Neonatal respiratory distress syndrome: mechanisms, findings, and support
THE CONTEXT
Respiratory distress syndrome (RDS)* is primarily caused by surfactant deficiency and is common in neonates born before 34 weeks of gestation.
Occurrence and risk factors
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The overall incidence is 10–15%, rising to as high as 80% in neonates born before 28 weeks.
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In addition to prematurity, risk factors include asphyxia, acidosis, maternal diabetes, and cesarean section.
Surfactant and disease mechanism
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Surfactant production starts around 20 weeks and peaks at 35 weeks of gestation; neonates born before 35 weeks are therefore prone to RDS.
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Type II alveolar cells produce surfactant, a lipoprotein containing phospholipids and proteins.
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Surfactant lowers alveolar surface tension and prevents alveoli from deflating at the end of expiration. Deficiency causes expiratory alveolar collapse and increases the effort required to reopen the alveoli.
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Increased work of breathing and hypoxemia cause acidosis, followed by pulmonary vasoconstriction and right-to-left shunting across the foramen ovale, producing further hypoxemia.
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Ischemic alveolar damage causes protein transudation and formation of a hyaline membrane.
Clinical and radiological findings
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Respiratory distress usually begins within the first 6 hours of life, with tachypnea, retractions, grunting, cyanosis, and decreased air entry.
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Chest X-ray findings include low-volume lungs, a reticulogranular pattern, ground glass opacity, and air bronchograms.
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Severe disease produces white-out lungs.
Management
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Affected neonates need neonatal intensive care unit admission, intravenous fluids, and appropriate respiratory support.
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Continuous positive airway pressure (CPAP)* is generally sufficient for mild to moderate disease.
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CPAP provides noninvasive support by applying continuous distending pressure of 5–7 cm H₂O at the nostrils to keep alveoli open in a spontaneously breathing neonate.