Uterine rupture is one of the most important obstetric emergencies, threatening the lives of both mother and fetus. There are two types of rupture: 1) complete, where the whole thickness of the uterine wall is involved, usually occurring in an unscarred uterus; and 2) incomplete, where the visceral peritoneum remains intact, as seen in scar dehiscence [3]. We could not categorize our case using either definition since it was somewhat different. The rupture seen in our case was not complete because only one-third of the uterine wall was involved, without communication between the uterine and the peritoneal cavities. We think that this may be the reason why excessive bleeding through the vaginal route was not seen. The rupture was not incomplete either, since the visceral peritoneum was not intact at that site. Although most cases in the literature were placed into one of these two categories, only a few were similar to ours in appearance. Langton et al reported a case of spontaneous uterine rupture that occurred in a nonlaboring uterus of a primigravid with no previous risk factors at 32 weeks and a tear extending into two-thirds of the uterine wall with small actively bleeding vessels was identified during laparotomy [4]. The patient in our case was a grandmultiparous woman at term and laboring.
The most common presentation is intrapartum, but rupture can be diagnosed ante- or postpartum. Intrapartum events are usually detected after a sudden increase in maternal pulse rate and a decrease in blood pressure together with vaginal bleeding and abdominal pain followed by fetal bradycardia [5]. However, in the postpartum period, a clinical diagnosis is difficult and a high index of suspicion is essential. Hruska et al described a patient who presented to the outpatient obstetrical clinic with worsening left lower quadrant abdominal pain 4 days postpartum of an uncomplicated, vaginal delivery involving low dose oxytocin stimulation and underwent a total abdominal hysterectomy due to a defect in the left lower uterine wall [6]. That patient stated that the pain had been present since after her delivery but had worsened in the past day and described the pain as a "burning" sensation radiating to her left back. In our case, the only positive signs in the patient were a transient drop in blood pressure during labor and orthostatic hypotension afterwards. The patient did not report any specific type of pain other than some pain thought to be related to parturition. However, the patient did not want to undergo surgery for some time when it was recommended after our preoperative diagnosis of uterine rupture.
Risk factors for uterine rupture include obstructed labor, grand multiparity, placenta percreta, induction of labor in a woman with a previously scared uterus, uterine anomalies, inappropriate prostaglandin and oxytocin usage, previous instrumental abortion, vacuum extraction and forceps delivery, vigorous fundal pressure, and intrauterine manipulations [1, 2]. In our patient, the identified risk factors were grand multiparity and fundal pressure.
Fundal pressure is the application of steady pressure on the fundus of the uterus and is considered among the most controversial maneuvers that are used in the second stage of labor since no confirmed benefit of the procedure has been documented and a few adverse events have been reported in association with its use.
Pan et al reported a case of uterine rupture due to traumatic fundal pressure in a primigravid woman with an unscarred uterus [1]. Wei et al also reported an unusual case associated with traumatic assisted fundal pressure related uterine rupture at 34 weeks of gestation in a pregnancy complicated by hydrops fetalis and shoulder dystocia [7]. In a review by Güney et al, 1 out of 8 ruptured unscarred uterus cases was found to be related to the application of fundal pressure [8]. A prospective study consisting of 63 patients with uterine rupture, among whom half had a uterine scar, revealed that fundal pressure, along with forceps and oxytocin use, was an iatrogenic factor associated with uterine rupture [9]. However, in that study, there was no control group and so it is unknown whether fundal pressure was an independent factor in causing uterine rupture [10]. In our case, the mother had an unscarred uterus and was not given any prostaglandin or oxytocin during labor. We applied assisted uterine fundal pressure during the delivery since fetal bradycardia was noted and the mother was too exhausted to push the baby properly. Thus, we tried to accelerate the second stage of labor in order to save the baby. However, Wei et al stated that they applied fundal pressure because of coexistent shoulder dystocia [7], but fundal pressure should be avoided if shoulder dystocia is identified. If applied in this circumstance, the shoulder will be further impacted and increase the chances of injury to the baby [11]. In this situation, fundal pressure possibly also increases the risk of uterine rupture.
