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,

. . .
isms by which this occurs have not yet been fully delineated. The synthesis of SP-A, SP-B, and SP-C ribonucleic acids and proteins increases with advancing gestation and may be induced by glucocorticoids (Morris, 1990, pp. 547-549). Normal breathing involves active inspiratory and passive expiratory phases. With inspiration, diaphragmatic contraction creates a negative pressure within the thoracic cavity. This negative pressure then inflates the lung. In contrast, expiration depends on the recoiling force of the lungs' elastic tissue and surface tension. Surface tension is caused by cohesive forces between adjacent liquid molecules. These forces are generally greater than those which occur between the liquid molecules and the gas outside the surface. According to the Young-Lapace relationship, with decreasing alveolar radius, the pressure generated by tissue elasticity and surface tension should increase. Such pressure, however, could exceed the transpulmonary pressure (i.e., the difference in pressure between the alveoli lumen and pleural cavity) and ultimately cause the alveoli to collapse. Pulmonary surfactant, however, reduces surface tensions to "as low as 0 dyn/cm in the alveolar zone and 30 dyn/cm in the large
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Approximate Pages = 7 (250 words per page)

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