Physiology, presentations, and clinical signs

Several newborn lung diseases present very similarly, whether in the preterm or the term infant. Varying combinations of tachypnea, apnea, nasal flaring, expiratory grunting, sternal or costal retractions, and a supplemental oxygen need or cyanosis are manifestations of “respiratory distress.” In the preterm infant, this usually results from surfactant deficiency which has come to be termed respiratory distress syndrome (RDS). Historically, this same disease process has been referred to as hyaline membrane disease (HMD) because of the histological appearance of the lung.

The newborn transition to extrauterine life is dominated by the need to mobilize lung fluid into the interstitial space and establish a functional residual capacity (FRC). A vivid illustration of mobilization of fetal lung fluid in an animal model from Hooper et al. [1] can be seen at www.fasebj.org/content/21/12/3329/ suppl/DC1. Post-natally, the struggle to recruit and maintain FRC in the preterm infant continues because of the combination of poorly alveolarized lungs and surfactant deficiency. To compound matters, both preterm and full-term infants have extremely compliant chest walls, which results in a tendency for the respiratory units to collapse at end-expiration.

Two other physiological features are relevant to the growth of the lung. First, the in utero lung is a secretory organ which contributes to the production of amniotic fluid.