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