Background: Intrahepatic cholestasis of pregnancy (ICP) has been increasingly associated with neonatal respiratory distress syndrome (RDS) in late preterm and term neonates, with an incidence of 17% - 29%, significantly higher than in the general neonatal population. Proposed mechanisms include bile acid-mediated disruption of fetal lung development and surfactant dysfunction.Case Presentation Summary: We report a late preterm male infant, delivered at 36 weeks’ gestation via cesarean section due to the progression of maternal ICP. Birth weight was 2750 g, length 48 cm, with Apgar scores of 8 and 8 at one and five minutes, respectively. Maternal history was significant for ICP, diagnosed at 34 weeks’ gestation (AST 93 U/L, ALT 150 U/L, ALP 172 U/L). At birth, the infant required a brief period of positive pressure ventilation using a face mask with a Neopuff device.The infant was admitted to the neonatal intensive care unit (NICU) for further monitoring and respiratory support. Antibiotics were administered empirically, but no evidence of sepsis was found. Persistent signs of respiratory distress (tachypnea and oxygen dependency) required initiation of non-invasive respiratory support with nasal continuous positive airway pressure (nCPAP). Chest radiography revealed findings consistent with neonatal RDS. Given the impaired ventilation and oxygenation, respiratory support was escalated from monophasic to biphasic nasal CPAP. On day of life 2, synthetic surfactant was administered via the INSURE method due to persistent need for high oxygen concentration.Gradual improvement in respiratory function followed. By day of life 4, supplemental oxygen was discontinued. The infant was weaned off respiratory support by day of life 5. He was discharged home on day of life 16, clinically stable, eupnoic, and maintaining normal oxygen saturation in room air.Learning Points Discussion: This case highlights the risk of RDS in late preterm infants born to mothers with ICP. Evidence suggests that elevated maternal bile acids (BA) in ICP may cross the placenta and interfere with fetal lung development and surfactant function. This bile acid–mediated mechanism is thought to contribute to respiratory symptoms independently of gestational age, highlighting a potential link between ICP and unexpected neonatal respiratory morbidity at all gestations. An alternative pathway may involve direct damage produced by BA on type II pneumocytes.This case reinforces the need for early recognition and rigorous monitoring of bile acid levels in ICP, optimizing delivery timing, and ensuring immediate availability of neonatal respiratory support. Further research is needed to clarify the role of ursodeoxycholic acid (UDCA)’s impact on neonatal outcomes and to establish standardized management strategies for both maternal and neonatal outcomes.
