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The Adnexa

The adnexa (ovaries, fallopian tubes, their suspensory mesenteric ligaments, and their vascular and lymphatic pedicles) are the lateralmost structures of the female reproductive tract.

See also The Uterus for the shared vascular and ligamentous pedicles; The Ureters for ureter-in-the-ovarian-fossa anatomy; and Pelvic Neuroanatomy for the superior hypogastric plexus through which adnexal autonomic fibers travel.

Ovarian follicle development stages

Follicle growth from primordial through pre-ovulatory stages; this illustration does not show ovulation or the corpus luteum.

The Ovary​

Location and surgical relations​

The ovary lies in the ovarian fossa (Waldeyer's fossa) on the lateral pelvic sidewall, a shallow peritoneal recess. Standard anatomic descriptions bound it as follows:

BoundaryStructure
SuperiorExternal iliac vessels (the fossa lies in the angle between the external and internal iliac arteries)
AnteriorObliterated umbilical artery and the broad ligament
PosteriorInternal iliac artery and the ureter. The ureter runs directly posterior to the ovary.
Floor (lateral)Obturator vessels and nerve and the internal obturator muscle, covered by parietal peritoneum

In adnexal surgery (oophorectomy, cystectomy, salpingo-oophorectomy, excision of endometrioma) the ureter is the closest significant structure to the ovary. Before transecting the infundibulopelvic (suspensory) ligament laterally or mobilizing a fixed mass, positively identify the ureter on the pelvic sidewall. Fixed endometriomas, ruptured dermoids, tubo-ovarian abscesses and radiation obliterate this plane, and distorted anatomy of this kind is the setting for many iatrogenic ureteric injuries in benign gynecologic surgery.

Typical dimensions are approximately 3–4 cm × 2–2.5 cm × 1–1.5 cm in reproductive-age women. The ovaries shrink to almond size after menopause.[1][2][3]

Ligamentous attachments​

Three structures anchor the ovary: the vessel-bearing IP ligament, the fibromuscular utero-ovarian ligament, and the mesovarium, which carries hilar vessels.[4][5][6][33]

StructureConnectsContents
Infundibulopelvic (IP) / suspensory ligament of the ovaryOvary to pelvic sidewallOvarian artery and vein, lymphatics, autonomic nerves; the pedicle secured at oophorectomy
Utero-ovarian (ovarian proper) ligamentOvary to uterine cornuaUtero-ovarian arterial anastomosis
MesovariumOvary to posterior broad ligamentHilar vessels, nerves, lymphatics

The IP ligament is the operative pedicle for oophorectomy; the utero-ovarian ligament is the pedicle that remains attached to the uterus after salpingo-oophorectomy. When the ovary is preserved at hysterectomy, the utero-ovarian ligament and its uterine vascular contribution are divided; the ovarian vessels in the IP ligament remain its principal supply.[38] When the ovary is removed, both pedicles must be secured.

Histology and tumor origin​

The ovary contains three functional tissues, each the origin of a distinct tumor family, which is relevant when an adnexal mass is encountered intraoperatively:[1]

TissueOrigin of
Surface epithelium (coelomic)Epithelial ovarian tumors (the large majority), including high-grade serous tumors, many of which appear to originate from the fallopian-tube fimbria rather than the ovarian surface
Sex cords / stroma (granulosa, theca, fibroblasts)Sex-cord / stromal tumors, often hormonally active (granulosa-cell, Sertoli–Leydig, fibroma / thecoma)
Germ cells (oocytes within follicles)Germ-cell tumors — mature teratoma, dysgerminoma, yolk-sac, choriocarcinoma

Vascular supply and the right-vs-left asymmetry​

  • Ovarian artery. Arises directly from the aorta below the renal arteries, traverses the retroperitoneum in the IP ligament, and enters the ovary at the mesovarium.
  • Utero-ovarian arterial anastomosis at the cornua: the uterine and ovarian arteries communicate. This anastomosis is the anatomic basis of uterine artery embolization failure in fibroids with dominant ovarian artery supply, and of persistent bleeding after unilateral ligation of either source.

Venous drainage has the same asymmetry seen with the testis:

  • Right ovarian vein drains directly into the IVC
  • Left ovarian vein drains into the left renal vein (at approximately 90°)

The two ovarian veins have different clinical patterns:

  • Pelvic congestion syndrome and ovarian-vein reflux are more common on the left.
  • Postpartum ovarian-vein thrombophlebitis is more common on the right, where the dextrorotated gravid uterus compresses the vein and the vein enters the IVC directly.

Lymphatic drainage — paraaortic and pelvic pathways​

Ovarian lymph commonly follows the IP ligament cephalad with the ovarian vessels to the paraaortic and paracaval nodes at the level of the renal vessels. Pelvic drainage also occurs.[7][8][9][10]

  • Right ovary drains to paracaval / interaortocaval nodes
  • Left ovary drains to preaortic / para-aortic nodes

A secondary pathway drains to pelvic (external iliac, internal iliac) nodes. In a cadaveric dye-injection study of 20 ovaries, the pelvic territory was stained in 50% of cases and the lumbo-aortic territory in 65%.[7] In a small isotopic lymphography series (8 premenopausal and 6 postmenopausal women), premenopausal ovaries drained to both lumbo-aortic and pelvic nodes, whereas after menopause lymphatic flow decreased and drainage was essentially aorto-lumbar.[8]

Ovarian cancer can involve paraaortic and pelvic basins, but whether and how to sample nodes depends on stage, histology and the oncologic operation. In advanced disease after complete macroscopic resection with non-suspicious nodes on imaging and at surgery, systematic pelvic and paraaortic lymphadenectomy is not recommended (LION randomized trial, 2019; ESGO/ESMO/ESP 2025).[26] Staging decisions in apparent early disease differ.[26][27]

The Fallopian Tube​

Segments and surgical landmarks​

The human uterine tube has four segments with distinct operative relevance.[1][16] A rabbit oviduct study distinguished five histologic regions, a separate animal scheme.[17]

SegmentLengthKey feature
Infundibulum + fimbriaeDistal trumpet with finger-like fimbriae; the ovarian fimbria touches the ovaryOpen communication with the peritoneal cavity; probable origin of many high-grade serous carcinomas (via serous tubal intraepithelial carcinoma, STIC); target of risk-reducing salpingectomy
Ampulla5–8 cm; widest; thin-walledSite of fertilisation and of most ectopic pregnancies
Isthmus2–3 cm; narrow, thick-walledSite of tubal sterilisation by ligation, fulguration, clips, or rings; previously placed Essure microinserts span the intramural and proximal isthmic portions at the uterotubal junction.[44]
Interstitial (intramural) portionTraverses the uterine wall at the cornuaSite of interstitial ectopic pregnancy, which can rupture with severe hemorrhage

Histology and vascular supply​

The folded mucosa contains ciliated and secretory cells; historically described peg (intercalated) cells may represent a secretory-cell variant. The muscularis has inner circular and outer longitudinal smooth muscle, and the serosa is continuous with the mesosalpinx.[15][16]

The tube receives ovarian and uterine arterial branches through anastomoses in the mesosalpinx; an anatomical study described segmental supply, and a 15-patient hysterectomy pilot assessed tubal perfusion. When removing a tube while retaining the ovary, preserve ovarian vascular branches. Ovarian function after salpingectomy at hysterectomy does not appear to be affected based on surrogate measures.[18][19][23]

Cyclic function — at surgical depth​

The tube picks up the oocyte at the fimbria via a combination of fimbrial motion and ciliary current, transports it to the ampulla for fertilization, nurtures the early embryo in a secretion-rich environment, and delivers the cleavage-stage embryo to the uterus over 3–4 days.[46] The blastocyst forms around day 5 after fertilization.[45] In mice lacking oviductal motile cilia, the infundibulum failed to pick up ovulated oocytes, whereas sperm still reached the ampulla and embryos still reached the uterus, with reduced efficiency; myosalpinx contractions contribute to egg transport along the oviduct.[20][21] Disruption of any of these steps, such as scarring from PID (chlamydia / gonorrhea), endometriosis, or surgery, produces tubal-factor infertility.

Adnexal Physiology — Kept to Operative Depth​

The hypothalamic-pituitary-ovarian axis​

A brief summary sufficient for counseling:[11][12]

  • GnRH from the hypothalamus pulses LH/FSH from the anterior pituitary.
  • FSH drives follicular recruitment and granulosa-cell proliferation; LH drives theca-cell androgen production and triggers ovulation.
  • Ovarian steroids (estradiol, progesterone, inhibin) feed back on the hypothalamus and pituitary.
  • A mid-cycle LH surge triggered by rising estradiol ovulates the dominant follicle; the collapsed follicle becomes the corpus luteum producing progesterone until luteolysis or pregnancy rescue by hCG.

The two-cell, two-gonadotropin model of steroidogenesis​

This underpins PCOS, adrenal-androgen differential diagnosis, and hormone-suppressive therapy:[13][14]

  • Theca cells (LH-responsive) produce androstenedione from cholesterol.
  • Granulosa cells (FSH-responsive) express aromatase (CYP19) and convert theca-derived androstenedione into estradiol.
  • Postovulation the corpus luteum produces progesterone under LH / hCG drive; progesterone withdrawal drives menstruation.

Menopause and its consequences for the pelvic floor​

Ovarian estrogen production falls sharply at menopause. The urogenital consequences make ovariectomy decisions relevant to the reconstructive surgeon:

  • Urogenital atrophy. Thinned vaginal and urethral epithelium, reduced lubrication and submucosal vascular seal, raised vaginal pH.
  • Urinary symptoms (including urgency and recurrent UTI) may coexist with genitourinary syndrome of menopause.
  • Native-tissue prolapse repair. Vaginal estrogen may improve atrophy symptoms and tissue appearance. In IMPROVE (199 randomized; 186 underwent native-tissue vaginal apical repair), model-estimated 12-month composite surgical failure was 19% with conjugated estrogen cream and 9% with placebo (adjusted HR 1.97, 95% CI 0.92–4.22); routine perioperative use was not shown to improve surgical success.[24] At 36 months, 164 of 186 surgical participants supplied data; model-estimated composite failure was 32.6% with estrogen versus 26.8% with placebo (adjusted HR 1.55, 95% CI 0.90–2.66).[47] In EVA (oestriol cream; 311 randomized, 293 had surgery and started treatment, 57 dropped out), anatomic outcomes and reintervention did not differ, but among women assessed at 12 months, 92% with oestriol versus 80% with placebo reported being “much” or “very much” improved on the PGI-I (p = 0.02).[25]
  • Surgical menopause (bilateral oophorectomy in premenopausal women) produces the same spectrum abruptly and often more severely. The tradeoff against cancer prevention and ovarian-vein pathology is discussed explicitly.

Clinical Correlations for the Reconstructive Surgeon​

  • Ureteric injury during adnexectomy. The ureter runs along the posterior boundary of the ovarian fossa, posterior to the ovary, and passes medial to the IP ligament as the ligament crosses the pelvic brim. Identifying the ureter before IP-pedicle clamping is the main injury-prevention step, particularly in endometrioma excision, tubo-ovarian abscess drainage, and any reoperation.
  • Opportunistic salpingectomy. The tubal origin of many high-grade serous carcinomas supports complete bilateral salpingectomy at benign hysterectomy for patients at population risk who have completed childbearing.[1][22] ACOG's 2026 Clinical Practice Update says obstetrician–gynecologists should routinely perform bilateral salpingectomy at hysterectomy, recommend it at other intraperitoneal gynecologic surgery for patients who do not desire future fertility, prefer complete bilateral salpingectomy for permanent contraception after shared decision making, and support other specialists offering it at nongynecologic surgery.[39] It reduces but does not eliminate ovarian-cancer risk. Technique: remove the tube to the uterotubal junction while preserving ovarian blood supply when ovaries remain.[23] Counseling on surgical route should consider whether complete salpingectomy can be achieved through each route.[39]
  • Risk-reducing salpingo-oophorectomy (RRSO). The indication and timing require gene-, age- and patient-specific counseling for BRCA1/2, Lynch syndrome and other inherited risks. At risk-reducing salpingo-oophorectomy, remove all ovarian and tubal tissue, inspect peritoneal surfaces, obtain pelvic washings, and request complete serial sectioning of the ovaries and tubes, including detailed fimbrial examination (SEE-FIM).[40] Discuss surgical-menopause and urogenital symptoms; vaginal estrogen can address appropriate atrophy symptoms, but should not be promised to improve later prolapse-repair durability.[23][24][25]
  • Adnexal torsion. The ovary and tube can twist on the IP-ligament / utero-ovarian ligament axis, causing venous engorgement and ischemia. Urgent evaluation is needed. In adolescents with suspected torsion, timely diagnostic laparoscopy is indicated even when Doppler flow is present.[28] In adolescents especially, detorsion and ovarian preservation are preferred regardless of a blue-black appearance, because Doppler flow and gross color do not reliably establish viability. Associated cyst management and oophoropexy are individualized.[28]
  • Ectopic pregnancy. In a population-based registry of 1,800 surgically treated ectopic pregnancies, 95.5% were tubal and 70.0% were ampullary.[37] RCOG supports expectant management for clinically stable patients with an ultrasound-confirmed tubal pregnancy and an initially <1500 IU/L, falling β-hCG (Grade B).[30] Systemic methotrexate may be offered to suitable women with a tubal ectopic pregnancy who can attend follow-up (Grade B), but should not be given at a first visit unless ectopic pregnancy is certain and a viable intrauterine pregnancy has been excluded.[30] For surgery, RCOG prefers salpingectomy (complete tube removal) when the other tube is healthy (Grade B); salpingostomy or salpingotomy (linear incision and evacuation with tube preservation) may be considered with fertility-reducing factors (Grade C) and requires β-hCG follow-up. Interstitial implantation in the intramural tube differs from cornual pregnancy in an anomalous uterine horn. Selected stable interstitial cases can receive expectant or medical management; operations described include cornual resection or salpingotomy, with attention to the vascular pedicle (Grade D).[30]
  • Pelvic inflammatory disease (PID) and tubo-ovarian abscess (TOA). PID can involve gonorrhea, chlamydia, anaerobes, and other organisms; salpingitis and TOA are possible manifestations.[41] Sequelae include tubal scarring, adhesions, tubal infertility, chronic pelvic pain, and ectopic pregnancy; a historical CDC estimate put ectopic risk at approximately sevenfold after one PID episode versus no PID history.[42] TOA warrants hospitalization and broad-spectrum antibiotics with anaerobic coverage. Drainage or surgery may be required according to severity and response; extensive disease may require adnexectomy in a pelvis with distorted ureteric anatomy.[41]
  • Ovarian vein thrombophlebitis. Postpartum septic thrombophlebitis is more common on the right (the dextrorotated gravid uterus compresses the right ovarian vein against the pelvic brim). It presents as persistent fever after negative infectious workup. CT shows a dilated thrombosed ovarian vein that may extend to the IVC or renal vein. Treat the septic component with broad-spectrum antibiotics; anticoagulation is commonly used for confirmed ovarian-vein thrombosis, although its added benefit in puerperal septic pelvic thrombophlebitis is uncertain.[48][49]
  • Pelvic congestion syndrome. Chronic pelvic pain worsened by standing, improved by recumbency; associated with ovarian-vein varicosities (more often left than right) and sometimes with nutcracker-syndrome left-renal-vein compression. For symptoms attributed to pelvic venous reflux after imaging evaluation, ovarian or pelvic-vein embolization is an option; comparative outcome evidence remains limited.[50][51] Surgical ovarian-vein ligation has also been studied in a small randomized comparison, and the reconstructive surgeon may participate with pelvic-venous specialists when relevant.[52]
  • Ovarian remnant syndrome. Recurrent cyclic pelvic pain and a palpable or imaging mass after prior oophorectomy, from residual ovarian tissue. Common after difficult oophorectomy through dense endometriotic or TOA-related adhesions. Reoperation in the lateral pelvis risks ureteric injury. Preoperative imaging can help localize the remnant; dissection may require retroperitoneal ureterolysis from the pelvic brim. Ureteric stents can be considered selectively but do not replace direct identification of the ureter.[53]
  • Ovarian cancer operations. Staging and cytoreduction are stage-, histology- and patient-specific gynecologic-oncology decisions; possible components include hysterectomy, bilateral salpingo-oophorectomy, omentectomy, washings/biopsies and selected node assessment. A blanket pelvic/paraaortic lymphadenectomy rule does not apply to completely resected advanced disease with clinically non-suspicious nodes.[26][27] Urologic involvement can include ureterolysis or urinary-tract reconstruction in extensive cases.
  • Incidental adnexal mass at pelvic reconstructive surgery. A mass known before surgery is characterized with pelvic ultrasound; CA-125 is considered according to malignancy risk, and suspicious findings warrant gynecologic-oncology consultation before planned reconstruction. A mass first found intraoperatively requires assessment at discovery, with subsequent imaging or consultation as indicated.[31][32]
  • Sterilization options and reversal. Tubal ligation (Pomeroy, Parkland), fulguration, and mechanical (Filshie clip, Hulka clip, Falope ring) remain in use; Essure devices are no longer available for implantation. When removal is indicated, first confirm insert location on preoperative imaging; laparoscopic salpingectomy, cornuectomy, and hysterectomy with en-bloc salpingectomy are described options, selected according to device location, procedural risks, and patient goals. Avoid transecting an insert or directly contacting it with active electrosurgery; inspect each removed insert for completeness and use intraoperative imaging if a fragment remains.[34][35][43] Reversal after surgical tubal sterilization depends on residual tube length, prior method, and female and male fertility factors. Essure should be considered irreversible because the safety and effectiveness of reversal surgery are unknown.[55]
  • Ectopic pregnancy after tubal ligation. In the prospective U.S. Collaborative Review of Sterilization (10,685 women), the 10-year cumulative probability of ectopic pregnancy was 7.3 per 1000 procedures.[29] It varied with method and age (31.9 per 1000 after bipolar coagulation before age 30 years vs 1.2 per 1000 after postpartum partial salpingectomy) and did not fall after the third year.[29]
  • Müllerian anomalies of the tube and ovary. Tubal agenesis, absence of a fimbriated end, accessory tubes or ostia, and supernumerary / ectopic ovaries are uncommon but can be encountered at reconstructive surgery. Tubo-ovarian agenesis can coexist with uterine and renal anomalies; assess the associated uterine and upper-tract anatomy when a broader developmental anomaly is present.[36]
  • Ovarian repositioning before pelvic radiotherapy. In selected premenopausal patients without elevated ovarian-metastasis risk, the reconstructive team may move an ovary outside the planned radiation field to preserve endocrine function. Transposition divides the utero-ovarian ligament while preserving the IP vascular pedicle; fix the ovary beyond the field without pedicle tension or torsion and mark its position with radiopaque clips. Ovariopexy may preserve uterine attachment when the planned field allows. Endocrine preservation varies, particularly with chemotherapy, and repositioning affects subsequent surgical access and fertility planning.[54]

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