Respiratory Distress Syndrome

Respiratory distress syndrome (RDS), also known as hyaline membrane disease, is the end result of a relative surfactant deficiency that, when combined with the compliant chest wall of the neonate, promotes alveolar atelectasis and prevents newborns from developing a normal functional residual capacity (Figure 102-1). The most significant risk factor for RDS is prematurity because surfactant production begins between 24 and 28 weeks of gestation and does not become fully functional until at least 35 weeks. Other risk factors for the development of RDS include maternal diabetes; early-onset sepsis; and less commonly, congenital surfactant deficiency. Fifty percent of infants with birth weights between 500 and 1500 g develop some degree of respiratory distress; however, survival is greater than 90% with the use of exogenous surfactant and antenatal steroids.

Figure 102-1 Respiratory distress syndrome of the newborn.

Transient Tachypnea of the Newborn

Transient tachypnea of the newborn (TTN) is one of the most common respiratory disorders of newborns with an incidence of 5.7 per 1000 deliveries. TTN occurs as a result of delayed reabsorption and clearance of fetal alveolar fluid from the airways. Throughout gestation, epithelial cells in the lung secrete alveolar fluid. In the late gestational period, epithelial ion channels shift from active secretion of sodium and chloride to active reabsorption caused by high circulating levels of maternal epinephrine. At birth, inspired oxygen increases gene expression of the sodium transporter, which further facilitates fluid shifts from the airways to the interstitium and intravascular space. Passive fluid reabsorption is also postulated to play a role. However, the accumulation of fluid in the interstitium can decrease lung compliance and prevent the establishment of functional residual capacity.

Factors that increase the likelihood of TTN include nonreassuring fetal status, instrumentation at delivery, Apgar score less than 7 at 1 minute, male sex, in vitro fertilization, multiple gestation, and macrosomia. Relevant maternal characteristics include history of maternal asthma, maternal diabetes, and nulliparity. Cesarean section poses a theoretical risk because of the absence of a “squeeze” effect created by passage through the vagina, which may increase the passive absorption of alveolar fluid. The risk of TTN in the setting of cesarean section increases with absence of labor before delivery and with delivery before 39 weeks.