ALTERATIONS IN BODY TEMPERATURE

I. INTRODUCTION
Body temperature is a routinely measured vital sign in all patients admitted to the
intensive care unit. Body temperature reflects the balance between the heat produced
and the heat loss from the body. Abnormal body temperature can be slight, such as low
grade fever or life threatening, as in severe cases of hypothermia or hyperthermia. The
nurse is often the person to monitor client‘s temperature, to identify deviations and to
report significant findings to the physician, so that appropriate therapy can be
instituted. Homoeothermic, humans capable of maintaining their body temperatures
within narrow limits. Biochemical reactions do not fluctuate due to the constant and
high temperatures. It is the somatic sensation of heat or cold. It is the degree of or
intensity of or intensity of heat of a body in relation to external environment. It is the
degree of hotness or coldness of a body or environment.
Body Temperature
In humans the traditional normal value for the temperature is 37°C. Various parts
of the body are at various temperatures.
II. Definition of body temperature
The body temperature is reflects the balance between the amount of heat produced
by the body processes and the amount of heat loss to the external environment.
Heat produced -Heat lost = Body temperature.

III. Types of Body Temperatures

Core temperature
It is the temperature of the interior body tissue below the skin and subcutaneous
tissue. The sites of measurement of core temperature are rectum, tympanic membrane,
oesophagus, pulmonary artery, urinary bladder.
Shell temperature
It refers to body temperature at the surface that is of the skin and subcutaneous
tissue. The sites of measurement of shell temperature are skin, axillae and oral.
Oral: 37°C (98.6°F)
Rectal: 37.5°C (99.6°F)
Tympanic: 375°C (99.5°F)
Axillary: 365°C (97.6°F)
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 Heat is continually produced in the body as a by-product of the chemical reactions
called metabolism. To convert Celsius to Fahrenheit, just multiply the temperature by
1.8 and then add 32 to the product. To convert temperature from Fahrenheit to Celsius,
subtract 32 from the number and then divide the difference by 1.8.Oct 21, 2012

IV. Regulation of temperature

The balance between the heat lost and heat produced or thermoregulation is
regulated by physiological and behavioural mechanisms.
A. Neural control
Body temperature is controlled by the hypothalamus. The hypothalamus detects
minor changes in body temperature and maintains the body temperature within the
critical level referred as set point. Neurons in both the pre-optic anterior hypothalamus
and the posterior hypothalamus receive two kinds of signals; one from peripheral
nerves that reflect warmth/cold receptors and the other from the temperature of the
blood bathing the region. These two types of signals are integrated by the
thermoregulatory centre of hypothalamus to maintain normal body temperature. When
these neurons detect the temperature of blood is too warm, signals radiate to the heat
loss centre located in the anterior portion of the hypothalamus which is mainly
composed of parasympathetic nerves that when stimulated initiate mechanism to
decrease body heat. If cold is detected signals are sent to the heat promoting centre in
the posterior hypothalamus which operates mainly through sympathetic nervous
system which stimulates mechanisms to produce body heat. In a neutral environment,
the metabolic rate of humans constantly produces more heat than is necessary to
maintain the core body temperature at 37°C.
B. Vascular control
The circulatory system functions as a transportation mechanism responsible for
carrying heat from body core to the skin surfaces from where it is transferred to the air
through radiation, evaporation, conduction and convection. In order to cool the body
the superficial blood vessels dilate which leads to increased blood flow to the skin and
is controlled by Peripheral nervous System. Sympathetic nervous system produces
vasoconstriction when body needs to conserve heat.
Heat production
Heat is produced in body by metabolism, which is the chemical reacxion in all
body cells. Food is the primary fuel source for metabolism. As metabolism increases
heat production increases and as it decreases less heat is produced. Heat production
occurs during rest, voluntary and involuntary shivering and no shivering
thermogenesis.
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  Rest
Basal metabolism accounts for the heat produced by the body at absolute rest. The
average basal metabolic rate (BMR) depends on the body surface area. Thyroid
hormones also affect the BMR by promoting the breakdown of body glucose and fat
they increase the chemical reactions in almost all the cells of the body. Stimulation of
sympathetic nervous system by nor epinephrine and epinephrine also increase the
metabolic rate of body tissues. These chemical mediators cause blood glucose to fall
which stimulates cells to manufacture glucose. The male sex hormone test osterone
increases BMR. Men have higher BMR than women.
 Voluntary movements
Voluntary movements such as muscular activity during exercise require additional
energy; during exercise, the glycogen which is stored in the body will be reduced and
broken down in to sugars with the release of energy. Heavier the exercise makes
greater heat production in the body. During exercise, the blood supply to the skin is
increased and the individual feels hot. The metabolic rate can increase up to 2000
times normal during exercise. Heat production can increase up to 50 times normal.
 Shivering
It is an involuntary body response to temperature differences in the body. The
skeletal muscle movement during the shivering requires significant energy. Shivering
can increase heat production up to 4-5 times greater than normal. The heat that is
produced assists in equalizing the body temperature, and the shivering ceases.
 Non shivering thermogenesis
It occurs primarily in neonates. Because neonates cannot shiver, a limited amount
of vascular brown tissue present at birth is metabolized for heat production.

Heat loss
Heat loss and heat production occurs simultaneously. The skin‘s structure and
exposure to the environment result in constant, normal heat loss through radiation,
conduction, convection and evaporation.
 Radiation (60%)
It is the transfer of heat from the surface of one object to the surface of another
without direct contact between the two. Radiation occurs because heat transfers
through electromagnetic waves Heat radiates from skin to any surrounding cooler
object. Radiation increases as the temperature difference between the object increases.
Blood flows from the core internal organs carrying heat to skin and surface blood
vessels. The amount of heat carried to the surface depends on the extent of
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vasoconstriction and vasodilatation regulated by the hypothalamus. Peripheral
vasodilatation increases blood flow to the skin to increase radiant heat loss. Peripheral
vasoconstriction minimizes radiant heat loss. Up to 8500 of the human body‘s surface
area radiates heat to the environment. However if the environment is warmer than the
skin, the body absorbs heat through radiation. The nurses increase the heat loss
through radiation by removing the clothing or blankets. The client‘s position enhances
radiation heat loss e.g. standing exposes a greater radiating surface area and lying in a
foetal position minimizes heat radiation. Covering body with dark, closely woven
clothing reduces the amount heat lost from radiation.
 Conduction (3%)
It is the transfer of heat from one object to another with direct contact. When a
warm skin touches a cooler object, heat is lost. When the temperature of two objects is
same, the conductive heat loss stops. Heat conducts through contact with solids,
liquids and gases. Conduction normally accounts for small amount of heat loss. The
nurse increases the conductive heat loss when applying an ice pack or bathing a client
with cools water. Applying several layers of clothing reduces conductive loss. The
body gains heat by conduction when contact is made with materials warmer than skin
temperature.
 Convection (15%)
It is the transfer of heat away by air movement. Heat is first conducted to air
molecules directly in contact with skin. Air currents carry away the warm air. As the
air current velocity increases, convective heat loss increases.
 Evaporation (22%)
It is the transfer of heat energy when a liquid is changed to a gas. The body
continuously lose heat by evaporation. About 600-900ml a day evaporates from the
skin and lungs, resulting in water and heat loss. This is normal loss and considered
insensible water loss and does not play a major role in temperature regulation. When
the body temperature rises, the anterior hypothalamus signals the sweat glands to
release sweat. Sweat evaporates from the skin surface resulting in heat loss. During
exercise and emotional and mental stress sweating is one way to lose excessive heat
produced by the increased metabolic rate.
C. Skin in temperature regulation
The skin‘s role in temperature regulation includes insulation of the
body, vasoconstriction and temperature sensation. The skin, subcutaneous tissue and
fat keep heat inside the body. In the human body, the internal organs produce heat and
during exercise and increased sympathetic stimulation. The amount of heat produced is
greater than the usual core temperature. Blood flows from the internal organs carrying
heat to the body surface. The skin is well supplied with the blood vessels esp., the
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areas of hands, feet and ears. Blood flow through these vascular areas of the skin may
vary from minimal flow to as much as 30% of the blood ejected from the heart, Heat
transfer from the blood through vessel walls, to the skin surface and is to environment
though the heat loss mechanisms.
The body‘s core temperature remains within the safe limits.
The degree of vasoconstriction determines the amount of blood flow and heat loss to
the skin. If the vasoconstriction is too high, the hypothalamus inhibits the
vasoconstriction. As a result the blood vessels dilate and more blood reaches the skin
surface. On a hot humid day the blood vessels in the hands are dilated and easily
visible. In contrast if the vasoconstriction becomes too low, the hypothalamus initiates
the vasoconstriction and blood flow to the skin lessens. Thus the body heat is
conserved. The skin is well supplied with heat and cold receptors. As the cold
receptors are plentiful in the skin, it functions primarily to detect cold surface
temperatures. When the skin becomes chilled, its sensors send information to the
hypothalamus. This initiates shivering to increase body heat production, inhibition of
sweating, and vasoconstriction.
D. Behavioural control
Humans voluntarily act to maintain comfortable body temperature when exposed
to temperature extremes. The ability of person to control body temperature depends on
degree of temperature extreme, the person‘s ability to sense feeling comfortable or
uncomfortable, thought processes or emotions. And the person‘s mobility or ability to
remove or add clothes. Infants can sense uncomfortable warm conditions but need
assistance in changing the environment. Older adults may need the help in detecting
cold environments and minimizing heat loss.
E. Mechanisms Activated by Cold
 Increased heat production by increase in BMR, muscle activity, thyroxin output,
epinephrine, nor epinephrine and sympathetic stimulation fever.
 Decreased heat loss by cutaneous vasoconstriction, and curling up.

F. Mechanisms Activated By Heat

 Increased heat loss by cutaneous vasodilatation, sweating, and increased respiration.
 Decreased heat production manifested by anorexia, apathy, illness.

V. Factors Affecting Body Temperature

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 Many factors affect the body temperature. Changes in body temperature within an
acceptable range occur when the relationship between the heat production and the heat
loss is altered by physiological or behavioural variables.
1. Age
At birth the newborn leaves a warm, relatively constant environment and
enters one in one in which temperature fluctuates widely. Temperature control
mechanisms are immature. An infant‘s temperature may respond drastically to changes
in the environment. Extra care is needed to protect the newborn from environmental
temperatures. Clothing must be adequate and exposure to the temperature extremes
must be avoided. A newborn loses up to 30% of body heat through the head and
therefore needs to wear a cap to prevent heat loss. The newborn‘s body temperature is
maintained within 35.5-37.5°C (95.9-99.5°F). Heat production steadily declines as the
infant grows into childhood.
Children‘s temperatures continue to be more variable than those of adults
until puberty. Older adults are particularly sensitive to temperature extremes because
of deterioration in control mechanisms particularly poor vasomotor control (control of
vasoconstriction and vasodilatation), reduced amounts of subcutaneous tissue, reduced
sweat gland activity and reduced metabolism, reduced intake of diet.
2. Exercise
Muscle activity requires an increased blood supply and an increased fat and
carbohydrate breakdown that causes increase in heat production. Any form of exercise
increases the heat production and thus the body temperature. Prolonged strenuous
exercise, such as long distance running, can temporarily raise body temperatures up to
41°C (105.8°F).
3. Hormone level
Women generally experience greater fluctuations in body temperature than men.
Hormonal variations during the menstrual cycle cause body temperature fluctuations.
Progesterone levels rise and fall cyclically during the menstrual cycle. When
progesterone levels are low, the body temperature is a few tenths of a degree below the
baseline level. The lower temperature persists until ovulation occurs. During ovulation,
greater amounts of progesterone enter the circulatory system and raise the body
temperature to previous baseline levels or higher by 0.3-0.6(0.5-l.0F). Body
temperature changes also occur in women during menopause (cessation of
menstruation). Women who have stopped menstruating may experience periods of
intense body heat and sweating lasting from 30 second to 5 minutes. There may be
intermittent increases in skin temperature of up to 4°C (72°F) during these periods,
referred to hot flashes. This is due to the instability of the vasomotor controls for
vasodilatation and vasoconstriction.

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 4. Circadian rhythm
Body temperature normally changes 0.5-1°C (0.91.8°F) during a 24 hour period.
The temperature is usually lowest between 1.004.00 am. During the daytime the
body temperature rises steadily up to 6.00pm and then declines to early morning
levels.
5. Stress
Physical and emotional stress increase body temperature through stimulation of
sympathetic nervous system due to increase in production of epinephrine and nor
epinephrine thereby increasing metabolic activity and heat production. A client who is
anxious could have an elevated body temperature for that reason.
6. Environment
Extremes of environment can affect a person‘s temperature regulatory systems. If
temperature is assessed in a warm room, a client may be unable to regulate body
temperature by heat loss mechanisms and the body temperature will be elevated.
Similarly, if the client has been outside in extremely cold weather without suitable
clothing the body temperature may be low.
7. Sickness
Disease condition is caused by the bacterial invasion. It is the productive action of
the body against the invading bacteria. The degree of temperature depends upon the
sensitivity of infection.

VI. F EVER
Fever is an elevation of body temperature that exceeds normally daily variation
and occurs in conjunction with an increase in the hypothalamic set point for e.g. 37°C-
39°C. Once the hypothalamic set point is raised, neurons in the vasomotor centre are
activated and vasoconstriction commences. The individual first notices
vasoconstriction in hands and feet. Shunting of blood away from the periphery to the
internal organs essentially decreases heat loss from the skin and the person feels cold.
For most fevers body temperature increases by l-2degree Celsius. Shivering which
increases heat production from muscles may begin at this time. Heat production from
liver also increases. In humans behaviour e.g. putting on more clothing or bedding
help raise body temperature.
The process of heat conservation (vasoconstriction) and heat production (shivering
and increased metabolic activity) continue until the temperature of blood bathing the
hypothalamic neurons match the new thermostat setting. Once the point is reached, the
hypothalamus maintains the temperature at febrile levels by same mechanism of heat
balance that is operative in a febrile state. The hypothalamic set point is again reset

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downward due to either the reduction in concentration of pyrogens or use of
antipyretics. The process of heat loss through vasodilatation and shivering are initiated.
Loss of heat by sweating and vasodilatation continues until the body temperature at the
hypothalamic level matches the lower settings. A fever of less than 41.50 (less than
106.7°F) is called hyperpyrexia. This abnormally high fever can develop in patients
with severe infection. But mostly occur in central nervous system haemorrhage. In
some rare cases, the hypothalamic set point is elevated as a result of local trauma,
haemorrhage, tumour or intrinsic hypothalamic malfunction. The term hypothalamic
fever is sometimes used to describe elevated temperature caused by abnormal
hypothalamic function. However, most patients with hypothalamic damage have
subnormal or equal but not subnormal body temperatures.
a) Causes of Fever
 Hot environment
 Excessive exercise
 Neurogenic factors like injury to hypothalamus
 Dehydration after excessive diuresis.
 As an undesired side effect of a therapeutic drug.
 Chemical substances e.g. caffeine and cocaine directly injected into the
bloodstream.
 Injection of proteins or other products.
 Infectious disease and inflammation.
 Severe haemorrhage.
b) Symptoms of fever
Flushed face: Hot dry skin; anorexia; headache; nausea and sometimes
vomiting; constipation and sometimes diarrhoea; body aches and scanty highly
coloured urine.
Clinical Signs of Fever
Increased heart rate, Respiratory rate and depth; shivering; pale cold skin; cyanotic
nail beds; cessation of sweating
c) Classification or Patterns of Fever
1. Intermittent fever: The temperature curve returns to normal during the day and
reaches its peak in the evening. Fluctuates greatly in 24 hours, may suddenly rise
above the normal then suddenly fall to or below the normal. E.g.: in septicaemia,
malaria, TB
2. Remittent fever: The temperature fluctuates but does not return to normal. E .g:
TB, viral diseases, bacterial infections.
3. Sustained fever: The temperature remains elevated with little fluctuation.

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 4. Relapsing fever: Periods of fever are interspersed with periods of normal
temperature.
. Tertian-When paroxysm occurs on 1st and 3rd days
. Quatrain Fever associated with paroxysm on first and fourth day. E.g. in malaria
d) Pathogenesis of Fever
1. Pyroxenes
Pyroxenes are any substance that causes fever. Exogenous pyroxenes are derived
from outside the patient; most are microbial products, toxins or microorganisms. E.g.:
lipopolysaccharide end toxin produced by all gram negative bacteria. Enterotoxins of
gram positive like staphylococcus aureus and Group. A and B Streptococcal toxins
2. Pyrogenic cytokines
Cytokines are small proteins that regulate immune, inflammatory and
hematopoietic processes. For e.g. stimulation of lymphocyte proliferation during any
immune response to vaccination is the result of the cytokines interleukin (IL) 2, IL-4,
IL-6, TNF (Tumour Necrosis Factor). Some cytokines cause fever and are called
pyrogenic cytokines including IL-l, lL-6, and interferon (IFN) alpha. Each cytokine is
encoded by a separate gene and each pyrogenic cytokine has been shown to cause
fever. The synthesis and release of endogen progeny cytokines are induced by
exogenous progeny which has recognizable bacteria or fungal sources. Viruses induce
progeny cytokines by infecting cells. In absence of microbial infection, inflammation,
trauma, tissue necrosis or antigen antibody complexes can induce the production of
progeny cytokines which individually or in combination trigger the hypothalamus to
raise the set point to febrile levels. The cellular sources of cytokines are primary
monocytes, neutrophils, lymphocytes although many other types of cells can
synthesize these molecules.
3. Elevation of hypothalamic set point by cytokines
During fever, levels of prostaglandin E2 (PG E2) are elevated in hypothalamic
tissue. Cytokines pass from circulation to brain. The endogenous and exogenous
pyroxenes interact with the endothelium of hypothalamus and raise set point of febrile
cells.
4. Production of cytokines in central nervous system
Several viral diseases produce active infection in the brain. Glial or neuronal cells
synthesize Interleukins TNF. Therefore central nervous system production of
cytokines raises hypothalamic set point.

e) Chronology of Events for Induction of Fever

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 FEVER

Microbial toxins
Heat conservation
heat production
Infection, microbial toxins,
mediators of inflammation,
immune reactions
Cyclic Elevated
AMP thermoregulatory
setpoint
Monocytes macrophages,
endothelial cells, others
PGE2

Pyogenic cytokines Hypothalamic

IL-1, IL-6, TNF, IFN endothelium

Circulation

f) Grades of Fever
l. Low grade fever: 37.1-38.2°C (98.8-100.6°F)
2. High grade fever: 38.2-40.5° C (100.6-104.9°F).
3. Hyperpyrexia: >40.5°C(104.9°CF)

g) PHASES OF FEVER
A febrile episode has three distinct phases:
1. Chill phase
The body‘s heat producing, mechanism attempts to increase the core
temperature. The client experiences cold and may shiver. Goose flesh caused by
contraction of erector pilli muscles m an attempt to trap air around body hairs, is
evident. Skin becomes pale and cool due to vasoconstriction

2. Fever phase

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 It occurs when fever reaches the new higher set point. The client‘s
skin feels neither hot nor cold. Cellular degeneration leads to fluid and electrolyte
losses. 1f fluid volume deficit has occurred the client may experience thirst.
Complaints of aching muscles, general malaise, and weakness can be there due to
increase of protein catabolism. Client may be drowsy or restless. An uncontrolled
fever can make the patient delirious and to suffer from convulsions due to cerebral
nerve cell irritation.
3. Flush or crisis phase
During this phase the client experiences profuse diaphoresis, decreased
shivering and possible fluid volume deficit. The client‘s skin appears flushed and
warm to touch because of vasodilatation.

VII. HYPERTHERMIA
Hyperthermia is characterized by an unchanged (normothermic) setting of the
thermoregulatory center in conjunction with an uncontrolled increase in body
temperature that exceeds the body‘s ability to lose heat. Exogenous heat exposure and
endogenous heat production are two mechanisms by which hyperthermia can result in
dangerously high internal temperatures. Excessive heat production can easily cause
hyperthermidespite physiologic and behavioural control of body temperature. For e.g.:
work and exercise in a hot environment can produce heat faster than peripheral
mechanisms can lose it. Although most patients with elevated body temperature have
fever, there are few circumstances in which elevated body temperature represents not
fever but hyperthermia.

a) Causes of Hyperthermia Syndromes

1. Heat stroke:
Caused by thermoregulatory failure in association with an arm environment may
be categorized as exceptional and no exceptional.
Exceptionals: it occurs in younger individuals who exercise in higher than normal
heat or humidity, dehydration
Non exceptional: It is caused by anticholinergic, including antihistamines, anti
parkinsonian drugs, diuretics, phenothiazines. It occurs in either very young or elderly
during heat waves, bedridden patients, elderly and taking drugs confined to poorly
ventilated and non AC environment.

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 2. Drug induced hyperthermia:
It’s due to increased use of psychotropic drugs. Monoamine oxidise inhibitors,
tricycle antidepressants, amphetamines, phencyclidine, lysergic acid diethylamide or
cocaine.
3. Malignant:
Occurs in individuals with inherited abnormality of skeletal muscle sarcoplasmic
reticulum that cause rapid increase in intracellular CA level in response to halothane
and other inhalation anaesthetics or to succinylcholine. In this there is elevated body
temperature, increased muscle metabolism, muscle rigidity, rhabdomyolysis, acidosis
and cardiovascular instability and is often fatal.
4. The narcoleptic malignant syndrome (NMS):
Occurs due to use of narcoleptic agents like anti-psychotic phenothiazines,
haloperidol, pro chlorprazine, metochlopramide or withdrawal of dopaminergic drugs
and is characterized by muscle rigidity (lead pipe), extra pyramidal side effects,
autonomic deregulation and hyperthermia. It is caused by inhibition of central
dopamine receptors in hypothalamus which results in increased heat generation and
decreased heat dissipation
5. Serotonin syndrome:
Seen in selective serotonin uptake inhibitors (SSRIs), MAO‘s and serotonergic
medications have overlapping features including hyperthermia but distinguished by
presence of diarrhoea, tremors, myoclonous rather than lead pipe rigidity.
6. Endocrinopathy:
Thyrotoxicosis and pheochromocytoma can lead to increased thermogenesis
7. Central nervous system damage:
Cerebral haemorrhage, status epileptics, hypothalamic injury can cause
hyperthermia
b) Assessment of the Patient

1. History
History of use of over the counter medications [OTC] or treatment such as
surgical/dental procedures. Nature of prosthetic materials or dental procedures.
Occupational history, exposure to animals, infectious agents, febrile or infected
individuals in the home, workplace geographic areas patient travelled, Use of tobacco,
IV drugs, trauma, animal bites, immunization, Family history of TB, arthritis,

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infectious disease, anaemia. Ethnic origin e.g. blacks are more likely to have
haemoglobinopathies
2. Physical examination
Vital signs, check skin, lymph nodes, eyes, nail beds, Cardiovascular System,
chest, abdomen, musculoskeletal system, nervous system, penis, scrotum, testes should
be examined carefully. Pelvic examination for Pelvic inflammatory disease and tubo-
ovarian abscess.
3. Laboratory tests
If a patient reveals more than a simple viral illness or pharyngitis then lab testing is
done:
Clinical pathology: Complete blood count, differential leukocyte count,
Neutrogena is present in some viral infections, drug reactions, Systemic lupus
erythematous, typhoid, leukaemia. Lymphocytosis with typhoid, brucellosis, TB and
viral diseases. Monocytosis in typhoid, TB, brucellosis, lymphoma, Eosinophilia in
hypersensitivity and drug reactions, Hodgkin‘s disease, adrenal insufficiency. Blood
smear for malarial pathogens, ESR, Urinalysis. Any abnormal fluid accumulation like
pleural fluid, peritoneum, joint is examined. Bone marrow biopsy for histopathologic
studies as well as culture in infiltration of marrow by pathogens or tumor cells. Stool
for occult blood, inspection for ova, parasites.
Chemistry: Electrolytes, blood glucose, blood urea nitrogen, creatinine, liver
function test
Microbiology: Smears and cultures of specimen from throat, urethra, anus, cervix,
vagina. When there are no localized findings or when findings suggest the involvement
of pelvis, GIT. If respiratory infection then sputum evaluation (Gram staining, staining
for AFB, culture). Cultures of blood, abnormal fluid collection, urine if fever reflects
more than uncomplicated viral illnesses. CSF examined and cultured if meningismus,
severe headache or change in medical status is there.
4. Radiology
A chest X-ray is part of evaluation for any significant febrile illness.
c) Management
a. Medical management
It is important to distinguish between fever and hyperthermia since hyperthermia
can be fatal and doesn‘t respond to antipyretics.
Pharmacological Management

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 1. Acetaminophen: adult: 325-650 mg PO q 4-6 hrs. Children: 10-15mg/kg body
weight q4-6 hrs.
2. Ibuprofen (NSAID) dosage: adult-200-400mg PO q6hrs; Children: 5mg/kg body
wt. for temp. <102.5°F;10 mg/kg body wt. for temp 102.5°F (not to exceed 40
mg/kg/day).
3. Indomethacin and naproxen (NSAID).
4. Aspirin: adult 325-650 mg PO q6hrs; children 10-20 mg q 6hrs.
5. Glucocorticosteroid: potent antipyretic inhibit PGEZ synthesis.
6. Meperidine, morphine sulphate, chlorpromazine. To manage severe rigors:
treatment of underlying cause, nutrition, rest, physical cooling: tepid bath,
hypothermia blankets
The attempt to lower the already normal hypothalamic set point is of little use.
Physical cooling with sponging, cooling blankets, cooling mattress or even ice bags
should be initiated immediately in conjunction with appropriate pharmacological
agents and intravenous fluids. Internal cooling can be achieved by gastric or peritoneal
lavage by iced saline. In extreme circumstances, haemodialys is or even cardio
pulmonary bypass with cooling of blood may be perfumed.
d) Nursing Management of Fever and Hyperthermia

o Monitor vital signs.

o Assess skin colour and temperature.
o Monitor white blood cell count, hematocrit value, and other pertinent
laboratory reports for indication of infection or dehydration.
o Remove excess blankets when the client feels warm, but provide extra
warmth when the client feels chilled.
o Provide adequate nutrition and fluids to meet the increased metabolic
demands and prevent dehydration.
o Measure intake and output.
o Reduce physical activity to limit heat production especially during the flush
stage.
o Administer antibiotics as ordered.
o Provide oral hygiene to keep the mucous membranes moist.
o Provide a tepid sponge bath to increase heat loss through conduction.
o Provide dry clothing and bed linens.
During chill phase
1. Risk for altered body temperature as evidenced by shivering and feeling cold

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 Monitor vital signs, restrict activity, monitor skin colour and temperature, apply
extra blankets, increase fluid intake, apply extra blankets, supply oxygen if client has
pre-existing cardiac or respiratory problem.
During fever phase
1. Hyperthermia related to invasion of microorganisms as evidenced by
increased body temperature >38.5°C, irritability, increased respiratory rate and dry
skin
Remove excess clothing and covers, cover with light warm clothing to avoid
chilling, monitor temperature as needed, encourage cool fluids, apply lubricant to dry
lips and nasal mucosa, increase air circulation to encourage cooling, control
environmental temperature not too cold, administer antipyretics as prescribed, cool
with tepid bath, adjust cooling measures on the basis of temperature, notify physician
of significant change.
2. Impaired comfort as evidenced by restlessness
Promote rest, restrict activity, assess client‘s response to pain management, and
take safety precautions if patient is delirious, monitor for decreasing level of
consciousness.
3. Impaired nutrition related to fever as evidenced by anorexia and lack of food
intake. Provide high calorie diet, encourage fluid intake, reduce iron intake
During flush phase
1. Altered fluid and electrolyte balance related to excessive sweating Monitor
intake and output, monitor electrolytes, replace fluids and electrolytes lost through
sweating, monitor temperature, and provide rest.
Heat cramps: These painful muscle cramps occur most commonly in the legs of
young people following vigorous exercise in the hot weather. There is no elevation of
core temperature. The mechanism is considered to be extracellular sodium depletion
following electrolyte losses a result of persistent sweating with replacement of water
but no salt. The syndrome is also encountered in miners undertaking heavy physical
work in hot conditions with very limited ventilation, which impairs the effect of
evaporative heat loss from sweating. Symptoms usually respond to salt replacement.
Heat exhaustion: Heat exhaustion occurs when there is an elevation in core
(rectal) temperature to between 37-40°C and is usually seen when the individual is
undertaking vigorous physical work in a hot environment. A high work rate, extreme
ambient temperature, impairing evaporative heat loss due to high humidity or
inappropriate clothing may all combine to overcome thermoregulatory control. The
diagnosis is based on the findings of an elevated core temperature associated with
hyperventilation and symptoms of tiredness or fatigue, muscular weakness, dizziness
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 and collapse. The blood analysis may show evidence of dehydration with mild
elevation of blood urea, sodium concentration and haematocrit. Treatment involves
removal of patient from the heat, active cooling using cool sponging, and fluid
replacement. This may be achieved by oral dehydration mixtures containing both salt
and water or intravenous isotonic saline. Adult patients may require 5 liters or more
positive fluid balance in the first 24 hours. Frequent monitoring of blood electrolytes is
important, especially in patients receiving I.V. replacement therapy.
Heat stroke: Heat stroke occur when the core body temperature rises above 40°C
and is a severe and life threatening condition provoked by failure of heat regulatory
mechanisms. The symptoms of heat exhaustion progress to include headache, nausea
and vomiting. Neurological manifestations include a coarse muscle tremor and
confusion, which may progress to loss of consciousness. The patient‘s skin feels very
hot, and sweat is often absent due to failure of thermoregulatory mechanisms. The
condition may progress from heat exhaustion or present acutely in a patient who has
become progressively dehydrated without symptoms. Coincidental illness age and
drug therapy, particularly phenothiazine diuretics and alcohol may be the contributory
factors. Complications include hypovolemic shock, lactic acidosis, and disseminated
intravascular coagulation. Rhabdomyolis is hepatic and renal failure and cerebral
edema. The patient should be managed in ICU with rapid cooling using ice packs,
careful fluid replacement and appropriate intravascular monitoring. Investigations
reflect the complications and include coagulation studies and muscle enzymes, in
addition to routine haematology and biochemistry

VIII. F EVER OF UNKNOWN ORIGIN

Fever of unknown origin (FUO) was defined by Peterson and Benson in 1961 as:
l. Temperatures of > 38.3 degree Celsius (>101 degree Fahrenheit) in several
occasions;
2. A duration of fever of > 3 weeks and;
3. Failure to reach a diagnosis despite 1 week of inpatient investigation.

a) Classification of F UO
Derrick and Street have proposed a new system for classification of F U0:
1. Classic FUO: Same as above criteria. E.g. infections, malignancy, inflammatory
diseases, drug fever.
2. Nosocomial FUO: A temperature of >= 38.30 C (>=101°F) develops on
several occasions in a hospitalized patient who is receiving acute care and in whom
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infection was not present at time of admission. For e.g. septic thrombophlebitis,
sinusitis, drug fever.
3. Neutropenic FUO: A temperature of >= 38.30 C (>=101°F) develops on
several occasions in a patient whose neutrophil count is < SOO/micro litre or is
expected to fall to that level in 1-2 days.
4. HIV associated FUO: A temperature of >= 383° C (>=101° F) develops on
several occasions over a period of > 4 weeks for outpatients or > 3 days for
hospitalized patients with HIV infection.
b) Causes of FUO
1. Infections
 Localized phylogenic infections: appendicitis, cholecystitis, dental abscess.
 Intravascular infections: bacterial endocarditis.
 Systemic bacterial infections: typhoid fever.
 Mycobacterium infections: tuberculosis.
 Fungal infections: candidiasis
 Viral infections: dengue, hepatitis A, B, C, D and E, HIV infection.
 Parasitic infections: ameobiasis, malaria.
 Rickettsial infections.
 Mycoplasmal infections.
 Chlamydial infections.
2. Neoplasms
a. Malignant: Colon cancer, gall bladder carcinoma, leukemia, renal cell
carcinoma.
b. Benign: Castle man‘s disease
3. Habitual hyperthermia
Exaggerated circadian rhythm
4. Collagen vascular/ Hypersensitivity diseases
Rheumatic fever, rheumatic arthritis, systemic lupus erythematous
5. Granulomatous Diseases
Cohn’s disease
6. Miscellaneous conditions
Drug fever, gout, haemo globinopathies, tissue infarction or necrosis
7. Inherited and metabolic diseases
Adrenal insufficiency, familial cold urticarial
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 8. Thermoregulatory Disorders
a. Central: Brain tumour, Cerebrovascular accident, encephalitis;
b. Peripheral: Hyperthyroidism, pheochromocytoma
c) Diagnosis of FUO
History and physical examination, blood investigations, tumor markers, purified
protein derivative for TB, semiogical studies, peripheral smears, multiple samples for
culture and sensitivity, X-Ray studies, bone marrow biopsy, Liver biopsy, G1 contrast
studies, CT scan, MR1, ultrasonography.
d) Treatment
The patients with classic FUO are continually observed and examined and not
given the empirical therapy. The antibiotic therapy given to the patient can delineate
the ultimate cause of FUO. If neutropenia and vital sign instability are present then
empirical therapy with fluoroquinolone and piperacillin is given. If PPD test is positive
or granuloma hepatitis is confimied then isoniazid and rifampicin for 6 weeks is given.
When no underlying source of infection is found even after 6 months the prognosis is
generally good. The debilitating symptoms are treated by NSAIDSs and
glucocorticoids.

IX. HYPOTHERMIA
Hypothermia is a state in which the core body temperature is lower than 35 degree
Celsius or 95 degree Fahrenheit. At this temperature many of the compensatory
mechanism to conserve heat begin to fall.
a) Classification
1. Primary hypothermia: It is a result of the direct exposure of a previously healthy
individual to the cold.
2. Secondary hypothermia: It is hypothermia that results due to a complication of a
serious systemic disorder.
3. Accidental hypothermia: It results from unintentional exposure to cold or wet
and windy climate with an ambient temperature less than 16 degree Celsius.
4. Induced hypothermia: It is deliberate lowering of temperature to a range of a 78-
900F (2632.50C) to reduce oxygen need during surgery (especially cardiovascular and
neurosurgical procedures) and in hypoxia, to reduce blood pressure and to alleviate
hyperthermia by administering drugs that depress the hypothalamic thermostat or by
encasting the client in a cooling blanket.

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 b) Causes
1. Exposure to cold environment in winter months and colder climates.
2. Occupational exposure or hobbies that entail extensive exposure to cold for
e.g. hunters, skiers, sailors and climbers.
3. Medications like ethanol, phenothiazine, barbiturates, benzodiazepines, cyclic
antidepressants, anesthetics.
4. Endocrine dysfunction: hypothyroidism, adrenal insufficiency, hypoglycemia.
5. Neurologic injury from trauma, Cerebral vascular accident, Subarachnoid
hemorrhage.
6. Sepsis.
c) Risk Factors for Hypothermia
1. Age extremes: Elderly, neonates.
2. Outdoor exposure: Occupational, sports-related, inadequate clothing.
3. Drugs and intoxicants: Ethanol, phenothiazines, barbiturates, anesthetics,
neuromuscular blockers and others.
4. Endocrine related: Hypoglycemia, hypothyroidism, adrenal insufficiency, and
hypopituitarism.
5. Neurologic related: Stroke, hypothalamic disorders, Parkinson‘s disease, spinal
cord injury.
6. Multisystem: Malnutrition, sepsis, shock, hepatic or renal failure.
7. Burns and exfoliative dermatologic disorders. 8. Immobility or debilitation. '
d) Clinical Presentation
Hypothermia leads to physiological changes in all organ systems.
 Mild hypothermia
Temperature 35-32.2°C (95-90“F)
CNS- Decreased cerebral metabolism, amnesia, Apathy, dysarthria, Impaired
judgement.
CVS- Tachycardia, vasoconstriction, increase in cardiac output and Blood
pressure.
Respiratory system- Tachypnoea, bradypnea, decline in oxygen consumption,
bronchospasm.
Renal and endocrine- Diuresis increase in metabolism with shivering.
Neuromuscular -Increased pre shivering muscle tone, fatiguing, ataxia

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  Moderate hypothermia
Temperature -<32.2-28°C (90-82.4“F)
CNS- EEG abnormalities, decreasing level of consciousness, pupillary dilatation,
hallucinations.
CVS- Decrease in pulse and cardiac output, increased atrial and ventricular
arrhythmias, prolonged systole. Respiratory system Hypoventilation, 50° 0 decrease in
carbon dioxide per 8°C drop in temp, Absence of protective airway reflexes, 50%
decrease in oxygen consumption.
Renal and endocrine- 50° 0 Increase in renal blood flow impaired insulin action .
Neuromuscular- Hyporeflexia, diminishing shiverin g induced thermogenesis,
rigidity.
 Severe hypothermia
Temperature -< 28°C (82.4°F)
CNS- Loss ofcerebrovascular auto regulation, decline in cerebral blood flow,
coma, loss of reflexes.
CVS- Decrease in BP, heart rate and cardiac output, a systole.
Respiratory system- Pulmonic congestion and edema, apnea.
Renal and endocrine- Decrease in renal blood flow, Extreme oliguria.
Neuromuscular- No motion, peripheral areflexia.
There is progressive deterioration, with apathy, poor judgment, ataxia, dysarthria,
drowsiness, pulmonary edema, acid-base abnormalities, coagulopathy, and eventual
coma. Shivering may be suppressed below a temperature of 322°C (90°F), because the
body‘s self-warming mechanisms become ineffective. The heartbeat and blood
pressure may be so weak that peripheral pulses become undetectable.
e) Diagnosis
Hypothermia is confirmed by measuring the core temperature, at two sites. Rectal
probes should be placed to a depth of 15 cm and not adjacent to cold faces. A
simultaneous oesophageal probe should be placed 24cm below the larynx; it may lead
to falsely high during heated inhalation therapy.
f) Management
Management consists of continuous monitoring, rewarding, and removal of wet
clothing, insulation, and supportive care.

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 Monitoring
The ABC‘s of basic life support are a priority. The patient‘s vital signs, central
venous pressure, urine output, arterial blood gas levels. Blood chemistry
determinations (BUN, creatinine. glucose, electrolytes), and chest X-Rays are
evaluated frequently. Body temperature is monitored with an esophageal, bladder, or
rectal thermostat. Continuous ECG monitoring is performed because cold induced
myocardial irritability leads to conduction disturbances. Especially ventricular
fibrillation. An arterial line is inserted and maintained to record BP and facilitate blood
sampling.
Rewarming
Rewarming methods include active core (internal) rewarming, active external
rewarming, and passive or spontaneous rewarming.
Core rewarming
Methods include cardiopulmonary by-pass, warm fluid administration, and warm
humidified oxygen by ventilator, and warmed peritoneal lavage. Core rewarming is
recommended for severe hypothermia i.e. poikilothermia. Monitoring for ventricular
fibrillation as the patient passes through 31C-32°C (88-90°F) is essential.
Passive external rewarming
It includes the use of warm blankets or over-the-bed heaters. Passive rewarming of
the extremities increases blood flow to the acidosis, anaerobic extremities.
Supportive care
External cardiac compression (only as directed in very cold patient). Defibrillation
of ventricular fibrillation. It is ineffective in patients with temperatures lower than
31°C (88°F). Mechanical ventilation with positive endexpiratory pressure (PEEP) and
heated humidified oxygen to maintain tissue oxygenation. Administration of warm
intravenous fluids (nonnal saline) to correct hypotension and maintain urine output and
core rewarding. Administration of sodium bicarbonate to correct metabolic acidosis 0
Administration of antiarrythmic medications bretyliumtosylate is safe. 0 Low dose
dopamine (2 -5 microgram/kg) to treat hypotension. Gastric tube insertion to prevent
dilation secondary to decreased bowel motility. lndwelling catheter to facilitate cold
induced diuresis.
g) Nursing Management of Hypothermia
Nursing diagnosis
Hypothermia as evidence by body temperature <35C, shivering, cool skin,
irritability etc.

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 Nursing interventions
 Provide extra covering and monitor temperature.
 Cover head properly.
 Use heat retaining blankets.
 Keep patient‘s linen dry.
 Control environmental temperature. Provide extra heat source (heat lamp,
radiant warmer, pads, and blankets).
 Carefully assess for hyperthermia or burn.
 Regulate heat source according to physical response.

X. Hypothermia in New born Babies

New born babies are often not able to keep themselves warm with low
environmental temperature resulting in hypothermia. Hypothermia continues to be a
very important cause of neonatal morbidity and mortality due to lack of attention by
the health care providers.
1. Handicaps of newborn in temperature regulation
A newborn is more prone to develop hypothermia because of a large surface area
per unit of body weight. A low birth weight baby has decreased thermal insulation due
to less subcutaneous fat and reduced amount of brown fat. Brown fat is a site of heat
production. It is localized around the adrenal glands, kidneys, nape of neck, inter
scapular and axillary region. Metabolism of brown fat results in heat production.
Blood flowing through the brown fat becomes warm and through circulation transfers
heat to other body parts of the body. This mechanism of heat production is called as
non-shivering thermogenesis. LBW babies lack this effective méchanism of heat
production.
ll. Mechanism of heat loss
Newborn loses heat by evaporation (particularly soon after birth due to evaporation
of amnioticfluid from skin surface), conduction (by coming in contact with cold
objects -cloth, tray etc), convection ( by air currents in which cold air from open
windows replaces warm air around babies), and radiation(to cooler solid objects in
vicinity walls). The process of heat gain is by conduction, convection and radiation in
addition to nonshivering thermogenesis.
Why newborns are prone to develop hypothermia?
. Large surface area.
. Decreased thermal insulation due to lack of subcutaneous fat.
. Reduced amount of brown fat.

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 Nursing Responsibility in Preventing the Heat Loss in Newborns and Infants
Evaporation

Keep the child dry, remove wet nappies, and minimize exposure during baths.
Conduction

e.g. weighing a baby. Put the baby on pre-warmed sheet and cover scales and X-
Ray diapers with warm diaper or blanket.

Radiation Keep the babies cots and incubators away from outside walls, air
conditioners; cover the baby if stable.
Convection

Avoid currents of air, manage babies inside incubator, and organize work to
minimize opening portholes, provide warm humidified oxygen.
XI. FROST BITE
Frost bite is the condition in which the tissue temperature drops below 0 degree
Celsius. It is trauma from exposure to freezing temperatures and actual freezing of the
tissue fluids in the cell and intracellular spaces. It results in cellular and vascular
damage. Body parts more frequently affected by frostbite include the digits of feet and
hands, tip of nose, and earlobes.
a) Predisposing factors
Contact with thermal conductors such as metal or volatile solutions, constrictive
clothing or shoes, immobility, careless application of cold packs, vasoconstrictive
medications, Raynaud‘s phenomenon.
b) Pathophysiology
In pre freeze phase plasma leaks out and microvascular contriction develops

The freeze phase begins with extra cellular crystallization

Water exits the cells and causes Intracellular dehydration, hyperosmolality And
cellular shrinkage

Damaged tissue releases thromboxame A2 and prostaglandin which produce

platelet aggregation and vasoconstriction

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 The microvasculature begins to colapse

Tissue ischemia and necrosis

c) Classification of Frost Bite

1. First degree frost bite: Causes only anaesthesia and erythematic.
2. Second degree frost bite: Appearance of superficial vesiculation surrounded
by edema leads to very cold extremities.
3. Third degree frost bite: Haemorrhagic vesicles due to serious
microvasculature injury which further leads to cyanosis.
4. Fourth degree frost bite: Damage in sub cuticular, muscular and osseous
tissue.
d) Symptoms
The injured area is white or mottled blue white, waxy and firm to the touch. There
is tingling and redness followed by pallor and numbness of the affected area. There are
three degrees: Transitory hyperaemia following numbness, formation of vesicles and
gangrene. The affected area is insensitive to touch.
e) Diagnosis
 Angiography and MRI to assess the potency of large vessels.
 Ultrasonography.
 Plethismography.
 Thermography to evaluate perfusion after rewarming.
 Technetium scintigraphy to assess perfusion.
f) Management of Frost Bite
Before thawing
Remove the client from cold environment. Stabilize core temperature and treat
hypothermia. Protect the frozen part and do not apply friction or massage.
During thawing
Provide parental analgesia e.g. keratolac. Immerse part in 37-40°C circulating
water containing an antiseptic soap for 10-45 minutes. Encourage patient to gently
move the part. Provide ibuprofen 40 mg PO.

After thawing

24
 Gently dry and protect the part and elevate it. Apply pledges between toes; if
macerated. If clear vesicles are intact aspirate the fluid or the fluid will reabsorb in
days; if broken then debride and dress with antibiotic. Leave haemorrhagic vesicle
intact to prevent infection. Continue analgesics Ibuprofen 400mg 8-12 hourly. Provide
tetanus prophylaxis and hydrotherapy at 37°C. The patient should be stimulated with
orally administered hot fluids such as tea and coffee. The patient should not be allowed
to smoke. Artificial respiration should be administered if the patients unconscious.
Non freezing cold injury
Trench foot or immersion foot is the less severe form of cold injury resulting from
prolonged exposure to cold and damp conditions the limb appears cold ischemic and
numb but there is no freezing of tissue, no rearming the limb appears mottled. There
after it becomes hyperthermia, swollen and painful. Recovery may take many months
and there may be chronic pain and sensitivity to cold. The pathology probably involves
endothelial injury. The pain and associated paraesthesia may be difficult to control
with normal analgesic. Hypothermia and hyperthermia are two major types of
alterations in body temperature. If well treated, it will cause no complications.
Otherwise it can be fatal.
XII. NURSING MANAGEMENT AND TERMOREGULATION

THERMOREGULATION PROBLEMS AND NEEDS

Problems

Actual Potential problems

problems

o Body temperature o Risk for infection

alteration o Risk for hypovolemia
o Hot, flushed skin o Risk for hypothermia/
o Increased respiratory hyperthermia.
rate o Risk for seizure
o Loss of appetite
o Malaise or weakness

Needs
General needs Specific needs

25
  Fluid management o Infection prevention
 Maintenance of o Maintain normal body
body temperature temperature
 Nurturing and o Maintain normal blood
bonding sugar
 Elimination needs o Maintain hydration
 Maintain hygiene o Maintain normal
 Sleeping respiration

NURSING DIAGNOSIS

Hyperthermia related to increased body temperature above usual range as evidenced

by flushed skin, warm skin to touch, increased pulse, and respiratory rate (Herpetic
lesion of the mouth)
Hypothermia related to decreased body temperature as evidenced by pale cool skin,
decreased pulse and respiratory rate & feeling of cold and chill.
Ineffective thermoregulation related age (older adults or infants) or weak inability to
adapt to environmental temperature.

a) INTERVENTIONS
 Nursing interventions for a patient with fever
 Assess the patients vital signs
 Assess for contributing factors such as dehydration, infection, or
environmental temperature.
 Assess skin temperature
Observe for shivering and diaphoresis.
Assess patient comfort and well-being
 Determine phase of fever—chill , plateau, fever break
 Remove excess blankets when the client feels warm, but provide extra
warmth when the client feels chilled.
 Promote heat loss and lower the temperature
Limit physical activity for reducing heat production
Reduces external covering for heat loss
Physical therapies including ice packs application; bathing with alcohol-
water solutions
 medications
26
 Observe therapeutic effect.
Administer antibiotics and antipyretics as per order
 Observe the intake of liquids and the output of urine.
Provide fluids at least 3000ml per day for patient with normal cardiac and
renal functional to compensate fluids lost through insensible water loss
and sweating.
 Promote comfort and prevent complications.
Provide oxygen therapy
Send diagnostic tests to find the cause of fever
Provide psychological support

 Nursing interventions for a patient with hypothermia

 Control environment temperature at 22-24C
 Elevate body temperature.
 Patients are monitored closely for cardiac irregularities and electrolyte
imbalances. Observe the vital signs, take temperature once at least per
hour until the temperature returned normal and stability.
 Eliminate pathogeny

XIII. SUMMARY

27
Temperature can be expressed as degree Celsius or Fahrenheit. Nerve malfunction and
protein denaturation seen with higher temperature. Measured under tongue, axilla or rectum.
Oral temperature is 0.5 C less than core body temperature (rectal temp). Internal temp varies
with activity pattern and changes in external temp. Circadian fluctuation of about 1C- lowest
at night and highest during the day. Women show higher temp during second half of
menstrual cycle. Fever occur in approximately half of the patients admitted to the ICU and is
reported to be associated with adverse outcome. Conversely, the beneficial effect of fever
may include reduction in bacterial growth and promotion of antibody and cytokine synthesis,
thereby actvating immune cells and improving survival.

28
XIV. CONCLUSION

29
 Body temperature is the degree of hotness or coldness of a body or environment.
It is the somatic sensation of heat or cold. It is the degree or intensity of heat of a
body in relation to external environment. Humans capable of maintaining their
body temperature within narrow limits. Body temperature abnormalities, which
occur because of several infectious and non-infectious aetiologies’ are among the
most commonly noted symptoms of critically ill patients. These abnormalities
frequently trigger changes in patient management. Body temperature is a
routinely measured vital sign

XV. BIBLIOGRAPHY

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 1. Basher. P. Shabeer, Khan Yaseen S.(2013). A Concise Textbook of
Advanced Nursing Practice. “psychosocial Pathology”.1 st Edition.
Emmess Medical Publishers. 241-255
2. Potter A Patrica, Anne Griffin Perry’. Fundamentals of Nursing II.
6th Edition. Elsevier India private ltd. 619-637
3. Nancy Sr. (2006). Fundamentals of Nursing.1st volume. Jaypee
medical publishers. 255-269
4. Basavanthappa BT. Textbook of Fundamentals of Nursing. “Vital
Signs”. 1st Edition. Jaypee Medical Publishers. 125-255
5. Navadeep kaur Brar & Rawat Hc. (2005). The text book of advanced
nursing practice. 1st Edition. India. Jaypee Brothers Medical (p) ltd.
6. James A Johnson. (2009). Health Organization: Theory, Behavior and
Development. 1st Edition. Toronto: Jones and Bartlett publishers, 109-
133
7. Neelam kumara and Madu Sharma. (2013). Nursing services and
administration. India: 1st Edition. PV books, 345-349
8.
Journal reference
1. Nakitende, T Namujwiga, ( October 2018)An International Journal
of Medicine. Volume 111, pages 691-697
2. W. Larry KENNEY, AND Thayne A. Munce. (2003). Journal of
Applied Physiology. Invited Review: Aging and human temperature
regulation. Pages 202- 230

Net reference
1. www.emedicine.medspace.com
2. www.medicinenet.com
3. www.nia.nih.gov

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