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Case Report Posterior Uterine Rupture Causing Fetal Expulsion Into the Abdominal Cavity: a Rare Case of Neonatal Survival

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Case Report Posterior Uterine Rupture Causing Fetal Expulsion Into the Abdominal Cavity: a Rare Case of Neonatal Survival Hindawi Publishing Corporation Case Reports in Obstetrics and Gynecology Volume 2011, Article ID 426127, 3 pages doi:10.1155/2011/426127 Case Report Posterior Uterine Rupture Causing Fetal Expulsion into the Abdominal Cavity: A Rare Case of Neonatal Survival K. Navaratnam, P. Ulaganathan, M. A. Akhtar, S. D. Sharma, and M. G. Davies Southport and Ormskirk Hospital, NHS Trust, Town Lane, Kew, Southport, Merseyside PR8 6PN, UK Correspondence should be addressed to K. Navaratnam, [email protected] Received 25 June 2011; Accepted 21 August 2011 AcademicEditors:Y.Ezra,K.Matsuo,andI.M.Usta Copyright © 2011 K. Navaratnam et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Uterine rupture is a potentially catastrophic complication of vaginal birth after caesarean section. We describe the sixth case of posterior uterine rupture, with intact lower segment scar, and the first neonatal survival after expulsion into the abdominal cavity with posterior rupture. Case Presentation. A multiparous woman underwent prostaglandin induction of labour for postmaturity, after one previous caesarean section. Emergency caesarean section for bradycardia revealed a complete posterior uterine rupture, with fetal and placental expulsion. Upon delivery, the baby required inflation breaths only. The patient required a subtotal hysterectomy but returned home on day 5 postnatally with her healthy baby. Discussion. Vaginal birth after caesarean section constitutes a trial of labour, and the obstetrician must be reactive to labour events. Posterior uterine rupture is extremely rare and may occur without conventional signs. Good maternal and fetal outcome is possible with a prompt, coordinated team response. 1. Introduction uneventful consultant-led care throughout her third preg- nancy. She attended counselling regarding mode of delivery, Uterine rupture is a recognised complication of vaginal with explicit discussion of postmaturity management, and birth after caesarean section (VBAC), with serious maternal specific risks of uterine rupture during spontaneous labour, and fetal outcomes. It is conventionally attributed to the induction, and augmentation. She chose to proceed with a structural compromise of the uterine scar, as depicted by trial of labour, with induction of labour if indicated. Third- the term “trial of scar.” The incidence of uterine rupture trimester ultrasound demonstrated a posterior placenta, and during VBAC is the lowest after one previous caesarean well-grown fetus, with cephalic presentation. section, with spontaneous, progressive labour not requiring At 42 weeks of gestation she was admitted, for Pros- augmentation. Prostaglandins and oxytocics to induce and taglandin induction, according to protocol. On admission, augment labour increase the risk of uterine rupture 2-3- her Bishop’s score was 4, and 1 mg prostaglandin E2 fold. We present a case of atypical uterine rupture of the was administered vaginally. After 12 hours she was 2 cm posterior uterine wall, with induced, augmented labour, dilated, and partially effaced, transferred to delivery suite and a discussion of the case characteristics and the existing for continuous fetal cardiotocography (CTG) and artificial literature. rupture of membranes (ARM). After ARM, uterine activity remained mild and incoordinate and induction of labour 2. Case Presentation was continued with oxytocin. She established in labour, with oxytocin titrated to uterine activity, with regular moderate A 38-year-old gravida 3, para 2 requested VBAC. She pre- contractions and a 3-minute pain-free interval. After 6 hours viously had a spontaneous vaginal delivery at term, followed of Oxytocin her cervix was effaced and 5 cm dilated, the by unstable lie in her second pregnancy, necessitating elective fetal head was in the left occipitotransverse position, and lower segment caesarean section at 37 weeks. There were station was −2. 18 minutes later she had a brisk antepartum no existing medical or antenatal problems, and she had haemorrhage (APH) of 150 mL, associated with persistent 2 Case Reports in Obstetrics and Gynecology fetal bradycardia to 80 bpm. She was rapidly assessed by perinatal death associated with uterine rupture is 1/20 and the specialist registrar. Uterine scar rupture was suspected, 1-2/100, respectively [1]; maternal death occurs in 1/100000 and a grade one emergency caesarean section conducted, cases [8]. under general anaesthetic, with the consultant obstetrician In scarred uteri, the vast majority of uterine dehiscence in attendance. and ruptures will occur via the uterine scar. The atrophic, Upon peritoneal entry, there was a large haemoperi- inelastic nature of the scar renders it less adaptive to forces in toneum and the uterus was well contracted with an intact labour, predisposing to scar rupture. However, a particularly lower segment scar. The fetus and placenta had been expelled rigid anterior lower segment may cause abnormal distribu- via a posterolateral uterine wall rupture, both were free in the tion of force. During retraction, the posterior wall may be posterior peritoneal cavity. A live male infant was promptly excessively shortened and thinned due to the rigid anterior delivered and handed to the neonatal team; the decision to uterine scar, catalysing atypical uterine rupture via healthy delivery interval was 13 minutes. tissue. Any factor compromising uterine structural integrity Initially the infant made no respiratory effort but main- or causing abnormal distribution of force can precipitate tained a heart rate of greater than 100 bpm. Three cycles uterine rupture. The site of uterine rupture is unpredictable of five inflation breaths were required. Apgar scores were 2 and may be atypical. at1minute,6at5minutes,and10at10minutes.Venous Five cases of posterior uterine rupture complicating vag- and arterial umbilical cord pHs were 6.988 with Base excess inal birth after caesarean section have been published from −13.4 and 6.958 with Base Excess −10.1, respectively. The 1997 to 2007 [9–13]. Recognised factors predisposing to birthweight was 3.26 kg. uterine rupture during VBAC are induction or augmenta- The 8 cm posterior uterine rupture extended into the left tion of labour, slow progress, labour dystocia, multiparity, lateral uterine wall, and the left infundibulopelvic ligament fetal malposition, short interdelivery interval (less than 24 was completely avulsed from its attachment. The infundibu- months), and placenta accreta [6]. In this case, the patient lopelvic vessels had retracted into the retroperitoneal space had one previous spontaneous vaginal delivery, followed by and were bleeding persistently. Due to severe uterine trauma a caesarean section for unstable lie. Two other women were with loss of pelvic attachments and haemorrhage, a subtotal multiparous with parity of three or greater [9, 13], one with a hysterectomy was required. A senior consultant was called previous twin pregnancy [13]. It is possible that uterine laxity to assist, and the consultant anaesthetist and haematologist or hyperdistension predisposes to atypical uterine rupture. were alerted. After completing the subtotal hysterectomy, the In addition to our patient’s case there are two reported retroperitoneal space was opened, to mobilise the infundibu- cases of posterior uterine rupture with prostaglandin induc- lopelvic vessels. The estimated intraoperative haemorrhage tion of labour, using prostaglandin E2 and dinoprostone [9, was 2000 mL. The patient had high-dependency obstetric 11]. Three cases of posterior uterine rupture in spontaneous care for 24 hours postoperatively, haemoglobin intraopera- labour are also recorded [10, 12, 13]. In our patient’s case tively was 5.0 g/dL and a transfusion of 4 units of packed red the fetal head was occipitotransverse prior to rupture. cells was commenced. The events were carefully explained Fetal malposition with an occipitoposterior position has by the operating consultant, and the patient recovered re- previously contributed to posterior uterine ruptures, as has markably quickly. She was discharged home with her baby malpresentation with a transverse lie and dead fetus [12, 13]. on day five postnatally and comprehensively debriefed by the Malposition alters the distribution of contractile force and obstetric team six weeks postnatally. increases labour dystocia; certain malpresentations cause uterine hyperdistension, which may also precipitate atypical 3. Discussion uterine rupture. In our experience, and that of two others, the first sign Uterine rupture is a defect involving the full thickness of the of posterior uterine rupture was a pathological CTG with myometrium and uterine serosa or myometrial disruption persistent fetal bradycardia [10, 11]. CTG abnormalities are extending to the bladder or broad ligament [1]. Uterine de- associated with 55–87% of uterine ruptures [14]. Other hiscence describes a partial thickness defect, with intact recognised signs of uterine rupture include loss of station of uterine serosa, which may progress to rupture [1]. Uterine presenting part and new inefficient contractility [6]. rupture occurring in an unscarred uterus is very rare, with APH, as in this case, often indicates uterine rupture an incidence of 0.5–2.0/10000, largely confined to labouring and may occur in association with shoulder tip pain due multiparas [2]. However, isolated
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