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LOCAL ANESTHESIA
IN DENTISTRY

1
CONTENTS
• Definition
• History
• Classification
• Properties of L.A
• Nerve physiology
• Mechanism of action
• Specific local anesthetics
• Local anesthetic techniques
• Maxillary
• Mandibular

• Complications
• Local
• Systemic
• Post operative

2
Definition of L.A
Local anaesthesia has been 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”.
(According to Moheims)

3
HISTORY

4
Early History of Regional Anaesthesia
 Koller and Gartner
report local anesthesia
(1884).
 In 1884,Koller was the
first, to use cocaine for
topical anaesthesia in
ophthalmological
surgery.
Carl Koller
1857 -1944
5
Early History Of Regional Anaesthesia
 1885 Halsted injects
cocaine directly into
mandibular nerve and
brachial plexus

William S. Halsted
6
Common Uses Of Local Anesthetic :

Excision

Dermatology

Spinal Anaesthesia

Dentistry

7
CLASSIFICATION

8
BASED ON SITE

Topical

Cocaine, Prilocaine, Lignocaine

Injectable

Lignocaine, Mepivacaine

9
BASED ON CHEMICAL STRUCTURE

ESTERS
• Cocaine
• Procaine
• Benzocaine
• Tetracaine

AMIDES
• Articaine
• Bupivacaine
• Lidocaine
• Mepivacaine
• Prilocaine
• Ropivacaine

10
BASED ON DURATION OF ACTION
Ultra Short
• 2% lignocane without vasoconstrictor
Duration
Short
duration
Intermediate
duration

Long duration

• Procaine,
• 2 % Lignocaine with 1:1,00,000
Epinephrine
•
•
•
•

Articaine
Mepivacaine
Prilocaine
2 % Lignocaine with 1:2,00,000
Epinephrine
• Bupivacaine
• Etidocaine
• 5 % Lignocaine with 1:2,00,000
Epinephrine

11
DIFFERENCES
AMIDES
• longer lasting analgesia.
• Produce more intense
analgesia.
• Rarely cause hypersensitivity
reactions- no cross reactivity
with ESTER L A s.
• Not hydrolyzed by Plasma
Cholinesterase, more slowly
destroyed by liver microsomal
P450 enzymes.

ESTERS
• Short duration of action
• Less intense analgesia
• Higher risk of
hypersensitivity ESTER
linked LA s are rarely used.
• Hydrolyzed by Plasma
Cholinesterase in blood.
• Rarely used for Infiltration
anesthesia
• But useful for topical
anaesthesia on mucous
membranes.

12
Properties of L.A
• It should not be irritating to the tissue to which it is
applied.
• It should not cause any permanent alteration of nerve
structure.
• Its systemic toxicity should be low.
• The time of onset of anaesthesia should be as short as
possible.
• The duration of action must be long enough to permit
completion of the procedure yet not so long as to
require an extended recovery.
According to Beneett an ideal properties of
local anaesthesia
• It should have potency sufficient to give complete
anaesthesia without the use of harmful concentrated
solutions.
• Its should be relatively free from producing allergic
reactions.
• It should be stable in solution &readily undergo
biotransformation in the body.
• It should either be sterile or capable of being
sterilized by heat without deterioration.
NERVE PHYSIOLOGY
AND MECHANISM OF
ACTION

15
Electrophysiology of nerve conduction
• Electrical events that occurs within a nerve during the
conduction of an impulse.
• A nerve possesses a resting potential. This is a
negative electrical potential of -70 mV that exists
across the nerve membrane, produced by differing
concentrations of ions on either side of the
membrane.
• A stimulus excites the nerve, in following sequence
of event –

16
Step 1a – an initial phase of slow
depolarization. The electrical
potential within the nerve becomes
slightly less negative.
1b –falling electrical potential
reaches a critical level, it give result
of rapid phase of depolarization.
This is termed threshold
potential, or firing threshold.
1c –this phase of rapid depolarization
results in a reversal of electrical
potential across the nerve
membrane. electrical potential
0f+40 mV exists on the interior of
the nerve cell.
17
Membrane excitation • Depolarization – Excitation of nerve segment leads to
an increase in permeability of the cell membrane to
sodium ions. The rapid influx of sodium ions to the
interior of the nerve cell causes depolarization of the
nerve membrane from its resting level to its firing
threshold of approx. -50 to -60 mV. Exposure of the
nerve to local anesthetic raises its firing threshold.

18
Repolarization • The action potential is terminated when the
membrane repolarizes. This is caused by the
inactivation of increased permeability to sodium. In
many cells potassium also increases, resulting in the
reflex of K+, and leading to more rapid membrane
repolarization and return to its resting potential.

19
Mechanism of action
A.
1.
2.
3.
4.
5.

Theories for mechanism of action of L.A are :
The Acetylcholine theory.
The calcium displacement theory.
The surface charge theory.
Membrane expansion theory.
Specific receptor theory.

20
THE ACETYLCHOLINE THEORY
• Started that acetylcholine was involved in nerve
conduction in addition to its role as a neurotransmitter
at nerve synapses .

THE CALCIUM DISPLACEMENT THEORY
• L.A nerve block was produced by the displacement
of calcium from some membrane site that controlled
permeability to sodium. That varying the
concentration of calcium ion bathing a nerve does
not affect local anesthetic potency has diminished
the credibility of this theory.
21
Membrane expansion theory
• Stated that L.A molecules diffuse to hydrophobic
regions of excitable membranes, producing a general
disturbance if the bulk membrane
structure, expending some critical regions in the
membrane & preventing an increase in the
permeability to sodium ions.

22
Specific receptor theory by strichartz 1987
 Drug molecules bind to specific receptors present
on the external or internal axoplasmic surface of
sodium channels & by acting directly on
them, decrease or eliminate permeability to Na2+
leading to interruption of nerve conduction.

23
B. Local anaesthesia act in following ways:

Displacement of calcium ions from the sodium channel
receptor site, which permits

Binding of the L.A molecules to the receptor site,
which thus produce

Blockade of the sodium channel

,

24
Decrease in sodium conductance, which lead to

Depression of the rate of electrical depolarization

Failure to achieve the threshold potential level, along
with
Lack of development of propagated action
potentials, which is called

Conduction blockade

25
CLINICAL
PROPERTIES OF
LOCAL ANESTHETICS

26
pKa
• ONSET = pKa
• pKa = pH at which 50% of drug is ionized
• LA’s <50% exists in the lipid soluble in non
ionized form
• Only the non ionized form crosses into the nerve
cell

27
pH influence
• Usually at range 7.4 -8.5
• Decrease in pH shifts equilibrium toward the
ionized form, delaying the onset action.
• Lower pH, solution more acidic, gives slower
onset of action.
Presence of Pus and inflammation will retard the
action of LA. ( probably low acidic pH) therefore
• LA are more ionized - don’t penetrate very well.
• Decreased ability of LA to produce effects.

28
VASODILATOR ACTIVITY
• Affects Anesthetic potency and duration
• Greater vasodilator activity = increased blood flow to
region =rapid removal of anesthetic molecule from
injection site ; thus decreased anesthetic potency and
duration.

29
Composition
Local Anesthetics solution contains :
1. Local anaesthetic agents –
Ester linkage – procaine, cocaine, tetracaine.
Amide linkage – lignocaine , prilocaine
, mepivacaine,
bupivacaine .

2. Vasoconstrictors –
Adrenaline – a synthesis substance similar to that
secreted in human body.

30
Advantages –
• Reduces toxic effect by retarding the absorption of the
constituents.
• It increases the depth & duration of anaesthesia and
produces bloodless field for surgical procedure.
3. Reducing agent- Sodium bimetasulphite.
• small quantity in the solution to prevents oxidation
of the vasoconstrictors as they are unstable in
solution especially on exposure to sunlight.

31
4. Preservative – Caprylhydrocupeinotoxin
• it helps to maintain sterility of the solution & also
increases its self life.
5. Fungicide – Thymol
• to prevents proliferation of minute fungi which
causes cloudiness of the solution.
6.Vehicle – Ringer’s solution.
• In which all constituent dissolves to minimizes
discomfort during injection of L.A.
32
DOSES AND DURATION OF BLOCK
Drug

Conc.

Total
dose(mg)

Dose(mg/k
g)

Duration of
block

Procaine

1-2%

400

6

30-60 min.

Lidocaine

0.5-2%

300

4.5

60-120 min.

Bupivacaine

0.25-0.5%

90

1.4

180-360
min.

Tetracaine

0.25-0.5%

80

1.3

180-480
min.

33
UNDESIRED EFFECTS
OF LOCAL
ANESTHETICS

34
CENTRAL NERVOUS SYSTEM
• CNS Stimulation:
(More sensitive than cardiac)
• Dose-related spectrum of effects
and all effects are due to depression
of neurons.
• First an apparent CNS stimulation
(convulsions most serious)
• Premonitory signs include: ringing
in ears, metallic taste, numbness
around lips
• Followed by CNS depression
(death due to respiratory
depression)
Cocaine - Euphoria
Lidocaine - Sedation even at nontoxic doses.
35
CARDIOVASCULAR SYSTEM
• ARRHYTHMIAS:
• Decrease cardiac excitability
and contractility
• Decreased conduction rate
• Increased refractory rate
(bupivicaine)
• ALL can cause arrhythmias
if conc. is high enough
Note: cocaine is
exception......it stimulates
heart

• HYPOTENSION: Arteriolar
dilation is a result of:
• Direct effect (procaine and
lidocaine have most effect)
• Block of postganglionic
sympathetic fiber function
• CNS depression
• Avoid by adding
vasoconstrictor to the
preparation
• Cocaine is exception:
produces vasoconstriction.
36
• Hypersensitivity:
• Common with ester-linked LA
• Rashes, angio-edema, dermatitis and rare anaphylaxis
• Sometimes typical asthmatic attack
• Neurotoxicity:
• LA can cause concentration-dependent nerve damage to
central and peripheral NS
• Mechanism(s) not clear
• Permanent neurological injury is rare
• May account for transient neurological symptoms.
37
SPECIFIC LOCAL
ANESTHETICS

38
PROCAINE (NOVOCAINE)
• First synthetic injectable local anesthetic.
• Produce the greatest vasodilation of all currently used
local anesthetics.
• Slower clinical onset (6-10 min.)
Used for
• Soft tissue anesthesia for 15- 30 min.
• Systemic toxicity negligible because rapidly destroyed
in plasma
• Max. recommended dose for peripheral nerve block
1000mg
39
LIDOCAINE

1:200000 conc. is safest
As well as potent

• The most popular contains
epinephrine 1:100,000 and
provides good anesthesia for
healthy patients.

• Lidocaine with epinephrine
1:50,000 is used for
hemostasis, but because of the
rebound effect noted earlier, it
should be used sparingly.
40
Lidocaine ( Xylocaine )
• Most widely used Amide linked LA and most
versatile anaesthesia.
• Has variety of applications like Local, nerve
block, topical.
• When used locally action starts within 3 min., more
profound anesthesia, has longer duration of action
and greater potency.
• Overdose causes muscle
twitching, convulsions, cardiac arrhythmias, fall in
BP, coma, respiratory arrest.
• Most popular anti arrhythmic drug
41
Maximum Dose of Lignocaine
• Without Vasoconstrictor :
4.4 mg / kg of body wt = 300 mg in a 70 kg individual
= 15 ml of solution
• With Vasoconstrictor :
7.2 mg / kg of body wt = 500 mg in a 70 kg individual
= 25 ml of solution
• For children with VC 3.2 mg/kg

42
MEPIVACAINE
• 3% Mepivacaine without a
vasoconstrictor is used as anesthetic
for patients who cannot take a
vasoconstrictor or for short
procedures.
• It is appropriate for pedodontics and
for use on geriatric patients.
• 2% Mepivacaine with
vasoconstrictor provides pulpal
anesthesia that is similar to lidocaine
with epinephrine, but hemostasis is
not as intense.
43
PRILOCAINE
• The action of prilocaine plain varies
with the area injected (longer with a
nerve block).
• Prilocaine with vasoconstrictor gives
good anesthetic effect and uses a
1:200,000 concentration of
epinephrine.

44
ARTICAINE
• Articaine is a newer anesthetic
typically given in a 4% solution with
1:100,000 epinephrine.
• However, concern has arisen about
its potential for tissue necrosis and
persistent nerve parasthesia.

45
BUPIVACAINE
• Bupivacaine is used when pulpal
anesthesia is desired for longer
appointments and when
postoperative pain is anticipated.
• Bupivacaine is not
recommended for children or
handicapped patients because of
the increased risk of
postoperative injury (chewing
on a numb lip).

46
• Available as 0.5% solu.1:2,00,000 (vc)
• Indication- Pulpal anesthesia >90- min.


Full mouth reconstruction.



Extensive oral and maxillofacial surgery, periosurgery.

• Duration –Pulpal - 90- 180 min.

Soft tissue- 4-12 hrs.
• Contra indication- Burning sensation at site of injection, in
children anticipating self trauma .

47
POSTPROCEDURAL PAIN
CONTROL
• Prescribe nonsteroidal antiinflammatory agents prior to the
appointment.
• Use an intermediate duration
anesthetic for the procedure.
• Inject bupivacaine just prior to the
patient's dismissal .
• Direct the patient to take oral
analgesics for a certain number of
days following the procedure.
48
LOCAL
ANAESTHESIA
TECHNIQUE

49
TOPICAL
• The local anesthetic solution is applied on the mucous
membrane or skin, through which it penetrates to
anesthetize superficial nerve endings.
e.g. - Ointments containing
5%lignocaine
-Viscous solution containing
lignocaine hydrochloride
-Ethyl chloride sprays
50
EMLA = Eutectic Mixture of Local Anesthetics
• Eutectic = two solid substances mixed together in equal quantities
by weight form a eutectic mixture
• The melting point of the mixture is lower than the melting points
of the individual components
• EMLA = lidocaine and prilocaine becomes an oily mixture

51
INFILTRATION
• Small terminal nerve endings in the area of dental treatment are
flooded with local anesthetic.
• The treatment is done in the same place where anesthetic is
deposited.

52
FIELD BLOCK
• Local anesthetic solution is deposited near the larger
terminal branches so the anesthetized area is well
circumscribed.
• Incision or treatment is done at an area away from the
site of injection of local anesthetic.

53
NERVE BLOCK
• Local anesthetic solution is deposited close to the main
nerve trunk, usually at a distance from the site of
operative intervention

54
SUPRA PERIOSTEAL INJECTION

55
POSTERIOR SUPERIOR ALVEOLAR
NERVE BLOCK
Nerves anaesthetized –
posterior superior alveolar and
branches.
Areas anaesthetized –
Pulps of the maxillary
third, second and first molars.
Buccal periodontium and bone
overlying these teeth.

56
Indications:
• When treatment involves two or more maxillary
molars.
• When supraperiosteal injection has proved
ineffective.
Contraindication:
• When the risk of hemorrhage is too high.

57
• Procedure –
• Insert the needle slowly in upward, inward and backward
direction.
• Upward: superiorly at 45-degree angle to the occlusal plane.
• Inward: medially toward the midline at a 45-degree angle to the
occlusal plane.
• Backward: posteriorly at a 45-degree angle to the long axis of the
second molar.

58
Sign and symptoms:
• Subjective: none
• Objective: absence of pain during therapy.
Complications:
• Hematoma
• Mandibular anesthesia

59
MIDDLE SUPERIOR ALVEOLAR
NERVE BLOCK
Nerves anaesthetized – middle
superior alveolar and terminal
branches.
Areas anaesthetized –
Pulps of the maxillary first
and second
premolars, mesiobuccal root
of the first molar.
Buccal periodontal tissues and
bone over the same teeth.
60
Indications –
• When infraorbital nerve block fails to provide pulpal
anaesthesia distal to the maxillary canine.
Indicated for both maxillary premolars only
Contraindication:
• Infection or inflammation in the areas of injection.
Sign and symptoms:
• Subjective: upper lip numb
• Objective: no pain during treatment
61
INFRAORBITAL NERVE BLOCK
Nerve anaesthetized –
•Anterior superior alveolar
•Middle superior alveolar
•Infraorbital nerve
a) inferior palpebral
b) Lateral nasal
c) Superior labial

62
Indications • Involving more than two maxillary teeth and their
overlying buccal tissues
• Infection or inflammation
• When supraperiosteal injections have been ineffective
because of dense cortical bone
Contraindications –
• Discrete treatment areas
• Hemostasis of localized area
63
64
Sign and symptoms –
Subjective – tingling and numbness of the lower
eyelid, side of the nose and upper lip
Objective – no pain during procedure

65
GREATER PALATINE NERVE BLOCK
Nerves anaesthetized – Greater palatine
Area anaesthetized – posterior portion of hard
palate, anteriorly upto first premolar and medially to the
midline

66
Indications –
• For pain control during periodontal or oral surgical
procedures involving the palatal soft and hard tissues.
Contraindications –
• Inflamation or infection at the injection site
• Smaller area of therapy.

67
Sign and symptoms –
• Subjective – numbness in the posterior portion of the
palate
• Objective – no pain during dental therapy.
Complications –
• Few of significance
• Ischemia and necrosis of soft tissues when highly
conc. vasoconstructing solution used for homeostasis
over a prolonged period.
• Hematoma is possible but rarely occur.
68
NASOPALATINE NERVE BLOCK
Nerves anaesthetized – nasopalatine nerves bilaterally.
Area anaesthetized – anterior portion of the hard palate
from the mesial of the right first premolar to the mesial
of the left first premolar.

69
Indications –
• For pain control during periodontal or oral surgical
procedures involving palatal soft and hard tissues.
• For subgingival restoration and insertion of matrix
bands (subgingivally).
Contraindications –
• Inflammation or infection at the injection site
• Smaller area of treatment i.e. one or two teeth
• Alternatives • Local infiltration into specific regions
• Maxillary nerve block.
70
Techniques –
• Target area – incisive foramen, beneath the incisive
papilla.
• Landmarks – central incisor and incisive papilla.

71
Signs and Symptoms –
• Subjective – numbness in the anterior portion of the
palate.
• Objective – no pain during dental treatment.
Complications –
• Necrosis of soft tissue occurs when highly concentrated
vasoconstriction solutions (norepinephrine).
• Interdental papilla tenderness are present sometimes
after few days of injection.

72
ANTERIOR MIDDLE SUPERIOR ALVEOLAR
NERVE BLOCK
Nerves anaesthetized –
•Anterior superior nerve
•Superior alveolar nerve, when present Sub neural dental
nerve plexus of the anterior and middle superior alveolar
nerves.
Areas anaesthetized –
•Pulpal anaesthesia of the max. Incisors, canines, and
premolars.
•Buccal attached gingival of the same teeth.
•Attached palatal tissues from midline
to free gingival margin on the
associated teeth.

73
Indications –
• Is easier performed with a CCLAD system.
• When maxillary anterior teeth involves any dental
procedure.
• When supraperiosteal injection is failed because
of dense cortical bone.
Contraindications –
• Patients with usually thin palatal tissues.
• Procedures requiring more than 90 min.

74
Signs and Symptoms –
Subjective • A sensation of firmness and numbness is immediately on
palatal tissue.
• Numbness of the teeth and associated soft tissues
Objectives –
• Blanching of the soft tissues of the palatal and facial
attached gingival from central incisor to premolar region.
• No pain during dental procedure.
Complications –
• Palatal ulcer at injection site after 1 to 2 days
postoperative.
• Density of injection site causing squirt – back of
anaesthetic and bitter taste.
75
MAXILLARY NERVE BLOCK
Nerves anaesthetized –
• Maxillary division of the trigeminal nerve

76
Indications –
• Pain control during extensive oral surgical, periodontal, or
restorative procedures.
• When tissue inflammation or infection precludes the use of other
regional nerve blocks.
Contraindications –
• Inexperienced administrator
• Paediatric patients
• Uncooperative patients
• Inflammation or infection of tissues overlying the injection site.

77
Procedure –
• Locate the greater palatine foramen at the region of the
second molar.
• It mostly located at the distal aspect of the second
molar.

78
Signs and symptoms –
Subjective –
• Sensation of numbness in the teeth and buccal and
palatal soft tissues on the side of injection.
Objectives –
• No pain during dental therapy.

Complications –
• Hematoma develops rapidly if the maxillary artery is
punctured during maxillary nerve block.

79
INFERIOR ALVEOLAR NERVE BLOCK
Nerves anaesthetized –
• Inferior alveolar, a branch of the posterior
division of he mandible
• Incisive
• lingual

80
Indication –
1. Multiple mandibular teeth in one quadrant.
2. When buccal soft tissue anaesthesia is necessary.
3. When lingual soft tissue anaesthesiais necessary.
Contraindication –
1. Infection or acute inflammation in the area of
injection.
2. Physically or handicapped adult or child.

81
Sign and symptoms –
Subjective – tingling or numbness of the lower lip.
Objective – no pain .
Complications –
1. Hematoma .
2. Trismus .
3. Facial paralysis .

82
BUCCINATOR / LONG BUCCAL NERVE
BLOCK

83
MENTAL NERVE BLOCK

84
GOW GATES TECHNIQUE
(MANDIBULAR N. BLOCK)
Nerves anaesthetized –
• Inferior alveolar
• Mental
• Incisive
• Lingual
• Mylohoyid
• Auricotemporal
• Buccal

85
Area anaesthetized –
• Mandibular teeth to the midline
• Buccal mucoperiosteum and mucous
membranes on the side of injection
• Anterior two thirds of the tongue and floor of
the oral cavity
• Lingual soft tissues and periosteum
• Body of the mandible, inferior portion of the
ramus

86
Indications –
1. multiple procedure on mandibular teeth
2. When buccal soft tissue anesthesia, from third
molar to the midline
3. For lingual soft tissue anesthesia
Contraindications –
1. Infection or acute inflammation in area of
injection.
2. In children, physically or mentally handicapped
patients
3. Patient who are unable to open their mouth wide
87
Target area – lateral side of the condylar neck, just
below the insertion of the lateral pterygoid muscle
Landmarks –
Extraoral –
• Lower border of tragus
• Corner of the mouth

88
Intraoral –
•Place the needle tip just below the mesiolingual cusp
of the maxillary second molar
•Penetrates soft tissues just distal to the maxillary
second molar.

89
Sign and symptoms –
Subjectives – tingling or numbness of the lower lip and
tongue
Objectives – no pain is felt during dental therapy.
Complications –
1. Hematoma
2. Trismus
3. Temporary paralysis of cranial nerves III, IV AND VI.

90
COMPLICATIONS OF
LOCAL
ANESTHETICS

91
COMPLICATIONS –
1. LOCAL COMPLICATIONS.
2. SYSTEMIC COMPLICATIONS.

92
LOCAL COMPLICATIONS
• Needle Breakage
• Prolonged anesthesia
• Facial nerve paralysis
• Trismus
• Soft- tissue injury
• Hematoma

• Pain on injection
• Burning on injection
• Infection
• Edema
• Sloughing of tissues

93
SYSTEMIC COMPLICATIONS
Adverse Drug Reactions
1) Side effects
2) Overdose reactions
3) Local toxic effects (most common)
4) Allergic reactions

94
Signs and Symptoms – Toxic Reaction to
Local Anesthesia
•Talkativeness
•Slurred speech
•Dizziness
•Nausea
•Depression
•Euphoria
•Excitement
•Convulsions
95
Overdose Reactions
Clinical signs and symptoms that develop as a
result of an over-administration of a drug.

96
Overdose Contributing Factors
•Age

•Weight
•Sex
•Presence of disease
•Mental attitude

97
Drug Factors
• Vasoactivity – All L.A currently used in dentistry
have vasodilating properties. Injection into the soft
tissues increases perfusion area which lead to an
increases rate of drug absorption .
• Dose – Larger the volume of L.A administered,
greater the no. of milligram injected which result in
increased circulating blood level.

98
• Concentration
• Vascularity of the injection site
• Presence of vasoconstrictors

99
Signs and Symptoms of Epinephrine Overdose
• Fear, anxiety
• Tenseness
• Restlessness
• Throbbing headache
• Tremor
• Weakness
• Dizziness
• Pallor
• Respiratory difficulty
• Palpitations
100
Management of Epinephrine Overdose
• Terminate dental procedure

• Sit patient upright in the dental chair
• Reassure patient

• Monitor blood pressure
• Administer oxygen

101
Allergic Reactions to Local Anesthetic Agents
•Hypersensitive state as a result of exposure to an
allergen.
•Re-exposure can heighten the initial reaction.

102
Clinical Manifestations of an Allergy
• Fever

• Angioedema
• Urticaria
• Dermatitis
• Depression of blood-forming organs
• Photosensitivity
• Anaphylaxis
103
Post anaesthetic complications –
Lip biting – commonly seen in children's.

104
Cheek biting

Blanching due to
vasoconstrictor

105
Hematoma due to local anaesthesia

106
Conclusion
Local anaesthesia is considered as a backbone of pain
control in dentistry. Research has continued in both
medical and dental to seek new and better means of
managing pain associated with mainly surgical
treatment.

107
References
1. Monheim's Local Anesthesia and Pain Control in Dental
Practice.
2. Handbook of local anesthesia Stanley F. Malamed , 6th
edition,2004.
3. Essentials of pharmacology for dentistry,KDTriphati,1st
edition,2005
4. Short textbook of anaesthesia, Ajay yadav,4th
edition, 2009.
5. Millers anaesthesia, 7th edition, Ronald. D Miller, 2010.

108
Thank You
109

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La seminar

  • 2. CONTENTS • Definition • History • Classification • Properties of L.A • Nerve physiology • Mechanism of action • Specific local anesthetics • Local anesthetic techniques • Maxillary • Mandibular • Complications • Local • Systemic • Post operative 2
  • 3. Definition of L.A Local anaesthesia has been 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”. (According to Moheims) 3
  • 5. Early History of Regional Anaesthesia  Koller and Gartner report local anesthesia (1884).  In 1884,Koller was the first, to use cocaine for topical anaesthesia in ophthalmological surgery. Carl Koller 1857 -1944 5
  • 6. Early History Of Regional Anaesthesia  1885 Halsted injects cocaine directly into mandibular nerve and brachial plexus William S. Halsted 6
  • 7. Common Uses Of Local Anesthetic : Excision Dermatology Spinal Anaesthesia Dentistry 7
  • 9. BASED ON SITE Topical Cocaine, Prilocaine, Lignocaine Injectable Lignocaine, Mepivacaine 9
  • 10. BASED ON CHEMICAL STRUCTURE ESTERS • Cocaine • Procaine • Benzocaine • Tetracaine AMIDES • Articaine • Bupivacaine • Lidocaine • Mepivacaine • Prilocaine • Ropivacaine 10
  • 11. BASED ON DURATION OF ACTION Ultra Short • 2% lignocane without vasoconstrictor Duration Short duration Intermediate duration Long duration • Procaine, • 2 % Lignocaine with 1:1,00,000 Epinephrine • • • • Articaine Mepivacaine Prilocaine 2 % Lignocaine with 1:2,00,000 Epinephrine • Bupivacaine • Etidocaine • 5 % Lignocaine with 1:2,00,000 Epinephrine 11
  • 12. DIFFERENCES AMIDES • longer lasting analgesia. • Produce more intense analgesia. • Rarely cause hypersensitivity reactions- no cross reactivity with ESTER L A s. • Not hydrolyzed by Plasma Cholinesterase, more slowly destroyed by liver microsomal P450 enzymes. ESTERS • Short duration of action • Less intense analgesia • Higher risk of hypersensitivity ESTER linked LA s are rarely used. • Hydrolyzed by Plasma Cholinesterase in blood. • Rarely used for Infiltration anesthesia • But useful for topical anaesthesia on mucous membranes. 12
  • 13. Properties of L.A • It should not be irritating to the tissue to which it is applied. • It should not cause any permanent alteration of nerve structure. • Its systemic toxicity should be low. • The time of onset of anaesthesia should be as short as possible. • The duration of action must be long enough to permit completion of the procedure yet not so long as to require an extended recovery.
  • 14. According to Beneett an ideal properties of local anaesthesia • It should have potency sufficient to give complete anaesthesia without the use of harmful concentrated solutions. • Its should be relatively free from producing allergic reactions. • It should be stable in solution &readily undergo biotransformation in the body. • It should either be sterile or capable of being sterilized by heat without deterioration.
  • 16. Electrophysiology of nerve conduction • Electrical events that occurs within a nerve during the conduction of an impulse. • A nerve possesses a resting potential. This is a negative electrical potential of -70 mV that exists across the nerve membrane, produced by differing concentrations of ions on either side of the membrane. • A stimulus excites the nerve, in following sequence of event – 16
  • 17. Step 1a – an initial phase of slow depolarization. The electrical potential within the nerve becomes slightly less negative. 1b –falling electrical potential reaches a critical level, it give result of rapid phase of depolarization. This is termed threshold potential, or firing threshold. 1c –this phase of rapid depolarization results in a reversal of electrical potential across the nerve membrane. electrical potential 0f+40 mV exists on the interior of the nerve cell. 17
  • 18. Membrane excitation • Depolarization – Excitation of nerve segment leads to an increase in permeability of the cell membrane to sodium ions. The rapid influx of sodium ions to the interior of the nerve cell causes depolarization of the nerve membrane from its resting level to its firing threshold of approx. -50 to -60 mV. Exposure of the nerve to local anesthetic raises its firing threshold. 18
  • 19. Repolarization • The action potential is terminated when the membrane repolarizes. This is caused by the inactivation of increased permeability to sodium. In many cells potassium also increases, resulting in the reflex of K+, and leading to more rapid membrane repolarization and return to its resting potential. 19
  • 20. Mechanism of action A. 1. 2. 3. 4. 5. Theories for mechanism of action of L.A are : The Acetylcholine theory. The calcium displacement theory. The surface charge theory. Membrane expansion theory. Specific receptor theory. 20
  • 21. THE ACETYLCHOLINE THEORY • Started that acetylcholine was involved in nerve conduction in addition to its role as a neurotransmitter at nerve synapses . THE CALCIUM DISPLACEMENT THEORY • L.A nerve block was produced by the displacement of calcium from some membrane site that controlled permeability to sodium. That varying the concentration of calcium ion bathing a nerve does not affect local anesthetic potency has diminished the credibility of this theory. 21
  • 22. Membrane expansion theory • Stated that L.A molecules diffuse to hydrophobic regions of excitable membranes, producing a general disturbance if the bulk membrane structure, expending some critical regions in the membrane & preventing an increase in the permeability to sodium ions. 22
  • 23. Specific receptor theory by strichartz 1987  Drug molecules bind to specific receptors present on the external or internal axoplasmic surface of sodium channels & by acting directly on them, decrease or eliminate permeability to Na2+ leading to interruption of nerve conduction. 23
  • 24. B. Local anaesthesia act in following ways: Displacement of calcium ions from the sodium channel receptor site, which permits Binding of the L.A molecules to the receptor site, which thus produce Blockade of the sodium channel , 24
  • 25. Decrease in sodium conductance, which lead to Depression of the rate of electrical depolarization Failure to achieve the threshold potential level, along with Lack of development of propagated action potentials, which is called Conduction blockade 25
  • 27. pKa • ONSET = pKa • pKa = pH at which 50% of drug is ionized • LA’s <50% exists in the lipid soluble in non ionized form • Only the non ionized form crosses into the nerve cell 27
  • 28. pH influence • Usually at range 7.4 -8.5 • Decrease in pH shifts equilibrium toward the ionized form, delaying the onset action. • Lower pH, solution more acidic, gives slower onset of action. Presence of Pus and inflammation will retard the action of LA. ( probably low acidic pH) therefore • LA are more ionized - don’t penetrate very well. • Decreased ability of LA to produce effects. 28
  • 29. VASODILATOR ACTIVITY • Affects Anesthetic potency and duration • Greater vasodilator activity = increased blood flow to region =rapid removal of anesthetic molecule from injection site ; thus decreased anesthetic potency and duration. 29
  • 30. Composition Local Anesthetics solution contains : 1. Local anaesthetic agents – Ester linkage – procaine, cocaine, tetracaine. Amide linkage – lignocaine , prilocaine , mepivacaine, bupivacaine . 2. Vasoconstrictors – Adrenaline – a synthesis substance similar to that secreted in human body. 30
  • 31. Advantages – • Reduces toxic effect by retarding the absorption of the constituents. • It increases the depth & duration of anaesthesia and produces bloodless field for surgical procedure. 3. Reducing agent- Sodium bimetasulphite. • small quantity in the solution to prevents oxidation of the vasoconstrictors as they are unstable in solution especially on exposure to sunlight. 31
  • 32. 4. Preservative – Caprylhydrocupeinotoxin • it helps to maintain sterility of the solution & also increases its self life. 5. Fungicide – Thymol • to prevents proliferation of minute fungi which causes cloudiness of the solution. 6.Vehicle – Ringer’s solution. • In which all constituent dissolves to minimizes discomfort during injection of L.A. 32
  • 33. DOSES AND DURATION OF BLOCK Drug Conc. Total dose(mg) Dose(mg/k g) Duration of block Procaine 1-2% 400 6 30-60 min. Lidocaine 0.5-2% 300 4.5 60-120 min. Bupivacaine 0.25-0.5% 90 1.4 180-360 min. Tetracaine 0.25-0.5% 80 1.3 180-480 min. 33
  • 35. CENTRAL NERVOUS SYSTEM • CNS Stimulation: (More sensitive than cardiac) • Dose-related spectrum of effects and all effects are due to depression of neurons. • First an apparent CNS stimulation (convulsions most serious) • Premonitory signs include: ringing in ears, metallic taste, numbness around lips • Followed by CNS depression (death due to respiratory depression) Cocaine - Euphoria Lidocaine - Sedation even at nontoxic doses. 35
  • 36. CARDIOVASCULAR SYSTEM • ARRHYTHMIAS: • Decrease cardiac excitability and contractility • Decreased conduction rate • Increased refractory rate (bupivicaine) • ALL can cause arrhythmias if conc. is high enough Note: cocaine is exception......it stimulates heart • HYPOTENSION: Arteriolar dilation is a result of: • Direct effect (procaine and lidocaine have most effect) • Block of postganglionic sympathetic fiber function • CNS depression • Avoid by adding vasoconstrictor to the preparation • Cocaine is exception: produces vasoconstriction. 36
  • 37. • Hypersensitivity: • Common with ester-linked LA • Rashes, angio-edema, dermatitis and rare anaphylaxis • Sometimes typical asthmatic attack • Neurotoxicity: • LA can cause concentration-dependent nerve damage to central and peripheral NS • Mechanism(s) not clear • Permanent neurological injury is rare • May account for transient neurological symptoms. 37
  • 39. PROCAINE (NOVOCAINE) • First synthetic injectable local anesthetic. • Produce the greatest vasodilation of all currently used local anesthetics. • Slower clinical onset (6-10 min.) Used for • Soft tissue anesthesia for 15- 30 min. • Systemic toxicity negligible because rapidly destroyed in plasma • Max. recommended dose for peripheral nerve block 1000mg 39
  • 40. LIDOCAINE 1:200000 conc. is safest As well as potent • The most popular contains epinephrine 1:100,000 and provides good anesthesia for healthy patients. • Lidocaine with epinephrine 1:50,000 is used for hemostasis, but because of the rebound effect noted earlier, it should be used sparingly. 40
  • 41. Lidocaine ( Xylocaine ) • Most widely used Amide linked LA and most versatile anaesthesia. • Has variety of applications like Local, nerve block, topical. • When used locally action starts within 3 min., more profound anesthesia, has longer duration of action and greater potency. • Overdose causes muscle twitching, convulsions, cardiac arrhythmias, fall in BP, coma, respiratory arrest. • Most popular anti arrhythmic drug 41
  • 42. Maximum Dose of Lignocaine • Without Vasoconstrictor : 4.4 mg / kg of body wt = 300 mg in a 70 kg individual = 15 ml of solution • With Vasoconstrictor : 7.2 mg / kg of body wt = 500 mg in a 70 kg individual = 25 ml of solution • For children with VC 3.2 mg/kg 42
  • 43. MEPIVACAINE • 3% Mepivacaine without a vasoconstrictor is used as anesthetic for patients who cannot take a vasoconstrictor or for short procedures. • It is appropriate for pedodontics and for use on geriatric patients. • 2% Mepivacaine with vasoconstrictor provides pulpal anesthesia that is similar to lidocaine with epinephrine, but hemostasis is not as intense. 43
  • 44. PRILOCAINE • The action of prilocaine plain varies with the area injected (longer with a nerve block). • Prilocaine with vasoconstrictor gives good anesthetic effect and uses a 1:200,000 concentration of epinephrine. 44
  • 45. ARTICAINE • Articaine is a newer anesthetic typically given in a 4% solution with 1:100,000 epinephrine. • However, concern has arisen about its potential for tissue necrosis and persistent nerve parasthesia. 45
  • 46. BUPIVACAINE • Bupivacaine is used when pulpal anesthesia is desired for longer appointments and when postoperative pain is anticipated. • Bupivacaine is not recommended for children or handicapped patients because of the increased risk of postoperative injury (chewing on a numb lip). 46
  • 47. • Available as 0.5% solu.1:2,00,000 (vc) • Indication- Pulpal anesthesia >90- min.  Full mouth reconstruction.  Extensive oral and maxillofacial surgery, periosurgery. • Duration –Pulpal - 90- 180 min. Soft tissue- 4-12 hrs. • Contra indication- Burning sensation at site of injection, in children anticipating self trauma . 47
  • 48. POSTPROCEDURAL PAIN CONTROL • Prescribe nonsteroidal antiinflammatory agents prior to the appointment. • Use an intermediate duration anesthetic for the procedure. • Inject bupivacaine just prior to the patient's dismissal . • Direct the patient to take oral analgesics for a certain number of days following the procedure. 48
  • 50. TOPICAL • The local anesthetic solution is applied on the mucous membrane or skin, through which it penetrates to anesthetize superficial nerve endings. e.g. - Ointments containing 5%lignocaine -Viscous solution containing lignocaine hydrochloride -Ethyl chloride sprays 50
  • 51. EMLA = Eutectic Mixture of Local Anesthetics • Eutectic = two solid substances mixed together in equal quantities by weight form a eutectic mixture • The melting point of the mixture is lower than the melting points of the individual components • EMLA = lidocaine and prilocaine becomes an oily mixture 51
  • 52. INFILTRATION • Small terminal nerve endings in the area of dental treatment are flooded with local anesthetic. • The treatment is done in the same place where anesthetic is deposited. 52
  • 53. FIELD BLOCK • Local anesthetic solution is deposited near the larger terminal branches so the anesthetized area is well circumscribed. • Incision or treatment is done at an area away from the site of injection of local anesthetic. 53
  • 54. NERVE BLOCK • Local anesthetic solution is deposited close to the main nerve trunk, usually at a distance from the site of operative intervention 54
  • 56. POSTERIOR SUPERIOR ALVEOLAR NERVE BLOCK Nerves anaesthetized – posterior superior alveolar and branches. Areas anaesthetized – Pulps of the maxillary third, second and first molars. Buccal periodontium and bone overlying these teeth. 56
  • 57. Indications: • When treatment involves two or more maxillary molars. • When supraperiosteal injection has proved ineffective. Contraindication: • When the risk of hemorrhage is too high. 57
  • 58. • Procedure – • Insert the needle slowly in upward, inward and backward direction. • Upward: superiorly at 45-degree angle to the occlusal plane. • Inward: medially toward the midline at a 45-degree angle to the occlusal plane. • Backward: posteriorly at a 45-degree angle to the long axis of the second molar. 58
  • 59. Sign and symptoms: • Subjective: none • Objective: absence of pain during therapy. Complications: • Hematoma • Mandibular anesthesia 59
  • 60. MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK Nerves anaesthetized – middle superior alveolar and terminal branches. Areas anaesthetized – Pulps of the maxillary first and second premolars, mesiobuccal root of the first molar. Buccal periodontal tissues and bone over the same teeth. 60
  • 61. Indications – • When infraorbital nerve block fails to provide pulpal anaesthesia distal to the maxillary canine. Indicated for both maxillary premolars only Contraindication: • Infection or inflammation in the areas of injection. Sign and symptoms: • Subjective: upper lip numb • Objective: no pain during treatment 61
  • 62. INFRAORBITAL NERVE BLOCK Nerve anaesthetized – •Anterior superior alveolar •Middle superior alveolar •Infraorbital nerve a) inferior palpebral b) Lateral nasal c) Superior labial 62
  • 63. Indications • Involving more than two maxillary teeth and their overlying buccal tissues • Infection or inflammation • When supraperiosteal injections have been ineffective because of dense cortical bone Contraindications – • Discrete treatment areas • Hemostasis of localized area 63
  • 64. 64
  • 65. Sign and symptoms – Subjective – tingling and numbness of the lower eyelid, side of the nose and upper lip Objective – no pain during procedure 65
  • 66. GREATER PALATINE NERVE BLOCK Nerves anaesthetized – Greater palatine Area anaesthetized – posterior portion of hard palate, anteriorly upto first premolar and medially to the midline 66
  • 67. Indications – • For pain control during periodontal or oral surgical procedures involving the palatal soft and hard tissues. Contraindications – • Inflamation or infection at the injection site • Smaller area of therapy. 67
  • 68. Sign and symptoms – • Subjective – numbness in the posterior portion of the palate • Objective – no pain during dental therapy. Complications – • Few of significance • Ischemia and necrosis of soft tissues when highly conc. vasoconstructing solution used for homeostasis over a prolonged period. • Hematoma is possible but rarely occur. 68
  • 69. NASOPALATINE NERVE BLOCK Nerves anaesthetized – nasopalatine nerves bilaterally. Area anaesthetized – anterior portion of the hard palate from the mesial of the right first premolar to the mesial of the left first premolar. 69
  • 70. Indications – • For pain control during periodontal or oral surgical procedures involving palatal soft and hard tissues. • For subgingival restoration and insertion of matrix bands (subgingivally). Contraindications – • Inflammation or infection at the injection site • Smaller area of treatment i.e. one or two teeth • Alternatives • Local infiltration into specific regions • Maxillary nerve block. 70
  • 71. Techniques – • Target area – incisive foramen, beneath the incisive papilla. • Landmarks – central incisor and incisive papilla. 71
  • 72. Signs and Symptoms – • Subjective – numbness in the anterior portion of the palate. • Objective – no pain during dental treatment. Complications – • Necrosis of soft tissue occurs when highly concentrated vasoconstriction solutions (norepinephrine). • Interdental papilla tenderness are present sometimes after few days of injection. 72
  • 73. ANTERIOR MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK Nerves anaesthetized – •Anterior superior nerve •Superior alveolar nerve, when present Sub neural dental nerve plexus of the anterior and middle superior alveolar nerves. Areas anaesthetized – •Pulpal anaesthesia of the max. Incisors, canines, and premolars. •Buccal attached gingival of the same teeth. •Attached palatal tissues from midline to free gingival margin on the associated teeth. 73
  • 74. Indications – • Is easier performed with a CCLAD system. • When maxillary anterior teeth involves any dental procedure. • When supraperiosteal injection is failed because of dense cortical bone. Contraindications – • Patients with usually thin palatal tissues. • Procedures requiring more than 90 min. 74
  • 75. Signs and Symptoms – Subjective • A sensation of firmness and numbness is immediately on palatal tissue. • Numbness of the teeth and associated soft tissues Objectives – • Blanching of the soft tissues of the palatal and facial attached gingival from central incisor to premolar region. • No pain during dental procedure. Complications – • Palatal ulcer at injection site after 1 to 2 days postoperative. • Density of injection site causing squirt – back of anaesthetic and bitter taste. 75
  • 76. MAXILLARY NERVE BLOCK Nerves anaesthetized – • Maxillary division of the trigeminal nerve 76
  • 77. Indications – • Pain control during extensive oral surgical, periodontal, or restorative procedures. • When tissue inflammation or infection precludes the use of other regional nerve blocks. Contraindications – • Inexperienced administrator • Paediatric patients • Uncooperative patients • Inflammation or infection of tissues overlying the injection site. 77
  • 78. Procedure – • Locate the greater palatine foramen at the region of the second molar. • It mostly located at the distal aspect of the second molar. 78
  • 79. Signs and symptoms – Subjective – • Sensation of numbness in the teeth and buccal and palatal soft tissues on the side of injection. Objectives – • No pain during dental therapy. Complications – • Hematoma develops rapidly if the maxillary artery is punctured during maxillary nerve block. 79
  • 80. INFERIOR ALVEOLAR NERVE BLOCK Nerves anaesthetized – • Inferior alveolar, a branch of the posterior division of he mandible • Incisive • lingual 80
  • 81. Indication – 1. Multiple mandibular teeth in one quadrant. 2. When buccal soft tissue anaesthesia is necessary. 3. When lingual soft tissue anaesthesiais necessary. Contraindication – 1. Infection or acute inflammation in the area of injection. 2. Physically or handicapped adult or child. 81
  • 82. Sign and symptoms – Subjective – tingling or numbness of the lower lip. Objective – no pain . Complications – 1. Hematoma . 2. Trismus . 3. Facial paralysis . 82
  • 83. BUCCINATOR / LONG BUCCAL NERVE BLOCK 83
  • 85. GOW GATES TECHNIQUE (MANDIBULAR N. BLOCK) Nerves anaesthetized – • Inferior alveolar • Mental • Incisive • Lingual • Mylohoyid • Auricotemporal • Buccal 85
  • 86. Area anaesthetized – • Mandibular teeth to the midline • Buccal mucoperiosteum and mucous membranes on the side of injection • Anterior two thirds of the tongue and floor of the oral cavity • Lingual soft tissues and periosteum • Body of the mandible, inferior portion of the ramus 86
  • 87. Indications – 1. multiple procedure on mandibular teeth 2. When buccal soft tissue anesthesia, from third molar to the midline 3. For lingual soft tissue anesthesia Contraindications – 1. Infection or acute inflammation in area of injection. 2. In children, physically or mentally handicapped patients 3. Patient who are unable to open their mouth wide 87
  • 88. Target area – lateral side of the condylar neck, just below the insertion of the lateral pterygoid muscle Landmarks – Extraoral – • Lower border of tragus • Corner of the mouth 88
  • 89. Intraoral – •Place the needle tip just below the mesiolingual cusp of the maxillary second molar •Penetrates soft tissues just distal to the maxillary second molar. 89
  • 90. Sign and symptoms – Subjectives – tingling or numbness of the lower lip and tongue Objectives – no pain is felt during dental therapy. Complications – 1. Hematoma 2. Trismus 3. Temporary paralysis of cranial nerves III, IV AND VI. 90
  • 92. COMPLICATIONS – 1. LOCAL COMPLICATIONS. 2. SYSTEMIC COMPLICATIONS. 92
  • 93. LOCAL COMPLICATIONS • Needle Breakage • Prolonged anesthesia • Facial nerve paralysis • Trismus • Soft- tissue injury • Hematoma • Pain on injection • Burning on injection • Infection • Edema • Sloughing of tissues 93
  • 94. SYSTEMIC COMPLICATIONS Adverse Drug Reactions 1) Side effects 2) Overdose reactions 3) Local toxic effects (most common) 4) Allergic reactions 94
  • 95. Signs and Symptoms – Toxic Reaction to Local Anesthesia •Talkativeness •Slurred speech •Dizziness •Nausea •Depression •Euphoria •Excitement •Convulsions 95
  • 96. Overdose Reactions Clinical signs and symptoms that develop as a result of an over-administration of a drug. 96
  • 98. Drug Factors • Vasoactivity – All L.A currently used in dentistry have vasodilating properties. Injection into the soft tissues increases perfusion area which lead to an increases rate of drug absorption . • Dose – Larger the volume of L.A administered, greater the no. of milligram injected which result in increased circulating blood level. 98
  • 99. • Concentration • Vascularity of the injection site • Presence of vasoconstrictors 99
  • 100. Signs and Symptoms of Epinephrine Overdose • Fear, anxiety • Tenseness • Restlessness • Throbbing headache • Tremor • Weakness • Dizziness • Pallor • Respiratory difficulty • Palpitations 100
  • 101. Management of Epinephrine Overdose • Terminate dental procedure • Sit patient upright in the dental chair • Reassure patient • Monitor blood pressure • Administer oxygen 101
  • 102. Allergic Reactions to Local Anesthetic Agents •Hypersensitive state as a result of exposure to an allergen. •Re-exposure can heighten the initial reaction. 102
  • 103. Clinical Manifestations of an Allergy • Fever • Angioedema • Urticaria • Dermatitis • Depression of blood-forming organs • Photosensitivity • Anaphylaxis 103
  • 104. Post anaesthetic complications – Lip biting – commonly seen in children's. 104
  • 105. Cheek biting Blanching due to vasoconstrictor 105
  • 106. Hematoma due to local anaesthesia 106
  • 107. Conclusion Local anaesthesia is considered as a backbone of pain control in dentistry. Research has continued in both medical and dental to seek new and better means of managing pain associated with mainly surgical treatment. 107
  • 108. References 1. Monheim's Local Anesthesia and Pain Control in Dental Practice. 2. Handbook of local anesthesia Stanley F. Malamed , 6th edition,2004. 3. Essentials of pharmacology for dentistry,KDTriphati,1st edition,2005 4. Short textbook of anaesthesia, Ajay yadav,4th edition, 2009. 5. Millers anaesthesia, 7th edition, Ronald. D Miller, 2010. 108