Uterine Rupture During VBAC Trial Of Labor: Risk Factors and Fetal Response

Nancy O'Brien-Abel, RNC, MN


J Midwifery Womens Health. 2003;48(4) 

In This Article

Timing of Birth and Neonatal Outcome

Several studies have attempted to evaluate the timing of birth and neonatal outcome in women with uterine rupture during VBAC-TOL. Bujold et al.[16] compared neonatal morbidity associated with uterine rupture during VBAC-TOL to neonatal morbidity following umbilical cord prolapse when the median time from the first manifestation to birth was comparable (18 versus 17 minutes). Although similar in response times, neonatal neurological morbidity was more significant with uterine rupture than with umbilical cord prolapse. Neonatal arterial blood pH less than 7.1 occurred in 47% of the uterine rupture cases compared to only 3% in the umbilical cord prolapse group (P < .005). Likewise, 5-minute Apgar scores less than 6 were found in 33% of the uterine rupture cases compared to 3% in the umbilical cord prolapsed group (P < .05). At 2- to 6-month follow-up, three (20%) of the newborns in the uterine rupture group were diagnosed with ischemic encephalopathy and major neurologic impairment compared to none in the cord prolapse group (P < .05).

Porter et al.[15] examined the neonatal outcome in 26 cases of uterine rupture occurring during VBAC-TOL in large hospitals in a single metropolitan region, all of which had 24-hour in-house anesthesia coverage. Six (23%) infants suffered either neonatal death or adverse neurologic sequelae as a result of the uterine rupture. Poor neonatal outcome was seen in 31% of the infants birthed within 30 minutes and in 33% of the infants birthed within 20 minutes of either severe variable decelerations or bradycardia.

In a larger study, Leung et al.[14] evaluated 78 cases of uterine rupture in a large tertiary care medical center and reported significant neonatal morbidity when 18 minutes or more elapsed between the onset of prolonged deceleration and birth. When the prolonged deceleration was preceded by severe late or variable decelerations, fetal asphyxia occurred as early as 10 minutes from the onset of prolonged deceleration.

Similarly, Bujold and Gauthier[17] examined 23 cases of uterine rupture in a tertiary care medical center with in-house obstetricians and anesthesiologists. Nine neonates (39%) had severe metabolic acidosis. Among these, four neonates had seizures, two had multiple organ failure, and three were diagnosed with hypoxic-ischemic encephalopathy. Within this group, one intrapartum death occurred. All three neonates with hypoxic-ischemic encephalopathy were outside the uterus at the time of laparotomy. Contrary to the findings of Leung et al., less than 18 minutes elapsed between the time of prolonged deceleration and delivery in two of the three neonates diagnosed with hypoxic-ischemic encephalopathy (15 and 16 minutes).

Prompt intervention does not always prevent severe, fetal metabolic acidosis or neonatal death. Even in facilities with immediate access to cesarean birth uterine rupture can result in catastrophic outcome. A non-reassuring FHR pattern, occurring prior to the time of uterine rupture, further decreases the amount of time available before fetal insult occurs.


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