A preterm infant born at 29 weeks develops grunting, nasal flaring, and cyanosis within hours of birth. Chest radiograph shows diffuse ground-glass opacities with air bronchograms. The fundamental defect accounting for the diffuse atelectasis is:
- A Persistent contraction of the ductus arteriosus raising pulmonary pressures
- B Excessive production of fetal hemoglobin reducing oxygen unloading
- C Deficient type II pneumocyte surfactant production due to immaturity ✓
- D Congenital absence of pulmonary lymphatic drainage
Explanation
Surfactant synthesis by type II pneumocytes matures late in gestation, so infants born before about 34 weeks have deficient surfactant. High alveolar surface tension then causes widespread atelectasis, low compliance, and the ground-glass radiograph of neonatal respiratory distress syndrome. Antenatal corticosteroids accelerate surfactant production. Ductal dynamics and hemoglobin type do not cause diffuse atelectasis.
Reference: Guyton and Hall Textbook of Medical Physiology, 14th ed.
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