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314
Pedunculated
Uterine
N. A. Keefe and Z. J Haskal
Fig. 28.1 Drawing
representation of submucosal, subserosal, intramural, and pedunculated broids
Intracavitary
Submucosal
Subserosal
artery
Intramural
Cervix
Vagina
Fig. 28.2 A 36-year-old female with a single large uterine broid
with signicant symptoms of menorrhagia and constipation. MRI T1-weighted post-contrast axial (a) image demonstrates the large broid (thick arrow) with uptake of contrast. Three months post­UAE the patient had signicant improvement in both symptoms.
Post-embolization T2-weighted sagittal (b) and T1-post contrast axial (c) images demonstrate a devascularized broid (thick arrow) which is decreased in size. No enhancement is seen. The rectum (thin arrow) and femoral vessels (arrowheads) are also visualized
28 Uterine Artery Embolization
315
Fig. 28.3 A 48-year-old female with uterine adenomyosis and signicant
symptoms of dysmenorrhea. Preoperative MRI T2-weighted sagittal (a) image demonstrates the characteristic stromal invasion of the myome­trium (thick arrow). The rectum is visualized posteriorly (thin arrow).
broids, adenomyosis can appear as a diffusely enlarged “boggy”uterus similar to how a pregnant uterus might look. It is estimated to affect 20% of women, although some studies suggest a much higher occurrence of 65% on microscopic examination [8]. An estimated 80% of patients with adenomy­osis also have broids [9].
Postpartum Hemorrhage
Post partum hemorrhage (PPH) is among the top three causes of maternal mortality, preceded by pulmonary embo­lism and hypertension. Risk factors include retained pla­centa; uterine atony; placenta accreta, previa, and percreta; iatrogenic laceration or instrumentation and induction of labor.
Post-procedural sagittal T1-weighted contrast-enhanced sagittal image (b) demonstrates successful treatment of adenomyosis (thick arrow) with sig­nicant improvement of symptoms post-procedurally (Images courtesy of Dr. Man-Deuk Kim, from Yeonsei University Hospital, South Korea)
Key Point
Indications for UAE
• Fibroids
• Adenomyosis
• Postpartum hemorrhage
• Uterine AV stula
• Dysfunctional uterine bleeding
• Trauma
Asymptomatic broids rarely, if ever, warrant embolization
or surgery unless impairing fertility. Treatment should be patient-specic, consider the severity of symptoms, as well as her age and desire for future fertility. There are numerous for­mal societal guidelines discussing indications for broid ther­apies. Figure 28.4 illustrates the American College of Obstetricians and Gynecologist (ACOG) guidelines [11].

Clinical Indication

Diagnosis of uterine broids usually results after a complaint of menorrhagia or infertility. All patients with an enlarged mass palpated on physical exam should undergo further imaging for evaluation of broids and to rule out ovarian masses or uterine cancers. Ultrasound and MRI are the two best imaging modalities for evaluation of broids (see Fig.28.2). These techniques establish size, location, number, and relation to the endometrial canal [10]. Gynecologists can also directly visualize submucosal and large intramural broids using hysteroscopy.

Conventional Therapy

Fibroids
As the majority of broids are identied incidentally, treat­ment is often not necessary [12]. Medical, surgical, and interventional options are available for symptomatic women, depending on preference and anatomic specics. Controlled trials assessing efcacy of medical therapies are few [13]. Some data suggest that treatment may be efcacious in men­orrhagia patients, although failure rates are high [14]. Arrays
316
N. A. Keefe and Z. J Haskal
Asymptomatic No treatment necessary
Mild symptoms
- Mild pain
- Mild bleeding
Moderate symptoms
- Urinary symptoms
- Menorrhagia
- Pain symptoms
- Constipation
Medical Management
Bleeding predominant symptoms
Diagnosis of Uterine Fibroids
Severe symptoms
- Severe bleeding
- Infertility
- Severe pain
Fig. 28.4 Uterine broid treatment algorithm
Bulk predominant symptoms
of hormonal and nonhormonal therapies have been used. Combined hormonal contraceptives can be used to regulate abnormal uterine bleeding but have little, if any, benet with bulk symptoms. Gonadotropin-releasing hormone agonists such as leuprolide are perhaps the most efcacious [15]. Their articially induced temporary menopause can be accompanied by undesirable symptoms such as hot ashes and mood swings. With the cessation of treatment, menses return with concomitant rapid increase in the size of the uterus and myomas back to baseline [16]. Long-term treat­ment can cause a loss of bone density. A trial of medical management can be useful in patients approaching meno­pause as well as for patients with mild symptoms to distin­guish if their symptoms are related to the broids or secondary to another condition [5].
Hysterectomy, rst performed in 1843, is the only denitive therapy for symptomatic broids [17, 18]. Today, nearly 30% of hysterectomies in white women and 50% in black women are performed for broids, accounting for more than 600,000 hysterectomies annually [19]. The procedure can be performed from the transabdominal or transvaginal approach. Hysterectomies have an increased morbidity and mortality including the development of pelvic oor abnormalities includ­ing vaginal prolapse, sexual dysfunction, premature meno­pause, adhesions, and wound infection [20, 21]. Furthermore, this can lead to body image issues in women both from the scar tissue, as well as potential incisional hernia development.
GnRH agonists
Combined OCPs/IUD
Mifepristone
Endometrial Ablation
Hysterectomy
Uterine Artery Embolization
Myomectomy
Hysterectomy
Uterine Artery Embolization
Myomectomy has advanced from open to more mini­mally invasive laparoscopic and robotic approaches. The conventional open technique involves a transabdominal inci­sion, removal of the broids, and surgical repair of the uterus. Laparoscopic technique is associated with signicantly less pain, shorter hospital stay, and less febrile morbidity than open myomectomy [22]. The broid is morcellated (ground up) and removed through the port site; this can lead to an increased risk of the spread of unsuspected cancerous tis­sues. Both the laparoscopic and open techniques hold a <1% risk of uterine rupture during pregnancy [23]. The rst reported hysteroscopic myomectomy was performed in 1976 using a urologic resectoscope. With advances in instruments and techniques, the procedure was further rened and is cur­rently an option to treat intracavitary broids (submucosal or intramural) as they must be visualized from the endometrial canal [24]. Initial success rates range from 70% to 99% but with a high rate of recurrence. Fertility rates vary widely; on average 50% of women who undergo myomectomy are able to subsequently conceive [25].
Endometrial ablation is an effective treatment used for menorrhagia caused by intracavitary broids or adenomyo­sis. The procedure destroys the endometrial lining through a device inserted into the uterine cavity that delivers a uniform thermal energy to the endometrium. Ablative therapy does not shrink the size of the broid nor the uterus [26]. Endometrial ablation is contraindicated in patients who desire future pregnancy [27].
28 Uterine Artery Embolization
317
Adenomyosis
Medical therapy for the treatment of adenomyosis is similar to broids. Surgical management includes hysterectomy or ablation.
Postpartum Hemorrhage
Treatment for postpartum hemorrhage begins with support­ive management. In the stable patient, initial management includes uterine packing to tamponade the site of bleeding. Oxytocin is used to cause contraction of the uterus and stem bleeding. Misoprostol can be used if oxytocin is not avail­able. In the unstable patient, initial supportive management should be performed including transfusion and pressure sup­port as needed. If bleeding still cannot be controlled, vessel ligation or, as a last resort, hysterectomy, may be used to stop the bleeding.
Key Point
Treatment options for postpartum hemorrhage
• Uterine packing
• Oxytocin
• Supportive management
• UAE
• Hysterectomy
• Vessel ligation
Fibroids
The Society of Interventional Radiology maintains a pro­spective UAE registry called the Fibroids Registry for Outcomes Data (FIBROID) which is the largest database to be reported on to date. Three-year follow-up data on over 2000 patients demonstrated that severely affected patients returned to normal quality of life after UAE.The baseline mean symptom score for patients was 58.61 as assessed with the uterine broid symptom scale with patients seeing on average an improvement in their score by 41.41 points (P<0.001). Similarly, the quality of life score improved by
41.47 points over their baseline at 3years, bringing them into a normal range [30]. A large-scale comparison of myomec­tomy and UAE (Cochrane review) suggests that myomec­tomy has better fertility outcomes, but the evidence was low quality [30]. During the 3-year duration of the study, hyster­ectomy, myomectomy, or repeat UAE was performed in
9.79%, 2.82%, and 1.83% of patients, respectively, compa­rable to surgical reintervention rates of 5% annually after myomectomy [30]. More recent and larger studies have sug­gested that UAE may be better at preserving fertility [22,
31]. Although UAE appears to destroy most of the broids
during the initial procedure, it does not change the underly­ing nature of the uterus to form new broids which can lead to delayed reintervention [32].
Key Point
UAE absolute contraindications
• Pregnancy
• Suspected malignancy (except pre‐op)

Interventional Therapy

Uterine artery embolization (UAE) is a minimally invasive therapy that blocks the blood supply to the uterus. UAE was originally introduced in the 1970s at UCLA as a treatment for postpartum hemorrhage [28]. It is used for the treatment of broids, adenomyosis, arteriovenous stula, arteriove­nous malformation, and placenta previa, percreta, or accreta. First reported in 1995 by Ravina, UAE can be used in the treatment of uterine broids, in which case it may be referred to as uterine broid embolization (UFE) [28]. The reduction of blood ow to the uterus results in selective infarction of the broids yielding improvements in both bulk- and bleed­ing-related symptoms. To date, no one fully understands why UAE infarcts broids but preserves surrounding normal uter­ine tissue [29].
UAE relative contraindications
• Coagulopathy
• Renal insufciency
• Contrast allergy
• Desire for pregnancy in 2years
UAE is performed as an outpatient or overnight proce­dure, depending on institution and provider preference. Post­embolization syndrome is a common prodrome characterized by pain and occasional nausea lasting 2–7days post-proce­durally. These symptoms can be managed by NSAIDs +/ narcotics combined with stool softeners, typically prescribed to all women prior to discharge. Rarely some women can experience passage of necrosed broid, occurring primarily in patients with submucosal broids [33]. Sometimes, if
318
N. A. Keefe and Z. J Haskal
The How To
Before the procedure, most interventional radiologists
obtain a contrast-enhanced pelvic MRI for character-
Here’s what you expect to see when you walk into the
angio suite:
1. A Foley bladder catheter may be placed pre­procedurally. Unilateral or bilateral femoral access
radial artery approach, which may occur in younger healthier patients or very obese patients.
2. The Seldinger technique is used to access the artery of choice (refer to Chap. 8 for a review of more information).
3. An aortogram may be performed for evaluation of ovarian feeding vessels; however, it is not routinely performed at all institutions. Internal iliac angio­gram delineates the origins of the uterine artery.
4. The side contralateral to the initial puncture is cath­eterized (if coming from a femoral approach), and the uterine artery is accessed using a microcatheter. The uterine artery and occasionally the ovarian
Fig. 28.5 A 48-year-old female with a large submucosal broid. Post-
embolization T1 sagittal MRI demonstrates sloughing of the broid from the endometrial lining (arrowheads) into the uterine cavity. This necrosed broid (thick arrow) was too large to remove via colposcopy and required hysterectomy. The rectum is visualized posteriorly (thin arrow)
these submucosal broids are too large, they may need to be removed via colposcopy (Fig.28.5). Inadvertent emboliza­tion of the ovary via ovarian artery embolization can lead to rare premature ovarian failure in premenopausal patients. Patients are seen in follow-up in IR clinic at 1-, 3-, and 6-month follow-ups, which can vary by institution.
Key Point
Complications
• Fibroid passage
• Pulmonary embolism
• Nontarget embolization
• Myometrial injury
• Ovarian failure (1–5%)
artery of the round ligament can be a source of blood supply to the uterus; this vessel arises from the infe­rior epigastric artery [29 ­cular compared to the uterus, when contrast is injected into the catheter, you will see serpiginous (snake-like) vessels spread out in a semicircular
28.6a, c).
5. Embolization is performed from a proximal uterine artery position using embolization particles (500–
µm). Typically, permanent microspheres are utilized. Gelfoam or polyvinyl alcohol particles can also be used. The goal of embolization is not com­plete occlusion of the main uterine artery, but occlu-
Completion of embolization can be demonstrated
-
28.6b, d).
6. If a bilateral femoral artery approach is employed, steps 4 and 5 are repeated from the other side.
7. If a unilateral femoral artery approach is used, the ipsilateral side (the initial side of puncture in the femoral approach) is accessed by the Waterman loop technique. This is done by bending the cathe­ter into a hairpin turn within the aorta and backing it down into the ipsilateral iliac artery.
8. then be interrogated to ensure complete embolization
28 Uterine Artery Embolization
Fig. 28.6 A 51-year-old
female with menorrhagia and large uterine broids. Pre-embolization imaging (a) and (c) demonstrate extensive tortuous uterine vessels (thick arrows) on the right and left side, respectively. Post­embolization imaging demonstrates no residual lling of the abnormal vessels (arrowhead) supplying the broid (b, d)
319
Adenomyosis
UAE is also used for successful treatment of adenomyosis. Many studies show initial success in the relief of bleeding and pain-related symptoms [34, 35]. Patients must be coun­seled prior to the procedure on the possibilities of treatment failure and possible need for reintervention.
Postpartum Hemorrhage
UAE is a lifesaving procedure, performed emergently or pro­phylactically (in high-risk patients) for postpartum hemor­rhage [36]. Initial management for postpartum bleeding
begins with uterine stimulants such as oxytocin combined with bimanual compression. Although conservative manage­ment is favored for uterine preservation, traditional surgical options include repair of genital tract lacerations, uterine hypogastric artery ligation, and hysterectomy [37]. Numerous studies have reported various success rates of UAE for post­partum hemorrhage ranging from 80% to 100% [3840]. Rarely and controversially, bilateral femoral catheters can beplaced prior to delivery for prophylactic therapy in high­risk patients (placenta previa, accreta, or percreta). Occlusion balloons are inated in the anterior division of the internal iliac artery during delivery to reduce blood loss (Fig.28.7). In the postdelivery patient in whom they cannot control hem­orrhage by traditional techniques, angiogram is aimed at
320
N. A. Keefe and Z. J Haskal
Fig. 28.7 A 26-year-old female with prenatal ultrasound demonstrat-
ing placenta percreta. Patient was taken to the hybrid OR and bilateral groin access was obtained. (a) Selective angiography demonstrated increased vascularity of the serosa (thick arrows). Fogarty balloons were inated in bilateral uterine arteries, and uterine artery emboliza-
tion was performed bilaterally using PVA particles. Caesarean section was then performed by the obstetrics surgical team. Following closure, a DSA run (b) was performed demonstrating no evidence of active bleeding. The bladder can be seen lling with contrast post-procedur­ally (thin arrow)
Fig. 28.8 A 38-year-old female status post-hysterectomy with persis-
tent active bleeding. (a) Angiography demonstrates active blush (thin arrow) arising from branches of the right internal iliac pelvic branches.
Coils were placed in the anterior division of the internal iliac artery. This was followed by embolization with Gelfoam and PVA. (b) Post­embolization demonstrates no evidence of active extravasation
28 Uterine Artery Embolization
321
Fig. 28.9 A 29-year-old female with arteriovenous stula following
dilation and curettage. (a) Aortography demonstrates an abnormal hypervascularity (thick arrows) originating from the right uterine artery.
identifying an area of “blush” (active extravasation) (Fig.28.8). That vessel is targeted using a microcatheter, and Gelfoam is used to embolize the area. Gelfoam is the pre­ferred agent as it is temporary (2–6weeks) but is sufcient to reduce hemorrhage. Each vessel supplying the uterus should be interrogated to ensure that all sites of active bleeding have been occluded.
AV Fistula
Arteriovenous stulae (also called uterine AVMs) are an unusual cause of abnormal uterine bleeding and can lead to severe hemorrhage [41]. Approximately 50% are congenital arteriovenous malformations, while the remainder are stu­lae that develop after uterine instrumentation, dilatation and curettage (D&C), uterine neoplasms, or maternal diethylstil­bestrol. Uterine artery embolization is the rst-line treatment for uterine AV stulae and has a 90% success rate (Fig.28.9) [42, 43]. The area of abnormality is located angiographi­cally. Any embolic agent (Gelfoam, PVA, EVOH, glue, microspheres, etc.) can be used to occlude the area. When coils are used, the microcatheter is parked adjacent to the area of interest and advanced. Several coils may be necessary to ll the area, and, occasionally, Gelfoam may be used after a coil to achieve complete stasis.
(b) Post-embolization angiography demonstrates no residual lling of the AV stula (arrowheads). Symptoms of metrorrhagia improved post-embolization

References

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15. Friedman AJ, Daly M, Juneau-Norcross M, Rein MS.Predictors of uterine volume reduction in women with myomas treated with a gonadotropin-releasing hormone agonist. Fertil Steril. 1992;58(2):413–5.
16. Letterie GS, Coddington CC, Winkel CA, Shawker TH, Loriaux DL, Collins RL. Efcacy of a gonadotropin- releasing hormone agonist in the treatment of uterine leiomyomata: long-term follow­up. Fertil Steril. 1989;51(6):951–6.
17. Amirikia H, Evans TN.Ten-year review of hysterectomies: trends, indications, and risks. Am JObstet Gynecol. 1979;134(4):431–7.
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19. Keshavarz H, Hillis SD, Kieke BA, Marchbanks PA.Hysterectomy aurveillance – United States, 1994–1999. MMWR. 2002;51(SS05):1–8.
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21. Jacoby VL, Jacoby A, Learman LA, Schembri M, Gregorich SE, Jackson R, etal. Use of medical, surgical and complementary treat­ments among women with broids. Eur JObstet Gynecol Reprod Biol. 2014;182:220–5.
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33. Abbara S, Spies JB, Scialli AR, Jha RC, Lage JM, Nikolic B. Transcervical expulsion of a broid as a result of uterine artery embolization for leiomyomata. J Vasc Interv Radiol. 1999;10(4):409–11.
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35. Kim MD, Kim S, Kim NK, Lee MH, Ahn EH, Kim HJ, etal. Long­term results of uterine artery embolization for symptomatic adeno­myosis. AJR Am JRoentgenol. 2007;188(1):176–81.
36. Bibi S, Ghaffar S, Memon S, Memon S. Severe acute maternal morbidity (SAMM) in postpartum period requiring tertiary hospital care. Iran JReprod Med. 2012;10(2):87–92.
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41. Fleming H, Ostör AG, Pickel H, Fortune DW.Arteriovenous mal­formations of the uterus. Obstet Gynecol. 1989;73(2):209–14.
42. Kim T, Shin JH, Kim J, Yoon HK, Ko GY, Gwon DI, et al. Management of bleeding uterine arteriovenous malforma­tion with bilateral uterine artery embolization. Yonsei Med J.2014;55(2):367–73.
43. Forssman L, Lundberg J, Scherstén T. Conservative treatment of uterine arteriovenous stula. Acta Obstet Gynecol Scand. 1982;61(1):85–7.

Prostate Artery Embolization

Bladder
Central
Peripheral
TimothyC.Huber, BenjaminN.Contrella, andAndreUacker
29

Pathophysiology

Benign Prostatic Hyperplasia
Benign prostatic hyperplasia (BPH) is characterized by development of discrete nodules in the transitional zone of the prostate gland [1]. Testosterone and dihydroxytestoster­one (DHT) potentiate the growth of the prostate gland which results in an enlarging gland with age [2]. Studies of cas­trated court ofcials in both Ottoman and Chinese courts demonstrated small to non-palpable prostates in males from 40 to 60years of age, supporting the role of hormonal inu­ence [3]. BPH occurs naturally with age with a strong hor­monal inuence, affecting approximately 25% of men 40–50 years of age and over 80% of men greater than 70years of age [4]. Risk factors for BPH include higher lev­els of endogenous androgens, family history, and Caucasian race; obesity, diabetes mellitus, alcohol consumption, physi­cal inactivity, high levels of insulin-like growth factor, and high levels of C-reactive protein have also been suggested to place individuals at risk [5, 6].
Lower urinary tract symptoms (LUTS) are a classic nd­ing in BPH and are comprised of obstructive and irritative symptoms (Table 29.1), which can decrease quality of life [6, 7].
The prostate is divided into three zones (Fig.29.1). In the normal prostate, the peripheral zone accounts for 70% of the volume, the central zone accounts for 25%, and the transi-
Table 29.1 Symptoms of benign prostatic hypertrophy (BPH) [5, 6]
Lower urinary tract symptoms of BPH Irritative/bothersome
symptoms Obstructive symptoms Increased frequency/urgency Poor urinary stream/straining to void Painful voiding Urinary hesitancy Nocturia Incomplete voiding Incontinence Urinary retention/bladder outlet
Sexual dysfunction Bladder dysfunction
zone
Fig. 29.1 Zonal anatomy of the prostate gland and its relation to adja-
cent structures
obstruction
Transition zone
Central zone
Urethra
gland
T. C. Huber · B. N. Contrella · A. Uacker (*) University of Virginia Health System, Department of Radiology and Medical Imaging, Charlottesville, VA, USA e-mail: th8mt@virginia.edu; BNC7CJ@hscmail.mcc.virginia.edu;
au2b@virginia.edu
© Springer International Publishing AG, part of Springer Nature 2018 N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_29
tional zone accounts for 5%. BPH causes growth of the tran­sitional zone through hypertrophy, while prostatic cancer most commonly affects the peripheral zone [810].
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