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Uterine rupture: Unscarred uterus

Uterine rupture: Unscarred uterus
Literature review current through: Jan 2024.
This topic last updated: Nov 30, 2023.

INTRODUCTION — Rupture of the pregnant uterus, similar to rupture of any internal organ, can be life-threatening. Both the mother and fetus are at risk for serious morbidity and mortality. Most uterine ruptures occur in patients who have had a previous transmyometrial surgical incision, typically for cesarean birth. Rupture of the unscarred uterus is rare, but the incidence is increasing and the rate of maternal and neonatal serious morbidity is higher than that after rupture of the scarred uterus [1].

This topic will review issues related to rupture of the unscarred uterus. Rupture of the scarred uterus is discussed separately. (See "Uterine rupture: After previous cesarean birth".)

INCIDENCE — Rupture of the unscarred pregnant uterus is a rare event, estimated to occur in 1 in 5700 to 1 in 50,000 pregnancies [1-7]. In a series of 75 ruptures (complete disruption of the uterine muscle and serosa) in unscarred uteruses (no previous cesarean or other uterine surgery), the incidence was 0.2 ruptures per 10, 000 births, 18 of the 75 ruptures occurred preterm and 6 of the 75 ruptures occurred prelabor (one was due to a ruptured horn of a bicornuate uterus at 18 weeks, the other five had no reported risk factors) [7].

The incidence of rupture of both scarred and unscarred uteruses has increased in recent decades [8]. Rupture of the unscarred uterus occurs more frequently in resource-limited countries where prompt access to cesarean and operative vaginal delivery is not widely available for management of obstructed labor [9-12]. Higher parity and frequency of contracted pelvises may also play a role.

ETIOLOGY

Trauma, such as from a motor vehicle crash or an obstetric maneuver (eg, internal or external cephalic version, fundal pressure, forceps-assisted birth)

Weakness of the myometrium

Congenital, such as from Ehlers-Danlos type IV [13-16] or osteogenesis imperfecta type 1 [7].

Acquired, such as from prolonged labor or use of uterotonic drugs, which place prolonged stress on the myometrium [17,18].

Overdistension of the uterine cavity, whether absolute or relative to the size of the cavity, may be the major physical factor provoking rupture when the myometrium is weakened for any reason.

RISK FACTORS

Overview — Reported risk factors include [1,6,7,18-26]:

Exposure to uterotonic drugs (oxytocin, prostaglandins) – Exposure to uterotonic drugs is a consistent risk factor for rupture of the unscarred uterus and more commonly associated with rupture of the unscarred uterus than the scarred uterus [1].

High parity (mean parity 3.6 in one study [1]).

Uterine anomaly.

Advanced maternal age.

Dystocia.

Macrosomia.

Multiple gestation.

Abnormal placentation (eg, placenta accreta spectrum).

Short interpregnancy interval.

Prior cerclage.

The presence of several risk factors likely compounds the risk of rupture. In one case report, for example, a grand multipara who experienced rupture of an unscarred uterus at 19 weeks of gestation also had placenta increta and used cocaine [27]. Two case reports have linked chronic glucocorticoid use with uterine rupture (one primigravid patient age 36 had systemic lupus erythematosus and a twin pregnancy at 23 weeks; the other patient was age 40, in her seventh pregnancy, at term, had psoriatic arthritis, and three previous vaginal births) [28,29]. A third report described two patients experiencing ruptures following prior curettage for placenta accreta spectrum [6].

Risk reduction — Given the rarity of rupture of the unscarred uterus, risk reduction strategies are limited to good obstetric practice.

Perform obstetric maneuvers with caution – Procedures that involve uterine manipulation, such as external cephalic version for malpresentation in a patient with a significant uterine anomaly, should be performed gently. (see "External cephalic version", section on 'Risks').

Avoid fundal pressure – Fundal pressure in the second stage should be avoided. It is not an effective approach to dystocia [2].

Use uterotonic agents judiciously – The safety of uterotonic drugs has improved with development of equipment for accurate drug delivery, timely recognition and appropriate treatment of excessive uterine activity, and better understanding of the indications for beginning and discontinuing these drugs. Nevertheless, rupture of the unscarred uterus has been reported even with low-dose and, presumably judicious, use of uterotonic drugs, particularly misoprostol with or without mifepristone in the second and third trimesters [18,30-32].

The use of low-dose oxytocin would seem prudent in a grand multipara, while a high-dose oxytocin protocol may be reasonable in a low-parity patient. The key factor is closely monitoring the progress of labor and fetal heart rate pattern, with timely intervention for protracted or arrested labor. In a meta-analysis of randomized trials of high- versus low-dose oxytocin for induction of labor at term, high-dose oxytocin was associated with a nonstatistical increase in the risk of uterine rupture (relative risk 3.10, 95% CI 0.50-19.3; three trials, 1429 women) [33]. There were only five ruptures in the induced cohort. Two occurred in patients with prior cesareans (each with two prior cesareans) undergoing oxytocin induction. Three of the ruptures occurred in patients with high parity from a single trial included in the meta-analysis. Use of low- and high-dose oxytocin protocols are described separately. (See "Induction of labor with oxytocin", section on 'Oxytocin administration'.)

Use mechanical methods of cervical ripening in high-risk patients – Rupture of the unscarred uterus appears to be increased but is still a rare event with use of either mechanical or pharmacologic methods of cervical ripening [34]. When induction of labor is indicated, it is prudent to consider whether the patient has other risk factors for rupture. The method of cervical ripening in patients with risk factors should be individualized, taking into account clinical factors, the likelihood of vaginal birth, and patient preferences. For example, high parity is a risk factor for rupture. Although misoprostol was not associated with rupture of the unscarred uterus in grand multiparas in small series [35,36], if additional risk factors (eg, macrosomia, twins) are present in a patient of high parity and vaginal birth is appropriate, some obstetric providers may choose to avoid prostaglandins for cervical ripening and use mechanical methods when cervical ripening is needed.

Perform an operative delivery (cesarean or assisted vaginal [if appropriate]) when criteria for labor arrest or prolonged second stage are met. Obstructed labor can eventually result in uterine rupture [37]. (See "Labor: Diagnosis and management of an abnormal first stage", section on 'Management' and "Labor: Diagnosis and management of a prolonged second stage", section on 'Management'.)

CLINICAL PRESENTATION AND MANIFESTATIONS — The clinical presentation of rupture can vary depending on the uterine site and the type of labor analgesia, so a high index of suspicion is needed. For example, rupture involving the posterior uterus or parametrium in a patient with epidural anesthesia may result in large vital sign changes, but minimal patient discomfort or vaginal bleeding, whereas rupture involving the cervix and upper vaginal wall may present with heavy vaginal bleeding, and rupture involving the bladder may present with the abrupt onset of hematuria [1,38]. Postpartum presentation is more common with the unscarred than the scarred uterus and suggests that the rupture occurred shortly before birth [39].

Antepartum — Pain is the major sign of antepartum uterine rupture. In one series, all eight antepartum complete ruptures among over two million patients with an unscarred uterus presented with acute abdominal pain [6].

Intrapartum

Fetal heart rate changes – Bradycardia, sometimes preceded by variable or late decelerations, is the most common clinical manifestation of uterine rupture. However, no fetal heart rate pattern is pathognomonic of rupture and fetal heart rate changes alone are not useful for detecting or excluding rupture [40].

Loss of station – A loss of station can be observed if all or part of the fetus passes through the rupture site and into the peritoneal cavity.

Abdominal pain with/without hemodynamic changes – Constant abdominal pain accompanied by signs of intra-abdominal hemorrhage (eg, hypotension, tachycardia, increasing abdominal girth) are consummate signs and symptoms of uterine rupture. However, the degree, character, and location of pain are often variable, and the signs and symptoms of intra-abdominal bleeding can be subtle [2,3,22]. Furthermore, rupture-related pain may be partially or completely masked by neuraxial analgesia for management of labor pain. The acute onset of pain after previously effective neuraxial anesthesia may be a sign of uterine rupture [41].

Uterine tenderness, cessation of contractions, and/or change in uterine shape – Rupture may be accompanied by these findings because of extrusion of all or part of the fetus and/or amniotic sac.

Intuitively, loss of integrity of the uterine wall should be associated with a reduction in intrauterine pressure, but case series where an intrauterine pressure catheter was in place at the time of rupture have generally not observed pressure changes significantly different from laboring patients without rupture [42,43]. Interestingly, an increase in baseline intrauterine pressure was seen in 4 of 39 patients in one series [42].

Vaginal bleeding – Vaginal bleeding may be modest, despite major intra-abdominal hemorrhage. Bleeding tends to be heavy when the cervix and upper vaginal wall are involved. Intraperitoneal bleeding may result in hypovolemic shock in the absence of excessive vaginal bleeding [44].

Hematuria – Hematuria may occur if the rupture extends into the bladder.

Postpartum — Maternal symptoms of uterine rupture are generally the same postpartum; however, a key potential additional postpartum finding is excessive vaginal bleeding that persists despite use of uterotonic drugs.

DIAGNOSTIC IMAGING AND LABORATORY TESTS — For the gravid patient with abdominal pain, hemodynamic instability, and a nonreassuring fetal heart rate pattern, stabilization and urgent delivery are generally indicated. In the rare stable patient with a subacute presentation (eg, no or mild abdominal pain, no or light vaginal bleeding, category I or II fetal heart rate tracing), ultrasound imaging of the abdomen may identify a defect in the uterine wall or another pathology accounting for the patient's symptoms [2,45]. Focused assessment with sonography in trauma (ie, "FAST" ultrasound) may detect large quantities of free fluid in the peritoneal cavity.

Laboratory testing is guided by the clinical setting (eg, estimated blood loss, suspected coagulopathy).

DIAGNOSIS — The diagnosis of uterine rupture is typically made at laparotomy by visualization of complete disruption of all uterine layers with active bleeding and hemoperitoneum [22]. Over 90 percent of uterine ruptures occur in the anterior lower uterine segment, but the corpus, cervix, vaginal wall, posterior uterus, or parametrium may be involved [38].

A high index of suspicion is needed preoperatively in patients with an unscarred uterus since rupture is rare and unexpected [3]. Not surprisingly, an unscarred uterus is an independent risk factor for delayed diagnosis of intrapartum uterine rupture [46]. A preoperative provisional diagnosis of rupture is not critical since urgent delivery is often indicated because of fetal heart rate abnormalities. Postpartum, laparotomy is often indicated because of maternal hemodynamic instability due to hemorrhage unresponsive to conservative therapy.

Intrapartum differential diagnosis

Placental abruption – Abruption is characterized by fetal heart rate changes, abdominal pain, and vaginal bleeding, and may not be distinguishable from uterine rupture before delivery. In contrast to uterine rupture, abruption is associated with increased uterine activity, and the uterus may be tetanic. Abruption can cause disseminated intravascular coagulation, whereas coagulopathy associated with rupture is due to loss of hemostatic factors because of massive hemorrhage. (See "Acute placental abruption: Pathophysiology, clinical features, diagnosis, and consequences".)

Ruptured viscus or vascular structure – Maternal hemodynamic instability may result from intra-abdominal bleeding from any source, including hepatic rupture, which can occur in preeclampsia with severe features or HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelet count), or rupture of a major vascular structure, such as a splenic artery aneurysm, which is more common during pregnancy.

Preeclampsia with severe features and HELLP syndrome are characterized by hypertension, proteinuria, elevated liver function tests, and thrombocytopenia, which are not findings associated with uterine rupture. (See "Preeclampsia: Clinical features and diagnosis" and "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)".)

The rupture of a vascular structure (eg, splenic, renal, ovarian, iliac) can present with pain (sometimes difficult to distinguish from labor pain), hypotension, tachycardia, free peritoneal fluid, and a category II or III fetal heart rate tracing. In contrast to uterine rupture, the uterus is not typically affected. (See "Approach to acute abdominal/pelvic pain in pregnant and postpartum patients".)

Intraamniotic infection/chorioamnionitis – Intraamniotic infection/chorioamnionitis can cause uterine tenderness and abdominal pain. However, fever is typically present and the fetal heart rate responds with tachycardia rather than bradycardia. (See "Clinical chorioamnionitis".)

Postpartum differential diagnosis — After a vaginal birth, patients with a ruptured uterus may have excessive bleeding and pain. The differential diagnosis of postpartum hemorrhage includes atony, trauma of the lower genital tract or cervix, and coagulopathy. (See "Overview of postpartum hemorrhage", section on 'Causes of postpartum hemorrhage'.)

The differential diagnosis of pelvic pain immediately after vaginal birth is broad. (See "Approach to acute abdominal/pelvic pain in pregnant and postpartum patients", section on 'Causes of postpartum acute abdominal pain'.)

The diagnosis of uterine rupture in patients with excessive bleeding or pain after delivery can be readily made or excluded by transvaginal physical examination of the uterine cavity.

MANAGEMENT

Initial approach to intrapartum uterine rupture — As discussed above, an abnormal fetal heart rate pattern is the most common clinical manifestation of uterine rupture and thus the dominant factor influencing management, whether or not uterine rupture is suspected.

Category III tracing and hemodynamically unstable mother

Initiate maternal resuscitation – Patients who are hemodynamically unstable should be given crystalloid, blood, and blood components, as appropriate, as they are prepared for an urgent cesarean birth/exploratory laparotomy. Fluid and blood resuscitation is similar to that for patients with postpartum hemorrhage. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Transfuse red blood cells, platelets, plasma'.)

Notify anesthesia and pediatrics – The anesthesia staff should be notified to assist with patient management and provide anesthetic support for delivery. General anesthesia is preferable to neuraxial anesthesia for these patients because maternal hypovolemia, potential coagulopathy, and acute fetal compromise are contraindications to neuraxial anesthesia. (See "Anesthesia for cesarean delivery", section on 'Choice of anesthetic technique'.)

The pediatric staff should be notified in case newborn resuscitation is needed.

Perform a midline abdominal incision for cesarean birth – A midline skin incision is preferable when the fetal heart rate pattern is abnormal and intra-abdominal bleeding is suspected. A midline incision slightly shortens the incision-to-delivery interval; in one study, median incision-to-delivery times were three minutes for midline incisions versus four minutes for Pfannenstiel incisions [47]. In addition, a midline incision provides good exposure for evaluating potential pathology involving the lower and upper uterus, pelvis, and upper abdomen, while a Pfannenstiel incision only provides good exposure for evaluating potential pathology of the lower uterine segment and pelvis.

Prepare for a possibly difficult fetal extraction – The fetus is delivered using conventional maneuvers, but delivery may be difficult if fetal parts have extruded through the site of rupture [2]. Providing adequate exposure and use of vacuum or other fetal extraction instruments may facilitate delivery. (See "Cesarean birth: Management of the deeply impacted head and the floating head", section on 'Floating fetal head'.)

Category II or III tracing and hemodynamically stable mother

Choice of anesthesia – Neuraxial anesthesia is reasonable in this setting when expeditious, but not urgent cesarean delivery is indicated because of an abnormal fetal heart rate pattern in a hemodynamically stable mother. The choice of neuraxial versus general anesthesia depends on case-specific factors including the specific fetal heart rate pattern and the estimated time to administer a safe and effective anesthetic.

Choice of abdominal incision – The choice of a midline versus Pfannenstiel incision depends on whether the obstetrician believes the incision-to-delivery time is critical. Intra-abdominal bleeding would not be suspected preoperatively in this setting, so choosing an incision that provides the best exposure of the upper abdomen would not be a consideration unless uterine rupture is suspected because of other clinical findings (eg, loss of station, abdominal pain, uterine tenderness, cessation of contractions, excessive vaginal bleeding); however, this is rare.

Fetal extraction – The fetus is delivered using conventional maneuvers.

The pediatric staff should be notified for a category III tracing and possibly for a category II tracing in case newborn resuscitation is needed.

Uterine repair versus hysterectomy — The uterus must be repaired, or occasionally removed, after rupture. Additional surgical goals are to control hemorrhage, identify damage to other organs (eg, urinary tract), and minimize early postsurgical morbidity.

The decision to perform hysterectomy is based on a combination of factors, including:

The patient's desire for future pregnancy

The extent of uterine damage from the rupture

The patient's intraoperative hemodynamic and anesthetic stability, and

The skill of the surgeon for repairing a complicated rupture

A long and difficult repair of an extensive laceration is not in the patient's best interests if they are hemodynamically unstable or the repair is at high risk of failure in a subsequent pregnancy. Single cases and small series report cesarean hysterectomy in 34 to 70 percent of patients [22,42,48]. Importantly, rupture of the unscarred uterus is an independent risk factor for hysterectomy [46]. (See "Peripartum hysterectomy for management of hemorrhage".)

Management of the repair — If the rupture site is repaired, the major challenge is reducing the risk of complications in future pregnancies. 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.

A reasonable approach is to repair the uterine defect in two or three layers with an absorbable suture, similar to repair of any hysterotomy. If the laceration extends to the bladder or there is any suspicion of ureteral injury from the laceration or its repair, we suggest an intraoperative consultation with an experienced urologic surgeon (eg, urologist, gynecologic oncologist).

MORBIDITY AND MORTALITY — Uterine rupture can lead to multiple adverse and interrelated maternal outcomes, including sequelae of severe hemorrhage, bladder laceration, hysterectomy, and death [1,49-51]. Perinatal complications include death or serious morbidity from prolonged intrauterine hypoxia [1,39,49,50,52]. The frequency of these outcomes depends on factors such as the size and location of the rupture (eg, lateral is more morbid than anterior) and speed of intervention.

In two studies, rupture of the unscarred uterus was associated with a higher risk of adverse maternal outcome (especially hemorrhage) than rupture of the scarred uterus [1,49]. At least 60 percent of patients with rupture of an unscarred uterine rupture had estimated blood loss greater than 1 liter and/or received a blood transfusion. The same studies reported discordant findings regarding which type of rupture was associated with a higher risk of adverse perinatal outcomes. A series limited to infant outcome after complete rupture reported intrapartum/neonatal death in 26 percent, hypoxic ischemic encephalopathy in 6 percent, and neonatal intensive care unit due to severe asphyxia (without encephalopathy) in 23 percent, without a significant difference between unscarred and scarred uteruses [39].

PREGNANCY AFTER UTERINE RUPTURE

Risk of recurrent rupture — A systematic review of 13 studies including 365 pregnancies after a previous complete uterine rupture reported the following findings [53]:

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 of management in 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). The location of the initial rupture is important because there is a higher risk of recurrence when the previous rupture was outside of the lower uterine segment [54,55]. Extrapolation of these data to inform management choices in subsequent pregnancies following rupture of the unscarred uterus seems reasonable.

A short interpregnancy interval following cesarean birth appears to be associated with a higher risk of uterine rupture in patients who attempt a trial of labor after a previous low transverse cesarean birth. Extrapolating from these data, we suggest an interpregnancy interval of at least 18 months for patients who desire pregnancy following repair of rupture of the unscarred uterus. (See "Interpregnancy interval: Optimizing time between pregnancies", section on 'After a cesarean birth'.)

Predicting recurrent rupture — Scar thickness and integrity may be assessed by ultrasound examination in future pregnancies. An intact, thick scar is reassuring of the integrity of the repair, and a thin scar or a defect is worrisome for recurrent rupture [56]. However, the quantitative risk of rupture associated with scar thickness has not been determined, and there are no data for normal myometrial thickness at sites other than the lower uterine segment. Furthermore, patients with normal lower uterine segment thickness antepartum have gone on to rupture the uterus when in labor [57].

Whether the use of imaging improves outcome needs to be validated, but the authors of this topic believe it is prudent. Ultrasound is performed at 18 to 20 weeks with attention to placental morphology and location. In the absence of an obvious disruption of the uterine wall or evidence of placenta accreta spectrum at that time, a follow-up scan is performed at approximately 32 weeks.

Timing of delivery — Recurrent rupture can occur as early as the second trimester and is difficult to predict [58]. Most obstetricians attempt to reduce the risk of recurrent rupture by recommending cesarean birth and scheduling the birth before the onset of labor. There is no consensus on the optimum timing of delivery. A reasonable approach is to plan repeat cesarean at 36+0 to 37+0 weeks [59], but the risks and benefits need to be considered on a case-by-case basis (eg, earlier in this window if a previous fundal rupture at term, later if a previous lower segment rupture at term). In general, morbidity in late preterm neonates is low and considered acceptable when compared with the potential maternal and fetal consequences of recurrent rupture in labor.

We administer a course of antenatal corticosteroids 48 hours before the cesarean if not previously administered. (See "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery", section on '34+0 or more weeks'.)

SUMMARY AND RECOMMENDATIONS

Incidence – Rupture of the unscarred pregnant uterus is a rare event, occurring in 1 in 5700 to 1 in 50,000 pregnancies. (See 'Incidence' above.)

Etiology and risk factors – Rupture of an unscarred uterus may be caused by trauma or congenital or acquired weakness of the myometrium. Contributing factors include dystocia resulting in prolonged labor, exposure to uterotonic drugs, placenta accreta, multiparity, multiple gestations, and advanced maternal age. (See 'Risk factors' above.)

Clinical manifestations -– An abnormal fetal heart rate pattern, particularly bradycardia, is the most common clinical manifestation of uterine rupture. Other potential findings include loss of station, abdominal pain with or without hemodynamic instability, uterine tenderness, cessation of contractions, change in uterine shape, vaginal bleeding, and hematuria. Postpartum, abdominal pain and vaginal bleeding unresponsive to uterotonic drugs are signs of rupture. (See 'Clinical presentation and manifestations' above.)

Diagnosis – A high index of suspicion is required to diagnose intrapartum rupture in patients with an unscarred uterus since it is a rare and unexpected event. The diagnosis of uterine rupture is typically made at laparotomy by visualization of complete disruption of all uterine layers with active bleeding. A preoperative provisional diagnosis of rupture is not critical since urgent delivery is often indicated in these patients because of fetal heart rate abnormalities. However, symptoms may be subtle in some cases. (See 'Diagnosis' above and 'Clinical presentation and manifestations' above.)

Management

Route of birth and anesthesia – In most patients, an abnormal fetal heart rate pattern is the dominant factor impacting the decision to perform a cesarean birth, whether or not uterine rupture is suspected. The choice of anesthesia and type of incision depends on the urgency of the clinical situation and whether upper abdominal pathology is suspected preoperatively. (See 'Initial approach to intrapartum uterine rupture' above.)

Hysterectomy versus repair

-The decision to perform hysterectomy or repair the defect is based on a combination of factors, including the patient's desire for future pregnancy, the extent of uterine damage from the rupture, the patient's intraoperative hemodynamic and anesthetic stability, and the skill of the surgeon for repairing a complicated rupture. (See 'Uterine repair versus hysterectomy' above.)

-If the defect is repaired, a reasonable approach is a two- or three-layer closure with an absorbable suture, similar to repair of any hysterotomy. If the laceration extends to the bladder or there is any suspicion of ureteral injury from the laceration or its repair, we suggest an intraoperative consultation with an experienced urologic surgeon. (See 'Uterine repair versus hysterectomy' above.)

Morbidity and mortality – Uterine rupture can lead to multiple adverse and interrelated maternal outcomes, including sequelae of severe hemorrhage, bladder laceration, hysterectomy, and death. Perinatal complications include death or serious morbidity from prolonged intrauterine hypoxia. Uterine rupture can lead to multiple adverse outcomes, including severe hemorrhage, bladder laceration, hysterectomy, and infant death or morbidity from prematurity of hypoxemia. (See 'Morbidity and mortality' above.)

Recurrent rupture – 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 likely associated with fundal rupture. We suggest an interpregnancy interval of at least 18 months for women who desire pregnancy following repair of rupture of the unscarred uterus. (See 'Pregnancy after uterine rupture' above.)

Timing of future cesarean births – In future pregnancies, cesarean birth should be scheduled before labor. We suggest delivery at 36+0 to 37+0 weeks. (See 'Timing of delivery' above.)

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Topic 14210 Version 30.0

References

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