Department of Obstetrics and Gynecology, Veterans General Hospital-Taipei and Institute of Clinical Medicine, National Yang-Ming University, Taipei 201, Section 2, Shih-Pai Road, Taipei 11217, Taiwan
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Abstract |
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Key words: Caesarean section/uterine rupture/vaginal birth
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Introduction |
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Case report |
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The labour course progressed smoothly. In this labour process, neither oxytocin nor prostaglandin augmentation was administered. During labour, no fetal distress was found and uterine contractions were without overt or abnormal contractions. The feto-tocomonitor proved a normal labour course. After a 3 h time lapse, the patient had 6 cm of the cervical dilation. Sudden onset of acute abdominal pain and drop of blood pressure occurred in the mother and at the same time fetal heartbeats were undetectable. Rapid progression to shock was noted, subsequent coma occurred, and initial resuscitation began. Simultaneously, the patient immediately received laparotomy within 15 min after initial resuscitation. Operative findings revealed a large haemoperitoneum (4000 ml of bloody ascites in the peritoneal cavity) and the fetus was completely out of the uterus.
After an urgent delivery of the fetus from the abdominal cavity, an 8 cm irregular laceration wound was found on the posterior uterine wall near the low segment of the uterus and on the opposite side from the scar due to previous Caesarean section. Active bleeding was noted at the laceration wound. The placenta was located in the fundal area. Neither abnormal placental implantation nor placental eruption could be identified. Congenital anomaly of the uterus was absent. Bilateral tubes and ovaries appeared healthy and were normally attached to the uterus. The Caesarean section scar on the anterior uterine wall had healed well. The fetus weighed 3150 g and had Apgar scores of 1, 1 and 1 at 1, 5 and 10 min respectively. Primary repair of the uterus and ligature of bilateral uterine vessels were performed. The total volume of blood loss was estimated at 12 000 ml. After appropriate treatment, the mother was discharged uneventfully 10 days after delivery, but the fetus died of encephalopathy and widespread necrotizing enterocolitis that may have been secondary to severe hypoxia. The patient is now well educated for future pregnancies. The most important thing would be to include intensive care during her whole pregnancy course and a repeat Caesarean section for delivery because she is not a good candidate for vaginal delivery.
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Discussion |
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A handful of cases addressing uterine rupture regardless of spontaneous or augmenting labour either on a possibly normal uterus or a on scarred uterus have been reported in the literature (McLellan, 1916; Nagy, 1989
; Saglamtas et al., 1995
; Levrant and Wingate, 1996
; Hawe and Olah, 1997
; Kindig et al., 1998
; Sciscione et al., 1998
; Wing et al., 1998
); however, only a very limited number of cases occurred in an area that was not anticipated (Hawe and Olah, 1997
), as in our patient. The patient denied any history of medical illnesses, and denied history of intrauterine device insertion. This is the first documented spontaneous rupture on the posterior wall on the opposite side from a previous Caesarean section in a uterus, to have occurred at 38 weeks gestation. The patient did not accelerate the labour course by any medication such as misoprostol or prostaglandin. The benefits and safety of VBAC have not been undermined because uterine rupture could occur at any time or in any position, even without evidence of risk factors. We suggest that it is necessary to repeat Caesarean section rapidly after attempting and failing VBAC and to encourage routine examinations of VBAC in women without contra-indications.
Others have concluded (Phelan et al., 1998) that uterine activity patterns and oxytocin use do not appear to be associated with the occurrence of intrapartum uterine rupture. In our case, the patient had a smooth and uneventful labour course, which was confirmed by routine feto-tocomonitor results. Many reports demonstrated that underlying pathological changes could be anticipated in the presence of certain risk factors; however, our patient was devoid of any of the following risk factors which might contribute to spontaneous uterine rupture, including multiparity, uterine anomaly, uterine diverticulae, placenta percreta, arteriovenous malformation, endometriosis, endometritis, precipitous labour or obstructed labour (McLellan, 1916
; Nagy, 1989
; Langton et al., 1997
; Imseis et al., 1998
; Kindig et al., 1998
). It was difficult for us to provide a reasonable explanation as to why the uterus would rupture in the area it did. In this patient, we did not perform biopsy during the emergency operation for an established wound, so we cannot really exclude any possibility of underlying pathological changes. However, we believe that the patient was an isolated case and had a normal uterus based on the operative findings. The findings included that the placenta was easily removed from the fundal area, the placenta did not invade the rupture site as established after careful examination of the uterus and the observation that it was grossly normal.
In conclusion, because this report is about an isolated and extremely rare case, the benefits and safety of VBAC have not been undermined. We should, however, bear in mind that prompt response to every woman during labour is of paramount importance to avoid repeating this type of incident.
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Acknowledgments |
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Notes |
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References |
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Submitted on August 23, 1999; accepted on January 27, 2000.