1 Department of Gynecology and Obstetrics, Meishan Women and Children’s Hospital, Sichuan University, 620010 Meishan, Sichuan, China
2 Department of Gynecology and Obstetrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, West China Second Hospital, Sichuan University, 610041 Chengdu, Sichuan, China
Abstract
To examine the mechanisms underlying changes in ovarian function after total hysterectomy, identify relevant risk factors, and summarize clinical management strategies for such changes.
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.
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).
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.
Keywords
- hysterectomy
- ovarian function
- ovarian reserve
- anti-Müllerian hormone (AMH)
- premature menopause
- surgical approach
Total hysterectomy is one of the most important surgical procedures in many gynecologic conditions [1]. However, changes in ovarian function after surgery (such as early menopause and hormonal disorders) can have significant impacts on the reproductive and long-term health of women, including cardiovascular and cognitive issues [2, 3]. There is currently a need for systematic integration of research on the mechanisms, risk stratification, and management strategies for total hysterectomy.
The aims of this study were to elucidate the pathophysiological mechanisms underlying ovarian dysfunction following total hysterectomy, systematically evaluate the clinical evidence and epidemiological characteristics of postoperative ovarian dysfunction, identify key risk factors affecting postoperative ovarian function, and provide evidence-based management strategies for preserving ovarian function and improving long-term health outcomes after total hysterectomy.
Articles were identified via searches of Embase, PubMed, and Web of Science from each database’s inception to June 2025, supplemented by manual screening of reference lists. The computerized search included only English-language articles, using the keyword combination: “Hysterectomy” paired with “Ovarian function” or “Ovarian Reserve”, and supplemented by “premature menopause”, “surgical approach”, “AMH/anti-Müllerian hormone”, etc.
This strategy initially yielded 383 records. After removing duplicates, we focused on screening for meta-analyses and clinical studies, while excluding abstracts (incomplete data) and review articles (non-original research); finally, 39 eligible studies were selected, categorized as follows: 7 on pathophysiologic mechanisms, 24 on clinical evidence and symptoms, and 8 on risk factors related to post-hysterectomy ovarian consequences.
The uterine artery contributes approximately 50–70% of the blood supply to the ovary. Multiple studies using Doppler ultrasound have reported elevated resistance index (RI) and pulsatility index (PI) post-hysterectomy, along with reduced peak flow velocity (PSV) in the ovarian arteries. These findings imply a diminished blood supply, possibly due to direct vessel injury or induction of thrombosis by the surgical procedures. Halmesmäki et al. (2007) [4] reported the results of a randomized controlled trial (n = 107) in which post-operative pelvic ultrasound revealed significant alterations in ovarian blood flow. Specifically, the PI showed a significant decrease (p = 0.01), potentially due to vascular dilation as a consequence of surgical tissue trauma. Lee et al. (2010) [5] conducted a prospective cohort study (evidence level II) comprising 32 patients who underwent hysterectomy and 21 control patients. Three months after hysterectomy with bilateral ovarian preservation, they found no significant changes in ovarian artery blood flow indices (PI, RI) using transvaginal Doppler ultrasound, and no change in anti-Müllerian hormone (AMH) level using the Enzyme-Linked Immunosorbent Assay (ELISA) method. Furthermore, no differences were found between the laparoscopically-assisted vaginal hysterectomy (LAVH) and total abdominal hysterectomy (TAH) groups. An animal model showed a 32% absolute reduction in endothelium-dependent vasodilatory function after ovariectomy, with impaired small-conductance Ca2+-activated K+ (SK3) channels activity suggested to be the key mechanism [6].
The uterus and ovaries are interconnected via the hypothalamic-pituitary-ovarian
(HPO) axis and the autonomic nervous system (ANS). This regulatory balance
between the HPO and ANS can be disrupted following hysterectomy. Postoperative
changes include significant increases in the levels of follicle-stimulating
hormone (FSH) and luteinizing hormone (LH), along with a decrease in estradiol
(E2), indicating ovarian hypoplasia. These hormonal shifts are most notable 3–6
months after surgery and may result from reduced negative feedback by ovarian
steroid hormones. Increased levels of sympathetic nerve activity trigger the
toll-like receptor 4 (TLR4)/Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome pathway, resulting in the release of Interleukin-1 beta (IL-1
Surgical trauma can elicit sustained inflammatory responses, fostering a pro-aging milieu. Inflammaging, denoted by chronic low-grade inflammation, is a pivotal factor in ovarian senescence, influencing oxidative stress, fibrosis, and immune cell infiltration [8, 9]. Elevated levels of ovarian oxidative stress driven by chronic inflammation can impede follicular maturation and development, thereby accelerating the depletion of ovarian reserve and egg quality [8, 9, 10]. Furthermore, chronic inflammation is associated with ovarian fibrosis, which disrupts the tissue architecture and compromises follicular growth. In addition, chronic inflammation exacerbates apoptosis and DNA damage during ovarian aging through molecular mechanisms such as activation of the NLRP3 inflammasome [7].
Following a total hysterectomy, patients may enter menopause 3–4 years earlier.
Siddle et al. (1987) [11] found that hysterectomy was associated with an
earlier onset of ovarian failure compared to natural menopause (mean age: 45.4
Since the uterine artery provides 50–70% of the blood supply to the ovaries,
surgical severance results in ischemic damage to these organs. Postoperative
Doppler ultrasound showed elevated ovarian artery RI and PI, and decreased PSV,
suggesting decreased blood supply [15]. Tapisiz et al. (2008) [16]
examined histopathological changes in ovarian tissues after hysterectomy in a rat
model. These authors observed a 50% reduction in primordial follicle number
(p = 0.01), and a 300% increase in atretic follicle number (p
= 0.02). Hu et al. (2006) [17] found that hysterectomy affected the
ovarian vasculature and gland function in women aged 32–45 years. A transient
increase in Vmax was observed 5 days after surgery (26.47 vs. 22.00 cm/s,
p
AMH is produced by small antral follicles and is
the most reliable circulating marker of ovarian reserve. Following total
hysterectomy, the concentration of AMH may decline by 20–30%, and even more in
patients with low reserve. Atabekoğlu et al. (2012) [18] reported
that total hysterectomy resulted in a larger decrease in the ovarian reserve, as
measured by AMH level, at 4 months after surgery. Specifically, the AMH level
decreased by 30% more than in the controls. A prospective cohort study by
Trabuco et al. (2016) [19] showed that hysterectomy resulted in a
significant decrease of almost 20% in the AMH level at 1 year compared with the
control group. The hysterectomy group also exhibited a significantly greater fall
in AMH (–40.7% vs. 20.9%, p
Serum FSH levels are significantly elevated in patients after hysterectomy.
Huang et al. (2023) [20] reported significantly elevated FSH levels in
the hysterectomy group compared to the control group (WMD = 2.96, 95% CI:
1.47–4.44, p
Inhibin B is secreted by growing follicles and negatively regulates pituitary
FSH secretion, with its decline indicating a diminished follicular pool. Studies
have consistently shown that inhibin B levels are significantly reduced after
hysterectomy. A meta-analysis conducted by Huang et al. (2023) [20]
revealed the test group showed a decrease of 14.34 pg/mL (95% CI: –24.69 to
–3.99, p
Women have a higher persistence of hot flashes and night sweats following hysterectomy. A prospective observational study by Maiti et al. (2018) [21] found that 34% of patients developed menopausal symptoms within one year following hysterectomy. The observed symptoms were somatic (30% of cases), psychological (19%), and genitourinary (12%) in nature. A longitudinal study of 6106 women over 17 years found that those with a history of hysterectomy had higher incidences of persistent hot flashes (30% vs. 15%) and night sweats (19% vs. 9%) than women without hysterectomy. Moreover, women with a history of hysterectomy had higher rates of persistent hot flashes (1.97%, 95% CI: 1.64–2.35) and persistent night sweats (2.09%, 95% CI: 1.70–2.55) compared to those without hysterectomy [24].
Several studies have found that about one-third of post-hysterectomy patients
subsequently develop genitourinary and vaginal prolapse problems. Following
hysterectomy, many patients experience lower urinary tract dysfunction (LUTD)
caused by synergistic dysfunction of the bladder detrusor muscle with the
urethral sphincter due to pelvic autonomic nerve injury. One study found that
about a third of post-hysterectomy patients develop genitourinary issues and
vaginal prolapse [25]. Patients may experience urinary frequency, dysuria
(56–64%), urgency and/or stress urinary incontinence (37–60%), and incomplete
bladder emptying (36.7%) [26]. Compared to standard hysterectomy, radical
hysterectomy has a higher incidence of urinary complications (odds ratio [OR] =
15.63, p = 0.001), residual urine sensation (OR = 10.37, p
Hysterectomy has been associated with a 27% reduction in carotid artery compliance (p = 0.004), independent of traditional cardiovascular risk factors [29]. A matched case-control study (n = 246; 123 matched pairs) conducted by Punnonen et al. (1987) [8] found that premenopausal hysterectomy tripled the risk of cardiovascular disease relative risk [RR] = 3.0, significant in McNemar test) compared to myomectomy controls. Notably, hypertension was more prevalent among hysterectomy cases (6/20) than controls (1/6). A nationwide cohort study by Lai et al. (2018) [9] on 4986 women, including 1083 bilateral salpingo-oophorectomy (BSO) cases, found that undergoing BSO during hysterectomy did not significantly increase the overall risk of stroke during a 13-year follow-up (HR = 0.84, 95% CI: 0.63–1.13). However, BSO decreased the risk of stroke by 64% (HR = 0.36, 95% CI: 0.16–0.79) in women aged 50 years or older who were using estrogen therapy. This protective effect in older women receiving estrogen therapy suggests that hormonal compensation may attenuate the cardiovascular risks following BSO, offsetting the effects of surgical menopause. No increase in risk was observed for either ischemic stroke (HR = 0.85, 95% CI: 0.61–1.18) or hemorrhagic stroke (HR = 0.82, 95% CI: 0.42–1.60). Analysis of the Nurses’ Health Study data by Parker et al. (2009) [30] revealed a 17% increase in the risk of coronary heart disease among women who had undergone hysterectomy (HR = 1.17, 95% CI: 1.02–1.35), irrespective of ovarian status. Gavin et al. (2012) [29] examined the relationship between hysterectomy (with or without bilateral oophorectomy) and large artery stiffness. Both hysterectomy alone and hysterectomy with bilateral oophorectomy were found to be associated with increased arterial stiffness, as indicated by reduced carotid compliance, and independently of traditional cardiovascular risk factors.
Phung et al. (2010) [10] conducted a nationwide historical cohort study (n = 2,313,388) to investigate the association between hysterectomy (with or without oophorectomy) and the risk of dementia. Their analysis revealed that hysterectomy was associated with an elevated risk of early-onset dementia (diagnosed before age 50), with the risk increasing progressively according to the extent of surgery: hysterectomy alone (RR = 1.38, 95% CI: 1.07–1.78), hysterectomy with unilateral oophorectomy (RR = 2.10, 95% CI: 1.28–3.45), and hysterectomy with bilateral oophorectomy (RR = 2.33, 95% CI: 1.44–3.77). Notably, the magnitude of risk exhibited a strong inverse relationship with age at surgery, with younger patients having a disproportionately higher risk.
Most studies have shown that simultaneous removal of the fallopian tubes during
hysterectomy (opportunistic salpingectomy (OS) or prophylactic bilateral
salpingectomy (PBS)) does not cause significant acute damage to ovarian reserve
markers (e.g., AMH, FSH, LH). Behnamfar and Jabbari (2017) [31] compared combined
BSO in hysterectomy with tubal preservation group, finding significantly higher
FSH and LH (p
The prospective cohort study (n = 67 patients) by Yuan et al. (2015) [39] revealed that TLH caused a greater decline in serum AMH levels than LSH at 4 months post-surgery (p = 0.017).
Women with bilateral ovarian preservation show a significantly higher 5-year
rate of normal ovarian function than those with unilateral preservation (89% vs.
66%). Intraoperative preservation of both ovaries is therefore recommended as a
priority. For women requiring unilateral ovarian removal, postoperative
monitoring of AMH should be performed every 6 months for early detection of
functional decline. A prospective randomized study by Bukovsky et al.
(1995) [40] found that abdominal hysterectomy with unilateral oophorectomy (USO)
resulted in a higher dysfunction rate (35% vs. 10%, p = 0.02) at the
6-month follow-up assessment compared to ovarian conservation. A prospective
cohort study by Farquhar et al. (2005) [13] involving 257 women in the
hysterectomy group and 259 controls found the 5-year menopausal rate was
significantly higher in women who retained one ovary (35.7%, 10/28) compared to
those retaining both ovaries (16.9%, p
Laparoscopic hysterectomy has been associated with substantial short-term
impacts on ovarian reserve function, possibly due to the thermal effects of
electrocoagulation during the procedure. In contrast, open surgical approaches or
techniques that preserve the ovarian blood supply may offer superior protection
of ovarian function. A prospective cohort study by Chun and Ji (2020) [41]
examined the impact of hysterectomy with ovarian preservation on ovarian reserve
in 86 premenopausal women aged 31–48 years. The results showed differential
effects during the early postoperative period depending on the surgical approach.
While the laparoscopic group experienced a greater reduction in AMH level (0.42
ng/mL) compared to the open group (0.01 ng/mL), this did not reach statistical
significance (p = 0.053). Cho et al. (2017) [42] prospectively
monitored the AMH level in 91 individuals and found no significant difference in
the rate of decline between TLH and non-TLH groups at 6
months postoperatively (TLH 42.1% vs. non-TLH 33.3%, p = 0.545).
However, the TLH group exhibited a sustained decrease in the mean AMH value (3.5
to 1.6 ng/mL), whereas the AMH level remained relatively stable in the non-TLH
group (2.4 to 2.6 ng/mL). The systematic review and meta-analysis of 9 studies by
Gelderblom et al. (2022) [34] found a significant decline of more than
40% in the AMH level at 2 months postoperatively in the TLH group (p =
0.042), compared to a 20% decline in the non-TLH group. This difference may be
attributable to thermal damage from the electrocoagulation equipment used in
laparoscopic procedures, which can adversely impact ovarian tissues or blood
vessels through heat diffusion. A randomized controlled trial (n = 100) conducted
by Cai et al. (2017) [43] compared traditional hysterectomy with a novel
hysterectomy technique that preserves the uterine blood supply (STHMUV, uterine
blood supply-preserving hysterectomy technique). Superior ovarian protection was
observed with the STHMUV technique, which maintained stable postoperative
estradiol (E2) levels (346.12 pg/mL to 298.34 pg/mL) over 2 years (p
Younger patients (
Cooper and Thorp (1999) [22] reported the impact of hysterectomy on FSH levels (OR = 1.5) was less pronounced than that of smoking (OR = 2.0), but significantly greater than the natural aging process. This finding underscores the importance of incorporating the effect of hysterectomy on the FSH level into postoperative management strategies.
The management of post-hysterectomy ovarian hypoplasia and associated complications requires a full-cycle approach, incorporating detailed preoperative evaluation, optimized surgical techniques, and extended postoperative monitoring. The following evidence-based strategy is recommended:
In patients of childbearing age or those concerned about endocrine function,
preoperative testing of AMH, FSH, and E2 should be conducted to evaluate the risk
of postoperative ovarian failure. The factors of age, BMI, and smoking history
should also be considered. Age
In the absence of clear ovarian pathology, bilateral preservation is favored (89% vs. 66% for unilateral preservation 5 years postoperatively) [13]. Patients undergoing unilateral oophorectomy should be informed of the 2–3-fold increased risk of postoperative POI (HR = 2.93) [14].
Opportunistic Salpingectomy (OS) does not cause significant acute damage to ovarian function, but may shorten the time to menopause (1.84 years in the OS group vs. 2.93 years in the preserved group) [32, 34], and should thus be considered in the context of the patient’s age and reproductive needs. When tubal resection is required, fine dissection should be used to avoid damage to the ovarian mesosalpinx vessels. AMH is monitored postoperatively until it stabilizes, usually after 3–6 months.
In benign conditions, extrafascial subtotal resection is favored over radical resection to minimize the decrease in AMH level (p = 0.001) and to maintain the ovarian blood supply provided by the uterine artery, which normally contributes 50–70% of the total supply [34].
Careful use of electrocoagulation equipment is required, with preference given to cold knife separation or low-power modes of energy instrumentation to minimize ovarian damage from heat spread [34, 43].
Surgical techniques that preserve the uterine vasculature, such as the STHMUV
procedure, are recommended to maintain postoperative estrogen homeostasis. These
modified approaches result in a less pronounced decrease in estradiol levels
(
In line with the 2022 European Society of Human Reproduction and
Embryology (ESHRE) Guidelines on the management of premature ovarian insufficiency
[46], as well as the expert consensus [20], the levels of AMH, FSH and E2 should
be monitored postoperatively. Intervals should be shortened for patients who
undergo laparoscopic hysterectomy, or who retained only one ovary. Annual
evaluation should focus on FSH levels that exceed 40 IU/L (indicative of
menopausal status), as well as the presence of perimenopausal symptoms such as
hot flashes and vaginal dryness. Particular consideration should be given to
interventions for individuals who experience early-onset menopause (
Postoperative screening of pelvic floor function, including urodynamics, is recommended from 6 months onward in patients undergoing transvaginal surgery or radical resection. These should have careful monitoring for vaginal prolapse (37.8% incidence) and urethral dysfunction such as stress urinary incontinence (41% incidence at five years postoperatively).
Post-hysterectomy ovarian function undergoes significant changes, including diminished ovarian reserve, menstrual alterations, and early menopausal symptoms. The impact of surgical techniques and adjunct procedures on ovarian function is varied, and can influence the patients’ quality of life and psychological well-being. Clinicians should consider factors such as age, fertility desires, and disease status when selecting surgical methods and devising treatment plans. Surgical benefits and drawbacks must be balanced with ovarian function to tailor patient-specific strategies. Careful monitoring and management of postoperative ovarian function are crucial to promptly address issues, thereby improving the quality of life and health of patients. Future research should focus on personalized surgical designs such as vascular refinement protection, novel biomarkers including inflammatory factor profiles, and targeted interventions such as antifibrotic drugs. Advances in these areas should help to refine clinical management and improve long-term patient outcomes.
AMH, anti-Müllerian hormone; FSH, follicle-stimulating hormone; STHMUV, uterine blood supply-preserving hysterectomy technique; HPO, hypothalamic-pituitary-ovarian; ANS, autonomic nervous system; PI, pulsatility index; RI, resistance index; PSV, peak flow velocity; LAVH, laparoscopically-assisted vaginal hysterectomy; TAH, total abdominal hysterectomy; LUTD, lower urinary tract dysfunction; OS, opportunistic salpingectomy; PBS, prophylactic bilateral salpingectomy; BSO, bilateral salpingo-oophorectomy; LH, luteinizing hormone; E2, estradiol; USO, unilateral oophorectomy; TLH, total laparoscopic hysterectomy; LSH, laparoscopic supracervical hysterectomy.
YC conceptualized and designed the review, conducted comprehensive literature search and selection, and compiled and synthesized the relevant data. LM not only provided critical advice on data collation and interpretation of the review findings, but also took the lead in formulating literature inclusion and exclusion criteria, participated in the quality assessment of included literature, and constructed the core argumentation. Both authors contributed to editorial changes in the manuscript. Both authors read and approved the final manuscript. Both authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.
Not applicable.
We would like to express our gratitude to all those who provided assistance during the writing of this manuscript. We also thank all peer reviewers for their valuable opinions and suggestions.
This research received no external funding.
The authors declare no conflict of interest.
References
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