Persistent Sacral Sensory Deficit Induced by Intrathecal Local Anesthetic Infusion in the Rat
Persistent Sacral Sensory Deficit Induced by Intrathecal Local Anesthetic Infusion in the Rat
复制标题
鞘内局麻药输注致大鼠持续性骶感觉缺失
作者：
K. Drasner;S. Sakura;V. Chan;A. Bollen;R. Ciriales
背景：最近报道了几例连续脊髓麻醉后出现马尾综合征的病例。一种可能的病因是由于鞘内大剂量局麻药的不均匀使用导致骶根中毒暴露。目前的实验旨在确定局部麻醉溶液，在鞘内注射以产生有限的麻醉分布，是否会导致骶骨缺损。此外，我们试图验证这样一个假设，即当鞘内给予等量麻醉时，三种常用麻醉溶液诱导感觉损伤的潜力存在显着差异。方法：32只大鼠采用鞘内置管反复输注局麻。动物被随机分为四组，每组8只，接受5%利多卡因加7.5%葡萄糖；0.75%布比卡因加8.25%葡萄糖；0.5%丁卡因加5%葡萄糖；或者生理盐水。各组大鼠依次注射1 h （60 μl）、2 h （120 μl）、4 h (240 μl)；两组注射后休息4天。感觉功能通过甩尾测试进行评估，该测试在每次输注前和最后一次输注后6天由一名不知道输注溶液的研究者进行。结果：四组的基线甩尾潜伏期无显著差异。与布比卡因、丁卡因和生理盐水组相比，利多卡因组甩尾潜伏期明显延长。这种差异在第一次输注后就很明显，并在整个研究过程中持续存在。结论：大鼠麻醉分布受限，可引起感觉障碍。这些发现进一步支持了局麻神经毒性对近期连续脊髓麻醉后临床损伤的病因学。所描述的功能模型似乎适合于局部麻醉神经毒性的体内研究。
Background:Several 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 of three commonly used anesthetic solutions to induce sensory impairment. Methods:Thirty-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 μl), a 2-h (120 μl), and a 4-h (240 μl) 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. Results:There 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. Conclusions:In 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.