Adnexal Masses & Ovarian Neoplasms
Age, ultrasound, and tumor markers sort benign cysts from cancer
Approach to the adnexal mass
First steps. Every adnexal mass in a reproductive-age patient starts with a pregnancy test (ectopic pregnancy and a corpus luteum of pregnancy are common mimics) and transvaginal ultrasound, which defines size, wall, septations, solid components, Doppler flow, and ascites. MRI is a second-line problem solver; CT is for staging suspected cancer. The differential also includes paratubal cysts, hydrosalpinx, tubo-ovarian abscess, and pedunculated fibroids.
Age sets the prior probability. In girls and adolescents most ovarian malignancies are germ cell tumors, and masses predispose to torsion. In reproductive-age women most masses are functional cysts, dermoids, or endometriomas. After menopause the risk of epithelial cancer rises and CA-125 becomes more informative.
| Scenario | Likely lesion | Next step |
|---|---|---|
| Girl or adolescent, solid or complex mass | Germ cell tumor | AFP, β-hCG, LDH, inhibin; ovary-sparing surgery |
| Reproductive age, simple or hemorrhagic cyst | Follicular or corpus luteum cyst | 5 cm or smaller: no follow-up (O-RADS); larger than 5 cm: repeat ultrasound in 8 to 12 weeks; OCPs do not speed resolution |
| Postmenopausal simple cyst <10 cm, normal CA-125 | Benign cyst | Serial ultrasound |
| Solid areas, thick septations, ascites, or high CA-125 | Possible malignancy | CT staging and gynecologic oncology surgery |
| Sudden pain and vomiting with a mass | Adnexal torsion | Urgent laparoscopic detorsion, preserve the ovary |
Red flags. Solid components with Doppler flow, papillary projections, thick septations (>3 mm), irregular walls, bilateral masses, ascites, omental or peritoneal nodules, and lymphadenopathy. CA-125 above 35 U/mL in a postmenopausal woman, or a markedly elevated value (e.g., >200 U/mL) before menopause, also warrants referral; surgery by a gynecologic oncologist improves survival.
CA-125 limitations. It rises with endometriosis, fibroids, PID, pregnancy, menstruation, cirrhosis, and any peritoneal irritation, so it is nonspecific before menopause, and it is normal in about half of stage I epithelial cancers. Its best uses are a postmenopausal mass and monitoring treatment response.
Do not aspirate or percutaneously biopsy a suspicious ovarian mass; remove it intact to avoid spilling tumor and upstaging the cancer.
Functional cysts and benign neoplasms
Functional cysts. Follicular cysts are simple, thin-walled, and anechoic. Corpus luteum cysts can bleed; rupture causes acute pain and hemoperitoneum. A hemorrhagic cyst has lacy, reticular internal echoes and a retracting clot with no internal flow. Most resolve over one or two cycles: per O-RADS, a classic simple or hemorrhagic cyst 5 cm or smaller in a premenopausal woman needs no follow-up, and a larger one gets repeat ultrasound in 8 to 12 weeks; combined OCPs do not hasten resolution. Theca lutein cysts are bilateral, multiloculated cysts driven by very high hCG (molar pregnancy, multiple gestation, ovarian hyperstimulation) and regress as hCG falls.
Postmenopausal simple cysts. A unilocular, thin-walled, anechoic cyst <10 cm with a normal CA-125 carries a very low risk of malignancy and can be followed with serial ultrasound.
Mature cystic teratoma (dermoid). The most common ovarian neoplasm in young women, containing all three germ layers—skin, hair, sebaceous material, teeth, and fat; about 10–15% are bilateral. Ultrasound shows an echogenic Rokitansky nodule, a fat-fluid level, hair lines, and shadowing calcifications; CT shows fat density. Torsion is the most common complication; rupture (chemical peritonitis) and squamous cell carcinoma in older women are rare. Struma ovarii (thyroid tissue) can cause hyperthyroidism, and neural tissue can trigger anti-NMDA receptor encephalitis. Treatment is ovarian cystectomy with preservation of the ovary.
Endometrioma. Ovarian endometriosis produces a "chocolate cyst" of old blood with homogeneous, low-level ("ground-glass") echoes and no internal flow. Patients report dysmenorrhea, dyspareunia, or infertility, and CA-125 is often mildly elevated. Options are hormonal suppression or laparoscopic cystectomy, performed carefully to protect ovarian reserve. Endometriosis slightly raises the risk of clear cell and endometrioid carcinoma.
Epithelial cystadenomas. Serous cystadenomas are thin-walled and often bilateral; mucinous cystadenomas are multiloculated and can grow very large.
Torsion. A mass acts as a lead point, especially dermoids and masses in children. Sudden unilateral pain with nausea and vomiting calls for urgent laparoscopy; normal Doppler flow does not exclude torsion. Detorsion with ovarian preservation is standard even when the ovary looks dusky or black—most recover.
Germ cell tumors
These arise in girls and young women, grow quickly, and are usually unilateral. Serum markers support the diagnosis and track treatment.
| Tumor | Marker | Histology and features |
|---|---|---|
| Mature cystic teratoma | None | Benign; all three germ layers; torsion |
| Dysgerminoma | LDH (± hCG) | Most common malignant germ cell tumor; fried-egg cells with lymphocytes; bilateral in ~10–15%; very chemo- and radiosensitive |
| Yolk sac tumor | AFP | Schiller-Duval (glomerulus-like) bodies; aggressive; young girls |
| Choriocarcinoma | β-hCG | Syncytio- and cytotrophoblast without villi; early hematogenous (lung) spread; can cause precocious puberty |
| Immature teratoma | ± AFP | Immature neuroectoderm; graded by amount of neural tissue |
Dysgenetic gonads. Dysgerminoma is the ovarian counterpart of testicular seminoma and arises in dysgenetic gonads that contain a Y chromosome (Swyer syndrome, 46,XY; Turner mosaicism with Y material), often through a gonadoblastoma—so these gonads are removed prophylactically.
Treatment. Fertility-sparing unilateral salpingo-oophorectomy with surgical staging preserves the uterus and contralateral ovary. Stage IA dysgerminoma and low-grade stage IA immature teratoma may need surgery alone; most others receive bleomycin, etoposide, and cisplatin (BEP), with high cure rates. Bleomycin causes pulmonary fibrosis and cisplatin causes nephrotoxicity and ototoxicity. The relevant marker is followed for recurrence.
Sex cord–stromal tumors
These tumors often announce themselves through hormones.
| Tumor | Hormone / marker | Clinical picture |
|---|---|---|
| Granulosa cell (adult) | Estrogen; inhibin | Peri- or postmenopausal bleeding, breast tenderness, endometrial hyperplasia or cancer; Call-Exner bodies, coffee-bean nuclei; late recurrence |
| Granulosa cell (juvenile) | Estrogen; inhibin | Isosexual precocious puberty in girls |
| Sertoli-Leydig cell | Testosterone | Young women; rapid virilization, oligo/amenorrhea; Reinke crystals may be seen |
| Fibroma | None | Benign solid tumor of older women; Meigs syndrome |
Granulosa cell tumor. Unopposed estrogen makes endometrial sampling mandatory. The juvenile form causes GnRH-independent precocious puberty with suppressed LH and FSH.
Sertoli-Leydig cell tumor. Months of hirsutism, clitoromegaly, deepening voice, and temporal balding with a testosterone level above about 200 ng/dL and a normal DHEA-S (an adrenal source would raise DHEA-S). Treatment is unilateral salpingo-oophorectomy.
Meigs syndrome. An ovarian fibroma with ascites and a (usually right-sided) pleural effusion that resolve once the tumor is removed—a benign mimic of metastatic cancer. Bilateral calcified fibromas in a young woman suggest Gorlin (nevoid basal cell carcinoma) syndrome.
Epithelial ovarian cancer
Biology and risk. Epithelial tumors account for about 90% of ovarian cancers. High-grade serous carcinoma, the most common subtype, often begins in the fallopian tube fimbria and shows psammoma bodies; endometrioid and clear cell types are linked to endometriosis. Risk factors: older age, BRCA1 (~40% lifetime risk) and BRCA2 (~15–20%) mutations, Lynch syndrome, nulliparity, infertility, and endometriosis. Anything that reduces ovulation or tubal exposure protects: combined OCPs, pregnancy, breastfeeding, and tubal ligation or salpingectomy.
Presentation. Symptoms are vague and easily dismissed: bloating, early satiety, pelvic or abdominal pain, and urinary urgency. Signs include ascites, omental caking, and a fixed, nodular pelvic mass. About 75% are diagnosed at stage III–IV because cells spread across the peritoneum early. Bilateral ovarian masses of signet-ring cells (Krukenberg tumor) are metastases, usually from the stomach.
- Image and marktransvaginal ultrasound, CA-125, CT of chest, abdomen, and pelvis
- Refergynecologic oncologist for surgical staging
- Cytoreductionhysterectomy, bilateral salpingo-oophorectomy, omentectomy, peritoneal biopsies, node assessment; goal is no gross residual disease
- Chemotherapycarboplatin plus paclitaxel for 6 cycles; neoadjuvant chemotherapy with interval debulking if disease is unresectable or the patient is frail
- MaintenancePARP inhibitor (olaparib, niraparib), especially with BRCA mutation or homologous-recombination deficiency; ± bevacizumab
- Surveillanceexam and CA-125 trend
PARP inhibitors. Blocking poly(ADP-ribose) polymerase prevents repair of single-strand DNA breaks, which become double-strand breaks that homologous-recombination-deficient (BRCA-mutated) cells cannot fix—synthetic lethality. Every woman with epithelial ovarian cancer should be offered germline genetic testing, regardless of family history.
Screening and prevention. Average-risk women should not be screened: CA-125 and transvaginal ultrasound do not lower mortality and lead to unnecessary surgery. BRCA1 carriers should have risk-reducing salpingo-oophorectomy at 35–40 after childbearing, and BRCA2 carriers at 40–45 (their cancers arise later); this lowers ovarian and tubal cancer risk by about 80%. Lynch syndrome carriers are offered hysterectomy with salpingo-oophorectomy after childbearing. Opportunistic salpingectomy at hysterectomy or sterilization reduces risk in average-risk women.