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eMedicine Specialties > Obstetrics and Gynecology >

Obstetrical Complications

Uterine Rupture in Pregnancy

Author: Gerard G Nahum, MD, FACOG, FACS, Adjunct Associate Professor of Obstetrics
and Gynecology, Uniformed Services University of the Health Sciences; Head of Global Clinical
Development, Women's Healthcare U.S., Bayer HealthCare Pharmaceuticals
Coauthor(s): Krystle Quynh Pham, MD, FACOG, Attending Faculty, Department of
Obstetrics and Gynecology, Santa Clara Valley Medical Center; Clinical Instructor, Department
of Obstetrics and Gynecology, Stanford University
Contributor Information and Disclosures

Updated: May 12, 2010

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Introduction
Uterine rupture in pregnancy is a rare and often catastrophic complication with a high incidence
of fetal and maternal morbidity. Several 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-
2009, 20 peer-reviewed publications that described the incidence of uterine rupture reported
1,864 cases among 2,863,330 pregnant women, yielding an overall uterine rupture rate of 1 in
1,536 pregnancies (0.07%).

The initial signs and symptoms of uterine rupture are typically nonspecific, which makes
diagnosis difficult and sometimes delays definitive therapy. From the time of diagnosis to
delivery, 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 inconsistent premonitory signs and the short time for instituting definitive therapeutic action
make uterine rupture a fearful event.

Definition

Uterine rupture during pregnancy is a rare occurrence that frequently results in life-threatening
maternal and fetal compromise, whereas uterine scar dehiscence is a more common event that
seldom results in major maternal or fetal complications. By definition, uterine scar dehiscence
constitutes separation of a preexisting scar that does not disrupt the overlying visceral
peritoneum (uterine serosa) and that does not significantly bleed from its edges. In addition, the
fetus, placenta, and umbilical cord must be contained within the uterine cavity, without a need
for cesarean delivery due to fetal distress.

By contrast, uterine rupture is defined as a full-thickness separation of the uterine wall and the
overlying serosa. Uterine rupture is associated with (1) clinically significant uterine bleeding; (2)
fetal distress; (3) expulsion or protrusion of the fetus, placenta, or both into the abdominal cavity;
and (4) the need for prompt cesarean delivery and uterine repair or hysterectomy.

Although a scar from cesarean delivery is a well-known risk factor for uterine rupture, most
events that involve disruption of the uterine scar result in uterine-scar dehiscence rather than
frank uterine rupture. These 2 entities must be clearly distinguished because the options for
clinical management and outcomes differ significantly.

Sources of information and study selection

The peer-reviewed literature was searched using the PubMed, Medline, and Cochrane databases
for all relevant articles published in the English language. The search terms were uterine rupture,
pregnancy and prior cesarean section, vaginal birth after cesarean, VBAC, trial of labor (TOL),
trial of labor after cesarean (TOLAC) uterine scar dehiscence, and pregnancy and myomectomy.
Standard reference tracing was also used.

Articles published from 1976-2010 that described the incidence of uterine rupture and that
included sufficient information regarding the authors' definitions of uterine rupture and of
uterine-scar dehiscence were incorporated for review. All studies were observational or reviews.
A total of 109 published articles were included for data extraction and analysis.

Incidence and risk factors

Meta-analysis of pooled data from 20 studies in the peer-reviewed medical literature published
from 1976-2009 indicated an overall incidence of pregnancy-related uterine rupture of 1 per
1,536 pregnancies (0.07%). When 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 potential success of a
TOL after a prior cesarean section, accurate models to predict the person-specific risk of uterine
rupture for individuals are not available.

Major patient characteristics for determining 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:

 Single low transverse (further subcategorized by 1-layer or 2-layer hysterectomy closure)

 Single low vertical
 Classic vertical
 Multiple previous cesarean deliveries

Scarred status may also include previous myomectomy (transabdominal or laparoscopic).

Uterine configuration may be normal or may involve a congenital uterine anomaly.

Pregnancy considerations include the following:

 Grand multiparity
 Maternal age
 Placentation (accreta, percreta, increta, previa, abruption)
 Cornual (or angular) pregnancy
 Overdistension (multiple gestation, polyhydramnios)
 Dystocia (fetal macrosomia, contracted pelvis)
 Trophoblastic invasion of the myometrium (hydatidiform mole, choriocarcinoma)

Previous pregnancy and delivery history may include the following:

 Previous successful vaginal delivery

 No previous vaginal delivery
 Interdelivery interval

Labor status is determined as follows:

 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:

 Instrumentation (forceps use)

 Intrauterine manipulation (external cephalic version, internal podalic version, breech
extraction, shoulder dystocia, manual extraction of placenta)
 Fundal pressure

Uterine trauma includes the following:

  Direct uterine trauma (motor vehicle accident, fall)
 Violence (gunshot wound, blunt blow to abdomen)

Rupture of the Unscarred Uterus

The normal, unscarred uterus is least susceptible to rupture. Grand multiparity, neglected labor,
malpresentation, breech extraction, and uterine instrumentation are all predisposing factors for
uterine rupture. A 10-year Irish study by Gardeil et al showed that the overall rate of unscarred
uterine rupture during pregnancy was 1 per 30,764 deliveries (0.0033%). No cases of uterine
rupture occurred among 21,998 primigravidas, and only 2 (0.0051%) occurred among 39,529
multigravidas with no uterine scar.1

A meta-analysis of 8 large, modern (1975-2009) studies from industrialized countries revealed

174 uterine ruptures among 1,467,534 deliveries. This finding suggested that the modern rate of
unscarred uterine rupture during pregnancy is 0.012% (1 of 8,434). This rate of spontaneous
uterine rupture has not changed appreciably over the last 40 years, and most of these events
occur at term and during labor. An 8-fold increased incidence of uterine rupture of 0.11% (1 in
920) has been noted in developing countries. This increased incidence of uterine rupture has
been attributed to a higher-than-average incidence of neglected and obstructed labor due to
inadequate access to medical care. When one assesses the risk of uterine rupture, this baseline
rate of pregnancy-related uterine rupture is a benchmark that must be used as a point of
reference.

Effect of maternal parity

Many authors have considered multiparity a risk factor for uterine rupture. Golan et al noted that,
in 19 of 61 cases (31%), uterine rupture occurred in women with a parity of more than 5.2
Schrinsky and Benson found that 7 of 22 women (32%) who had unscarred uterine rupture had a
parity of greater than 4.3 In a study by Mokgokong and Marivate, the mean parity for women
who had pregnancy-related uterine rupture was 4.4 Despite the apparent increase in the risk of
uterine rupture associated with high parity, Gardeil et al found only 2 women with uterine
rupture among 39,529 multigravidas who had no previous uterine scar (0.005%).1

Rupture of the unscarred uterus before labor versus during labor

Schrinsky and Benson reported 22 cases of uterine rupture in gravidas with unscarred uteri.
Nineteen occurred during labor (86%), and 3 occurred before labor (14%). This percentage was
markedly different from that of gravidas with a previous uterine scar, for whom the timing of
uterine rupture between labor and the antepartum period was nearly evenly distributed.3

Oxytocin augmentation and induction of labor in the unscarred uterus

Although distinguishing oxytocin use for labor induction versus labor augmentation is useful,
many researchers who have investigated the use of oxytocin and the risk of uterine rupture in
unscarred uteri unfortunately have not made this distinction.
In 1976, Mokgokong and Marivate reported 260 uterine ruptures among 182,807 deliveries that
involved unscarred uteri, and 32 of the 260 (12%) were associated with oxytocin use.4 Rahman et
al similarly found that oxytocin was administered in 9 of 65 cases (14%) that involved unscarred
uterine rupture.5 Golan et al noted that, among 126,713 deliveries, oxytocin was used in 26 of 61
cases (43%) that involved unscarred uterine rupture.2 However, Plauche et al attributed only 1 of
23 unscarred uterine ruptures (4%) to the use of oxytocin.6

Therefore, 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).

Congenital uterine anomalies

In a review article, Nahum reported that congenital uterine anomalies affected approximately 1
in 200 women.7 In such cases, the walls of the abnormal uteri tend to become abnormally thin as
pregnancies advance, and the thickness can be inconsistent over different aspects of the
myometrium.8,9,10,11

Ravasia et al reported an 8% incidence of uterine rupture (2 of 25) in women with congenitally

malformed uteri compared with 0.61% (11 of 1,788) in those with normal uteri (P =.013) who
were attempting VBAC.12 Both cases of uterine rupture involved labor induction with
prostaglandin E2. Pregnancies implanted in the rudimentary horn of the uterus pose special risk
for those women undergoing induction of labor, with a uterine rupture rate of up to 81% (387 of
475).13 Importantly, 80% of ruptures occurred before the third trimester, with 67% occurring
during the second trimester.

In contrast, a study of 165 patients with Müllerian duct anomalies who underwent spontaneous
labor after 1 prior cesarean delivery reported no cases of uterine rupture.14 Of note, in this study
36% (60 of 165) had only a minor uterine anomaly (arcuate or septate uterus), and 64% (105 of
165) had a major uterine anomaly (unicornuate, didelphys, or bicornuate uterus). Moreover, only
6% (10 of 165) of patients with Müllerian duct anomalies underwent induction of labor. The
decision of induction of labor in women with congenitally anomalous uteri and a previous
cesarean section must therefore be considered carefully given the higher incidence of uterine
rupture reported in this patient population.

Although the uterine rupture rate in anomalous, unscarred uteri during pregnancy appears to be
increased relative to that for normal uteri, the precise risk for different uterine malformations
remains uncertain.

Previous Uterine Myomectomy and Uterine Rupture

Previous myomectomy by means of laparotomy

Nearly all uterine ruptures that involved uteri with myomectomy scars have occurred during the
third trimester of pregnancy or during labor. Only 1 case of a spontaneous uterine rupture has
been reported before 20 weeks of gestation.15 Brown et al reported that among 120 term infants
delivered after previous transabdominal myomectomy, no uterine ruptures occurred, and 80% of
the infants were delivered vaginally.16 In contrast, Garnet identified 3 uterine ruptures among 83
women (4%) who had scars from a previous myomectomy and who underwent elective cesarean
delivery because of previous myomectomy.17

Such reports do not often delineate the factors that were deemed important for assessing the risk
of subsequent uterine rupture (eg, number, size, and locations of leiomyomata; number and
locations of uterine incisions; entry of the uterine cavity; type of closure technique). Further
studies to investigate these issues are needed.

Previous laparoscopic myomectomy

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 finding suggests that additional investigations with long-term follow-up are needed.

Rupture of the Scarred Uterus Due to Previous Cesarean

Delivery
The effect of previous cesarean delivery on the risk of uterine rupture has been studied
extensively. In a meta-analysis, Mozurkewich and Hutton used pooled data from 11 studies and
showed that the uterine rupture rate for women undergoing a TOL after previous cesarean
delivery was 0.39% compared with 0.16% for patients undergoing elective repeat cesarean
delivery (odds ratio [OR], 2.10; 95% CI, 1.45-3.05). Restricting the meta-analysis to 5
prospective cohort trials generated similar results (OR, 2.06; 95% CI, 1.40-3.04).26
Hibbard et al examined the risk of uterine rupture after previous cesarean delivery in 1324
women who underwent a subsequent TOL. They reported a significant difference in the risk of
uterine rupture between women who achieved successful vaginal birth compared with women in
whom attempted vaginal delivery failed (0.22% vs 1.9%; OR, 8.9; 95% CI, 1.9-42).27 The effect
of previous cesarean delivery on the rate of subsequent pregnancy-related uterine rupture can be
further examined according to additional subcategories, which are summarized in Table 1.

Previous classic cesarean delivery

Classic cesarean delivery via vertical midline uterine incision is infrequently performed in the
modern era and currently account for 0.5% of all births in the United States.28 In a meta-analysis,
Rosen et al reported an 11.5% absolute risk of uterine rupture (3 of 26 cases) in women with
classic vertical cesarean scars who underwent an unplanned TOL.29 For women who underwent
repeat cesarean section, Chauhan et al reported that the uterine rupture rate for 157 women with
prior classical uterine cesarean scars was 0.64% (95% CI, 0.1-3.5%). All patients in that study
underwent repeat cesarean delivery, but a high rate of preterm labor resulted in 49% of the
patients being in labor at the time of their cesarean delivery.28

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.30 These rates of frank uterine rupture in women with classic cesarean
deliveries are in contrast to the higher rates of 4-9% 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%).28 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.

Previous low vertical cesarean delivery

A meta-analysis of pooled data from 5 studies demonstrated a 1.1% absolute risk (12 of 1,112
cases) of symptomatic uterine rupture in women undergoing a TOL with a low vertical cesarean
scar.31,32,33,34,30 Compared to women with low transverse cesarean scars, these data suggest no
significantly increased risk of uterine rupture or adverse maternal and perinatal outcomes.

Interpretation of these studies is hampered by inconsistencies in how high the lower uterine
segment could be cut before it was considered a classic incision. Even when the lower uterine
segment is already well developed as a result of active labor, a low vertical incision of adequate
length is often impossible to permit fetal delivery. Naef et al arbitrarily defined a 2-cm extension
into the upper segment as a classic extension. For 322 pregnancies that occurred after a low
vertical cesarean delivery, the overall rate of uterine rupture was 0.62%. This rate could be
further divided as 1.15% for 174 women who underwent a TOL compared with no ruptures
among 148 women who underwent elective repeat cesarean delivery.31

Unknown uterine scar

In many instances, the type of incision used for a prior cesarean delivery cannot be confirmed
due to unavailability of the operative report. Under these circumstances, the assessment of
uterine rupture risk may sometimes be guided by the obstetric history to infer the most probable
type of uterine scar. For example, a patient with a history of a preterm cesarean delivery at 28
weeks’ gestation has a much higher likelihood of having had a vertical uterine incision than a
patient who underwent a cesarean section for an indication of arrest of fetal descent at term. 

It has been argued that because most cesarean deliveries in the United States are accomplished
via low-transverse uterine incisions, the risk of uterine rupture for patients with an unknown scar
is similar to that for women who have previously undergone a low-transverse hysterotomy. This
logic depends on the high ratio of low-transverse to vertical incisions performed for cesarean
section, but it ignores the varying probability with which different types of uterine incisions are
made under different obstetrical circumstances, as well as differences that occur due to varying
medical resources and the prevailing local practitioner practices in countries other than the
United States (eg, practices that occur in other countries, such as Mexico or Brazil).
Nevertheless, the vast majority of cesarean deliveries performed in the United States are
accomplished via low-transverse uterine incisions.

In a small case-control study of 70 patients by Leung et al, no association was found between an
unknown uterine scar and the risk of uterine rupture; however, given the rarity of uterine rupture
(see Table 1), this study was vastly underpowered to detect such a difference.35 Two additional,
but similarly underpowered, case series have also reported comparable rates of uterine rupture
and VBAC success in women with unknown uterine cesarean delivery scars versus those with
documented previous low-transverse hysterotomies.36,37 The Maternal-Fetal Medicine Units
(MFMU) Network cesarean delivery registry reports a 0.5% risk (15 of 3,206) of uterine rupture
for patients who underwent a TOL with an unknown uterine scar.30

For cases in which there are 1 or 2 unknown prior uterine incisions, there is a single small,
randomized, controlled trial by Grubb et al that compared labor augmentation with oxytocin
(n=95) with no intervention (n=93) in women with prior cesarean deliveries involving either 1 or
2 unknown uterine incisions. Four uterine dehiscences and 1 uterine rupture occurred, all in the
group that underwent labor augmentation. In the 1 case of uterine rupture, the unknown uterine
scar was in a patient with 2 prior cesarean deliveries, one of which involved a vertical incision.
Had the uterine scar status for this patient been known in advance, it would have represented a
contraindication to a TOL.38

Previous low transverse cesarean delivery

The risk of uterine rupture after a low transverse cesarean delivery varies depending on whether
patients undergo a TOL 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.

Previous cesarean delivery without a subsequent trial of labor

In a study of 20,095 women by Lydon-Rochelle et al, the spontaneous uterine rupture rate among
6,980 women with a single cesarean delivery scar who underwent scheduled repeat cesarean
delivery without a TOL was 0.16%.39 This finding indicates that uteri with cesarean scars have an
intrinsic propensity for rupture that exceeds that of the unscarred organ during pregnancy, which
is 0.012% (OR increase of approximately 12-fold). Therefore, all other uterine rupture rates in
women with a previous cesarean delivery should be referenced to this expected baseline rate.

Previous cesarean delivery with subsequent spontaneous labor

A study by Lydon-Rochelle et al showed that the uterine rupture rate among 10,789 women with
a single previous cesarean delivery who labored spontaneously during a subsequent singleton
pregnancy was 0.52%.39 This rate of uterine rupture implies an increased relative risk (RR) of 3.3
(95% CI, 1.8-6.0) for women who labor spontaneously compared with women who undergo
elective repeat cesarean delivery.

In a study by Ravasia et al of 1,544 patients with a previous cesarean delivery who later labored
spontaneously, the uterine rupture rate was 0.45%.40 Zelop et al found that, among 2,214 women
with 1 previous cesarean delivery who labored spontaneously, the uterine rupture rate was
0.72%.41 The authors of this article performed a meta-analysis of 29,263 pregnancies from 9
studies from 1987-2004 and showed that the overall risk of uterine rupture was 0.44% for
women who labor spontaneously after a previous cesarean delivery.

Previous cesarean delivery with subsequent augmentation of labor

Despite the clinical heterogeneity and different VBAC success rates for women undergoing
spontaneous labor rather than either labor augmentation or induction, very few studies have
stratified their data by labor augmentation versus labor induction and the data that do exist are
conflicting. There is wide variance in the frequency of clinical use of oxytocin as well as in the
dose and dosing schedules of oxytocin that are used. As a result, there is a paucity of specific
evidence-based clinical guidelines for the use of oxytocin in VBAC trials.

Previous cesarean delivery with subsequent induction of labor

Emerging data indicate that induction of labor after a prior cesarean delivery appears to be
associated with an increased risk of uterine rupture.

Zelop et al found that the rate of uterine rupture in 560 women who underwent labor induction
after a single previous cesarean delivery was 2.3% compared with 0.72% for 2,214 women who
had labored spontaneously (P =.001).41

In a study by Ravasia et al of 575 patients who underwent labor induction, the uterine rupture
rate was 1.4% compared with 0.45% for women who labored spontaneously (P =.004).40

Blanchette et al found that the uterine rupture rate after previous cesarean delivery when labor
was induced was 4.0% compared with 0.34% for women who labored spontaneously.42 This last
finding suggests a 12-fold increased risk of uterine rupture for women who undergo labor
induction after previous cesarean delivery.

Data on mechanical methods of labor induction for cervical ripening are limited but reassuring.
In a small case series, Bujold et al found no statistically significant difference among the uterine
rupture rates of 1.1% for spontaneous labor, 1.2% for induction by amniotomy with or without
oxytocin, and 1.6% for induction by transcervical Foley catheter (P =0.81).43

Conversely, Hoffman et al reported a 3.67-fold increased risk of uterine rupture (95% CI, 1.46-
9.23) with Foley catheter use for preinduction cervical ripening. Importantly, however, many of
these patients received concomitant oxytocin together with application of the transcervical Foley
catheter.44

Of particular note is that a recent randomized controlled trial by Pettker et al found that the
addition of oxytocin to the use of a transcervical Foley catheter for labor induction does not
shorten the time to delivery and has no effect on either the likelihood of delivery within 24 hours
or the vaginal delivery rate.45 In light of these findings, induction of labor with a transcervical
Foley catheter alone may be a reasonable option for women undergoing a TOLAC with an
unfavorable cervix.

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 TOL after previous cesarean delivery. 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.39

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.46
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.40

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 PGE2.47 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 PGE2 and patients with previous cesarean scars who labored
spontaneously (1.1 vs 0.3%; P =.15).48
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).30

Previous cesarean delivery with previous successful vaginal delivery

Several studies have shown a protective association of previous vaginal birth on uterine rupture
risk in subsequent attempts at vaginal birth after previous cesarean delivery. Zelop et al
compared 1,021 women who underwent a TOL after a single previous cesarean delivery with 1
previous vaginal delivery with 2,762 women who underwent a TOL with no previous vaginal
delivery. The uterine rupture rate was 0.2% versus 1.1% (P =.01).49

Among women with a single uterine scar, those with at least 1 previous vaginal delivery had one
fifth the risk for uterine rupture compared with women without a previous vaginal delivery (OR,
0.2; 95% CI, 0.04-0.8). Caughey et al found that women with a previous vaginal delivery were
about one fourth as likely as patients without a previous vaginal delivery to have a uterine
rupture (OR, 0.26; 95% CI, 0.08-0.88).50 In a study of 205 patients who underwent a TOL after 1
previous cesarean delivery, Kayani and Alfirevic noted that all 4 of their cases of uterine ruptures
occurred in women with no previous vaginal delivery.51

A study of 11,778 women by members of the Maternal-Fetal Medicine Units (MFMU) Network
found that in women with no prior vaginal delivery who underwent a TOL, there was an
increased risk of uterine rupture with induction versus spontaneous labor (1.5% vs 0.8%, P
=0.02). In contrast, no statistically significant difference was shown for women with a prior
vaginal delivery who underwent spontaneous TOL compared with labor induction (0.6% vs
0.4%, P =0.42).52

Previous cesarean delivery with subsequent successful VBACs

Multiple studies suggest a protective advantage with regard to the uterine rupture rate if a woman
has had a prior successful VBAC attempt. Multiple potential explanations exist, but the 2 most
obvious are that a successful prior VBAC attempt assures that (1) the maternal pelvis is tested
and that the bony pelvis is adequate to permit passage of the fetus and (2) the integrity of the
uterine scar has been tested previously under the stress/strain conditions during labor and
delivery that were adequate to result in vaginal delivery without prior uterine rupture.

Mercer et al found that the rate of uterine rupture decreased after the first successful VBAC, but
that there was no additional protective effect demonstrated thereafter: the uterine rupture rate
was 0.87% with no prior VBACs, 0.45% for those with one successful prior VBAC, and 0.43%
for those with 2 or more successful prior VBACs (P =.01).53 Pooled data from 5 studies indicate
an increased uterine rupture rate of 1.4% (1 per 73) in failed VBAC attempts that required a
repeat cesarean section in labor.30,42,54,55,56

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).57 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).58

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 TOL after 1 previous
cesarean delivery (OR, 3.0; 95% CI, 1.2-7.2).59 The authors controlled for maternal age, public
assistance, length of labor, gestational age of ³41 weeks, and induction of augmentation of labor
with oxytocin.

In additional support of this observation, 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).60 After adjusting for confounding
variables, the odds ratio for a uterine rupture during a subsequent TOL 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).

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 TOL with a previous classic midline
cesarean scar.

One-layer versus 2-layer hysterotomy closure

In a Canadian study of 1,980 women who underwent a TOL after a single previous low
transverse cesarean delivery, Bujold et al found a 4- to 5-fold increased risk of uterine rupture for
women who had a previous single-layer uterine closure compared with those having a 2-layer
closure. Uterine rupture occurred in 3.1% (15 of 489 cases) of single-layer closure versus 0.5%
(8 of 1,491 cases) of double-layer closure (P <.001). Using stepwise multivariate logistic
regression, the authors concluded that the OR for uterine rupture in women who had undergone a
single previous 1-layer cesarean hysterotomy closure was 3.95 (95% CI, 1.35-11.49) compared
with those who had a 2-layer closure.61

Durnwald and Mercer found that 182 patients with single-layer hysterotomy closure did not have
an increased rate of uterine rupture, but the rate of uterine windows at subsequent delivery was
increased to 3.5% versus 0.7% for those who had a multi-layer closure (P =.046).62
Gyamfi et al reported an 8.6% (3 of 35) rate of uterine rupture in patients with a single-layer
closure compared with 1.3% (12 of 913) in those with double-layer closure (P =0.015). Although
the single-layer group had a shorter interdelivery interval, the uterine rupture rate remained
significantly elevated even when the time interval was controlled for using logistic regression
(OR 7.20, 95% CI, 1.81-28.62, P =0.005).63

Multiple prior cesarean deliveries

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 TOL, 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].64

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 TOL, 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).65

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, 0.08-0.88).50

In contrast, Landon et al reported through the MFM 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).66 However, in this study there was a much
lower TOL rate of 9% for women with multiple prior cesarean deliveries compared with the 27%
rate in the report of Macones et al65 and the 73% rate in Miller’s study64 . 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 TOL rate in their 12-year data analysis.50

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.67 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 suggests that in women with 2 previous cesarean deliveries, only those
with a previous vaginal delivery should be considered candidates for a TOL.68
Fetal macrosomia

Elkousy et al found that, in 9,960 women who underwent a TOL after 1 previous cesarean
delivery, the risk of uterine rupture was significantly greater for fetuses that weighed >4000 g
(2.8%) than in those weighing <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 >4000 g compared to women with a fetal weight of <4000 g (RR
2.3, P <.001).69

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).70 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 <3500 g, 3500-3999 g, and ≥4000 g, respectively (P <.05).71

Maternal age

Shipp et al showed that increasing maternal age has a detrimental effect on the rate of uterine
rupture. In a multiple logistic regression analysis that was designed to control for confounding
factors, the overall rate of uterine rupture in 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).72

Table 1. Absolute Rates of Uterine Rupture for Different Patient Subgroups

Open table in new window

[ CLOSE WINDOW ]

Table

Subcategory Uterine Rupture

Total Years No.
General Total No. of Data of
References
Category Major Minor Deliveri Rate in Sub- Collectio Studie
es categor n s
y
All NA NA 2,863,33 1 per 1,864 1973- 20 Gardeil
0 1536 2006 1994, Golan
(0.07%) 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
Unscarred In NA 1,467,53 1 per 174 1975- 8 Gardeil
uterus industrializ 4 8,434 2006 1994,
ed countries (0.013%) Plauche
1984,
Gregory
1999,
Rageth
1999, Yap
2001,
Miller
1997,
Kieser
2002,
Zwart, 2009
In NA 399,314 1 per 920 434 1966- 4 Golan,
developing (0.11%) 2006 1980,
countries Mokgokong
1976,
Rahman
 1985, Gupta
2010
Elective NA 17,209 1 per 13 1995 1 Gregory
primary 1,324 1999
cesarean (0.08%)
delivery
TOL NA 452,720 1 per 91 1995 1 Gregory
4,975 1999
(0.02%)
Labor with NA 401,387 1 per 27 1995 1 Gregory
vaginal 14,866 1999
delivery (0.01%)
Failed labor NA 51,333 1 per 802 64 1995 1 Gregory
with (0.12%) 1999
primary
cesarean
delivery
Congenitall Previous NA 190 1 per 95 2 1992- 2 Ravasia
y low (1.1%) 2002 1999, Erez
anomalous transverse 2007
uterus cesarean
delivery
Normal NA NA 1,001 1 per 143 7 1930- 10 Brown,
uterus, (.70%) 2006 1956,
previous Garnet
myomecto 1964,
my Dubuisson
2000,
Seinera
2000,
Nezhat
1999,
Seracchioli
2000,
Seracchioli
2006,
Kumakiri
2008, Sizzi
2007,
Makino
2008
Trans- NA 179 1 per 60 3 1930- 2 Brown
abdominal (1.7%) 1960 1956,
myomecto Garnet 1964
my
 Laparoscop NA 822 1 per 4 1989- 8 Dubuisson
ic 206(0.49 2006 2000,
myomecto %) Seinera
my 2000,
Nezhat,
1999,
Seracchioli
2000,
Seracchioli
2006,
Kumakiri
2008, Sizzi
2007,
Makino
2008
Normal NA NA 172,397 1 per 236 732 1983- 13 Gardeil
uterus, (0.42%) 2002 1994,
previous Landon
cesarean 2004,
delivery Lydon-
Rochelle
2001,
Blanchette
2001,
Grobman
2007,
Rageth
1999,
Miller
1994, Yap
2001,
Leung
1993,
Kieser
2002,
Flamm
1994,
Cowan
1994, Lin
2004
Elective NA 90,360 1 per 623 145 1982- 10 Gardeil
repeat (0.16%) 2002 1994,
cesarean Mozurkewi
delivery ch 2000,
Landon
2004,
 Lydon-
Rochelle
2001,
Blanchette
2001,
Gregory
1999,
McMahon
1996,
Rageth
1999,
Kieser
2002, Lin
2004
TOL NA 168,609 1 per 174 970 1982- 22 Gardeil
(0.58%) 2002 1994,
Mozurkewi
ch 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 71,470 1 per 581 123 1976- 9 Landon
previous (0.17%) 2002 2004,
successful Blanchette
VBAC* 2001,
Mercer
2008,
Gregory
1999,
McMahon
1996,
Rageth
1999, Yap
2001,
Leung
1993,
Asakura
1995
No history of 20,191 1 per 125 161 1983- 2 Mercer
previous (0.80%) 2002 2008,
successful Leung 1993
VBAC
Failed 25,922 1 per 356 1983- 5 Landon
VBAC or 73 (1.4%) 2002 2004,
repeat Blanchette
cesarean 2001,
delivery in Gregory
labor 1999,
McMahon
1996,
Rageth
1999
Spontaneous 29,263 1 per 225 130 1979- 9 Landon
TOL (0.44%) 2002 2004,
Lydon-
Rochelle
2001,
 Ravasia
2000, Zelop
1999,
Blanchette
2001,
Delaney
2003, Lin
2004,
Locatelli
2006,
Molloy
1987
Augmented 15,666 1 per 144 109 1979- 6 Landon
TOL (0.70%) 2002 2004, Zelop
(oxytocin) 1999,
Blanchette
2001,
Rageth
1999,
Molloy
1987,
Flamm
1990
Induced 3,658 1 per 125 54 1983- 5 Landon
TOL (0.80%) 2002 2004, Zelop
(oxytocin) 1999,
Blanchette
2001,
Taylor
2002, Lin
2004
Induced 6,768 1 per 125 54 1983- 5 Rageth
TOL (non- (0.80%) 2002 1999,
prosta- Landon
glandin) 2004,
Lydon-
Rochelle
2001,
Raasia
2000,
Bujold 2004
Induced 1,817 1 per 29 1984- 12 Landon
TOL (prosta- 63 (1.6%) 2002 2004,
glandin) Lydon-
Rochelle
2001,
 Ravasia
2000, Zelop
1999,
Blanchette
2001,
Taylor,
2002,
Delaney
2003, Lin,
2004,
Locatelli
2006,
Choy-Hee
2001, Plaut
1999, Wing
1998
Combined 924 1 per 16 1984- 5 Ravasia
prostaglandi 58 (1.7%) 2000 2000, Zelop
n-oxytocin 1999,
induction Banchette
2001,
Taylor
2002,
Flamm
1997
Normal NA NA 134,556 1 per 196 686 1975- 13 Plauche
uterus, (0.51%) 2000 1984,
single Lydon-
previous Rochelle
cesarean 2001, Zelop
delivery 1999,
Delaney
2003,
McMahon
1996,
Rageth
1999,
Miller
1994,
Macones
2005,
Elkousy
2003,
Leung
1993,
Kieser
 2002,
Bujold
2002,
Asakura
1995
Before NA 6,980 1 per 635 11 1987- 1 Lydon-
labor (0.16%) 1996 Rochelle
2001
With labor NA 28,698 1 per 173 166 1984- 6 Lydon-
(0.58%) 2002 Rochelle
2001, Zelop
1999,
Delaney
2003,
Grobman
2007,
Bujold
2002, Lin
2004
Labor NA 7,757 1 per 92 84 1984- 6 Lydon-
induction (1.1%) 2002 Rochelle
2001, Zelop
1999,
Delaney
2003,
Grobman
2007, Lin
2004,
Locatelli
2006
Successful 1,110 1 per 1 1987- 1 Asakura
vaginal 1,110 1991 1995
delivery (0.09%)
Classic NA 428 1 per 5 1980- 4 Chauhan
midline 86 (1.2%) 2002 2002,
cesarean Landon
delivery 2004,
Patterson
2002,
Bethune
1997
Successful NA 7,070 1 per 244 29 1984- 4 Zelop 2000,
previous (0.41%) 2002 Kayani
vaginal 2005,
delivery Grobman
2007,
 Hendler
2004
No NA 12,805 1 per 137 1984- 5 Ravasia
previous 93 (1.1%) 2002 2000, Zelop
vaginal 2000,
delivery Kayani
2005,
Grobman
2007,
Hendler
2004
Successful NA 526 1 per 526 1 1988- 2 Kayani
previous (0.19%) 2002 2005,
VBAC Hendler
2004
Low NA 29,501 1 per 142 208 1984- 6 Landon
transverse (0.68%) 2002 2004, Shipp
cesarean 1999, Zelop
delivery 1999,
Delaney
2003,
Bujold
2002,
Menihan
1998
With labor 22,855 1 per 143 160 1988- 6 Zelop 1999,
(0.70%) 2002 Delaney
2003,
Grobman
2007,
Bujold
2002,
Locatelli
2006,
Yogev 2004
Spontaneous 13,381 1 per 188 71 1992- 4 Delaney
TOL (0.53%) 2002 2003,
Grobman
2007,
Locatelli
2006,
Yogev 2004
Induced 3,224 1 per 35 1992- 2 Delaney
TOL 92 2000 2003,
(oxytocin) (1.09%) Grobman
2007
 Induced 724 1 per 241 3 1992- 4 Delaney
TOL (0.41%) 2002 2003,
(prostaglandi Grobman
n) 2007,
Locatelli
2006,
Yogev 2004
TOL with 1,071 1 per 26 1988- 4 Stamilio
interdelivery 41 (2.8%) 2000 2007, Shipp
interval ≤2 y 2001,
Bujold
2002,
Huang 2002
TOL with 1- 776 1 per 18 1988- 4 Bujold
layer 43 (2.3%) 2001 2002,
hysterotomy Durnwald
closure 2003,
Gyamfi
2006,
Chapman
1997
TOL with 2- 2,819 1 per 117 24 1988- 4 Bujold
layer (0.85%) 2001 2002,
hysterotomy Durnwald
closure 2003,
Gyamfi
2006,
Chapman
1997
Fetal 1,915 1 per 42 1984- 3 Elkousy
macrosomia 39 (2.6%) 2004 2003, Zelop
>4000 g 2001,
Jastrow
2010
Unknown NA 3,698 1 per 218 17 1999- 4 Landon
uterine scar (0.5%) 2002 2004, Pruett
1988, Beall
1984,
Grubb 1996
Low NA 1,355 1 per 15 1981- 6 Landon
vertical 90 (1.1%) 2002 2004, Naef
cesarean 1995, Adair
delivery 1996,
Martin
1997, Shipp
1999, Zelop
 1999
With labor 933 1 per 104 9 1981- 3 Naef 1995,
(0.96%) 1997 Martin
1997, Shipp
1999
Normal NA NA 6,279 1 per 116 1983- 10 Blanchette
uterus, 54 2002 2001, Zelop
multiple (1.85%) 2000,
previous Caughey
cesarean 1999,
deliveries Miller
1994,
Macones
2005,
Landon
2006,Leung
1993,
Cowan
1994,
Asakura
1995, Cahill
2010
Spontaneou NA 523 1 per 131 4 1996- 1 Lin 2004
s TOL (0.76%) 2002
Induced NA 54 1 per 1 1996- 1 Lin 2004
TOL 54 (1.8%) 2002
(oxytocin)
Induced NA 19 1 per 1 1996- 1 Lin 2004
TOL 19 (5.3%) 2002
(prosta-
glandin)
Subcategory Uterine Rupture
Total Years No.
General Total No. of Data of
References
Category Major Minor Deliveri Rate in Sub- Collectio Studie
es categor n s
y
All NA NA 2,863,33 1 per 1,864 1973- 20 Gardeil
0 1536 2006 1994, Golan
(0.07%) 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
Unscarred In NA 1,467,53 1 per 174 1975- 8 Gardeil
uterus industrializ 4 8,434 2006 1994,
ed countries (0.013%) Plauche
1984,
Gregory
1999,
Rageth
1999, Yap
2001,
Miller
1997,
Kieser
2002,
Zwart, 2009
In NA 399,314 1 per 920 434 1966- 4 Golan,
developing (0.11%) 2006 1980,
countries Mokgokong
1976,
 Rahman
1985, Gupta
2010
Elective NA 17,209 1 per 13 1995 1 Gregory
primary 1,324 1999
cesarean (0.08%)
delivery
TOL NA 452,720 1 per 91 1995 1 Gregory
4,975 1999
(0.02%)
Labor with NA 401,387 1 per 27 1995 1 Gregory
vaginal 14,866 1999
delivery (0.01%)
Failed labor NA 51,333 1 per 802 64 1995 1 Gregory
with (0.12%) 1999
primary
cesarean
delivery
Congenitall Previous NA 190 1 per 95 2 1992- 2 Ravasia
y low (1.1%) 2002 1999, Erez
anomalous transverse 2007
uterus cesarean
delivery
Normal NA NA 1,001 1 per 143 7 1930- 10 Brown,
uterus, (.70%) 2006 1956,
previous Garnet
myomecto 1964,
my Dubuisson
2000,
Seinera
2000,
Nezhat
1999,
Seracchioli
2000,
Seracchioli
2006,
Kumakiri
2008, Sizzi
2007,
Makino
2008
Trans- NA 179 1 per 60 3 1930- 2 Brown
abdominal (1.7%) 1960 1956,
myomecto Garnet 1964
my
 Laparoscop NA 822 1 per 4 1989- 8 Dubuisson
ic 206(0.49 2006 2000,
myomecto %) Seinera
my 2000,
Nezhat,
1999,
Seracchioli
2000,
Seracchioli
2006,
Kumakiri
2008, Sizzi
2007,
Makino
2008
Normal NA NA 172,397 1 per 236 732 1983- 13 Gardeil
uterus, (0.42%) 2002 1994,
previous Landon
cesarean 2004,
delivery Lydon-
Rochelle
2001,
Blanchette
2001,
Grobman
2007,
Rageth
1999,
Miller
1994, Yap
2001,
Leung
1993,
Kieser
2002,
Flamm
1994,
Cowan
1994, Lin
2004
Elective NA 90,360 1 per 623 145 1982- 10 Gardeil
repeat (0.16%) 2002 1994,
cesarean Mozurkewi
delivery ch 2000,
Landon
2004,
 Lydon-
Rochelle
2001,
Blanchette
2001,
Gregory
1999,
McMahon
1996,
Rageth
1999,
Kieser
2002, Lin
2004
TOL NA 168,609 1 per 174 970 1982- 22 Gardeil
(0.58%) 2002 1994,
Mozurkewi
ch 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 71,470 1 per 581 123 1976- 9 Landon
previous (0.17%) 2002 2004,
successful Blanchette
VBAC* 2001,
Mercer
2008,
Gregory
1999,
McMahon
1996,
Rageth
1999, Yap
2001,
Leung
1993,
Asakura
1995
No history of 20,191 1 per 125 161 1983- 2 Mercer
previous (0.80%) 2002 2008,
successful Leung 1993
VBAC
Failed 25,922 1 per 356 1983- 5 Landon
VBAC or 73 (1.4%) 2002 2004,
repeat Blanchette
cesarean 2001,
delivery in Gregory
labor 1999,
McMahon
1996,
Rageth
1999
Spontaneous 29,263 1 per 225 130 1979- 9 Landon
TOL (0.44%) 2002 2004,
Lydon-
Rochelle
2001,
 Ravasia
2000, Zelop
1999,
Blanchette
2001,
Delaney
2003, Lin
2004,
Locatelli
2006,
Molloy
1987
Augmented 15,666 1 per 144 109 1979- 6 Landon
TOL (0.70%) 2002 2004, Zelop
(oxytocin) 1999,
Blanchette
2001,
Rageth
1999,
Molloy
1987,
Flamm
1990
Induced 3,658 1 per 125 54 1983- 5 Landon
TOL (0.80%) 2002 2004, Zelop
(oxytocin) 1999,
Blanchette
2001,
Taylor
2002, Lin
2004
Induced 6,768 1 per 125 54 1983- 5 Rageth
TOL (non- (0.80%) 2002 1999,
prosta- Landon
glandin) 2004,
Lydon-
Rochelle
2001,
Raasia
2000,
Bujold 2004
Induced 1,817 1 per 29 1984- 12 Landon
TOL (prosta- 63 (1.6%) 2002 2004,
glandin) Lydon-
Rochelle
2001,
 Ravasia
2000, Zelop
1999,
Blanchette
2001,
Taylor,
2002,
Delaney
2003, Lin,
2004,
Locatelli
2006,
Choy-Hee
2001, Plaut
1999, Wing
1998
Combined 924 1 per 16 1984- 5 Ravasia
prostaglandi 58 (1.7%) 2000 2000, Zelop
n-oxytocin 1999,
induction Banchette
2001,
Taylor
2002,
Flamm
1997
Normal NA NA 134,556 1 per 196 686 1975- 13 Plauche
uterus, (0.51%) 2000 1984,
single Lydon-
previous Rochelle
cesarean 2001, Zelop
delivery 1999,
Delaney
2003,
McMahon
1996,
Rageth
1999,
Miller
1994,
Macones
2005,
Elkousy
2003,
Leung
1993,
Kieser
 2002,
Bujold
2002,
Asakura
1995
Before NA 6,980 1 per 635 11 1987- 1 Lydon-
labor (0.16%) 1996 Rochelle
2001
With labor NA 28,698 1 per 173 166 1984- 6 Lydon-
(0.58%) 2002 Rochelle
2001, Zelop
1999,
Delaney
2003,
Grobman
2007,
Bujold
2002, Lin
2004
Labor NA 7,757 1 per 92 84 1984- 6 Lydon-
induction (1.1%) 2002 Rochelle
2001, Zelop
1999,
Delaney
2003,
Grobman
2007, Lin
2004,
Locatelli
2006
Successful 1,110 1 per 1 1987- 1 Asakura
vaginal 1,110 1991 1995
delivery (0.09%)
Classic NA 428 1 per 5 1980- 4 Chauhan
midline 86 (1.2%) 2002 2002,
cesarean Landon
delivery 2004,
Patterson
2002,
Bethune
1997
Successful NA 7,070 1 per 244 29 1984- 4 Zelop 2000,
previous (0.41%) 2002 Kayani
vaginal 2005,
delivery Grobman
2007,
 Hendler
2004
No NA 12,805 1 per 137 1984- 5 Ravasia
previous 93 (1.1%) 2002 2000, Zelop
vaginal 2000,
delivery Kayani
2005,
Grobman
2007,
Hendler
2004
Successful NA 526 1 per 526 1 1988- 2 Kayani
previous (0.19%) 2002 2005,
VBAC Hendler
2004
Low NA 29,501 1 per 142 208 1984- 6 Landon
transverse (0.68%) 2002 2004, Shipp
cesarean 1999, Zelop
delivery 1999,
Delaney
2003,
Bujold
2002,
Menihan
1998
With labor 22,855 1 per 143 160 1988- 6 Zelop 1999,
(0.70%) 2002 Delaney
2003,
Grobman
2007,
Bujold
2002,
Locatelli
2006,
Yogev 2004
Spontaneous 13,381 1 per 188 71 1992- 4 Delaney
TOL (0.53%) 2002 2003,
Grobman
2007,
Locatelli
2006,
Yogev 2004
Induced 3,224 1 per 35 1992- 2 Delaney
TOL 92 2000 2003,
(oxytocin) (1.09%) Grobman
2007
 Induced 724 1 per 241 3 1992- 4 Delaney
TOL (0.41%) 2002 2003,
(prostaglandi Grobman
n) 2007,
Locatelli
2006,
Yogev 2004
TOL with 1,071 1 per 26 1988- 4 Stamilio
interdelivery 41 (2.8%) 2000 2007, Shipp
interval ≤2 y 2001,
Bujold
2002,
Huang 2002
TOL with 1- 776 1 per 18 1988- 4 Bujold
layer 43 (2.3%) 2001 2002,
hysterotomy Durnwald
closure 2003,
Gyamfi
2006,
Chapman
1997
TOL with 2- 2,819 1 per 117 24 1988- 4 Bujold
layer (0.85%) 2001 2002,
hysterotomy Durnwald
closure 2003,
Gyamfi
2006,
Chapman
1997
Fetal 1,915 1 per 42 1984- 3 Elkousy
macrosomia 39 (2.6%) 2004 2003, Zelop
>4000 g 2001,
Jastrow
2010
Unknown NA 3,698 1 per 218 17 1999- 4 Landon
uterine scar (0.5%) 2002 2004, Pruett
1988, Beall
1984,
Grubb 1996
Low NA 1,355 1 per 15 1981- 6 Landon
vertical 90 (1.1%) 2002 2004, Naef
cesarean 1995, Adair
delivery 1996,
Martin
1997, Shipp
1999, Zelop
 1999
With labor 933 1 per 104 9 1981- 3 Naef 1995,
(0.96%) 1997 Martin
1997, Shipp
1999
Normal NA NA 6,279 1 per 116 1983- 10 Blanchette
uterus, 54 2002 2001, Zelop
multiple (1.85%) 2000,
previous Caughey
cesarean 1999,
deliveries Miller
1994,
Macones
2005,
Landon
2006,Leung
1993,
Cowan
1994,
Asakura
1995, Cahill
2010
Spontaneou NA 523 1 per 131 4 1996- 1 Lin 2004
s TOL (0.76%) 2002
Induced NA 54 1 per 1 1996- 1 Lin 2004
TOL 54 (1.8%) 2002
(oxytocin)
Induced NA 19 1 per 1 1996- 1 Lin 2004
TOL 19 (5.3%) 2002
(prosta-
glandin)

NA=Not applicable
TOL=Trial of labor
VBAC=Vaginal birth after cesarean delivery

Signs and Symptoms of Uterine Rupture During Pregnancy

The signs and symptoms of uterine rupture largely depend on the timing, site, and extent of the
uterine defect. Uterine rupture at the site of a previous uterine scar is typically less violent and
less dramatic than a spontaneous or traumatic rupture because of their relatively reduced
vascularity.

The classic signs and symptoms of uterine rupture are (1) fetal distress (as evidenced most often
by abnormalities in fetal heart rate), (2) diminished baseline uterine pressure, (3) loss of uterine
contractility, (4) abdominal pain, (5) recession of the presenting fetal part, (6) hemorrhage, and
(7) shock. However, modern studies show that some of these signs and symptoms are rare and
that many may not be reliably distinguished from their occurrences in other, more benign
obstetric circumstances (see Table 2).

Table 2. Conditions Associated With Uterine Rupture

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Table

Incidence
Cases in Patients
Years No.
Total With With
Condition of Data of References
Cases Uterine Uterine
Collection Studies
Rupture Rupture,
%
Abnormal pattern 344 187 54 1973-2002 8 Gardeil 1994, Golan
in fetal heart rate 1980, Rahman 1985,
Blanchette 2001, Taylor
2002, Rageth 1999, Yap
2001, Bujold 2002
Prolonged 143 114 80 1983-2002 4 Miller 1994, Leung
deceleration in 1993, Bujold 2002,
fetal heart rate or Menihan 1998
bradycardia
Uterine 30 12 40 1994-1999 2 Blanchette 2001, Phelan
tachysystole* or 1998
hyper-stimulation
Loss of 144 6 4 1973-1999 3 Golan 1980, Blanchette
intrauterine 2001, Eden 1986
pressure or
cessation of
contractions
Abnormal labor or 169 49 29 1983-1996 2 Rageth 1999, Leung
failure to progress 1993
Abdominal pain 454 118 26 1931-2000 9 Golan 1980, Rahman
1985, Blanchette 2001,
Yap 2001, Leung 1993,
Miller 1997, Bujold
2002, Rodriguez 1989,
Eden 1986
Vaginal bleeding 381 140 37 1931-2000 8 Gardeil 1994, Golan
1980, Rahman 1985,
 Yap 2001, Leung 1993,
Miller 1997, Bujold
2002, Eden 1986
Shock 213 71 33 1931-1993 3 Golan 1980, Rahman
1985, Eden 1986
Incidence
Cases in Patients
Years No.
Total With With
Condition of Data of References
Cases Uterine Uterine
Collection Studies
Rupture Rupture,
%
Abnormal pattern 344 187 54 1973-2002 8 Gardeil 1994, Golan
in fetal heart rate 1980, Rahman 1985,
Blanchette 2001, Taylor
2002, Rageth 1999, Yap
2001, Bujold 2002
Prolonged 143 114 80 1983-2002 4 Miller 1994, Leung
deceleration in 1993, Bujold 2002,
fetal heart rate or Menihan 1998
bradycardia
Uterine 30 12 40 1994-1999 2 Blanchette 2001, Phelan
tachysystole* or 1998
hyper-stimulation
Loss of 144 6 4 1973-1999 3 Golan 1980, Blanchette
intrauterine 2001, Eden 1986
pressure or
cessation of
contractions
Abnormal labor or 169 49 29 1983-1996 2 Rageth 1999, Leung
failure to progress 1993
Abdominal pain 454 118 26 1931-2000 9 Golan 1980, Rahman
1985, Blanchette 2001,
Yap 2001, Leung 1993,
Miller 1997, Bujold
2002, Rodriguez 1989,
Eden 1986
Vaginal bleeding 381 140 37 1931-2000 8 Gardeil 1994, Golan
1980, Rahman 1985,
Yap 2001, Leung 1993,
Miller 1997, Bujold
2002, Eden 1986
Shock 213 71 33 1931-1993 3 Golan 1980, Rahman
1985, Eden 1986
*
Defined as > 6 contractions during 2 consecutive 10-minute periods of observation.
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.60 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.73 Rodriguez et al found that fetal distress was
the most common finding associated with uterine rupture, occurring in 78%.74 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.73,75,76,60

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 TOL, only 22% of complete uterine
ruptures presented with abdominal pain and 76% presented with signs of fetal distress diagnosed
by continuous electronic fetal monitoring.77

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.60 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. A guideline from ACOG from 2004
suggests there is no absolute contraindication to epidural anesthesia for a TOL because epidurals
rarely mask the signs and symptoms of uterine rupture.68

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.78 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.74

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.2,5,79

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 TOL after a previous cesarean delivery. 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.80

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.81

Consequences of Uterine Rupture

Overview

The consequences of uterine rupture during pregnancy depend on the time that elapses from the
rupture until the institution of definitive therapy. Definitive therapy for the fetus is delivery and
must generally be accomplished with alacrity to avoid major fetal morbidity and mortality.
Conversely, therapy for the mother can generally be supportive and resuscitative until surgical
intervention can be undertaken to arrest the often life-threatening uterine hemorrhage.

Several studies have shown that delivery of the fetus within 10-37 minutes of uterine rupture is
necessary to prevent serious fetal morbidity and mortality.73,76,82,42,60 If proper supportive measures
(including fluid resuscitation and blood transfusion), are available to treat the mother, the time
for definitive surgical intervention before the onset of major maternal morbidity and mortality
may often be substantially longer than that for the fetus.

Therefore, the consequences of uterine rupture may be divided into 2 major categories,
depending on whether they apply to the fetus or to the mother (see Table 3).
Table 3. Fetal and Maternal Consequences of Uterine Rupture

Open table in new window

[ CLOSE WINDOW ]

Table

Incidence
Cases in Patients
Years No.
Total With With
Consequence of Data of Studies References
Cases Uterine Uterine
Collection Reviewed
Rupture Rupture,
%
Fetal or Neonatal
Hypoxia or 231 19 8 1983-2002 3 Landon 2004, Leung
anoxia 1993, Kieser 2002
Acidosis 252 83 33 1976-2002 5 Landon 2004, Ravasia
(Umbilical artery 2000, Yap 2001, Leung
cord pH <7) 1993, Menihan 1998
Depressed Apgar 349 90 26 1976-2002 9 Landon 2004, Shipp
scores (Five- 1999, Blanchette 2001,
minute Apgar Caughey 1999, Yap 2001,
score <7) Leung 1993, Miller 1997,
Kieser 2002, Menihan
1998
Admission to 164 71 43 1976-2002 4 Landon 2004, Miller
neonatal 1997, Kieser 2002,
intensive care Menihan 1998
unit
Perinatal death, 548 39 7 1975-2002 14 Gardeil 1994, Plauche
industrialized 1984, Landon 2004,
countries Shipp 1999, Lydon-
Rochelle 2001,
Blanchette 2001,
Caughey 1999, Esposito
2000, Yap 2001, Leung
1993, Kieser 2002,
Flamm 1994, Lieberman
2001, Flamm 1990
Perinatal death, 524 388 74 1966-1980 3 Golan 1980, Mokgokong
developing 1976, Rahman 1985
countries
Maternal
Severe blood 286 67 23 1976-1998 7 Gardeil 1994, Shipp
loss or 1999, Lydon-Rochelle
transfusion 2001, Yap 2001, Leung
1993, Kieser 2002,
Menihan 1998
Cystotomy 311 45 11 1976-1998 7 Gardeil 1994, Shipp
1999, Lydon-Rochelle
2001, Caughey 1999, Yap
2001, Leung 1993, Kieser
2002
Need for 518 109 21 1973-2000 14 Gardeil 1994, Golan
hysterectomy 1980, Plauche 1984,
Shipp 1999, Lydon-
Rochelle 2001,
Blanchette 2001,
Caughey 1999, Esposito
2000, Yap 2001, Leung
1993, Kieser 2002,
Menihan 1998,
Lieberman 2001, Flamm
1990
Death, 313 1 0.32 1975-2000 11 Gardeil 1994, Plauche
industrialized 1984, Shipp 1999,
countries Caughey 1999, McMahon
1996, Yap 2001, Leung
1993, Kieser 2002,
Flamm 1994, Lieberman
2001, Spaulding 1979
Death, 524 41 8 1966-1980 3 Golan 1980, Mokgokong
developing 1976, Rahman 1985
countries
Incidence
Cases in Patients
Years No.
Total With With
Consequence of Data of Studies References
Cases Uterine Uterine
Collection Reviewed
Rupture Rupture,
%
Fetal or Neonatal
Hypoxia or 231 19 8 1983-2002 3 Landon 2004, Leung
anoxia 1993, Kieser 2002
Acidosis 252 83 33 1976-2002 5 Landon 2004, Ravasia
(Umbilical artery 2000, Yap 2001, Leung
cord pH <7) 1993, Menihan 1998
Depressed Apgar 349 90 26 1976-2002 9 Landon 2004, Shipp
scores (Five- 1999, Blanchette 2001,
minute Apgar Caughey 1999, Yap 2001,
score <7) Leung 1993, Miller 1997,
Kieser 2002, Menihan
1998
Admission to 164 71 43 1976-2002 4 Landon 2004, Miller
neonatal 1997, Kieser 2002,
intensive care Menihan 1998
unit
Perinatal death, 548 39 7 1975-2002 14 Gardeil 1994, Plauche
industrialized 1984, Landon 2004,
countries Shipp 1999, Lydon-
Rochelle 2001,
Blanchette 2001,
Caughey 1999, Esposito
2000, Yap 2001, Leung
1993, Kieser 2002,
Flamm 1994, Lieberman
2001, Flamm 1990
Perinatal death, 524 388 74 1966-1980 3 Golan 1980, Mokgokong
developing 1976, Rahman 1985
countries
Maternal
Severe blood 286 67 23 1976-1998 7 Gardeil 1994, Shipp
loss or 1999, Lydon-Rochelle
transfusion 2001, Yap 2001, Leung
1993, Kieser 2002,
Menihan 1998
Cystotomy 311 45 11 1976-1998 7 Gardeil 1994, Shipp
1999, Lydon-Rochelle
2001, Caughey 1999, Yap
2001, Leung 1993, Kieser
2002
Need for 518 109 21 1973-2000 14 Gardeil 1994, Golan
hysterectomy 1980, Plauche 1984,
Shipp 1999, Lydon-
Rochelle 2001,
Blanchette 2001,
Caughey 1999, Esposito
2000, Yap 2001, Leung
1993, Kieser 2002,
Menihan 1998,
Lieberman 2001, Flamm
1990
Death, 313 1 0.32 1975-2000 11 Gardeil 1994, Plauche
industrialized 1984, Shipp 1999,
countries Caughey 1999, McMahon
 1996, Yap 2001, Leung
1993, Kieser 2002,
Flamm 1994, Lieberman
2001, Spaulding 1979
Death, 524 41 8 1966-1980 3 Golan 1980, Mokgokong
developing 1976, Rahman 1985
countries

Fetal and Neonatal Consequences of Uterine Rupture

Fetal hypoxia or anoxia

Leung et al found that 5 of 99 neonates (5%) born to women who had uterine ruptures developed
neonatal asphyxia (defined as umbilical-artery pH <7 with seizures and multiorgan dysfunction).
No neonate had clinically significant perinatal morbidity when delivery was accomplished within
17 minutes of an isolated and prolonged deceleration of fetal heart rate. If severe late
decelerations preceded prolonged deceleration, perinatal asphyxia was observed as soon as 10
minutes from the onset of the prolonged deceleration to delivery.73

In a study by Menihan, 6 of 11 fetuses born after uterine rupture had bradycardias occur between
18-37 minutes prior to delivery. Although the rate of fetal acidosis was high (91%), no
permanent neurologic injuries or neonatal deaths occurred.76

In 23 cases of uterine rupture, Bujold and Gauthier found that, even with rapid (<18-min)
intervention between prolonged deceleration in fetal heart rate and delivery, 2 neonates
developed hypoxic-ischemic encephalopathies with impaired motor development. They
concluded that, though rapid intervention did not always prevent severe metabolic acidosis and
serious neonatal disease, it probably did limit the occurrence of neonatal death.60

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 3.73

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.76

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).76
Kieser and Baskett found an NICU admission rate for newborns 45% (8 of 18) after uterine
rupture.83 Landon et al found a similar NICU admission rate of 32% (46 of 144 newborns) after
uterine rupture.30

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.42

Leung et al reported that 6 perinatal deaths (6%) occurred among 99 patients who had uterine
rupture.73 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.39 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.30

Maternal Consequences of Uterine Rupture

Severe maternal blood loss or anemia

Cowan et al found that, among 5 patients who developed uterine rupture, mean blood loss was
1,500 mL and great enough to be symptomatic in 3 patients (60%).84 In a study by Shipp et al,
25% (7 of 28 women) who had uterine rupture during a TOL after a previous cesarean delivery
received a blood transfusion.34

Kieser and Baskett found that 44% (8 of 18 patients) who had a complete uterine rupture
required blood transfusion.83 Leung et al found that 29% of patients (29 of 99) who had uterine
rupture required a blood transfusion.73

Hypovolemic shock

In a study of 93 uterine ruptures by Golan et al, 29% of women who experienced a uterine
rupture developed signs and symptoms of hypovolemic shock.2 Rahman et al reported that, of 96
women who had uterine rupture, 33 (34%) developed hypovolemic shock.5

These modern rates of maternal shock after uterine rupture appear to be reduced compared with
the early rates reported in a 53-year review of the literature by Eden et al; their observed
incidence was 46% (11 of 24 cases).79

Maternal bladder injury

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).39 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.34

In a study by Kieser and Baskett, 17% of women (3 of 18) who developed uterine rupture had a
cystotomy.83 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%.73

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.85 Kieser and Baskett found that 1 of 18 patients (6%) who developed
complete uterine rupture required hysterectomy.83 Blanchette et al reported that hysterectomy
was necessary in 17% of women (2 of 12) who developed uterine rupture.42 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.73

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%.5,4

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.73

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

Management of the Ruptured Uterus

Treatment

The most critical aspects of treatment in the case of uterine rupture are establishing a timely
diagnosis and minimizing the time from the onset of signs and symptoms until the start of
definitive surgical therapy. Once a diagnosis of uterine rupture is established, the immediate
stabilization of the mother and the delivery of the fetus are imperative.

As a rule, the time available for successful intervention after frank uterine rupture and before the
onset of major fetal morbidity is only 10-37 minutes.73,76,82,42,86 Therefore, once the diagnosis of
uterine rupture is considered, all available resources must quickly and effectively be mobilized to
successfully institute a timely surgical treatment that results in favorable outcomes for both the
newborn and the mother.

After the fetus is successfully delivered, the type of surgical treatment for the mother should
depend on the following factors:

 Type of uterine rupture

 Extent of uterine rupture
 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:

 Desire for future childbearing

 Low transverse uterine rupture
 No extension of the tear to the broad ligament, cervix, or paracolpos
 Easily controllable uterine hemorrhage
 Good general condition
 No clinical or laboratory evidence of an evolving coagulopathy

Hysterectomy should be considered the treatment of choice when intractable uterine bleeding
occurs or when the uterine rupture sites are multiple, longitudinal, or low lying.

Because of the short time available for successful intervention, the following 2 premises should
always be kept firmly in mind: (1) Maintain a suitably high level of suspicion regarding a
potential diagnosis of uterine rupture, especially in high-risk patients, and (2) when in doubt, act
quickly and definitively.

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:

 Multiple previous cesarean deliveries

 Previous classic midline cesarean delivery
 Previous low vertical cesarean delivery
 Previous low transverse cesarean delivery with a single-layer hysterotomy closure
 Previous cesarean delivery with an interdelivery interval of less than 2 years
 Previous low transverse cesarean delivery with a congenitally abnormal uterus
 Previous cesarean delivery without a previous history of a successful vaginal birth
 Previous cesarean delivery with either labor induction or augmentation
 Previous cesarean delivery in a woman carrying a macrosomic fetus weighing >4000 g
 Previous uterine myomectomy accomplished by means of laparoscopy or laparotomy

If a gravida falls into any of these categories, her risk for uterine rupture is increased to more
than 1 in 200, and a clinical management plan should be specifically designed with this increased
risk in mind.

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.

Keywords
uterine rupture, pregnancy-related uterine rupture, ruptured uterus, fetal anoxia, uterine scar
dehiscence, uterine scar, prior cesarean section, prior cesarean delivery, vaginal birth after
cesarean delivery, VBAC, myomectomy, congenital uterine anomalies, hysterotomy closure,
induced labor, labor induction, grand multiparity, prior uterine myomectomy, fetal macrosomia,
uterine trauma, neglected labor, breech extraction, uterine instrumentation, oxytocin, labor
augmentation

More on Uterine Rupture in Pregnancy

References
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Further Reading
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Keywords
uterine rupture, pregnancy-related uterine rupture, ruptured uterus, fetal anoxia, uterine scar
dehiscence, uterine scar, prior cesarean section, prior cesarean delivery, vaginal birth after
cesarean delivery, VBAC, myomectomy, congenital uterine anomalies, hysterotomy closure,
induced labor, labor induction, grand multiparity, prior uterine myomectomy, fetal macrosomia,
uterine trauma, neglected labor, breech extraction, uterine instrumentation, oxytocin, labor
augmentation

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Contributor Information and Disclosures

Author

Gerard G Nahum, MD, FACOG, FACS, Adjunct Associate Professor of Obstetrics and

Gynecology, Uniformed Services University of the Health Sciences; Head of Global Clinical
Development, Women's Healthcare U.S., Bayer HealthCare Pharmaceuticals
Gerard G Nahum, MD, FACOG, FACS is a member of the following medical societies:
American Association of Gynecologic Laparoscopists, American College of Obstetricians and
Gynecologists, American College of Surgeons, American Society for Reproductive Medicine,
and Association of Professors of Gynecology and Obstetrics
Disclosure: Algorithmic Bioscience Inc. Ownership interest Board membership; Biomedical
Decision Support Inc. Ownership interest Board membership

Coauthor(s)

Krystle Quynh Pham, MD, FACOG, Attending Faculty, Department of Obstetrics and

Gynecology, Santa Clara Valley Medical Center; Clinical Instructor, Department of Obstetrics
and Gynecology, Stanford University
Krystle Quynh Pham, MD, FACOG is a member of the following medical societies: American
Association for the Advancement of Science, American College of Obstetricians and
Gynecologists, American Medical Association, American Medical Women's Association,
American Society for Reproductive Medicine, Association of Professors of Gynecology and
Obstetrics, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor
Bryan D Cowan, MD, Professor and Chairman, Department of Obstetrics and Gynecology,
University of Mississippi College of Medicine; Consulting Staff, Department of Obstetrics and
Gynecology, Veterans Affairs Medical Center; Medical Director, Wiser Hospital for Women,
University of Mississippi Medical Center
Bryan D Cowan, MD is a member of the following medical societies: American Association of
Gynecologic Laparoscopists, American College of Obstetricians and Gynecologists, American
Gynecological and Obstetrical Society, American Medical Association, American Society for
Reproductive Medicine, Association of Professors of Gynecology and Obstetrics, Central
Association of Obstetricians and Gynecologists, Endocrine Society, Sigma Xi, Society for
Assisted Reproductive Technologies, Society for Gynecologic Investigation, Society for the
Study of Reproduction, and Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Managing Editor

Richard S Legro, MD, Professor, Department of Obstetrics and Gynecology, Division of

Reproductive Endocrinology, Pennsylvania State University College of Medicine; Consulting
Staff, Milton S Hershey Medical Center
Richard S Legro, MD is a member of the following medical societies: American College of
Obstetricians and Gynecologists, American Society for Reproductive Medicine, Endocrine
Society, Phi Beta Kappa, and Society of Reproductive Surgeons
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical

Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of
Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

David Chelmow, MD, Professor and Chair, Department of Obstetrics and Gynecology, Virginia
Commonwealth University Medical Center
David Chelmow, MD is a member of the following medical societies: American College of
Obstetricians and Gynecologists, American Medical Association, Association of Professors of
Gynecology and Obstetrics, Massachusetts Medical Society, Phi Beta Kappa, Sigma Xi, Society
for Gynecologic Investigation, and Society for Medical Decision Making
Disclosure: Nothing to disclose.
 medscapecme

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