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Fifth stage
Pediatric
Lec-8
.د
بسام
21/12/2015
NEONATAL SEPSIS
Neonatal sepsis can be either:
Early neonatal sepsis:
-Acquired transplacentally
-Ascending from the the vagina,
-During birth (intrapartum infection)
Or late neonatal sepsis:
-postnatally acqired from the environment or contact with others.
Risk factors for early-onset neonatal sepsis:
-Prolonged rupture of membranes >18hr, especially if preterm.
-Signs of maternal infection, e.g. maternal fever, chorioamnionitis, UTI.
-Vaginal carriage or previous infant with group B streptococcus.
-Preterm labour; foetal distress.
-Skin and mucosal breaks.
Risk factors for late-onset sepsis:
-Central lines and catheters.
-Congenital malformations, e.g. spina bifida.
-Severe illness, malnutrition, or immunodeficiency.
Early-onset neonatal infection:
Infection is caused by organisms acquired from the mother, usually GBS, E. coli, or Listeria.
Other possibilities include herpes virus,
H. influenza, anaerobes, Candida, and Chlamydia trachomatis.

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Presentation (symptomatic):
Includes temperature instability, lethargy, poor feeding, respiratory distress, collapse, DIC,
and osteomyelitis or septic arthritis.
Investigations:
These include blood culture, cerebrospinal fluid (glucose, protein, cell
count and culture), CBC, CXR.
The diagnostic value of CRP in early neonatal sepsis is unclear. .
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.
Prognosis:
Up to 15% mortality (up to 30% if VLBW).
Late-onset neonatal infection:
Infection is caused by environmental organisms such as coagulase –ve staphylococci, Staph.
aureus, E. coli, and other Gram –ve bacilli, Candida spp., and GBS.
Investigations:
CBC, blood culture, urinalysis (clean catch) and urine culture, CSF glucose, protein, cell count
and culture.
Treatment:
In addition to supportive therapy, start vancomycin + gentamicin, or vancomycin+ cefotaxime
if meningitis is suspected.
Duration is 2 weeks if no meningitis and for 3 weeks if meningitis is present.

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General measures to prevent neonatal sepsis:
-Good hand washing with antiseptic solutions and use of gloves.
-Avoidance of overcrowding.
-Low nurse to patient ratio.
-Patient isolation and barrier nursing.
-Minimal handling.
-Rational antibiotic use.
-Minimize indwelling vascular access
TORCH infections “Congenital Infections”:-
TORCH refers to toxoplasmosis,rubella, cytomegalovirus,and herpes,some includes syphilis,
parvovirus,HIV,and hepatitis B.
Presentation:
TORCH infection: SGA, jaundice, hepatitis, hepatosplenomegaly, purpura, chorioretinitis,
micro-ophthalmos, cerebral calcification, micro/macrocephaly, hydrocephalus.
Rubella and CMV: also cause deafness, cataracts, congenital heart disease, osteitis (rubella
only).
Parvovirus B19: rubella-like rash, aplastic anaemia +/– hydrops.
Herpes zoster: cutaneous scarring, limb defects, multiple structural defects.
Congenital syphilis: SGA, jaundice, hepatomegaly, 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: spiramycin (4–6wks 100mg/kg/day) alternating with pyrimethamine (3wks
1mg/kg/day) plus sulfadiazine (1yr 50–100mg/kg/day).
Syphilis: benzylpenicillin 14 days 30mg/kg 12-hourly IV.
Symptomatic CMV: IV ganciclovir then oral valganciclovir