Local anesthesia
History;
The leaves of the coca plant were traditionally used as a
stimulant in Peru. It is believed[by whom?] that the local anesthetic
effect of coca was also known and used for medical purposes.
Cocaine was isolated in 1860 and first used as a local anesthetic
in 1884. The search for a less toxic and less addictive substitute
led to the development of the aminoester local anesthetic
procaine in 1904. Since then, several synthetic local anesthetic
drugs have been developed and put into clinical use, notably
lidocaine in 1943, bupivacaine in 1957 and prilocaine in 1959.
Shortly after the first use of cocaine for topical anesthesia, blocks
on peripheral nerves were described. Brachial plexus anesthesia
by percutaneous injection through axillary and supraclavicular
approaches was developed in the early 20th century. The search
for the most effective and least traumatic approach for plexus
anesthesia and peripheral nerve blocks continues to this day. In
recent decades, continuous regional anesthesia using catheters
and automatic pumps has evolved as a method of pain therapy.
Intravenous regional anesthesia was first described by August
Bier in 1908. This technique is still in use and is remarkably safe
when drugs of low systemic toxicity such as prilocaine are used.
Spinal anesthesia was first used in 1885 but not introduced into
clinical practice until 1899, when August Bier subjected himself to
a clinical experiment in which he observed the anesthetic effect,
but also the typical side effect of postpunctural headache. Within
a few years, spinal anesthesia became widely used for surgical
anesthesia and was accepted as a safe and effective technique.
Although atraumatic (non-cutting-tip) cannulas and modern
drugs are used today, the technique has otherwise changed very
little over many decades.
LOCAL ANESTHETICS are used in dentistry to
anesthetize teeth and portions of your jaw so as to
maximize comfort during dental procedures.
Dental anesthetics are dispensed in individual,
sterile cartridges into which a sterile needle is
inserted.
Typical dental anesthetics are "-caine type agents" such
as xylocaine, lidocaine, carbocaine, and marcaine.
Novocaine was perhaps the first widely used local
anesthetic but it is no longer available. Some anesthetics
contain epinephrine (adrenalin), a vasoconstrictor
(reduces blood flow), to decrease bleeding in the site and
increase anesthetic potency.
Dentists inject anesthetic into spaces near nerves that
innervate (supply sensation) the area to be treated. The
goal is to let the anesthetic gently diffuse into the desired
region.
As a patient, you will feel the needle go in and the
pressure of the solution being injected into the tissues.
Generally, the slower the injection, the less the
discomfort.
Topical Anesthetic is a -caine type ointment applied before
the injection to diminish the prick of the needle.
Each patient is anatomically unique; therefore, it is
possible to inject directly into a nerve. This situation
causes sudden, sharp "shock" followed by immediate
anesthesia.
It is also possible to inject into a blood vessel. In those
circumstances, you may feel your heart pound faster.
This is due to the epinephrine (Adrenalin) in the
anesthetic. You may also swell and bruise (hematoma).
Local anesthetic can block almost every nerve between the
peripheral nerve endings and the central nervous system. The
most peripheral technique is topical anesthesia to the skin or
other body surface. Small and large peripheral nerves can be
anesthetized individually (peripheral nerve block) or in
anatomic nerve bundles (plexus anesthesia). Spinal
anesthesia and epidural anestem merges into the central
nervous system.
Injection of local anesthetics is often painful. A number of
methods can be used to decrease this pain including
buffering of the solution with bicarb and warming.[1]
Surface anesthesia - application of local anesthetic
spray, solution or cream to the skin or a mucous
membrane. The effect is short lasting and is limited to
the area of contact.
Infiltration anesthesia - injection of local anesthetic
into the tissue to be anesthetized. Surface and
infiltration anesthesia are collectively topical
anesthesia.
Field block - subcutaneous injection of a local
anesthetic in an area bordering on the field to be
anesthetized.
Peripheral nerve block - injection of local
anesthetic in the vicinity of a peripheral nerve to
anesthetize that nerve's area of innervation.
Plexus anesthesia - injection of local anesthetic
in the vicinity of a nerve plexus, often inside a
tissue compartment that limits the diffusion of
the drug away from the intended site of action.
The anesthetic effect extends to the innervation
areas of several or all nerves stemming from the
plexus.
Physiology
To achieve conduction anesthesia a local anesthetic is injected
or applied to a body surface. The local anesthetic then diffuses
into nerves where it inhibits the propagation of signals for pain,
muscle contraction, regulation of blood circulation and other
body functions. Relatively high drug doses or concentrations
inhibit all qualities of sensation (pain, touch, temperature etc.) as
well as muscle control. Lower doses or concentrations may
selectively inhibit pain sensation with minimal effect on muscle
power. Some techniques of pain therapy, such as walking
epidurals for labor pain use this effect, termed differential block.
Pathophysiology
Reviewing the physiology of nerve conduction is important
before any discussion of local anesthetics. Nerves transmit
sensation as a result of the propagation of electrical impulses;
this propagation is accomplished by alternating the ion gradient
across the nerve cell wall, or axolemma.
In the normal resting state, the nerve has a negative
membrane potential of -70 mV. This resting potential is
determined by the concentration gradients of 2 major
ions, Na+ and K+, and the relative membrane
permeability to these ions (also known as leak currents).
The concentration gradients are maintained by the
sodium/potassium ATP pump (in an energy-dependent
process) that transports sodium ions out of the cell and
potassium ions into the cell. This active transport creates
a concentration gradient that favors the extracellular
diffusion of potassium ions. In addition, because the
nerve membrane is permeable to potassium ions and
impermeable to sodium ions, 95% of the ionic leak in
excitable cells is caused by K+ ions in the form of an
outward flux, accounting for the negative resting
potential. The recently identified 2-pore domain
potassium (K2P) channels are believed to be responsible
for leak K+ currents.
Dentistry (surface anesthesia, infiltration anesthesia or
intraligamentary anesthesia during restorative
operations or extractions, regional nerve blocks during
extractions and surgeries.)