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Anesth Analg 2005;101:1847-1848
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000184126.57327.C3


REGIONAL ANESTHESIA

Persistent Cauda Equina Syndrome with No Identifiable Facilitating Condition After an Uneventful Single Spinal Administration of 0.5% Hyperbaric Bupivacaine

Thouraya Chabbouh, MD, Claude Lentschener, MD, Mathieu Zuber, MD, Nicole Jude, MD, Bernard Delaitre, MD, and Yves Ozier, MD

Université Paris-Descartes, Faculté de Médecine; Assistance Publique – Hôpitaux de Paris, Hôpital Cochin; Université Paris-Descartes, Faculté de Médecine; Hôpital Sainte Anne, Paris, France

Address correspondence to Claude Lentschener, MD, Department of Anesthesia and Critical Care, Hôpital Cochin, 27 rue du Faubourg Saint Jacques, 75679 Paris Cedex 14, France. Address e-mail to claude.lentschener{at}cch.ap-hop-paris.fr.


    Abstract
 Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
We diagnosed cauda equina syndrome 15 h after uneventful single spinal administration of 0.5% hyperbaric bupivacaine 12.5 mg through a 27-gauge pencil-point type needle. No preexisting neurologic disorder was recorded. There was no pain or paresthesia during needle placement or drug injection. The sensory levels were bilateral, symmetric, and caudal to T8. Resolution of most of the symptoms occurred within a few days but some foot drop persisted for 2 yr after the procedure. Bupivacaine neurotoxicity is suggested by the absence of any other identifiable cause for this neurologic deficit.


    Introduction
 Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
To our knowledge, only one well documented case of persistent lumbo-sacral nerve root deficit after a single spinal administration of bupivacaine has been reported (1). That clinical case recorded several conditions that had previously been reported to facilitate maldistribution of local anesthetic in cerebrospinal fluid (CSF) (1). We report a case of persistent cauda equina syndrome in the absence of any predisposing factors after uneventful single intrathecal administration of bupivacaine.


    Case Report
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 Abstract
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 Case Report
 Discussion
 References
 
A 72-yr-old, 172-cm, 70-kg, ASA physical status I patient underwent elective inguinal hernia repair. No history of radicular pain or back pain was reported, nor was the presence of preexisting neurologic disorder reported. With the patient in the sitting position, the lumbar area was disinfected with a solution of 10% povidone-iodine (Betadine; Viatris Manufacturing, Merignac, France). After removing excess moisture from the disinfected site, spinal anesthesia was performed at the L3-4 interspace using a 27-gauge pencil-point tip needle (B. Braun Melsungen, AG D-34209 Melsungen, Germany). Clear CSF was obtained after the first puncture and 2 mL of CSF was aspirated before injecting 0.5% hyperbaric bupivacaine 12.5 mg (Marcaine, Astra Pharmaceutical Products, Rueil-Malmaison, France). One ampoule of 0.5% hyperbaric bupivacaine contains 80 mg glucose and 5 mg of bupivacaine hydrochloride (0.5%) per mL of solution. There was no pain or paresthesia during needle placement or drug injection. Twenty minutes after bupivacaine administration, the sensory levels were bilateral, symmetric, and caudal to T8, as assessed using the pinprick method. The 90-min surgical procedure was conducted uneventfully with the patient in the supine position. Throughout the procedure, his arterial blood pressure remained within 20 percent of baseline. One-hundred-twenty minutes after surgery, lower limb motility was noted to be adequate and the patient was discharged from the postanesthesia care unit. The next morning the patient had difficulty in defecation and complained of urinary retention requiring bladder catheterization and impaired ambulation. Neurological examination by the third author documented impaired sensation to pinprick in both L5 dermatomes, in the perineal region, and on the posterior part of the left calf. Reflexes in the knee and ankle joints were diminished when compared with reflexes recorded in the upper limbs. Lasegue’s test was negative. Bilateral steppage gait resulting from foot-drop was observed. Lumbosacral magnetic resonance imaging revealed no spinal stenosis and no compression on the cauda equina nerve roots. Cauda equina syndrome was diagnosed. One month postoperatively, the patient could void normally and had recovered bowel function. He continued to complain of an intermittent aching pain in the first right toe and of painful dysesthesia in the right L5 dermatome, and he still could not walk normally. Electromyography, also obtained 1 mo postoperatively, showed various degrees of bilateral denervation and reinnervation in the L4, L5, and S1 roots. Two years after the procedure, the patient still complained of paresthesia in the dorsal part of the right foot. Nocturnal aching cramps associated with involuntary extension of the first right toe altered his sleep. A moderate steppage gait impaired walking.


    Discussion
 Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
Most cases of cauda equina syndrome after spinal anesthesia have been reported in association with the administration of lidocaine (2,3). Limited cephalad extension of sensory block, suggesting the restricted distribution of lidocaine in the CSF and likely to have resulted in local anesthetic toxicity, was obtained in clinical reports of cauda equina syndromes after spinal lidocaine (2,4). Local anesthetic toxicity is believed to occur mainly in the cauda equina because the sacral root sheaths (a) are substantially longer (and larger for S1) than neighboring lumbar roots, (b) are devoid of protective sheaths, and (c) given their dorsal position in the thecal sac (especially L-5, S-1, and S-2), they are more exposed to hyperbaric anesthetic pooling (5).

To our knowledge, only one case of persistent cauda equina syndrome following the single intrathecal administration of bupivacaine 3.6 mL, with glucose 5 mg/mL has been completely documented (1). In contrast to our case, the previously reported case noted several clinical conditions previously reported with complaints of cauda equina syndrome (1). The patient’s history included acute meningitis, a condition likely to cause spinal adhesion. After administration of spinal bupivacaine 18 mg, poor cephalad spread was recorded, indicating maldistribution of the local anesthetic. Spinal stenosis at the L2-3 level was diagnosed (1).

Other potential causes of neurologic injuries associated with spinal anesthesia were not identified in our case. No flashing pain or paresthesia was noted on needle placement or bupivacaine injection, as is the case in direct needle-induced trauma to the spinal cord or intraneural injection (3). The spinal anesthetic was performed awake, allowing the patient to respond to painful stimuli (3). Spinal cord compression by an expanding hematoma was excluded in this case by magnetic resonance imaging (3). There was no evidence of infection (6). The risk of chemically induced injury was minimized by the routine use of disposable syringes and needles and of high-quality heat-sterilized local anesthetics (7). Also, the antiseptic used to clean the skin was supplied in a single-use disposable bottle and the skin was, as usual, carefully dried before skin puncture (7). Spinal cord ischemia was also unlikely because the patient had no microvascular disease, remained hemodynamically stable, and vasoconstrictors were not administered (8). Coincident postoperative exacerbation of a preexisting neurologic disease was also inconsistent with the conditions of this clinical case (9). Finally, the neurological examination was not consistent with a neurological injury from improper patient positioning or surgical trauma (10).

In conclusion, we report a case of cauda equina syndrome after uneventful single spinal administration of bupivacaine. Bupivacaine neurotoxicity is suggested by the absence of any other identifiable cause for this neurologic deficit.


    Footnotes
 
Accepted for publication June 29, 2005.


    References
 Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 

  1. Kubina P, Gupta A, Oscarsson A, et al. Two cases of cauda equina syndrome following spinal-epidural anesthesia. Reg Anesth 1997;22:447–50.[Web of Science][Medline]
  2. Rigler ML, Drasner K, Krejcie TC, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 1991;72:275–81.[Abstract/Free Full Text]
  3. Cheney FW, Domino KB, Caplan RA, Posner KL. Nerve injury associated with anesthesia: a closed claims analysis. Anesthesiology 1999;90:1062–9.[Web of Science][Medline]
  4. Rigler ML, Drasner K. Distribution of catheter-injected local anesthetic in a model of the subarachnoid space. Anesthesiology 1991;75:684–92.[Web of Science][Medline]
  5. Hogan Q. Anatomy of spinal anesthesia: some old and new findings. Reg Anesth Pain Med 1998;23:340–3.[Web of Science][Medline]
  6. Bouhemad B, Dounas M, Mercier FJ, Benhamou D. Bacterial meningitis following combined spinal-epidural analgesia for labour. Anaesthesia 1998;53:292–5.[Web of Science][Medline]
  7. Seige TD. Aseptic meningitis following spinal anesthesia. Anesthesia 1970;25:402–7.
  8. Auroy Y, Narchi P, Messiah A, et al. Serious complications related to regional anesthesia: results of a prospective survey in France. Anesthesiology 1997;87:479–86.[Web of Science][Medline]
  9. Warren TM, Datta S, Ostheimer GW. Lumbar epidural anesthesia in a patient with multiple sclerosis. Anesth Analg 1982;61:1022–3.[Abstract/Free Full Text]
  10. Irvin W, Andersen W, Taylor P, Rice L. Minimizing the risk of neurologic injury in gynecologic surgery. Obstet Gynecol 2004;103:374–82.[Medline]



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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2005 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press