Maternal Obesity and Labor Progression: A Comprehensive Review

Abstract

Maternal obesity alters labor physiology, prolonging labor and increasing rates of induction, oxytocin use, and cesarean delivery. Mechanisms include excess pelvic soft tissue, disrupted estrogen-progesterone balance, elevated leptin, impaired cortisol-corticotropin-releasing hormone signaling, and myometrial dysfunction characterized by reduced myocyte density, lipid infiltration, and delayed connexin-43-mediated gap junction formation. These changes produce asynchronous uterine contractions, lower intrauterine pressures, and altered pushing efficiency. Patients with obesity often achieve vaginal delivery through increased cumulative pushing efforts, highlighting the limitations of standard time-based labor definitions. Recognizing obesity as a modifier of labor physiology supports individualized management, including optimized induction timing, combined cervical ripening, and tailored oxytocin protocols, with the potential to reduce unnecessary operative intervention and improve maternal and neonatal outcomes.