Uterine rupture: After previous cesarean birth

INTRODUCTION — Uterine rupture is a life-threatening pregnancy complication for both the mother and fetus. Most uterine ruptures in resource-rich countries are associated with a trial of labor after cesarean birth (TOLAC). This topic will review clinical findings, risk factors, prediction, and management of uterine rupture in patients attempting TOLAC. Other important issues related to TOLAC are discussed separately:

●(See "Choosing the route of delivery after cesarean birth".)

●(See "Trial of labor after cesarean birth: Intrapartum management".)

●(See "Cervical ripening and induction of labor after a prior cesarean birth".)

In resource-limited countries, many uterine ruptures are related to obstructed labor and lack of access to operative delivery. Rupture of the unscarred uterus is also discussed separately. (See "Uterine rupture: Unscarred uterus".)

TERMINOLOGY: RUPTURE VERSUS DEHISCENCE

●Rupture – We use the term "rupture" to refer to a clinically significant uterine disruption, which can be defined as a complete disruption of all uterine layers, including the serosa, leading to changes in maternal or fetal status.

●Dehiscence – We use the term "dehiscence" to refer to a clinically occult uterine disruption (or uterine window), which can be loosely defined as an incomplete disruption that is not readily discernible by signs or symptoms and does not lead to any serious maternal or neonatal consequences. It is often discovered incidentally at cesarean birth.

Others have used the terms rupture and dehiscence interchangeably.

PATHOPHYSIOLOGY OF MYOMETRIAL WOUND HEALING — Little is known about the histopathology of myometrial wound healing and its effects on scar strength and other biomechanical properties. A systematic review of human and animal studies found that the histology of uterine scars was characterized by disorganized smooth muscle, fibrosis with collagen fibers, and few endometrial glands [1]. The inflammation phase of the uterine healing process was important for optimal organization and maturation of collagen, and a mathematical model indicated that collagen fiber orientation was the most important factor for the biomechanical properties of a scarred uterus [2].

INCIDENCE — The overall incidence of uterine rupture in patients with a prior cesarean birth is approximately 0.3 percent (3 ruptures per 1000 deliveries), regardless of mode of delivery in the pregnancy in which the rupture occurs. However, uterine rupture is far more common among women who undergo a trial of labor after cesarean (TOLAC) than in those who undergo planned repeat cesarean delivery (PRCD) [3]. The authors of a systematic review estimated that 468 uterine ruptures would occur in a hypothetical group of 100,000 patients of any gestational age planning TOLAC compared with an estimated 26 uterine ruptures among 100,000 women planning PRCD [4].

RISK FACTORS

Factors that increase the risk of rupture — The primary risk factors for uterine rupture after a previous cesarean birth are:

●Previous uterine rupture – Data are limited [5,6]. In a case series including 59 pregnancies among 37 pregnant patients with a prior uterine rupture (clinically apparent complete scar separation), there were no cases of uterine rupture, but 19 percent of the patients had a uterine dehiscence (incomplete uterine scar separation with intact serosa) noted at the time of repeat cesarean birth [6]. In the 75 pregnancies among 50 patients with a history of uterine dehiscence in a prior pregnancy, there was one incidental uterine rupture noted when the patient with a unicornuate uterus and three prior cesarean births went into labor prior to a scheduled cesarean birth. Of note, the authors' routine practice in this case series was to perform repeat cesarean births at 36 to 37 weeks in patients with a prior uterine rupture and between 37 and 39 weeks in those with a prior uterine dehiscence. (See 'Recurrence risk' below.)

●Previous fundal or high vertical hysterotomy – The incidence of rupture is higher in patients with a previous high vertical, especially fundal, hysterotomy. This includes an inverted T or J incision or extension of a low transverse incision into the upper uterine segment. After a previous classical (fundal) cesarean hysterotomy, the reported risk of rupture varies widely in the literature, from 1 to 12 percent [7].

•In the prospective National Institutes of Health (NIH) Maternal-Fetal Medicine Units Network Study of almost 46,000 patients with singleton gestations undergoing a trial of labor after cesarean birth (TOLAC), the uterine rupture rate was 1.9 percent (2 in 105) in those with a prior classical, inverted T, or J incision who either presented in advanced labor or refused a repeat cesarean birth versus 0.7 percent (105 in 14,483) in those with a prior low transverse incision [8].

•In a cross-sectional analysis of over 25,000 patients in the 2016-2019 National Inpatient Sample database who had a classical cesarean birth followed by a live singleton birth at ≥24 weeks, uterine rupture occurred in 10.6 percent of the 1785 patients who experienced labor compared with 0.3 percent of those who did not [9].

●Patients with a previous low vertical hysterotomy – Although few studies have evaluated the risk of uterine rupture in patients with a previous low vertical incision, these studies have reported similar rates of uterine rupture as in patients with a low transverse incision [10,11].

●Induction – The incidence of rupture is higher in patients with a prior cesarean birth who undergo induction than in those who experience spontaneous labor (2010 NIH state-of-the science statement: 1.5 versus 0.8 percent [12]; 2015 systematic review: rupture/dehiscence odds ratio [OR] 1.62, 95% CI 1.13-2.31 [13]). However, the incidence varies among institutions due to variations in indications for delivery and induction protocols (eg, choice of drugs, dosing, use of mechanical cervical ripening).

•Misoprostol – The risk of rupture with use of misoprostol was sufficiently high (approximately 5 to 10 percent [14-16]) in a few small studies that the American College of Obstetricians and Gynecologists advised against its use for labor induction in patients at term with a previous cesarean birth [17]. Other prostaglandins have also been associated with an increased risk for uterine rupture, although methodologic limitations to these data make it more difficult to define the level of risk associated with their use. Some guidelines allow use of prostaglandin E2 for cervical ripening in patients with a previous cesarean birth. These data and guidelines are reviewed separately. (See "Cervical ripening and induction of labor after a prior cesarean birth", section on 'Use of prostaglandins'.)

•Oxytocin alone – Induction of labor with oxytocin alone appears to be associated with only a marginally increased risk for uterine rupture (risk of rupture 1.1 percent in two studies [18,19]). Most experts do not consider induction of labor with oxytocin contraindicated in patients with a previous cesarean birth. (See "Cervical ripening and induction of labor after a prior cesarean birth", section on 'Issues related to use of oxytocin'.)

Data on mechanical methods of cervical ripening in this population are limited by small sample size and retrospective analysis. These data are generally reassuring, but uterine ruptures have occurred, as they have occurred during labors in most other settings. (See "Cervical ripening and induction of labor after a prior cesarean birth", section on 'Issues related to use of mechanical methods of cervical ripening'.)

●Labor – The incidence of rupture is higher in patients who undergo a TOLAC than in women who undergo planned repeat cesarean delivery (PRCD; at term: 0.78 percent with TOLAC and 0.02 percent with PRCD in the 2010 NIH state-of-the science statement [12]). Risk factors for rupture during labor include a low Bishop score on admission to the labor and delivery unit; dystocia [20-22], particularly at advanced dilation (>7 cm) [23]; slower cervical dilation in the first stage of labor; and a longer second stage [22].

Observational studies have generally reported that augmentation of labor with oxytocin during TOLAC is associated with a higher risk of uterine rupture than spontaneous labor [8,24-27]. However, there is uncertainty regarding the relative and absolute risks of rupture, thus cautious use of oxytocin augmentation is considered acceptable in the management of patients with a prior cesarean birth. Higher doses of oxytocin may be associated with an increased risk of uterine rupture [28], but there is no consensus on an absolute threshold dose that should not be exceeded.

Possible risk factors — Factors inconsistently reported to be associated with an increased risk of rupture include [29-37]:

●Increasing maternal age

●Gestational age >40 weeks

●Birth weight >4000 grams

●Interdelivery interval less than approximately 18 months (and particularly <6 months)

●Single-layer uterine closure, especially if locked

●More than one previous cesarean birth

●Previous second-trimester cesarean birth

None of these possible risk factors, alone or in combination, is sufficiently reliable to be clinically useful for prediction of rupture. (See "Cesarean birth: Surgical technique", section on 'Single- versus double-layer closure of lower uterine segment incisions'.)

One study observed that uterine rupture in the subsequent pregnancy occurred more frequently among patients whose primary cesarean birth was at 20 to 26 weeks of gestation versus at term (8 in 456 [1.8 percent] versus 38 in 10,505 [0.4 percent], OR 4.9, 95% CI 2.3-10.6), and the relationship was not confounded by incision type at the index delivery or induction or augmentation in the subsequent pregnancy [37]. In contrast, other studies have not found an association between prior preterm cesarean birth and an increased risk of uterine rupture [38,39].

In a systematic review of studies, the frequency of uterine rupture during a trial of labor after one versus two previous cesarean births was 0.72 and 1.59 percent, respectively (OR 0.42, 95% CI 0.29-0.60); however, the definition of rupture varied among studies [34]. The marginal increase in the rate of rupture with two prior cesarean births does not preclude TOLAC. Data are limited regarding rupture rates in patients with more than two prior cesarean births undergoing TOLAC [40]. (See "Choosing the route of delivery after cesarean birth", section on 'Two prior low transverse uterine incisions'.)

Factors that decrease the risk of rupture — A prior vaginal delivery, either before or after the prior cesarean birth, significantly reduces, but does not eliminate, the risk of uterine rupture (OR 0.26-0.62 for prior vaginal delivery, OR 0.52 for prior successful TOLAC) [29].

PREDICTING UTERINE RUPTURE — There is no reliable method for predicting uterine rupture in patients with a prior cesarean birth. Because of the great concern for uterine rupture in patients undergoing a trial of labor after cesarean birth, investigators have conducted sophisticated analyses with the goal of using risk factors to predict the likelihood of uterine rupture in specific patients. A number of predictive models for uterine rupture using a combination of risk factors have been described, but none has proven reliable or clinically useful [29,30].

Antepartum imaging of the hysterotomy scar — In our clinical practice, we do not routinely measure the lower uterine segment thickness in patients with a prior cesarean birth. The utility of measuring the lower uterine segment thickness was evaluated in a multicenter randomized trial [41]. In the group randomly assigned to ultrasound assessment, cesarean birth was encouraged if the thickness was ≤3.5 mm at 36 to 38 weeks of gestation and a trial of labor was encouraged if the thickness was >3.5 mm; thickness was not measured in the control group. The composite risk of adverse pregnancy outcome was similar in the group in which the sonographic measurement guided recommendations and the control group (3.4 versus 4.3 percent, relative risk [RR] 0.78, 95% CI 0.15-1.19). The incidence of uterine rupture in the study and control groups was 0.4 percent (5 out of 1472) and 0.9 percent (13 out of 1476), respectively (RR 0.43; 95% CI 0.15–1.19). Given that this trial was underpowered, we believe that further prospective research regarding the use of lower uterine segment measurements and its effect on obstetric outcomes is necessary before this sonographic technique becomes part of standard obstetric care.

If scar thickness is measured, at least three measurements of the lower uterine segment thickness should be obtained near term and the lowest value reported [42]. One caliper is placed at the interface between the urine and the bladder wall and the other is placed at the interface between amniotic fluid (or fetal scalp) and decidua. Either a transabdominal or transvaginal approach can be used. The 10^th, 25^th, and 50^th percentiles of lower uterine segment thickness are approximately 2, 2.3, and 3.2 mm, respectively, near term [42]. There are no data defining normal myometrial thickness at sites other than the lower uterine segment.

Although an intact, thick scar is reassuring of the integrity of the repair while a thin scar or a defect is worrisome that the area of the scar might rupture, a systematic review (21 studies) found that no myometrial thickness threshold value performed adequately to use in clinical practice to predict whether a hysterotomy scar will rupture or remain intact [43]. The quantitative risk of rupture associated with scar thickness has not been determined. A thin lower uterine segment has a low positive predictive value for rupture [44], and patients with normal lower uterine segment thickness have gone on to rupture their uterus when in labor [45,46].

Despite limitations of available data, some authors consider a full lower uterine segment thickness <2 mm predictive of an increased risk of rupture or dehiscence [47] and incorporate this information into clinical counseling [42,43].

Interpregnancy imaging of the hysterotomy scar — U or V wedge-shaped hypoechoic uterine defects (also called niches) have been observed on imaging studies several months after birth. On ultrasound, the defect appears as a hypoechogenic or nonechogenic area in a region of the myometrial thinning [48,49]. The defect is typically covered by a thin layer of myometrium and/or peritoneum. Hysteroscopic confirmation is diagnostic. Nonpregnant patients with these defects may be asymptomatic or present with lower abdominal pain, dysmenorrhea, or abnormal uterine bleeding (often postmenstrual spotting) [50,51].

The natural history of uterine scar defects identified months after delivery in patients who subsequently become pregnant is unknown and no guidelines are available for management of patients with these defects, as available data are limited by small numbers. Management should therefore be decided on a case-by-case basis.

Repair of the defect, including excision of the fibrotic tissue and vaginal or laparoscopic closure of the anterior uterine wall, has been described, and subsequent successful pregnancies delivered by planned cesarean have been reported [50,52,53], but the need for this approach has not been proven. One study performed ultrasound examinations of the uterine scar at 6 to 9 months postpartum in 162 patients who delivered by cesarean, and then collected delivery outcome data for those who became pregnant [54]. Results of the ultrasound study were not available to the patient or clinician. In the first subsequent pregnancy after ultrasound examination, most (10 out of 13) patients with deep uterine scar defects had no scar problems at birth: Four underwent uncomplicated vaginal birth, two had an assisted vaginal birth, and four had a cesarean birth with no signs of uterine dehiscence or rupture. Four uterine dehiscences/ruptures were detected during the 26 repeat cesarean births: One occurred among the 19 patients with an intact scar or shallow scar defect and three occurred among the seven patients with deep scar defects.

CLINICAL MANIFESTATIONS OF UTERINE RUPTURE

Patient presentation

Antepartum and intrapartum — Signs of uterine rupture may include some or all of the following, listed from most to least common [55]:

●Abnormal fetal heart rate (FHR) – Sudden development of a concerning category II or a category III FHR pattern is consistently reported in patients with uterine rupture, but no FHR pattern is pathognomonic of rupture. The most common FHR abnormality in rupture is fetal bradycardia [56,57], which may be sudden or preceded by significant variable or prolonged decelerations. Category III FHR tracings may occur in the hour preceding diagnosis of rupture [58]. Given these observations, continuous FHR monitoring is routinely recommended during a trial of labor after cesarean (TOLAC) [17].

●Abdominal pain – Rupture may be associated with the sudden onset of abdominal pain, but this pain may be partially masked by neuraxial analgesia administered for management of labor pain. Patients who attempt TOLAC with epidural anesthesia may ask for additional epidural doses and require frequent dosing because of pain from an unrecognized rupture [59]. Therefore, clinicians should be mindful that the acute onset of pain after previously effective neuraxial anesthesia may be a sign of uterine rupture [60].

●Vaginal bleeding – Vaginal bleeding may occur but is not a cardinal symptom as it may be modest or even absent despite major intraabdominal hemorrhage.

●Loss of station of the fetal presenting part, if the fetus is partially extruded through the rupture or possibly from myometrial relaxation.

●Hematuria, if the rupture extends into the bladder.

●Hemodynamic instability – Intraabdominal hemorrhage from the site of rupture can lead to rapid maternal hemodynamic deterioration (hypotension and tachycardia).

●Changes in contraction patterns – Both increased uterine contractility and loss of uterine tone have been described in association with uterine rupture [61]. Another external tocodynamometry finding that has been reported is a gradual decrease in the amplitude of consecutive contractions, the so-called "staircase sign" [62]. Nevertheless, a consistent change in uterine contraction patterns at the time of uterine rupture has not been identified, and utilization of an intrauterine pressure catheter may fail to show any abnormality [63].

Postpartum — In postpartum patients, occult uterine rupture that occurred during birth is characterized by pain and persistent vaginal bleeding despite use of uterotonic agents. Hematuria may occur if the rupture extends into the bladder.

Findings on imaging — Imaging is generally not performed intrapartum because uterine rupture is an obstetric emergency. If the fetal and maternal conditions are stable and rupture is suspected, assessment with sonography may be used to look for hemoperitoneum [64].

Patients who are not in labor may undergo imaging studies of the uterus because of mild symptoms or as part of a trauma evaluation. Imaging studies may show one or more of the following: disruption of the myometrium [65], a hematoma adjacent to the hysterotomy scar [66], extrauterine fluid-distended fetal membranes [65,67,68], free peritoneal fluid [65,69], anhydramnios [70], an empty uterus [69,71], fetal parts outside of the uterus [69,72], and/or fetal demise.

Computed tomography or magnetic resonance imaging performed as part of a trauma evaluation may detect peritoneal air, as well as pathology associated with rupture, such as ileus [73] and abscess [74].

Intraoperative findings — A uterine rupture is usually immediately recognized upon opening the abdomen. Hemoperitoneum is usually present and fetal parts or membranes are often visible.

DIAGNOSIS

●When to suspect rupture – Uterine rupture should be suspected in patients undergoing trial of labor after cesarean birth with one or more of the following signs and symptoms: a concerning category II or category III fetal heart rate (FHR) tracing, hemodynamic instability, sudden or worsening abdominal pain, loss of fetal station, vaginal bleeding, hematuria, or changes in uterine contraction patterns. A preoperative provisional diagnosis of rupture is not critical since urgent delivery is often indicated in these patients because of concerning FHR changes and/or hemodynamic instability.

●Criteria for definitive diagnosis – The diagnosis of uterine rupture is based on identification of a complete disruption of all uterine layers (including the serosa) on imaging or at laparotomy.

Differential diagnosis — The differential diagnosis of uterine rupture is based on the presenting signs and symptoms.

●In patients with acute abdominal pain, vaginal bleeding, and a concerning category II or a category III FHR tracing, abruption is the leading diagnosis and may not be distinguishable from uterine rupture prior to laparotomy. (See "Acute placental abruption: Pathophysiology, clinical features, diagnosis, and consequences", section on 'Clinical features of acute abruption'.)

●In patients with acute abdominal pain and hemodynamic instability without vaginal bleeding, the possibility of severe intraabdominal bleeding from any source must be considered, particularly hepatic rupture, which can occur in preeclampsia with severe features and HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets). In contrast to uterine rupture, preeclampsia with severe features and HELLP syndrome do not have an acute onset and are often associated with hypertension, proteinuria, epigastric or right upper quadrant pain, and low platelets. Laparotomy after maternal stabilization allows both diagnosis and therapeutic intervention of hepatic rupture [75]. (See "Preeclampsia: Clinical features and diagnosis" and "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)".)

●Neuraxial anesthesia-induced sympathetic blockade can cause a decrease in systemic vascular resistance, peripheral blood pooling with decreased venous return to the heart, or both, which can result in maternal hypotension and FHR abnormalities. These changes have a temporal relationship with administration of the anesthetic drug and, in contrast to uterine rupture, the changes are transient and rapidly respond to administration of fluids and/or a vasopressor, and contraction frequency is not affected. (See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Hypotension'.)

MANAGEMENT

Management of patients in whom rupture is suspected before delivery — Uterine rupture may be suspected antepartum or intrapartum because of the sudden onset of abdominal pain accompanied by fetal heart rate (FHR) abnormalities and maternal hemodynamic instability, as discussed above (see 'Antepartum and intrapartum' above). FHR abnormalities, maternal hemodynamic instability, and severe abdominal pain generally require urgent delivery, regardless of the underlying etiology.

●Stabilize patients with hemodynamic instability – Hemodynamically unstable patients should be stabilized with fluids and blood transfusion, as appropriate, and prepared urgently for cesarean birth. Patient preparation and fluid and transfusion management are similar to that for undelivered pregnant patients with disseminated intravascular coagulation. (See "Disseminated intravascular coagulation (DIC) during pregnancy: Management and prognosis", section on 'Management of hemodynamically unstable patients'.)

●Notify the anesthesia service – The anesthesia staff should be notified for assistance with patient management and to provide anesthetic support for delivery. The choice of regional versus general anesthesia is based on the clinical stability of the patient and urgency of delivery. Spinal analgesia or a newly placed epidural are generally inadvisable in patients who require urgent delivery because of the time required to achieve an adequate level and are contraindicated in patients with a severe bleeding diathesis because of the risk of epidural or spinal hematoma.

●Notify the neonatology service – Personnel who are adequately trained in neonatal resuscitation should be readily available to perform neonatal resuscitation, if needed.

●Prepare for unexpected findings at laparotomy – The choice of abdominal incision is based on the leading diagnoses and suspicion for other etiologies as well as provider preference [76]. A Pfannenstiel incision only provides good exposure of the lower uterine segment and pelvis. Many consider a midline incision preferred if hemoperitoneum is suspected because it provides good exposure of the uterine fundus (which extends above the umbilicus by the late second trimester) and for comprehensive abdominal exploration.

Management of patients with uterine rupture at laparotomy

Repair versus hysterectomy — A major decision facing the surgeon in any case of uterine rupture is whether the uterus can be repaired or must be removed.

Hysterectomy — Obviously, the patient's desire for future pregnancies needs to be considered, but this desire may be superseded by the need for prompt, lifesaving measures, such as hysterectomy. The decision to perform hysterectomy is based on a combination of factors, including the patient's desire for future pregnancy, the patient's intraoperative hemodynamic and anesthetic stability, whether the uterine defect can be repaired, whether hemostasis can be achieved, and the skill of the surgeon for repairing a complicated rupture. The technique is reviewed separately. (See "Peripartum hysterectomy for management of hemorrhage".)

Uterine repair — The goals of conservative surgery are to repair the uterine defect, control hemorrhage, identify damage to other organs (eg, urinary tract), minimize early postsurgical morbidity, and reduce the risk of complications in future pregnancies.

The surgeon can try to close the uterine defect using a technique similar to that for traditional hysterotomy closure, with additional interventions as needed to achieve hemostasis. The optimal repair technique has not been established due to the rarity of uterine rupture, variability in location and extent of damage, and scarcity of long-term follow-up data. In general, medial ruptures that do not involve the adnexal vasculature can often be repaired successfully by primary closure, while lateral ruptures and very large ruptures require ligation of the adnexal vasculature, and often hysterectomy.

Following delivery of the fetus and placenta, primary single- or double-layer closure with a delayed absorbable suture is a straightforward, rapid technique for repairing the rupture and closing the incision [72,77-79]. The optimal technique for uterine closure at the time of cesarean (single- versus double-layer closure, locking versus unlocked closure) is controversial (see "Cesarean birth: Surgical technique"); no trials have addressed the optimal closure after uterine rupture. Whichever closure technique is used, the goal is to adequately close the defect and obtain hemostasis. Several other techniques for primary closure and innovative approaches to avoid hysterectomy have been described in numerous case reports. These reports often come from countries where rupture of the gravid uterus is more common but also include ruptures unrelated to previous cesarean birth [70,72,77,78,80-82].

Management of coexistent complications

●Atony – Concomitant uterine atony may result in persistent bleeding, which is managed by standard methods (uterotonic agents, hemostatic sutures, intrauterine balloon tamponade or low-level vacuum to induce uterine contraction [77]). (See "Postpartum hemorrhage: Management approaches requiring laparotomy".)

●Bladder trauma – Uterine rupture may lead to bladder injury [83]. If the uterine laceration extends to the bladder or a ureteral injury is suspected, we suggest an intraoperative consultation with an experienced urologic surgeon (eg, urologist, gynecologic oncologist) [84]. Large anterior ruptures that extend into the bladder are repaired in two layers followed by urethral and/or suprapubic catheter placement for up to 14 days [83]. (See "Urinary tract injury in gynecologic surgery: Identification and management", section on 'Bladder injury'.)

●Pelvic organ injury – Injuries to blood vessels and other pelvic organs are repaired using standard techniques; intraoperative consultation with an experienced pelvic surgeon, vascular surgeon, or general surgeon is advised, as needed. (See "Complications of gynecologic surgery".)

●Placenta accreta spectrum – Uterine rupture may be associated with placenta accreta spectrum [67,85-92]. Management of placenta accreta spectrum is reviewed separately. (See "Placenta accreta spectrum: Management".)

OUTCOME

Maternal mortality and morbidity

●Mortality – The 2010 National Institutes of Health (NIH) Consensus Development Conference statement on vaginal birth after cesarean birth found no reports of maternal death associated with uterine rupture [12], but a 10-year review of severe maternal outcomes in Canada reported four maternal deaths among 1879 cases of uterine rupture in patients with no major preexisting medical conditions (1 death per 500 uterine ruptures) [93].

●Morbidity – Maternal morbidity was assessed in a literature review of 880 cases of uterine rupture during 142,075 trials of labor after cesarean birth (TOLAC) [94]. The two major morbidities associated with uterine rupture were transfusion of packed red blood cells and need for hysterectomy; the frequency of these complications after rupture were not reported.

Others have reported that 14 to 33 percent of patients with a uterine rupture undergo hysterectomy; comorbidities of hysterectomy include operative injuries such as urinary tract or bowel lacerations, blood transfusion, and postoperative infection. (See "Peripartum hysterectomy for management of hemorrhage".)

Perinatal mortality and morbidity — The reported perinatal death rate associated with uterine rupture ranges from 5 to 26 percent [12,95-100]. Death is most likely in cases of placental separation and/or fetal extrusion [96,100,101].

●In a prospective study by the NIH Maternal-Fetal Medicine Units Network, the incidence of neonatal hypoxic-ischemic encephalopathy associated with uterine rupture was seven cases among 114 infants born after uterine rupture (6 percent) and two of these seven neonates died [8]. There were no neonatal deaths or cases of hypoxic-ischemic encephalopathy among infants of women undergoing planned repeat cesarean birth. Prompt intervention after uterine rupture did not always prevent severe acidosis and neonatal morbidity and mortality [96].

●In two studies of TOLAC, neonatal morbidity increased when the interval between recognition of fetal heart rate abnormalities and delivery was ≥18 minutes [101,102]. This supports recommendations by many organizations that TOLAC should be performed in facilities capable of performing an emergency cesarean birth [103-105]. In particular, planned TOLAC in the home should be avoided and has been associated with higher rates of low Apgar scores, neonatal seizures [106,107], and neonatal death [108].

The key message is that delivery should be accomplished as soon as safely possible if a uterine rupture is suspected. Eighteen minutes should not be considered a reliable threshold whereby later delivery is certain to be associated with adverse neonatal outcome and earlier delivery is certain to be without risk. Reports have described hypoxic-ischemic encephalopathy in 2 of 23 neonates with an intervention time <18 minutes [96] and two deaths in infants delivered at 10 minutes [100]. It is not surprising that prompt intervention will not always successfully prevent these adverse outcomes because outcome severity depends largely on the extent of placental separation following uterine rupture. This exists as a spectrum varying from no separation to total placental abruption, and partial degrees of separation may increase over time. At its worst, acute total placental separation as an immediate consequence of rupture would require delivery of the fetus almost immediately to reduce the risk of fetal death or hypoxic-ischemic encephalopathy, a nearly impossible task in any delivery unit.

RECURRENCE RISK — Data on future pregnancies after repair of a ruptured scarred uterus are derived from small case series. Reports of the risk of recurrent rupture vary widely (range 0 to 33 percent) [109]. The risk of recurrent rupture appears to be highest when the previous rupture was in the fundus or longitudinal (in one study: 3 out of 3 versus 2 out of 9 with transverse rupture [5]). Recurrent rupture can occur as early as the second trimester and is difficult to predict. (See 'Predicting uterine rupture' above.)

A systematic review of 13 studies including 365 pregnancies after a previous complete uterine rupture (defined as destruction of all layers of the uterus, including the serosa) reported the following findings [109]:

●Incidence of recurrent uterine rupture: 10 percent (95% CI 6-17)

●Mean gestational age at the time of recurrent uterine rupture: 32.5 weeks (95% CI 29.9-35.1)

●Mean gestational age at the time of delivery without recurrent uterine rupture: 35.8 weeks (95% CI 34.9-36.6)

●Maternal mortality rate: 5 percent (95% CI 2-11)

●Neonatal mortality rate: 5 percent (95% CI 3-10)

Limitations of the analysis included possible publication bias, lack of uniformity in the management of pregnancies after uterine rupture, and missing information (eg, whether patient had a previous cesarean or myomectomy scar, uterine location of previous rupture, whether patient labored in the subsequent pregnancy, maternal morbidity in subsequent pregnancy).

MANAGEMENT OF SUBSEQUENT PREGNANCIES — Most obstetricians attempt to reduce the risk of recurrent rupture by recommending cesarean birth for subsequent pregnancies and scheduling the delivery before the onset of labor.

Timing of delivery — In patients with uterine rupture in a previous pregnancy, the American College of Obstetricians and Gynecologists suggests delivery at 36+0 to 37+0 weeks of gestation, with individualization based on the clinical setting [17]. We generally agree with this recommendation but perform delivery before 36+0 weeks of gestation on a case-by-case basis, considering factors such as whether there has been preterm labor in the current pregnancy and whether there is a history of preterm or antepartum uterine rupture in a prior pregnancy.

For patients with a history of a uterine dehiscence without full thickness rupture, we generally perform a repeat cesarean at 37+0 to 38+0 weeks (prior to the onset of labor), but this is largely based on expert opinion.

We administer a course of antenatal corticosteroids 48 hours before planned preterm delivery in patients who have not received a previous course. (See "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery", section on '34+0 or more weeks'.)

Recurrent rupture — If recurrent rupture is suspected, emergency cesarean birth is indicated. The urgency of delivery depends on the obstetrician's assessment of the maternal and fetal status and his/her assessment of the likelihood of the diagnosis versus other causes of abdominal pain, fetal heart rate abnormalities, vaginal bleeding, and hemodynamic instability.

ANTEPARTUM UTERINE DEHISCENCE

Presentation — Uterine dehiscence (or uterine window) is a clinically occult and incomplete disruption that does not lead to any serious maternal or neonatal consequences. Most uterine dehiscences are diagnosed incidentally at repeat cesarean birth, but some are identified during prenatal ultrasound examination, sometimes with extrusion of a sac containing fetal membranes and amniotic fluid. A defect in the scar may be seen as early as the first trimester, with the possibility of "cesarean scar" pregnancy [110] (see "Cesarean scar pregnancy"). Scar defects and uterine windows have also been detected in the nonpregnant uterus [48,49].

Management — Management of antepartum dehiscence is influenced by gestational age (eg, previable, preterm viable, term), but there is insufficient evidence to make firm recommendations. Near term, repeat cesarean birth before the onset of labor is probably the safest option to avoid progression to rupture. Remote from term, case reports have described successful outcomes with expectant management with close monitoring and early delivery [6,67,68,111-114]. There is no standard or optimum approach; if the pregnancy is continued, the patient should be thoroughly counseled about potential risks to her and to the fetus.

Repair of the uterine defect by a layered suture closure or a patch with successful outcome has also been described [115-119], including in rare patients with symptomatic rupture remote from term [118]. No conclusions can be made about the efficacy of these approaches, given the complexity and rarity of such cases. We would not attempt antepartum repair in such cases because of the potential for maternal mortality or significant morbidity.

SUMMARY AND RECOMMENDATIONS

●Terminology – Uterine rupture refers to complete disruption of all uterine layers, including the serosa. It is an obstetric emergency. Uterine dehiscence (or uterine window) is a clinically occult and incomplete disruption that does not lead to any serious maternal or neonatal consequences. (See 'Terminology: rupture versus dehiscence' above.)

●Uterine rupture

•Incidence – The risk of uterine rupture is approximately 0.3 percent in patients with a prior cesarean birth, regardless of mode of delivery in the current pregnancy. A systematic review of similar data estimated 468 uterine ruptures in a hypothetical group of 100,000 patients of any gestational age undergoing a trial of labor after cesarean birth (TOLAC). (See 'Incidence' above.)

•Risk factors – The primary risk factors for uterine rupture after a previous cesarean birth are, from highest to lowest risk, previous uterine rupture, previous fundal or vertical hysterotomy extending into the upper uterine segment, and induction of labor (particularly with misoprostol). A short interdelivery interval also appears to increase risk. A prior vaginal birth, either before or after the prior cesarean birth, is associated with a reduced risk of uterine rupture. However, uterine rupture remains an unpredictable event. (See 'Risk factors' above.)

•Predicting rupture by antepartum imaging – There is no reliable way to predict uterine rupture in patients with a prior cesarean birth. On imaging studies, an intact, thick scar is reassuring of the integrity of the repair and a thin scar or a defect is worrisome for recurrent rupture, but neither finding is strongly predictive of outcome. (See 'Predicting uterine rupture' above.)

•Clinical presentation

-Clinical signs of uterine rupture may include fetal heart rate (FHR) abnormalities (a concerning category II or category III tracing), vaginal bleeding, sudden or worsening abdominal pain, need for frequent epidural dosing (in patients with epidural anesthesia), changes in contraction patterns, loss of station, hemodynamic instability, and hematuria. (See 'Patient presentation' above.)

-No FHR pattern is pathognomonic of rupture. The most common FHR abnormality is fetal bradycardia, which may be sudden or preceded by significant variable or prolonged decelerations. (See 'Patient presentation' above.)

-Intraabdominal hemorrhage can lead to rapid maternal hemodynamic deterioration. Vaginal bleeding may be modest, despite major intraabdominal hemorrhage. Uterine contractions may gradually decrease in amplitude and there may be loss of station of the fetal presenting part. Pain related to uterine rupture may be partially or completely masked by neuraxial analgesia administered for management of labor pain. (See 'Patient presentation' above.)

-In postpartum patients, abdominal pain and persistent vaginal bleeding despite use of uterotonic agents should prompt consideration of uterine rupture. (See 'Postpartum' above.)

•Diagnosis – The diagnosis of uterine rupture is based on clinical or radiologic identification of complete disruption of all uterine layers, including the serosa. It should be suspected in patients undergoing TOLAC with one or more of the following signs and symptoms: sudden development of FHR abnormalities, sudden or worsening abdominal pain, vaginal bleeding, hemodynamic instability. A preoperative provisional diagnosis of rupture is not critical since urgent delivery is often indicated in these patients because of nonreassuring FHR changes and/or hemodynamic instability. (See 'Diagnosis' above.)

•Management – Definitive surgical management involves hysterectomy. Uterine repair may be possible. The decision to attempt repair depends on patient plans for future pregnancies, extent of uterine damage, hemodynamic stability, and the surgeon's skills. The goals of conservative surgery are to repair the uterine defect, control hemorrhage, identify damage to other organs (eg, urinary tract), minimize early postsurgical morbidity, and reduce the risk of complications in future pregnancies. (See 'Repair versus hysterectomy' above.)

•Outcome – Uterine rupture can lead to multiple adverse outcomes, including severe hemorrhage, bladder laceration, hysterectomy, and rarely death for the mother, and death or neurologic morbidity for the fetus/neonate. (See 'Outcome' above.)

•Future pregnancies – There is an increased probability of recurrent rupture in a future pregnancy. The risk is related to the site of rupture with the highest risk in patients with fundal or longitudinal rupture. For women with a previous rupture that occurred during labor, at term, and in the lower uterine segment, a scheduled cesarean birth at 36+0 to 37+6 weeks is the preferred approach. (See 'Recurrence risk' above and 'Timing of delivery' above.)

●Uterine dehiscence

•Most uterine dehiscences are incidentally identified at repeat cesarean birth, but some have been detected during prenatal ultrasound examination.

•Management is repeat cesarean with repair of the defect; timing of delivery depends on the gestational age when the dehiscence is detected, but delivery is recommended at or near term prior to the onset of labor. (See 'Antepartum uterine dehiscence' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Christopher T Lang, MD, who contributed to an earlier version of this topic review.