ALTERATIONS IN

BODY
TEMPERATURE
JOSEPHINE JOJO
I MSC NURSING
 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

• Temperature of the interior body tissue below the skin and subcutaneous tissue.

• The sites of measurement: 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.
 THERMOREGULATION
•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.
 THERMOREGULATION….
 NEURAL CONTROL  HEAT PRODUCTION

 VASCULAR CONTROL - REST

- VOLUNTARY MOVEMENT
 SKIN TEMPERATURE REGULATION
- INVOLUNTARY SHIVERING

 BEHAVIOURAL CONTROL - NON SHIVERING THERMOGENESIS

 MECHANISMS ACTIVATED BY COLD  HEAT LOSS

- RADIATION
 MECHANISMS ACTIVATED BY HEAT
- CONDUCTION
- CONVECTION
- EVAPORATION.
 THERMOREGULATION….
 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.
 REGULATION
 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 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.
 REGULATION…

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.
 REGULATION…

• 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.
 REGULATION…

• 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.
 REGULATION…

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.
 REGULATION…

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.
 REGULATION…

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.
 HEAT LOSS…

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.
 HEAT LOSS…
 The amount of heat carried to the surface depends on the extent
of 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.
 HEAT LOSS…
 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.
 HEAT LOSS…
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.

 Heat conducts through contact with solids, liquids and gases.

 Conduction normally accounts for small amount of heat loss.

 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.
 HEAT LOSS…
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.
 HEAT LOSS…
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.
 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.
 REGULATION…
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 during exercise
and increased sympathetic stimulation.
 REGULATION…
 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.
 REGULATION…
 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.
 REGULATION…
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.
 REGULATION…
•
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.

 REGULATION…

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

1. Age

2. Exercise
3. Hormone level
4. Circadian rhythm
5. Stress
6. Environment
 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 .

 FEVER

 For most fevers body temperature increases by 1-2degree

Celsius.

 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.
 FEVER

 The process of heat conservation (vasoconstriction) and heat production (shivering and increased
metabolic activity) continue until the temperature match the new THERMOSTAT SETTING.

 Once the point is reached, the hypothalamus maintains the temperature at febrile levels

 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.
 FEVER….

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 & central nervous
system haemorrhage.

 Rarely 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.
 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 - Caffeine and cocaine directly injected into the bloodstream.

 Injection of proteins or other products.

 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: normal during the day and 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.
 CLASSIFICATION OR PATTERNS OF FEVER…

 Tertian- when paroxysm occurs on 1st and 3rd days

 Quatrain- fever associated with paroxysm on first and fourth day. E.G., In
malaria
 PATHOGENESIS OF FEVER
1. PYROXENES
 Pyroxenes are any substance that causes fever.

 Exogenous pyroxenes: 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
 PATHOGENESIS OF FEVER…

2. PYROGENIC CYTOKINES

 Cytokines are small proteins that regulate immune, inflammatory and hematopoietic
processes.

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..
 PATHOGENESIS OF FEVER…

 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.
 PATHOGENESIS OF FEVER…

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.
 PATHOGENESIS OF FEVER…

4. PRODUCTION OF CYTOKINES IN CNS

 Several viral diseases produce active infection in the brain.

 Glial or neuronal cells synthesize interleukins TNF.

 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)

3.HYPERPYREXIA : 40.5°C(104.9°F)
 PHASES OF FEVER

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.

• Skin becomes pale and cool due to vasoconstriction

 PHASES OF FEVER…

1. 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.

 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.
 PHASES OF FEVER…

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

 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 result in dangerously high internal temperatures.
 HYPERTHERMIA…

Excessive heat production can easily cause hyperthermia despite physiologic

and behavioural control of body temperature. 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

Exceptional: exercise in higher than normal

heat or humidity, dehydration

• Non exceptional: drug induced.

 CAUSES OF HYPERTHERMIA
SYNDROMES…
2. DRUG INDUCED HYPERTHERMIA:
psychotropic drugs- Monoamine oxidise inhibitors,
tricycle antidepressants,
amphetamines, phencyclidine,
lysergic acid diethylamide or
cocaine.
 CAUSES OF HYPERTHERMIA SYNDROMES…

•3. MALIGNANT:
•individuals with inherited abnormality of skeletal muscle sarcoplasmic
reticulum
•that cause rapid increase in intracellular calcium level in response to
halothane and other inhalation anaesthetics or to succinylcholine.
•elevated body temperature, increased muscle metabolism, muscle
rigidity, rhabdomyolysis, acidosis and cardiovascular instability and is
often fatal.
 CAUSES OF HYPERTHERMIA SYNDROMES…

•4. THE NARCOLEPTIC MALIGNANT SYNDROME (NMS):

• Occurs due to use of narcoleptic agents like antipsychotics
• characterized by muscle rigidity (lead pipe), extra pyramidal side
effects, autonomic deregulation and hyperthermia.
•caused by inhibition of central dopamine receptors in
hypothalamus which results in increased heat generation and
decreased heat dissipation
 CAUSES OF HYPERTHERMIA SYNDROMES…

• SEROTONIN SYNDROME:
Seen in selective serotonin uptake inhibitors (SSRIS),
MAOS and serotonergic medications have overlapping
features including hyperthermia but distinguished by
presence of diarrhoea, tremorsCAUSES OF
HYPERTHERMIA SYNDROMES…
 CAUSES OF HYPERTHERMIA SYNDROMES…

• ENDOCRINOPATHY:
• Thyrotoxicosis and pheochromocytoma can lead to increased
thermogenesis

• CENTRAL NERVOUS SYSTEM DAMAGE:

• Cerebral haemorrhage, status epileptics, hypothalamic Injury

can cause hyperthermia
 APPROACHES TO THE PATIENT

• 1. HISTORY

 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

 APPROACHES TO THE PATIENT

• . PHYSICAL EXAMINATION

 Vital signs

 Pelvic examination for pelvic inflammatory disease.

• . LABORATORY TESTS

 CLINICAL PATHOLOGY:

• - COMPLETE BLOOD COUNT, DIFFERENTIAL LEUKOCYTE COUNT

- BLOOD SMEAR FOR MALARIAL PATHOGENS

• ESR

- URINALYSIS.

- BONE MARROW BIOPSY

 APPROACHES TO THE PATIENT

• CHEMISTRY:-Electrolytes , blood glucose ,BUN , creatinine , LFT

• MICROBIOLOGY:

- -Cultures of blood-

• CSF.

• RADIOLOGY
 MEDICAL MANAGEMENT

• Distinguish between fever and hyperthermia

• 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).

• 3. INDOMETHACIN AND NAPROXEN (NSAID).

 MEDICAL MANAGEMENT…

• 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.

 Physical cooling Management of Hyperthermia

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 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

 Measure intake and output.

 Reduce physical activity

 Administer antibiotics as ordered.

 Provide oral hygiene

 NURSING MANAGEMENT OF FEVER AND
HYPERTHERMIA
• DURING CHILL PHASE

1. Risk for altered body temperature as evidenced by shivering and feeling cold

 Monitor vital 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.

 NURSING MANAGEMENT OF FEVER AND
HYPERTHERMIA

• 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

2.Provide comfort

3.Administer adequate nutrition

 NURSING MANAGEMENT OF FEVER AND
HYPERTHERMIA

• DURING FLUSH PHASE

• 1. Altered fluid and electrolyte balance related to excessive sweating

• HEAT CRAMPS:

 These painful muscle cramps

 There is no elevation of core temperature.

 The mechanism is considered to be extracellular sodium depletion

 Symptoms usually respond to salt replacement.

 NURSING MANAGEMENT OF FEVER AND
HYPERTHERMIA

• 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.
hyperventilation and symptoms of tiredness or fatigue, muscular weakness, dizziness and
collapse.
The blood analysis - mild elevation of blood urea, sodium concentration and haematocrit.
 NURSING MANAGEMENT OF FEVER AND
HYPERTHERMIA

• TREATMENT INVOLVES:

 Removal of patient from the heat

 Active cooling using cool sponging

 Fluid replacement.

 Adult patients may require 5 litters or more positive fluid balance in the first 24
hours.

 Frequent monitoring of blood electrolytes

•HEAT STROKE:
• Heat stroke occur when the core body temperature rises above 40°C and is a severe and
life threatening
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
Complications include hypovolemic shock, lactic acidosis, and disseminated intravascular
coagulation.
hepatic and renal failure and cerebral oedema.
managed in ICU with rapid cooling using ice packs, careful fluid replacement
 FEVER OF UNKNOWN ORIGIN

• 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

. CLASSIC FUO: Infections, malignancy, inflammatory diseases, drug fever.

• 1

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

a hospitalized patient

• 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
• . 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.

• Chlamydial infections
 CAUSES OF FUO…
• 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

 CAUSES OF FUO…
• 4.COLLAGEN VASCULAR/ HYPERSENSITIVITY DISEASES

• Rheumatic fever, rheumatic arthritis, systemic lupus erythematous

• 5. GRANULOMATOUS DISEASES

• Crohn’s disease

• 6. MISCELLANEOUS CONDITIONS

• gout, haemoglobinopathies, tissue infarction or necrosis

 CAUSES OF FUO…

. INHERITED AND METABOLIC DISEASES

7

•Adrenal Insufficiency, Familial Cold Urticaria

•8. THERMOREGULATORY DISORDERS
•A. Central: Brain Tumour, Cerebrovascular Accident,
Encephalitis;
•B. Peripheral: Hyperthyroidism, Pheochromocytoma
 DIAGNOSIS OF FUO

 Multiple samples for culture and sensitivity

 History and physical examination
 X-ray studies
 Blood investigations
 Bone marrow biopsy
 Tumour markers
 Liver biopsy
 Purified protein derivative for TB
 GI contrast studies
 Serological studies
 CT scan, MRI, ultrasonography.
 Peripheral smears
 TREATMENT

Classic FUO are continually observed and examined and not given the empirical therapy.

 The antibiotic therapy.

If neutropenia and vital sign instability - 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 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: Direct exposure of a previously healthy individual to the cold.

2.SECONDARY HYPOTHERMIA: 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
•To reduce oxygen need during surgery (Especially cardiovascular and neurosurgical procedures
•in hypoxia, to reduce blood pressure
•to alleviate hyperthermia by administering drugs.
 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.
 CLINICAL PRESENTATION

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
 CLINICAL PRESENTATION…

• 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.

 CLINICAL PRESENTATION…
• 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.

• NEUROMUSCULAR - No motion, peripheral areflexia

 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
 MANAGEMENT
• Management consists of :

• continuous monitoring

• rewarming, and

• removal of wet clothing, insulation

• supportive care.
 MANAGEMENT…

• MONITORING

o ABCs

o vital signs ,CVP, urine output, ABG, 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 for ventricular fibrillation.

o An arterial line is inserted and maintained to record BP and facilitate blood sampling.
 MANAGEMENT…

• REWARMING

• Rewarming methods include:

 Active core (internal) rewarming

 Active external rewarming,

 Passive or spontaneous rewarming.

 MANAGEMENT…

• CORE REWARMING

• cardiopulmonary by-pass, warm fluid administration, and warm humidified oxygen

by ventilator, and warmed peritoneal lavage.

• 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 anaerobic

extremities.
 MANAGEMENT…

• 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

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.

 HYPOTHERMIA IN NEW BORN BABIES

• I. HANDICAPS OF NEWBORN IN TEMPERATURE

REGULATION
•Large surface area per unit of body weight.
•Non-shivering thermogenesis
• A low birth weight
 HYPOTHERMIA IN NEW BORN BABIES…

• II. MECHANISM OF HEAT LOSS

• EVAPORATION
• CONDUCTION
• CONVECTION
• RADIATION
 HYPOTHERMIA IN NEW BORN BABIES…

• 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 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
tissue temperature drops below 0 degree Celsius.

exposure to freezing temperatures and actual freezing of the

tissue fluids in the cell and intracellular spaces.

cellular and vascular damage.

more frequently affected parts 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.
 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.

• 4.FOURTH DEGREE FROST BITE: Damage in sub cuticular, muscular and

osseous tissue.
 FROST BITE…
• 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.

 FROST BITE…
• 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.

 MANAGEMENT OF FROST BITE…

• 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 40mg PO.

 MANAGEMENT OF FROST BITE…

• 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.

 MANAGEMENT OF FROST BITE…

 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

- less severe form

- prolonged exposure to cold and damp

- appears cold ischemic and numb

- no freezing of tissue

- There after it becomes hyperemic, swollen and painful.

- Recovery may take many months and there may be chronic pain and sensitivity to cold.

- endothelial injury.

- The pain and associated paraesthesia.  

 
 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.
•