A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A newborn presents with central cyanosis, nasal flaring, and subcostal retractions following a scheduled cesarean delivery. He was born to a healthy 29-year-old G-1-P-1 mother due to cervical incompetence at 34 weeks gestation; the pregnancy was otherwise uneventful. Appearance, Pulse, Grimace, Activity, and Respiration (APGAR) scores were 6 and 8 at 1 and 5 minutes, respectively and his birth weight was 3,200 g. The umbilical cord had 3 vessels and the placenta was tan-red with all cotyledons intact. Fetal membranes were tan-white and semi-translucent. Currently, the vital signs include: temperature 36.9°C (98.4°F), blood pressure 70/40 mm Hg, pulse 190/min, and respiratory rate 68/min. On auscultation, breath sounds are decreased. Diffuse ground-glass opacifications are identified on chest X-ray. Which of the factors listed below most likely contributed to this infant’s current condition?
-
A
Gestational diabetesCorrect. Maternal gestational diabetes increases fetal insulin, which antagonizes cortisol-driven surfactant maturation in type II pneumocytes, predisposing to NRDS even at near-term gestational age.
-
B
Alcohol abuseIncorrect. Fetal alcohol syndrome causes facial dysmorphism, microcephaly, and developmental delay — not surfactant deficiency or ground-glass infiltrates.
-
C
Down syndromeIncorrect. Down syndrome can cause respiratory issues via cardiac defects or pulmonary hypoplasia, but it does not produce surfactant deficiency or the diffuse ground-glass pattern of NRDS.
-
D
LithiumIncorrect. Lithium exposure in utero is associated with Ebstein anomaly (tricuspid valve malformation), not neonatal surfactant deficiency.
-
E
Maternal smokingIncorrect. Maternal smoking is associated with intrauterine growth restriction, placental abruption, and SIDS — not directly with surfactant deficiency producing diffuse ground-glass infiltrates.
↑ Tap an answer to reveal the reasoning
Answer: A. A late-preterm (34-week) infant delivered by elective cesarean section (without labor) who develops respiratory distress with central cyanosis, retractions, and diffuse ground-glass opacities on chest X-ray has neonatal respiratory distress syndrome (NRDS) from surfactant deficiency. Surfactant production by type II pneumocytes accelerates after 32–34 weeks and is functionally mature by ~35 weeks; without adequate surfactant, alveolar surface tension is high, leading to diffuse microatelectasis (the ground-glass / 'reticulogranular' appearance) and impaired gas exchange.
Maternal risk factors include prematurity itself, male sex, and importantly maternal diabetes (gestational or pregestational). Hyperinsulinemia in the fetus (from maternal hyperglycemia) antagonizes cortisol's effect on surfactant synthesis, delaying lung maturation. Cesarean delivery without labor also reduces the catecholamine surge that helps clear fetal lung fluid, compounding the problem.
Management: antenatal corticosteroids before delivery (now too late), and postnatal exogenous surfactant (e.g., beractant), supplemental oxygen, and respiratory support (CPAP/mechanical ventilation as needed).
**Why each option:**
**A.** Correct. Maternal gestational diabetes increases fetal insulin, which antagonizes cortisol-driven surfactant maturation in type II pneumocytes, predisposing to NRDS even at near-term gestational age.
**B.** Fetal alcohol syndrome causes facial dysmorphism, microcephaly, and developmental delay — not surfactant deficiency or ground-glass infiltrates.
**C.** Down syndrome can cause respiratory issues via cardiac defects or pulmonary hypoplasia, but it does not produce surfactant deficiency or the diffuse ground-glass pattern of NRDS.
**D.** Lithium exposure in utero is associated with Ebstein anomaly (tricuspid valve malformation), not neonatal surfactant deficiency.