Position best seen with empty-bladder (distended bladder may compress and distort); may be ante- or retro-verted (depending on orientation of cervix); ante- or retro-flexed (folding at the body, retroflexed may mimic fundal fibroid); midline or tilted to the right or left. Physiological changes:
- Neonatal uterus affected by maternal hormones for several weeks, with prominent fundus.
- Prepubertal uterus cigar-shaped, cervix ~2/3 of uterus length.
- Postpubertal uterus smooth, pear-shaped (max 90x60x40 CC/lat/AP, larger in multiparous women), cervix ~1/3 of length, uniform mid-echogenic myometrium, thin hypoechoic junctional zone (innermost myometrium or myometrial-endometrial boundary), echogenic endometrium (endometrial stripe/complex, thickness is added anterior and posterior layers excluding cavity fluid/blood). Serosal surface may have prominent anechoic subserosal veins (normal variant, more commonly multiparous). Endometrium has basal (adjacent to myometrium) and functional (thickens then sloughs) layers. Proliferative/oestrogen phase endometrial thickness 4-8mm (thicker with lengthened phase). May have striated triple-layer/trilaminated appearance with three hyperechoic lines at mid cycle, signifying when endometrium most receptive to implantation. Secretory/progesterone phase after ovulation progressively thickens up to 15mm, more uniformly echogenic but less defined. With menses endometrium sloughs with stripe thinning out. At at end of menstruation it is discrete and thin (2-4mm). Endometrium high T2, junctional zone low T2 (low water content), bulk of myometrium intermediate T2; all of uterus low T1. The cervical central zone (epithelium and endocervical canal) is of high T2, cervical stroma wide band of low T2 (fibrous tissue), outermost stroma is thin intermediate T2 (smooth muscle).
- Postmenopause (>1yr after cessation of menses, ~55yo) uterus is ~ 60x20x20mm, gradually atrophies over 15-20yrs to prepubertal size. Endometrial atrophy to uniformly thin double-layer echogenic <5mm; most common cause of postmenopausal bleeding. Endometrium may thicken by 1-2mm with HRT. Tamoxifen-induced changes via oestrogenic effect may cause cystic endometrial hyperplasia (may extend into subendometrial region) with increased risk for endometrial carcinoma, difficult to destinguish between on US hence may need biopsy.
Abnormal PV bleeding doesn’t require biopsy if endometrial thickness is normal (most likely from endometrial atrophy if postmenopausal). Dysfunctional uterine bleeding (DUB) is bleeding not caused by any organic/structural abnormality; includes anovulatory cycle, ovulatory dysfunctional bleeding (eg inadequate luteal phase), irregular shedding. Postmenopausal bleeding (PMB) with endometrial thickness (ET) >5mm is high risk, requiring biopsy or SHG; may be caused by endometrial/glandular hyperplasia, carcinoma, polyps, endometritis, tamoxifen therapy, incomplete abortion, metastatic carcinoma, submucosal leiomyoma or pregnancy.
Endometrial cavity fluid may be blood (haematometra of uterus, haematocolpos of vagina, haematometrocolpos of both), mucous or pus (pyometros). Premenstrual fluid is usually obstruction from imperforate hymen, vaginal septum, or vaginal/cervical atresia. Later it may be due to cervical stenosis/PID, instrumentation, radiation, carcinoma (cervical or endometrial), menorrhagia, endometrial polyps, pyometrium or pregnancy/RPOC. It is a never normal finding if postmenopausal, is usually from cervical stenosis or obstructing tumour (eg endometrial or cervical). Collections can become infected (pyometra); if untreated can cause sepsis, uterine rupture.
Mullerian Duct Fusion Anomalies
Paired mullerian ducts form the uterus, cervix and fallopian tubes. Anomalies are associated with urinary tract abnormalities in 20-50%.
- Uterus didelphys – 2 uteri, 2 cervices, 2 vaginas.
- Bicornuate uterus – 2 uterine horns, 1 (unicollis) or 2 (bicollis) cervices, 1 vagina.
- Arcuate/septate uterus – Midline septum dividing into 2 cavities, no surface indentations at the fundus (cf bicornuate).
- Uterine agenesis – Arrested development -> uterine aplasia or unicornuate uterus with single fallopian tube (associated with unilateral renal agenesis in 5-20%).
- Bartholin cyst – Obstructed Bartholin glands (post-lat to vaginal opening), up to 30-50mm, may become infected. Tx excision or marsupialization.
- Gartner duct cysts – Along lateral walls of vagina, derived from wolffian/mesonephric duct rests. 10-20mm submucosal cysts.
- Nabothian cysts – Obstruction of ducts of mucous-secretic glands lining cervix causing retention cysts. Anechoic, often multiple, 2-40mm.
- Paratubal cysts – 1-20mm cysts along the fallopian tube ?remnants of the mullerian duct and of no significance. Large cysts near the fibria are termed hydatids of Morgagni.
- Subendometrial cysts – from adenomyosis or tamoxifen related change (cystic thickened irregular endometrium).
Remnant endocervical type columnar epithelium in the upper vagina, persisting as red granular areas.
Endometrial abnormalities are rare prepubertal. Hydrocolpos (vaginal) or hydrometrocolpos (vaginal and uterine) from mucosal secretions and fluid or blood (at time of menses), from vaginal atresia, vaginal septum or imperforate hymen.
Inflammation and Infection
At menarche oestrogen stimulates cervical and vaginal squamous mucosa to form intracellular glycogen vacuoles; shedding of these cells provide a rich substrate for aerobic and anaerobic microbes. Normal vaginal and cervical flora is dominated by lactobacilli, producing lactic acid and hydrogen peroxide maintaining a pH <4.5 suppressing pathogenic organisms. Alkaline pH from bleeding, sexual intercourse, vaginal douching, antibiotics allow overgrowth of other organisms causing cervicitis/vaginitis. Infection with Candida, Trichomonas and Gardnerella are extremely common; may cause discomfort but no serious sequalae. Infections with gonococci, chalmydia, mycoplasma, or HSV may cause significant disease.
- Candida – Normal vaginal microflora. Symptomatic disease occurs with disturbance in normal vaginal microbial ecosystem with diabetes, antibiotics, pregnancy, cell-mediated immunocompromise.
- Trichomonas vaginalis – Protazoa causing vaginal and cervical mucosal infection with frothy yellow vaginal discharge.
- Gardnerella vaginalis – Gram-positive bacillus, most common cause of vaginitis. May cause premature labour.
- Chlamydia trachomatis – Most cause cervicitis, but may ascend to cause endometritis, salpingitis
- Genital HSV (generally HSV2) – Very common (20% by 40yo) with symptoms in 1/3. Vesicles then coalescent ulcers over vulva, vagina, cervix.
- Molluscum contagiosum (MSV) – Poxvirus infection of skin and mucous membranes over genitals, lower abdomen, buttocks, inner thighs with papules; esp 2-12yo
- Mycoplasma hominisand Ureaplasma urelyticum – Vaginitis and cervicitis, may cause chorioamniotis and premature delivery.
Uncommon. Acute endometritis is usually bacterial infection (haemolytic strep, staph) after birth or miscarriange, esp RPOC. Chronic endometritis occurs with chronic PID, RPOC, IUCD or TB (esp TB salpingitis).
Asherrman’s syndrome (uterine synechiae/adhesions) – trauma to the basal layer of endometrium with subsequent scarring, from previous pregnancy, D&C/instrumentation, surgery, infection. May cause infertility, pregnancy loss, menstraum abnormalities, pain. Irregular linear filling defects are usually hyperechoic, low T2. Resists endometrial cavity distention.
Ectopic benign endometrial glands and stroma within the myometrium (‘internal endometriosis’). Common in multiparous women >30yo. Dysmenorrhoea or menorrhagia. Best seen on MRI, not usually seen on CT, US commonly subtle/nonspecific.
- Diffuse (most common) – Islands of endometium scattered throughout with abnormal hypoechoic or heterogeneous myometrial echotexture, poorly defined/nodular endometrial-myometrial junction with regular/irregular ‘moth-eaten’ myometrial thickening >12mm, subendometrial echogenic nodules, myometrial or subendometrial cysts (1-5mm), hypoechoic linear striations, Venetian blind shadowing, uterus usually enlarged.
- Adnomyoma – Focal/localised within the myometrium with low T2 mass (but less mass effect than fibroid), occasionally high T1 haemorrhage, poorly defined (cf leiomyomas), no large peripheral vessel (cf fibroid).
Small inflammatory mass at the external urethral meatus, typically older females. Extremely friable.
Benign exophytic growths present in 2-5%, composed of loose fibromyxomatous stroma and mucus-secreting endocervical glands. May cause irregular PV spotting/bleeding. Most are in the endocervical canal, up to 50mm protruding through the os.
Most common 30-60yo. May cause PV bleeding if ulcerates or necrosis. Hyperplastic polyps are asscosiated with endometrial hyperplasia; atrophic polyps (mostly postmenopausal) are probably atrophic hyperplastic polyps. Increased risk with tamoxifen. Malignant transformation in 1-4%. Multiple in ~20%. Focal echogenic polypoid mass or diffuse endometrial thickening, may see a feeding vessel. Saline sonohystereography (SHG) may demonstrate polypoid nature.
Proliferation of endometrial glands with increased gland-to-stroma ratio. Unopposed/prolonged oestogren stimulation from anovulation, endogenous production or exogenous oestrogen; incresaed risk with obesity, menopause, PCOS, functioning granulosa cell ovarian tumours, cortical stromal hyperplasia, prolonged oestrogen replacement therapy. Thickened, heterogeneous endometrium, small cysts common. Biopsy required to distinguish from carcinoma.
- Simple hyperplasia without atypia (cystic/mild hyperplasia) – Glands of various sizes and shapes with cystic dilatation. 1% progress to adenocarcinoma. May lead to cystic atrophy when oestrogen is withdrawan.
- Simple hyperplasia with atypia – Uncommon, more rounded cells. 8% progress to carcinoma.
- Complex hyperplasia without atypia – Increased number and size of glands with marked crowding. 3% progress to carcinoma.
- Complex hyperplasia with atypia – Similar to low-grade endometrioid carcinoma, with 25% progressing to this. Tx hysterectomy.
(Fibroid). Benign smooth muscle tumour (with some fibrous tissue) of the myometrium with a whorled grey-white appearance; large tumours have red softening/degeneration. 50% of women of reproductive age. More common in African-Americans, older women. Most asymptomatic, may cause excessive bleeding, pain, mass symptoms, infertility. Most multiple. Continue to grow, accelerated with hormones esp pregnancy; involute with menopause. Intramural (most), subserosal or submucosal (beneath endometrium, prone to ulcerate -> severe menorrhagia). May be pedunculated (may appear adnexal), predominantly extrauterine, may torse. Vascular supply contiguous with myometrium. Typically hypoechoic and heterogeneous, but can be any echogenicity. Acousting shadowing due to solid mass. Distorts uterine contour and junctional zone. Best seen on T2WI being low T1/T2, discrete rim of low signal. CT hypo/iso/hyper-dense. May undergo atrophy, internal haemorrahge, cystic degeneration, fibrosis or calcification (‘popcorn’ with dense, clumped, coalescing being characteristic). Less fibrous component equates to increased enhancement. Unable to be distinguished from the rare leiomyosarcoma. Ovaries may be difficult to identify as they may be displaced or represent a pedunculated fibroid. May have low-resistance arterial weveforms mimicing some ovarian tumours.
Extramammary Paget Disease
Rare lesion of vulva, occasionally perianal. Similar to Paget disease of the breast. Red, crusty, sharply demarcated geographic region on labia majora. Intraepithelial malignancy confined to the epidermis and skin appendages. May persist for years/decades before rare deeper invasion/mets.
Uncommon, most are SCC. Types include:
- Basaloid/warty carcinomas (30%) – Develop from classic vulvar intraepithelial neoplasia (classic VIN, previously CIS, Bowen disease). From HPV infection (most HPV16), similar risk factors as cerical cancer.
- Keratinizing SCC (70%) – Not related to HPV. Usually arising from chronic lichen sclerosis or squmous cell hyperplasia (white plaque lesions of unkown aetiology). Mean 76yo. Premalignant lesion is differentiated VIN (VIN simplex).
Invasive cancer spreads to LN (inguinal, pelvic, iliac, periaortic), metastases to lungs, liver etc.
Rare, almost all SCC arising from vaginal intraepithelial neoplasia (VIN) due to HPV. Most in upper posterior vagina esp along junction with ectocervix. Lower 2/3 lesions spread to inguinal nodes; upper 1/3 spread to iliac nodes.
(Sarcoma botryoides). Uncommon vaginal tumour in <5yo. Grapelike clusters of polypoid, rounded, bulky masses occasionally projecting out of vagina. Spread into peritoneeal cavity, may cause urinary obstruction. Tx conservative surgery and chemotherapy.
Most common non-invasive gynaecologic malignancy. Peak age 45yo. Almost all develop from high oncogenic risk HPV (esp 16 and 18), increased risk with multiple sexual partners, male partner with current/previous partners, young age at first intercourse, high parity, immunosuppression, OCP, smoking. Reducing incidince of invasive carcinoma with cervical Pap smear screening, with >50% detected in those not participating in regular screening. Spread to vagina, paracervical, parametrial, bladder, rectum. LN common (>10mm short axis or central necrosis) along internal/external iliac, presacral, paraaortic chains; may involve nodes without enlargement. Late haematogenous metastases to lung, bone, liver, brain.
- Squamous cell carcinoma (80%) – The large areas of immature squamous metaplastic epithleium at the junctional zone is vulnerable to infection, causing koilocytic cellular atypia, low grade squamous intraepithelial lesion (LSIL, previously cervical intraepithelial neoplasia CIN I). 10% of LSILs progresses to high grade SIL (HSIL, previously CIN II and III), a premalignant lesion with 10% progressing to invasive carcinoma.
- Adenocarcinoma (15%) – Develop from precursor adenocarcinoma in situ (from HPV). Tends to present with more advanced disease. Pap screening is less effective.
- Adenosquamous carcinoma
- Neuroendocrine carcinoma
Staging best done by MRI. Carcinoma is isointense to myometrium T1, but higher T2. CT 50% isodense to cervix on contrast and noncontrast, may be heterogeneously hypodense on postcontrast.
- Stage 0 – Carcinoma in situ (HSIL)
- Stage I – Confined to cervix. Ia microinvasive <5mm deep and <7mm wide (Tx cone biopsy, 95% 5-yr survival); Ib >5mm deep or >7mm wide (90% survival).
- Stage II – Beyond cervix or invasion of upper 2/3 vagina (loss of normal thin rind of low T2 vaginal muscle). IIa without parametrial invasion (contiuous rind of low signal cervical stroma surrounding tumour); IIb with parametrial invasion (high T2 signal). 75% 5-yr survival
- Stage III – To pelvic wall, lower 1/3 vagina or hydronephrosis. IIIa no extension to pelvic side wall; IIIb to pelvic side wall (tumour abutting/extending within 3mm of muscles) or hydronephrosis. <50% 5-yr survival.
- Stage IV – IVa invasion of mucosa of bladder/rectum or pelvic side walls; IVb distant metastases, para-aortic or inguinal lymphadenopathy.
Most common invasive gynaecological malignancy. 95% adenocarcinomas. Postmenopausal bleeding.
- Type I carcinomas (80%, endometrioid carcinoma) – 55-65yo, from endometrial hyperplasia hence increased risk wth with unopposed oestrogen, obesity, diabetes (impaired glucose tolerance in 60%), HTN, infertility. Most well or moderately differentiated. 20% have foci of squamous differentiation. Indolent spread via direct extension and lymphatics.
- Type II carcinomas (15%) – 65-75yo, arising from endometrial intraepithelial carcinoma (EIC) in the setting of endometrial atrophy. By definition are poorly differentiated (all grade 3), usually with extrauterine spread at diagnosis with worse prognosis. Tend to be superficial, spreading by tubal/intraperitoneal or lymphatics. Subtypes include serous carcinoma (most), clear cell and malignant mixed mullerian tumour
- Malignant mixed mullerian tumour (MMMT, previously carcinosarcoma with sarcomatous elements) – Large, solid, prominent necrosis and haemorrhage expanding uterine cavity, myometrial invasion. LN and peritoneal spread common.
- Tumours with stromal differentiation (5%)
- Adenosarcomas – Usually large broad-based polypoid growths, may prolapse through the os. 30s-40s. Generally low grade, almost always confined to the pelvis.
- Stromal tumours – Benign stromal nodules are well-circumscribed nodules of endometrial stromal cells in the myometrium of little consequence. Stroma sarcomas are malignant endometrial stroma within the myometrium with diffuse infiltration or lymphatic invasion (previously endolymphatic stromal myosis).
Staging better on MR, signal similar to normal endometrium being isointense to myometrium T1, hyperintense T2, variable enhancement. May be diffuse with ill-defined irregular thickening, or less likely localised polypoid tumour. Primary spread myometrium (seen on contrast and T2, intact junctional zone indicates absent invasion) and cervix (sag T2 and contrast, enhancing tumour in dark cervix), LN (unlikely if myometrial invasion <50%), broad ligaments, parametrium (best seen on T1), ovaries. Peritoneal seeding when penetrates uterine serosa. Late haematogenous metastases to lung, bone, liver, brain.
- Stage 0 – Carcinoma in situ
- Stage I – Limited to uterus. Ia <50% thickness myometrium; Ib >50%. (Old staging was Ia limited to endometrium; Ib <50% thickness myometrium; Ic >50%).
- Stage II – Cervix. IIa cervical mucosa; IIb cervical stroma.
- Stage III – Outside uterus, but limited to true pelvis. IIIa parametrial fat or positive peritoneal cytology; IIIb vagina; IIIc regional lymphadenopathy.
- Stage IV – Outside true pelvis or into bladder/rectum. IVa bladder/bowel mucosa; IVb distant metastases, malignant ascites, peritoneal seeding or abdominal/inguinal lymphadenopathy.
Rare. Rapidly growing pelvic mass, within the uterine wall or polypoid mass into the uterine lumen. Uterine enlargement, markedly heterogeneous mass with extensive necrosis, haemorrhage, frequent calcification. Unable to distinguish from degenerated benign leiomyoma. Tend to recur after resection, >50% metastasize to lungs, bone, brain etc. 40% 5-yr survival.
Uterine Arteriovenous Fistula
Uncommon, may be congenital or aquired (surgery, GTD, post-partum). Most are of reproductive age with PV bleeding, may have pulsatile PV mass. Hypoechoic mass/chennels within the myometrium, highly vascular with mosaic colour doppler flow (turbulence), high velocity with low resistive index, arterialised veins. Tx embolisation.
Arcuate Artery Calcification
Discrete echogenic foci in outer 1/3 of postmenopausal myometrium esp diabetes or HTN.
- Intrauterine contraceptive device (IUCD) – Plastic (two parallel echogenic lines of equal intensity) and/or copper (single bright echogenic line with posterior reverberation), 7- or T-shaped. Should be midline within endometrial canal unless fibroids present; if not seen may represent expulsion or perforation into/through myometrium. Obliquely positioned IUCD may be from fibroids or partial perforation. If there is concomitent pregnancy, IUCD should be removed if possible, as it may provide source of infection, best done under US guidance. Increased risk of ectopic pregnancy.
- Essure device – Permanent, inserted hysteroscopically under LA, crosses tubo-uterine junction inducing fibrosis. Not funtional for 3 months and should be checked with XR, ultrasound or hysterosalpingogram.
US, CT or MR. Primarily to assess fallopian tubes (cf US endometrium, MRI myometrium) for infertility; other indications recurrent abortions, postop tubal ligation, preop myomectomy. Heavily T2 weighted MRI inadequate resolution to detect normal tube. Contraindications include pregnancy and active pelvic infection. NSAID 1hr prior (may induce cramping). Supine lithotomy position, 5F HSG cathter into cervical canal with balloon inflated. Water soluble contrast instilled under fluoroscopy; spot images at early filling (for filling defects), full distention (uterine shape), fallopian tubes and free intraperitoneal spillage views. Oblique views may elongate the tubes. Further view after catheter removed to evaluate low uterine segment (balloon may obscure this). Evaluation includes:
- Congenital variants – Unicornuate, bicornuate, septate, arcuate uterus.
- Luminal filling defects – Best seen on early filling view, may be obscured on complete filling. Air bubbles are non-dependent mobile/transient. Uterine folds are normal variant infolding of myometrium parallelling long axis. Synechiae are intrauterine adhesions from post-traumatic/iatrogenic scarring, irregular/linear filling defects connecting walls, may be associated with Asherman syndrome. C-section scars are usually transvere in lower uterine segment, may be linear filling defect or wedge-shaped outopuching/diverticulum. Endometrial polyps are well-defined.
- Abnormal uterine contour – Submucosal leiomyomas may cause filling defect. Adenomyosis focal adenomyoma and/or small diverticula extending into myometrium.
- Fallopian tubes – 100-120mm divided into interstitial/cornuate short segment (traversing myometrium), longer isthmus (narrow like spaghetti) and wider ampullary segment (confirmed with mucosal folds) near ovary with a funnel-shaped fibriated end (not usually seen on HSG). Should be thin smooth lines, vary in degree of tortuosity, should have free spillage into peritoneal cavity. Venous/lymphatic intravasation of contrast (beaded channels with ascending course) from previous surgery or increased intrauterine pressure may mimic free peritoneal spillage. Abnormalities include congenital, spasm, occlusion or infection.
- Salpingitis isthmica nodosum (SIN) – Unknown aetiology associated with infertility, PID, ectopic pregnancy. Small outpouchings/diverticular from isthmus or one/both tubes.
- Cornual spasm – Uterine smooth muscle contraction at the interstitial segment obstructing flow of contrast, indistinguishable from true occlusion. Spasmolytic agent (glucagon, GTN spray, hyoscine) may relax the muscle.
- Tubal occlusion – Abrupt cutoff affecting any portion of the tube. May cause hydrosalpinx if occluded at ampulla. Most commonly from PID sequalae.
- Peritubal adhesions with loculations of contrast around the ampullary portion and inhibiting free peritoneal spillage. Usually from PID sequala.
- Surgery – Tubal ligation causes abrupt termination +/- mild proxmial bulbous expansion, with no peritoneal spillage. HSG may be useful to docoment tubal patency without extravasation after reversal of ligation. Hysteroscopically inserted Essure devices obstructed the interstitial segment.
- Tubal polyps – Rare ectopic endometrial tissue in the interstitial segment. Smooth rounded filling defects.
- Ectopic pregnancy – Should not be seen.
Isotonic saline instilled into uterine cavity while being examined by TVUS. If during fertile years should be done within 1st wek of cycle to ensure normal endometrial lining is as thin as possible. Does not allow evaluation of the tubes unless contrast enhanced (even then is only partial).