this is a summary of the important points to consider in local anesthesia . most of the information in this jandout are taken from handbook of local anethesia by malamed

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Local anesthesia summary handout
Done by : Dr.khalil raziq
BDS, MFDRCSI (Ireland),diploma in research and
methodology

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Local anesthesia for students
Anesthesia
Definition :
Local anesthesia can be defined as loss of sensation in circumscribed
area of the body caused by depression of excitation in nerve endings
or inhibition of the conduction process in peripheral nerves.
An important feature of local anesthesia is that it produces this loss of
sensation without inducing a loss of consciousness .
Mode of action :
Background
. In 1860, cocaine, the oldest anesthetic, was extracted from the leaves of the
Erythroxylon coca bush.
Procaine, a synthetic alternative to cocaine, was not developed until 1904.
Procaine is an ester of para-aminobenzoic acid (PABA). As procaine is
metabolized, PABA, a known allergen, is released as a metabolic product. The
potential for severe allergic reactions limits the use of procaine and other ester-
type anesthetic agents. Tetracaine, another ester-type anesthetic, was
introduced in 1930. Tetracaine is more potent than procaine, and it causes
similar allergic reactions.
In 1943, an alternative class of anesthetics was discovered when Lofgren
developed lidocaine. This agent is an amide derivative of diethylaminoacetic
acid, not PABA; therefore, it has the benefit of a low allergic potential. Since
then, multiple amide-type anesthetics have been introduced into clinical use.
Slight chemical alterations to the compounds have imparted beneficial
characteristics, including increased duration and potency, to each. These
compounds offer the surgeon more choices, and anesthetics can be
appropriately matched to different procedures.

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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.
When a nerve is stimulated, depolarization of the nerve occurs, and impulse
propagation progresses. Initially, sodium ions gradually enter the cell through
the nerve cell membrane. The entry of sodium ions causes the transmembrane
electric potential to increase from the resting potential. Once the potential
reaches a threshold level of approximately -55 mV, a rapid influx of sodium ions
ensues. Sodium channels in the membrane become activated, and sodium ion
permeability increases; the nerve membrane is depolarized to a level of +35 mV
or more.

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Once membrane depolarization is complete, the membrane becomes
impermeable to sodium ions again, and the conductance of potassium ions into
the cell increases. The process restores the excess of intracellular potassium and
extracellular sodium and reinstates the negative resting membrane potential.
Alterations in the nerve cell membrane potential are termed the action
potential. Leak currents are present through all the phases of the action
potential, including setting of the resting membrane potential and
repolarization.

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Mechanism of action
Local anesthetics inhibit depolarization of the nerve membrane by interfering
with both Na+
and K+
currents. The action potential is not propagated because
the threshold level is never attained.
Although the exact mechanism by which local anesthetics retard the influx of
sodium ions into the cell is unknown,
2 theories have been proposed:
1) The membrane expansion theory postulates that the local anesthetic is
absorbed into the cell membrane, expanding the membrane and leading to
narrowing of the sodium channels. This hypothesis has largely given way to the
2)specific receptor theory: This theory proposes that the local anesthetic
diffuses across the cell membrane and binds to a specific receptor at the
opening of the voltage-gated sodium channel. The local anesthetic affinity to
the voltage-gated Na+
channel increases markedly with the excitation rate of
the neuron. This binding leads to alterations in the structure or function of the
channel and inhibits sodium ion movement. Blockade of leak K+
currents by
local anesthetics is now also believed to contribute to conduction block by
reducing the ability of the channels to set the membrane potential.
On the basis of their diameter, nerve fibers are categorized into 3 types:
1) Type A fibers are the largest and are responsible for conducting pressure and
motor sensations.
2) Type B fibers are myelinated and moderate in size.
3) Type C fibers, which transmit pain and temperature sensations, are small and
unmyelinated. As a result, anesthetics block type C fibers more easily than they
do type A fibers. Therefore, patients who have blocked pain sensation still feel
pressure and have mobility because of the unblocked type A fibers.

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Mode of action :
Kinetics of local anesthesia ,onset and duration of action :
Barriers to diffusion of the solution :
Aperipheral nerve is composed of hundreds to thousands of tightly
packed axons .these axons are protected ,supported and nourished by
several layers of fibrous and elastic tissues.nutrients blood vessels
and lymphatics course through out these layers
Individual nerve fibers (axon) is covered by and also separated from
one another by the endoneurium . The perineurim then binds these

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nerve fibers into fasciculi . each fasciuli contains between 500 and
1000 individual nerve fibers.
The thickness of the perineurium varies with the amount of fasciulis is
surrounds .the thicker the perineurium the slower the rate of local
anesthetic diffusion across it .
The fasciculi are contained within loose connective tissue called
epineuriam .the epineurium constitutes between 30 and 75% of the
total cross section of the nerve.LA are readily able to diffuse through
the epineuriem because of loose consistency .nutrients blood vessels
and lymphatics traverse the epineurium .
Summary:
Within a nerve, each axon is surrounded by a layer of connective
tissue called the endoneurium. The axons are bundled together into
groups called fascicles, and each fascicle is wrapped in a layer of
connective tissue called the perineurium.
Induction of local anesthesia :
During the induction phase of anesthesia ,the local anesthetic moves
from its extraneural site of deposition towards the nerve .this process
is known as diffusion . it’s the unhindered migration of molecules or
ions from through a fluid medium under the influence of the
concentration gradient . Penetration of an anatomical barrier to
diffusion occurs when drug passes through a tissue that tends to
restrict free molecular movement. The perineuriem is the greatest
barrier to penetration of LA.

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Diffusion:
The rate of diffusion is governed by many factors but mainly its
governed by the concentration gradient .
Fasciculi that are located near the surface of the nerve are termed
mantle bundles . mantle bundles are the first to be reached by the
local anesthetic and are exposed to a higher concentration of it.
Mantle bundles are usually blocked completely shortly after the
injection of a local anesthetic .
Fasciculi found near the center of the nerve are called core bundles .
core bundles are contacted by local anesthetic only after much delay
and by lower concentration because of greater distance the solution
must traverse and the greater number of barriers it must cross.
As local anesthetic diffuse into the nerve it becomes extremely
diluted by tissue fluids and is absorbed by capillaries and lymphatics
;ester anesthetics undergo almost immediate enzymatic hydrolysis.
Thus core fibers sre exposed to decreased conc of LA .a fact may
explain the clinical situation of inadequate pulpal anesthesia
developing in the presence of subjective symptoms of adequate soft
tissue anesthesia .complete conduction block of all nerve fibers in
aperipheral nerve requires that an adequate volume as well as an
adequate concentration .
Fibers near the surface the nerve (mantle fibers) tend to innervate
more proximal regions ( the molar area with inferior alveolar nerve
block ) where is fibers in the core bundles innervate the more distal
points of nerve distribution (e.g central and lateral incisors with
inferior alveolar block)

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So the local anesthetic faces many challenges before its able to get to
the nerve like:
1)some of the drug is absorbed by non neural tissues (muscle and fat)
2)some are diluted by interstitial fluid
3)some is removed by capillaries and lymphatics from injection site
4)Ester-type anesthetic are hydrolyzed
Induction time:
It’s the period from deposition of the anesthetic to complete
conduction blockade. Several factors control the induction time of a
given drug.
Those under operator control :
1)concentration of drug
2)PH of LA
Those not under operator control:
Diffusion constant of the anesthetic drug and the anatomical diffusion
barriers

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Physical properties and clinical actions:
1)effect of PKa (the PH when unionized and ionized are equal ) the
lower the PKa the more unionized the greter the lipid solubility so the
faster the onset
2)Lipid solubility :increased lipid solubility permits the anesthetic to
penetrate the nerve membrane more easily.this is reflected
biologically in an increased potency of the anesthetic. Local anesthetic
with greater lipid solubility produce more effective conduction
blockade at lower concentration (lower percentage solutions or
smaller volumes deposited)
3)protein binding : the degree of protein binding of local anesthetic to
plasma proteins (mainly albumin) is responsible for the duration of
local anesthetic activity .
4)vasoactivity : affects both the potency and the duration of
anesthesia provided the drug.injection of local anesthetic ,such as
procaine ,with greater vasodilating properties increases the profusion
of the local site with blood. The local anesthetic is therefore absorbed
into the cardiovascular compartment more rapidly and carried away
from injection site and from the nerve ,thus providing for a shortened
duration of anesthesia as well as decreased potency of drug .

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Order of recovery from local anesthesia:
Follows the same diffusion patterns as induction only in reverse order
.mantle fibers lose anesthesia before the core bundles and so third
molars will regain sensation before the incisors if inferior alveolar
nerve block was administered .
Recovery is usually is aslower process than induction because the
local anesthetic is bound to the drug receptor site in sodium channel
and is therefore released more slowly than its absorbed
So factors affecting the duration of local anesthetic :
1)protein binding property
2)vascularity of injection site ( duration is increased in less
vascularized area)
3)presence or absence of vasoactive substance

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Components of local anesthesia :
1)local anesthetic drug
2)vasoconstrictor drug
3)preservative of vasocnstricor (sodium metabisulphate)
4)sodium chloride
5)distilled water
6)general preservative

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Local anesthetic agent :
2 main groups :
The main difference between the ester and amide LA is their
Metabolism :
Esters are hydrolyzed in the plasma by the enzyme
pseudocholinestrase . the rate at which hydrolysis has an impact on
the potential toxicity of local anesthetic . choloroprocaine ,the most
rapidly hydrolyzed is the least toxic , where as tetracaine is
hydrolyzed 16 times more slower than choloroprocaine thus has the
greatest potential toxicity .
Procaine undergoes hydrolysis to para-aminobenzoic acid (PABA)
which is most common reason of allergy .
Approximately 1 out of every 2800 persons has an atypical form of
pseudocholinestarse .which causes inability to hydrolyze ester local
anesthetic and other chemically related drugs (e.g succinylcholine) its
presence leads to prolongation of higher blood levels of the local
anesthetic and increased potential for toxicity.

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Amide local anesthetic:
The metabolism of amide local anesthetic is more complx than that of
esters.the primary site of biotransformation is the liver. Virtually the
entire metabolic process occurs in the liver for lidocaine , articane ,
mepivicane and bupivicane.
Prilocaine undergoes primary metabolism in liver ,with possibility
occurring in lungs.
Liver function and hepatic blood flow therefore is significantly
influence the rate of biotransformation of an amide local anesthetic.
Approximately 70% of dose injected lidocaine undergoes
biotransformation in pts with healthy liver function . pts with lower
than usual hepatic blood flow( hypotension , congestive heart failure )
or poor liver function (cirrhosis) are unable to biotransform amide
local anesthetic at a normal rate . this slower than normal
biotransformation rate leads to increased anesthetic blood levels and
potentially increased toxicity .
Prilocaine and articane have a serious side effect and that is their by
products may induce METHEAMGLOBINEMIA.

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Metheamglobinemia :
is acondition in which cyanosis like state develops in the absence of
cardiac or respiratory abnormalities . when condition is sever the
blood appears chochlate brown ,and clinical signs and symptoms
including respiratory depression and syncope,maybe noted ;death
though unlikely can result.
Etiology :
I the heamoglobin molecule ,iron is usually is present in the reduced
ferrous state (Fe++) . in the ferrous state heamoglobin can carry
oxygen that is available to the tissues. Because hemoglobin in the
erythrocyte is inherently unstable its continuously being oxidized to
the ferric state (Fe+++) , in which state the oxygen molecule is more
firmly attached and cannot be released to the tissues . this form of
hemoglobin is called methemoglobin. To permit an adequate oxygen-
carrying capacity in the blood an enzyme system is present which
continually reduces the ferric form to ferrous state . in usual clinical
situations the approximately 97%-99% of hemoglobin is found in
ferrous state and only 1-3% is found in ferric state (methemoglobin)
this enzyme system is called methemoglobin reductase and it acts to
reconvert the iron from ferric to ferrous state maintaining a level less
than 1% methemoglobin in blood at any given time. As blood level of
methemoglobin increases ,clinical signs and symptoms of cyanosis
and respiratory distress may become noticeable . in most instances it
will not be noticed until a mrthhemoglobin blood level of 10-20% is
reached
Treatment: -IV of methylene blue - or ascorbic acid IV or IM

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- All local anesthetic agents are vasodialtary except cocaine
So how to choose which local anesthetic agent?
A rational approach to the selection of LA for apt includes a
consideration of the length of procedure . here is the usual used La
agents and their soft tissue and pulpal anesthesia
A second consideration is the requirement of pain control following
treatment .long duration LA can be administered when postoperative
pain is though to be a factor. Drugs providing shorter duration of soft
tissue anesthesia can be used for non traumatic procedures .
For pts in whom postoperative anesthesia is apotential hazard
,shorter duration anesthetic shoukd be used. These include younger
children and physically or mentally disabled ,who might accidentally
bite or chew their lips or tongue
Athird factor the need for hemostasis during procedure . anesthetic
solution containing epinephrine are recommended
A fourth factor: medical status of pt
So in summary the choice of local anesthetic depends on ;
1)length of treatment
2)the need of pain control after treatment
3)need for hemostasis
4)medical status of pt.

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Table 1. Duration of Injectable Local Anesthetics (in minutes).3
Anesthetic Pulp Soft Tissue
Lidocaine 2%
1:100,000 epi
60 minutes 180-240 minutes
Mepivacaine 3%
Plain I (infiltration)
5-10 minutes 90-120 minutes
Articaine 4%
1:200,000 epi
1:100,000 epi
45-60 minutes
60-75 minutes
180-240 minutes
180-300 minutes
Prilocaine 4% plain
Infiltration
Block
10-15 minutes
60-120 minutes
40-60 minutes
120-240 minutes
Prilocaine 4% + epi
1:200,000 epi
60-90 minutes 180-480 minutes
2) Vasoconstrictor :
Vasocnstrictors are drugs that constrict the blood vessels and thereby
control tissue perfusion. They are added to local anesthetic solutions
to oppose the vasodilating actions of the local anesthetic .
vasoconstrictors are highly important additions to alocal anesthetic
solutions for the following reasons :
1)by constrictiong blood vessels , vasoconstrictors decrease the blood
flow to the site of injection
2)absorption of LA in to cardiovascular system is slowed , thus
decreseing the level of LA in blood
3)lower LA in blood decreases the risk of LA toxicity
4)prolong the duration of LA
5)decrease bleeding at the site of administration and are useful when
bleeding is anticipated

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Vasoconstrictors used are : 1) epinephrine and 2) fleypressin
The main difference between the 2 is that epinephrine works on
arterial blood vessels while flypressin works with V1 receptors in
smooth muscles
Epinephrine is most commonly used ,and usually used with lidocaine
It comes in 1:50,000 or 1:80,000,or 1:100,000
Flypressin if used it will be with prilocaine (its contraindicated in
pregnant ladies because it induces uterine contraction)
Average duration of local anesthetic without the use of
vasoconstrictor :
2% lidocaine : 5-10mins
3%mepivcaine: 20-40 mins
4%prilocaine:5-15mins (infiltration)
Upto 60 mins (block)

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3)preservative of vasoconstrictor : ( oxidizing agent)
The antioxidant most frequently used is sodium metabisulphate . it
prevents the biodegradation of the vasoconstrictor by oxygen.which
maight be present in the cartridge during manufacture or which can
be diffused through the semi permeable diaphragm
4)sodiumchloride:
Is added to make the solution isotonic with the tissue in of the body.
In the past isolated cases have been reported in which LA solutions
containing too much sodium chloride (hypertonic solution) produced
tissue edema or paresthesia sometimes persisting months
5)Distilled water: used as the diluent to provide the volume of
solution of cartridge
6)general preservative :
Methylparaben is a bacteriostatic agent .it has been removed in the
united states in 1984 because of its allergic reactions it causes .
7)fungicide : thymol.

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Local Complications of local anesthesia:
1)needle breakage:
Causes: a) smaller needles (i.e 30 Gauge) are more likely to break than
larger needles (25-gauge)
b)needles that have been previously bent are weakend and
more likely to break
c)needles may prove to be defective in manufacture
2)pain on injection:
Causes: 1)careless injection technique
2)needle can become dull after multiple injections
3)rapid deposition of the anesthetic soloution may cause
tissue damage
3)burning sensation:
Causes : 1) mainly is the PH of the soloution the lower the PH the
more burning sensation
2)Rapid injection of LA
3)contamination of LA cartridges (when stored in alcohol or
other sterilizing solutions )
4)solution is warm

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4)persistant anesthesia
Causes: 1) trauma to nerve during injection
2) hemorrhage into or around the neural sheath is another
cause .
5)Trismus
Causes: trauma to muscle or blood vessel in the infratemporal fossa is
the most common cause
, 6)hematoma
Causes: a rather large hematoma may result from either arterial or
venous puncture following posterior superior alveolar nerve or
inferior alveolar nerve block. The tissues surrounding these vessles
more readily accommodate significant volume of blood. The blood
effuses from vessles until extravascular exceeds intravascular
pressure or clotting occurs. Hematoma following inferior alveolar
nerve is usually intraoral, while superior alveolar nerve is extraoral.
7)infection
8)edema: swelling of tissues is not a syndrome it’s a sign
Causes: -trauma during injection
-infection
-allergy , -hemorrhage

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9)soft tissue injury:self inflicted trauma to the lips or tongue is
frequently caused by th patient inadvertently biting or chewing these
tissues while still anesthetized
-frequently occurs with mentally or physically disabled children
The primary cause is that soft tissue anesthesia lasts significantly
longer than pulpal anesthesia .the pt will be dismissed with his lips
still numb
10)facial nerve paralysis: transient facial paralysis is commonly caused
by the introduction of the local anesthetic into the capsule of the
parotid gland ,which is located at the posterior border of the
mandibular ramus clothed by the medial pterygoid ,and masster
muscle .
Systemic complications of local anesthesia:
Complications OF LA:
Systemic Complications
• Toxicity.
• Syncope.
• Allergic Reaction.
• Vasoconstrictors effects.

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Calculation of dose local anesthesia :
The maximum dose for lidocaine is 4.4 mg /kg of body weight with
vasoconstrictor
The anesthetic carpule conatins 2% lidocaine which = 20mg/ml
And the volume of one carpule is 1.8 ml or 2.2 ml (in some books)
So the amount of LA in one carpule is : 20 *1.8= 36mg per carpule .
Example 1 :
20kg child can tolerate maximum dose of 1.8ml of 2% lidocaine with
vasoconstrictor is ?
Maximum dose of lidocaine is 4.4 mg per kg
So the maximum dose for this pt is 20*4.4=88mg
So how many carpules ? if one carpule contains 36mg (as calculated
above ) then this child needs: 88mg/36mg= 2.4 carpule = 2 carpules
maximum

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Example 2 :
A70kg man can tolerate maximum dose of 2.2 ml of 2% lidocaine with
vasoconstrictor is:
Maximum dose is 4.4 mg per kg
So the maximum dose for this pt is 70kg *4.4= 308 mg
So how many carpules can this pt take ?
1 carpule = 2.2ml * 20ml(because its 2% lidocaine) = 44mg
And the maximum dose for this pt is 308mg so =
308/44= 7 carpules
Failure to obtain anesthesia:
1.poor technique and inadequate volume of anesthesia
2.injection into muscle
3.injection into infected area
4.intravascular injection
5.dense compact bone