JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Röhm, K. D. Articles by Boldt, J. Search for Related Content PubMed PubMed Citation Articles by Röhm, K. D. Articles by Boldt, J.

---

LETTER TO THE EDITOR

Persisting Neurological Symptoms After Uncomplicated Intrathecal Bupivacaine

Department of Anesthesiology and Critical Care Medicine; Klinikum Ludwigshafen; Ludwigshafen, Germany; k.d.roehm{at}web.de

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.

REFERENCES

1. Chabbouh T, Lentschener C, Zuber M, et al. Persistent cauda equina syndrome with no identifiable facilitating condition after uneventful single spinal administration of 0.5% hyperbaric bupivacaine. Anesth Analg 2005;101:1847–8.[Abstract/Free Full Text]
2. Zaric D, Christiansen C, Pace NL, Punjasawadwong Y. Transient neurological symptoms (TNS) following spinal anaesthesia with lidocaine versus other local anaesthetics. Cochrane Database Syst Rev 2003;(2):CD003006.
3. Bauer H, Röhm K, Grau A. Transient toxic cauda-syndrome after uncomplicated spinal anaesthesia with hyperbaric bupivacaine 0.5%. Akt Neurol 2005;32: 143–8.
4. Ganem EM, Vianna PT, Marques M, et al. Neurotoxicity of subarachnoid hyperbaric bupivacaine in dogs. Reg Anaesth 1996;21:234–8.
5. Takenami T, Yagishita S, Murase S, et al. Neurotoxicity of intrathecally administered bupivacaine involves the posterior roots/posterior white matter and is milder than lidocaine in rats. Reg Anesth Pain Med 2005;30:464–72.[ISI][Medline]
6. Drasner K, Sakura S, Chan VW, et al. Persistent sacral sensory deficit induced by intrathecal local anesthetic infusion in the rat. Anesthesiology 1994;80:847–52.[ISI][Medline]
7. Radwan IA, Saito S, Goto F. The neurotoxicity of local anesthetics on growing neurons: a comparative study of lidocaine, bupivacaine, mepivacaine, and ropivacaine. Anesth Analg 2002;94:319–24.[Abstract/Free Full Text]
8. Paech MJ. Unexplained neurologic deficit after uneventful combined spinal and epidural anaesthesia for cesarean delivery. Reg Anaesth 1997;22:479–82.
9. Navarro JL, Soria A, Herrera P, Montero R. Cauda equina syndrome after intradural anesthesia with bupivacaine. Rev Esp Anestesiol Reanim 2001;48:337–9.[Medline]
10. Zeidan AM, Samii K. A case of unusually prolonged hyperbaric spinal anesthesia. Acta Anaesth Scand 2005;49:885.[ISI][Medline]

This article has been cited by other articles:

				T. Chabbouh and C. Lentschener Persisting Neurological Symptoms After Uncomplicated Intrathecal Bupivacaine Anesth. Analg., October 1, 2006; 103(4): 1047 - 1047. [Full Text] [PDF]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Röhm, K. D. Articles by Boldt, J. Search for Related Content PubMed PubMed Citation Articles by Röhm, K. D. Articles by Boldt, J.

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999