Post-Hysterectomy Ovarian Consequences: Mechanisms, Risks, and Clinical Management Strategies—A Narrative Review

Objective(s): To examine the mechanisms underlying changes in ovarian function after total hysterectomy, identify relevant risk factors, and summarize clinical management strategies for such changes. Mechanism: The pathogenesis of impaired ovarian function post-total hysterectomy involves three key pathways: (1) reduced ovarian blood supply due to uterine artery ligation; (2) neuroendocrine imbalance caused by abnormal gonadotropin levels; (3) oxidative stress and fibrosis induced by chronic inflammation. Findings in Brief: Total hysterectomy is associated with diminished ovarian reserve, including a 20–30% decrease in anti-Müllerian hormone (AMH), elevated serum follicle-stimulating hormone (FSH) levels, and an approximate 3–4-year acceleration of menopause. Risk factors include the surgical approach (e.g., laparoscopic electrocoagulation decreases AMH by 40% vs. 20% with open surgery), unilateral ovarian preservation (increases the risk of menopause by 2.93-fold compared to bilateral preservation), and age <40 years (increases the risk of postoperative ovarian failure). Conclusions: Personalized clinical management, including preoperative assessment of AMH levels and ovarian blood flow, preference for ovarian and uterine artery-preserving techniques (e.g., STHMUV, uterine blood supply-preserving hysterectomy technique), and postoperative hormone/pelvic floor function monitoring may mitigate damage to ovarian function. To optimize long-term outcomes, future research should focus on vasoprotective strategies and precision interventions guided by biomarkers.