RDS may develop immediately in the delivery room in extremely immature infants at 26 to 30 weeks of gestation. Some more mature infants (34 weeks’ gestation) may not show signs of RDS until 3 to 4 hours after birth, correlating with the initial release of stored surfactant at the onset of breathing accompanied by the ongoing inability to replace the surfactant owing to inadequate stores. Manifestations of RDS include cyanosis, tachypnea, nasal flaring, intercostal and sternal retractions, and grunting. Grunting is caused by closure of the glottis during expiration, the effect of which is to maintain lung volume (decreasing atelectasis) and gas exchange during exhalation. Atelectasis is well documented by radiographic examination of the chest, which shows a ground-glass haze in the lung surrounding air-filled bronchi (the air bronchogram) (Fig. 61-2). Severe RDS may show an airless lung field (whiteout) on a radiograph, even obliterating the distinction between the atelectatic lungs and the heart.
During the first 72 hours, infants with untreated RDS haveincreasing distress and hypoxemia. In infants with severeRDS, the development of edema, apnea, and respiratoryfailure necessitates assisted ventilation. Thereafter, uncomplicated cases show a spontaneous improvement that oftenis heralded by diuresis and a marked resolution of edema. Complications include the development of a pneumothorax,a patent ductus arteriosus (PDA), and bronchopulmonarydysplasia (BPD). The differential diagnosis of RDS includesdiseases associated with cyanosis and respiratory distress (seeTable 58-10).
Strategies to prevent preterm birth include maternal cervical cerclage, bed rest, treatment of infections, and administration of tocolytic medications. In addition, prevention of neonatal cold stress, birth asphyxia, and hypovolemia reduces the risk of RDS. If premature delivery is unavoidable, the antenatal administration of corticosteroids (e.g., betamethasone) to the
Figure 61-2 Respiratory distress syndrome. The infant is intubated, and the lungs show a dense reticulonodular pattern with air bronchograms (A). To evaluate rotation on the frontal chest, the lengths of the posterior ribs are compared from left to right (arrows). Because the infant is supine, the side of the longer ribs indicates to which side the thorax is rotated. In this case, the left ribs are longer, and this radiograph is a left posterior oblique view. Surfactant was administered, resulting in significant improvement in the density of the lung (B). The right lung is slightly better aerated than the left. Uneven distribution of clearing is common. (From Hilton S, Edwards D: Practical Pediatric Radiology, ed 2, Philadelphia, 1994, Saunders.) mother (and thus to the fetus) stimulates fetal lung production of surfactant; this approach requires multiple doses for at least 48 hours.
After birth, RDS may be prevented or its severity reduced by intratracheal administration of exogenous surfactant immediately after birth in the delivery room or within a few hours of birth. A mammalian-derived surfactant is currently preferred. Exogenous surfactant can be administered repeatedly during the course of RDS in patients receiving endotracheal intubation, mechanical ventilation, and oxygen therapy. Additional management includes the general supportive and ventilation care presented in Table 61-3.
The Pao2 level should be maintained between 60 and 70 mm Hg (oxygen saturation 90%), and the pH should be maintained above 7.25. An increased concentration of warm and humidified inspired oxygen administered by a nasal cannula or an oxygen hood may be all that is needed for larger premature infants. If hypoxemia (Pao2 <50 mm Hg) is present, and the needed inspired oxygen concentration is 70% to 100%, nasal continuous positive airway pressure should be added at