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Fifth stage
Pediatric
Lec. 9
د. رياض
14/12/2016
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.
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Early-onset neonatal sepsis:
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.
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),umbilical, nasopharyngeal swab 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.
Or, cefotaxime with ampicillin
If meningitis confirmed or strongly suspected then treatment
continue for 3 weeks.
Prognosis:
Up to 15% mortality (up to 30% if VLBW).
Late-onset neonatal sepsis:
Infection is caused by environmental organisms such as coagulase
–ve staphylococci, Staph. aureus, E. coli, and other Gram –ve bacilli,
Candida spp., and Group B Streptococcus.
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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.
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
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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
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
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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