Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

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Figure 12.23. Adenomyosis. Sagittal T2-weighted image identifies an enlarged uterus containing multiple hyperintense myometrial foci (arrowheads). (Source: Imaoka I,Wada A, Matsuo M, Yoshida M, Kitagaki H, Sugimura K. MR imaging of disorders associated with female infertility: use in diagnosis, treatment, and management. RadioGraphics 2003;23:1401–1421, with permission from the Radiological Society of North America.)

nomyomas have a T2-weighted tumor signal intensity similar to that of adenomyosis. Adenomyotic cysts are filled with heterogeneous, often hyperintense fluid on T1-weighted images; some have a hypointense rim on T2weighted images.

Uterine artery embolization is alternate therapy for women with menorrhagia due to adenomyosis. Studies suggest an improvement in symptoms and quality of life (69). Contrast enhanced MRI after uterine artery embolization reveals adenomyosis devascularization (70).

Leiomyomatous Tumors

Clinical

Uterine leiomyomas, also called fibroids and myomas, are well-marginated tumors consisting of smooth muscle and fibrous connective tissue. They do not have a true capsule. A familial pre-

disposition exists to uterine leiomyomas. Their prevalence increases with age and they are more common in black than in white women.

Leiomyoma growth is variable and unpredictable. Increased tumor vascularity appears to predispose to growth; a leiomyoma with a detectable feeding artery is more prone to increase in volume than one without an identifiable feeding artery (71). With growth, ischemia leads to necrosis, hemorrhage, fibrosis, and calcification. Leiomyomas often grow during pregnancy; growth tends to be greatest during the first trimester. Following pregnancy, some myomas revert to their prepregnancy size. Some decrease in size after discontinuation of oral contraceptives.

Leiomyomas range in location from intraluminal, to intramural, to subserosal, some even being pedunculated. Intramural ones are confined to myometrium, submucosal tumors extend into the uterine cavity, and subserosal ones extend from the outer margin (exophytic). Intramural leiomyomas are the most common but the least often symptomatic. Larger myomas distort the uterine cavity but tend not to interfere with pregnancy unless they are located in the lower uterine segment or cervix. A submucosal location is the least common, but these are most often symptomatic, resulting in dysmenorrhea and infertility. An occasional pedunculated submucosal leiomyoma protrudes into the cervix. Some subserosal leiomyomas become pedunculated and mimic an extrauterine tumor or extend laterally into the broad ligament and mimics an ovarian tumor.

Lipoleiomyoma

Fat is normally not present in the myometrium, but is occasionally found in regions of degeneration or metaplasia. Fat is also detected in some leiomyomas, and pathologists label these mesenchymal neoplasms lipoleiomyomas. They constitute about 1% of all leiomyomas. Some pathologists believe that uterine lipoleiomyomatous tumors do not constitute a single entity but represent two distinct neoplasms: lipoleiomyoma and angiolipoleiomyoma. The former probably originates from lipomatous metaplasia within a leiomyoma, while the latter is analogous to a renal angiomyolipoma.

Magnetic resonance findings of uterine lipoleiomyomas vary considerably depending

on predominant tumor composition; some are even hyperintense on T2-weighted images.

Imaging

Intramural myomas are usually evaluated by transabdominal US and occasionally by endovaginal US, MRI, and hysteroscopy. Their follow-up is with US, although if a uterinesparing myomectomy is contemplated and number and specific location of these myomas is needed, greater accuracy and sensitivity of MRI is advantageous.

Larger leiomyomas calcify and have a characteristic conventional radiographic appearance familiar to most radiologists.

Computed tomography shows a homogeneous, lobular uterine tumor, with any necrotic regions appearing hypodense. Aside from

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necrosis, most myomas enhance with contrast similar to normal myometrium, while most carcinomas are hypodense, although overlap exists (Fig. 12.24). Submucosal myomas growing into the uterine lumen tend to have a complex appearance, contain a hypervascular component, and at times mimic a carcinoma or sarcoma.

In women with uterine tumors, endovaginal US achieves a sensitivity of 90% to 95% in diagnosing leiomyomas. Specificity varies considerably, depending on false-positive rate. Although endovaginal US is more accurate than transabdominal US in a number of conditions, this may not be true for leiomyomas, especially those originating from the fundus and transabdominal US is indicated.

The sonographic diagnosis of most uterine myomas is straightforward. Most appear as

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hypoechoic solid tumors having discrete margins. With cystic degeneration, especially in the submucosa, US reveals a “honeycomb” pattern mimicking endometrial hyperplasia. Some leiomyomas produce discrete acoustic shadowing with both transabdominal and endovaginal US (72). This shadowing originates from fibroid, muscle, and connective tissue transitional zones. Central hypoechoic foci and no detectable Doppler blood flow in some exophytic leiomyomas presumably represent necrosis.

Endovaginal color Doppler US provides myoma blood flow data. Intratumoral blood flow has a negative correlation with myoma size. Some myomas have PI values <1.0, similar to some malignancies. In general, neither PI nor RI can differentiate a myomatous from a nonmyomatous uterus.

Magnetic resonance imaging appears superior to US in detecting and localizing leiomyomas and establishing their relationship to the uterus. Nondegenerated leiomyomas are isointense to hypointense on T1and also hypointense on T2-weighted images. Tumor margin is usually well defined, with an occasional hyperintense rim identified on T2weighted images. Degeneration results in a variable appearance, with hemorrhage having a higher signal intensity on T1-weighted images and cystic degeneration being hypointense on T1and hyperintense on T2-weighted images. Cystic regions do not enhance after intravenous (IV) contrast. Some initially nonenhancing regions postcontrast do eventually enhance on delayed images, probably due to vascular insufficiency. If needed, different imaging planes are useful to show that a pedunculated leiomyoma connects to the uterus.

Flow voids are detected by MRI between the uterus and some larger leiomyomas (73); pathologically, these flow voids are believed to represent dilated feeding arteries located outside of the leiomyoma.

The ovaries should be identified if a suspected leiomyoma has an atypical appearance or location. If the tumor cannot be separated from the ovaries, an ovarian fibroma/thecoma is in the MR differential diagnosis.

Complications

Clinically, some degenerated uterine leiomyomas mimic acute appendicitis; US aids in

differentiating between these two conditions. Torsion, most often with a pedunculated subserosal leiomyoma, and hemorrhagic infarct of a leiomyoma lead to ischemia and an acute abdomen. Magnetic resonance imaging identifies a hyperintense rim on T1and a hypointense rim on T2-weighted images, probably representing dilated blood vessels at the periphery.

Occasionally a large leiomyoma results in urinary retention. Similarly, a more posterior one can compress the rectum and result in constipation. A myomatous uterus compressing pelvic veins can induce pelvic vein thrombosis.

A leiomyosarcoma develops de novo either from smooth muscle cells or from sarcomatoid degeneration of a leiomyoma; the latter is rare but should be suspected if a myoma increases rapidly in size.

A rare uterine leiomyomatosis extends into the vena cava and even intracardiac.

Therapy

Medical therapy of fibroids ranges from nonsteroidal antiinflammatory drugs (NSAIDs) to hormonal therapy. Tumors do shrink in size but generally regrow after cessation of therapy.

Surgical options range from hysterectomy to myomectomy, including laparoscopic and hysteroscopic approaches.

Since the initial description in 1995 of selective arterial embolization of myomas with Ivalon particles (74), uterine artery embolization has evolved as viable therapy for symptomatic myomas. Considerable literature confirms that it is a less invasive and is safer in women with symptomatic leiomyomas than a myomectomy (75). Myoma feeding arteries are endarteries, while the myometrium is supplied by a collateral network. Thus myometrial vascularity tends to be preserved even in the face of myoma ischemia and necrosis. Presence of adenomyosis is not a contraindication to uterine artery embolization because similar therapy is also beneficial in women with adenomyosis. Postprocedure MR suggests that successful embolization results in hemorrhagic infarction (Fig. 12.25). Most investigators embolize polyvinyl alcohol particles, although gelatin microspheres, used in neuroradiology, appear promising. Most embolizations are bilateral; bilateral uterine artery embolization

can be performed using a single femoral approach.

First-pass postcontrast MRI can monitor uterine perfusion after fibroid embolization (76). The clinical utility of such monitoring is not clear. Arterial spin tagging MRI assesses uterine fibroid perfusion before and after arterial embolization (77); this technique provides an estimate of tumor volume and perfusion changes after embolization.

Reported symptomatic improvement ranges from 80% to 85%, results similar to those

obtained with myomectomy. Pain and fever are common after the procedure. An occasional postprocedure infection requires hysterectomy. Sloughed fibroids (78), uterine necrosis (79) and even death secondary to overwhelming sepsis after embolization have been reported (80). Uterine artery embolization can lead to loss of ovarian arterial perfusion, but US reveals that most women reestablish perfusion and do not develop ovarian failure (81). Amenorrhea develops in a minority. On the other hand, embolization avoids surgery in most patients, and

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menstrual periods return to normal in menorrhagic women. Full-term pregnancy has occurred after embolization.

Postprocedure imaging follow-up, if deemed necessary, consists of measuring decrease in myoma volume, uterine volume, or change in uterine blood flow. All require that a similar preprocedure imaging study be available. A marked reduction in fibroid volume occurs after successful embolization, with mean myoma volume continuing to decrease for a number of months. Follow-up US shows about a 50% eventual reduction in uterine volume. Serial gadolinium-enhanced MRI reveals that completely infarcted uterine fibroids eventually decrease in size considerably, but partially infarcted ones can regrow and result in recurrent symptoms (82). Interestingly, a preembolization high signal intensity on T1-weighted images predicted a poor response and a high signal intensity on T2-weighted images a good response, but the degree of contrast enhancement did not correlate with myoma volume reduction (83).

Another therapeutic option is laser ablation of uterine fibroids using an open MR scanner for needle guidance. One study achieved a mean fibroid volume decrease of 38% at 3 months (84); a percutaneous approach under local anesthetic was used.

Neither US nor MRI differentiates between a leiomyoma and a leiomyosarcoma, and one concern is embolizing a leiomyosarcoma. A biopsy is generally not helpful. A rationale for continuing to perform embolization is the very low prevalence of sarcomatous degeneration, but a sarcoma is in the differential diagnosis if a tumor continues to grow after embolization; sarcomas tend to develop an extensive parasitic blood supply (85).

Lipoma

Lipomatous uterine tumors include pure lipomas, fibrolipomyomas, and lipoleiomyomas (discussed previously). These tumors are not common. With some, a correct preoperative diagnosis can be suggested by imaging. Differentiation between a lipomatous uterine tumor and an ovarian dermoid has clinical significance, because most lipomatous tumors can be observed. A dermoid, on the other hand, is associated with more complications and is

usually resected. The boundaries and origin of a large lipomatous tumor are difficult to establish with endovaginal US; therefore, in this setting transabdominal US with its better global definition is worthwhile.

Ultrasonography shows a homogeneous, hyperechoic tumor, similar to a dermoid. Doppler US reveals lack of blood flow. To differentiate between the two, a tumor site of origin needs to be established; a lipomatous tumor originates from uterine myometrium, while most dermoids are ovarian in origin.

Hemangiopericytoma

Uterine hemangiopericytomas are rare. They are readily confused with a highly vascular leiomyoma or leiomyosarcoma. There is no specific imaging finding for these tumors.

Adenomatoid Tumor/Benign

Mesothelioma

These are rare, benign tumors usually presenting as a focal mass. An occasional one infiltrates the myometrium diffusely.

Cervical Cysts

Nabothian cysts, or inclusion cysts, of the cervix are common. They vary in size considerably. Although most are incidental findings, the larger ones and multiple cysts tend to enlarge the cervix.

T2-weighted MR images reveal a hyperintense signal, reflecting the cystic nature of these lesions. They are sharply marginated and do not enhance postcontrast.

Hydrometrocolpos

Hydrometrocolpos means a nonsanguineous fluid-filled uterus and vagina. The most common cause is an imperforate hymen, although it may also be secondary to undetected vaginal atresia. Hydrometra and hematometra occur with cervical obstruction. A unilateral hydroor hematometrocolpos develops in a bicornuate uterus with an obstructing partial vaginal septum.

Ultrasonography of hydrometrocolpos reveals a cystic, anechoic structure. Residual

blood products lead to an increase in echogenicity.

Pyometra

The imaging findings of pus in the uterine cavity, or pyometra, are similar to those seen with hydrometra or hematometra.

Malignant Tumors of the Uterus and Cervix

A majority of endometrial malignancies are adenocarcinomas. Less common are adenoacanthomas, transitional cell carcinomas, adenosquamous carcinomas, and squamous carcinomas.

Adenocarcinoma

Clinical

The most frequent gynecologic malignancy in women is an endometrial adenocarcinoma. Initially detected tumors are mostly stages I and II. Overall, they are associated with a relatively good prognosis, with a 5-year disease-free survival being over 80%. Most develop in postmenopausal women. Premenopausal women with these tumors are prone to develop synchronous ovarian malignancies.

An association between human papilloma virus (HPV) infection and ovarian and endometrial carcinomas is controversial. Some studies point to only a limited association, while others have found HPV sequences in roughly half of ovarian carcinomas and some endometrial carcinomas. The biologic significance of such infection is yet to be determined.

Conditions believed to be risk factors for endometrial carcinoma include those that result in unopposed endometrial stimulation by estrogen and include obesity, hypertension, diabetes mellitus, polycystic disease (SteinLeventhal syndrome), long-standing estrogen use, and functioning granulosa cell tumors and thecomas. In premenopausal women some forms of endometrial hyperplasia evolve into an adenocarcinoma. On rare occasion an endometrial adenocarcinoma develops in a setting of an intrauterine pregnancy. In postmenopausal women, unopposed estrogen replacement therapy is associated with these tumors. An

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estrogen antagonist, tamoxifen, is used for adjuvant therapy of breast cancer. Tamoxifen has an estrogenic effect on the endometrium, and therapy increases the risk of endometrial carcinoma, endometrial polyps, and cystic hyperplasia.

Even if an endometrial cancer shows no myometrial invasion, hysterectomy does not necessarily result in cure; recurrence, peritoneal dissemination, and lymph node metastases are possible due to earlier spread.

With growth, some endometrial carcinomas obstruct the cervix and result in hydrometra or hematometra.

Screening for endometrial cancer consists mostly of measuring endometrial thickness with endovaginal US, especially in postmenopausal women (discussed in a previous section).

Pathologic Study

Common endometrial adenocarcinomas predominate. Less often found are papillary, serous, mucinous, and clear-cell adenocarcinomas. A rare oxyphilic cell variant of endometrioid adenocarcinoma is believed to represent an early stage of adenocarcinoma. The rare hepatoid adenocarcinoma is discussed in a later section.

Detection

The diagnostic approach to a woman with postmenopausal bleeding and suspected endometrial carcinoma consists of endometrial and endocervical curettage performed under anesthesia, often on an outpatient basis. A hysteroscopic approach is used if the above procedure is unsatisfactory.

Hysterosalpingography is rarely performed for suspected endometrial carcinoma. The incidentally detected carcinoma appears as a single or multiple irregular tumor extending into the uterine cavity.

Computed tomography reveals an endometrial carcinoma either as a focal or diffuse uterine wall thickening. These cancers show less contrast enhancement than normal myometrium or cervix. Cervical canal obstruction is inferred by detecting intraluminal fluid, although obstruction may be due to benign