A Case Series of Uterine Rupture: Lessons to be Learned for Future Clinical Practice

Abstract

Objective: In this article, we try to discuss risk factors and diagnostic difficulties for uterine rupture.

Methods: Case series of 12 cases of uterine rupture observed in the Norfolk and Norwich University Hospital in the UK, with an average yearly birth rate of 6,000 deliveries, over a 6-year period.

Results: In the present case series, there was no maternal mortality, and uterine rupture was a rare occurrence (12 in 36,000 births). Uterine rupture is associated with clinically significant uterine bleeding, fetal distress, expulsion or protrusion of the fetus, placenta or both into the abdominal cavity, and the need for prompt cesarean delivery and uterine repair or hysterectomy. The risk factors for rupture include previous cesarean sections, multiparity, malpresentation and obstructed labor, uterine anomalies, and use of prostaglandins for induction of labor. Previous cesarean section is, however, the most commonly associated risk factor. The most consistent early indicator of uterine rupture is the onset of a prolonged, persistent, and profound fetal bradycardia.

Conclusion: In this case series, we suggest that the signs and symptoms of uterine rupture are typically nonspecific, which makes diagnosis difficult. Delay in definitive therapy causes significant fetal morbidity. The inconsistent signs and the short time in prompting definitive treatment of uterine rupture make it a challenging event. For the best outcome, vaginal birth after previous cesarean section needs to be looked after in an appropriately staffed and equipped unit for an immediate cesarean delivery and advanced neonatal support.

Keywords: Previous cesarean section; Prolonged bradycardia; Risk factor; Uterine rupture.

Fig. 1

Preterminal CTG trace

Fig. 2

Example of normal CTG

Fig. 3

Bradycardia on CTG

Fig. 4

Atypical variable decelerations on CTG

Fig. 5

Atypical variable decelerations with reduced variability CTG

Fig. 6

Deep decelerations on CTG

Fig. 7

Pathological CTG

Chart 1

Flow chart of management of VBAC