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• W2607854429 abstract "One of the most serious complications encountered during fetal surgery is fetal bradycardia, which may result in premature delivery or abandonment of the intervention. We report on two cases of fetal bradycardia encountered during and after fetoscopic repair of a myelomeningocele (MMC). Both patients elected to undergo experimental fetoscopic repair of MMC using the technique previously described by our group1. In both cases, maternal hypothermia was identified and fetal bradycardia was resolved with correction of maternal temperature. The first patient was a 37-year-old woman (gravida 2, para 1) presenting at 24 weeks' gestation. Fetal heart rate (FHR) was noted to be 104 bpm 45 min after induction of general anesthesia and prior to skin incision. Because cardiac function remained stable, we elected to continue with surgery. However, after uterine ports were inserted, but prior to starting MMC repair, FHR decreased to 92–94 bpm, prompting the decision to abandon the intervention. Intrauterine fetal resuscitation was initiated, which resulted in sustained FHR response, and the abdominal incision was closed. During the case debrief, we postulated prolonged exposure to deep general anesthesia as the cause of bradycardia, given that maternal hypotension, placental and umbilical cord compression, and uterine overdistension had been considered and eliminated during the procedure. However, a review of this case following the second case showed maternal hypothermia (35.2 °C) that had been present as early as 45 min after induction of general anesthesia; the maternal core temperature ranged between 34.8 °C and 35.2 °C during the attenuated surgery. The pregnancy continued in an uncomplicated fashion; the neonate was delivered at 38.3 weeks and underwent postnatal MMC repair. The second patient was a 22-year-old woman (gravida 3, para 2) with short stature (144.8 cm), body weight 46.8 kg and a body mass index of 22.3 kg/m2, who presented at 25 weeks of gestation. Forty-five minutes into the maintenance of general anesthesia (sevoflurane in oxygen at minimum alveolar concentration 0.6), fetal echocardiographic monitoring demonstrated bradycardia, ranging between 100 and 110 bpm, with good cardiac function maintained throughout the procedure. Intravenous magnesium sulfate was administered (6-g loading dose and 2 g/h continuous infusion) for tocolysis when the neurosurgical portion of the repair was complete. Following conclusion of the surgery, the patient had persistent muscle weakness which prevented tracheal extubation for approximately 75 min. During this period, the maternal temperature was not continuously monitored; however, intermittent FHR monitoring demonstrated a slowly decreasing rate that ultimately stabilized in the 80–90 bpm range. The decreasing FHR prompted repeat fetal echocardiography, which demonstrated preservation of reassuring cardiac function parameters. Given the reassuring cardiac function, we elected not to deliver the fetus. During this observation period, maternal temperature was noted to be 34.4 °C. Efforts were immediately directed toward re-establishing maternal normothermia; the increasing maternal temperature was associated with a progressive increase in FHR (Figure 1). The pregnancy continued in an uncomplicated fashion. The neonate was delivered at 40 weeks and had a favorable neurological outcome with no ventriculoperitoneal shunt required. Identifying maternal hypothermia as the cause of delayed emergence from anesthesia in the second patient prompted focus on the effect of maternal temperature on FHR. In the setting of reassuring fetal cardiac function, and with no other explanation for the fetal bradycardia, we elected to correct the underlying temperature issue in lieu of immediate delivery or in-utero resuscitation with epinephrine or atropine (as in the first patient). Seeing that the FHR responded positively to maternal rewarming in the second patient, the earlier bradycardia case was reviewed, revealing maternal hypothermia, which suggests that the fetal bradycardia seen in both cases was caused by significant maternal hypothermia. This conclusion was supported by observing that the bradycardia progressively resolved with the correction of maternal temperature. In the first patient, the procedure was aborted in accordance with the preset FHR critical level; however, we now believe it likely that correction of the maternal temperature intraoperatively could have allowed completion of the surgery. The relationship between FHR and maternal core temperature in the second patient (Figure 1) suggests that FHR decreases dramatically when maternal core temperature falls below 35.5 °C and that FHR responds to administration of anti-muscarinic (atropine) drugs; however, the anti-muscarinic effect is reduced dramatically when maternal core temperature is below 35.5 °C. This reduced effect appears to involve both the absolute increase in FHR and the duration of its elevation. Patient positioning and preparation time for these procedures is significant, often 45–60 min from induction of anesthesia to being ready for surgical incision. During this time, the gravid abdomen is potentially exposed to cold ultrasound gel, cold alcohol-based sterilizing solutions and a cold ambient room environment. Each of these factors may compound the radiant heat loss expected under general anesthesia. Fetal bradycardia has been reported previously with maternal hypothermia2-4; in each case, rewarming corrected the fetal bradycardia. Magnesium sulfate tocolysis, frequently used in fetal intervention procedures, can also lead to maternal hypothermia5. We considered this, but do not accept that the magnesium sulfate directly caused the hypothermia in these cases. The bradycardia was observed before the magnesium sulfate was administered; however, it may ultimately have had an additive effect. We believe that several factors may have contributed to maternal hypothermia in our cases. These include: a relatively cold ambient room temperature (23.3 °C); polyhydramnios (in the second case) with exposure of a large and highly vascular uterine surface area for heat exchange; monitoring the maternal skin temperature in lieu of a true core temperature; inadequate warming measures to counter radiant heat loss under general anesthesia during the prolonged surgical preparation and delayed emergence periods; and possibly the lack of an adjusted magnesium sulfate dose based on the patient's body weight in the second case. As a result, our protocol has been modified: the ambient room temperature is maintained at 26.6 °C from patient entry to exit; the maternal core temperature is monitored; the patient's head is wrapped to minimize radiant heat loss; a humidifier is included in the anesthesia circuit to minimize evaporative heat loss; warmed saline is used to irrigate the exposed uterus; and magnesium sulfate dosing is adjusted to body weight." @default.
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• W2607854429 date "2018-03-01" @default.
• W2607854429 modified "2023-09-24" @default.
• W2607854429 title "Fetal bradycardia associated with maternal hypothermia after fetoscopic repair of neural tube defect" @default.
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• W2607854429 doi "https://doi.org/10.1002/uog.17501" @default.
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