Local Anesthesia in Oral and Maxillofacial Surgery

LOCAL ANAESTHESIA
Dept Of Oral And Maxillofacial Surgery
VSPM’S Dental College, Nagpur
Presented by: Guided by:
Dr. Sapna K Vadera Dr. S.R.Shenoi
(P.G. Student) (Prof, Guide and H.O.D)

CONTENT
 Introduction
 History
 Definition
 Desirable properties
 Mode of impulse transmission
 Mechanism of action of L.A
 Factors affecting L.A action
 Classification
 Pharmacology

 Composition of L.A
 Systemic effects of L>A
 Topical Local anesthetics
 Containdications of L.A
 Vasocontrictors
 Clinical aspects
 Complications
 Future Directions
 Summary
CONTENT

INTRODUCTION
The efforts of human kind to find the means to control pain presents as
one of the greatest challenges in medicine. Pain is the phenomenon
wisely instituted by nature as a warning sign of a condition that may be
detrimental to our bodies.
Pain-free operating is of obvious benefit to the patient, it also helps the
operator as treatment can be performed in a calm, unhurried manner.
Joseph A et al,pharmacology of Local Anesthetics used in oral surgery ,Anesthesia:Oral and Maxillofacial clinics of North America;
Volume 25, Issue 3, Pages 453-466 (August 2013)

Local anaesthesia is the mainstay of pain control for outpatient oral surgical
procedures.
The ability to provide safe, effective local anaesthesia is the cornerstone of
clinical oral surgical practice. Its use and effectiveness depends on patient
considerations, the extent and duration of the procedure, the choice of drug and
technique, and the skill and experience of the practitioner.
INTRODUCTION

 Alcohol is the oldest known sedative. It was used in the ancient
Mesopotamia thousands of years ago.
 3400 B.c-The ‘Euphoric’ effect of Opium was discovered by
Summerians.
 Joseph Priestly(1733-1804)- discovered various gases like- nitrous
oxide, ammonia, oxygen.
HISTORY
Fonseca J Raymond,Chapter 3; Local aneasthetics,Vol 1: Anesthesia and pain control, Dentoalveolar Surgery, Practice Managment,
Implant Surgery, oral and maxillofacial Surgery,pg- 35-55,vol 1,2nd edition,2009, Saunders, Elsevier

 1801-Humphry Davy
- Anesthetic properties of nitrous oxide.
-Coined the term ‘laughing gas’.
 Dec 10,1844- Sir Horace Well attended lecture on ‘Chemical
Phenomenon’ by Gardner.(nitrous oxide)
HISTORY

 Dec 11,1844, Nitrous oxide was
administered to Dr. Horace Well,
rendering him unconcious & able
to have wisdom tooth extracted
without awareness of pain.
HISTORY
T. Y. Euliano,J. S. Gravenstein, Essential Anesthesia -From Science to Practice:United States of America by Cambridge University
Press, New York;2004: Introduction A very short history of anesthesia;p.1-4

 16th oct, 1846, ether was
administered by Sir William Morton
for the removal of mandibular
tumor.
 Experiment was published in Boston
daily journal. And led to the
discovery of Surgical anesthesia.
HISTORY

 1850’s Cocaine isolated, hypodermic needle developed
 1853 Chloroform used as anesthetic by Dr.John Snow
Chloroform being used as anesthesia
HISTORY

 1884 Carl Koller introduces cocaine into
medical practice
 1884 Halsted injected cocaine directly into
mandibular nerve and brachial plexus
Carl Koller
(1857 -1944)
William
Halsted
HISTORY

 1905 Procaine synthesized by Einhorn
 1948 First amide L.A (Lidocaine) synthesized by Lofgren
 1960 Mepivacaine
 1983 Bupivacaine
 2000 Articaine
HISTORY
Joseph A et al,pharmacology of Local Anesthetics used in oral surgery ,Anesthesia:Oral and Maxillofacial clinics of
North America; Volume 25, Issue 3, Pages 453-466 (August 2013)

DEFINITION
Loss of pain sensation over a specific area of the
anatomy without loss of consciousness but also to the
interruption of all other sensations ,including
temperature, pressure, and motor function.
Bennett Richard C.,Monheim’s Local Anesthesia and Pain Control in Dental Practice 7th edition page
no.2,CBS publishers and distributers

DEFINITION
Local anesthesia is defined as a loss of sensation in a
circumscribed area of the body caused by a
depression of excitation in nerve endings or an
inhibition of the conduction process in peripheral
nerves.
Malamed F Stanley,pg-1,Chapter I, Neurophysiology, Handbook of local anesthesia,Sixth edition,2013, An
imprint of Elsevier.

DESIRABLE
PROPERTIES
 Non irritating.
 No permanent alteration of nerve structure.
 Low systemic toxicity.
 Must be effective ( injected or applied locally)
 Short onset of anaesthesia.
 Long duration of action.

 Potency sufficient to give complete anesthesia.
 Free from producing allergic reactions.
 Stable in solution and readily undergo biotranformation in
the body.
 Sterile and capable of being sterlized.
DESIRABLE
PROPERTIES

MODE OF IMPULSE
CONDUCTION
Malamed F Stanley,pg-1,Chapter I, Neurophysiology, Handbook of local anesthesia,Sixth edition,2013, An imprint of Elsevier.

https://o.quizlet.com/hvC0vHrO8QZrEu-2pi6iXQ_m.png
MODE OF IMPULSE
CONDUCTION

MODE OF IMPULSE
CONDUCTION
http://hyperphysics.phy-astr.gsu.edu/hbase/biology/imgbio/actpot4.gif

http://cnx.org/resources/09ab17c9199ed6fb925c5fae201df4bcfac9b846/Figure_35_02_01.jpg
RESTING MEMBRANE
POTENTIAL

RESTING MEMBRANE
POTENTIAL
https://upload.wikimedia.org/wikipedia/commons/9/91/1218_Voltage-gated_Channels.jpg

 ACETYLCHOLINE THEORY
MECHANISM OF ACTION OF
LOCAL ANESTHESIA

 CALCIUM DISPLACEMENT
THEORY
LOCAL ANESTHESIA
https://wikispaces.psu.edu/download/thumbnails/42338579/image2.jpg?version=1&modificationDate=1248755004
000&api=v2

LOCAL ANESTHESIA
 SURFACE CHARGE THEORY

LOCAL ANESTHESIA
 MEMBRANE EXPANSION THEORY

LOCAL ANESTHESIA
 SPECIFIC RECEPTOR THEORY

RNH+
==== RN+ H+
low pH RNH+
> RN+
+ H+
high pH RNH+
< RN + H+
 Henderson Hasselbalch equation
Log base/acid = pH - pKa
DISSOCIATION OF
LOCAL ANESTHETICS

Mechanism of action of L.A molecule.
Anesthetic pKa of 7.9; tissue pH of 7.4
Effect of decreased pH on action of L.A
CLINICAL IMPLICATIONS

Factor Action affected Description
pKa Onset Lower pKa = more rapid onset of action, more uncharged molecules present to diffuse
through nerve sheath.
Lipid solubility Anesthetic potency Increased lipid solubility = increased potency
Protein binding Duration Increased protein binding allows anesthetic cations to be more firmly attached to protein
located at receptor sites, thus duration of action is increased
Non-nervous
tissue
diffusibility
Onset Increased diffusibility = decreased time of onset
Vasodilator
activity
Anesthetic potency
and duration
Greater vasodilator activity = increased blood flow to region = rapid removal of anesthetic
molecules from injection site, thus decreased anesthetic potency and decreased duration
FACTORS AFFECTING LOCAL
ANESTHETIC ACTION

CLASSIFICATION
 A) BASED ON DURATION OF ACTION:
1) Ultra Short acting anesthetics (less than 30 mins)
2) Short acting anesthetics(45 to 75 mins)
3) Medium acting anesthetics (90-150 mins)
4) Long acting anesthetics (180 mins or longer)

 B)SURFACE ANESTHETICS:
1)Soluble agents- E.g. Cocaine,
Lidocaine,
Tetracaine
2)Insoluble agents- E.g. Benzocaine,
Oxethazine
CLASSIFICATION

 C) BASED ON BIOLOGICAL SITE
1) CLASS A- Agents acting at receptor site on external
surface of nerve membrane.
E.g. Biotoxins
2) CLASS B- Agents acting at receptor sites on internal
surface of nerve membrane.
E.g. lidocaine
CLASSIFICATION

CLASSIFICATION

3) CLASS C- Agents acting by a receptor
independent, physicochemical agents.
E.g. Benzocaine.
4) CLASS D- Agents acting by combination of
receptor and receptor independent
mechanisms.
E.g. Articaine , Prilocaine.
CLASSIFICATION

Based on the chemistry
Esters Amides Quinilones
e.g. Articaine e.g. centbucridine
Lidocaine
Bupivacaine
Mepivacaine ,prilocaine
Benzoic Paraaminobenzoic
e.g. Butacaine e.g. Procaine
Cocaine Cloroprocaine
Benzocaine Propoxycaine
Tetracaine
Piperocaine

PHARMACOLOGY
 UPTAKE
• Degree of vasoactivity
• Vasodialating properties.
• Procaine is a potent vasodialator.
• Cocaine - only L.A having vasoconstriction action
• Vasodilatation -  the rate of absorption of L.A. into
the blood - duration and depth of anesthesia.

 ORAL ROUTE
• Except cocaine , L.A are absorbed poorly , if at all from the G.I.
tract
• 72% OF drug undergoes significant hepatic first pass effect.
 TOPICAL ROUTE
• Applied to intact skin- No anesthetic action.
• Damaged or sunburn skin- anesthetic effect
• EMLA-can be used on intact skin
PHARMACOLOGY

 INJECTION
• Rate of uptake after s.c., i.m., or i.v., is related to the
vascularity at the site of injection and vasoactivity of
the drug.
• I.V administration of L.A., is used for the management
of ventricular dsyrhythmias
PHARMACOLOGY
ROUTE TIME TO PEAK LEVEL
(MIN)
INTRAVENOUS 1
TOPICAL 5
INTRAMUSCULAR 5-10
SUBCUTANEOUS 30 - 90

 DISTRIBUTION
 Plasma conc. Of local anasthetics have significant
effect on potential toxicity of the drug.
PHARMACOLOGY
Blood level of anaesthetics depends on-
• 1.Rate at which drug is absorbed into CVS.
• 2. Rate of distribution of drug from vascular
compartment to tissues.
• 3.Elimination of drug through metabolic or excretory
pathway.

Esters - Hydrolyzed in plasma by enzyme Pseudocholinesterase
Procaine hydrolyzed by pseudo cholinesterase's
Para amino benzoic acid Diethylamine
Excreted unchanged urine further transformed-urine
• Atypical Pseudocholinesterase
PHARMACOLOGY

Amide
 Mostly gets metabolised in Liver
 Relative contraindication for patient with liver
dysfuction.
PHARMACOLOGY

EXCRETION
 KIDNEYS
 Esters readily undergo biotransformation-small conc.
in urine as parent compound compared to amide.
 Renal impairment- Relative contraindication
PHARMACOLOGY

COMPOSITION
 Local anesthetic drug –eg lignocaine . 21.3 mg/ml
 Vasopressor drug - eg adrenaline.1:80,000, 1:20,0000
 Reducing agent - eg Sodium meta bi sulfide. 0.4-0.5mg
 Preservative – eg Methyl paraben.0.1%
 For isotonicity – Normal Saline . 6mg
 Diluting agent – Distal water

SYSTEMIC EFFECTS
 CNS
• Easily crosses blood brain barrier.
• Causes CNS depression at low doses.
Blood level Effect
• 0.5-4μg/ml - Anticonvulsant action, direct depression
Increase in seizure threshold.
• 4.5-7μg/ml - Preseizure signs and symptoms caused by
depression of inhibitory neuron
• > 7.5μg/mi - Tonic clonic seizure.
entire blokage of inhibitory neuron.

 CVS
• Causes myocardial depression.
• Produces peripheral vasodialation and hypotension.
• Maximum dose-
4.4 mg/kg body weight (plain)
7 mg/kg body weight (with adrenaline)
SYSTEMIC EFFECTS

 RESPIRATORY SYSTEM
 Dual effect.
 Low doses- direct relaxant action on bronchial smooth
muscles.
 High doses- Respiratory arrest as a result of CNS
depression
SYSTEMIC EFFECTS

49
NotesMain unwanted effectsPlasma
half-life
Tissue
penetration
DurationOnsetDrug
Rarely used, only as spray for
upper respiratory tract
Cardiovascular and CNS
effects due to block of
amine uptake
~1hGoodMediumMediumCocaine
No longer usedCNS: restlessness,
shivering, anxiety,
occasionally convulsions
followed by respiratory
depression
CVS: bradycardia and
decreased cardiac output,
vasodilatation, which can
cause cardiovascular
collapse
<1hPoorShortMediumProcaine
(2-4%)
Widely used for local
anaesthesia .Also used i.V.
For treating ventricular
arrhythmias mepivacaine is
similar
Less tendency to cause
CNS effects
~2hGoodMediumRapidLignocaine
(lidocaine)
(2%)
Widely used because of long
duration of action.
Ropivacaine is similar, with
less cardiotoxicity
As lingocaine, but greater
cardiotoxicity
~2hModerateLongSlowBupivacaine
(0.5%)
Widely used, not for obstetric
analgesia because of risk of
neonatal
methaemoglobinaemia
No vasodilator activity, can
cause
methaemoglobinaemia
~2hModerateMediumMediumPrilocaine

TOPICAL
ANAESTHESIA
Insoluble in water- soluble in vehicle such as alcohol,
polyethylene glycol, propylene glycol, or carboxymethyl
cellulose – can be used for surface application
Advantage
1. By incorporating the anesthetic into a viscous liquid, a gel, or
an ointment, they remain in contact with the area for a longer
period, thereby increasing the duration of action.
2. poorly absorbed into the circulation,

 BENZOCAINE
• Poor solubility in water
• Poor absorption into CVS
• Remains longer at the site of application
• Prolonged use – localized allergic
reaction
• Availability as: Aerosol, Gel, Gel patch,
Ointment , Solution
TOPICAL
ANAESTHESIA

 EMLA
• Cream (Lidocaine 2.5% +Prilocaine 2.5%)
• Emulsion in which oil phase is eutectic mix of
lidocaine and prilocaine in a ratio of 1:1 by wt
• Supplied as 5g or 30 gm tube or as an EMLA
disc.
• Can be used to provide surface anesthesia o
intact skin.
• Contraindicated-pts with congenital idiopathic
methhemogloulinemia.
TOPICAL
ANAESTHESIA

 LIGNOCAINE
• Lidocaine base- poorly soluble in
water-5%, used on ulcerated,abraded
and lacerated wound.
• Lidocaine hydrochloride- water soluble
-2%.
• Aerosol spray, gel, ointment, patch,
solution.
• Topical form-20mg/ml
TOPICAL
ANAESTHESIA

CONTRINDICATIONS
 ABSOLUTE
• Local anaesthetic allergy
• Bisulfite allergy
 RELATIVE
• Atypical plasma cholinesterase
• Methemoglobinemia
• Significant cardiovascular, liver or renal disease.

VASOCONSTRICTOR
 Need for vasoconstrictor
• ↑ absorption of L.A into CVS → removal from injection site
• Rapid diffusion of L.A from inj site → ↓ duration of action &
depth of anesthesia.
• Higher plasma level of L.A → ↑ risk of toxicity
• ↑ bleeding at inj site.

 Addition of vasoconstrictor
• Constriction of blood vessels → ↓ tissue perfusion
• Slow absorption into CVS → low anesthetic blood level → ↓
risk of toxicity.
• Higher volume of L.A around nerve → ↑ duration of action
• ↓ bleeding at inj site
VASOCONSTRICTOR

 Adrenergic system- α and β receptors.
 β - β1 and β2
 α – α1 and α2
 β1 - Heart
 β2 - Vascular beds of skeletal muscle and pulmonary
vasculature.
 α1 - peripheral vasculature.
 α2 - CNS
SYSTEMIC EFFECTS

Vasoconstrictor Β1 selectivity Β2 selectivity Relative α
potency
Epinephrine 50% 50% 100%
Norepinephrine 85% 15% 25%
Levonordefrin 75% 25% 15%
Phenylephrine 95% 5% 5%
SYSTEMIC EFFECTS

CLINICAL ASPECTS
Max dose of lidocaine without adrenaline is = 300mg
Max dose of LA with adrenaline = 500mg
Max safe dose of adrenaline =0.2mg/visit
2% Lignocaine= 2g in 100 ml
2000mg in 100 ml
20 mg in 1ml - 1 mg= 1/20
500mg=1/20500= 25ml can be given safely for a normal pt
Adrenaline present in our vials is in conc. of 1:200,000
1ml=1/200,000=0.005mg
0.005mg-1ml
As MRD-0.2mg , so for normal pt- 0.2 mg=1/0.0050.2= 40ml of LA can be
administered safely

COMPLICATIONS
 LOCAL
 SYSTEMIC

 [A] LOCAL COMPLICATIONS:-
 Needle breakage
 Pain on injection
 Burning on injection
 Parasthesia or persistent anesthesia
 Trismus
 Hematoma
 Infection
 Sloughing of tissues
 Soft tissue injury
 Facial nerve paralysis
 Post anesthetic intra-oral lesions

 B. Systemic
 Drug allergy
 Toxicity
 Cvs and respiratory complications

 1.Needle breakage
 Use of larger needles for nerve blocks.
 Use longer needles when sufficient
depth injections are to be given.
 As hub is the weakest part, avoid
inserting a needle into the tissues to its
hub.
 Do not redirect the needle, instead
withdraw almost completely and then
redirect it.

 2. PAIN ON INJECTION
 Proper technique.
 Usage of topical anesthesia.
 Slowly injecting local anesthetic.
 Correct temperature of L.A.
 Management:
 No Management generally required only reassurance is
given to the patient.

3. BURNING ON INJECTION:
 pH of solution.
 Rapid injection of L.A. to adherent tissues like palate.
 Contamination of local anesthetic solution.
 Warmed solution.
Prevention:
 Slowing of injection should help.
 Ideal rate : 1 ML per minute.
 Max. rate : 1.8 ML per minute.
 Storage of solution at room temperature.

4. TRISMUS
Cause:
 Most common : Trauma to muscles or blood vessels in infratemporal
fossa.
 Usually, injury to medial pterygoid muscles, also superior constrictor
of pharyna and masseter muscles can cause trismus.
 L.A. into which alcohol or cold sterilizing solutions have diffused, may
produce irritation and cause this problems.
• The injection of L.A. either intramuscularly or supramuscularly lead to rapidly
progressive necrosis of exposed muscle fibres.
• Haemorrhage.
• Low grade infection.
• Multiple needle penetration at the same site.
• Excessive volumes of solution deposited in a restricted area produces
distention causing trismus.

 Prevention:
 Use of sharp, sterile, disposable needles.
 Proper care for and handle dental L.A. cartridges.
 Use aseptic technique.
 Practice atraumatic insertion and injection technique.
 Use minimum effective volumes of solution.
 Avoid repeat injections and multiple insertion in the same
area.

 Management:
 Heat Therapy
 Warm saline rinse
 Analgesics:
 Muscle relaxant
 Physiotherapy consisting of opening and closing the mouth as well
as lateral exursion of mandible
 Complete recovery : About six weeks(range: 4-20 weeks)

1. Toxicity
 Too large dose of local anesthetic drug
 Unusually rapid absorption of the drug
 Accidental intravenous injection
 High concentration of drug
 Unusually slow biotransformation
 Slow elimination
 Injection of solution In highly vascular area without the
addition of vasoconstrictor

Early symptoms
 On cerebral cortex
a. Talkativeness
b. Restlessness
c. Apprehension
d. disorientation
e. Tremors of hands and feet
 On Medulla
a. Lethargy
b. Sleepiness
c. Drowsiness
d. Muscular weakness

Late symptoms
 On cerebral cortex
a. Increased blood pressure
b. Increased pulse rate
c. Increased respiratory rate
d. Generalized seizure
 On medulla
a. Decrease blood pressure
b. Decrease pulse rate
c. Decease heart rate
d. Respiration depression
e. Unconsciousness

Cortical depression
a. Unresponsiveness
b. Unconsciousness
c. Stupor
d. coma
Medullary depression
a. Depression of cardiovascular function
b. Respiratory depression
c. hypoxia

Prevention
 Pre analgesic evaluation of the patient
 Use the weakest possible concentration of drug
 Use vasoconstrictor whenever possible
 Use of least possible volume
 Aspirate before injection
 Slow injection
 Monitor the patient carefully after injection

In slow onset (5min after administration)
-Position (supine with feet elevated slightly)
-Assess and maintain airway
-Assess breathing
-Assess circulation
-Definitive care
1. Reassure the patient
2. Oxygen administration to prevent acidosis
3. Monitor and record vital signs
4. Diazepam administered slowly intravenously (5mg/min)
Treatment

 In severe overdose reaction (rapid onset)
-Assess breathing
-Assess circulation
-Definitive care in the presence of tonic clonic seizure
1.Protect patient’s arms ,legs and head.Loosen tight clothing.
2.Administer oxygen
3. Administer anticonvulsant –IV Diazepam at rate 5mg/min
or midazolam 1mg/min.

 Postseizure (postictal) phase
-Assess breathing
-Assess circulation
-Definitive care
1.Administer IV fluids
2.Allow the patient to rest until recovery

Drug Allergy may be defined as a specific type of
hypersensitivity to drug or chemical compound
brought about by an alteration in the body’s reaction
to an antigenic substance.
2. Allergy

Type Mechanism Principle
Antibody
Or cell
Time of
reaction
Clinical
examples
I Anaphylaxis (Immediate,
Homocytochromic , antigenic
induced , antibody mediated)
IgE Sec to min -Anaphylaxis
-Atopic bronchial asthma
-Allergic rhinitis
-Urticaria
-Angioedema
-Hay fever
II Cytotoxic(antimembrane) IgG
IgM
- -Transfusion reaction
-Autoimmune hemolysis
-Hemolytic anemia
-Certain drug reaction
III Immune complex(Serum sickness
like)
IgG 6-8 hrs -Membranous
glomerulonephritis
-Serum sickness
-Acute Viral hepatitis
Classification of allergic diseases

Type mechanism Principle
antibody
Time of
reaction
Clinical examples
IV Cell mediated (delayed) or
Tuberculin type response
- 48 hrs -Allergic contact dermatitis
-Infectious
granulomas(tuberculosis
,mycoses)
-Tissue graft rejection
-Chronic hepatitis
Classification of allergic diseases

1. Early phase –Skin reactions
a. Pt complains of feeling sick
b. Intense itching
c. Flushing(erythema)
d. Urticaria over the face and upper chest
e. Angioedema
2. GI disturbances related to smooth muscle spasm
a. Severe abdominal cramps
b. Nausea and vomiting
c. Diarrhea
Typical Reaction Progression of Generalized
Anaphylaxis

3. Respiratory Symptoms
a. Respiratory distress
b. Dyspnea
c. Wheezing
d. Flushing
e. Cyanosis
f. Perspiration
g. Tachycardia
h. Possible laryngeal edema
4. Cardiovascular system
a. Pallor
b. Lightheadedness
c. Tachycardia
d. Hypotension
e. Cardiac dysrhythmias
f. Unconsciousness
g. Cardiac arrest
Typical Reaction Progression of Generalized
Anaphylaxis

Recognize problem
( itching, hives, edema,flushed skin)
Discontinue dental treatment
Activate office emergency team
P –Position patient comfortably
A-B-C-Assess and perform basic life support as needed
Activate emergency medical service if recovery not immediate
D- Provide definitive management as needed
In more generalized slow onset skin reaction
Observe patient Administer oral Administer IM or IV +oral
histamine blocker histamine blocker every 4-6 hrly
50 mg diphenhydramine or 10mg
Chlorpheniramine
Medical consultation prior to future dental care
Management of delayed onset ,allergic skin reaction

Recognize problem
( itching, hives, edema,flushed skin ,conjunctivitis ,Rhinitis)
Discontinue dental treatment
Activate office emergency team
P –Position patient comfortably
A-B-C-Assess and perform basic life support as needed
Activate emergency medical service if recovery not immediate
D- Provide definitive management as needed
management of more rapid onset allergic reaction is predicted on presence or absence of signs of
respiratory or cardiovascular involvement
(Monitor vital signs)
(no CVS or respiratory involvement) (CVS or respiratory involvement)
Administer Oral or IM
Histamin blocker (50 mg diphenhydramine or P-reposition patient
10 mg chlorpheniramine
Allow recovery and discharge patient
Management of rapid onset ,allergic skin reaction

CVS involvement No CVS involvement
Hypotension
Supine position with legs elevated Comfortable
Administer Oxygen
Administer 0.3 ml epinephrine IM every 5-20 min .as needed to a total of 3
doses.
Summon medical assistance
Administer histamine blocker 50 mg diphenhydramine (IM)
Permit recovery and discharge of patient

FUTURE DIRECTION
OF LOCAL
ANESTHETICS

BUFFERED LOCAL
ANESTHESIA

MICROPARTICULATE
FORMULATIONS

REVERSAL OF LOCAL
ANESTHESIA
 Formulation of phentolamine mesylate (OraVerse)
 a-adrenergic antagonist
 1.7 ml cartridges containing 0.4 mg phentolamine
mesylate.

ELECTRONIC DENTAL
ANESTHESIA

SINGLE TOOTH
ANESTHESIA/COMPUDENT
Orrett E. Ogle,et al Advances in Local Anesthesia in Dentistry Dent Clin N Am 55 (2011) 481–499

INTRAOSSEOUS INJECTION,
STABIDENT
Orrett E. Ogle,et al Advances in Local Anesthesia in Dentistry Dent Clin N Am 55 (2011) 481–499

SUMMARY
Local anesthesia remains the foundation of pain control in dentistry
especially when combined with moderate-deep sedation for invasive
and painful procedures in the contemporary oral and maxillofacial
surgical model.
Dentistry has never had the choice of local anesthetic drugs and
techniques that can be tailored to individual patients and procedures
as are available today

Local anesthetics remain the safest and most effective drugs in
medicine and dentistry to relieve introperative and
postoperative pain.
It is only with a through understanding of pharmacology and
anatomy that clinicians have the basic clinical foundation to
enhance the care of patients.
SUMMARY

Local Anesthesia in Oral and Maxillofacial Surgery

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