Respiratory Distress Syndrome in the Neonate
Neonatal respiratory distress syndrome involves a pathophysiologic deficit of pulmonary surfactant. This complex mixture of phospholipids, neutral lipids, and protein normally increases lung compliance and facilitates gas exchange. Preterm infants born with this disorder often develop life-threatening complications.
During the 1970s and 1980s, significant advances were made in neonatology. As a result, the survival of very-low-birth-weight, premature infants improved from three- to sevenfold. Unfortunately though, this success gave rise to an increase in ventilator-dependent infants suffering from severe chronic lung disease (Cheu, 1990, p. 561).
Respiratory distress syndrome (RDS) was originally referred to as hyaline membrane disease. The disorder results from premature lungs' lack of pulmonary surfactant. The symptoms of RDS occur soon after birth. In general, these comprise the multiple signs of respiratory distress. They may include cyanosis, tachypnea, and retractions. Moreover, neonates may also exhibit nasal flaring, and grunting (Morris, 1990, pp. 547-549).
The incidence of RDS is inversely proportional to gestational age. Obviously, the most important factor in the disease's etiology is lung maturity. Infants born at less than 28 weeks gestation have about a 60 percent to 80 percent chance of developing RDS; whereas, only about 5 percent of infants born after 37 weeks develop the disease. Moreover, male infants seem to be affected twice as often as females, and infants born to diabetic mothers are at increased risk (Morris, 1990, pp. 547-549).
RDS complications can impair a child's maturation. For example, the disease's cardiovascular, cerebral, and gastrointestinal complications may include patent ductus arteriosus, intracranial hemorrhage, and necrotizing enterocolitis. In addition, stricken infants may develop a chronic emphysemic lung disea...