While a common complication during the first VBAC, uterine rupture decreases during the subsequent VBACs . When present, ruptured uterus is often associated with induction/augmentation of labour [2–4, 6, 7], fundal pressure  and some form of labour dystocia especially after 7 cm of cervical dilatation [1, 5]. Intrapartum, the point of uterine rupture is usually indicated by onset of foetal bradycardia and tender maternal abdomen [4, 6].
Shoulder dystocia has been reported in association with uterine rupture, both as a precipitant  and as a result . There are also recorded cases of transvaginal omental and bowel herniation after third stage as the first signs of uterine rupture [7, 8].The case by Sighal and colleagues  was associated with prostaglandin E2 labour induction and fundal pressure while Guasch and colleagues  reported a case of previous repeated uterine curettage as the possible risk for the uterine rupture.
This patient could not tell the exact indication for the caesarean section she had undergone, only saying she had laboured for a day at a health centre before she was referred to a hospital for the caesarean section. Vacuum delivery was not attempted prior to the operation. Her first and second babies weighed 3500 grams and 3000 grams respectively. Since both prior deliveries did not occur in our hospital, it was not possible to cross check her medical records. Neither was it possible to establish if a partograph was used during her first delivery and what pattern of labour it showed. The decision to transfuse the patient despite a near-normal haemoglobin and mild pallor may have been unnecessary for this patient.
The uniqueness of this case lies in its presentation in the form of vaginal omental herniation. That the woman presented with no perceivable foetal heart rate means the rupture could have occurred earlier whence foetal life was lost. The bradycardia and subsequent loss of foetal heart rate occurs due to placental detachment and uterine contraction  following rupture. If this had already happened to this patient, it is logical to imagine that the foetus would have been expelled through the 10 cm tear into the peritoneal cavity. There is also the possibility that the shoulder dystocia could have led to the uterine rupture. If this was the case, then the cause of foetal demise remains unknown. The placenta was not yet detached and active management of third stage of labour was done. Overzealous vaginal delivery in the setting of shoulder dystocia can also cause uterine rupture .
With excellent haemodynamic status intra-op, the sudden post-operative death of the mother is a shock in an operation gone just well. The last recorded blood pressure was 100/82mmHg, less than an hour before death. The shortness of breath and tachycardia, coupled with the rapidity of deterioration of cardiorespiratory status in the hands of resuscitating staff points to a possibility of pulmonary embolism. Pulmonary embolism is a leading cause of mortality following gynaecologic surgery and cesarean section . It is also likely to have been due to reaction to the blood transfusion.
In this part of Kenya, it is not uncommon to find women presenting to hospital in advanced labour, not to mention those delivering at home. Had this patient presented earlier for delivery at hospital, probably a non-reassuring foetal heart rate would have been picked and the baby saved through an emergency caesarean delivery. As there was no post mortem examination, the exact cause of death could not be established.
It is not common to experience uterine rupture among women attempting repeat VBAC. Uterine rupture is often associated with poor foetal outcome. When it occurs, it may not always follow the known pattern intra-partum. It is important that women with a previous caesarean delivery present to hospital for delivery so that good labour monitoring and appropriate intervention is done. This was a unique case of a successful second VBAC complicated with uterine rupture that did not present classically.