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Neonatal respiratory distress syndrome (RDS) is the most common cause of respiratory failure in preterm infants. Its incidence is inversely related to gestational age and increases to as high as 95% in infants born at 22 to 24 weeks of gestation. Over time, the outcome of infants suffering from RDS has changed dramatically. Forty years ago, approximately 50% of infants with RDS died. However, significant improvements in both prevention and treatment of RDS over the last 4 decades have markedly reduced mortality. As a consequence, the focus of improving outcome has now shifted from mortality to preventing (pulmonary) morbidity following RDS and its treatment.


The main feature of RDS is compromised lung function caused by both structural and biochemical immaturity of the lung.

Structural Immaturity

Lung development during fetal life occurs in different stages. Following organogenesis in the first 2 stages (embryonic and pseudoglandular) of lung development, the canalicular stage, starting at approximately 16 weeks after conception, is the first step in lung differentiation, involving formation of an actual air-blood barrier. Differentiation continues in both the saccular and alveolar stages of lung development starting at 24 and 36 weeks’ postconceptional age, respectively. This means that, at the time of birth, lung development of most preterm infants is still at the saccular stage, resulting in a reduced surface area for gas exchange and limited diffusion capacity due to thickened membranes at the air-blood interface.

Biochemical Immaturity

The hallmark of RDS is a deficiency of pulmonary surfactant, a complex mixture of lipids (90%) and proteins (10%) that is synthesized in alveolar epithelial type II cells. Type II cells are 1 of the 2 epithelial cell types that line the alveolus. The most important function of surfactant is lowering of the alveolar surface tension, the force directed from the wall to the center of the alveolus at the air-liquid interface. This function is mainly attributed to the surfactant phospholipid dipalmitoylphosphatidylcholine and the surfactant hydrophobic proteins B and C. The hydrophilic surfactant proteins A and D play a role in innate host defense. Synthesis and storage of surfactant begins at about 16 weeks’ gestation, and lung homogenates have high concentrations of surfactant by 20 weeks. However, surfactant is not secreted until later, appearing in amniotic fluid at approximately 28 weeks’ gestation, although this may vary greatly among individuals. This explains why some infants with a gestational age of less than 30 weeks do not develop neonatal RDS while other infants, born at a more advanced gestation, do.

The high alveolar surface tension accompanying surfactant deficiency will increase the elastic recoil forces of the lung and decrease compliance of the respiratory system. As a result, preterm infants with RDS need to create large transpulmonary pressures to establish an adequate tidal volume. The absence of surfactant will also compromise lung volume ...

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