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15.neonatal Infection

Neonatal infection is a clinical syndrome in infants aged 0 to 28 days, characterized by systemic signs of infection and isolation of a bacterial pathogen from the bloodstream. It is classified into early-onset (before 7 days) and late-onset (≥7 days) infections, with common etiological agents including Group B Streptococcus and Escherichia coli. Management typically involves supportive measures and antibiotic therapy, with specific regimens based on the timing and suspected pathogens.

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0% found this document useful (0 votes)
97 views40 pages

15.neonatal Infection

Neonatal infection is a clinical syndrome in infants aged 0 to 28 days, characterized by systemic signs of infection and isolation of a bacterial pathogen from the bloodstream. It is classified into early-onset (before 7 days) and late-onset (≥7 days) infections, with common etiological agents including Group B Streptococcus and Escherichia coli. Management typically involves supportive measures and antibiotic therapy, with specific regimens based on the timing and suspected pathogens.

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Kandy Emmy
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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NEONATAL INFECTION

Prof. Melvis
Bernis Maren
KIU-TH
DEFINITION
Neonatal infection is a
clinical syndrome in a baby
between 0 to 28 days of life,
manifested by systemic signs
of infection and isolation of a
bacterial pathogen from the
blood stream.
DEFINITION
Neonatal infection is classified according to
the baby’s age at the onset of symptoms.
1.Early-onset infection is defined as the onset
of symptoms before 7 days of age, although
some experts limit the definition to
infections occurring within the first 72 hours
of life
DEFINITION
1. Late-onset infection is
generally defined as the onset of
symptoms at ≥7 days of age. Similar
to early-onset sepsis, there is
variability in its definition, ranging
from an onset at >72 hours of life to
≥7 days of age
DEFINITION
Systemic inflammatory response
syndrome — The systemic inflammatory
response syndrome (SIRS) is a
widespread inflammatory response that
may or may not be associated with
infection. The presence of two or more
of the following criteria (one of which
must be abnormal temperature or
leukocyte count) defines SIRS
DEFINITION
●Core temperature (measured by
rectal, bladder, oral, or central
probe) of >38.5°C or <36°C
●Tachycardia, defined as a mean
heart rate more than two standard
deviations above normal for age, or
for children younger than one year
of age, bradycardia defined as a
mean heart rate <10th percentile
DEFINITION
●Mean respiratory rate more
than two standard deviations
above normal for age or
mechanical ventilation for an
acute pulmonary process
●Leukocyte count elevated or
depressed for age, or >10
percent immature neutrophils
DEFINITION
Sepsis: The systemic
inflammatory response
syndrome in the presence of
suspected or proven
infection constitutes sepsis.
DEFINITION
Severe sepsis: Sepsis is considered
severe when it is associated with
cardiovascular dysfunction, acute
respiratory distress syndrome (ARDS),
or dysfunction in two or more other
organ systems as defined in the
section on multiple organ failure
below. The diagnostic criteria for
ARDS are discussed elsewhere.
DEFINITION
Septic shock: Septic shock
refers to sepsis with
cardiovascular
dysfunction that persists
despite the administration
of ≥40 mL/kg of isotonic
fluid in one hour .
DEFINITION
1. Refractory septic shock –
There are two types of
refractory septic shock: fluid-
refractory septic shock exists
when cardiovascular
dysfunction persists despite at
least 60 mL/kg of fluid
resuscitation.
DEFINITION
2. And catecholamine-resistant
septic shock exists when shock
persists despite therapy with
dopamine ≥10 mcg/kg per min
and/or direct-acting
catecholamines (epinephrine,
norepinephrine)
PATHOGENESIS
Early-onset infection is usually due to vertical
transmission by ascending contaminated amniotic
fluid or during vaginal delivery from bacteria in the
mother's lower genital tract.
•Maternal chorioamnionitis is a well-recognized risk
factor for early-onset neonatal sepsis.
•Maternal group B streptococcal (GBS) colonization is
another important risk factor.
PATHOGENESIS
Late-onset infections can be acquired
by the following mechanisms
•Vertical transmission, resulting in initial
neonatal colonization that evolves into
later infection
•Horizontal transmission from direct
contact with care providers or
environmental sources
EPIDEMIOLOGY
•The overall incidence of neonatal infection
ranges from one to five cases per 1000 live
births.
•Infection rates increase with decreasing
gestational age.
•The incidence of early-onset infection has
decreased primarily due to reduction in
group B streptococcal (GBS) infections
owing to the use of intrapartum antibiotic
RISK FACTORS
Risk factors associated with an increased risk of
early onset sepsis:
•Low birth weight (less than 2500 grams)
•Febrile illness in the mother with evidence of
bacterial infection within 2 weeks prior to the
delivery
•Foul smelling and/or meconium stained liquor
•Rupture of membranes > 24 hours
RISK FACTORS
Risk factors associated with an
increased risk of early onset sepsis:
•Single unclean or > 3 sterile vaginal
examination (s) during labour
•Prolonged labour
•Perinatal asphyxia (Apgar score <4
at 1 minute)
RISK FACTORS
Risk of nosocomial infection include
•Low birth weight
•Prematurity
•Admission in intensive care unit
•Mechanical ventilation
RISK FACTORS
•Risk of nosocomial infection
include
•Invasive procedures
•Administration of parenteral
fluids
•Use of stock solutions
RISK FACTORS
Risk of community-acquired
Sepsis
•Poor hygiene
•Poor cord care
•Bottle-feeding
•Prelacteal feeds
ETIOLOGIC AGENTS
Group B Streptococcus (GBS) and Escherichia coli
(E. coli) are the most common causes of both
early- and late-onset infection
Other bacterial agents associated with neonatal
sepsis include
Listeria monocytogenes
Staphylococcus aureus
ETIOLOGIC AGENTS
Other gram-negative bacteria
including Klebsiella, Enterobacter,
and Citrobacter
Pseudomonas aeruginosa are
associated with late-onset infection,
especially in infants admitted to
neonatal intensive care units
ETIOLOGIC AGENTS
Common non-bacterial agents associated
with neonatal sepsis include:
• Herpes simplex virus
• Enterovirus
• parechovirus
• Candida
MANIFESTATIONS
Respiratory Gastrointestin Neurologic
and al symptoms
cardiocirculato
ry
Tachypnea Feed Lethargy
intolerance

Grunting Vomiting Poor tone

Nasal flaring Diarrhea Poor feeding


CLINICAL MANIFESTATIONS
Respiratory Gastrointestin Neurologic
and al symptoms
cardiocirculat
ory

Use of Addominal Irritability


accessory distention
muscles
Tachycardia Paralytic ileus Seizures
MANIFESTATIONS
Hepatic Renal Hematologic Skin changes
al

Hepatomegaly Reduced Bleeding Multiple pustule


urine output

Direct Petechiae Abscess


hyperbilirubinemi
a

Purpura Mottling

Umbilical
Lab Exams
•Blood culture
•Lumbar puncture (if the baby is clinically
stable enough to tolerate the procedure)
•Complete blood count with differential and
platelet count
•Chest radiograph (if respiratory symptoms
are present)
Lab Exams
•Urine culture
•Cultures from any other potential
focus of infection (eg, tracheal
aspirates if intubated, purulent
eye drainage, or pustules)
•Cultures from tracheal aspirates
if intubated
MANAGEMENT
•Support measures (depend the
signs and symptom)
Incubator (Hypothermia)
Oxygen (difficulty in breathing)
Fluids ( Dehydration or refuse breastfeeding)
Phenobarbitone (convulsion)
MANAGEMENT
•Antibiotic
The combination of Ampicillin and
Gentamicin is effective in treating
most common pathogens that
cause neonatal sepsis, including
group B Streptococcus (GBS),
Listeria, Enterococcus, and most
isolates of Escherichia coli
ANTIBIOTIC
Ampicillin and Gentamicin are preferred over ampicillin
and a third-generation cephalosporin based upon the
following:
•The regimen of Ampicillin and a third-generation
cephalosporin is not more effective than the combination
of ampicillin and Gentamicin
•The emergence of cephalosporin-resistant gram-negative
organisms (eg, Enterobacter cloacae, Klebsiella, and
Serratia species) can occur when Cefotaxime is used
ANTIBIOTIC
•Ampicillin and Gentamicin are synergistic
in treating infections caused by GBS and
Listeria monocytogenes. Cephalosporins
are not active against L. monocytogenes
•In a large cohort study, infants who
received Ampicillin plus Cefotaxime had a
1.5-fold increase in mortality compared
with those treated with ampicillin plus
Gentamicin
ANTIBIOTIC
Antibiotic Dose
Ampicillin 50-75mg/kg/dose
6 hours (7 day)
Gentamicin 4
Staphylococcusmg/kg/day (7
day)
•Cefazolin 50-100mg/kg/day
•Vancomycin
40-60mg/kg/day
•Cloxacillin 50-100mg/kg/day
ANTIBIOTIC
Empiric therapy Antibiotic regimen
Early onset (<7 days) Ampicillin AND gentamicin
Late onset (≥7 days): Ampicillin AND gentamicin
Admitted from the
community
Late onset (≥7 days): Gentamicin AND
Hospitalized since birth vancomycin
Special circumstances
Suspected meningitis - early Ampicillin AND gentamicin
onset
Suspected meningitis - late Ampicillin, gentamicin, AND
onset, admitted from the cefotaxime
community
Suspected meningitis - late Gentamicin, vancomycin, AND
onset, hospitalized since birth cefotaxime
Suspected pneumonia Ampicillin AND gentamicin
ALTERNATIVES Ampicillin AND cefotaxime
(Pneumonia)
Vancomycin AND cefotaxime,
Special circumstances
Suspected infection of soft tissues, Vancomycin or vancomycin AND
skin, joints, or bones (S. aureus is a nafcillin
likely pathogen)
Suspected intravascular catheter- Vancomycin AND gentamicin
related infection
Suspected infection due to organisms Ampicillin, gentamicin, AND
found in the gastrointestinal tract (eg,
anaerobic bacteria) clindamycin

ALTERNATIVES Ampicillin, gentamicin, AND


(From above) metronidazole OR
Piperacillin-tazobactam AND gentamicin
COMPLICATIONS
• SepticShock
•Disseminated intravascular coagulation
• Multiorganic failure
Discharge Criteria
48 hours with normal
temperature
• Breastfeeding well
• Increasing of weight
• Asymptomatic
WE NEED TO SERVE/WORK
for the health of children
because they love and they
are the hope of the world.
THANK YOU
Prof. Melvis

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