AJR AJR-based Continuing Ed for Technologists
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Verma, S. K.
Right arrow Articles by Parker, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Verma, S. K.
Right arrow Articles by Parker, L.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
Hotlight (NEW!)
Right arrow
What's Hotlight?
DOI:10.2214/AJR.07.3312
AJR 2008; 190:1220-1226
© American Roentgen Ray Society


Original Research

Submucosal Fibroids Becoming Endocavitary Following Uterine Artery Embolization: Risk Assessment by MRI

Sachit K. Verma1, Diane Bergin1,2, Carin F. Gonsalves1, Donald G. Mitchell1, Anna S. Lev-Toaff1,3 and Laurence Parker1

1 Department of Radiology, Thomas Jefferson University Hospital, 396C Main Bldg., 111 S 10th St., Philadelphia, PA 19107.
2 Present address: Department of Radiology, Galway University Hopital, Newcastle Rd., Galway, Co. Galway, Ireland.
3 Present address: Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, PA.

Received October 17, 2007; accepted after revision November 29, 2007.

 
Address correspondence to D. Bergin (dianebergin{at}yahoo.com).

Address correspondence to D. Bergin (dianebergin{at}yahoo.com).


Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
OBJECTIVE. The purpose of our study was to assess the relationship between the endometrium and submucosal fibroids before and after uterine artery embolization (UAE).

MATERIALS AND METHODS. Contrast-enhanced pelvic 1.5-T MRI was performed in 49 women before and after UAE over a 2-year period. Dominant (largest diameter) fibroids in intramural, submucosal, subserosal, pedunculated subserosal, and endocavitary locations were assessed on pre- (baseline) and postembolization MRI. Size, locations of dominant fibroids relative to endometrium and serosa before and after embolization were compared. The ratio between the largest endometrial interface and the maximum dimension of the dominant submucosal fibroid (interface–dimension ratio) was determined on baseline MRI. The infarction rate for dominant fibroids was estimated after UAE.

RESULTS. One hundred forty dominant fibroids were identified on baseline MRI. Forty-nine (35%) were intramural, 39 (28%) were submucosal, 34 (24%) were subserosal, eight (6%) were pedunculated subserosal, and 10 (6%) were endocavitary in location on preembolization MRI. After UAE, of 39 dominant submucosal fibroids, 13 (33%) became endocavitary: complete (n = 4), partial (n = 9) on the basis of European Society of Gynaecological Endoscopy (ESGE) classification. The preembolization mean interface–dimension ratio and mean diameters for dominant fibroids that became endocavitary were significantly greater than for those that did not become endocavitary after embolization (0.65 vs 0.32, p < 0.005; 8 vs 5.4 cm, p < 0.05, respectively). All dominant submucosal fibroids showed 100% infarction after UAE.

CONCLUSION. Submucosal fibroids with an interface–dimension ratio of greater than 0.55 are more likely to migrate into the endometrial cavity after UAE. The majority of these are expelled spontaneously without significant symptoms. Rarely, submucosal fibroids greater than 6 cm in size that become endocavitary may cause postprocedural complications requiring further intervention and medical treatment.

Keywords: embolization • fibroids • MRI • uterine artery


Introduction
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Uterine fibroids (myomas or leiomyomas) are benign growths of uterine muscle that are common in women of reproductive age [1]. The location of fibroids, whether submucosal, subserosal, pedunculated subserosal, intramural, or endocavitary, is important because signs and symptoms may be determined by location [24]. Uterine artery embolization (UAE) for many patients is an effective alternative treatment to surgical therapy for fibroid tumors [57].

Pretreatment evaluation of a patient with suspected myomas by means of pelvic MRI includes determining size, location, and contrast enhancement of uterine fibroids as well as coexistent or alternative unsuspected pelvic abnormality. This pretreatment assess ment has improved patient selection and reduced treatment failure or potential complications such as pyometrium, acute endometritis, ischemic injuries, and expulsion of submucosal fibroids [813]. Pedunculated subserosal fi broids with a narrow pedicle may slough off, becoming a potential source of infection in the peritoneal cavity. After UAE, submucosal and endocavitary fibroids may be associated with symptoms including pain, bleeding, infection, and vaginal discharge for prolonged periods of time [1419]. Spontaneous expulsion of infarcted fibroids has been described after childbirth, laparoscopic uterine artery occlusion, and UAE. The rate of fibroid expulsion after UAE has been estimated to be 3% to 12% [16, 17].

We have noted that fibroids deemed to be submucosal on preembolization MRI may become endocavitary after embolization. We found no published data evaluating the imaging features of submucosal fibroids on preprocedural imaging that may predict increased risk of the fibroids becoming endocavitary after treatment. The purpose of our study was to retrospectively assess the change in location of dominant fibroids relative to the serosa and endometrium before and after UAE and to assess what factors determine which submucosal fibroids may become endocavitary after UAE.


Materials and Methods
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Subjects
With institutional board approval, a retrospective analysis was performed of 74 consecutive symptomatic women (mean age, 42 years; age range, 32–52 years) who presented for UAE at our institution in a 24-month period from December 2004 to November 2006. All women were premenopausal and had symptoms including menorrhagia, pelvic pain, and mass-related symptoms that were not controlled by conservative measures. Fifteen women did not proceed with embolization for the following reasons: declined embolization treatment (n = 4); history of anaphylaxis to iodinated contrast agent (n = 2); comorbid conditions including adenomyosis, untreated pelvic infection (n = 5), and suspicion of uterine, ovarian, or cervical malignancy (n = 4). Ten other women were excluded from the study because preembolization MRI was not performed at our institution (n = 10) and thus not available for review. Thus our study group consisted of 49 women (mean age, 42 years; age range, 32–46 years).

Before UAE, a complete gynecologic examination and clinical evaluation were performed by the referring gynecologist. All women had documented negative results of cervical Pap smears. Endometrial biopsies performed for abnormal uterine bleeding in 19 of 49 women were also negative. Fifteen women who received hormonal therapy before UAE discontinued it at least 6 weeks before embolization. The majority of women (n = 38/49, 78%) had pelvic sonography performed at an outside facility before being referred for UAE; these images were not available for review.

Initial assessment by the interventional radiologist included a written patient questionnaire recording the women's baseline clinical symptoms [20]. All women had contrast-enhanced pelvic MRI approximately 1–2 months before UAE (mean, 36 days; range, 15–65 days). Contrast-enhanced pelvic MRI was routinely performed after UAE in all women (range, 40–140 days; mean interval, 125 days). Clinical follow-up for each woman was obtained through health records maintained by the treating interventional radiologist; telephone correspondence with referring physicians; and, in some cases, directly with the patient. Recurrence was defined clinically as recurrence of symptoms or anatomically with an increase in fibroid size or detection of new fibroids by imaging.

Embolization Procedure
One radiologist with 8 years of experience in interventional radiology performed UAE in all women. Informed consent was obtained from each woman after all risks associated with the procedure were explained. UAE was performed in the following manner. Conscious sedation was achieved with midazolam (Versed, Roche Laboratories) and fentanyl citrate (Fentanyl, Elkins-Sinn). The patient's right groin was prepared and draped using a sterile technique. Lidocaine hydrochloride 2% plain (Xylocaine, Laboratoire Roger Bellon) was used for local anesthesia. The right common femoral artery was the preferred approach for access in all women. Bilateral selective uterine artery catheterization was performed using a 3-French Renegade microcatheter (Boston Scientific/Medi-tech) and a 70° angled tip guidewire that were passed coaxially through a 4-French Cobra catheter (Cordis, Johnson & Johnson). Digital subtraction arteriography was performed. Embolization was performed by using either 500- to 700-µm polyvinyl alcohol (PVA) particles (Contour, Boston Scientific) or 500- to 700-µm tris-acryl gelatin microspheres (Embospheres, Biosphere Medical), as determined by the performing inter ventional radiologist, with the end point being stasis or near stasis in the artery and with no large uterine artery branches remaining patent. All women tolerated the procedure well and there were no com pli cations. After the UAE procedure, each woman remained in the hospital at bedrest for 6 hours and a majority were discharged the same day.

Pre- and Postembolization MRI
MRI was performed with a 1.5-T superconducting unit (Signa, GE Healthcare; or Intera, Philips Medical Systems) using a pelvic coil. Sagittal fat-suppressed and axial 2D fast spin-echo T2-weighted (TR range/TE range, 2,500–4,000/80–90) and spoil ed dual gradient-echo T1-weighted in- and out-of-phase (120–200/2.3–4.6, 90° flip angle) MR images were obtained. Parameters for 2D images included a section thickness of 5–6 mm with an intersection gap of 0–1 mm; matrix, 256 x 160–192; and field of view, 20–24 cm with one or two signals acquired. Three-dimensional dynamic enhanced spoiled gradient-echo MR images were obtained with 4-mm section thickness in 2.5-mm increments by using zero interpolation; 4–6/2.1–3; 10–15° flip angle parameters; matrix, 256 x 160; 0.5 signals acquired; and field of view, 24 cm. Gadopentetate dimeglumine (20 mL) (Magnevist, Bayer HealthCare) was administered IV by using a power injector at 2 mL/s followed by a 20-mL saline flush. Breath-hold dynamic imaging was performed with initial acquisition acquired immediately at the end of the saline flush and a second acquisition immediately thereafter. Delayed contrast-enhanced imaging after approximately 3–5 minutes was performed using contiguous 5-mm-thick fat-suppressed 2D single-section technique (TR/TE, 22/2; flip angle, 30°; matrix, 256 x 160; and field of view, 24 cm with one signal acquired in the sagittal plane).

Review of MR Images
All MR images were evaluated in consensus by two radiologists with more than 3 and 10 years of experience, respectively, in abdominal and pelvic MRI. Images were reviewed without knowledge of the clinical history or findings at embolization. Three-dimensional maximal measurements of the entire uterus and fibroids were obtained on axial and sagittal planes using an independent computer monitor with a PACS workstation. On preembolization (baseline) MRI, the dominant fibroids, defined as fibroids with the largest dimensions, in each of the following locations: intramural, submucosal, subserosal, and endocavitary were identified and measured. Both the dominant pedunculated and nonpedunculated subserosal fibroids when present were also measured. The volumes of the entire uterus and dominant submucosal fibroid (in cubic centimeters) were calculated on pre- and postembolization MRI by using the formula for a prolate ellipse (length x width x depth x 0.5233). The relative difference in uterine and dominant submucosal fibroid volume before and after embolization was calculated and expressed as a percentage, as follows: 100 x [(Volume pre – Volume post) / Volume pre], where Volume pre and Volume post are the volumes before and after UAE, respectively.

A fibroid was defined as submucosal if any portion of the fibroid contacted the endometrium. A fibroid was defined as intramural when it was completely surrounded by myometrium. A fibroid was defined as completely endocavitary when surrounded by endometrium or partially endocavitary if greater than 50% of the surface area of the fibroid was surrounded by endometrium, in accordance with the European Society of Gynaecological Endoscopy (ESGE) classification [21]. A subserosal fibroid was defined as a fibroid with a partial or complete lack of surrounding myometrium and abutting or deforming the serosal layer. Pedunculated subserosal fibroids were defined as those with a pedicle diameter 50% narrower than the diameter of the fibroid.


Figure 1
View larger version (114K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 1 56-year-old woman with fibroids. Baseline sagittal fat-suppressed fast spin-echo T2-weighted MR image shows calculation of interface of fibroid with endometrium (em) (xy + yz = xz) and maximum submucosal fibroid dimension (ab). Interface–dimension ratio calculated by (xz / ab).

 
For the selected dominant submucosal fibroid in each woman, the largest interface with the endometrium and the maximum dimension in the same plane on MRI were measured with electronic caliper before embolization. A ratio of the largest endometrial interface to the largest dimension of the selected dominant submucosal fibroid was then determined (interface–dimension ratio) on baseline MRI (Fig. 1).

After embolization, the same dominant fibroid in an intramural, submucosal, subserosal, and endocavitary location was reevaluated with regard to its location relative to the endometrium and serosa. These dominant fibroids were remeasured to assess change in size after embolization. The extent of postembolization dominant fibroid infarction was subjectively rated as 100%, 50% to 100%, and less than 50% of the total fibroid volume on contrast-enhanced T1-weighted images. We defined devascularization (infarction) of the fibroid if the signal intensity on unenhanced and contrast-enhanced MR images was similar, indicating no enhancement.

Statistical Analyses
To assess the difference in total uterine volume before and after UAE, dominant submucosal fibroid volume, dominant submucosal fibroid size, interface–dimension ratio, and paired Student's t tests were performed. Statistical analysis was performed using software (Excel 2003, Microsoft); p values of less than 0.05 were considered statistically significant.


Results
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Pre- and Postembolization MRI Observations
A total of 140 dominant fibroids were identified and measured in 49 women. The number of dominant fibroids in each woman on baseline MRI ranged from one to five (mean, four). Of 49 women, 48 (97%) had no other coexistent gynecologic abnormality on MRI. One patient (2%) had adenomyosis and fibroids confirmed on MRI before embolization

Of 140 dominant fibroids examined, 49 (35%) were intramural, 39 (28%) were submucosal, 34 (24%) were subserosal, eight (6%) were pedunculated subserosal, and 10 (7%) were endocavitary in location on preembolization MRI. The distribution and maximum dimension of the dominant fibroids before and after embolization are shown in Table 1. The mean reduction in volume of dominant submucosal fibroids was 53% (range, 18–100%) from 541 to 254 cm3 (p < 0.001) and of overall uterine volume was 40% (range, 18–62%) from 615 to 363 cm3 (p < 0.001), when pre- and postembolization MRI examinations were compared.


View this table:
[in this window]
[in a new window]

 
TABLE 1: Distribution and Maximum Dimension of Dominant Fibroids Before and After Uterine Artery Embolization (UAE)

 

Of 39 dominant submucosal fibroids identified on preembolization MRI, 13 (33%) became endocavitary (complete [n = 4] or partial [n = 9]) after embolization (Table 2). The mean interface–dimension ratio on preembolization MRI of dominant submucosal fibroids that subsequently became endocavitary whether complete or partial was 0.65 (range, 0.55–0.83), which was significantly greater than the interface–dimension ratio of the submucosal fibroids that did not become endocavitary, 0.32 (range, 0.10–0.47; p < 0.005) (Table 3). The mean diameter of dominant submucosal fibroids on preembolization MRI that became endocavitary was 8 cm (range, 3–17 cm) greater than the diameter of submucosal fibroids that did not become endocavitary, 5.4 cm (range, 1.6–12 cm; p = 0.03). The mean preembolization interface–dimension ratio for dominant submucosal fibroids that became completely endocavitary after UAE was higher, 0.81 (range, 0.76–0.83) than for those that did not (Fig. 2A, 2B). The mean preembolization interface–dimension ratio for dominant submucosal fibroids on baseline MRI that became partially endocavitary after UAE was 0.67 (range, 0.55–0.69) (Fig. 3A, 3B).


View this table:
[in this window]
[in a new window]

 
TABLE 2: Location of Dominant Submucosal Fibroids After Uterine Artery Embolization (UAE)

 

View this table:
[in this window]
[in a new window]

 
TABLE 3: Maximum Dimension and Interface–Dimension Ratio of Submucosal Fibroids on MRI Before Uterine Artery Embolization (UAE) Relative to Their Location After UAE

 

Figure 2
View larger version (121K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 2A 43-year-old woman with submucosal (SM) fibroid. Sagittal fat-suppressed fast spin-echo T2-weighted MR image (TR/TE, 2,800/85) before uterine artery embolization (UAE) shows submucosal fibroid with broad interface with endometrium (em) (arrows). Interface–dimension ratio is 0.76.

 

Figure 3
View larger version (125K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 2B 43-year-old woman with submucosal (SM) fibroid. Sagittal fat-suppressed fast spin-echo T2-weighted MR image (2,800/85) after UAE shows submucosal fibroid that became completely endocavitary (EC). em = endometrium.

 

Figure 4
View larger version (134K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 3A 41-year-old woman with submucosal fibroid. Axial T2-weighted fast spin-echo image (TR/TE, 2,800/85) before uterine artery embolization (UAE) shows submucosal fibroid (asterisk) with interface–dimension ratio of 0.67.

 

Figure 5
View larger version (149K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 3B 41-year-old woman with submucosal fibroid. Axial T2-weighted fast spin-echo image (2,800/85) after UAE shows submucosal fibroid (asterisk), which became partially endocavitary.

 

Two of 49 (4%) dominant intramural fibroids became submucosal after UAE (Fig. 4A, 4B). Two of 10 (20%) dominant endocavitary fibroids were not evident at postembolization MRI, likely secondary to spontaneous expulsion. There was no change in location of dominant subserosal and pedunculated subserosal fibroids between pre- and post embolization MRI. Forty-nine of 49 (100%) dominant intramural, 39 of 39 (100%) dom inant submucosal, 32 of 34 (91%) dominant subserosal, six of eight (75%) dominant pe dunculated subserosal, and eight of 10 (80%) dominant endocavitary fibroids were com pletely infarcted after embolization. Two of 10 endocavitary fibroids completely disappeared. Two of 34 (6%) dominant subserosal and two of eight (25%) dominant pedunculated sub serosal fibroids had partial persistent enhancement (Table 4).


Figure 6
View larger version (169K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 4A 42-year-old woman with intramural fibroid. Axial T2-weighted fast spin-echo image (TR/TE, 4,000/90) before uterine artery embolization (UAE) shows intramural fibroid within myometrium (arrows). IM = intramural fibroid, em = endometrium.

 

Figure 7
View larger version (158K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 4B 42-year-old woman with intramural fibroid. Axial fast spin-echo T2-weighted MR image (4,000/90) after UAE shows intramural fibroid that became submucosal (SM). em = endometrium.

 

View this table:
[in this window]
[in a new window]

 
TABLE 4: Infarcted Rate of Dominant Fibroids After Embolization

 

Clinical Outcomes
Forty-five of 49 (92%) women had resolution of preembolization symptoms and no significant postprocedural symptoms. Four (8%) of 49 had significant post-procedural symptoms (menorrhagia, acute pelvic pain, or persistent vaginal discharge). These four women had dominant submucosal fibroids on baseline MRI that subsequently became endocavitary after embolization. The mean preembolization interface–dimension ratio of these submucosal fibroids on baseline MRI was 0.81 (range, 0.76–0.83), with a maximum fibroid dimension range of 6–17 cm (mean, 12 cm). The mean reduction in volume of these dominant submucosal fibroids that were both symptomatic and endocavitary after embolization was 58% (range, 659–275 cm3; p < 0.001).

One woman with a 12-cm dominant submucosal fibroid on baseline MRI with a preembolization interface–dimension ratio of 0.82 that became endocavitary and measured 11 cm after embolization reported persistent pelvic pain that required analgesic medication. Hysteroscopic removal of the endocavitary fibroid was advised, but she was subsequently lost to follow-up. A second woman with a 6-cm dominant submucosal fibroid on baseline MRI and a preembolization interface–dimension ratio of 0.83 complained of persistent vaginal discharge after embolization. Follow-up MRI showed that the submucosal fibroid was endocavitary and measured 5.5 cm. She was treated with antibiotics, although there was no documentation of fever and no organism was cultured. Her symptoms were alleviated after spontaneous expulsion of tissue fragments. Two women who had dominant submucosal fibroids measuring 16 cm and 17 cm with preembolization interface–dimension ratios of 0.81 and 0.76, respectively, complained of persistent pelvic pain and heavy menstrual bleeding. In both, the submucosal dominant fibroids seen on baseline MRI were endocavitary, measuring 11 and 16 cm on post-embolization MRI follow-up. One of these patients refused further treatment and was discharged on antibiotics. The other patient had hysteroscopic myomectomy for a necrotic endocavitary prolapsing fibroid with subsequent resolution of symptoms (Fig. 5).


Figure 8
View larger version (87K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 5 Hysteroscopic resection of necrotic fibroid in 43-year-old woman. Fibroid changed location from submucosal to endocavitary after uterine artery embolization. Photomicrograph of fibroid shows coagulative necrosis. (H and E, x400)

 

Discussion
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Symptomatic fibroids are a major health concern for women. UAE is now increasingly used as a means of treatment for symptomatic fibroids and as an alternative to surgery [57, 21]. UAE leads to interstitial edema followed by coagulative necrosis and hyaline degeneration within the fibroids. Hyaline de generation represents a permanent end point in the natural history of a uterine fibroid [11, 22, 23]. UAE is an effective method of causing fibroid necrosis and alleviating symptoms in 80% to 96% [57, 13]. In our study, 92% (45/49) of women had resolution of symptoms after UAE. The mean 40% reduction in uterine volume after UAE in our patient group is similar to results from other studies [24].

Pretherapeutic imaging is important to define the location of uterine fibroids before UAE [9, 2527]. MRI has excellent tissue contrast and its multiplanar capabilities allow precise definition of fibroid location. The use of IV contrast media allows accurate assessment of the vascularity of fibroids. Because of the large field of view, MRI also allows comprehensive assessment of the remainder of the pelvic contents [2427]. Central fibroids frequently obscure visualization of the endometrium at sonography making accurate localization of fibroids relative to the endometrium difficult. MRI has therefore become the imaging technique of choice for assessing the myomatous uterus before embolization. Prior studies report additional pelvic abnormalities detected on MRI in 2% of patients [24]. This is similar to our patient group, 2% of whom had adenomyosis.

In our study, the dominant fibroid in a submucosal location constituted 28% of all the dominant fibroids; this is a higher proportion of submucosal fibroids than the reported incidence of 11% [27]. This increased incidence in our group is also reflective of a symptomatic group of women, all of whom had failed conservative treatment. Although successful UAE leads to necrosis of submucosal fibroids, the pretreatment loca tion of these necrotic fibroids can lead to additional symptoms and potential complications after treatment.

Complications of UAE are infrequent; however, 2% to 3% of women may expel small pieces of fibroid tissue after UAE [12, 17]. This is more commonly associated with submucosal and endocavitary fibroids [8, 17]. Thinning of the myometrium after embolization results in changes in fibroid location relative to the endometrium and serosa [11, 22, 23]. Submucosal fibroids after embolization can communicate with the endometrial cavity because of sloughing of the overlying endometrium. Communication of a cavitating necrotic submucosal fibroid with the endometrial cavity can result in prolonged vaginal discharge of necrotic tissue and vaginal bleeding [8, 12, 28]. Spies et al. [12] reported fibroid tissue passage as the most common reason for hospital readmission after UAE. Although many endocavitary fibroids are expelled spontaneously, some remain firmly attached to the uterine wall and require dilation and evacuation, transfusion, hysteroscopic myomectomy, and possible dilation and curettage or hysterectomy [13].

In our study, we observed that submucosal fibroids on baseline MRI with an interface–dimension ratio of 0.55–0.83 (mean, 0.65) and maximum dimension of 3–17 cm (mean, 8 cm) are more likely to become endocavitary after UAE. Of those patients who had submucosal fibroids that became endocavitary, a small group with preembolization submucosal fibroids with a mean interface–dimension ratio of 0.81 (range, 0.76–0.83) and maximum fibroid dimension 6–17 cm (mean, 12 cm) had significant symptoms. Smaller submucosal fibroids that become endocavitary are likely expelled without significant symptoms. Rarely, however, larger fibroids that do become endocavitary can lead to postprocedural complications [9]. We found that 33% (13/39) of dominant submucosal fibroids became endocavitary and four of these women (4/13, 31%) had significant symptoms on follow-up. One of these women required hysteroscopic resection of endocavitary fibroids. We also noted that 4% (2/49) of dominant intramural fibroids changed location after UAE and were submucosal on follow-up MRI. This thinning or loss in volume of myometrium after embolization is similar in mechanism to the secondary effect of UAE described on the junctional zone and as a potential treatment for adenomyosis [29]. A change in location of fibroids after UAE that is appreciable on follow-up MRI therefore has potential clinical significance for the patient.

We acknowledge the following limitations of our study. This was a retrospective study with a small patient group. Nonetheless, to the best of our knowledge, the results of this study describe for the first time the importance of the relative interface between a submucosal fibroid and the endometrium on baseline MRI and the subsequent post-embolization risk of becoming endocavitary, potentially increasing patient morbidity. Ideally the relationship of the sub mucosal endometrial interface relative to fibroid volume would be more accurately assessed by determining the endometrial surface area of the fibroid. However, lack of endometrial cavity distention limits assessment of the true surface area of a submucosal fibroid.

We believe that the largest endometrial interface (the interface–dimension ratio) on multiplanar images relative to the corresponding largest dimension of the submucosal fibroid has the greatest reproducibility and on a practical basis is more easily achieved during routine interpretation in a busy radiology practice. Future prospective studies can address the potential role and utility of 3D volumetric analyses. Also, because all of the women had multiple fibroids, it was not practical to analyze each individual fibroid. Small submucosal fibroids are likely to become endocavitary but would likely be expelled spontaneously without significant symptoms. In this study, we have shown that submucosal fibroids with an interface–dimension ratio greater than 0.55 on baseline MRI may become endocavitary after embolization. The majority of these did not cause significant postprocedural symptoms. Submucosal fibroids greater than 6 cm in size that become endocavitary had a higher association with significant symptoms requiring further treatment or intervention.

In conclusion, in this pilot study we found that submucosal fibroids with an interface–dimension ratio on preprocedural MRI of greater than 0.55 are more likely to migrate into the endometrial cavity. The majority of these do not cause significant additional symptoms. Larger submucosal fibroids greater than 6 cm that become endocavitary can occasionally lead to postprocedural complications requiring further intervention and medical treatment.


Acknowledgments
 
We thank Marianne Hamel, Department of Pathology, for her pathology assistance.


References
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 

  1. Vollenhoven BJ, Lawrence AS, Healy DL. Uterine fibroids: a clinical review. Br J Obstet Gynaecol 1990;97 : 285–298[Medline]
  2. Buttram VC, Reiter RC. Uterine leiomyomata: etiology, symptomatology and management. Fertil Steril1981; 36:433 –445[Medline]
  3. Spies JB, Roth AR, Jha RC, et al. Leiomyomata treated with uterine artery embolization: factors associated with successful symptom and imaging outcome. Radiology 2002;222 : 45–52[Abstract/Free Full Text]
  4. Salerno S, Belli AM. Percutaneous treatment of uterine fibroleiomyomas: analysis of complications and quality of life after embolization [in Italian]. Radiol Med (Torino)2001; 101:360 –364[Medline]
  5. Goodwin S, McLucas B, Lee M, et al. Uterine artery embolization for the treatment of uterine leiomyomata: midterm results. J Vasc Interv Radiol 1999; 10:1159 –1165[Medline]
  6. Spies J, Ascher SA, Roth AR, et al. Uterine artery embolization for leiomyomata Obstet Gynecol 2001;98 : 29–34[CrossRef][Medline]
  7. Walker WJ, Pelage JP. Uterine artery embolisation for symptomatic fibroids: clinical results in 400 women with imaging follow up. BJOG 2002; 109:1262 –1272[Medline]
  8. Berkowitz RP, Hutchins FL Jr, Worthington-Kirsch RL. Vaginal expulsion of submucosal fibroids after uterine artery embolization: a report of three cases. J Reprod Med 1999;44 : 373–376[Medline]
  9. Mayer DP, Shipilov V. Ultrasound and magnetic resonance imaging of uterine fibroids. Obstet Gynecol Clin North Am1995; 22:667 –725[Medline]
  10. Jha RC, Ascher SM, Imaoka I, Spies JB. Symptomatic fibroleiomyomata: MR imaging of the uterus before and after uterine arterial embolization. Radiology 2000;217 : 228–235[Abstract/Free Full Text]
  11. Aziz A, Petrucco OM, Makinoda S, et al. Transarterial embolization of the uterine arteries: patient reactions and effects on uterine vasculature. Acta Obstet Gynecol Scand 1998;77 : 334–340[CrossRef][Medline]
  12. Spies JB, Spector A, Roth AR, et al. Complications after uterine artery embolization for leiomyomas. Obstet Gynecol2002; 100:873 –880[CrossRef][Medline]
  13. McLucas B, Adler L, Perrella R. Uterine fibroid embolization: non surgical treatment for symptomatic fibroids. J Am Coll Surg 2001; 192:95 –105[CrossRef][Medline]
  14. Lumsden MA, Wallace EM. Clinical presentation of uterine fibroids. Baillieres Clin Obstet Gynaecol 1998;12 : 177–195[CrossRef][Medline]
  15. Golzarian J, Lohle P, Walker WJ, Lampmann L, Pelage JP. Uterine fibroid embolization for large symptomatic fibroids. J Vasc Interv Radiol 2003;14 [suppl]:S38
  16. Khilnani NM, Min RJ, Golia P. The response of menorrhagia in patients with fibroids in different locations after UFE. J Vasc Interv Radiol 2004;14 [suppl]:S83
  17. Abbara S, Spies JB, Scialli AR, et al. Transcervical expulsion of a fibroid as a result of uterine artery embolization for leiomyomata. J Vasc Interv Radiol 1999;10 : 409–411[Medline]
  18. Wegienka G, Baird DD, Hertz-Picciotto I, at al. Self-reported heavy bleeding associated with uterine leiomyomata. Obstet Gynecol 2003; 101:431 –437[CrossRef][Medline]
  19. D'Angelo AD, Amso NN, Wood A. Spontaneous multiple pregnancy following uterine artery embolisation for uterine fibroid: a case report. Eur J Obstet Gynecol Reprod Biol 2003;110 : 245–246[CrossRef][Medline]
  20. Spies JB, Coyne K, Guaou Guaou N, Boyle D, Skyrnarz-Murphy K, Gonsalves SM. The UFS-QOL: a new disease-specific symptom and health-related quality of life questionnaire for leiomyomata. Obstet Gynecol 2002; 99:290 –300[CrossRef][Medline]
  21. Wamsteker K, Emanuel MH, deKruif JH. Transcervical hysteroscopic resection of submucous fibroids for abnormal uterine bleeding: results regarding the degree of intramural extension. Obstet Gynecol 1993; 82:736 –740[Medline]
  22. McCluggage WG, Ellis PK, McClure N, Walker WJ, Jackson PA, Manek S. Pathologic features of uterine leiomyomas following uterine artery embolization. Int J Gynecol Pathol 2000;19 : 342–347[Medline]
  23. Siskin GP, Eaton LA Jr, Stainken BF, Dowling K, Herr A, Schwartz J. Pathologic findings in a uterine leiomyoma after bilateral uterine artery embolization. J Vasc Interv Radiol 1999;10 : 891–894[Medline]
  24. Katsumori T, Nakajima K, Tokuhiro M. Gadolinium-enhanced MR imaging in the evaluation of uterine fibroids treated with uterine artery embolization. AJR 2001;177 : 303–307[Abstract/Free Full Text]
  25. Hurley V. Imaging techniques for fibroid detection. Baillieres Clin Obstet Gynaecol 1998;12 : 213–224[CrossRef][Medline]
  26. Griffin KW, Ellis MR, Wilder L, DeArmond L. Clinical inquiries: what is the appropriate diagnostic evaluation of fibroids? J Fam Pract 2005; 54:458 –462[Medline]
  27. Banovac F, Ascher SM, Jones DA, Black MD, Smith JC, Spies JB. Magnetic resonance imaging outcome after uterine artery embolization for leiomyomata with use of tris-acryl gelatin microspheres. J Vasc Interv Radiol 2002; 13:681 –688[Medline]
  28. Payne JF, Haney AF. Serious complications of uterine fibroid embolization for conservative treatment of fibroids. Fertil Steril 2003; 79:128 –131[CrossRef][Medline]
  29. Siskin GP, Tublin ME, Stainken BF, Dowling K, Dolen EG. Uterine artery embolization for the treatment of adenomyosis: clinical response and evaluation with MR imaging. AJR 2001;177 : 297–302[Abstract/Free Full Text]

Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
Am. J. Roentgenol.Home page
F. Burbank
Are Fibroids That Become Endocavitary After Uterine Artery Embolization Necessarily a Complication?
Am. J. Roentgenol., May 1, 2008; 190(5): 1227 - 1230.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Verma, S. K.
Right arrow Articles by Parker, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Verma, S. K.
Right arrow Articles by Parker, L.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
Hotlight (NEW!)
Right arrow
What's Hotlight?


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS