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March 29, 2001
Cauda Equina Syndrome After Spinal Anesthesia with Hyperbaric
5% Lignocaine: A Review of the Six Cases of Cauda Equina Syndrome Reported
to the Swedish Pharmaceutical Insurance 1993-1997
Loo CC, Irestedt L. Acta Anaesthesiol Scand
1999;43:371-379
Commentary by Kathryn
McGoldrick, M.D.
Ever since August Bier pioneered spinal anesthesia in 1898, the
safety of drugs administered intrathecally has been debated vigorously. Although
uncommon, neurological complications after spinal anesthesia can be devastating.
These can include such serious entities as spinal cord ischemia, arachnoiditis,
and cauda equina syndrome (CES). CES is characterized by varying degrees of
saddle anesthesia, sphincter dysfunction resulting in bowel or urinary problems,
and paraplegia.
Auroy and colleagues, [1] after a prospective survey of 40,640 spinal anesthetics
administered in France in 1994, found five cases of CES as a result of spinal
anesthesia (1 in 8,128 blocks). During the past decade there has been particular
concern about the potential direct neurotoxicity of hyperbaric 5% lidocaine
and its possible role in the development of CES. However, most cases involving
lidocaine-associated CES have been attributed to sacral maldistribution with
microcatheters (removed from the market in the United States in the early
1990s) and the administration of excessive doses of hyperbaric 5% lidocaine
via the continuous spinal anesthesia technique [2-4] rather than to a unique
neurotoxic property of the drug per se. Then in 1997 Gerancher described
CES after a single spinal administration of 5% hyperbaric lidocaine through
a 25-gauge Whitacre needle. [5]
The current publication by Loo and Irestedt describes five cases of CES after
"single-shot spinal" with hyperbaric 5% lidocaine and one case of
CES after two doses of spinal hyperbaric 5% lidocaine that were reported to
the Swedish Pharmaceutical Insurance from 1993 to 1997. The dose of hyperbaric
5% lidocaine administered ranged from 60 to 120 mg, and the ages of the patients
ranged from 31 to 59 years.
Clearly, as the authors so appropriately underscore, the diagnosis of direct
local anesthetic neurotoxicity is one of exclusion. Care must be exercised
to rule out trauma; spinal cord ischemia (localized or global); infection;
compression by hematoma, abscess, prolapsed intervertebral disc and spondylolisthesis;
contamination of local anesthetics; and injurious surgical positioning. With
regard to the latter phenomenon, it is important to point out that the lithotomy
position stretches the cauda equina and may jeopardize perfusion of the nerves,
rendering them vulnerable to neurotoxicity.
Loo and Irestedt considered that three of the cases were most probably the
result of direct neurotoxicity of hyperbaric 5% lidocaine. Furthermore, in
the other three cases, direct neurotoxicity was also probable, but a compressive
etiology could not be excluded owing to the omission of appropriate radiological
studies.
Both animal and epidemiologic studies indicate that lidocaine neurotoxicity
is concentration- and dose-dependent. Drasner has suggested that there is
little justification for administering more than 60 mg lidocaine, [6] and
it is important to appreciate that Astra USA wrote a "Dear Doctor"
letter in 1995, revising its prescribing information for hyperbaric 5% lidocaine,
wherein they suggested mixing the drug with an equal volume of CSF or preservative-free
saline solution thereby producing a concentration of 2.5 percent [7]. Emphasizing
that no cases of CES have been linked to hyperbaric lidocaine in concentrations
less than 5% when administered in doses not greater than 100 mg, Loo and Irestedt,
taking a conservative approach in the context of serious potential risk, recommend
that hyperbaric lidocaine should be administered in concentrations not greater
than 2% and a total dose preferably not exceeding 60 mg.
References
- Auroy Y, Narchi P, Messiah A, Litt L, Rouvier B, Samii K. Serious complications
related to regional anesthesia: Results of a prospective survey in France.
Anesthesiology 1997;87:479-486. Click
here for abstract
- Lambert DH, Hurley RJ. Cauda equina syndrome and continuous spinal anesthetic.
Anesth Analg 1991;72:817-819.
- Rigler ML, Drasner K, Krejcie TC, et al. Cauda equina syndrome after continuous
spinal anesthesia. Anesth Analg 1991;72:275-281. Click
here for abstract
- Schell RM, Brauer FS, Cole DJ, Applegate RL. Persistent sacral root deficits
after continuous spinal anaesthesia. Can J Anaesth 1991;38:908-911.
Click
here for abstract
- Gerancher J. Cauda equina syndrome following a single spinal administration
of 5% hyperbaric lidocaine through a 25-gauge Whitacre needle. Anesthesiology
1997;87:687-689.
- Drasner K. Lidocaine spinal anesthesia: A vanishing therapeutic index?
(Editorial) Anesthesiology 1997;87:469-472.
- "Dear Doctor" letter. Important new prescribing information
enclosed. Westborough, MA: Astra USA, June 12, 1995.
ABSTRACT
Cauda Equina Syndrome
After Spinal Anesthesia with Hyperbaric 5% Lignocaine: A Review of the Six
Cases of Cauda Equina Syndrome Reported to the Swedish Pharmaceutical Insurance
1993-1997
AUTHORS:
Loo CC, Irestedt
L.
SOURCE:
Acta
Anaesthesiol Scand 1999;43:371-379
ABSTRACT:
Six
cases of cauda equina syndrome with varying severity were reported to the
Swedish Pharmaceutical Insurance during the period 1993-1997. All were associated
with spinal anaesthesia using hyperbaric 5% lignocaine. Five cases had single-shot
spinal anaesthesia and one had a repeat spinal anaesthetic due to inadequate
block. The dose of hyperbaric 5% lignocaine administered ranged from 60
to 120 mg. Three of the cases were most likely caused by direct neurotoxicity
of hyperbaric 5% lignocaine. In the other 3 cases, direct neurotoxicity
was also probable, but unfortunately radiological investigations were not
done to definitely exclude a compressive aetiology. All cases sustained
permanent neurological deficits. We recommend that hyperbaric lignocaine
should be administered in concentrations not greater than 2% and at a total
dose preferably not exceeding 60 mg.
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