Local Anesthetic Neurotoxicity : Cauda Equina Syndrome

Definition

As the term cauda equina syndrome (CES) implies, clinical manifestations are related to injury to the nerve roots below the conus medullaris. Consequently, CES results in varying degrees of bowel and bladder dysfunction, perineal sensory loss, and lower extremity motor weakness. Although there are multiple potential causes, two are of concern to anesthesiologists: (1) compressive injuries (e.g., epidural or spinal hematoma/abscess), and (2) direct toxicity of substances administered into the intrathecal space. Clinical experience and experimental data suggest that, under certain circumstances, local anesthetics in current clinical use have the potential to induce neurotoxic damage and CES. We review the problem in this chapter.

Recognition

The medical literature has the occasional report of significant neurologic injury associated with spinal and epidural anesthesia and has led to further understanding about local anesthetic neurotoxicity. Early reports of CES were associated with continuous spinal anesthesia (CSA) with microcatheters. These CSA-related cases shared two common elements: restricted sacral block that required repetitive doses of local anesthetic to achieve adequate surgical anesthesia, and the cumulative dose far exceeded that commonly used with single-injection spinal anesthesia. It was suggested that the combination of maldistribution and high dose of anesthetic led to neurotoxic concentrations in a restricted area of the subarachnoid space, a mechanism supported by subsequent in vitro and in vivo experimental data. Although most of the injuries involved the administration of 5% lidocaine through small-bore microcatheters, not all were associated with lidocaine, and some involved intrathecal delivery of anesthetic through an epidural catheter. Therefore withdrawal of microcatheters from clinical practice has not eliminated the risk of injury, as practitioners remain at liberty to use epidural equipment for CSA. Further, some clinicians routinely convert to a continuous spinal technique if dural puncture accidentally occurs during attempted epidural placement.

Factors that lead to neurotoxic injury with CSA are not unique to this technique; they also apply to single-injection spinal anesthesia. Specifically, inadequate sensory block with single-injection spinal anesthesia is often the result of maldistribution. Under such circumstances, there is the potential for repeat injections to distribute in the same pattern, resulting in neurotoxic concentrations of local anesthetic within a restricted area of the subarachnoid space. Case reports and review of the closed claims database appear to support this concern.

There is a third mechanism by which high doses of anesthetic may be administered into the subarachnoid space. If a practitioner is administering an epidural anesthetic and fails to appreciate that the needle or catheter has traversed the dura or arachnoid, the doses administered may achieve neurotoxic concentrations in the subarachnoid space. Such doses may be sufficient to induce injury even in the absence of maldistribution, as evidenced by case reports.

Reports of neurologic injury with CSA, repetitive injection after failed spinal anesthesia, and inadvertent intrathecal injection of anesthetic intended for the epidural space established the potential toxicity of anesthetics administered at a dose exceeding the usual clinical range for spinal anesthesia. More surprising, two reports raised the suspicion that neurologic deficits might occur with the administration of lidocaine at doses recommended for single-injection spinal anesthesia. One was a case report of CES after the intrathecal injection of 100 mg of lidocaine with epinephrine. The second was a prospective study of regional anesthesia from France. In both reports there were persistent deficits after single injections of lidocaine that could not be otherwise explained. In all cases, relatively high doses (≥75 mg) were used, and cases of permanent injury occurred only after injection of the maximum recommended clinical dose (100 mg).