PERSISTENT SACRAL SENSORY DEFICIT INDUCED BY INTRATHECAL LOCAL-ANESTHETIC INFUSION IN THE RAT

Background: Several cases of cauda equina syndrome after continuous sp inal anesthesia have been recently reported. One possible etiology is toxic exposure of the sacral roots resulting from intrathecal maldistr ibution of a relatively large dose of local anesthetic. The current ex periments sought to determine whether a local anesthetic solution, inj ected 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, s ignificant differences exist in the potential of three commonly used a nesthetic solutions to induce sensory impairment. Methods: Thirty-two rats were implanted with intrathecal catheters to permit repetitive in fusion of local anesthetic. Animals were randomly assigned to four gro ups 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 mu l), a 2-h (120 mu l), and a 4-h (240 mu l) infusion; the infusions were separate d by a 4-day test period. Sensory function was assessed using the tan- flick test, which was performed immediately before each infusion and 6 days after the last infusion by an investigator blinded to the soluti on infused. Results: There was no significant difference in baseline t ail-flick latencies for the four groups. Tail-flick latency for the li docaine group was significantly prolonged when compared with the bupiv acaine, tetracaine, and saline groups. This difference was apparent af ter the first infusion and persisted throughout the study. Conclusions : In the rat, restricted anesthetic distribution can be achieved, and sensory impairment may result. These findings further support an etiol ogy of local anesthetic,eurotoxicity for recent clinical injuries afte r continuous spinal anesthesia. The functional model described appears to be suitable for in vivo study of local anesthetic neurotoxicity.