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11 Torsion oftheGravid Uterus
a
Fig. 11.7 Vital post-Cesarean section uterus didelphys: (a) before detorsion, and (b) after detorsion. (Reproduced with permission from [14] under the CC Attribution License)
b
double layer of delayed-absorbable suture (polyglycolic acid suture 2-0).
Uterotonics are given to estimate the vital-
ity of the uterus [82]. A hysterectomy is
recommended if the uterus is atonic and
nonviable, with the potential of necrosis or
subsequent bleeding [64, 82].
Fig. 11.8 Exteriorized uterus after untwisting, posterior side. Opening of the right broad ligament and section of the branches of the right uterine artery (rhombus). Posterior transversal hysterorrhaphy (rectangle). Myoma below hysterorrhaphy (ellipse). (Reproduced with permis­sion from [47])
organs. After delivery, manual correction is easy. Any predisposing factors such as adhe­sions, broids, or ovarian cysts should be removed to prevent a postpartum recurrence. After deliberate posterior transverse cesarean hysterotomy, the round ligament plication may prevent recurrent UT in the immediate puerpe­rium [71, 81]. Incorporating into routine prac­tice the palpation of round ligaments at the time of CS would most likely prevent inadvertent hysterotomy at sites other than the anterior lower segment [10]. The uterine incision is closed in a standard fashion (Fig.11.8) with a
Some administer uterotonics for intrauterine fetal death before hysterotomy to minimize bleeding [82], while others give uterotonics after hysterotomy and the extraction of the dead fetus [64].
11.7.1.3 Hysterectomy
Hysterectomy is indicated if [83, 84]:
• The uterus is not viable,
• Women past the reproductive age,
• Women do not desire more pregnancies,
• Unsuccessful uterotonics during the third stage of labor.
It is, however, challenging to determine whether the ischemic injury affecting the uterus is reversible, especially because puerperal UT is rare [14]. When low hemoglobin is encountered, and the fetus is dead, bilateral uterine artery liga­tion before proceeding with conventional CS after untwisting the uterus reduces intraoperative
11.8 Prognosis
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blood loss [85]. The ischemic single-sided uterus of twisted uterus didelphys bicollis mandates one-side subtotal hysterectomy (commonly with ipsilateral adnexectomy due to gangrenous changes) to preserve fertility [58, 77].
11.7.2 Obstetric Management
Obstetric decisions depend on gestational age. Beyond 34weeks, CS is the procedure of choice. At an earlier stage (before 23–24weeks), the caus­ative factor should be corrected if possible, and the pregnancy is allowed to continue to term. In the interval between the limit of fetal viability at 23–24weeks’ gestation and the 34th week or the rare instance when imaging accurately establishes the preoperative diagnosis and signs and symp­toms are not compelling, the best management is unclear. After successful uterine derotation into the anatomic position, the gynecologist must bal­ance the unknown risk of maternal or fetal compli­cations if the delivery is not accomplished against the immediate risk of substantial prematurity.
11.8 Prognosis
11.8.1 Maternal Outcome
11.8.1.1 Morbidity andMortality
During the 1970s, the maternal mortality rate associated with gravid UT was 13%, and when UT was accompanied by malpresentation, the mortality rose to 20%. Mortality is directly related to the duration of gestation and the degree of UT. Under 5 months, it was 0%, whereas at term, it reached 18.5% [9, 32, 52]. In 1951, it was
7.4% in UT of 90–180° and increased to 50% when it was 180–360° [9, 76]. Until 1960, for UT >180, maternal mortality was 44% [9]. Between 1960 and 1976, only one mother died [9]. The two last cases of maternal mortality were in 2005 (the delay in UT treatment) [68] and 2020 (pro­longed hemorrhagic shock) [86]. Since 2006, the maternal outcome in twin pregnancies is not increased [33]. Table11.5 shows maternal mor- tality from 1876 to 2020.
Table 11.5 Maternal mortality with gravid uterine tor­sion (1876–2020) [9–11, 33]
Year 1876–
1899 1900– 1929 1930– 1959 1960– 1990 1966– 2006 2006– 2020
Recovery (%)
57 29 14 0
83 17 0 13
89 11 0 16
98 1 1 1
97.4 2.6 0 No data
97.5 2.5 0 7.3
Fatal (%)
Unknown (%)
Torsion >180° (%)
Pulmonary embolism has been described after uterine detorsion [51, 56].
11.8.1.2 Future Pregnancy
The women with UT treated without hysterectomy have normal fertility and can have normal future pregnancies. There are no evidence-based recom­mendations for women who have had a UT and wish for future pregnancies. The risk of uterine rup­ture with a prior posterior lower segment incision versus the risk following an anterior lower segment incision remains unknown. Recommendations fol­lowing vertical posterior hysterotomy for future pregnancies are similar to anterior classic CS [47,
48]. Theoretically, a repeated CS is safer because it
avoids the possibility of a labor-associated uterine rupture [10] or repeated UTs. Between 1966 and 2006, 2/36 cases had described subsequent preg­nancies. Both had successful CS [10].
11.8.2 Fetal Outcome
Perinatal mortality increases with the following:
• Higher UT degree,
• Longer UT duration,
• Uterine malformations,
• Increasing gestational age until midgestation,
• Earlier decades during the twentieth century.
Until 1956, it was 24% when the uterus was rotated 90–180° and reached 75% with torsion
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11 Torsion oftheGravid Uterus
of >180° [45]. Then, until 1992 it was 20% for UT ≤90°, 71% for 90–180°, 71% for 180–360°, and 83% for >360° [9]. It declined from 37.5% from 1876 to 1911 to 24.1% from 1941 to 1956 [45]. The fetal mortality rate of 18% in (English language reports) cases from 1966 to 2006 [10] was higher than 12% reported (in a variety of countries) from 1876 to 1992 [9]. Since 2006, perinatal mortality has been 22% [11]. Gestational age has also been found to impact perinatal outcomes. Perinatal mortality was 19% before the fth month, 50% in the fth to sixth, 35% in the seventh to eighth, and 19% at term [9, 45]. UT associated with uterine mal­formations (bicornuate uterus, uterus didel­phys, etc.) is also associated with other adverse pregnancy outcomes like preterm labor, IUGR, a spontaneous uterine rupture, and obstructed labor due to the rudimentary horn [43, 64]. Since 2006, only two cases have been reported on IUGR [33]. It can be underreported, or the incidence is low due to the acuity of the condi­tion without enough time for IUGR to develop. Since 2006, twin pregnancies have not increased fetal mortality [33].
There are no data about fetal morbidity. During UT, blood supply is decreased to the uterus. Initially, obstruction of venous blood ow raises the pressure in the placental cotyledons, leading to fetal distress and abruption. If arterial blood ow is compromised, fetal demise may ensue [72]. Therefore, increased fetal morbidity is expected. There are cases of clubfeet deformity [80].
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30. Kawakami K, Sagoh T, et al. Uterine deformity caused by surgery during pregnancy. J Comput Assist Tomogr. 1994;18:272–4.
31. Kremer P, etal. Torsion of the pregnant uterus with a change in placental localization on ultrasound; a case report. Eur J Obstet Gynecol Reprod Biol. 1989;31:273–5.
32. Rabbiner B. Torsion of the pregnant uterus in patients with kyphotic pelvis. Am J Obstet Gynecol. 1935;30:136.
33. Ferrari F, Ferrari FA, Negri B, Forte S, Franceschetti L, Sartori E, et al. Uterine torsion and intrauterine growth restriction: case report and systematic literature review. J Obstet Gynaecol Res. 2021;47(12):4224–31.
34. Oláh K.Classical caesarean section through the pos­terior uterine wall- a complication of complete uter­ine torsion. J Obstet Gynaecol. 1996;16:32–3.
35. Rudloff LA, etal. Irreducible uterine torsion at cae­sarean section: how to deliver? J Obstet Gynaecol. 2003;23:76–7.
36. Tian N, Fan L. Diagnosis and treatment of pla­cental abruption. Chin J Pract Gynecol Obstet. 2016;32:1167–71.
37. Ulu İ, Güneş MS, Kiran G, Gülşen MS.A rare cause of placental abruption: uterine torsion. J Clin Diagn Res. 2016;10(1):QD06–7.
38. Lahood J, You W. Uterine torsion and subsequent rupture in a gravid bicornuate uterus associated with an elevated alpha-fetoprotein. BMJ Case Rep. 2018;2018:bcr2018224388.
39. Rasquinha SB, Rasquinha VC, Aithal V, etal. A twist in the tale– rare case of uterine torsion. Int J Biomed Res. 2012;3:435–6.
40. Huang MM, Zhang J, Yao L. Uterine torsion with placental abruption in late pregnancy: a case report and literature review. Chin J Pract Gynecol Obstet. 2017;33:991–2.
41. Berger A, Ritter M, Fessler S.Uterine torsion in preg­nancy. Arch Gynecol Obstet. 2020;302(4):791–2.
42. Oláh K. Uterine torsion and ischaemia of one horn of a bicornute uterus: a rare cause of failed second trimester termination of pregnancy. Br J Obstet Gynaecol. 2002;109:585–6.
43. Chundawat R, Rastogi R, Tak A.Torsion of gravid horn of bicornuate uterus: a rare case report. Int J Reprod Contracept Obstet Gynecol. 2016;5:2428–30.
44. Jain M, Tripathi R, Jain S, Verma A, Bajpai N. Spontaneous rupture of bicornuate uterus caused by levorotation due to congenital band. Nepal J Obstet Gynaecol. 2013;8:57–9.
45. Nesbitt GW, et al. Torsion of the human pregnant uterus. Obstet Gynecol Surv. 1956;11:311–32.
46. Farhadifar F, Nikkhoo B, Shahgheibi S, Soozadeh N, Rezaie M.Asymptomatic uterine torsion in a pregnant woman. Indian J Surg. 2014;76(4):321–2.
47. Carrier M, Korb D, Morin C, Sibony O.Asymptomatic uterine torsion diagnosed after two unevent­ful pregnancies. J Gynecol Obstet Hum Reprod. 2018;47(10):583–5.
48. Homam S, Alizadeh M, et al. Asymptomatic tor­sion of a gravid uterus. Taiwan J Obstet Gynecol. 2013;52:599–601.
49. Nielsen T. Torsion of the pregnant human uterus without symptoms. Am J Obstet Gynecol. 1981;141: 838–9.
50. Tripathi Y, et al. 180 degrees torsion of the term gravid uterus –a case report on this rare obstetric emergency. J Evol Med Dent Sci. 2013;2:4055–7.
51. Biswas P, Schultis SA, et al. Torsion of the gravid uterus. A report of two cases. J Reprod Med. 1990;35:194–7.
52. Koh CR, etal. Torsion of the pregnant uterus. Can Med Assoc J. 1977;117:501.
53. Smith C. Pathologic uterine torsion: a catastrophic event in late pregnancy. Am J Obstet Gynecol. 1975;123:32–3.
54. Visser MV, Heyns A, Marais C, etal. Torsion of the gravid uterus. Case reports. Br J Obstet Gynaecol. 1993;90:87–9.
55. Bakos O, et al. Pathologic torsion of the pregnant uterus. Acta Obstet Gynecol Scand. 1987;66:85–6.
56. Cook SM, et al. Pathologic uterine torsion associ­ated with placental abruption, maternal shock, and intrauterine fetal demise. Am J Obstet Gynecol. 2005;192:2082–3.
57. El-Taher IY, et al. Unexpected torsion of the gravid uterus. J Obstet Gynaecol. 2004;24:177.
58. Parmar DC, Kadikar GK, Kalathiya BG, Bajaj P.Torsion of pregnant uterus in case of uterus didel­phys bicollis. Int J Res Med. 2016;5:137–9.
59. Yin FL, Huang HX, Zhang M, Xia XK, Xu H, Liu T, etal. Clinical analysis of uterine torsion and broids in full-term pregnancy: a case report and review of the literature. J Int Med Res. 2020;48:1–7.
60. Greening RP, et al. Torsion of the pregnant uterus. Report of a case. Obstet Gynecol. 1963;21:421–2.
61. Zullino S, Paganelli AM, Ferrazzi E, et al. A case of abruptio placentae due to the torsion of gravid uterus. Case Rep Obstet Gynecol. 2014;2014:
801616.
62. Evans J, Masson GM, etal. Incarceration of the retro­verted gravid uterus at term. Case report. Br J Obstet Gynaecol. 1986;93:883–5.
63. Siegler KM, etal. Torsion of a pregnant uterus with rupture. Am J Obstet Gynecol. 1948;55:1053–7.
64. Rathod AT. Torsion of gravid uterus due to uterine asymmetry associated with placental abruption, intra­uterine fetal demise, and maternal shock. Int J Infertil Fetal Med. 2014;5:64–5.
65. Androutsopoulos G, Gkogkos P, Papadopoulos V, Adonakis G, Tsapanos V, Vassilakos P, et al. Mid-trimester maternal serum markers in predict­ing adverse pregnancy outcome. Clin Exp Obstet Gynecol. 2009;36:237–40.
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66. Dugoff L.First-and second-trimester maternal serum markers for aneuploidy and adverse obstetric out­comes. Obstet Gynecol. 2010;115:1052–61.
67. Davies J.Case report: torsion of a nongravid nonmyo­matous uterus. Clin Radiol. 1998;53:780–2.
68. Guié R, Nguessan E, etal. Uterine torsion with mater­nal death: our experience and literature review. Clin Exp Obstet Gynecol. 2005;32:245–6.
69. Fatih FF, Gowri V, Rao K.Uterine torsion in second trimester of pregnancy followed by a successful-term pregnancy. BMJ Case Rep. 2012;2012:1–3.
70. Nicholson CC, McCoy MC, Semelka RC, et al. Pelvic magnetic resonance imaging in the evaluation of uterine torsion. Obstet Gynecol. 1995;85(5 Pt 2): 888–90.
71. Pelosi MA 3rd, Pelosi MA.Managing extreme uter­ine torsion at term. A case report J Reprod Med. 1998;43(2):153–7.
72. Deshpande G, Kaul R. A case of torsion of gravid uterus caused by leiomyoma. Case Rep Obstet Gynecol. 2011;2011:206418.
73. Sachan R, Patel ML, Sachan P, Arora A. Complete axial torsion of pregnant uterus with leiomyoma. BMJ Case Rep. 2014;2014:bcr2014205558.
74. Dragosloveanu T, Moisa M, Vladareanu S, et al. Torsion of term gravid uterus in a pregnancy obtained by intrauterine insemination. A case report. Ginecoeu. 2014;10:136–8.
75. Bissa U, Shyam KR.Complete axial torsion of gravid uterus by 720°. J Dent Med Sci. 2013;7:12–5.
76. Wrubel NN, Greenberg MW, Beilly JS. Interstitial pregnancy with torsion of uterus and spontaneous amputation of adnexa and round ligament. N Y State J Med. 1951;51(21):2533–4.
77. Suseela TL, Jyothi SJ, Rabbani P, Jhonsi C.Axial rota­tion of gravid uterus in uterus didelphys bicollis- a rare case report. Eur J Pharm Med Res. 2016;3:417–8.
78. Mustafa F, Sporrong B, et al. Extreme torsion of the pregnant uterus. Aust N Z J Obstet Gynaecol. 1999;39:360–3.
79. Aviram O, Fejgin M, et al. Posterior wall caesar­ean section following chronic uterine torsion. Int J Gynaecol Obstet. 1995;51:59–60.
80. Picone A, Doumerc S, Frydman R, etal. Caesarean delivery by posterior hysterotomy due to torsion of the pregnant uterus. Obstet Gynaecol. 2006;107(2 Pt
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81. Albayrak A, Ozdemir I, et al. Deliberate posterior low transverse incision at cesarean section of a gravid uterus in 180 degrees of torsion: a case report. J Reprod Med. 2011;56:181–3.
82. Inderjeet P, Ramona P, Neha S. Torsion of gravid uterus managed by obstetric hysterectomy with the fetus in situ. Indian J Appl Res. 2015;5:520–1.
83. Acharya PC, etal. Acute axial torsion of gravid uterus by 360 degrees– a rare case report and an unpredict­able complication of pregnancy. J Dent Med Sci. 2013;3:4–6.
84. Qureshi U, Bansal B, Singh N, etal. Torsion of the preterm gravid uterus: a case report. Int J Case Rep Imag. 2013;4:392–5.
85. Gowri D.Torsion of gravid uterus: alternate manage­ment options. J Obstet Gynaecol India. 2015;65:68.
86. Darido J, Grevoul Fesquet J, Diari J, El Haddad C, Bouzid N, Abou El Hassan N, et al. Hemorrhagic shock due to irreducible uterine torsion in a third tri­mester twin pregnancy: a case report. Clin J Obstet Gynecol. 2020;3(2):085–9.
Symptomatic Uterine Myoma
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Abstract
Uterine broids (leiomyomas or myomas) are the most common benign uterine neoplasms, especially over the age of 30. Myomas are increasing found in pregnancy because many women delay childbearing. Uterine myoma can be asymptomatic or symptomatic. Presentations include red degeneration, spon­taneous bleeding, obstructed labor, broid tor­sion, and gravid uterine torsion. It is essential to dene the type of uterine myoma presenta­tion. All presentations can be dened by trans­abdominal or transvaginal sonography. Abdominal MRI is used in unequivocal cases. Bleeding myomas are treated with radiologic or surgical interventions. Red degeneration is treated conservatively based on analgesia. Torsion of the gravid uterus should be detorsed immediately to minimize fetal hypoxia and death. The potential of obstructed labor is a complex issue that should be diagnosed before the labor starts to prevent emergency obstetric interventions.
12.1 Denition andClassication
Uterine broids (UF), also known as leiomyoma or myoma, is the most common uterine neo­plasm, especially over the age of 30. These benign monoclonal tumors of smooth muscle
origin have varying amounts of brous connec­tive tissue [1]. UF usually arise in the myome­trium and occasionally in the cervix, broad ligament, or ovaries [1, 2]. UF are multiple in up to 84% [3], with prevalence increasing with age, from 40–60% at 35years to 70–80% at 50years old. The highest prevalence is in black women, who also often have the more severe disease [4, 5]. UF usually decrease in size after meno­pause. Early age at menarche and obesity are risk factors for developing UF, likely due to increased exposure to estrogen [6].
UF are classied according to their location as submucosal, intramural, or subserosal [1]. Submucosal broids are the least common, accounting for 5% of UF [7], but are most likely symptomatic since they project into the endome­trial cavity. Submucosal broids can become pedunculated and prolapse into the cervical canal or vagina [8]. Intramural broids are the most common but usually asymptomatic; however, they may cause infertility due to compression of the fallopian tubes. Subserosal broids project exophytically into the abdomen or pelvis and can become pedunculated and confused with ovarian tumors.
Large UF often degenerate as they outgrow their blood supply. Dead UF cells are often replaced by collagen. This type of degeneration is called hyaline degeneration. Degeneration in UF may be hyaline (the most common), myxoma­tous, cystic, fatty, hemorrhagic, or malignant
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 G. Augustin, Acute Abdomen During Pregnancy, https://doi.org/10.1007/978-3-031-26021-6_12
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316
100
Leiomyoma prevalence (%)
or
older
Age (years)
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12 Symptomatic Uterine Myoma
[7, 9, 10]. The type of degenerative change depends on the degree and rapidity of the onset of vascular insufciency. Calcication tends to occur following necrosis [10].
Although most UF are benign, some uterine leiomyosarcomas arise in a subset of UF [11]. Only 0.23–0.7% of benign UF turn out to be leio­myosarcomas on pathologic examination [12,
13]. Most leiomyosarcomas arise de novo. A
leiomyosarcoma can be difcult to distinguish from a benign UF, particularly during rapid UF growth.
12.2 Incidence
Edema and softening may result from changes dur-
ing pregnancy.
(Adolf Ludwig Sigismund Gusselow, 1885)
The mean maternal age is higher among women with UF than in the general obstetric pop­ulation [14]. In Canada, for all births, the average age of mothers at childbirth has been over 30 since 2010 (30.8years in 2016). The average age of mothers at rst birth was 28.7years in 2012 and 29.2years in 2016. It has been rising steadily since the mid-1960s [15]. This resulted in an increased UF occurrence in pregnancy [3, 16]. In contrast, others claim the decreasing incidence of submucosal UF during pregnancy, especially in
larger sizes, because of their removal before pregnancy [14]. UF affect 0.1–12.3% of pregnant women [14, 17–20]. The prevalence differs with ethnicity (Fig.12.1) (18% in African–American women, 8% in white women, and 10% in Hispanic women) [21]. In older women undergo­ing ovum donor-recipient in vitro fertilization (IVF), the incidence rises to 25% [22, 23].
The inaccuracy of different UF types or loca­tions during pregnancy is due to the lack of data. The pedunculated UF were reported in 11%, sub­serosal or intramural UF in 7.6%, and in the remaining cases, the UF type was not reported [24].
12.2.1 Red Degeneration
Enlarging UF can outgrow its blood supply and undergo degeneration (muscular infarction). Red degeneration (aseptic necrobiosis, carneous degeneration, and hemorrhagic infarction) is common during pregnancy. Even before 1913, a relationship between red degeneration of UF and pregnancy was evident [25]. In the 1920s, the estimated occurrence was 0.7% [26]. Monro Kerr and Chassar Moir found an incidence of
0.8%. Between 1930 and 1954, the incidence was approximately 0.35% [27]. The incidence of UF during pregnancy varies greatly from 0.01%
Fig. 12.1 Prevalence of uterine myomas during the rst trimester among Black and White Women. Prevalence is for 2-year intervals (18=17 and 18-year­olds; 20=19 and 20-year-olds, etc.). Patients with assisted reproduction techniques are excluded. (Reproduced with permission from [21])
Blacks
80
60
40
20
0
Whites
18 20 22 24 26 28 30 32 34 36 38 40 41
12.3 Natural History
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[19] to 1.6–2% [28]. A signicant number of patients gave a history of infertility (43%) and spontaneous abortions (25%) [19]. Having an accurate number of red degeneration cases is complex [29].
12.2.2 Spontaneous Bleeding
Spontaneous hemoperitoneum is extremely rare despite increased vascularization of the uterus during pregnancy and up to 12.3% of the preg­nant woman with UF [14, 17–20]. Carl von Rokitansky reported the rst case discovered at the autopsy of a girl who had died from internal abdominal bleeding. It is rare even in the general female population, with 125 cases published from 1902 to 2020 [30]. The numbers could be higher because Hasskarl, in 1949, collected 60 cases [31].
Ernest Lambert published the rst cases of pregnancy in 1870 and Gaillard Thomas in 1875. Adolf Ludwig Sigismund Gusselow, an editor of the journal Archives of Gynecology, in 1878, described a 27-year-old pregnant woman in a profound shock that resulted in death from bleed­ing UF.Spontaneous abortion of a 4-month dead fetus took place 40h before symptoms [32]. Until 2020, 115 cases of spontaneous bleeding from UF in the general population have been collected [30], while over 20 were during pregnancy [32–47].
12.2.3 Uterine Fibroid Torsion
The rst descriptions were by Carl von Rokitansky, Turner, and then James Cappie, who presented the fatal case at the Obstetrical Society of Edinburgh in 1874 and published it in 1875 [48]. UF torsion during pregnancy is exception­ally rare [48–53].
12.2.4 Gravid Uterus Torsion
See Chap. 11.
12.3 Natural History
Large or multiple broids exert pressure on … the uterus itself… and hence an enlargement of the blood vessel which may be further stretched and occasionally be torn. In this manner, it has been noted that a tear of a subserosal vein in a broid led to hemorrhage into the peritoneal cavity.
(Karl von Rokitansky, 1861 [54])
12.3.1 Uterine Fibroid Growth
Most ultrasound (US) studies have shown that most of the UF during pregnancy (60–78%) do not show signicant changes in their volume. UF that did increase their volume (22–32%), the growth was limited to the rst trimester [55]. UF increases 12±6% of the initial size, up to 25%. At 4weeks postpartum, the size of the UF did not differ signicantly from the size during pregnancy [55]. However, the magnitude of UF enlargement differs across studies [56, 57]. In one study, the volume of the UF more than doubled within 6–7weeks’ gestation [58]. One case showed nor­mal pregnancy without any signs of UF during ve gestational weeks. At the seventh week of pregnancy, a 3.5-cm subserosal UF was found. At the 12th week of pregnancy, the US showed a sub­serous pedunculated UF 15×10.9cm on the left edge of the uterine fundus [59].
Differently, there are contradictory data about the modications of UF during the sec­ond trimester of pregnancy. The most likely is a nonlinear trend of growth of UF. UF may undergo a progressive slowdown during the second trimester, up to stabilization and subse­quent regression. Some UF may start to reduce in size earlier (at the beginning of the second trimester) and others signicantly later (during the second half of gestation), probably concern­ing their initial size (with larger lesions starting to reduce in size earlier in comparison to smaller lesions) [56].
Similarly, discrepancies exist for UF growth during the third trimester. Some claim that UF increase in size, while others claim to decrease.
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The third option is that small UF (<4cm) enlarge or do not change, while UF >4cm decrease in size [56].
Infarction of UF secondary to uterine involu­tion in the postpartum period facilitates this com­plete regression of small UF in puerperium [60]. This is supported by epidemiologic data that par­ity is protective against the incidence and further development of UF [4].
The remarkable growth of UF during the ini­tial pregnancy could be related to other pregnancy- related hormones rather than sex ste­roids because serum concentrations of estrogen and progesterone are higher in the second half of pregnancy [58, 61]. One hypothesis is that the “LH-hCG myomal receptors hyperstimulation” due to serum embryonic-hCG increases in early gestation [61]. Nevertheless, given the possible histological heterogeneity of UF in terms of the percentage of smooth muscle cells and collage­nous matrix, the expression of LH receptors may differ, leading to a wide range of sensitivity to hCG stimulation [58]. However, many other hor­mones, enzymes, and growth factors secreted by the maternal and fetoplacental compartments markedly increase during early pregnancy, with potential effects. Similarly, factors such as UF– placental site relationship and UF location (sub­mucosal, intramural, or subserosal) may inuence their growth trend [56].
12 Symptomatic Uterine Myoma
Fig. 12.2 Twisted subserosal pedunculated uterine broid in the 35th week of pregnancy. Excision with Cesarean section was performed. (Reproduced with per­mission from [51] under the CC BY 4.0)
severe abdominal pain. Torsion is more likely in the rst trimester [64] and after delivery [53] when a large space in the abdominal pelvic cavity permits UF twisting, although it can develop throughout pregnancy [51].
12.3.2 Acute Red Degeneration
Acute red degeneration of a UF occurs almost exclusively during pregnancy. It usually occurs between the tenth and 20th weeks, during the fastest uterine growth [19, 62]. The rst trimester is a period of the most signicant UF growth. Rapid UF growth can result in a relative decrease in perfusion, leading to ischemia and necrosis (red degeneration) and the release of prostaglan­dins, causing pain [63].
12.3.3 Uterine Fibroid Torsion
Pedunculated subserosal UF can undergo torsion and consequent infarction (Fig.12.2), resulting in
12.3.4 Spontaneous Bleeding
Spontaneous bleeding UF during the rst trimes­ter [35, 37] or a term or the immediate postpartum period is most common [33, 34, 38, 41, 43, 44], although sporadic cases are present throughout pregnancy [36, 46, 47]. The hypothesis is that involution of the uterus after delivery promoted compression of venous drainage but not arterial ow [41, 44]. Spontaneous bleeding presents as (1) free subserosal UF bleeding into the abdomi­nal cavity (Fig.12.3) or (2) intrabroid bleeding resulting in fast-growing, very large UF (Fig.12.4) commonly with underlying red degeneration [41]. Bleeding can also result from UF rupture [65, 66].
Subserosal UF are prone to free intra-
abdominal bleeding [37]. The risk factor for spon-
12.4 Clinical Presentation
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posterior wall UF are at higher risk, as trauma or delivery from direct contact with the sacral prom­ontory can result in rupture and hemoperitoneum [33]. The dual effect of increased vascularity and venous congestion with mechanical extrusion of the UF can aggravate the condition and the force of tension created on the surface of the UF.This can lead to a tear of the supercial veins [67].
12.3.5 Uterine Incarceration
See Sect. 28.1.
Fig. 12.3 A 10-week gravid uterus with pedunculated myoma. Large ruptured vein causing massive intra­abdominal bleeding. (Reproduced with permission from [35] under the CC BY 2.0)
Fig. 12.4 Rapidly growing uterine broma extirpated during puerperium. The cut surface shows a dark red area of bleeding. (Reproduced with permission from [44])
taneous intrabroid bleeding is red degeneration [44]. This could lead to blood sequestration from maternal circulation into large UF, resulting in hypovolemia without hemoperitoneum [30]. The venous drainage of large UF courses over their surface and enters the supporting myometrium at the periphery of the UF.In most cases, the bleed­ing occurs from torn, enlarged veins coursing over the surface of subserosal UF [37, 67]. A sud­den increase in venous pressure is a risk factor for venous bleeding: Uterine manipulation [33], straining at stool, lifting heavy weights, and vio­lent coitus can provoke bleeding. In pregnancy,
12.4 Clinical Presentation
12.4.1 Medical History
Most UF are small and remain asymptomatic. However, 10–40% will have symptomatic UF-related complications in pregnancy [68], with at least some discomfort. Very large UF can change the shape of the abdomen or present with lumps (Fig.12.5). More than 50% present with abdominal pain without bleeding [68]. Approximately 5–21% require hospitalization during pregnancy for pain control [69], and>25% with UF >5cm experience pelvic pain of signi­cant intensity to require narcotic analgesics [20].
The pain of UF acute red degeneration is often sudden, severe, and localized to the site of the UF, usually in the pelvic area. The severe pain often lasts for 2–4weeks. Unlike torsion of an ovarian mass, there is no direct correlation between the size of the UF and the degree of pain, but most UF associated with abdominal pain have a volume>200cm3 [70]. Vomiting and dehydration are self-limiting. A similar presenta­tion is found with UF torsion [49, 51, 64].
Bleeding presents as intra-abdominal bleed­ing, including intrabroid bleeding or vaginal bleeding. Vaginal bleeding mainly correlates with UF position and size, especially if >5 cm [20]. Intra-abdominal bleeding is the rarest pre­sentation. Depending on the bleeding severity, only falls in hematocrit and hemoglobin can be detected [35], or hypovolemic shock results from massive free intra-abdominal bleeding.
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