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ALTERATIONS IN BODY TEMPERATURE

INTRODUCTION
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.
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Body Temperature

In humans the traditional normal value for the temperature is 37°C. Various parts of the body
are at various temperatures.

Physiology

The body temperature is the difference 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.

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.

Rectal

Oral : 37°C (98.6°F)

Rectal : 37.5°C (99.6°F)

Tympanic : 37.5°C (99.5°F)

Axillary : 36.5°C (97.6°F)

Heat is continually produced in the body as a by- product of the chemical reactions called
metabolism.

Regulation

The balance between the heat lost and heat produced or thermoregulation is regulated by
physiological and behavioural mechanisms.
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• Neural control
• Vascular control
➢ Heat production - Rest
- Voluntary movement
- Involuntary shivering
- Non shivering thermogenesis
➢ Heat loss - radiation
- conduction
- convection
- evaporation.
• Skin temperature regulation
• Behavioural control
• Mechanisms activated by cold
• Mechanisms activated by heat

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 send to the heat promoting centre in the posterior
hypothalamus stimulated initiate mechanism to decrease body heat. If cold is detected
signals are sent to the heat promoting centre in the posterior hypothalamus which
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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 reaction 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.

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 testosterone increases BMR. Men have higher BMR than
women.
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Voluntary movements

• Voluntary movements such as muscular activity during exercise require additional

energy.
• 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 vasoconstriction and
vasodilatation regulated by the hypothalamus.
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• Peripheral vasodilatation increases blood flow to the skin to increase radiant heat loss.
Peripheral vasoconstriction minimizes radiant heat loss. Up to 85% of the human
body’s surface area radiates heat to the environment.
• 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 cool 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.
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• 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 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 transfers from the blood through vessel walls, to the skin’s surface and is lost to
the environment through 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’s
surface.
• On a hot humid day the blood vessels in the hands are dilated and easily visible.
• If the vasoconstriction becomes too low, the hypothalamus initiates the
vasoconstriction and blood flow to the skin lessens. Thus, 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
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the skin becomes chilled, its sensors send information to the hypothalamus. This initiate
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 vaso- constriction, curling up.

F. Mechanisms Activated by Heat

• Increased heat loss by cutaneous vasodilatation, sweating, increased respiration

• Decreased heat production: manifested by anorexia, apathy, illness.

Factors Affecting Body Temperature

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
which temperature fluctuates widely.
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• 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(0.5-1.0°F).
• 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
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intermittent increases in skin temperature of up to 4°C (7.2°F) during these periods,

referred to hot flashes. This is due to the instability of the vasomotor controls for
vasodilatation and vasoconstriction.

4. Circadian rhythm

• Body temperature normally changes 0.5-1°C (0.9- 1.8°F) during a 24 hour period.
• The temperature is usually lowest between 1.00- 4.00 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.

FEVER

• 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 feels cold.
• For most fevers body temperature increases by 1-2degree Celsius.
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• Shivering which increases heat production from muscles may begin at this time. Heat
production from liver also increases.
• In human 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 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.
Hyperpyrexia
• 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.
• Most patients with hypothalamic damage have subnormal or equal but not supernormal
body temperatures.

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.
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• Infectious disease and inflammation.

• Severe haemorrhage.

Symptoms of fever

• Flushed face
• Hot dry skin
• Anorexia
• Headache
• nausea and sometimes vomiting
• constipation and sometimes diarrhoea
• body aches
• 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

Classification or Patterns of Fever

1. Intermittent fever: The temperature curve returns to normal during the day and
reaches its peak in the evening. E.g.: in septicaemia.

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.

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
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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-1, IL-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 bacterial 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 (PGE2) 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.

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• Glial or neuronal cells synthesize Interleukins TNF.

• Therefore, central nervous system production of cytokines raises hypothalamic set
point.

Chronology of Events for Induction of Fever

Grades of Fever

1. 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)
[Link]: >40.5°C(104.9°F)

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 flush caused by contraction of
erector Pilli muscles in an attempt to trap air around body hairs, is evident.
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• Skin becomes pale and cool due to vasoconstriction.

2. Fever phase
• 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.
• If fluid volume deficit has occurred the client may experience thirst. Complaints of
aching muscles, general malaise, 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.

HYPERTHERMIA

• Hyperthermia is characterized by an unchanged (normothermic) setting of the

thermoregulatory centre 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 hyperthermia despite 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.

Causes of Hyperthermia Syndromes

1. Heat stroke: Caused by thermoregulatory failure in association with an arm environment

may be categorized as exceptional and non exceptional.
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Exceptional: it occurs in younger individuals who exercise in higher than normal heat or
humidity, dehydration

Non exceptional: It is caused by anti cholinergic, 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.

2. Drug induced hyperthermia: 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
antipsychotic 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), MAOs and
serotonergic medications have overlapping features including hyperthermia but distinguished
by presence of diarrhoea, tremors, myoclonus 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

Approaches to the Patient

1. History
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• 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, 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
erythematosus, 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 tumour cells.
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- 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.

Medical Management

It is important to distinguish between fever and hyperthermia since hyperthermia can be fatal
and doesn’t respond to antipyretics.

Pharmacological Management

1. Acetaminophen: adult: 325-650 mg PO q4-6 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).
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3. Indomethacin and naproxen (NSAID).

4. Aspirin: adult 325-650 mg PO q6hrs; children 10- 20 mg q 6hrs.

5. Glucocorticosteroid: potent antipyretic inhibits PGE2 synthesis.

6. Meperidine, morphine sulphate, chlorpromazine.

To manage severe rigors: treatment of underlying cause

nutrition, rest,

physical cooling: tepid bath, hypothermia blankets

Management of Hyperthermia

❖ Cause of hyperthermia should be treated.

❖ Dantrolene and procainamide should be given for malignant hyperthermia. 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, haemodialysis is or even cardio pulmonary bypass with
cooling of blood may be performed.

Nursing Management of Fever and Hyperthermia

✓ Monitor vital signs.

✓ Assess skin colour and temperature.
✓ Monitor white blood cell count, haematocrit value, and other pertinent laboratory
reports for indication of infection or dehydration.
✓ Remove excess blankets when the client feels warm, but provide extra warmth when
the client feels chilled.
✓ Provide adequate nutrition and fluids to meet the increased metabolic demands and
prevent dehydration.
✓ Measure intake and output.
✓ Reduce physical activity to limit heat production especially during the flush stage.
✓ Administer antibiotics as ordered.
✓ Provide oral hygiene to keep the mucous membranes moist.
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✓ Provide a tepid sponge bath to increase heat loss through conduction.

✓ Provide dry clothing and bed linens.

During chill phase

1. Risk for altered body temperature as evidenced by shivering and feeling cold
✓ Monitorvital signs
✓ restrict activity
✓ monitor skin colour and temperature
✓ apply extra blankets
✓ increase fluid intake
✓ 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. Altered comfort as evidenced by restlessness
✓ Promote rest
✓ restrict activity
✓ assess client’s response to pain management,
✓ take safety precautions if patient is delirious
✓ monitor for decreasing level of consciousness.
3. Altered nutrition related to fever as evidenced by anorexia and lack of food intake
✓ Provide high calorie diet
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✓ 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
✓ 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
✓ 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
and collapse.
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✓ 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
✓ Fluid replacement. This may be achieved by oral dehydration mixtures containing both
salt and water or intravenous isotonic saline.
✓ Adult patients may require 5 litters 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 oedema.
• 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

FEVER OF UNKNOWN ORIGIN

 23

Fever of unknown origin (FUO) was defined by Peterson and Benson in 1961 as:

1. Temperatures of >38.3 degree Celsius (>101-degree Fahrenheit) in several occasions

2. A duration of fever > 3 weeks and

3. Failure to reach a diagnosis despite 1 week of inpatient investigation.

Classification of FUO

Derrick and Street have proposed a new system for classification of FUO: -

1. Classic FUO: Same as above criteria. E.g., infections, malignancy, inflammatory diseases,
drug fever.

2. Nosocomial FUO: A temperature of >=38.3° C (>=101°F) develops on several occasions in

a hospitalized patient who is receiving acute care and in whom infection was not present at
time of admission. For e.g., septic thrombophlebitis, sinusitis, drug fever.

3. Neutropenic FUO: A temperature of >= 38.3° C (>=101° F) develops on several occasions

in a patient whose neutrophil count is <500/micro litre or is expected to fall to that level in 1-
2 days.

4. HIV-associated FUO: A temperature of >= 38.3° C (>=101° F) develops on several

occasions over a period of > 4 weeks for outpatients or > 3 days for hospitalized patients with
HIV infection.

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: amoebiasis, malaria.
• Rickettsial infections.
• Mycoplasmal infections.
 24

• Chlamydial infections.

2. Neoplasms

a. Malignant: Colon cancer, gall bladder carcinoma, leukaemia, renal cell carcinoma.

b. Benign: Castle man’s disease

3. Habitual hyperthermia

Exaggerated circadian rhythm

[Link] vascular/ Hypersensitivity diseases

Rheumatic fever, rheumatic arthritis, systemic lupus erythematous

5. Granulomatous Diseases

Crohn’s disease

6. Miscellaneous conditions

Drug fever, gout, haemoglobinopathies, tissue infarction or necrosis

7. Inherited and metabolic diseases

Adrenal insufficiency, familial cold urticaria

8. Thermoregulatory Disorders

a. Central: Brain tumour, Cerebrovascular accident, encephalitis;

b. Peripheral: Hyperthyroidism, pheochromocytoma

Diagnosis of FUO

✓ History and physical examination

✓ blood investigations
✓ tumour markers
✓ purified protein derivative for TB
✓ serological studies
✓ peripheral smears,
✓ multiple samples for culture and sensitivity
✓ X-Ray studies
✓ bone marrow biopsy
 25

✓ Liver biopsy
✓ GI contrast studies
✓ CT scan, MRI, ultrasonography.

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 confirmed 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.

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.

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 16degree Celsius.
4. Induced hypothermia: It is deliberate lowering of temperature to a range of a 78-90°F
(26- 32.5°C) to reduce oxygen need during surgery
(especially cardiovascular and neurosurgical procedures)
and in hypoxia, to reduce blood pressure and to
 26

alleviate hyperthermia by administering drugs that depress

the hypothalamic thermostat or by encasting the client in
a cooling blanket.

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, anaesthetics.

4. Endocrine dysfunction: hypothyroidism, adrenal insufficiency, hypoglycaemia.

5. Neurologic injury from trauma, Cerebral vascular mill accident, Subarachnoid haemorrhage.

6. Sepsis.

Risk Factors for Hypothermia

1. Age extremes: Elderly, neonates.

2. Outdoor exposure: Occupational, sports-related, inadequate clothing.

3. Drugs and intoxicants: Ethanol, phenothiazines, barbiturates, anaesthetics, neuromuscular

blockers and others.

4. Endocrine related: Hypoglycaemia, 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.

Clinical Presentation

Hypothermia leads to physiological changes in all organ systems.

Mild hypothermia

Temperature - 35-32.2°C (95-90°F)

 27

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

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% decrease in carbon dioxide per 8°C drop in temp,

Absence of protective airway reflexes, 50% decrease in oxygen consumption.

Renal and endocrine - 50% Increase in renal blood flow impaired insulin action.

Neuromuscular - Hyporeflexia, diminishing shivering induced thermogenesis, rigidity.

Severe hypothermia

Temperature - < 28°C (82.4°F)

CNS-Loss of cerebrovascular auto regulation, decline in cerebral blood flow, coma, loss of
reflexes.

CVS - Decrease in BP, heart rate and cardiac output, asystole.

Respiratory system - Pulmonic congestion and oedema, apnoea.

Renal and endocrine - Decrease in renal blood flow, Extreme oliguria.

 28

Neuromuscular - No motion, peripheral areflexia. There is progressive deterioration, with

apathy, poor judgment, ataxia, dysarthria, drowsiness, pulmonary oedema, acid-base
abnormalities, coagulopathy, and eventual coma. Shivering may be suppressed below a
temperature of 32.2°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.

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.

Management

Management consists of continuous monitoring, rewarding, and removal of wet clothing,

insulation, and supportive care.

Monitoring

o The ABCs of basic life support are a priority.

o 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.
o Body temperature is monitored with an oesophageal, bladder, or rectal thermostat.
o Continuous ECG monitoring is performed because cold induced myocardial irritability
leads to conduction disturbances, especially ventricular fibrillation.
o 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,
 29

▪ 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 end- expiratory pressure (PEEP) and heated
humidified oxygen to maintain tissue oxygenation.
➢ Administration of warm intravenous fluids (normal saline) to correct hypotension and
maintain urine output and core rewarding.
➢ Administration of sodium bicarbonate to correct metabolic acidosis
➢ Administration of antiarrhythmic medications bretyliumtosylate is safe.
➢ Low dose dopamine (2-5 microgram/kg) to treat hypotension.
➢ Gastric tube insertion to prevent dilation secondary to decreased bowel motility.
➢ Indwelling catheter to facilitate cold induced diuresis.

Nursing Management of Hypothermia

Nursing diagnosis

Hypothermia as evidence by body temperature <35°C, shivering, cool skin, irritability

etc.

Nursing interventions

➢ Provide extra covering and monitor temperature.

 30

➢ 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.

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.

I. 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 a fat result in heat production. Blood flowing through the brown
fat becomes warm and through circulation transfers heat to other body [Link]
mechanism of heat production is called as non-shivering thermogenesis.
➢ LBW babies lack this effective mechanism of heat production.

II. Mechanism of heat loss

➢ Newborn loses heat by evaporation (particularly soon after birth due to evaporation of
amniotic fluid 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 non-
shivering thermogenesis.
 31

Why newborns are prone to develop hypothermia?

▪ Large surface area.

▪ Decreased thermal insulation due to lack of subcutaneous fat.
▪ Reduced amount of brown fat.

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.

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.

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.
 32

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

The microvasculature begins to collapse

Tissue ischemia and necrosis

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 oedema

leads to very cold extremities.

3. Third degree frost bite: Haemorrhagic vesicles due to serious microvasculature injury
which further leads to cyanosis.

[Link] degree frost bite: Damage in sub cuticular, muscular and osseous tissue.

Symptoms

▪ The injured area is white or mottled blue white, waxy and firm to the touch.
 33

▪ 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.

Diagnosis

▪ Angiography and MRI to assess the potency of large vessels.

▪ Ultrasonography.
▪ Plethysmography.
▪ Thermography to evaluate perfusion after rewarming.
▪ Technetium scintigraphy to assess perfusion.

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 401 PO.

After thawing

▪ 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.
 34

▪ 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 hyperemic, 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

CONCLUSION

Body temperature is the degree of hotness or coldness of a body 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.

RESEARCH REFERANCE

• Measurement and evaluation of body temperature: Implications for clinical practice Märtha
Sund-Levander Department of Medicine and Care, Division of Clinical Physiology, Faculty of
Health Sciences. Linköping University, SE-581 85 Linköping, Sweden Department of Welfare
and Care, Faculty of Health Sciences, Linköping University, SE-601 74 Norrkoping, Sweden

The general aim was to explore factors influencing the normal variation and
measurement of body temperature. Additional aims were to study morbidity, mortality
and the clinical presentation of pneumonia and predictors for survival in elderly
nursing-home residents. Two hundred and thirty-seven non-febrile nursing home
residents (aged 66-99 years) and 87 healthy adults (aged 19-59 years) were included.
In elderly individuals, the morning ear and rectal body temperature was measured at
 35

baseline and pneumonia and survival was observed at one- two and three-year. In
healthy adults the rectal, ear, oral and axillary temperature were measured
simultaneously on one morning and repeated measurements were performed in three
subjects. Overall, the range of normal body temperature was wider then traditionally
stated. In elderly nursing home residents, functional and cognitive impairment and BMI
< 20 were related to a lower body temperature and medication with analgesics to a
higher. Compared to adults < 60 years elderly persons had a higher average ear and a
lower rectal temperature. Men and postmenopausal women < 60 years had lower body
temperature than premenopausal women. The repeated measurements showed a wide
individual variability irrespective of the site of measurement, and that replicated
measurements do not improve accuracy. When comparing the rectal temperature with
oral, ear and axillary readings the average difference was > 0.5°C with a wide individual
variation. The yearly incidence of nursing-home acquired pneumonia varied between
6.9% and 13.7%. Functional impairment, chronic obstructive pulmonary disease
(COPD) and male sex were related to a higher risk of acquiring pneumonia and
presenting non-specific symptoms were common. Age and functional impairment
predicted mortality, irrespective of gender, while cerebral vascular insult, a lower body
mass index and malnutrition in women and heart disease, COPD, medication with
sedatives and mortality rate index in men were gender specific predictors. Surviving
women had a higher baseline body temperature than non-surviving, while no such
difference was found in men. When assessing body temperature, it is important to
consider the site of measurement, technical design, operator technique, age and gender
and, in elderly nursing-home residents, physical and cognitive impairment, body
constitution and medication with analgesics. The best approach is to use an unadjusted
mode, without adjusting to another site. To prevent a delayed diagnosis of pneumonia,
one should be aware of a low baseline body temperature and lack of specific clinical
symptoms in elderly nursing-home residents. Preserving and/or improving functional,
cognitive, nutritional status and preventing agitation and confusion would improve
survival in nursing-home residents.

• Effect of Altered Core Body Temperature on Glottal Closing Force October 2011 The
Annals of otology, rhinology, and laryngology 120(10):669-73
DOI:10.1177/000348941112001007 Source PubMed Authors: Mikhail Wadie Juan Li
Clarence T Sasaki
 36

A basic function of the larynx is to provide sphincteric protection of the lower airway,
initiated by a brain stem-mediated glottal closure reflex. Glottal closing force is defined
as the measured pressure generated between the vocal folds during glottal closure. One
of the factors thought to affect the glottal closure reflex is a variation in core body
temperature. Four adult male Yorkshire pigs were used in this study. The subjects were
studied under control conditions (37 degree C, hyperthermic conditions (38 degrees C
to 41 degrees C), and hypothermic conditions (36 degrees C to 34 degrees C). We
demonstrated that the glottal closing force increased significantly with an increase in
core body temperature and also decreased significantly with decreased core body
temperature. These results are supported by neurophysiological changes demonstrated
by other studies in pups and adult dogs in response to altered core body temperatures.
The mechanism for these responses is thought to reside centrally, rather than in the
peripheral nervous system. We hope that a better understanding of these aspects of
glottal closure will alter the care of many patients with postanaesthetic hypothermia
and many sedated inmates and will also further enhance preventive measures needed to
decrease the incidence of sudden infant death syndrome in overheated or febrile infants

BIBLIOGRAPHY

▪ Shabeer P Basheer a concise text book of advanced nursing practice 2nd edition2017
EMMESS medical publishers Bangalore, page no: 246-259
▪ Potter and Perry fundamentals of nursing