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Objective: Myelomeningocele is a neural tube defect resulting in an exposed spinal cord, which leads to irreversible neurologic damage at birth. We proposed development of a fetal rabbit model of myelomeningocele to study in utero spinal cord injury and repair strategies. Methods: New Zealand white rabbits (n = 10) at 22 days of gestation (term = 31 days) underwent laparotomy to expose the gravid uterus; a hysterotomy exposed the fetal hindlimbs and back. A three to four level lumbar laminectomy was performed, and the dura over the posterior spinal cord was removed. At 30 days of gestation, the does underwent C-section for fetal harvest, and total fetal number, length, weight, and the presence or absence of a spinal defect were recorded for all viable fetuses. Results: All injured fetuses were smaller and weighed less than the nonoperated littermate controls, and histologic examination confirmed a spina bifida-like lesion of their spinal cords. Conclusions: We successfully created an exposed spinal cord defect in the fetal rabbit model similar to the lesion found in humans. Advantageous because of low animal cost, relatively large fetal size, multiple fetuses per pregnancy, and short total gestation, this model will allow us to study the mechanism of injury to the exposed spinal cord, and perhaps develop strategies to repair human myelomeningoceles.

Advances in prenatal diagnosis including improvements in ultrasonography have revealed the natural history of fetal sacrococcygeal teratomas, and this natural history differs substantially from that for postnatally diagnosed sacrococcygeal teratoma. A fetal sacrococcygeal teratoma may lead to perinatal morbidity and mortality by a variety of mechanisms. Adverse clinical sequelae of a sacrococcygeal teratoma can be prevented by accurate prenatal assessment and appropriate obstetrical and perinatal management. Development of fetal hydrops and/or placentomegaly predicts fetal demise. Fetal surgical intervention has proven successful in highly selected cases.

Sonographic detection of chorioamniotic membrane separation (CMS) has been considered a benign incidental finding. We now report 6 cases of CMS identified by prenatal ultrasound; 1 in an otherwise normal pregnancy and 5 following fetal surgery. Following membrane separation, amniotic bands formed and compromised the umbilical cord in 4 cases leading to 2 fetal deaths.In the first case, a CMS was detected by ultrasound at 22 weeks’ gestation in an otherwise uncomplicated pregnancy. Because CMS was considered benign and umbilical cord blood flow was ample, the mother was followed by intermittent sonographic examinations. Fetal demise occurred 2 weeks later, clearly due to umbilical cord strangulation by an amniotic band. Surprised by this unexpected outcome, we reviewed our experience with CMS after hysterotomy for fetal surgery. Out of more than 40 fetal surgical cases, we have 5 cases in which CMS was recognized after hysterotomy. Three of these fetuses had umbilical cord compromise by a band of amniotic membrane leading to 1 fetal death.This experience demonstrates that membrane separation may be associated with amniotic band formation which can lead to cord strangulation and fetal compromise. Following fetal surgery, serial ultrasound evaluation and close fetal monitoring are indicated. In otherwise unremarkable pregnancies, clinician awareness of the possibility of amniotic band formation following CMS should be heightened. In either situation, knowledge of this potentially life-threatening complication may identify cases in which cord compromise requires emergent delivery or fetoscopic release of the strangulating amniotic band.

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