Rupture of the Uterus

Uterine rupture may be primary, defined as occurring in a pre-viously intact or unscarred uterus, or may

be secondary and associated with a preexisting myometrial inci- sion, injury, or anomaly. Some of the

etiologies associated with uterine rupture are presented in Table 41-3. Importantly, the contribu- tion of

each of these underlying causes has changed remarkably during the past 50 years. Specifically, before

1960, when the cesarean delivery rate was much lower than it is cur- rently and when women of great

parity were numerous, primary uterine rupture predomi- nated. As the incidence of cesarean delivery

increased and especially as a subsequent trial of labor in these women became prevalent through the

1990s, uterine rupture through the cesarean hysterotomy scar became pre- eminent. As discussed in

detail in Chapter 31 (p. 617), along with diminished enthusiasm for trial of labor in women with prior

cesarean delivery, the two types of rupture likely now have equivalent incidences. Indeed, in a 2006 study

of 41 cases of uterine rupture from the Hospital Corporation of America, half were in women with a prior

cesarean delivery (Porreco, 2009).

Predisposing Factors and Causes

In addition to the prior cesarean hysterotomy incision already discussed, risks for uterine rupture include

other previous operations or manipulations that traumatize the myo- metrium. Examples are uterine

curettage or perforation, endometrial ablation, myomec- tomy, or hysteroscopy (Kieser, 2002; Pelosi,

1997). In the study by Porreco and colleagues (2009) cited earlier, seven of 21 women with- out a prior

cesarean delivery had undergone prior uterine surgery.

In developed countries, the incidence of rupture was cited by Getahun and associates (2012) as 1 in 4800

deliveries. The frequency of primary rup- ture approximates 1 in 10,000 to 15,000 births (Miller, 1997;

Porreco, 2009). One reason is a decreased incidence of women of great parity (Maymon, 1991; Miller,

1997). Another is that excessive or inappropriate uterine stimulation with oxy- tocin—previously a

frequent cause—has mostly disappeared. Anecdotally, however, we have encountered primary uterine

rupture in a disparate number of women in whom labor was induced with prostaglandin E 1.
Pathogenesis. Rupture of the previously intact uterus during labor most often involves the thinned-out

lower uterine segment. When the rent is in the immediate vicinity of the cervix, it fre- quently extends

transversely or obliquely. When the rent is in the portion of the uterus adjacent to the broad ligament, the

tear is usually longitudinal. Although these tears develop primarily in the lower uterine segment, it is not

unusual for them to extend upward into the active segment or downward through the cervix and into the

vagina (Fig. 41-13). In some cases, the bladder may also be lacerated (Rachagan, 1991). If the rupture is

of suf- ficient size, the uterine contents will usually escape into the peritoneal cavity. If the presenting

fetal part is firmly engaged, however, then only a portion of the fetus may be extruded from the uterus.

Fetal prognosis is largely dependent on the degree of placental separation and magnitude of maternal

hemorrhage and hypovolemia. In some cases, the overlying peritoneum remains intact, and this usually is

accompanied by hemorrhage that extends into the broad ligament to cause a large retroperitoneal

hematoma with extensive blood loss.

Occasionally, there is an inherent weakness in the myo- metrium in which the rupture takes place. Some

examples include anatomical anomalies, adenomyosis, and connective- tissue defects such as Ehlers-

Danlos syndrome (Arici, 2013; Nikolaou, 2013).

Management and Outcomes. The varied clinical presenta- tions of uterine rupture and its management

are discussed in detail in Chapter 31 (p. 617).

In the most recent maternal mortality statistics from the Centers for Disease Control and Prevention,

uterine rupture accounted for 14 percent of deaths caused by hemorrhage (Berg, 2010). Maternal

morbidity includes hysterectomy that may be neces- sary to control hemorrhage. There is also

considerably increased perinatal morbidity and mortality associated with uterine rup- ture. A major

concern is that surviving infants develop severe neurological impairment (Porreco, 2009).

Traumatic Uterine Rupture

Although the distended pregnant uterus is surprisingly resistant to blunt trauma, pregnant women

sustaining such trauma to the abdomen should be watched carefully for signs of a rup- tured uterus

(Chap. 47, p. 954). Even so, blunt trauma is more likely to cause placental abruption as described
subsequently. In a study by Miller and Paul (1996), trauma accounted for only three cases of uterine

rupture in more than 150 women.

Other causes of traumatic rupture that are uncommon today are those due to internal podalic version and

extraction, dif- ficult forceps delivery, breech extraction, and unusual fetal enlargement such as with

hydrocephaly.

Classification

Uterine rupture typically is classified as either (1) complete when all layers of the uterine wall are

separated, or (2) incomplete when the uterine muscle is separated but the visceral perito- neum is intact.

Incomplete rupture is also commonly referred to as uterine dehiscence. As expected, morbidity and

mortality rates are appreciably greater when rupture is complete. The greatest risk factor for either form

of rupture is prior cesarean delivery. In a review of all uterine rupture cases in Nova Scotia between 1988

and 1997, Kieser and Baskett (2002) reported that 92 percent were in women with a prior cesarean

birth. Holmgren and associates (2012) described 42 cases of rupture in women with a prior hysterotomy.

Of these, 36 were in labor at the time of rupture.

Diagnosis

Progress of labor in women attempting VBAC is similar to reg- ular labor, and there is no specific pattern

that presages uterine rupture (Graseck, 2012; Harper, 2012b). Before hypovolemic shock develops,

symptoms and physical findings in women with uterine rupture may appear bizarre unless the possibility

is kept in mind. For example, hemoperitoneum from a rup- tured uterus may result in diaphragmatic

irritation with pain referred to the chest—directing one to a diagnosis of pulmo- nary or amnionic fluid

embolism instead of uterine rupture. The most common sign of uterine rupture is a nonreassuring fetal

heart rate pattern with variable heart rate decelerations that may evolve into late decelerations and

bradycardia as shown in Figure 31-4 (American Academy of Pediatrics and American College of

Obstetricians and Gynecologists, 2012). In 36 cases of such rupture during a trial of labor, there were fetal

signs in 24, maternal in eight, and both in three (Holmgren, 2012). Few women experience cessation of
contractions fol- lowing uterine rupture, and the use of intrauterine pressure catheters has not been

shown to assist reliably in the diagnosis (Rodriguez, 1989).

In some women, the appearance of uterine rupture is iden- tical to that of placental abruption. In most,

however, there is remarkably little appreciable pain or tenderness. Also, because most women in labor

are treated for discomfort with either narcotics or epidural analgesia, pain and tenderness may not be

readily apparent. The condition usually becomes evident because of fetal distress signs and occasionally

because of mater- nal hypovolemia from concealed hemorrhage.

If the fetal presenting part has entered the pelvis with labor, loss of station may be detected by pelvic

examination. If the fetus is partly or totally extruded from the uterine rupture site, abdominal palpation

or vaginal examination may be helpful to identify the presenting part, which will have moved away from

the pelvic inlet. A firm contracted uterus may at times be felt alongside the fetus.

Decision-to-Delivery Time

With rupture and expulsion of the fetus into the peritoneal cavity, the chances for intact fetal survival are

dismal, and reported mortality rates range from 50 to 75 percent. Fetal condition depends on the degree to

which the placental implan- tation remains intact, although this can change within minutes. With rupture,

the only chance of fetal survival is afforded by immediate delivery—most often by laparotomy—

otherwise, hypoxia is inevitable. If rupture is followed by immediate total placental separation, then very

few intact fetuses will be sal- vaged. Thus, even in the best of circumstances, fetal salvage will be impaired.

The Utah experiences are instructive here (Holmgren, 2012). Of the 35 laboring patients with a uterine

rupture, the decision-to-delivery time was 18 minutes in 17, and none of these infants had an adverse

neurological outcome. Of the 18 born 18 minutes from decision time, the three infants with long-term

neurological impairments were delivered at 31, 40, and 42 minutes. There were no deaths, thus severe

neo- natal neurological morbidity developed in 8 percent of these 35 women with uterine rupture.

In a study using the Swedish Birth Registry, Kaczmarczyk and colleagues (2007) found that the risk of

neonatal death following uterine rupture was 5 percent— a 60-fold increase in risk compared with

pregnancies not complicated by uterine rupture. In the Network study, seven of the 114 uterine
ruptures—6 percent— associated with a trial of labor were com- plicated by the development of neonatal

hypoxic ischemic encephalopathy (Spong,

Maternal deaths from rupture are uncommon. For example, of 2.5 mil- lion women who gave birth in

Canada between 1991 and 2001, there were 1898 cases of uterine rupture, and four of these—0.2

percent—resulted in maternal death (Wen, 2005). In other regions of the world, however, maternal

mortality rates associated with uterine rupture are much higher. In a report from rural India, for example,

the maternal mortality rate associated with uterine rupture was 30 percent (Chatterjee, 2007).

Hysterectomy versus Repair

With complete rupture during a trial of labor, hysterec- tomy may be required. In the reports by

McMahon (1996) and Miller (1997) and their coworkers, 10 to 20 percent of such women required

hysterectomy for hemostasis. In selected cases, however, suture repair with uterine preserva- tion may

be performed. Sheth (1968) described outcomes from a series of 66 women in whom repair of a uterine

rup- ture was elected rather than hysterectomy. In 25 instances, the repair was accompanied by tubal

sterilization. Thirteen of the 41 mothers who did not have tubal sterilization had a total of 21 subsequent

pregnancies. Uterine rupture recurred in four of these—approximately 25 percent. Usta and associates

(2007) identified 37 women with a prior complete uterine rupture delivered during a 25-year period in

Lebanon. Hysterectomy was performed in 11, and in the remaining 26 women, the rupture was repaired.

Twelve of these women had 24 subsequent pregnancies, one third of which were complicated by

recurrent uterine rupture. In another study, however, women with a uterine dehiscence were not more

likely to have uterine rupture with a subse- quent pregnancy (Baron, 2013b).

Because of the concerns with attempting a trial of labor—even in the woman with excellent criteria that

forecast successful VBAC—most women in the United States undergo elective repeat cesarean delivery.

This choice is not without several sig- nificant maternal complications, and rates of these increase in

women who have multiple repeat operations. The incidences of some common complications for women

with one prior trans- verse cesarean delivery who undergo an elective repeat cesarean delivery were
shown in Table 31-2. Finally, half of cesarean hysterectomies done at Parkland Hospital are in women

with one or more prior cesarean deliveries (Hernandez, 2013).

The Network addressed issues of increased morbidity in a cohort of 30,132 women who had from one to

six repeat cesarean deliveries (Silver, 2006). This report addressed a list of morbidities, most of which

increased as a trend with increasing number of repeat operations. The rates of some of the more common

or serious complications are depicted in Figure 31-5. In addition to the ones shown, rates of bowel or

bladder injury, admission to an intensive care unit or ventilator therapy, and maternal mortality, as well

as operative and hospitalization length, showed significantly increasing trends. Similar results have been

reported by others (Nisenblat, 2006; Usta, 2005). More difficult to quantify are risks for bowel

obstructions and pelvic pain from peritoneal adhesive disease, both of which increase with each

successive cesarean delivery (Andolf, 2010; Mankuta, 2013).

Cook and colleagues (2013) from the United Kingdom Obstetric Surveillance System (UKOSS) described

adverse sequelae of women with multiple cesarean deliveries. Outcomes of those undergoing a fifth or

greater operation were compared with those from women having a second through fourth pro- cedure.

Those having five or more cesarean deliveries had sig- nificantly increased rates of morbidity compared

with rates in women having fewer than five procedures. Specifically, the major hemorrhage rate

increased 18-fold; visceral damage, 17-fold; critical care admissions, 15-fold; and delivery 37 weeks,

sixfold. Much of this morbidity was in the 18 percent who had placenta previa or accrete syndromes

(Chap. 41, p. 799). A percreta may invade the bladder or other adjacent structures. With this, dif- ficult

resection carries an inordinately high risk of hysterectomy, massive hemorrhage with transfusion, and

maternal mortality.