2.1.

Historical Aspect

The origin of local anaesthesia is credited to Carl Koller, an ophthalmologist, who demonstrated
the used of topical cocaine for surgical anaesthesia of the eye in 1884. August Bier is credited
with administrating the first planned spinal anaesthesia in 1898; he used 3ml of 0.5% cocaine
intrathecally. He soon abandoned the technique because of the toxicity of cocaine and its short
duration of action. The development of procaine, a much safer agent, in 1904 by Einhorn enabled
spinal anaesthesia to gain popularity (Morgan et al., 2002).
Procaine was synthesized in 1904 by Alfred Einhorn and within a year used clinically as
a local anaesthetic by Heinrich Braun. Additional local anaesthetics subsequently introduced
clinically included dibucaine (1930), lidocaine (1947), chloroprocaine (1955), mepivacaine
(1957), prilocaine (1960), bupivacaine (1963), and etidocaine (1972) (Morgan & Paul, 1994).
Ropivacaine and levovupivacaine, isomers of bupivacaine are newer agents with the same
duration of action as bupivacaine but less cardiac toxicity (Morgan et al, 2006).
Bupivacaine is a member of the homologous series of n-alkyl substituted pipecholyl
xylidines first synthesized by Ekenstam in 1957, and was used clinically in 1963. Debutylation
of bupivacaine results in the production of a xylide metabolite. This metabolite undergoes further
breakdown.
In recent years, there has been a steady increased in the popularity of spinal block for
surgery. In UK, bupivacaine is now the analgesic drug readily available for intrathecal injection.
Experience shows that the technique is safe in expert hands and is to preferred to general
anaesthesia for certain operation and in groups of patients.
By 1909, however, anaesthesiologists were already realizing that they needed to restrict
the degree of sympathetic blockade produced by spinal anaesthesia and so ameliorate the ensuing
cardiovascular disturbance. The underlying supposition has been that if one can confine the
anaesthesia to the nerve roots relevant to the operative field one can achieve a more stable
cardiovascular profile.
In fact, the definitive studies were performed nearly 100 years ago by Arthur Baker, a
London surgeon who was the first to use solutions made hyperbaric by the addition of glucose,
but his principle have had to be re-learned virtually each time a new drug has been introduced for
the technique (Hocking & Wildsmit, 2004).
 In practice, there are a number of tasks that need to be performed successfully to achieve
this goal. One needs to deposit the local anaesthetic solution in the relevant area, prevent its
mixture’s spread in the cerebrospinal fluid, and have sufficient volume and concentration of local
anaesthetic to render the patient amenable to surgery but not so much as to result in
cardiovascular derangement. Finally one needs to be able to do this in a manner that is practical
in a clinical setting and acceptable to patients.
The problem was recognized from the beginning, even Bier referring to the waywardness
of the technique. Since then there has been a progressive, almost exponential growth of research
in this field, but a clear understanding of the mechanism of spread of drugs through the
subarachnoid space has remained elusive. The variability between patients relates to both extent
and duration of block, and occurs even when technically identical injection techniques are used.
The search to identify and control the factors influencing this variability began shortly after
Bier’s pioneering work. Barker, a London based surgeon, was the first to examine the problem
systematically using a glass model of the spinal column as well as clinical observation. He
deduced that gravity and the curves of the vertebral column could be used to influence the spread
of a solution with a density which differed from that of cerebrospinal fluid. As a result, he
devised a solution that was hyperbaric and could be used with predictable effects. Babcock,
meanwhile, took the opposite approach using a solution that was less dense than cerebrospinal
fluid so that it would “float” (Connolly & Wildsmith, 1998).
In 1984, when injecting hyperbaric and isobaric bupivacaine in the sitting position, then
placing the subject in a dorsal decubitus position, Bengtsson failed to find any difference in
block spread. In order to elucidate these findings Lui et al, compared hyperbaric with isobaric
lidocaine in a glass spine model placed in the vertical position. With this model, the hyperbaric
solution was more concentrated at the lower end of the column, whereas the isobaric formulation
tended to concentrated around the site of injection. They concluded that Bengtsson’s findings
were not only related to baricity, but also to the effect of the spinal curvature. However, the
patients in Bengtsson’s study were moved to the dorsal decubitus position two minutes after
injection. Therefore, if Lui et al., had moved their model to the horizontal position after
injection, their findings may have been different.
In 1990, Toft published a study similar to that of Bengtsson, but with 80 mg of either 2%
isobaric or 5% hyperbaric xylocaine. He found that concentration, volume and baricity had no
effect on the cephalad spread of the block. Other studies using bupivacaine found that cephalad
spread was greater by an average of two dermatomes when a hyperbaric formulation was used.
Unlike Bengtsson’s experiment, the subjects were injected in the lateral decubitus position and
not the sitting position.
Zundert, injected subjects in the lateral decubitus position with a constant dose of
lidocaine (70 mg), but at different concentrations (0.5, 1, 2, 5, 10%) of which only the 10% was
hyperbaric. He reported that baricity had no effect on cephalad spread, as long as the dose was
kept constant. This suggested that there was a difference between lidocaine and bupivacaine
when injected in the lateral decubitus position (Jankowska et al., 2000).

2.2. Subarachnoid Anaesthesia

The temporary axonal blockage produced by subarachnoid injection of a local anaesthetic

solution into CSF is termed subarachnoid anaesthesia. The injection of local anaesthetic solution
into the CSF induces a temporary paralysis of the autonomic, sensory and motor nerve fibers in
both the anterior and posterior nerve roots, which meet in contact with anaesthetic solution. The
technique of subarachnoid anaesthesia is basically that of lumber puncture, but the knowledge of
factors which effect the extent and duration of anaesthesia and experience in patient management
are essential (Lee, 2001).
Spinal anaesthesia requires a small volume of drug, virtually devoid of systemic
pharmacologic effects to produce profound, reproducible sensory analgesia. Other impediments
to the effective use of neuraxial blockades are the predictable decrease in arterial blood pressure
and heart rate through the accompanying sympathectomy with vasodilatation and blockade of
cardio accelerator fibers. Maintaining arterial blood pressure and heart rate at normal values
during these blocks often requires administration of vasoactive drugs and intravenous fluids.
Anaesthesiologists continue to face confusion about balancing the risks and benefits of spinal
anaesthesia (David, 2000).
Although spinal anaesthesia has long been considered a safe technique, it is not without
risk or side effects. Hypotension, nausea, vomiting are occurred during spinal anaesthesia, with
incidences ranging from 7 to 42 percent. Similarly severe bradycardia, cardiac arrest and
dysarrhythemia occur during spinal anaesthesia although the incidence of these events is not well
established (Carpenter et al, 1992).
Spinal anaesthesia is a simple, and popular anaesthetic technique, yet much remains
unknown regarding pertinent anatomy, physiology and pharmacology. Investigations into
physiologic effects of spinal anaesthesia reveal complex action on multiple organ systems. Safety
of spinal agents and complications from spinal anaesthesia continue to be examined to improve
safety (Liu et al, 2001).