of
heat; with vigorous exertion, sweat loss can be as
much as 2.5 L/h. This mechanism is also limited as
Health conditions that inhibit sweat production or
evaporation and increase susceptibility to heat disorders
include obesity, generalized skin diseases, diminished
cutaneous blood flow, dehydration, malnutrition, hypotension,
and reduced cardiac output. Medications that impair
the sweating mechanism are the anticholinergics, antihistamines,
phenothiazines, tricyclic antidepressants, monoamine
oxidase inhibitors, and diuretics; reduced cutaneous
blood flow results from use of vasoconstrictors and
- adrenergic blocking agents; and dehydration results
from use of alcohol. Illicit drugs eg, phencyclidine,
LSD, amphetamines, and cocaine - can cause increased
muscle activity and thus generate increased body heat.
Drug withdrawal syndromes may have the same effect,
as may prolonged seizures.
The risk of heat disorder also increased with age,
impaired cognition, concurrent illness, reduced physical
fitness, and insufficient acclimatization.
evaluation and monitoring should be used to identify
individuals at increased risk of heat disorders. The
exposed public should be made aware of the early symptoms
and signs of heat disorders. It is not recommended
to make salt tablets available for use without medical
supervision; close monitoring of fluid and electrolyte
intake may be necessary in situations necessitating
activity in hot environments. Athletic events should
be organized and managed with attention to thermoregulation:
the WBGT Index should be encouraged, and medical support
should be immediately accessible. Competition is not
recommended when the WBGT exceeds 28 C. Workers should
not begin work in hot temperatures without proper
acclimatization and should be encouraged to drink
water or balanced electrolyte fluids frequently.
Protective cooled suits have been used successfully
in industry for prolonged work in environment up to
Acclimatization is achieved by scheduled regulated
exposure to hot environments and by gradually increasing
the duration of exposure and the work load until the
body adjusts by starting to produce sweat of lower
salt content in greater amounts at later ambient temperatures.
Acclimatization is accompained by increased plasma
volume, cardiac output, and cardiac stroke volume
and a slower heart rate.
SYNDROMES DUE TO HEAT EXPOSURE
unconsciousness can result from cutaneous vasodilation
with consequent systemic and cerebral hypotension.
Systolic blood pressure is usually less than 100 mm
Hg, and there is typically a history of vigorous physical
activity for 2 hours or more just preceding the episode.
The skin is typically cool and moist and the pulse
Treatment consist of rest and recumbency in a cool
place, with fluids by mouth
and electrolyte depletion can result in slow, painful
skeletal muscle contractions and even severe muscle
spasms lasting 1 - 3 minutes, usually of the muscles
most heavily used. Cramping results from salt depletion
as sweat losses are replaced with water alone. The
skin is moist and cool, and the muscles are tender.
There may be muscle twitching. The victim is alert,
with stable vital signs, but may be agitated and complaining
of pain. The body temperature may be normal or slightly
increased. Involved muscle groups are hard and lumpy.
There is almost always a history of vigorous activity
just preceding the onset of symptoms. Laboratory evaluation
may show low serum sodium, hemoconcentration, and
elevated urea and creatinine.
The patient should be moved to a cool environment
and given oral saline solution to replace both salt
and water. Because of their slower absorption, salt
tablets are not recommended. The victim may have to
rest for 1 - 3 days with continued dietary salt supplementation
before returning to work or resuming strenuous activity
in the heat.
exhaustion results from prolonged heavy activity with
inadequate salt intake in a hot environment and is
characterized by dehydration, sodium depletion, or
isotonic fluid loss with accompanying cardiovascular
The diagnosis is based on prolonged symptoms and a
rectal temperature over 37.8 C, increased pulse rare
- usually more than half again the patient's normal
rate - and moist skin. Symptoms associated with heat
syncope and heat cramps may also be present. The patient
may be quite thirsty and weak, with central nervous
system symptoms such as headache, fatigue, and, in
cases due chiefly to water depletion, anxiety, paresthesias,
impaired judgment, hysteria, and occasionally psychosis.
Hyperventilation secondary to heat exhaustion can
lead to respiratory alkalosis. Heat exhaustion may
progress to heat stroke if sweating ceases.
Treatment consist of patient location in a shaded,
cool environment, providing adequate hydration, salt
replenishment - orally, if possible - and active cooling
if necessary. Physiologic saline or isotonic glucose
solution can be administered intravenously in severe
cases or when oral administration is not appropriate.
Intravenous 3% saline may be necessary if sodium depletion
is severe. At least 24 hours of rest is recommended.
stroke is a life - threatening medical emergency resulting
from failure of the thermoregulatory mechanism. Heat
stroke is imminent when the core temperature approaches
41 C. It presents in one of two forms: Classic heat
stroke occurs in patients with compromised hoemostatic
mechanism: exertional heat stroke occurs in previously
healthy persons undergoing strenuous exertion in a
thermally stressful environment. Morbidity or even
death can result from cerebral , cardiovascular, hepatic,
or renal damage.
The hallmarks of heat stroke are cerebral dysfunction
with impaired consciousness, high fever, and absence
of sweating. Persons at greatest risk are the very
young, the elderly or chronically infirm, and patients
receiving medications that interfere with heat-dissipating
Exertional heat stroke and exertion - related illnesses,
including rhabdomyolysis, are appearing more frequently
as including rhabdomyolysis, are appearing more frequently
as complications of participation by unconditioned
amateurs in strenuous athletic activities such as
marathon running and triathlon competition.
Symptoms and Signs
Failure of the heat dissipation mechanism for any
reason result in dizziness, weakness, emotional liability,
nausea and vomiting, diarrhea, confusion, delirium,
blurred vision, convulsions, collapse, and unconsciousness.
The skin is hot and initially covered with perspiration.
Later it dries. The pulse is strong initially. Blood
pressure may be slightly elevated at first, but hypotension
develops later. The core temperature is usually over
41 C. As with heat exhaustion, hyperventilation can
occur, leading to respiratory alkalosis.
Exertional heat stroke may present with sudden collapse
and loss of consciousness followed by irrational behavior.
Anhidrosis may not be present. Twenty-five percent
of heat stroke victims have prodromal symptoms for
minutes to hours that may include dizziness, weakness,
nausea, confusion, disorientation, drowsiness, and
Laboratory Findings :
Laboratory evaluation may reveal dehydration leukocytosis,
elevated BUN, hyperuricemia, hemoconcentration, acid-base
abnormalities, and decreased serum potassium, sodium,
calcium, and phosphorus; urine is concentrated, with
elevated protein, tubular casts, and myoglobinuria.
Thrombocytopenia, increased bleeding and clotting
times, fibrinolysis, and consumption coagulopathy
may also be present. Rhabdomyolysis and myocardial,
hepatic, or renal damage may be identified by elevated
serum creatine kinase and aminotransferase levels
and BUN and by the presence of anuria, proteinuria,
and hematuria. Electrocardiographic findings may include
ST - T changes consistent with myocardial ischemia.
Treatment is aimed at reducing the core temperature
rapidly and controlling the secondary effects. Evaporative
cooling is rapid and effective and is easily performed
in most emergency settings. The patient's clothing
should be removed and the entire body sprayed with
water while cooled or ambient air is passed across
the patient's body with large fans or other means
at high velocity. The patient should be in the lateral
recumbent position or supported in a hands - and -
knees position to expose as much skin surface as possible
to the air. Other alternatives include use of cold
wet sheets accompained by fanning or immersion in
chilled water. Cardiopulmonary bypass provides rapid
cooling but is often not practical.
Immersion is an ice-water bath as initial treatment
is no longer preferred because of its greater potential
for complications of hypotension and shivering. However,
it should be considered if core temperature is not
decreased rapidly in response to other treatment.
Alternatives include hand forearm immersion in cold
water, ice packs, and iced gastric lavage, though
these are much less effective than evaporative cooling.
Treatment should be continued until the rectal temperature
drops to 30 C. The temperature remains stable in most
cases, but it should continue to be monitored for
24 hours. Chlorpromazine or diazepam can be give initially
and then every 4 hours to control shivering and other
muscular activity associated with increased heat load.
Antipyretics have no effect on environmentally induced
hyperthermia and are contraindicated.
Hypovolemic and cardiogenic shock must be carefully
distinguished, as either or both may occur. Central
venous or pulmonary artery wedge pressure should be
monitored. Five percent destrose in half-normal or
normal saline should be administered for fluid replacement.
The patient should also be observed for renal failure
due to rhabdomyolysis, hypokalemia, cardiac arrhythmias,
disseminated intravascular coagulation, and hepatic
failure. Hypokalemia frequently accompanies heat stroke
but may not appear until rehydration. Maintenance
of extracellular hydration and electrolyte balance
should reduce the risk of renal failure due to rahbdomyolysis.
Fluid administration to ensure a high urine output,
mannitol administration , and alkalinizing the urine
are recommended. Corticosteroids have not been shown
to be of value.
Fluid output should be monitored through the use of
an indwelling urinary catheter.
Because sensitivity to high environmental temperature
continues in some patients for prolonged periods following
an episodes of heat stroke, immediate reexposure should