DEPT.OF ORAL &MAXILLOFACIAL SURGERY

Presented By Dr Haneef

LOCAL ANAESTHESIA

HistoryArmamentariumDefinition &ClassificationComposition Different Agents , Vasoconstrictors Mechanism of ActionBio Transformation Systemic Action

Contents

INTRODUCTION

Ancient time – dental treatment associated with painEarliest pain relief – Coca shrub mood elevator

Incas

Cocoa shrub – foot hills of AndesIntroduced by Europeans to South AmericaCocaine

1855 – Gaedicke extracted alkaloid Erythroxylin

1860 – Dr. Scherzer cocaine from this alkaloid

1844 – Francis Rynd (Dublin) Acetate of morphine + CreosoteSkin incision TGN treatmentFirst time liquid used - intradermally

1884 – marks birth of LA

Sigmund Freud Carl Koller Cocaine for eye operation

William Steward Halsted Cocaine for inferior dental nerve

1886 – BDJ William Alfred Hunt et alCocaine - dental anesthetic documented

1901 – E Mayers Vasoconstrictor + cocaine

190513 lives claimed – addictionA Einhorn & E Uhlfelder(Sweden)

Synthesized Procaine hydrochlorideProcaine sterilizable, non-additive, non-toxic

1943N Lofgren(Sweden)

Synthesized Anilide called LignocaineLignocaine – amide linked synthetic derivative

1946 – Lignocaine introduced Dental practice

1948 – Lignocaine ; published in BDJ – Lofgren

Sweden – Birth place of newer LA agents

Bupivacaine

Ropivacaine

Pain and pain control

DEFINITION --

It is defined as an unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specific neural pathway to the central nervous system where it is interpreted as such.

Methods of pain control.Accupuncture Analgesia --

Originated-CHINA,between600BC to 200ADHypnotism –

Still employed—susceptible patients,Time consuming, lasts for less time

Audio Analgesia –1959 Gardner and lickliderLoud noise used to produce analgesia

Electric analgesia -- Peripheral nerve- Direct electric currentElos-1,powered by 18v battery- SiemensNever more than 30 ma

ArmamentariumSyringe-

Breech loading, metallic cartridge-aspirating

Advantage

Visible cartridge

Aspiration- 1 hand

Autoclavable

Rust resistance, Long lasting

Disadvantage

Weight

Size-Too big

Possibility of infection

PISTON WITH HARPOON

FINGER GRIP

THUMB RING

SYRINGE BARRELNEEDLE ADAPTOR

Breech loading plastic cartridge-aspirating

Advantage

Light weight

Cartridge visible

Rust resistance, Long lasting

Low cost

Disadvantage

Size – Too big / small

Possibility of infection

Repeated autoclaving – Plastic looses its properties

PLASTIC REUSABLE SYRINGE

Breech loading metallic cartridge-Self aspirating

Advantage

Cartridge visible

Autoclavable

Easier to aspirate

Piston is scored – Qty Known

Disadvantage

Weight

Possibility of infection

Finger has to be moved from thumb ring to disc-Aspiration

Takes time to accustom

SELF ASPIRATING SYRINGE

Pressure syringe --

Advantage

Measured dose

Overcomes tissue resistance

Non threatening – Cartridge protected

Disadvantage

Cost

Inject too rapidly -Possibility

PRESSURE SYRINGE

WILCOX- JEWETT OBTUNDER

Jet injectors

Advantage

Does not require – needle

Very small volume – Delivered

Topical anesthesia-effective

Disadvantage

Inadequate – Pulpal / Regional block

Patient disturbed by jolt of jet.

Cost

PDL damage – common

JET INJECTOR

Disposable syringe

Advantage

Single use

Sterile-Till opened

Light weight

Disadvantage

Does not accept – Dental cartridge

Aspiration – Difficult – 2 hands

NeedleType – Stainless steel – Disposable

Platinum

Iridium platinum

Ruthenium platinum

Parts – Bevel

Shank

Hub-Leur lock, Friction grip.

Rubber diaphragm

Aluminum cap

NECK

GLASS TUBE

RUBBER PLUNGER

Additional Armamentarium –

Topical antiseptic

Topical anesthetic

Cotton Gauge

Hemostat

Applicator Stick.

It is defined as a transient loss of sensation to a

painful or potentially painful stimulus, resulting from a

reversible interruption of peripheral conduction along a

specific neural pathway to its central integration and

perception in the brain.

Definition of L.A --

IDEAL REQUIREMENTS OF LOCAL ANESTHETICS

Its action must be reversibleIt must be nonirritating to the tissues and produce no secondary local reactionIt should have a low degree of systemic toxicityIt should have a potency sufficient duration to be advantageous.It should have a potency sufficient to give complete anesthesia without the use of harmful concentrated solutionsIt should have sufficient penetrating properties to be effective as a topical anesthetic.It should be relatively free from producing allergic reactions.It should be stable in solution and undergo biotransformation readily within the bodyIt should be either sterile or capable of being sterlized by heat without deterioration.

INDICATIONS OF LAROOT CANAL TREATMENT FOR PULPAL

ANESTHESIAPERIODONTAL SURGERYORTHODONTIC EXTRACTIONSEXTRACTION OF CARIOUS ,PRE PROSTHETIC

EXTRACTIONS,MALPOSED AND IMPACTED TEETH.PREPROSTHETIC SURGERYSURGICAL EXCISION AND INSICION OF

PATHOLOGICAL LESIONS.ORTHOGNATHIC SURGERYMAXILLARY ND MANDIBULAR # REDUCTIONS

OPEN/CLOSED

CONTRAINDICATIONS OF LA

ABSOLUTE:

DRUG ALLERGY OR HYPERSENSTIVITY REACTION

RELATIVE CONTRAINDICATION IN HEPATIC FAILURE PATIENTS Amides are

metabolized in the liver. Patients with significant liver disease who have poor hepatic blood flow will have trouble metabolizing amides and other agents.

Patients administered prilocaine may develop methemoglobinemia.

HEART FAILURE (ASA IV OR VI) LIDOCAINE is used as an ACLS drug for patients with

ventricular dysrythmias. However high levels of lidocaine will decrease contractility and cardiac output and can lead to circulatory collapse. Systemic actions on the central nervous system include CNS depression, seizures and analgesia.

In addition, one of the metabolites of lidocaine may actually cause some sedation. These metabolites are excreted in the kidney.IN RENAL FAILURE PATIENTS HAS TO BE USED WITH CAUTION.

ATYPICAL PSEUDOCHOLINESTERASE. BLEEDING DISORDERS PERTICULARLY REGIONAL

BLOCKS

TYPES OF LOCAL ANESTHESIATopical Surface contact.Paste, ethyl chloride. May be adequate for simple incision and drainage,

preinjection,Infiltration Deposition of solution at or close to site of surgery.a) Sub mucous - for simple soft tissue surgery - includes long buccal

infiltration.Not suitable for pulpal anaesthesia.b) Supraperiosteal - the commonest technique - solution diffusesthrough cortical bone into apical area. Usually adequate especiallyin maxilla but adult mandibles to thick in posterior buccal cortex.c) Subperiosteal - painful! - use if (b) fails.d) Intraosseous - very painful! again use if (b) fails. Drill smallaccess hole over appropriate tooth apex and deposit 0.25ml oflocal anaesthetic.

e) Intraseptal - variation of (d) - similar indications but inject through

softer crestal bone to reach apex.

f) Intraligamentous - painful but occasionally very useful especially

for acute pulpitis where regional block fails to give adequate depth

of anaesthesia. Must use special syringe to avoid breaking

cartridge. Push needle along root surface to apex - inject small

volume of solution - effect is rapid so proceed with surgery

C.FIELD BLOCKS

D.NERVE BLOCKS

E.Regional Block: Remote from site of surgery.

Contraindicated in patients with bleeding diatheses even if controlled!Success depends on knowledge of local anatomy and good technique.

Based on composition – A) Natural – eg – cocaine. B) synthetic nitrogenous compd –

para amino benzoic acid-procaine,

benzocaine.

acetanilide - lignocaine

quinoline - cinchocoline C) non Nitrogenous compounds -

benzyl alcohol D) miscellaneous – clove oil , phenol .

Classification--

Based on intermediate group --

Esters –

Benzoic acid Para Amino benzoic Acid

Butane Chloroprocaine

Cocaine Procaine

Benzocaine Propoxycaine

Hexylcaine

Tetracaine

Amides –

Articaine

Bupivacaine

Dibucaine

Lignocaine

Mepivacaine

Prilocaine

According to biological site and mode of action—Class A Class B

Class C

Class D

Agents acting at receptor site –external surface.

Agents acting at receptor site- internal surface..

Agents acting at receptor independent physico chemical mechanism.

Agents acting in combn of receptor and independent mechanism.

Biotoxin -eg tetrodotoxin

Quaternary amonium-scorpion venom

Benzocaine

Clinically useful agents –Lignocaine etc

Injectables -- Surface -- Ultra short acting *Soluble - eg <80 min eg Lignocaine Cocaine

Lignocaine Short acting 45-50 *Insoluble- egMin 2% ligno with Benzocaine1:1 lakh VC Medium acting 90-1502% ligno with Vc or4% prilocaine with 1:2 epin Long acting > 180 5% Bupivacaine with 1:2 epin

Composition--Local anesthetic agent This is the active ingredient in the solution, but despite

the constant development of new drugs, the ideal L.A. agent is yet to be introduced into clinical practice.

Vasoconstrictor Merits Reduces toxic effects by retarding the absorption of the

constituents By confining the anesthetic agent to a localized area it

increases the depth and duration of anesthesia. It produces a relatively blood less field of operation for

surgical procedures.

Demerits In higher doses can cause systemic effects that are undesirable,

practically in individuals suffering from cardiovascular disease.

Vasoconstrictor may also cause a delay in wound healing, edema and tissue necrosis. This is because sympathomimetic amines may increase O2 consumption of tissues. This, together with vaso constriction leads to hypoxia and local tissue damage.

The vasoconstrictors in general uses are Adrenaline. Noradrenaline Felypressin

Anti oxidant Most often is sodium meta-bi sulphite Amount varies from 0.0065 to 0.002 mg/CC. Since this substance is more readily oxidized than adrenaline or noradrenaline it

protects their stability. Preservative

Modern LA solutions are very stable and have a shelf – life of 2 years or more. Most frequently used bacteriostatic agents are methylparaben, propylparaben

and chlorobutanol. Fungicide Thymol is added. Vehicle The anaesthetic agent and the additives are dissolved in modified Ringer’s

solution. This automatic vehicle minimizes the discomfort during injection.

Anesthetic 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

Lignocaine-- Classified under – Amide2-diethylamino 2,6 acetoxylidide hcl1943 – Nils Lofgrens- intro 1948(dentistry) Metabolised- Liver by microsomal fixed function oxidases

to monoethyl glycerine and xylidide Excretion -<10% unchanged, >80%-metabVasodilaton ->Procaine, <MepivacainePka –7.9 , ph(plain)-6.5,ph(with Vc)5 –5.5,Onset of action

2-3 min,Anesthetic half life 1.6hrs,topical anesthetic -yes

Individual Agents --

NH.CO.CH2.N

CH3

CH3

C2H5

C2H5

LIGNOCAINE

Recommended dose – 7mg/kg not>500mg with VC 4.4mg/kg not>300mgFor children with VC 3.2 mg/kg Council for dental therapeutics- ADA 4.4mg/kgIt is non allergic available in three formulations Ligno2% with out Vc Ligno2% with VC 1:80,000 Ligno2% with VC 1:100,000Adverse reactions- CNS stimulation then

Depression,Overdose causes unconsciousness and respiratory arrest.

Bupivacaine –Classified under amide

1-butyl 2,6 pipecoloxylidide

Toxicity <4 times – Lignocaine, Mepivacaine

Metabolism –Liver by Amidases

Excretion by kidney (16% unchanged)

Vasodilation- relatively significant

Pka-8.1,ph(plain)- 4.5-6, ph(vc)- 3-4.5

Onset of action –6-10 min,Anesthetic half life-2.7hrs,Dose

1.3mg/kg ,Maximum dose-not >40mg,Absolute maximum dose-

not> 90mg

N

NH.CO

C4H9

CH3

CH3

BUPIVACAINE

Available as 0.5% soln 1:2,00,000 (vc)

Indicaton- pulpal anesthesia->90- min.

Full mouth recontruction.

Extensive perio surgery.

management of post op pain.

Duration –Pulpal- 90- 180 min

Soft tissue-4-12 hrs

Contra indication- burning sensation at site of injecton, in children-

anticipating self trauma .

Procaine- Classified under –Esters

2Diethylamino ethyl 4aminobenzoate hcl

Metabolised-in Plasma by plasma pseudocholine esterases

Excretion >2%unchanged, 90% -PABA,8% diethyl aminoethanol in

urine.

Pka-9.1,High degree of vasodilation, 2% procaine 15-30min soft

tissue LA

no pulpal anesthesia , > incidence allergy, drug of choice for intra

arterial injection and accidents.

Mepivacine- classified -amide type

1 Methyl 2,6 pipecoloxylidide hcl

Metabolism-microsomal fixed funcn oxidasea in liver.

Maximum dose 4.4 mg/kg , absolute max dose-300mg.

Excretion-1-10% unchanged urine.

Pka-7.6,Anesthetic half life-90min,

Mild vasodilator, 3% mepivacaine used in patients with vc

contraindicaton. Low reported cases-allergy.over dose CNS

stimulation followed by depression.

Articaine- classified- Amide2 Carboxymethoxy 4 methylthiophene hclMetabolised- Liver Excretion – Kidney 10% - unchanged.Pka 7.8, Anesthetic half life-1.2-2 hrs, Maximum dose – 1mg/kg , Absolute maximum dose –

500mgfirst LA Agent with thiophene ring,little potential to diffuse

through soft tissue.Adverse reaction-methymoglobinemia-Rx by using

methylene blue 1mg/kg.

Etidocaine- classified –Amide

Metabolism –Liver

Excretion –urine- Kidney

Pka 7.7 ,Anesthetic half life-56 min.

Maximum dose 8mg /kg, Absolute max dose 400 mg

Employed mainly in epidural or caudal regional block.

Added – to counteract vasodilation effect of injectable

L.A

Decreases rate of absorption

Reduces the risk of overdose reaction

Increases duration of action

Reduces bleeding at the site

VASOCONSTRICTORS

CLASSIFICATION OF V.C

Catecholamines EpinephrineNor epinephrineDopamine

Non catecholaminesAmphetamineMeta amphetamine

Based on chemical stc (Catechol nucleus)

Based on mode of action

Direct acting Epinephrine Nor epinephrine

Indirect acting Amphetamine Tyramine

Mixed acting Ephedrine

Proprietary name

Mode of action

Systemic 1) CVS

EPINEPHRINEAdrenaline

α1& β receptors

Systolic & Diastolic pressure Heart rate Oxygen consumption Stroke volume

FELYPRESSINOctopressin

Direct stimulation of vasculatureNo direct effect onMyocardium Non-arrythmagenicHigh doses – impaired coronary flow

2) CNS

3) RS4) Vasculature

5)Metabolism

CNS stimulation

Bronchodilator α1 – vasoconstrictionβ 2 – vasodilation oxygen consumption blood sugar level

Adrenergic nerve – no effect

Vasoconstriction – coronary blood vessels

Anti-diuretic action Oxytocin like action – uterus

6) Clinical

application

7) Max

dose

8) Side

effect

Allergy, hemostasis

0.2 mg – healthy

0.04mg – CVS impaired

CVS & CNS symptoms

Cerebral hemorrhage

As vaso-constrictor in

L.A

0.04mg

Rate Non-myelinated 1.2m/s Myelinated 14.8 – 120m/s

Site of action Outer bimolecular lipoprotein layer in nerve membrane

Altering the basic RMP of nerve

Altering the threshold potential

Decreasing the rate of depolarization

Prolonging rate of repolarization

MODE OF ACTION

ACTEYLCHOLINE THEORY:Involved in nerve conduction in addition to its role as a

neurotransmitter at nerve synapsesNo such evidence

CALCIUM DISPLACEMENT THEORY:L.A causes nerve block by displacement of Ca from some

membrane site that controls entry of NaVarying conc. Of Ca in nerve – not seen

THEORIES OF ACTION OF L.A

SURFACE CHARGE THEORY:Action by binding to nerve membrane and changing its

electric potential.Cationic molecules aligned at membrane water interface –surface

elec potn more positively charged - electric potn , threshold potn.

Demerits- RMP not altered by LA.

LA act on nerve channel rather than surface –cannot explain how uncharged LA molecule causes nerve blockage.

Membrane expansion theory-LA lipid soluble – enters nerve membr and changes

configuration of membr. There by reduced space for sodium

to enter and thus cause inhibition.Explains how non ionised drug causes- blockade, nerve

membrane do expand and become more fluid when exposed to

LA .No evidence to tell that the whole blockade is due to this

phenomenon.

Specific receptor theory—

LA act by binding to specific receptors- sodium channel-on

external/ axoplasmic surface.

Once it binds there is no permeability of sodium- no conduction.

LA molecule replace calcium molecule at calcium gate – thus

prevent sodium entry.

This is by far the most accepted theory.

All LA are available as acid salt of weak bases.

Weak base(BNHOH) combined with acid (HCL) to give

acid salt(BNHCL)& water.

In mucosa BNHCL dissociates into BNH and CL . Normal

tissue PH 7.4 is necessary for conversion of acid salt to free

base.

BNH which is hydrophilic further dissociates to BN and H.

BN is now lipophilic.

Mechanism of action.

Lipophilic BN diffuses through nerve membrane (lipid).

Inside the nerve it combines with intrinsic H. (H in nerve

formed by buffering action.)

Newly formed ionised BNH displaces calcium from the

sodium channel receptor site to cause conduction blockade.

LA Solution .

Biotransformation. Esters- eg- Procaine-

hydrolyzed to pseudo cholinesterase's

Para amino benzoic acid Diethyl amino alcohol

Excreted unchanged urine further transformed-urine

Atypical cholinesterase's --- increase toxicity

Amide eg lidocaine --

Mono ethyl xylidide

Glycine xylidide xylidide

Xylidide

Hydroxy xylidide. Excreted kidney .

Significant renal diseases – contra indication.

Systemic action.CNS –

Low levels – no action Toxic dose – tonic clonic convulsionsBlood- 0.5-4.0 mg/ml-no complication 4.5-7.0 mg/ml-pre seizure sign/

symptom >7.5mg/ml-tonic clonic seizures.Anti convulsive property –As it causes depression of CNS.Seizure threshold- excitability nerve

CVS-Action on Heart

Electrical excitability of myocardium .

conduction rate

Tone of contraction.

clinically effective level-1.8-5mg/ml –anti arrhythmic

used in premature ventricular contractures , arrhythmias.

Action on vasculature-

normal value no change.

over dose- hypo tension.( myocardial contractility)

Lethal dose- cardio vascular collapse

( myocardial contractility, massive peripheral vaso dilatation )

Action on Respiratory system– Normal levels- no over dose- bronchial muscles relaxation .Over dose – Respiratory arrest due to CNS depression.

DEPT.OF ORAL &MAXILLOFACIAL SURGERY

Presented By Dr Haneef

LOCAL ANAESTHESIApart II

Anatomical considerationsLocal anaesthesia technique- MaxillaLocal anaesthesia technique- MandibleComplicationsFuture trends

CONTENTS

The right and left trigeminal nerves provide among other functions, the overwhelming majority of sensory innervation from the teeth, bone, soft tissues of the oral cavity.

Two parts:-

i. Motor:- a. Masseter

b. temporalis

c. lateral/medial pterygoid d. Mylohyoid

e. Anterior belly of digastric f. Tensor tympani g. Tensor veli palatiniii. Sensory: V1 Opthalmic nerve V2 Maxillary division V3 mandibular division

ANATOMICAL COSIDERATIONS

Opthalmic division V1

Maxillary nerve V2

Mandibular nerve V3

Use a Sterile Sharp Needle

Check The flow of Solution

Determine Whether to Warm solution before use or not.

Position the patient

Dry the tissue/ wipe once.

Apply topical anesthetic

Basic points To keep in mind

Communicate with patient apply firm hand rest

Inject few drops of soln, communicate with patient,

Advance to the target slowly ,aspirate , inject

Withdraw the needle slowly

Observe the patient & check for anesthetic symptoms

Intra Oral injection techniquesSupraperiosteal injection Intralegimentry injection Intraspetal injection Intraosseus injectionPosterior superior alveolar nerve blockMiddle superior alveolar nerve blockAnterior superior alveolar nerve blockMaxillary nerve blockGreater palatine nerve blockNasopalatine nerve block

Exta oral injection techniques Ifraorbital nerve block – anterior, middle superior alveolar nerve blockMaxillary nerve block

Maxillary injection techniques

Supra periosteal injection:

Anaesthetize buccal soft tissue & hard tissue

Nerves anaesthetized – large terminal branches

Indication :

1 or 2 teeth need to be anaesthetized / small area

Teclhnique for Maxillary Block

Contra-indication :

Infection

Dense bone covering

Target area :

Behind apices of tooth

Landmarks :

Muco-buccal fold

Crown & root length

Area anaesthetized:Maxillary 3rd, 2nd & 1st molar (except mesio-buccal root of 1st

molarBone & periodontium over these

Indication:Treatment of 2 or more molars required Supra-periosteal injection – ineffective Acute inflammation

Posterior Superior Alveolar Nerve Block

Contra-indication:Pt with bleeding disorders

Disadvantage:More of soft tissue landmarks used2nd injection for 1st molar

Landmarks:Mucobuccal foldZygomatic process of maxillaInfratemporal surface of maxillaAnterior border and coronoid process of mandibleTuberosity of maxilla

Complications:

Hematoma –

Non visible - pterygoid plexus posteriorly

Visible – buccal aspect

Accidental mandibular Anaesthesia

Orbital contents – anaesthetized accidentally

Accidental - parotid gland facial nerve affected

Only in present in about 20% of the poplation thereby limiting its clinical usefulness of this block.

Area anaesthetized:Mesiobuccal root of the 1st molar, pulps of maxillary first 1st and

2nd premolarBuccal periodontal tissues

Indication:When ifra orbital block fails to provide anaesthesia to maxillary

canineDental procedures involving both maxillary premolars

contraindication:When infection or inflammation

Middle Superior Alveolar Nerve Block

Areas anaesthetizedPulp of maxillary C.Is – CanineBuccal periodontium, lower eyelid, lateral aspect of nose Upper lip

IndicationsMore than 2 anterior teeth

ContraindicationsDiscreet treatment areas Hemostasis of localized area – not adequately achieved

Anterior superior alveolar nerve block ( ifra orbital nerve block)

Landmarks

Mucobuccal fold,lforamen supra –orbital notch infra-orbital

notch, infra-orbital foramen, mental foramen

2 methods:

Intra-oral

Premolar approach

Incisal approach

1.Nasopalatine nerve block/spenopalatine nerve block/ incisive nerve blockAreas anaesthetized

Anterior portion of Hard palate and over lying structures back to the bicuspid area.

IndicationsAnterior palatal procedures supplementing infraorbital nerve

blocksAnaesthesia of nasal septum

LandmarksCentral incisor & incisive papilla

Palatal Anaesthesia

Complications Hematoma

Necrosis

Technique Single needle penetration

Multiple needle penetration

Usually most discomforting block for patient – very painful

2.Greater palatine nerve block/ anterior palatine nerve blockAreas anaesthetized

Palatal soft tissue – posterior aspectPalatal hard tissue

IndicationSurgical procedures posterior portion of hard palatePalatal Anaesthesia in conjunction with posterior superior

alveolar nerve block. Landmarks

Greater palatine foramen – junction of the maxillary alveolar process & palatine bone

Between the 2nd & 3rd molars – 1-1.5cms away from gingival margin

First reported by freidman and hochman in 1997 during development of CCLAD system

Muscles of facial expression and upper lip anesthesized.Nerves anesthetized

ASA and MSAAreas anesthetized

Pulpal anesthesia of maxillary incisors,canines and premolarsBuccal and palatal attached gingiva

Indications Performed with CCLADWhen anterior cosmetic procedures are performedWhen anesthesia is desired from a single injection

contraindications Patients with thin palatal tissuesPatients who cannot tolerate the 3-4 minute adminstration timeLong procedures >90 mins

Anterior middle superior alveolar nerve block

AdvantageLess amount of LA is deposited 0.5ml/minAllows for accurate smile line assesment in case of aesthetic

restorationsDisadvantage

Very slow adminstrationCan cause operator fatigueMaybe uncomfortable for the patientTechnique sensitive

Anterior middle superior alveolar nerve block

Nerve anaesthetized Maxillary division of trigeminal nerve

Areas anaesthetized Pulpal Anaesthesia Maxillary teeth – 1 side Periodontium / soft tissue – 1 side

Indications Extensive oral / periodontal / endodontal procedures Other regional nerve blocks not possible Therapeutic procedure to diagnose neuralgias

Maxillary nerve block

Contra-indicationsPediatric patients Inexperience operatorsInfection / inflammationHemorrhage – anticipated Greater palatine canal approach not possible – bony obstr.

Landmarks Mucobuccal fold distal to maxillary 2nd molar Maxillary tuberosityZygomatic process Greater palatine foramen

Complications Hematoma Penetration into orbit

Volume – displaces orbital structures, periorbital swelling, proptosis, 6th nr block – diplopia, transient loss of vision, optic nerve blocked, retrobulbar block producing mydriasis, corneal anesthesia / hemorrhage, opthalmoplegias (common)

Penetration into nasal cavityPatient complains – LA running down the throat – to

prevent keep mouth wide open Technique

High tuberosity approachGreater palatine canal approach

I. Anterior and middle superior alveolar nerve block – Nerves anaesthetized

Infraorbital nerveInferior palpebral, lateral nasal and superior labial nerves

Area anaesthetizedIncisors and bicuspids on the effected sideLabial alveolar plate and associated tissues

Anatomical landmarksPupil of the eyeInfraorbital ridgeInfrorbital notchInfraorbital depression

IndicationsWhen Intra oral route is not feasableWhen attempts of intra oral anaesthesia have been ineffective

Extra Oral nerve blocks

II. Maxillary nerve block – Areas anaesthetised

Anterior temporal & zygomatic regionLower eyelidSide of noseAnterior cheekUpper lipMaxillary teeth / alveolar bone & overlying structures – 1side Hard & soft palate Tonsils – parts of pharynxNasal septum – floor of nose

Extra Oral nerve blocks

Indications Extensive surgery – 1 half of maxilla Others blocks not possibleTherapeutic purposes

Techniquemid point of zygomatic processNeedle gently contact lateral pterygoid plate Maximum length of 4.5cms directed slightly upward & forward

Note:In final position – internal maxillary artery – inferior to needleTemporal vessels on either sides Posteriorly foramen ovale with mandibular nerve & foramen spinosum

with middle meningeal artery Anteriorly pterygomaxillary fissure

MANDIBULAR NERVE BLOCK

INFERIOR ALVEOLAR NERVE BLOCKOther common name- Mandibular block

Different techniques are:

DIRECT METHOD. INDIRECT METHOD. METHOD OF CLARKE & HOLMES METHOD OF ANGELO SARGENTI VAZIRANI- AKINOSI TECHNIQUE GOW-GATE’S TECHNIQUE KURT THOMA EXTERNAL APPROACH

Classical inferior alveolar nerve block Nerves anaesthetised- inferior alveolar nerve block and its

subdivisionsAreas anaesthetised

Mandibular teeth upto midline Body of mandibleInferior portion of ramus Buccal periosteum & mucous membrane Lingual soft tissue Anterior 2/3rd of tongue

IndicationsMultiple mandibular teeth – proceduresBuccal / Lingual soft tissue anaesthesia

Mandibular Nerve Blocks

ContraindicationsInfection / acute inflammation Young children / mentally handicapped

Landmarks Coronoid notch Mucobuccal foldExternal oblique ridgeRetromolar triangleInternal oblique ridgePterygomandibular raphe Occlusal plane of posterior mandibular teeth

Complication Hematoma Trismus Transient facial paralysis (parotid gland)

Anatomical structures - final position Disadvantages:• Rate of indequate anesthesia is high 10-20%• Intra oral landmarks are not consistently reliable• Highest positive aspiration of about 10-20%• Partial anesthesia where bifid inferior alveolar nerve and bifid

mandibular canal are present

INDIRECT METHOD:

Stages in the indirect technique :- Initial insertion of the needle more laterally,thus immediately strikes the bone, needle is partially withdrawn after touching the bone, syringe is moved parallel to the lower molars on the other side, insertion of the needle beyond theinternal oblique ridge, the syringe is returned to it’s original direction, ie over the lower premolars and deposit 1.5ml of solution in the pterygomandibular space.

METHOD OF CLARKE & HOLMES

It involves deposition of solutions @ a higher level than usual. It is a

modification of indirect technique. In the standard direct/indirect technique,

the analgesic is placed immediately behind the mandibular foramen, which

is 1cm above the occlusal plane of molar teeth. At this level the nerve is

concealed by lingula & sphenomandibular ligament. Depositing the

solution at a higher level causing complete anesthesia.

Method of angelo sargenti This technique is a modification of direct method. The difference is that the

nerve is approached from a higher level than usual.

TECHNIQUE: Syringe with 1 5/8 inch 26gauge needle is used.The index finger is placed in the retro molar fossa with nail facing lingually. The needle is inserted opposite to the mid point of the finger nail. The barrel of the syringe is now placed between and in contact with the upper premolars of the opposite side. Needle is slowly inserted in a downwards & backwards direction until it touches the bone, depth is 1cm. 1.5ml of solution is deposited.

Closed mouth/ Akinosis technique (1977)—Nerves anesthetized – inferior alveolar nerve, lingual nerve

buccinator nervesArea anesthetized

one half of mandible upto mid line including lingual tissue and inferior portion of the ramus of the mandible.

Land mark- occluding plane of the teeth.Muco gingival junction maxillary teeth.Antr border of ramus.Orientation of bevel must be oriented away from the bone of mandibulaar

ramus (bevel faces toward mid line).More popular now

Land marks easyOne prick – mandibular, buccal, lingual n anesthetised.Patient more comfortable.

Advantages• Atraumatic, • pats. with restricted mouth opening.• fewer post op complications.• Disadvantages• Difficult to visualize the path of needle and depth of

insertion. • Complications• hematoma, transient facial n. paralysis.

Nerves anaesthetised – inferior alveolar, mental,

incisive, lingual, mylohyoid, auriculotemporal and buccal.Area –all mandibular hard and soft tissue Upto mid line.Indications- multiple procedures on mandibular teeth,

buccal soft tissue anaesthesia from third molar to midline, conventional inf. alv. n. block is unsuccessful.

Contraindications – infection or acute inflammation in the area of infection, pats. with restricted mouth opening.

Gow gates technique– 1973 (mandibular n. block)

Land marks-

Extraoral- corner of mouth, lower border of the tragus, intertragic

notch

Intraoral – height of injection established by placement of

needle tip just below the mesiolingual cusp of max. 2nd molar,

penetration of soft tissue distal to 2nd molar at the same height.

Final position needle is just inferior to condyle and insertion of lateral

pterygoid.

Gained popularity – single needle penetration, relies on soft tissue

landmarks – differ from patient to patient

OTHER NAME Buccal nerve block or buccinator nerve block.TARGET AREA Buccal nerve as it passes over the anterior border of the ramusLAND MARKS External oblique ridge Retromolar triangle Distal to 3rd molarTECHNIQUE 1” 25 gauge needle is inserted in to the buccal mucosa just distal to the

lower 3rd molar. 0.25 to 0.5ml of solution is deposited.

Long buccal nerve block

Lingual nerve block – Area anaesthetised –

Anterior 2/3rd tongue, floor of mouth, lingual mucoperiosteum Only used singly to operate on tongue, floor of mouth

Buccinator / long buccal nerve blockArea anaesthetised –

Buccal mucosa & mandibular molar – mucoperiosteum Land marks

External oblique ridge, retromolar triangle

Mental & Incisive nerve blockArea anaesthetised

Mandibular hard & soft tissue – labial aspect with lower lip Landmarks

Bicuspid teeth, lower ridge of body of mandibleSupra & infra orbital notch Pupil of the eye

2 inch 22 gauge needle used & introduced slightly anteriorly & downwards

Mandibular nerveArea anaesthetised

Temporal region with auricle of ear & external auditory meatusTMJ, salivary glands Anterior 2/3rd of tongue Mandible – hard & soft tissue – midline

Landmarks mid point of zygomatic arch Zygomatic notch Cornoid process of mandible Lateral pterygoid plate

Extra Oral Technique

Indications

When need to anaesthetise entire mandibular nerve

Infection / trauma – makes terminal anaestheisa not possible

Diagnostic / therapeutic

The needle is pointed posteriorly & to a greater depth of 5

cms

Professor Kurt Thoma external approach

This technique is used when there is severe limitation of opening of the jaws in case of ankylosis of TMJ.

Anatomical land marks/ surface markings: Lowest point on the anterior border of the masseter Tragus Posterior border of the ascending ramus

Anterior border of masseter is located by clenching the teeth.The point is marked and a line drawn connecting this with the tragus of the ear.The mid point of this line shows the position of the mandibular foramen.

Needle Used 21 gauge,7 to 8cm long.

Definition

An anaesthetic complication may be defined as any

deviation from the normal expected pattern during or after

securing regional anaesthesia

2 typesLocal

Systemic

Complications

LOCAL COMPLICATIONSNeedle breakagePain on injectionBurning on injectionPersistent anaesthesia or paresthesia TrismusHematoma Sloughing of the tissue / soft tissue injuryFacial nerve paralysis

SYSTEMIC COMPLICATIONS

Toxicity

Idiosyncracy

Allergy

Anaphylactoid reaction

Syncope

Classification Primary / secondary

Primary – caused & manifested at time of anaesthesiaSecondary – manifested later

Mild / severeMild – exhibit slight change from normal expected pattern

- reverses itself without treatment Severe – manifests itself – pronounced deviation

- requires specific treatment

Transient / permanent Transient – is one that is severe at occurrence – no residual

effectsPermanent – residual effect; lasts for a life time even though it is

mild

Complications could be a combination of any of the above

mentioned types

Majority are either Primary Mild & Transient or Secondary Mild &

Transient

Complications

Attributed to solutions – toxicity, allergy, idiosyncrasy,

anaphylactoid reaction, local irritation

Attributed to technique / needle – syncope, muscle trismus,

pain, edema, hematoma

Cause –

Unexpected movement – patient (if patient movement is

opposite to path of needle insertion)

Multiple used needle

Defective manufacture of needles/barbed needles

smaller gauge – more likely to break

Needle breakage

Prevention Correct gauge – 25 gauge Long needles – prevent penetration till hub Not to redirect when in tissue

Management Patient – not to move – hand in the mouth – mouth openFragment visible – remove it Fragment not visible – inform patient – not necessary for

intervention immediately – Radiograph suggested

Precautions

Avoid bony contact

Avoid heavy pressure

Avoid movement of needle and patient

Causes – Careless injection technique Multiple used needle Rapid deposition

Problems –Pain – patient anxiety – unexpected movements

Prevention –Proper technique – sharp needles Enter topical anaesthetics Inject slowly – solution sterilized Check temperature of solution

Pain on injection

Causes Due to pH of solution 5 (LA) – 3 (LA+VC)Rapid injection Contamination Warm solution

ProblemspH disappears upon LA action – no residual effectContaminated solution other complications – trismus,

edema, paraesthesia

Burning on injection

Prevention

Slow injection – 1ml / minute

Cartridge stored at room temperature – away from containers with

alcohol / other agents

Causes Direct trauma to nerve – bevel of needle LA solution containing neurotoxic substance – alcoholInjection of wrong solutionHemorrhage / infection – near to nerve

ProblemPersistent anaesthesia – usually rare Biting / thermal / chemical insult – without patient

awareness When lingual nerve is involved – taste impaired

Persistent anaesthesia / paresthesia

Prevention Proper care & handling of dental cartridgeAdherence to injection protocol

Management Usually resolve in 8 weeks Periodic recall & check up of patients Persistence – consult neurosurgeon TENSRecall patient every 2 months for check up

Definition “difficulty in opening the jaws due to muscle spasm”

Causes Trauma – muscle / blood vessel Irritating solution hemorrhage InfectionMultiple needle puncturesLA have been known to have slight myotoxicity Excessive volume – distension of tissues

Problems Pain / hypomobility

Trismus

Prevention

Use of sharp, sterile, disposable needle

Aseptic technique

Practice atraumatic methods

Avoid repeated injections

Use minimum volume

Control infection

Management Heat therapy

Warm saline rinses, moist hot packs Analgesics

Aspirin, Codeine (30-60mg), muscle relaxantsInitial physiotherapy

Thrice a dayAntibiotic regime

Possibility of infection

“effusion of blood into extra-vascular spaces”Causes

Arterial & venous puncture – common in PSA & Inf. Alv. nerve blocks

Patients with bleeding disordersProblem

Bruise – may / may not be visible extra-orallyComplications – pain & trismus Swelling & discoloration

Prevention Knowledge of normal anatomy – proper technique Shorter needle – PSA, minimize the number of penetrationDiscard defective needles- barbed needles

Hematoma

Management Immediate – apply firm pressure 5-10minutes

Inf. Alv. Nr. Block – medial aspect of ramusInfra orbital, Mental, Incisive block – directly over foramen PSA – pressure on soft tissue with finger as posteriorly as tolerated by

patient – medial superior direction Patient to be reviewed after 24 hours, advice analgesics, cold application

upto 4-6 hours, warm- pack application next day

Comparitively rare complication

Instrument needle solution to be as aseptic as possible

Area & operative hands – cleaned

Avoid passing needle through infected area

Use disposable syringes

Infection

Causes Trauma during injection Infection, hemorrhage Allergy (Angioedema)Injection of irritating solution

Problems Pain & dysfunction Airway obstruction

Edema

PreventionProper care & handling of armamentarium Atraumatic injection technique Complete medical evaluation prior to injection

Management Trauma – resolve in few days without therapy Hemorrhage – resolve slowly 7-14 daysAllergy – life threatening, airway impairment – basic life

support, call medical help, Epinephrine – 0.3mg, Antihistamine, Corticosteroids

Total airway obstruction – Tracheostomy / Cricothyroidectomy

CausesEpithelial desquamation – topical anaesthesia – long time,

heightened sensitivity to LASterile abscess – secondary to prolonged ischemia – VC in

LA site – hard palate Problems

Pain & infection Prevention

Topical – for not more than 1-2 minutes VC – minimal concentration in solution

Sloughing of tissue

Management

Symptomatic – pain – analgesia

Epithelial desquamation – resolve few days

Sterile abscess resolve 7-10 days

CausesTrauma occurs – frequently mentally / physically challenged

children Primary cause – significantly longer duration of action

Problem Pain & swellingInfection of soft tissue

Prevention Cotton roll between lip & teeth Patient – guarded against eating / drinking Warning sticker

Soft tissue injury

CauseLA solution into parotid gland – usually while giving Inf

Alv Nr. Block, Akinosis technique Problem

Ipsilateral loss of motor control – Buccinator muscle Inability to raise the corner of Mouth, close Eye lid

Prevention Needle tip to contact bone, redirection of needle to be done

only after complete withdrawal

Facial nerve paralysis

Management Reassure the patient Resolves after action of LA is overEye patches to the affected – eye drops Contact lenses if any – removed

Toxicity / toxic overdose“Signs and symptoms that result from an overly high blood

level of a drug in various target organs and tissues”Predisposing factors

Age – any age Weight – greater the body weight greater is the amount of dose

tolerated before overdose reaction Sex – during pregnancy – renal function disturbed – females more

affected at this time Diseases – hepatic & renal dysfunction reduced breakdown Congestive heart failure – less liver perfusionGenetics – pseudocholinesterase deficient – toxicity - Ester LA

Systemic complications

Drug factors – Vasoactivity – vasodilation – increase in blood

concentration

More concentration – greater risk

Dose- smaller dose should always be preferred

Route of Administration – Intravascular – increased toxicity

Rate of injection – slower rate preferred

Vascularity of injection site – more vascular – greater absorption

Presence of Vasoconstrictor – with VC less absorption

Causes of toxicity – Biotransformation usually slow Drug – slowly eliminated by kidney Too large a total dose Absorption from injection site - rapid Accidental intra-vascular injection

Symptoms –CNS – cerebral cortical stimulation – talkative, restless,

apprehensiveness, convulsions Cerebral cortical depression – lethargy, sleepiness,

unconsciousness Medullary stimulation – increased B.P, Pulse rate, Respiration

Medullary depression – mild fall in B.P– severe cases drops to 0 , Pulse , Respiration – similar effect

Treatment Mild overdose reaction – slow onset reaction – > 5 mins administer

Oxygen (prevent acidosis), monitor vital signs, in case of convulsions – anti-convulsants (diazepam/midazolam infusion)

Slower onset - >15 mins – same procedure Severe overdose reaction – rapid onset – 1 minute –

unconsciousness with or without convulsion, patient in supine position, convulsions – protect hand, leg, tongue, BLS, administer anti-convulsant,use of vasopressor(phenyl ephrine) i.m if hypotensiom presists.

post seizure – CNS depression usually present

“It is an adverse response that is neither an overdose

nor an allergic reaction”

Common cause – some underlying

pathology/psychological /genetic mechanism

Psychotherapy may be helpful

Treatment – symptomatic ..ABC

Idiosyncrasy

“transient loss of consciousness that is caused due to cerebral

ischemia (neurogenic shock)”

Anxiety – increased blood supply to muscles, sitting position

2mm Hg, less pressure – cerebral arteries

Clinically pallor, light headedness, dizziness, tachycardia &

palpitation – may further lead to Unconsciousness

Treatment – discontinue procedure, supine position-

(trendelenburg position), deep breathing, O2 administration if

required, BLS

Syncope

“hypersensitive state acquired through exposure to a particular allergen reexposure to which produces a heightened capacity to react”

1 % of all reaction in LA is allergyPredisposing factors

Hyper sensitivity to ester more common-procaineMost of patients allergic to methyl paraben Recently allergy to sodium meta bi sulfide is also increasingPrecautions--- Ho of allergy to be recordedHo any asthmatic attack to be noted.Always better to test the patient for allergy before treatment.

Allergy

Consultation and allergy testingRefer doubtful cases for allergic skin test – sub cutaneous test most

sensitive.Informed consent that includes cardiac arest end death to be included.

Signs and symptoms of allergy.Dermatological------ urticaria –wheal and smooth elevated patch seen,

------angio oedema—localised swelling – face hands, common Respiratory– broncho spasm, respiratory distress,

dysnea, wheezing, flushing, tachycardia etc.

Laryngeal edema – type of angio neurotic oedema- life threating.Edema upper air way – laryngeal edema Lower air way affect broncioles- small.

Managementskin reactions-

Delayed – non life threatening - oral histamine blockers- 50 mg diphenhidramine,10 mg chlorpheniramine 3-4 days.

Immediate reaction—with conjunctivitis rhinitis- vigorous management.

0.3 mg epinephrine. IM 50 mg diphenhydramine Im medical help summoned.

Observe patient for minimum of 60 minOral histamine blockers for 5 days.Respiratory reaction –

patient in comfortable position. administer - oxygenAdmn epinephrine- bronchodilator Observe for 60 min , advise anti histamines to prevent relapse.Histamine blockers Im

Laryngeal edema-Patient position ,oxygen, broncho-dilator, iv anti histamines.If condition not improving cricothyrotomy - achieve patent air

way if necessary give artificial ventilation.

Patient with confirmed allergy status- if patient allergic to any one type of anesthetic ester /

amide use the other.Use histamine blocker like diphenhydramine as anesthetic. General anesthesia alternative method of pain control –

electric anesthesia / hypnosis.

Efforts have been made to improve to increase the ability of the anesthetic to cross intact skin

Attempts at making the experience more comfortable for the patients

The addition of hyalurodinase for deeper penetration than plain solutions

Local anaesthesia without the use of needlesExploring the possibility of reversing local anaesthesia at

the conclusion of dental procedure

Future trends in pain control

Centbucridine-5-8 time potency of lidocaineDoesn’t effect CNS or CVS except in large dosesWhen adminstered in overdose the drug acts as a true

stimulant of nervous system0.5% concentratio effective to 2% lignocaine

RopivacaineAmide anaesthetic similar to mepivicaine and bupvicaineHas greater margin of safetyDecrease cardiotoxicity as compared to others

Local anaesthetics

Its an oil in water emulsion containing high concentrations of lidocaine and prilocaine in base form

Provides enouh anaesthesia of intact skin to permit a venipuncture

Consists of 5% cream containing 25mg/g lidocaine and prilocaine respectively

Eutectic mixture of local anaesthetics

The adminsteration of local anaesthetic is usually

uncomfortable for the patient due to difference in PHAddition of sodium bicarbonate provides more rapid onset

of block, but it has decreased stabilityCO2 enhances diffusion, as it increase intracellular PH.

Unstable solution, has short life

PH alterations

First used described in 1949Provides more rapid onset of anaesthesiaDecrease duration of actionPossibility for allergic reactions

Use of hyaluronidase

Precursor for TENSIt acts by working at low frequency of 2 HzIt serotonin, endomorphin levels in bloodIt takes about 10 minutes for sufficient rise of blood levelsIt causes dilation of vesselsIt can be used to reverse partially of totally the effects of local

anaesthesiaCan be used in patients who have needle phobiaIts being used with increasing success in chronic TMJ painIts contraindicated in patients having cardiac pacemakers,

pregnancy, young and old age patients

Electronic dental anaesthesia

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