Complications Associated with Drug Toxicity
Absorption of excessive amounts of local anesthet-ics can produce toxic
blood levels (see “Intravascu-lar Injection”). Excessive absorption from
epidural or caudal blocks is rare when appropriate doses of local anesthetic
are used.
First described in 1993, transient
neurologicalsymptoms (TNS), also referred to
as transient radic-ular irritation, are characterized by back pain radi-ating
to the legs without sensory or motor deficits, occurring after the resolution
of spinal anesthesia and resolving spontaneously within several days. It is most
commonly associated with hyperbaric lido-caine (incidence up to 11.9%), but has
also been reported with tetracaine (1.6%), bupivacaine (1.3%), mepivacaine,
prilocaine, procaine, and subarach-noid ropivacaine. There are also case
reports of TNS following epidural anesthesia. The incidence of this syndrome is
greatest among outpatients, particularly males undergoing surgery in the
lithotomy position, and least among inpatients undergoing surgery in positions
other than lithotomy. The pathogenesis of TNS is believed to represent
concentration-depen-dent neurotoxicity of local anesthetics.
CES was associated with the use of continuous
spinal catheters (prior to their withdrawal) and 5% lido-caine (see “Spinal
Catheters”). CES is characterizedby bowel and bladder dysfunction together with
evi-dence of multiple nerve root injury. There is lower motor neuron type
injury with paresis of the legs. Sensory deficits may be patchy, typically
occurring in a peripheral nerve pattern. Pain may be similar to that of nerve
root compromise. Animal studies sug-gest that pooling or “maldistribution” of
hyperbaric solutions of lidocaine can damage the nerve roots of the cauda
equina. However, there are reports of CES occurring after uneventful single
shot lidocaine spi-nals. CES has also been reported following epidural
anesthesia.
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