GYNECOLOGIC EMERGENCIES: BEYOND TORSION Monisha Shetty MD, Syed Zafar H. Jafri MD, FACR Beaumont Health, Royal Oak, MI OUWB School of Medicine, Rochester, MI Society of Abdominal Radiology Annual Meeting, San Diego, CA 2015 DISCLOSURES

• The speakers have no relevant financial relationships which may be considered conflicts of interest in regards to this workshop. TEACHING GOALS

• To present imaging examples of uterine, fallopian tubal ovarian and vaginal pathology as well as entities in the setting of early pregnancy that can present acutely

• To highlight specific imaging features that can aid in the diagnosis of these entities

• To focus on more rare acute entities, recognizing that the more common entities, including ovarian torsion, are well covered in the literature BACKGROUND

• Gynecologic emergencies most often present with pelvic pain and/or vaginal bleeding • These symptoms frequently send patients to the ER for assessment • Additional information to seek out includes the following: – ß‐HCG – past pelvic surgical history – pregnancy history • While US is the first‐line modality of choice for female pelvic complaints, symptoms may be non‐specific, leading to a CT as the initial imaging study in the ER • Recognition of acute gynecologic conditions on CT as well as US is valuable for this reason UTERINE ENTITIES WILL INCLUDE:

• Neglected IUD with infection • Ectopically located IUD • Uterine perforation • Fibroid complications including prolapse, torsion • Uterine inversion, uterine torsion • UAE complications including retained abdominal fibroid • Utero‐enteric fistula • Uterine dehiscence • Pyometra/endometritis • Hematometra • Trauma • CA NEGLECTED IUD WITH ACTINOMYCOSIS • Background: Actinomyces commonly present in normal vaginal flora although can cause endometritis, pelvic inflammatory disease, pelvic abscess, retroperitoneal fibrosis • Approximately 7 % of women using an IUD have actinomyces‐like organisms on a Papanicolaou (Pap) test ; only half of these women will have positive actinomyces cultures • Presentation: If asymptomatic, likely represents colonization • Infection occurs when mucosa is disrupted • Treatment: If woman shows signs or symptoms of pelvic infection: – Antibiotics – Culture IUD anaerobically – Remove IUD (Acitomyces grows preferentially on foreign bodies) • Increased duration of IUD thought to increase risk of infection – In one study, duration of 8 years on average • Imaging findings are not specific to this microbe, but it can cause fistulas IUD PERFORATION

• Presentation: Patients may be asymptomatic or have pain/bleeding • Risk factors include the following: – Clinician inexperience – Immobile uterus – Retroverted uterus – Myometrial defect • Pre‐existing or created by uterine sound or IUD insertion device • Imaging: US may reveal IUD embedded in myometrium or in pelvic cul‐de‐ sac – If not seen, obtain radiograph to exclude expulsion • Management: – If in myometrium, can remove hysterscopically – If in peritoneal cavity, requires laparoscopy or laparotomy • Usually embeds in adhesions, next to sigmoid colon, in omentum or in cul‐de‐sac • Reports of bladder perforation • Bowel perforation not reported with newer IUDs UTERINE PERFORATION AFTER D & C • Presentation: History of gynecologic intervention, with abdominal pain (usually not bleeding) • Background: Uterine perforation causes: – Iatrogenic : dilatation and curettage, hysteroscopy, endometrial ablation, insertion of intrauterine contraceptive devices – Spontaneous causes (less common): gestational trophoblastic disease, pyometra, placenta accreta, degenerating myoma • WHO reports risk of uterine perforation with D & C to be 0.07‐1.2 % • Most common site of myometrial perforation in uterine surgeries is relatively avascular anterior or posterior midline surfaces • Imaging: Hypoechoic or anechoic/hypoattenuating transmural myometrial defect +/‐ small bowel filling the defect, free fluid, extrauterine fetal parts if D & C done for abortion – Look for evidence of associated bowel perforation FIBROID COMPLICATIONS

• Degeneration of a fibroid when it outgrows its blood supply can present with acute pain • Imaging: Cystic components within fibroid with hypoenhancement

• Red degeneration is another type of acute fibroid degeneration caused by thrombosis of the venous outflow – Seen in pregnancy and in patients on the oral contraceptive pill – Results in a rapid increase in fibroid size with acute hemorrhagic infarction – Imaging: Features unique to this entity best appreciated by MRI

• Torsion of a pedunculated fibroid • Imaging: Fibroid on a stalk with absent enhancement +/‐ free fluid

• Prolapse of a submucosal fibroid – Can rarely lead to uterine inversion, although more commonly a post‐partum complication (look for mirror image of uterus, pseudostripe, target sign) • Imaging: Stalk of fibroid with internal vessels coursing into endocervical canal or vagina FALLOPIAN TUBE ENTITIES WILL INCLUDE: • PID including: – TOA – Pyosalpinx – Fitz‐Hugh Curtis Syndrome • Hydrosalpinx/Hematosalpinx • Tubal torsion • Fallopian tube CA PELVIC INFLAMMATORY DISEASE (PID)

• Background: Infection that typically spreads via cervix and endometrium into fallopian tubes, ovaries and peritoneum • Gonorrhea and chlamydia most common pathogens • Increased risk of PID with IUD • Less common causes: – Direct extension from regional infection (appendicitis, diverticulitis) – Post‐partum or post‐abortion complication – Hematogenous spread (TB) • Imaging: – Normal early in course – Endometrial thickening/fluid (endometritis) – Dilated tube with complex fluid or fluid‐pus level (pyosalpinx) • Wall thickness of ≥ 5mm suggests acute disease • Cogwheel sign • Beads on a string • Incomplete septa • Waist sign—best to discriminate hydrosalpinx from other masses – Enlarged, multi‐cystic ovaries with indistinct margins – Echogenic fluid (pus) in cul‐de‐sac TUBO‐OVARIAN ABSCESS (TOA)

• Background: Result of progressing infection – Periovarian adhesions form – Fusion of tube and ovary • Structures may be indistinguishable from each other • Cannot be separated by transvaginal transducer pressure • Can mimic other adnexal masses— “clinical correlation” required • Presentation: Clinical findings of fever, leukocytosis, and cervical motion tenderness very important • Imaging: CT findings – Thick‐walled, low‐attenuation adnexal mass with thick septations, fluid‐debris levels, regional fat infiltration – Gas bubbles are the most specific radiologic sign of abscess but are unusual in tubo‐ovarian abscess – +/‐ associated ileus, hydroureteronephrosis, intraperitoneal abscesses secondary to rupture • US findings – Thick‐walled adnexal mass containing complex fluid, with thick septations, increased echogenicity of regional fat • Treatment: ABX or drainage ISOLATED FALLOPIAN TUBE TORSION • Background: Presents with acute pain; definitive diagnosis rarely made pre‐operatively • Incidence: – 1 in 1.5 million women • Right > left; theorized due to tubal immobilization by sigmoid mesocolon • Intrinsic causes include: dilated fallopian tube, chronic PID with adhesions, prior pelvic surgery, congenital tubal abnormalities, paratubal cysts • Extrinsic causes include: adnexal mass, uterine enlargement • Course: Congestion, necrosis and gangrene/superinfection and peritonitis • Imaging: Midline cystic mass (either superior to uterus or in cul‐de‐sac) with a NORMAL ipsilateral ovary OVARIAN ENTITIES WILL INCLUDE:

• Ovarian hyperstimulation • Theca lutein cysts • Ovarian cyst rupture with hemoperitoneum • Inguinal hernia containing ovary • Ovarian abscess from diverticulitis • Ruptured endometrioma • Ovarian CA presenting acutely OVARIAN HYPERSTIMULATION • Background: Rare, potentially fatal complication following ovulation induction • Causative medications include: – Injectable gonadotropins – Clomiphene citrate – Gonadotropin‐releasing hormone • Pregnancy can exacerbate condition • High estradiol levels and large number of follicles can lead to: – Ascites and pleural effusions – Depletion of intravascular volume – Oliguria – Thromboembolic symptoms (arterial and venous reported) – Ovarian torsion /hemorrhage/cyst rupture • Imaging features include: – Increased ovarian volume – Numerous large follicles often with thin echogenic borders – Increased blood flow – Ascites, pleural effusions • Management: Close monitoring by US necessary to tailor exogenous hormones – Abort treatment cycle – Withhold hormones for 1‐3 days before oocyte aspiration OVARIAN CYST RUPTURE • Background: Most functional ovarian cysts asymptomatic and resolve in 1 to 2 menstrual cycles • Although rupture and hemorrhage of an ovarian cyst may be a self‐limited process, significant hemoperitoneum is a potential complication • Hemodynamic status or amount of hemoperitoneum may guide operative versus conservative management • Can mimic a ruptured ectopic pregnancy – Correlation with LMP and ß‐HCG essential • Imaging: – Hemoperitoneum—hematocrit level in free fluid or internal echoes/high attenuation – May see active extravasation on CECT – Corpus luteum—thick walled, peripherally vascular, < 3cm, internal echoes, crenulated – Hemorrhagic cyst—internal reticulation, retractile clot with concave margins, no internal flow, variable wall thickness INGUINAL HERNIA CONTAINING OVARY

• Background: Inguinal hernias occur in less than 5% of women—may not be recognized – Typically indirect (neck lateral to inferior epigastric artery origin) – Hernia contents most commonly omentum or bowel • Adnexal herniation is rare and more common in infants due to anatomy including a short inguinal canal • Risk factors include: – Abnormalities of the fallopian tube or ovary causing weighted descent – Lengthening of the broad, uterine, or ovarian suspensory ligaments in high parity patients resulting in displacement of adnexal structures – High intra‐abdominal pressures from frequent Valsalva maneuvers in patients with chronic cough or frequent heavy lifting • Potential complications of hernia include: – Incarceration (trapped organs) – Strangulation (disruption of blood flow) – US may confirm hernia but CT may aid in complication detection • Presentation: Diagnosis of inguinal hernia often made by history and physical exam alone – Painless or painful bulging in the groin – Exacerbation of symptoms with Valsalva maneuver • Imaging: Ovary in inguinal canal; can confirm its identity by looking for follicles, following gonadal vein, noticing absence of ovary in expected location in adnexa VAGINAL ENTITIES WILL INCLUDE:

• Foreign body • Fistulas including: – Cecovaginal – Vesicovaginal – Ureterovaginal – Rectovaginal • Labial cellulitis • Bartholin’s abscess VAGINAL FISTULAS

• Background: Rectovaginal fistula is the moost common GI fistula involving the genital tract in women • Causes: obstetric complications, inflammatory bowel disease, gynecologic malignancy, surgery, radiation • Presentation: Presents as passage of feces through vagina • Imaging: – Vaginography , CT and MR are useful modalities • On CT, look for air or oral contrast in vagina – GI study may not demonstrate communication unless large • Treatment: Complex surgical repair – At least temporary colonic diversion often necessary • Cecovaginal fistula: Uncommon, but reported in literature as a result of cecal diverticulitis VAGINAL FISTULAS

• Background: Ureterovaginal fistula causes: – GYN procedures, most commonly hysterectomy – Coexistent vesicovaginal fistula common • Urine collects in the pelvis and dissects into the vaginal suture line • Vesicovaginal fistulas causes: – GYN procedures, most commonly hysterectomy – Less commonly, radiation, trauma – In developing countries, childbirth and infection • Presentation: Patients present with urinary incontinence per the vagina +/‐ fever • Imaging: – Vaginography, excretory urography, and retrograde pyelography, as well as with CT and MR – Ureterovaginal fistula: Excretory urography , contrast enhanced CT with delayed images may reveal extravasation of contrast material in a collection outside the ureter, eventually draining into vagina – Vesicovaginal fistula:Excretory urography, contrast enhanced CT with delayed images or US with microbubbles may show communication LABIAL CELLULITIS/ABSCESS

• Background: Vulvar infection pedisposing factors include edema (often seen in pregnant patients), obesity, DM – Reported increase in community acquired MRSA, an organism that causes tissue necrosis • Imaging: Edema (comparison to contralateral side may help) and fluid collection • Treatment: ABX active against MRSA, I & D if abscess has developed

• Beware of potential progression to Fournier Gangrene, a rapidly progressing infection of superficial fascia and subcutaneous tissues • Imaging: early stages may not demonstrate gas • Gas may extend to the inguinal regions, thighs, body wall, and retroperitoneum

• Also consider hydradenitis suppurativa: – Chronic disease of follicular occlusion and secondary involvement of apocrine glands; can become infected – Can manifest with abscesses, fistulas, sinus tracts and scarring in the intertriginous areas of body (axillary, inframammary and anogenital) – Infection can become systemic EARLY PREGNANCY‐RELATED ENTITIES WILL INCLUDE: • Ectopic pregnancy: – Tubal, bilateral, heterotopic, interstitial, c‐section, ovarian • Retained products of conception • Arteriovenous malformation • Molar pregnancy/choriocarcinoma DIAGNOSTIC CRITERIA FOR NON‐ VIABLE PREGNANCY OVERVIEW • Diagnosis of pregnancy failure by TVUS: – Embryonic crown‐rump length ≥7 mm and no heartbeat – Mean gestational sac diameter ≥25 mm and no embryo present – No embryo with heartbeat ≥2 weeks after TVUS showed a gestational sac without a yolk sac – No embryo with heartbeat ≥11 days after TVUS showed a gestational sac with a yolk sac

• For evaluation and management of a woman with pregnancy of unknown location when TVUS reveals no intrauterine fluid and no obvious adnexal abnormalities – A single hCG assessment, regardless of level, does not reliably determine a pregnancy's location or viability – hCG levels in women with nonviable IUPs, viable IUPs, and EPs overlap substantially) – A single hCG level <3000 mIU/mL should not elicit treatment for presumed EP – A single hCG ≥3000 mIU/mL indicates that viable IUP is possible but unlikely. At least one additional hCG level should be measured before initiating treatment for EP

• For pregnant women in whom TVUS has not been performed, hCG level does not predict probability of EP rupture • For high clinical suspicion of EP, TVUS should be performed even if hCG level is low ECTOPIC PREGNANCY • Background: Tubal: Most common (95%) – Distinguish from CL—CL wall will be less echogenic than endometrium and CL will be intraovarian – Adherent ectopic or exophytic CL—short term followup will reveal a CL to evolve rapidly in its appearance • Labs: ß‐HCG will not rise normally; increase by less than 50% over 48 hours highly suggestive of non‐viable pregnancy (intra‐ or extrauterine) • Imaging: – Extrauterine GS with yolk sac or embryo (100% specific) – Tubal ring (100%) – Complex adnexal mass separate from ovary (92‐99%) – Echogenic fluid (96%) – Desidual cast (92%) • These features have varying sensitivities, with complex adnexal mass being the most sensitive (89‐100%); abdominal pressure combined with TV probe pressure may aid in separating ovary from ectopic pregnancy – Endometrial thickness will be varied – +/‐ pseudosac (10%)—ovoid, centrally located in cavity, poorly defined, absent desidual reaction and single desidual layer compared to early IUP ECTOPIC PREGNANCY

• C‐section: Sac implants in the myometrium through a dehiscence and myometrium continues to thin as sac grows; tx includes abortion followed by repair of the uterine defect • Intersitial: Sac implants in intramyometrial segment of fallopian tube; sac can grow silently until later rupture; myometrium is < 5mm in thickness in one plane; interstitial line in continuity with sac (80% sensitive; 98% specific); eccentric sac can be misleading (fibroids ,contractions, uterine anomalies can cause this) • Cervical: Sac with peritrophoblastic flow or live embryo (vs. AB—sac will change shape) • Abdominal: Typically develops in broad ligament and recruits blood supply from omentum or regional organs • Heterotopic: In high risk patients (fertility treatment); presence of IUP does not elimiinate need for careful inspection of adnexa • Ovarian: Ovum is fertilized and retained in ovary; strong association with IUDs; may be difficult to distinguish from a CL RPOC

• Background: RPOC is defined as residual fetal or placental tissue remaining after delivery, miscarriage, or termination • Presentation: RPOC is a cause of secondary post‐partum hemorrhage (occurring > 24 hours and < 6 weeks after delivery) • Imaging: – Avascular (type 0)markedly vascular (type 3) • 45% of the patients with type 0 vascularity had RPOC; 86% of those with type 1 had RPOC; 100% of those with types 2 and 3 had RPOC • Type 3 can mimic AVM—inform OB because D & C can lead to hemorrhage – Echogenic mass (distinguishable from endometrium) had a moderate positive predictive value (80%) but low sensitivity (29%) for RPOC • Could represent blood clot – Peak systolic velocities ranged from 10 to 108 cm/s (average, 36.1 cm/s) – Resistive indices in arterial waveforms ranged from 0.33 to 0.7 (average, 0.5) – Thickened endometrium (8‐13 mm) • ß‐HCG value should be taken into account AVM

• AVM defined as an abnormal connection between artery and vein without an intervening capillary bed • In uterus, acquired much more common than congenital – D & C, therapeutic AB, uterine surgery, direct uterine trauma, endometrial/cervical CA, GTD • Present with intermittent but severe bleeding, suggesting an arterial source • ß‐HCG will be negative; no source of production • Imaging: – Myometrial heterogeneity or anechoic spaces – Tangle of vessels with multi‐directional flow • High velocity (average 60 cm/sec in one study) • Low resistance (average 0.40 in one study) • Management: Anemia or hemodynamic instability will prompt embolization; otherwise, conservative management as traumatic AVMs may spontaneously regress • Misdiagnosis as RPOC with subsequent D & C could be catastrophic – Type 3 RPOC vascularity can be robust and extend into the myometrium GESTATIONAL TROPHOBLASTIC DISEASE • Background: Encompasses: Complete and partial hydatidiform mole, invasive mole, chorioCA and placental site trophoblastic tumor • Diagnosis often made sonographically, before there is clinical suspicion for GTD • Therefore, familiarity with imaging features is essential, but early imaging features can be non‐specific • In one study, only 40% of HM were diagnosed pre‐evacuation; the remainder were diagnosed at missed AB • Presentation: Irregular bleeding, large uterine size, hyperemesis, expulsion of hydropic vesicles • ß‐HCG is useful more to diagnose and manage persistent GTD, not to make the initial diagnosis due to large variations in values • Imaging: – Heterogeneous intrauterine mass with varied anechoic spaces with high velocity, low resistance flow – Invasive mole and chorioCA—myometrial invasion – ChorioCA‐‐mass enlarging uterus, necrosis and hemorrhage