Placenta percreta is a condition associated with significant maternal and fetal mortality, estimated to be 6–7% and 9–19%, respectively1, 2. Diagnosis of placenta percreta is often established late when attempts are made at the time of Cesarean section to separate the adherent placenta from the uterine wall and occasionally even the bladder. This maneuver can cause massive exsanguinating hemorrhage3. Preoperative diagnosis allows the planning of multidisciplinary management, including the conservative approach of leaving the placenta untouched followed by the use of methotrexate and/or uterine artery embolization. This more conservative approach is associated with less maternal morbidity, such as a significantly lower hysterectomy rate, a reduced need for blood transfusion and a lower incidence of disseminated intravascular coagulation4. We describe a case of placenta previa percreta treated conservatively and present the antenatal and postnatal ultrasonographic findings. The patient was a 30-year-old Caucasian woman with two previous Cesarean sections. She was referred at 35 weeks' gestation because of the suspicion of placenta accreta after an episode of antepartum hemorrhage. On transabdominal and transvaginal ultrasound examination the placenta was anterior, low lying and reaching the internal cervical os. There were lacunae in the placental substance. A 4-cm diameter bulge in the lower segment of the uterus was noted protruding towards the bladder. There was no clear demarcation observed between the placental substance and the anterior uterine wall musculature in the lower segment (Figure 1a, 1b, 1c). The bladder wall overlying this area was very vascular (Figure 1d, 1e) and irregular (Figure 1e). Branching (Figure 1d) and communicating (Figure 1e) vessels between the lower anterior uterine wall and bladder wall were seen. Placenta percreta was diagnosed. Elective classical Cesarean section and bilateral tubal ligation were performed at 37 weeks' gestation. Placenta percreta was confirmed intraoperatively. The lower segment of the uterus was replaced by placental tissue and the vascular bladder wall was adherent to the placenta. The placenta was left in situ. Methotrexate (50 mg) was administered intraoperatively followed by postoperative bilateral uterine artery embolization. Postoperatively the patient responded well with rapid decline of serum beta-human chorionic gonadotropin level. She had episodes of vaginal bleeding associated with passage of placental tissue. However, no blood transfusion was required. At 2 months post-delivery, some placental tissue including the bulge in the lower anterior uterine wall was still observed in situ on ultrasound examination (Figure 2). However, blood vessels running between the placental tissue in the lower uterine wall and bladder wall could no longer be observed. Antenatal ultrasound examination revealed the presence of placental lacunae and no definite intervening uterine musculature between the placenta and posterior bladder wall on transabdominal (a, b) and transvaginal scans (c). The interface between the uterine muscular wall and the placental tissue could be identified at the upper margin of the placenta. From about 2–3 cm below the upper placental margin this interface could not be clearly identified (a), and uterine musculature could not be definitely delineated in the ‘anterior uterine wall’ below this point on both the transabdominal and transvaginal scans (b, c). There was marked vascularity and branching vessels between the posterior bladder wall and anterior uterine wall on the transabdominal scan (d) and interruption of the posterior bladder wall–uterine interface and communicating vessels on the transvaginal scan (e). Transvaginal ultrasound examination at 2 months post-delivery still showed the placental tissue in the uterus including the bulge in the lower anterior uterine wall. BL, bladder; PL, placenta. The patient's menstruation returned shortly after passage of another piece of infarcted placental tissue. At 5 months post-delivery the uterus had regained a normal contour. The calcified placental tissue became incorporated into the whole thickness of the lower anterior uterine wall (Figure 3) with some extension to higher levels of the uterus. Transvaginal ultrasound examination 5 months post-delivery demonstrated a hyperechogenic mass with calcifications in the lower anterior uterine wall at the site previously occupied by the placenta. Extensions of this mass to higher levels in the uterus could also be observed. We have reported a case of placenta percreta treated conservatively with success. In carefully selected cases, placenta percreta can be treated by leaving the placenta in situ following delivery and by subsequent treatment with methotrexate and/or uterine artery embolization. When managed as such, the placental tissue is reabsorbed and/or incorporated into the uterine wall spontaneously as demonstrated sonographically in this case. H. S. Wong*, S.
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