• K Drasner, S Sakura, V W Chan, A W Bollen, and R Ciriales.
• Department of Anesthesia, University of California, San Francisco.
• Anesthesiology. 1994 Apr 1; 80 (4): 847-52.

BackgroundSeveral cases of cauda equina syndrome after continuous spinal anesthesia have been recently reported. One possible etiology is toxic exposure of the sacral roots resulting from intrathecal maldistribution of a relatively large dose of local anesthetic. The current experiments sought to determine whether a local anesthetic solution, injected intrathecally to produce a restricted distribution of anesthesia, could result in a sacral deficit. In addition, we sought to test the hypothesis that, when equal volumes are administered intrathecally, significant differences exist in the potential to three commonly used anesthetic solutions to induce sensory impairment.MethodsThirty-two rats were implanted with intrathecal catheters to permit repetitive infusion of local anesthetic. Animals were randomly assigned to four groups of eight to receive either 5% lidocaine with 7.5% dextrose; 0.75% bupivacaine with 8.25% dextrose; 0.5% tetracaine with 5% dextrose; or normal saline. Each rat received, in sequence, a 1-h (60 microliters), a 2-h (120 microliters), and a 4-h (240 microliters) infusion; the infusions were separated by a 4-day rest period. Sensory function was assessed using the tail-flick test, which was performed immediately before each infusion and 6 days after the last infusion by an investigator blinded to the solution infused.ResultsThere was no significant difference in baseline tail-flick latencies for the four groups. Tail-flick latency for the lidocaine group was significantly prolonged when compared with the bupivacaine, tetracaine, and saline groups. This difference was apparent after the first infusion and persisted throughout the study.ConclusionsIn the rat, restricted anesthetic distribution can be achieved, and sensory impairment may result. These findings further support an etiology of local anesthetic neurotoxicity for recent clinical injuries after continuous spinal anesthesia. The functional model described appears to be suitable for in vivo study of local anesthetic neurotoxicity.

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