Adnexa = ovaries, fallopian tubes, broad ligament, ovarian and uterine vessels. Fallopian tubes not seen unless enlarged; broad ligament seen when outlined by fluid.
Ovaries ~40x30x20mm, maximum of 40mm in any direction; 6-10mL menstruating and 3-6mL postmenopausal (length x width x height x 0.5), but can be up to 20mL (esp during pregnancy) depending on follicles. Outer cortex with stromal cells, follicles and connective tissue; inner medulla is loose mesenchymal tissue with remnant mesonephric duct and clusters of epithelioid/hilus cells. Usually in shallow ovarian fossa (betw external iliac vessels anteriolaterally, ureter and internal iliac posteriorly, fallopian tubes draped over/around), if displaced by uterus (dextro/levo-version, fibroids, pregnancy) then usually deviated superolaterally, occasionally into cul-de-sac and may remain there.
- Post menstruation ovaries are smallest with follicles <5mm
- Oestrogen phase follicles grow to 10-15mm with dominant graafian follicle (up to 20-25mm midcycle, contains small echogenic cumulus oophorus soft tissue/cyst with ovum) appearing by day 10 and most other follicles starting to regress.
- Ovulation with luteinising hormone surge at mid-cycle -> rupture -> corpus luteum (recent -> senescent corpura albicans), fluid pooling in cul-de-sac, remaining follicles involute in progesterone phase.
- Postmenopausal ovaries are atrophic, lack follicles, difficult to see, volume 8mL (40-44yo) -> 1mL (70yo); max 6mL, abnormal if one is twice the size of the other. Focal calcifications in otherwise normal ovaries are common and benign. T2 of cortex darker than medulla, follicles high T2/low T1.
Absent/streak ovary – absence of a second X chromosome (45XO, 46XY) from dysgenetic testis (gonadal dysgenesis). Increased risk of gonadoblastoma, seminoma/dysgerminoma.
Non-Neoplastic and Functional Ovarian Cysts
Functional/physiological ovarian cysts are low T1, high T2, uniform thin dark T2 wall (which may enhance). Physiological ovarian follicles are <40mm and should regress by beginning of next cycle; pathological follicular cysts are >40mm from excessive accumulation of fluid or internal haemorrhage from failure to regress.
- Corpus luteal cyst – 15-20mm, uni/bi-lateral, ring-of-fire on colour Doppler.
- Theca letual cysts – from excessive HCG (GTD, twin pregnancy) or IVF.
- Simple cysts – anechoic, no wall thickening or internal echoes, good distal acousting enhancement. Follicle cysts are from unruptured or ruptured and immediately sealed graafian follicle. May rupture or undergo torsion. Round, smooth usually unilocular, resolve on follow-up after 1-2 cycles. Premepausal follow up if >40mm; postmenopausal if >30mm. If a simple cyst persists, it is considered nonfunctioning (not under hormonal influence), if <60mm is almost always benign, but should be followed to confirm stability; if >60mm may represent cystic neoplasm or endometrioma.
- Complex cysts – irregular, thickened walls, internal echoes or septations with maintaned acoustic enhancement (otherwise is most likely solid). May represent haemorrhagic cyst (functioning or nonfunctioning), endometrioma, dermoid, ovarian torsion, abscess, pyosalpinx/hydrosalpinx, cystic neoplasm.
- Haemorrhagic ovarian cyst – bleed into corpus luteum or other follicle. Cystic mass measuring up to 150mm with internal echoes (depending on state of haemorrahge), maintain good through-transmission, variable wall thickness (2-20mm), blood flow in wall common, may appear solid but no internal blood vessels on colour Doppler, clots may adhere to wall mimicing neoplasia (but lacking flow), weblike lacy internal echoes (cobweb-like) characteristic. Variable MR signal depending on age of blood (methaemoglobin, RBC lysis). Should completely resolve within 2 cycles (8-10 weeks).
- Postmenopausal cysts – in 15-20%, being benign serous inclusions cysts. Small <50mm, smooth uniform thin walls <3mm, anechoic contents, absence of septations nodules or soft tissue component. May remain stable, regress or disappear, some develop new cysts.
- Broad ligament (paraovarian) cysts – Wolffian duct remanants. Cystic lesion separate to ovary.
Polycystic Ovary Syndrome (PCOS)
(PCO disease PCOD, previously Stein-Leventhal syndrome SLS). 3-6% of women of reproductive age. Clinical diagnosis of hirsutism, amenorrhoea, infertility and obesity. Failure of follicles to mature. Rotterdam 2003 criteria for PCOS include 2 out of 3 of: oligo/an-ovulation, hyperandrogenism and polycystic ovary (PCO). PCO must ”’>/=12 follicles 2-9mm in one slice and/or ovarian volume >10mL”’; but no cyst > 10mm or corpus luteum; may or may not be associated with PCOS. 70% bilateral, follicles just under the capsule (”’string of pearls”’), echogenic stroma (innumerable follicle cysts from follicular hyperthecosis/hyperplasia. In 30% of PCOS ovary appears completely normal. DDx anovulatory menstrual cycles esp COCP, young female athletes, but lacks clinical features.
Stroma hyperthecosis (cortical stromal hyperplasia) – mostly postmenopausal women, associated with earlier PCOS. Uniformly enlarged ovary (up to 70mm) with hypercellular stroma. Similar clinical presentation as PCOS, virilisation usually worse.
Ovarian Hyperstimulation Syndrome (OHS)
Fertility meds eg clomiphine for maturation of multiple follicles up to 20mm. US used to identify and measure these; if they are of appropriate size then luteinising hormone is given or cyst aspiration for harvesting. Ovarian hyperstimulation syndrome (OHS) is overstimulation causing bilateral ovarian enlargement with follicles being easily palpable, may be >200mm. Increased capillary permeability causing 3rd spacing with ascites and pleural effusions. When no identifiable ovarian tissue remains, LH or pregnancy induction should be avoided until ovaries revert to normal. May also be seen in GTD, multiple pregnancies.
Infection and Inflammation
Pelvic collections are usually round/oval cf bladder triangular on sagittal (posterior indentation from uterus), can be confirmed with lack of emptying with micturition.
Aberrant endometrial glands and/or stroma outside the uterus (in tiny deposits, sheets or focal masses), 20s/30s with infertility, dysmenorrhoea, dyspaereunia. Responds to hormonal stimulation -> recurrent bleeding, inflamamtion, fibrosis.Metastatic theory (most likely) – retrograde menstruation; metaplastic theory – primitive coelemic epithelium differentiates into endometrium. There is profound inflammation and also oestrogen production by the implants. Tiny 1-2mm peritoneal implants usually not seen on imaging. In descending order implants occur on ovaries, uterine ligaments, rectovaginal septum, cul-de-sac, pelvic peritoneium, small/large bowel and appendix, mucosa of cervix/vagina/fallopain tubes, laparotomy scars. Endometriomas (‘chocolate cyst’) – large deposits -> cystic masses with old echogenic blood (diffuse low-level homogeneous internal echoes in ground glass appearance, rarely anechoic), single or multiple and usually bilateral, echogenic foci in wall of echogenic cyst is characteristic, blood products of various age but characteristically high T1 low T2 (‘T2 shading sign’), low signal wall (fibrous tissue or haemosiderin), does not resolve within 2/12 (cf haemorhagic cyst). Generally the more ovoid/irregular shape, unusual/varied echogenicity the more likely it is an endometrioma. Adhesions are common, hydrosalpinx in 30%. DDx PID. Increased risk of endometrial adenocarcinoma.
Pelvic Inflammatory Disease (PID)
Acute or chronic inflammation of tubes (always affected), ovaries and pelvic peritoneum, usually teenager or 20s. Pain, fever and vaginal discharge. From gonococcus, chlamydia, anaerobic bacteria, Tb. Complex ill-defined adnexal mass, swollen ovary, adhesions to adjacent structures, fluid in cul-de-sac, parametrial and paraovarian stranding, margins of pelvic structures become ill-defined. DDx endometriosis. Risk of recurrent infection and ectopic pregnancy significantly increased, heterotopic pregnancies as high as 1/4,000. Peritonitis and bacteraemia, may spread to endocarditis, meningitis, septic arthritis.
- Myometritis – Tx medical.
- Acute suppurative salpingitis – congested tubal mucosa with inflammatory infiltration.
- Pyosalpinx – Thickwalled hydrosalpinx containing complex fluid with internal echoes, occasionally with fluid-debris level.
- Salpingo-oophoritis – Spillage of infection to ovaries.
- Tubo-ovarian abscess – Thick-walled fluid-filled adnexal mass incorporating ovary and dilated fallopian tube. Occaional gas bubbles (highly indicative of abscess). Tx surgery.
- Fitz-Hugh-Curtis syndrome – Perihepatic inflammation occasionally seen with gonorrhea, hypoechoic rim between liver and adjacent ribs.
- Chronic follicular salpingitis – Sequalae of infection with denuded epithelium forming adhesions and scarring, blind pouches. May cause hydrosalpinx, infertility.
- Tubuerculous salpingitis – Rare
Hydrosalpinx – From occlusion (ampullary ± interstitial portions) by sequalae of infection (most common), surgery or endometriosis. Thin or thick-walled tubular mass, elongated and folded on itself, may simulate septa from ovarian tumour, sausage/C/S-shaped. Fluid is commonly echogenic. Normal tubes are not usually seen (but occasionally thin 5mm soft tssue band from uterine fundus can be seen on axial-coronal).
Peritoneal Inclusion Cysts
Common inflammatory cysts of peritoneal cavity from adhesions enveloping the ovary. Diseased peritoneum is unable to absorb fluid, so secretions from active ovary are confined by the adhesions -> expanding cystic mass, pain. Most have Hx of pelvic surgery, infection, trauma or endometriosis. Complex fluid collection in pelvic recesses, angulated boundaries, containing ovary ± septations, loculations, particulate matter.
20% malignant, 2/3 cystic, 25% bilateral (hence always look at the other ovary). 20-45yo tend to be benign; 45-65yo malignant. Insidious onset, silent growth with advanced disease at presentation in 70% with poor prognosis. CA-125 elevated in 80%, but only in 25-50% of stage I; useful for follow-up.
Signs of malignancy include solidity (solid increases risk: walls >3mm, multiple septations, thick septations, irregular wall thickness, papillary projections or mural nodules, poor transmission of sound), size >100mm (<50mm likely benign), enlarged or change in size of ovaries (>20mL), blood vessels within papillary projections or septations (flow in wall may be benign), increased age, extension outside ovary (to uterus, broad ligament etc), ascites, metastases (peritoneal implants, omental cake, LNs). No imaging is reliable to differentiate between benign and malignant disease. Spread is primarily by peritoneal seeding with nodules on peritoneum, mesentery, omentum, ascites. Secondary spread includes direct extension to adjacent structures, lymph nodes, late haematogenous to lung, liver or bone. On ultrasound should always check for ascites, liver metastases, hydronephrosis (ureteric obstruction), other ovary.
Colour Dopper of small aa centrally suggests malignancy. Cancers also tend to have lower-resistence Dopper with RI <0.4 (DDx inflammatory masses, trophoblastic tissue from ectopic) due to neovascularity. An early diastolic notch indicates arterial rebound hence normal smooth muscle wall and benignity. In 1st 7 days of cycle ovaries have greatest vascular resistance, resistive index reducing later in the cycle, esp dominant ovary. Hence, if low RI then repeat in 1st week of cycle.
Ovarian cancer staging usually by laparotomy; initial radiographic staging only for clearly advanced disease.
- Stage I – limited to ovaries. Ia to one ovary; Ib to both ovaries; Ic malignant ascites or peritoneal washings.
- Stage II – pelvic extension. IIa uterus and/or fallopian tubes; IIb other pelvic tissues; IIc with malignant ascites or peritoneal washings.
- Stage III – peritoneal extension outside pelvis or LN. IIIa microscopic peritoneal metastases outside pelvis; IIIb macroscopic <20mm; IIIc >20mm and/or regional LN.
- Stage IV – distant metastases.
Epithelial Tumours (65-70%)
From epithelial covering of ovary ?derived from inclusion cysts of coelomic epithelium which otherwise normally differentiate into serous (tubal), endometrioid (endometrium) and mucinous (cervical) epithelia. Most are cystic masses, benign/malignant differentiation sometimes difficult. Commonly bilateral, esp if malignant. May be mixed tumours.
- Serous cystadenoma and cystadenocarcinoma (serous adenocarcinoma) – 30% of ovarian tumours. 60% are benign cystadenomas, 15% borderline, 25% malignant cystadenocarcinoma. Increased risk with low or nulliparity, FHx, BRCA1/2; reduced risk with OCP or tubal ligation. Tends to be superficial. Cystadenomas are thin-walled, usually unilocular, anechoic fluid, 20% bilateral. Cystadenocarcinomas are multiloculated, thick walled, thick septa, papillary projections (may be echogenic), blood flow in septa and papilla, 66% bilateral.
- Mucinous cystadenoma and cystadenocarcinoma (mucinous adenocarcinoma) – 20% of ovarian tumours. 80% are benign cystadenomas, 10% borderline, 10% malignant. Increased risk with smoking. Don’t tend to involve the surface, only 5% are bilateral (hence if bilateral must look for non-ovarian origin). Larger cysts which may be huge, filling pelvis extending into abdomen. Most have multiple septations, echogenic fluid (mucin). Rupture -> mucin-secreting cells through peritoneum, may -> pseudomyxoma peritonei (most are actually ruptured appendiceal mucinous tumours with secondary ovarian spread).
- Endometrioid adenocarcinoma – Almost all malignant, 20% of all ovarian cancers. 15-20% also have endometriosis, 15-30% have concurrent endometrial carcinoma (second primary rather than metastasis). 40% are bilateral, usually implying extension beyond the genital tract. Most are cystic masses with papillary projections.
- Clear cell adenocarcinoma – Almost all malignant. Occasionally associated with endometriosis or endometrioid ovarian carcinoma. Solid or cystic. Typically unilocular cyst with mural nodule. Associated with DVT.
- Cystadenofibroma – Variant with more pronounced fibrous stroma proliferation. Benign, usually small, multilocular. May have mucinous, serous, endometrioid or transitional/Brenner epithelium.
- Brenner tumour – Adenofibromas in which the epitheium is transitional cell resembling urothelium. Solid or cystic, only 10% bilateral. Most are benign, solid.
- Undifferentiated epithelial tumour (malignant mixed mullerian tumour, MMMT) – Aggressive, ill-defined, cystic or solid.
Germ Cell Tumors (15-20%)
Derived from germ cells that migrate to the ovary from the yolk sac, are pluripotent. Most are benign cystic teratomas.
- Mature/benign cystic teratoma (dermoid cyst) – Benign, present from birth but slow growing and usually detected 10-30yo, most incidental asymptomatic. May be associated with paraneoplastic syndromes eg inflammatory limbic encephalitis. Bilateral in 10-15%. Predominantly cystic, complex with mature endoderm, mesoderm and ectodermal elements, varied appearance. Cystic mass with complex fluid, usually unilocular, fluid-fluid level (fatty sebum floating on liquid). Rokitansky/mural nodule (dermoid plug) – echogenic rounded area within a hypoechoic mass; containing hair, teeth, bone and/or cartilage. ‘Tip of the iceberg’ appearance with echogenic mass fading into acoustic shadowing (sound absorption from multiple internal interfaces). Multiple fine echogenic strands (hair) in cyst. Non-dependent fat (diagnostic) confirmed on MR in-and-out-of-phase GRE or fat sat. Rarely might be almost completely anechoic, esp adolescents. 1% undergo malignant transformation (most SCC, others thyroid carcinoma, melanoma). Occasionally are incorporated within the wall of a mucinous cystadenoma.
- Monodermal/specialised teratoma – Rare, always unilateral. Most are struma ovarii (thyroid tissue, may cause hyperthyroidism) or carcinoid (unilateral cf bilateral in almost all mets).
- Immature/malignant teratoma – Rare, tissue resembles embryonal/fetal tissue (cf benign teratomas). Most young adolescents. Rapid growth, may have immature neuroepithelium, cartilage, bone, muscle.
- Dysgerminoma – Similar to testicular seminoma. Young females, may be associated with gonadal dysgenesis (eg pseudohermaphroditism). Usually unilateral, small nodule to massive, soft and fleshy. All are malignant, but only 1/3 aggressive hence excellent prognosis if hasn’t breached the ovarian capsule, good response to chemotherapy.
- Yolk sac tumour (endodermal sinus tumour) – Rare, mostly children or young females. Produces α-fetoprotein and α1-antitrypsin. Histological glomerulus-like structures with central vessels (Schiller-Duval bodies). Rapid aggressive growth.
- Choriocarcinoma – Almost all coexist with other germ cell tumours. Aggressive, usually has metastasized to lungs, liver, bone etc. Hgih HCG. Usually unresposive to chemotherapy and are fatal (cf placental choriocarcinomas).
- Mixed germ cell tumours
Sex Cord Stromal Tumours (5-10%)
Arise from endocrine apparatus of the postnatal ovarian stroma. Solid hypoechoic mass often causing striking sound attenuation. May be masculinising or feminising depending on released oestrogens/androgens. DDx pedunculated leiomyomas (these have vascular connection to uterus).
- Granulosa-theca cell tumour – Varying proportions of granulosa and theca cell differentiation. 2/3 discovered postmenopausal. Hormonally active tumours are yellow due to intraceuular lipid. Granulosa cells may secrete large amounts of oestrogen causing precocious puberty (juvenile granulosa cell tumours), endometrial hyperplasia, cystic disease of the breast, endometrial carcinoma (in 10-15%). Occasionoally secretes androgens causing masculinization. 5-25% of granulosa cell tumours are malignant.
- Gonadal stromal tumours – Contain fibrobasts (fibromas, most), plump spindle cells with lipid droplets (thecomas) or both (fibromathecomas). Solid masses, most benign. Well-defined ovarian mass low T1/low T2. Scattered high T2 (focal oedema/cystic change).
- Fibromas (most) – Usually unilateral, hard mass. 40% associated with ascites, may also cause pleural effusions (usually right). Meigs syndrome – ovarian tumour, hydrothorax, ascites. May be associated with basal cell nevus syndrome.
- Thecoma – Pure thecomas are rare, produce oestrogen. Contains lipid.
- Sertoli-Leydig cell tumour (androblastoma) – Unilateral, malignant in 10-20%. Most cause masculinisation or defeminisation, may block normal female sexual development in children.
Metastases to the Ovary (5%)
Most common site of metastases to the pelvis. Commonly GI and breast primaries. Krukenberg tumour – metastasis from mucin-producing tumour of GIT (most gastric). Most metastases are bilateral. Stomach, biliary tract, gallbladder, and pancreatic metastases tend to be solid; rectosigmoid metastases tend to be cystic.
Carcinoma of the Fallopian Tube
Rare malignant adnexal mass.
Axial rotation of ovary and/or tube around vascular pedicle causing arterial occlusion and venous stasis. Contralateral torsion in 10%. Ovary enlarged from oedema, haemorrhage, often necrotic, central echogenic stroma. May have cyst or mass lead point. Torsion very unlikely when ovary is of normal size and echogenicity. Fallopian tube torsion has complex appearance, amorphous mass or tube with thick walls. Uterine deviation towards torsed adnexa. Free fluid in cul-de-sac. Doppler flow not reliable (normal variations in adnexal flow, intermittent torsion common -> hyperaemia), but reduced/absent flow is suggestive. Central venous flow indicates ovarian viability. Haemorrhagic infarction -> marked wall thickening >10mm, haemorrhage in the mass and twisted tube, haemoperitoneum. DDx complex ovarian mass.
Pelvic Congestion Syndrome
Chronic abdominal/pelvic pain, esp multiparous pre-menopausal. Prevalence up to 10%. From proximal venous obstruction eg retroaortic left renal vein, compression of left renal vein by SMA or right iliac vein, incompentent valves in the ovarian vein. Tx coil embolisation.
Ovarian Vein Thrombosis
(Puerperal/post-partum ovarian vein thrombosis, POVT/PPOVT). Most postpartum, may cause PE. Usually acute pelvic pain, may have fever. 80-90% involves right ovarian vein.