I would like to narrate a few cases. A woman pregnant for the second time with a previous normal, uneventful delivery presented in labour. I examined her at admission. The vitals were normal. She was not anaemic. Abdomen revealed a singleton term foetus with moderate contractions. The foetal heart sound was 120 dropping to 100/min. On vaginal examination, she was fully dilated with vertex at +2 station and a normal pelvis. There was no caput or moulding. I admitted her and informed the sister to take her delivery immediately. The dropping foetal heart sound worried me. I got a call from the sister half an hour later that she has not delivered, and the foetal heart sound is no longer heard. I rushed to attend to her. She was stable. Pulse was 100/min. BP was 120/70 mm of Hg. There were no contractions, and the foetal heart sound was absent. On vaginal examination, the head had receded to 0 station. There was no bleeding from the vagina. When I inserted a urinary catheter, there was frank haematuria. I wheeled her for immediate laparotomy which confirmed a rent in the left lateral wall (Fig. 3.1) involving both the upper and lower segments. The rent had involved the bladder, and the foetus was lying in the peritoneal cavity. I had to resort to a hysterectomy. The bladder rent was repaired.

Unlike the bladder rents following obstructed labour or involving previous scars, in this case, the edges of the bladder rent did not seem to be oedematous or friable. On later questioning, she gave a history of curettage for a previous spontaneous abortion. I presume there must have been a low perforation with the bladder getting adhered to it. It is very important to understand that the uterus is likely to rupture in the second stage after going through the whole labour if there is a weak point in the lower segment. Xia and colleagues [20] reported two cases, one of whom had a scarring due to placenta accreta and the other without apparent cause. Both these cases also had manifested with foetal bradycardia before manifesting rupture. Foetal heart rate abnormalities were found to be the most frequent manifestation [6] among the 25 cases with complete rupture in a retrospective analysis of ruptures over 20 years. The gradual diminution of amplitude of uterine contraction followed by severe prolonged bradycardia has been described as staircase sign by Matsuo and colleagues [9].

The case emphasizes the need to monitor and be vigilant even in the second stage of a woman who appears to be a low-risk case in labour.

I would like to detail another case I had managed about 10 years back. The case was handed over to me in the labour room as a third gravida with previous two normal deliveries. She had been admitted half an hour earlier with term pregnancy in the second stage with foetal demise. There was no history of bleeding. She had been started on oxytocin drip as there had been no contractions observed at admission. When I examined the woman, she appeared peaceful and comfortable. Her pulse was 90/min. Blood pressure was 120/80 mm of Hg. She was mildly anaemic. Abdominal examination revealed term size uterus with expected foetal weight of 3 kg. The contour was well made out. There were no contractions. The foetal heart sound was absent. Vaginal examination revealed a fully dilated and effaced cervix. The vertex was at 0 station. There was no caput or moulding. There was no bleeding. The pelvis was normal gynaecoid. She did not have any pain. In fact, she requested me to do a caesarean as she had not delivered in spite of 1 h of being in the second stage. I reassured her and counselled for oxytocin drip and vaginal delivery. I continued the oxytocin drip. The patient’s condition remained the same. The labour had come to a standstill. Contractions failed to establish, so I took her up for a caesarean section as she refused any destructive operation. On opening the abdomen, I observed that the lower segment had completely given way with the shoulders presenting at the edges of the rupture. The foetal trunk and breech were still inside the upper segment. There was minimal haemoperitoneum. The shoulders had probably tamponade the ruptured edges (Fig. 3.2).

It indeed made me feel miserable to have missed rupture. In this case, foetal demise and the loss of uterine contractions in established labour especially in the second stage were the features signalling possible rupture. In the previously discussed case, the sequence of events happened right after admission, and the changing findings with the contractions ceasing, the station receding, and the foetal heart disappearing were clear features of rupture. Thus even though the woman is stable without any other features of rupture, these two important findings of cessation of contractions and foetal demise in labour in a multigravid woman may be the only clue for suspecting rupture especially when the previous record of the station of the presenting part is not available. I still vividly remember the name and face of the patient and her earnest request for caesarean. Fortunately, I did not try any instrumentation or destructive procedure. The adage that when a multiparous woman feels that something is not well with her in established labour, we need to heed to her, is so true for this case. There was no other cause for this rupture other than the fact that she was a multiparous woman.

I would like to narrate two cases that bring out a close differential diagnosis confusing the picture and delaying the diagnosis.

A woman in her third pregnancy presented at term pregnancy with bleeding from the vagina. It was the first episode of bleeding. She was in shock at admission. Abdominal examination, however, revealed a lax abdominal wall with a poor tone of the rectus muscle. The contour was made out. The foetal parts were not superficially palpable but were easily palpable. There were no uterine contractions. The duty resident made a diagnosis of placenta previa with intrauterine foetal demise. The patient was quickly resuscitated and wheeled for caesarean. At laparotomy it was realized that the uterus had ruptured, the foetus was in the amniotic sac with fluid pockets around it, and the back of the foetus was under the abdominal wall resulting in a false sign of maintained contour of the uterus. What was perceived as low-lying placenta on sonography was the retracted uterus. In this case, the definitive management was immediate laparotomy as she was in shock. So the exact preoperative diagnosis may be inconsequential.

I would like to narrate yet another interesting case we recently managed in our hospital. A woman pregnant for the third time, with previous two normal deliveries, was referred from a primary health centre as a case of suspected abruption. She was 32 weeks pregnant and complained of sudden onset painful bleeding followed by loss of foetal movements. She was not hypertensive. There was no history of trauma or previous fibroids. She had been transfused a pint of blood in the primary health centre 16 h before she came to our hospital. Her pregnancy was so far unsupervised. There was no history of prior caesarean/abortions/uterine procedures.

At admission to our hospital, her pulse was 100/min and blood pressure was 110/70 mm of Hg. She was moderately pale, ill-nourished, and asthenic. The admitting resident made a diagnosis of abruption because the uterus was 32 weeks size with normal contour and slight tenderness. The foetal heart sound was absent. The cervix was uneffaced and closed, and there was no bleeding observed. Urinary catheter revealed high-coloured but adequate urine. We transfused one more pint of whole blood as the baseline investigations revealed moderate anaemia with a haemoglobin of 6.5 g%. The coagulation profile and blood urea and creatinine were normal. Labour induction was started with 50 μg of misoprostol sublingually. The junior consultant reviewed the case and concurred with the clinical findings. The bedside sonography by the consultant revealed a foetus with signs of spalding, with adequate liquor around the foetus. The foetus was presenting as vertex high up. The placenta was found anterior, but a succenturiate lobe of the placenta was found to be overlying the os. There was no free fluid. The revised diagnosis was as placenta previa with foetal demise. The patient had not responded to labour induction. The case was discussed with me and I saw the woman nearly 36 h after admission. I observed that she was asthenic, ill-nourished, and not in pain. Her pulse had settled to 90/min. and BP was stable at 120/80. There was adequate urine output. Abdominal examination revealed a 32-week size relaxed uterus with absent foetal heart sounds. Vaginal examination revealed a closed cervix but no presenting part from the fornices. We discussed, and since she was stable with a macerated foetus, with placenta previa, with no further bleed, we took a calculated risk of extra-amniotic saline instillation after counselling and discussing with the woman. The same was performed uneventfully. She was under strict observation for any bleeding. Facilities for immediate caesarean section were kept ready in the case of bleeding. She remained status quo for the next 24 h. I must confess I was internally reflecting with the finding of no presenting part from the fornices gnawing at me, when in the middle of the night I woke up agonized when it dawned on me that we have missed ruptured uterus. I felt miserable. Laparotomy confirmed a longitudinal rupture of the anterior wall of the upper segment (Fig. 3.3).

The foetus was lying in the peritoneal cavity with intact membranes and amniotic fluid. The placenta was anterior and so was the back of the foetus. There was about 400 ml haemoperitoneum.