Management of extensive placenta percreta with induced fetal demise and delayed hysterectomy

Background

Abnormal placentation is a source of significant perinatal morbidity [1]. The rate of abnormal placentation is estimated to be 1 in 533 [2, 3]. While traditional management of abnormal placentation has been peripartum hysterectomy, there is a growing literature to support conservative management strategies [4, 5]. We describe a case of an invasive intra-abdominal placenta percreta that was treated with pregnancy termination with a demised fetus remaining in situ, and a delayed gravid hysterectomy performed 4 months later.

Case report

This is a 35-year-old G4P2012 with a history of two prior cesarean deliveries who presented with an elevated maternal serum alpha-fetoprotein. Ultrasound at 21 weeks gestational age revealed a complete placenta previa and no anatomic abnormalities of the fetus. The placenta demonstrated large placental lakes throughout the lower uterus extending into the bladder and the anterior fornix of the vagina. Magnetic resonance imaging (MRI) revealed a widespread extra-uterine placenta percreta involving the bladder, cervix, upper vagina, anterior abdominal wall, sigmoid, rectum, pelvic sidewall, and sciatic neurovascular bundle (Figures 1–3).

Figure 1:

MRI sagittal image.

Anterior abdominal wall (arrowhead) involvement by the placenta percreta and loss of fat plane between the placenta and the bladder (black arrowheads) suggesting bladder invasion.

Figure 2:

MRI axial image.

Lateral pelvic wall involvement (double arrows) and loss of fat plane with the rectum (black arrow).

Figure 3:

MRI oblique sagittal image.

Involvement of the cervix (arrows) with loss of normal architecture and replacement by T2 hyperintense areas which were consistent with vasculature and placenta (* denotes the fetus).

Maternal fetal medicine, gynecologic oncology, neonatology, interventional radiology, and anesthesiology were consulted given the early extensive presentation of placenta percreta. After full counseling regarding treatment and delivery options at various gestational ages, the patient requested termination of pregnancy as she did not wish to proceed with the risks of a progressing pregnancy. Termination of pregnancy was performed by fetal demise through fetal intracardiac potassium chloride administration. This was followed by systemic methotrexate administration. Prior to initiating methotrexate, her serum Beta-human chorionic gonadotropin (HCG) was 14,847 mIU/mL, hemoglobin 10.7 g/L, and platelets 172,000/µL, with normal coagulation studies. She received 3 weekly intramuscular injections of 85 mg methotrexate (dose: 50 mg/m²).

Surgery was delayed to allow for resorption of placental tissue. Pelvic embolization was not initially performed due to concern that the sudden devascularization could precipitate uterine irritability. Placental volume and vascularity were followed by monthly MRI. Maternal status was followed with weekly beta HCG levels, complete blood cell count (CBC), and coagulation studies, and she was monitored for any clinical signs of labor, infection, and bleeding.

She remained hospitalized for 122 days. Her HCG dropped to 197 mIU/mL on day 50, with a nadir of 13 mIU/mL on day 113. Her weekly CBC and coagulation studies remained normal. Her fourth MRI on hospital day 112 showed that placental volume had significantly decreased, now involving only a small portion of the anterior abdominal wall and posterior bladder. Two days after this MRI, while planning definitive surgical management at the equivalent of 41 weeks gestational age, she developed a fever to 39.0 Celsius and uterine tenderness. White blood cell count was 6.43×10³/μL and coagulation studies were within normal limits. Urine analysis was negative. Chorioamnionitis was suspected. Intravenous antibiotic therapy with a 3^rd generation cephalosporin was begun.

At this time, the patient underwent bilateral uterine artery embolization immediately prior to laparotomy and gravid hysterectomy. Operative findings included necrotic intrauterine contents with necrosis of the anterior myometrium. The lower uterine segment had evidence of prior dehiscence with necrotic placental tissue visibly extruding through the uterine serosa. The bladder was adherent to the anterior uterus and placenta. There was minimal residual placental tissue outside of the uterus. Pathologic examination revealed extensive placenta percreta protruding from the uterine body with extension through the serosa (Figure 4). Histology confirmed bacterial colonization within the amniotic membranes.

Figure 4:

Pathology specimen of uterus, cervix, and placenta.

An unavoidable cystotomy was performed to extract the placenta percreta and complete the hysterectomy. Estimated blood loss was 800 mL, and she received a total of two units of packed red blood cells. Antibiotics were continued for 48 h postoperatively. She was afebrile postoperatively. She received postoperative prophylactic heparin.

Her initial postoperative course was uncomplicated, and she was discharged home on postoperative day 8 with a Foley catheter in place. She was re-admitted on postoperative day 12 with flank pain. CT scan of the abdomen/pelvis revealed a left renal vein thrombosis with extension to the inferior vena cava; the ureters were without obstruction. She was afebrile with a negative urine culture and normal white blood cell count. Therapeutic anticoagulation was initiated. She was discharged from this hospitalization on hospital day 7. The Foley catheter was removed on postoperative day 14 after a normal retrograde cystourethrogram.

An outpatient visit 8 weeks after her hysterectomy was uneventful without pain or urinary difficulties. Her physical exam was normal. She was tolerating therapeutic anticoagulation without difficulty.

Discussion

In this case, the extensive placental intra-abdominal invasion at 21 weeks of pregnancy presented a significant risk for a catastrophic hemorrhage. The patient ultimately requested termination of pregnancy due to her desire to limit maternal morbidity [6, 7]. Our goal was to reduce extra-uterine placental mass preoperatively. We elected not to proceed with immediate hysterectomy after induced fetal demise due to the residual burden of vascularized placental tissue.

Current conservative management strategies focus on decreasing blood loss and surgical complications after delivery of the infant. Such strategies include leaving the placenta in situ to allow spontaneous regression, serial embolization, hypogastric or uterine artery ligation, over-sewing the placental bed, and use of methotrexate [4, 5, 8]. The usefulness of conservative management strategies for invasive placentation is limited in the antepartum setting by the viability of the fetus. This case is unique in that induction of fetal demise and methotrexate administration with delayed gravid hysterectomy was a successful strategy. We found monthly MRIs to be useful in determining the resolution of extra-uterine placenta tissue. Our strategy provides an alternative option for potentially reducing the placental bulk prior to surgical intervention.

Given the very high maternal morbidity and potential mortality with abnormal placentation, safe management options are critical. This case describes a potential strategy for the management of an extensively invasive placenta percreta detected in the mid-second trimester. The case is not without morbidity, as our patient was hospitalized for four months, experienced a cystotomy, venous thrombosis, and chorioamnionitis. However, we propose that antepartum management of highly invasive placenta percreta with desire for pregnancy termination can be achieved with induction of fetal demise and delayed laparotomy with gravid hysterectomy.