FEVER is protective and adaptive reaction of one’s organism developing as an answer on pathogenic

factors influence and characterized by thermoregulation processes rebuilding which leads in body temperature
increase with stimulating of corresponding reactivity of an organism.
Hyperthermia is increasing of body temperature with no rebuilding of thermoregulation.
Thermoregulatory center includes several parts of the brain. They are: thermosensitive zone (contains
complex of neurons receiving information from thermoreceptors of skin and blood); thermosetting point
(consists of complex of neurons which integrate an information of the thermosensitive zone and head the
activity of heath production and heath output centers; heath production centers (neurons of the behind part of
hypothalamus); heath output center (neurons of frontal part of hypothalamus).
Body temperature increasing is marked rather more often in children than in adults. This is caused by
physiological peculiarities of thermoregulation in childhood. Last time majority of investigators consider the
temperature to be increased if its index exceeds 37,20C (by the results of axillary measurement).
Fever – is general reaction of an organism, developing in many diseases of the childhood as a result of
influence of different exo- and endogenous factors (pyrogens) and accompanying by activation of the protective
response of an organism. According to UNICEF, fever is increasing of body temperature more than 37,50C.
Accordingly to body temperature increasing degree fever is divided into subfebrile (below 38,0 0C), febrile
(38,10C – 39,00C), pyretic, or high febrile (39,10C – 41,00C) and hyperpyretic (above 41,00C) ones.
In diseases accompanied by prolonged fever rippling of the temperature submit to a daily two-phase
rippling of body temperature: its maximal indexes are marked at 5.00 – 7.00 p.m. and minimal ones – at 4.00 –
6.00 a.m. In pathological conditions the following fever types are marked:
 Constant (febris continua) – temperature daily rippling doesn’t exceed 10C and is marked in
tuberculosis and croupous pneumonia;
 Remittent (febris remittens) – temperature daily rippling exceeds 10C and is typical for rheumatic
fever and sepsis
 Intermittent (febris intermittens) – during some certain time body temperature increasing is changed
by its decreasing to normal indexes. It is characteristic of sepsis, malaria and spread (disseminated) tuberculosis
 Hectic (exhausting; febris hectic) fever is characterized by episodes of marked hyperthermia and its
fast decrease which may be detected two or three times during some certain period and often accompanies
sepsis and tuberculosis;
 Recurrent (febris recurrens) fever is characterized by long periods (lasting many hours) of
hyperthermia (to 39 – 400C), repeating every day or three days and changing by apyretic periods; it is typical
for malaria and epidemic typhus;
 Inverted (febris inverse) – perversion of daily rhythm of body temperature with its maximal indexes
in the morning;
 Incorrect (febris atipica) is characterized by the absence of body temperature rippling regularity in
different time of the day; it may take place in rheumatic fever, dysentery and influenza.
There are three periods in fever. The first period is characterized by body temperature increase, moderate
shiver and worsening of child’s general condition. It is worthwhile to warm the child during this period by
applying hot-water bag to child’s legs or giving warm tea and covering the child.
Second period – is a time of maximal body temperature increase characterized by rising intoxication,
intensive headache, thirst and general weakness. On the background on physiological reaction as an answer on
hyperthermia the patient’s skin gets brightly pink color (due to peripheral vessels distension), moderate or high
moisture; child’s extremities get warm. General condition is not severely violated. In this type of fever heat
production corresponds to heat emission. This type of fever is called “red” one and is common for majority of
pathological cases. Paleness of skin and its marble image, cold limbs (sign of peripheral vessels spasm and
blood circulation centralization), general condition worsening (development of flabbiness, headache, shiver and
vomiting) testifies to “white” fever, which is resulted by imbalanced heat production and heat emission
processes caused by different factors. The most dangerous is fever in infants of first months of life, immature
newborns and newborns with pathologic damage of central nervous system as far as in some cases it may lead
in hallucinations and/or convulsions development. For peripheral blood circulation improvement and heat
emission induce the child is heated with a hot-water bag.
Patient with hyperthermia must not be stay with no observation as far as he may fall down from the bed
and traumatize. At the time of “red” fever it is reasonable to use physical methods of hypothermia in order to
increase emission of heat: the child is uncovered, blow off with ventilator and his skin is rubbed with acetic or
alcohol solution.
Third period – period of body temperature decrease – may have different course: critical (characterized by
fast decrease of body temperature from high to normal indexes within some hours) or lytic one (gradual
decreasing of body temperature during several days and more so that each following day it gets down on
0,50C). Critical decrease of body temperature general weakness and massive sweating are marked; extremities
get cold and there is pulsus filiformis detected. All these may be explained by accompanying arterial
hypotension. In this case the child should put on dry and clean clothes, be warmed with hot-water bag and
given to drink sweat tea. Gradual decreasing of body temperature is accompanied by mild signs of general
weakness and sweating.
Biological role of fever:
 Activation of immunobiological protection
 Prevention of pathogenic microorganisms reproduction
 Induction of phagocytic activity of leukocytes and macrophages
 Activation of enzymatic systems participating in viruses’ reproduction inhibition
 Stimulation of immunoglobulins and interferone production
 Reduction of microorganisms’ resistance against drugs
 Reduction of child’s activity leading in decresing of loads on main organs and systems and contributing
to faster recovery

Group of risk on fever’s possible complications:

 Hyperpyrexia (body temperature higher than 39.00C)
 Children of the first 3 years of life if bode temperature exceeds 38.30C
 Congenital heart and other organs’ defects
 Sepsis, influenza, intestinal infections, meningitis, meningoencephalitis, shock
 Febrile convulsions in the anamnesis
 Congenital metabolic diseases (phenylketonuria, galactosemia, glycogenoses)
 CNS pathology (encephalopathies, hydrocephaly, convulsions, brain’s defects).
Temperature is ultimately regulated in the hypothalamus. A trigger of the fever, called a pyrogen, causes
a release of prostaglandin E2(PGE2). PGE2 then in turn acts on the hypothalamus, which generates a systemic
response back to the rest of the body, causing heat-creating effects to match a new temperature level.
In many respects, the hypothalamus works like a thermostat. When the set point is raised, the body
increases its temperature through both active generation of heat and retention of heat.
Peripheral vasoconstriction both reduces heat loss through the skin and causes the person to feel cold. If these
measures are insufficient to make the blood temperature in the brain match the new set point in the
hypothalamus, then shivering begins in order to use muscle movements to produce more heat. When the
hypothalamic set point moves back to baseline either spontaneously or with medication, the reverse of these
processes (vasodilation, end of shivering and nonshivering heat production) and sweating are used to cool the
body to the new, lower setting.
This contrasts with hyperthermia, in which the normal setting remains, and the body overheats through
undesirable retention of excess heat or over-production of heat. Hyperthermia is usually the result of an
excessively hot environment (heat stroke) or an adverse reaction to drugs. Fever can be differentiated from
hyperthermia by the circumstances surrounding it and its response to anti-pyreticmedications.
 A pyrogen is a substance that induces fever. These can be either internal (endogenous)
or external (exogenous) to the body. The bacterial substance lipopolysaccharide (LPS), present in the cell wall
of some bacteria, is an example of an exogenous pyrogen. Pyrogenicity can vary: In extreme examples, some
bacterial pyrogens known as superantigens can cause rapid and dangerous fevers. Depyrogenation may be
achieved through filtration, distillation, chromatography, or inactivation.
In essence, all endogenous pyrogens are cytokines, molecules that are a part of the immune system. They
are produced by activated immune cells and cause the increase in the thermoregulatory set point in the
hypothalamus. Major endogenous pyrogens are interleukin 1(α and β) and interleukin 6 (IL-6). Minor
endogenous pyrogens include interleukin-8, tumor necrosis factor-β, macrophage inflammatory protein-α and
macrophage inflammatory protein-β as well as interferon-α, interferon-β, and interferon-γ. Tumor necrosis
factor-α also acts as a pyrogen. It is mediated by interleukin 1 (IL-1) release.
These cytokine factors are released into general circulation, where they migrate to the circumventricular
organs of the brain due to easier absorption caused by the blood–brain barrier's reduced filtration action there.
The cytokine factors then bind with endothelial receptors on vessel walls, or interact with local microglial cells.
When these cytokine factors bind, the arachidonic acid pathway is then activated.
One model for the mechanism of fever caused by exogenous pyrogens includes LPS, which is a cell wall
component of gram-negative bacteria. An immunological protein called lipopolysaccharide-binding
protein (LBP) binds to LPS. The LBP–LPS complex then binds to the CD14 receptor of a nearby macrophage.
This binding results in the synthesis and release of various endogenous cytokine factors, such as interleukin 1
(IL-1), interleukin 6 (IL-6), and the tumor necrosis factor-alpha. In other words, exogenous factors cause
release of endogenous factors, which, in turn, activate the arachidonic acid pathway.
PGE2 release
PGE2 release comes from the arachidonic acid pathway. This pathway (as it relates to fever), is mediated
by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase. These
enzymes ultimately mediate the synthesis and release of PGE2.
PGE2 is the ultimate mediator of the febrile response. The set point temperature of the body will remain
elevated until PGE2 is no longer present. PGE2 acts on neurons in thepreoptic area (POA) through
the prostaglandin E receptor 3 (EP3). EP3-expressing neurons in the POA innervate the dorsomedial
hypothalamus (DMH), the rostral raphe pallidus nucleus in the medulla oblongata (rRPa), and
the paraventricular nucleus (PVN) of the hypothalamus . Fever signals sent to the DMH and rRPa lead to
stimulation of the sympathetic output system, which evokes non-shivering thermogenesis to produce body heat
and skin vasoconstriction to decrease heat loss from the body surface. It is presumed that the innervation from
the POA to the PVN mediates the neuroendocrine effects of fever through the pathway involving pituitary
gland and various endocrine organs.
Hypothalamus
The brain ultimately orchestrates heat effector mechanisms via the autonomic nervous system. These may
be:
 Increased heat production by increased muscle tone, shivering and hormones like epinephrine (adrenaline)
 Prevention of heat loss, such as vasoconstriction.
In infants, the autonomic nervous system may also activate brown adipose tissue to produce heat (non-
exercise-associated thermogenesis, also known as non-shivering thermogenesis). Increased heart rate and
vasoconstriction contribute to increased blood pressure in fever.

Fever in the infant and toddler is one of the most common problems and greatest challenges faced by
those caring for them. This material addresses the most common etiologies of fever in these age groups and the
appropriate clinical prediction rules for identifying infants and toddlers at lowest risk for serious bacterial
infections.
 Neonates (≤28 d) with fever may have few clues on history and physical examination to guide therapy;
however, 3% have a serious bacterial infection. Obtaining the pertinent medical history from the mother
regarding the pregnancy, delivery, and early neonatal life of the febrile neonate is essential. Typically,
infections that occur in the first 7 days of life are secondary to vertical transmission, and those infections
occurring after the first 7 days are usually community acquired or hospital acquired.
Definitive identification of a serious bacterial infection requires laboratory investigation; a
full sepsis evaluation; and a positive result in blood culture, cerebrospinal fluid (CSF), and/or urine. Bacterial
meningitis is more common in the first month of life than at any other time. An estimated 5-10% of neonates
with early onset group B streptococcal (GBS) sepsis have concurrent meningitis.
The general approach to fever in a febrile infant aged 28-60 days includes maintaining a high index of
suspicion, because these patients often lack clues on physical examination. The prevalence of a serious bacterial
infection in an infant younger than 3 months is approximately 6-10%, most often urinary tract infections
(UTIs). Interestingly, infants aged 3 months or younger with a confirmed viral infection are at lower risk for a
serious bacterial infection when compared with those in whom a viral infection is not identified; although a UTI
is still a significant concurrent infection in infants with bronchiolitis.
According to guidelines from the Agency of Health Care Policy and Research published in 2012, in
infants younger than 3 months with rectal temperatures 38oC or higher, the prevalence of serious bacterial
infection reported in studies conducted in North American emergency departments or primary care practices
ranged from 4.1-25.1%.
Historically, children aged 3 months to 3 years with rectal temperatures of 38.5 o C or higher had a risk of
2-4% for occult bacteremia. The leading cause of bloodstream infection was Streptococcus
pneumoniae, followed by Haemophilus influenzae type b. With the introduction of effective vaccines for these
pathogens, the incidence and epidemiology of childhood bacteremia in the immunologically normal host has
changed considerably; only 1 in 200 (0.5%) febrile children are now found to be bacteremic.
The incidence of occult bacteremia in this population now ranges from 0.25-0.7%; moreover, 2 of every 3
blood isolates from these children represent an artifact (contamination) and not a true pathogen. S.
pneumoniae and Escherichia coli are the most common pathogens, accounting for two thirds of cases. In infants
with S. pneumoniae, many isolates are strains not covered by the currently available heptavalent conjugate
vaccine.
Children with pneumococcal bacteremia may present with acute otitis media, pneumonia, symptoms of
sinusitis, meningitis, febrile seizures, cellulitis (including orbital or facial cellulitis), or nonspecific febrile
illnesses. E coli bacteremia is most common in children younger than 1 year and is usually associated with
urinary tract infection (UTI). Staphylococcus aureus accounts for 15% of bloodstream infections and may be
associated with skin, soft tissues, or musculoskeletal infections. Salmonella species, Neisseria meningitides,
and S. pyogenes account for most of the remaining infections.
As with most patients, the approach to the febrile child aged 3 months to 3 years consists of a targeted
medical history, a complete physical examination, and the judicious use of the laboratory tests.
History and examination of neonates
A thorough history is essential for all neonates with fever. Associated symptoms may be system specific
(eg, diarrhea, cough) or nonspecific (eg, poor feeding, irritability, lethargy). Seizures have been reported in 20-
50% of neonates with meningitis. Exposures to sick contacts in the household or daycare should be ascertained,
as well as a recent history of a previous illness, immunization, or antibiotic use while in the birth hospital or
since discharge.
Prenatal history
A review of the prenatal history, including maternal history of sexually transmitted infections (human
immunodeficiency virus [HIV], hepatitis B and hepatitis C, syphilis, gonorrhea, chlamydia, herpes simplex),
maternal group B Streptococcus(GBS) status and prophylaxis, mode of delivery, prolonged rupture of
membranes, and history of maternal fever should be noted.
A birth weight of less than 2500 g, rupture of membranes before the onset of labor, septic or traumatic
delivery, fetal hypoxia, maternal peripartum infection, and galactosemia are all risk factors for a serious
bacterial infection in the neonate. Gestational age should be determined, because premature infants are at
increased risk for serious bacterial infections.
Nursery course
 The neonate’s nursery course should be noted, including the age at which the patient went home from the
nursery, whether or not a male neonate has been circumcised, and the use of peripartum or antepartum
antibiotics. Any underlying diseases or conditions, as well as the use of medications that may increase the risk
of infection, should be ascertained. Diet (ie, quantity and description of milk consumed; breast milk vs formula;
and, if pertinent, the method the caregiver uses for preparing and storing the formula) and sleep histories should
be obtained, because decreased oral intake or an acute change in sleep patterns may be clues to an invasive
infection.
Household contacts
Any ill contacts in the household should also be noted. Exposure to any animals inside the home of the
caregiver or outside the home (eg, in daycare facility) should be determined. The vaccination status of
household members should be determined. A history of maternal fetal loss or death due to an infectious disease
in a previous infant increases the suspicion of congenital anomalies and primary immunodeficiencies.
Identifying who is in the neonate’s household, who is the primary caregiver, contact with recent
immigrants, and exposure to homelessness and poverty all impact the care the neonate receives.
Review of systems and physical examination
A thorough review of systems must be obtained to identify any other symptoms associated with the fever.
A complete physical examination including vital signs (temperature 38°C = 100.4°F), pulse oximetry, and
growth parameters with percentiles is necessary. General appearance should be noted for activity level, color,
tone, and irritability. Signs of localized infection should be identified via a thorough examination of the skin,
mucous membrane, ear, and extremities.
The presence of an umbilical stump after age 4 weeks should be noted, because it is a potential clue
to leukocyte adhesion deficiency, and the lack of a circumcision in males should be noted, because it increases
the risk for a urinary tract infection (UTI). In addition to fever, the most common clinical features of a UTI in a
neonate include failure to thrive, jaundice (typically secondary to conjugated hyperbilirubinemia from
cholestasis), and vomiting. Irritability, inconsolability, poor perfusion, poor tone, decreased activity, and
lethargy can be signs of a serious infection in this age group.
Most neonates with bacterial meningitis have a full fontanelle with normal neck flexion at the time of
presentation. Remember that neonates younger than 28 days with significant bacterial infections can appear to
be at low risk when analyzing history, physical examination findings, and laboratory values; thus, a high index
of suspicion must be maintained.
Febrile infant aged 28-60 days may have symptoms that are nonspecific (eg, poor feeding, irritability,
lethargy) or specific symptoms (eg, diarrhea, cough). History of exposure to sick contacts in the household or
daycare should be obtained, as well as a recent history of a previous illness, immunization, and recent antibiotic
use.
Past medical history and household contacts
The past medical history needed is essentially the same as in neonates. A prenatal, perinatal, and neonatal
history should be obtained. Underlying diseases or conditions and the use of medications that may increase the
risk of infection should be ascertained. In addition, as with neonates, diet and sleep histories should be
obtained, because decreased oral intake or an acute change in sleep patterns may be clues to an invasive
infection.
Exposure to any animals inside the home of the caregiver or outside the home such as in the daycare
facility should be determined. A travel history of all household contacts should be obtained. The vaccination
status of household members should also be determined.
As with neonates: (1) a family history of a previous death in a young infant from an infectious disease
increases the suspicion of congenital anomalies and primary immunodeficiencies, and (2) identifying who lives
in the household, who is the primary caregiver, exposure to any recent immigrants, and exposure to
homelessness and poverty helps establish risk for infection and how to manage the patient.
Review of systems and physical examination
 A thorough review of systems must be obtained to identify any other symptoms associated with the fever.
A complete physical examination including vital signs (temperature 38°C = 100.4°F), pulse oximetry, and
growth parameters with percentiles is necessary. A heart rate of more than 160 beats per minute in infants and a
respiratory rate of more than 60 beats per minute are associated with an increased mortality risk and often
signal the development of septic shock.
As with a neonate, general appearance should be noted for activity level, color, tone, and irritability.
Irritability, inconsolability, poor perfusion, poor tone, decreased activity, and lethargy can be signs of a serious
infection. Likewise, signs of localized infection should be identified via a thorough examination of the skin,
mucous membranes, ear, and extremities. Lack of a circumcision in males should be noted.
Unfortunately, bacterial meningitis is often associated with minimal signs and symptoms in this age
group, and a bulging fontanelle is a late sign. Nuchal rigidity is only present in 27% of infants younger than 6
months.
History and Examination of Children Aged 3 Months to 3 Years
The medical history should focus on factors that would predispose the infant or toddler to serious
bacterial infection.
History of present illness
Documentation of the child’s temperature and how it was measured is essential. A rectal temperature of
more than 38.5o C (101o F) is abnormal in this age group. In addition to identifying when the fever started and
how long it has lasted, a detailed search should be made for other symptoms, including but not limited to
diarrhea, vomiting, rhinorrhea, cough, rash, and changes in weight or feeding habits.
Past medical history
Every effort should be made to identify previous infectious episodes and risk factors for serious bacterial
infections. Underlying chronic diseases, previous surgery, history of urinary tract infections (UTIs), and
incomplete immunization to Streptococcus pneumoniae or Haemophilus influenzae type b must be specifically
delineated. In children younger than 9 months, neonatal and perinatal history is also important.
Family history
Episodes of recurrent infections among siblings and first cousins or a history of maternal fetal loss raises
suspicion of primary immunodeficiencies. Parental human immunodeficiency (HIV) status is essential
information. A history of chronic infections (eg, hepatitis B, hepatitis C, tuberculosis) in the immediate or
extended family is also important to obtain. The presence of acute illness in the family, such as croup or
respiratory infection, is also important information.
Social history and household contacts
Animal, insect, and sylvan exposure; exposure to contaminated potable water and sewage; recent travel
(particularly international travel); and attendance at daycare provide epidemiologic and environmental clues to
the etiology of fever. Exposure to sick individuals outside of the household is also critical information.
Review of systems and physical examination
A detailed review of systems helps to identify other symptoms associated with fever. Important
associations include rash, conjunctivitis, ear pain or drainage, lymphadenopathy, respiratory symptoms,
changes in appetite, weight loss, diarrhea, vomiting, changes in frequency of voiding, pain with voiding, failure
to bear weight, pain on passive motion of an extremity, and overt neurologic symptoms.
A careful and thorough physical examination is essential in the evaluation of the febrile child. Vital signs,
including length and weight with percentiles, should be part of the evaluation. The child’s general state of
nutrition, level of activity, and level of arousal should be noted.
Physical examination findings that suggest serious bacterial infections in febrile children (aged 3-36 mo)
include ill appearance, fever, vomiting, tachypnea with retractions, and delayed capillary refill. These findings
are associated with bacterial infection in more than 39.5% of febrile children aged 24-36 months and in more
than 39% of children aged 3-24 months.
 Close examination of the skin, lymphatics, eyes, ears, nose, and throat is necessary, because many febrile
infants have viral infections with associated rashes or associated respiratory symptoms. Inspection and
auscultation of the chest should be included in all evaluations. The abdomen should be inspected for signs of
distention. Auscultation may reveal signs of ileus or hyperactivity. The extremities should be evaluated for
capillary refill; range of motion, signs of infection, and local tenderness should be evaluated. Neurologic and
developmental examinations appropriate for age should be performed.
The clinical management of infants and toddlers with fever is based on their age groups.
Neonates and young infants should be hospitalized with intravenous antibiotics pending results of
laboratory tests and cultures.
For the most part, management should be individualized based on risk factors, clinical appearance, and
clinical judgment. Ill-appearing children with poor capillary refill and children who have clinical signs and
symptoms suggestive of meningitis need to be managed in hospital and perhaps in the critical care setting.
Children with focal infections such as sinusitis and pneumonia need to be managed with appropriate
antimicrobial therapy.
With the widespread use of pneumococcal vaccine in young children, the incidence of occult bacteremia
in febrile children aged 3 months to 3 years has fallen from 4.6% to less than 1%. As such, the evaluation has
become more extensive to prevent overtreatment. In the absence of focal findings, any child in the target age
group who appears ill or has excessive fever, vomiting, or tachypnea with retractions should be evaluated
further.
Parents and medical professionals who want to supplement physical measures with medication in order to
maximize the time that children spend without fever should use ibuprofen first and weigh the use of
paracetamol plus ibuprofen over 24 hours.
All febrile infants aged 28-60 days, after having a sepsis evaluation, should be hospitalized and
empirically started on intravenous antibiotics pending culture results. The antibiotic spectrum of coverage must
include both community-acquired pathogens (eg, Streptococcus pneumoniae, Haemophilusinfluenzae,
Moraxella catarrhalis, Neisseria meningitidis, late-onset group B Streptococcus [GBS], Staphylococcus
aureus), perinatally acquired organisms (eg, early onset GBS, Escherichia coli, and other gram-negative
organisms and Listeria monocytogenes), or hospital-acquired organisms in the neonate or infant who was
recently hospitalized (eg, enteric gram-negative organisms, S aureus).
Empiric antibiotics
Ampicillin and gentamicin, or ampicillin and cefotaxime for the neonate, covers GBS, E
coli, Listeria, and most S pneumoniae and N meningitides. For infants aged 1-2 months, recommended empiric
coverage includes ampicillin, cefotaxime, and vancomycin to provide adequate coverage for community-
acquired pathogens. All antibiotic dosages should be adequate to treat meningitis. For infants older than 2
months, vancomycin and cefotaxime are the empiric antibiotic choices. Vancomycin is especially important if
the patient has evidence of soft-tissue infection, given the increasing prevalence of methicillin-resistant S
aureus (MRSA), or a cerebrospinal fluid (CSF) profile consistent with bacterial meningitis to cover for
antibiotic-resistant S pneumoniae.
Well-appearing and relatively well-appearing infants
Relatively well-appearing febrile infants younger than 28 days who are diagnosed with a viral respiratory
illness should have a septic workup that includes cultures of blood, urine, and CSF. These infants should
receive empiric antibacterial therapy in hospital until culture results are known.
Infants older than 28 days who look well and whose history, physical examination, and laboratory
evaluation findings classify them as low risk can be treated as outpatients with ceftriaxone (50 mg/kg in a single
intramuscular dose), as long as 24-hour follow-up can be ensured.
Infants older than 28 days who are diagnosed with bronchiolitis or influenza and are relatively well-
appearing should undergo a limited laboratory evaluation, including complete blood cell (CBC) count with
differential, blood culture, urinalysis, and urine culture. If the CBC count and urinalysis findings are benign,
these patients can be initially managed without antibacterial therapy.
 Ill-appearing neonates
Acyclovir (60 mg/kg/d divided every 8 h) is recommended for febrile neonates who appear ill, have
mucocutaneous vesicles, experience seizures, or have a CSF pleocytosis.[12] In addition, viral cultures and direct
fluorescent antigen detection should be performed on skin vesicles and conjunctival, nasopharyngeal, and rectal
mucous membranes. CSF should be assessed for herpes simplex virus (HSV) and undergo polymerase chain
reaction (PCR) and viral culture.
Empiric antimicrobial therapy in non-toxic children aged 3 months to 3 years is not recommended. For
those requiring hospitalization, antimicrobial therapy must provide coverage against the suspected pathogens
and must achieve high and sustained serum concentrations.[20] In this setting, a single intramuscular (IM) dose
of ceftriaxone has been shown to prevent sustained bacteremia in children whose initial blood culture has
yielded Streptococcus pneumoniae.
In vitro, ceftriaxone is also effective against most strains of Escherichia coli, thus supporting the empiric
use of this agent until bacterial culture results are known (see Workup). Children at risk for Staphylococcus
aureus infections should receive clindamycin as well. Limited data are available regarding the use of alternative
agents.
The most effective way to treat fever is to use a medication such as acetaminophen (sample brand name:
Tylenol) or ibuprofen (sample brand names: Advil, Motrin). These treatments can reduce the child's discomfort
and lower the child's temperature by 2 to 3ºF (1 to 1.5ºC). Aspirin is not recommended for children under age
18 years due to concerns that it can cause a rare but serious illness known as Reye syndrome.
Acetaminophen may be given every four to six hours as needed, but should not be given more than five
times in a 24-hour period. Acetaminophen should not be used in children younger than three months of age
without consultation with a healthcare provider. The dose of acetaminophen should be calculated based upon
the child's weight (not age).
Ibuprofen may be given every six hours. Ibuprofen should not be used in children younger than six
months of age. The dose of ibuprofen should be calculated based upon the child's weight (not age).
Giving combinations of acetaminophen and ibuprofen or alternating acetaminophen and ibuprofen
increases the chance of giving the wrong dose of one or the other of the medications.
Fever-reducing medications should only be given as needed, and discontinued once bothersome
symptoms have resolved.
Increase fluids — Having fever can increase a child's risk of becoming dehydrated. To reduce this risk,
parents should encourage their child to drink an adequate amount of fluids. Children with fever may not feel
hungry, and it is not necessary to force them to eat. However, fluids such as milk (cow's or breast), formula, and
water should be offered frequently. Older children may eat flavored gelatin, soup, or frozen popsicles. If the
child is unwilling or unable to drink fluids for more than a few hours, the parent should consult the child's
healthcare provider.
Rest — Having a fever causes most children to feel tired and achy. During this time, parents should
encourage their child to rest as much as the child wants. It is not necessary to force the child to sleep or rest if
he or she begins to feel better. Children may return to school or other activities when the temperature has been
normal for 24 hours.
Sponging and baths — Sponging is not as effective as medications for fever and generally is not
recommended. Alcohol should not be used for sponging because of the risk of toxicity if it is absorbed through
the skin.