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.)