Fever

The aim of thermoregulation is to maintain
the actual core temperature of the body at
the set level of about 37°C (with diurnal
variations).
In contrast to passive hyperthermia, the set
level is raised in fever, and the
thermoregulatory mechanisms are thus
responsible for maintaining the raised
temperature. This becomes noticeable
when the fever rises: because the actual level
deviates from the suddenly raised set level,
heat loss is reduced by a decrease in
cutaneous blood flow, resulting in cooling of
the skin (feeling cold). Additionally, heat
production is increased by shivering (tremor).
This lasts until the actual level has
approached the new set level (plateau).
When the fever falls, the set level again falls,
so that now the actual level is too high and
cutaneous blood flow increases, resulting in
the person feeling hot and sweating
profusely.

CORE TEMPERATURE of most females
increases approximately 0.5°C to 1.0°C
during postovulation time of their
menstrual cycle.
CORE BODY TEMPERATURE (i.e., intracranial,
intrathoracic, & intraabdominal) normally is
maintained within a range of 36.0°C to
37.5°C (97.0°F to 99.5°F). Within this range,
there are individual differences.
Indeed, a NUDE PERSON can be exposed
to temperatures as low as 55°F (12,78 °C)
or as high as 130°F (54,44 °C) in dry air
and still maintain an almost constant
core temperature.
The SKIN TEMPERATURE, in contrast to
the CORE TEMPERATURE, rises and falls
with the temperature of the
surroundings. The skin temperature is
the important temperature when we
refer to the skin’s ability to lose heat to
the surroundings.

Temperatures differ in various parts of
the body, with core temperatures being
higher than those at the skin surface.
The rectal temperature is used as a measure
of core temperature and is considered the
most accurate parameter. Rectal
temperatures usually range from 37.3°C
(99.1°F) to 37.6°C (99.6°F).
The oral temperature, taken sublingually, is
usually 0.2°C (0.36°F) to 0.51°C (0.9°F) lower
than the rectal temperature.
The axillary temperature also can be used as
an estimate of core temperature.
However, the parts of the axillary fossa must
be pressed closely together for an extended
period (5 to 10 minutes for a glass
thermometer) because this method requires
considerable heat to accumulate before the
final temperature is reached.
Ear-based thermometry uses an infrared
sensor to measure the flow of heat from the
tympanic membrane and ear canal.

EXERCISE can increase metabolic heat production
10-fold. Thankfully, thermoregulatory responses
such as sweating simultaneously increase heat loss,
and thus keep body temperature from rising
dangerously high.
Shivering increases metabolic heat production.
BODY TEMPERATURE reflects the difference between
heat production and heat loss and varies with
exercise and extremes of environmental temperature.
ICE CRYSTALS can form in tissues exposed to very
cold and damp ambient temperatures.
The failure to adequately manage heat production
and/or loss results in devastating consequences.
Very high temperatures (+45°C, 113° F) cause
proteins to coagulate and/or aggregate.
Systemic changes in body temperature can be
equally devastating, leading to tissue damage, organ
failure, coma, and even death.

THE BASAL NUCLEI SOME OF THE NUCLEI OF THE HYPOTHALAMUS
The part of the brain which lies below the thalamus, forming the major portion of the
ventral region of the diencephalon and which functions to regulate bodily temperature,
water balance, carbohydrate and fat metabolism among other metabolic processes, and
autonomic activities and also contributes to the regulation of internal homeostasis by
neurosecretory functions which control the activity of the pituitary gland.
6 aspects of internal homeostasis coordinated by the hypothalamus:
1. BODY TEMPERATURE
2. food intake/hunge
5. water and electrolyte balance
6. thirst
3. biological rhythms and drives
4. regulates output of pituitary
gland = hypophysis

Temperature-regulating centers located in the hypothalamus:
preoptic and anterior hypothalamic nuclei, posterior
hypothalamic area
The anterior hypothalamic
preoptic area contain large
numbers of heat-sensitive neurons
as well as about one third as many
cold-sensitive neurons (temperature
sensors function for controlling
body temperature).
The heat-sensitive neurons increase their firing
rate 2- to 10-fold in response to a 10°C increase
in body temperature.
The cold-sensitive neurons, increase their firing
rate when the body temperature falls.
Even though many °t sensory signals
arise in peripheral receptors, these
signals contribute to body °t control
mainly through the hypothalamus.
The area of the hypothalamus that they
stimulate is located bilaterally in the
posterior hypothalamus approximately
at the level of the mammillary bodies.
The °t sensory signals from the
anterior hypothalamic-preoptic area
are also transmitted into this posterior
hypothalamic area. Here the signals
from the preoptic area & the signals
from elsewhere in the body are
combined & integrated to control the
heat-producing & heat-conserving
reactions of the body.

The skin is endowed with both cold and warmth receptors. There are far more cold
receptors than warmth receptors—in fact, 10 times as many in many parts of the skin.
Peripheral detection of °t mainly concerns detecting cool & cold instead of warm
temperatures. When the skin is chilled over the entire body, immediate reflex effects
are invoked and begin to increase the ºt of the body in several ways:
1) by providing a strong stimulus to cause shivering, with a resultant increase in the
rate of body heat production;
2) by inhibiting the process of sweating, if this is already occurring;
3) by promoting skin vasoconstriction to diminish loss of body heat from the skin.
 Deep body temperature receptors are found mainly in the spinal cord, in the abdominal
viscera, and in or around the great veins in the upper abdomen and thorax.
 These deep receptors function differently from the skin receptors because they are exposed
to the body core °t rather than the body surface temperature.
 Skin °t receptors, they detect mainly cold rather than warmth.
 It is probable that both the skin and the deep body receptors are concerned with preventing
hypothermia—that is, preventing low body °t.

1) Neurons of the “THERMOSTAT” is a group of thermosensitive neurons,
which perceive the temperature of blood which flows through
hypothalamus.
The information from skin and organs thermoreceptors comes here too.
A “thermostat” provides the middle temperature of body core.
2) Neurons of the “SET LEVEL OF TEMPERATURE” are a group of thermo
nonsensitive neurons which program the level of temperature of body core.
Information from a “thermostat” comes to the neurons of the “set level of
temperature”, where comparing of present temperature of core to the
programmed level.
3) HEAT PRODUCTION CENTER. It neurons are localized in dorso- and
ventromedial nucleus of hypothalamus. Their irritation causes multiplying
formation of heat.
4) The center of HEAT EMISSION is disposed in the preoptic area of
hypothalamus. At it irritation leads to calorification by an organism.

•• Metabolic rate of each cell
•• Any factor that may  the basal
metabolic rate (BMR), such as that
caused by muscle activity
•• Extra metabolism caused by
hormones (thyroxine, growth
hormone, testosterone).
•• Any extra metabolism caused by
the sympathetic nervous system
(SNS) stimulation on cells
•• Extra metabolism caused by 
cellular chemical activity
•• Thermogenic effect of food
digestion, absorption, or storage.
The CHEMICAL REACTIONS that occur during the ingestion and metabolism
of food & those required to maintain the body at rest (basal metabolism) require
energy & produce heat. These processes occur in the body core (primarily the
liver) & are in part responsible for the maintenance of core temperature.
There is a 0.55°C (1°F) increase in body °t for every 7% increase in metabolism.
The sympathetic neurotransmitters, epinephrine and norepinephrine, which are released when an
increase in body °t is needed, act at the cellular level to shift body metabolism to heat production
rather than energy generation. This may be one of the reasons fever tends to produce feelings of
weakness and fatigue.
Thyroid hormone increases cellular metabolism, but this response usually requires several weeks
to reach maximal effectiveness.
Metabolism is the body’s main source of heat production or thermogenesis.
Many factors impact the metabolic rate, including:

Skeletal muscles produce heat through two mechanisms:
GRADUAL INCREASE IN
MUSCLE TONE
PRODUCTION OF RAPID MUSCLE OSCILLATIONS
(SHIVERING— WHICH DOES NOT OCCUR IN NEONATES)
Both increasing muscle tone and shivering are controlled by the posterior
hypothalamus and occur in response to cold.
As peripheral temperature drops, muscle tone increases and shivering begins.
Shivering is a fairly effective method for increasing heat production because
no work is performed and all the energy produced is retained as heat, and
increases the use of oxygen by approximately 40%.
The first muscle change that occurs with shivering is a general  in muscle
tone, followed by an oscillating rhythmic tremor involving the spinal-level
reflex that controls muscle tone. Physical exertion  body °t.
Muscles convert most of the energy in the fuels they consume into heat
rather than mechanical work. With strenuous exercise, more than ¾ of the 
metabolism resulting from muscle activity appears as heat within the body,
and the remainder appears as mechanical work.

Chemical thermogenesis, also called nonshivering thermogenesis or
adrenergic thermogenesis, results from the release of epinephrine &
norepinephrine.
Epinephrine and norepinephrine produce a rapid, transient increase in heat
production by raising the body’s basal metabolic rate.
Chemical thermogenesis seems to be different from hormone-triggered
increases in the basal metabolic rate.
Chemical thermogenesis produces a quick, brief rise in basal metabolic
rate, whereas the hormone thyroxine triggers a slow, prolonged rise.
Chemical thermogenesis occurs in brown adipose tissue.
Brown adipose tissue is rich with mitochondria and blood vessels & is
essential for nonshivering thermogenesis.
White and brown adipocytes are found together in visceral & subcutaneous
tissue.
White adipocytes store energy and brown adipocytes produce heat.
Adipocytes demonstrate transdifferentiation & such plasticity allows direct
conversion of one cell type into the other.
With chronic cold exposure white-to-brown conversion increases
thermogenesis, whereas excessive food consumption induces brown-to-white
conversion to meet the need for energy storage..

1. Vasodilation of skin blood vessels. In almost all areas of the body, the skin
blood vessels become intensely dilated. This is caused by inhibition of the
sympathetic centers in the posterior hypothalamus that cause
vasoconstriction. Full vasodilation can increase the rate of heat transfer to the
skin as much as eightfold.
3. Sweating. The effect of
increased body temperature
shows a sharp increase in the
rate of evaporative heat loss
resulting from sweating when
the body core temperature
rises above the critical level of
37°C (98.6°F).
An additional 1°C increase in
body temperature causes
enough sweating to remove
10 times the basal rate of
body heat production.
2. Decrease in heat production. The mechanisms that cause excess heat
production, such as shivering and chemical thermogenesis, are strongly
inhibited.

RADIATION
CONDUCTION
CONVECTION
VASODILATION
DECREASED
MUSCLE TONE
EVAPORATION
INCREASED
PULMONARY
VENTILATION
VOLUNTARY
MEASURES
ADAPTATION TO
WARMER
CLIMATES

Radiation is the transfer of heat through air or a vacuum. Heat from the sun is carried by
radiation. Heat loss by radiation varies with the temperature of the environment.
Environmental temperature must be less than that of the body for heat loss to occur. In a
nude person sitting inside a normal-temperature room, approximately 60% of body heat
typically is dissipated by radiation.
During strenuous physical activities, such as skiing (a) or running (c), the dermal blood vessels
dilate and sweat secretion increases (b). These mechanisms prevent the body from
overheating. In contrast, the dermal blood vessels constrict to minimize heat loss in response
to low temperatures (b).

Conduction refers to heat loss by direct molecule-to-
molecule transfer from one surface to another.
 Through conduction, the warmer surface loses heat
to the cooler surface. Thus the skin loses heat
through direct contact with cooler air, water, or
another surface. In the same manner, the core of the
body loses heat to the cooler body surface.
 Cooling blankets or mattresses that are used for
reducing fever rely on conduction of heat from the
skin to the cool surface of the mattress.
 Heat also can be conducted in the opposite
direction—from the external environment to the
body surface.
 For instance, body temperature may rise slightly
after a hot bath.
 Water has a specific heat several times greater than air, so water absorbs far greater amounts
of heat than air does. The loss of body heat can be excessive and life threatening in situations of
cold water immersion or cold exposure in damp or wet clothing.
 The conduction of heat to the body’s surface is influenced by blood volume. In hot weather,
the body compensates by increasing blood volume as a means of dissipating heat.
 A mild swelling of the ankles during hot weather provides evidence of blood volume expansion.
 Exposure to cold produces a cold diuresis and a reduction in blood volume as a means of
controlling the transfer of heat to the body’s surface.

Vasodilation.
Peripheral vasodilation increases heat loss by diverting core-warmed blood to the
surface of the body. As the core-warmed blood passes through the periphery, heat
is transferred by conduction to the skin surface and from the skin to the surrounding
environment. Because heat loss through conduction depends on the surrounding
temperature, it is minimal to nonexistent if the surrounding air or water is warmer
than the body surface.
Vasodilation occurs in response to autonomic stimulation under the control of the
hypothalamus. It is useful in instances of moderate temperature elevation.
As core temperature increases, vasodilation increases until maximal dilation is
achieved. At that point the body must use additional heat loss mechanisms.
Convection is the transfer of heat through
currents of gases or liquids. It greatly aids heat
loss through conduction by exchanging warmer air
at the surface of the body with cooler air in the
surrounding space.
Convection occurs passively as warmer air at the
surface of the body rises away from the body and
is replaced by cooler air, but the process may be
aided by fans or wind. (The combined effect of
conduction and convection by wind is
conventionally measured as the windchill factor.)

Evaporation of body water from the surface of the skin and the linings of the mucous
membranes is a major source of heat reduction.
Even when a person is not sweating, water still evaporates insensibly from the skin and lungs
at a rate of about 600 to 700 ml/day. Heat is lost as surface fluid is converted to gas, so that
heat loss by evaporation is increased if more fluids are available at the body surface.
To speed this process, fluids are actively secreted through the sweat glands. As much as 2.2 L
of fluid per hour may be lost by sweating. Electrolytes are lost with the water.
Therefore, loss of large volumes through sweating may result in decreased plasma volume,
decreased blood pressure, weakness, and fainting.
Like other heat reduction mechanisms, stimulation of sweating occurs in response to
sympathetic neural activity and depends on a favorable temperature difference between the
body and the environment. In addition, heat loss through evaporation is affected by the
relative humidity of the air. If the humidity is low, sweat evaporates quickly, but if the
humidity is high, sweat does not evaporate and instead remains on the skin or drips off.
Anything that prevents adequate evaporation when the surrounding temperature is higher
than the skin temperature will cause the internal body temperature to rise.
This occurs occasionally in human beings who are born with congenital absence of sweat
glands. These people can stand cold temperatures as well as normal people can, but they
are likely to die of heatstroke in tropical zones because without the evaporative
refrigeration system, they cannot prevent a rise in body temperature when the air
temperature is above that of the body.

DECREASED MUSCLE TONE. To decrease heat production, muscle tone may be moderately reduced and
voluntary muscle activity curtailed. These mechanisms explain in part the “washed-out” feeling
associated with high temperatures and warm weather. Decreased muscle tone and reduced activity have
a limited effect on decreasing heat production, however, because muscle tone and heat production
cannot be reduced below basal body requirements.
INCREASED PULMONARY VENTILATION. Exchanging air with the environment through the normal
pulmonary ventilation provides some heat loss, although it is minimal in humans. As air is inhaled, the air
draws heat from the upper respiratory tract. The air is further warmed in the alveoli by blood in the
microcirculation. This warmed air then is exhaled into the environment. This normal process occurs faster
at higher body temperatures through an increase in ventilatory rates. Thus hyperventilation is
associated with hyperthermia.
VOLUNTARY MECHANISMS. In response to high body temperatures, people physically “stretch out,”
thereby increasing the body surface area available for heat loss. They also “slow down” or “take it easy,”
thereby decreasing skeletal muscle work, and they “dress for warm weather” with light-colored, loose-
fitting garments to reflect heat and promote convection, conduction, and evaporation.
ADAPTATION TO WARMER CLIMATES. The body of an individual who moves from a cooler to a much
warmer climate undergoes a period of adjustment, a process that takes several days to weeks. At first the
individual experiences feelings of lassitude, weakness, and faintness with even moderate activity. Body
temperatures rise with any work. Within several days, however, the individual experiences an earlier
onset of sweating, the volume of sweat is increased, and the sodium content is lowered. Heart rate is
decreased and stroke volume increased so that cardiac output remains unchanged. Extracellular fluid
volume increases, as does plasma volume. These physiologic adaptations result in improved warm
weather functioning and decreased symptoms of heat intolerance. People’s work output, endurance, and
coordination increase, and their subjective feelings of discomfort decrease.

1. Skin vasoconstriction throughout the body. This is caused by stimulation
of the posterior hypothalamic sympathetic centers.
2. Piloerection. Piloerection means hairs “standing on end.”
Sympathetic stimulation causes the arrector pili muscles attached to the
hair follicles to contract, which brings the hairs to an upright stance. This
is not important in human beings, but in lower animals, upright projection
of the hairs allows them to entrap a thick layer of “insulator air” next to the
skin, so that transfer of heat to the surroundings is greatly depressed.
3. Increase in thermogenesis (heat
production). Heat production by
the metabolic systems is
increased by promoting shivering,
sympathetic excitation of heat
production, and thyroxine
secretion.
These methods of increasing heat
require additional explanation,
which follows.

I. INCREASE OF
TEMPERATURE
(ST. INCREMENTI)
II. SAVING OF THE
PROMOTED TEMPERATURE
(ST. FASTIGII)
III. DECLINE OF
TEMPERATURE
(ST. DECREMENTI).
Fever, or pyrexia, describes an elevation in body temperature that
is caused by an upward displacement of the thermostatic set
point of the hypothalamic thermoregulatory center.
Temperature is one of the most frequent physiologic responses
to be monitored during illness.
FEVER is a typical pathological process which arises up for higher warm-blooded
animals and man at influence on the organism of pyrogenic irritants.
Fevers that are regulated by the hypothalamus
usually do not rise above 41°C (105.8°F),
suggesting a built-in thermostatic safety
mechanism. Temperatures above that level are
usually the result of superimposed activity, such
as convulsions, hyperthermic states, or direct
impairment of the temperature control center.

INFECTIOUS UNINFECTIOUS NATURAL PRIMARYARTIFICIAL
SECONDARYEndotoxins
(LPS)
Exotoxin
Products of
activity of
pathogenic
mushrooms
Rickettsia
Viruses
Components
of the
incompatible
blood
(transfusion
fever)
Exogenous
proteins
(protein of
milk)
Products of
disintegration
of tissues
Pyrogens
exist in
nature or
appear in
natural way
from
unpyrogenic
matters
Pyrogens get
from bacterial
toxins and
use with a
medical
purpose
(pyrotherapy)
Exogenous
pyrogens entered
from outside
Endoenous
pyrogens appear
in an organism:
IL 1α, 1β, 6, 8, and
11, INFα2 & γ, TNFα
(cachectin) & TNFβ
(lymphotoxin), the
macrophage-
inflammatory
protein MIP 1

S aureus strains
growing on mucous
membranes (eg, the
vagina in association
with menstruation) or
in wounds
TOXIC SHOCK
SYNDROME
•shock, high fever,
•diffuse red rash that later
desquamates;
•Involved multiple other organ
systems
characterized by
Super antigen stimulates
T-cells to produce large
amounts of IL-2 & TNF
PYROGENIC EXOTOXIN A
(similar/same as
streptococcal
ERYTHROGENIC TOXIN
SCARLET FEVER
Clinical manifestations
similar to staphylococcal
toxic shock syndrome
LPS (ENDOTOXIN)
of gram-negative
bacteria (bacterial
cell wall components
that are often liberated
when the bacteria
lyse)
In the bloodstream is
initially bound to
circulating proteins,
which then interact
with receptors on
macrophages
neutrophils & other
reticuloendothelial
cells
IL-1, IL-6, IL-8, TNF-α, and other cytokines
are released, & the complement &
coagulation cascades are activated
fever, leukopenia, & hypoglycemia;
hypotension &shock resulting in impaired
perfusion of essential organs (eg, brain,
heart, kidney); intravascular coagulation; &
death from massive organ dysfunction.
Some strains of
group A β-hemolytic
streptococci

When a brain surgeon operates
in the region of the hypothalamus:
 severe fever almost always occurs;
 rarely, hypothermia, occurs.
Demonstrate both the potency of the
hypothalamic mechanisms for body
°t control & the ease with which
abnormalities of the hypothalamus
can alter the set-point of
temperature control.
Prolonged high ºt is compression
of the hypothalamus by a brain tumor.
Brain damage from a fever generally
will not occur unless the fever is over
107.6 °F (42 °C). Untreated fevers
caused by infection will seldom go over
105 °F unless the child is overdressed
or trapped in a hot place.

During fever, arginine vasopressin (AVP), α-melanocytestimulating hormone (α-MSH), and corticotropin-releasing
factor are released from the brain, and systemic anti-Inflammatory cytokines (i.e., IL-1 receptor agonist and IL-10) can
act as endogenous cryogens or antipyretics to help diminish the febrile response.This antipyretic effect constitutes
a negative-feedback loop.The antipyretic effect may help explain fluctuations in the febrile response.When the fever
breaks, the set point is returned to normal.The hypothalamus responds by signaling a decrease in heat production and
an increase in heat-reduction mechanisms.The result is decreased muscle tone, peripheral vasodilation, flushed skin,
and sweating.The individual feels very warm, replaces warm clothing with cooler clothes, throws off the covers, and
stretches out. Once the body has returned to a normal temperature, the individual feels more comfortable and the
hypothalamus adjusts thermoregulatory mechanisms to maintain the new temperature.
At this point, PGE2 binds to receptors in the hypothalamus to induce  in the thermostatic set point through the
second messenger cyclic adenosine monophosphate (cAMP). In response to the  in its thermostatic set point, the
hypothalamus initiates shivering and vasoconstriction that raise the body’s core °t to the new set point, and fever is
established. Peripheral vasoconstriction occurs with shunting of blood from the skin to the body core. Epinephrine
release  metabolic rate, and muscle tone .  release of vasopressin reduces the volume of body fluid to be heated.
Shivering also may occur. The individual dresses more warmly,  body surface area by curling up, and may go to bed in
an effort to get warm. Body °t is maintained at the new level until the fever “breaks.”
These cytokines induce prostaglandin E2 (PGE2), which is a metabolite of arachidonic acid (an intramembrane fatty
acid). It is hypothesized that when interleukin (IL-1B) interacts with the endothelial cells of the blood–brain barrier in
the capillaries of the organum vasculosum laminae terminalis (OVLT), which is in the third ventricle above the optic
chiasm, PGE2 is released into the hypothalamus.
These phagocytic cells digest the bacterial products and then release pyrogenic cytokines, principally interleukin-1
(IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), into the bloodstream for transport to the
hypothalamus, where they exert their action.
When bacteria or breakdown products of bacteria are present in blood or
tissues, phagocytic cells of the immune system engulf them.

The endogenous pyrogens mediate a number of other
responses.
For example, IL-1 and TNF-α are inflammatory mediators
that produce other signs of inflammation such as
leukocytosis, anorexia, and malaise.
Many noninfectious disorders, such as myocardial
infarction, pulmonary emboli, and neoplasms, produce
fever. In these conditions, the injured or abnormal cells
incite the production of endogenous pyrogens. For
example, trauma and surgery can be associated with up to
3 days of fever.
Some malignant cells, such as those of leukemia and
Hodgkin disease, secrete chemical mediators that function
as endogenous pyrogens.
A fever that has its origin in the central nervous
system is sometimes referred to as a NEUROGENIC
FEVER. It usually is caused by damage to the
hypothalamus due to central nervous system trauma,
intracerebral bleeding, or an increase in intracranial
pressure.
NEUROGENIC FEVER is characterized by a high
temperature that is resistant to antipyretic therapy
and is not associated with sweating.

Characteristics of Febrile Conditions Chills.
 When the set-point of the hypothalamic temperature-
control center is suddenly changed from the normal level to
higher than normal (as a result of tissue destruction,
pyrogenic substances, or dehydration), the body temperature
usually takes several hours to reach the new temperature
set-point.
 Because the blood temperature is now less than the set-
point of the hypothalamic temperature controller, the usual
responses that cause elevation of body temperature occur.
 During this period, the person experiences chills and feels
extremely cold, even though his or her body temperature may
already be above normal.
 Also, the skin becomes cold because of vasoconstriction,
and the person shivers.
 Chills can continue until the body temperature reaches the
hypothalamic set-point of 103°F. Then the person no longer
experiences chills but instead feels neither cold nor hot.
 As long as the factor that is causing the higher set-point of
the hypothalamic temperature controller is present, the body
temperature is regulated more or less in the normal manner,
but at the high temperature set-point level.

Heat emission is more or less equal to thermoproduction. This balance of thermo
regulative processes is set at more high level, as a norm, that provides maintenance of
the promoted temperature of body.
Duration of fever can be a few hours, days and even years.
After a level the increases of temperature distinguish the followings types of febris:
a) mild pyrexia, (subfebrile) is an increase of temperature to 38ºC;
b) moderate (febrile) - 38-39ºC;
c) high (pyretic) - 39-41ºC;
d) very high (hyperpyretic) - 41-42ºC.
It is known that the temperature of body of man have day's (circadian) oscillation:
 maximal temperature in 5-7 hours of evening,
 minimum - in 4-6 hours of morning.
This temperature rhythm is saved in most cases of fever.

36.6 °C (97.88 F) - NORMAL
37-38 °C (98.6 – 100.4 F) -
SUBFEBRILE
39-41 °C (102.2 – 105.8 F) -
PYRETIC
38-39 °C (100.4 – 102.2 F) -
FEBRILE
over 41 °C (more than 105.8 F) -
HYPERPYRETIC
Formulas for conversion
of both Celsius to Fahrenheit
and Fahrenheit to Celsius are
as follows:
(X°C × 9/5) + 32 =Y°F;
(X°F – 32) × 5/9 =Y°C
As a consequence of fever, heart rate is
 8–12 min–1/ °C) and energy metabolism raised,
resulting in fatigue, joint aches and headaches

A. Febris Continua (Continous fever) in which the
elevated °t for the some time persists at a high level, the
difference between the morning and evening °t not
exceed 1°C. (Typhoid fever, croupous pneumonia, typhus)
B. Febris Remittens (Remittent fever) in which the
difference between the morning and evening °t exceeds
1°C, but the °t never falls to normal level. (Typhoid fever,
catarrhal pneumonia, sepsis, etc.)
C. Febris Intermittens (Intermittent fever) which is
characterized by regular alternation of brief attacks of
fever (paroxysms) with feverless periods (apyrexia). High
°t persists for several h, drops to normal and then rises
again. The length of the feverless periods may vary
(Malaria). Attacks – occurs every 3rd day (f. quartana),
every 2nd day (f. tertiana) or every day (f. quotidiana)
D. Febris Recurrens (Recurrent fever) which is
characterized by longer periods of pyrexia then
intermittent f. (5-6 days). The duration of these periods
corresponds to that of the periods of normal °t (Borreliosis
– relapsing fever; Treponematoses, Tularemia,
Meningococcemia, Malaria, rat-bite fever).
E. Febris Hectica (Hectic fever) in which the swings are 3 to 5 °C (Sepsis, severe Tbc, malignant tumors)
F. Febris Inversa (Inverse fever) is a fever with perverted course, for ex. elevation of °t in the morning and a
drop in the evening (Sepsis, Tbc)

A mechanism of decline of body temperature in the III
stage of fever.
As soon as an action is halted IL-1 on the
termoregulative center, maintenance of PgE diminishes in the
neurons of the “set level of temperature”, that lead to restore
sensitiveness of neurons to the "thermostat" signals.
The temperature of “core” begins to be perceived as
promoted, as a result of what the center of heat emission is
activated and the heat production center of is repressed.
Two types of physiologic reactions have most value:
a) expansion of skin vessels and extremities vessels;
b) multiplying hidropoiesis and sweating [sweat secretion;
perspiration]. These reactions are reason of multiplying heat
emission and diminishing of body temperature.
Distinguish 2 variants of decline of temperature:
1) critical decline is the sharp diminishing of temperature
during a few hours;
2) a lytic decline is the gradual diminishing of temperature
during a few days.
At the critical decline of temperature there is
hyperhidrosis with acute expansion of peripheral vessels, which
can lead to falling of arterial pressure and development of acute
vascular insufficiency (collapse).

Most febrile illnesses are due to common infections and are relatively easy to diagnose.
In certain instances, however, it is difficult to establish the cause of a fever. A prolonged
fever for which the cause is difficult to ascertain is often referred to as fever of
unknown origin (FUO) or unexplained persistent fever.
FUO is defined as a temperature elevation of 38.3°C (101°F) or higher that is present
for 3 weeks or longer and includes 1 week of comprehensive diagnostic testing that
does not identify a diagnosis. Among the causes of FUO are malignancies (i.e.,
lymphomas, metastases to the liver and central nervous system); infections such as
human immunodeficiency virus, tuberculosis, or abscessed infections; and drug fever.
Malignancies, particularly non-Hodgkin lymphoma, are important causes of FUO in the
elderly. Cirrhosis of the liver is another cause of FUO.

Recurrent or periodic fevers may occur in predictable intervals or without
any discernible time pattern. They may be associated with no discernible
cause, or they can be the presenting symptom of several serious illnesses,
often preceding the other symptoms of those diseases by weeks or
months. Conditions in which recurrent fevers occur but do not follow a
strictly periodic pattern include genetic disorders such as familial
Mediterranean fever.
FAMILIAL MEDITERRANEAN FEVER, an autosomal recessive disease, is
characterized by an early age of onset (<20 years) of acute episodic bouts
of peritonitis and high fever with an average duration of less than 2 days.
In some cases pleuritis, pericarditis, and arthritis are present.
The primary chronic complication is the presence of serum antibodies
that can result in kidney or heart failure.
Other conditions that present with recurrent fevers occurring at irregular
intervals include repeated viral or bacterial infections, parasitic and fungal
infections, and some inflammatory conditions, such as lupus
erythematosus or Crohn disease.
The clinical challenge is in the differential diagnosis of periodic or recurrent
fever. The initial workup usually requires a thorough history and physical
examination designed to rule out the more serious medical conditions that
present initially with fever.

Fever occurs frequently in infants and young children and is a common reason for visits to the emergency
department. Infants and young children have decreased immunologic function and are more commonly
infected with virulent organisms. Also, the mechanisms for controlling temperature are not as well developed in
infants as they are in older children and adults. Even though infants with fever may not appear ill, this does not
imply an absence of bacterial disease.
In infants younger than 3 months, a mild elevation in temperature (i.e., rectal temperature of 38°C
[100.4°F]) can indicate serious infection.
Although the differential diagnosis of fever is quite broad and includes both infectious and noninfectious
causes, the majority of febrile children have an underlying infection.
The most common causes are minor or more serious infections of the respiratory system, gastrointestinal
tract, urinary tract, or central nervous system. The epidemiology of serious bacterial disease has changed
dramatically with the introduction of the Haemophilus influenzae and Streptococcus pneumoniae vaccines
in developed countries.
H. influenzae type b has been nearly eliminated, and the incidence of pneumococcal disease caused by
vaccine and crossreactive vaccine serotypes has declined substantially. Fever in infants and children can be
classified as low risk or high risk, depending on the probability of the infection progressing to bacteremia or
meningitis and signs of toxicity.
Infants between the ages of 1 and 28 days with a fever should be considered to have a bacterial infection
that can cause bacteremia or meningitis. Signs of toxicity include lethargy, poor feeding, hypoventilation,
poor tissue oxygenation, and cyanosis. A white blood cell count with differential and blood cultures usually
is taken in high-risk infants and children to determine the cause of fever. A chest radiograph should be obtained
in febrile infants younger than 3 months of age with at least one sign of a respiratory illness (e.g.,
tachypnea, crackles, decreased breath sounds, wheezing, coughing).
Febrile children who are younger than 1 year of age and girls between 1 and 2 years of age should be
considered at risk for a urinary tract infection.
The approach to treatment of the young child who has a fever without a known source varies depending on
the age of the child. High-risk infants and infants who are younger than 28 days are often hospitalized for
evaluation of their fever and treatment.

In the elderly, even slight elevations in temperature may indicate serious infection or
disease, most often caused by bacteria. This is because the elderly often have a lower baseline
temperature, and although they increase their temperature during an infection, it may fail to reach
a level that is equated with significant fever.
Normal body temperature and the circadian pattern of temperature variation often are altered
in the elderly.
Fever in the older adult does increase the older adult’s immunological response, but it is
generally a much weaker response compared to younger people.
It has been suggested that 20% to 30% of older adults with serious infections present with
an absent or blunted febrile response. The probable mechanisms for the blunted fever
response include a disturbance in sensing of temperature by the thermoregulatory center in the
hypothalamus, alterations in release of endogenous pyrogens, and the failure to elicit responses
such as vasoconstriction of skin vessels, increased heat production, and shivering that increase
body temperature during a febrile response.
Absence of fever may delay diagnosis and initiation of antimicrobial treatment.
Therefore, it is important to perform a thorough history and physical examination focusing on
other signs of infection and sepsis in older adults. Signs of infection in older adults when fever is
absent include unexplained changes in functional capacity, worsening of mental status,
weakness and fatigue, and weight loss.
Another factor that may delay recognition of fever in older adults is the method of temperature
measurement. It has been suggested that rectal and tympanic membrane methods are more
effective in detecting fever in the elderly. This is because conditions such as mouth breathing,
tongue tremors, and agitation often make it difficult to obtain accurate oral temperatures in older
adults.

Fever is a disease symptom, its manifestation suggests the need for diagnosis and 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, but caution is necessary so the person is not cooled too quickly.
It is better to bring the person to a health care practice to obtain advice on whether the person may
need intravenous lines for hydration and other medical attention.
More profound cooling can be accomplished through the use of forced air blankets or a cooling
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 the cooling method does not produce vasoconstriction
and shivering that decrease heat loss and increase heat production.
Adequate fluids and sufficient amounts of simple carbohydrates are needed to support the
hypermetabolic state and prevent the tissue breakdown that is characteristic of fever.
Additional replacement fluids are needed for sweating and to balance the insensible water losses from
the lungs that accompany an increase in respiratory rate. Fluids also are needed to maintain an adequate
vascular volume for heat transport to the skin surface.
Antipyretic drugs, such as aspirin, ibuprofen, and acetaminophen, often are used to alleviate the
discomforts of fever and protect vulnerable organs, such as the brain, from extreme elevations in body
temperature. It is thought that these drugs act by resetting the set point of the temperature-regulating
center in the hypothalamus to a lower level, presumably by blocking the activity of cyclooxygenase, an
enzyme that is required for the conversion of arachidonic acid to PGE2.
However, evidence suggests that the routine administration of antipyretics does not decrease the
duration of the fever or illness.
Because of the risk of Reye syndrome, the Centers for Disease Control and Prevention, U.S. Food and
Drug Administration, and American Academy of Pediatrics Committee on Infectious Diseases advise
against the use of aspirin and other salicylates in children with influenza or chickenpox.

TYIENOL (Acetaminophen)
Tylenol is approved for use in children as young as 2 months old, but should
never be given to a child under 3 months without first speaking to a doctor.
ADVIL or MOTRIN (Ibuprofen)
Ibuprofen is approved for use in children as young as 6 months.
Aspirin
Aspirin should never be given to children under 18 years of age, unless
specifically recommended by a doctor, because of the risk of a rare but possibly
fatal illness called Reye’s Syndrome.

Hyperthermia (marked warming of core temperature) can produce nerve
damage, coagulation of cell proteins, and death.
At 41° C (105.8° F), nerve damage produces convulsions in the adult.
At 43° C (109.4° F), death results.
Hyperthermia is not mediated by pyrogens, and there is no resetting of the
hypothalamic set point. Hyperthermia may be accidental or therapeutic.
Therapeutic hyperthermia is a form of local or general body-induced
hyperthermia. Its purpose is to destroy pathologic microorganisms or tumor
cells by facilitating the host’s natural immune process through elevated
body temperature.
As a form of treatment, it is generally controversial.
The four forms of accidental hyperthermia are:
1) HEAT CRAMPS,
2) HEAT EXHAUSTION,
3) HEAT STROKE,
4) MALIGNANT HYPERTHERMIA

Heat Cramps
Heat cramps are slow, painful, skeletal muscle cramps and spasms, usually
occurring in the muscles that are most heavily used and lasting for 1 to 3 minutes.
Cramping results from salt depletion that occurs when fluid losses from heavy
sweating are replaced by water alone.
The muscles are tender, and the skin usually is moist. Body temperature may be
normal or slightly elevated. There almost always is a history of vigorous activity
preceding the onset of symptoms.
Heat Exhaustion
Heat exhaustion is related to a gradual loss of salt and water, usually after
prolonged and heavy exertion in a hot environment.
The symptoms include thirst, fatigue, nausea, oliguria, giddiness, and finally
delirium.
Gastrointestinal flulike symptoms are common.
Hyperventilation in association with heat exhaustion may contribute to heat
cramps and tetany by causing respiratory alkalosis. The skin is moist, the rectal
temperature usually is higher than 37.8°C (100°F) but below 40°C (104°F), and
the heart rate is elevated. Signs of heat cramps may accompany heat exhaustion.

HEAT STROKE is a potentially lethal result of a breakdown in
control of an overstressed thermoregulatory center.
The brain cannot tolerate temperatures over 40.5°C (104.9° F).
When core temperature reaches or exceeds 40.5°C (104.9° F),
the brain may be preferentially cooled by maximal blood flow
through the veins of the head and face, specifically the forehead.
Sweat production on the face is maintained even during
dehydration.
Evaporation of the sweat cools the blood in the veins of the face
and forehead; the blood then is returned to the endocranial
venous network and sinus cavernosus, cooling the blood in the
cerebral arterial vessels that lie in proximity.
Fanning the face enhances this mechanism. In this way the brain
can be maintained temporarily at 40°C (104°F), even when core
temperatures are higher. In instances of very high core
temperatures (40° to 43°C [104° to 109.4° F]), the
cardiovascular and thermoregulatory centers may cease to
function appropriately.
Sweating ceases, and the skin becomes dry and flushed. The
individual may be irritable, confused, stuporous, or comatose.
Visual disturbances may occur.
As heat loss through the evaporation of sweat ceases, core
temperatures increase rapidly. High core temperatures and
vascular collapse produce cerebral edema, degeneration of the
CNS, swollen dendrites, and renal tubular necrosis.
Treatment: removing the person from the warm environment, if
possible, and using a cooling blanket or cool water bath.
DEATH results
unless immediate,
effective treatment
is initiated.

Children are more susceptible
to heat stroke than adults
because:
1) they produce more metabolic
heat when exercising,
2) they have a greater surface
area: mass ratio,
3) their sweating capacity is less
than that of adults.

Drugs can induce fever by several mechanisms.:
o interfere with heat dissipation,
o alter temperature regulation by the
hypothalamic centers,
o act as direct pyrogens,
o injure tissues directly/induce an immune
response.
 Exogenous thyroid hormone increases the
metabolic rate & can increase heat production &
body temperature.
 PROPYLTHIOURACIL (PTU) has several side
effects including fever & that use of PTU can
induce fever and cause interstitial pneumonia.
 Peripheral heat dissipation can be impaired by
ATROPINE & ANTICHOLINERGIC drugs,
antihistamines, phenothiazine antipsychotic
drugs, & tricyclic antidepressants, which 
sweating, or by AMPHETAMINEs (especially
ecstasy), COCAINE, & sympathomimetic drugs,
which produce peripheral vasoconstriction.
Intravenously administered drugs can lead to
infusion-related phlebitis with production of
cellular pyrogens that produce fever.
TREATMENT with anticancer drugs → release of endogenous pyrogen from destroyed cancer
cells. Overdoses of serotonin reuptake inhibitors or use in people taking monoamine oxidase
(MOA) inhibitors can cause agitation, hyperactivity, and hyperthermia (Serotonin syndrome).
The most common cause of drug fever is a hypersensitivity reaction. Hypersensitivity drug
fevers signs: arthralgias, urticaria, myalgias, gastrointestinal discomfort, and rashes.
Temperatures of 38.9°C to 40.0°C (101.8°F to 104.0°F) are common in drug fever.
coinciding with the administration
of a drug & disappearing after the
drug has been discontinued

 autosomal dominant metabolic disorder;
 heat generated by uncontrolled skeletal muscle contraction can
produce severe & potentially fatal hyperthermia;
 mutation involves the RYR1 gene on chr. 19q13.1.2;
 muscle contraction is caused by an abnormal release of
intracellular Ca2+ from the sarcoplasmic reticulum through calcium
release channels.
  Ca2+ leads to a sustained hypermetabolic rate & a subsequent loss
of cellular integrity:
 excess lactate production,
 high adenosine triphosphate (ATP) consumption,
 increased oxygen consumption;
  carbon dioxide production;
 elevated heat production.
 An episode of malignant hyperthermia is triggered by exposure to
certain stresses or general anesthetic agents (acute/insidious onset of
symptoms).
 MH is associated with the halogenated anesthetic agents
(halothane) & the depolarizing muscle relaxant succinylcholine.
Nonoperative precipitating factors: trauma, exercise, environmental
heat stress, & infection.
 Dangerous in a young person (large muscle mass to generate
heat).
 Steady  in end-tidal carbon dioxide levels (initial sign, when the
condition occurs during anesthesia, is skeletal muscle rigidity).
 Cardiac arrhythmias and a hypermetabolic state;
 TREATMENT: measures to cool the body, cardiopulmonary support, &
the administration of dantrolene, a muscle relaxant drug that acts by
blocking the release of calcium from the sarcoplasmic reticulum.

BROMOCRIPTINE (a dopamine agonist)
& DANTROLENE (a muscle relaxant) may
be used as part of the treatment regimen.

The extent of the total body surface area
(TBSA) burn is estimated using the “rule
of nines. First-degree burns are not
included in the TBSA estimate. The
surface area of the palm, including palmar
finger surface, averages 1% of the body
surface area over a wide range of ages;
thus it can be used to estimate burn areas
of irregular size and shape.

SECOND DEGREE THIRD DEGREE
CHARACTE-
RISTIC
FIRST
DEGREE
SUPERFICIAL PARTIAL
THICKNESS
DEEP PARTIAL THICKNESS FULL THICKNESS
MORPHOLOGY
Destruction of
epidermis only
Destruction of
epidermis & some
dermis
Destruction of epidermis &
dermis, leaving only skin
appendages
Destruction of epidermis,
dermis, & underlying
subcutaneous tissue
SKIN FUNCTION Intact Absent Absent Absent
TACTILE AND
PAIN SENSORS
Intact Intact Intact but diminished Absent
BLISTERS
Present only
after first 24 hr
Present within
minutes, thin walled
and fluid filled
May appear as fluid-filled
blisters; often is layer of flat,
dehydrated “tissue paper”
that lifts off in sheets
Blisters rare; usually is a
layer of flat, dehydrated
“tissue paper” that lifts
off easily
APPEARANCE
OF WOUND
AFTER INITIAL
DÉBRIDEMENT
Skin peels at
24-48 hr, normal
or slightly red
underneath
Red to pale ivory,
moist surface
Mottled with areas of waxy
white, dry surface
White, cherry red, or
black; may contain visible
thrombosed veins; dry,
hard leathery surface
HEALING TIME 3-5 days 21-28 days 30 days to many months
Will not heal; may close
from edges as secondary
healing if wound is small
SCARRING None
May be present; low
incidence
influenced by
Genetic predisposition
Highest incidence because
of slow healing rate
promoting scar tissue
development; also
influenced by genetic
predisposition
Skin graft; scarring
minimized by early
excision and grafting;
influenced by genetic
predisposition

Acute Burn Injury
Direct tissue injury
Increased capillary
permeability
Systemic injury response
Increased capillary
permeability
Tissue injury
Endothelial injury
Leukocyte
sequestration
 Acidosis
 Depressed cardiac function
 Multiorgan dysfunction
Edema
Tissue ischemia
Hypovolemia and
hyperviscosity

Hypothermia is defined as a core temperature (i.e., rectal, esophageal, or tympanic) less than
35°C (95°F). Accidental hypothermia may be defined as a spontaneous decrease in core
temperature, usually in a cold environment and associated with an acute problem but without a
primary disorder of the temperature-regulating center.
In children, the rapid cooling process, in addition to the diving reflex that triggers apnea and
circulatory shunting to establish a heart–brain circulation, may account for the surprisingly high
survival rate after submersion. The diving reflex is greatly diminished in adults.
Systemic hypothermia may result from exposure to prolonged cold (atmospheric or
submersion). The condition may develop in otherwise healthy people in the course of accidental
exposure. Because water conducts heat more readily than air, body temperature drops rapidly
when the body is submerged in cold water or when clothing becomes wet. In people with
altered homeostasis due to debility or disease, hypothermia may follow exposure to relatively
small decreases in atmospheric temperature.
Many underlying conditions can contribute to the development of hypothermia. Malnutrition
decreases the fuel available for heat generation, and loss of body fat decreases tissue insulation.
Alcohol and sedative drugs dull mental awareness to cold and impair judgment to seek shelter
or put on additional clothing. Alcohol also inhibits shivering. People with cardiovascular disease,
cerebrovascular disease, spinal cord injury, and hypothyroidism also are predisposed to
hypothermia.

I Stage of excitement (mild hypothermia, 32–35°C): maximal muscle tremor,
resulting in a marked increase in resting metabolic rate, all sources of glucose are
utilized (hyperglycemia), and O2 consumption is increased up to six fold.
Tachycardia and vasoconstriction cause a rise in blood pressure; sacral
vasoconstriction causes pain. The person is at first fully awake, later confused and
even apathetic, and ultimately judgment becomes impaired.
II Stage of exhaustion (moderate hypothermia, 32-28°C): the sources of
glucose become exhausted (hypoglycemia); bradycardia, arrhythmia, and
depressed breathing occur and the person begins to hallucinate and to behave
perplexingly, soon losing consciousness and no longer feeling pain.
III Stage of paralysis (severe hypothermia, < ca.28°C): coma; no pupillary
reflexes (but no sign of brain death); ultimately ventricular fibrillation, asystole,
and apnea. The lower the temperature until cerebral blood flow ceases, the longer
the brain will tolerate circulatory arrest (30°C: 10–15min; 18°C: 60–90 min). This
is why some persons have survived extreme hypothermia (< 20°C). The long time
of circulatory arrest tolerated at low temperature is also of use in induced
therapeutic hypothermia (during open-heart surgery and preservation of organs
for transplantation).
THE ACUTE SEQUELAE AND SYMPTOMS OF HYPOTHERMIA CAN BE
DIVIDED INTO THREE STAGES (I–III):

 Infants are particularly at risk for
hypothermia because of their high ratio of
surface area to body mass.
 Relative to body weight, the body surface area
of an infant is three times that of an adult, and in
infants with low birth weight, the insulating layer
of subcutaneous fat is thinner.
 The newborn infant is particularly at risk, but
the premature newborn is at greatest risk for
heat loss and hypothermia.
 Under the usual delivery room conditions
(20°C to 25°C [68°F to 77°F]), an infant’s skin
temperature falls approximately 0.3°C/minute and
deep body temperature by approximately
0.1°C/minute.
 The heat loss occurs by convection to the
cooler surrounding air, by conduction to cooler
materials on which the infant is resting, by
radiation to nearby cooler solid objects, and by
evaporation from the moist skin.
The unstable body temperature of a preterm
infant can drop precipitously after delivery, and
this hypothermia is associated with an increase
in morbidity and mortality.
Neonatal Hypothermia

The newborn infant does have one
important process to fight against hypothermia.
This process is called nonshivering
thermogenesis, and it occurs primarily in
the liver, brown fat tissue, and brain.
 Brown fat differs from regular adipose
tissue because it has a high number of
mitochondria.
 Newborns have this brown fat tissue in
their necks and upper back.
 The brown fat has an uncoupling protein
called UCP1 (thermogenin), which allows
oxidation of fatty acids to produce heat.
 The extreme cold temperature stimulates a
release of epinephrine & TSH, which causes a
release of T3 and T4.
 Epinephrine activates the 5´/3´-
monodeiodinase, which assists with the
conversion of T4 to the more rapid-acting T3.
 The T3 acts in the brown fat to release the
mitochondrial oxidation from
phosphorylation. This, in turn, causes more
heat production.

Used to slow metabolism;
Preserve ischemic tissue after brain
trauma or during brain surgery;
After cardiac arrest;
In neonatal hypoxic encephalopathy.
Hypothermia protects the brain by:
Reduction in metabolic rate;
ATP consumption and oxidative stress;
Reduction of the critical threshold for
oxygen delivery;
Modulation of excitotoxic
neurotransmitters;
Calcium antagonism;
Preservation of protein synthesis;
Preservation of the blood-brain barrier;
Decreased edema formation;
Modulation of the inflammatory
response.
Survival from accidental hypothermia
has been reported in individuals with core
°t at 16° C (60.8° F) & from therapeutic
hypothermia with °t at 9° C (48.2° F).
Aneurysm opened with hypothermia & distal anastamosis completed

COMPLICATION MECHANISM
Acidosis
Rewarming stimulates peripheral vasodilation;
peripheral blood, returning to the core from the ischemic
peripheral tissues, causes a reduction in the pH of core
blood
Rewarming
shock
As rewarming and vasodilation progress, the body is
unable to maintain blood pressure because of reduced
fluid volume (from “cold diuresis”), catecholamine
depletion (prolonged shivering), and myocardial injury
Deep-ended
hypothermia
As colder surface blood is returned to the core, core
temperature may drop; this is also referred to as “after
fall” or “after drop”
Dysrhythmia
Rewarming places an additional stress on an already
severely stressed myocardium

CNS TRAUMA
ACCIDENTAL
INJURY
THERMAL BURNS
HEMORRHAGIC
SHOCK
MAJOR SURGERY
Major body trauma has varying
effects on temperature regulation,
depending on the body systems
involved.
CNS damage, inflammation
 intracranial pressures, or intracranial bleeding
Fever greater than 39°C (102.2°F)
NEUROGENIC FEVER
with/ without relative
bradycardia & is not
caused by infection
°t is sustained, not induce
sweating, resistant to
antipyretic therapy

Slight elevation in core temperature
Severe injuries result in
peripheral vasoconstriction with
decreased surface and core
temperatures
Core °t is inversely related to
the severity of the injury &may
be a result of decreased
oxygen transport to the tissues
In severe injuries, shivering is
absent & some alteration in
thermoregulation is evident
Volume expansion with warmed solutions is
recommended to prevent the deleterious
effects of hypothermia on cardiac output,
cardiac rhythm, and the immune system
Loss of blood volume
in hemorrhage
Peripheral vasoconstriction
& hypoxia contributing to
hypothermia
Risk for subsequent  in core °t occurs
treated with unwarmed, volume-expanding
solutions & surgery

Significant hypothermia through exposure of body
cavities to the relatively cool operating room environment;
Irrigation of body cavities with room °t solutions;
Infusion of room °t intravenous solutions;
Use of drugs that impair thermoregulatory mechanisms;
Inhalation of unwarmed anesthetic agents.
Anesthesia
Induces
hypothermia
Reduces platelet function
Impairs the coagulation
cascade contributing to
transfusion requirements
& postoperative
complications
Reduces
intraoperative
hypothermia &
postoperative
complications
Use of irrigating;
warmed intravenous solutions;
perioperative forced air;
other warming procedure.

Large burn injuries produce
significant hypothermia
because of the loss of the skin
barrier to fluid evaporation &
the loss of control of the
microcirculation in the skin.
Severe burns also
compromise the normal
insulation of the skin &
subcutaneous tissues.

Even with mild hypothermia and/or low
ambient temperature the perfusion of skin and
limbs is markedly reduced, with intermittent and
brief increases (Lewis reaction: about every 20
min at a skin temperature < 10°C). None the
less, frostbite may occur:
1st degree (at first pallor and loss of sensation;
swelling and pain after rewarming);
2nd degree (blister formation after 12–24 h
followed later by healing);
3rd degree (after days and weeks: extensive
tissue necrosis with healing by scar).

The mapping exercise produced
what you might expect: an angry
hot-head, a happy person
lighting up all the way through
their fingers and toes, a
depressed figurine that was
literally blue (meaning they felt
little sensation in their limbs).
Almost all of the emotions
generated changes in the head
area, suggesting smiling,
frowning, or skin temperature
changes, while feelings like joy
and anger saw upticks in the
limbs—perhaps because you’re
ready to hug, or punch, your
interlocutor. Meanwhile,
“sensations in the digestive
system and around the throat
region were mainly found in
disgust,” the authors wrote. It's
worth noting that the bodily
sensations weren't blood flow,
heat, or anything else that could
be measured objectively—they
were based solely on physical
twinges subjects said they
experienced.

Fever

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