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.

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.

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

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