LOCAL ANESTHESIA

DR.PRIYANKA SHARMA

II YEAR MDS

PUBLIC HEALTH DENTISTRY

JSSDCH

CONTENTS Introduction Historical background Definition Methods of inducing local anesthesia Desirable properties Electrophysiology of nerve conduction Impulse propagation and spread Theories of mechanism of action of local

anesthesia Dissociation of local anesthesia

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Classification of local anesthetic according to biological site and mode of action

Mode and site of action of local anesthesia

Mechanism of action of local anesthesia

Local anesthetics descriptionArmamentariumInjection techniquesLocal & Systemic complications Special care groupsRecent advancementsConclusionReferences

Historical background

• COCAINE -first local anesthetic agent-isolated

by Nieman -1860 -from the leaves of the coca

tree.

• Its anesthetic action was demonstrated by Karl

Koller in 1884.

• First effective and widely used synthetic local

anesthetic -PROCAINE -produced by Einhorn in

1905 from benzoic acid and diethyl amino

ethanol.

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• It anesthetic properties were identified by Biberfield

and the agent was introduced into clinical practice by

Braun.

• LIDOCAINE- Lofgren in 1948.

• The discovery of its anesthetic properties was

followed in 1949 by its clinical use by T. Gordh

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DEFINITION:

Local anesthesia is defined as a loss of sensation in a

circumscribed area of the body caused by depression

of excitation in nerve endings or an inhibition of the

conduction process in peripheral nerves.

An important feature of local anesthesia is that it

produces:

LOSS OF SENSATION WITHOUT

INDUCING LOSS OF CONSCIOUSNESS..

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METHODS OF INDUCING LOCAL

ANESTHESIA:

Low temperature

Mechanical trauma

Anoxia

Neurolytic agents such as alcohol & phenol

Chemical agents such as local anesthetics

PROPERTIES OF LOCAL ANESTHESIA

I==It should not be irritating to tissue to which it is applied

N==It should not cause any permanent alteration of nerve structure

S==Its systemic toxicity should be low

T==Time of onset of anesthesia should be short

E== It should be effective regardless of whether it is injected into the tissue or applied locally to mucous membranes

D==The duration of action should be long enough to permit the completion of procedure

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It should have the potency sufficient to give

complete anesthesia with out the use of harmful

concentration solutions

It should be free from producing allergic

reactions

It should be free in solution and relatively

undergo biotransformation in the body

It should be either sterile or be capable of being

sterilized by heat with out deterioration.

ELETROPHYSIOLOGY OF NERVE CONDUCTION

• There is an electrical charge across the membrane.

• This is the membrane potential.

• The resting potential (when the cell is not firing)

is a negative electrical potential of -70mv that

exists across the nerve membrane, produced by

different concentrations of either side of the

membrane.

• The interior of nerve is NEGATIVE in relation to

exterior. 10

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inside

outside

Resting potential of neuron = -70mV+

-

+

-

+

-

+

-

+

-

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Action Potentials

• At rest: Na+& K+ channels closed. -70mV• Fibre stimulated: Na+channel opens, Na+ enters

cell. Potential rising• Cell depolarised, Na+ channel closes. +20mV• K+ channel opens, K+ exits cell, potential falling• Fibre repolarised, Na+& K+ channels closed.

Na/K pump restores balance. -70mV• Result is a voltage gradient along axon, causing

a current. This causes configurational change in Na-channels in the next segmentconduction

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SLOW DEPOLARIRIZATION

RAPID DEPOLARIZATION:

The interior of nerve is POSITIVE in relation to exterior.

REPOLARIZATION:

.

• Depolarization takes 0.3 msec

• Repolarization takes 0.7 msec

SODIUM PUMPenergy comes from the oxidative

metabolism of ATP

• The entire process require 1 msec15

IMPULSE PROPOGATION

IMPULSE SPREAD

The propagated impulse travels along the nerve membrane towards CNS. The spread of impulse differs in myelinated and unmyelinated nerve fibers.

UNMYELINATED NERVES: The high resistance cell membrane and extra cellular media produce a rapid decrease in density of current with in a short distance of depolarized segment.

The spread of the impulse is characterized as a slow forward-creeping process.

Conduction rate is 1.2m/sec

DEPOLARIZED SEGMENT ADJACENT RESTING AREA

MYLINATED NERVES:

Impulse conduction in myelinated nerves occurs by means of current leaps from nodes to node this process is called as SALTATORY CONDUCTION.

It is more rapid in thicker nerves because of increase in thickness of myelin sheath and increase in distance between adjacent nodes of ranvier.

If conduction of impulse is blocked at one node the local current will skip over that node and prove adequate to raise that membrane potential at next node to its firing potential and produce depolarization.

Conduction rate of myelinated fibers is 120m/sec.

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MODE AND SITE OF ACTION OF LOCAL ANESTHETICS

Local anesthetic agent interferes with excitation process in a nerve membrane in one of the following ways:

Altering the basic resting potential of nerve membrane

Altering the threshold potential Decreasing the rate of depolarizationProlonging the rate of repolarization

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THEORIES MECHANISM OF ACTION OF LOCAL

ANESTHETICSMany theories have been promulgated over

the years to explain the mechanism of action of local anesthetics.

ACETYLECHOLINE THEORY: Stated that acetylcholine was involved in nerve conduction in addition to its role as a neurotransmitter at nerve synapses. There is no evidence that acetylcholine is involved in neural transmission.

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CALCIUM DISPLACEMENT THEORY:

States that local anesthetic nerve block was produced by displacement of calcium from some membrane site that controlled permeability of sodium.

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SURFACE CHARGE (REPULSION) THEORY:

Proposed that local anesthetic acted by binding to nerve

membrane and changing the electrical potential at

the membrane surface. Cationic drug molecule were

aligned at the membrane water interface, and since

some of the local anesthetic molecule carried a net

positive charge, they made the electrical potential at

the membrane surface more positive, thus

decreasing the excitability of nerve by increasing

the threshold potential. Current evidence indicate

that resting potential of nerve membrane is unaltered

by local anesthetic.22

MEMBRANE EXPANSION THEORY

• It states that local anesthetic molecule diffuse to

hydrophobic regions of excitable membranes,

producing a general disturbance of bulk membrane

structure, expanding membrane, and thus preventing

an increase in permeability to sodium ions. Lipid

soluble LA can easily penetrate the lipid portion of

cell membrane changing the configuration of

lipoprotein matrix of nerve membrane. This results

in decreased diameter of sodium channel, which

leads to inhibition of sodium conduction and neural

excitation.23

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MEMBRANE EXPANSION THEORY

SPECIFIC RECEPTOR THEORY:

The most favored today, proposed that local anesthetics

act by binding to specific receptors on sodium

channel the action of the drug is direct, not mediated

by some change in general properties of cell

membrane. Biochemical and electrophysiological

studies have indicated that specific receptor sites for

local anesthetic agents exists in sodium channel

either on its external surface or on internal

axoplasmic surface. Once the LA has gained access

to receptors, permeability to sodium ion is decreased

or eliminated and nerve conduction is interrupted.25

CLASSIFICATION OF LOCAL ANESTHETIC SUBSTANCES

ACCORDING TO BIOLOGICAL SITE AND MODE OF ACTION

CLASS A: Agents acting at receptor site on external surface of nerve membrane

Chemical substance: Biotoxins (e.g., tetrodotoxin and saxitoxin)

CLASS B: Agents acting on receptor sites on internal surface of nerve membrane

Chemical substance: Quaternary ammonium analogues of lidocaine, scorpion venom

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CLASS C: Agents acting by receptor independent of physiochemical mechanism

Chemical substance: Benzocaine

CLASS D: Agents acting by combination of receptors and receptor independent mechanisms

Chemical substance: most clinically useful anesthetic agents (e.g., lidocaine, mepivacaine, prilocaine)

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BASED ON THE SOURCE• NATUAL• SYNTHETIC• OTHERS

BASED ON MODE OF APPLICATION• INJECTABLE• TOPICAL

• BASED ON DURATION OF ACTION

• ULTRA SHORT• SHORT• MEDIEM• LONG

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BASED ON ONSET OF ACTION• SHORT• INTERMEDIATE• LONG

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DISSOCIATION OF LOCAL ANESTHETICS

• Local anesthetics are available as salts (usually hydrochlorides) for clinical use.

• The salts, both water soluble and stable, is dissolved in either sterile water or saline.

• In this solution it exists simultaneously as unchanged molecule (RN), also called base and positively charged molecules (RNH+) called cations.

RNH+ ==== RN+ H+

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• The relative concentration of each ionic form in the solution varies in the pH of the solution or surrounding tissue.

• In the presence of high concentration of hydrogen ion (low pH) the equilibrium shifts to left and most of the anesthetic solution exists in cationic form.

RNH+ > RN+ + H+

• As hydrogen ion concentration decreases (higher pH) the equilibrium shifts towards the free base form.

RNH+ < RN + H+

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• The relative proportion of ionic form also depends on pKa or DISSOCIATION CONSTANT, of the specific local anesthetic.

• The pKa is a measure of molecules affinity for H+

ions.• When the pH of the solution has the same value as

pKa of the local anesthetic, exactly half the drug will exists in the RNH+ form and exactly half in RN form.

• The percentage of drug existing in either form can be determined by Henderson Hasselbalch equation

Log base/acid = pH - pKa

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• Henderson hasselbach equation Determines how much of a local anesthetic will be in a non-ionized vs ionized form . Based on tissue pH and anesthetic Pka .

• Injectable local anesthetics are weak bases (pka=7.5-9.5) When a local anesthetic is injected into tissue it is neutralized and part of the ionized form is converted to non-ionized The non-ionized base is what diffuses into the nerve.

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• Hence if the tissue is infected, the pH is lower (more acidic) and according to the HH equation; there will be less of the non-ionized form of the drug to cross into the nerve (rendering the LA less effective)

• Once some of the drug does cross; the pH in the nerve will be normal and therefore the LA re-equilibrates to both the ionized and nonionized forms; but there are fewer cations which may cause incomplete anesthesia.

MECHANISM OF ACTION OF LOCAL ANESTHETICS

The following sequence is proposed mechanism of action of LA:

Displacement of calcium ions from the sodium channel receptor site

Binding of local anesthetic molecule to this receptor site

Blockade of sodium channel

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Decrease in sodium conductance

Depression of rate of electrical depolarization

Failure to achieve the threshold potential level

Lack of development of propagated action potential

Conduction blockade…36

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Na +Na +

LOCAL ANESTHETIC

AGENT

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COMERCIALLY PREPARED LOCAL ANESTHESIA CONSISTS OF:

Local anesthetic agent (xylocaine, lignocaine 2%)

Vasoconstrictor (adrenaline 1: 80,000)

Reducing agent (sodium metabisulphite)

Preservative (methylparaben,capryl hydrocuprienotoxin)

Fungicide (thymol)Vehicle (distillde water,NaCl)

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REDUCING AGENT

• Vasoconstrictors are unstable in solution and

may oxidize especially on prolong exposure to

sunlight this results in turning of the solution

brown and this discoloration is an indication that

such a solution must be discarded.

• To overcome this problem a small quantity of

sodium metabisulphite is added - competes for

the available oxygen.

• SHELF LIFE INCRESES

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PRESERVATIVE

• Modern local anesthetic solution are very stable

and often have a shelf of two years or more.

Their sterility is maintained by the inclusion of

small amount of a preservative such as capryl

hydrocuprienotoxin.

• Some preservative such as methylparaben have

been shown to allergic reaction in sensitized

subjects.

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FUNGICIDE

• In the past some solutions tended to become cloudy due to the proliferation of minute fungi.

• In several modern solutions a small quantity of

thymol is added to serve as fungicide and prevent this occurrence.

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VEHICLE

• The anesthetic agent and the additives referred to

above are dissolved in distilled water & sodium

chloride.

• This isotonic solution minimizes discomfort

during injection.

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. The chemical characteristics are so balanced that they have both lipophilic and hydrophilic properties.

If hydrophilic group predominates, the ability to diffuse into lipid rich nerves is diminished. If the molecule is too lipophilic it is of little clinical value as an injectable anesthetic, since it is insoluble in water and unable to diffuse through interstitial tissue.

LOCAL ANESTHETIC AGENT

The local anesthetics used in dentistry are divided into two groups:

ESTER GROUP

AMIDE GROUP

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ESTER GROUP:It is composed of the followingAn aromatic lipophilic groupAn intermediate chain containing an ester linkageA hydrophilic secondary or tertiary amino group

AMIDE GROUP:It is composed of the followingAn aromatic, lipophilic groupAn intermediate chain containing amide linkageA hydrophilic secondary or tertiary amino group

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CLASSIFICATION OF LOCAL ANESTHETICS

ESTERS

Esters of benzoic acidButacaine

Cocaine

Benzocaine

Hexylcaine

Piperocaine

Tetracaine

Esters of Para-amino benzoic acid

Chloroprocain

Procaine

Propoxycaine

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AMIDES

Articaine

Bupivacaine

Dibucaine

Etidocaine

Lidocaine

Mepivacaine

Prilocaine

Ropivacaine

QUINOLINE

Centbucridine

ABCDE LMPR

PHARMACOKINETICS OF LOCAL ANESTHETICS

UPTAKE: When injected into soft tissue most local anesthetics

produce dilation of vascular bed.

Cocaine is the only local anesthetic that produces

vasoconstriction, initially it produces vasodilation

which is followed by prolonged vasoconstriction.

Vasodilation is due to increase in the rate of

absorption of the local anesthetic into the blood, thus

decreasing the duration of pain control while

increasing the anesthetic blood level and potential for

over dose.50

ORAL ROUTE:

Except cocaine, local anesthetics are poorly absorbed

from GIT

Most local anesthetics undergo hepatic first-pass effect

following oral administration.

72% of dose is biotransformed into inactive

metabolites

TOCAINIDE HYDROCHLORIDE an analogue of

lidocaine is effective orally

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TOPICAL ROUTE:

Local anesthetics are absorbed at different rates after

application to mucous membranes, in the tracheal

mucosa uptake is as rapid as with intravenous

administration.

In pharyngeal mucosa uptake is slow

In bladder mucosa uptake is even slower

Eutectic mixture of local anesthesia (EMLA) has been

developed to provide surface anesthesia for intact

skin.52

INJECTION:

The rate of uptake of local anesthetics after injection is related to both the vascularity of the injection site and the vasoactivity of the drug.

IV administration of local anesthetics provide the most rapid elevation of blood levels and is used for primary treatment of ventricular dysrhythmias.

RATES AT WHICH LOCAL ANESTHETICS ARE ABSORBED AND REACH THEIR PEAK BLOOD LEVEL

ROUTE TIME TO PEAK LEVEL (MIN)

INTRAVENOUS 1TOPICAL 5

INTRAMUSCULAR 5-10

SUBCUTANEOUS 30 - 90

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DISTRIBUTION

Once absorbed in the blood stream local anesthetics

are distributed through out the body to all tissues.

Highly perfused organs such as brain, head, liver,

kidney, lungs have higher blood levels of anesthetic

than do less higher perfused organs.

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The blood level is influenced by the following

factors:

Rate of absorption into the blood stream.

Rate of distribution of the agent from the

vascular compartment to the tissues.

Elimination of drug through metabolic and/or

excretory pathways.

All local anesthetic agents readily cross the

blood-brain barrier, they also readily cross the

placenta.

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METABOLISM

(BIOTRANSFORMATION)ESTER LOCAL ANESTHETICS:• Ester local anesthetics are hydrolyzed in

the plasma by the enzyme pseudocholinesterase.

• Chloroprocaine the most rapidly hydrolyzed, is the least toxic.

• Tertracaine hydrolyzed 16 times more slowly than Chloroprocaine ,hence it has the greatest potential toxicity.

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AMIDE LOCAL ANESTHETICS

The metabolism of amide local anesthetics is more

complicated then esters. The primary site of

biotransformation of amide drugs is liver.

Entire metabolic process occurs in the liver for

lidocaine, articaine, etidocaine, and bupivacaine.

Prilocaine undergoes more rapid biotransformation

then the other amides.

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EXCREATIONKidneys are the primary excretory organs for both the

local anesthetic and its metabolites

A percentage of given dose of local anesthetic drug is

excreted unchanged in the urine.

Esters appear in only very small concentration as the

parent compound in urine.

Procaine appears in the urine as PABA (90%) and 2%

unchanged.

10% of cocaine dose is found in the urine unchanged.

Amides are present in the urine as a parent compound

in a greater percentage then are esters.

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MRD

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VASOCONSTRICTORS• Constrict vessels and decrease blood

flow to the site of injection. • Absorption of LA into bloodstream

is slowed, producing lower levels in the blood.

• Lower blood levels lead to decreased risk of overdose (toxic) reaction.

• Higher LA concentration remains around the nerve increasing the LA's duration of action.

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• Minimize bleeding at the site of administration.

• Naturally Occurring Vasoconstrictors:- Epinephrine - Norepinephrine• Vasoconstrictors should be included

unless contraindicated.• Mode of Action - Attach to and directly

stimulate adrenergic receptors . Act indirectly by provoking the release of endogenous catecholamine from intraneuronal storage sites.

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• Concentrations of Vasoconstrictor in Local Anesthetics - 1:50,000 ,1:100,000, 1:200,000 - 0.020mg/ml ,0.010mg/ml, 0.005 mg/ml

• Calculation 1:50,000= 1gram/50,000ml= 1000mg/50,000ml= 1mg/50ml= 0.02mg/ml

• Levonordefrin - One fifth as active as epinephrine

• Vasoconstrictors - Unstable in Solution Sodium metabisulfite added Known allergen

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• Max dose of vasoconstrictors - Healthy patient approximately

0.2mg- Patient with significant

cardiovascular history: 0.04mg • Max Dose for Vasoconstrictors (CV

patient) 1 carpule = 1.8cc 1:100,000=.01mg/cc

0.01 X 1.8cc= 0.018mg 0.04/0.018=2.22 carpules

• In a healthy adult patient 0.2/0.018=11.1 carpules

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Local Anesthesia Armanterium

1.) The Syringe

2.) The Needle

3.) The Cartridge

4.) Other Armamentarium - Topical Anesthetic (strongly

recommended) -ointments, gels, pastes, sprays

- Applicator sticks- Cotton gauze

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TYPES OF SYRINGES

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Plastic disposable syringe

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Syringe Components

1.) Needle adapter

2.) Piston with harpoon

3.) Syringe barrel

4.) Finger grip

5.) Thumb ring

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• American Dental Association (ADA) criteria

for acceptance of LA syringes:

1-Durable and re-sterilzable or packaged in a

sterile container (if disposable).

2-Accept a wide variety of cartridges and needles

of different manufactures (universal use)

3-Inexpensive, light weight, and simple to use with

one hand.

4-Provide effective aspiration and the blood be

easily observed in the cartridge. The incidence of

positive aspiration may be as high as 10%-15%

in some injection techniques.

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Needle

• The Needle Gauge: the larger the gauge the smaller the internal diameter of the needle Usual dental needle gauges are 25,27, & 30 Length:

1-Long(approximately 40 mm "32-40 mm"), for NB.

2-Short(20-25 mm).

3-Extra-short(approximately 15 mm), for PDL.

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Components of needle

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Cartridge

• The Cartridge Components:

- Cylinder, plunger, diaphragm

- Types: Standard – Self aspirating, plastic, Glass

- Contents: LA, VC, Vehicle, preservative.

- Volume: 1.8, 2.00 & 2.2 ML.

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• The Cartridge:

- Should not be autoclaved Stored at

room temperature (21°C to 22°C

(70°F to 72°F)

- Should not soak in alcohol

- Should not be exposed to direct

sunlight

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INJECTION TECHNIQUES

• MAXILLARY :

1) Supraperiosteal

2) PDL

3) Intraseptal Injection

4) Intracrestal Injection

5) Intraosseous Injection

6) PSA Nerve Block

7) MSA Nerve Block

8) ASA Nerve Block

9) Maxillary Nerve Block

10) Greater Palatine Nerve Block

11) Nasopalatine Nerve Block

12) AMSA Nerve Block

13) P-ASA Nerve Block

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Supraperiosteal injection

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Posterior superior alveolar nerve block

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Anterior superior alveolar nerve block

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Palatal Anasthesia• Greater palatine

nerve block• Nasopalatine

nerve block

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• MANDIBULAR INJECTION TECHNIQUES:

1) IANB Nerve block

2) Buccal Nerve Block

3) Mandibular nerve block techniques:

- Gow Gates technique- Vazirani Akinosi closed mouth

mandibular block

4) Mental Nerve block

5) Incisive nerve block

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Inferior alveolar nerve block

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Buccal nerve block

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Gow gates technique

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Vazirani-Akinosi technique

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Mental nerve block

INCISIVE NERVE BLOCK

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Local Complications

1) Needle breakage :

Prevention• Do not use short needles for inferior alveolar

nerve block in adults or larger children.• Do not use 30-gauge needles for inferior

alveolar nerve block in adults or children.• Do not bend needles when inserting them into

soft tissue.• Do not insert a needle into soft tissue to its hub,

unless it is absolutely essential for the success of the injection.

• Observe extra caution when inserting needles in younger children or in extremely phobic adult or child patients.

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2) Prolonged Anesthesia or Paresthesia• Strict adherence to injection protocol• Most paresthesias resolve within approximately

8 weeks to 2 months without treatment.• Determine the degree and extent of paresthesia.• Explain to the patient that paresthesia• Record all findings • Second opinion• Examination every 2 months• It would be prudent to contact your liability

insurance carrier should the paresthesia persist without evident improvement beyond 1 to 2 months.

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3) Facial Nerve palsy• Reassure the patient• Contact lenses should be removed until

muscular movement returns.• An eye patch should be applied to the

affected eye until muscle tone returns• Record the incident on the patient's chart.• Although no contraindication is known to

reanesthetizing the patient to achieve mandibular anesthesia, it may be prudent to forego further dental care at this appointment.

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4) Trismus• Prescribe heat therapy, warm saline

rinses, analgesics (Aspirin 325 mg)• If necessary, muscle relaxants to manage

the initial phase of muscle spasm - Diazepam (approximately 10 mg bid)

• Initiate physiotherapy• Antibiotics should be added to the

treatment regimen described and continued for 7 full days

• Patients report improvement within 48 to 72 hours

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5) Soft tissues injury• Analgesics, antibiotics, lukewarn

saline rinse, petroleum jelly• Cotton roll placed between lips and

teeth, secured with dental floss, minimizes risk of accidental mechanical trauma to anesthetized tissues.

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6) Hematoma :• Hematoma is not always preventable. Whenever

a needle is inserted into tissue, the risk of inadvertent puncturing of a blood vessel is present.

• When swelling becomes evident during or immediately after a local anesthetic injection, direct pressure should be applied to the site of bleeding.

• For most injections, the blood vessel is located between the surface of the mucous membrane and the bone; localized pressure should be applied for not less than 2 minutes. This effectively stops the bleeding.

• Ice may be applied to the region immediately on recognition of a developing hematoma.

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7) Pain on injection• Adhere to proper techniques of injection,

both anatomic and psychological.• Use sharp needles.• Use topical anesthetic properly before

injection.• Use sterile local anesthetic solutions.• Inject local anesthetics slowly.• Make certain that the temperature of the

solution is correct• Buffered local anesthetics, at a pH of

approximately 7.4, have been demonstrated to be more comfortable on administration

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8) Burning on Injection• By buffering the local anesthetic solution

to a pH of approximately 7.4 immediately before injection, it is possible to eliminate the burning sensation that some patients experience during injection of a local anesthetic solution containing a vasopressor.

• Slowing the speed of injection also helps

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9) Infection :• Use sterile disposable needles.• Properly care for and handle

needles.• Properly prepare the tissues before

penetration.• Prescribe 29 (or 41, if 10 days)

tablets of penicillin V (250-mg tablets).

• Erythromycin may be substituted if the patient is allergic to penicillin.

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10) Edema

If edema occurs in any area where it compromises breathing, treatment consists of the following:

• P (position): if unconscious, the patient is placed supine.• A-B-C (airway, breathing, circulation): basic life support is administered,

as needed.• D (definitive treatment): emergency medical services (e.g., 9-1-1) is

summoned.• Epinephrine is administered: 0.3 mg (0.3 mL of a 1:1000 epinephrine

solution) (adult), 0.15 mg (0.15 mL of a 1:1000 epinephrine solution) (child [15 to 30 kg]), intramuscularly (IM) or 3 mL of a 1:10,000 epinephrine solution intravenously (IV-adult), every 5 minutes until respiratory distress resolves.

• Histamine blocker is administered IM or IV.• Corticosteroid is administered IM or IV.• Preparation is made for cricothyrotomy if total airway obstruction

appears to be developing. This is• extremely rare but is the reason for summoning emergency medical

services early.• The patient's condition is thoroughly evaluated before his or her next

appointment to determine the cause of the reaction.

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10) Sloughing of tissue• Usually, no formal management is

necessary for epithelial desquamation or sterile abscess. Be certain to reassure the patient of this fact.

• For pain, analgesics such as aspirin or other NSAIDs and a topically applied ointment (Orabase)

• The course of a sterile abscess may run 7 to 10 days

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11) Postanesthetic Intra-oral lesion:• Primary management is symptomatic• No management is necessary if the pain is not

severe• Topical anesthetic solutions (e.g., viscous

lidocaine)• A mixture of equal amounts of diphenhydramine

(Benadryl) and milk of magnesia rinsed in the mouth effectively coats the ulcerations and provides relief from pain.

• Orabase, a protective paste, without Kenalog can provide a degree of pain relief.

• A tannic acid preparation (Zilactin) can be applied topically to the lesions extraorally or intraorally (dry the tissues first).

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Systemic complications

Adverse drug reaction• Toxicity Caused by Direct Extension of the Usual

Pharmacologic Effects of the Drug:

1) Side effects

2) Overdose reactions

3) Local toxic effects• Toxicity Caused by Alteration in the Recipient of the

Drug:

1) A disease process (hepatic dysfunction, heart failure, renal dysfunction)

2) Emotional disturbances

3) Genetic aberrations (atypical plasma cholinesterase, malignant hyperthermia)

4) Idiosyncrasy• Toxicity Caused by Allergic Responses to the Drug

CLINICAL MANIFESTATION OF LOCAL ANESTHETIC OVERDOSE

SIGNS:LOW TO MODERATE OVERDOSE LEVELS: Confusion Talkativeness Apprehension Excitedness Slurred speech Generalized stutter Muscular twitching, tremor of face and extremities Elevated BP, heart rate and respiratory rate

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MODERATE TO HIGH BLOOD LEVELS: Generalized tonic clonic seizure, followed by Generalized CNS depression Depressed BP, heart rate and respiratory rate

SYMPTOMS: Headache Light headedness Auditory distrurbances Dizziness Blurred vision Numbness of tongue and perioral tissues Loss of consciousness

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Management of systemic complications

1) Basic emergency management : A-B-C-D approach

2) Allergy : Medical history questionnaire is important.

3) Elective dental care

4) Emergency dental care:- Protocol no.1 : no treatment of an invasive

nature- Protocol no.2 : use general anesthesia- Protocol no.3: Histamine blockers- Protocol no.4 : Electronic dental

anesthesia/hypnosis

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LA Management For Special Patients

• Uncooperative childThe maximum safe dose of

lidocaine for a child is 4.5 mg/kg per dental appointment.

Local infiltration of anesthesia is sufficient for all dental treatment procedures in 90% of cases even in the mandible.

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• Handicapped Patient• retarded patientschoose a shorter needle

and/or a larger gauge needle which is less likely to be bent or broken.

better to use general anesthesia

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• Patients receiving anticoagulation or suffering from bleeding disorders

Oral procedures must be done at the beginning of the day & must be performed early in the week, allowing delayed re-bleeding episodes, usually occurring after 24-48 h, to be dealt with during the working weekdays.

Local anesthetic containing a vasoconstrictor should be administered by infiltration or by intraligamentary injection wherever practical.

X Regional nerve blocks should be avoided when possible.

Local vasoconstriction may be encouraged by infiltrating a small amount of local anesthetic containing adrenaline (epinephrine) close to the site of surgery.

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PREGNANCY

• Lidocaine + vasoconstrictor: most common local anesthetic used in dentistry extensively used in pregnancy with no proven ill effects, Esters are better to be used.

• Accidental intravascular injections of lidocaine pass through the placenta but the concentrations are too low to harm fetus.

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GERIATRIC PATIENT

– When choosing an anesthetic, we are largely concerned with the effect of the anesthetic agent upon the patient's cardiovascular and respiratory systems.

– increased tissue sensitivity to drugs acting on the CNS

– Decreased hepatic size and blood flow may reduce hepatic metabolism of drugs

– hypertension is common and can reduce renal function

– Same prevention procedures used with children

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LIVER DISORDERS– Advanced liver diseases include:Liver cirrhosis - Jaundice

- Potential complications:

1 . Impaired drug detoxication e.g. sedative, analgesics, general anesthesia.

2. Bleeding disorders ( decrease clotting factors, excess fibrinolysis, impaired vitamin K absorption).

3. Transmission of viral hepatitis.

Management– Avoid LA metabolized in liver: Amides

(Lidocaine, Mepicaine), esters should be used

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DRUG-DRUG INTERACTION

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RECENT ADVANCEMENTS

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Recent developments in local anesthesia and oral sedation.

2003 Journal of anesthesia• Yagiela JA.

Abstract• This article reviews 3 recent developments in anxiety and

pain control with significant potential for altering dental practice. First is the introduction of articaine hydrochloride as an injectable local anesthetic. Although articaine is an amide, its unique structure allows the drug to be quickly metabolized, reducing toxicity associated with repeated injections over time. The second development is the formulation of a lidocaine and prilocaine dental gel for topical anesthesia of the periodontal pocket. This product may significantly reduce the need for anesthetic injections during scaling and root planing. Finally, the use of triazolam as an oral sedative/anxiolytic is reviewed. The recent administration of triazolam in multiple doses has extended the availability of anxiety control to many dental patients, but unknowns about the safety of the technique as practiced by some dentists remains a concern.

Eutectic mixture of local anesthesia (EMLA)

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surface anesthesia for intact skin.

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• DentiPatch (lidocaine transoral delivery system) Preinjection – 10-15 minutes exposure prior to injection - Root scaling/planing – apply 5-10 minutes prior to beginning procedure.

• PRESSURE SYRINGE :Used in IL injection techniques,

especially in mandibular teeth (types: pistol-grip, pen-grip).

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CONCLUSION• Please Remember !!! - Principle 1- No drug ever exerts a

single action - Principle 2- No clinically useful

drug is entirely devoid of toxicity - Principle 3- The potential toxicity of

a drug rests in the hands of the user

References

• Handbook of local anesthesia – Stanley F Malamed – 6th edition

• Essentials of Local Anesthetic Pharmacology : Daniel E Becker : Anesth Prog. 2006 Fall; 53(3): 98–109.

• Vasoconstrictors in local anesthesia for dentistry: A. L. Sisk; Anesth Prog. 1992; 39(6): 187–193.

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• Local anesthetic failure associated with inflammation: verification of the acidosis mechanism and the hypothetic participation of inflammatory peroxynitrite : Takahiro Ueno et al ; Journal of Inflammation Research; November 2008 Volume 2008:1 Pages 41 - 48

• Advanced techniques and armamentarium for dental local anesthesia; Clark TM; Dent Clin North Am. 2010 Oct;54(4):757-68 119

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• Advances in dental local anesthesia techniques and devices: An update ; Payal Saxena et al: National Journal of Maxillofacial Surgery | Vol 4 | Issue 1 | Jan-Jun 2013.

THANK YOU!

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