SYNDROME INCIDENCE • occurs primarily in premature infant; incidence is inversely related to AOG and BW
• occurs 60-80% of infants in <28wks AOG; in
15-30% of those between 32-36 wks and rarely in >37 wks. RISK FOR DEVELOPMENT OF RDS Increases with: • maternal diabetes • multiple births • CS • precipitous delivery • asphyxia • cold stress • maternal hx of prev affected infants ETIOLOGY • Surfactant deficiency- primary cause of RDS • Mature levels of pulmonary surfactant are present usually after 35 wks AOG. • Asphyxia, hypoxemia, and pulmonary ischemia may suppress surfactant synthesis. CLINICAL MANIFESTATIONS • tachypnea, prominent (often audible) grunting, intercostal, and subcostal retractions, nasal flaring, and cyanosis are noted. • breath sounds may be normal or diminished with a harsh tubular quality, and on deep inspiration, fine rales may be heard. • Apnea and irregular respirations are ominous signs requiring immediate intervention. DIAGNOSIS • X-ray findings: low lung volume Diffuse “ground glass” appearance with air bronchogram PREVENTION • Avoidance of unnecessary or poorly timed cesarean section (<39 weeks) • Prediction of pulmonary immaturity • Antenatal and intrapartum fetal monitoring for fetal asphyxia • Administration of antenatal corticosteroids to women before 34 weeks of gestation TREATMENT/ MANAGEMENT • Early supportive care • Mechanical ventilation – CPAP: reduces alveolar atelectasis • If persistent, intubated and surfactant is given via endotracheal tube