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Transcript
Background
 Neonatal sepsis is one of the leading problem of
neonatal death, causes the neonatal morbidity and
mortality.
 The incidences of neonatal death due to neonatal
sepsis varies from 3 – 14 per 1000 newborns.
 It is higher in preterm babies(up to 26 per 1000 live
babies).
 Incidence is even higher in the underdeveloped
countries like Bangladesh, where the proper
treatment facility is not sufficient
Definition
 Neonatal sepsis is a clinical syndrome of systemic
illness accompanied by bacteremia in the first 28 day’s
of life.
 Early Onset Sepsis (EOS):
 Culture proven infection within the first 72 hours of life
 85% present within 24 hrs ,5% present in between 24-
48 hrs, a small % present in between 48-72 hrs.
 Late Onset Sepsis (LOS):
 Culture proven infection after 72 hours of life
Etiology
 Infectious agents associated with neonatal sepsis
have changed since the mid-20th century
 1950 - S. aurus, E. coli; later s. aurus replaced by GBS
 1990 – GBS and E .coli
 Now – coagulase-negative S. epidamis frequently
observed
 Can also be caused by adenovirus, enterovirus,
coxsakie virus.
 Gonorrhea, syphilis, herpes simplex virus, CMV,
hepatitis, HIV, TORCH infection have also been
implicated in neonatal infection.
Early-onset Sepsis
 Associated with acquisition of microorganisms
from the mother – transplacental infection or
ascending infection
Onset is most rapid in premature neonates
 GBS, E. coli, Coagulase-negative Staphylococcus,
Stepto coccus , H. influenzae, L. monocytogenes are
common pathogens.
 In Bangladesh context Klebsiella, Pseudomonas,
E.coli, Acinobactor are common
 Pneumonia is more common in early-onset sepsis
Risk Factors of Early-onset Sepsis
 Maternal GBS colonization (especially if
untreated during labor)
 Premature rupture of membranes
(PROM)
 Prolonged rupture of membranes
 Prematurity
 Maternal urinary tract infection
 Chorioamnionitis
Etiology of Late-onset Sepsis
 Acinetobacter
 Klebsiella
 E coli
Meningitis and
 Serratia
bacteremia are
 Pseudomonas
 S. aureus
more common in
 Enterobacter
late-onset sepsis
 Candida
 GBS
 Anaerobes
 Coagulase negetive staphilococcus
Risk Factors of Late-onset Sepsis
 Prematurity
 Central venous catheterization
(duration >10 days)
 Nasal cannula or continuous positive airway
pressure (CPAP)
 H 2 -receptor blocker or proton pump inhibitor
(PPI)
 GI tract pathology
Numerous host factors in
Neonatal sepsis




Cellular immunity
Humeral immunity
Complement factors
And other Barrier function
Clinical Examination
 Clinical signs of neonatal sepsis are nonspecific
and are associated with
 Characteristics of the causative organism
 Body’s response to the invasion.
 These nonspecific clinical signs are also
associated with other neonatal diseases
 Respiratory distress syndrome (RDS)
 Metabolic disorders
 Intracranial hemorrhage
 Traumatic delivery
Clinical Symptoms
Common /Non-specific
Respiratory distress (90%) - RR, apnea (55%),
hypoxia/vent need (36%), flaring/grunting
Temperature instability, feeding problems
Lethargy-irritability (23%)
Gastrointestinal – poor feeding, vomiting, abdominal
distention, ileus, diarrhea
Color—Jaundice, pallor, mottling
Hypo- or hyperglycemia,Metabolicacidosis
Cardiovascular – Hypotension (5%), hypo perfusion,
tachycardia,overt shock with pallor & odema.
This late signs of shock are indicative of severe
compromise & strongly associated with mortality
NICHD data
 Less com
 Seizure
 DIC
 Petechiae
 Hepatosplenomegaly
 Sclerema
 Meningitis symptoms
 Buiging anterior frontanele
 Irritability, lethargy, poorly responsive
 Changes in muscle tone, etc.
Differential Diagnoses


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
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Bowel Obstruction in the Newborn
Congenital Pneumonia
Heart Failure, Congestive
Hemolytic Disease of Newborn
Meconium Aspiration Syndrme
Necrotizing Enterocolitis
Pediatric Congenital Diaphragmatic Hernia
Pediatric Infective Pericarditis
Pulmonary Hypoplasia Imaging
Respiratory Distress Syndrome
Approach Considerations
 Complete blood count (CBC) and differential
 Blood culture
 Quantity measurement of CRP and possibly other
infection markers
 In some cases, serial CBC and CRP studies may be
appropriate
 Gram stain provides early identification of the
gram-negative or gram-positive status of the
organism for preliminary identification
 CSF analysis and culture
Approach Considerations contd…
 Emerging technology using PCR could eventually
help achieve faster identification of causative
organism. Rapid pathogen detection with multiplex
PCR may facilitate more timely selection of
targeted antibiotic therapy while limiting exposure
to broad-spectrum antibiotics
 Imaging studies may include:
 Chest radiography to evaluate pulmonary
involvement
 CT scan, MRI and ultrasonography of the head in
cases of meningitis
Results “Trigger Points”
 CBC
 WBC <5.0, or > 22.0, abs neutro <1,750, bands >2.0
 I/T ratio > 0.2*
 Platelets < 100,000
 CRP > 1.0 mg/dl
 CSF > 20 WBC’s with few or no RBC’s
 Radiographs: infiltrates on CXR, ileus on KUB,
periosteal elevation, etc.
Treatment & Management
 When neonatal sepsis is suspected, treatment should




be initiated immediately because of the neonate’s
relative immunosuppression
Begin antibiotics as soon as diagnostic tests are
performed
Cardiopulmonary support and parenteral nutrition
may be required during the acute phase of the illness
until the infant’s condition stabilizes
Monitoring BP & vital signs, HCT, platelets, and
coagulation studies is vital
Not uncommonly, blood product transfusion, including
packed red blood cells, platelets and FFP are indicated
Treatment & Management contd…
 Infant
with
temperature
instability
needs
thermoregulatory support with a radiant warmer or
incubator. Once the infant is stable from a
cardiopulmonary point, parental contact is important,
kangaroo management can be applicable in this regard
 Surgical consultation for central line placement may be
necessary in infants who require prolonged IV
antimicrobial therapy
 If an abscess is present, surgical drainage may be
necessary; IV antibiotic therapy cannot adequately
penetrate an abscess, and antibiotic treatment alone is
ineffective
Treatment & Management contd…
 The infant may require transfer to a level III
perinatal center, especially if he or she requires
cardiopulmonary support, parenteral nutrition, or
prolonged IV access. The multidisciplinary services
available at larger centers may be necessary if the
neonate’s condition is acutely compromised
 Additional therapies can be apply for the treatment
of neonatal sepsis, including granulocyte
transfusion, IVIg infusion, exchange transfusion,
and the use of recombinant cytokines
Antibiotic Therapy
 In the United States and Canada, the current
approach to the treatment of early-onset neonatal
sepsis includes combined IV aminoglycoside and
expanded-spectrum penicillin antibiotic therapy
 The specific antibiotics to be used are chosen on
the basis of maternal history and prevalent trends
of
organism
colonization
and
antibiotic
susceptibility in individual nurseries
Antibiotic Therapy contd…
 If an infection appears to be nosocomial (late-onset
sepsis), antibiotic coverage should be directed at
organisms
implicated
in
hospital-acquired
infections, including S. aureus, S epidermidis, and
pseudomenous sp.
 Vancomycin has been favored for this coverage;
however, concern exists that overuse of this drug
may lead to vancomycin-resistant organisms, For
this reason, some clinicians prefer oxacillin therapy
in this setting.
Antibiotic Therapy contd…
 Cephalosporins are attractive in the treatment of
nosocomial infection because lack of dose-related
toxicity and ability to reach adequate serum and
CSF concentrations; however, their use has led to
resistance in gram-negative organisms. Ceftriaxone
displaces bilirubin from serum albumin and should
be used with caution in infants with significant
hyperbilirubinemia
 Aminoglycosides and vancomycin both have the
potential to produce ototoxicity and nephrotoxicity
and should therefore be used with caution
Prognosis
 Mortality from neonatal sepsis may be as high as 50% for infants





who are not treated.
Low birth weight and gram-negative infection are associated with
adverse outcomes.
In preterm infants who have had sepsis, impaired
neurodevelopment is a concern.
Residual neurologic damage occurs in 15-30% of neonates with
septic meningitis.
preterm infants with sepsis who did not have meningitis had higher
rates of cognitive deficits, cerebral palsy, and other neuro
developmental disabilities than infants who did not have sepsis.
Infants with meningitis may acquire hydrocephalus or
periventricular leukomalacia. They may also have complications
associated with the use of aminoglycosides, such as hearing loss or
nephrotoxicity.
Long time -Follow Up
Follow up- The primary care provider (PCP) should evaluate the
infant with neonatal sepsis within 1 week of discharge from the
hospital.
1st week, Then Two weekly up to 3 Month
Monthly up to 18 month
If need to continue
The PCP should evaluate growth and determine whether the
feeding regimen and activity have returned to normal.




ROP Screening,
Hearing test- audiology test, audio screen
RSV prophylaxis
Neonatal sepsis is associated with meningitis, prolong hypoxia, ECMO
therapy or brain abscess should be folowed for several yrs,
Prevention
 HAND-WASHING- the gold slandered measure for
prevention
 Aseptic precaution during examination
 For GBS antibiotic treatment & prophylaxis during
labor and delivery
 Pediatrician especially neonatologist all over the
world continuously pay great attention to the unsolved
questions of new born babies with sepsis, to reduce
neonatal morbidity & mortality of this contingent of
babies, hope to reduce to single digit.