The intrathecal lidocaine enigma: On the brink of cauda equinopathy

Abstract

HE 1990s have not been kind to spinal anesthesia, the introduction, via lumbar puncture, of local anesthetic into spinal fluid. The first of many tremors to come rumbled from over a dozen instances of persistent cauda equina syndrome following continuous catheter spinal anesthesia (mostly with hyperbaric 5% lidocaine). No sooner had the microbore catheter issue been resolved when heavy xylocaine itself was snared in controversy over alleged neurotoxicity. Aftershocks from that eruption fanned out when neurotoxicity was implied not only for 5%, but also for 2.5% and even plain 2% lidocaine. As if that weren't enough, yet another tremor hit home when other local anesthetics (bupivacaine, mepivacaine, and even tetracaine) too became implicated in neurotoxicity, although lidocaine still tops the list. With so many reports of radicular irritation, venting one after another in short order, dawned a growing professional concern over the imputed radiculotoxicity of local anesthetics as a pharmacologic species. Ever since the seminal 1954 report by Dripps and Vandam? intrathecal injection of local anesthetics was considered both safe and efficacious, and lidocaine specifically so in the epochal 1969 multicenter study by Phillips et al.2 One cannot help but wonder what, if anything, has changed about spinal anesthesia in the intervening decades. Did the old masters, in searching out major neurologic complications perhaps overlook or shortchange the minor transient sequelae? Has our practice changed with new techniques, better drugs, and sharper tools for detecting borderline events? Or are we simply paranoid, hyping minor postoperative backache into a major media frenzy that threatens to deny future access to one of the safest and simplest methods of anesthesia? These are the fundamental issues that will be considered in this review.