MRI of the Ovaries and Adnexa

Technique

Similar to cervical and uterine lesions, the potentially small size of ovarian lesions necessitates the need for high resolution imaging; the examination justifies the use of a high field strength system (≥1.0 T). As delineated in Chapter 9 diagnostic images can be obtained with systems of lower field strength.

Imaging evaluation is similar to that employed for the uterus. A combination of T1-weighted, T2-weighted, and fat-saturated sequences suffices to solve most problems encountered in the pelvis. T2-weighted images are the mainstay of pelvic imaging. T2-weighted images confer conspicuity to the ovaries and most adnexal lesions, especially cystic lesions. T2-weighted images highlight cystic adnexal lesions and any potential septa, mural nodules, or other complex features. T1-weighted images depict hemorrhage and lipid, and the addition of fat-saturated sequences allows for differentiating between blood and fat (which both appear hyperintense in T1-weighted images without fat suppression). In- and out-of-phase images serve as a time-saving alternative to spin echo T1-weighted images (approximately 20 seconds compared with 3–5 minutes) with sensitivity to both intracellular fat and susceptibility artifact, although potentially degraded by low signal-to-noise in low field strength systems.

Gadolinium-enhanced images provide additional information regarding the complexity and/or blood supply of a lesion and its tissue content and often increase lesion conspicuity. Enhancement of an ovarian lesion confirms its neoplastic etiology. Enhancement patterns provide diagnostic information. For example, arterial enhancement characterizes an arteriovenous fistula and delayed enhancement characterizes fibrous lesions ( Table 10.1 ), such as an ovarian fibroma. Dynamic imaging provides a reliable time frame to assess enhancement patterns, whereas static pre- and postgadolinium images yield only binary information (enhancement versus no enhancement). Quantitative evaluation of fibroid vascularity demands dynamic images.

TABLE 10.1

Adnexal Lesion Enhancement Patterns

Lack of enhancement	Simple/functional cyst Paroovarian cyst Ovarian torsion
Mild rim enhancement	Corpus luteal Endometrioma Some cystadenoma ± Ovarian torsion
Marked rim enhancement	Some cystadenoma/cystadenocarcinoma Tuboovarian abscess
Solid enhancement
Early arterial	Arteriovenous malformation Malignant > benign epithelial ovarian neoplasms
Delayed	Fibroma Benign > malignant epithelial ovarian neoplasms

Three-dimensional fat-saturated gradient echo images offer the best spatial resolution and tissue contrast. Approximately 20 mL of gadolinium (0.1 mmol/kg) is administered intravenously at approximately 1 to 2 mL/second. A timing bolus or timing sequence triggers the arterial phase of the acquisition and one or two additional phases obtained in succession suffice. A delayed T1-weighted (preferably fat-saturated) sequence detects delayed enhancement, if present.

Interpretation

If pictures are worth a thousand words, imagine how much the hundreds of images in the multiimage set of a female pelvis MR study are worth. This much information compels the use of a directed search pattern ( Box 10.1 ). First of all, assess the technical adequacy of the examination. Review the localizer sequence, which usually includes large field-of-view coronal images, and ensure that coil placement is adequately reflected by the highest signal emanating from the region of interest. Note whether gadolinium was administered and whether enhancement is perceptible. Assess the degree of motion artifact and any other artifact that degrades image quality.

BOX 10.1

Female Pelvis Checklist

Technical

• Magnetic field strength

• Coil position

  • Signal—optimal signal corresponding to pelvis

  • Kidneys—at least one large FOV coronal to include kidneys

• Enhancement—note amount and type of contrast agent

  • Inspect vessels for adequate enhancement

• Artifacts

  • Bowel peristalsis

  • Susceptibility—surgical hardware, gas (ie, bowel)

  • Motion—bulk motion, vascular flow artifacts

  • Conductivity/dielectric effects—focal signal loss

Adnexa

• Ovaries

  • Dimensions

  • Cystic lesions

    • Size

    • Hemorrhage

    • Shading

    • Lipid

    • Rim enhancement

    • Solid component/complexity

  • Solid lesions

    • T2 signal

    • Unilateral vs bilateral involvement

• Parovarian region

  • Cystic lesions

  • Vascular lesions

  • Lymphadenopathy

Other Anatomy

• Bladder

• Bowel

• Musculoskeletal structures

  • Bony pelvis

  • Lower lumbar spine

  • Muscles—gluteal, adductors, hip flexors, piriformis

  • Tendons—iliopsoas, rectus femoris, hamstring

Look for the ovaries, often a difficult task as a result of their small size in prepubertal and older women and to their variable location. The presence of ovarian cysts often attracts your attention to their location. In the absence of an easily identifiable ovariform structure, remember the relevant anatomy tethering the ovaries in the pelvis ( Fig. 10.1 ). The suspensory ligament contains the vascular structures and originates from the pelvic sidewall in the region of the iliac bifurcation connecting to the ovary. The round “ligament” (actually composed largely of smooth muscle) is the female equivalent of the spermatic cord and courses from the uterine cornua into the inguinal canal through the deep inguinal ring in an effort to maintain anteversion. The proper ovarian ligament originates adjacent to the round ligament, but unfortunately usually averts detection as a discrete structure. Measure the ovaries in three planes, and record measurements of any associated ovarian lesions.

Parenthetically, MRI occasionally supplements ultrasound in detecting acute ovarian/adnexal pathology. Under acute circumstances, consider the possibility of (ectopic) pregnancy, tuboovarian abscess, or torsion and rupture of a preexisting ovarian lesion (such as dermoid) ( Box 10.2 ). Pay particular attention to fluid-sensitive sequences (such as T2-weighted fat-saturated and inversion recovery sequences), which most vividly portray the edema, inflammation, and/or fluid, almost always associated with acute pathology.

BOX 10.2

Acute Adnexal Pathology

Ectopic pregnancy

Ovarian torsion

Tuboovarian abscess

Ruptured cystic lesion (eg, ruptured dermoid cyst)

Leiomyoma degeneration

Assess the quantity of free fluid in the pelvis, and remember that a small quantity is physiologic in reproductive-age females. Especially if there is a history of (ovarian) carcinoma, exclude the presence of peritoneal thickening, enhancement, or nodularity/implants. Look for pelvic lymph nodes, and record any enlarged nodes.

Normal Anatomy

The adnexa include the ovaries and everything else—paired fallopian tubes, broad and other parametrial ligaments, and the associated vascular structures. Only the ovaries are consistently well visualized and of clinical relevance—disorders of the supporting structures are beyond the scope of this text. The size and appearance of the normal ovary depend on the menstrual status ( Fig. 10.2 and Box 10.3 ). Female hormones induce growth and functional cyst development in the ovary, and normal ovarian features are listed in Fig. 10.3 .

BOX 10.3

Normal Ovarian Volume (0.523 × length × width × thickness)

Premenstrual: 3.0 mL

Reproductive age: 9.8 mL (2.5–5.0 × 1.5–3.0 × 1.0–2.0 cm)

Postmenopausal: 5.8 mL

The first task is to find the ovaries, usually located in proximity to the iliac vessels, near the bifurcation. However, the ovaries are not rigidly tethered. Medially, they are adherent to the fallopian tubes, caudally to the broad ligament, medially to the proper ovarian ligament, and superolaterally to the suspensory ligament, which contains the ovarian vessels ( Fig. 10.4 ). Usually T2-weighted images provide the best anatomic roadmap and chance of finding the ovaries. First just scour the adnexa for an ovariform structure with or without cysts. Next trace the ovarian vein caudally over the iliac vessels into the suspensory ligament hopefully into a recognizable ovary. If that fails, try to find the round ligament entering the internal inguinal os and follow it posteromedially—proximally, it courses along the anterior edge of the broad ligament in the vicinity of the ovary and abuts the proper ovarian ligament ( Figs. 10.1 and 10.4 ). Inevitably loops of (usually small) bowel occupy the adnexal regions and complicate the process. As long as you exclude the presence of an underlying adnexal mass, you have accomplished your mission.

Ovarian lesion characterization and diagnosis figure prominently among the major indications for pelvic MRI and boast a high probability of success. A major discriminator is solid (or at least partially solid) versus cystic. Cystic lesions are far more common, and the approach should focus on two things—cyst content and complexity (differentiating neoplastic from nonneoplastic cysts) ( Table 10.2 and Box 10.4 ).

TABLE 10.2

Differential Diagnosis of Cystic Ovarian Lesions

Lesion	Tissue Content
T2 Hyperintense Adnexal Lesions
Pedunculated leiomyomata	Collagen
Endometrioma (shading)	Concentrated blood products
Ovarian torsion	Hemorrhage
Ectopic pregnancy	Hemorrhage
Vascular lesions	Signal voids
Cystadenofibroma (cystic components dominate)	Fibrous tissue
Fibroma/fibrothecoma	Fibrous stroma
Brenner tumor	Fibrous stroma
T1 Hyperintense Adnexal Lesions
Hemorrhagic cyst	Hemorrhage
Endometrioma	Hemorrhage
Pedunculated leiomyoma with hemorrhagic degeneration	Hemorrhage
Ovarian torsion (peripheral hyperintensity)	Hemorrhage
Dermoid cyst (hypointense with fat suppression)	Fat
Bilateral Adnexal Lesions
Functional ovarian cysts
Ovarian epithelial neoplasms
Metastases (Krukenberg’s tumor)
Endometriosis
Estrogenic Adnexal Lesions
Granulosa cell tumor (most common)
Thecoma/Fibrothecoma
Virilizing Adnexal Lesions
Sertoli-Leydig tumor
Cystic teratoma
Metastases

BOX 10.4

Age-Predictive Probability Scheme for Cystic Ovarian Lesions

From Gant NF, Cunningham FG. Basic Gynecology and Obstetrics. Norwalk, CT: Appleton and Lange, 1993.

Prepubertal	Reproductive	Menopausal
Germ cell, 80%	Functional, 70%	Malignant, 50%
Malignant, 10%	Endometrioma, 10%
	Neoplastic, 20%
	Benign, 85%
	Malignant, 15%

Cystic Lesions

First of all, to call a lesion cystic, you must exclude a change in intensity between T1-weighted pre- and postgadolinium images (which is an analog to perfusion, implying solid tissue). Catalog the signal intensity in the various pulse sequences. Using these data, almost all cysts fall into one of three broad categories based on their content: 1) water, 2) hemorrhage, and 3) lipid.

Cystic ovarian lesions cannot be assessed in one pulse sequence alone. Accurate classification requires binary information from various pulse sequences. The T2-weighted axial sequence portrays cystic lesions consistently as round hyperintense foci—albeit mildly variable depending on cyst content (water > blood and fat). Next note the signal intensity in a T1-weighted sequence without fat saturation—hypointensity connotes water and hyperintensity indicates lipid or blood. Finally, review T1-weighted fat-saturated images to distinguish between fat and blood; signal cancellation indicates fat. Although this seems redundant, following this scheme avoids errors in characterization. Some common errors include: designating a T1 hyperintense lesion as a hemorrhagic cyst or endometrioma without noting signal suppression in fat-saturated images, or misclassifying a T2 hyperintense lesion with no signal in T1-weighted fat-saturated images as a dermoid without considering the possibility of a simple cyst with no signal in T1-weighted images without fat saturation.

Water Content

Of course to equate water with ovarian cyst content of any etiology is an oversimplification. Nonetheless this construct serves its purpose to identify a population of ovarian cysts that are further subclassified. “Water” defines the limits of hyperintensity in T2-weighted images with commensurate hypointensity in T1-weighted images. Enhancement is absent ( Fig. 10.5 ). Under these circumstances, as long as the size of the lesion does not violate physiologic limits and there is no evidence of wall thickening, septation, or mural nodularity to suggest an underlying neoplasm, no further analysis is necessary.

Functional Ovarian Cysts

The normal menstrual cycle involves the recruitment of a cohort of functional (or follicular) cysts that are generally smaller than 1 cm. A single dominant cyst enlarges up to 3.0 cm and usually undergoes ovulation, evolving into the corpus luteal cyst. Hemorrhagic cysts join the other two categories of functional cysts (follicular and corpus luteal) and reflect blood from a ruptured vessel in the wall of a follicular cyst (see the Cystic Lesions section— Blood Content ). Even the postmenopausal ovary often continues to produce cysts that are usually spherical, simple, and unilocular. Therefore regardless of age, simple ovarian cysts up to 3.0 cm in diameter require no follow-up ( Box 10.5 ). This includes corpus luteal cysts, which characteristically exhibit a rim of enhancement and a nonspherical shape ( Fig. 10.6 ). Although the internal contents often approximate simple fluid, hemorrhage occasionally may coexist, resulting in T1 hyperintensity (without T2 hypointensity—or shading—which indicates concentrated, or long-standing blood products characteristic of endometriomas, to be considered later).

BOX 10.5

Ovarian Cyst Management

<3.0 cm → no follow-up necessary (regardless of age)

3.0–7.0 cm → yearly ultrasound follow-up

>7.0 cm → suggest surgical management (risk of torsion)

Ovarian Inclusion Cyst

An ovarian inclusion cyst is an equally benign, incidental lesion common in menopause and during the reproductive years. Imagine the ovarian surface epithelium invaginating, forming a self-enclosed cavity, and losing its connection with the surface from which it arose (which likely occurs during ovulation)—that is the etiology of an ovarian inclusion cyst. Although ovarian inclusion cysts may be a precursor to ovarian epithelial neoplasms, they exhibit simple features indistinguishable from a follicular cyst, usually measuring no more than 1.5 cm. Because of the absence of physiologic ovarian cysts and the relative prevalence of postmenopausal cystic ovarian neoplasms, surveillance of postmenopausal ovarian cysts has been observed historically, according to different, often institutionally driven, guidelines. Follow-up algorithms informed by the features of inclusion cysts and the risk of torsion with increasingly large lesion size generally conform to the following guidelines: 1) <30 mm, no follow-up; 2) 31 mm to 7 cm, yearly follow-up; and 3) ≥7 cm, surgical evaluation. However, the burden of evidence indicates an exceedingly low likelihood of neoplasm associated with cystic lesions regardless of age. Consequently cystic ovarian lesions up to 3 cm generally require no surveillance.

Peritoneal Inclusion Cyst

Another variety of inclusion cysts, developing in the appropriate clinical setting, are actually extraovarian. The peritoneal inclusion cyst should only be considered when a history of pelvic surgery or trauma (or possibly endometriosis) is confirmed. The necessary precursors to a peritoneal inclusion cyst are adhesions and active ovarian tissue. Ovarian secretions gradually accumulate as traumatized, reactive, mesothelial tissue absorbs fluid less freely forming locules between leaves of peritoneum and/or adhesions. As a consequence of this pathogenesis and growth pattern, peritoneal inclusion cyst margins are at least partially spatially defined by anatomic structures; they fill (potential) spaces rather than create their own space, like tumors or endothelially derived cystic lesions do. Obtusely angulated margins with adjacent structures are observed, because they insinuate around instead of displacing structures. They are usually located around (occasionally surrounding) or in proximity to the ovary. Their contents usually approximate simple fluid (T1 hypo- and T2 hyperintense) with no enhancement ( Fig. 10.7 ).

The problem with this diagnosis is the protean appearance of peritoneal inclusion cysts, which overlaps with the appearance of multiple other lesions, including ovarian neoplasms, hydro- or pyosalpinx, and parovarian cysts. First of all this diagnosis should not be considered without the appropriate preexisting condition—history of peritoneal injury/manipulation. Secondly an extraovarian location must be established. With septation, or other evidence of complexity (which is usually relatively sparse and often attributable to the envelopment of adjacent structures), stability on prior or follow-up examinations is confirmatory. Finally margins that conform to extralesional structures, such as the pelvic sidewall, loops of bowel, or the uterus, are characteristic of peritoneal inclusion cysts.

Parovarian Cysts

True parovarian cysts are uncommon, are usually simple, water-containing cysts, and occasionally simulate simple ovarian cysts. They arise in the mesosalpinx, between the ovary and fallopian tube. Parovarian cysts are usually mesothelial or embryologic remnants (usually paramesonephric versus mesonephric). Their clinical importance lies in their frequent symptomatic nature and diagnostic confusion with primary ovarian pathology.