A newborn delivered at 30 weeks gestation develops progressive respiratory distress within 4 hours of birth. Chest radiograph shows a 'ground-glass' pattern. The primary pathophysiological defect is:
- A Surfactant deficiency causing increased alveolar surface tension, alveolar collapse, and reduced lung compliance ✓
- B Immaturity of the respiratory centres causing central apnoea with secondary atelectasis
- C Persistence of fetal lung fluid due to immature epithelial sodium channels delaying fluid absorption
- D Pulmonary hypertension causing right-to-left shunting through the foramen ovale, reducing PaO2
Explanation
Surfactant (primarily dipalmitoylphosphatidylcholine, DPPC) is produced by type II pneumocytes and reduces alveolar surface tension, preventing alveolar collapse at end-expiration. Surfactant synthesis accelerates after 32 weeks (stimulated by cortisol); before this, surfactant deficiency in preterm neonates causes neonatal respiratory distress syndrome (NRDS/hyaline membrane disease). Without surfactant, surface tension increases markedly (LaPlace's law: P = 2T/r; small alveoli collapse), leading to diffuse atelectasis, reduced lung compliance, V/Q mismatch, and hypoxia. The ground-glass appearance reflects diffuse atelectasis with air bronchograms. Options B–D are separate conditions and not the primary defect in NRDS.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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Written and medically reviewed by the StethoPrep medical team.