Z Chen1, S Lin2, W Shao1. 1. Department of Anesthesiology, Yantaishan Hospital, No. 91 Jiefang Road, Yantai, 264001, China. 2. Department of Anesthesiology, Yantaishan Hospital, No. 91 Jiefang Road, Yantai, 264001, China. linsheng760401@163.com.
Abstract
OBJECTIVE: The aim of this study was to evaluate the effects of different doses of dexmedetomidine (Dex) compounded propofol and fentanyl on intraoperative somatosensory evoked potential (SEP) and motor evoked potential (MEP) monitoring on senile patients. METHODS:Forty-five patients undergoing elective spinal surgery were randomly divided into three groups: group C, group D1 (Dex, 0.3 μg kg(-1) h(-1)), and group D2 (Dex, 0.8 μg kg(-1) h(-1)). Anesthesia administration: midazolam, propofol, fentanyl, and cisatracurium. Anesthesia maintenance: propofol and fentanyl. No muscle relaxant was used throughout the operation. When muscle relaxation was T 4/T 1 > 75%, SEPs and MEPs were monitored for the baseline. In group D1, Dex (0.3 μg/kg, loading dose) was administered, followed by a 0.3 μg kg(-1) h(-1) infusion of said drug until the end of surgery. In group D2, Dex (0.8 μg/kg, loading dose) was injected, followed by a 0.8 μg kg(-1) h(-1) infusion of said drug. RESULTS: Compared with group C, no significant difference was observed in the amplitude and latency of SEP (P15-N20) waves in groups D1 and D2 (P > 0.05). In groups C and D1, the MEP waveform did not disappear at every stage. In group D2, three patients lost the MEP waveform after the Dex loading dose, while four patients lost it during the Dex infusion stage. A significant difference was observed between groups C and D1. The median time to recover the MEP waveform was 47 min. CONCLUSIONS:Dex did not affect SEPs of senile patients, but inhibited MEPs when larger doses were administered.
RCT Entities:
OBJECTIVE: The aim of this study was to evaluate the effects of different doses of dexmedetomidine (Dex) compounded propofol and fentanyl on intraoperative somatosensory evoked potential (SEP) and motor evoked potential (MEP) monitoring on senile patients. METHODS: Forty-five patients undergoing elective spinal surgery were randomly divided into three groups: group C, group D1 (Dex, 0.3 μg kg(-1) h(-1)), and group D2 (Dex, 0.8 μg kg(-1) h(-1)). Anesthesia administration: midazolam, propofol, fentanyl, and cisatracurium. Anesthesia maintenance: propofol and fentanyl. No muscle relaxant was used throughout the operation. When muscle relaxation was T 4/T 1 > 75%, SEPs and MEPs were monitored for the baseline. In group D1, Dex (0.3 μg/kg, loading dose) was administered, followed by a 0.3 μg kg(-1) h(-1) infusion of said drug until the end of surgery. In group D2, Dex (0.8 μg/kg, loading dose) was injected, followed by a 0.8 μg kg(-1) h(-1) infusion of said drug. RESULTS: Compared with group C, no significant difference was observed in the amplitude and latency of SEP (P15-N20) waves in groups D1 and D2 (P > 0.05). In groups C and D1, the MEP waveform did not disappear at every stage. In group D2, three patients lost the MEP waveform after the Dex loading dose, while four patients lost it during the Dex infusion stage. A significant difference was observed between groups C and D1. The median time to recover the MEP waveform was 47 min. CONCLUSIONS:Dex did not affect SEPs of senile patients, but inhibited MEPs when larger doses were administered.
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