C h a p t e r 3
Inflammation, the Inflammatory Response, and Fever
67
Manifestations of Fever
The physiologic behaviors that occur during the develop-
ment of fever can be divided into four successive stages:
a prodrome; a chill, during which the temperature rises;
a flush; and defervescence (see Fig. 3-9). During the
first
or
prodromal
period, there are nonspecific complaints,
such as mild headache and fatigue, general malaise,
and fleeting aches and pains. During the
second stage
or
chill,
there is the uncomfortable sensation of being
cold and the onset of generalized shaking, although the
temperature is rising. Vasoconstriction and piloerection
usually precede the onset of shivering. At this point the
skin is pale and covered with goose flesh. There is an
urge to put on more clothing or covering and to curl up
in a position that conserves body heat. When the shiver-
ing has caused the body temperature to reach the new
set point of the temperature control center, the shiver-
ing ceases, and a sensation of warmth develops. At this
point, the
third stage
or
flush
begins, during which cuta-
neous vasodilatation occurs and the skin becomes warm
and reddened. The
fourth,
or
defervescence,
stage of the
febrile response is marked by the initiation of sweat-
ing. Not all persons proceed through all four stages of
fever development. Sweating may be absent, and fever
may develop gradually, with no indication of a chill or
shivering.
Common manifestations of fever are anorexia, myal-
gia, arthralgia, and fatigue. These discomforts are worse
when the temperature rises rapidly or exceeds 39.5°C
(103.1°F). Respiration is increased, and the heart rate
usually is elevated. Dehydration occurs because of
sweating and the increased vapor losses caused by the
rapid respiratory rate. The occurrence of chills com-
monly coincides with the introduction of pyrogen into
the circulation. This is one of the reasons that blood
cultures to identify the organism causing the fever are
usually drawn during the first signs of a chill.
Many of the manifestations of fever are related to
the increases in the metabolic rate, increased need for
oxygen, and use of body proteins as an energy source.
During fever, the body switches from using glucose (an
excellent medium for bacterial growth) to metabolism
based on protein and fat breakdown. With prolonged
fever, there is increased breakdown of endogenous fat
stores. If fat breakdown is rapid, metabolic acidosis may
result (see Chapter 8).
Headache is a common accompaniment of fever and
is thought to result from the vasodilatation of cerebral
vessels occurring with fever. Delirium is possible when
the temperature exceeds 40°C (104°F). In the elderly,
confusion and delirium may follow moderate elevations
in temperature. Because of the increasingly poor oxy-
gen uptake by the aging lung, pulmonary function may
prove to be a limiting factor in the hypermetabolism
that accompanies fever in older persons. Confusion,
incoordination, and agitation commonly reflect cere-
bral hypoxemia. Febrile seizures can occur in some
children.
39
They usually occur with rapidly rising tem-
peratures and/or at a threshold temperature that differs
with each child.
Herpetic lesions, or fever blisters, develop in some
persons during fever. They are caused by a separate
infection by the type 1 herpes simplex virus that estab-
lished latency in the regional ganglia and is reactivated
by a rise in body temperature.
Management of Fever
Fever usually is a manifestation of a disease state, and
as such, determining the cause of a fever is an impor-
tant aspect of its treatment. Sometimes it is difficult to
establish the cause. A prolonged fever for which the
cause is difficult to ascertain is often referred to as
fever
of unknown origin
(FUO). Fever of unknown origin is
defined as a temperature of 38.3°C (101°F) or higher that
is present for 3 weeks or longer.
40,41
Among the causes
of FUO are malignancies (i.e., lymphomas, metastases
to the liver or central nervous system); infections such
as human immunodeficiency virus or tuberculosis, or
abscessed infections; and drug fever. Malignancies, par-
ticularly non-Hodgkin lymphoma, are important causes
of FUO in the elderly. Cirrhosis of the liver is another
cause of FUO.
The methods of fever treatment focus on modifica-
tions of the external environment intended to increase
heat transfer from the internal to the external environ-
ment, support of the hypermetabolic state that accom-
panies fever, protection of vulnerable body organs and
systems, and treatment of the infection or condition
causing the fever. Because fever is a disease symptom,
its manifestation suggests the need for treatment of the
primary cause.
Modification of the environment ensures that the
environmental temperature facilitates heat transfer
away from the body. Sponge baths with cool water or
an alcohol solution can be used to increase evaporative
heat losses. More profound cooling can be accomplished
through the use of a cooling blanket or mattress, which
facilitates the conduction of heat from the body into the
coolant solution that circulates through the mattress.
Care must be taken so that cooling methods do not pro-
duce vasoconstriction and shivering that decrease heat
loss and increase heat production.
Adequate fluids and sufficient amounts of simple
carbohydrates are needed to support the hypermeta-
bolic state and prevent the tissue breakdown that is
characteristic of fever. Additional fluids are needed for
sweating and to balance the insensible water losses
from the lungs that accompany an increase in respira-
tory rate. Fluids also are needed to maintain an ade-
quate vascular volume for heat transport to the skin
surface.
Antipyretic drugs, such as aspirin, ibuprofen, and
acetaminophen, often are used to alleviate the discom-
forts of fever and protect vulnerable organs, such as the
brain, from extreme elevations in body temperature.
These drugs act by resetting the hypothalamic tem-
perature control center to a lower level, presumably by
blocking the activity of cyclooxygenase, an enzyme that
is required for the conversion of arachidonic acid to
prostaglandin E
2
.
