Pharmacology of local anesthetics

Why are local anesthetics different??

Local anesthetic, when used for the management of pain, differs from other drugs used in dentistry in one important regard i.e. almost all other drugs reach blood stream & exert their effect, while the action of local anesthetics ceases when these enter the blood stream.

Uptake of local anesthetic..

When injected into soft tissue, L.A. exerts action on blood vessels of the area.

Mostly producing vasodilatation, only some can produce vasoconstriction.. E.g.

Cocaine.

Procaine is probably the most potent vasodilator, this property is used clinically in accidental i.a. injection of thiopental.

Vasodilatation increases the rate of absorption of L.A into blood.

Decrease in duration & quality of pain control.

Rotes of administration..

1. ORAL…. All L.A. Except cocaine are poorly

absorbed from G.I.T. These undergo significant hepatic first

pass. e.g lidocaine. Approx 72% of the absorbed dose is converted to inactive metabolites..thereby hampering its use as oral antidysarhythmic.

Tocainide hydrochloride, analogue of lidocaine is used.

2. Topical.…Different rates of absorption for

different mucosaTracheal mucosa- as rapid as i.vPharyngeal mucosa- slowEsophageal mucosa- slower then

pharyngeal.Eg. Solarcaine, E.M.L.A – provides

anesthetic action to intact skin.

3. Injection….Intravenous.. Clinically used in primary management of ventricular dysrhythmias. Eg. Premature ventricular contractions.but these may cause toxic reactions as well.

Distribution…

From blood, L.A is distributed to body tissues.Highly perfused organs are:-BrainLiver KidneysLungsSpleen Skeletal muscle, although not highly

perfused has higher distribution due to larger surface area.

Blood levels of l.A depend on…

rate of absorption into C.V.S. rate of distribution to tissues rate of elimination.Elimination half life of some L.A agents:-• Procaine -0.1 hrs• Lidocaine-1.6 hrs• Bupivacaine-3.5 hrsAll L.A readily cross B.B.B & placenta.

Metabolism/biotransformation…

There are two types of local anesthetic

esters amideswith different types of

metabolism..

esters

Hydrolyzed in plasma by enzyme pseudocholinesterase.

Rate of hydrolysis is different for different compounds.

e.g. chlorprocaine is most rapidly hydrolysed while tetracaine is hydrolysed 16 times slowly.

PABA is the metabolic product causing most of the allergic reactions.

Approx. 1 in 2800 people have atypical form of pseudocholinesterase

Inability to hydrolysed LA & other chemically related drugs.

atypical form of pseudocholinesterase is hereditary trait so family history is important.

amides

Biotransformation products

Significant in cases of renal & cardiac failure.e.g. orthotoluidine, a metabolite of prilocaine , may cause clinically significant methemoglobinemia.Also, metabolites of lidocaine i.e. monoethylglycinexylidide &glycine xylidide may produce sedation.

excretion

Kidneys are primary excretory organs.A small dose may appear unchanged in urine.Esters are usually present as metabolites while amides as parent compounds.

Patients with severe renal impairment pose a potential of toxicity

Relative contraindication

Action of L.A.

Systemic local

L.A reversibly blocks action potential in all membranes & thus C.V.S & C.N.S are susceptible to their effects.

The actions of L.A depend on the plasma concentration of the drug.

Central nervous system

Rapidly cross BBB.Pharmacologic action is depression.1. Anticonvulsive property

Used especially in interrupting status epilepticus at a dose of 2-3 mg/kg body wt, given at a rate of 40-50mg/min.

Blood levels of lidocaine- anticonvulsive

anticonvulsive 0.5-4µg/mlpreseizure signs & symptoms 4.5-7µg/mltonic clonic seizures >7.5µg/ml

2. Analgesia Earlier used as i.v. analgesic but not

used now due to low safety margin.3. Mood elevationCocaine has been long used for

inducing euphoria & lessening fatigue. Since cocaine causes habituation it is no longer used.

Cardiovascular system

L.A. have direct action on myocardium & peripheral vasculature.

1. DIRECT ACTION ON MYOCARDIUM:-L.A. produce myocardial depression,

decrease the conduction rate, decrease the force of contraction.

Therapeutic advantage of this is taken in managing the hyperexcitable myocardium.

Therapeutic plasma levels for lidocaine are1.8-6µg/ml. levels >6µg/ml lead to overdose symptoms.

2. Direct effect on peripheral vasculature.

Cocaine causes vasoconstriction, ropivacaine causes cutaneous vasoconstriction, almost all others cause vasodilatation.

The primary effect of L.A. on blood pressure is hypotension- depression of myocardium & relaxation of smooth muscles.

Non overdose levels

Slight increase or no change in B.P.

Levels approaching yet still below overdose

Mild hypotensionRelaxation of smooth muscles

Overdose levels Profound hypotensionDecreased myocardial contractility, cardiac output, peripheral resistance.

Lethal levels C.V.S. collapseMassive peripheral vasodilatationDecreased myocardial contractility & heart rate.

Local actions

No / minimal local irritant action.Injected around a nerve cause

anesthesia.Both sensory & motor nerves are

equally sensitive.Order of pain blockade is pain,

temperature, touch, deep pressure sense.

Applied to tongue bitter taste is lost first, followed by sweet & sour, and salty taste is lost last of all.

INDVIDUAL DRUGS IN LOCAL ANESTHESIA & LOCAL ANESTHESTICS IN DENTISRY

What are local anesthetics?

• Local anesthetic: drugs that have little no irritating effects when injected into the tissues & that will temporarily interrupt conduction when absorbed into the nerve.

CLASSIFICATION OF LOCAL ANESTHETICS

• ESTERS AMIDES Procaine Lidocaine Prpoxycaine Etidocaine 2-chloroprocaine Bupivacaine Tetracaine Mepivacaine

Structures of Amides and Esters• The amine end is hydrophilic (soluble in water), anesthetic molecule

dissolve in water in which it is delivered from the dentist’s syringe into the patient’s tissue. It’s also responsible for the solution to remain on either side of the nerve membrane.

• The aromatic end is lipophilic (soluble in lipids). Because nerve cell is made of lipid bilayer it is possible for anesthetic molecule to penetrate through the nerve membrane.

Differences of Esters and Amides

ESTERS AMIDES result from the combination results from the combination of para- amino benzoic acid of an aromatic amine & an & an amino alcohol. Amino acid.

unstable in a solution stable in a solution diffuse poorly through diffuse readily through tissues tissues.

Pka value high pka value low

rmetabolised by plasma metabolised in liver only cholinestrases & liver. produce less intense & produce more intense & shorter lasting anaesthesia longer lasting anaesthesia.

allergic rxn can occur rarely cause allergic rxn

Mechanism• The mechanism of local anesthetics involves the ion channels, nerve, and

depolarization.• Local anesthetics block the conduction in peripheral nerves that inhibited the

nerve to get excited and creates anesthesia.• The anestheic is having a reversible action. • The anesthetics inhibit the sodium ion influx across the neuronal cell

membrane .

• As a result, the nerve loses depolarization and the capacity to create the impulse, the patient loses sensation in the area supplied by the nerve.

Factors Affect the action of Local Anesthetics

Lipid solubility• All local anesthetics have weak bases. Increasing the lipid solubility leads to

faster nerve penetration, block sodium channels, and speed up the onset of action.

• The more tightly local anesthetics bind to the protein, the longer the duration of onset action.

• Local anesthetics have two forms, ionized and nonionized. The nonionized form can cross the nerve membranes and block the sodium channels.

• More non ionised form present lead to faster onset of action.

pH influence• Usually at range 7.6 – 8.9• Decrease in pH shifts equilibrium toward the ionized form, delaying the

onset action.• Lower pH, solution more acidic, gives slower onset of action

Factors Affect the Reaction of Local Anesthetics (cont.)

Vasodilation greater vasodilator activity = increased blood flow through the region=rapid

removal of anesthetic molecule from the injection site. thus decreased anesthetic potency & decreased duration

• Vasoconstrictor is a substance used to keep the anesthetic solution in place at a longer period and prolongs the action of the drug

• vasoconstrictor delays the absorption which slows down the absorption into the bloodstream

• Lower vasodilator activity of a local anesthetic leads to a slower absorption and longer duration of action

• Vasoconstrictor used the naturally hormone called epinephrine (adrenaline). Epinephrine decreases vasodilation.

Side effects of epinephrine• Epinephrine acts on the heart, causes the heart beat stronger and faster,

and makes people feel nervous.

Factors of circulation levels• Factors of circulation levels are the rates of

absorption,, distribution and metabolism.• . Absorption depends on the speed of administration

and levels of the doses.• Distribution allows absorption to occur in three

phases. First, the drug occurs at highly vascular tissues in the lungs and kidneys. Then it appears in less vascular, muscle and fat.

• Then the drug is metabolized.• Metabolism involves in the chemical structure based

on two classes, amide and ester as discussed earlier.• Rapid metabolism leads to decreased toxicity.

Toxicity• Toxicity is the peak circulation levels of local anesthetics• Levels of local anesthetic concentration administered to patients are

varied according to age, weight, and health.• Maximum dose for an individual is usually between 70mg to 500mg• The amount of dose also varied based on the type of solution used and

the presence of vasoconstrictorExample:---For adult whose weight is 150lbs and up, maximum dose Articaine and

lidocaine is about 500mg---For children, the dosage reduced to about 1/3 to ½ depending on their

weight.The doses are not considered lethal.Some common toxic effects: --light headedness ---shivering or twitching --seizures--hypotension (low blood pressure) --numbness

HISTORY• Cocaine was the first drug tried to produce surface anaesthesia.

• An ophthalmologist Carl Koller realized the importance of the alkaloid’s anesthetic effect on mucous membranes.

• In 1884, he used the first local anesthetic on a patient with glaucoma.

• Freud, Halsted, and Koller became addicted to the drug through self-experimentation.

• Though having strong addicting CNS action but it was widely Used, neverthless for 30 yr.

• Modification of cocaine molecule has been responsible for producing vast no of local anesthetichs.

• Certain structural changes may increase toxicity or irritancy without Increasing potency.

Aim in synthesis of new compound is to produce more potent drug With decreased systemic & local toxicity

• However,if the structural change responsible for increased potency also increases the rate of biotransformation, the toxicity of new compound may be decreased.

Procaine replaced Novocaine cocaine Problems

• In 1898, Professor Heinrich Braun introduced procaine as the first derivative of cocaine, also known as the first synthetic local anesthetic drug

• Trade name is Novocaine®

• Took too long to set (i.e. to produce the desired anesthetic result)

• Wore off too quickly, not nearly as potent as cocaine

• Classified as an ester; esters have high potential to cause allergic reactions

• Caused high conc. of adrenaline resulted in increasing heart rate, make people feel nervous

Most dentists preferred not to used any local anesthetic at all that time; they used nitrous oxide gas.

Today, procaine is not even available for dental procedures.

PROCAINE(NOVACAINE)

• A diethyl amino ethyl ester of PABA• Synthesised by german chemist EINHON 1905• POTENCY-1( Procaine=1)• TOXICITY- 1(procaine=1)• METABOLISM-hydrolysed in plasma by plasma pseudocholine -estrase.• EXCREATION- more than 2% unchanged in urine.• VASODILATING PROPERTIES-produces the greatest vasodilatation of all curently used local anesthetics. ONSETOF ACTION- 6TO 10 min. EFECTIVE DENTAL CONC-2% to 4% SYSTEMIC EFFECTS- CNS- crosses blood brain barrier it first stimulate the CNS & Latter on can produce CNS depression. CVS- no effect on CVS except vasodilatation of the microcirculation in the injectin site. RESPIRATORY SYSTEM-Large doses depresees the system

• PROPOXYCAINE 2 –CHLOROPOCAINE• CHEMICAL FORMULA 2-diethyl amino ethyl -4 amino beta – diethyl amino ethyl 2-prpoxy benzoate hydrochloride 2- chloro 4- amino benzoate POTENCY-7to8(procaine) 2 times potent than procaine TOXICITY-7to8(procaine) less toxic than that of procaine because of rapid hydrolysis. METABOLISM- hydrolysed in the both hydrolysed in the presence plasma & the liver of plasma choline estrases

Lidocaine• In 1940, the first modern local anesthetic agent

came in use that is lidocaine , trade name Xylocaine®

• It developed as a derivative of xylidine• dental surgeries• Belongs to the amide class, cause little

allergenic reaction; it’s hypoallergenic• Sets on quickly and produces a desired

anesthesia effect for several hours• It’s accepted broadly as the local anesthetic in

United States today• POTENCY-2( compared with procaine)• TOXICITY-2( Compared with procaine)• METABOLISM-In liver by microsomal fixed function oxidases , to mono ethyl glycerine & xylidine. EXCREATION- Via kidneys VASODILATING PROPERTIES-Less than that of procaine. ONSET OF ACTION- Rapid( 2 to 3 min)

SYSTEMIC EFFECTS• NERVOUS SYSTEM- Lidocaine, in toxic doses,first produces stimulation then depression of the CNS. Lidocaine administer I.V is capable of producing a degree of analgesia & even general anesthesia. RESPIRATORY SYSTEM- small doses of lidocaine have a mild bronchodilating effect respiratory arrest is the most common cause of death related to over dose of local anesthetics. CARDIOVASCULAR SYSTEM- Effect of lidocaine on the cvs varies in acc with dose - the drug, indoses of 50 to 100mg (1.5mg /kg) is givaen I.V during general anesthesia & surgery to correct ventricular arrhythmias. In general moderately large doses produces a -decrease in the electrical excitability force of of the myocardium -decrease in the force of contraction( negative inotropic effect) -decrease in the rate of electrical impulse conduction( negative chronotropic effect) Although these effects make lidocaine one of the most popular anti arrhythmic

agent.

Three special drugs used in dental anesthesia• Bupivicaine (Marcaine®--Produce very long acting anesthetic effect to delay the post operative pain from the surgery for as

long as possible--0.5% solution with vasoconstrictor--toxicity slowed because the pKa is very basic--Onset time is longer than other drugs b/c most of the radicals (about 80%) bind to sodium channel

proteins effectively--less than four times that of lidocaine.

• Prilocaine (Citanest®)--Identical pKa and same conc. with lidocaine--Almost same duration as lidocaine--Less toxic in higher doses than lidocaine b/c small vasodilatory activity

• Articaine (Septocaine®) --newest local anesthetic drug approved by FDA in 2000--Same pKa and toxicity as lidocaine, but its half life is less than about ¼ of lidocaine--Used with vasoconstrictor.--Enters blood barrier smoothly--The drug is widely used in most nations today

ConclusionAnesthetic pKa Onset Duration

(with Epinephrine) in minutes

Max Dose (with Epinephrine)

Procaine 9.1 Slow 45 - 90 8mg/kg – 10mg/kg

Lidocaine 7.9 Rapid 120 - 240 4.5mg/kg – 7mg/kg

Bupivacaine 8.1 Slow 4 hours – 8 hours

2.5mg/kg – 3mg/kg

Prilocaine 7.9 Medium 90 - 360 5mg/kg – 7.5mg/kg

Articaine 7.8 Rapid 140 - 270 4.0mg/kg – 7mg/kg

COMPLICATIONS OF LA.

Dr. Manu Gupta M.D.S – I

Deptt. Of Oral & Maxillofacial Surgery

Reactions to Local Anesthesia

• Syncope

• Toxic

• Loss of blood flow-fainting-Trendelburg position

• High level of drug in circulation-agitation-restless-HR& BP up-then CNS depression-nonester have depression only

Reactions to Local Anesthesia

• Allergic• Immediate- target lungs and circulatory• Delayed-minor type-hours to days after - IM or

IV or oral antihistamines- Benadryl 50 mg either IM or per oral

• Document patient chart

Complications of Injections

• Injury to nerve– Inferior alveolar block– Burning sensation lip

• Injury to blood vessels– Torn vessel-hematoma– warm rinse/warm compress reduce swelling

• Blanching of skin– spasm, time heals

• Broken needle– Infrequent,removal

• Infections– previously used needle– passage of needle thru infected area

• Idiosyncrasy– unknown reaction

Anesthetic complications

Anesthetic complication may be defined as any deviation from the normally expected pattern during or after the securing of regional analgesia.CLASSIFICATION OF COMPLICATIONS: These complications may be classified as follows.

Primary or secondary Mild or severe Temporary or permanent

Complications may be further subdivided into two groups. – These attributed to the solution used. – These attributed to the insertion of the needles.

COMPLICATION OF LOCAL ANESTHETICS SOLUTION • Syncope (fainting) • Muscle trismus • Pain or hyperalgesia an infections. • Edema • Infections • Broken needles • Prolonged anaesthesia • Hematoma • Sloughing of tissues • Facial nerve paralysis • Soft tissue injury • Bizarre neurological symptoms

Broken needles

Hematoma

Soft tissue injury

Effects of over dosage of local anesthesia On CNS

•Anxiety, restlessness

•Sighing respiration, tremors

•Generalized convulsions

•Disorganized respiration

•Over stimulated CNS, finally depressed

On CVS

•Cardiac muscle beats less effectively

•Cardiac output falls

•Many LA’s produce vasodilatation leading to pallor of skin & fall in BP

Death

Overdose Predisposing factors

I. Patient factors

1. Age

2. Weight

3. Other drugs

4. Sex

5. Presence of disease

6. Genetics

7. Mental attitude & environment.

II. Drug factors

1. Concentration

2. Dose

3. Route of ad.

4. Rate of injection

5. Vascularity of the injection site

6. Presence of vacsoconstrictors.

Causes of Overdose1. Biotransformation & elimination.2. Excessive total dose.3. Rapid absorption into the circulation. 4. Intravascular injection.

Classification of Orofacial anesthetic techniques:

I. LOCAL INFILTRATIONII. FIELD BLOCKIII. NERVE BLOCK

I. LOCAL INFILTRATION• Technique that anesthetizes the terminal nerve

endings of the dental plexus.

• The procedure is performed in the direct vicinity of the site of infiltration.

• Anesthetic fluid is injected deep the vestibular fold and deposited on the periosteum of the alveolar bone overlying the root apex (supraperiosteal injection).

• In general, a localized tooth block may be attempted on any tooth that has a vestibular alveolar plate of bone thin enough to permit diffusion of the solution to the apical nerves.

II. FIELD BLOCK• anesthetizes the terminal nerve branches in the

area.

• The deposition of local anesthetic at the apex of a tooth for the purposes of achieving pulpal and soft tissue anesthesia is often employed by many dental and maxillofacial professionals.

• While this is commonly termed “local infiltration,” it is important to note this is a misnomer. Terminal nerve branches are anesthetized in this technique and it is therefore correctly termed a field block.

III. NERVE BLOCK

• Larger areas and several teeth may be anesthetized by blocking a main nerve.

• The anesthetic solution is deposited adjacent to a main peripheral nerve.

• Will obviously produce a greater effect because the farther proximally a nerve is blocked, the greater the area anesthetized.

Equipments

Topical Anesthetic Cartridge

anesthesia cartridge containers

SYRINGE and NEEDLE

• t

Needle assembling

Techniques of Maxillary Regional Anesthesia

I. Local Infiltrationa. Supraperiosteal Injectionb. Periodontal Ligament Injectionc. Intraseptal Injectiond. Intrapulpal Injectione. Local Palatal infiltration

II. Nerve blocka. PSAN blockb. ASAN block or Infraorbital Nerve blockc. Greater Palatine Nerve blockd. Nasopalatine Nerve block

Techniques of Anesthesia for Treatment of a Localized Area or 1 or 2 Teeth

TECHNIQUE AREA ANESTHETIZED

1. Supraperiosteal Injection

2. Periodontal Ligament Injection

3. Intraseptal Injection4. Intrapulpal Injection5. Palatal Infiltration

- Individual teeth and buccal soft tissue- Individual teeth and buccal soft tissue - Localized soft tissue- Individual tooth- palatal tissue in the area of injection.

Supraperiosteal (Local) Infiltration- simplest and most commonly employed

Injection Site: Height of the mucobuccal fold above the

tooth

Technique:• Insert the needle at the injection site to a depth of

no more than to a depth of no more than a few millimeters and aspirate. Then inject one third to one half (0.6-1.2cc) of a cartridge of anesthetic solution slowly, over the course of thirty seconds.

Supraperiosteal (Local) Infiltration

Periodontal Ligament (Intraligamentary Injection)

- useful adjunct to the nerve block.

Injection Site: Sulcus between the gingiva and the tooth

Technique:• Insert the needle (bevel facing the root), to the

depth of the gingival sulcus • Advance the needle until resistance is met. A small

amount of anesthetic (0.2cc) is then administered slowly over the course of twenty to thirty seconds. It is normal to experience resistance to the flow of anesthetic.

Periodontal Ligament (Intraligamentary Injection)

Intrapulpal Injection

- involves anesthesia of the nerve within the pulp canal of the individual tooth to be treated. - may be used once the pulp chamber is open.

Injection Site: Pulp Chamber

Technique:• Advance the needle into the pulp canal and

deposit another 0.2cc of local anesthetic solution.• It may be necessary to bend the needle in order

to gain access to the chamber.

Local Palatal Infiltration Injection Site: five to ten millimeters palatal

area of tooth

Technique: • While maintaining pressure behind the

injection site, deposit anesthetic solution as the soft tissue is penetrated. Advance the needle until bone is contacted

Local Palatal Infiltration

Techniques of Anesthesia for Treatment of Upper Quadrant for Multiple Teeth

TECHNIQUE AREA ANESTHETIZED

1. Posterior Superior Alveolar Nerve Block

Max. molars (with exception of mesiobuccal root of max. 1st molar in some cases), hard and soft tissue on buccal aspect

2. Middle Superior Alveolar Nerve Block

Mesiobuccal root of max. 1st molar (in some cases),premolars and surrounding hard and soft tissue on buccal aspect

3. Anterior Superior Alveolar Nerve Block/Infraorbital Nerve Block

Max. central and lateral incisors and canine, surrounding hard and soft tissue on buccal aspect, mesiobuccal root of max. 1st molar (in some cases)

4. Greater Palatine Nerve Block

Palatal mucosa and hard palate from 1st premolar anteriorly to posterior aspect ofthe hard palate, and to midline medially

5. Nasopalatine Nerve Block

Hard and soft tissue of lingual aspect of maxillary anterior teeth from distal ofcanine on one side to distal of canine on the contralateral side

6. Maxillary Nerve Block

Hemimaxilla on side of injection (teeth, hard and soft, buccal and lingual tissue)

PSAN Block• Also known as the tuberosity block or the

zygomatic block,

Injection site: height of the mucobuccal fold over the

2nd molar

Technique:• Insert the needle at the injection site at a 45 degree

angle directed superiorly, medially, and posteriorly (one continuous movement).

• Advance the needle, aspirate, and inject • Prior to injecting, one should aspirate in two planes

to avoid accidental injection into the pterygoid plexus

Posterior Superior Alveolar Nerve Block

Anterior Superior Alveolar Nerve Block/Infraorbital Nerve Block

• the ASA nerve may also innervate the premolar teeth and mesiobuccal root of the 1st molar.

Injection site: ht. of the mucobuccal fold above the max. 1st premolar

Technique:• Identify the infraorbital notch and inferior to it is the

infraorbital foramen in line with the second premolar.

• Insert the needle at the injection site and The

syringe should be angled toward the infraorbital foramen and kept parallel with the long axis of the 1st premolar to avoid hitting the maxillary bone prematurely.

Anterior Superior Alveolar Nerve Block/Infraorbital Nerve Block

Greater Palatine Nerve Block

• is useful when treatment is necessary on the palatal aspect of the maxillary premolar and molar dentition.

• This technique targets the area just anterior to the

greater palatine canal.

• The greater palatine nerve exits the canal and travels forward between the bone and soft tissue of the palate.

• Location of the greater palatine foramen is done by placing it on a cotton swab the palatal tissue approximately one centimeter medial to the junction of the 2nd and 3rd molar

Greater Palatine Nerve Block

Nasopalatine Nerve Block• known as the incisive nerve block and

sphenopalatine nerve block,• anesthetic solution is deposited in the area of the

incisive foramen.

Injection Site: lateral to the incisive papilla is the injection site

Technique-:• With a cotton swab, hold pressure over the incisive

papilla. • Insert the needle just lateral to the papilla with the

bevel against the tissue. • Advance the needle slowly toward the incisive

foramen while depositing small volumes of anesthetic and maintaining pressure on the papilla.

Nasopalatine Nerve Block

Techniques of Mandibular Regional Anesthesia

I. Local Infiltrationa. Supraperiosteal Injectionb. Periodontal Ligament Injectionc. Intraseptal Injectiond. Intrapulpal Injection

• are executed in the same manner as described above for maxillary

anesthesia.

II. Nerve blocka. Inferior Alveolar Nerve Block b. Buccal Nerve Block c. Gow-Gates Technique d. Vazirani-Akinosi Closed Mouth Mandibular Block

e. Mental Nerve Block f. Incisive Nerve Block

Techniques of Anesthesia for Treatment of Lower Quadrant for

Multiple TeethTECHNIQUE AREA ANESTHETIZED

1. Inferior Alveolar Nerve Block

Mandibular teeth on side of injection, buccal and lingual hard and soft tissue, lower lip

2.Buccal Nerve Block Buccal soft tissue of molar region

3. Gow-Gates Mandibular Nerve Block

Mandibular teeth to midline, hard and soft tissue of buccal and lingual aspect, anterior 2/3 of tongue, FOM, skin over zygoma, posterior aspect of cheek, and temporal region on side of injection

4. Vazirani-Akinosi Closed Mouth

Mandibular teeth to midline, hard and soft tissue of buccal aspect, anterior 2/3 of tongue, FOM

5. Mental  Nerve BlockBuccal

Buccal soft tissue anterior to mental foramen, lower lip, chin

6. Incisive Nerve Block

Premolars, canine and incisors, lower lip, skin over the chin, buccal soft tissue anterior to the mental foramen

Inferior Alveolar Nerve Block

Most commonly employed technique

This technique carries a high failure rate

The target for this technique is the mandibular nerve as it travels on the medial aspect of the ramus, prior to its entry into the mandibular foramen.

The lingual, mental, and incisive nerves are also anesthetized.

A 25 gauge long needle is preferred for this technique.

Inferior Alveolar Nerve Block

• Technique- With the mouth open maximally, identify the coronoid notch and the pterygomandibular raphe.

• Bring the needle to the injection site from the contralateral premolar region.

• Advance the needle until bone is contacted. Once bone is contacted, withdraw the needle 1mm and redirect the needle posteriorly by bringing the barrel of the syringe towards the occlusal plane .

• Advance the needle to three quarters of its depth, aspirate, and inject three quarters of a cartridge of anesthetic solution slowly over the course of one minute. As the needle is withdrawn, continue to deposit the remaining one quarter of anesthetic solution so as to anesthetize the lingual nerve

Inferior Alveolar Nerve Block

The buccal nerve block

• The buccal nerve block, otherwise known as the long buccal or buccinator block

Technique- • Identify the most distal molar tooth on the

side to be treated. The tissue just distal and buccal to the last molar tooth is the target area for injection . Needle should parallel to the occlusal plane on the side of the injection. The needle is inserted into the soft tissue and a few drops of anesthetic solution are administered.

• 0.2cc of local anesthetic solution is deposited.

The buccal nerve block

Mental Nerve Block

• The mental nerve block is indicated for procedures where manipulation of buccal soft tissue anterior to the mental foramen is necessary.

Technique-

• The target area is the height of the mucobuccal fold over the mental foramen .

• The foramen can be manually palpated by applying gentle finger pressure to the body of the mandible in the area of the premolar apicies.

• The needle is directed toward the mental foramen with the bevel facing the bone.

Mental Nerve Block

Thank you.