Predictive Value of Abdominal Subcutaneous Fat Thickness for Dinoprostone-Induced Labor Success in Obese Pregnant...

Background: While maternal obesity is a well-established risk factor for labor induction failure, the specific impact of regional fat distribution and its direct influence on prostaglandin dose-response profiles remain under-investigated. Relying solely on generalized anthropometric metrics like Body Mass Index (BMI) may obscure the true physiological variations in tissue bioavailability. Therefore, this study aimed to compare dinoprostone-induced labor outcomes between obese pregnant women and non-obese controls, and to evaluate whether ultrasonographically measured abdominal subcutaneous fat thickness (ASFT) can serve as a more precise, independent predictor of induction success and cumulative prostaglandin dose requirements. Methods: This prospective two-center observational study was conducted with 200 single-term pregnant women, comprising an obese study group (n = 100, BMI ≥ 30 kg/m²) and a symmetrical non-obese control group (n = 100, BMI 18.5-29.9 kg/m²). Maternal ASFT was measured via high-resolution ultrasonography at the infraumbilical midline prior to labor induction. All participants initially received a 10 mg dinoprostone vaginal insert governed by a standardized institutional induction protocol. Primary outcomes included successful labor induction (defined as achieving vaginal delivery within 24 h) and cumulative prostaglandin dose requirements. Secondary analyses involved comparative evaluation stratified by obesity classes (Class 1 vs. Class 2-3) and an exploratory ASFT threshold (<30 mm vs. ≥30 mm). Results: Obese women demonstrated significantly lower successful labor induction rates (defined as vaginal delivery within 24 h) compared to the non-obese control group (59.0% vs. 86.0%, p = 0.001). The cumulative dinoprostone dose required for cervical ripening was significantly higher in the obese cohort than in controls (16.8 ± 4.5 mg vs. 12.4 ± 2.2 mg, p < 0.001). Similarly, induction-to-delivery intervals were significantly prolonged in obese parturients (19.2 ± 6.1 vs. 14.6 ± 4.8 h, p < 0.001). Subgroup analysis within the obese cohort revealed that patients with ASFT ≥ 30 mm required higher prostaglandin doses (18.08 ± 3.40 mg vs. 14.14 ± 3.08 mg, p < 0.001) and exhibited lower vaginal delivery rates (45.7% vs. 70.4%, p = 0.012) than those with ASFT < 30 mm. Multivariate logistic regression analysis encompassing the entire study population (n = 200) confirmed that ASFT remained a strong independent predictor of induction failure (Adjusted OR: 1.14; 95% CI: 1.05-1.24, p = 0.002). Conversely, generalized obesity metrics via BMI did not maintain independent significance in the multivariate model (p = 0.420). Conclusions: Increased maternal ASFT is directly associated with blunted drug responsiveness, higher cumulative dinoprostone requirements, and a lower likelihood of successful labor induction. Compared with generalized metrics such as BMI, ultrasonographic measurement of ASFT provides a more precise and clinically relevant assessment of regional maternal adiposity. These findings suggest that incorporating pre-induction ASFT evaluation into routine obstetric practice could improve risk stratification and help clinicians design individualized, precision-based dosing strategies for obese parturients.