Survivors of stage 3 hypoxic-ischemic encephalopathy have ahigh incidence of seizures and serious neurodevelopmental handicaps. The prognosis of severe asphyxia also depends on otherorgan system injury (see Table 58-6). Another indicator of poorprognosis is time of onset of spontaneous respiration as estimatedby Apgar score. Infants with Apgar scores of 0 to 3 at 10 minuteshave a 20% mortality and a 5% incidence of cerebral palsy; if thescore remains this low by 20 minutes, the mortality increases to60%, and the incidence of cerebral palsy increases to 57%.
Systemic and local infections (lung, cutaneous, ocular, umbilical, kidney, bone-joint, and meningeal) are common in the newborn period. Infection may be acquired in utero through the transplacental or transcervical routes and during or after birth. Ascending infection through the cervix, with or without rupture of the amniotic fluid membranes, may result in amnionitis, funisitis (infection of the umbilical cord), congenital pneumonia, and sepsis. The bacteria responsible for ascending infection of the fetus are common bacterial organisms of the maternal genitourinary tract, such as group B streptococci, Escherichia 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.
Maternal humoral immunity may protect the fetus against some neonatal pathogens, such as group B streptococci and HSV. Nonetheless, various deficiencies of the neonatal antimicrobial defense mechanism probably are more important than maternal immune status as a contributing factor for neonatal infection, especially in the low birth weight infant. The incidence of sepsis is approximately 1:1500 in full-term infants and 1:250 in preterm infants. The sixfold-higher rate of sepsis in preterm infants 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.
Preterm infants before 32 weeks of gestational age have notreceived the full complement of maternal antibodies (IgG),which cross the placenta by active transport predominantly inthe latter half of the third trimester. In addition, although lowbirth weight infants may generate IgM antibodies, their ownIgG response to infection is reduced. These infants also havedeficiencies of the alternate and, to a smaller degree, the classiccomplement activation pathways, which results in diminishedcomplement-mediated opsonization. Newborn infants alsoshow a deficit in phagocytic migration to the site of infection (tothe lung) and in the bone marrow reserve pool of leukocytes.In addition, in the presence of suboptimal activation of complement, neonatal neutrophils ingest and kill bacteria less effectively than adult neutrophils do. Neutrophils from sick infants seem to have an even greater deficit in bacterial killing capacitycompared with phagocytic cells from normal neonates.
Defense mechanisms against viral pathogens also may be deficient in a newborn. Neonatal antibody-dependent, cell-mediated immunity by the natural killer lymphocytes is deficient in the absence of maternal antibodies and in the presence of reduced interferon production; reduced antibody levels occur in premature infants and in infants born during a primary viral infection of the mother, such as with enteroviruses, HSV-2, or cytomegalovirus. In addition, antibody-independent cytotoxicity may be reduced in lymphocytes of newborns.