NM-284
Management of Fetal Cardiac Dysfunction During Fetal Surgery
Miller I, Hoffman G
Childrens Hospital of Wisconsin, Milwaukee, WI, US
Prenatal surgery for congenital anomalies balances the hope of improvement in long-term outcome with an increased risk of fetal and maternal complications including fetal demise. Open fetal surgeries have unique anesthetic concerns including induction of profound uterine relaxation, maintaining uterine-placenta perfusion, fetal resuscitation, and limited monitoring and intervention capability. In-utero intervention for closure of neural cord defects exemplifies these competing risk and benefits, with demonstrated improved fetal-infant neurodevelopmental with a 10% burden of fetal bradycardia but no increased fetal mortality[1]. We describe the intrauterine repair of a myelomeningocele [MMC] complicated by acute intraoperative fetal cardiac dysfunction.
A 34 year old G3P1 healthy women with singleton male fetus at 24 weeks gestation underwent intrauterine MMC repair. General endotracheal anesthesia was induced and maintained with sevoflurane (0.5-1 MAC), propofol, and remifentanyl[2]. Utero-placental perfusion pressure was augmented with phenylephrine. Fetal wellbeing was assessed with near-continuous ultrasonographic interrogation of ventricular rate, contractility, stroke volumes, and aortic and umbilical doppler. Upon fetal manipulation to localize the MMC within hysterotomy, severe fetal bradycardia and hypokinesis occurred. Uterine blood flow was augmented with maternal phenylephrine and volatile anesthetics decreased. Intramuscular epinephrine, atropine, vecuronium and fentanyl were delivered to the fetus with restoration of FHR however ventricular function remained compromised. Umbilical vein doppler windows were not adequate to fully assess placental perfusion. With persistent cardiac dysfunction additional epinephrine was delivered prior to uterine closure. Transabdominal fetal ultrasound in the PACU revealed return of normal fetal echocardiographic parameters. On POD 1 severe bradycardia recurred; consistent with preoperative plans, no postoperative intervention was performed and fetal demise ensued.
A detailed understanding of the fetal cardiovascular system and utero-placental interface is essential for optimal management of mother and fetus during fetal intervention. Monitoring of fetal oxygen supply-demand is typically dependent on the presence or absence of fetal bradycardia, often the result of prolonged or profound myocardial hypoxia. Prevention of hormonal stress response with opioid administration reduces fetal oxygen consumption, while fetal immobility promotes both fetal positioning and surgical intervention. Volatile anesthetics depress fetal myocardium. Fetal catecholamine administration while encouraging cardiac output further increases myocardial demand and afterload. Continuous, quantitative assessment of in-utero fetal circulation remains limited, and development or application of better monitoring modalities may permit more rational guided intervention to maintain or improve fetal oxygen supply-demand economy.
1) Adzick NS, MOMS Investigators. A randomized trial of prenatal versus postnatal repair of myelomingocele. PMID: 21306277
2) Boat A, Supplementing desflurane with intravenous anesthesia reduces fetal cardiac dysfunction during open fetal surgery. PMID: 20670239
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