INTRODUCTION —
Uterine rupture is a life-threatening pregnancy complication for both the pregnant person and fetus. Most uterine ruptures in resource-rich countries are associated with a trial of labor after cesarean birth (TOLAC). This topic will review issues related to 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, rupture of an unscarred uterus may be related to lack of access to cesarean birth for managing an obstructed labor. Rupture of the unscarred uterus is also discussed separately. (See "Uterine rupture of the unscarred uterus: Risk factors, clinical manifestations, management, and outcome".)
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 discernable 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.
Some studies 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]. However, further research is needed to better understand the pathologic processes of wound healing that increase the risk of subsequent uterine rupture.
RISK FACTORS —
Risk factors for rupture are described in the table (table 1).
INCIDENCE OF RUPTURE —
The overall incidence of uterine rupture in pregnant patients with a prior cesarean birth is approximately 300 ruptures per 100,000 deliveries [3]. However, the incidence varies widely depending on factors such as exposure to labor, the location of the hysterotomy (fundal versus lower uterine segment), and history of prior rupture. These data are reviewed in detail separately. (See "Choosing the route of delivery after cesarean birth", section on 'Prior transfundal uterine incision' and "Choosing the route of delivery after cesarean birth", section on 'Prior uterine rupture or dehiscence'.)
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 (TOLAC), 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 [4,5].
Antepartum imaging of the hysterotomy scar — In our 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 [6]. 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 TOLAC 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). As the trend is concerning and the trial was underpowered, 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 [7]. One caliper is placed at the interface between 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 10th, 25th, and 50th percentiles of lower uterine segment thickness are approximately 2, 2.3, and 3.2 mm, respectively, near term [7]. There are no data defining normal myometrial thickness at sites other than the lower uterine segment.
The quantitative risk of rupture associated with scar thickness has not been determined. Although an intact, thick scar is reassuring of the integrity of the repair and a thin scar or a defect is worrisome that the scar might rupture, a systematic review (21 studies) found no myometrial thickness threshold value that performed adequately to use in clinical practice to predict whether a hysterotomy scar will rupture or remain intact [8].
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 [9] and incorporate this information into clinical counseling [7,8].
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 giving birth. On ultrasound, the defect appears as a hypoechogenic or nonechogenic area in a region of the myometrial thinning [10,11]. 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 symptoms (termed cesarean scar disorder), which may include lower abdominal pain, dysmenorrhea, abnormal uterine bleeding (often postmenstrual spotting), or secondary unexplained infertility [12]. They are also at risk for cesarean scar pregnancy and placenta accreta spectrum. (See "Cesarean scar pregnancy".)
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 [13-15], but the need for repair has not been established. 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 [16]. 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 more common to less common [17]:
●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 [18,19], 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 [20]. Given these observations, continuous FHR monitoring is routinely recommended during a trial of labor after cesarean (TOLAC) [21].
●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 [22]. Therefore, clinicians should be mindful that the acute onset of pain after previously effective neuraxial anesthesia may be a sign of uterine rupture [23].
●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 – Loss of station can result from partial extrusion of the fetus through the rupture, or possibly from myometrial relaxation.
●Hematuria – A rupture that extends into the bladder may cause hematuria.
●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 [24]. Another external tocodynamometry finding that has been reported is a gradual decrease in the amplitude of consecutive contractions, the so-called "staircase sign" [25]. Nevertheless, a consistent change in uterine contraction patterns at the time of uterine rupture has not been identified, and an intrauterine pressure catheter, if utilized, may fail to show any abnormality [26].
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, sonographic assessment may be used to look for hemoperitoneum [27].
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 [28], a hematoma adjacent to the hysterotomy scar [29], extrauterine fluid-distended fetal membranes [28,30,31], free peritoneal fluid [28,32], anhydramnios [33], an empty uterus [32,34], fetal parts outside of the uterus [32,35], and/or fetal demise.
In addition to these findings, computed tomography (CT) or magnetic resonance imaging (MRI) performed as part of a trauma evaluation may detect peritoneal air, as well as pathology associated with rupture, such as ileus [36]. In a case report, CT of a patient two weeks postcesarean who presented to the emergency department with abdominal pain and fever revealed a uterine perforation with an adjacent abscess [37].
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 (TOLAC) 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 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 with 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 [38]. (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 staff – 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 staff – 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 [39]. Many clinicians choose a midline incision when 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. A Pfannenstiel incision only provides good exposure of the lower uterine segment and pelvis.
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 for peripartum hysterectomy 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 (especially the 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 also require ligation of the adnexal vasculature and often require 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 [35,40-42]. 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 [33,35,40,41,43-45].
In rare patients in the second trimester, repair of the uterine defect by a layered suture closure or a patch with ongoing pregnancy and successful outcome has also been described [46].
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 [40]). (See "Postpartum hemorrhage: Management approaches requiring laparotomy".)
●Bladder trauma – Uterine rupture may lead to bladder injury [47]. 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) [48]. 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. (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 [30,49-56]. 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 a previous cesarean found no reports of maternal death associated with uterine rupture [57], 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) [58].
●Morbidity – Maternal morbidity was assessed in a literature review of 880 cases of uterine rupture during over 142,000 trials of labor after cesarean birth (TOLAC) [59]. The two major morbidities associated with uterine rupture were transfusion of packed red blood cells and need for hysterectomy, but the frequency of these complications after rupture were not provided.
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 perinatal death rate associated with uterine rupture ranges from 5 to 26 percent in case series [57,60-65]. Death is most likely in cases of placental separation and/or fetal extrusion [61,65,66].
●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 [67]. There were no neonatal deaths or cases of hypoxic-ischemic encephalopathy among infants of patients undergoing planned repeat cesarean birth. Prompt intervention after uterine rupture did not always prevent severe acidosis and neonatal morbidity and mortality [61].
●In two studies of TOLAC, neonatal morbidity increased when the interval between recognition of fetal heart rate abnormalities and delivery was ≥18 minutes [66,68]. This supports recommendations by many organizations that TOLAC should be performed in facilities capable of performing an emergency cesarean birth [69-71]. In particular, planned TOLAC in the home should be avoided and has been associated with higher rates of low Apgar scores, neonatal seizures [72,73], and neonatal death [74].
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 [61] and two deaths in infants delivered at 10 minutes [65]. 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 separation, 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 —
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 [21]. 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 preterm labor in the current pregnancy, gestational age at prior rupture, and whether the prior rupture was antepartum or intrapartum. If delivery is planned prior to 37+0 weeks, 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'.)
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.
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 their assessment of the likelihood of the diagnosis versus other causes of abdominal pain, fetal heart rate abnormalities, vaginal bleeding, and hemodynamic instability. Management of the uterine rupture with repair of the hysterotomy versus hysterectomy is performed as previously described, with consideration of the interoperative findings, the patient's hemodynamic stability, and their desire for future pregnancy. (See 'Management of patients with uterine rupture at laparotomy' above.)
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 scar defect may be seen as early as the first trimester, with the possibility of cesarean scar pregnancy [75] (see "Cesarean scar pregnancy"). As discussed above, scar defects and uterine windows have also been detected in the nonpregnant uterus [10,11]. (See 'Interpregnancy imaging of the hysterotomy scar' above.)
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 [30,31,76-80]. There is no standard or optimum approach; if the pregnancy is continued, the patient should be thoroughly counseled about potential maternal and fetal risks.
Repair of the uterine defect by a layered suture closure or a patch with successful outcome has also been described [46,81-84]. 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 of rupture' above.)
•Risk factors – Risk factors for uterine rupture after a previous cesarean birth are described in the table (table 1). 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 patients 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.