(16) The Impact of Dexmedetomidine vs. Morphine Sedation and Bradycardia on Cerebral Oxygenation During Neonatal Therapeutic Hypothermia Treatment

Devon Swofford, Washington University in St. Louis School of Medicine, Webster Groves, MO, United States; Zachary A. Vesoulis, Washington University School of Medicine, St. Louis, MO, United States; Christopher McPherson, St. Louis Children's Hospital, United States; Halana Whitehead, Washington University in St. Louis, United States; Steve Liao, Washington University in St. Louis, United States

Background: Dexmedetomidine is a non-opioid sedative agent increasingly used in neonates. In 2021, we changed from morphine to dexmedetomidine as first-line sedation for neonates undergoing therapeutic hypothermia. Although bradycardia is a known side effect of both dexmedetomidine and therapeutic hypothermia, it is not currently known if low heart rate in this population results in impaired cerebral blood flow or cerebral oxygenation.

Objectives: Our objectives were: 1) To compare overall mean heart rates and cerebral saturation (using near-infrared spectroscopy, StO2) of infants receiving either morphine or dexmedetomidine and 2) to determine if there was a decrease in cerebral perfusion when heart rate (HR) was less than 70 or 100 beats per minute.

Design/Methods: Infants treated with therapeutic hypothermia for moderate or severe neonatal encephalopathy underwent single-channel cerebral NIRS monitoring with simultaneous capture of HR starting as soon as feasible through completion of rewarming (96h postnatal age). All data were collected at 0.5 Hz. All infants born before November 2021 received morphine while all infants after received dexmedetomidine.
Infants were divided by sedation type and matched on gestational age and sex. Mean HR and StO2 were calculated for each infant over the entire recording. Mean cerebral saturation during bradycardia was also calculated for two different thresholds (HR < 100 and HR < 70). Means were compared for statistical significance using the Mann-Whitney U-Test.

Results: A total of 6 infants in each group (8 male, 4 female) were included in the study. Mean GA was 37.3 weeks, mean BW was 3001g, and median 5 min Apgar score was 5. As anticipated, a lower mean HR was noted in the dexmedetomidine vs. morphine group (105 vs. 114 bpm). However, there was no statistical difference in overall mean StO2 (86 vs 85%) between the groups, nor was there a difference in cerebral saturations at either bradycardia threshold (Table 1).

Conclusion: Although dexmedetomidine is associated with a lower mean HR, there is no detectable difference in cerebral oxygenation overall or during bradycardia at either the 100 or 70 bpm threshold. These pilot data suggest that dexmedetomidine associated bradycardia is not associated with a decrease in cerebral oxygenation. Further study in a larger sample is needed.