t was a warm June morning when the harried
and hurried father strapped his five-month-
old son Bryan into the backseat of his car and
headed for work. Tragically, the father forgot to
drop his son oF
at the babysitter’s. When his wife
called him at work late that afternoon to inquire
why the child was not at the sitter’s, the shocked
father realized his mistake and hurried down to his
parked car. But it was too late—Bryan had died.
Left for ten hours in the car in the sun, all windows
shut, the baby’s temperature had quickly soared.
Two hours after he was discovered, the child’s tem-
perature still exceeded 41°C (106°±).
Sarah L.’s case of elevated body temperature
was more typical. She awoke with a fever of 40°C
(104°±) and a terribly painful sore throat. At the
doctor’s office, a test revealed that Sarah had a
infection. The fever was her body’s
attempt to ²
ght the infection.
The true cases of Bryan and Sarah illustrate
two reasons why body temperature may rise—
inability of the temperature homeostatic mecha-
nism to handle an extreme environment and an
immune system response to infection. In Bryan’s
case, sustained exposure to very high heat over-
whelmed the temperature-regulating mechanism,
resulting in hyperthermia. Body heat built up faster
than it could dissipate, and body temperature rose,
even though the set point of the thermostat was
normal. His blood vessels dilated so greatly in an
attempt to dissipate the excess heat that after a
few hours, his cardiovascular system collapsed.
±ever is a special case of hyperthermia
in which temperature rises in response to an
elevated set point. In fever, molecules on the
surfaces of the infectious agents (usually bacte-
ria or viruses) stimulate phagocytes to release
a substance called interleukin-1 (also called
endogenous pyrogen, meaning “²
re maker from
within”). The bloodstream carries interleukin-1 to
the hypothalamus, where it raises the set point
controlling temperature. In response, the brain
signals skeletal muscles to increase heat pro-
duction, blood ³
ow to the skin to decrease, and
sweat glands to decrease secretion. As a result,
body temperature rises to the new set point, and
fever develops. The increased body temperature
helps the immune system kill the pathogens.
Rising body temperature requires diF
treatments, depending on the degree of eleva-
tion. Hyperthermia in response to exposure to
intense, sustained heat should be rapidly treated
by administering liquids to replace lost body
fluids and electrolytes, sponging the skin with
water to increase cooling by evaporation, and
covering the person with a refrigerated blanket.
±ever can be lowered with ibuprofen or acet-
aminophen, or aspirin in adults. Some health
professionals believe that a slightly elevated tem-
perature should not be reduced (with medication
or cold baths) because it may be part of a normal
immune response. A high or prolonged fever,
however, requires medical attention.
Elevated Body Temperature
Slightly burned skin, such as from a minor sunburn, may
become warm and reddened (erythema) as dermal blood
vessels dilate. This response may be accompanied by mild
edema, and, in time, the surface layer of skin may be shed.
A burn injuring only the epidermis is called a
Healing usually occurs
within a few days to two weeks, with no scarring.
A burn that destroys some epidermis as well as some
underlying dermis is a
deep partial-thickness
±luid escapes from damaged dermal capillaries, and as
it accumulates beneath the outer layer of epidermal cells,
blisters appear. The injured region becomes moist and F rm
and may vary in color from dark red to waxy white. Such a
burn most commonly occurs as a result of exposure to hot
objects, hot liquids, fl
ames, or burning clothing.
The healing of a deep partial-thickness burn depends
upon stem cells that are associated with accessory struc-
tures of the skin. These structures include hair follicles,
sweat glands, and sebaceous glands. They survive the injury
because they are derived from the epidermis located deep in
the dermis. During healing, the stem cells divide, and their
daughter cells grow out onto the surface of the dermis, spread
over it, and differentiate as new epidermis. In time, the skin
usually completely recovers, and scar tissue does not develop
unless an infection occurs.
Acute sunburn (solar erythema) is an in³
ammatory reaction of the
skin to excessive exposure to ultraviolet radiation in sunlight. The
skin becomes very red, swollen, and painful, with discomfort peaking
between 6 and 48 hours after exposure. Within a few days the skin
may peel, as surface cells die and are shed. Peeling, an example of
apoptosis (programmed cell death), prevents cancer from develop-
ing by ridding the body of susceptible cells. Microscopic skin changes
begin within a half hour of intense sun exposure, including damage
to cells in the upper, epidermal layer of the skin, and swelling of blood
vessels in the deeper, dermal layer.
Treatment for acute sunburn includes frequent cool baths, per-
haps with oatmeal or baking soda added to soothe. Do not wash the
area with a harsh soap, and avoid products with benzocaine, which
can cause allergic reactions. Apply aloe for the ²
rst two days, but do
not use petroleum jelly, ointments, or butters—these lock in the heat.
Seek medical care if fever, blistering, dizziness, or visual disturbances
develop, which are signs of sun poisoning.
To avoid sunburn, stay out of the sun between the hours of
. and 3
., and when exposed, apply sunblock with an SP± fac-
tor of at least 15—even on a cloudy day. Certain medications can has-
ten or intensify the skin’s reaction to sun. Tanning lotions, re³
sunlamps, or tanning booths may pose a risk for sunburn.
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