Skip to main content

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. For the reconstructive pelvic surgeon they matter less as reproductive organs than as the posterolateral neighbor of the ureter, the source of the ovarian vascular pedicle (IP ligament), and the territory of opportunistic salpingectomy, adnexal torsion, and risk-reducing surgery. They generate three distinct reconstructive problems: (1) iatrogenic ureteric injury in the ovarian fossa / IP ligament, (2) the pelvic-congestion and ovarian-vein thrombophlebitis presentations that a pelvic reconstructive specialist sees, and (3) the long-term pelvic-floor and urogenital consequences of surgical menopause when both adnexa are removed. This article prioritises those surgical anatomy and perioperative issues, and compresses folliculogenesis, steroidogenesis, tubal cell biology, and reproductive cycle detail to the depth the reconstructive urologist or urogynecologist needs.

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 development stages — from primordial follicle to 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 bounded by:[1][2]

BoundaryStructure
AnteriorExternal iliac vessels
PosteriorInternal iliac vessels and the ureter — the ureter runs in the floor of the fossa, directly posterior to the ovary
SuperiorBifurcation of the common iliac artery
MedialUterus
Inferior / lateralObturator nerve and internal obturator muscle (covered by parietal peritoneum)
The ureter lies on the floor of the ovarian fossa

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 mobilising a fixed mass, positively identify the ureter on the pelvic sidewall. Fixed endometriomas, ruptured dermoids, tubo-ovarian abscesses, and radiation all obliterate this plane and account for most iatrogenic ureteric injuries in benign gynecologic surgery.

Typical dimensions: ~3–4 cm × 2–2.5 cm × 1–1.5 cm in reproductive-age women; they shrink to almond size postmenopausally.[1][2][3]

Ligamentous attachments​

Three connective-tissue attachments anchor the ovary — each a vessel-carrying mesentery rather than a fibrous cord:[4][5][6]

StructureConnectsContents
Infundibulopelvic (IP) / suspensory ligament of the ovaryOvary to pelvic sidewallOvarian artery and vein, lymphatics, autonomic nerves — the critical pedicle of 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 and IP ligament vessels remain the ovarian blood supply; when it 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 — the operatively decisive fact when an intra-operative adnexal mass is encountered:[1]

TissueOrigin of
Surface epithelium (coelomic)Epithelial ovarian tumors — the large majority, including high-grade serous (most of which now appear to originate from the fallopian-tube fimbria rather than the ovarian surface)
Sex cords / stroma (granulosa, theca, fibroblasts)Sex-cord / stromal tumors — 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 — uterine and ovarian arteries communicate. This is the anatomic basis of UAE failure in fibroids (ovarian artery dominant supply), and of persistent bleeding after unilateral ligation of either source.

Venous drainage has the same asymmetry seen with the testis:

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

The left-sided drainage into the renal vein, with the same nutcracker geometry, is why:

  • Pelvic congestion syndrome is more common on the left.
  • Left ovarian-vein thrombophlebitis is classically the postpartum presentation of pelvic thrombosis — though right-sided is actually more common because of dextrorotation of the gravid uterus.

Lymphatic drainage — paraaortic, not pelvic​

Ovarian lymph follows the IP ligament cephalad with the ovarian vessels to the paraaortic / paracaval nodes at the level of the renal vessels — not the pelvic nodes.[7][8][9][10]

  • Right ovary → paracaval / interaortocaval
  • Left ovary → preaortic / para-aortic

A secondary pathway drains to pelvic (external iliac, internal iliac) nodes in ~50% of cases, particularly in premenopausal women.[7][8] After menopause, lymphatic flow decreases and drainage is essentially paraaortic.

Clinical consequence: staging lymphadenectomy for ovarian cancer targets the paraaortic basin up to the renal vessels, with pelvic nodes added per template. Contrast this with uterine cancer, which drains primarily pelvic.

The Fallopian Tube​

Segments and surgical landmarks​

Four segments, each with distinct operative relevance:[1][16][17]

SegmentLengthKey feature
Infundibulum + fimbriaeDistal trumpet with finger-like fimbriae; the ovarian fimbria touches the ovaryPeritoneal open communication with the abdomen; origin of most HGSOC (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 (ligation, fulguration, clips / rings, Essure)
Interstitial (intramural) portionTraverses the uterine wall at the cornuaCornual/interstitial ectopic pregnancy — catastrophic rupture risk

Histology and vascular supply​

Mucosa contains ciliated, secretory (peg), and intercalated cells on highly folded epithelium; muscularis has inner circular and outer longitudinal smooth muscle; serosa continuous with the mesosalpinx.[15][16]

The tube is perfused from the ovarian and uterine arteries via anastomoses within the mesosalpinx; segmental rather than marginal in its distribution — which is the reason ovary-preserving hysterectomy and salpingectomy can often be done safely without ovarian devascularization.[18][19]

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 blastocyst to the uterus over 3–4 days. The myosalpinx rather than ciliary beating is the dominant transport mechanism — which is why even heavily ciliopathic tubes can carry sperm and embryos but still fail at oocyte pickup.[20][21] Disruption of any of these steps — 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​

Worth knowing because it 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 collapses at menopause. The urogenital consequences are the reason ovariectomy decisions matter to the reconstructive surgeon:

  • Urogenital atrophy — thinned vaginal and urethral epithelium, reduced lubrication and submucosal vascular seal, raised vaginal pH.
  • Stress urinary incontinence worsens through loss of mucosal coaptation and reduced urethral closure pressure.
  • Overactive bladder and recurrent UTI increase in frequency.
  • Native-tissue prolapse repair is less durable on atrophic tissue — addressed by perioperative topical vaginal estrogen.
  • Surgical menopause (bilateral oophorectomy in premenopausal women) produces the same spectrum abruptly and severely; the tradeoff against cancer prevention / ovarian-vein pathology should be discussed explicitly.

Clinical Correlations for the Reconstructive Surgeon​

  • Ureteric injury during adnexectomy. The ureter lies on the floor of the ovarian fossa, immediately posterior to the ovary, and passes medial to the IP ligament as the ligament crosses the pelvic brim. Identification before IP-pedicle clamping is the definitive injury-prevention step — particularly in endometrioma excision, tubo-ovarian abscess drainage, and any reoperation.
  • Opportunistic salpingectomy. The recognition that serous tubal intraepithelial carcinoma (STIC) in the fimbria is the origin of most high-grade serous ovarian cancers has made bilateral opportunistic salpingectomy the standard adjunct to benign hysterectomy or sterilization in women who have completed childbearing. Technique: divide the tubal mesentery close to the tube, preserve the utero-ovarian arterial anastomosis, leave the ovary in situ to preserve endocrine function.[1][22]
  • Risk-reducing salpingo-oophorectomy (RRSO). Indicated for BRCA1/2, Lynch syndrome, and other high-penetrance hereditary ovarian-cancer syndromes. The standard operation: bilateral salpingectomy + oophorectomy with detailed sectioning and extensive examination (SEE-FIM protocol) of the fimbria. Reconstructive-surgical implications: counseling about urogenital atrophy, stress incontinence, and prolapse; plan perioperative vaginal estrogen for later native-tissue repair if indicated.
  • Adnexal torsion. The ovary and tube can twist on the IP-ligament / utero-ovarian ligament axis, causing venous engorgement, arterial compromise, and ischemic necrosis. Typical presenting population: reproductive-age women with a functional cyst, dermoid, or paratubal cyst >5 cm. Emergency. Detorsion (not oophorectomy) is the preferred approach whenever the ovary has any evidence of residual perfusion; blue/black appearance alone is not a mandate for resection. Cystectomy and oophoropexy follow in selected cases.
  • Ectopic pregnancy. ~95% implant in the fallopian tube, dominantly in the ampulla. Management: methotrexate (medical) for small, unruptured, stable ectopics; salpingostomy (linear incision, evacuation, tube preservation) or salpingectomy (complete tube removal) for surgical cases. Interstitial (cornual) ectopics require wedge resection or cornuostomy with attention to the uterine-cornual vascular pedicle.
  • Pelvic inflammatory disease (PID) and tubo-ovarian abscess (TOA). Ascending infection (gonorrhea, chlamydia) → salpingitis → TOA. Sequelae: tubal scarring, adhesions, tubal infertility, chronic pelvic pain, 6–10× risk of ectopic pregnancy. TOA is a reconstructive problem: drainage, antibiotics, and — when disease is extensive — adnexectomy in a potentially hostile pelvis with distorted ureteric anatomy.
  • Ovarian vein thrombophlebitis. Postpartum septic thrombophlebitis — right-sided more common (dextrorotation of gravid uterus compresses the right ovarian vein against the pelvic brim), though classically discussed as left. Presents as persistent fever after negative infectious workup. Imaging (CT) shows dilated thrombosed ovarian vein extending to the IVC or renal vein. Management: anticoagulation + broad antibiotics.
  • Pelvic congestion syndrome. Chronic pelvic pain worsened by standing, improved by recumbency; associated with ovarian-vein varicosities (left >> right) and sometimes with nutcracker-syndrome left-renal-vein compression. Treatment: ovarian / internal iliac vein embolization or surgical ligation, with the reconstructive surgeon increasingly involved as an interdisciplinary contributor.
  • Ovarian remnant syndrome. Recurrent cyclic pelvic pain + a palpable / 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 carries substantial ureteric-injury risk — preoperative imaging and ureteric stents are standard.
  • Ovarian cancer surgical staging. Full staging includes total abdominal hysterectomy with bilateral salpingo-oophorectomy, omentectomy, peritoneal washings, multiple peritoneal biopsies, and paraaortic + pelvic lymphadenectomy. Paraaortic dissection up to the renal vessels follows the ovarian-lymphatic pathway described above. Urologic involvement: ureterolysis, partial cystectomy, occasional bowel / urinary-tract reconstruction in extensive cases.
  • Incidental adnexal mass at pelvic reconstructive surgery. Discovered adnexal masses during prolapse or fistula surgery should be evaluated preoperatively with TV-US and CA-125; if malignancy cannot be excluded, refer to gynecologic oncology rather than proceeding with the reconstructive step.
  • Sterilization options and reversal. Tubal ligation (Pomeroy, Parkland), fulguration, and mechanical (Filshie clip, Hulka clip, Falope ring) remain in use; Essure hysteroscopic devices have been withdrawn but their removal (salpingectomy with cornual resection) is a not-uncommon referral. Reversal depends on residual tube length, prior method, and female / male fertility factors.
  • Tubal ectopic pregnancy after tubal ligation. If ligation fails, ~30–40% of subsequent pregnancies are ectopic — part of the informed-consent discussion.
  • 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. Associated genitourinary anomalies (renal agenesis, ureteral duplication) are found in ~30% and warrant upper-tract imaging.
  • Oophoropexy for pediatric / adolescent patients undergoing pelvic radiation. The reconstructive team is occasionally asked to reposition ovaries out of a planned radiation field to preserve endocrine function — a technical procedure with implications for subsequent surgical access and fertility planning.

References​

1. Sisodia RC, Del Carmen MG. "Lesions of the Ovary and Fallopian Tube." N Engl J Med. 2022;387(8):727–736. doi:10.1056/NEJMra2108956

2. Campo H, López-Martínez S, Cervelló I. "Decellularization Methods of Ovary in Tissue Engineering." Adv Exp Med Biol. 2021;1345:129–139. doi:10.1007/978-3-030-82735-9_11

3. Outwater EK, Talerman A, Dunton C. "Normal Adnexa Uteri Specimens: Anatomic Basis of MR Imaging Features." Radiology. 1996;201(3):751–755. doi:10.1148/radiology.201.3.8939226

4. Saksouk FA, Johnson SC. "Recognition of the Ovaries and Ovarian Origin of Pelvic Masses With CT." Radiographics. 2004;24 Suppl 1:S133–S146. doi:10.1148/rg.24si045507

5. Kaniewska M, Gołofit P, Heubner M, Maake C, Kubik-Huch RA. "Suspensory Ligaments of the Female Genital Organs: MRI Evaluation With Intraoperative Correlation." Radiographics. 2018;38(7):2195–2211. doi:10.1148/rg.2018180089

6. Bazot M, Deligne L, Boudghène F, et al. "Correlation Between Computed Tomography and Gross Anatomy of the Suspensory Ligament of the Ovary." Surg Radiol Anat. 1999;21(5):341–346. doi:10.1007/BF01631336

7. Murris F, Weyl A, Ouldamer L, et al. "Contribution of the Cadaveric Recirculation System in the Anatomical Study of Lymphatic Drainage of the Ovary: Applications in the Management of Ovarian Cancer." Surg Radiol Anat. 2024;46(8):1155–1164. doi:10.1007/s00276-024-03406-w

8. Vanneuville G, Mestas D, Le Bouedec G, et al. "The Lymphatic Drainage of the Human Ovary In Vivo Investigated by Isotopic Lymphography Before and After the Menopause." Surg Radiol Anat. 1991;13(3):221–226. doi:10.1007/BF01627990

9. Negishi H, Takeda M, Fujimoto T, et al. "Lymphatic Mapping and Sentinel Node Identification as Related to the Primary Sites of Lymph Node Metastasis in Early Stage Ovarian Cancer." Gynecol Oncol. 2004;94(1):161–166. doi:10.1016/j.ygyno.2004.04.023

10. Benedetti-Panici P, Greggi S, Maneschi F, et al. "Anatomical and Pathological Study of Retroperitoneal Nodes in Epithelial Ovarian Cancer." Gynecol Oncol. 1993;51(2):150–154. doi:10.1006/gyno.1993.1263

11. Barbieri RL. "The Endocrinology of the Menstrual Cycle." Methods Mol Biol. 2014;1154:145–169. doi:10.1007/978-1-4939-0659-8_7

12. Buffet NC, Bouchard P. "The Neuroendocrine Regulation of the Human Ovarian Cycle." Chronobiol Int. 2001;18(6):893–919.

13. McNatty KP, Makris A, DeGrazia C, Osathanondh R, Ryan KJ. "The Production of Progesterone, Androgens, and Estrogens by Granulosa Cells, Thecal Tissue, and Stromal Tissue From Human Ovaries In Vitro." J Clin Endocrinol Metab. 1979;49(5):687–699. doi:10.1210/jcem-49-5-687

14. Szołtys M. "Hormonal Regulation of Ovarian Function In Vivo and In Vitro." J Physiol Pharmacol. 1992;43(4 Suppl 1):51–56.

15. Csöbönyeiová M, Varga I, Lapides L, et al. "From a Passive Conduit to Highly Dynamic Organ. What Are the Roles of Uterine Tube Epithelium in Reproduction?" Physiol Res. 2022;71(Suppl 1):S11–S20.

16. Crow J, Amso NN, Lewin J, Shaw RW. "Morphology and Ultrastructure of Fallopian Tube Epithelium at Different Stages of the Menstrual Cycle and Menopause." Hum Reprod. 1994;9(12):2224–2233. doi:10.1093/oxfordjournals.humrep.a138428

17. Pedrero-Badillo F, Anaya-Hernández A, Corona-Quintanilla DL, et al. "Morphohistological Characteristics of Rabbit Oviduct: A Proposal for a Single Regionalization." Anim Reprod Sci. 2013;143(1–4):102–111. doi:10.1016/j.anireprosci.2013.09.011

18. Tamash Y, Hammer N, Varga I, Supilnikov A, Iukhimetc S. "Arterial Blood Supply of the Mesosalpinx Appears Segmentally Organized in Absence of Uterine Tubes Arteries." Physiol Res. 2022;71(Suppl 1):S107–S113.

19. Farag S, Frazzini Padilla P, Smith KA, et al. "Fallopian Tube Perfusion in Ex-Vivo and In-Vivo Laparoscopic Hysterectomy Specimens: Potential Application for Uterine Transplantation." Hum Reprod. 2018;33(12):2232–2240. doi:10.1093/humrep/dey307

20. Yuan S, Wang Z, Peng H, et al. "Oviductal Motile Cilia Are Essential for Oocyte Pickup but Dispensable for Sperm and Embryo Transport." Proc Natl Acad Sci U S A. 2021;118(22):e2102940118. doi:10.1073/pnas.2102940118

21. Dixon RE, Hwang SJ, Kim BH, Sanders KM, Ward SM. "Myosalpinx Contractions Are Essential for Egg Transport Along the Oviduct and Are Disrupted in Reproductive Tract Diseases." Adv Exp Med Biol. 2019;1124:265–294. doi:10.1007/978-981-13-5895-1_11

22. Sowamber R, Nelson O, Dodds L, et al. "Integrative Transcriptome Analyses of the Human Fallopian Tube: Fimbria and Ampulla — Site of Origin of Serous Carcinoma of the Ovary." Cancers. 2020;12(5):1090. doi:10.3390/cancers12051090