Respiratory distress syndrome (RDS) in the newborn, previously known as hyaline membrane disease, results from a deficiency of surfactant (a naturally occurring substance that lines the alveoli of the lung and is produced by type 2 pneumocytes) due to lung immaturity. Surfactant reduces the surface tension of alveoli, preventing their collapse during expiration. Without this protection, gas exchange is significantly impaired due to alveolar collapse. This can also lead to lung inflammation due to pulmonary edema and increased airway resistance. Hypoxemia is caused by a mismatch between ventilation and perfusion.

The most common cause of surfactant deficiency is premature birth. Less commonly, genetic mutations in surfactant protein (SP) B, SP-C, and adenosine triphosphate (ATP)-binding cassette (ABC) transporter can decrease surfactant production. These mutations can cause RDS in full-term infants. Partial mutations in surfactant proteins can lead to interstitial lung disease in children.

Symptoms of RDS occur within several minutes to hours after birth. Symptoms include cyanosis, tachypnea, nasal flaring, grunting, and accessory muscle use. RDS typically progresses for 48-72 hours and resolves in 1 week.

Treatment is with exogenous surfactant and supportive care. Complications of RDS include pulmonary air leak due to ruptured alveoli, which can cause pneumomediastinum or pneumothorax and bronchopulmonary dysplasia (BPD).

Related topic: acute respiratory distress syndrome