DESCRIPTION

Respiratory distress syndrome (RDS) is a developmental lung disease affecting primarily premature infants. Disease is characterized by alveolar collapse due to a lack of pulmonary surfactant owing to lung immaturity that results in increased work of breathing, hypoxemia, and respiratory acidosis. The term hyaline membrane disease (HMD) is often used synonymously, referring to the distinctive pathology, although hyaline membranes can be seen in other disorders.

EPIDEMIOLOGY

• RDS is the most common lung disease in premature infants, affecting approximately 60,000 to 80,000 infants per year in the United States.
• Risk increases with the degree of prematurity, with nearly 100% of infants born at <26 weeks’ gestation affected.
• For near-term infants delivered operatively without benefit of labor, the risk of developing RDS increases roughly 2-fold for every week <39 weeks’ gestation.

RISK FACTORS

• Prematurity
• Low birth weight
• Maternal diabetes
• Delivery without labor
• Absence of antenatal corticosteroid (ANCS) administration
• Male gender
• Northern European ancestry
• Perinatal depression

GENERAL PREVENTION

• Prevention of prematurity
• Maternal ANCS

PATHOPHYSIOLOGY

• Insufficient or dysfunctional surfactant results in alveolar instability and atelectasis, causing hypoventilation and ventilation–perfusion mismatch, leading to hypoxemia and respiratory acidosis.
• The lack of surfactant in conjunction with pulmonary immaturity also leads to transudation of fluid and alveolar edema.
• Surfactant inactivation from transudation of proteins or other substances into the alveolus
• Increased work of breathing generates high negative intrathoracic pressures to overcome alveolar collapse. Retractions result from the highly compliant newborn rib cage combined with poorly compliant lungs.
• Expiratory grunting is due to glottic closure at the end of expiration to prevent end-expiratory atelectasis and maintain functional residual capacity.
• Infants with a well-developed pulmonary arterial muscular bed can develop secondary pulmonary hypertension, with hypoxemia leading to pulmonary vasoconstriction.