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Learning Objectives
The student will be able to describe the clinical features of the neonatal respiratory distress syndrome (RDS) and how those features relate to the physiology of increased alveolar surface tension.
The student will be able to provide the scientific bases of medical therapies for neonatal RDS including prenatal steroids, continuous positive airway pressure, mechanical ventilation, and exogenous surfactant.
The student will be able to characterize the diving response and laryngeal chemoreceptor reflex as used to study the sudden infant death syndrome (SIDS).
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NEONATAL RESPIRATORY DISTRESS SYNDROME (RDS)
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Introduction to Neonatal RDS
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Normal intrauterine lung development is comprised of stages featuring both cellular proliferation to increase total lung size, and cellular differentiation by which the airway and alveolar architectures are elaborated from primordial organ buds (Chaps. 2 and 37). By the time the fetus reaches normal term gestation (~38 weeks), there is ongoing alveolarization and normally the lungs are structurally and biochemically prepared for the transition to extrauterine function in gas exchange. Among the most profound changes in the lung at the time of birth are: (1) the replacement of fluid with gas in the airways, with consequent generation of alveolar surface tension forces that must be overcome; and (2) a fall in pulmonary vascular resistance, with consequent increase in pulmonary blood flow. These changes must occur over a relatively short time frame for normal pulmonary function. As an additional challenge, the newborn's lungs are surrounded by ribs and related thoracic structures that are considerably more compliant than in the adult, owing to their incomplete ossification. This greater thoracic compliance at birth limits the expansive traction that can be exerted by the chest wall on the lungs' visceral pleura, and thus alters the inherent equilibrium that defines FRC and the work of breathing (Chap. 6). Given these challenges, it is no surprise that respiratory failure is a major contributor to newborn morbidity and mortality.
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By far, the most common cause of life-threatening respiratory disease in newborns is prematurity. Insufficient development and maturation of the type 2 surfactant-secreting epithelial cells leaves the preterm lung unprepared to overcome surface tension forces at the alveolar gas-fluid interface, as described by the law of Laplace (Chap. 5). The consequences of surfactant insufficiency in the preterm lung and the clinical treatment to overcome these consequences will be discussed in depth here. As these are elaborated below, the student should remember that surfactant dysfunction contributes to the pathogenesis of lung disease beyond the immediate postnatal period, such as ALI and ARDS (Chap. 28), emphasizing the broader implications of the concepts outlined in this chapter.
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Historical Perspective: Failure of Oxygen Treatment
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Before discussing the pathophysiology of RDS and the current modalities of treatment, it is useful first to consider why the historical mode of treatment, administration of oxygen, was ...