Neonatal Respiratory Distress Syndrome

Overview
  • Neonatal Respiratory Distress Syndrome is a relatively common cause of respiratory distress in neonates, especially those born prematurely, due to insufficient synthesis of surfactant in the lungs. Newborns are at greater risk if the mother displays Type II Diabetes as insulin appears to inhibit surfactant synthesis. However, conditions that boost corticosteroids during gestation appear to reduce the risk of NRDS as glucocorticoids induce surfactant synthesis.
Pathogenesis
  • As described in lung compliance, surfactant chemicals are critical for reducing the elastic recoil of the lung and thus increasing lung compliance. Surfactant synthesis, performed by type II pneumocytes, is one of the last stages of neonatal development and may not be fully completed in premature newborns. In the absence of sufficient surfactant, alveoli require significantly more pressure to remain open and often collapse on themselves. Consequently, expansion of the lung during inspiration requires significantly more effort in these newborns who first become tachypnic but may then become rapidly exhausted after birth.
  • Widespread collapse of alveoli results in the development of atelectatic areas within the lung, yielding hypoxemia due to right-left Shunting of blood and areas of ventilation-perfusion defect. Additionally, the alveolar membrane of collapsed alveoli undergoes hypoxic damage, resulting in breakdown of the membrane and leakage of plasma fluid and proteins into the alveolar space, yielding pulmonary edema.
Morphology
  • NRDS is characterized by fluid-filled alveoli that display "Hyaline Membranes", representing aggregations of leaked plasma proteins along with necrotic cellular debris. Unlike ARDS, the lungs of neonates with NRDS do not display any inflammatory changes.