A major cause of death in neonates.
Associated with brain damage and disability, especially among preterm infants.
Black infants have an increased incidence of group B streptococcal sepsis and late-onset sepsis.
The incidence is higher in males than in females.
Premature infants, and low-birth weight infants have an increased incidence.
Categorized as early or late onset disease with 85% of early-onset infections present within 24 hours, 5% present at 24-48 hours, and a lesser percentage presenting within 48-72 hours.
Premature neonates have rapid onset sepsis.
Early onset sepsis associated with acquisition of infection from the mother transplacentally or by ascending infection from the cervix.
Organisms most commonly associated with early-onset infection include group B Streptococcus, Escherichia coli, coagulase-negative Staphylococcus,Haemophilus influenzae, and Listeria monocytogenes.
Recent studies suggest group B Streptococcus sepsis infections are decreasing due to intrapartum antibiotic prophylaxis in at risk situation.
Late-onset sepsis syndrome refers to infection at 4-90 days of life and is acquired from the environment.
Microorganisms in late-onset sepsis syndrome include coagulase-negative staphylococci, Staphylococcus aureus, E coli, Klebsiella, Pseudomonas, Enterobacter, Candida, group B Streptococcus, S2242atia, Acinetobacter, and anaerobes.
Late-onset sepsis associated with an increase in coagulase-negative Streptococcal infections.
Neonatal skin, respiratory tract, mucous membranes, or the GI tract may become colonized leading to the possibility of late-onset sepsis.
Colonizated vascular or urinary catheters or contact from caregivers with bacterial colonization may be the source of late-onsert infections.
Pneumonia is more common in early onset sepsis.
Meningitis and bacteremia are more common in late-onset sepsis.
Premature and ill infants have an increased risk.
Clinical signs of neonatal sepsis are nonspecific.
Signs of neonatal sepsis associated with characteristics of the causative organism and the neonates response to the infection.
Incidence of culture proven sepsis is approximately 2 per 1000 live births.
Of the 7-13% of neonates who are evaluated for neonatal sepsis, only 3-8% have culture proven sepsis.
Many neonates are asymptomatic and undergo evaluation based on risk factors because the mortality rate of untreated sepsis can be as high as 50%.
Treatment is often initiated before confirmation by positive blood cultures.
Hypoglycemia, hyperglycemia, metabolic acidosis, and jaundice are metabolic signs that are commonly seen with neonatal sepsis syndrome.
Jaundice occurs in response to decreased hepatic glucuronidation caused by both hepatic dysfunction and increased red blood cell destruction.
Meningitis is the common manifestation, and is primarily associated with group B streptococci, E coli, and Listeria species infections, although other organisms may be associated.
Infarction of the brain may be seen in neonatal meningitisand occurs in 30% of infants who die.
Meningitis due to early onset neonatal sepsis usually occurs within 24-48 hours.
Meningitis signs include stupor and irritability, but overt signs of meningitis occur in only 30% of cases.
Late-onset disease is more likely to demonstrate neurologic signs with impairment of consciousness, coma, seizures, bulging anterior fontanel, extensor rigidity, focal cerebral signs, cranial nerve signs, and nuchal rigidity.
Many physical findings are subtle or nonapparent in the neonate.
CSF findings in infectious neonatal meningitis are an elevated WBC count, an elevated protein level, a decreased CSF glucose concentration, and positive culture results.
Hypoglycorrhachia is more severe in late-onset disease and with gram-negative organisms.
The CSF WBC count, protein and glucose concentrations are more often abnormal in gram negative infections than with gram positive meningitis.
Temperature instability with hypothermia, poor feeding, poor muscle tone and lethargy commonly seen with neonatal meningitis.
Neurologic hyperactivity is more likely seen with late-onset meningitis.
The platelet count in the healthy newborn is rarely less than 100,000/µL in the first 10 days of life and the presence of thrombocytopenia may be a presenting sign in neonatal sepsis.
WBC counts and ratios are more sensitive in determining the presence pf neonatal sepsis than platelet counts, but have low positive predictive value as the count may be normal in 50% of culture positive patients.
Some patients with neonatal sepsis present with neutropenia.
Disseminated intravascular coagulation, and necrotizing enterocolitis can occur in neonatal sepsis.
Mortality for neonatal sepsis may be as high as 50% for infants who are not treated.
Neonatal sepsis contributes to 13-15% of all neonatal deaths.
Neonatal meningitis occurs in 2-4 cases per 10,000 live births, and is responsible for 4% of all neonatal deaths.
Inflammatory mediators associated with neonatal sepsis may contribute to brain injury and poor neurodevelopmental.
Polyvalent IgG immune globulin may help to prevent or treatinfection in infants, particularly preterm infants with low serum IgG levels.
Prophylactic use of intravenous immune globulin in a review of 19 trials involving more than 5000 preterm below birth weight, inference reduced the rate of late onset infection by 3% with no significant reduction in rates of death and adverse effects (Ohlsson A et al).
A review of seven trials of intravenous immune gamma globulin involving 338 newborns with suspected or proven sepsis showed no difference in mortality (Alahandria MM et al).
In a double-blind, randomized, controlled trial of adjunctive human nonspecific polyvalent IgG intravenous immune globulin, compared with placebo in newborn infants suspected of or with proven sepsis, who were receiving antibiotic therapy with an enrollment of 3493 infants: therapy with intravenous immune gamma globulin had no affect on outcomes of suspected or proven neonatal sepsis (INIS Collaborative Group).
Intrapartum oral azithromycin does not prevent neonatal sepsis and total mortality.