A 29-week preterm neonate develops progressive respiratory distress within 2 hours of birth: expiratory grunting, subcostal retractions, nasal flaring, and cyanosis. CXR shows bilateral ground-glass opacification with air bronchograms. What is the primary biochemical deficiency, and which surfactant proteins are deficient in this condition?
- A Deficiency of lecithin (dipalmitoyl phosphatidylcholine); SP-B and SP-C are primarily deficient ✓
- B Deficiency of phosphatidylcholine synthesis; SP-A and SP-D deficient
- C Deficiency of phosphatidylglycerol only; SP-A is deficient
- D Deficiency of all phospholipids due to type II pneumocyte immaturity; SP-A is the key deficient protein
Explanation
Respiratory Distress Syndrome (RDS) of the preterm newborn is caused by surfactant deficiency. The primary surface-active phospholipid is dipalmitoyl phosphatidylcholine (DPPC = lecithin), which reduces alveolar surface tension. Surfactant protein B (SP-B) and SP-C are hydrophobic proteins critical for spreading and stabilizing surfactant; SP-B deficiency alone causes lethal surfactant deficiency. SP-A and SP-D are hydrophilic collectins involved in host defense and surfactant recycling, not primarily in surface tension reduction. The lecithin-to-sphingomyelin (L/S) ratio in amniotic fluid ≥2 indicates fetal lung maturity; below this ratio, RDS risk is high.
Reference: Ghai Essential Pediatrics, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.