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Changes in Plasma Glial Fibrillary Acidic Protein in Children Receiving Sevoflurane Anesthesia: A Preliminary
Eun-Hee Kim1, Young-Eun Jang1, Sang-Hwan Ji1
1Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 03080, Korea.
Insights
Sevoflurane anesthesia in young children did not elevate plasma glial fibrillary acidic protein, a marker of neuronal injury. Dexmedetomidine infusion may increase this biomarker over time, warranting further investigation.
Area of Science:
- Anesthesiology
- Pediatric Neurology
- Biomarkers
Background:
- Assessing anesthetic-induced neurotoxicity in pediatric patients is crucial.
- Glial fibrillary acidic protein (GFAP) is a potential biomarker for neuronal injury.
Purpose of the Study:
- To investigate changes in plasma GFAP during sevoflurane anesthesia induction in children under 3 years old.
- To determine the effect of co-administered dexmedetomidine on plasma GFAP levels.
Main Methods:
- A preliminary randomized trial involving 60 pediatric patients undergoing sevoflurane anesthesia for over 3 hours.
- Patients were randomized into dexmedetomidine or control groups.
- Plasma GFAP levels were measured at multiple time points post-induction.
Main Results:
- Plasma GFAP levels did not significantly change over time during sevoflurane anesthesia (p = 0.759).
- A significant increase in plasma GFAP was observed after 180 minutes of dexmedetomidine infusion compared to 30 minutes (p = 0.04).
Conclusions:
- Sevoflurane anesthesia for three hours in pediatric patients under 3 years old did not indicate neuronal injury via plasma GFAP.
- Further research is needed on the impact of prolonged dexmedetomidine infusion on anesthetic-induced neuronal injury.
Abstract:
We investigated changes in plasma glial fibrillary acidic protein concentration during sevoflurane anesthesia induction in children < 3 years old and determined the effect of co-administering dexmedetomidine. This preliminary randomized trial included 60 pediatric patients who received sevoflurane anesthesia for >3 h. Patients were assigned to dexmedetomidine or control groups at a 1:1 ratio. The primary outcome was changes in plasma glial fibrillary acidic protein concentration of dexmedetomidine and control groups over time. Fifty-five patients were included in the final analysis. The median (interquartile range (IQR)) of the plasma glial fibrillary acidic protein level was 387.7 (298.9-510.8) pg·mL-1 immediately after anesthetic induction, 302.6 (250.9-412.5) pg·mL-1 at 30 min, and 321.9 (233.8-576.2) pg·mL-1 at 180 min after the first sample. These values did not change over time (p = 0.759). However, plasma glial fibrillary acidic protein increased after 180 min of infusion of dexmedetomidine compared with values at 30 min infusion (p = 0.04, mean difference and 95% confidence interval of 221.6 and 2.2 to 441.0 pg·mL-1). In conclusion, three hours of sevoflurane anesthesia in pediatric patients < 3 years old did not provoke neuronal injury assessed by the plasma biomarker. Further studies regarding the effect of prolonged dexmedetomidine infusion on anesthetic neuronal injury are required.
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