BACKGROUND/ PURPOSE: Peripheral deafferentation induced by neuraxial anesthesia reduces the degree of cortical arousal. This study investigated whether epidural analgesia blockade decreased sedation, as measured by the rapidly extracted auditory evoked potentials index, A-line autoregressive index (AAI) and Ramsay Sedation Scale (RSS) in sedated surgical intensive care patients, and looked at whether this was a concentration-dependent effect of lidocaine. METHODS:Forty patients underwent major lower abdominal surgery and receivedepidural analgesia in the surgical intensive care unit. Patients were continuously sedated with propofol to achieve an RSS value of 3, randomly divided into two groups, and received epidural analgesia with 10 mL of 0.5% or 1% lidocaine. Sedation was evaluated using the RSS and AAI, and analgesia was evaluated using a visual analog scale (VAS). RSS, AAI, electromyography (EMG) activity of AAI and VAS values were recorded at 5 minutes before and 30, 60 and 90 minutes after epidural lidocaine administration. RESULTS:Epidural 0.5% lidocaine produced a reduction of AAI, EMG and VAS at 30, 60 and 90 minutes after administration. For 1% epidural lidocaine administration, AAI, EMG and VAS were also reduced at 30, 60 and 90 minutes after epidural lidocaine administration. However, there was no difference in the AAI between the two concentrations; moreover, no significant change was observed in the RSS. CONCLUSION:Epidural lidocaine analgesia could potentiate sedation in patients evaluated by the AAI, but had no effect on the RSS. The present study suggests that the AAI could provide an objective and more precise index than the RSS in evaluation of sedation level in patients who are undergoing epidural pain management in the intensive care unit. 2010 Formosan Medical Association & Elsevier. Published by Elsevier B.V. All rights reserved.
RCT Entities:
BACKGROUND/ PURPOSE: Peripheral deafferentation induced by neuraxial anesthesia reduces the degree of cortical arousal. This study investigated whether epidural analgesia blockade decreased sedation, as measured by the rapidly extracted auditory evoked potentials index, A-line autoregressive index (AAI) and Ramsay Sedation Scale (RSS) in sedated surgical intensive care patients, and looked at whether this was a concentration-dependent effect of lidocaine. METHODS: Forty patients underwent major lower abdominal surgery and received epidural analgesia in the surgical intensive care unit. Patients were continuously sedated with propofol to achieve an RSS value of 3, randomly divided into two groups, and received epidural analgesia with 10 mL of 0.5% or 1% lidocaine. Sedation was evaluated using the RSS and AAI, and analgesia was evaluated using a visual analog scale (VAS). RSS, AAI, electromyography (EMG) activity of AAI and VAS values were recorded at 5 minutes before and 30, 60 and 90 minutes after epidural lidocaine administration. RESULTS: Epidural 0.5% lidocaine produced a reduction of AAI, EMG and VAS at 30, 60 and 90 minutes after administration. For 1% epidural lidocaine administration, AAI, EMG and VAS were also reduced at 30, 60 and 90 minutes after epidural lidocaine administration. However, there was no difference in the AAI between the two concentrations; moreover, no significant change was observed in the RSS. CONCLUSION: Epidural lidocaine analgesia could potentiate sedation in patients evaluated by the AAI, but had no effect on the RSS. The present study suggests that the AAI could provide an objective and more precise index than the RSS in evaluation of sedation level in patients who are undergoing epidural pain management in the intensive care unit. 2010 Formosan Medical Association & Elsevier. Published by Elsevier B.V. All rights reserved.