5neonate6-539857398bbhg933459349759.pptx

neonate

1. Sepsis and Meningitis

2. Neonatal infections are unique: (1)Infectious agents can be transmitted from the mother to the fetus or newborn infant by diverse modes. ( 2) Newborn infants are less capable of responding to infection because of 1 or more immunologic deficiencies. ( 3) Coexisting conditions often complicate the diagnosis and management of neonatal infections.

3. (4) The clinical manifestations of newborn infections vary and include subclinical infection, mild to severe manifestations of focal or systemic infection, ( 5) Maternal infection that is the source of transplacental fetal infection is often undiagnosed (6) A wide variety of etiologic agents infect the newborn, including bacteria, viruses, fungi, protozoa, and mycoplasmas. (7) Immature, very low birthweight (VLBW) newborns have improved survival but remain in the hospital for a long time in an environment that puts them at continuous risk for acquired infections.

4. The bacteria responsible for ascending infection of the fetus are common bacterial organisms of the maternal geni-tourinary tract, such as group B streptococci GBS, E. coli, Haemophilus influenzae , and Klebsiella . Herpes simplex virus (HSV)-1 or more often HSV-2 also causes ascending infection that at times may be indistinguishable from bacterial sepsis. Syphilis and Listeria monocytogenes are acquired by transplacental infection

5. The incidence of sepsis is approximately 1:1500 in full-term infants and 1:250 in preterm infants. This relates to the more immature immunologic systems of preterm infants and to their prolonged periods of hospitalization, which increase risk of nosocomially acquired infectious diseases. Neonatal antibody-dependent, cell-mediated immunity by the natural killer lymphocytes is deficient in the absence of maternal antibodies

6. Preterm infants before 32 weeks of gestational age have not received the full complement of maternal antibodies ( IgG ). These infants also have deficiencies of the alternate and, to a smaller degree, the classic complement activation pathways, which results in diminished complement-mediated opsonization . Newborn infants also show a deficit in phagocytic migration to the site of infection (to the lung) and in the bone marrow reserve pool of leukocytes. Neutrophils from sick infants seem to have an even greater deficit in bacterial killing capacity compared with phagocytic cells from normal neonates

7. The incidence of meningitis is approximately 1 in 20 cases of sepsis. The causative organisms : group B streptococci, E. coli, and L. monocytogenes . Gram-negative organisms, such as Klebsiella and Serratia marcescens , are more common in less developed countries, and coagulase-negative staphylococci need to be considered in VLBW infants . Male more than female infants. Neonates in the neonatal ICU live in a hostile environment,

8. Early-onset sepsis O ften begins in utero and usually is a result of infection caused by the bacteria in the mother's genitourinary tract. Organisms related to this sepsis include group B streptococci, E. coli, Klebsiella , L. monocytogenes , and nontypable H. influenzae . Most infected infants are premature show nonspecific cardiorespiratory signs, such as grunting, tachypnea, and cyanosis at birth. Risk factors for early-onset sepsis include vaginal colonization with group B streptococci, prolonged rupture of the membranes (>24 hours), amnionitis , maternal fever or leukocytosis, fetal tachycardia, and preterm birth

9. overwhelming multiorgan system disease frequently manifested as respiratory failure, shock, meningitis (in 30% of cases), DIC, acute tubular necrosis, and symmetric peripheral gangrene. Early manifestations-grunting, poor feeding, pallor, apnea, lethargy, hypothermia, or an abnormal cry-may be nonspecific. In the initial stages of early-onset septicemia in a preterm infant, it is often difficult to differentiate sepsis from RDS. Because of this difficulty, premature infants with RDS receive broad-spectrum antibiotics.

10. diagnosis 1-Serial complete blood counts should be performed to identify neutropenia, an increased number of immature neutrophils (bands), and thrombocytopenia. 2-C-reactive protein levels are often elevated in neonatal patients with bacterial sepsis 3- blood and CSF cultures, CSF Gram stain, cell count, and protein and glucose levels. Normal newborns generally have an elevated CSF protein content (100 to 150 mg/ dL ) and may have 25 to 30/mm3 white blood cells (mean 9/mm3), which are 75% lymphocytes in the absence of infection. 4- rapid antigensity test. 5-The PCR test primarily is used to identify viral infections . 6- CXR

11. TREATMENT A combination of ampicillin and an aminoglycoside (usually gentamicin) for 10 to 14 days is effective treatment against most organisms responsible for early-onset sepsis. The combination of ampicillin and cefotaxime also is proposed as an alternative method of treatment. If meningitis is present, the treatment should be extended to 21 days or 14 days after a negative result from a CSF culture. If gram-negative meningitis is present, some authorities continue to treat with an effective penicillin derivative combined with an aminoglycoside, whereas most change to a third-generation cephalosporin . High-dose penicillin (250,000 to 450,000 U/kg/24 hr ) is appropriate for group B streptococcal meningitis.

12. Inhaled nitric oxide, ECMO (in term infants), or both may improve the outcome of sepsis-related pulmonary hypertension . Intratracheal surfactant may reverse respiratory failure. Intrapartum penicillin empirical prophylaxis for group B streptococcal colonized mothers or mothers with risk factors (e.g., fever, preterm labor, previous infant with group B streptococci, and amnionitis ) has reduced the rate of early-onset infection. SUPPORTIVE CARE ( ventilatory , nutritional…)

13. Late-onset sepsis ( 8 to 28 days) usually occurs in a healthy full-term infant who was discharged in good health from the normal newborn nursery. Clinical manifestations may include lethargy, poor feeding, hypotonia , apathy, seizures, bulging fontanel, fever, and direct-reacting hyperbilirubinemia . In addition to bacteremia, hematogenous seeding may result in focal infections, such as meningitis (in 75% of cases), osteomyelitis (group B streptococci, S. aureus ), arthritis (gonococcus, S. aureus , Candida albicans , gram-negative bacteria), and urinary tract infection (gram-negative bacteria).

14. The evaluation of infants with late-onset sepsis is similar to that for infants with early-onset sepsis, with special attention given to a careful physical examination of the bones Because of the increased rate of resistance of H. influenzae and pneumococcus to ampicillin, some centers begin treatment with ampicillin and a third-generation cephalosporin (and vancomycin if meningitis is present) when sepsis occurs in the last week of the first month of life. The treatment of late-onset neonatal sepsis and meningitis is the same as that for early-onset sepsis.

15. Nosocomially acquired sepsis (8 days to discharge) occurs predominantly in premature infants in the neonatal ICU; many of these infants have been colonized with the multidrug-resistant bacteria indigenous to the neonatal ICU. The risk of such serious bacterial infection is increased by frequent treatment with broad-spectrum antibiotics for sepsis and by the presence of central venous indwelling catheters, endotra-cheal tubes, umbilical vessel catheters, and electronic monitoring devices. Epidemics of bacterial (coagulase-negative staphylococci, fungi, enteric bacteria) or viral sepsis, bacterial or aseptic meningitis, staphylococcal bullous skin infections, cellulitis, pneumonia, omphalitis and diarrhea are common in the neonatal ICU and in the nursery for well infants

16. Clinical manifestations The initial clinical manifestations of nosocomial infection in a premature infant may be subtle and include apnea and bradycardia , temperature instability, abdominal distention, and poor feeding . In the later stages, signs of infection are shock, DIC, worsening respiratory status, and local reactions, such as omphalitis , eye discharge, diarrhea, and bullous impetigo.

17. treatment Because S. aureus (occasionally methicillin-resistant), Staphylococcus epidermidis (methicillin-resistant), and gram-negative pathogens are common nosocomial bacterial agents in many nurseries, a combination of vancomycin or oxacillin / nafcillin (some use ampicillin) with an aminoglycoside (gentamicin or tobramycin ) is appropriate. Persistent signs of infection despite antibacterial treatment suggest candidal or viral sepsis.

18. Congenital Infections

19. Many of the clinical manifestations of congenital infections are similar, including IUGR, nonimmune hydrops , anemia, thrombocytopenia, jaundice, hepatosplenomegaly , chorioretinitis , and congenital malformations. Evaluation of patients thought to have a congenital infection should include attempts to isolate the organism by culture (for rubella, CMV, HSV, gonorrhea, and M. tuberculosis), to identify the antigen of the pathogen (for hepatitis B and C. trachomatis), to identify the pathogen's genome with PCR, and to identify specific fetal production of antibodies ( IgM or increasing titer of IgG for Toxoplasma, syphilis, parvovirus, HIV, or Borrelia ).