Frequently asked questions about rupture of uterus in pregnancy

Uterine rupture in pregnancy is a rare and often catastrophic complication with a high incidence of fetal and maternal morbidity. Several factors are known to increase the risk of uterine rupture, but, even in high-risk subgroups, the overall incidence of uterine rupture is low.
The initial signs and symptoms of uterine rupture are typically nonspecific, which makes diagnosis difficult and sometimes delays definitive therapy. From the time of diagnosis to delivery, only 10-37 minutes are available before clinically significant fetal morbidity becomes inevitable. Fetal morbidity occurs as a result of catastrophic hemorrhage, fetal anoxia, or both. The inconsistent premonitory signs and the short time for instituting definitive therapeutic action make uterine rupture a fearful event.

Definition

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

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

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

Incidence and risk factors

Congenital uterine anomalies, multiparity, previous uterine myomectomy, the number and type of previous cesarean deliveries, fetal macrosomia, labor induction, uterine instrumentation, and uterine trauma all increase the risk of uterine rupture, whereas previous successful vaginal delivery and a prolonged inter-pregnancy interval after a previous cesarean delivery may confer relative protection. In contrast to the availability of models to predict the potential success of a TOL after a prior cesarean section, accurate models to predict the person-specific risk of uterine rupture for individuals are not available.
Major patient characteristics for determining risk of uterine rupture are noted below.

Uterine status is either native (unscarred) or scarred. Scarred status may include previous cesarean delivery, including the following:

Previous pregnancy and delivery history may include the following:

Labor status is determined as follows:

Obstetric management considerations include the following:

Uterine trauma includes the following:

Maternal age

Increasing maternal age has a detrimental effect on the rate of uterine rupture. The rate of uterine rupture in women differed significantly.

The signs and symptoms of uterine rupture largely depend on the timing, site, and extent of the uterine defect. Uterine rupture at the site of a previous uterine scar is typically less violent and less dramatic than a spontaneous or traumatic rupture because of their relatively reduced vascularity.
The classic signs and symptoms of uterine rupture are:
(1) Recession of the presenting fetal part,
(2) diminished baseline uterine pressure,
(3) Fetal distress (as evidenced most often by abnormalities in fetal heart rate),
(4) Abdominal pain,
(5)  Loss of uterine contractility,
(6) Hemorrhage, and
(7) Shock.

Prolonged, late, or recurrent variable decelerations or fetal bradycardias are often the first and only signs of uterine rupture. Sudden or atypical maternal abdominal pain occurs more rarely than fetal heart rate decelerations or bradycardia. Moreover, abdominal pain was the first sign of rupture in patients and occurred in women who developed uterine rupture without epidural analgesia but not in women who received an epidural block. Thus, abdominal pain is an unreliable and uncommon sign of uterine rupture.

Diagnosis

Because of the short time available to diagnose uterine rupture before the onset of irreversible physiologic damage to the fetus, time-consuming diagnostic methods and sophisticated imaging modalities have only limited use. Therefore, uterine rupture is most appropriately diagnosed on the basis of standard signs and symptoms.
Despite this limitation, various diagnostic techniques have been used to attempt to assess the individual risk of uterine rupture in selected patients. Amniography, radiopelvimetry, and pelvic examination have all proven unsuitable for predicting the risk of uterine rupture in women who desire a TOL after a previous cesarean delivery. In addition, imaging modalities such as CT and MRI have not been clinically useful in diagnosing acute uterine rupture because of the time constraints involved in establishing the diagnosis. Given this limitation, MRI is thought to be superior to CT for evaluating the status of a uterine incision because of its increased soft tissue contrast.

Several reports have suggested that trans-abdominal, trans-vaginal, or sonohysterographic ultrasonography may be useful for detecting uterine-scar defects after cesarean delivery. The risk of uterine rupture after previous cesarean delivery was directly related to the thickness of the lower uterine segment, as measured during trans-abdominal ultra-sonography at 36-38 weeks of gestation. The risk of uterine rupture increased significantly when the uterine wall was thinner than 3.5 mm.

Overview 

The consequences of uterine rupture during pregnancy depend on the time that elapses from the rupture until the institution of definitive therapy. Definitive therapy for the fetus is delivery and must generally be accomplished with alacrity to avoid major fetal morbidity and mortality. Conversely, therapy for the mother can generally be supportive and resuscitative until surgical intervention can be undertaken to arrest the often life-threatening uterine hemorrhage. Several studies have shown that delivery of the fetus within 10-37 minutes of uterine rupture is necessary to prevent serious fetal morbidity and mortality. If proper supportive measures (including fluid resuscitation and blood transfusion), are available to treat the mother, the time for definitive surgical intervention before the onset of major maternal morbidity and mortality may often be substantially longer than that for the fetus.

Therefore, the consequences of uterine rupture may be divided into 2 major categories, depending on whether they apply to the fetus or to the mother.

Fetal Consequences of Uterine Rupture

Fetal hypoxia or anoxia

No neonate had clinically significant perinatal morbidity when delivery was accomplished within 17 minutes of an isolated and prolonged deceleration of fetal heart rate. If severe late decelerations preceded prolonged deceleration, perinatal asphyxia was observed as soon as 10 minutes from the onset of the prolonged deceleration to delivery.

Fetal acidosis

The most important factor for the development of fetal acidosis was complete extrusion of the fetus and placenta into the maternal abdomen.

Maternal Consequences of Uterine Rupture

Severe maternal blood loss or anemia

Patients, who developed uterine rupture, mean blood loss was 1,500 mL and great enough to be symptomatic and patient who had uterine rupture during a TOL after a previous cesarean delivery received a blood transfusion. Many patients, who had a complete uterine rupture, required blood transfusion.

Maternal death

The availability of modern medical facilities in developed nations is likely to account for this difference in maternal outcomes.
The maternal mortality rate associated with uterine rupture largely depends on whether the diagnosis is established before or after delivery.

Treatment

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

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

Uterine bleeding is typically most profuse when the uterine tear is longitudinal rather than transverse. Conservative surgical management involving uterine repair should be reserved for women who have the following findings:

Hysterectomy should be considered the treatment of choice when intractable uterine bleeding occurs or when the uterine rupture sites are multiple, longitudinal, or low lying. Because of the short time available for successful intervention, the following 2 premises should always be kept firmly in mind: (1) Maintain a suitably high level of suspicion regarding a potential diagnosis of uterine rupture, especially in high-risk patients, and (2) when in doubt, act quickly and definitively.

Prevention

The absolute risk of uterine rupture in pregnancy is low, but it is highly variable depending on the patient subgroup. Women with normal, intact uteri are at the lowest risk for uterine rupture. The most direct prevention strategy for minimizing the risk of pregnancy-related uterine rupture is to minimize the number of patients who are at highest risk. The salient variable that must be defined in this regard is the threshold for what is considered a tolerable risk. Although this choice is ultimately arbitrary, it should reflect the prevailing risk tolerance of patients, physicians, and of society as a whole. the categories of patients that exceed critical value are those with the following:

Uterine rupture is a rare but often catastrophic obstetric complication. The vast majority of uterine ruptures occur in women who have uterine scars, most of which are the result of previous cesarean deliveries. Other subgroups of women who are at increased risk for uterine rupture are those who have a previous single-layer hysterotomy closure, a short inter-pregnancy interval after a previous cesarean delivery, a congenital uterine anomaly, a macrosomic fetus, prostaglandin exposure, and a failed previous trial of a vaginal delivery.

Surgical intervention after uterine rupture in less than 10-37 minutes is essential to minimize the risk of permanent perinatal injury to the fetus. However, delivery within this time cannot always prevent severe hypoxia and metabolic acidosis in the fetus or serious neonatal consequences.
The most consistent early indicator of uterine rupture is the onset of a prolonged, persistent, and profound fetal bradycardia. Other signs and symptoms of uterine rupture, such as abdominal pain, abnormal progress in labor, and vaginal bleeding, are less consistent and less valuable than bradycardia in establishing the appropriate diagnosis.

The general guideline that labor-and-delivery suites should be able to start cesarean delivery within 20-30 minutes of a diagnosis of fetal distress is of minimal utility with respect to uterine rupture. In the case of fetal or placental extrusion through the uterine wall, irreversible fetal damage can be expected before that time; therefore, such a recommendation is of limited value in preventing major fetal and neonatal complications. However, action within this time may aid in preventing maternal exsanguination and maternal death, as long as proper supportive and resuscitation methods are available before definitive surgical intervention can be successfully initiated.

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Last Editorial Review: November 2nd 2009
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