Abstract Objective Despite the high incidence of fetal growth restriction (FGR) in gastroschisis (GS) associated with placental fetal vascular malperfusion (FVM), the underlying mechanism remains unclear. We aimed to investigate whether umbilical vein (UV) stenosis at the abdominal wall defect impairs fetoplacental circulation, leading to FGR. Methods A single‐center retrospective review of magnetic resonance imaging (MRI) scans in fetuses with GS was performed. The presence of FGR and complex GS was recorded after birth. Systematic measurements of UV diameter were collected, as well as placental characteristics. Multivariable analysis identified in‐uter o risk factors for FGR. Area under the receiver‐operating‐characteristics curves (AUC) for the predictive performance of predictors of FGR was calculated. In addition, 1:1 age‐matched omphalocele and healthy control cases were included for comparison with GS cases with and without FGR, examining UV diameter, placental features and T2* signal intensity (SI) differences between the left and right hepatic lobes. Co‐occurrence network analysis integrated prenatal MRI findings with postnatal outcomes. Results A total of 86 GS cases, 27 omphalocele cases and 27 age‐matched healthy control cases were included. The incidence of FGR was 66.3% (57/86) in all GS cases, 86.7% (26/30) in complex GS cases and 18.5% (5/27) in omphalocele cases. Multivariable analysis identified the following independent risk factors for FGR: Z ‐score of UV diameter at the defect (adjusted odds ratio (aOR), 0.76 (95% CI, 0.65–0.89); P = 0.001); placental thickness (aOR, 1.57 (95% CI, 1.13–2.05); P = 0.015); placental lobulation (aOR, 1.84 (95% CI, 1.45–2.32); P = 0.026); and the presence of complex GS (aOR, 2.33 (95% CI, 1.85–2.96); P = 0.003). The Z ‐score of the UV diameter at the abdominal wall defect had an AUC of 0.81 (95% CI, 0.73–0.84) for the presence of FGR. Compared to the GS without FGR, omphalocele and healthy control groups, the GS with FGR group exhibited significantly reduced UV diameter at the abdominal wall defect, greater placental thickness, increased placental lobulation and larger T2* SI differences between the left and right hepatic lobes, reflecting hypoxia‐driven circulatory redistribution. Network analysis demonstrated interdependencies among UV stenosis, FGR, placental FVM and adverse outcomes. Conclusion There is strong association between UV stenosis at the abdominal wall defect and the development of FGR in cases of GS. UV diameter measurements and placental assessment may constitute important imaging biomarkers for FGR prediction in cases of GS. Ultimately, future research is required to evaluate potential benefits of fetal intervention to reduce severe UV stenosis. © 2026 The Author(s). Ultrasound in Obstetrics & Gynecology published by John Wiley & Sons Ltd on behalf of International Society of Ultrasound in Obstetrics and Gynecology.
Shi et al. (Fri,) studied this question.