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Fifth stage
vM
Pediatrics
mv
Lec :11
Dr.Athal
10/11/2016
NEONATAL SEPSIS
Early neonatal sepsis (birth to 7 days) :
• Acquired transplacentally
• Ascending from the vagina
• During birth (intrapartum infection)
late neonatal sepsis:
• After birth, neonates are exposed to infectious agents in the nursery or in the
community (including family). by direct contact with hospital personnel, the mother,
or other family members; from breast milk (HIV, CMV); or from contaminated
equipment. The most common source of postnatal infections in hospitalized newborns
is hand contamination of healthcare personnel, underscoring the importance of hand
washing.
Early Onset Neonatal Sepsis
Risk factors for early-onset neonatal sepsis:
1. PROM >18hr.
2. Preterm
3. Vaginal colonization with group B streptococci.
4. Signs of maternal infection, e.g. maternal fever, chorioamnionitis, UTI &
leukocytosis.
5. Fetal tachycardia & distress.
6. African American race.
7. Male sex.
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Etiology of ENS:
• Infection is caused by organisms acquired from the mother, usually GBS, E. coli,
klebsiella or other possibilities include herpes virus( HSV1, HSV2), H. influenza,
anaerobes, Candida, and Chlamydia trachomatis. Transplacental transferred
infection(syphilis, listeria)
Presentation:
• ENS is an overwhelming multiorgan system disease frequently manifested as
respiratory failure, shock, meningitis, DIC, acute tubular necrosis, and symmetrical
peripheral gangrene.
• Early manifestations may be “non specific” grunting, poor feeding, pallor, apnea,
lethargy, hypothermia, or an abnormal cry.
Investigations:
• Septic screen (blood culture, GUE & urine culture, GSE & stool culture, CSF
examination & culture.)
• CXR to exclude pneumonia.
• CBC (neutropenia, thrombocytopenia)
• CRP
• Blood urea & serum electrolytes
• Arterial blood gas analysis
Treatment:
• Supportive (may require ventilation, volume expansion, inotropes).
• Broad-spectrum antibiotics, e.g. ampicillin 300mg/kg/day with gentamicin
5mg/kg/day for 2 weeks.
• If meningitis confirmed or strongly suspected then treatment with cefotaxime with
ampicillin for 3 weeks.
• Intratracheal surfactant may reverse respiratory failure.
Prognosis
:
Up to 15% mortality (up to 30% if VLBW).
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Late onset neonatal infection
Risk factors for late-onset sepsis:
• Central lines and catheters.
• Frequent blood drawing for lab.
• Endotracheal intubation.
• Congenital malformations, e.g. spina bifida.
• Severe illness, malnutrition, or immunodeficiency.
Etiology:
• Infection is caused by environmental organisms such as coagulase -ve staphylococci,
Staph. Aureus.
• Same pathogens as early-onset sepsis, but infants exhibiting sepsis late in the neonatal
period.
• May have infections caused by the pathogens usually found in older infants (H.
influenzae, S. pneumoniae, and Neisseria meningitidis).
• Viral agents as (HSV, CMV, or enteroviruses)
Presentation:
• Non specific: lethargy, poor feeding, hypotonia, apathy, seizures, bulging fontanelle,
fever, and direct-reacting hyperbilirubinemia.
• localized symptoms more common than in early onset sepsis as osteomyelitis, arthritis,
UTI, cellulitis & omphalitis.
Investigations:
Same as early onset sepsis with specific investigation for localized infection.
Treatment:
• Supportive therapy.
• Antibiotics:
o vancomycin + gentamicin for 2 week.
o vancomycin+ cefotaxime for 3 weeks if meningitis is present.
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General measures to prevent neonatal sepsis:
1. Good hand washing with antiseptic solutions and use of gloves.
2. Avoidance of overcrowding.
3. Low nurse to patient ratio.
4. Patient isolation and barrier nursing.
5. Minimal handling.
6. Rational antibiotic use.
7. Minimize indwelling vascular access
• Congenital infections, an infection acquired transplacentally during gestation include a
well-known group of fungal, bacterial, and viral pathogens.
TORCH
: (Toxoplasmosis, rubella, CMV, HSV) in addition to VZV, congenital syphilis,
parvovirus, HIV, hepatitis B, Neisseria gonorrhoeae, Chlamydia, and Mycobacterium
tuberculosis.
Presentation
:
• IUGR
• Jaundice
• Anaemia
• TCP, HSM
• Purpura
• Nonimmune hydrops
• Chorioretinitis
• Congenital malformation.
TOXOPLASMOSIS
The classic findings of hydrocephalus, chorioretinitis, and intracerebral calcifications
suggest the diagnosis of congenital toxoplasmosis.
Affected infants tend to be SGA, develop early onset jaundice, HSM, generalized
maculopapular rash. Seizures are common, and skull films may reveal diffuse cortical
calcifications.
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RUBELLA
The most common characteristic abnormalities associated with congenital rubella
include:
• Eye: cataracts, retinopathy, and glaucoma.
• Ear: sensorineural hearing loss.
• Cardiac: PDA, peripheral PS.
• CNS: behavioral disorders ,meningoencephalitis, and MR.
• Others: growth retardation, HSM, jaundice, TCP, and skin lesions.
CYTOMEGALOVIRUS
CMV is the most common congenital infection and the leading cause of:
• Sensorineural hearing loss.
• Retinal disease.
• MR.
• CP
Parvovirus B19:
rubella-like rash, aplastic anaemia +/– hydrops.
Herpes zoster
: cutaneous scarring, limb defects, multiple structural defects.
Congenital syphilis:
SGA, jaundice, HSM, rash, rhinitis, bleeding mucous
membranes, osteochondritis, meningitis.
Investigations:
• Blood culture.
• Pathogen-specific IgM and IgG.
• Venereal Disease Research Laboratory (test)(VDRL).
• Maternal-specific serology.
• Urine CMV culture.
• Skin vesicle viral culture and electron microscopy
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Treatment:
• Most congenital infections have no specific treatment. General treatment is supportive
and involves careful follow-up to identify sequelae, e.g. deafness.
• Toxoplasma: For symptomatic and asymptomatic congenital infections, initial therapy
should include pyrimethamine (supplemented with folic acid) combined with
sulfadiazine. Duration of therapy is often prolonged even up to 1 year.
• Syphilis: benzylpenicillin 14 days.
• Symptomatic CMV: IV ganciclovir then oral valganciclovir.
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