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contents
 Terms
 Pain
 Neurophysiology & neuroanatomy
 Local anesthesa
 History
 Classification
 Composition
 Mode of action
 Metabolism
 Local Anesthetic agents
3
terms
 Analgesia: refers to loss of pain sensation without
loss of consciousness.
 Regional analgesia: refers to loss of pain
sensation over a portion of anatomy without loss
of consciousness.
 Regional anesthesia: refers to loss of all
sensations i.e. pain as well as temperature,
pressure and motor function without the loss of
consciousness.
4
terms
 Local Anesthesia: Loss of sensation in a
circumscribed area of the body caused by a
depression of excitation in nerve ending or an
inhibition of conduction process in peripheral
nerve.
Malamed
 General Anesthesia: A reversible state of
unconsciousness from where a person cannot be
aroused by external stimulus.
Anaesthesia & Analgesia in dentistry
5
terms
 Nerve block: this method consists of depositing LA
solution within close proximity to a main trunk and thus
preventing afferent impulses traveling beyond that point.
 Field block: consisting of depositing LA solution in close
proximity to a large terminal nerve branch so that area to be
anaesthetized is walled off circumscribed to prevent central
passage of afferent impulses.
 Local infiltration: small terminal nerve branches in the
area of surgery are flooded with LA solution rendering
them insensible to pain or preventing them from becoming
stimulated and creating an impulse. The incision made in
the same region in which the solution has been deposited.
6
terms
 Intraligamentary technique: this technique is
injected to provide single tooth anaesthesia and
consists of forcing LA solution under pressure
into periodontal membrane space of teeth.
 Topical anaesthesia: it renders the free nerve
endings in accessible structure (intact mucous
membrane, abraded skin, cornea of eye)
incapable of stimulation by the application of a
suitable solution directly to the surface area.
7
Pain
 An unpleasant sensory & emotional experience
associated with actual or potential tissue damage
or described in terms of such damage
INTERNATIONALASSOCIATION FOR THE
STUDY OF PAIN
 An unpleasant emotional experience usually
initiated by noxious stimulus & transmitted over
specialized neural network to CNS where it is
interpreted as such
MONHEIM
8
9
Specificity theory (Von Fray)
late 19th century
 A pain centre was thought to exist within the brain,
which was responsible for all overt manifestation
of the unpleasant experience.
10
Pattern theory (Goldscheider, 1894)
 Central summation and stimulus intensity are
the critical determinants of pain.
 Pain results when the total output of cells
exceeds the critical levels.
11
Gate control theory (Melzack and Wall, 1965)
 Briefly stated this theory postulates the following:
 Information about the presence of injury is
transmitted to the CNS by small peripheral nerves.
 Cells in the spinal cord, which are excited by these
injury signals, are also facilitated or inhibited by
other large peripheral nerves
 Descending control systems originating in the brain
modulate the excitability of the cells
12
 Therefore, the brain receives information
about injury by way of gate control system,
which is influenced by:
Injury signals
Other types of afferent impulses
Descending control
13
CLASSIFICATION OF NERVE
FIBRES
14
A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
 Substantia gelatinosa [SG] (located in dorsal horn of
spinal cord) acts as gatekeeper for transmission of pain
impulses
Fast
Slow
15
A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
 Step 1: without any painful stimulation;
the gate is closed – therefore no pain
transmission
16
A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
 Step 2: with non-painful stimulation, large
nerve fibers are primarily activated; both the
SG and T cell are activated; activation of SG
closes gate – no pain
O
F
F
17
A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
 Step 3: with painful stimulation, A-delta & C fibers
are primarily activated; the SG is inhibited and T cell
are activated; inhibition of SG opens gate – pain
transmitted to brain
O
N
18
A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
 Rubbing the skin stimulates large diameter
nerves, exciting the SG, closing the gate.
 Result: reduction of pain.
O
F
F
ON
19
A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
 There are multiple gates in the dorsal horn
of the spinal cord.
 Closing one gate reduces some pain
transmission
 Relatively impossible to close all gates
20
Methods of pain control
 Removing the cause
 Blocking the pathway of painful impulses.
 Raising the pain threshold
 Preventing the pain reaction by cortical
depression
21
NEUROPHYSIOLOGY AND
NEUROANATOMY
22
Neuron
Sensory Motor
23
24
NEUROPHYSIOLOGY
25
ElectroPhysiology of Nerve
Conduction
26
27
 Resting state
 Slightly permeable to Na+
 Freely permeable to K+ & Cl+
 Depolarization
 Slow depolarization
 Firing threshold
 Rapid depolarization
 Repolarization
Electrochemstry of Nerve Conduction
28
29
depolarization
30
31
repolarizaton
32
33
Local anesthesia
 Loss of sensation in a circumscribed area of the
body caused by a depression of excitation in nerve
ending or an inhibition of conduction process in
peripheral nerve.
-Malamed 6th Ed
34
history
35
History
ALBERT NIEMANN
IN 1860
36
History
CARL KOLLER IN 1884
37
 Einhorn in 1905
History
38
History
 NILS LOFGREN in
1943
39
History
 Mepivacaine
 Bupivacaine
 Prilocaine
 Etidocaine
 Ropivacaine
40
CLASSIFICATION
(MALAMED)
Esters
Benzoic acid:
Butacaine
Cocaine
Ethyl
aminobenzoate
Benzocaine
Piperocaine
Tetracaine
Para-aminobenzoic
acid:
Chloroprocaine
Procaine
Propoxycaine
Quinolone
Centbucridine
Amide
Articaine
Bupivacaine
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
Prilocaine
41
Structure
Fundamental structural features is
common
42
Injectable
a. Low potency, short duration
Procaine
Chloroprocaine
b. Intermediate potency and
duration
Lidocaine
Mepivacaine
c. High potency, long duration
Tetracaine
Bupivacaine
Surface anesthetic
a. Soluble
Cocaine
Lidocaine
Tetracaine
b. Insoluble
Benzocaine
Butyl aminobenzoate
43
According to duration of action
 Ultra Short Acting: acting for < 30 mins
e.g Procaine without vasoconstrictor
 Short Acting: acting for 45 -75 mins
e.g 4% prilocaine with 1: 200,000 epinephrine
 Medium Acting: acting for 90 – 150 mins
e.g. 2% lidocaine with 1: 100,000 epinephrine
 Long acting: acting for 180 mins or longer
e.g. 0.5% Bupivacaine with 1: 200,000 epinephrine
44
Desirable Properties
 Must be reversible
 Should not be irritating to tissue
 Should not cause any permanent alteration of
nerve structure
 Low systemic toxicity
 Must be effective-injection/ topical
 Onset as short as possible.
 Long duration of action
45
Composition of LA solution
 Local anesthetic agent
 Vasoconstrictor
 Reducing agent
 Preservative
 Fungicide
 The vehicle
46
1. Local Anesthetic Agent
○Lidocaine
○Mepivacaiine
○Prilocaine
○Etidocaine
○Bupivacane
47
2. Vasoconstrictor
This is sometimes included to delay the
removal of the anesthetic from the tissues by
decreasing the blood flow through adjacent
blood vessels
48
Advantages
 It 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 bloodless field of
operation for surgical procedures.
[DCNA2002]
49
The choice of selection of
vasoconstrictors depends on:
 Length of dental procedures
 Requirements for haemostasis
 Medical status of a patient
50
Vasoconstrictors In
General Use
 Adrenaline: a synthetic alkaloid almost identical with
the natural secretion of the adrenal medulla.
 Nor-adrenaline: a synthetic substance similar to the
pressor amine secreted in the human body
51
 Felypressin: is a synthetically produced
polypeptide similar to that secreted from the
human posterior pituitary gland.
 Only available in a concentration of 0.03
IU/ml.
Vasoconstrictors In General Use
52
 Both depth and duration of anesthesia can be
modified by the amount of vasoconstrictor in
solution.
 Lidocaine solution containing adrenaline / nor-
adrenaline in concentrations of 1:50,000; 1:
80,000 or 1: 1,00,000
53
Dilutions Of Vasoconstrictors
 A conc. of 1:1000 means that there is 1 gm of solute
in 1000ml of solution
 Therefore 1:1000 ratio means 1000mg in 1000 ml or
1.0mg / ml of solution
 To produce a 1:10000 solution a 1:1000 solution of
1ml is mixed with 9 ml of solvent
 so 1:10000 is 0.1mg/ml
 To produce a 1:100000 solution a 1ml solution of
1:10000 is diluted in 9 ml of solvent
54
3. Reducing agent
 Vasoconstrictors are unstable in solution
 This results in solution turning brown and
must be discarded
 Sodium metabisulphite
 It is more readily oxidized
55
4. PRESERVATIVE
Small amount of preservative
Methylparaben have been shown to produce allergic
reactions in sensitized subjects
5. Fungicide
In the past some solutions tended to become cloudy due to
the proliferation of minute fungae
In several modern solutions a small quantity of thymol is
added to serve as a fungicide.
56
6. The vehicle
 The anesthetic agent and the additives referred to
above are dissolved in modified ringer’s solution
 This isotonic vehicle minimizes discomfort during
injection
57
COMPOSITON OF NIRCAINE – ADR
(Lignocaine 2%, adrenaline 1:2,00,000)
 Lignocane hydrochlorde - 21.3 mg
 Adrenalne bitartarate - .005 mg
 Sodium chloride - 6.0 mg
 Sodium metabisulphite - 0.5 mg
 Methylparaben - 1.0 mg
 Water for injection
58
Mode & site of action
Nerve membrane is the site of action of the local
anesthetics.
 Altering the basic resting potential of the nerve
membrane
 Altering the threshold potential
 Decreasing the rate of depolarization
 Prolonging the rate of repolarization
59
Evolution Of Theories For Mode Of Action
 Acetylcholine theory
 Calcium displacement theory
 Surface charge (repulsion) theory
 Membrane expansion
 Specific receptor theory
60
ACETYL CHOLINE THEORY
61
Membrane Expansion theory
62
Specific Receptor Theory
63
 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 ammonium-
scorpion venom
Benzocaine
Clinically useful agents
–Lignocaine etc
According to biological site and mode of action - MALAMED
64
65
How local anesthetic works?
66
RNH+ displaces calcium ions for the sodium channel receptor site.
↓ which causes
Binding of the local anesthetic molecules to this receptor site
↓ which produce
Blockade of sodium channel
↓ and
Decrease in sodium conduction
↓ which leads to
Depression of the rate of electrical depolarization
↓ and
Failure to achieve the threshold potential level

Lack of development of propagated action potentials
↓ called
Conduction blockade
67
Effect of pH
 Acidic environment (low pH)
RNH+ > RN + H+
 Basic environment (higher pH)
RNH+ < RN + H+
68
69
BLOOD LEVELS OF LOCALANESTHETICS
ARE INFLUENCED BY THE FOLLOWING
FACTORS
Rate at which the drug is absorbed into the
cardiovascular system
Rate of distribution of the agent from the vascular
compartment to the tissues
 Elimination of the drug through metabolism /
excretory pathways.
70
METABOLISM / BIOTRANSFORMATION
 A significant difference between the two
major types of local anesthetics, the esters
and the amides, is the method by which
they undergo metabolic breakdown.
71
ESTERS:
 They are hydrolyzed in the plasma by the
enzyme pseudocholinesterase.
AMIDES:
 The primary site of biotransformation of
amide agents is the liver.
72
EXCRETION
 Kidneys
 Esters appear only in very small concentrations as
parent compound in urine.
 Amides are usually present in the urine as the parent
compound in greater percentage than esters, primarily
because they have a complex biotransformation.
73
 Classification: Ester
 Prepared by: Alfred Einhorn (1904-1905)
 Potency: 1
 Toxicity: 1
 Metabolism: Hydrolyzed rapidly in plasma, by
plasma pseudocholinesterase.
 Excretion: 2% unchanged in urine
90% as para amino benzoic acid
8% as diethylaminoethanol
74
A. Procaine
 Vasodilatation property: produces the greatest
vasodilatation of all currently employed local
anesthetics.
 pKa : 9.1
 Onset of action: 6-10 min’s
 Effective dental concentration: 2% - 4%
 Topical action: not in clinically acceptable
concentrations.
 Actions:
It was the 1st injectable local anesthetic to be
synthesized
75
Propoxycaine
 Classification: Ester
 Prepared by: Clinton and Laskowski, 1952
 Potency: 7-8
 Toxicity: 7-8
 Metabolism: Hydrolysed both in plasma and liver
 Excretion: Kidneys (almost entirely hydrolyzed)
 Vasodilatation property: Present
 pKa : Not available
 Onset of action: Rapid (2-3 min’s)
 Effective dental concentration: 0.4 %
 Topical action: Not in clinically acceptable concentrations
76
Chloroprocaine
 Classification: Ester
 Potency: 2
 Toxicity: ½ of procaine
 Metabolism: by rapid hydrolysis in serum
 Excretion: Kidneys
 Vasodilatation property: < procaine
 pKa : 8.7
 Onset of action: Moderate (6-12 min’s)
 Effective dental concentration: 2%
 Anesthetic ½ life: sec’s to min’s (extremely rapid)
 Topical action: not in clinically acceptable
concentrations.
77
AMIDES
A. Lidocaine
 Classification: Amide
 Prepared by: Nils Lofgren, 1943
 Introduced in: 1948
 Potency: 2 (compared to procaine). Today Lidocaine
is used as standard of comparison.
78
79
 Toxicity: 2 (compared to procaine)
 Metabolism: Liver
(Lidocaine Monoethylglycerine + Xylidide).
Xylidide is a local anesthetic and is toxic.
 Excretion: Kidneys. < 10% unchanged, 80%
metabolites.
 Vasodilatation property: < Procaine but >
Prilocaine
 pKa : 7.9
 Onset of action: Rapid (2-3 min’s)
80
 Effective dental concentration: 2%
 Anesthetic ½ life: 90 min’s
 Topical anesthetic action: Present
 Action: (2% lidocaine + 1: 1,00,000 epinephrine)
60 min’s pulpal anesthesia.
 3-5 hrs. - Soft tissue anesthesia
 Less bleeding in the area of injection
 Epinephrine conc. : 0.01 mg / ml or 0.018 mg. /
cartridge
81
B. Mepivacaine
 Classification: Amide
 Prepared by: A.F. Ekenstam, 1957
 Introduced in: 1960, 2% with vasoconstrictor
1961, 3% without vasoconstrictor.
 Potency: 2
 Toxicity: 1.5 – 2
 Metabolism: Liver
 Excretion: Kidneys 1% -16% unchanged form
 Vasodilatation property: Slight
 pKa : 7.6
 Onset of action: Rapid (1 ½ - 2 min’s)
82
83
 Effective dental conc. : 3% without vasoconstrictor
 2% with vasoconstrictor
 Anesthetic ½ life: approx 90 min’s
 Topical anesthetic action: Not in clinically
acceptable concentrations.
 Action: Mepivacaine plain is most often
administered in pediatric dentistry and is very
appropriate in management of geriatric patients.
84
Bupivacaine
 Classification: Amide
 Prepared by: A.F. Ekenstam, 1957
 Potency: 4 (compared to lidocaine)
 Toxicity: < 4 times that of lidocaine
 Metabolism: Liver
 Excretion: Kidneys (16% unchanged)
 Vasodilatation property: > lidocaine, < procaine
85
 pKa : 8.1
 Onset of action: similar to that of lidocaine but occasionally
requires longer time (6-10 min’s)
 Effective dental conc: 0.5%
 Anesthetic ½ life: 76 min’s
 Topical action: Not in clinically acceptable concentrations
Action:
 Lengthy dental procedures (pulpal anesthesia > 90 min’s)
 Procedures in which post operative discomfort is
anticipated. Example: - Endodontic surgeries [JOE,2005,AL
READER]
86
87
ARTICAINE
 Classification : amide
 Prepared by: A. Rusching
 Potency:1.5 times that of lignocaine
 Toxicity :similar to that of lignocaine
 Metabolism :articaine is the only amide type local
anesthetic that causes metabolism in both liver and
plasma
 Excretion: via kidneys, 5-10% unchanged, app 90%
metabolites
 Vasodilating properties similar to that of lignocaine
88
 pka-7.8
 ph of vaso constrictor containing substance-4.4-5.2
 Onset of action: 1-2 mins
 Effective dental concentration -4%
 Originally known as carticaine and is available in 2
formulations of 4%.
 It has been claimed that articaine can better diffuse
through hard and soft tissues than other anesthetics
89
90
 TOPICAL ANESTHETICS
91
 Lidocaine: (available in 2 forms)
Lidocaine base
Water-soluble preparation
 Benzocaine:
Poorly soluble in water
Poor absorption
Systemic toxic reactions unknown
Prolonged duration of action
Not suitable for injection
Reported to inhibit antibacterial action of
sulfonamides
92
EMLA-EUTECTIC MIXTURE OF LOCAL
ANESTHETICS
 Recently introduced topical anesthetic agent.
 Medical use to achieve anesthesia of skin.
 Posses a local anesthetic effect on the oral
mucosa also.
 Contents:
 Lidocaine 25 mg /ml
 Prilocaine 25mg. /ml
93
Tetracaine Hydrochloride
Highly water soluble
Applied topically, 5-8 times more potent than cocaine
Slow onset of action (topically)
Duration of action: approximately 45 min’s
Metabolized in Liver and plasma
Injectable: 0.15 % concentration
Topically: 2% concentration.
Rapidly absorbed through mucous membrane
Greater potential for toxicity.
94
armamentarium
95
syringes
The syringe is a vehicle by which the local
anesthetic is delivered
96
97
 -Non disposable
 Breech loading, metallic, catridge type, aspirating
 Breech loading, plastic, catridge type, aspirating
 Breech loading, metallic, catridge type, self aspirating
 Pressure syringe
 Jet injector
 -Disposable
 -Safety
 -Computer controlled
TYPES
Breech loading, metallic, catridge type, aspirating
98
 It is a metallic syringe where the needle is attached to
the barrel of the syringe at the needle adaptor.
 The end of the needle then penetrates the barrel of
syringe and pierces the rubber diaphragm on the
cartridge of anesthetic sol.
 The screw hub is removable and sometimes
inadvertently discarded with needle when the needle
is removed and discarded.
99
100
Breech loading, plastic, catridge type, aspirating
101
Breech – loading, metallic, self aspirating cartridge
102
The self aspirating
syringes obtain the
required negative
pressure for
aspiration by means
of elasticity of the
rubber diaphragm of
the syringe which
directs the needle
into the cartridge
103
 Pressure acting directly on the cartridge
through the thumb disk or indirectly through
the plunger shaft stretches the rubber
diaphragm.
 When that pressure is released, sufficient
negative pressure is produced with in the
cartridge to achieve aspiration.
 The use of self aspirating dental syringe
permits easy, multiple aspirations throughout
the period of local anesthetic deposition.
104
105
JET INJECTOR
 It was introduced by Figge & Scherer in 1947.
 Jet injections is based on the principle that liquids
forced through very small openings, called jets, at
very high pressure can penetrate skin or mucous
membrane
106
107
Syrijet mark II MadaJet
Pressure syringe
 These syringes introduced in the late 1970 was
primarily used for periodontal injections
 All pressure syringes encase in a glass or metal
container
 Help in achieving pulpal anesthesia of a single tooth
108
Plastic disposable syringe
 Plastic disposable syringes are available in a variety
of sizes and with an assortment of needle gauges.
They are most often employed for intramuscular or
intravenous drugs administration but also useful for
intra oral injections.
109
110
 These syringes contain luer – lock screw on
needle attachment but no aspirating tip. These
syringes do not accept the dental cartridges.
 The needle, attached to the syringe must be
inserted into a vial or cartridge of local
anesthetic drug and an appropriate volume of
solution removed.
Safety syringes
 These type of syringes posess “locks” which
prevent the operator from accidental needle pricks
 All safety syringes are meant for single use
111
In 1997 the first computer
controlled injection system
was introduced into dentistry
Hochman and associates were
the first to demonstrate the
ability of this delivery system
Fukayama and associates in a
controlled study reported less
or no pain on palatal injection
The wand
112
The needle
 The needle directs the local anesthetic solution
from the dental cartridge into the tissues
surrounding the needle tip.
TYPES OF NEEDLES
•Reusable/Autoclavable
•Disposable
•Winged
113
114
Part of the needle
Bevel
Shank
Hub
1 Bevel  Defines the point or tip of the needle
2 Shank  Or shaft of the needle consists of the
diameter of the needle lumen and the length of the
shank from it points to the hub.
3 Hub  It is a plastic or metal piece through which
the needle is attacked to the syringe.
115
Length
 Needles are available in two lengths
 Long-32 mm
 Short-20mm
Care and handling
 Needles must never be reused
 Needles should be changed after several penetrations
 Needles should be covered with protective sheath
 It should be properly disposed
116
117
118
CARTRIDGE
 The dental cartridge is a glass cylinder that contains,
among other ingredients, the local anesthetic drug.
 The dental cartridge is commonly referred to as
“CARPULE”.
119
 Components
Cylindrical glass tub
Rubber stopper
Aluminium cap
Rubber diaphragms
 Rubber stopper:- Is located at the end of the cartridge
that receives the harpoon of the syringe. The harpoon is
imbedded in the plunger by gentle finger pressure on the
thumping of the syringe. The rubber plunger occupies
little more than 0.2 ml of the volume of the entire
cartridge.
120
 Aluminium Cap :- Is located on the opposite end of
the cartridge from the rubber plunger. It fits tightly
around the neck of the glass cartridge, holding the
thin rubber diaphragm in position.
 Rubber diaphragm:- Is a permeable membrane
through which the cartridge end of the needle
penetrates. When properly prepared, the hole made
by the needle is centrically located and hound,
forming a tight seal around the needle.
121
Care While Handling Cartridges
 Some local anesthetic cartridges come vacuum sealed in a tin
container of fifty cartridges. The glass dental cartridge should
not be autoclaved.
 The seals on the cartridge cannot withstand the extreme
temperatures of autoclaving, and the heat labile
vasoconstrictors will be destroyed in the process.
 The cartridges are moistened with (not immersed) wither 91%
is isopropyl or 70% ethyl alcohol. There must be no alcohol
present around the cartridge.
122
Seminar / table clinic
TECHNIQUES OF MAXILLARY
ANESTHESIA
 Dr. Sangam Mittal
 Dr. Niti Shah
Techniques
Three major types of local anesthetic injection can be
differentiated
 Local infiltration
 Field block
 Nerve block
Local Infiltration
 Small terminal nerve endings in the area of dental
treatment are flooded with local anesthetic
solution
Field block
 Local anesthetic solution is deposited near the
larger terminal nerve branches so the
anesthetised area will be circumscribed,
preventing the passage of impulses from the
tooth to the C.N.S.
 Incision (or treatment) is made into an area
away from the site of injection of the anesthetic
eg. maxillary injections administered above the
apex of the tooth
Nerve block
 Local anesthetic is deposited close to a main
nerve trunk, usually at a distance from the site
of operative intervention
 Post sup alv., inf. Alv. and nasopalatine
MAXILLARY INJECTION TECHNIQUES
Supra periosteal injection
 Nerves anaesthetized – large terminal branches
 Anaesthetize buccal soft tissue & hard tissue
Indication :
1 or 2 teeth need to be anaesthetized / small
area
Contra-indication :
Dense bone covering
 Target area :
 Behind apices of tooth
 Landmarks :
 Muco-buccal fold
 Crown & root length
Signs & symptoms
 Subjective : Feeling of numbness in the area of
administration
 Objective: Use of EPT with no response from
tooth
 Absence of pain during treatment
Failures of anesthesia
 Needle tiip lies below the apex
 Needle tip lies too far from the bone
Posterior superior alveolar
 Area anaesthetized:
 Maxillary 3rd, 2nd & 1st molar (except mesio-buccal root
of 1st molar
 Bone & periodontium over these
Indication:
Treatment of 2 or more molars required
Supra-periosteal injection – ineffective
Acute inflammation
Contra-indication:
Pt with bleeding disorders
Landmarks:
Mucobuccal fold
Zygomatic process of maxilla
Maxillary tuberosity
Signs & symptoms
 Subjective : usually none
 Objective: Use of EPT with no response from
tooth
 Absence of pain during treatment
Failures of anesthesia
 Needle too lateral
 Needle not high enough
 Needle too far posterior
Complications
Hematoma
Pterygoid plexus posteriorly
Visible – buccal aspect of mandibular
region
Accidental mandibular Anaesthesia
Middle superior alveolar
Signs & symptoms
 Subjective : usually lip numb
 Objective: Use of EPT with no response from
tooth
 Absence of pain during treatment
Failures of anesthesia
 Deposited high above the apex of the 2nd PM
 Too far from the max bone
Complications
Hematoma (rare)
Anterior superior alveolar
Areas anaesthetized
Pulp of maxillary CI through the canine
Buccal periodontium, bone
Lower eyelid, lateral aspect of nose , upper lip
Indications
More than 2 anterior teeth
Contraindications
Discreet treatment areas
Hemostasis of localized area – not
adequately achieved
Landmarks
Mucobuccal fold, infra-orbital notch, infra-
orbital foramen
Locate infraorbital foramen
Signs & symptoms
 Subjective : Tingling and numbness
 Subjective & Objective: numbness in the teeth &
soft tissues along the distribution of ASA & MSA
nerves
 Objective: Use of EPT with no response from tooth
 Absence of pain during treatment
Failures of anesthesia
 Needle contacting bone below the infraorbital
foramen
 Needle deviation medial or lateral to the
infraorbital foramen
Complications
Hematoma (rare)
Greater palatine
Areas anaesthetized
Palatal soft tissue – posterior aspect
Palatal hard tissue
Indication
Surgical procedures posterior portion of hard
palate
Palatal Anaesthesia in conjunction with
posterior superior alveolar nerve block.
Landmarks
Greater palatine
foramen
Junction of the
maxillary alveolar
process & palatine
bone
Signs & symptoms
 Subjective : Numbness in posterior portion of the
palate
 Objective: Absence of pain during treatment
Failures of anesthesia
 Deposited too far anterior to the foramen
Nasopalatine
 Areas anaesthetized
 Anterior portion of Hard palate and over lying
structures back to the bicuspid area.
Indications
Anterior palatal procedures supplementing
infraorbital nerve blocks
Landmarks
Central incisor & incisive papilla
Signs & symptoms
 Subjective : Numbness in anterior portion of the
palate
 Objective: Absence of pain during treatment
Failures of anesthesia
 Unilateral anesthesia
 Inadequate palatal soft tissue anesthesia in the
area of the maxillary canine and first premolar.
Complications
Hematoma
Necrosis
Anteroir middle superior alveolar
nerve block
Signs & symptoms
 Subjective : Numbness on the palatal tisses
 Subjective: Numbness of the teeth and asso soft
tissues
 Objective: Use of EPT
 Objective: Absence of pain during treatment
Failures of anesthesia
 May need supplemental anesthesia for central and
lateral incisors
Complications
Palatal ulcer
Unexpected contact with nasopalatine
nerve
Maxillary nerve block
High tuberosity approach
Greater palatine canal
approach
 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
 Contra-indications
 Pediatric patients
 Infection / inflammation
 Hemorrhage – anticipated
 Greater palatine canal approach not possible – bony
obstr.
Landmarks
Mucobuccal fold distal to maxillary 2nd
molar
Maxillary tuberosity
Zygomatic process
Complications
Hematoma
Penetration into orbit
Penetration into nasal cavity
 Maxillary nerve block – Extra Oral
 Areas anaesthetised
 Anterior temporal & zygomatic region
 Lower eyelid
 Side of nose
 Anterior cheek
 Upper lip
 Maxillary teeth / alveolar bone & overlying structures
– 1side
 Hard & soft palate
 Tonsils – parts of pharynx
 Nasal septum – floor of nose
 Indications
 Extensive surgery – 1 half of maxilla
 Others blocks not possible
 Therapeutic purposes
 Technique
 Mid point of zygomatic process
 Needle gently contact lateral pterygoid plate
 Maximum length of 4.5cms directed slightly upward & forward
 Note:
 In final position – internal maxillary artery – inferior to needle
 Temporal vessels on either sides
 Posteriorly foramen ovale with mandibular nerve & foramen
spinosum with middle meningeal artery
 Anteriorly pterygomaxillary fissure
Seminar / table clinic
MANDIBULAR INJECTION TECHNIQUE
Dr. Sangam Mittal
Dr. Niti Shah
Inferior alveolar nerve block
 Areas anaesthetised
 Mandibular teeth upto midline
 Body of mandible
 Inferior portion of ramus
 Buccal periosteum & mucous membrane
 Lingual soft tissue
 Anterior 2/3rd of tongue
 Indications
 Multiple mandibular teeth
 Buccal / Lingual soft tissue anaesthesia
 Contraindications
 Infection / acute inflammation
 Young children / mentally handicapped
 Landmarks
 Coronoid notch
 Pterygomandibular raphe
 Occlusal plane of posterior mandibular teeth
If Bone Is Contacted Too Soon
If Bone Is Not Contacted
Signs & symptoms
 Subjective : Tingling and numbness of the lower lip
 Subjective: Tingling and numbness of the tongue
 Objective: Use of EPT with no response from tooth
 Absence of pain during treatment
Complication
Hematoma
Trismus
Transient facial paralysis (parotid gland)
buccal nerve block
 Area anaesthetised –
 Buccal mucosa of mandibular molars
Signs & symptoms
 Subjective : usually none
 Objective: instrumentation in the area without
pain
Complication
Hematoma
Gow-gates technique
George Edwards Gow Gates - 1973
Area anesthetized
 All mandibular hard and soft tissue upto mid line
 Anterior 2/3rd of the tongue
Indications
 Multiple procedures on mandibular teeth,
 Buccal soft tissue anaesthesia from third molar to midline
 Conventional inferior alveolar nerve block is
unsuccessful
Contraindications
 Infection or acute inflammation in the area of infection
 Patients with restricted mouth opening
Signs & symptoms
 Subjective : Tingling and numbness of the lower lip
 Subjective: Tingling and numbness of the tongue
 Objective: Use of EPT with no response from tooth
 Absence of pain during treatment
Complication
Hematoma
Trismus
Transient facial paralysis (parotid gland)
Vazirani-Akinosi
Area anesthetized
 Mandibular teeth to the midline
 Body of mandible & inferior portion of ramus
 Mucous membrane ant to mental foramen
 Anterior 2/3rd of tongue & floor of the oral cavity
Signs & symptoms
 Subjective : Tingling and numbness of the lower lip
 Subjective: Tingling and numbness of the tongue
 Objective: Use of EPT with no response from tooth
 Absence of pain during treatment
Failure of anesthesia
 Almost always present because of falure to
apprecate the flarng nature of the ramus
 Needle insertion point too low
 Underinsertion or overinsertion of the needle
Complication
Hematoma
Trismus
Transient facial paralysis (parotid gland)
Mental nerve
Areas anaesthetised
 Lower lip, mucous membrane – anterior to mental
foramen
Landmarks
 Mandibular bicuspids
Locating the mental foramen
Signs & symptoms
 Subjective : Tingling and numbness of the lower
lip
 Objective: Absence of pain during treatment
Complication
Hematoma
Paresthesia of lip / chin
Incisive nerve block
Locating the mental foramen
Signs & symptoms
 Subjective : Tingling and numbness of the lower
lip
 Objective: Absence of pain during treatment
Complication
Hematoma
Paresthesia of lip / chin
SUPPLIMENTAL INJECTION TECHNIQUES
INTRALIGAMENTARY INJECTION
Indication for the PDL injection
 The need for anesthesia of one or two mandibular
teeth
 Treatment of isolated teeth
 Treatment of children
 Its use as a possible aid in the diagnosis
 Nerve block is contraindicated
 As an adjunctive technique after nerve block
anesthesia
CONTRA-INDICATION TO THE PDL
INJECTION
 Infection or severe inflammation at the injection
site.
 Primary teeth, when permanent tooth bud is
present is present
Advantages
 Prevents anesthesia of lip, tongue, and other
soft tissue
 Minimum dose of local anesthetic necessary
 An alternative to partially successful regional
nerve block
 Rapid onset
 Less traumatic
Disadvantages
 Proper needle placement is difficult to achieve
 Leakage of local anesthetic solution
 Excessive pressure or overly rapid injection
 A special syringe may be necessary
 Excessive pressure can produce focal tissue damage
 Post injection discomfort may persist
 The potential for extrusion of a tooth exists
Signs & symptoms
Subjective : No adequate sign is present
A. ischemia of soft tissue at the injection site.
B. resistance to injection of solution
 Objective: use of EPT with no response
Failure of anesthesia
Infected or inflammed tissues
Solution not retained
INTRASEPTAL INJECTION
Indication
When both pain control and
haemostasis are desired for soft tissue
and osseous periodontal treatment
Contraindication
Infection or severe inflammation at
the injection site
Signs and symptoms
 No objective symptoms. The anesthetized area
is too circumscribed.
 There is absence of pain during the treatment.
 Subjective Resistance to the injection of solution
is felt.
Failure of Anesthesia
 Infected or inflammed tissue
 Solution not retained in the tissue
INTRAOSSEOUS INJECTION
 It has been in use since the start of twentieth
century.
 The technique traditionally was a two-step
procedure used to deliver anesthetic into the
cancellous bone near the apex of the targeted
tooth.
 Nerves Anesthetized :Terminal nerve endings at
the site of injection and in the adjacent soft and
hard tissue.
 Areas Anesthetized : Bone, soft tissue, and root
structure in the area of injection
 Indication : Pain control for dental treatment on
single or multiple teeth in a quadrant.
 Contraindication : Infection or severe
inflammation at the injection site.
Lateral perforation
1.At a point 2mm apical to the intersection of lines
drawn horizontally along the gingival margins of
the teeth and a vertical line through the
interdental papilla.
2.The site should be located distal to the tooth to be
treated, if possible
Vertical perforation
 Perforate at a point on the alveolar crest either
mesial or distal to the treatment area
Radiograph of potential intraosseous injection site in the
maxilla.
Signs and symptoms
Subjective : Ischemia of the soft tissues at the
injection site
Objective: Use of EPT
Failures of Anesthesia
Infected or inflammed tissues
Inability to perforate cortical bone
INTRAPULPAL INJECTION
 Nerves Anesthetized
Terminal nerve endings at the site of injection in the
pulp chamber and canals of the involved tooth.
 Areas Anesthetized
Tissues within the injected tooth
 Indication
When pain control is necessary for pulp
extirpation or other endodontic treatment in the
absence of adequate anesthesia from other
techniques
 Contraindication
None.
Signs and Symptoms
 Subjective: There are no subjective symptoms
that can ensure adequate anesthesia. The area is
too circumscribed.
 Objective The endodontically involved tooth
may be treated painlessly.
Failuresof Anesthesia
 Infected or inflamed tissues
 Solution not retained in tissue
Complication
Discomfort during the injection of anesthetic
Definition
An anaesthetic complication may be defined as any
deviation from the normal expected pattern during
or after securing regional anaesthesia
Local
Systemic
LOCAL COMPLICATIONS
Needle
breakage
Pain on
injection
Burning
on
injection
Persistent
anaesthesia or
paresthesia
Trismus
Hematoma
Sloughing of
the tissue / soft
tissue injury
Facial
nerve
paralysis
SYSTEMIC COMPLICATIONS
Toxicity
Idiosyncracy
Allergy
Anaphylactoid
reaction
Syncope
Classification
Primary / Secondary
Transient / Permanent
Mild / Severe
Attributed to solution/technique
Needle breakage
causes
 Unexpected movement
 Long needles
 Defective manufacture of needles
 Smaller gauge – more likely to break
Prevention
Correct gauge – 25 gauge
Long needles – prevent penetration till hub
Not to insert a needle into soft tissue to its
hub
Do not bend needles
Management
Patient – not to move
Fragment visible – remove it
Fragment not visible – inform patient
Radiograph suggested
Persistent anaesthesia / paresthesia
Causes
• Direct trauma to nerve
• LA solution containing neurotoxic substance –
alcohol
• Injection of wrong solution
• Hemorrhage / infection – near to nerve
Problem
 Persistent anaesthesia – usually rare
 Biting / thermal / chemical insult – without patient
awareness
 When lingual nerve is involved – taste impaired
Prevention
 Proper care & handling of dental cartridge
 Adherence to injection protocol
Management
 Usually resolve in 8 weeks
 Periodic recall & check up of patients
 Persistence – consult neurosurgeon
 Recall patient every 2 months for check up
Facial nerve paralysis
Cause
 LA solution into parotid gland – usually while giving
Inferior Alveolar Nerve 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
Management
Reassure the patient
Resolves after action of LA is over
Eye patches to the affected – eye drops
Contact lenses if any – removed
Trismus
“Difficulty in opening the jaws due to
muscle spasm”
Causes
 Trauma – muscle / blood vessel
 Irritating solution
 Hemorrhage
 Multiple needle punctures
 Excessive volume – distension of tissues
Prevention
 Use of sharp, sterile, disposable needle
 Aseptic technique
 Practice atraumatic methods
 Avoid repeated injections
 Use minimum volume
Management
Heat therapy
Analgesics
Initial physiotherapy
Antibiotic regime
Soft tissue injury
Causes
 Trauma occurs – frequently mentally / physically
challenged children
 Primary cause – significantly longer duration of action
Problem
Pain
Swelling
Prevention
Hematoma
 “Effusion of blood into extra-vascular spaces”
Causes
Arterial & venous puncture
Patients with bleeding disorders
Problem
Bruise – may / may not be visible extra-
orally
Complications – pain & trismus
Swelling & discoloration
Prevention
Knowledge of normal anatomy – proper
technique

Shorter needle – PSA
Minimize the number of penetration
Management
 Immediate – apply firm pressure
 Inf. Alveolar Nerve Block – medial aspect of ramus
 Infra orbital, Mental, Incisive block – directly over
foramen
 PSA – pressure on soft tissue with finger as posteriorly
as tolerated by patient
 Patient to be reviewed after 24 hours
Pain on injection
Causes
Careless injection technique
Multiple used needle
Rapid deposition
Prevention
 Proper technique
 Sharp needles
 Enter topical anaesthetics
 Inject slowly
 Check temperature of solution
Burning on injection
Causes
Problems
 pH  disappears upon LA action – no residual effect
 Contaminated solution , rapid injection, warm
solution
 Other complications – trismus, edema, paraesthesia
Prevention
 Slow injection – 1ml / minute
 Cartridge stored at room temperature
Infection
 Comparatively rare complication
 Instrument needle solution to be as aseptic as
possible
 Area & operative hands – cleaned
 Avoid passing needle through infected area
 Use disposable syringes
Edema
Causes
 Trauma during injection
 Infection, hemorrhage
 Allergy (Angioedema)
 Injection of irritating solution
Problems
 Pain & dysfunction
 Airway obstruction
Prevention
 Proper care & handling of armamentarium
 Atraumatic injection technique
 Complete medical evaluation prior to injection
Management
 Trauma – resolve in few days without therapy
 Hemorrhage – resolve slowly over 7-14 days
 Allergy – life threatening
 Total airway obstruction – Tracheostomy /
Cricothyroidectomy
Sloughing of tissue
Causes
 Epithelial desquamation
 Sterile abscess
Problems
 Pain & infection
Prevention
 Topical – for not more than 1-2 minutes
 Vaso - constrictors – minimal concentration in
solution
Management
Symptomatic – pain – analgesia
Epithelial desquamation – resolve few days
Sterile abscess resolve  7-10 days
Overdose reactions
Allergy
Idiosyncrasy
overdose
 Overdose reactions are those clinical signs and
symptoms that manifest as a result of an
absolute or relative over - administration of a
drug, which leads to elevated blood levels of
the drug in its target organs
Predisposing factors
 Age
 Weight
 Sex
 Diseases
 Congestive heart failure
 Genetics
 Mental Attitude
Drug factors
Vasoactivity
Concentration
Dose
Route of Administration
Rate of injection
Vascularity of injection site
Presence of Vasoconstrictor
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
Drug Formulaton MRD (mg/kg)
Articaine With epinephrine -- 7.0
Lidocaine Plain 300 4.4
With epinephrine 500 7.0
Mepivacaine Plain 400 5.7
With epinephrine 400 5.7
Prilocaine Plain 600 8.8
With epinephrine 600 8.8
Symptoms
Central Nervous System
0.5 – 4 µg / ml
> 4.5 µg / ml
> 7.5 µg / ml
Cardiovascular system
Less sensitive
1.8 µg / ml – 5 µg / ml
5 - 10 µg / ml
> 10 µg / ml
Treatment
Mild Overdose Reacton
Slow onset – 5-10 mins
Slower onset - >15 mins
P
A
B
C
D
Definitive Care
 Reassure the patient
 Administer oxygen
 Montor & record vital signs
 Establish IV infusion (optional)
 Permit the patient to recover
 Consider emergency medical assistance
Severe Overdose Reacton
Rapid Onset : within 1 min
P
A
B
C
D
Definitive Care
 Protect patient’s arms, legs & hand
 Loosen tight clothes
 Summon emergency medical assistance
 Continue basic life support
 Administer an anti-convulscant
Idiosyncrasy
 “It is an adverse response that is neither an overdose
nor an allergic reaction”
 Treatment – symptomatic ..remember ABC’s!
Syncope
 “Transient loss of consciousness that is caused due to
cerebral ischemia (neurogenic shock)”
Treatment
Discontinue procedure, supine position, deep
breathing, O2 administration if required, BLS
Allergy
 “Hypersensitive state acquired through exposure to
a particular allergen, re-exposure to which produces
a heightened capacity to react”
TYPE MECHANISM ANTIBODY
/ CELL
TIME OF
REACTION
CLINICAL EXAMPLES
I Anaphylactic IgE Sec to min Anaphylaxis
Asthma
Allergic rhinitis
Hay fever
II cytotoxic IgG
IgM
-- Transfusion rxns
Autoiimmune hemolysis
III Immune
complex
IgG 6-8 hrs Serum sickness
Lupus nephtitis
IV Cell mediated -- 48 hrs Allergic dermatitis
Infectious franulomas
Classification of allergic diseases
Allergic responses
 Dermatitis
 Bronchospasm
 Systemic anaphylaxis
 Localized dermatologic reactions
 Life threatening allergic responses
Sodium bisulfite allergy
 Antioxidant for vasoconstrictor
 Bronchospasm
 LA solution without a vasopresson should be
used
Prevention
Questionnaire
 Are you allergic or made sick by penicillin, aspirin,
codeine or any other medications?
 Have you ever had asthma, hay fever, sinus trouble?
 Describe exactly what happened?
 What treatment was given?
 What was the time consequence of events?
Prevention
Questionnaire
 Were the services of emergency medical
personnel necessary?
 What drug was used?
 What volume of the drug was administered?
 Did the local anesthetic contain a
vasoconstrictor?
 Details of the doctor?
Allergy testing
 No form : 100 % reliable
 Skin testng : primary mode
 Intracutaneous injections : most reliable
 0.1 ml test sol into patients forearm
Signs And Symptoms Of Allergy
Dermatological reactions
Urticaria
Angioedema
Respiratory reactions
Bronchospasm
Laryngeal edema
Generalised anaphylaxis
Delayed skin reactions
Non life threatening
Oral histamine blocker
Immediate skin reactions
Conjunctivitis, rhinitis, urticaria
50 mg diphenhydramine IM
Record vital sgns
Observe for 60 mins
Oral histamine for 3 days
Respiratory reaction
Terminate dental treatment
Patient in comfortable position.
Administer - oxygen 5-6 lts / mns
Administer epinephrine/bronchodilator
Observe for 60 min , advise anti histamines to
prevent relapse
Laryngeal edema
 Oxygen
 Broncho-dilator,
 Epinephrine 0.3mmd IM/SC,
 Anti histamines
 If condition not improving : cricothyrotomy
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Local Anesthesia Guide: Pain, Neurophysiology, Agents & Techniques

  • 1. 1
  • 2. 2
  • 3. contents  Terms  Pain  Neurophysiology & neuroanatomy  Local anesthesa  History  Classification  Composition  Mode of action  Metabolism  Local Anesthetic agents 3
  • 4. terms  Analgesia: refers to loss of pain sensation without loss of consciousness.  Regional analgesia: refers to loss of pain sensation over a portion of anatomy without loss of consciousness.  Regional anesthesia: refers to loss of all sensations i.e. pain as well as temperature, pressure and motor function without the loss of consciousness. 4
  • 5. terms  Local Anesthesia: Loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve ending or an inhibition of conduction process in peripheral nerve. Malamed  General Anesthesia: A reversible state of unconsciousness from where a person cannot be aroused by external stimulus. Anaesthesia & Analgesia in dentistry 5
  • 6. terms  Nerve block: this method consists of depositing LA solution within close proximity to a main trunk and thus preventing afferent impulses traveling beyond that point.  Field block: consisting of depositing LA solution in close proximity to a large terminal nerve branch so that area to be anaesthetized is walled off circumscribed to prevent central passage of afferent impulses.  Local infiltration: small terminal nerve branches in the area of surgery are flooded with LA solution rendering them insensible to pain or preventing them from becoming stimulated and creating an impulse. The incision made in the same region in which the solution has been deposited. 6
  • 7. terms  Intraligamentary technique: this technique is injected to provide single tooth anaesthesia and consists of forcing LA solution under pressure into periodontal membrane space of teeth.  Topical anaesthesia: it renders the free nerve endings in accessible structure (intact mucous membrane, abraded skin, cornea of eye) incapable of stimulation by the application of a suitable solution directly to the surface area. 7
  • 8. Pain  An unpleasant sensory & emotional experience associated with actual or potential tissue damage or described in terms of such damage INTERNATIONALASSOCIATION FOR THE STUDY OF PAIN  An unpleasant emotional experience usually initiated by noxious stimulus & transmitted over specialized neural network to CNS where it is interpreted as such MONHEIM 8
  • 9. 9
  • 10. Specificity theory (Von Fray) late 19th century  A pain centre was thought to exist within the brain, which was responsible for all overt manifestation of the unpleasant experience. 10
  • 11. Pattern theory (Goldscheider, 1894)  Central summation and stimulus intensity are the critical determinants of pain.  Pain results when the total output of cells exceeds the critical levels. 11
  • 12. Gate control theory (Melzack and Wall, 1965)  Briefly stated this theory postulates the following:  Information about the presence of injury is transmitted to the CNS by small peripheral nerves.  Cells in the spinal cord, which are excited by these injury signals, are also facilitated or inhibited by other large peripheral nerves  Descending control systems originating in the brain modulate the excitability of the cells 12
  • 13.  Therefore, the brain receives information about injury by way of gate control system, which is influenced by: Injury signals Other types of afferent impulses Descending control 13
  • 15. A-beta fiber afferents A-delta and C fiber afferents + - + + - - SG T cell Brain  Substantia gelatinosa [SG] (located in dorsal horn of spinal cord) acts as gatekeeper for transmission of pain impulses Fast Slow 15
  • 16. A-beta fiber afferents A-delta and C fiber afferents + - + + - - SG T cell Brain  Step 1: without any painful stimulation; the gate is closed – therefore no pain transmission 16
  • 17. A-beta fiber afferents A-delta and C fiber afferents + - + + - - SG T cell Brain  Step 2: with non-painful stimulation, large nerve fibers are primarily activated; both the SG and T cell are activated; activation of SG closes gate – no pain O F F 17
  • 18. A-beta fiber afferents A-delta and C fiber afferents + - + + - - SG T cell Brain  Step 3: with painful stimulation, A-delta & C fibers are primarily activated; the SG is inhibited and T cell are activated; inhibition of SG opens gate – pain transmitted to brain O N 18
  • 19. A-beta fiber afferents A-delta and C fiber afferents + - + + - - SG T cell Brain  Rubbing the skin stimulates large diameter nerves, exciting the SG, closing the gate.  Result: reduction of pain. O F F ON 19
  • 20. A-beta fiber afferents A-delta and C fiber afferents + - + + - - SG T cell Brain  There are multiple gates in the dorsal horn of the spinal cord.  Closing one gate reduces some pain transmission  Relatively impossible to close all gates 20
  • 21. Methods of pain control  Removing the cause  Blocking the pathway of painful impulses.  Raising the pain threshold  Preventing the pain reaction by cortical depression 21
  • 24. 24
  • 27. 27
  • 28.  Resting state  Slightly permeable to Na+  Freely permeable to K+ & Cl+  Depolarization  Slow depolarization  Firing threshold  Rapid depolarization  Repolarization Electrochemstry of Nerve Conduction 28
  • 29. 29
  • 31. 31
  • 33. 33
  • 34. Local anesthesia  Loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve ending or an inhibition of conduction process in peripheral nerve. -Malamed 6th Ed 34
  • 38.  Einhorn in 1905 History 38
  • 40. History  Mepivacaine  Bupivacaine  Prilocaine  Etidocaine  Ropivacaine 40
  • 43. Injectable a. Low potency, short duration Procaine Chloroprocaine b. Intermediate potency and duration Lidocaine Mepivacaine c. High potency, long duration Tetracaine Bupivacaine Surface anesthetic a. Soluble Cocaine Lidocaine Tetracaine b. Insoluble Benzocaine Butyl aminobenzoate 43
  • 44. According to duration of action  Ultra Short Acting: acting for < 30 mins e.g Procaine without vasoconstrictor  Short Acting: acting for 45 -75 mins e.g 4% prilocaine with 1: 200,000 epinephrine  Medium Acting: acting for 90 – 150 mins e.g. 2% lidocaine with 1: 100,000 epinephrine  Long acting: acting for 180 mins or longer e.g. 0.5% Bupivacaine with 1: 200,000 epinephrine 44
  • 45. Desirable Properties  Must be reversible  Should not be irritating to tissue  Should not cause any permanent alteration of nerve structure  Low systemic toxicity  Must be effective-injection/ topical  Onset as short as possible.  Long duration of action 45
  • 46. Composition of LA solution  Local anesthetic agent  Vasoconstrictor  Reducing agent  Preservative  Fungicide  The vehicle 46
  • 47. 1. Local Anesthetic Agent ○Lidocaine ○Mepivacaiine ○Prilocaine ○Etidocaine ○Bupivacane 47
  • 48. 2. Vasoconstrictor This is sometimes included to delay the removal of the anesthetic from the tissues by decreasing the blood flow through adjacent blood vessels 48
  • 49. Advantages  It 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 bloodless field of operation for surgical procedures. [DCNA2002] 49
  • 50. The choice of selection of vasoconstrictors depends on:  Length of dental procedures  Requirements for haemostasis  Medical status of a patient 50
  • 51. Vasoconstrictors In General Use  Adrenaline: a synthetic alkaloid almost identical with the natural secretion of the adrenal medulla.  Nor-adrenaline: a synthetic substance similar to the pressor amine secreted in the human body 51
  • 52.  Felypressin: is a synthetically produced polypeptide similar to that secreted from the human posterior pituitary gland.  Only available in a concentration of 0.03 IU/ml. Vasoconstrictors In General Use 52
  • 53.  Both depth and duration of anesthesia can be modified by the amount of vasoconstrictor in solution.  Lidocaine solution containing adrenaline / nor- adrenaline in concentrations of 1:50,000; 1: 80,000 or 1: 1,00,000 53
  • 54. Dilutions Of Vasoconstrictors  A conc. of 1:1000 means that there is 1 gm of solute in 1000ml of solution  Therefore 1:1000 ratio means 1000mg in 1000 ml or 1.0mg / ml of solution  To produce a 1:10000 solution a 1:1000 solution of 1ml is mixed with 9 ml of solvent  so 1:10000 is 0.1mg/ml  To produce a 1:100000 solution a 1ml solution of 1:10000 is diluted in 9 ml of solvent 54
  • 55. 3. Reducing agent  Vasoconstrictors are unstable in solution  This results in solution turning brown and must be discarded  Sodium metabisulphite  It is more readily oxidized 55
  • 56. 4. PRESERVATIVE Small amount of preservative Methylparaben have been shown to produce allergic reactions in sensitized subjects 5. Fungicide In the past some solutions tended to become cloudy due to the proliferation of minute fungae In several modern solutions a small quantity of thymol is added to serve as a fungicide. 56
  • 57. 6. The vehicle  The anesthetic agent and the additives referred to above are dissolved in modified ringer’s solution  This isotonic vehicle minimizes discomfort during injection 57
  • 58. COMPOSITON OF NIRCAINE – ADR (Lignocaine 2%, adrenaline 1:2,00,000)  Lignocane hydrochlorde - 21.3 mg  Adrenalne bitartarate - .005 mg  Sodium chloride - 6.0 mg  Sodium metabisulphite - 0.5 mg  Methylparaben - 1.0 mg  Water for injection 58
  • 59. Mode & site of action Nerve membrane is the site of action of the local anesthetics.  Altering the basic resting potential of the nerve membrane  Altering the threshold potential  Decreasing the rate of depolarization  Prolonging the rate of repolarization 59
  • 60. Evolution Of Theories For Mode Of Action  Acetylcholine theory  Calcium displacement theory  Surface charge (repulsion) theory  Membrane expansion  Specific receptor theory 60
  • 64.  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 ammonium- scorpion venom Benzocaine Clinically useful agents –Lignocaine etc According to biological site and mode of action - MALAMED 64
  • 65. 65
  • 66. How local anesthetic works? 66
  • 67. RNH+ displaces calcium ions for the sodium channel receptor site. ↓ which causes Binding of the local anesthetic molecules to this receptor site ↓ which produce Blockade of sodium channel ↓ and Decrease in sodium conduction ↓ which leads to Depression of the rate of electrical depolarization ↓ and Failure to achieve the threshold potential level  Lack of development of propagated action potentials ↓ called Conduction blockade 67
  • 68. Effect of pH  Acidic environment (low pH) RNH+ > RN + H+  Basic environment (higher pH) RNH+ < RN + H+ 68
  • 69. 69
  • 70. BLOOD LEVELS OF LOCALANESTHETICS ARE INFLUENCED BY THE FOLLOWING FACTORS Rate at which the drug is absorbed into the cardiovascular system Rate of distribution of the agent from the vascular compartment to the tissues  Elimination of the drug through metabolism / excretory pathways. 70
  • 71. METABOLISM / BIOTRANSFORMATION  A significant difference between the two major types of local anesthetics, the esters and the amides, is the method by which they undergo metabolic breakdown. 71
  • 72. ESTERS:  They are hydrolyzed in the plasma by the enzyme pseudocholinesterase. AMIDES:  The primary site of biotransformation of amide agents is the liver. 72
  • 73. EXCRETION  Kidneys  Esters appear only in very small concentrations as parent compound in urine.  Amides are usually present in the urine as the parent compound in greater percentage than esters, primarily because they have a complex biotransformation. 73
  • 74.  Classification: Ester  Prepared by: Alfred Einhorn (1904-1905)  Potency: 1  Toxicity: 1  Metabolism: Hydrolyzed rapidly in plasma, by plasma pseudocholinesterase.  Excretion: 2% unchanged in urine 90% as para amino benzoic acid 8% as diethylaminoethanol 74 A. Procaine
  • 75.  Vasodilatation property: produces the greatest vasodilatation of all currently employed local anesthetics.  pKa : 9.1  Onset of action: 6-10 min’s  Effective dental concentration: 2% - 4%  Topical action: not in clinically acceptable concentrations.  Actions: It was the 1st injectable local anesthetic to be synthesized 75
  • 76. Propoxycaine  Classification: Ester  Prepared by: Clinton and Laskowski, 1952  Potency: 7-8  Toxicity: 7-8  Metabolism: Hydrolysed both in plasma and liver  Excretion: Kidneys (almost entirely hydrolyzed)  Vasodilatation property: Present  pKa : Not available  Onset of action: Rapid (2-3 min’s)  Effective dental concentration: 0.4 %  Topical action: Not in clinically acceptable concentrations 76
  • 77. Chloroprocaine  Classification: Ester  Potency: 2  Toxicity: ½ of procaine  Metabolism: by rapid hydrolysis in serum  Excretion: Kidneys  Vasodilatation property: < procaine  pKa : 8.7  Onset of action: Moderate (6-12 min’s)  Effective dental concentration: 2%  Anesthetic ½ life: sec’s to min’s (extremely rapid)  Topical action: not in clinically acceptable concentrations. 77
  • 78. AMIDES A. Lidocaine  Classification: Amide  Prepared by: Nils Lofgren, 1943  Introduced in: 1948  Potency: 2 (compared to procaine). Today Lidocaine is used as standard of comparison. 78
  • 79. 79
  • 80.  Toxicity: 2 (compared to procaine)  Metabolism: Liver (Lidocaine Monoethylglycerine + Xylidide). Xylidide is a local anesthetic and is toxic.  Excretion: Kidneys. < 10% unchanged, 80% metabolites.  Vasodilatation property: < Procaine but > Prilocaine  pKa : 7.9  Onset of action: Rapid (2-3 min’s) 80
  • 81.  Effective dental concentration: 2%  Anesthetic ½ life: 90 min’s  Topical anesthetic action: Present  Action: (2% lidocaine + 1: 1,00,000 epinephrine) 60 min’s pulpal anesthesia.  3-5 hrs. - Soft tissue anesthesia  Less bleeding in the area of injection  Epinephrine conc. : 0.01 mg / ml or 0.018 mg. / cartridge 81
  • 82. B. Mepivacaine  Classification: Amide  Prepared by: A.F. Ekenstam, 1957  Introduced in: 1960, 2% with vasoconstrictor 1961, 3% without vasoconstrictor.  Potency: 2  Toxicity: 1.5 – 2  Metabolism: Liver  Excretion: Kidneys 1% -16% unchanged form  Vasodilatation property: Slight  pKa : 7.6  Onset of action: Rapid (1 ½ - 2 min’s) 82
  • 83. 83
  • 84.  Effective dental conc. : 3% without vasoconstrictor  2% with vasoconstrictor  Anesthetic ½ life: approx 90 min’s  Topical anesthetic action: Not in clinically acceptable concentrations.  Action: Mepivacaine plain is most often administered in pediatric dentistry and is very appropriate in management of geriatric patients. 84
  • 85. Bupivacaine  Classification: Amide  Prepared by: A.F. Ekenstam, 1957  Potency: 4 (compared to lidocaine)  Toxicity: < 4 times that of lidocaine  Metabolism: Liver  Excretion: Kidneys (16% unchanged)  Vasodilatation property: > lidocaine, < procaine 85
  • 86.  pKa : 8.1  Onset of action: similar to that of lidocaine but occasionally requires longer time (6-10 min’s)  Effective dental conc: 0.5%  Anesthetic ½ life: 76 min’s  Topical action: Not in clinically acceptable concentrations Action:  Lengthy dental procedures (pulpal anesthesia > 90 min’s)  Procedures in which post operative discomfort is anticipated. Example: - Endodontic surgeries [JOE,2005,AL READER] 86
  • 87. 87
  • 88. ARTICAINE  Classification : amide  Prepared by: A. Rusching  Potency:1.5 times that of lignocaine  Toxicity :similar to that of lignocaine  Metabolism :articaine is the only amide type local anesthetic that causes metabolism in both liver and plasma  Excretion: via kidneys, 5-10% unchanged, app 90% metabolites  Vasodilating properties similar to that of lignocaine 88
  • 89.  pka-7.8  ph of vaso constrictor containing substance-4.4-5.2  Onset of action: 1-2 mins  Effective dental concentration -4%  Originally known as carticaine and is available in 2 formulations of 4%.  It has been claimed that articaine can better diffuse through hard and soft tissues than other anesthetics 89
  • 90. 90
  • 92.  Lidocaine: (available in 2 forms) Lidocaine base Water-soluble preparation  Benzocaine: Poorly soluble in water Poor absorption Systemic toxic reactions unknown Prolonged duration of action Not suitable for injection Reported to inhibit antibacterial action of sulfonamides 92
  • 93. EMLA-EUTECTIC MIXTURE OF LOCAL ANESTHETICS  Recently introduced topical anesthetic agent.  Medical use to achieve anesthesia of skin.  Posses a local anesthetic effect on the oral mucosa also.  Contents:  Lidocaine 25 mg /ml  Prilocaine 25mg. /ml 93
  • 94. Tetracaine Hydrochloride Highly water soluble Applied topically, 5-8 times more potent than cocaine Slow onset of action (topically) Duration of action: approximately 45 min’s Metabolized in Liver and plasma Injectable: 0.15 % concentration Topically: 2% concentration. Rapidly absorbed through mucous membrane Greater potential for toxicity. 94
  • 96. syringes The syringe is a vehicle by which the local anesthetic is delivered 96
  • 97. 97  -Non disposable  Breech loading, metallic, catridge type, aspirating  Breech loading, plastic, catridge type, aspirating  Breech loading, metallic, catridge type, self aspirating  Pressure syringe  Jet injector  -Disposable  -Safety  -Computer controlled TYPES
  • 98. Breech loading, metallic, catridge type, aspirating 98
  • 99.  It is a metallic syringe where the needle is attached to the barrel of the syringe at the needle adaptor.  The end of the needle then penetrates the barrel of syringe and pierces the rubber diaphragm on the cartridge of anesthetic sol.  The screw hub is removable and sometimes inadvertently discarded with needle when the needle is removed and discarded. 99
  • 100. 100
  • 101. Breech loading, plastic, catridge type, aspirating 101
  • 102. Breech – loading, metallic, self aspirating cartridge 102 The self aspirating syringes obtain the required negative pressure for aspiration by means of elasticity of the rubber diaphragm of the syringe which directs the needle into the cartridge
  • 103. 103  Pressure acting directly on the cartridge through the thumb disk or indirectly through the plunger shaft stretches the rubber diaphragm.  When that pressure is released, sufficient negative pressure is produced with in the cartridge to achieve aspiration.  The use of self aspirating dental syringe permits easy, multiple aspirations throughout the period of local anesthetic deposition.
  • 104. 104
  • 105. 105
  • 106. JET INJECTOR  It was introduced by Figge & Scherer in 1947.  Jet injections is based on the principle that liquids forced through very small openings, called jets, at very high pressure can penetrate skin or mucous membrane 106
  • 108. Pressure syringe  These syringes introduced in the late 1970 was primarily used for periodontal injections  All pressure syringes encase in a glass or metal container  Help in achieving pulpal anesthesia of a single tooth 108
  • 109. Plastic disposable syringe  Plastic disposable syringes are available in a variety of sizes and with an assortment of needle gauges. They are most often employed for intramuscular or intravenous drugs administration but also useful for intra oral injections. 109
  • 110. 110  These syringes contain luer – lock screw on needle attachment but no aspirating tip. These syringes do not accept the dental cartridges.  The needle, attached to the syringe must be inserted into a vial or cartridge of local anesthetic drug and an appropriate volume of solution removed.
  • 111. Safety syringes  These type of syringes posess “locks” which prevent the operator from accidental needle pricks  All safety syringes are meant for single use 111
  • 112. In 1997 the first computer controlled injection system was introduced into dentistry Hochman and associates were the first to demonstrate the ability of this delivery system Fukayama and associates in a controlled study reported less or no pain on palatal injection The wand 112
  • 113. The needle  The needle directs the local anesthetic solution from the dental cartridge into the tissues surrounding the needle tip. TYPES OF NEEDLES •Reusable/Autoclavable •Disposable •Winged 113
  • 114. 114
  • 115. Part of the needle Bevel Shank Hub 1 Bevel  Defines the point or tip of the needle 2 Shank  Or shaft of the needle consists of the diameter of the needle lumen and the length of the shank from it points to the hub. 3 Hub  It is a plastic or metal piece through which the needle is attacked to the syringe. 115
  • 116. Length  Needles are available in two lengths  Long-32 mm  Short-20mm Care and handling  Needles must never be reused  Needles should be changed after several penetrations  Needles should be covered with protective sheath  It should be properly disposed 116
  • 117. 117
  • 118. 118
  • 119. CARTRIDGE  The dental cartridge is a glass cylinder that contains, among other ingredients, the local anesthetic drug.  The dental cartridge is commonly referred to as “CARPULE”. 119
  • 120.  Components Cylindrical glass tub Rubber stopper Aluminium cap Rubber diaphragms  Rubber stopper:- Is located at the end of the cartridge that receives the harpoon of the syringe. The harpoon is imbedded in the plunger by gentle finger pressure on the thumping of the syringe. The rubber plunger occupies little more than 0.2 ml of the volume of the entire cartridge. 120
  • 121.  Aluminium Cap :- Is located on the opposite end of the cartridge from the rubber plunger. It fits tightly around the neck of the glass cartridge, holding the thin rubber diaphragm in position.  Rubber diaphragm:- Is a permeable membrane through which the cartridge end of the needle penetrates. When properly prepared, the hole made by the needle is centrically located and hound, forming a tight seal around the needle. 121
  • 122. Care While Handling Cartridges  Some local anesthetic cartridges come vacuum sealed in a tin container of fifty cartridges. The glass dental cartridge should not be autoclaved.  The seals on the cartridge cannot withstand the extreme temperatures of autoclaving, and the heat labile vasoconstrictors will be destroyed in the process.  The cartridges are moistened with (not immersed) wither 91% is isopropyl or 70% ethyl alcohol. There must be no alcohol present around the cartridge. 122
  • 123.
  • 124. Seminar / table clinic TECHNIQUES OF MAXILLARY ANESTHESIA  Dr. Sangam Mittal  Dr. Niti Shah
  • 125. Techniques Three major types of local anesthetic injection can be differentiated  Local infiltration  Field block  Nerve block
  • 126. Local Infiltration  Small terminal nerve endings in the area of dental treatment are flooded with local anesthetic solution
  • 127.
  • 128. Field block  Local anesthetic solution is deposited near the larger terminal nerve branches so the anesthetised area will be circumscribed, preventing the passage of impulses from the tooth to the C.N.S.  Incision (or treatment) is made into an area away from the site of injection of the anesthetic eg. maxillary injections administered above the apex of the tooth
  • 129.
  • 130. Nerve block  Local anesthetic is deposited close to a main nerve trunk, usually at a distance from the site of operative intervention  Post sup alv., inf. Alv. and nasopalatine
  • 131.
  • 133.
  • 134. Supra periosteal injection  Nerves anaesthetized – large terminal branches  Anaesthetize buccal soft tissue & hard tissue
  • 135. Indication : 1 or 2 teeth need to be anaesthetized / small area Contra-indication : Dense bone covering
  • 136.  Target area :  Behind apices of tooth  Landmarks :  Muco-buccal fold  Crown & root length
  • 137. Signs & symptoms  Subjective : Feeling of numbness in the area of administration  Objective: Use of EPT with no response from tooth  Absence of pain during treatment
  • 138. Failures of anesthesia  Needle tiip lies below the apex  Needle tip lies too far from the bone
  • 139.
  • 141.  Area anaesthetized:  Maxillary 3rd, 2nd & 1st molar (except mesio-buccal root of 1st molar  Bone & periodontium over these
  • 142. Indication: Treatment of 2 or more molars required Supra-periosteal injection – ineffective Acute inflammation Contra-indication: Pt with bleeding disorders
  • 143. Landmarks: Mucobuccal fold Zygomatic process of maxilla Maxillary tuberosity
  • 144.
  • 145.
  • 146. Signs & symptoms  Subjective : usually none  Objective: Use of EPT with no response from tooth  Absence of pain during treatment
  • 147. Failures of anesthesia  Needle too lateral  Needle not high enough  Needle too far posterior
  • 148. Complications Hematoma Pterygoid plexus posteriorly Visible – buccal aspect of mandibular region Accidental mandibular Anaesthesia
  • 150.
  • 151.
  • 152.
  • 153.
  • 154. Signs & symptoms  Subjective : usually lip numb  Objective: Use of EPT with no response from tooth  Absence of pain during treatment
  • 155. Failures of anesthesia  Deposited high above the apex of the 2nd PM  Too far from the max bone
  • 158. Areas anaesthetized Pulp of maxillary CI through the canine Buccal periodontium, bone Lower eyelid, lateral aspect of nose , upper lip
  • 159. Indications More than 2 anterior teeth Contraindications Discreet treatment areas Hemostasis of localized area – not adequately achieved
  • 160. Landmarks Mucobuccal fold, infra-orbital notch, infra- orbital foramen
  • 161.
  • 163.
  • 164. Signs & symptoms  Subjective : Tingling and numbness  Subjective & Objective: numbness in the teeth & soft tissues along the distribution of ASA & MSA nerves  Objective: Use of EPT with no response from tooth  Absence of pain during treatment
  • 165. Failures of anesthesia  Needle contacting bone below the infraorbital foramen  Needle deviation medial or lateral to the infraorbital foramen
  • 168. Areas anaesthetized Palatal soft tissue – posterior aspect Palatal hard tissue
  • 169. Indication Surgical procedures posterior portion of hard palate Palatal Anaesthesia in conjunction with posterior superior alveolar nerve block.
  • 170. Landmarks Greater palatine foramen Junction of the maxillary alveolar process & palatine bone
  • 171.
  • 172.
  • 173.
  • 174.
  • 175. Signs & symptoms  Subjective : Numbness in posterior portion of the palate  Objective: Absence of pain during treatment
  • 176. Failures of anesthesia  Deposited too far anterior to the foramen
  • 178.  Areas anaesthetized  Anterior portion of Hard palate and over lying structures back to the bicuspid area.
  • 179. Indications Anterior palatal procedures supplementing infraorbital nerve blocks Landmarks Central incisor & incisive papilla
  • 180.
  • 181.
  • 182.
  • 183.
  • 184.
  • 185. Signs & symptoms  Subjective : Numbness in anterior portion of the palate  Objective: Absence of pain during treatment
  • 186. Failures of anesthesia  Unilateral anesthesia  Inadequate palatal soft tissue anesthesia in the area of the maxillary canine and first premolar.
  • 188. Anteroir middle superior alveolar nerve block
  • 189.
  • 190.
  • 191. Signs & symptoms  Subjective : Numbness on the palatal tisses  Subjective: Numbness of the teeth and asso soft tissues  Objective: Use of EPT  Objective: Absence of pain during treatment
  • 192. Failures of anesthesia  May need supplemental anesthesia for central and lateral incisors
  • 194. Maxillary nerve block High tuberosity approach Greater palatine canal approach
  • 195.  Areas anaesthetized  Pulpal Anaesthesia  Maxillary teeth – 1 side  Periodontium / soft tissue – 1 side
  • 196.  Indications  Extensive oral / periodontal / endodontal procedures  Other regional nerve blocks not possible  Therapeutic procedure to diagnose neuralgias  Contra-indications  Pediatric patients  Infection / inflammation  Hemorrhage – anticipated  Greater palatine canal approach not possible – bony obstr.
  • 197. Landmarks Mucobuccal fold distal to maxillary 2nd molar Maxillary tuberosity Zygomatic process
  • 198.
  • 200.
  • 201.  Maxillary nerve block – Extra Oral  Areas anaesthetised  Anterior temporal & zygomatic region  Lower eyelid  Side of nose  Anterior cheek  Upper lip  Maxillary teeth / alveolar bone & overlying structures – 1side  Hard & soft palate  Tonsils – parts of pharynx  Nasal septum – floor of nose
  • 202.  Indications  Extensive surgery – 1 half of maxilla  Others blocks not possible  Therapeutic purposes  Technique  Mid point of zygomatic process  Needle gently contact lateral pterygoid plate  Maximum length of 4.5cms directed slightly upward & forward  Note:  In final position – internal maxillary artery – inferior to needle  Temporal vessels on either sides  Posteriorly foramen ovale with mandibular nerve & foramen spinosum with middle meningeal artery  Anteriorly pterygomaxillary fissure
  • 203.
  • 204. Seminar / table clinic MANDIBULAR INJECTION TECHNIQUE Dr. Sangam Mittal Dr. Niti Shah
  • 205.
  • 207.  Areas anaesthetised  Mandibular teeth upto midline  Body of mandible  Inferior portion of ramus  Buccal periosteum & mucous membrane  Lingual soft tissue  Anterior 2/3rd of tongue
  • 208.  Indications  Multiple mandibular teeth  Buccal / Lingual soft tissue anaesthesia  Contraindications  Infection / acute inflammation  Young children / mentally handicapped
  • 209.  Landmarks  Coronoid notch  Pterygomandibular raphe  Occlusal plane of posterior mandibular teeth
  • 210.
  • 211.
  • 212.
  • 213.
  • 214.
  • 215. If Bone Is Contacted Too Soon
  • 216. If Bone Is Not Contacted
  • 217. Signs & symptoms  Subjective : Tingling and numbness of the lower lip  Subjective: Tingling and numbness of the tongue  Objective: Use of EPT with no response from tooth  Absence of pain during treatment
  • 219. buccal nerve block  Area anaesthetised –  Buccal mucosa of mandibular molars
  • 220.
  • 221.
  • 222.
  • 223. Signs & symptoms  Subjective : usually none  Objective: instrumentation in the area without pain
  • 226. Area anesthetized  All mandibular hard and soft tissue upto mid line  Anterior 2/3rd of the tongue
  • 227. Indications  Multiple procedures on mandibular teeth,  Buccal soft tissue anaesthesia from third molar to midline  Conventional inferior alveolar nerve block is unsuccessful Contraindications  Infection or acute inflammation in the area of infection  Patients with restricted mouth opening
  • 228.
  • 229.
  • 230.
  • 231.
  • 232. Signs & symptoms  Subjective : Tingling and numbness of the lower lip  Subjective: Tingling and numbness of the tongue  Objective: Use of EPT with no response from tooth  Absence of pain during treatment
  • 235. Area anesthetized  Mandibular teeth to the midline  Body of mandible & inferior portion of ramus  Mucous membrane ant to mental foramen  Anterior 2/3rd of tongue & floor of the oral cavity
  • 236.
  • 237.
  • 238. Signs & symptoms  Subjective : Tingling and numbness of the lower lip  Subjective: Tingling and numbness of the tongue  Objective: Use of EPT with no response from tooth  Absence of pain during treatment
  • 239. Failure of anesthesia  Almost always present because of falure to apprecate the flarng nature of the ramus  Needle insertion point too low  Underinsertion or overinsertion of the needle
  • 242. Areas anaesthetised  Lower lip, mucous membrane – anterior to mental foramen
  • 244.
  • 246.
  • 247. Signs & symptoms  Subjective : Tingling and numbness of the lower lip  Objective: Absence of pain during treatment
  • 250.
  • 251.
  • 253.
  • 254. Signs & symptoms  Subjective : Tingling and numbness of the lower lip  Objective: Absence of pain during treatment
  • 258. Indication for the PDL injection  The need for anesthesia of one or two mandibular teeth  Treatment of isolated teeth  Treatment of children  Its use as a possible aid in the diagnosis  Nerve block is contraindicated  As an adjunctive technique after nerve block anesthesia
  • 259. CONTRA-INDICATION TO THE PDL INJECTION  Infection or severe inflammation at the injection site.  Primary teeth, when permanent tooth bud is present is present
  • 260. Advantages  Prevents anesthesia of lip, tongue, and other soft tissue  Minimum dose of local anesthetic necessary  An alternative to partially successful regional nerve block  Rapid onset  Less traumatic
  • 261. Disadvantages  Proper needle placement is difficult to achieve  Leakage of local anesthetic solution  Excessive pressure or overly rapid injection  A special syringe may be necessary  Excessive pressure can produce focal tissue damage  Post injection discomfort may persist  The potential for extrusion of a tooth exists
  • 262.
  • 263.
  • 264.
  • 265. Signs & symptoms Subjective : No adequate sign is present A. ischemia of soft tissue at the injection site. B. resistance to injection of solution  Objective: use of EPT with no response
  • 266. Failure of anesthesia Infected or inflammed tissues Solution not retained
  • 268. Indication When both pain control and haemostasis are desired for soft tissue and osseous periodontal treatment Contraindication Infection or severe inflammation at the injection site
  • 269.
  • 270.
  • 271. Signs and symptoms  No objective symptoms. The anesthetized area is too circumscribed.  There is absence of pain during the treatment.  Subjective Resistance to the injection of solution is felt.
  • 272. Failure of Anesthesia  Infected or inflammed tissue  Solution not retained in the tissue
  • 273. INTRAOSSEOUS INJECTION  It has been in use since the start of twentieth century.  The technique traditionally was a two-step procedure used to deliver anesthetic into the cancellous bone near the apex of the targeted tooth.
  • 274.  Nerves Anesthetized :Terminal nerve endings at the site of injection and in the adjacent soft and hard tissue.  Areas Anesthetized : Bone, soft tissue, and root structure in the area of injection
  • 275.  Indication : Pain control for dental treatment on single or multiple teeth in a quadrant.  Contraindication : Infection or severe inflammation at the injection site.
  • 276. Lateral perforation 1.At a point 2mm apical to the intersection of lines drawn horizontally along the gingival margins of the teeth and a vertical line through the interdental papilla. 2.The site should be located distal to the tooth to be treated, if possible
  • 277. Vertical perforation  Perforate at a point on the alveolar crest either mesial or distal to the treatment area
  • 278.
  • 279.
  • 280. Radiograph of potential intraosseous injection site in the maxilla.
  • 281. Signs and symptoms Subjective : Ischemia of the soft tissues at the injection site Objective: Use of EPT
  • 282. Failures of Anesthesia Infected or inflammed tissues Inability to perforate cortical bone
  • 283. INTRAPULPAL INJECTION  Nerves Anesthetized Terminal nerve endings at the site of injection in the pulp chamber and canals of the involved tooth.  Areas Anesthetized Tissues within the injected tooth
  • 284.  Indication When pain control is necessary for pulp extirpation or other endodontic treatment in the absence of adequate anesthesia from other techniques  Contraindication None.
  • 285.
  • 286. Signs and Symptoms  Subjective: There are no subjective symptoms that can ensure adequate anesthesia. The area is too circumscribed.  Objective The endodontically involved tooth may be treated painlessly.
  • 287. Failuresof Anesthesia  Infected or inflamed tissues  Solution not retained in tissue
  • 288. Complication Discomfort during the injection of anesthetic
  • 289.
  • 290.
  • 291.
  • 292. Definition An anaesthetic complication may be defined as any deviation from the normal expected pattern during or after securing regional anaesthesia Local Systemic
  • 293. LOCAL COMPLICATIONS Needle breakage Pain on injection Burning on injection Persistent anaesthesia or paresthesia Trismus Hematoma Sloughing of the tissue / soft tissue injury Facial nerve paralysis
  • 295. Classification Primary / Secondary Transient / Permanent Mild / Severe Attributed to solution/technique
  • 297. causes  Unexpected movement  Long needles  Defective manufacture of needles  Smaller gauge – more likely to break
  • 298. Prevention Correct gauge – 25 gauge Long needles – prevent penetration till hub Not to insert a needle into soft tissue to its hub Do not bend needles
  • 299. Management Patient – not to move Fragment visible – remove it Fragment not visible – inform patient Radiograph suggested
  • 300.
  • 301. Persistent anaesthesia / paresthesia Causes • Direct trauma to nerve • LA solution containing neurotoxic substance – alcohol • Injection of wrong solution • Hemorrhage / infection – near to nerve
  • 302. Problem  Persistent anaesthesia – usually rare  Biting / thermal / chemical insult – without patient awareness  When lingual nerve is involved – taste impaired
  • 303. Prevention  Proper care & handling of dental cartridge  Adherence to injection protocol
  • 304. Management  Usually resolve in 8 weeks  Periodic recall & check up of patients  Persistence – consult neurosurgeon  Recall patient every 2 months for check up
  • 306. Cause  LA solution into parotid gland – usually while giving Inferior Alveolar Nerve Block, Akinosis technique
  • 307. Problem  Ipsilateral loss of motor control – Buccinator muscle  Inability to raise the corner of mouth, close eye lid
  • 308.
  • 309. Prevention Needle tip to contact bone, redirection of needle to be done only after complete withdrawal
  • 310. Management Reassure the patient Resolves after action of LA is over Eye patches to the affected – eye drops Contact lenses if any – removed
  • 311. Trismus “Difficulty in opening the jaws due to muscle spasm”
  • 312. Causes  Trauma – muscle / blood vessel  Irritating solution  Hemorrhage  Multiple needle punctures  Excessive volume – distension of tissues
  • 313. Prevention  Use of sharp, sterile, disposable needle  Aseptic technique  Practice atraumatic methods  Avoid repeated injections  Use minimum volume
  • 315. Soft tissue injury Causes  Trauma occurs – frequently mentally / physically challenged children  Primary cause – significantly longer duration of action
  • 317.
  • 319. Hematoma  “Effusion of blood into extra-vascular spaces”
  • 320. Causes Arterial & venous puncture Patients with bleeding disorders
  • 321. Problem Bruise – may / may not be visible extra- orally Complications – pain & trismus Swelling & discoloration
  • 322. Prevention Knowledge of normal anatomy – proper technique  Shorter needle – PSA Minimize the number of penetration
  • 323. Management  Immediate – apply firm pressure  Inf. Alveolar Nerve Block – medial aspect of ramus  Infra orbital, Mental, Incisive block – directly over foramen  PSA – pressure on soft tissue with finger as posteriorly as tolerated by patient  Patient to be reviewed after 24 hours
  • 325. Causes Careless injection technique Multiple used needle Rapid deposition
  • 326. Prevention  Proper technique  Sharp needles  Enter topical anaesthetics  Inject slowly  Check temperature of solution
  • 328. Problems  pH  disappears upon LA action – no residual effect  Contaminated solution , rapid injection, warm solution  Other complications – trismus, edema, paraesthesia
  • 329. Prevention  Slow injection – 1ml / minute  Cartridge stored at room temperature
  • 330. Infection  Comparatively rare complication  Instrument needle solution to be as aseptic as possible  Area & operative hands – cleaned  Avoid passing needle through infected area  Use disposable syringes
  • 331. Edema Causes  Trauma during injection  Infection, hemorrhage  Allergy (Angioedema)  Injection of irritating solution
  • 332. Problems  Pain & dysfunction  Airway obstruction
  • 333. Prevention  Proper care & handling of armamentarium  Atraumatic injection technique  Complete medical evaluation prior to injection
  • 334. Management  Trauma – resolve in few days without therapy  Hemorrhage – resolve slowly over 7-14 days  Allergy – life threatening  Total airway obstruction – Tracheostomy / Cricothyroidectomy
  • 335. Sloughing of tissue Causes  Epithelial desquamation  Sterile abscess
  • 336.
  • 337. Problems  Pain & infection Prevention  Topical – for not more than 1-2 minutes  Vaso - constrictors – minimal concentration in solution
  • 338. Management Symptomatic – pain – analgesia Epithelial desquamation – resolve few days Sterile abscess resolve  7-10 days
  • 339.
  • 341. overdose  Overdose reactions are those clinical signs and symptoms that manifest as a result of an absolute or relative over - administration of a drug, which leads to elevated blood levels of the drug in its target organs
  • 342. Predisposing factors  Age  Weight  Sex  Diseases  Congestive heart failure  Genetics  Mental Attitude
  • 343. Drug factors Vasoactivity Concentration Dose Route of Administration Rate of injection Vascularity of injection site Presence of Vasoconstrictor
  • 344. 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 Drug Formulaton MRD (mg/kg) Articaine With epinephrine -- 7.0 Lidocaine Plain 300 4.4 With epinephrine 500 7.0 Mepivacaine Plain 400 5.7 With epinephrine 400 5.7 Prilocaine Plain 600 8.8 With epinephrine 600 8.8
  • 345. Symptoms Central Nervous System 0.5 – 4 µg / ml > 4.5 µg / ml > 7.5 µg / ml Cardiovascular system Less sensitive 1.8 µg / ml – 5 µg / ml 5 - 10 µg / ml > 10 µg / ml
  • 346. Treatment Mild Overdose Reacton Slow onset – 5-10 mins Slower onset - >15 mins P A B C D
  • 347. Definitive Care  Reassure the patient  Administer oxygen  Montor & record vital signs  Establish IV infusion (optional)  Permit the patient to recover  Consider emergency medical assistance
  • 348. Severe Overdose Reacton Rapid Onset : within 1 min P A B C D
  • 349. Definitive Care  Protect patient’s arms, legs & hand  Loosen tight clothes  Summon emergency medical assistance  Continue basic life support  Administer an anti-convulscant
  • 350. Idiosyncrasy  “It is an adverse response that is neither an overdose nor an allergic reaction”  Treatment – symptomatic ..remember ABC’s!
  • 351. Syncope  “Transient loss of consciousness that is caused due to cerebral ischemia (neurogenic shock)”
  • 352. Treatment Discontinue procedure, supine position, deep breathing, O2 administration if required, BLS
  • 353. Allergy  “Hypersensitive state acquired through exposure to a particular allergen, re-exposure to which produces a heightened capacity to react”
  • 354. TYPE MECHANISM ANTIBODY / CELL TIME OF REACTION CLINICAL EXAMPLES I Anaphylactic IgE Sec to min Anaphylaxis Asthma Allergic rhinitis Hay fever II cytotoxic IgG IgM -- Transfusion rxns Autoiimmune hemolysis III Immune complex IgG 6-8 hrs Serum sickness Lupus nephtitis IV Cell mediated -- 48 hrs Allergic dermatitis Infectious franulomas Classification of allergic diseases
  • 355. Allergic responses  Dermatitis  Bronchospasm  Systemic anaphylaxis  Localized dermatologic reactions  Life threatening allergic responses
  • 356. Sodium bisulfite allergy  Antioxidant for vasoconstrictor  Bronchospasm  LA solution without a vasopresson should be used
  • 357. Prevention Questionnaire  Are you allergic or made sick by penicillin, aspirin, codeine or any other medications?  Have you ever had asthma, hay fever, sinus trouble?  Describe exactly what happened?  What treatment was given?  What was the time consequence of events?
  • 358. Prevention Questionnaire  Were the services of emergency medical personnel necessary?  What drug was used?  What volume of the drug was administered?  Did the local anesthetic contain a vasoconstrictor?  Details of the doctor?
  • 359. Allergy testing  No form : 100 % reliable  Skin testng : primary mode  Intracutaneous injections : most reliable  0.1 ml test sol into patients forearm
  • 360. Signs And Symptoms Of Allergy Dermatological reactions Urticaria Angioedema Respiratory reactions Bronchospasm Laryngeal edema Generalised anaphylaxis
  • 361.
  • 362. Delayed skin reactions Non life threatening Oral histamine blocker
  • 363. Immediate skin reactions Conjunctivitis, rhinitis, urticaria 50 mg diphenhydramine IM Record vital sgns Observe for 60 mins Oral histamine for 3 days
  • 364. Respiratory reaction Terminate dental treatment Patient in comfortable position. Administer - oxygen 5-6 lts / mns Administer epinephrine/bronchodilator Observe for 60 min , advise anti histamines to prevent relapse
  • 365. Laryngeal edema  Oxygen  Broncho-dilator,  Epinephrine 0.3mmd IM/SC,  Anti histamines  If condition not improving : cricothyrotomy