{"paper_id":"7eac57a0-93f5-4931-9359-98b4249f1346","body_text":"177\n13\nBenign Disease of the Uterus\nHelen Addley and Fiona Fennessy\n13.1  Introduction\nBenign diseases of the uterus are common and can be debili-\ntating for patients with severe symptoms. Imaging is instru -\nmental in diagnosing these conditions, ultrasound being the \nfirst-line investigation of choice. Correctly identifying con -\ngenital abnormalities of the uterus leads to optimal manage-\nment, which in some cases can lead to a successful pregnancy \noutcome. Correct high-quality imaging performed optimally \nis therefore fundamental to patient management.\n13.2  Modalities for Imaging the Uterus\n13.2.1  Ultrasound\nPelvic ultrasound is the first-line examination in the investi-\ngation for gynecological symptoms both in pre- and post-  \nmenopausal patients [ 1]. Pelvic ultrasound is therefore the \ninitial diagnostic test of choice for the investigation of symp-\ntoms that are due to benign diseases of the uterus. The most \ncommon of these are dysmenorrhea and menorrhagia. \nUltrasound examination of the pelvis should include trans -\nvaginal examination (TVUS) which clearly demonstrates the \nuterus and its components, i.e., the myometrium, endome -\ntrium, and the myometrial/endometrial interface. The posi -\ntion of the uterus (anteverted, axial, or retroverted) should be \nassessed as well as uterine size (in longitudinal and trans -\nverse sections). The myometrium should be assessed for \nfocal fibroids and diffuse heterogeneity. Heterogeneity of the \nmyometrium and difficulty visualizing the myometrial and \nendometrial interface should raise the possibility of adeno -\nmyosis. The endometrial thickness should be measured as \nstandard on the longitudinal section and the correlation with \nthe pre-menopausal date in the cycle or post-menopausal sta-\ntus be made as routine.\nLearning Objectives\n• Recognize the normal appearances of the uterus and \navoid benign pitfall appearances, e.g., myometrial \ncontractions.\n• Diagnose common benign disease processes of the \nuterus, e.g., fibroids, adenomyosis, endometriosis, \nand endometrial pathology.\n• Understand how congenital anomalies of the uterus \nare classified.\nKey Points\n• The diagnosis of DIE requires the presence of both \nmorphological and signal intensity anomalies.\n• Uterine leiomyomas use the FIGO classification \nsystem and are classified according to their loca -\ntion, to provide a uniform description to facilitate \nclinical care and research. It subdivides fibroids into \nsubmucosal, other (intramural and subserosal), and \nhybrid types.\n• The Mullerian duct abnormality classification sys -\ntem is clinically orientated, based on anatomy. The \nexternal uterine contour and the uterine wall thick -\nness—defined as the distance between the interos -\ntial line and a parallel line on the top of the \nfundus-are important considerations to appreciate.\nH. Addley (*) \nDepartment of Radiology, Cambridge University Hospitals NHS \nFoundation Trust, Cambridge, Cambridgeshire, UK\ne-mail: helenclare.addley@nhs.net \nF. Fennessy \nDepartment of Radiology, Brigham and Women’s Hospital, \nHarvard Medical School, Boston, MA, USA\ne-mail: ffennessy@bwh.harvard.edu\n© The Author(s) 2023\nJ. Hodler et al. (eds.), Diseases of the Abdomen and Pelvis 2023-2026, IDKD Springer Series, \nhttps://doi.org/10.1007/978-3-031-27355-1_13\n\n178\n13.2.2  MR/CT\nMR imaging is utilized as second-line imaging following \npelvic ultrasound with a focused question. When determin -\ning optimal fibroid treatment options, such as uterine artery \nembolization or MR-guided focused ultrasound surgery, MR \nimaging provides necessary pre-procedure anatomical and \nvascular supply detail. Similarly, MR imaging helps to plan \nthe optimal surgical technique, such as open myomectomy \nversus hysteroscopic resection. In addition, MR imaging \ndepicts the many different types of degeneration clearly, e.g., \ncystic, hyaline, or hemorrhagic, and may raise suspicious \nfeatures for leiomyosarcoma which cannot be appreciated on \npelvic ultrasound imaging.\nMR imaging for endometriosis is required for surgical \nmapping of endometriosis patients prior to surgical resec -\ntion. Subtle features of endometriosis, not apparent on US \nimaging, are often seen with MR imaging, such as thin endo-\nmetriotic plaques and distortion.\nThe MR imaging protocol depends upon the study indica-\ntion. Planning for uterine artery embolization or MR-guided \nfocused ultrasound ablation, intravenous contrast adminis -\ntration is required. Most of the remaining indications for \nbenign diseases of the uterus do not typically require intrave-\nnous contrast medium administration but require good prep-\naration and technique for high-quality imaging interpretation. \nPatients should ideally be asked to empty their bladder at \narrival for their appointment so that when their examination \nis started the bladder is not full or completely empty. This \nwill help to decrease difficulty with movement artifact dur -\ning the examination. An antiperistaltic agent, e.g., buscopan \nmay be used, subject to contraindications, to also decrease \nmovement artifact. The key sequences are multiplanar \nT2-weighted sequences in both sagittal and axial planes and \nthen also T1-weighted sequences for the assessment of blood \nproducts. Dual-phase T1-weighted imaging (in-phase/out-  \nof- phase) fat-saturated images allow for greater conspicuity \nof small areas of blood products in the assessment of endo -\nmetriotic deposits and adenomyosis. A small field of view \n(FOV) axial oblique sequence perpendicular to the long axis \nof the uterus is required for optimal assessment of the endo-\nmetrium and is also helpful for true assessment of the thick-\nness of the junctional zone. This plane is also used to assess \nthe fundal contour when suspicious of uterine anomaly \nsequence, which also requires evaluation of the upper \nabdominal in either a coronal or axial plane to visualize the \nkidneys fully to diagnose associated renal anomalies and \nagenesis.\nThere is no role for CT in the investigation of benign \ndiseases of the uterus. However, benign diseases of the \nuterus are often incidentally identifiable on CT e.g. calcifi -\ncation of uterine fibroids. In addition, given the nature of the \npresentation of endometriosis with pelvic pain, it is impor -\ntant that the radiologist remains vigilant in the assessment \nof possible pathology during CT examinations for other \nrequests.\n13.3  Normal Anatomy\nThe flexion (angle between the longitudinal axis of the uter-\nine fundus and cervix) and version (angle between the longi-\ntudinal axis of the cervix and vagina) are most commonly \nanteverted and anteflexed, but any of the four variants (ante-\nverted and anteflexed, anteverted and retroflexed, retroverted \nand anteflexed, and retroverted and retroflexed) are consid -\nered normal. The size of the uterus is variable but typically \nbetween 6 and 9 cm in length. The pre-menopausal uterus \ndemonstrates zonal anatomy (Fig.  13.1) from the central \nendometrial cavity (high signal intensity on T2-weighted \nMR imaging), inner myometrium junctional zone (low sig -\nnal intensity on T2-weighted MR imaging) and the outer \nmyometrium (higher signal intensity than the junctional \nzone on T2-weighted imaging). The outer serosal surface of \nthe uterus is thin and of low signal intensity on T2-weighted \nimaging. On ultrasound examination, the endometrial cavity \nand myometrium are well demonstrated, and a thickened \njunctional zone can be seen as heterogeneity and difficulty in \ndelineating the crisp endometrial margin with the myome -\ntrium. On MR imaging the zonal anatomy is best depicted on \nFig. 13.1  Sagittal T2 weighted image demonstrating normal zonal \nanatomy of the anteverted and anteflexed uterus. Endometrium ( *), \ninner myometrium (junctional zone white arrow), and outer myome -\ntrium (black arrow)\nH. Addley and F. Fennessy\n\n179\na b\nFig. 13.2 Sagittal T2 weighted image (a) and localizer image (b) The \nlow signal “band-like” area (white arrow) extending from the endome-\ntrial and myometrial interface into the myometrium may be mistaken \nfor adenomyosis but correlation to the localizer images demonstrates a \ntransient appearance in keeping with myometrial contraction. MR \nimaging in this case was performed for the ovarian cyst\nsagittal T2-weighted imaging. The normal thickness of the \njunctional zone on MR imaging is approximately 8 mm with \n>12  mm in keeping with adenomyosis. A pitfall is when \nthere is uterine contraction which can cause “band-like” arti-\nfact and subjective increases in thickness of the junctional \nzone. It is helpful to review the localizer sequences which in \ntransient uterine contraction will demonstrate a normal junc-\ntional zone thickness on another sequence in the same exam-\nination (Fig.  13.2).\nThe endometrial thickness varies depending upon the \nmenstrual cycle in the pre-menopausal uterus. During the \nproliferative phase, the endometrial thickness increases to \nbecome trilaminar in the mid-cycle which is seen clearly on \nultrasound examination. The thickness in this phase is typi -\ncally between 3 and 8 mm. In the latter secretory phase, the \nendometrium becomes more echogenic on ultrasound and \nincreased in thickness to 8–12 mm. In the post-menopausal \nuterus, an endometrial thickness of >4 mm is used to guide \nfurther direct assessment of the endometrial cavity with hys-\nteroscopy and sampling. The increased usage of hormone \nreplacement therapy (HRT) tamoxifen has increased the \nreferral of post-menopausal patients with endometrial thick-\nness >4 mm, but this threshold remains for consideration of \nendometrial sampling to exclude a malignant cause. In addi-\ntion to a decrease in endometrial thickness, the uterus \ndecreases in size following menopause.\n13.4  Benign Disease Processes\n13.4.1  Endometriosis\nEndometriosis is defined as ectopic functional endometrial \nglands and stroma outside of the uterus. The repeated bleed-\ning of these areas causes fibrosis and anatomical distortion.\nIn recent years there has been increased awareness and \nsupport regarding the importance of earlier detection of \nendometriosis to avoid the delayed diagnoses of these \npatients who are typically in pain for many years prior to \ntheir ultimate diagnosis. This has led to increased imaging \nfor pelvic pain and abnormal uterine bleeding at an earlier \nstage. First-line examination with ultrasound should ideally \naddress four components as described from the IDEA \n(International Deep Endometriosis Analysis) group [ 2], \nnamely: (1) routine examination of the uterus and adnexae \n(features for position of uterus, adenomyosis, and endome -\ntriomas); (2) evaluation of TVUS “soft-markers,” e.g., site-  \nspecific tenderness; (3) assessment of status of pouch of \nDouglas using real-time ultrasound-based “sliding sign” \nand; (4) assessment for deep infiltrating endometriosis (DIE). \nInvolvement of the torus uterinus from endometriosis with \nplaque formation is an example of deep infiltrating endome-\ntriosis and can extend to involve the adjacent rectosigmoid \ncolon (Fig.  13.3a, b). Similarly, involvement of the retrocer-\n13 Benign Disease of the Uterus\n\n180\na b\nFig. 13.3 Sagittal T2 weighted image (a) and axial T2 weighted image \n(b) demonstrating low signal intensity stellate plaque extending from \nposterior aspect of torus uterinus (a white arrow) in keeping with deep \ninfiltrating endometriosis with anatomical distortion and tethering of \nboth ovaries and rectosigmoid colon (b white arrow)\nvical region into the pouch of Douglas can cause immobility \nand therefore restricted sliding sign. The features of these \ndeposits on ultrasound and restricted movement can be sub -\ntle and therefore proactive examination and assessment is \nrequired by an experienced practitioner. DIE nodules can be \nseen most typically at the torus uterinus, retrocervical area, \nuterovesical area, and uterosacral ligaments. DIE nodules on \nultrasound are seen as hypoechoic areas and should be mea-\nsured in three orthogonal planes.\nMR imaging for endometriosis has also been optimized \nby clear guidelines from the ESUR [ 3]. MR imaging for \nendometriosis mapping of disease sites prior to surgical \nresection has improved surgical morbidity and led to \nimproved patient outcomes. The importance of a multidisci-\nplinary approach with the involvement of radiology, gyne -\ncology and colorectal or urological surgery when required \nhelps to ensure optimal discussion of treatment options for \nthese patients. The ESUR guidelines agreed that the diagno-\nsis of DIE required the presence of both morphological and \nsignal intensity anomalies. The signal intensity depends \nupon the age of the hemorrhage and therefore can have vary-\ning appearances [ 4]. The typical appearance involving the \nuterus is adhesions and DIE nodules. Adhesions are seen as \nlow signal intensity plaques (similar to fibrosis) on the poste-\nrior aspect of the uterus at the torus uterinus or retrocervical \nregion extending to the posterior compartment. Associated \nfeatures of anatomical distortion and tethering are common. \nDIE nodules contain endometrial glands and stroma and in \ncontradistinction to the adhesions which are low signal \nintensity on T1 and T2-weighted imaging these endometri -\notic deposits will typically demonstrate areas of focal high \nT1 signal intensity foci. Due to the multifocal nature of the \ndisease, it is important to assess all pelvic compartments for \nendometriosis which is out of the scope for this chapter.\n13.4.2  Adenomyosis\nAdenomyosis is the presence of ectopic endometrial glandu-\nlar cells within the myometrium. Adenomyosis may also be \npresent in patients with leiomyomas or with endometriosis. In \na recent study looking at the coexistence of leiomyomas, ade-\nnomyosis, and endometriosis and their risk for endometrial \nmalignancy, >50% of patients with leiomyomas also had \nadenomyosis and half of the patients with endometriosis also \nhad adenomyosis [ 5]. Differentiation of adenomyosis from \nleiomyomas is easier when adenomyosis is diffuse rather than \nfocal but is very accurate on MR imaging. In focal adeno -\nmyosis there is less surrounding mass effect of the lesion rela-\ntive to its size, e.g., distortion of the endometrial cavity for the \nsize of the adenomyoma compared to leiomyomas, their out-\nline is more indistinct, they appear more elliptical in shape \ncompared to spherical leiomyomas and the adenomyoma \ncontains typical key signal intensity characteristic with hyper-\nH. Addley and F. Fennessy\n\n181\nintense foci on T2-weighted imaging and often striations out \nfrom the endometrial and myometrial junction (Fig.  13.4a). \nIn diffuse adenomyosis, the thickness of the junctional zone \n>12  mm representing smooth muscle hyperplasia predicts \ndiffuse adenomyosis with high accuracy (85%) [6]. In addi-\ntion to the hyperintense foci on T2 weighted imaging, adeno-\nmyosis may also demonstrate high T1 signal intensity foci (in \napproximately 20% of cases) which represent small punctate \nhemorrhagic foci within ectopic endometrial tissue and has a \n95% positive predictive value for adenomyosis. Cystic adeno-\nmyosis is less common and needs to be differentiated from \ncystic degeneration of a leiomyoma.\nIn comparison to MR imaging, which is highly accurate \nfor diagnosis of adenomyosis, ultrasound appearances can be \nchallenging in subtle cases such as mild diffuse adenomyo -\nsis. Given ultrasound is the first-line test it is important to be \nfamiliar with the appearances that raise suspicion for adeno-\nmyosis. The consensus statement from the morphological \nuterus assessment (MUSA) group [7] describes the key fea-\ntures on TVUS examination for adenomyosis as asymmetri-\ncal thickening of the myometrium (globular shaped uterus), \npresence of cystic areas within the myometrium, hyperechoic \nislands, fan-shaped shadowing, echogenic subendometrial \nlines and buds, translesional vascularity, irregular junctional \nzone and interrupted junctional zone (Fig.  13.4b).\n13.4.3  Uterine Fibroids\nUterine fibroids (leiomyomas, myomas) are benign mono -\nclonal tumors of uterine smooth muscle and are the single \nimportant indication for hysterectomy. Approximately 25% \nof women of reproductive age and over 70% of women by \nthe time they reach menopause are symptomatic with uterine \nfibroids. Their growth is dependent on estrogen and proges -\nterone, and they may enlarge with pregnancy and oral contra-\nceptive use, and usually request during menopause. They are \ncommonly multiple, and their size can vary greatly.\nUltrasound is usually the initial imaging test of choice for \nsymptomatic patients. However, MRI provides a more accu-\nrate assessment of the location, number, and type of uterine \nfibroids and is often used for complex cases or to help decide \noptimal therapy [ 8, 9]. MRI is also helpful as a problem-  \nsolving tool to distinguish uterine fibroids from adenomyo -\nsis, myometrial contractions, and malignant disease entities \nsuch as leiomyosarcoma [10].\n13.4.3.1  Imaging Features on Ultrasound\nBoth transabdominal and transvaginal ultrasounds are often \nneeded to adequately evaluate the uterus. Large or subse -\nrosal pedunculated fibroids may be missed by transvaginal \nimaging alone, whereas transvaginal ultrasound is often \nbest to adequately evaluate submucosal fibroids. On ultra -\nsound, fibroids typically appear as solid masses which are \nhypoechoic compared to the normal myometrium. They are \noccasionally hyperechoic and may have some foci of calci -\nfication. When there are many fibroids, or the fibroids are \nlarge and extend out of the pelvis, accurate assessment and \nmeasurement by ultrasound may be difficult.\n13.4.3.2  Imaging Features on MRI\nMRI is the most accurate modality for determining the size, \nnumber, location, and cellular characteristics of fibroids. \nMost commonly, uterine fibroids are well-circumscribed and \na b\nFig. 13.4 Sagittal T2 weighted image (a) demonstrating thickening of \nthe junctional zone and hyperintense focal punctate areas in keeping \nwith extensive diffuse adenomyosis. Corresponding TVUS transverse \nsection (b) of the uterus demonstrates the heterogeneity of the myome-\ntrium, indistinct endometrial and myometrial interface and focal small \ncystic areas\n13 Benign Disease of the Uterus\n\n182\nof low signal intensity on T2-weighted imaging compared to \nthe surrounding myometrium. They are usually isointense on \nT1-weighted imaging and commonly enhance to the same or \nslightly less extent than the myometrium post-contrast \nadministration.\nUterine leiomyomas are classified according to their loca-\ntion. The FIGO classification system (Fig.  13.5 and \nTable  13.1) was developed to provide a uniform description \nof location to “facilitate communication, clinical care and \nresearch” [11], and allows clinicians to determine the best \ntreatment plan. Submucosal fibroids (FIGO 0, 1, and 2) are \nlocated beneath the mucosal lining: FIGO 0 are peduncu -\nlated intracavitary and attached to the endometrium by a \nstalk; FIGO 1 (Fig.  13.6) are ≥50% submucosal and <50% \nintramural, whereas FIGO 2 leiomyomas are <50% submu -\ncosal and ≥50% intramural. Differentiating FIGO 1 from \nFIGO 2 can be helpful to gynecologists during hysteroscopic \nresection as it provides a better understanding of the intra -\nmural extent. FIGO classifies all remaining leiomyomas that \ndo not have a submucosal component as “other.” FIGO 3 \nleiomyomas (Fig.  13.6) are 100% intramural but may contact \nthe endometrium with mass effect, but do not extend into the \nendometrial cavity. FIGO 4 leiomyomas (Fig.  13.6) are also \n100% intramural but without any endometrial or serosal con-\ntact. Distinguishing FIGO 2 from FIGO 3 and 4 is important \nas the surgical approach is different, with FIGO 3 and 4 \n7\n6 1\n2\n2-5\n05\n3\n4\n8\nFig. 13.5 FIGO fibroid subtypes. Submucosal fibroids (shown in red) \ninclude Type 0 (pedunculated intracavitary), Type 1 (≥ 50% submuco-\nsal), Type 2 (< 50% submucosal), and hybrid fibroids (here depicted as \na Type 2–5 fibroid). Fibroids without submucosal components (shown \nin blue) include Type 3 (100% intramural fibroid with endometrial con-\ntact), Type 4 (100% intramural fibroid with no endometrial contact), \nType 5 (≥ 50% intramural fibroid with subserosal component), Type 6 \n(< 50% intramural fibroid with subserosal component), Type 7 (pedun-\nculated subserosal), and Type 8 (non-myometrial location, such as cer-\nvical, broad ligament, or parasitic fibroids) (Permission requested from \nSpringer journals. Original  Fig.  13.1 from Abdominal Radiology \n(2021) 46: 2146–2155. https://doi.org/10.1007/s00261- 020- 02882- z)\nGroup\nSubmucosal 0\n1\n2\n3\n4\n5\n6\n7\n8\nX-X\nPedunculated intracavitary\n< 50% intramural (≥ 50% submucosal)\n≥ 50% intramural (< 50% submucosal)\n100% intramural, contacting endometrium\n100% intramural, no endometrial or subserosal contact\nSubserosal, ≥ 50% intramural\nSubserosal, < 50% intramural\nPedunculated subserosal\nNon-myometrial location: e.g., cervical, broad ligament, parasitic\nBoth submucosal and subserosal components. First number\ndesignates the submucosal component and second number\ndesignates the subserosal component \nOther\nHybrid\nType DescriptionTable 13.1 FIGO fibroid \nclassification system. Permission \nrequested from Springer journals. \nOriginal Table 1 from Abdominal \nRadiology (2021) 46: 2146–\n2155. https://doi.org/10.1007/\ns00261- 020- 02882- z\nFig. 13.6  Coronal T2-weighted image depicting numerable uterine \nleiomyomas. They are classified as FIGO 1 (#1): ≥50% submucosal \nand < 50% intramural; FIGO 4 (#4): intramural without any serosal or \nendometrial contact; FIGO 5 (#5): ≥50% intramural and < 50% subse -\nrosal; FIGO 6 (#6): <50% intramural and  ≥ 50% subserosal\nH. Addley and F. Fennessy\n\n183\nbeing removed via laparoscopy or laparotomy. Subserosal \nleiomyomas are divided into FIGO 5, 6, or 7 depending on \nthe extent of subserosal involvement: FIGO 5 leiomyomas \n(Fig.  13.6) are ≥50% intramural and <50% subserosal, \nwhereas FIGO 6 (Fig.  13.6) are <50% intramural and ≥50% \nsubserosal. FIGO 7 leiomyomas are pedunculated without \nany intramural component. As they enlarge, they are at risk \nof torsion. Treatment options for subserosal fibroids usually \ninclude uterine artery embolization or myomectomy. Any \nextrauterine leiomyomas are classified as FIGO 8, including \nthose arising from the cervix, broad ligament, or those para-\nsitized in the pelvis. When a leiomyoma extends from the \nsubmucosal to the subserosal surface they are considered \n“hybrid” and denoted by two numbers (X-X), the first repre-\nsenting the submucosal component and the second repre -\nsenting the subserosal component. These are usually large \nand treatment options may include MR-guided focused \nultrasound surgery, uterine artery embolization or hysterec -\ntomy. MRI is the preferred modality to assess for response \npost MR-guided focused ultrasound surgery or uterine artery \nembolization.\nThere are many different forms of degeneration that can \noccur in uterine fibroids and are usually well depicted on \nMRI. The most common form is that of hyaline degeneration \nwhich occurs when the smooth muscle is replaced by fibrous \nconnective tissue. Areas of very low signal intensity, some -\ntimes speckled, are identified within the fibroid on \nT2-weighted imaging and there is usually less enhancement \nafter administration of gadolinium compared to the remain -\nder of the uterine fibroid.\nThe clinical presentation and symptoms of leiomyomas \nmay overlap with those of a rare though aggressive malig -\nnant smooth muscle tumor, leiomyosarcoma [12]. The rate of \ntumor growth cannot differentiate benignity from malig -\nnancy, nor can specific serum markers such as lactate dehy -\ndrogenase [ 13] or CA-125 [ 14]. However, more recent \nstudies have suggested that specific MR features such as \nintra-tumoral hemorrhage, ill-defined border with the myo -\nmetrium and enhancing finger-like projections post-contrast \nare associated with leiomyosarcoma [10]. It is also suggested \nthat diffusion weighted imaging (with a b value of 1000 s/\nmm2) and apparent diffusion coefficient mapping should also \nbe used for the detection of leiomyosarcoma [ 15]. This dif-\nferentiation is important, as although rare, leiomyosarcoma \ncan have a devastating outcome.\n13.4.4  Endometrial Pathology\nEndometrial pathology is readily assessed with TVUS. The \ncorrelation with thickness of the expected appearance during \nthe menstrual cycle is vital and if there is debate between \nnormal appearances and pathology then further TVUS just \nshortly following menstruation when the endometrium \nshould be at its thinnest can be helpful. Most endometrial \npolyps are seen in the postmenopausal patient group, and \nfollowing ultrasound will undergo hysteroscopy and endo -\nmetrial sampling.\nEndometrial polyps are common causes of abnormal uter-\nine bleeding. On ultrasound, these appear as a well-defined \narea within the endometrium and are typically homogeneous \nand isoechoic to the background endometrium. The ability to \ndemonstrate a central feeding vessel on color doppler \nincreases accuracy to >90% [16] (Fig.  13.7a). On MR imag-\ning polyps are typically of intermediate T1 signal intensity \nbut can be of heterogenous signal intensity on T2-weighted \nimaging as their size increases (Fig.  13.7b, c, d). The central \nfibrous core demonstrates low T2 signal intensity. Resection \nof the polyp is required to exclude malignancy or foci of \natypical hyperplasia.\nEndometrial hyperplasia is characterized by the prolifera-\ntion of endometrial glands and is commonly seen in unop -\nposed estrogen stimulation or in tamoxifen therapy. In \npostmenopausal patients, the TVUS appearances of a thick -\nened endometrium >4 mm require further assessment with \nhysteroscopy and endometrial sampling. There are no defini-\ntive features on imaging currently which can differentiate \nbenign endometrial hyperplasia from complex atypical \nhyperplasia or endometrial carcinoma and therefore a thick -\nened endometrium should prompt cellular sampling.\nAsherman’s syndrome is an inflammatory response caus-\ning adhesions within the endometrial cavity typically fol -\nlowing previous intervention or from previous repeated \ninflammatory events. In severe cases, fibrous adhesions \nwithin the cavity can cause cavity obliteration. This can be a \ncause of infertility or pregnancy loss. On TVUS, adhesions \nare identified as echogenic bands extending transversely \nacross the endometrium. MR imaging is more accurate for \nthis diagnosis and demonstrates obliteration of the endome -\ntrial cavity and fibrous signal intensity. Hysterosalpingogram \nor sonohysterography, which distends the endometrial cavity, \ncan be helpful in demonstrating the extent of involvement.\n13 Benign Disease of the Uterus\n\n184\na\nc\nb\nd\nFig. 13.7  TVUS transverse section ( a) of the uterus demonstrates \nincreased endometrial thickness (white arrow) with central vascularity. \nHysteroscopy and subsequent pathology confirmed benign endometrial \npolyp. Corresponding MR examination sagittal T2 weighted image (b) \nand axial T2 weighted image ( c) and T1 weighted image ( d) demon-\nstrate large central endometrial polyp (white arrow)\n13.5  Mullerian Duct Anomalies \nof the Uterus\nMullerian duct anomalies (MDAs) are congenital disorders \nthat arise from arrested development, incomplete fusion, or \nincomplete resorption of the mesonephric ducts. The \nMüllerian ducts undergo descent, fusion, and septum resorp-\ntion to form the uterus, fallopian tubes, cervix, and upper \ntwo-third of the vagina. The ovaries and external genitalia/\ndistal one-third of the vagina are spared because they origi -\nnate from the primitive yolk sac and sinovaginal bud, \nrespectively. MDAs are usually identified incidentally, and \nless commonly are identified as causes of infertility, endo -\nmetriosis, recurrent miscarriages, or an obstructed repro -\nductive tract. The prevalence of Mullerian duct anomalies in \nthe general fertile population is 6.7%, versus 7.3% in the \ninfertile population, and 13–17% in women with miscar -\nriages [17].\nThe European Society of Human Reproduction and \nEmbryology (ESHRE) and the European Society for \nGynecological Endoscopy (ESGE) developed a clinically \norientated classification system, based on anatomy [18]. US \nis commonly performed and may be diagnostic, especially \nwhen 3D US is used. MRI can be reserved for those cases in \nwhich the US is non-diagnostic or for complex cases. This \nsystem sorts the anomalies into classes based on increasing \ndeviation from anatomical deviations (Fig.  13.8). Anomalies \nare classified into the following main classes, expressing \nuterine anatomical deviations deriving from the same embry-\nological origin: U0, normal uterus; U1, dysmorphic uterus; \nH. Addley and F. Fennessy\n\n185\nFig. 13.8 Schematic drawing of the ESHRE/ESGE classification system of uterine congenital anomalies from Ref. [18], dividing uterine anoma-\nlies into six classes\nU2, septate uterus; U3, bicorporeal/bicornuate uterus; U4, \nhemi-uterus; U5, aplastic uterus; U6, for unclassified cases. \nUterine wall thickness (UWT) is an important parameter and \na reference point for the definitions of dysmorphic T-shaped, \nseptate, and bicorporeal uteri, and is defined as the distance \nbetween the tubal ostia (interostial line) and a parallel line on \nthe top of the fundus [19] (Fig.  13.9).\n13.5.1  Class U0\nThe normal uterus (U0) has either a straight or curved inter-\nostial line with an internal indentation ≤50% of the UWT at \nthe fundal midline.\n13.5.2  Class U1\nClass U1 (dysmorphic uterus) has a normal uterine outline, \nbut an abnormally shaped cavity (excluding septal abnor -\nmalities). An example is a T-shaped U1 which has thickened \nlateral walls. As with U0, the midline, fundal, inner indenta-\ntion is <50% UWT.\n13.5.3  Class U2\nClass U2 uteri also have a normal outer contour, but there is \nabnormal resorption of the midline septum (either partial or \ncomplete) following normal Mullerian duct fusion. As such, \nfor U2 cases there is midline, fundal, inner indentation is \n>50% of the UWT.\n13.5.4  Class U3\nClass U3 (bicorporeal) is due to abnormal fusion of the \nMullerian ducts and has an abnormal outer contour with \nexternal indentation at the fundal midline >50% of the \nUWT.  The extent to which the external fundal indentation \ndivides the uterus above or to the level of the internal os \ndefines partial or complete U3a vs U3b.\n13.5.5  Class U\nClass U4 category is unilateral uterine horn development, \nwith associated incomplete (U4a) or absent (U4b) contralat-\neral uterine horn remnant.\n13 Benign Disease of the Uterus\n\n186\nab\ncd\nFig. 13.9 Coronal 3D ultrasound views of the uterus depicting a nor -\nmal uterus (a), a partial septate uterus (b), a complete septate uterus (c) \nand a bicornual uterus ( d). Measurement 1  =  uterine wall thickness: \ndistance between tubal ostia and a parallel line on the top of the uterine \nfundus. Measurement 2  =  internal midline indentation: distance \nbetween the tubal ostia and a parallel line on top of the indentation\nH. Addley and F. Fennessy\n\n187\n13.5.6  Class U5\nIn Class U5 there is uterine aplasia, with no fully developed \nor unilaterally developed uterus. There may be a functional \nrudimentary horn or horns (U5a) or no functioning rudimen-\ntary horns (U5b).\n13.5.7  Class U6\nThis class is reserved for subtle or combined abnormalities \nthat do not fit into classes 0-5.\n13.6  Concluding Remarks\nUltrasound is usually the first imaging modality in the assess-\nment of benign diseases of the uterus. MRI is an important \nadjunct, especially for patients with complicated congenital \nanatomy, for the detection of deep infiltrating endometriosis \nor pre-operative intervention.\nReferences\n1. Benacerraf BR, et  al. Consider ultrasound first for imaging the \nfemale pelvis. Am J Obstet Gynecol. 2015;212:450–5.\n2. Guerriero S, et al. Systematic approach to sonographic evaluation \nof the pelvis in women with suspected endometriosis, including \nterms, definitions and measurements: a consensus opinion from \nthe International Deep Endometriosis Analysis (IDEA) group. \nUltrasound Obstet Gynecol. 2016;48:318–32.\n3. Bazot M, et  al. European society of urogenital radiology (ESUR) \nguidelines: MR imaging of pelvic endometriosis. Eur Radiol. \n2017;27:2765–75.\n4. Foti PV , et al. Endometriosis: clinical features, MR imaging find -\nings and pathologic correlation. Insights Imaging. 2018;9:149–72.\n5. Johnatty SE, et  al. Co-existence of leiomyomas, adenomyosis \nand endometriosis in women with endometrial cancer. Sci Rep. \n2020;10:3621.\n6. Novellas S, et  al. MRI characteristics of the uterine junctional \nzone: from normal to the diagnosis of adenomyosis. AJR Am J \nRoentgenol. 2011;196:1206–13.\n7. Van den Bosch T, et  al. Terms, definitions and measurements to \ndescribe sonographic features of myometrium and uterine masses: \na consensus opinion from the Morphological Uterus Sonographic \nAssessment (MUSA) group. Ultrasound Obstet Gynecol. \n2015;46:284–98. https://doi.org/10.1002/uog.14806.\n8. Hossain MZ, et  al. A Comparative study of magnetic resonance \nimaging and transabdominal ultrasonography for the diagnosis and \nevaluation of uterine fibroids. Mymensingh Med J. 2017;26:821–7.\n9. Dueholm M, Lundorf E, Hansen ES, Ledertoug S, Olesen \nF. Accuracy of magnetic resonance imaging and transvaginal ultra-\nsonography in the diagnosis, mapping, and measurement of uterine \nmyomas. Am J Obstet Gynecol. 2002;186:409–15.\n10. Jagannathan JP, et  al. Differentiating leiomyosarcoma from leio -\nmyoma: in support of an MR imaging predictive scoring system. \nAbdom Radiol. 2021;46:4927–35.\n11. Munro MG, Critchley HOD, Broder MS, Fraser IS, FIGO Working \nGroup on Menstrual Disorders. FIGO classification system (PALM- \nCOEIN) for causes of abnormal uterine bleeding in nongravid \nwomen of reproductive age. Int J Gynaecol Obstet. 2011;113:3–13.\n12. Skorstad M, Kent A, Lieng M. Preoperative evaluation in women \nwith uterine leiomyosarcoma. A nationwide cohort study. Acta \nObstet Gynecol Scand. 2016;95:1228–34.\n13. Goto A, Takeuchi S, Sugimura K, Maruo T. Usefulness of Gd-DTPA \ncontrast-enhanced dynamic MRI and serum determination of LDH \nand its isozymes in the differential diagnosis of leiomyosarcoma \nfrom degenerated leiomyoma of the uterus. Int J Gynecol Cancer. \n2002;12:354.\n14. Juang CM, et al. Potential role of preoperative serum CA125 for \nthe differential diagnosis between uterine leiomyoma and uterine \nleiomyosarcoma. Eur J Gynaecol Oncol. 2006;27:370–4.\n15. Hindman N, et al. MRI evaluation of uterine masses for risk of leio-\nmyosarcoma: a consensus statement. Radiology. 2022;306:e211658. \nhttps://doi.org/10.1148/radiol.211658.\n16. Jakab A, et al. Detection of feeding artery improves the ultrasound \ndiagnosis of endometrial polyps in asymptomatic patients. Eur J \nObstet Gynecol Reprod Biol. 2005;119:103–7.\n17. Saravelos SH, Cocksedge KA, Li TC. Prevalence and diagnosis of \ncongenital uterine anomalies in women with reproductive failure: a \ncritical appraisal. Hum Reprod Update. 2008;14:415–29.\n18. Grimbizis GF, et al. The ESHRE/ESGE consensus on the classifi -\ncation of female genital tract congenital anomalies. Hum Reprod. \n2013;28:2032–44.\n19. Grimbizis GF, et al. The Thessaloniki ESHRE/ESGE consensus on \ndiagnosis of female genital anomalies. Hum Reprod. 2016;31:2–7.\nTake-Home Message\nUltrasound examination is the first-line investigation \nfor benign disease of the uterus. MR imaging is focused \non a particular question, often for complex diagnoses \nor for surgical planning, and may require specific pro-\ntocol as a result.\nOpen Access  This chapter is licensed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.\norg/licenses/by/4.0/), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropri-\nate credit to the original author(s) and the source, provide a link to the Creative Commons license and indicate if changes were made.\nThe images or other third party material in this chapter are included in the chapter's Creative Commons license, unless indicated otherwise in \na credit line to the material. If material is not included in the chapter's Creative Commons license and your intended use is not permitted by statu-\ntory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.\n13 Benign Disease of the Uterus","source_license":"CC0","license_restricted":false}