In one line
Most adnexal masses are benign, so the consultant task is not diagnosis but disciplined risk stratification — using transvaginal ultrasound morphology, age/menopausal status and the right marker — to separate the benign mass that can be watched or removed simply from the one that must reach a gynae-oncologist before a single incision, and to do that without either under-triaging a cancer or over-treating a follicular cyst.
The groundwork on simple cyst types and the differential of pelvic pain is assumed here; revise it at genital tract cysts. The focus is the exit-level judgement: stratifying risk and defending a plan.
Mechanism & pathophysiology
Adnexal masses are a spectrum, and reasoning about risk starts with knowing what each lesion is and how its biology shows on the screen.
Functional cysts are not neoplasms at all — they are exaggerated physiology. A follicular cyst is a dominant follicle that fails to rupture and keeps growing under FSH drive; a corpus luteum cyst is a corpus luteum that fails to involute and may bleed into itself (the haemorrhagic cyst, with its lace-like retracting clot on ultrasound). Both are oestrogen- or progesterone-supported transient structures, which is exactly why most resolve within two to three cycles once the hormonal stimulus passes. Theca-lutein cysts are the extreme of this logic — bilateral, multiloculated ovaries driven by very high β-hCG (multiple/molar pregnancy, ovarian hyperstimulation), which regress as hCG falls. Understanding functional cysts as physiology, not pathology, is what licenses watchful waiting.
Benign epithelial tumours arise from the ovarian surface epithelium (or, on the current pathogenesis model, from tubal/secondary müllerian epithelium). A serous cystadenoma is typically unilocular, thin-walled and anechoic; a mucinous cystadenoma is often large, multilocular, with low-level internal echoes from mucin. They matter because their malignant counterparts (serous and mucinous carcinoma) share the morphological vocabulary — locules, septa, solid areas — so the same ultrasound features that define the benign lesion are the ones that, when they tip over (thick septa, solid papillary projections, vascularity), signal malignancy.
Benign germ-cell tumours are dominated by the mature cystic teratoma (dermoid) — the commonest ovarian neoplasm in women under 30. It contains tissue from all three germ layers (skin, hair, sebaceous material, teeth, occasionally thyroid), which gives its pathognomonic ultrasound signs: the echogenic Rokitansky nodule, hyperechoic lines and dots (hair), and acoustic shadowing from fat/calcium. Its biology drives its complications — fat content makes it buoyant and torsion-prone, and rare malignant transformation (usually squamous carcinoma in older women) is the reason a large or atypical dermoid is not entirely a non-event.
Endometrioma is ectopic endometrium that bleeds cyclically into a cyst, producing the homogeneous low-level "ground-glass" echoes of altered blood. It links directly to the endometriosis story (assume that groundwork) and carries two specific consultant concerns: it distorts pelvic anatomy and impairs fertility, and a small but real subset undergoes malignant transformation to clear-cell or endometrioid carcinoma — a new solid nodule with vascularity inside a long-standing endometrioma is the warning.
Sex-cord-stromal tumours are hormonally active and that is the diagnostic clue. Granulosa-cell tumours secrete oestrogen and inhibin (presenting with postmenopausal bleeding, endometrial hyperplasia, or precocious puberty in girls); Sertoli-Leydig tumours secrete androgens (virilisation). Fibromas/thecomas are benign solid ovarian tumours; a fibroma with ascites and a pleural effusion is Meigs syndrome — a benign cause of the picture that otherwise screams ovarian cancer, and a classic trap.
Para-ovarian and paratubal cysts arise from mesonephric or paramesonephric remnants in the broad ligament; they sit beside a normal ovary, which is the key to recognising them (the "split sign" — separately identifiable ipsilateral ovary). They are almost always benign.
Tubo-ovarian abscess is the inflammatory mass that does not belong to the neoplastic spectrum but is mistaken for it: a complex, often bilateral, multiloculated adnexal mass with thick walls, fever, raised inflammatory markers and a pelvic-infection history. In SA, where HIV and tuberculosis are common, a complex adnexal mass with constitutional symptoms must prompt consideration of pelvic/genital TB before anyone reaches for an oncology operation — granulomatous tubo-ovarian disease can radiologically and biochemically (raised CA-125, ascites) mimic ovarian cancer precisely, and the management is antituberculous therapy, not laparotomy.
The malignant lesions to exclude run alongside this list: epithelial ovarian cancer (the bulk, including high-grade serous, which on the current pathogenesis model arises largely from a precursor lesion at the fimbrial end of the fallopian tube — serous tubal intraepithelial carcinoma — rather than from the ovary itself), the malignant germ-cell tumours of the young (dysgerminoma, yolk-sac, immature teratoma, choriocarcinoma), malignant sex-cord-stromal tumours, and secondary metastases (the Krukenberg tumour — bilateral solid ovarian metastases, classically signet-ring gastric primary). The tubal-origin model matters clinically because it underpins opportunistic salpingectomy as a prevention strategy and explains why removing the tubes, not just the ovaries, reduces future cancer risk. Risk stratification is the discipline of reading this whole spectrum and placing the patient in front of you on it. For the malignant end and its staging and treatment, see Ovarian malignancy.
Assessment
History and examination orient the probability before any test:
- Age and menopausal status are the single most powerful modifiers — the same morphology carries a far higher malignancy risk in a 65-year-old than a 25-year-old, and the marker that helps differs by age. In a woman under ~30 with a solid or mixed mass, think germ-cell tumour and send germ-cell markers; in a postmenopausal woman, think epithelial cancer and the CA-125–based tools.
- Symptoms: most masses are asymptomatic and incidental. Acute severe pain suggests torsion, rupture or haemorrhage; chronic pelvic pain with dysmenorrhoea suggests endometrioma; bloating, early satiety, urinary frequency, weight loss and a palpable mass — especially with ascites — are the sinister cluster of advanced ovarian cancer. Hormonal symptoms (postmenopausal bleeding, virilisation, precocious puberty) point to a sex-cord-stromal tumour.
- Examination: abdominal mass, ascites, an immobile/fixed or bilateral adnexal mass, and nodularity in the pouch of Douglas raise malignancy concern. A normal examination never excludes a mass — imaging is decisive.
Transvaginal ultrasound is the cornerstone investigation. It is far more than "cyst present"; the consultant reads the specific morphological features that the structured tools depend on:
- Reassuring (benign) features: unilocular, anechoic, thin smooth wall, ≤10 cm, no solid component, no vascularity, acoustic shadows (dermoid/calcification), ground-glass content (endometrioma), or a clear single classic pattern recognised by an experienced examiner.
- Concerning (malignant) features: solid components, irregular/thick septa (>3 mm), papillary projections (≥3), bilaterality, ascites, strong internal Doppler flow, irregular solid tumour, and large size.
Where ultrasound is indeterminate, MRI characterises soft tissue best (fat, blood, solid enhancement); CT is for staging suspected malignancy (omental/peritoneal/nodal disease), not for characterising the mass itself.
Tumour markers — interpret, do not just measure.
- CA-125 is the workhorse but its caveats are the exam point. It is a non-specific epithelial glycoprotein raised by many benign conditions — endometriosis, fibroids, pelvic inflammatory disease, menstruation, pregnancy, ascites of any cause, and peritoneal irritation — so it is far less specific in premenopausal women, where these conditions are common. Conversely it is insensitive for early-stage and for mucinous, clear-cell and germ-cell tumours, so a normal CA-125 never excludes cancer. Its real value is in the postmenopausal woman and as one input into a structured index, not as a standalone test.
- HE4 and the ROMA algorithm combine HE4 (less elevated by benign gynaecological disease, so more specific) with CA-125 and menopausal status. HE4/ROMA improve specificity over CA-125 alone, particularly in distinguishing endometriosis and fibroids from cancer, but are less sensitive in premenopausal women, and ROMA cut-offs are assay- and menopause-dependent. HE4/ROMA are not uniformly available in the SA public sector.
- In the young woman with a solid/complex mass, send germ-cell and stromal markers, not CA-125: AFP (yolk-sac tumour, some immature teratomas), β-hCG (choriocarcinoma, dysgerminoma), LDH (dysgerminoma), and inhibin/oestradiol (granulosa-cell tumour). Missing these in a young woman by reflexively ordering CA-125 is a recurrent error.