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B. W. Rackow
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35. Nawroth F, Rahimi G, Nawroth C, Foth D, Ludwig M, Schmidt T. Is there an association between septate uterus and endometriosis? Hum Reprod. 2006;21:542–4.
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37. Mazouni C, Girard G, Deter R, Haumonte JB, Blanc B, Bretelle F. Diagnosis of Müllerian anoma­lies in adults: evaluation of practice. Fertil Steril. 2008;89:219–22.
38. Sanlippo JS, Wakim NG, Schikler KN, Yussman MA.Endometriosis in association with uterine anom­aly. Am J Obstet Gynecol. 1986;154:39–43.
39. Acien P. Reproductive performance of women with uterine malformations. Hum Reprod. 1993;8:122–6.
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41. Hua M, Odibo AO, Longman RE, Macones GA, Roehl KA, Cahill AG. Congenital uterine anoma­lies and adverse pregnancy outcomes. Am J Obstet Gynecol. 2011;205:558 e1–5.
42. Acien P.Incidence of Müllerian defects in fertile and infertile women. Hum Reprod. 1997;12:1372–6.
43. Homer HA, Li TC, Cooke ID. The septate uterus: a review of management and reproductive outcome. Fertil Steril. 2000;73:1–14.
44. Fedele L, Bianchi S, Marchini M, Franchi D, Tozzi L, Dorta M. Ultrastructural aspects of endometrium in infertile women with septate uterus. Fertil Steril. 1996;65:750–2.
45. Fedele L, Bianchi S. Hysteroscopic metroplasty for septate uterus. Obstet Gynecol Clin N Am. 1995;22:473–89.
46. Andrews MC, Jones HW Jr. Impaired reproductive performance of the unicornuate uterus: intrauterine growth retardation, infertility, and recurrent abortion in ve cases. Am J Obstet Gynecol. 1982;144:173–6.
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48. Candiani GB, Fedele L, Zamberletti D, De Virgiliis D, Carinelli S.Endometrial patterns in malformed uteri. Acta Eur Fertil. 1983;14:311–8.
49. Golan A, Langer R, Wexler S, Segev E, Niv D, David MP.Cervical cerclage: its role in the pregnant anoma­lous uterus. Int J Fertil. 1990;35:164–70.
50. Ghi T, Casadio P, Kuleva M, Perrone AM, Savelli L, Giunchi S, etal. Accuracy of three-dimensional ultra­sound in diagnosis and classication of congenital uterine anomalies. Fertil Steril. 2009;92:808–13.
51. Faivre E, Fernandez H, Defeux X, Gerviase A, Frydman R, Levaillant JM. Accuracy of three­dimensional ultrasonography in differential diagnosis of septate and bicornuate uterus compared with ofce hysteroscopy and pelvic magnetic resonance imaging. J Minim Invasive Gynecol. 2012;19:101–6.
52. Reuter KL, Daly DC, Cohen SM.Septate versus bicor­nuate uteri: errors in imaging diagnosis. Radiology. 1989;172:749–52.
53. Grimbizis GF, DiSpezio Sardo A, Saravelos SH, Gordts S, Exacoustos C, Van Schoubroeck D, et al. The Thessaloniki ESHRE/ESGE consensus on diag­nosis of female genital anomalies. Hum Reprod. 2016;31:2–7.
54. Nicolini U, Bellotti M, Bonazzi B, Zamberletti D, Candiani GB.Can ultrasound be used to screen uter­ine malformations? Fertil Steril. 1987;47:89–93.
55. Caliskan E, Ozkan S, Cakiroglu Y, Sarisoy HT, Corakci A, Ozeren S. Diagnostic accuracy of real­time 3D sonography in the diagnosis of congenital Müllerian anomalies in high-risk patients with respect to the phase of the menstrual cycle. J Clin Ultrasound. 2010;38:123–7.
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57. Troiano RN. Magnetic resonance imaging of Müllerian duct anomalies of the uterus. Top Magn Reson Imaging. 2003;14:269–79.
58. Pellerito JS, McCarthy SM, Doyle MB, Glickman MG, DeCherney AH. Diagnosis of uterine anoma­lies: relative accuracy of MR imaging, endovaginal sonography, and hysterosalpingography. Radiology. 1992;183:795–800.
59. Letterie GS, Haggerty M, Lindee G.A comparison of pelvic ultrasound and magnetic resonance imaging as diagnostic studies for Müllerian tract abnormalities. Int J Fertil Menopausal Stud. 1995;40:34–8.
60. Fedele L, Dorta M, Brioschi D, Massari C, Candiani GB. Magnetic resonance evaluation of double uteri. Obstet Gynecol. 1989;74:844–7.
61. Carrington BM, Hricak H, Nuruddin RN, Secaf E, Laros RK Jr, Hill EC.Müllerian duct anomalies: MR imaging evaluation. Radiology. 1990;176:715–20.
62. Jurkovic D, Geipel A, Gruboeck K, Jauniaux E, Natucci M, Campbell S. Three-dimensional ultra­sound for the assessment of uterine anatomy and detection of congenital anomalies: a comparison with hysterosalpingography and two-dimensional sonogra­phy. Ultrasound Obstet Gynecol. 1995;5:233–7.
63. Raine-Fenning N, Fleischer AC.Clarifying the role of three-dimensional transvaginal sonography in repro­ductive medicine: an evidence-based appraisal. J Exp Clin Assist Reprod. 2005;2:10.
64. Salim R, Woelfer B, Backow M, Regan L, Jurkovic D. Reproducibility of three-dimensional ultrasound diagnosis of congenital uterine anomalies. Ultrasound Obstet Gynecol. 2003;21:578–82.
65. Raga F, Bonilla-Musoles F, Blanes J, Osborne NG. Congenital Müllerian anomalies: diagnostic accuracy of three-dimensional ultrasound. Fertil Steril. 1996;65:523–8.
66. Graupera B, Pascual MA, Hereter L, Browne JL, Ubeda B, Rodriguez I, et al. Accuracy of three­dimensional ultrasound compared with magnetic resonance imaging in diagnosis of Mullerian duct anomalies using ESHRE-ESGE consensus on the classication of the female genital tract. Ultrasound Obstet Gynecol. 2015;46:616–22.
67. Ergenoglu AM, Sahin C, Simsek D, Akdemir A, Yeniel AO, Yerli H, etal. Comparison of three-dimensional ultrasound and magnetic resonance imaging diagno­sis in surgically proven Mullerian duct anomaly cases. Eur J Obstet Gynecol Reprod Biol. 2016;197:22–6.
68. Reichman DE, Laufer MR.Congenital uterine anoma­lies affecting reproduction. Best Pract Res Clin Obstet Gynaecol. 2010;24:193–208.
69. Marcus S, al-Shawaf T, Brinsden P.The obstetric out­come of invitro fertilization and embryo transfer in women with congenital uterine malformation. Am J Obstet Gynecol. 1996;175:85–9.
70. Taylor E, Gomel V. The uterus and fertility. Fertil Steril. 2008;89:1–16.
71. Dabirashra H, Bahadori M, Mohammad K, Alavi M, Moghadami-Tabrizi N, Zandinejad K, et al. Septate uterus: new idea on the histologic features of the sep­tum in this abnormal uterus. Am J Obstet Gynecol. 1995;172:105–7.
72. Reichman D, Laufer MR, Robinson BK. Pregnancy outcomes in unicornuate uteri: a review. Fertil Steril. 2009;91:1886–94.
73. Heinonen PK, Saarikoski S, Pystynen P.Reproductive performance of women with uterine anomalies: an evaluation of 182 cases. Acta Obstet Gynecol Scand. 1982;61:157–62.
74. Jacobsen LJ, DeCherney A. Results of conven­tional and hysteroscopic surgery. Hum Reprod. 1997;12:1376–81.
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76. Practice Committee of the American Society of Reproductive Medicine. Uterine septum: a guideline. Fertil Steril. 2016;106:530–40.
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78. Fedele L, Arcaini L, Parazzini F, Vercellini P, Di Nola G.Reproductive prognosis after hysteroscopic metro­plasty in 102 women: life-table analysis. Fertil Steril. 1993;59:768–72.
79. Mollo A, De Franciscis P, Colacurci N, Cobellis L, Perino A, Venezia R, et al. Hysteroscopic resection of the septum improves the pregnancy rate of women with unexplained infertility: a prospective controlled trial. Fertil Steril. 2009;91:2628–31.
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Uterine Fibroids

BradleyS.Hurst
9

Background

The identication of uterine broids during eval­uation for infertility or in preparation for assisted reproductive technology can present a perplexing problem for patients and their providers, espe­cially when broids are asymptomatic. The con­cern is well-deserved, since unnecessary surgery for broids exposes the patient to risks, has a high potential to result in adhesion formation, may require future cesarean delivery, and may reduce fertility if adhesions compromise the tubo-ovarian relationship or distort the uterine cavity. However, failure to treat broids could impair spontaneous conception, compromise out­comes of fertility treatments, or increase the risk of miscarriage and pregnancy-related complica­tions. The goal of this chapter will be to provide rational treatment options for women with uter­ine broids, based on the best available data.
A uterine broid is a monoclonal growth of brovascular cells that arise from the myome­trium. Estrogen and progesterone receptors are present in broids, and both hormones stimulate broid proliferation. Fibroids are surrounded by a dense vascular pseudocapsule, and larger
B. S. Hurst (*) Carolinas Medical Center, Department of Obstetrics and Gynecology, Reproductive Endocrinology and Infertility, Charlotte, NC, USA e-mail: brad.hurst@atriumhealth.com
masses usually have a greater vascular supply [1]. Factors within the pseudocapsule stimulate broid growth, including a local overexpression of aromatase, which converts androgens to estro­gens [2]. Estrogen stimulates growth factors in the pseudocapsule, including EGF, IGF-1, bFGF, GH, TGF-β, PDGF, endothelin A, and VEGF [3]. Vitamin D deciency appears to stimulate broid growth [4].
The prevalence of broids peaks during the fourth decade because of the cumulative effects of estrogen, progesterone, and growth factors on myoma growth during the reproductive years [5]. Fibroids are more numerous and larger in African­Americans. Ultrasound studies have found a cumulative incidence of broids in approximately 80% of African-American women by age 50 [6]. However, broids are common in all ethnicities, including a cumulative incidence of 70% in Caucasian women. There is great interest in iden­tifying dietary and environmental factors that contribute to broid growth. There is increasing evidence that hypertension, a family history of broids, time since last birth, food additives, and soybean milk consumption increase the risk of uterine broids [7]. Oral contraceptives, depot medroxyprogesterone acetate, smoking, and increased parity reduce the risk of broids.
The broid deforms the surrounding tissues as it grows. A broid that develops in the myometrial wall is considered an “intramural” myoma (Fig. 9.1). A broid that protrudes into the
© Springer Nature Switzerland AG 2019 L. A. Stadtmauer, I. Tur-Kaspa (eds.), Ultrasound Imaging in Reproductive Medicine,
https://doi.org/10.1007/978-3-030-16699-1_9
137
138
Fig. 9.1 Saline infusion
sonohysterography with intramural broid
endometrial mucosa is a “submucous” myoma. Fibroids that protrude the serosal surface of the uterus are called “subserosal” myomas (Fig.9.2). Other terms sometimes used to describe the loca­tion of broids include “sessile,” a type of submu­cous myoma that is located in the myometrium but also distorts the endometrium (Fig.9.3). A “pedun­culated” broid is located primarily outside of the uterus, connected to the uterus by a brovascular stalk (Fig.9.4). In this chapter, the terms broid, myoma, and leiomyoma are used interchangeably.
In 2011, the International Federation of Gynecology and Obstetrics (FIGO) published a classication system further describing the loca­tion of broids [8], and clinical studies often refer to this classication. There are eight broid types. Submucous broids are divided into Type 0 (completely intracavitary), Type 1 (>50% intra­cavitary), and Type 2 ( 50% intramural) (Fig.9.5). A Type 3 broid is intramural but con­tacts the endometrium, Type 4 is intramural and entirely within the endometrium, and Type 5 is intramural and distorts the serosa but is ≤50% subserosal. A Type 6 broid is partly intramural but >50% subserosal, and a Type 7 broid is sub­serosal pedunculated. A Type 8 broid is not attached to the uterus and may include other loca­tions such as the cervix or could be a parasitic broid. Finally, a “Hybrid 2–5” broid distorts
B. S. Hurst
Fig. 9.2 Transvaginal ultrasound demonstrating subsero-
sal broid
the endometrium and the serosa but is <50% sub­mucosal and <50% subserosal.
Symptoms attributed to broids are deter-
mined by the size and the location of the
9 Uterine Fibroids
Fig. 9.3 Transvaginal
ultrasound demonstrating several uterine broids, including one submucous myoma with deection of the endometrial cavity
Fig. 9.4 Transvaginal
ultrasound demonstrating pedunculated broid
139
masses. Most intramural, subserosal, and pedunculated broids are asymptomatic. However, large broids may cause bulk symp­toms such as abdominal pressure, bloating, or distention. A myoma that presses against the bladder may cause urinary frequency, urgency, or nocturia. A broid that compresses the rec­tum may cause constipation, diarrhea, or alter­nating symptoms. Infarction of a broid may cause severe acute pain, and the inammation caused by degenerating myoma may cause adhesions. Fibroids located in the posterior cul-
de-sac may cause dyspareunia. Occasionally, broids are associated with chronic, intermit­tent, or cyclic pain.
Submucous myomas often cause abnormal uterine bleeding (Fig.9.6). Symptoms of submu­cous broids include menorrhagia, dysmenor­rhea, clotting, and intermenstrual bleeding [9]. When bleeding is severe, anemia may occur. With the high prevalence of broids and the mul­titude of symptoms that may be attributed to broids, it is not surprising that broids are the leading indication for hysterectomy. However,
140
B. S. Hurst
Leiomyoma subclassification system
3
2-5
6
5
Fig. 9.5 International Federation of Gynecology and Obstetrics (FIGO) published a classication system further
describing the location of broids [8]. (Reprinted with permission from Munro etal. [8])
4
0
1
2
7
SM - Submucosal
O - Other
Hybrid leiomyomas
(impact both endometrium and serosa)
0Pedunculated intracavitary
1
<50% intramural
50% intramural
2
3
Contacts endometrium; 100% intramural
4
Intramural
Subserosal 50% intramural
5
6
Subserosal <50% intramural
7
Subserosal pedunculated
8
Other (specify e.g. cervical, parasitic)
Two numbers are listed separated by a hyphen. By convention, the first refers to the relationship with the endometrium while the second refers to the relationship to the serosa. One example is below
2–5
Submucosal and subserosal, each with less than half the diameter in the endometrial and peritoneal cavities, respectively.
broids increases with age, fertility declines with age, and many women with broids conceive spontaneously.
The location of broids is important in deter­mining the impact on fertility. In some circum­stances, broids impair fertility by mechanically distorting the uterine cavity, altering the endome­trium and impairing embryo implantation and growth. Other obvious causes of broid-related infertility may include mechanical obstruction of the tubal ostia.
Submucous myomas directly impair fertility and cause adverse reproductive outcomes by sev­eral potential mechanisms [9]. These broids alter the vascular supply and development of the endometrium with intramural myomas or alter growth factors and inammatory substances that
Fig. 9.6 Three-dimensional mapping of a submucosal
broid
may impair implantation or fetal growth. The mechanical distortion of the endometrial cavity almost certainly has a direct effect on fertility. In general, greater endometrial distortion more
other treatment options must be considered for women who are interested in childbearing.
clearly results in compromised fertility. Myomectomy improves fertility in these cases.
Intramural broids reduce fertility when they are 4cm or larger, and myomectomy appears to
Fibroids andFertility
restore fertility [10]. Additionally, FIGO Type 3 intramural broids 2cm or larger that touch the
It is difcult to determine the direct impact of broids on fertility, since the incidence of uterine
endometrium impair fertility [11]. Another study found that fertility was reduced in women who
9 Uterine Fibroids
Fig. 9.7 Transvaginal
ultrasound demonstrating multiple intramural broids; the entire endometrium is difcult to visualize
141
had two or more intramural broids, or for intra­mural broids that are 3 cm or larger [12]. However, there is no clear evidence that myo­mectomy enhances fertility in women with intra­mural myomas [13, 14]. Subserosal broids do not impair fertility [15].
Many women have multiple broids, and the different size, location, number, and relative rela­tionship to the endometrium increase the dif­culty in establishing the effect of broids on fertility, as no two individuals are directly com­parable (Fig. 9.7). As such, the relative useful­ness of myomectomy in these situations cannot be established with certainty.
Fibroids andIVF
Studies of the impact of broids in IVF cycles are helpful to establish the impact, since many fac­tors impacting fertility are either controlled, such as male infertility, or directly evaluated, such as the impact of age on cycle outcome. Submucosal broids have long been recognized to reduce IVF pregnancy and birth rates [16, 17]. Furthermore, hysteroscopic myomectomy improves pregnancy rates, with outcomes comparable to women with a normal uterine cavity [18].
The effect of medium and large intramural myomas on IVF outcomes is unclear, and some studies have shown little clinical effect. When IVF outcomes are generally poor, IVF live birth rates were not improved by myomectomy in one small retrospective study: IVF “ongoing” preg­nancy rates were 17% after myomectomy (n=47), 21% with untreated broids (n=11), and 19% in normal controls [17]. However, 50% of women with broids experienced a spontane­ous abortion, compared to 34% after myomec­tomy, suggesting that broids compromise pregnancy outcomes. A study of 46 IVF cases with intramural and subserosal broids showed that outcomes were similar to controls, but broid size was not assessed [19]. Other investigators found that myomas, 73% of which were subsero­sal, had no effect on conception in 39 women [20]. A study of 119 women with asymptomatic intramural or subserosal broid found that myo­mas smaller than 5cm did not compromise IVF pregnancy or birth rates when matched to con­trols [21]. The outcome was not changed when the group was limited to those with intramural myomas.
Contrary to these reports, increasing evidence suggests that some intramural broids are associ­ated with lower ART live birth rates. A retrospec-
142
B. S. Hurst
tive study found a signicant decrease in IVF live birth rates in women under age 40 years with intramural broids (49% and 58%, respectively) [22]. In 2005, a meta-analysis showed a signi­cantly lower implantation rate with intramural broids compared to controls, 16.4 vs. 27.7%, respectively (OR 0.62, 0.48–0.8), and a signi­cantly lower birth rate per embryo transfer with broids compared to controls, 31.2% and 40.9% (OR 0.69, 0.50–0.95) [23]. In a retrospective study of 91 IVF cycles in women with intramural or subserosal broids, Stovall etal. found a sig­nicantly lower pregnancy rate with broids (37%) compared to matched controls (53%) [24]. The broids size ranged from 8 to 54mm, with a mean diameter of 29mm, and 95% were intra­mural. The implantation rate was 14% with broids, signicantly lower than the 20% implan­tation rate in controls without broids. Another study found that women with intramural broids had signicantly lower pregnancy rates com­pared to women without broids, 16% and 34%, respectively, p < 0.05 [16]. Implantation rates were more than 50% lower with intramural broids compared to the controls (p < 0.005), even though the mean diameter of the broids was 24mm. A meta-analysis assessed 19 obser­vational studies comprising 6087 IVF cycles and found a signicantly lower IVF live birth (RR=0.79, 95% CI 0.70–0.88, p<0.0001) and clinical pregnancy rate (RR=0.85, 95% CI 0.77–
0.94, p = 0.002) in women with intramural broids compared to those without broids [25]. The authors concluded that non-cavity-distorting intramural broids are associated with adverse pregnancy outcomes in women undergoing IVF. Oliveira etal. found a signicantly lower preg­nancy rate with IVF only when intramural broids were 4cm or larger [10].
Recent studies have identied characteristics that impair ART live birth rates. A case-control study of 151 women with FIGO Type 3 intramu­ral broids found that broids 2cm or larger that touch the endometrium impair IVF pregnancy and live birth rates, but smaller broids do not compromise outcomes [11]. Finally, one case­controlled study women undergoing IVF found that the live birth rate was reduced in women who
had two or more intramural broids (OR 0.47; 95% CI 0.26–0.83) or if intramural broids that are 3cm or larger (OR 0.41; 95% CI 0.19–0.89) [12]. There was no difference in pregnancy out­comes in those with one intramural broid <3cm. Subserosal broids do not impair fertility [15].
Egg donation provides an opportunity to study the effect of implantation while minimizing the effect of confounding factors of maternal age and male fertility. There is evidence that egg donation outcomes are lower in African-American women compared to other populations, although the pop­ulations are too small to conclude that broids are the primary explanation for this effect [26]. It is possible that uterine broids could provide a possible explanation for this observation.
Uterine broids may increase the difculty of the oocyte retrieval or embryo transfer and either may lower IVF outcomes. A broid may raise the ovary out of the pelvis, especially large masses. If this occurs, it may be necessary to perform lapa­roscopic oocyte retrieval or ultrasound-directed transabdominal retrieval. A broid may increase the difculty of the embryo transfer in one of sev­eral ways: distorting the position of the cervix in a way that it is difcult or impossible to expose the cervix with a speculum, by markedly altering the endocervical course or causing endocervical stenosis (Fig. 9.8). Finally, a large broid may make visualization of embryo transfer difcult or impossible when an abdominal ultrasound­guided procedure is performed. This can be criti­cal since increasing difculty or tortuosity of the endocervix makes it difcult to visualize the transfer catheter to conrm optimal placement.
Myomas andObstetrical Outcomes
While the impact of broids on fertility is still debated, obstetrical outcomes appear to be com­promised by uterine broids in some [9] but not all studies. A population-based retrospective study by Sheiner et al. [27] found that women with broids had a 3.5-fold increased incidence of intrauterine growth restriction (6.8% vs.
1.9%), a 4-fold increase in placental abruption (2.8% vs. 0.7%), a 5-fold higher incidence of
9 Uterine Fibroids
Fig. 9.8 Transvaginal
ultrasound demonstrating large broid in the lower uterus and cervix
143
transverse lie or breech presentation (16.9% vs.
2.4%), a 5 times higher cesarean section rate (57.7% vs. 10.8%), 70% higher risk of premature rupture of membranes (9.6% vs. 5.5%), and were 3 times more likely to receive transfusion (4.2% vs. 1.4%). All of these outcomes were signicant, with p<0.001. Adjusting for maternal age, par­ity, gestational age, and malpresentation, preg­nancies with broids still had a 6.7 times higher risk of cesarean delivery, with 95% CI 5.5–8.1, p<0.01). Placental abruption and preterm deliv­eries remained signicantly more common with broids. The size and locations of the broids were not assessed in this study, but other investi­gators have found that broids adjacent to the placenta increase the risk of bleeding and prema­ture rupture of membranes [28].
A retrospective study in 2012 supports the hypothesis that broids have a detrimental impact on pregnancy, especially when the broids are large [29]. The mean gestation age at delivery for women with broids larger than 5cm was 36.5weeks, signicantly earlier than women with smaller broids or no broids. Other signicant effects included shortened cer­vix, premature preterm rupture of membranes, preterm delivery, blood loss during delivery, and the need for postpartum transfusion. Considering these and other publications, authors of a litera­ture review concluded that pregnancy outcomes
are compromised in women who have intramural broids [30].
Uterine broids tend to enlarge during preg­nancy, regardless of size and maternal age [31]. Although the growth or degeneration of a broid is not linear throughout the course of pregnancy, there is remarkable growth during the early preg­nancy. This was demonstrated in a prospective case-controlled study of women with broids undergoing IVF, in which broids were serially measured by ultrasound in 25 women who con­ceived and in 25 who failed to become pregnant [32]. A signicant 34% increase in the mean diameter of broids was found in early preg­nancy, compared to a 2% increase in those who failed to conceive. There was no correlation between ovarian response to stimulation and broid growth. Therefore, the growth was attrib­uted solely to pregnancy-associated factors. The observation that broids grow in diameter by approximately 30–35% during the early preg­nancy is concerning, as it is possible that an asymptomatic or seemingly “innocent” broid near the endometrium could enlarge and lead to unexpected problems during pregnancy. Approximately 70% of broids grow by a vol­ume of 10% or more between the rst and second and second and third trimesters [31]. However, there is limited evidence that treatment improves outcomes.
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Myomectomy could be justied in some cir­cumstances to reduce the risk of adverse preg­nancy outcomes [33]. Unfortunately, the benet of myomectomy for intramural broids has not been denitively proven. The most compelling evidence for intramural myomas appears to be cases with large broids, 4 cm or larger, and tumors close to the uterine cavity. It is important to clarify this issue since myomectomy for intra­mural broids has a risk of morbidity and adhe­sion formation, and surgery should not be considered unless the benets outweigh the risks.
Some studies have questioned the relationship between uterine broids and miscarriage and poor pregnancy outcomes. A study of over 500 women with uterine broids found no increase in risk of miscarriage after adjusting for confound­ing factors (adjusted hazard ratio = 0.83, 95% condence interval: 0.63, 1.08) [34]. Furthermore, a meta-analysis that utilized ve studies that included 1394 women with broids and 20,435 without found no increase in risk of spontaneous abortion (risk ratio 0.83, 95% CI 0.68–0.98) [35]. No characteristic of broids was associated with risk in these studies.
Despite the contradictory literature, myoma size, location, and number are key factors when considering treatments such as myomectomy. However, size, location, and number are not sep­arable for an individual patient, and the provider must weigh the cumulative impact of all three factors when deciding if how and when to treat an infertile woman with uterine broids.
Diagnosis ofUterine Fibroids
A focused history and physical examination may provide suspicion of uterine broids. Symptoms related to broids may include menorrhagia, dys­menorrhea, menstrual clotting, intermenstrual bleeding, pelvic pain, pressure, progressive con­stipation or alternating constipation and diarrhea, abdominal distention, or urinary frequency. However, other conditions can cause any of these symptoms, and broids are often asymptomatic. On examination, the uterus is often enlarged and irregular with uterine broids due to the distor-
tion from the individual masses. A rectovaginal examination may be helpful to identify posterior broids. However, other conditions, such as ade­nomyosis, can cause uterine enlargement, and a clinically signicant broid may be present, even if the examination is normal. Diagnostic testing with ultrasound is appropriate for any women with infertility and is considered an important component of the infertility evaluation.

Ultrasound

Transvaginal ultrasound provides better image quality than abdominal ultrasound, but both meth­ods might be necessary if the uterus is markedly enlarged with uterine broids. Since overlying bowel may limit the visualization of the uterus, abdominal ultrasound is performed with the blad­der full enough to provide a “window” for the uterus. Vaginal ultrasound studies are performed with an empty bladder for patient comfort.
Careful examination of the endometrium and myometrium is needed to assess anatomic abnor­malities. A submucous myoma is easily identi­ed when the endometrium has a preovulatory “triple stripe” pattern. If there is no endometrial distortion, or deection of trilaminar endome­trium, a submucous broid is unlikely. In the early follicular phase and after ovulation, when the endometrium is more homogeneous, endo­metrial distortion is more difcult to assess, and saline infusion sonohysterography should be per­formed if a submucous broid is suspected [33].
Uterine broids have several variations in ultrasound appearance, depending on the charac­teristics of the mass. For example, a calcied myoma has a bright echogenic pattern and distor­tion or “artifact” beyond the mass (see Fig.9.7). Although calcied broids are easily identied, distortion that occurs beyond the mass may “hide” the endometrium or other broids. Uterine broids are sometimes visible as “hypoecho­genic” oval masses in the myometrium. Less often, a broid may have the same echogenic pat­tern as the surrounding myometrium and be iden­tied by nding a deection of the endometrial or the serosal surface of the uterus. Subtle or uncer-