Anesthesia for In Utero Repair of Myelomeningocele
* Assistant Professor, Department of Anesthesia and Perioperative Care, † Professor, Department of Obstetrics, Gynecology and Reproductive Sciences, ‡ Professor, Department of Surgery, Division of Pediatric Surgery, § Associate Professor, Departments of Anesthesia and Perioperative Care and Surgery, University of California San Francisco, San Francisco, California.Anesthesiology (Impact Factor: 5.88). 03/2013; 118(5). DOI: 10.1097/ALN.0b013e31828ea597
Recently published results suggest that prenatal repair of fetal myelomeningocele is a potentially preferable alternative when compared to postnatal repair. In this article, the pathology of myelomeningocele, unique physiologic considerations, perioperative anesthetic management, and ethical considerations of open fetal surgery for prenatal myelomeningocele repair are discussed. Open fetal surgeries have many unique anesthetic issues such as inducing profound uterine relaxation, vigilance for maternal or fetal blood loss, fetal monitoring, and possible fetal resuscitation. Postoperative management, including the requirement for postoperative tocolysis and maternal analgesia, are also reviewed. The success of intrauterine myelomeningocele repair relies on a well-coordinated multidisciplinary approach. Fetal surgery is an important topic for anesthesiologists to understand, as the number of fetal procedures is likely to increase as new fetal treatment centers are opened across the United States.
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ABSTRACT: Gastroschisis requires surgical repair, which is generally performed after birth. We report a case in which a fetus with gastroschisis underwent the abdominal wall defect repair before birth. To ensure reliable operating conditions for the repair (to prevent fetal movement and crying), the fetus received deep anesthesia via placental transfer of maternally administered anesthetics. Meanwhile, the ex utero intrapartum treatment procedure was performed to ensure fetal oxygen supply, which was likely to be compromised by the deep fetal anesthesia. The procedure last for 23 minutes and the gastroschisis was successfully repaired before the neonate was delivered. Maternal hemodynamics was kept stable during this surgical procedure. The prenatal repair of abdominal wall defect is safe for the mother and the fetus, which could potentially improve the neonatal outcomes.
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ABSTRACT: Background: Advances in surgery and technology have resulted in increased in-utero procedures. However, the effect of anesthesia on the fetal brain is not fully known. The inhalational anesthetic agent, isoflurane, other gamma amino butyric acid (GABA) agonists (benzodiazepines, barbiturates, propofol, other inhalation anesthetics) and N-methyl D aspartate (NMDA) antagonists e.g. ketamine have been shown to induce neuroapoptosis. The ovine model has been used extensively to study maternal-fetal physiologic interactions and to investigate different surgical interventions on the fetus. Objective: The purpose of this study was to determine effects of different doses and duration of isoflurane on neuroapoptosis in mid-gestation fetal sheep. We hypothesized that repeated anesthetic exposure and high concentrations of isoflurane would result in increased neuroapoptosis. Study design: Time-dated, pregnant sheep at 70 days gestation (G70; term=145 days) received either isoflurane 2% x 1 hour, 4% x 3 hours, or 2% x 1 hour every other day for three exposures (repeated exposure group). Euthanasia occurred following anesthetic exposure and fetal brains were processed. Neuroapoptosis was detected by immunohistochemistry using anti-caspase-3 antibodies. Fetuses unexposed to anesthesia served as controls. Another mid-gestation group with repeated 2% isoflurane exposure was examined at day 130 (G130; long term group) and neuronal cell density compared to age-matched controls. Representative sections of the brain were analyzed using Aperio Digital imaging. Data, reported by number of neurons per cubic millimeter of brain tissue are presented as means and standard error of the mean (SEM). Data were analysed using the Mann-Whitney U and Kruskal Wallis tests as appropriate. Results: Thirty-four fetuses were studied. There was no significant difference in neuroapoptosis observed in fetuses exposed to 2% isoflurane for 1 hour or 4% isoflurane for 3 hours. Increased neuroapoptosis was observed in the frontal cortex following repeated 2% isoflurane exposure compared to controls (1.57 x 10(6)/mm(3)±0.22 x 10(6) vs. 1.01 x 10(6)/mm(3)±0.44 x 10(6), p=0.02). G70 fetuses with repeated exposure demonstrated decreased frontal cortex neurons at G130 when compared to age matched controls (2.42 x 10(5)/mm(3)±0.3 x 10(5) vs. 7.32 x 10(5)/mm(3)±0.4 x 10(5), p = 0.02). No significant difference in neuroapoptosis was observed between the repeated exposure group and controls in the hippocampus, cerebellum or basal ganglia. Conclusion: Repeated isoflurane exposure in mid-gestation sheep resulted in increased frontal cortex neuroapoptosis. This persisted into late gestation as decreased neuronal cell density. While animal studies should be extrapolated to humans with caution, our findings suggest that the number of anesthetic/sedative exposures should be considered when contemplating the risks and benefits of fetal intervention as certain fetal therapies may need to be repeated.
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