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10 Uterine Rupture andPerforation
vulva, vagina, uterus (nonpregnant), uterus (pregnant), fallopian tube, and ovary. J Trauma. 1995;39:
1069–70.
361. Williams JK, McClain L, Rosemurgy AS, Colorado
NM. Evaluation of blunt abdominal trauma in the
third trimester of pregnancy: maternal and fetal considerations. Obstet Gynecol. 1990;75(1):33–7.
362. Onwudiegwu U, Okonofua FE, Omole-Ohonsi
A. Rupture of the gravid uterus following a
road trafc accident. Int J Gynecol Obstet.
1990;33(3):273–4.
363. Danso D, Dimitry ES. Perforated 26 weeks
pregnant uterus at appendicectomy. BJOG.
2004;111(6):628–9.
364. Friedman PS, Ramin KD, Berry C, et al.
Pneumoamnion and pregnancy loss after secondtrimester laparoscopic surgery. Obstet Gynecol.
2002;99:512–3.
365. Joumblat N, Grubbs B, Chmait RH.Incidental fetoscopy during laparoscopy in pregnancy: management
of perforation of the gravid uterus. Surg Laparosc
Endosc Percutan Tech. 2012;22(2):e76.
366. Post RJ, Friedrich E, Amaya KE, Chmait
RH. Inadvertent perforation of a gravid uterus
during laparoscopy. J Soc Laparoendosc Surg.
2019;23(3):e2019.00026.
367. Friedman JD, Ramsey PS, Ramin KD, Berry
C.Pneumoamnion and pregnancy loss after secondtrimester laparoscopic surgery. Obstet Gynecol.
2002;99(3):512–3.
368. Reedy MB, Galan HL, Richards WE, Preece CK,
Wetter PA, Kuehl TJ. Laparoscopy during pregnancy. A survey of laparoendoscopic surgeons. J
Reprod Med. 1997;42(1):33–8.
369. Barnett DT. Complication of laparoscopy during
early pregnancy. BMJ. 1974;1:328.
370. Graves CE, Harrison MR, Padilla BE.Minimally
invasive fetal surgery. Clin Perinatol.
2017;44:729–51.
371. Yamamoto M, El Murr L, Robyr R, Leleu F,
Takahashi Y, Ville Y.Incidence and impact of perioperative complications in 175 fetoscopy-guided
laser coagulations of chorionic plate anastomoses in
fetofetal transfusion syndrome before 26 weeks of
gestation. Am J Obstet Gynecol. 2005;193:1110–6.
372. Or K, Sheiner E, Levy A, Katz M, Mazor
M.Uterine rupture: risk factors and pregnancy outcome. Am J Obstet Gynecol. 2003;189(4):1042–6.
Torsion oftheGravid Uterus
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Abstract
Torsion of the gravid uterus, a frequent disorder in veterinary obstetrics, is extremely rare
in humans but is more common than torsion
of a nongravid uterus. Physiological dextrorotation is common in pregnancy. If additional risk factors for uterine torsion are
present, such as uterine anomalies, myomas,
or fetal disproportions, uterine torsion has a
higher incidence of occurrence. The clinical
presentation of uterine torsion is variable and
nonspecic. Symptoms depend on the degree
of torsion, the speed at which the torsion
develops, duration of torsion, and stage of
pregnancy, labor, or puerperium. Differential
diagnosis is almost always obstetric, mostly
spontaneous uterine rupture or obstructed
labor. The diagnosis should be made promptly
for two reasons: (1) to save the fetus and (2)
to prevent ischemic uterine changes, which
could lead to uterine necrosis, indicating hysterectomy. Before irreversible uterine ischemic changes occur, early intervention
enables uterus preservation with the possibility of normal future pregnancies. Detorsion
is a method of choice. If not successful, hysterotomy with Cesarean delivery helps in
uterine detorsion.
11.1 Historical Perspective
No tumor, no torsion.
(J.Barozzi, 1907 [1])
No uterine abnormality, no torsion.
(Leyland A.Robinson and
Muriel H.Duvall, 1931 [2])
The earliest report of uterine torsion (UT) in
pregnancy was made by an Italian veterinarian,
Hippiaper Columbi, in 1662 [3] because gravid
UT is more common in animals (cattle). Almost
200years later, in 1863, Virchow reported the rst
case of the nongravid UT in a human at postmortem examination [4]. Léon Labbé (1832–1916), a
French surgeon from Paris, rst described this
abnormality with maternal survival in 1876 and
then Leopold Reinprecht in Germany in 1899 [5].
11.2 Incidence
Uterine torsion is the rotation of the uterus
on its longitudinal axis ≥45°.
Gravid UT, a frequent disorder in veterinary
obstetrics, is extremely rare in humans [6–8] but
is more common than nongravid UT.During the
© 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_11
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11 Torsion oftheGravid Uterus
long period between 1876 and 1992, there were
212 cases [9]. Between 1996 and 2006, Wilson
etal. found another 38 cases [10]. Between 2006
and 2020, 41 gravid UT have been reported [11].
Therefore, 300 cases have been published in the
last 150years.
Most UT is detected in the third trimester [10,
11]. The earliest reported period for UT during
pregnancy is in the sixth gestational week; the
latest is in the 43rd week. Most UTs diagnosed at
term are during the rst stage of labor. Only six
cases of puerperal UT exist [12–14].
11.3 Etiopathogenesis
In its normal state, the uterus has little mobility
and is rmly held by the broad and uterosacral
ligaments. These widely distributed supports
resist any tendency to UT.The uterus becomes an
abdominal organ during pregnancy with exaggerated congenital and physiological rotations and
obliquities of the normal uterus. During pregnancy, a relatively small increase in the length of
the broad ligaments causes the uterus to curve
around the attachment point. This anatomical
arrangement permits increased uterine mobility
in late gestation with a predisposition to UT.An
additional factor is an elongated cervix with
structural weakness and angulation in the isthmic
region leading to UT. The structural weakness
may be developmental or acquired [15].
Physiological dextrorotation occurs commonly in pregnancy with a normal orientation of
the myometrium bers. Approximately 80%
include dextrorotation, while levorotation is present in 20% [16]. A degree of more than 30° is
considered pathological during pregnancy, but it
is insufcient to obstruct the normal uterus’
blood supply [17]. Further rotation will give rise
to symptoms depending on the degree of UT, the
stage of pregnancy, and the speed at which the
UT develops [18].
In most cases, the degree of torsion is 180°
[16]. Since 1985, only 46 cases during pregnancy
were published, and none with a rotation of
≥270° [19]. However, there were cases with the
rotation of 540° [20, 21] and even 720° [22],
which results rst in venous engorgement
(Fig.11.1), and then, when arterial blood supply
is arrested, in uterine necrosis [16, 24].
11.3.1 General Population
The presence of a uterine tumor was believed to
be the main etiological factor in the development
of UT, and in 1907, Barozzi made the statement
“no tumor, no torsion” [1]. Leyland A.Robinson
and Muriel H. Duvall, in 1931, modied that
statement to “no uterine abnormality, no torsion,”
and they presented the hypothesis that uterine
rotation in the absence of gross disease was due
to a developmental asymmetry of the myometrium [2]. Uterine anomalies occur in 0.1–0.5%
of all women [25, 26]. The most common are
symmetric or duplication anomalies, including
didelphic, bicornuate, and septate uteri.
Bicornuate and septate uteri occur more frequently than didelphic uteri. In malformed uteri,
the discrepancy in uterine vascularity and the
Fig. 11.1 Untwisted 180° levorotated gravid uterus with
venous engorgement. (Reproduced with permission from
[23])
11.3 Etiopathogenesis
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development of one-sided muscular and brous
attachments cause the pregnant horn to develop a
high degree of mobility. Even abdominal trauma
during pregnancy can be the cause [27]. For
example, a large, heavy broid of the subperitoneal type attached near the fundus of the uterus
and well above the pelvic brim may rotate and
exert traction on the uterus. It has inertia and a
wide eld of movement, and the more spherical
its shape, the more easily it can rotate. Sessile
leiomyoma increases the risk of UT [28].
However, as early as 1935, Reis and Chaloupka
found UT unassociated with any uterine abnormalities during normal pregnancy and within a
typical pelvis [19, 29]. In approximately 20%, no
causative factor is apparent [28], although a common feature in many cases has been a previous
cesarean section (CS). MRI studies proved that
defective isthmic healing after lower uterine segment CS might result in suboptimal restoration of
normal cervical length [27, 30]. This may result
in an elongated cervix with structural weakness
and angulation in the isthmic region and may predispose to UT.Sometimes intrinsic pelvic pathology is the cause.
11.3.2 Pregnancy
The common risk factors reported in association
with UT are often nonspecic. Changes due to
pregnancy play an important role, but the phenomenon is more common in nulliparous women,
while maternal age and parity seem to play no
part in UT [9, 31]. In 1931, intrinsic intrapelvic
pathology was responsible for 66% of UT during
pregnancy [2], and a kyphotic pelvis was an
occasional cause of gravid UT [32]. According to
Piot et al., 31.8% had uterine myomas, 14.9%
had uterine anomalies, especially the bicornuate
uterus, 8.4% had pelvic adhesions, 7% had ovarian cysts, 4.6% had an abnormal presentation and
fetal anomalies, 2.8% had abnormalities of spine
and pelvis, and no discoverable causes in the rest
of the cases were found [16]. Since 2006, 10%
were twin pregnancies [33].
With sudden falls, sudden pushes from other
people, and bumpy movements during transpor-
tation, the fetus in the advanced pregnant uterus
may respond with violent movements exposing
the unstable pregnant uterus to torsion.
Contractions of the abdominal muscles or the
degree of lling of the bladder and distension of
the intestines could contribute. Possibly excessively lax abdominal wall muscles allow UT to
occur [34, 35]. A reduced amount of amniotic
uid decreases the distance between a fetus and
the uterine wall. The fetus feels abrupt movements of the dam as a painful stimulus and, in
response, performs strong reexive movements
that may cause the rotation of the uterus. A
reduced amount of amniotic uid also decreases
the size of the uterus, allowing free intraabdominal uterine movements. The twisting of
the uterus puts pressure on the middle uterine
vein, which results in disturbances in the venous
circulation and increases the CO2 tension in fetal
blood. As a result, the fetus makes vigorous
movements, which aggravates the condition and
causes the uterus to be turned to a higher degree.
This presses upon the middle uterine artery and
decreases the O2 going to the fetus. If the case is
neglected, the fetus dies and may undergo maceration or mummication.
UT can lead to occlusion of the blood circulation of the uterus and appendages, and placental
ischemic injury can lead to decidual necrosis
with vascular rupture and bleeding, followed by
preterm labor and separation of the decidua and
placenta [36]. Furthermore, severe acute UT can
lead to placental abruption [37] and intrauterine
fetal death [38].
The point of UT usually occurs at the level of
the uterine isthmus [28], with three possible consequences (Fig.11.2): (1) Rotation of the uterus
may cause narrowing to complete obstruction of
the birth canal. The fetus is unable to enter the
cervix, stopping stage 2 of labor; (2) vascular
compromise renders the uterine wall congested
and fragile (Fig. 11.1); and (3) the diagnostic
delay results in the delivery of a dead fetus since
hypoxia can result from placental separation, due
to venous congestion, even with intact membranes [39].
UT in the third trimester of pregnancy correlates with an abnormal fetal position, older
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Fig. 11.2 Posterior view of the uterus. (A) Fibroid situated
upon the fundus of the uterus; (B) left broad ligament
(wrapped around the body of the uterus); (C) right broad ligament; (D) rectum. (Reproduced with permission from [28])
maternal age, uterine ligament relaxation [40], or
prepregnancy (partial) resection of broad ligaments due to endometriosis [41]. UT with a
bicornuate uterus occurs between 21 and
33weeks of gestation [38, 42–44]. This may be
due to unilateral muscular attachments providing
decreased stability and increased mobility, which
puts the uterus at increased risk of UT [42].
Decreased uterine rotational stability can result
in UT in subsequent pregnancies [41].
The causative factors in pregnancy are listed
in Table11.1.
11 Torsion oftheGravid Uterus
Table 11.1 Causes of gravid uterus torsion [27, 28, 35,
38, 41, 45]
Uterine myomas
Uterine anomalies, especially the bicornuate uterus
Congenital weakness at the junction of the cervix and
uterus
Previous cesarean section(s)
Pelvic adhesions
Abnormal pelvic architecture
Ovarian neoplasms
Abnormal fetal presentation or anomalies
Abnormalities of the spine or pelvis
Abdominal trauma
Sudden maternal movements
Peristaltic movements of the sigmoid colon
Bowel distension
Excessive abdominal wall muscle contraction
External cephalic version
Hydramnios
Multiple gestations
Hyperactive fetus
Interstitial pregnancy
Resection of ligaments stabilizing uterus
No discoverable cause
11.4 Clinical Presentation
11.4.1 Pregnancy
11.4.1.1 Medical History
The clinical presentation of UT is variable and
nonspecic. Symptoms depend on the [18]
following:
11.3.3 Puerperium
The risk factors for UT during the puerperium
include xation of the uterus by adhesions, ovarian tumor, uterine myomas, large neoplasms, and
uterine Müllerian anomalies. MRI evaluation following low transverse CS suggested that, occasionally, poor healing of the hysterotomy scar
may result in suboptimal restoration of normal
cervical length and strength, predisposing to UT
[30]. Sometimes, the association of two or more
factors determines UT—for example, uterus
didelphys and iatrogenic adhesion between one
of the uteri and the pelvic wall [14].
• Degree of torsion,
• Speed at which the torsion develops,
• Duration of torsion,
• Stage of pregnancy, labor, or puerperium.
Therefore, the disease may be asymptomatic,
acute, subacute, chronic, or intermittent. The
severity of the disease ranges from asymptomatic
to mild abdominal pain and cramping to shock
and maternal death.
Asymptomatic cases (11%) [45] are mostly
found during elective CS for other maternal [39]
or fetal indications [46, 47], commonly fetal distress [19, 48, 49].
11.4 Clinical Presentation
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Asymptomatic UT is ≤180° [9, 46, 47].
The gradual type is usually 90–200° and often
presents as obstructed labor [11]. The acute or
fulminating type is usually ≥180°. The main clinical features are pain in the lower abdomen,
shock (maternal pallor, tachycardia [11], breathlessness, and sweating [50]), intestinal and urinary symptoms, obstructed labor, and secondary
vaginal bleeding due to placental abruption. In
cases when clinical features exacerbate progressively, patients present with an acute abdomen.
When gravid UT arrests the uterine circulation, it
leads to acute maternal symptoms and threatens
fetal survival. Thus, it is usually associated with
placental abruption [51]. Other obstetric diagnoses can confound the examination, such as abnormal fetal heart rate [27, 49, 51–55] and failure to
Table 11.2 Most common symptoms of gravid uterine
torsion
% of
Symptoms at
presentation n=28
Abdominal pain 23 82.1 56.1
Vaginal bleeding 3 10.7 7.3
Nausea/vomiting 4 14.3 9.8
Decreased fetal
movement
Fetal distress 11 39.3 26.8
Hemodynamic
instability/syncope
Uterine size greater
than dates or rapidly
enlarging uterus
Labor obstruction
Reproduced with permission from [11]
a
Both cases with labor obstruction had no other symp-
toms upon presentation
a
symptomatic
cases
4 14.3 9.8
12 42.9 29.3
3 10.7 7.3
2 n/a 4.9
% of
total
cases
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progress in labor [53, 54, 56, 57]. Urinary symptoms include urgency, frequency, nocturia, oliguria, and hematuria. Pyrexia can result from red
broid degeneration as a leading point of UT [12,
13]. UT presenting in labor [17] may manifest by
the failure of cervical dilation despite strong uterine contractions or fetal distress due to a reduction in uterine blood ow. The symptoms are
listed in Table 11.2, while symptoms related to
the degree of UT are listed in Table11.3.
11.4.1.2 Physical Examination
Examination reveals an abnormal pendulous
shape of the abdomen [35]. The round ligament
is palpably stretched across the maternal abdomen. Uterine hypertonia can be present with
uterine tenderness on palpation. On pelvic
examination, the uterine artery is perceived as
pulsating anteriorly. A vaginal examination
may reveal vaginal bleeding, uterine tenderness, spiral twisting of the vaginal or cervical
canal with a high cervical position, stenosis of
the vagina, uterine artery pulsating anteriorly,
and urethral displacement [15, 58, 59]. The dorsal commissure of the vulva may be pulled forward and to the left or right (twisting of the
vulva).
The transverse fetal lie is common with UT
[35, 49, 60, 61].
Rectal examination reveals that the broad ligament on one side is pulled strongly downward
and under the twisted uterine body and cervix.
The opposite broad ligament is pulled tightly
Table 11.3 Symptoms (%) related to the degree of gravid uterine torsion
Degree of torsion Pain Shock Intestinal Urinary Bleeding Obstructed laboraOther symptoms No symptoms
<90° 65 6 15 8 9 11 20 14
90°–180° 75 18 14 8 11 16 29 11
>180°–360° 100 43 50 0 7 21 21 0
>360° 100 100 0 33 17 100 0 0
Unknown 100 50 0 0 0 0 0 0
Reproduced with permission from [9]
a
Although obstructed labor was not mentioned in any of the cases with torsion of >180°, it could nevertheless be a fac-
tor in all such cases
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11 Torsion oftheGravid Uterus
across the uterine body and cervix. John Grønkjær
Jensen described four pathognomonic clinical
ndings of UT [9]:
• Round ligament palpably stretching
across the abdomen,
• Uterine artery pulsating anteriorly on
vaginal examination,
• Twisting of the vagina or the cervical
canal with the urethra displaced
laterally,
• Twisting of the rectum.
In addition to the clinical presentation,
unsuccessful labor induction should raise the
suspicion of UT. The failure of the uterus to
respond to oxytocics is due to ischemia of the
myometrium [42].
11.4.2 Puerperium
The clinical presentation of puerperal UT is nonspecic and may differ from UT during pregnancy. The most common symptom is abdominal
pain varying from mild abdominal tenderness to
symptoms of an acute abdomen, making diagnosis difcult. In the puerperium, a signicant
decrease in postpartum discharge (lochia) and a
sudden complete stop of vaginal bleeding and
discharge several days after delivery are highly
suggestive of puerperal UT [14].
11.5 Dierential Diagnosis
Due to the rarity, the nonspecic clinical presentation with variable severity makes correct preoperative diagnosis challenging. The differential
diagnoses are presented in Table11.4.
Table 11.4 Differential diagnosis of gravid uterine torsion [6, 16, 62]
Ectopic pregnancy
Acute hydramnios
Obstructed labor
Placental abruption
Abdominal hemorrhage
Torsion of a pelvic tumor
Peritonitis
Concealed accidental hemorrhage
Tonic uterine contraction
Degenerating bromyomata
Uterine retroversion or incarceration
Uterine inversion
11.6 Diagnosis
The preoperative diagnosis of UT is challenging,
and the diagnosis is primarily intraoperative. Up
to 1948, there was no instance of this condition
being diagnosed preoperatively [63]. A severe
UT can cause irreversible ischemic injury, thrombotic accidents, and fetal wastage. Hence, it is
crucial to diagnose this condition quickly. In
women who are known to have uterine anomalies
that have acute severe abdominal pain in pregnancy, the possibility of UT should be considered. When fetal distress without a known cause
is present, asymptomatic UT should be excluded
[19, 48].
11.6.1 Laboratory Findings
There is no specic laboratory test for
UT.Leukocytosis is present, especially if UT is
complicated, such as uterine rupture [38]. Low
hemoglobin levels are present with associated
bleeding, as with placental abruption or uterine
rupture. The severity of maternal shock is mostly
greater than expected for the initial hemoglobin
level [64]. Maternal serum alpha-fetoprotein
(MSAFP) screening was originally used to detect
11.6 Diagnosis
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aneuploidy and fetal malformations such as neural tube and abdominal wall defects. Also,
MSAFP elevation in the second trimester is associated with an increased risk of pregnancy complications and adverse obstetrical outcomes,
including pre-eclampsia, preterm labor, intrauterine growth restriction, intrauterine fetal demise
[65], and even UT [38]. A proposed explanation
for this nding in the context of a structurally
normal fetus includes fetal–placental insufciency [66].
11.6.2 Plain Abdominal X-Ray
On plain abdominal radiographs, gas in the uterine cavity has been described as a feature of UT
in a nongravid patient [67]. Possibly, it can be
applied to the gravid uterus, but no images exist
in the literature.
11.6.3 Abdominal Ultrasound
Ultrasound (US) is not specic for UT in pregnancy. Comparison with previous US scans can
reveal broids that have changed position, implying a torsion of a myomatous uterus [67]. Also, a
change in placental position [31, 61, 68] or
abnormal position of ovarian or uterine vessels
across the uterus on the Doppler examination
[68] may be signs of UT.The hyperechoic area
behind the placenta suggests placental abruption,
and UT was never a working diagnosis [37, 38,
56, 69]. No US images of gravid UT exist in the
literature.
11.6.4 Abdominal CT
On an abdominal CT, gas in the uterine cavity is
a feature of UT in a nongravid patient [67]. It can
be applied to the gravid uterus, but no images
exist. This diagnostic imaging is rarely performed
because the indication for exploration or CS is
based on the emergent clinical ndings of maternal acute abdomen, shock, or fetal distress.
11.6.5 Abdominal MRI
Emergent MRI provides an accurate evaluation
when the equipment and personnel are available. Nicholson et al., in 1995, detected the
rst case of UT in pregnancy by MRI [70]. The
wall of the upper vagina changes from a normal H conguration to an X-shaped conguration in UT (Figs.11.3 and 11.4), but the plane
should be at the level of the vagina on abdominal MRI [71].
Fig. 11.3 Schematic
representation of uterine
torsion at the level of the
upper vagina.
(Reproduced with
permission from [70])
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11 Torsion oftheGravid Uterus
a
Fig. 11.4 Transverse section MRI of the vagina (v), ure-
thra (u), and anal canal (a). (a) Distorted anatomy in uterine torsion (X-shaped conguration). (b) Normal
anatomic position at the level of the inferior vagina
11.7 Treatment
UT in pregnancy is an absolute indication of
emergent operation due to several goals:
• Prevent or stop uterine ischemia,
• Prevent or stop the adnexal ischemia,
• Prevent placental abruption due to venous sta-
sis and ischemia,
• Prevent or stop fetal hypoxia/anoxia.
In animals, non-surgical methods are (1) rotation of fetus and uterus when hands may pass
through the twisted portion (for lesser degree torsion), (2) very fast rolling, and (3) rolling using
plank (Schaffer’s method).
If the diagnosis is known or suspected preoperatively, the patient could be offered simultaneous tubal ligation [34]. These situations include
when no further pregnancies are planned or to
eliminate the risk of similar complications in
subsequent pregnancies.
11.7.1 Operative Treatment
11.7.1.1 Uterine Detorsion
The only therapy for a successful maternal and
fetal outcome is laparotomy, CS, and UT correction (Figs. 11.5, 11.6, 11.7, and 11.8). During
exploration, the anterior aspect of the uterus has
b
(H-shaped conguration). The lower vagina is xed at the
introitus, so the normal H-shaped conguration is maintained. (Reproduced with permission from [70])
abnormal implantation of the uterine adnexa,
which is morphologically identical to the normal
posterior aspect of the uterus implicating UT
[74]. Adnexa is commonly congested [75] or
could even be ischemic/necrotic [75, 76]. With
UT, the uterovesical fold cannot be identied [59,
77], dilated veins on the lower uterine segment
(Fig.11.1), and excessively stretched round ligament that crosses the midline are present. The
routine practice of palpating the round ligament
at the time of CS would most likely prevent inadvertent hysterotomy at sites other than the anterior lower segment [43]. With previous delivery
by CS, bladder adherence to the lower aspect of
the posterior surface of the uterus (torsion of
180°) would suggest that the UT could have
taken place in the previous pregnancy just after
CS [39]. With uterus didelphys, the torsion of one
horn is easier to detect (Fig.11.7). The vitality of
the uterus is checked after detorsion. Detorsed
parts (horn, one side of uterus didelphys) atonic
after intraoperative uterotonics should be resected
[43].
After detorsion, or even prophylactically after
CS in patients with risk factors for UT, the uterus
xation in the usual anatomic position is questionable. Bilateral plication of the uterosacral
ligaments prevents immediate postpartum recurrence of UT [69, 71]. This may help keep the
uterus in its natural position and reduce the effect
of iatrogenic uterine adhesion. It may provide
11.7 Treatment
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309
a
Fig. 11.5 (a) posterior wall uterus with vital left adnexa turned to right; (b) detorsed uterus with myoma after suturing.
(Reproduced with permission from [72] under the CC Attribution License)
b
important to note the position of round ligaments
anteriorly before hysterotomy. If UT is not identied, the incision would be given inadvertently
in the lateral wall of the uterus, leading to hematoma formation. Both vertical and transverse posterior uterine incisions are indicated depending
on the circumstances.
The posterior vertical Cesarean hysterotomy
is recommended when the lower segment of a
twisted uterus is inaccessible due to dense
adhesions or covered with engorged venous vessels [9]. Sometimes, the low transverse incision
Fig. 11.6 Gangrenous ovaries due to venous stasis
caused by 360° torsion of a 17-week pregnant uterus with
myoma. After detorsion, ovaries became vital.
(Reproduced with permission from [73])
cannot be made due to a narrow and twisted
lower uterine segment, and a vertical incision is
the only option [34, 64]. It also minimized the
risk of ureteral injury. In these cases, a classical
posterior hysterotomy should carry the least risk
resistance to UT and prevent long-term recurrence [78]. The third option is the bilateral plication of the uterosacral and round ligaments [9].
With UT recognized at term and successful manual detorsion, CS with standard anterior
Cesarean hysterotomy is recommended.
of injury to vascular structures of the broad
ligament.
On the other hand, the risk of rupture, blood
loss, and operating time of a posterior trans-
verse cesarean hysterotomy are theoretically
less than a posterior vertical incision [35]. The
data on the long-term consequences of posterior
11.7.1.2 Hysterotomy
Sometimes the detorsion is initially impossible,
especially near the term. Then, the hysterotomy
in the form of CS allows detorsion after delivery
of the viable or nonviable fetus [35, 43]. It is
uterine incisions, particularly on the outcome of
subsequent pregnancies, do not exist [35, 79,
80]. The anatomical landmarks should be
dened before the uterine incision to prevent
accidental injury to blood vessels or other
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