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Flashcards in OBGYN Deck (38)
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1
Q

Primary amenorrhoea

A
  1. Constitutional delay.
  2. Polycystic ovarian syndrome (PCOS).
  3. Congenital genitourinary malformation—broad range of anomalies,
    see Fig. 10.2.
  4. Gartner duct cyst.
  5. Complete androgen insensitivity syndrome (CAIS)—Y chromosome
    present but external genitalia are of female phenotype due to
    complete insensitivity of cells to androgens.
  6. Hyperprolactinaemia secondary to a pituitary tumour.
  7. Androgen-secreting ovarian or adrenal tumour.
  8. Pregnancy—always consider in a female who is over the expected
    age of menarche and is not menstruating.
2
Q

Secondary amenorrhoea

A
  1. Pregnancy.
  2. Premature ovarian failure.
  3. Prolonged oral contraceptive pill or implant.
  4. Significant weight loss or low body mass index.
  5. Cervical stenosis/adhesion.
  6. Iatrogenic—e.g. Asherman syndrome, surgery, chemotherapy or
    radiotherapy.
  7. PCOS.
  8. Androgen-secreting ovarian or adrenal tumour.
  9. Other endocrine disorders—e.g. hypothyroidism, pituitary
    disease, etc
3
Q

Postmenopausal bleeding (PMB)

A

Definition: vaginal bleeding >12 months following menopause.
1. Endometrial/vaginal atrophy.
2. Endometrial cancer, hyperplasia or polyp.
3. Cervical cancer or polyp.
4. Oestrogen-secreting ovarian lesion—e.g. Brenner tumour,
granulosa cell tumour.
5. Endometritis.
6. Anticoagulants

4
Q

Acute pelvic pain

A
  1. Complicated ovarian cyst—haemorrhage, rupture or torsion. If
    haemorrhagic rupture, accompanied by high density ascites
    (>20 HU).
  2. Adnexal torsion—enlarged ovary with central oedema, peripherally
    placed follicles and a twisted pedicle.
  3. Acute pelvic inflammatory disease (PID)—e.g. pyosalpinx,
    tuboovarian abscess.
  4. Complicated fibroid—e.g. degeneration, torsion (if pedunculated).
  5. Ectopic pregnancy—particularly tubal location or ruptured ectopic.
  6. Ovarian hyperstimulation—enlarged multicystic ovaries in a woman
    undergoing IVF.
  7. Nongynaecological causes—e.g. appendicitis, diverticulitis, Crohn’s
    disease, cystitis and urolithiasis.
  8. Acute exacerbation of chronic pelvic pain
5
Q

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

A
  1. Adhesions—due to previous pelvic inflammation, surgery or trauma. May be associated with peritoneal inclusion cysts (pelvic fluid collections entrapped by adhesions).
  2. Endometriosis and adenomyosis—pre/perimenopausal women.
  3. Chronic PID—e.g. hydrosalpinx.
  4. Fibroids.
  5. Pelvic congestion syndrome—dilated veins in uterus, broad
    ligament and ovarian plexus.
  6. Nongynaecological causes—e.g. musculoskeletal, neurological
6
Q

Raised Ca-125 (normal <35 U/mL)
Ca-125 is a nonspecific marker that increases in response to
peritoneal irritation

A
  1. Ovarian malignancy—invasive or borderline; note invasive
    mucinous tumours are less likely to elevate Ca-125.
  2. Other primary malignancies with peritoneal dissemination—e.g.
    fallopian tube, breast, GI tract and pancreas.
  3. Pregnancy.
  4. Endometriosis.
  5. Pelvic inflammatory disease.
  6. Peritoneal inclusion cyst.
  7. Nongynaecological—e.g. congestive cardiac failure, cirrhosis,
    pancreatitis, abdominopelvic tuberculosis, sarcoidosis and
    peritoneal dialysis patients
7
Q

HSG

Abnormal uterine cavity

A

. Fibroid—submucosal fibroids create a well-defined smooth
rounded filling defect. Large intramural fibroids distort the normal
contour of the uterine cavity.
2. Endometrial polyp—well-defined filling defect indistinguishable
from a submucosal fibroid.
3. Congenital Müllerian duct anomalies—see Section 10.2.
4. 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.
5. Adenomyosis—may see endometrial irregularity with tiny
diverticula.
6. 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.
7. Unsuspected pregnancy—very rare. The gestational sac creates a
filling defect.
8. Air bubbles—can mimic a polyp. Mobile, nondependent location.

8
Q

Tubal abnormality

3

A
  1. Dilated fallopian tube—i.e. hydrosalpinx or haematosalpinx. Due
    to distal tubal obstruction in the ampullary portion. No contrast
    spillage into the peritoneal cavity.
    (a) PID—most common cause. Results in hydrosalpinx in the
    chronic setting (HSG contraindicated in acute infection).
    (b) Endometriosis*.
    (c) Tubal malignancy—primary or secondary.
  2. Failure to opacify the whole fallopian tube.
    (a) 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.
    (b) Tubal spasm—tube does not fill beyond the cornual portion.
    Indistinguishable from cornual tubal occlusion. Spasmolytic
    agents may help.
    (c) 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.
  3. Tubal irregularity.
    (a) Salpingitis isthmica nodosa (SIN)—idiopathic. Multiple tiny
    tubal diverticula arising from the isthmic portion. Can affect
    one or both tubes.
    (b) 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.
    (c) Tubal polyp—rare, located in the cornual portion. Smooth,
    rounded <1 cm filling defect. May be bilateral.
9
Q

Diffusely thickened endometrium

A
  1. Normal secretory phase—homogeneously echogenic on US and
    T2 hyperintense on MRI.
  2. Early pregnancy—gestation sac can be seen after 5 weeks; if not
    visible consider ectopic.
  3. 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).
  4. Endometrial carcinoma—usually heterogeneous and irregular, but
    can mimic (or coexist with) hyperplasia.
  5. Endometritis—typically in the postpartum period + clinical signs
    of sepsis; occasionally due to PID. Intrauterine fluid or gas may also
    be seen.
  6. 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)
10
Q

Focal endometrial mass

A
  1. Endometrial carcinoma—typically in postmenopausal women
    with a history of bleeding. Usually heterogeneous and irregular. 308 Aids to Radiological Differential Diagnosis
    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.
  2. Endometrial polyp—benign, well-defined, homogeneously
    hyperechoic ± cystic change ± vascular stalk. On MRI, slightly T2
    hypointense relative to endometrium.
  3. Submucosal fibroid—well-defined, usually hypoechoic on US and
    T2 hypointense on MRI.
  4. Focal endometrial hyperplasia—mimics a sessile polyp or early
    cancer on imaging.
  5. Lesions related to pregnancy.
    (a) Pregnancy or missed miscarriage—visible gestation sac.
    (b) Retained products of conception (RPOC)—heterogeneously
    echogenic, usually contain Doppler flow; enhance on MRI.
    (c) Intrauterine blood clot—in the postpartum period.
    Heterogeneous, no internal Doppler flow or enhancement.
    (d) Gestational trophoblastic disease—see Section 10.16.
  6. 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.
    (a) 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.
    (b) 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.
  7. Metastasis to the endometrium—rare, most commonly from
    breast or stomach.
11
Q

Abnormality involving both endometrium and myometrium

4

A
  1. Adenomyosis—thickening of the junctional zone with irregularity
    of the endometrial–myometrial interface. May mimic endometrial
    thickening on US.
  2. Submucosal fibroid.
  3. Invasive endometrial malignancy.
  4. Gestational trophoblastic disease
12
Q

Diffuse myometrial abnormality

A
  1. Adenomyosis—best seen on MRI. Thickening of the T2
    hypointense junctional zone (>12 mm is diagnostic; <8 mm is
    normal) that may be diffuse, asymmetrical (often posterior) or
    focal (adenomyoma). T2 hyperintense subendometrial cysts and
    linear striations are often visible ± myometrial foci of T1
    hyperintensity (haemorrhage).
  2. Leiomyomatosis—numerous ill-defined T2 hypointense fibroids
    diffusely replacing the myometrium ± areas of degeneration.
  3. Postpartum appearance—after delivery the uterus reduces in size
    slowly over several weeks. In the first 30 hours the myometrium is
    heterogeneous with multiple dilated vessels. The junctional zone is
    usually not visible in the first 6 weeks (or longer after caesarean
    section).
  4. Oral contraceptives—can result in diffuse T2 hyperintensity
    throughout the myometrium ± endometrial atrophy.
  5. Infiltrative malignancy—rare, mainly lymphoma and leukaemia.
    Diffuse enlargement and infiltration of the uterus by a
    homogeneous mildly T2 hyperintense tumour + restricted
    diffusion. The endometrium is usually spared, but adjacent organs
    may be involved ± pelvic lymphadenopathy. Aggressive sarcomas
    can also diffusely replace the uterus but are heterogeneous on
    imaging.
13
Q

Focal myometrial mass

7

A
  1. Fibroid (leiomyoma)—very common, particularly in Afro-Caribbeans. Typically hypoechoic on US and T1/T2 hypointense on MRI with homogeneous enhancement and no restricted diffusion. Well-defined, rounded + pseudocapsule. May be intramural, subserosal or submucosal (± pedunculated). Many different variants and forms of degeneration, giving a variety of appearances. Regress after the menopause.
    (a) Degeneration—more common in larger fibroids due to outgrowth of blood supply. Calcification is common after hyaline degeneration and suggests chronicity.
    (i) Hyaline—most common. Heterogeneous T2 hypointensity and enhancement within the fibroid on MRI, may be difficult to see.
    (ii) Cystic—internal well-defined cystic spaces (T2
    hyperintense, T1 hypointense, no enhancement).
    (iii) Myxoid—similar in appearance to cystic degeneration but usually appears more complex + internal enhancement.
    (iv) Red—haemorrhagic infarction, usually occurs in pregnancy. Heterogeneous T2 signal with no enhancement and areas of T1 hyperintensity (haemorrhage or thrombosed veins).
    (v) Infection (pyomyoma)—usually postpartum or after
    instrumentation. Clinical features of sepsis. Fluid and gas
    within a degenerated fibroid + restricted diffusion +
    surrounding fat stranding.
    (b) Variants.
    (i) Lipoleiomyoma—well-defined, contains a mixture of
    smooth muscle and fat. May be almost completely fatty.
    Markedly hyperechoic on US. CT and T1/fatsat MRI are
    diagnostic. If exophytic, may mimic ovarian teratoma.
    May rarely transform to liposarcoma.
    (ii) Cellular leiomyoma—often larger and more T2
    hyperintense than a normal leiomyoma due to minimal
    collagen. Can show restricted diffusion, mimicking
    leiomyosarcoma, but usually less heterogeneous and
    typically well-defined.
    (iii) Angioleiomyoma—rare. Usually large with prominent
    intratumoural vessels ± internal haemorrhage.
    (iv) Very rare variants—atypical leiomyoma (mimics
    cystic degeneration), myxoid leiomyoma (mimics
    myxoid degeneration), smooth muscle tumour of
    uncertain malignant potential (STUMP; mimics cellular
    variant).
    (c) Extrauterine manifestations.
    (i) Parasitic leiomyoma—due to torsion and detachment of
    a pedunculated subserosal leiomyoma, which then
    attaches onto another site in the peritoneal cavity,
    usually in the pelvis, e.g. broad ligament. More
    commonly occurs post myomectomy or hysterectomy
    due to peritoneal implantation of small leiomyoma
    fragments.
    (ii) Disseminated peritoneal leiomyomatosis—multiple
    benign peritoneal leiomyomas, T1/T2 hypointense on
    MRI with homogeneous enhancement. Rare, occurs in
    premenopausal women; mimics peritoneal metastases but
    without ascites and no solid organ involvement apart
    from uterus and ovaries. No increased uptake on PET.
    (iii) Benign metastasizing leiomyoma—usually seen post
    hysterectomy performed for fibroids. Typically manifests
    as multiple discrete lung nodules histologically identical
    to benign uterine fibroids. Cavitation ± pneumothorax
    can occur. Less commonly involves retroperitoneum or
    lymph nodes.
    (iv) Intravenous leiomyomatosis—benign uterine fibroids
    can rarely invade adjacent pelvic veins, and may even
    extend into the IVC ± right heart. The vascular invasion
    makes it hard to differentiate from endometrial stromal
    sarcoma.
  2. Adenomyoma—focal form of adenomyosis; best seen on MRI.
    Ill-defined T2 hypointense mass ± small cystic spaces ± foci of T1
    hyperintensity. Usually continuous with junctional zone but can be
    subserosal or submucosal and pedunculated. May rarely appear
    predominantly cystic with internal haemorrhage, mimicking a
    fibroid with red degeneration.
  3. Other myometrial tumours.
    (a) Leiomyosarcoma—usually solitary, large and heterogeneous
    with areas of haemorrhage and necrosis. Mimics a
    degenerating fibroid, but features suggesting malignancy
    include irregular or invasive margins, restricted diffusion and
    rapid growth, particularly in a postmenopausal woman.
    (b) Metastases—rare, usually from breast or stomach. Direct
    invasion from an adjacent tumour (e.g. cervix, colon, bladder)
    is more common.
    (c) Lymphoma*/leukaemia—usually diffuse; can rarely be focal.
    (d) Other rare tumours—e.g. melanoma (may be T1
    hyperintense), haemangioma (may contain phleboliths),
    perivascular epithelioid cell tumour (PEComa), inflammatory
    pseudotumour, nerve sheath tumour, neuroendocrine tumour,
    plasmacytoma, solitary fibrous tumour.
  4. External invasive endometriosis—typically in the pouch of
    Douglas.
  5. Caesarean section haematoma—in the postpartum period,
    located at the incision site in the lower anterior wall. In the chronic
    setting there is focal myometrial thinning or a defect.
  6. Arteriovenous malformation—usually in young women, often
    related to previous pregnancy or surgery. US/MRI shows focal
    ill-defined myometrial thickening with multiple dilated tortuous
    vessels (high flow and low resistance on Doppler, avid early filling
    on postcontrast MRI).
  7. Transient physiological myometrial contraction (mimic)—focal
    area of T2 hypointense myometrial thickening inseparable from the
    junctional zone; mimics focal adenomyosis but does not contain
    cystic spaces and often disappears on subsequent sequences.
14
Q

Cystic cervical lesion

A
  1. Nabothian cyst—mucous retention cyst related to chronic
    cervicitis. Typically unilocular but can be multiple and clustered.
    Anechoic on US and T2 bright on MRI; mucin content shows
    variable T1 signal and may create low-level echoes on US. Typically
    superficial with preservation of the underlying T2 hypointense
    cervical stroma, but can occasionally extend into the stroma. No
    vascularity or enhancement (cf. adenoma malignum).
  2. Cervical endometriosis—can be cystic (T1/T2 hyperintense) or
    solid (T2 hypointense) in appearance. Other sites of involvement
    are usually also present.
  3. Postbiopsy haematoma—T1 hyperintense.
  4. Adenoma malignum—mucinous adenocarcinoma of the cervix.
    Presents as a multilocular cystic mass arising from epithelial glands
    and invading the underlying cervical stroma, with enhancing septa
    + solid components. Peritoneal metastases are common. Associated
    with Peutz-Jeghers syndrome.
  5. Ectopic pregnancy—gestation sac in the endocervical canal,
    usually with a closed internal os. Can mimic a miscarriage in
    progress, but in the latter there is no fetal heartbeat and the
    internal os is usually open. Repeat US should be considered
15
Q

Solid cervical lesion

8

A
  1. Primary cervical carcinoma—most are squamous; less commonly
    adenocarcinoma or other rarer variants. Arises from epithelium of
    ectocervix (younger women) or endocervix (older women).
    Typically homogeneously T2 hyperintense on MRI + restricted
    diffusion + enhancement; invades and disrupts the underlying T2
    hypointense cervical stroma. Can invade the uterus (± obstruction),
    vagina, parametrium or other adjacent structures.
  2. Cervical polyp—well-defined polypoid mass within and expanding
    the endocervical canal without stromal invasion. Echogenic on US,
    T2 hypointense on MRI with avid enhancement ± small cystic
    spaces. Usually pedunculated with a vascular stalk on US; may
    prolapse into the vagina. Usually benign but may contain foci of
    noninvasive cancer.
  3. Cervical fibroid—usually within the cervical stroma but can rarely
    be pedunculated and endocervical. Identical imaging features to
    uterine fibroids.
  4. Endocervical hyperplasia—diffuse T2 hyperintense thickening of
    cervical epithelium ± cystic change. Can mimic adenoma malignum,
    but does not show stromal invasion and is usually hypovascular.
  5. Prolapsed endometrial mass—e.g. polyp (benign or malignant),
    fibroid, mixed Müllerian tumour. Distends cervical canal.
  6. Primary endometrial or vaginal tumour invading the cervix—
    bladder and rectal tumours may also invade the cervix.
  7. Other rare cervical tumours—nearly all rare uterine tumours can
    also arise from the cervix, e.g. lymphoma (homogeneous and
    diffusely infiltrative, spares cervical epithelium), melanoma (often
    T1 hyperintense), sarcoma (often large, heterogeneous T2
    hyperintensity and enhancement), metastasis (e.g. from breast,
    stomach), NET (± paraneoplastic syndrome), etc.
  8. Iatrogenic lesions—e.g. postbiopsy inflammation
16
Q

Physiological and functional ovarian cysts

Only occur in premenopausal women

A

•Developing follicle: <1 cm, unilocular, anechoic.
•Dominant follicle: 1–3 cm, unilocular, anechoic. There may be
one or more smaller cysts around the periphery of the dominant
follicle (‘cumulus oophorus’)—this suggests imminent ovulation
and must not be mistaken for a multilocular cystic neoplasm.
•Corpus luteal cyst: >3 cm by definition (normal corpus luteum is
<3 cm). Typically <5 cm but can reach 8 cm. Thick hypervascular
wall (‘ring of fire’), crenulated edges, can be haemorrhagic (may
appear solid on US).
• Follicular cyst: persistent unruptured follicle; >3 cm by definition,
usually <5 cm but can be up to 20 cm. Unilocular anechoic cyst.
Usually resolves spontaneously within 2–3 months.
Some adnexal masses have characteristic US appearances allowing
a definitive diagnosis:
•Unilocular cyst with smooth walls <10 cm in diameter → simple
cyst or cystadenoma.
•Unilocular cyst with ground-glass echogenicity in a premenopausal
woman → endometrioma.
• Unilocular cystic mass with mixed echogenicity and acoustic
shadows in a premenopausal woman → benign cystic teratoma.
•Other unilocular cysts with smooth walls → haemorrhagic
cyst (contains echoes and thin lacy strands) or hydrosalpinx
(contains incomplete ‘septa’ representing folds of the fallopian
tube).
• Mass with ascites and at least moderate Doppler flow in a
postmenopausal woman → malignant tumour.

17
Q

US features of benign adnexal masses:

A
B features:
•	 Unilocular cyst
•	 Solid components
<7 mm in largest
diameter
•	 Presence of acoustic
shadows
•	 Smooth multilocular
cystic mass <10 cm in 
largest diameter
•	 No blood flow
18
Q

US features of malignant adnexal masses

A
M features:
•	 Irregular solid tumour
•	 Presence of ascites
•	 >3 papillary structures 
>3 mm in height
•	 Irregular multilocular
cystic-solid tumour 
≥10 cm
•	 Very strong blood
flow
 Peritoneal implants, or
•	 Solid tissue with a type 3
enhancement curve (initial 
increase in signal intensity 
steeper than that of 
myometrium)
19
Q

Unilateral enlarged ovary, no dominant mass

A
  1. Acute adnexal torsion—oedematous ovary (hyperechoic on US,
    T2 hyperintense on MRI) with peripheral follicles and a twisted
    pedicle + free fluid. The ovary is usually displaced from its normal
    location, often sited closer to the midline anterior or posterior to
    the uterus. Haemorrhage may be seen on CT/MRI, suggesting
    necrosis. Doppler flow may be normal, or absent in advanced
    cases. Most cases occur in the presence of a mass, e.g. large cyst
    or dermoid; torsion of a normal ovary most commonly occurs in
    children due to developmental hypermobility.
  2. Massive ovarian oedema—due to chronic intermittent partial
    torsion; clinical presentation is usually subacute with intermittent
    pelvic pain (in contrast to acute severe pain in acute torsion).
    Imaging appearance is similar to torsion, except Doppler flow is
    typically present and ascites is less common. In some chronic
    cases, areas of T2 hypointensity may be seen, representing ovarian fibromatosis—this may be peripheral and ring-like (‘black garland’
    appearance).
20
Q

Bilateral enlarged ovaries, no dominant mass

A
  1. Polycystic ovarian morphology (PCOM)—ovaries ≥10 cm3
    in
    volume with ≥25 subcapsular follicles, typically measuring
    2–9 mm. Hormonal and clinical correlation is required for
    diagnosis of PCOS.
  2. Ovarian hyperstimulation syndrome—complication of exogenous
    hormonal stimulation for IVF. Grossly enlarged ovaries with
    multiple peripheral follicles of varying size (typically >1 cm)
    creating a ‘spoke-wheel’ appearance. This may mimic a
    multilocular cystic mass but the bilaterality and clinical context are
    indicative. Ascites and pleural ± pericardial effusions may be
    present and suggest increasing severity.
  3. Hyperreactio luteinalis (theca lutein cysts)—due to high levels of
    endogenous human chorionic gonadotropin (hCG), typically
    caused by gestational trophoblastic disease, but occasionally seen
    in multifetal pregnancy. Similar on imaging to ovarian
    hyperstimulation syndrome, but free fluid is usually absent.
  4. Stromal hyperplasia/hyperthecosis—clinical features similar to
    PCOS but typically occurs in postmenopausal women. Ovaries may
    be enlarged with hyperechoic stromal expansion and T2
    hypointensity; the number of follicles is not increased
21
Q

Simple cystic adnexal lesion

A
  1. Follicular cyst—premenopausal women only; >3 cm by definition,
    usually <5 cm. May show smooth wall enhancement on MRI.
    Resolves spontaneously, usually within 2–3 months.
  2. Paraovarian cyst—separate from ovary, within broad ligament.
    Usually <5 cm.
  3. Ovarian inclusion cyst—in postmenopausal women. Benign,
    typically ≤1 cm.
  4. Serous cystadenoma—usually >5 cm, unilocular and anechoic ±
    smooth wall enhancement. Occasionally bilateral. Does not resolve
    spontaneously. Cystadenofibromas and mucinous cystadenomas
    can also rarely be unilocular.
  5. Hydrosalpinx—tubular with partial ‘septa’ representing folding of
    the fallopian tube.
  6. Peritoneal inclusion cyst—premenopausal women only, typically
    with a history of pelvic surgery or inflammation. Caused by
    peritoneal adhesions that entrap fluid released by physiological
    rupture of ovarian follicles, resulting in loculated peritoneal fluid
    adjacent to or surrounding the ovary; often has an unusual shape,
    following the contours of adjacent structures without much masseffect. Can be large ± bilateral, may contain thin septa that are
    mobile (‘flapping sail’ sign).
  7. Dermoid cyst—can rarely appear anechoic if filled with sebum
    and fluid
22
Q

Unilocular cyst with internal echoes on US or T1

hyperintensity on MRI

A
  1. Haemorrhagic functional cyst—typically solitary and unilocular.
    On US, contains low-level echoes and thin lacy fibrin strands
    (‘cobweb’ appearance) ± fluid–fluid level or echogenic retracting
    clot. Hypervascularity of the wall is common but internal flow is
    absent. May occasionally appear solid on US, but posterior acoustic
    enhancement and absent internal vascularity help exclude a solid
    mass. On unenhanced CT, the cyst is typically hyperattenuating.
    MRI often shows T1 hyperintensity (best seen on T1 fatsat) and T2
    hyperintensity ± restricted diffusion but no signal voids on SWI.
    Retracting clots, if present, show lower T1/T2 signal but do not
    enhance. Typically resolves within 2–3 months; if persistent,
    consider endometrioma or haemorrhagic cystic neoplasm.
  2. Endometrioma—usually in premenopausal women. Often
    multiple, may be septated, do not usually resolve over time. On
    US, typically contain diffuse low-level echoes giving a ground-glass
    appearance ± echogenic avascular foci adherent to the cyst wall.
    The wall is usually hypovascular ± calcification. On MRI, contents
    typically show uniform T1 hyperintensity and reduced T2 signal
    (T2 shading—may be uniform or layered) ± restricted diffusion +
    signal voids in the wall on SWI. A characteristic nonenhancing T2
    dark spot adherent to the wall may be seen. A mural nodule which
    is not T2 hypointense and shows enhancement or Doppler flow is
    suspicious for malignant change, or if pregnant, a decidualized
    endometrioma (in which case the nodule should be isointense to
    the placenta on all sequences and regress postpartum).
  3. Corpus luteal cyst—develops after ovulation; >3 cm, thick
    hypervascular wall (‘ring of fire’ on Doppler), crenulated edges.
    Can be haemorrhagic and may appear solid on US.
  4. Dermoid cyst—typically found in young patients. Variable
    appearance on US depending on contents. Usually a unilocular
    cyst containing multiple linear echoes (hair) and a characteristic
    very echogenic, densely shadowing, mural nodule (dermoid plug).
    Densely packed hair can create a ‘dermoid mesh’ appearance. The
    acoustic shadowing created by a large dermoid plug may obscure
    the rest of the lesion (‘tip of the iceberg’ sign). Fluid–fluid levels,
    floating balls of fat/keratin and foci of calcification may also be
    seen. No internal vascularity. Pathognomonic appearance on CT/
    MRI: well-defined adnexal mass containing fat, fluid, soft tissue
    and calcification (often tooth-like). Restricted diffusion may be
    present. Usually does not enhance except in rare cases, e.g. ifthyroid or carcinoid tissue is present. Can be complicated by
    torsion, rupture (free intraperitoneal fat) and malignant
    transformation (foci of avid enhancement or extramural invasion
    are suggestive).
  5. Haematosalpinx/pyosalpinx—due to haemorrhage or infection
    respectively. Tubular cystic structure with internal echoes on US. T1
    hyperintensity is more common in haematosalpinx. With a
    pyosalpinx there is hypervascularity and wall thickening (>5 mm,
    often has a ‘cogwheel’ appearance on US in cross-section) +
    restricted diffusion on MRI.
  6. Haemorrhage within a cystic neoplasm—e.g. cystadenoma.
23
Q

Multilocular cystic lesion

A
  1. Mucinous ovarian tumours—typically unilateral, large and
    multilocular + low-level echoes ± ‘stained-glass’ appearance on MRI
    due to differing amounts of proteinaceous material in different
    locules. Smooth enhancement of the wall and septa. Difficult to
    differentiate benign from borderline and malignant varieties on
    imaging, but bilaterality or high locularity makes malignancy more
    likely. Serous cystadenomas can also occasionally be multilocular.
  2. Tuboovarian abscess—complication of PID; pain and clinical
    features of infection are indicative. Complex cystic mass containing
    debris and septations ± gas, with a thick hypervascular wall. On
    MRI, contents are heterogeneous and usually show restricted
    diffusion. May be bilateral, and may be associated with
    perihepatitis (Fitz-Hugh-Curtis syndrome). If there is diffuse
    peritoneal thickening, consider TB.
  3. Ovarian cystadenofibroma—solid components may be absent in
    some cases. Septa are characteristically T2 hypointense.
  4. Benign cystic mesothelioma—separate from ovary, arises from
    pelvic peritoneum.
  5. Ovarian lymphangioma—very rare, more commonly arises from
    retroperitoneum. Multilocular, no or minimal vascularity.
  6. Hydatid cyst—very rare.
24
Q

Solid-cystic lesion

A
  1. Epithelial ovarian tumours—including serous borderline tumours,
    serous and mucinous cystadenocarcinomas and endometrioid and
    clear cell carcinomas—the imaging features of these overlap.
    Typically presents in peri- or postmenopausal women as a
    multilocular cystic mass with papillary projections or solid
    components showing vascularity and restricted diffusion. Gynaecology and obstetrics 319
    10
    Bilaterality or calcification, if present, suggests a serous tumour.
    Small papillary projections can rarely be seen in serous
    cystadenomas, but are larger and more numerous in borderline
    and malignant serous tumours. Endometrioid and clear cell
    carcinomas can arise within endometriomas (rapid growth or
    enhancing nodules are suspicious). Endometrioid carcinomas may
    be accompanied by uterine endometrial hyperplasia or
    synchronous carcinoma.
  2. Ovarian metastasis—usually from a signet-ring adenocarcinoma of
    the GI tract (Krukenberg metastasis). Typically bilateral. Solid
    components enhance and may be T2 hypointense. Usually occurs
    in the presence of disease elsewhere, especially the peritoneum.
  3. Ovarian cystadenofibroma—cystic mass with fibrous septa and
    mural nodules that cause acoustic shadowing on US and are very
    T2 hypointense on MRI + enhancement + internal cystic change
    (characteristic ‘black sponge’ appearance). Typically no restricted
    diffusion (in contrast to ovarian carcinoma).
  4. Granulosa cell tumour—malignant stromal tumour, usually seen
    in peri- or postmenopausal women but a rare juvenile form also
    exists. Variable appearance, usually large; can be solid ± numerous
    small cystic spaces (‘Swiss cheese’ appearance) or can be cystic
    with a rind of soft tissue. Secretes oestrogen, causing endometrial
    hyperplasia, polyps or carcinoma.
  5. Primary fallopian tube carcinoma—rare. May present as a
    hydrosalpinx containing nodular enhancing components, or as a
    predominantly solid sausage-shaped mass. Often mimics ovarian
    carcinoma. There may be a suggestive history of colicky pelvic pain
    and an intermittent serosanguinous vaginal discharge that relieves
    the pain.
  6. Struma ovarii—rare subtype of mature teratoma composed mostly
    of thyroid tissue; usually found in premenopausal women, may
    present with hyperthyroidism. Multilocular cystic-solid mass +
    hypervascular nodules on imaging; nonenhancing areas of very
    high attenuation (>90 HU on unenhanced CT) and very low T2
    signal on MRI are suggestive, representing colloid.
25
Q

Purely/mainly solid lesion, T2 hypointense

A
  1. Fibrothecoma spectrum—composition ranges from purely fibrous
    (fibroma) to purely theca cells (thecoma). Apart from pure
    thecomas, these are typically solid and hypoechoic ± acoustic
    shadowing on US, and T2 hypointense on MRI with minimal
    enhancement. Cystic change and calcification may be seen.
    Fibromas can be associated with ascites and pleural effusions
    (Meigs syndrome), and are common in women with Gorlin-Goltz
    syndrome (usually bilateral).320 Aids to Radiological Differential Diagnosis
  2. Brenner tumour—benign transitional cell tumour. Typically <2 cm
    (smaller than fibrothecomas) + characteristic amorphous
    calcification. T2 hypointense on MRI + mild-moderate enhancement.
    May coexist with a cystadenoma. Malignant form (TCC) is rare
    and indistinguishable from other malignant epithelial tumours.
  3. Uterine fibroid—separate from the ovary; either pedunculated
    and projecting into the adnexa (± vessels extending to the uterus)
    or parasitic (attached to broad ligament). T2 hypointense on MRI,
    enhances more than ovarian fibroma.
  4. Ovarian adenofibroma—solid form of cystadenofibroma. T2
    hypointense + enhancement.
  5. Ovarian fibromatosis (mimic)—peripherally located follicles are
    indicative.
  6. Lithopaedion—rare; also known as ‘stone baby’. Results from an
    abdominal ectopic pregnancy where the dead fetus is too large to
    be broken down and absorbed by the mother’s body, so it
    becomes heavily calcified instead. Characteristic appearance on
    plain film and CT.
26
Q

Adnexal

Purely/mainly solid lesion, not T2 hypointense

A
  1. Ovarian metastasis—e.g. from breast, stomach or uterus. Typically
    bilateral and usually in the presence of disease elsewhere.
  2. Ovarian stromal tumours.
    (a) Pure thecoma—rare, usually seen in postmenopausal women. Well-defined, intermediate T2 signal + moderate enhancement. May show microscopic fat on in/out of phase sequences. Secretes oestrogen so can cause endometrial thickening.
    (b) Sertoli-Leydig cell tumour—usually presents in young women with virilization. Typically a heterogeneous hypervascular mass ± foci of T2 hypointensity and/or cystic change.
    (c) Sclerosing stromal tumour—rare, benign, typically seen in young women with menstrual irregularity. Heterogeneously T2 hyperintense solid mass ± small cysts. Characteristic avid peripheral enhancement with centripetal filling.
  3. Malignant ovarian germ cell tumours—typically in children or young adults. Usually solid but cystic change can occur due to haemorrhage and necrosis. Note that there may be a mixture of cell types.
    (a) Dysgerminoma—solid, intermediate T2 signal with avidly enhancing T2 hypointense fibrovascular septa ± calcification.
    (b) Immature teratoma—usually contains small foci of fat and calcification.
    (c) Yolk sac tumour—large hypervascular mass + prominent intratumoural vessels. Often appears solid-cystic due to haemorrhage and necrosis. Raised serum αFP.
    (d) Choriocarcinoma—aggressive, rare (more commonly metastatic from an intrauterine primary). Large hypervascular mass + central necrosis/haemorrhage. Raised serum ß-hCG.
    (e) Embryonal carcinoma—very rare in pure form. Nonspecific large solid mass with areas of necrosis and haemorrhage. Raised serum ß-hCG.
  4. Primary ovarian carcinomas—can occasionally be mainly solid.
  5. Pelvic actinomycosis—subacute presentation, associated with a
    longstanding IUD. Bilateral predominantly solid tuboovarian abscesses + ill-defined infiltrative soft tissue invading adjacent structures—this can be extensive ± fistulae with bowel or skin.
  6. Lymphoma*—usually secondary, often bilateral. Homogeneous ovarian masses without ascites. Disease elsewhere is usually present.
  7. Polypoid endometriosis—rare form, histologically similar to an endometrial polyp. T2 hyperintense enhancing mass with a T2 hypointense rim.
  8. Carcinosarcoma—rare, aggressive, usually metastatic at presentation. Heterogeneous enhancing solid mass ± cystic change/necrosis ± invasion of adjacent structures.
  9. Carcinoid tumour—rare, usually in peri- or postmenopausal women. Solid hypervascular mass; may arise within a mature cystic teratoma. Carcinoid syndrome is common.
  10. Massive ovarian oedema (mimic)—peripherally located follicles
    are indicative.
27
Q

Bilateral adnexal masses

A
  1. PID—bilateral hydrosalpinx or tuboovarian abscesses.
  2. Endometriosis*—bilateral endometriomas ± haematosalpinx. The
    ovaries are often pulled towards the midline by adhesions and may
    touch (‘kissing’ ovaries).
  3. Invasive/borderline ovarian malignancy—particularly serous
    tumours. Stage 1b if bilateral. Benign serous cystadenomas can
    also be bilateral.
  4. Metastases—including lymphoma. Typically bilateral.
  5. Germ cell tumours—dermoid cysts and dysgerminomas are
    bilateral in 10%–20%.
  6. Ovarian hyperstimulation syndrome/theca lutein cysts—clinical
    context is indicative.
  7. Ovarian hyperthecosis—mildly enlarged T2 hypointense ovaries.
  8. Sarcoidosis*—very rare.
28
Q

GYNAECOLOGICAL FISTULAE

A
  1. GI inflammation—e.g. Crohn’s disease (enterovaginal),
    diverticulitis (colovaginal), anal fistula (anovaginal).
  2. Iatrogenic—e.g. hysterectomy (ureterovaginal), obstetric trauma
    (vesicovaginal).
  3. Malignancy—of gynaecological tract or other pelvic organs.
  4. Infective—e.g. actinomycosis, TB.
  5. Post radiotherapy.
  6. Endometriosis*.
  7. Congenital—e.g. high imperforate anus + rectovaginal fistula.
    Seen in neonates.
29
Q

NONGYNAECOLOGICAL PELVIC

MASS LESION

A
  1. Bowel origin—e.g. diverticular/Crohn’s abscess, colorectal cancer,
    appendix mass, GIST.
  2. Bladder origin—e.g. tumour, malakoplakia.
  3. Nodal mass—e.g. lymphoma.
  4. Peritoneal origin—e.g. inclusion cyst, cystic mesothelioma,
    metastases, desmoid tumour.
  5. Retroperitoneal origin—e.g. lymphocele, haematoma,
    lymphangioma, liposarcoma, neurogenic tumour, solitary fibrous
    tumour.
  6. Presacral—e.g. chordoma, epidermoid cyst, tailgut cyst,
    myelolipoma, extramedullary haematopoiesis.
30
Q

Cystic vaginal/vulval mass

A
  1. Gartner duct cyst/Müllerian cyst—indistinguishable on imaging, both typically located in the anterolateral wall of the upper vagina, above the lower margin of the symphysis pubis. Gartner duct cysts arise from Wolffian ducts, so can be associated with
    renal anomalies.
  2. Epidermal inclusion cyst—due to previous trauma or surgery. Usually in the posterolateral wall of the lower vagina or vulva.
  3. Bartholin cyst—in the posterolateral wall of the lower vagina/introitus, medial to the labia minora.
  4. Skene duct cyst—lateral to the urethral meatus.
  5. Urethral diverticulum—periurethral cystic lesion, usually at the level of the midurethra. Often has a horseshoe configuration ±stones. Due to Skene gland infection and abscess formation that then ruptures into the urethra, forming a diverticulum.
  6. Hydrocele of the canal of Nuck—due to a patent processus vaginalis resulting in encysted fluid within the inguinal canal that
    can extend into the labia majora.
  7. Vulvar abscess—higher risk in diabetics and pregnancy. Clinical features of infection. Complex cystic lesion + wall enhancement and surrounding fat stranding. Note that the other cysts in this list can also become infected and form an abscess.
  8. Vascular lesions of the vulva—varicosities of the labia or round
    ligament can develop in pregnancy. Vascular malformations, including lymphangiomas, can involve the vulva.
  9. Haematocolpos—distended vagina filled with menstrual blood. Due to either an imperforate hymen, vaginal atresia, a transverse vaginal septum or a longitudinal vaginal septum + obstructed hemivagina. Presents in adolescence after menarche.
  10. Ectopic ureterocoele—can insert onto the urethra.
  11. Periurethral collagen injection—treatment for stress incontinence. Can mimic a urethral diverticulum. Other periurethral bulking agents can mimic a mass or calcification.
  12. Endometrioma—rare; can be superficial (related to surgery, e.g.
    episiotomy) or deep (usually in the posterior fornix, related to
    pelvic endometriosis).
31
Q

Solid vaginal/vulval mass

A
  1. Secondary vaginal malignancy—more common than primary
    tumours; usually via contiguous spread. Common sources include
    ovaries, cervix, endometrium and anorectum.
  2. Primary vaginal malignancy—usually SCC; enhancing infiltrative
    mass with intermediate T2 signal, most commonly arising from
    the upper vaginal wall in postmenopausal women. Less
    commonly adenocarcinoma (young women, T2 hyperintense),
    melanoma (usually postmenopausal, lower vagina, may be T1
    hyperintense), leiomyosarcoma (discrete heterogeneous
    submucosal mass + haemorrhage and necrosis),
    rhabdomyosarcoma (in children), yolk sac tumour (<3 years old),
    lymphoma (homogeneous mass; more commonly secondary).
  3. Leiomyoma—can arise from submucosa of vagina (usually
    anterior wall) or urethra. Well-defined, low or intermediate T2
    signal, homogeneous enhancement.
  4. Aggressive angiomyxoma—arises from vulval/perineal soft
    tissues; usually large and extends cranially through the pelvic
    floor between the pelvic viscera without invading them. Gynaecology and obstetrics 325
    10
    Heterogeneously T2 hyperintense with a characteristic swirled
    appearance + avid enhancement. Benign but high rate of local
    recurrence. Similar but less invasive variants (cellular
    angiofibroma, angiomyofibroblastoma) can also occur—these are
    usually smaller (<5 cm), limited to the vulva/perineum, and tend
    to appear more homogeneous on MRI but can also have a
    swirled appearance.
  5. Fibroepithelial polyp—usually small and polypoid, arising from
    the lateral wall of the lower vagina.
  6. Condyloma acuminatum—due to HPV infection. Large irregular
    superficial carpet-like mass involving the anus and vulva ± vagina.
    Can be invasive and transform to SCC.
  7. Endometriosis*—can appear solid and T2 hypointense.
  8. Labial haematoma—e.g. due to surgery or straddle injuries.
  9. Lichen sclerosus—diffuse T2 hypointensity in the perineum and
    labia + mild enhancement.
  10. Urethral caruncle—benign ectropion of urethra. Cuff of T2
    hyperintense tissue surrounding urethral meatus.
  11. Other rare tumours not specific to the vagina/vulva—e.g.
    lipoma, haemangioma, solitary fibrous tumour, nodular fasciitis,
    nerve sheath tumour, paraganglioma, hidradenoma, Merkel cell
    tumour
32
Q

ULTRASOUND FEATURES OF A NORMAL

INTRAUTERINE PREGNANCY

A

4.5 weeks: visible gestational sac (2–5 mm).
• 5.5 weeks: visible yolk sac (should be seen when gestational sac is
12 mm).
• 6 weeks: embryonic pole is visible and heart rate may be seen
• 6.5 weeks: normal sac growth 1.2 mm per day (on transvaginal
scanning). Embryo 4–10 mm with a heartbeat. If not seen, missed
miscarriage highly likely.
• 7 weeks: crown–rump length (CRL) 11–16 mm. Cephalad and
caudal poles distinguished.
• 8 weeks: CRL 17–23 mm. Forebrain, midbrain, hindbrain and limb
buds visible.

33
Q

FEATURES OF MISCARRIAGE

ON ULTRASOUND

A

• Threatened miscarriage—live fetus visible; pregnancy will be subsequently lost in 15%.
• Missed miscarriage—retention of gestational sac following fetal
death. Typically asymptomatic. Most reliable US features to confirm fetal death are:
Gestational sac: mean sac diameter ≥25 mm without a yolk sac or fetal pole.
Fetal pole: CRL ≥7 mm without detectable cardiac activity.
Other signs include deformity or abnormally low position of the gestational sac.
Incomplete miscarriage—pregnancy has incompletely discharged.
RPOC have variable appearances and vascularity on US, and can be hard to differentiate from blood clots. Clinical and biochemical correlation essential to exclude ectopic pregnancy.
•Complete miscarriage—no residual uterine pregnancy. Empty
uterus with normal endometrial thickness (may be subtly irregular).
Difficult to diagnose, as an empty uterus can also be seen in ectopic pregnancy and very early intrauterine pregnancy

34
Q

US findings of ectopic pregnancy

A
  1. No evidence of an intrauterine pregnancy—highly suggestive if
    ß-hCG >1800 IU/L.
  2. Endometrial thickening—pseudogestational sac may be seen in
    10%–29%; this is a small amount of intrauterine fluid that can
    mimic a gestational sac (but tends to have an irregular shape).
  3. Fluid in pelvis—often slightly echogenic as it is usually blood.
  4. Adnexal mass—often complex and vascular.
  5. Live fetus/fetal cardiac activity outside uterus occurs in about 10%.
  6. No ultrasound abnormality does not exclude ectopic gestation.Gynaecology and obstetrics 327
    10
  7. Live intrauterine gestation normally excludes the diagnosis of
    ectopic pregnancy but beware the coincidental ectopic twin
    gestation (~1:30,000 in unstimulated population).
  8. Location of ectopic pregnancy can vary:
    (a) Tubal—most common (>90%), usually in the ampullary
    portion. Implantation in the isthmic or interstitial portions has
    a higher risk of rupture.
    (b) Abdominal—usually implants on the pelvic ligaments or pouch
    of Douglas, but can be found anywhere in the peritoneal
    cavity (may need CT/MRI to locate). Can obtain blood supply
    from abdominal organs. Higher risk of mortality.
    (c) Ovarian—can mimic a corpus luteal cyst in the early stages.
    (d) Cervical—can mimic a miscarriage in progress. Features
    favouring miscarriage include absent fetal heartbeat, an
    irregular sac and an open cervical os. Repeat US may be
    required.
    (e) Caesarean scar—gestational sac located anteriorly in the lower
    uterus; may look similar to cervical ectopic. High risk of uterine
    rupture
35
Q

PLACENTAL ABNORMALITIES

A

. Placental abruption—premature separation of a normally sited
placenta, resulting in antepartum haemorrhage. Associated with
maternal hypertension, smoking, drug abuse, trauma, fibroids and
other risk factors. Haematoma may be hyperechoic (acute),
isoechoic or hypoechoic (subacute) relative to placenta, and is
usually located at the placental margin; less commonly
retroplacental or preplacental. If isoechoic, mimics placental
thickening; if hypoechoic, can mimic focal myometrial contraction
(transient), uterine fibroid, venous lake or chorioangioma.
Haematoma is avascular on Doppler, aiding differentiation from
mimics. Note that in many cases a haematoma is not seen—this
does not exclude the diagnosis.
2. Placenta praevia—a portion of the placenta covers the internal
cervical os; high risk of maternal and fetal haemorrhage during
labour. US diagnosis at the 18–20 week scan is far greater than
incidence at term due to differential growth of the lower uterine
segment. ‘Low-lying placenta’ and ‘touching the os’ are terms no
longer advised on the 18–20 week scan. The placenta must cross
the internal os to initiate a follow-up scan (NICE).
3. Vasa praevia—abnormal fetal vessels coursing through the
membranes over the internal cervical os; high risk of fetal
haemorrhage during labour. Usually associated with velamentous
insertion of the umbilical cord (i.e. inserting directly onto the
membranes), but can also occur in placentas with >1 lobe where
vessels traverse the membranes to connect the lobes.328 Aids to Radiological Differential Diagnosis
4. Morbidly adherent placenta—abnormal myometrial adherence or
invasion by placental chorionic villi. Caused by a focal decidual
defect typically related to previous caesarean section(s) or other
uterine interventions; often occurs in the presence of placenta
praevia. High risk of catastrophic maternal haemorrhage during
labour. Depth of invasion determines subtype, but this is often
difficult to classify on imaging—general features on US include
multiple turbulent linear vascular channels (lacunae) extending
from placenta into myometrium, loss of the retroplacental
hypoechoic clear space and myometrial thickness <1 mm. On MRI,
the placenta may contain heterogeneous T2 signal with
hypointense bands of fibrosis, and there may be focal bulging or
interruption of the myometrium.
(a) Placenta accreta—placenta is attached to myometrium (rather
than decidua) without direct invasion. Commonest form, least
severe.
(b) Placenta increta—placenta partially invades myometrium.
(c) Placenta percreta—placenta invades full thickness of
myometrium ± adjacent structures, e.g. bladder. Suggestive
imaging features include loss of the fat plane between uterus
and bladder, increased vascularity in the bladder wall or direct
extension of placental tissue beyond the uterus. Least common
form, most severe—high risk of uterine rupture.
5. Placental masses—excluding abruption (avascular haematoma,
see above).
(a) Placental lake—well-defined hypoechoic vascular space
containing slow nonturbulent blood flow (cf. lacunae). May
thrombose (intervillous thrombus).
(b) Placental cyst—well-defined, anechoic, avascular. Usually
asymptomatic unless large (>4.5 cm) or multiple.
(c) Chorioangioma—benign hamartoma, most common
placental tumour. Well-defined, hypoechoic and hypervascular;
usually located on the fetal side of placenta close to the
umbilical cord. Fetal complications can occur if >5 cm or
diffuse in nature (chorioangiomatosis).
(d) Gestational trophoblastic disease—see Section 10.16.
(e) Placental mesenchymal dysplasia—large thick placenta
containing multiple cysts. Can cause fetal growth restriction,
death or preterm delivery. Associated with
Beckwith-Wiedemann syndrome. Mimics partial molar
pregnancy, but multiple fetal anomalies and markedly elevated
ß-hCG levels are usually seen in a partial mole.
(f) Placental metastases—rare, most commonly from maternal
melanoma, lymphoma, breast or lung cancer, or fetal
neuroblastoma.
(g) Placental teratoma—very rare; usually on the fetal side of
placenta. Well-defined heterogeneous mass + calcification with minimal internal flow on Doppler. Can mimic an acardiac
twin—absence of organized fetal structures or umbilical vessels
aids differentiation

36
Q

GESTATIONAL TROPHOBLASTIC DISEASE

6

A
  1. Complete hydatidiform mole—most common, due to fertilization
    of an empty ovum. Large complex echogenic hypervascular
    multicystic mass with no identifiable fetal tissue. May mimic
    placental hydropic degeneration after a failed pregnancy, but is
    usually more vascular with higher ß-hCG levels. Rarely, a complete
    mole may coexist with a normal twin, thereby mimicking a partial
    mole or placental mesenchymal dysplasia—but the presence of a
    second normal placenta helps exclude these.
  2. Partial hydatidiform mole—due to fertilization of a normal ovum
    by two sperm. Similar appearance to a complete mole except
    fetal tissue is present, albeit growth-restricted with multiple
    anomalies.
  3. Invasive mole—most commonly develops after evacuation of a
    hydatidiform mole. Heterogeneous echogenic hypervascular mass
    ± small cysts or foci of haemorrhage and necrosis. Locally invades
    the myometrium ± adjacent structures, but does not typically
    metastasize.
  4. Gestational choriocarcinoma—similar appearance to an invasive
    mole but often metastasizes (most commonly to lungs). The
    primary tumour may be very small. 50% develop after a molar
    pregnancy, the rest after abortion, miscarriage or normal
    pregnancy (usually within 1 year, but can be longer).
  5. Placental site trophoblastic tumour—rare. Similar appearance to
    choriocarcinoma but produces little ß-hCG and is chemoresistant,
    requiring surgery.
  6. Epithelioid trophoblastic tumour—very rare, produces little
    ß-hCG. Can occur many years after pregnancy.
37
Q

MATERNAL COMPLICATIONS DURING PREGNANCY

7

A
  1. Nongynaecological—e.g. appendicitis, urinary tract infection or
    obstruction, biliary obstruction or infection. CT is best avoided, US
    ± MRI are preferable. In the case of suspected pulmonary embolus,
    low-dose perfusion-only scintigraphy is recommended unless the
    CXR is abnormal, in which case low-dose CTPA is preferable.
  2. Red degeneration of a uterine fibroid—not uncommon,
    particularly in large fibroids. Contains cystic spaces on US with
    internal echoes and absent internal Doppler flow. Contains T1
    hyperintensity on MRI.
  3. Adnexal torsion—usually occurs at 12–14 weeks gestation.
  4. HELLP syndrome—complication of preeclampsia characterized by
    Haemolysis, Elevated LFTs and Low Platelets, which can result in
    hepatic subcapsular haemorrhage, rupture or infarction.
  5. Hyperreactio luteinalis
  6. Ovarian luteoma—rare benign ovarian tumour that occurs in
    pregnancy and can cause maternal virilization. Solid, hypoechoic
    and vascular on US. Regresses after delivery.
  7. Ectopic deciduosis—this can occur in two settings (both regress
    after delivery):
    (a) Within preexisting endometriomas, creating enhancing mural
    nodules that are isointense to the placenta on all sequences
    on MRI.
    (b) In the peritoneum, due to progesterone-induced metaplasia of
    mesenchymal cells, creating peritoneal nodules (mainly in the
    pelvis) that can mimic metastatic disease. If peritoneal
    deciduosis occurs on the serosal surface of the appendix, it
    can mimic appendicitis.
38
Q

POSTPARTUM COMPLICATIONS

A
  1. Haemorrhage—causes include uterine atony, RPOC, morbidly
    adherent placenta and uterine rupture or dehiscence. Intrauterine
    blood clots may be seen on imaging.
  2. Endometritis—pelvic pain and clinical features of sepsis; more
    common after caesarean section. Can be related to RPOC or
    intrauterine blood clots. Imaging features are nonspecific and
    overlap with normal postpartum state, so mainly a clinical
    diagnosis. Intrauterine fluid, gas, debris and RPOC ± increased
    vascularity may be seen.
  3. RPOC—can occur postpartum or after miscarriage or abortion.
    Heterogeneous echogenic material within endometrial cavity that
    usually demonstrates vascularity on US/MRI (cf. intrauterine blood
    clots which are avascular and usually more hypoechoic). May
    contain calcification. Note that a normal postpartum uterus may
    contain fluid and echogenic foci.
  4. Uterine rupture/dehiscence—rupture usually occurs during labour
    at a previous caesarean-section site, but can be delayed and occur
    postpartum. A myometrial defect ± haematoma ±
    haemoperitoneum may be seen on imaging. Dehiscence of a
    recent caesarean-section incision is often due to infection and can
    be associated with a bladder flap haematoma (situated between
    the bladder and uterus).
  5. Adnexal torsion—can occur as the uterus returns to the pelvis.
  6. Ovarian vein thrombosis—R>L, usually due to endometritis
    leading to ascending septic pelvic thrombophlebitis. High
    attenuation thrombus within a distended ovarian vein on
    unenhanced CT ± surrounding fat stranding. Hypoattenuating on
    postcontrast CT, may be mistaken for a dilated ureter