Fetal Adrenal Gland Enlargement and Ophthalmic Artery Doppler as Complementary Markers of Adaptation in Fetal Growth Restriction.

Background Fetal growth restriction (FGR), also referred to as intrauterine growth restriction (IUGR), results primarily from placental insufficiency and is associated with chronic fetal hypoxemia and adverse perinatal outcomes. Doppler surveillance traditionally focuses on umbilical artery and middle cerebral artery (MCA) indices to identify cerebral blood flow redistribution ("brain sparing"). However, these markers reflect only part of the fetal adaptive response and may not fully capture the systemic and chronic nature of fetal compromise. Objective To evaluate ophthalmic artery (OA) Doppler indices in fetuses with FGR, to examine their relationship with established MCA Doppler markers, and to describe fetal adrenal gland enlargement as a complementary structural marker of chronic intrauterine stress in the same cohort. Methods This observational study included 32 singleton pregnancies diagnosed with FGR in the third trimester. All fetuses underwent standardized Doppler ultrasound assessment of the MCA and OA. OA waveforms were analyzed for peak systolic velocity of the first and second systolic peaks, and the OA peak systolic velocity ratio (PSV2/PSV1) was calculated. MCA pulsatility index (PI), resistance index (RI), and cerebroplacental ratio (CPR) were interpreted using gestational age-specific reference ranges. In addition, fetal adrenal gland size was assessed using two-dimensional ultrasound, and whole adrenal gland volumes were calculated and corrected for estimated fetal weight. Results Fetuses with FGR demonstrated consistent alterations in cerebral and carotid-related hemodynamics, characterized by reduced MCA PI and CPR and increased OA PSV ratios, indicating cerebral redistribution and altered distal carotid vascular resistance. A significant inverse association was observed between OA PSV ratio and MCA PI. In parallel, corrected adrenal gland volumes were generally higher than values reported in published studies of normally grown fetuses, consistent with structural endocrine adaptation to chronic intrauterine stress. A qualitative trend was observed suggesting that fetuses with more pronounced cerebral redistribution may exhibit larger adrenal gland volumes, suggesting concurrent vascular and endocrine adaptive responses to chronic intrauterine hypoxia. Conclusion In fetuses with growth restriction, ophthalmic artery Doppler and fetal adrenal gland enlargement reflect complementary aspects of fetal adaptation to placental insufficiency. While OA and MCA Doppler indices characterize cerebral hemodynamic redistribution, adrenal gland enlargement represents a structural marker of sustained endocrine stress. Integrating vascular and structural markers may provide a more comprehensive evaluation of fetal adaptation in IUGR than cerebral Doppler assessment alone.