Ever since the introduction of Spinal anesthesia in 1898 by the German surgeon August Bier,
the approach gained wide acceptance by the anesthesia community 1. Since that time, the
technique has evolved to accommodate a wide variety of surgical procedures, making it one of
the most common regional anesthesia modalities used. The advancement of the anesthesia field
has led to the advancement of the technique it self, specially the drugs used in it.
A wide range of local anesthetics has been introduced after the initial successful
intrathecal use of cocaine. Starting with amylocaine, and later with the introduction of
various local anesthetics such as procaine, 2-chloroprocaine, lidocaine, tetracaine,
mepivacaine, prilocaine, bupivacaine, with ropivacaine and levobupivacaine being introduced
last. Many of these drugs have fallen out of favour due to various reasons, with Lidocaine,
procaine, mepivacaine, ropivacaine and bupivacaine still being used in clinical practice 2.
The choice of the local anesthetic used depends on many factors such as the duration of the
operation, the type of surgery and the degree of motor blockade desired. With the advancement
of surgery and the increase in day surgical cases, a need for a fast acting, short in
duration local anesthetic that allows fast recovery and early discharge has emerged. Of all
the local anesthetic drugs available, Lidocaine is one of the drugs that fulfills these
needs.
Common complications associated with the use of this technique include headache (5%),
backache (11%), hypotension, bradycardia, nausea and vomiting (20%), urinary retention,
hypothermia and transient neurological syndrome (TNS). More serious complications include
total spinal, infection (meningitis/ encephalitis) and epidural hematoma (<1 in 150,000). On
the other hand, complications related to receiving General Anesthesia for the same procedure
are similar, with higher chances of nausea and vomiting or airway problems.
TNS is defined as back pain and/or dysesthesia radiating bilaterally to the legs or buttocks
after total recovery from spinal anesthesia, manifesting within 24 hours after the surgery
and typically lasting less than a week. The etiology of TNS is unknown. Possible contributing
factors to the development of TNS include sciatic nerve stretching causing neural ischemia,
vasoconstriction of spinal cord arteries, patient positioning, direct needle injury and
pooling of local anesthetic in the sacral region. The pathophysiology of TNS is unknown, and
there is no specific lab test to diagnose this complication. Treatment of TNS, includes bed
rest, administration of nonsteroidal anti inflammatory drugs and sometimes the addition of an
opioid is needed 3.
All local anesthetics have been shown to cause TNS, with lidocaine appearing to have the
greatest risk. The first reported case of TNS after the single shot administration of 5%
hyperbaric lidocaine was published by Schneider and colleagues in 1993 4, which was confirmed
later by several other studies 5-9. The reported incidence of TNS after the administration of
lidocaine ranges from 10%-40% 10-13. In a more resent study done by F. Salazar et al. the
incidence of TNS with lidocaine was reported to be 2.5%, much lower than what was previously
described in the literature 14.
Furthermore, in an internal audit done at the MGH looking at all spinal anesthesia cases
performed by Dr. Asenjo in the past two years, TNS incidence was found to be 2.7%, far less
than what the literature describes, and correlates more with what F. Salazar et al. found in
their study. We want to clarify this discrepancy in the incidence of TNS with lidocaine since
this is a very inexpensive agent, with a short to intermediate duration of action and readily
available world wide. With this purpose we have designed a randomized controlled trial to
test the hypothesis that the incidence of TNS after spinal anesthesia with lidocaine is much
lower than what was previously described in the literature. This trial will also look at the
natural course of the symptoms of TNS.