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Uterine rupture in pregnancy is a rare and often catastrophic complication with a high incidence of fetal and
maternal morbidity. Numerous factors are known to increase the risk of uterine rupture, but even in high-risk
subgroups, the overall incidence of uterine rupture is low. From 1976-2012, 25 peer-reviewed publications
described the incidence of uterine rupture, and these reported 2,084 cases among 2,951,297 pregnant women,
yielding an overall uterine rupture rate of 1 in 1,146 pregnancies (0.07%).
The initial signs and symptoms of uterine rupture are typically nonspecific, which makes the diagnosis difficult
and sometimes delays definitive therapy. From the time of diagnosis to delivery, generally only 10-37 minutes
are available before clinically significant fetal morbidity becomes inevitable. Fetal morbidity occurs as a result of
catastrophic hemorrhage, fetal anoxia, or both.
The premonitory signs and symptoms of uterine rupture are inconsistent, and the short time for instituting
definitive therapeutic action makes uterine rupture in pregnancy a much feared event for medical practitioners.
Definition
Uterine rupture during pregnancy is a rare event and frequently results in life-threatening maternal and fetal
compromise. It can either occur in women with (1) a native, unscarred uterus or (2) a uterus with a surgical scar
from previous surgery.
Uterine rupture occurs when a full-thickness disruption of the uterine wall that also involves the overlying
visceral peritoneum (uterine serosa) is present. By definition, it is associated with the following:
the studies were limited to a subset of 8 that provided data about the spontaneous rupture of unscarred uteri in
developed countries, the rate was 1 per 8,434 pregnancies (0.012%).
Congenital uterine anomalies, multiparity, previous uterine myomectomy, the number and type of previous
cesarean deliveries, fetal macrosomia, labor induction, uterine instrumentation, and uterine trauma all increase
the risk of uterine rupture, whereas previous successful vaginal delivery and a prolonged interpregnancy
interval after a previous cesarean delivery may confer relative protection. In contrast to the availability of
models to predict the success of a vaginal delivery after a TOLAC, accurate models to predict the personspecific risk of uterine rupture in individual cases are not available.
The major patient characteristics for determining the risk of uterine rupture are noted below.
Uterine status is either native (unscarred) or scarred. Scarred status may include previous cesarean delivery,
including the following:
Grand multiparity
Maternal age
Placentation (accreta, percreta, increta, previa, abruption)
Cornual (or angular) pregnancy
Uterine overdistension (multiple gestation, polyhydramnios)
Dystocia (fetal macrosomia, contracted pelvis)
Gestation longer than 40 weeks
Trophoblastic invasion of the myometrium ( hydatidiform mole, choriocarcinoma)
Previous pregnancy and delivery history may include the following:
Not in labor
Spontaneous labor
Induced labor - with oxytocin, with prostaglandins
Augmentation of labor with oxytocin
Duration of labor
Obstructed labor
Obstetric management considerations include the following:
Fundal pressure
Uterine trauma includes the following:
Based on this type of limited information, the increased risk of uterine rupture attributable to the use of oxytocin
in gravidas with unscarred uteri is uncertain. However, women who have had a cesarean delivery appear to
have an increased risk of uterine rupture associated with the use of oxytocin, both when it is used for labor
augmentation and labor induction (see Table 1).
Dubuisson et al reported 100 patients who underwent laparoscopic myomectomy and found 3 uterine ruptures
during subsequent pregnancies.[18] Only 1 rupture occurred at the site of the previous myomectomy scar,
resulting in the conclusion that the risk of pregnancy-related uterine rupture attributable to laparoscopic
myomectomy is 1% (95% CI, 0-5.5%). However, the rarity of spontaneous uterine rupture raises the issue of
whether the 2 uterine ruptures at sites that were not coincident with previous myomectomy scars were
attributable to the previous myomectomies. If so, a markedly higher 3% uterine rupture rate is associated with
previous laparoscopic myomectomy.
Different authors reported no pregnancy-related uterine ruptures in 4 studies of 320 pregnancies in women who
previously underwent laparoscopic myomectomy.[19, 20, 21, 22] However, in all 4 studies, the number of patients who
were allowed to labor was low, and a high percentage of deliveries were by scheduled cesarean delivery (80%,
79%, 75%, and 65%, respectively).
In a prospective study from Japan, there were no uterine ruptures among 59 patients with a successful vaginal
delivery after a prior laparoscopic myomectomy.[23] In a multicenter study in Italy with 386 patients who achieved
pregnancy after laparoscopic myomectomy, there was 1 recorded spontaneous uterine rupture at 33 weeks'
gestation (rupture rate 0.26%).[24]
Uterine rupture has been reported to occur as late as 8 years after laparoscopic myomectomy.[25] This find
Landon et al reported a 1.9% absolute uterine rupture rate (2 of 105 cases) in women with a previous classic,
inverted T, or J incision who either presented in advanced labor or refused repeat cesarean delivery.[32] These
rates of frank uterine rupture in women with classic cesarean deliveries are in contrast to the higher rates of 49% that the American College of Obstetricians and Gynecologists (ACOG) had historically reported for women
with these types of uterine scars. However, Chauhan et al observed a 9% rate of asymptomatic uterine scar
dehiscence (95% CI, 5-15%).[30] This result suggests that disruptions of uterine scars might have been
misclassified as true ruptures instead of dehiscences in previous studies; this error may explain the bulk of the
discrepancy.
The risk of uterine rupture after a low transverse cesarean delivery varies depending on whether patients
undergo a TOLAC or an elective repeat cesarean delivery and on whether labor is induced or spontaneous, as
well as other factors. The vast majority of cesarean deliveries in the United States are of the low transverse
type. For women who have had 1 previous cesarean delivery, examining the various risk factors for uterine
rupture is instructive. These absolute risks for uterine rupture are discussed below, as well as in Table 1.
1.06-14.52) was noted. The attributable risk of uterine rupture associated with oxytocin use was 2.9% and 3.6%
for the maximum oxytocin dose ranges of more than 20 mU/min and more than 30 mU/min, respectively.
The authors did not find a significant risk association between time (in terms of both duration of oxytocin
exposure and duration of labor) and uterine rupture risk.They suggest an upper limit of 20 mU/min of oxytocin
for use in VBAC trials and a judicious approach to the use and monitoring of oxytocin for both labor
augmentation and induction.
The benefit of intrauterine pressure catheter (IUPC) monitoring of uterine contractions in VBAC trials is unclear,
with only a single small case series failing to detect differences in fetal or maternal morbidity/mortality
associated with uterine rupture when an IUPC was used instead of external tocodynamometry. Nevertheless,
many institutions have found the IUPC useful in allowing careful titration of oxytocin dosing, especially when
maternal habitus poses a limit to the accurate external monitoring of uterine contractions in women undergoing
a TOLAC.
Use of prostaglandins for cervical ripening and induction of labor after previous cesarean delivery
Current ACOG guidelines discourage the use of prostaglandins to induce labor in most women with a previous
cesarean delivery. This recommendation is based on considerable evidence for an increased risk of uterine
rupture associated with prostaglandins. Lydon-Rochelle et al reported a 15.6-fold increased risk for uterine
rupture (95% CI, 8.1-30) when prostaglandins were used in gravidas who underwent a TOLAC. In 366 women
with scars from a previous cesarean delivery who underwent labor induction with prostaglandins, the uterine
rupture rate was 2.45% compared with 0.77% without prostaglandin use. [41]
Taylor et al identified 3 uterine ruptures among 58 patients with 1 previous cesarean delivery who received
prostaglandin E2 (PGE2) alone for labor induction. The uterine rupture rate was 5.2% (3 of 58) compared with
1.1% (8 of 732) among patients not treated with prostaglandin.[50] Ravasia et al found that 3 ruptures occurred
among 172 patients who underwent labor induction with PGE2 alone (1.7%), which was significantly higher than
0.45% (7 of 1,544) women who labored spontaneously.[42]
In contrast, Flamm et al found a uterine rupture rate of 1.3% (6 of 453) in patients with a previous cesarean
delivery who were treated with PGE2 in combination with oxytocin. This result was not significantly different
from the rate of 0.7% (33 of 4,569) in women who were not treated with PGE 2.[51] In a small study, Delaney and
Young also did not find a significant difference in uterine rupture rates between patients with scars from a
previous cesarean delivery who underwent labor induction with PGE 2 and patients with previous cesarean
scars who labored spontaneously (1.1 vs 0.3%; P =.15).[52]
Landon et al reported no uterine ruptures among 227 patients who underwent induction with prostaglandins
alone. Although the study was underpowered to detect small differences, the particular type of prostaglandin
administered did not appear to significantly affect the uterine rupture rate (52 patients received misoprostol;
111, dinoprostone; 60, PGE2 gel; and 4, combined prostaglandins).[32]
Interdelivery interval
In a case-control study by Esposito et al, an interpregnancy interval between cesarean delivery and a
subsequent pregnancy of < 6 months was nearly 4 times as common among patients who had uterine rupture
than in control subjects (17.4 vs 4.7%; OR, 3.92; 95% CI, 1.09-14.3). Among 23 patients who had uterine
rupture after a previous cesarean delivery, the mean interpregnancy interval was 20.4 15.4 months compared
with 36.5 30.4 months for control patients (P =.01).[61]Stamilio et al recently confirmed a similar uterine rupture
rate of 2.7% in women with an interdelivery interval of < 6 months compared with 0.9% for those having
interdelivery intervals of 6 months (adjusted OR 2.66, 95% CI, 1.21-5.82). [62]
Shipp et al similarly found that the risk of symptomatic uterine rupture was increased 3-fold in women with
interdelivery intervals of< 18 months when they underwent a TOLAC after 1 previous cesarean delivery (OR,
3.0; 95% CI, 1.2-7.2).[63] The authors controlled for maternal age, public assistance, length of labor, gestational
age of 41 weeks, and induction of augmentation of labor with oxytocin.
In additional support of this observation, a Canadian study by Bujold et al reported on 1,527 women who
underwent a TOL after a single previous low-transverse cesarean delivery, finding that 2.8% of patients who
had an interdelivery interval of 24 months had a uterine rupture compared with 0.9% for those with an
interdelivery interval of >24 months (P < .01).[64] After adjusting for confounding variables, the odds ratio for a
uterine rupture during a subsequent TOLAC was 2.65 for women who had an interdelivery interval of 24
months compared with women who had a longer interdelivery interval (95% CI, 1.08-5.46).
In a follow-up study, the same authors examined the risk of uterine rupture between 18-24 months. After
adjustment for confounding factors, they found that an interdelivery interval shorter than 18 months was
associated with a significant increase of uterine rupture (odds ratio [OR], 3; 95% confidence interval [CI], 1.3
7.2), whereas an interdelivery interval of 18-24 months was not (OR, 1.1; 95% CI, 0.43.2). In agreement with
the findings by Shipp et al, the study by Bujold et al concludes that an interdelivery interval shorter than 18
months but not between 18-24 months should be considered as a risk factor for uterine rupture. [65]
The authors speculated that a prolonged interpregnancy interval may allow time for the previous cesarean
delivery scar to reach its maximal tensile strength before the scar undergoes the mechanical stress and strain
with a subsequent intrauterine pregnancy. Interestingly, the authors also observed that the combination of a
short interdelivery interval of 24 months and a single-layer hysterotomy closure was associated with a uterine
rupture rate of 5.6%. This is comparable to the rate of uterine rupture for patients undergoing a TOLAC with a
previous classic midline cesarean scar.
For women with a history of 2 or more cesarean deliveries, 10 studies published from 1993-2010 showed that
the risk of uterine rupture in a subsequent pregnancy ranged from 0.9-6.0% (1 per 17-108 pregnancies). This
risk is increased 2- to 16-fold compared to women with only a single previous cesarean delivery. In a study of
17,322 women with scars from cesarean delivery, Miller et al found that, when women underwent a TOLAC,
uterine rupture was 3 times more common with 2 or more scars (1.7%) than with 1 scar (0.6%) [OR, 3.06; 95%
CI, 1.95-4.79; P < .001].[70]
In the largest analysis to date, Macones et al reviewed data from 17 tertiary and community hospitals and
found that, in 1,082 women with 2 uterine scars who underwent a TOLAC, the risk of uterine rupture was
increased 2-fold compared with women with only 1 uterine scar (absolute rupture risk 1.8% vs 0.9%; adjusted
OR, 2.3; 95% CI, 1.37-3.85).[71]
In the only study to control for potential confounding variables, Caughey et al concluded that in women who
had 2 previous cesarean deliveries who then attempted vaginal birth, the risk of uterine rupture was almost 5
times the risk of those with only 1 previous cesarean delivery (3.7% vs 0.8%; P =.001). The study controlled for
several key covariates, including the use of prostaglandin E2 gel, oxytocin induction, oxytocin augmentation,
length of labor, and epidural use. They also found that women with a previous vaginal delivery were about one
fourth as likely to have a uterine rupture as women without a previous vaginal delivery (OR, 0.26; 95% CI, 0.080.88).[54]
In contrast, Landon et al reported through the MFMU Network that there was no significant difference in the
uterine rupture rate for women with multiple prior cesarean deliveries versus 1 prior cesarean delivery (0.9% vs
0.7%; P= 0.37).[72]However, in this study there was a much lower TOLAC rate of 9% for women with multiple
prior cesarean deliveries compared with the 27% rate in the report of Macones et al [71] and the 73% rate in
Millers study.[70] This indicates that there were much more stringent inclusion/exclusion criteria applied by
Landon et al, and that this difference may account for the apparent discrepancy in outcomes. Caughey et al did
not report the TOLAC rate in their 12-year data analysis. [54]
A recent meta-analysis of 17 studies including 5,666 patients undergoing a TOL after 2 or more cesarean
deliveries demonstrated a 1.36% uterine rupture rate. [73]This is similar to the result of our pooled data analysis
from 10 studies published from 1993-2010, which shows a 1.81% uterine rupture rate for patients with multiple
previous cesarean delivery scars.
A 2004 ACOG guideline suggested that in women with 2 previous cesarean deliveries, only those with a
previous vaginal delivery should be considered candidates for a TOLAC. [74] This ACOG recommendation was
subsequently revised in an updated 2010 guideline to suggest that women with two previous low transverse
cesarean deliveries may be considered candidates for TOLAC regardless of their prior vaginal delivery status. [28]
Maternal age
Shipp et al showed that advancing maternal age is associated with an increased rate of uterine rupture. In a
multiple logistic regression analysis designed to control for confounding factors, the overall rate of uterine
rupture among 3,015 women with 1 previous cesarean delivery was 1.1%. The rate of uterine rupture in women
older than 30 years (1.4%) versus younger women (0.5%) differed significantly (OR, 3.2; 95% CI, 1.2-8.4). [75]
Multiple gestation
Most large series of VBAC with twin gestations report similar rates of uterine rupture for twin and singleton
gestations. In an analysis of the largest database of inpatient hospitalizations available in the United States
from 1993-2002, Ford et al studied 1,850 women with twin gestations attempting VBAC and found similar
uterine rupture rates compared with singleton gestations (0.9% vs 0.8%). [76]
Similarly, Cahill et al compared 535 twin pregnancies with 24,307 singleton pregnancies and reported a
comparable uterine rupture rate of 1.1% for twin vs 0.9% for singleton pregnancies (OR, 1.2; 95% CI, 0.3-4.6)
in women with at least 1 previous cesarean delivery undergoing TOLAC. [77] Additionally, they found that patients
with twins were less likely to attempt a TOLAC (OR, 0.3; 95% CI 0.2-.04), but no more likely to have a VBAC
failure (OR, 1.1; 95% CI, 0.8-1.6), or major maternal morbidity (OR, 1.6; 95% CI, 0.7-3.7).
Overall, women with multifetal gestations attempting VBAC did not incur any greater risk of uterine rupture than
their singleton controls. In a nested case-control study of the MFMU cesarean registry, Varner et al compared
cases of women undergoing TOLAC with one previous cesarean delivery with a multifetal pregnancy versus
controls with one previous cesarean delivery with a singleton pregnancy.[78]A similar uterine rupture rate of 0.7%
was found in both multifetal (4/556) versus singleton groups (99/13,923) [ORadj 1.19 (0.43-3.30)] . In a smaller
study, Aaronson et al reported no cases of uterine rupture among 134 twin pregnancies undergoing a TOLAC
with a single prior cesarean section.[79] The ACOG 2010 guidelines for VBAC recommend that women with one
previous cesarean delivery with a low transverse incision, who are otherwise appropriate candidates for twin
vaginal delivery, may be considered candidates for TOLAC. [28]
Fetal macrosomia
Elkousy et al found that, in 9,960 women who underwent a TOLAC after 1 previous cesarean delivery, the risk
of uterine rupture was significantly greater for fetuses that weighed more than 4000 g (2.8%) than in those
weighing less than 4000 g (1.2%; RR 2.3, P < .001). For women with 1 previous cesarean delivery and no
previous vaginal deliveries, the uterine rupture rate was 3.6% for women with a fetal weight of more than 4000
g compared to women with a fetal weight of < 4000 g (RR 2.3, P < .001).[80] More recently, Jastrow et al showed
that birth weight was directly correlated with the rate of uterine rupture, with uterine rupture rates of 0.9%,
1.8%, and 2.6% for birth weights of less than 3500 g, 3500-3999 g, and 4000 g or larger, respectively (P < .05).
[81]
Zelop et al reported that the rate of uterine rupture for women delivering neonates weighing >4000 g was 1.6%
versus 1% for newborns 4000 g, but that the difference was not statistically significant (P =0.24).[82] Flamm et al
examined TOLAC risks in a cohort of 301 women and reported no difference between the rates of uterine
rupture for women with neonates weighing 4000 gm versus < 4000 gm. [83] The ACOG 2010 VBAC guidelines
suggest that suspected fetal macrosomia alone should not preclude the possibility of TOLAC. [28]
Subcategory
Uterine Rupture
Years
No.
of Data
Collection
of
Studies
Total No.
General Category
All
Normal uterus,
previous myomectomy
Normal uterus,
previous cesarean
delivery
References
Minor
Total
Deliveries
Rate
NA
NA
2,951,297
1 per 1,426
(0.07%)
2,084
1973-2010
25
Gardeil 1994, Golan 1980, Schrinsky 1978, Mokgokong 1976, Rahman 1985, Plauche 1984,
Landon 2004, Gregory 1999, McMahon 1996, Rageth 1999, Elkousy 2003, Yap 2001, Leung
1993, Miller 1997, Kieser 2002, Bujold 2002, Ofir 2004, Flamm 1994, Menihan 1998, Zwart
2009
In industrialized
countries
NA
1,467,534
1 per 8,434
(0.013%)
174
1975-2006
Gardeil 1994, Plauche 1984, Gregory 1999, Rageth 1999, Yap 2001, Miller 1997, Kieser
2002, Zwart, 2009
In developing
countries
NA
399,314
1 per 920
(0.11%)
434
1966-2006
Elective primary
cesarean delivery
NA
17,209
1 per 1,324
(0.08%)
13
1995
Gregory 1999
TOLAC
NA
452,720
1 per 4,975
(0.02%)
91
1995
Gregory 1999
27
1995
Gregory 1999
Unscarred uterus
Congenitally
anomalous uterus
in Subcategory
Major
NA
401,387
1 per 14,866
(0.01%)
NA
51,333
1 per 802
(0.12%)
64
1995
Gregory 1999
Previous low
transverse cesarean
delivery
NA
190
1 per 95
(1.1%)
1992-2002
NA
NA
1,001
1 per 143
(.70%)
1930-2006
10
Brown, 1956, Garnet 1964, Dubuisson 2000, Seinera 2000, Nezhat 1999, Seracchioli 2000,
Seracchioli 2006, Kumakiri 2008, Sizzi 2007, Makino 2008
Trans-abdominal
myomectomy
NA
179
1 per 60
(1.7%)
1930-1960
1989-2006
Dubuisson 2000, Seinera 2000, Nezhat, 1999, Seracchioli 2000, Seracchioli 2006, Kumakiri
2008, Sizzi 2007, Makino 2008
Laparoscopic
myomectomy
NA
822
1 per
206(0.49%)
NA
NA
172,397
1 per 236
(0.42%)
732
1983-2002
13
Gardeil 1994, Landon 2004, Lydon-Rochelle 2001, Blanchette 2001, Grobman 2007, Rageth
1999, Miller 1994, Yap 2001, Leung 1993, Kieser 2002, Flamm 1994, Cowan 1994, Lin 2004
Elective repeat
cesarean delivery
NA
90,360
1 per 623
(0.16%)
145
1982-2002
10
Gardeil 1994, Mozurkewich 2000, Landon 2004, Lydon-Rochelle 2001, Blanchette 2001,
Gregory 1999, McMahon 1996, Rageth 1999, Kieser 2002, Lin 2004
NA
168,609
1 per 174
(0.58%)
970
1982-2002
22
Gardeil 1994, Mozurkewich 2000, Hibbard 2001, Landon 2004, Lydon-Rochelle 2001,
Ravasia 2000, Zelop 1999, Blanchette 2001, Taylor 2002, Grobman 2007, Gregory 1999,
McMahon 1996, Rageth 1999, Leung 1993, Kieser 2002, Flamm 1994, Menihan 1998,
Phelan 1987, Asakura 1995, Lieberman 2001, Locatelli 2006
History of previous
successful VBAC *
71,470
1 per 581
(0.17%)
123
1976-2002
Landon 2004, Blanchette 2001, Mercer 2008, Gregory 1999, McMahon 1996, Rageth 1999,
Yap 2001, Leung 1993, Asakura 1995
No history of previous
successful VBAC
20,191
1 per 125
(0.80%)
161
1983-2002
356
1983-2002
Landon 2004, Blanchette 2001, Gregory 1999, McMahon 1996, Rageth 1999
TOLAC
1 per
25,922
Spontaneous TOLAC
29,263
1 per 225
(0.44%)
130
1979-2002
Landon 2004, Lydon-Rochelle 2001, Ravasia 2000, Zelop 1999, Blanchette 2001, Delaney
2003, Lin 2004, Locatelli 2006, Molloy 1987
Augmented TOLAC
(oxytocin)
15,666
1 per 144
(0.70%)
109
1979-2002
Landon 2004, Zelop 1999, Blanchette 2001, Rageth 1999, Molloy 1987, Flamm 1990
3,658
1 per 125
(0.80%)
54
1983-2002
Landon 2004, Zelop 1999, Blanchette 2001, Taylor 2002, Lin 2004
6,768
1 per 125
(0.80%)
54
1983-2002
Rageth 1999, Landon 2004, Lydon-Rochelle 2001, Raasia 2000, Bujold 2004
29
1984-2002
12
Landon 2004, Lydon-Rochelle 2001, Ravasia 2000, Zelop 1999, Blanchette 2001, Taylor,
2002, Delaney 2003, Lin, 2004, Locatelli 2006, Choy-Hee 2001, Plaut 1999, Wing 1998
16
1984-2000
Ravasia 2000, Zelop 1999, Banchette 2001, Taylor 2002, Flamm 1997
73 (1.4%)
Induced
TOLAC (oxytocin)
1 per
Induced TOLAC
(prosta-glandin)
Combined
prostaglandin-oxytocin
induction
1,817
924
63 (1.6%)
1 per
58 (1.7%)
NA
NA
134,556
1 per 196
(0.51%)
686
1975-2000
13
Plauche 1984, Lydon-Rochelle 2001, Zelop 1999, Delaney 2003, McMahon 1996, Rageth
1999, Miller 1994, Macones 2005, Elkousy 2003, Leung 1993, Kieser 2002, Bujold 2002,
Asakura 1995
Before labor
NA
6,980
1 per 635
(0.16%)
11
1987-1996
Lydon-Rochelle 2001
28,698
1 per 173
(0.58%)
166
1984-2002
Lydon-Rochelle 2001, Zelop 1999, Delaney 2003, Grobman 2007, Bujold 2002, Lin 2004
NA
7,757
1 per 92
(1.1%)
84
1984-2002
Lydon-Rochelle 2001, Zelop 1999, Delaney 2003, Grobman 2007, Lin 2004, Locatelli 2006
Successful vaginal
delivery
1,110
1 per 1,110
(0.09%)
1987-1991
Asakura 1995
1980-2002
29
1984-2002
137
1984-2002
Ravasia 2000, Zelop 2000, Kayani 2005, Grobman 2007, Hendler 2004
With labor
NA
Labor induction
Classic
midline cesarean
delivery
Successful previous
vaginal delivery
1 per
NA
428
NA
7,070
86 (1.2%)
1 per 244
(0.41%)
1 per
93 (1.1%)
No previous vaginal
delivery
NA
12,805
Successful previous
VBAC
NA
526
1 per 526
(0.19%)
1988-2002
NA
29,501
1 per 142
(0.68%)
208
1984-2002
Landon 2004, Shipp 1999, Zelop 1999, Delaney 2003, Bujold 2002, Menihan 1998
With labor
22,855
1 per 143
(0.70%)
160
1988-2002
Zelop 1999, Delaney 2003, Grobman 2007, Bujold 2002, Locatelli 2006, Yogev 2004
Spontaneous TOLAC
13,381
1 per 188
(0.53%)
71
1992-2002
35
1992-2000
1992-2002
40
1988-2004
18
1988-2001
Low
transverse cesarean
delivery
1 per
Induced TOLAC
(oxytocin)
3,224
Induced TOLAC
(prostaglandin)
724
92 (1.09%)
1 per 241
(0.41%)
1 per
TOLAC with
interdelivery interval
24 months
1,516
38 (2.6%)
1 per
43 (2.3%)
776
2,819
1 per 117
(0.85%)
24
1988-2001
2,216
1 per
44
1984-2004
Fetal macrosomia
4000 g
44
(2.3%)
Unknown uterine
scar
3,289
1 per 137
(0.73%)
24
1985-2007
Miller 1996, Myles 2001, Sansregret 2003, Varner 2005, Cahill 2005, Ford 2006, Varner
2007, Aaronson 2010
Multiple gestation
Without TOLAC
(ERCD)
5,229
1 per 1,1046
(0,10%)
1985-2007
Miller 1996, Sansregret 2003, Varner 2005, Ford 2006, Aaronson 2010
Fetal macrosomia
4000 g
2,216
1 per 44
(2.3%)
44
1984-2004
Flamm 1989
Gestation beyond 40
weeks
6,746
1 per 77
(1.3%)
88
1984-2002
Induced labor
578
1 per 34
(2.9%)
17
1984-2002
Spontaneous labor
1,488
1 per 78
(1.3%)
19
1984-2002
3,698
1 per 218
(0.5%)
17
1999-2002
15
1981-2002
Landon 2004, Naef 1995, Adair 1996, Martin 1997, Shipp 1999, Zelop 1999
1981-1997
116
1983-2002
10
Blanchette 2001, Zelop 2000, Caughey 1999, Miller 1994, Macones 2005, Landon
2006,Leung 1993, Cowan 1994, Asakura 1995, Cahill 2010
1996-2002
Lin 2004
1996-2002
Lin 2004
1996-2002
Lin 2004
NA
1 per
NA
1,355
With labor
933
90 (1.1%)
Low vertical
cesarean delivery
1 per 104
(0.96%)
1 per
NA
NA
6,279
Spontaneous TOL
NA
523
54 (1.85%)
1 per 131
(0.76%)
1 per
Normal uterus,
multiple previous
cesarean deliveries
Induced TOL
(oxytocin)
NA
54
54 (1.8%)
1 per
Induced TOL
(prosta-glandin)
NA
19
19 (5.3%)
NA=Not applicable
Table 2. Conditions Associated With Uterine Rupture (Open Table in a new window)
Incidence
Years
No.
of Data
Collection
of
Studies
References
in Patients
Total
Cases
Cases With
Uterine
Rupture
344
187
54
1973-2002
Prolonged deceleration in
fetal heart rate or bradycardia
143
114
80
1983-2002
Uterine tachysystole* or
hyper-stimulation
30
12
40
1994-1999
144
1973-1999
169
49
29
1983-1996
Abdominal pain
454
118
26
1931-2000
Vaginal bleeding
381
140
37
1931-2000
Shock
213
71
33
1931-1993
Condition
With Uterine
Rupture, %
Prolonged, late, or recurrent variable decelerations or fetal bradycardias are often the first and only signs of
uterine rupture. Bujold and Gauthier showed that abnormal patterns in fetal heart rate were the first
manifestations of uterine rupture in 87% of patients.[64] In a study by Leung et al, prolonged decelerations in fetal
heart rate occurred in 79% of cases and were the most common finding associated with uterine rupture.
[88]
Rodriguez et al found that fetal distress was the most common finding associated with uterine rupture,
occurring in 78%.[89] Overall, in 4 studies from 1983-2000, prolonged decelerations of fetal heart rate or
bradycardias occurred in 114 (80%) of 143 cases of uterine rupture. In cases that involved the extrusion of the
placenta and fetus into the abdominal cavity, prolonged decelerations in fetal heart rate invariably occurred. [64, 88,
90, 91]
Sudden or atypical maternal abdominal pain occurs more rarely than fetal heart rate decelerations or
bradycardia. In 9 studies from 1980-2002, abdominal pain occurred in 13-60% of cases of uterine rupture. In a
review of 10,967 patients undergoing a TOLAC, only 22% of complete uterine ruptures presented with
abdominal pain and 76% presented with signs of fetal distress diagnosed by continuous electronic fetal
monitoring.[92]
Moreover, in a study by Bujold and Gauthier, abdominal pain was the first sign of rupture in only 5% of patients
and occurred in women who developed uterine rupture without epidural analgesia but not in women who
received an epidural block.[64] Thus, abdominal pain is an unreliable and uncommon sign of uterine rupture.
Initial concerns that epidural anesthesia might mask the pain caused by uterine rupture have not been verified
and there have been no reports of epidural anesthesia delaying the diagnosis of uterine rupture. The ACOG
guideline from 2010 suggests there is no absolute contraindication to epidural anesthesia for a TOLAC
because epidurals rarely mask the signs and symptoms of uterine rupture.
Phelan et al found that abnormal patterns of uterine activity, such as tetany and hyperstimulation, are often not
associated with uterine rupture. In their study, in which monitoring of uterine activity was limited to external
tocodynamometry, tetany was defined as a contraction lasting longer than 90 seconds, and hyperstimulation
was defined as more than 5 contractions in 10 minutes.[93]Rodriguez et al found that the usefulness of
intrauterine pressure catheters (IUPCs) for diagnosing uterine rupture was not supported. In 76 cases of
uterine rupture, the classic description of decreased uterine tone and diminished uterine activity was not
observed in any patients, 39 of whom had IUPCs in place. In addition, rates of fetal and maternal morbidity and
mortality associated with uterine rupture did not differ with the use of an IUPC compared with external
tocodynamometry.[89]
In 8 reports published from 1980-2002 in which investigators examined the frequency of vaginal bleeding in
cases of uterine rupture, vaginal bleeding occurred in 11-67% of cases. In 3 studies, maternal shock from
hypovolemia was associated with uterine rupture in 29-46% of cases. [2, 5, 94]
Diagnosis
Because of the short time available to diagnose uterine rupture before the onset of irreversible physiologic
damage to the fetus, time-consuming diagnostic methods and sophisticated imaging modalities have only
limited use. Therefore, uterine rupture is most appropriately diagnosed on the basis of standard signs and
symptoms (see Table 2).
Despite this limitation, various diagnostic techniques have been used to attempt to assess the individual risk of
uterine rupture in selected patients. Amniography, radiopelvimetry, and pelvic examination have all proven
unsuitable for predicting the risk of uterine rupture in women who desire a TOLAC. In addition, imaging
modalities such as CT and MRI have not been clinically useful in diagnosing acute uterine rupture because of
the time constraints involved in establishing the diagnosis. Given this limitation, MRI is thought to be superior to
CT for evaluating the status of a uterine incision because of its increased soft tissue contrast. All studies of
these methods are limited by their retrospective design and their lack of surgical confirmation of true uterine
dehiscence.
Several reports have suggested that transabdominal, transvaginal, or sonohysterographic ultrasonography may
be useful for detecting uterine-scar defects after cesarean delivery. Rozenberg et al prospectively examined
642 women and found that the risk of uterine rupture after previous cesarean delivery was directly related to
the thickness of the lower uterine segment, as measured during transabdominal ultrasonography at 36-38
weeks of gestation. The risk of uterine rupture increased significantly when the uterine wall was thinner than
3.5 mm. Using a 3.5 mm cutoff, the authors had a sensitivity of 88%, specificity of 73.2%, positive predictive
value of 11.8%, and a negative predictive value of 99.3% in predicting subsequent uterine rupture. [95]
In a study of 722 women, Gotoh et al reported that a uterine wall thinner than 2 mm, as determined with
ultrasonography performed within 1 week of delivery, significantly increased the risk of uterine rupture. Positive
and negative predictive values were 73.9% and 100%, respectively.[96]
Incidence
Years
No.
of Data
Collection
of Studies
Reviewed
References
in Patients
Consequence
Total
Cases
Cases With
Uterine
Rupture
With Uterine
Rupture, %
Fetal or Neonatal
Hypoxia or anoxia
231
19
1983-2002
Acidosis (Umbilical
artery cord pH < 7)
252
83
33
1976-2002
349
90
26
1976-2002
Admission to neonatal
intensive care unit
164
71
43
1976-2002
Perinatal death,
industrialized countries
548
39
1975-2002
14
Perinatal death,
developing countries
524
388
74
1966-1980
286
67
23
1976-1998
Cystotomy
311
45
11
1976-1998
518
109
21
1973-2000
14
Death, industrialized
countries
313
0.32
1975-2000
11
Death, developing
countries
524
41
1966-1980
Maternal
always prevent severe metabolic acidosis and serious neonatal disease, it probably did limit the occurrence of
neonatal death.[64]
Fetal acidosis
In 99 cases of uterine rupture, Leung et al found that 43 newborns (43%) had an umbilical-artery pH level of
less than 7, and 25 of these newborns had a pH level of less than 6.8. In association with these pH levels, 39
newborns (39%) had 5-minute Apgar scores of less than 7, 12 of whom had 5-minute Apgar scores of less than
3.[88]
Menihan found that 10 of 11 fetuses (91%) who were born after uterine rupture had an umbilical-artery cord pH
level of less than 7.0, and 5 (45%) had 5-minute Apgar scores of less than 7. The most important factor for the
development of fetal acidosis was complete extrusion of the fetus and placenta into the maternal abdomen. [91]
Admission to a neonatal intensive care unit
Menihan found that 8 of 11 newborns (73%) delivered after uterine rupture required admission to the neonatal
intensive care unit (NICU).[91]
Kieser and Baskett found an NICU admission rate for newborns 45% (8 of 18) after uterine rupture. [98] Landon et
al found a similar NICU admission rate of 32% (46 of 144 newborns) after uterine rupture. [32]
Fetal or neonatal death
In studies reported before 1978, the fetal mortality rate associated with uterine rupture was high. In a review of
33 studies by Schrinsky and Benson, 960 cases of uterine rupture resulted in 620 infant deaths, yielding a
perinatal mortality rate of 65%.[3] Blanchette et al reported that 2 neonates (17%) died among 12 women who
had uterine rupture and that 1 of these neonates died after a decision-to-delivery time of only 26 minutes after
the acute onset of fetal bradycardia, lower abdominal pain, and vaginal bleeding, which signaled the acute
uterine rupture.[44]
Leung et al reported that 6 perinatal deaths (6%) occurred among 99 patients who had uterine rupture. [88] In a
study by Lydon-Rochelle et al, the perinatal death rate among fetuses in 91 cases of uterine rupture was 5.5%
compared with 0.5% in control subjects.[41] Landon et al reported a perinatal death rate from uterine rupture of
2% (2 of 124) among 19 academic centers in the United States. These studies indicate that the incidence of
perinatal death associated with uterine rupture is decreasing in the modern era. [32]
Lydon-Rochelle et al reported significant maternal bladder injuries in 8% of women (7 of 91) whose uteri
ruptured compared with 240 of 20,004 control patients (1.2%) in whom rupture did not occur (P =.001).[41] Shipp
et al found that bladder injuries occurred in 18% of women (5 of 28) who had a uterine rupture after previous
low transverse cesarean delivery.[36]
In a study by Kieser and Baskett, 17% of women (3 of 18) who developed uterine rupture had a cystotomy.
[98]
Leung et al found that 12% (12 of 99) who experienced a uterine rupture had incidental cystotomies at the
time of surgery, and 7 more (7%) had either a ruptured bladder or an accidental cystotomy; the combined total
urologic injury rate was 19%.[88]
Need for hysterectomy
In a study from South Africa, 78% of women (261 of 335) who had uterine rupture were treated with
hysterectomy.[4] Flamm et al found that 3 of 39 patients (8%) who developed uterine rupture required
hysterectomy.[100] Kieser and Baskett found that 1 of 18 patients (6%) who developed complete uterine rupture
required hysterectomy.[98] Blanchette et al reported that hysterectomy was necessary in 17% of women (2 of 12)
who developed uterine rupture.[44] Hibbard et al found that 6 hysterectomies (60%) were necessary in 10 women
who had a uterine rupture.[27]
Leung et al reported that 19% of patients (19 of 99) who experienced a uterine rupture required hysterectomy.
Thirteen hysterectomies (68%) were performed because the uterus was not deemed repairable, 4 (21%) for
irremediable uterine atony, and 1 (5%) because of placenta accreta. [88]
Maternal death
Maternal death as a consequence of uterine rupture occurs at a rate of 0-1% in modern developed nations, but
the mortality rates in developing countries are 5-10%. [4, 5]
The availability of modern medical facilities in developed nations is likely to account for this difference in
maternal outcomes. In a South African study from 1976, 22 of 260 women who had pregnancy-related rupture
of an unscarred uterus died (mortality rate 8.5%). These deaths could be further subdivided into mortality for
women with longitudinal uterine tears (15 of 183 patients [8.2%]), transverse tears (2 of 49 patients [4%]),
posterior-wall tears (2 of 16 patients [13%]), and multiple uterine tears (3 of 12 patients [25%]).
Golan et al reported no deaths among 32 mothers who experienced rupture of a scarred uterus compared with
9 deaths among 61 women with an intact uterus (15%).[2] In a study from Los Angeles in which Leung et al
reported on 99 patients with uterine ruptures, 1 woman (1%) died. [88]
Mokgokong and Marivate noted that the maternal mortality rate associated with uterine rupture largely depends
on whether the diagnosis is established before or after delivery; these rates were 4.5% and 10.4%,
respectively.[4]
Degree of hemorrhage
General condition of the mother
Mother's desire for future childbearing
Uterine bleeding is typically most profuse when the uterine tear is longitudinal rather than transverse.
Conservative surgical management involving uterine repair should be reserved for women who have the
following findings:
Prevention
The absolute risk of uterine rupture in pregnancy is low, but it is highly variable depending on the patient
subgroup (see Table 1). Women with normal, intact uteri are at the lowest risk for uterine rupture (1 in 8,434
pregnancies [0.012%]).
The most direct prevention strategy for minimizing the risk of pregnancy-related uterine rupture is to minimize
the number of patients who are at highest risk. The salient variable that must be defined in this regard is the
threshold for what is considered a tolerable risk. Although this choice is ultimately arbitrary, it should reflect the
prevailing risk tolerance of patients, physicians, and of society as a whole. If this threshold is chosen as 1 in
200 women (0.5%) (see Table 1), the categories of patients that exceed this critical value are those with the
following:
Conclusion
Uterine rupture is a rare but often catastrophic obstetric complication with an overall incidence of approximately
1 in 1,536 pregnancies (0.07%). In modern industrialized countries, the uterine rupture rate during pregnancy
for a woman with a normal, unscarred uterus is 1 in 8,434 pregnancies (0.012%).
The vast majority of uterine ruptures occur in women who have uterine scars, most of which are the result of
previous cesarean deliveries. A single cesarean scar increases the overall rupture rate to 0.5%, with the rate for
women with 2 or more cesarean scars increasing to 2%. Other subgroups of women who are at increased risk
for uterine rupture are those who have a previous single-layer hysterotomy closure, a short interpregnancy
interval after a previous cesarean delivery, a congenital uterine anomaly, a macrosomic fetus, prostaglandin
exposure, and a failed previous trial of a vaginal delivery.
Surgical intervention after uterine rupture in less than 10-37 minutes is essential to minimize the risk of
permanent perinatal injury to the fetus. However, delivery within this time cannot always prevent severe
hypoxia and metabolic acidosis in the fetus or serious neonatal consequences.
The most consistent early indicator of uterine rupture is the onset of a prolonged, persistent, and profound fetal
bradycardia. Other signs and symptoms of uterine rupture, such as abdominal pain, abnormal progress in
labor, and vaginal bleeding, are less consistent and less valuable than bradycardia in establishing the
appropriate diagnosis.
The general guideline that labor-and-delivery suites should be able to start cesarean delivery within 20-30
minutes of a diagnosis of fetal distress is of minimal utility with respect to uterine rupture. In the case of fetal or
placental extrusion through the uterine wall, irreversible fetal damage can be expected before that time;
therefore, such a recommendation is of limited value in preventing major fetal and neonatal complications.
However, action within this time may aid in preventing maternal exsanguination and maternal death, as long as
proper supportive and resuscitation methods are available before definitive surgical intervention can be
successfully initiated.