Page 221 - Encyclopedia of Nursing Research

188 n FEVEr/FEBrILE rESPONSE

cease. Finally, falling pyrogen levels lead to
Fever/Febrile response the defervescence phase, with diaphoresis and
F vasodilation.
Nurses have managed fever through-
Fever is an abnormally high body tempera- out history, yet the scientific evidence sup-
ture that occurs as part of a host response to porting care decisions is relatively recent.
pyrogens (fever producers). An alternate term The lag between basic research findings and
for fever is pyrexia, with hyperpyrexia refer- clinical application is documented in the
ring to high fever. It is misleading to define absence of evidence-based hospital proto-
fever simply in terms of temperature eleva- cols and the lack of consensus among nurses
tion, however, because it emphasizes only in some setting for appropriate fever man-
the thermal manifestations of the nonspecific agement approaches (Thompson, Kirkness,
systemic host defense called the acute phase & Mitchell, 2007). reluctance of many nurses
response. Acute phase response is triggered to change methods of care is often seated in
by endogenous release of cytokines, includ- misunderstanding. Early traditions of cool-
ing interleukin-1, interleukin-6, and tumor ing febrile patients were empirically based
necrosis factor that cause a cascade of bio- on the limited state of scientific knowledge
chemical events, autonomic reactions, and and the erroneous fear that elevated body
immune responses including heat genera- temperature was the cause, rather than the
tion. Some promote immunostimulant prop- result, of febrile illness. Intervention was
erties against infectious disease and tumors therefore geared toward lowering body tem-
(Holtzclaw, 2002). perature. Current knowledge confirms that
Pyrogens readjust hypothalamic reg- fever is the host response to illness or inva-
ulatory centers to a higher set-point range, sion. Cooling the body is counterproductive,
so that body temperature is maintained at distressful to patients, and may cause com-
higher levels. In true fever, other cytokines, pensatory overwarming. Evidence of fever’s
hormones, and endogenously produced bio- host benefits led investigators to focus on
chemicals act as cryogens with antipyretic methods to reduce distressful febrile symp-
properties that limit temperature elevation toms rather than reducing temperature.
in fever. Controlled temperature elevation Febrile shivering is among the most distress-
and intact thermoregulatory function dif- ful and energy-consuming symptoms of
ferentiate fever from hyperthermia, a poten- fever, particularly in immunosuppressed
tially lethal condition in which unregulated patients with opportunistic infections or
thermoregulatory function can produce those receiving antigenic drugs or blood
neurologically damaging high tempera- products. Vigorous shivering is sometimes
tures. Fever occurs in three phases, reflect- described by patients as “bone shaking.”
ing the rise and fall of circulating pyrogens. Nonpharmacological nursing interventions
Initially, the chill phase occurs when ther- are based primarily on thermoregulatory
mostatic mechanisms are activated to raise dynamics to (a) insulate thermosensitive
body temperature to the newly elevated areas of skin from cooling to reduce shiv-
set-point range. Vasoconstriction decreases ering, (b) facilitate heat loss from less ther-
skin perfusion, conserving heat but mak- mosensitive regions without chilling, and
ing skin feel cold. Shivering generates heat (c) restore fluid volume and improve capil-
and is stimulated by sensory inputs that lary blood flow to skin. Fear of neural dam-
detect discrepancies between existing tem- age due to protein denaturation during high
peratures and the new set point. The plateau fevers is justified at temperatures of more
phase follows when body temperature rises than 42°C. However, true fevers are usu-
to the new set point and warming responses ally self-limiting and remain well below this