Pneumonia
Gross Ian
Pneumonia in the newborn period may arise during the first 2 to 3 days after birth (early onset) or after the first week (late onset). It may occur as an isolated infection or in association with septicemia. Pneumonia that develops shortly after birth is probably acquired in utero or intrapartum by hematogenous spread from the mother, by ascending infection from the vagina and cervix, or by aspiration of contaminated secretions immediately after birth. Late-onset pneumonia, similar to other nosocomial infections in the newborn unit, can be transmitted by the infant’s caretakers. The most common pathogens are group B streptococci and gram-negative organisms such as Escherichia coli and Klebsiella, but a wide variety of organisms may be involved. During the 1970s, the group B streptococci emerged as a major cause of pneumonia and septicemia in newborns. Although group B streptococcal infection is still a significant problem, it now occurs with about the same frequency as infection with gram-negative enteric organisms.
CLINICAL MANIFESTATIONS AND COMPLICATIONS
Infants with early-onset pneumonia usually have respiratory distress within the first few hours after birth. If they are
premature, the symptoms may be indistinguishable from those of respiratory distress syndrome (RDS). Features that suggest pneumonia rather than RDS include maternal chorioamnionitis, prolonged rupture of the membranes, early onset of apnea, and poor perfusion and shock. The amniotic fluid lecithin-to-sphingomyelin ratio, if available, also is useful in differentiating pneumonia from RDS (a “mature” ratio rules out RDS).
premature, the symptoms may be indistinguishable from those of respiratory distress syndrome (RDS). Features that suggest pneumonia rather than RDS include maternal chorioamnionitis, prolonged rupture of the membranes, early onset of apnea, and poor perfusion and shock. The amniotic fluid lecithin-to-sphingomyelin ratio, if available, also is useful in differentiating pneumonia from RDS (a “mature” ratio rules out RDS).
The clinical course of neonatal pneumonia varies considerably. Some infants have fulminant disease with a rapid downhill course and early death. More commonly, moderate respiratory distress develops and assisted ventilation may be required for a few days, after which the baby recovers. The course may be different from that of RDS, which tends to become progressively more severe and to peak at 48 to 72 hours; pneumonia usually follows a more level course. In addition to parenchymal lung disease, some infants also have severe pulmonary hypertension, presumably secondary to pulmonary vasospasm, with right-to-left shunting of blood. These babies may be critically ill and tend to have a labile PaO2 with marked hypoxia disproportionate to the severity of their parenchymal lung disease as reflected by the chest radiograph. This complication is associated with significant morbidity and mortality.
DIAGNOSIS
Radiographic Appearance
At least four different radiographic appearances have been described in newborn infants with pneumonia and include extensive coarse infiltrates scattered throughout both lungs and lobar consolidation (Fig. 45.1). Also possible is an RDS-like pattern (Fig. 45.2); the radiographic appearance of pneumonia in premature infants, particularly that caused by the group B streptococci, may be indistinguishable from that seen in RDS. It is possible that some of these infants have both RDS and pneumonia. Additionally, scattered small infiltrates may develop in one or both lungs (more commonly in mature than in premature infants).
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