Persisting Neurological Symptoms After Uncomplicated Intrathecal Bupivacaine

Abstract

To the Editor: Chabbouh et al. (1) presented a case of persistent neurological impairment after an uncomplicated spinal anesthesia with bupivacaine. Transient neurological symptoms (TNS), typically persisting over 1–3 days have been reported after the use of bupivacaine at an incidence of up to 1% (2), but persisting symptoms have been rarely addressed in this context. We also have observed a case of cauda equina syndrome after intrathecal bupivacaine with persisting neurological derangements lasting over a period of 2 wk (3), without abnormalities on magnetic resonance imaging such as hematoma or spinal stenosis. Risk factors were not identified on a postoperative analysis, and symptoms were reversible without further interference. We too concluded that the conus medullaris syndrome was due to a direct neurotoxicity of hyperbaric bupivacaine. Animal (4–6) and in vitro (7) studies showed bupivacaine neurotoxicity as a function of concentration, demonstrated by significantly increased glutamate levels, as well as lesions in the posterior roots and motor neurons seen in histopathological preparation (5). We are highly concerned about the increasing number of reports on neurological deficits after hyperbaric spinal bupivacaine, suggesting that this topic has been underestimated in the past (2,8–10). In the early period of neurological deficit after spinal anesthesia, both TNS and persisting neurological symptoms primarily present with a comparable impairment in motor and/or sensory block. A distinction between transient, mostly normalizing within 1–2 days, and prolonged deficit can only be realized by the investigation of the time course. On the basis of the reported neurotoxicity of bupivacaine, future investigations should focus on the identification of potential risk factors to avoid neurological symptoms. The amount of aspirated cerebrospinal fluid (“Barbotage”) during placement of spinal anesthesia, as well as the concentration of bupivacaine at nerve roots seem to be important factors in this context. An adequate treatment of transient and persisting neurological deterioration without anatomic equivalence still has to be identified. Kerstin D. Röhm, MD Joachim Boldt, MD Department of Anesthesiology and Critical Care Medicine Klinikum Ludwigshafen Ludwigshafen, Germany [email protected]