The incidence of pneumonia in the newborn appears to be inversely proportional to gestational age, occurring in up to 4% of premature infants <1000 g. The most common pathogens in this age group currently include Escherichia coli, group B streptococcus, and staphylococcus species. Although alveolar infiltrates may be seen in the premature infant with pulmonary infection (Fig. 3), both the clinical signs and the radiographic features of pneumonia may be indistinguishable from those of hyaline membrane disease.

Transient tachypnea of the newborn is one of the most common causes of respiratory distress in the older premature and full-term infant. The basic underlying patho-physiology is one of delayed clearing of fetal lung fluid. Risk factors include prematurity and birth by cesarean section, usually without preceding labor. Respiratory difficulties begin within a few hours of birth, lasting between a few hours up to 2 days in uncomplicated cases. Chest radiographs typically show increased perihilar bronchovascular markings and fluid in the pulmonary fissures (Fig. 4). The lungs may vary in their degree of inflation, from normal to hyperinflated.

Meconium aspiration syndrome consists of fetal acidosis and subsequent hyperperistalsis, passage of meconium, fetal gasping, and aspiration of meconium into the trachea and lungs [2]. Thick meconium may cause physical obstruction of the distal airways, resulting in patchy, alternating areas of pulmonary overinflation and atelectasis. Meconium also inactivates surfactant and causes secondary surfactant deficiency and poor lung compliance. The clinical course of many patients with meconium aspiration syndrome is complicated by pulmonary hypertension, which increases illness severity and worsens clinical outcomes. The radiographic features of meconium aspiration vary widely, depending on the severity of aspiration. The mildest cases manifest as pulmonary hyperinflation with scattered interstitial pulmonary opaci ties, while in more severe cases patchy alveolar and interstitial infiltrates and more pronounced hyperinflation are seen, often together with pneumothorax and pneumomediastinum as complications (Fig. 5).

Pulmonary air leaks are complications of greatest concern in newborns receiving positive pressure ventilation. They can manifest as pulmonary interstitial emphysema, pneumomediastinum, pneumothorax, and intravascular gas. As alveoli become overdistended and rupture, gas is forced into the connective tissues of the lung and can dissect along the interlobular septae toward the hilum of the lung. This pattern is of flame-shaped lucencies that may be bilateral or unilateral and is characteristic of pulmonary interstitial emphysema (PIE). Increasing distention can progress to plural or mediastinal air collections with or without PIE. In rare cases, gas is forced through lymphatic channels into the vascular tree, resulting in cardiovascular collapse (Fig. 6).