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ALTERATIONS IN BODY TEMPERATURE

INTRODUCTION
Temperature is the hotness or coldness. The body temperatures is the difference
between the amount of heat produced and the amount of heat lost to the external
environment.
BODY TEMPERATURE: In humans the traditional normal value for the temperature is
37C. 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
Core temperature: - 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, esophagus, pulmonary artery, urinary bladder.
Shell temperature: - it refers to body temperature at the surface that is of the skin and
subcutaneous tissue. The sites of measurement of shell temperature are skin, axillae and
oral.
Oral: 37C (98.6F)
Rectal: 37.5C (99.5F)
Tympanic: 37.5C (99.5F)
Axillary: 36.5C (97.6F)
Heat is continually produced in the body as a by-product of the chemical reactions called
metabolism
Temperature calculation:
C=(f-32)5/9
F= (C x 9/5)+ 32
REGULATION
The balance between the heat lost and heat produced or thermoregulation is regulated by
physiological and behavioral mechanisms.
Neural control
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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 points. Neurons in both the preoptic anterior hypothalamus and the
posterior hypothalamus receive two kinds of signals; one from peripheral nerves that
reflect warmth/cold receptors and the other from the temperature of the blood bathing the
region. These two types of signals are integrated by the thermoregulatory centre of
hypothalamus to maintain normal body temperature. When these neurons detect the
temperature of blood is too warm, signals radiate to the heat loss centre located in the
anterior portion of the hypothalamus which is mainly composed of parasympathetic
nerves that when stimulated initiate mechanism to decrease body heat. If cold is detected
signals are sent to the heat promoting centre in the posterior hypothalamus which
operates mainly through sympathetic nervous system which stimulates mechanisms to
produce body heat. In a neutral environment, the metabolic rate of humans constantly
produces more heat than is necessary to maintain the core body temperature at 37C.
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 PNS. SNS 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
thermo genesis.
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 SNS 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.
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: 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
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heat that is produced assists in equalizing the body temperature, and the shivering
ceases.
No shivering thermo genesis: 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 skins structure and
exposure to the environment result in constant, normal heat loss through radiation,
conduction, convection and evaporation.
Radiation (60%): 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. However if the environment is warmer
than the skin, the body absorbs heat through radiation. The
nurses increase the heat loss through radiation by removing the
clothing or blankets. The clients position enhances radiation
heat loss e.g. standing exposes a greater radiating surface area
and lying in a fetal position minimizes heat radiation. Covering
body with dark, closely woven clothing reduces the amount
heat lost from radiation.
Conduction (3%): it is the transfer of heat from one object to
another with direct contact. When a warm skin touches a cooler
object, heat is lost. When the temperature of two objects is
same, the conductive heat loss stops. Heat conducts through
contact with solids, liquids and gases. Conduction normally
accounts for small amount of heat loss. The nurse increases the
conductive heat loss when applying an ice pack or bathing a
client with cools water. Applying several layers of clothing
reduces conductive loss. The body gains heat by conduction
when contact is made with materials warmer than skin
temperature.

Convection (15%): it is the transfer of heat away by air


movement. Heat is first conducted to air molecules directly in
contact with skin. Air currents carry away the warm air. As the
air current velocity increases, convective heat loss increases.

Evaporation (22%): it is the transfer of heat energy when a


liquid is changed to a gas. The body continuously loose heat by
evaporation. About 600-900ml a day evaporates from the skin
and lungs, resulting in water and heat loss. This is normal loss
and considered insensible water loss and does not play a major
role in temperature regulation. When the body temperature
rises, the anterior hypothalamus signals the sweat glands to
release sweat. Sweat evaporates from the skin surface resulting
in heat loss. During exercise and emotional and mental stress
sweating is one way to lose excessive heat produced by the
increased metabolic rate.
Skin in temperature regulation
The skins 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 skins surface and is lost to the environment through the heat loss
mechanisms. The bodys 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 skins surface. On a hot humid day
the blood vessels in the hands are dilated and easily visible. In contrast if the
vasoconstriction becomes too low, the hypothalamus initiates the vasoconstriction and
blood flow to the skin lessens. Thus body heat is conserved.
The skin is well supplied with heat and cold receptors. As the cold receptors. Are
plentiful the skin functions primarily to detect cold surface Temperatures. When the skin
becomes chilled, its sensors send information. To the hypothalamus, this initiates
shivering to increase body heat. Production, inhibition of sweating, and vasoconstriction.
Behavioral control
Humans voluntarily act to maintain comfortable body temperature when exposed to
temperature extremes. The ability of person to control body temperature depends no:
degree of temperature extreme, the persons ability to sense feeling comfortable or
uncomfortable, thought processes or emotions. And the persons 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.
Mechanisms Activated By Cold:
Increased heat production: increase in BMR, muscle activity, thyroxin output,
epinephrine, nor epinephrine and sympathetic stimulation, fever.
Decreased heat loss by coetaneous vasoconstriction, curling up.
Mechanisms Activated By Heat:
Increased heat loss by cutaneous vasodilatation, sweating, increased respiration
Decreased heat production: manifested by anorexia, apathy, illness.
FACTORS AFFECTING THE BODY TEMPERATURE
Many factors affect the body temperature. Changes in body temperature within an
acceptable within an acceptable range occur when the relationship between the heat
production and the heat loss is altered by physiological or behavioral variables.
1. Age: at birth the newborn leaves a warm, relatively constant environment and enters
one in one in which temperature fluctuates widely. Temperature control mechanisms are
immature. An infants 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 newborns body temperature is maintained
within 35.5-37.5C (95.9-99.5F). Heat production steadily declines as the infant grows
into childhood. Childrens 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 increases in heat production. Any form of exercise
increase the heat production and thus the body temperature. Prolonged strenuous
exercise, such as long distance running, can temporarily raise body temperatures up to
41C (105.8F).
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
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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(0.5-1.0F). Body temperature
changes also occur in women during menopause (cessation of menstruation). Women
who have stopped menstruating may experience periods of intense body heat and
sweating lasting from 30 second to 5 minutes. There may be intermittent increases in skin
temperature of up to 4C (7.2F) 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 0.5-1C (0.9-1.8F) 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 persons 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. 37C-39C.
CAUSES OF FEVER
Hot environment.
Excessive exercise.
Neurogenic factors like injury to hypothalamus.
Dehydration after excessive dieresis.
As an undesired side effect of a therapeutic drug.
Chemical substances e.g. caffeine and cocaine directly injected into the
bloodstream.
Injection of proteins or other products.
Infectious disease and inflammation.
Severe hemorrhage.

SYMPTOMS OF FEVER
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Flushed face; hot dry skin; anorexia; headache; nausea and sometimes vomiting;
constipation and sometimes diarrhea; body aches and scant highly colored 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 septicemia
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
PATHOGENESIS OF FEVER:
1. Pyroxenes: progeny is any substance that causes fever. Exogenous pyroxenes are
derived from outside the patient; most are microbial products, toxins or micro-organisms.
E.g.: lip polysaccharide end toxin produced by all gram negative bacteria. Enter toxins of
gram positive like staphylococcus aurous and Group. A and B Streptococcal toxins
2. Phylogenic 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 (Tumor Necrosis Factor). Some cytokines cause fever
and are called phylogenic cytokines including IL-1, IL-6, and interferon (IFN) alpha.
Each cytokine is encoded by a separate gene and each phylogenic cytokine has been
shown to cause 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.
4. Production of cytokines in CNS: several viral diseases produce active infection in the
brain. Glial or neuronal cells synthesize IL-1, IL-6, and TNF. Therefore CNS production
of cytokines raises hypothalamic set point.
GRADES OF FEVER
1. low grade fever: 37.1-38.2C(98.8-100.6F)
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2. high grade fever: 38.2-40.5C(100.6-104.9F)


3. hyperpyrexia: >40.5C(104.9F)
PHASES OF FEVER
A febrile episode has three distinct phases:1. Chill phase: the bodys heat producing, mechanism attempt to increase the core
temperature. The client experiences cold and may shiver. Goose flesh 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.
2. Fever phase: it occurs when fever reaches the new higher set point. The clients skin
feels neither hat nor cold. Cellular degeneration leads to fluid and electrolyte losses. If
fluid volume deficit has occurred the client may experience thirst. Complains of aching
muscles, general malaise weakness can be there due to increased 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 clients skin appears flushed
and warm to touch because of vasodilatation.
HYPERTHERMIA
Hyperthermia is characterized by an unchanged (normothermic) setting of the
thermoregulatory center in conjunction with an uncontrolled increase in body temperature
that exceeds the bodys ability to lose heat. Exogenous hest 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 behavioral 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.
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 in very young or
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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
oxidizes inhibitors, tricycle antidepressants, amphetamines, phencyclidine, lysergic acid
diethylamide or cocaine.
3. malignant: occur 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 anesthetics 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): occur due to use of narcoleptic agents
like antipsychotic phenothiazines, haloperidol, pro chlorprazine, meto chlopramide 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 diarrhea, tremors, myoclonous rather than lead pipe rigidity.

6. endocrinopathy: thyrotoxicosis and pheochromocytoma can lead to increased


thermogenesis
7. central nervous system damage: cerebral hemorrhage, status epileptics, hypothalamic
injury can cause hyperthermia
APPROACH TO THE PATIENT
1. History: history of use of OTC medications, 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/O geographic areas patient traveled. Use of tobacco, IV drugs, trauma, animal
bites, immunization. Family history of TB, arthritis, infectious disease, anemia. Ethnic
origin e.g. blacks are more likely to have haemoglobinopathies
2. Physical examination: vital signs, check skin, lymph nodes, eyes, nail beds, CVS,
chest abdomen, musculoskeletal system, nervous system, penis, scrotum, testes should be
examined carefully. Pelvic examination for PID and tubo-ovarian abscess.

3. laboratory tests: if a patient reveals more than a simple viral illness or pharangitis
then lab testing is done:

CLINICAL PATHOLOGY
CBC, DLC. Neutrogena is present in some viral infections, drug reactions, SLE, typhoid,
leukemia. Lymphocytosis will be presenting with typhoid, brucellosis, TB and viral
diseases. Monocytosis in typhoid, TB, brucellosis, lymphoma. Eosinophilia in
hypersensitivity and drug reactions, Hodgkins disease, adrenal insufficiency. Blood
smear for malarial pathogens, ESR. Urinalysis. Any abnormal fluid accumulation like
pleural fluid, peritoneum, joint is examined. Bone marrow biopsy for histopathologic
studies as well as culture in infiltration of marrow by pathogens or tumor cells. Stool for
occult blood, inspection for ova, parasites.
Chemistry: electrolytes, blood glucose, BUN, creatinine, LFT
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 than 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 MSE is there.
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
rapidly fatal and doesnt respond to antipyretics.
Pharmacological management
1. Acetaminophen: adult: 325-650 mg PO q 4-6 hrs. Children: 10-15mg/kg body weight
q4-6 hrs.
2. Ibuprofen (NSAID) - dosage: adult-200-400mg PO q6hrs; children: 5mg/kg body wt
for temp. <102.5F; 10 mg/kg body wt. for temp 102.5F (not to exceed 40 mg/kg/day).
3. Indomethacine and naproxen (NSAID).
4. Aspirin: adult 325-650 mg PO q6hrs; children 10-20 mg q 6hrs.
5. Glico corticosteroid: potent antipyretic inhibit PGE2 synthesis.
6. Mepridine, morphine sulphate, chlorpromazine.
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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. Dandroline 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, hemo dialysis or
even CPB with cooling of blood may be performed.
Nursing management of fever and hyperthermia
Monitor vital signs.
Assess skin color and temperature.
Monitor white blood cell count, hematocrit 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.
Provide a tepid sponge bath to increase heat loss through conduction.
Provide dry clothing and bed linens.
During chill phase
Risk for altered body temperature as evidenced by shivering and feeling cold:
Monitor vital signs, restrict activity, monitor skin color and temperature, apply extra
blankets, increase fluid intake, apply extra blankets, supply oxygen if client has
preexisting cardiac or respiratory problem.

During fever phase


Hyperthermia as evidenced body temperature >38.5C, 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
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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.
Altered comfort as evidenced by restlessness: Promote rest, restrict activity, assess
clients response to pain management, and take safety precautions if patient is delirious,
monitor for decreasing level of consciousness.
Altered nutrition related to fever as evidenced by anorexia and lack of food intake:
Provide high calorie diet, encourage fluid intake, reduce iron intake
During flush phase:
Altered fluid and electrolyte balance related to excessive sweating: Monitor intake
and output, monitor electrolytes, replace fluids and electrolytes lost through sweating,
monitor temperature, and provide rest.
HEAT CRAMPS
These painful muscle cramps occur most commonly in the legs of young people
following vigorous exercise in the hat weather. There is no elevation of core temperature.
The mechanism is considered to be extracellular sodium depletion following electrolyte
loss a result of persistent sweating with replacement of water but no salt. The syndrome is
also encountered in miners undertaking heavy physical work in hat 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
37-40C and is usually seen when the individual is undertaking vigorous physical work in
a hat 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 no the findings of an elevated
core temperature associated with hyperventilation and symptoms of tiredness or fatigue,
muscular weakness, dizziness and collapse. The blood analysis may show evidence of
dehydration with mild elevation of blood urea, sodium concentration and hematocrit.
Treatment involves removal of patient from the heat, active cooling using cool sponging,
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and fluid replacement. This may be achieved by oral dehydration mixtures containing
both salt and water or intravenous isotonic saline . Adult patients may require 5 liters or
more positive fluid balance in the first 24 hours. Frequent monitoring of blood
electrolytes is important, esp. in patients receiving I.V. replacement therapy.
HEAT STROKE
Heat stroke occur when the core body temperature rises above 40C 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 patients skin feels very hot, and sweating 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 phenothiazines
diuretics and alcohol may be the contributory factors. Complications include
Hypovolemic shock, lactic acidosis, and disseminated intravascular coagulation.
Rhabdomyolisis, hepatic and renal failure and cerebral edema. The patient should be
managed in ICU with rapid cooling using ice packs, careful fluid replacement and
appropriate intravascular monitoring. Investigations reflect the complication sand include
coagulation studies and muscle enzymes and in addition to routine hematology and
biochemistry

FEVER OF UNKNOWN ORIGIN

DEFINITION:
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 of > 3 weeks and; (3) failure to reach a diagnosis despite 1 week of
inpatient investigation.
CLASSIFICATION OF FUO:
Derrick and Street have purposed a new system for classification of FUO:1. Classic FUO: same as above criteria. E.g. infections, malignancy, inflammatory
diseases, drug fever.

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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 liter 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 endocarditic.
Systemic bacterial infections: typhoid fever.
Mycobacterium infections: tuberculosis.
Fungal infections: candidacies.
Viral infections: dengue, hepatitis A, B, C, D and E, HIV infection.
Parasitic infections: amebiasis, malaria.
Rikettsial infections.
Mycoplasmal infections.
Chlamydial infections.
2. Neoplasms:
(a) malignant: colon cancer, gall bladder carcinoma, leukemia, renal cell carcinoma.
(b) benign: castle mans disease
3. Habitual hyperthermia: exaggerated circadian rhythm
4. Collagen vascular/ Hypersensitivity diseases: rheumatic fever, rheumatic arthritis,
systemic lupus erythematous
5. Granulomatous Diseases: crohns disease

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6. Miscellaneous conditions: drug fever, gout, haemo globinopathies, tissue infarction or


necrosis
7. Inherited and metabolic diseases: adrenal insufficiency, familial cold urticaria
8. Thermoregulatory Disorders:
(a) Central: brain tumor, Cerebro vascular accident, encephalitis;
(b) Peripheral: hyperthyroidism, pheochromocytoma
DIAGNOSIS OF FUO:
History and physical examination, blood investigations, tumor markers, PPD for TB,
serological studies, peripheral smears, multiple samples for culture and sensitivity, X-Ray
studies, bone marrow biopsy, 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 fluroquinolone and piperacillin is given. If PPD test is positive or granuloma
hepatitis is confirmed then isoniazid and rifampcin 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 and 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 16 degree Celsius.
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4. Induced hypothermia: it is deliberate lowering of temperature to a range of a 78-90F


(26-32.5C) to reduce oxygen need during surgery (esp. cardiovascular and neurosurgical
procedures) and in hypoxia, to reduce blood pressure and to alleviate hyperthermia by
administering drugs that depress the hypothalamic thermostat or by encasting the client in
a cooling blanket.
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, phenothiazines, barbiturates, benzodiazepines, cyclic
antidepressants, anesthetics.
4. Endocrine dysfunction: hypothyroidism, adrenal insufficiency , hypoglycemia
5. Neurologic injury from trauma, Cerebral vascular accident, Subarachnoid hemorrhage
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, anesthetics,
neuromuscular blockers and others.
4) Endocrine related: hypoglycemia, hypothyroidism, adrenal insufficiency, and
hypopituitarism.
5) Neurologic related: stroke, hypothalamic disorders, Parkinsons 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

16

35-32.2C (95-90F)

Decreased cerebral Metabolism


Amnesia
Apathy
Dysarthria
Impaired judgement
Tachycardia
Vasoconstriction
Increase in cardiac output and Blood pressure
Tachypne,
Bradypnea
Decline Oxygen consumption
Bronchospasm
Diuresis
Increase in metabolism with shivering
Increased preshivering Muscle tone
Fatiguing
Ataxia

Moderate
<32.2-28C (90-82.4F)

EEG abnormalities
Decrease in pulse and cardiac output
Hypoventilation
50% decrease in carbon
50% Increase in renal blood flow
Hyporeflexia,
Diminishinglevel of consciousness,
Pupillary dilatation
Hallucinations
Increased atrial and ventricular arrhythmias
Absence of protective airway reflexes
50% decrease in oxygen consumption
Impaired insulin action
Shivering- induced thermogenesis,
Rigidity

Severe
17

<28C (82.4F)

Loss of cerebro- vascular auto regulation


Decline in cerebral blood flow
Coma,
Loss of reflexesdecrease in BP, heart rate and cardiac output
Pulmonic congestion and edema
Apnea
Decrease in renal blood flow,
Extreme oliguria
Peripheral areflexia.

There is progressive deterioration, with apathy, poor judgment, ataxia, dysarthria,


drowsiness, pulmonary edema, acid-base abnormalities, coagulopathy, and eventual
coma. Shivering may be suppressed below a temperature of 32.2C (90F), because the
bodys 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
esophageal 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: the ABCs of basic life support are a priority. The patients vital signs, CVP,
urine output, arterial blood gas levels, blood chemistry determinations (BUN, creatinine,
glucose, electrolytes), and chest X-Rays are evaluated frequently. Body temperature is
monitored with an esophageal, bladder, or rectal thermostat. Continuous ECG monitoring
is performed because cold induced myocardial irritability leads to conduction
disturbances, esp. ventricular fibrillation. An arterial line is inserted and maintained to
record BP and facilitate blood sampling.
Rewarming: rewarming methods includes: active core (internal) rewarming, active
external rewarming, and passive or spontaneous rewarding.
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-32C (88-90F) is essential.
18

Passive external rewarding: 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 31C (88F).
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 antiarrythmic medications bretylium tosylate 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 <35C, shivering, cool skin, irritability etc.
Nursing interventions:

Provide extra covering and monitor temperature.


Cover head properly.
Use heat retaining blankets.
Keep patients 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 NEWBORN 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:

19

A newborn is more prone to develop hypothermia because of a large surface area per unit
of body weight. A low birth weight baby has decreased thermal insulation due to less
subcutaneous fat and reduced amount of brown fat. Brown fat is a site of heat production.
It is localized around the adrenal glands, kidneys, nape of neck, inter scapular and
axillary region. Metabolism of brown fat results in heat production. Blood flowing
through the brown fat becomes warm and through circulation transfers heat to other body
parts of the body. This mechanism of heat production is called as non-shivering thermo
genesis. LBW babies lack this effective mechanism of heat production.
ii. Mechanism of heat loss:
Newborn looses 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 nonshivering thermo genesis.
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 prewar med 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
20

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, vaso constrictive medications,
Raynauds phenomenon
CLASSIFICATION OF FROST BITE
1. First degree frost bite: causes only anesthesia and erythematic.
2. Second degree frost bite: appearance of superficial vesiculation surrounded by edema
leads to very cold extremities.
3. Third degree frost bite: hemorrhagic vesicles due to serious microvasculature injury
which further leads to cyanosis.
4. Fourth 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. There is
tingling and redness followed by pallor and numbness of the affected area. There are
three degrees: transitory hyperemia 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,
plethismography, thermography to evaluate perfusion after rewarming. Technetium
scientigraphy 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 40 mg 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
21

in days; if broken then debride and dress with antibiotic. Leave hemorrhagic vesicle
intact to prevent infection. Continue analgesics Ibuprofen 400mg 8-12 hourly. Provide
tetanus prophylaxis and hydrotherapy at 37C. 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 patient is unconscious.
NON FREEZING COLD INJURY
Trench foot or immersion foot this 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 rewarding the limb appears mottled. There after
becomes hyperemic swollen and painful recovery may take many months and there may
be chronic pain and sensitivity to cold. The pathology provably involves endothelial
injury. The pain and associated par aesthesia may be difficult to control with normal
analgesic.
CONCLUSION
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 clients temperature, to identify deviations and to report significant
findings to the physician, so that appropriate therapy can be instituted.
INSOMNIA
DEFINITION
Sleep disorder - insomnia; Learned insomnia; Chronic insomnia; Primary insomnia
Insomnia is trouble falling asleep or staying asleep through the night.
Episodes may come and go (episodic), last up to 3 weeks (short-term), or be long-lasting
(chronic).
TYPES OF INSOMNIA
Insomnia can be classified as transient, acute, or chronic.
1. Transient insomnia lasts for less than a week. It can be caused by another
disorder, by changes in the sleep environment, by the timing of sleep,
severe depression, or by stress. Its consequences sleepiness and impaired
psychomotor performance are similar to those of sleep deprivation.
2. Acute insomnia is the inability to consistently sleep well for a period of less than
a month. Insomnia is present when there is difficulty initiating or maintaining
22

sleep or when the sleep that is obtained is non-refreshing or of poor quality. These
problems occur despite adequate opportunity and circumstances for sleep and they
must result in problems with daytime function.
3. Chronic insomnia lasts for longer than a month. It can be caused by another
disorder, or it can be a primary disorder. People with high levels of stress
hormones or shifts in the levels ofcytokines are more likely to have Chronic
insomnia. Its effects can vary according to its causes. They might include
muscular fatigue, hallucinations, and/or mental fatigue. Some people that live
with this disorder see things as if they are happening in slow motion, wherein
moving objects seem to blend together.Chronic insomnia can cause double vision.
PATTERNS OF INSOMNIA
Sleep-onset insomnia is difficulty falling asleep at the beginning of the night, often a
symptom of anxiety disorders or the delayed sleep phase disorder.
Nocturnal awakenings are characterized by difficulty returning to sleep after awakening
in the middle of the night or waking too early in the morning: middle-of-the-night
insomnia and terminal insomnia. The former may be a symptom of pain disorders or
illness; the latter is often a characteristic of clinical depression.
Poor sleep quality
Poor sleep quality can occur as a result of, for example, restless legs, sleep
apnea or major depression. Poor sleep quality is caused by the individual not reaching
stage 3 or delta sleep which has restorative properties.
Major depression leads to alterations in the function of the hypothalamic-pituitaryadrenal axis, causing excessive release of cortisol which can lead to poor sleep quality.
Nocturnal polyuria, excessive nighttime urination, can be very disturbing to sleep.
Subjective insomnia
Some cases of insomnia are not really insomnia in the traditional sense. People
experiencing sleep state misperception often sleep for normal durations, yet severely
overestimate the time taken to fall asleep. They may believe they slept for only four hours
while they, in fact, slept a full eight hours.

23

CAUSES, INCIDENCE, AND RISK FACTORS


Sleep habits we learned as children may affect our sleep behaviors as adults. When we
repeat these behaviors over many years, they become habits.
Poor sleep or lifestyle habits that may cause insomnia or make it worse:

Going to bed at different times each night

Daytime napping

Poor sleeping environment, such as too much noise or light

Spending too much time in bed while awake

Working evening or night shifts

Not getting enough exercise

Using the television, computer, or smartphone in bed

The use of some medications and drugs may also affect sleep:

Alcohol or other drugs

Heavy smoking

Too much caffeine, especially late in the day

Getting used to certain types of sleep medications

Some cold medications and diet pills

Other medicines, herbs, or supplements prescribed by a health care provider or


bought on your own

Physical, social, and mental health issues can affect sleep patterns, including:

Anxiety disorders
Bipolar disorder
Certain medical conditions, such as thyroid disease

Feeling sad or depressed. Often, insomnia is the symptom that causes people
with depression to seek medical help.

Physical pain or discomfort

Stress, whether it is short-term or long-term. For some people, the stress caused
by the insomnia makes it even harder to fall asleep.
24

With age, sleep patterns tend to change. Many people find that aging causes them to have
a harder time falling asleep, and that they wake up more often.

SYMPTOMS AND COMORBIDITIES


Symptoms of insomnia can be caused by or can be co-morbid with:

Use
of psychoactive
drugs (such
as stimulants),
including
certain medications, herbs, caffeine, nicotine, cocaine, amphetamines, methylphenidat
e, aripiprazole, MDMA, modafinil, or excessive alcohol intake.

Use of fluoroquinolone antibiotic drugs, see fluoroquinolone toxicity, associated


with more severe and chronic types of insomnia[13]

Restless Legs Syndrome, which can cause sleep onset insomnia due to the
discomforting sensations felt and the need to move the legs or other body parts to
relieve these sensations.

Periodic limb movement disorder (PLMD), which occurs during sleep and can
cause arousals that the sleeper is unaware of.

Pain: An injury or condition that causes pain can preclude an individual from
finding a comfortable position in which to fall asleep, and can in addition cause
awakening.

Hormone shifts
during menopause

Life events such as fear, stress, anxiety, emotional or mental tension, work
problems, financial stress, birth of a child and bereavement.

Mental disorders such as bipolar disorder, clinical depression, generalized anxiety


disorder, post traumatic stress disorder, schizophrenia, obsessive compulsive disorder,
or dementia.

Disturbances of the circadian rhythm, such as shift work and jet lag, can cause an
inability to sleep at some times of the day and excessive sleepiness at other times of
the day. Chronic circadian rhythm disorders are characterized by similar symptoms.

such

as

those

that

precede menstruation and

those

Certain neurological disorders, brain lesions, or a history of traumatic brain injury


25

Medical conditions such as hyperthyroidism and rheumatoid arthritis[16]


Abuse of over-the counter or prescription sleep aids (sedative or depressant drugs)
can produce rebound insomnia
Poor sleep hygiene, e.g., noise
Parasomnias,
which
include
such
disruptive
sleep
events
as nightmares, sleepwalking, night terrors, violent behavior while sleeping, and REM
behavior disorder, in which the physical body moves in response to events within
dreams

A rare genetic condition can cause a prion-based, permanent and eventually fatal
form of insomnia called fatal familial insomnia.
Physical exercise. Exercise-induced insomnia is common in athletes, causing prolonged

TESTS
Your health care provider will do a physical exam and ask you questions about your
current medications, drug use, and medical history. Usually, these are the only methods
needed to diagnose insomnia.
Polysomnography, an overnight sleep study, can help rule out other types of sleep
disorders (such as sleep apnea).
TREATMENT
It is important to identify or rule out medical and psychological causes before deciding on
the treatment for insomnia. Attention to sleep hygieneis an important first line treatment
strategy and should be tried before any pharmacological approach is
considered. Pharmacological treatments have been used mainly to reduce symptoms in
acute insomnia; their role in the management of chronic insomnia remains unclear.
Non-pharmacological
Non-pharmacological strategies are superior to hypnotic medication for insomnia
because tolerance develops to the hypnotic effects
Stimulus control therapy is a treatment for patients who have conditioned
themselves to associate the bed, or sleep in general, with a negative response. As
26

stimulus control therapy involves taking steps to control the sleep environment, it
is sometimes referred interchangeably with the concept of sleep hygiene.
A component of stimulus control therapy is sleep restriction, a technique that aims
to match the time spent in bed with actual time spent asleep. This technique
involves maintaining a strict sleep-wake schedule, sleeping only at certain times of
the day and for specific amounts of time to induce mild sleep deprivation.
Complete treatment usually lasts up to 3 weeks and involves making oneself sleep
for only a minimum amount of time that they are actually capable of on average,
and then, if capable (i.e. when sleep efficiency improves), slowly increasing this
amount (~15 min) by going to bed earlier as the body attempts to reset its internal
sleep clock.
Bright light therapy, which is often used to help early morning wakers reset their
natural sleep cycle, can also be used with sleep restriction therapy to reinforce a
new wake schedule. Although applying this technique with consistency is difficult,
it can have a positive effect on insomnia in motivated patients.
Paradoxical intention is a cognitive reframing technique where the insomniac,
instead of attempting to fall asleep at night, makes every effort to stay awake (i.e.
essentially stops trying to fall asleep).
Cognitive Behavioral Therapy for Insomnia
A recent study found that Cognitive Behavioral Therapy for Insomnia (CBT-I) is more
effective than hypnotic medications in controlling insomnia. In this therapy, patients are
taught improved sleep habits and relieved of counter-productive assumptions about sleep.
MEDICATIONS
Benzodiazepines
The most commonly used class of hypnotics prescribed for insomnia are the
benzodiazepines.
Non-benzodiazepines

27

Nonbenzodiazepine sedative-hypnotic drugs, such as zolpidem, zaleplon, zopiclone,


and eszopiclone, are a newer classification of hypnotic medications indicated for mild to
moderate insomnia.
Alcohol
Alcohol is often used as a form of self-treatment of insomnia to induce sleep. However,
alcohol use to induce sleep can be a cause of insomnia.
Opioids
Opioid medications such as hydrocodone, oxycodone, and morphine are used for
insomnia
that
is
associated
with pain due
to
their analgesic properties
and hypnotic effects.
Antidepressants
Some antidepressants such as amitriptyline, doxepin, mirtazapine, and trazodone can
often have a very strong sedative effect, and are prescribed off label to treat insomnia [58]
Melatonin and melatonin agonists
The hormone melatonin, sold as a "dietary supplement" in some countries or as a slowrelease prescription drug (Circadin) in Europe, is effective in several types of insomnia.
Antihistamines
The antihistamine diphenhydramine is widely used in nonprescription sleep aids such as
Benadryl.
Atypical antipsychotics
Low doses of certain atypical antipsychotics such as quetiapine, olanzapine,
and risperidone are also prescribed for their sedative effect, but the danger of
neurological, metabolic, and cognitive side-effects makes these drugs a poor choice to
treat insomnia.

28

Other substances
Some
insomniacs
use herbs such
marijuana, valerian, chamomile, lavender, hops, and passion-flower.
undergone multiple studies and appears to be modestly effective.[67][68][69]

as medical
Valerian has

Insomnia may be a symptom of magnesium deficiency, or low magnesium levels, but this
has not yet been proven. A healthy diet containing magnesium can help to improve sleep
in individuals without an adequate intake of magnesium.
EXPECTATIONS (PROGNOSIS)
Most people are able to sleep by practicing good sleep hygiene. See a doctor if you have
insomnia that does not improve.
CONCLUSSION
It is most common sleep disorder. Insomnia is a perception of inadequate sleep and
characterized by difficulty in initiating sleep and frequent awakening from sleep

29