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Polycystic ovarian syndrome (PCOS).
Congenital genitourinary malformation—broad range of anomalies, see Fig. 10.2 .
Gartner duct cyst.
Complete androgen insensitivity syndrome (CAIS)—Y chromosome present but external genitalia are of female phenotype due to complete insensitivity of cells to androgens.
Hyperprolactinaemia secondary to a pituitary tumour.
Androgen-secreting ovarian or adrenal tumour.
Pregnancy—always consider in a female who is over the expected age of menarche and is not menstruating.
Pregnancy.
Premature ovarian failure.
Prolonged oral contraceptive pill or implant.
Significant weight loss or low body mass index.
Cervical stenosis/adhesion.
Iatrogenic—e.g. Asherman syndrome, surgery, chemotherapy or radiotherapy.
PCOS.
Androgen-secreting ovarian or adrenal tumour.
Other endocrine disorders—e.g. hypothyroidism, pituitary disease, etc.
Definition: vaginal bleeding >12 months following menopause.
Endometrial/vaginal atrophy.
Endometrial cancer, hyperplasia or polyp.
Cervical cancer or polyp.
Oestrogen-secreting ovarian lesion—e.g. Brenner tumour, granulosa cell tumour.
Endometritis.
Anticoagulants.
Complicated ovarian cyst—haemorrhage, rupture or torsion. If haemorrhagic rupture, accompanied by high density ascites (>20 HU).
Adnexal torsion—enlarged ovary with central oedema, peripherally placed follicles and a twisted pedicle.
Acute pelvic inflammatory disease (PID)—e.g. pyosalpinx, tuboovarian abscess.
Complicated fibroid—e.g. degeneration, torsion (if pedunculated).
Ectopic pregnancy—particularly tubal location or ruptured ectopic.
Ovarian hyperstimulation—enlarged multicystic ovaries in a woman undergoing IVF.
Nongynaecological causes—e.g. appendicitis, diverticulitis, Crohn's disease, cystitis and urolithiasis.
Acute exacerbation of chronic pelvic pain.
Definition: cyclical or noncyclical pain in the lower abdomen or pelvis of >6 months duration that limits activities of daily living; may be continuous or intermittent.
Adhesions—due to previous pelvic inflammation, surgery or trauma. May be associated with peritoneal inclusion cysts (pelvic fluid collections entrapped by adhesions).
Endometriosis and adenomyosis—pre/perimenopausal women.
Chronic PID—e.g. hydrosalpinx.
Fibroids.
Pelvic congestion syndrome—dilated veins in uterus, broad ligament and ovarian plexus.
Nongynaecological causes—e.g. musculoskeletal, neurological.
Ca-125 is a nonspecific marker that increases in response to peritoneal irritation.
Ovarian malignancy—invasive or borderline; note invasive mucinous tumours are less likely to elevate Ca-125.
Other primary malignancies with peritoneal dissemination—e.g. fallopian tube, breast, GI tract and pancreas.
Pregnancy.
Endometriosis.
Pelvic inflammatory disease.
Peritoneal inclusion cyst.
Nongynaecological—e.g. congestive cardiac failure, cirrhosis, pancreatitis, abdominopelvic tuberculosis, sarcoidosis and peritoneal dialysis patients.
The normal uterus is generally anteverted but can be retroverted or retroflexed. The degree of bladder filling affects flexion of the uterus. Normal ranges for uterine size (in cm):
Infantile | Prepubertal | Reproductive a | Postmenopausal | ||
---|---|---|---|---|---|
Uterus | Length | 1.5–2 | 2–5.4 | 5–12 | 3.5–6.5 |
Width | 0.8–1 | 1–2.2 | 4 | 1.2–1.8 | |
AP diameter | 1 | 3 | 1.5–2 |
a These values all increase, on average by 1.2 cm, following pregnancy.
The female reproductive organs develop from the Müllerian ducts in the absence of testosterone. The caudal portions of the Müllerian ducts fuse to form the uterus, cervix and upper two-thirds of the vagina, whereas the cranial portions remain separate forming the fallopian tubes. The lower third of the vagina develops from the urogenital sinus.
Abnormal development or fusion of the Müllerian ducts results in a spectrum of anomalies (see Fig. 10.2 ). These are often accompanied by renal and ureteric anomalies due to a common embryological origin.
The ovaries develop separately from the primitive yolk sac, so are typically normal in the presence of Müllerian duct anomalies.
Some are better assessed by US, MRI or sonohysterography.
Fibroid —submucosal fibroids create a well-defined smooth rounded filling defect. Large intramural fibroids distort the normal contour of the uterine cavity.
Endometrial polyp —well-defined filling defect indistinguishable from a submucosal fibroid.
Congenital Müllerian duct anomalies —see Section 10.2 .
Synechiae —intrauterine adhesions, most commonly caused by dilation and curettage procedures. Other causes include previous pregnancy, IUD, radiotherapy or infection (TB, schistosomiasis). Present as linear, angular or stellate filling defects. TB can cause marked distortion of the endometrial cavity. Multiple synechiae + infertility = Asherman syndrome.
Adenomyosis —may see endometrial irregularity with tiny diverticula.
Previous surgery —a caesarean-section scar may be visible as a transverse linear filling defect in the lower uterus. Previous myomectomy can cause focal irregularity or a diverticulum.
Unsuspected pregnancy —very rare. The gestational sac creates a filling defect.
Air bubbles —can mimic a polyp. Mobile, nondependent location.
HSG is still the best imaging test.
Dilated fallopian tube —i.e. hydrosalpinx or haematosalpinx. Due to distal tubal obstruction in the ampullary portion. No contrast spillage into the peritoneal cavity.
PID —most common cause. Results in hydrosalpinx in the chronic setting (HSG contraindicated in acute infection).
Endometriosis *.
Tubal malignancy —primary or secondary.
Failure to opacify the whole fallopian tube .
Tubal occlusion —most commonly due to PID; this can occlude any part of one or both tubes, or cause loculation of spilled contrast around the ampulla. Other causes include endometriosis, TB and fallopian tube malignancy.
Tubal spasm —tube does not fill beyond the cornual portion. Indistinguishable from cornual tubal occlusion. Spasmolytic agents may help.
Previous surgery —tubal ligation results in an abrupt cut-off in the isthmic portion of the fallopian tubes ± mild bulbous dilatation proximally. Hysteroscopically inserted occlusion devices result in total tubal occlusion with a radiopaque linear microinsert visible within the tubes.
Tubal irregularity .
Salpingitis isthmica nodosa (SIN) —idiopathic. Multiple tiny tubal diverticula arising from the isthmic portion. Can affect one or both tubes.
Tuberculosis *—usually bilateral. In the acute phase, causes tubal diverticula that tend to be larger and less uniform than in SIN. In the chronic phase, typically causes multiple short tubal constrictions giving a beaded appearance, ± isthmico-ampullary junction obstruction ± peritubal adhesions resulting in a fixed distorted ‘corkscrew’ tube. Diffuse pipe-stem narrowing can be seen in advanced cases.
Tubal polyp —rare, located in the cornual portion. Smooth, rounded <1 cm filling defect. May be bilateral.
Normal cyclical values of endometrial thickness in premenopausal women:
During menstruation: <5 mm (echogenic line)
Proliferative phase (day 6–14): 5–7 mm (echogenic stripe)
Late proliferative phase (periovulation): up to 11 mm (multilayered appearance)
Secretory phase (day 15–28): 7–16 mm (homogeneously echogenic)
Normal values in postmenopausal women:
Without postmenopausal bleeding: <12 mm
With postmenopausal bleeding: <5 mm
Note that abnormal postmenopausal endometrial thickening usually requires biopsy to exclude malignancy.
Normal secretory phase —homogeneously echogenic on US and T2 hyperintense on MRI.
Early pregnancy —gestation sac can be seen after 5 weeks; if not visible consider ectopic.
Endometrial hyperplasia —usually homogeneously echogenic ± cystic change, but can be focal or irregular, mimicking malignancy. Due to increased or unopposed oestrogen, e.g. obesity, PCOS, drugs (e.g. Tamoxifen; can cause hyperplasia, polyps, cystic change or, rarely, endometrial cancer), or hormone-secreting ovarian tumour (e.g. fibrothecoma or granulosa cell tumour).
Endometrial carcinoma —usually heterogeneous and irregular, but can mimic (or coexist with) hyperplasia.
Endometritis —typically in the postpartum period + clinical signs of sepsis; occasionally due to PID. Intrauterine fluid or gas may also be seen.
Intrauterine fluid —can mimic endometrial thickening on CT (both hypoattenuating), but not on US (anechoic). Usually related to menstruation or pregnancy in premenopausal women (or infection if clinically septic). In postmenopausal women, usually due to benign cervical stenosis or an obstructing cervical or endometrial tumour/polyp (requires biopsy).
Endometrial carcinoma —typically in postmenopausal women with a history of bleeding. Usually heterogeneous and irregular. On MRI, T2 hypointense relative to normal endometrium, hyperintense relative to junctional zone of myometrium. Enhances less than normal myometrium. Myometrial invasion, if present, is diagnostic.
Endometrial polyp —benign, well-defined, homogeneously hyperechoic ± cystic change ± vascular stalk. On MRI, slightly T2 hypointense relative to endometrium.
Submucosal fibroid —well-defined, usually hypoechoic on US and T2 hypointense on MRI.
Focal endometrial hyperplasia —mimics a sessile polyp or early cancer on imaging.
Lesions related to pregnancy .
Pregnancy or missed miscarriage —visible gestation sac.
Retained products of conception (RPOC) —heterogeneously echogenic, usually contain Doppler flow; enhance on MRI.
Intrauterine blood clot —in the postpartum period. Heterogeneous, no internal Doppler flow or enhancement.
Gestational trophoblastic disease —see Section 10.16 .
Endometrial stromal tumours —rare. Benign forms are nonspecific on imaging, mimicking endometrial polyps. Malignant forms are usually larger than endometrial carcinomas with more avid enhancement, and tend to greatly distend the uterine cavity; high-grade forms are very invasive and aggressive ± metastases.
Mixed Müllerian tumours —contain both epithelial and stromal components; can be benign (adenofibroma), low-grade malignant (adenosarcoma) or high-grade (carcinosarcoma). Adenosarcoma is typically solid-cystic and confined to the uterus, carcinosarcoma is heterogeneous (haemorrhage and necrosis) + restricted diffusion ± extrauterine invasion and metastases. Both may protrude into the endocervical canal.
Pure stromal tumours —can be benign (stromal nodule), low-grade malignant (endometrial stromal sarcoma) or high-grade (undifferentiated endometrial sarcoma). Low-grade sarcoma is heterogeneously T2 hyperintense ± nodular myometrial invasion with characteristic T2 hypointense bands of preserved myometrium. High-grade sarcoma shows more diffuse myometrial invasion. Vascular invasion is common in both malignant forms.
Metastasis to the endometrium —rare, most commonly from breast or stomach.
Adenomyosis —thickening of the junctional zone with irregularity of the endometrial–myometrial interface. May mimic endometrial thickening on US.
Submucosal fibroid .
Invasive endometrial malignancy .
Gestational trophoblastic disease.
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