(S-239) Newton, D.E., Monday 9:15
TITLE: TRAMADOL CAUSES EEG ACTIVATION IN ANAESTHETISED PATIENTS BUT NO CHANGE IN THE AUDITORY EVOKED RESPONSE
AUTHORS: David J. Vaughan, MB BS FRCA, Douglas Newton, MB BS FRCA, Anjalee Gondhia, MB BS FRCA, Christine Thornton, Ph D, Michael D. Brunner, MB BS FRCA
AFFILIATION: Imperial College School of Medicine, Harrow, United Kingdom.
Tramadol is a centrally acting, opioid-like analgesic commonly used during anaesthesia. Previous studies have suggested it causes increased awareness during surgery [1] and significant dose dependant electroencephalograph (EEG) activation [2]. A British Journal of Anaesthesia editorial described this perceived risk as 'a major drawback' [3].
AIM OF STUDY: To assess whether tramadol causes lightening of anaesthesia using EEG and auditory evoked response (AER) analysis.
METHOD: Informed consent was obtained from 29 ASA I-II patients (ages 18-63) attending our hospital for routine surgery. After induction with propofol 2 mg kg-1 and vecuronium 0.1 mg kg-1, the subjects were ventilated to normocapnoea via a laryngeal mask. Anaesthesia was maintained with 50% nitrous oxide in oxygen and 0.6 MAC isoflurane (age adjusted). After 20 mins of stable anaesthesia, the subjects were randomised to one of 3 groups: group T1 (100mg tramadol iv, n=10), group T2 (200mg tramadol iv, n=10) and group S (saline iv, n=9).
The EEG mean frequency (MF), 95% spectral edge (SE) and early cortical AER to a 6 Hz click stimulus were recorded from forehead and mastoid electrodes. The MF, SE and AER data were printed out and analysed for 1 pre injection period as a baseline, and 3 post injection periods (+ 5, 10 and 15 mins).
RESULTS: Significant, dose graduated haemodynamic changes were seen; heart rate deceased (p<0.001) and systolic blood pressure increased (p<0.001) after tramadol. Similar EEG changes to those reported by Coetzee et al [2] were also seen; both MF (p< 0.01) and SE (p<0.01) increased post tramadol. No significant changes in Pa amplitude (p=0.96), Pa latency (p=0.61), Nb amplitude (p=0.63) or Nb latency (p=0.51) were detected.
CONCLUSION: Tramadol causes reproducible EEG activation in anaesthetised patients, but no significant change in anaesthetic depth as indicated by the AER. This study supports clinical evidence that tramadol does not antagonise the hypnotic effects of volatile anaesthesia [4].
REFERENCES:
1. Lehmann KA, Horrichs G, Hoeckle W. Anaesthetist 1985; 34: 89-107.
2. Coetzee JF, Maritz JS, du Toit JC. Br. J Anaesth. 1996; 76: 415-8.
3. Eggers KA, Power I. Br. J Anaesth 1995; 74: 247-8.
4. Coetzee JF, van Loggerenberg H. Br. J Anaesth 1998; 81: 737- 41.